The liberation of large amounts of myoglobin and other muscle cell contents in the blood leads to hyperkalemia, hyperphosphatemia, hypocalcemia, and metabolic acidosis (Table. ...2). These abnormalities begin when serum urea and creatinine concentrations are still within normal limits. Hyperkalemia may cause life-threatening ventricular arrhythmias, justifying continuous electrocardiographic monitoring.
Table 2 Flow of solutes and water across skeletal muscle cell membrane in rhabdomyolysis
Myoglobinuria associated with intravascular volume depletion, which is seen in crush syndrome, leads to acute tubular necrosis. The latter is the consequence of renal hypoperfusion, acid urine pH, tubular obstruction caused by precipitation of heme proteins, and possibly tubular cell anoxia. Delayed volume replacement, even if adequate in quantity, results in the development of acute renal failure within a day.
Patients with acute renal failure in this setting have a high-anion-gap metabolic acidosis, hyperuricemia, and hyperphosphatemia. Hemoconcentration and occasionally thrombocytopenia may suggest the onset of disseminated intravascular coagulation (DIC).
Factors predicting the development of acute renal failure have been identified as peak creatine phosphokinase elevation, degree of serum potassium elevation on admission, degree of phosphate elevation on admission, decrease in serum albumin, and clinical evidence of dehydration. Acute renal failure has been seen in patients with a mean creatine phosphokinase level of 40 500 lU/l accompanied by significant hypovolemia, or in patients with urinary myoglobin concentrations in excess of 1000 ng/ml. None of these factors have been confirmed prospectively.
Within minutes of trauma, intramuscular pressure in injured muscle may exceed arterial blood pressure. Ischemic interference with the regulation of muscle cell volume causes cell swelling, which results from the accumulation of intracellular solutes, an increase in the leakiness of the cell membrane, and a reduction in active ionic extrusion. Intracompartmental pressure rises rapidly in muscle groups confined in tight fibrous sheaths with low compliance, such as the calf or forearm. The compartment syndrome appears when intracompartmental pressure exceeds arteriolar perfusion pressure, obliterating the circulation to the affected region and causing muscle and myoneuronal ischemic damage within hours. Stretching of the muscle increases the leakiness of the skeletal muscle cells and nerve cells to calcium ions, which may explain the vulnerability and sensitivity of skeletal muscle to mechanical pressure of short duration. The intramuscular pressure in patients with compressed or wedged limb injuries may increase to more than 240 mmHg, causing rhabdomyolysis independent of ischemia. Full-blown rhabdomyolysis and anterior tibial compartment syndrome may occur in such patients despite normal arterial pedal pulses and warm skin.
Many symptoms may mimic spinal injury. However, the neurological examination reveals normal anal sphincter and urinary bladder function, which may help to exclude the presence of an acute spinal cord lesion in chemically or organically paralyzed patients with rhabdomyolysis. Diagnosis relies upon repeated physical examination and measurement of the intramuscular compartment pressure. Severe worsening of myalgias, development of paresthesias, and tense muscle compartments with myoedema should provoke the measurement of the intramuscular pressure by means of manometry using a probe and a transducer. Values in excess of 30 to 40 mm Hg confirm the diagnosis and prompt the need for decompression (e.g. fasciotomy, escherotomy).
Rhabdomyolysis is often associated with hypocalcemia due to a shift of extracellular calcium into the injured muscle. Sarcolemmic Na +,K+-ATPase activity is impaired in damaged muscle. Attenuating the activity of this ion pump would diminish the extrusion of sodium from the sarcoplasm and interfere indirectly with the efflux of calcium from the cell (Table2). Thus an increase in the cytosolic free-calcium level would activate neutral proteases which, in turn, disrupt myofibrils and lead to muscle damage with rhabdomyolysis. Serum monitoring may initially show hypocalcemia. A 99mTc-diphosphate scan would confirm the calcium shift. Release of muscle-fixed calcium leads to secondary hypercalcemia with elimination of calcium excess by the kidneys as the syndrome resolves. Secondary hypercalcemia of less than 3 mmol/l is clinically uneventful and may be secondary to abnormal control of 1,25-(OH) 2-vitamin D3 metabolism. Therefore monitoring of serum (and urinary) calcium levels at regular intervals during the course of acute traumatic rhabdomyolysis is recommended.
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