Gastrointestinal Perforation

Introduction

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.

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

Aetiology

There are multiple causes of gastrointestinal perforation, including

• Diverticulitis (most common in higher-income countries)
• Peptic ulcer disease
• Gastrointestinal malignancy, mainly gastric or colorectal (Fig. 1)
• 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 Clostridum Difficile or Ulcerative Colitis)
• Excessive vomiting (Boerhaave Syndrome), leading to oesophageal perforation

By Jiri.pekhart [CC BY-SA 3.0], via Wikimedia Commons

Figure 1 – Endoscopic image of colorectal adenocarcinoma

Clinical Features

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.

Investigations

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.

Hellerhoff, CC BY-SA 3.0 , via Wikimedia Commons

Figure 2 – CT scan showing a patient with perforated sigmoid diverticulitis

*The sensitivity in detecting perforation on eCXR is around 70%, meaning 3 out of every 10 patients with a gastrointestinal perforation will have no signs on plain film radiograph

CXR and AXR Features

A eCXR may show air under the diaphragm in cases of pneumoperitoneum (Fig. 3a), whilst an AXR may show either Rigler’s sign (both sides of the bowel visible, Fig. 3b), or psoas sign (loss of the sharp delineation of the psoas muscle border)

Adapted from work by Scott1751 and Clinical_Cases [CC BY-SA 2.5], via Wikimedia Commons

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

Management

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 an nasogastric tube considered. Provide adequate intravenous fluid resuscitation and appropriate analgesia.

Following this standard initial approach, management becomes highly individualised, 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.

Adapted from Ekrem Musalar on Flickr (CC BY-NC-SA 2.0)

Figure 4 – CT scan showing free intra-peritoneal gas (arrows)

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 generalised peritonism
• Elderly frail patients with extensive co-morbidities who would be very unlikely to survive surgery

*An estimated size less than 5cm on CT scan 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

Appendix – 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 oversew due to tissue inflammation
• Small bowel perforations can be accessed via a midline laparotomy; small perforations can be oversewn 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