Back to top

Bowel Obstruction

Presentations in this section include:


Bowel obstruction occurs when the normal flow of intraluminal contents is interrupted. Obstruction can be mechanical or functional and may occur in the small or large bowel. The small bowel is involved in about 80 percent of cases of mechanical intestinal obstruction. Ischemia, which complicates up to 42 percent of bowel obstructions, significantly increases mortality associated with bowel obstruction.

Mechanical bowel obstruction may be classified as partial (incomplete) or complete (see Table 1), simple or complicated (see Table 2). A complete bowel obstruction may progress to complicated bowel obstruction when intestinal ischaemia, necrosis, and/or perforation develop.

Table 1: Partial vs Complete bowel obstruction

Partial Bowel Obstruction

Complete Bowel Obstruction

Partial passage of flatus or stool

Failure to pass flatus or stool

Not usually associated with peritonitis

Generally associated with peritonitis

Table 2: Simple vs Complicated bowel obstruction

Simple Bowel Obstruction

Complicated Bowel Obstruction

Absence of peritonitis

Associated with perionitis

Generally reflects early or partial obstruction

Obstruction has progressed to intestinal ischaemia/ gangrene and/or perforation

Small bowel obstruction

Acute, mechanical small bowel obstruction is a common surgical emergency. Without resolution it is fatal, progressing to intestinal necrosis, perforation, sepsis, and multisystem organ failure.

Step 1: Pathway Entry

Symptoms to consider: Abdominal pain, bloating, nausea, vomiting, inability to pass flatus or stool

Signs to consider: Abdominal distension, abdominal tenderness, peritonitis, hyperactive and high pitched bowel sounds, presence of hernias

Common risk factors in adults:

  • Previous abdominal or pelvic surgery (with the formation of intra-abdominal adhesions).
  • Abdominal wall or groin hernia, such as inguinal hernia with incarceration
  • Intestinal inflammation, such as diverticulitis or Crohn's disease
  • Intestinal malignancy (prior hx or risk factors for neoplasm)

Rare causes include radiation enteritis, foreign body ingestion, intra-abdominal abscess (e.g. perforated appendicitis/diverticulitis), gallstone ileus, intestinal bezoar, intussusception and volvulus.

Step 2: Is the Patient Stable?

  • Initiate resuscitation measures if required.
  • Consideration of other life-threatening diagnoses with similar symptoms (Perforated viscus, Pancreatitis, AAA)
  • In the stable patient a thorough assessment is the next step including a detailed history, a detailed examination, blood tests including FBC, EUC, LFTs, lipase, BSL, an ECG and a CXR. Beta-HCG in women of childbearing age, VBG for lactate.
  • If an alternative diagnosis is made at this time then the steps further down the pathway can be curtailed.

Step 3: Detailed Initial Assessment

Step 4: Imaging

Plain films: Initial imaging should include upright CXR and erect/supine AXR films (or lateral decubitus film if the patient cannot sit upright) - these have a sensitivity of 70-83% and specificity of 67-83% for small bowel obstruction. Plain film findings that suggest small bowel obstruction include:

  • Dilated loops of small bowel proximal to the obstruction > 3 cm
  • Predominantly central dilated loops
  • Three instances of dilatation > 2.5 - 3 cm
  • Valvulae conniventes are visible
  • Gas-fluid levels if the study is erect, especially suspicious if >2.5 cm in width and in same loop of bowel but at different heights (> 2 cm difference in height).

However, obstruction (which may be high-grade mechanical obstruction) may also present with the following features:

  • Gasless abdomen: gas within the small bowel is a function of vomiting, NG tube placement and level of obstruction
  • String-of-beads sign: small pockets of gas within a fluid-filled small bowel

CT abdomen: provides more information than plain films. May be useful to identify the specific site (i.e. transition point) and severity of the obstruction (partial vs complete). It will also give information about the aetiology, by identifying hernias, masses or inflammatory changes, and potential complications, such as ischaemia or perforation.

Step 5: Management

Emergency surgery is indicated in:

  • Perforation or impending perforation
  • Strangulated small bowel obstruction

Patients considered for emergency surgery should be receive preoperative antibiotic prophylaxis and made NBM in preparation for surgery in addition to supportive case detailed below.

All patients should receive supportive care:

  • NBM until surgical review
  • IV fluids
  • Monitoring of urine output
  • Analgesia
  • Anti-emetics can be a useful for emesis and/or nausea in cases where surgery is contraindicated (ondansetron 4mg IV q8H prn)
  • Consider NG tube for gastric decompression (vomiting or severe symptoms of gastric distension)

The need for gastrointestinal decompression varies from patient to patient and remains a matter of clinical judgment. It is suggested with significant distension, nausea, and/or vomiting. Such patients likely have complete or high-grade obstruction; decompression of the distended stomach improves patient comfort and also minimizes the passage of swallowed air, which can worsen distension.

