Sciatic Nerve block from Hell

A healthy (ASA I) 48 year old male presents for ORIF of ankle (bi malleolar fracture). Location is fast paced surgical hospital 1st case. Anesthetic Plan: placement of sciatic nerve catheter in OR before case begins, GA, and then saphenous nerve block post operatively in OR.

The posterior (Labat) approach was used. Sedation was provided with 150 mcg fentanyl and 2 mg of Versed in divided doses by an assistant. The stimulating current was initially set to 1 mA. Initial twitch was strong and the current was reduced to 0.2 mA. A dorsiflexion twitch was still present, therefore the 17 G stimuplex needle was withdrawn slightly. Now at 0.3 mA, a very slight twitch was visible and after aspiration 30 mL of 0.5% ropivacaine was injected containing 1:400k epinepherine. The patient did not complain of severe pain during injection. Because of time constraints the patient was immediately placed supine and GA was induced w/ Propofol and an LMA was placed without difficulty. The lateral aspect of the ankle was reduced and plated first. No additional fentanyl was required during this portion of the case. During the placement of screws into the medial malleolar fracture, an additional 100 mcg of fentanyl was required. At the end of surgery, the LMA was removed, and 0.5% Ropivacaine was injected at just deep to the sartorius muscle for 7 mL and then an additional 5 mL was injected just medial to the tibial tuberosity.

In the PACU the patient complained of pain and was given an additional 100 mcg of fentanyl for pain. The ankle was tightly wrapped and braced, but sensory exam using ice revealed a dense block on the lateral leg just below the knee. The patient was discharged soon after to home.

At 9 pm on the day of surgery, the patient was contacted by phone for follow up. The patient complained of urinary retention that lasted until aproximately 7:30pm (from time of discharge at 12 pm). Although the patient was able to urinate, he stated that it was very difficult and that he was experiencing severe numbness of his entire right lower extremity, right buttocks and his entire penis. The patient described a very dense block in the sciatic nerve distribution, however, he was experiencing 8 to 10 out of 10 pain at the surgical incision site on the lateral portion of the ankle. The patient had numbness that went down to just below the mid portion of the lateral leg and then stopped. The patient self d/c'd the continuous infusion of bupivacaine 0.25% at 7:30pm.

On POD 1, the patient still complained of numbness to his buttocks and groin area, and entire right upper leg. He felt that the numbness was less dense however. He did not experience any further problems with urinary retention, and his penis had nearly returned to normal.

On POD 2, the patient described a significant improvement. He described a circumferential area of slight tingling and dysesthesia of the upper leg. He estimated that it was about 90% back to normal in terms of sensation. The patient did not complain of any motor deficits.


Discussion:
Using the labat approach for sciatic block for ankle surgery may not be the best approach. I choose this approach for a few reasons. 1) Less local anesthetic is needed at this level adequate block, 2) time of onset is faster according to one study, 3) more reliable block and 4) I can place a sciatic block more quickly using the labat or posterior approach when compared to a lateral popliteal or posterior popliteal approach. Nevertheless, this may not be the ideal block for ankle surgery for a patient destined to return home given that a more proximal sciatic nerve block makes ambulation more difficult and may result in urinary retention. In this patient it is likely that an intraneuronal injection occurred. With an intraneuronal injection, local anesthetic was not able to spread around the nerve to the same degree as it would with an injection outside of the nerve sheath (epinuerium). The local anesthetic then tracked proximally and distally. Clinically this resulted in urinary retention and a dense penile block. The duration of anesthesia was also atypical (lasting nearly 48 hrs). This is expected with an intraneuronal injection of local anesthetic. The patient seemed to develop only anesthesia to the common peroneal nerve componenent of the sciatic nerve. During the case, I injected after seeing dorsiflexion. Although, there is not much published information dealing with anesthesia of a single component of the sciatic nerve, this seems to represent a case of a common peroneal nerve block, sparing almost completely the tibal componenet. The skin overlying the ankle is served by the sural nerve which is a continuation of the tibial nerve. This portion was not numb according to the patient despite a dense block at other locations of the leg. Therefore, when performing a sciatic nerve block, consider whether the surgical site will include the common peroneal nerve or the tibial nerve. For ankle surgery, accepting plantarflexion would allow blockade of the tibial component and thus result in higher rate of success. The common peroneal nerve serves the lateral leg just below the knee and the dorsal aspect of the foot, and stimulation of this component results in dorsiflexion.

