INTRODUCTION — Perforation of the gastrointestinal tract may be suspected based upon the patient's clinical presentation, or the diagnosis becomes obvious through a report of extraluminal "free" gas or fluid or fluid collection on diagnostic imaging performed to evaluate abdominal pain or another symptom. Clinical manifestations depend somewhat on the organ affected and the nature of the contents released (gas, succus entericus, stool), as well as the ability of the surrounding tissues to contain those contents.
Intestinal perforation can present acutely or in an indolent manner (eg, abscess or intestinal fistula formation). A confirmatory diagnosis is made primarily using abdominal imaging studies, but on occasion, exploration of the abdomen (open or laparoscopic) may be needed to make a diagnosis. Specific treatment depends upon the nature of the disease process that caused the perforation. Some etiologies are amenable to a nonoperative approach, while others will require surgery.
An overview of the clinical features, diagnosis, and management of the patient with alimentary tract perforation is reviewed here. Specific etiologies are briefly reviewed below and discussed in the linked topic reviews in more detail. (See 'Risk factors' below and 'Specific organs' below.)
GENERAL PRINCIPLES
Pathophysiology — Perforation requires full-thickness injury of the bowel wall; however, partial-thickness bowel injury (eg, electrocautery, blunt trauma) can progress over time to become a full-thickness injury or perforation, subsequently releasing gastrointestinal contents.
Full-thickness injury and subsequent perforation of the gastrointestinal tract can be due to a variety of etiologies, including:
●Instrumentation (eg, endoscopy, instillation of contrast, cautery application during surgery)
●Trauma (blunt or penetrating)
●Bowel obstruction
●Neoplasms (particularly colon carcinoma), besides by causing bowel obstruction, can also cause perforation by direct penetration of the tumor through the bowel wall or from complete bowel obstruction, ischemia from increased intra-luminal pressure, and subsequent perforation.
Other etiologies are less common [1-4]. Spontaneous perforation can be related to inflammatory changes or tissues weakened by inflammatory bowel disorders, infections, or connective tissue disorders. Esophageal, gastric, or duodenal perforations may also be associated with peptic ulcer disease, corrosive agents, vasculitis, or certain types of medications. Ulceration and perforation can also occur after certain types of bowel anastomoses (eg, gastrojejunostomy) and are called "marginal ulcers." (See 'Risk factors' below.)
With bowel obstruction, perforation occurs proximal to the obstruction as pressure builds up within the bowel, exceeding intestinal perfusion pressure, and leading to ischemia and subsequently necrosis. When perforation is proximal to a colon obstruction, it usually occurs in the cecum (the thinnest-walled portion of the large bowel) in the presence of a competent ileocecal valve, which does not allow retrograde decompression of the cecum. Enteroliths and gallstones can also cause perforation by direct pressure or indirectly by leading to obstruction resulting in a proximal perforation [5,6].
Alternatively, the excess pressure can cause the musculature of the bowel to fail mechanically; in other words, to simply split (diastatic rupture) without any obvious necrosis. Intestinal pseudo-obstruction (Ogilvie syndrome) can also lead to perforation by these mechanisms. (See "Acute colonic pseudo-obstruction (Ogilvie's syndrome)".)
As free gas accumulates in the peritoneal cavity, it can compress intra-abdominal veins or lead to respiratory insufficiency by compromising diaphragmatic function [7]. Such a tension pneumoperitoneum (valvular pneumoperitoneum) can result from iatrogenic or pathologic processes. Perforation and subsequent inflammation can also cause abdominal compartment syndrome [8].
Anatomic considerations — Knowledge of gastrointestinal anatomy and anatomic relationships to adjacent organs helps predict symptoms and to interpret imaging studies in patients with a possible gastrointestinal perforation. Whether or not gastrointestinal perforation leads to free fluid and diffuse peritonitis or is contained, resulting in an abscess or fistula formation, depends upon location along the gastrointestinal tract and the patient's ability to mount an inflammatory response to the specific pathologic process. As an example, retroperitoneal perforations are more likely to be contained. Immunosuppressive and anti-inflammatory medications impair this response.
In brief, the relationship of the gastrointestinal tract to itself and other structures is as follows:
●The esophagus begins in the neck and descends adjacent to the aorta through the esophageal hiatus to the gastroesophageal junction (figure 1). Perforations of the esophagus due to foreign body ingestion usually occur at the narrow areas of the esophagus such as the cricopharyngeus muscle, aortic arch, left main stem bronchus, and lower esophageal sphincter.
●The stomach is located in the left upper quadrant of the abdomen but can occupy other areas of the abdomen, depending upon its degree of distention, phase of diaphragmatic excursion, and the position of the individual. Anteriorly, the stomach is adjacent to the left lobe of the liver, diaphragm, colon, and anterior abdominal wall. Posteriorly, the stomach is in close proximity to the pancreas, spleen, left kidney and adrenal gland, splenic artery, left diaphragm, transverse mesocolon, and colon (figure 2 and figure 3).
●The small bowel is anatomically divided into three portions: the duodenum, jejunum, and ileum. The duodenum is retroperitoneal in its second and third portion and forms a loop around the head of the pancreas. The jejunum is in continuity with the fourth portion of the duodenum beginning at the ligament of Treitz; there are no true lines of demarcation that separate the jejunum from ileum. The ileocecal valve marks the beginning of the colon in the right lower quadrant. The appendix hangs freely from the cecum, which is the first portion of the colon (figure 3). Foreign bodies that perforate the small intestines most commonly occur at sites of gastrointestinal fixation (eg, duodenum).
●The ascending and descending colon are retroperitoneal, while the transverse colon, which extends from the hepatic flexure to the splenic flexure, is intraperitoneal. The sigmoid colon (intraperitoneal) continues from the descending colon, ending where the teniae converge to form the rectum. The anterior upper two-thirds of the rectum are located intraperitoneally, and the remainder is extraperitoneal. The rectum lies anterior to the three inferior sacral vertebrae, coccyx, and sacral vessels and is posterior to the bladder in men and the vagina in women. Foreign bodies that perforate the colon tend to occur at transition zones from an intraperitoneal location to fixed retroperitoneal locations, such as the cecum.
RISK FACTORS — Factors that increase the risk for gastrointestinal perforation are discussed below and are important to assess when taking the history of any patient suspected of having gastrointestinal perforation.
●Instrumentation/surgery – Instrumentation of the gastrointestinal tract is the main cause of iatrogenic perforation and may include upper endoscopy (especially rigid endoscopy), sigmoidoscopy, colonoscopy [9,10], stent placement [9,10], endoscopic sclerotherapy [11], nasogastric intubation [12], esophageal dilation, and surgery.
