Intolerance to enteral feeding in the brain-injured patient

Abstract

Calorie and protein supplementation improves nutritional status. This support may improve outcome and decrease morbidity and mortality in acutely brain-injured patients. Investigators have observed a poor tolerance to enteral feedings after brain injury and have noted that this persists for approximately 14 days postinjury. This delay has been attributed to increased gastric residuals, prolonged paralytic ileus, abdominal distention, aspiration pneumonitis, and diarrhea. In the present investigation, 23 brain-injured patients with an admission 24-hour peak Glasgow Coma Scale (GCS) score between 4 and 10 were studied for 18 days from hospital admission. The mean duration from injury to initiation of full-strength, full-rate enteral feeding was 11.5 days. Seven of the 23 patients tolerated enteral feedings within the first 7 days following hospital admission (mean 4.3 days), four patients tolerated feedings between 7 and 10 days postadmission (mean 9 days), and 12 patients did not tolerate feedings until after 10 days postinjury (mean 15.9 days). There was a marginally significant relationship between low GCS scores on admission and length of days to enteral feeding tolerance (p = 0.07). A significant inverse relationship was observed between daily peak intracranial pressure (ICP) and time to tolerance of feedings (p = 0.02). There was no significant relationship between feeding tolerance and days to return of bowel sounds (p = 0.12). Serum albumin levels decreased during the investigation (mean +/- standard error to the mean: 3.2 +/- 0.12 gm/dl on Day 1; 2.7 +/- 0.23 gm/dl on Day 16; normal = 3.5 to 5.0 gm/dl), whereas the percentage of patients tolerating feedings increased over the course of the study. The authors conclude that patients with acute severe brain injury do not adequately tolerate feedings via the enteral route in the early postinjury period. Tolerance of enteral feeding is inversely related to increased ICP and severity of brain injury. It is suggested that parenteral nutritional support is required following brain injury until enteral nutrition can be tolerated.

RETRACTED CHAPTER: Brain Trauma and Nutritional Support

“…However, patients with TBI often have severe impairment of gastrointestinal passage despite the use of different therapies to improve tolerance for enteral feeding. In some patients, parenteral or supplemented nutrition (enteral feeding with parenteral components on top to reach the required nutrition goals) has to be applied (Norton et al 1988). A later supplementation may be associated with a better outcome than early supplementation (Casaer et al 2011).…”

Lesões cerebrais agudas e sua influência sobre a motilidade gastrintestinal

“…(32)(33)(34) However, enteral nutrition has been reported to be more beneficial than parenteral nutrition, given its lower cost, lower infection risk, protection of intestinal epithelium integrity, improvement of immunocompetence and attenuation of the metabolic stress response during the illness critical phase. (35) Some severe HT patients, however, cannot tolerate enteral nutrition and show increased gastric residues, prolonged paralytic ileus, abdominal distension and diarrhea. (35) In this clinical condition, enteral nutrition success appears to be inversely correlated with the ICP and trauma severity.…”

“…(35) Some severe HT patients, however, cannot tolerate enteral nutrition and show increased gastric residues, prolonged paralytic ileus, abdominal distension and diarrhea. (35) In this clinical condition, enteral nutrition success appears to be inversely correlated with the ICP and trauma severity. The mechanism of this relationship may be multi-factorial.…”

Traumatic Brain Injury and the Gastrointestinal Tract: The Role of Female Sexual Hormones

“…Motility disorders in brain injured patients include gastroesophageal reflux related to reduced tone in the lower esophageal sphincter and deferred gastric emptying [8,9]. Some studies showed that moderate TBI with no substantial mucosal damage causes a delayed significant decrease in intestinal contractile activity that occurs primarily in the ileum due to decreased contraction amplitude.…”

“…The association between the severity of brain injury and the intolerance of enteral feeding suggests a strong link between the central nervous system and the nonfunctional gut [6,7]. More than 50% of patients with severe head injuries do not tolerate enteral feedings [8]. The intolerance is presented by vomiting, abdominal distention, delayed gastric emptying [9], esophageal reflux [10], and decreased intestinal peristalsis indicating that GI dysfunction is a common phenomenon following TBI [11].…”