tag:blogger.com,1999:blog-51603303395528329072024-03-06T12:02:46.214-08:00Case Reports in AnesthesiaBlog with interesting cases and/or problems related to anesthesia with discussion based on best evidence in the literature.Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.comBlogger79125tag:blogger.com,1999:blog-5160330339552832907.post-62950761401617389482024-02-23T06:57:00.000-08:002024-02-23T06:57:40.073-08:00DIEP flaps at our institution<p> I recently started a new position at a facility that performs a fair number of DIEP flaps after breast cancer surgery. The surgeries are very adamant that the anesthesia provider avoid all vasopressors and give at minimum 4 to 5 liters of fluid regardless, and also use additional repaid fluid infusion to treat and prevent hypotension. This approach is actually written down as instructions to the anesthesia providers on how to approach their patients. In my previous practice we did flap repairs but never received direct instructions from the surgeons involved with an algorithm to treat hemodynamic perturbations. Therefore, when I arrived here and received a "recipe" for the approach to treatment of hypotension, I was surprised.</p><p>The concept of "loading the patient with crystalloid" as indicated by our plastic surgeons derives from the idea in free flap physiology related to maintain low SVR in a relative sense with elevated cardiac output. It is clear that, when a patient is hypovolemic, the natural response in the healthy intact human is to see elevated levels of ANP and sympathetic nervouse system output resulting in vasoconstriction. Therefore, the fear of a patient having a large sympathetic response with significant vasoconstriction and low cardiac output prompts the concept of giving large amounts of fluids to avoid this. Unfortunately, this ignores the idea that in patients who are appropriately anesthetized, the baroreceptor response is blunted, and sympathetic response is severely mitigated. Patients under GA find themselves in a state of low SVR although cardiac output is often not increased as desired by the free flap surgeon. Unfortunately, large volume crystalloid may be harmful. In an elegant review on the endothelial and endothelial glycocalyx physiology by Millford et al. [11], one can see how infusing large volumes of crystalloid may or may not remain in the intravascular space depending on the intrinsic intra capillary pressure. As this pressure increases, any crystalloid infused will simply be "pressed" out of the intravascular space and into the interstitial space. Here, excess fluid will then interefere with tissue oxygenation and thus degrade perfusion of the free flap intended to protect. Furthermore, there is evidence that diluting albumin with large volume crystalloid intereferes with the endothelial glycocalyx integrity. In theory this will allow a greater flux of fluid across the endothelial lining of capillaries resulting in greater interstitial fluid accumulation. In research that highlights this physiology, it has been shown that when healthy volunteers are hemorrhaged 900 mL, an equal amount to 2 x 's this volume of balanced crystalloid can restore normovolemia. This is an example of unique microcirculation physiology, where the intracapillary pressure is decreased by hemorrhage, thus allowing infusing crystalloid to remain in the intravascular space. In comparison, when crystalloid in infused to induce hypervolemia, only 17% (+/-) 10% remains in the intravascular space, the rest being pushed (squeezed) into the interstitial space. If the endothelial glycocalyx is damaged, the amount of crystalloid OR colloid infused will now be pushed into the interstitial space at lower pressures in the capillaries. With severe endothelial glycocalyx degradation, both colloids and crystalloids will move out of the intravascular space into the interstitial space in equal volumes. The amount of fluid that is lost across the endothelial membrane is then largely a function of elevated pressure within the microvascular space AND intactness of the glycocalyx. There is evidence to suggest that large volume crystalloid infusion can disrupt or cause breakdown of the glycocalyx. Furthermore, albumin carries the phospholipid sphingosine 1 phosphate (S1P), which is essential in the maintenance of the endothelial glycocalyx structure. There is evidence that demonstrates that as the albumin concentration decreases thus interrupting S1P transport endothelial glycocalyx suffers significantly degradation. It has been demonstrated that in absence of albumin, 25 times less S1P is released from RBC's (its primary source). Furthermore, there is some evidence in animal models suggesting that albumin infusion can restore the glycocalyx. However, it is clear that albumin is not likely to be able to restore glycocalyx function directly, rather, it is the S1P that the albumin coaxes out of RBCs or the S1P in the albumin solution infused that mediates repair. On the other hand, FFP has clearly been demonstrated to be restorative to the glycocalyx structure via upregulation of endothelial glycocalyx component production.</p><p><br /></p><p> Thus, preserving endothelial glycocalyx structure is critical when caring patients undergoing DIEP flap (or any other free flap). This goal is put at risk when we are asked to rapidly administer high volume crystalloid solutions (and in particular when the crystalloid consists of NS). The damage done may be less when administering large amounts of crystalloid to patients who are hypotensive, at least while microvascular pressures remain low. However, there can be a reversal in the post operative period when baroreceptor function returns and microvascular pressures return to normal resulting in a relative hypervolemia in contradistinction to the relative HYPOvolemia produced by induction of anesthesia.</p><p>Above is a practical physiologic rationale for avoiding large volume crystalloid. However, I wanted to see if there was good clinical evidence from real world studies that support avoidance of large volume crystalloid infusions. Karamanos et al. [1] performed a retrospective review of 126 patients undergoing DIEP flap. One group had received 5.5 mL/kg/hr vs liberal fluid group who had received 10.2 mL/kg/hr. The group who received liberal fluids (more fluid) had more wound complications (76% vs 15%). Furthermore, the flap oximetry readings were lower in the liberal fluid group over the 24 hours following surgery (41% vs 56%). No difference in AKI between groups. It is interesting to note that the flap oximetry readings were lower in the liberal fluid regimen group. This is direct evidence of the extra fluid finding its way into the interstitial space thus harming tissue oxygen tissue levels. In another retrospective review on breast reconstruction surgery by Sjöberg, T et al. [2] a moderate fluid therapy group was compared to liberal fluid therapy. It should be noted that radiotherapy was more frequent in the group that received the moderate fluid making them at higher risk for post op complications with wound healing. Neverthless, despite this, the study found that intraop and post op complications were more frequent in the liberal fluid group. The moderate fluid therapy group included noriepi as part of the protocol to treat hypotension. Zhong T, et al. did a retrospective multivariate analysis and found that extremes of crystalloid infusions predicted post operative complications (p=0.03). This analysis carefully controlled for a multitude of different possible causes of post op complications.</p><p>On the other hand, if one follows the general theme outlined above, it is likely that low blood pressure may in some cases require intervention. Allowing lower MAP during a free flap has very likely negative impacts on flap perfusion which is highly sensitive to perfusion pressure given that local innervation is erradicated when the flap is removed from its native neurovascular bundle. On the other hand, free flap surgeons often consider all vasopressors to be contraindicated. This concept is not supported by general hemodyanamic physioglogy however. In particular, in patients whose stressed volume has been shifted to the unstressed vasculature after induction of and during maintenance of anesthesia, small doses of phenylephrine has been shown to increase cardiac output by shifting blood from the unstressed compartment (i.e. venous reservoir) into the stressed compartment. To state in other words, in normovolemic patients whose cardiac output is depressed due to decreased venous return, phenylephrine will predominantly increase blood pressure by increasing cardiac output via increased preload. This increase in cardiac output will improve perfusion pressure to organs who are flow dependent for perfusion of oxygen. It has been documented, that in normal physiology, venous vasculature has a larger number of alpha receptors than that located on arteries and arterioles. Obviously, improving venous return via alpha 1 agonism depends exquisitely on ensuring normovolemia in your patients. Nevertheless, basic clinical research suggests that in general anesthesiologists should use vasopressors as needed in this patient population based on a perusal of a number of studies. For example Motakef et al. [3] published a systematic review of literature where they found that there is a high level of evidence that fluid should be between 3.5 ml/kg/hr up to max of 6 mL/kg/hr. Vasopressor use do not harm outcomes and may improve flap flow (highest level of evidence). Chen et al. [4] performed a retrospective review on 187 patients and found that vasopressor use not associated with any negative consequences of any type. Eltorai et al. [5] also found this. In a retrospective review they showed that <span face="BlinkMacSystemFont, -apple-system, "Segoe UI", Roboto, Oxygen, Ubuntu, Cantarell, "Fira Sans", "Droid Sans", "Helvetica Neue", sans-serif" style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-size: 16px;">Ephedrine treatment for hypotension during DIEP flap cases is associated with decreased intraoperative flap complication rates compared with controls who did not receive vasopressors, whereas phenylephrine has no significant association.</span><span face="BlinkMacSystemFont, -apple-system, "Segoe UI", Roboto, Oxygen, Ubuntu, Cantarell, "Fira Sans", "Droid Sans", "Helvetica Neue", sans-serif" style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-size: 16px;"> In a </span>systematic review of studies done in head and neck free flaps the authors [6] looked at the effect of using vasopressors for BP control to determine if this increased risk of complications. The review included one prospective and nine retrospective studies. Authors concluded that administration of phenylephrine and/or ephedrine was not associated with any complications which included: free flap failures, pedicle thrombosis, or other flap complications. In a prospective observational study in 169 ENT free flap surgeries Monroe et al. concluded that vasopressor use does not increase the risk of pedicle loss or complications in this population [7]. In yet another review of 320 patients who received vasopressors (phenylephrine and ephedrine) during free flap surgery for head and neck Harris et al. [8] determined that the administration of vasopressors were not associated with any complications or increased failure rate of flaps. In a different surgical population a retrospective review of 110 jejunal flaps for pharyngeal tumors was completed. Chen et al. [9] were able to show that when phenylephrine and ephedrine were used there was no increase risk of complications or flap failures.</p><p><br /></p><p>Therefore, optimizing perfusion of free flaps shares the same physiological approach utilized everyday by anesthesiologists whose is to optimize perfusion of all organs. While it is true that due to denervation of the free flap perfusion pressure may not be automatically controlled by intrinsic bodily physiology, anesthesia providers can easily overcome this obstacle as they do in other scenarios (i.e perfusion of placenta in obstetric anesthesia). Evidence suggest strongly that maintaining normovolemia by judicious use of a balanced crystalloid solution with careful titration of vasopressors when needed is the best approach to free flap microsurgery anesthesia based on current evidence.</p><p><br /></p><p><br /></p><p><br /></p><p><span style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-family: Roboto, "Helvetica Neue", Arial, Tahoma; font-size: 17px;">1. Karamanos E, Walker R, Wang HT, Shah AR. Perioperative Fluid Resuscitation in Free Flap Breast Reconstruction: When Is Enough Enough? Plast Reconstr Surg Glob Open. 2020 Mar 28;8(3)</span></p><p><span style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-family: Roboto, "Helvetica Neue", Arial, Tahoma; font-size: 17px;"><br /></span></p><p><span style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-family: Roboto, "Helvetica Neue", Arial, Tahoma; font-size: 17px;">2. </span>Sjöberg, Thomas MD*,†; Numan, Anmar MD†,‡; de Weerd, Louis MD, PhD*,†. Liberal versus Modified Intraoperative Fluid Management in Abdominal-flap Breast Reconstructions. A Clinical Study. Plastic and Reconstructive Surgery - Global Open 9(9):p e3830, September 2021. | DOI: 10.1097/GOX.0000000000003830</p><p><br /></p><p>3. <span face="BlinkMacSystemFont, -apple-system, "Segoe UI", Roboto, Oxygen, Ubuntu, Cantarell, "Fira Sans", "Droid Sans", "Helvetica Neue", sans-serif" style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-size: 16px;">Motakef S, Mountziaris PM, Ismail IK, Agag RL, Patel A. Emerging paradigms in perioperative management for microsurgical free tissue transfer: review of the literature and evidence-based guidelines. Plast Reconstr Surg. 2015 Jan;135(1):290-299. doi: 10.1097/PRS.0000000000000839. PMID: 25539313.</span></p><p><span face="BlinkMacSystemFont, -apple-system, "Segoe UI", Roboto, Oxygen, Ubuntu, Cantarell, "Fira Sans", "Droid Sans", "Helvetica Neue", sans-serif" style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-size: 16px;"><br /></span></p><p><span face="BlinkMacSystemFont, -apple-system, "Segoe UI", Roboto, Oxygen, Ubuntu, Cantarell, "Fira Sans", "Droid Sans", "Helvetica Neue", sans-serif" style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-size: 16px;">4. </span><span face="BlinkMacSystemFont, -apple-system, "Segoe UI", Roboto, Oxygen, Ubuntu, Cantarell, "Fira Sans", "Droid Sans", "Helvetica Neue", sans-serif" style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-size: 16px;">Chen C, Nguyen MD, Bar-Meir E, Hess PA, Lin S, Tobias AM, Upton J 3rd, Lee BT. Effects of vasopressor administration on the outcomes of microsurgical breast reconstruction. Ann Plast Surg. 2010 Jul;65(1):28-31. doi: 10.1097/SAP.0b013e3181bda312. PMID: 20548236.</span></p><p><span face="BlinkMacSystemFont, -apple-system, "Segoe UI", Roboto, Oxygen, Ubuntu, Cantarell, "Fira Sans", "Droid Sans", "Helvetica Neue", sans-serif" style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-size: 16px;">5. </span><span face="BlinkMacSystemFont, -apple-system, "Segoe UI", Roboto, Oxygen, Ubuntu, Cantarell, "Fira Sans", "Droid Sans", "Helvetica Neue", sans-serif" style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-size: 16px;">Szabo Eltorai A, Huang CC, Lu JT, Ogura A, Caterson SA, Orgill DP. Selective Intraoperative Vasopressor Use Is Not Associated with Increased Risk of DIEP Flap Complications. Plast Reconstr Surg. 2017 Jul;140(1):70e-77e. doi: 10.1097/PRS.0000000000003444. PMID: 28654605.</span></p><p><br /></p><p><br /></p><p><span style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-family: Roboto, "Helvetica Neue", Arial, Tahoma; font-size: 17px;">6. Naik AN, Freeman T, Li MM, Marshall S, Tamaki A, Ozer E, Agrawal A, Kang SY, Old MO, Seim NB. The Use of Vasopressor Agents in Free Tissue Transfer for Head and Neck Reconstruction: Current Trends and Review of the Literature. Front Pharmacol. 2020 Aug 28;11:1248. doi: 10.3389/fphar.2020.01248. PMID: 32982724; PMCID: PMC7485519.</span></p><p><span style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-family: Roboto, "Helvetica Neue", Arial, Tahoma; font-size: 17px;">7. </span><span face="Arial, sans-serif" style="background-color: white; caret-color: rgb(34, 34, 34); color: #222222; font-size: 13px;">Monroe, M.M., Cannady, S.B., Ghanem, T.A., Swide, C.E. and Wax, M.K., 2011. Safety of vasopressor use in head and neck microvascular reconstruction: a prospective observational study. </span><i style="caret-color: rgb(34, 34, 34); color: #222222; font-family: Arial, sans-serif; font-size: 13px;">Otolaryngology--Head and Neck Surgery</i><span face="Arial, sans-serif" style="background-color: white; caret-color: rgb(34, 34, 34); color: #222222; font-size: 13px;">, </span><i style="caret-color: rgb(34, 34, 34); color: #222222; font-family: Arial, sans-serif; font-size: 13px;">144</i><span face="Arial, sans-serif" style="background-color: white; caret-color: rgb(34, 34, 34); color: #222222; font-size: 13px;">(6), pp.877-882.</span></p><p><span face="Arial, sans-serif" style="color: #222222; font-size: x-small;"><span style="background-color: white; caret-color: rgb(34, 34, 34);">8. </span></span><span face="Arial, sans-serif" style="background-color: white; caret-color: rgb(34, 34, 34); color: #222222; font-size: 13px;">Harris, L., Goldstein, D., Hofer, S. and Gilbert, R., 2012. Impact of vasopressors on outcomes in head and neck free tissue transfer. </span><i style="caret-color: rgb(34, 34, 34); color: #222222; font-family: Arial, sans-serif; font-size: 13px;">Microsurgery</i><span face="Arial, sans-serif" style="background-color: white; caret-color: rgb(34, 34, 34); color: #222222; font-size: 13px;">, </span><i style="caret-color: rgb(34, 34, 34); color: #222222; font-family: Arial, sans-serif; font-size: 13px;">32</i><span face="Arial, sans-serif" style="background-color: white; caret-color: rgb(34, 34, 34); color: #222222; font-size: 13px;">(1), pp.15-19.</span></p><table style="border-collapse: collapse; border: 0px; caret-color: rgb(34, 34, 34); color: #222222; empty-cells: show; font-family: Arial, sans-serif; font-size: 13px; margin: -8px 0px 0px; padding: 0px; width: 438px;"><tbody><tr></tr><tr><td style="line-height: 1.24; padding: 8px 0px; vertical-align: top;"><div class="gs_citr" style="border: 0px; margin: 0px; padding: 0px;" tabindex="0">9. Chan, J.Y.W., Chow, V.L.Y. and Liu, L.H.L., 2013. Safety of intra‐operative vasopressor in free jejunal flap reconstruction. <i>Microsurgery</i>, <i>33</i>(5), pp.358-361.</div><div class="gs_citr" style="border: 0px; margin: 0px; padding: 0px;" tabindex="0"><br /></div><div class="gs_citr" style="border: 0px; margin: 0px; padding: 0px;" tabindex="0">10. <span face="BlinkMacSystemFont, -apple-system, "Segoe UI", Roboto, Oxygen, Ubuntu, Cantarell, "Fira Sans", "Droid Sans", "Helvetica Neue", sans-serif" style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-size: 16px;">Swanson EW, Cheng HT, Susarla SM, Yalanis GC, Lough DM, Johnson O 3rd, Tufaro AP, Manson PN, Sacks JM. Intraoperative Use of Vasopressors Is Safe in Head and Neck Free Tissue Transfer. J Reconstr Microsurg. 2016 Feb;32(2):87-93. doi: 10.1055/s-0035-1563381. Epub 2015 Sep 4. PMID: 26340760.</span></div><div class="gs_citr" style="border: 0px; margin: 0px; padding: 0px;" tabindex="0"><br /></div><div class="gs_citr" style="border: 0px; margin: 0px; padding: 0px;" tabindex="0">11. <span face="BlinkMacSystemFont, -apple-system, "Segoe UI", Roboto, Oxygen, Ubuntu, Cantarell, "Fira Sans", "Droid Sans", "Helvetica Neue", sans-serif" style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-size: 16px;">Fang L, Liu J, Yu C, Hanasono MM, Zheng G, Yu P. Intraoperative Use of Vasopressors Does Not Increase the Risk of Free Flap Compromise and Failure in Cancer Patients. Ann Surg. 2018 Aug;268(2):379-384. doi: 12.1097/SLA.0000000000002295. PMID: 28489683.</span></div><div class="gs_citr" style="border: 0px; margin: 0px; padding: 0px;" tabindex="0"><br /></div><div class="gs_citr" style="border: 0px; margin: 0px; padding: 0px;" tabindex="0">13. Milford EM, Reade MC. Resuscitation Fluid Choices to Preserve the Endothelial Glycocalyx. Crit Care. 2019 Mar 9;23(1):77. doi: 10.1186/s13054-019-2369-x. PMID: 30850020; PMCID: PMC6408751.</div></td></tr><tr><th class="gs_cith" scope="row" style="-webkit-user-select: none; color: #777777; font-weight: normal; padding: 8px 16px 8px 0px; text-align: right; user-select: none; vertical-align: top; white-space: nowrap;"><br /></th><td style="line-height: 1.24; padding: 8px 0px; vertical-align: top;"></td></tr></tbody></table>Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-45032992206995086072023-06-28T20:43:00.003-07:002023-06-29T13:44:59.896-07:00complex robot VHR in patient with smoking induced COPD<p> a 59 year old male presented with a complex VHR via robot laparoscopy. He had a prior history of drug abuse, hepatitis C and a long smoking history resulting in mild undiagnosed and untreated COPD. </p><p><br /></p><p>The patient was given a GETA anesthetic with sevoflurane, rocuronium, dilaudid, and low dose ketamine. During the anesthetic, his minute ventilation was unusually large for this 71 kg male. His peak airway pressures were also elevated despite no trendelenburg positioning requested from the surgeon. The procedure began at approximately 7:45am and closure was completed just prior to 5:00pm. Multiple ventilation manipulations were provided in an atttempt to improve ventilation, decrease airway pressures including driving pressure as well as minute ventilation.</p><p>In the October 2020 Journal <i>Anesthesiology [1], </i>An article on ventilation in obese patients undergoing laparoscopy surgery appeared. This article discussed a new paradigm emerging in ventilatory medicine to improve ventilation while reducing the incidence of ventilator induced lung injury (VILI). Dozens of studies showed reduced mortality in ICU patients who were ventilated due to ARDS when they were treated with low plateau pressure (Pplat) which often required reducing tidal volumes (Vt) to around 6 to 8 mL/kg and permissive hypercapnia. This has evolved over the years and there are now several studies indicating that the improvement in outcomes may be related more to reducing the driving pressure (Pdrive) rather than a purely low Vt permissive hypercapnea strategy.</p><p><br /></p><p>It is noted that Transpulmonary pressure is the pressure felt by the lung tissue itself and therefore the main concern when attempting to limit or avoid VILI. It has been identified that during robotic surgery in particular, airway pressures generated when attempting to ventilate the patient are not similar to a patient who is undergoing non robotic surgery. In particular, the airway pressure measured by the ventilator is diverted from the lungs to the chest wall. This occurs because during robotic surgery, chest wall compliance can decrease by up to 300% while lung tissue compliance decreases by only 50%, and thus. To restate, <span face="Lato, Helvetica, Arial, sans-serif" style="background-color: white; caret-color: rgb(56, 54, 54); color: #383636; font-size: 16px;">higher chest wall stiffness results in a lower fraction of airway pressure distributed to the lungs during the Trendelenburg position and docked robot condition than after intubation. Measurements in non obese patients, after docking and insufflation of the abdomen, found that the fractional pressure presented to the lungs by mechanical ventilation is reduced (48% from 63% immediately after intubation). In the obese patient (BMI 30-40), the decrease is from 80% after intubation to 56% after docking. In essence, because the chest wall compliance decreases dramatically after docking the robot, the lungs are now "protected" or shielded to a degree from high "airway pressures". To illustrate, lets take an example patient with BMI of 40 whose plateau pressures immediately after intubation are 27 cmH2O. If 80% of this pressure is distributed to the lungs, they would be impacted by (0.8 x 27)= 21.6 cmH2O while the rest would be distributed to the chest wall. Now, after docking, and pneumoperitoneum has been established the Plat increases from 27 cmH2O to 35 cmH2O. If we now calculate the fractional pressure applied to the lungs we see that it is (0.56 x 35) = 19.6 cmH20. The other pressure is applied to the chest wall (35 cmH2O - 19.6 cmH2O)= 15.4 cmH2O. Obviously, these numbers are explanatory only to make a point. However, it is important to understand that this occurs due to the differential change in compliance of the chest wall (decreased by up to 300%) vs the decrease in compliance of the lungs (up to 50%). </span></p><p><sup style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 0.625rem; line-height: 1; margin: 0px; padding: 0px;"> </sup><span face="Lato, Helvetica, Arial, sans-serif" style="background-color: white; caret-color: rgb(56, 54, 54); color: #383636; font-size: 16px;"> Overzealous limitation of PEEP or tidal volume to maintain plateau pressures less than 28 to 30 cm H</span><sub style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 0.625rem; line-height: 1; margin: 0px; padding: 0px;">2</sub><span face="Lato, Helvetica, Arial, sans-serif" style="background-color: white; caret-color: rgb(56, 54, 54); color: #383636; font-size: 16px;">O in such cases could expose patients to unnecessary hypoxemia, hypoventilation, and mechanical injury. </span></p><p><span face="Lato, Helvetica, Arial, sans-serif" style="color: #383636;"><span style="background-color: white;">After the benefits of lower tidal volumes and permissive hypercapnea were realized, a large number of studies attempting to translate these results into clinical anesthesia were published. Unfortunately, the results were scattered with many studies unable to clearly show </span>definite and meaningful benefits with "lung protective ventilation" strategies during routine clinical mechanical ventilation. In general, patients were divided into groups of high vs. low Vt (i.e. 10-12 ml/kg vs. 6-8 ml/kg) and groups of standard PEEP or no PEEP. The PEEP applied was usually standardized in the group that received PEEP anywhere from 2 up to 10 cmH20. Another recent trial found that PEEP of 12 cmH2O vs. 2 or less provided no benefit to patients undergoing open abdominal surgery. While there was no improvement in post op pulmonary complications (PPCs), the high PEEP group experienced more hemodynamic instability and required more fluid. This led many to recommend low PEEP. However, Tharp et al. [1], showed that individualizing applied PEEP, improves mechanical ventilation parameters. Tharp et al found that in patients with normal BMI, optimal PEEP was 9.7 cm H2O (+/- 3.7), whereas, for obese patients (BMI >= 40), optimal PEEP was 21.3 cmH2O (+/- 7.4). High PEEP has been shown beneficial in other studies of obese patients with ARDS, where PEEP as high as 20 cm H2O showed benefit[3]. The real takeaway from the Tharp paper [1], is the observed high variability in optimal PEEP between patients.</span></p><p><span face="Lato, Helvetica, Arial, sans-serif" style="color: #383636;">Post operative pulmonary complications and VILI can be understood by stress and strain placed on the alveoli. Excessive alveolar strain during ventilation may result in injury, and in predisposed patients will lead to post operative pulmonary complications (PPCs). Strain to the alveoli can be quantified and understood via the equation Vt/FRC ratios. Since the strain is equal to the ratio of change in volume to initial volume, understanding that if FRC drops in your patient as you anesthetize them, total alveolar strain will increase. As example, if you have a two patients both with Vt of 500ml but different FRCs, they will experience large differences in total alveolar strain during ventilation.</span></p><p><span face="Lato, Helvetica, Arial, sans-serif" style="color: #383636;"><br /></span></p><p><span face="Lato, Helvetica, Arial, sans-serif" style="color: #383636;">Patient 1: Vt=500mL and FRC 2000mL strain = 25%</span></p><p><span face="Lato, Helvetica, Arial, sans-serif" style="color: #383636;">Patient 2: Vt=500mL and FRC 500mL (due to ARDS) strain = 100% (four fold increase)</span></p><p><span face="Lato, Helvetica, Arial, sans-serif" style="color: #383636;"></span></p><div class="separator" style="clear: both; text-align: center;"><span face="Lato, Helvetica, Arial, sans-serif" style="color: #383636;"><a href="https://blogger.googleusercontent.com/img/a/AVvXsEhz5fOs1hHD_CoankDguW7HkoMYqR-UPbJm_pihCFOA7-2bQNR8lOGae8_6QgzQoWLpJ_Y1PkggvbVrNfTkUgvuRuu1rcaUVyFaSX_CRRo2DrlnO6FvG0R4dUYV_bNHmBNMQqQaj0jy7MblAfIE8YXuGBbgdfBdLOtdH_42y-J712ZQsBgUo6Qezk63dA" style="margin-left: 1em; margin-right: 1em;"><img data-original-height="1778" data-original-width="1850" height="614" src="https://blogger.googleusercontent.com/img/a/AVvXsEhz5fOs1hHD_CoankDguW7HkoMYqR-UPbJm_pihCFOA7-2bQNR8lOGae8_6QgzQoWLpJ_Y1PkggvbVrNfTkUgvuRuu1rcaUVyFaSX_CRRo2DrlnO6FvG0R4dUYV_bNHmBNMQqQaj0jy7MblAfIE8YXuGBbgdfBdLOtdH_42y-J712ZQsBgUo6Qezk63dA=w640-h614" width="640" /></a></span></div><span face="Lato, Helvetica, Arial, sans-serif" style="color: #383636;"><br />Intraop, we can't directly measure strain, although this variable is obviously incredibly important in causing lung injury if elevated. However, we can indirectly get clues as to the strain we are applying to the airways by measuring the driving pressure. Simply, Driving pressure (Pdrive) is the plateau pressure (Pplat) minus PEEP. Pplat is measured at the end of an inspiratory pause during volume controlled ventilation. The inspiratory pause is important as no flow can occur during measurement for accuracy. Fortunately, all modern anesthesia ventilators can apply this after each breath in order to measure Pplat. As we learn more about our ability to measure ventilation parameters and how to change those parameters to improve outcomes, anesthesiologists will find greater roles in controlling outcomes. Pdrive is a concept that is gaining greater traction. Essentially, Pdrive is expressed as the ratio between Vt and respiratory system compliance (Crs). Crs correlates closely with the aerated lung volume. Recent studies have demonstrated that Pdrive is a better indicator than purely Vt management to predict pulmonary outcomes. in 2015, a large analysis of patients with ARDS [4] was completed where it was shown that independent changes in Vt or PEEP were not independently associated with survival. However, Pdrive was associated independently with survival EVEN in patients receiving protective Pplat and Vt. In this study, the cut off point where risk was increased was Pdrive of 15 cmH2O. One year after the above was published a large meta analysis was completed looking at studies using "protective ventilation" to reduce post operative pulmonary complications [5]. They included data from 17 RCT with 2250 patients. A multivariate analysis suggested that Pdrive was associated with PPCs (there was a 13% increased probability of PPCs for every 1 cmH2O increase in Pdrive). There was no association at all with Vt or PEEP. </span><p></p><p><span face="Lato, Helvetica, Arial, sans-serif" style="color: #383636;">Unfortunately, Pdrive as a surrogate for acquiring measurement of transpulmonary pressure (what we are really after) can be unreliable in situations where Chest wall compliance is dramatically altered. This occurs as mentioned above during laparoscopy especially when robotic and in steep trendelenburg positioning. For example, increasing intraabdominal pressure increased Pplat by 50% of the applied intraabdominal pressure, but produced minimal change in transpulmonary pressure (Plung) in healthy lungs. In contrast, in the presence of lung injury, both Pdrive and Plung increased with increasing intra-abdominal pressure. In obese patients undergoing robotic laparoscopic surgeries, adequate mechanical ventilation may be difficult. In these situations there is a push to use esophageal manometry to directly measure pleural pressure which allows a direct measurement of transpulmonary pressure. Unfortunately, esophageal manometry is unavailable in routine clinical anesthesia. Therefore, given the tools at our disposal, how does one determine the "ideal" PEEP so as to decrease Pdrive when it becomes a challenge. As made clear above, routine application of 5 cmH2O of PEEP is likely not what any given patient will need. Previous studies have shown that "ideal" PEEP in obese patients ranged from 13 to 25 cmH2O. Tharp found using individualized PEEP titration using esophageal manometry that not all obese patients require higher PEEP settings. High PEEP can reduce venous return, right ventricular after load, cerebral perfusion pressure, and increase the potential for barotrauma and increased ICP. Therefore, much consideration should be given prior to simply increasing PEEP beyond 10 cmH2O when one encounters troublesome ventilation parameters. Finding "ideal" PEEP was highlighted by an article in the journal <i>Anesthesiology </i>[6], where it was demonstrated that when 'ideal' PEEP was identified using electrical impedance tomography intraoperative oxygenation, Pdrive, and post operative lung collapse were all improved. They also determined that ideal PEEP varied greatly between patients, and those receiving 'ideal' PEEP had no adverse affects. These authors were also able to demonstrate that applying a uniform level of PEEP to all patients can be problematic. During their recruitment process they were able to observe that a fixed PEEP of 6 cmH2O caused a wide range of lung collapse from 3 to 33% of the lung volume. At the other extreme, a fixed-PEEP of 16 cmH2O caused 5 to 52% of lung hyper distention. This study was also able to demonstrate a strong correlation between increasing BMI and higher ideal PEEP, but again, there was large variability. Tharp was [10] also able to demonstrate, that PEEP requirements also increase with the trendelburg position.</span></p><p><span face="Lato, Helvetica, Arial, sans-serif" style="color: #383636;">Unfortunately, the above technique of electrical impedance tomography is not available clinically. However, Park et al.[7] studied PEEP titration to Pdrive in an RCT of patients undergoing one lung ventilation for esophagectomy. One group received "protective" ventilation parameters by using 6 mL/kg of IBW Vt and PEEP of 5 cmH2O with recruitment maneuvers while the test group had their PEEP titrated. Starting at a PEEP of 2 cmH2O, they calculated Pdrive for the patient by using an inspiratory hold of 30% of inspiratory time to measure Pplat and then subtracted PEEP (Pdrive =Pplat-PEEP). After every change in PEEP, then allowed ten breath cycles to occur, and then used the Pplat of the last cycle for the measurement. After they tried PEEP 2 through 10 cmH2O, they used the PEEP at which the Pdrive was the lowest. PPCs were decreased from 12.2% in the protected ventilation group to 5.5% in the titration of Pdrive group which was statiscally significant (OR 0.4). A meta analysis of various set PEEP levels compared to individualized PEEP found that individualized PEEP was superior to set PEEP values (from low to high) in terms of oxygenation and lung compliance. In another RCT [8] in elderly patients undergoing laparoscopic surgery, titration of best PEEP from 4 to 10 cmH2O was compared to a convention group (Vt 10 ml/kg no PEEP) and a protective ventilation group (Vt ml/kg IBW and PEEP of 6 cmH2O). The CV and PV groups had similar post op pulmonary profiles vs much improved profiles in patients whose PEEP was titrated to the lowest Pdrive. Similar results were found in patients having a lapx chole [9]. </span></p><p><span face="Lato, Helvetica, Arial, sans-serif" style="color: #383636;">Unfortunately, while it seems clear that reducing Pdrive and titrating PEEP to the lowest Pdrive in patients improve pulmonary profiles, several questions remain: In which patients should we use these procedures, which types of surgeries, what PEEP level should be tried, what Pdrive is too high, and how often should we reverify ideal PEEP Intraoperatively?</span></p><p><span style="color: #383636;">My patient had high Peak airway pressures as well as high Pdrive. I tried to titrate my PEEP higher and this did help reduce Pdrive, but it remained around 14 to 16 cmH2O with a PEEP as 12 to 14 cmH2O. My patient was having a robotic VHR. </span></p><p><br /></p><p>1. Tharp WG et al. <i>Anesthesiology </i>V133, issue 4, 2020</p><p>2. Bao X, Vidal Melo M. <i>Anesthesiology</i> V133, issue4, 2020</p><p>3. <span face="BlinkMacSystemFont, -apple-system, "Segoe UI", Roboto, Oxygen, Ubuntu, Cantarell, "Fira Sans", "Droid Sans", "Helvetica Neue", sans-serif" style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-size: 16px;">Florio G, Ferrari M, Bittner EA, De Santis Santiago R, Pirrone M, Fumagalli J, Teggia Droghi M, Mietto C, Pinciroli R, Berg S, Bagchi A, Shelton K, Kuo A, Lai Y, Sonny A, Lai P, Hibbert K, Kwo J, Pino RM, Wiener-Kronish J, Amato MBP, Arora P, Kacmarek RM, Berra L; i <i>Crit Care. </i>2020 Jan 15;24(1):4. </span></p><p><span face="BlinkMacSystemFont, -apple-system, Segoe UI, Roboto, Oxygen, Ubuntu, Cantarell, Fira Sans, Droid Sans, Helvetica Neue, sans-serif" style="color: #212121;"><span style="background-color: white; caret-color: rgb(33, 33, 33);">4. </span></span><span face="BlinkMacSystemFont, -apple-system, "Segoe UI", Roboto, Oxygen, Ubuntu, Cantarell, "Fira Sans", "Droid Sans", "Helvetica Neue", sans-serif" style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121; font-size: 16px;">Amato MB, Meade MO, Slutsky AS, Brochard L, Costa EL, Schoenfeld DA, Stewart TE, Briel M, Talmor D, Mercat A, Richard JC, Carvalho CR, Brower RG. <i>N Engl J Med.</i> 2015 Feb 19;372(8):747-55.</span></p><p><span style="font-family: arial; font-size: x-small;"><span style="background-color: white; caret-color: rgb(33, 33, 33); color: #212121;">5. </span><span style="background-color: white; caret-color: rgb(48, 48, 48); color: #303030;">Neto AS, Hemmes SN, Barbas CS, Beiderlinden M, Fernandez-Bustamante A, Futier E, Gajic O, El-Tahan MR, Ghamdi AA, Gunay E, Jaber S, Kokulu S, Kozian A, Licker M, Lin WQ, Maslow AD, Memtsoudis SG, Reis Miranda D, Moine P, Ng T, Paparella D, Ranieri VM, Scavonetto F, Schilling T, Selmo G, Severgnini P, Sprung J, Sundar S, Talmor D, Treschan T, et al.: </span><span style="background-color: white; caret-color: rgb(48, 48, 48); color: #303030;">. </span><span class="ref-journal" style="box-sizing: inherit; caret-color: rgb(48, 48, 48); color: #303030; font-style: italic;">LancetRespiratory Med</span><span style="background-color: white; caret-color: rgb(48, 48, 48); color: #303030;"> 2016; </span><span class="ref-vol" style="box-sizing: inherit; caret-color: rgb(48, 48, 48); color: #303030;">4</span><span style="background-color: white; caret-color: rgb(48, 48, 48); color: #303030;">:272–80 </span></span></p><p><span style="font-family: arial; font-size: x-small;"><span style="background-color: white;"><span style="color: #303030;"><span style="caret-color: rgb(48, 48, 48);">6. Pereira S, Tucci M, Morais C, Simons C, Tonelotto B, Pompeo M, Kay F, Pelosi P, Vieira J, Amato M. </span></span></span></span><span face="Lato, Helvetica, Arial, sans-serif" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; font-size: 12px; font-style: italic; margin: 0px; padding: 0px; vertical-align: baseline;">Anesthesiology</span><span face="Lato, Helvetica, Arial, sans-serif" style="background-color: white; caret-color: rgb(56, 54, 54); color: #383636; font-size: 12px;"> December 2018, Vol. 129, 1070–1081.</span></p><p><span face="Lato, Helvetica, Arial, sans-serif" style="background-color: white; caret-color: rgb(56, 54, 54); color: #383636; font-size: 12px;">7. Park et al. <i>Anesthesiology. </i>March 2019, Vol. 130, issue 3</span></p><p><span face="Lato, Helvetica, Arial, sans-serif" style="background-color: white; caret-color: rgb(56, 54, 54); color: #383636; font-size: 12px;">8. Xu Q <i><b>BMC</b> Anesthesiology</i>. 2022; 22:72.</span></p><p><span face="Lato, Helvetica, Arial, sans-serif" style="background-color: white; caret-color: rgb(56, 54, 54); color: #383636;"><span style="font-size: 12px;">9</span><span style="font-family: arial;">. </span></span><span style="background-color: white; color: #303030; white-space: pre-wrap;"><span style="font-family: arial;"> D’Antini D, Rauseo M, Grasso S, et al. Physiological effects of the open lung approach during laparoscopic cholecystectomy: focus on driving pressure. Minerva Anestesiol. 2018;84(2):159–67.</span></span></p><p><br /></p>Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-145464393271460322022-02-19T15:13:00.000-08:002022-02-19T15:13:02.132-08:00pituitary adenoma coming for surgery<p> 59 year old female for D&C and hysteroscopy with a history of pituitary adenoma, empty sella syndrome, Adrenal insufficiency, HTN, OSA, and BMI of 31. The patient was taking cabergoline to inhibit the secretion of prolactin via agonism of dopamine receptors. The patient also had a history of PONV and was very concerned with this prior to surgery.</p><p><br /></p><p>The patient had been followed for several years for her pituitary adenoma and had had no recent changes in her medical status. I verified that her labs were within normal limits and proceeded with a general anesthetic with LMA.</p><p><br /></p><p><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;">The pituitary gland occupies the sella turcica of the sphenoid bone at the base of the skull, the roof of which is created by an incomplete fold of dura, the diaphragma sella, through which passes the pituitary stalk.</span></p><p><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;"><br /></span></p><table style="background-color: #fafafa; border-bottom-color: initial; border-bottom-style: initial; border-collapse: collapse; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-spacing: 0px; border-top-color: rgb(207, 213, 228); border-top-style: solid; border-width: 1px 0px 0px; color: #2a2a2a; font-family: "Source Sans Pro", Helvetica, Arial, sans-serif; font-size: 0.9375rem; font-stretch: inherit; font-variant-east-asian: inherit; font-variant-numeric: inherit; line-height: inherit; margin: 0px 0px 1rem; padding: 0px; vertical-align: baseline;"><thead style="background-color: #f5f7fa; border-bottom-color: initial; border-bottom-style: initial; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: rgb(207, 213, 228); border-top-style: solid; border-width: 1px 0px 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: 700; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><th style="background-color: #f2f5f9; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; text-align: left; vertical-align: baseline;">Hormone and site of production</th><th style="background-color: #f2f5f9; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; text-align: left; vertical-align: baseline;">Target organ and function</th></tr></thead><tbody style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td colspan="2" style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"><b style="background-color: #fcff01;">Anterior pituitary </b></td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">ACTH pars distalis </td><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"><em style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Adrenal glands</em>: stimulates the glands to produce glucocorticoids and aldosterone </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">GH pars distalis </td><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"><em style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Musculoskeletal system</em>: anabolic effects on bone and muscle. Promotes lipolysis, increases free fatty acid levels, and impairs glucose utilization and cellular sensitivity to insulin </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td rowspan="2" style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-bottom-width: 1px; border-bottom: 1px solid rgb(207, 213, 228); border-image: initial; border-left-style: none; border-left: none; border-right-color: rgb(207, 213, 228); border-right-style: solid; border-right-width: 1px; border-right: 1px solid rgb(207, 213, 228); border-top-width: 0px; border-top: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Prolactin pars distalis </td><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"><em style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Mammary glands</em>: stimulates the glands to produce milk </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"><em style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Ovary</em>: inhibits the actions of gonadotropins on the ovary </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">FSH and LH pars tuberalis </td><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"><em style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Gonads</em>: stimulate the testes to produce sperm and testosterone, and the ovaries to produce eggs and oestrogen </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">TSH pars tuberalis </td><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"><em style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Thyroid</em>: stimulates the gland to produce thyroid hormones </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Beta-melanocyte-stimulating hormone pars intermedia </td><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"><em style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Skin</em>: causes increased pigmentation </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Endorphins and encephalins pars intermedia </td><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"><em style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Brain and immune system</em>: inhibits pain sensations </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td colspan="2" style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"><b style="background-color: #fcff01;">Posterior pituitary</b><span style="background-color: white; font-weight: inherit;"> </span></td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Antidiuretic hormone </td><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"><em style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Kidneys</em>: regulates the amount of water excreted by the kidneys and maintains water balance in the body </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td rowspan="2" style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-bottom-width: 1px; border-bottom: 1px solid rgb(207, 213, 228); border-image: initial; border-left-style: none; border-left: none; border-right-color: rgb(207, 213, 228); border-right-style: solid; border-right-width: 1px; border-right: 1px solid rgb(207, 213, 228); border-top-width: 0px; border-top: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Oxytocin </td><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"><em style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Uterus</em>: contracts the uterus during childbirth and immediately after delivery </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="background-color: white; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: initial; border-top-style: initial; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"><em style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-variant-alternates: inherit; font-variant-caps: inherit; font-variant-east-asian: inherit; font-variant-ligatures: inherit; font-variant-numeric: inherit; font-variant-position: inherit; font-variant: inherit; font-weight: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Mammary glands</em>: stimulates contractions of the milk ducts in the breast leading to the let-down reflex, which moves milk to the nipple in lactating women </td></tr></tbody></table><br /><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif;">The posterior pituitary is regulated directly by the hypothalamic axons which project to it and synapse with its cells. The anterior pituitary is regulated by hypothalamic tropic hormones that reach it via the portal venous system. The hypothalamic influence is mainly stimulatory, which is in turn regulated by negative feedback control exerted at the pituitary and hypothalamic level, the classical example being the feedback regulation of thyroid-stimulating hormone (TSH) by the thyroid hormones</span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif;"><br /></span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif;">There are two main categories that facilitate tracking the practical considerations of approaching a patient with a pituitary adenoma. Macroadenomas (>10mm) and microadenomas (<10mm). </span><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif;"> </span><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif;">Larger tumours can cause hypopituitarism, cranial nerve palsies, and hydrocephalous due to blockage of third ventricle outflow.</span><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif;"> </span><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif;">Microadenomas may present with symptoms of hormonal excess, the classic example being Cushing's disease [excess of adrenocorticotropic hormone (ACTH)] or very rarely thyrotoxicosis (excess of TSH). </span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif;"><br /></span></div><div><span style="color: #2a2a2a; font-family: Merriweather, serif;"><span style="background-color: white;">The three most common hypersecreting hormonal syndromes from pituitary adenomas include:</span></span></div><div><span style="color: #2a2a2a; font-family: Merriweather, serif;"><span style="background-color: white;"><br /></span></span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif;">1) Acromegaly: 20% of pituitary adenomas. These are macroadenomas secreting excess GH resulting in a constellation of comorbidities.</span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif;">Patients coming to surgery with this type of tumor will be on medications to inhibit GH production such as Somatostatin analogues, Octreotide, lanreotide or GH receptor antagonist (Pegvisomant).</span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif;">2) Cushing's disease: A pituitary corticotroph adenoma secreting excess ACTH. These represent about 7% of pituitary adenomas. These patients may arrive to surgery taking </span><span style="background-color: white; font-family: "Times New Roman", stixgeneral, serif;">ketoconazole, metyrapone, mitotane, or aminoglutethimide. These medications inhibit the enzymes in the adrenal gland that make up the chain of synthesis of cortisol and therefore, are able to reduce hypercortisolemia. Patient's may be arriving to surgery to undergo bilateral adrenalectomy which is required for non resesectable ACTH hypersecreting microadenomas. These patients often suffer from HTN, DM and osteoporosis (40% of patients).</span></div><div><span style="background-color: white; font-family: "Times New Roman", stixgeneral, serif;"><span>In particular, patients with Cushing's disease may present with hypokalemic metabolic alkalosis. </span></span><span style="background-color: white; font-family: "Times New Roman", stixgeneral, serif;">Hypokalemia occurs due to overwhelming of the enzyme 11-beta-hydroxysteroid dehydrogenase by excessive circulating cortisol, resulting in inappropriate activation of the mineralocorticoid receptor. This receptor allows for retention of sodium at the expense of spilling potassium and hydrogen ions into the urine at the distal convoluted tubule of the kidney.</span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif;">3) Prolactinoma: Medical therapy is first line with bromocriptine or cabergoline (inhibit prolactin secretion). These medications will often resolve hyperporlactinemia and reduce tumor size. There are no perioperative care issues caused by the physiological affects of prolactinomas. These tumors are far more common in females. In men, they are often macro adenomas.<div class="separator" style="clear: both; text-align: center;"><br /></div><br /></span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;"><br /></span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;">Hormone Hyposecretion</span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;"><br /></span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;">1) Adrenal cortical insufficiency: This is also known as secondary adrenal insufficiency and </span><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;">differs from Addison's disease in that the electrolyte disturbances are less severe. In the perioperative period IV hydrocortisone along with IV normal saline +/- IV glucose is indicated for support to avoid hypotension.</span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;"><br /></span></div><div><span style="background-color: white;"><span style="color: #2a2a2a; font-family: Merriweather, serif;"><span style="font-size: 15px;">As cortisol is produced in the </span><span style="caret-color: rgb(42, 42, 42); font-size: 15px;">adrenal</span><span style="font-size: 15px;"> cortex in the zone </span></span></span><span style="color: #2a2a2a; font-family: Merriweather, serif;"><span style="font-size: 15px;">fasciculate via stimulation from ACTH, in some rare cases (i.e. pituitary apoplexy), the pituitary gland is rendered incapable of producing ACTH. While in secondary adrenal insufficiency the sodium and potassium are often normal, although in some instances, a dilution hyponatremia develops due to excess ADH secretion from absence of cortisol. Dehydration and hyperkalemia are typical of primary adrenal cortical insufficiency due to faulty aldosterone secretion as well. However, aldosterone is not primarily under the control of the PG, and therefore, not typical of secondary adrenal </span><span style="caret-color: rgb(42, 42, 42); font-size: 15px;">insufficiency.<br /><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/a/AVvXsEjQxEe8aWrRcYezf8hLItx5PBUN3u-_RSFuywFs8Xcn2eEKaK7oBNe5n11MseeSbbzw65FvZ4rH0qNHhzEtfIKqBE5OSjSduk0lI8iQqFAdSxbfXJFHP3RLRnTshAKfG-ovyEmZsjwhq9HxcpCXxHN-pO8LBi2sTZJskUkxj2im-smpybJLTw56XWYFyg" style="margin-left: 1em; margin-right: 1em;"><img alt="" data-original-height="1904" data-original-width="2600" height="234" src="https://blogger.googleusercontent.com/img/a/AVvXsEjQxEe8aWrRcYezf8hLItx5PBUN3u-_RSFuywFs8Xcn2eEKaK7oBNe5n11MseeSbbzw65FvZ4rH0qNHhzEtfIKqBE5OSjSduk0lI8iQqFAdSxbfXJFHP3RLRnTshAKfG-ovyEmZsjwhq9HxcpCXxHN-pO8LBi2sTZJskUkxj2im-smpybJLTw56XWYFyg" width="320" /></a></div><br /></span></span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;"><br /></span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;"><br /></span><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/a/AVvXsEiAsmRlCCv8c3-JuXtMBWqr9qYAiWEi_Y98wNc1ujg_tVOCdz-BF9VLFp9W0Ih2G_KcZOr2HIJO_txZbVLSeUXHDOzQfrOXsP6xCX6wmJvUcFw5N0xey48YtGzUoHEv7NZ6JjlO_fCdQpURmhfUxBY9U7xP8TWh0OGH6USgh9OyISTTUNGLtOGFr4joJA" style="margin-left: 1em; margin-right: 1em;"><img data-original-height="692" data-original-width="1404" height="198" src="https://blogger.googleusercontent.com/img/a/AVvXsEiAsmRlCCv8c3-JuXtMBWqr9qYAiWEi_Y98wNc1ujg_tVOCdz-BF9VLFp9W0Ih2G_KcZOr2HIJO_txZbVLSeUXHDOzQfrOXsP6xCX6wmJvUcFw5N0xey48YtGzUoHEv7NZ6JjlO_fCdQpURmhfUxBY9U7xP8TWh0OGH6USgh9OyISTTUNGLtOGFr4joJA=w400-h198" width="400" /></a></div></div><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: left;">In cases of addisonian crisis from secondary adrenal insufficiency as seen from a PG problem can be treated with dexamethasone 8 mg or hydrocortisone. Since in secondary adrenal insufficiency aldosterone is adequate, the mineralocorticoid effects of hydrocortisone are not critical, and a pure glucocorticoid such as decadron is adequate for treatment. However, NS should be infused as well, as opposed to LR, as hyponatremia may accompany this syndrome from SIADH.</div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;"><br /></span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;">2) Hypothyroidism: Pituitary hypothyroidism tends to be less severe than primary thyroid failure. However, patients will be more sensitive to and less able to metabolize anesthetic medications. This can result in induction of anesthesia with very low dosages as well as prolonged sleep after discontinuation of anesthetic medications. </span><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;">Clinical response to thyroid replacement therapy may take 10 days, although more rapid correction can be achieved with i.v. </span><span class="small-caps" style="background-color: white; border: 0px; box-sizing: border-box; color: #2a2a2a; font-family: Merriweather, serif; font-size: 0.825em; font-stretch: inherit; font-variant-east-asian: inherit; font-variant-numeric: inherit; letter-spacing: 0.05em; line-height: inherit; margin: 0px; padding: 0px; text-transform: uppercase; vertical-align: baseline;">L</span><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;">-iodothyronine (T3). Unfortunately, there is a significant risk of precipitating myocardial ischaemia and heart failure. Furthermore, </span><span style="background-color: white; font-family: "Times New Roman", stixgeneral, serif; font-size: 15.9991px;">Thyroid hormone replacement has to be done very cautiously in patients with impaired adreno-corticotrophic hormone ACTH reserves as it can precipitate an adrenal crisis. Therefore, glucocorticoid cover is essential before proceeding with thyroid hormone replacement.</span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;"><br /></span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;">3) Central Diabetes Insipidus: Far less likely to be encountered in the perioperative period. T</span><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;">he result of failure of secretion of ADH. It is treated with desmopressin, a synthetic analogue of ADH that has a longer half life and which lacks the vasoconstricting properties of the endogenous hormone. Although desmopressin is usually administered orally or intra-nasally, after operation it can be given as a subcutaneous or intra-muscular injection. Failure to secrete oxytocin only becomes clinically evident during and after childbirth, and is not relevant in the acute setting.</span><span face=""Source Sans Pro", Helvetica, Arial, sans-serif" style="background-color: white; border: 0px; box-sizing: border-box; color: #2a2a2a; font-size: 0.75rem; font-stretch: inherit; font-variant-east-asian: inherit; font-variant-numeric: inherit; line-height: normal; margin: 0px; padding: 0px; position: relative; top: -0.75em; vertical-align: baseline;"><span class="xrefLink" id="jumplink-MKR014C7" style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; line-height: inherit; margin: 0px; padding: 0px; position: relative; top: -55px; vertical-align: baseline; visibility: hidden;"></span><a class="link link-ref link-reveal xref-bibr" data-open="MKR014C7" reveal-id="MKR014C7" style="border: 0px; box-sizing: border-box; color: #006fb7; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; font: inherit; hyphens: auto; line-height: inherit; margin: 0px; overflow-wrap: break-word; padding: 0px; vertical-align: baseline; word-break: break-word;">7</a></span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;"> </span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;"><br /></span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;">Surgical stress and hormonal changes</span></div><div><span style="background-color: white; color: #2a2a2a; font-family: Merriweather, serif; font-size: 15px;"><div class="table-wrap-title" data-id="TBL2" id="TBL2" style="border: 0px; box-sizing: border-box; caret-color: rgb(0, 0, 0); color: black; font-family: inherit; font-size: 0.9375rem; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px 0px 0.65rem; padding: 0px; vertical-align: baseline;"><br /></div><div class="table-overflow" style="border: 0px; box-sizing: border-box; caret-color: rgb(0, 0, 0); color: black; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px 0px 0.5em; overflow-x: auto; padding: 0px; vertical-align: baseline;"><table style="border-collapse: collapse; border-spacing: 0px; border-top-color: rgb(207, 213, 228); border-top-style: solid; border-width: 1px 0px 0px; box-sizing: border-box; font-family: "Source Sans Pro", Helvetica, Arial, sans-serif; font-size: 0.9375rem; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline; white-space: nowrap; width: 849.8875122070312px;"><thead style="background-color: #f5f7fa; border-top-color: rgb(207, 213, 228); border-top-style: solid; border-width: 1px 0px 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: 700; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; font-weight: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><th style="background-color: #f2f5f9; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: baseline;"><hr style="background-color: #cfd5e4; border: 0px; box-sizing: border-box; height: 1px;" /></th><th style="background-color: #f2f5f9; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: baseline;">Pituitary<hr style="background-color: #cfd5e4; border: 0px; box-sizing: border-box; height: 1px;" /></th><th style="background-color: #f2f5f9; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: baseline;">Adrenal<hr style="background-color: #cfd5e4; border: 0px; box-sizing: border-box; height: 1px;" /></th><th style="background-color: #f2f5f9; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: baseline;">Pancreatic<hr style="background-color: #cfd5e4; border: 0px; box-sizing: border-box; height: 1px;" /></th><th style="background-color: #f2f5f9; border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: baseline;">Others<hr style="background-color: #cfd5e4; border: 0px; box-sizing: border-box; height: 1px;" /></th></tr></thead><tbody style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Increased secretion </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Growth hormone (GH) </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Catecholamines </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Glucagon </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Renin </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Adrenocorticotrophic hormone (ACTH) </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Cortisol </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">β-Endorphin </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Aldosterone </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Prolactin </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Arginine vasopressin (posterior pituitary) (AVP) </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Unchanged secretion </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Thyroid stimulating hormone (TSH) </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Luteinizing hormone (LH) </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Follicle stimulating hormone (FSH) </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Decreased secretion </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Insulin </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Testosterone </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Oestrogen </td></tr><tr style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;"> </td><td style="border-bottom-color: rgb(207, 213, 228); border-bottom-style: solid; border-width: 0px 0px 1px; box-sizing: border-box; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: 1.3em; margin: 0px; padding: 0.65em; vertical-align: top;">Tri-iodothyronine (T<sub style="border: 0px; box-sizing: border-box; font-family: inherit; font-size: 0.75rem; font-stretch: inherit; font-style: inherit; font-variant-caps: inherit; line-height: normal; margin: 0px; padding: 0px;">3</sub>)</td></tr></tbody></table></div></span></div><div><br /></div><div>Opioids can suppress the hypothalamic and pituitary hormone response to surgery. However, to cause complete suppression, very large doses are required (i.e. ~50 mcg/kg).