Constipation and diarrhoea

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Chapter 14 Constipation and diarrhoea

P. Rutter

Key points

Constipation

• About 90% of people defaecate between three times a day and once every 3 days.
• Constipation is considered infrequent bowel action when it happens twice a week or less that involves straining to pass hard stools accompanied by a sensation of pain or incomplete evacuation.
• Constipation is usually not caused by a serious disease and is corrected by non-drug treatment.
• Non-drug treatment involves increasing fibre intake, increasing fluid intake and encouraging exercise.
• The four main groups of drugs used to treat constipation (bulk forming, stimulant, osmotic and faecal softener) all have proven efficacy compared to placebo.

Diarrhoea

• Diarrhoea is the passage of loose or watery stools, at least three times in a 24-h period, which may be accompanied by anorexia, nausea, vomiting, abdominal cramps or bloating.
• Gastroenteritis is the most common cause of diarrhoea in all age groups.
• In the UK, rotavirus and small round structured virus (SRSV) are the most common causes of gastroenteritis in children.
• In adults, Campylobacter followed by rotavirus are the most common causes.
• Blood in diarrhoea is classed as dysentery and indicates the presence of an invasive organism such as Campylobacter, Salmonella, Shigella or Escherichia coli O157.
• Dehydration is the main complication of acute diarrhoea. Oral rehydration solution is the mainstay of treatment, particularly in children and the elderly.
• Antimotility agents, for example, loperamide, diphenoxylate, codeine, may be given to adults with mild-to-moderate diarrhoea but are not recommended for use in children.

Constipation and diarrhoea are two of the most common disorders of the gastro-intestinal tract. Most adults will suffer from these disorders at some time in their life and while they are often self-limiting, they can cause significant morbidity or occur as a secondary feature to a more serious disorder. For example, constipation may be secondary to hypothyroidism, hypokalaemia, diabetes, multiple sclerosis or gastro-intestinal obstruction. Likewise, diarrhoea may be secondary to ulcerative colitis, Crohn’s disease, malabsorption or bowel carcinoma. Both constipation and diarrhoea can also be drug induced and this should be considered when trying to identify a likely cause and determine effective management.

Constipation

In Western populations, 90% of people defaecate between three times a day and once every 3 days. It is clear, therefore, that to base a definition of constipation on frequency alone is problematic. What is perceived to be constipation by one individual may be normal to another. Most definitions of constipation include infrequent bowel action of twice a week or less that involves straining to pass hard faeces and which may be accompanied by a sensation of pain or incomplete evacuation. A pragmatic definition would simply be the passage of hard stools less frequently than the patient’s own normal pattern. Standard criteria for the diagnosis of diarrhoea are available (Longstreth et al., 2006), although they are seldom used in practice.

Incidence

Constipation affects all age groups but is more common in the elderly: up to 20% of elderly people, compared to 8% of middle-aged and 3% of young people, seek medical advice for constipation. In the elderly, poor diet, insufficient intake of fluids, lack of exercise, concurrent disease states and use of drugs that predispose to constipation have all been identified as contributory factors.

Constipation is reported to be twice as common in women than men, although this probably reflects the greater likelihood that they seek medical advice. Constipation is, however, common in late pregnancy (up to 40% of women) due to increased circulating oestrogens, reduced gastro-intestinal motility and delayed bowel emptying caused by displacement of the uterus against the colon. It has also been reported that between 5% and 10% of children have constipation and it is more common in formula-fed babies.

Aetiology

The digestive system can be divided into the upper and lower gastro-intestinal tract. The upper gastro-intestinal tract starts at the mouth and includes the oesophagus and stomach and isresponsible for the ingestion and digestion of food. The lower gastro-intestinal tract consists of the small intestine, large intestine (colon), rectum and anus (Fig. 14.1) and is responsible for the absorption of nutrients, conserving body water and electrolytes, drying the faeces and elimination.

image

Fig. 14.1 The lower gastro-intestinal tract.

