Quail consumption can be harmful

Background: Intoxication due to quail consumption is rarely seen. Such a toxicological syndrome (also called coturnism) occurs during the migration of quails from north to south, when they consume hemlock seeds. The clinical symptoms and laboratory results are indicative of acute rhabdomyolysis. Objectives: Acute rhabdomyolysis has a wide range of etiologies. Coturnism is a rare cause of acute rhabdomyolysis that can be lethal due to renal failure and shock. To avoid severe complications, coturnism may be considered if the history is appropriate. Case Report: We report four cases of coturnism from quail consumption; the patients were admitted with some combination of symptoms including muscle tenderness, extremity pain, nausea, and vomiting. They were treated with vigorous isotonic crystalloid hydration and urine alkalinization. Consequently, the laboratory results returned to normal ranges and the clinical symptoms disappeared. Conclusion: Although coturnism is a rarely seen toxicological syndrome that causes rhabdomyolysis, we present this case to increase awareness that it may present with symptoms of muscle tenderness, extremity pain, nausea, and vomiting after quail consumption.     

Rhabdomyolysis with concurrent atorvastatin and diltiazem

OBJECTIVE: To report a case of rhabdomyolysis and acute hepatitis associated with the coadministration of atorvastatin and diltiazem. CASE SUMMARY: A 60-year-old African American man with a significant past medical history presented to the emergency department with acute renal failure secondary to rhabdomyolysis. In addition, liver enzymes were elevated to greater than 3 times normal. The only change in medication was the initiation of diltiazem 3 weeks earlier for atrial fibrillation to a complicated medication regimen that included atorvastatin. DISCUSSION: Rhabdomyolysis has been reported in patients receiving hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors when coadministered with agents that may inhibit their metabolism. Atorvastatin is the most potent of this class of agents currently available and is commonly used in the treatment of hyperlipidemia. Rhabdomyolysis resulting from the drug interaction between diltiazem and other HMG-CoA reductase inhibitors has been described in the literature. However, no report has specifically associated this adverse event with atorvastatin and diltiazem. We describe a patient with a complex medication regimen who was admitted for rhabdomyolysis and accompanying acute renal failure, along with acute hepatitis, thought to be secondary to a drug interaction between atorvastatin and diltiazem. CONCLUSIONS: While optimizing the patient's lipid profile should be the primary factor in choosing one statin over another, the potential for drug interactions requires close attention. All patients beginning HMG-CoA reductase inhibitor therapy should be counseled regarding the signs and symptoms of muscle injury; particular attention should be paid to those patients who are taking medications that may interact.     

Rhabdomyolysis and acute renal failure following an ethanol and diphenhydramine overdose

OBJECTIVE: To report a case of nontraumatic rhabdomyolysis complicated by oliguric, acute renal failure following an intentional overdose of ethanol and diphenhydramine. CASE SUMMARY: A 21-year-old white man was admitted through the emergency department following an intentional overdose of ethanol and diphenhydramine. The patient subsequently developed acute renal failure, and a diagnosis of nontraumatic rhabdomyolysis was made. With the absence of other common causes in this case, the rhabdomyolysis was believed to be due to the combined ethanol and diphenhydramine overdose. DISCUSSION: Rhabdomyolysis is a severe and life-threatening syndrome caused by various insults to skeletal muscle, including drug-induced injury. Early detection and institution of effective treatments are essential to minimizing the complications of this syndrome. A delay in establishing the diagnosis in this case likely contributed to the severity of the renal failure. CONCLUSIONS: Nontraumatic rhabdomyolysis is an uncommon adverse outcome of drug and toxin ingestion. Due to the potential severity of the complications of this syndrome and the importance of early recognition and treatment to prevent renal failure, clinicians should have a high index of suspicion for rhabdomyolysis following overdoses that involve alcohol or antihistamines.     