</div><div><br /></div><div>Acute IV opioid administration can have a stimulatory effect on prolactin secretion mediated by the mu-,Kappa-, and sigmoid opioid receptors in the hypothalamus. In cases of prolactinemia induced by opioids, bromocriptine has been used successfully to decrease prolactin levels.</div><div><br /></div><div>This patient was taking cabergoline a dopamine 2 receptor agonist. Cabergoline has been found to be effective in 80% of women with prolactinomas. Bromocriptine has lost favor mainly due to pharmacokinetic issues where it is required up to 3 or 4 times a day. Cabergoline is long acting requiring dosing as little as twice a week. It is important to note that PONV can be affected by stimulation of D2 and D3 receptors. Antagonism of these receptors may decrease PONV. <span style="background-color: white;"><span style="font-family: Times New Roman, stixgeneral, serif;"><span style="font-size: 15.999099731445312px;">The mechanism involves blocking adenylate cyclase to reduce the amount of cAMP in neurons in the nucleus tractus solitarius and area postrema. Commonly used D2 antagonists include reglan, and a newer agent name Barhemsys (amusulpride). In this patient with a concern for PONV and taking a D2 receptor agonist that was long acting, rescue treatment with any D2 receptor blocker may prove less effective. Therefore, with the patient's permission a scopolamine patch was placed on the skin prior to rolling into the operating room. Opioids were minimized, ketorolac was provided to reduce opioid requirements, dexamethasone 4mg and </span></span></span><span style="font-family: Times New Roman, stixgeneral, serif;"><span style="font-size: 15.999099731445312px;">zoltan 4 mg were given as prophylaxis. The patient did not experience any PONV. If the patient had required rescue therapy, promethazine was ordered for rescue. Barhemsys is a newer alternative which has been shown to be moderately effective for rescue therapy in patients who have already received prophylaxis. Unfortunately, Barhemsys is a D2/3 antagonist which presents two potential concerns in this patient. 1) it may not be able to bind to the D2 receptor given the presence of cabergoline (d2 agonist). 2) It can induce increased prolactin levels in normal patients. However, it is not clear at all, that this would be a problem in a patient who is already properly treated with cabergoline.</span></span></div><div><span style="font-family: Times New Roman, stixgeneral, serif;"><span style="font-size: 15.999099731445312px;"><br /></span></span></div><div><span style="font-family: Times New Roman, stixgeneral, serif;"><span style="font-size: 15.999099731445312px;">Pituitary adenomas represent a potential large constellation of syndromes and diseases processes. A careful understanding of the type of adenoma along with its included pathophysiology is important prior to providing anesthesia. Fortunately, most pituitary adenomas are prolactinomas which tend to be benign and very responsive to medical therapy with dopamine 2 agonists. It must be recognized that alternative pharmacotherapy for PONV must be considered as the d2 agonist in these patients will likely make antagonism of the D2 receptor impossible.</span></span></div><div><br /></div>Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-40435963294331235932022-02-07T12:49:00.000-08:002022-02-07T12:49:07.136-08:00Twins in patient with thrombocytopenia<p> A 28 year G3P2 carrying twins vertex vertex, presents the day before induction for consultation with anesthesia. She states that she was diagnosed with thrombocytopenia by MFM, and started on 10 mg of prednisone for a platelet count of 71K. She has had two prior deliveries without epidural analgesia. She plans on vaginal delivery this pregnancy without epidural analgesia. </p><p><br /></p><p>In a recent study published in the NEJM, 2,804 women were followed with twin pregnancy. Those who planned for vaginal birth ended up getting a c-section 44% of the time. This study looked at mortality and morbidity in women and fetuses who had planned c-section v. planned vaginal delivery. There was no difference between groups in terms of outcome. The study did exclude any patients whose twin A was in the breech position, in which case, those patients were delivered by c-section. Another study did show that a major risk factor for unplanned c-section in twin pregnancy is nulliparity and breech twin B.</p><p>While twin pregnancy is rare, so also is thrombocytopenia. While up to 12% of obstetric patients may have some degree of thrombocytopenia, only 1% meet the definition of moderate to severe thrombocytopenia (<100,000 x 10^6/L). An anesthesiologist confronting a parturient with thrombocytopenia is most likely to be dealing with one of three main etiologies: 1) gestational thrombocytopenia 2) Immune thrombocytopenia (ITP) or 3) thrombocytopenia associated with hypertensive disorders of pregnancy (i.e. pre eclampsia; hemolysis, elevate liver enzymes, low platelet count [HELLP] syndrome). It is estimated that of parturients who are diagnosed with Thrombocytopenia, 80% of these cases are a result of gestational thrombocytopenia (affects 5-11% of pregnant patients). Some important diagnostic clues include onset in the mid second semester to third semester, mild Thrombocytopenia (not usually less than 75K), no outward symptoms (easy bruising etc), and no prior history of Thrombocytopenia. The diagnosis can only be made by exclusion of other causes. The other main cause of Thrombocytopenia during pregnancy is that related to hypertensive disease of pregnancy. This comprises 8 to 21% of patients with Thrombocytopenia during pregnancy. In these cases platelet function can be impaired in addition to decreased in number. The etiology of Thrombocytopenia in both of these conditions in unknown.</p><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhMgQ_aAfjV29eouEKOJkTnOg4RlZdyy3QdCUSGnQf5x7-S1_c9DhMLQ_qGZ-u_EOEj7_ro90Q7eQyYAha2koHx_RgpHv_Nx8wTenNQdMEVr6QNFE0rt8DH7Yyz4Is8qiSnVZdmlT4SyAIy/" style="margin-left: 1em; margin-right: 1em;"><img data-original-height="978" data-original-width="1812" height="346" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhMgQ_aAfjV29eouEKOJkTnOg4RlZdyy3QdCUSGnQf5x7-S1_c9DhMLQ_qGZ-u_EOEj7_ro90Q7eQyYAha2koHx_RgpHv_Nx8wTenNQdMEVr6QNFE0rt8DH7Yyz4Is8qiSnVZdmlT4SyAIy/w640-h346/Screen+Shot+2021-12-09+at+3.15.19+PM.png" width="640" /></a></div><br /><p></p><p>Unfortunately, given the low number of parturients presenting with thrombocytopenia who need neuraxial anesthesia, we do not have good numbers to determine the absolute risk (probability) of any one patient developing an epidural hematoma. It should be noted, that thrombocytopenia refers simply to how many platelets are available, but tells us nothing of platelet function which may be normal, reduced or even increased. Indeed, in pre eclampsia, platelet function is often impaired. However, in general we know that the risk of epidural hematoma with neuraxial anesthesia is about 1:250,000 in all comers. In a meta analysis reviewing 7509 neuraxial procedures, most epidural hematomas occurred in patients with platelet counts < 50,000 x 10^6/L. Of women with platelet counts < 100,000 x 10^6/L there were a total of 33 epidural hematomas, and 5 of these occurred in women with platelet counts between 44,000 and 91,000. However, ALL five of these had other ongoing issues [1 with AVM, 1 was coagulopathic on top of the low platelet count, 2 had HELLP syndrome, and 1 had full blown eclampsia). </p><p>In another study, 1524 patients received neuraxial anesthesia with no epidural hematomas noted. The authors, however, estimated the upper limits of the 95% CI for the risk of spinal epidural hematoma stratified by platelet count.</p><p></p><ul style="text-align: left;"><li>70K to 100K ....0.2% risk</li><li>50K to 69K ....3% risk</li><li><50K .........11%</li></ul>Unfortunately, it is not clear exactly how to use this information in clinical practice except to say that it appears risk is relatively low when platelets are above 70K. <div><br /></div><div><br /></div><div>Thromboelastography (TEG) or rotational thromboelastometry (ROTEM) have been studied as it relates to neuraxial anesthesia with thrombocytopenia. These studies were able to show no spinal epidural hematomas in patients with thrombocytopenia AND normal parameters on the TEG or ROTEM. However, other studies in oncologic patients with thrombocytopenia have reported no correlation between TEG and ROTEM parameters and clinical bleeding unless platelet levels were below 50,000 x 10^6/L.</div><div><br /></div><div>The platelet function analyzer (PFA)-100 test platelet function. Time to platelet plug formation is measured and labeled closure time (CT). An abnormal CT may be found in patients with counts <100,000 x 10^6/L, anemia, or significant qualitative platelet defects. However, at the end of the day, the consensus statement from the Society for Obstetric Anesthesia and Perinatology Interdisciplinary Consensus statement on Neuraxial Procedures in Obstetric Patients with thrombocytopenia can not recommend any of the above tests to determine the safety of neuraxial anesthesia.</div><div><br /></div><div>Platelet transfusion:</div><div>A 1 unit apheresis transfusion is expected to raise the platelet count between 30,000 to 50,000 x 10^6/L, although the end result is often variable depending on the disease in question. In particular, in HELLP or pre eclampsia, the end result may be much less than what was expected after transfusion. In ITP, transfusion of platelets alone is likely ineffective and requires concomitant treatment with IVIG and/or corticosteroid therapy. It should be noted that platelet transfusions in platelet consumption disease such as ITP is short lived.</div><div><br /></div><div>It is currently recommended [1] that the anesthesiologist confronting a parturient with thrombocytopenia should determine whether the patient has a known etiology for the thrombocytopenia. In addition, it is critical to determine if there is a history of easy or prolonged bleeding with the thrombocytopenia. In particular, the clinician should be confident that the etiology of the thrombocytopenia is not related to DIC or other highly morbid and evolving conditions. If it is suspected or confirmed that this is a case of gestational, autoimmune (idiopathic) thrombocytopenia or related to confirmed diagnosis of hypertensive disorder of pregnancy, then verifying that a recent platelet count is above 70,000 x 10^6/L would allow the clinician to have a rather high confidence that neuraxial anesthesia is safe. With a platelet count between 50K and 70K, a more careful cost benefit analysis should be carried out. If the platelet count if less than 50K, the guidelines recommend avoiding neuraxial anesthesia.</div><div><br /></div><div>The SOAP guidelines can be summarized in this algorithm which I found very helpful.</div><div><br /></div><div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhHc_kDQcU8YeYYuLf1sB8kMRGk-yyuY4IAutdIXfOPmvlQge0hOGtrTROtj2IKchRZ6IJuDZHvY0Owqws82gJSWcDcT-31ER1wadJGd-BIeXDLfI5jevYFLVNA751oCtx5NDIWP8nCr7hp/" style="margin-left: 1em; margin-right: 1em;"><img alt="" data-original-height="2048" data-original-width="2039" height="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhHc_kDQcU8YeYYuLf1sB8kMRGk-yyuY4IAutdIXfOPmvlQge0hOGtrTROtj2IKchRZ6IJuDZHvY0Owqws82gJSWcDcT-31ER1wadJGd-BIeXDLfI5jevYFLVNA751oCtx5NDIWP8nCr7hp/w637-h640/Screen+Shot+2021-12-11+at+7.11.30+PM.png" width="637" /></a></div><br /><br /></div><div><br /></div><div><br /></div><div>1. <span style="font-family: OpenSansRegular;">The Society for Obstetric Anesthesia and Perinatology Interdisciplinary Consensus Statement on Neuraxial Procedures in Obstetric Patients With Thrombocytopenia. <i>A&A</i> N. 132 2021 Pg 1531.</span><div><p></p><p><br /></p></div></div>Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-81265575756563681272021-06-09T19:21:00.004-07:002021-07-17T17:06:51.071-07:00Waste anesthesia Gases<p> The other day I arrived to our main hospital to relieve one of my partners who was working with several CRNAs. One of the CRNAs had just arrived in the cath lab where we had been asked to anesthetize a patient for a cardiac catheterization procedure. We induced general anesthesia with an ETT. Shortly thereafter I was called to the room for an alarm with warning indicator of "<span> PEEP high. Blockage?,"</span>. I quickly determined that there was high pressure in the 3 Liter scavenging system bag and this was a result of not having the vacuum line connected to a central vacuum. I thought it odd that the anesthesia machine had been placed in the cath lab without having been connected to the central vacuum for scavenging of waste anesthesia gases (WAGs). But it turns out there are no connections for vacuum in this particular room.</p><p><br /></p><p>In the typical OR, the anesthesia machine has a scavenging system set up so that all WAGs are emitted into the atmosphere and do not contaminate the OR. Below is a figure with the basic outline of how this system would be set up.</p><p>Because all modern ORs are built the same most anesthesia providers take it for granted that WAGs will be scavenged. </p><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhrg5i6M339uNUyJgocdxMiaJmugVkr8thxdoRsRPktBHtvRQafJQTGwWUGc2-TmFtHswAkwQHKHxgY9t5n2ElefeXoccZ0h4o0kEgGUVcd8livf5wnSJHhiznL1l3kFu6X2xY2iqeQqrco/s502/scavenging-1_fmt.png" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" data-original-height="344" data-original-width="502" height="274" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhrg5i6M339uNUyJgocdxMiaJmugVkr8thxdoRsRPktBHtvRQafJQTGwWUGc2-TmFtHswAkwQHKHxgY9t5n2ElefeXoccZ0h4o0kEgGUVcd8livf5wnSJHhiznL1l3kFu6X2xY2iqeQqrco/w400-h274/scavenging-1_fmt.png" width="400" /></a></div><br /><p>However, at times we are asked to provide anesthesia services outside of the OR setting. In this case, the anesthesia tech for the hospital placed an anesthesia machine in a site that had no medical gas column therefore, no site for suction for the anesthesia suction hook up. Therefore, the hose leading from the scavenging system meant for active suction of anesthetic gases from the machine to the environment was placed on the ground. The frequency of the build up of pressure could be decreased by using low flows (less than 1 L/m). However, this did not eliminate pressure build up. Therefore, periodically we were forced to disconnect the circuit from the anesthesia machine as a manual vent of a pressure build up in the anesthesia. The rationale for this will be discussed in more detail below.</p><p>The rationale for scavenging of WAGs comes from a number of studies on small concentrations of anesthetics on animals (predominantly rats) and humans. </p><p>Nitrous Oxide has been shown to increase fetal death in rats and also to result in an increased rate of rib and vertebral defects. In humans, dental assistants exposed to nitrous oxide in a setting without a scavenging system had a 59% decrease in fertility vs unexposed females. Dental assistants working with nitrous oxide and using a scavenging system had no decrease in fertility rates. The exposure limit resulting in fertility problems was at least 5 hours per week of work with nitrous oxide. Likewise, similar findings were noted for the occurrence of spontaneous abortion in exposed workers (at least 3 hours of exposure per week) vs un exposed female dental assistants (working with a scavenging system). The relative risk of spontaneous abortion was 2.6. In humans, there is no clear evidence for an increase rate of congenital abnormalities in females exposed to nitrous oxide. </p><p>Halogenated agents:</p><p>Dental assistants exposed to 8 hours per week of halogenated agents had an elevated rate of spontaneous abortion (19.1 per 100 pregnancies) vs dental assistants who worked with a scavenging system (8.1 per 100 pregnancies). The wives a dentists with heavy exposure to halogenated agents also experienced spontaneous abortion at higher rates than non exposed females (10.2 vs 6.7 events per 100 pregnancies). A subsequent study found that spontaneous abortion was increased in exposed females and spouses of exposed males to halogenated anesthetics. In this study, they are were able to determine that congenital abnormalities were also increased in female workers exposed as well as to spouses of male exposed workers. </p><p>Unfortunately, due to the difficulties in conducting an RCT that is prospective, all of the data we have currently related to the harmful effects of anesthetics are retrospective in nature and therefore, not robust. However, there are multiple different studies in both animals and humans plus the biologic plausibility of danger related to long term chronic exposure to anesthetics that lend to the credibility of the current evidence available to us.</p><p>In the above studies, it is important to note that the groups who suffered an increase in spontaneous abortion from anesthetic agents (presumably) were working in an environment where waste anesthetic gases were not scavenged, whereas, they were often times compared to workers who had access to scavenging of waste anesthetic gases. Modern day anesthesia machines all come equipped with a scavenging system to dispose of all waste anesthetic gases to the environment. It should be noted that ALL air flow (oxygen, air or nitrous) that is not consumed and metabolized by the patient will make its way into the scavenging system. Therefore, much of the problem with waste anesthetic gases can be mitigated by low flow anesthesia. The scavenging system is made up of several parts with complicated names that are not terribly helpful in understanding their function. </p><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjw5uTqItoJzsDeR3DBDJOK6k23gwAERd70gdPfkqbSFknSEQtwR8S2TejagMfRSPgpmqOjmh406CmNlopp-hyQQdqrDQTSwryLg2Didy06oPGRrKiA53alEmZpmf3ILFGgwJoBKvvivlQE/s718/Screen+Shot+2021-06-06+at+2.08.26+PM.png" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="677" data-original-width="718" height="604" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjw5uTqItoJzsDeR3DBDJOK6k23gwAERd70gdPfkqbSFknSEQtwR8S2TejagMfRSPgpmqOjmh406CmNlopp-hyQQdqrDQTSwryLg2Didy06oPGRrKiA53alEmZpmf3ILFGgwJoBKvvivlQE/w640-h604/Screen+Shot+2021-06-06+at+2.08.26+PM.png" width="640" /></a></div><div class="separator" style="clear: both; text-align: left;">The above diagram highlights how the scavenging system is incorporated into the anesthesia machine. It should be noted that when the anesthesia machine is in manual or bag ventilation mode, when the APL value "pop-off" valve is opened all the way to relieve "pressure" in the reservoir bag, the excess flow is directed into the scavenging system (which contains another reservoir bag [see figure above]). Modern day OR's have active scavenging systems. In other words, the excess flow from the anesthesia machine is hooked up to the hospital vacuum system (see figure above), and the excess gas is actively suctioned off. If there is any obstruction to this vacuum system or its tubing, you will quickly develop a build up of pressure in the reservoir bag (see figure above). This will create a back up of pressure leading to the ventilator piston (setting off an alarm as indicated above) or to the reservoir bag on the anesthesia machine. Opening the APL valve "pop-off valve", to relieve the reservoir bag will not help the problem at all since the "pop-off" valve simply leads directly to the scavenging system reservoir bag, the source of the high pressure. The scavenging interface on anesthesia machines come in two varieties. An open interface system has no valves between the interface and the outside vent. Therefore, this provides a safety mechanism in that there are no valves that can malfunction leading to pressure build up to the patient. Our anesthesia machine, The Datex Ohmeda Asys CS2, has a scavenging interface that is a closed system, and therefore, relies on a positive pressure and negative pressure relief valve. In our particular case, after removing the patient from the anesthesia ventilator, and opening the APL valve to vent excess pressure to no avail, it became evident that pressure was building up distal to the APL valve, which would be the scavenging system. The scavenging interface allowed pressure to build up until 10 cmH2O, when the positive pressure valve vented excess pressure, but after 15 seconds of continuous pressure greater than 10 cmH2O, the "PEEP high" alarm is triggered on the machine.</div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiZ5qotSwp4wA-rveRmZvS_Ws6UgnOCqcyXDmSfjHaso81NAR4PiYeNzG2VhkyECJ8NDFhSeCDySO8aVuLKj4NOtVJ9e7Epg5DCME0ZJbJ30DPjtE-RbbikCKXyP52SfgqA_zL4RKg8KRI7/s1984/Screen+Shot+2021-06-09+at+9.00.39+PM.png" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1984" data-original-width="1242" height="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiZ5qotSwp4wA-rveRmZvS_Ws6UgnOCqcyXDmSfjHaso81NAR4PiYeNzG2VhkyECJ8NDFhSeCDySO8aVuLKj4NOtVJ9e7Epg5DCME0ZJbJ30DPjtE-RbbikCKXyP52SfgqA_zL4RKg8KRI7/w400-h640/Screen+Shot+2021-06-09+at+9.00.39+PM.png" width="400" /></a></div><div class="separator" style="clear: both; text-align: left;">It turns out that the Asys CS2 also has an option for an open scavenging interface system. In this system, there would be no alarm because there would be no build up of pressure in the case of insufficienct extraction of WAGs. In these systems, they are designed so that extraction flow is greater than average waste gas flow, therefore, the hospital vacuum entrains OR air during anesthesia. There is a 2L reservoir bag to hold WAGs should extraction flow fall below waste anesthesia gas flow for any amount of time. Should this state continue until the reservoir bag is full, then WAGs would be vented to the OR proper.</div><div class="separator" style="clear: both; text-align: left;">In our situation, we needed to proceed without the ability to scavenge.We recognized the need to attempt to perfectly match the anesthesia gas flow to the patient's metabolic rate of oxygen (closed anesthesia system) or periodically vent excess pressure with disconnects of the patient from the anesthesia machine. </div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;">While modern day ORs all have active scavenging systems, there are passive systems as well. A passive system would have tubing allowing the passive flow of the WAGs from the anesthesia machine into the environment or other collecting system. All modern day ORs also must have high air exchange in order to reduce the concentration of anesthetic gases. Despite active scavenging, waste anesthesia gases (WAGs) may escape from the machine during mask ventilation, or any time the patient is disconnected from the ventilator. Obviously, high flows should be avoided to reduce excess WAGs into the ambient room air during cases when the patient can be disconnected from the anesthesia.</div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;">Low flow anesthesia (usually considered to be 1 L/m of fresh gas flow as elaborated by Foldes in 1952) and minimal flow (@ 0.5L/m) was defined by virtue in 1972. These techniques can reduce WAGs dramatically. There are the additional advantages of cost savings on the volatile anesthetics, reduction of the drying affects of high fresh gas flows on mucous membranes and avoidance of cooling the patient, as well as the reduction of WAGs in the atmosphere. Open circuit anesthesia (FGF exceeds minute ventilation (V<span style="font-size: xx-small;">m</span>), can be compared to closed circuit anesthesia where FGFs is set as low as the metabolic rate of the patient, and would, in theory, maximize the above benefits noted. There are three main contraindications to using minimal or closed circuit anesthesia. These include patients acutely intoxicated with alcohol, patients in decompensated diabetic metabolic acidosis, and patients suffering from acute carbon monoxide poisoning. The rationale is simply that the patients would be rebreathing the alcohol, acetones, or carbon monoxide respectively. Desflurane is capable of being used in low flow anesthesia with little controversy. Sevoflurane has been shown to produce compound A at low flows which caused acute tubular necrosis in rats at concentrations greater than 250 ppm. At FGFs of 1 L/min compound A is usually fond to be around 15 ppm in clinical anesthesia but the amount of compound A produced is a function of the concentration of sevoflurane delivered, the duration of exposure to the absorbent, lower FGFs, the temperature and desiccated absorbents. Since the reaction that eliminates CO2 is an exothermic reaction, as the amount of CO2 absorbed increases temperature increases linearly producing greater degradation of sevoflurane to compound A. Therefore, in spontaneously breathing patients with significant hypercarbia, the risk of elevated compound A is elevated. Howeve, recent evidence suggests that compound A is not as clinically relevant with soda lime absorbers vs baralyme [2]. Furthermore, the studies raising concerns initially, were invalidated due to the marked difference between rat and human renal biochemistry. Nevertheless, The FDA issued a lower limit FGF rate when using sevoflurane at 2 L/m when using sevoflurane for greater than 2 MACs hours. Typically, to be safe, clinicians set FGFs to at least 2 L/m when using sevoflurane. However, this doubles the cost and production of WAGs when compared to a setting of 1 L/m. I have created a quick calculator to help a clinician determine how long the anesthetic may continue with sevoflurane at low flow (1 L/min) before exceeding the FDA recommendation of 2 MAC hours (see calculator <a href="https://docs.google.com/spreadsheets/d/1zEpy_8zB6Bes1hhGxImpruJnpHW0TEiygnkcUgHwQHc/edit#gid=1808800771">here</a>). It should be noted that the studies the FDA relied upon to publish a warning label on sevoflurane were problematic and it is not clear at all that there is significant real clinical risk from compound A to humans at low FGFs. <span style="font-family: inherit;">In fact, <span style="background-color: white; caret-color: rgb(56, 54, 54); color: #383636; font-size: 16px;">The Brigham and Women’s Hospital Anesthesiology Clinical Practice Committee approved the use of sevoflurane at any fresh gas flow when CO</span><sub style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; font-size: 0.625rem; line-height: 1; margin: 0px; padding: 0px;">2</sub><span style="background-color: white; caret-color: rgb(56, 54, 54); color: #383636; font-size: 16px;"> absorbents are used that limit the added strong base. The justification was that these products permit safe, effective and planet-friendly use of low-flow or closed-circuit delivery of anesthetic agents. Similarly, the University of California, San Francisco implemented a fresh gas flow alert within the electronic medical record that notifies providers if their flows exceed 1 liter per minute and does not require a minimum fresh gas flow for sevoflurane.</span> </span></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;">Regulatory bodies:</div><div class="separator" style="clear: both; text-align: left;">OSHA does not mandate any particular scavenging system for WAGs. However, I did find this reference related to Joint commission where it states that they mandate scavenging be used when WAGs could be a problem (i.e. they are used for anesthesia). [1] In 1977, the national institute of safety and health (NIOSH) made a recommendation that workers should not be exposed to a greater than eight hour time weighted average of 2 ppm of halogenated agents. The limit is only 0.5 ppm if nitrous oxide is being used. The limit for nitrous oxide is eight hours time weighted average of 25 ppm. Obviously, the ability to make these calculations on the fly and track it is not done in the real world and would be expensive and difficult requiring the workers wear a badge of some sort that could record the exposure and then maintain that reading. To me, the message is that there is really little tolerance for any exposure and a scavenging system is mandatory for inhalation anesthesia.</div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;">The scavenging system on modern anesthesia machines actively emits anesthetics into the atmosphere. Therefore, there is a plausible concern of the effects of these hydrofluorocarbons in the atmosphere. Indeed, anesthetic gases are recognized as green house gases (GHGs). The US health care sector is responsible for about 10% of US GHG emissions. If the US healthcare sector were a country, it would rank 13th in the world for GHG emissions, ahead of the entire United Kingdom. <span style="background-color: white; caret-color: rgb(56, 54, 54); font-size: 16px;"><span style="font-family: inherit;">Kaiser Permanente, one of the nation’s largest non-governmental health care systems, has a robust sustainability program. Anesthetic gases account for 3% of the organization’s greenhouse gas emissions – over half of which was from desflurane [3].</span></span> In 2014, WAGs stood at the equivalent of 3 million tons of carbon dioxide. Greenhouse Gases (GHGs) differ in their abilities to trap heat. The effect of this heat trapping over a 100-year period is described using a scale called the global warming potential over 100 years (GWP<span style="font-size: xx-small;">100</span>). This allows a direct comparison a variety of different gases using CO2 as a baseline with a value of 1.</div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: center;">GWP<span style="font-size: xx-small;">100 </span>for several anesthetics</div><div class="separator" style="clear: both; text-align: left;">CO<span style="font-size: xx-small;">2 </span> ......................1</div><div class="separator" style="clear: both; text-align: left;">Methane..................30</div><div class="separator" style="clear: both; text-align: left;">SEVO......................130</div><div class="separator" style="clear: both; text-align: left;">N<span style="font-size: xx-small;">2</span>O ........................298</div><div class="separator" style="clear: both; text-align: left;">ISO ......................510</div><div class="separator" style="clear: both; text-align: left;">DES ......................2540</div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;">SEVO is much lower than DES in part because it remains in the atmosphere for 1.1 years vs. 14 years for Desflurane. Nitrous remains in the atmosphere for about 150 years making its GWP<span style="font-size: xx-small;">100 </span> fairly high.</div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;">To use another analogy to better put in perspective the GHG effect of anesthetics vs CO<span style="font-size: xx-small;">2</span> it is helpful to compare a typical anesthetic to driving a car some distance. As an example, a two hour anesthetic with desflurane with fresh gas flow (FGF) of 1 L/min using a 1 MAC setting would be the equivalent of driving a car 378 miles (from Los Angeles to Phoenix). The same anesthetic with sevoflurane but at double the FGF would be the equivalent of driving about 16 miles. see chart below:</div><div class="separator" style="clear: both; text-align: center;"><table border="1" cellpadding="0" cellspacing="0" style="border-collapse: collapse; border-spacing: 0px; border: 1px solid black; box-sizing: border-box; color: black; font-family: sans-serif; font-size: 16px; width: 600px;"><tbody style="box-sizing: border-box;"><tr style="box-sizing: border-box;"><td style="box-sizing: border-box; padding: 0px;"><br /><table bgcolor="#ffffff" border="0" cellpadding="6" cellspacing="0" style="border-collapse: collapse; border-spacing: 0px; border: none; box-sizing: border-box; line-height: 17.6px; width: 598px;"><tbody style="box-sizing: border-box;"><tr style="box-sizing: border-box;"><td colspan="5" style="box-sizing: border-box; font-size: 14px; font-weight: bold; line-height: 17px; padding: 6px;" valign="top">Table. One hour of anesthetic is like driving a car [how many?] miles.<span style="box-sizing: border-box; font-size: 0.6em; line-height: 0; position: relative; top: -0.6em; vertical-align: baseline;">a</span></td></tr><tr class="table_headers" style="background-color: black; box-sizing: border-box; color: white; font-size: 12px; font-weight: bold; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding-top: 3px; vertical-align: text-bottom;"><td class="table_headers" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; vertical-align: bottom;"><strong style="box-sizing: border-box;">Dose (1-MAC-hr)</strong></td><td class="table_headers" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: bottom;"><strong style="box-sizing: border-box;">Sevoflurane 2.2%</strong></td><td class="table_headers" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: bottom;"><strong style="box-sizing: border-box;">Isoflurane 1.2%</strong></td><td class="table_headers" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: bottom;"><strong style="box-sizing: border-box;">Desflurane 6.7%</strong></td><td class="table_headers" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: bottom;"><strong style="box-sizing: border-box;">N<span style="bottom: -0.25em; box-sizing: border-box; font-size: 0.6em; line-height: 0; position: relative; top: 0.2em; vertical-align: baseline;">2</span>O<span style="box-sizing: border-box; font-size: 0.6em; line-height: 0; position: relative; top: -0.6em; vertical-align: baseline;">b</span> 0.6 MAC-hour</strong></td></tr><tr class="table_text" style="box-sizing: border-box; font-size: 12px; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding-top: 3px; vertical-align: text-top;"><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; vertical-align: top;"><strong style="box-sizing: border-box;">0.5 L/min</strong></td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">—</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">4</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">93</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">29</td></tr><tr class="table_text" style="background-color: #b9e4ff; box-sizing: border-box; font-size: 12px; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding-top: 3px; vertical-align: text-top;"><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; vertical-align: top;"><strong style="box-sizing: border-box;">1.0 L/min</strong></td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">4</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">7</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">189</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">57</td></tr><tr class="table_text" style="box-sizing: border-box; font-size: 12px; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding-top: 3px; vertical-align: text-top;"><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; vertical-align: top;"><strong style="box-sizing: border-box;">2.0 L/min</strong></td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">8</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">15</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">378</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">112</td></tr><tr class="table_text" style="background-color: #b9e4ff; box-sizing: border-box; font-size: 12px; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding-top: 3px; vertical-align: text-top;"><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; vertical-align: top;"><strong style="box-sizing: border-box;">5.0 L/min</strong></td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">19</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">38</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">939</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">282</td></tr><tr class="table_text" style="box-sizing: border-box; font-size: 12px; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding-top: 3px; vertical-align: text-top;"><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; vertical-align: top;"><strong style="box-sizing: border-box;">10.0 L/min</strong></td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">38</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">74</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">1,876</td><td class="table_text" colspan="1" style="box-sizing: border-box; line-height: 16px; margin-bottom: 0px; margin-top: 0px; padding: 3px 6px 6px; text-align: center; vertical-align: top;">564</td></tr><tr class="table_refs" style="box-sizing: border-box;"><td class="table_refs" colspan="5" style="border-top-color: black; border-top-style: solid; border-top-width: 1px; border-top: 1px solid black; box-sizing: border-box; font-size: 10px; line-height: 13px; margin-bottom: 0px; margin-top: 0px; padding: 6px; vertical-align: top;"><div -0.6em="" 0.6em="" baseline="" font-size:="" position:="" relative="" style="box-sizing: border-box; padding-left: 8px; text-indent: -8px;" top:="" vertical-align:="">a Assumes EPA 2012 fuel efficiency average of 23.9 miles per gallon.</div><div -0.6em="" 0.6em="" baseline="" font-size:="" position:="" relative="" style="box-sizing: border-box; margin-top: 5px; padding-left: 8px; text-indent: -8px;" top:="" vertical-align:="">b Because N<span style="bottom: -0.25em; box-sizing: border-box; font-size: 0.6em; line-height: 0; position: relative; top: 0.2em; vertical-align: baseline;">2</span>O cannot be delivered at 100%, the more typical percentage of 60% is used. In combination, 0.6 MAC-hour of N<span style="bottom: -0.25em; box-sizing: border-box; font-size: 0.6em; line-height: 0; position: relative; top: 0.2em; vertical-align: baseline;">2</span>O would be added to 0.4 MAC-hour of a volatile.</div><div style="box-sizing: border-box; margin-top: 5px;"><strong style="box-sizing: border-box;">EPA,</strong> Environmental Protection Agency; <strong style="box-sizing: border-box;">MAC,</strong> minimal alveolar concentration; <strong style="box-sizing: border-box;">N<span style="bottom: -0.25em; box-sizing: border-box; font-size: 0.6em; line-height: 0; position: relative; top: 0.2em; vertical-align: baseline;">2</span>O,</strong> nitrous oxide</div></td></tr></tbody></table></td></tr></tbody></table></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;">After the choice of anesthetic, the FGF used is the next most important determinant of the carbon footprint of a typical anesthetic. Any anesthetic with FGF beyond the metabolic needs and system requirements will be vented into the atmosphere as described earlier via the scavenging system. Thus, if you double the FGF of sevoflurane from 1 l/m to 2 l/m, the output of CO2 equivalent GHG is doubled for sevoflurane and for desflurane. Adding N<span style="font-size: xx-small;">2</span>O to the anesthetic, but keeping the FGFs equivalent, will increase the CO<span style="font-size: xx-small;">2</span> equivalent emissions by 20 times. Therefore, the ability to decrease the concentration of the halogenated agent because of the N<span style="font-size: xx-small;">2</span>O does not come close to compensating. Furthermore, N<span style="font-size: xx-small;">2</span>O is known to deplete the ozone layer in the atmosphere.</div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;">However, to put this all into perspective, an equivalent of 6% of global carbon dioxide emissions result from nitrous oxide, where 1% of these are medicinal. Furthermore, as a waste anesthetic gas, N<span style="font-size: xx-small;">2</span>O contributes roughly 0.1% of the whole GHG. In addition, N<span style="font-size: xx-small;">2</span>O contributes by far, the largest amount to GHG when compared to all waste anesthetic gases as the consumption values of N<span style="font-size: xx-small;">2</span><span style="font-size: medium;">O far exceed those of other anesthetic gases.</span></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;">From a GHG perspective the perfect inhalation anesthetic would be Xenon which acts via inhibition of calcium pumps in cell membranes which may increase intraneuronal calcium concentrations altering excitability. Xenon also inhibits NMDA receptors, as well as nicotinic acetylcholine receptors. Other beneficial characteristics of Xenon include:</div><div class="separator" style="clear: both; text-align: left;"><ul style="text-align: left;"><li>non-flammable and non-explosive</li><li>Rapid onset/offset (partition co-efficient of 0.12 (lowest of all anesthetics)</li><li>Zero metabolism, low toxicity, and devoid of teratogenicity.</li><li>Produces high regional blood flow in brain, liver, kidney and intestine.</li><li>Neuroprotective</li><li>Lacks cardiovascular depression</li></ul>So why doesn't Xenon replace all current inhalation anesthetics? It costs $10.00/Liter, far more than current inhalation agents.</div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;">In summary, when performing anesthesia outside of the regular OR, the anesthesia provider will be forced to determine if WAGs are scavenged as it is likely this component has been forgotten. WAGs have a real, although small, negative health effect over time on exposed personnel. Regulatory bodies demand that WAGs be eliminated in the anesthetizing location as best as possible which requires scavenging. Anesthesia technique, utilizing low FGFs, etc can reduced exposure of the OR worker as well as mitigate to some degree contaminants into the environment.</div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;">1. <a href="https://healthprofessions.udmercy.edu/academics/na/agm/10.htm">https://healthprofessions.udmercy.edu/academics/na/agm/10.htm</a></div><div class="separator" style="clear: both; text-align: left;">2. <span style="background-color: white; font-family: "Times New Roman", stixgeneral, serif; font-size: 15.9991px;">Kharasch ED, Powers KM, Artru AA. Comparison of Amsorb, Sodalime, Baralyme degradation of volatile anesthetics and formation of carbon monoxide and compound in swine </span><em style="font-family: "Times New Roman", stixgeneral, serif; font-size: 15.9991px;">in vivo</em><span style="background-color: white; font-family: "Times New Roman", stixgeneral, serif; font-size: 15.9991px;">. </span><span style="font-family: "Times New Roman", stixgeneral, serif; font-size: 15.9991px;"><span class="ref-journal" style="font-style: italic;">Anesthesiology. </span>2002;<span class="ref-vol">96</span>:173–82</span></div><div class="separator" style="clear: both; text-align: left;"><span style="font-family: "Times New Roman", stixgeneral, serif; font-size: 15.9991px;">3. <a href="https://pubs.asahq.org/monitor/article/84/4/14/108428/Inhaled-Anesthetic-2020-Challenge-Reduce-Your">https://pubs.asahq.org/monitor/article/84/4/14/108428/Inhaled-Anesthetic-2020-Challenge-Reduce-Your</a></span></div><div class="separator" style="clear: both; text-align: left;"><span style="font-family: "Times New Roman", stixgeneral, serif; font-size: 15.9991px;"><br /></span></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;"><a href="https://docs.google.com/spreadsheets/d/1zEpy_8zB6Bes1hhGxImpruJnpHW0TEiygnkcUgHwQHc/edit?usp=sharing">cost of different settings: dollars and CO2 equivalent warming</a></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;"><br /></div><div class="separator" style="clear: both; text-align: left;"><br /></div><br /><p></p><p><br /></p><p><br /></p>Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-63068814759025823932020-05-18T18:35:00.001-07:002020-05-21T18:03:04.599-07:00severe bronchospasm after induction in obese female<span style="font-family: Georgia, Times New Roman, serif;">Sunday afternoon the friendly GI doc boarded a case for an urgent ERCP in a 31 year old female with choledokolithiasis. She had elevated liver enzymes and he was concerned that she might develop ascending cholingitis. The patient had hypothyroidism and was morbidly obese with a weight of apporoximately 320 lbs and was 5'3". We proceeded to the OR after 2 mg versed, 100 mcg fentanyl and 4 mg decadron were given as a premed. In the OR after monitors were applied, pre oxygenation in the reverse T - burg position with HOB up at 30 degrees was accomplished. Induction with 150 mg of propofol and succinylcholine (100mg) was used. Intubation was easy grade I view. However, She immediately desaturated (less than 60 seconds). Manual ventilation was begun to expand lung units, and sevoflurane was begun and saturations slowly climbed to the high 90's. Within 4 to 5 minutes, the patient began moving slightly. I immediately went to increase the sevoflurane, but noticed at this point that the vaporizer was completely empty. Unfortunately, the machine only allowed one vaporizer at a time to be inserted into the port. Therefore, I had to remove the sevo cartridge and insert the cartridge with desflurane. The patient was now starting to move and cough, causing her to desaturate again. I overpressurized the desflurane to quickly deepen the anesthetic to prevent further coughing and bucking on the ETT. The patient, again desaturated significantly (down into the 60's). With careful and aggressive manual ventilation to expand all alveoli units, her sats slowly started to climb and the desflurane was able to be delivered. In an attempt to quickly deepen the anesthesia, I had turned the desflurane up to 10%. After getting her sats back up into the 90's, I switched again to machine ventilation with pressure control of 29 and PEEP of 9 mmHg. However, within a short period, her sats began to fall again. I decreased the desflurane to 6% and once again took over manual ventilation. I perceived that indeed her compliance was very poor. I quickly verified once again that her ETT was not in too deep (i.e. right main stemmed), and that there were no kinks in the ETT. I also gave 40 mg of rocuronium to ensure that she wasn't fighting the ventilator and rule out any chest wall contribution to poor compliance. With careful high pressure ventilation I was able to achieve large tidal volumes (not achievable with the anesthesia machine despite high pressure settings in pressure control ventilation). Her saturations again trailed down into the 60's. At this time the ERCP was underway, and the endo team was particularly involved with the procedure. The anesthesia tech had left for the day (I'm not sure why). I suspected bronchospasm at this point (previously thinking I was dealing with atelectisis with shunt due to morbid obesity). Therefore, I asked for help in filling the vaporizer. During this time I was forced to put her back on the ventilator with saturations in the 80's. I quickly filled the sevo vaporizer, and switched the desflurane cartridge for sevoflurane. I dialed in a 4% concentration with high FGF (i.e. 5 l/m). After about five minutes, her compliance began to improve, her saturations slowly improved for the remainder of the case. Now that I could rely on mechanical ventilation, I was free to grab some albuterol and hook up a make shift nebulizer treatment via the ETT and ventilator which required some creative hookups to achieve success. The case lasted about 50 min. At the end of the case, compliance was pretty near normal levels with normal saturation's. However, the patient was still weak from the very large dose of rocuronium given to ensure improved compliance. Given that she only had one twitch and the Concern for airway patency, I administered 200 mg suggamadex. I followed this dose with a subsequent dose of 100 mg to achieve full reversal in about 3 minutes. The patient went to PACU extubated on face mask O2 and saturations at 100%. </span><br />
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<span style="font-family: Georgia, Times New Roman, serif;">This case highlights the interplay of obesity, asthma (bronchospasm/reactive airway disease) and desflurane. </span><br />
<span style="font-family: Georgia, Times New Roman, serif;">Obesity has reached epidemic proportions in the US. Super obese patients require surgery for a variety of problems and can present unique problems for the anesthesia team. In this case, the patient reported no significant past medical history with the exception of hypothyroidism. However, severe hypoxemia was encountered almost immediately after induction, which was exacerbated by significant bronchospasm likely brought on by high (overpressurization) concentrations of desflurane. </span><br />
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<span style="font-family: Georgia, Times New Roman, serif;">Pathophysiology of the obese state</span><br />
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<span style="font-family: Georgia, Times New Roman, serif;"><span style="background-color: white;">Excess adipose tissue is associated with the production of various proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1-β (IL-1β), and interleukin-6 (IL-6).</span><span style="background-color: white;"> TNF-α plays a critical role in the inflammatory response of the immune system as well as in the apoptosis of adipose cells, lipid metabolism, hepatic lipogenesis, and the induction of oxidative stress. Increased levels of TNF-α promote a response via the release of IL-6, another proinflammatory molecule, and the reduction of levels of anti-inflammatory cytokines such as adiponectin. TNF-α also increases the interaction of electrons with oxygen, generating superoxide anions. TNF-α levels are elevated in obese individuals and decrease with weight loss [1]. Furthermore, </span><span style="color: #333333; font-family: "georgia" , "palatino" , serif; font-size: 18px;">Adipose tissue is a source of several bioactive adipokines, including leptin, adiponectin, visfatin, resistin, apelin, and type I plasminogen activation inhibitor (PAI-I). These adipokines are directly associated with physiological and pathological processes involving oxidative stress [2]. </span><span style="background-color: white;">Rasslan et al. [3</span><span style="background-color: white;"><span style="color: #333333; font-family: "georgia" , "palatino" , serif; font-size: small;"><span style="caret-color: rgb(51, 51, 51);">] observed that adipose tissue is an endocrine and paracrine organ that produces many cytokines and bioactive mediators, resulting in a pro-inflammatory state that may be associated with pulmonary hypoplasia, atopy, hyper reactive bronchi, and increased risk of asthma in obese individuals. Leptin is one hormone elevated in the obese state, likely related to leptin resistance and consequent overproduction. </span></span></span><span style="background-color: white;"> L</span><span style="background-color: white;">eptin crosses the blood brain barrier and serves as an afferent signal, originating from the adipose tissue, engaging distinct hypothalamic effector pathways to suppress appetite and augment energy expenditure. Therefore, leptin is an important negative feedback loop in controlling appetite to prevent obesity. </span><span style="background-color: white;"><span style="color: #333333; font-family: "georgia" , "palatino" , serif; font-size: small;"><span style="caret-color: rgb(51, 51, 51);">Leptin resistance has been shown to enhance parasympathetic tone which increases airway reactivity and obesity associated asthma [8]. </span></span></span><span style="background-color: white;">In addition, hyperleptinemia was proposed to be a crucial factor leading to respiratory failure in leptin-resistant obese subjects [9]. </span><span style="background-color: white;"> </span><span style="background-color: white;"><span style="color: #222222; font-family: "lora" , "palatino" , "times" , "times new roman" , serif; font-size: small;">Meta-analyses have further implicated a positive relationship between serum leptin and the risk of asthma. Of note, the link with obesity and airway hyper responsiveness is much stronger in females than males. Furthermore, it has been shown that </span></span><span style="background-color: white;">Leptin expression is inhibited by testosterone, whereas it is increased by ovarian sex steroids</span><span style="background-color: white;"><span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445312px;"> and therefore, leptin is higher in females than age and body mass index (BMI) matched males. Of note, leptin also plays a role in central respiratory function. Injection of leptin into the nucleus of the tractuss solitarius increases minute ventilation in addition to enhanced bioelectrical activity of the respiratory muscles. This seems to indicate that in obesity with leptin resistance, patients will be at much higher risk for OSA partially related to the inability of the brain to react to high leptin levels. </span></span></span><span style="background-color: white;">In obese patients, hyperleptinemia is associated with a reduction in respiratory drive and hypercapnic response, irrespective of anthropometric measurements</span><span style="background-color: white;"><span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445312px;"> while circulating leptin is a predictor for the presence of hypercapnia. Furthermore, as discussed </span></span></span><span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445312px;">above, high leptin levels result in the production of a number of cytokines that induce inflammation. A</span></span><span style="background-color: white;">dministration of leptin to wild-type mice enhances O</span><span style="bottom: -0.25em; line-height: 1.6363em; position: relative; top: 0.25em; vertical-align: baseline;">3</span><span style="background-color: white;">-induced airway inflammation (in other words, airways are hyper reactive in mice who are given exogenous leptin). In summary, while the evidence relating leptin levels to lung and respiratory pathology is mixed, there seems to be a general preponderance of studies linking obesity, leptin resistance (i.e. elevated leptin levels) and hyper responsive airways. </span></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEijVz7r6PSfM4hlJVKbCXHIeEkq2ZrrhW7uaV_XoKr5CLGT1T42JZ0NLHR5qJla8m1ogtlW_7qjXQXiA8lM027PLFJwsOBQgD3m2WlMxFyM8BTTVRqsOjlWkubot_wU13CMY0otuFMscoqQ/s1600/Screen+Shot+2020-05-15+at+9.03.21+PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><span style="color: black; font-family: Georgia, Times New Roman, serif;"><img border="0" data-original-height="1178" data-original-width="1600" height="470" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEijVz7r6PSfM4hlJVKbCXHIeEkq2ZrrhW7uaV_XoKr5CLGT1T42JZ0NLHR5qJla8m1ogtlW_7qjXQXiA8lM027PLFJwsOBQgD3m2WlMxFyM8BTTVRqsOjlWkubot_wU13CMY0otuFMscoqQ/s640/Screen+Shot+2020-05-15+at+9.03.21+PM.png" width="640" /></span></a></div>
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<span style="font-family: Georgia, Times New Roman, serif;">However, the situation is yet more complicated. It is known that obese women have higher levels of estrogen than their non obese counterparts. Elevated estrogen is also known to be an independent risk factor for asthma. Furthermore, adiponectin seems to have the exact opposite effect as leptin in the body, i.e. inhibits the production of IL-6, TNA-alpha and other pro inflammatory mediators. <span style="color: #666666; font-family: "open sans" , sans-serif;"><span style="caret-color: rgb(102, 102, 102);"> Studies have noted that adiponectin levels are reduced in asthma </span></span><span style="color: #666666; font-family: "open sans" , sans-serif; font-size: 16px;"> and reduced in subjects with low lung function. However, this was true only in women. Low adiponectin levels are found in obese patients. </span></span><br />
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<span style="color: #666666; font-family: "open sans" , sans-serif; font-size: 16px;">Therefore, the obese state creates altered hormonal levels from the non obese state that have a pro inflammatory effect and promote hyper responsive airways.</span></span><br />
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<span style="font-family: Georgia, Times New Roman, serif;">In addtion to the above described endocrine pathology of obesity, Mafort et al. evaluated 30 patients and showed that the primary change in lung volume was reduced end respiratory volume. In the morbidly obese, FVC and FEV1 were both reduced. However, obesity has been associated with a higher incidence, prevalence and severity of asthma and with altered pulmonary function, poor treatment response, and high morbidity. The increased incidence is correlated with BMI in that there is a 35% increase in the risk of asthma with each 3 unit increase in BMI. Further derangements of lung function in obese individuals have been identified. Radial traction of lung parenchymal attachments around the airways is attenuated at low lung volumes contributing to airway collapse. Breathing at low lung volume is a hallmark of respiration in morbid obesity. When an obese patient goes from standing to supine, there is no further decrease in FRC and expiratory reserve volume (contrary to what is seen in lean people). But, Airway resistance increases with decreased expiratory flow. As intrinsic (or auto) PEEP develops, work of breathing (WOB) increases and the supine obese patient develops a mixed respiratory pathology of restrictive and obstructive etiology. In the supine obese patient oxygenation is particularly affected by breathing at low lung volumes where expiratory reserve volume approaches residual volume. A decreased expiratory capacity seems to be the primary cause of decreased ventilation/perfusion ratios causing significant and rapid hypoxemia after induction of anesthesia. Therefore, pre oxygenation with pressure support and PEEP in a head up (at least 25 degrees), can increase safe apnea time. After intubation, recruitment maneuvers with titrated PEEP can optimize oxygenation. Obese patients are far more susceptible to ventilator induced lung injury (VILI) due to the potential for high driving pressures to ensure adequate ventilation. The dual concepts of static stress and dynamic strain on the lungs come into play both adding to the risk of VILI. By titrating PEEP appropriately, both of these can be mitigated to a degree. Large PEEP values (at least 12 cmH20) may be needed, however. As the degree of end expiratory lung pressures increase, the right ventricle will be exposed to increased afterload. However, at very low lung volumes, right afterload is also increased due to collapsed vasculature. Therefore, the obese patient will need to be well hydrated to counter act the potential negative CV effects of increased levels of PEEP.</span><br />
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<span style="font-family: Georgia, Times New Roman, serif;">There is evidence that metabolic syndrome (obesity, insulin resistance, atherogenic dyslipidemia and hypertension), is a key contributor to worsening lung function. Metabolic syndrome shares a great deal of pathologic features with polycystic ovary syndrome. This 31 y/o female also had PCOS. See graph: </span></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi9n9sSAVplCHQVeKDjAbVt6660ontZJDSga2EFW0qMa8TDMNxqqO6f_DSzBobIahAtjfbI8DMnNFxdmRm_Od-Rp_KhiWsOjIb9LpBK_luSWfg8kPvj2lkxbQeRdozFgJQ62i2CDYe3OMay/s1600/Screen+Shot+2020-05-15+at+9.23.39+PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><span style="color: black; font-family: Georgia, Times New Roman, serif;"><img border="0" data-original-height="1048" data-original-width="1052" height="636" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi9n9sSAVplCHQVeKDjAbVt6660ontZJDSga2EFW0qMa8TDMNxqqO6f_DSzBobIahAtjfbI8DMnNFxdmRm_Od-Rp_KhiWsOjIb9LpBK_luSWfg8kPvj2lkxbQeRdozFgJQ62i2CDYe3OMay/s640/Screen+Shot+2020-05-15+at+9.23.39+PM.png" width="640" /></span></a></div>
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<span style="font-family: Georgia, Times New Roman, serif;">In the end, airway hyperesponsiveness, reduced lung volume, air trapping, auto peep, increased inflammation, and increased work of breathing all contribute to reduced pulmonary reserve in obese individuals with worsening pathology at greater BMIs. Airway hyperresponsiveness was found in a study of obese patients undergoing laparoscopic surgery. In this study, obese patients had an incidence of bronchospasm of 12% vs. 0% in non obese patients. </span></div>
