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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

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Sep 2020. | This topic last updated: Nov 26, 2019.

INTRODUCTION

Perforation of the gastrointestinal tract may be suspected based upon the patient's clinical
presentation, or the diagnosis becomes obvious through a report of extraluminal "free" gas
or fluid or fluid collection on diagnostic imaging performed to evaluate abdominal pain or
another symptom. Clinical manifestations depend somewhat on the organ affected and the
nature of the contents released (gas, succus entericus, stool), as well as the ability of the
surrounding tissues to contain those contents.

Intestinal perforation can present acutely, or in an indolent manner (eg, abscess or intestinal
fistula formation). A confirmatory diagnosis is made primarily using abdominal imaging
studies, but on occasion, exploration of the abdomen (open or laparoscopic) may be needed
to make a diagnosis. Specific treatment depends upon the nature of the disease process that
caused the perforation. Some etiologies are amenable to a nonoperative approach, while
others will require 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).

● The small bowel is anatomically divided into three portions: the duodenum, jejunum,
and ileum. The duodenum is retroperitoneal in its second and third portion and forms a
loop around the head of the pancreas. The jejunum is in continuity with the fourth
portion of the duodenum beginning at the ligament of Treitz; there are no true lines of
demarcation that separate the jejunum from ileum. The ileocecal valve marks the
beginning of the colon in the right lower quadrant. The appendix hangs freely from the
cecum, which is the first portion of the colon ( figure 3). Foreign bodies that perforate
the small intestines most commonly occur at sites of gastrointestinal 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, coccyx, and sacral vessels and is posterior to the bladder
in men and the vagina in women. Foreign bodies that perforate the colon tend to occur
at transition zones from an intraperitoneal location to fixed retroperitoneal locations
such as the cecum.

RISK FACTORS

Factors that increase the risk for gastrointestinal perforation are discussed below and are
important to assess when taking the history of any patient suspected of having
gastrointestinal perforation.

● Instrumentation/surgery – Instrumentation of the gastrointestinal tract is the main

cause of iatrogenic perforation and may include upper endoscopy (especially rigid
endoscopy), sigmoidoscopy, colonoscopy [9,10], stent placement [9,10], endoscopic
sclerotherapy [11], nasogastric intubation [12], esophageal dilation, and surgery.
 The incidence of perforation related to endoscopy increases with procedural complexity.
Perforation is less common with diagnostic compared with therapeutic procedures [13].
A perforation rate of 0.11 percent for rigid endoscopy contrasts with a 0.03 percent rate
for flexible endoscopy [14,15]. When iatrogenic perforation occurs, there is often
significant associated pathology. As an example, in the esophagus, there may be
stricture, severe esophagitis [16], or a diverticulum, and the presence of cervical
osteophytes also increases the risk [15]. The area of the esophagus at most risk for
instrumental perforation is Killian's triangle [17], which is the part of the pharynx formed
by the inferior pharyngeal constrictor and cricopharyngeus muscle. During endoscopy,
perforations are frequently recognized at the time of the procedure. At other times, the
perforation remains occult for several days. (See "Overview of upper gastrointestinal
endoscopy (esophagogastroduodenoscopy)", section on 'Perforation' and "Overview of
colonoscopy in adults", section on 'Perforation'.)

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
[18]. (See "Inpatient placement and management of nasogastric and nasoenteric tubes
in adults".)

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 "Etiologies,
clinical manifestations, and diagnosis of mechanical small bowel obstruction in adults"
and "Overview of treatment for inguinal and femoral hernia in adults" and "Surgical
management of paraesophageal hernia" and "Gastric volvulus in adults" and
"Postgastrectomy complications", section on 'Afferent and efferent loop syndrome'.)
● Inflammatory bowel disease – Crohn disease has a propensity to perforate slowly,
leading to formation of entero-enteric or enterocutaneous fistula formation [52,53]. (See
"Operative management of Crohn disease of the small bowel, colon, and rectum" and
"Surgical management of ulcerative colitis".)

● Appendicitis – A portion of appendicitis results in perforation, which can lead to life-

threatening complications if left untreated, including intra-abdominal infection, sepsis,
intraperitoneal abscesses, and, rarely, death [54]. In adults, the risk of perforated
appendicitis increases with male gender, increasing age and comorbidity, and lack of
medical insurance coverage [55]. The diagnosis and management of perforated
appendicitis are discussed elsewhere. (See "Acute appendicitis in adults: Diagnostic
evaluation", section on 'Perforation' and "Management of acute appendicitis in adults",
section on 'Perforated appendicitis'.)

