Overview of gastrointestinal tract perforation

INTRODUCTION — 

Perforation of the gastrointestinal tract is suspected on clinical presentation with the presence of extraluminal "free" gas or fluid, or fluid collection on diagnostic imaging performed to evaluate abdominal pain or another symptom. Clinical manifestations 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 and the nature of host-pathogen interactions.

Intestinal perforation may 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 (see 'Definitive management' below) and discussed in the linked topic reviews in more detail.

ANATOMY — 

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 or instrumentation usually occur at the site of esophageal constrictions 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 (figure 2). 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 3).

●The small bowel is anatomically divided into three portions: the duodenum, jejunum, and ileum (figure 4). The duodenum is retroperitoneal in its second and third portions 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 the ileum. Foreign bodies that perforate the small intestines most commonly occur at sites of gastrointestinal fixation (eg, duodenum or the terminal 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 5).

●The ascending and descending colon are retroperitoneal, while the transverse colon, which extends from the hepatic flexure to the splenic flexure, is intraperitoneal (figure 6). 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 males and the vagina in females (figure 7). Foreign bodies that perforate the colon tend to occur at transition zones from an intraperitoneal location to fixed retroperitoneal locations, such as the cecum.

ETIOLOGIES AND RISK FACTORS — 

Etiologic and risk 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. (See 'History' below.)

Etiologies by mechanisms — Gastrointestinal perforations in adults are most commonly caused by injury or bowel obstruction. Other etiologies (eg, inflammation) are numerous but less common.

Bowel injury — Perforation requires full-thickness injury of the bowel wall. Additionally, partial-thickness bowel injury (eg, electrocautery, blunt trauma) can progress over time to become a full-thickness injury or perforation, subsequently releasing gastrointestinal contents. Bowel injury can be caused by:

●Instrumentations – Instrumentation of the gastrointestinal tract is the main cause of iatrogenic perforation and may include endoscopy, percutaneous procedures, and surgery.

•Endoscopic procedures – The gastrointestinal tract is routinely instrumented by flexible and rigid upper endoscopy, endoscopic retrograde cholangiopancreatography, sigmoidoscopy, colonoscopy, as well as endoscopic procedures such as biopsy, dilation, stent placement, sclerotherapy, and endoscopic ultrasound. Endoscopy-related 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 'Adverse events'.)

•Percutaneous procedures – Many other percutaneous interventional procedures can also be complicated with gastrointestinal perforation, such as chest tube insertion low in the chest [1], peritoneal dialysis catheter insertion [2], percutaneous gastrostomy [3], paracentesis, diagnostic peritoneal lavage, and percutaneous drainage of fluid collections or abscesses.

Additionally, nasogastric tube placement can cause perforation of the esophagus or stomach. 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 [4]. (See "Inpatient placement and management of nasogastric and nasoenteric tubes in adults".)

•Surgery – Gastrointestinal perforation can occur during or after any abdominal surgery.

-Intraoperative – Perforation can occur at the initial entry into the abdomen, during mobilization of the organs, during the takedown of adhesions, or as a result of thermal injury from electrocautery devices [5,6]. (See "Complications of laparoscopic surgery", section on 'Bowel injuries'.)

-Postoperative – Gastrointestinal leakage can also occur postoperatively as a result of anastomotic disruption [7-14]. Immunosuppressed individuals and patients with serious medical illnesses such as diabetes and cirrhosis may be at increased risk for dehiscence and deep organ space infection following surgery [15]. Enterocutaneous fistula can develop after direct injury or spontaneously in the open abdomen. (See "Management of anastomotic complications of colorectal surgery", section on 'Dehiscence and leaks' and "Enterocutaneous and enteroatmospheric fistulas", section on 'Etiology and pathogenesis'.)

●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".)

●Caustic ingestions, foreign bodies, medications – Ingested substances (caustic injury), foreign bodies (ingested or medical devices), and medications 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 [16-19]. (See "Ingested foreign bodies and food impactions in adults" and "Internal concealment of drugs of abuse (body packing)".)

•Surgically implanted foreign bodies such as hernia mesh [20], stents, and artificial vascular grafts [21,22] can cause perforation with subsequent abscess and fistula formation or vasculoenteric fistulas. (See "Hernia mesh", section on 'Mesh-associated morbidities' and "Aortoenteric fistula: Recognition and management".)