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<span style="font-family: Georgia, Times New Roman, serif;">The anatomy of airway hyper responsiveness as experienced in this case of acute intraoperative bronchospasm is demonstrated with the following graphic.</span></div>
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<span style="font-family: Georgia, Times New Roman, serif;">While obesity does increase airway responsiveness, anesthetic vapors also effect airway responsiveness. Back in 1997, Rooke at al. [5] showed that Sevoflurane reduced airway resistance after intubation more than Halothane or Isoflurane. In 2000, Desflurane was compared head to head with Sevoflurane to determine airway resistance after intubation, and shown to increase airway resistance while Sevoflurane was able to reduce airway resistance [6]. (see graphic)</span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEisUgz6ErL-7kjMURN2yiKlYZCbPrWjFvuc9eGvx0BTNgMrq4_iE_Jtp4lnFhI2mio3LEarmKT1wj2tXTuOKkcaGkDy-0G03L_xkk4wm-A0umjKEswEJogfK30jrAWx_kSXV54xndGieyqn/s1600/Screen+Shot+2020-05-16+at+4.10.44+PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><span style="color: black; font-family: Georgia, Times New Roman, serif;"><img border="0" data-original-height="580" data-original-width="1600" height="232" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEisUgz6ErL-7kjMURN2yiKlYZCbPrWjFvuc9eGvx0BTNgMrq4_iE_Jtp4lnFhI2mio3LEarmKT1wj2tXTuOKkcaGkDy-0G03L_xkk4wm-A0umjKEswEJogfK30jrAWx_kSXV54xndGieyqn/s640/Screen+Shot+2020-05-16+at+4.10.44+PM.png" width="640" /></span></a></div>
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<span style="background-color: white; font-family: Georgia, Times New Roman, serif;">It should be noted, that the majority of the increase in degree of airway resistance in patients receiving Desflurane were in those who were smokers. Even still, non smoking patients who received Desflurane saw no decrease in airway resistance like those who received Sevoflurane. In 2008, a study [7] in pediatric patients comparing Desflurane to Sevoflurane in normal patients and in those with airway senstivities was able to show that Sevoflurane decreased airway resistance slightly in both groups, while Desflurane increased airway resistance. (graphic)</span><br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhJ1gxM4sIOhuvjiMjhS1wWCbiXiM3xD-GXvX4Ox25rTFCmQl9MMeqxOXNVp_fMmCWEWBRBVY6M5x1uIxj8CxZK6xHeuz96EajlPANUQq9zdEgNFYDyfFgg3Pe6EeijNIgYkwelBtldlhOI/s1600/Screen+Shot+2020-05-16+at+4.22.18+PM.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><span style="color: black; font-family: Georgia, Times New Roman, serif;"><img border="0" data-original-height="676" data-original-width="1474" height="292" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhJ1gxM4sIOhuvjiMjhS1wWCbiXiM3xD-GXvX4Ox25rTFCmQl9MMeqxOXNVp_fMmCWEWBRBVY6M5x1uIxj8CxZK6xHeuz96EajlPANUQq9zdEgNFYDyfFgg3Pe6EeijNIgYkwelBtldlhOI/s640/Screen+Shot+2020-05-16+at+4.22.18+PM.png" width="640" /></span></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="font-family: Georgia, Times New Roman, serif; font-size: small;">light bar is normal patient, and the dark bar are patients with airway sensitivity.</span><br />
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<span style="font-family: Georgia, Times New Roman, serif;"><span style="background-color: white;"><br /></span><span style="background-color: white;">More recently, a case series in the PICU was able to show that in six children with life threatening asthma exacerbations, Sevoflurane successfully relieved bronchospasm and all children made improvement except one who was later diagnosed with ARDS and required NO. Consequently, while desflurane has a superior recovery profile vs Sevoflurane in obese patients due to its very low solubility co efficient in blood and fat, in some patients, the potential for increased airway resistance may present problems. In my patient, who was super obese, a severe bronchospasm was elicited after introduction of Desflurane with overpressurization. Sevoflurane was able to break this bronchospasm successfully. The patient was required to return for a lap chole three days after her ERCP. The team used sevoflurane. I arrived towards the end of the case to relieve the provider who had started the case. On the hand over report I was told that she had saturated in the high 80's for much of the case, but this improved to mid 90's after the evacuation of the pneumoperitoneum. She was maintained on Sevoflurane, and upon emergence and transfer to the PACU she did well although she required oxygen. On POD #2, she required an additional ERCP due to more stones found in the duct. After intubation, recruitment breaths were used, and she was placed on 9 cmH20 of PEEP with pressure control ventilation of 30 cm H20. Sevoflurance at 2.4% was used. She did not experience any evidence of bronchospasm, and saturations were maintained at 98% on Fio2 of 0.85. She was extubated at the end of the case and went to PACU without incident. </span></span><br />
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<span style="background-color: white;">1. </span><span style="background-color: white;">Möller K, Ostermann AI, Rund K, Thoms S, Blume C, Stahl F, et al.</span><span style="background-color: white;"> </span><span style="background-color: white;">Acids. 2016;106:39–49.</span></span><br />
<span style="font-family: Georgia, Times New Roman, serif;"><span style="background-color: white;">2. </span><span style="background-color: white;">Marseglia L, Manti S, D’Angelo G, Nicotera A, Parisi E, Di Rosa G, et al.</span><span style="background-color: white;"> </span><span style="background-color: white;">Int J Mol Sci. 2014;16:378–400.</span></span><br />
<span style="background-color: white; font-family: Georgia, Times New Roman, serif;">3. Rasslan Z, Stirbulov R, Lima CA, Saad JR. Lung function and obesity. Rev Bras Clínica Médica. 2009;7:36–9.</span><br />
<span style="color: #333333; font-family: "georgia" , "palatino" , serif;"><span style="background-color: white; caret-color: rgb(51, 51, 51); font-family: Georgia, Times New Roman, serif;">4. Grassi L, Kacmarek R, Berra L. <i>Anesthesiology.</i> 2020;132:1246-56.</span></span><br />
<span style="font-family: Georgia, Times New Roman, serif;"><span style="color: #333333; font-family: "georgia" , "palatino" , serif;"><span style="background-color: white; caret-color: rgb(51, 51, 51);">5. </span></span><span style="background-color: white;">Rooke GA, Choi J-H, Bishop MJ: . <i>anesthesiology </i>1997; 86:1294–9</span></span><br />
<span style="font-family: Georgia, Times New Roman, serif;"><span style="background-color: white;">6. Goff MJ, et al. </span><span class="journal-name" style="box-sizing: border-box; line-height: 1.4; word-wrap: break-word;"><i>Anesthesiology</i></span><span style="box-sizing: border-box; line-height: 1.4; word-wrap: break-word;"> 2000, Vol.93, 404-408</span></span><br />
<span style="font-family: Georgia, Times New Roman, serif;"><span style="box-sizing: border-box; line-height: 1.4; word-wrap: break-word;">7. von Ungern-Sternberg BS, Saudan S, Petek F. et al. </span><span class="journal-name" style="box-sizing: border-box; line-height: 1.4; word-wrap: break-word;"><i>Anesthesiology</i></span><span style="box-sizing: border-box; line-height: 1.4; word-wrap: break-word;"> 2008, Vol.108, 216-224</span></span><br />
<span style="font-family: Georgia, Times New Roman, serif;"><span style="box-sizing: border-box; line-height: 1.4; word-wrap: break-word;">8. </span><span style="background-color: white;">Arteaga-Solis, E. </span><i style="caret-color: rgb(34, 34, 34); color: #222222; font-family: Lora, Palatino, Times, "Times New Roman", serif; font-size: 16px;">et al</i><span style="background-color: white;">. </span><i style="caret-color: rgb(34, 34, 34); color: #222222; font-family: Lora, Palatino, Times, "Times New Roman", serif; font-size: 16px;">Cell Metab<span style="background-color: white;">. 2013;</span></i><span style="color: #222222; font-family: "lora" , "palatino" , "times" , "times new roman" , serif; font-size: 16px;">17</span><span style="background-color: white;">, 35–48 </span></span><br />
<span style="font-family: Georgia, Times New Roman, serif;"><span style="background-color: white;">9. </span><span style="background-color: white;">Phipps, P. R., Starritt, E., Caterson, I. & Grunstein, R. R. </span><i style="caret-color: rgb(34, 34, 34); color: #222222; font-family: Lora, Palatino, Times, "Times New Roman", serif; font-size: 16px;">Thorax</i><span style="background-color: white;"> </span><span style="color: #222222; font-family: "lora" , "palatino" , "times" , "times new roman" , serif; font-size: 16px;">57</span><span style="background-color: white;">, 75–76 (2002).</span></span><br />
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Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-30209229031701329892020-05-01T16:00:00.000-07:002020-05-01T16:00:42.844-07:00ramping up elective cases as COVID-19 ramps up as wellAs the Anesthesia Chair at a small community hospital I have been involved in helping to make decisions about how to ramp up elective cases as Government Abbot's decision to cancel elective cases comes to an end. We are scheduled to begin regular cases on May 1st as we certified that we would comply with all of the requirements in order to do so.<br />
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I work for a large anesthesia group that has communicated recommendations on how we should protect ourselves as we ramp up. Some of the recommendations have caused me to think about the rationale behind them a little more in depth to see whether they may apply to our community hospital.<br />
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The current recommendation in general is that all patients should be tested using RT PCR as well as tested for IgM/IgG antibodies. The idea behind this is to reduce the chance of transmission of infection from an asymptomatic patient who has COVID-19 and also reduce the burden of PPE burden. The general recommendation however, continues on that it is recommended in asymptomatic patients who test negative via both serology and PCR (also known as molecular testing) that providers who intubate/place an LMA for surgery should don an N95 mask and gloves per the usual method as we now do for untested patients. Furthermore, it is still recommended to don maximal barrier protection (i.e. face shield, double gloves, gown, n95 or PAPR) in cases on the respiratory tract such as bronchoscopies, ent etc even if the patient has tested negative using both PCR and serology.<br />
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The argument put forward for this recommendation relates to the sensitivity of the two tests. Our gurus have quoted a sensitivity of 98.6 % when the two tests are done together. However, I do not believe this gives us a full picture of the actual risk to any given patient under our care. First of all, as clinicians in practice, we really don't care about the sensitivity of any test except to use it in the calculation of the negative predictive value of our test. The negative predictive value relates to Baye's rule where the pretest probability of the disease is considered. In this case, we are concerned with asymptomatic patients, no known contact with a COVID-19 positive patient living in our local community who has not traveled or taken excessive risk related to work environment etc. The pretest probability in this case is simply the current prevalence of disease in the community. Unfortunately, we don't really know the current prevalence in real time because it is changing everyday. Fortunately, my county publishes daily the prevalence in all of the individual surrounding communities. Currently, the prevalence is 1%. This can be doubled (to account for positive patients who have not been tested). After considering the prevalence, the negative predictive value can change dramatically given the same sensitivity.<br />
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Understanding why we do what we do in the OR to prevent transmission of infection is important and should be based on rational science underlying infectious disease. The first principal of infectivity of any pathogen has to do with inoculum: A larger inoculum of pathogen is more likely to cause an infection than a lower inoculum. The second principal considers how virulent the pathogen is.<br />
The reason that Sars CoV-2 has been so easily transmitted is tied to the ability of the host's viral load to reach near peak levels prior to the symptom onset. (See graph)<br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjtk-MAe5QkZfjafx1DQ-GgLblqB08RWhmKRUrOOiAyOHl0baYxRyanxufgYAMQngAqfh8x5ajLcxb739ROhXtRSGYPAPY8fmdP2t_bLYaTlfZEKbNG0SaktxFAwy7jcCjOXepTFNcbr2IP/s1600/Screen+Shot+2020-04-29+at+3.09.54+PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="521" data-original-width="919" height="362" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjtk-MAe5QkZfjafx1DQ-GgLblqB08RWhmKRUrOOiAyOHl0baYxRyanxufgYAMQngAqfh8x5ajLcxb739ROhXtRSGYPAPY8fmdP2t_bLYaTlfZEKbNG0SaktxFAwy7jcCjOXepTFNcbr2IP/s640/Screen+Shot+2020-04-29+at+3.09.54+PM.png" width="640" /></a></div>
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From ASA townhall</div>
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Therefore, SARS-CoV-2 is very contagious largely because asymptotic individuals can have very high viral loads allowing them to deliver a large inoculum without realizing it. Therefore, the ability to detect viral burden in a patient without symptoms can aid us in determining how to handle the person in question. Unfortunately, as per the slide above, PCR will only detect virus (turn positive) if the viral load is relatively high AND the test is done correctly. When the specimen is collected in appropriately, or the viral load is low ( i.e. it's day one of the infection), then the test will indicate negative while the patient is really infected. This results in published sensitivities of anywhere from 60% to 90%. The important point to keep in mind about sensitivity and specificity is that they are characteristics of the test, and have nothing to say about the population the test is used in. (Sensitivity = Tp/Tp+Fn) We really need to calculate the negative predictive value of our negative result. For this we need to know the prevalence in our community (or the community in which the patient resides and spends most of their time). In my community, the current prevalence is less than 1%, but I'm going to assume 2% for a margin of safety and to presume a higher real prevalence due to lack of testing of all individuals in the community. So lets go through what we are looking at with negative predictive value: </div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhDA5ECb6ETr9M-nx_UIZvua8U9v5XGz1X-gyjEy3g4bSj7bYzM_Fqopkv9S80lMymFqRcLOAXAVK_nODBRbnUQPY3A69CrAkXxhjexMuu0XdhTXmFfqyTPSp-c6a29Xcqkt9c98E4YAUHZ/s1600/Screen+Shot+2020-04-29+at+3.40.34+PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="379" data-original-width="829" height="292" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhDA5ECb6ETr9M-nx_UIZvua8U9v5XGz1X-gyjEy3g4bSj7bYzM_Fqopkv9S80lMymFqRcLOAXAVK_nODBRbnUQPY3A69CrAkXxhjexMuu0XdhTXmFfqyTPSp-c6a29Xcqkt9c98E4YAUHZ/s640/Screen+Shot+2020-04-29+at+3.40.34+PM.png" width="640" /></a></div>
The above graphic illustrates our example and shows the relevant formulas to calculate the relevant results. In our hypothetic case, if we assume that the PCR test has a sensitivity of 85% and we assume a prevalence of 2%, the negative test result tells us that the the actual chance of you actually encountering a patient who is infected is three patients for every 1,000 you care for. Of course, that is still not the whole story. You also have to consider the risk for you personally. For example, are you a healthy 35 year old female? Are you a 60 year male on corticosteroids for a chronic disease, with hypertension, DM and obesity? The 35 year female who is infected with SARS-CoV-2 is likely to have a very different clinical course than the 60 year male as described. It should be noted that males who acquire SARS-CoV-2 tend to have a much higher mortality. It could be argued however, that wearing an N95 mask for intubation and extubation is still reasonable. It could be argued that guidance to have OR staff stay clear of the patient during intubation and extubation is also reasonable. However, some facilities have taken a very conservative stance and are demanding that after intubation or extubation, a full 20 minutes should pass prior to allowing any OR staff to enter the room. I will touch on this policy at the end of this article. additional cost was invested into having the patient arrive 72 hours prior to scheduled surgery to have a swab performed for PCR testing. (The test should be done at least 72 hours prior to surgery because of the above graph showing how patients may be in the early phase of infection resulting in low viral shedding and thus a negative PCR test). This is where the prevalence in your community plays a role. If the prevalence is 15% in the community and the patient is known to have a known COVID-19 contact, the NPV is different: see graph:<br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhbglbOILhnCyuSnkUB2wODPFuZJ3geLxf_vMe5IGhZ6nafhnlfafM1SePh9Yhb9KH1WO4P7JdN9ZXHQW2NkcOBAHbXt45u1rfIv7Tdl03QiK1YMXgUpmL7zzqiaDmJh9e-WDDqIxItmjL1/s1600/Screen+Shot+2020-04-29+at+3.56.41+PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="380" data-original-width="827" height="294" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhbglbOILhnCyuSnkUB2wODPFuZJ3geLxf_vMe5IGhZ6nafhnlfafM1SePh9Yhb9KH1WO4P7JdN9ZXHQW2NkcOBAHbXt45u1rfIv7Tdl03QiK1YMXgUpmL7zzqiaDmJh9e-WDDqIxItmjL1/s640/Screen+Shot+2020-04-29+at+3.56.41+PM.png" width="640" /></a></div>
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(prevalence 20% is due to known positive contact: best guess)</div>
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However, at this point perhaps it is reasonable to move forward with the more conservative approach. What would you do? Would you don full PPE (i.e. double glove, PAPR throughout entire case, gown entire case, videolargyngoscope for intubation)? I personally would be comfortable using an N95 for intubation and extubation with eye shield and gloves. But during the remainder of the case I would not don an N95 if the case was not considered to be aerosolize generating.</div>
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Fortunately, I live in an area with a known prevalence of less than 1%. Obviously, there are probably a fair number of asymptomatic individuals who have the virus and could show up for surgery. The other side of the coin is to consider that there is a cost to using full scale PPE, the resource is limited, there are few surgeries that are elective to the point that they are never needed (i.e. eventually the patient needs their surgery), and the longer we go without providing services for elective surgeries, the larger the back log of cases will be. Therefore, ramping up will require an intelligent approach utilizing a full understanding of the true risk associated with caring for asymptomatic patients.</div>
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At my small private hospital the intention is to provide both molecular (PCR) testing and serology (antibody) testing for all patients. PCR testing is recommended to be done about 48 to 72 hours prior to surgery. This is because the test will be negative in an infected patient very early on in infection due to low viral load. Please see the above graph showing how the viral load ramps up over 5 days or so. Serology testing is recommended to be done just prior to surgery with enough time to get results. This is because it can take several days to weeks for IgM antibodies to appear and up to four weeks for IgG antibodies to appear. A recent study was able to show that when PCR alone was used the sensitivity of test was 51.9%, but when adding serology (IgM) testing into the mix, the sensitivity improved dramatically (98.6%). So lets look at the graph below with this new sensitivity and we will assume a very conservative prevalence of 5%.</div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiuT30eRsP3xfQ1mamOufrQJXngVaXTATCLq7IjxrSLp2zm9YNdL5xUbQPu_7t-RlcRoOHHdVRkyTQAKPK6k3miNMjqzyUtdDJZXxGZS-oU0uH7bd-6jW5ZpRKDOlOstuxBRS5hfupfttBF/s1600/Screen+Shot+2020-04-30+at+8.35.56+AM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="356" data-original-width="812" height="280" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiuT30eRsP3xfQ1mamOufrQJXngVaXTATCLq7IjxrSLp2zm9YNdL5xUbQPu_7t-RlcRoOHHdVRkyTQAKPK6k3miNMjqzyUtdDJZXxGZS-oU0uH7bd-6jW5ZpRKDOlOstuxBRS5hfupfttBF/s640/Screen+Shot+2020-04-30+at+8.35.56+AM.png" width="640" /></a></div>
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In raw numbers, I would have to care for 1,000 patients before I ran into one patient who was a false negative. Some practices are busy enough that this isn't good enough. Therefore, the cost benefit of depleting PPE for every case becomes questionable. I personally do not think it unreasonable to approach a healthy patient coming from a low prevalence area to this particular facility with routine universal precautions if they are negative for SARS-CoV-2 after both PCR test (done 72 hrs prior to surgery) and a serology test done no more than 24 hours prior to surgery. The critical piece to this is to have access to updated prevalence data from the community from which the patient resides and to verify that the patient has not traveled in the last 14 days nor had contact with others who might have traveled or had symptoms similar to COVID-19. This could be accomplished prior to surgery by simply asking the patient a few questions.</div>
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In the real world different facilities are currently planning different testing patters. In my area, a large nationwide hospital chain is not requiring ANY test prior to elective surgery in asymptomatic patients with no known risk factors. They are asking the surgeons to request the test (PCR) and then it will be done. As an example, the Mayo clinic is performing dual testing (PCR/serology) on all asymptomatic patients 48 hours prior to surgery. However, vanderbilt is using just the PCR test. This is also true of other major institutions. Cost is likely to be a major factor in making this decision. Each test can be around $100.00. In addition, different facilities are requiring different levels of PPE depending on the test results. Again, Vanderbilt who is performing the PCR nasal swab, will not require N95 if the patient tests negative. UCSF (also using single molecular testing) will allow the provider to opt out of N95, but allows the provider to choose if the patient tests negative. Mayo, (dual testing), still requires N95 regardless of test results. The takeaway, we still really don't know what the right answer is. However, I believe the pre test probability (baye's rule) should be a large factor in determining whether you believe the test. In a patient who has been living with a COVID-19 patient in close quarters, and comes for elective surgery, testing would allow you to decide to proceed with surgery should it be negative, but the NPV of the test would likely be low. In that case, the testing would not impact my decision to use enhanced PPE. </div>
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There are also questions related to what actually results in aerosolization of SARS-CoV-2. The current recommendations for PPE during intubation and extubation are largely based on the experience of HCW during the SARS-CoV-1 outbreak. During that outbreak, HCW doing intubations had a higher rate of infection than others. Other data comes form the recent experience in Wuhan. For example, there is anecdotal evidence of cases of contracting SARS-CoV-2 after an arduous intubation where nasal intubation was ultimately required. In this case, several HCWs contracted SARS-CoV-2 despite the use of N95 masks. However, the anesthesiologist, who was utilizing a PAPR, did not contract the disease. Other anecdotes are similar, for example, all HCWs contracted SARS-CoV-2 after transphenoidal puitary surgery except the anesthesiologist who again was using a PAPR. The takeaway for me is that first, there is a lot we don't know right now about how different procedures may lead to different aerosolized viral particles. Second, a one size fits all approach is not the best. Thirdly, as far as I can tell, at least I could not find any published papers, where someone measure the amount of aerosolized particles after an intubation. It is clear that difficult and prolonged airway manipulation will lead to higher risk (i.e. prolonged ongoing surgery using a high speed drill (Transphenoidal pituitary surgery). However, gently placing a blade into the mouth, with careful ETT placement may cause very little in the way of a viral plume. Extubation can be much more dangerous. The main documentary evidence leading to the recommendation of N95's indicates that HCW doing intubations were more likely to contract SARS CoV-1, but did not specify whether the exposure might have occurred during extubation. There is some data that the virus can be aerosolized but the study was unable to determine the amount of viable virus in the aerosolized form only that in some cases viral particles may remain viable for several hours in aerosol form. This same<a href="https://wwwnc.cdc.gov/eid/article/26/7/20-0885_article"> study</a> also found that the floor is the most contaminated surface due to droplets migrating to the ground via gravity. The study seemed to indicate that the quantity of viable virus decreases significantly with distance from the source. </div>
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Many facilities want to preserve PPE. In a drastic maneuver to do this, they are demanding that all staff not required for intubation/extubation remain out of the OR for varying amounts of time. The rational is by allowing the viral particles to clear via air exchange, the OR crew may enter and perform the surgery without enhanced PPE. It is not clear to me whether the decrease in throughput, expense of staff and OR for additional time, risk to patient who must remain under anesthesia for a longer period and other factors may outweigh the benefit. Or would dual testing be cheaper and do away with this requirement for negative patients? Furthermore, the wait times vary from institution to institution and the prescribed wait time seems arbitrary. It is not clear if the times are based on good data, or whether a best guess. The CDC published the following related to this topic:</div>
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<tr style="box-sizing: border-box;"><th class="text-center" style="background-color: #4ebaaa; border-color: rgb(222, 226, 230); border-style: solid; border-width: 1px 1px 2px; box-sizing: border-box; color: black; padding: 0.75rem; text-align: center; vertical-align: bottom;">ACH </th><th class="text-center" style="background-color: #4ebaaa; border-color: rgb(222, 226, 230); border-style: solid; border-width: 1px 1px 2px; box-sizing: border-box; color: black; padding: 0.75rem; text-align: center; vertical-align: bottom;">Time (mins.) required for removal<br style="box-sizing: border-box;" />99% efficiency</th></tr>
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<tr style="box-sizing: border-box;"><td class="text-center" style="border: 1px solid rgb(222, 226, 230); box-sizing: border-box; padding: 0.75rem; text-align: center; vertical-align: top;">10<span style="box-sizing: border-box; font-size: 0.65em; line-height: 1.15; position: relative; top: -0.5em; vertical-align: baseline;">+</span></td><td class="text-center" style="border: 1px solid rgb(222, 226, 230); box-sizing: border-box; padding: 0.75rem; text-align: center; vertical-align: top;">28</td></tr>
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<tr style="box-sizing: border-box;"><td class="text-center" style="border: 1px solid rgb(222, 226, 230); box-sizing: border-box; padding: 0.75rem; text-align: center; vertical-align: top;">12<span style="box-sizing: border-box; font-size: 0.65em; line-height: 1.15; position: relative; top: -0.5em; vertical-align: baseline;">+</span></td><td class="text-center" style="border: 1px solid rgb(222, 226, 230); box-sizing: border-box; padding: 0.75rem; text-align: center; vertical-align: top;">23</td></tr>
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ACH-air changes per hour (dependent upon each facilities air conditioning units)</div>
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<span style="box-sizing: border-box; font-size: 18.700000762939453px; text-align: center;"><span style="font-family: inherit;">The above equation is used to calculate the time listed above and is highly dependent on the volume of the room. The C relates to the viral concentration. This is totally unknown and will be much higher for certain intubations than others. I would also argue, that the initial viral load will be much higher after extubation than intubation.</span></span></div>
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<span style="box-sizing: border-box; text-align: center;"><span style="font-family: inherit; font-size: medium;">In summary, SARS-CoV-2 is a novel virus that has an Ro of around 3 or higher. This indicates that it is highly contagious. Current tests are not uniformly highly sensitive (i.e. PCR), but dual testing patients provides sensitivity of 98.6%. In low </span><span style="font-size: medium;">prevalence</span><span style="font-size: medium;"><span style="font-family: inherit;"> areas, the NPV can be as as high as 99.9% after dual testing. For providers in low prevalence areas providing care to small to moderate numbers</span> of patients, forgoing enhanced PPE during cases where the patient was negative on two different tests (rt PCR and serology) may be reasonable. The decision to preserve PPE may also depend on the type of case (i.e. an airway case with prolonged manipulation of the airway with high impact equipment). The requirement for requiring staff to wait outside the OR during intubation and extubation likewise could depend on other factors as well? Local prevalence, what kind of testing was done, was the intubation difficult or very smooth and non traumatic, did the patient have any known risk factors to raise your </span></span><span style="font-size: medium;">suspicion etc. Furthermore, N95's are susceptible to failure in certain high viral load environments. However, PAPRs are total overkill for routine non airway surgeries in COVID-19 negative patients or unknown but low risk patients. </span></div>
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<span style="font-size: medium;">Please feel free to use the below link to a web based calculator to help you individualize your care. Please note that patients who have SARS-CoV-2 contact, or symptoms (such as fever, cough, SOB, dyguesia, anosmia, headache) should be assumed to be positive no matter what the test states when determining whether to use enhanced PPE. This tool is related to asymptomatic patients with no known contact with a SARS-CoV-2 positive patient.</span></div>
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<a href="https://docs.google.com/spreadsheets/d/1Zpiotc72XGD2RET3r9I9iowrTZHUV_57OXBbeRkkr-0/edit?usp=sharing" target="_blank"> <span style="font-size: x-large;">Link NPV tool</span></a></div>
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<br />Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-89293783444099702312020-04-20T08:34:00.001-07:002020-04-20T08:34:06.472-07:00HIV + patient for urgent c/s<br />
<span style="font-family: Times, Times New Roman, serif;">A 26 year old female diagnosed with HIV for several years was urgently brought to the OR for a c/s for NRFHT. The patient was being treated by quadruple anti viral therapy for her HIV. She was also on bactrim presumably as a prophylactic against PCP +/- toxoplasmosis. After successful spinal anesthesia, the patient was laid down and oxygen applied. I discarded of all sharps, and then went to dispose of the remaining packaging. As I did so, my index finger received a superficial puncture from a needle that had not been visible in the remaining packaging. I discovered that it was the needle used for the local anesthetic injection prior to the spinal injection. The cap had fallen off exposing the needle.</span><br />
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<span style="font-family: Times, Times New Roman, serif;"><span style="background-color: white;">HIV is a Lentivirus that belongs to a group of retroviruses. R</span><span style="background-color: white;">everse transcriptase is an enzyme that enables retroviruses such as HIV to transcribe their own RNA into DNA. This DNA can then been incorporated into the host genome to produce large quantities of new HIV RNA. HIV attacks the cells containing antigens CD4 (T-helper lymphocytes and macrophages) on their surface and then destroys them, which leads to immunodeficiency, increased incidence of opportunistic infections, and malignancies. </span><span style="background-color: white;"> </span></span><br />
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<span style="font-family: Times, Times New Roman, serif;"><span style="background-color: white;">According to the International Health Care Worker Safety Center (IHCWSC), approximately 295,000 hospital-based healthcare workers experience occupational percutaneous injuries annually. Other studies put the risk of </span><span style="font-family: "georgia" , "times new roman" , "dejavu" serif , serif;">needle stick injuries at 83% annually. There are more than 20 blood borne pathogens that might be transmitted from a contaminated sharp, but the ones most commonly affecting health care workers (HCW) are HCV, HBV, and HIV.</span></span><br />
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<span style="font-family: Times, Times New Roman, serif;">List of potential pathogens transmitted after needle stick injury</span></div>
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<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Human T lymphotrophic retroviruses (HTLV I and II)</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Hepatitis D virus (HDV or delta agent, which is activated in the presence of HBV)</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Hepatitis G virus (GB virus or GBV-C)</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Cytomegalovirus (CMV)</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Epstein-Barr virus (EBV)</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Parvovirus B19</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Transfusion-transmitted virus (TTV)</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">West Nile virus (WNV)</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Malarial parasites</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Prion agents</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Blastomycosis</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Cryptococossis</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Diptheria</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Ebola</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Leptosprirosis</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Mycobacterium tuberculosis</span></li>
<li style="box-sizing: border-box; margin: 0px 0px 10px;"><span style="font-family: Times, Times New Roman, serif;">Toxoplasmosis</span></li>
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<span style="font-family: Times, Times New Roman, serif;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEje-uGFYXbgRdCMOhhAUlvQxqWQaBCsciI66YdWYTDz_qTKXL9sMBlk0S1XVLcu6aQ0cfWwMo-d36EOp-di23wYHYdkgfpOjdkIih1cNcQB_CMpjNop1EFOZEvA_iajO5cE5elmmEC7I-Hd/s1600/Screen+Shot+2020-04-16+at+3.55.16+PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1052" data-original-width="1600" height="420" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEje-uGFYXbgRdCMOhhAUlvQxqWQaBCsciI66YdWYTDz_qTKXL9sMBlk0S1XVLcu6aQ0cfWwMo-d36EOp-di23wYHYdkgfpOjdkIih1cNcQB_CMpjNop1EFOZEvA_iajO5cE5elmmEC7I-Hd/s640/Screen+Shot+2020-04-16+at+3.55.16+PM.png" width="640" /></a></span></div>
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<span style="font-family: Times, Times New Roman, serif;">The biggest concern after a needle stick in the health care setting is typically related to hepatitis B, hepatitis C and HIV. Fortunately, today, virtually everyone working in the US health care system has been vaccinated against HBV. There is no vaccine for hepatitis C, but it can be cured with medication. Unfortunately, the medication used to cure Hepatitis C is extremely expensive. HIV is not curable, but can be managed effectively with expensive pharmacotherapy.</span><br />
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<span style="font-family: Times, Times New Roman, serif;">Fortunately, for me the source patient was HCV negative and I have immunity to HBV (although the patient was also negative for HBV). My immediate focus was determining my probability for seroconversion to HIV positive. I finished the case about 60 min after the percutaneous puncture, and went to the ER. I received one dose in the ER of two reverse transcriptase inhibitors (emtricitabine and tenofovir) and one integrase inhibitor (Raltegravir) as part of the standard PEP regimen.</span><br />
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<span style="font-family: Times, Times New Roman, serif;">Contacting HIV after a needle stick injury is rare fortunately. From 1981 through 2006, the CDC documented only 57 cases of HIV transmission in HCWs following occupational exposure and identified an additional "possible" 140 cases. There are no high quality human studies to provide us any guidance on understanding the probability of seroconversion after a needle stick. The commonly cited risk of 0.3% transmission was from a study done in the late 80's and 90's where HAART therapy was non existent, thus creating a higher risk study population vs. today. In 1997, Cardo and colleagues identified four factors associated with increased risk for seroconversion:</span><br />
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<li><span style="font-family: Times, Times New Roman, serif;">Deep injury (Odds Ratio=15)</span></li>
<li><span style="font-family: Times, Times New Roman, serif;">Injury with a device visibly contaminated with source patient blood (Odds ratio=6.2)</span></li>
<li><span style="font-family: Times, Times New Roman, serif;">Injury from a needle that was in blood vessel (Odds ratio=4.3).</span></li>
<li><span style="font-family: Times, Times New Roman, serif;">Exposure to a source patient who died of AIDS two months following the occupational exposure (Odds ratio=5.6)</span></li>
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<span style="font-family: Times, Times New Roman, serif;">Many sources declare that risk from a hollow bore needle stick exposure is greater than that of an exposure from a suture style needle. In a retrospective case-control trial published in the NEJM, the authors state that "no significant difference in risk was found between exposure involving a hollow-bore needle and that involving a suture needle" after univariate analysis. This same study found after univariate analysis that risk of exposure to a large bore needle carried increased risk (14 times increased odds of seroconversion). However, the authors noted that this meant a gauge of 16 or less. In studies of needle sharing during IV drug use, the per use risk of transmission of HIV was only 0.67%. </span><br />
<span style="font-family: Times, Times New Roman, serif;"><span style="font-family: "georgia" , "times new roman" , serif;">While the amount of blood contaminating a needle after a needle stick injury is an important consideration, so is the viral load of a source patient. The viral load is greater during early HIV infection, before the immune system has had a chance to mount a response. </span><span style="background-color: white;"> Pilcher et al. estimated that viral load reaches its peak at 17 days after seroconversion in blood [2].</span><span style="font-family: "georgia" , "times new roman" , serif;"> Likewise, in late stage AIDS, viral load will increase as the viral replication overwhelms the host patient's immune defenses. The viral load varies from patient to patient but has a large effect on the conversion rates, where it is as low as 0.01% with viral loads less than 1,700 copies / mL, but closer to 0.3% when the viral load is greater than 38,000 copies / mL. This may explain the rate of seroconversion that occurs with a blood transfusion from an HIV infected blood source of 95%. While this is high, why is it not 100%? You are receiving 300 to 350 mL of blood after all. I suspect that it relates to the viral load of the source blood. The next highest risk activity to result in HIV infection is the birth process at 13 to 45%. In decreasing risk, you then have needle sharing for IV drug use, unprotected receptive anal intercourse (0.5%), needle stick injury (0.3%), and </span><span style="font-family: "georgia" , "times new roman" , serif;">exposure of mucous membranes to contaminated blood (0.09%).</span><span style="font-family: "georgia" , "times new roman" , serif;"> Of course, the probablities listed are averages from studies. After a needle stick injury, the risk for serconversion in that one event could be wildly different from that quoted due to all of the unknowns. However, the good news is that it is low.</span></span><br />
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<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white;">During acute HIV infection, the viral doubling time is approximately 10 hours and approximately 19 newly infected cells will develop from each HIV infected cell. Therefore, within 48 hours of infection, there will be more than 1.3 x 10^6 HIV infected cells. HIV is also readily incorporated into the DNA of resting lymphocytes, where it exists in a non duplicating state. This is important because this DNA is not susceptible to anti retroviral therapy. This relates to the recommendations of what actions to take after a needle stick injury from an HIV infected patient. The CDC currently recommends that after a needle stick injury from a known HIV infected patient to start triple drug pharmacotherapy within two hours of the accident and not greater than 72 hours after the injury. It is recommeneded to continue this therapy for 28 days. This recommendation is based on a variety of studies. The only human study we have relates to post exposure treatment mentioned above with ZDV [1]. In this case-control study, there was an 79% reduction in seroconversion when the HCW took zidovudine. Animal models are also illuminating. therese studies when therapy was begun immediately or within a few hours and continued for days to weeks it was effective in reducing rates of seroconversion. Pharmacotherapy was ineffective if begun after 72 hours. In animals treated with chemoprophylaxis within 24 hours of inoculation infection was prevented. However, if there was a delay of 48 hours, 1/2 of the animals became infected and half again became infected if the delay was 72 hours. Others studies have found a similar result. Likewise, therapy lasting only three days in animals resulted in 100% rate of seroconversion whereas, therapy lasting 10 days resulted in a seroconversion rate of 50%, whereas a 28 day course of chemoprophylaxis prevented infection in all animals tested. In Africa there have been several retrospective studies tracking HCWs exposed to HIV and using PEP. The PEP regimens were typically based on zidovudine, plus one or two additional medications. In these small studies there were zero cases of seroconversion despite a large number of those exposed failing to complete their PEP regimen. </span></span></span><br />
<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;">Currently the CDC is recommending triple drug regimen for PEP. This is based on two concepts. 1) it is likely that the effectiveness of PEP is related to the host's immunological response and ability to clear the HIV virus from the body, indicating that PEP is more a treatment than a prophylactic, and 2) in more robust studies looking at vertical transmission in pregnancy there is a study showing that rates of transmission are 20%,10%, 3.8% and 1.2% if mothers received no therapy, ZDV mono therapy, two drug therapy, and triple therapy respectively. </span></span><br />
<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;">Understanding cases of post exposure prophylaxis (PEP) failure is also illuminating. There have been 24 cases of reported failure that can be verified in the literature as of 2014. In these cases, 75% of the patients used single agent zidovudine as their PEP. There has been only six cases of failure with multiple agent prophylaxis regimens. There are also cases of failure of PEP in HCW only to discover after further testing that the HCW was infected by another source outside of work after the completion of PEP or that PEP was not continued. (as Hard as that is to believe-I mean who gets exposed to HIV at work, starts PEP, and then contracts HIV in the community?)</span></span><br />
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<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;">The take home message on PEP is this: If it is to be effective, the number of drugs you take is probably less important than making sure the full 28 day course is completed. If a triple drug regimen is stopped early due to side effects/toxicity, then clearly mono therapy or dual therapy would be more effective if tolerated the full 28 days. This fact is born out in studies showing that triple drug therapy is cause for a greater number of side effects and issues with toxicity. However, the issues related to toxicity have been greatly diminished with newer medications (see below). However, the newer medications are also extremely expensive which can also be a barrier to full treatment.</span></span><br />
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<span style="background-color: white;"><span style="font-family: Times, Times New Roman, serif;">The first line PEP regimen is Truvada + Isentress. Truvada (Gilead) is a combination of emtricitabine and tenofovir. These medications are in the class if HIV drugs known as NRTIs or nucleoside reverse transriptase inhibitors. They block HIV's ability to convert its RNA into DNA.</span></span><br />
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<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg4gCev_-ITH8n0fuJXprvUp9NGUmCPSFA41zHZq9Uc9RpM2A_rmD7GMTDoFt8U715FaEV_hJBYrb92_xUuKFbpQw0eXEMzUXAABcuUuXllXyFfv8cGSEz9w014G-DkFW6y8ajGkwMgCviG/s1600/NNRTI-and-NRTI-intervention-600.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="771" data-original-width="600" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg4gCev_-ITH8n0fuJXprvUp9NGUmCPSFA41zHZq9Uc9RpM2A_rmD7GMTDoFt8U715FaEV_hJBYrb92_xUuKFbpQw0eXEMzUXAABcuUuXllXyFfv8cGSEz9w014G-DkFW6y8ajGkwMgCviG/s320/NNRTI-and-NRTI-intervention-600.jpg" width="249" /></a></span></span></div>
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<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;">Insetress (Raltegravir) is an integrase inhibitor. After HIV has successfully used its own enzyme <i>reverse transcriptase</i> to make make a copy of its RNA into DNA, raltegravir inhibits this DNA's ability to integrate into the host's DNA.</span></span></div>
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<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjREIqgVVvu6ZotLfZQGYEnw_Y0yWjvpqm2b9LCIxKJhJhZ5gtWmESWHLw_oljRWFUeMyVQPOOdKJAJzcFlq4n4Dgne-4JONZi5ETN2MSgOgS-r7509_a8evVla0AnHcwwogkI6WYjkReRP/s1600/3-s2.0-B978143770310800018X-f26.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="916" data-original-width="372" height="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjREIqgVVvu6ZotLfZQGYEnw_Y0yWjvpqm2b9LCIxKJhJhZ5gtWmESWHLw_oljRWFUeMyVQPOOdKJAJzcFlq4n4Dgne-4JONZi5ETN2MSgOgS-r7509_a8evVla0AnHcwwogkI6WYjkReRP/s640/3-s2.0-B978143770310800018X-f26.jpg" width="258" /></a></span></span></div>
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<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;">There are now a large number of different anti-HIV medications available. What exactly one should use for PEP may depend on a number of factors and may require consultation with an infectious disease specialist. However, if the source patient has an undetectable viral load, PEP is not necessary. An undetectable viral load means that a real time PCR is unable to detect any virus free in the blood. The PCR test today can detect down to a threshold of 20 copies of RNA / mL of blood. Another issue to consider is the cost. Truvada costs around $1500 for a 28 day regimen. raltegravir is another $1200 or so. No studies have been done to show that using a triple drug regimen is better than single drug PEP. The only evidence we have in humans for PEP comes from a case control study with zidovudine where HIV serconversion was decreased by 79% [1]. In my case, I looked at the factors that increase risk. I was stuck fairly superficially (not deep) with a small gauge (25g) needle with no evidence of visible blood on the needle after a SQ injection of local anesthetic (i.e. needle was not placed directly into a blood vessel). The patient's viral load was detectable (at the time of exposure we had no lab value as such), but she was taking four different medications for HIV. Since she was also pregnant, I presumed that she was likely fairly compliant as she was likely motivated by her unborn child to reduce the chance of perinatal transmission of HIV. I also considered that I began therapy (truvada + isentress) early after exposure (2 hrs). Because I was financially responsible for the PEP regiment thereafter and discovering that GILEAD offered a free 28 day supply of truvada, I opted for this. It is recommended with newer tests that you can test for HIV after four weeks. I tested negative at 4 weeks. At 12 weeks, I will test again. However, if the first test is negative, there is a 95% chance the second test will also be negative.</span></span></div>
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<span style="font-family: times new roman, stixgeneral, serif;"><span style="background-color: white;">Patients coming to surgery requiring anesthesia who are on antiviral therapy for HIV should be evaluated for toxicity from this therapy. Fortunately, newer agents used today are far less toxic than their older counter parts. Nevertheless, potential toxicity exists for many of these agents and include problems such as:</span></span></span><br />
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<li><span style="font-family: times new roman, stixgeneral, serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;">dyslipidemia</span></span></li>
<li><span style="font-family: times new roman, stixgeneral, serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;">hyperglycemia</span></span></li>
<li><span style="font-family: times new roman, stixgeneral, serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;">insulin resistance</span></span></li>
<li><span style="font-family: times new roman, stixgeneral, serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;">osteopenia/osteoporosis</span></span></li>
<li><span style="font-family: times new roman, stixgeneral, serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;">anemia, neutropenia and thrombocytopenia</span></span></li>
<li><span style="font-family: times new roman, stixgeneral, serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;">lactic acidosis</span></span></li>
<li><span style="font-family: times new roman, stixgeneral, serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;">hepatic toxicity</span></span></li>
<li><span style="font-family: times new roman, stixgeneral, serif;"><span style="background-color: white; font-family: Times, Times New Roman, serif;">peripheral neuropathy</span></span></li>
</ul>
<span style="font-family: Times, Times New Roman, serif;">Potential interactions with antiviral therapy and anesthetics must also be considered. Propofol and NRTIs may both potentially promote mitochondrial toxicity and lactic acidosis. Enzyme induction or inhibition (CYP450 3A4) must also be considered.</span><br />
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<li><span style="font-family: Times, Times New Roman, serif;">rionavir/darunavir (protease inhibitors) can enhance the affect of opoiods and ketamine due to inhibition of liver enzyme CYP 3A4.</span></li>
<li><span style="font-family: Times, Times New Roman, serif;">Saquinavir/ritonavir/darunavir (protease inhibitor) may inhibit midazolam metabolism and oral administration is particularly problematic; IV midazolam should be used with caution.</span></li>
<li><span style="font-family: Times, Times New Roman, serif;">Ca2+ channel blockers (amlodipine, diltiazem) may be enhanced due to enzyme inhibition from darunavir (protease inhibitor)</span></li>
<li><span style="font-family: Times, Times New Roman, serif;">Lidocaine and other amide local anesthetics (bupivacaine) may have increased blood levels due to enzyme inhibition since they are metabolized by CYP 3A4 if given to someone on darunavir or ritonavir.</span></li>
<li><span style="font-family: Times, Times New Roman, serif;">Neuromuscular blocker effects may be prolonged due to inhibition of metabolism.</span></li>
<li><span style="font-family: Times, Times New Roman, serif;">Aprepitant is metabolized by CYP 3A4 therefore, darunavir could increase aprepitant concentrations.</span></li>
<li><span style="font-family: Times, Times New Roman, serif;">Dexamethasone is a CYP 3A4 inducer and therefore, at high doses over a long period of time can reduce the effectiveness of both darunavir and ritonavir in treatment of HIV. This should not be a problem with a single preoperative dose for PONV prophylaxis however.</span></li>
<li><span style="font-family: Times, Times New Roman, serif;">Dexmedetomidine undergoes extensive hepatic metabolism and therefore, theoretically both darunavir and ritonavir could decrease dexmedetomidine blood concentrations requiring a larger dose.</span></li>
<li><span style="font-family: Times, Times New Roman, serif;">Ergotamine is metabolized by CYP 3A4 and darunavir/ritonavir may lead to toxic levels if multiple doses are given. This could lead to a life threatening event due to the narrow therapeutic window of ergotamine.</span></li>
<li><span style="font-family: Times, Times New Roman, serif;">Labetaolol </span></li>
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<span style="font-family: Times, Times New Roman, serif;">Conclusion</span></div>
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<span style="font-family: Times, Times New Roman, serif;">HCW are at high risk today to exposure to a number of infectious agents. Needlevstick injuries continue to occur in HCW despite universal precautions. HIV represents only one of these. HIV infection continues to quietly cause a large number of infecctions worldwide and is an ongoing epidemic despite receiving little press. Although HIV can now be managed with medications, life with HIV significantly altered and complex when considering the complexity of the drug regimens, ability of the virus to become resistant, ongoing potential to infect others around you, expense of lifelong medications and infectious disease consultation, etc etc. Therefore, needle stick injuries in the HCW produce a large degree of anxiety. However, it is clear that the risk for seroconversion overall is low and is largely dependent degree of virus in the source patient's blood, amount of blood on the source needle, and degree of injury from the needle itself. The risk of seroconversion can be further modified by determining the need for PEP within two hours of exposure, taking an appropriate regimen based on risk profile of exposure, and continuing the prescribed regimen for the full course (likely 28 days). Testing for HIV should be done at time point zero, 4 weeks, and again at 12 weeks to determine if serovconversion occurred. In most cases of seroconversion, patients will experience full like symptoms associated with viral replication and the immune system's response to the virus. HCW who experience a work related needle injury of low risk, and take the prescribed PEP as recommended have a very low risk of seroconversion, but unfortunately, the probability is not quantified due to lack of studies.</span><ul>
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<span style="background-color: white;"><span style="font-size: small;">1. Bell, DM. et al. <i>NEJM. </i>1997; 337:21:1485-1490.</span></span></span><br />
<span style="font-family: Times, Times New Roman, serif;"><span style="background-color: white;"><span style="font-size: small;">2. P</span></span><span style="background-color: white;">ilcher CD, Joaki G, Hoffman IF, et al. AIDS 2007;21(13):1723-30.</span></span></div>
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<br />Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-17191500300902147122020-03-16T12:29:00.001-07:002020-03-16T13:10:20.480-07:00Patient requesting labor epidural and a history of Idiopathic Intracranial HypertensionThis morning while watching the news showing the DOW plunging by another 2000 + points in the midst of a panicked public related to the spread of the novel corona virus, I was called up to L and D to place an epidural. The patient was a G3P2 31 year old patient who was otherwise healthy with the exception of a reported prior history of Idiopathic Intracranial Hypertension. She reported that she had been told that she could have an epidural by an anesthesiologist, but not a spinal. Upon further questioning, I was able to determine that the patient had been treated by doxycycline for a routine URI or sinus infection. Thereafter, she developed changes in her ability to see and sought medical care. She was diagnosed with a reaction to the doxycycline and underwent lumbar puncture as part of the work up and therapy. She states that after the lumbar puncture, she developed a headache which she had not suffered prior. She was started on diamox and this was discontinued after a period of time.<br />
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At first glance, this seemed to be a case of primary idiopathic intracranial hypertension, when in fact, it was likely a case of secondary intracranial hypertension, meaning, caused by an external known cause rather than from a completely unknown cause. Idiopathic intracranial hypertension is a diagnosis of exclusion. It typically affects females who are middle aged and obese. Upon LP, opening pressures of greater than 25 cm of H20 would be considered typical (normal opening pressure is 10 to 15 cm of H2O). Patients with IIH can develop partial or complete blindness of one or both eyes if not treated. In severe cases, when therapeutic LP or medicine like diamox or corticosteroids are not working, surgical placement of an LP shunt is required.<br />
<br />
For the OB anesthesiologist, any patient with potential intracranial pathology should be approached with caution. Prior to any neuraxial procedure, it is important to fully understand the cause and natural history of any intracranial abnormality due to the potential catastrophic risk of brain tissue herniation. An excellent review of the approach to the OB patient with intracranial pathology can be found <a href="https://anesthesiology.pubs.asahq.org/article.aspx?articleid=1918202">here</a>. In summary, patients who have obstruction to flow of CSF from the brain into the spinal canal are at high risk for any type of puncture of the dura mater. In the normal scenario when a puncture occurs of the dura mater in the lumbar portion of the spine, CSF will flow out and to compensate, CSF from the brain fills the space to equalize pressure throughout the continuous space. Any obstruction to this flow from from the cerebral ventricular system into the spinal canal will result in herniation.<br />
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However, patients with idiopathic intracranial hypertension (IIH) do not have a problem of obstruction of flow, and thus are not at risk for herniation after a dural puncture whether with a large bore or small bore needle. As mentioned, LP is a therapeutic modality used to relieve headaches in these patients. In patients with significant symptomatic IIH who wish neuraxial anesthesia for labor, there is a risk for potential exacerbation of symptoms (to include: pupillary changes or asymmetry, eye movement abnormalities, papilledema, hemiparesis, facial weakness, somnolence). This is due to displacement of CSF from the lumbar spinal canal back up into the cerebral area. Furthermore, pregnancy and labor have been found to increase the baseline lumbar epidural pressure which it is thought is caused by engorged epidural veins. In studies of patients with elevated ICP, a 10 mL bolus of LA given over 20 to 30 s caused an average increase of 21 mmHg in ICP lasting 4.5 min vs an average increase of 6 mmHg for 2.3 min in a patient with normal pre injection ICP. Therefore, this possibility should be discussed, and it may be a potential indication for a CSE, where a small IT dose can be given, and then a low volume infusion with PCEA can be offered to the patient to create a slow transition into epidural analgesia via lumbar epidural catheter. Indeed there are numerous case reports of successful neuraxial anesthesia for patients with IIH for both labor epidurals and cesarean sections. In this <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2044.2006.04891.x">case report</a>, the practictioner used the tuohy needle to drain 25 mLs of CSF prior to placement of an intrathecal catheter for labor analgesia. It was noted that the patient had excellent analgesia for labor and delivery, and did not suffer a PDPH, although the patient did complain of a headache. Indications for an IT catheter might include patients where avoidance of GETA is important and likelihood of cesarian is also high. The authors of the case report felt that their patient fell into this category. They also noted that in a patient with difficult to control increased intracranial pressure, bolus doses through an epidural catheter may not be tolerated.<br />
