• Lifetime prevalence: ~5–10% of the population will develop a peptic ulcer ^[2].
• Male predominance (M:F ≈ 3:1), although the gap is narrowing with ageing populations and increased NSAID use in women ^[2].
• Duodenal ulcers (DU) account for ~75% of peptic ulcers; gastric ulcers (GU) ~20%; the remainder occur at other sites (oesophagus, Meckel's diverticulum, anastomotic sites) ^[2].
• In Hong Kong, PUD remains the most common cause of upper GI bleeding ^[1][3], largely driven by:
  • High prevalence of H. pylori infection (declining but still significant in older cohorts — historically > 50% seroprevalence in adults > 60 years).
  • Widespread NSAID and aspirin use in an ageing population with cardiovascular and musculoskeletal disease.
  • Stress-related mucosal disease in ICU patients.
• PUD is the leading cause of death among peptic ulcer complications — specifically haemorrhage ^[3].

High Yield: Peptic ulcer is the most common cause of UGIB ^[1]. The four major risk factors are H. pylori, NSAIDs, stress, and excess gastric acid ^[1][3].

• Overall incidence of PUD has declined due to H. pylori eradication and PPI use.
• However, NSAID/aspirin-related ulcers are increasing relative to H. pylori ulcers as eradication rates rise but antiplatelet/anticoagulant use expands.
• The proportion of "idiopathic" ulcers (neither H. pylori nor NSAID) is rising — now ~10–20% of DU and ~5–10% of GU in some series.

The stomach is divided into five anatomical regions (proximal → distal):

The duodenum is divided into four parts (D1–D4). D1 (the duodenal bulb/cap) is the most common site for duodenal ulcers because it receives the highest concentration of gastric acid exiting the pylorus before alkaline pancreatic/biliary secretions neutralise it in D2 ^[2].

Understanding the arterial anatomy is critical because ulcer haemorrhage occurs when the ulcer erodes into an artery.

Greater curvature:

• Short gastric arteries (from splenic artery)
• Left gastro-omental (gastroepiploic) artery (from splenic artery)
• Right gastro-omental (gastroepiploic) artery (from gastroduodenal artery)

Lesser curvature:

• Left gastric artery (from coeliac trunk — the largest blood supply to the stomach)
• Right gastric artery (from common hepatic artery / proper hepatic artery)

Duodenum (D1):

• Supplied by branches of the gastroduodenal artery (GDA), which runs behind the first part of the duodenum.

Gastric ulcers on the lesser curvature can erode into the left gastric artery — the largest arterial supply to the stomach — causing catastrophic haemorrhage.

Sympathetic supply:

• Greater splanchnic nerve (T5–T9 sympathetic trunk) → coeliac ganglion → stomach
• Function: inhibits peristalsis, constricts pyloric sphincter, reduces secretions

Parasympathetic supply (Vagus nerve, CN X):

• Anterior vagal nerve: innervates the stomach, pylorus, and liver (gives off the hepatic branch, then continues as the anterior nerve of Latarjet along the lesser curvature) ^[2]
• Posterior vagal nerve: innervates the stomach and the entire foregut/midgut down to the splenic flexure (gives off the coeliac branch, then continues as the posterior nerve of Latarjet) ^[2]

The nerve of Latarjet (anterior and posterior) runs along the lesser curvature and provides the principal motor and secretory innervation to the antrum and pylorus. It is the key structure in highly selective vagotomy (HSV), where only the parietal cell branches are divided while preserving the nerve of Latarjet to maintain antral motility and pyloric function ^[3].

High Yield for surgery: In truncal vagotomy, both vagal trunks are divided at the oesophageal hiatus. This abolishes the pyloric relaxation reflex → must add a drainage procedure (pyloroplasty or gastrojejunostomy). In highly selective vagotomy, the nerve of Latarjet is preserved so pyloric function is maintained and no drainage is needed — but the operation is technically difficult ^[3].

Understanding PUD requires understanding the balance between aggressive and protective factors:

Aggressive factors ("Offence"):

1. Hydrochloric acid (HCl) — secreted by parietal cells, stimulated by:
   • Gastrin (from G cells in antrum) — endocrine pathway
   • Histamine (from enterochromaffin-like [ECL] cells in corpus) — paracrine pathway via H₂ receptors
   • Acetylcholine (from vagal nerve endings) — neural pathway via M₃ receptors
2. Pepsin — secreted as inactive pepsinogen by chief cells; activated by acid (pH < 2); digests proteins including mucosal tissue
3. Bile acids — refluxed bile can disrupt the mucosal barrier (relevant in post-gastrectomy states)

Defensive factors ("Defence"):

