Constipation and diarrhoea

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Chapter 14 Constipation and diarrhoea

Key points

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.

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.

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

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.

Diarrhoea

Diarrhoea is defined as the increased passage of loose or watery stools relative to the person’s usual bowel habit. It may be accompanied by anorexia, nausea, vomiting, abdominal cramps or bloating. It is not a disease but a sign of an underlying problem such as an infection or gastro-intestinal disorder. The most likely cause of diarrhoea in all age groups is viral or bacterial infection; therefore, the following section primarily focuses on acute infective gastroenteritis but also includes reference to drug-induced diarrhoea. Diarrhoea can be associated with other conditions, for example, irritable bowel syndrome, inflammatory bowel disease, colorectal cancer and malabsorption syndromes, but these will not be covered here.

Acute gastroenteritis is most common in children but the precise incidence is not known because many cases are self-limiting and not reported. Nevertheless, diarrhoeal illness in children leads to high consultation rates with primary care doctors and accounts for one in five consultations in the 0–4 age group. It has been estimated that children under the age of 5 years have between one and three bouts of diarrhoea per year. Children in the same age range account for over 5% of consultations to primary care doctors, with 18,000 children a year in England and Wales being admitted to hospital with rotavirus infection.

The incidence of diarrhoea in adults is, on average, just under one episode per person each year. Many of these cases are thought to be food related, with 22% of those consulting a doctor claiming to have ‘food poisoning’. Traveller’s diarrhoea is another common cause of diarrhoea. For high-risk travel to areas such as Africa, Asia and South America, the reported incidence is more than 20%. Over recent years, Escherichia coli O157 has gained prominence because of a number of outbreaks in different communities associated with severe disease and even death. It is, however, an uncommon cause of diarrhoea, accounting for only 0.1% of all cases.

Aetiology

In the UK, rotavirus and small round structured virus (SRSV) are the most common identified causes of gastroenteritis in children. In adults, Campylobacter followed by rotavirus are the most common causes, although rates of norovirus have reported to be on the increase. Other identified causes include: the bacteria E. coli, Salmonella, Shigella, Clostridium perfringens enterotoxin; viruses such as adenovirus and astrovirus; and the protozoa Cryptosporidium, Giardia and Entamoeba. These pathogens produce diarrhoea via a number of methods: for example, enterotoxigenic E. coli produce enterotoxins that affect gut function with secretion and loss of fluids; by interfering with normal mucosal function, for example, adherent enteropathogenic E. coli; or by causing injury to the mucosa and deeper tissues, for example, enteroinvasive E. coli or enterohaemorrhagic E. coli such as E. coli O157. Other organisms, for example, Staphylococcus aureus and Bacillus cereus, produce preformed enterotoxins which on ingestion induce rapid-onset diarrhoea and vomiting that usually last less than 12 h.

So-called traveller’s diarrhoea frequently affects people travelling from an area of more developed standards of hygiene to a less developed area. In many instances, the cause remains unknown, even after stool culture, but where a pathogen is identified, bacterial infection is responsible in over 80% of cases, and associated with ingestion of contaminated food or water and occurs during or shortly after travel. Bacterial pathogens commonly isolated include E. coli, Shigella, Salmonella, Campylobacter, Vibrio and Yersinia species. Viruses (10–15% of cases) and parasites (2–10% of cases), such as norovirus, Giardia, Cryptosporidium and Entamoeba, account for the remainder.

Many medicines, particularly broad-spectrum antibiotics such as ampicillin, erythromycin and neomycin, induce diarrhoea secondary to therapy (Table 14.3). With these antibiotics the mechanism involves the overgrowth of antibiotic-resistant bacteria and fungi in the large bowel after several days of therapy. The diarrhoea is generally self-limiting. However, when the overgrowth involves Clostridium difficile and the associated production of its bacterial toxin, life-threatening pseudomembranous colitis may be the outcome.

