Upper and Lower Gastrointestinal Bleeding Thomas A Kintanar

Upper and Lower Gastrointestinal Bleeding Thomas A Kintanar, MD FAAFP/ABFM

Learning Objectives At the end of this session, participants will be able to: 1. Identify the symptoms and possible underlying causes of upper and lower GI bleeds. 2. Perform tests to determine the site of an upper or lower GI bleed and recommend further testing or treatment as necessary to discover underlying conditions responsible for bleeds. 3. Determine the location of severe or acute GI bleeds while keeping the patient stable, and treat the patient in a timely manner to avoid excessive blood loss and/or shock.

Definition l l Gastrointestinal (GI) bleeding refers to any bleeding that starts in the gastrointestinal tract Divided into upper GI bleeding, which includes the esophagus, stomach, and duodenum Lower GI bleeding includes much of the small intestine, large intestine or bowels, rectum, and anus Acute vs occult or obscure GI Bleeding Upper Lower Acute versus occult Or obscure

Acute vs Chronic Upper or Lower? l l l Signs and symptoms of bleeding in the upper or lower digestive tract depend on the site and severity Can include bright red blood in vomit, black or tarry stool, or bloody stool. Signs of acute bleeding may include weakness, dizziness, shortness of breath, abdominal pain and cramping, and/or diarrhea Acute GI bleeding can be life threatening and may cause a person to go into shock, hospitalization is often required. Chronic bleeding may be accompanied by fatigue, lethargy, and shortness of breath and can also lead to anemia

Major Presenting Factors of Upper GI Bleed l Hematemesis (either red blood or coffee-ground emesis) suggests bleeding proximal to the ligament of Treitz l The majority of melena (black, tarry stool) originates proximal to the ligament of Treitz (90 percent) l It may also originate from the small bowel or right colon [3]. Melena may be seen with variable degrees of blood loss, being seen with as little as 50 ml of blood l Hematochezia (red or maroon blood in the stool) may occur in cases of upper GI bleeding although seen in lower GI bleeds more commonly Sudden, severe bleeding is called acute bleeding. If acute bleeding occurs, symptoms may include l weakness l dizziness or faintness l shortness of breath l crampy abdominal pain l diarrhea l paleness

Major Causes of Upper GI Bleed: Ulcers Peptic ulcer disease l Idiopathic l Drug induced: Aspirin Nonsteroidal antiinflammatory drugs l Infectious: Helicobacter pylori, Cytomegalovirus, Herpes simplex virus l Stress-induced ulcer l Zollinger Ellison syndrome

Portal hypertension: Varices l Esophageal varices l Gastric varices l Duodenal varices l Portal hypertensive gastropathy l Cirrhosis the most common cause of these anomalies l In a series of 1000 patients at the UCLA and West Los Angeles Veterans Administration Medical Centers found that esophagogastric varices were the second most common cause of UGI bleeding, accounting for 14 percent of episodes

Gastritis l l NSAIDs and other drugs Infections Crohn's disease Illness and injuries

Esophagitis l Peptic l Infectious: Candida albicans, Herpes simplex virus, Cytomegalovirus, Miscellaneous Pill-induced : Alendronate Tetracycline Quinidine Potassium chloride Aspirin Nonsteroidal antiinflammatory drugs

Benign tumors and Cancer l l Adenomas and other benign tumors Gastric or Esophageal cancer

Other Causes of Upper GI Bleed Arterial, venous, or other vascular malformations l Idiopathic angiomas l Osler-Weber-Rendu syndrome l Dieulafoy's lesion l Watermelon stomach (gastric antral vascular ectasia) l Radiation-induced telangiectasia l Blue rubber bleb nevus syndrome Traumatic or post-surgical l Mallory-Weiss tear l Foreign body ingestion l Post-surgical anastamosis l Aortoenteric fistula l Post gastric/duodenal polypectomy

Other Causes of Upper GI Bleed: Tumors Benign Miscellaneous l Leiomyoma l Hemobilia l Lipoma l Hemosuccus pancreaticus l Polyp (hyperplastic, adenomatous, hamartomatous) Malignant l Adenocarcinoma l Mesenchymal neoplasm l Lymphoma l Kaposi's sarcoma l Carcinoid l l Melanoma Metastatic tumor

Major causes of Lower GI tract Bleeding l l l Diverticulosis — 5 to 42 percent Ischemia — 6 to 18 percent Anorectal (hemorrhoids, anal fissures, rectal ulcers) — 6 to 16 percent Neoplasia (polyps and cancers) — 3 to 11 percent Angiodysplasia — 0 to 3 percent Postpolypectomy — 0 to 13 percent – – – Inflammatory bowel disease — 2 to 4 percent Radiation colitis — 1 to 3 percent Other colitis (infectious, antibiotic associated, colitis of unclear etiology) — 3 to 29 percent Small bowel/upper GI bleed — 3 to 13 percent Other causes — 1 to 9 percent Unknown cause — 6 to 23 percent

