The metabolic response to spinal cord injury

• Published in: Spinal cord 1997-09, Vol.35 (9), p.599-604
• Main Authors: Rodriguez, Donna J, Benzel, Edward C, Clevenger, Frederick W
• Format: Article
• Language: English
• Subjects: Adult; Aged; Anatomy; Biological and medical sciences; Biomedical and Life Sciences; Biomedicine; Calorimetry, Indirect; Diarrhea - etiology; Dietary Proteins - administration & dosage; Energy Intake; Energy Metabolism; Female; Foods, Specialized; Human Physiology; Humans; Injuries of the nervous system and the skull. Diseases due to physical agents; Male; Medical sciences; Middle Aged; Neurochemistry; Neuropsychology; Neurosciences; Nitrogen - metabolism; Nutritional Support - adverse effects; original-article; Spinal Cord Injuries - metabolism; Spinal Cord Injuries - therapy; Traumas. Diseases due to physical agents
• ISSN: 1362-4393; 1476-5624
• DOI: 10.1038/sj.sc.3100439

The metabolic response to trauma, including neurotrauma in general, has been studied extensively, but the acute metabolic response to spinal cord injury (SCI) has not. Therefore, 12 patients with SCI are presented in whom intensive nutrition assessment and management were instituted immediately after injury. Nitrogen balance (NB), predicted energy expenditure (PEE), and actual energy expenditure (MEE) were calculated or measured in each patient. A persistent negative NB was observed in all but one of the 12 patients. The single patient who did not exhibit persistent negative NB (no positive NB from week 2 to week 4 in the face of appropriate feeding) had an incomplete myelopathy, thus implying that the degree of motor dysfunction correlates with the obligatory nature of the negative NB. The negative NB observed in several of the patients did not occur until the second or third post-injury week. In addition, calculations of PEE by successively multiplying the Harris-Benedict equation by an activity factor of 1.2 and then by a stress factor of 1.6, resulted in excessive feeding (as assessed by metabolic cart measurements; ie indirect calorimetry) in the majority of the patients. In all of the 11 patients with persistent negative NBs, protein administration in the amount of 2 g/k of ideal body weight and aggressive caloric delivery did not alter the negative pattern of the NBs. Therefore, it is concluded that the negative NB following SCI is obligatory. Furthermore, the extent of SCI (extent of myelopathy or of neurological injury) correlates with the obligatory nature of the negative NB. In addition, the results from using the above method for estimating caloric requirements and the delayed manifestation of the negative NB may cause an additional tendency to acutely overfeed SCI patients. Therefore, eliminating the activity factor of 1.2 (due to the diminished activity arising from paralysis) and a diminution of the stress factor is recommended for initial PEE calculations. Serial metabolic cart (indirect calorimetry) measurements are recommended to accurately assess the patient's subsequent metabolic requirements.