Bowel Perforation

Etiology

Bowel perforations can be categorized by anatomic location, as the underlying etiologies often differ between the stomach/small bowel and the large bowel. Importantly, several causes, including neoplasms, foreign bodies, obstruction, trauma, and iatrogenic injury, may affect either region.

Stomach and Small Bowel

Common causes include erosion from gastric or duodenal ulceration, neoplasms, infection or abscess, Meckel diverticulum, hernia with strangulation, volvulus, inflammatory bowel disease/colitis, mesenteric ischemia, foreign body ingestion, mechanical obstruction, medication or radiation-induced injury, iatrogenic perforation, and blunt or penetrating abdominal trauma.

Large Bowel

Frequent etiologies include neoplasms, diverticulitis, appendicitis, localized or disseminated infection/abscess, inflammatory bowel disease/colitis, foreign body, obstruction, volvulus, iatrogenic injury, medication or radiation-related injury, and blunt or penetrating abdominal trauma.[2]

Epidemiology

The etiology of bowel perforation varies considerably by patient age and anatomical location. In premature infants, necrotizing enterocolitis is the leading cause of perforation.[3][4] Among children and adolescents, appendicitis is the most frequent etiology, while in the pediatric trauma population, the incidence of bowel perforation is approximately 10% to 12%.[5] Foreign body ingestion accounts for perforation in 1% to 5.6% of cases, and colorectal cancer is associated with perforation in 3% to 10% of patients. Iatrogenic injury is another important contributor, with reported perforation rates after colonoscopy ranging from 0.01% to 6.7%.[6]

In adults, etiologies shift toward inflammatory, neoplastic, and iatrogenic causes. Approximately 1% to 2% of patients with acute diverticulitis develop free perforation, while up to 30% present with contained perforation and abscess formation.[7] Perforated peptic ulcer disease occurs in 2% to 10% of cases, with about 60% involving the duodenum and 40% involving the stomach.[8] Colonoscopy-related perforation is reported in 0.9% to 2% of patients undergoing colonoscopy.[9] Inflammatory bowel disease also carries a significant risk, with perforation rates reaching up to 20% in severe ulcerative colitis and 1% to 3% in Crohn disease.[10][11]

Pathophysiology

Bowel perforation results from a full-thickness disruption of the gastrointestinal wall, leading to spillage of luminal contents—gas, fluid, bile, or feces—into the peritoneal cavity (see Image. Abdomen With Free Air, Radiograph). The bowel functions as a closed system, and once this barrier is breached, the degree of contamination and inflammatory response depends on the location of the perforation, the underlying etiology, and the rapidity of diagnosis. Small perforations may cause localized peritonitis with minimal leakage, whereas large or unrecognized perforations can result in gross feculent peritonitis, rapid bacterial translocation, and septic shock. This means that pain may be gradual or sudden, but it typically progresses in severity, and patients often develop abdominal distension and muscular rigidity, consistent with evolving peritonitis.[12]

The pathophysiology is multifactorial and linked to the underlying insult. Inflammatory conditions such as diverticulitis, appendicitis, or inflammatory bowel disease weaken the intestinal wall through transmural inflammation and necrosis. Ischemic injury compromises mucosal and muscular integrity, increasing susceptibility to rupture. Obstruction, whether due to tumor, volvulus, or hernia, causes progressive intraluminal pressure and bowel distension; once the intramural blood supply is compromised, ischemic necrosis and subsequent perforation occur. Trauma (blunt or penetrating) and iatrogenic injuries disrupt the bowel wall directly. In contrast, chronic insults from medications (eg, nonsteroidal anti-inflammatories, steroids), radiation enteritis, or foreign bodies may cause focal weakening over time that eventually results in perforation.

Once perforation occurs, peritoneal contamination triggers a cascade of systemic inflammatory responses. Initially, peritonitis is localized by the omentum and adjacent bowel loops, but continued leakage or delayed diagnosis allows bacterial proliferation, toxin release, and widespread peritoneal inflammation. If untreated, this can progress to systemic inflammatory response syndrome, bacteremia, and multiorgan dysfunction. Even after repair, the inflammatory injury to the peritoneum and bowel increases the risk for long-term sequelae, including adhesions, abscesses, anastomotic leaks, and fistula formation.

