Critical care nephrology · KIMS Secunderabad
Rhabdomyolysis — When Muscle Breakdown Threatens the Kidneys
Rhabdomyolysis is the rapid breakdown of skeletal muscle — releasing the muscle cell's contents into the bloodstream. The most clinically dangerous of these contents is myoglobin, a haem-containing protein from muscle cells that is freely filtered by the kidneys. At high concentrations, myoglobin precipitates in the renal tubules, causing direct tubular toxicity and obstruction — the mechanism of rhabdomyolysis-induced acute kidney injury (AKI). The urine turns dark brown or cola-coloured from myoglobin excretion, and without immediate, aggressive treatment, oliguric AKI requiring dialysis develops within 12 to 24 hours.
Rhabdomyolysis has multiple causes — from the dramatic (crush injuries, severe electric shock, drowning) to the unexpectedly common (statin-induced myopathy, alcohol, seizures, extreme exertion). In India, trauma-related rhabdomyolysis is the most frequent severe presentation — road traffic accidents causing crush injury, entrapment, and compartment syndrome. Awareness of rhabdomyolysis as a cause of AKI is critical because the treatment — massive IV fluid hydration to flush myoglobin through the kidneys — is time-sensitive: delay of even a few hours significantly worsens kidney outcomes.
Causes of rhabdomyolysis
Trauma
Road traffic accidents with crush injury · Entrapment · Falls from height · Electrical injury · Burns · Prolonged immobilisation (coma, drug overdose) causing compartment syndrome.
Exertion
Extreme unaccustomed exercise · Marathon running · Military training · Status epilepticus (prolonged seizures) · Hyperthermic emergencies (heat stroke — relevant to Indian summers).
Drug and toxin-related
Statins (statin myopathy — rare but important, particularly with rosuvastatin at high doses or statin-fibrate combinations) · Alcohol excess · Cocaine · MDMA (ecstasy) · Snake venom · Haemolytic toxins.
Infections
Viral myositis (influenza, coxsackie, EBV, HIV) · Bacterial sepsis with severe muscle involvement · Leptospirosis (important in India — severe leptospirosis commonly causes rhabdomyolysis + AKI) · Tetanus.
Metabolic and genetic
Hyponatraemia or hyperosmolarity · Hypothyroidism · Hypokalemia · Glycogen storage diseases (McArdle disease) · CPT2 deficiency.
Clinical features
Dark brown or cola-coloured urine — the most visually dramatic symptom, caused by myoglobin excretion. The urine may be brown without visible haematuria — myoglobin causes a positive dipstick reaction for blood (because the haem group reacts with the dipstick reagent) but urine microscopy shows no red blood cells. This dipstick-positive, microscopy-negative haematuria distinguishes myoglobinuria from true haematuria.
Muscle pain, tenderness, and swelling — in the affected muscle groups. Diffuse myalgia in exertion or drug-related rhabdomyolysis; localised tenderness and swelling over the crushed or compressed muscle in trauma.
Weakness — profound in severe rhabdomyolysis affecting large muscle groups.
Oliguria or anuria — as AKI develops from tubular myoglobin precipitation and ischaemia.
Systemic features — fever, nausea, tachycardia, and haemodynamic instability in severe cases, particularly trauma-related rhabdomyolysis with fluid sequestration into damaged muscle.
Key investigations
Serum creatine kinase (CK)
The principal diagnostic marker. CK is released from damaged muscle cells and rises dramatically in rhabdomyolysis — typically above 1,000 U/L (five times the upper limit of normal) and often above 10,000 to 100,000 U/L in severe cases. The CK level correlates roughly with the degree of muscle injury. CK peaks at 24 to 72 hours after injury and falls by 50% every 1 to 2 days with treatment.
Urine dipstick and microscopy
Positive for blood (from myoglobin) with no red cells on microscopy. The combination confirms myoglobinuria.
Serum creatinine and eGFR
Rising creatinine indicates developing AKI. Note: in rhabdomyolysis, creatinine may rise faster than in typical AKI — because damaged muscle also releases creatine, which is converted to creatinine in the body, artificially elevating serum creatinine beyond the level explained by kidney dysfunction alone.
Serum potassium
Hyperkalaemia is common and can be life-threatening. Damaged muscle releases massive quantities of potassium. ECG monitoring is essential if potassium is above 5.5 mEq/L.
Serum calcium and phosphate
Hypocalcaemia (from calcium entering damaged muscle cells and phosphate release from muscle) is common in the oliguric phase. Hypercalcaemia may occur during the recovery phase (as calcium mobilises from damaged muscle).
Urine myoglobin
A specific but less widely available test than CK. Not required for diagnosis when the clinical picture and CK are clear.
