Upper Gastrointestinal (GIT) Bleeding - Complete Clinical Review

CAUSES / ETIOLOGY

IMPORTANT HISTORY POINTS

• Hematemesis - bright red blood in vomitus = active or recent bleeding
• Coffee-ground emesis - digested blood, suggests slower or stopped bleeding
• Melena - black, tarry, malodorous stools - strongly suggests UGIB (especially in patients <50 years)
• Hematochezia - bright red blood per rectum - can arise from UGIB in ~14% of cases when bleeding is massive and rapid

1. Prior GI bleeding episodes - up to 60% of recurrent UGIBs arise from the same lesion
2. History of peptic ulcer disease or H. pylori infection
3. Alcohol use and liver disease - cirrhotic patients have a 30% chance of variceal bleeding; ~60% rebleed within 12 months
4. NSAID / aspirin / anticoagulant use - most patients presenting with UGIB used aspirin or an NSAID in the preceding week; half use these OTC
5. Retching and vomiting before hematemesis - classic for Mallory-Weiss tear (also seen with DKA, chemotherapy, alcohol binge)
6. History of aortic graft surgery - "herald bleed" (self-limited initial hematemesis) preceding massive hemorrhage = aortoenteric fistula
7. Iron or bismuth ingestion - can simulate melena (stool guaiac will be negative)
8. Red-dye liquids or beets - can simulate hematochezia
9. Smoking, alcohol, GERD - risk factors for esophageal cancer
10. Known varices, prior TIPS, banding - high-risk endoscopic history
11. Syncope, weakness, angina, confusion - may be the only presenting feature without overt bleeding

CLINICAL FEATURES

Symptoms

• Hematemesis (bright red or coffee-ground)
• Melena
• Hematochezia (in massive UGIB)
• Syncope, dizziness, weakness
• Angina or palpitations (demand ischemia from blood loss)

Signs - Vital Signs

• Tachycardia (often first sign)
• Hypotension / orthostatic hypotension
• Decreased pulse pressure
• Tachypnea
• Paradoxical bradycardia can occur even with significant hemorrhage
• Younger patients without comorbidities may tolerate substantial volume loss with minimal vital sign changes

Signs - Physical Examination

• Pallor, cool clammy extremities (hypovolemia)
• Jaundice, spider angiomas, palmar erythema, splenomegaly, ascites - suggest liver disease and variceal bleeding
• Epigastric tenderness - suggests peptic ulcer disease
• Digital rectal exam - assess stool color (melena vs. hematochezia) and confirm rectal bleeding

Postural (Orthostatic) Vital Signs

• Drop in systolic BP >10 mmHg OR rise in HR >20 bpm on standing suggests >15% volume loss

INVESTIGATIONS

Bedside / Initial Assessment

• Nasogastric aspirate (NG tube) - red blood or coffee-ground material confirms UGIB; useful when diagnosis is not clinically apparent (no strong evidence it provokes variceal bleeding)
• Stool guaiac / FOBT - confirms blood in stool; differentiates true melena from iron/bismuth ingestion

Laboratory Studies

Scoring Systems (Risk Stratification)

• Predicts need for clinical intervention (transfusion, endoscopy, surgery)
• Score 0 = very low risk; can consider outpatient management

• Albumin <3.0 g/dL
• INR >1.5
• Mental status alteration
• Systolic BP <90 mmHg
• Age >65 years
• Score ≥2 = higher mortality, longer stay, higher cost

• Score 0-2 = low risk, consider early discharge
• Correlates well with mortality

Imaging and Endoscopy

1. Upper GI Endoscopy (EGD) - gold standard - diagnostic AND therapeutic
   • Perform within 24 hours of presentation in most patients with overt bleeding after adequate resuscitation
   • Identifies stigmata of recent haemorrhage (SRH): active spurting, visible vessel, adherent clot, flat spot, clean base
   • Can be performed urgently (<12 hours) in haemodynamically unstable or high-risk patients
   • Side-viewing duodenoscope for suspected duodenal/ampullary bleeding not seen on standard scope
2. CT angiography (CTA) - when endoscopy is non-diagnostic or not feasible; detects bleeding >0.3-0.5 mL/min
3. Mesenteric angiography - for active bleeding; can be therapeutic (coil embolization)
4. Scintigraphy (tagged RBC scan) - detects slow intermittent bleeding (>0.1 mL/min)

MANAGEMENT

Step 1: Immediate Resuscitation ("ABC" First)

• Airway - consider prophylactic endotracheal intubation if massive active bleeding, altered consciousness, or aspiration risk; use smaller induction agent doses to minimize peri-intubation hypotension
• IV access - two large-bore IVs (16-gauge or larger)
• IV fluids - crystalloid resuscitation while awaiting blood products
• Oxygen - supplemental O2 in all patients

Step 2: Blood Transfusion

• Correct coagulopathy: FFP if INR elevated; platelets if <50,000; vitamin K if on warfarin
• Correct thrombocytopenia aggressively in active bleeding

