5/29/25, 11:16 AM Overview of gastrointestinal tract perforation

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Overview of gastrointestinal tract

perforation
Author: All topics are updated as new evidence
Stephen R Odom, MD becomes available and our peer review
Section Editors: process is complete.
Martin Weiser, MDKrishnan Raghavendran, Literature review current through: Apr
MD, FACS 2025.
Deputy Editor: This topic last updated: Jul 05, 2023.
Wenliang Chen, MD, PhD

INTRODUCTION
Perforation of the gastrointestinal tract may be suspected based upon the patient's
clinical presentation, or the diagnosis becomes obvious through a report of
extraluminal "free" gas or fluid or fluid collection on diagnostic imaging performed to
evaluate abdominal pain or another symptom. Clinical manifestations depend
somewhat on the organ affected and the nature of the contents released (gas, succus
entericus, stool), as well as the ability of the surrounding tissues to contain those
contents.
Intestinal perforation can present acutely or in an indolent manner (eg, abscess or
intestinal fistula formation). A confirmatory diagnosis is made primarily using
abdominal imaging studies, but on occasion, exploration of the abdomen (open or
laparoscopic) may be needed to make a diagnosis. Specific treatment depends upon the
nature of the disease process that caused the perforation. Some etiologies are
amenable to a nonoperative approach, while others will require surgery.
An overview of the clinical features, diagnosis, and management of the patient with
alimentary tract perforation is reviewed here. Specific etiologies are briefly reviewed
below and discussed in the linked topic reviews in more detail. (See 'Risk factors' below
and 'Specific organs' below.)

GENERAL PRINCIPLES
PathophysiologyPerforation requires full-thickness injury of the bowel wall; however,
partial-thickness bowel injury (eg, electrocautery, blunt trauma) can progress over time

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to become a full-thickness injury or perforation, subsequently releasing gastrointestinal

contents.
Full-thickness injury and subsequent perforation of the gastrointestinal tract can be due
to a variety of etiologies, including:
●Instrumentation (eg, endoscopy, instillation of contrast, cautery application during
surgery)
●Trauma (blunt or penetrating)

●Bowel ischemia

●Bowel obstruction

●Neoplasms (particularly colon carcinoma), besides by causing bowel obstruction, can

also cause perforation by direct penetration of the tumor through the bowel wall or
from complete bowel obstruction, ischemia from increased intra-luminal pressure, and
subsequent perforation.
Other etiologies are less common [1-4]. Spontaneous perforation can be related to
inflammatory changes or tissues weakened by inflammatory bowel disorders,
infections, or connective tissue disorders. Esophageal, gastric, or duodenal perforations
may also be associated with peptic ulcer disease, corrosive agents, vasculitis, or certain
types of medications. Ulceration and perforation can also occur after certain types of
bowel anastomoses (eg, gastrojejunostomy) and are called "marginal ulcers." (See 'Risk
factors' below.)
With bowel obstruction, perforation typically occurs proximal to the obstruction as
pressure builds up within the bowel, exceeding intestinal perfusion pressure, and
leading to ischemia and subsequently necrosis. Perforation may also occur at the site of
the narrowing such as a tight adhesive band causing focal ischemia. When perforation
is proximal to a colon obstruction, it usually occurs in the cecum (the thinnest-walled
portion of the large bowel) in the presence of a competent ileocecal valve, which does
not allow retrograde decompression of the cecum. Enteroliths and gallstones can also
cause perforation by direct pressure or indirectly by leading to obstruction resulting in a
proximal perforation [5,6].
Alternatively, the excess pressure can cause the musculature of the bowel to fail
mechanically; in other words, to simply split (diastatic rupture) without any obvious
necrosis. Intestinal pseudo-obstruction (Ogilvie syndrome) can also lead to perforation
by these mechanisms. (See "Acute colonic pseudo-obstruction (Ogilvie's syndrome)".)
As free gas accumulates in the peritoneal cavity, it can lead to reduction in venous
return and respiratory insufficiency by compromising diaphragmatic function [7]. Such a
tension pneumoperitoneum (valvular pneumoperitoneum) can result from iatrogenic or

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pathologic processes. Perforation and subsequent inflammation can also cause

