All You Want To Know About Diarrhoea

Diarrhoea
Diarrhoea is defi ned as the passing of increased amounts of loose stools (more than 300 g in 24 hours in adults). There are several causes, but the condition is usually short-lived and symptoms can be treated with over-the-counter medication.
Causes
Acute diarrhoea (infective diarrhoea, gastroenteritis)
  Acute diarrhoea is caused by bacterial or viral infection, usually from contaminated food.
  Damage to cells in the intestinal mucosa causes infl ammation and prevents absorption of water from the intestine into the blood stream, and the fl uid is evacuated in watery stools.
  The condition is self-limiting and normally resolves within 72 hours.
Traveller’s diarrhoea
  This is the term given to diarrhoea experienced by travellers or holidaymakers.
Causes, and the severity of symptoms, vary with location.
  Attacks are normally short-lived, lasting up to 4–7 days, and begin early in a trip, although they can occur at any time.
  Some infections can cause persistent or recurrent diarrhoea and systemic complications.
  More serious microbial infections, such as typhoid and cholera, and parasitic infections, such as giardiasis and amoebic dysentery, may be contracted in tropical and subtropical areas.
  Up to 15% of patients with traveller’s diarrhoea have dysentery (bloody diarrhoea).
Chronic diarrhoea
  Recurrent or persistent: there are several causes and chronic diarrhoea requires medical investigation.
  Causes include:
–  irritable-bowel syndrome (IBS) – a common functional bowel disorder of unknown aetiology, of which diarrhoea is a common symptom (see Chapter 14)
– infl ammatory bowel disease (for example, Crohn’s disease, ulcerative colitis)
–  malabsorption syndromes (such as coeliac disease)
– bowel tumour
–  metabolic disease (diabetes, hyperthyroidism)
– side-effects of drugs
– laxative abuse.
Epidemiology
Acute diarrhoea
  The exact incidence is unknown, but it is very common and everybody is thought to have a bout at least once in their life.
Traveller’s diarrhoea
  Between 30 and 80% of all travellers are estimated to suffer.
  In up to about 60% of cases no pathogenic cause is found. Of the rest, the causative organisms are:
– enterotoxigenic Escherichia coli – responsible for 40–75% of traveller’s diarrhoea from an infectious cause; most common in Africa and Central America
– enterohaemorrhagic E. coli and Shigella  species – up to 15%, most common in Africa and Central America
–  Salmonella species – up to 10%
–  Campylobacter jejuni  – up to 10%, more common in travellers in Asia
–  viruses (for example, rotavirus, Norwalk virus), protozoa and helminths – up to 10%
–  Giardia lamblia (especially occurs in travellers in Eastern Europe)
–  Entamoeba histolytica – up to 3%.
Signs and symptoms
Acute diarrhoea
  rapid onset
  watery stools, passed frequently
  resolves spontaneously within 72 hours
  there may be:
–  abdominal cramps and fl  atulence
–  nausea and vomiting
–  weakness and malaise
– fever
–  in babies and young children, diarrhoea may be associated with respiratory symptoms.
Traveller’s diarrhoea
  early onset, usually within fi rst 3 days of trip
  normally of short duration: mean 4 days, maximum 7 days
  bloody diarrhoea in about 15% of cases
  other symptoms as for acute diarrhoea.