History and Physical

Historical factors are beneficial when making the diagnosis of bowel perforation. Patients most often present with acute abdominal pain that may be sudden and severe, as seen with peptic ulcer or traumatic perforation, or more gradual in onset and progressive, as in diverticulitis or inflammatory bowel disease–related perforation. A pain-free interval followed by worsening pain can sometimes occur, representing decompression of an inflamed or injured bowel segment immediately after the perforation. The pain is usually diffuse and persistent, but it may initially localize before spreading as peritonitis develops. Patients frequently describe abdominal distension and bloating, often accompanied by nausea, vomiting, anorexia, fever, and obstipation. Lower chest or abdominal pain following recent instrumentation—such as colonoscopy, endoscopy, or abdominal surgery—should raise particular concern for iatrogenic perforation. A detailed medical, surgical, and social history should be obtained, including prior hernia, bowel obstruction, known or suspected malignancy, history of foreign body ingestion or insertion, abdominal trauma, and substance use. Medication history is equally important, as nonsteroidal anti-inflammatory drugs, corticosteroids, and chemotherapy increase the risk of perforation.

On physical examination, patients often appear ill, with tachycardia, tachypnea, fever, and evolving signs of sepsis, though vital signs may be normal early in the course.[13] The abdomen may exhibit progressive distension, and palpation typically reveals diffuse tenderness that can be difficult to localize due to the widespread spillage of air and intestinal contents. Gentle percussion or even jostling the stretcher can elicit peritoneal irritation. As the disease advances, patients develop involuntary guarding, rigidity, and rebound tenderness, classic signs of diffuse peritonitis. Bowel sounds are usually diminished or absent, reflecting ileus. In more localized or contained perforations, tenderness may be confined to 1 quadrant. A digital rectal exam may reveal heme-positive stool in malignancy or feculent material with distal colonic perforation. Importantly, elderly, immunocompromised, or critically ill patients may lack overt peritoneal findings, making a high index of suspicion critical.

Evaluation

Diagnosing bowel perforation requires integrating clinical suspicion with laboratory and imaging studies. Laboratory evaluation is nonspecific but helpful in assessing severity, systemic response, and potential underlying etiologies. Common findings include leukocytosis with a left shift, suggestive of infection; however, severe sepsis or immunosuppression may present with normal or even depressed white blood cell counts. Elevated C-reactive protein and procalcitonin can support the diagnosis of systemic inflammation or sepsis. Electrolyte abnormalities, such as hypokalemia or metabolic alkalosis from vomiting or metabolic acidosis from shock, are often present. Serum lactate is a critical marker of tissue hypoperfusion and may indicate evolving mesenteric ischemia or systemic shock. Blood cultures should be obtained in patients with suspected sepsis. In select cases, serum amylase or lipase levels may help differentiate between perforation and pancreatitis.

Imaging plays the central role in confirming the diagnosis. An upright chest x-ray or left lateral decubitus abdominal radiograph may reveal free intraperitoneal air beneath the diaphragm in 50% to 70% of cases, a classic but not universally present finding. The Rigler sign, which is the visualization of both sides of the bowel wall due to free intraperitoneal air, may also be seen. Abdominal radiographs may show dilated bowel loops, air-fluid levels, or loss of psoas margins in cases of retroperitoneal perforation. However, computed tomography (CT) with oral and intravenous contrast is the gold standard for diagnosis, as it can detect even small volumes of extraluminal air, extraluminal contrast leak, peritoneal fluid collections, and the underlying etiology, such as diverticulitis, tumor, or ischemia. CT also provides guidance for potential percutaneous drainage in cases of localized abscess. In rare instances when perforation is suspected but imaging is equivocal, diagnostic laparoscopy may be necessary for definitive evaluation. Together, laboratory data help stratify severity and systemic impact, while imaging defines the presence, location, and etiology of the perforation, guiding the urgency and type of intervention.

Treatment / Management

The management of bowel perforation requires prompt recognition, rapid resuscitation, early antibiotic therapy, and timely surgical evaluation. Initial treatment should focus on hemodynamic stabilization, with large-bore intravenous (IV) access, aggressive IV crystalloid resuscitation, and supplemental oxygen. In patients presenting with sepsis or septic shock, early vasopressor support may be necessary. Broad-spectrum antibiotics should be initiated immediately, covering gram-negative and anaerobic organisms, with options such as piperacillin-tazobactam, a carbapenem, or a third-generation cephalosporin combined with metronidazole. Antifungal coverage may be considered in high-risk or immunocompromised individuals. A multimodal analgesic regimen should be used for pain control, while patients are maintained on nothing per os. Nasogastric tube decompression can be placed for ileus or obstruction. Still, if gastric or duodenal perforation is strongly suspected, placement should be deferred until the patient is in the operating room to avoid worsening contamination.

