Gastroduodenal Perforation

Gastroduodenal perforation may be spontaneous or traumatic and the majority of spontaneous perforation is due to peptic ulcer disease.

Improved medical management of peptic ulceration has reduced the incidence of perforation, but still remains a common cause of peritonitis.

The classic sub-diaphragmatic air on chest x-ray may be absent and computed tomography scan is a more sensitive investigation in the stable patient. The management of perforated peptic ulcer disease is still a subject of debate. The majority of perforated peptic ulcers are caused by Helicobacter pylori, so definitive surgery is not usually required.

Perforated peptic ulcer is an indication for operation in nearly all cases except when the patient is asymptomatic or unfit for surgery. However, non-operative management has a significant incidence of intra-abdominal abscesses and sepsis. Primary closure is achievable in traumatic perforation, but the management follows the Advanced Trauma Life Support (ATLS) principles.

Gastrointestinal perforation may occur at any anatomical location from the upper oesophagus to the anorectal junction.

Delay in resuscitation and definitive surgery will progress rapidly into septic shock, multi organ dysfunction, and death, hence it should be one of the first diagnoses considered in all patients who present with acute abdominal pain.


  • Diverticulitis (most common in higher-income countries)
  • Peptic ulcer disease
  • Gastrointestinal malignancy, mainly gastric or colorectal
  • Iatrogenic, such as during routine endoscopy
  • Trauma, either through penetrating or blunt mechanisms
  • Foreign body (e.g. battery or caustic soda)
  • Appendicitis or Meckel’s Diverticulitis
  • Mesenteric ischaemia
  • Obstructing lesions (e.g. cancer, bezoar, or faeces/sterocoral)
    • Results in bowel obstruction, with subsequent ischaemia and necrosis
  • Severe colitis, such as Crohn’s Disease
    • Includes toxic megacolon from ClostridumDifficile or Ulcerative Colitis)
  • Excessive vomiting (Boerhaave Syndrome), leading to oesophageal perforation.
  • The main feature of gastrointestinal perforation is pain. Typically this is rapid onset and sharp in nature. Patients are systemically unwell and may also have associated malaise, vomiting, and lethargy.
  • On examination, patients will look unwell and often have features of sepsis. They will have features of peritonism, which may be localised or generalized (a rigid abdomen); generalised peritonitis implies diffuse contamination of the abdomen and the patient will be very unwell.
  • Laboratory Tests
  • Any patient with an acute abdomen will require urgent blood tests, including FBC, U&Es, LFTs, CRP, clotting, and G&S.
  • Raised WCC and CRP are common features, dependent on timing and degree of contamination, and amylase is often mildly elevated in perforation (although non-specific).
  • Imaging
  • The gold standard for Diagnosis of any perforation is with a CT scan (Fig. 2) confirming the presence of free air and suggesting a location of the perforation (as well as a possible underlying cause).
  • Historically, both a plain film erect chest radiograph (eCXR) and abdominal radiograph (AXR) were used for Diagnosis, however are much less specific* compared to CT imaging. As such, in suspected cases, a CT scan should always be performed.

How is it managed?

The management of any suspected gastrointestinal perforation warrants an early assessment and resuscitation, rapid Diagnosis, and early definitive Treatment.

Broad spectrum antibiotics should be started early. Patients should be placed nil by mouth (NBM) and nasogastric tube considered. Provide adequate intravenous fluid resuscitation and appropriate analgesia.

Following this standard initial approach, management becomes highly individualized, taking into account the site of perforation and patient factors. Most patients with a perforated viscus will require theatre for repair and control of contamination.

Surgical Intervention

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

  • Identification of the underlying cause 
  • Appropriate management of perforation (see Appendix)
  • Thorough washout

Conservative Management

Select physiologically well patients may be managed conservatively, including patients with:

  • Localised diverticular perforation* with only localised peritonitis and tenderness, and no evidence of generalised contamination on imaging
  • Patients with a sealed upper GI perforation on CT imaging without generalized peritonism
  • Elderly frail patients with extensive co-morbidities who would be very unlikely to survive surgery
Gastroduodenal Perforation

How is it treated?

Surgical Techniques in GI Perforation

The surgical technique employed varies depending on the pathology and the anatomical location involved. The most important aspect of any surgery for perforation however remains the intra-operative washout

  • Any peptic ulcer perforation can be accessed typically via an upper midline incision (or laparoscopically if feasible) and a patch of omentum (termed a “Graham patch”) is tacked loosely over the ulcer, which would otherwise be difficult to oversaw due to tissue inflammation
  • Small bowel perforations can be accessed via a midline laparotomy; small perforations can be overseen if the bowel is viable, yet any doubt about condition of bowel should lead to bowel resection +/- primary anastomosis +/- stoma formation
  • Large bowel perforations can be accessed via midline laparotomy; anastomosis in the presence of faecal contamination and an unstable patient is not recommended, so a resection with stoma formation is often the preferred option.
Postoperative and Rehabilitation Care

Patients who present early after perforation normally recover well and may be fed a day or two after the operation and discharged once they are tolerated sufficient intake. Patients who present late in a septic state or have multiple comorbidities may have a more protracted recovering including time in the ICU to treat them for their sepsis.

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