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Duodenal Perforation

Author: Connor Foote Editor: Richard A. Lopez Updated: 8/17/2026 1:40:51 AM

Introduction

Anatomically, the duodenum is the proximal portion of the small intestine, located between the stomach and jejunum. The duodenum includes 4 segments:

  1. The proximal segment is the duodenal bulb, which connects to the liver via the hepatoduodenal ligament containing the hepatic artery, portal vein, and the common bile duct.
  2. The second, or descending, segment surrounds the pancreatic head.
  3. The third segment is the horizontal segment with the superior mesenteric vessels located ventral to it.
  4. The fourth segment continues as the jejunum.

Duodenal perforation is a rare but potentially lethal condition. Please see StatPearls' companion reference, "Anatomy, Abdomen and Pelvis: Duodenum," for further information. The mortality rate ranges from 8% to 25% in published reports.[1][2][3] In 1688, Muralto described a perforated duodenal ulcer, which was reported by Lenepneau.[4]

Subsequently, in 1894, Dean reported the first successful surgical closure of a perforated duodenal ulcer.[5] In 1929, Cellan-Jones described a technique for repairing perforations using an omental patch, and Graham later modified it in 1937.[4][6] Duodenal perforation can be classified as free or contained. Free perforation occurs when bowel contents leak into the abdominal cavity, causing diffuse peritonitis.

Contained perforation occurs when the ulcer creates a full-thickness defect, but adjacent organs, such as the pancreas, wall off the area and prevent free leakage.[4] Peptic ulcer disease is a significant cause of duodenal perforation.[7] Typically, patients with duodenal ulcers experience nocturnal abdominal pain or hunger.

Perforation usually causes a sudden onset of severe upper abdominal pain.[8] However, clinical signs may be subtle or absent in immunocompromised individuals and older adults, delaying diagnosis. Imaging plays an essential role in early diagnosis, which supports prompt resuscitation. Appropriate treatment selection and risk assessment can reduce morbidity and mortality.[9]

Etiology

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Etiology

Underlying Duodenal Pathology

  • Peptic ulcer disease: Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs are the 2 major causes of peptic ulcer disease and subsequent duodenal perforation.[7] Although the incidence of peptic ulcer disease has decreased in recent years, the condition remains the main cause of duodenal perforation.[10]
    • Additional risk factors for perforated peptic ulcers include smoking, physiological stress, a history of peptic ulcer disease, and corticosteroid use.[11]
    • Alcohol consumption increases gastrin secretion and damages the gastric mucosa. However, results from studies did not show that alcohol causes peptic ulcer disease.[12]
  • Duodenal diverticula [13]
  • Infectious disease: tuberculosis, rotavirus, norovirus, and Ascaris lumbricoides infection [14][15][16]
  • Autoimmune conditions: systemic sclerosis, Crohn disease, and polyarteritis nodosa involving the abdomen [17][18][19]
  • Duodenal ischemia [20]
  • Gallstones impacted within the duodenum [21]
  • Chemotherapy [22][23]
  • Tumors [24]

Iatrogenic perforation: The widespread use of endoscopic procedures has increased the frequency of iatrogenic duodenal perforation.[25] The following are examples of iatrogenic causes of duodenal perforation:

  • Endoscopic perforations: Perforation is often due to diagnostic and therapeutic procedures. The incidence of perforation is higher in therapeutic procedures.  
  • Operative injury: Surgical instruments can cause duodenal perforation. Laparoscopic cholecystectomy can cause duodenal perforation in 0.015% of procedures through electrocautery-related thermal injury or blunt or sharp dissection.[26][27]

Trauma: Isolated duodenal injuries are uncommon and usually occur in association with injuries to other organs.[28] 

Foreign bodies: Thin, sharp foreign bodies are associated with a higher risk of perforation.[29]

Spontaneous perforation: Spontaneous duodenal perforation may occur in neonates without an identifiable underlying cause.[30]

Epidemiology

Although the incidence of peptic ulcer disease (PUD) has decreased in recent years, this condition is the leading cause of duodenal perforation.[10] Annually, PUD affects 4 million people worldwide, with an incidence of 1.5% to 3%.[31][32] The decline in PUD incidence is attributed to eradication therapy for Helicobacter pylori infection and the use of proton pump inhibitors.

