Adynamic
obstruction
Paralytic ileus
This may be defined as a state in which there
is failure of transmission of peristaltic waves secondary to neuromuscular
failure [i.e. in the myenteric (Auerbach) and the submucous (Meissner)
plexuses]. The resultant stasis leads to accumulation of fluid and gas within
the bowel with associated distension, vomiting, absence of bowel sounds and
absolute constipation.
Varieties
The following varieties are recognised.
•
Postoperative — a degree of ileus usually occurs after any abdominal
procedure and is self-limiting with a variable duration of 24—72 hours.
Postoperative ileus may be prolonged in the presence of hypoproteinaemia or
metabolic abnormality (vide in Ira).
•
Infection — intra-abdominal sepsis may give rise to localized or
generalised ileus. Resultant adhesions may contribute a mechanical element to
the initial neurogenic aetiology.
•
Reflex ileus — may occur following fractures of the spine or ribs,
retroperitoneal haemorrhage or even the application of a plaster jacket.
•
Metabolic — uraemia and hypokalaemia are the commonest contributory
factors.
Clinical features
Paralytic ileus takes a clinical significance
if 72 hours after laparotomy:
•
there has been no return of bowel sound on auscultation;
•
there has been no passage of flatus.
Abdominal distension becomes more marked and
tympanitic. Pain is not a feature. In the absence of gastric aspiration,
effortless vomiting may occur. Radiologically, the abdomen shows gas-filled
loops of intestine with multiple fluid levels.
Management
The essence of treatment is prevention, with
the use of nasogastric suction and restriction of oral intake until bowel
sounds and the passage of flatus return. Electrolyte balance must be maintained.
Specific
treatment is directed towards the cause, but the following general principles
apply:
•
the primary cause must be removed;
•
gastrointestinal distension must be relieved by decompression;
•
close attention to fluid and electrolyte balance is essential;
•
there is no place for routine use of peristaltic stimulants. Rarely,
medical therapy with the adrenergic blocking agent in association with
cholenergic stimulation, e.g. neostigmine (the Catchpole regime), may be used
in resistant cases provided that an intraperitoneal cause has been excluded;
•
if paralytic ileus is prolonged and threatens life, a laparotomy should
be considered to exclude a hidden cause and facilitate bowel decompression.
Pseudo-obstruction
This condition describes an obstruction,
usually of the colon, in the absence of a mechanical cause or acute
intra-abdominal disease. It is associated with a variety of syndromes where
there is an underlying neuropathy and/or myopathy. A variety of causes has been
described (Table 58.7).
Small
intestinal pseudo-obstruction
This condition may be primary (i.e. idiopathic
or associated with familial visceral myopathy) or secondary. The clinical
picture consists of recurrent subacute obstruction. The diagnosis is made by the
exclusion of a mechanical cause. Treatment consists of initial correction of any
underlying disorder. Metoclopramide and erythromycin may be of use but cisapride,
which increases the local concentration of acetylcholine with the smooth
muscle, is the drug of choice.
Colonic
pseudo-obstruction
This may occur in an acute or a chronic form.
The former, also known as Ogilvie syndrome, presents as acute large bowel
obstruction. Abdominal radiographs show evidence of colonic obstruction with
marked caecal distension being a common feature. Indeed, caecal perforation is a
well-recognised complication. The absence of a mechanical cause requires urgent
confirmation by colonoscopy or a single contrast water-soluble barium enema.
Once confirmed, pseudo-obstruction should be treated by colonoscopic
decompression. This may recur in 25 per cent of cases requiring further
colonoscopy with simultaneous placement of a flatus tube. When colonoscopy fails
or is unavailable, a tube caecostomy may be required. The chronic form may
respond to cisapride but continued symptoms may benefit from surgical
intervention with subtotal colectomy and ileorectal anastomosis.
Acute
mesenteric ischaemia
Mesenteric vascular disease may be classified
as acute intestinal ischaemia — with or without occlusion — venous,
chronic arterial, central or peripheral. The superior mesenteric vessels are
likeliest of the visceral vessels to be affected by embolisation or thrombosis,
with the former being most common. Occlusion at the origin of the superior
mesenteric artery (SMA) is almost invariably the result of thrombosis, whilst
emboli lodge at the origin of the middle colic artery. Inferior mesenteric
involvement is usually clinically silent owing to a better collateral
circulation.
Possible
sources for the embolisation of the SMA include the left atrium associated with
fibrillation, a mural myocardial infarct, an atheromatous plaque from an
aortic aneurysm and a mitral valve vegetation associated with endocarditis.
Primary
thrombosis is associated with atherosclerosis or thromboangitis obliterans.
Primary
thrombosis of the superior mesenteric veins may occur in association with factor
V leiden, portal hypertension, portal pyaemia, sickle cell disease and in
women taking the contraceptive pill.
Irrespective
of whether the occlusion is arterial or venous, haemorrhagic infarction occurs.
The mucosa is the only layer of the intestinal wall to have little resistance to
ischaemic injury. The intestine and its mesentery become swollen and oedematous.
Blood-stained fluid exudes into the peritoneal cavity and bowel lumen. If the
main trunk of the SMA is involved the infarction covers an area from just distal
to the duodenojejunal flexure to the splenic flexure. Usually a branch of the
main trunk is implicated and the area of infarction is less.
Clinical features
The most important clue to an early diagnosis
is the sudden onset of severe abdominal pain in a patient with atrial fibrillation
or atherosclerosis. The pain is typically central and out of all proportion to
physical findings. Persistent vomiting and defecation occur early with the
subsequent passage of altered blood. Hypovolaemic shock rapidly ensues.
Abdominal tenderness may be mild initially with rigidity being a late feature.
Investigation
will usually reveal a profound neutrophil leucocytosis with an absence of gas in
the thickened small intestine on abdominal radiograph. The presence of gas
bubbles in the mesenteric veins is rare but pathognomnonic.
Treatment
needs to be tailored to the individual. In conjunction with full resuscitation,
in early embolic cases embolectomy via the ileo-colic artery or
revascularisation of the SMA may be considered. The majority of cases, however,
is diagnosed late. In the young all affected bowel should be resected, whilst in
the elderly or infirm the situation may be deemed incurable. Anticoagulations
should be implemented early in the postoperative period.
After
extensive enterectomy it is usual for patients to require intravenous
alimentation. The young, however, may sometimes develop sufficient intestinal
digestive and
absorptive function to lead relatively normal
lives. In selected cases, consideration may be given to small bowel transplantation,
but at present this must be considered experimental.
Infarction
of the large intestine alone is relatively rare. Involvement of the middle colic
artery territory should be treated by transverse colectomy and exteriorisation
of both ends, with an extended right hemicolectomy in selected cases.
Ischaemic
colitis describes the structural changes which occur in the colon as a result of
the deprivation of blood. They are commonest in the splenic flexure whose blood
supply is particularly tenuous. They have been classified by Marston into
gangrenous, stricturing and transient forms. Acute presentation is with lower
abdominal pain and the passage of blood per rectum. The differential diagnosis
is usually from a carcinoma, Crohn’s disease or ulcerative colitis. In those
patients without evidence of peritonism, most cases resolves spontaneously. In a
few, a permanent stricture develops requiring elective resection.