● Peptic ulcer disease – Peptic ulcer disease (PUD) is the most common cause of stomach
and duodenal perforation but occurs in a small percentage of patients with PUD [56]. 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 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 may complain of chest or abdominal pain to

some degree. Sudden, severe chest or abdominal pain following instrumentation or surgery
is very concerning for perforation. Patients on immunosuppressive or anti-inflammatory
agents may have an impaired inflammatory response, and some may have little or no pain
and tenderness. Many patients will seek medical attention with the onset or worsening of
significant chest or abdominal pain, but a subset of patients will present in a delayed fashion.
These patients may present with an abdominal mass reflecting abscess formation, or fistula
drainage, and some may present with abdominal sepsis. (See 'Acute pain' below and 'Fistula
formation' below and 'Abdominal/pelvic mass' below and 'Sepsis' below.)

Acute pain — Inflammation of the gastrointestinal tract, as a result of perforation by a

variety of etiologies, usually leads to some degree of neck pain (or dysphagia), or chest or
abdominal discomfort.

The patient with a free perforation often notes with precision the time of the onset of the
perforation. The patient may relate a sudden worsening of pain, followed by complete
dissipation of the pain as perforation decompresses the inflamed organ, but relief is usually
temporary. As the spilled gastrointestinal contents irritate the mediastinum or visceral
peritoneum, a more constant pain will develop.

Acute symptoms associated with free perforation depend upon the nature and location of
the gastrointestinal spillage (mediastinal, intraperitoneal, retroperitoneal). Cervical
esophageal perforation can present with pharyngeal or neck pain associated with
odynophagia, dysphagia, tenderness, or induration. Perforation of upper abdominal organs
can irritate the diaphragm, leading to pain radiating to the shoulder. If perforation is
confined to the retroperitoneum or lesser sac (eg, duodenal perforation), the presentation
may be more subtle. Retroperitoneal perforations often lead to back pain.

Because the pH of gastric contents is 1 to 2 along the gastric luminal surface, a sudden
release of this acid into the abdomen causes severe and sudden peritoneal irritation and
severe pain. The 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 "Enterocutaneous and enteroatmospheric fistulas".)
 Sepsis — Sepsis can be the initial presentation of perforation, but its frequency is difficult
to determine. The ability of the peritoneal surfaces to wall off a perforation may be impaired
in patients with severe medical comorbidities, particularly frail, 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".)

Timely and adequate peritoneal source control is the most important determinant in the
management of patients with acute peritonitis/abdominal sepsis. In the Physiological
Parameters for Prognosis in Abdominal Sepsis (PIPAS) study, the overall in-hospital mortality
rate of 3137 patients was 8.9 percent. Ten independent variables were associated with
mortality: malignancy, severe cardiovascular disease, severe chronic kidney disease,
respiratory rate >22 breaths/minute, systolic blood pressure <100 mmHg, unresponsiveness,
room air oxygen saturation level <90 percent, platelet count <50,000/microL, and serum
lactate level >4 mmol/L. These variables were used to create the PIPAS severity score. The
overall mortality was 2.9 percent for patients with scores of 0 to 1, 22.7 percent for 2 to 3,
46.8 percent for 4 to 5, and 86.7 percent for 7 to 8 [74].

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 gas, and auscultation
and percussion of the chest for signs of effusion. Mediastinal gas might be heard as a
systolic "crunch" (Hamman's sign) at the apex and left sternal border with each heartbeat (
movie 1) [51]. Palpation reveals crepitus in 30 percent of patients with thoracic esophageal
perforation and in 65 percent of patients with cervical esophageal perforation [75]. 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, lactate, amylase, and/or lipase.

Serum amylase may be elevated in patients with intestinal perforation due to absorption of
amylase from the intestinal lumen [76]. 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 [77] or colorectal surgery [78,79]. It has also been useful for diagnosing
perforation associated with typhoid fever [80]. (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 [81]. Drain studies are generally unnecessary. In addition, most surgeons do not
routinely place drainage tubes in the abdomen.

