Rhabdomyolysis


Rhabdomyolysis

Description, Causes and Risk Factors:

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.

Approximately 26,000 cases of rhabdomyolysis are reported annually in the United States. Prompt recognition and early intervention are vital. Full recovery can be expected with early diagnosis and treatment of the many complications that can develop in patients with this syndrome.

Clinical features of rhabdomyolysis may be absent initially, and its most serious complication, acute renal failure, is common. Many patients develop dialysis-dependent acute renal failure associated with the misuse of alcohol or other drugs. The nephrotoxicity of myoglobin is decreased by forced alkaline diuresis. Critically ill patients with acute renal failure are also likely to develop multiorgan failure syndrome, with a resultant increase in mortality.

Several investigators have attempted to categorize the many diverse causes and risk factors for rhabdomyolysis. The most common causes are alcohol abuse, muscle overexertion, muscle compression and the use of certain medications or illicit drugs.

Other significant causes of rhabdomyolysis include electrical shock injury and crush injury. In crush injury, rhabdomyolysis occurs because of the release of necrotic muscle material into the circulation after compression is relieved in, for example, persons trapped in crashed cars or collapsed buildings. Heat-stroke and sporting activities, especially in previously untrained persons, are also common causes of the syndrome. Heat dissipation impairment from wearing heavy sports equipment or exercising in humid, warm weather increases the risk of rhabdomyolysis.

Infectious causes:

    Viruses: influenza virus B, parainfluenza virus, adenovirus, coxsackievirus, echovirus, herpes simplex virus, cytomegalovirus, Epstein-Barr virus, human immunodeficiency virus.

  • Bacteria: Streptococcus, Salmonella, Legionella, Staphyloccus and Listeria species.

Inflammatory causes

    Polymyositis.

  • Dermatomyositis.

  • Capillary leak syndrome.

  • Snake bites (mostly in South America, Asia and Africa).

Metabolic and endocrinologic causes

    Electrolyte imbalances: hyponatremia, hypernatremia, hypokalemia, hypophosphatemia, hypocalcemia.

  • Hypothyroidism.

  • Thyrotoxicosis.

  • Diabetic ketoacidosis.

  • Nonketotic hyperosmolar syndrome.

Genetic Causes of Rhabdomyolysis

    Lipid metabolism: Carnitine palmitoyltransferase deficiency, Carnitine deficiency, Short-chain and long-chain acyl-coenzyme A dehydrogenase deficiency.

  • Carbohydrate metabolism: Myophosphorylase deficiency (McArdle's disease), Phosphorylase kinase deficiency, Phosphofructokinase deficiency, Phosphoglycerate mutase deficiency, Lactate dehydrogenase deficiency (characteristic elevation of creatine kinase level with normal lactate dehydrogenase level).

  • Purine metabolism: Myoadenylate deaminase deficiency, Duchenne's muscular dystrophy.

Symptoms:

Symptoms may include:

    Muscle pain.

  • Tea-colored urine.

  • Tenderness.

  • Fever.

  • Swelling.

  • Malaise.

  • Bruising.

  • Nausea.

  • Weakness.

  • Emesis.

  • Confusion.

  • Agitation.

  • Delirium.

  • Anuria.

Diagnosis:

Because patients may present without any obvious history or physical sign of rhabdomyolysis, clinicians must be aware of the potentially subtle presentation and keep the possibility of rhabdomyolysis in mind. In the evaluation of blunt trauma in children, it is vital to remain vigilant for signs of child abuse (nonaccidental injury). Consider rhabdomyolysis in cases of child abuse, drug-overdoses, heat-related events and pediatric orthopedic injuries.

Failure to consider this diagnosis could result in the most severe complication of rhabdomyolysis: pigment-associated renal injury. Rhabdomyolysis accounts for 5-25% of cases of acute kidney injury (AKI) in adult patients; rates in pediatric patients are unknown.

Useful laboratory tests that should be ordered include the following:

    Complete blood count (CBC), including hemoglobin, hematocrit, and platelets.

  • Serum chemistries, including blood urea nitrogen (BUN), creatinine, glucose, calcium, potassium, phosphate, uric acid, and liver function tests (LFTs).

  • Prothrombin time (PT).

  • Activated partial thromboplastin time (aPTT) - Thromboplastin released from injured myocytes can cause disseminated intravascular coagulation (DIC).

  • Serum aldolase.

  • Lactate dehydrogenase (LDH).