1. Mucus-bicarbonate barrier — surface mucous cells secrete a thick gel layer of mucus + bicarbonate ions, creating a pH gradient from ~2 in the lumen to ~7 at the epithelial surface
2. Prostaglandins (especially PGE₂ and PGI₂) — produced via COX-1 in mucosal epithelial cells; prostaglandins:
   • Stimulate mucus and bicarbonate secretion
   • Maintain mucosal blood flow (vasodilation)
   • Promote epithelial cell turnover and repair
   • Inhibit gastric acid secretion
3. Mucosal blood flow — washes away back-diffused H⁺ ions and delivers oxygen/nutrients for repair
4. Epithelial cell turnover — the gastric epithelium renews every 3–5 days; rapid restitution after injury
5. Surface phospholipids — create a hydrophobic layer that repels acid

PUD occurs when aggressive factors overwhelm defensive factors.

H. pylori is the single most important aetiological factor worldwide.

Microbiology:

• Microaerophilic, Gram-negative, curved/spiral-shaped rod (coccobacillus)
• Possesses flagella → motility through the viscous mucus layer
• Produces mucolytic enzymes → facilitates penetration to the epithelial surface
• Has strong urease activity → this is vital for survival and colonisation:
  • Bacterial urease hydrolyses gastric luminal urea → ammonia (NH₃) + CO₂
  • Ammonia neutralises surrounding gastric acid, creating a protective alkaline cloud around the organism
  • This is the basis for the rapid urease test (CLO test) and the urea breath test (UBT) used diagnostically ^[2]

Pathogenesis of DU vs GU — the two patterns of H. pylori gastritis:

Why does antral-predominant gastritis increase acid?

• H. pylori infection of antral G cells → ↑ gastrin release
• H. pylori infection of antral D cells → ↓ somatostatin (the "brake" on acid secretion is lost)
• Net effect: hypergastrinaemia → parietal cell hyperplasia in the (unaffected) body → acid hypersecretion

Why does pangastritis decrease acid?

• Inflammation extends to the body → direct damage to parietal cells → atrophic gastritis → loss of acid-secreting capacity
• Compensatory ↑ gastrin occurs but there are fewer functioning parietal cells to respond

Virulence factors of H. pylori:

• CagA (cytotoxin-associated gene A) — injected into host cells via a type IV secretion system; disrupts cell signalling, promotes inflammation, and is strongly associated with ulcers and gastric cancer
• VacA (vacuolating cytotoxin A) — induces vacuolation and apoptosis in epithelial cells
• Urease — as above, neutralises acid
• Flagella and adhesins (e.g., BabA, SabA) — enable colonisation

High Yield: H. pylori is found in ~90–95% of DU and ~60–80% of GU ^[2]. Eradication of H. pylori dramatically reduces ulcer recurrence from ~80% to < 5% per year.

NSAIDs are the second most common cause of PUD.

Pathogenesis:

1. Systemic prostaglandin inhibition (the main mechanism):

   • Gastric and duodenal mucosa rely on COX-1 (constitutive) for the synthesis of prostaglandins (especially PGE₂ and PGI₂)
   • Prostaglandins protect the mucosa by: mucin production, bicarbonate secretion, maintaining mucosal blood flow, inhibiting acid secretion, and promoting epithelial cell turnover
   • Non-selective NSAIDs inhibit both COX-1 and COX-2 → impaired prostaglandin production → disruption of mucosal barrier → increased mucosal permeability to H⁺ ions → intramural acidosis → cell death → ulceration ^[2]
   • This is a systemic effect — even parenteral or rectal NSAIDs cause gastric ulcers (not just direct topical injury)

2. Topical injury (minor contribution):

   • Many NSAIDs are weak acids that are non-ionised in the acidic gastric lumen → they diffuse into mucosal cells where the neutral intracellular pH causes them to ionise and become trapped ("ion trapping") → direct cellular toxicity

3. Impaired platelet function:

   • COX-1 inhibition in platelets → ↓ thromboxane A₂ → impaired platelet aggregation → if an ulcer forms, bleeding is more severe and harder to stop

Why selective COX-2 inhibitors (e.g., celecoxib, etoricoxib) are safer:

• COX-2 is mainly induced in inflammatory cells and is not the dominant isoform in gastric mucosa
• Selective COX-2 inhibition spares COX-1-dependent prostaglandin production in the stomach
• However, COX-2 inhibitors still carry some GI risk (COX-2 contributes to mucosal healing) and importantly increase cardiovascular risk (↓ PGI₂ in endothelium while TXA₂ production is preserved)

Risk factors for NSAID-related peptic ulcers ^[2]:

• Advanced age ( > 75 years)
• Prior history of clinical ulcer disease or ulcer complications
• High dose / long duration / relatively toxic NSAIDs
• Concurrent use of corticosteroids, anticoagulants, or antiplatelet agents
• Concomitant H. pylori infection (synergistic risk)
• Concurrent use of SSRIs (impair platelet serotonin uptake → worse bleeding)

"Stress ulcers" occur in critically ill patients (burns, trauma, major surgery, sepsis, ICU patients on mechanical ventilation). This is physiological stress, not psychological stress.

