Emergency Medicine Hub / Gastrointestinal & Abdominal • 3 min read • 2 sections

Peptic Ulcer Disease & Perforated Viscus

Comprehensive emergency evaluation and protocolized resuscitation of peptic ulcer disease (PUD) complications and acute gastrointestinal perforation: Helicobacter pylori infection vs. COX-1 NSAID-induced mucosal ulceration, sudden onset excruciating epigastric pain progressing to diffuse chemical and purulent peritonitis ('board-like' abdominal rigidity), radiographic detection of free intraperitoneal air (pneumoperitoneum: subdiaphragmatic crescent on upright CXR, Rigler's sign, falciform ligament sign on CT), rapid blood resuscitation, IV proton pump inhibitors, broad-spectrum IV antimicrobials, and emergent surgical laparotomy.

Resuscitation Quick Actions • First 2 Minutes

High-Acuity

Perforation Clinical Triad

Sudden instantaneous onset severe epigastric pain + 'Board-like' abdominal wall rigidity + Subdiaphragmatic free air on CXR/CT

Subdiaphragmatic Air on CXR

Upright chest X-ray is more sensitive than supine KUB; detect as little as 1 mL of free air under the right hemidiaphragm

Rigler's Double-Wall Sign

On supine KUB: both the inner (luminal) and outer (serosal) borders of the bowel wall are clearly outlined by gas = PNEUMOPERITONEUM

Stat Sepsis Antibiotics

Piperacillin-Tazobactam 4.5g IV OR Ceftriaxone 2g IV + Metronidazole 500 mg IV stat within 60 min of diagnosis

High-Dose IV PPI

Pantoprazole 80 mg IV push, followed by continuous infusion at 8 mg/hr to suppress gastric acid secretion

NG Tube Decompression

Insert 16–18 French sump nasogastric tube to low continuous wall suction to halt ongoing acid leakage into peritoneum

Bottom-Line Clinical Pearl

Perforated peptic ulcer is a hyperacute, time-critical surgical emergency with mortality reaching 30% if surgical source control is delayed > 12–24 hours. The classic presentation is sudden, instantaneous, excruciating epigastric pain that spreads across the abdomen, accompanied by profound physical 'board-like' abdominal rigidity and absent bowel sounds (gastroduodenal acid chemical peritonitis). Upright chest radiography reveals subdiaphragmatic free air (pneumoperitoneum) in 75–85% of cases; non-contrast or IV contrast CT abdomen is the definitive gold standard (> 98% sensitive). Immediate resuscitation requires: (1) Two large-bore IVs with aggressive balanced crystalloid boluses, (2) Large-bore nasogastric (NG) tube placement to evacuate remaining gastric acid, (3) High-dose IV Proton Pump Inhibitor (Pantoprazole 80 mg IV bolus + 8 mg/hr infusion), (4) Immediate broad-spectrum IV antibiotics (Piperacillin-Tazobactam 4.5g IV), and (5) Stat surgical consult for emergent exploratory laparotomy and Graham omental patch repair.

1. Pathophysiology: Chemical vs. Bacterial Peritonitis

Peptic ulcer disease stems from an imbalance between aggressive gastric luminal factors (gastric acid, pepsin, NSAID inhibition of mucosal protective prostaglandins, and Helicobacter pylori chronic inflammation) and mucosal protective barriers (bicarbonate secretion, mucous layer, mucosal blood flow).

When an ulcer erodes through the full thickness of the anterior duodenal bulb (most common site of perforation) or gastric antrum, gastroduodenal contents spill into the lesser sac and peritoneal cavity. The clinical course evolves in three distinct pathophysiological stages:

Stage of Perforation	Timing Post-Perforation	Pathophysiologic Mechanism & Clinical Exam
Stage 1: Acute Chemical Peritonitis	0 to 2 Hours	Spillage of caustic, acidic gastric juice (pH 1.0–2.0) chemically burns the parietal and visceral peritoneum. Sudden, instantaneous, severe epigastric pain (patients often identify the exact second of onset); profound physical 'board-like' rigidity, shallow breathing, tachycardia.
Stage 2: The 'Lucid' Intermediate Illusion	2 to 12 Hours	Peritoneal exudate and transudate dilute the acidic gastric juice, leading to temporary subjective pain reduction. However, severe abdominal wall guarding persists; liver dullness is lost due to free air capping the hepatic dome.
Stage 3: Secondary Bacterial Peritonitis & Septic Shock	> 12 to 24 Hours	Overgrowth of enteric bacteria (E. coli, Klebsiella, Bacteroides) converts the chemical peritonitis into diffuse purulent peritonitis, abdominal distension, septic shock, multi-organ failure, and death without surgery.

2. Radiographic Signs of Pneumoperitoneum

Radiographic Sign	Imaging Modality	Anatomical & Physical Appearance
Subdiaphragmatic Free Air	Upright Chest Radiograph (CXR)	Thin, crescent-shaped lucency beneath the right hemidiaphragm (seen between liver and diaphragm; left diaphragm air can be confused with gastric bubble). Have patient sit upright for 10–15 min prior to film to allow air to rise.
Left Lateral Decubitus Air	Left Lateral Decubitus Abdomen Film	Indicated if patient is too unstable to sit upright; free air outlines the lateral edge of the liver against the right lateral abdominal wall.
Rigler's Sign ('Double-Wall Sign')	Supine Abdominal Film (KUB)	Gas is present on BOTH the inside (luminal) and outside (peritoneal) surfaces of the bowel wall, outlining the intestinal wall as a crisp, distinct white stripe.
Falciform Ligament Sign	Supine Abdomen Film/CT	Free gas outlines the falciform ligament as a thin vertical linear density over the upper mid-abdomen.
Abdominal CT with IV Contrast	Definitive Gold Standard (> 98% sensitive)	Detects micro-pneumoperitoneum (< 1 mL of gas), identifies the exact site of ulcer perforation, and excludes alternative causes (pancreatitis, diverticular rupture).

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