Intestinal Perforation



Upper-bowel perforation can be described as either free or contained. Free perforation occurs when bowel contents spill freely into the abdominal cavity, causing diffuse peritonitis (eg, duodenal or gastric perforation). Contained perforation occurs when a full-thickness hole is created by an ulcer, but free spillage is prevented because contiguous organs wall off the area (as occurs, for example, when a duodenal ulcer penetrates into the pancreas).

Lower-bowel perforation (eg, in patients with acute diverticulitis or acute appendicitis) results in free intraperitoneal contamination.

Lau and Leow have indicated that perforated peptic ulcer was clinically recognized by 1799, but the first successful surgical management of gastric ulcer was by Ludwig Heusner in Germany in 1892. In 1894, Henry Percy Dean from London was the first surgeon to report successful repair of a perforated duodenal ulcer.[1]

Partial gastrectomy, although performed for perforated gastric ulcer as early as 1892, did not become a popular treatment until the 1940s. This was carried out as a result of the perceived high recurrence rate of ulcer symptoms after simple repair. The physiologic effects of truncal vagotomy on acid secretion had been known since the early 19th century, and this approach was introduced to the treatment of chronic duodenal ulcer in the 1940s.

The next development in the management of peptic ulcer disease was the introduction of high selective vagotomy in the late 1960s. However, neither of these approaches proved to be useful, and several postoperative complications, including high rates of ulcer recurrence, have limited their use. Currently, in patients with gastric perforation, simple closure of perforated ulcers is more commonly performed than is gastric resection.[2]

During World War I, the mortality following isolated injuries of the small intestine and colon was approximately 66% and 59%, respectively. The possible reasons for the high mortality and morbidity rates at that time may have been related to the following factors:

During the early years of World War II, Ogilvie, a leading surgeon in the British Army, recommended colostomy for management of all colonic injuries. This notion was supported by a publication from the office of the Surgeon General of the United States. However, the data presented in Ogilvie's series were not convincing. He reported a mortality rate of 53% for colonic injuries treated with colostomy, a rate similar to that observed during World War I.

According to Ogilvie, colostomy apparently failed to improve the mortality rate in World War II because primary repairs were used to treat less-severe injuries during World War I. Many patients in World War I were treated expectantly and were not included in the mortality data. On the other hand, Ogilvie's data included all patients with bowel injuries. These apparent differences in the methodology used convinced surgeons to continue using colostomies in such injuries after World War II.

Several reports clearly indicated that surgeons used colostomy during the Korean and Vietnam wars, particularly in the management of left colonic injuries. However, in civilian injuries, it has been reported that primary repair can be successfully used. By the end of 1980s, primary repair was considered to the management strategy of choice, and it has replaced the use of colostomies in the treatment of civilian patients in most hospitals in the United States, the United Kingdom, Europe, and Australia. At present, primary repairs are widely used for such bowel injuries.


The peritoneal cavity is lined with a single layer of mesothelial cells, connective tissue (including collagen), elastic tissues, macrophages, and fat cells. The parietal peritoneum covers the abdominal cavity (ie, abdominal wall, diaphragm, pelvis); the visceral peritoneum covers all of the intra-abdominal viscera, forming a cavity that is completely enclosed except at the open ends of the fallopian tubes.

The peritoneal cavity is divided by the transverse mesocolon. The greater omentum extends from the transverse mesocolon and from the lower pole of the stomach to line the lower peritoneal cavity. The pancreas, duodenum, and ascending and descending colon, are located in the anterior retroperitoneal space; the kidneys, ureters, and adrenal glands are found in the posterior retroperitoneal space. The liver, stomach, gallbladder, spleen, jejunum, ileum, transverse colon, sigmoid colon, cecum, and appendix are found within the peritoneal cavity.

A small amount of fluid sufficient to allow movement of organs is usually present in the peritoneal space. This fluid is normally serous (protein content of < 30 g/L, < 300 WBCs/µL). In the presence of infection, the amount of this fluid increases, its protein content climbs to more than 30 g/L, and the white blood cell (WBC) count increases to more than 500/µL; in other words, the fluid becomes an exudate.