•Glucocorticoids [23], other immunosuppressive or biologic drugs (eg, tocilizumab) [24], or cancer chemotherapy in patients with metastases have been associated with gastrointestinal perforations. Anti-inflammatory medications such as ketorolac have been associated with increased anastomotic leak after surgery.

Bowel obstruction — Abdominal wall, groin, diaphragmatic, internal, and paraesophageal hernia, as well as 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'.)

With bowel obstruction, perforation typically occurs proximal to the obstruction as pressure builds up within the bowel, exceeding intestinal perfusion pressure, and leading to ischemia and subsequent necrosis. Perforation may also occur at the site of the narrowing, such as a tight adhesive band, causing focal ischemia. As an example, in patients with gallstone ileus, enteroliths and gallstones can cause small bowel perforation either by direct pressure or indirectly by leading to obstruction, resulting in a proximal perforation [25,26]. (See "Gallstone ileus", section on 'Pathogenesis'.)

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)".)

Others — Other etiologies are numerous but less common [27-30].

●Inflammatory diseases – Acute and chronic inflammation can weaken the bowel wall and predispose to subsequent perforation. As an example, Crohn disease can cause inflammation of the entire alimentary tract. It has a propensity to perforate slowly, leading to the formation of enteroenteric or enterocutaneous fistula formation [31,32]. (See "Clinical manifestations, diagnosis, and prognosis of Crohn disease in adults", section on 'Features of transmural inflammation' and "Clinical manifestations, diagnosis, and prognosis of ulcerative colitis in adults", section on 'Acute complications'.)

Organ-specific inflammatory diseases (eg, appendicitis, diverticulitis) are discussed below. (See 'Etiologies by organs' below.)

●Neoplastic diseases – 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 [33-35]. Delayed perforations in patients with malignancy can be related to stent placement for malignant obstruction. (See "Endoscopic stenting for palliation of malignant esophageal obstruction" and "Enteral stents for the management of malignant colorectal 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 [36-38]. (See "Ehlers-Danlos syndromes: Clinical manifestations and diagnosis" and "Genetics, clinical features, and diagnosis of Marfan syndrome and related disorders".)

●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 [39]. (See "Overview of intestinal ischemia in adults".)

●Spontaneous intestinal perforation – This entity occurs in the neonate or in premature infants. No demonstrable cause is appreciated. (See "Spontaneous intestinal perforation of the newborn".)

Etiologies by organs

●Esophagus – More than half of esophageal perforations are iatrogenic following endoscopic (eg, biopsy, sclerotherapy, or dilation) or surgical procedures (eg, esophagectomy, hiatal hernia repair, thyroidectomy, pulmonary procedures, or vagotomy). Other causes include spontaneous (Boerhaave syndrome; 15 percent), foreign body or caustic ingestion (12 percent) [16,17], intrinsic esophageal disease such as pill esophagitis [27,28], Crohn disease [29], eosinophilic esophagitis [30], and trauma (9 percent). (See "Esophageal perforation", section on 'Etiology'.)

When the esophagus is perforated during upper endoscopy, there is often significant associated pathology, such as stricture, severe esophagitis [40], diverticulum, or the presence of cervical osteophytes. The area of the esophagus at most risk for instrumental perforation is the Killian triangle, which is the part of the pharynx formed by the inferior pharyngeal constrictor and cricopharyngeus muscle, and is a common site for the development of Zenker diverticulum (see "Zenker's diverticulum"). (See "Adverse events related to endoscopic dilation of esophageal strictures", section on 'Esophageal perforation'.)

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. (See "Spontaneous esophageal rupture (Boerhaave syndrome)".)

Nonsteroid anti-inflammatory drugs, antibiotics, and potassium or iron supplements are also common causative medications for pill-induced esophageal ulcer or injury [28,41-43].

●Stomach and duodenum – Peptic ulcer disease is the most common cause of stomach and duodenal perforation, which occurs in a small percentage of patients with peptic ulcer disease [44]. Despite the worldwide increase in the use of proton pump inhibitors, the incidence of perforation from peptic ulcer disease has not decreased appreciably [45]. Marginal ulceration leading to perforation may also complicate surgeries that create a gastrojejunostomy (eg, partial gastric resection, Roux-en-Y gastric bypass). 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 [46]. (See "Peptic ulcer disease: Clinical manifestations and diagnosis", section on 'Perforation'.)