Symptoms and circumstances for referral
  duration:
–  more than 72 hours in older children and adults
–  more than 48 hours in children under 3 years and elderly patients
–  more than 24 hours in people with diabetes
–  more than 24 hours in babies under 1 year
–  babies under 3 months: refer immediately.
  diarrhoea associated with severe vomiting and fever
  history of change in bowel habit
  recurrent diarrhoea
  presence of blood or mucus in stools
  suspected adverse drug reaction
  alternating constipation and diarrhoea in elderly patients – may indicate faecal impaction
  signs of dehydration in babies: dry skin, sunken eyes and fontanelle, dry tongue, drowsiness, less urine than normal.
Treatment
Oral rehydration therapy
  The first line of treatment for acute diarrhoea is fluid and electrolyte replacement by oral rehydration therapy (ORT).
  Normal faeces contain 60–85% water, and the body loses between 70 and 200 ml of water per day through defecation. In diarrhoea, water loss of up to four times
this volume per loose stool occurs, and sodium and potassium alkaline salts are excreted along with it, leading to a fall in plasma pH (acidosis). This can have serious metabolic consequences, particularly in the very young and the elderly.
Fluid and electrolyte losses are increased if vomiting also occurs.
  Oral rehydration salts are not intended to relieve symptoms but are designed to replace water and electrolytes lost through diarrhoea and vomiting.
  They contain sodium and potassium to replace these essential ions and citrate and/or bicarbonate to correct acidosis.
  Glucose is also an important ingredient as it acts as a carrier for the transport of sodium ions, and hence water, across the mucosa of the small intestine, as well as providing the energy necessary for that process.
  ORT can be recommended for patients of any age, even when referral to a doctor is considered necessary.
  There are no contraindications unless the patient is vomiting frequently and unable to keep the solution down, in which case intravenous fl  uid and electrolyte replacement may be necessary.
  Fluid overload from excessive administration of ORT is highly unlikely, but possible if it is continued in babies and young children for more than 48 hours. Fluid overload is recognised by the eyelids becoming puffy, and is rapidly corrected by withholding ORT and other liquids.
Antimotility agents
  Non-prescription medicines are available containing the opioid drugs loperamide, morphine and diphenoxylate.
  One of the effects of opioid drugs is to cause constipation by increasing tone of both the small and large bowel and reducing intestinal motility.
They also increase sphincter tone and decrease secretory activity along the gastrointestinal tract. Decreased motility enhances fluid and electrolyte reabsorption and decreases the volume of intestinal contents.
Loperamide
  Loperamide has a high affinity for, and exerts a direct action on, opiate receptors in the gut wall.
  It also has a high first-pass metabolism so little reaches the systemic circulation, and at the restricted dosage permitted for non-prescription use it is unlikely to cause any of the side-effects associated with opiates.
  It is not licensed for non-prescription use in children under 12 years.
Morphine
  Morphine acts promptly on the intestine (within 1 hour of administration), because of its direct action on intestinal smooth muscle and quick absorption from the gastrointestinal tract.
  Its action peaks within 2–3 hours and lasts about 4 hours.
  Morphine is not well absorbed orally and its availability may be reduced in combination products because of its adsorption on to other constituents.
  The morphine content of diarrhoea preparations may also be subtherapeutic.
  Morphine, particularly in Kaolin and Morphine Mixture, is subject to abuse and many pharmacists severely restrict its sale.
Diphenoxylate
  Diphenoxylate is a synthetic derivative of pethidine.
  It has little or no central action but acts selectively on gastrointestinal smooth muscle. It takes longer to act than loperamide.
  Diphenoxylate is combined with atropine as co-phenotrope. Atropine is included at a subtherapeutic dose to discourage abuse, on the premise that unpleasant antimuscarinic effects will be experienced if higher than recommended doses are taken. 
  Co-phenotrope is not licensed for non-prescription use in children under 16 years.
Adsorbents
  The rationale behind the use of adsorbents is that they are capable of adsorbing microbial toxins and microorganisms onto their surfaces. Because these substances are not absorbed from the gastrointestinal tract, the toxins and microorganisms are thereby excreted in the stool.
  This lack of absorption also means that adsorbents are relatively harmless and safe to use, but there is little evidence that they are effective.
  Adsorption is a non-specific process and, as well as adsorbing toxins, bacteria and water, the drugs may interfere with the absorption of other drugs from the intestine. This should be borne in mind if recommending adsorbent antidiarrhoeals to patients taking other medicines.
  The adsorbents used in antidiarrhoeals are kaolin, attapulgite and bismuth salicylate.
  Bismuth subsalicylate is claimed to possess adsorbent properties, and some studies have shown it to be effective in treating diarrhoea. Large doses are required and salicylate absorption may occur. It should be avoided by individuals sensitive to aspirin.

