Upper gastrointestinal bleeding (UGIB) is a major medical emergency defined as luminal hemorrhage originating from the upper gastrointestinal tract, specifically proximal to the ligament of Treitz 1, 3. It accounts for a significant proportion of acute hospital admissions globally, associated with a substantial morbidity and mortality rate ranging between 2% and 10% 6. Prompt triage, aggressive haemodynamic resuscitation, risk stratification using validated clinical scoring systems, and urgent endoscopic intervention within 24 hours (or within 12 hours in suspected variceal hemorrhage) are critical to improving patient survival and minimizing rebleeding rates 4, 6.
1. Etiology & Risk Factors
- Peptic Ulcer Disease (PUD): Accounts for approximately 50% of all UGIB cases. Gastric and duodenal ulcers are frequently exacerbated by Helicobacter pylori infection and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) 3.
- Esophageal and Gastric Varices: Secondary to portal hypertension, predominantly driven by advanced liver cirrhosis. Variceal bleeding carries a high risk of massive hemorrhage and significant mortality 6.
- Mallory-Weiss Syndrome: Longitudinal mucosal lacerations at the gastroesophageal junction typically precipitated by severe retching, vomiting, or coughing.
- Erosive Gastroduodenitis & Esophagitis: Caused by mucosal irritation from NSAIDs, systemic stress, alcohol abuse, or severe gastroesophageal reflux disease (GERD).
- Vascular Malformations & Neoplasms: Dieulafoy lesions (abnormally large submucosal arteries), gastric antral vascular ectasia (GAVE), angiodysplasias, and ulcerated upper GI malignancies (adenocarcinoma, gastrointestinal stromal tumors) 3.
- Systemic Risk Factors: Advanced age, prior history of UGIB, concurrent use of antiplatelet agents (aspirin, P2Y12 inhibitors), anticoagulants (warfarin, DOACs), chronic kidney disease, and severe systemic comorbidities 3.
2. Pathophysiology
The pathophysiological process begins with structural disruption of the protective mucosal barrier or increased vascular fragility within the upper gastrointestinal tract 1. In peptic ulcer disease, gastric acid and pepsin breach the mucosal defenses, exposing underlying submucosal blood vessels—such as the gastroduodenal artery in posterior duodenal ulcers—to enzymatic and mechanical erosion. Once the vessel wall is compromised, arterial or venous pressure drives luminal blood loss 6. In portal hypertension, increased hepatic sinusoidal resistance leads to portosystemic collateral formation, engorging submucosal veins in the distal esophagus and gastric fundus until wall tension exceeds structural limits, resulting in catastrophic variceal rupture 6. Acute blood loss triggers compensatory sympathetic nervous system activation, increasing systemic vascular resistance and tachycardia to maintain vital organ perfusion. Concurrently, digestion of extravasated blood protein within the small intestine releases urea into the bloodstream, elevating the serum urea-to-creatinine ratio 3.
3. Clinical Presentation & Classic Clinical Signs
- History & Cardinal Symptoms:
- Haematemesis: Vomiting of bright red blood or dark "coffee-ground" material, indicating gastric retention and partial oxidation of hemoglobin by stomach acid 4.
- Melaena: Black, tarry, foul-smelling stools resulting from the bacterial degradation of hemoglobin as it traverses the gastrointestinal tract (typically requiring at least 50–100 mL of blood loss and several hours in the lumen) 7.
- Haematochezia: Passing of bright red or maroon stools, typically seen in massive, brisk upper GI bleeding with rapid intestinal transit 4, 7.
- Systemic Symptoms: Lightheadedness, dizziness, presyncope, syncope, exertional dyspnea, and angina reflecting acute intravascular volume depletion and anaemia 3.
- Physical Examination & Named Clinical Signs:
- Haemodynamic Instability: Tachycardia, orthostatic hypotension, resting hypotension, tachypnea, cold clammy extremities, and oliguria indicating class III or IV hemorrhagic shock.
- Stigmata of Chronic Liver Disease: Jaundice, palmar erythema, spider angiomata, ascites, splenomegaly, caput medusae, and asterixis, pointing toward a variceal etiology 5, 6.
- Abdominal Examination: Epigastric tenderness in peptic ulcer disease; peritoneal signs (guarding, rigidity) suggest perforation. Digital rectal exam confirms melaena or haematochezia 3.