Other causes include iatrogenic (endoscopy, surgery), trauma [1,39,47], ingested foreign bodies [18], neoplasm (particularly during chemotherapy) [33,34], tuberculosis [48], and perforated duodenal diverticulum. Gastric perforation during cardiopulmonary resuscitation can also occur [39].

●Small bowel – Perforation of the small intestine can be related to small bowel obstruction, acute mesenteric ischemia, inflammatory bowel disease [49], 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 [50]. Severe pain or sepsis after a laparoscopic procedure should be investigated promptly. (See "Complications of laparoscopic surgery", section on 'Bowel injuries'.)

Perforations caused by the tumor (eg, lymphoma [35]) 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 [25,26], or, more rarely, migrated stents (eg, esophageal, biliary).

Perforation of a diverticulum of the small intestine, such as Meckel diverticulum, can occur and may lead to abscess formation. Occasionally, jejunal diverticula can become inflamed and perforate [51]. 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 have produced jejunal perforations [52]. (See "Small bowel diverticula: Clinical manifestations, diagnosis, and management" and "Meckel's diverticulum".)

Typhoid, tuberculosis, and schistosomiasis can cause perforation of the small intestine [53,54]. With typhoid, the perforation is usually in a single location (the ileum at necrotic Peyer patches), but it can be multiple [55,56]. Typhoid perforation is more common in children, adolescents, or young adults. (See "Enteric (typhoid and paratyphoid) fever: Epidemiology, clinical manifestations, and diagnosis", section on 'Gastrointestinal manifestations'.)

Cytomegalovirus, particularly in an immunosuppressed patient, can cause intestinal perforation [57]. (See "AIDS-related cytomegalovirus gastrointestinal disease", section on 'Clinical manifestations'.)

Some reports have suggested that coronavirus disease 2019 (COVID-19) infections can be associated with spontaneous bowel perforation [58]. (See "COVID-19: Gastrointestinal symptoms and complications", section on 'Mesenteric ischemia'.)

●Appendix – Approximately 30 percent of appendicitis can result in perforation, which, if left untreated, can lead to intra-abdominal infection, sepsis, intraperitoneal abscesses, and, rarely, death [59]. In adults, the risk of perforated appendicitis increases with male sex, increasing age, comorbidity, and lack of medical insurance coverage [60]. Younger children and older adults often have atypical or vague symptoms and are more likely to present after perforation has occurred [61,62]. The diagnosis and management of perforated appendicitis are discussed elsewhere. (See "Management of acute appendicitis in adults", section on 'Perforated appendicitis'.)

●Colon and rectum – Colon and rectal perforation is most commonly due to diverticulitis, neoplasm, iatrogenic (endoscopy and surgery), and trauma. The colon is the most perforated gastrointestinal organ during endoscopy. The incidence of perforation increases with procedural complexity; perforation is less common with diagnostic compared with therapeutic procedures [63]. (See "Overview of colonoscopy in adults", section on 'Perforation'.)

Because colonic diverticulosis is common in resource-abundant countries, sigmoid diverticulitis is most prevalent. All clinical cases of diverticulitis represent some degree of perforation of the thinned diverticular wall, leading to inflammation of the adjacent parietal peritoneum [64]. Free perforations leading to generalized peritonitis require urgent surgical intervention. (See "Acute colonic diverticulitis: Surgical management", section on 'Perforation'.)

A myriad of other etiologies can lead to colonic or rectal perforation. The use of aspirin, nonsteroidal anti-inflammatory drugs, and some disease-modifying antirheumatic drugs has been associated with serious diverticular perforation [65,66], with diclofenac and ibuprofen being the most commonly implicated drugs [67]. Glucocorticoids are also associated with diverticular perforation. Colonic perforations, particularly involving the transverse colon, can be a result of infected pancreatic necrosis and subsequent postinflammatory ischemia [68]. Stercoral perforation, caused by ischemic necrosis of the intestinal wall by stool, is also possible, particularly in older individuals [69,70]. Perforation after barium enema or colonoscopy has been reported in patients with collagenous colitis [71]. Foreign bodies, either ingested or inserted, can cause colorectal perforation [72]. Colon perforation can also be related to collagen-vascular diseases such as Ehlers-Danlos syndrome type IV [73,74], Behçet syndrome [75], and eosinophilic granulomatosis with polyangiitis (Churg-Strauss) [76]. Perforation has been reported with anorectal manometry in the setting of a rectal anastomosis [77]. Perforation is also associated with invasive amebiasis of the colon [78].

