Chapter 29
Gastrointestinal Bleeding (Case 22)
Melissa Morgan DO, Michael Share MD, and Marc Zitin MD
Case: A 70-year-old woman with a past medical history of coronary artery disease, hypertension, and hyperlipidemia presents to the ED complaining of rectal bleeding that has been present all day. Earlier in the day she had a bowel movement and noted bright red blood mixed in with her stool. She complains of dizziness and light-headedness. Her outpatient daily medications include aspirin, simvastatin, and metoprolol. She also admits to taking ibuprofen twice daily for the past week for pain in her knees. She admits to “occasional” drinking and one cocktail each night after dinner.
Differential Diagnosis
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Peptic ulcer disease |
Arteriovenous malformation |
Colon cancer |
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Hemorrhoids |
Esophagogastric varices |
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Gastric cancer |
Diverticulosis |
Speaking Intelligently
When asked to see a patient with GI bleeding, it is important to remember to first stabilize the patient. It is also important to know whether the bleeding is coming from the upper or lower GI tract; this will affect both acute management and treatment. Upper GI bleeding commonly presents with hematemesis and/or melena. In comparison, lower GI bleeding presents with hematochezia. However, these distinctions are not absolute. A massive upper GI hemorrhage can also present with hematochezia, and a proximal lower GI bleed can present with melena.
PATIENT CARE
Clinical Thinking
• As stated previously, the management of the patient strongly depends on the cause of bleeding. Patients who are having a massive upper GI hemorrhage will most likely require intubation and observation in the ICU.
History
• Has the patient ever had an endoscopic procedure such as colonoscopy or upper endoscopy?
• Did the patient have bloody vomitus or coffee-grounds emesis?
• Was there blood only on the toilet paper or in the toilet bowl as well?
• Does the patient have abdominal pain? If so, determine duration.
Physical Examination
• Check the vital signs: Tachycardia and/or hypotension indicates an active or ongoing hemorrhage.
Tests for Consideration
| Clinical Entities | Medical Knowledge |
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Peptic Ulcer Disease |
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Pφ |
PUD occurs when the caustic effects of acid and pepsin in the GI lumen overwhelm the ability of the mucosa to resist their effects. Most ulcers occur when the process of mucosal protection is disrupted by Helicobacter pylori infection or use of NSAIDs. |
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Although gastric and duodenal ulcers are associated with epigastric pain 66% of the time, often the diagnosis is not made until complications such as hemorrhage or perforation occur. Hemorrhage will be evident by melena, hematemesis, or coffee-grounds emesis. Perforation will cause severe abdominal pain and usually presents as an acute abdomen with peritonitis, requiring surgery. |
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Dx |
Endoscopy is the most accurate diagnostic test for PUD and is the appropriate first diagnostic test for GI bleeding. Mucosal biopsies should also be obtained for rapid urease tests to determine whether Helicobacter pylori is present; histologic staining should be done for patients with a negative rapid urease test or for instances when the urease test is not available. However, if the concern is for a perforated ulcer presenting with free intraperitoneal air, endoscopy should not be performed and the treatment is surgical. |
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Tx |
The majority of upper GI bleeds due to PUD will stop spontaneously, but certain findings on endoscopy will predict the risk of repeat hemorrhage and should prompt early intervention: (1) a visible vessel in the ulcer bed, (2) an adherent clot, and (3) active bleeding. EGD is not only a diagnostic procedure but a therapeutic one as well; bleeding is often stopped by injection of epinephrine, use of electrocautery, and/or clips placed endoscopically. It is recommended that at least two of the above therapies be used to fully control and prevent repeat bleeding. The use of a proton pump inhibitor (PPI) infusion is helpful during an upper GI hemorrhage secondary to PUD. Raising the pH in the stomach enhances stabilization of clot formation. In patients with demonstrated infection with H. pylori, appropriate antimicrobial therapy should also be added. See Cecil Essentials 37. |
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Arteriovenous Malformation |
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Pφ |
Also called angiodysplasia, these abnormalities consist of ectatic, dilated, thin-walled vessels that are composed of either endothelium alone or endothelium with a small component of smooth muscle. Although the pathogenesis is not completely understood, one theory is that development occurs because of intermittent obstruction of submucosal veins in the muscularis propria, which causes dilation. AVMs can occur anywhere throughout the GI tract. They are seen in patients with numerous conditions, including end-stage renal disease, von Willebrand disease, and aortic stenosis. |
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Presentation varies based on the location of the AVM. AVMs in the stomach can cause melena or hematemesis. Those located in the small intestine or right side of the colon can cause melena, bright red blood per rectum, or even anemia with occult bleeding. Presentation depends on how extensively they bleed. Coagulopathy or platelet dysfunction can lead to more overt bleeding. |
