Exertional rhabdomyolysis associated with decerebrate posturing

A case is presented in which decerebrate posturing after a head injury led to rhabdomyolysis and renal failure. Exertional rhabdomyolysis is caused by an energy deficient state in overworked musculature that leads to a loss of integrity of the muscle cell. The resultant myoglobin in serum leads to acute renal failure. This condition should be suspected in a comatose patient with fever, brown discoloration of the urine, and edema of the extremities. Laboratory results will show orthotoluidine positive urine with a clear serum, elevated serum creatine phosphokinase, and serum creatinine elevation out of proportion to blood urea nitrogen. Management consists of fluids and diuretics with dialysis if necessary. Rhabdomyolysis with head injury and decerebracy may occur more frequently than has been previously reported.     

Rhabdomyolysis

Key points Rhabdomyolysis describes the destruction or disintegrationof striated muscle; it is an important cause of acute renalfailure. Creatinine kinase concentration is the most sensitiveand useful indicator of muscle injury in rhabdomyolysis. Themost important intervention is early aggressive crystalloidfluid resuscitation. Life-threatening hyperkalaemia is a commoncause of death and must be treated promptly. Myoglobin-inducedrenal failure has an excellent prognosis.   The term rhabdomyolysis describes the breakdown or disintegrationof striated muscle. Although a broad range of conditions canresult in rhabdomyolysis, the final common pathway of myocytenecrosis involves a rapid increase in intracytoplasmic calcium.This leads to the release of myocyte constituents into the circulation,which can produce life-threatening complications including acutehyperkalaemia and acute renal failure (ARF). Rhabdomyolysis is a common cause of ARF, especially in timesof conflict or after major disasters     

Acute Renal Failure Due to Rhabdomyolysis in Diabetic Patients

We report a 32-year-old Black man, admitted to the ICU with coma and severe metabolic disturbances due to diabetic ketoacidosis. During the admission, rhabdomyolysis and acute renal failure (ARF) were diagnosed. After metabolic control and gradual decrease of creatine kinase levels, he presented a progressive improvement of renal function. We emphasize nontraumatic rhabdomyolysis as a poorly recognized pathogenetic factor for ARF in diabetic ketoacidosis and suggest that a better understanding of its mechanisms and an early application of protective measures is necessary.     

Rhabdomyolysis and severe muscle weakness secondary to colistin therapy

Rhabdomyolysis is a clinical condition that causes renal failure up to 40%. Rhabdomyolysis may be traumatic or nontraumatic. Colistin (polymyxin E) is an effective antibiotic. Nephrotoxicity is a frequently encountered side effect. The nephrotoxic effect of colistin is thought to be associated with increased membrane permeability, cell swelling and lysis, and the development of acute tubular necrosis. Here, we report a case of nontraumatic rhabdomyolysis associated with the use of colistin. There is only one report of rhabdomyolysis secondary to colistin in the literature, and there is no report of a case developing severe tetraparesis, as in our case.     

Pheochromocytoma presenting with rhabdomyolysis and acute renal failure: a case report

Rhabdomyolysis ranges from an asymptomatic illness with elevated creatine kinase levels to a life-threatening condition associated with extreme elevations in creatine kinase, electrolyte imbalances, acute renal failure, and disseminated intravascular coagulation. The most common causes are crush injury, overexertion, alcohol abuse, certain medicines, and toxic substances. A number of electrolyte abnormalities and endocrinopathies, including hypothyroidism, thyrotoxicosis, diabetic ketoacidosis, nonketotic hyperosmolar state, and hyperaldosteronism, cause rhabdomyolysis. Rhabdomyolysis and acute renal failure are unusual manifestations of pheochromocytoma. There are a few case reports with pheochromocytoma presenting rhabdomyolysis and acute renal failure. Herein, we report a case with pheochromocytoma crisis presenting with rhabdomyolysis and acute renal failure.     

Hyperosmolal state associated with rhabdomyolysis

We report a case of nonketotic hyperosmolal state associated with rhabdomyolysis. None of the known predisposing factors for rhabdomyolysis, e.g. coma, potassium or phosphate depletion, were present in this patient. We propose that severe hyperosmolality per se may represent another predisposing factor for nontraumatic rhabdomyolysis.     

Hypokalemia causing rhabdomyolysis resulting in life-threatening hyperkalemia

Hyperkalemia is commonly associated with renal failure and is rare if renal function is normal. It is rarely caused by rhabdomyolysis and can be life threatening if unrecognized. Rhabdomyolysis is caused by many disorders, including hypokalemia. The available literature, both for human beings and experimental animals, contains evidence of hypokalemia causing rhabdomyolysis and rhabdomyolysis leading to hyperkalemia. Hypokalemia as a cause of rhabdomyolysis often goes unnoticed, because of the counteracting effect of rhabdomyolysis on serum potassium. There are no pediatric reports showing hypokalemia as a cause of rhabdomyolysis leading to life-threatening hyperkalemia. This case emphasizes the vigilance required toward the occurrence of rhabdomyolysis, which if not detected promptly may prove fatal.     