The remains of undigested food are swept along the gastro-intestinal tract by waves of muscular contractions called peristalsis. These peristaltic waves eventually move the faeces from the colon to the rectum and induce the urge to defaecate. By the time the stool reaches the rectum it generally has a solid consistency because most of the water has been absorbed.

Normally there is a net uptake of fluid in the intestine in response to osmotic gradients involving the absorption and secretion of ions, and the absorption of sugars and amino acids. This process is under the influence of the autonomic nervous system (sympathetic and parasympathetic). In those situations where absorption increases, this will generally lead to constipation, whereas a net secretion will result in diarrhoea.

Agents that alter intestinal motility, either directly or by acting on the autonomic nervous system, affect the transit time of food along the gastro-intestinal tract. Since the extent of absorption and secretion of fluid from the gastro-intestinal tract generally parallels transit time, a slower transit time will lead to the formation of hard stools and constipation. Motility is largely under parasympathetic (cholinergic) control, with stimulation bringing about an increase in motility while antagonists such as anticholinergics, or drugs with anticholinergic side effects, decrease motility and induce constipation. This mechanism is distinct from that of the other major group of drugs that induce constipation, the opioids. Opioids cause constipation by maintaining or increasing the tone of smooth muscle, suppressing forward peristalsis, raising sphincter tone at the ileocaecal valve and anal sphincter, and reducing sensitivity to rectal distension. This delays passage of faeces through the gut, with a resultant increase in absorption of electrolytes and water in the small intestine and colon.

It is normally the lower section of the gastro-intestinal tract that becomes dysfunctional during constipation. For convenience, many classify constipation as originating from within the colon and rectum, or externally. Causes directly attributable to the colon or rectum include obstruction from neoplasm, Hirschsprung’s disease (absence of neurons in the diseased segment of the internal anal sphincter), outlet obstruction due to rectal prolapse or damage to the pudendal nerve, typically during childbirth. Causes of constipation outside the colon include poor diet, inadequate fibre intake, inadequate water intake, excessive intake of caffeine, use of medicines with constipating side effects or systemic disorders such as hypothyroidism, diabetic autonomic neuropathy, spinal cord injury, cerebrovascular accident, multiple sclerosis or Parkinson’s disease.

Differential diagnosis

Constipation is a symptom and not a disease and can be caused by many different factors (Table 14.1) but the overwhelming majority of cases in non-elderly patients will be due to lack of dietary fibre. To aid diagnosis, questions need to be asked about the frequency and consistency of stools, nausea, vomiting, abdominal pain, distension, discomfort, mobility, diet and other concurrent symptoms or disorders the patient may be experiencing. It may also be necessary to ask about access to a toilet or commode. The individual with limited mobility may suppress the urge to defaecate because of difficulty in getting to the toilet. Likewise, lack of privacy or dependency on a nurse or carer for toileting may result in urge suppression that precipitates constipation or exacerbates an underlying predisposition. Patients with unexplained constipation of recent onset or a sudden aggravation of existing constipation associated with abdominal pain and the passage of blood or mucus, and long-standing constipation unresponsive to treatment require further investigation. Investigations include sigmoidoscopy/colonoscopy, barium enema, full blood count and biochemical monitoring including thyroid function tests (Fig. 14.2).

