# Perforated Peptic Ulcer

## Overview

Perforated peptic ulcer (PPU) is a life-threatening surgical emergency occurring in approximately 2 to 10% of patients with peptic ulcer disease. Despite advances in acid suppression therapy and *H. pylori* eradication, PPU remains a significant cause of morbidity and mortality, with overall mortality of 5 to 25% that rises to 30 to 50% in elderly patients with delayed presentation. Prompt recognition, resuscitation, and surgical repair are essential.

## Epidemiology and Risk Factors

The annual incidence of PPU is 3 to 14 per 100,000 population. Duodenal ulcer perforations are more common than gastric ulcer perforations. A critical anatomic point is that anterior duodenal ulcers perforate into the peritoneal cavity, whereas posterior ulcers erode into the gastroduodenal artery and present with bleeding. Risk factors include NSAID use (the most important modifiable risk factor), *H. pylori* infection, smoking, alcohol use, corticosteroid use, physiologic stress (in ICU patients, burn patients, and those with traumatic brain injury), crack cocaine use, and Zollinger-Ellison syndrome.

## Pathophysiology

Perforation occurs when an ulcer penetrates through all layers of the bowel wall. Chemical peritonitis develops immediately as gastric or duodenal contents spill into the peritoneum, with bacterial peritonitis following within 6 to 12 hours. The most common site of perforation is the **anterior duodenal wall** (60%), which results in free perforation into the peritoneal cavity. Anterior gastric wall perforations along the lesser and greater curvature also occur. In some cases, the omentum or adjacent organs wall off the leak, creating a sealed or contained perforation that may present as a localized abscess.

## Clinical Presentation

### Classic Presentation

The hallmark is **sudden onset of severe, diffuse abdominal pain** -- patients can often identify the exact moment the pain began. Pain typically begins in the epigastrium and rapidly becomes generalized. The patient lies motionless, consistent with peritonitis. Some patients have a prior history of dyspepsia or known ulcer disease, but many perforations occur without preceding symptoms. Nausea and vomiting are variable.

### Physical Examination

**Board-like rigidity** (involuntary guarding of the entire abdomen) is the hallmark physical finding. Diffuse tenderness with rebound is present, and bowel sounds are absent. Tachycardia and hypotension develop in advanced cases. Fever may be absent early. Referred shoulder pain results from diaphragmatic irritation by free air or fluid.

### Three-Phase Clinical Course

The clinical course follows three phases described by Boas. The **phase of contamination** (0 to 2 hours) features sudden severe pain and peritoneal irritation. The **phase of reaction** (2 to 12 hours) may produce a deceptive improvement -- the "treacherous interval" -- as localized fluid dilutes the chemical irritants. The **phase of peritonitis** (beyond 12 hours) brings fever, sepsis, abdominal distension, and clinical deterioration.

## Diagnostic Workup

### Laboratory Studies

The CBC shows leukocytosis. The BMP may reveal dehydration markers with elevated BUN and creatinine. Amylase may be mildly elevated from leaked duodenal contents. Lactate is elevated in sepsis or shock. A type and crossmatch should be sent.

### Imaging

An **erect chest X-ray** demonstrates pneumoperitoneum (free air under the diaphragm) in 70 to 80% of cases, with the left lateral decubitus or erect CXR being the most sensitive views. However, absence of free air does not exclude perforation, as 20 to 30% of cases are negative. **CT abdomen/pelvis** has a sensitivity exceeding 95% for detecting free air, even in tiny amounts, and identifies the site of perforation, free fluid, and abscess formation. Oral contrast leak may be visible. CT is the study of choice when the diagnosis is uncertain and can exclude other diagnoses such as pancreatitis, appendicitis, and mesenteric ischemia.

