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.
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
—
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).