The incidence of perforation related to endoscopy increases with procedural complexity. Perforation is less common with diagnostic compared with therapeutic procedures [13]. A perforation rate of 0.11 percent for rigid endoscopy contrasts with a 0.03 percent rate for flexible endoscopy [14,15]. When iatrogenic perforation occurs, there is often significant associated pathology. As an example, in the esophagus, there may be stricture, severe esophagitis [16], or a diverticulum, and the presence of cervical osteophytes also increases the risk [15]. The area of the esophagus at most risk for instrumental perforation is Killian's triangle [17], which is the part of the pharynx formed by the inferior pharyngeal constrictor and cricopharyngeus muscle. During endoscopy, perforations are frequently recognized at the time of the procedure. At other times, the perforation remains occult for several days. (See "Overview of colonoscopy in adults", section on 'Perforation' and "Overview of upper gastrointestinal endoscopy (esophagogastroduodenoscopy)", section on 'Complications'.)
When the normal anatomy of the esophagus or stomach has been disturbed, such as after Roux-en-Y gastric bypass, great care should be taken with nasogastric intubation to avoid iatrogenic perforation [18]. (See "Inpatient placement and management of nasogastric and nasoenteric tubes in adults".)
Many other procedures can also be complicated with perforation, such as chest tube insertion low in the chest [19], peritoneal dialysis catheter insertion [20], percutaneous gastrostomy [21], paracentesis, diagnostic peritoneal lavage, and percutaneous drainage of fluid collections or abscess.
With surgery, perforation can occur during essentially any portion of the case, including initial laparoscopic access, during mobilization of the organs or during the takedown of adhesions, or as a result of thermal injury from electrocautery devices [22-24]. Gastrointestinal leakage can also occur postoperatively as a result of anastomotic breakdown [25-32]. Immunosuppressed individuals may be at increased risk for dehiscence and deep organ space infection following surgery [33]. Medical illnesses such as diabetes, cirrhosis, and HIV are associated with an increased risk of anastomotic leak after colon resection for trauma [34]. Enterocutaneous fistula can develop after direct injury or spontaneously in the open abdomen. (See "Complications of laparoscopic surgery", section on 'Gastrointestinal puncture' and "Complications of laparoscopic surgery", section on 'Gastrointestinal injury' and "Management of anastomotic complications of colorectal surgery" and "Enterocutaneous and enteroatmospheric fistulas".)
●Penetrating or blunt trauma – Traumatic perforation of the gastrointestinal tract is most likely a result of penetrating injury, although blunt perforation can occur with severe abdominal trauma acutely related to pressure effects or as a portion of the gastrointestinal tract is compressed against a fixed bony structure, or more slowly as a contusion develops into a full-thickness injury. (See "Overview of esophageal injury due to blunt or penetrating trauma in adults" and "Traumatic gastrointestinal injury in the adult patient".)
●Medications, other ingestions, foreign body – Medications or other ingested substances (caustic injury) and foreign bodies (ingested or medical devices) can lead to gastrointestinal perforation. Foreign bodies, such as sharp objects (toothpicks), food with sharp surfaces (eg, chicken bones, fish), or gastric bezoar more commonly cause perforation, compared with dislodged medical implants [35-38]. Button batteries as an esophageal foreign body have a more pronounced perforation risk [39,40]. Surgically implanted foreign bodies such as hernia mesh [41] and artificial vascular grafts [42,43] can cause perforation with subsequent abscess and fistula formation or vasculoenteric fistulas. (See "Caustic esophageal injury in children" and "Caustic esophageal injury in adults" and "Foreign bodies of the esophagus and gastrointestinal tract in children" and "Ingested foreign bodies and food impactions in adults".)
Aspirin and nonsteroidal anti-inflammatory drug (NSAID) use has been associated with perforation of colonic diverticula, with diclofenac and ibuprofen being the most commonly implicated drugs [44]. Some disease-modifying antirheumatic drugs (DMARDs) have been associated with lower intestinal perforations [45]. Rarely, NSAIDs have produced jejunal perforations [46]. Glucocorticoids, particularly in association with NSAIDs, are particularly problematic [47,48]. Further, because steroids suppress the inflammatory response, detection of a perforation can be delayed. Interleukin-6 inhibiting drugs (eg, tocilizumab) and other biologic agents have been associated with bowel perforation [49]. Anti-inflammatory medications such as ketorolac have been associated with increased anastomotic leak after surgery.
NSAIDs, antibiotics, and potassium supplements are also common causative medications for pill-induced esophageal ulcers [50]. Other medication-induced injury leading to perforation has been reported for immunosuppressive therapies, cancer chemotherapy in patients with metastases, and for iron supplementation causing esophageal injury [2,51,52].
●Violent retching/vomiting – Violent retching/vomiting can lead to spontaneous esophageal perforation, known as Boerhaave syndrome. This occurs because of failure of the cricopharyngeal muscle to relax during vomiting or retching causing an increased intraesophageal pressure in the lower esophagus [53]. (See "Boerhaave syndrome: Effort rupture of the esophagus".)
●Hernia/intestinal volvulus/obstruction – Abdominal wall, groin, diaphragmatic, internal hernia, paraesophageal hernia, and volvulus (gastric, cecal, sigmoid) can all lead to perforation either related to bowel wall ischemia from strangulation, or pressure necrosis. Perforation can also occur with afferent loop obstruction after Roux-en-Y reconstruction. (See "Overview of abdominal wall hernias in adults" and "Etiologies, clinical manifestations, and diagnosis of mechanical small bowel obstruction in adults" and "Overview of treatment for inguinal and femoral hernia in adults" and "Surgical management of paraesophageal hernia" and "Gastric volvulus in adults" and "Postgastrectomy complications", section on 'Afferent and efferent loop syndrome'.)
●Inflammatory bowel disease – Crohn disease has a propensity to perforate slowly, leading to formation of entero-enteric or enterocutaneous fistula formation [54,55]. (See "Surgical management of Crohn disease" and "Surgical management of ulcerative colitis".)
●Appendicitis – Appendicitis can result in perforation, which, if left untreated, can lead to intra-abdominal infection, sepsis, intraperitoneal abscesses, and, rarely, death [56]. In adults, the risk of perforated appendicitis increases with male sex, increasing age and comorbidity, and lack of medical insurance coverage [57]. The diagnosis and management of perforated appendicitis are discussed elsewhere. (See "Acute appendicitis in adults: Diagnostic evaluation", section on 'Perforation' and "Management of acute appendicitis in adults", section on 'Perforated appendicitis'.)
●Peptic ulcer disease – Peptic ulcer disease (PUD) is the most common cause of stomach and duodenal perforation, which occurs in a small percentage of patients with PUD [58]. In spite of the introduction of proton pump inhibitors, the incidence of perforation from PUD has not changed appreciably [59]. Marginal ulceration leading to perforation may also complicate surgeries that create a gastrojejunostomy (eg, partial gastric resection, bariatric surgery). (See "Overview of complications of peptic ulcer disease".)