abdominal compartment syndrome [8].
Anatomic considerationsKnowledge 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 site of esophageal
constrictions such as the cricopharyngeus muscle, aortic arch, left main stem bronchus,
and lower esophageal sphincter.
●The stomach is located in the left upper quadrant of the abdomen but can occupy
other areas of the abdomen, depending upon its degree of distention, phase of
diaphragmatic excursion, and the position of the individual. Anteriorly, the stomach is
adjacent to the left lobe of the liver, diaphragm, colon, and anterior abdominal wall.
Posteriorly, the stomach is in close proximity to the pancreas, spleen, left kidney and
adrenal gland, splenic artery, left diaphragm, transverse mesocolon, and colon (figure 2
and figure 3).
●The small bowel is anatomically divided into three portions: the duodenum, jejunum,
and ileum. The duodenum is retroperitoneal in its second and third portion and forms a
loop around the head of the pancreas. The jejunum is in continuity with the fourth
portion of the duodenum beginning at the ligament of Treitz; there are no true lines of
demarcation that separate the jejunum from ileum. The ileocecal valve marks the
beginning of the colon in the right lower quadrant. The appendix hangs freely from the
cecum, which is the first portion of the colon (figure 3). Foreign bodies that perforate
the small intestines most commonly occur at sites of gastrointestinal fixation (eg,
duodenum).
●The ascending and descending colon are retroperitoneal, while the transverse colon,
which extends from the hepatic flexure to the splenic flexure, is intraperitoneal. The
sigmoid colon (intraperitoneal) continues from the descending colon, ending where the
teniae converge to form the rectum. The anterior upper two-thirds of the rectum are
located intraperitoneally, and the remainder is extraperitoneal. The rectum lies anterior
to the three inferior sacral vertebrae, coccyx, and sacral vessels and is posterior to the
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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 and is a
common site for the development of Zenker’s diverticulum. During endoscopy,
perforations are frequently recognized at the time of the procedure. At other times, the
perforation remains occult for several days. (See "Overview of colonoscopy in adults",
section on 'Perforation' and "Overview of upper gastrointestinal endoscopy
(esophagogastroduodenoscopy)", section on 'Adverse events'.)
When the normal anatomy of the esophagus or stomach has been disturbed, such as
after Roux-en-Y gastric bypass, great care should be taken with nasogastric intubation
to avoid iatrogenic perforation [18]. (See "Inpatient placement and management of
nasogastric and nasoenteric tubes in adults".)
Many other procedures can also be complicated with perforation, such as chest tube
insertion low in the chest [19], peritoneal dialysis catheter insertion [20], percutaneous
gastrostomy [21], paracentesis, diagnostic peritoneal lavage, and percutaneous
drainage of fluid collections or abscess.
With surgery, perforation can occur during essentially any portion of the case, including
initial laparoscopic access, during mobilization of the organs or during the takedown of
adhesions, or as a result of thermal injury from electrocautery devices [22-24].
Gastrointestinal leakage can also occur postoperatively as a result of anastomotic
breakdown [25-32]. Immunosuppressed individuals may be at increased risk for
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dehiscence and deep organ space infection following surgery [33]. Medical illnesses
such as diabetes, cirrhosis, and HIV are associated with an increased risk of
anastomotic leak after colon resection for trauma [34]. Enterocutaneous fistula can
develop after direct injury or spontaneously in the open abdomen. (See "Complications
of laparoscopic surgery", section on 'Bowel injuries' and "Management of anastomotic
complications of colorectal surgery" and "Enterocutaneous and enteroatmospheric
fistulas" and "Complications of laparoscopic surgery", section on 'Dissection-related
bowel injuries'.)
●Penetrating or blunt trauma – Traumatic perforation of the gastrointestinal tract is
most likely a result of penetrating injury, although blunt perforation can occur with
severe abdominal trauma acutely related to pressure effects or as a portion of the
gastrointestinal tract is compressed against a fixed bony structure, or more slowly as a
contusion develops into a full-thickness injury. (See "Overview of esophageal injury due
to blunt or penetrating trauma in adults" and "Traumatic gastrointestinal injury in the
adult patient".)
●Medications, other ingestions, foreign body – Medications or other ingested
substances (caustic injury) and foreign bodies (ingested or medical devices) can lead to
gastrointestinal perforation. Foreign bodies, such as sharp objects (toothpicks), food
with sharp surfaces (eg, chicken bones, fish), or gastric bezoar more commonly cause
perforation, compared with dislodged medical implants [35-38]. Button batteries as an
esophageal foreign body have a more pronounced perforation risk [39,40]. Surgically
implanted foreign bodies such as hernia mesh [41], stents and artificial vascular grafts
[42,43] can cause perforation with subsequent abscess and fistula formation or
vasculoenteric fistulas. (See "Caustic esophageal injury in children" and "Caustic
esophageal injury in adults" and "Foreign bodies of the esophagus and gastrointestinal
tract in children" and "Ingested foreign bodies and food impactions in adults".)
Aspirin and nonsteroidal anti-inflammatory drug (NSAID) use has been associated with
perforation of colonic diverticula, with diclofenac and ibuprofen being the most
commonly implicated drugs [44]. Some disease-modifying antirheumatic drugs
(DMARDs) have been associated with lower intestinal perforations [45]. Rarely, NSAIDs
have produced jejunal perforations [46]. Glucocorticoids, particularly in association with
NSAIDs, are particularly problematic [47,48]. Further, because steroids suppress the
inflammatory response, detection of a perforation can be delayed. Interleukin-6
inhibiting drugs (eg, tocilizumab) and other biologic agents have been associated with
bowel perforation [49]. Anti-inflammatory medications such as ketorolac have been
associated with increased anastomotic leak after surgery.
NSAIDs, antibiotics, and potassium supplements are also common causative
medications for pill-induced esophageal ulcers [50]. Other medication-induced injury
leading to perforation has been reported for immunosuppressive therapies, cancer
chemotherapy in patients with metastases, and for iron supplementation causing
esophageal injury [2,51,52].
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●Violent retching/vomiting – Violent retching/vomiting can lead to spontaneous

