5.1 Upper & Lower Gastrointestinal Bleeding: Evaluation & Management

Anatomical Delineation & Clinical Presentations

Gastrointestinal (GI) hemorrhage is among the most frequent medical emergencies encountered in casualty departments and inpatient medical wards across the Caribbean. Clinical management begins with rapid anatomical localization:

• Upper Gastrointestinal Bleeding (UGIB): Defined as bleeding originating proximal to the ligament of Treitz (the suspensory muscle of the duodenum at the duodenojejunal junction). Etiologies include peptic ulcer disease (gastric and duodenal ulcers), gastroesophageal varices, Mallory-Weiss mucosal tears, Dieulafoy lesions, gastric antral vascular ectasia (GAVE), and upper GI malignancies.
• Lower Gastrointestinal Bleeding (LGIB): Defined as bleeding arising distal to the ligament of Treitz, encompassing the jejunum, ileum, colon, rectum, and anal canal. Major causes include colonic diverticular bleeding, angiodysplasia (arteriovenous malformations), ischemic colitis, hemorrhoids, colorectal polyps or carcinomas, and inflammatory bowel disease (IBD).

Classical Clinical Manifestations

1. Hematemesis: Vomiting of gross blood (bright red or dark brown with clots), or "coffee-ground" emesis caused by the conversion of hemoglobin to brown hematin by gastric hydrochloric acid. Hematemesis pathognomonically confirms an upper GI source.
2. Melena: The passage of black, tarry, foul-smelling stools resulting from the degradation of blood by enteric bacteria and digestive enzymes. A minimum of 50 to 100 mL of blood entering the upper GI tract and remaining for at least 14 hours is required to generate melena. Although melena almost always signifies UGIB, slow-transit bleeding from the right colon or terminal ileum can occasionally produce melena.
3. Hematochezia: The passage of fresh, bright red or maroon blood per rectum, with or without clots. Hematochezia typically indicates an LGIB source. However, 10% to 15% of patients presenting with massive hematochezia have a brisk, life-threatening UGIB (e.g., eroding gastroduodenal artery aneurysm or torrential variceal hemorrhage) with rapid intestinal transit. An upper GI source must be suspected whenever hematochezia is accompanied by orthostatic hypotension, tachycardia, or shock.
4. Blood Urea Nitrogen to Creatinine Ratio: In acute UGIB, the digestion and intestinal absorption of large volumes of blood proteins, coupled with pre-renal hypoperfusion, elevates serum urea out of proportion to creatinine, yielding a BUN/Creatinine ratio > 30:1 when both are expressed in mg/dL, which strongly supports an upper GI etiology.

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Initial Resuscitation & Hemodynamic Stabilization

Resuscitation takes absolute precedence over diagnostic investigations or endoscopy. The primary goal is restoring effective circulating volume and preventing ischemic end-organ injury.

Airway & Vascular Access

• Airway Protection: Elective endotracheal intubation should be performed prior to endoscopy in patients with active massive hematemesis, depressed consciousness (Glasgow Coma Scale <= 8), severe agitation, or advanced hepatic encephalopathy to prevent catastrophic pulmonary aspiration.
• Large-Bore Intravenous Access: Insert two 14-gauge or 16-gauge peripheral IV cannulae in the antecubital fossae. Flow rate through a short 14G peripheral catheter is substantially higher than through a standard 20 cm triple-lumen central venous line (Poiseuille's law: flow is inversely proportional to catheter length and directly proportional to the fourth power of catheter radius).
• Fluid Resuscitation: Infuse isotonic crystalloids (e.g., Ringer's lactate or 0.9% normal saline) titrated to blood pressure and urine output (> 0.5 mL/kg/h). In patients with suspected variceal hemorrhage, avoid aggressive over-transfusion and volume overloading, as excessive central venous and portal pressures precipitate rebleeding and worsen mortality.

Restrictive Transfusion Strategy

• Landmark randomized trials (Villanueva et al.) established that a restrictive red blood cell (RBC) transfusion strategy achieves significantly lower 6-week mortality, lower rebleeding rates, and fewer adverse events compared to a liberal strategy.
• General Target: Transfuse packed red blood cells (PRBCs) when hemoglobin falls below 70 g/L (7.0 g/dL), maintaining a target hemoglobin of 70 to 80 g/L (7.0-8.0 g/dL).
• Cardiovascular Disease / Ongoing Shock: Individualize transfusion with cardiology/gastroenterology input; cardiovascular disease commonly warrants a higher threshold (around 80 g/L), with a higher target according to ischemia and clinical status. Resuscitate ongoing major hemorrhage by perfusion and bleeding severity rather than waiting for a fixed hemoglobin value.
• Correction of Coagulopathy: Transfuse platelets if the platelet count is < 50 x 10^9/L in active hemorrhage. Administer Prothrombin Complex Concentrate (PCC) or fresh frozen plasma (FFP) alongside intravenous vitamin K (10 mg) in patients receiving warfarin with life-threatening bleeding. The routine administration of tranexamic acid (TXA) is not recommended in acute GI bleeding, as the HALT-IT trial demonstrated no reduction in mortality and a significant increase in venous thromboembolic events.

