Epigastric Pain

• H. pylori infection — major risk factor for PUD and gastric cancer (see below)
• NSAIDs / aspirin — dose-dependent mucosal injury
• Smoking — doubles PUD risk, increases gastric cancer risk (~11%) ^[5]
• Alcohol — gastritis, pancreatitis, liver disease
• Age — increasing risk of malignancy
• Obesity — GERD, gallstones, pancreatic cancer
• Hereditary factors — E-cadherin mutation (hereditary diffuse gastric cancer), HNPCC, FAP ^[5][6]

Why is foregut pain felt in the epigastrium? The foregut (stomach, duodenum D1–D2, liver, gallbladder, pancreas, spleen) is innervated by the coeliac (splanchnic) plexus, which enters the spinal cord at T5–T9. The brain interprets this afferent input as coming from the T5–T9 dermatomes, which map to the epigastrium. This is why gastric ulcer pain, biliary colic, and early appendicitis (midgut = T10) all start as poorly localised midline pain before parietal peritoneal involvement causes localisation.

The stomach is a J-shaped muscular organ with the following regions: cardia (entry point from oesophagus), fundus (dome-shaped superior portion), body/corpus (largest part), antrum (distal narrowing), and pylorus (sphincter controlling gastric outflow).

Arterial supply ^[1][3]:

• Greater curvature: short gastric arteries, left gastro-omental (gastroepiploic) artery, right gastro-omental (gastroepiploic) artery
• Lesser curvature: left gastric artery (largest contributor), right gastric artery

All these are branches or indirect branches of the coeliac trunk — this rich anastomotic supply means the stomach rarely infarcts but ulcer erosion into an artery (e.g., left gastric artery or gastroduodenal artery posteriorly in DU) causes torrential haemorrhage.

Nerve supply ^[1]:

• Sympathetic: greater splanchnic nerve (T5–T9 sympathetic trunk) — mediates visceral pain
• Parasympathetic:
  • Anterior vagal nerve: Stomach + Pylorus + Liver
  • Posterior vagal nerve: Stomach + Foregut and midgut down to splenic flexure

The vagus nerve stimulates gastric acid secretion (via acetylcholine on parietal cells and gastrin release from G cells). This is why vagotomy was historically used to treat PUD — cutting the vagal supply reduces acid output.

The stomach maintains a balance between aggressive factors (acid, pepsin) and protective mechanisms (mucus-bicarbonate barrier, mucosal blood flow, prostaglandins, epithelial cell turnover) ^[1][3]:

1. Mucus layer — secreted by surface epithelial cells; forms an unstirred gel layer trapping bicarbonate
2. Bicarbonate secretion — creates a pH gradient (pH 1–2 at lumen surface → pH 6–7 at epithelial surface)
3. Mucosal blood flow — delivers oxygen and nutrients, washes away back-diffused H⁺ ions
4. Prostaglandins (PGE₂, PGI₂) — synthesised via COX-1; stimulate mucus and bicarbonate secretion, maintain mucosal blood flow, promote epithelial restitution
5. Rapid epithelial cell turnover — gastric epithelium renews every 3–7 days

The pancreas is a retroperitoneal organ lying transversely across the posterior abdominal wall at the level of L1–L2. It has a head (nestled in the C-loop of the duodenum), uncinate process (hooks behind the superior mesenteric vessels), neck, body, and tail (extending to the splenic hilum).

Key vascular relationships ^[7][8]:

• The superior mesenteric artery (SMA), hepatic artery, coeliac trunk, superior mesenteric vein (SMV), and portal vein (PV) all pass in close proximity — this is why pancreatic tumours can encase these vessels making them unresectable ^[7][8]
• The common bile duct (CBD) passes through the head of the pancreas before joining the main pancreatic duct (of Wirsung) at the ampulla of Vater — this is why head of pancreas tumours cause painless obstructive jaundice ^[7][8]

Pancreatic ducts:

• Main pancreatic duct (of Wirsung) joins the CBD at the ampulla of Vater
• Accessory duct (of Santorini) drains via the minor papilla
• Pancreatic divisum: MC congenital anomaly — failure of fusion of dorsal and ventral ductal systems

Why does pancreatic pain radiate to the back? The pancreas is retroperitoneal, lying directly anterior to the aorta and vertebral bodies (T12–L2). Inflammatory or neoplastic processes irritate the retroperitoneal nerve plexuses (coeliac and superior mesenteric plexuses), causing referred pain to the back.