Additional adviceFor patients suffering from diarrhoea

  Drink plenty of clear fl uids, such as water and diluted fruit squash.
  Avoid drinks high in sugar as these can prolong diarrhoea.
  Avoid milk and milky drinks, as a temporary lactose intolerance occurs due to damage done by infecting organisms to the cells lining the intestine, making diarrhoea worse.
  Many people with acute diarrhoea do not feel like eating, but those who do will probably benefi t from eating light, easily digested food.
  Babies should continue to be fed as normal, whether by breast or bottle. Formula feeds should be diluted to quarter-strength, and built back up to normal over 3 days. During this period, babies should be fed more frequently than normal and feeds should be supplemented with ORT. To avoid traveller’s diarrhoea in areas of risk
  Always wash the hands thoroughly with soap and dry in the air or with a clean towel before using them to put anything in the mouth. Carry antiseptic wipes or hand-cleaning gel in case washing facilities are not available.
  Avoid the local drinking water, even for cleaning teeth; drink only bottled mineral water. Avoid ice cubes, dairy products, ice cream and home-distilled drinks.
  Eat only fresh foods that have been directly and suffi ciently heat-treated.
  Avoid unpeeled fruit and vegetables and uncooked meat.
  Do not eat salads that have been washed in the local drinking water.
  Avoid shellfi sh and fi sh unless you are sure they are fresh and have not been living in water near to a sewage outlet.
  Avoid food from street stalls unless you can be sure this is fresh and cooked instantly.
  Try to eat only in establishments that are clean and hygienically run. Try to look inside the kitchen to ensure that there are no fl  ies and no left-over food in pots, and that the staff have no visible sores or boils.
  Generally follow the dictum: cook it, boil it, peel it – or leave it

Constipation, Causes, Epidemiology, Signs, symptoms, Differential diagnosis and Treatment

Constipation
Constipation is the infrequent or diffi cult evacuation of faeces. There is no exact defi nition, but it is a reduction in normal stool frequency accompanied by hardening of stools. Constipation that is not secondary to underlying disease or caused by factors such as side-effects of drugs or laxative abuse is known as simple or functional constipation and may be self-treated with advice from a pharmacist.
Causes
Constipation can be broadly divided into two types:
1.   Simple (functional): constipation with no underlying pathology. There are various causes but it is often due to insuffi cient fl uid or fi  bre in the diet, or reduced mobility. It can usually be corrected with dietary or lifestyle measures or short-term use of laxatives. Several drugs also cause constipation as a side-effect.
2.   Secondary: constipation with an underlying pathological cause. It requires referral for medical investigation.
Epidemiology
  Constipation is common; it is thought to affect a quarter of the population at some time.
  Women are three times more likely to suffer than men.
  The condition is especially prevalent in the elderly, with up to 40% of people over 65 suffering.
Signs and symptoms
Bowel frequency reduced below normal for the individual (‘normal’ can be from twice or three times daily to once or twice weekly).
  Straining in attempt to defecate, with possible abdominal pain and a feeling of incomplete emptying of the bowel.
Stools are harder than normal.
There may be abdominal bloating and discomfort.
  Stools may be specked with bright blood, due to bleeding from haemorrhoids caused by straining.
Children with constipation may be irritable and lose their appetite.
Differential diagnosis
Causes of secondary constipation include:
  bowel obstruction
  carcinoma
  faecal impaction
  irritable-bowel syndrome
  hypothyroidism
  drug side-effects.
(See Symptoms and circumstances for referral below for further details of signs and symptoms of these conditions.)
Symptoms and circumstances for referral
  constipation for more than 7 days with no identifi  able cause
  recurrent constipation
  colicky pain, nausea and vomiting, and abdominal distension (may indicate bowel obstruction)
  constipation accompanied by weight and appetite loss (may indicate carcinoma)
  blood in stools, which appear tarry and red or black (may indicate carcinoma)
  bright blood on stools or in lavatory pan. This usually indicates haemorrhoids, which is often not serious but should be diagnosed by a doctor
  alternating constipation and diarrhoea in elderly patients, which may indicate faecal impaction and overfl ow. In younger patients, alternating constipation and diarrhoea may indicate irritable-bowel syndrome
  constipation with associated weight gain, lethargy, coarse hair or dry skin (may indicate hypothyroidism)
  suspected adverse drug reaction. Constipation is a common side-effect of drugs with antimuscarinic actions, including:
–  older antidepressant drugs, such as amitriptyline and imipramine
–  antiparkinsonian drugs, such as orphenadrine, procyclidine and trihexphenidyl (benzhexol)
–  antipsychotics, such as chlorpromazine and other phenothiazines.
Other drugs that can cause constipation include:
  opioid analgesics (morphine, codeine, dihydrocodeine)
  aluminium-containing antacids
  antihypertensives (such as verapamil)
  iron.
Treatment
Laxatives can be broadly classified into five groups depending on their mode of action:
1.  bulk-forming
2.  stimulant
3.  osmotic
4.  faecal softeners
5.  faecal lubricants.

