Chronic diarrhoea

What counts as chronic diarrhoea

Diarrhoea becomes chronic at four weeks. The working definition used internationally is stools that are persistently loose, types 5 to 7 on the Bristol stool chart, passed more than three times a day, going on for at least four weeks. Below that threshold most episodes are infections that clear on their own.

The four-week mark matters because it changes what is likely. An illness that has lasted a month is rarely still the gastro that started it, even when that is how it began.

What needs looking at sooner

Most chronic diarrhoea is not dangerous. A short list of features changes that, because they raise the chance of an underlying structural or inflammatory cause and they shorten the sensible waiting time:

• Blood in the stool, or black tarry stools.
• Diarrhoea that wakes you at night. Functional causes generally leave people alone once they are asleep. Diarrhoea that does not is worth taking seriously.
• Weight loss that was not intended, fever or drenching night sweats.
• Pain that is getting worse rather than fluctuating.
• Symptoms that started after the age of 50, particularly when there was no previous bowel trouble.
• Iron deficiency, or a raised inflammatory marker on a blood test.
• A family history of bowel cancer, coeliac disease or inflammatory bowel disease.

None of these means something serious is present. Each one shifts the balance towards investigating properly rather than treating and waiting, and together they are the main reason a referral is made early rather than late.

Bleeding in particular has its own page, because the causes and the urgency differ from diarrhoea alone. There is more on it under rectal bleeding.

What causes it

In Australia and comparable countries the common causes cluster into a handful of groups.

The common ones

• Irritable bowel syndrome with diarrhoea as the dominant symptom. The commonest single explanation, and a positive diagnosis rather than a leftover once everything else is excluded. Covered on the irritable bowel syndrome page.
• Inflammatory bowel disease, meaning Crohn's disease and ulcerative colitis. Usually, though not always, with blood, weight loss or raised inflammatory markers. Covered under inflammatory bowel disease.
• Coeliac disease, which is far more variable than the textbook description and sometimes presents with almost nothing except loose stools and tiredness. See coeliac disease.
• Lactose intolerance and other carbohydrate intolerances, where the pattern follows what is eaten.
• Medicines, which are behind more chronic diarrhoea than most people expect, and which are easy to overlook precisely because they were started for something else.

The ones that get missed

• Microscopic colitis, which is invisible at colonoscopy and diagnosed only on biopsies. Summarised below and covered in full on its own page.
• Bile acid diarrhoea, including the diarrhoea that starts after gallbladder surgery. Also below.
• Persistent infection, particularly Giardia, which can settle in for months and which ordinary stool culture does not reliably find.
• Small intestinal bacterial overgrowth, where too many bacteria colonise the small bowel. Genuine, but harder to prove than the amount written about it suggests, and covered in its own section below.
• Diarrhoea after an infection, where the original bug has gone but the bowel has not returned to normal. This is common enough to have a name, post-infectious irritable bowel syndrome, and it is covered on the irritable bowel syndrome page.
• An overactive thyroid, which is a blood test away and is worth excluding early because it is easy to treat.

Less common causes, including pancreatic and hormone-secreting conditions, exist and are looked for when the picture calls for it rather than in everyone.

The first round of tests

The initial set is small, cheap and mostly done through the GP. The purpose is not to find everything at once. It is to separate the people who need a colonoscopy from the people who do not.

• Blood tests. A full blood count, thyroid function, iron studies and coeliac serology. Coeliac testing is the one with the strongest evidence behind it in this setting and it is the one most often left out.
• A stool test for Giardia. The evidence for testing for this specifically is stronger than for any other stool test in chronic diarrhoea. It is a notifiable infection in New South Wales and it is diagnosed here regularly, with the highest rates in young children. Broad testing for other parasites, by contrast, is not recommended unless something in the history points to it.
• Faecal calprotectin, in the right person. This measures inflammation in the bowel and is the single most useful test for separating inflammatory bowel disease from irritable bowel syndrome.

Two tests that are often ordered are worth less than their reputation. C-reactive protein performs poorly at telling irritable bowel syndrome from inflammatory bowel disease and is a fallback rather than a first choice. Testing stool for white cells is an older test that is no longer used for this purpose: it misses too many people who do have inflammation, and it has never been properly validated in long-standing diarrhoea. Faecal calprotectin is what is used instead.