### Boey Score

The Boey score provides prognostic information based on three risk factors (one point each):

| Risk Factor | Points |
|------------|--------|
| Major medical illness (ASA III–V) | 1 |
| Preoperative shock (SBP <90 mmHg) | 1 |
| Duration of perforation >24 hours | 1 |

| Boey Score | Predicted Mortality |
|-----------|-------------------|
| 0 | ~1% |
| 1 | ~10% |
| 2 | ~45% |
| 3 | ~100% |

A score of 0 predicts mortality of approximately 1%; score 1, approximately 10%; score 2, approximately 45%; and score 3, approximately 100%.

## Management

### Initial Resuscitation

Initial management includes NPO status, nasogastric decompression, aggressive IV fluid resuscitation, broad-spectrum antibiotics (covering gram-negatives and anaerobes), PPI infusion (IV pantoprazole), Foley catheter for urine output monitoring, and correction of electrolyte abnormalities.

### Operative Management

#### Graham Patch Repair (Omental Patch)

The **Graham patch repair** is the most commonly performed procedure for PPU. Three interrupted sutures are placed across the perforation, incorporating full-thickness healthy tissue on either side. A free omental pedicle (tongue of omentum) is laid over the perforation, and the sutures are tied over the omentum, sealing the defect. This technique is applicable to both duodenal and gastric perforations and is simple, rapid, and effective. It is followed by lifelong PPI therapy and *H. pylori* eradication.

#### Laparoscopic Repair

Laparoscopic repair is increasingly the preferred approach when expertise is available. The same principles as the open Graham patch apply, with benefits including reduced wound complications, less postoperative pain, and shorter hospital stay. Leak rates are comparable to open repair in experienced hands. Contraindications to the laparoscopic approach include hemodynamic instability, delayed presentation beyond 24 hours with extensive peritoneal contamination, and large perforations exceeding 2 cm.

#### Definitive Ulcer Surgery

Definitive acid-reducing surgery is rarely performed in the PPI era. Historical procedures include truncal vagotomy with pyloroplasty (incorporating the perforation repair), truncal vagotomy with antrectomy (Billroth I or II reconstruction), and highly selective vagotomy (parietal cell vagotomy) with patch closure. Definitive surgery is considered only for patients with documented PPI non-compliance and recurrent ulcer disease, patients unable to take or access PPI therapy long-term, or giant duodenal ulcers requiring resection.

#### Gastric Ulcer Perforation

Perforated gastric ulcers require biopsy or excision to exclude malignancy, as 10 to 15% harbor cancer. Small perforations can be managed with wedge excision of the ulcer edge and patch closure, while large or suspicious perforations require distal gastrectomy. The approach is guided by ulcer location according to the Johnson classification:

| Johnson Type | Location | Acid Status | Surgical Procedure |
|-------------|----------|-------------|-------------------|
| I | Lesser curve, body | Low/normal acid | Excisional biopsy or distal gastrectomy |
| II | Gastric body + duodenal ulcer | High acid | Vagotomy with antrectomy |
| III | Prepyloric | High acid | Vagotomy with antrectomy |
| IV | High lesser curve (near GEJ) | Low/normal acid | Subtotal gastrectomy |

Type I (lesser curve, body) requires excisional biopsy or distal gastrectomy; Type II (gastric body combined with duodenal ulcer) and Type III (prepyloric) require vagotomy with antrectomy; and Type IV (high lesser curve) requires subtotal gastrectomy.

### Non-Operative Management (Taylor Method)

Non-operative management is appropriate only in selected cases: sealed perforations in clinically stable patients without generalized peritonitis. Components include NPO status, nasogastric decompression, IV PPI, and IV antibiotics. A water-soluble contrast study confirms the perforation is sealed. Close monitoring with serial abdominal examinations is essential, with a low threshold for operative intervention if deterioration occurs. The success rate is 70 to 80% in highly selected patients, but there is a higher risk of intra-abdominal abscess.