DIAGNOSIS

General approach — Gastrointestinal perforation may be suspected based upon history and

physical examination findings, but a diagnosis relies upon imaging that demonstrates gas
outside the gastrointestinal tract in the abdomen (ie, pneumoperitoneum) or mediastinum
(ie, pneumomediastinum), or complications associated with perforation, such as an intra-
abdominal or mediastinal abscess, or gastrointestinal fistula formation [82]. Other studies
may be needed to confirm a clinical suspicion. Further evaluation for a specific diagnosis
differs depending upon the potential etiologies, which may be suggested by the patient's
clinical presentation in combination with determining the specific organ that has perforated.
If a diagnosis of perforation is strongly suspected but imaging remains equivocal, abdominal
exploration may be necessary. (See 'Indications for abdominal exploration' below and
'Further evaluation of specific organs' below.)
The diagnostic evaluation of most patients with abdominal complaints often begins with
upright radiographs of the chest and abdomen. Supine and lateral decubitus films can be
obtained in patients who cannot sit or stand. Chest films are helpful in the diagnosis of a
patient with chest or abdominal pain approximately 90 percent of the time, but plain films
cannot rule out a perforation. The reported sensitivity for detecting extraluminal gas on plain
radiography ranges from 50 to 70 percent [83-86]. The yield of an upright plain chest film to
detect free gas may be improved by having the patient sit fully upright or in a left lateral
decubitus position for at least 10 to 20 minutes (if possible) prior to taking the film [84,85].

Another disadvantage of plain radiography is that, although perforation may be

demonstrated, the source of the perforation usually cannot be localized. However, if there is
a large amount of free gas on plain abdominal films (in the absence of recent surgery) and
abdominal tenderness, the patient should be taken directly to surgery for exploration. If
there is free gas and no abdominal pain (in the absence of immunosuppressive therapies),
the cause for pneumoperitoneum could be benign, and additional studies may be warranted
if there remain any concerns. (See "Evaluation of the adult with abdominal pain" and
'Differential diagnosis' below.)

If subcutaneous emphysema is identified in anteroposterior or posteroanterior projections

on chest radiograph, the neck region should be carefully examined (if subcutaneous
emphysema was not obvious beforehand), and lateral neck films should be obtained to
determine if gas can be seen in prevertebral fascial planes.

Ultrasound has also been studied and shows some excellent potential for identifying
pneumoperitoneum. Some studies show detection rates at or above chest films, especially in
supine films, which may be the only option for certain patients [87-90].

The most useful imaging modality is computed tomography (CT), which is highly sensitive
and specific for extraluminal gas, and which can usually be obtained quickly [58,91,92].
Patients suspected of a gastrointestinal tract perforation should be evaluated by abdominal
CT scan. Compared with plain films, CT scans are more sensitive and can demonstrate
smaller amounts of extraluminal gas, which may be best appreciated using lung windows.
Since the peritoneal cavity can be divided into various compartments, the location of gas on
abdominal CT scan can help suggest the site and cause of the perforation [83,93]. CT helps
localize the site by identifying discontinuity of the bowel wall, the site of luminal contrast
leakage, level of bowel obstruction, and gas in the bowel wall or bowel wall thickening with
or without an associated inflammatory mass or abscess, or fistula [83]. 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 [94].
However, at times, the foreign body may migrate a distance from the initial perforation, and
thus, its location does not necessarily correspond with the site of the perforation. In general,
the volume of free gas within the abdomen or mediastinum varies with the extent and
duration of the perforation.

Although demonstration of free intra-abdominal gas on imaging studies is a sign of

perforation, this may not be helpful in the postoperative period, particularly after
laparoscopic surgery, because approximately 40 percent of patients will have more than 2 cm
of free gas at 24 hours postlaparoscopy, despite lack of any clinical evidence of bowel
perforation [95-97]. However, because laparoscopy utilizes carbon dioxide to insufflate the
abdomen, any residual gas in the peritoneum should be absorbed quickly. After laparotomy,
however, free intra-abdominal gas often may be seen on a radiograph up to a week
postoperatively, but the volume should gradually decrease with time. Increasing amounts of
intra-abdominal gas during a period of observation is concerning, and a finding of increasing
free intra-abdominal gas suggests perforation until proven otherwise.

Other imaging modalities can identify extraluminal gas. Gas can also be detected by
ultrasound, although ultrasound is infrequently used for this purpose in the United States.
Other findings on ultrasound that may signal perforation include the presence of free fluid,
reduced peristaltic activity in the intestines, and localized abscess. Magnetic resonance
imaging can also be used, but it is more time consuming, and a lack of generalized
availability limits its usefulness.

