Seminars in gastrointestinal disease最新文献

The incidence of esophageal adenocarcinoma has increased dramatically in developed countries during the past 2 decades, and prognosis remains very poor. Gastroesophageal reflux disease is an important risk factor for this cancer that develops in patients with specialized esophageal metaplasia (Barrett's esophagus). Careful periodic endoscopic examinations, with random biopsy sampling of the entire mucosal surface, are usually recommended for the surveillance of these patients. Several innovative techniques have recently been developed to improve the accuracy of diagnosis of intestinal metaplasia, dysplasia, and early adenocarcinoma in Barrett's esophagus. Some of these techniques (eg, chromoendoscopy, magnifying endoscopy, and light-induced fluorescence endoscopy) are intended to identify suspicious areas of the mucosa not visible during conventional endoscopic examination and to perform targeted biopsies toward these areas to avoid sampling errors. Optical coherence tomography and confocal laser scanning microscopy are other powerful techniques that provide real-time cross-sectional tissue images at a resolution close to that of histology. They allow tissue characterization based solely on optical properties and are likely to replace excisional biopsies. Although promising, none of these techniques is currently recommendable for routine surveillance of patients with Barrett's esophagus. Further evaluation is warranted to define the optimal method and standardize the procedures.

The incidence of esophageal adenocarcinoma has increased dramatically in Western societies over the last 20 years. Most patients present with advanced disease. Stage-dependent treatment protocols require the most complete and accurate staging possible. With all esophageal cancers (ie, adenocarcinomas and squamous carcinomas), it is perhaps most important to identify patients who are unlikely to benefit from aggressive treatment. The performance characteristics and clinical utility of CT scanning, endoscopic ultrasound, FDG-PET, and minimally invasive surgery in staging esophageal cancer are reviewed, including issues relating specifically to staging of adenocarcinomas. These investigations are not mutually exclusive and each has its own strengths and shortcomings. Accurate staging often requires the use of multiple modalities. The optimal staging algorithm for a given practice setting (if it exists) will be determined largely by local variables that include patient population, available technology, and local expertise in applying such technology. A lack of consensus on the effectiveness of therapeutic alternatives (particularly surgical v nonsurgical methods) may also affect the perceived value of the various staging modalities and how they are used.

Liver transplantation has become the procedure of choice for a wide variety of patients with end-stage liver disease. Perioperative morbidity and mortality have decreased dramatically over the past two decades, and superior graft and patient survival rates are now routine. Despite these advances, however, there remain several potentially lethal possibilities that may complicate the immediate postoperative period. Failure of the graft to regain any useful metabolic activity is known as primary nonfunction, and almost uniformly requires retransplantation for any hope of survival. Lesser degrees of immediate dysfunction require experienced clinical judgment as to the probability of sustaining long-term patient viability. Another potentially catastrophic development is thrombosis of the grafted hepatic artery. This is sometimes successfully managed by surgical reconstruction. It may develop immediately, or present insidiously much later. Thrombosis of the portal vein, while not usually fatal, can significantly complicate the immediate course, carrying with it a significant risk of sepsis. Close monitoring of patients in the period following liver transplantation is crucial, as prompt diagnosis and early intervention directly affects the patient's chances of survival.

Acute gastrointestinal bleeding is a common disorder with a wide spectrum of presentations that may encompass multiple clinical scenarios. Initial hemodynamic assessment and resuscitation are critical. Once accomplished, the source of bleeding should be localized, active bleeding should be stopped, the underlying abnormality should be treated, and recurrent bleeding should be prevented. The means to accomplish these goals depends on the specific clinical situation. For most forms of upper gastrointestinal bleeding, early endoscopy is the cornerstone of diagnosis and management. It can predict and improve clinical outcomes. A variety of endoscopic and pharmacologic modalities are effective at achieving and maintaining hemostasis. The optimum means of evaluation and treatment of acute lower gastrointestinal bleeding is less clear and is now evolving. Endoscopy (usually expectant, less often early) is widely used and effective for diagnosis but has unproven therapeutic benefits. Angiography is effective (diagnostically and/or therapeutically) in certain situations. Surgery offers the opportunity for definitive therapy at the cost of higher morbidity. At this time, the approach to evaluation and management should be based on the specific clinical situation and available local expertise.