esophageal perforation, known as Boerhaave syndrome. This occurs because of failure
of the cricopharyngeal muscle to relax during vomiting or retching causing an
increased intraesophageal pressure in the lower esophagus [53].
●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 "Etiologies, clinical manifestations, and diagnosis of mechanical
small bowel obstruction in adults" and "Overview of treatment for inguinal and femoral
hernia in adults" and "Surgical management of paraesophageal hernia" and "Gastric
volvulus in adults" and "Postgastrectomy complications", section on 'Afferent and
efferent loop syndrome'.)
●Inflammatory bowel disease – Crohn disease has a propensity to perforate slowly,
leading to formation of entero-enteric or enterocutaneous fistula formation [54,55].
Perforations are also rare in ulcerative colitis. However the incidence of perforation in
IBD significantly increases following a colonoscopy [56]. (See "Surgical management of
Crohn disease" and "Surgical management of ulcerative colitis".)
●Appendicitis – Appendicitis can result in perforation, which, if left untreated, can lead
to intra-abdominal infection, sepsis, intraperitoneal abscesses, and, rarely, death [57]. In
adults, the risk of perforated appendicitis increases with male sex, increasing age and
comorbidity, and lack of medical insurance coverage [58]. The diagnosis and
management of perforated appendicitis are discussed elsewhere. (See "Acute
appendicitis in adults: Diagnostic evaluation", section on 'Diagnostic evaluation when CT
is available' and "Management of acute appendicitis in adults", section on 'Perforated
appendicitis'.)
●Peptic ulcer disease – Peptic ulcer disease (PUD) is the most common cause of
stomach and duodenal perforation, which occurs in a small percentage of patients with
PUD [59]. In spite of the introduction of proton pump inhibitors, the incidence of
perforation from PUD has not changed appreciably [60]. 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 [61]. (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
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perforate, which may lead to abscess formation. Nonoperative management of small

bowel diverticulitis is much less successful than for colonic diverticulitis. (See "Meckel's
diverticulum".)
●Cardiovascular disease – Any process that reduces the blood flow to the intestines
(occlusive or nonocclusive mesenteric ischemia) for an extended period of time
increases the risk for perforation, including embolism, mesenteric occlusive disease,
cardiopulmonary resuscitation, and heart failure that leads to gastrointestinal ischemia
[62]. (See "Overview of intestinal ischemia in adults".)
●Infectious disease – Typhoid, tuberculosis, and schistosomiasis can cause perforation
of the small intestine [63,64]. With typhoid, the perforation is usually in a single location
(ileum at necrotic Peyer's patches), but it can be multiple [65,66]. Typhoid perforation is
more common in children, adolescents, or young adults. Cytomegalovirus, particularly
in an immunosuppressed patient, can cause intestinal perforation [67]. Some reports
have suggested that COVID-19 infections can be associated with spontaneous bowel
perforation [68]. (See "COVID-19: Gastrointestinal symptoms and complications",
section on 'Mesenteric ischemia'.)
●Neoplasms – Neoplasms can perforate by direct penetration and necrosis or by
producing obstruction. Perforations related to tumors can also occur spontaneously,
following chemotherapy, or as a result of radiation treatments when the tumor involves
the wall of a hollow viscus organ [69-71]. 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 [72-74]. (See "Ehlers-Danlos
syndromes: Clinical manifestations and diagnosis" and "Genetics, clinical features, and
diagnosis of Marfan syndrome and related disorders".)
●Spontaneous intestinal perforation – This entity occurs in the neonate or in
premature infants. No demonstrable cause is appreciated [75].

CLINICAL FEATURES
HistoryA 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.)

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PresentationsPatients 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 painInflammation of the gastrointestinal tract, as a result of perforation by a
variety of etiologies, usually leads to some degree of neck pain (or dysphagia) or chest
or abdominal discomfort.
The patient with a free perforation often notes with precision the time of the onset of
the perforation. The patient may relate a sudden worsening of pain, followed by
complete dissipation of the pain as perforation decompresses the inflamed organ, but
relief is usually temporary. As the spilled gastrointestinal contents irritate the
mediastinum or visceral peritoneum, a more constant pain will develop.
Acute symptoms associated with free perforation depend upon the nature and location
of the gastrointestinal spillage (mediastinal, intraperitoneal, retroperitoneal). Cervical
esophageal perforation can present with pharyngeal or neck pain associated with
odynophagia, dysphagia, tenderness, or induration. Perforation of upper abdominal
organs can irritate the diaphragm, leading to pain radiating to the shoulder. If
perforation is confined to the retroperitoneum or lesser sac (eg, duodenal perforation),
the presentation may be more subtle. Retroperitoneal perforations often lead to back
pain.
Because the pH of gastric contents is 1 to 2 along the gastric luminal surface, a sudden
release of this acid into the abdomen causes severe and sudden peritoneal irritation
and severe pain. The acidity of the stomach contents is often buffered by recent food
consumption. The leakage of small intestinal contents into the peritoneal cavity causes
severe abdominal pain and peritonitis (ie, the "acute abdomen").
Abdominal/pelvic massIt is not uncommon for perforation to lead to abscess or
phlegmon formation that can be appreciated on examination as an abdominal mass or
with abdominal exploration. A pelvic abscess caused by a perforation can sometimes be
felt on digital rectal examination. Diverticulitis is the most common etiology leading to
intra-abdominal abscess formation. (See "Clinical manifestations and diagnosis of acute
colonic diverticulitis in adults".)
Fistula formation (discussed below) can lead to a mass felt in the abdominal wall prior
to spontaneous decompression and drainage.