• Gallbladder sits on the visceral surface of the liver (segments 4b and 5)
• Hartmann's pouch: infundibulum of the gallbladder where stones commonly impact
• Cystic duct → joins the common hepatic duct to form the common bile duct (CBD)
• CBD descends behind the first part of the duodenum and through the head of the pancreas
• Courvoisier's Law: In painless jaundice with an enlarged gallbladder, the cause is unlikely to be gallstone — because a gallbladder chronically inflamed by stones becomes fibrotic and cannot distend; therefore think of periampullary tumours ^[9]

GERD: Condition that develops when reflux of stomach contents causes troublesome symptoms and/or complications (Montreal definition, 2006) ^[4].

Pathophysiology ^[1][4]:

• Incompetent lower oesophageal sphincter (LES): transient LES relaxation (early) or persistent weakness (late)
• Increased intra-abdominal pressure: obesity, pregnancy, chronic cough, constipation
• Hiatus hernia: sliding type (Type 1) — upper stomach slides up through oesophageal hiatus → loss of intra-abdominal oesophageal segment → loss of the "pinch" effect → functional LES weakness
• Delayed oesophageal clearance: defective peristalsis → prolonged acid exposure
• Gastric dysmotility: delayed gastric emptying

Why does GERD cause epigastric pain? The refluxed acid contacts the squamous epithelium of the lower oesophagus (which lacks the protective mucus-bicarbonate layer of the stomach), causing chemical irritation → oesophagitis → retrosternal burning (heartburn). Some patients present with an "acid feeling in the stomach" or epigastric burning rather than classic heartburn — this is the atypical presentation more common in Asians ^[4].

Risk factors ^[1][4]:

• ↓ LES tone: genetic determinants, hiatus hernia, alcohol, caffeine, smoking
• Drugs: NSAIDs, CCBs, beta-blockers, nitrates, anticholinergics
• ↑ Intra-abdominal pressure: pregnancy, obesity, chronic cough, constipation

Functional dyspepsia (FD): dyspepsia in the absence of detectable organic disease ^[2].

Rome IV Subtypes ^[2]:

1. Postprandial distress syndrome (PDS): postprandial fullness + early satiety (≥ 3 days/week)
2. Epigastric pain syndrome (EPS): epigastric pain or burning (≥ 1 day/week)
3. Overlap of both

Pathophysiology (not well understood, multifactorial) ^[2]:

• Gastric dysmotility and impaired compliance → distension-like feeling
• Visceral hypersensitivity → ↓ threshold for pain even with normal gastric compliance
• H. pylori infection → evidence weak but eradication relieves symptoms in a minority
• Altered gut microbiome
• Psychological factors → anxiety and depression strongly associated
• Diet and genetics

Epidemiology: ↓ trend globally but ↑ in Asia; 6th in incidence, 4th in cancer mortality; adenocarcinoma (90%) > lymphoma (5%) > GIST, metastasis; site: distal stomach (antrum/pylorus) > cardia (↑ trend) > OGJ ^[5][6].

Risk factors ^[5][6]:

• Compensatory epithelial cell proliferation:
  • H. pylori → chronic atrophic gastritis → intestinal metaplasia → body/distal CA (intestinal type)
  • Chronic gastric reflux (e.g., Barrett's oesophagus) → proximal CA
  • History of gastric resection → bile reflux (e.g., Billroth II) → chronic gastritis
  • Chronic atrophic gastritis associated with pernicious anaemia and Ménétrier's disease
• Environmental factors: smoking, smoked/pickled food, nitrosamines, alcohol
• Host factors: hereditary diffuse gastric carcinoma (HDGC: E-cadherin mutation), HNPCC, FAP, Peutz-Jeghers syndrome ^[5][6]
• Adenomatous polyps ^[6]
• Previous partial gastrectomy ( > 20 years) ^[6]
• EBV infection (~10%) ^[5]
• Industrial exposure (dusty, high temperature, rubber, coal mining, metal processing, chromium production) ^[6]
• Pernicious anaemia ^[6]
• Common variable immunodeficiency (CVID) ^[6]

Classification (Lauren) ^[5]:

Pathophysiology of epigastric pain in gastric cancer: The tumour invades the gastric wall → serosal irritation and involvement of the coeliac plexus → constant, dull epigastric pain. Antral tumours may cause gastric outlet obstruction → distending pain with vomiting. Ulceration within the tumour mimics peptic ulcer pain.