This patient complained a circumferential numbness around the thigh. It is likely that some of the numbness in the femoral nerve distribution was a result of the tourniquet used during surgery for aproximately 2 hours at 300 mmHg. Indeed, nerve injuries from tourniquet use, especially at times greater than 2 hours, are well documented. Paralysis from tourniquet use has been estimated to occur with an incidence of 1:8000. Less severe and subclinical neuropraxias likely develop with far greater frequency. Recommendations include maintaining pressure at no greater than 150 mmHg greater than the systolic blood pressure and deflation after no more than 90 to 120 min. Nerve damage from tourniquet use may also occur despite following these guidelines. For example, a healthy patient suffered severe conduction block of both sensory and motor fibers localized to the margins of a tourniquet after hand surgery. The tourniquet was at 300 mmHg for 45 minutes, well within the current recommendations for tourniquet use.
Peripheral nerve injury is classified into three degrees of severity:
A) Neuropraxia-myelin damage
B) axonotmesis-loss of axonal continuity with intact endoneurium.
C) Neurotmesis-loss of axonal and endoneurial continuity.

This patient suffered a neuropraxia-nerve dysfunction that lasted longer than clinically expected from the local anesthetic block alone. In this case, the nerve axons and fascicles remained intact, and injury was likely a result of pressure induced ischemia. Although, neuropraxia may result in months of nerve dysfunction, this patient was essentially back to normal after three days. In order to cause more permanent neurologic injury, an injection must disrupt the nerve fascicles causing a disruption of axons.

In this case all steps to avoid neurologic damage were followed: the patient was lightly sedated, injection only occurred at >0.2 mA, injecting against excessive resistance was avoided, and a blunt tuohy styled needle was used. Nevertheless, following these recommendations religiously will not prevent all intraneuronal injections and severe nerve damage can still ocurr, although the likelyhood is decreased tremendously. Recently, in the journal Anesthesiology, Tsui and colleagues published their measurements using electrical impedance (EI). This was done in a pig model, but is probably relavent to humans. In their study, the EI increased by greater than 50% from baseline when the needle entered a nerve. I did not measure EI in this case and it would have been interesting to see whether this parameter would have been an early clue that an intraneuronal injection was about to occurr. I am currently measuring EI in all my nerve blocks to see if this might be clinically useful.

Options available to the clinician facing a possible nerve injury after peripheral nerve block

If a patient complains of pain, weakness and/or paresthesias after surgery, consideration should be given to all possible causes, as opposed to assuming the cause to be the nerve block. If a patient still has significant complaints 1 to 2 days after surgery which do not appear to be resolving, consideration of nerve conduction studies should be given. Nerve conduction studies will only detect injury to myelinated nerves and so will not be useful in patients' whose only complaint is pain. If the study is normal, a neuropraxia is likely and expectant management is indicated. If abnormal, then electromyography (EMG) studies can be used to localize the lesion. It takes 2 to 4 week after injury for EMG to detect injury.

Fortunately nerve injury following peripheral nerve blockade is extremely rare. The commonly sited incidenc is 0.4%. However, vigilance and impeccable technique is still required to avoid what could be a devestating injury.

