Acute Rhabdomyolysis ✅

Related Subjects: | Acute Kidney Injury | Acute Rhabdomyolysis |Hypovolaemic or Haemorrhagic Shock |Obstructive Shock |Septic Shock and Sepsis |Shock (General Assessment) |Toxic Shock Syndrome

⚡ Rhabdomyolysis is the rapid breakdown of skeletal muscle fibres leading to release of intracellular contents into the circulation — including myoglobin, creatine kinase (CK), potassium, and phosphate. 🩸 The released myoglobin can precipitate within renal tubules, causing acute kidney injury (AKI). 🔎 A classic diagnostic clue is urine dipstick positive for “blood” but with no red blood cells on microscopy, indicating myoglobinuria rather than haematuria.

🚑 Immediate Management (ED/Acute Ward/HDU ideally)

• 🩺 Perform ABCDE assessment.
• 💉 Establish two large-bore IV lines.
• 📊 Check serum creatine kinase (CK) – levels ≥1000 U/L support diagnosis.
• ⚠️ CK >5000 U/L indicates increased risk of renal complications.
• 🚽 Consider urinary catheter for strict monitoring of urine output.

• 📊 FBC, U&E, creatinine. 🧪 CK level and serial CK monitoring.
• 🧬 LFTs (AST often elevated due to muscle injury).
• 🧪 Coagulation profile.
• 🧪 Lactate and venous/arterial blood gas.
• 🧫 Urinalysis (myoglobinuria).
• 🩸 Group and save if trauma suspected.

• 💧 Aggressive IV crystalloid fluids are the cornerstone of treatment and can significantly reduce risk of AKI. Aim for 200 mL/hour in severe rhabdomyolysis or orhtrwise 1–2 mL/kg/hour generally. Best done in a HDU with close monitoring to avoid overload in older patients or those with heart failure with a high CK
• 🔥 Hyperkalaemia can be fatal so watch out and treat
• 🦠 Alkalinisation is adjunct, not substitute: evidence is mixed, but considered in high-risk cases.

• 🚑 Trauma or crush injury.
• 💊 Stop offending drugs (e.g., statins).
• 🔥 Treat heat stroke or malignant hyperthermia.
• 🦠 Treat sepsis if present.
• 🧠 Manage seizures if causative.

• ⚡ Hyperkalaemia (life-threatening arrhythmia risk).
• 🩸 Disseminated intravascular coagulation (DIC).
• 🫁 Acute respiratory distress syndrome (ARDS).
• 🧠 Compartment syndrome.
• 🩺 Acute kidney injury.

🧬 Pathophysiology

• 💥 Muscle injury causes breakdown of sarcolemma membranes.
• Intracellular components enter the bloodstream:
  • Creatine kinase
  • Myoglobin
  • Potassium
  • Phosphate
  • Uric acid
• Myoglobin is filtered by the kidneys and causes damage via:
  • 🚽 Tubular obstruction (myoglobin–Tamm-Horsfall protein casts)
  • 🧨 Oxidative injury via heme-mediated reactive oxygen species
  • 📉 Renal vasoconstriction
• These mechanisms together produce acute tubular necrosis.

🩸 Causes of Rhabdomyolysis

• Traumatic Causes
  • 🚑 Crush injuries
  • Prolonged immobilisation
  • Compartment syndrome
• Exertional Causes
  • 🏋️ Extreme exercise
  • Seizures
  • Heat stroke
• Drug-related Causes
  • 💊 Statins (especially with CYP3A4 inhibitors)
  • Alcohol
  • Cocaine
  • Heroin
  • Amphetamines
• Toxic Causes
  • ☠️ Carbon monoxide
  • Ethylene glycol
  • Methanol
• Medical Causes
  • 🧬 Polymyositis / dermatomyositis
  • ⚡ Neuroleptic malignant syndrome
  • 🔥 Malignant hyperthermia
  • 🦠 Severe infection or sepsis
  • 🧪 Electrolyte disorders (hypokalaemia, hypophosphataemia)
  • 🩸 Diabetic ketoacidosis

🧍 Clinical Features

• 💪 Muscle pain and tenderness
• 🧠 Generalised weakness
• 🟤 Dark “tea-coloured” urine
• 🦵 Muscle swelling
• 🌡️ Fever (if infectious cause)
• ⚡ Arrhythmia symptoms due to hyperkalaemia

⚠️ The classic triad (pain, weakness, dark urine) is present in **less than 10% of patients**, so diagnosis requires a high index of suspicion.

