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Print version ISSN 0034-7094
On-line version ISSN 1806-907X
Rev. Bras. Anestesiol. vol.56 no.1 Campinas Jan./Feb. 2006
Rhabdomyolysis in morbidly obese patient submitted to gastric bypass and during upper limb revascularization of pediatric patient. Case reports*
Rabdomiólisis en paciente obeso mórbido sometido a gastroplastia reductora y durante revascularización del miembro superior en paciente pediátrico. Relato de los casos
Maria Angélica Abrão, TSAI-II; Renata Gomes FerreiraI; Paulo Alípio Germano Filho, TSAII; Luiz Cláudio Lerner, TSAI
IAnestesiologista do Hospital Universitário
Clementino Fraga Filho, UFRJ
IIAnestesiologista do Hospital Geral de Bonsucesso
BACKGROUND AND OBJECTIVES:
Rhabdomyolysis is a syndrome caused by skeletal muscle injury. Its etiology
is broad with special interest when it is manifested as intra or post-anesthetic
complication. This report aimed at describing two cases of rhabdomyolysis in
the postoperative period of long procedures in morbidly obese and trauma injury
patients, emphasizing its correlation with anesthesia.
CASE REPORTS: The first case is a 39-year old, morbidly obese patient, BMI 62, submitted to laparoscopic gastric bypass under general anesthesia. In the postoperative period patient presented upper and lower limbs muscle weakness and changes in sensitivity evolving with muscle pain and reddish urine. Increased creatinokinase (CK) plasma levels confirmed the diagnosis of rhabdomyolysis. Patient was treated with forced and diuretic hydration, has not evolved with renal failure, but was discharged with muscular and neurological sequelae. The second case is a 7-year old child victim of accident with a glass door, who was submitted to emergency procedure for left upper limb revascularization. During anesthesia urine color has changed becoming reddish. Intravenous sodium bicarbonate and mannitol were administered to alkalinize the urine and increase urinary output. Patient was referred to the ICU where rhabdomyolysis was confirmed by increased CK enzyme and myoglobinuria. Patient was discharged 10 days later without sequelae.
CONCLUSIONS: Cases have shown risk factors for rhabdomyolysis and their relationship with anesthesia and surgery. Early diagnosis is critical for a fast and aggressive treatment to prevent more severe complications.
Key Words: ANESTHESIA, Pediatric; COMPLICATIONS: rhabdomyolysis; DISEASES, Morbid obesity; SURGERY, Abdominal: gastric bypass
JUSTIFICATIVA Y OBJETIVOS:
La rabdomiólisis es un síndrome derivado de la lesión el músculo
esquelético. Su etiología es variada, y tiene interés particular
en nuestra especialidad cuando se manifiesta como complicación perioperatoria.
El objetivo de este relato es mostrar dos casos de rabdomiólisis durante
el post-operatorio de intervenciones quirúrgicas prolongadas, en un paciente
con obesidad mórbida y otro con lesión traumática, enfatizando
su relación con la anestesia.
RELATO DE LOS CASOS: El primer caso es un paciente de 39 años, obeso mórbido con IMC 62, programado para gastroplastia reductora por laparotomía con anestesia general. En el post-operatorio presentó debilidad muscular en miembros superiores e inferiores con alteración de la sensibilidad. En la evolución hubo dolor muscular y orina rojiza. El diagnóstico de rabdomiólisis fue confirmado por el aumento de la enzima creatin-quinasa (CK) en el plasma. Tratado con hidratación y diuréticos no desarrolló insuficiencia renal pero tuvo alta con secuelas muscular y neurológica. El segundo caso es un niño de 7 años, víctima de un accidente con puerta de vidrio y fue operado de urgencia para revascularizar el miembro superior izquierdo. Presentó alteración del color de la orina, que se tornó rojiza durante la anestesia. Fue administrado bicarbonato de sodio y manitol por vía venosa, con el objetivo de alcalinizar la orina y aumentar el gasto urinario. Fue enviado al CTI donde se confirmó la hipótesis de rabdomiólisis por aumento de la enzima CK y por la mioglobinuria. Tuvo alta al 10º día de internación, sin secuelas.
