ABSTRACT. Background: There is a paucity of data evaluating the efficacy of nutrition support in traumatic brain-injured patients induced into barbiturate coma for refractory intracranial hypertension. Our objective was to evaluate the efficacy of enteral nutrition in a select group of trauma patients. Methods: Prospective data were collected on severe traumatic brain-injured patients over a 4-year period. Patients were stratified by whether or not they were induced into a barbiturate coma. Barbiturate coma was defined as per American Association of Neurological Surgeons (AANS) guidelines. All patients were initially fed via the enteral route via a nasogastric feeding tube. Patients who did not tolerate feedings within 48 hours started receiving prokinetic agents. Feeding tolerance was defined as ability to tolerate enterai feedings with 72 hours. Results: Fifty-seven patients were induced into a barbiturate coma. All were victims of blunt-force trauma. Forty-two of 57 (74%) patients were men, with a mean age of 37 ± 12 years and a mean injury severity score of 24 ± 10. Thirty-eight of the 57 (67%) patients had an isolated traumatic brain injury. All 57 patients failed enteral nutrition via the nasogastric route after the first 48 hours of nutrition initiation after barbiturate coma was fully achieved by protocol criteria. Prokinetic agents demonstrated no improvement in feeding tolerance after the subsequent 48-72 hours. Of the 12 patients who had a postpyloric feeding tube placed, only 25% tolerated enteral nutrition for >48 hours. Conclusions: Patients with traumatic brain injury induced into barbiturate coma develop a significant ileus that is refractory to prokinetic agents. Only a marginal improvement is seen when the postpyloric route is obtained. Early parenteral nutrition should be considered in this patient population. (Journal of Parenteral and Enteral Nutrition 30:503-506, 2006)

Nutrition support in the traumatic brain-injured patient continues to be a very important factor in the care of these unique high-risk patients. Because of various factors, including multiple surgeries and aggressive treatment modalities, that may hinder gastric emptying, nutrition support is often compromised. This increases the risk of poor outcome and, thus, may negatively affect outcome. The traumatic braininjured patient who has intractable intracranial hypertension represents a unique patient population that is at the far end of the spectrum in terms of risk and adverse outcome.

The traumatic brain-injured patient rapidly becomes the paradigm of unchecked metabolism and catabolism.1 A hypermetabolic and hypercatabolic state ensues, and daily caloric and protein needs may be in excess of twice the normal predicted basal caloric and protein needs. Impaired immune function may result as a consequence of this hypermetabolic response and inadequate nutrition, leading to increased susceptibility to infection and adverse outcome.2 Early nutrition in these patients has been demonstrated to ameliorate the profound negative nitrogen balance caused by this excessive protein catabolism.1′3

The ability to provide adequate nutrition support is often hindered when patients require neuromuscular blockers and other sedative agents as major components of their clinical management.4′5 Both traumatic brain injury and these classes of medications impair gastric emptying and thus lead to intolerance of gastric feeding.6 Pentobarbital-induced coma is a treatment strategy reserved for the traumatic brain-injured patient with refractory intracranial hypertension. This treatment modality decreases the tone and amplitude of contractions of the gastrointestinal tract and is mediated centrally and peripherally. Therefore, patients are more likely to not tolerate enterai nutrition.

There is a paucity of data evaluating the efficacy of nutrition support in traumatic brain-injured patients induced into barbiturate coma for refractory intracranial hypertension. Our objective was to evaluate the efficacy of enterai nutrition in a select group of trauma patients.

METHODS

Prospective data were collected over a 4-year period (1999-2003) on 57 consecutive severely traumatic brain-injured patients admitted to the R. Adams Cowley Shock Trauma Center who were induced into a barbiturate coma due to refractory intracranial hypertension. Barbiturate coma was denned as per American Association of Neurological Surgeons (AANS) guidelines (Table I). Feeding tolerance was not evaluated until there was a physical examination consistent with barbiturate coma (no cough or gag reflex) or burst suppression by electroencephalogram (EEG) measurements. All patients were initially fed with an immuneenhanced formula via the enterai route using a nasogastric feeding tube. Patients who did not tolerate enterai feedings within 48 hours of barbiturate coma initiation began receiving a standard prokinetic regimen (Reglan, AH Robins Co., Division of American Home Products, Madison, NJ; 10 mg IV every 6 hours) and switched over to a semielemental or elemental formula as per the staff clinical nutritionist. Placement of nasal-jejunal tubes, either blindly or endoscopically assisted, in patients that failed to tolerate enterai feedings despite prokinetic therapy was at the discretion of the intensive care unit (ICU) attending physician. Feeding tolerance was defined as the ability to tolerate enterai feedings with 72-hour period from initiation of barbiturate coma. Patients who did not tolerate gastric feedings within 72 hours started receiving parenteral nutrition (PN) via the central venous route. Caloric requirements and rates of nutrition infusion were determined in a multidisciplinary fashion by the critical care physician, critical care nutritionist, and trauma physician.