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Infections associated with regional anesthesia may be more prevalent than previously thought and are associated with various risk factors. In general, central neuraxial block should not be performed in patients with untreated systemic infection except in the most extraordinary circumstances. Strict adherence to aseptic technique, including masks and gloves, skin disinfection, and maintaining sterility of equipment, is critical to avoid infection and colonization of potentially harmful bacteria. Epidural abscess is most likely to occur in immunocompromised patients with prolonged durations of epidural catheterization, with the most common causative organism being S. aureus. In contrast, meningitis following neuraxial blockade occurs more frequently in healthy individuals who have undergone uneventful spinal anesthesia. In general, neuraxial blocks in patients with preexisting viral disease (herpes, HIV) or who are immunocompromised are safe; however, the usual precautions and safety measures are still recommended. The patient care team must be vigilant of any signs or symptoms of infection so that the source can be identified and treatment be initiated as early as possible.

Although individual cases have been reported in the literature, serious infections of the central nervous system (CNS) such as arachnoiditis, meningitis, and abscess following spinal or epidural anesthesia are rare. However, recent epidemiologic series from Europe suggest that the frequency of infectious complications associated with neuraxial techniques may be increasing. Importantly, while meningitis and epidural abscess are both complications of neuraxial block, the risk factors and causative organisms are disparate. For example, staphylococcus is the organism most commonly associated epidural abscess; often these infections occurred in patients with impaired immunity. Conversely, meningitis follows dural puncture, and is typically caused by alpha-hemolytic streptococci, with the source of the organism the nasopharynx of the proceduralist. In order to reduce the risk of serious infection following neuraxial blockade, the clinician must be knowledgeable in the pathogenesis of CNS infections, patient selection, and use of meticulous aseptic technique. Finally, since delay in the diagnosis may result in morbidity and even death, it is crucial to be aware of the presenting signs and symptoms of meningitis and epidural abscess.

Summary Background: It is assumed that those children with known or suspected neuromuscular disorders (NMD) are at increased risk for malignant hyperthermia (MH). Despite the lack of conclusive data, most of these children are managed with a nontriggering anesthetic. This study examined the risk of MH in children exposed to a triggering anesthetic while undergoing muscle biopsy for suspected NMD. Methods: Between 1992 and 2005, the medical records of 351 children under 21 years of age were identified as having undergone muscle biopsy for suspected NMD. Of these, only 274 received a volatile anesthetic agent or succinylcholine and were included for study. Records were examined for evidence of MH or rhabdomyolysis. Results: No patient exhibited signs or symptoms suggestive of MH. One patient was found, by muscle biopsy, to have evidence of rhabdomyolysis prior to exposure to a volatile anesthetic. Of 274 patients, only three received succinylcholine. None developed MH or rhabdomyolysis. The estimated risk of a patient with suspected NMD developing MH as a result of exposure to volatile anesthetic agents during muscle biopsy is 1.09% or less. Conclusion: The estimated risk of MH or rhabdomyolysis is 1.09% or less in a diverse population of children with suspected NMD.

Thyrotoxic periodic paralysis (TPP) is a disease characterized by recurrent episodes of paralysis and hypokalemia during a thyrotoxic state. The disease primarily affects people of Asian descent, but can affect other ethnic groups. In Asians, the symptoms of thyrotoxicosis are distinct and usually precede the first paralytic episode, whereas in non-Asian populations, paralysis is the presenting symptom. If TPP has not been diagnosed and the patient has a surgical procedure during general or regional anesthesia, symptoms of the disease may be confused with other adverse perioperative events such as delayed recovery from neuromuscular paralysis. No specific anesthetic regimen is superior. Current TTP treatment recommendations involve treating the underlying hyperthyroid state. Other modalities such as beta-blockade and potassium replacement are also important in the acute paralytic state. Future diagnostic and treatment innovations may lie in the genetic and molecular understanding of this disease. We present a case of an Asian male with known TPP undergoing general anesthesia, a brief case series involving 5 patients, and a review of the literature.