In pediatric populations, bacterial colitis, particularly with nontyphoid Salmonella, can lead to perforation [79]. Neutropenic enterocolitis is defined as severe inflammation associated with neutropenia, typically associated with chemotherapeutic agents. They usually involve the cecum and the right colon. Rarely, they lead to perforation, which carries a high mortality [80]. (See "Neonatal necrotizing enterocolitis: Management and prognosis", section on 'Surgical management'.)

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, recent instrumentation (nasogastric tube, endoscopy) or abdominal trauma, and prior surgery. Sudden, severe chest or abdominal pain following instrumentation or surgery is very concerning for perforation. (See 'Etiologies and risk factors' above.)

The history should also inquire about possible ingested foreign bodies (eg, fish or chicken bone), malignancy, and other medical conditions (eg, peptic ulcer disease, medical device implants), including medications (nonsteroidal anti-inflammatory drugs, glucocorticoids) that predispose to gastrointestinal perforation. Patients on immunosuppressive or anti-inflammatory agents may have an impaired inflammatory response, and some may have little or no pain and tenderness.

Presentations — The severity of the patient's discomfort depends on whether the perforation is free or contained.

Free perforation — The patient with a free perforation into the peritoneal cavity can often pinpoint the precise time of onset. 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 is likely to develop.

●Cervical esophageal perforation can present with pharyngeal or neck pain associated with odynophagia, dysphagia, neck 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").

●As free gas accumulates in the peritoneal cavity, it can lead to a reduction in venous return and respiratory insufficiency by compromising diaphragmatic function [81]. Such a tension pneumoperitoneum (valvular pneumoperitoneum) can result from iatrogenic or pathologic processes. Perforation and subsequent inflammation can also cause abdominal compartment syndrome [82]. (See "Abdominal compartment syndrome in adults".)

Contained perforation — While many patients will seek immediate medical attention with the onset or worsening of significant chest or abdominal pain, a subset of patients will present in a delayed fashion. These patients may present with an abdominal mass reflecting abscess formation, or fistula drainage. Some may present with abdominal sepsis.

●Abscess formation – 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 colonic diverticulitis in adults", section on 'Abscess'.)

●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 or other gastrointestinal 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 erode into adjacent organs, 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 (see "Enterocutaneous and enteroatmospheric fistulas"). In other cases, intestines can fistulize to many organs or spaces (eg, bladder, uterus, other portions of the intestine, etc). (See "Diverticular fistulas" and "Colovesical fistulas" and "Urogenital tract fistulas in females".)

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 [83]. Thus, it can occur with either free or contained perforation. Furthermore, sepsis in itself can contribute to the causation of perforation by reducing intestinal wall perfusion [84].

Septic patients could appear ill, may or may not be febrile, and may be hemodynamically unstable with altered mental status. Organ dysfunction may be present, including acute respiratory distress syndrome, acute kidney injury, and disseminated intravascular coagulation. Timely diagnosis and adequate peritoneal source control are the most important determinants in the management of patients with acute peritonitis/abdominal sepsis [85]. (See "Antimicrobial approach to intra-abdominal infections in adults", section on 'Source control and drainage'.)

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 sign) at the apex and left sternal border with each heartbeat (movie 1) [86]. Palpation reveals crepitus in 30 percent of patients with thoracic esophageal perforation and in 65 percent of patients with cervical esophageal perforation [87]. 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 intraperitoneal contamination. With free intraperitoneal perforation, typical signs of 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 [88].

Laboratory studies — Laboratory studies are typically obtained in patients who present with acute abdominal pain including complete blood count, electrolytes, blood urea nitrogen, creatinine, liver function tests, lactate, amylase or lipase, and an inflammatory marker (eg, C-reactive protein or procalcitonin).

●Although laboratory abnormalities can vary depending on the timing and severity of the condition, typical findings reflect inflammation, infection, and possibly sepsis, and include leukocytosis (with possible left shift), high anion gap metabolic (lactic) acidosis, and abnormal electrolytes (eg, hyponatremia, hypokalemia).

●Liver function tests will be normal for an isolated perforation but may be elevated when the perforation is near the liver (eg, gallbladder or duodenum), or when in septic shock (due to hypoperfusion of the liver).