What Medicare covers

Faecal calprotectin attracts a Medicare rebate in specific circumstances. The diagnostic items apply to a patient not older than 50, with symptoms suggestive of inflammatory or functional bowel disease for more than six weeks, where infection has been excluded, the likelihood of cancer is low and there are no alarm features. A separate item was added on 1 November 2025 for monitoring someone who already has a diagnosis of inflammatory bowel disease, requested by or on behalf of a specialist, with a schedule fee of $75.

Outside those situations the test can still be done and is paid for privately. The rules change, so it is worth asking the requesting doctor rather than assuming.

Why a normal calprotectin does not end the conversation

This is the part that matters most, and it is the reason this page exists.

A normal faecal calprotectin is genuinely reassuring about inflammatory bowel disease. It is not reassuring about everything. The two conditions covered in the next two sections, microscopic colitis and bile acid diarrhoea, both typically produce a normal calprotectin, a normal blood count and a colon that looks entirely normal through the camera.

There is a second gap worth naming. The Medicare criteria for the diagnostic calprotectin items stop at age 50. Microscopic colitis is diagnosed at a median age above 60. So the rebated test that sorts out most chronic diarrhoea does not apply to the age group most likely to have the diagnosis that the test would not detect anyway.

Microscopic colitis

Microscopic colitis is inflammation of the lining of the colon that cannot be seen. The bowel looks normal at colonoscopy, and the diagnosis exists only in the biopsies, under the microscope, which is where the name comes from.

It is not rare. Pooled across studies, it is found in 12.8 per cent of people having a colonoscopy for unexplained watery diarrhoea, so roughly one in eight. It is typically diagnosed after 60 and affects women about two and a half times as often as men. The symptoms are watery diarrhoea without blood, six to seven times a day on average, with urgency in about half and a need to open the bowels overnight in about a third.

Three things keep it hidden. The colon looks normal, so an endoscopist not thinking of it has no prompt to biopsy. Faecal calprotectin is not a reliable marker for it, so the test that reassures about inflammatory bowel disease does not cover this. And the symptoms overlap almost completely with irritable bowel syndrome. The guidelines are explicit that biopsies should be taken from at least the right and the left side of the colon, which is why a full colonoscopy is preferred to a shorter examination of the left colon alone when microscopic colitis is a possibility.

Treatment, when it is needed, is usually a steroid that works locally in the bowel and is largely broken down before it reaches the rest of the body, which is why it is tolerated better than conventional steroid tablets. Most people respond. It does not raise the risk of bowel cancer.

Bile acid diarrhoea

Bile acids are made by the liver to help digest fat. Almost all of them are reabsorbed at the end of the small bowel and recycled. When more than usual reach the colon, they draw water and salt into it, and the result is watery diarrhoea.

It is common and under-recognised. Among people carrying a diagnosis of irritable bowel syndrome with diarrhoea, pooled testing puts the prevalence at around 28 per cent, and guideline estimates for chronic diarrhoea generally sit between a quarter and a third.

The patterns that suggest it

• Diarrhoea that started after the gallbladder was removed and never settled. Without a gallbladder, bile drains continuously into the bowel rather than in a meal-sized release. Reported rates after gallbladder surgery vary enormously between studies, and in many people it improves over weeks to months on its own.
• Diarrhoea after surgery or disease affecting the end of the small bowel, which is why it is common in Crohn's disease affecting that segment, and after radiotherapy to the abdomen.
• Urgency, often in the morning or after meals, and diarrhoea that eases when not eating, because less bile is being released.
• No identified cause at all. This is the largest group and the one usually labelled irritable bowel syndrome.

How it is sorted out here

The nuclear medicine retention test used for this in the United Kingdom is not readily available in Australia, and there is no simple blood or stool test that replaces it in routine practice. Guidelines written for countries in the same position accept that a carefully monitored trial of treatment may be the only practical route to the diagnosis, and that is how it is usually approached here.

The treatment is a medicine that binds bile acids in the bowel so they cannot irritate it. When the diagnosis is right the response is usually quick and obvious, which is what makes the trial informative. It needs to be taken away from other medicines, because it binds those too, and that detail is the commonest reason a trial appears to fail.

Small intestinal bacterial overgrowth

The small bowel normally carries far fewer bacteria than the colon. When the population there grows too large, the bacteria ferment food before it can be absorbed properly, and the result is bloating, wind, discomfort and often diarrhoea. Bloating is the commonest symptom rather than diarrhoea, and where the overgrowth produces methane the bowel tends to slow down, so some people present with constipation instead.

