Fulminant Rhabdomyolysis Research Articles

A Case of Dermatomyositis presenting with Fulminant Rhabdomyolysis without Myoglobinuric Acute Kidney Injury-A Rare Clinical Manifestation

Rhabdomyolysis and myoglobinuria are a rare complication of dermatomyositis. Rhabdomyolysis has a wide range of presentations, from asymptomatic to life-threatening. The most dramatic presentation can result in acute renal failure, electrolyte imbalances, and/or disseminated intravascular coagulation (DIC). Recognition of this fact has important therapeutic implications as patients require immunotherapy in addition to the symptomatic treatment for renal failure.

Exertional Sickling Deaths in Army Recruits With Sickle Cell Trait

Exertional sickling from sickle cell trait (SCT) can pose a grave risk for some military recruits and is a troubling cause of death in college athletes. We report the cases of two U.S. Army recruits with undetected SCT who collapsed and soon died from metabolic complications of exertional sickling as they struggled to finish in time the 2-mile run of the Army Physical Fitness Test, having failed this test on prior attempts. These cases are similar to other military cases and to recent sickling deaths in college track and football. Research shows how and why, in the face of SCT, during intense exercise bouts, sickle cells can quickly form and lead to fulminant rhabdomyolysis that can be fatal. Increasing evidence suggests that, in the military and in sports, the proximate trigger for most cases of fatal sickling collapse is intensity. If this hypothesis is correct, that sickling collapse is an intensity syndrome, it raises vital questions about how best to train military recruits with SCT.

Sickle Cell Trait and Fatal Rhabdomyolysis in Football Training

We report the athletic, the clinical, and the pathological details of a case of fatal rhabdomyolysis during training in a college football player with sickle cell trait (SCT) who collapsed minutes after running 16 successive sprints of 100 yd each. The player, 19 yr old, African American, was apparently healthy when he took the field for the conditioning run. No exertional heat illness was present. After collapsing on-field, the player soon went into coma and developed fulminant rhabdomyolysis, profound lactic acidosis, acute myoglobinuric renal failure, refractory hyperkalemia, and disseminated intravascular coagulation. Despite intensive care in the hospital, he died about 15 h after admission, likely from a hyperkalemic cardiac arrhythmia; the terminal rhythm was pulseless electrical activity. The forensic autopsy confirmed that the cause of death was acute exertional rhabdomyolysis associated with SCT. Counting this case, at least 15 college football players with SCT have died from complications of exertional sickling, as have younger football players and other athletes. In SCT, maximal, sustained exercise evokes four forces that can foster sickling: hypoxemia, acidosis, hyperthermia, and red cell dehydration. The setting, the clinical and laboratory features, and the clinicopathological correlation here suggest that the fulminant rhabdomyolysis and its fatal sequelae were from exertional sickling. These data suggest that screening and simple precautions for SCT may be warranted to prevent tragedies like this and enable all athletes with SCT to thrive in their sports.

Youth Football: Heat Stress and Injury Risk

Michael F. Bergeron, Ph.D., FACSM (Co-Chair)Douglas B. McKeag, M.D., FACSM (Co-Chair)Douglas J. Casa, Ph.D., ATC, FACSMPriscilla M. Clarkson, Ph.D., FACSMRandall W. Dick, FACSME. Randy Eichner, M.D., FACSMCraig A. Horswill, Ph.D., FACSMAnthony C. Luke, M.D., MPHFrederick Mueller, Ph.D., FACSMThayne A. Munce, Ph.D.William O. Roberts, M.D., FACSMThomas W. Rowland, M.D., FACSM

Acute rhabdomyolysis as a complication of cytarabine chemotherapy for acute myeloid leukemia: case report and review of literature.

Rhabdomyolysis is an unusual complication of chemotherapy that can lead to substantial morbidity through such complications as renal failure, infections, and disseminated intravascular coagulation. The syndrome has been described after treatment with cyclophosphamide, 5-azacytidine, interleukin-2, and interferon and after bone marrow transplantation. We report a patient with acute myeloid leukemia who developed fulminant rhabdomyolysis after treatment with a cytarabine-containing regimen. The syndrome was complicated by acute renal failure requiring hemodyalisis, respiratory insufficiency, and pancreatitis. We suggest that the muscle damage might be related to the known ability of cytarabine to trigger the release of cytochrome c from the mitochondria, which could lead to uncoupling of the oxidative phosphorylation with subsequent depletion of ATP reserves at the skeletal muscle and rhabdomyolysis.