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Clinical Risk Stratification Scores

Objective risk scores guide decisions regarding hospital admission, timing of endoscopy, and level of monitoring.

Glasgow-Blatchford Score (GBS)

• Calculated prior to endoscopy utilizing readily available clinical and laboratory variables: blood urea, hemoglobin, systolic blood pressure, pulse rate, presentation with melena, syncope, hepatic disease, and cardiac failure.
• Scores range from 0 to 23 points.
• Score 0 to 1: Identifies very low-risk patients with a < 1% risk of requiring intervention (blood transfusion, endoscopic therapy, or surgery). These patients can be safely discharged from the casualty department for elective outpatient investigation.
• Score >= 2: Mandates hospital admission and inpatient endoscopy.
• Higher Scores: Indicate increasing risk of hospital-based intervention, including blood transfusion; the score does not specifically predict a need for endoscopic or surgical therapy.

Rockall Score

• Incorporates clinical variables (age, hemodynamic shock, comorbidities) and post-endoscopy findings (endoscopic diagnosis, stigmata of recent hemorrhage).
• Pre-endoscopy score (0-7) and complete post-endoscopy score (0-11). A complete score <= 2 indicates low risk of rebleeding and mortality (< 5%), whereas a score >= 8 confers high mortality (> 40%).

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Non-Variceal Upper GI Bleeding: Endoscopy & Pharmacotherapy

Peptic ulcer disease accounts for over 50% of non-variceal UGIB cases. Mucosal ulceration erodes into underlying submucosal arterioles or arteries (e.g., gastroduodenal artery on the posterior duodenal wall, or left gastric artery on the lesser gastric curvature).

Pharmacological Acid Suppression

• Proton Pump Inhibitors (PPIs): Gastric acid impairs clot stabilization by inhibiting platelet aggregation and accelerating fibrinolysis via pepsin activation at pH < 6.0. Suppressing intragastric pH > 6.0 promotes clot formation and stability.
• Dosing: Administer intravenous Omeprazole (or Pantoprazole) 80 mg bolus, followed by an 8 mg/hour continuous IV infusion for 72 hours, or high-dose intermittent therapy (40 mg IV twice daily). Following 72 hours, transition to high-dose oral PPI therapy.
• Test for Helicobacter pylori at index endoscopy and eradicate confirmed infection. Repeat initially negative tests after recovery, withholding PPI for at least 2 weeks before repeat testing.

Timing & Modalities of Endoscopy

• Perform diagnostic and therapeutic upper GI endoscopy within 24 hours of presentation following adequate hemodynamic resuscitation. Urgent endoscopy within 12 hours is reserved for patients with severe persistent shock or suspected variceal hemorrhage.
• Forrest Classification of Ulcer Hemorrhage:
  • Forrest Ia: Active spurting arterial bleeding (rebleeding risk 90%). Requires immediate endoscopic hemostasis, usually combination therapy.
  • Forrest Ib: Active oozing bleeding (rebleeding risk 10-30%). Requires endoscopic hemostasis, usually combination therapy.
  • Forrest IIa: Non-bleeding visible vessel (rebleeding risk 40-50%). Treat with thermal or mechanical therapy, alone or with epinephrine.
  • Forrest IIb: Adherent clot (rebleeding risk 20-30%). Consider clot irrigation/removal by an endoscopist able to manage provoked bleeding; treat exposed high-risk stigmata.
  • Forrest IIc: Flat pigmented spot (rebleeding risk 5-10%). Does not require endoscopic therapy; oral PPI is sufficient.
  • Forrest III: Clean ulcer base without stigmata (rebleeding risk < 5%). No endoscopic therapy indicated; early hospital discharge.
• Endoscopic Hemostasis: Active bleeding (Ia/Ib) is usually treated with dilute epinephrine (1:10,000 or 1:20,000) plus clips or contact thermal therapy; selected over-the-scope clip or hemostatic-forceps monotherapy is an alternative. A non-bleeding visible vessel (IIa) may receive thermal therapy or clips alone or with epinephrine. Epinephrine alone is unacceptable because of high rebleeding rates.

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Variceal Upper GI Bleeding: Emergency Protocol

Esophageal and gastric variceal bleeding represents a catastrophic complication of portal hypertension in cirrhotic patients, carrying an immediate 6-week mortality of 15% to 20%.