CONCLUSIONES: Los casos presentados muestran algunos factores de riesgo para rabdomiólisis durante anestesia y cirugía. El diagnóstico precoz es importante y el tratamiento debe ser rápido y agresivo para evitar complicaciones más graves.
Rhabdomyolysis is a clinical and laboratorial syndrome caused by skeletal muscle injury, with the release in circulation of potentially toxic intracellular substances1.
It has a broad etiology, including trauma, drugs, muscle diseases, inherited enzymatic defects, malignant hyperthermia, infections and excessive physical exercise2. Clinical manifestation of the syndrome may vary from asymptomatic plasma increase of muscle enzymes to more severe cases associated to hydroelectrolytic disorders, compartmental syndrome and acute renal failure3.
It is more common than one can imagine4 because anesthesia promotes some risk situations such as prolonged immobilization, long surgical procedures and anatomically forced surgical positions3,5-10. In addition, obesity has been considered a risk factor 3,11,12.
Journals of anesthesia have few references to this type of complication5 and discussions on the subject are scarce. In pediatric patients, intraoperative rhabdomyolysis is still more seldom reported, being considered an uncommon disease for this age, with an incidence of 0.26%13.
Early diagnosis is critical for the early beginning of a compulsorily fast and aggressive treatment in an attempt to prevent more severe complications, such as acute renal failure and even death8,10.
This study describes two cases of rhabdomyolysis of different etiologies associated to the anesthetic period.
Male, African-Brazilian, morbidly obese patient, 39 years old, submitted to vertical laparoscopic Capella-Fobi gastric bypass. Obesity started 12 years ago reaching a maximum weight of 202 kg two years ago. At surgery, having lost 42 kg with diet and drugs, patient weighed 160 kg, was 1.74 m high with body mass index (BMI) of 62.
Patient presented systemic hypertension and diabetes mellitus type II, being under regular enalapril, metformin and glibenclamide. Preoperative blood count, coagulogram and electrolytes were normal and respiratory function test revealed mild restrictive disorder. Patient was not premedicated according to hospitals anesthesia rules for bariatric surgery. Patient received low molecular weight heparin 12 hours before anesthesia.
Monitoring consisted of cardioscopy, noninvasive blood pressure, pulse oximetry and capnography. Lactated Ringers infusion was started after venous puncture with 18G catheter. Baseline parameters were blood pressure 140 x 90 mmHg, heart rate 86 bpm, oxygen saturation 97% and sinusoidal cardiac rhythm.
Puncture at T10-T11 interspace was performed with patient in the sitting position and was followed by cephalad epidural catheter insertion after the second attempt. Patient received 3 mg epidural morphine. Patient was placed in 100% oxygen under mask for 5 minutes, followed by rapid sequence induction with thiopental, fentanyl and succinylcholine followed by eventless tracheal intubation. Anesthesia was maintained with 50% enantiomeric excess bupivacaine (S75-R25) in intermittent infusion by the epidural catheter, associated to inhalational anesthesia with O2, N2O and enflurane, and neuromuscular block with pancuronium. At the end of surgery, neuromuscular block reversal was attempted with intravenous neostigmine and atropine, but failed. Anesthesia lasted 8h30 minutes without intercurrences.
Patient was extubated in the ICU in the first postoperative day, remaining with the epidural catheter. Patient complained of upper limbs weakness`, which has evolved to lower limbs in subsequent days with difficulty to move in bed. Neurological evaluation has revealed upper limbs paresia, especially proximal, and lower limbs paresia, more severe on feet. Tactile, thermal and painful sensitivities were changed in forearms, arms and feet. Chest region was unchanged. Upper and lower limbs arterial pulses were normal.
On the 5th ICU day, patient started referring severe gluteus and lower limbs pain, in addition to preexisting neurological complaints. At this moment, urine became dark and reddish.
Rhabdomyolysis was confirmed by plasma creatinophosphokinase (CPK) enzyme dosage with levels of 32,l256 U/L. Other changes were seen in potassium (6/2 ,Eq/L) in the 7th postoperative day; TGO (529 U/L) and TGP (359 U/L) in the 4th day; and creatinine (1,8) in the 1st day. Urine test for abnormal elements and sediments (AES) showed hematuria and hemoglobinuria, however myoglobin was not dosed.