A case of fulminant rhabdomyolysis after total removal of a craniopharyngioma

We reported a case of fulminant rhabdomyolysis with a high fever of more than 40°C which occured 4 days after total removal of a craniopharyngioma. After admission to the ICU, the patient was treated with surface cooling, wash-out therapy and continuous hemodiafiltration, together with the administration of dantrolene, methyl prednisolone, gabexate mesilate and ulinastatin.The patient became afebrile with this treatment, but multiple organ failure and severe metabolic acidosis led to death on the 2nd ICU day. We suspect that the cause of rhabdomyolysis was hyperthermia caused by the failure of the thermoregulatory center a few days after surgery for craniopharyngioma.

Sickle Cell Trait, Heroic Exercise, and Fatal Collapse.

In brief Although sickle cell trait is generally benign and consistent with peak athleticism, it poses a small risk of gross hematuria and splenic infarction at altitude. More alarming is the growing evidence that, in some people with sickle cell trait, maximal exercise-especially in hot weather or when new at altitude-can evoke a life-threatening syndrome of sickling, fulminant rhabdomyolysis, lactic acidosis, collapse, acute renal failure, and hyperkalemia. More than 30 such cases are described, along with practical tips for recognition and prevention.

Clinical features, pathogenesis and management of drug-induced rhabdomyolysis.

Striated musculature is considered unusually tolerant to all kinds of injuries, and rhabdomyolysis associated with drug overdose or chronic drug intake is a rare event. This may be because striated musculature, in contrast to other tissues such as liver and kidney, shows little affinity for most drugs. Several different types of drug-induced rhabdomyolysis may be distinguished, and the clinical features of the condition may vary widely, from moderate myalgia to involvement of groups of muscles to involvement of the total skeletal musculature. In clinically asymptomatic rhabdomyolysis, early diagnosis is only made if routine laboratory tests include determination of serum creatine kinase. Determination of myoglobin in serum and urine is more sensitive and allows earlier diagnosis of muscle necrosis. Myoglobinaemia may lead to toxin-induced tubular necrosis, and impairment of renal function or even acute renal failure. About 10% of all cases of acute renal failure are due to rhabdomyolysis. Fulminant rhabdomyolysis may be associated with excessive hyperkalaemia and hypocalcaemia which may induce further life-threatening complications. Therefore, early diagnosis of rhabdomyolysis is most important for prevention of its potentially life-threatening sequelae. Therapy of rhabdomyolysis consists of supportive and specific measures. Early diagnosis may help to prevent life-threatening sequelae like acute renal failure, electrolyte imbalance and shock. Withdrawal of the incriminated drug or detoxification in drug overdose should be followed by supportive measures including infusion therapy and correction of dehydration and electrolyte imbalances. Forced diuresis with sodium bicarbonate may protect the kidney function from acidosis and precipitation of myoglobin in tubules. Elimination of myoglobin from plasma may be enhanced by plasmapheresis. In patients with acute renal failure, haemodialysis is necessary. In malignant hyperthermia, immediate infusion of dantrolene sodium is required. This drug also seems to have a beneficial effect in neuroleptic malignant syndrome. The repair mechanisms of striated musculature function extremely well. The prognosis of muscular atrophy after the acute stage of rhabdomyolysis is excellent. The same is true for the prognosis of acute renal failure. However, the extent of complications or survival of the acute stage of rhabdomyolysis strongly depend on early diagnosis and start of adequate therapy.

Depletion of serum hemopexin in fulminant rhabdomyolysis. Evidence for an interaction of hemopexin with myoglobin-derived heme.

Hemopexin is a normal serum glycoprotein that functions as a carrier for intravascularly liberated free heme. Although its role is well established in the reutilization of hemoglobin-derived heme, there have been no previous clinical data to support its suspected interaction with heme released in the degradation of myoglobin. In a patient with fulminant rhabdomyolysis, we found depletion of serum hemopexin in the presence of high serum levels of myoglobin with normal levels of haptoglobin and hemoglobin. This combination of laboratory findings is evidence for an interaction between myoglobin-derived heme and hemopexin and implies a role for hemopexin in the catabolism of myoglobin. These findings support the proposed induction mechanism for observed increases of serum hemopexin in Duchenne muscular dystrophy and in polymyositis.