To describe the anesthetic management of a patient with extreme obesity undergoing bariatric surgery whose intraoperative narcotic management was entirely substituted with dexmedetomidine.We describe a 433-kg morbidly obese patient with obstructive sleep apnea and pulmonary hypertension who underwent Roux-en-Y gastric bypass. Because of the concern that the use of narcotics might cause postoperative respiratory depression, we substituted their intraoperative use with a continuous infusion of dexmedetomidine (0.7 microg.kg(-1).hr(-1)). The anesthesia course was uneventful, and the intraoperative use of dexmedetomidine was associated with low anesthetic requirements (0.5 minimum alveolar concentration). After completion of the operation and after tracheal extubation, the dexmedetomidine infusion was continued uninterrupted throughout the end of the first postoperative day. The analgesic effects of dexmedetomidine extended narcotic-sparing effects into the postoperative period; the patient had lower narcotic requirements during the first postoperative day [48 mg of morphine by patient-controlled analgesia (PCA)] while still receiving dexmedetomidine, compared to the second postoperative day (morphine 148 mg by PCA) with similar pain scores.Dexmedetomidine may be a useful anesthetic adjunct for patients who are susceptible to narcotic-induced respiratory depression. In this morbidly obese patient the narcotic-sparing effects of dexmedetomidine were evident both intraoperatively and postoperatively.

Neuraxial anesthesia and analgesia provide several advantages over systemic opioids, including superior analgesia, reduced blood loss and need for transfusion, decreased incidence of graft occlusion, and improved joint mobility following major knee surgery. 1-4 New challenges in the management of patients undergoing neuraxial block have arisen over the last 2 decades, as medical standards for the prevention of perioperative venous thromboembolism were established. 5,6 Concern for patient safety in the presence of potent antithrombotic drugs has resulted in avoidance of regional anesthesia. Indeed, perioperative anesthesia and analgesia are often determined by the antithrombotic agent. 7 Conversely, although the anesthesia community is well aware of the potential for spinal bleeding, other specialties have only recently become cognizant of the risk, as documented by case reports

Partly based on magnetic resonance imaging studies, the "plumb-bob" approach for brachial plexus block was designed to minimize the risk of pneumothorax. Nevertheless, the risk of pneumothorax has remained a concern. We analyzed magnetic resonance images from 10 volunteers to determine whether the risk of pneumothorax was decreased with this method. The recommended initial needle direction is anteroposterior through the junction between the lateral-most part of the sternocleidomastoid muscle and the superior edge of the clavicle. If the initial placement is not successful, the brachial plexus may be sought in sectors 20 degrees -30 degrees cephalad or caudad to the anteroposterior line in a sagittal plane through the insertion point. We found that the anteroposterior line reached the pleura in 6 of 10 volunteers without prior contact with the subclavian artery or the brachial plexus, but always with contact with the subclavian vein. To reach the middle of the brachial plexus, a mean cephalad redirection of the simulated needle by 21 degrees was required (range from 41 degrees cephalad to 15 degrees caudad in one case). We conclude that the risk of contacting the pleura and the subclavian vessels may be reduced by initially directing the needle 45 degrees cephalad instead of anteroposterior. If the brachial plexus is not contacted, the angle should be gradually reduced.In magnetic resonance images of volunteers, simulated needle passes with the "plumb-bob" approach to the supraclavicular brachial plexus block were analyzed for precision and risk profile. To avoid needle contact with the lung, the subclavian vein, and the subclavian artery, our results suggest a change in the method's initial needle direction.

In Christian legend, the Holy Grail was the cup used by Jesus at the Last Supper. It was said to possess miraculous powers, and in Medieval times its acquisition became the quest of every worthy knight, requiring dedication, single-mindedness, and vision. Not surprisingly, with such lofty prerequisi