<br />
It is known that tetracycline, doxycycline and minocycline can all result in elevated intracranial hypertension. Therefore, anytime a patient is treated with these antibiotics, any headache should prompt careful evaluation for this diagnosis. Currently it is unknown how these antibiotics can result in this disorder, although there is speculation that the antibiotics interfere with the production of ATP at the site of CSF absorption into the venous sinuses known as the arachnoid granulations.<br />
<br />
My patient had been treated with Diamox or Acetazolamide, which is a carbonic anhydrase inhibitor. It is often noted that this action is predominantly effective at the renal tubule to reduce hydrogen ion secretion and increase the excretion of sodium, potassium, bicarbonate, and water. Other uses include the treatment of glaucoma, seizures, and metabolic alkalosis due to its ability to dump bicarb and retain hydrogen ions. Diamox also inhibits carbonic anhydrase in the brain, and specifically in the choroid plexus, the site of CSF production, causing a decrease. Unfortunately, patients with IIH who are controlled with diamox will often be told to discontinue the medication while they are pregnant due to some case reports of congenital abnormalities and literature in animal models showing potential teratogenicity. However, a recent <a href="https://journals.lww.com/jneuro-ophthalmology/Fulltext/2013/03000/The_Use_of_Acetazolamide_During_Pregnancy_in.3.aspx">study</a> found no evidence for harmful effects of diamox in human pregnancy. Therefore, when a patient arrives for delivery, it is possible that she is still taking diamox to control her symptoms. If this is the case, it will be important to consider the effects of diamox on a potential anesthetic, primarily the risk of hypokalemia.<br />
<br />
Patients who arrive for labor are always at risk for the potential to require anesthesia for cesarian section. While neuraxial anesthesia is the preferred method overall, GETA may be required for a number of reasons. In this case, there is a question as to whether succinylcholine should be used as it may cause a minor increase in ICP. Furthermore, careful consideration of PaCO2 managment will be important as any increase in ICP will accompany hypercarbia. <span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">Definitive measures used for decreasing the ICP include, mild head elevation, maintain EtCO</span><span style="background-color: white; bottom: -0.25em; font-family: "times new roman" , "stixgeneral" , serif; font-size: 0.8461em; line-height: 1.6363em; position: relative; top: 0.25em; vertical-align: baseline;">2</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"> between 25 mmHg and 30 mmHg, I.V. mannitol, continuous infusion of propofol, avoid hypoxia, hypercarbia, hyperthermia and hypotension.</span><br />
<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"><br /></span>
<span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="background-color: white; font-size: 15.9991px;">Anesthesia OB management for patients with IIH is generally straightforward, but careful history and a detailed understanding of the patients history and manifestation are important to avoid confusion with other intracerebral pathology that may also present during the peripartum period, such as PDPH and venous sinus thrombosis that can make diagnosis more challenging. </span></span><br />
<br />Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-29016061884285529552020-02-23T17:57:00.005-08:002023-03-10T19:15:53.117-08:00Severe toxic Megacolon secondary to Ischemic ColitisA 76 Year old male was admitted to the hospital after a syncopal episode during a BM at home. The patient was found to be constipated and admitted for further testing. The patient deteriorated in a day and a half and required intubation due to ventalitaory failure. Pressors were required in low dose shortly thereafter, with accompanying renal failure. The GI physician was called in on Sunday morning to attempt colonic decompression via a colonoscopy and I was called into the hospital to provide anesthesia. I explained to the GI doctor, that giving additional sedation to the patient might cause additional decompensation. Therefore, I ordered the ICU nurse to given 30 mg of Rocuronium, so the GI doc could proceed without any movement from the patient. This was done about 8:30am without problems. However, the patient continued to deteriorate requiring max dose of Norepinephrine (30mcg/min) and vasopressin at 0.02u/min. Patient was taken emergently to the OR at about 4:30pm sunday afternoon for ex lap and total colectomy with ileostomy.<br />
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Upon transport to the OR, the patient was receiving the above mentioned infusions, plus insulin 4 u/hr, diltiazem for new onset AF, Bicarbonate drip, and precedex at 0.2 mcg/kg/hr. These were all continued during surgery with the exception of the diltiazem.<br />
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Upon arrival to the OR I placed a left radial arterial catheter for invasive pressure monitoring. US was used and visualizing of the artery revealed a virtually pulseless distal artery despite NIBP blood pressures reading 100/50 mmHg. After cannulation, there was almost no pulistile flow from the catheter causing me to question whether I had cannulated the artery or a vein. After connection to the transducer, an obviously arterial tracing was visualized on the monitor. However, there was a very wide discrepancy between the NIBP reading and the AL reading. In general, the NIBP of the same arm was 45 mmHg higher for systolic pressures. All attempts to reduce this discrepancy failed. The waveform was not dampened, there was excellent blood flow when withdrawing from the AL, the transducer was carefully zeroed twice, and placed at a similar level as the NIBP cuff. The cuff was on the same arm as the AL. Therefore, throughout the case, the AL was used mostly for trending, while I chose to accept the NIBP reading as more indicative of the actual pressure experienced by the patient.<br />
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Here are some serial ABGs<br />
The patients labs were as follows: (day of surgery was 2/16).<br />
ABGs (serial)<br />
2/13--7.2<br />
2/14--7.37<br />
2/15--7.5<br />
2/15--7.3 19:00 (lactate 7.2)<br />
2/16--7.013<br />
2/17--7.027<br />
Na+: 138 mEq/L<br />
K+: 4.2 mEq/L<br />
Cl-: 99 mEq/L<br />
CO2: 21<br />
BUN: 54 mg/dL<br />
Cr: 4.3 mg/dL<br />
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The patient was on a bicarb infusion and I continued this to the OR. I admit that I found this unusual and wondered what the evidence was to support treating severe lactic acidosis from severe ischemic colitis with bicarbonate therapy. Indeed, severe metabolic acidosis is feared by clinicians for good reason. Low pH (<7.2) predicts mortality in ICU. It is also associated with impaired <span style="background-color: white; caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif;">cardiac contractility, systemic vasodilatation, pulmonary vasoconstriction, arrhythmias, altered oxygen delivery, altered renal blood flow, cerebral edema, diaphragm dysfunction, energy failure with decreased adenosine triphosphate production, and immune response impairment. However, the intuitive therapy of sodium bicarbonate given IV does not always prove therapeutic. Multiple studies </span><span style="background-color: white;"><span style="color: #383636; font-family: Lato, Helvetica, Arial, sans-serif;"><span style="caret-color: rgb(56, 54, 54);"> in critically ill patients with metabolic acidosis have not found any benefit to bicarbonate therapy for improving outcomes. As an example, a robust study of 1700 patients was unable to find any benefit for those who received sodium bicarbonate for treatment of severe metabolic acidosis in the setting of sepsis [7]. This was replicated in two other large multi center RCTs where sodium bicarb did not prove beneficial [8]. Other studies have also not shown benefit. And, in a retrospective study, sodium bicarbonate infusion actually was an independent predictor of increased mortality [9]. However, in one small study, patients with lactic acidosis AND AKI did have improved mortality when treated with bicarb [1]. In studies on patients in code situations, bicarb therapy has not improved outcome and is likely contraindicated. Bicarb is most definitely indicated for patients with RTA I, or proximal RTA where bicarbonate is wasted, or not efficiently reabsorbed by the kidneys. However, RTA I leads to a chronic metabolic acidosis and is not relevant to our patients condition. To me, it is not clear that our patient met the criteria of the patients in the study that found a benefit of bicarb therapy. Prior to surgery the patient was anuric and had near complete renal failure, as opposed to AKI. In the above mentioned study, it should be noted that the authors found that in patients who did not have AKI and were treated with sodium bicarb, there was an increase in mortality after correction for disease severity. The authors noted that this may be related to the fact that severe acidosis inhibits the enzyme phosphofructokinase which is responsible for the production of lactate. By increasing pH, this enzyme is unleashed to continue to produce additional lactate worsening the acidemia unless the underlying cause of the production of lactate is corrected. It is of note, that in the cited above study, patients treated with sodium bicarb did not see a reduction of blood lactate levels to the degree of those patients with a similar acidemia who did not receive sodium bicarb therapy. It should be noted that in non mechanically ventilated patients, sodium bicarb therapy for metabolic acidosis can be particularly detrimental since this therapy rapidly increases gaseous CO2 in the blood. As PaCO2 increases, a respiratory acidosis may ensue, and as CO2 rapidly enters cells, intracellular acidosis may become significant evens as blood HCO3- decrease.</span></span></span><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj7msp6HJ-jMeU0udD-fsLfrqdty8Bf3DaEdgfYPN5RZlsdgltw_BdmpvhbprogLU81ZUP96rn3fpDsSJc_fczEJBJ6zWmDaUQT0OZzP_wcj650vnkSrg1CIFVIZFm3dEbaEcSi8pHczfUz55lYo8tS-Lp45lAx1evtjmg27B1CGS7OiTs7mtRnAxN6Cg/s533/Screen%20Shot%202023-03-10%20at%208.52.17%20PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="312" data-original-width="533" height="374" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj7msp6HJ-jMeU0udD-fsLfrqdty8Bf3DaEdgfYPN5RZlsdgltw_BdmpvhbprogLU81ZUP96rn3fpDsSJc_fczEJBJ6zWmDaUQT0OZzP_wcj650vnkSrg1CIFVIZFm3dEbaEcSi8pHczfUz55lYo8tS-Lp45lAx1evtjmg27B1CGS7OiTs7mtRnAxN6Cg/w640-h374/Screen%20Shot%202023-03-10%20at%208.52.17%20PM.png" width="640" /></a></div><br /><br /><br /><br />
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It is noteworthy, that prior to surgery, my patient's lactate was 7.2 mg/dL, after surgery it had jumped to 12.2 mg/dL. Lactate clearance has been shown to be a much better predictor of mortality than other predictors [2]. In the ARISE trial, septic patients with high lactate levels had higher mortality than those who presented with hypotension only [6]. This massive increase also lends weight to the evidence described above that bicarb therapy may worsen lactate production, although, in this case the patient's on going significant disease burden most likely greatly contributed to the rocketing lactate levels seen. Indeed, 24 hours later, his lactate level had jumped to 18.9 mg/dL and the patient expired not long after this. <br />
<br />
Another question that arose early in the case was related to the dose of vasopressin. Due to low blood pressure and the already high dose of norepinephrine, I attempted to increase the infusion rate of vasopressin to 0.05 u/min. The pump had been preprogrammed to disallow this dose. Therefore, I was forced by the pump to limit my infusion to 0.04 u/min. To me this seemed too low of a dose. An excellent review of the pharmacology and endocrinology of vasopressin can be located <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3145307/">here.</a> In an early study on vasopressin for septic shock, the dose used to show benefit was 0.07 u/min. In hemorrhagic shock, it is recommended to use doses near 0.4 u/min and in post cardiac surgery vasodilatory shock a dose of 0.1 u/min is recommended and was found to be devoid of adverse effects. Therefore, evidence exists to allow for higher infusion rates of vasopressin when combined with norepinephrine in a patient in severe shock.<br />
<br />
<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif;">Pre-pro-AVP is synthesized in magnocellular neurosecretory neurons (also known as neurohypophyseal neurons) in the supraoptic and paraventricular nuclei (known as osmoreceptors) of the anterior hypothalamus. It migrates along the supraoptic-hypophyseal tract to the posterior pituitary gland, where it is stored in neurosecretory vesicles and is then secreted in response to decreased stretch on atrial, aortic and carotid body </span><span style="font-family: "times new roman" , "stixgeneral" , serif;"><span>mechano receptors. Vasopressin acts on receptors labeled V1, V2 and V3. V1 receptors are located on vascular endothelium, kidneys, platelets, and brain and V2 receptors are predominantly located in the kidney collecting duct where they cause an increase in aquaporin insertion in the walls of the collecting ducts to allow increased water reabsorption into the blood. </span></span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif;"> In refractory shock, the enhanced sensitivity to exogenous vasopressin may be attributable to its ability to block K</span><span style="bottom: -0.25em; font-family: "times new roman" , "stixgeneral" , serif; line-height: 1.6363em; position: relative; top: 0.25em; vertical-align: baseline;">ATP</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif;"> channels, interfere with NO signaling, bind avidly to V</span><span style="bottom: -0.25em; font-family: "times new roman" , "stixgeneral" , serif; line-height: 1.6363em; position: relative; top: 0.25em; vertical-align: baseline;">1</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif;">receptors, and potentiate the effects of adrenergic agents at the level of vascular smooth muscle in shock states.</span><br />
<span style="font-family: "times new roman" , "stixgeneral" , serif;"><span><br /></span></span>
<span style="font-family: "times new roman" , "stixgeneral" , serif;"><span>Vasopressin has increased in popularity in ICUs in large part because of large and well done studies such as VASST, where vasopressin (low dose 0.01 to 0.03 mcg/min) was found to be beneficial (decreased mortality by nearly 10%) in patients with low severity shock [4]. </span></span> Furthermore, in a post hoc analysis of the data from this large study, Gordon found that patients who received vasopressin were less likely to advance to the loss or dialysis categories of RIFLE scoring system if they already had AKI (21% vs 40%) [5]. Unfortunately, in the VASST study, no difference in mortality could be found in those receiving vasopressin in addition to norepinephrine vs norepinephrine alone in patients with more severe sepsis, as was the case in our patient.<br />
<br />
The surgery lasted approximately four hours. The patient received seven liters of crystalloid (LR), 1L of albumin and was essentially anuric. Blood loss was minimal. The patient was transported to the ICU ventilated, paralyzed with max pressors continued. The patients lactate nearly doubled within 24 hours, the INR went to 4, d-dimer went very high, Hgb dropped despite no obvious blood loss, liver enzymes went to nearly 5,000, and K+ levels went to 6.9 mEq/L, while albumin dropped to less than 2 mg/dL. The patient was placed on CRRT and it became obvious that he was not going to survive. The patient expired on POD #2 after apparent multi organ failure with DIC.<br />
<br />
<br />
<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">1. Kim HJ, Son YK, An WS. </span><span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"><span class="ref-journal">PLoS One. </span>2013;<span class="ref-vol">8</span>:65283</span><br />
<span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">2. </span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"> <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4686961/">Lee SM, Kim SE, Kim E Bin, Jeong HJ, Son YK, An WS. </a></span><span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4686961/"><span class="ref-journal">PLoS One. </span>2015;<span class="ref-vol">10</span>:145181</a></span><br />
<span style="font-family: inherit;">3. <span style="background-color: white; color: #303030; font-style: italic;">Dünser MW, Mayr AJ, Ulmer H, Knotzer H, Sumann G, Pajk W, Friesenecker B, Hasibeder WR</span></span><br />
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<span style="font-family: inherit;">4. <span style="font-size: 13px;">Russell JA, Walley KR, Singer J, Gordon AC, Hébert PC, Cooper DJ, Holmes CL, Mehta S, Granton JT, Storms MM, Cook DJ, Presneill JJ, Ayers D, VASST Investigators.</span></span><br />
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<span style="font-family: inherit;">5. </span><span style="color: black; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"> </span><span class="element-citation" style="color: black; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">Gordon AC, Russell JA, Walley KR, Singer J, Ayers D, Storms MM, et al. The effects of vasopressin on acute kidney injury in septic shock. <span class="ref-journal">Intensive Care Med. </span>2010;<span class="ref-vol">36</span>:83–91.</span><br />
<span class="element-citation" style="color: black; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"><span style="background-color: #fcfcfc; caret-color: rgb(51, 51, 51); color: #333333; font-family: Georgia, Palatino, serif; font-size: 16px;">6. Gotmaker R, Peake SL, Forbes A, Bellomo R, ARISE Investigators (2017) Mortality is greater in septic patients with hyperlactatemia than with refractory hypotension. Shock 48:294–300</span></span></div><div class="citation" style="font-size: 13px; margin-bottom: -0.3em; margin-top: 0.5em;"><span class="element-citation" style="color: black; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"><span style="background-color: #fcfcfc; caret-color: rgb(51, 51, 51); color: #333333; font-family: Georgia, Palatino, serif; font-size: 16px;">7. </span></span><span class="person-group" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Zhang</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Z</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Zhu</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">C</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Mo</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">L</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Hong</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Y</div></span></span><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;">: </span><i><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;"> </span><div class="source" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Intensive Care Med</div><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;">. </span></i><div class="year" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">2018</div><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;">; </span><div class="volume" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">44</div><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;">:</span><div class="fpage" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">1888</div><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;">–</span><div class="lpage" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">95</div></div><div class="citation" style="font-size: 13px; margin-bottom: -0.3em; margin-top: 0.5em;"><div class="lpage" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">8. </div><span class="person-group" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Jung</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">B</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Rimmele</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">T</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Le Goff</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">C</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Chanques</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">G</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Corne</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">P</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Jonquet</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">O</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Muller</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">L</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Lefrant</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">JY</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Guervilly</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">C</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Papazian</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">L</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Allaouchiche</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">B</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Jaber</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">S</div></span></span><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;">; </span><div class="collab" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">AzuRea Group</div><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;">: </span><i><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;"> </span><div class="source" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Crit Care</div></i><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;"><i>.</i> </span><div class="year" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">2011</div><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;">; </span><div class="volume" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">15</div><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;">:</span><div class="fpage" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">R238</div></div><div class="citation" style="font-size: 13px; margin-bottom: -0.3em; margin-top: 0.5em;"><div class="fpage" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">9. </div><span class="person-group" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Kim</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">HJ</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">Son</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">YK</div></span>, <span class="name string-name" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;"><div class="surname" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">An</div> <div class="given-names" style="border: 0px; display: inline; font-size: 1rem; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">WS</div></span></span><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;">: </span><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;"> </span><div class="source" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">PLoS One</div><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;">. </span><div class="year" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">2013</div><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;">; </span><div class="volume" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">8</div><span style="caret-color: rgb(56, 54, 54); color: #383636; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px;">:</span><div class="fpage" style="border: 0px; caret-color: rgb(56, 54, 54); color: #383636; display: inline; font-family: Lato, Helvetica, Arial, sans-serif; font-size: 16px; margin: 0px; padding: 0px; vertical-align: baseline; word-break: break-word;">e65283</div></div>
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Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-28900214995602890202020-01-16T10:53:00.004-08:002021-04-15T15:52:10.918-07:0072 year old male with gastric outlet obstructionOn a Saturday call I was called in to take care of a 72 year old gentleman who had undergone a six hour paraesophageal hernia repair and extensive lysis of adhesions 10 days prior. He was now suffering from abdominal pain with radiological studies that showed extensive colon dilation with stool and lack of movement from the stomach to the duodenum leading to a diagnosis of gastric outlet obstruction. The patient had an NG tube in place which was on suction. The patient was alert and orientated able to answer questions with no signs of obtundation or lethargy.<br />
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Lab values were significant for the following:<br />
<ul>
<li>Sodium level of 150 mmol/L</li>
<li>Potassium level of 3.2 mmol/L</li>
<li>Chloride of 116 mmol/L</li>
<li>BUN of 26.</li>
<li>Magnesium level of 1.7 mmol/L</li>
<li>Calcium (total) 7.9 mg/dL</li>
<li>Phosphate 1.8 mg/dL</li>
<li>Creatinine 0.8 mg/dL (down from 2.8 10 days earlier after AKI)</li>
</ul>
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Post op labs</div>
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<ul>
<li>Sodium down to 140 mmol/L</li>
<li>Potassium level increased to 4 mmol/L</li>
<li>Chloride slightly decreased to 114 mmol/L</li>
<li>BUN of 25</li>
<li>creatinine 1.2 mg/dL</li>
<li>Magnesium of 1.6 mmol/l</li>
<li>Calcium 7.4 mg/dL</li>
<li>Phosphate 4.0 mg/dL</li>
</ul>
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Gastric outlet obstruction is typically considered a medical emergency not a surgical emergency as serious electrolyte abnormalities are typical along with significant alkalosis if not treated. The standard textbook presentation of gastric outlet obstruction (GOO), is a dehydrated patient with a metabolic alkalosis, hypochloremia, hypokalemia and hyponatremia. Initially, the kidneys will dump bicarbonate into the urine to avoid serious alkalosis and retain chloride ions. However, this process is overwhelmed as dehydration ensues. At this point, the kidneys agressively attempt to retain fluid by holding onto sodium at the expense of secreting potassium and hydrogen ions. This leads to a paradoxical acidic urine and further exacerbates the alkalemia and hypokalemia. Alkalosis leads to a reduction in circulating calcium levels. This patient, despite a diagnosis of GOO, did not have the typical biochemical abnormalities associated with this syndrome.<br />
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Firstly the patient had significant hypernatremia (Na greater than 144 mmol/L). Clinically,<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"> </span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">the sensation of intense thirst that protects against severe hypernatremia in health may be absent or reduced in patients with altered mental status or with hypothalamic lesions affecting their sense of thirst and in infants and elderly people. Non-specific symptoms such as anorexia, muscle weakness, restlessness, nausea, and vomiting tend to occur early. More serious signs follow, with altered mental status, lethargy, irritability, stupor, and coma. Patients with chronic hypernatremia (hyperosmolar states) have adapted their brains via "idiogenic osmoles" to avoid neuronal shrinkage. Idiogenic osmoles are organic molecules such as myo-inositol, taurine, glycerylphosphorylcholine, and betaine which are accumulated via extracellular fluid uptake via activation of sodium-dependent cotransporters. Because of this adaptation to chronic hypernatremia, rapid correction of the free water deficit would result in rapid cerebral edema due to the relative hyperosmolarity inside the neuron.</span><br />
In a systematic review, hypernatremia has been found to be associated with increased 30 day mortality and morbidity [1]. Hypernatremia may result in severe metabolic derangements, myocardial depression and injury, neurologic impairment, venous thromboembolism, and poor wound healing. Although there is an association, it is not proven that preoperative treatment of hypernatremia will improve outcome. It is clear that the rate of change in sodioum levels is very important. One study showed that slow rates of improvement (less than 0.25 mmol/L/hr) were typically inadequate with a 3-fold increased risk of 30 day mortality compared to those with a more rapid rate of correction (0.25 to 0.5 mmol/L/hr).<br />
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The most likely reason for this patient's hypernatremia was loss of hypotonic body fluids with addition of hypertonic TPN. Rapid and aggressive fluid volume replacement should have been started immediately to correct his likely volume deficit. Also, the free water deficit needed to be replaced. The formula to determine the free water deficit (L)=[0.6 x IBW] x [(current [Na+]/140)-1]. The deficit should be corrected in the short term by 1/2 or 50% of the deficit with the remainder corrected over the next 24 to 36 hours to minimize cerebral edema.<br />
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Therefore, in my patient, his estimated free water deficit at the start of the case was (in liters): 0.6 x 70kg= 42 x (150/140)-1 = 2.99 L. During the case in order to avoid truly catastrophic cerebral edema while under GETA, I planned a very mild correction and estimated that slowly infusing 1/2 NS would help provide a small amout of free water while volume ressuscitation for the case with some 5% albumin (250 mL) and LR (3.5 L). LR contains 130 mEq/L of sodium, 4 mEq/L of potassium, 2.7 mEq/L of Calcium, 109 mEq/L of Chloride and finally lactate 28 mEq/L.<br />
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The Adrogue Formula will allow you to determine how much the serum sodium level will change based on the fluid you infuse: Change in serum Na+= (infused Na+ - serum Na+)/(TBW +1). For my patient using 1/2 NS and plugging in the data, the expected change in serum sodium after the six hour case was (75 - 150)/(0.6 x 70kg)+1 = 1.74 mmol. If my target is to reduce the serum sodium by about 0.3 mmol/hr, after 6 hours (approximate length of the case), I would want to have reduced the serum from 150 mmol/L to 148.2 mmol/L. It turns out that I didn't use the above formulas, nor make the calculations listed above. I guestimated that giving 1 L of 1/2 NS would be safe and help reduce to some degree the amount of hypernatremia. It turns out that the 1 L of 1/2 NS I infused over the six hour procedure was predicted to reduce the serum sodium by 1.74 mmol/L and my goal based on the above equations was to decrease it by 1.8 mmol after six hours.<br />
In retrospect, I do not believe the goal should be focused at all on reducing serum sodium when taking a patient with chronic hypernatremia who is not suffering any symptoms, into major abdominal surgery. This was likely an error of judgement on my part.<br />
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In fact, the patient also had LR infusing, and this was contributing to the reduction in Na+ as well. I infused 3.5 L of LR and the estimated reduction in serum sodium from this therapy would be (130-150)/42+1 = 0.46 mmol/L x 3.5 L = 1.62 mmol total. This shows that I actually overshot my goal by using LR aggressively during the case. Therefore, when facing a patient with likely chronic hypernatremia undergoing major abdominal surgery, the best therapy is to use LR as needed.<br />
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My patient also suffered from hypomagnesemia. Magnesium (Mg2+) plays a major role in a number of pathways in the human body including serving as a co factor for a number of processes (i.e. protein synthesis, neuromuscular function etc.), is an endogenous regulator of several electrolytes, in particular it is a calcium channel antagonist. In addition, Mg2+ is important in maintaining Calcium levels because low levels of Mg2+ result in end organ resistance to parathyroid hormone and in parathyroid secretion. Furthermore, Mg2+ also modulates sodium and potassium currents thus affecting membrane potentials. In the CNS, Mg2+ exerts depressant effects by antagonizing the NMDA receptor and also inhibiting catecholamine release.<br />
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Magnesium levels are primarily affected in the small bowel via absorption (passive and active transport) and re absorption in the thick ascending limb of the loop of henle.<br />
Hypomagnesemia results mainly from inadequate dietary intake and/or GI and renal losses. Hypomagnesemia is often associated with diarrhea, vomiting, use of loop and thiazide diuretics, ACE inhibitors, cisplatin, aminoglycosides,or other nephrotoxic drugs, and several endocrine like parathyroid diseases, hyperaldosteronism, and chronic alcoholism. In addition, during major abdominal surgery, intraoperative crystalloid infusion may lead to a decrease in the passive magnesium transport, thus leading to a decrease in plasma magnesium concentrations. The incidence of hypomagnesemia is as high as 65% for patients in the ICU, where hypoalbuminemia, TPN, and the use of magnesium-wasting medications are commonly present. Patients with head injuries also seem to be at high risk for hypomagnesemia secondary to polyuria. Hypokalemia and hypocalcemia are also frequently associated with hypomagnesemia. <br />
There has been an effort to associate hypomagnesemia with increased mortality. Several studies have been able to link the two, however, careful analysis and high quality studies have suggested that hypomagnesemia may be an epiphenomenon of critically ill patients who suffer increased mortality. Therefore, treating low magnesium levels is not likely to reduce mortality. However, replenishing magnesium levels in surgical patients can have other benefits. For example, reduction in cardiac dysrhythmias, primary atrial tachyarrhythmias, reduced anesthetic need (MgSO4 as an adjunct anesthetic/analgesic) inhibition of platelet dependent thrombosis, attenuate adverse cardiovascular effects during laryngoscopy, and intubation. The treatment of hypomagnesemia takes several days of IV therapy because nearly all magnesium is intracellular. In fact, in critically ill patients, 4 to 6 grams of IV Magnesium per day will likely be required to maintain a serum magnesium level of near 2 Gm/dL. In addition, IV magnesium can take up to 48 hours to redistribute into the cells, causing serum levels after IV administration to be falsely elevated.<br />
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The patient was also suffering from hypophosphatemia. Hypophosphatemia is a very common disorder in critically ill patients occurring in up to 100% of patients in some studies. Particularly relevant to this patient, TPN can result in sudden and profound hypophosphatemia. This usually is due to providing TPN to patients who are malnourished, have initial low phosphate levels and then suddenly receive glucose via TPN which supports a sudden increase in the formation of ATP. With TPN initiation, a sudden acute rise in glucose transport across cell membranes occurs accompanied by oxidative phosphorylation resulting in a large demand on intracellular phosphate for support of ATP production. This results in "refeeding syndrome" where rapid changes in fluids and electrolytes occurs. Commonly, this changes result in hypophosphatemia, hypomagnesemia and hypokalemia. Low phosphate levels can have wide ranging clinical effects including myocardial dysfunction, diaphragmatic weakness, seizures, coma, rhabdomyolysis, and red blood cell dysfunction from tissue hypoxia (by decreased RBC 2,3-DPG). Furthermore, there is some evidence that hypophasphatemia is associated with longer ICU and hospital stays and increased risk of arrythmias. A recent retrospective analysis found that hypophosphatemia was associated with increased 28 day mortality in the ICU [2]. The authors of this study concluded based on their analysis that independent of illness severity, hypophosphatemia still resulted in increased mortality. This patient had significant hypophosphatemia, and I elected to replace phosphate during the case. It is important to consider the calcium levels of patients who receive phosphate repletion because the calcium level will likely decrease as phosphate is replaced.<br />
My patient went to the ICU intubated post op. No problems were evident related to his severe electrolyte abnormalities. He required prolonged post operative care in the ICU with mechanical ventilation. However, after about two weeks he was extubated and made progress. <br />
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Memorizing the dosing of all electrolyte replacements is tedious and unnecessary. I have included a simple calculator that can be stored on one's home screen of their smart phone for easy use to determine the appropriate dose to give a patient assuming IV administration.<br />
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<a href="https://docs.google.com/spreadsheets/d/1cxiq8kdqUsRWAItuyusM36RhfeMGVFvDnOP11EkdysE/edit?usp=sharing">Lyte Calculator</a><br />
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1. Leung AA, McAlister FA, et al. <i>Amer J Medicine</i>. V. 126(10): 2013. p 877-885<br />
2. Wang L, Xiao C, Chen L, Zhang X, Kou Q. <i>BMC Anesthesiology</i>. 86;2019.</div>
Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-27291958746768717992019-08-21T14:42:00.000-07:002019-08-23T15:02:34.999-07:00Post op MI after lap h/h repairA 61 year old mail presented for repair of a hiatal hernia for symptomatic GERD via a laparoscopic approach and LINX placement. The patient had a history of HTN, hyperlipidemia and CAD with stents placed in 2013 and 2016. He was no longer on any anticoagulants and had a negative stress test 9 months previous. The patient stated that he was in his usual state of health at the time of surgery with no chest pain, limitations of activity due to shortness of breath, or otherwise. The patient was otherwise active capable of doing more than 4 METS of work.<br />
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The patient was induced in the usual fashion and provided GETA with desflurane. The anesthetic was complicated by severe hypotension and bradycardia when placed in reverse T-burg at the beginning of the case which was treated with glycopyrrolate (0.2mg) and ephedrine 15mg in 5 mg increments. Aproximately 45 min into the case the patient developed tachycardia of 109 or so BPM and this was treated with a bolus of 100 mcg fentanyl and esmolol 30 mg. Towards the end of the case the patient developed significant hypotension again and this was treated with a very small dose of phenyephrine given via slow drip.<br />
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The surgical time was a little over one hour. The patient emerged from anesthesia without complications, was extubated in the OR and taken to PACU in excellent condition. The patient appeared comfortable and care was transferred to the PACU nurse. After approximately 30 min I went back to see how the patient was doing. He appeared comfortable, sleeping in bed. I finished my paper work and signed out to the nurse and headed for the door. About 10 min later as I had just pulled out of the facility I was called by the nurse stating that the patient was having chest pain and his EKG tracing appeared abnormal. The nurse told me she had already ordered and EKG. I asked her to call me with results. I was called about 5 min later by a panicked nurse stating the patient's EKG showed a STEMI. The ER doc had already been called and given them orders to begin a code STEMI. Patient was transferred to a nearby hospital for further care where an occluded stent was encountered and treated with stenting.<br />
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This is a picture of the patients lesion prior to a stent being placed.</div>
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This patient had an acute coronary syndrome (ACS) further specified as ST segment elevation myocardial infarction. There are two other ACS subtypes, non-ST segment elevation myocardial infarction (NSTEMI) and unstable angina.<br />
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<ol>
<li>Unstable angina-New onset chest pain that is cardiac in nature or chest pain that is getting progressively worse without any elevation in cardiac specific enzymes.</li>
<li>NSTEMI-EKG changes consistent with ischemia, and elevation in cardiac specific enzymes indicating myocardial damage.</li>
<li>STEMI-EKG changes where at least a 1 mm elevation in the ST segment is encountered that is new and associated with elevation in cardiac specific enzymes and should be in contiguous leads.</li>
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The patient in this case report complained of chest pain. Unfortunately, 100% of patients experience chest pressure and pain after lapx hiatal hernia repair. So this complaint is non specific. <br />
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In our case, we had ST elevation in the septal, anterior and lateral leads.</div>
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<ul>
<li>Septal leads (V1/V2)</li>
<li>Anterior leads (V3/V4)</li>
<li>Lateral leads (V5/V6)</li>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEglmOuPMkyzq8_18i_yytnRdVAqOq2Tv3JSn0oCI7dG7NE_9yOnwr6kgVKAyqzxMiQh7Bi8DPD8X_b4wMp_GJhVNaU2ZrYW_1lg_-eQA5b0HO0GGFmGxxu0Er24v4-r36FZ6eVNAgu4zpWj/s1600/Screen+Shot+2019-08-19+at+4.29.08+PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="566" data-original-width="922" height="245" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEglmOuPMkyzq8_18i_yytnRdVAqOq2Tv3JSn0oCI7dG7NE_9yOnwr6kgVKAyqzxMiQh7Bi8DPD8X_b4wMp_GJhVNaU2ZrYW_1lg_-eQA5b0HO0GGFmGxxu0Er24v4-r36FZ6eVNAgu4zpWj/s400/Screen+Shot+2019-08-19+at+4.29.08+PM.png" width="400" /></a>(sample)</div>
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Above is an example of anterolateral STEMI with some septal involvement (V2).</div>
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Post op MI tends to occur early-see below. </div>
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<ul>
<li>44% day of surgery</li>
<li>34% POD 1</li>
<li>16% POD 2</li>
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Prior to surgery, the risk for a major adverse cardiac event (MACE) in this patient can be estimated using the revised cardiac risk index (RCRI):</div>
<div>
<ol>
<li>high risk surgery = 1 pt</li>
<li>Ischemic heart disease (coronary artery disease) = 1 pt</li>
<li>history of congestive heart failure = 1 point</li>
<li>history of cerebral vascular disease (h/o of CVA or TIA) = 1 pt</li>
<li>diabetes requiring insulin treatment = 1 pt</li>
<li>preoperative creatinine greater than 2 mg/dl = 1 pt</li>
</ol>
<span style="caret-color: rgb(46, 46, 46); color: #2e2e2e;"><span style="font-family: "georgia" , "times new roman" , serif;"></span></span><br />
<div>
<span style="caret-color: rgb(46, 46, 46); color: #2e2e2e;"><span style="font-family: "georgia" , "times new roman" , serif;">This patient had one risk factor (ischemic heart disease) on the RCRI scale and therefore, was awarded 1 point. Therefore, the patient's risk for major cardiac morbidity would be 0.9% (see here): </span></span><span style="background-color: white; color: #333333; font-family: "georgia" , "times new roman" , serif;">0 – 0.4% 1 – 0.9% 2 – 6.6% 3 or more – 11%</span></div>
</div>
<br />
<br />
<span style="font-family: "georgia" , "times new roman" , serif;">T<span style="caret-color: rgb(46, 46, 46); color: #2e2e2e;">he RCRI has a moderately good ability to discriminate patients who will develop cardiac events from those who will not after mixed noncardiac surgical procedures (area under the curve [AUC] 0.75), it is less accurate in patients undergoing vascular surgical procedures (AUC, 0.64), and it is less able to predict all-cause mortality (median AUC, 0.62). Recently a published geriatric sensitive RCRI performed better on patients over age 65 than the original RCRI [2].</span></span><br />
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<span style="font-family: "georgia" , "times new roman" , serif;"><span style="caret-color: rgb(46, 46, 46); color: #2e2e2e;">To overcome these limitations of RCRI, the National Surgical Quality Improvement Program (NSQIP) score was developed and validated on 211,410 surgical patients. This model includes age, ASA class, functional status, abnormal serum creatinine, and a novel and more appropriate organ-based categorization of surgery. Risk may be quantified by a risk calculator on the Internet. The discriminative or predictive ability of the NSQIP score is significantly better as compared with RCRI (AUC, 0.88), and it works well also in vascular surgical patients.</span> The NSQIP calculator is very labor intensive making it somewhat impractical to use by the bedside clinician. However, I input the data from this case into the online calculator available for free. The result indicated that the patient was at less than 1 % risk for cardiovascular complications.</span><br />
<span style="font-family: "georgia" , "times new roman" , serif;"><br /></span>
<span style="font-family: "georgia" , "times new roman" , serif;">The preop EKG in patient's with cardiac disease</span><br />
<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; color: #232323; font-size: 16px;"><br /></span></span>
<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; color: #232323; font-size: 16px;">ECG abnormalities are not part of either the revised cardiac risk index (RCRI) or the National Surgical Quality Improvement Plan (NSQIP) because of the lack of prognostic specificity associated with these findings.</span></span><br />
<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; color: #232323; font-size: 16px;"><br /></span></span>
<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; color: #232323; font-size: 16px;">The rationale for obtaining a preoperative ECG comes from the utility of having a baseline ECG should a postoperative ECG be abnormal.</span></span><br />
<br />
<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white;"><span style="color: #232323;"><span style="caret-color: rgb(35, 35, 35);">Subjective assessment of cardiopulmonary reserve (i.e. evaluation of METs) prior to surgery suffers from poor sensitivity (i.e. falsely labels high risk patients as low risk). Therefore, in patients with more than 4 METs where there is an otherwise high index of suspicion for disease, a low threshold for further evaluation should exist. On the other hand, patients with a low MET score (i.e. inability to engage in activities equivalent to at least 4 METs) is very good at predicting a patient at higher risk. However, this method is also not used in the formal scoring systems for predicting post operative cardiac risk.</span></span></span></span><br />
<br />
<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white;"><span style="color: #232323;"><span style="caret-color: rgb(35, 35, 35);">According to the recent ACC/AHA guidelines, stress testing is not indicated unless it would be done regardless of the planned </span></span></span></span><span style="color: #232323; font-family: "georgia" , "times new roman" , serif;">surgery. In addition, resting echocardiography is not indicated unless needed regardless of planned surgery to evaluate ongoing dyspnea or evaluate valve function in a patient with a murmur.</span><br />
<span style="color: #232323; font-family: "georgia" , "times new roman" , serif;"><br /></span>
<span style="color: #232323; font-family: "georgia" , "times new roman" , serif;"><span style="caret-color: rgb(35, 35, 35);">On <i>UpToDate</i>, a summary of the preoperative approach to cardiac evaluation includes the following general principles:</span></span><br />
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<ul>
<li><span style="font-family: "georgia" , "times new roman" , serif;">All patients scheduled to undergo noncardiac surgery should have an assessment of the risk of a cardiovascular perioperative cardiac event and the patient’s functional status is an important determinant of risk. </span></li>
</ul>
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<div class="bulletIndent1" style="caret-color: rgb(35, 35, 35); clear: both; color: #232323; line-height: 1.625; margin-left: 2em; position: relative;">
<span class="glyph" style="left: -15px; line-height: 2; position: absolute;"><span style="font-family: "georgia" , "times new roman" , serif;">●</span></span><span style="font-family: "georgia" , "times new roman" , serif;">We use either the revised cardiac risk index (RCRI), also referred to as the Lee index, or the American College of Surgeons National Surgical Quality Improvement Program (NSQIP) risk prediction rule to establish the patient’s risk. </span></div>
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<div class="bulletIndent1" style="caret-color: rgb(35, 35, 35); clear: both; color: #232323; line-height: 1.625; margin-left: 2em; position: relative;">
<span class="glyph" style="left: -15px; line-height: 2; position: absolute;"><span style="font-family: "georgia" , "times new roman" , serif;">●</span></span><span style="font-family: "georgia" , "times new roman" , serif;">We obtain an electrocardiogram (ECG) in patients with cardiac disease (except in those undergoing low-risk surgery) in large part to have a baseline available should a postoperative test be abnormal.</span></div>
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<div class="bulletIndent1" style="caret-color: rgb(35, 35, 35); clear: both; color: #232323; line-height: 1.625; margin-left: 2em; position: relative;">
<span class="glyph" style="left: -15px; line-height: 2; position: absolute;"><span style="font-family: "georgia" , "times new roman" , serif;">●</span></span><span style="font-family: "georgia" , "times new roman" , serif;">For patients with known or suspected heart disease we only perform further cardiac evaluation (echocardiography, stress testing, or 24-hour ambulatory monitoring) if it is indicated <b>in the absence of proposed surgery.</b></span></div>
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<span style="font-family: "georgia" , "times new roman" , serif;">In a 2007 study, it was found that the only preoperative EKG abnormality that was predictive of post op MI was a bundle branch block (right or left). However, this abnormality did not improve prediction beyond risk factors identified in patient history.</span>
<span style="font-family: "georgia" , "times new roman" , serif;"><br /></span><br />
<span style="font-family: "georgia" , "times new roman" , serif;">In the immediate post operative period anticoagulation may be contraindicated for treatment of ACS. </span><br />
<span style="font-family: "georgia" , "times new roman" , serif;"><br /></span>
<span style="font-family: "georgia" , "times new roman" , serif;">There are two main types of MI that anesthesiologists are likely to encounter in the preoperative period: Type I MI and Type II MI. A type I MI occurs when a thrombus forms with a plaque rupture in a coronary artery and causes acute obstruction to blood flow. Type II MI occurs when there is a demand supply imbalance of oxygen. In general, the literature suggests that both types can occur in the preoperative period with a frequency that varies largely based on the reference study. </span><span style="background-color: white; color: #232323; font-family: "arial" , "helvetica neue" , "helvetica" , sans-serif; font-size: 16px;">In one angiographic study, nearly 50 percent of patients with perioperative acute coronary syndrome had evidence of plaque rupture [</span><a class="abstract_t" href="https://www.uptodate.com/contents/perioperative-myocardial-infarction-or-injury-after-noncardiac-surgery/abstract/3" style="background-color: white; color: #00905a; font-family: Arial, "Helvetica Neue", Helvetica, sans-serif; font-size: 16px;">3</a><span style="background-color: white; color: #232323; font-family: "arial" , "helvetica neue" , "helvetica" , sans-serif; font-size: 16px;">]. However, in this case presentation, the patient had what could be called a type 4b MI (stent thrombosis). In a recent retrospective study, Helwani et al. [1], showed that 72% of post operative MIs were Type II, while 25% were of type I (acute plaque rupture). They also found an event rate of 2.1% for type 4b (stent thrombosis). </span><br />
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Type 4b MI, or stent thrombosis, is a greater risk shortly after stent placement. Recommendations currently state that dual antiplately therapy should continue for 30 to 45 days after a bare metal stent because the stent undergoes reendothelialization quickly. In the updated guidelines of 2016, the period of mandatory DAPT after a second generation DES has been shortened to six months for patients with stable CAD. These second generation DES appear to be much safer when it comes to stent thrombosis. Even newer DES are pushing the window back even further to only 1 month. However, experts are recommending that aspirin therapy be continued into the operative period whenever possible. The last time a stent had been placed in the above patient was 2016 and therefore, the patient was not required to continue DAPT during the surgical period.<br />
<span style="font-family: "georgia" , "times new roman" , serif;"><br /></span>
<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">Mortality from myocardial infarction (MI) after noncardiac surgery[</span><a aria-expanded="false" aria-haspopup="true" class=" bibr popnode tag_hotlink tag_tooltip" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4173430/#ref2" id="__tag_402151990" rid="ref2" role="button" style="color: #642a8f; font-family: "Times New Roman", stixgeneral, serif; font-size: 15.999099731445313px;">2</a><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">] is believed to be 10 to 15%. High-risk patients experience perioperative MI 3.0% of the time.</span></span><br />
<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;"><br /></span></span>
<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">Once a diagnosis is made management consists of the following general themes:</span></span><br />
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<ul>
<li><span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">Antiplatelet agents-ASA, plavix, GP IIb/IIIa inhibitors</span></span></li>
<li><span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">Anticoagulation-Heparin, LMWH, Fondaparinux, Bivalirudin</span></span></li>
<li><span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">Anti ischemic therapy-B blockers, nitrates, CCB</span></span></li>
<li><span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">Statins</span></span></li>
<li><span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">Ace inhibitors</span></span></li>
<li><span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">O2*</span></span></li>
<li><span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">Transfusion as needed</span></span></li>
</ul>
<div>
* There is some evidence that hyperoxia in patients with STEMI may not be beneficial, but rather harmful [3]. In an RCT, patients given supplemental oxygen in the prehospital treatment of STEMI, had an increase in infarct size at six months after diagnosis of MI.<br />
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In the PACU, the patient was given IV heparin 1000 units, nitroglycerine infusion for elevated blood pressure, and aspirin to chew (325mg). The treatment of ACS with ST elevation generally includes immediate (less than 2 hours) cardiology consultation for PCI, which is what occurred with my patient. A stent was placed and the patient was discharged home on POD #2 in good condition.<br />
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Lastly, in patients who are considered at risk of MACE in the perioperative period, it might make sense to use a volatile anesthetic as the major component of anesthesia due to the proven ability of these agents to condition cardiomyocytes (as well as neurons) against ischemic damage. The mechanisms behind anesthetic preconditioning relate to reduction in inflammation, cytokines, and a cascade of enzymes that prevent ischemic reperfusion damage.<br />
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<span style="font-family: Georgia, Times New Roman, serif;"><span style="background-color: white;">A meta-analysis of randomized clinical trials involving 1922 patients undergoing cardiac surgery showed that, in comparison with total intravenous anesthesia (TIVA), desflurane and sevoflurane achieved significant reductions of myocardial infarctions [2.4% in the VA group vs 5.1% in the TIVA group, odds ratio (OR) 0.51] and all-cause mortality (0.4% vs 1.6%, OR 0.31) [4]. Furthermore, a</span><span style="background-color: white; caret-color: rgb(51, 51, 51); color: #333333;">n international consensus conference provided expert opinion support for the use of VA in hemodynamically stable cardiac surgery patients [</span>5<span style="background-color: white; caret-color: rgb(51, 51, 51); color: #333333;">] as a means to reduce myocardial damage and death. The pre conditioning affect appears to be dose dependent, and benefits are typical found at a usual clinical dose of 1 MAC.</span></span><br />
<span style="font-family: Georgia, Times New Roman, serif;"><br /></span>
<span style="font-family: Georgia, Times New Roman, serif;">This case highlights that patient coming to surgery with apparent low risk (RCRI of 1 pt = 0.9% risk of MACE) are still vulnerable and a high index of suspicion is required so that if a MI type 4b occurs, rapid transfer to the cath lab will occur for definitive therapy. Anesthesiologists need to be aware of and ready to institute the first line of therapy in preparation for PCI which includes beta blockade, anti platelet agents (asa), nitro as tolerated and pain control with morphine or an equivalent.</span><br />
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<span style="font-family: "georgia" , "times new roman" , serif;"><br /></span><span style="font-family: Georgia, Times New Roman, serif;"><span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; color: #333333;">1. Helwani, MA, Amin, A, Lavigne, P, Rao, S, Oesterreich, S, Samaha, E, Brown, JC, Nagele, P Etiology of acute coronary syndrome after noncardiac surgery. </span><span style="box-sizing: border-box; color: #333333; font-style: italic; line-height: inherit;">A<span style="box-sizing: border-box; font-variant-alternates: normal; font-variant-caps: small-caps; font-variant-east-asian: normal; font-variant-ligatures: normal; font-variant-numeric: normal; font-variant-position: normal;">nesthesiology</span></span><span style="background-color: white; color: #333333;"> 2018; </span><span style="box-sizing: border-box; color: #333333; font-style: italic; line-height: inherit;">128</span><span style="background-color: white; color: #333333;">:1084–91</span></span>
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<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white; color: #333333;">2. Alrezk R, Jackson N, Al Rezk M, Elashoff R, Weintraub N, Elashoff D, Fonarow GC: <i>J Am Heart Assoc.</i> 2017;6:e006648</span></span></span><br />
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<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: white;"><span style="color: #333333; font-family: georgia, times new roman, serif;">3.</span><span style="font-family: Georgia, Times New Roman, serif;"> </span></span></span><span style="font-family: Georgia, Times New Roman, serif;">D. Stub, K. Smith, S. Bernard, Z. Nehme, M. Stephenson, J.E. Bray, et al., Air versus ox- ygen in ST-segment-elevation myocardial infarction, Circulation 131 (2015) 2143–2150.</span></span><br />
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<span style="font-family: Georgia, Times New Roman, serif;"><span style="font-family: Georgia, Times New Roman, serif;"><span style="background-color: white; caret-color: rgb(48, 48, 48); color: #303030;">4. </span></span><span style="background-color: white; caret-color: rgb(48, 48, 48); color: #303030; font-style: italic;">Landoni G, Biondi-Zoccai GG, Zangrillo A, Bignami E, D'Avolio S, Marchetti C, Calabrò MG, Fochi O, Guarracino F, Tritapepe L, De Hert S, Torri G. </span><span style="background-color: white; caret-color: rgb(48, 48, 48); color: #303030; font-style: italic;">J Cardiothorac Vasc Anesth. </span><span style="background-color: white; caret-color: rgb(48, 48, 48); color: #303030;">2007 Aug; 21(4):502-11</span><span style="background-color: white; caret-color: rgb(48, 48, 48); color: #303030; font-style: italic;">.</span></span><br />
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<span style="font-family: Georgia, Times New Roman, serif;"><span style="color: #303030;"><span style="background-color: white; caret-color: rgb(48, 48, 48);">5 .</span></span><span style="background-color: white; caret-color: rgb(51, 51, 51); color: #333333;">Landoni G, Augoustides JG, Guarracino F, Santini F, Ponschab M, Pasero D, Rodseth RN, Biondi-Zoccai G, Silvay G, Salvi L, Camporesi E, Comis M, Conte M, Bevilacqua S, Cabrini L, Cariello C, Caramelli F, De Santis V, Del Sarto P, Dini D, Forti A, Galdieri N, Giordano G, Gottin L, Greco M, Maglioni E, Mantovani L, Manzato A, Meli M, Paternoster G: Mortality reduction in cardiac anesthesia and intensive care: results of the first International Consensus Conference. Acta Anaesthesiol Scand. 2011, 55 (3): 259-266.</span></span><br />