Normally, the stomach is relatively free of bacteria and other microorganisms because of its high intraluminal acidity. Most persons who experience abdominal trauma have normal gastric functions and are not at risk of bacterial contamination following gastric perforation. However, those who have a preexisting gastric problem are at risk of peritoneal contamination with gastric perforation.

Leakage of acidic gastric juice into the peritoneal cavity often results in profound chemical peritonitis. If the leakage is not closed and food particles reach the peritoneal cavity, chemical peritonitis is succeeded by gradual development of bacterial peritonitis. Patients may be free of symptoms for several hours between the initial chemical peritonitis and the later occurrence of bacterial peritonitis.

The microbiology of the small bowel changes from its proximal to its distal part. Few bacteria populate the proximal part of the small bowel, whereas the distal part of the small bowel (the jejunum and ileum) contains aerobic organisms (eg, Escherichia coli) and a higher percentage of anaerobic organisms (eg, Bacteroides fragilis). Thus, the likelihood of intra-abdominal or wound infection is increased with perforation of the distal bowel.

The presence of bacteria in the peritoneal cavity stimulates an influx of acute inflammatory cells. The omentum and viscera tend to localize the site of inflammation, producing a phlegmon. (This usually occurs in perforation of the large bowel.) The resulting hypoxia in the area facilitates growth of anaerobes and produces impairment of bactericidal activity of granulocytes, which leads to increased phagocytic activity of granulocytes, degradation of cells, hypertonicity of fluid forming the abscess, osmotic effects, shift of more fluids into the abscess area, and enlargement of the abdominal abscess. If untreated, bacteremia, generalized sepsis, multiorgan failure, and shock may occur.


Causes of intestinal perforation include the following:


In children, small-bowel injuries following blunt abdominal trauma are infrequent, with an incidence of 1-7%. Evidence shows, however, that the incidence of these injuries is increasing.

In adults, perforations of peptic ulcer disease were a common cause of morbidity and mortality with acute abdomen until the latter half of the 20th century. The rate has fallen in parallel with the general decline in the prevalence of peptic ulcer disease. Duodenal ulcer perforations are 2-3 times more common than are gastric ulcer perforations. About a third of gastric perforations are due to gastric carcinoma.

Approximately 10-15% of patients with acute diverticulitis develop free perforation. Although most episodes of perforated diverticulum are confined to the peridiverticular region or pelvis, patients occasionally present with signs of generalized peritonitis. The overall mortality is relatively high (~20-40%), largely because of complications, such as septic shock and multiorgan failure.

In elderly patients, acute appendicitis has a mortality of 35% and a morbidity of 50%. A major contributing factor to morbidity and mortality in these patients is the presence of 1 or more severe medical conditions coexisting with, but predating, the appendicitis.

Endoscopy-associated bowel injuries are not a common cause of perforation. For example, perforations related to ERCP occur in about 1% of patients.[5]


Outcome is improved with early diagnosis and treatment. The following factors increase the risk of death:


A careful medical history often suggests the source of the problem, which is subsequently confirmed by clinical examination and radiologic study findings. Possible etiologies include the following:

With regard to abdominal pain, it is important to ask patients about the time of onset of pain, the duration and location of pain, the characteristics of pain, relieving and aggravating factors, and other symptoms associated with abdominal pain. A history of similar attacks may also suggest the etiology.

Sharp, severe, sudden-onset epigastric pain that awakens the patient from sleep often suggests perforated peptic ulcer. Differentiate this from conditions such as cholecystitis and pancreatitis. Painless perforation of a peptic ulcer can occur with steroid use. The presence of shoulder pain suggests involvement of the parietal peritoneum of the diaphragm.

In elderly patients, consider the possibility of perforated diverticulitis or ruptured acute appendicitis if the pain is located in the lower abdomen. Approximately 30-40% of elderly patients with acute appendicitis present more than 48 hours after the onset of abdominal pain. (Delayed presentation is usually associated with increased risk of perforation.) Elderly patients may have minimal pain.