Types: ductal adenocarcinoma (90%); cystic tumours, ampullary tumours, islet cell tumours (better prognosis); metastasis from RCC (MC), lung, breast ^[7][8].

Sites: head (60%), body (15%), tail (5%), diffuse (20%) ^[7].

Risk factors ^[7][8]:

• Smoking (3× risk)
• DM, chronic pancreatitis
• Family history
• Pre-malignant conditions: pancreatic intraepithelial neoplasia (PanIN)
• Hereditary cancer syndromes: Lynch syndrome

Pathophysiology ^[7][8]:

• Head tumours obstruct the CBD → painless progressive obstructive jaundice (the classic presentation) ^[7][8]
• Body/tail tumours infiltrate the retroperitoneum → severe epigastric pain radiating to the back (because the coeliac plexus sits directly behind the pancreas) ^[7]
• Pancreatic duct obstruction → pancreatic exocrine insufficiency → steatorrhoea, maldigestion, new-onset diabetes
• Trousseau syndrome: hypercoagulable state → migratory superficial thrombophlebitis (mucin-secreting adenocarcinomas release tissue factor and other procoagulant substances) ^[7]

Definition: Acute inflammation of the pancreatic parenchyma ^[1][9].

Aetiology (mnemonic: GAME ID) ^[9]:

• G — Gallstone (MC): impacted stone at ampulla → duct obstruction → reflux + duct hypertension → premature enzyme activation
• A — Alcohol: direct toxic effect on acinar cells + increases ductal permeability
• M — Metabolic: hypertriglyceridaemia, hypercalcaemia
• E — ERCP (reduced by PR NSAID or temporary pancreatic stenting)
• I — Idiopathic (10%)
• D — Drugs (NSAIDs, steroids, azathioprine, ACEi, valproate)
• Others: trauma, infections (mumps), autoimmune (SLE), pregnancy, scorpion venom, pancreatic divisum

Pathophysiology ^[1][9]:

1. Initial insult: unregulated premature activation of pancreatic enzymes (especially trypsinogen → trypsin) within acinar cells
2. Autodigestion: trypsin activates other zymogens → autodigestion of pancreatic parenchyma → necrosis
3. Extension: autodigestion extends into retroperitoneum → fat necrosis (fatty acids bind calcium = saponification → hypocalcaemia → tetany)
4. Systemic response: NF-κB pathway → cytokines (TNF-α, IL-1, IL-6) → SIRS → organ dysfunction (ARDS, AKI, shock)
5. Enzymes in bloodstream: amylase and lipase leak into blood (diagnostic) → distant organ injury

Biliary colic ^[9]:

• Transient obstruction of Hartmann's pouch or cystic duct by gallstone → gallbladder contracts against obstruction → steady (not truly colicky — gallbladder has no peristalsis) RUQ/epigastric pain
• Worse after fatty meals (fat in duodenum → CCK release → gallbladder contraction)
• Usually resolves < 6 hours; if > 6 hours → suspect acute cholecystitis

Acute cholecystitis ^[9]:

• Calculous (95%): persistent cystic duct obstruction → gallbladder distension → ↑ intraluminal pressure → mucosal ischaemia → secondary bacterial infection
• Acalculous (5%): critically ill patients (dehydration, shock, TPN) → gallbladder stasis and ischaemia

Definition: clinical syndrome characterised by epigastric pain and post-prandial vomiting due to mechanical obstruction ^[10].