Major Presenting Factors and Symptoms of Lower GI Bleed l l • Black or tarry stool Dark blood mixed with stool Stool mixed or coated with bright red blood l l l Diverticular disease. This disease is caused by diverticula—pouches in the colon wall. Colitis. Infections, diseases such as Crohn's disease, lack of blood flow to the colon, and radiation cause colitis— inflammation of the colon. Hemorrhoids or fissures. Hemorrhoids are enlarged veins in the anus or rectum that can rupture and bleed. Fissures, or ulcers, are cuts or tears in the anal area. Angiodysplasia. Aging causes angiodysplasia—abnormalities in the blood vessels of the intestine. Polyps or cancer. Benign growths or polyps in the colon are common and may lead to cancer. Colorectal cancer is the third most common cancer in the United States and often causes occult bleeding

Diverticular disease l Results from progressive injury to the artery supplying that segment l As diverticulum herniates, the penetrating vessel responsible for the wall weakness at that point becomes draped over the dome of the diverticulum, separated from the bowel lumen only by mucosa l Vasa recta exposed to injury along its luminal aspect, leading to eccentric intimal thickening and thinning of the media l Rupture!

Colitis l l l Inflammatory: Chron’s/ UC Infectious: C diff Collagenous/Lymphocytic: Colonic Ischemia Diversion colitis: segment lacks short chain fa’s Colonic Ischemia

The Microscopic Colitis’ l Lymphocyctic Colitis l Main symptom of this disease is chronic watery diarrhea Colonoscopy finding normal Histopathologic findings include an increased amount of intraepithelial lymphycytes and other signs of chronic inflammation Association between this disease and celiac disease noteworthy Limited treatment experience Sulfasalazine, 5 -ASA-preparations and cortison can be effective, loperamide is used as symptomatic treatment l l l Collagenous colitis l characterized by a thickened subepithelial collagenous band in the colonic mucosa that varies in thickness from 7 to as much as 100 µm (normal is 1 to 7 µm, with a more prominent band in the rectum) l Same colonscopy findings as Lymphocytic l May be associated with abnormal collagen metabolism, Nsaids, bacterial toxins, diabetes, Other meds ie: simvastatin, lansoprazole (with associated linear mucosal defects [58]), omeprazole, esomeprazole, and ticlopidine

Hemorrhoids l External hemorrhoids arise from the inferior hemorrhoidal plexus and are located beneath the dentate line. They are covered with squamous epithelium l Internal hemorrhoids arise from the superior hemorrhoidal cushion. Their three primary locations (left lateral, right anterior, and right posterior) correspond to the end branches of the middle and superior hemorrhoidal veins

Anal Fissures l l Tear in the lining of the anal canal distal to the dentate line, which most commonly occurs in the posterior midline Medical therapy The majority of anal fissures are caused by local trauma to the anal canal, such as after passage of hard stool l Oral nifedipine l Oral diltiazem l Topical diltiazem or bethanechol l Surgical Intervention: Lateral sphincterotomy / Incontinence. Seen with Crohn's disease, tuberculosis, and leukemia Noted cyclic sphincter spasm, stretching of damaged area, with slowing of healing, continued pain and chronicity l Topical nitroglycerin l Botulinum toxin

Angiodysplasia Most common vascular anomaly in the GI tract Vascular tumors or angiomas 1 of 3 classifications l Most prominent feature in angiodysplasias is the presence of dilated, tortuous submucosal veins l Vascular anomalies associated with congenital or systemic diseases 2/3 l l Acquired and sporadic lesions 3/3 Small arteriovenous communications are also present and are due to incompetence of the precapillary sphincter l Resulting av communications may be responsible for the occasional brisk bleeding that may ensue l l l Composed of ectatic, dilated, thin-walled vessels that are lined by endothelium alone or endothelium along with small amounts of smooth muscle

Angiodysplasia

Polyps l l l Hyperplastic Polyps Adenomatous Polyps Tubular adenomas Peutz-Jeghers Familial Polyposis

Colon Cancer

Clinical Case of Lower GI Bleed: Bonnie l l l 78 yo WF widow had 3 month history of not “feeling like herself”. No evidence of abdominal pain or discomfort Had culminated in black tarry and maroon colored stools. Weakness and inability to ambulate well prompting her daughter to transport to rural hospital ER. Hgb was 6. 3 on admission and was noted to have normal vital signs except pulse of 98 l l l Initial approach included CT scan which was negative 3 units of PRBC’s given to bolster Hgb to 10. 4 Pt taken to endoscopy suite by surgeon for upper endoscopy Endoscopy negative Transported to our facility for completion of workup