In young adults with pain in the lower abdominal quadrant, consider perforated appendicitis as a possible diagnosis. Acute appendicitis with sudden perforation is usually associated with illness of several hours. The pain is typically localized in the right lower quadrant of the abdomen, unless the disease process has progressed to generalized peritonitis. In young women, also consider ruptured ovarian cyst and ruptured tubo-ovarian abscess in the differential diagnosis.

Physical Examination

Assess the patient's general appearance, take vital signs, and assess for any hemodynamic changes. (Take pulse and blood pressure measurements with the patient lying in bed and sitting, and note any postural changes.)

Examine the abdomen for any external signs of injury, abrasion, and/or ecchymosis. Observe patients' breathing patterns and abdominal movements with breathing, and note any abdominal distention or discoloration. (In perforated peptic ulcer disease, patients lie immobile, occasionally with knees flexed, and the abdomen is described as boardlike.)

Carefully palpate the entire abdomen, noting any masses or tenderness. Tachycardia, fever, and generalized abdominal tenderness may suggest peritonitis. Abdominal fullness and doughy consistency may indicate intra-abdominal hemorrhage. Tenderness on percussion may suggest peritoneal inflammation. Bowel sounds are usually absent in generalized peritonitis.

Rectal and bimanual vaginal and pelvic examinations may help in assessing conditions such as acute appendicitis, ruptured tubo-ovarian abscess, and perforated acute diverticulitis.

Laboratory Studies

A complete blood count (CBC) may reveal parameters suggestive of infection (eg, leukocytosis), though leukocytosis may be absent in elderly patients. Elevated packed blood cell volume suggests a shift of intravascular fluid. Blood culture for aerobic and anaerobic organisms is indicated. Findings from liver function and renal function tests may be within reference ranges (or nearly so) if no preexisting disorder is present.

Imaging Studies


Erect radiographs of the chest are recognized as the most appropriate first-line investigation when a perforated peptic ulcer is considered likely.[15] However, in approximately 30% of patients, no free gas can be identified. Thus, an erect posteroanterior chest radiograph is not sufficiently sensitive to rule out pneumoperitoneum in patients presenting with upper abdominal pain.

Plain supine and erect radiographs of the abdomen are the most common first steps in the diagnostic imaging evaluation of patients presenting with medical history and/or clinical signs suggestive of bowel perforation. Findings suggestive of perforation include the following:

Water-soluble radiologic contrast media administered orally or through a nasogastric tube can be used as an adjunct diagnostic tool to detect any intraperitoneal leak.

The perforation has sealed at presentation in approximately 50% of patients. For those who favor a nonoperative approach, contrast radiology is routine in the management of these patients.


Localized gas collection related to bowel perforation may be detectable on ultrasonography (US), particularly if it is associated with other visible abnormalities (eg, thickened bowel loop). The site of bowel perforation can be detected by US (eg, gastric vs duodenal perforation, perforated appendicitis vs perforated diverticulitis). Ultrasonograms of the abdomen can also provide rapid evaluation of the liver, spleen, pancreas, kidneys, ovaries, adrenals, and uterus.

Computed tomography

Computed tomography (CT) of the abdomen can be a valuable investigative tool, providing differential morphologic information not obtainable with plain radiography or ultrasonography.

CT scans may provide evidence of localized perforation (eg, perforated duodenal ulcer) with leakage in the area of the gallbladder and right flank with or without free air being apparent. They may show inflammatory changes in the pericolonic soft tissues and focal abscess due to diverticulitis (may mimic perforated colonic carcinoma). CT scans may not provide definitive radiographic evidence of perforated Meckel diverticulitis.


Laparoscopy may significantly improve surgical decision making in patients with acute abdominal pain, particularly when the need for operation is uncertain.

Peritoneal diagnostic tap may be useful in determining the presence of intra-abdominal blood, fluid, and pus.