●Serum amylase may be elevated in patients with intestinal perforation due to absorption of amylase from the intestinal lumen [89] or in patients with pancreatitis. As such, 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 [90], particularly after bariatric surgery [91] or colorectal surgery [92,93]. It has also been useful for diagnosing perforation associated with typhoid fever [94]. (See "Management of anastomotic complications of colorectal surgery", section on 'Definition and manifestations'.)

Clinical instruments for prognostication in abdominal sepsis — 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 [95].

DIAGNOSTIC EVALUATION — 

Gastrointestinal perforation may be suspected based on 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 [96]. 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.

Imaging modalities — 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. Although a large amount of free gas on a plain film may diagnose a gastrointestinal perforation, negative plain films cannot exclude a gastrointestinal perforation or localize its source. (See 'Plain films' below.)

Stable patients should be further evaluated by chest/abdominal/pelvic computed tomography (CT). Compared with plain films, CT scans are much more sensitive and are more likely to localize the source of the perforation. (See 'Computed tomography' below.)

In patients undergoing CT scan for suspected gastrointestinal perforation, intravenous contrast is generally recommended, but oral contrast may not be necessary and may even be discouraged in some settings [97]. However, in patients with suspected postoperative leak, interloop abscess, or fistula, giving oral contrast with delayed scanning ("long-prep" CT) might provide more information than a noncontrast CT.

Plain films — 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 [98-101]. The yield of a 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 [99,100].

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 with signs of peritonitis (guarding, rebound tenderness), the patient can be taken directly to surgery for exploration. If there is free gas but 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.

Computed tomography — The most useful imaging modality is CT, which is highly sensitive and specific for extraluminal gas [64,102-104]. Compared with plain films, CT scans can demonstrate small amounts (1 cm³) 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 an abdominal CT scan can help suggest the site and cause of the perforation [98,105]. 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 [106]. 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 [107]. 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 [108]. The presence of free air 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 air at 24 hours post-laparoscopy, despite the lack of any clinical evidence of bowel perforation [109,110]. 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 [111], but the volume should gradually decrease with time. An increasing amount of intra-abdominal gas during a period of observation is concerning and may indicate perforation. Similarly, intra-abdominal gas is routinely noticed following a percutaneous endoscopic gastrostomy tube placement.

Others — Other imaging modalities can identify extraluminal gas but are less commonly used than CT.

●Ultrasound has been studied but is infrequently used for this purpose in the United States, although it shows some excellent potential for identifying pneumoperitoneum at the point of care [112,113]. 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 [114].

Imaging signs of perforation — Imaging signs of gastrointestinal tract perforation are listed for plain radiography and CT.

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 [115].

-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) [116].

•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 [117].

-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 [98,106,107,118].

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, contrast studies, and dye studies [119].

●Endoscopies – Endoscopy is an important tool for evaluating patients with suspected esophageal perforation, particularly following instrumentation, or related to noniatrogenic trauma [120,121]. 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 increasing the size of the perforation. Nevertheless, in most cases, CT is obtained first because of its sensitivity and wide availability [122]. (See "Spontaneous esophageal rupture (Boerhaave syndrome)", section on 'Diagnosis' and "Overview of esophageal injury due to blunt or penetrating trauma in adults", section on 'Esophagoscopy and esophagography'.)

●Contrast studies – Depending on the involved organ, fluoroscopic contrast studies are called esophagography, upper gastrointestinal series, or contrast enema. It is important to note that for suspected perforation, water-soluble contrast is preferred over barium for the risk of mediastinitis or granulomatous peritonitis associated with barium [119]. 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 [123].

●Dye studies – Dye studies may be useful for evaluating patients with a pleural effusion and a thoracostomy tube who are suspected of 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 — 

The differential diagnosis of pain is broad and needs to be narrowed down by clinical reasoning, lab work, and imaging studies. Although gastrointestinal perforation is usually diagnosed by imaging evidence of gas outside of the alimentary tract, the converse is not always true. Pneumoperitoneum and pneumomediastinum may not be a result of perforation. This is important because surgical intervention should be avoided when there is no perforation.

Pain — 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. (See "Causes of abdominal pain in adults" and "Evaluation of the adult with nontraumatic abdominal or flank pain in the emergency department".)

The etiology of chest pain is similarly broad, including a wide variety of conditions. (See "Approach to the adult with nontraumatic chest pain in the emergency department".)