This is a real condition. It is also the one on this page where the gap between what is written about it online and what can actually be proven is widest, and it is worth being straight about that.

Why it happens

Overgrowth is usually secondary to something that has changed the small bowel rather than a problem in its own right. The recognised causes are worth knowing because they are what makes the diagnosis plausible in a given person:

• Slowed movement of the small bowel, from long-standing diabetes affecting the nerves, from scleroderma or from strong pain medicines
• Altered anatomy, including previous bowel surgery, adhesions, strictures and small bowel diverticulosis, all of which create places where contents sit still
• Reduced stomach acid, from long-term acid-suppressing medicine or from autoimmune gastritis. Acid is part of what keeps the upper bowel relatively sterile
• Conditions affecting immunity or digestion, including immunoglobulin deficiency and pancreatic insufficiency

The problem with the test

Breath testing is how the diagnosis is usually made. The person swallows a sugar and the hydrogen and methane in their breath is measured over two hours, on the principle that human cells do not produce those gases, so their appearance means bacteria are fermenting the sugar earlier than they should.

Measured against small bowel aspirate culture, which is the reference standard, the breath test does not perform well. Pooled across studies, the glucose breath test has a sensitivity of 54.5 per cent and a specificity of 83.2 per cent. The lactulose version is worse, at 42.0 per cent and 70.6 per cent.

In plain terms: roughly half the people who have the condition will test negative, and a meaningful minority of people who do not have it will test positive. The reference standard it is being compared against is itself invasive and gives inconsistent results, so the true picture is not even as firm as those numbers imply.

If you have been booked for a breath test

The preparation changes the result more than most people are told, and a test done without it is close to uninterpretable. Antibiotics should be avoided for four weeks beforehand, and laxatives and medicines that speed the bowel up for one week. Complex carbohydrates and dairy are avoided for twelve hours, followed by a fast of eight to twelve hours. Smoking and strenuous exercise on the morning of the test both alter the readings and should be avoided.

What treatment achieves, and what it does not

Treatment is a course of antibiotics, usually around ten to fourteen days, chosen to act mainly within the bowel rather than throughout the body. It works reasonably often. Pooled across trials, antibiotics normalised the breath test in about half of people compared with one in ten on placebo, which is a real effect and a modest one.

Two things are worth knowing before starting, because they are the source of most of the disappointment around this diagnosis.

• A single course does not settle it for everyone. The breath test returns to normal in about half of those treated, and even among the people whose test does clear, a proportion still have symptoms. That does not necessarily mean the treatment failed. It often means overgrowth was not the whole explanation, which is why persistent symptoms after two courses is a reason to look again at the diagnosis rather than to keep repeating it.
• It comes back. In a study following 80 people after successful treatment, the overgrowth had returned in 13 per cent by three months, 28 per cent by six months and 44 per cent by nine months. Recurrence was more likely in older people, in those who had had their appendix removed and in those on long-term acid-suppressing medicine.

That recurrence rate is the argument for the part of treatment that gets least attention. Antibiotics clear the bacteria; they do nothing about the reason the bacteria were able to accumulate. Where there is a treatable underlying cause, or a medicine slowing the bowel or suppressing acid that could reasonably be reviewed, that is what determines whether the problem stays away.

On the things people commonly try alongside, probiotics are a mixed picture rather than a flat no. Pooling 18 studies, they did not prevent overgrowth developing and did not reduce how often people opened their bowels. They did clear the overgrowth more often than no probiotic, lower the hydrogen on breath testing and reduce abdominal pain scores, although the pain result only just reached significance. So they are not a substitute for treatment, and they are not useless either. The low FODMAP diet helps bloating in irritable bowel syndrome, but the evidence for it in bacterial overgrowth specifically is lacking.

What the colonoscopy adds

Not everyone with chronic diarrhoea needs a colonoscopy. It becomes the right test when there are alarm features, when the first round of tests has not produced an answer, when inflammatory bowel disease is suspected, when there is iron deficiency, or when microscopic colitis is on the list, which in practice means most people over 50 with persistent watery diarrhoea.

Two things happen during it that a shorter examination does not provide. The end of the small bowel can be entered and inspected, which is where Crohn's disease most often sits. And biopsies can be taken from the right and left colon, which is what makes microscopic colitis findable.

What the procedure itself involves, including the preparation and the sedation, is set out on the colonoscopy page. Where a gastroscopy is added, usually to take small bowel biopsies when coeliac disease is suspected, that is covered under gastroscopy.