Corticosteroids in the treatment of alcohol-induced rhabdomyolysis

Rhabdomyolysis is a common condition with potentially devastating complications, including acute renal failure, arrhythmias, and death. The standard of care is to use supportive measures such as aggressive fluid repletion to prevent kidney injury and attenuate clinical symptoms. Besides fluid management, few therapeutic options are available for the treatment of acute rhabdomyolysis. As a result, acute and refractory cases remain difficult to manage. We report a case of alcohol-induced rhabdomyolysis that responded dramatically to high-dose corticosteroids. A 55-year-old man presented to the emergency department for evaluation of diffuse muscle pain, weakness, and darkening urine. On admission, his creatine kinase (CK) level was 50,022 U/L. Despite aggressive fluid repletion, his CK level continued to increase, peaking at 401,280 U/L with a concomitant increase in muscle pain and urine darkening. On administration of high-dose corticosteroids, clinical symptoms and CK levels improved dramatically, and the patient was discharged 36 hours later with complete resolution of muscle pain and weakness. Given their low toxicity profile, short-term high-dose corticosteroids may be a valid treatment option for recurrent rhabdomyolysis unresponsive to fluid repletion.     

Cyclobenzaprine in the treatment of acute muscle spasm: review of a decade of clinical experience

Cyclobenzaprine hydrochloride became available for the treatment of acute skeletal muscle spasm ten years ago. The initial clinical trials conducted during the premarketing evaluation of this drug showed that it was significantly superior to placebo in relieving the signs and symptoms of acute skeletal muscle spasm. In addition, cyclobenzaprine was found to have a more rapid onset of action than diazepam. Data obtained both in controlled clinical investigations and in a postmarketing surveillance program indicated that cyclobenzaprine treatment was associated with few serious adverse experiences. Cyclobenzaprine represents a cost-effective approach to the management of acute muscle spasm, primarily because of the rapid symptomatic relief that it provides.     

Acute rhabdomyolysis associated with ofloxacin/levofloxacin therapy

OBJECTIVE: To report a case of ofloxacin/levofloxacin-induced rhabdomyolysis and to compare other reported cases from the literature. CASE SUMMARY: A 19-year-old male patient developed ofloxacin/levofloxacin-induced rhabdomyolysis during admission for periorbital cellulitis. Symptoms of myalgia, weakness, and swelling of the arms developed after 3 days of treatment with ofloxacin 800 mg/day. Laboratory analysis confirmed the presence of urine myoglobin (381.2 microg/L) and a marked increase in serum myoglobin (590.8 microg/L), along with marked elevations in serum creatine kinase (up to 16 546 IU/L). DISCUSSION: In addition to ruling out other possible etiologic factors one by one, we assessed the probability of ofloxacin/levofloxacin-induced rhabdomyolysis by observing the close time relationship between drug administration and the development of symptoms/signs, as well as the close time relationship between drug withdrawal and the disappearance of symptoms/signs. An objective causality assessment by use of the Naranjo probability scale revealed that the adverse drug reaction was probable. CONCLUSIONS: Although ofloxacin/levofloxacin-induced rhabdomyolysis appears to be rare, patients with muscle pain, swelling, or weakness during therapy should be closely monitored for this adverse effect.     

Rhabdomyolysis in a patient complicated with hypopituitarism and multiple organ dysfunction syndrome and the literature review

Introduction

Muscular symptoms, including stiffness, myalgia, cramps, and fatigue, are present in the majority of the patients with hypopituitarism, adrenal insufficiency and hypothyroidism, but rhabdomyolysis, the rapid breakdown of skeletal muscle, is a rare manifestation. In most patients who develop rhabdomyolysis, precipitating factors, such as strenuous exercise or use of lipid-lowering drugs, can be identified.

Reversible Myoglobinuric Renal Failure Following Rhabdomyolysis as a Rare Complication of Cardioversion

CAVUSOGLU, Y., et al .: Reversible Myoglobinuric Renal Failure Following Rhabdomyolysis as a Rare Complication of Cardioversion. Reversible myoglobinuric renal failure following rhabdomyolysis that was related to repeated countershocks delivered for the treatment of refractory recurrent VT and VF attacks during acute myocardial infarction is presented in this case report, in which scan with technetium-99m pyrophosphate has been used for in the diagnosis of extensive skeletal muscle damage. (PACE 2003; 26[Pt. I]:645–646)     

Acute kidney injury due to rhabdomyolysis and renal replacement therapy: a critical review

Rhabdomyolysis, a clinical syndrome caused by damage to skeletal muscle and release of its breakdown products into the circulation, can be followed by acute kidney injury (AKI) as a severe complication. The belief that the AKI is triggered by myoglobin as the toxin responsible appears to be oversimplified. Better knowledge of the pathophysiology of rhabdomyolysis and following AKI could widen treatment options, leading to preservation of the kidney: the decision to initiate renal replacement therapy in clinical practice should not be made on the basis of the myoglobin or creatine phosphokinase serum concentrations.     