Bulk-forming laxatives
  Bulk-forming laxatives contain ispaghula husk (the seed coats of a species of plantain), sterculia (a gum from a tropical shrub) or methylcellulose (a semisynthetic hydrophilic colloid).
  These contain polysaccharides or cellulose derivatives that pass through the gastrointestinal tract undigested. They increase faecal volume through three mechanisms:
1.  adding directly to the volume of the intestinal contents
2. softening the faeces
3.  adding to faecal mass by acting as substrates for the growth of colonic bacteria.
  They provide the closest approximation to the natural process of increasing faecal volume and are normally the first-line recommendation for functional constipation.
  They usually act within 24 hours, but 2–3 days of medication may be required for a full effect.
  They are not absorbed so have no systemic effects. They do not interact with other medicines and do not appear to interfere significantly with drug absorption.
Adverse effects and disadvantages are relatively minor. They include:
–  risk of oesophageal and intestinal obstruction if preparations are not taken with suffi  cient water
–  abdominal distension and flatulence
–  some bulk laxatives contain glucose, which needs considering in diabetes
–  they may not be suitable for patients who must restrict their fluid intake severely.
Stimulant laxatives
Stimulant laxatives are thought to act mainly by stimulating the intestinal mucosa to secrete water and electrolytes, through one or both of two mechanisms:
1.  inhibition of the sodium pump (the enzyme sodium/potassium adenosine triphosphatase), preventing sodium transport across the intestinal wall, leading to the accumulation of water and electrolytes in the gut lumen
2.  increased production of fluid in the intestine through action on cyclic adenosine monophosphate and prostaglandins, which promote active secretory processes in the intestinal mucosa.
  Stimulant laxatives may also cause direct damage to mucosal cells, thereby increasing their permeability and allowing fluid to leak out, increasing fl uid volume in the intestine.
  The length of time for individual stimulant laxatives to take effect following oral administration varies according to their site of action, which may be in the small intestine, the large intestine, or both, but they normally work within
4–12 hours of administration. Doses are usually taken at bedtime to produce an effect the next morning. Suppositories produce much faster results, usually within an hour.
The main adverse effects of stimulant laxatives are:
–  griping and intestinal cramps
–  following prolonged use, fluid and electrolyte imbalance and loss of colonic smooth-muscle tone resulting in a vicious circle in which larger and larger doses are needed to produce evacuation, until eventually the bowel ceases to respond at all and constipation becomes permanent. Stimulant laxatives should therefore be used for only short periods of a few days at most, to re-establish bowel habit.
Stimulant laxatives are not contraindicated in pregnancy, but should be avoided in the first trimester. They are generally not recommended, and most are not licensed, for use in children under 5.
  Stimulant laxatives fall into two main groups: diphenylmethane derivatives and anthraquinones.
Diphenylmethane derivatives
  Compounds available are bisacodyl and sodium picosulfate.
Bisacodyl
Bisacodyl acts mainly via stimulation of the mucosal nerve plexus of the large intestine, so takes longer to act (6–10 hours after oral administration) than laxatives acting in the small intestine. It is minimally absorbed and appears to exert no systemic effects. It causes gastric irritation; there are therefore no oral liquid presentations and tablets are enteric-coated.
Sodium picosulfate
Sodium picosulfate becomes active following metabolism by colonic bacteria so it has a relatively slow onset of action, usually within 10–14 hours. It can be used in young children.
Anthraquinones
  Anthraquinones are naturally occurring glycosides used in the form of standardised plant extracts. They are thought to act through a combination of direct stimulation of the intramural nerve plexus and interference with absorption of water across the intestinal wall.
  Dantron and senna are the only anthraquinone laxatives in current use.
  Based on studies in rodents, dantron is believed to be potentially carcinogenic. It is a prescription-only medicine (POM) and is indicated for use only in terminally ill patients. It is available in combination with poloxamer ‘188’ (an organic osmotic laxative) as co-danthramer, and with docusate (see below) in co-danthrusate.
  Senna is widely used.
  Senna is secreted in breast milk and large doses may cause increased gastric motility and diarrhoea in infants, so it should therefore be avoided by nursing mothers.
  Senna is excreted via the kidney and may colour the urine a yellowish-brown to red colour depending on its pH.
Osmotic laxatives
  Osmotic laxatives are either inorganic salts or organic compounds which are poorly absorbed and create a hypertonic state in the intestine. To equalise osmotic pressure, water is drawn from the intestinal wall into the lumen, raising the intraluminal pressure by increasing the volume of the contents, thus stimulating peristalsis and promoting evacuation.
Inorganic salts
Inorganic salts used as osmotic laxatives are:
– magnesium sulphate
– magnesium hydroxide
– sodium sulphate.