Table 14.3 Examples of medicines known to cause diarrhoea (defined as very common [>10%] or common [1–10%])

α-Blocker Prazosin
ACE inhibitor Lisinopril, perindopril
Angiotensin receptor blocker Telmisartan
Acetylcholinesterase inhibitor Donepezil, galantamine, rivastigmine
Antacid Magnesium salts
Antibacterial All
Antidiabetic Metformin, acarbose
Antidepressant SSRIs, clomipramine, venlafaxine
Antiemetic Aprepitant, dolasetron
Antiepileptic Carbamazepine, oxcarbagepine, tiagabine, zonisamide, pregabalin, levtiracetam
Antifungal Caspofungin, fluconazole, flucytosine, nystatin (in large doses), terbinafine, voriconazole
Antimalarial Mefloquine
Antiprotozoal Metronidazole, sodium stibogluconate
Antipsychotic Aripiprazole
Antiviral Abacavir, emtricitabine, stavudine, tenofovir, zalcitabine, zidovudine, amprenavir, atazanavir, indinavir, lopinavir, nelfinavir, saquinavir, efavirinez, ganciclovir, valganciclovir, adefovir, oseltamivir, ribavrin, fosamprenavir
β-Blocker Bisoprolol, carvedilol, nebivolol
Bisphosphonate Alendronic acid, disodium etidronate, ibandronic acid, risedronate, sodium clodronate, disodium pamidronate, tiludronic acid
Cytokine inhibitor Adalimumab, infliximab
Cytotoxic All classes of cytotoxics
Dopaminergic Levodopa, entacapone
Growth hormone antagonist Pegvisomant
Immunosuppressant Ciclosporin, mycophenolate, leflunomide
NSAID All
Ulcer healing All proton pump inhibitors
Vaccine Pediacel (5 vaccines in 1), haemophilus, meningococcal
Miscellaneous Calcitonin, strontium ranelate, colchicine, dantrolene, olsalazine, anagrelide, nicotinic acid, pancreatin, eplerenone, acamprosate

Signs and symptoms

Acute-onset diarrhoea is associated with loose or watery stools that may be accompanied by anorexia, nausea, vomiting, abdominal cramps, flatulence or bloating. When there is blood in the diarrhoea this is classed as dysentery and indicates the presence of an invasive organism such as Campylobacter, Salmonella, Shigella or E. coli O157.

The history of symptom onset is important. The duration of diarrhoea, whether other members of the family and contacts are ill, recent travel abroad, food eaten, antibiotic use and weight loss are all important factors to elucidate. The possibility of underlying diseases such as AIDS or infective proctitis in homosexual men must also be considered.

Dehydration is a common problem in the very young and frail elderly and the signs and symptoms must be recognised.In children, the severity of dehydration is most accurately determined in terms of weight loss as a percentage of body weight prior to the dehydrating episode. Unfortunately, in the clinical situation pre-illness weight is rarely known; therefore, clinical signs of dehydration must be assessed. National Institute for Health and Clinical Excellence (2009) has issued guidance on assessing the level of dehydration in children under 5 years of age and appropriate fluid management depending on the level of dehydration. Symptoms that could indicate mild dehydration are vague and include tiredness, anorexia, nausea and light-headedness.

Symptoms become more prominent in moderate dehydration and include dry mucous membranes, sunken eyes, decreasedskin turgor (pinch test of 1–2 s or longer), tachycardia, apathy, dizziness and postural hypotension. In severe dehydration, the above symptoms are more marked and may also include hypovolaemic shock, oliguria or anuria, cold extremities, a rapid and weak pulse and low or undetectable blood pressure.

Treatment

Acute infective diarrhoea, including traveller’s diarrhoea, is usually a self-limiting disorder. However, depending on the causative agent, a number of complications may have to be dealt with. Dehydration and electrolyte disturbance can be readily treated but may, if severe, progress to acidosis and circulatory failure with hypoperfusion of vital organs, renal failure and death. Toxic megacolon due to infective colitis has been documented; associated arthritis or Reiter’s syndrome may complicate the invasive diarrhoeas of Campylobacter and Yersinia; Salmonella species may infiltrate bones, joints, meninges and the gallbladder; and E. coli infection may, for example, be complicated by haemolytic uraemic syndrome.

General measures

Patients should be advised on handwashing and other hygiene-related issues to prevent transmission to other family members. Promotion of handwashing has been shown to decrease diarrhoeal episodes by approximately one-third (Ejemot et al., 2008). Exclusion from work or school until the patient is free of diarrhoea is advised. In acute, self-limiting diarrhoea, children, healthcare workers and food handlers should be symptom free for 48 h before returning to school or work. More exacting criteria for return to work, such as testing for negative stool samples, are rarely required.

In both children and adults, normal feeding should be restarted as soon as possible. In weaned and non-weaned children with gastroenteritis, early feeding after rehydration has been shown to result in higher weight gain, no deterioration or prolongation of the diarrhoea and no increase in vomiting or lactose intolerance (Conway and Ireson, 1989, Sandhu et al., 1997). Similarly, breast-feeding infants should continue to feed throughout the rehydration and maintenance phases of therapy. Avoidance of milk or other lactose-containing food is seldom justified.

Dehydration treatment

Since diarrhoea results in fluid and electrolyte loss, it is important to ensure the affected individual maintains adequate fluid intake. Most patients can be advised to increase their intake of fluids, particularly fruit juices with their glucose and potassium content, and soups because of their sodium chloride content. High-carbohydrate foods such as bread and pasta can also be recommended because they promote glucose and sodium co-transport.

Young children and the frail elderly are prone to diarrhoea-induced dehydration and use of an oral rehydration solution (ORS) is recommended. The formula recommended by the World Health Organization (WHO) contains glucose, sodium, potassium, chloride and bicarbonate in an almost isotonic fluid. A number of similar preparations are available commercially in the form of sachets that require reconstitution in clean water before use (Table 14.4). Glucose concentrations between 80 and 120 mmol/L are needed to optimise sodium absorption in the small intestine. Glucose concentrations in excess of 160 mmol/L will cause an osmotic gradient that will result in increased fluid and electrolyte loss. High sodium solutions, in excess of 90 mmol/L, may lead to hypernatraemia, especially in children, and should be avoided. Until recently, the WHO ORS contained 90 mmol/L sodium, as cholera is more common in developing countries and associated with rapid loss of sodium and potassium. However, a systematic review of trials using a reduced osmolarity ORS (Hahn et al., 2002) concluded that solutions with a reducedosmolarity compared to the standard WHO formula were associated with fewer unscheduled intravenous infusions, a trend towards reduced stool output and less vomiting in children with mild-to-moderate diarrhoea. Based on this and other findings, the WHO ORS now has a reduced osmolarity of 245 mOsm/L and contains 75 mmol of sodium.

Commercially available solutions in the UK contain lower sodium concentrations as diarrhoea tends to be isotonic, and therefore replacement of large quantities of sodium is less important and indeed may be harmful. The presence of potassium prevents hypokalaemia occurring in the elderly, especially in those taking diuretics. ORS should be routinely used in both primary and secondary care settings. There appears to be no significant difference between intravenous and oral rehydration (Gavin et al., 1996).

For healthy adults, an appropriate substitute for a rehydration sachet is 1 level teaspoonful of table salt plus 1 tablespoon of sugar in 1 L of drinking water. The volume of ORS to be taken in treating mild-to-moderate diarrhoea is dependent on age. In adults, 2 L of oral rehydration fluid should be given in the first 24 h, followed by unrestricted normal fluids with 200 mL of rehydration solution per loose stool or vomit. For children, 30–50 mL/kg of an ORS should be given over 3–4 h. This can be followed with unrestricted fluids, either with normal fluids alternating with ORS or normal fluids with 10 mL/kg rehydration solution after each loose stool or vomit (Murphy, 1998). The solution is best sipped every 5–10 min rather than drunk in large quantities less frequently.

Care is required in diabetic patients who may need to monitor blood glucose levels more carefully.

Drug treatment

Antimicrobials

Antibiotics are generally not recommended in diarrhoea associated with acute infective gastroenteritis. Inappropriate use will only contribute further to the problem of resistant organisms. There is, however, a place for antibiotics in patients with positive stool culture where the symptoms are not receding or for travellers’ diarrhoea (De Bruyn et al., 2000). In patients presenting with dysentery or suspected exposure to bacterial infection, treatment with a quinolone, for example, ciprofloxacin, may be appropriate. However, quinolones are not without their problems: they may cause tendon damage or induce convulsions in epileptics, in situations that predispose to seizures, and in patients taking NSAIDs. Their use in adolescents is also not recommended because of an association with arthropathy.

Where Campylobacter is the suspect causative organism, patients with severe symptoms or dysentery should receive early treatment with erythromycin or ciprofloxacin. Severe symptoms or dysentery associated with Shigella can also be treated with ciprofloxacin. Nalidixic acid can be used in children and trimethoprim may be appropriate in pregnant women where resistance is not a problem.

