《消化道出血》word版.doc

Acute gastrointestinal (GI) hemorrhage is a common clinical problem with diverse manifestations. Such bleeding may range from trivial to massive and can originate from virtually any region of the GI tract, including the pancreas, liver, and biliary tree. Although no demographic group is spared, the annual incidence of about 170 cases per 100,000 adults increases steadily with advancing age, and the disease is slightly more common in men than women.1 Furthermore, GI hemorrhage accounts for 1% to 2% of acute admissions, resulting in more than 300,000 annual hospitalizations in the United States.2 It is also a common complication in patients hospitalized for other illness, especially surgical patients. Although the total economic burden of GI hemorrhage has not been formally assessed, annual estimates suggest that diverticular bleeding alone costs in excess of 1.3 billion dollars.3Management of these patients is frequently multidisciplinary, involving emergency medicine, gastroenterology, intensive care, surgery, and interventional radiology. The importance of early surgical consultation in the care of these patients cannot be overemphasized.4 In addition to aiding in the resuscitation of the unstable patient, in some settings the surgical endoscopist establishes the diagnosis and initiates therapy. Even when the gastroenterologist assumes this role, the early collaboration of the surgeon permits the establishment of goals and limits for initial nonoperative therapy. Ultimately 5% to 10% of patients hospitalized for bleeding require operative intervention, and prompt surgical consultation permits more time for preoperative preparation and evaluation as well as patient and family education should urgent surgery become necessary.1Most patients with an acute GI hemorrhage stop bleeding spontaneously. This allows time for a more elective evaluation. However, in almost 15% of cases, major bleeding persists, requiring emergent resuscitation, evaluation, and treatment.5 Improvements in the management of these patients, primarily by early endoscopy and directed therapy, has significantly reduced the length of hospitalization. Despite this, the mortality rate remains greater than 5% and is significantly higher in those patients initially hospitalized for other reasons. This discrepancy between therapeutic advances and outcomes is probably related to the aging of the population with an increase in its comorbidities. Currently, the patient requiring operative intervention is both older and sicker than in the past.Hemorrhage can originate from any region of the GI tract and is typically classified based on the location relative to the ligament of Treitz. Upper GI hemorrhage (proximal to the ligament of Treitz) accounts for more than 80% of acute bleeding.1 Peptic ulcer disease (PUD) and variceal hemorrhage are the most common etiologies. Most lower GI bleeding originates from the colon, with diverticula and angiodysplasias accounting for the majority of cases. In less than 5% of patients, the small intestine is responsible.1 Obscure bleeding is defined as hemorrhage that persists or recurs after negative endoscopy. Occult bleeding is not apparent to the patient until presentation with symptoms related to the anemia. Determination of the site of bleeding is important for directing diagnostic interventions with minimal delay. However, attempts to localize the source never precede appropriate resuscitative measures.APPROACH TO THE PATIENT WITH ACUTE GASTROINTESTINAL HEMORRHAGE In patients with GI bleeding, several fundamental principles of initial evaluation and management must be followed. A well-defined and logical approach to the patient with GI hemorrhage is outlined in Figure 46-1 . On presentation, a rapid initial assessment permits a determination of the urgency of the situation. Resuscitation is initiated with stabilization of the patients hemodynamic status and the establishment of a means for monitoring ongoing blood loss. A careful history and physical examination provides clues to the etiology and source of the bleeding and identifies any complicating conditions or medications. Specific investigation then proceeds to refine the diagnosis. Therapeutic measures are then initiated, and bleeding is controlled and recurrent hemorrhage prevented. Figure 46-1 General approach to the patient with acute GI hemorrhage. Initial Assessment Adequacy of the patients airway and breathing takes first priority. After this is assured, the patients hemodynamic status becomes the dominant concern and forms the basis for further management. The presentation of GI bleeding is variable, ranging from hemoccult-positive stool on rectal exam to exsanguinating hemorrhage. Initial evaluation focuses on rapid assessment of the magnitude of both the preexisting deficits and ongoing hemorrhage. Continuous reassessment of the patients circulatory status determines the aggressiveness of subsequent evaluation and intervention. The history of the bleeding, both its magnitude and frequency, also provides some guidance.The