Rhabdomyolysis after correction of hyponatremia in psychogenic polydipsia possibly complicated by ziprasidone

OBJECTIVE: To report a case of rhabdomyolysis related to correction of hyponatremia secondary to psychogenic polydipsia, possibly complicated by the use of ziprasidone. CASE SUMMARY: A 50-year-old white man treated for 3 weeks with ziprasidone 40 mg twice daily for chronic paranoid schizophrenia was admitted to the intensive care unit after a witnessed generalized seizure. Marked hypotonic hyponatremia was present secondary to psychogenic polydipsia. After correction of hyponatremia with intravenous NaCl 0.9%, he developed a substantial elevation in the creatine kinase level without any evidence of muscle trauma, stiffness, or swelling or any signs of neuroleptic malignant syndrome. Renal failure or compartment syndrome did not complicate the clinical picture. DISCUSSION: It is well known that severe hyponatremia can cause neurologic complications such as stupor, seizures, and even coma. Hyponatremia from water intoxication (n = 28) and its correction with intravenous fluids (n = 2) may cause non-neurologic complications such as rhabdomyolysis. An explanation may lie within the calcium-sodium exchange mechanism across the skeletal myocyte or the failure of cell volume regulation secondary to extracellular hypo-osmolality. Neuroleptic medications have been linked to the development of rhabdomyolysis, with antipsychotics being the primary offenders. As of August 2005, there has been only one reported case of rhabdomyolysis related to correction of hyponatremia complicated by an atypical antipsychotic (clozapine). It is possible that ziprasidone, like clozapine, may enhance muscle cell permeability leading to rhabdomyolysis under similar conditions. CONCLUSIONS: Psychiatric patients treated with atypical antipsychotic medications should be closely monitored for rhabdomyolysis during correction of hyponatremia, thus permitting prompt therapy to limit its complications.     

Alcoholic skeletal myopathy, a clinical and pathological study

One hundred and fifty-one inpatients with a history of chronic heavy alcohol intake were examined for evidence of muscle disease. Ninety-two patients (60 per cent) had histologically abnormal biopsies of the quadriceps muscle. The most common abnormality, which was often severe, was type II muscle fibre atrophy. Seven patients (5 per cent) had histological evidence of acute myopathy, one of whom presented with the full clinical picture of acute rhabdomyolysis. Twenty-three patients had cirrhosis, 36 were significantly malnourished and 98 had evidence of a peripheral neuropathy. None of these features, however, were sufficient to account for the muscle abnormalities. There was no clear relationship between musculo-skeletal symptoms and muscle biopsy histology. Serum creatine kinase activity was elevated in only 23 subjects and was an insensitive indicator of subclinical acute myopathy and of chronic alcoholic myopathy. Follow-up studies after abstinence from alcohol invariably showed both objective and subjective improvement of muscle function - often in the absence of any clinical recovery from the peripheral neuropathy. Continued alcohol consumption was accompanied by persistence and often deterioration of muscle fibre atrophy. It is concluded that chronic skeletal myopathy is a frequent consequence of alcohol abuse and may result from a direct toxic effect of ethanol on muscle fibres.     

Acute rhabdomyolysis due to prolonged exposure to the cold

Rhabdomyolysis represents an acute skeletal muscle injury and may be accompanied by acute renal failure due to myoglobinuria. This disorder has many potential causes. We describe the case of a 75-year-old man who developed rhabdomyolysis after prolonged exposure to cold but without associated hypothermia. This unusual case highlights that an appropriate investigation for rhabdomyolysis such as serum CK measurement should be performed in patients presenting with a history of prolonged exposure to cold, even in the absence of an obvious precipitating factor.     