  The effects of the inorganic salts are rapid: large doses produce a semifluid or watery evacuation within 3 hours and smaller doses act in 6–8 hours.
  Magnesium salts are also believed to act by stimulating the secretion of the hormone cholecystokinin, which promotes fluid secretion and motility in the intestine.
  Some absorption of inorganic laxative salt ions occurs but in normal, healthy individuals the amounts are too small to be toxic and the ions are rapidly excreted via the kidney.
  Accumulation of magnesium ions can occur in the presence of renal impairment, causing toxic effects in the central nervous system and altered neuromuscular function through hypermagnesaemia. As renal function tends to decline with age, elderly patients should be advised against regular use of
magnesium-containing laxatives.
  Absorption of sodium salts can result in water retention and a rise in blood pressure, and chronic use should be avoided in patients with renal insufficiency, oedema, high blood pressure or congestive heart failure.
  The main side-effects of inorganic osmotic laxatives are nausea and vomiting.
  Large doses of inorganic laxatives can produce dehydration, so enough water should always accompany a dose to avoid a net loss of body water.
Organic osmotic laxatives
Lactulose
  Lactulose is a synthetic disaccharide.
  It is broken down by colonic bacteria, mainly to lactic acid, to produce a local osmotic effect and therefore takes much longer to act than inorganic osmotic laxatives.
72 hours of regular dosing may be required to produce an effect, which may be seen as a disadvantage by patients seeking rapid results.
  Lactulose has a sweet taste, which makes it more palatable for children, to whom it can be safely given, but many adults find the large dose volumes required (up to 30 ml) sickly and a deterrent to compliance.
  Serious adverse effects with lactulose are rare. Relatively minor side-effects, although they may be sufficient to discourage compliance, occur in about 20% of patients taking full doses and include flatulence, cramp and abdominal discomfort, particularly at the start of treatment.
  Lactulose is a disaccharide of galactose and fructose and includes some lactose, so cannot be used by patients with galactose or lactose intolerance and must be used with caution in diabetes.
Macrogols
  Macrogols (polyethylene glycols, PEGs), are condensation polymers of ethylene oxide and water.
  They are presented as powders that are dissolved in water and taken as a single daily dose.
  They appear to act more effectively and rapidly than lactulose, and have been suggested as the laxative of fi rst choice for children.
Glycerol
  Glycerol is a highly hygroscopic trihydric alcohol that appears to attract water of hydration into the intestine. It is also believed to have a direct mild irritant effect and may have some lubricating and softening actions.
  It is inactive by mouth as it is readily absorbed and extensively metabolised in the liver.
  Glycerol is administered in the form of suppositories, which usually act within 15–30 minutes.
  It is a useful laxative for babies and young children.
Faecal softener
Docusate sodium
  Docusate sodium is an anionic surfactant that lowers the surface tension of the intestinal contents, allowing fluid and fat to penetrate, emulsify and soften faecal material for easier elimination. Evacuation is achieved without straining. It is also thought to be a stimulant similar to the anthraquinones. A laxative effect usually occurs within 1–3 days.
  Used alone docusate is a weak laxative, but it is considered useful for patients who must avoid straining, for example, following an operation or myocardial infarction.
  Docusate is non-absorbable and non-toxic but it is believed to facilitate the transport of other drugs across the intestine, and could thereby increase their
action and adverse effects.
Faecal lubricant Liquid paraffi n
  Liquid paraffi n is a purifi ed mixture of liquid hydrocarbons obtained from petroleum.
  It is indigestible and absorbed only to a small extent. It penetrates and softens faeces, coating the surface with an oily film that facilitates its passage through the intestine.
It has limited usefulness as an occasional laxative where straining must be avoided.
It has several drawbacks that make it unsuitable for regular use:
–  It can seep from the anus and cause irritation.
–  It may interfere with the absorption of fat-soluble vitamins.
–  It is slightly absorbed into the intestinal wall where it may set up foreign-body granulomatous reactions.
–  It may enter the lung through aspiration and cause lipoid pneumonia.
  It should not be used in the presence of abdominal pain, nausea or vomiting and should never be used for children.
Additional advice
To help prevent constipation:
–  Eat a diet high in fi bre, including wholegrains, fruits and vegetables.
–  Cut down on food low in fi  bre, such as white bread, cakes and sugar.
–  Drink plenty of fl uids, the equivalent of at least 8–10 glasses of water a day. Hot drinks may stimulate bowel movements.
–  Take regular exercise to improve digestion and bowel function and reduce stress, which can cause constipation.
–  Establish a regular bowel habit. The best time to try for a bowel motion is usually the fi  rst hour after breakfast, when the gastrocolic refl ex is activated. Be patient and sit for at least 10 minutes if necessary, regardless of whether you manage to pass a stool. Don't strain.

