PubMed · 8642750
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C H Organ, R J Bold. 1996-06-19. Surgery.. https://pubmed.ncbi.nlm.nih.gov/8642750/
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Progressive liver failure in parenteral nutrition (PN)-dependent children with short bowel syndrome carries significant morbidity and mortality. The authors retrospectively reviewed 47 consecutive patients with short bowel syndrome diagnosed from October 1985 through October 1995. All patients were treated according to a protocol designed to promote intestinal motility and discourage bacterial translocation. Elements of the protocol included the use of taurine, vigilant prevention and aggressive treatment of sepsis, meticulous catheter care, early PN cycling, appropriate enteral feeding, and measures designed to inhibit gastrointestinal bacterial translocation, especially gram-negative rods. Complete blood counts and serum liver function studies were compiled from both clinic visits and hospital admissions for each patient every 3 to 6 months while they were on PN. Three patients were lost to follow-up after they had moved out of state. The length of time on PN ranged from 3 months to 9.4 years with an average of 2.2 years. Elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and glutamyltransferase (GGT) were present in 82%, 66%, and 84% of patients, respectively. Alkaline phosphatase was elevated in 58% of patients. Eight patients (18%) are still on PN, and 31 (70%) have been weaned off PN. Five patients have died (11%). Three patients (7%) developed cholecystitis requiring cholecystectomy. No patients developed progressive liver failure. These results suggest that PN-related liver failure may be prevented in most patients with short bowel syndrome. Specific measures to prevent PN-related cholestatic jaundice need further investigation.
BACKGROUND: Critically ill patients are susceptible to injury of the intestinal mucosa, changes in gut permeability, and failure of intestinal defense mechanisms. These conditions put the patients at risk for infection and multiple organ dysfunction syndrome. Specific therapies are needed to prevent gut failure during critical illness. OBJECTIVE: The purpose of this literature review is to provide a better understanding of the normal defense mechanisms of the gut and alterations associated with ischemia-reperfusion injury, risk of infection, and the link to multiple organ dysfunction syndrome in critically ill patients. Implications for early enteral stimulation and nutrition are included. METHODS: Medical and nursing studies on the intestinal response to critical illness and on the implications for early enteral nutrition in critically ill patients were reviewed. RESULTS: Significant advances have been made in understanding the normal defense mechanisms of the gut, including barrier and immune functions. Translocation of bacteria, mediators of the inflammatory response, and the microcirculation play a role in the response to critical illness. Enteral nutrition that includes glutamine and arginine enhances gut function and improves patients' outcomes in some clinical states. DISCUSSION: Further research should focus on specific strategies to enhance gut function, prevent loss of gut integrity, and improve patients' outcomes. These strategies include maintaining mesenteric blood flow, using gastric tonometry to assess oxygenation, inhibiting inflammatory mediators, and using growth factors to modify the metabolic state in patients who are critically ill.
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