Imaging signs of perforation — Imaging signs of gastrointestinal tract perforation are

listed for the various imaging modalities.

Chest imaging

● Plain chest films (or chest CT scout film).

• Pneumomediastinum (in the absence of tracheal injury).

- The "V" sign of Naclerio is free gas in the mediastinum outlining the diaphragm (
image 1) and is seen in approximately 20 percent of cases [98].

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

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

• Free gas under the diaphragm on upright films ( image 3).

• Pleural effusion may represent leaked esophageal contents ( image 4).

• Pneumothorax is a rare finding in esophageal perforation and is thought to occur by

the spread of gas along tissue planes (Macklin effect).  

• Subcutaneous emphysema may be seen in some cases.

 ● Chest CT: Pneumothorax, pneumomediastinum (in the absence of tracheal injury),
pleural effusion, mediastinal abscess.

Abdominal imaging

● Plain abdominal films (or abdominal CT scout film).

• The appearance of pneumoperitoneum on plain films depends on the location of the

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

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

- Cupola sign (inverted cup) is an arcuate lucency over the lower thoracic spine
[99].

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

- Psoas sign is gas in the retroperitoneal space outlining the psoas muscle.

- Urachus sign is gas in the preperitoneal space outlining the urachus or umbilical
ligaments.

● Abdominal CT – Signs of perforation on abdominal CT scanning include extraluminal gas

( image 6); extraluminal oral contrast; free fluid or food collections; and discontinuity
of the intestinal wall, fistula, or intra-abdominal abscess often associated with irregular
adjacent bowel wall thickening [83,94,100,101].

Neck imaging

● Plain films – Signs of perforation on plain neck imaging include subcutaneous

emphysema tracking into the neck ( image 2), anterior displacement of the trachea,
and gas in the prevertebral fascial planes on lateral view ( image 7).

Further evaluation of specific organs — Additional studies may be indicated as a means to

further investigate a suspected perforation in a specific organ. Other imaging studies include
endoscopy (upper, lower), esophagography, upper gastrointestinal series, ultrasound,
contrast enema, and dye studies [102]. 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 [102]. 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 [103].

Endoscopy is an important tool for evaluating patients with suspected esophageal

perforation, particularly following instrumentation, or related to noniatrogenic trauma
[104,105]. 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 [106].

Dye studies may be useful for evaluating patients with a pleural effusion and a thoracostomy
tube who are suspected to have an esophageal leak. Methylene blue introduced cautiously
via a nasoesophageal tube will make or confirm the diagnosis by causing blue discoloration
of the chest tube drainage.

DIFFERENTIAL DIAGNOSIS

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

Pneumoperitoneum — A small subset of patients may have findings of pneumoperitoneum,

identified typically on computed tomography (CT) scanning, that is not associated with
abdominal discomfort. A nonsurgical etiology may be the cause of pneumoperitoneum in up
to 10 percent of patients [107]. 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 [108]. On occasion, bacterial peritonitis has been associated with
pneumoperitoneum [109,110], 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 [111]. 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 [112]. (See "Epidemiology, clinical
manifestations, and diagnosis of Pneumocystis pneumonia in HIV-uninfected patients" and
"Clinical presentation and diagnosis of Pneumocystis pulmonary infection in patients with
HIV".)

Placement of a percutaneous gastrostomy tube (PEG) can be the cause of intraperitoneal

gas. The true incidence of pneumoperitoneum after PEG is unknown. In one review, among
those who had imaging within five days after percutaneous endoscopic gastrostomy, the
incidence of pneumoperitoneum was 12 percent [113]. 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 [114]. 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 "Enterocutaneous
and enteroatmospheric fistulas".)

Antibiotics — Broad-spectrum antibiotic therapy is initiated. The antibiotic regimen should

be chosen based on the suspected site of perforation. If the level of perforation is unknown,
a broad-spectrum antibiotic regimen can be initiated; precise regimen selection depends on
patient risk factors for resistant bacteria and adverse outcomes. This is discussed in detail
elsewhere. (See "Antimicrobial approach to intra-abdominal infections in adults", section on
'Regimens'.)

Conservative care — A subset of patients may not require immediate surgery to manage
gastrointestinal perforation. Traditionally, conservative management of gastrointestinal
perforation (including esophagus) was used only for patients who were deemed so ill that
they would not likely survive surgery. The positive results achieved catalyzed extension of
conservative management to other patients.