Pathogenesis:

• Splanchnic hypoperfusion → mucosal ischaemia → breakdown of mucosal defence
• ↓ Mucosal blood flow → ↓ bicarbonate delivery → ↓ wash-out of back-diffused H⁺
• Reperfusion injury with free radical generation worsens mucosal damage

Eponymous types:

• Curling ulcer — associated with severe burns (named after Thomas Blizard Curling). Mechanism: hypovolaemia → splanchnic vasoconstriction → mucosal ischaemia. Typically in the duodenum.
• Cushing ulcer — associated with CNS injury/neurosurgery (named after Harvey Cushing). Mechanism: ↑ vagal tone from raised ICP → ↑ gastric acid secretion. Unique in that these ulcers have high acid as a driver. Typically deep, single ulcers that perforate.

• Impairs mucosal blood flow (nicotine → vasoconstriction)
• Reduces bicarbonate secretion from the pancreas and duodenal mucosa
• Promotes duodenogastric reflux of bile
• May enhance H. pylori colonisation
• Delays ulcer healing and increases recurrence

• Direct topical mucosal irritant → disrupts the mucosal barrier
• Stimulates acid secretion (especially at low concentrations)
• Causes acute gastritis (mucosal haemorrhage) rather than true chronic PUD per se, but exacerbates ulcers

A rare but important cause of refractory/unusual ulcers.

• Caused by a gastrinoma (gastrin-secreting neuroendocrine tumour) — most commonly in the duodenum (60–80%) or pancreas (20–40%), in the "gastrinoma triangle"
• Pathophysiology: Autonomous hypersecretion of gastrin → massive acid hypersecretion → overwhelms mucosal defences → multiple, refractory ulcers
• ↑ Gastrin also causes gastric epithelial cell (ECL cell and parietal cell) hyperplasia

When to suspect ZES ^[2]:

• Recurrent ulcers despite adequate treatment
• Ulcers in unusual locations (D2, jejunum)
• Complicated PUD without H. pylori or NSAID use
• Multiple ulcers simultaneously
• Ulcers associated with diarrhoea (massive acid inactivates pancreatic lipase → steatorrhoea; acid damages small bowel mucosa)
• Association with MEN1 (multiple endocrine neoplasia type 1) — parathyroid adenoma + pituitary adenoma + pancreatic/duodenal neuroendocrine tumour

Diagnosis: Fasting serum gastrin level (markedly elevated, typically > 1000 pg/mL) in the presence of high gastric acid output (to distinguish from the hypergastrinaemia of achlorhydria/PPI use, where gastrin rises as a compensatory response to low acid) ^[2].

• Corticosteroids — alone they have minimal ulcerogenic potential, but in combination with NSAIDs they significantly increase risk
• Crack cocaine, methamphetamines — mesenteric vasoconstriction → mucosal ischaemia
• Radiation — to upper abdomen
• Crohn's disease — can cause duodenal or gastric ulcers
• CMV/HSV — in immunocompromised patients (e.g. HIV/AIDS, post-transplant)
• Gastric cancer — a gastric ulcer may be malignant (always biopsy GU; DU is almost never malignant)
• Idiopathic ulcers — rising proportion; possibly related to mucosal hypersensitivity, visceral hyperalgesia, or unidentified pathogens

This classification is based on anatomical location and acid-secretory status and is particularly useful for guiding surgical management of GU.

This endoscopic classification grades the stigmata of recent haemorrhage (SRH) and predicts rebleeding risk — critical for guiding endoscopic therapy. Briefly:

A. Epigastric Pain — the cardinal symptom ^[2]

• Character: Gnawing, burning, or aching pain localised to the epigastrium.
• Pathophysiological basis: Exposed submucosal nerve endings in the ulcer crater are stimulated by gastric acid and pepsin contact; also local inflammation with release of inflammatory mediators (prostaglandins, bradykinin, substance P) activating visceral nociceptors.
• The relationship of pain to meals differs classically between DU and GU:

• Periodicity: PUD pain classically waxes and wanes over weeks to months, with symptom-free intervals. This reflects cycles of ulcer healing and relapse.
• Radiation to the back: Atypical but important — suggests posterior penetration (DU penetrating into the pancreas; GU penetrating into the pancreatic body). Persistent back pain in PUD is a red flag ^[2].