PINAL HEMATOMA is a rare and potentially catastrophic complication of spinal or epidural anesthesia. The actual incidence of neurologic dysfunction resulting from hemorrhagic complications associated with central neural blockade is unknown; however, the incidence cited in the literature is estimated to be less than 1 in 150,000 epidural and less than 1 in 220,000 spinal anesthetic cases. 1 Hemorrhage into the spinal canal most commonly occurs in the epidural space because of the prominent epidural venous plexus. Although hemorrhagic complications can occur after virtually all regional anesthetic techniques, bleeding into the 'spinal canal is perhaps the most serious hemorrhagic complication associated with regional anesthesia because the spinal canal is a concealed and-nonexpandable space. Spinal cord compression from spinal hematoma may result in nenrologic ischemia and paraplegia. Spinal hematoma may occur due to vascular trauma from needle or catheter placement into the subarachnoid or epidural space (Fig 1). However, it also may occur in association with neoplastic disease or pre-existing vascular abnormalities. Of special interest to the anesthesiologist are those spinal hematomas that have occurred spontaneously with or without the presence of antiplatelet or anticoagulation therapy. Over 100 spontaneous epidural hematomas have been reported, 25% of which are associated with anticoagulation therapy. 2 In a review of the reports appearing in the literature between 1906 and 1994, Vandermeulen et al 3 discussed 61 cases of spinal hematoma associated with epidural or spinal anesthesia. In 42 of the 61 (68%) patients, the spinal hematomas associated with central neural blockade occurred in patients with evidence of hemostatic abnormality. Twenty-five of the patients had received intravenous or subcutaneous heparin; as they were undergoing a vascular surgical procedure, an additional five patients were presumably administered heparin. In addition, 12 patients had evidence of coagulopathy or thrombocytopenia or were treated with antiplatelet medications (aspirin, indomethacin, ticlopidine), oral anticoagulants (phenprocoumone), thrombolytics (urokinase), or dextran 70 immediately before or after the spinal or epidural anesthetic. Needle and catheter placement was reported to be difficult in 15 (25%) or bloody in 15 (25%) patients. Thus, in 53 of the 61 (87%) cases, either a clotting abnormality or needle placement difficulty was present. To reduce the risk of spinal hematoma associated with central neural blockade, it is necessary to understand the mechanisms of blood coagulation, the pharmacologic properties of the anticoagulant and antiplatelet medications, and the clinical studies involving patients undergoing central neural blockade while receiving these medications. While this discussion will deal mainly with continuous techniques of major conduction blocks and anticoagulants, the same principles apply to all regional anesthetic techniques.

We describe 49 neurologically asymptomatic patients with persistently increased serum creatine kinase (CK) levels (idiopathic hyperCKemia or IHCK) who were referred to our institution for diagnostic muscle biopsy, including malignant hyperthermia (MH) susceptibility testing between 1979 and 1993. Muscle biopsy samples of the vastus lateralis were obtained for histologic analysis and MH contracture testing with halothane and caffeine. From 1979 to November 1987, patients were tested for MH in accordance with a standardized institutional protocol. After November 1987, contracture testing was performed according to the recently adopted North American MH Group protocol. In both protocols, a patient was considered to be MH susceptible (MHS) if one or more muscle strip demonstrated an abnormal contracture response after exposure to 3% halothane, 2% halothane, or caffeine alone. Twenty-four of the 49 IHCK patients (49%) had positive contracture tests. No significant correlation was found between the magnitude of CK increase and the incidence of MHS or histologic abnormalities. Unexplained persistently increased CK levels in an otherwise healthy patient should alert the anesthesiologist to the possibility of MHS and/or myopathy.