●Diverticular disease – Colonic diverticulosis is common in the developed world. All clinical cases of diverticulitis represent some degree of perforation of the thinned diverticular wall, leading to inflammation of the adjacent parietal peritoneum [60]. (See "Acute colonic diverticulitis: Surgical management" and "Overview of colon resection", section on 'Primary closure versus ostomy'.)
Perforation can also occur with duodenal or small intestinal diverticula (jejunal, Meckel's). These diverticula can become inflamed, much as in colonic diverticulitis, and perforate, which may lead to abscess formation. Nonoperative management of small bowel diverticulitis is much less successful than for colonic diverticulitis. (See "Meckel's diverticulum".)
●Cardiovascular disease – Any process that reduces the blood flow to the intestines (occlusive or nonocclusive mesenteric ischemia) for an extended period of time increases the risk for perforation, including embolism, mesenteric occlusive disease, cardiopulmonary resuscitation, and heart failure that leads to gastrointestinal ischemia [61]. (See "Overview of intestinal ischemia in adults".)
●Infectious disease – Typhoid, tuberculosis, and schistosomiasis can cause perforation of the small intestine [62,63]. With typhoid, the perforation is usually in a single location (ileum at necrotic Peyer's patches), but it can be multiple [64,65]. Typhoid perforation is more common in children, adolescents, or young adults. Cytomegalovirus, particularly in an immunosuppressed patient, can cause intestinal perforation [66]. Some reports have suggested that COVID-19 infections can be associated with spontaneous bowel perforation [67]. (See "COVID-19: Gastrointestinal symptoms and complications", section on 'Mesenteric ischemia'.)
●Neoplasms – Neoplasms can perforate by direct penetration and necrosis or by producing obstruction. Perforations related to tumors can also occur spontaneously, following chemotherapy, or as a result of radiation treatments when the tumor involves the wall of a hollow viscus organ [68-70]. Delayed perforations of the esophagus or duodenum in patients with malignancy can be related to stent placement for malignant obstruction.
●Connective tissue disease – Spontaneous perforation of the small intestine or colon has been reported in patients with underlying connective tissue diseases (eg, Ehlers-Danlos syndrome), collagen vascular disease, and vasculitis [71-73]. (See "Clinical manifestations and diagnosis of Ehlers-Danlos syndromes" and "Genetics, clinical features, and diagnosis of Marfan syndrome and related disorders".)
●Spontaneous intestinal perforation – This entity occurs in the neonate or in premature infants. No demonstrable cause is appreciated [74].
CLINICAL FEATURES
History — A careful history is important in evaluating patients with neck, chest, and abdominal pain. The history should include questioning about prior bouts of abdominal or chest pain, prior instrumentation (nasogastric tube, abdominal trauma, endoscopy), prior surgery, malignancy, possible ingested foreign bodies (eg, fish or chicken bone ingestion), and medical conditions (eg, peptic disease, medical device implants), including medications (nonsteroidal anti-inflammatory drugs [NSAIDs], glucocorticoids) that predispose to gastrointestinal perforation. (See 'Risk factors' above.)
Presentations — Patients with perforation may complain of chest or abdominal pain to some degree. Sudden, severe chest or abdominal pain following instrumentation or surgery is very concerning for perforation. Patients on immunosuppressive or anti-inflammatory agents may have an impaired inflammatory response, and some may have little or no pain and tenderness. Many patients will seek medical attention with the onset or worsening of significant chest or abdominal pain, but a subset of patients will present in a delayed fashion. These patients may present with an abdominal mass reflecting abscess formation, or fistula drainage, and some may present with abdominal sepsis. (See 'Acute pain' below and 'Fistula formation' below and 'Abdominal/pelvic mass' below and 'Sepsis' below.)
Acute pain — Inflammation of the gastrointestinal tract, as a result of perforation by a variety of etiologies, usually leads to some degree of neck pain (or dysphagia) or chest or abdominal discomfort.
The patient with a free perforation often notes with precision the time of the onset of the perforation. The patient may relate a sudden worsening of pain, followed by complete dissipation of the pain as perforation decompresses the inflamed organ, but relief is usually temporary. As the spilled gastrointestinal contents irritate the mediastinum or visceral peritoneum, a more constant pain will develop.
Acute symptoms associated with free perforation depend upon the nature and location of the gastrointestinal spillage (mediastinal, intraperitoneal, retroperitoneal). Cervical esophageal perforation can present with pharyngeal or neck pain associated with odynophagia, dysphagia, tenderness, or induration. Perforation of upper abdominal organs can irritate the diaphragm, leading to pain radiating to the shoulder. If perforation is confined to the retroperitoneum or lesser sac (eg, duodenal perforation), the presentation may be more subtle. Retroperitoneal perforations often lead to back pain.
Because the pH of gastric contents is 1 to 2 along the gastric luminal surface, a sudden release of this acid into the abdomen causes severe and sudden peritoneal irritation and severe pain. The acidity of the stomach contents is often buffered by recent food consumption. The leakage of small intestinal contents into the peritoneal cavity causes severe abdominal pain and peritonitis (ie, the "acute abdomen").
Abdominal/pelvic mass — It is not uncommon for perforation to lead to abscess or phlegmon formation that can be appreciated on examination as an abdominal mass or with abdominal exploration. A pelvic abscess caused by a perforation can sometimes be felt on digital rectal examination. Diverticulitis is the most common etiology leading to intra-abdominal abscess formation. (See "Clinical manifestations and diagnosis of acute diverticulitis in adults".)
Fistula formation (discussed below) can lead to a mass felt in the abdominal wall prior to spontaneous decompression and drainage.
Fistula formation — A fistula is an abnormal communication between two epithelialized surfaces. It can occur from bowel injury during instrumentation or surgery, anastomotic leak, or foreign body erosion. Fistulas are often related to inflammatory bowel diseases such as Crohn disease. Rarely, perforated colon carcinomas can fistulize to adjacent structures or to the abdominal wall.
When the initial gastrointestinal perforation is contained between two loops of bowel, subsequent inflammatory changes lead to the abnormal communication, which spontaneously decompresses any fluid collection or abscess that has formed. Patients who develop an external fistula will complain of the sudden appearance of drainage from a postoperative wound, or from the abdominal wall or perineum in the case of spontaneous fistulas. Intestines can fistulize to many organs or spaces (eg, bladder, uterus, other portion of the intestine, etc). (See "Enterocutaneous and enteroatmospheric fistulas".)
