Seminars in gastrointestinal disease最新文献

Critically ill patients are at increased risk of developing stress-related mucosal lesions. The pathogenesis of stress-related mucosal disease is not entirely clear, but probably is associated with impairment of mucosal protective mechanisms due to compromised gastric mucosal microcirculation. Acid also plays an integral role. The incidence of gastrointestinal bleeding among intensive care unit patients has been declining over the past 30 years. Only a small proportion of patients with stress-related mucosal lesions develop clinically overt bleeding, and the majority of the overt bleedings do not lead to hemodynamic instability. However, the presence of gastrointestinal bleeding in a critically ill patient predicts markedly increased mortality. Prolonged mechanical ventilation and coagulopathy are the most important predictors of stress ulcer related bleeding. Critically ill patients with stress ulcer related bleeding should be managed in the acute setting just as patients presenting with upper gastrointestinal bleeding. Available evidence supports the use of stress ulcer prophylaxis in patients with risk factors for bleeding. Both histamine 2 receptor antagonists and sucralfate are effective forms of stress ulcer bleeding prophylaxis. More potent acid suppression by proton pump inhibitors may offer additional benefit in the prevention of stress ulcer bleeding.

Intensive care unit patients present a difficult challenge in the diagnosis and treatment of complications related to the biliary tract. Altered mental status interferes with the patient's ability to communicate symptoms and give a reliable physical examination. Laboratory data are often nonspecific in diagnosing complications of biliary tract disease because of the high incidence of cholestasis in intensive care unit patients. Likewise, routine radiographic evaluation has a marked decreased sensitivity and specificity in evaluating biliary tract disorders. Taken together, these factors often lead to a delay in diagnosis of biliary tract problems in the intensive care unit patient. Intervention in these patients is associated with high morbidity and mortality when compared to the ambulatory setting. This article reviews the clinical presentation, differential diagnosis, and management options of biliary tract complications in this complex patient population.

Fulminant hepatic failure is a challenging medical condition that requires intensive care management to prevent-major complications (cerebral edema, infections, and multi-system organ failure) and assistance from a liver transplant team when it is believed that liver regeneration is unlikely. Unfortunately, there are no specific medical therapies or devices to correct all of the functions of a liver. N-acetylcysteine is used for the treatment of acetaminophen overdose, but for most other causes of fulminant hepatic failure therapy is supportive care. This case illustrates many of the problems that are encountered during medical management of fulminant hepatic failure.

Esophageal varices develop in patients with cirrhosis once portal pressure, measured by hepatic venous pressure gradient, and exceeds 10 mm Hg. At a portal pressure of 12 mm Hg, variceal bleeding may develop that is associated with a mortality of 30% to 50% per episode. In addition to an elevated portal pressure, other risk factors for the development of variceal hemorrhage include: variceal size, endoscopic features on the variceal wall (i.e., red wales), and Child-Pugh class. In patients with suspected variceal hemorrhage, the treatment of the acute episode includes intravascular volume expansion, hemostasis through the use of pharmacological agents and endoscopy, and the prevention and treatment of potential complications associated with variceal hemorrhage such as aspiration pneumonia, spontaneous bacterial peritonitis and hepatic encephalopathy. Given a high rate of rebleeding, long-term prevention through secondary prophylaxis should be instituted in all patients who have survived an episode of variceal bleeding. Current prophylactic options include: non-selective beta-blockers alone (first line) or in combination with long-acting nitrates (isosorbide mononitrate) and/or endoscopic variceal obliteration achieved through sclerotherapy or preferably, band ligation.

"Malabsorption" syndrome is the term widely used to describe the end result of either impaired breakdown of nutrients (maldigestion) or defective mucosal uptake and transport of adequately digested nutrients (true malabsorption). The latter may affect a broad range of nutrients (ie, panmalabsorption) or individual nutrients or groups of nutrients (ie, specific malabsorption). This review discusses the etiology and pathophysiology of malabsorption. A diagnostic approach to malabsorption is proposed. Other articles review specific disorders such as celiac disease, bacterial overgrowth, and chronic pancreatitis.

Tropical malabsorption remains an important clinical problem for both the indigenous population of tropical countries and for short-term visitors and longer-term residents from the industrialized world. In young children, persistent diarrhea and malabsorption can result in severe retardation of growth and development. The most common cause is an intestinal infection notably the small intestinal protozoa including Giardia intestinalis, Cryptosporidium parvum, Isospora belli, Cyclospora cayetanensis, and the microsporidia. Tropical sprue still remains an important diagnostic option but is less common than it was 20 to 30 years ago. It is important to attempt to make a specific microbiological diagnosis as this will influence the choice of antibiotic. However, if laboratory facilities are not available, it is possible to offer empirical therapy although this may involve a trial of more than one antibiotic.

