Section 5 Gastrointestinal Tract and Abdomen
5 Gastrointestinal BleedingEric S. Hungness, MD, FACS
Northwestern University Feinberg School of Medicine
and Attending Physician
Northwestern Memorial Hospital, Chicago, IL
10.2310/7800.S05C05
Despite recent advances in therapeutic endoscopy and the widespread use of antisecretory medications, upper gastrointestinal bleeding (UGIB)—defined as bleeding that occurs proximal to the ligament of Treitz—continues to be one of the more common reasons for surgical consultation. It also remains a significant source of mortality for both emergency admissions (11%) and inpatients (33%).
1 The most common causes of UGIB are esophageal (varices and Mallory-Weiss tears), gastric (acute hemorrhagic gastritis, varices, ulcers, and neoplasms), and duodenal (ulcers) [see Discussion and Management of Specific Sources of UGIB, below]. Less common causes include various other gastrointestinal (GI) conditions and certain hepatobiliary and pancreatic disorders.Lower gastrointestinal bleeding (LGIB)—defined as abnormal hemorrhage into the lumen of the bowel from a source distal to the ligament of Treitz—usually derives from the colon; however, the small bowel is identified as the source of bleeding in as many as one-third of cases,2 and UGIB is identified as the source in as many as 11% of patients presenting with hematochezia.3 The most common causes of LGIB are colonic, with diverticular disease being the most common and accounting for 30 to 40% of all cases.4 Arteriovenous malformations (AVMs), although extensively described in the literature, are considerably less common causes, accounting for 1 to 4% of cases.5 Other significant causative conditions are inflammatory bowel disease (IBD), benign and malignant neoplasms, ischemia, infectious colitis, benign anorectal disease, coagulopathy, use of nonsteroidal antiinflammatory drugs (NSAIDs), radiation proctitis, AIDS, and small bowel disorders.
Presentation and Initial ManagementGastrointestinal bleeding (GIB) may present as severe bleeding with hematemesis (UGIB), hematochezia (UGIB or LGIB), and hypotension; as gradual bleeding with melena (UGIB); or as occult bleeding detected by positive tests for blood in the stool. The initial steps in the evaluation of patients with GIB are based on the perceived rate of bleeding and the degree of hemodynamic stability. Hemodynamically stable patients who show no evidence of active bleeding or comorbidities and in whom endoscopic findings are favorable may be treated on an outpatient basis,
6 whereas patients who show evidence of serious bleeding should be managed aggressively and hospitalized.The airway, breathing, and circulation should be rapidly assessed, and the examiner should note whether the patient has a history of or currently exhibits hematemesis, melena, or hematochezia. Blood should be drawn for a complete blood count, blood chemistries (including tests of liver function and renal function), and measurement of the prothrombin time and the partial thromboplastin time. Blood should be sent to the blood bank for typing and crossmatching.
If the patient is stable and shows no evidence of recent or active hemorrhage, the surgeon may proceed with the workup. If, however, the patient is stable but shows evidence of recent or active bleeding, short, large-bore intravenous lines should be placed before workup is begun to ensure that immediate intravenous (IV) access is possible should the patient subsequently become unstable.
If the patient is unstable, he or she should be taken to an intensive care unit and resuscitated immediately. Resuscitation of an unstable patient is begun by establishing a secure airway and ensuring adequate ventilation.7 Oxygen should be given, with a low threshold for endotracheal intubation. Much as in trauma resuscitation, either short, large-bore, peripheral IV lines or a single-lumen 8 French catheter in the femoral vein should then be placed, through which lactated Ringer solution or 0.9% normal saline should be infused at a rate high enough to maintain tissue perfusion. A urinary catheter should be inserted and urine output monitored. Blood products should be given as necessary, and any coagulopathies should be corrected. It is all too easy to forget these basic steps in a desire to evaluate and manage massive GI hemorrhage.
Every effort should be made to resuscitate and stabilize the patient sufficiently to allow clinical evaluation and diagnostic testing to help determine the cause of the bleeding and direct subsequent care. Only if the patient remains unstable and continues to bleed despite maximal supportive measures should he or she be taken to the operating room for intraoperative diagnosis as a last resort. If UGIB is the etiology, the abdomen should be opened through an upper midline incision, and an anterior gastrotomy should be performed. If inspection does not reveal the source of the bleeding or if bleeding is observed beyond the pylorus, a duodenotomy is made, with care taken to preserve the pylorus if possible. Bleeding from the proximal stomach may be difficult to verify, but it should be actively sought if no other bleeding site is identified. Intraoperative endoscopy should be considered in this situation.
For LGIB, intraoperative options for bleeding-site localization include colonoscopy (to allow for this option, patients should always be placed in the lithotomy position), esophagogastroduodenoscopy (EGD), and transoral passage of a pediatric colonoscope for enteroscopy with simultaneous intraperitoneal assistance for small bowel manipulation [see 5:18 Gastrointestinal Endoscopy]. If the bleeding site is identified, directed segmental resection is the procedure of choice: it is associated with rebleeding rates less than 10% and low mortality rates ranging from 0 to 13%.8 Blind segmental colectomy should never be performed; it is associated with rebleeding rates as high as 75% and mortality rates as high as 50%.9 If the bleeding site still cannot be accurately localized, subtotal colectomy is the procedure of choice. This procedure is associated with high morbidity,10 which underscores the importance of accurate preoperative localization of bleeding before surgical intervention.
Clinical EvaluationOnly after the initial measures to protect the airway and stabilize the patient have been completed should an attempt be made to establish the cause of the bleeding. The history should focus on known causes of GIB (e.g., previous GIB, peptic ulcer disease, diverticulosis, AVM, esophageal varices, and IBD) and on the possible use of medications that interfere with coagulation (e.g., warfarin, aspirin, and NSAIDs) or alter hemodynamics (e.g., beta blockers and antihypertensive agents). Of particular importance in taking the history is to ascertain the nature and duration of the bleeding, including stool color and frequency. The patient should also be asked about any associated symptoms of potential significance (e.g., abdominal pain, changes in bowel habits, fever, urgency, tenesmus, or weight loss). Knowledge of the patient's cardiac history is useful to assess the patient's ability to withstand varying degrees of anemia.
The physical examination is seldom of much help in determining the exact site of bleeding, but determination of postural vital signs can accurately estimate intravascular volume status. A drop in the orthostatic blood pressure greater than 10 mm Hg or an increase in the pulse rate greater than 10 beats/min indicates that more than 800 mL of blood (> 15% of the total circulating blood volume) has been lost. Marked tachycardia and tachypnea in association with hypotension and depressed mental status indicate that more than 1,500 mL of blood (> 30% of the total circulating blood volume) has been lost. A complete abdominal examination, including digital rectal examination and anoscopy, should be performed as it may reveal jaundice, ascites, or other signs of hepatic disease; a tumor mass; or a bruit from an abdominal vascular lesion.
A nasogastric tube should be placed for gastric lavage. If lavage yields positive results (i.e., the aspirate contains gross blood or so-called coffee grounds), EGD is indicated. An aspirate that contains copious amounts of bile is strongly suggestive of an LGIB, and the workup proceeds accordingly. The choice is less clear-cut with a clear aspirate. In the absence of bile, such an aspirate cannot rule out a duodenal source for the bleeding. Accordingly, there is some degree of latitude for clinical judgment: depending on the overall clinical picture, the surgeon may choose either to perform EGD to rule out a duodenal bleeding source or to proceed with colonoscopy on the assumption that the source of the bleeding is in the lower GI tract.
