Crush syndrome

Definition

Crush syndrome/rhabdomyolysis is defined as the systemic manifestation of injury(prolonged severe crushing) of the skeletal muscles of such a severity as to cause a disruption of cellular integrity & release of its contents(creatine kinase, lactic acid, myoglobin, & potassium) into the circulation.
This causes hypovolemia, hyperkalemia, metabolic acidosis, renal hypoperfusion, & ischemia resulting in acute renal failure (ARF).

Pathophysiology

-Crush injury can lead to crush syndrome.
-in crush injury, ischaemia followed by reperfusion (reperfusion injury)-the main mechanism of muscle injury in crush syndrome (traumatic rhabdomyolysis)
-Muscle injury causes release of large quantities of potassium, phosphate, myoglobin, creatine kinase & urate into the circulation.
-excess myoglobin is filtered by the kidneys & can cause renal tubular obstruction & renal damage (nephrotoxic)
-Intravascular volume depletion & renal hypoperfusion, combined with myoglobinuria-→ Renal dysfunction
-Hypovolaemic shock (sequestration of water in the injured muscle cells)
-Hyperkalaemia (K release by the injured muscle cells)
-Metabolic acidosis (release of phosphate & sulphate by the injured muscle cells)
-Acute Renal Injury
-DIC

Clinical feaures

-Petechiae, blisters, muscle bruising, & superficial injuries
-Crushing injury to a large mass of skeletal muscle
-Sensory & motor disturbances in the compressed limbs, which later on become tense & swollen.
-The limb/body part may be pulseless.
-Tea/cola coloured urine (due to Myoglobinuria and/or haemoglobinuria)
-Oliguria with hypovolaemic shock(Renal failure)
-Fever, cardiac arrythmia, Pneumonia
-Nausea, Vomiting, Confusion, agitation/irritability & delirium (due to deranged-elevated urea, creatinine, uric acid, potassium, phosphate & creatine kinase & hypocalcaemia)

Management

RESCUE & RESUSCITATION at the site of Injury
-safety of self and others.
-assessment of patient considering him/her as a severely injured person.
ABCDE protocol(Airway, Breathing & Circulation) should be followed.
-Monitor vital signs & O2 saturation level & administer oxygen through a non-rebreather mask.
-assessment of limbs for ‘5 Ps'(pain, paraesthesia, paralysis, pallor & pulselessness), to estimate extent of ischaemic injury.
-attention to life-threatening injuries.
– IV access, if possible, before the trapped limb is freed & decompressed.
-Preserve body heat.
-Apply a tourniquet prior to release if compression has been more than 30 minutes(an arterial tourniquet if compression less than 30 minutes).
-a saline infusion of 1,500 ml/hour(in adult), should be initiated during extrication. Early, vigorous hydration (≥10 litres/day) helps preserve renal function.
-a Foley’s catheter insertion for urine output monitoring.
-analgesia should be provided(e.g. nitrous oxide is better than oral/IV analgesia)

Investigations
-Urea, Creatinine, Electrolytes including potassium
-Ca (hypocalcaemia), Phosphate.
-Creatine kinase (rhabdomyolysis is confirmed when total creatine kinase levels 5-10 times above normal in a patient with typical symptoms &/or risk factors)
-Serum creatinine kinase (CKMM) levels more than 1000 U/L with associated clinical features is an indicator of crush syndrome, (Normal range is 25-175 U/L), usually rises 2-12 hrs after a crush, peaks in 1 to 3 days and declines after 3 to 5 days.
-Serum myoglobin & myoglobin degradation products- highly sensitive tests
-Uric acid
-CBC & clotting profiles (DIC).
-LFTs (hepatic dysfunction).
– ABG(arterial blood gases).
-ECG
-Intracompatmental pressure measurement
-Doppler studies

Further Management

Medical
-it mainly includes Fluid replacement and monitoring; Diuresis; Dialysis; Hyperbaric oxygen; & Antibiotics.
-maintain urine output at 300 ml/hr until myoglobinuria has ceased
-forced mannitol-alkaline diuresis (Mannitol enhances renal perfusion & reduce muscle injury too).
-Urinary alkalinisation with Na-bicarbonate
-Treatment of hyperkalaemia
-Renal dialysis may be required
-treatment of DIC with FFP, cryoprecipitate & platelets.
-Hyperbaric Oxygen
-Antibiotics (Broad spectrum non nephrotoxic antibiotics)
-Tetanus immunisation

Surgical
-Laparotomy & thoracotomy for wide & ruthless debridement of all necrosed muscles followed by delayed primary or secondary suturing.
-Fasciotomy for increased compartment pressure-Early fasciotomy is better, as fasciotomies after 8-10 hrs of crush have necessitated amputations
Fracture fixation & conservative amputation of crushed limbs (Early amputation may prevent crush syndrome)

Rehabilitation
-for muscle contracture & for any limb amputation

For more details, lease see the following articles:
1. Crush Injuries and the Crush Syndrome
by S Rajagopalan

2. Crush Syndrome
by Dr Laurence Knott