However, peptic ulcer perforation remains a significant concern. The aging population, overuse of nonsteroidal anti-inflammatory drugs (NSAIDs), and interactions between NSAIDs, selective serotonin reuptake inhibitors, and corticosteroids may contribute to the persistently high incidence of perforation.[3][33] Furthermore, results from studies have shown that the prevalence of H pylori infection ranges from 50% to 80% in patients with perforated duodenal ulcers.[34] Results from other studies also showed that ulcer perforation occurs more frequently in the morning, possibly because of circadian variation in gastric acid secretion.[9]

The reported incidence of duodenal perforation after endoscopic retrograde cholangiopancreatography (ERCP) ranges from 0.09% to 1.67%.[35][36] Sphincter of Oddi dysfunction, older age, precut sphincterotomy, anatomical abnormalities, and contrast medium injection increase the risk of duodenal perforation after ERCP.[37][38] Reported rates of leakage after suturing a duodenal ulcer range from 1% to 13%, whereas rates after endoscopic mucosal resection range from 6% to 13%.[39]

  • Fewer than 2% of traumatic abdominal injuries involve the duodenum.[40]
  • Fewer than 1% of ingested foreign bodies can cause gastrointestinal tract perforation.[41]

Pathophysiology

Underlying Duodenal Pathology

The leading causes of perforated peptic ulcers are NSAID use and H pylori infection.[10] NSAIDs can reduce prostaglandin synthesis by inhibiting cyclooxygenase-1 in the gastrointestinal tract, leading to gastroduodenal mucosal injury. The risk of gastroduodenal mucosal injury associated with NSAID use increases in patients older than 65 and those with heart disease, a history of peptic ulcer disease, or concurrent use of antiplatelet medications, corticosteroids, or anticoagulants.[42]

Prolonged NSAID use and high NSAID doses are additional risk factors for gastroduodenal mucosal injury. Furthermore, results from studies showed that piroxicam and ketorolac have the greatest mucosal injury effects among NSAIDs.[43] H pylori infection also contributes to the development of duodenal ulcers. H pylori may cause duodenal injury and subsequent perforation by inducing gastric metaplasia, stimulating immune responses and gastric acid secretion, and reducing mucosal defenses.[44]

Iatrogenic Perforation

The Stapfer classification categorizes duodenal perforations after ERCP into 4 types. Type I perforations involve the lateral or medial duodenal wall and are caused by the endoscope. Type II perforations are periampullary injuries that occur during sphincterotomy. Type III perforations involve the distal bile duct and result from basket or guidewire instrumentation. Type IV perforations are characterized by retroperitoneal air on imaging and are usually asymptomatic.[45] Type III and IV perforations can be treated conservatively or surgically, with favorable outcomes.[46] 

Duodenal perforation can be free or contained. Free perforation occurs when bowel contents leak freely into the abdominal cavity, causing diffuse peritonitis. Contained perforation occurs when the ulcer creates a full-thickness defect, but adjacent organs, such as the pancreas, wall off the area and prevent free leakage.[4]

In duodenal perforation, gastric acid initially leaks into the peritoneal cavity, leading to profound chemical peritonitis. During this phase, patients may have few or no symptoms. If the perforation does not seal, food particles can enter the peritoneal cavity, and bacterial peritonitis may gradually develop, producing abdominal symptoms.[4]

History and Physical

To obtain a thorough history, clinicians should ask patients about risk factors for perforated peptic ulcer disease. However, once a perforated peptic ulcer occurs, the patient’s history does not alter the treatment plan.[8] Typical symptoms of a perforated peptic ulcer include the sudden onset of persistent abdominal pain that does not completely subside with medications taken before evaluation. The classic triad in patients with a perforated peptic ulcer consists of tachycardia, sudden-onset abdominal pain, and abdominal rigidity.[8] 

The clinical manifestations of a perforated peptic ulcer progress through 3 phases. During the initial phase, within 2 hours after symptom onset, characteristic findings include tachycardia, epigastric pain, and cold extremities. During the second phase, 2 to 12 hours after onset, pain becomes generalized and worsens with movement.

