Unanswered questions of "ProCon"etic therapy.

T he provision of enteral nutrition shortly after admission to the intensive care unit (ICU) is associated with beneficial outcomes. The development of high residual volumes frequently impedes the delivery of gastric feeding and may be associated with deleterious outcomes. 3 The most common therapeutic option for managing high gastric residual volumes is the initiation of prokinetic therapy with either metoclopramide or erythro-mycin. Several studies have demonstrated greater gastric motility and feeding tolerance when these agents are used for this indication. 4-7 However, few data exist that define residual volume that signifies intolerance, delineate the relationship between residual volume and clinical outcomes , or assess the optimal role of prokinetic agents in various patient populations. Moreover, these agents have side effects; metoclopramide may cause extrapyramidal movement disorders, whereas erythromycin is associated with hepatic drug interactions, QT interval prolongation, and possibly microbial resistance. 6 In this volume of the Journal of Parenteral and Enteral Nutrition (JPEN), Dickerson et al demonstrated in trauma patients that: (1) patients with brain injury are approximately 1.8 times more likely to develop feeding intolerance than other trauma patients; (2) metoclopramide frequently fails to maintain residual volume low enough to advance the feeding rate in trauma patients with intolerance ; and (3) the presence of brain injury is associated with a 2.9-fold higher rate of metoclopramide therapy failure. 8 These results mandate close monitoring of gastric feeding and aggressive therapy when intolerance is present in this patient population. Although this study was retrospective in design, its strength involves the systematic manner in which nutrition support was provided and gastric residual volumes managed. Others have demonstrated that feeding intolerance is common when neu-rologic injury is present and that subsequent therapy with metoclopramide may not be effective. The Dickerson study, however, is the first to label traumatic brain injury as an independent predictor of therapy failure, specifically with metoclopramide. Patients with metoclopramide failure had higher measurements of intracranial pressure, further suggesting that a centrally mediated neurologic insult limits gastric motility. The mechanism may involve the suppression of vagal activity to disturb the migrating motor complex (MMC) that originates in the gastric antrum. 4,5 Similarly, cardiovascular abnormalities as a result of altered vagal activity may occur after traumatic brain injury. Although Dickerson et al showed similar rates of successful feeding over 7 days regardless of the degree of head injury, whether improved neurologic recovery was associated with greater metoclopramide response …