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Dx |
Diagnosis can be made during upper endoscopy or colonoscopy if the lesions are within reach of the endoscope or colonoscope. If a cause of bleeding cannot be found, patients will undergo a video capsule study or double-balloon enteroscopy (DBE), to visualize the entire small bowel, including the jejunum and ileum. |
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Tx |
AVMs can be treated endoscopically using electrocautery or argon plasma coagulation. The choice of treatment varies on location of the lesion as well as the preference of the endoscopist. The right side of the colon is extremely thin-walled and more likely to perforate during treatment compared to other parts of the GI tract. If a hemorrhage is particularly aggressive, other options for treatment include surgery and angiography with embolization. See Cecil Essentials 34. |
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Diverticulosis |
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Pφ |
A diverticulum is a saclike protrusion of the colonic wall that does not contain all of the layers of the wall; the mucosa and submucosa herniate through the muscle layer. Diverticula develop at four points along the circumference of the colon, where the blood vessels (vasa recta) penetrate the circular muscle layer. The blood vessel can become irritated and rupture into the diverticulum, causing a brisk hemorrhage. These account for 30% to 50% of brisk rectal bleeding. A diet low in fiber can predispose a patient to diverticular disease. A low-fiber diet can cause increased intraluminal pressure in the colon, and this can lead to the formation of diverticula. |
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TP |
Painless rectal bleeding is the main presentation. This most commonly occurs in those >60 years of age but can occur in younger patients as well. As many as 50% may have had a previous episode. |
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Dx |
Diagnosis can be made via colonoscopy. If the patient has had a previous colonoscopy with documented diverticulosis and presents with a brisk lower GI hemorrhage, the bleeding will most likely be diverticular in nature. To diagnose the exact site of bleeding, colonoscopy can again be useful. However, if a significant amount of blood is present, it may be difficult to localize the bleeding. A tagged-RBC scan can aid in localization. |
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Bleeding will cease spontaneously in 75% of episodes. If bleeding does not stop, a colonoscopy can be performed to try to localize the diverticulum involved, and a clip can be placed. However, if the bleeding cannot be localized via colonoscopy, a tagged-RBC scan followed by angiography and embolization is necessary. If the patient continues to bleed despite these efforts, surgical intervention may be necessary. See Cecil Essentials 34. |
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Hemorrhoids |
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Pφ |
Hemorrhoids arise from a plexus of dilated veins located in the submucosal layer of the rectum and are classified as internal or external based on their location from the pectinate line. Those that are above the pectinate line are considered internal, and those below are external. A patient may have both. Hemorrhoids are classically associated with advanced age, chronic constipation, pregnancy, prolonged sitting, and diarrhea. |
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TP |
Internal hemorrhoids can cause painless bleeding that can be described most often as either a slow drip into the toilet or blood that is seen solely on the toilet paper. External hemorrhoids generally lead to pruritus and the formation of skin tags, and they cause acute rectal pain when they become thrombosed. |
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Dx |
Diagnosis of external hemorrhoids is made by visual inspection of the anus. At times internal hemorrhoids can be palpated on rectal examination; they are best visualized by performing anoscopy or sigmoidoscopy. |
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Tx |
Conservative measures to treat hemorrhoids include adding fiber to the diet to add bulk to the stools, thereby lessening constipation and minimizing bleeding. Hydrocortisone suppositories and sitz baths can help with symptoms of pain and pruritus. If symptoms persist despite conservative treatment, more invasive measures may be required. Most external hemorrhoids require no further intervention. When acute thrombosis occurs, the patient may benefit from surgical evacuation of the clot and excision of the hemorrhoid within the first 48 hours. Internal hemorrhoids that persistently bleed can be treated with rubber-band ligation; if this is unsuccessful, hemorrhoidectomy becomes appropriate. See Cecil Essentials 34. |
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Pφ |
Varices develop as a consequence of portal hypertension, usually from cirrhosis. Normal portal pressure is approximately 9 mm Hg compared to an inferior vena cava pressure of 2–6 mm Hg. Therefore, a normal portal→caval gradient is 3–7 mm Hg. At gradients >10 mm Hg, blood flow through the hepatic portal system is redirected from the liver to areas with lower venous pressures. This causes extremely dilated submucosal veins that can be present in the stomach or esophagus. Isolated gastric varices can be present from obstruction of the splenic vein. |
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TP |
