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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.

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.

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.

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.

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

Masseter muscle rigidity has been identified as a possible risk factor for malignant hyperthermia (MH) and is usually noted in children receiving intravenously administered succinylcholine chloride after mask induction with halothane. Nondepolarizing muscle relaxants are considered safe for persons susceptible to MH. In this article, we present a case of clinically recognized jaw rigidity in the absence of succinylcholine after administration of a non-depolarizing muscle relaxant that was reported to the Malignant Hyperthermia Association of the United States hot line. The patient had recurrent jaw rigidity during subsequent anesthesia when a different non-depolarizing muscle relaxant was given. The North American MH Registry was then reviewed for similar cases. Three cases of masseter muscle rigidity in the presence of nondepolarizing muscle relaxants were discovered. Two of the patients were not found to be susceptible to MH; however, the third patient had positive findings on muscle biopsy. These cases do not provide enough information to confirm the ability of nondepolarizing muscle relaxants to cause jaw rigidity in the absence of MH.

SUMMARY Retrospective chart review (1978–1993) of 179 children less than age 18 (10.0 ± 3.8 SD yrs) undergoing muscle biopsy for determination of susceptibility to malignant hyperthermia provided data. One hundred and forty-six patients received femoral and lateral femoral cutaneous nerve blocks as their primary anaesthetic. We examined age, weight, duration of surgery, time to discharge from hospital, choice and dosage of local anaesthetics, choice and dosage of sedation, postoperative pain medications, and complications. All children receiving this form of anaesthesia remained outpatients. Between 1978 and 1985 procaine (10 mg·kg-1) with hyaluronidase or 2-chloroprocaine (12 mg·kg-1) provided nerve blockade; after 1985, lignocaine (6.8 mg·kg-1), or a combination of lignocaine or mepivacaine and 2-chloroprocaine, were the preferred agents. More recently the combination of 2-chloroprocaine and bupivacaine has been popular. Three patients required admission to the recovery room postoperatively, due to heavy sedation. Forty-three children (29%) received pain medication during recovery. Femoral and lateral femoral cutaneous block anaesthesia with light to moderate sedation is well tolerated in children undergoing anterior thigh procedures.

The relative safety of epidural catheter placement with subsequent heparinization has been well documented. However, what is the risk of neurologic sequelae in such patients who receive warfarin perioperatively? This study retrospectively evaluates the risk of spinal hematoma in patients receiving postoperative epidural analgesia while receiving low-dose warfarin after total knee replacement. All patients received low-dose warfarin to prolong the prothrombin time (PT) to 15.0-17.3 s (normal 10.9-12.8 s). There were 192 epidural catheters placed in 188 patients. All catheters were advanced through an 18-gauge needle. In 13 instances, blood was noted during needle and/or catheter placement. In addition to warfarin, 36 patients with indwelling catheters received nonsteroidal antiinflammatory drugs (NSAIDs). Epidural catheters were left indwelling 37.5 +/- 15 h (range 13-96 h). The mean PT was not increased beyond the normal range until the third postoperative day and did not reach 15 s until the seventh postoperative day. Cumulative warfarin dose at that time was 20.0 +/- 7.6 mg. Mean PT at the time of epidural catheter removal was 13.4 +/- 2 s. There were no signs of spinal hematoma. Although epidural catheter placement and subsequent anticoagulation with warfarin appears relatively safe, there is a large variability in patient response to warfarin; therefore, coagulation status should be monitored to avoid excessive prolongation of the PT, and the patient should be watched closely for evidence of spinal hematoma.

The purpose of this study was to gain new insights in the role of succinylcholine in the initiation of malignant hyperthermia (MH). The intravenous (i.v.) administration of succinylcholine (2.0 mg/kg) induced fasciculations and masseter spasm in both normal swine and those susceptible to MH. However, the amplitudes and durations of generalized fasciculations were significantly greater in the susceptible animals that subsequently developed a fulminant episode of MH: succinylcholine induced not only tachycardia, hyperthermia, contractures, and increases in PaCO2 and lactate, all classic indicators of an episode, but also an initial severe hypotension. The mean arterial pressure in these swine decreased from 115 +/- 6 mm Hg to 60 +/- 12 mm Hg (mean +/- SD), 1 min after the administration of succinylcholine. Normal swine developed neither cardiovascular effects nor altered metabolism in response to succinylcholine. The pretreatment of animals with a nondepolarizing muscle relaxant (pancuronium 0.1 mg/kg) minimized fasciculations induced by succinylcholine, but did not prevent the hypotension nor episodes of MH in the susceptible swine. In the pretreated and untreated susceptible swine, dantrolene was an equally effective treatment. Plasma catecholamine levels after succinylcholine administration were increased only in the susceptible swine without the pancuronium pretreatment. We concluded that the effects of succinylcholine on skeletal muscle and/or on other tissues play a significant role in the initiation of a MH episode in swine with this genetic disorder, and that these effects are not dependent on an abnormal sensitivity for succinylcholine-induced skeletal muscle fasciculations in these animals.