B. Nausea and Vomiting

• More common in GU than DU.
• Pathophysiology: gastric mucosal inflammation → visceral afferent stimulation → nausea; if there is pyloric oedema or spasm from a peri-pyloric ulcer, gastric emptying is delayed → vomiting.
• Projectile, non-bilious vomiting of undigested food → suggests gastric outlet obstruction (GOO) due to chronic scarring/fibrosis at the pylorus ^[3].

C. Early Satiety and Postprandial Fullness

• Due to gastric inflammation, impaired accommodation (fundus fails to relax normally), or pyloric oedema causing delayed emptying.

D. Belching and Bloating

• Aerophagia from repeated swallowing (a reflex response to nausea/pain); also gaseous distension from delayed emptying.

E. Anorexia and Weight Loss

• More common with GU (food avoidance due to pain).
• Must always exclude gastric malignancy in a patient with GU + weight loss.

F. Fatty Food Intolerance

• Fat delays gastric emptying and stimulates cholecystokinin (CCK) → may exacerbate symptoms.

G. Heartburn (Not a Primary Symptom of PUD)

• Heartburn (retrosternal burning) is more suggestive of GERD but may coexist — the two conditions share risk factors ^[2].

H. Symptoms of Complications (presenting features in some patients):

• Haematemesis / melaena → haemorrhage (the most common complication presenting acutely)
• Sudden severe epigastric pain ("thunderclap") radiating to the whole abdomen → perforation
• Persistent vomiting of old food, succussion splash → gastric outlet obstruction

High Yield: Up to 70% of NSAID-related ulcers are asymptomatic — the first presentation may be a life-threatening haemorrhage or perforation. This is because NSAIDs also have analgesic properties that mask ulcer pain ^[2].

A. General Examination — Often Normal in Uncomplicated PUD

In uncomplicated PUD, physical examination may be entirely unremarkable. This is important to recognise: the diagnosis of uncomplicated PUD is clinical (history) + endoscopic, not based on physical signs.

B. Epigastric Tenderness

• Mild, localised epigastric tenderness on palpation — the most common (but non-specific) sign.
• Pathophysiology: visceral inflammation in the upper GI tract → referred somatic pain/tenderness in the T6–T8 dermatome distribution (epigastrium).
• Absence of tenderness does NOT exclude PUD; its presence does not confirm it.

C. Signs of Complications:

D. Signs Suggesting Alternative Diagnoses (Important Negatives):

• Jaundice → think biliary disease, pancreatic head malignancy, hepatocellular disease
• Lymphadenopathy (Virchow's node — left supraclavicular) → gastric malignancy
• Palpable mass → gastric cancer, not uncomplicated PUD
• Hepatomegaly / ascites → consider liver disease with portal hypertensive gastropathy or variceal bleeding mimicking PUD

For patients who receive endoscopic therapy for Forrest Class Ia, Ib, IIa, or IIb ulcer bleeding:

IV esomeprazole (or pantoprazole) 80 mg stat bolus → 8 mg/hour continuous infusion for 72 hours ^[3]

Why this protocol?

• Platelet aggregation and clot stability are pH-dependent — platelet function is optimal at pH > 6.0. Below pH 5.4, platelet aggregation is abolished; below pH 4, fibrin clots dissolve (pepsin-mediated fibrinolysis).
• High-dose IV PPI maintains intragastric pH > 6 for a sustained period → stabilises the haemostatic clot over the bleeding vessel → reduces rebleeding.
• After 72 hours, switch to oral PPI (e.g., esomeprazole 40 mg daily).

Two major scores are used to stratify patients with UGIB:

The three pillars of uncomplicated PUD management are:

1. Remove the cause (H. pylori eradication, NSAID withdrawal)
2. Heal the ulcer (acid suppression with PPI)
3. Prevent recurrence (confirm eradication, prophylaxis if NSAIDs cannot be stopped)

A. Medication Alteration

• NSAID users ^[2]:

  • Switch to less ulcerogenic NSAIDs or COX-2 selective inhibitors — COX-2 inhibitors (e.g., celecoxib) spare COX-1-mediated prostaglandin synthesis in the gastric mucosa, preserving the mucosal barrier. Why does this work? Because the ulcer is caused by systemic COX-1 inhibition reducing PGE₂; removing the offending agent allows prostaglandin levels to recover.
  • Withdraw NSAIDs during PPI treatment — healing is dramatically impaired if the causative agent continues ^[2].