Varices result in massive hematemesis, which is usually painless. Patients often demonstrate signs of systemic shock with hypotension and tachycardia on initial presentation due to the large amount of blood loss. Only 50% of patients with an acute variceal hemorrhage will stop bleeding spontaneously; 30% of patients will die during their first acute hemorrhage. |
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Dx |
Diagnosis is based on clinical history as well as endoscopic findings. If a patient is a known cirrhotic (although they can certainly develop other disease entities such as PUD), it is important to treat aggressively, as their mortality from a variceal hemorrhage is high. |
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Tx |
Treatment varies from pharmacologic, endoscopic, Blakemore tube placement (a tube with multiple balloons designed to accomplish tamponade of proximal gastric and/or esophageal varices), or transjugular intrahepatic portosystemic shunt (TIPS). All variceal hemorrhage patients should be intubated for airway protection before any intervention. A somatostatin analogue can be infused to induce splanchnic vasoconstriction and decrease portal inflow. Endoscopy should be performed as soon as possible. Therapy consists of band ligation or sclerotherapy, which consists of injecting a sclerosant solution into the bleeding varix. Blakemore tube placement is a temporizing measure, and the tube can be left in place for 24–48 hours before complications such as esophageal necrosis occur. TIPS is used as a last resort to decompress the portal system for bleeding that cannot be controlled with any of the aforementioned therapies. See Cecil Essentials 34, 45. |
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Pφ |
Environmental and genetic factors increase the likelihood of developing colorectal cancer. The proposed mechanism is that most cancers arise from adenomatous polyps in the colon. Polyps can progress to dysplastic polyps and ultimately to adenocarcinoma. The lifetime risk of colorectal cancer in an average-risk person is 5%. More than 90% of colorectal cancers occur in persons over the age of 50 years. |
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TP |
The majority of patients who are symptomatic from colorectal cancer present with hematochezia, abdominal pain, change in bowel habits, or unexplained iron deficiency anemia. Hematochezia is more commonly caused by a rectal rather than a colon cancer. |
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Dx |
Colonoscopy is the single best test to diagnose colon cancer. Although barium enema combined with flexible sigmoidoscopy can be used for colorectal cancer screening, the yield is much lower than with colonoscopy. Colonoscopy is considered the gold standard for the symptomatic patient. |
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Tx |
Once the diagnosis of colon cancer is made, treatment such as chemotherapy, surgery, or radiation therapy varies based on the stage of the disease. If a patient is experiencing symptoms such as hematochezia, interventions such as electrocautery can be utilized for pure palliation of bleeding. However, most lesions are friable, and definitive treatment would consist of surgical intervention. See Cecil Essentials 39, 57. |
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Gastric Cancer |
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Pφ |
Gastric cancer is the second leading cause of cancer deaths in the world. Risk factors include smoking, obesity, infection with Helicobacter pylori, and diet consisting of high-salt and high-nitrosamine compounds. |
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TP |
The most common presenting symptoms are weight loss and abdominal pain. Tumors located at the gastroesophageal junction, or cardia of the stomach, will present with dysphagia. Those that are located more distally in the antrum can cause gastric outlet obstructive symptoms, such as nausea and vomiting. |
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Dx |
Large tumors can be seen during an upper GI series or on CT scan. Definitive diagnosis is made endoscopically with biopsy. |
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Treatment options are based on stage of disease. Surgery may be curative if there are no lymph nodes involved. Often patients have advanced disease at the time of diagnosis. For patients who undergo surgery and prove to have positive lymph nodes, adjuvant postoperative therapy with combination chemotherapy and radiation therapy may be of benefit. See Cecil Essentials 39, 57. |
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Practice-Based Learning and Improvement: Evidence-Based Medicine
Title
Effect of intravenous omeprazole on recurrent bleeding after endoscopic treatment of bleeding peptic ulcers
Authors
Lau JY, Sung JJ, Lee KK, et al.
Institution
Chinese University of Hong Kong
Reference
N Engl J Med 2000;343:310–316
Problem
After endoscopic treatment of bleeding peptic ulcers, bleeding recurs in 15% to 20% of patients.
Intervention
Endoscopic therapy of bleeding peptic ulcers and then randomization to continuous infusion of omeprazole vs. placebo
Prospective randomized trial of 240 patients with 120 patients in each group of treatment and placebo.
Outcome/effect
Bleeding recurred within 30 days in 8 patients (6.7%) in the omeprazole group, as compared with 27 (22.5%) in the placebo group.
Historical significance/comments
This information has helped clinicians substantially in treating bleeding PUD. A constant infusion of a proton pump inhibitor significantly decreases the risk of recurrent bleeding and leads to decreased morbidity and mortality from bleeding PUD. This has become one of the mainstays of treatment presently.