The anesthesiologist and surgical site infection!
A 65 year old male for emergent hemicolectomy secondary to massive bleeding. Pt has remote history of testicular cancer (age 30), now with HTN, DM and obesity (BMI 32). Current BP is 100/70, HR is 85, AF, RR 27. Plan is GETA w/ RSI and Cricoid Pressure.The anesthesiologist often does not consider surgical site infection as a main theme or criteria when deciding what medications to give or in developing the anesthetic plan. In many cases, issues of surgical site infection (SSI) are simply to give preop antibiotics and go no further. However, there are special cases as the one above, where your patient has an above average potential for developing a surgical site infection and the anesthesiologists role is directly relevant to this outcome. Although, maintaining normothermia, adminstering effective prophylactic antimicrobials prior to incision, and maintaining blood flow to tissues are obvious and well known to be critical in reducing the risk of surgical site infections, there are other methods that are important, particularly in higher risk patients that are less known and understand by many anesthesia providers who have a great amount of experience.The first step in playing an active role in reducing the probability of a SSI post op is estimating your patients risks which implies understanding those factors that increase risk.the following is a general list of risk factors but does not quantify how much each factor increases risk:hypovolemiadiabetesobesitymalnourishmentblood trasnfusioninadequate pain controlantibiotic prophylaxisprolonged surgical timehost immune systemair in OR (ultraclean, negative pressure)hypothermialow SC Oxygen tensionThis article will focus on the few modifiable risk factors that exist with an emphasis on those that are predominantly under the control of the anesthesiologist. These will include:pain control-briefantibiotic prophylaxis-briefpatient temp-briefSub Q oxygen tension- emphasisPain Control: at this point I will limit my comments to a simple better pain control is better. The 'why' will be touched upon under the heading of Sub Q oxygen tension (improved w/ pain control).Antibiotic prophylaxis: appropriate antibiotics should be given within one hour of surgical incision. Giving antibiotics after incision is has questionable benefit.Patient temp: normothermia is critical. This is often very difficult in a scenario as described above because patients come to the OR emergently and time is spent placing lines in a pt who is not being warmed in a cold OR. Often by the time the drapes go up and surgery commences the patient has become hypothermic. Evidence for the importance of normothermia comes from a RCT published in the NEJM demonstrating an absolute risk reduction (ARR) of 13% by maintaining normothermia (37C vs. 34.5C)(1). Sub Q oxygen tension: Most anesthesiologists do not consider this data when performing anesthesia. Indeed, it is usually not important information for the vast majority of anesthetics. However, as arterial lines are appropriate to place in some patients, the information gained from sub q oxygen tension can be quite important. Unfortunately there is no clinical method available to monitor this parameter. Nevertheless, it is important to understand what is normal, what is abnormal, and how this will affect your patient. In a normal volunteer breathing room air, it sits around 65 mmHg. Surgical patients when measured average about 49 mmHg with large variability. Post surgical patients breathing oxygen through NC (~0.4 to 0.6 FiO2) average around 69 mmHg, whereas a normal volunteer given the same amount of oxygen will increase their TsqO2 to ~130 mmHg (2). This is important to understand because it turns out that tissue healing and bacteria killing are dependent on an oxygen tension in the tissues and vary in direct proportion to the tissue oxygen tension (PsqO2). In fact it has been experimentally verified that oxidative killing is oxygen dependent from 0 to 150 mmHg PsqO2 (3). Furthermore, when bacteria are introduced and phagocytes begin utilizing NADPH to reduce O2, this results in a dramatic reduction in PsqO2, that is from the normal of ~60 mmHg down to 0-10 mmHg. Bacterial contamination also alters PsqO2 by altering perfusion of tissues independently of oxygen utilization. In rats where lesions have been experimentally created and then inoculated it has was demonstrated that low FiO2 compared to high FiO2 was an independent variable in determining infection size and was no less