Small bowel obstruction

Contributed by Dr Helena Brown, FY2 in general surgery, Basildon and Thurrock University Hospitals NHS Foundation Trust and Mr Joe Dawson, specialist registrar in general surgery, North East Thames.

Section 1 Epidemiology and aetiology
Small bowel obstruction (SBO) is a common surgical emergency accounting for approximately 5 per cent of acute hospital admissions. Even simple cases uncomplicated by strangulation are associated with mortality rates as high as 10 per cent, and even higher in cases involving ischaemic bowel.

In the Western world the most common cause of SBO is adhesions, accounting for 60 per cent of cases. The majority of these will be secondary to previous abdominal or pelvic surgery. 1

Other important causes include strangulated hernias (20 per cent), malignancy (5 per cent) and volvulus (5 per cent). Intussusception and hernias are more common causes of SBO in young children. 2, 3

SBO is classified into mechanical or functional obstruction. Mechanical obstruction is characterised by physical impedance of intestinal contents. Functional obstruction is due to decreased bowel motility rather than a blockage.

Up to nine litres of fluid a day passes through the small bowel as a combination of oral intake, saliva and secretions from the stomach, small intestine and pancreas. During obstruction this fluid accumulates within the bowel lumen, combined with air that has been swallowed or produced by the gut flora. This results in distended loops of small bowel proximal to the obstructing lesion.

As the bowel dilates it triggers an increase in peristaltic activity to try to overcome the obstruction. This is responsible for the colicky abdominal pain experienced and the tinkling bowel sounds on auscultation. Inhibition of these motor reflexes leads to an absence of peristalsis.

Increased intraluminal pressure caused by the sequestered fluid increases the pressure in the bowel wall, restricting mucosal lymphatic drainage. This leads to ischaemic necrosis of the bowel wall. The resulting gangrenous segment then perforates, with ensuing peritonitis.4

Causes of small bowel obstruction
Site of lesionCauses
  • Adhesions
  • Congenital bands
  • Hernias (internal and external)
  • Volvulus
  • Non-GI tumours causing extrinsic compression of bowel (eg ovarian, lymphoma, nodes)
  • GI tumours
  • Intussusception
  • Strictures (Crohn's/previous surgery/radiotherapy/ischaemia)
  • Foreign bodies (especially in children)
  • Gallstone
  • Faecal impaction
  • Meconium
  • Bezoar
  • Post-operative
  • Electrolyte disturbances
  • Infection

Section 2 Diagnosis
Clinical features

The classic features of SBO are rapid-onset colicky abdominal pain, a distended abdomen, vomiting and absolute constipation (ie flatus and stool).

The level of obstruction will affect the presentation, and constipation may be a very late symptom with a proximal obstruction, with vomiting a late symptom in distal obstruction. It is important to note that the absence of these symptoms does not rule out the diagnosis.

A more detailed history may give an indication as to the aetiology of the obstruction, as summarised in the box in section 1.

Features to note on examination are the presence of scars, hernias, and a distended, tympanic and tender abdomen with either tinkling (early) or absent (late) bowel sounds.

In addition, there may be signs of dehydration due to vomiting, third space losses and fluid sequestration into the bowel, such as tachycardia, hypotension, oliguria, acidosis, hypokalaemia and hypoalbuminaemia. Signs such as fever, tachycardia and peritonism are more serious as they suggest ischaemic bowel.

Distinguishing between simple and strangulated SBO is vital as the mortality for untreated strangulated obstruction approaches 100 per cent.5

Blood tests may demonstrate renal impairment due to dehydration and hypokalaemia due to third space losses rich in potassium. A raised white count, CRP and lactate may indicate strangulation, although a closed-loop obstruction may not be evident on blood tests.

A single supine abdominal X-ray is the initial investigation of choice. The typical findings in SBO are multiple, centrally placed dilated loops of bowel ([s40]3cm diameter) with valvulae conivente shadows cross the entire width of the lumen.

Care must be taken, however, as this classical picture occurs in around 60 per cent of cases.6

Traditionally both supine and erect X-rays were taken; the erect images demonstrating multiple air and fluid levels in SBO.

However, this was found not to enhance the sensitivity so it has become normal practice to perform only supine films.

The most useful radiological investigation is a CT with oral contrast as this has a very high sensitivity and specificity.

Section 3 Management
The correct management for SBO depends largely on the cause.

