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.