Under certain conditions, colonic bacterial flora can colonize the upper small bowel in concentrations sufficient to cause mucosal damage and malabsorption of nutrients, vitamin B12, and fat-soluble vitamins. This situation, known as small bowel bacterial overgrowth syndrome (SBBOS) may be an under-appreciated cause of malnutrition in elderly people. The diagnosis of SBBOS should be considered when patients with known or suspected predisposing conditions have symptoms or findings compatible with this syndrome. However, proof of small bowel bacterial overgrowth requires specialized testing that is not readily available. Moreover, disagreement persists as to how best to test definitively for this disease. Therefore, on a practical level and despite the potential drawbacks of such a decision, SBBOS is usually diagnosed when a compatible syndrome responds to an empirical trial of appropriate oral antibiotics. Improvements on this approach to SBBOS will be built on more widespread access to sensitive, specific, and less cumbersome testing than is currently available.

Patients with chronic pancreatitis may suffer from maldigestion and malnutrition. Longstanding inflammation and fibrosis in the gland can destroy exocrine tissue, leading to inadequate delivery of digestive enzymes to the duodenum in the prandial and postprandial period and subsequent maldigestion. Maldigestion is augmented by inadequate bicarbonate delivery to the duodenum, with secondary inactivation of enzymes and bile acids by gastric acid. Abdominal pain, sitophobia, nausea, vomiting, postprandial satiety, and on-going alcohol abuse may contribute to poor oral intake. Gastric dysmotility and mechanical gastric outlet obstruction from fibrosis in the pancreatic head may contribute to malnutrition and clinical decline. Patients with chronic pancreatitis may at times experience profound steatorrhea and weight loss. In this article, we examine the natural history of exocrine insufficiency in chronic pancreatitis, outline the important nutritional issues in these patients, review the methods of diagnosis of maldigestion, and discuss the approach to therapy.

Short bowel syndrome is an uncommon disease that results from extensive intestinal resection. Short bowel patients develop severe malabsorption of macronutrients, micronutrients, electrolytes and water, and pose difficult management problems. This report describes a typical patient with the short bowel syndrome and how each component of the malabsorption syndrome is managed to maintain nutritional, electrolyte, and water balance. In practice, some short bowel patients become dependent on parenteral nutrition for life, while others become independent with time due to intestinal adaptation and can be managed on oral intake and supplementations. Short bowel patients are at risk of developing gallstones, oxalate kidney stones and, rarely, d-lactic acidosis, and the pathophysiology of these disease processes is outlined. A minority of short bowel patients may ultimately require intestinal transplantation due to irreversible complications, and the current status of this intervention is reviewed. Finally, growth factors that stimulate intestinal growth and, thus, enhance absorptive capacity, are currently being identified and may eventually be introduced in the treatment of these patients.

Celiac sprue, celiac disease, or gluten-sensitive enteropathy, is a malabsorption disorder of the small intestine that occurs after ingestion of wheat gluten in genetically susceptible individuals. This disease is characterized by intestinal malabsorption associated with villous atrophy of the small intestinal mucosa, clinical and histological improvement after adherence to strict gluten free diet, and relapse when gluten is reintroduced. Celiac sprue has a high prevalence in Western Europe and North America where it is estimated to affect 1:120 to 1:300 individuals. The pathogenesis of celiac sprue is related to inappropriate intestinal T-cell activation in HLA-DQ2 positive individuals triggered by antigenic peptides from wheat gluten or prolamins from barley and rye. Although previously thought to be mainly a disease of childhood onset, the diagnosis is increasingly being made in adults. There are a wide variety of presentations, which range from asymptomatic forms to severe diarrhea, weight loss and nutritional deficiencies. Extraintestinal manifestations including anemia, osteopenia or neurological disorders and associated conditions such as diabetes or hypothyroidism are commonly present. The availability of highly sensitive and specific serologic markers has dramatically facilitated the diagnosis of celiac sprue. However, the demonstration of characteristic histological abnormalities in a biopsy specimen of the small intestine remains the mainstay of diagnosis. Treatment consists of life-long avoidance of dietary gluten to control symptoms and to prevent both immediate and long-term complications.