Altered Bowel Habit

Altered bowel habit is very common and can be acute or chronic.

For further information, also see the articles diarrhoea and constipation

 
















Causes

-          Acute gastroenteritis

-          Simple constipation

-          Irritable bowel or diverticular disease

-          Colonic Malignancy

-          Inflammatory bowel disease

-          Maldigestion / malabsorption

Constipation -

There are various definitions of constipation, but these are not very useful in clinical situations.

What is important is an alteration in bowel habit. Has there been a change? What kind of change? What is the frequency and consistency of the stool?

               

-          Causes

o   Dietary / drug induced

§      Opiates and analgesics are particularly common, but there are loads more!

§      Calcium intake is also very important.

§      Cationic compounds

o   Functional – e.g. IBS

o   Mechanical obstruction – e.g. strictures

o   Metabolic /systemic disease – e.g. thyroid disease – particularly common is under active thyroid in older age.

o   Local anorectal dysmotility – Anismus

o   Neurological disorders

               

-          Prevelance of functional constipation

o   This is a condition where there is no underlying pathological condition

o   It affects 3% of the population

o   Often these people won’t go to GP, they will just go to chemist and get laxatives

-          Disease associated with chronic constipation

o   Often constipation is a consequence of lack of mobility, rather than a direct consequence of the disease itself. This is particularly common in neurological conditions, e.g. parkinsons

o   Systemic diseases such as thyroidism.

o   Ano-rectal dysmotility (aka anismus) – this is common in younger people, particularly women. They will present at the stage where they are already taking lots oflaxatives and controlling their diet (e.g. taking lots offluids and eating lots of fibre). It is caused by an in-co-ordination of muscles actions. When they try to defacate, instead of the rectal angle decreasing and straightening up, instead the angle will increase, and thus making it virtually impossible to defacate.

Taking the History

-          Determine onset, evolution and related symptoms

-          If the patient seems vague, consider a diary of symptoms

-          Does the patient’s definition of constipation match your definition? Ask the patient exactly what they mean, and exactly what their symptoms are.

-          If it is long standing – why have they presented now.

-          Are there any co-factors? Psychological, stress, dietary, environmental.

 Examination

-          Signs of systemic disease? E.g. in hypothyroidism – look at facial features – coarsening official features, weight gain.

-          Any abdominal mass, or faecal loading?

-          Anal disease? Haemorrhoids or fissure? A fissure can be caused by something hard in the faeces – it causes damage to the colonic wall. Often it will just cause acute constipation

-          You should always do a rectal exam!

-          Neuromuscular disease

Investigations

-          Blood tests – TFT’s and calcium

-          Plain abdo X-ray

-          Sigmoidoscopy – this excludes a mechanical cause. You don’t need to do a full colonoscopy.

-          Do a colonic transit study. Get them to eat markers on different days, and then a weekor so later, do an x-ray. You can see how far round the markers have got! Normal transit should be less than 5 days.

Hirschprung’s disease

Common in teenagers / children (neonates). It is caused by neural disease,  and prevents peristalsis of the colon. Sometimes the section of colon is very small, and you can remove it. This disease is often not picked up quickly if the section of bowel affected is small – you might just think they have a bit of constipation.

Management

-          High fibre diet, increase fluid intake, and avoid constipating drugs

-          Identify and treat metabolic or structural diseases.

-          Consider some patients for psychological help.

Laxatives

There are loads of these on the market!!

The most common are the bulk forming. They basically perform the same role as dietary fibre. They attract fluid and form a nice bulk that can be easily passed through the colon.

-          Osmotic laxatives – these are much more aggressive at keeping fluid in the bowel. The active ingredient in many of these is movicol. Often these are dissacharides that have no enzyme in the human to break them down. They are broken down by bacteria into osmotic compounds that help hold fluid in the colon.

-          Stimulants – these should be avoided if at all possible. Senna is a common one. It is an anthraquinones. They can damage young people’s colon, but generally in adults there is no evidence they cause any damage.

-          Softeners – these make the stool more soft and sqooshy making it easier to pass.

Diarrhoea -

-          Again there are various things used to classify this, but again the most important thing is a change in bowel habit.

-          Accounts for 10% of GP visits and 1.5% of adult hospital admission.

-          Worldwide it is the second most common cause of death. Most cases are due to infection. They can be viral / bacterial / amoebic (rare) / protozoa (e.g. giardia lamblia)

-          Chronic diarrhoea – this has existed for over a month. This occurs in 5% of the population. It is common in IBS.

-          Beware particularly old people will say they have ‘bad diarrhoea’ when in actual fact they have faecal incontinence. This is a very disabling condition (socially).

Mechanisms

-          Osmotic – something is causing too much liquid to be held in the gut

-          Secretory – due to abnormal ion transfer across the gut – the small bowel secretes about a litre of fluid across the gut with each day. Normally you absorb about 4L. In cholera, you secret up to 8L a day, but still only absorb 4L

o   Deficiency of lactase – about 10% of the population are lactase deficient. As part of the weaning process, mammals normally lose lactase. If you have no lactase then you can’t break down lactose, and thus it will be broken down by gut bacteria and cause diarrhoea

-          Dysmotility – reduced or increased gut transit time.

In many cases of diarrhoea there is more than one mechanism in action. In some cases it is purely one.

Celiac ulcers and ulcerative colitis often cause diarrhoea.

C. difficile can also cause diarrhoea. It produces a toxin that will damage the membrane of the colon. It causes a condition called pseudomembranous colitis. It is common in hospital with acquired C. difficile.

Immunosupressed patients will be at more risk from diarrhoea. These patients will often be affected by viruses that don’t affect normal people.

Villous adenoma – this is a rare cause of diarrhoea. It secretes large amounts of fluid and thus causes secretory diarrhoea.

Traveller’s diarrhoea

-          Up to 50% of travellers experience this.

-          Symptoms tend to last 3-4 days.

-          Most common causing agent is E. Coli. (40%)

-          Specific pathogen is identified 50-80% of the time.

Dysmotility related diarrhoea

-          Increased intestinal transit time – can be caused by small bowel overgrowth (found in diabetes and scleroderma)

-          Reduced intestinal transit time

Fictitious diarrhoea

It is not that rare. In this condition, these people will take laxatives to cause diarrhoea, and then deny they eve take them. If you have done loads of tests, and can’t find anything wrong, it is worthwhile doing a ‘laxative screen’ – test the patient’s urine and stools for laxatives.

It occurs in 4-15% of patients with chronic diarrhoea. It may account for up to 1/3 of patients referred to GI specialist for diarrhoea.

The psychology is poorly understood. There are two main groups of people who present with it.