important than giving prophylactic antibiotics. In other words, utilizing a FiO2 after bacterial inoculation was just as effect maintaining normal (0.21) FiO2 but giving antibiotics (4,5). So who do we give oxygen to and in what dose? The first step that should be taken in any patient going to the OR where a surgical incision will be made is to make a valid determination of the risk of SSI to the patient. Although the above risk factors as listed are pertinent, considering them provides no quantitative probability of a particular patient developing a SSI post operatively. A crude, but simple tool that has been used in research is the SENIC scoring system. See below:1 pt: intraperitoneal abdominal surgery1 pt: duration of surgery >2 hrs.1 pt: 3 or more co morbidities (i.e. hypertension, pulmonary disease, diabetes)1 pt: contaminated wound/surgery- (i.e. abscess, colon surgery non prepped)Predicted infections rates are as follows depending on score:0=1% 1pt=3.6% risk 2pts.=9% 3pts.=17% 4pts.=27%However, in 1997 Hopf and colleagues published a paper in the Archives of Surgery demonstrating that this scoring system was not nearly as effective at predicting the risk for SSI as was measuring the PsqO2 on patients(6). Among their findings were the following:· If baseline PsqO2 was >70 mmHg, no SSI occurred.· If baseline PsqO2 was 40 mmHg or less, SSI rate was 40%· Rate of infection varied inversely with both baseline PsqO2 and with post operative maximal PsqO2.There are three main factors which determine PsqO2, two of which are under the control of the anesthesiologist. These are vascular anatomy at the site of inoculation (surgical site), vasomotor control (vasoconstricted vs. vasodilated), and PaO2 which varies directly w/ PsqO2 assuming normal blood flow to tissues.The first factor is beyond our control, however, vasomotor control and the PaO2 can be manipulated by us to a much greater degree. Controlling PaO2: Two large RCTs in colon surgery patients both demonstrated that indeed, by providing a FiO2 (80% vs. 30%), and therefore increasing PsqO2, indeed decreases the rate of SSI in colon surgical patients although the decrease was modest (7,8). Patients in both of these large studies had significantly lower SSI rates when given 80% FiO2 both during surgery and afterwards for 2 or 6 hours depending on the study.Vasomotor state: Okca et al(9) demonstrated that in patients undergoing surgery w/ FiO2 of 0.4 received an average increase of ~30 mmHg (from 63 to 89 mmHg) if the etCO2 was maintained at 45 mmHg vs. 30 mmHg. Note that is quite common for the etCO2 to be maintained at ~30 mmHg in patients who are paralyzed and mechanically ventilated. Patients already receiving FiO2 of 0.8 also benefit however(10), going from PsqO2 of 84 mmHg to 116 mmHg and more importantly, an intestinal oxygen tension went from 53 mmHg to 107 mmHg.Hypovolemia is detrimental to PsqO2. In fact, if you give provide a higher FiO2 to a patient with goal of raising PsqO2 and thus decreasing chance of SSI, but do not adequately resuscitate your patient, it has been shown that despite your good intentions, the PsqO2 will not increase. It’s only after adequate volume status has been restored that raising FiO2 will prove beneficial (11). Others have shown that indeed an aggressive fluid regimen can augment PsqO2 in abdominal surgical patients (12), but a follow up study on this same cohort of patients found that this increase in PsqO2 did not result in a decrease in the rate of SSI (13). Despite these findings, hypovolemia must be avoided and fluid therapy should be adequate to ensure this. In the above study looking at an aggressive fluid regimen vs. a standard protocol of 8 to 10 mL/kg/hr a balanced crystalloid solution was used. However, Lang et al (14). showed that LR in large volumes (11L) caused a 59% decrease in the PsqO2, however, giving a HES in addition to the LR at lower volumens (3 L each) PsqO2 was increased by 23%. The take home message from these studies is avoid hypovolemia, but caution she be used when this requires large volumes of crystalloid (i.e. >8 or 9 L) and consideration should be given to other fluid types. Inadequate pain control has been shown to have a significant effect on decreasing the PsqO2 by around ~24 mmHg (15). Morphine and its derivatives effective at reducing pain, however, they also can cause respiratory depression and lead to decreased PaO2 which reduces PsqO2. Furthermore, meta analyses have shown that PCA with narcotic pain medications are inferior to PCEA after many different kinds of