Immediate Medical Management (Before Endoscopy)

1. Vasoactive Drug Infusion: Initiate immediately upon clinical suspicion, prior to endoscopy:
   • Terlipressin: Synthetic vasopressin analog; IV bolus 2 mg every 4 hours, titrated down to 1 mg every 4 hours once bleeding is controlled (causes splanchnic arterial vasoconstriction, lowering portal inflow and pressure).
   • Octreotide: Somatostatin analog; IV bolus 50 mcg followed by continuous IV infusion of 50 mcg/hour for 2 to 5 days.
2. Prophylactic Intravenous Antibiotics: Administer IV Ceftriaxone 1 g once daily for 7 days (or oral ciprofloxacin). Cirrhosis with GI bleeding carries a high risk of bacterial infection, partly related to gut bacterial translocation. Prophylactic antibiotics significantly reduce infectious complications, rebleeding, and in-hospital mortality.

Endoscopic Intervention

• Perform emergency endoscopy within 12 hours of admission.
• Endoscopic Band Ligation (EBL): The definitive intervention for esophageal varices. Bands are deployed starting at the gastroesophageal junction and spiraling proximally. Sclerotherapy carries higher complication rates (perforation, strictures) and is reserved only when EBL is technically impossible.
• Gastric Variceal Bleeding: Fundal varices (GOV2, IGV1) respond poorly to banding. Treatment involves endoscopic injection of cyanoacrylate tissue adhesive (glue) or early Transjugular Intrahepatic Portosystemic Shunt (TIPS).

Rescue Therapy for Refractory Variceal Hemorrhage

• Balloon Tamponade: Insertion of a Sengstaken-Blakemore tube or Minnesota tube provides temporary mechanical compression of bleeding varices. After confirming intragastric position, inflate to the device-specific recommended volume and apply gentle traction to tamponade the GE junction. Tamponade is strictly a temporary bridge (maximum 24 hours) due to risks of esophageal ulceration, pressure necrosis, and airway obstruction.
• Transjugular Intrahepatic Portosystemic Shunt (TIPS): Creates a low-resistance shunt between the portal vein and hepatic vein using an expandable stent. Indicated as rescue therapy for uncontrolled variceal bleeding, or as "early/preemptive TIPS" within 72 hours for high-risk cirrhotics (Child-Pugh C 10–13 points, Child-Pugh B 8–9 with active bleeding at initial endoscopy, or HVPG >20 mmHg).

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Lower Gastrointestinal Bleeding (LGIB)

LGIB accounts for approximately 20% to 30% of all major GI bleeding episodes. In over 80% of cases, LGIB resolves spontaneously with supportive resuscitation.

Differential Diagnosis

• Diverticular Bleeding (30-40%): Sudden onset of painless, large-volume hematochezia caused by arterial rupture at the neck of a colonic diverticulum. Right-sided diverticula bleed more frequently despite left-sided preponderance.
• Angiodysplasia (10-15%): Dilated, tortuous submucosal venules, most commonly located in the cecum and ascending colon of elderly patients. Associated with severe aortic stenosis (Heyde syndrome, where sheer stress cleaves high-molecular-weight von Willebrand factor multimers, causing acquired coagulopathy).
• Ischemic Colitis (10-15%): Transient bowel hypoperfusion (hypotension, heart failure, vascular surgery) affecting vulnerable watershed territories: Griffiths' point (splenic flexure) and Sudeck's point (rectosigmoid junction). Characterized by abrupt crampy lower abdominal pain followed within 24 hours by bloody diarrhea.
• Colorectal Neoplasms (10%): Intermittent, low-volume hematochezia or occult blood loss with microcytic iron-deficiency anemia and altered bowel habits.
• Anorectal Lesions: Internal hemorrhoids, anal fissures, and radiation proctitis.

Diagnostic & Interventional Algorithm for LGIB

1. Hemodynamically Unstable LGIB:
   • Assess for brisk UGIB and perform urgent upper endoscopy when an upper source is suspected; a negative nasogastric aspirate cannot exclude it.
   • Perform CT Angiography (CTA): Rapid, non-invasive, detects active extravasation at rates >= 0.3 to 0.5 mL/min.
   • Catheter-Directed Mesenteric Angiography: Allows selective catheterization and transcatheter arterial embolization (TAE) using microcoils or polyvinyl alcohol particles without requiring bowel preparation.
2. Hemodynamically Stable LGIB:
   • Perform oral bowel preparation (polyethylene glycol) followed by nonemergent inpatient colonoscopy in most hospitalized patients to identify mucosal bleeding sites and provide endoscopic hemostasis (clips, thermal probes, or band ligation).
   • Technetium-99m Labeled Red Blood Cell Scintigraphy: Highly sensitive, detecting hemorrhage rates as low as 0.1 mL/min; useful for intermittent, obscure bleeding, though anatomical localization is less precise than CTA.

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Summary Matrix: Forrest Classification & Endoscopic Stigmata