Peritoneal lavage is more valuable in the presence of a history of blunt abdominal trauma. The presence of blood or purulent material or the detection of bacteria on Gram stain suggests the need for early surgical exploration. Alkaline phosphatase concentration in the peritoneal lavage is a helpful and sensitive test that may be used to detect occult blunt intestinal injuries. A concentration greater than 10 IU/L has been shown to be a sensitive and reliable test in the detection of occult small bowel injuries.

Fine-catheter peritoneal cytology involves the insertion of a venous cannula into the peritoneal cavity, through which a fine umbilical catheter is inserted while the patient is under local anesthesia. Peritoneal fluid is aspirated, placed on a slide, and stained for examination under a light microscope for percentage of polymorphonuclear cells. A value greater than 50% suggests a significant underlying inflammatory process. This test, however, provides no clue as to the exact cause of inflammation.

Approach Considerations

The mainstay of treatment for intestinal perforation is surgery.[16] Surgery for intestinal perforation is contraindicated in the presence of general contraindications to anesthesia and major surgery, such as severe heart failure, respiratory failure, or multiorgan failure. It is also contraindicated if the patient refuses the operation and no evidence of generalized peritonitis exists. Finally, surgery is contraindicated if a contrast meal confirms spontaneous sealing of the perforation (eg, perforated duodenal ulcer) and the patient prefers a nonsurgical approach.[17]

Medical Therapy

Treatment is primarily surgical. Emergency medical care includes the following steps:

However, if symptoms and signs of generalized peritonitis are absent, a nonoperative policy may be used with antibiotic therapy directed against gram-negative and anaerobic bacteria.[18, 19]


Antibiotics have proved effective in decreasing the rate of postoperative wound infection and improving outcomes in patients with intraperitoneal infection and bloodstream infection.

Metronidazole is typically used in combination with an aminoglycoside to provide broad gram-negative and anaerobic coverage. It is reduced to a product that interacts with deoxyribonucleic acid (DNA) to cause a loss of helical DNA structure and strand breakage, resulting in inhibition of protein synthesis and cell death in susceptible organisms. Adult dosing is 7.5 mg/kg IV before surgery. Pediatric dosing is 15-30 mg/kg/day IV divided bid/tid for 7 days. Metronidazole is a pregnancy category B drug.

Gentamicin is an aminoglycoside antibiotic with gram-negative coverage. It is used in combination with both an agent against gram-positive organisms and one that covers anaerobes. Although it is not the drug of choice, it should be considered if penicillins or other less toxic drugs are contraindicated, when clinically indicated, and in mixed infections caused by susceptible staphylococci and gram-negative organisms.

Gentamicin dosing regimens are numerous; the dosage is adjusted on the basis of creatinine clearance (CrCl) and changes in volume of distribution. It may be given IV or intramuscularly (IM). In adults, the loading dose before surgery is 2 mg/kg IV; thereafter, the dosage is 3-5 mg/kg/day divided tid/qid. In infants, the dosage is 7.5 mg/kg/day IV divided tid. In children, the dosage is 6-7.5 mg/kg/day IV divided tid. Gentamicin is a pregnancy category C drug.

Cefotetan is a second-generation cephalosporin that inhibits bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins. It inhibits the final transpeptidation step of peptidoglycan synthesis, resulting in cell wall death. Adult dosing is 2 g IV once before surgery. In children younger than 3 months, dosing is not established. In those older than 3 months, dosing is 30-40 mg/kg IV once before surgery. Cefotetan is a pregnancy category B drug.

Cefoxitin is also a second-generation cephalosporin that inhibits bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins. It inhibits the final transpeptidation step of peptidoglycan synthesis, resulting in cell wall death. Adult dosing is 2 g IV once before surgery, followed by 4 doses of 2 g IV q4-6hr. In children younger than 3 months, dosing is not established. In those older than 3 months, dosing is 30-40 mg/kg IV before surgery, followed by 3 doses of 2 g IV q4-6hr for 24 hr. Cefoxitin is a pregnancy category B drug.

