Rhabdomyolysis & Crush Syndrome

📘 1 · Washington Manual of Critical Care

Definition, Causes & the Classic Triad

Rhabdomyolysis is the breakdown of skeletal muscle with release of its intracellular contents — creatine kinase, myoglobin, potassium and phosphate — into the circulation. The classic triad of muscle pain, weakness and dark "tea-coloured" urine is present in a minority; most cases are picked up on a raised creatine kinase in the right clinical setting. The threat to life comes not from the muscle injury itself but from what leaks out of it: potassium, and the myoglobin that poisons the kidney.

Summarised from the Washington Manual of Critical Care — Rhabdomyolysis.

Diagnosis

Creatine kinase (CK) > ~5× the upper limit of normal (usually >1000 U/L); the risk of AKI rises as CK climbs, particularly above ~5000 U/L.
Myoglobinuria — urine dipstick positive for "blood" but few/no red cells on microscopy (the dipstick detects myoglobin as well as haemoglobin) — a useful bedside clue.
Supportive: raised potassium, phosphate, urate; low calcium early; raised AST/LDH.

Causes — "trauma and everything else"

Traumatic / compression

Crush injury, prolonged immobility ("long lie", collapse, surgery)
Compartment syndrome, tourniquet, burns, electrocution

Exertional / thermal

Extreme exertion, seizures, agitation, dystonia
Heat stroke, neuroleptic malignant syndrome, malignant hyperthermia

Toxic / metabolic / other

Alcohol, statins/fibrates, cocaine, opioids (immobile)
Hypokalaemia/-phosphataemia, myopathies, infections, snakebite

📗 2 · Marino's The ICU Book, 5th Edition (2025)

Why Myoglobin Injures the Kidney

Filtered myoglobin damages the kidney through three overlapping mechanisms: it causes renal vasoconstriction, it precipitates with Tamm–Horsfall protein to form obstructing casts in the tubule, and its heme moiety generates oxidative injury to tubular cells. All three are made dramatically worse by hypovolaemia and by acidic urine. This is why the single most effective treatment is early, generous fluid — restoring renal blood flow and flushing the pigment through before it can precipitate.

Summarised from Marino PL. The ICU Book, 5th Ed — Myoglobinuric Acute Kidney Injury.

🔬 From muscle injury to pigment AKI

TriggerMuscle necrosis (crush, exertion, toxin, ischaemia)

Release of myoglobin, K⁺, PO₄³⁻, CK, urate + fluid sequestration into muscle

Hypovolaemia → renal hypoperfusion & concentrated, acidic urine

Renal vasoconstriction

Tubular cast obstruction (Tamm–Horsfall)

Heme oxidative injury

Pathological statePigment (myoglobinuric) AKI + life-threatening hyperkalaemia

📗 Marino — the electrolyte rollercoaster

Hyperkalaemia — released from dying muscle, worsened by AKI: the immediate killer. Compounded by hyperphosphataemia.
Early hypocalcaemia — calcium is deposited in damaged muscle; do not correct it unless symptomatic or needed for hyperkalaemia, because…
…rebound hypercalcaemia occurs in the recovery phase as that calcium is released — over-replacing early makes it worse.

📗 Marino — crush syndrome & the reperfusion trap

In crush syndrome, the systemic illness often begins when the compressing force is released: reperfusion floods the circulation with potassium and acid and shifts litres of fluid into the injured limb, precipitating hyperkalaemic arrest and shock. In entrapment/disaster settings, start aggressive IV fluids before or at the moment of extrication — resuscitation cannot wait for the patient to reach hospital.

📋 3 · Guidelines — Fluids, Urine & the Controversies

Evidence-Based Management

Early aggressive fluid resuscitation — the cornerstone STRONG

Start IV isotonic fluid early and generously — often 1–2 L/h initially, then titrated (commonly aiming for the order of ~200–300 mL/h urine output, i.e. a target diuresis rather than a fixed volume). Total requirements can reach several litres to >10 L/day in crush injury. Balanced crystalloid or 0.9% saline are both used — avoid potassium-containing fluids while hyperkalaemic; monitor closely for fluid overload once oliguric AKI is established.

Urinary alkalinisation & mannitol — optional, not proven WEAK / individualise

Sodium bicarbonate (to alkalinise urine to pH >6.5) and mannitol are traditional adjuncts intended to reduce cast formation and act as an osmotic diuretic — but no trial has shown they add benefit over adequate saline volume alone, and both carry risks (bicarbonate worsens hypocalcaemia and causes alkalosis; mannitol can precipitate AKI if the patient is volume-depleted or already oliguric). If used, only after volume repletion and an established urine output, and stop if there is no response.