Sepsis — Sepsis can be the initial presentation of perforation, but its frequency is difficult to determine. The ability of the peritoneal surfaces to wall off a perforation may be impaired in patients with severe medical comorbidities, particularly frail, older, and immunosuppressed patients, resulting in free spillage of gastrointestinal contents into the abdomen, generalized abdominal infection, and sepsis [75]. Sepsis in itself can contribute to the causation of perforation by reducing intestinal wall perfusion [76].
These patients are very ill appearing, may or may not be febrile, and may be hemodynamically unstable with altered mental status. Anastomotic leak (eg, colon surgery) can be associated with increased fluid and blood transfusion requirements [77]. Organ dysfunction may be present, including acute respiratory distress syndrome, acute kidney injury, and disseminated intravascular coagulation. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis" and "Evaluation and management of suspected sepsis and septic shock in adults".)
Timely and adequate peritoneal source control is the most important determinant in the management of patients with acute peritonitis/abdominal sepsis [78]. In the Physiological Parameters for Prognosis in Abdominal Sepsis (PIPAS) study, the overall in-hospital mortality rate of 3137 patients was 8.9 percent. Independent variables associated with mortality include malignancy, severe cardiovascular disease, severe chronic kidney disease, respiratory rate >22 breaths/minute, systolic blood pressure <100 mmHg, unresponsiveness, room air oxygen saturation level <90 percent, platelet count <50,000/microL, and serum lactate level >4 mmol/L. These variables were used to create the PIPAS severity score. The overall mortality was 2.9 percent for patients with scores of 0 to 1, 22.7 percent for 2 to 3, 46.8 percent for 4 to 5, and 86.7 percent for 7 to 8 [79].
Physical examination — Physical examination should include vital signs; a thorough examination of the neck, chest, and abdomen; and rectal examination. In patients with gastrointestinal perforation, vital signs may initially be normal or reveal mild tachycardia or hypothermia. As the inflammatory response progresses, fever and other signs of sepsis may develop.
Palpation of the neck and chest should look for signs of subcutaneous gas and auscultation and percussion of the chest for signs of effusion. Mediastinal gas might be heard as a systolic "crunch" (Hamman's sign) at the apex and left sternal border with each heartbeat (movie 1) [53]. Palpation reveals crepitus in 30 percent of patients with thoracic esophageal perforation and in 65 percent of patients with cervical esophageal perforation [80]. Patients with esophageal rupture caused by barotrauma can have facial swelling.
The abdominal examination can be relatively normal initially or reveal only mild focal tenderness, as in the case of contained or retroperitoneal perforations. The abdomen may or may not be distended. Distention is common in patients with perforation related to small bowel obstruction but can also be from ileus secondary to free intra-peritoneal contamination. When free intraperitoneal perforation has occurred, typical signs of focal or diffuse peritonitis are present.
The rectal examination may be normal, as with contained upper abdominal gastrointestinal perforation, or reveal a palpable mass in the cul-de-sac, representing a phlegmon or abscess. There may also be rectal tenderness as well as bogginess secondary to inflammation.
Administration of opiate pain medication should not be withheld during the evaluation of acute abdominal pain. While physical examination can be affected, pain management is better and clinical outcomes are not significantly affected [81].
Laboratory studies — Laboratory studies are typically obtained in patients who present with acute abdominal pain including complete blood count (CBC), electrolytes, blood urea nitrogen (BUN), creatinine, liver function tests, lactate, amylase, and/or lipase.
Serum amylase may be elevated in patients with intestinal perforation due to absorption of amylase from the intestinal lumen [82]. However, this finding is nonspecific. Alterations in serum amylase can be due to a variety of conditions (table 1), and many drugs affect serum amylase values (table 2). (See "Approach to the patient with elevated serum amylase or lipase".)
C-reactive protein levels may help to diagnose gastrointestinal leak [83], particularly after bariatric surgery [84] or colorectal surgery [85,86]. It has also been useful for diagnosing perforation associated with typhoid fever [87]. (See "Management of anastomotic complications of colorectal surgery", section on 'Strictures'.)
Some inflammatory markers in drain fluid have also been associated with anastomotic leak following colorectal surgery. Although a diagnosis of gastrointestinal leak was made in the APPEAL study, it was done in conjunction with imaging studies or because of stool in the effluent [88]. Drain studies are generally unnecessary. In addition, most surgeons do not routinely place drainage tubes in the abdomen.
DIAGNOSIS
General approach — Gastrointestinal perforation may be suspected based upon history and physical examination findings, but a diagnosis relies upon imaging that demonstrates gas outside the gastrointestinal tract in the abdomen (ie, pneumoperitoneum) or mediastinum (ie, pneumomediastinum), or complications associated with perforation, such as an intra-abdominal or mediastinal abscess, or gastrointestinal fistula formation [89]. Other studies may be needed to confirm a clinical suspicion. Further evaluation for a specific diagnosis differs depending upon the potential etiologies, which may be suggested by the patient's clinical presentation in combination with determining the specific organ that has perforated. If a diagnosis of perforation is strongly suspected but imaging remains equivocal, abdominal exploration may be necessary. (See 'Indications for abdominal exploration' below and 'Further evaluation of specific organs' below.)
The diagnostic evaluation of most patients with abdominal complaints often begins with upright radiographs of the chest and abdomen. Supine and lateral decubitus films can be obtained in patients who cannot sit or stand. Chest films are helpful in the diagnosis of a patient with chest or abdominal pain approximately 90 percent of the time, but plain films cannot rule out a perforation. The reported sensitivity for detecting extraluminal gas on plain radiography ranges from 50 to 70 percent [90-93]. The yield of an upright plain chest film to detect free gas may be improved by having the patient sit fully upright or in a left lateral decubitus position for at least 10 to 20 minutes (if possible) prior to taking the film [91,92].
Another disadvantage of plain radiography is that, although perforation may be demonstrated, the source of the perforation usually cannot be localized. However, if there is a large amount of free gas on plain abdominal films (in the absence of recent surgery) and abdominal tenderness, the patient should be taken directly to surgery for exploration. If there is free gas and no abdominal pain (in the absence of immunosuppressive therapies), the cause for pneumoperitoneum could be benign, and additional studies may be warranted if there remain any concerns. (See "Evaluation of the adult with abdominal pain" and 'Differential diagnosis' below.)
If subcutaneous emphysema is identified in anteroposterior or posteroanterior projections on chest radiograph, the neck region should be carefully examined (if subcutaneous emphysema was not obvious beforehand), and lateral neck films should be obtained to determine if gas can be seen in prevertebral fascial planes.
Ultrasound has also been studied and shows some excellent potential for identifying pneumoperitoneum. Some studies show detection rates at or above chest films, especially in supine films, which may be the only option for certain patients [94-97].