UGIB Investigative Testsesophagogastroduodenoscopy
EGD [see 5:18 Gastrointestinal Endoscopy] almost always reveals the source of UGIB; its utility and accuracy have been well documented in the literature.11 Performance of this procedure requires considerable skill: identification of bleeding sites in a blood-filled stomach is far from easy. Hematemesis is an indication for emergency EGD, usually within 1 hour of presentation. If the rate of bleeding is high, saline lavage may be performed to clear the stomach of blood and clots. If the rate of bleeding is moderate or low, as is often the case in patients with melena, urgent EGD is indicated.
EGD is not only an excellent diagnostic tool but also a valuable therapeutic modality. Indeed, most UGIBs may be controlled endoscopically, although the degree of success to be expected in individual cases varies according to the expertise of the endoscopist and the specific cause of the bleeding. Therapeutic endoscopic maneuvers include injection, thermal coagulation, and mechanical occlusion of bleeding sites (clip application or variceal banding). The choice of therapy depends on the cause, the site, and the rate of bleeding.
other ugib imagingTagged red blood cell (RBC) scans may confirm the presence of an active bleeding site; however, scans are fairly nonspecific with respect to determining the anatomic location of the bleeding.
12 Arteriography may demonstrate that a lesion is present, but it cannot reliably identify a bleeding site unless the bleeding is brisk (> 1 mL/min). Occasionally, arteriography reveals the cause of the bleeding even if the bleeding has stopped. Angiography may also be considered as a therapeutic modality for high-risk surgical patients.6 These tests, in conjunction with EGD, should allow the surgeon to establish the cause of UGIB more than 90% of the time.LGIB Investigative TestsA number of diagnostic techniques are available for determining the source of LGIB, including colonoscopy [see 5:18 Gastrointestinal Endoscopy], radionuclide scanning, computed tomography (CT), and angiography (in the form of selective mesenteric arteriography), enteroscopy, and capsule endoscopy (CE). The goal of these tests is to locate the site of bleeding accurately so that definitive therapy can be properly directed as the potential source ranges from the ligament of Treitz to the anus. Which diagnostic test is chosen for a specific patient depends on several factors, including the hemodynamic stability of the patient, the bleeding rate, patient comorbidities, therapeutic options, and local expertise available. Unlike radionuclide and CT scanning, arteriography and colonoscopy provide a therapeutic option. Arteriography has a lower diagnostic yield and a higher complication rate than colonoscopy does; therefore, it is reasonable to attempt colonoscopy first and to reserve angiography for patients in whom the volume of bleeding is such that colonoscopy would be neither safe nor accurate.13
colonoscopySeveral large series that evaluated the diagnostic utility of colonoscopy in patients with LGIB found this modality to be moderately to highly accurate, with overall diagnostic yields ranging from 53 to 97%.
3,14,15 Those studies that reported morbidity found colonoscopy to be safe, with an average complication rate of 0.5%. Colonoscopy has both a higher diagnostic yield and a lower complication rate than arteriography in this setting and thus would appear to be a more attractive initial test in most circumstances.3,16 An argument has been made that colonoscopy should be considered the procedure of choice for structural evaluation of LGIB and that arteriography should be reserved for patients with massive, ongoing bleeding in whom endoscopy is not feasible or colonoscopy fails to reveal the source of the hemorrhage.17The merits of colonic purging have been extensively debated in the literature.3,18 Although no firm conclusion has been reached, adequate colonic purging may improve both the diagnostic yield and the safety of colonoscopy. Given the absence of any definitive data suggesting that colonic purging either reactivates or increases bleeding, one should consider administering an oral purge after the patient has been adequately resuscitated.
If the entire colon has been adequately visualized and no source for the bleeding has been identified, the ileum should be intubated; fresh blood in this region suggests a possible small bowel source. If no active bleeding is observed in the ileum, upper GI endoscopy should be performed to rule out a UGIB site.
When colonoscopy identifies a bleeding source, endoscopic treatment may be an option [see 5:18 Gastrointestinal Endoscopy]. Endoscopic modalities used to treat LGIB include use of thermal contact probes, laser photocoagulation, electrocauterization, injection of vasoconstrictors, application of metallic clips, and injection sclerotherapy. The choice of a specific modality often depends on the nature of the offending lesion and on the expertise and resources available locally. A 1995 survey of members of the American College of Gastroenterology found that endoscopic therapy was used in 27% of patients presenting with LGIB.19
radionuclide scanning |
| Figure 1 |
Radionuclide scanning is highly sensitive for lower LGIB, capable of detecting bleeding at rates as slow as 0.1 to 0.4 mL/min.20 The patient's RBCs are labeled with technetium-99m (99mTc), which can be detected on images as long as 24 to 48 hours after injection [seeFigure 1]. The high sensitivity of 99mTc-labeled RBC scanning—80 to 98%—is well attested, but there is considerable disagreement in the literature with regard to its specificity in identifying the anatomic site of bleeding.21,22 For example, on the one hand, a 1997 study found radiolabeled RBC scanning to be 97% accurate for localizing bleeding in 37 patients undergoing surgical resection22; on the other hand, a 1990 study reported a 42% rate of incorrect resection when surgical therapy was based solely on this modality.21 In 2005, one group retrospectively reviewed 127 bleeding scans in an effort to identify factors that might predict a positive scan.23 The investigators found that tagged RBC scans were 48% accurate in localizing bleeding sites later confirmed by endoscopy, surgery, or pathologic evaluation. Multivariate analysis demonstrated that both the number of units of blood transfused in the 24 hours preceding the scan and the lowest recorded hematocrit differed significantly between patients with positive scans and those with negative scans. However, the clinical significance of a positive scan was unclear in this study in that the rate of endoscopy was not significantly different between patients who had positive scans and those who did not.
To date, no prospective, randomized trials have compared radionuclide scanning with colonoscopy as the initial diagnostic procedure for patients with lower GI hemorrhage. Given that radionuclide scanning has no therapeutic intervention capabilities, its best use is in patients with non–life-threatening LGIB as a prelude and a guide to mesenteric angiography after active hemorrhage has been confirmed.
Radionuclide scanning is also useful for diagnosing Meckel diverticulum, a rare cause of LGIB. Patients are injected with 99mTc pertechnetate, which is taken up by the ectopic gastric mucosa. Although studies in the pediatric population have demonstrated high diagnostic accuracy, the sensitivity of the scan is only 60 to 70% in the adult population.24
angiography |
| Figure 2 |
Selective mesenteric arteriography is somewhat less sensitive than radionuclide scanning for lower GI hemorrhage: bleeding must be occurring at a rate of at least 1.0 to 1.5 mL/min to be detectable with this test.25 The procedure involves percutaneous placement of a transfemoral arterial catheter for evaluation of the superior mesenteric, inferior mesenteric, and celiac arteries. A positive test result is defined as extravasation of contrast into the lumen of the bowel. Once the bleeding vessel has been localized angiographically, the area must be marked so that it can be successfully identified intraoperatively; this is commonly accomplished by infusing methylene blue into the bleeding artery [seeFigure 2].26
In several large series, the overall diagnostic yield of arteriography ranged from 27 to 67%.8,22,27,28 The complication rate for arteriography performed for LGIB ranges from 2 to 4%.2,26 Reported complications include contrast allergy, renal failure, bleeding from arterial puncture, and embolism from a dislodged thrombus.17 Diagnostic use of angiography in patients with LGIB can often be followed by angiographic therapy. The two main angiographic treatment options are intra-arterial injection of vasopressin and transcatheter embolization.
