Presentation

Classic presentation

• While motor vehicle collisions, pedestrians being struck by motor vehicles, and industrial accidents are the most common causes of a crush injury, a large number of life-threatening crush injuries occur as a result of natural disasters. Injury is often clear from chief complaint and mechanism.
  
• Arterial injuries can present broadly, from a simple hematoma to profound hemorrhagic shock. The clinical presence of “the 5 Ps” (pain, pallor, pulselessness, paresthesias, and paralysis) should be attributed to arterial injury.
  
• Open fractures are typically obvious with significant disruption of the original anatomy and visible bony structures. The main concerns are arterial injury compromising the viability of the extremity and deep tissue and joint space contamination that can lead to long-term complications, such as osteomyelitis.

Critical presentation

• The “crush syndrome” comprises the systemic manifestations that arise as a result of a crush injury once the external force is removed. The patient can develop hypovolemia, shock, compartment syndrome, lactic acidosis, or renal failure from traumatic rhabdomyolysis. Rhabdomyolysis can cause acute renal failure in up to 40% of patients with crush injuries.
  
• Arterial injury can lead to hypotension if the hemorrhage is not addressed aggressively with source control and resuscitation with fluids.
  
• The mangled extremity severity score (MESS) is the most widely validated classification system of the lower extremity when evaluating the severity of open fractures. Limb viability is related to vascular status, patient age, duration of ischemia, and absorbed energy. A score of 6 or less predicts limb viability while a score of 7 or higher predicts the need for amputation. MESS has high specificity but low sensitivity. As yet, there is no scoring system that reliably predicts the need for amputation.

Diagnosis and evaluation

• Crush injury
  
  
  
  • Electrolyte abnormalities such as low calcium and elevated serum potassium, phosphate, and uric acid that results from massive cellular damage.
    
  • Venous (or arterial) blood gas will reveal metabolic lactic acidosis.
    
  • Creatine phosphokinase (CPK), as the surrogate marker to assess the extent of muscle damage.
    
  • Urine studies will determine the presence of myoglobin indirectly. Myoglobin in the urine will be detected as “blood” on the urine dipstick but there will be no red blood cells noted on the urine analysis.
    
  • Evaluate for manifestations of hyperkalemia by obtaining an ECG. The increase in serum potassium is most severe in the first 12–36 hours after muscle injury. Initially, there may be peaked T waves and prolonged PR interval. At levels between 7–8 mEq/L, the ECG may reveal a widened QRS and flattened P waves. For potassium levels >8 mEq/L, the ECG may degenerate into a sine wave pattern (see Figure 14.1), then ventricular fibrillation, followed by cardiac arrest.

Severe hyperkalemia on ECG (Figure 14.1)

Figure 14.1. Severe hyperkalemia on ECG.

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