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<br />Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-85615234329186362122019-03-10T17:25:00.000-07:002019-03-21T07:44:24.289-07:005,10 methylenetetrahydrofolate reductase deficiency in my patientThis past month I have suddenly had two teenagers present for surgery claiming to have 5,10 methylenetetrahydrolate reductase deficiency. Ironically, I had just reviewed two articles on this exact issue in my past journals of anesthesiology. This was nice, because it allowed me to offer a degree of comfort to the patients by appearing to be informed of the disease and potential pitfalls. What made me particularly interested in doing a write up about this particular genetic polymorphism was that the mother of the second patient gave me a paper claiming that these patients should avoid propofol, epinephrine, lactated ringers, and N20. <a href="https://raisingnaturalkids.com/mthfr-and-anesthesia/?unapproved=32667&moderation-hash=adc444274056be98eb55f4bae6524905#comment-32667">(here is the link) </a>The mother was hyper anxious and emotionally charged in discussing the anesthetic. She appeared ready to defend her position and stated that her daughter had an "allergy" to propofol and lactated ringers. I reassured her that it would be no problem to avoid propofol and nitrous oxide for her anesthetic and the mother appeared to back down in a somewhat disappointed manner as if she was hoping for more push back from the doctor which could provide her an opportunity to demonstrate to her other family members her superior intellect. However, I was intrigued enough to spend some time looking at the anesthetic literature related to this deficiency to better understand how propofol, bupivacaine, lactated ringers or epinephrine might have been included in the list of things to avoid by this very concerned mother.<br />
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In general, the main concern related to 5,10 methylenetetrahydrofolate reductase (MTHFR) deficiency is related to increased homocysteine in the blood. Homocysteine is an amino acid that has been associated with increased cardiovascular disease. In a large cohort [4] of (~18,000 men and woman) in western Norway, total plasma homocysteine was associated with increased risk of cardiovascular morbidity, general mortality, and depression with neurocognitive deficits in the elderly. This cohort study, demonstrated an association, but cannot be said to prove that elevated total plasma homocysteine caused these outcomes. However, other case control studies have also found an association with elevated plasma homocysteine levels and increased vascular disease. Graham IM et al. showed in a case control study that increased plasma total homocysteine levels is an independent risk factor for vascular diseases similar to that conferred from smoking or hyperlipidemia. It also was shown to powerfully increase the already elevated risk associated with smoking and hypertension [5]. It is estimated that plasma levels above 10 micromol/L are associated with a doubling of vascular risk and levels greater than 20 micromol/L can confer a TEN fold increased risk of vascular disease. Furthermore, acute increases have also been shown to cause endothelial dysfunction and provide procoagulant effects [6]. Chambers et al. hypothesize that hypomethylation is the major biochemical mechanism in homocystinemia vascular disease in addition to inhibition of HDL biosynthesis in humans.<br />
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Hyperhomocysteinemia can result from a number of causes. These include vitamin deficiencies such as Vitamin B6 (pyridoxine), Vitamin B12, and folic acid. Renal insuficiency can also be a culprit. Genetic defects that are relevant to homocysteine levels and anesthesia practice include methyltetrahydrofolate reductase deficiency and cystathionine β synthase deficiency. <br />
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Cystanthionine β Synthase deficiency is a congenital disorder that is also known as homocystinuria and is associated with defects in collagen such that patients suffer from a marfanoid like body with defects in bone and issues with the eyes. They are prone to hypoglycemia, therefore, patients having surgery will require short fasting periods and supplementation during fasting with IV dextrose. Furthermore, thromboembolic complications are high and measures must be taken to reduce these complications in the perioperative period.<br />
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Acute increases in homocysteine were found to occur in patients given nitrous oxide. These acute increases of homocysteine levels were associated with cardiovascular damage in a 2000 clinical study. Badner et al [7] looked at patients undergoing carotid endarterectomy who were randomized to a nitrous oxide(N2O) group (more than 50%) vs. no nitrous. They found that in those receiving N2O, homocysteine levels were significantly increased from an average baseline of 12.7 μmol/L to 15.5 μmol/L in the PACU. Although, this was a very slight increase, it was statistically greater than the non N2O group. Furthermore, this resulted in patients in the N2O group experiencing more frequent episodes of ischemia in the first 48 hours post op and a longer average duration of ischemia post op. There was no increased cardiovascular morbidity noted although this wasn't an end point of the study. Importantly, they found that the univariate predictors of myocardial ischemia in these patients were N2O use (RR 1.9), homocysteine greater than 17 μmol (RR 2.0), and pre and intraop ischemia (RR 3.7). These same authors noted that the potential causes of elevated ischemic risk in the patients with elevated homocysteine can be traced back to homocyteine's effects on the vascular endothelial lining and known procoagulant effects such as increased platelet adhesivness, factor V activation, protein C inhibition and antithrombin and plasminogen activator binding. It is likely that these effects are mediated by the consumption of nitric oxide (potent vasodilator).<br />
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N2O inhibits vitamin B12 (cobalamin) by irreversibly oxidizing the cobalt atom (from +1 to +3 valence state) of cobalamin. This leads to subsequent inhibition of enzymes requiring cobalamin in its coenzyme form. Because this is an irreversible inhibition, the reduction of cobalamin lasts several days. Among the many enzymes, methionine synthase is crucial because it's located at the juncture of two pathways: homocysteine remethylation and the folate cycle. (fee fig)<br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEge-OF1ASUqfrAGo2wiSmGPUKxM-5rw2atHGXFl1IB3hxiAetWWHvjJAl4-fKNc9w6K0tB5kD84YAZNmd-FOqM5g1R4aLMckTdcbbPSlq7jvoXaXTnvtMIxdSyPROya0a1syMHeOoP4YFbk/s1600/folate.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="405" data-original-width="1033" height="250" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEge-OF1ASUqfrAGo2wiSmGPUKxM-5rw2atHGXFl1IB3hxiAetWWHvjJAl4-fKNc9w6K0tB5kD84YAZNmd-FOqM5g1R4aLMckTdcbbPSlq7jvoXaXTnvtMIxdSyPROya0a1syMHeOoP4YFbk/s640/folate.png" width="640" /></a></div>
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fig (see reference 8.)<br />
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Therefore, when cobalamin is oxidized via N2O, homocysteine can no longer be converted into methionine and builds up in the blood. As noted in the above chart, a multitude of problems can now arise, because purines, thymidine, and RNA/DNA methylation all depend on the proper function of this pathway (see fig). In particular, S-adenosylmethionine (from methionine) is critical in the methylation of myelin sheath phospholipids resulting in decreased myelin formation. Furthermore, elevated homocysteine levels are thought to lead to increased concentrations of S-adenosyl homocysteine (SAH), a feedback inhibitor of methylation reactions. In this case, patients with severe vitamin B12 deficiency exposed to nitrous oxide are at particular risk of subacute combined degeneration of the spinal cord. Degeneration in the spinal cord occurs primarily in the posterior and lateral columns, but can in rare occasions occur in peripheral nerves and white matter in the brain. There have been a number of case reports related to this in susceptible individuals in the literature. In general, patients in the case reports are found to 1) be deficient in vitamin B12, or 2) abuse N2O. Patients present from days to weeks after an exposure to N2O with ataxia, sensory deficits that are symmetrical, with deficitis of propioception and vibration sensory discrimination (posterior columns). These patients often have a megalobastic anemia (or no anemia, but elevated MCV) which goes along with vitaminB12 defiency. In severe cases, death or permanent disability are the result. In many cases, high doses of vitamin B12 can result in a resolution.<br />
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The methylenetetrahydrofolate reductase gene (see fig above) (MTHFR) has two distinct polymorphisms that result in deficits and have a combined prevalence of 20% in the Western European population. Two prominent case reports [9,10] related these polymorphisms to catastrophic neurologic outcomes in children which have lead to further studies being conducted. In a 2008 study, [8], 140 healthy patients were carefully evaluated to determine how the above two polymorphisms affected homocysteine levels after N2O (66%) anesthesia. They found significantly higher homocysteine levels in patients who were homozygous for MTHFR 677T or MTHFR 1298C (5.6 increase vs. 1.8 <u>μM)</u><br />
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<span style="color: blue;"><strong style="background-color: #eeeeee; box-sizing: border-box; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">Fig. 2. Plasma homocysteine concentrations in the different groups based on methylenetetrahydrofolate reductase (</strong><span style="background-color: #eeeeee; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> </span><strong style="background-color: #eeeeee; box-sizing: border-box; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;"><em style="box-sizing: border-box; line-height: inherit;">MTHFR</em> </strong><strong style="background-color: #eeeeee; box-sizing: border-box; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">) 677/1298 genotype at three different time points: preoperative, after 2 h of anesthesia, and at the end of surgery. </strong><span style="background-color: yellow;"><strong style="box-sizing: border-box; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">Both homozygous groups developed significantly higher homocysteine concentrations than the other groups (***</strong><span style="font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> </span><strong style="box-sizing: border-box; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;"><em style="box-sizing: border-box; line-height: inherit;">P</em> </strong><strong style="box-sizing: border-box; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">< 0.001)</strong></span><strong style="background-color: #eeeeee; box-sizing: border-box; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">. Genotype combinations (</strong><span style="background-color: #eeeeee; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> </span><strong style="background-color: #eeeeee; box-sizing: border-box; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;"><em style="box-sizing: border-box; line-height: inherit;">MTHFR</em> </strong><strong style="background-color: #eeeeee; box-sizing: border-box; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">677/1298): wt/wt: CC/AA; het/wt: CT/AA; wt/het: CC/AC; het/het: CT/AC; wt/hom: CC/CC; hom/wt: TT/AA</strong></span><br />
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This same study was also able to show that even in patients with normal genetic (wild type) function at the MTHFR locus, prolonged (greater than four hours) exposure to N2O could substantially increase homocysteine levels. In this group of patients with prolonged exposure, there was an approximate 80% increase in homocysteine levels which is similar to the increase experienced by those with the shorter exposures but homozygous for MTHFR polymorphisms.<br />
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More recently, a study of pediatric patients was conducted who had known MTHFR deficiency. In this cohort, they found 12 patients with known MTHFR defiency (ages 3.5 months to 9 years). All twelve patients had normal homocysteine levels preoperatively. The authors found no increase in homocysteine levels in these twelve at risk patients. Four of the twelve had a TIVA with propofol and the remainder underwent sevoflurane anesthesia. Nitrous oxide was avoided in all twelve. Although this study seems to suggest that in healthy pediatric patients with MTHFR deficiency, anesthesia is safe and homocysteine levels are not increased, there are reports of morbidity from MTHFR deficiency after "safe" no nitrous anesthesia. A case report from 2007 describes a patient who underwent urgent surgery with a preoperative diagnosis of homogyzous MTHFR deficiency. The patient was apparently well managed with coumadin and folic acid for prevention of ischemic insults. In the post operative period this patient developed a coronary ischemic insult and renal artery thrombosis [11].<br />
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Finally, there is evidence to suggest that despite acute elevations in homocysteine with adminstration of N2O, it may not be clinically relevant. In 2013, Nagele et al. published results in <i>Anesthesiology </i> [13], showing that even in patients with with at least two cardiovascular risk factors AND being homozygous for MTHFR deficiency, there was no difference in increase in Troponin I increases for 72 hours post operatively. They did find that patients homozygous for MTHFR deficiency had an increase in post operative homocysteine as has been previously shown. There were two arms of randomization (n=250) in patients determined to be homozygeous for MTHFR deficiency. One arm received 1mg vitamin B12 and 5 mg folic acid (before and after surgery) and the other arm received a saline placebo. All patients received a balanced anesthetic with 60% nitrous oxide for procedures lasting at least two hours. The results indicated that although vitamin supplementation did lower homocysteine levels,the incidence of elevation of troponin I was not different between groups.<br />
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This study provided further evidence that N2O results in an increase in homocysteine plasma levels and that these levels can be decreased by vitamin B12 supplementation. However, the study may have diminished concerns that an acute elevation of homocysteine levels after a short interval of anesthesia (~2 hrs) will lead to myocardial damage. The authors noted that there is a growing consensus that homocysteine may be a marker, rather than a cause of atherosclerotic disease and increased cardiovascular risk. The authors also noted that in this study, N2O did not result in an increase in homocysteine to a greater degree in MTHFR homozygous patients vs wild type genotype. They concluded that this difference was related to national mandatory folate fortification of all grain products in the US which can reduce the effects of MTHFR polymorphisms. This is in contrast to the study population in an earlier study conducted in Austria, a country without mandatory folate fortification.<br />
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In my case, I was presented with documentation by the mother that she apparently obtained from the web that indicated that I needed to avoid propofol, lactated ringers, bupivacaine and epinephrine in order to provide safe anesthesia. It is clear, after consulting the literature and gaining a greater understanding of the biochemicals pathways involved in MTHFR deficiency, that propofol, lactated ringers and epinephrine would not increase risk. It seems clear after reading the report that the authors seemed to have conflated MTHFR deficiency and a general mitochondrial disease. Indeed, there are a number of different congenital mitochondrial diseases and depending on the type encountered, propfol, lactated ringers, bupivacaine and epinephrine may be a relative contraindication. Mitochondrial diseases can be broken down into two major groups of related diseases. These are defects of the respiratory chain and defects in fatty acid transfer and metabolism. Propofol may have been on the list due to its relation to propofol infusion syndrome (PRIS) which leads to mitochondrial dysfunction and lactic acidosis. In fact, propofol is unque among parenteral anesthetics in that it is known to affect mitochondrial metabolism by at least four separate mechanisms. It can uncouple oxidative phosphorylation and inhibit complexes I, II, and IV. However the strongest effect of propofol is its inhibition of transport of long-chain acylcarnitine esters via inhibition of acylcarnitine transferase (carnitine palmitoyl transferease I). However, reveiws note that even in patients with mitochondrial defects, a limited one time bolus of propofol for induction of anesthesia seem generally well tolerated. The number and manifestations of mitochondrial disease are enormous and protean. Fortunately, MTHFR is not related to the function of the mitochondria and even patients homozygous for the defective gene of this enzyme seem to tolerate anesthesia without significant complications, even when given nitrous oxide. Now, I feel I would be better equipped to have a more involved and informative conversation with the mother. This will allow to me to push to maintain the freedom to use propofol, bupivacaine, LR, and epinephrine if I feel that they would be important to use.<br />
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<span style="font-family: inherit;">1. <span style="background-color: white;">Shay H, Frumento RJ, Bastien A.<i> </i></span><span style="background-color: white;"><span class="ref-journal"><i>J Anesth.</i> </span>2007;<span class="ref-vol">21</span>:493–6.</span></span><br />
<span style="font-family: inherit;"><span style="background-color: white;">2. </span><span style="background-color: white;"> </span><span class="element-citation" style="background-color: white;">Badner NH, Beattie WS, Freeman D, Spence JD.<i> </i><span class="ref-journal"><i>Anesth Analg</i>. </span>2000;<span class="ref-vol">91</span>:1073–9</span></span><br />
<span class="element-citation" style="background-color: white;"><span style="font-family: inherit;">3. Nur Orhon Z, Koltka EN, Tufekci S, Buldag C, Kisa A, Durakbasa CU, and Celik M. <i>Turk, J Anaesthesiol Reanim. </i>2017;45(5):277-281.</span></span><br />
<span style="font-family: inherit;"><span class="element-citation" style="background-color: white;">4. </span><span class="BibAuthorName" style="background-color: #fcfcfc; box-sizing: border-box; color: #333333; letter-spacing: 0.102px;">Ueland, PM, </span><span class="BibAuthorName" style="background-color: #fcfcfc; box-sizing: border-box; color: #333333; letter-spacing: 0.102px;">Nygard, O, </span><span class="BibAuthorName" style="background-color: #fcfcfc; box-sizing: border-box; color: #333333; letter-spacing: 0.102px;">Vollset, SE, </span><span class="BibAuthorName" style="background-color: #fcfcfc; box-sizing: border-box; color: #333333; letter-spacing: 0.102px;">Refsum, H </span><span class="Year" style="background-color: #fcfcfc; box-sizing: border-box; color: #333333; letter-spacing: 0.102px;">2001</span><span class="ArticleTitle" style="background-color: #fcfcfc; box-sizing: border-box; color: #333333; display: inline; letter-spacing: 0.102px;">The Hordaland Homocysteine Studies<i> </i></span><span class="JournalTitle" style="background-color: #fcfcfc; box-sizing: border-box; color: #333333; letter-spacing: 0.102px;"><i>Lipids. </i> 2001; </span><span class="VolumeID" style="background-color: #fcfcfc; box-sizing: border-box; color: #333333; letter-spacing: 0.102px;">36</span><span class="FirstPage" style="background-color: #fcfcfc; box-sizing: border-box; color: #333333; letter-spacing: 0.102px;">S33-</span><span class="LastPage" style="background-color: #fcfcfc; box-sizing: border-box; color: #333333; letter-spacing: 0.102px;">S39</span></span><br />
<span class="LastPage" style="background-color: #fcfcfc; box-sizing: border-box; color: #333333; letter-spacing: 0.102px;"><span style="font-family: inherit;">5. Graham IM, Daly LE, Refsum HM, et al. <i>JAMA. </i>1997;277:1775-81.</span></span><br />
<span class="LastPage" style="background-color: #fcfcfc; box-sizing: border-box; color: #333333; letter-spacing: 0.102px;"><span style="font-family: inherit;">6. Chambers JC, McGregor A, Jean-Marie J, Kooner JS. <i>Lancet. </i>1998;351:36-7.</span></span><br />
<span class="LastPage" style="background-color: #fcfcfc; box-sizing: border-box; color: #333333; letter-spacing: 0.102px;"><span style="font-family: inherit;">7. badner NH, Beattie WS, Freeman D and Spence JD. <i>Anesth Analg. </i>2000; 91:1073-9.</span></span><br />
<span style="background-color: #fcfcfc; color: #333333; letter-spacing: 0.102px;"><span style="font-family: inherit;">8. Nagele P, Zeugswetter B, Wiener C, Burger H, Hupfl M. <i>Anesthesiology. </i>2008;109:36-43.</span></span><br />
<span style="font-family: inherit;"><span style="background-color: #fcfcfc; color: #333333; letter-spacing: 0.102px;">9. </span><span style="background-color: white; color: #333333;">Lacassie HJ, Nazar C, Yonish B, Sandoval P, Muir HA, Mellado P:<i> Br J Anaesth</i> 2006; 96:222–5</span></span><br />
<span style="background-color: white; color: #333333;"><span style="font-family: inherit;">10. Lacassie, HJ Nazar, C Yonish, B Sandoval, P Muir, HA Mellado, P</span></span><br />
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<span style="font-family: inherit;">Selzer RR, Rosenblatt DS, Laxova R, Hogan K: . <i>N Engl J Med</i> 2003; 349:45–50</span></div>
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<span style="font-family: inherit;"><span style="background-color: white; font-size: 15.9991px;">11. </span><span style="color: #303030;">Shay H, Frumento RJ, Bastien </span><i><span style="color: #303030;">J Anesth</span><span style="color: #303030;">.</span></i><span style="color: #303030; font-style: italic;"> 2007; 21(4):493-6.</span></span><br />
<span style="color: #303030;">12. </span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"> </span><span class="element-citation" style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">Badner NH, Freeman D, Spence JD. Preoperative <span class="ref-journal"><i>Anesth Analg.</i> </span>2001;<span class="ref-vol">93</span>:1507–10.</span><br />
<span class="element-citation" style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">13. Nagele P, Brown F, Francis A, Scott M, Gage BF, Miller JP. <i>Anesthesiology. </i> 2013;119:19-28.<br />14. Hsieh VC, Krane EJ, Morgan PG. <i>Jour inborn Error Metabolism & Screening</i>. 2017;5:1-5.</span>Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-71301956765469734752019-03-01T18:53:00.002-08:002020-01-15T14:06:26.105-08:00fluid resuscitation in an open bowel resection<div style="text-align: center;">
61 year old male presents with perforation of sigmoid colon secondary to diverticulitis</div>
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On my saturday call, a 61 year old male presented after several days on the floor for open sigmoid colectomy secondary to a perforation of the large bowel. Versed and fentanyl were given in preparation to go to the OR. The patient was otherwise stable and talkative in the preoperative area. After 2mg of versed and 100 mcg of fentanyl, the patient was more somnolent than expected for the given dose. The patient had a history of coronary artery disease. A review of his cardiac history revealed that he had had an angioplasty nearly 10 years ago with a repeat angiogram eight years ago. His repeat angiogram revealed restenosis of his RCA lesion now occluded at 30 to 40%. The patient had disease of two other coronary arteries as well. The patient was receiving nitrates to control angina. He reported that he was currently asymptomatic. He was a diabetic using insulin. He also admitted to drinking vodka each day. Based on this history his RCRI would be 3 pts (1 pt for ischemic cardiac disease, 1 pt for diabetes requiring insulin and 1 pt for high risk surgery <emergency colon="" for="" intraabdominal="" of="" perforation="" surgery="">). By using this tool located <a href="https://www.mdcalc.com/revised-cardiac-risk-index-pre-operative-risk">here</a> you can derive his preoperative expected risk of major cardiac event at 15%. </emergency></div>
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Induction was with 50 mg of propofol and succinylcholine with rapid sequence intubation. His abdomen was very distended and appeared to have ascites. After intubation, a right radial arterial line was placed. Blood pressure was stable with induction, however, very shortly after beginning the inhalation agent, the blood pressure dropped down into the 60's systolic. A phenylephrine drip was begun while decreasing the concentration of desflurane. A foley catheter was placed, however, no urine returned into the foley bag. I also noticed that the pulse pressure was large, with very low diastolic pressures (consistently in the 40's). </div>
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Trying to determine the volume status of this patient was a challenge. The blood pressure was low, and required ongoing low dose phenylephrine as an infusion. The main question thus became, what was the main etiology of this patient's continued hypotension. Vasoplegia secondary to sepsis syndrome, hypovolemia from capillary leak, and inadequate cardiac contractility were all possibilities. Determining fluid management can be a challenge in situations where multiple sources of hypotension may coincide.</div>
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The current recommendations in surviving sepsis guidelines recommend immediate infusion of 30 mL/kg of crystalloid in suspected sepsis with hypotension (about 2 Liters of fluid in the normal adult). If hypotension continues, a vasopressor should be added. The general gestalt for most anesthesiologists treating a patient with a known perforation of the colon for emergency surgery would consider using rapid infusion of crystalloids as a mainstay for continued hypotension. During my residency training, it was often stated and taught that giving vasopressors to a hypovolemic patient could results in vasoconstriction that leads to organ ischemia, and aggressive fluid (cyrstalloid) administration should continue during surgery.</div>
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However, more recently, clinicians are reconsidering and evolving the resuscitation methods during large and extensive surgery. A large number of studies have looked at the detrimental effects of large amounts of crystalloids given to patients. Another group of studies have specifically looked at restrictive volume strategies to improve outcomes in elective bowel surgery patients. Another group of studies have utilized a large number of methods to measure or estimate cardiac output to provide fluids in a goal directed manner to improve outcomes. To date, there is still confusion as to what constitutes best practice. What remains clear is that under resuscitated patients, or those who are hypovolemic for extended periods of time, suffer morbidity. What has started to become equally clear, is that over hydration, can be equally detrimental. </div>
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My patient had very little urine and what did appear was very concentrated. Therefore, I pushed forward with a presumptive diagnosis of hypovolemia as at least one major cause of his ongoing hypotension. I therefore began an aggressive fluid resuscitation with lactated ringers. After four liters given over about 1.5 hours, there was little if any change in any of the patients parameters. In fact, there was almost no urine output. At this point I gave 250 mL of 5% albumin. Blood loss was not substantial, however, there was an approximate 3 liter loss of fluid from the peritoneal cavity of presumptive ascites. It was noted that the patient had a visibly cirrhotic liver. Large volume paracentesis is known to lead to arteriolar vasodilation and an increase in cardiac output. It is widely recognized that paracentesis induced circulatory dysfunction can lead to significant morbidity in patients with liver disease. Management recommendations include post removal treatment with 125 mL of 5% albumin volume replacement per liter of ascitic fluid removed (if more than 5L is removed), and consideration of vasopressors such as terlipressin for continued hypotension.<br />
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Recently, a large number of studies have attempted to determine the best way to manage volume status in patients with or at risk for hypotension. Maintaining perfusion pressure and thus DO2 to tissues is critical to avoid organ damage secondary to hypoxic injury. However, some studies have also shown harm to patients associated with overhydration. In Anesthesiology, a study [1] in radical cystectomy patients found that the rate of complications was 52% in a group of patients who received a low volume of LR vs a high volume of LR where the rate of complications was 73%. The low volume group received LR at 1 mL/kg/hr until completion of cystectomy and then 3 mL/kg/hr until the end of surgery plus low dose norepinephrine. The high volume group received 6 mL/kg/hr plus 250 mL fluid boluses as need during surgery. Post op fluid therapy was similar between groups. The rationale for using 6 mL/kg/hr in this study likely came from traditional teaching in textbooks such as Stoelting where we are taught that 6 to 8 mL/kg/hr should be used to maintain hydration in patients undergoing major abdominal surgery [2]. In 2003, Brandstrup et al was able to show a reduction in complications by using a low volume algorithm in elective colorectal surgery. In that study, the high volume group received 7 mL/kg/hr x 1 hour, then 5 mL/kg/hr x 2 hours, and then 3 mL/kg/hr thereafter. Blood loss was replaced by NS up to an EBL of 500 mL, and then colloid up to an EBL of 1500 mL. The restrictive group only received 500 mL D5W and 6% Hetastarch for blood loss up to 1500 mL. The standard group received 5.4 L overall and the restrictive fluid group received only 2.7L. Cardiopulmonary complications were reduced in the restrictive fluid group from 24% to 7% and the incidence of tissue healing complications was reduced from 31% to 16%. In 2018 a large international RCT trial compared a restrictive fluid therapy regimen to a liberal strategy (RELIEF study) in patients having major abdominal surgery. In the liberal group crystalloid was given at 10 ml/kg during induction of anesthesia, followed by an 8 ml/kg/hr infusion until the end of surgery. Post op patients received 1.5 ml/kg/hr for 24 hours. The restrictive regimen was designed to provide a net zero fluid balance. An infusion of crystalloid at a dose of 5 ml/kg/hr was administered until the end of surgery. Post op fluids were given at 0.8 ml/kg/hr. During surgery, colloid or blood was given to replace blood loss in a 1:1 ratio. The primary outcome measure was rate of disability free survival at 1 year. There were no differences between groups for this outcome. The secondary outcome was AKI which occurred in 8.6% of the restrictive group and 5% of the liberal group. The median fluid load given in the restrictive group was 1.7L for average surgery duration of 3.2 h while the fluid volume was 3L in the liberal group. It seems likely, that in this study at least, restrictive was too restrictive and the liberal group was more like the restrictive group of past studies. <0 .001="" 1.7l.="" 13.6="" 16.5="" 1="" 30-day="" 3="" 3l="" 40="" a="" abdominal="" about="" administered="" administration="" aki.="" an="" and="" anesthesiologists="" another="" appropriate="" as="" associated="" association="" average="" be="" between="" both="" but="" by="" can="" case.="" challenges="" characterized="" complications="" concluded="" consistently="" costs="" crystalloid="" defined="" difference="" differences="" during="" enough="" equates="" estimates.="" find="" fluid="" for="" found="" group="" hand="" have="" having="" he="" highest="" his="" hour="" in="" incidence="" intraoperatively="" l="" length="" less="" liberal="" lowest="" major="" moderate="" mortality="" n="" nbsp="" ndeed="" needle="" observational="" observed="" of="" on="" optimal="" other="" outcome.="" outcomes="" p="" patients="" postoperative="" quintile="" received="" regimen="" relief="" respiratory="" restrictive="" revealed="" same="" second="" secondary="" sick="" significantly="" small="" stay.="" strategy="" study="" surgery.="" surgery="" textbook="" than="" that="" the="" therapy="" there="" this="" threading="" to="" traditional="" trial="" u-shaped="" underscores="" volume="" volumes="" was="" we="" were="" whereas="" while="" with="">Traditional thresholds for intraoperative oliguria do not predict acute kidney injury (AKI). In a meta analysis [4] done in 2016 of 28 trials including both surgical and critically ill patients, less renal dysfunction was noted in patients receiving goal directed fluid therapy without the use of oliguria to guide fluid administration. Another meta analysis by Cochrane concluded, "The balance of current evidence does not support widespread implementation of this approach to reduce mortality but does suggest that complications and duration of hospital stay are reduced." Specifically they showed that GDT reduced the rate of renal failure, respiratory failure and wound infection. Typically, goal directed therapy for fluid management has relied upon esophageal doppler technology to estimate stroke volume. This technology is not readily available however. Technology to analyze the arterial waveform to estimate pulse pressure variation (PPV) and stroke volume variation (SVV) as as well as systolic pressure variation (SPV) has been developed and is making inroads into many operating rooms. However, these technologies are not wide spread and easily applied. In 2012 Thiele et al published a study showing that anesthesia providers were able to make correct diagnostic decisions in 96% of situations using a simple visual "eyeball" review of systolic blood pressure waveforms attempting to estimate systolic blood pressure variation. This provides evidence that in patients who have an arterial line in place, anesthesiologists who do not have access to higher level arterial waveform analysis technology can be "good enough" in lower acuity situations to determine which patients need more fluid.<br />
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Goal directed therapy using stroke volume variation (SVV) or pulse pressure variation (PPV) and arterial waveform analysis has been studied intensely in the last decade. The general concept relates to an attempt to determine if a patient who is hypotensive would respond to a fluid challenge (best is 3 to 4 mL/kg) by increasing stroke volume by about 10 to 15%. During mechanical ventilation there is a rise in pleural pressure during the inspiratory phase which impedes blood return to the right atrium and thus the right ventricle. At the same time as right heart preload is decreased, right heart afterload is increasing during the inspiratory phase in conjunction with increased pleural pressure. However, left ventricular preload increases while left ventricular afterload decreases. This transient alteration in right heart and left heart preload and afterload leads to a decrease in LV output a few heartbeats after completion of mechanical insufflation (or expiratory phase of mechanical ventilation). The changes in the RV and LV stroke volume with each mechanical breath are larger on the steep compared with the flat portion of the Frank Starling curve for four main reasons: 1) the SVC is more collapsible in hypovolemia, 2) the inspiratory increase in right atrial pressure is greater in hypovolemic states secondary to the greater transmission of pleural pressures to the more compliant right atrium, 3) the effect of mechanical inspiration on RV after load is greater because of higher trans alveolar pressures in the setting of hypovolemia, and 4) the ventricles are more sensitive to preload when they are operating on the steep portion of the frank starling curves. To validate this Michard et al studied 40 patients with sepsis on mechanical ventilation. This study found higher variations in pulse pressure (24% vs 7%) in a group of patients who responded to volume expansion (defined by a 15% increase in CI) vs those that did not. They showed that if pulse pressure varied by more than 13% there was a 94% sensitivity (low false negative) and a 96% specificity (low false positive) in predicting volume responsiveness [5]. Nine years after this initial study, a meta analysis was completed by Marik et al [5]. This group looked at 29 clinical studies. They found that the area under the ROC curve was 0.94 for PPV and 0.86 for SVV. All other strategies utilized for determining volume status (CVP, global end-diastolic volume index, LVEDA index) performed poorly. They also found a very consistent threshold for defining fluid responsiveness of 12 to 13%. They also noted that there is a gray zone of 9 to 13% where fluid responsiveness cannot be predicted reliably and this 'gray zone' may affect up to 25% of patients during general anesthesia. Furthermore, in order to perform arterial waveform analysis using current technology, patients must be in sinus rhythm, be mechanically ventilated with tidal volumes greater than 7 mL/kg and not be receiving vasopressors.<br />
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When confronting a patient whose volume status is in question and hypotension is at hand, a detailed conceptual construct is helpful in understanding how to proceed. This construct aids in understanding the mechanisms of how fluid therapy can be harmful or helpful and when. One concept that was previously highlighted in the journal <i>Anesthesiology</i> divides total blood volume into the stressed and unstressed volumes within the body. The 'unstressed' volume is that volume of blood that fills the blood vessels without causing a rise in pressure. The 'stressed' volume is any additional volume that results in a rise in pressure AND elastic distention of the vessel wall. Therefore, when a clinican administers a fluid challenge, they are aiming to expand the 'stressed' volume. Whether the fluid challenge leads to a rise in pressure or not is dependent upon whether it fills the 'unstressed' volume or the 'stressed' volume. This is dependent upon the overall venous compliance. In 1894, Bayliss and Starling first described the concept of mean systemic filling pressure (Pmsf) in a dog model. This is defined as the pressure in the vascular system when the heart is stopped and there is no blood flow. Pmsf is a critical element in determining venous return along with right atrial pressure and resistance to venous return. The driving pressure for venous return is the pressure gradient between Pmsf and central venous pressure (CVP) which then determines cardiac output.<br />
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It should be noted that with the induction of anesthesia, or other physiologic changes the unstressed volume can suddenly increase. A sudden increase in the unstressed volume (see above figure) would then lead to a decrease in the Pmsf and thus reduce venous return and thus cardiac output. In a patient who undergoes a temporary state (i.e. general anesthesia) where the unstressed volume is suddenly increased due to sympathectomy, and this is filled aggressively with fluid, and then thereafter, the unstressed volume returns to its previous state (emergence), the patient could now be in a sudden state of fluid overload as the fluid placed into the unstressed volume is now recruited into the stressed volume per force. Therefore, the above conceptual framework allows clinicians to visualize the potential negative effects of overly aggressive fluid therapy. Conceptually, one might consider what happens to the Pmsf in a patient suffering a vasodilatory state such as sepsis. In this scenario, once again, the unstressed volume is dramatically increased leading to a decrease in Pmsf which will decrease venous return and thus cardiac output. If the treatment modality is only additional fluid to fill the unstressed volume, there is a real risk of too much fluid. Therefore, the correct therapeutic modality in treating an unnatural increase in the venous capacitance or unstressed volume are vasopressors. Vasopressors in this setting serve to return the unstressed volume back to its "natural" volume, at which time, additional fluid therapy can fill the "stressed" volume leading to an increase in Pmsf which would be clinically observable with an increase in SV or CO leading to improved blood pressure.<br />
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The above case represents a perfect example of a patient who had vasoplegia secondary to sepsis and therefore, a very large unstressed volume. In addition, the patient was also likely suffering from a capillary leak syndrome leading to loss of intravascular fluid into the interstitium. This fluid would need to be replaced. However, the vasodilated state required Alpha 1 adrenergic therapy. There is evidence that early fluid therapy will do more than just increase the mean systemic filling pressure (Pmsf) promoting increased right heart filling pressures. Early aggressive fluid therapy in sepsis can also shift the cytokine response towards a more anti-inflammatory balance [8] and is associated with reduced mortality in septic patients [9].<br />
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In my patient after about 6 liters of crystalloid I infused 250 mL of human 5% albumin. There is a great deal of controversy related to the type of fluids. Currently, there is no clear evidence that crystalloid (balanced salt solution) leads to greater mortality than colloid. In addition hespan has fallen out of favor because it has been linked to AKI in critically ill adults. Risk of HES-induced renal toxicity depends primarily on the molar substitution. For example, the commonly available Hespan or hydroxylethyl starch 6% has a MW of 600 and degree of substitution of 0.75. This formulation started to fall out of favor initially in 2003 when the FDA required that a new label be applied to 6% hetastarch (HESPAN) that recommended against HESPAN in bypass patients due to concerns related to coagulopathy. Newer HES solutions (tetrastarch 130/0.4) are considered far less toxic to the kidneys. A recent [10] observational study compared a newer HES (130/0.4) to crystalloid and found that HES was not associated with an increased frequency of post op kidney failure. Also, in-hospital mortality and ICU requirements were not different between groups. This was a mixed cohort of elective surgical patients. Another study comparing HES 130/0.4 to 5% albumin found no differences in renal function in a small RCT in patients undergoing cystectomy. Another study of HES 130/0.4 found that this formulation could reduce the inflammatory response in patients undergoing major surgery compared to a purely crystalloid based volume regimen. In larger meta analyses where a large number of different types of starches were compared to crystalloids, the incidence of RRT was greater in the patients receiving starches. In another study using pentastarch (200/0.5) vs LR there was a larger incident of AKI in the starch group. However, on subgroup analysis it was found that patients suffering the negative renal outcome were given a larger than usual volume of pentastarch. Patients given less than 22 mL/kg of pentastarch actually suffered a significantly lower mortality (31% vs 58%) vs high dose penta starch and vs. LR (41% mortality). Furthermore, starches, especially those with a high degree of molar substitution (i.e. 0.75) are associated with a greater risk of bleeding and transfusions as per large meta analyses. Fortunately, once again, lower molar substitution products (tetra starch=0.4) seem to have a smaller effect on hemostasis. Avoiding these products (starches in general) would likely be important in particular in the above case as it was found that the patient had a fairly large amount of ascites upon opening the abdomen with a liver that appeared markedly cirrhotic. Although the patient had normal coagulation parameters prior to surgery with no evidence of decreased liver function, it is possible that the patient had some degree of platelet dysfunction from his liver disease which would be a relative contraindication to any form a starch fluid therapy.<br />
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In 2008, a lengthy review article was published on periopeartive fluid management in <i>Anesthesiology </i>[109;723-740]. In addition to being an excellent general review of the literature on perioperative fluid management, the author reviews the importance of the glycocalyx and it's part in forming the enodthelial surface layer (ESL) (see fig).<br />
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<span style="font-family: "georgia" , "times new roman" , serif;">This layer is critical in avoiding platelet aggregation, leukocyte adhesion and increased endothelial permeability. The ESL can be damaged by ischemia reperfusion, proteases, TNF-alpha, oxidized LDL lipoproteins, and atrial natriueretic peptide. Therefore, two important things should be noted: 1) overly aggressive fluid hydration even in healthy volunteers may damage the ESL leading to pathologic fluid losses via damage to the ESL. 2) Major surgery and/or patients in a state of sepsis where a large inflammatory response is expected will also have a damaged ESL and pathologic shift of fluids into the interstitial space. Quoting the article from Chappell in Anesthesiology, "</span><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 16px;">Consequently, the primary indication of crystalloids is replacement of fluid losses </span><span style="box-sizing: border-box; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 16px; font-style: italic; line-height: inherit;">via</span><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 16px;"> (1) insensible perspiration and (2) urinary output. Colloids, by contrast, are indicated to replace plasma deficits due to (2) acute blood loss or (2) protein-rich fluid shifts toward the interstitial space (pathologic type 2 shift)."</span><span style="background-color: white; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 16px;"> </span><span style="font-family: "georgia" , "times new roman" , serif;"><span style="caret-color: rgb(51, 51, 51);">Therefore, for major surgery, crystalloids would be indicated to replace insensible losses estimated to be about 1 mL/kg/hr (per chappell article). All other fluid needs (i.e. from pathologic type 2 shift (shift of fluid across the endothelial glycocalyx into the interstitium) should be replaced by a colloid solution. Unfortunately, HESPAN is no longer available and HES (130/0.4) is likely to be unavailable as well. 5% albumin is the only choice available in our hospital. Given that the current evidence does not seem to indicate a clear and defined cut off for crystalloid where it is clear that you are killing patients, heavy use of crystalloid is still the mainstay given a lack of alternatives.</span></span><br />
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<span style="font-family: "georgia" , "times new roman" , serif;"><span style="caret-color: rgb(51, 51, 51);">Therefore, in the above case, I might have selected a larger 5% albumin dose, maybe 1 liter, but ultimately, given the degree of the fluid needs, I would have been forced to use a fairly large volume of crystalloid. Unfortunately, the vast majority of this crystalloid found its way into the interstitial space (chappell estimates it's actually 5:1 into the interstitial space not 3:1 as historically taught). Patients with sepsis are also suffering from vasoplegia. Therefore, using the above definition, there unstressed volume will be pathologically increased. An IV vasopressor infusion to decrease the unstressed volume was also critical in facilitating the fluid resuscitation.</span></span><br />
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<span style="font-family: "georgia" , "times new roman" , serif;"><span style="caret-color: rgb(51, 51, 51);">In summary, this case represents a patient with a perforation of the large bowel presenting with a significant systemic inflammatory response resulting in shock requiring emergent open abdominal surgery and aggressive fluid therapy. In addition, the patient had co morbidities of liver disease, coronary artery disease, and insulin requiring diabetes. Fluid management was reviewed and an understanding of the mechanisms of how to determine the volume status of patients using objective measures such as PPV to achieve a goal directed infusion of fluids was highlighted. Furthermore, the pros and cons of crystalloid vs colloids was addressed highlighting that crystalloids should in general be reserved to treat ongoing insensible fluid losses while colloids should be utilized for all type II or pathologic fluid losses (including hemorrhage and fluid crossing the endothelial layer into the interstitial space.</span></span><br />
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1. Wuethrich P, Burkhard F, Thalmann G, Stueber F, Studer U. <i>Anesthesiology</i>. 2014 FEB<br />
2. <span style="background-color: whitesmoke;"><span style="font-family: "georgia" , "times new roman" , serif;">Stoelting et. al. Basics of Anesthesia, 5th ed. Elsevier – China, p. 349, 2007</span></span><br />
<span style="background-color: whitesmoke;"><span style="font-family: "georgia" , "times new roman" , serif;">3. </span></span><span style="background-color: whitesmoke;"><span style="font-family: "georgia" , "times new roman" , serif;">Brandstrup B et. al. Ann Surg 238: 641, 2003</span></span><br />
<span style="font-family: "georgia" , "times new roman" , serif;"><span style="background-color: whitesmoke;">4. Egal M, Erler NS, de Geus HR, Van Bommel J, Groenevald AB. <i>Anesth </i></span><i>Analg</i>. 2016; 122:173-185.</span><br />
<span style="font-family: "georgia" , "times new roman" , serif;">5. Michard F, Boussat S, Chemla D. et al. <i>Am J Resp Grit Care Med</i>. 2000; 162: 134-138.</span><br />
<span style="font-family: "georgia" , "times new roman" , serif;">6. Myles PM et al. <i>NEJM.</i> 2018; 378:2263-2274.</span><br />
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<span style="font-family: "georgia" , "times new roman" , serif;">7. Shin CH, Long DR, McLean D, et al. Ann Surg 2017 Mar 10</span><br />
<span style="font-family: "georgia" , "times new roman" , serif;">8. </span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">Dorresteijn MJ, van Eijk LT, Netea MG, et al. </span><span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;"><span class="ref-journal"><i>J Endotoxin Res.</i> </span>2005;<span class="ref-vol">11</span>:287–293.</span><br />
<span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">9. </span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">Lee SJ, Ramar K, Park JG, et al. </span><span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;"><span class="ref-journal"><i>Chest.</i> </span>2014;<span class="ref-vol">146</span>:908–915.</span><br />
<span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">10. Pagel JI, Rehm M, Kammerer T, Hulde N, Speck E, Briegel J, Reinholz F, Crispin A, Hofmann-Kiefer KF. <i>Anesth Analg</i>. 2018; 126(6): 1949</span></div>
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Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-51653057918797437712018-11-14T15:33:00.000-08:002019-09-11T11:23:26.615-07:0034 year old female who is 15 weeks pregnant for cerclageA 34 year old female required cerclage for incompetent cervix and presented to the OR for the procedure. I discussed the pros and cons of GA vs. regional neuraxial anesthesia and we proceeded with spinal anesthesia. The patient was taken to the OR, 6.5mg of hyperbaric bupivacaine + 20 mcg fentanyl was administered via 25 G whitakre needle. The patient remained seated for aproximately 1 minute and then was layed supine. The patient tolerated the procedure without sedation.<br />
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The patient went to PACU able to move her legs but complaining of sinificant pruritis for which she requested treatment. She was discharged after 2 hours and 37 min in the PACU after a case that was 30 min in duration. </div>
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Management of the pregnant patient brings about a lot of questions for the anesthesiologist. Determining what anesthetics are safe and if needed what can be used to treat common side effects of anesthesia must be considered. For example, in our patient, pruritis is typically treated with benadryl. This medication may not be appropriate for the parturient however. In general, I prefer to provide spinal anesthesia for cerclage. While there is currently no evidence to indicate that anesthetics are teratogenic, there is a growing literature demonstrating that anesthetics are neurotoxic to the fetus or early developing brain. While large human studies in pediatric patients seem to indicate that there is no significant increased risk to the brain, we have no good studies to indicate that there is not alteration to neurogenesis in the fetus. Furthermore, even though we do not have evidence of harmful fetal affects of anesthetics, we also lack good solid randomized controlled trials to prove an absence of negative effects. If you perform an anesthetic on a patient who is pregnant who goes on to deliver a newborn with obvious defects, not otherwise explained, you carry potential legal risk unless you can establish that general anesthesia was truly your only option. </div>
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Giving spinal anesthesia to a patient who is to be discharged the same day creates panic in surgeons and facility administrators who are convinced that the patient will require prolonged care due to inability to void. Therefore, in some cases overcoming this concern can be prohibitive. Avoiding prolonged PACU stays (due to post operative urinary retention [POUR]) is accomplished by modification of typical intrathecal doses.</div>
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The control of micturition is a complex process involving multiple afferent and efferent neural pathways, reflexes and central and peripheral neurotransmitters. It is well known that bupivacaine and tetracaine delay return of bladder function beyond the resolution of sensory anesthesia, and may lead to distention of the bladder beyond its normal functioning capacity. This may result in bladder damage. The normal bladder has a capacity of between 400 mL and 600 mL. The detrusor muscle is innervated by efferent somatic, sympathetic and parasympathetic fibers. The parasympathetic fibers cause contraction of the detrusor and relaxation of the spinchter, permitting micturition. The sympathetic fibers produce detrusor relaxation and internal urethral sphincter closure. The two systems are governed by spinal reflexes and two pontine brain stem centers. General anesthesia casues bladder atony. Volatile anesthetics as well as sedative-hypnotics inhibit the pontine micturition center and voluntary cortical control center of the bladder. IT injection of bupivacaine will block afferent and efferent neural transmission from and to the spinal segments (S2-S4). Typically, complete normalization of detrusor strength occurs 1 to 3.5 h after ambulation. IT injection of opioid decreases the urge sensation and detrusor contraction largely by opioid effect on opioid receptors in the spinal cord that decrease parasympathetic firing. Theses effects as well as others, can be reversed with naloxone administration. It is understood that opioids added to IT local anesthetic increases the rate of POUR. This concept was looked at in an article by Niazi et al. [1]. They compared three groups of patients who received hyperbaric bupivacaine 0.5% (15 mg) (S1), bupi 15 mg + fentanyl 20 mcg (S2) or GA (G). The incidence of POUR was 20% in group S1, 35% in group S2, and 8% in group G. There incidence of 35% of POUR in the local + fentanyl group was much higher than another study [2] where the group with fentanyl given IT had POUR of only 20%. This is likely because in this study only 7.5 mg of bupivacaine was used and 25 mcg of fentanyl. The impact of bupivacaine dose was considered in a study that compared bupivacaine with lidocaine for spinal anesthesia for cervical cerclage. In this study, the bupivacaine dose was 5.25 mg with 20 mcg of fentanyl added. This was compared to lidocaine 30 mg + fentanyl 20 mcg [3]. They did not detect any difference between the two anesthetics with regard to onset and recovery time. They concluded that low dose bupivacaine (5.25 mg) offered a similar recovery profile to lidocaine IT 30 mg. They did have 2 of 30 women in the lidocaine group with complaints consistent with TNS that resolved in 48 hours. Indeed, lidocaine is really the gold standard in regards to outpatient spinal anesthesia. Due to its reputation of causeing TNS, it has fallen into disuse. TNS or transient neurological symptoms is described as transient buttock pain, radicular lower extremity pain, and dysesthesias that present within the first 24 hours following recovery from spinal anesthesia. Some have reported an incidence as high as 40% with lidocaine. There is also some who speculate that the hyperbaric lidocaine solution (5% hyperbaric could be the cause) of TNS. A recent study of 50 patients using 2% isobaric lidocaine as a single IT dose did not find a single case of TNS [4]. Unfortunately, this paper did not disclose the lidocaine dose. This is important, because some studies suggest that the incidence of TNS is dose dependent [6]. In fact, some research or analysis of research suggests that using a lidocaine dose of less than 25 mg might prevent TNS from lidocaine. The above study failed to cite another study performed in 1998 (<i>Anesthesiology [5]). </i>In this publication isobaric lidocaine 60 mg at a 2% concentration was compared to mepivacaine 1.5 %. They found a 22.2% incidence of TNS with this formulation of lidocaine vs 0% in the mepivacaine group. Another group used 10 mg lidocaine for spinal anesthesia and found a 0% incidence of TNS [7] with good operating conditions for prostate bx. Another group compared knee arthroscopy in patients who received IT unilateral bupivacaine 3 mg + fentnayl 10 mcg vs bilateral lidocaine 20 mg + fentanyl 25 mcg [8]. In this study no patients in either group suffered TNS (each group had n=25). The incidence of pruritis was 5/25 patients and 7/25 patients in the bupi group vs the lido group. Urinary retention not requiring bladder catheterization was found in 2/25 patients in the bupivacaine group (however the p value was 0.149). They reported 100% excellent operating conditions for knee arthroscopy, with a duration of sensory block of 157 min in the bupivacaine group and 129 min in the lidocaine group. Time spent in the PACU was 39 min vs 0 min in the bupivacaine vs lidocaine group, time to ambulate was 159 min vs 3.6 min and time to home readiness was 184 min vs 153 min in the bupivacaine vs lidocaine group respectively. while this was a small study, it seems to emphasize that with 20 mg of lidocaine + fentnayl, you can achieve a very short PACU stay, nominal risk for urinary retention, with very low chance of TNS. Unfortunately, in many institutions, spinal lidocaine is simply not available. Therefore, low dose bupivacaine is an alternative. I opted for 6 mg of bupivacaine, but as mentioned there is some evidence that 5.25 mg of bupivacaine is sufficient for cerclage. </div>
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1. Niazi AAA, Taha MAA. <i>Egyptian Journal of Anesthesia. </i>2015. 31:65-9.</div>
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2. Gupta A, Axelsson K, Thorns, E, et al. <i>Acta Anaesthesiol Scand</i> 2003;47:13-9.</div>
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3. Beilin Y, Zahn J, Abramovitz S, Bernstein HH, Hossain S, Bodian C. <i>Anesth Analg. </i>2003; 97: 56-61.</div>
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4. Frisch NB, Darrith B, Hansen DC, Wells A, Sanders S, Berger RA. <i>Arthroplast Today. </i>2018;4:236-39.</div>
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5. Liguori GA, Zayas VM, Chisholm MF. <i>Anesthesiology</i> 1998. 88; 619-23.</div>
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6. Buckenmaier CC III, Nielsen KC, Pietrobon R, et al. <i>Anesth Analg</i> 2002;95:1253-7.</div>
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7. Nishikawa K. et al. <i>Jour of Clinical Anesthesia </i>2007;19:25-9.</div>
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8. Hassan HIEA, <i>Anesth Essays Res</i> 2015. 9:21-27.</div>
Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-38811982697096245282018-11-14T06:18:00.000-08:002018-11-14T06:18:18.279-08:0026 year old on TPN for major bowel surgery<span style="font-family: inherit;">A 26 year old female with previous bowel surgery for superior mesenteric artery (SMA) syndrome, presents to have a revision of her gastrojejunal anastomossis. SMA syndrome occurs when the aorta and superior mesenteric artery wrap around the duodenum in such a way as to compromise the passage of food through the narrowed part. The syndrome is often related to loss of the mesenteric fat pad in the area. In this case the patient suffered from anxiety and a history of anorexia nervosa likely leading to the loss of the mesenteric fat pad. During two previous abdominal surgeries the patient suffered complications of post operative pain unrelieved by post operative thoracic epidural analgesia and multimodal analgesia. She was also persistently nauseous and struggled to tolerate food post op. She had to return to the OR a second time due to the development of a stricture post op in her small intestine. The second surgery also resulted in a similar challenge of pain control with severe nausea. The patient is now scheduled for a third surgery, a revision gastrojejunal anastomosis and gastrojejunostomy.</span><br />
<span style="font-family: inherit;"><br /></span>
<span style="font-family: inherit;">Given that the patient is very likely to suffer as in her prior surgeries with significant pain, I have decided to consider an aggressive multimodal pain regimen for post op pain. Currently, many surgeons are requesting transversus abdominal pain blocks (often with catheters) for post op pain control after abdominal surgery. In many cases, it appears that this method of pain control is supplanting TEA as the primary regional technique for pain control after abdominal surgery. Unfortunately, I have had less success with the TAP technique for open abdominal surgery in particular with upper (above the umbilicus) abdominal surgery. It is well known that the transverses abdominal plane block (TAP) provides somatic analgesia to the skin and anterior abdominal wall. Unfortunately, pain sensation from the viscera and peritoneum are not blocked with this technique as it is with epidural analgesia (EA). Recently a head to head trial comparing TAP vs EA was published [1]. The authors found that in lower abdominal surgery, TAP had similar pain control to EA patients for the first 16 hours. After 16 hours up to 48 hours, the group with epidural analgesia had better pain control. For incisions above the umbilicus, it is recommended that a subcostal technique be used. However, for long incisions, it is often difficult to get enough spread of local anesthetic in the transversus abdominis plane to block all of the necessary nerves. Nevertheless, Rao et al. were able to show that after major abdominal surgery, TAP catheters were equal to EA in terms of pain scores, opioid requirements, and patient satisfaction [2]. In another study of open laparotomy patients (n=51)[3], Ganapathy et al. found that TAP catheters were essentially equivalent to EA during 72 hours in terms of pain control. However, in another study, TAP catheters were inferior to EA for pain control after major open abdominal surgery [4]. A small meta analysis of four studies was unable to find any significant differences in pain control or opioid use after abdominal surgery when comparing TAP catheters with EA [5]. However, there was a trend toward increased morphine use in the TAP catheter group. All, in all, it would appear that for abdominal surgery TAP catheters can be a reliable alternatively to EA when pain control is the only outcome of interest. However, multiple studies and a cochrane review have shown that for the important endpoint of reduction in post operative ileus, EA is helpful. <a href="https://www.cochrane.org/CD001893/ANAESTH_epidural-local-anaesthetics-prevention-postoperative-gastrointestinal-paralysis-vomiting-and-pain"> (see here for cochrane review).</a> In this particular case, post operative ileus is a major concern. The patient is currently on TPN, due to continued poor oral intake. It will be imperative to maximize her chances of avoiding a prolonged post operative ileus. Therefore, EA would be an ideal choice. However, this patient is likely to still have significant post operative pain as she did after her prior two abdominal surgeries despite having a functioning thoracic epidural. There is evidence that in patients with difficult to treat pain, that ketamine can be helpful. There is a large literature related to ketamine use in the perioperative period. In 2010, a Cochrane review found that sub-anesthetic ketamine reduced analgesic requirements and/or pain scores in 27 of 37 RCTs [10]. Currently, most guidelines suggest giving a bolus of 0.5 mg/kg at the beginning of the case plus an infusion of 0.25mg/kg/hr during surgery. De Koch et al. found that intraoperative ketamine ( 0.5 mg/kg bolus + 0.25 mg/kg/hr infusion) reduced morphine consumption in patients having abdominal surgery [6]. Importantly, this occurred even though all patients received aggressive EA. Furthermore, they were able to show that secondary hyperalgesia was reduced in the ketamine group and that in this group, chronic post operative pain was significantly less at 6 months after surgery. Himmeslseher et al. published a meta analysis on ketamine for post operative pain control. They recommend ketamine to reduce post operative pain and provided the following recommendations:</span><br />
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<span style="font-family: inherit;">Major surgery: 0.5 mg/kg bolus prior to incision and 0.5 mg/kg/hr infusion until end of surgery. then post op infusion of 0.12 mg/kg/hr x 24 hours in the post operative period.</span><br />
<span style="font-family: inherit;"><br /></span>
<span style="font-family: inherit;">Minor surgery: 0.25 mg/kg bolus prior to incision + 0.25 mg/kg/hr infusion until the end of surgery.</span><br />
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<span style="font-family: inherit;">Dosages above are fairly aggressive, and it is clear that post operative hallucinations, vivid dreams and other cognitive affects are more frequent and more severe at higher doses. Therefore, I tend to decrease the doses from those recommended above.</span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiapx7XLwlO5Rq4pDFWtpXQrb5bRTTaAREou_Je7NbQWms_2RN3q5oHAGkw_Bcojr3tbEGgGBbosxA9yMCbnXo6UKwAroJXIrqmMm7_7b2gUk-iggnNySRoM0jbFb7WomgZa252CB5vT2yf/s1600/pain+p-way.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="466" data-original-width="697" height="213" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiapx7XLwlO5Rq4pDFWtpXQrb5bRTTaAREou_Je7NbQWms_2RN3q5oHAGkw_Bcojr3tbEGgGBbosxA9yMCbnXo6UKwAroJXIrqmMm7_7b2gUk-iggnNySRoM0jbFb7WomgZa252CB5vT2yf/s320/pain+p-way.jpg" width="320" /></a></div>
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Multipmodal analgesia will be very important so I will given IV Tylenol during the surgery and then q 8 hours post op.<br />
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Another option is an IV infusion of Magnesium. Magnesium as an adjunct for pain control has been considered for decades. A large number of clinical studies looking at the use of magnesium for post operative pain control have been published with mixed results. A systematic review in 2007 that included 14 studies could not detect a beneficial effect of systemic magnesium administration on post operative pain control [8]. In 2013, another systematic review was undertaken and was able to demonstrate a beneficial effect of magnesium on pain control [9]. The largest improvement was the reduction in morphine consumption as noted in the figure below. Most of the studies utilized a 30 mg/kg bolus or a 50 mg/kg bolus +/- an infusion of between 8 mg/kg/hr to 15 mg/kg/hr intraoperatively or a few even post operatively.<br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhRFGqOEl3JKSMVyMU98rf2WuQd6cr5uwtS_8DiB26KqMv0tLijCKxEIux9vEHFJpWmvRxtJwN8X4GeQ8sbCJk3A7kch5P1W4ztHNxTR3gMYrGItTv76HCoYN6YOx_4qRa50nCa7Ru0KYUL/s1600/mg+opioids.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="498" data-original-width="1000" height="198" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhRFGqOEl3JKSMVyMU98rf2WuQd6cr5uwtS_8DiB26KqMv0tLijCKxEIux9vEHFJpWmvRxtJwN8X4GeQ8sbCJk3A7kch5P1W4ztHNxTR3gMYrGItTv76HCoYN6YOx_4qRa50nCa7Ru0KYUL/s400/mg+opioids.png" width="400" /></a>Fig 1 post operative morphine consumption is reduced with magnesium.</div>
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Magnesium acts as an NMDA antagonist to reduce the perception and duration of pain.<br />
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Recently, more and more groups have started to take interest in the possibility of gabapentin reducing post operative pain and/or analgesic opioid requirements. In 2013, an article in <a href="http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1918108">Anesthesiology</a> stated that the current evidence suggested that gabapentinoids (gabapentin and pregabalin) could reduce preoperative acute pain/analgesic requirements and the incidence of post surgical chronic pain development.<br />
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gabapentinoid pharmacology: these are not active at the GABA-a receptor although they are GABA structural analgues.</h4>
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<span style="font-family: inherit;">These GABA analogues actually bind to the alpha 2-delta subunit of pre synaptic P and Q type voltage gated calcium channels. Doesn't make much sense, but that's how they cause the effect we are looking for. This is believed to modulate the release of excitatory neurotransmitter from activated nociceptors. So, by inhibiting Calcium induced release of glutamine, these agents can inhibit pain transmission and/or decrease central sensitization. <span style="background-color: white; color: #333333; font-size: 16px;">Alternatively, some evidence indicates that their antinociceptive mechanism may arise through activation of noradrenergic pain-inhibiting pathways in the spinal cord and brain. (see figure)</span></span></div>
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In 2016 a meta analysis of gabapentinoids [11] in dosages from 300 mg to 1200 mg found that they were helpful in reducing morphine consumption for the first 24 hours after surgery. They did report increased sedation levels in patients who received gabapentinoids, and there was no decrease in side effects such as pruritus, nausea or vomiting. Two different studies looked at gabapentin as a part of a multimodal analgesia program and both concluded that it was of questionable benefit in this context. The first of these two studies was a RCT in TKA with gabapentin [12]. In this study patients were given 600 mg gabapentin preop with 200 mg q8 hours post op along with morphine, ketorolac and tylenol. Morphine consumption and VAS scores were similar between groups. Monks et al. [13] looked at gabapentin in post cesarean section patients at dose of 600 mg preop and 200 mg q8 hours post op. Patients received spinal morphine. There was a very slight decrease in morphine consumption in the group receiving gabapentin and the authors concluded that gabapentin is of questionable benefit in cesarean section patients. One consideration that is important is to understand that gabapentin is an oral medication and was not possible to use in our case in a patient requiring TPN due to an inability to tolerate oral intake. In addition, I was planning an aggressive multimodal pain program to include regional anesthesia, toradol, tylenol IV, magnesium infusion and a ketamine infusion, thereby making gabapentin an unlikely success in further reducing post op pain scores or opioid consumption.</div>
One day prior to the scheduled surgery the pre admissions testing nurse called me to report that the patient had a lab drawn and that her potassium was 2.9 mEq/L. The nurse at the PAT clinic reported that the patient had a PICC line where she receives TPN in addition to potassium replacement. The nurse also revealed that the patient suffers from orthostatic hypotension for which she is prescribed midorine and fludrocortisone. I instructed the nurse to call the patient and have her stop her fludrocortisone the day before surgery and to come in early for repeat K+ lab draw with an order to start 20 mEq of postassium if her K+ level was below 3.1 mEq/L.<br />
<span style="font-family: inherit;"><span style="background-color: white; color: #333333; font-size: 16px;"><br /></span>
<span style="color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif;"><span style="background-color: white; font-family: inherit;">Orthostatic hypotension is often caused by failure of the autonomic nervous system. There are a variety of reasons for failure of the autonomic nervous system including:</span></span></span><br />
<ul>
<li><span style="color: #333333; font-family: inherit;">Multiple system atrophy</span></li>
<li><span style="color: #333333; font-family: inherit;">familial dysautonomia</span></li>
<li><span style="color: #333333; font-family: inherit;">dementia with lewy bodies</span></li>
<li><span style="font-family: inherit;">Shy-Drager's syndrome</span></li>
<li><span style="font-family: inherit;">Parkinson's disease</span></li>
<li><span style="font-family: inherit;">longstanding diabetes</span></li>
<li><span style="font-family: inherit;">Vitamin deficiencies (our patient)</span></li>
<li><span style="font-family: inherit;">Amyloidosis</span></li>
<li><span style="font-family: inherit;">Bronchogenic carcinoma</span></li>
<li><span style="font-family: inherit;">Pure autonomic failure</span></li>
</ul>
<span style="font-family: inherit;">Treatment for othorstatic hypotension can include a dire</span>ct vasocontrictor. My patient was taking midodrine, which is a prodrug and acts on the alpha 1 adrenergic receptor to cause vasoconstriction. Unfortunutely, this can lead to supine hypertension that is severe in some patients. This supine hypertension can result in pressure natriuresis leading to a worsening of orthostatic hypotension. In patients taking midodrine for autonomic failure, there is typically an associated denervation hypersensitivity making these patients exquisitely sensitive to norepinephrine. Patients with autonomic failure have other clinical manifestations as well. These may include post prandial hypotension, urinary bladder dysfunction leading to urinary retention, and decreased gastrointestinal motility.<br />
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Fludrocortison is a mineralocorticoid used in patients with orthostatic hypotension. It results in fluid retention and patients often will gain 2 to 3 Kg of water weight before receiving full benefit of this medication. Fludrocortisone does have some glucocorticoid activity above dosages of 0.3 mg per day and this must be considered as to whether the HPA axis may be inhibited. Mineralocorticoids act by mimicking aldosterone (binding to the aldosterone receptor in the cell necleus) which causes sodium retention at the expense of excretion of potassium and hydrogen ions. The action occurs in the renal collecting tubules. This can lead to severe hypokalemia and metabolic alkalosis. In addition, about 10% of patients also suffer from hypomagnesemia with chronic fludrocortisone therapy. Because fludrocortisone does have some glucocorticoid activity, I could not ensure that the patient's HPA axis was not suppressed, and therefore, in addition to 4 mg of dexamethosone (purely glucocorticoid activity) I gave a one time dose of solucortef 50 mg. This medication has both glucocorticoid and mineralocorticoid activity. <br />
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On the day of surgery the patient arrived and a repeat potassium level came back at 3.3 mEq/L. Therefore, KCL infusion was not required prior to proceeding as I was worried might happen. As discussed above, there is evidence that EA and bilateral subcostal TAP catheters are equivalent. It was decided to proceed with GETA and post operative placement of subcostal TAP catheters. The patient weight was 50 kg. The patient was given 2 mg of versed and 2 mg of dilaudid and we rolled to the OR. Induction was with propofol and rococuronium. The patient was given ketamine in 25 mg increments to a total of 100 mg. She was given MgSO4 2 GM intraoperatively, and another 1 GM was infused post operatively. She also received decadron 4 mg, solocortef (to add some mineralocorticoid activity) 50 mg, IV tyelonol 1000mg, and zofran 4 mg. The open laparotomy with revision of gastrojejunal anastomosis was uneventful and the patient arrived in the PACU extubated and breathing comfortably. After 30 min the patient was interviewed and complained of 8/10 pain. The nurse administered opioid pain medications. A post operative ketamine infusion was begun at 5 mg/hr with a magnesium infusion of 250 mg/hr. She received an additional amount of magnesium in her TPN solution. The surgeon also prescribed a PCA with hydromorphone. On POD 1, the patient appeared comfortable in her bed but complained of 8/10 pain. It should be noted that on the first night on the day of surgery, the nurses called me to tell me that the patient had respiratory depression and that they had d/c'd all of her pain medications until she woke up. It was decided to restart her magnesium and ketamine infusion, and cut her hydromorphone dose in half. The patient requested EA, however, the surgeon intervened to avoid this. The patients was NPO and therefore, not receiving fludrocortisone or midodrine, both oral medications. Her blood pressures were low normal.<br />
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In this case, EA is likely to have been a better choice than TAP catheters. Particularly on POD 1 when it became apparent that the patient had an event of respiratory depression from opioids requiring adjustment of the medication. In addition, the patient perceived that her pain control was not adequate nor being addressed. She stated that the TAP catheters were not working. A test with ice to the skin around the incision was unable to detect any decrease in sensation or perception of cold. This is a fairly good indicator of failure of block. I have a long experience with the placement of TAP catheters and doing the subcostal block. This patient was thin, and the US guided block went flawless, with excellent landmarks that were well visualized. However, the subcostal approach relies on local anesthetic spreading throughout the transversus abdominis plane and finding the nerves as they run along to their destination. The actual nerves are not visualized and it is impossible to guarantee that all of the nerves will be bathed in local anesthetic (LA). This is also true for EA, however. The patient did state that the block was patchy. To me this indicated that indeed the LA was located around several nerves, but that there were others not reached by the LA. This, to me constitutes a general weakness of the TAP approach than my technique. On POD 2 the patient appeared much more comfortable and in fact had reduced the amount of opioid pain medication she was consuming.<br />
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1. <span style="font-family: inherit;"><span style="font-size: 12.999268531799316px; white-space: nowrap;">Sadasivan Shankar Iyer</span><span style="font-size: 12.999268531799316px;">,</span><span style="font-size: 0.8461em; line-height: 1.6363em; position: relative; top: -0.5em; vertical-align: baseline;"></span><span style="font-size: 0.8461em; line-height: 1.6363em; position: relative; top: -0.5em; vertical-align: baseline;"></span><span style="font-size: 12.999268531799316px;"> </span><span style="font-size: 12.999268531799316px; white-space: nowrap;">Harshit Bavishi</span><span style="font-size: 12.999268531799316px;">,</span><span style="font-size: 12.999268531799316px;"> </span><span style="font-size: 12.999268531799316px; white-space: nowrap;">Chadalavada Venkataram Mohan</span><span style="font-size: 12.999268531799316px;">,</span><span style="font-size: 0.8461em; line-height: 1.6363em; position: relative; top: -0.5em; vertical-align: baseline;"></span><span style="font-size: 12.999268531799316px;"> </span><span style="font-size: 12.999268531799316px;">and</span><span style="font-size: 12.999268531799316px;"> </span><span style="font-size: 12.999268531799316px;"> </span><span style="font-size: 12.999268531799316px; white-space: nowrap;">Navdeep Kaur, Anesth Essays Res. 2017 (11)7: 670-675</span></span><br />
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<span style="font-family: inherit;"><span style="font-size: 12.999268531799316px; white-space: nowrap;">2. </span></span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">Rao Kadam V, Van Wijk RM, Moran JI, Miller D. </span><span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;"><span class="ref-journal">Anaesth Intensive Care. </span>2013;<span class="ref-vol">41</span>:476–81.</span><br />
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<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">3. Ganapathy S, Sondekoppam RV, Terlecki M, et al. </span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">. </span><span class="ref-journal" style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">Eur J Anaesthesiol </span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">2015;</span><span class="ref-vol" style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">32</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">:797–804</span><br />
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<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">4. </span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">Wahba SS, Kamal SM. </span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">. </span><span class="ref-journal" style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">J Anesth</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;"> 2014;</span><span class="ref-vol" style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">28</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">:517–23.</span><br />
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<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">5. Zhang P, Deng XQ, Zhang R, Zhu T. </span><span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;"><span class="ref-journal">Br J Anaesth. </span>2015;<span class="ref-vol">114</span>:339.</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;"> </span><br />
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<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px; white-space: nowrap;">6. </span><span style="background-color: whitesmoke; font-family: "trebuchet ms" , "verdana" , sans-serif; font-size: 13px; text-indent: 10px;">De Kock M, Lavand'homme P, Waterloos H. Pain 92(2001) 373-380.</span><br />
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<span style="background-color: whitesmoke; font-family: "trebuchet ms" , "verdana" , sans-serif; font-size: 13px; text-indent: 10px;">7. </span><span style="background-color: whitesmoke; font-family: "trebuchet ms" , "verdana" , sans-serif; font-size: 13px; text-indent: 10px;">Himmeslseher S, durieux ME. Ketamine for perioperative Pain Management. Anesthesiology. 2005; (102):211-20.</span><br />
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<span style="background-color: whitesmoke; font-family: "trebuchet ms" , "verdana" , sans-serif; font-size: 13px; text-indent: 10px;">8. </span><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">Lysakowski, C, Dumont, L, Czarnetzki, C, Tramèr, MR . </span><span style="box-sizing: border-box; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px; font-style: italic; line-height: inherit;">Anesth Analg</span><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">. (2007). </span><span style="box-sizing: border-box; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px; font-style: italic; line-height: inherit;">104</span><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> 1532–9</span><span class="crossrefDoi" style="box-sizing: border-box; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> </span><br />
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<span class="crossrefDoi" style="box-sizing: border-box; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">9</span><span style="font-family: inherit;"><span class="crossrefDoi" style="box-sizing: border-box; caret-color: rgb(51, 51, 51); font-size: 14px;">. </span><span class="wi-fullname brand-fg" style="box-sizing: border-box; caret-color: rgb(34, 34, 34); font-size: 16px;"><span style="box-sizing: border-box; font-size: 0.875rem; line-height: 1.45;">Gildasio S. De Oliveira, Jr, M.D., M.S.C.I.</span></span><span style="background-color: white; caret-color: rgb(34, 34, 34); font-size: 16px;">; </span><span class="wi-fullname brand-fg" style="box-sizing: border-box; caret-color: rgb(34, 34, 34); font-size: 16px;"><span style="box-sizing: border-box; font-size: 0.875rem; line-height: 1.45;">Lucas J. Castro-Alves, M.D.</span></span><span style="background-color: white; caret-color: rgb(34, 34, 34); font-size: 16px;">; </span><span class="wi-fullname brand-fg" style="box-sizing: border-box; caret-color: rgb(34, 34, 34); font-size: 16px;"><span style="box-sizing: border-box; font-size: 0.875rem; line-height: 1.45;">Jamil H. Khan, B.S.</span></span><span style="background-color: white; caret-color: rgb(34, 34, 34); font-size: 16px;">; </span><span class="wi-fullname brand-fg" style="box-sizing: border-box; caret-color: rgb(34, 34, 34); font-size: 16px;"><span style="box-sizing: border-box; font-size: 0.875rem; line-height: 1.45;">Robert J. McCarthy, Pharm.D.</span></span><span class="crossrefDoi" style="box-sizing: border-box; caret-color: rgb(51, 51, 51); font-size: 14px;"> </span><span class="journal-name" style="box-sizing: border-box; font-size: 0.9375rem; line-height: 1.4; word-wrap: break-word;">Anesthesiology</span><span style="box-sizing: border-box; font-size: 0.9375rem; line-height: 1.4; word-wrap: break-word;"> 07 2013, Vol.119, 178-190</span></span><br />
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<span style="font-size: 15px;">10. </span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">Bell RF, Dahl JB, Moore RA, Kalso E. Perioperative ketamine for acute postoperative pain. </span><span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;"><span class="ref-journal">Cochrane Database Syst Rev. </span>2006</span><br />
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<span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">11. </span><span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="color: #642a8f;"><span style="font-size: 12.999268531799316px; white-space: nowrap;">Sudha Arumugam</span></span><span style="background-color: white; font-size: 12.999268531799316px;">,</span><span style="background-color: white; font-size: 12.999268531799316px;"> </span><span style="color: #642a8f;"><span style="font-size: 12.999268531799316px; white-space: nowrap;">Christine SM Lau</span></span><span style="background-color: white; font-size: 12.999268531799316px;">,</span><span style="background-color: white;"><span style="font-size: x-small;"> </span></span><span style="background-color: white; font-size: 12.999268531799316px;">and </span><span style="color: #642a8f;"><span style="font-size: 12.999268531799316px; white-space: nowrap;">Ronald S Chamberlain</span></span><span style="font-size: x-small;">. </span><span role="menubar" style="font-size: 10.99868106842041px;"><span style="color: #642a8f;">J Pain Res</span></span><span style="background-color: white; font-size: 10.99868106842041px;">. 2016; 9: 631–640.</span></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="background-color: white; font-size: 10.99868106842041px;">12. </span></span><span style="font-family: "arial"; font-size: 10pt;">Paul JE, Nantha-Aree M, Buckley N, Cheng J, Thabane L, Tidy A, DeBeer J, Winemaker M, Wismer D, Punthake D, Avram V; Gabapentin does not improve multimodal analgesia outcomes for total knee arthroplasty: a randomized controlled trial; </span><span style="font-family: "arial,italic"; font-size: 10pt;">Canadian Journal of Anesthesia </span><span style="font-family: "arial"; font-size: 10pt;">2013, 60:423-431</span><br />
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<span style="font-family: "arial"; font-size: 10pt;">13. </span><span style="font-family: "arial"; font-size: 10pt;">Monks DT, Hoppe DW, Downey K, Shah V, Bernstein P, Carvalho JCA; </span><span style="font-family: "arial,italic"; font-size: 10pt;">A perioperative dose of gabapentin does not produce a clinically meaningful improvement is analgesia after cesarean delivery; </span><span style="font-family: "arial"; font-size: 10pt;">Anesthesiology 2015 August, 123(2): 320-326</span>Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-52275227904542617702018-07-23T07:28:00.001-07:002019-09-20T09:27:22.869-07:00super obese patient for shoulder surgeryRecently my partner placed an interscalene brachial plexus block with catheter in a patient who had a BMI of greater than 60. The patient was at risk for post operative respiratory insufficiency due to the known complication of phrenic nerve palsy on the ipsilateral side of the block, which results in an elevated diaphragm on chest x ray. (see figure 1).<br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEglXTMIWyWAKiq5_njcCbWaEe8XQ3eilB3xzZqtl-RlrqW8dmVYPVvt1A4-dT8Zr0zdzngbcTHm2DsZUotmLfQQAbvCU46fHNdKjPJC5rGwgvo4clmdAyFS4UnW6JoaLcdeFCZEWgRg1L6Y/s1600/hemidiaphragm.jpeg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="575" data-original-width="623" height="295" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEglXTMIWyWAKiq5_njcCbWaEe8XQ3eilB3xzZqtl-RlrqW8dmVYPVvt1A4-dT8Zr0zdzngbcTHm2DsZUotmLfQQAbvCU46fHNdKjPJC5rGwgvo4clmdAyFS4UnW6JoaLcdeFCZEWgRg1L6Y/s320/hemidiaphragm.jpeg" width="320" /></a></div>
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fig 1</div>
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Patients having arthroscopic shoulder surgery are most commonly scheduled for day surgery, and admission to the hospital for hypoxia associated phrenic nerve paralysis is suboptimal. Patients with intrinsic lung disease are at risk for this complication. Patients who are morbidly obese are also at risk for this complication [1]. Unfortunately, it is not always easy to tell ahead of the block who will develop clinically relevant complications as a result of phrenic nerve palsy after interscalene block. A large retrospective review was published on cases of outpatient interscalene catheter usage (n=509) [12]. Adverse events were recorded in 6.7% of patients. Of these only 0.6% (3 patients) had problems or complaints of dyspnea all of which were after discharge to home. However, the mean BMI was 24, with no patient having a BMI greater than 29. In addition, all patients with any lung disease were not included in the study. </div>
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At the level of the interscalene block, the phrenic nerve lies in close association with the brachial plexus cords/trunks. (see fig 2). Its course is most proximate to the brachial plexus at the level of the interscalene block where it typically is 18 to 20 mm away from the C5 nerve root at the level of cricoid cartilage. </div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEidZQrbBoL70xOA6Fkm81gSfm6996To2fZ3RTRTarK5uONqdGU5WfQgu2JpTNAyO7Ag3o_6_osNoULoPlI_IyL23DWrgCWzz0mntktzu-4Vfy8FvBLXAt0NtwhYKiGgIiQNI651M2vro36R/s1600/11_1_c_Neck-Phrenic-Nerve_labels.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="720" data-original-width="900" height="256" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEidZQrbBoL70xOA6Fkm81gSfm6996To2fZ3RTRTarK5uONqdGU5WfQgu2JpTNAyO7Ag3o_6_osNoULoPlI_IyL23DWrgCWzz0mntktzu-4Vfy8FvBLXAt0NtwhYKiGgIiQNI651M2vro36R/s320/11_1_c_Neck-Phrenic-Nerve_labels.jpg" width="320" /></a></div>
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fig 2</div>
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However, as one moves caudad, the phrenic nerve moves an additional 3 mm further away from the plexus for every cm that it descends over the anterior scalene muscle. </div>
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A review article on the options for avoidance of significant phrenic nerve block was published in the journal <i>Anesthesiology</i> in 2017 [2]. This article is highly recommended for the practioner who desires a more in depth understanding of brachial plexus and phrenic nerve anatomy.</div>
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<span style="font-family: inherit;"><span style="background-color: white; color: #333333; font-size: 16px;">Patients who are obese are more likely to experience dyspnea in association with phrenic nerve palsy. Furthermore, it is likely that morbid obesity will also increase the risk of hypoxemia in association with dyspnea. There are several strategies to reduce the chances of this outcome and will be reviewed briefly. Traditional training of the ISB has recommeneded high volumes (30 to 40 mLs) to ensure complete blockade of the brachial plexus. Reducing this amount could reduce the incidence of phrenic nerve palsy.</span> H</span>owever, most studies indicated that volumes of 20 mL or greater will inevitably result in phrenic nerve palsy if the injection occurs around the C5-C6 nerve roots. US guided techniques have allowed practitioners to be more precise in the placement of the local anesthetic permitting a lower volume to achieve shoulder analgesia after interscalene block. In particular, one study found that after 10 mL was injected, the chance of phrenic nerve palsy could be reduced from 100% to 60% [3]. Reducing the injected volume to 5 mL can lower the chance of phrenic nerve palsy to as low as 27% [4] without compromising the block effectiveness for up to 24H. However, it is well known that introducing a greater volume tends to increase the chances for success, and therefore, using 5 mL as a routine is likely to lead to suboptimal outcomes in some cases. Furthermore, given the problems with admitting a patient from an outpatient facility to a hospital secondary to respiratory compromise, an incidence of phrenic nerve palsy of 27% may seem high. Nevertheless, further improvements seem possible if the concentration is reduced. To provide dense surgical anesthesia and prolonged dense post operative analgesia, I typically opt for 0.5% bupivacaine or Ropivacaine. By halving the concentration to 0.25%, AL-Kaisy et al was able to reduce the incidence of phrenic nerve palsy from 100% to 17% [4]. However, this study only had 5 volunteers in each group. In a slightly larger group of patients (30), Thackeray et al.[5] were able to reduce the incidence of phrenic nerve palsy from 78% to 21% by halving the bupivacaine concentration with a 20 mL injection. This reduction in concentration seemed to come at the expense of more opioid requirements over a 72 hour time frame and also a shorter block duration (18 hr vs. 11.9 hr) [6]. To add confusion to the previous studies, Zhai et al. couldn't find a significant differenence in phrenic nerve palsy when using a fixed dose of 50 mg of Ropivacaine for US guided interscalene block using concentrations of 0.25, 0.5 or 0.75% [7].</div>
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Perhaps more effective, is an injection of local anesthetic around the C7 nerve root. When using 5 mL of a 0.75% concentration of Ropivacaine, no patients (n=20) had any diaphragmatic paresis after 2 hours post injection [8]. The calculated ED 95 was 3.6 mL of 0.75% ropivacaine for this study when injected around the C7 nerve root.</div>
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Performing a supraclavicular block has been studied as a method of reducing phrenic nerve palsy. More specifically, targeting the superior trunk of the brachial plexus (formed by the union of the C5/C6 nerve roots), has been reported in two case reports to provide analgesia after shoulder surgery without blocking the phrenic nerve. At this level the phrenic nerve has migrated away from the brachial plexus. An approach to target the superior trunk is to do a supraclavicular brachial plexus block. Mulltiple studies have looked at the supraclavicular block and the results are somewhat equivocal. For example, with injection volumes of 20 to 30 mL, phrenic nerve palsy occured in 25 to 51% of patients. Furthermore, in some of the studies, patients receiving a supraclavicular block had inferior post op analgesia. On the other hand, Kim et al. were able to show that a supraclavicular block performed equally to ISB for patients having shoulder surgery without GA in terms of conversion to GA (0 patients) or fentanyl requirements [14]. Given the above data, I have begun to modify my block for shoulder surgery, seeking to do what I consider to be a high supraclavicular block or perhaps a low ISB. I further modify my block in patients who I consider to be at higher risk for phrenic nerve palsy by reducing the volume of local anesthetic and perhaps also decreasing the concentration. </div>
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The above techniques may reduce the incidence of phrenic nerve palsy, but don't seem to eliminate the risk altogether. The risk of phrenic nerve palsy may be completely eliminated by avoiding any injection around the brachial plexus. In 2012, Siegenthaler et al. desribed a novel approach to the suprascapular nerve [9]. In their study, a comparison study was done between locating the suprascapular nerve in the supraclavicular space vs. in the suprasspinous fossa. They determined that suprascapular nerve identification was much better in the supraclavicular space (81% identified vs. 36%). In my own practice, attempts at identification of the correct space using the supraspinous fossa (also known as the suprascapular notch) proved very difficult due to the greater amount of thick tissue overlying the area. Furthermore, This approach requires a cooperative patient who can sit upright in order for the approach. Lastly, I found that due to the depth of the area to be blocked, an acute angle was required making visualization of the needle problematic for accurate injection. </div>
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The suprascapular nerve provides aproximately 70% of the innervation to the glenohumeral joint. The majority of the remaining 30% derives from the axillary nerve. Two recent studies published in <i>Anesthesiology</i> have looked at the effectiveness of suprascapular nerve block vs. interscalene block to determine non inferiority. One was a meta analysis comparing the two approaches [10]. The meta analysis determined that a suprascapular nerve block alone was not inferior to an ISB. In this meta analysis, only one study utilized a supraclavicular block in the supraclavicular fossa (all other studies approached the nerve from supraspinous fossa). The primary outcome for which the blocks were compared and found to be similar were for post operative morphine consumption (24H) and the cumulative difference between ISB and SSNB in the area under the curve for rest pain during the first 24H interval. This meta analysis did note, however, that during a 1 hour interval in the PACU, ISB provided superior pain control. At 6,12,24, and 48hr there was no statistical difference. In this same meta analysis, it was found that ISB was associated with more respiratory complications, undesirable blockades, and block-related complications. </div>
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This month (july 2018), a head to head to head trial was published comparing analgesic efficacy between the anterior suprascapular, supraclavicular and interscalene nerve blocks [11]. The primary outcome was pain scores in the PACU. The pain scores were 1.9,2.0 and 2.3 for the ISB, anterior suprascapular, and supraclavicular blocks respectively. The authors concluded that the anterior suprascapular nerve block was non inferior to the ISB. They also concluded that the supraclavicular block did not meet their prespecified criteria for non inferiority. They also found a significant decrease in respiratory function (measuring VC) for the ISB. (see fig 3).</div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhPcavgBNr9hhFOTEG3wpEq_1KkcD3YQZDeCdonQI-nxKUfY2pXDMQ-0oy9RPIzNUPR16rG8FRr41CNnJxHOS5t3gyhDArlTBkQwzmsf-smjwWWzT-R8XAqsfQ9PfyS0inCxDruIrk2SgWX/s1600/Screen+Shot+2018-07-14+at+12.08.38+PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="701" data-original-width="661" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhPcavgBNr9hhFOTEG3wpEq_1KkcD3YQZDeCdonQI-nxKUfY2pXDMQ-0oy9RPIzNUPR16rG8FRr41CNnJxHOS5t3gyhDArlTBkQwzmsf-smjwWWzT-R8XAqsfQ9PfyS0inCxDruIrk2SgWX/s400/Screen+Shot+2018-07-14+at+12.08.38+PM.png" width="376" /></a></div>
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In general, ISB is the gold standard for providing effective and consistent post op analgesia for shoulder surgery. However, in day surgery patients who are likely to become hypoxemic (sat less than 90%) on room air after phrenic nerve block, the ISB is a relative contraindication. Current research indicates that the only method found to virtually provide a 0% incidence of phrenic nerve palsy is a suprascapular nerve block. Fortunately, several studies indicate that this block is likely non inferior to ISB in providing ample pain control.</div>
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Technique-Anterior Surpascapular nerve block:</div>
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place US probe in standard location as you would for ISB. Move the probe in a caudad direction as you follow the brachial plexus. (see figures below).</div>
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After determining the location of isolated SCN, only 3 to 4 mL are required to block this nerve at this level. Furthermore, due to the location of the nerve, a catheter could easily be inserted and secured in this location.</div>
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1. Hartrick CT et al. <i>BMC Anesthesiol </i>2012;12:6.</div>
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2. Deborah Culley <i>Anesthesiology</i> 2017;127:173-91.</div>
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3. <span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">Lee, JH, Cho, SH, Kim, SH, Chae, WS, Jin, HC, Lee, JS, Kim, YI R </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">Can J Anaesth</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> 2011; </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">58</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">:1001–6</span></div>
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<span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">Stundner, O, Meissnitzer, M, Brummett, CM, Moser, S, Forstner, R, Koköfer, A, Danninger, T, Gerner, P, Kirchmair, L, Fritsch, G </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">Br J Anaesth</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> 2016; </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">116</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">:405–12</span></div>
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<span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">4. </span><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">Al-Kaisy, AA, Chan, VW, Perlas, </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">Br J Anaesth</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> 1999; </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">82</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">:217–20</span></div>
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<span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">5. </span><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">Thackeray, EM, Swenson, JD, Gertsch, MC, Phillips, KM, Steele, JW, Burks, RT, Tashjian, RZ, Greis, PE </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">J Shoulder Elbow Surg</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">2013; </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">22</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">:381–6</span></div>
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<span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">6.</span><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">Wong, AK, Keeney, LG, Chen, L, Williams, R, Liu, J, Elkassabany, NM </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">Pain Med</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> 2016; </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">17</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">:2397–403</span></div>
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<span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">7.</span><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">Zhai, W, Wang, X, Rong, Y, Li, M, Wang, H </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">BMC Anesthesiol</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> 2016; </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">16</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">: 1–8</span></div>
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<span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">8. </span><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">Renes, SH, van Geffen, GJ, Rettig, HC, Gielen, MJ, Scheffer, GJ </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">Reg Anesth Pain Med</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> 2010; </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">35</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">:529–34</span><span class="crossrefDoi" style="background-color: white; box-sizing: border-box; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> </span></div>
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<span class="crossrefDoi" style="background-color: white; box-sizing: border-box; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">9. </span><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">Siegenthaler, A, Moriggl, B, Mlekusch, S, Schliessbach, J, Haug, M, Curatolo, M, Eichenberger, U </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">Reg Anesth Pain Med</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> 2012; </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">37</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">:325–8</span><span class="crossrefDoi" style="background-color: white; box-sizing: border-box; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> </span></div>
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10. Hussain N, Goldar G, Ragina N, Banfield L, Laffey J and Abdallah F. <i>Anesthesiology</i> 2017;127:998-1013.</div>
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11. Auyong DB, Hanson NA, Joseph RS, Schmidt BE, Slee AE, and Yuan SC. <i>Anesthesiology</i> 2018;129:47-57.</div>
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12. Marhofer P, Anderl W, Heuberer P, Fritz M, Kimberger O, Marhofer D, Klug W, and Blast J. <i>Anaesthesia</i> 2015, 70, 41-46.</div>
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13.<span style="background-color: white; color: #303030; font-family: "arial" , "helvetica" , "clean" , sans-serif; font-size: 13px;">Urmey WF, Talts KH, Sharrock NE</span><span style="background-color: white; color: #303030; font-family: "arial" , "helvetica" , "clean" , sans-serif; font-size: 13px; font-style: italic;"> </span><span style="background-color: white; color: #303030; font-family: "arial" , "helvetica" , "clean" , sans-serif; font-size: 13px; font-style: italic;">Anesth Analg. </span><span style="background-color: white; color: #303030; font-family: "arial" , "helvetica" , "clean" , sans-serif; font-size: 13px;">1991 Apr; 72(4):498-503.</span></div>
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<span style="background-color: white; color: #303030; font-family: "arial" , "helvetica" , "clean" , sans-serif; font-size: 13px;">14.</span><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">Ryu, T, Kil, BT, Kim, JH </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">Medicine (Baltimore)</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"> 2015; </span><em style="background-color: white; box-sizing: border-box; color: #333333; font-family: Lato, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 14px; line-height: inherit;">94</em><span style="background-color: white; color: #333333; font-family: "lato" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;">:e1726</span></div>
Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-10979539870486780772018-03-04T06:29:00.001-08:002019-09-20T09:02:08.744-07:0063 year old male for shoulder arthroscopy and polycythemia veraToday I was informed by the orthopedic surgeon that the next patient scheduled for shoulder surgery had a Hgb of 19.4 g/dL. He was 63 and appeared to be in poor health. He was on several medications including:<br />
<br />
<ul>
<li>ASA 81 mg</li>
<li>Buprion 300 mg qd</li>
<li>Citalopram 20 mg </li>
<li>Fluoxetine 40 mg</li>
<li>Gaba 300 mg</li>
<li>Glipizide 5 mg</li>
<li>Lantus 50 units qd</li>
<li>NPH 30 units qd</li>
<li>Metformin 1000 mg</li>
<li>pravastatin 40 mg</li>
</ul>
<div>
Labs:</div>
<div>
<ul>
<li>Na+ 141</li>
<li>K+ 4.8</li>
<li>BUN 10</li>
<li>Cr 0.83</li>
<li>Glucose (finger stick) 63 mg/dL patient without symptoms of hypoglycemia.</li>
<li>Hct 57.8</li>
<li>Platelets 245,000</li>
<li>total CO2 33</li>
</ul>
</div>
In addition to untreated HTN, depression and diabetes, the patient had significant OSA. <br />
The surgeon was eager to proceed with surgery. Therefore, I had a conversation with the patient in an attempt to determine the etiology of his polycythemia. He admitted to a chronic smoking history, but denied any trouble with SOB, orthopnea or lung disease. His room air sat was 94%. He had previously been made aware of his elevated Hgb levels, and it was recommended to him to donate blood. However, he stated that he had never donated blood because they would not accept his blood due to his diabetes. I explained to him the importance of immediate follow up with his doctor to treat his condition. I made a presumptive diagnosis of polycythemia vera since I could not find any obvious source of hypoxemia in this patient. A formal diagnosis requires that several criteria be met as listed below.<br />
<br />
I placed an interscalene catheter under US guidance. In the meantime, as we waited for surgery, I gave the patient 2 L of LR in order to mitigate his PV to a small degree. We also planned to extract a small amount of blood once we arrived to the OR (between 60 and 100 mL's). The patient underwent an uneventful shoulder scope with a surgical time of 63 min with un uneventful PACU stay.<br />
<br />
Polycythemia Vera (PV) is a myeloproliferative disease which results in excessive production of RBCs. In addition, it can also lead to luekocytosis and thrombocytosis. Other myeloproliferative disorders include essential thrombysthenia and primary myelofibrosis. PV is considered when the Hct is greater than 48% in women and 52% in men. This is an important disease to recognize in the perioperative period because patients with this condition are at greater risk for venous and arterial thrombosis, and hemorrhage [1,2], due to hyperviscosity of the blood and dysfunctional platelets. Diagnosis can be challenging and is not easily made at the bedside. <span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">In order to be positively diagnosed with polycythemia vera, two major criteria and one minor criterion must be present</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">. </span><br />
<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"><br /></span>
<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">Major criteria include:</span><br />
<br />
<ol>
<li><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">hemoglobin greater than 18.5 g/dl in men, greater than 16.5 g/dl in women</span></li>
<li><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">presence of the JAK2 V617F or similar mutation.</span></li>
</ol>
<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">Minor criteria include: </span><br />
<div>
<ol>
<li><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">bone marrow biopsy showing myeloproliferation. </span></li>
<li><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">serum erythropoietin level below the normal range.</span></li>
<li><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">endogenous erythroid colony formation in vitro [3]. </span></li>
</ol>
<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"></span><br />
<div>
<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">In additioon, in patients who do NOT have the JAK2 mutation, but do have elevated Hgb, AND two minor criteria, a positive diagnosis of PV can be made.</span></span></div>
<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">
<div>
<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"><br /></span></div>
The only available information from the above list in my patient was a Hbg of 19.4 md/dL. My patient also had significant OSA. I questioned whether this might account for his polycythemia rather than polycythemia vera. A recent retrospective analysis of polycythemia in patients with OSA considered over 527 patients who had polysomnography indicating OSA. The authors concluded that the incidence of polycythmia in OSA patients was indeed very rare. They also reported that severity of OSA did not correlate with greater increases in Hgb levels. The authors did concede that, "</span><span style="background-color: white; color: #4f4f4f; font-family: "lucida sans unicode" , "lucida sans" , "lucida grande" , "arial" , "helvetica" , sans-serif; font-size: 14.98px;">In those rare polycythemic OSA patients, polycythemia is corrected by CPAP therapy in the majority." </span><span style="font-family: inherit;"><span style="background-color: white;"> </span><span style="background-color: white;">In addition, my patient had diabetes and a finger strip glucose reading prior to surgery read 63 mg/dL. I did not treat this as the patient stated that he had no symptoms and usually did not feel bad until his sugar reading fell below 50 mg/dL. It should be noted, that glucose bedside monitors can read artificially low levels of glucose in patients with elevated hematocrits.</span></span><br />
<span style="font-family: inherit;"><span style="background-color: white;"><br /></span>
<span style="background-color: white;">Polycythemia results in hyper viscous blood. It should be recognized that Poiseuille's equation indicates that flow through a tube is proportional to the fourth power of the radius, the pressure differential, and inversely proportional to the length and viscosity of the fluid. Therefore, as viscosity increases with increasing hematocrit, the pressure differential must increase in the exact amount to maintain an equal blood flow. Unfortunately, as the hematocrit increases it results in a semilogarithmic increase in the blood's viscosity. In fact, as the hematocrit hits 45%, it can be said that the increase in viscosity "takes off". (see figure)</span></span><br />
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<span style="background-color: white; color: #4f4f4f; font-family: inherit; font-size: 14.98px;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh9FYug7CI0rz0ecd6QVU05xt07Lk32yk65OnNz3UtUOpB65cvGcbpGIj1DgONksgmd4xb-yv738Lp5Tl3neNJOY2HS29VMYjKet9zi_mP3bbp-Zd0JmQ9O9dpyw0bf6HPNN4VefG3nuheG/s1600/Screen+Shot+2018-02-28+at+7.23.35+PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="980" data-original-width="976" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh9FYug7CI0rz0ecd6QVU05xt07Lk32yk65OnNz3UtUOpB65cvGcbpGIj1DgONksgmd4xb-yv738Lp5Tl3neNJOY2HS29VMYjKet9zi_mP3bbp-Zd0JmQ9O9dpyw0bf6HPNN4VefG3nuheG/s320/Screen+Shot+2018-02-28+at+7.23.35+PM.png" width="318" /></a></span></div>
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<span style="background-color: white; color: #4f4f4f; font-family: inherit; font-size: 14.98px;"><br /></span></div>
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<span style="background-color: white; font-family: inherit;">Therefore, cardiac work must increase to maintain forward flow, and indeed, as polycythemia progresses much beyond a hematocrit of 45% cardiac output decreases. Clinically, this can manifest as SOB, lack of energy, tiredness, and even angina. Therefore, a careful history is critical in these patients. It should be noted that hyperviscous blood is particularly problematic for the small capillaries which can lead to ischemia especially in patients with poor heart function.</span></div>
<span style="background-color: white; font-family: inherit;"><br /></span>
<span style="background-color: white;"><span style="font-family: inherit;">Polycythemia Vera can also result in paradoxical hemorrhage. This is believed to be a result of platelet dysfunction. Acquired Von Willebrand's diesease could be another cause of increased bleeding tendency in these patients. Most authors recommend the avoidance of neuraxial anesthesia in patients with PV unless a coagulation profile is normal (i.e.thromboeslastography) due to known platelet dysfunction.</span></span><br />
<span style="background-color: white;"><span style="font-family: inherit;"><br /></span></span>
<span style="background-color: white;">These patients may be at high risk for complication and death after surgery. In a review from 1963, patients with uncontrolled polycythemia had a 79% rate of complications and a mortality rate of 36% [4]. However, patients who were treated had their rate of complications decreased to 28% and mortality rate to 5%. Another study found that the incidence of thrombosis was 7.7% and that of major hemorrhage was 7.3% [5].</span><br />
<span style="background-color: white; font-family: "lucida sans unicode" , "lucida sans" , "lucida grande" , "arial" , "helvetica" , sans-serif;"><br /></span>
<span style="font-family: inherit;"><span style="background-color: white;">Treatment</span></span><br />
<span style="background-color: white;">A lower hematocrit can be favorable in the perioperative period. The increased viscosity of blood is particularly problematic during this period. Some evidence suggests that the brain oxygenation and brain oxygen delivery is optimized when the hematocrit is decreased to below 45% [5].</span><br />
<span style="font-family: inherit;"><span style="background-color: white;">In several case reports dealing with patients who have presumptive PV, the authors desribe performing acute normovolemic hemodulition. The formula that should be used in order to arrive at the proper Hgb level preoperatively is V=EBV X (Ho - Hf)/Have. </span></span><br />
<span style="font-family: inherit;"><span style="background-color: white;"><br /></span></span>
<span style="font-family: inherit;"><span style="background-color: white;">V=volume of blood to extract</span></span><br />
<span style="font-family: inherit;"><span style="background-color: white;">EBV = Estimated Blood Volume (in adult males 70 mL/kg is often used)</span></span><br />
<span style="font-family: inherit;"><span style="background-color: white;">Ho= starting Hematocrit level of patient </span></span><br />
<span style="font-family: inherit;"><span style="background-color: white;">Hf= final Hematocrit or minimal allowable (around 40 to 45%).</span></span><br />
<span style="font-family: inherit;"><span style="background-color: white;">Have= the average between the start and final hematocrit.</span></span><br />
<span style="font-family: inherit;"><span style="background-color: white;"><br /></span></span>
<span style="font-family: inherit;"><span style="background-color: white;">An equivalent volume to replace the blood withdrawn should be infused during the extraction of blood. I.e. if 500 mL of blood is extracted, then 500 mL of colloid might be infused. In general, the goal is to reduce the viscosity of blood, and generous intravenous fluids (LR or NaCl) should be infused.</span></span><br />
<br />
Even in patients that have normalized their hematocrit prior to surgery there is elevated risk of thrombosis. A retrospective review of patients with either PV or ET and receiving anticoagulation therapy during their surgery estimated that the incidence of DVT after major surgery was increased 5-fold. Unfortunately, the risk of major bleeding was also increased in this retrospective review demonstrating the paradoxical risk of hemorrhage in PV. The authors recommended using LMWH for prevention of DVT during the perioperative period.<br />
<br />
One final note on this particular patient was his list of medications. He was taking bupropion, a norepinephrine/dopamine reuptake inhibitor for depression, citalopram a norepinephrine/serotonin reuptake inhibitor and fluoxetine a selective serotonin reuptake inhibitor. This patient was therefore, at some risk for serotonin syndrome. <span style="background-color: white; color: #2a2a2a; font-family: "merriweather" , serif; font-size: 16px;">This syndrome is characterized by changes in autonomic, neurological, and cognitive behavioral functions and appears to result from over-stimulation of 5-HT</span><sub style="border: 0px; box-sizing: border-box; color: #2a2a2a; font-family: Merriweather, serif; font-size: inherit; font-stretch: inherit; line-height: inherit; margin: 0px; padding: 0px;">1a</sub><span style="background-color: white; color: #2a2a2a; font-family: "merriweather" , serif; font-size: 16px;"> and 5-HT</span><sub style="border: 0px; box-sizing: border-box; color: #2a2a2a; font-family: Merriweather, serif; font-size: inherit; font-stretch: inherit; line-height: inherit; margin: 0px; padding: 0px;">2</sub><span style="background-color: white; color: #2a2a2a; font-family: "merriweather" , serif; font-size: 16px;"> receptors in the central grey nuclei and medulla.</span><span style="background-color: white; font-size: 12px;"><span style="color: #006fb7; font-family: "source sans pro" , sans-serif;"> </span></span> Therefore, Demerol, tramadol and dextromethorphan would be relatively contraindicated in this patient. Furthermore, as mentioned, this patient had a glucose reading of 63 mg/dL preop. There are a number of articles and case reports indicating the risk of hypoglycemia in patients taking SSRIs. It has been shown that SSRIs can enhance insulin sensitivity in man [7-10]. Therefore, this patient had three possible causes of low blood sugar: 1) too much diabetic medication plus a missed meal, 2) polycythemia induced misreading of glucometer, and 3) SSRI induced insulin enhanced sensitivity.<br />