Manage the electrolytes & know when to dialyse KDIGO

Treat hyperkalaemia aggressively (see Electrolyte Emergencies) — it is the acute cause of death. Do not routinely correct hypocalcaemia (deposition now, rebound later) unless symptomatic or treating hyperkalaemia. Renal replacement therapy for the usual indications — refractory hyperkalaemia, severe acidosis, fluid overload, uraemia (see AKI & RRT). Note that most CK/myoglobin is not effectively cleared by conventional dialysis — RRT is for the complications, not to "remove myoglobin".

Look for & treat compartment syndrome

Rhabdomyolysis and compartment syndrome drive each other. Suspect it with a tense, painful limb, pain out of proportion and pain on passive stretch (pulses and sensation are late signs). Measure compartment pressures if unsure; urgent fasciotomy for established acute compartment syndrome — but avoid unnecessary fasciotomy of a non-viable crush limb (infection risk). Involve surgery early.

🇮🇳 Indian Context

Rhabdomyolysis is common from trauma and road-traffic crush injuries, building collapses, prolonged "found-down" states, heat stroke, seizures, strenuous unaccustomed exertion, and snakebite (several Indian snake venoms are directly myotoxic — see Snakebite). In mass-casualty crush disasters (earthquakes/building collapse), begin high-volume IV fluids at the scene, before extrication, to pre-empt reperfusion hyperkalaemia. Where dialysis access is limited, early aggressive fluids to prevent AKI is the highest-value, lowest-cost intervention — and the reason to start volume the moment rhabdomyolysis is suspected.

💊 4 · Drug Doses

Fluids, Electrolyte & Adjunct Therapy

Drug / Fluid	Indication	Dose	Notes
0.9% saline / balanced crystalloid	Resuscitation (cornerstone)	1–2 L/h initially, then titrate to urine ~200–300 mL/h	Start early/at extrication; avoid K⁺-containing fluids while hyperkalaemic; watch overload if oliguric
Calcium gluconate 10%	Hyperkalaemic ECG changes / symptomatic ↓Ca²⁺	10 mL IV (repeat as needed)	Cardiac membrane stabilisation; don't routinely correct asymptomatic hypocalcaemia
Insulin + dextrose	Hyperkalaemia (shift)	10 U soluble insulin + 25 g glucose IV	Monitor glucose; see Electrolyte Emergencies
Salbutamol neb	Hyperkalaemia (shift)	10–20 mg nebulised	Adjunct to insulin-dextrose
Sodium bicarbonate	Optional urinary alkalinisation / severe acidosis	Titrate to urine pH >6.5 (only after volume repletion)	Unproven benefit over saline; worsens hypocalcaemia; stop if no response
Mannitol	Optional osmotic diuretic	Only after euvolaemia & established urine output	Unproven; avoid if oliguric/hypovolaemic (can worsen AKI)
Renal replacement therapy	Refractory K⁺ / acidosis / overload / uraemia	Standard indications (KDIGO)	For complications — does not effectively clear myoglobin

🗺 5 · Clinical Flowchart

Management Algorithm

Recognise & check the killers first

CK >5× ULN in context; dip "blood" positive with no RBCs; myalgia/weakness/dark urine
ECG + potassium immediately — hyperkalaemia is the acute threat

Fluids early & generously

Isotonic crystalloid 1–2 L/h, then titrate to urine output ~200–300 mL/h
In crush/entrapment: start fluids before extrication
Insert a urinary catheter; monitor U&E, CK, Ca²⁺, PO₄³⁻, ABG, fluid balance closely

Treat electrolytes & the cause

Aggressive hyperkalaemia treatment; don't over-correct calcium
Stop the offending drug/toxin; cool heat stroke; control seizures/agitation; treat sepsis

Consider adjuncts & complications

Bicarbonate/mannitol only after volume repletion & urine output — and only if they help
Assess for compartment syndrome → urgent fasciotomy if established; involve surgery

Support the kidney & watch the rebound

RRT for refractory hyperkalaemia/acidosis/overload/uraemia
Anticipate rebound hypercalcaemia in recovery; most non-oliguric AKI recovers with time

⚠️ 6 · Common Mistakes

Common Mistakes in Rhabdomyolysis

❌ Mistake 1 — Under-resuscitating with fluid

Timid fluids are the commonest error. Early, high-volume isotonic fluid — titrated to a brisk urine output — is the single intervention that prevents pigment AKI. Start before extrication in crush injury.

