Metabolic Consequences of Spinal Cord Injury

THE clinical course of many patients after severe trauma to the spinal cord is often marked by the inability to ingest adequate amounts of protein and the failure to assimilate fully protein which is ingested or administered parenterally (1, 2). It is not a rare occurrence to see a patient who is paraplegic as the result of injury to the spinal cord, literally “die of starvation,” despite vigorous attempts to supply adequate nutrients (Case 6). Our study was undertaken to gain further factual insight into the pathogenesis of the derangement of protein metabolism in such cases. In addition we have recorded clinical observations of gynecomastia, testicular atrophy and other endocrinologic variations which have been reported in cases of paraplegic men (3, 4). Clinical and metabolic studies were made of the cases of 16 men who had suffered injury to the spinal cord. The investigation was limited to hospitalized patients, who, for the purpose of this report, were divided into 3 groups, depending on the interval which elapsed from the time of injury until the time the essential data were recorded. These arbitrary groups included cases in which the condition of the patient was 1) acute (recent), being observed during the first two weeks after injury, 2) postacute, with examination from two weeks to six months after injury and 3) chronic, observed six months or longer after injury. Four patients are considered in more than one of these categories.