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Fistula formationA 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 and other GI carcinomas can fistulize to
adjacent structures or to the abdominal wall.
When the initial gastrointestinal perforation is contained between two loops of bowel,
subsequent inflammatory changes lead to an abnormal communication, which
spontaneously decompresses any fluid collection or abscess that has formed. Patients
who develop an external fistula will complain of the sudden appearance of drainage
from a postoperative wound, or from the abdominal wall or perineum in the case of
spontaneous fistulas. Intestines can fistulize to many organs or spaces (eg, bladder,
uterus, other portion of the intestine, etc). (See "Enterocutaneous and
enteroatmospheric fistulas".)
SepsisSepsis can be the initial presentation of perforation, but its frequency is difficult
to determine. The ability of the peritoneal surfaces to wall off a perforation may be
impaired in patients with severe medical comorbidities, particularly frail, older, and
immunosuppressed patients, resulting in free spillage of gastrointestinal contents into
the abdomen, generalized abdominal infection, and sepsis [76]. Sepsis in itself can
contribute to the causation of perforation by reducing intestinal wall perfusion [77].
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
[78]. 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 [79]. In the
Physiological Parameters for Prognosis in Abdominal Sepsis (PIPAS) study, the overall
in-hospital mortality rate of 3137 patients was 8.9 percent. Independent variables
associated with mortality include malignancy, severe cardiovascular disease, severe
chronic kidney disease, respiratory rate >22 breaths/minute, systolic blood pressure
<100 mmHg, unresponsiveness, room air oxygen saturation level <90 percent, platelet
count <50,000/microL, and serum lactate level >4 mmol/L. These variables were used to
create the PIPAS severity score. The overall mortality was 2.9 percent for patients with
scores of 0 to 1, 22.7 percent for 2 to 3, 46.8 percent for 4 to 5, and 86.7 percent for 7 to
8 [80].
Physical examinationPhysical examination should include vital signs; a thorough
examination of the neck, chest, and abdomen; and rectal examination. In patients with

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gastrointestinal perforation, vital signs may initially be normal or reveal mild

tachycardia or hypothermia. As the inflammatory response progresses, fever and other
signs of sepsis may develop.
Palpation of the neck and chest should look for signs of subcutaneous gas and
auscultation and percussion of the chest for signs of effusion. Mediastinal gas might be
heard as a systolic "crunch" (Hamman's sign) at the apex and left sternal border with
each heartbeat (movie 1) [53]. Palpation reveals crepitus in 30 percent of patients with
thoracic esophageal perforation and in 65 percent of patients with cervical esophageal
perforation [81]. Patients with esophageal rupture caused by barotrauma can have
facial swelling.
The abdominal examination can be relatively normal initially or reveal only mild focal
tenderness, as in the case of contained or retroperitoneal perforations. The abdomen
may or may not be distended. Distention is common in patients with perforation related
to small bowel obstruction but can also be from ileus secondary to free intra-peritoneal
contamination. When free intraperitoneal perforation has occurred, typical signs of
diffuse peritonitis are present.
The rectal examination may be normal, as with contained upper abdominal
gastrointestinal perforation, or reveal a palpable mass in the cul-de-sac, representing a
phlegmon or abscess. There may also be rectal tenderness as well as bogginess
secondary to inflammation.
Administration of opiate pain medication should not be withheld during the evaluation
of acute abdominal pain. While physical examination can be affected, pain
management is better and clinical outcomes are not significantly affected [82].
Laboratory studiesLaboratory 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 [83]. 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 [84], particularly
after bariatric surgery [85] or colorectal surgery [86,87]. It has also been useful for
diagnosing perforation associated with typhoid fever [88]. (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
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of stool in the effluent [89]. Drain studies are generally unnecessary. In addition, most
surgeons do not routinely place drainage tubes in the abdomen.

DIAGNOSIS
General approachGastrointestinal 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 [90]. 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 [91-94]. 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 [92,93].
Another disadvantage of plain radiography is that, although perforation may be
demonstrated, the source of the perforation usually cannot be localized. However, if
there is a large amount of free gas on plain abdominal films (in the absence of recent
surgery) and abdominal tenderness with signs of peritonitis, 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 [95-98].
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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
[61,99-101]. 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 [91,102]. 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 [91]. 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 [103]. 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 [104-106]. 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. Similarly intra-abdominal gas is routinely noticed following a
percutaneous endoscopic gastrostomy tube placement.
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 [107].
Imaging signs of perforationImaging 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).