<br />
In general, the approach to patients with PV with scheduled surgery needs to consider any clinical symptoms resulting from the PV, current medical condition of the patient, age, degree of polycythemia, and stress and duration of surgery. Therefore, a patient having a relatively short procedure, with no evidence of any symptoms from the polycythemia and in otherwise decent health may tolerate surgery with acute preoperative normovolemic hemodilution. A patient with uncontrolled PV undergoing major surgery on the other hand may need to be delayed to allow for a hematologist consult for preoperative treatment.<br />
<br />
<br />
<div class="ref-cit-blk half_rhythm" id="B2" style="background-color: white; font-family: "Times New Roman", stixgeneral, serif; font-size: 15.9991px; margin: 0.6923em 0px;">
<span class="element-citation">1. Berk PD, Goldberg JD, Donovan PB, Fruchtman SM, Berlin NI, Wasserman LR. Therapeutic recommendations in polycythemia vera based on Polycythemia Vera Study Group protocols. <span class="ref-journal">Semin Hematol. </span>1986;<span class="ref-vol">23</span>:132–143.</span></div>
<div class="ref-cit-blk half_rhythm" id="B3" style="background-color: white; font-family: "Times New Roman", stixgeneral, serif; font-size: 15.9991px; margin: 0.6923em 0px;">
2. <span class="element-citation">Ruggeri M, Rodeghiero F, Tosetto A, Castaman G, Scognamiglio F, Finazzi G, et al. Postsurgery outcomes in patients with polycythemia vera and essential thrombocythemia: a retrospective survey. <span class="ref-journal">Blood. </span>2008;<span class="ref-vol">111</span>:666–671.</span></div>
<div class="ref-cit-blk half_rhythm" id="B3" style="background-color: white; margin: 0.6923em 0px;">
<div style="font-family: "times new roman", stixgeneral, serif; font-size: 15.9991px;">
<span class="element-citation">3. </span><span style="font-size: 15.9991px;">Wadleigh M, Tefferi A. Classification and diagnosis of myeloproliferative neoplasms according to the 2008 World Health Organization criteria. </span><span style="font-size: 15.9991px;"><span class="ref-journal">Int J Hematol. </span>2010;<span class="ref-vol">91</span>:174–179.</span><span style="font-size: 15.9991px;"> </span></div>
<div style="font-family: "times new roman", stixgeneral, serif; font-size: 15.9991px;">
<span style="font-size: 15.9991px;"><br /></span>
<span style="font-size: 15.9991px;">4. </span><span style="background-color: #f8f8f8; color: #373737; font-family: "arial" , "helvetica" , sans-serif; font-size: 14px;">Wasserman LR, Gilbert HS.<i> Ann New York Acad Sci </i>1964;115:122-38.</span></div>
<div style="font-family: "times new roman", stixgeneral, serif; font-size: 15.9991px;">
<span style="background-color: #f8f8f8; color: #373737; font-family: "arial" , "helvetica" , sans-serif; font-size: 14px;"><br /></span>
<span style="background-color: #f8f8f8; color: #373737; font-family: "arial" , "helvetica" , sans-serif; font-size: 14px;">5. </span><span style="font-size: 15.9991px;">Thomas DJ, Marshall J, Russell RW, Wetherley-Mein G, du Boulay GH
et al. <i>Lancet. </i>1977;2(8045): 941-943</span></div>
<div style="font-family: "times new roman", stixgeneral, serif; font-size: 15.9991px;">
<span style="font-size: 15.9991px;"><br /></span>
<span style="font-size: 15.9991px;">6. </span><span style="font-size: 15.9991px;">Ruggeri M, Rodeghiero F, Tosetto A, Castaman G, Scognamiglio F, et al. <i>Blood</i> </span><span style="font-size: 15.9991px;">2008; </span><span style="font-size: 15.9991px;">111(2): 666-671</span></div>
<div style="font-family: "times new roman", stixgeneral, serif; font-size: 15.9991px;">
<span style="font-size: 15.9991px;"><br /></span></div>
<span style="font-family: inherit;"><span style="font-size: 15.9991px;">7. </span>Araya V, Contreras P, Aguirre C, Depix MS, Zura ML. The effect of fluoxetine on insulin resistance in nondiabetic obese patients [in Spanish]. <em style="box-sizing: border-box;">Rev Med Chil.</em> 1995;123(8):943-947.</span><br />
<div style="box-sizing: border-box; margin-bottom: 10px;">
<span style="font-family: inherit;"><br /></span></div>
<div style="box-sizing: border-box; margin-bottom: 10px;">
<span style="font-family: inherit;">8. Potter van Loon BJ, Radder JK, Frölich M, Krans HM, Zwinderman AH, Meinders AE. Fluoxetine increases insulin action in obese nondiabetic and in obese non-insulin-dependent diabetic individuals. <em style="box-sizing: border-box;">Int J Obes Relat</em> <em style="box-sizing: border-box;">Metab Disord</em>. 1992;16(2):79-85.</span></div>
<div style="box-sizing: border-box; margin-bottom: 10px;">
<span style="font-family: inherit;">9. Lustman PJ, Clouse RE, Nix BD, et al. Sertraline for prevention of depression recurrence in diabetes mellitus: a randomized, double-blind, placebo-controlled trial. <em style="box-sizing: border-box;">Arch Gen Psych</em>. 2006;63(5):521-529.</span></div>
<div style="box-sizing: border-box; margin-bottom: 10px;">
<span style="font-family: inherit;">10. Paile-Hyvärinen M, Wahlbeck K, Eriksson JG. Quality of life and metabolic status in mildly depressed women with type 2 diabetes treated with paroxetine: a single-blind randomised placebo controlled trial. <em style="box-sizing: border-box;">BMC Fam Pract.</em> 2003;4:7.</span></div>
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Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-42689719807386611652018-02-01T14:51:00.001-08:002018-02-01T14:52:22.364-08:00WPW syndrome in patient with significant intraoperative hyperthermia<div style="text-align: left;">
Recently I relieved one of our CRNAs. The patient was undergoing a marathon thyroidectomy which had started at 9:30 that morning. It was now 3pm. The report I received indicated that the patient had developed hyperthermia with a temperature (esophageal) of 38.8 C. The patient was receiving sevoflurane in oxygen and the HR was 110's. BP was stable, and etCO2 was 36 mmHg with a minute ventilation of close to 5 to 6 L/min. </div>
<div style="text-align: left;">
<br /></div>
<div style="text-align: left;">
I immediately verified that the room temperature was turned down and that the bear hugger was blowing cool air.</div>
<div style="text-align: left;">
<br /></div>
<div style="text-align: left;">
The main considerations when confronted with sudden intraoperative hyperthermia are:</div>
<div style="text-align: left;">
</div>
<ul>
<li>malignant hyperthermia</li>
<ul>
<li>in this case ruled out by normal minute ventilation and etPCO2, and lack of muscle rigidity.</li>
</ul>
<li>Thyroid Storm</li>
<ul>
<li>A possibility in this case, considering that the patient was having a thyroidectomy that required nearly seven hours of surgery. </li>
<li>often causes tachycardia, hyperthermia, hyper or hypotension, hypokalemia and significant mental status changes that would not be evident until emergence.</li>
</ul>
<li>cocaine abuse</li>
<ul>
<li>excessive preoperative use can result in hyperpyrexia along with other symptoms like tachycardia, seizures, tachypnea, and dysrhythmias can often mimic MH.</li>
</ul>
<li>sepsis</li>
<ul>
<li>usually clinical history can clue in to this cause as well as tachycardia and hypotension.</li>
</ul>
<li>pheochromocytoma</li>
<ul>
<li>clinical history of headaches, sudden onset hypertension and tachycardia will lead the clinician to suspect this diagnosis</li>
<li>Catecholamine excess usually results in significant tachycardia and hypertension intraoperatively, but hyperthermia may also be present.</li>
</ul>
<li>excessive medication administration</li>
<ul>
<li>ketamine, atropine, dopamine, droperidol, or tricyclics </li>
</ul>
<li>Neuroleptic malignant syndrome (NMS)</li>
<ul>
<li>from central dopaminergic blockade</li>
<li>butyrophenones, phenothiazines, metoclopramide, lithium, tricyclics, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, and haloperidol.</li>
<li>clinical symptoms similar to MH; tachycardia, hyperthermia, metabolic acidosis, and increased muscle tone.</li>
<li>The only possible way to distinguish NMS from MH is that severe hypercapnia is not seen with NMS.</li>
</ul>
</ul>
This patient also was diagnosed with Wolf Parkinson White (WPW) syndrome and was currently tachycardic. WPW is a pre excitation syndrome where atrial cardiac impulses may bypass the AV node via Kent's bundle which can lead to pre excitation of the ventricle leading two main arrythmias: parosxymal supraventricular tachycardia (PSVT) or atrial fibrillation (AF). The accessory pathway (Kent's bundle) utilizes a sodium-dependent fast inward current for electrical impulse transmission, thus conducting signals more quickly from the atrium to the ventricle than the AV node, where a calcium-dependent slow inward current slows conduction. Therefore, the general goal is to increase the refractory period of the bundle of kent relative to the AV node. However, conduction of cardiac impulses may travel in either a retrograde or anterograde direction through the bundle of Kent creating a clinical challenge in both diagnosis and proper treatment of pathologic tachycardias in patients with WPW syndrome. In some cases The bundle of kent conducts impulses in only a retrograde direction as seen below in the graphic. In this case, no delta wave is visible on a normal EKG.<br />
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However, the vast majority of WPW patients can experience both anterograde and retrograde conduction via the accessory pathway. This is important because the EKG appearance is altered by the direction of conduction of cardiac impulses through the accessory pathway. Patients with WPW syndrome who develop PSVT will have a regular R to R interval and may have a narrow complex tachycardia. However, Antidromic AVRT can lead to wide complex tachycardia that is very difficult to differentiate from ventricular tachycarida (VT). Antidromic AVRT is rare (~5% of PSVT in WPW). Orthodromic AVRT is more common and results in a narrow complex tachycardia (200 to 300 bpm). Patients with WPW syndrome and AF have an irregularly irregular wide complex tachycardia. (see graphic of AF in WPW below).</div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgVlqFwhZrpFpTUsiiX-fwcFlvOBONQICIbAQ99eu7fkuMyx8eedvCwLmlSIBsLkjYmKM80_Y_IFKx_lAd-PcUMOTWqmV8O-f2Jb9KldnNzy2e4tQebWcIKhPiL3COmWJM_03fdxi0Q7qGp/s1600/WPW-ecg-004.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="558" data-original-width="1024" height="174" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgVlqFwhZrpFpTUsiiX-fwcFlvOBONQICIbAQ99eu7fkuMyx8eedvCwLmlSIBsLkjYmKM80_Y_IFKx_lAd-PcUMOTWqmV8O-f2Jb9KldnNzy2e4tQebWcIKhPiL3COmWJM_03fdxi0Q7qGp/s320/WPW-ecg-004.jpg" width="320" /></a></div>
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Therefore, the approach to a patient who develops pathologic tachycardia and has WPW syndrome in the preoperative period requires determining most importantly whether there is a regular R to R interval (see discussion below). In many cases, amiodarone is the preferred for treatment of pathologic tachycardia in WPW only because amiodarone can be safely used regardless of the etiology, i.e. AF, VT, PSVT. If a clear diagnosis is possible from the cardiac tracing or 12 lead EKG, then a more selective medication may be chosen. For example, it may be best to begin treatment of PSVT with vagal maneuvers if the patient is otherwise stable. These include valsalva, gag reflex (fingers in throat), or ice on face (diving reflex). If prompt attempts at vagal maneuvers fail, then medications that can abruptly prolong the refractory period of the AV node (PSVT) such as adenosine 3 to 12 mg IV, verapamil 2.5 to 10 mg IV, or esmolol 50 to 100 mg IV can be tried. It should be noted that several case reports of WPW syndrome patients receiving general anesthesia have commented on the use of lidocaine to prevent re entrant tachycardia. It is unlikely that lidocaine will play a significant role in preventing re entrant tachycaridias in this patient population as noted in a paper published by Barrett et al. [2] In another study, the authors showed that in patients with WPW syndrome in A Fib with RVR, lidocaine was likely to increase (make worse) the ventricular rate, or have no beneficial effect [3]. Lidocaine is a class IB anti arrhythmic (blocks Na+ channels), but unlike procainamide (used in WPW syndrome with A fib), lidocaine decreases the effective refractory period (procainamide class IA increases the effective refractory period). Therefore, lidocaine based on its pharmacology alone would be predicted to be less useful in treating supra ventricular tachycardias as compared to procainamide. In the case of WPW with AF, the goal is exactly the opposite of that in a non WPW syndrome patient with AF. i.e. the goal in non WPW A fib is to slow conduction through the AV node, via medications such as verapamil. In WPW AF, verapamil (and digitalis), which slows AV node conduction, is strictly contraindicated. Procainamide, on the other hand, can be used since it prolongs the refractory period of the accessory pathway. In daily clinical practice, procainamide may not be readily available. Amiodarone is a class III anti arryhmic and indeed can treat AF in WPW. However, a 2010 review [4] found several studies that were able to identify a small risk of ventricular fibrillation (similar to the concern when using lidocaine for AF in WPW syndrome). The study, therefore, concluded that amiodarone was not superior to procainamide in rate control for WPW with AF and could be dangerous.<br />
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In any patient who becomes unstable due to the arrhythmia, synchronized cardioversion is the treatment of choice. <span style="background-color: white; color: #1b1b1b; font-family: "georgia";">Opioids like fentanyl, benzodiazepines including midazolam have been found to have no effect on the EP effects of the accessory pathway. There is a case report of disappearance of delta wave after propofol administration making it the induction drug of choice if GETA is required [1]. Both isoflorane and sevoflorane do not have any effect on AV node conduction, however, desflurane if given at greater than a 6% concentration initially can lead to increased sympathetic output. Therefore, if desflurance is chosen, slowly increasing the concentration would be required. </span><br />
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<span style="background-color: white; color: #1b1b1b; font-family: "georgia";"><span style="color: black; font-family: -webkit-standard;">Typically, the anesthetic management of a patient with WPW calls for the avoidance of increased sympathetic activity (pain, anxiety, fear, stress response from any cause, lighter planes of anesthesia, hypovolemia and the avoidance of anticholinergic medications. Since the avoidance of lighter planes of anesthesia is critical in these cases, monitoring anesthesia depth with a BIS monitor would not be unreasonable in any patient with WPW syndrome who has not had the accessory pathway ablated. </span></span><br />
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<span style="background-color: white; color: #1b1b1b; font-family: "georgia";">In this patient who was at risk for thyroid storm having a prolonged thyroidectomy surgery, significant hyperthermia with sinus tachycardia and WPW syndrome, presumptive treatment for thyroid storm was reasonable. It turns out that many of the indicated treatments for a patient with possible thyrotoxicosis are also indicated to modify the risk in a patient having surgery with WPW syndrome. An esmolol infusion is recommended to control HR in thyroid storm [5], and is not a bad choice to control HR and attenuate the sympathetic nervous syndrome in a WPW syndrome patient. Also recommended for patients suspected of thyroid storm and persistent hypotension is cortisol IV (100 to 200 mg). Decadron may inhibit the conversion of T4 to T3 (T3 is the main culprit in promoting symptomatology in thyrotoxicosis) [5]. </span><br />
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<span style="background-color: white; color: #1b1b1b; font-family: "georgia";">In the end, the patient was extubated and taken to PACU. Despite efforts to cool the patient, the temperature was still elevated in the PACU. Fortunately, other than hyperthermia, the patient suffered no apparent ill effect from the surgery and recovered without sequelae. However, vigilance and the ability to prioritize treatments in patients who present with two or more conditions simultaneously in the OR requires a more intimate understanding of the underlying goals at a mechanistic level. In this case, the treatments recommended were beneficial for both conditions.</span><br />
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<span style="background-color: white; color: #1b1b1b; font-family: "georgia";">1. </span><span style="background-color: white; color: #1b1b1b; font-family: "georgia"; font-size: 18px;">8. </span><span style="color: #1b1b1b; font-family: "georgia"; font-size: 18px; max-width: 100%;">Seki S, Ichimiya T, Tsuchida H, Namiki A. A case of normalization of Wolff-Parkinson-White syndrome conduction during propofol anaesthesia. <span style="max-width: 100%;"><span style="max-width: 100%;">Anesthesiology. </span>1999;<span style="max-width: 100%;">90</span>:1779–81.</span></span></div>
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<span style="color: #1b1b1b; font-family: "georgia"; font-size: 18px; max-width: 100%;"><span style="max-width: 100%;">2. Barrett PA, Laks MM, Mandel WJ, Yamaguchi I. <i>Am Heart J</i>. 1980. Jul;100(1):23-33.</span></span></div>
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<span style="color: #1b1b1b; font-family: "georgia"; font-size: 18px; max-width: 100%;"><span style="max-width: 100%;">3. Akhtar M, Gilbert CJ, and Shenasa M. <i>Circulation</i> 1981. Vol. 63(2):435-441.</span></span><br />
<span style="color: #1b1b1b; font-family: "georgia"; font-size: 18px; max-width: 100%;"><span style="max-width: 100%;">4. Simonian SM, Lotfipour S, wall C, and Langdorf MI. <i>Intern Emerg Med. </i>2010, 5(5): 421-6.</span></span><br />
<span style="color: #1b1b1b; font-family: "georgia"; font-size: 18px; max-width: 100%;"><span style="max-width: 100%;">5. Stoelting RK.<i> Anesthesia and Co Existing Disease. </i>p. 349</span></span></div>
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Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-87940981082783299262017-09-21T15:41:00.000-07:002017-11-09T15:10:29.785-08:00Three cases of spinal for c-section; an eval of each one.Last weekend on call I had three sections during the night. The first case was a young nurse, healthy with excellent anatomy for placing a spinal anesthetic. She was admitted around 4pm and went to c-section at 10:00pm for lates and variables. <br />
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CASE 1<br />
I performed a spinal in my usual fashion. The hospital supplies us with Spinocan spinal trays. These contain a 25 G spinocan needle, 2 mL of 0.75% hyperbaric bupivacaine, Lidocaine 1% 5 cc and a 3 cc syringe plus a 5 cc syringe for drawing the intrathecal dose. I also administer 12 mg bupivacaine mixed with 20 mcg of fentanyl + 150 mcg of preservative free morphine (duramorph). I also, always grab a 25 G whitacre needle from the anesthesia cart to decrease the risk of PDPH.<br />
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CASE 2<br />
I finished this case at 11:15pm and went to bed. At 12:30am I was called by the obstetrician who told me she had a drop in patient with severe PIH. She planned on delivering her, but she her platelets went from 88K to 84K. She wanted to know what I thought. I told her I would place a spinal in this patient as long as the platelets were greater than 75K. We rolled back to the OR at 2:10am and finished at 3:30am. In this patient, due to challenging anatomy (obese patient with lots of adiposity in the lumbar back), I was unable to get the spinal needle (once again a spinocan) into the space with just 2 to 3 attempts. Due to the relative urgency of the case, I opted to use a touhy needle (18G) to locate the midline and use a gertie marx 26G spinal needle through the touhy to inject my usual mix. With the touhy, I rapidly (with one pass) identified the midline and epidural space, inserted the spinal needle, and got a great spinal. The case went smoothly, and blood pressures after spinal normalized almost immediately with no further issues.<br />
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CASE 3<br />
At 5:30am, I was called for an urgent c-section. A young healthy patient who was schedule for c-section that very morning but at 10:00am had arrived to the hospital early contracting. She had been scheduled because she was carrying twins who were breech. Because of the urgency, the obstetrician was standing at my side during the spinal placement. I noticed that her anatomy was also very poor for easy identification of the midline. She was obese, with the vast majority of her adipose tissue located in the lumbar region. Palpation of a midline area was very challenging. The patient was also in terrible pain due to near constant uterine contractions and had trouble sitting and holding her position. I elected to immediately start with a tuohy needle as I sensed that I might again have a difficult time identifying the midline by feel with a thin 25G spinal needle. I inserted the touhy needle to a moderate depth without feeling any resistance that I could identify as ligament or bone. No sooner had I got the touhy to a moderate depth (approximately 4.5 cm) did I notice a flash of clear liquid at the hub. I feared a wet tap, so I removed the stylet from the touhy, without any CSF flow. It was clear that there was however some residual clear liquid in the touhy. I removed the touhy and retried with no luck. After searching a minute or two for the midline, I again noticed a small flash of clear liquid in the hub and withdrew the stylet. This time clear fluid drained from the tuohy. While disappointed in this result, my only real option at this time was to inject the spinal cocktail I had prepared. I attached my syringe, aspirated to verify continued CSF drainage, and once this was verified, I injected the anesthetic (12 mg bupivacaine, 20 mpg fentanyl, 150 mpg duramorph). The patient laid down, and very slowly the contractions eased, but did not go away completely. Very quickly it was evident, that the patient did not develop a proper spinal block. GETA via rapid sequence was rapidly induced and the twins were delivered without incident. We finished at 7:05am, the end of my shift.<br />
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Case 1 breakdown- discussion of spinocan vs other needle types.<br />
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This case went as uneventful as you might expect in a healthy 28 year old female having her 2nd child for NRFHT. The only difference in this cases was that I was forced to use a spinocan needle (cutting type tip) rather than my usual choice of a whitacre. This case was performed at 10PM. I visited the patient on POD 2 at about 4:30pm. She was complaining of a headache which started mid morning on POD 1. It was gone in the morning of POD 2 after a good nights sleep, but returned with a vengeance by early afternoon. It was totally relieved by lying down, and clearly aggravated when the head was elevated. <br />
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<span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">Modifiable risk factors of PDPH include the needle size, needle shape, bevel orientation and inserting angle, stylet replacement, and operator experience.</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;"> Needle size might be the most significant factor in the development of PDPH. In our hospital, we only have access to 25G needles. </span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">A previous meta-analysis published in 2000 has compared the frequency of PDPH between Quincke (a cutting-point spinal needle) and pencil-point spinal needles which suggested that pencil-point spinal needle will significantly reduce PDPH rate compared with Quincke spinal needles. They found a RR of PDPH of 0.38 if a pencil point needle was used. Criticism of this meta </span><span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">analysis related to its small size (only 15 PDPH occurred in the study), and only two needle types compared (Quincke vs whitacre). One study estimated that the incidence of PDPH when a 25 G cutting needle is used (Quincke) is about 23% [1] but may be less than 2% if a 27G needle is used. However, a more recent study [3] a prospective comparison of 5 needle types showed that PDPH went from an incidence of 8% in the quincke style needle to 3% with a whitacre. The requirement for blood patch in this study went from 12.5% with a 25G quincke to 0% with a whitacre. Studies also find that there is less chance of successful spinal anesthesia when smaller gauge needles are used, therefore, the law of diminishing returns becomes significantly apparent with needles smaller than 27G. In a recent meta analysis looking at over six thousands patients, an overall incidence of 4.6% was found for PDPH [2]. The incidence of PDPH was 6.6% for cutting type needles, and 2.6% for pencil point styled needles. This resulted in a RR of PDPH of 2.5 when a cutting style needle was used based on the studies included in this meta analysis.</span></span><br />
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<span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">Other risk factors for PDPH include female sex, younger age, and pre existing headache. Pregnancy may be yet another risk factor for developing PDPH. Ironically, it is this patient population that is most exposed to dural puncture. In this case, the patient suffered a PDPH likely avoided if a pencil point styled needle was used. She was treated with a blood patch on POD 2, and her headache was relieved.</span></span><br />
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<span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">Case 2 breakdown- low plateles requiring urgent delivery due to sever PIH</span></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg9-rh8ETFoDrI_XSbzaSGHl-i7esIAWltpEXBhi0_Fa3H7OVw6Io67YvrRe5MFgeTBmEDNy1jvvRqkg48YIXOOyJ8PtDL_A3J-lGO-y-uHglpvqo8dzUuyiD2jlf0GzppEN8FEWa74pUfX/s1600/IMG_2519.JPG" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1600" data-original-width="1200" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg9-rh8ETFoDrI_XSbzaSGHl-i7esIAWltpEXBhi0_Fa3H7OVw6Io67YvrRe5MFgeTBmEDNy1jvvRqkg48YIXOOyJ8PtDL_A3J-lGO-y-uHglpvqo8dzUuyiD2jlf0GzppEN8FEWa74pUfX/s400/IMG_2519.JPG" width="300" /></a></div>
<span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;"><br /></span></span><span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">For a general review on PIH and anesthesia click <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3127293/">here. </a> There is no evidence to support any arbitrary cut off when performing neuraxial anesthesia in a patient whose platelets are low (i.e. less than 150k). However, we have indirect evidence that there is some risk associated with neuraxial anesthsia in thrombocytopenic patients. In PIH about 30% of patients will develop thrombocytopenia. The cause is unknown, but damage to the endothelium has been implicated. This is known to cause the release of thromboxane and serotonin from activated platelets and a platelet consumption cascade ensues. As an anesthesia resident, I was taught that below 100k platelets, neuraxial anesthesia is contraindicated in PIH. However, practice patterns are changing. In a small retrospective study of 30 parturients, epidural anesthesia was conducted when platelets were between 69K and 98K [4]. in 1989, Rasmus et al. [5] found 14 parturients who received neuraxial anesthesia with platelet counts ranging from 15K to 99K. No reports of epidural hematoma were found in this review. In a more recent review Goodier et al. [6] looked at 174 parturients with low platelet count (less than 100K) and neuraxial anesthesia and found no cases of hematoma formation. Nevertheless, at this time, the numbers of patients documented to have neuraxial anesthesia with platelets less than 100k (~499) is small. In a review by Vandermuelen et al revealed that in cases of epidural hematoma, 75% were in patients who had EA instead of SAB. This rare condition may still be a relevant concern given that it may lead to permanent paraplegia. In the past, many have advocated for epidural anesthesia in PIH or severe PIH for Cesarean delivery to avoid severe hypotension by using a gradual block onset. This is related to the fact that in PIH, intervillous blood flow is decreased, therefore, making these patients particularly vulnerable to hypotension. However, in clinical practice this has not born out. Dyer at al stated that current evidence suggests that parturients with PIH have less susceptibility to hypotension and perhaps less impairment of cardiac output vs their healthy counterparts [7]. In a recent prospective study, hypotension was more frequent in SAB vs. EA for C-section, however, the duration of hypotension was short (less than 1 min) in both groups. Also, hypotension was easily treated in both groups, and the study concluded that SAB was safe for C-section in patients with severe pre eclampsia [9]. In severe PIH, a major concern for maternal health is the avoiding severe hypertension that can result in cerebral bleeding. Ramanathan et al. showed that neuraxial anesthesia is superior to GA in avoiding hypertension during cesarean delivery [8]. Therefore, in patients with severe PIH and low platelets requiring urgent cesarean delivery, SAB is better than EA is probably better than GA. </span></span><br />
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<span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">Case 3 breakdown:</span></span><br />
<span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">This case was FUBAR. Some of the issues making this case difficult, included: a patient in near hysterics due to near constant contractions, significant obesity located to the lower back area, and the fact that I was exhausted by this point having been working on and off for the last 24 hours. Nevertheless, my decision to use a touhy needle (a routine for me) as my first attempt in a difficult spinal was a problem. It lead to an immediate dural puncture. Unfortunately, when I removed the stylet to verify my suspicion, there was no flow of CSF. The next "dural puncture" was likely not a dural puncture after all. Although there was flow of CSF from the tuohy, no level was achieved. My explanation for this is that a pool of CSF must have built itself up in the epidural space from the initial dural puncture. I therefore, had plenty of CSF flow and could withdraw CSF prior to injection, but the injection was placed into the epidural space. The very slight relief of pain that occurred just a few minutes after my "spinal injection" is likely attributed to some medication finding its way through the dural tear into the IT space. In hind site, and going forward, I will always make my first attempt at spinal anesthesia with the standard 25 g spinal needle (pencil point type). In this case, I did have some redemption in choosing the tuohy first for two reasons: 1) I had had to resort to a touhy in the previous spinal after multiple failed attempts with the spinal needle and this had solved immediately my difficulty with gaining access to the IT space, and 2) we had 5 inch gertie marx needles (pencil point styled) which are meant to be inserted through the touhy after gaining access to the epidural space, but I only 3.5 inch 25 G spinocan needles for a straight IT approach. (BTW, i have since talked to the anesthesia tech to ensure that we have a large supply of 25G whitacre needles in each OB OR). </span></span><br />
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<span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="font-size: 15.999099731445313px;">In summary, in one night on OB call, I performed 3 anesthetics. Case one was a straight forward very forgettable spinal anesthetic that resulted in an early and severe PDPH requiring blood patch. Case two was a severe PIH patient with very low platelets that underwent uneventful spinal anesthesia despite unfavorable anatomy using a pencil point spinal needle with no sequelae. Case three was a healthy breech twin parturient in extreme pain who suffered a dural puncture with 18G touhy needle with accompanied failed SAB requiring conversion to GETA via RSI. She developed a PDPH 36 hours after puncture and eventually requested a blood patch which resolved her headache. </span></span><br />
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1. <span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">Castrillo A, Tabernero C, Garcia-Olmos LM, et al</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">. </span><span class="ref-journal" style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">Spine J</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;"> 2015;</span><span class="ref-vol" style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">15</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">:1571–6</span><br />
<span style="background-color: white;"><span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">2.</span><span style="font-family: inherit;"> </span></span><span style="font-family: inherit;"><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Xu%20H%5BAuthor%5D&cauthor=true&cauthor_uid=28383416" style="color: #642a8f;">Hong Xu</a><span style="background-color: white;">, MD, </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Liu%20Y%5BAuthor%5D&cauthor=true&cauthor_uid=28383416" style="color: #642a8f;">Yang Liu</a><span style="background-color: white;">, MD, </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Song%20W%5BAuthor%5D&cauthor=true&cauthor_uid=28383416" style="color: #642a8f;">WenYe Song</a><span style="background-color: white;">, MD, </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Kan%20S%5BAuthor%5D&cauthor=true&cauthor_uid=28383416" style="color: #642a8f;">ShunLi Kan</a><span style="background-color: white;">, MD, </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Liu%20F%5BAuthor%5D&cauthor=true&cauthor_uid=28383416" style="color: #642a8f;">FeiFei Liu</a><span style="background-color: white;">, MD, </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Zhang%20D%5BAuthor%5D&cauthor=true&cauthor_uid=28383416" style="color: #642a8f;">Di Zhang</a><span style="background-color: white;">, MD, </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Ning%20G%5BAuthor%5D&cauthor=true&cauthor_uid=28383416" style="color: #642a8f;">GuangZhi Ning</a><span style="background-color: white;">, PhD,</span><span style="line-height: 1.6363em; position: relative; top: -0.5em; vertical-align: baseline;">∗</span><span style="background-color: white;"> and </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Feng%20S%5BAuthor%5D&cauthor=true&cauthor_uid=28383416" style="color: #642a8f;">ShiQing Feng</a><span style="background-color: white;">, PhD </span><span role="menubar"><a aria-expanded="false" aria-haspopup="true" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5411200/#" role="menuitem" style="color: #642a8f;">Medicine (Baltimore)</a></span><span style="background-color: white;">. 2017 Apr; 96(14): </span></span><br />
<span style="font-family: inherit;"><span style="background-color: white;">3. </span></span><span style="font-family: inherit;">Vallejo MC<span style="background-color: white; line-height: 1.6363em; position: relative; top: -0.5em; vertical-align: baseline;">1</span><span style="background-color: white;">, </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Mandell%20GL%5BAuthor%5D&cauthor=true&cauthor_uid=11004048" style="background-color: white; border-bottom: 0px; color: #660066;">Mandell GL</a><span style="background-color: white;">, </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Sabo%20DP%5BAuthor%5D&cauthor=true&cauthor_uid=11004048" style="background-color: white; border-bottom: 0px; color: #660066;">Sabo DP</a><span style="background-color: white;">, </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Ramanathan%20S%5BAuthor%5D&cauthor=true&cauthor_uid=11004048" style="background-color: white; border-bottom: 0px; color: #660066;">Ramanathan S</a><span style="background-color: white;">. </span><span role="menubar" style="background-color: white;"><a abstractlink="yes" alsec="jour" alterm="Anesth Analg." aria-expanded="false" aria-haspopup="true" href="https://www.ncbi.nlm.nih.gov/pubmed/11004048/#" role="menuitem" style="border-bottom: 0px; color: #660066; outline: 0px;" title="Anesthesia and analgesia.">Anesth Analg.</a></span><span style="background-color: white;"> 2000 Oct;91(4):916-20.</span></span><br />
<span style="font-family: inherit;"><span style="background-color: white;">4. </span></span><span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;"> </span><span class="element-citation"><span style="font-family: inherit;">Beilin Y, Zahn J, Comerford M. Safe epidural analgesia in 30 parturients with platelet count between 69000 and 98000 cumm-1. <span class="ref-journal">Anesth Analg. </span>1997;<span class="ref-vol">85</span>:385–8. <span class="nowrap ref pubmed" style="white-space: nowrap;">[<a href="https://www.ncbi.nlm.nih.gov/pubmed/9249118" ref="reftype=pubmed&article-id=3127293&issue-id=198100&journal-id=1510&FROM=Article%7CCitationRef&TO=Entrez%7CPubMed%7CRecord&rendering-type=normal" style="color: #642a8f;" target="pmc_ext">PubMed</a>]</span></span></span><br />
<span style="font-family: inherit;"><span style="white-space: nowrap;">5. </span>Rasmus KT, Rottman RL, Kotelko DM, Wright WC, Stone JJ, Rosenblatt RM. Unrecognised thrombocytopenia and regional anaesthesia in parturients: A retrospective review.</span><span style="font-family: inherit;"> </span><span class="ref-journal" style="font-family: inherit;">Obstet Gynecol. </span><span style="font-family: inherit;">1989;</span><span class="ref-vol" style="font-family: inherit;">73</span><span style="font-family: inherit;">:943–6.</span><span style="font-family: inherit;"> </span><span style="font-family: inherit;"> </span><span class="nowrap ref pubmed" style="font-family: inherit; white-space: nowrap;">[<a href="https://www.ncbi.nlm.nih.gov/pubmed/2726116" ref="reftype=pubmed&article-id=3127293&issue-id=198100&journal-id=1510&FROM=Article%7CCitationRef&TO=Entrez%7CPubMed%7CRecord&rendering-type=normal" style="color: #642a8f;" target="pmc_ext">PubMed</a>]</span><br />
<span class="nowrap ref pubmed" style="font-family: inherit; white-space: nowrap;">6. Goodier CG, Lu JT, Hebbar L, Segal BS, Goetz L. <i>Anesth Analg </i>2015 Oct;121(4):988-91.</span><br />
<span class="nowrap ref pubmed"><span style="font-family: inherit;"><span style="white-space: nowrap;">7. Dyer RA, Piercy JL, Reed AR. </span></span><span style="font-style: italic; white-space: nowrap;">Currently</span><span style="font-family: inherit; font-style: italic;"><span style="white-space: nowrap;"> </span></span><span style="font-style: italic; white-space: nowrap;">Open</span><span style="font-family: inherit;"><span style="white-space: nowrap;"><i> Anaesthesiol. </i>2007 Jun;20(3): 168-74.</span></span></span><br />
<span class="nowrap ref pubmed"><span style="font-family: inherit;"><span style="white-space: nowrap;">8. </span></span></span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">Ramanathan J, Coleman P, Sibai B. Anesthetic modification of hemodynamic and neuroendocrine stress responses to caesarean delivery in women with severe preeclampsia. </span><span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;"><span class="ref-journal">Anesth Analg. </span>1991;<span class="ref-vol">73</span>:772–9.</span><br />
<span style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">9. </span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">15. </span><span class="element-citation" style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.999099731445313px;">Visalyaputra S, Rodanant O, Somboonviboon W, Tantivitayatan K, Thienthong S, Saengchote W. Spinal versus Epidural anaesthesia for caesarean delivery in severe pre-eclampsia: A prospective randomised multicenter study. <span class="ref-journal">Anesth Analg. </span>2005;<span class="ref-vol">101</span>:862–8.</span><br />
<br />Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-22758702637730325222017-09-03T17:23:00.002-07:002017-09-07T11:31:53.024-07:00preoperative hypokalemia, replace and proceed or cancel?The other morning, while I was in the middle of my first of three scheduled cases I received a call from a nurse to report that the K+ level was 2.8 mEq/L on my next scheduled patient. The patient was a 76 year old female who had a history of Afib, CHF, CAD. Previously, an AICD was placed for unclear reasons. The patient stated that she believed the reason for the AICD was due to her poor cardiac function. She reported no history of previous ventricular fibrillation/tachycardia. She was on diuretics, with oral potassium supplements. <br />
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Basic Science review: Potassium homeostasis<br />
Total body stores of K+ are approximately 3000 to 4000 meq with 98% of this located inside the cells. This concentration differential is maintained by the Na+-K+ ATPase pump, located in the cell membrane which pumps out 3 Na+ ions for every 2 K+ions pumped in. K+ plays an important role in cell metabolism, and therefore, a myriad of cellular functions deteriorate with an imbalance of K+ ion concentration. For example, significant hypokalemia can result in polyuria due to a reduced sensitivity to ADH. Also critical is the intracellular to extracellular concentration gradient which largely determines resting membrane potential. <br />
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Em=-61 log r[K+]cell+0.01 [Na+]cell / r[K+]ecf + 0.01[Na+]ecf</div>
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Alterations in relative concentrations of K+ inside versus outside cells can significantly alter the resting membrane potential leading to cardiac arrhythmia as well as other skeletal muscular symptoms.</div>
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The maintenance of whole body potassium stores is handled by the kidney, in particular by the principal cells of the cortical collecting tubule. Here aldosterone (secreted in response to a minimal rise in serum potassium) stimulates increased activity of the Na+-K+ ATPase pump located in the basolateral membrane of the principal cell. This pump pulls K+ from the extracellular space and pumps it into the principal cell while exchanging this for Na+ (3 Na+ : 2 K+ ratio). As the intracellular K+ ion concentration increases inside the principal cells, K+ passively leaves the principal cell into the collecting tubule lumen as it follows its concentration gradient. Also in the collecting tubules are located the intercalated cells. These cells work to reabsorb K+ (exactly opposite the Principal cells). These cells are particularly important in hypokalemic patients where an H+-K+ ion pump located in the luminal membrane actively exchanges intracellular H+ ions for K+ ions, allowing K+ to be reabsorbed back into the plasma. As mentioned above, ADH, plays a role in K+ ion secretion by increasing the number of luminal K+ ion channels in the collecting tubules. The K+ ion itself can mimic all of the changes in the kidney that aldosterone initiates. In other words, elevated K+ levels produce an aldosterone like effect where K+ excretion and Na+ reabsorption are enhanced in the principal cells. This is due to increased luminal membrane permeability to Na+ and K+ (by increasing the number of open channels for passive diffusion) and increased activity of the Na+-K+ ATPase pump located on the basolateral membrane.<br />
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Also critical to K+ homeostasis is the urine flow rate in the cortical collecting tubule. There are two mechanisms that allow a greater urinary flow rate in the cortical collecting tubule to increase net K+ secretion leading to hypokalemia. 1) increased flow lowers the intraluminal (inside the collecting tubule) K+ concentration, favoring the passive movement of K+ out of the principal down its concentration gradient via the K+ channels in the luminal membrane of the principal cells. 2) increased flow through the kidney brings more Na+ to the collecting tubule leading to increased Na+ reabsorption in the collecting tubule causing the lumen to become more electronegative favoring passive K+ diffusion to maintain electroneutrality. Furthermore, as more Na+ is reabsorbed into the principal cell, the Na+-K+ ATPase pump removes the Na+ from the cell back into the body, leading to increased K+ entry into the principal cell which increases the intracellular K+ concentration of the principal cells of the collecting tubule. Increased distal flow of urine in the collecting tubule seems to be the mechanism by which the loop and thiazide diuretics induce hypokalemia. These agents increase distal flow by diminishing Na+ and water reabsorption in the loop of Henle and distal tubule respectively.</div>
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<span style="font-family: inherit;">Clinically, chronic K+ alterations from so called normal levels are not as likely to cause outward clinical symptoms. This is because, the intracellular to extracellular gradient is the more important than the overall measured serum concentration. Nevertheless, hypokalemia does result in symptoms even if chronic in nature. W</span><span style="color: #231f20; font-family: inherit;">hen considering the hypokalemic patient in the immediate </span><span style="color: #231f20;">preoperative</span><span style="color: #231f20; font-family: inherit;"> period, it is important to consider three main things: 1) degree of hypokalemia, 2) Invasiveness of surgery and 3) patient's co morbid conditions (i.e. concomitant coronary artery disease or congestive heart failure). </span><span style="color: #231f20; font-family: "arial";"> </span><span style="background-color: white;">Per </span><em style="background-color: white; box-sizing: inherit;">Miller’s Anesthesia</em><span style="background-color: white;">, p. 1107, “As a rule, all patients undergoing elective surgery should have normal serum potassium levels. However, we do not recommend delaying surgery if the serum potassium level is above 2.8 mEq/L or below 5.9 mEq/L, if the cause of the potassium imbalance is known, and if the patient is in otherwise optimal condition.”</span><br />
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<span style="background-color: white;">Patients without underlying cardiac disease are unlikely to suffer myocardial effects, even at levels below 3.0 mEq/L. However, those with ischaemic heart disease, heart failure or left ventricular dysfunction are at risk of arrhythmias with only mild or moderate hypokalaemia. This fact was highlighted in 1981 when Hulting followed patients admitted for treatment of an MI. This paper showed that patients who had a baseline risk of arrhythmia of 3.5% increased to 8% if their serum K+ was less than 3.5 mEq/L. They also found that no patients suffered arrhythmias if their serum potassium was greater than 4.6 mEq/L.</span><br />
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<span style="color: #231f20; font-family: "arial";"><br /></span><span style="color: #231f20; font-family: inherit;"><span style="font-family: inherit;">I</span>n patients undergoing very quick surgeries such as cataract, egd, etc, it is routine to not check labs in the first place so that hypokalemia if it existed would be unknown to the provider. In patients who require diuretics undergoing intermediate or high risk surgery, checking potassium levels is common and hypokalemia should prompt a decision tree based on the degree of hypokalemia, patient co morbidities, and type of surgery.</span><br />
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<span style="color: #231f20; font-family: inherit;">By far the most common cause of hypokalemia in the preoperative period is diuretic use. Diuretic induced hypokalemia has been associated with an increased rate of arrhythmias [4]. Furthermore, diuretic therapy in hypertension and heart failure has been associated with an increased rate of arrhythmic death that can be prevented by a K+ sparing diuretic and therefore, may be related to K+ depletion [5,6]. In the Framingham Heart Study [10], they reported increased frequency of PVCs to be associated with hypokalemia. They estimated that the arrhythmia increased by 27% wit each 0.5 mEq/L decrease in K+ level. Understanding diuretic physiology makes sense given its importance in both inducing and treating hypokalemia. A brief primer on diuretics follows:</span><br />
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<span style="color: #231f20; font-family: inherit;"><b>Loop Diuretics </b><i>(furosemide, bumetanide, torsemide, and ethacrynic acid)</i></span><br />
<br />
<ul>
<li><span style="color: #231f20;">may lead to the excretion of 20 to 25% of filtered Na+ at max doses.</span></li>
<li><span style="color: #231f20;">Act in thick ascending limb of loop of henle. </span></li>
<li><span style="color: #231f20;">loop diuretics inhibit Na+ reabsorption by binding to Cl- site of the Na+-K+-2Cl- carrier on luminal membrane. The carrier only works when all four sites are occupied.</span></li>
<li><span style="color: #231f20;">Secondarily inhibit Ca2+ reabsorption which is passive down an electronegative gradient by the absorption of Na+/K+, which leads to a caliuresis.</span></li>
<li><span style="color: #231f20;">Ca2+ effects make loop diuretics excellent method of treating hypercalcemia when combined with saline loading.</span></li>
</ul>
<span style="color: #231f20;"><b>Thiazide type diuretics</b></span><br />
<br />
<ul>
<li><span style="color: #231f20;">primarily inhibit NaCl transport in the DCT</span></li>
<li><span style="color: #231f20;">at max doses only inhibit up to 3 to 5% of filtered Na+ (far less potent than loop diuretics).</span></li>
<li><span style="color: #231f20;">Diuresis offset by increased reabsorption in the cortical collecting tubule.</span></li>
<li><span style="color: #231f20;">Thiazide type diuretics also compete with Cl- at the Na+-Cl- cotransporter</span></li>
<li><span style="color: #231f20;">In contrast to loop diuretics, thiazide type diuretics can increase the reabsorption of Ca2+ in the DCT and early collecting tubule which may be useful in the treatment of recurrent kidney stones due to hypercalciuria.</span></li>
</ul>
<span style="color: #231f20;"><b>Potassium Sparing Diuretics </b><i>(Amiloride, Spironolactone, Triamtere)</i></span><br />
<br />
<ul>
<li><span style="color: #231f20;">Act in principal cell in the cortical collecting tubule where Na+ reabsorption occurs passively through Na+ channels (which are increased via aldosterone)</span></li>
<li><span style="color: #231f20;">amiloride and triamterene directly decrease the number of open Na+ channels decreasing Na+ reabsorption leading to decreased K+ (and H+) secretion. </span></li>
<li><span style="color: #231f20;">Spironolactone competitively inhibits aldosterone resulting in same result.</span></li>
<li><span style="color: #231f20;">Weak natriuretic effect (1 to 2% of filtered Na+).</span></li>
<li><span style="color: #231f20;">Amiloride is very effective in the treatment of polyuria/polydipsia from lithium-induced nephrogenic diabetes insipidus where the tubular cells of the collecting ducts become insensitive to ADH from the accumulation of lithium.</span></li>
<li><span style="color: #231f20;">Triamterene is a potential nephrotoxin, possibly leading to crystalluria and cast formation which in severe cases has lead to renal failure particularly if given in conjunction with NSAIDs.</span></li>
</ul>
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<span style="color: #231f20; font-family: inherit;"><b><br /></b></span>
<span style="color: #231f20; font-family: inherit;"><br /></span>
<span style="color: #231f20; font-family: inherit;"> In a patient with hypokalemia not taking any loop or thiazide diuretics, other causes should be considered. The next most common cause would be increased GI losses, either from diarrhea, vomiting or NG suction. Magnesium levels should also be checked. The loop and thiazide diuretics also result in Mg2+ wasting, and hypomagnesemia promotes K+ wasting. The mechanism whereby Mg2+ effects K+ homeostasis is unclear. However, replacement with MgSO4 (as is common in the perioperitve period) could be problematic. The sulfate acts as a non resorbable anion in the collecting tubule (leading to a greater negative intraluminal charge). The negative charge in the lumen prevents the passive diffusion of K+ out of the lumen into luminal cells of the collecting tubules leading to increased K+ losses. Repletion with magnesium chloride or magnesium lactate would avoid this problem. </span><br />
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<span style="color: #231f20; font-family: inherit;">In the patient who is hypokalemic prior to anesthesia, it is important for the anesthesiologist to consider all of the ways in which acute shifts of K+ into the intracellular space may occur exacerbating the pre existing hypokalemia. Avoidance of respiratory or metabolic alkalemia. is very important since alkalemia results in a transfer of H+ ions from the intracellular space into the plasma to counter act a rising pH. To preserve electroneutrality, Na+ and K+ ions enter cells. In general the plasma concentration falls less than 0.4 meq/L for 0.1 unit increase in pH. Therefore, a patient with a serum potassium of 3.1 meq/L who develops a respiratory alkalosis to a pH of 7.5 due to inadvertent hyperventilation, will potentially see an acute intracellular shift of K+ ions leading to a serum K+ concentration of 2.7 meq/L. </span><br />
<span style="font-family: inherit;"><span style="color: #231f20; font-family: "arial";"><br /></span>
<span style="color: #231f20; font-family: "arial";">Insulin directly stimulates the entry of K+ ions into skeletal muscle and hepatic cells via a Na+-K+ ATPase pump. Thusly, it would be important to avoid using a dextrose solution to replace potassium, as the dextrose can stimulate insulin release causing a paradoxical further decrease in the serum potassium concentration.</span></span><br />
<span style="color: #231f20; font-family: "arial";"><br /></span>
<span style="color: #231f20; font-family: inherit;">The Na+-K+ -ATPase pump is also stimulated by beta 2 adnergic receptors. This is a particular concern in the preoperative period when stress related events causes a surge in catecholamines. In fact, a catecholamine surge can acutely lower the plasma K+ concentration by approximately 0.5 to 0.6 meq/L. This large change in serum K+ ion concentration may be partially due to the effects of insulin which is secreted in response to increased B2 adrenergic activity. Prompt recognition of this may be treated by adequate opioids +/- non selective beta blockers (i.e. propranolol). Administration of beta agonists such as albuterol for a breathing treatment, may induce a 0.5 to 1 meq/L drop in serum K+ concentration.</span><br />
<span style="font-family: inherit;"><span style="color: #231f20; font-family: "arial";"><br /></span></span>
<span style="font-family: inherit;"><span style="background-color: white;">Clinical studies looking at preoperative K+ levels and patient outcomes</span></span><br />
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<span style="font-family: inherit;"><span style="color: #231f20; font-family: "arial";">One study done on patients with coronary artery disease who underwent non-cardiac surgery suggested that a pre-operative serum potassium level of less than 3.5meq/ L was </span><span style="color: #231f20; font-family: "arial";">independently associated with peri-operative mortality. Other studies have failed to find any increased incidence of arrhythmia in patients at high risk (major vascular or cardiac surgery with cardiac disease) who also had significantly decreased K+ levels [2]. However, this study was probably under powered. They examined only 447 patients, and of these only 9% had significant hypokalemia (less than or equal to 3.0 mEq/L). In contrast to this, another study of 2402 patients undergoing CABG, were followed for a variety of outcomes. In this study, a serum potassium level less than 3.5 mEq/L was a predictor of serious perioperative arrhythmia (OR 2.2), intraoperative arrhythmia (OR 2.0) and post operative atrial fibrillation/flutter (OR 1.7) [8]. In another study looking at patients undergoing non cardiac surgery were analyzed for predictors of preoperative myocardial infarction (PMI) or cardiac death. They found that among several risk factors hypokalemia (serum level less than 3.5 mEq/L) was identified as a predictor of these outcomes [9]. Myocardial ischemia seems to be a significant risk factor leading to arrhythmias in the setting of hypokalemia [3,7]. Therefore, it becomes particularly important to monitor potassium levels in any patient at significant risk for preoperative ischemia.</span></span></div>
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<span style="font-family: inherit;"><span style="color: #231f20; font-family: "arial";"><br /></span><span style="color: #231f20; font-family: "arial";">Repletion of K+ prior to surgery is fraught with problems due to the logistics of K+ administration. KCl is painful in peripheral IVs and can cause severe phlebitis. In my patient, she could not tolerate KCl being infused in her peripheral IV at a concentration of 20 mEq per 100 mL any faster than 50 mL per hour (or 20 mEq per 2 hour time period). Therefore, it was decided to delay surgery until later that afternoon to allow adequate time for her to receive 40 mEq (requiring 4 hours) and to recheck her potassium level. After 5 hours, we returned to perform her surgery. Her repeat potassium was 3.3 mEq/L. She underwent GETA with Sevoflurane. Because she had a medtronic AICD, defibrillator pads were placed prior to surgery and a magnet was placed over the device to disable anti tachycardia therapy. The anesthetic was uneventful and she was observed overnight in the hospital.</span>
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<span style="color: #231f20; font-family: "arial";">1. </span><span style="color: #231f20; font-family: "arial";">Shah, K.B., Klienman, B.S., Rao, T.L., Jacobs,
H.K., Mestan, K. and Schaafsma, K. (1990)
Angina and other risk factors in patients with
cardiac diseases undergoing non-cardiac
operations. Anesth. Analg., 70, 240-247. </span><br />
<span style="color: #231f20; font-family: "arial";"><br /></span>
<span style="color: #231f20; font-family: "arial";">2.</span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Hirsch%20IA%5BAuthor%5D&cauthor=true&cauthor_uid=3341565" style="border-bottom-width: 0px; color: #660066; font-family: arial, helvetica, clean, sans-serif; font-size: 11.99899959564209px;">Hirsch IA</a><span style="font-family: "arial" , "helvetica" , "clean" , sans-serif; font-size: 0.8461em; line-height: 1.6363em; position: relative; top: -0.5em; vertical-align: baseline;">1</span><span style="background-color: white; font-family: "arial" , "helvetica" , "clean" , sans-serif; font-size: 11.99899959564209px;">, </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Tomlinson%20DL%5BAuthor%5D&cauthor=true&cauthor_uid=3341565" style="border-bottom-width: 0px; color: #660066; font-family: arial, helvetica, clean, sans-serif; font-size: 11.99899959564209px;">Tomlinson DL</a><span style="background-color: white; font-family: "arial" , "helvetica" , "clean" , sans-serif; font-size: 11.99899959564209px;">, </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Slogoff%20S%5BAuthor%5D&cauthor=true&cauthor_uid=3341565" style="border-bottom-width: 0px; color: #660066; font-family: arial, helvetica, clean, sans-serif; font-size: 11.99899959564209px;">Slogoff S</a><span style="background-color: white; font-family: "arial" , "helvetica" , "clean" , sans-serif; font-size: 11.99899959564209px;">, </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Keats%20AS%5BAuthor%5D&cauthor=true&cauthor_uid=3341565" style="border-bottom-width: 0px; color: #660066; font-family: arial, helvetica, clean, sans-serif; font-size: 11.99899959564209px;">Keats AS</a><span style="background-color: white; font-family: "arial" , "helvetica" , "clean" , sans-serif; font-size: 11.99899959564209px;">. </span><span role="menubar" style="font-family: "arial" , "helvetica" , "clean" , sans-serif; font-size: 11.004500389099121px;"><a abstractlink="yes" alsec="jour" alterm="Anesth Analg." aria-expanded="false" aria-haspopup="true" href="https://www.ncbi.nlm.nih.gov/pubmed/3341565#" role="menuitem" style="border-bottom-width: 0px; color: #660066;" title="Anesthesia and analgesia.">Anesth Analg.</a></span><span style="background-color: white; font-family: "arial" , "helvetica" , "clean" , sans-serif; font-size: 11.004500389099121px;"> 1988 Feb;67(2):131-6.</span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="background-color: white;">3. </span><span style="color: #231f20;">Hulting, J. (1981) In hospital ventricular
fibrillation and its relation to serum potassium.
