Gastrointestinal Bleeding

Department of Surgery

Hadassah-Hebrew University Medical Center

Asaf Kedar M.D.

Introduction 1-2% of acute hospital admissions. Leading diagnosis in patients admitted to ICU. Mortality overall – 5-12%, with persistent or

recurring hemorrhage – 40%. Up to 85% cease spontaneously. Hemorrhage can arise in any part of the GI track

from nose / mouth to anus, including organs that empty into the GI.

Ligament of TreitzJejunumDuodenu

m

Portal vain

Superior Mesenteric

vessels

Cisterna ChyliCeliac Ganglia

Aorta

Introduction Upper Gastrointestinal

Bleeding (UGIB) – Proximal to the ligament of Treitz.

Lower Gastrointestinal Bleeding (LGIB) – Distal to the ligament of Treitz.

>85% of major bleeding are d/t: PUD Variceal hemorrhage Colonic diverticulosis Angiodysplasia.

Introduction Only age is a risk factor for hemorrhage Surgery is required in 5-10% of patients

hospitalized with GI bleeding. Four primary goals in initial management of a

patient with acute GIB:1. Patient assessment – Hemodynamic status

and identification of significant comorbidities.2. Resuscitation and monitoring.3. Identification of the source of bleeding.4. Specific therapy

Initial Patient Assessment Characteristics of bleeding:

1. Hematemesis2. Melena3. Hematochezia

Associated symptoms: dizziness, syncope, antecedent dyspepsia, crampy

abdominal pain, wt. loss. Medications:

Salicylates, NSAIDs, clopidogrel (plavix), warfarin, clexan, ß blockers, Ca-channel blockers, anti-hypertensives.

Past Medical History: GIB, dysphagia, GERD, H.pylori infection, PUD, liver

disease, alcohol abuse, IBD, diverticulosis, malignancy.

Co-morbid medical conditions: Renal insufficiency, IHD, CHF, chronic

respiratory disease, liver disease, CNS disability.

Physical examination: Determine the degree of blood loss, Rectal examination exclude nasopharyngeal bleeding. Assesment of cirrhosis – Jaundice, ascitis,

palmar erythema, caput medusa.

Initial Patient Assessment

Class I Class II Class III Class IV

Estimated blood loss (% of volume)

< 15% 15% - 30% 30% - 40% > 40%

Typical pulse rate < 100 > 100 > 120 > 140

Typical blood pressure

Normal mean Normal mean Decreased Markedly decreased

Pulse pressure Normal Narrowed Narrowed Unobtainable

Mental status Normal to slightly anxious

Mildly anxious Anxious and confused

Confused or lethargic

Urine output Normal ~ 0.5 ml/kg/hr < 0.5 ml/kg/hr Nil

Volume required Often none Crystalloid Crystalloid and blood Blood

Hypovolemic shock classification

Melanin spots on lips, oral mucosa and digits, small intestinal polyposis Peutz – Jeghers syndrome.

Cutaneous telangiectasias. Osler – Weber – Rendu Syndrome

Initial Patient Assessment

Initial Patient Assessment Initial Laboratory Assessment:

Biochemistry profile CBC Coagulation profile Type and cross-matching

HGb less than 10g/100ml is associated with increased risk for morbidity and mortality.

Resuscitation 2 large-bore IV lines Crystalloids Colloids Packed cells and other blood products Foley catheter Central venous or pulmonary artery catheter. Endotracheal intubation for massive hematemesis

and mental obtundation, hemodynamically unstable patient.

Patient with GIB rarely die from hemorrhage – they die from multisystem organ failure d/t shock Treat fast to prevent and reverse these processes ASAP

Identification of Source of Bleeding

Nasogastric tube (NGT) of large caliber.

Identification of Source of Bleeding

Patients with suspected upper GIB require upper endoscopy with diagnostic and therapeutic capabilities.

Timing of examination – from immediately to within 24h for stable patients.

Identification of Source of Bleeding

Patients with suspected lower GIB require colonoscopy with diagnostic and therapeutic capabilities (after colonic purging).

Hemodynamically stable patient with hematochezia / melena with negative upper gastrointestinal examination may be presumed to have acute lower GIB, choice of initial diagnostic test remain controversial.

Identification of Source of Bleeding

Selective visceral angiography: Selective injection of radiographic contrast into

vessels. ID bleeding at a rate of 0.5ml/min or greater. Identify arterial hemorrhage in 45-75% of patient

with active bleeding. GIB may be intermittent in nature. Some advocate evocative testing (inappropriate

in 90% of cases). Complication rate – 10%: Stroke, Renal failure,

femoral artery thrombosis, lower extremity immobilization, hematoma.

Identification of Source of Bleeding Technetium 99m-red Blood Cell Scintigraphy:

Noninvasive. The patient’s RBC are labeled with a technetium

isotope and reintroduced into circulation. Labeled blood is shed into the GI lumen, creating

an isotope focus. Images are obtained within first 2h, thereafter at 4-

6h intervals or if clinical evidence of rebleed. ID bleeding at a rate of 0.1ml/min or greater. Identify arterial hemorrhage in 85% of patient with

active bleeding. Serve primarily to target the subsequent

therapeutic act.