Ertapenem is indicated for complicated intra-abdominal infections in adults and children aged 3 years or older. It is a carbapenem that inhibits cell-wall synthesis by binding to penicillin-binding proteins. It is resistant to most beta-lactamases. Dosing in adults and adolescents is 1 g IV or IM once daily for 5-14 days. The dosage for children aged 3-12 years is 15 mg/kg IV or IM q12hr for 5-14 days.

Eravacycline is a synthetic fluorocycline antibiotic belonging to the tetracycline class. It disrupts bacterial protein synthesis by binding the 30S ribosomal subunit, thus preventing incorporation of amino acid residues into elongating peptide chains. It is indicated in adults for treatment of complicated intra-abdominal infections caused by the following susceptible bacteria:

Dosing is 1 mg/kg IV every 12 hours for 4-14 days. Dosage modifications are required in patients with severe hepatic impairment or if coadministered with strong CYP3A inducers. Approval for complicated intra-abdominal infections was based on results from the IGNITE-1 clinical trial (N = 541), which demonstrated that eravacycline was noninferior to ertapenem.[20]

Surgical Therapy

The goals of surgical therapy are as follows:

Operative details

Preoperatively, correct any fluid or electrolyte imbalance. Replace extracellular fluid losses by administering Hartmann solution or a similar solution that has an electrolyte composition similar to plasma. Central venous pressure (CVP) monitoring is essential in critically ill and/or elderly patients, in whom cardiac impairment may be exacerbated by large fluid loss.

Administer systemic antibiotics (eg, ampicillin, gentamicin, or metronidazole), making a best estimation regarding the likely organisms. Nasogastric suction is required to empty the stomach and reduce the risk of further vomiting. Urinary catheterization is used to assess urinary flow and fluid replacement. Administer analgesics, such as morphine, in small IV doses, preferably as a continuous infusion.

Operative management depends on the cause of perforation. Perform urgent surgery either on patients not responding to resuscitation or following stabilization and maintenance of adequate urine output. All necrotic material and contaminated fluid should be removed and accompanied by lavage with antibiotics (tetracycline 1 mg/mL). Decompress distended bowel via a nasogastric tube.

Laparoscopic or laparoscopic-assisted (minilaparotomy) surgery is also being increasingly performed, with outcomes comparable to those of conventional laparotomy.[21] Experience and advances in accessories have enabled endoscopic repair of a significant number of intestinal perforations, such as iatrogenic perforation. Management of such cases must be individualized to the patient.

In a study involving 934 patients with sigmoid diverticulitis, Ritz et al found that the risk of free perforation in acute sigmoid diverticulitis decreases with the increases in the number of previous episodes of sigmoid diverticulitis. They concluded that the first episode has the highest risk for a free perforation. Therefore, the indication for colectomy should not be made on the basis of the potential risk of free perforation.[22]

Postoperative Care

Intravenous replacement therapy

The aim of IV replacement therapy is to maintain intravascular volume and hydrate the patient. Monitor by CVP measurement and urinary output.

Nasogastric drainage

Perform nasogastric drainage continuously until drainage becomes minimal. At that stage, the nasogastric tube may be removed.


Continue administration of the antibiotics commenced preoperatively unless the results of cultures taken at the time of the operation reveal that the causative organisms are resistant to them.

The goal of antibiotic therapy is to achieve levels of antibiotics at the site of infection that exceed the minimum inhibitory concentrations for the pathogens present.

In the presence of intra-abdominal infections, GI function is often impaired; therefore, oral antibiotics are not efficacious, and intravenous antibiotics are recommended.

If no obvious improvement in the patient's condition occurs within 2-3 days, consider the following possibilities:


Analgesics, such as IV morphine, should be given continuously or in small doses at frequent intervals.


Wound infection rates correlate with the bacterial load in the bowel; accordingly, this complication occurs more often with colonic perforation (eg, perforated diverticulitis). The judicious use of prophylactic antibiotics has been demonstrated to reduce the incidence of wound infection in contaminated and potentially contaminated wounds.