Aetiology: malignant until proven otherwise ^[10]:

• Malignant (80%): gastric cancer (MC), lymphoma; extraluminal compression (CA head of pancreas, CA ampulla, cholangioCA)
• Benign (20%): PUD-related pyloric stenosis (2nd MC), gastric volvulus, SMA syndrome, foreign body/bezoar, Bouveret syndrome (gallstone in duodenum), chronic pancreatitis, Crohn's disease

Perforated peptic ulcer ^[3]:

• Anterior duodenal ulcer perforates → gastric acid leaks into peritoneal cavity → chemical peritonitis (immediate, intense pain) → secondary bacterial peritonitis (hours later)
• Pain starts in epigastrium → generalises to the whole abdomen
• Board-like rigidity, pneumoperitoneum on CXR

Acute myocardial infarction (inferior wall) ^[11]:

• The inferior wall of the left ventricle sits on the diaphragm → ischaemia/infarction → afferent fibres travel with the phrenic nerve and sympathetic chain → referred pain to the epigastrium
• Especially common in diabetics (autonomic neuropathy masks typical chest pain)
• Always do an ECG in any patient with epigastric pain, especially if risk factors for IHD

Abdominal aortic aneurysm (AAA) rupture:

• Aorta lies retroperitoneally at the level of the epigastrium → expanding or leaking AAA → sudden epigastric/back pain + haemodynamic collapse
• Classic triad: abdominal pain + hypotension + pulsatile abdominal mass

Gastric volvulus ^[10]:

• Abnormal rotation of stomach > 180° → closed-loop obstruction ± strangulation
• Usually secondary to diaphragmatic/hiatal hernia (rolling type)
• Borchardt's triad: severe epigastric pain, retching without vomiting, inability to pass NG tube below diaphragm

High Yield: When distinguishing pancreatitis from PUD — PUD has long-standing intermittent epigastric pain, NSAID use/HP infection, and normal amylase and lipase; PPU has early florid peritoneal signs, free gas under diaphragm on erect CXR, and lipase/amylase < 3× ULN ^[16].

Think surgical emergency until proven otherwise:

• Perforated peptic ulcer
• Acute pancreatitis
• Ruptured AAA
• Acute mesenteric ischaemia
• Acute MI (inferior)
• Gastric volvulus
• Boerhaave's perforation (oesophageal rupture — after forceful vomiting)

Think organic vs functional:

• Functional dyspepsia (most common — 60% of dyspepsia presentations) ^[1]
• PUD (H. pylori, NSAIDs)
• GERD
• Chronic pancreatitis
• Gastric/pancreatic cancer (if alarm features)
• Drug-induced dyspepsia
• Coeliac disease, Crohn's disease (less common)

Think hepatobiliary/pancreatic:

• Choledocholithiasis ± cholangitis
• CA head of pancreas (painless jaundice) / body-tail (painful jaundice)
• Acute hepatitis
• Cholangiocarcinoma
• Periampullary tumour

Think mucosal pathology:

• PUD (MC cause of UGIB) ^[12]
• Gastritis / duodenitis (erosive)
• Oesophageal varices (portal hypertension)
• Gastric cancer
• Mallory-Weiss tear
• Dieulafoy's lesion
• Angiodysplasia

Think malignancy or malabsorption:

• Gastric cancer
• Pancreatic cancer
• Chronic pancreatitis (malabsorption)
• Coeliac disease
• Functional dyspepsia (afraid to eat → weight loss, but mild)

Functional dyspepsia (FD) is a diagnosis of exclusion — you must first rule out organic disease ^[1][2].

Rome IV diagnostic criteria (updated from Rome III) ^[1][2]:

Presence of one or more of the following, with no evidence of structural disease (including at upper endoscopy) to explain the symptoms:

• Bothersome postprandial fullness
• Bothersome early satiation
• Bothersome epigastric pain
• Bothersome epigastric burning

Criteria fulfilled for the last 3 months with symptom onset ≥ 6 months before diagnosis.

Two subtypes:

• Postprandial distress syndrome (PDS): postprandial fullness and/or early satiation occurring ≥ 3 days/week
• Epigastric pain syndrome (EPS): epigastric pain and/or burning occurring ≥ 1 day/week

Supportive remarks ^[1]:

• Pain may be induced or relieved by ingestion of a meal, or may occur while fasting
• Pain does not fulfil biliary pain criteria
• Vomiting warrants consideration of another disorder
• Heartburn is not a dyspeptic symptom but may often coexist
• Symptoms relieved by evacuation of faeces or gas should generally not be considered as part of dyspepsia

Diagnostic criteria: ≥ 2 out of 3 ^[9][16]:

Key points ^[9][16]:

• Pancreatic enzyme elevation is NOT indicative of severity — it tells you the diagnosis, not the prognosis ^[9]
• Imaging is usually only needed if the diagnosis is in doubt (i.e., amylase/lipase is equivocal but clinical suspicion is high) ^[16]
• Early CT scan ( < 3 days) will not show necrotic/ischaemic areas — necrosis takes 48–72 hours to demarcate ^[16]

Diagnostic criteria (Sensitivity 91.2%, Specificity 96.9%) ^[18][19]:

Interpretation ^[18][19]:

• Suspected diagnosis = 1× item in A + 1× item in B
• Definite diagnosis = 1× item in A + 1× item in B + 1× item in C

Why this structure? Because you want both clinical and radiological confirmation — clinical signs alone have limited specificity (Murphy's sign: Sens 50–65%, Spec 79–96%), and imaging alone may show incidental cholecystitis in asymptomatic patients ^[19].

Detection of rise and/or fall of cardiac biomarkers (preferably cTn) with ≥ 1 value above 99th percentile URL, PLUS ≥ 1 of ^[11][20]:

1. Symptoms of ischaemia
2. New or presumed new significant ST-T changes or new LBBB
3. Development of pathological Q waves
4. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
5. Identification of an intracoronary thrombus by angiography or post-mortem

This is critical because inferior MI can present as isolated epigastric pain — you diagnose it by ECG + troponin, not by abdominal examination.

PUD is diagnosed by direct visualisation at upper endoscopy (OGD) with biopsy ^[1][3]. There are no validated clinical diagnostic criteria — history alone cannot reliably distinguish PUD from functional dyspepsia or gastric cancer. This is why OGD is the definitive investigation.

GERD can be diagnosed clinically when typical symptoms (heartburn + regurgitation) are present ^[4]. A PPI therapeutic trial (1–4 weeks) serves as both diagnostic and therapeutic — symptom improvement strongly suggests GERD ^[1]. Definitive testing (pH monitoring, impedance) is reserved for refractory cases.

The approach to a patient with epigastric pain depends on two critical decision points:

1. Is this an acute emergency? → Stabilise first, then investigate
2. Are alarm features present? → Determines urgency and type of investigation

1. Why ECG first in acute epigastric pain?

Because inferior MI can mimic an acute abdomen, and the treatment (reperfusion) is time-critical. An ECG takes 30 seconds and can save a life. Always ECG + cardiac enzymes to rule out basal MI ^[3][11][18].

2. Why erect CXR?

Erect CXR looks for free gas under diaphragm → pneumoperitoneum → perforation ^[3][18]. This is the fastest way to diagnose a perforated peptic ulcer. Also evaluates for: left-sided pleural effusion (pancreatitis, Boerhaave's), widened mediastinum (aortic dissection), basal pneumonia.

3. Why amylase/lipase?

Because acute pancreatitis requires ≥ 3× ULN for diagnosis — and the treatment pathway (aggressive fluid resuscitation, aetiology-directed therapy) is completely different from PUD or biliary colic ^[9][16].

4. The age threshold for OGD

In Hong Kong, age ≥ 40 years with new-onset dyspepsia warrants OGD (lower than Western guideline of ≥ 55) due to higher gastric cancer prevalence in East Asia ^[2].

5. Test-and-treat for H. pylori

In young patients ( < 40) without alarm features, a non-invasive H. pylori test (urea breath test or stool antigen test) is the first step — because HP eradication can cure a subset of both PUD and functional dyspepsia without needing endoscopy ^[2].

Upper Endoscopy (OGD — Oesophago-gastro-duodenoscopy)

OGD is the definitive investigation for the upper GI tract. It is both diagnostic and therapeutic ^[1][3].

Indications ^[1]:

• Symptom-based: anaemia, haematemesis, melaena, epigastric pain, dysphagia, acid reflux, indigestion
• Disease-based: PUD follow-up, suspected oesophageal/gastric cancer, oesophageal variceal treatment, foreign body ingestion

Contraindications ^[1]: Known/suspected perforation; recent MI

Key findings and their significance ^[1]:

Forrest classification — endoscopic stigmata of recent haemorrhage (SRH), used to prognosticate rebleeding risk and guide therapy ^[1]:

High Yield: Forrest Class I and IIa/IIb are high risk and require endoscopic haemostasis. Class IIc and III are low risk and can be managed with acid suppression alone ^[1].

