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" air 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 (air, 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 emergent 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, commonly
instrumentation (particularly with cautery) or surgery, blunt or penetrating injury, and
bowel obstruction. In addition to causing obstruction, neoplasms (particularly colon
carcinoma) can also cause perforation by direct penetration of the tumor through the
bowel wall. Other etiologies are less common [1-4]. Spontaneous perforation can be
related to inflammatory changes or tissues weakened by medications or connective
tissue disorders. Esophageal, gastric, or duodenal perforations may also be
associated with peptic ulcer disease, corrosive agents, or particular medications.
(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 in the presence of a competent ileocecal
valve. 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 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).
 ●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 [9].

●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 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 immobility (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 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, the 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 [10,11], stent placement [10,11],
endoscopic sclerotherapy [12], nasogastric intubation [13], 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 [14]. A perforation rate of 0.11 percent for rigid endoscopy contrasts with
a 0.03 percent rate for flexible endoscopy [15,16]. When iatrogenic perforation
occurs, there is often significant associated pathology. As an example, in the
esophagus, there may be stricture, severe esophagitis [17], or a diverticulum, and the
presence of cervical osteophytes also increases the risk [16]. The area of the
esophagus at most risk for instrumental perforation is Killian's triangle [18], 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 upper gastrointestinal endoscopy
(esophagogastroduodenoscopy)", section on 'Perforation' and "Overview of
colonoscopy in adults", section on 'Perforation'.)

Other procedures can also be complicated with perforation, such as chest tube
insertion low in the chest [19], peritoneal dialysis catheter insertion, percutaneous
gastrostomy [20], paracentesis, diagnostic peritoneal lavage, and percutaneous
drainage of fluid collections or abscess.

With surgery, perforation can occur during initial laparoscopic access, during
mobilization of the organs or during the takedown of adhesions, or as a result of
thermal injury from electrocautery devices [21-23]. Gastrointestinal leakage can also
occur postoperatively as a result of anastomotic breakdown [24-31].
Immunosuppressed individuals may be at increased risk for dehiscence and deep
organ space infection following surgery [32]. Medical illnesses such as diabetes,
cirrhosis, and HIV are associated with an increased risk of anastomotic leak after
colon resection for trauma [33]. (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".)

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
perforation due to blunt or penetrating trauma" 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 [34-37]. Button
batteries as an esophageal foreign body have a more pronounced perforation risk
[38,39]. Surgically implanted foreign bodies such as hernia mesh [40] and artificial
vascular grafts [41,42] 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 [43]. Some disease-modifying antirheumatic drugs
(DMARDs) have been associated with lower intestinal perforations [44]. Rarely,
NSAIDs have produced jejunal perforations [45]. Glucocorticoids, particularly in
association with NSAIDs, are particularly problematic [46,47]. Further, because
steroids suppress the inflammatory response, detection of a perforation can be
delayed.

NSAIDs, antibiotics, and potassium supplements are also common causative

medications for pill-induced esophageal ulcers [48]. 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 [2,49,50].

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 [51]. (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 "Epidemiology, clinical features, 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 [52,53].
(See "Operative management of Crohn disease of the small bowel, colon, and
rectum" and "Surgical management of ulcerative colitis".)

Appendicitis — Overall in the United States in 2010, approximately 30 percent of

hospital stays for appendicitis involved a perforated appendix [54-56]. Rates for
perforated appendix in children have not significantly changed from 2001 to 2010
(approximately 300/1000 appendicitis discharges), whereas the rate has declined 12
percent for adults (from 307/1000 to 270/1000 appendicitis discharges). (See "Acute
appendicitis in children: Clinical manifestations and diagnosis" and "Acute
appendicitis in adults: Clinical manifestations and differential diagnosis".)

Peptic ulcer disease — Peptic ulcer disease (PUD) is the most common cause of
stomach and duodenal perforation but occurs in less than 10 percent of patients with
PUD. In spite of the introduction of proton pump inhibitors, the incidence of
perforation from PUD has not changed appreciably [57]. Marginal ulceration leading
to perforation may also complicate surgeries that create a gastrojejunostomy (eg,
partial gastric resection, bariatric surgery). (See "Overview of the 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 [58].
(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. (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 [59]. (See "Overview of intestinal ischemia in adults".)

Infectious disease — Typhoid, tuberculosis, and schistosomiasis can cause

perforation of the small intestine [60,61]. With typhoid, the perforation is usually in a
single location (ileum at necrotic Peyer's patches), but it can be multiple [62,63].
Typhoid perforation is more common in children, adolescents, or young adults.
Cytomegalovirus, particularly in an immunosuppressed patient, can cause intestinal
perforation.

Neoplasms — Neoplasms can perforate by direct penetration and necrosis, or by

producing obstruction. Perforations related to tumor can also occur spontaneously,
following chemotherapy, or as a result of radiation treatments when the tumor
involves the wall of a hollow viscus organ [64-66]. 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 [67-69].
(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

premature infants. No demonstrable cause is appreciated [70].