Hemolytic uremic syndrome and rhabdomyolysis in a patient with succinate coenzyme Q reductase (complex II) deficiency

Hemolytic uremic syndrome (HUS) is characterized by microangiopathic hemolytic anemia, thrombocytopenia and acute renal failure. Besides diarrhea-associated HUS, due to verotoxin-producing Escherichia coli, in children HUS without prodromal diarrhea may be associated with other infectious and autoimmune diseases, genetic defects of the complement-regulator alternative-pathway, and inborn errors of vitamin B12 metabolism. Rhabdomyolysis is the dissolution of skeletal muscle due to various causes, including inborn errors of metabolism. Recurrent rhabdomyolysis and HUS have been previously described in one patient with a genetic defect of oxidative phosphorylation. We report the case of a 2-year-old boy with recurrent HUS and rhabdomyolysis in whom a succinate coenzyme Q reductase (complex II) deficiency was diagnosed. We hypothesize that defects of oxidative phosphorylation could be another etiological factor in atypical HUS.     

Preliminary identification of prognostic factors from clinical outcome in 38 cases of rhabdomyolysis

Background Rhabdomyolysis is a systemic metabolic disorder caused by leakage of muscle cell constituents into the blood after necrosis of skeletal muscle due to traumatic and nontraumatic causes. This study was done to identify the significant prognostic factors for rhabdomyolysis. Methods The relationship between the outcomes and various clinical characteristics was investigated retrospectively from January 1991 to December 1996, in 38 patients with rhabdomyolysis (29 men and 9 women). Results Among the 8 patients who died, old age, diabetes mellitus, acute renal failure, and disseminated intravascular coagulation were significantly more common than in the 30 survivors. The BUN, serum sodium, serum potassium, serum phosphorus, and blood glucose levels were also significantly higher in the patients who died. There was no significant correlation between the outcome and the patient's sex, the serum levels of creatine phosphokinase and other enzymes leaking from muscle, the blood and urine pH, base excess, and blood pressure, or the use of hemodialysis. Conclusions In patients with rhabdomyolysis, advanced age, diabetes mellitus, acute renal failure, and disseminated intravascular coagulation were factors associated with a poor prognosis, and so require aggressive treatment.     

Rhabdomyolysis: need for high index of suspicion

Rhabdomyolysis, both traumatic and nontraumatic, may be defined as a triad of skeletal muscle injury, pigmented urine, and acute renal failure. Nontraumatic rhabdomyolysis may be more of a subtle diagnosis and requires a high index of suspicion. Pertinent findings in the history as well as clinical evidence of muscle injury with a marked elevation of creatinine kinase will suggest the diagnosis. A disproportionate elevation of serum creatinine to blood urea nitrogen may also occur. Treatment consists of adequate hydration to help prevent oliguric or anuric renal failure without additional calcium or bicarbonate supplementation in most cases. Radiologic studies involving intravenous contrast media as well as urologic instrumentation should be avoided in the acute setting. With early diagnosis and prompt treatment the prognosis for recovery is excellent.     

Severe lactic acidosis and rhabdomyolysis following metformin and ramipril overdose

We report the case of a 46-yr-old male who developed severelactic acidosis, cardiorespiratory arrest, and rhabdomyolysisfollowing an overdose of metformin and ramipril. The lacticacidosis was successfully treated with early high-volume continuousveno-venous haemofiltration. Rhabdomyolysis and lower limb compartmentsyndrome developed later. The patient otherwise made a goodrecovery. We discuss the management of severe lactic acidosissecondary to metformin overdose and the association with rhabdomyolysis.     

Acute Renal Failure Secondary to Fenofibrate Monotherapy-Induced Rhabdomyolysis

Fenofibrate, a fibric acid derivative, is used to treat diabetic dyslipidemia, hypertriglyceridemia, and combined hyperlipidemia alone or in combination with statins. Rhabdomyolysis is defined as a pathological condition of skeletal muscle cell damage leading to the release of toxic intracellular material into the circulation. Its major causes include trauma, ischemia, toxins, metabolic disorders, infections, and drugs. Rhabdomyolysis associated with fenofibrate is extremely rare. In nearly all of the presented cases, there was a predisposing factor for rhabdomyolysis such as diabetes, older age, renal insufficiency, and hypothyroidism. Here, we report a nondiabetic, nonhypothyroidic young female patient without any known prior renal disease presenting with acute renal failure developing after fenofibrate treatment.     

Acute renal failure secondary to fenofibrate monotherapy-induced rhabdomyolysis

Fenofibrate, a fibric acid derivative, is used to treat diabetic dyslipidemia, hypertriglyceridemia, and combined hyperlipidemia alone or in combination with statins. Rhabdomyolysis is defined as a pathological condition of skeletal muscle cell damage leading to the release of toxic intracellular material into the circulation. Its major causes include trauma, ischemia, toxins, metabolic disorders, infections, and drugs. Rhabdomyolysis associated with fenofibrate is extremely rare. In nearly all of the presented cases, there was a predisposing factor for rhabdomyolysis such as diabetes, older age, renal insufficiency, and hypothyroidism. Here, we report a nondiabetic, nonhypothyroidic young female patient without any known prior renal disease presenting with acute renal failure developing after fenofibrate treatment.     

