Extensive muscle crush injury culminating in the crush syndrome (CS) is often lethal unless promptly and vigorously treated. The causes of death in the CS are extreme hypovolemic shock, hyperkalemia, hypocalcemia, metabolic acidosis, acute myoglobinuric renal failure, and the compartment syndrome. Treatment consists of early massive volume replacement, preferably administered in the field, followed by forced alkaline solute (mannitol) diuresis. With this regimen, it is possible to increase substantially the survival of lives and limbs and to prevent acute myoglobinuric renal failure in patients suffering from the CS. Preliminary experience suggests that intravenous hypertonic mannitol is protective also to the injured muscle and can be used as a noninvasive adjunct in the management of compartment syndrome in humans. Moreover, by preserving muscular integrity, mannitol can conceivably reduce sarcolemmal leakage of the nephrotoxic myoglobin urate and phosphate and thus further defend kidney function. Furthermore, mannitol reduces the plasma pool of these nephrotoxic metabolites by increasing urinary elimination.

Uremic patients undergoing chronic hemodialysis demonstrate a secondary systemic carnitine deficiency. We studied the effect of carnitine replacement with high doses (L-carnitine, 3 g/day) similar to those used in the treatment of primary systemic carnitine deficiency. 10 uremic patients on hemodialysis were randomly selected into a control group (4 patients) treated by placebo and a treatment group (6 patients) treated by L-carnitine. Plasma lipoprotein concentration and composition as well as platelet aggregation were studied before and after treatment. Following carnitine administration, a paradoxical rise in plasma triglyceride concentration from 180 ± 66 to 219 ± 88 mg% (p < 0.05) was noted. No other significant changes in lipoprotein concentration and composition or in plasma apoprotein A-I and B concentration were observed. Carnitine treatment caused a significant rise in platelet aggregation induced by epinephrine, ADP, and thrombin. These findings suggest a harmful effect of L-carnitine replacement therapy when given in high doses, causing aggravation of uremic hypertriglyceridemia and increased platelet aggregation in patients predisposed to thromboembolic phenomena.

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An 11‐year follow‐up of a patient with malignant pheochromocytoma of the organ of Zuckerkandl (M.P.O.Z.) is reported. The long survival was probably due to treatment by α and β blocking agents, preventing a cardiovascular catastrophy. The patient ultimately succumbed to diffuse metastatic spread. Radiologic and cytotoxic treatment did not have any appreciable effect on the course of the disease.