Vasopressin acts to control bleeding by causing arteriolar vasoconstriction and bowel wall contraction. Once the bleeding site has been localized angiographically, the catheter is positioned in the main trunk of the vessel. Infusion of vasopressin is initiated at a rate of 0.2 U/min and can be increased to a rate of 0.4 U/min. Within 20 to 30 minutes, angiography is performed again to determine whether the bleeding has ceased. If the bleeding is under control, the catheter is left in place and vasopressin is continuously infused for 6 to 12 hours. If the bleeding continues to be controlled, infusion is continued for an additional 6 to 12 hours at 50% of the previous rate. Finally, vasopressin infusion is replaced by continuous saline infusion, and if bleeding does not recur, the catheter is removed.29
The vasoconstrictive action of vasopressin can have deleterious systemic side effects, including myocardial ischemia, peripheral ischemia, hypertension, dysrhythmias, mesenteric thrombosis, intestinal infarction, and death. Occasionally, simultaneous intravenous administration of nitroglycerin is necessary to counteract these systemic effects. The reported success rate of vasopressin in controlling LGIB ranges from 60 to 100%, and the incidence of major complications ranges from 10 to 20%.30–32 Rebleeding rates as high as 50% have been reported.30,31
An alternative for patients with coronary vascular disease, severe peripheral vascular disease, or other comorbidities that prevent safe administration of vasopressin is transcatheter embolization. In this technique, a catheter is superselectively placed into the identified bleeding vessel and an embolizing agent (e.g., a gelatin sponge, a microcoil, polyvinyl alcohol particles, or a balloon) is injected. Several small series found this technique to be 90 to 100% successful at stopping bleeding.32–34 Equally impressive was the finding that the rebleeding rates in these series were 0%. The complication rates of this procedure are generally reasonable as well; however, intestinal infarction has been reported.8,35
The use of small microcatheters and the ability to superselectively embolize individual vessels have reduced the potential for ischemic perforation. It is possible that as more experience is gained with these techniques, superselective embolization may replace catheter-directed vasoconstrictive therapy, thus obviating the potential deleterious systemic effects of vasopressin administration. Some researchers have suggested that with the exception of cases of diffuse bleeding lesions or cases whose demands exceed the technical limitations of superselective catheterization, embolization therapy should be the first choice for angiographic treatment of LGIB.35,36
In a minority of patients, obscure bleeding persists despite negative findings from endoscopy, mesenteric arteriography, and radiolabeled RBC scanning. This obscure bleeding presents a considerable diagnostic challenge, which some investigators have proposed addressing by means of so called provocative angiography.37 Provocative angiography involves the use of short-acting anticoagulant agents (unfractionated heparin, vasodilators, thrombolytics, or combinations thereof) in association with angiography. Once the bleeding point has been localized (in up to 89% of cases in a recent study),38 superselective embolization can be attempted or methylene blue is injected and the patient is immediately brought to the operating room (OR) for surgical treatment.
computed tomographyWith the ongoing improvements in high-speed abdominal CT scanning, interest has been growing in the evaluation of GIB with CT.
39 Helical CT scanners can provide direct or indirect evidence of the source of GIB. Typical findings that can facilitate localization of bleeding sites include spontaneous hyperdensity of the peribowel fat, contrast enhancement of the bowel wall, vascular extravasation of the contrast medium, thickening of the bowel wall, polyps, tumors, and vascular dilatation.CT evaluation of GIB has several noteworthy advantages: the scanners typically are readily available, mobilization of special teams or units is not required, the scans can be completed rapidly in the emergency department, and bowel preparation is unnecessary. In one experimental study, CT scanners were able to detect arterial bleeding at rates as low as 0.07 mL/min, which suggests that CT scanning is more sensitive than angiography for this purpose.40 In addition, CT scans are noninvasive and carry little morbidity. Unfortunately, like radionuclide scanning, CT has no therapeutic capability.
A 2003 study of 19 patients with GI hemorrhage compared triphasic helical CT evaluation with colonoscopy and surgery for localization of bleeding sites.40 In this series, 5 patients had small bowel bleeding sites, and 14 patients had colonic sites. Helical CT scanning correctly identified 4 of the 5 small bowel lesions and 11 of the 14 colonic lesions. These findings, although preliminary, suggest that CT is a potentially valuable evaluation method in certain cases of GIB. Perhaps CT scanning can eventually replace radionuclide scanning, which is often inaccurate. One potential drawback to the use of CT in this setting is the excessive dye load if angiography is employed as well.
enteroscopyWhen other tests fail to locate a bleeding source, enteroscopy may be helpful to localize the LGIB. This procedure can be carried out in several ways. It can be performed purely endoscopically with a pediatric colonoscope. Termed 'push' endoscopy, this approach generally requires a high level of skill on the part of the endoscopist in that the lack of retroperitoneal attachments of the small intestine makes endoscopic navigation extremely challenging. In most cases, only the proximal 150 cm of the small intestine can be evaluated in this way. Depending on the indication and on the technique employed, the diagnostic yield from push enteroscopy has ranged from 13 to 78%.
41 Typically, yields are highest (40 to 60%) in patients with significant GI hemorrhage.Recently, double-balloon enteroscopy (DBE) has evolved as an effective method of identifying and endoscopically treating occult LGIB. Using this technique, the entire length of the small intestine can be examined in up to 50% of cases using combined antegrade (transoral) and retrograde (transanal) insertion by milking the bowel in a push/pull technique between two balloons.42 A recent study demonstrated that 66% of occult bleeding sources were identified using DBE. DBE should be considered the first choice in stable patients with occult active bleeding.
capsule endoscopyAnother option for stable patients with occult GIB is CE, in which a miniature camera is swallowed and intermittent images are taken along the entire length of the GI tract as the capsule advances. Recent studies, including a prospective, blinded trial and several meta-analyses, have demonstrated that the diagnostic yield of CE is similar to that of DBE, although CE does not allow for therapeutic intervention.
42–44 Because it is less invasive, however, CE should be considered the first choice in stable patients in whom occult bleeding has stopped.Discussion and Management of Specific Sources of UGIBduodenal ulcer
The development of effective medical regimens for controlling uncomplicated duodenal ulcers has led to a drastic reduction in the number of elective surgical procedures performed for this purpose. Nevertheless, the incidence of bleeding from duodenal ulcers that is severe enough to necessitate emergency endoscopic or operative intervention has not decreased over the past decade.45
Once EGD has demonstrated that a duodenal ulcer is the source of the bleeding, the first question that must be addressed is whether active bleeding is present. If it is, an attempt should be made to control the hemorrhage endoscopically [seeFigure 1]. Because ongoing blood loss eventually leads to coagulopathies, the surgeon must exercise good judgment in deciding how long to pursue endoscopic treatment before concluding that such treatment has failed and that surgical treatment is necessary. In general, substantial bleeding (6 units or more) or bleeding that is not controlled endoscopically is an indication for surgical intervention. Likewise, ongoing hemorrhage in a hemodynamically unstable patient (especially an elderly one) calls for immediate surgical therapy. In addition, certain patients whose bleeding is controlled endoscopically (e.g., those with a visible vessel, active bleeding, or an adherent clot,46 as well as those with giant ulcers) should be strongly considered for surgical therapy.