Step 3: Pharmacological Treatment

Step 4: Endoscopic Therapy (Definitive for Most)

• Injection therapy - adrenaline/epinephrine injection (local vasoconstriction + tamponade), tissue adhesives (e.g., cyanoacrylate for gastric varices)
• Mechanical therapy - hemostatic clips, band ligation (variceal banding), suturing devices
• Thermal therapy:
  • Contact: electrocoagulation, thermocoagulation (heater probe)
  • Non-contact: argon plasma coagulation (APC), Nd:YAG laser photocoagulation
• Combination therapy (e.g., epinephrine + thermal/clip) is superior to monotherapy for high-risk lesions

• Esophageal varices - endoscopic band ligation (EBL) is first-line
• Gastric varices - cyanoacrylate glue injection or thrombin

Step 5: Management of Refractory Bleeding

Step 6: Secondary Prevention

• H. pylori eradication - test-and-treat in all peptic ulcer bleeders
• Stop NSAIDs - if not possible, add PPI prophylaxis
• PPI long-term - for high-risk ulcers or ongoing NSAID use
• Beta-blockers (propranolol/carvedilol) + EBL - for variceal bleed secondary prevention
• TIPS - for refractory or recurrent variceal bleeding in cirrhosis

RISK STRATIFICATION SUMMARY

KEY PROGNOSTIC FACTS

• Bleeding is self-limited in 80% of UGIB patients even without specific therapy
• Of the remaining 20% who rebleed, mortality is 30-40%
• Overall UGIB mortality is 5-10% (unchanged since the 1970s despite advances, due to older and sicker patient population)
• Variceal bleeding carries 20% mortality per episode; ~60% rebleed within 12 months
• Peptic ulcer most common cause (~35-50%); varices carry highest per-episode mortality

RECENT EVIDENCE UPDATES

Differentials of Upper GIT Bleeding and How to Rule Each Out

1. True UGIB causes - conditions within the upper GIT that genuinely bleed (need to be distinguished from each other)
2. Pseudo-UGIB / Mimics - conditions that simulate UGIB but do not originate there

CATEGORY 1: TRUE UGIB DIFFERENTIALS

1. Peptic Ulcer Disease (PUD) - Most Common (~35-50%)

• Chronic, recurring epigastric/burning pain - often relieved by food or antacids (duodenal ulcer), or worsened by food (gastric ulcer)
• History of NSAID, aspirin, or steroid use - most patients used NSAIDs the week before
• History of H. pylori infection or previous ulcer
• Tobacco smoking history
• Middle-aged to elderly patient
• Melena more common than hematemesis (unless actively bleeding)
• Coffee-ground emesis typical

• EGD (gold standard) - shows discrete ulcer crater with clean base, flat spot, adherent clot, visible vessel, or active bleeding
• H. pylori testing (CLO test at endoscopy, urea breath test, stool antigen)
• Elevated BUN:Creatinine ratio supports upper GI source
• Absence of liver disease signs argues against varices

2. Esophageal / Gastric Varices (Second Most Common, Highest Mortality per Episode)

• Known cirrhosis / chronic liver disease - alcoholic, viral hepatitis, NAFLD
• Physical signs of portal hypertension: jaundice, spider angiomas, palmar erythema, caput medusae, splenomegaly, ascites, hepatomegaly or small shrunken liver
• Sudden, massive, painless hematemesis of bright red blood - often torrential
• Altered sensorium (hepatic encephalopathy)
• No preceding epigastric pain (unlike PUD)
• History of alcohol binge; prior known varices; prior banding/sclerotherapy
• Coagulopathy (raised INR, low platelets from hypersplenism)

• EGD - shows dilated tortuous submucosal veins at lower esophagus or gastric fundus; red-wale signs indicate high bleed risk
• LFTs, albumin, INR - deranged in liver disease
• Platelets typically low (hypersplenism)
• Abdominal USS/Doppler - portal vein diameter >13 mm, reversal of flow, splenomegaly
• MELD or Child-Pugh score to quantify liver disease severity
• No ulcer crater on endoscopy distinguishes from PUD
• Note: cirrhotic patients bleed from non-variceal sources ~40% of the time, so EGD remains mandatory

3. Mallory-Weiss Tear

• Classic triad: repeated forceful vomiting → THEN hematemesis (the nonbloody vomiting comes first)
• History of alcohol binge, DKA, chemotherapy, bowel preparation
• Can also occur with Valsalva (coughing, seizures, lifting)
• Usually younger patients
• Bleeding often self-limiting and less severe than varices
• No prior GI history
• Sometimes hiatal hernia is present

• EGD - shows longitudinal mucosal laceration at the gastroesophageal junction, often extending into a hiatal hernia; best seen on retroflexed view
• Single or occasionally multiple tears
• Tear heals spontaneously within ~48 hours in most cases
• Absence of cirrhosis signs distinguishes from variceal bleeding
• No chronic pain history distinguishes from PUD