The most useful imaging modality is computed tomography (CT), which is highly sensitive and specific for extraluminal gas, and which can usually be obtained quickly [60,98-100]. Patients suspected of a gastrointestinal tract perforation should be evaluated by abdominal CT scan. Compared with plain films, CT scans are more sensitive and can demonstrate smaller amounts of extraluminal gas, which may be best appreciated using lung windows. Since the peritoneal cavity can be divided into various compartments, the location of gas on abdominal CT scan can help suggest the site and cause of the perforation [90,101]. CT helps localize the site by identifying discontinuity of the bowel wall, the site of luminal contrast leakage, level of bowel obstruction, and gas in the bowel wall or bowel wall thickening with or without an associated inflammatory mass or abscess, or fistula [90]. Calcific vascular lesions and strangulating small bowel obstruction can also be seen. If perforation has been caused by a foreign body or enterolith, the object or stone may also be appreciated [102]. However, at times, the foreign body may migrate a distance from the initial perforation, and thus, its location does not necessarily correspond with the site of the perforation. In general, the volume of free gas within the abdomen or mediastinum varies with the extent and duration of the perforation.
Although demonstration of free intra-abdominal gas on imaging studies is a sign of perforation, this may not be helpful in the postoperative period, particularly after laparoscopic surgery, because approximately 40 percent of patients will have more than 2 cm of free gas at 24 hours postlaparoscopy, despite lack of any clinical evidence of bowel perforation [103-105]. However, because laparoscopy utilizes carbon dioxide to insufflate the abdomen, any residual gas in the peritoneum should be absorbed quickly. After laparotomy, however, free intra-abdominal gas often may be seen on a radiograph up to a week postoperatively, but the volume should gradually decrease with time. Increasing amounts of intra-abdominal gas during a period of observation is concerning, and a finding of increasing free intra-abdominal gas suggests perforation until proven otherwise.
Other imaging modalities can identify extraluminal gas. Gas can also be detected by ultrasound, although ultrasound is infrequently used for this purpose in the United States. Other findings on ultrasound that may signal perforation include the presence of free fluid, reduced peristaltic activity in the intestines, and localized abscess. Magnetic resonance imaging can also be used, but it is more time consuming, and a lack of generalized availability limits its usefulness [106].
Imaging signs of perforation — Imaging signs of gastrointestinal tract perforation are listed for the various imaging modalities.
Chest imaging
●Plain chest films (or chest CT scout film).
•Pneumomediastinum (in the absence of tracheal injury).
-The "V" sign of Naclerio is free gas in the mediastinum outlining the diaphragm (image 1) and is seen in approximately 20 percent of cases [107].
-Ring-around-the-artery sign (image 2).
-Widening of the mediastinum is sometimes seen with esophageal perforation.
•Free gas under the diaphragm on upright films (image 3).
•Pleural effusion may represent leaked esophageal contents (image 4).
•Pneumothorax is a rare finding in esophageal perforation and is thought to occur by the spread of gas along tissue planes (Macklin effect) [108].
•Subcutaneous emphysema may be seen in some cases.
●Chest CT: Pneumothorax, pneumomediastinum (in the absence of tracheal injury), pleural effusion, mediastinal abscess.
Abdominal imaging
●Plain abdominal films (or abdominal CT scout film).
•The appearance of pneumoperitoneum on plain films depends on the location of the gas and patient positioning. Gas outside the gastrointestinal tract (pneumoperitoneum) can be located freely in the peritoneal cavity (ie, free gas), in the retroperitoneal spaces, in the mesentery, or in ligaments of organs. Extraluminal gas may not be apparent if the perforation is small, has self-sealed, or has been contained by adjacent organs. Nonsurgical sources can also cause gas in the peritoneal cavity. (See 'Differential diagnosis' below.)
-Free gas under the diaphragm in upright abdominal films (image 3), gas over the liver (right lateral decubitus) or spleen (left lateral decubitus) or anteriorly on supine films (football sign) is indicative of gastrointestinal perforation.
-The Cupola sign (inverted cup) is an arcuate (bow-shaped) lucency over the lower thoracic spine in the supine patient secondary to air accumulating under the central tendon of the diaphragm [109].
-The Rigler sign (double-wall sign) is seen as gas outlining the inner and outer surfaces of the intestine (image 5).
-The Psoas sign is gas in the retroperitoneal space outlining the psoas muscle.
-The Urachus sign is gas in the preperitoneal space outlining the urachus or umbilical ligaments.
●Abdominal CT – Signs of perforation on abdominal CT scanning include extraluminal gas (image 6); extraluminal oral contrast; free fluid or food collections; and discontinuity of the intestinal wall, fistula, or intra-abdominal abscess often associated with irregular adjacent bowel wall thickening [90,102,110,111].
Neck imaging
●Plain films – Signs of perforation on plain neck imaging include subcutaneous emphysema tracking into the neck (image 2), anterior displacement of the trachea, and gas in the prevertebral fascial planes on lateral view (image 7).
Further evaluation of specific organs — Additional studies may be indicated as a means to further investigate a suspected perforation in a specific organ. Other imaging studies include endoscopy (upper, lower), esophagography, upper gastrointestinal series, ultrasound, contrast enema, and dye studies [112]. It is important to note that for suspected perforation, barium should not be used initially as an oral contrast agent, because it can produce granulomas in the tissues if it leaks out, and it can obscure abdominal findings on other imaging studies [112]. However, if extravasation has not been demonstrated on initial water-soluble contrast studies and suspicion for perforation remains high, barium can be administered orally or transrectally depending on the suspected site of perforation, provided additional CT or arteriography is not planned [113].
Endoscopy is an important tool for evaluating patients with suspected esophageal perforation, particularly following instrumentation, or related to noniatrogenic trauma [114,115]. Endoscopy allows direct inspection of the perforation and, in some cases, a therapeutic option. Endoscopy may show local erythema or spasm and essentially excludes the presence of the mucosal lesion. The disadvantage is the potential for causing a perforation with instrumentation. Nevertheless, in most cases, CT is obtained first because of its sensitivity and wide availability [116].
Dye studies may be useful for evaluating patients with a pleural effusion and a thoracostomy tube who are suspected to have an esophageal leak. Methylene blue introduced cautiously via a nasoesophageal tube will make or confirm the diagnosis by causing blue discoloration of the chest tube drainage.
DIFFERENTIAL DIAGNOSIS — Abdominal pain that is not associated with complaints such as nausea, vomiting, or diarrhea may be due to an etiology not related to the gastrointestinal tract. The etiology of chest pain is similarly broad, including a wide variety of conditions. (See "Causes of abdominal pain in adults".)