surgery with regard to pain scores (16, 17). Therefore, whenever appropriate regional anesthesia should be considered as a method not only for pain control but also as an intervention with the goal of decreasing SSI risk. In addition to the improvement provided by improved pain control to the PsqO2 of nearly 24 mmHg as shown, the vasodiliation that results from the sympathectomy of regional anesthesia induces a further increase in PsqO2 of from 9 mmHg to 31 mmHg depending on the method and study (18, 19, 20, & 21).Obesity is associated with a greater risk of post op SSI. Studies looking at the PsqO2 in obese patients (BMI >30), showed that to no one’s surprise, a much greater FiO2 was required to maintain a certain PaO2 (22, 23). However, more surprising was the studies findings that once obese and non obese patients achieved an equal PaO2, PsqO2 were still much lower in the obese patient by approximately 20 to 30 mmHg depending on the PaO2 that was used as the starting measurement. Both studies indicated that obese patients require FiO2 of >0.95) in order to maintain PsqO2 around ~47 mmHg, which is still low enough to be associated with risk. Furthermore, simply raising FiO2 in this population results in an underwhelming increase of PsqO2 of 13 mmHg, which is half the benefit their non obese counterparts experience. Adding PEEP may be necessary if tolerated in order to increase PaO2 to >300 mmHg, the maximum tested in these studies.Although PsqO2 is an excellent predictor of risk of SSI, and two RCT have demonstrated benefit to hyperoxia, the practice of delivering high FiO2 is not standard of care. Many cite a study showing that hyperoxia was associated with worse outcome in a study of general surgical patients (24). This study however suffered from methodological flaws: the experimental group (hyperoxia) had a greater number of obese patients, were more likely to be intubated at the end of surgery (likely sicker) and underwent longer and more complicated surgery. Simply put, the groups were not equal. Nevertheless, performing a metanalysis of the three studies shows that hyperoxia is beneficial. Another common concern among clinicians is that of absorption atelectasis resulting in post operative pulmonary complications. Although, this is a known feature of high FiO2, a study looking specifically at this problem in a clinical setting demonstrated that this concern is likely unfounded (25).In conclusion, it is my current practice to utilize every maneuver possible to maximize PaO2 in at risk patients who present to the OR. I generally estimate risk utilizing a combination of factors including the SCENIC score (although I do not necessarily chart of format pt value for each patient), surgical setting (emergent/elective), type of operation (bowell vs. highly vascular site) surgical duration etc. In most cases FiO2 for short duration is harmless, and therefore that is my default. I typically avoid Nitrous (not necessarily because N2O has been shown to be a risk factor for SSI itself [26], but because it requires FiO2< 1.0.
JAMA. 2003 Nov 12;290(18):2455-63.17. Wu CL, Cohen SR, Richman JM, Rowlingson AJ, Courpas GE, Cheung K, Lin EE, Liu SS.Anesthesiology. 2005 Nov;103(5):1079-88; quiz 1109-10.18. Treschan TA et al. Effects of Epidural and General Anesthsia on Tissue Oxygenation. Anesth Analg 2003; 96: 155319. Buggy DJ. Paraveterbral anesthesia increases post op flap tissue oxygen tension….compared to IV opioids analgesia. Anesthesiology 2004; 100;37520. Buggy DJ, Dougherty DL. Postoperative Wound oxygenation with epidural or intravenous Analgesia. Anesthesiology 2002; 97:952.21. Kabon B et al. Thoracic Epidural Anesthesia Increases Tissue Oxygenation During Major Abdominal Surgery. Anesth Analg 2003; 97:1812 .22. Fleischman E. et al. Tissue oxygenation in obese and non-obese patients during laparoscopy. Obes Surg. 2005 Jun-Jul;15(6):813-923. Kabon B, Nagele A, Reddy D, Eagon C, Fleshman JW, Sessler DI, Kurz A. Obesity decreases perioperative tissue oxygenation Anesthesiology. 2004 Feb;100(2):274-80.24. Pryor KO, Fahe TJ et al. Surgical Site infectin and the Routine Use of Perioperative Hyperoxia in a General Surgical Population: RCT. JAMA. Vol 291, No.1 Jan 2004.25. Akca O, Podolsky A, Eisen huber E et al. Comparable postoperative pulmonary atelectasis in patient given 30% or 80% oxygen during and 2 hours after colon resection. Anesthesiology 1999;91:991-8.26. Fleischmann E. Et al. Lancet 2005;366:1101-1107
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anesthesia for liposuction