BACKGROUND Desflurane (difluoromethyl 1-fluoro 2,2,2-trifluoroethyl ether) is a new inhalational anesthetic currently under investigation for use in humans. Recently, the authors showed that desflurane is a trigger of malignant hyperthermia (MH) in susceptible swine. To date, there has been no in vivo comparison of the relative ability of inhalational anesthetics to trigger MH. The effects of desflurane, isoflurane, and halothane on six MH-susceptible purebred and six MH-susceptible mixed-bred Pietrain swine were examined. METHODS The animals were exposed to 1 MAC and 2 MAC (if MH was not triggered after 1 MAC hour) doses of each of the three volatile anesthetics in random sequence at 7-10-day intervals and changes in end-tidal CO2, arterial blood gases, serum lactate, core and muscle temperature, blood pressure, and heart rate were measured. RESULTS There was a statistical difference between anesthetics in the time required to trigger MH; halothane exposure resulted in the fastest onset of an MH episode (20 +/- 5 min), compared with isoflurane (48 +/- 24 min) and desflurane (65 +/- 28 min), both of which required significantly longer exposures. There was no statistical difference between the MH purebred and mixed-bred swine in the time required to trigger MH (defined as a PaCO2 of 70 mmHg) with a given agent, and time to triggering was also independent of the order of exposure to the three anesthetics. Malignant hyperthermia susceptibility was confirmed in ten surviving animals, by both in vivo succinylcholine challenge and in vitro contracture testing. CONCLUSIONS Although all three volatile anesthetics triggered MH, exposure to halothane resulted in significantly shorter times to MH triggering when compared with desflurane and isoflurane.

The in vitro contracture test determines the sensitivity of freshly obtained skeletal muscle specimens to caffeine or halothane applied to a bathing solution. Muscles from persons susceptible to malignant hyperthermia have lower contracture thresholds for these agents than do normal muscle. Thus, known concentrations of these agents must be accurately administered. We describe a system in which the bath concentrations of halothane (0 to 3%) are reproducible within 0.2% halothane from month to month. With use of this system, which includes an on-line gas analyzer, the measured halothane concentration within the bathing solution was independent of the performance of the vaporizer. The system is inexpensive and stable. The methods used to determine the bath concentrations of halothane and caffeine are reviewed. Finally, experimental equipment and a new recording system are described.

Desflurane (difluoromethyl 1-fluoro 2,2,2-trifluoroethyl ether: CF2-H-O-CFH-CF3) is a potent inhalation anesthetic agent being investigated for possible clinical use. The authors examined the effects of this agent on normal swine and those from a special breeding program that were considered purebred for susceptibility to malignant hyperthermia (MH). Animals were exposed to 1 or 2 MAC or both doses of desflurane and observed for changes in end-tidal CO2, arterial blood gases, lactate, catecholamines, core temperature, blood pressure, and heart rate. All normal swine tolerated exposure to desflurane without clinical signs of MH, but significant changes in heart rate and blood pressure were noted. In contrast, of six MH susceptible swine tested, two had unequivocal MH reactions to deflurane, defined by significant increases of end-tidal CO2 (greater than 50 mmHg), an increase in PaCO2 (greater than 70 mmHg), a decrease in blood pH (less than 7.30), an increase in blood lactate concentration, and an increase in core temperature. Two other susceptible swine showed equivocal signs of MH but not until desflurane had been administered for 40-60 min. Finally, two other susceptible swine showed no signs of MH after 60 min of exposure to 2 MAC desflurane. These latter four animals all developed episodes of MH immediately after intravenous succinylcholine (2 mg/kg). The increased PaCO2, blood lactate concentrations, and temperature, and the decrease in pH induced by desflurane, were successfully treated with dantrolene and supportive measures. All surviving animals were biopsied 1 to 2 weeks after the exposure to desflurane for in vitro contracture testing to confirm MH susceptibility.(ABSTRACT TRUNCATED AT 250 WORDS)

Peroneal nerve palsy is a rare complication of total knee arthroplasty (TKA). Previous studies have investigated surgical variables contributing to the development of peroneal nerve palsy after TKA, but have ignored potential medical and anesthetic risk factors. The charts of all patients undergoing TKA over a 1-yr period were retrospectively studied to identify medical, surgical, and anesthetic risk factors contributing to the development of peroneal nerve palsy after TKA; 361 TKAs were performed on 292 patients. There were eight peroneal nerve palsies in seven patients representing an overall incidence of 2.2%. A preoperative valgus deformity > or = 10 degrees, total tourniquet time > 120 min, the diagnosis of a preexisting neuropathy, and postoperative bleeding complications were identified as significant risk factors. Postoperative epidural analgesia was used in 108 cases and was not a significant risk factor for the development of peroneal palsy. However, all cases of peroneal nerve palsy with motor deficits and partial neurologic recovery occurred in patients receiving postoperative epidural analgesia and were diagnosed after discontinuation of the epidural infusion. Since diagnosis of peroneal nerve palsy may be delayed in patients with postoperative epidural analgesia, these patients must be monitored closely. A dilute local anesthetic or an opioid infusion is recommended for patients at increased risk, such as those with preexisting neuropathies.