Other Investigations

In every case of suspected rhabdomyolysis a full blood count (FBC) and clotting test must be performed in addition to renal function and CK.

Full blood count and clotting test

A full blood count must be obtained in all cases of rhabdomyolysis:

• Disseminated Intravascular Coagulation (DIC) can occur and serial coagulation and platelet studies with prothrombin time (PT) are required
• Activated Partial Thromboplastin Time (APTT), fibrin degradation products and fibrinogen may need to be monitored to direct therapeutic intervention

Always obtain a full blood count and clotting test.

DIC and its attendant complications carry a poor prognosis.

In the ED, the muscle damage can be determined by imaging.

Imaging

In the imaging investigations the considerations are that:

• MRI is more sensitive at detecting muscle damage than ultrasound or CT
• There are clear logistical problems in obtaining MRI
• Ultrasound shows decreased echogenicity compared with normal muscle imaging

In addition, other investigations are carried out to identify the following:

Myoglobinuria

Myoglobinuria does not have to be present to make the diagnosis. Healthy patients that are well hydrated can clear myoglobin quickly with preserved renal function.
The initial clue to the presence of rhabdomyolysis may be a dipstick positive for blood but with no red cells present in the urine. When the dipstick and a requested urinalysis do not correspond, myoglobinuria and rhabdomyolysis are likely to be present.

Potassium

Hyperkalaemia can be life threatening in rhabdomyolysis. Early measurement and frequent monitoring are necessary. The high level of serums potassium released by necrosed muscle are further elevated by the development of renal failure and acidosis.

Renal function

Serum Creatinine and Urea will be elevated and the ratio of creatinine is increased relative to urea as large amounts are released from the damaged muscle.

Calcium

Calcium levels may be low in serum initially as calcium is deposited in necrotic muscle tissue. Symptoms of hypocalcaemia are, however, rare early in the course of the disease. This calcium is later released into the circulation and symptoms of hypercalcaemia may occur.

Clearly caution must be exercised if calcium is to be administered in cases where hyperkalaemia is a feature.

Phosphate

When muscle damage occurs myocytes release Phosphate which can bind with calcium forming calcium phosphate. This can exacerbate hypocalcaemia.

Urate

Muscle cells release purines that the liver can convert to urate. Fluid rehydration will facilitate excretion.

Other enzyme levels, such as lactate dehydrogenase, aldolase, and hydroxybutyric dehydrogenase may all be elevated but these are non-specific to the condition.