Malignant hyperthermia (MH) is a rare genetic trait characterized by potential life-threatening episodes of hypermetabolism, hyperthermia, and muscle rigidity when susceptible humans or animals are exposed to triggering drugs. The role of norepinephrine (NE) in triggering MH is controversial. The purpose of this study was to show that NE does not initiate nor speed the onset of MH in susceptible swine exposed to known triggering drugs. Three groups of MH susceptible (MHS) pigs were exposed to two times the minimum alveolar anesthetic concentrations (MAC) halothane (2%) for 60 min and monitored continuously until a PaCO2 of 70 mm Hg was obtained as an end point for fulminant MH. This dose of halothane is associated with significant hypotension which was addressed by three modalities: no treatment; NE infusion at 8 micrograms.kg-1.min-1; and intraaortic balloon pump (IABP) with 1:1 augmentation (7.0-mL balloon catheter). NE and epinephrine (Epi) plasma levels were determined at 15-min intervals and at trigger time. All animals developed signs of MH during the study. There was no difference in pHa, lactate, PaCO2, or temperature at control or trigger times between groups. Time to trigger was longer in the untreated group compared to both the NE and the IABP groups which were equal. The NE group had greater NE and Epi plasma levels at all times than either the untreated or IABP group and the levels increased at each sample time. The IABP group had increased NE levels at time of trigger compared to control time period, however, Epi levels did not increase. In the untreated group, individual animals had marked increases in NE levels, but extreme variability in response prevented achievement of a single mean change. This group showed no increase in plasma Epi levels throughout the study. There was no difference in NE levels between the untreated and IABP groups. Three animals in the untreated group died prior to trigger due to complications of hypotension. In conclusion, addition of exogenous NE in high doses did not enhance triggering of MH. The large dose NE infusion resulted in increased total catecholamines throughout the study in the NE group with no effect on time to MH trigger compared to animals where mean arterial pressure (MAP) was maintained by IABP. Animals in all three groups with times to trigger of less than 30 min had significantly higher MAPs at control, 15 min, and trigger time than those with times to trigger of greater than 30 min. We conclude that NE does not trigger MH and that severe reduction of MAP delays the the onset of MH in susceptible swine.

Objective To compare side effects after intravenous administration of dantrolene sodium in subjects susceptible to and those nonsusceptible to malignant hyperthermia (MHS and MHN, respectively). Design We studied two groups, six patients thought to be MHS and six assumed MHN subjects, and analyzed their responses to intravenously administered dantrolene. Material and Methods Dantrolene (3 mg/kg) was administered slowly into an antecubital vein, and blood samples were withdrawn from the other arm at 5 and 25 minutes after infusion. Shortly thereafter, all subjects underwent a clinical neurologic assessment, and side effects were graded subjectively by the study participants. RESULTS Side effects occurred in all subjects. Visual symptoms occurred more commonly in MHN than in MHS subjects. Subjective muscle weakness of the extremities, dizziness, and fatigue occurred more commonly and were more severe in MUS patients than in MHN subjects. Conclusion In patients recovering from an episode of malignant hyperthermia for which dantrolene has been administered, these side effects should be considered. Although the presence of side effects does not outweigh the usefulness of this drug in treating malignant hyperthermia, it may be a consideration in deciding whether to administer dantrolene prophylactically before surgical procedures in known or suspected MHS patients.

One thousand orthopedic procedures in 924 patients given spinal or epidural anesthesia were prospectively studied to determine the risk of hemorrhagic complications associated with regional anesthesia. A history of excessive bruising or bleeding was elicited in 115 (12%) patients. Preoperative antiplatelet medications were taken by 386 (39%) patients. Aspirin was the most frequently reported antiplatelet drug and was taken by 193 patients. Subcutaneous heparin was administered to 22 patients before surgery on the operative day. One patient of 774 tested had a preoperative platelet count less than 100,000/mm3. In addition, 26 of 171 preoperative prothrombin times and 10 of 115 preoperative activated partial thromboplastin times were longer than normal. Only 31 preoperative bleeding times were performed; five were prolonged. There were no documented spinal hematomas (major hemorrhagic complications). Blood was noted during needle or catheter placement (minor hemorrhagic complication) in 223 (22%) patients, including 73 patients with frank blood in the needle or catheter. Preoperative antiplatelet therapy did not increase the incidence of minor hemorrhagic complications. However, female gender, increased age, a history of excessive bruising/bleeding, surgery to the hip, continuous catheter anesthetic technique, large needle gauge, multiple needle passes, and moderate or difficult needle placement were all significant risk factors. The lack of correlation between antiplatelet medications and bloody needle or catheter placement (producing clinically insignificant collections of blood in the spinal canal or epidural space) is strong evidence that preoperative antiplatelet therapy is not a significant risk factor for the development of neurologic dysfunction from spinal hematoma in patients who undergo spinal or epidural anesthesia while receiving these medications.