Biopsy protocol at OGD:

• All gastric ulcers must be biopsied (to exclude malignancy) — duodenal ulcers are rarely malignant and do not routinely need biopsy
• H. pylori testing should be done on biopsy sample (rapid urease test / histology) ^[2]
• Follow-up OGD for gastric ulcers at 6–8 weeks to confirm healing and re-biopsy if not healed

H. pylori testing is central to the diagnostic approach to epigastric pain, because it determines management for both PUD and functional dyspepsia ^[1][2].

Why stop PPI before HP testing? PPIs suppress H. pylori replication and reduce urease activity → false-negative results on urease-based tests (CLO test, UBT). Always stop PPI ≥ 2 weeks and antibiotics ≥ 4 weeks before testing ^[1][2].

Any patient presenting with acute severe epigastric pain needs the ABCDE approach before any specific treatment ^[23][24]:

When epigastric pain is accompanied by haematemesis/melaena ^[23][24]:

• Bloods: CBC (baseline Hb), clotting, cross-match, LRFT, VBG (acidosis)
• RFT: elevated urea:creatinine ratio ( > 100:1) — because Hb digestion in the gut generates urea + reduced renal perfusion from hypovolaemia ^[23]
• Pre-endoscopic PPI: IV esomeprazole 80 mg stat → 8 mg/h infusion until OGD (only if early endoscopy cannot be arranged; raising gastric pH stabilises clots) ^[23]
• Risk stratification:

Definitive treatment: Early laparoscopic cholecystectomy (LC) — ideally within 72 hours of symptom onset. This is supported by current guidelines because:

• Early LC has comparable morbidity to delayed LC
• ↓ Overall hospital stay
• ↓ Risk of recurrent attacks while waiting for interval surgery

First-line approach: Endoscopic retrograde cholangiopancreatography (ERCP) ± biliary stenting ^[28]

• IV broad-spectrum antibiotics (cover Gram-negatives: e.g., piperacillin-tazobactam, or ceftriaxone + metronidazole)

• ERCP for biliary decompression: sphincterotomy + stone extraction + stenting

• Potential complications of ERCP: perforation, bleeding from papillotomy, pancreatitis ^[28]

• Relative contraindications for ERCP: altered GI anatomy e.g., Billroth II gastrectomy, Roux-en-Y ^[28]

• If ERCP not feasible: PTBD (percutaneous transhepatic biliary drainage) or surgical exploration of CBD

• Prevent recurrence: elective LC after recovery

High Yield: Reinvestigate by OGD if symptoms persist despite multiple treatments — do not keep treating empirically indefinitely ^[2].

Criteria for unresectability ^[5]:

• Distant metastasis
• Invasion of major vascular structures (aorta)
• Encasement/occlusion of coeliac axis, proximal splenic artery, or hepatic artery (distal splenic artery involvement is NOT a contraindication)

Assess resectability — this is the central decision point ^[7][8]:

Vascular encasement by SMA, hepatic artery, coeliac trunk, SMV, or portal vein determines resectability on CT pancreas protocol ^[7][8].

• Acute: NPO, analgesia (NSAIDs preferred — e.g., diclofenac IM; opioids if severe), antiemetics ^[9]
• Definitive: Elective laparoscopic cholecystectomy — to ↓ risk of future complications (cholecystitis, cholangitis, pancreatitis) ^[9]

The leading cause of death in peptic ulcer disease (5–15% mortality) ^[1][10].

Pathophysiology: The ulcer erodes through the mucosa and submucosa into a submucosal or serosal artery. Posterior duodenal ulcers classically erode into the gastroduodenal artery (GDA) because the GDA runs directly behind the first part of the duodenum ^[1][10]. Gastric ulcers may erode into the left gastric artery or splenic artery.

