Section 1: Epidemiology and aetiology
Large bowel obstruction, an int-erruption in the flow of colonic contents, accounts for approximately 15 per cent of all cases of intestinal obstruction,1 and most commonly involves the sigmoid colon.
It occurs predominantly in the elderly due to the higher incidence of causative pathology in this age group - but it can occur in all age groups.
The causes of large bowel obstruction can be divided into two groups: dynamic (mechanical obstruction) or adynamic (pseudo-obstruction). The causes of mechanical obstruction may be further considered as luminal, mural or extramural.
In developed countries, colorectal cancer accounts for more than 60 per cent of mechanical large bowel obstruction, with the majority of the remainder due to benign strictures or sigmoid volvulus.1
Adynamic obstruction, or acute colonic pseudo-obstruction, refers to loss of peristalsis with consequent dilatation of the colon in the absence of an obstructing lesion.
Although the exact pathophysiology remains unclear in the majority of patients, it is thought to result from an autonomic imbalance of decreased parasympathetic tone and exc-essive sympathetic output. It may occur post-operatively, but can also occur in a wide range of medical conditions.
The clinical presentation of large bowel obstruction is det-ermined by underlying pathophysiological changes.
As mechanical obstruction becomes established, the proximal bowel produces increasingly vigorous contractions in an effort to overcome the obstruction. This accounts for the abdominal colicky pain.
The proximal bowel then begins to dilate, initially due to accumulation of air and increased intestinal secretions. Stagnation of fluid encourages anaerobic bacterial overgrowth leading to fermentation and production of gas, manifesting as dilated bowel loops seen on plain abdominal radiograph.
The products of fermentation in the bowel lumen also increase the osmotic gradient causing intraluminal fluid and electrolyte shifts, which compounds the problem leading to abdominal distension. The bowel distal to the obstruction eventually evacuates its contents and collapses, accounting for eventual absence of flatus and faeces (absolute constipation). Vomiting may occur as this process evolves. The timing of onset depends on the level of obstruction. The vomitus contains gastric contents initially, then becomes bile stained, and finally faeculent.
With increased intraluminal pressure the tension in the bowel wall increases, which subsequently impairs venous drainage of the bowel, leading to capillary congestion and mural oedema.
Arterial inflow becomes compromised leading to ischaemia. This results in loss of the bowel's innate immunoprotective mechanism, predisposing to translocation of intraluminal bacteria into the circulation with associated signs of sepsis.
This process is more likely in a 'closed loop obstruction' whereby a closed loop is formed between the proximal and distal segments of the obstructed bowel.
Section 2: Making the diagnosis
The cardinal features of acute intestinal obstruction are abd-ominal pain, distension, vomiting and absolute constipation.
In mechanical large bowel obstruction, abdominal distension tends to dominate the clinical picture.
The abdomen is usually tympanic with high-pitched or 'tinkling' bowel sounds. Constipation may also occur and is absolute in complete obstruction, particularly with more distal obstructing lesions.
Vomiting is less common and is usually a late symptom.
Colonic obstruction is characterised by colicky abdominal pain in the central and lower abdomen. If pain becomes continuous and severe this may indicate ischaemia and imminent perforation.
Likewise, localised or generalised peritonitis suggests infarction or perforation. Other non-specific signs that may be present include dehydration, with associated tachycardia and eventual hypotension. Digital rectal examination may reveal a tumour, the presence or absence of stool, and a capacious rectum.
Pseudo-obstruction usually presents in elderly patients, often with multiple comorbidities and acute illness (see box).
|Risk factors for colonic pseudo-obstruction|
|Surgery||Laparotomy, hip/pelvic surgery, thoracic surgery, renal transplantation|
|Trauma||Multiple fractures (especially lumbar spine/pelvis)
|Cardiac||MI, cardiogenic shock|
|Neurological||Spinal cord injury, multiple sclerosis, Alzheimer's disease|
|Medical||Chest infection, infarction, cerebrovascular event, renal failure, retroperitoneal malignancy|
The clinical picture strongly resembles that of mechanical bowel obstruction, except that pain may not be such a feature.
An FBC may demonstrate leukocytosis, which if elevated suggests underlying perforation. Iron deficiency anaemia may be due to malignancy, while derangement of U&Es points towards dehydration, with associated renal impairment.
A plain abdominal radiograph is often diagnostic, with the colon characteristically demonstrating a 'picture-frame' outline of the abdominal cavity, but often may demonstrate large bowel loops throughout the abdomen.
A 'cut-off' point from dilated to collapsed bowel can occasi-onally be seen, signifying the point of obstruction. An erect chest radiograph is mandatory in all patients, in order to exclude free intraperitoneal air secondary to perforation.
Contrast studies are useful in delineating the level, degree and nature of the obstruction.2 A single-contrast enema can differentiate mechanical and pseudo-obstruction, and in the emergency setting is preferable to a double-contrast study.