There are several techniques used to perform liposuction. See table.1The wet technique was introduced in the 1980s, and the superwet technique was introduced in 1980 and advocated by fodor. With this technique, infiltration was injected in equal volume to aspirated liposuction. In the same year, the tumescent technique, introduced by Klein, was described and the injectate volume was now 2 to 3.1 to 12 part aspirated and required only local anesthesia.3 Some have liberalized the tumescent technique using ratios from 3-7:1.6 Blood loss was minimal with the tumescent technique and deemed safe.4 While these techniques have been accepted by surgeons, there is still controversy regarding the resuscitation of these patients, typified by the stances of Klein and Pitman. Klein considers (for the tumescent technique) the fluid injected into the tissues sufficient for volume resuscitation hypothesizing that this fluid makes its way into the intravascular space.5 In fact, this process is known as hypodermoclysis. Hypodermoclysis is the mechanism described by which SQ fluid migrates to the intravascular space. This process is estimated to take around 2 ½ hours for 1 liter of fluid infiltrated into medial thigh.11 Unfortunately, this data is from only one study and therefore, the true rate may be quite different. Authors have tried to quantify how much of the infiltrate is removed in the aspirate and have estimated that only 2212 to 29%13 of the aspirated fluid contains the original fluid infiltrated. This view contrasts with Pitman, who advocates a 2:1 ratio (IV + injected SQ:aspirate).7 Neither author reports complications from fluid overload, and there is only one reported case of fluid overload.8 Other reports of death have been documented.9-10 A prospective observational trial of 53 patients who underwent USG liposuction using a superwet technique, where the ratio was 1:1 (infiltrate:aspirate) was used.1 Fluid was replaced per preoperative deficits, and then given to maintain VS and UO WNL, and finally per protocol of 1:1 ratio of infused crystalloid:aspirate after >4L of aspirate. Infiltrate solution contained 0.03% lidocaine plus 0.01% epinephrine (1:1,000,000), and given to maximum of 4,000 mL (lidocaine 1200 mg=17 mg/kg assuming 70kg). In this study the average aspirated volume was ~4.5 L (range 300 mL to 15.5 L). The average UO for both small volume (<4l)>4L) aspirate liposuction was > 1.5cc/kg/hr. There were 3 episodes of transient hypotension responsive to fluid in the PACU and 3 more on the floor. See table 2.average volume used on per kg per hour basis.The authors for this study used a reference for fluid replacement of 5 to 6 cc/kg/hr based on the stoelting and miller textbooks of anesthesia stating this type of surgery represented moderate trauma. Based on this study the authors gave the following recommendations based on the fact that the large volume patients seemed to be slightly over resuscitated by virtue of the UO all greater than 1 cc/kg/hr in OR and PACU.1. Pre op deficits as needed.2. IVF per VS and UO3. infiltrate solution4. 0.25 mL per mL infiltrated after 4 L aspirated.This same group followed up their first study with a review of 89 patients14 using their own recommendations for IVF therapy from the previous study in an attempt to avoid the slight over resuscitation that occurred. They did modify the regimen only slightly by not starting to give IVF 0.25 mL/mL aspirated until after 5 L of aspirate. Of these 89 pts only 21 underwent large volume liposuction (>5 L aspiration). This group used a super wet technique with a similar lidocaine + epinephrine mixture as detailed in their first study, but this was given up to a total of 5 L of infiltrate after which lidocaine was removed from the LR. See table for volume resuscitation:The average intraop fluid ratio (total volume in/total volume aspirated) was 1.8 for the small volume group (<5l)>5L). UO ave was 1.5 cc/kg/hr and 1.7 