Gastrointestinal Perforation

Gastrointestinal (GI) perforation may occur at any anatomical location from the upper oesophagus to the anorectal junction. It should be a diagnosis considered in all patients with an acute abdomen.

In GI perforation, the potential to cause peritonitis and a responding inflammatory cascade are constant factors. An untreated patient with can progress rapidly from a systemic inflammatory response to septic shock, multi organ dysfunction, and death.

In this article, we shall look at the causes, clinical features and management of gastrointestinal perforation.


These are several causes of gastrointestinal perforation, which can be broadly categorised into ‘inflammatory/ischaemic’ or ‘traumatic’:

Inflammatory or Ischaemic

  • Chemical
    • Peptic ulcer disease
    • Foreign body (e.g. battery or caustic soda)
  • Fig 1 - Endoscopic image of colorectal adenocarcinoma. GI cancers can cause peforation via obstruction, or via direct invasion of the bowel wall.

    Fig 1 – Endoscopic image of colorectal adenocarcinoma. GI cancers can cause peforation via obstruction, or via direct invasion of the bowel wall.


    • Appendicitis
    • Diverticulitis
    • Cholecystitis
    • Meckel’s Diverticulum
  • Ischaemia
    • Mesenteric ischaemia
    • Obstructive lesions (e.g. cancer*, bezoar or faeces (sterocoral)), resulting in bowel distension and subsequent ischaemia and necrosis
  • Colitis
    • Fistula formation (e.g. Crohn’s Disease)
    • Toxic Megacolon (e.g. Clostridum Difficile or Ulcerative Colitis)

 *GI malignancies are also capable of local invasion through the bowel wall leading to perforation.


  • Iatrogenic
    • Recent surgery (including anastomotic leak)
    • Endoscopy or overzealous NG tube insertion
  • Penetrating or blunt trauma
    • Shear forces from acceleration-deceleration or high forces over small surface area (e.g. a handle bar)
  • Direct rupture
    • Excessive vomiting leading to oesophageal perforation (Boerhaave Syndrome)

Clinical Features

The presentation is dictated mostly by the anatomical location of the perforation.


Any intra-peritoneal gastrointestinal rupture presents with abdominal pain, typically crescendo in nature, beginning as a generalised pain, then focused to the affected region, before spreading as the organ perforates. There is usually an accompanying generalised abdominal tenderness, worse on movement – known as the rigid abdomen.

On examination, the abdomen will be distended and peritonitic. A palpable mass may be present, depending on the underlying cause (e.g. appendiceal mass or malignancy).


A retroperitoneal perforation can be insidious in onset. The presentation can vary and patients may complain of right shoulder tip pain referred from diaphragm irritation, back pain or right iliac fossa pain (right paracolic phenomenon*) representing retroperitoneal duodenal ulcer, or pelvic or left lower quadrant pain – suggesting diverticulitis.

Importantly, there may only be minimal or focal tenderness on palpation, with an otherwise normal examination.

*Gastric content settles in the right paracolic gutter due to gravity, and may mimic appendicitis.


Any thoracic region perforation will present with pain, ranging from chest pain or neck pain to pain radiating to the back or pain on inspiration. There may be associated vomiting (however this may also be preceding if an oesophageal rupture), and respiratory symptoms.

On examination, auscultation and percussion may reveal signs of a pleural effusion, with the potential for palpable crepitus.

Fig 2 - Referred pain chart. Note how diaphragmatic irritation can result in shoulder-tip pain.

Fig 2 – Referred pain chart. Note how diaphragmatic irritation can result in shoulder-tip pain.

Differential Diagnosis

The list of potential differentials is vast.

Important differentials to consider are acute pancreatitis, myocardial infarction, tubo-ovarian pathology, or a ruptured aortic aneurysm.


Laboratory Tests

Any patient with an acute abdomen will require routine baseline blood tests. In a GI perforation, the bloods may show (depending on the underlying cause):

  • FBC – Anaemia, secondary to malignancy or bleeding peptic ulcer. Raised WCC, dependent on timing and degree of contamination.
  • CRP – Raised CRP, dependent on timing and degree of contamination.
  • Amylase – Elevated in perforation (not specific).
  • LFTs – Deranged secondary to gall bladder pathology or metastatic disease.

A urinalysis should be routinely performed to exclude both renal and tubo-ovarian pathology.


