Case #039

The whole case turns on one line of the urinalysis. The dipstick is strongly positive for blood, yet microscopy finds no red cells, and that combination has a single explanation: the dipstick detects haem, so it reads positive for myoglobin exactly as it does for haemoglobin. What is colouring this urine is muscle pigment, not bleeding. That immediately separates it from the glomerular causes of dark urine, where dysmorphic red cells and red cell casts are the finding. A creatine kinase of 84,000 confirms the source, and levels above roughly 5,000 mark the point where kidney injury becomes likely. The mechanism of the injury is threefold: myoglobin casts obstruct the tubules, haem is directly toxic to tubular cells, and fluid sequestered into swollen muscle leaves the patient intravascularly dry, driving renal vasoconstriction. The electrolytes are simply the contents of broken muscle cells appearing in the blood, which is why potassium and phosphate rise together while calcium falls as it deposits in damaged muscle. The raised AST is muscle in origin rather than liver, a common source of confusion. The precipitant here is unaccustomed exertion in someone deconditioned and dehydrated, the classic exertional pattern, and the ECG is the reminder that the potassium, not the kidney, is what can kill him in the next hour: the T waves across the praecordial leads are tall, narrow and symmetrically peaked on a QRS that is still narrow, the earliest change of hyperkalaemia and the one that precedes the widening QRS and sine wave pattern that follow if it is left alone. So the potassium is treated first and in parallel: calcium gluconate to stabilise the myocardium, insulin with dextrose to drive potassium back into cells. The kidney is then saved with volume. Early, large-volume crystalloid is the only intervention shown to prevent the injury, flushing myoglobin through the tubules before it can obstruct them, titrated to a urine output of 200 to 300 mL per hour, which often means several litres on the first day. Hartmann's and other potassium-containing fluids are avoided while the potassium is high. Bicarbonate and mannitol are traditional additions on weak evidence, and dialysis is held back for refractory hyperkalaemia, acidosis or anuria.