• Aspirin users ^[2]:

  • Bleeding peptic ulcer: Resume aspirin with PPI treatment once haemostasis is secured — the rationale is to minimise cardiovascular risk. Studies show that withholding aspirin for > 7 days after ulcer haemostasis is associated with increased cardiovascular events (MI, stroke) without significant benefit in reducing rebleeding ^[2][3].
  • Non-bleeding peptic ulcer: Continue aspirin with PPI treatment — no need to stop aspirin if the ulcer is not actively bleeding ^[2].

• Antithrombotic management principles ^[3]:

  • Withhold all antithrombotics stat +/- reversal agents in acute bleeding
  • Resume aspirin after OGD; clopidogrel 5–7 days later ^[3] — aspirin is resumed early because its cardiovascular benefit outweighs the small rebleeding risk once endoscopic haemostasis is achieved.

B. Lifestyle Modification ^[2]

• Smoking cessation — smoking impairs mucosal blood flow, reduces bicarbonate secretion, promotes duodenogastric reflux, and delays ulcer healing. It also increases recurrence rates even after successful H. pylori eradication.
• Limit alcohol intake — alcohol is a direct mucosal irritant and stimulates acid secretion.

This is a high-yield topic — the prevention strategy depends entirely on the underlying cause:

Most common site: anterior wall of D1 ^[3].

Management Algorithm [3]

Step 1: Resuscitation

• NPO
• IV fluids
• NG tube decompression (may have co-existing GOO) ^[3]
• IV broad-spectrum antibiotics (e.g., augmentin) — to cover the bacterial peritonitis that develops within 6 hours ^[3]
• IV PPI / H₂ blocker (suppress acid production, limit ongoing chemical peritonitis) ^[3]

Step 2: Surgery ^[3]

Treatment options: H. pylori eradication + surgery + peritoneal lavage ( > 6L NS) after repair ^[3]

Biopsy ulcer edge for ALL gastric ulcers to rule out malignancy ^[3]

Indications to convert laparoscopic to open ^[3]:

• Haemodynamically unstable → shorter operative time with open
• Large defect ( > 1 cm) → difficult laparoscopic suturing
• Gross contamination → limited laparoscopic peritoneal lavage capacity

Post-operative management ^[3]:

• NPO until no signs of leakage and return of bowel function
• Complete full course of antibiotics
• Continue PPI until follow-up OGD
• FU OGD 6–8 weeks after surgery to confirm healing and check H. pylori status ^[3]

Prognosis: Boey's Score (3 points) ^[3]:

GOO results from chronic scarring and fibrosis at the pylorus/D1 from repeated ulcer-healing cycles, or from acute oedema and spasm during active ulceration. Prolonged obstruction can lead to gastric atony (the dilated stomach loses its contractile ability) ^[2].

GOO is malignant until proven otherwise — 80% malignant (gastric cancer is the most common cause), 20% benign (PUD-related pyloric stenosis is the 2nd most common overall cause) ^[3].

Management [2][3]

Step 1: Medical ("Drip and Suck") ^[2][3]

• NPO
• Nasogastric (NG) tube — decompress the stomach, relieve vomiting
• Fluid resuscitation
• Correction of electrolyte abnormality ^[2]:
  • Normal saline + KCl — prolonged vomiting causes hypochloraemic hypokalaemic metabolic alkalosis ^[2]
  • Why NS specifically? Because this is a chloride-responsive alkalosis — the kidneys need chloride to excrete excess bicarbonate; until Cl⁻ is replaced, the alkalosis cannot correct
• IV PPI — antisecretory agents remain the mainstay of initial treatment (e.g., pantoprazole) ^[2]

Step 2: OGD after decompression ^[3]

• Once the stomach is adequately decompressed → OGD to biopsy the pylorus and establish whether GOO is benign (PUD) or malignant ^[3]

Step 3: Definitive Treatment ^[2][3]

Surgical options for benign GOO ^[2][3]:

• GU: Antrectomy with Billroth I/II reconstruction ^[2]
• DU: Truncal vagotomy + Antrectomy with Billroth I/II reconstruction ^[2]
• Alternative: Bypass (gastrojejunostomy), pyloroplasty ^[3]

• Penetration = ulcer erodes through the bowel wall without free perforation — the adjacent organ "seals" the defect, preventing spillage into the peritoneal cavity ^[2]
• Occurs in descending order of frequency: Pancreas > Lesser omentum > Biliary tract > Liver > Greater omentum > Mesocolon > Colon > Vascular structures ^[2]
• Leads to complications such as pancreatitis (most common — posterior DU penetrating into pancreas) or cholangitis
• Clinical clue: pain becomes more intense, longer-lasting, localised to the back, and is NOT relieved by food or antacids (unlike uncomplicated DU) ^[2]
• Surgical treatment is NOT recommended ^[2] — manage conservatively with IV PPI and treat the secondary complication (e.g., pancreatitis). Surgery is only considered if the penetration leads to uncontrollable haemorrhage or fistula formation.