Pneumoperitoneum — A small subset of patients may have findings of pneumoperitoneum, identified typically on computed tomography (CT) scanning, that is not associated with abdominal discomfort. A nonsurgical etiology may be the cause of pneumoperitoneum in up to 10 percent of patients [117]. In patients on respiratory support, pneumoperitoneum can be due to continuous positive airway pressure (CPAP) or positive end-expiratory pressure (PEEP). Endoscopy, paracentesis, peritoneal dialysis, and vaginal instrumentation can also cause pneumoperitoneum [118]. On occasion, bacterial peritonitis has been associated with pneumoperitoneum [119,120], which is important to distinguish in cirrhotic patients, since exploratory surgery is associated with a mortality rate of approximately 80 percent in this patient population [121]. Pulmonary etiologies of pneumoperitoneum include pulmonary abscess and ruptured pulmonary alveoli.
Pneumatosis cystoides intestinalis is usually secondary to a surgical disease process. It manifests most commonly as gas-containing cysts in the wall of the small intestine or colon. Although most cases should be treated with operation, the absence of an elevated white count and C-reactive protein (CRP) in combination with benign abdominal examination leaves the option for nonoperative management [122]. (See "Epidemiology, clinical manifestations, and diagnosis of Pneumocystis pneumonia in patients without HIV" and "Clinical presentation and diagnosis of Pneumocystis pulmonary infection in patients with HIV".)
Placement of a percutaneous gastrostomy tube (PEG) can be the cause of intraperitoneal gas. The true incidence of pneumoperitoneum after PEG is unknown. In one review, among those who had imaging within five days after percutaneous endoscopic gastrostomy, the incidence of pneumoperitoneum was 12 percent [123]. Surgical intervention was required in only 0.83 percent. In this study of 722 patients who had a PEG procedure, 39 patients had intraperitoneal gas on postprocedural imaging. Of these, six (15 percent) had a serious complication requiring surgery. (See "Gastrostomy tubes: Complications and their management".)
Pneumomediastinum — Nonesophageal causes of pneumomediastinum include infection, asthma, trauma, cocaine abuse, and other rare etiologies such as high-speed air turbine drilling during dental procedures, or may be idiopathic [124]. In addition to causing pneumoperitoneum, perforated duodenal ulcer can also result in pneumomediastinum.
INITIAL MANAGEMENT — Initial management of the patient with gastrointestinal perforation includes intravenous (IV) fluid therapy, cessation of oral intake, and broad-spectrum antibiotics. Monitoring should initially take place in an intensive care unit. The administration of intravenous proton pump inhibitors is appropriate for those suspected to have upper gastrointestinal perforation.
Patients with intestinal perforation can have severe volume depletion. The severity of any electrolyte abnormalities depends upon the nature and volume of material leaking from the gastrointestinal tract. Surgical management of patients with free perforation should be expedited to minimize such derangements.
Electrolyte abnormalities are common among those who have developed a fistula as a result of perforation (eg, metabolic alkalosis from gastrocutaneous fistula). (See "Enterocutaneous and enteroatmospheric fistulas".)
Antibiotics — Broad-spectrum antibiotic therapy is initiated. The antibiotic regimen should be chosen based on the suspected site of perforation. If the level of perforation is unknown, a broad-spectrum antibiotic regimen can be initiated; precise regimen selection depends on patient risk factors for resistant bacteria and adverse outcomes. This is discussed in detail elsewhere. (See "Antimicrobial approach to intra-abdominal infections in adults", section on 'Regimens'.)
Conservative care — A subset of patients may not require immediate surgery to manage gastrointestinal perforation. Traditionally, conservative management of gastrointestinal perforation (including esophagus) was used only for patients who were deemed so ill that they would not likely survive surgery. The positive results achieved catalyzed extension of conservative management to other patients.
Patients chosen for nonoperative management are those with contained perforation, gastrointestinal fistula formation, or limited contamination as judged by imaging, in those who have no signs of systemic sepsis [125]. Not surprisingly, since patients chosen for conservative management in contemporary series are generally less ill, conservative management is often associated with lower rates of morbidity and mortality compared with surgical management.
A conservative approach including antibiotic therapy combined with drainage (effusion, abscess), provision for nutritional support (eg, gastrostomy, feeding jejunostomy), or stent placement may be an appropriate initial management strategy for patients with the following [126-128]:
●Perforated esophagus – (See "Surgical management of esophageal perforation", section on 'Alternatives to primary surgical repair' and "Overview of esophageal injury due to blunt or penetrating trauma in adults", section on 'Conservative treatment'.)
●Perforated appendicitis [129] – (See "Management of acute appendicitis in adults", section on 'Nonoperative management'.)
●Perforated colonic diverticulum – (See "Acute colonic diverticulitis: Surgical management", section on 'Perforation'.)
Indications for abdominal exploration — Many patients will require urgent surgical intervention to limit ongoing abdominal contamination and manage the perforated site. Immediate surgical consultation is appropriate whenever perforation is confirmed or even strongly suspected to determine if immediate surgical intervention is needed and the interval of time to surgery.
Patients with evidence of perforation and the following clinical signs benefit from immediate surgery:
●Abdominal sepsis, worsening or continuing abdominal pain, and/or signs of diffuse peritonitis. (See "Evaluation and management of suspected sepsis and septic shock in adults" and "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis".)
●Bowel ischemia. (See "Overview of intestinal ischemia in adults".)
●Complete or closed-loop bowel obstruction. (See "Management of small bowel obstruction in adults" and "Large bowel obstruction".)
SPECIFIC ORGANS
Esophagus — Perforations of the esophagus range from minute piercings, often following biopsy or sclerotherapy, to large-scale rupture of the esophageal wall, and presenting signs and symptoms also cover a wide range. The onset of pain related to esophageal perforation may be sudden or insidious. Pain on swallowing (ie, odynophagia) is the most frequent symptom [130]. Mortality related to esophageal perforation is highest for thoracic esophageal perforation at approximately 18 percent, followed by cervical esophageal perforation, then perforation at the gastroesophageal junction. (See 'Clinical features' above.)
Perforation of the esophagus is more often iatrogenic (endoscopy or related to surgery) or due to noniatrogenic penetrating or blunt traumatic mechanisms. Other causes include tumors, foreign body or caustic ingestion [35,36], pneumatic injury, peptic ulceration, intrinsic esophageal disease such as pill esophagitis [1,2], Crohn disease [3], eosinophilic esophagitis [4], or, more rarely, it is spontaneous (Boerhaave's syndrome). During surgery, the esophagus can be injured during operations such as hiatal hernia repair, thyroidectomy, pulmonary procedures, and vagotomy.