Table 14.1 Causes of constipation

Cause Comment
Poor diet Diets high in animal fats, for example, meats, dairy products, eggs, and refined sugar, for example, sweets, but low in fibre predispose to constipation
Irritable bowel syndrome Spasm of colon delays transit of intestinal contents. Patients have a history of alternating constipation and diarrhoea
Poor bowel habit Ignoring and suppressing the urge to have a bowel movement will contribute to constipation
Laxative abuse Habitual consumption of laxatives necessitates increase in dose over time until intestine becomes atonic and unable to function without laxative stimulation
Travel Changes in lifestyle, daily routine, diet and drinking water may all contribute to constipation
Hormone disturbances For example, hypothyroidism, diabetes. Other clinical signs should be more prominent, for example, lethargy and cold intolerance in hypothyroidism and increased urination and thirst in diabetes
Pregnancy Mechanical pressure of womb on intestine and hormonal changes, for example, high levels of progesterone
Fissures and haemorrhoids Painful disorders of the anus often lead patients to suppress defaecation, leading to constipation
Diseases Many disease states may have constipation as a symptom, for example, scleroderma, lupus, multiple sclerosis, depression, Parkinson’s disease, stroke
Mechanical compression Scarring, inflammation around diverticula and tumours can produce mechanical compression of intestine
Nerve damage Spinal cord injuries and tumours pressing on the spinal cord affect nerves that lead to intestine
Colonic motility disorders Peristaltic activity of intestine may be ineffective, resulting in colonic inertia
Medication See Table 14.2
Dehydration Insufficient fluid intake or excessive fluid loss. Water and other fluids add bulk to stools, making bowel movements soft and easier to pass
Immobility Prolonged bedrest after an accident, during an illness or general lack of exercise
Electrolyte abnormalities Hypercalcaemia, hypokalaemia
image

Fig. 14.2 A diagnostic algorithm for constipation.

General management

In uncomplicated constipation, education and advice on diet and exercise are the mainstays of management and may adequately control symptoms in many individuals. Typically this advice will include reassurance that the individual does not have cancer, that the normal frequency of defaecation varies widely between individuals, and that mild constipation is not in itself harmful.

If the patient is taking medication for a concurrent disorder this must be assessed for its propensity to cause constipation. In the UK, over 700 medicinal products, including ophthalmic preparations, have constipation listed as a possible side effect. Common examples of medicines involved are presented in Table 14.2.

Table 14.2 Examples of medicines known to cause constipation (frequency defined as very common [>10%] or common [1–10%])

α-Blocker Prazosin
Antacid Aluminium and calcium salts
Anticholinergic Trihexyphenidyl, hyoscine, oxybutynin, procyclidine, tolterodine
Antidepressant Tricyclics, SSRIs, reboxetine, venlafaxine, duloxetine, mirtazepine
Antiemetic Palonosetron, dolasetron, aprepitant
Antiepileptic Carbamazepine, oxcarbazepine
Antipsychotic Phenothiazines, haloperidol, pimozide and atypical antipsychotics such as amisulpride, aripiprazole, olanzapine, quetiapine, risperidone, zotepine, clozapine
Antiviral Foscarnet
β-Blocker Oxprenolol, bisoprolol, nebivolol; other β-blockers cause constipation more rarely
Bisphosphonate Alendronic acid
CNS stimulant Atomoxetine
Calcium channel blocker Diltiazem, verapamil
Cytotoxic Bortezomib, buserelin, cladribine, docetaxel, doxorubicin, exemestane, gemcitabine, irinotecan, mitozantrone, pentostatin, temozolomide, topotecan, vinblastine, vincristine, vindesine, vinorelbine
Dopaminergic Amantadine, bromocriptine, carbegolide, entacapone, tolcapone, levodopa, pergolide, pramipexole, quinagolide
Growth hormone antagonist Pegvisomant
Immunosuppressant Basiliximab, mycophenolate, tacrolimus
Lipid-lowering agent Colestyramine, colestipol, rosuvastatin, atorvastatin (other statins uncommon) gemfibrozil
Iron Ferrous sulphate
Metabolic disorder Miglustat
Muscle relaxant Baclofen
NSAID Meloxicam; other NSAIDs, for example, aceclofenac, and COX-2 inhibitors reported as uncommon
Smoking cessation Bupropion
Opioid analgesic All opioid analgesics and derivatives
Ulcer healing All proton pump inhibitors, sucralfate