Fluid moving along the right paracolic gutter can lead to right lower quadrant tenderness and abdominal rigidity. During the third phase, more than 12 hours after onset, patients may develop abdominal distension, fever, and hypotension.[12] Patients with retroperitoneal perforation may present more indolently, without signs of peritoneal irritation.[4]

Evaluation

Laboratory Tests

Laboratory tests commonly used to evaluate patients and exclude differential diagnoses include the following:

  • Elevated serum amylase levels, even when less than 4 times the upper limit of the reference range, may be associated with perforated peptic ulcers.[47]
  • Serum gastrin levels are useful for diagnosing Zollinger-Ellison syndrome in patients with a history of recurrent ulcers.[12]
  • Leukocytosis and elevated C-reactive protein levels indicate inflammation or infection.[48]
  • Blood cultures should be obtained before antibiotic therapy is initiated.[49]
  • Arterial blood gas analysis assesses the degree of metabolic compromise in those with sepsis.[9]

Radiography

In patients with acute upper abdominal pain, urgent upright chest radiography is an essential initial test for suspected duodenal perforation. Upright chest radiography demonstrates subdiaphragmatic free air in 75% of patients. However, radiographic findings may be normal, especially in patients who present soon after symptom onset.[50]

Subdiaphragmatic free air on upright chest radiography in a patient with abdominal symptoms establishes the diagnosis of a perforated peptic ulcer. Abdominal radiography may demonstrate the Rigler sign, defined as air outlining both sides of the intestinal wall; the football sign, characterized by a large, oval collection of intraperitoneal gas; or gas outlining soft tissue structures, such as the falciform ligament or liver edge.[51] Please see StatPearls' companion reference, "Anatomy, Abdomen and Pelvis, Falciform Ligament," for further information. Normal upright radiographic findings do not exclude duodenal perforation. Stable patients with clinical findings suspicious for duodenal perforation should undergo CT scanning.[4] 

The diagnostic accuracy of CT for detecting perforated peptic ulcers is approximately 98%.[52] A CT scan with oral and intravenous contrast is the most useful imaging method for diagnosing duodenal perforation.[53] CT findings of perforation include duodenal wall thickening, extravasation of oral contrast, extraluminal air, fat stranding, and a periduodenal fluid collection.[53] 

However, a noncontrast CT scan can demonstrate free air beneath the anterior abdominal wall in patients with acute kidney injury who cannot receive contrast. Oral diatrizoate can help diagnose a perforated peptic ulcer when CT is unavailable and upright chest radiography does not demonstrate free air. However, the absence of contrast extravasation does not exclude a perforated peptic ulcer because the perforation can seal spontaneously.[54]

Treatment / Management

Treatment of duodenal perforations depends on the type of perforation. Perforations are classified as contained or noncontained. Noncontained perforations are further classified as minor or major.

Contained Perforations

Contained perforations occur when adjacent organs, such as the pancreas, wall off the perforation, preventing free leakage. Conservative treatment is feasible for contained perforations. Before initiating conservative treatment, clinicians should perform a diatrizoate study to confirm the absence of leakage.

Conservative treatment includes intravenous fluid therapy, nothing by mouth, intravenous proton pump inhibitors, broad-spectrum antibiotics, Helicobacter pylori eradication therapy, and repeated clinical assessments.[4] Results from studies showed that somatostatin may facilitate enterocutaneous fistula closure.[55] Among patients with contained perforations, study results showed mortality rates of 3% with conservative treatment and 6.2% with surgical treatment.[56] The essential components of conservative treatment can be summarized as the 6 Rs: repeated clinical examination, radiologically undetected leak, repeated blood investigations, resources for monitoring, respiratory and renal support, and readiness to operate.[12](A1)

