Case Reports in Anesthesia

Blog with interesting cases and/or problems related to anesthesia with discussion based on best evidence in the literature.

November 14, 2018

34 year old female who is 15 weeks pregnant for cerclage

A 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 + 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 received no sedation via the intravenous route.  The patient tolerated the procedure without any problems.

The patient went to PACU able to move her legs but complaining of sinificant pruritis for which she reqeusted treatment.  She was discharged after a 2 hours and 37 min in the PACU after a case that was 30 min in duration.  

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 indicated that there is no significant increased risk to the brain, we have no good studies to indicated that there is not alteration to neurogenesis in the fetus.  Furthermore, even thought 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.  Juries do not evaluate the potential cause of harm to the fetus like you or I, and therefore, the legal risk is greater than you might expect.  

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 case 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.

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 pontine 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 bupicacaine was used and 25 mcg of fentanyl.  The impact of bupicavaine 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 (Anesthesiology [5]). 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.  

1.  Niazi AAA, Taha MAA. Egyptian Journal of Anesthesia. 2015. 31:65-9.

2. Gupta A, Axelsson K, Thorns, E, et al. Acta Anaesthesiol Scand 2003;47:13-9.

3. Beilin Y, Zahn J, Abramovitz S, Bernstein HH, Hossain S, Bodian C.  Anesth Analg. 2003; 97: 56-61.

4. Frisch NB, Darrith B, Hansen DC, Wells A, Sanders S, Berger RA. Arthroplast Today. 2018;4:236-39.

5. Liguori GA, Zayas VM, Chisholm MF. Anesthesiology 1998. 88; 619-23.

6. Buckenmaier CC III, Nielsen KC, Pietrobon R, et al. Anesth Analg 2002;95:1253-7.

7. Nishikawa K. et al. Jour of Clinical Anesthesia 2007;19:25-9.

8. Hassan HIEA, Anesth Essays Res 2015. 9:21-27.

26 year old on TPN for major bowel surgery

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.

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.  (see here for cochrane review). 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:

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.

Minor surgery: 0.25 mg/kg bolus prior to incision + 0.25 mg/kg/hr infusion until the end of surgery.

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.

Multipmodal analgesia will be very important so I will given IV Tylenol during the surgery and then q 8 hours post op.

 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.

Fig 1 post operative morphine consumption is reduced with magnesium.

Magnesium acts as an NMDA antagonist to reduce the perception and duration of pain.

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 Anesthesiology 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.

gabapentinoid pharmacology: these are not active at the GABA-a receptor although they are GABA structural analgues.

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.  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)

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.
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.

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:

  • Multiple system atrophy
  • familial dysautonomia
  • dementia with lewy bodies
  • Shy-Drager's syndrome
  • Parkinson's disease
  • longstanding diabetes
  • Vitamin deficiencies (our patient)
  • Amyloidosis
  • Bronchogenic carcinoma
  • Pure autonomic failure
Treatment for othorstatic hypotension can include a direct 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.

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. 

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.

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.

1. Sadasivan Shankar Iyer, Harshit Bavishi, Chadalavada Venkataram Mohan, and  Navdeep Kaur,  Anesth Essays Res. 2017 (11)7: 670-675

2. Rao Kadam V, Van Wijk RM, Moran JI, Miller D. Anaesth Intensive Care. 2013;41:476–81.

3. Ganapathy S, Sondekoppam RV, Terlecki M, et al. Eur J Anaesthesiol 2015;32:797–804

4. Wahba SS, Kamal SM. J Anesth 2014;28:517–23.

5. Zhang P, Deng XQ, Zhang R, Zhu T.  Br J Anaesth. 2015;114:339. 

6.  De Kock M, Lavand'homme P, Waterloos H.  Pain 92(2001) 373-380.

7. Himmeslseher S, durieux ME. Ketamine for perioperative Pain Management. Anesthesiology. 2005; (102):211-20.

8.  Lysakowski, C, Dumont, L, Czarnetzki, C, Tramèr, MR . Anesth Analg. (2007). 104 1532–9 

9Gildasio S. De Oliveira, Jr, M.D., M.S.C.I.Lucas J. Castro-Alves, M.D.Jamil H. Khan, B.S.Robert J. McCarthy, Pharm.D. Anesthesiology 07 2013, Vol.119, 178-190

10. Bell RF, Dahl JB, Moore RA, Kalso E. Perioperative ketamine for acute postoperative pain. Cochrane Database Syst Rev. 2006

11. Sudha Arumugam, Christine SM Lau, and  Ronald S ChamberlainJ Pain Res. 2016; 9: 631–640.

12. 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; Canadian Journal of Anesthesia 2013, 60:423-431

13. Monks DT, Hoppe DW, Downey K, Shah V, Bernstein P, Carvalho JCA; A perioperative dose of gabapentin does not produce a clinically meaningful improvement is analgesia after cesarean delivery; Anesthesiology 2015 August, 123(2): 320-326

July 23, 2018

super obese patient for shoulder surgery

Recently 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).
fig 1
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.  