Isolated pneumoperitoneum — A small subset of patients may have findings of pneumoperitoneum, identified typically on CT, that is not associated with abdominal discomfort. A nonsurgical etiology may be the cause of pneumoperitoneum in up to 10 percent of patients [124]. These include:

●In patients on respiratory support, pneumoperitoneum can be due to continuous positive airway pressure or positive end-expiratory pressure.

●Endoscopy, paracentesis, peritoneal dialysis, and vaginal instrumentation can also cause pneumoperitoneum [125].

●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 [126]. 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".)

●On occasion, bacterial peritonitis has been associated with pneumoperitoneum [127,128], 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 [129].

●Pneumoperitoneum (on CT) is expected after surgical exploration of the abdomen for up to one week. (See 'Computed tomography' above.)

Nonesophageal causes of pneumomediastinum — Nonesophageal causes of pneumomediastinum include infection, asthma, trauma, cocaine use, and other rare etiologies such as high-speed air turbine drilling during dental procedures, or may be idiopathic [130]. In addition to causing pneumoperitoneum, a perforated duodenal ulcer can also result in pneumomediastinum by tracking through the retroperitoneum into the mediastinum [131,132].

MANAGEMENT

Initial management — Initial management of the patient with gastrointestinal perforation includes intravenous fluid therapy, cessation of oral intake, and broad-spectrum antibiotics. The administration of intravenous proton pump inhibitors is appropriate for those with suspicion of upper gastrointestinal perforation.

●Fluid resuscitation – Patients with intestinal perforation can have severe volume depletion, and the increased fluid requirement is also a result of poor oral intake. Thus, intravenous fluid resuscitation is required. (See "Maintenance and replacement fluid therapy in adults".)

●Correction of electrolyte deficits – The severity of any electrolyte abnormalities depends upon the nature and volume of the leakage from the gastrointestinal tract. Electrolyte abnormalities are common among those who have developed a fistula (eg, metabolic alkalosis from gastrocutaneous fistula (table 3)). (See "Enterocutaneous and enteroatmospheric fistulas".)

●Antibiotics – Following a gastrointestinal perforation, broad-spectrum antibiotic therapy is initiated; routine use of antifungal therapy is not required. The antibiotic regimen should be chosen based on whether the patient has mild (table 4) or severe infection (table 5), and if the infection is community or hospital acquired (table 6). This is discussed in detail elsewhere. (See "Antimicrobial approach to intra-abdominal infections in adults", section on 'Approach to empiric antibiotic selection'.)

Definitive management — Once gastrointestinal perforation is diagnosed, patients with abdominal sepsis, worsening or continuing abdominal pain, and/or signs of diffuse peritonitis require urgent surgical exploration. The purpose of surgery is to limit ongoing abdominal contamination and manage the perforated site (ie, source control). (See "Evaluation and management of suspected sepsis and septic shock in adults" and "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis".)

A subset of patients may not require immediate surgery to manage gastrointestinal perforation. Patients are chosen for nonoperative management based on the absence of systemic signs of sepsis, especially those with contained perforation and gastrointestinal fistula [133]. Nonoperative management usually entails a combination of percutaneous drainage (effusion, abscess), provision for nutritional support (eg, gastrostomy, feeding jejunostomy), and endoscopic clipping/stenting/vacuum therapy where applicable [134-136]:

The definitive treatment of gastrointestinal perforation is discussed in the context of a specific organ and etiology of perforation below.

Esophagus — An esophageal perforation can be managed surgically, endoscopically, or medically. The appropriate treatment is selected based on the etiology of the perforation and the patient's condition (algorithm 1). This is discussed in detail elsewhere. (See "Esophageal perforation", section on 'Definitive management'.)

Stomach and duodenum — Most perforations of the stomach and duodenum require surgical repair. The most common surgery for a perforated peptic ulcer is oversewing the ulcer or the use of a Graham patch, which is used because suturing an inflamed ulcer can be difficult or impossible. Biopsy of the gastric perforations is typically recommended to rule out malignancy and evaluate the presence of Helicobacter pylori. Surgery can be performed via an open or minimally invasive approach [137-144]. (See "Surgical management of peptic ulcer disease".)

A subtotal gastrectomy with a Billroth II or Roux-en-Y reconstruction is sometimes used when extensive inflammation is present in the region of gastroduodenal perforation. Treatment for a 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.