If bleeding is controlled endoscopically, then a proton pump inhibitor (PPI), such as pantoprazole, should be given intravenously, either in a bolus twice daily or by continuous infusion.47 In addition, antibiotic therapy directed against Helicobacter pylori (e.g., a 14-day course of metronidazole, 500 mg p.o., t.i.d.; omeprazole, 20 mg p.o., b.i.d.; and clarithromycin, 500 mg p.o., b.i.d.) should be considered if the organism is present; such therapy has been shown to reduce rebleeding rates after antacid medication has been stopped.48 Food need not be withheld unless the likelihood of rebleeding is high, because resumption of oral feeding does not appear to affect rebleeding rates.49 If bleeding recurs despite medical and endoscopic therapy, a second attempt at endoscopic control should be made. Repeat endoscopic treatment reduces the need for surgery without increasing the risk of death and is associated with fewer complications than is surgery.50
Surgical management may be accomplished either laparoscopically or via an open approach [see 5:20 Procedures for Benign and Malignant Gastric and Duodenal Disease]. The latter begins with an upper midline incision. The duodenum is mobilized, and an anterior longitudinal duodenotomy is performed over the site of the ulcer. The bleeding vessel, which is usually on the posterior wall of the first portion of the duodenum, is ligated with nonabsorbable sutures at sites proximal and distal to the bleeding point. A third stitch is placed posterior to the bleeding vessel. Pains must be taken to avoid injury to the common bile duct during the placement of these sutures. The duodenotomy is then closed. If a truncal vagotomy is to be performed, the duodenotomy should extend through the pylorus and be closed transversely to perform a pyloroplasty. Frozen section to confirm the presence of nerve tissue is helpful for ensuring that the vagotomy is complete.
The recommendation for truncal vagotomy is based on data from studies done before PPIs and H. pylori therapy came into use. Subsequent studies and a 2004 Cochrane review that evaluated rebleeding rates with current medical regimens demonstrated much lower rebleeding rates.51 Furthermore, it seems probable that long-term PPI therapy (the medical equivalent of vagotomy), in conjunction with eradication of H. pylori and avoidance of NSAIDs, should reduce rebleeding rates significantly. Studies from the United States45 and the United Kingdom52 have shown that a vagotomy is performed less than 50% of the time during surgical treatment of an acute bleeding duodenal ulcer. Therefore, although there are no prospective, randomized studies to support it, one may consider an alternative treatment approach in patients who have not been receiving ulcer therapy before the bleeding began—namely, ligation of the bleeding vessel, postoperative administration of PPIs, and H. pylori therapy. This approach avoids the complications associated with truncal vagotomy.
Another option for preventing postvagotomy symptoms when operating on stable patients for bleeding duodenal ulcer is to perform a highly selective vagotomy (HSV) [see 5:20 Procedures for Benign and Malignant Gastric and Duodenal Disease]. This procedure is considered preferable to truncal vagotomy because of the decreased incidence of gastric atony, alkaline reflux gastritis, dumping, and diarrhea; however, HSV is associated with a higher recurrence rate than is truncal vagotomy and takes significantly longer to perform.53
gastric ulcerGastric ulcers are classified according to their location and to the role (if any) that gastric acid hypersecretion plays in their development. Type I ulcers are located on the lesser curvature and are not associated with acid secretion. Type II ulcers are associated with high acid secretion and are located on the lesser curvature, occurring in synchrony with duodenal ulcers. Type III ulcers are also associated with acid hypersecretion but occur in the prepyloric region. Type IV ulcers are not associated with acid secretion and are located in the cardia near the esophagogastric junction. Type V ulcers are diffuse and are related to the use of medications (e.g., NSAIDs) [see Acute Hemorrhagic Gastritis, below].
Bleeding is less common than with duodenal ulcers, but initial management of a bleeding gastric ulcer is the same as that of a duodenal ulcer (i.e., endoscopic control) [see
Figure 1]. To prevent aggravation of the bleeding, early biopsy generally is not recommended; repeat endoscopy and biopsy are done at a later date. The indications for emergency surgical intervention for gastric ulcers are the same as those for duodenal ulcers.Bleeding gastric ulcers that necessitate operative intervention should be treated with resection. For type I ulcers, wedge resection is typically performed. For type II and III ulcers, the usual approach consists of antrectomy with Billroth I reconstruction and truncal vagotomy [see 5:20 Procedures for Benign and Malignant Gastric and Duodenal Disease]. Type IV ulcers can pose a technical challenge as a consequence of their close proximity to the esophagogastric junction. A distal gastrectomy with a tongue-shaped extension upward along the lesser curvature to incorporate the ulcer, followed by a Roux-en-Y reconstruction (the Csendes procedure), is often required.54 Another option is ligation of the left gastric artery, followed by biopsy and oversewing of the ulcer.
esophageal varicesThe value of endoscopy in the diagnosis and management of variceal bleeding cannot be overemphasized. Even in patients with known varices, the site of bleeding is frequently nonvariceal; endoscopy is therefore essential.
55 If bleeding varices are identified, rubber banding or intravariceal sclerotherapy with a sclerosing agent (1.5% sodium tetradecyl sulfate, ethanolamine, sodium morrhuate, or absolute alcohol) is performed [seeFigure 2].56 If these measures do not control the hemorrhage, balloon tamponade is indicated.57 Patients who are to undergo this procedure require an endotracheal tube. The preferred tube to use for balloon tamponade is the four-port Minnesota tube, although the Sengstaken-Blakemore tube is also acceptable. The Minnesota tube has a gastric balloon, an esophageal balloon, and aspiration ports for the esophagus and the stomach. The gastric balloon is inflated first and placed on traction. If the bleeding is not controlled, the esophageal balloon is then inflated to a set pressure. The pressure in the balloons should be released in 24 to 48 hours to prevent necrosis of the esophageal or the gastric wall. Successful balloon tamponade is followed by endoscopic variceal injection or variceal banding.Intravenous somatostatin (250 µg bolus, followed by infusion of 250 µg/hr) should be administered in conjunction with the above-mentioned steps. Vasopressin (10 U/hr) may also be given; however, it causes diffuse vasoconstriction, and nitroglycerin may be required to alleviate cardiac side effects. Somatostatin has proved superior to placebo in controlling variceal hemorrhage when used in conjunction with endoscopic sclerotherapy.58 It is as effective as vasopressin while giving rise to fewer side effects. Octreotide, a synthetic analogue of somatostatin, shares many of the properties of somatostatin but perhaps not all. Both agents decrease secretion of gastric acid and pepsin; however, the decreased gastric blood flow observed with somatostatin administration has not been reported with octreotide administration. Nevertheless, some clinicians in the United States elect to use octreotide (25 to 50 µg/hr) in place of IV somatostatin because the former tends to be more widely available. Several prospective, randomized trials showed that propranolol (40 mg b.i.d., p.o.) decreased the incidence of first-time variceal bleeding and the incidence of recurrent variceal bleeding.59,60 Propranolol should not be used during active bleeding but should be started once bleeding stops.