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.  
fig 2
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.  
A review article on the options for avoidance of significant phrenic nerve block was published in the journal Anesthesiology 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.

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 blockaded of the brachial plexus. Reducing this amount could reduce the incidence of phrenic nerve palsy. However, 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 reduciton in  concentration seemed to come at the expense of more opioid requirements over a 72 hours 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].
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.
Performing a supraclavicular block as 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. 
    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.  
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 Anesthesiology 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. 
    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).

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.

Technique-Anterior Surpascapular nerve block:

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).

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.
1. Hartrick CT et al. BMC Anesthesiol 2012;12:6.
2.  Deborah Culley Anesthesiology 2017;127:173-91.
3. Lee, JH, Cho, SH, Kim, SH, Chae, WS, Jin, HC, Lee, JS, Kim, YI R Can J Anaesth 2011; 58:1001–6
Stundner, O, Meissnitzer, M, Brummett, CM, Moser, S, Forstner, R, Koköfer, A, Danninger, T, Gerner, P, Kirchmair, L, Fritsch, G  Br J Anaesth 2016; 116:405–12
4. Al-Kaisy, AA, Chan, VW, Perlas, Br J Anaesth 1999; 82:217–20
5. Thackeray, EM, Swenson, JD, Gertsch, MC, Phillips, KM, Steele, JW, Burks, RT, Tashjian, RZ, Greis, PE  J Shoulder Elbow Surg2013; 22:381–6
6.Wong, AK, Keeney, LG, Chen, L, Williams, R, Liu, J, Elkassabany, NM Pain Med 2016; 17:2397–403
7.Zhai, W, Wang, X, Rong, Y, Li, M, Wang, H BMC Anesthesiol 2016; 16: 1–8
8. Renes, SH, van Geffen, GJ, Rettig, HC, Gielen, MJ, Scheffer, GJ  Reg Anesth Pain Med 2010; 35:529–34 
9.  Siegenthaler, A, Moriggl, B, Mlekusch, S, Schliessbach, J, Haug, M, Curatolo, M, Eichenberger, U Reg Anesth Pain Med 2012; 37:325–8 
10. Hussain N, Goldar G, Ragina N, Banfield L, Laffey J and Abdallah F. Anesthesiology 2017;127:998-1013.
11. Auyong DB, Hanson NA, Joseph RS, Schmidt BE, Slee AE, and Yuan SC. Anesthesiology 2018;129:47-57.
12. Marhofer P, Anderl W, Heuberer P, Fritz M, Kimberger O, Marhofer D, Klug W, and Blast J. Anaesthesia 2015, 70, 41-46.
13.Urmey WF, Talts KH, Sharrock NE Anesth Analg. 1991 Apr; 72(4):498-503.
14.Ryu, T, Kil, BT, Kim, JH  Medicine (Baltimore) 2015; 94:e1726

March 4, 2018

63 year old male for shoulder arthroscopy and polycythemia vera

Today 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:

  • ASA 81 mg
  • Buprion 300 mg qd
  • Citalopram 20 mg 
  • Fluoxetine 40 mg
  • Gaba 300 mg
  • Glipizide 5 mg
  • Lantus 50 units qd
  • NPH 30 units qd
  • Metformin 1000 mg
  • pravastatin 40 mg
  • Na+ 141
  • K+ 4.8
  • BUN 10
  • Cr 0.83
  • Glucose (finger stick) 63 mg/dL patient without symptoms of hypoglycemia.
  • Hct 57.8
  • Platelets 245,000
  • total CO2 33
In addition to untreated HTN, depression and diabetes, the patient had significant OSA.
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.

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.

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. In order to be positively diagnosed with polycythemia vera, two major criteria and one minor criterion must be present

Major criteria include:

  1. hemoglobin greater than 18.5 g/dl in men, greater than 16.5 g/dl in women
  2. presence of the JAK2 V617F or similar mutation.
Minor criteria include: 
  1. bone marrow biopsy showing myeloproliferation. 
  2. serum erythropoietin level below the normal range.
  3. endogenous erythroid colony formation in vitro [3].  
In additioon, in patients who NOT have the JAK2 mutation, but do have elevated Hgb, AND two minor criteria, a positive diagnosis of PV can be made.

