Gastrointestinal Bleeding (Case 22)
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.
Peptic ulcer disease
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.
• 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.
• The rectal exam is important: black tarry stools (melena) will most likely mean an upper GI source of bleeding; bright red blood usually indicates a lower GI source. Are there masses or hemorrhoids present?
• Placement of an NG tube can be helpful when there is concern for an upper GI source of bleeding. Keep in mind that if the fluid aspirated from the tube is clear, this does not exclude an upper GI source. It is important to have bilious return to rule out a duodenal source. If the return is bloody, this indicates an upper GI hemorrhage.
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Peptic Ulcer Disease
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Large tumors can be seen during an upper GI series or on CT scan. Definitive diagnosis is made endoscopically with biopsy.
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.
a. Dieulafoy lesion: A dilated, aberrant submucosal vessel that erodes the underlying epithelium in the absence of an ulcer. It accounts for less than 1% of severe upper GI hemorrhages. Both diagnosis and treatment can be done endoscopically. The vessel most likely requires dual therapy with injection and electrocautery or clipping.
b. Mallory-Weiss tear: Longitudinal mucosal tears at the distal esophagus and proximal stomach usually caused by retching. Retching increases the intra-abdominal pressure and causes the tear. Diagnosis is made by endoscopy. Most tears heal spontaneously. If a tear is actively bleeding, the usual modes of endoscopic treatment can be utilized.
c. Gastric antral vascular ectasia (GAVE) syndrome: This disorder is also known as watermelon stomach. The term comes from the endoscopic appearance of the stomach with longitudinal flat red stripes that radiate from the pylorus into the antrum and resemble the stripes on a watermelon. Most cases are idiopathic. Treatment consists of endoscopic ablation with argon plasma coagulation. Multiple treatments are usually necessary.