After the acute variceal bleeding has been controlled, any remaining varices should be subjected to injection sclerotherapy or banding at 2-week intervals until they too are obliterated.
The main indications for surgical intervention in patients with bleeding esophageal varices are uncontrolled hemorrhage and persistent rebleeding despite endoscopic and medical therapy. When such intervention is considered, it is essential to determine whether the patient is a transplant candidate. If so, operation should be avoided and bleeding managed by decompressing the portal venous system with a transjugular intrahepatic portosystemic shunt (TIPS) [see 5:10 Portal Hypertension]. TIPS significantly reduces rebleeding rates, but it poses a risk of encephalopathy.61
If the patient is not a transplant candidate and is not actively bleeding, a distal splenorenal shunt (DSRS) is preferable.62 Arteriograms with views of the portal vein and the left renal vein are obtained to assess for suitable anatomy. Alternatively, CT angiography with three-dimensional reconstruction may be performed. If the venous anatomy is suitable—that is, if the diameter of the splenic vein is greater than 0.75 cm (preferably greater than 1.0 cm) and the vein is within one vertebral body of the renal vein on venography—a DSRS procedure should be feasible. If the venous anatomy is not suitable, then esophageal transection, a mesocaval venous graft, or a portacaval shunt is required.
In the emergency setting, a central portacaval shunt, usually in a side-to-side orientation or with a short polytetrafluoroethylene (PTFE) interposition graft, may be placed. Esophageal transection is also a reasonable choice. This procedure is associated with a lower incidence of encephalopathy than a portacaval shunting procedure; however, it is associated with higher rates of rebleeding (particularly late rebleeding), and it can be difficult to perform when active bleeding is present. Suture ligation of the bleeding varices with devascularization (the Sugiura procedure) [see 5:10 Portal Hypertension] should also be considered.
In general, prognosis is related to the underlying liver disease. For example, patients with varices that are secondary to chronic extrahepatic portal venous or splenic venous occlusion generally have a much better prognosis than those whose portal hypertension is secondary to hepatic parenchymal causes. The severity of the cirrhosis also determines short-term and long-term survival and may influence the decision whether to perform a shunting procedure. For varices that are secondary to splenic vein thrombosis (sinistral portal hypertension), splenectomy is usually curative; the procedure may be performed laparoscopically [see 5:25 Splenectomy].63
gastric varicesGastric varices are managed in much the same way as esophageal varices [see
Figure 2], although they are less amenable to sclerotherapy.64 Other endoscopic treatments (e.g., ligation or sclerotherapy plus ligation) and interventional radiologic treatments (e.g., TIPS or intravascular balloon occlusion) should be considered before surgical management (i.e., DSRS, portosystemic shunting, or suture ligation with gastric devascularization). If the patient is a suitable candidate, liver transplantation may be performed as an alternative to shunting.mallory-weiss tearsMallory-Weiss tears are linear mucosal tears at the esophagogastric junction that are usually caused by vomiting. Any patient who presents with vomiting that initially is not bloody but later turns so should be suspected of having a Mallory-Weiss tear. As a rule, these lesions stop bleeding without therapy. If bleeding is substantial or persistent, however, endoscopic injection, clipping, banding, or coagulation may be necessary.
65,66 In rare instances, the tear will have to be oversewn at operation. This is accomplished via an anterior gastrotomy and direct suture ligation of the tear.acute hemorrhagic gastritisBleeding from gastritis is virtually always managed medically with H2 blockers, PPIs, sucralfate, or antacids (either alone or in combination), along with antibiotics if H. pylori is present.
67 Somatostatin may be beneficial. Sometimes, administration of vasopressin via the left gastric artery is needed to control bleeding. In rare cases, total or near-total gastrectomy [see 5:20 Procedures for Benign and Malignant Gastric and Duodenal Disease] is required; however, the mortality associated with this operation in this setting is high. Stress ulcer prophylaxis in severely ill or traumatized patients is essential to prevent this problem.68 The gastric pH should be kept as close to neutral as possible. If the gastritis is relatively mild, a biopsy specimen should be obtained and tested for H. pylori. Treatment consists of acid reduction and H. pylori therapy.neoplasmsBenign tumors of the upper GI tract (e.g., gastrointestinal stromal tumors [GISTs], hamartomas, and hemangiomas) occasionally bleed [see 5:8 Tumors of the Stomach, Duodenum, and Small Bowel]. Wedge excision of the offending lesion is the procedure of choice. GISTs (previously classified as leiomyomas or leiomyosarcomas) run the gamut from benign to highly aggressive. They typically present as a submucosal mass that may cause bleeding as a result of mucosal ulceration. The bleeding may be treated with wedge excision of the tumor, which can be challenging when the GIST is located in the gastric cardia. Such excision can often be accomplished laparoscopically [see 5:20 Procedures for Benign and Malignant Gastric and Duodenal Disease] or even through a laparoscopic intragastric approach.
69 Some surgeons now perform full-thickness wedge resections endoscopically with the use of a flexible stapler.70Bleeding from malignant neoplasms, whether early stage or late stage, generally can be controlled initially by endoscopic means; however, rebleeding rates are high.71 If the lesion is resectable, it should be excised promptly once the patient is stable (provided that it has been appropriately staged). If disease is advanced, however, surgical options are limited, and a nonoperative approach, although necessarily imperfect, is preferable.
hiatal herniaNot infrequently, the source of chronic enteric blood loss is a hiatal hernia. Major bleeding is rare in this condition but may occur as a result of linear erosions at the level of the diaphragm (Cameron lesions),
72 gastritis within the hernia, or torsion of a paraesophageal hernia. Endoscopy is generally diagnostic, although the sources of chronic blood loss are not always obvious. Recognition that the bleeding derives from a Cameron lesion should incline the surgeon toward operative intervention [see 4:7 Open Esophageal Procedures and 4:8 Minimally Invasive Esophageal Procedures]; this lesion is usually mechanically induced and therefore tends to be less responsive to antacid therapy.Chronic bleeding from a type I hiatal hernia should be treated initially with a PPI. H. pylori therapy should be added if biopsy shows this organism to be present. Operative management (i.e., laparoscopic Nissen fundoplication [see 4:8 Minimally Invasive Esophageal Procedures]) should be considered for fit patients who have complications associated with their hiatal hernia and for all symptomatic patients with type II, III, or IV hiatal hernias (laparoscopic paraesophageal hernia repair).73
dieulafoy lesionA Dieulafoy lesion is the rupturing of a 1 to 3 mm bleeding vessel through the gastric mucosa without surrounding ulceration. This lesion is most commonly found high on the lesser curvature, but it can also occur anywhere throughout the GI tract. Histologic studies have not revealed any intrinsic abnormalities either of the mucosa or of the vessel.
Initial treatment consists of either endoscopically based coagulation of the bleeding vessel with a heater probe or mechanical control with clips or rubber bands; local injection of epinephrine may help control acute hemorrhage while this is being done. In skilled hands, endoscopic therapy has a 95% success rate, and long-term control is excellent. If endoscopic therapy fails, surgical options, including ligation or excision of the vessel involved, come into play.
74 Having the endoscopist mark the site with India ink is helpful for localization.hemobiliaHemobilia should be suspected in all patients who present with the classic triad of epigastric and right upper quadrant pain, GIB, and jaundice; however, only about 40% of patients with hemobilia present with the entire triad. Endoscopy demonstrating blood coming from the ampulla of Vater points to a source in the biliary tree or the pancreas (hemosuccus pancreaticus).