Non-drug treatment

Non-drug treatment is advocated as first-line therapy for all patient groups, except those who are terminally ill. This often includes advising an increase in fluid intake at the same time as reducing strong or excessive intake of tea or coffee, since these act as a diuretic and serve to make constipation worse.It is generally recommended that fibre intake in the form of fruit, vegetables, cereals, grain foods, wholemeal bread, etc. be increased to about 30 g/day. The amounts of fibre in commonly eaten foods have been published (MeReC, 2004). Such a diet should be tried for at least 1 month to determine if it has an effect. Most will notice an effect within 3–5 days. Unfortunately, a high-fibre diet is not without problems, with patients complaining of flatulence, bloating and distension, although these effects should diminish over a period of several months. Patients who increase their fibre intake must also be advised to drink 2 L of water a day. Where an intake of this volume cannot be ingested it will be necessary to avoid increasing dietary fibre. An increased level of exercise should also accompany the raised fibre intake as this is thought to help relax and contract the abdominal muscles and help food move more efficiently through the gut.

A high-fibre diet is not recommended in those with megacolon or hypotonic colon/rectum because they do not respond to bulk in the colon. Similarly, a high-fibre diet may not be appropriate in those with opioid-induced constipation.

Drug treatment

Drug treatment is indicated where there is faecal impaction, constipation associated with illness, surgery, pregnancy, poor diet, where the constipation is drug induced, where bowel strain is undesirable, and as part of bowel preparation for surgery. The various laxatives available can be classified as bulk forming, stimulant, osmotic and faecal softeners. A systematic review (Tramonte et al., 1997) identified 36 trials involving 1815 participants that met their inclusion criteria. Twenty of the trials compared laxative against placebo or regular diet, 13 of which demonstrated statistically significant increases in bowel movement. The remaining 16 trials compared different types of laxatives with each other. The review concluded that laxative use was superior to placebo but due to a lack of comparative data could not conclude which laxative group was most efficacious. Further, more recent reviews have found good evidence that macrogols are effective, as are ispaghula husk and bisacodyl, although data is still lacking on which laxative is best (Frizelle and Barclay, 2007).

In general, the fit, active, elderly person should be treated as a younger adult. In contrast, management of constipation in children is often complex. Early treatment is required in children to avoid developing a megarectum, faecal impaction and overflow incontinence. Encouraging the child to use the toilet after meals and increasing dietary fibre have a role alongside oral drug treatment. Depending on circumstances, behavioural therapy may be indicated. In pregnancy, if drug treatment is required, bulk-forming laxatives are first choice, but if stools remain hard then either changing to or adding in lactulose or a macrogol is advocated. Conversely, if stools are soft but the woman still finds difficulty in passing stools then a stimulant laxative should be considered.

Bulk-forming agents

Ispaghula, methylcellulose, sterculia and bran are typical bulk-forming agents and are usually taken as granules, powders or tablets. Their use is most appropriate in situations where dietary intake of fibre cannot be increased and the patient has small hard stools, haemorrhoids or an anal fissure.

The mechanism of action for bulk-forming agents involves polysaccharide and cellulose components that are not digested and which retain fluid, increase faecal bulk and stimulate peristalsis. They may also encourage the proliferation of colonic bacteria and this helps further increase faecal bulk and stool softness. Following ingestion it usually takes 12–36 h before any effect is seen but it may take longer. An adequate volume of fluid should also be ingested to avoid intestinal obstruction. Bulk-forming agents can be used safely long term, during pregnancy or breast feeding but many users will experience problems with flatulence and distension. The use of bulk-forming agents is not recommended in patients with colonic atony, intestinal obstruction or faecal impaction and they are less effective, or may even exacerbate constipation, in those who lack mobility.

Stimulant laxatives

Drugs in this group include bisacodyl, senna and dantron. They directly stimulate colonic nerves that cause movement of the faecal mass, reduce transit time and result in the passage of stool within 8–12 h. As a consequence of their time to onset, oral dosing at bedtime is generally recommended. For a rapid action (within 20–60 min), suppositories can be used. Abdominal cramps are common as an immediate side effect of stimulant laxatives, while electrolyte disturbances and an atonic colon may result from chronic use.

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