cc/kg/hr for the small and large volume groups respectively. In the PACU, UO was 1.6 and 1.7 for the small and large volume groups respectively, while fluid given was 3.8 and 4.4 mL/kg/hr for the small and large volume groups respectively. On the floor, fluid was required for 10 hrs and 16 hrs for the small and large volume groups respectively, while fluid given was 1.6 and 1.3 mL/kg/hr for the small and large volume groups respectively. UO was 2.9 and 2.5 mL/kg/hr for the small and large volume groups respectively.They did not have any major complications in this study, and no transfusion was given. This group reports that they have never had pulmonary edema as a complication in over 700 patients, but are still yet wary of this complication.The graphs below depict comparison from the first cohort on 1st protocol (1 mL IVF given for each mL of aspiration after 4000 mL) compared to the current protocol. The original protocol is blue and revised protocol in purple.the original protocol is represented by the yellow, and revised by the light blue. The authors note that in the second graph, UO peaked in the RR in the original protocol, which could represent a more sudden and abrupt IV volume shift as compared to the more delayed and gradual shift as occurred with the current protocol. They also note that UO was still high representing a slight over resuscitation which might be modified by not replacing aspirate with IVF therapy at all.Although this group does not report morbidity from high volumes of fluid, the tumescent technique has potential for harm. Gilliland reports a case of pulmonary edema in a 55 year old ASA 1 male who returned for a 3rd liposuction surgery.8 He received a 7900 mL SQ and 2200 mL IV. He develop hypoxemia in the PACU and required 2 doses of lasix after which he urinated approximately 5 L over the ensuing several hours improving saturations from the 80s to 100. Pitman submitted a response to this case report stating that he believes the imminent cause of this patient’s pulmonary edema to be the 2200 mL of IV fluid.15 He then describes a formula that has been shown to be safe for tumescent liposuction of up to 6 L. He suggests limiting IVF intraop to KVO max 100 to 300 cc. He uses 0.5% lidocaine + 1:1,000,000 epinephrine for the injectate solution and typically gives up to 40 mg/kg. see fig from pitman. At the conclusion of surgery the aspirate is measure and compared to the total injectate seeking a 2:1 ratio for injectate (infiltrate):aspirate. If this ratio is <2:1,>2:1, then no IVF are given. He states that he has experienced no adverse events in over 1000 patients using this formula. Pitman also states that for his procedures using the tumescent technique, he has calculated blood loss at 7.8% of aspirate volume (78cc blood per 1000cc aspirated).Grazer has written about the dangers associated with the tumescent technique and reports that most morbidity and mortality is associated with poorly trained physicians performing very large aspiration (~10L) in office type settings. Furthermore, large amounts of lidocaine (40 to 70 mg/kg) are being used in these procedures resulting in toxicity of both lidocaine and epinephrine. He also emphasized pulmonary edema as a problem. In another review, Grazer discussed lidocaine toxicity. He points out that therapeutic plasma lidocaine levels are between 1.5 mcg/mL and 5 mcg/mL total lidocaine, and this is different from reported levels that only measure active drug (unbound) which is 0.5 to 1.5 mcg/mL. Lidocaine is only active when unbound, and 60 to 70% is bound in healthy individuals: to alpha 1 glycoprotein (50%), albumin 25%, and other miscellaneous proteins (25%). Grazer notes that patients undergoing liposuction have increased FFA levels which displace lidocaine from its binding sites on proteins, which will increase the unbound active fraction, increasing the potential for toxicity. They also note that with lidocaine dosages in the