Arteriography may provide the definitive diagnosis: a bleeding tumor, a ruptured artery from trauma, or another cause. Arteriographic embolization of the affected portion of the liver is the preferred treatment option; hepatic artery ligation (selective if possible) or hepatic resection [see 5:23 Hepatic Resection] may be required.
hemosuccus pancreaticusBleeding into the pancreatic duct, generally from erosion of a pancreatic pseudocyst into the splenic artery, is signaled by upper abdominal pain followed by hematochezia.
75 If endoscopy is performed when hematochezia is present, the bleeding site may not be seen; however, if endoscopy is performed when pain is first noted, blood may be seen coming from the ampulla of Vater. The combination of significant GIB, abdominal pain, a history of alcohol abuse or pancreatitis, and hyperamylasemia should suggest the diagnosis. If there are no pancreatitis-related indications for surgery, angiographic embolization can be definitive treatment.76 If there are pancreatitis-related indications for operation, angiographic embolization may allow an elective operative procedure based on the structural changes observed in the pancreas. If embolization fails, pancreatic resection is usually required, often on an emergency basis [see 5:24 Procedures for Benign and Malignant Pancreatic Disease].aortoenteric fistulaAortoenteric fistulas may occur spontaneously as a result of rupture of an aortic aneurysm or perforation of a duodenal lesion (primary); more often, they arise after aortic surgery (secondary).
77 A common initial manifestation of an aortoenteric fistula is a small herald bleed that is followed a few days later by a massive hemorrhage. Patients often present with the triad of GI hemorrhage, a pulsatile mass, and infection; however, not all of these symptoms are invariably present. A high index of suspicion facilitates diagnosis. Endoscopy may show an aortic graft eroding into the enteric lumen, but this is an uncommon finding. CT scanning is the procedure of choice for diagnosis. The finding of air around the aorta or the aortic graft is diagnostic and is an indication for emergency exploration. The preferred surgical treatment is resection of the graft with extra-abdominal bypass. Some authorities, however, advocate resection of the graft with in situ graft replacement.78 Some now advocate endovascular stent repair for high-risk patients without evidence of infection.79vascular ectasiasVascular ectasias (also referred to as vascular dysplasia, angiodysplasia, angiomata, telangiectasia, and AVMs) may bleed briskly. As a rule, gastric lesions can be readily identified and the bleeding controlled by endoscopic means.
80 Lesions that continue to bleed, either acutely or chronically, despite endoscopic measures should be excised. Some patients have multiple and extensive lesions that necessitate resection of large portions of the stomach. Pharmacotherapy and hormone therapy have been tried; the results have been mixed.duodenal diverticulaDuodenal diverticula are rare causes of UGIB. Accurate identification of a bleeding site within a given diverticulum is difficult, but an attempt should be made to accomplish this by means of per oral enteroscopy or video-CE. Excision is the preferred treatment and is accomplished by means of segmental resection.
81 Great care must be taken in the treatment of duodenal diverticula in the region of the ampulla of Vater to ensure that the pancreatic duct and the bile ducts are not injured during excision.Discussion and Management of Specific Sources of LGIBdiverticulosis
The vast majority of colonic diverticula are actually false diverticula (pseudodiverticula) that contain only serosa and mucosa [see 5:12 Diverticulitis]. They occur at weak points in the colonic wall where the vasa recta penetrate the muscularis to supply the mucosa; as the diverticulum expands, these vessels are displaced. A 1976 anatomic study of colonic specimens from patients with diverticular bleeding used angiography to demonstrate that in all cases, the vasa recta overlying the diverticulum ruptured into the lumen of the diverticulum, not into the peritoneum.82
It has been estimated that approximately 17% of patients with colonic diverticulosis experience bleeding, which may range from minor to severe and life-threatening. Fortunately, most diverticular hemorrhages stop spontaneously. In one series, surgery was unlikely to be necessary if fewer than 4 units of packed RBCs were transfused in a 24-hour period, whereas 60% of patients receiving more than 4 units of packed RBCs in a 24-hour period required surgical intervention.83 Semielective surgical therapy is usually offered after a second diverticular bleeding episode because once a second such episode has occurred, the risk that a third will follow exceeds 50%. In a series of 83 conservatively managed cases of diverticular disease, the predicted yearly recurrence rates were 9% at 1 year, 10% at 2 years, 19% at 3 years, and 25% at 4 years.84
In general, patients who require more than 4 units of blood in a 24-hour period to remain hemodynamically stable, who have not stopped bleeding after 72 hours, or who experience rebleeding within 1 week after an initial episode should undergo surgery.18
Endoscopic treatment of diverticular hemorrhage can be difficult because of the high bleeding rate and the location of the bleeding point within the diverticulum. In 2000, one group of investigators reported their experience with endoscopic therapy for severe hematochezia and diverticulosis in a prospective series of 121 patients.85 In this series, none of the patients treated endoscopically with epinephrine injections, bipolar coagulation, or both required surgery and none experienced recurrent bleeding episodes. A 2001 study from another group, however, reported high rates of recurrent bleeding episodes in both the early and the late posttreatment periods.86 In the absence of prospective, randomized trials, it is difficult to draw definitive conclusions about the utility of endoscopic therapy in treating diverticular hemorrhage.
colonic avmsThe term arteriovenous malformation includes vascular ectasias, angiomas, and angiodysplasias. AVMs are ectatic blood vessels seen in the mucosa and submucosa of the GI tract. They are degenerative lesions of the GI tract, occurring more frequently with advancing age.
18 In patients older than 50 years, the incidence of colonic AVMs is estimated to range from 2 to 30%.87Colonic AVMs are believed to derive from chronic colonic wall muscle contraction, which leads to chronic partial obstruction of the submucosal veins, causing the vessels to become dilated and tortuous. This process eventually renders the precapillary sphincters incompetent, resulting in direct arterial-venous communication. Colonic AVMs are most commonly found in the cecum. They have been associated with several systemic diseases, including atherosclerotic cardiovascular disease, aortic stenosis, chronic renal disease, collagen vascular disease, von Willebrand disease, chronic obstructive pulmonary disease, and cirrhosis of the liver; to date, however, no definite causal relationship to any of these conditions has been established.21
The diagnosis of a colonic AVM is made at the time of angiography or colonoscopy. During angiography, visualization of ectatic, slow-emptying veins, vascular tufts, or early-filling veins establishes the diagnosis.88 During endoscopy, angiodysplasias appear as red, flat lesions about 2 to 10 mm in diameter, sometimes accompanied by a feeding vessel.4,21
Typically, the bleeding caused by colonic AVMs is chronic, slow, and intermittent. Although these lesions can cause severe lower GI hemorrhage, they are a relatively uncommon cause. The bleeding stops spontaneously in 85 to 90% of cases,88 but it recurs in 25 to 85%.89 Accordingly, definitive surgical or colonoscopic treatment should be rendered once the lesion has been identified.