SUMMARY Unexplained significant intraoperative hyperthermia can be caused by a variety of diverse conditions. Some of these, such as pheochromocytoma, sepsis, thyrotoxicosis, and hypermetabolism associated with osteogenesis imperfecta, may closely mimic MH. Determination of the etiology is important in determining appropriate management of the patient as well as family counseling and subsequent evaluation. Other causes of hyperthermia in the operating room include central nervous system dysfunction, blood transfusion reactions, iatrogenic overheating, and genetic conditions associated with abnormal thermoregulatory control. Core temperature monitoring is an important feature of safe anesthetic management. Understanding of the non-MH causes of intraoperative hyperthermia will aid the anesthesiologist in managing this infrequent but worrisome event.

The diagnosis of an acute malignant hyperthermia reaction by clinical criteria can be difficult because of the nonspecific nature and variable incidence of many of the clinical signs and laboratory findings. Development of a standardized means for estimating the qualitative likelihood of malignant hyperthermia in a given patient without the use of specialized diagnostic testing would be useful for patient management and would promote research into improved means for diagnosing this disease.Using the Delphi method and an international panel of 11 experts on malignant hyperthermia, a multifactor malignant hyperthermia clinical grading scale comprising standardized clinical diagnostic criteria was developed for classification of existing records and for application to new patients.This scale ranks the qualitative likelihood that an adverse anesthetic event represents malignant hyperthermia (malignant hyperthermia event rank) and that, with further investigation of family history, an individual patient will be diagnosed as malignant hyperthermia susceptible (malignant hyperthermia susceptibility rank). The assigned rank represents a lower bound on the likelihood of malignant hyperthermia. The clinical grading scale requires the anesthesiologist to judge whether specific clinical signs are appropriate for the patient's medical condition, anesthetic technique, and surgical procedure.The malignant hyperthermia clinical grading scale is recommended for use as an aid to the objective definition of this disease. It use may improve malignant hyperthermia research by allowing comparisons among well-defined groups of patients. This clinical grading system provides a new and comprehensive clinical case definition for the malignant hyperthermia syndrome.

Numerous studies have documented the safety of neuraxial anesthesia and analgesia in the anticoagulated patient. Patient management is based on appropriate timing of needle placement and catheter removal relative to the timing of anticoagulant drug administration. Familiarity with the pharmacology o

Summary Regional anesthesia can be safely performed in patients receiving anticoagulant or antiplatelet therapy as attested by studies reported by Rao and El-Etr,26 Horlocker et al,11 and Odoom and Sih.21 Therefore, based on the available information, we believe the following recommendations are appropriate: 1. It is generally agreed that in the absence of extraordinary indications, spinal and epidural anesthesia are contraindicated in patients within 24 hours of receiving thrombolytic therapy, having known coagulopathies, or having significant thrombocytopenia. 2. Although the data by Odoom and Sih21 are reassuring, central neuraxis blockade should probably be avoided in fully anticoagulated patients. However, patients who have received only one or two doses of an oral anticoagulant will not have an increased prothrombin time and may safely undergo regional anesthesia. A prothrombin time may be measured before needle placement if necessary. 3. Patients fully anticoagulated with a continuous heparin infusion should have the infusion discontinued 4 to 6 hours before needle or catheter placement. Subcutaneous low-dose heparin should also not be administered within 4 to 6 hours of a spinal or epidural anesthetic to allow for normalization of the activated partial thromboplastin time. Laboratory verification may be performed before initiation of regional blockade. 4. Epidural or spinal anesthesia followed by systemic heparinization is probably safe, provided adequate precautions are taken.18, 26 Heparinization should not be initiated for at least an hour after needle placement.18, 28 In addition, patients also receiving antiplatelet medications who will undergo subsequent heparinization appear to be at increased risk for spinal hematoma and need to be followed closely. Rao and El-Etra26 recommended careful monitoring of the activated clotting time during heparinization. If needle placement is traumatic or difficult, the decision to proceed with surgery should be reevaluated. Removal of an indwelling epidural catheter in a patient receiving intravenous or subcutaneous heparin should occur 4 to 6 hours after the last heparin dose, and anticoagulation should not be initiated for at least 1 hour after catheter removal. 5. Epidural and spinal anesthesia can be safely performed in a patient receiving antiplatelet therapy.11 Patients with a history of bleeding or bruising may be further evaluated with a preoperative bleeding time. 6. The use of small-gauge needles and the midline approach (thereby avoiding the lateral aspect of the epidural venous plexus) allows more atraumatic needle placement. Epidural catheters should not be inserted more than 3 to 4 cm into the epidural space in order to minimize trauma to the epidural venous structures. 7. Short-acting local anesthetics should be used in patients at increased risk in order to promptly evaluate their neurologic status postoperatively. Likewise, an epidural blockade should be allowed to regress sufficiently before initiating a continuous local anesthetic infusion for postoperative analgesia. A narcotic rather than local anesthetic infusion would allow continuous monitoring of neurologic function and may be a more prudent choice in these patients. It is also worth noting that epidural hematomas have also occurred spontaneously in patients on anticoagulant or antiplatelet medications in the absence of trauma or needle placement.15 The decision to perform spinal or epidural anesthesia on a patient receiving these medications should be made on an individual basis, weighing the risks of hemorrhagic complications and benefits of regional anesthesia for a specific patient. The patient's history should be reviewed to discover any underlying medical conditions with associated bleeding tendencies that would increase the risk. Because it is difficult to predict an individual patient's response to antiplatelet or anticoagulant therapy, laboratory verification may be helpful before initiation of spinal or epidural anesthesia (Table 1). It is most useful clinically to evaluate coagulation parameters that are specific to the clotting defect expected such as the prothrombin time in patients on oral anticoagulants or the activated thromboplastin time in heparinized patients. Although the role of tests such as the thromboelastogram, which measure overall coagulation function, has not been defined at this time, they may prove useful in the future. Needle and catheter placement should be accomplished as atraumatically as possible, and subsequent anticoagulation should be carefully monitored to minimize hemorrhagic complications. The patient should be monitored closely in the perioperative period for early signs of cord compression such as backache or neurologic dysfunction, and any clinical or radiologic evidence of cord compression should be followed by an immediate decompressive laminectomy because recovery is unlikely if surgery is delayed for more than 12 hours.8

