Rhabdomyolysis is a serious medical condition that occurs when skeletal muscle tissue breaks down rapidly, releasing muscle components into the bloodstream. This process releases substances such as myoglobin, creatine kinase (CK), electrolytes, and other enzymes that can damage organs, particularly the kidneys. While some cases are mild, severe cases can lead to life-threatening complications including acute kidney injury (AKI), electrolyte disturbances, and dangerous heart rhythm problems. 

Historically, rhabdomyolysis was described in soldiers after long marches or in victims of crush injuries. Today, it remains clinically important and may result from trauma, strenuous exercise, certain drugs, toxins, and infections. Because it can progress quickly, early recognition and treatment are critical. 

Rhabdomyolysis is defined as the breakdown of striated muscle fibers, leading to the leakage of their contents into the blood. The most important laboratory marker is a significant rise in creatine kinase (CK), often more than five times the upper limit of normal. Myoglobin release is central to the disease, as it can clog kidney tubules and cause direct toxicity, leading to kidney injury. 

Electrolyte disturbances such as increased potassium and phosphate, and shifts in calcium, can result in dangerous metabolic and heart complications. The condition ranges in severity, from silent laboratory abnormalities to life-threatening illness with multiorgan failure. 

Rhabdomyolysis can develop from both direct muscle injury and indirect triggers. The wide range of potential causes makes careful evaluation essential in every case. For clarity, these causes are usually divided into three main groups: traumatic, exertional, and non-traumatic factors. 

Traumatic causes: 

Crush injuries, such as those seen in earthquakes or building collapses, can damage muscle tissue severely. Prolonged immobilization, often after coma or drug overdose, can lead to muscle breakdown. Compartment syndrome, where pressure builds up in muscle compartments, may trigger rhabdomyolysis. Electrical injuries, such as lightning strikes or high-voltage shocks, can damage muscle. Severe burns may destroy muscle fibers and release toxins. 

Exertional causes: 

Extreme physical exertion, especially in untrained individuals or hot environments, can trigger muscle breakdown. Seizures may damage muscles due to intense, sustained contractions. Alcohol withdrawal delirium and heat stroke are additional causes. 

Non-traumatic, non-exertional causes: 

Drugs such as statins, especially when combined with fibrates, can cause rhabdomyolysis. Alcohol, cocaine, amphetamines, and heroin can directly injure muscle. Certain antipsychotics, especially in neuroleptic malignant syndrome, are linked to rhabdomyolysis. Toxins such as snake or insect venom may cause muscle breakdown. Metabolic and genetic conditions, including glycogen storage diseases and mitochondrial myopathies, increase risk. Infections such as influenza, HIV, and bacterial illnesses like Legionella may trigger rhabdomyolysis. Electrolyte disturbances like severe hypokalemia or hypophosphatemia can also contribute. 

Environmental factors such as heat, dehydration, and fasting worsen risk. Rarely, autoimmune diseases or paraneoplastic syndromes are implicated. 

The key event in rhabdomyolysis is damage to the muscle cell membrane, known as the sarcolemma. This damage allows calcium to flood into muscle cells, which sets off destructive processes: 

• Enzymes such as proteases and phospholipases are activated and break down muscle tissue. 

• Mitochondrial damage and oxidative stress increase injury. 

• Damaged cells release myoglobin, CK, potassium, phosphate, uric acid, and other contents into the bloodstream. 

The kidneys are particularly affected: 

• Myoglobin forms harmful casts with proteins in the kidney tubules, blocking them and causing injury. 

• Reduced blood flow to the kidneys (vasoconstriction) further damages tissue. 

• The heme component of myoglobin is directly toxic to kidney cells. 

Electrolyte imbalances, especially high potassium, increase the risk of dangerous arrhythmias and sudden cardiac arrest. Recent research suggests that inflammation and oxidative stress also worsen the condition once it begins. 

The classic triad of rhabdomyolysis includes muscle pain, muscle weakness, and dark-colored urine from myoglobinuria. However, this triad is seen in fewer than 10% of patients, making diagnosis challenging. 

Common symptoms include: 

• Patients often report pain in large muscle groups such as the shoulders, thighs, or lower back. 

• Muscle weakness is frequently present. 

• Urine may become dark brown or tea-colored due to myoglobin. 

• Some patients develop swelling in affected muscles. 

• Nausea, vomiting, and fever may also occur. 

• Severe cases may involve confusion, altered mental status, or decreased urine output, which suggests kidney involvement. 

On examination, affected muscles may be swollen, tender, or firm. Compartment syndrome can develop in severe cases, requiring urgent surgery. 

Diagnosis relies on laboratory tests, urinalysis, and imaging studies when needed. Clinicians combine blood and urine tests with physical findings to confirm the diagnosis and monitor disease severity. 