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, "
In those rare polycythemic OSA patients, polycythemia is corrected by CPAP therapy in the majority."  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.

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)

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.

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.

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].

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].
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.    

V=volume of blood to extract
EBV = Estimated Blood Volume (in adult males 70 mL/kg is often used)
Ho= starting Hematocrit level of patient 
Hf= final Hematocrit or minimal allowable (around 40 to 45%).
Have= the average between the start and final hematocrit.

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.

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.

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 should. This syndrome is characterized by changes in autonomic, neurological, and cognitive behavioral functions and appears to result from over-stimulation of 5-HT1a and 5-HT2 receptors in the central grey nuclei and medulla.  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.

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.

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. Semin Hematol. 1986;23:132–143.
2. 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. Blood. 2008;111:666–671.
3. Wadleigh M, Tefferi A. Classification and diagnosis of myeloproliferative neoplasms according to the 2008 World Health Organization criteria. Int J Hematol. 2010;91:174–179. 

4. Wasserman LR, Gilbert HS. Ann New York Acad Sci 1964;115:122-38.

5. Thomas DJ, Marshall J, Russell RW, Wetherley-Mein G, du Boulay GH et al.  Lancet. 1977;2(8045): 941-943

6. Ruggeri M, Rodeghiero F, Tosetto A, Castaman G, Scognamiglio F, et al.  Blood 2008; 111(2): 666-671

7. Araya V, Contreras P, Aguirre C, Depix MS, Zura ML. The effect of fluoxetine on insulin resistance in nondiabetic obese patients [in Spanish]. Rev Med Chil. 1995;123(8):943-947.

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. Int J Obes Relat Metab Disord. 1992;16(2):79-85.
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. Arch Gen Psych. 2006;63(5):521-529.
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. BMC Fam Pract. 2003;4:7.

February 1, 2018

WPW syndrome in patient with significant intraoperative hyperthermia

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.  

I immediately verified that the room temperature was turned down and that the bear hugger was blowing cool air.

The main considerations when confronted with sudden intraoperative hyperthermia are:
  • malignant hyperthermia
    • in this case ruled out by normal minute ventilation and etPCO2, and lack of muscle rigidity.
  • Thyroid Storm
    • A possibility in this case, considering that the patient was having a thyroidectomy that required nearly seven hours of surgery. 
    • often causes tachycardia, hyperthermia, hyper or hypotension, hypokalemia and significant mental status changes that would not be evident until emergence.
  • cocaine abuse
    • excessive preoperative use can result in hyperpyrexia along with other symptoms like tachycardia, seizures, tachypnea, and dysrhythmias can often mimic MH.
  • sepsis
    • usually clinical history can clue in to this cause as well as tachycardia and hypotension.
  • pheochromocytoma
    • clinical history of headaches, sudden onset hypertension and tachycardia will lead the clinician to suspect this diagnosis
    • Catecholamine excess usually results in significant tachycardia and hypertension intraoperatively, but hyperthermia may also be present.
  • excessive medication administration
    • ketamine, atropine, dopamine, droperidol, or tricyclics 
  • Neuroleptic malignant syndrome (NMS)
    • from central dopaminergic blockade
    • butyrophenones, phenothiazines, metoclopramide, lithium,  tricyclics, monoamine oxidase inhibitors, selective serotonin  reuptake inhibitors, and haloperidol.
    • clinical symptoms similar to MH; tachycardia, hyperthermia, metabolic acidosis, and increased muscle tone.
    • The only possible way to distinguish NMS  from MH is that severe hypercapnia is not seen with NMS.
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.
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).
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.
  In any patient who becomes unstable due to the arrhythmia, synchronized cardioversion is the treatment of choice.   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. 

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.  

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]. 

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.

1. 8. Seki S, Ichimiya T, Tsuchida H, Namiki A. A case of normalization of Wolff-Parkinson-White syndrome conduction during propofol anaesthesia. Anesthesiology. 1999;90:1779–81.
2. Barrett PA, Laks MM, Mandel WJ, Yamaguchi I. Am Heart J. 1980. Jul;100(1):23-33.
3. Akhtar M, Gilbert CJ, and Shenasa M. Circulation 1981. Vol. 63(2):435-441.
4. Simonian SM, Lotfipour S, wall C, and Langdorf MI.  Intern Emerg Med. 2010, 5(5): 421-6.
5. Stoelting RK. Anesthesia and Co Existing Disease. p. 349