Nutritional Support after Spinal Cord Injury

Hypermetabolism, an accelerated catabolic rate and rampant nitrogen losses are
consistent sequelae to major trauma, particularly acute traumatic brain injury and acute spinal
cord injury. (7,9-11,13,18,20,23). A well-documented hypermetabolic, catabolic injury cascade
is initiated immediately after central nervous system injury which results in depletion of whole
body energy stores, loss of lean muscle mass, reduced protein synthesis, and ultimately in loss of
gastrointestinal mucosal integrity and compromise of immune competence. (5,9,10,12,18,20,23).

Severely injured brain and spinal cord injury patients, therefore, are at risk for prolonged
nitrogen losses and advanced malnutrition within two to three weeks following injury with
resultant increased susceptibility for infection, impaired wound healing and difficulty weaning
from mechanical ventilation. (6,9,13,18,20,23). These factors added to the inherent immobility,
denervation and muscle atrophy associated with spinal cord injury provide the rationale for
nutritional support of spinal cord injured patients following trauma.

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