The use of antibiotics in patients with Salmonella is not generally recommended because of the likelihood that excretionis prolonged. Antibiotics may, however, be indicated in the very young and the immunocompromised. The benefit of antibiotic use in enterohaemorrhagic infection, for example, E. coli O157, is less clear. In this situation, there is evidence that antibiotics cause toxins to be released which may lead to haemolytic uraemic syndrome.

In both amoebic dysentery and giardiasis, metronidazole is the drug of choice. Diloxanide is also used in amoebic dysentery to ensure eradication of the intestinal disease. Antibiotics are not indicated in the treatment of cryptosporidiosis in immunocompromised individuals.

Zinc

The use of zinc has been reviewed in the treatment of diarrhoea in children in developing countries (Lazzerini et al., 2008). In this context, zinc has been shown to be of value in children older than 6 months, probably because they have some prior, underlying deficiency of zinc.

Rotavirus vaccine

Rotavirus vaccine has been shown to protect against the most common strains of rotavirus (G1 and G3), although the benefits of the vaccine are dependant on the type of vaccine used, with rhesus and human rotavirus the most efficacious (Soares-Weiser, 2004).

Some of the common therapeutic problems in the management of individuals with constipation and diarrhoea are outlined in Table 14.5.

Table 14.5 Common therapeutic problems in constipation and diarrhoea

Problem Comment
Constipation
Bulk laxative, for example ispaghula, taken at bedtime Drugs such as ispaghula should not be taken before going to bed because of risk of oesophageal blockage
Urine changes colour Anthraquinone glycosides, for example senna, are excreted by the kidney and may colour urine yellowish-brown to red colour, depending on pH
Patient claims dietary and fluid advice ineffective in resolving constipation May find high-fibre diet difficult to adhere to, socially unacceptable, and expect result in less than 4 weeks
Patient taking docusate complains of unpleasant aftertaste or burning sensation Advise to take with plenty of fluid after ingestion
Sterculia as Normacol® and Normacol Plus® granules or sachets The granules should be placed dry on the tongue and swallowed immediately with plenty of water or a cool drink. They can also be sprinkled onto and taken with soft food such as yoghurt
Methylcellulose (Celevac®) Each tablet should be taken with at least 300 mL of liquid
Diarrhoea
Antimotility agent requested for a young child Antimotility agents must be avoided in young children or patients with severe gastroenteritis or dysentery
Antimotility agent requested by patient with persistent diarrhoea (>10 days) Antimotility agent inappropriate. Stool culture required to exclude parasitic infection such as Giardia, Entamoeba and Cryptosporidium
Adult with diarrhoea stops eating and drinking to allow diarrhoea to settle Patient should eat and drink as normally as possible. Plenty of fluids required to prevent dehydration. Fruit juice (glucose and potassium), soup (salt), bread and pasta (carbohydrate) are of particular benefit
Reconstitution of oral rehydration solution Each sachet of Diorolyte® and Electrolade® requires 200 mL of water. They should be discarded after 1 h after preparation unless stored in a fridge when they may be kept for 24 h

Case studies

Answers

1. This patient probably has haemolytic uraemic syndrome caused by E. coli O157. Haemolytic uraemic syndrome is the most common form of acquired renal insufficiency in young children. It is characterised by nephropathy, thrombocytopenia and microangiopathic haemolytic anaemia. Although there are a number of potential causative factors, the most common is the toxin-producing O157 strain of E. coli. In 1996, 21 people died from E. coli O157 after eating contaminated meat from a butcher’s shop in Scotland. In 2001, 13 Girl Guides and their leader contracted E. coli O157 after camping in a field in Inverclyde, Scotland, previously grazed by sheep and in 2005 more than 158 children from 42 schools in South Wales were affected by eating contaminated meat, one of whom died.

The syndrome typically has a pro-drome of bloody diarrhoea occurring 5–7 days before onset of renal insufficiency. Colonoscopy is usually non-specific and shows haemorrhagic colitis. At diagnosis most children are pale and very irritable. Hypertension and hyponatraemia may be associated with convulsions and are generally a consequence of a disorder of fluid and salt balance. Laboratory findings may include anaemia and thrombocytopenia, hyponatraemia, hyperkalaemia, hypocalcaemia and metabolic acidosis. The kidney typically shows signs of glomerular endothelial injury. Capillary thrombosis is quite prominent but with no evidence of immune complex deposition. Similar findings can usually be seen in all other organs including the brain, liver and intestine.

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