Clinical features ^[1]:

• Haematemesis: vomiting of red blood (rapid bleed) or coffee-ground material (slow bleed — Hb oxidised to acid haematin by gastric acid)
• Melaena: black tarry stools (Hb digested by gut bacteria → dark pigment)
• Haematochezia: fresh red blood per rectum in massive upper GI bleeding (transit too rapid for digestion)
• Postural hypotension, tachycardia, syncope (hypovolaemia)

Signs of rebleeding ^[1]: haematemesis, fresh melaena, tachycardia, falling Hb trend, fresh blood from NGT

Why does bleeding recur after initial haemostasis? The clot that forms over the eroded vessel is unstable in an acidic environment — gastric acid (pH < 6) inhibits platelet aggregation and promotes clot fibrinolysis. This is why IV PPI (to raise gastric pH above 6) after endoscopic haemostasis is critical for clot stabilisation ^[1][24].

Pathophysiology: The ulcer erodes through the full thickness of the gastric or duodenal wall into the peritoneal cavity. Anterior duodenal ulcers perforate (because there is no adjacent solid organ to seal them off — they face the free peritoneal cavity), whereas posterior duodenal ulcers bleed (they face the retroperitoneum and the GDA) ^[1][3].

Sequence of events ^[3]:

1. Chemical peritonitis (immediate): Gastric acid (pH 1–2) spills into the peritoneal cavity → intense chemical irritation → sudden excruciating epigastric pain → board-like rigidity
2. "Silent interval" (4–6h): Acid becomes diluted by peritoneal fluid → pain and guarding may paradoxically decrease — but the peritonitis is still progressing
3. Bacterial peritonitis (late): Gut flora contaminate the peritoneal cavity → sepsis, systemic toxicity

Clinical features ^[1][3]:

• Fever, tachycardia, hypotension
• Acute onset of severe diffuse abdominal pain (initially epigastric → generalises)
• Board-like rigidity; ↓ liver dullness on percussion (pneumoperitoneum)
• Erect CXR: free gas under diaphragm

Pathophysiology: The ulcer erodes through the bowel wall without free perforation — the base of the ulcer penetrates into an adjacent solid organ that seals it off. This is because the inflammatory process creates adhesions between the ulcer base and the adjacent organ before full-thickness perforation occurs ^[1].

Sites of penetration (in descending order of frequency) ^[1]:

• Pancreas (most common) → pancreatitis
• Lesser omentum
• Biliary tract → cholangitis
• Liver
• Greater omentum
• Mesocolon
• Colon → fistulisation
• Vascular structures → haemorrhage

Clinical features ^[1]:

• Change in pain character: more intense, longer duration
• Shift from vague visceral discomfort to localised intense pain in the back (pancreatic penetration)
• NOT relieved by food or antacids (unlike uncomplicated PUD)

Pathophysiology: Two mechanisms, often coexisting ^[1]:

1. Acute: Inflammation and oedema from active ulcer → duodenal spasm → reversible obstruction
2. Chronic: Repeated cycles of ulceration → healing with fibrosis and scarring → fixed pyloric/duodenal stenosis → irreversible obstruction

Clinical features ^[1][10]:

• Epigastric pain after eating, early satiety, bloating, nausea and vomiting
• Non-bilious projectile vomiting of undigested food (obstruction is proximal to ampulla of Vater → no bile in vomitus)
• Succussion splash on examination (retained gastric content)
• Weight loss, dehydration
• Metabolic consequences: prolonged vomiting → loss of H⁺, Cl⁻, K⁺ → hypokalaemic, hypochloraemic metabolic alkalosis ^[1]

Pathophysiology: Chronic ulcer penetrates completely through the bowel wall into an adjacent hollow viscus, creating an abnormal communication ^[1].

Why does infected necrosis develop? Pancreatic necrosis creates a devitalised tissue bed — an ideal medium for bacterial colonisation. Gut bacteria (mainly Gram-negative bacilli) translocate across the inflamed, permeable intestinal wall into the peripancreatic tissue via the portal circulation or lymphatics. This typically occurs after > 7–10 days of disease onset ^[27].

General ^[29]:

• Immediate: bleeding, injury to nearby organs (pancreas, duodenum)
• Early: wound infection, chest infection, post-op ileus
• Late: recurrence (usually at gastric bed)

Anastomosis-Related ^[1][5][29]:

Motility-Related ("Post-Gastrectomy Syndromes") ^[1][5][29]:

Nutritional Deficiencies ^[5][29]: