Rhabdomyolysis, Obstetric Emergencies, Obesity and Failure to Thrive

Rhabdomyolysis: Assessment, Electrolyte Dynamics, and Renal Protection

Rhabdomyolysis is characterized by skeletal muscle necrosis with the release of intracellular contents into the systemic circulation, including myoglobin, potassium, phosphorus, and creatine kinase. A creatine kinase level greater than five times the upper limit of normal supports the diagnosis in the appropriate clinical setting; however, the bedside nurse must recognize that this level may be normal early after muscle injury. Myoglobinuria can cause dark reddish-brown urine, but visible discoloration is absent in many patients with rhabdomyolysis. In the laboratory and bedside setting, this causes a urine dipstick to test positive for blood despite the microscopic absence of intact red blood cells.

Major mechanisms of acute kidney injury in rhabdomyolysis include renal vasoconstriction, direct myoglobin-mediated tubular toxicity, and tubular obstruction by myoglobin-containing casts. Early electrolyte derangements include life-threatening hyperkalemia, hyperphosphatemia, hyperuricemia, and initial hypocalcemia caused by calcium precipitation into damaged muscle tissue. Later in the clinical course, hypercalcemia can occur as this sequestered calcium is mobilized back into the extracellular space during tissue recovery. Continuous cardiac monitoring and serial electrolyte tracking are essential to detect these rapid shifts before lethal arrhythmias emerge.

Early intravenous crystalloid administration is the cornerstone of therapy. Critical care nurses monitor urine output and volume status while titrating ordered fluids toward an individualized goal, commonly 1 to 3 mL/kg/hr up to about 300 mL/hr, while remaining vigilant to prevent fluid overload. Routine sodium bicarbonate infusion to alkalinize the urine has not been shown to prevent acute kidney injury. If sodium bicarbonate is ordered for another clinical indication, the nurse must closely monitor acid-base status and serum electrolytes, watching specifically for worsening hypocalcemia and arterial metabolic alkalosis.

Skeletal muscle breakdown also places patients at high risk for extremity compartment syndrome. Nurses must assess frequently and report early warnings: severe pain out of proportion to the examination, pain triggered by passive stretch, and paresthesias. Pallor, coolness, paralysis, and loss of pulses are late findings, and peripheral pulses may remain fully palpable despite dangerous pressures. When intracompartmental pressure reaches at least 30 mmHg, or the perfusion delta pressure drops to 30 mmHg or less, the nurse must notify the surgical team immediately for emergency assessment of possible fasciotomy.