## Postoperative Management

Postoperative care includes continuing IV PPI with transition to oral PPI when tolerating a diet. **H. pylori testing and treatment** is critical to prevent recurrence -- testing can be performed by biopsy at the time of surgery or with a stool antigen or urea breath test postoperatively. Eradication reduces recurrence from approximately 60% to less than 5%. NSAIDs should be stopped permanently if possible; if an NSAID is required, a COX-2 selective agent with PPI co-therapy is used. Repeat endoscopy at 6 to 8 weeks is necessary for gastric ulcers to confirm healing and exclude malignancy.

## Complications

Complications include intra-abdominal abscess (subphrenic, pelvic, or interloop) in 5 to 10% of cases, managed by percutaneous or surgical drainage. Wound infection rates are higher with contamination and the open approach. Reperforation or leak occurs in 2 to 5% and requires reoperation. Postoperative ileus usually resolves with conservative management. Sepsis and multiorgan failure are the major causes of mortality.

<image>Erect chest X-ray demonstrating pneumoperitoneum with free air visible as a lucent crescent beneath both hemidiaphragms in a patient with perforated peptic ulcer. Include a comparison panel showing a CT scan axial image with extraluminal free air anterior to the liver and a focal defect in the anterior duodenal wall indicating the site of perforation. Label the free air, duodenal wall defect, and adjacent free fluid.</image>

<image>Surgical illustration demonstrating the Graham omental patch repair technique for a perforated duodenal ulcer. Show the step-by-step procedure: (1) identification of the anterior duodenal perforation, (2) placement of three interrupted full-thickness sutures across the perforation, (3) mobilization and positioning of a pedicled omental tongue over the defect, and (4) final result with sutures tied over the omentum creating a sealed repair. Include anatomical landmarks (pylorus, duodenum, gallbladder).</image>

<image>Classification diagram of gastric ulcer types (Johnson classification): Type I (lesser curvature, body), Type II (gastric body combined with duodenal ulcer), Type III (prepyloric), and Type IV (high lesser curvature near GEJ). Show each type on a stomach outline with the associated acid production status (low acid for Type I, high acid for Types II and III) and the recommended surgical procedure for each type when perforation occurs.</image>

## Clinical Pearls

A patient who can identify the exact moment their abdominal pain began likely has a visceral perforation until proven otherwise. Board-like rigidity is the hallmark physical finding of free perforation with generalized peritonitis. Absence of free air on erect CXR does not exclude perforation -- CT is far more sensitive and should be obtained when clinical suspicion remains. In the PPI era, simple Graham patch repair with postoperative PPI therapy and *H. pylori* eradication has largely replaced definitive acid-reducing surgery. All perforated gastric ulcers must be biopsied or excised to exclude malignancy, as 10 to 15% harbor cancer. The Boey score (medical comorbidity, shock, perforation duration beyond 24 hours) reliably predicts mortality risk. The "treacherous interval" at 2 to 12 hours post-perforation may create a false sense of clinical improvement before peritonitis becomes established. NSAID cessation and *H. pylori* eradication are the two most important measures to prevent recurrence after PPU repair. Laparoscopic repair is feasible and preferred when expertise is available, but should be converted to open for hemodynamic instability, large perforations, or extensive contamination.

## References

- Soreide K, Thorsen K, Harrison EM, et al. Perforated peptic ulcer. *Lancet*. 2015;386(10000):1288-1298.
- Lau JY, Sung J, Hill C, et al. Systematic review of the epidemiology of complicated peptic ulcer disease: incidence, recurrence, risk factors and mortality. *Digestion*. 2011;84(2):102-113.
- Bertleff MJ, Lange JF. Perforated peptic ulcer disease: a review of history and treatment. *Dig Surg*. 2010;27(3):161-169.
- Thorsen K, Glomsaker TB, von Meer A, et al. Trends in diagnosis and surgical management of patients with perforated peptic ulcer. *J Gastrointest Surg*. 2011;15(8):1329-1335.