Patients chosen for nonoperative management are those with contained perforation,
gastrointestinal fistula formation, or limited contamination as judged by imaging, in those
who have no signs of systemic sepsis [115]. 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 [116-118]:

● 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 'Perforation'.)

Indications for abdominal exploration — Many patients will require urgent surgical

intervention to limit ongoing abdominal contamination and manage the perforated site.
Immediate surgical consultation is appropriate whenever perforation is confirmed or even
strongly suspected to determine if immediate surgical intervention is needed and the
interval of time to surgery.

Patients with evidence of perforation and the following clinical signs benefit from immediate
surgery:

● Abdominal sepsis, worsening or continuing abdominal pain, and/or signs of diffuse

peritonitis. (See "Evaluation and management of suspected sepsis and septic shock in
 adults" and "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation,
diagnosis, and prognosis".)

● Bowel ischemia. (See "Overview of intestinal ischemia in adults".)

● Complete or closed-loop bowel obstruction. (See "Management of small bowel

obstruction in adults" and "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 [119]. 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 [120]. 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], 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 [121]. 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 [122].

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 [51,119]. 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 [123].

Other causes include iatrogenic (endoscopy, surgery [open or laparoscopic]) or noniatrogenic

trauma [13,19,59], ingested foreign bodies [36], neoplasm (particularly during
chemotherapy) [64,65], tuberculosis [124], 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) [125-133]. 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 [134-136]. 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 [137]. 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

[138], 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 [139]. The management of perforated appendicitis is
discussed in detail separately. (See "Management of acute appendicitis in adults", section on
'Perforated appendicitis' and "Acute appendicitis in children: Management", section on
'Advanced appendicitis'.)

Colon and rectum — Colon and rectal perforation is more commonly due to diverticulitis,
neoplasm, and iatrogenic and noniatrogenic traumatic mechanisms, including surgery (eg,
anastomotic leak). Colonic diverticulosis is common in the developed world, affecting up to
50 percent of adults, most with left-sided disease. In Asian countries, by contrast, the most
common cause of right-sided colonic perforation is diverticulitis [140]. 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 [141].
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 [142]. In one series, the rectosigmoid area was most
commonly perforated (53 percent), followed by the cecum (24 percent) [143]. 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 [144,145]. Perforation after barium enema or
colonoscopy has been reported in patients with collagenous colitis [142]. Foreign bodies,
either ingested or inserted, can cause colorectal perforation [146]. Colon perforation can also
be related to collagen-vascular diseases such as Ehlers-Danlos syndrome type IV [147,148],
Behcet syndrome [149], and eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
[150]. Perforation has been reported with anorectal manometry in the setting of a rectal
anastomosis [151]. Perforation is also associated with invasive amebiasis of the colon [152].
In pediatric populations, bacterial colitis, particularly with nontyphoid Salmonella, can lead to
perforation [153].

Colon perforations can be treated by simple suture if the perforation is small, often using a
laparoscopic approach [154]. If the perforation is larger and devascularizing the colonic wall,
colon resection will be necessary [155]. Patients with a perforated colon due to neoplasm
also require resection [156]. Laparoscopic treatment of complicated disease is feasible but
has a higher rate of conversion to open operation compared with uncomplicated disease
[157]. A primary anastomosis is preferred, whenever feasible [141,158]. Primary anastomosis
may be combined with proximal "protective" ostomy in those with complicated diverticulitis
or malignancy. Colonic perforation due to Ehlers-Danlos syndrome is best treated with
resection or exteriorization, or subtotal colectomy. (See "Overview of colon resection",
section on 'Primary closure versus ostomy'.)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Gastrointestinal
perforation".)

SUMMARY AND RECOMMENDATIONS

● 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 (gas, succus entericus, stool), as well as the ability of
the surrounding tissues to contain those contents. Whether or not gastrointestinal
perforation leads to free fluid and diffuse peritonitis or is contained, resulting in an
abscess or fistula formation, depends upon location along the gastrointestinal tract and
the patient's ability to mount an inflammatory response to the specific pathologic
process. Immunosuppressive and anti-inflammatory medications impair this response.
(See 'Pathophysiology' above and 'Anatomic considerations' above.)

● A careful history is important in evaluating patients with neck, chest, and abdominal
pain. The history should include questioning about the factors known to predispose to
gastrointestinal perforation, listed above. (See 'Risk factors' above.)