4. Dieulafoy Lesion

• Intermittent, recurrent, massive hematemesis or melena with absolutely NO precipitating factor and NO history of liver disease or NSAID use
• Patient has often had multiple previous negative endoscopies ("serial negative workups")
• Classically in the proximal stomach within 6 cm of the GEJ, but can be anywhere
• No epigastric pain; no alcohol history; no cirrhosis
• Any age, but more common in older males with cardiovascular comorbidities
• Bleeding can be profuse and life-threatening from normal-looking mucosa

• EGD - profuse bleeding from an area of apparently normal mucosa is the hallmark
• When not bleeding: only a subtle vascular protuberance (1-3 mm) visible; overlying mucosa appears normal
• Doppler endoscopic probe (DEP) can detect submucosal arterial blood flow even when the lesion is not visually apparent
• Mark the site with submucosal ink tattoo if found - aids relocation during rebleed
• Angiography can demonstrate the culprit vessel if endoscopy fails

(Brisk bleeding from a Dieulafoy lesion in the gastric fundus)

5. Erosive Gastritis / Duodenitis / Esophagitis

• Coffee-ground emesis more than frank hematemesis (usually oozing rather than arterial)
• History of alcohol, aspirin, NSAIDs (stress-related mucosal disease)
• Critical illness - sepsis, trauma, mechanical ventilation (stress ulcers)
• Dysphagia or odynophagia with heartburn suggests erosive esophagitis
• Immunocompromised patients (HIV, transplant): esophagitis from Candida, HSV, CMV
• Pill-induced esophagitis: doxycycline, bisphosphonates, potassium, NSAIDs
• Rarely causes massive bleeding; more often occult or minor

• EGD - multiple superficial erosions without a discrete deep ulcer crater (distinguishes from PUD)
• No vascular lesion (distinguishes from Dieulafoy and varices)
• Biopsy for infection in immunocompromised patients (Candida plaques, viral inclusions)

6. Upper GIT Neoplasm (Gastric / Esophageal Cancer, GIST)

• Older patient (>50), progressive symptoms over weeks to months
• Weight loss, anorexia, dysphagia (esophageal cancer), early satiety
• Chronic, unremitting, occult bleeding leading to iron-deficiency anaemia - rarely torrential
• History of smoking, alcohol, GERD (esophageal SCC/adenocarcinoma)
• Family history of gastric cancer; H. pylori-related
• Palpable epigastric mass, left supraclavicular lymph node (Virchow's node), Sister Mary Joseph nodule
• GISTs (gastrointestinal stromal tumors) may present with massive UGIB in 20-30% of cases

• EGD with biopsy - irregular, firm, ulcerated mass; rolled edges in gastric cancer
• CT chest/abdomen/pelvis - staging, lymph nodes, metastases
• Endoscopic ultrasound (EUS) - depth of invasion, GIST characterisation
• Absence of discrete ulcer with surrounding normal mucosa distinguishes from PUD
• Elevated tumour markers (CEA, CA 19-9) in advanced disease

7. Aortoenteric Fistula (Rare but Lethal - Must Not Miss)

• History of prior aortic surgery (AAA repair, aortic graft) - typically 3-5 years prior
• Or known abdominal aortic aneurysm (AAA)
• Classic "herald bleed" - initial self-limited, mild hematemesis or hematochezia hours to months before catastrophic exsanguination
• Pulsatile abdominal mass on exam
• Most commonly involves the 3rd portion of the duodenum

• Urgent CT angiography with IV contrast or MR angiography is first-line in stable patients - shows inflammation around graft, may demonstrate the fistula
• EGD / push enteroscopy to directly visualize the 3rd part of duodenum for compression, blood, or graft material
• Endoscopic therapy plays NO role - surgical vascular intervention is required
• Do NOT delay with endoscopy alone if clinical suspicion is high

8. Angioectasia / Hereditary Haemorrhagic Telangiectasia (HHT / Osler-Weber-Rendu)

• Recurrent episodes of obscure GI bleeding with iron-deficiency anaemia
• HHT: visible telangiectasias on lips, tongue, buccal mucosa, fingers - autosomal dominant family history; frequent epistaxis since childhood
• Patients with CREST syndrome, scleroderma, Turner syndrome, or radiation injury
• Often elderly patients with no liver disease or NSAID history
• Chronic, indolent course; rarely catastrophic

• EGD shows flat, reddish, spider-like vascular lesions in stomach/duodenum (vs. normal mucosa around a Dieulafoy, vs. varices at GEJ)
• HHT: genetic testing for ENG or ALK-1 mutations
• Clinical criteria for HHT (Curacao criteria): epistaxis + telangiectasias + visceral lesions + positive family history

CATEGORY 2: PSEUDO-UGIB MIMICS (Rule These Out First)

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