Imaging is vital to confirm the suspected diagnosis (by demonstrating air outside the gastrointestinal tract). Radiographs alone can dictate a visit to the operating theatre, yet further imaging is usually warranted.

A plain erect CXR (eCXR) can show free air under the diaphragm (sensitivity around 70%). Pneumomediastinum or widened mediastinum may also be present if the perforation is thoracic in origin. An abdominal X-Ray (AXR) can show signs including:

  • Rigler’s sign – both sides of the bowel wall can be seen, due to free intra-abdominal air acting as an additional contrast.
  • Psoas sign – loss of the sharp delineation of the psoas muscle border, secondary to fluid in the retroperitoneum.

The gold standard for diagnosis of any perforation is with a CT scan, confirming any free air presence and suggesting a location of the perforation (as well as a possible underlying cause). A contrast swallow is also useful for assessing any suspected oesophageal perforation.

Fig 3 - Radiographic evidence of pnuemoperitoneum. a) Free air under the diaphragm; and b) Rigler's sign.

Fig 3 – Radiographic evidence of pnuemoperitoneum. a) Free air under the diaphragm; and b) Rigler’s sign.


The management of any suspected GI perforation warrants an early assessment and resuscitation as necessary. Broad spectrum antibiotics should be started early, especially in patients deemed to need surgery for contamination.

Patients should be placed nil by mouth, and an nasogastric tube should be considered. Provide adequate IV fluid support and patient analgesia.

Following this standard initial approach, management becomes highly individualised, taking into account the site of perforation and patient factors.

Conservative Management

Fig 4 - Oesophageal stents can be used as part of the conservative treatment of perforation.

Fig 4 – Oesophageal stents can be used as part of the conservative treatment of perforation.

A trial of conservative treatment may be considered for the systemically ‘well’ patient with no overt signs of sepsis or peritonitis, when contrast-enhanced imaging has confirmed the site of perforation and the leak appears contained. Examples of this include:

  • Oesophageal perforation – May be treated with a endoscopically placed stent or simple bowel rest with an alternative source of nutrition such as NG tube feeding.
  • Peptic Ulcer perforation  May heal with bowel rest and PPI therapy.
  • Diverticular abscess perforation – An estimated size less than 5cm on CT is an accepted cut off for conservative treatment in these patients, who may respond to antibiotics alone or may be amenable to guided percutaneous drainage.

Surgical Intervention

Any patient who is systemically unwell with confirmed or suspected perforation (or who has failed conservative management) should be rapidly assessed for theatre. The P-Possum Score is useful in these situations as a predictor of post-operative morbidity and mortality, and can help facilitate communication and decision making for clinicians and patients.

The key aspects of any surgical intervention for a GI perforation are:

  • Thorough washout.
  • Diagnosis and management of underlying cause where possible (e.g. relief of obstruction).
  • Appropriate management of perforation:
    • Primary repair of perforations which can heal spontaneously.
    • Resection of area of disease with anastomosis or (more commonly) stoma formation.

Surgical Techniques in GI Perforation

The surgical technique employed varies depending on the pathology and the anatomical location involved.

The oesophagus can be accessed via neck incision, thoracotomy, or upper abdominal incision, with primary repair of small defects performed where possible. Defects not amenable to repair may require drainage and alternative feeding in form of gastrostomy or jejunostomy.

Any stomach or duodenum perforation can be accessed typically via an upper midline incision (but can be done laparoscopically). A perforated peptic ulcer is often the most common cause found, whereby a patch of omentum (Graham Patch) is often sufficient to close an ulcer which would otherwise be difficult to oversew due to tissue inflammation.

Small bowel perforations can be accessed via midline laparotomy. Small perforations can be oversewn if the bowel is viable, yet any doubt about condition of bowel should lead to resection and primary anastomosis.

Large bowel perforations can also be accessed via midline laparotomy. Once any underlying cause is managed, a primary anastomosis is preferred, with or without covering/divergent stoma in proximal bowel. The formation of an end stoma and distal stump with intention to rejoin later is also an option, such as a Hartmanns’ Procedure.

The most important aspect of any surgery for perforation is the intraoperative washout. This should be copious to reduce the bacterial load, and further administration of post operative antibiotics is imperative.


The most important and severe complications of a GI perforation are infection (peritonitis and sepsis) and haemorrhage, with incidence depending on the site involved.

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