Acute intestinal ischemia is a gastrointestinal emergency resulting from a sudden decrement in intestinal blood flow. It may occur as a consequence of mesenteric vascular occlusion and/or hypoperfusion and may involve the small intestine or colon. Bowel infarction, sepsis, and death may result, making prompt diagnosis and management imperative. Acute mesenteric ischemia generally stems from interruption of blood flow within the superior mesenteric artery or vein, and leads to small intestinal hypoperfusion and infarction. It carries with it a mortality rate of approximately 70%, but improved survival may be achieved as a result of early diagnostic consideration, undelayed angiography, and surgical intervention, when appropriate. Acute colonic ischemia occurs typically as a result of a transient mismatch between intestinal blood flow and the metabolic demands of the colon. Although infarction may occur, colonic ischemia is often a reversible condition with mortality rates considerably lower than those witnessed in acute mesenteric ischemia. This article reviews the pathophysiology, clinical features, diagnostic, and therapeutic options applicable to patients with acute intestinal ischemia.

The term "fulminant hepatic failure" (FHF) encompasses a pattern of clinical symptoms and pathophysiological responses associated with rapid arrest of normal hepatic function. The syndrome is defined by the presence of hepatic encephalopathy in association with coagulopathy and jaundice. In many cases, the clinical picture is complicated by cerebral edema, renal impairment, sepsis, and multiorgan failure. In this review, we examine the specific causes of FHF, including acetaminophen-related hepatotoxicity, drug- and viral-related FHF, and other less common causes of FHF such as pregnancy and vascular related disease. The approach to FHF should be multidisciplinary and requires a thorough understanding of the biochemical, metabolic, and physiological changes associated with hepatic necrosis. Also examined are management issues pertinent to these complex situations and the role of liver transplantation and liver assist devices are considered.

The most common cause of acute pancreatitis is gallstones, although many other etiological factors have been identified. The management of the initial episode depends on the severity of the attack and the etiology. In most patients, acute pancreatitis has a benign, self-limited course. However, in the minority who develop infected pancreatic necrosis the mortality can reach 25%. The early assessment of severity and aggressive management of these patients is critical. The roles of endoscopic retrograde cholangiopancreatography, surgical intervention, enteral feeding and use of antibiotics in acute pancreatitis are discussed in this article. Finally, the origin of recurrent acute pancreatitis is discussed, with particular reference to conditions such as pancreas divisum and sphincter of Oddi dysfunction whose role in the development of acute pancreatitis is controversial, and to hereditary or familial pancreatitis.

Acute colonic pseudo-obstruction is a syndrome of massive dilation of the colon without mechanical obstruction that develops in hospitalized patients with serious underlying medical and surgical conditions. Increasing age, cecal diameter, delay in decompression, and status of the bowel significantly influence mortality, which is approximately 40% when ischemia or perforation is present. Evaluation of the markedly distended colon in the intensive care unit setting involves excluding mechanical obstruction and other causes of toxic megacolon such as Clostridium difficile infection, and assessing for signs of ischemia and perforation. The risk of colonic perforation in acute colonic pseudo-obstruction increases when cecal diameter exceeds 12 cm and when the distention has been present for greater than 6 days. Appropriate management includes supportive therapy and selective use of neostigmine and colonoscopy for decompression. Early recognition and management are critical in minimizing complications.

While aspiration is a fairly common event for critically ill patients on enteral tube feeding, progression to aspiration pneumonia is difficult to predict due to variation in host factors and characteristics of the aspirate material. Aspiration of oropharyngeal secretions is of equal if not greater importance than aspiration of gastric contents. Monitors for aspiration such as glucose oxidase, blue food coloring, and gastric residual volumes are insensitive and unreliable. A number of clinical risk factors can be identified at the bedside. A variety of management strategies may be used in the intensive care unit to reduce risk of aspiration, while efforts continue to provide sufficient volume of enteral nutrients.