Patients with gastroduodenal perforations, where at surgery, the perforation is noted to be completely covered by omental adhesions, could be left alone with placement of intraperitoneal drains. (See "Partial gastrectomy and gastrointestinal reconstruction".)

Treatment of postbariatric surgery leaks depends on the procedure and patient condition. Details are discussed in other topics. (See "Metabolic and bariatric operations: Early morbidity and mortality", section on 'Gastrointestinal leak'.)

Small intestine — Small intestinal perforation requires surgical repair, which is performed by closing the perforation in one or two layers if the perforation is clean and small. Small bowel injuries involving more than half the circumference, the presence of significant inflammation, or patients with significant hemodynamic instability often warrant bowel resection. The timing and nature of subsequent reconstruction, including adopting a damaged control approach, is based on the general status of the patient and underlying comorbidities. In patients with ileal perforations and severe hemodynamic instability due to septic shock, it may be wise to perform an end ileostomy rather than an ileocolic anastomosis. (See "Bowel resection techniques" and "Traumatic gastrointestinal injury in the adult patient".)

Appendix — Perforated appendicitis is treated with upfront surgery or antibiotics plus drainage, depending on the patient's presentation (algorithm 2). This is discussed in detail separately. (See "Management of acute appendicitis in adults", section on 'Perforated appendicitis' and "Acute appendicitis in children: Management", section on 'Complicated appendicitis'.)

Colon and rectum — A perforated colon or rectum typically requires surgical resection. Primary anastomosis is preferable, but a diverting colostomy or ileostomy may be necessary in some clinical scenarios (eg, septic patients, local tissue inflammation/edema, or severe comorbidities). The management of colorectal perforation is also discussed separately by etiologies:

●Perforated diverticulitis – Colonic diverticulosis is common in resource-abundant countries, affecting up to 50 percent of adults, most with left-sided disease. In Asian countries, the most common cause of right-sided colonic perforation is diverticulitis [145]. 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 frank or free perforation (algorithm 3). The management of perforated diverticulitis can be found elsewhere. (See "Acute colonic diverticulitis: Surgical management", section on 'Perforation'.)

●Colonoscopy – The incidence of perforation during colonoscopy increases as the complexity of the procedure increases (1:10000 to 1:1000 for screening colonoscopy and higher for therapeutic colonoscopies). If perforation is suspected, immediate abdominal and chest radiographs or CT should be obtained to look for free air under the diaphragm, retroperitoneal air, pneumomediastinum, pneumothorax, or subcutaneous emphysema (see 'Diagnostic evaluation' above). A confirmed perforated colon or rectum can be managed surgically (resection), endoscopically (clipping of the perforation), or medically (antibiotics), depending on the patient's condition. (See "Overview of colonoscopy in adults", section on 'Perforation'.)

●Anastomotic leak – The overall incidence of anastomotic leaks after colorectal surgery is 2 to 7 percent. Most leaks become apparent between five and seven days postoperatively. A suspected leak should be characterized by a CT scan. A free intraperitoneal leak requires surgical repair, diversion, or both. A large, contained leak may be managed with percutaneous drainage or endoluminal vacuum therapy (if accessible). A small, contained leak (subclinical) may be managed with antibiotics. (See "Management of anastomotic complications of colorectal surgery", section on 'Dehiscence and leaks'.)

●Perforated colorectal cancer – Colorectal neoplasms can cause perforation by direct penetration of the tumor through the bowel wall or from complete bowel obstruction, ischemia from increased intraluminal pressure, and subsequent perforation. 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. Treatment of a perforated colorectal cancer is typically surgical and consists of resection, diversion, or both, depending on the patient's presentation. (See "Large bowel obstruction", section on 'Patients requiring immediate surgery'.)

Perforation not identified at surgical exploration — Patients in whom no clear site of perforation is identified at laparotomy or laparoscopic evaluation could be managed by placement of intraperitoneal drains and subsequent gastrointestinal evaluation by contrast enterography [146].

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".)

INFORMATION FOR PATIENTS — 

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Gastrointestinal tract perforation (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Etiologies and risk factors – Gastrointestinal perforations are most commonly caused by injury or bowel obstruction. (See 'Etiologies and risk factors' above.)

•The bowel can be injured by instrumentation (endoscopy, percutaneous procedures, surgery), trauma (penetrating or blunt), or ingestion (foreign substance, medical device, medications). (See 'Bowel injury' above.)