Identification of Source of Bleeding Other available modalities:

CT ± CT angio CT mannitol Double Balloon Enteroscopy Video Capsule Endoscopy Intraoperative Endoscopy.

Institution of specific therapy For the 15% of patients with ongoing GIB and

hemodynamic instability the time interval to specific intervention should be 2h.

Specific treatment according to the etiology.

Upper Gastrointestinal

BleedingDepartment of Surgery

Hadassah-Hebrew University Medical Center

Bleeding is proximal to the ligament of Treitz. 85% of GIB.

Definition & Incidence

Ligament of TreitzJejunumDuodenu

m

Portal vain

Superior Mesenteric

vessels

Cisterna ChyliCeliac Ganglia

Aorta

Etiology Gastroduodenal Ulcer Disease – 50% Varices (secondary to portal hypertension) – 10-

20% Acute mucosal lesions (Gastritis, Duodenitis) -

found in 15-30% of patients with UGIB. Mallory – Weiss mucosal tears – 8-10% Esophagitis – 3-5% Malignancy – 3% (esophagus, stomach, duodenum) Dieulafoy’s Lesion – 1-3% Other (Aortoduodenal fistula, AVM, CD, Hemobilia,

hemorrhage from pancreas)

Clinical Presentation Hematemesis Melena Massive bleeding may be

associated with Hematochezia

Upper Endoscopy is the mandatory initial diagnostic test.

Increase risk during examination (cardiopulmonary, aspiration).

Bleeding Peptic Ulcer Most common cause of UGIB 5% of patients with PUD have bleeding as initial

manifestation. 20% of patient with PUD will experience bleeding. Caused by acid-peptic erosion into submucosal or

extraluminal vessels.

Bleeding Peptic Ulcer Stomach – small

submucosal artery (D=0.7mm).

Larger arteries Larger bleeding and may be refractory to endoscopy.

M/C bleeding from Lt gastric a. territory.

1.

4.

3.

5.

2.

Duodenum – m/c in posterior ulcers. M/C Major bleeding arises from branches of Gastroduodenal and Sup

Pancreaticoduodenal arteries

Bleeding Peptic Ulcer

2.

1.

3.

4.

5.

H. pylori – responsible for 40-50% of cases. NSAIDs – responsible for 50-60% 30% of patients with NSAIDs will have H. pylori

infection. Physiologic Acid Hypersecretion in cases were

there is no NSAIDs and no H. pylori Zollinger – Ellison syndrome – 1-2% of patients with

ulcer disease.

Bleeding Peptic Ulcer - Etiology

Clinical Prognostic Features: Overall – 5-8% Age: >60 - 10-15%; >80 - 25-30% Systolic BP on presentation: 80-90 - 12-15%;

<80 - 30-35% NGT Aspirate on presentation: Coffee-ground -

6-10%; Red blood - 18-20% Transfusion requirements >10 units – 28-34% Co-morbidities (Renal, Liver, Pulmonary,

Cardiac)

Bleeding Peptic Ulcer

Bleeding Peptic Ulcer Endoscopic Prognostic Features:

Clean ulcer base – rarely rebleed Flat pigmented spot on the ulcer surface

(purple, brown, black) – 10% will rebleed Adherent clot –

20% will rebleed

Visible vessel – 40-80% will rebleed

Active bleeding Ulcer greater

than 2cm are at high risk

Cessation of NSAIDs H. pylori eradication (Amoxicillin 1g bid

[Metronidazole 500mg bid], Clarithromycin 500mg bid, Omeprazole 20mg bid for 14d)

H2-receptor antagonist – Ranitidine (Zantac), Famotidine

Proton Pump Inhibitor (PPI) – Omeprazole (Losec) PPI (IV) as adjuncts to endoscopy. Hospitalization

Bleeding Peptic Ulcer –Medical Management

Diagnostic and Therapeutic procedure. Coagulation (Bipolar electro-coagulation, LASER) Injection of Sclerosing and Vasoconstricting agents:

Alcohol, Epinephrine, Fibrin glue, Polidocanol.

Bleeding Peptic Ulcer –Endoscopic Management

Initial success rate of 95% 20% will rebleed, 97% of those rebleed within 96h

of the initial endoscopic therapy. In 20% of patient 1st endoscopy fails (failure to stop

a bleeding or early rebleed). Risk of endoscopy (Rate 0.5%):

1. Perforation2. Bleeding

In gastric ulcer – repeat endoscopy + biopsy within 6 weeks.

Bleeding Peptic Ulcer –Endoscopic Management

Required in 10% of patients with bleeding ulcer. Indication:

1. Hemorrhage not responsive to endoscopic treatment

2. Significant recurrent hemorrhage3. Ongoing transfusion requirements (>6 PC in

24h)

Bleeding Peptic Ulcer –Surgical Management

Bleeding Duodenal Ulcer: Exposure of the ulcer by Duodenotomy or

duodenopyloromyotomy. Direct suture ligation Four-quadrant suture ligation around the

perimeter of the bleeding ulcer. Ligation of gastroduodenal a. In stable patients – Truncal vagotomy or Parietal

cell vagotomy.