Bonnie l l Past history: Hyperlipidemia, s/p ectopic pregnancy laparotomy, blepharoplasty, peripheral neuropathy, hypovitaminosis D Family/Soc history: Negative for Etoh, and smoking. Widowed l l l ROS: fatigue over 2 months VS: BP 112/55, P 99 PE: Skin: pale. Chest: clear, CV: RRR no murmur Data base: hemoccult positive, Pancytopenia: rbc: 2. 76, wbc: 3. 3, plates 4. 7, mpv: 7, few atypical lymphs, rouleaux formation Patient scheduled for upper and lower endo. Hematology consult obtained

Diagnostic Approach to the Patient with GI Bleeding Esophagogastroduodenoscopy inspects the esophagus, stomach and duodenum. Tissue can also be biopsied during this test. • Colonoscopy. Studies show colonoscopy can identify definitive bleeding sites in more than 70 percent of patients with lower GI bleeding. • Capsule endoscopy. A small pill containing a video camera transmits images of the small intestine. • Balloon-assisted enteroscopy. A wireless scope inspects parts of the small intestine that EGD and colonoscopy can't reach. • Endoscopic ultrasound. An ultrasound probe attached to an endoscope shows all the layers of tissue in the digestive tract. • Endoscopic retrograde cholangiopancreatography. An X-ray visualizes the ducts of the liver and pancreas • l CT enterography involves ingestion of a neutral contrast agent to distend the small bowel, followed by CT imaging of the abdomen l MR enterography an alternative to CT enterography. It has the advantage of not using ionizing radiation, which allows for sequential imaging of the small bowel l Nuclear GI Bleed Scan a methodology employing nuclear radioiodide imaging to identify active hemorrhage

Bonnie l l l Colonoscopy to cecum performed with identification of blood in rectal vault Cecal intubation reveals 2 angiodysplastic lesions which required heater probe fulguration with copious irrigation. Procedure lasting nearly 1 hour 10 minutes Hemostasis successfully achieved l l EGD revealed patchy areas of erythema. Consistent with gastritis Appearance very similar to angiodysplastic lesions seen in cecum. Capsule endoscopy evaluation held pending consult from hematology. 3 units of PRBC administered to approximate nearly normal H/H.

What to Do When the diagnostic Answer is not clear? l l When the source of bleeding cannot be identified by endoscopic, radiographic, or nuclear intervention, the patient may need exploratory laparotomy In most circumstances this is accompanied by intraoperative endoscopy, which has a sensitivity of more than 70 percent for identifying sources of bleeding and limits the extent ofsurgery in up to 10 percent of cases When rectal bleeding stops before the source is identified, evaluation can proceed in the outpatient setting in patients who remain stable Repeat endoscopic evaluation may be necessary in certain cases

Bonnie l l l Hematology consult obtained Noted increasing protein count with decreasing albumin Hematology notes elevated protime and lower fibrinogen l l l Diagnosis of Waldenstrom’s macroglobulinemia made Plans for plasma exchange and chemotherapy made Continued melanotic stools noted but less in volume than in past few days

Summary l l A Good History and Physical exam always is our best arsenal piece The initial clinical presentation gives us the idea of how urgent the workup must be The broad range of diagnostic tools aside from the H and P are elements easily employed or referred out for further evaluation Aside from procedural components of workup, the Family Medicine team is well equipped to work their patient up to achieve a fairly accurate diagnosis thus serving our patients best interest

Questions?

Thank You!

References l 1. Gastrointestinal bleeding. Medline. Plus. National Institutes of Health. January 2011. Available at http: //www. nlm. nih. gov/medlineplus/ency/article/003133. htm. l 2. Bleeding in the Digestive Tract. National Digestive Diseases Information Clearinghouse. January 2010. Available at http: //digestive. niddk. nih. gov/ddiseases/pubs/bleeding/. 3. Gastrointestinal Bleeding. Mayo Clinic. Accessed August 2011. Available at http: //www. mayoclinic. org/gastrointestinal-bleeding/diagnosis. html. 4. Manning-Dimmitt LL, Dimmitt SG, Wilson GR. Diagnosis of Gastrointestinal Bleeding in Adults. American Family Physician. American Academy of Family Physicians. April 2005. Available at http: //www. aafp. org/afp/2005/0401/p 1339. html. 5. Krumberger JM. How to Manage an Upper GI Bleed. Modern Medicine. March 2005. Available at http: //www. modernmedicine. com/modernmedicine/article. Detail. jsp? id=150046. 6. Barnert J, Messmann H. Diagnosis and management of lower gastrointestinal bleeding. Nature Reviews. Medscape CME. November 2009. Available at http: //www. nature. com/nrgastro/journal/v 6/n 11/full/nrgastro. 2009. 167. html l l