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 invariably 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, invariably 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 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 pH of the stomach contents is often buffered by recent
food consumption. The leakage of small intestinal contents into the peritoneal cavity
may also cause severe pain, and for this reason, any severe pain after, particularly, a
laparoscopic procedure should cause the surgeon to suspect leakage.

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
carcinoma can fistulize to adjacent structures or to the abdominal wall.
The initial gastrointestinal perforation is contained between two loops of bowel, and
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. (See "Overview of enteric 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,
elderly, and immunosuppressed patients, resulting in free spillage of gastrointestinal
contents into the abdomen, generalized abdominal infection, and sepsis [71]. Sepsis
in itself can contribute to the causation of perforation by reducing intestinal wall
perfusion [72]. 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 [73]. 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".)

Physical examination — Physical exam 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 air, and
auscultation and percussion of the chest for signs of effusion. Mediastinal air might
be heard as a systolic "crunch" (Hamman's sign) at the apex and left sternal border
with each heartbeat [51]. Palpation reveals crepitus in 30 percent of patients with
thoracic esophageal perforation and in 65 percent of patients with cervical
esophageal perforation [74]. 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 those patients with perforation
related to small bowel obstruction. 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.

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, amylase, and
lipase.

Serum amylase may be elevated in patients with intestinal perforation due to

absorption of amylase from the intestinal lumen [75]. 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, particularly after
bariatric surgery [76] or colorectal surgery [77,78]. It has also been useful for
diagnosing perforation associated with typhoid fever [79]. (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 [80]. 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 air 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 [81]. 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 typically 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 air on plain radiography ranges from 50 to 70 percent [82-85].
The yield of an upright plain chest film to detect free air 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 [83,84].

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 air 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 air 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 air can often 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 [86-89].

The most useful imaging modality is computed tomography (CT), which is highly
sensitive and specific for extraluminal air, and which can usually be obtained quickly
[58,90,91]. 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 [82,92]. CT helps localize the site by identifying
discontinuity of the bowel wall, the site of luminal contrast leakage, level of bowel
obstruction, and air in the bowel wall or bowel wall thickening with or without an
associated inflammatory mass or abscess, or fistula [82]. 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
[93]. 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 air within the abdomen or mediastinum
varies with the extent and duration of the perforation.

Although demonstration of free intra-abdominal air 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 air at 24 hours postlaparoscopy, despite lack of any clinical
evidence of bowel perforation [94-96]. Free intra-abdominal air 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 air during a period of observation is
concerning, and a finding of increasing free intra-abdominal air suggests perforation
until proven otherwise.

Other imaging modalities can identify extraluminal air. 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.

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 air in the mediastinum outlining the
diaphragm (image 1) and is seen in approximately 20 percent of cases
[97].

-Ring-around-the-artery sign (image 2).

 -Widening of the mediastinum is sometimes seen with esophageal
perforation.

•Free air 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).

•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 air and patient positioning. Air outside the gastrointestinal
tract (pneumoperitoneum) can be located freely in the peritoneal cavity (ie,
free air), in the retroperitoneal spaces, in the mesentery, or in ligaments of
organs. Extraluminal air may not be apparent if the perforation is small, has
self-sealed, or has been contained by adjacent organs. Nonsurgical
sources can also cause air in the peritoneal cavity. (See 'Differential
diagnosis' below.)

-Free air under the diaphragm in upright abdominal films (image 3), air
over the liver (right lateral decubitus) or spleen (left lateral decubitus),
anteriorly on supine films (football sign).

-Cupola sign (inverted cup) is an arcuate lucency over the lower

thoracic spine [98].

-Rigler sign (double-wall sign) is seen as gas outlines the inner and
outer surfaces of the intestine (image 5).

-Psoas sign is air in the retroperitoneal space outlining the psoas

muscle.

-Urachus sign is air in the preperitoneal space outlining the urachus or

umbilical ligaments.
 ●Abdominal CT – Signs of perforation on abdominal CT scanning include
extraluminal air (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
[82,93,99,100].

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 air 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 [101]. 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 [101]. 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 [102].

Endoscopy is an important tool for evaluating patients with suspected esophageal

perforation, particularly following instrumentation, or related to noniatrogenic trauma
[103,104]. 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 [105].

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
blueintroduced 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" and "Outpatient evaluation of the adult with chest pain", section on
'Etiologies'.)

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 [106]. 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 [107]. On occasion, bacterial peritonitis has been associated with
pneumoperitoneum [108,109], 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. Pulmonary etiologies of pneumoperitoneum include
pulmonary abscess and ruptured pulmonary alveoli.

Pneumatosis cystoides intestinalis is usually secondary to a surgical disease

process. It is manifest 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
[110]. (See "Epidemiology, clinical manifestations, and diagnosis of Pneumocystis
pneumonia in HIV-uninfected patients" and "Clinical presentation and diagnosis of
Pneumocystis pulmonary infection in HIV-infected patients".)

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 [111].
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 [112]. 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. Drainage, gastrostomy, and feeding jejunostomy may be
appropriate depending upon the level of the perforation. 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 "Overview of enteric 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 the 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 [113]. 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 [114-116]:
 ●Perforated esophagus – (See "Surgical management of esophageal
perforation", section on 'Alternatives to primary surgical repair' and "Overview of
esophageal perforation due to blunt or penetrating trauma", section on
'Conservative treatment'.)

