Crush syndrome pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
It is a reperfusion injury that appears after the release of the crushing pressure. The mechanism is believed to be the release into the bloodstream of muscle breakdown products—notably myoglobin, potassium and phosphorus—that are the products of rhabdomyolysis (the breakdown of skeletal muscle damaged by ischemic conditions).
The specific action on the kidneys is not understood completely, but may be due partly to nephrotoxic metabolites of myoglobin.
Seigo Minamistudied the pathology of three soldiers who died in World War I from insufficiency of the kidney. The renal changes were due to methohemoglobin infarction, resulting from the destruction of muscles, which is also seen in persons who are buried alive. The progressive acute renal failure is because of acute tubular necrosis.
The most devastating systemic effects can occur when the crushing pressure is suddenly released, without proper preparation of the patient, causing reperfusion syndrome. Without proper preparation, the patient, with pain control, may be cheerful before extrication, but die shortly thereafter. This sudden decompensation is called the "smiling death." [1]
These systemic effects are caused by a traumatic rhabdomyolysis. As muscle cells die, they absorb sodium, water and calcium; the rhabdomyolysis releases potassium, myoglobin, phosphate, thromboplastin, creatine and creatine kinase.
Compartment syndrome can be secondary to crush syndrome. Monitor for the classic 5 P’s: pain, pallor, parasthesias, pain with passive movement, and pulselessness.
References
- ↑ Nancy Caroline (2007), Nancy Caroline's Emergency Care in the Streets: Trauma Medical, 2 (6th ed.), p. 19-13, ISBN 9780763742393