The ulcer starts at the mucosa and erodes progressively deeper: mucosa → muscularis mucosae → submucosa → muscularis propria → serosa. The submucosa contains a rich vascular plexus. Once the ulcer breaches the muscularis mucosae and enters the submucosa, it encounters arteries and veins. If the ulcer erodes even deeper through the full wall thickness posteriorly, it can reach named arteries behind the bowel wall.

• DU bleeding usually locates at the posterior duodenal wall within 2 cm of the pylorus and typically erodes into the gastroduodenal artery (GDA) ^[2][3] — the GDA runs behind D1, so a posterior DU bores straight into it.
• GU bleeding on the lesser curvature can erode into the left gastric artery (the largest arterial supply to the stomach).
• The clinical presentation depends on the rate and volume of bleeding: slow ooze → occult blood loss → iron-deficiency anaemia; brisk bleed → haematemesis (vomiting red blood or coffee-ground material — coffee-ground appearance results from haemoglobin being denatured to haematin by gastric acid) and/or melaena (black, tarry stool — the result of haemoglobin being digested through the entire GI tract and converted to haematin and other pigments by gut bacteria).

These are testable and clinically important — they identify patients who need close monitoring or early surgical/IR referral:

Risk factors for recurrent bleeding ^[1]:

• Patient already hospitalised (stress, comorbidities, NSAIDs)
• Large ulcer
• Ulcer on posterior D1 (proximity to GDA)
• Ulcer on higher posterior lesser curve (proximity to left gastric artery)

Additional risk factors ^[2]:

• Age > 60
• Coagulopathy or anticoagulant use
• Hb < 8.0 g/dL on presentation
• Shock on presentation
• Need for blood transfusion

After initial endoscopic haemostasis, continuous vigilance is required:

• Haematemesis or fresh melaena
• Tachycardia (the earliest haemodynamic sign — the body compensates by increasing heart rate before blood pressure drops)
• Falling Hb trend on serial monitoring (anaemia developing despite transfusion)
• Blood in the NG tube ^[2]

This has been covered in detail in the management section; here is a concise summary of the escalation ladder:

Step 1: Resuscitate → ABC, 2 large-bore IV, fluids, blood if Hb < 7 (or < 9 if high-risk)

Step 2: Endoscopy → Dual therapy (adrenaline 1:10,000 [tamponade + vasoconstriction + platelet aggregation] + heater probe [coaptive effect: pressure + heat] or metal clip) for Forrest Ia, Ib, IIa, IIb ^[1][3]

• Clean base → start feeding, early discharge ^[1]
• Injection therapy should NOT be used as monotherapy ^[2][3]

Step 3: Post-OGD → IV PPI infusion (80 mg stat → 8 mg/h × 72h) — higher pH stabilises clot since platelet function depends on normal pH ^[3]

Step 4: If rebleed → Re-scope + repeat endoscopic therapy

Step 5: If 2nd endoscopy fails → Surgery or TAE ^[1][2][3]

Surgery for bleeding ulcer — indications ^[1]:

• Therapeutic endoscopist not available
• Massive bleeding
• Failed endoscopic therapy
• Rebleed after endoscopic therapy

Surgery = Plication of bleeder + additional procedure ^[1]:

• DU: V+P (truncal Vagotomy + Pyloroplasty) ^[1]
• GU: partial gastrectomy ^[1] (because GU may harbour malignancy)

TAE (transcatheter arterial embolisation): equally effective as surgery for patients who failed endoscopic therapy; fewer complications; should be considered in patients unfit for surgery ^[2][3]

Limitations of endoscopic haemostasis ^[3]:

• Massive bleeding obscuring view
• Large bleeding artery ( > 3.2 mm)
• Large ulcer ( > 2 cm)

When the ulcer erodes through all layers of the bowel wall (mucosa → submucosa → muscularis propria → serosa) and there is no adjacent organ to seal the defect, the luminal contents spill freely into the peritoneal cavity. This causes:

1. Chemical peritonitis (first 4–6 hours) — gastric acid (pH ~1–2), pepsin, bile, and food particles directly irritate the peritoneum. This produces the classic sudden, severe, "thunderclap" epigastric pain and board-like rigidity (reflex tonic contraction of the abdominal wall muscles to splint the inflamed peritoneum).