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-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 [108].
-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) [109].
•Subcutaneous emphysema may be seen in some cases.
●Chest CT: Pneumothorax, pneumomediastinum (in the absence of tracheal injury),
pleural effusion, mediastinal abscess.
Abdominal imaging
●Plain abdominal films (or abdominal CT scout film).

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

gas and patient positioning. Gas outside the gastrointestinal tract (pneumoperitoneum)
can be located freely in the peritoneal cavity (ie, free gas), in the retroperitoneal spaces,
in the mesentery, or in ligaments of organs. Extraluminal gas may not be apparent if
the perforation is small, has self-sealed, or has been contained by adjacent organs.
Nonsurgical sources can also cause gas in the peritoneal cavity. (See 'Differential
diagnosis' below.)
-Free gas under the diaphragm in upright abdominal films (image 3), gas over the liver
(right lateral decubitus) or spleen (left lateral decubitus) or anteriorly on supine films
(football sign) is indicative of gastrointestinal perforation.
-The Cupola sign (inverted cup) is an arcuate (bow-shaped) lucency over the lower
thoracic spine in the supine patient secondary to air accumulating under the central
tendon of the diaphragm [110].
-The Rigler sign (double-wall sign) is seen as gas outlining the inner and outer surfaces
of the intestine (image 5).
-The Psoas sign is gas in the retroperitoneal space outlining the psoas muscle.
-The Urachus sign is gas in the preperitoneal space outlining the urachus or umbilical
ligaments.

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●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 [91,103,111,112].
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 organsAdditional 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 [113]. 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 [113]. 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 [114].
Endoscopy is an important tool for evaluating patients with suspected esophageal
perforation, particularly following instrumentation, or related to non-iatrogenic trauma
[115,116]. 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 [117].
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".)
PneumoperitoneumA small subset of patients may have findings of
pneumoperitoneum, identified typically on computed tomography (CT) scanning, that is
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not associated with abdominal discomfort. A nonsurgical etiology may be the cause of
pneumoperitoneum in up to 10 percent of patients [118]. 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 [119]. On occasion,
bacterial peritonitis has been associated with pneumoperitoneum [120,121], 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 [122].
Pulmonary etiologies of pneumoperitoneum include pulmonary abscess and ruptured
pulmonary alveoli.
Pneumatosis cystoides intestinalis is usually secondary to a surgical disease process. It
manifests most commonly as gas-containing cysts in the wall of the small intestine or
colon. Although most cases should be treated with operation, the absence of an
elevated white count and C-reactive protein (CRP) in combination with benign
abdominal examination leaves the option for nonoperative management [123]. (See
"Epidemiology, clinical manifestations, and diagnosis of Pneumocystis pneumonia in
patients without HIV" and "Epidemiology, 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 [124].
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".)
PneumomediastinumNon-esophageal causes of pneumomediastinum include infection,
asthma, trauma, cocaine use, and other rare etiologies such as high-speed air turbine
drilling during dental procedures, or may be idiopathic [125]. In addition to causing
pneumoperitoneum, perforated duodenal ulcer can also result in pneumomediastinum.

INITIAL MANAGEMENT
Initial management of the patient with gastrointestinal perforation includes
intravenous (IV) fluid therapy, cessation of oral intake, and broad-spectrum antibiotics.
Monitoring should initially take place in an intensive care unit. The administration of
intravenous proton pump inhibitors is appropriate for those suspected to have upper
gastrointestinal perforation.
Patients with intestinal perforation can have severe volume depletion. The severity of
any electrolyte abnormalities depends upon the nature and volume of material leaking

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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".)
AntibioticsFollowing a gastrointestinal perforation, broad-spectrum antibiotic therapy is
initiated; routine use of antifungal therapy is not required. The antibiotic regimen
should be chosen based on 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 'Approach to empiric antibiotic selection'.)
Conservative careA 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 [126]. 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 [127-129]:
●Perforated esophagus – (See "Esophageal perforation", section on 'Alternative surgical
techniques' and "Overview of esophageal injury due to blunt or penetrating trauma in
adults", section on 'Conservative treatment'.)
●Perforated appendicitis [130] – (See "Management of acute appendicitis in adults",
section on 'Nonoperative management'.)
●Perforated colonic diverticulum – (See "Acute colonic diverticulitis: Surgical
management", section on 'Perforation'.)
Indications for abdominal explorationMany 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

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or even strongly suspected to determine if immediate surgical intervention is needed

and the interval of time to surgery.
Patients with evidence of perforation and the following clinical signs benefit from
immediate surgery:
●Abdominal sepsis, worsening or continuing abdominal pain, and/or signs of diffuse
peritonitis. (See "Evaluation and management of suspected sepsis and septic shock in
adults" and "Sepsis syndromes in adults: Epidemiology, definitions, clinical
presentation, diagnosis, and prognosis".)
●Bowel ischemia. (See "Overview of intestinal ischemia in adults".)

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

obstruction in adults" and "Large bowel obstruction".)

