Overview of gastrointestinal tract perforation

Author:
Michael J Cahalane, MD
Section Editors:
Martin Weiser, MD
Lillian S Kao, MD, MS
Deputy Editor:
Wenliang Chen, MD, PhD

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer
review process is complete.
Literature review current through: Dec 2017. | This topic last
updated: Nov 29, 2017.

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 blue introduced cautiously via a nasoesophageal tube will
make or confirm the diagnosis by causing blue discoloration of the chest
tube drainage.

DIFFERENTIAL DIAGNOSIS — Abdominal pain that is not associated with

complaints such as nausea, vomiting, or diarrhea may be due to an
etiology not related to the gastrointestinal tract. The etiology of chest pain is
similarly broad, including a wide variety of conditions. (See "Causes of
abdominal pain in adults" 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", section on
'Initial management'.)

Antibiotics — Broad-spectrum antibiotic therapy is initiated if the level of

perforation is unknown (table 3) but, when possible, should be chosen
based on the suspected site of perforation. Antibiotic management for
specific etiologies is discussed in separate topic reviews.

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 "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 ibuprofen being 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's 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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