Imaging studies generally play little role in the initial diagnosis of rhabdomyolysis. However, radiographs should be obtained when fractures are suspected. Computed tomography (CT) of the head may be necessary on a case-by-case basis when a patient with an altered sensorium is evaluated. Patients with significant head trauma may require head CT. A head CT scan may also be obtained in patients with first-time seizure activity or prolonged seizures or in patients with neurologic deficits of unknown etiology.

Magnetic resonance imaging (MRI) may be useful in distinguishing various etiologies of myopathy. One study suggests that bacterial myositis, focal myositis, and idiopathic rhabdomyolysis show a characteristic gadolinium enhancement on MRI. Abscesses were found only in bacterial myositis. Polymyositis and dermatomyositis have a characteristic uniform distribution pattern with emphasis on the quadriceps muscles.

MRI is the imaging modality of choice for evaluating the distribution and extent of injury of affected muscles, especially when fasciotomy or involvement of deep compartments is considered.

ECG should be performed early in the course of evaluation to evaluate for cardiac dysrhythmias related to hyperkalemia or hypocalcemia. ECG may reveal changes reflective of acute hyperkalemia, including peaked T waves, prolongation of the PR and QRS intervals, and loss of the P wave or the sine wave. Specific disease testing may be indicated to determine definitive causes during or after short-term management of rhabdomyolysis.

The compartment pressures should be measured in any patient with severe focal muscle tenderness and a firm muscle compartment. A fasciotomy may be needed if compartment pressures in excess of 25-30 mm Hg are sustained.

Histology demonstrates necrotic muscle fibers in patients with rhabdomyolysis. A muscle biopsy may be required to demonstrate immunohistochemical features of necrosis only if underlying and often inherited muscle disease is a concern. Immunoblotting, immunofluorescence, and genetic studies may be necessary to find evidence of inflammatory conditions or dystrophinopathies.

Treatment:

The treatment of rhabdomyolysis is primarily directed at preserving renal function. Up to 12 L of fluid may be sequestered in the necrotic muscle tissues, thereby contributing to hypovolemia, which is one cause of renal failure in patients with rhabdomyolysis.

Intravenous (IV) hydration must be initiated as early as possible. In the patient with a crush injury, IV fluids should be started even before the trapped limb is freed and decompressed, and certainly no later than six hours after decompression. The longer it takes for rehydration to be initiated, the more likely it is that oliguric renal failure (less than 500 mL of urine per day) or anuric renal failure (less than 50 mL of urine per day) will be established. Investigators in one study found that forced diuresis within the first six hours of admission prevented all episodes of acute renal failure.

Initially, normal saline should be given at a rate of 1.5 L/hr. Urine output should be maintained at 300 mL per hour until myoglobinuria has ceased. High rates of IV fluid administration should be used at least until the CK (creatine kinase) level decreases to or below 1,000 units per L. If these measures successfully thwart the development of oliguria, the patient can be switched to 0.45 percent saline with the addition of one or two ampules of sodium bicarbonate (40 mEq) and 10 g per L of mannitol. Diuretics (loop or other types) should not be used because they do not improve, and may actually compromise, the final renal outcome.

The objectives are to alkalinize urine to a pH of greater than 6.5 (thereby decreasing the toxicity of myoglobin to the tubules) and to enhance the flushing of myoglobin casts from renal tubules by means of osmotic diuresis. However, these measures should not be employed if oliguria is established despite initial generous hydration with normal saline. The use of mannitol remains controversial as it is mostly supported by experimental animal studies and retrospective clinical studies. In one study, mannitol did not confer additional protection compared with normal saline alone. There are also some concerns about the use of sodium bicarbonate, because it may worsen hypocalcemia or precipitate calcium phosphate deposition on various tissues.

Elderly patients should be treated in an intensive care unit so that vital signs, intake and hourly output can be closely monitored and fluid overload can be quickly detected. Invasive hemodynamic monitoring is critical to fine-tune treatment in patients with comorbid cardiovascular disorders or preexisting chronic renal dysfunction.

Hemodialysis may be a therapeutic modality. Despite treatment, patients with rhabdomyolysis often develop oliguric acute tubular necrosis. In this situation, hemodialysis should be started and carried on aggressively, frequently on a daily basis. If given enough time, many patients partially or completely recover renal function. The chances of recovery are obviously much higher in the absence of preexisting renal insufficiency.

Finally, initial hypocalcemia should not be corrected unless a patient is symptomatic. It is important to avoid further aggravating the hypercalcemia that commonly develops during the recovery phase of rhabdomyolysis, when calcium deposited in the injured muscles is mobilized back to the extracellular space.29

NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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