❌ Mistake 2 — Missing hyperkalaemia

Potassium pours out of dying muscle and rises further with AKI; it, not the CK, is what causes arrest. Get an early ECG and potassium and treat aggressively.

❌ Mistake 3 — Over-correcting early hypocalcaemia

Calcium is deposited in injured muscle early and released later. Replacing it routinely worsens the rebound hypercalcaemia of the recovery phase — treat only if symptomatic or for hyperkalaemia.

❌ Mistake 4 — Relying on bicarbonate/mannitol instead of volume

Neither is proven superior to adequate saline, and both harm if the patient is under-filled or oliguric. Volume comes first; adjuncts are optional and stopped if they don't work.

❌ Mistake 5 — Interpreting dip "blood" as haematuria

A urine dipstick positive for blood with no red cells on microscopy is myoglobinuria, not bleeding — a valuable clue that is often misread.

❌ Mistake 6 — Forgetting compartment syndrome

Pain out of proportion and pain on passive stretch precede the loss of pulses. Missing acute compartment syndrome causes limb loss and perpetuates the rhabdomyolysis — assess actively and get surgery involved.

❌ Mistake 7 — Expecting dialysis to "clear the myoglobin"

Conventional RRT does not remove myoglobin effectively. Dialysis is for the metabolic complications (K⁺, acidosis, overload, uraemia), not as a treatment for the pigment itself.

🎓 7 · Exam Pearls — DrNB / PDCC / IFCCM / EDIC

Exam Pearls

Q: How is rhabdomyolysis diagnosed?
CK >5× ULN (usually >1000 U/L) in the right setting; AKI risk climbs above ~5000 U/L. Urine dip positive for "blood" with no red cells = myoglobinuria.

Q: How does myoglobin cause AKI?
Three mechanisms — renal vasoconstriction, tubular cast obstruction (with Tamm–Horsfall protein), and heme-mediated oxidative tubular injury — all amplified by hypovolaemia and acidic urine.

Q: What is the cornerstone of treatment?
Early, aggressive isotonic IV fluids (1–2 L/h initially) titrated to a high urine output (~200–300 mL/h) — started as early as possible, before extrication in crush injury.

Q: Do bicarbonate and mannitol help?
Not proven superior to adequate saline volume; both carry risks. Use only after volume repletion and an established urine output, and stop if there is no benefit.

Q: Explain the calcium changes.
Early hypocalcaemia (calcium deposits in damaged muscle) then rebound hypercalcaemia in recovery. Do not routinely correct the early hypocalcaemia unless symptomatic or treating hyperkalaemia.

Q: What is crush syndrome, and why is extrication dangerous?
The systemic effects (hyperkalaemia, acidosis, hypovolaemic shock) of reperfusing a crushed limb on release of compression — hence start IV fluids before/at extrication to pre-empt hyperkalaemic arrest.

Q: Which electrolyte disturbance is the acute killer?
Hyperkalaemia (with hyperphosphataemia) — treat aggressively with calcium, insulin-dextrose, salbutamol and RRT if refractory.

Q: Does dialysis remove myoglobin?
No — conventional RRT does not clear it effectively; dialyse for the complications (refractory K⁺, acidosis, fluid overload, uraemia).

📚 8 · References

References

Bosch X, Poch E, Grau JM. Rhabdomyolysis and Acute Kidney Injury. N Engl J Med. 2009;361:62–72.
Chavez LO, Leon M, Einav S, Varon J. Beyond muscle destruction: a systematic review of rhabdomyolysis for clinical practice. Crit Care. 2016;20:135.
Sever MS, Vanholder R (RDRTF of ISN Work Group). Recommendations for the management of crush victims in mass disasters. Nephrol Dial Transplant. 2012;27(Suppl 1):i1–i67.
Scharman EJ, Troutman WG. Prevention of kidney injury following rhabdomyolysis: a systematic review. Ann Pharmacother. 2013;47:90–105.
KDIGO AKI Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl. 2012;2:1–138.
Marino PL. The ICU Book, 5th Edition. Acute Kidney Injury / Myoglobinuria. Wolters Kluwer; 2025.
Washington Manual of Critical Care, 4th Edition. Kollef MH, Witt CA (eds). Rhabdomyolysis. Wolters Kluwer; 2023.