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Albany Medical College Albany, NY 12180 E-mail: howardl{at}mail.amc.edu
This text provides a comprehensive overview of intestinal failure, both acute and chronic, and its pathophysiology and management. The authors are chiefly from the United Kingdom and Europe, and their cooperation on this book reflects the cooperation they have exercised in research pertinent to intestinal failure. This is said with some envy because in the United States fiscal pressures on academic health science centers are relentlessly emphasizing clinical work over scientific work.
Early chapters focus on the many different conditions that lead to intestinal failure, including inflammatory processes, loss of bowel surface area, and impaired motility. Also included is a chapter on iatrogenic intestinal failure used as a treatment for morbid obesity.
The book makes a serious effort to present established knowledge about intestinal adaptation to massive bowel resection, stressing the relative lack of adaptation in the short bowel with an end-jejunostomy and the substantial adaptation provided by a retained colon. This is an important orientation for new students. But the book also captures the interest of old students because it is peppered with new nuggets awaiting more scientific confirmation. For example, the chapter on the short bowel discusses how lack of peptide YY and glucagon-like peptide 2 may in part explain the poor adaptation with an end-jejunostomy. The chapter describes how reduced mucosal mass results in reduced citrulline formation, potentially leading to impaired ammonia detoxification. The chapter on intestinal adaptation discusses a potential role for bovine colostrum, which is a rich source of growth factors and antibacterial peptides. The chapter on dietary treatment describes the use of cholylsarcosine, a synthetic bile acid that is resistant to bacterial deconjugation and hydroxylation.
Every serious effort unfortunately has a few errors. In the chapter on the short bowel, figure 12.2 (183) is incorrectly shaded. It shows the patient with 101–200 cm of jejunum and incontinuity colon as the most likely to remain dependent on parenteral nutrition. In fact, exactly the opposite is true, as is indicated in the figure legend. The home parenteral nutrition chapter states (415) that "in the USA 23% of Medicare patients received IDPN [intradialytic parenteral nutrition] during dialysis." This is not correct. IDPN is not considered a part of home parenteral nutrition because it is administered in hemodialysis centers by professionals, not self-administered in the patient's home. By 1992 IDPN accounted for 23% of the parenteral nutrition Medicare beneficiaries were receiving outside the hospital (eg, in their homes, in nursing homes, in dialysis centers, and in infusion clinics). In 1992 there were 40000 home parenteral nutrition patients in the United States and 27% were Medicare beneficiaries. None of these patients were receiving IDPN.
Most available texts on intestinal failure stress the management of intestinal failure and focus on parenteral and enteral nutrition therapy. This text opens the gate wider by considering the many pathophysiologic components of intestinal failure and hence new avenues for the treatment of intestinal failure.