Malignant hyperthermia (MH) is a rare clinical syndrome characterized by hypermetabolism and triggered by specific anesthetic agents. The mechanism of this abnormal reaction is due to uncontrolled calcium flux in the skeletal muscles resulting in a variable clinical syndrome of muscle rigidity, respiratory and metabolic acidosis, and elevation of temperature. The specific genetic defect underlying this condition has not been identified in humans, though in susceptible swine a mutation of the gene for the ryanodine receptor, a large protein which comprises the calcium channel in the sarcoplasmic reticulum, has been identified recently. Inheritance in humans appears to be autosomal dominant with variable penetrance. Patients with MH rarely have physical or laboratory signs of muscle disease. However, scattered case reports and investigations of individuals with known myopathies and other muscle related problems, such as acute rhabdomyolysis or idiopathic persistently elevated creatine kinase, suggest a possible association of MH with a variety of neuromuscular diseases and stress syndromes. This association is very strong in the case of central core disease (CCD) where it is supported by clinical and laboratory evidence, including the proximity of the CCD gene to the ryanodine receptor gene on chromosome 19. A variety of other diseases have been implicated and can be classified as possibly associated (King-Denborough syndrome, Duchenne muscular dystrophy) or unlikely to be associated (myotonia congenita, sudden infant death syndrome, limb girdle dystrophy, neuroleptic malignant syndrome, etc.).(ABSTRACT TRUNCATED AT 250 WORDS)

IMPLICATIONS Atrial septal defect is usually diagnosed and surgically repaired in childhood. We present a case of previously asymptomatic atrial septal defect that presented during total hip arthroplasty during general anesthesia in a 72-yr-old woman. Intraoperative transesophageal echocardiography assisted in the diagnosis and in determining the appropriate treatment.