Treatment at KIMS — the urgency of hydration
Aggressive IV fluid resuscitation
The cornerstone of treatment. The goal is to maintain urine output above 200 to 300 ml/hour — high urine flow dilutes myoglobin in the tubules, reduces its concentration below the precipitation threshold, and washes it through before tubular obstruction occurs. IV 0.9% normal saline at 1 to 1.5 litres per hour initially, adjusted to maintain the urine output target. Isotonic sodium bicarbonate solution may be alternated with normal saline to alkalinise the urine (alkaline pH reduces myoglobin precipitation in the tubular lumen and reduces its oxidative toxicity). Total fluid requirements in severe rhabdomyolysis may reach 10 to 20 litres in the first 24 hours.
Electrolyte management
Hyperkalaemia is the most dangerous electrolyte complication — treated with calcium gluconate (membrane stabilisation), insulin-dextrose, and sodium bicarbonate. Dialysis for potassium above 6.5 mEq/L with ECG changes. Hypocalcaemia in the oliguric phase: avoid aggressive calcium supplementation — asymptomatic hypocalcaemia is not treated (the calcium is being taken up by damaged muscle and will be released during the recovery phase, potentially causing hypercalcaemia if supplemented).
CRRT for severe AKI
Patients with rhabdomyolysis-AKI who develop oliguric renal failure, life-threatening hyperkalaemia, or severe fluid overload despite aggressive hydration require dialysis support. At KIMS, CRRT (continuous renal replacement therapy) provides continuous fluid removal and electrolyte control in haemodynamically unstable patients. CRRT also provides some myoglobin clearance through high-volume haemofiltration, though the primary treatment remains IV hydration.
Treat the underlying cause
Compartment syndrome — emergency fasciotomy to decompress the muscle compartment and prevent further ischaemia. Trauma-related rhabdomyolysis — surgical management of the injury. Statin-related — immediate statin cessation. Infection — appropriate antibiotics.
Emergency Nephrology at KIMS — 24/7 for Rhabdomyolysis and AKI
Frequently Asked Questions — Rhabdomyolysis
Yes — exercise-induced rhabdomyolysis is increasingly recognised, particularly with the popularity of high-intensity training, CrossFit, long-distance running, and military fitness regimens in India. Extreme unaccustomed exertion — particularly eccentric muscle loading (downhill running, plyometrics, heavy squat sessions) in untrained individuals — causes sarcolemmal damage and myoglobin release. Warning signs: severe generalised muscle pain and weakness appearing 12 to 48 hours after extreme exercise, along with dark or reduced urine output. Exercise-induced rhabdomyolysis that requires hospitalisation is not rare — anyone who develops dark-coloured urine after extreme exertion should seek emergency evaluation immediately.
Statin-induced rhabdomyolysis is rare but real — occurring in approximately 1 in 10,000 patients on standard statin doses. The risk is higher with: high-dose statins (rosuvastatin 40mg, atorvastatin 80mg), combination of a statin with a fibrate (particularly gemfibrozil — a pharmacokinetic interaction increases statin plasma levels), concurrent use of CYP3A4 inhibitors (certain antibiotics, antifungals, and grapefruit juice with simvastatin and atorvastatin), and pre-existing muscle disease. Any patient on a statin who develops significant myalgia (muscle pain that is new and disproportionate) with weakness should have a CK checked — and the statin should be withheld until the CK result is available.
The brown or cola-coloured urine of rhabdomyolysis is caused by myoglobin — a haem-containing protein released from damaged muscle cells that is freely filtered by the kidneys and excreted in the urine. Myoglobin imparts a brown colour to urine (similar to how blood in the urine turns it red — both contain haem). The urine dipstick tests positive for blood (the haem group reacts with the dipstick reagent), but urine microscopy shows no red blood cells — because the brown colour comes from myoglobin molecules, not intact red cells. This discordance — positive dipstick, negative microscopy — is the classic diagnostic finding of myoglobinuria.
The volume is large — typically 6 to 12 litres of IV fluid in the first 24 hours, and sometimes up to 20 litres in severe trauma-related rhabdomyolysis. The target is urine output above 200 to 300 ml/hour — not a specific volume of fluid given. Fluid is titrated to urine output. Patients with massive rhabdomyolysis can sequester enormous volumes of fluid into the damaged muscle ('third-space fluid loss'), requiring proportionally larger volumes of replacement to maintain intravascular volume and renal perfusion. Under-resuscitation — giving too little fluid because the volumes seem alarming — is the most common error in rhabdomyolysis management.
KIMS Secunderabad — Dr. E. Ravi (Senior Consultant Nephrologist, critical care nephrology), 24/7 emergency nephrology, CRRT in ICU for severe rhabdomyolysis-AKI, high-volume IV fluid protocol with urine output monitoring, CK and potassium monitoring, ECG monitoring for hyperkalaemia, fasciotomy coordination with orthopaedic surgery for compartment syndrome. Emergency line: 040-4488-5000.