SPECIFIC ORGANS
EsophagusPerforations of the esophagus range from minute piercings, often following
biopsy or sclerotherapy, to large-scale rupture of the esophageal wall, and presenting
signs and symptoms also cover a wide range. The onset of pain related to esophageal
perforation may be sudden or insidious. Pain on swallowing (ie, odynophagia) is the
most frequent symptom [131]. 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 non-iatrogenic penetrating or blunt traumatic mechanisms. Other causes
include tumors, foreign body or caustic ingestion [35,36], pneumatic injury, peptic
ulceration, intrinsic esophageal disease such as pill esophagitis [1,2], Crohn disease [3],
eosinophilic esophagitis [4], or, more rarely, it is spontaneous (Boerhaave's syndrome).
During surgery, the esophagus can be injured during operations such as hiatal hernia
repair, thyroidectomy, pulmonary procedures, and vagotomy.
As an element of conservative care, covered stents are increasingly being used to
manage some patients with esophageal perforation. Placed endoscopically, the stent
covers the perforation while healing occurs. Complications associated with stents
include bleeding, fistula and injury to adjacent structures, kinking, erosion, and reflux.
Stents also have a tendency to migrate, which occurred in 33 percent of patients in one
series [132]. 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 [133].

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Notwithstanding innovations in conservative care for esophageal perforation, open

surgery remains the mainstay of treatment. Surgical options for esophageal perforation
include primary repair, repair over a drain, and, in the case of severe stricture or tumor,
esophagectomy and esophageal exclusion [53,131]. The approach to open surgical
repair depends upon the level of the perforation and may involve a neck incision and/or
thoracotomy and, for lower esophageal perforation, potentially an upper abdominal
incision as well. Specific management is reviewed in detail elsewhere. (See "Endoscopic
stenting for palliation of malignant esophageal obstruction" and "Esophageal
perforation", section on 'High-risk perforation or unstable patients' and "Esophageal
perforation" and "Overview of esophageal injury due to blunt or penetrating trauma in
adults".)
Stomach and duodenumPeptic 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 [60]. 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 [134].
Other causes include iatrogenic (endoscopy, surgery [open or laparoscopic]) or
noniatrogenic trauma [13,19,62], ingested foreign bodies [37], neoplasm (particularly
during chemotherapy) [69,70], tuberculosis [135], and perforated duodenal
diverticulum. Gastric perforation during cardiopulmonary resuscitation can also occur
[62].
Most perforations of the stomach and duodenum require surgical repair (open or
laparoscopic) [136-144]. 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 [145-147]. 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".)

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Small intestinePerforation of the small intestine can be related to bowel obstruction,

acute mesenteric ischemia, inflammatory bowel disease [55], or due to iatrogenic
(laparoscopic access, takedown of adhesions, endoscopy) or non-iatrogenic traumatic
mechanisms. Injuries to the small intestine during laparoscopic procedures are often
not recognized during the procedure [23]. Severe pain or sepsis after a laparoscopic
procedure should be investigated promptly [24]. Perforations caused by the tumor (eg,
lymphoma [71]) can occur spontaneously or after chemotherapy. Furthermore, because
glucocorticoids suppress the inflammatory response, detection of a perforation can be
delayed. Other causes of small intestinal perforation include foreign body ingestion,
enteroliths/gallstones [5,6], or, more rarely, migrated stents (eg, esophageal, biliary).
Perforation of a diverticulum of the small intestine, such as in perforated Meckel's
diverticulum, can occur and may lead to abscess formation. Occasionally, jejunal
diverticula can become inflamed and perforate [148]. These rare diverticula are located
along the mesenteric aspect of the proximal jejunum and decrease in number with
increasing distance from the duodenal-jejunal junction. Rarely, nonsteroidal anti-
inflammatory drugs (NSAIDs) have produced jejunal perforations [46].
Occasionally, particularly in resource-limited countries, diseases such as typhoid,
tuberculosis [149], or schistosomiasis [64] can perforate the small intestine. In typhoid,
the perforation is usually single but can be multiple 28 to 37 percent of the time [65,66].
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, affected more than half of
its circumference, associated with shock and hemodynamic instability, or if it has been
long-standing, producing significant induration, a small bowel resection with primary
anastomosis is performed. In patients with ileal perforations and severe hemodynamic
instability due to septic shock, it may be wise to perform an end ileostomy rather than
an ileocolic anastomosis. (See "Bowel resection techniques" and "Traumatic
gastrointestinal injury in the adult patient".)
AppendixApproximately 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 [150]. 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 'Complicated appendicitis'.)