4. Diagnostic Workup & Interpretation (Laboratory, Imaging & ECG/Pathology)
| Diagnostic Modality / Test | Expected Clinical & Radiological / Laboratory Finding |
|---|---|
| Gold-Standard Investigation | Oesophagogastroduodenoscopy (OGD / EGD): Performed within 24 hours of presentation (within 12 hours for suspected varices) after hemodynamic stabilization; allows direct visualization, risk stratification (Forrest classification), and therapeutic intervention 4, 6. |
| Laboratory Panel | Complete Blood Count (CBC): Initial haemoglobin may be deceptively normal due to acute volume contraction; significant drop manifests over 24-48 hours with hemodilution. Coagulation Profile & Renal Function: Elevated INR/PTT indicating coagulopathy; elevated Blood Urea Nitrogen (BUN) and disproportionately high BUN-to-creatinine ratio (>30:1) due to upper GI protein digestion and prerenal azotaemia 3. |
| Imaging / Radiology (X-ray, US, CT, MRI) | CT Angiography (CTA): Indicated in massive ongoing hemorrhage where endoscopy is unsuccessful or non-diagnostic, or to plan transjugular intrahepatic portosystemic shunt (TIPS) / embolization. Abdominal Ultrasound: Evaluates signs of chronic liver disease, portal hypertension, and ascites 3, 6. |
| ECG / Histopathology / Procedural | 12-Lead ECG: Evaluates for myocardial ischemia precipitated by acute oxygen supply-demand mismatch in vulnerable patients. Histopathology: Biopsies taken during OGD to rule out malignancy and test for H. pylori (rapid urease test or histology) 3. |
5. Staging, Classification & Clinical Scoring Systems
| Criterion / Score Component | Clinical Threshold, Points & Management Implication |
|---|---|
| Glasgow-Blatchford Score (GBS) | Assesses pre-endoscopic risk using blood urea, hemoglobin, systolic blood pressure, heart rate, melaena, syncope, hepatic disease, and cardiac failure. A score of 0 indicates patients who are safe for early discharge and outpatient management 3, 6. |
| Rockall Score | Combines clinical parameters (age, shock, co-morbidities) and endoscopic findings (diagnosis, stigmata of recent hemorrhage). Used post-endoscopy to predict rebleeding risk and mortality. |
| Forrest Classification (Endoscopic) | Ia: Spurting hemorrhage (high risk); Ib: Oozing hemorrhage; IIa: Non-bleeding visible vessel; IIb: Adherent clot; IIc: Flat pigmented spot; III: Clean base (low risk). High-risk lesions (Ia-IIa) mandate immediate endoscopic therapy 6. |
6. Differential Diagnosis
| Differential Condition | Distinguishing Clinical, Biochemical & Imaging Features |
|---|---|
| Lower Gastrointestinal Bleeding (LGIB) | Bleeding distal to the ligament of Treitz. Typically presents with bright red blood per rectum (haematochezia) or maroon stools, normal BUN-to-creatinine ratio, and negative upper endoscopy. |
| Haemoptoic / Pseudo-haematemesis | Blood originating from the respiratory tract (hemoptysis) coughed up rather than vomited. Confirmed by history of pulmonary disease, bright frothy blood mixed with sputum, and normal OGD. |
| Dietary & Medication Mimetics | Ingestion of bismuth compounds, iron supplements, activated charcoal, blueberries, or dark chocolate can cause black stools mimicking melaena, but without hemodynamic instability or fecal occult blood positivity. |
| Aortoenteric Fistula | Rare, catastrophic communication between the aorta and the GI tract (usually duodenal third/fourth portion), often presenting as a "sentinel bleed" followed by massive exsanguinating hemorrhage in patients with prior aortic graft surgery. |
7. Management & Treatment Protocol
- Initial Stabilization & Resuscitation:
- Establish secure large-bore intravenous access (two peripheral lines of 16-gauge or larger or central venous access).
- Perform aggressive volume resuscitation using crystalloids cautiously, and institute a restrictive red blood cell (RBC) transfusion threshold of haemoglobin <70 g/L (targeting 70–90 g/L), except in patients with acute coronary syndrome where a threshold of <90 g/L may be utilized 3, 6.
- Reverse coagulopathies promptly (platelet transfusion for counts <50,000/mcL, fresh frozen plasma or prothrombin complex concentrates for warfarin reversal, and vitamin K) 3.
- First-Line Medical / Pharmacological Therapy:
- Non-Variceal Bleeding: High-dose intravenous proton pump inhibitor (PPI) therapy (e.g., pantoprazole 80 mg bolus followed by 8 mg/hour continuous infusion for 72 hours, or intermittent high-dose IV boluses) to stabilize clot formation and promote mucosal healing 4, 6.
- Variceal Bleeding: Immediate initiation of vasoactive drugs (Terlipressin 2 mg IV every 4 hours initially, or Octreotide 50 mcg IV bolus followed by 50 mcg/hour infusion) maintained for 2–5 days to reduce portal pressure 6.
- Antibiotic Prophylaxis: Mandatory short-term intravenous broad-spectrum antibiotics (e.g., Ceftriaxone 1 g IV daily for 5–7 days) in patients with cirrhosis and acute UGIB to prevent bacterial infections and improve survival 5, 6.
- Prokinetics: Erythromycin (250 mg IV administered 30–60 minutes prior to endoscopy) may be used to clear gastric contents and improve endoscopic visualization 4, 6.
- Surgical / Interventional Indications:
- Therapeutic OGD with combined endoscopic modalities (e.g., epinephrine injection combined with mechanical clipping, bipolar electrocoagulation, or thermal probes) for high-risk non-variceal lesions 4, 6.
- Endoscopic variceal band ligation (EVL) for esophageal varices and tissue glue (cyanoacrylate) injection for gastric varices 6.
- Transjugular intrahepatic portosystemic shunt (TIPS) or balloon-occluded retrograde transvenous obliteration (BRTO) for refractory variceal bleeding.
- Urgent interventional radiology angiography with superselective embolization or surgical intervention (ulcer oversewing, partial gastrectomy) for refractory arterial hemorrhage failing endoscopic control 6.
8. Complications & Prognosis
- Acute Complications: Rebleeding (typically occurring within 48–72 hours), hypovolemic shock, aspiration pneumonia, acute kidney injury (prerenal azotaemia or hepatorenal syndrome), hepatic encephalopathy (triggered by blood protein breakdown in the gut), and multi-organ dysfunction syndrome 1, 3.
- Prognosis & Mortality: Overall mortality remains 2% to 10%, rising significantly in elderly patients, those with underlying liver cirrhosis, active malignancy, or multi-organ failure. Prompt risk stratification via the Glasgow-Blatchford score and timely multidisciplinary intervention dramatically optimize clinical outcomes 3, 6.
