Rhabdomyolysis

Rhabdomyolysis is the dissolution of skeletal muscle. Breakdown of the myocyte causes the extravasation of intracellular constituents, leading to a clinical syndrome--the classic triad of brown urine, muscle pain, and weakness. The pathogenesis of rhabdomyolysis is presented.     

Rhabdomyolysis

Rhabdomyolysis is a potentially life-threatening syndrome resulting from the breakdown of skeletal muscle fibers with leakage of muscle contents into the circulation. The most common causes are crush injury, overexertion, alcohol abuse and certain medicines and toxic substances. Several inherited genetic disorders, such as McArdle's disease and Duchenne's muscular dystrophy, are predisposing factors for the syndrome. Clinical features are often nonspecific, and tea-colored urine is usually the first clue to the presence of rhabdomyolysis. Screening may be performed with a urine dipstick in combination with urine microscopy. A positive urine myoglobin test provides supportive evidence. Multiple complications can occur and are classified as early or late. Early complications include severe hyperkalemia that causes cardiac arrhythmia and arrest. The most serious late complication is acute renal failure, which occurs in approximately 15 percent of patients with the syndrome. Early recognition of rhabdomyolysis and prompt management of complications are crucial to a successful outcome.     

Hypophosphatemia and Rhabdomyolysis

Clinical observations suggest that overt rhabdomyolysis may occur if severe hypophosphatemia is superimposed upon a pre-existing subclinical myopathy. To examine this possibility, a subclinical muscle cell injury was induced in 23 dogs by feeding them a phosphorus- and calorie-deficient diet until they lost 30% of their original weight. To induce acute, severe hypophosphatemia in the animals after partial starvation, 17 of the dogs were given large quantities of the same phosphorus-deficient diet in conjunction with an oral carbohydrate supplement, which together provided 140 kcal/kg per day.     

Rhabdomyolysis in Isoniazid Poisoning

Background: Rhabdomyolysis is one of the reported complications of isoniazid poisoning, but relevant data are limited. Methods: A retrospective study was conducted on isoniazid poisoning cases seen at the Philippine General Hospital over 5 years (1992–1997). Patients excluded from the study were those who coingested other substances, including hepatotoxic and nephrotoxic drugs, those with underlying medical illnesses, and those without creatine phosphokinase muscle fraction determinations. Results: Out of the 270 cases of isoniazid poisoning, 52 patient records were reviewed. Common clinical manifestations were seizures (100%), depressed sensorium (53%), and vomiting (45%). Laboratory results showed leukocytosis (74.5%), metabolic acidosis (29%), and impaired liver function tests (21%). Creatine phosphokinase muscle fraction was elevated in 59.6% of cases, beginning at a dose of 2.4 g. Values peaked on days 5 and 6 and declined on days 7 and 8. Statistically significant correlations were observed for the elevation of creatine phosphokinase muscle fraction with the duration/amount of drug ingested and the frequency of seizure. No correlation was observed between the frequency of seizures and elevated creatine phosphokinase muscle fraction nor between the time delay in consultation and elevation of creatine phosphokinase muscle fraction. Conclusions: The incidence of rhabdomyolysis in isoniazid poisoning was 3/100 cases a year. The findings suggesting its direct toxic effect on the muscles may not be clinically relevant.     

Rhabdomyolysis associated with naltrexone

OBJECTIVE: To report a possible association between naltrexone therapy and the development of rhabdomyolysis in one patient. CASE SUMMARY: A 28-year-old white man in good physical health was started on naltrexone 50 mg/d for inpatient treatment of alcohol dependence and depression. A routine serum chemistry panel obtained on day 9 of naltrexone therapy showed marked new elevations in creatine kinase and aspartate aminotransferase. The patient remained asymptomatic and did not develop renal insufficiency. The serum enzyme concentrations returned to normal within eight days of naltrexone discontinuation. DISCUSSION: Rhabdomyolysis has not been previously reported to occur in patients during treatment with naltrexone. Alcoholism may result in a reversible acute muscle syndrome, but our patient did not fit the appropriate clinical profile for such a syndrome. Additionally, the other prescribed medications could not be implicated as possible causative agents. CONCLUSIONS: This case report illustrates a possible association between naltrexone therapy and rhabdomyolysis.     

横纹肌溶解综合征合并急性肾功能衰竭

病史摘要患者,女,19岁。因少尿5d,伴心悸、呼吸困难转至我院。患者2d前因左下肢海绵状血管瘤在当地医院行血管硬化剂治疗(含有锂,鱼肝油酸钠等药物),治疗当天局部疼痛较剧烈,无发热。第4天出现恶心、呕吐,并在家中突然昏倒,同时伴胸闷、心悸、呼吸困难及尿量减少,当地医院诊断为成人呼吸窘迫综合征(ARDS),当时呼吸30～40次/分,心率130次/分(无奔马律),血压120/80mmHg,肝肿大,颈静脉怒张,肝颈静脉回流征阳性,下肢水肿。给予呋塞米(速尿)和毛花苷丙(西地兰)治疗效果不佳,心电图示室性早搏,V1、VR、V4、V5导联呈QR波型,伴心肌酶谱增高,疑…