Fungal nail infection (onychomycosis)

Fungal nail infection (onychomycosis)

Causes
  Onychomycosis is infection of the nails of the fi ngers or toes caused by dermatophytes (fungi that live on the outer keratinous layer of the skin), yeasts or moulds.
  90% of toenail and 50% of fi ngernail infections are caused by the same Trichophyton and Epidermophyton  species that cause athlete’s foot.
  Predisposing factors include: increasing age, male gender, diabetes, nail trauma, excessive sweating, peripheral vascular disease, poor hygiene, athlete’s foot, immunodefi ciency and chronic exposure of the nails to water.
Epidemiology
  Onychomycosis accounts for one-third of all fungal skin infections.
  Prevalence in adults is estimated at between 3 and 8% and there are more than 1 million sufferers in the UK.
  Infection rates in children are about 30 times lower than in adults, and in patients with diabetes about three times higher. Immunosuppressed and immunocompromised individuals also have a high susceptibility to infection.
  The main form of fungal nail infection is distal and lateral subungual onychomycosis (DLSO). It is 20–30 times more common on toenails than fi ngernails.
Signs and symptoms

  The nail is thickened and has turned yellow or white.
  Changes usually start at the top of the nail but may spread across to the sides and down towards the nail base.
  Debris created as a result of the infection accumulates under the nail.
  There is scaling and distortion of the nail.
  The nail may become brittle and some or all of it may break off.