Colonic AVMs are usually amenable to endoscopic treatment. That these lesions are frequently found in the right colon makes perforation a concern; this complication is reported in approximately 2% of patients. Good success rates have been reported with both injection and thermal methods.90 In one series, endoscopic fulguration was successful in 87% of patients, and no rebleeding episodes occurred over a 1- to 7-year follow-up period.90 Bleeding from multiple telangiectatic lesions in the distal colon resulting from radiation injury can be treated with thermal contact probes, lasers, or noncontact devices such as the argon plasma coagulator.
neoplasiaSignificant GIB from colorectal neoplasia [see 5:15 Adenocarcinoma of the Colon and Rectum] accounts for 7 to 33% of cases of severe lower GI hemorrhage.
3,18 Such bleeding is believed to result from erosions on the luminal surface. Adenomatous polyps are implicated in 5 to 11% of cases of acute LGIB.91LGIB, either immediate or delayed, is the most common reported complication after endoscopic polypectomy, occurring in 0.2 to 6% of cases.3,84 Immediate postpolypectomy bleeding is believed to result from incomplete coagulation of the stalk before transection. Delayed bleeding has been reported as long as 15 days after polypectomy and is thought to be secondary to sloughing of the coagulum; it is less common than immediate bleeding, occurring in only 0.3% of cases.92 Postpolypectomy hemorrhage can often be successfully treated by endoscopic means. Methods used include simple resnaring of the stalk while pressure is maintained92; electrocauterization, with or without epinephrine injection; endoscopic band ligation; and placement of metallic clips.
benign anorectal diseaseHemorrhoids, ulcer or fissure disease, and fistula in ano [see 5:17 Benign Rectal, Anal, and Perineal Problems] must not be overlooked as causes of GI hemorrhage: in one review comprising almost 18,000 cases of LGIB, 11% were attributable to anorectal pathology. It is therefore imperative to perform a digital rectal examination and anoscopy in all patients with LGIB. However, identification of a benign anorectal lesion does not eliminate the possibility of a more proximal cause of hemorrhage. Patients with hemorrhoids identified on physical examination should therefore still undergo thorough endoscopic evaluation of the colon to rule out other pathologic conditions. For patients whose bleeding is attributable to benign anorectal causes, endoscopic therapy may include epinephrine injection, sclerosant injection, or band ligation of internal hemorrhoids.93
Portal hypertension [see 5:10 Portal Hypertension], congestive heart failure, and splenic vein thrombosis can cause colonic or anorectal varices, which can result in massive lower GI hemorrhage. The reported incidence of anorectal varices in patients with portal hypertension ranges from 78 to 89%.94 If local measures fail to control hemorrhage, some form of portosystemic shunting is indicated.
colitisThe broad term colitis includes IBD, infectious colitis, radiation colitis, and idiopathic ulcers. IBD, in turn, includes Crohn disease [see 5:11 Crohn Disease] and ulcerative colitis [see 5:13 Fulminant Ulcerative Colitis]. Patients with IBD usually present with bloody diarrhea that is not life-threatening; however, 6 to 10% of patients with ulcerative colitis have LGIB severe enough to necessitate emergency surgical resection,
95 and 0.6 to 1.3% of patients with Crohn disease have acute life-threatening LGIB.95 In one review, 50% of patients with intestinal hemorrhage from IBD experienced spontaneous cessation of bleeding.95 Approximately 35% of patients whose bleeding stops without intervention will have another bleeding episode. Because of this high recurrence rate, semielective surgery is recommended after the first episode of severe GIB secondary to IBD.Colitis caused by various infectious agents (e.g., typhi, Escherichia coli O157:H7, Clostridium difficile, and cytomegalovirus) can result in severe LGIB, but this is a relatively rare occurrence.
Increasing use of radiation therapy to treat pelvic malignancies has led to a corresponding increase in the incidence of chronic radiation proctitis. Radiation therapy damages bowel mucosa, resulting in the formation of vascular ectasias that are prone to bleeding. From 1 to 5% of cases of acute LGIB from radiation-induced proctocolitis are severe enough to necessitate hospitalization.84 In a survey of patients with prostate cancer who underwent pelvic irradiation, 5% of the patients reported hematochezia daily.96 Initial therapy for clinically significant hematochezia related to radiation proctitis should include some form of endoscopic treatment (e.g., argon-beam coagulation). Surgery should be reserved for unstoppable hemorrhage or other major complications, such as fistulas and strictures.
coagulopathyLGIB can be a presenting symptom for both patients with iatrogenic coagulopathy from heparin or warfarin therapy and patients with a hematologic coagulopathy from thrombocytopenia [see 1:4 Bleeding and Transfusion]. It is unclear, however, whether severe coagulopathy leads to spontaneous hemorrhage or whether it predisposes to bleeding from an existing lesion.
97 In an early series of leukemic patients with thrombocytopenia and severe GI hemorrhage, 50% of bleeding patients had platelet counts lower than 20,000/µL without any identifiable mucosal lesions; furthermore, when the platelet count rose above 20,000/µL, the incidence of bleeding decreased to 0.8%.97 The investigator concluded that severe thrombocytopenia led to spontaneous GI hemorrhage. Other investigators subsequently challenged this conclusion, arguing that spontaneous bleeding from coagulopathy is, in fact, rare. In one report, the distribution of pathologic lesions in patients with GIB who were taking heparin or warfarin was essentially equivalent to that in the general population.98 Regardless of what the precise relation between coagulopathy and GI hemorrhage may be, a thorough investigation for an anatomic lesion is imperative in the workup of patients with LGIB even in the face of coagulopathy or thrombocytopenia.colonic ischemiaAcute LGIB can also be a presenting symptom of colonic ischemia. In several large series, colonic ischemia accounted for 3 to 9% of cases of acute lower GI hemorrhage.
84,91 Other vascular diseases reported as potential causes are polyarteritis nodosa, Wegener granulomatosis, and rheumatoid vasculitis. The resultant vasculitis can cause ulceration, necrosis, and, ultimately, hemorrhage.More than 80% of patients with colonic ischemia respond to bowel rest, IV fluids, and antibiotics and do not require surgical intervention.99 When exploration is indicated because of peritonitis or recalcitrant disease, all questionable bowel should be resected with stoma creation unless a second-look operation is planned.
small intestinal sourcesSmall intestinal sources account for 0.7 to 9% of cases of acute LGIB.
3,84 About 70 to 80% of cases of small bowel hemorrhage are attributable to AVMs; other, less common causes are jejunoileal diverticula, Meckel diverticulum, neoplasia, regional enteritis, and aortoenteric fistulas. Accurate localization of a bleeding site in the small intestine can be highly challenging: the length and the free intraperitoneal position of the small bowel make endoscopic examination difficult, and the nature of the overlying loops makes angiographic localization imprecise. For these reasons, the small intestine is usually left for last in the attempt to localize the source of LGIB and is examined only after sources in the colon, upper GI tract, and anorectum have been ruled out.aidsThe etiology of LGIB in patients with AIDS differs from that in the general population. In AIDS patients, LGIB is caused predominantly by conditions related to the underlying HIV infection. Cytomegalovirus colitis is the most common cause of such bleeding in this population, occurring in 39% of cases. AIDS patients with hemorrhoids or anal fissures often experience significant bleeding as a result of HIV-induced thrombocytopenia. A 1998 study reported that in 23% of AIDS patients hospitalized for LGIB, benign anorectal disease was the cause.
100 Other significant causes of lower GI hemorrhage in this population are colonic histoplasmosis, Kaposi sarcoma of the colon, and bacterial colitis.100nsaidsThe association between NSAID use and UGIB is well known. Current data suggest that NSAIDs have a toxic effect on colonic mucosa as well. An epidemiologic study estimated the incidence of NSAID-associated large bowel bleeding to be 7 in 100,000.
