Funnel plot – way of spotting if small negative trials have gone missing in actionLeft – spurious false negative; right – spurious false positive
AngiodysAnorectalDiverticIBDIschemiaOther causesOther colitisPostpolyRadioUpper GI
1. GI Bleeds:What does theevidence show? Brian A. Wells, MD, MPH, MSM March 1st, 2013
2. Warm-up Question Asymptomatic 24 year old. Is there an abnormality? Is it pathologic? What is it likely to be? How common is it?
3. Warm-up question What classic sign is seen in this CT? Of what disease is it a sign? Is the disease active? I love the alphabet. You forgot to thank Berg and Lesniowski.
4. GI bleeds:What does the evidence show? There seems to be no study too fragmented, no hypothesis too trivial, no literature too biased or too egotistical, no design too warped, no methodology too bungled, no presentation of results too inaccurate, too obscure, and too contradictory, no analysis too self- serving, no argument too circular, no conclusions too trifling or too unjustified, and no grammar and syntax too offensive for a paper to end up in print. - Drummond Rennie, MD, Deputy Editor of JAMA
5. ―Medicine as a computational science… as a probability science.‖
6. Why talk about GI bleeds? • Frequent cause of hospitalization • Upper GI Bleeding accounts for approximately 350,000 hospitalizations per year. • In a study, patients with UGI bleeds experienced significantly higher 12- month health-resource utilization and costs than patients without UGI bleeds. • UGI-related healthcare utilization and total healthcare, medical, and pharmacy costs incurred by the UGI-bleed cohort were significantly greater (p< 0.0001) than those incurred by the general population cohort (mean of $20,405 vs. 3,652), even after excluding the initial hospitalization costs (mean of $11,228 vs. 3,652).The economics of upper gastrointestinal bleeding in a US managed-care setting: a retrospective, claims-based analysis.J Med Econ. 2010 Mar;13(1):70-7. doi: 10.3111/13696990903526676. http://www.ncbi.nlm.nih.gov/pubmed/20047365
7. GI Bleed – Trends and Economics • From 1998 to 2006 – For patients with either a principal or secondary GI bleed diagnosis, the number of hospitalizations for upper GI bleeding per 100,000 people decreased by 14%. However, hospitalizations for lower GI bleeding increased 8%, yielding a 4% overall decrease in the hospitalization rate per 100,000 people for GI bleeding. – Possible reasons for the decrease in upper GI bleeding may include the increased use of proton pump inhibitors to decrease gastric acid secretion, antibiotic treatment of gastric ulcers caused by Helicobacter pylori bacteria, and increased use of selective COX-2 inhibitors for arthritis or other pain.Agency for Healthcare Research and Quality. Hospitalizations for Gastrointestinal Bleeding in 1998 and 2006.HCUP Statistical Brief #65. Published online December 2008.
8. GI Bleed – Trends and Economics • From 1998 to 2006 – The largest decreases in the rate of hospital stays for GI bleeding were for upper GI ulcers (25% decrease) and gastritis/duodenitis (31% decrease). – The largest increases in the rate of hospital stays for GI bleeding were for angiodysplasia, which is a relatively infrequent cause of GI bleeding (38% increase), and hemorrhage of the rectum and anus (41% increase). – For patients with a principal diagnosis of GI bleeding, the number of inpatient deaths decreased from 20,013 in 1998 to 16,344 in 2006, with a 23% decrease in inpatient death rate from 3.9% to 3.0%. – For patients aged 30 to 44 years, the inpatient death rate for gastrointestinal bleeding decreased by 31%, from 1.6% in 1998 to 1.1% in 2006.Agency for Healthcare Research and Quality. Hospitalizations for Gastrointestinal Bleeding in 1998 and 2006.HCUP Statistical Brief #65. Published online December 2008.
9. GI Bleeds• Unfortunately, far too extensive to cover everything in the time we have• Will attempt to give an overview of upper and lower• Will talk about – Classification – Etiology – Management
10. Types of GI Bleeds (i.e. our agreed-upondefinitions)• Upper v. Lower• Divided by the ligament of Treitz – The suspensory muscle of duodenum, also known as the ligament of Treitz (named for Vaclav Treitz), connects the duodenum to the diaphragm. – It arises from the right crus as it passes around the esophagus, continues as connective tissue around the stems of the celiac trunk and SMA and inserts into the third and fourth portions of the duodenum and frequently into the duodenojejunal flexure as well.• Upper – 70% of GI bleeds (some variation in this data, will also find values like 60/40 in the literature)• Lower – 30% of GI bleeds
11. Fun Slide!• An abnormally low and fixed position of the ligament of Treitz is a known cause of ______?
12. Upper GI Bleed• Upper gastrointestinal bleeding is a common medical condition that results in high patient morbidity and medical care costs.• In a study, the annual incidence of hospitalization for acute upper gastrointestinal bleeding was approximately 100 per 100,000 adults; the incidence was twice as common in males as in females and increased with age Longstreth, GF. Epidemiology of hospitalization for acute upper gastrointestinal hemorrhage: a population-based study. Am J Gastroenterol. 1995;90(2):206.
