Clinical features and intestinal complications

2 Clinical features and intestinal complications

Clinical features of ulcerative colitis

The onset of ulcerative colitis is usually gradual, and its natural history chronic, with relapses and remissions over many years. Between attacks, patients are usually free of symptoms. The features of active disease depend on the extent as well as the activity of disease. Although for formal epidemiological and clinical trial purposes various classifications of ulcerative colitis have been proposed (see Key references), they are rarely used in routine clinical practice. The main features of the disease are as described below.

Acute severe ulcerative colitis most commonly occurs in patients with extensive colonic involvement and causes profuse frequent diarrhea (six or more loose stools per day) with blood and mucopus, peridefecatory abdominal pain, fever, malaise, anorexia and weight loss. On external examination the patient is thin, anemic, fluid-depleted, febrile and tachycardic. In the few (now very rare) patients who develop acute colonic dilatation (previously called toxic megacolon) and/or perforation, further deterioration is usually obvious, with sudden worsening of abdominal pain, distension, fever, tachycardia, sepsis and shock.

Moderately active ulcerative colitis is commonly left-sided, causes rectal bleeding and discharge of mucopus accompanied by diarrhea (fewer than six loose stools daily), urgency and abdominal pain. Patients may experience malaise, but examination is usually normal.

Active proctitis causes rectal bleeding and mucous discharge, often with tenesmus and pruritus ani. Patients may have diarrhea, but often well-formed stools. Indeed, many patients with refractory proctitis are constipated (see Chapter 7). Patients usually maintain general health.

Clinical features of Crohn’s disease

The symptoms and signs of Crohn’s disease depend on the affected site and the predominant pathological process in each patient. As for ulcerative colitis, a consensus meeting held in Montreal in 2005 proposed a classification based on disease site and behavior, but this is rarely used for routine clinical purposes. However, the classification does take into account an important feature of the natural history of Crohn’s, which is its tendency to progress from an inflammatory phenotype in most patients at diagnosis, to intestinal stricturing and then fistula and/or abscess formation (so-called ‘penetrating’ disease) as the years go by. Fistulation most commonly occurs between loops of bowel (entero-enteric), bowel and skin (enterocutaneous), and bowel and urogenital tract (e.g. enterovesical, rectovaginal). Fistulation and abscess are particularly common in patients with perianal disease (see below).

Patients likely to have a poor prognosis tend to demonstrate the following clinical features at diagnosis:

• age, younger than 40 years

• ileocolonic disease

• early treatment with corticosteroids

• cigarette smoking

• weight loss of more than 5 kg

• perianal disease.

Active ileocecal and terminal ileal Crohn’s disease patients usually present with pain and/or a tender mass in the right iliac fossa, with or without diarrhea and weight loss. Common mechanisms of diarrhea include mucosal inflammation, bile-salt malabsorption (see pages 31 and 136) and bacterial overgrowth proximal to a stricture (Table 2.1). In patients with symptoms predominantly due to inflammation or abscess, the pain tends to be constant, often with fever. In those with small-bowel obstruction, whether due to active inflammation or to fibrosis and stricture formation in the healing phase, the pain is more generalized, intermittent and colicky, and associated with loud borborygmi (abdominal gurgling sounds), abdominal distension, vomiting and eventually absolute constipation. Enterocutaneous fistulas are clinically obvious, but direct questions about pneumaturia, fecaluria and feculent vaginal discharge may be necessary to identify enterovesical or enterovaginal fistulas. Presentation as an acute abdomen, with peritonitis due to free perforation, is rare.

TABLE 2.1 Mechanisms of diarrhea in Crohn’s disease
Mechanism	Treatment
Inflammation	Anti-inflammatory drugs
Small-bowel bacterial overgrowth	Antibiotics
Bile-salt diarrhea	Colestyramine (cholestyramine), colesevalam, low fat diet
Lactase deficiency	Avoid lactose
Short-bowel syndrome	See Table 2.2
Internal fistula	Surgery
Antibiotic-related	Stop antibiotics
Intercurrent infection (e.g. Clostridium difficile)	Appropriate antibiotic
Coincident disorders (e.g. irritable bowel syndrome, celiac disease)	As appropriate