Noncontained Perforations

Noncontained perforations occur when bowel contents leak freely into the abdominal cavity. This group includes minor and major perforations.[4](B3)

Minor noncontained perforations: Endoscopic treatment and simple surgical repair are the 2 primary treatment strategies. Endoscopic options include through-the-scope clips, over-the-scope clips, detachable snare loops with clips, and self-expandable metal stents.[4] Through-the-scope clips are suitable for linear perforations less than 1 cm in diameter, whereas over-the-scope clips, detachable snare loops with clips, and self-expandable metal stents are appropriate for perforations measuring 1 to 3 cm.[57](B3)

Simple surgical repair is another option and may be performed with or without an omental patch. Alternatively, a free omental plug, known as a Graham patch, or a pedicled omental flap, known as a Cellan–Jones repair, can be sutured into the perforation.[4][6] Results from a meta-analysis showed that laparoscopic Graham patch repair was associated with lower morbidity and mortality than open repair; however, the analysis was subject to inherent selection bias. [58] Findings from other studies did not show a benefit from drain placement after surgical repair.[59](A1)

Endoscopic vacuum therapy should be considered when the defect contains a cavity. Traditional endoscopic vacuum therapy uses a sponge sutured to a nasogastric tube, which is placed endoscopically within the defect. Negative pressure seals the cavity, drains intestinal contents, and promotes granulation tissue formation. The system can be replaced every 3 to 5 days under endoscopic guidance until the defect closes.[60]

Major noncontained perforations: Major noncontained perforations usually require reconstructive surgical procedures, including duodenoduodenostomy as the first option, Roux-en-Y duodenojejunostomy as the second option, and a Billroth II procedure as a third option.[40] Perforations involving the first or proximal portion of the second segment may require a Billroth II procedure.[61](B3)

Differential Diagnosis

Before diagnostic imaging, the differential diagnosis of epigastric abdominal pain should be considered, including:

  • Abdominal aortic aneurysm
  • Acute coronary syndrome
  • Aortic dissection
  • Pancreatitis
  • Appendicitis
  • Boerhaave syndrome
  • Cholecystitis
  • Cholelithiasis 
  • Diverticulitis
  • Duodenitis
  • Esophagitis
  • Gastroesophageal reflux disease
  • Foreign body ingestion
  • Gastritis
  • Hepatitis
  • Ventral hernia
  • Mesenteric ischemia
  • Small bowel obstruction
  • Volvulus
  • Pneumonia

Prognosis

Reported mortality rates among patients with perforated peptic ulcers range from 1.3% to 20%.[62][63][64] Results from other studies showed that the 30-day mortality rate may reach 20%.[33] The primary prognostic factor is the interval between duodenal perforation and treatment. An interval greater than 24 hours increases mortality.[4]

The American Society of Anesthesiologists score and Boey score are the most commonly validated scoring systems for predicting outcomes in duodenal perforation.[12] Factors included in the Boey score are concomitant severe medical illness, preoperative shock, and a perforation duration greater than 24 hours. When all 3 factors are present, the total score is 3 and predicts a mortality rate of 38% and a morbidity rate of 77%.[65]

The American Society of Anesthesiologists score uses the severity of systemic disease and comorbidities to predict outcomes in patients with perforated peptic ulcers.[65] Significant risk factors for increased mortality include comorbidities, resection procedures, shock at admission, female sex, older age, metabolic acidosis, presentation delayed by more than 24 hours, acute kidney injury, hypoalbuminemia, smoking, and underweight status.[66][67]

Results from other studies showed that mortality is higher among patients older than 65 than among younger patients.[66] The postoperative mortality rate among patients with perforated peptic ulcers is estimated to be 6% to 10%.[68] Treatment delays greater than 24 hours, age older than 60, concomitant diseases, and systolic blood pressure less than 100 mm Hg are the main risk factors for increased mortality.[69]