101 A retrospective review found that patients who had experienced LGIB were twice as likely to have taken NSAIDs as those who had not.102 NSAIDs have also been linked to diverticular hemorrhage. The exact mechanism of NSAID-induced colonic injury is unknown.References1. Rockall TA, Logan RF, Devlin HB: Incidence of and mortality from acute upper gastrointestinal haemorrhage in the United Kingdom. Steering Committee and members of the National Audit of Acute Upper Gastrointestinal Haemorrhage BMJ 1995 311:222, . [PMID 15871677]
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Section 5 Gastrointestinal Tract and Abdomen
2 Upper Gastrointestinal BleedingEric S. Hungness, MD, FACS
DOI 10.2310/7800.S05C05
Upper and lower gastrointestinal bleeding require different diagnostic tests and treatments.
Upper and lower gastrointestinal (GI) bleeding, proximal and distal to the ligament of Treitz, respectively, are two common reasons for surgical consultation. Upper GI bleeding is generally esophageal (varices and Mallory-Weiss tears), gastric (acute hemorrhagic gastritis, varices, ulcers, and neoplasms), and duodenal (ulcers). Lower GI bleeding can be colonic, with diverticular disease being the most common, or develop from a range of other causes, including inflammatory bowel disease, benign and malignant neoplasms, ischemia, infectious colitis, and many others.
The diagnostic test for upper GI bleeding is primarily esophagoduodenoscopy. A range of tests exist for lower GI bleeding, including colonoscopy, radionuclide scanning, angiography, computed tomography, enteroscopy, and capsule enteroscopy. Treatments for these conditions range from laparo-scopic or open surgery (for certain ulcers or neoplasms) to medications (for gastritis) to minimal treatments like bowel rest and IV fluids (for colonic ischemia).
Gastrointestinal Bleeding
Question 1 A 35-year-old gentleman has presented with massive upper gastrointestinal bleeding. He has received seven units of packed red blood cells and is hemodynamically unstable, with hypotension and tachycardia. Upper gastrointestinal endoscopy (esophagogastroduodenoscopy [EGD]) reveals a giant duodenal ulcer as the source of active bleeding.
Regarding the recommended management approach for this patient, which of the following statements is not true?
Please choose the single most appropriate answer to the question - Persisting with an endoscopic approach is justifiable provided that adequate blood replacement is done
This is correct.
Key Concept/Objective: To learn about the optimum approach in the management of an actively bleeding giant duodenal ulcerIf the EGD confirms duodenal ulcer to be the cause of active upper gastrointestinal bleeding, persisting with endoscopic management in a patient who is hemodynamically unstable is not recommended. The initial management may be endoscopic, but in the event of ongoing blood loss or massive blood loss (more than 6 units), as in the presented scenario, a delay in surgery is not recommended. In patients with giant ulcers, even if the endoscopic treatment has controlled the bleeding from a visible bleeding vessel, surgical therapy should be strongly considered. - Immediate surgical therapy is indicated in this case
Sorry, this is incorrect. Try again!
- Initial treatment may be endoscopic; surgery is indicated if the bleeding persists
- Surgical therapy is indicated even after the bleeding has been controlled endoscopically
Question 2 A 65-year-old woman has presented with active gastrointestinal bleeding.
Regarding arteriography as a localizing modality, which of the following statements is not true? Please choose the single most appropriate answer to the question - Cannot reliably identify a bleeding site unless the bleeding is brisk (> 1 mL/min)
- May reveal the cause (lesion) of bleeding even if the bleeding has stopped
- Can be used as a therapeutic modality
- Reliably and accurately predicts the bleeding site even if the bleeding is minimal
Key Concept/Objective: To learn about the utility of angiography as a modality to localize the bleeding site in gastrointestinal bleedingAmong various modalities to localize the bleeding site, arteriography is a useful diagnostic and therapeutic modality. Although arteriography may demonstrate that a lesion is present, it cannot reliably identify a bleeding site unless the bleeding is brisk (> 1 mL/min). Arteriography may sometimes reveal the cause (lesion) of bleeding even if the bleeding has stopped. Angiography may serve as a therapeutic modality for performing embolization using a foam or coil for high-risk surgical patients.
Question 3 A 33-year-old woman presents to the emergency department after experiencing an episode of hematemesis. She has a history of peptic ulcer disease. She has no other relevant medical history.
For this patient, which of the following statements regarding vagotomy and pyloroplasty is true? Please choose the single most appropriate answer to the question - Two traction sutures are placed in the anterior aspect of the pylorus, one superiorly and one inferiorly
- The bleeding ulcer bed is directly oversewn with at least three sutures
- Gastric outlet obstruction may occur secondary to either scarring or edema at the operative site
- All of the above
Key Concept/Objective: To understand vagotomy and pyloroplasty for bleeding ulcerTruncal vagotomy with pyloric drainage via pyloroplasty is rarely employed as primary therapy for peptic ulcer disease, but it does play a role in the emergency management of bleeding duodenal ulcers. This approach to acid suppression fits well with the proximal duodenotomy used to control the hemorrhage. Exposure of the first portion of the duodenum via a longitudinal incision in the pylorus is combined with truncal vagotomy; the pylorus is then closed in a transverse fashion to prevent the development of gastric outlet obstruction. A Kocher maneuver is performed. The pylorus is identified through palpation and through identification of the pyloric vein as it courses anteriorly. Two traction sutures are placed in the anterior aspect of the pylorus, one superiorly and one inferiorly. A longitudinal incision is made that extends approximately 2 to 3 cm on either side of the pylorus. The bleeding ulcer bed is directly oversewn with at least three sutures. Figure-eight sutures are placed on the superior and inferior borders of the ulcer bed to ligate the gastroduodenal artery proximal and distal to the ulcer, and a third figure-eight suture is placed medially to control the transverse pancreatic branch. Leakage from a pyloroplasty is rare. Gastric outlet obstruction may occur secondary to either scarring or edema at the operative site; often, it is relieved by nasogastric decompression and conservative management.
Question 4 A 55-year-old male who is critically ill has presented with stress gastritis.
What would be the ideal prevention and management strategies for this patient? Please choose the single most appropriate answer to the question - Stress ulcer prophylaxis is essential in prevention
- In mild cases, a biopsy for Helicobacter pylori should be obtained
- In severe cases, a total or near-total gastrectomy is indicated
- All of the above
Key Concept/Objective: To understand the prevention and management of stress gastritisBleeding from gastritis is virtually always managed medically with H2 blockers, PPIs, sucralfate, or antacids (either alone or in combination), along with antibiotics if Helicobacter pylori is present. Somatostatin may be beneficial. Sometimes, administration of vasopressin via the left gastric artery is needed to control bleeding. In rare cases, total or near-total gastrectomy [see 5:20 Procedures for Benign and Malignant Gastric and Duodenal Disease] is required; however, the mortality associated with this operation in this setting is high. Stress ulcer prophylaxis in severely ill or traumatized patients is essential to prevent this problem. The gastric pH should be kept as close to neutral as possible. If the gastritis is relatively mild, a biopsy specimen should be obtained and tested for Helicobacter pylori. Treatment consists of acid reduction and Helicobacter pylori therapy.
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