Wound failure (partial or total disruption of any or all layers of the operative wound) may occur early (ie, wound dehiscence) or late (ie, incisional hernia). The following factors are associated with wound failure:

Localized abdominal abscess may develop.

Multiorgan failure and septic shock may develop. Septicemia (bloodstream infection) is defined as proliferation of bacteria in the bloodstream resulting in systemic manifestations such as rigors, fever, hypothermia (in gram-negative septicemia with endotoxemia), leukocytosis or leukopenia (in profound septicemia), tachycardia, and circulatory collapse. Septic shock is associated with a combination of the following:

Gram-negative infections are associated with a much worse prognosis than gram-positive infections, possibly because of associated endotoxemia.

Renal failure and fluid, electrolyte, and pH imbalance may occur.

Gastrointestinal mucosal hemorrhage is usually associated with failure of multiple organ systems and is probably related to a defect in the protective gastric mucosa.

Mechanical obstruction of the intestine is most often caused by postoperative adhesions.

The following factors may cause a predisposition to postoperative delirium:

Long-Term Monitoring

For patients treated with a nonsurgical approach, follow-up care consists of the following:

What is intestinal perforation?What is the history of surgical management procedures for intestinal perforation?Which factors contributed to a high mortality rate for intestinal perforation during World War I?How did colostomy become the treatment of choice for intestinal perforation during the World War II?When did primary repair of intestinal perforation become the treatment of choice?What is the anatomy of the peritoneal cavity relative to intestinal perforation?What is the pathophysiology of intestinal perforation?What are the etiologies of intestinal perforation?What is the incidence of intestinal perforation in children?What is the incidence of intestinal perforation in adults?What is the incidence of intestinal perforation in elderly patients?Which factors increase the risk of death from intestinal perforation?What should be the focus of medical history in the evaluation of intestinal perforation?How is the history of pain used to determine the underlying etiology of intestinal perforation?What is included in the physical exam of a patient with suspected intestinal perforation?What are the differential diagnoses for Intestinal Perforation?What is the role of lab studies in the diagnosis of intestinal perforation?What is the role of radiography in the diagnosis of intestinal perforation?What is the role of ultrasonography in the diagnosis of intestinal perforation?What is the role of CT scanning in the diagnosis of intestinal perforation?Which procedures are performed in the workup of intestinal perforation?When is surgery contraindicated in the treatment of intestinal perforation?What is included in emergency medical care for intestinal perforation?What is the role of antibiotics in the treatment of intestinal perforation?Which antibiotics are used as treatment for intestinal perforation?What are the goals of surgical therapy for intestinal perforation?What is included in preoperative care for intestinal perforation?When is urgent surgery indicated in the treatment of intestinal perforation?What is the role of laparoscopic surgery in the treatment of intestinal perforation?What is the aim of IV replacement therapy for intestinal perforation?When is nasogastric drainage performed in the treatment of intestinal perforation?When are antibiotics administered in the treatment of intestinal perforation?What is the goal of antibiotic therapy during postoperative care for intestinal perforation?What should be considered in patients with intestinal perforation who have not improved following surgery?How is pain managed during postoperative care of intestinal perforation?What are the complications of intestinal perforation surgery?What are complications of intestinal perforation?Which factors may cause postoperative delirium in patients with intestinal perforation?What is included in monitoring of patients with intestinal perforation who did not undergo surgery?


Samy A Azer, MD, PhD, MPH, Professor of Medical Education, Chair of Medical Education Research and Development Unit, Faculty of Medicine, Universiti Teknologi MARA, Malaysia; Visiting Professor of Medical Education, Faculty of Medicine, University of Toyama, Japan; Former Senior Lecturer in Medical Education, Faculty Education Unit, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne and University of Sydney, Australia

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

John Geibel, MD, MSc, DSc, AGAF, Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, Professor, Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow; Fellow of the Royal Society of Medicine

Disclosure: Nothing to disclose.


Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons

Disclosure: Nothing to disclose.


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