Rhabdomyolysis secondary to lovastatin therapy

We report a case of lovastatin-induced rhabdomyolysis and resulting life-threatening renal failure. Lovastatin, a hypocholesterolemic agent, decreases endogenous cholesterol synthesis by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase (EC 1.1.1.88). This agent has been implicated in causing rare serious side effects in various clinical settings; however, the mechanism of these adverse reactions is not understood. The clinical course of our patient was characterized by profound muscle weakness with marked increases in serum creatine kinase and myoglobin. Light- and electron-microscopic studies of skeletal muscle of our patient demonstrated a noninflammatory myopathy suggestive of ongoing rhabdomyolysis with vacuolization and focal degeneration of myocytes. The patient's symptoms and the laboratory values referable to rhabdomyolysis resolved after discontinuation of the drug. We speculate that the rhabdomyolysis was due to mitochondrial damage secondary to inadequate synthesis of coenzyme Q and heme A, members of the electron-transport system of the inner mitochondrial membrane.     

The role of mitochondrial uncoupling in 3,4-methylenedioxymethamphetamine-mediated skeletal muscle hyperthermia and rhabdomyolysis

Use of the popular club drug ecstasy (3,4-methylenedioxymethamphetamine, MDMA) can result in life-threatening hyperthermia and rhabdomyolysis. Recent studies show a link between skeletal muscle uncoupling proteins in MDMA-mediated hyperthermia. The mechanisms by which MDMA interacts with skeletal muscle mitochondria are largely unknown. The present study was designed to comprehensively evaluate the effects of MDMA on bioenergetics and toxicity of skeletal muscle. Using (31)P nuclear magnetic resonance (NMR) and serum creatine kinase levels, we demonstrate evidence for uncoupling of oxidative phosphorylation in the skeletal muscle of MDMA (40 mg/kg)-treated rats. In vivo, rats treated with MDMA had significantly elevated serum creatine kinase levels, a marker of rhabdomyolysis, 4 h post-MDMA treatment (955 +/- 132 IU/l) compared with saline-treated controls (373.2 +/- 59 IU/l). beta-ATP signal areas after MDMA treatment showed significant reductions (15%) from the baseline values with corresponding increases in inorganic phosphate (88% increases) and decreases in intracellular pH. Clark electrode experiments on isolated skeletal muscle mitochondria in vitro (1-5 mM MDMA) and ex vivo in MDMA-treated animals demonstrated no evidence of uncoupling of oxidative phosphorylation. In vitro experiments using L6 myotubules cocultured with primary hepatocytes demonstrated the presence of uncoupling protein-3 in the L6 myotubules, but no evidence of a direct effect of MDMA or its potential metabolites on cellular creatine kinase concentrations. These findings suggest that MDMA uncouples skeletal muscle mitochondria in vivo but that this uncoupling is the result of indirect mechanisms.     

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.     

Rhabdomyolysis: two pediatric case reports

We report two pediatric cases of rhabdomyolysis. This disease involves the destruction of skeletal muscle, which can present with myalgia and a brown-pigmented urine. The first patient presented with acute renal failure, hypertension, and hyponatremia. The second patient was pyrexic, hypernatremic, and hypokalemic, and later developed hypertension. Evidence of rhabdomyolysis in both patients included dark, o-tolidine-positive urine, granular casts in the urinary sediment, and grossly increased activities of creatine kinase (greater than 60 000 U/L) in serum. An uncommonly recognized entity in the pediatric age group, rhabdomyolysis often presents as an acute disease with severe onset but can be diagnosed with relatively simple laboratory tests.     

Successful management of rhabdomyolysis with acute infection resulting from chronic sacrococcygeal pressure ulcers in a paraplegic patient: a case report

Rhabdomyolysis, a potentially life-threatening syndrome, is caused by the breakdown of skeletal muscle cells and leakage of intramyocellular contents into the bloodstream. The treatment of rhabdomyolysis resulting from chronic sacrococcygeal pressure ulcers has been rarely reported. A 62-year-old man developed a high fever and dark-colored urine. For the past 30 years, he had lived with paraplegia, which led to his immobility. Physical examination showed evidence of repeated dehiscence and exudation of the wound on his sacrococcygeal region with loss of skin sensation. Upon corroboration of the physical examination findings and laboratory test results, the patient was diagnosed with rhabdomyolysis with an acute infection resulting from sacrococcygeal pressure ulcers. We first debrided the necrotic tissue and then repaired the chronic ulcer. The wound dressing was changed frequently, and antimicrobial therapy and nutritional support were included in the treatment. The fever and dark-colored urine gradually resolved postoperatively. The patient’s renal function also improved according to the typical laboratory indicators, and the size of the pressure ulcers decreased to some extent. The patient was discharged after 1 month of hospitalization. This case highlights that accurate diagnosis is critical for administration of precise treatment to paraplegic patients with progressive rhabdomyolysis.     