For patients with recurrent SBO who have undergone multiple prior operations, and in whom another operation is felt to be particularly risky, nasogastric decompression is a component of conservative management to avoid further surgery.

Patients who do not require emergency surgery are initially treated conservatively for 48-72 hours. Failure to respond to conservative treatment would lead to consideration for surgery.

Gastrografin may be diagnostic and therapeutic in SBO due to surgical adhesions. The appearance of water-soluble contrast in the colon on an abdominal X ray within 24 hours of its administration predicts resolution of an adhesive small bowel obstruction. While gastrografin does not reduce the need for surgery it does reduce hospital stay in those patients who do not require surgery.

Large bowel obstruction

Acute colonic distension can occur due to the following causes:

  • Mechanical obstruction
  • Toxic megacolon (eg, as a complication of inflammatory bowel disease or Clostridium difficile infection)
  • Acute colonic pseudo-obstruction (Ogilvie's syndrome)

This pathway deals with large bowel obstruction due to mechanical causes.

Step 1: Pathway Entry


  • Abdominal pain (normally colicky), bloating, change in bowel habit, tenesmus, rectal bleeding, recent weight loss, nausea and vomiting


  • Abdominal distension, tympanic abdomen, abdominal tenderness, abdominal rigidity, palpable rectal mass or empty rectum

Risk factors:

  • Malignancy (colorectal cancers and other neoplasms e.g. pancreatic ca, ovarian ca, lymphoma)
  • Prior abdominal surgery, especially prior colorectal resection and stricture formation
  • Volvulus - common in institutionalised elderly patients (5%)
  • Rare causes include hernia, foreign body, benign neoplasm, gynaecological neoplasm, pelvic abscess, or endometriosis
  • Initiate resuscitation measures if required.
  • Consideration of other life-threatening diagnoses with similar symptoms (Perforated viscus, Pancreatitis, AAA)
  • Strictures (i.e. diverticular, inflammatory, ischaemic, radiation-induced, or anastomotic)

Step 2: Is the Patient Stable?

  • Initiate resuscitation measures if required.
  • Consideration of other life-threatening diagnoses with similar symptoms (Perforated viscus, Pancreatitis, AAA)

Step 3: Detailed Initial Assessment

In the stable patient a thorough assessment is the next step including a detailed history, a detailed examination, blood tests including FBC, EUC, LFTs, lipase, BSL, an ECG and a CXR. Beta-HCG in women of childbearing age, VBG for lactate.

If an alternative diagnosis is made at this time then the steps further down the pathway can be curtailed.

Step 4: Imaging

Signs on plain films that may demonstrate large bowel obstruction include:

  • Colonic distension: gaseous secondary to gas-producing organisms in faeces
  • Collapsed distal colon: very few or no air-fluid levels are found in the large bowel because water is reabsorbed
  • Small bowel dilatation, which depends on duration of obstruction, incompetence of the ileocaecal valve
  • No air in the rectum has little or no air

In advanced cases one may see the stigmata of an ischaemic colon, namely:

  • Intramural gas (pneumatosis coli)
  • Portal venous gas
  • Free intra-abdominal gas (pneumoperitoneum)

CT abdomen: more sensitive and specific for colorectal obstruction than plain films (>90% each). Will also distinguish between true obstruction and pseudo-obstruction, as well as determine the cause of obstruction and complications.

Step 5: Management

Supportive care

  • NBM
  • IV fluids
  • Monitor urine output
  • Analgesia
  • NG tube usually unnecessary, may be used if there is severe distension and vomiting

If there is evidence of perforation or impending perforation, emergency surgery is indicated. In the absence of perforation, definitive treatment depends on cause. Treatment in most cases of mechanical large bowel obstruction is surgery, with the exception of:

  • Sigmoid volvulus, where first line treatment is flexible or rigid sigmoidoscopy and insertion of a rectal tube.
  • Benign strictures, which should be treated based on the severity of symptoms, the underlying disease process, and the patient's general condition.

Toxic megacolon

Toxic megacolon is a complication of inflammatory bowel disease (IBD) or infectious colitis that is characterized by colonic dilatation and systemic toxicity. The diagnosis of toxic megacolon should be considered in all patients presenting with abdominal distension and acute or chronic diarrhoea. The diagnosis is clinical, based upon the finding of an enlarged dilated colon accompanied by severe systemic toxicity. The initial evaluation should be aimed at establishing the diagnosis and at determining the underlying cause.

Clinical assessment is similar to that for large bowel obstruction, additionally stool specimens should be sent for culture and CDT. X-rays are important in the diagnosis. CT scanning may occasionally be of value in determining the aetiology of megacolon.