Bleeding Peptic Ulcer –Surgical Management

Bleeding Gastric Ulcer: Ulcer excision Ulcers of incisura, antrum and distal body –

distal gastrectomy.

Bleeding Peptic Ulcer –Surgical Management

Bleeding Gastric Ulcer: Ulcers higher than the lesser curvature are

treated with Subtotal gastrectomy or local ulcer excision and distal gastrectomy.

Bleeding Peptic Ulcer –Surgical Management

Responsible for 33% of all deaths in patients with cirrhosis & Portal hypertension.

90% of cirrhotic patients will develop esophageal varices.

25-30% of patients with varices will bleed. Mortality rate – 25%

per bleeding episode. Rebleed rate – 70%

Bleeding Varices

Clinical presentation: Massive hematemesis Melena, occasionally – hematochezia Hemodynamic instability

Initial management: Resuscitation – correction of volume deficit,

coagulopathy and AW. Treatment in ICU.

Bleeding Varices

Emergency endoscopy – Diagnostic and Therapeutic

Sclerotherapy and rubber band ligation. Complications: Esophageal ulceration, bleeding

perforation, mediastenitis, pleural effusion, and pulmonary edema.

Somatostatin – decreases splanchnic blood flow decreasing portal and variceal pressure (w/o eliciting coronary vasoconstriction)

Vasopressin ± nitroglycerin - decreases splanchnic blood flow.

Sclerothrapy + somatostatin are effective in 80-90% of cases

Bleeding Varices - Treatment

If treatment not effective – insertion of Sengstaken-Blakemore tube

Bleeding Varices - Treatment

Transjugular Intrahepatic Shunt (TIPS) Creating an intrahepatic portosystemic fistula for

decompression of portal hypertension

Bleeding Varices - Treatment

(1) cannulating a hepatic vein (usually the right hepatic vein) via the internal jugular vein, (2) passing a needle from the hepatic vein through the liver parenchyma and into a portal vein branch, (3) passing a guide wire through the needle, (4) dilating the needle tract with a balloon passed over the guide wire, and (5) stenting the tract to a desired diameter, thus effectively constructing a nonselective side-to-side portosystemic shunt.

Emergency decompressive surgery.

Bleeding Varices - Treatment

Acute Gastric Mucosal Lesions (AGML)

Characterized by: Mucosal pallor, petechiae, and

erosions Mucosal injury. Predominantly found in the

body of the stomach. Bleeding is the clinical

presenting sign in the critically ill patients.

Broad category of acute erosive mucosal conditions, develop in the cortically ill patients.

AKA: Stress Gastritis, Acute mucosal ischemia, Erosive gastritis, Stress ulcer.

Risk factors: All critically ill patients Sepsis Respiratory failure Hemodynamic instability Coma following head injury Intracranial operation Burn (>35% BSA) Multiple trauma Particularly lethal in post-OP cardiovascular

patients & patients in sepsis with multiorgan failure

Acute Gastric Mucosal Lesions (AGML)

Pathogenesis: Gastric acid and activated pepsin injuring the mucosa. Exacerbated by mucosal ischemia (d/t hypotension).

Prophylaxis Treatment:

treat underlining condition. Resuscitation, transfusion, correction of

coagulopathy. Emergency upper endoscopy Angiography

Recurrent bleeding is common.

Acute Gastric Mucosal Lesions (AGML)

Mallory – Weiss Tears Represent 10% of UGIB Tear in the proximal gastric mucosa near the E-G

junction. Clinical presentation - Vomiting, retching or

coughing followed by hematemesis.

Mallory – Weiss Tears Mean age >60 Men (80%) >>> Women Risk factors: Alcoholism, hiatal hernia, NSAIDs

and disease related bleeding diatheses. 90% will stop spontaneously. Initial assessment and treatment:

History and physical examination Resuscitation Endoscopic evaluation and treatment Acid reduction with anti secretory agents

Rebleeding is 30% within 24h for patients with coagulation disorders.

Esophageal Sources Source for < 3% of UGIB. Etiology:

Infectious esophagitis GERD Barrett’s epithelium Malignancy Medication induced

erosions Crohn’s disease Radiation

Dieulafoy’s Lesion A vascular malformation. Large submucosal or

mucosal vessels MC lesser curvature in the

mid-stomach Superficial erosions

Bleeding cease spontaneously

Treatment by wedge resection of gastric wall after marking with India ink injection

Aortoenteric Fistula Uncommon condition Inflammatory tract develops b/w the aorta and GIT Infectious aortitis Inflammatory aortic aneurysm Secondary process following aortic replacement

with synthetic graft (MC). Develop in 1% of patient after AAA repair.

A herald (כרוז) bleed occurs hours to days prior to exsanguinating hemorrhage.

Dx by Endoscopy, CT, Angiography

Thank you!