tumescent technique, they have measured total lidocaine plasma levels at <1 href="http://www.blogger.com/post-create.g?blogID=8800896920630287466#jong">16 states that the most common cause of mortality from liposuction is PE, thus spawning the practice of giving 5% etOH in D5W although this is only supported by anecdotal evidence.In summary, the approach to a patient who is to undergo liposuction under anesthesia care requires consideration of more than the standard preoperative history and physical, intraoperative monitoring and post operative care. There should be awareness of the liposuction technique used (superwet, tumescent) and more importantly an understanding of the injectate to aspirate ratio to expect during the procedure since this is critical in determining the volume status of your patient. A clear awareness of expected and actual aspirate volumes is necessary as well to determine fluid requirements and foresee potential risks to the patient. Also, a general understanding of L.A. toxicity is necessary as well as the amount of lidocaine your patient receives on a per kg basis. In addition the amount of epinephrine is important since this is almost universally used in wetting solutions. Finally, some surgeons may ask for a 5% alcohol in dextrose solution be used. Extensive searches in pub med and on the web by myself have proven futile in turning up any articles dedicated to the use of this technique in liposuction. Only peripheral mention of this technique is made in several articles which discuss liposuction and it is noted in each of the articles that there is no evidence to suggest that it is beneficial. Nevertheless, if the surgeon requests this infusion, (in hopes to reduce the risk of fat embolism or pulmonary embolism), it1. Trott SA, Beran SJ, Rohrich RJ, Kenkel JM et al. Safety considerations and fluid resuscitation in liposuction: An analysis of 53 consecutive patients Plast Reconst Surg. 1998; 102: 2220-29.Klein, J. A. Tumescent technique for local anesthesia improves safety in large-volume liposuction. Plast. Reconstr. Surg. 92: 1085, 1993Klein, J. A. The tumescent technique: Anesthesia and modified liposuction technique. Dermatol. Clin. 8: 425, 1990Lillis, P. The tumescent technique for liposuction surgery. Dermatol. Clin. 8: 439, 1990Klein, J. A. Tumescent technique for regional anesthesia permits lidocaine doses of 35 mg/kg for liposuction. J. Dermatol. Surg. Oncol. 16: 248, 1990Fodor, P. B. Wetting solutions in aspirate lipoplasty: A plea for safety in liposuction (Editorial). Aesthetic Plast. Surg. 19: 379, 1995.Pitman, G. H. The role of subcutaneous infiltration in suction-assisted lipoplasty: A review (Discussion). Plast. Reconstr. Surg. 99: 520, 1997.Gilliland MD, and Coates N. Tumescent liposuction complicated by pulmonary edema. Plast. Reconstr. Surg. 99: 215, 1997.Grazer FM, and Meister FL. Complications of the tumescent formula for liposuction (Editorial). Plast. Reconstr. Surg. 100: 1893, 1997.Grazer, F. M., and Meister, F. L. Factors contributing to adverse effects of the tumescent technique (surgical strategies). Aesthetic Surg. J. 17: 411, 1997Finley, R. K. and Shaffer, J. M. Parenteral fluid administration beneath the fascia lata. Am. J. Surg. 63: 337, 1944Pitman, G. H., Aker, J. S., and Tripp, Z. D. Tumescent liposuction. Clin. Plast. Surg. 23: 633, 1996.Samdal, F., Amland, P. F., and Bugge, J. F. Blood loss during liposuction using the tumescent technique. Aesthetic Plast. Surg. 18: 157, 1994.Rohrich RJ, Leedy JE, Swamy RBA, Brown SA, Coleman J. Fluid resuscitation in liposuction: A retrospective Review of 89 consecutive patients. Plast Reconstr Surg. 2006; 117: 431-5.Rohrich RJ, Leedy JE, Swamy RBA, Brown SA, Coleman J. Fluid resuscitation in liposuction: A retrospective Review of 89 consecutive patients. Plast Reconstr Surg. 2006; 117: 431-5.Grazer FM, De Jong RH. Perioperative management of Cosmetic liposuction. Plast Reconstr Surg. 2001; april.