Patient was treated with vigorous hydration and loop diuretic (furosemide), with no need for other therapeutic measures due to favorable response with adequate diuresis and no signs of acute renal failure.
Patient was discharged 12 days later with improved pain and lab test results, however still with neurological symptoms of flaccid paresia on upper and lower limbs, in addition to paresthesias specially on hands and feet. Electroneuromyography performed seven months later showed predominantly sensory polineuropathy in all limbs, in more advanced phase in lower limbs.
Male, Caucasian patient, 7 years old, 29 kg, physical status ASA IE, victim of accident with a glass door. Patient presented multiple cuts on left forearm with fingers ischemia, decreased turgor, lack of fingers and fist flexion and anesthesia in autonomous areas of median and ulnar nerves of fingers.
Diagnosis was left forearm devascularization, median and ulnar nerves injuries and flexor mucle-tendinous injuries. Accident had happened 12 hours ago, with first aid at another hospital where 300 mL of packed red cells were infused. Patient arrived to the operating center lucid, oriented and with 34.8% hematocrit. Except for allergy to dipirone, nothing of clinical relevance was observed during preanesthetic evaluation.
Monitoring consisted of noninvasive blood pressure, pulse oximetry and capnography. General anesthesia was induced with 125 mg intravenous thiopental, followed by neuromuscular block with 15 mg atracurium and tracheal intubation. Anesthesia was maintained with O2/N2O/sevoflurane associated to axillary brachial plexus anesthesia with 37.5 mg of 0.25% bupivacaine, 1:200 000 epinephrine and 30 mg clonidine. At 7 anesthetic hours, urine became reddish. Hemodynamic and respiratory parameters were stable throughout the procedure with blood pressure of 100 x 60 mmHg, heart rate between 90 and 100 bpm, PETCO2 of 28 to 32 mmHg and SpO2 100%.
Rhabdomyolysis was suspected due to trauma, and mannitol and 8.4% sodium bicarbonate were started in the doses of 0.5 g.kg-1 and 100 mEq/m² in 24 hours, respectively, in addition to hydration with lactated Ringers. Total diuresis during the procedure was 1320 mL. Dosage of CPK, CK-MB, electrolytes, urea and creatinine was requested but has shown no changes at that moment (CPK = 153 U/L and CK-MB= 33U/L). Anesthesia lasted 9 hours and surgery consisted of broad débridement, flexor myorrhaphy and tenorrhaphy, median and ulnar nerves graft with sural nerve and ulnar and radial arteries revascularization with saphenous vein graft.
After the end of surgery, perivascular subclavian continuous brachial plexus block was performed with 0.125% bupivacaine in infusion pump for revascularized limb vasodilation and analgesia. Patient was extubated and referred to the pediatric ICU where over-hydration with 3000 mL/m2 crystalloids and 8.4% sodium bicarbonate was maintained with diuresis at approximately 200 m L/hour. There has been CPK levels increase in the 1st postoperative day (357 U/L - N < 170 U/L), peaking in the 2nd day (828 U/L). Myoglobin has followed CPK curve reaching 421 ng/mL (normal value = 19-92 ng/mL), also in the 2nd day.
There has been no change in CK-MB and in TGO, TGP, urea and creatinine. Electrolytes showed low potassium levels (K+ = 2,4) which were replaced. Urine remained dark in the 1st postoperative day, showing at urianalysis hemoglobin +++ and uncountable red cells. Hourly diuresis was maintained in approximately 5 to 6 mL/kg/hour. Patient evolved satisfactorily with CPK and myoglobin normalization and not developing other complications. Patient was discharged 10 days later with no sequelae.
Among different bariatric surgery complications, rhabdomyolysis has until recently been not emphasized by surgeons and anesthesiologists, may be due to lack of identification, especially considering subclinical cases where only CK and myoglobin changes and mild electrolytic changes point to the disease, being necessary a high suspicion index3,9 for the correct diagnosis which very often goes unnoticed. Khurana et al., in a retrospective analysis of 353 morbidly obese patients submitted to laparoscopic gastric bypass, have found 1.4% postoperative rhabdomyolysis.