Nonoperative care may be considered in carefully selected, hemodynamically stable individuals with contained perforations and no evidence of peritonitis. These patients require inpatient admission, close monitoring with serial physical exams, vital signs, and laboratory evaluation. Normalization of laboratory results, stable vital signs, and a benign abdominal exam may allow for eventual discharge. If symptoms persist, repeat CT imaging with IV contrast may be warranted after 72 hours to assess for progression or the formation of an abscess. Contained perforations often present with intra-abdominal abscesses, which may be amenable to percutaneous drainage by interventional radiology if the abscess is 3 cm or greater (generally, 3 cm is the smallest size that can be effectively drained) and a safe access window exists.[14] Failure of nonoperative management, clinical deterioration, or hemodynamic instability warrants immediate surgical consultation and intervention.(A1)

Surgical management is indicated for patients presenting with free perforation, diffuse peritonitis, or clinical deterioration.[15] Early involvement of the surgical team during presentation is essential, as timely operative intervention remains the strongest determinant of improved morbidity and mortality.[16] The approach depends on stability, etiology, and extent of contamination. Minimally invasive laparoscopy may suit stable individuals with localized contamination and favorable anatomy, enabling diagnosis and repair. However, exploratory laparotomy remains the standard in unstable individuals, those with diffuse peritonitis, or in cases of diagnostic uncertainty, as it allows thorough evaluation, definitive repair or resection, and infection control.[17] Operative strategies include primary closure of small defects, omental (Graham) patch repair in peptic ulcer disease, segmental bowel resection with or without anastomosis, or damage-control surgery with diversion and temporary abdominal closure in unstable or septic patients.(B3)

Postoperative management requires ongoing sepsis monitoring, nutritional support, and vigilance for complications such as intra-abdominal abscess, anastomotic leak, fistula formation, or multiorgan dysfunction. A multidisciplinary approach involving critical care, infectious disease, nutrition, and interventional radiology teams is essential to optimize outcomes. Early surgical involvement is critical in any patient with abdominal pain, hemodynamic instability, or signs of clinical deterioration, as delays in intervention markedly increase morbidity and mortality.

Differential Diagnosis

The differential diagnoses for bowel perforation include: 

• Acute biliary disorders (cholecystitis/choledocholithiasis/cholangitis)
• Acute gastroenteritis
• Acute pancreatitis
• Kidney stones
• Bacterial peritonitis
• Appendicitis
• Constipation
• Crohn disease
• Ulcerative colitis
• Diverticulitis
• Endometriosis
• Fallopian tube disorders
• Ectopic pregnancies
• Pelvic inflammatory disease

Prognosis

The patient’s medical state before the perforation occurs best predicts general prognosis. In patients without multiple comorbidities, the outcomes are more favorable. Management of the underlying etiology is key to preventing further episodes.[18]

Complications

Bowel perforation carries a high risk of morbidity and mortality, and complications may arise both in the acute setting and during the postoperative or recovery period. These complications can be broadly categorized into early and late sequelae, reflecting the timeline and clinical consequences of the disease process and its management. Early complications are primarily related to the systemic inflammatory response and infectious burden of peritonitis and sepsis. If not promptly addressed, hemodynamic instability may progress rapidly to hypoperfusion, septic shock, and multiorgan system failure.[19] Infectious complications can manifest as localized intra-abdominal abscesses, diffuse peritonitis, or systemic bacteremia, each of which substantially increases morbidity and prolongs hospitalization.[19] In addition, acute renal failure, respiratory compromise, and disseminated intravascular coagulation may develop in critically ill patients.

Late complications often result from surgical intervention or the body’s healing response. These include delayed wound healing and postoperative adhesions, which may predispose patients to recurrent bowel obstruction. Structural complications such as fistula formation, anastomotic leaks, and ventral or incisional hernias can occur and may require further surgical or interventional management.[15] Patients who undergo damage-control laparotomy with delayed closure are particularly at risk for hernia formation and fistulization. Additionally, intra-abdominal abscesses or recurrent sepsis may present in a delayed fashion, necessitating vigilant postoperative surveillance. The severity and likelihood of complications are influenced by multiple factors, including the timing of diagnosis and intervention, the patient’s underlying comorbidities, the extent of contamination, and the surgical strategy employed. Early recognition, aggressive resuscitation, timely source control, and meticulous postoperative care are crucial in mitigating these risks and improving survival outcomes.