Management of Crush‑Injury–Induced Compartment Syndrome and Crush Syndrome

Diagnosis of Acute Compartment Syndrome

Severe pain out of proportion to injury and pain on passive stretch of fingers/wrist are key clinical signs of forearm compartment syndrome【1】.
Compartment pressures ≥ 30 mmHg, or a differential pressure (diastolic blood pressure – compartment pressure) < 30 mmHg, confirm the diagnosis【1】.

Prolonged entrapment (≥ 2 hours) in a crush injury markedly increases the risk of rhabdomyolysis and subsequent acute kidney injury【2】.
Young adult males (< 35 years) are a demographic group frequently affected by severe crush‑injury outcomes【1】.

Aggressive isotonic crystalloid therapy (3–6 L of 0.9 % saline in the first 24 h) is recommended to maintain urine output of 200–300 mL/h until myoglobinuria resolves【3】.
Continuous cardiac monitoring is advised because hyperkalemia from rhabdomyolysis can precipitate life‑threatening arrhythmias【3】.

Immediate fasciotomy is the definitive treatment for diagnosed compartment syndrome; delays beyond 6–8 h significantly raise the risk of irreversible muscle/nerve damage, limb loss, and death【1】.
Elevating the affected limb above heart level should be avoided, as it reduces perfusion pressure and worsens compartment syndrome【1】.

Serial measurement of serum creatinine and BUN is essential for early detection of acute kidney injury in crush patients【2】.
Urine output and color should be monitored hourly, targeting 200–300 mL/h; myoglobinuria (tea‑colored urine) indicates ongoing renal risk【3】.

Hyperbaric oxygen therapy has no proven benefit in reversing muscle necrosis once compartment syndrome is established and should not replace emergent fasciotomy【1】.
Routine urine alkalinization is not recommended; aggressive fluid resuscitation alone provides adequate renal protection【3】.

Even with optimal early management, a 2‑hour entrapment duration confers a high likelihood of poor functional outcome, including Volkmann’s contracture【2】.
Overall mortality in crush‑injury patients is approximately 20 %, with acute kidney injury being the second most common cause of death after direct trauma【2】.

The incidence of crush syndrome varies widely according to the amount of muscle necrosis, duration of compression, timing of fluid resuscitation, and individual patient characteristics such as baseline volume status and renal function. 4
Among earthquake victims, the proportion who develop crush syndrome is highly variable, demonstrating that not every crush injury leads to systemic complications. 4

Initiating intensive crystalloid therapy (e.g., 3–6 L of 0.9 % saline within the first 24 h, begun while the victim is still trapped) can restore renal function and completely prevent myoglobinuric acute kidney injury, often eliminating the need for dialysis. 5, 6
Aggressive early fluid management alone is sufficient to avert dialysis in crush victims who would otherwise progress to myoglobinuric AKI. 5

Low ambient temperatures at the disaster site lower metabolic demand, which may reduce the extent of muscle necrosis and therefore lessen the required intensity of fluid therapy. 5
In large‑scale disasters where close monitoring is impractical, fluid administration may be constrained to 3–6 L per day, potentially affecting the adequacy of resuscitation. 5
Chaotic rescue operations and delayed recognition of crush injury often cause the critical time window for effective fluid resuscitation to be missed, increasing the risk of myoglobinuric AKI. 4, 5