•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 'Bowel obstruction' above.)

•Less often, spontaneous perforation can also occur and is related to inflammatory changes or weakening of the tissues from connective tissue disorders or drug effects. (See 'Others' above.)

Etiologies specific to individual organs are discussed above. (See 'Etiologies by organs' above.)

●Clinical features – Depending 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, patients can present with either a free or a contained perforation, and with or without abdominal sepsis. (See 'Presentations' above.)

•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, recent instrumentation (nasogastric tube, endoscopy), abdominal trauma, and prior surgery. (See 'History' above.)

•Physical findings – Physical examination should include vital signs; a thorough examination of the neck, chest, and abdomen; and a rectal examination. (See 'Physical examination' above.)

•Laboratory studies – Laboratory studies typically obtained in patients who present with acute abdominal pain include complete blood count, electrolytes, blood urea nitrogen, creatinine, liver function tests, lactate, amylase or lipase, and an inflammatory marker (eg, C-reactive protein or procalcitonin). (See 'Laboratory studies' above.)

●Diagnostic evaluation – A diagnosis relies upon imaging that demonstrates gas outside the gastrointestinal tract in the abdomen (ie, pneumoperitoneum) or mediastinum (ie, pneumomediastinum; typically CT), or complications associated with perforation, such as an intra-abdominal or mediastinal abscess or gastrointestinal fistula formation. (See 'Imaging modalities' above.)

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 'Further evaluation of specific organs' above.)

●Differential diagnosis – Many patients present with chest or abdominal pain that is not due to a gastrointestinal etiology. (See 'Pain' above.)

A nonsurgical etiology may be the cause of pneumoperitoneum in up to 10 percent of patients. Additionally, free intra-abdominal gas often may be seen on imaging up to one week postoperatively, but the volume should gradually decrease with time. (See 'Isolated pneumoperitoneum' above.)

Nonesophageal causes of pneumomediastinum include infection, asthma, trauma, cocaine use, and idiopathic conditions. (See 'Nonesophageal causes of pneumomediastinum' above.)

●Initial management – Initial management of the patient with gastrointestinal perforation includes intravenous fluid resuscitation, cessation of oral intake, and broad-spectrum antibiotics. The administration of intravenous proton pump inhibitors is appropriate for those suspected of having upper gastrointestinal perforation. Antibiotic selection is discussed in separate topic reviews. (See 'Initial management' above and "Antimicrobial approach to intra-abdominal infections in adults", section on 'Approach to empiric antibiotic selection'.)

●Definitive management – Once gastrointestinal perforation is diagnosed, patients with abdominal sepsis, worsening or continuing abdominal pain, and/or signs of diffuse peritonitis require urgent surgical exploration. The purpose of surgery is to limit ongoing abdominal contamination and manage the perforated site (ie, source control). (See 'Definitive management' above.)

Patients may not require immediate surgery to manage gastrointestinal perforation if they have a contained perforation, gastrointestinal fistula, or limited contamination as judged by imaging, and they have no signs of systemic sepsis. Nonoperative management usually entails a combination of percutaneous drainage (effusion, abscess), provision for nutritional support (eg, gastrostomy, feeding jejunostomy), and endoscopic clipping/stenting/vacuum therapy of the perforation where applicable.

Detailed discussion of definitive treatment of gastrointestinal perforation of specific organs can be found in the following topics:

•Esophagus – (See "Esophageal perforation", section on 'Definitive management'.)

•Stomach and duodenum – (See "Surgical management of peptic ulcer disease" and "Metabolic and bariatric operations: Early morbidity and mortality", section on 'Gastrointestinal leak'.)

•Small intestine – (See "Bowel resection techniques" and "Traumatic gastrointestinal injury in the adult patient".)

•Appendix – (See "Management of acute appendicitis in adults", section on 'Perforated appendicitis' and "Acute appendicitis in children: Management", section on 'Complicated appendicitis'.)

•Colon and rectum – (See "Acute colonic diverticulitis: Surgical management", section on 'Perforation' and "Overview of colonoscopy in adults", section on 'Perforation' and "Management of anastomotic complications of colorectal surgery", section on 'Dehiscence and leaks' and "Large bowel obstruction", section on 'Patients requiring immediate surgery'.)

ACKNOWLEDGMENT — 

The UpToDate editorial staff acknowledges Michael J Cahalane, MD, who contributed to an earlier version of this topic review.