The most widely radiographic criteria for the clinical diagnosis of toxic megacolon are:

  • Radiographic criteria:
    • Dilated colon (>6cm, sometimes up to 15cm), commonly in the right or transverse colon but sometimes involving the descending colon
    • Multiple air-fluid levels in the colon with disturbance of the colonic haustrae
    • Deep mucosal ulcerations may appear as air-filled crevices between large pseudopolypoid projections extending into the colonic lumen
  • PLUS at least three of the following:
    • Fever >38ºC
    • Heart rate >120 beats/min
    • Neutrophilic leukocytosis >10,500/microL
    • Anaemia
  • PLUS at least one of the following:
    • Dehydration
    • Altered sensorium
    • Electrolyte disturbances
    • Hypotension

The main goal of treatment is to reduce the severity of colitis in order to restore normal colonic motility and decrease the likelihood of perforation. Initial treatment is medical, which is successful in preventing surgery in up to 50 percent of patients. However the surgical team should be involved early in the patient’s care.


Paralytic ileus and colonic pseudo-obstruction (Ogilvie's syndrome) cause functional obstruction, because of uncoordinated or attenuated intestinal muscle contractions. Functional bowel obstruction is characterized by signs and symptoms of a mechanical obstruction of the small or large bowel in the absence of an anatomic lesion that obstructs the flow of intestinal contents.

Paralytic ileus occurs to some degree after almost all open abdominal operations. Other causes include peritonitis, trauma, intestinal ischemia, and medications (eg, opiates, anticholinergics). It is exacerbated by electrolyte disorders, particularly hypokalemia. Symptoms are similar to that of mechanical obstruction. However, on imaging there is air in the colon and rectum, and on CT abdomen there is no demonstrable mechanical obstruction. Treatment is dependent on the cause. Prolonged post-operative ileus often responds to conservative treatment with bowel rest, correction of electrolyte disorders and reduction of opioid medications, and drug induced ileus responds to cessation of the precipitating drug.

Acute colonic pseudo-obstruction, or Ogilvie's syndrome, is a variant of ileus, characterized by massive colonic dilatation (discussed later). Chronic idiopathic pseudo-obstruction may be due to an underlying neuropathic disorder (involving the enteric nervous system or extrinsic nervous system) or a myopathic disorder (involving the smooth muscle).

Acute colonic pseudo-obstruction is associated with an underlying disease in 93% of patients including: postoperative status in 23.1%, cardiopulmonary disease in 17.5%, nonoperative trauma in 11.2%, neurologic disease in 8%, malignancy in 5.4%, intra-abdominal pathology in 4.6%, obstetric disorders in 4.4%, and retroperitoneal pathology in 3.5%. Narcotics and electrolyte disorders are frequent contributing factors.

Plain and upright abdominal radiographs show a dilated colon, often from the caecum to the splenic flexure, and occasionally to the rectum; haustral markings are normal. A CT scan is needed to confirm the diagnosis and to exclude mechanical obstruction and toxic megacolon. Treatment aims to relieve discomfort and prevent perforation or ischemia. Treatment in the first instance is supportive care with removal of precipitants. Conservative therapy can be continued for 24 to 48 hours provided that there is no pain or extreme (>12 cm) colonic distension.

If conservative treatment fails, then the following options may be considered:

  • Neostigmine and erythromycin have been reported as effective in the treatment of this condition.
  • Decompression in patients with Ogilvie's syndrome may consist of endoscopic decompression with or without placement of a decompression tube, or percutaneous tube caecostomy.
  • Surgery is rarely required. It is reserved for patients who fail medical and endoscopic management, and for those who develop signs of peritonitis or perforation.

Further resources and references

Online Resource:

BMJ Best Practice Small bowel obstruction and Large bowel obstuction.(Available through CIAP)


  1. Abbas S, Bissett IP, Parry BR. Oral water soluble contrast for the management of adhesive small bowel obstruction. Cochrane Database Syst Rev. 2005;(1):CD004651.
  2. Batke M, Cappell MS. Adynamic ileus and acute colonic pseudo-obstruction. Med Clin North Am. 2008 May;92(3):649-70.
  3. Daneshmand S, Hedley CG, Stain SC. The utility and reliability of computed tomography scan in the diagnosis of small bowel obstruction. Am Surg. 1999;65:922-926.
  4. Maglinte DD, Reyes BL, Harmon BH, et al. Reliability and role of plain film radiography and CT in the diagnosis of small-bowel obstruction. AJR Am J Roentgenol. 1996;167:1451-1455.
  5. Lopez-Kostner F, Hool GR, Lavery I. Management and causes of acute large bowel obstruction. Surg Clin North Am. 1997;77:1265-1290.
  6. Maung AA, Johnson DC, Piper GL, et al; Eastern Association for the Surgery of Trauma. Evaluation and management of small-bowel obstruction: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg. 2012;73(suppl 4):S362-S369.
  7. Tintinalli, Judith E, Tintinalli's emergency medicine : a comprehensive study guide, 9TH edition

© Agency for Clinical Innovation 2023