Cerivastatin and gemfibrozil-associated rhabdomyolysis

OBJECTIVE: To report a case of rhabdomyolysis resulting from concurrent use of cerivastatin and gemfibrozil. CASE SUMMARY An 82-year-old white man presented to the emergency department with severe muscle weakness and inability to walk approximately one month after starting cerivastatin. He had been taking gemfibrozil for several years without any known adverse effects. Both medications were discontinued and the patient recovered. He was discharged with a diagnosis of rhabdomyolysis secondary to his medications. DISCUSSION: Four previous reports describing rhabdomyolysis in patients on concomitant cerivastatin and gemfibrozil have been cited. Although monotherapy with cerivastatin is well tolerated and has a low frequency of adverse events, the combination with nicotinic acid (i.e., niacin) or a fibric-acid derivative (i.e., gemfibrozil, fenofibrate) may result in severe skeletal muscle toxicity and rhabdomyolysis. CONCLUSIONS: According to the Naranjo scale, a probable relationship exists between the concomitant use of gemfibrozil and cerivastatin with the resulting development of rhabdomyolysis. Concurrent use of gemfibrozil and cerivastatin is therefore contraindicated.     

Fluvastatin-induced rhabdomyolysis

OBJECTIVE: To demonstrate a case of rhabdomyolysis with acute renal failure in a patient receiving fluvastatin and to present evidence that this was an adverse drug reaction to fluvastatin. CASE SUMMARY: A 51-year-old white man with a past medical history significant for hyperlipidemia treated with fluvastatin presented with malaise, myalgias, nausea, and lumbar back pain. The patient had azotemia with elevated creatine kinase (CK), lactate dehydrogenase, and transaminases. He developed hematuria and proteinuria. Laboratory results demonstrated a normal antinuclear antibody, rheumatoid factor, angiotensin-converting enzyme, antineutrophil cytoplasmic antibody, and thyroid-stimulating hormone. Cytomegalovirus and Epstein-Barr virus titers were negative for recent infection. There were no signs of systemic infection; the white blood cell count was normal and blood and urine cultures were negative. Renal ultrasound showed hyperechoic renal cortices with no obstruction. The discontinuation of fluvastatin and hemodialysis led to a rapid decrease in CK and improvement in symptoms. DISCUSSION: Hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors have the potential to cause rhabdomyolysis. However, fluvastatin is rarely associated with rhabdomyolysis when compared to other statins. Differences in biochemical and pharmacokinetic properties between fluvastatin and other HMG-CoA reductase inhibitors may be important in the development of rhabdomyolysis. CONCLUSIONS: Fluvastatin was the precipitating factor causing rhabdomyolysis in this case report. This patient had no other findings to suggest infection or other disorder inducing rhabdomyolysis. An objective causality assessment revealed that the adverse drug reaction was probable as determined by the Naranjo probability scale. Fluvastatin has the potential to cause serious adverse effects. Therefore, a heightened awareness by the patient and physician for potential signs of myopathy is recommended.     

Isolated exercise-induced rhabdomyolysis of brachialis and brachioradialis muscles: an atypical clinical case

OBJECTIVE AND PATIENT: To report an atypical case of exercise-induced bilateral brachialis and brachioradialis rhabdomyolysis in a 25-year-old woman. DISCUSSION AND CONCLUSION: Persistent focal muscle pain, atypical by its duration and intensity, even after moderate exercise, should prompt the search for rhabdomyolysis and discuss the possibility of acute compartment syndrome. MRI images can validate the muscle edema. Progressive and adapted training as well as respecting individual limits are necessary measures to prevent rhabdomyolysis.