In three-quarters of patients, adhesional SBO will resolve spontaneously with conservative treatment, and the real skill is in deciding which patients require emergency surgery and which are safe to be managed conservatively.

Conservative treatment
The management of adhesional SBO commences with conservative management unless there are signs of bowel ischaemia.

This is colloquially known as 'drip and suck' - consisting of a nasogastric tube to decompress the bowel, and IV fluids.

A urinary catheter is used to monitor fluid balance and an accurate fluid balance chart is vital. It is important to monitor the patient's electrolytes and correct any disturbances.

It is essential that these patients are reviewed regularly to assess their progress and ensure there are no signs of peritonism or toxicity indicative of strangulation, ischaemia or peritonitis.

A trial of conservative treatment for up to 48 hours may be suitable in patients with incomplete obstruction, previous surgery, advanced malignancy, ileus or diagnostic doubt.

Surgery should be considered in patients who are deteriorating or have not improved after 48 hours despite optimum conservative management.

Absolute indications for surgery include peritonitis, an incarcerated hernia or evidence of ischaemia such as increasing pain, peritonism, fever, tachycardia and a leukocytosis.

Relative indications include a palpable mass, a virgin abdomen or failure to improve on conservative treatment.

Laparoscopic surgery
With the advent of laparoscopic surgery, trials have been undertaken to evaluate the role of laparoscopic adhesionolysis in SBO. Studies have shown that this procedure can result in shorter hospital stay with a lower rate of wound infections.

It is important to note, however, that benefits are only incurred with a suitably trained and experienced surgeon, as this remains a very challenging operation with a significant risk of bowel perforation due to the reduced intra-peritoneal space for pneumoperitoneum.

Section 4 Prognosis and follow-up

The morbidity and mortality associated with SBO depends very much on its cause and management. Uncomplicated SBO secondary to adhesions will usually resolve spontaneously with conservative management.

Conversely, the mortality from a strangulated obstruction remains significant, even with appropriate surgical intervention.

If the patient is operated on within 36 hours mortality is 8 per cent. This rises to 25 per cent if surgery is postponed beyond this time. Left untreated, strangulated SBO is universally fatal.

Patients treated conservatively for adhesional obstruction do not necessarily require any follow up. Patients that have undergone surgery for SBO are usually followed up in the outpatient clinic, and have a 20-30 per cent lifetime risk of recurrent obstruction.

Patients who have had non-adhesional SBO may require further investigations and treatment depending on the cause of obstruction.

Due to the significant morbidity and mortality caused by adhesions, a considerable amount of research has focused on attempts to develop products that may be applied at the time of surgery to prevent their formation.

Two Cochrane reviews have been published evaluating evidence to support the use of such products. One focused on preventing adhesion formation after gynaecological surgery and reported that one agent, Interceed, reduced the incidence of pelvic adhesions.7

However, there was not enough evidence to suggest that this translated into improved clinical outcomes.

A second review studied adhesion formation following general surgical procedures.8 It reported that a hyaluronic acid/carboxymethylcellulose membrane reduced the incidence, extent and severity of adhesions.

However, this also did not correlate with improved outcomes in terms of reducing the incidence and severity of subsequent intestinal obstruction.

Both reviews concluded that there is a need for further research to show evidence of clinical benefit from reduction in adhesions.


1. Moran B. Adhesion related small bowel obstruction. Colorectal Dis 2007; 9 Suppl 2: 39-44.

2. Waseem M, Rosenberg H K. Intussusception. Pediatr Emerg Care 2008; 24(11): 793-800.

3. Shalkow J, Asz J, Shorter N A, Friedburg B, Antillon M, Tsou T. Small bowel obstruction - Paediatrics. Emedicine Nov 2008.

4. Brunicardi F C, Andersen D K, Billiar T R et al. Schwarz's Principles of Surgery 8th edition.

5. Nobie B. Small bowel obstruction. Emedicine Sept 2007.

6. Silva A, Pimenta M, Guimaraes L. Small Bowel Obstruction - what to look for. Radiographics 2009; 29(2): 423-39.

7. Ahmad G, Duffy J M, Farquhar C et al. Barrier agents for adhesion prevention after gynaecological surgery. Cochrane Database Syst Rev 2008; (2): CD000475.

8. Kumar S, Wong P F, Leaper D J. Intra-peritoneal prophylactic agents for preventing adhesions and adhesive intestinal obstruction after non-gynaecological abdominal surgery. Cochrane Database Syst Rev 2009; (1): CD005080.

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