Laboratory tests: 
Creatine kinase (CK) levels are the most important marker. Levels greater than 5,000 IU/L are strongly suggestive. Myoglobin may be detected in blood or urine, although it clears quickly. Electrolyte testing often shows high potassium and phosphate and low calcium. Kidney function tests may show elevated creatinine and BUN. Liver enzymes (AST, ALT) can also rise due to muscle injury. 

Urinalysis: 
A urine dipstick often tests positive for blood, but no red blood cells are seen under the microscope, which indicates myoglobin. Urine is frequently brown or tea-colored. 

Other tests: 
An ECG may detect dangerous arrhythmias from high potassium. Imaging such as ultrasound or MRI may be used if compartment syndrome is suspected. 

Several conditions can resemble rhabdomyolysis and should be considered. Some of these mimic the muscle weakness or laboratory abnormalities, while others overlap in their complications. Differentiating between them is important because treatment strategies can differ significantly. 

Polymyositis and dermatomyositis can also present with muscle weakness and elevated enzymes. Guillain-Barré syndrome can mimic weakness but is neurological rather than muscular. Myasthenia gravis causes muscle weakness but not muscle breakdown. Acute compartment syndrome may cause swelling without systemic muscle breakdown. Other causes of acute kidney injury may mimic complications of rhabdomyolysis. 

Management is focused on rapid treatment to prevent kidney failure and correct metabolic problems. Treatment typically starts with fluid resuscitation and continues with careful monitoring of electrolytes and kidney function. Addressing the underlying cause is just as important as supportive care. 

Immediate priorities include: 
Patients are given aggressive intravenous fluids, usually isotonic saline, to keep urine output high. Early fluid treatment within six hours can reduce the risk of kidney injury. Electrolyte abnormalities must be corrected. High potassium is treated with calcium gluconate, insulin with glucose, and other agents. Low calcium is treated only if symptoms occur. Medications that harm the kidneys, such as NSAIDs and contrast dye, should be stopped. In some cases, sodium bicarbonate is used to alkalinize the urine, although benefits are debated. Diuretics such as mannitol may be used selectively but have limited evidence. The underlying cause, such as trauma, drugs, or infection, must be treated directly. 

Severe cases may require intensive care, dialysis, or surgery. Nutritional support and rehabilitation help patients recover and prevent long-term complications. 

Rhabdomyolysis can lead to serious health problems. These complications often arise quickly and can be life-threatening if not addressed. Recognizing them early allows clinicians to intervene before permanent damage occurs. 

Acute kidney injury develops in up to 60% of hospitalized patients. Severe hyperkalemia can cause fatal cardiac arrhythmias. Disseminated intravascular coagulation (DIC) may occur. Compartment syndrome may cause permanent muscle or nerve damage. Patients may develop metabolic acidosis, hypovolemic shock, or liver dysfunction. Rarely, acute respiratory distress syndrome (ARDS) or peripheral neuropathies may complicate the course. 

Outcomes depend on the severity of the muscle injury, the timeliness of fluid treatment, and whether kidney injury develops. Prognosis varies widely, but early recognition and treatment usually lead to good outcomes. Patients with more severe complications require close follow-up and may face long-term risks. 

Many patients recover fully with early management and never develop lasting kidney damage. Severe cases with multiorgan failure may require prolonged intensive care and dialysis. Patients who develop kidney failure requiring dialysis are at higher risk for chronic kidney disease and future cardiovascular disease. 

Prevention plays a key role in lowering the risk of rhabdomyolysis, especially in individuals who are more vulnerable. By addressing common triggers and promoting healthy habits, clinicians and patients can work together to reduce complications. Public education, early detection, and consistent monitoring are also essential parts of preventive care. 

• Athletes and military personnel should build exercise tolerance gradually and stay well-hydrated. 

• Strenuous activity should be avoided in extreme heat. 

• Doctors should monitor patients on drugs like statins for early signs of muscle toxicity. 

• Immobilized patients should be repositioned frequently to avoid prolonged pressure on muscles. 

• Disaster response planning should include measures to reduce crush injuries. 

• At-risk individuals, including laborers, athletes, and soldiers, should be taught the early warning signs of muscle injury and the importance of hydration. 

• Clinicians should maintain high suspicion for rhabdomyolysis in trauma, postoperative, or critically ill patients. 

Rhabdomyolysis is a dangerous condition that requires rapid recognition and treatment. The consequences of delayed intervention include acute kidney injury, electrolyte imbalances, and even death. A multidisciplinary approach involving emergency physicians, nephrologists, critical care specialists, and rehabilitation teams ensures the best outcomes. 

Ongoing research continues to improve our understanding of the condition, its biomarkers, and the best treatments. Prevention and education remain equally important in lowering the risk and improving outcomes. 

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