Medicines, diet and the things worth checking first

Before anything invasive, two lists are worth going through carefully, because between them they explain a fair proportion of chronic diarrhoea and neither requires a test.

Medicines and supplements

A great many medicines loosen the bowels, and the connection is easy to miss when the medicine was started months earlier for an unrelated reason. Magnesium-containing supplements and antacids, some diabetes medicines, some blood pressure medicines, antibiotics taken recently and long-term anti-inflammatory painkillers are all worth noting. So is anything bought without a prescription, which people often do not think to mention. Nothing should be stopped without asking the doctor who prescribed it.

Diet

Three dietary causes account for most of the rest:

• Lactose, where symptoms follow dairy and settle when it is avoided. GESA has a patient fact sheet on it.
• Sugar alcohols, particularly sorbitol and related sweeteners in sugar-free gum, mints, lollies and some medicines. These are a genuinely common cause and an easy one to test by stopping them.
• Fermentable carbohydrates more broadly, which is the basis of the low FODMAP diet. It is effective for the right person and it is restrictive, so it is best done with a dietitian and for a defined period rather than indefinitely.

Caffeine and alcohol both speed the bowel up and are worth a fortnight's honest trial before concluding they are irrelevant.

When the answer is irritable bowel syndrome

For a large proportion of people, the tests come back normal and the diagnosis is irritable bowel syndrome with diarrhoea. That is a real diagnosis made on a recognisable pattern, not a verdict of nothing being wrong, and there is a good deal that helps.

The important qualification is that the label should be revisited if things change. Symptoms that begin later in life, that wake someone at night, that come with weight loss, or that have not responded to reasonable treatment all deserve another look rather than a repeat of the same reassurance. Microscopic colitis and bile acid diarrhoea are both frequently found in people who have carried an irritable bowel syndrome label for years.

The irritable bowel syndrome page covers diagnosis, diet and the treatments used once the diagnosis is settled.

Managing symptoms while the cause is being worked out

Treating the cause is the aim, but there is usually a gap between the first appointment and the answer, and it is reasonable to be more comfortable during it.

• Fluid and salt. Persistent diarrhoea loses both. Water alone does not replace what is lost; oral rehydration preparations from a pharmacy do.
• An anti-diarrhoeal. Loperamide, commonly known as Imodium, slows the bowel and is available without prescription. It is reasonable for symptom control, taken before the times of day that cause the most trouble rather than only after an episode. It should not be used where there is fever or blood, and it is worth telling the specialist that it is being taken, because it changes what the symptom pattern looks like.
• Keep a short diary. A fortnight of what was eaten, how many stools, whether any were at night, and any blood, is more useful at the appointment than a general description, and it frequently identifies a dietary trigger on its own.

Anti-diarrhoeals mask rather than treat, so a good response is a reason to keep looking for the cause, not a reason to stop.

Getting the most out of the appointment

A gastroenterology appointment for chronic diarrhoea is largely a history-taking exercise, and the history is where the diagnosis usually comes from. Bringing the following makes a substantial difference:

• Every blood and stool result already done, including the ones reported as normal. Normal results narrow the field and stop tests being repeated
• A complete medicine list, including supplements, herbal preparations and anything bought over the counter
• Any previous endoscopy or colonoscopy reports, and the pathology that went with them if it is available
• When it started, and what was happening then. Travel, an episode of gastro, a course of antibiotics, an operation or a new medicine in the weeks beforehand are all informative
• Whether it wakes you at night, which is one of the more useful single questions in this whole assessment

A specific diagnosis is reached in the large majority of people with chronic diarrhoea. The path to it is usually a short sequence of ordinary tests rather than anything exotic, and the main reason it takes longer than it should is that the two conditions described above are not considered early.

Appointments need a referral from a GP or another specialist. There is more on that, and on what the costs look like, under fees and rebates.

Where chronic diarrhoea is assessed in Sydney

A/Prof Viraj Kariyawasam is a consultant gastroenterologist and hepatologist whose practice is focused on inflammatory bowel disease. Diarrhoea lasting more than four weeks is assessed at consultation in Norwest, Rouse Hill, Pennant Hills and Macquarie Park.

The colonoscopy with biopsies is performed at Norwest Private Hospital, Macquarie University Hospital and Pennant Hills Day Surgery. A referral from your GP is needed for a consultation.