● Patients with perforation invariably complain of chest or abdominal pain to some

degree, though patients on immunosuppressive therapy or anti-inflammatory agents
may have an impaired inflammatory response, and some may have little or no pain and
tenderness. The patient with a free perforation often notes with precision the time of the
onset of the perforation. A subset of patients will present in a delayed fashion,
presenting with an abdominal mass reflecting abscess formation, or fistula drainage,
and some may present initially with abdominal sepsis. (See 'Clinical features' above.)

● A diagnosis relies upon imaging that demonstrates gas outside the gastrointestinal tract
in the abdomen (ie, pneumoperitoneum) or mediastinum (ie, pneumomediastinum) on
imaging (typically abdominal computed tomography [CT]), or complications associated
with perforation, such as an intra-abdominal or mediastinal abscess or gastrointestinal
fistula formation. 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 gas often may be seen on a radiograph up to one week

postoperatively, but the volume should gradually decrease with time. Increasing
amounts of intra-abdominal gas during a period of postoperative observation is
concerning, and a finding of increasing free intra-abdominal gas suggests perforation
until proven otherwise. (See 'Imaging signs of perforation' above.)

● A nonsurgical etiology may be the cause of pneumoperitoneum in up to 10 percent of

patients. Etiologies include continuous positive airway pressure (CPAP) or positive end-
expiratory pressure (PEEP), percutaneous gastrostomy placement, paracentesis,
peritoneal dialysis, vaginal instrumentation, bacterial peritonitis, pulmonary abscess,
and ruptured pulmonary alveoli. Pneumomediastinum can be due to infection, asthma,
trauma, cocaine abuse, 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 gas 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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Topic 15075 Version 15.0

GRAPHICS

Anatomy of the esophagus

The esophagus has three anatomical points of narrowing that are prone to
perforation. These sites include the cricopharyngeus muscle, the broncho-aortic
constriction, and the esophagogastric junction. The esophagogastric junction is the
most common site of perforation.

Graphic 54206 Version 4.0

Anatomy of the stomach

The relationship of the stomach to surrounding structures is depicted in the figure. The arterial supply
to the stomach is derived primarily from the celiac axis. The celiac axis arises from the proximal
abdominal aorta and typically branches into the common hepatic, splenic, and left gastric arteries. The
common hepatic artery usually gives rise to the gastroduodenal artery (in approximately 75 percent of
people), which, in turn, branches off into the right gastroepiploic artery and the anterior and posterior
superior pancreaticoduodenal arteries, which supply the pancreas. The right gastroepiploic artery joins
with the left gastroepiploic artery, which emanates from the splenic artery in 90 percent of patients.
The right gastric artery branches from the hepatic artery and anastomoses with the left gastric artery
along the lesser curvature of the stomach. Because of its highly redundant blood supply, stomach
ischemia is rare.

Graphic 56689 Version 5.0

Anatomic relationship of colon to surrounding structures

This figure depicts the relationship of the large intestine to the overlying and underlying organs and
vessels.

Graphic 60998 Version 1.0

Conditions associated with a high serum amylase

Pancreatic disease
Pancreatitis

Complications of pancreatitis (pseudocysts, abscess)

Trauma

Surgery

Endoscopic retrograde cholangiopancreatography (ERCP)

Ductal obstruction

Pancreatic carcinoma

Cystic fibrosis

Salivary disease
Infection

Trauma

Radiation

Ductal obstruction

Gastrointestinal disease
Perforated or penetrating peptic ulcer

Perforated bowel

Obstructed bowel

Mesenteric infarction

Appendicitis

Cholecystitis

Liver disease

Severe gastroenteritis

Celiac disease

Gynecologic disease
Ruptured ectopic pregnancy

Ovarian or fallopian cysts

Pelvic inflammatory disease

Neoplasms
Solid tumors of the ovary, prostate, lung, esophagus, breast, and thymus

Multiple myeloma

Pheochromocytoma

Other
Renal failure

Alcoholism

Macroamylasemia

Burns

Type 2 diabetes mellitus

Acidosis (ketotic and nonketotic)

Pregnancy

Acquired immune deficiency syndrome (AIDS)