Complications

Sepsis is common and accounts for 40% to 50% of fatalities among patients with perforated peptic ulcers. At the time of arrival in the operating room, about 30% to 35% of these patients have sepsis. Within the first month after the surgical procedure, more than 25% of patients develop septic shock, which is associated with a mortality rate of 50% to 60%.[9] Postoperative complications occur in approximately 30% of patients.[70] Reported risk factors for increased postoperative complication rates include age older than 40 years, a history of shock, and a larger perforation size, which increases the rate of postoperative complications.[71] 

Common postoperative complications include pneumonia, wound dehiscence, peritonitis, incisional hernia, enterocutaneous fistula, intra-abdominal fluid collection or abscess, surgical site infection, and ileus. Surgical site infection, occurring in 32% of patients, is the most common complication after surgery.[71] Challenges associated with endoscopic vacuum therapy for duodenal perforations include safely accessing the defect, substantial resource requirements, and displacement of the endoscopic vacuum device because of intestinal motility.[72]

Postoperative and Rehabilitation Care

A nonrandomized study reported that a treatment protocol implemented from admission through 3 days after laparoscopic repair reduced the 30-day mortality rate from 27% to 17%. The protocol included minimizing surgical delay and preventing, detecting, and treating sepsis.[9] Results from small randomized clinical trials conducted in Türkiye showed that early tube removal and initiation of oral intake reduced the hospital stay by approximately 3 days among patients with an American Society of Anesthesiologists score of I or II.[73] Results from a meta-analysis by Wong et al showed that Helicobacter pylori eradication significantly reduced the incidence of recurrent ulcer at 8 weeks and 1 year among patients who underwent surgical treatment for duodenal ulcer perforation.[74] Follow-up endoscopy is not recommended after duodenal ulcer perforation because these patients have a low risk of malignant neoplasm.[9]

Consultations

Following a diagnosis of duodenal perforation, clinicians should consult a gastroenterologist and gastrointestinal surgeon.

Deterrence and Patient Education

Patients should be aware of modifiable risk factors for duodenal perforation and take steps to reduce their risk. Peptic ulcer disease remains the leading cause, making its prevention central to preventing duodenal perforation.

  • Patients should avoid NSAIDs when possible.
  • If NSAID therapy is necessary, patients should use the lowest effective dose for the shortest possible duration.
  • Clinicians should consider prophylactic therapy with a proton pump inhibitor or histamine-2 receptor antagonist when prolonged NSAID use is necessary.
  • Patients with peptic ulcer disease should follow the recommendations of their gastroenterologist.
  • Patients should stop smoking.

Enhancing Healthcare Team Outcomes

PUD can be treated with medications. However, perforation may occur and is associated with a high risk of mortality. The classic triad of perforated peptic ulcer disease consists of sudden-onset abdominal pain, abdominal rigidity, and tachycardia. Clinicians should recognize that normal upright chest radiographic findings do not exclude duodenal perforation. Early diagnosis, prompt resuscitation, and urgent surgical intervention are crucial for improving outcomes. Experienced teams should direct conservative treatment. Exploratory laparotomy with omental patch repair remains the standard surgical treatment. During the hospital stay, nurses monitor patients’ vital signs and educate patients and their families.

After discharge, the healthcare team should educate patients about lifestyle modifications, including smoking cessation and, whenever possible, avoiding nonsteroidal anti-inflammatory drugs. Patients with confirmed Helicobacter pylori infection should receive eradication therapy, which may reduce mortality. Gastroenterology nurses should monitor patients after discharge, provide education, and communicate changes in their condition to the interprofessional team. Pharmacists should discuss the importance of adherence to prescribed medications, including proton pump inhibitors, histamine-2 receptor antagonists, and H pylori eradication therapy, and counsel patients to limit nonsteroidal anti-inflammatory drug use.

An interprofessional approach can reduce morbidity and mortality associated with duodenal perforation. Older age, shock, surgical delay, definitive surgical procedures, and a higher American Society of Anesthesiologists score are associated with poor outcomes among patients undergoing emergency surgical procedures for perforated peptic ulcers. Therefore, improving outcomes requires prompt resuscitation from shock, minimizing surgical delays, reserving definitive surgical procedures for selected patients, and addressing modifiable perioperative risks.[66][67]

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