severity of the hemorrhage can be generally determined based on simple clinical parameters. Obtundation, agitation, and hypotension (systolic blood pressure 60 yr Comorbid disease Renal failure Liver disease Respiratory insufficiency Cardiac disease Magnitude of the hemorrhage Systolic blood pressure 100 mm Hg on presentation Transfusion requirement Persistent or recurrent hemorrhage Onset of hemorrhage during hospitalization Need for surgery Considerable recent effort has been devoted to the development of risk scoring tools to facilitate patient triage. These scoring systems have been used to predict the risk for rebleeding and mortality, to evaluate the need for intensive care unit (ICU) admission, and to determine the need for urgent endoscopy. For example, the BLEED classification schema uses five criteria8: ongoing bleeding; a systolic blood pressure of less than 100 mm Hg; a prothrombin time of greater than 1.2 times control; altered mental status; and an unstable comorbid disease process that would require ICU admission. If any one of these criteria is present, the model predicts an about three-fold increase in the risk for either recurrent hemorrhage, the need for surgical intervention, or death. Such scoring systems have been almost exclusively used in research studies and are significantly more accurate when endoscopic findings are included. Until these schema have been prospectively validated for everyday clinical practice, they are only applied in the context of clinical judgment.Resuscitation The more severe the bleeding, the more aggressive the resuscitation. In fact, the single leading cause of morbidity and mortality in these patients is multiorgan failure related to inadequate initial or subsequent resuscitation. Intubation and ventilation are initiated early if there is any question of respiratory compromise. In patients with evidence of hemodynamic instability and those in whom ongoing bleeding is suspected, two large-bore intravenous lines are placed, preferably in the antecubital fossae. Unstable patients receive a 2 L bolus of crystalloid solution, usually lactated Ringers, which most closely approximates the electrolyte composition of whole blood. The response to the fluid resuscitation is noted. Blood is sent immediately for type and crossmatch, hematocrit, platelet count, coagulation profile, routine chemistries, and liver function tests. A Foley catheter also is inserted for assessment of end-organ perfusion. In elderly patients and those with significant cardiac, pulmonary, or renal disease, placement of a central venous or pulmonary artery catheter is considered for closer monitoring. The oxygen-carrying capacity of the blood can be maximized by administering supplemental oxygen. Frequently, these patients benefit from early admission to and management in the ICU.The decision to transfuse blood depends on the response to the fluid challenge, the age of the patient, whether concomitant cardiopulmonary disease is present, and whether the bleeding continues. The initial effects of crystalloid infusion and the patients ongoing hemodynamic parameters are the primary criteria. Once again, this process requires clinical judgment. For example, a young, healthy patient with an estimated blood loss of 25% who responds to the fluid challenge with a normalization of hemodynamics may not need any blood products, whereas an elderly patient with a significant cardiac history and the same blood loss probably requires transfusion. Although the hematocrit may require 12 to 24 hours to fully equilibrate, it is commonly employed as one index of the need for blood replacement. In general, the hematocrit is maintained above 30% in elderly patients and above 20% in young, otherwise healthy patients. Likewise, the propensity of the suspected lesion to continue bleeding or to rebleed must play a role in this decision. For example, esophageal varices are very likely to continue to bleed, and transfusion might be considered earlier than in a patient with a Mallory-Weiss tear, which has a low rebleeding rate. In general, packed RBCs are the preferred form of transfusion, although whole blood, preferably warmed, may be employed in circumstances of massive blood loss.History and Physical Examination After the severity of the bleeding is assessed and resuscitation initiated, attention is directed to the history and physical examination. The history helps to make a preliminary assessment of the site and cause of bleeding and of significant medical conditions that may determine or alter the course of management.Obviously, the characteristics of the bleeding provide important clues. The time of onset, volume, and frequency are important in estimating blood loss. Hematemesis, melena, and hematochezia are the most common manifestations of acute hemorrhage. Hematemesis is the vomiting of blood and is usually caused by bleeding from the upper GI tract, although rarely bleeding from the nose or pharynx can be responsible. It may be bright red or older and therefore take on the appearance of coffee grounds. Melena, the