This provides sodium 90 mmol/L, potassium 20 mmol/L, chloride 80 mmol/L, citrate 10 mmol/L, glucose 111 mmol/L (total osmolarity 311 mmol/L). Several other formulations exist, some with less sodium (see national formularies).

Of note, it can be seen that attempted rehydration therapy with commercial soft drinks alone will fail because their sodium content is too low (usually less than 4 mmol/L).

Most cases respond adequately with assiduous attention to oral intake but fluid and electrolyte depletion are especially dangerous in children and the elderly, who may need intravenous fluid replacement. Antimotility drugs are inappropriate for severe diarrhoea; hazardous adverse effects (see below) counterbalance any marginal benefit.

Antidiarrhoeal drugs

There are two types of drug which are often used in combination. They should only be considered in benign cases of diarrhoea for short-term symptomatic benefit; in infective or inflammatory diarrhoea their use may be harmful.

Antimotility drugs

Codeine, diphenoxylate and loperamide all activate opiate receptors on the smooth muscle of the bowel to reduce peristalsis and increase segmentation contractions. The actions of all three drugs are antagonised by naloxone. Loperamide and diphenoxylate are relatively enterospecific and do not cross the blood–brain barrier (except diphenoxylate in large doses). These drugs should also be avoided in patients with active inflammatory bowel disease, for they may cause paralytic ileus and toxic megacolon. The abdominal bloating produced by antimotility drugs may be less acceptable than the loose stools for which they are prescribed.

Drugs that directly increase the viscosity of gut contents

Kaolin and chalk are adsorbent powders. Their therapeutic efficacy is marginal as is shown by the fact that they are often combined with an opioid; they should not be used routinely. Bulk forming agents such as ispaghula, methylcellulose and sterculia ¹ (see above) are useful for diarrhoea in diverticular disease, and for reducing the fluidity of faeces in patients with ileostomy and colostomy.

Infectious diarrhoea

This includes travellers’ diarrhoea, where up to half of the diarrhoea that afflicts visitors to tropical and subtropical countries is associated with enterotoxigenic strains of Escherichia coli; other bacteria including Shigella and Salmonella spp., viruses including the Norwalk family, and parasites (particularly Giardia lamblia) have also been implicated.

Transmission is almost invariably by ingestion of contaminated food and water, which indicates the most effective way of reducing risk.

Infectious diarrhoea as a rule is self-limiting and oral rehydration is generally all that is required. Antimotility agents are relatively contraindicated due to concerns of reduced pathogen clearance and toxic megacolon but may be permissible in mild cases. The use of antibiotics is controversial as even in cases of bacterial dysentery they do not reduce duration of symptoms by more than 48 hours, and there is hard in vitro as well as anecdotal evidence that their use in patients with certain bacterial infections (e.g. E. coli O175) can precipitate haemolytic-uraemic syndrome (HUS), which can be life-threatening. Antibiotics may be indicated if the patient is toxic or immunosuppressed, or if invasive infections (e.g. Shigella) are suspected or confirmed. Many regimens are used (commonly ciprofloxacin) but macrolides are theoretically less prone to precipitating HUS in susceptible patients.

Chemotherapy is available for certain specific organisms if enteric infection is confirmed on stool culture, e.g. amoebiasis, giardiasis (see Index).

Diarrhoea due to Clostridium difficile (‘C. diff’)

C. diff infection may range from an offensive but limited diarrhoeal illness to a life-threatening toxic pseudomembranous colitis, and for this reason occupies such a prominent place in the public consciousness. The major risk factors for infection are older age, significant co-morbidites, recent antibiotic use and a history of recent (within 3 months) hospitalisation. Virtually all antibiotics have been implicated as a risk factor for C. diff infection (including, rarely, metronidazole, one of the mainstays of treatment), but clindamycin, quinolones, cephalosporins and other β-lactams are particularly notorious.

First-line treatment has traditionally consisted of 7–14 days of metronidazole by mouth. There is better evidence for a prolonged (4-week) tapering course of oral vancomycin, although this tends to be reserved for severe, refractory or relapsed infections. The tapering course allows the killing of reactivated spores which may have survived initial treatment. Vancomycin not absorbed from the GI tract is excreted renally; it must therefore be given orally (125 mg four times daily initially; occasionally doubled) and monitoring of serum levels is unnecessary.

There are also some data supporting the use of more novel treatments, although solid evidence is lacking. Probiotics and faecal enemas (prepared using normal faeces from unaffected donors), for example, are thought to work by recolonising the bowel with non-pathogenic bacterial flora, whereas intravenous immunoglobulin probably works by neutralising pathogenic toxins.

Drug-induced diarrhoea

Innumerable drugs have diarrhoea as a side-effect. Antimicrobials are the commonest drugs that cause diarrhoea. This is usually due to a benign alteration of bowel flora, but occasionally this will allow latent C. diff colonisation to result in overt colitis (see above).

Secretory diarrhoea due to vasoactive peptides

Octreotide, a synthetic somatostatin analogue (see p. 549), inhibits the release of peptides that mediate certain alimentary secretions, and may be used to relieve diarrhoea due to neuroendocrine tumours such as carcinoids and VIPomas (tumours that produce VIP).