Rhabdomyolysis due to red yeast rice (Monascus purpureus) in a renal transplant recipient

Rhabdomyolysis is a known complication of hepatic 3-methylglutaryl coenzyme A reductase (HMG-CoA) inhibitor (statin) therapy for posttransplant hyperlipidemia, and thus monitoring for this effect is indicated. We report a case of an herbal preparation-induced rhabdomyolysis in a stable renal-transplant recipient, attributed to the presence of red yeast rice (Monascus purpureus) within the mixture. The condition resolved when consumption of the product ceased. Rice fermented with red yeast contains several types of mevinic acids, including monacolin K, which is identical to lovastatin. We postulate that the interaction of cyclosporine and these compounds through the cytochrome P450 system resulted in the adverse effect seen in this patient. Transplant recipients must be cautioned against using herbal preparations to lower their lipid levels to prevent such complications from occurring.     

Brauner Urin

Rhabdomyolysis is a rare but well-known complication of statin therapy. The risk is considerably increased when concomitant drugs are administered that inhibit metabolism and breakdown via the cytochrome CYP3A4. We report a case of myoglobin-induced acute renal failure secondary to the concomitant use of simvastatin and amiodarone. The risk of rhabdomyolysis is mainly determined by the statin dose; in the case of the concomitant use of CYP3A4 inhibitors, a maximal daily dose of 20 mg is recommended to avoid harmful drug interactions.     

Pregabalin- and azithromycin-induced rhabdomyolysis with purpura: An unrecognized interaction: A case report

IntroductionRhabdomyolysis associated with the use of pregabalin or azithromycin has been demonstrated to be a rare but potentially life-threatening adverse event. Here, we report an extremely rare case of rhabdomyolysis with purpura in a patient who had used pregabalin and azithromycin.Presentation of caseWe present the case of a 75-year-old woman with a history of fibromyalgia who was admitted with mild limb weakness and lower abdominal purpura. She was prescribed pregabalin (75 mg, twice daily) for almost 3 months to treat chronic back pain. Her medical history revealed that 3 days before admission, she began experiencing acute bronchitis and was treated with a single dose of azithromycin (500 mg). She had developed rapid onset severe myalgia, mild whole body edema, muscle weakness leading to gait instability, abdominal purpura and tender purpura on the lower extremities. Laboratory values included a white blood cell count of 25,400/mL and a creatinine phosphokinase (CPK) concentration of 1250 IU/L. Based on these findings and the patient’s clinical history, a diagnosis of pregabalin- and azithromycin-induced rhabdomyolysis was made.DiscussionThe long-term use of pregabalin and the initiation azithromycin therapy followed by a rapid onset of rhabdomyolysis is indicative of a drug interaction between pregabalin and azithromycin.ConclusionWe report an extremely rare case of rhabdomyolysis with purpura caused by a drug interaction between pregabalin and azithromycin. However, the mechanisms of the interactions between azithromycin on the pregabalin are still unknown.     

A case of rhabdomyolysis induced acute renal failure secondary to statin-fibrate-derivative combination and occult hypothyroidism

Rhabdomyolysis is a syndrome characterized by muscle necrosis and the release of intracellular muscle contents into the systemic circulation. We hereby report a patient proved to be a case of unrecognized hypothyroidism presenting with rhabdomyolytic acute renal failure precipitated by the combined use of statin and fenofibrate. A 63-year-old woman was referred to our department because of fatigue, diffuse muscle pain and oliguria. On the basis of pathogenesis, clinical and laboratory examination the diagnoses of acute renal failure secondary to the statin-fibrate-derivative combination induced rhabdomyolysis and auto-immune thyroiditis induced hypothyroidism were made. Although saline, furosemide and sodium bicarbonate infusions enabled diuresis and have led to a rapid recovery of renal function and normalization of blood pressure in five days (creatinine level decreased from 4.5 mg/dl to 1.2 mg/dl), only thyroid replacement therapy (0,1 mg thyroxine) that begun after the exclusion of adrenal insufficiency resulted in complete resolution of rhabdomyolysis. This prompted the diagnosis of background, clinically silent rhabdomyolysis aggrevated by the statin-fibrate-derivative combination. To our knowledge this case illustrates the first example of rhabdomyolytic acute renal failure induced by a statin-fibrate-derivative combination with underlying hypothyroidism which was responsible for the basal clinically unobservable rhabdomyolysis.     

Acute renal failure in a hypothyroid patient with rhabdomyolysis

A 49-year-old hypothyroid man developed rhabdomyolysis and acute renal failure. He had been on thyroid replacement therapy for 17 years following removal of a benign pituitary tumor. Rhabdomyolysis was diagnosed by elevated liver enzymes, CPK, and creatinine. The case illustrates how hypothyroidism can cause rhabdomyolysis and subsequently, acute renal failure.