passage of black, tarry, and foul-smelling stool, generally suggests bleeding from the upper GI tract. Although the melanotic appearance typically results from both the gastric acid, which converts hemoglobin to hematin, and the actions of digestive enzymes and luminal bacteria in the small intestine, blood loss from the distal small bowel or right colon may have this appearance, particularly if transit is slow. Melena must not be confused with the greenish character of the stool in patients taking iron supplements. These can be distinguished by performing a guaiac test, which tests negative in those on iron supplementation. Hematochezia refers to bright red blood from the rectum that may or may not be mixed with stool. Although this typically reflects a distal colonic source, if the magnitude is significant, even upper GI hemorrhage may produce hematochezia.The medical history may provide clues to the diagnosis. Chronic blood loss may lead to non-GI end-organ symptoms such as syncope, angina, and even myocardial infarction. Antecedent vomiting may suggest a Mallory-Weiss tear, whereas weight loss raises the specter of malignancy. Even demographic data may prove useful: elderly patients bleed from lesions such as angiodysplasias, diverticula, ischemic colitis, and cancer, whereas younger patients bleed from peptic ulcers, varices, and Meckels diverticulum. A history of GI disease, bleeding, or operation immediately begins to focus the differential diagnosis. Antecedent epigastric distress may point to a peptic ulcer, whereas previous aortic surgery suggests the possibility of an aortoenteric fistula. A history of liver disease prompts a consideration of variceal bleeding. Medication use may also be revealing. A history of ingestion of salicylates, nonsteroidal anti-inflammatory drugs (NSAIDs), or selective serotonin-reuptake inhibitors (SSRIs) is common, particularly in elderly patients.9 These medications are associated with GI mucosal erosions seen typically in the upper GI tract, but occasionally they can occur in the small bowel and colon. GI bleeding in the setting of anticoagulation therapy, either warfarin or low-molecular-weight heparin, is still most commonly the result of GI pathology and is not ascribed to the anticoagulation alone.10Physical examination may also be revealing. Bleeding from the oropharynx and nose can occasionally simulate symptoms of a more distal source and must always be examined. Abdominal examination is only occasionally helpful, but it is important to exclude masses, splenomegaly, and adenopathy. Epigastric tenderness is suggestive, but not diagnostic, of gastritis or peptic ulceration. The stigmata of liver disease, including jaundice, ascites, palmar erythema, and caput medusae, may suggest bleeding related to varices, although these patients commonly bleed from other sources as well. Occasionally the physical exam may reveal clues to more obscure diagnoses such as the telangiectasias of Osler-Weber-Rendu disease or the pigmented lesions of the oral mucosa in Peutz-Jeghers syndrome. A rectal exam and anoscopy are performed to exclude a low-lying rectal cancer or bleeding from hemorrhoids.Localization Subsequent management of the patient with acute GI hemorrhage depends on localization of the site of the bleeding. An algorithm for the diagnosis of acute GI hemorrhage is shown in Figure 46-2 . Figure 46-2 Algorithm for the diagnosis of acute GI hemorrhage. EGD, esophagogastroduodenoscopy; RBC, red blood cell. Although melena is usually the result of bleeding from the upper GI tract, it can be the result of bleeding from the small bowel or colon. Likewise, hematochezia is sometimes the consequence of brisk upper GI bleeding. The first step in distinguishing these possibilities is the insertion of a nasogastric (NG) tube and examination of the aspirate. Although hematemesis is usually diagnostic of an upper GI bleed, the tube is still useful to assess the rate of ongoing bleeding and to remove blood from the stomach to permit endoscopy. If the aspirate is positive, this effectively localizes the lesion. The presence of red blood or coffee-ground appearance suggests an upper source. Testing for occult blood is rarely necessary. The return of bile from a gastric aspirate suggests that the duodenum has been sampled. Although a bilious nonbloody gastric aspirate generally excludes the upper GI tract, these findings can occasionally be misleading. One study found that only 6 of 10 yellow-green NG aspirates tested positive for bile.11 Likewise, almost 20% of patients with a clear aspirate are still bleeding from an upper GI source.2 In patients with melena or even hematochezia from an upper lesion, the NG aspirate may be negative in the presence of significant duodenal bleeding and a competent pylorus preventing duodenogastric reflux. These considerations suggest that, although the findings of the NG aspirate can be helpful, virtually all patients with significant bleeding need to undergo upper endoscopy.Esophagogastroduodenoscopy (EGD) under these circumstances is highly acc