13. Upper GI Bleed• The most common causes of upper gastrointestinal bleeding include the following: – Gastric and/or duodenal ulcers (20% - 30%) – Esophagogastric varices with or without portal hypertensive gastropathy (10%) – Esophagitis (5%) – Erosive gastritis/duodenitis (5 – 10%) – Mallory-Weiss syndrome (3%) – Angiodysplasia – Mass lesions (polyps/cancers) (1%) – Dieulafoys lesion
14. Upper GI Bleed• Less common causes of upper gastrointestinal bleeding include: – Hemobilia – Hemosuccus pancreaticus – Aortoenteric fistula – Cameron lesions• Because of the overall incidence of upper gastrointestinal bleeding is high, the less common causes of upper gastrointestinal bleeding are still frequently encountered, and as such their recognition and appropriate management are important.
15. Duodenal Ulcer
18. Esophageal Malignancy
19. Upper GI Bleed• 50% present with hematemesis• NGT with positive blood on aspirate• 11% of brisk bleeds have hematochezia• Melena (black tarry stools)—this develops with approximately 150-200cc of blood in the upper GI tract. – Stool turns black after 8 hours of sitting within the GI tract.
20. Lower GI Bleed• The causes of lower gastrointestinal bleeding (LGIB) may be grouped into several categories: – Anatomic (diverticulosis) – Vascular (angiodysplasia, ischemic, radiation-induced) – Inflammatory (IBD, infectious) – Neoplastic (polyp, carcinoma) – Other (hemorrhoid, ulcer, post-biopsy or polypectomy)Strate, LL. Lower GI bleeding: epidemiology and diagnosis. Gastroenterol Clin North Am. 2005;34(4):643.
21. Lower GI Bleed• In a meta-anaysis including several large studies, the following bleeding sources were identified: Cause % Cause %Angiodysplasia 0% – 3% Other causes 1% – 9%Anorectal 6 – 16% Other colitis (infectious, 3% – 29%(hemorrhoids, anal antibiotic associated,fissure, rectal ulcer) colitis of unclear etiology)Diverticulosis 5 – 42% Postpolypectomy 0% – 13%IBD 2% – 4% Radiation colitis 1% – 3%Ischemia 6 – 18% Small bowel/upper GI 3% – 13% Unknown – 6 – 23% Strate LL. Lower GI bleeding: epidemiology and diagnosis. Gastroenterol Clin North Am 2005; 34:643.
23. Colonic Polyps
26. Lower GI Bleed• Blood originating from the left colon typically is bright red.• By comparison, bleeding from the right side of the colon usually appears dark or maroon-colored and may be mixed with stool.• However, rapid transit of blood from the right side of the colon or massive upper GI bleeding can appear red, and bleeding from the cecum may rarely present with melena.• Thus, although helpful, the distinctions based upon stool color are not absolute.• Patients with high-risk features including hemodynamic instability (shock, orthostatic hypotension), persistent bleeding, and/or significant comorbid illnesses should be admitted to an intensive care unit for resuscitation, close observation, and possible therapeutic interventions.
27. Lower GI Bleed• In patients with severe hematochezia, it is important to exclude upper GI bleeding, particularly if the bleeding is associated with orthostatic hypotension.• Patients suspected of having an upper GI bleed should undergo an upper endoscopy once appropriately resuscitated.• Nasogastric lavage may be carried out if there is doubt as to whether a bleed originates from the upper GI tract. A nasogastric lavage that yields blood- or coffee ground-like material confirms upper GI bleeding.• However, false negative aspirates can occur if bleeding has ceased or arises beyond a closed pylorus.
28. Lower GI Bleed• Acute LGIB: <3d• Chronic LGIB: > several days• Hematochezia• Blood in Toilet• Clear NGT aspirate• Normal Renal Function• Usually Hemodynamically stable – <200ml : no effect on HR** – >800ml: SBP drops by 10mmHg, Hr increases by 10 – >1500ml: possible shock OR – 10% Hct: tachycardia – 20% Hct: orthostatic hypotension – 30% Hct: shockStops spontaneously (80 - 85% of the time) **Barnet J and H Messmann H. Nat Rev Gastroenterol Hepatol 6, 637-646 (2009).