As an element of conservative care, covered stents are increasingly being used to manage some patients with esophageal perforation. Placed endoscopically, the stent covers the perforation while healing occurs. Complications associated with stents include bleeding, fistula and injury to adjacent structures, kinking, erosion, and reflux. Stents also have a tendency to migrate, which occurred in 33 percent of patients in one series [131]. However, stenting provides a window of time that may allow initial stabilization and healing, and conversion to open repair is always an option should the stent fail [132].
Notwithstanding innovations in conservative care for esophageal perforation, open surgery remains the mainstay of treatment. Surgical options for esophageal perforation include primary repair, repair over a drain, and, in the case of severe stricture or tumor, esophagectomy and esophageal exclusion [53,130]. The approach to open surgical repair depends upon the level of the perforation and may involve a neck incision and/or thoracotomy and, for lower esophageal perforation, potentially an upper abdominal incision as well. Specific management is reviewed in detail elsewhere. (See "Endoscopic stenting for palliation of malignant esophageal obstruction" and "Surgical management of esophageal perforation", section on 'Principles of surgical management' and "Surgical management of esophageal perforation" and "Overview of esophageal injury due to blunt or penetrating trauma in adults".)
Stomach and duodenum — Peptic ulcer disease is the most common cause of stomach and duodenal perforation. Marginal ulcers may complicate procedures involving a gastrojejunostomy (eg, partial gastrectomy, bariatric surgery). Although the frequency of elective surgery for peptic ulcer disease has declined, the incidence of peptic perforation has remained the same or is increasing [59]. Perforated duodenal ulcers are located on the anterior or superior portions of the duodenum and typically rupture freely, causing severe acute abdominal pain. Perforated gastric ulcer is associated with a higher mortality, possibly related to delays in diagnosis [133].
Other causes include iatrogenic (endoscopy, surgery [open or laparoscopic]) or noniatrogenic trauma [13,19,61], ingested foreign bodies [37], neoplasm (particularly during chemotherapy) [68,69], tuberculosis [134], and perforated duodenal diverticulum. Gastric perforation during cardiopulmonary resuscitation can also occur [61].
Most perforations of the stomach and duodenum require surgical repair (open or laparoscopic) [135-143]. The most common surgery for perforated peptic ulcer disease is oversewing the ulcer or the use of a Graham patch, which is used because suturing an inflamed ulcer can be difficult or impossible. The advent of natural orifice transluminal endoscopic surgery (NOTES) has led to the development of several methods of endoscopic gastric closure [144-146]. Regardless of whether an open, laparoscopic, or NOTES approach is used to provide local control or perform a definitive ulcer operation, it is important to obtain a biopsy of the ulcer margins in all patients with a gastric perforation to rule out gastric carcinoma. (See "Surgical management of peptic ulcer disease".)
Treatment for perforated duodenal diverticulum is usually diverticulectomy with closure of the duodenum. Omental fat can be used to buttress the repair with drainage tubes to permit egress of residual infected fluid. A subtotal gastrectomy with a Billroth II procedure or Roux-en-Y is sometimes used when extensive inflammation is present in the region. (See "Partial gastrectomy and gastrointestinal reconstruction".)
Small intestine — Perforation of the small intestine can be related to bowel obstruction, acute mesenteric ischemia, inflammatory bowel disease [55], or due to iatrogenic (laparoscopic access, takedown of adhesions, endoscopy) or noniatrogenic traumatic mechanisms. Injuries to the small intestine during laparoscopic procedures are often not recognized during the procedure [23]. Severe pain or sepsis after a laparoscopic procedure should be investigated promptly [24]. Perforations caused by the tumor (eg, lymphoma [70]) can occur spontaneously or after chemotherapy. Furthermore, because glucocorticoids suppress the inflammatory response, detection of a perforation can be delayed. Other causes of small intestinal perforation include foreign body ingestion, enteroliths/gallstones [5,6], or, more rarely, migrated stents (eg, esophageal, biliary).
Perforation of a diverticulum of the small intestine, such as in perforated Meckel's diverticulum, can occur and may lead to abscess formation. Occasionally, jejunal diverticula can become inflamed and perforate [147]. These rare diverticula are located along the mesenteric aspect of the proximal jejunum and decrease in number with increasing distance from the duodenal-jejunal junction. Rarely, nonsteroidal anti-inflammatory drugs (NSAIDs) have produced jejunal perforations [46].
Occasionally, particularly in resource-limited countries, diseases such as typhoid, tuberculosis [148], or schistosomiasis [63] can perforate the small intestine. In typhoid, the perforation is usually single but can be multiple 28 to 37 percent of the time [64,65]. The perforations usually occur in the ileum at necrotic Peyer's patches. Typhoid perforation is more common in children, adolescents, or young adults and has a high mortality (3 to 72 percent), reflecting, in part, the severity of the illness these patients have in addition to the effects of the perforation. A reperforation rate of 21.3 percent has been reported for typhoid perforation closure. Cytomegalovirus, particularly in an immunosuppressed patient, can also cause intestinal perforation.
Treatment of small intestinal perforation is performed by closing the perforation in one or two layers. If an injury has devitalized the small intestine or if it has been long-standing, producing indurated tissue, a small bowel resection is performed. (See "Bowel resection techniques" and "Traumatic gastrointestinal injury in the adult patient".)
Appendix — Approximately 30 percent of those with acute appendicitis present with perforation. Younger children often have atypical or vague symptoms and are more likely to present after perforation has occurred [149]. The management of perforated appendicitis is discussed in detail separately. (See "Management of acute appendicitis in adults", section on 'Perforated appendicitis' and "Acute appendicitis in children: Management", section on 'Advanced appendicitis'.)
Colon and rectum — Colon and rectal perforation is more commonly due to diverticulitis, neoplasm, and iatrogenic and noniatrogenic traumatic mechanisms, including surgery (eg, anastomotic leak). Colonic diverticulosis is common in the developed world, affecting up to 50 percent of adults, most with left-sided disease. In Asian countries, by contrast, the most common cause of right-sided colonic perforation is diverticulitis [150]. Several options exist for treating perforated diverticulitis. Most cases of diverticulitis with contained perforation or small abscess can be treated nonoperatively with antibiotics with or without percutaneous drainage. Resection is usually required for more severe diverticular complications [151].
The incidence of perforation during colonoscopy increases as the complexity of the procedure increases and is estimated at 1:1000 for therapeutic colonoscopy and 1:1400 for overall colonoscopies. The presence of collagenous colitis appears to predispose to perforation during colonoscopy [152]. In one series, the rectosigmoid area was most commonly perforated (53 percent), followed by the cecum (24 percent) [153]. In this series, most perforations were due to blunt injury, 27 percent of perforations occurred with polypectomy, and 18 percent of perforations were produced by thermal injury. Almost 25 percent of patients presented in a delayed fashion (after 24 hours). Polypectomy patients, in contrast to screening patients, were more likely to present in a delayed fashion. Most of the postprocedural perforations occurred in patients who had undergone bowel preparation, making primary anastomosis feasible. A poorly prepared bowel was a predictor of feculent peritonitis.