2. Bacterial peritonitis (after 6 hours) — gut flora colonise the contaminated peritoneal fluid → systemic inflammatory response → sepsis → multi-organ failure if untreated ^[3].

Most common site: anterior wall of D1 ^[3] — because the anterior wall faces the free peritoneal cavity with nothing to tamponade or seal the defect (contrast with the posterior wall which is retroperitoneal and abutted by the pancreas).

• Sudden onset severe generalised abdominal pain — the patient can often pinpoint the exact onset time (unlike gradual-onset pain of pancreatitis or cholecystitis) ^[3]
• Board-like rigidity with patient lying completely still (any movement worsens peritoneal irritation)
• +/- RLQ pain (Valentino's sign): GI contents track down the right paracolic gutter to the RIF, mimicking appendicitis ^[3]
• Progression: Shock → fever — chemical peritonitis in first 4–6 hours → bacterial peritonitis after 6 hours ^[3]
• Loss of liver dullness on percussion (Jobert sign) — free gas between the liver and abdominal wall

• Erect CXR: free gas under diaphragm in 60–70% of cases (require sitting upright for ≥ 10 minutes before film) ^[3]
• CT thorax + abdomen with contrast: rule out other DDx; detect small amounts of free gas and fluid that CXR may miss
• Bloods: CBC (Hb for GIB, WCC), LRFT, T&S, clotting, amylase (↑ due to pancreatic irritation by leaked duodenal contents — but typically a mild elevation; if markedly elevated, suspect acute pancreatitis as the primary diagnosis instead) ^[3]
• Do NOT attempt OGD: may convert sealed-off perforation to real perforation ^[3]

Resuscitation:

• NPO, IV fluids, NG tube decompression
• IV broad-spectrum antibiotics (e.g., Augmentin) — to cover emerging bacterial peritonitis
• IV PPI / H₂ blocker — suppress acid production, limit ongoing chemical peritonitis

Surgery ^[3]:

• Biopsy ulcer edge for ALL gastric ulcers to rule out malignancy ^[3]
• H. pylori eradication should be included in the treatment plan ^[3]

Convert to open if ^[3]:

• Haemodynamically unstable (shorter operative time)
• Large defect ( > 1 cm) (difficult laparoscopic suture)
• Gross contamination (limited laparoscopic peritoneal lavage)

Post-op management ^[3]:

• NPO until no signs of leakage and return of bowel function
• Complete full course of antibiotics
• Continue PPI until OGD
• FU OGD 6–8 weeks after surgery for healing + H. pylori status ^[3]

Prognosis — Boey's Score (3 points) ^[3]:

GOO from PUD occurs through three mechanisms working in sequence:

1. Acute oedema and spasm — active ulceration at or near the pylorus/D1 causes inflammatory swelling and smooth muscle spasm → functional narrowing. This component is potentially reversible with acid suppression and anti-inflammatory treatment.

2. Chronic fibrosis and scarring — repeated cycles of ulceration and healing deposit collagen in the pyloric/duodenal wall → fixed structural narrowing. This is irreversible and requires mechanical intervention (dilatation or surgery).

3. Gastric atony — prolonged obstruction leads to chronic gastric distension → the gastric wall muscle becomes over-stretched and loses contractile ability → even after the obstruction is relieved, the stomach may not empty properly ^[2].

• Waxing-and-waning epigastric pain (pain worsens after eating as the obstructed stomach distends, then partially subsides as some content trickles through)
• Repeated non-bilious projectile vomiting of undigested food — "non-bilious" because the obstruction is proximal to the ampulla of Vater (bile enters in D2, but the obstruction is at the pylorus/D1). "Undigested" because the food never reaches the small bowel for digestion. "Projectile" because the stomach builds up high pressure behind the obstruction ^[3]
• Early satiety, weight loss — the patient cannot eat without vomiting
• Succussion splash — audible splash heard with a stethoscope when shaking the patient's abdomen > 4 hours after the last meal; indicates retained gastric fluid. Pathophysiology: the dilated, atonic stomach retains food and fluid like a water balloon, and shaking it produces the characteristic sloshing ^[2]

This is a high-yield exam topic — the electrolyte disturbance in GOO is pathognomonic:

Hypochloraemic hypokalaemic metabolic alkalosis +/- paradoxical aciduria ^[2][3]

Step-by-step mechanism:

1. Repeated vomiting of HCl → loss of H⁺ and Cl⁻ → metabolic alkalosis + hypochloraemia
2. Volume depletion → kidney activates RAAS → aldosterone → proximal tubule Na⁺ reabsorption in exchange for K⁺ and H⁺ secretion → hypokalaemia + paradoxical aciduria (the kidneys excrete acid despite the body being alkalotic, because Na⁺ salvage takes priority over acid-base balance)
3. Cl⁻ deficit prevents the kidney from excreting HCO₃⁻ (because Cl⁻ is needed for HCO₃⁻ exchange in the proximal tubule) → alkalosis is maintained = "chloride-responsive alkalosis"
4. Hypokalaemia itself worsens alkalosis: in the distal tubule, K⁺ depletion causes H⁺ to be secreted instead of K⁺, further contributing to paradoxical aciduria and perpetuating alkalosis
5. Hypocalcaemia may develop → tetany (alkalosis increases protein-binding of ionised Ca²⁺, reducing the free fraction) ^[3]

Correction: IV normal saline (0.9% NaCl) + KCl — NS provides both volume and chloride, allowing the kidneys to finally excrete excess bicarbonate. KCl corrects hypokalaemia and enables H⁺/K⁺ exchange to normalise ^[2].

Step 1: Medical ("Drip and suck")

• NPO, NG tube decompression, IV fluid resuscitation
• Correction of electrolytes — NS + KCl ^[2]
• IV PPI (e.g., pantoprazole) — reduces acid secretion, may reduce acute inflammatory oedema component ^[2]

Step 2: OGD after decompression

• Biopsy to exclude malignancy — GOO is malignant until proven otherwise (80% malignant, 20% benign) ^[3]

Step 3: Definitive treatment

• Benign: Endoscopic balloon dilatation ^[2] +/- stenting; if fails → surgery
• Malignant: treat underlying CA; palliative bypass (gastrojejunostomy) or SEMS ^[3]

Surgical options for benign GOO ^[2]:

• GU: Antrectomy with Billroth I/II reconstruction
• DU: Truncal vagotomy + Antrectomy with Billroth I/II reconstruction

Penetration is essentially a "sealed perforation" — the ulcer erodes through the full thickness of the bowel wall, but instead of spilling into the free peritoneal cavity, the adjacent organ acts as a plug, preventing free leakage. The ulcer crater extends into the parenchyma of the neighbouring organ.

Order of frequency of penetration ^[2]: Pancreas > Lesser omentum > Biliary tract > Liver > Greater omentum > Mesocolon > Colon > Vascular structures

Why is the pancreas most common? Because posterior DU sit directly against the head of the pancreas (the pancreatic head is immediately retroperitoneal to D1). As the ulcer bores posteriorly, the first structure it encounters is the pancreas.

• Pain becomes more intense, longer duration
• Shift from typical vague visceral discomfort to localised intense pain radiating to the back — this back radiation occurs because the pancreas is a retroperitoneal organ, and inflammation of retroperitoneal structures causes somatic pain referred to the back (T10–L1 dermatomes)
• Pain is NOT relieved by food or antacids — unlike uncomplicated DU, where food buffers acid and provides temporary relief, in penetration the inflammatory process in the adjacent organ is ongoing and unrelated to intraluminal acid levels ^[2]
• Secondary complications: pancreatitis (most common — from DU penetrating into pancreas), cholangitis (if penetrating into biliary tract) ^[2]

• Surgical treatment is NOT recommended ^[2]
• Conservative management: IV PPI (high-dose acid suppression to halt further ulcer progression), H. pylori eradication if positive, treat the secondary complication (e.g., manage pancreatitis per standard protocol)
• Surgery reserved only for: uncontrollable haemorrhage from vascular erosion, fistula formation that does not resolve, or failure of conservative therapy

Fistulisation represents the most extreme form of penetration — the ulcer erodes completely through the bowel wall AND through the wall of an adjacent hollow organ, creating an abnormal communication (fistula) between two luminal structures.

Types:

• Gastrocolic fistula — stomach → transverse colon (the transverse colon lies immediately inferior to the greater curvature)
• Duodenocolic fistula — duodenum → colon
• Choledochoduodenal fistula — CBD → duodenum (can lead to gallstone ileus via this route)

The symptoms are dramatic because colonic content now refluxes into the stomach:

• Feculent vomiting — the patient vomits material with faecal odour/character (colonic bacteria + faecal matter refluxing into the stomach). This is nearly pathognomonic of a gastrocolic/duodenocolic fistula
• Postprandial diarrhoea — food bypasses the small bowel absorptive surface by directly entering the colon through the fistula → malabsorption + osmotic diarrhoea
• Dyspepsia and weight loss — chronic malabsorption and ongoing inflammation
• Halitosis (faecal breath)

• Nutritional optimisation (patients are often severely malnourished)
• Surgery: resection of the fistulous tract with repair of both organs involved; typically requires partial gastrectomy or duodenal repair + colonic resection
• IV PPI + H. pylori eradication as adjuncts