Section 3: Managing the condition
The principles of management of intestinal obstruction include replacement of fluid losses, correction of electrolyte imb-alances, decompression and surgery if indicated. Emphasis is now on adequate fluid resuscitation and in some cases non-operative decompression prior to definitive surgery.
Patients are dehydrated due to a lack of oral intake, vomiting and third-space losses in the non-functioning bowel. Adequate fluid resuscitation requires a nasogastric tube, IV fluids, a catheter and accurate fluid balance recordings.
Electrolytes (sodium and pot-assium) must be corrected and monitored, and crystalloids are infused to replace fluid losses.
In malignant obstruction, if patients can be decompressed using non-surgical conservative measures, definitive surgery can be undertaken when the patient is in an optimised physiological condition.
Such measures include Nd-YAG laser therapy, expandable metal stents and transanal endoscopic decompression tubes to traverse the obstruction. In the small number of studies on such modalities the subsequent mortality rates were far less than those associated with emergency surgery, which are approximately twice those of elective surgery.3
Such non-operative techniques are highly dependent on local availability and expertise. In the absence of such facilities, or if ischaemia or perforation are suspected, then urgent surgery is undertaken. In the case of obstructing colon malignancy, the site of obstruction guides the operation.
The surgical options include removal of the tumour and primary anastomosis (with or without a covering defunctioning ileostomy), or a colostomy (such as Hartmann's procedure for left-sided lesions).
The decision is based on the patient's general condition, the condition of the bowel, the presence of any peritoneal contamination, and the surgeon's expertise. Peri-operative considerations include broad-spectrum antibiotics to counter the potential translocation of bacteria, thromboprophylaxis and stoma marking and counselling.
Sigmoid and caecal volvulus
Non-surgical decompression of a sigmoid volvulus should be attempted either using a rigid sigmoidoscope and catheter or flexible sigmoidoscopy, unless there are signs of colonic strangulation.
This has the advantage of avoiding surgery, but can be hazardous if there is a gangrenous segment with a perforation risk. There is also a significant incidence of recurrence. Surgical options include sigmoid colectomy and colostomy or resection with a primary anastomosis.
Caecal volvulus is much less common, and again colonoscopic decompression should be attempted if there are no signs of gangrene.
Surgical options include a right hemicolectomy and primary anastomosis, double-barrelled stoma, caecostomy and caecopexy.
If pseudo-obstruction has been definitively diagnosed by gastrografin enema, surgery is rarely indicated as around 80 per cent of patients have resolution of symptoms with conservative treatment within 24-72 hours.4
Treatment measures include fluid balance and electrolyte correction, identifying and treating any contributing factors, avoiding exacerbating medication (for example, opiates, anticholinergics and psychotropics), and placement of a rectal tube to aid decompression.
The use of IV neostigmine (a parasympathomimetic) has been shown to be effective in relieving the colonic distension,5 but should be given in the presence of cardiac monitoring, as bradycardia can occur.
However, if these therapies fail then colonoscopic decompression may be attempted. If the patient demonstrates signs of impending perforation, or a grossly distended caecum, then a laparotomy and subsequent resection may be indicated, depending on the patient's overall condition.
Section 4: Prognosis and follow-up
Large bowel obstruction from all causes carries an appreciable mortality and morbidity risk owing to the nature of the disease process and the health of the patient groups affected.
Prognosis is dependent on the patient's physiological status, coexisting comorbidities, and the underlying disease.
In cases of malignant obstruction, survival can be predicted according to histological and radiological staging, which take into account evidence of local and distant spread.
In those patients with colonic volvulus, endoscopic decompression alone is associated with relatively high recurrence rates.
In addition, morbidity and mortality increase with each successive episode requiring intervention.6
Colorectal cancer patients presenting with large bowel obstruction are followed-up clinically and endoscopically for at least five years.
Colonoscopy is performed to exclude synchronous lesions that were not identified at the time of emergency surgery.
Metachronous lesions are identified by surveillance colonoscopy.
No formal monitoring is necessary for patients following resection, volvulus or diverticular stricture once the colon has been confirmed to be disease-free by colonoscopy.
Following discharge, pat-ients may require follow-up by stoma therapists, dietitians, and colorectal nurse specialists as well as colorectal surgeons.
1. Majid AA, Kingsnorth A (Eds). Advanced surgical practice, 2003 Greenwich Medical Media, London.
2. Macutkiewicz C, Carlson G. Acute abdomen: intestinal obstruction. Surgery (Oxford) 2008; 26: 102-7.
3. Simon Paterson-Brown (Ed). Core topics in general and emergency surgery. A companion to specialist surgical practice, third Edition, Elsevier Saunders.
4. Cameron JL (Ed). Current Surgical Therapy. Ninth edition. 2008 Mosby/Elsevier, Philadelphia, USA.
5. Ponec RJ, Saunders MD, Kimmey MB. Neostigmine for the treatment of acute colonic pseudo-obstruction. 1999. N Engl J Med 341: 137.
6. Gibney EJ. Volvulus of the sigmoid colon. Surg Gynecol Obstet 1991. 173: 243-55.