Iron released from the heme generates reactive oxygen species, damaging the kidney cells. In addition to the myoglobinuria, two other mechanisms contribute to kidney impairment: low blood pressure leads to constriction of the blood vessels and therefore a relative lack of blood flow to the kidney, and finally uric acid may form crystals in the tubules of the kidneys, causing obstruction. Together, these processes lead to acute tubular necrosis, the destruction of the cells of tubules. Glomerular filtration rate falls and the kidney is unable to perform its normal excretory functions. This causes disruption of electrolyte regulation, leading to a further rise in potassium levels, and interferes with vitamin D processing, further worsening the low calcium levels. Diagnosis
A diagnosis of rhabdomyolysis may be suspected in anyone who has sustained trauma, crush injury or prolonged immobilization, but it may also be identified at a later stage due to deteriorating kidney function (abnormally raised or increasing creatinine and urea levels, falling urine output) or reddish-brown discoloration of the urine. General investigations
The most reliable test in the diagnosis of rhabdomyolysis is the level of creatine kinase (CK) in the blood. This enzyme is released by damaged muscle, and levels above 1000 U/L (5 times the upper limit of normal (ULN)) indicate rhabdomyolysis. More than 5,000 U/L indicates severe disease but depending on the extent of the rhabdomyolysis, concentrations up to 100,000 U/l are not unusual. CK concentrations rise steadily for 12 hours after the original muscle injury, remain elevated for 1–3 days and then fall gradually.
A crush injury is injury by an object that causes compression of the body. This form of injury is rare in normal civilian practice, but common following a natural disaster. Other causes include industrial accidents, road traffic collisions, building collapse, accidents involving heavy plant, disaster relief or terrorist incidents. Presentation
Complications
Hypovolaemic Shock. Loss of plasma volume across damaged cell membranes and capillary walls can lead directly to severe hypovolaemia. Furthermore, shock can develop from myocardial depression following release of intracellular electrolytes. In addition, as a result of the mechanism of injury, blood loss from pelvic or long bone fractures may also co-exist. Hyperkalaemia and electrolyte imbalance. Disruption of cell membranes can result in a significant release of potassium, which is a largely intracellular cation that can precipitate cardiac arrest. Sequestration of plasma calcium into injured tissue can lead to a relative hypocalcaemia, which may worsen disruption of clotting abilities and shock. Metabolic acidosis may result from reperfusion injury and hypoperfusion related to shock. Compartment syndrome. Compartment syndrome is a common complication of crush injury as a consequence of oedematous tissue injury, redistribution of fluid into the intracellular compartment and bleeding. Established compartment syndrome may result in worsened systemic crush syndrome and irreversible muscle cell death. Acute Kidney Injury. Release of myoglobin by injured muscle leads to rhabdomyolysis coupled with shock leads to a significant rate of acute kidney injury, estimated as up to 15%. Acute kidney injury leads to a significantly higher mortality.