Acta Med. Scand. Suppl., 647, 109-116.</span></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="color: #231f20;">4. Kuller LH, Hülle SB, Cohen JD, Neaton J. <i>Circulation </i>73:114, 1986</span></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="color: #231f20;">5. Siscovick DS, Raghunathan TE, Psaty BM, et al. <i>N Engl J Med </i>330:1852, 1994</span></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="color: #231f20;">6. Pitt B, Zannad F, Remme WJ, et al. <i>N Engl J Med</i> 341:709, 1999</span></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="color: #231f20;">7. </span></span><span style="color: #333333; font-family: "guardian textsans web" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 16px;">Nordrehaug JE, von der Lippe G. Hypokalaemia and ventricular fibrillation in acute myocardial infarction. </span><i style="box-sizing: inherit; color: #333333; font-family: 'Guardian TextSans Web', 'Helvetica Neue', Helvetica, Arial, sans-serif; font-size: 16px;"> Br Heart J.</i><span class="ref-text" style="box-sizing: inherit; color: #333333; font-family: "guardian textsans web" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 16px;">1983;50:525-529.</span><br />
<span class="ref-text" style="box-sizing: inherit; color: #333333; font-family: "guardian textsans web" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 16px;">8. Wahr JA, Parks R, Boisvert D et al. <i>JAMA</i> 1999; 28(23):2203-10.</span><br />
<span class="ref-text" style="box-sizing: inherit; color: #333333; font-family: "guardian textsans web" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 16px;">9. S</span><span style="color: #333333; font-family: "guardian textsans web" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 16px;">hah KB, Kleinman BS, Rao TL, Jacobs HK, Mestan K, Schaafsma K. </span><i style="box-sizing: inherit; color: #333333; font-family: 'Guardian TextSans Web', 'Helvetica Neue', Helvetica, Arial, sans-serif; font-size: 16px;"> Anesth Analg.</i><span class="ref-text" style="box-sizing: inherit; color: #333333; font-family: "guardian textsans web" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 16px;">1990;70:240-247.</span><br />
<span class="ref-text" style="box-sizing: inherit; color: #333333; font-family: "guardian textsans web" , "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 16px;">10. Tsuji H, Venditti FJ Jr, Evans JC, et al. <i>Am J Cardiol</i> 74:237, 1994</span><br />
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Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-85166919608146755392017-05-10T16:51:00.002-07:002023-06-29T13:41:30.141-07:0035 year old female with history of alcohol abuseThe other day a 35 year old female presented for surgery for lipoma excision from the posterior neck. She reported a history of severe alcohol abuse in the past for which she was taking naltrexone 100mg qd. The patient also reported a severe allergy to all steroids. When I asked for details, she reported that she had severe manic exacerbations with steroids and that this had happened with a one time dose given prior to surgery in the past. The patient had also experienced at least two seizures in the past, one occurring after surgery. She was told that this seizure could have been related to the anesthetic she had. She also reported another seizure episode in the past related to severe depletion of vitamin B12. She was taking several medications for anxiety, bipolar, alcoholism and PTSD. These included:<br />
<br />
<ul>
<li>Seroquel</li>
<li>Tegretol</li>
<li>Prozac</li>
<li>Prazosin</li>
<li>Klonipin</li>
</ul>
In addition, the patient was concerned because in the past, she had experienced very severe and unpleasant emergence anxiety and agitation.<br />
<br />
<br />
There were several issues that played a role in choosing an anesthetic for this patient. First she requested that she did not receive a steroid which I commonly give to female patients (especially non smokers) as they are at increased risk for PONV. In addition, She was medicated with naltrexone for alcoholism. Therefore, there was likely to be challenges with pain control in this patient. Lastly, the patient had had previous seizures following anesthesia during emergence as reported. She was on a number of medications that could potentially also activate her liver enzymes causing her to be a rapid metabolizer of anesthetics such as propofol, midazolam and fentanyl.<br />
<br />
This patient described a past experience of severe agitation and anxiety upon emergence. Emergence delirium (ED) is not uncommon in pediatrics. However, it has not been well studied in adults. One review of the literature estimated an incidence of 3% in adult patients. Another study found an incidence of 4.7% among adult patients [1]. However, in those at risk for PTSD an incidence of 20% is more likely [3]. Emergence delirium in adults can be a significant problem as they are capable of self injury. A recent case report details a severe episode of emergence delirium in a patient with PTSD [4], and subsequent case where changes were made to help mitigate this issue. In this patient with a self described episode of emergence delirium and history of PTSD and bipolar disorder, several considerations would be important. One consideration is the recommendation to avoid midazolam in particular in this patient group. Some literature suggests that Midazolam in particular can enhance the memory of events surrounding the trauma [5]. If a benzodiazepine is desired, lorazepam may be preferred. While it has been traditional teaching that ketamine can excerbate PTSD, and should be avoided during anesthesia in these patients, recent literature suggests that ketamine may not be a problem [6], or may be helpful in the prevention of PTSD [7]. Currently, prazosin, an alpha 1 blocker is used in the treatment for PTSD, but also is effective in the treatment in reducing alcohol intake in alcoholics. Therefore, it would be important to verify that this patient continued to take this medication on their usual schedule prior to anesthesia. Prazosin, as an alpha 1 blocker, can cause sudden drops in blood pressure, and this is particularly problematic when patients stand up suddenly. In pediatrics, there is quite a large amount of literature looking at interventions that can prevent or decrease the chances of emergence delirium (ED). Propofol decreased the incidence from 38% after sevoflurane to 0% in pediatrics. In the pediatric literature, other studies have corroborated the benefit of propofol in reducing ED. In adults, propofol also was able to decrease the incidence of ED, from 45% to 10% [10]. Another study in the pediatric literature showed that 2 mck/kg of IV Clonidine after induction significantly reduced the incidence of ED. Like Clonidine, Dexmedetomidine may also be a useful (although expensive) adjuvant to help prevent ED. Given that the patient had already experienced a significantly negative ED event in the past, had a post anesthetic seizure, and was also allergic to steroids, so that decadron was unavailable for PONV prophylaxis, I opted to utilize a propofol infusion for anesthesia maintenance. Unfortunately, in a patient taking naltrexone for alcoholism, maintaining anesthesia with routine anesthetic dosages could be fraught with problems. Therefore, I opted to utilize a BIS monitor as an aid in verifying the depth of anesthesia. The BIS system is a proprietary system using data from a processed EEG signal to produce a dimentionless number that correlates with the depth of anesthesia in a sense. It is presumed that a number between 40 and 60 represents general anesthesia and would thus have a low incidence of recall. It is not clear if an alcoholic or patient who is taking naltrexone will respond in the same fashion to a typical anesthetic. In this patient, 200 mg of propofol was given for induction along with 100 mcg of fentanyl and 2 mg of versed. The BIS went from 87 to 34. This change in BIS was as expected. Shortly thereafter, with an infusion of propofol running at 200 mcg/kg/min and the BIS reading 34, an injection of local anesthetic by the surgeon was performed at the site of the lipoma. The patient immediately started moving requiring an additional bolus of propofol and another 100 mcg of fentanyl. This would be an atypical response at a BIS of 34. However, given that propofol does not inhibit spinal reflexes like the potent inhalational agents, this could be considered within normal limits. Given the patient movement at a BIS of 34, the BIS was maintained in the high 30's for the remainder of the very short case. A propofol infusion of 200 mcg/kg/min was sufficient. after 30 min the case was over and the BIS reading was 36. The propofol infusion was discontinued and in 4 minutes, the BIS had jumped from 36 to 74 and the patient began responding to commands and was extubated. This rapid emergence could likely be explained by rapid hepatic metabolism of the propofol as well as residual naltrexone binding of mu opioid receptors decreasing the efficacy of fentanyl. The patient was transported to the PACU with no evidence of emergence delirium and seemingly in good spirits with good pain control. However, 30 minutes later the PACU nurse called me to report that she had given an additional 200 mcg of fentanyl in PACU for pain control and the patient was reporting 10/10 pain. This was unusual in that the small lipoma excision had been anesthetized with local anesthetic. Hydromorphone was ordered and no more calls were forthcoming.<br />
<br />
Currently there is an epidemic occurring in America with opioid abuse. It is becoming ever more likely that we will be required to care for one of these patients. Many of these patients will require therapy such as suboxone to prevent cravings of opioid. Suboxone is a combination of buprenorphine and naloxone where the ratio is 4 parts buprenorphine to 1 part naloxone. The naloxone is included to prevent the crushing and snorting or intravenous injection and is not considered to be active when suboxone is taken as intended. Buprenorphine is a partial agonist at the mu receptor. It is also a kappa antagonist. These receptors are predominantly located in the spinal cord. As a partial agonist, buprenorphine has a ceiling affect which occurs at about 32 mg / day. Most patients who are on buprenorphine (suboxone) for maintenance therapy, are on doses that are higher than for treatment of chronic pain (i.e 16 mg for maintenance vs 2 to 4 mg for chronic pain therapy). There are two issues that anesthesiologists need to understand when patients arrive for surgery on suboxone. First is the underlying pharmacokinetics. Suboxone, if provided as a patch takes a full seven days to clear. Buprenorphine is also prescribed to be taken sublingual where the bioavailability is 30 to 50%. The half life of high dose buprenorphine (as used for maintenance therapy in opioid dependent patients) is 20 to 70 hours. However, the half-life is highly variable and depends on patient characteristics as well as the dosing regimen. It is clear from case reports that maintaining suboxone in the preoperative period will lead to very poor pain control amid escalating pure mu opioid agonist requirements. For elective surgery, where significant post op pain is anticipated, it used to be recommended that patients discontinue suboxone therapy for five days. However, currently experts are recommending the continuation of suboxone during the perioperative period citing the serious risks of relapse when the medication is discontinued. Furthermore, Buprenorphine provides significantly analgesia in its own right despite the ceiling effect. Further clarification has come from recent studies that looked at the Mu receptors available in the CNS when patients are on different doses of suboxone (buprenorphine) (see figure):<div><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiL_CMTr9P8bGg6ja_vciHOQ_dvfODHbr5gARZ2T7qww41ynicWB6wavMfA-P-x7EBsllTkER27DTVHTqGJWifBrbL7UC4k5SFUgkV8PFnYa5qWGCWG47sfV4IALNMC3fbEUmiAETYQ-zGYp1iiNhXVm40l103ronX6Fm1gJpmzQJUcRKqNYJIb6906mgSu/s1134/Screen%20Shot%202023-06-28%20at%209.33.47%20AM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="588" data-original-width="1134" height="332" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiL_CMTr9P8bGg6ja_vciHOQ_dvfODHbr5gARZ2T7qww41ynicWB6wavMfA-P-x7EBsllTkER27DTVHTqGJWifBrbL7UC4k5SFUgkV8PFnYa5qWGCWG47sfV4IALNMC3fbEUmiAETYQ-zGYp1iiNhXVm40l103ronX6Fm1gJpmzQJUcRKqNYJIb6906mgSu/w640-h332/Screen%20Shot%202023-06-28%20at%209.33.47%20AM.png" width="640" /></a></div><br /><div>In the above figure, patients receiving 2 mg of buprenorphine per day still maintain 59% of mu opioid receptors available for binding to other mu agonists. At 32 mg per day, the number of receptors is decreased down to 16%. However, it is stated by experts that even when only 16% of receptors are available for binding, this allows for successful analgesia via other mu opioid receptors.</div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiGo35zszx-XA4HNhW6BJnWxl-RMrdODLhO2sxDIwbZxS8s8OoR_tNdijlypm3F8oENNgv5thhwtiLv9N1lB6WFgwG1CanOjB3QHz8EOq38JcyMHjw7fJ1IErCC0VIwMF2ZCAms7yk50fV4Q6PdC1shlwjVHRkCu9T9GBE3DZPSoKbmFLvjSn8JZOviglY3/s716/Screen%20Shot%202023-06-28%20at%209.34.50%20AM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="598" data-original-width="716" height="534" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiGo35zszx-XA4HNhW6BJnWxl-RMrdODLhO2sxDIwbZxS8s8OoR_tNdijlypm3F8oENNgv5thhwtiLv9N1lB6WFgwG1CanOjB3QHz8EOq38JcyMHjw7fJ1IErCC0VIwMF2ZCAms7yk50fV4Q6PdC1shlwjVHRkCu9T9GBE3DZPSoKbmFLvjSn8JZOviglY3/w640-h534/Screen%20Shot%202023-06-28%20at%209.34.50%20AM.png" width="640" /></a></div><br /><div> The above graph indicates similar data, and demonstrates that a typical dose (8mg per day) of buprenorphine for maintenance, just over 30% of receptors may be available in certain parts of the brain.</div><div><br /></div><div>As mentioned, buprenorphine binds to the mu opioid receptor more tightly than conventional opioids. Therefore, in some cases, the clinician might expect that using typical opioids at typical clinical doses would be unable to "knock" the buprenorphine off of the mu receptors to provide analgesia. However, certain opioids bind just as tightly and can in theory effectively "knock" the buprenorphine off of the receptor. The following graphic highlights the different binding abilities of different opioids. Note, Sufentanil is the only opioid that has a larger affinity than buprenorphine on the list.</div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjzYybEjh8ysIEo2--O2jze3OojokIDyiGjp8ihmVYH3vjcQon049CGMMsle7YWO7yznDkhdAwTwhoP0n0tWyrUAmtZ1wlIAEtA-XFle5o5AyVloQYU-1BgejJ3XYjHqLbdOQ6P_zTeswmu1E23uEAn_j2PwMYVmHiCrLqC9n7C_fgr92h17Xd6_I__zAOe/s900/Screen%20Shot%202023-06-27%20at%207.22.44%20PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="580" data-original-width="900" height="412" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjzYybEjh8ysIEo2--O2jze3OojokIDyiGjp8ihmVYH3vjcQon049CGMMsle7YWO7yznDkhdAwTwhoP0n0tWyrUAmtZ1wlIAEtA-XFle5o5AyVloQYU-1BgejJ3XYjHqLbdOQ6P_zTeswmu1E23uEAn_j2PwMYVmHiCrLqC9n7C_fgr92h17Xd6_I__zAOe/w640-h412/Screen%20Shot%202023-06-27%20at%207.22.44%20PM.png" width="640" /></a></div><div><br /></div>In summary, patients taking buprenorphine (i.e. suboxone) should continue the medication thoughout the perioperative period. The clinician should expect reasonably good analgesia for post op pain when the daily dose taken by the patient is around 16 mg or higher. Hydromorphone and sufentanil are excellent choices for perioperative opioids due to their relatively high affinity for the mu opioid receptor as compared to buprenorphine. (on the chart, the Ki represents the binding affinity of the different opioids listed with a lower number meaning a higher affinity).<div><br /></div><div>It is important for the perioperative physician to be aware that patients treated with buprenorphine for chronic pain require very low doses for analgesia. For example, the mucoadhesive formulation (belbuca) is dosed at 75 mcg, whereas suboxone as a sublingual film has a max dose of 12 mg. As mentioned, the larger dosages are used for maintenance therapy for individuals with OUD.<br /><div><br /><div><br /></div><div><br />Some patients with opioid use disorder will be taking naltrexone. As a mu antagonist, it was anticipated that override could be difficult. While, indeed, higher doses of fentanyl than typical were required, the requirements were not extraordinary. Once again, an understanding of pharmacokinetics is important to determine how difficult it might be to override any naltrexone present at the mu receptor. A single oral dose of 25 mg of naltrexone has an apparent half-life (t1/2) of 14 hours. Veberey et al. [2], looked at naltrexone effectiveness in blockade of heroin 25 mg. After a 100 mg oral dose of naltrexone, there was 96% blockade at 24 hours, 86.5% blockade at 48 hours, and 46.6% at 72 hours. Therefore, it would seem prudent to recommend that patients avoid naltrexone for 72 hours prior to any surgery where it is anticipated post op pain control will require opioid therapy. In patients who have chronically taken naltrexone for maintenance therapy, there is up regulation of mu receptors in the brain [8]. Therefore, patients who discontinue naltrexone, may be resistant or more susceptible to opioids depending on how much naltrexone remains in the system compared to the degree of mu opioid receptor upregulation. While naltrexone is a mu opioid antangonist, it is approved by the FDA for treatment of alcoholism because it reduces the euphoria and positive reinforcing effects of ethanol use [9].<br />
Lastly, this patient had a history of vitamin B12 deficiency. Vitamin B12 is an integral part of two biochemical reactions: the conversion of L-methylmalonyl coenzyme A into succinylcholine coenzyme A and the formation of methionine by methylation of homocysteine. These reactions are critical for the synthesis of DNA and to the maintenance of the myelin sheath by methylation of myelin basic protein. Active Vitamin B12 contains cobalt in its reduced form (Co+). Nitrous oxide produces irreversible oxidation to the Co++ form leading to inactive Vitamin B12. The result is an irreversible inactivation of the enzyme methionine synthase There are several case reports in the literature of patients developing subacute combined degeneration of the spinal cord following nitrous oxide anesthesia [11,12,13]. In these case reports, the diagnosis of subacute combined degeneration of the spinal cord was made several weeks post op after otherwise routine and uneventful anesthesia. Subacute combined degeneration of the spinal cord is characterized by degeneration of the posterior and lateral columns. The avoidance of nitrous oxide in patients with anemia of unknown cause or in patients at risk of vitamin B12 depletion is recommended. A significant risk factor for Vitamin B12 depletion is alcoholism for two reasons. 1) alcohol abuse leads to poor nutrition and therefore, vitamin B12 intake is reduced, and 2) excessive alcohol use leads to atrophic gastritis. Atrophic gastritis is characterized by inflammation and dysfunction on the cells lining the stomach so that production and secretion of intrinsic factor is compromised. Intrinsic Factor (IF) is essential for the absorption of vitamin B12. Atrophic gastritis also decreases the production of hydrochloric acid. The increase in pH leads to overgrowth of different bacterial strains that consume vitamin B12 and reduction in efficiency of food breakdown that is necessary for the release of vitamin B12 from the diet for absorption into the body.<br />
<br />
Lastly, her seizure episode following anesthesia should be addressed more fully in context of her history of alcoholism. While there are case reports of severe vitamin B12 deficiency leading to seizures, this isn't typical. What is more common in alcoholics undergoing surgery is alcohol withdrawal syndrome (AWS). AWS can result in an incidence of mortality of around 15% if untreated [14]. In patients who abuse alcohol, AWS more commonly manifests during stress such as surgery [15]. It has been suggested that in operative patients, hypotension, hypoxia, or uncontrolled pain in the PACU may precipitate AWS [16]. The key features of AWS include hyperexcitability of the CNS due to reduced GABA activity and increased glutaminergic action [17]. Increased noradrenergic activity can lead to hypertension, tachycardia, sweating, tremor, and hallucinations. Lastly, seizures can occur. Seizures typically occur early in the process, i.e. 6 to 8 hours after stopping alcohol intake. This is long before the most severe manifestations of AWS, which may take 3 to 4 days. Attributing this patient's prior post anesthetic seizure to AWS may be reasonable, but can't be proven.<br />
<br />
In conclusion, this patient had multiple medical issues that were impactful on making an anesthetic plan. These included a history of seizures related to anesthesia and vitamin b12 depletion, alcoholism treated with naltrexone and prazosin, as well as high anxiety with a history of severe emergence delirium requiring treatment. In this patient, using TIVA, local anesthesia for the surgery site, along with a BIS monitor allowed for an uneventful anesthetic and emergence.<br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: x-small;"><span style="color: #2a2a2a; font-family: "times" , "times new roman" , serif;"><span style="background-color: white;">1. Lepouse c et al. Emergence delirium in adults in the post-anesthesia care unit, <i>BJA</i>, 2006, vol. 96(6), 747-53.</span></span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: x-small;"><span style="color: #2a2a2a; font-family: "times" , "times new roman" , serif;"><span style="background-color: white;">2. </span></span></span><span face=""arial" , "helvetica" , "clean" , sans-serif" style="background-color: white; color: #303030; font-size: 13px; font-style: inherit;">Verebey K. The clinical pharmacology of naltrexone: pharmacology and pharmacodynamics. </span><span class="ref-journal" face=""arial" , "helvetica" , "clean" , sans-serif" style="color: #303030; font-size: 13px; font-style: inherit;">NIDA Res Monogr</span><span face=""arial" , "helvetica" , "clean" , sans-serif" style="background-color: white; color: #303030; font-size: 13px; font-style: inherit;"> 1981;</span><span class="ref-vol" face=""arial" , "helvetica" , "clean" , sans-serif" style="color: #303030; font-size: 13px; font-style: inherit;">28</span><span face=""arial" , "helvetica" , "clean" , sans-serif" style="background-color: white; color: #303030; font-size: 13px; font-style: inherit;">: 147-58.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: x-small;"><span style="color: #2a2a2a; font-family: "times" , "times new roman" , serif;"><span style="background-color: white;">3. Curtis D, Stevens WC. Recovery from general anesthesia. <i>Int. Anesthsiol. Clin, 1991;29(2):1-11.</i></span></span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: x-small;"><span style="color: #2a2a2a; font-family: "times" , "times new roman" , serif;"><span style="background-color: white;"><i>4. </i>Lovestrand D, Phipps S, and Lovestrand S. Posttraumatic stress disorder and Anesthesia Emergence. <i>AANA Journal, 2013(81).3. 199-203.</i></span></span></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: x-small;"><span style="color: #2a2a2a;">5. </span>McGhee LL, Maani CV, Garza TH, DeSocio PA, Gaylord KM, Black IH.
The relationship of intravenous midazolam and posttraumatic stress
disorder development in burned soldiers. <span style="font-style: italic;">J Trauma Inj Infect Crit Care.
</span>2009;66(4 suppl):S186-S190 </span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: x-small;">6. </span><span style="font-family: "berkeley"; font-size: 8pt;">Wilson JT, Pokorny ME. Experiences of military CRNAs with ser-
vice personnel who are emerging from general anesthesia. </span><span style="font-family: "berkeley"; font-size: 8pt; font-style: italic;">AANA J.
</span><span style="font-family: "berkeley"; font-size: 8pt;">2012;80(4):260-265.</span><br />
<span style="font-family: "berkeley"; font-size: 8pt;">7. </span><span style="font-family: "berkeley"; font-size: 8pt;">McGhee LL, Maani CV, Garza TH, DeSocio PA, Gaylord KM, Black IH.
The correlation between ketamine and posttraumatic stress disorder
in burned service members. </span><span style="font-family: "berkeley"; font-size: 8pt; font-style: italic;">J Trauma Inj Infect Crit Care. </span><span style="font-family: "berkeley"; font-size: 8pt;">2008;64(2
suppl):S195-S199.</span><br />
<span style="font-family: "berkeley"; font-size: xx-small;">8. </span><span face=""arial" , "helvetica" , "clean" , sans-serif" style="background-color: white; color: #303030; font-size: 13px;">Yoburn BC, Luke MC, Pasternak GW, Inturrisi CE. Upregulation of opioid receptor subtypes correlates with potency changes of morphine and DADLE. </span><span class="ref-journal" face=""arial" , "helvetica" , "clean" , sans-serif" style="color: #303030; font-size: 13px;">Life Sciences</span><span face=""arial" , "helvetica" , "clean" , sans-serif" style="background-color: white; color: #303030; font-size: 13px;"> 1988;</span><span class="ref-vol" face=""arial" , "helvetica" , "clean" , sans-serif" style="color: #303030; font-size: 13px;">43</span><span face=""arial" , "helvetica" , "clean" , sans-serif" style="background-color: white; color: #303030; font-size: 13px;">: 1319-24.</span><br />
<span face=""arial" , "helvetica" , "clean" , sans-serif" style="background-color: white; color: #303030; font-size: 13px;">9. </span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">Volpicelli JR, Alterman AL, Hayashida M, O'Brien CP. Naltrexone in the treatment of alcohol dependence. </span><span class="ref-journal" style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">Arch Gen Psych</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;"> 1992;</span><span class="ref-vol" style="font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">49</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px;">: 876-80</span><br />
<span style="font-family: "times new roman" , "stixgeneral" , serif;"><span style="background-color: white; font-size: 15.9991px;">10. </span></span>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408515/<br />
11. https://www.ncbi.nlm.nih.gov/pubmed/19169627<br />
12. https://www.ncbi.nlm.nih.gov/pubmed/11455686<br />
13. http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1949600<br />
14. http://journals.lww.com/anesthesia-analgesia/Citation/1999/04000/Alcohol_Withdrawal_in_the_Surgical_Patient_.50.aspx<br />
15. <span style="background-color: white; font-family: "minion w08 regular_1167271" , "times"; font-size: 17px; text-align: justify;">C. Spies, H. Tønnesen, S. Andreasson, A. Helander, and K. Conigrave, “Perioperative morbidity and mortality in chronic alcoholic patients,” </span><span style="background-color: white; font-family: "minion w08 italic"; font-size: 17px; text-align: justify;">Alcoholism</span><span style="background-color: white; font-family: "minion w08 regular_1167271" , "times"; font-size: 17px; text-align: justify;">, vol. 25, no. 5, pp. 164S–170S, 2001.</span><span class="reflinks" style="background-color: white; border: 0px; font-family: "minion w08 regular_1167271" , "times"; font-size: 17px; margin: 0px; outline: 0px; padding: 0px; text-align: justify;"> </span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: x-small;">16. https://www.hindawi.com/journals/cria/2013/761527/</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: x-small;">17. http://search.proquest.com/openview/252f427f24a32c20bff649b85e2cd535/1?pq-origsite=gscholar&cbl=2031130</span></div>
</div></div></div>Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-71086313052356017332016-08-09T08:31:00.002-07:002016-08-09T08:31:16.091-07:00elevated preoperative BNP, what do I do now?A rather unhealthy and unkept gentleman of about 54 years of age presented to the ER after a 'fall'. He presented to the preop area as an add for intertrochanteric nail by our friendly orthopedic surgeon.<br />
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I was assigned the case and went over to look through the chart. <br />
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I noted a cardiology note that indicated that his troponin levels were very slightly elevated and an echocardiogram was recommended by the cardiology NP. Since this gentleman, had an injury that was better treated sooner than later (more discussion on this below), and he did not have an EKG with any indication of ischemia, I was not convinced that delaying his surgery for an additional day to perform an echo was absolutely required. I continued to look for more information to determine the liklihood that an his slight bump in troponins represented something truly sinister, or was perhaps more benign in nature. It was known that he was likely homeless, dehydrated, and had a mild elevation in his BUN and creatinine consistent with pre renal azotemia in a dehydrated (hypovolemia) patient.<br />
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A further review of his chart revealed that he also had a BNP of over 1200 pg and lasix had been ordered by the ER physician, but not yet administered due to various logistical issues. At this point, I decided to call the Ortho surgeon and have a conversation with him. After discussing it with him, a decision was made to cancel the surgery until his volume level could be better determined, and optimized.<br />
Patients in heart failure are poor candidates for surgery. Post operative morbidity and mortality is significantly higher; and any elective surgery is contraindicated when if patients are in failure. is predictor of poor outcome in non cardiac surgery. Typically, it is best to post pone non emergent surgery in patients suspected or known to be in hear failure. Unfortunately, clinical signs of heart failure (dyspnea, jugular vein distention, leg swelling etc) are not perfect indicators of a patient's status. Current evidence suggests that hip fracture patients have better outcomes when the fracture is repaired within 24 hours of admission. Therefore, an anesthesiologist who makes a decision to delay hip fracture surgery may potentially increase overall risk to the patient in an attempt to improve the patients perceived short term risks. <br />
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Atrial Natriuretic Peptide (ANP) was originally isolated from rat atrial myocardium. In humans, it is secreted predominantly by atrial myocytes. BNP was subsequently isolated from porcine brains. In humans it is secreted by both atrial and ventricular myocytes, but it is predominantly the ventricular myocytes that secrete BNP. These natriuretic peptides have several functions in normal physiology. When cardiac myocytes are stretched due to increased load or volume, secretion of these peptides results in: 1) down regulation of the sympathetic nervous system, and the renin-angiotensin-aldosterone system, 2) improved natriuresis and diuresis via afferent and efferent hemodynamic mechanisms of the distal tubule of the kidney, 3) decreasing peripheral vascular resistance via relaxation of smooth muscle. A BNP precursor is secreted by left ventricular myocytes which is synthesized into proBNP. This short lived molecule is cleaved into the biologically active C terminal portion and biologically inactive N-terminal (NT-proBNP) portion.<br />
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In a observational study, BNP was found to be an independent predictor of increased cardiac events after non cardiac surgery and performed better than a preoperative scoring system after abdominal surgery [1].<br />
It is known that BNP levels correlate with demodynamic parameters such as right atrial pressure, PCWP, and left ventricular end diastolic pressures. Echo studies looking at the correlation of BNP levels with ventricular function have also been done. Usuing the NYHA classificaiton system we find that in class I, BNP averages 240 pg, II 390 pg, III; 640 pg and IV 820 pg. This indicates that higher levels do seem to correlate with more significant cardiac dysfunction.<br />
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In 2002, the national breathing not properly (BNP) trial was completed and was able to show that plasma BNP measurement was able to differentiate between CHF and non CHF causes of dyspnea (area under receiver operating characteristic curve = 0.91) [2]. In this trial, a single BNP measurement was also more accurate than two commonly used methods of determining cardiac causes of SOB, the National Health and Nutritional Examination score and Franghiham (see below).<br />
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Using data from this same study, a patient presenting with SOB, and a BNP less than 50 pg/mL has an 7% chance that the cause is heart failure. If the BNP is between 50 pg/mL and 150 pg/mL, the chance that heart failure is the causes rises to 36%. With a BNP of greater than 150 pg/mL, there is an 83% chance of heart failure. Later, another study concluded that if the BNP level was less than 100 pg/mL, there was a low liklihood for congestive heart failure. Alternatively, in this study, they concluded that blood levels greater than 500 pg/mL made a diagnosis of heart failure extremely likely [3].</div>
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In another smaller study, dao et al. showed that a BNP of less than 80 pg/mL had a 98% negative predictive value. In this same trial, patients with dyspnea and diagnosed with CHF had a mean BNP of 1076 pg/mL while patients who had dyspnea but were found not to be in heart failure had a mean BNP of only 38 pg/mL. </div>
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A study of patients undergoing non cardiac surgery found that an elevated BNP measurement was an independent predictor of postoperative cardiac events. In this study, BNP measurements outperformed the goldman multifactorial clinical index in predicting cardiac adverse events after non cardiac surgery. (fee figures below for a great summary of this study).</div>
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They showed that a BNP level of 0 to 100 pg/mL had zero risk, BNP levels of 201-300 pg/mL was considered low risk (5% event rate), intermediate risk (12% event rate) was from 200 to 300 pg/mL, and high risk (greater than 300 pg/mL) had an event rate of 81% [4]. This was followed up with another study that was able to demonstrate that BNP levels greater than 40 pg/mL was associated with a seven fold increase in cardiac events in the early post operative period and longer hospital stay [5]. Yeh et al. found that pre operative NT pro-BNP independently predicted cardiac complications in non cardiac surgery (greater than 450 ng/L) with 100% sensitivity and 83% specificy [6].</div>
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The clinician should recognize that there are several causes other than heart failure that can result in elevated BNP levels. These include renal failure (decreased clearance), pulmonary embolism, pulmonary hypertension, and chronic hypoxia. Furthermore, BNP increases along with age. A trial was able to determine five independent predictors of elevated BNP in patients without heart failure. They were 1) low hemoglobin values, 2) low BMI, 3) history of A fib 4) radiographic cardiomegaly, and 5) advanced age. This is why this test has been found to have very good sensitivity, but not great specificity. Put another way, if the BNP is normal, the clinician has very high confidence that the patient is not currently in CHF or that cardiac complications will be low. However, the opposite is not true; if the BNP is elevated, the clinician cannot be as confident that the case should be cancelled or delayed because of certain CHF in the patient. However, ruling out the above other causes of elevated BNP can aid the clinician in ruling out other sources of an elevated BNP.</div>
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BNP also tracks appropriate therapy. Therefore, patients being treated with ACE inhibitors and diuretics will have lower than typical BNP levels, while other medications may increase BNP (beta blockers and digoxin).</div>
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Unfortunately, at this point, rigorous testing in the preoperative setting to determine cut off points for BNP levels in order to determine whether cases should be cancelled or not have not been done. In "up to date" the following quote relays the current recommendations regarding the use of BNP in the preoperative period to aid in evaluation of the patient: "<span style="font-family: "arial" , "helvetica neue" , "helvetica" , sans-serif; font-size: 13.44px; line-height: 18.816px;">However, it is unknown whether or which changes in perioperative management would improve outcomes in surgical patients with elevated BNP or NT-proBNP levels".</span></div>
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<span style="font-family: inherit;"><span style="line-height: 18.816px;">Determining when to delay or cancel hip fracture surgery is often a challenge for the anesthesiologist. Particularly since this population of patients generally have significant co morbidities that would result in cancelation or delay in purely elective surgery. Orthopedists are becoming more aggressive in trying to bring their patients to surgery within 24 hours of injury because of numerous observational trials indicating that early hip fracture surgical repair leads to better functional outcome and lower rates of complications and mortality. In fact, current guidelines recommend surgery within 24 hours of injury [6]. </span><span style="background-color: white; color: #333333; line-height: 25px;"> </span><span style="background-color: white; color: #333333; line-height: 25px;">Early surgery has also been included as a quality marker in the highly disseminated set of Inpatient Quality Indicators from the Agency for Healthcare Research and Quality [7].</span><span style="line-height: 18.816px;"> So, would my patient be better off, overall, if I had administered lasix in the holding area, and proceeded to surgery within the next 30 minutes to hour?</span></span></div>
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<span style="line-height: 18.816px;">Observational trials are prone to selection bias, attrition and detection bias. Prospective observational trials are more robust generally than retrospective trials, but a recent systematic review found that currently, 65% of studies addressing this issue are retrospective, and therefore, subject to confounding and biased ascertainment of outcomes. One of the most obvious problems with retrospective observational trials is that patient who are sicker are more likely to be delayed and therefore, have a larger time delay between the injury and the surgery. Therefore, it is likely that patients will have better outcomes in the 'early' surgery group vs. the later surgery group because the early surgery group is a healthier cohort. As an example, a recent large [8] retrospective observational trial in Spain looked at over 81,000 patients who had hip fracture surgery. They found a positive correlation with early surgery and lower in hospital mortality. However, after correcting for a multitude of variables, they found that indeed, patients at much higher risk had delayed surgery, and after correcting for this, there was no longer any effect on mortality from delaying surgery. In another study, the authors were able to demonstrate that individualizing the timing of surgery to medically optimize patients at higher risk led to improved outcomes [9]. Vidan et al. and Khan et al also showed that when controlling for medical co-morbidities, timing of surgery ceased to be a factor in mortality difference between groups [10,11]. Still, while it seems difficult to say that mortality is improved with early surgery after injury (within 24 hours), other important metrics may be apt for improvement. Investigators have found that time to discharge was 10.9 days earlier if surgery is performed within 48 hours [12], and another study concluded that surgery within 24 hours decreased LOS by 4 days [13]. Other clinically relevant benefits found with early surgery include a decrease in the incidence of decubitus ulcer formation and an increased likelihood of return to independent living.</span></div>
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<span style="line-height: 18.816px;">In summary, at this point, due to lack of prospective RCTs, it is not clear that early surgery (within 24 to 48 hours of injury) can reduce mortality. However, other parameters, such as LOS, pressure ulcer formation and long term functional recovery may be improved by early surgery. While guidelines recommend that patients go to the OR for operative repair within 24 to 48 hours of injury, the anesthesiologist should feel confident that a delay in surgery to allow for medical optimization of severe evolving medical conditions is warranted. Each case should be judged by its own merits and the anesthesiologists should play a role in not obstructing early surgery unless truly necessary. As an example, I recently reported on a case where a patient with a hip fracture was admitted for operative repair, but the gastroenterologist recommended a transfer because the patient had severe liver dysfunction. The orthopedist called me and I recommended proceeding with surgery given the enormous delay caused by a transfer and lack of evidence that further optimization could improve the patients outcome. This case proceeded as scheduled, although, the gastroenterologist, inked in the chart that he recommended a spinal which created a medico legal issue for the anesthesiologist.</span></div>
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<span style="font-family: inherit;">1. Mercantini P, et al. Preoperative brain natriuretic peptide (BNP) is a better predictor of adverse cardiac events compared to preoperative scoring system in patients who underwent abdominal surgery. <i>World J Surg</i> 2012 Jan;36(1):24-30.</span><br />
<span style="font-family: inherit;"><span style="background-color: white; font-size: 14px; line-height: 21px;">2. Maisel AM, Krishnaswamy P, Nowak R, et al. Bedside B-type natriuretic peptide in the emergency diagnosis of heart failure: primary results from the Breathing Not Properly (BNP) Multinational study. Paper presented at: 51st Annual Scientific Session of the American College of Cardiology;March 17–20,</span><span class="cit-pub-date" style="background-color: white; box-sizing: border-box; font-size: 14px; line-height: 21px;">2002;</span><span style="background-color: white; font-size: 14px; line-height: 21px;"> Atlanta, Ga.</span></span><br />
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<li style="border: 0px; color: #222222; display: inline; font-size: 1.1em; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px 0px 1em; outline-style: none; padding: 0.3em 0px; vertical-align: baseline;"><span style="font-family: inherit;"><span class="cit-auth" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"><span class="cit-name-surname" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">3. Mueller</span> <span class="cit-name-given-names" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">C</span></span>, </span></li>
<span style="font-family: inherit;">
<li style="border: 0px; color: #222222; display: inline; font-size: 1.1em; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px 0px 1em; outline-style: none; padding: 0.3em 0px; vertical-align: baseline;"><span class="cit-auth" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"><span class="cit-name-surname" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">Scholer</span> <span class="cit-name-given-names" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">A</span></span>, </li>
<li style="border: 0px; color: #222222; display: inline; font-size: 1.1em; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px 0px 1em; outline-style: none; padding: 0.3em 0px; vertical-align: baseline;"><span class="cit-auth" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"><span class="cit-name-surname" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">Laule-Kilian</span> <span class="cit-name-given-names" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">K</span></span>, </li>
<li style="border: 0px; color: #222222; display: inline; font-size: 1.1em; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px 0px 1em; outline-style: none; padding: 0.3em 0px; vertical-align: baseline;"><span class="cit-etal" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">et al</span></li>
<cite style="background-color: white; border: 0px; display: inline; font-size: 12.32px; font-style: normal; line-height: 16.016px; margin: 0.25em 0px 0px; outline-style: none; padding: 0px; vertical-align: baseline;">. <span class="cit-article-title" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea</span>. <abbr class="cit-jnl-abbrev" style="border: none; display: inline; font-size: inherit; font-weight: inherit; line-height: inherit; margin: 0px 0.1em 0px 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">N Engl J Med</abbr> <span class="cit-pub-date" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">2004</span>;<span class="cit-vol" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">350</span>:<span class="cit-fpage" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">647</span>-<span class="cit-lpage" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">54</span>.</cite></span><br />
<ol class="cit-auth-list" style="background-color: white; border: 0px; color: #222222; display: inline; font-size: 11.088px; line-height: inherit; list-style: none; margin: 0px; outline-style: none; padding: 0px; vertical-align: baseline;"><span style="font-family: inherit;">
<li style="border: 0px; display: inline; font-size: 1.1em; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px 0px 1em; outline-style: none; padding: 0.3em 0px; vertical-align: baseline;"><span class="cit-auth" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"><span class="cit-name-surname" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">4. Dernellis</span> <span class="cit-name-given-names" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">J</span></span>, </li>
<li style="border: 0px; display: inline; font-size: 1.1em; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px 0px 1em; outline-style: none; padding: 0.3em 0px; vertical-align: baseline;"><span class="cit-auth" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"><span class="cit-name-surname" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">Panaretou</span> <span class="cit-name-given-names" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">M </span></span></li>
</span></ol>
<span style="font-family: inherit;"><span class="cit-article-title" style="background-color: white; border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">Assessment of cardiac risk before non-cardiac surgery: brain natriuretic peptide in 1590 patients</span><span style="background-color: white; font-size: 12.32px; line-height: 16.016px;">.</span><span style="background-color: white; font-size: 12.32px; line-height: 16.016px;"> </span><abbr class="cit-jnl-abbrev" style="background-color: white; border: none; display: inline; font-size: inherit; font-weight: inherit; line-height: inherit; margin: 0px 0.1em 0px 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">Heart</abbr><span style="background-color: white; font-size: 12.32px; line-height: 16.016px;"> </span><span class="cit-pub-date" style="background-color: white; border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">2006</span><span style="background-color: white; font-size: 12.32px; line-height: 16.016px;">;</span><span class="cit-vol" style="background-color: white; border: 0px; display: inline; font-size: inherit; font-style: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">92</span><span style="background-color: white; font-size: 12.32px; line-height: 16.016px;">:</span><span class="cit-fpage" style="background-color: white; border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">1645</span><span style="background-color: white; font-size: 12.32px; line-height: 16.016px;">-</span><span class="cit-lpage" style="background-color: white; border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">50</span></span><br />
<div>
<ol class="cit-auth-list" style="background-color: white; border: 0px; color: #222222; display: inline; font-size: 11.088px; line-height: inherit; list-style: none; margin: 0px; outline-style: none; padding: 0px; vertical-align: baseline;"><span style="font-family: inherit;">
<li style="border: 0px; display: inline; font-size: 1.1em; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px 0px 1em; outline-style: none; padding: 0.3em 0px; vertical-align: baseline;"><span class="cit-auth" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"><span class="cit-name-surname" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">5. Cuthbertson</span> <span class="cit-name-given-names" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">BH</span></span>, </li>
<li style="border: 0px; display: inline; font-size: 1.1em; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px 0px 1em; outline-style: none; padding: 0.3em 0px; vertical-align: baseline;"><span class="cit-auth" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"><span class="cit-name-surname" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">Amiri</span> <span class="cit-name-given-names" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">AR</span></span>, </li>
<li style="border: 0px; display: inline; font-size: 1.1em; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px 0px 1em; outline-style: none; padding: 0.3em 0px; vertical-align: baseline;"><span class="cit-auth" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"><span class="cit-name-surname" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">Croal</span> <span class="cit-name-given-names" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">BL</span></span>, </li>
<li style="border: 0px; display: inline; font-size: 1.1em; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px 0px 1em; outline-style: none; padding: 0.3em 0px; vertical-align: baseline;"><span class="cit-etal" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">et al</span></li>
</span></ol>
<span style="font-family: inherit;"><cite style="background-color: white; border: 0px; display: inline; font-size: 12.32px; font-style: normal; line-height: 16.016px; margin: 0.25em 0px 0px; outline-style: none; padding: 0px; vertical-align: baseline;">. <span class="cit-article-title" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">The utility of B-type natriuretic peptide in predicting perioperative cardiac events in patients undergoing major non-cardiac surgery</span>. <abbr class="cit-jnl-abbrev" style="border: none; display: inline; font-size: inherit; font-weight: inherit; line-height: inherit; margin: 0px 0.1em 0px 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">Br J Anaesth</abbr> <span class="cit-pub-date" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">2007</span>;<span class="cit-vol" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">99</span>:<span class="cit-fpage" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">170</span>-<span class="cit-lpage" style="border: 0px; display: inline; font-size: inherit; font-style: inherit; font-weight: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;">6</span>.</cite><span style="border: 0px; color: #222222; font-size: 12px; font-weight: 700; line-height: 15px; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Yeh HM</span><span style="color: #222222; font-size: 12px; line-height: 15px;">, Lau HP, Lin JM, </span><em style="border: 0px; color: #222222; display: inline; font-size: 12px; line-height: 15px; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">et al.</em><span style="color: #222222; font-size: 12px; line-height: 15px;"> Preoperative plasma N-terminal pro-brain natriuretic peptide as a marker of cardiac risk in patients undergoing elective non-cardiac surgery. </span><span class="cit-source" style="border: 0px; color: #222222; display: inline; font-size: 12px; font-style: italic; line-height: 15px; margin: 0px 0.1em 0px 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Br J Surg</span><span class="cit-pub-date" style="border: 0px; color: #222222; display: inline; font-size: 12px; line-height: 15px; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">2005</span><span style="color: #222222; font-size: 12px; line-height: 15px;">;</span><span class="cit-vol" style="border: 0px; color: #222222; display: inline; font-size: 12px; line-height: 15px; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">92</span><span style="color: #222222; font-size: 12px; line-height: 15px;">:</span><span class="cit-fpage" style="border: 0px; color: #222222; display: inline; font-size: 12px; line-height: 15px; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">1041</span><span style="color: #222222; font-size: 12px; line-height: 15px;">–5</span></span><br />
<span style="font-family: inherit;">6. Fractured neck of femur. Prevention and management. Summary and recommendations of a report of the royal college of physicians. <i>J R Coll Physicians Lond</i> 1989 Jan:23(1):8-12</span><br />
<span style="font-family: inherit;">7. <span style="background-color: #fefefe; color: #333333; font-size: 14px; line-height: 21.875px;">Department of Health and Human Services. Agency for Healthcare Research and Quality: AHRQ Quality Indicators. Guide to Inpatient Quality Indicators: Quality of Care in Hospitals - Volume, Mortality, and Utilization. Version 3.1, March 12, 2007</span></span><br />
<span style="font-family: inherit;"><span style="background-color: #fefefe; color: #333333; font-size: 14px; line-height: 21.875px;">8. </span><span style="color: #333333;"><span style="font-size: 14px; line-height: 21.875px;">http://bmchealthservres.biomedcentral.com/articles/10.1186/1472-6963-12-15</span></span></span><br />
<span style="font-family: inherit;"><span style="color: #333333;"><span style="font-size: 14px; line-height: 21.875px;">9. </span></span><span style="background-color: white; font-size: 15.9991px; line-height: 21.9988px;"> </span><span class="element-citation" style="background-color: white; font-size: 15.9991px; line-height: 21.9988px;">Zagrodnick J, Kaufner HK. Decreasing risk by individualized timing of surgery of para-articular femoral fractures of the hip in the elderly.</span></span><br />
<span style="font-family: inherit;"><span class="element-citation" style="background-color: white; font-size: 15.9991px; line-height: 21.9988px;">10. </span></span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">Vidán MT, Sánchez E, Gracia Y, Marañón E, Vaquero J, Serra JA.. </span><span class="ref-title" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">Causes and effects of surgical delay in patients with hip fracture: a cohort study</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">. </span><span class="ref-journal" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">Ann Intern Med</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">. 2011;</span><span class="ref-vol" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">155</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">(</span><span class="ref-iss" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">4</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">):226–233</span><br />
<span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">11. </span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">Khan SK, Kalra S, Khanna A, Thiruvengada MM, Parker MJ.. </span><span class="ref-title" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">Timing of surgery for hip fractures: a systematic review of 52 published studies involving 291,413 patients</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">. </span><span class="ref-journal" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">Injury</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">. 2009;</span><span class="ref-vol" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">40</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">(</span><span class="ref-iss" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">7</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">):692–697</span><br />
<span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">12. </span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">Siegmeth AW, Gurusamy K, Parker MJ.. </span><span class="ref-title" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">Delay to surgery prolongs hospital stay in patients with fractures of the proximal femur</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">. </span><span class="ref-journal" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">J Bone Joint Surg Br</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">. 2005;</span><span class="ref-vol" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">87</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">(</span><span class="ref-iss" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">8</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">):1123–1126</span><br />
<span class="nowrap ref pubmed" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px; white-space: nowrap;">13. </span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">Al-Ani AN, Samuelsson B, Tidermark J, et al. . </span><span class="ref-title" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">Early operation on patients with a hip fracture improved the ability to return to independent living. A prospective study of 850 patients</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">. </span><span class="ref-journal" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">J Bone Joint Surg Am</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">. 2008;</span><span class="ref-vol" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">90</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">(</span><span class="ref-iss" style="font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">7</span><span style="background-color: white; font-family: 'Times New Roman', stixgeneral, serif; font-size: 16px;">):1436–1442</span><br />
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Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-86148671112421672962016-07-25T08:29:00.000-07:002016-07-25T08:29:11.000-07:00cysto after laparoscopic surgery to verify ureter patencyA 37 year old female presented for diag laparoscopy for suspected ectopic pregnancy and mass in the left adnexa.<br />
<br />
The procedure was uneventful, however, the surgeon was unable to visualize the ureters after performing a left salpingectomy. She was concerned about the ureters enough to perform a post operative cystoscopy to verify that both ureters remained functional. We verified that the only dye available to us was indocyanine green and methylene blue. I was given methylene blue and injected 3 1/2 mLs. After 20 minutes, no visible dye appeared in the bladder and the procedure was terminated with the plan to follow carefully her course.<br />
<br />
There are three common dyes that anesthesiologist are asked to inject patients in order for diagnostic purposes. The anesthesiologist should have familiarity with the properties of any medication they inject. A review of information on these dyes revealed a deficit in my own knowledge in this regard.<br />
<br />
Methylene Blue can be used to test ureteral patency after laparoscopic surgery. However, it is not commonly used for this indication. The recommended dose is 50 mg (it comes as a 10mg/mL concentration) for this purpose. Methylene blue does not have FDA approval for this use, and the package insert only asserts its use as a treatment for methemoglobinemia. <br />
<br />
Methylene blue is the only medication known to be effective for the treatment of methemoglobinemia, which is the oxidation of the iron in hemoglobin to the ferric form. Normally, the blood has a 1% concentration of methemoglobin (hemoglobin in the ferric form). When the concentration of methemoglobin rises to about 15%, symptoms become apparent and require treatment. The negative effects of this disorder result from hypoxia, as oxygen cannot be efficiently carried by methemoglobin. Symptoms include ashen color skin or cyanosis (methemoglobin from 3 to 20%), headache, dyspnea, lightheadedness (up to 50%), arrhythmias, unconsciousness etc (greater than 50% methemoglobin level). Treatment dose of methylene blue is 1 mg to 2 mg/kg. Ironically, at doses greater than 7 mg/kg can lead to the inducement of methemoglobinemia.<br />
<br />
Methylene blue inhibits monoamine oxidase enzyme, and therefore, can result in serotonin syndrome and should be used if with caution in patients taking serotonin reuptake inhibitors or MAO inhibitors. <br />
<br />
As methylene blue can be used for verification of ureteral patency via cystoscopy as the urine should turn blue after 10 to 20 min of IV injection, I thought it curious that we had no evidence of blue urine after 30 min. However, joel et al. did publish a look at two cases where injection of methylene blue did not result in any change in urine color [1]. The authors suspected that rapid metabolism of methylene blue to leulomethylene (a colorless metabolite was the cause of this anomaly). Since indigo carmine does not undergo any metabolism prior to excretion into the urine, it would be a superior alternative to methylene blue for detection of ureteral patency using cystoscopy. Indigo carmine's package insert asserts its primary use is for detecting change in urine color after IV injection. There are no drug interactions with indigo carmine, making it a safer alternative as well. The dose recommended is the full 5 mL ampule.<br />
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Indocyanine Green is another dye that may be encountered. It's used for determination of cardiac output, hepatic function and ophthalmic angiography (5mg, 0.5 mg/kg, and 40 mg respectively). It is bound to plasma proteins and taken up by hepatocytes without metabolism, and secreted in the bile unchanged. There are reports of the use of indocyanine green to detect ureteral patency via cystoscopy, however, it has been reported to be used in robotic surgery to detect ureters with near infrared light with success. However, the dye was injected directly into the ureters. Recently, I was involved in a case where a patient had an internal hernia with small bowel strangulation leading to questionable viability of the small bowel. Indocyanine green was injection IV and a laser was used to evaluate blood flow and vascular patency to the bowel. This technique is known as laser florescence angiography and uses the florescence properties of indocyanine green to visualize vessels that need to be verified as patent. With the laser set in place, the room lights off, an injection of indocyanine green is given IV, and within a few moments, the area of interest should light up white on the proper viewing screen where vessels are patent. Using this technique, we the surgeons were quickly able to verify that all vessels to the bowel section of interest were patent.<br />
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Anesthesiologists are often asked to inject substances that lie outside our typical armamentarium. We have an obligation to understand the possible ramifications of what we inject, and not always assume that it is proper and safe. <br />
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<span style="background-color: #6294ca; color: #555555; font-family: 'Open Sans', arial, sans-serif; font-size: 13px;">Joel AB, Mueller MD, Pahira JJ, Mordkin RM. Nonvisualization of intravenous methylene blue in patients with clinically normal renal function. Urology 2001; 58: 607vii. - See more at: http://www.ashp.org/menu/DrugShortages/CurrentShortages/Bulletin.aspx?id=27#sthash.ado1taUN.dpuf</span>Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0tag:blogger.com,1999:blog-5160330339552832907.post-3908354271681968462016-07-07T07:16:00.001-07:002016-07-07T07:16:22.479-07:00end tidal CO2, what intraoperative role can it play?Today I had a 64 year old male, with no reported medical history, who presented for L4-5 laminectomy. The patient reported that he walked regularly, up to 2 miles with no history of SOB, chest pain or other symptoms. The patient was taken to the OR and given 2 mg versed, 100 mcg fentanyl, 180 mg propofol, 5 mg rocuronium, and 100 mg succinylcholine. IV decadron was also given (8mg). Intubation proceeded without event and the patient was placed in the prone position. After turning prone, several issues arose at the same time. First, pulse oximetry revealed 93% saturation. Simultaneously, the blood pressure read 50/20 mmHg. ECG appeared normal with SR at 74 bpm. The pulse plethysmograph waveform appeared robust without obvious issues aberrations.<br />
Ausculation of the lungs was challenging due to a large tissue mass making breath sounds difficult to detect. However, it was noted by myself, that there appeared to be no breath sounds on the left, and therefore, the ETT was pulled back slightly. This resulted in an improvement of the arterial saturation as measured by pulse oximetry. However, simultaneous troubleshooting of the significant apparent hypotension occurred. The blood pressure cuff was recycled, and low blood pressure was verified. Also of note, the capnogram was reading 20 mmHg. The patient was noted to be ventilated at 700 mL with RR of 10. The patient weighed approximately 100 to 105 kg. It was immediately apparent that elevated minute ventilation was not likely the sole contributor to the issues related to the hypocapnea.<br />
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While multiple issues were at play at once in this case (endobronchial intubation along with severe hypotension), a deeper exploration of how the capnogram can be helpful in the diagnosis of the issues at hand.<br />
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In general, end tidal carbon dioxide (etCO2), is a function of PaCO2. However, a multitude of parameters can cause a gap (this is dead space [Vd], written as (a-ET)PCO2). In general, healthy patients without significant lung disease will have up to a 5 mmHg difference, where the etCO2 will be less than actual measure PaCO2. This gap increases with age, emphysema or any state that increass dead space ventilation (Vd), like low cardiac output (from hypovolemia) or pulmonary embolism. On the other hand, (a-ET)PCO2 can actually be positive (i.e. etCO2 is greater than PaCO2) in pregnancy and children (from 1 to 3 mmHg). In general clinical practice, we do not have access to the (a-ET)PCO2 because we do not routinely measure arterial blood gases. However, we do follow the trend of the etCO2, and thus, in general, if we see a sudden decrease in the etCO2 on the capnogram, we assume that we may be hyperventilating the patient, or that there has been a sudden increase in dead space ventilation. However, it must be understood, that there are several parameters other than Vd that can cause a decrease in etCO2. For example, decrease in metabolism or VCO2 will result in decrease in etCO2 if minute ventilation is constant. VCO2 is a function of depth of anesthesia relative to surgical stimulus, and body temperature. Alternatively, an increase in minute ventilation, if metabolic rate is constant will cause etCO2 to decrease. Importantly, the (a-ET)PC02, will remain the same in the two above situations. Another, more sutbtle and less recognized mechanism for (a-ET)PCO2 to be affected is via FiO2. Yamauchi et al. demonstrated that increasing the FiO2 from room air to very high caused an ever increasing (a-ET)PCO2. [8] They found that Vd increased as the FiO2 was increased in their anesthetized patients. They presumed that the mechanism of the increase in Vd was an increase in pulmonary vascular dilation with increased oxygen tension. This occurs predominantly in highly perfused alveolar units resulting in a shunt of blood away from low perfused alveolar units to high perfused alveolar units. Of course, this shunt created from increasing FiO2 is not related to physiologic shunts that might occur with something like ARDS. In this case, only large shunts of greater than 30 to 40% will cause a significant change in the (a-ET)PCO2.<br />
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However, a state of low cardiac output can also result in a reduced pulmonary artery blood flow. This results in increased Vd, and thus the (a-ET)PC02 increases. This manifests in the operating room as a sudden decrease of etCO2. This pattern was looked at by Askrog and colleagues where an inverse linear correlation was found between pulmonary artery pressure and (a-ET)PCO2. [1] Things that can cause this include pulmonary emboli (air, debris, clots), sudden massive hemorrhage leading to reduced venous blood return, vasodilation, mechanical obstruction to blood flow, reduced cardiac contractility, etc. In general, in the OR, mechanical ventilation and anesthetic depth are maintained at a reasonably constant level allowing us to remove these as a cause in theory.<br />
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In my patient, the simultaneous low blood pressure and sudden drop in etCO2, indicated two things: the blood pressure was real (i.e. it was not artifactual), and the drop in etCO2 was most likely due to decreased CO, in this case the cause being overdose of anesthesia. Of course other causes of a precipitous drop in etCO2 include PE or other mechanical obstruction to pulmonary blood flow. As it turns out the percent decrease in etCO2 is directly correlated with the percent decrease in CO (assuming that the metabolic rate and alveolar ventilation are unchanged). This was demonstrated in an article published in A and A. [2] It should be noted that after sustained or constant low CO, (i.e. after 10 to 20 min) CO2 begins to accumulate in the peripheral tissues leading to an increase in CO2 delivery to the pulmonary vasculature. This will cause the etCO2 to return to baseline if all other factors remain unchanged. The relationship of etCO2 and pulmonary blood flow was also studied in patients coming off cardiopulmonary bypass. [3] Here, an etCO2 greater than 30 mmHg (the study did not include patients with significant lung disease), was associated with CO of greater than 4 L/min (CI of 2 L/m). When etCO2 was greater than 34 mmHg, pulmonary blood flow (a good surrogate for CO) was greater than 5 L/min. Once again, minute ventilation was carefully maintained.<br />
Recently, a large volume of literature has been produced looking at measurements of indices that indicate a patient who is hypovolemic. Pulse pressure variation and stroke volume variation via measurement and analysis of the arterial waveform in ventilated patients in sinus rhythm has proven effective at determing which patients are likely going to respond with increased cardiac output if a fluid bolus is given. Unfortunately, the equipment is costly, requires a fair amount of data input, and is usually not routinely available. Recently, Monnet et al. [4] was able to show that etCO2 was better than arterial pressure for predicting volume responsiveness when using a passive leg raising test. Using a similar methodology in patients with acute circulatory failure in the ICU, monge garcia et al. showed that etCO2 after passive leg raise maneuver could be used to track changes in CO for the prediction of fluid responsiveness. [5] Recently, a group in France was able to demonstrate that after 500 mL hetastarch, an increasae of 2 mmHg in the etCO2 could diagnose fluid responsiveness (specificity 98%, sensitivity 60%). Obviously, it is critical to undertand that other changes to CO2 production and elimination must be held constant for this to be a valid clinical indicator. It should be recognized that in clinical anesthesia this can be difficult. In fact, very recently, I took care of patient having an open partial colectomy with small bowell resection. Her BP trailed lower early in the case. Based on this article, I decided to carefully track etCO2 and maintain other parameters unchanged (i.e. CO2 production and minute ventilation). I quickly boluses in 500 mL of hetastarch as used in the above mentioned article. While I did notice that etCO2 trailed higher with this bolus, I realized that in clinical practice, there are so many other factors occurring that it can be challenging to feel confident that other parameters are not the cause of the change you see reading on the capnogram. However, importantly, in this same study, HR variation, MAP variation, and PP variation were not predictive of volume responsiveness. In summary, these authors showed that after a rapid infusion of 500 mL colloid, an increase of 5.8% (or about 2 mmHg) of etCO2 predicted fluid responsiveness in 100% of their patients. If the etCO2 increased less than 5.8%, no conclusions could be drawn. [6] In real clinical practice, a bolus must be given very rapidly, to ensure that other parameters don't account for any subtle changes seen on the etCO2.<br />
Others have demonstrated that etCO2 can be predictive of mortality after out of hospital cardiac arrest (OHCA). In the NEJM [7], an observational study was published looking at etCO2 monitoring following OHCA to determine effectiveness of ACLS. They found that in this patient population, if after 20 minutes of ACLS, the etCO2 was less than 10 mmHg, there was a 100% specificity and specificity to determine non survival to hospital admission. If the etCO2 was greater than 20 mmHg, this indicates survival (at least in this study), but it does not guarantee it. In this article, it was noted that in low flow states (i.e. low cardiac output), etCO2 becomes a much better surrogate for cardiac output. <br />
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Having an in depth understanding of etCO2 can help us in ways that we might not otherwise expect. <br />
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[1] <span style="background-color: white; font-family: "tahoma"; letter-spacing: -0.2px; text-align: justify; text-indent: -48px;">Askrog V. Changes in (a-A)CO2 difference and pulmonary artery pressure in anesthetized man. J Appl Physiol 1966;;21:1299-1305.</span><br />
<span style="background-color: white; font-family: "tahoma"; letter-spacing: -0.2px; text-align: justify; text-indent: -48px;">[2] </span><span style="font-family: "tahoma"; letter-spacing: -0.2px;">Shibutani K, Muraoka M, Shirasaki S, Kabul K, Sanchala VT, Gupte P. Do changes in end-tidal PCO2 quantitatively reflect changes in cardiac output? Anesth Analg 1994;79:829-33.</span><br />
<span style="font-family: "tahoma";"><span style="letter-spacing: -0.2px;">[3] </span></span><span style="font-family: "tahoma"; letter-spacing: -0.2px; text-align: justify; text-indent: -48px;">Maslow A, Stearns G, Bert A, Feng W, Price D, Schwartz C, Mackinnon S, Rotenberg F, Hopkins R, Cooper G, Singh A, Loring SH. Monitoring end-tidal carbon dioxide during weaning from cardiopulmonary bypass in patients without significant lung disease. Anesth Analg 2001;92:306-13.</span><br />
<span style="font-family: "tahoma"; letter-spacing: -0.2px; text-align: justify; text-indent: -48px;">[4] </span><span style="background-color: #fefefe; color: #333333; font-family: sans-serif; font-size: 14px; line-height: 21.875px;">Monnet X, Bataille A, Magalhaes E, Barrois J, Le Corre M, Gosset C, Guerin L, Richard C, Teboul J-L. End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test. Intensive Care Med 2013;39: 93–100.</span><span style="background-color: #fefefe; color: #333333; font-family: sans-serif; font-size: 14px; line-height: 21.875px;"> </span><br />
[5] <span style="background-color: #fefefe; color: #333333; font-family: sans-serif; font-size: 14px; line-height: 21.875px;">Monge García MI, Gil Cano A, Gracia Romero M, Monterroso Pintado R, Pérez Madueño V, Díaz Monrové JC. Non-invasive assessment of fluid responsiveness by changes in partial end-tidal CO</span><span style="background-color: #fefefe; bottom: -0.25em; box-sizing: border-box; color: #333333; font-family: sans-serif; font-size: 10.5px; line-height: 0; position: relative; vertical-align: baseline;" xmlns="http://www.w3.org/1999/xhtml">2</span><span style="background-color: #fefefe; color: #333333; font-family: sans-serif; font-size: 14px; line-height: 21.875px;"> pressure during a passive leg-raising maneuver. Ann Intensive Care. 2012;2:9</span><br />
[6] Jacquet-Lagreze M, baudin F, David JS, Fellahi JL, Hu PB, Lilot Ma, Piriou V. End -tidal carbond dioxide variation after a 100- and a 500-ml fluid challenge to assess fluid responsiveness. <i>Annals of Intensive Care</i> 2016 6:37.<br />
[7]Levine R, et al. End Tidal Carbon Dioxide and Outcome of Out-of-Hospital Cardiac Arrest. NEJM; 337(5):301.<br />
[8] Yamauchi H, Ito S, Sasano H, Azami T, Fisher T, Sobue K. Dependence of the gradient between arterial and end-tidal PCO2 on the fraction of inspired oxygen. <i>BJA</i>. 2011.107(4):631-5.Rex Russellhttp://www.blogger.com/profile/13217822438784447144noreply@blogger.com0