29. Obscure GI Bleed• Obscure gastrointestinal bleeding accounts for approximately 5% of patients with gastrointestinal bleeding.• In approximately 75% of these patients, the source is in the small bowel. The remainder of cases are due to missed lesions in either the upper or lower gastrointestinal tract.• Most common presentation is iron deficiency anemia• Etiology: – Younger than 40 • Tumors • Meckel’s diverticulum • Dieulafoy’s lesion • Crohn’s Disease • Celiac Disease – Greater than 40 • Angioectasia • NSAID enteropathy • Celiac Gerson LB. Clin Gastroenterol & Hepatol 2009;7:828-833.
30. Localization of Bleeding• History• NG Tube• EGD• Colonoscopy• Radionuclide imaging – Bleeding at a rate of 0.1 to 0.5 mL/minute – Most sensitive radiographic test for GI bleeding – Can only localize bleeding to a general area of the abdomen (accuracy 24 – 91%)• Angiography – Bleeding at a rate of 0.3 to 0.5 mL/minute can be detected with CT angiography (Sn/Sp/Acc 82%/95%/100%) – Requires active blood loss of 1 to 1.5 mL/minute for normal angiography – No bowel preparation; accurate anatomic localization – Superselective embolization is feasible in 80 percent, and bleeding is successfully controlled in 97 percent; however, risk of intestinal infarct.
31. Management of Upper GI Bleed• Assess the severity of the bleed• Identify potential sources of the bleed• Determine if there are conditions present that may affect subsequent management.• Patients should be asked about prior episodes of upper GI bleeding, since up to 60 percent of patients with a history of an upper GI bleed are bleeding from the same lesion• Medication and symptom review (NSAIDS, anticoagulants, pain location, tachycardia, etc.)
32. Management of Upper GI Bleed• Medications – Acid suppression with intravenous PPI at presentation until confirmation of the cause of bleeding – Prokinetics like erythromycin to improve gastric visualization prior to endoscopy – Somatostatin or octreotide for variceal bleeding – Antibiotics for patient with cirrhosis (20% have infections; 50% develop an infection while hospitalized)
33. Management of Upper GI Bleed• Risk scoring – Rockall score is based upon age, the presence of shock, comorbidity, diagnosis, and endoscopic stigmata of recent hemorrhage – Modified Glasgow Blatchford score (used on first presentation), is calculated using only the blood urea nitrogen, hemoglobin, systolic blood pressure, and pulse (assess likelihood of the need for urgent endoscopic intervention). – AIMS65 - high accuracy for predicting inpatient mortality • Albumin < 3, INR >1.5, AMS, SBP < 90, Age > 65
34. Management of Upper GI Bleed• Provision of supplemental oxygen by nasal cannula• Nothing per mouth• Two large caliber (16 gauge or larger) peripheral catheters or a central venous line• Placement of a pulmonary artery catheter should be considered in patients with hemodynamic instability or who need close monitoring during resuscitation
35. Evidence for Transfusion• Withholding transfusions until hemoglobin levels are lower than 7%, rather than 9%, improves overall survival by 45% in patients with acute upper gastrointestinal (GI) bleeding, according to a study published in the January 3 issue of the New England Journal of Medicine.Transfusion Strategies for Acute Upper Gastrointestinal Bleeding. N Engl J Med. 2013;368:11-21, 75-76.
36. Management of Lower GI Bleed• Patients with high-risk features, particularly those with hemodynamic instability, ongoing active bleeding, and significant comorbid illnesses should be managed in the intensive care unit with aggressive resuscitation and early interventions.• A gastroenterologist, a general surgeon, and possibly an interventional radiologist should be involved early in the hospital course of high-risk individuals.• Two large caliber (18 gauge or larger) peripheral catheters or a central venous line should be inserted for intravenous access.• Patients with heart failure or valvular disease may benefit from pulmonary catheter monitoring to minimize the risk of fluid overload.
37. Management of GI Bleed• Oxygen• IV Access-central line or two large bore peripheral IV sites• Isotonic saline for volume resuscitation• Start transfusing blood products if the patient remains unstable despite fluid boluses.• Airway Protection• Altered Mental Status and increased risk of aspiration with massive upper GI bleed.
38. Management of GI Bleed• ICU admit indications – Significant bleeding (>2u pRBC) with hemodynamic instability• Transfusion – Brisk Bleed, transfusing should be based on hemodynamic status, not lab value of Hgb. – Cardiopulmonary symptoms-cardiac ischemia or shortness of breath, decreased pulse ox• 1 unit PRBC increases Hgb by 1mg/dL and increase Hct by 3%• FFP for INR greater than 1.5• Platelets for platelet count less than 50K
39. Obscure GI Bleed• Work Up – EGD, Colonoscopy both negative – Repeat – Proximal jejunum? Distal ileum? – Angiography AGA Institute. AGA Institute Medical Position Statement on Obscure Gastrointestinal Bleeding. Gastroenterology 2007;133:1694-1696