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Colon and rectumColon 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
[151]. 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 [152].
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 [153]. In one series, the rectosigmoid area was most
commonly perforated (53 percent), followed by the cecum (24 percent) [154]. In this
series, most perforations were due to blunt injury, 27 percent of perforations occurred
with polypectomy, and 18 percent of perforations were produced by thermal injury.
Almost 25 percent of patients presented in a delayed fashion (after 24 hours).
Polypectomy patients, in contrast to screening patients, were more likely to present in a
delayed fashion. Most of the postprocedural perforations occurred in patients who had
undergone bowel preparation, making primary anastomosis feasible. A poorly prepared
bowel was a predictor of feculent peritonitis.
A myriad of other etiologies can lead to colonic or rectal perforation. NSAID use has
been associated with serious diverticular perforation, with diclofenac and ibuprofen
being the most commonly implicated drugs [44]. Glucocorticoids are also associated
with diverticular perforation. Stercoral perforation, caused by ischemic necrosis of the
intestinal wall by stool, is also possible, particularly in older individuals [155,156].
Perforation after barium enema or colonoscopy has been reported in patients with
collagenous colitis [153]. Foreign bodies, either ingested or inserted, can cause
colorectal perforation [157]. Colon perforation can also be related to collagen-vascular
diseases such as Ehlers-Danlos syndrome type IV [158,159], Behcet syndrome [160], and
eosinophilic granulomatosis with polyangiitis (Churg-Strauss) [161]. Perforation has
been reported with anorectal manometry in the setting of a rectal anastomosis [162].
Perforation is also associated with invasive amebiasis of the colon [163]. In pediatric
populations, bacterial colitis, particularly with nontyphoid Salmonella, can lead to
perforation [164].
Neutropenic enterocolitis (NEC) is defined as severe inflammation associated with
neutropenia typically associated with chemotherapeutic agents. They usually involve
cecum and the right colon. Rarely they lead to perforation that carry a high mortality
[165].
Colon perforations can be treated by simple suture if the perforation is small, often
using a laparoscopic approach [166]. If the perforation is larger and devascularizing the
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colonic wall, colon resection will be necessary [167]. Patients with a perforated colon
due to neoplasm also require resection [168]. Laparoscopic treatment of complicated
disease is feasible but has a higher rate of conversion to open operation compared with
uncomplicated disease [169]. A primary anastomosis is preferred, whenever feasible
[152,170]. Primary anastomosis may be combined with proximal "protective" ostomy in
those with complicated diverticulitis or malignancy. Colonic perforation due to Ehlers-
Danlos syndrome is best treated with resection or exteriorization, or subtotal
colectomy. (See "Overview of colon resection", section on 'Primary closure versus
ostomy'.)

SOCIETY GUIDELINE LINKS

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

SUMMARY AND RECOMMENDATIONS

●General principles and risk factors – Perforation of the gastrointestinal tract leading
to release of gastrointestinal contents requires full-thickness injury of the bowel wall.
Partial-thickness bowel injury can progress over time to become full-thickness injury.
Full-thickness injury and perforation of the gastrointestinal tract can be due to a variety
of etiologies, commonly instrumentation or other trauma, and bowel obstruction. Other
etiologies are less common. Spontaneous perforation can also occur and is related to
inflammatory changes or weakening of the tissues from connective tissue disorders or
drug effects. (See 'General principles' above and 'Risk factors' above.)
●Clinical manifestations – Clinical manifestations of gastrointestinal perforation
depend on the organ affected and the nature of the contents released (gas, succus
entericus, stool), as well as the ability of the surrounding tissues to contain those
contents. Whether or not gastrointestinal perforation leads to free fluid and diffuse
peritonitis or is contained, resulting in an abscess or fistula formation, depends upon
location along the gastrointestinal tract and the patient's ability to mount an
inflammatory response to the specific pathologic process. Immunosuppressive and
anti-inflammatory medications impair this response. (See 'Pathophysiology' above and
'Anatomic considerations' above.)
•A careful history is important in evaluating patients with neck, chest, and abdominal
pain. The history should include questioning about the factors known to predispose to
gastrointestinal perforation listed above. (See 'Risk factors' above.)
•Patients with perforation invariably complain of chest or abdominal pain to some
degree, though patients on immunosuppressive therapy or anti-inflammatory agents
may have an impaired inflammatory response, and some may have little or no pain and
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tenderness. The patient with a free perforation often notes with precision the time of
the onset of the perforation. A subset of patients will present in a delayed fashion,
presenting with an abdominal mass reflecting abscess formation, or fistula drainage,
and some may present initially with abdominal sepsis. (See 'Clinical features' above.)
●Diagnosis – A diagnosis relies upon imaging that demonstrates gas outside the
gastrointestinal tract in the abdomen (ie, pneumoperitoneum) or mediastinum (ie,
pneumomediastinum) on imaging (typically abdominal computed tomography [CT]), or
complications associated with perforation, such as an intra-abdominal or mediastinal
abscess or gastrointestinal fistula formation. Further evaluation for a specific diagnosis
differs depending upon the potential etiologies, which may be suggested by the
patient's clinical presentation in combination with determining the specific organ that
has perforated. If a diagnosis of perforation is strongly suspected but imaging remains
equivocal, abdominal exploration may be necessary. (See 'Diagnosis' above and
'Imaging signs of perforation' above.)
●Imaging – Free intra-abdominal gas often may be seen on a radiograph up to one
week postoperatively, but the volume should gradually decrease with time. Increasing
amounts of intra-abdominal gas during a period of postoperative observation are
concerning, and a finding of increasing free intra-abdominal gas suggests perforation
until proven otherwise. (See 'Imaging signs of perforation' above.)
A nonsurgical etiology may be the cause of pneumoperitoneum in up to 10 percent of
patients. Etiologies include continuous positive airway pressure (CPAP) or positive end-
expiratory pressure (PEEP), percutaneous gastrostomy placement, paracentesis,
peritoneal dialysis, vaginal instrumentation, bacterial peritonitis, pulmonary abscess,
and ruptured pulmonary alveoli. Pneumomediastinum can be due to infection, asthma,
trauma, cocaine use, or other rare etiologies, or it may be idiopathic. (See 'Differential
diagnosis' above.)
●Initial management – Initial management of the patient with gastrointestinal
perforation includes resuscitation with intravenous fluids and correction of metabolic
acidosis using serum lactate as a measure of resuscitation. Patients should be made nil
per os. Broad-spectrum antibiotic therapy should be initiated if the level of perforation
is unknown but, when possible, should be chosen based upon the site of perforation.
Antibiotic management for specific etiologies is discussed in separate topic reviews.
(See 'Initial management' above.)
●Definitive management – Many patients will require urgent surgical intervention to
limit ongoing abdominal contamination and manage the perforated site. Immediate
surgical consultation is appropriate whenever perforation is confirmed or even strongly
suspected. If there is a large amount of free gas on plain abdominal films (in the
absence of recent surgery) and abdominal tenderness, urgent surgical treatment will
most likely be required. Patients with evidence of perforation and complete or closed

