Dynamic obstruction

The diagnosis of intestinal obstruction is based on the classic quartet of pain, distension, vomiting and absolute constipation.

Obstruction may be classified clinically into two types:

small bowel obstruction — high or low;

large bowel obstruction.

In high small bowel obstruction vomiting occurs early and is profuse with rapid dehydration. Distension is minimal with little evidence of fluid levels on abdominal radiography.

In low small bowel obstruction pain is predominant with central distension. Vomiting is delayed. Multiple central fluid levels are seen on radiography.

In large-bowel obstruction distension is early and pronounced. Pain is mild and vomiting and dehydration are late. The proximal colon and caecum are distended on an abdominal radiograph.

The nature of presentation will also be influenced by whether the presentation is:

acute;

   • chronic;

   • acute on chronic;

   • subacute.

  Acute obstruction usually occurs in small bowel obstruction with sudden onsets of severe colicky central abdominal pain, distension, with early vomiting and constipation.

Chronic obstruction is usually seen in large bowel obstruction with lower abdominal colic and absolute constipation, followed by distension.

In acute on chronic obstruction there is a short history of distention and vomiting against a background of pain and constipation.

Subacute obstruction implies an incomplete obstruction. Presentation will be further influenced by whether the obstruction is:

simple — where the blood supply is intact;

  • strangulating/strangulated — where there is direct interference to blood flow, usually by hernial rings or intra­peritoneal adhesions/bands.

The common causes of intestinal obstruction in Western countries and their relative frequency are shown in Fig. 58.1. The underlying mechanisms are shown in Table 58.1.

Pathophysiology

Irrespective of aetiology or acuteness of onset, the proximal bowel dilates and develops an altered motility. Below the obstruction, the bowel exhibits normal peristalsis and absorption until it becomes empty, when it contracts and becomes immobile. Initially, proximal peristalsis is increased to overcome the obstruction, with the length of time it remains vigorous being proportional to the distance of the obstruc­tion. If the obstruction is not relieved the bowel begins to dilate causing a reduction in peristaltic strength, ultimately resulting in flaccidity and paralysis. This is a protective phenomenon to prevent vascular damage secondary to increased intraluminal pressure.

The distension proximal to an obstruction is produced by two factors:

Gas — regardless of the level of obstruction, there is a significant overgrowth of both aerobic and anaerobic organisms resulting in considerable gas production. Following the reabsorption of oxygen and carbon dioxide, the majority is made up of nitrogen (90 per cent) and hydrogen sulphide.

Fluid — this is made up of the various digestive juices (Table 58.2). Following obstruction, fluid accumulates within the bowel wall and any excess is secreted into the lumen, whilst absorption from the gut is retarded. Dehydration and electrolyte loss are therefore due to:

       reduced oral intake;

       defective intestinal absorption;

      losses due to vomiting;

      sequestration in the bowel lumen.

Strangulation

When strangulation occurs the viability of the bowel is threatened secondary to a compromised blood supply. This may be due to:

external compression (hernial orifices/adhesions/bands);

interruption of mesenteric flow (volvulus, a twist of bowel loop on its mesenteric pedicle or intussusception where a segment of bowel invaginates into an adjacent segment);

rising intraluminal pressure (closed-loop obstruction);

primary obstruction of intestinal circulation (mesenteric infarction).

The venous return is compromised before the arterial supply unless primary obstruction is present. The resultant increase in capillary pressure leads to local mural distension with loss of intravascular fluid and red blood cells intramurally and intra-and extraluminally. Once the arterial supply is impaired, haemorrhagic infarction occurs. As the viability of the bowel wall is compromised there is marked translocation and systemic exposure to aerobic and anaerobic organisms with their associated toxins. The associated danger is far greater for intraperitoneal strangulation than that of an external hernia where there is a smaller absorptive surface.

The morbidity and mortality associated with strangulation are dependent on age and extent. In strangulated external hernias the segment involved is short and the resultant blood and fluid loss is small. When bowel involvement is extensive the loss of blood and circulatory volume will cause peripheral circulatory failure.

Closed-loop obstruction

This occurs when the bowel is obstructed at both the proximal and distal point (Fig. 58.2). It is present in many cases of intestinal strangulation. Unlike cases of nonstrangulating obstruction, there is no early distension of the proximal intestine. When gangrene of the strangulated segment is imminent, retrograde thrombosis of the mesenteric veins results in distension on both sides of the strangulated segment.

A classic form of closed-loop obstruction is seen in the presence of a tight carcinomatous stricture of the colon with a competent ileocaecal valve (present in up to a third of individuals). The inability of the distended colon to decompress itself into the small bowel results in an increase in luminal pressure, greatest at the caecum, with subsequent impairment of blood supply. Unrelieved, this results in necrosis and perforation (Fig. 58.3).