Cerebral trauma
 Abdominal aortic aneurysm

Anorexia nervosa, bulimia

Postoperative

Drug induced

Idiopathic

Following double-balloon enteroscopy

Myocardial infarction

Graphic 63497 Version 5.0

Drugs affecting serum amylase values

Increase Increase (cont.) Decrease

Adrenocorticotropic hormone Fluorides Citrates

Aminosalicylic acid Iodine-containing contrast media Intravenous dextrose

Some antibiotics (eg, nitrofurantoin) Lamivudine Oxalates

Some antineoplastics (eg, asparaginase) Meperidine Saquinavir

Aspirin Methylcholine

Atovaquone Methyldopa

Calcium salts Metoclopramide

Chloride salts Metronidazole

Chlorpromazine Pegaspargase

Chlorthalidone Prochlorperazine

Cholinergics (eg, bethanechol) Sulfonamides

Cimetidine Sulindac

Codeine Sunitinib

Cyproheptadine Sorafenib

Didanosine Thiazide diuretics

Estrogens Triprolidine/pseudoephedrine

Ethacrynic acid Valproic acid

Ethanol

Graphic 64829 Version 4.0

Esophageal perforation

Chest film from a patient with Boerhaave syndrome reveals free mediastinal air along
the esophageal contour (arrow).

Courtesy of Robert E Mindelzun, MD, Department of Radiology, Stanford University.

Graphic 67560 Version 3.0

Pneumomediastinum with ring around the artery sign on chest radiograph

Plain chest radiographs of a 22-year-old-woman who presented to the emergency department with 10 days of
sore throat and cough.
(A) A radiograph of the chest in the posteroanterior projection reveals linear lucencies overlying the upper chest
and neck (arrows) consistent with pneumomediastinum.
(B) A radiograph of the chest in the lateral projection reveals the "ring around the artery" sign (arrow), a finding
seen in pneumomediastinum.
(C) A magnified view of the "ring around the artery" sign (arrow).

Courtesy of Anna Ellermeier, MD.

Graphic 90041 Version 2.0

Chest radiograph of intraperitoneal free air

This plain PA radiograph of the chest taken with the patient upright reveals a small
amount of free air under the right hemidiaphragm confirming the diagnosis of a
perforated abdominal viscus. The lucent, crescent-shaped free air is noted between
the arrows. The dome of the liver (arrow) and the soft tissue shadow of the right
hemidiaphragm (arrowhead) border the free air.

PA: posterior-anterior.

Graphic 83050 Version 4.0

Esophageal perforation

CT scan of the chest in a patient with spontaneous esophageal perforation. There is

widening of the mediastinum, air in the mediastinum (appearing as black dots,
arrows), and bilateral pleural effusions.

CT: computed tomography.

Courtesy of Robert E Mindelzun, MD, Department of Radiology, Stanford University.

Graphic 81791 Version 3.0

Decubitus x-ray of intraperitoneal free air

The plain film examination of the abdomen in decubitus position reveals a large amount of free air collecting
in the right flank, clearly outlining the bowel wall (open arrows). When air is present on both sides of the
bowel, the wall is outlined with clear distinction because of the contrast differences created on both sides.
This is called Rigler's sign and is pathognomonic for free air in the peritoneal cavity. The yellow arrows show
air-fluid levels in distended bowel.

Reproduced with permission from: Daffner RH. Clinical Radiology: The Essentials, 3rd Edition. Philadelphia: Lippincott
Williams & Wilkins, 2007. Copyright © 2007 Lippincott Williams & Wilkins.

Graphic 83043 Version 1.0

Perforated duodenal ulcer

Computed tomographic scan showing free air in the anterior peritoneal space (white
arrows), in the ligamentum venosum (black arrow), and in the hepatogastric ligament
(small black arrow) resulting from a perforation of a duodenal peptic ulcer.

Courtesy of Jonathan B Kruskal, MD, PhD.

Graphic 76267 Version 3.0

Lateral neck radiograph of a child with pneumomediastinum

In this lateral neck radiograph of a young child with pneumomediastinum,

characteristic findings include retropharyngeal lucency (arrowheads), and
subcutaneous emphysema of the anterior and posterior neck and anterior chest wall
(arrows).

Courtesy of Ibrahim Janahi and Ammar Saadoon.

Graphic 69984 Version 4.0

Contributor Disclosures
Michael J Cahalane, MD Nothing to disclose Martin Weiser, MD Nothing to disclose Lillian S Kao,
MD, MS Nothing to disclose Wenliang Chen, MD, PhD Nothing to disclose

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