🔍 Laboratory Findings

• Normal: ~40–200 U/L
• ⚪ Mild: 1,000–5,000 U/L
• 🟡 Moderate: 5,000–15,000 U/L
• 🔴 Severe: >15,000 U/L

• ⬆️ Creatine kinase
• ⬆️ Potassium (hyperkalaemia)
• ⬆️ Phosphate
• ⬆️ Uric acid
• ⬇️ Calcium initially (later rebound hypercalcaemia may occur)

📊 McMahon Score (Predicts AKI Risk)

• Age ≥50 years
• Female sex
• Creatinine >2.2 mg/dL
• Calcium <7.5 mg/dL
• Phosphate >5.4 mg/dL
• Bicarbonate <19 mmol/L
• CK >40,000 U/L
• Non-exertional cause

🛠️ Advanced Management – Detailed Commentary

• 💧 Early aggressive IV fluids Initiate as soon as rhabdomyolysis is suspected, ideally within 6 hours. Normal saline is first-line. The goal is to maintain a urine output of 1–2 mL/kg/hr. Early fluids dilute myoglobin and free radicals, reducing the risk of myoglobin-induced acute kidney injury (AKI). Avoid potassium-containing solutions, as hyperkalaemia is common.
• ⚡ Treat hyperkalaemia urgently Rhabdomyolysis releases intracellular potassium. ECG monitoring is critical. Immediate management includes IV calcium gluconate for membrane stabilization, insulin with glucose, and nebulised salbutamol if needed. Severe or refractory cases may require renal replacement therapy.
• 🧪 Urinary alkalinisation with sodium bicarbonate Consider in severe rhabdomyolysis (CK > 5000 U/L, dark urine) or when myoglobinuria threatens AKI. Alkalinising urine (target pH > 6.5) can reduce cast formation and tubular toxicity. Monitor serum sodium and volume status carefully—avoid fluid overload, especially in elderly or cardiac patients.
• 🚽 Catheterisation to monitor urine output Hourly urine output guides fluid titration and early detection of oliguric AKI. Urine dipstick may show heme positivity without RBCs, consistent with myoglobinuria. In hospital settings, this allows rapid intervention for declining renal function.
• ✂️ Fasciotomy for compartment syndrome Rare but serious complication of severe crush injury or limb trauma. Suspect if there is tense swelling, severe pain out of proportion, or neurological deficits. Early recognition prevents irreversible muscle necrosis and secondary renal injury.
• 🩺 Nephrology referral Essential if there is:
  • Progressive AKI despite fluids
  • Persistent hyperkalaemia or metabolic complications
  • Oliguria (<0.5 mL/kg/hr)
  Early nephrology involvement can improve outcomes and guide **renal replacement therapy timing**.
• 🩸 Renal replacement therapy (dialysis) Indicated in refractory AKI, severe electrolyte disturbances, or fluid overload. Intermittent haemodialysis or continuous therapies may be used depending on patient stability. Dialysis removes toxins and corrects severe hyperkalaemia but does **not clear myoglobin**; supportive measures remain critical.

📚 References

• Torres PA, Helmstetter JA, Kaye AM, Kaye AD. Rhabdomyolysis: Pathogenesis, Diagnosis and Treatment. Ochsner Journal. 2015;15(1):58-69.
• Huerta-Alardín AL, Varon J, Marik PE. Bench-to-bedside review: Rhabdomyolysis. Critical Care. 2005;9:158-169.
• McMahon GM et al. A risk prediction score for kidney failure in rhabdomyolysis. JAMA Internal Medicine. 2013;173(19):1821-1828.
• Long B, Koyfman A. Rhabdomyolysis: Emergency department management. Journal of Emergency Medicine. 2017.