All five patients were male, with mean BMI of 56 and presented in the immediate postoperative period myalgia in dependent regions and increased plasma creatinokinase (CK) enzyme levels, mean value of 19.680 U/L3. The author emphasizes that a higher incidence could have been found if CK dosage were a routine for these patients. Bostanjian et al.11 have reported six cases of rhabdomyolysis in 650 morbidly obese patients submitted to laparoscopic gastric bypass (0.9% incidence). All six cases started with gluteus bed wounds reaching mean CK levels of 26 000 U/L. Three cases (50%) evolved to acute renal failure needing dialysis and progressed to death.
Myocite injury, which is the early rhabdomyolysis phenomenon, may be caused by insufficient oxygen supply to the muscle or by its increased consumption. Clinical situations able to promote ischemia, hypotension or vasospasm would help triggering the syndrome6. During malignant hyperthermia (MH) excessive energetic consumption would start cell dysfunction. Another important etiologic factor is reperfusion, where increased free radicals in the circulation coming from temporarily ischemic tissues would injury microcirculation5.
During obese patients anesthesia, continuous and prolonged pressure of body weight against the hard operating table could injury skeletal muscles. Prolonged dependent areas pressure, such as gluteus, back and shoulders, decreases fascio-muscular compartment size, increasing compartmental pressure and impairing blood irrigation5.
Compartment pressure at rest varies from 9 to 15 mmHg5. Some authors consider that mean blood pressure in microcirculation is close to diastolic pressure and that 10 to 30 mmHg decrease would be enough to promote ischemia14. According to some total ischemia experiments, neurological injuries would be seen within 30 minutes of ischemia and muscle injuries within 2 hours; capillary endothelial changes and myoglobinuria within four hours5. However, in humans, most clinical ischemias maintain partial perfusion, which could increase the time for the beginning of tissue injury, making it unpredictable5.
Owen et al., in a study with healthy volunteers, have measured intracompartmental pressures through catheters inserted in forearm and leg, simulating some body positions with muscle compression15. When the muscle was submitted to external compression, there were changes in normal compartmental pressure at rest, reaching 200 to 225 mmHg in positions where the forearm was compressed by the body, or in forced genopectoral positions. Protection with 2.5 cm pads attenuated this pressure increase in just 16% and 23% in forearm and leg, respectively. Distal arterial pulse at compression remained palpable, except in some cases of genopectoral position and when forearm was compressed by the body.
In spite of that, there was blood flow impairment with pressures above 30 mmHg, causing muscle ischemia and evolving to necrosis if maintained for 4 to 8 hours. Increased hydrostatic pressure in a closed compartment, such as the fascia-muscle set, is able to decrease tissue capillary perfusion causing ischemia, necrosis and cell membrane injury, leading to the building up of fluid in tissues and to hypovolemia, triggering a vicious cycle where increased compartmental pressure and muscle tissue ischemia alternate. So, the compartmental syndrome, defined as increased hydrostatic pressure in the muscle, may follow rhabdomyolysis and vice-versa6. Some authors suggest that compartmental syndrome, rhabdomyolysis and crush syndrome would be variations of the same disease15.
Patients immobility and possibly long surgeries and anesthesia-inherent situations are primary risk factors for muscle injury and should be taken into consideration. There are literature reports on compartmental syndrome and rhabdomyolysis caused by forced anatomic positions during surgical procedures, such as patients submitted to lithotomy, especially during urologic and proctologic procedures, some of them followed by acute renal failure with the need for dialysis5,8,10,16,17. Prolonged surgery was common to all cases5,7,9,10 and obesity was present in some cases.
In forced lithotomy position, two factors may cause ischemia: marked knee and hip flexion bending vessels and decreased perfusion pressure at the raised extremity5. Other positions associated to muscle injury are prone9,18,19, lateral7,14,20 and supine21. Long surgical procedures are also major risk factors7,8,10,14,16,18-21. Most surgery-related rhabdomyolysis are associated to procedures lasting 4 to 11 hours, although critical time above which injuries are established is still to be determined16.