Differential diagnosis
  Psoriasis of the nails may appear similar to DLSO but it is also usually present at other skin sites. There is usually fi  ne pitting on the nail surface, small salmon-coloured ‘oil drops’, and fi  ngernails on both hands are affected.
 (onychomycosis)
  Lichen planus is an infl ammatory skin condition, the main features of which are itchy, fl at-topped papules, usually on the inner surfaces of the wrists and the lower legs. Nail involvement occurs in about 10% of patients (usually in more serious cases) and fi  ne ridging or grooving can be seen, with severe dystrophy or even complete destruction of the nail bed.
  Contact dermatitis occasionally resembles onychomycosis. Asking the patient about contact with possible irritants and fi nding the presence of contact dermatitis elsewhere on the body should differentiate the condition from DLSO.
  Nail trauma: repeated damage to the nail can cause distal onycholysis (loosening of the nail, starting at the free edge and spreading to the root). This leads to colonisation by microorganisms and pigmentation of the area. If the onycholytic nail is clipped and the nail bed examined, it will appear normal with no subungual debris.
  Yellow-nail syndrome is characterised by yellow nails and is commonly associated with lung disorders. The nails lack a cuticle, grow slowly and are loose or detached. All nails are affected.
Symptoms and circumstances for referral
  Patients:
–  with conditions that predispose to fungal infections (e.g. immunosuppression, diabetes, peripheral circulatory disorders)
–  under 18 years of age
–  with nail conditions other than clearly identifi  ed DLSO
–  with more than two infected nails
–  with nail dystrophy or a destroyed nail
–  showing no improvement after 3 months’ treatment.
  Pregnant or breastfeeding women.
Treatment
  Onychomycosis is one of the most diffi cult fungal infections to treat because of the time it takes for the nail to grow, the hardness of the nail plate and location of the infectious process (between the nail bed and plate).
Prescription treatments
  Oral therapies. Terbinafi ne and itraconazole are considered the systemic treatments of choice.
  Tioconazole 28% cutaneous solution is licensed for topical treatment of onychomycosis, but there is little clinical evidence of its effectiveness.
Non-prescription treatment: amorolfi ne 5% nail lacquer
  Amorolfi ne 5% nail lacquer is licensed for pharmacy sale for the treatment of mild cases of DLSO, affecting up to two nails, in patients aged 18 years or over.

  Amorolfi ne is a morpholine derivative, used topically as an antifungal, with a broad spectrum of activity against dermatophytes, other fungi and yeasts. Its fungicidal action is based on ergosterol depletion and the accumulation of ignosterol in fungal cytoplasmic membrane, which causes the fungal cell wall to thicken and chitin to be deposited.
  The nail lacquer formulation builds a non-water-soluble fi lm on the nail plate that remains at the application site for a week, acting as a depot for the drug.
  The product must be used weekly for up to 9 months, until all the infected nail has grown out and been replaced by healthy nail tissue.
  A clinical trial demonstrated an overall cure in nearly 50% of patients after weekly treatment for 6 months, with overall improvement in a further 25%.
  Adverse effects are rare and minor, amorolfi ne is not systematically absorbed and there are no known interactions with other drugs.
Additional advice
  A cure cannot be achieved overnight. It is important that treatment is continued and directions are followed.
  Wash and thoroughly dry feet every day.
  To prevent the infection spreading to other toes, avoid tight-fi tting or occlusive shoes.
  Rest shoes periodically to limit exposure to infectious fungi.
  Use antifungal powders once a week to help keep shoes free from pathogens.
  Exercise good nail care and be alert for infection recurrence.
  Visit a podiatrist regularly.
  Infection can be passed to others through contamination of shared facilities, so do not go barefoot in the family bathroom or public places.