With true diarrhoea there is an increase in stool weight to greater than 300 g per day. This is usually accompanied by increased stool frequency. Patients often interpret the word ‘diarrhoea’ in different ways.


OSMOTIC DIARRHOEA. The gut mucosa acts as a semipermeable membrane and fluid enters the bowel if there are large quantities of non-absorbed hypertonic substances in the lumen. This occurs because:
1 The patient has ingested a non-absorbable substance,  e.g. a purgative such as magnesium sulphate or magnesium- containing antacid.
2 The patient has generalized malabsorption so that high concentrations of solute, e.g. glucose, remain in the lumen.
3 The patient has a specific absorptive defect, e.g. disaccharidase deficiency or glucose-galactose malabsorption.

The volume of diarrhoea produced by these mechanisms is reduced by the absorption of fluid by the ileum and colon. The diarrhoea stops when the patient stops eating or the malabsorptive substance is discontinued.
SECRETORY DIARRHOEA. In this disorder there is both active intestinal secretion of fluid and electrolytes as well as decreased absorption. The mechanism of intestinal secretion is shown (a). Common causes of secretory diarrhoea are:

• Enterotoxins, e.g. cholera, E. coli (thermolabile or thermostable toxin).
• Hormones, e.g. VIP in the Verner-Morrison syndrome
• Bile salts (in the colon) following ileal resection
• Fatty acids (in the colon) following ileal resection
• Some laxatives, e.g. dioctyl sodium sulphosuccinate With secretory diarrhoea, the stool volumes may be very high. Food does not affect the diarrhoea and it therefore continues during fasting.

(a) Mechanisms of diarrhoea. Small intestinal cell. Cholera toxin binds to its receptor (monosialoganglioside GM,) via its B subunits.
(a) Mechanisms of diarrhoea. Small intestinal cell.
Cholera toxin binds to its receptor (monosialoganglioside GM,) via its B subunits.

(b) Mechanisms of diarrhoea. Colonic mucosal cell. This demonstrates one of the mechanisms by which an invasive pathogen, e.g. Shigella, acts. Following penetration, the pathogens generate cytotoxins which lead to mucosal ulceration and cell death.

(b) Mechanisms of diarrhoea. Colonic mucosal cell. This demonstrates one of the mechanisms by which an invasive pathogen, e.g. Shigella, acts. Following penetration, the pathogens generate cytotoxins which lead to mucosal ulceration and cell death.

Diarrhoea occurs because of damage to the intestinal mucosal cell so that there is a loss of fluid and blood. In addition, there is defective absorption of fluid and electrolytes. Common causes are infective conditions, e.g. dysentery due to Shigella, and inflammatory conditions, e.g. ulcerative colitis .
ABNORMAL MOTILITY (usually not true diarrhoea).
Diabetic, postvagotomy and hyperthyroid diarrhoea are all due to abnormal motility of the upper gut. In many of these cases the volume and weight of the stool is not all that high, but frequency of defecation occurs; this therefore is not true diarrhoea.
Causes of diarrhoea are shown It should be noted that the irritable bowel syndrome and diverticular disease are not mentioned as they do not cause ‘true’ diarrhoea, even though the patients may complain of diarrhoea. Worldwide, infection and infestation are a major problem and these are discussed under the causative organisms
ACUTE DIARRHOEA (excluding cholera, which is discussed on p. 29). Diarrhoea of sudden onset is very common, often short-lived and requires no investigation or treatment. This type of diarrhoea is seen after dietary indiscretions, but diarrhoea due to viral agents also lasts 24-48 hours . The causes of other infective diarrhoeas are shown on p. 31. Traveller’s diarrhoea, which affects people travelling outside their own countries, particularly to developing countries, usually lasts 2- 5 days; it is discussed on p. 31. Clinical features associated with the acute diarrhoeas include fever, abdominal pain and vomiting. If the diarrhoea is particularly severe, dehydration can be a problem; the very young and very old are at special risk from this. Investigations are necessary if the diarrhoea has lasted more than 1 week. Stools (up to three) should be sent immediately to the laboratory for culture and examination for ova, cysts and parasites. If the diagnosis has still not been made, a sigmoidoscopy and rectal biopsy should be performed and radiological studies should be considered.

Causes of diarrhoea (see text).
Causes of diarrhoea (see text).

Oral fluid replacement is of prime importance in the treatment. Special oral rehydration solutions, e.g. sodium chlo ride and glucose powder (see Table 1.16), are available for use in severe episodes of diarrhoea in infants. These compounds were initially developed for use in cholera but are valuable in all severe diarrhoeas. Antidiarrhoeal drugs are thought to impair the clearance of any pathogen from the bowel but may be necessary for shortterm relief, e.g. codeine phosphate 30 mg four times daily or loperamide 2 mg three times daily; antibiotics are sometimes given

Chronic diarrhoea

This always needs investigation. All patients should have a sigmoidoscopy and rectal biopsy. The flow diagram  is illustrative; whether the large or the small bowel is investigated first will depend on the clinical story of, for example, bloody diarrhoea or steatorrhoea. The investigations and treatment are described in detail under the individual diseases.

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