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5/29/25, 11:16 AM Overview of gastrointestinal tract perforation

loop bowel obstruction, clinical sepsis, or signs of intestinal ischemia benefit from
immediate surgery (See 'Indications for abdominal exploration' above.)
A subset of patients may not require immediate surgery to manage gastrointestinal
perforation. Antibiotic therapy combined with drainage (eg, effusion, abscess cavity)
may be an appropriate initial management strategy for patients with perforated
esophagus, perforated appendicitis with abscess/phlegmon, and perforated colonic
diverticulum with abscess/phlegmon. (See 'Conservative care' above and 'Specific
organs' above.)

ACKNOWLEDGMENT
The UpToDate editorial staff acknowledges Michael J Cahalane, MD, who contributed to
an earlier version of this topic review.
Use of UpToDate is subject to the Terms of Use.

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Contributor Disclosures
Stephen R Odom, MDNo relevant financial relationship(s) with ineligible companies to
disclose.Martin Weiser, MDNo relevant financial relationship(s) with ineligible companies to
disclose.Krishnan Raghavendran, MD, FACSNo relevant financial relationship(s) with
ineligible companies to disclose.Wenliang Chen, MD, PhDNo relevant financial relationship(s)
with ineligible companies to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When
found, these are addressed by vetting through a multi-level review process, and through
requirements for references to be provided to support the content. Appropriately referenced
content is required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

Graphics

Conditions associated with a high serum amylase

Pancreatic disease
Pancreatitis
Complications of pancreatitis (pseudocysts, abscess)

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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

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5/29/25, 11:16 AM Overview of gastrointestinal tract perforation

Macroamylasemia
Burns
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 4.0

Drugs affecting serum amylase values

Increase Increase (cont.) Decrease
Adrenocorticotropic hormone Fluorides Citrates
Aminosalicylic acid Iodine-containing contrast Intravenous
media 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) Ranitidine
Cimetidine Sulfonamides
Codeine Sulindac
Cyproheptadine Sunitinib

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Didanosine Sorafenib
Estrogens Thiazide diuretics
Ethacrynic acid Triprolidine/pseudoephedrine
Ethanol Valproic acid
Graphic 64829 Version 3.0

Hamman sign audio

Hamman sign is an auscultatory finding associated with mediastinal emphysema. It is a

crackling or rasping sound that is synchronous with the heartbeat, heard over the precordium
mainly during systole and particularly in the left lateral decubitus position, and, in many
occasions, associated with muffling of heart sounds.
From Annals of Internal Medicine, Reijnders G, de Ridder S. The Hamman Sign: Case Report With Audio Recording. Ann
Intern Med 2020; 172:435. Copyright © 2020 American College of Physicians. All Rights Reserved. Reprinted with the
permission of American College of Physicians, Inc.
Graphic 127478 Version 2.0

Anatomy of the esophagus

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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

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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

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This figure depicts the relationship of the large intestine to the overlying and underlying
organs and vessels.
Graphic 60998 Version 1.0

Esophageal perforation

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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

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Plain chest radiographs of a 22-year-old-woman who presented to the Emergency Department

with 10 days of sore throat and cough. Image A is a radiograph of the chest in the PA
projection and reveals linear lucencies overlying the upper chest and neck (arrows) consistent
with pneumomediastinum. Image B is a radiograph of the chest in the lateral projection and
reveals the 'ring around the artery' sign (arrow), a finding seen in pneumomediastinum.
Image C is a magnified view of the 'ring around the artery' sign (arrow).
Courtesy of Anna Ellermeier, MD.
Graphic 90041 Version 1.0

Chest radiograph of intraperitoneal free air

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This plain AP 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.
AP: anterior-posterior; PA: posterior-anterior.
Graphic 83050 Version 3.0

Esophageal perforation

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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

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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

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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

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