A myriad of other etiologies can lead to colonic or rectal perforation. NSAID use has been associated with serious diverticular perforation, with diclofenac and ibuprofen being the most commonly implicated drugs [44]. Glucocorticoids are also associated with diverticular perforation. Stercoral perforation, caused by ischemic necrosis of the intestinal wall by stool, is also possible, particularly in older individuals [154,155]. Perforation after barium enema or colonoscopy has been reported in patients with collagenous colitis [152]. Foreign bodies, either ingested or inserted, can cause colorectal perforation [156]. Colon perforation can also be related to collagen-vascular diseases such as Ehlers-Danlos syndrome type IV [157,158], Behcet syndrome [159], and eosinophilic granulomatosis with polyangiitis (Churg-Strauss) [160]. Perforation has been reported with anorectal manometry in the setting of a rectal anastomosis [161]. Perforation is also associated with invasive amebiasis of the colon [162]. In pediatric populations, bacterial colitis, particularly with nontyphoid Salmonella, can lead to perforation [163].
Colon perforations can be treated by simple suture if the perforation is small, often using a laparoscopic approach [164]. If the perforation is larger and devascularizing the colonic wall, colon resection will be necessary [165]. Patients with a perforated colon due to neoplasm also require resection [166]. Laparoscopic treatment of complicated disease is feasible but has a higher rate of conversion to open operation compared with uncomplicated disease [167]. A primary anastomosis is preferred, whenever feasible [151,168]. Primary anastomosis may be combined with proximal "protective" ostomy in those with complicated diverticulitis or malignancy. Colonic perforation due to Ehlers-Danlos syndrome is best treated with resection or exteriorization, or subtotal colectomy. (See "Overview of colon resection", section on 'Primary closure versus ostomy'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Gastrointestinal perforation".)
SUMMARY AND RECOMMENDATIONS
●General principles and risk factors – Perforation of the gastrointestinal tract leading to release of gastrointestinal contents requires full-thickness injury of the bowel wall. Partial-thickness bowel injury can progress over time to become full-thickness injury. Full-thickness injury and perforation of the gastrointestinal tract can be due to a variety of etiologies, commonly instrumentation or other trauma, and bowel obstruction. Other etiologies are less common. Spontaneous perforation can also occur and is related to inflammatory changes or weakening of the tissues from connective tissue disorders or drug effects. (See 'General principles' above and 'Risk factors' above.)
●Clinical manifestations – Clinical manifestations of gastrointestinal perforation depend on the organ affected and the nature of the contents released (gas, succus entericus, stool), as well as the ability of the surrounding tissues to contain those contents. Whether or not gastrointestinal perforation leads to free fluid and diffuse peritonitis or is contained, resulting in an abscess or fistula formation, depends upon location along the gastrointestinal tract and the patient's ability to mount an inflammatory response to the specific pathologic process. Immunosuppressive and anti-inflammatory medications impair this response. (See 'Pathophysiology' above and 'Anatomic considerations' above.)
•A careful history is important in evaluating patients with neck, chest, and abdominal pain. The history should include questioning about the factors known to predispose to gastrointestinal perforation listed above. (See 'Risk factors' above.)
•Patients with perforation invariably complain of chest or abdominal pain to some degree, though patients on immunosuppressive therapy or anti-inflammatory agents may have an impaired inflammatory response, and some may have little or no pain and tenderness. The patient with a free perforation often notes with precision the time of the onset of the perforation. A subset of patients will present in a delayed fashion, presenting with an abdominal mass reflecting abscess formation, or fistula drainage, and some may present initially with abdominal sepsis. (See 'Clinical features' above.)
●Diagnosis – A diagnosis relies upon imaging that demonstrates gas outside the gastrointestinal tract in the abdomen (ie, pneumoperitoneum) or mediastinum (ie, pneumomediastinum) on imaging (typically abdominal computed tomography [CT]), or complications associated with perforation, such as an intra-abdominal or mediastinal abscess or gastrointestinal fistula formation. Further evaluation for a specific diagnosis differs depending upon the potential etiologies, which may be suggested by the patient's clinical presentation in combination with determining the specific organ that has perforated. If a diagnosis of perforation is strongly suspected but imaging remains equivocal, abdominal exploration may be necessary. (See 'Diagnosis' above and 'Imaging signs of perforation' above.)
●Imaging – Free intra-abdominal gas often may be seen on a radiograph up to one week postoperatively, but the volume should gradually decrease with time. Increasing amounts of intra-abdominal gas during a period of postoperative observation are concerning, and a finding of increasing free intra-abdominal gas suggests perforation until proven otherwise. (See 'Imaging signs of perforation' above.)
A nonsurgical etiology may be the cause of pneumoperitoneum in up to 10 percent of patients. Etiologies include continuous positive airway pressure (CPAP) or positive end-expiratory pressure (PEEP), percutaneous gastrostomy placement, paracentesis, peritoneal dialysis, vaginal instrumentation, bacterial peritonitis, pulmonary abscess, and ruptured pulmonary alveoli. Pneumomediastinum can be due to infection, asthma, trauma, cocaine abuse, or other rare etiologies, or it may be idiopathic. (See 'Differential diagnosis' above.)
●Initial management – Initial management of the patient with gastrointestinal perforation includes intravenous fluid therapy and cessation of oral intake. Broad-spectrum antibiotic therapy should be initiated if the level of perforation is unknown but, when possible, should be chosen based upon the site of perforation. Antibiotic management for specific etiologies is discussed in separate topic reviews. (See 'Initial management' above.)
●Definitive management – Many patients will require urgent surgical intervention to limit ongoing abdominal contamination and manage the perforated site. Immediate surgical consultation is appropriate whenever perforation is confirmed or even strongly suspected. If there is a large amount of free gas on plain abdominal films (in the absence of recent surgery) and abdominal tenderness, urgent surgical treatment will most likely be required. Patients with evidence of perforation and complete or closed loop bowel obstruction, clinical sepsis, or signs of intestinal ischemia benefit from immediate surgery (See 'Indications for abdominal exploration' above.)
A subset of patients may not require immediate surgery to manage gastrointestinal perforation. Antibiotic therapy combined with drainage (eg, effusion, abscess cavity) may be an appropriate initial management strategy for patients with perforated esophagus, perforated appendicitis with abscess/phlegmon, and perforated colonic diverticulum with abscess/phlegmon. (See 'Conservative care' above and 'Specific organs' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Michael J Cahalane, MD, who contributed to an earlier version of this topic review.