Early complaints vary from severe myalgias, muscle weakness, paresthesias, changes in sensitivity, or just signs of flare, ecchymosis, skin ulcers or limb edema. The most common and also more severe electrolytic disorder is hyperpotassemia, able to trigger arrhythmias1,22,23. Other changes are hyperphosphatemia, hypovolemia and oliguria22. Myoglobin deposition in renal tubules forms intraluminal cylinders leading to acute renal failure (ARF)8,23. More severe cases may be followed by disseminated intravascular coagulation, and lung and liver dysfunction1. In conscious patients, symptoms are absent in 50% of cases, even with expressive CK increase. Change in urine color indicating myoglobinuria should be investigated1 being an important alert in the anesthetized patient. In the pediatric patient of our report, this was the first symptom observed still during surgery and allowing for early treatment.
Classic rhabdomyolysis diagnosis depends on the identification of risk factors, on the presence of muscle pain, reddish or brown urine, and especially on the presence of muscle injury, CK and myoglobin indicators1,2,4. Final diagnosis is laboratorial and CT scan or MRI may be indicated to locate affected muscles when there is indication for surgical debridement22 or just to evaluate the severity of the injury.
CK plasma increase to 5 times its normal value (45-260 Ul/L) is enough for the diagnosis6,10,13. If the injury has a positive evolution, plasma decrease of approximately 39% a day is to be expected1. The primary objective of treating rhabdomyolysis is to prevent complications such as ARF and to control electrolytic disorders9. ARF in rhabdomyolysis patients has an incidence of 20% to 50%10 and is the major cause of disease-related death6. Relative hypovolemia, renal vasoconstriction and myoglobinuria are the three causal factors of ARF during rhabdomyolysis8. Myoglobin becomes nephrotoxic in the acid urine (pH < 5.6), when it is degraded in ferrohematin and globin16. Ferrohematin has a direct toxic effect on renal tubular epithelium6,16. Crystalloid infusion is titrated aiming at hourly diuresis of 100 to 500 mL.h-1.
Urine alkalinization is achieved with 8.4% sodium bicarbonate and pH should be maintained above 6.58. Frequent plasma and urinary pH lab control is important because they may not correlate23. If there is metabolic alkalosis (pH > 7.5), with urine pH < 6, acetalozamide, a carbonic anidrase inhibitor, may be added to increase bicarbonate excretion8,23. Urine alkalinization makes myoglobin more soluble, helping its excretion. Its normal solubility of 2% in acid pH of 5, increases to 80% with pH = 88. The attempt to remove myoglobin by plasmapheresis was not effective for the treatment, in spite of its plasma level decrease23.
Most popular diuretics are mannitol and furosemide. Mannitol has some advantages over loop diuretics not acidifying urine, being a plasma expander producing renal vasodilation, increasing glomerular filtration rate and being effective as free radicals carrier23. Fasciotomy may be indicated, depending on intra-compartmental pressure and on peripheral circulation involvement, however it increases infection and hospital stay indices6 and its indication should be carefully evaluated.
Skeletal muscle has notorious recovery ability, leaving no sequelae in most cases25. Sometimes, however, complaints of myalgia, muscle weakness and paresthesia persist for a long period9,10,14,16-18. In those cases, electroneuromyography is indicated to diagnose muscular or neurological injuries22.
Rhabdomyolysis in children may be associated to inherited muscle diseases, malignant hyperthermia and propofol continuous infusion syndrome being common heart arrest by hyperpotassemia4,25-28. Our pediatric patient had no signs of hypermetabolism during anesthesia, had no history of muscle diseases and has not received propofol So, evidences point to direct muscle trauma as the cause of myoglobinuria and rhabdomyolysis, although there are HM cases without a classic acute intraoperative episode29, manifested just by myoglobinuria, increased CK and postoperative ARF30,31.
Preventive measures to avoid or attenuate muscle injury may be directly related to intraoperative approaches, being the anesthesiologists responsibility to evaluate the risk-benefit ratio of forced surgical positions, especially when associated to long procedures, and to protect the areas exposed to pressure.
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Dra. Maria Angélica Abrão
Av. Américas, 17.500 rua 01 nº 60 casa 01 Recreio
22790-700, Rio de Janeiro, RJ
Submitted for publication June 25, 2005
Accepted for publication Novembrer 29, 2005
* Received from Hospital Universitário Clementino Fraga Filho da Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, RJ