●Perforated appendicitis – (See "Management of acute appendicitis in adults",

section on 'Evidence for nonoperative management'.)

●Perforated colonic diverticulum – (See "Acute colonic diverticulitis: Surgical

management", section on 'Indication for emergency surgery'.)

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 or worsening or continuing abdominal pain and/or signs of

diffuse or extensive 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 "Overview of management of

mechanical small bowel obstruction in adults" and "Overview of mechanical
colorectal 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,
dysphagia) is the most frequent symptom [117]. 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 [118].
Other causes include tumors, foreign body or caustic ingestion [34,35], pneumatic
injury, peptic ulceration, intrinsic esophageal disease such as pill esophagitis [1,2],
Crohn disease [3], eosinophilic esophagitis [4], foreign body ingestion, 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 [119]. 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 [120].

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 [51,117]. 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 "Use of expandable stents in the esophagus" and "Surgical
management of esophageal perforation", section on 'Principles of surgical
management' and "Surgical management of esophageal perforation" and "Overview
of esophageal perforation due to blunt or penetrating trauma".)

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 [57]. 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 [121].
Other causes include iatrogenic (endoscopy, surgery [open or laparoscopic]) or
noniatrogenic trauma [14,19,59], ingested foreign bodies [36], neoplasm (particularly
during chemotherapy) [64,65], tuberculosis [122], and perforated duodenal
diverticulum. Gastric perforation during cardiopulmonary resuscitation can also occur
[59].

Most perforations of the stomach and duodenum require surgical repair (open or
laparoscopic) [123-131]. 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 [132-134]. 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 [53], 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 [22]. Severe
pain or sepsis after a laparoscopic procedure should be investigated promptly [23].
Perforations caused by the tumor (eg, lymphoma [66]) can occur spontaneously or
after chemotherapy. Further, 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 [135]. 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 [45].

Occasionally, particularly in developing countries, diseases such as typhoid,

tuberculosis [136], or schistosomiasis [61] can perforate the small intestine. In
typhoid, the perforation is usually single but can be multiple 28 to 37 percent of the
time [62,63]. 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 [137]. 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 in Western countries. A younger
age group is affected in left-sided diverticulitis, and it is more common in men. With
increasing age, the number of diverticuli, which predominate in the sigmoid and left
colon, increases with the disease moving more proximally. In Asian countries, the
most common cause of right-sided colonic perforation is diverticulitis [138]. 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 [139].
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 [140]. In one series, the rectosigmoid
area was most commonly perforated (53 percent), followed by the cecum (24
percent) [141]. 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 ibuprofenbeing the most commonly implicated drugs [43].
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 [142,143]. Perforation after barium enema or
colonoscopy has been reported in patients with collagenous colitis [140]. Foreign
bodies, either ingested or inserted, can cause colorectal perforation [144]. Colon
perforation can also be related to collagen-vascular diseases such as Ehlers-Danlos
syndrome type IV [145,146], Behcet syndrome [147], and eosinophilic
granulomatosis with polyangiitis (Churg-Strauss) [148]. Perforation has been
reported with anorectal manometry in the setting of a rectal anastomosis [149].
Perforation is also associated with invasive amebiasis of the colon [150]. In pediatric
populations, bacterial colitis, particularly with nontyphoid Salmonella, can lead to
perforation [151].

Colon perforations can be treated by simple suture if the perforation is small, often
using a laparoscopic approach [152]. If the perforation is larger and devascularizing
the colonic wall, colon resection will be necessary [153]. Patients with a perforated
colon due to neoplasm also require resection [154]. Laparoscopic treatment of
complicated disease is feasible but has a higher rate of conversion to open operation
compared with uncomplicated disease [155]. A primary anastomosis is preferred,
whenever feasible [139,156]. 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'.)

SUMMARY AND RECOMMENDATIONS

●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 of gastrointestinal perforation depend on the organ

affected and the nature of the contents released (air, 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.)

●A diagnosis relies upon imaging that demonstrates air 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.
Imaging signs of gastrointestinal tract perforation are listed above for the various
imaging modalities. 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.)

●Free intra-abdominal air 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 air during a period of postoperative observation is
concerning, and a finding of increasing free intra-abdominal air 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,
other rare etiologies, or may be idiopathic. (See 'Differential diagnosis' above.)

●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.)

●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 air on plain abdominal films (in the
absence of recent surgery) and abdominal tenderness, the patient should be
taken directly to surgery for exploration. Patients with evidence of perforation
and the following clinical signs benefit from immediate surgery (see 'Indications
for abdominal exploration' above):
 •Complete or closed-loop bowel obstruction

•Abdominal sepsis

•Intestinal ischemia

●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 a perforated esophagus, perforated appendicitis
with abscess/phlegmon, and perforated colonic diverticulum
with abscess/phlegmon. Specific organ management is reviewed briefly above
and by specific etiology in accompanying topic reviews. (See 'Conservative
care' above and 'Specific organs' above.)

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