Interpersonal and Communication Skills
Communication Is the Cornerstone of Multidisciplinary Care
When managing a patient with GI bleeding, all specialties must work together. It may be the job of the medicine service or the ED team to stabilize the patient, while the gastroenterologist attempts to identify the cause of the bleeding. In patients with significant hypotension, endoscopy cannot be performed; therefore, the surgical team should be involved should there be a need to operate urgently. If the BP can be stabilized, upper endoscopy can be performed. If the gastroenterologist cannot find the source of bleeding, he or she needs to discuss options with the surgeon and the interventional radiologist. If the patient’s condition is unstable, the team should determine whether an emergent operation or emergent angiogram for embolization is most appropriate under the particular circumstances. Good communication among the various specialties is essential to provide the best possible care.
Remain Nonjudgmental and Treat All Patients with Respect
When approaching a patient with a history of alcohol use who is actively bleeding and suspected of having cirrhosis, it is important to remain nonjudgmental. As much as possible, make the patient feel at ease, particularly as you inquire about social habits such as alcohol consumption and use of injection drugs. If patients feel they cannot trust you, they may not be forthcoming with the information required to treat them, and they may also refuse treatment. Variceal hemorrhage can be deadly and thus has to be treated quickly and aggressively; treatment requires a cooperative patient. Placing patients at ease and showing genuine concern will make them comfortable and more likely to agree to treatment.
Systems-Based Practice
GI Bleeding: Develop a Time-Efficient, Systems-Based Approach to Diagnosis
When we see a patient with GI bleeding in the Emergency Department, we try to keep in mind which areas of the hospital system will need to be mobilized in order to achieve expeditious diagnosis and treatment. Our initial focus is on localizing the source to either the upper or lower GI tract (i.e., proximal or distal to the ligament of Treitz). If the patient’s history (e.g., hematemesis, melenic stool) and physical exam (e.g., hemodynamic instability, NG lavage with copious blood) are strongly suggestive of an upper GI hemorrhage, proceed with EGD, which can be both diagnostic and therapeutic.
NG lavage can be useful in a patient with an upper GI bleed, as return of blood or coffee-grounds–like material confirms the diagnosis of upper GI bleeding and predicts whether bleeding is caused by a high-risk lesion. However, a negative lavage does not exclude an upper GI hemorrhage, as a duodenal lesion may not cause duodenal-gastric reflux. If the EGD is unable to localize a source, proceed with colonoscopy to look for a lower tract source.
In a similar fashion, when a patient presents with a history consistent with lower GI bleeding, it is important to first rule out upper GI bleeding, as 10% to 15% of upper GI hemorrhages present with signs and symptoms of a lower GI hemorrhage. In a stable patient, after excluding an upper source with EGD (with or without NG lavage), proceed with colonoscopy.
Because many patients with lower GI bleeding will stop bleeding spontaneously (recurrent bleeding occurs in only 10% to 40% of patients), diagnosis can often be quite challenging. When the diagnosis cannot be made with endoscopic measures, radiologic imaging studies such as radionuclide scintigraphy and angiography serve their greatest purpose. In scintigraphy, the patient’s RBCs are tagged with technetium-99m (99mTc), and then a gamma camera follows flow and looks for signs of RBC leakage. Scintigraphy is very sensitive to bleeding, recognizing rates as low as 0.1 mL/min, and the radionuclide tag persists for 6 hours, allowing prolonged or repeat imaging. However, scintigraphy does not promote specific anatomic localization of lesions. In the past, scintigraphy has been used as a screening test for angiography, but inconsistent and inaccurate localization of bleeding sites, as well as recent promulgation of wireless capsule enteroscopy (WCE) and DBE, have dramatically decreased its use. Currently, its most appropriate use is in the patient who has intermittent, recurrent bleeding in which we can take advantage of the 6-hour duration of the tag to get a rough idea of lesion location.
Angiography is less sensitive, able to recognize bleeding rates of 0.5 mL/min. However, angiography is not only able to define exact anatomy of a lesion, but can also be therapeutic with localized vasopressin injection or vessel embolization. A patient must be actively bleeding at the time of this study, so it should be used accordingly in a patient with an active bleeding source whose hemodynamic stability is threatened.
The majority of diagnoses and therapies in patients with GI bleeding are achieved with endoscopy, but there is still a role for radiologic imaging to be used in specific situations.
Suggested Readings
Aljebreen AM, Fallone CA, Barkun AN. Nasogastric aspirate predicts high-risk endoscopic lesions in patients with acute upper-GI bleeding. Gastrointest Endosc 2004;59:172–178.
Strate LL. Lower GI bleeding: epidemiology and diagnosis. Gastroenterol Clin North Am 2005;34:643–664.
Westerhof J, Weersma RK, Koornstra JJ. Investigating obscure gastrointestinal bleeding: capsule endoscopy or double balloon enteroscopy? Neth J Med 2009;67:260–265.