Halothane, in a dose-dependent manner, induced the release of intracellular Ca2+ in hepatocytes prepared from swine. The magnitude of the release induced by halothane was greater for hepatocytes prepared from animals susceptible to malignant hyperthermia (MH) than for those from normal swine. Two different methods were used to ascertain the release of Ca2+ induced by halothane: 1) the release of 45Ca2+ from nonmitochondrial stores of saponin-permeabilized hepatocytes was measured; and 2) changes in luminescence from intact hepatocytes loaded with the Ca2(+)-sensitive photoprotein aequorin were recorded. It was also observed that, although 1,4,5-inositol trisphosphate (IP3), guanosine-5-triphosphate, and arachidonic acid all induced a significant release of 45Ca2+ from permeabilized swine hepatocytes, only the quantities of 45Ca2+ released by IP3 were significantly greater for the hepatocytes prepared from the animals susceptible to MH. These data indicate an abnormal Ca2+ homeostasis in hepatocytes isolated from swine susceptible to MH, which supports the hypothesis that membrane systems from multiple organs may be affected in this genetic disorder.

Neurologic complications associated with regional anesthesia and pain medicine practice are extremely rare. The ASRA Practice Advisory on Neurologic Complications in Regional Anesthesia and Pain Medicine addresses the etiology, differential diagnosis, prevention, and treatment of these complications. This Advisory does not focus on hemorrhagic and infectious complications, because they have been addressed by other recent ASRA Practice Advisories. The current Practice Advisory offers recommendations to aid in the understanding and potential limitation of neurologic complications that may arise during the practice of regional anesthesia and pain medicine.

A potentially fatal condition, yet preventable, malignant hyperthermia (MH) lacks a satisfactory noninvasive diagnostic test. Studying the effects of intravenous dantrolene (3 mg/kg) on electrically stimulated skeletal muscle, we found that this approach does not conclusively distinguish between normal humans and those susceptible to malignant hyperthermia but nonetheless yielded important information about the action of dantrolene in man and in MH. Supramaximal single- and multiple-pulse stimulation of the common peroneal nerve produced stable torque responses of the dorsiflexor muscles (monitored in vivo), which dantrolene suppressed. With the multiple-pulse stimulation (5-6 pulses) this torque suppression was significantly less in MH-susceptible subjects than in control subjects. This distinction, also observed in MH swine, confirms this animal as a good model for human MH. That dantrolene's effect in MH can be more completely reversed with high frequency stimulation is intriguing; presumably, excitation-contraction coupling differs in MH and normal muscle.

Infectious complications may occur after any regional anesthetic techniques, but are of greatest concern if the infection occurs around the spinal cord or within the spinal canal. Possible risk factors include underlying sepsis, diabetes, depressed immune status, steroid therapy, localized bacterial colonization or infection, and chronic catheter maintenance. Bacterial infection of the central neural axis may present as meningitis or cord compression secondary to abscess formation. The infectious source for meningitis and epidural abscess may result from distant colonization or localized infection with subsequent hematogenous spread and central nervous system (CNS) invasion. The anesthetist may also transmit microorganisms directly into the CNS by needle/catheter contamination through a break in aseptic technique or passage through a contiguous infection. An indwelling neuraxial catheter, although aseptically sited, may be colonized with skin flora and consequently serve as a source for ascending infection to the epidural or intrathecal space.

Perioperative hyperthermia is a serious and potentially life-threatening condition. The least common but most serious type, malignant hyperthermia (MH), is well documented in the literature. Some more common causes of perioperative hyperthermia include septicernia,' neuroleptic malignant syndrome.' thyrotoxic crisis," iatrogenic causes," and idiosyncratic drug reactions. With the exception of MH, these conditions are usually diagnosed by history and clinical examination and are rarely present initially during general anesthesia. Postoperative hyperthermia, probably the result of an episode of MH, was reported in the literature as early as 1900 by Moschowitz' and again by Ombredanne in 1929 and Guedel in 1937. Since that time, numerous articles have contributed to the understanding, diagnosis, and treatment of this rare genetic problem. MH is characterized by a hypennetabolic state following the administration of a "triggering" anesthetic that results in an increase in carbon dioxide production, heart rate, and later core temperature. This potentially life-threatening reaction is caused by a defect in the calcium-control mechanism in the sarcoplasmic reticulum of skeletal muscle. Under the appropriate triggering conditions, there is an increase in the concentration of myoplasmic calcium, failure of the sarcoplasmic reticulum to take up the calcium, and subsequent sustained muscle contraction associated with hypermetabolism. The adenosine triphosphate pump mechanism responsible for recycling calcium in the sarcoplasmic reticulum exhausts the available ox