doi:10.1111/jpc.

14986

REVIEW ARTICLE

Chronic diarrhoea in children: A practical algorithm-based

approach
Sahana Shankar1,2 and Jeremy Rosenbaum 2

1
Consultant Pediatric Gastroenterologist, Department of Pediatrics, Mazumdar Shaw Medical Centre, Narayana Health, Bangalore, India and 2Department
of Gastroenterology and Clinical Nutrition, Royal Children’s Hospital, Melbourne, Victoria, Australia

Diarrhoea is a leading cause of morbidity and mortality world-wide. Most diarrhoeal episodes are acute and infectious in origin. Diarrhoea lasting
for longer than 4 weeks with no discernible infectious aetiology warrants thorough evaluation. The aim of this review is to elucidate an approach
to evaluation of diarrhoea based on its pathophysiologic mechanisms with focus on aetiology, investigation and management of chronic diar-
rhoea. It includes a brief description of normal fluid homeostasis in the gut and pathophysiology of diarrhoea. Further, diarrhoea is classified as
‘watery’, ‘fatty’ and ‘bloody’ based on stool characteristics. Relevant history, physical examination findings, first and second-line investigations
which help in differentiating the different types of diarrhoea are listed and an algorithmic approach to individual types of diarrhoea has been
devised. Principles of management and recent advances in diagnostics and therapeutics of diarrhoea are briefly discussed.

Key words: adolescent; algorithm; children; diarrhoea; practical.

Diarrhoea remains an important cause of morbidity and mor-
tality world-wide. Around half a million children succumbed to
diarrhoeal diseases in 2016, making diarrhoea the fifth leading
cause of under-five mortality, with most deaths occurring in Sub-
Saharan Africa and South Asia.1,2 It is projected that if current
trends continue, around 4.4 million children will die before their
fifth birthday in 2030.1 Around 9% of those deaths would be
attributable to diarrhoea.1
Key Points
1 History, physical examination and basic stool investigations
help characterise the type of diarrhoea as watery, osmotic or
secretory, fatty or bloody. Characterising the type of diarrhoea
defines approach to investigation and management.
2 Infections are the commonest cause for diarrhoea in all age
groups. Coeliac disease can manifest at any age once exposed
to gluten and needs to be ruled out conclusively.
3 Chronic diarrhoea in the absence of red flags on history, exam-
ination and investigations is likely due to functional diarrhoea
or irritable bowel syndrome and does not warrant further inva-
sive testing.
Correspondence: Dr Jeremy Rosenbaum, Department of Gastroenterol-
ogy and Clinical Nutrition, Royal Children’s Hospital, 50, Flemington road,
Parkville, Vic. 3052, Australia. Fax: +61 39345 6240; email: jeremy.
rosenbaum@rch.org.au
Conflict of interest: None declared.
Accepted for publication 10 May 2020.
Although diarrhoea in high-income countries such as Australia
rarely leads to death, it remains a leading cause of
hospitalisation.3,4 The introduction of rotavirus vaccine was a
sentinel event, contributing to a 7% reduction in diarrhoea-
related mortality and hospitalisation rates in high-income coun-
tries.2,5 Notably, Clostridium difficile is emerging as a new threat,
responsible for most diarrhoeal deaths under 5 years of age in
high-income regions of the world.2 It is suggested that diarrhoea
by impairing growth can indirectly contribute to 40% of DALYs
(disability-adjusted life years) globally.6
In contrast to acute diarrhoea which is often infectious in ori-
gin, there is little epidemiological data regarding chronic diar-
rhoea, which can be equally distressing as symptoms are
remittent and aetiologies, often diverse and elusive. In this
review, we provide an overview of basic pathophysiologic mech-
anisms of diarrhoea, clinical approach and management strate-
gies, with specific focus on chronic diarrhoea.
Definition and Classification of Diarrhoea
Defining diarrhoea in children is challenging. Not only does stool
frequency vary with age and diet, it also varies considerably from
person to person within the same age group. A normal breastfed
infant can pass up to 12 stools in a day to one stool in a week.7
An older child rarely passes more than three stools per day.8
Stool weight increases with age; however, stool water content
remains constant.7 Diarrhoea is defined by an increase in the vol-
ume and water content of stools. An operative definition of diar-
rhoea as proposed by World Health Organization refers to
passage of three or more loose or liquid stools per day or more
frequently than is normal for the individual.9 Frequent passing of
formed stools is not diarrhoea, nor is the passing of loose, ‘pasty’
stools by breastfed babies.10,11 In an infant, change in frequency

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Chronic diarrhoea in children
and consistency of bowel actions from every infant’s ‘normal’ is
more indicative of diarrhoea.
The duration of diarrhoea offers a clue to the underlying
aetiology. Acute diarrhoea usually lasts <7 days, occasionally up
to but not longer than 14 days and is often infectious in origin.
Some authors refer to a diarrhoeal episode lasting >7 days but
<14 days as prolonged diarrhoea.12 An episode of acute
diarrhoeal illness lasting for longer than 14 days is qualified as
persistent diarrhoea.11 Persistent diarrhoea is a consequence of
multiple simultaneous or sequential enteric infections which lead
to mucosal injury resulting in a vicious cycle of further diarrhoea,
malnutrition and infections. The terms ‘prolonged’ and ‘persistent’
diarrhoea are epidemiologically relevant in low- to middle-income
countries as it identifies those children likely to experience sub-
stantial diarrhoea-related morbidity and mortality.11,13
Chronic diarrhoea, on the other hand, is a term used to define
diarrhoea without a demonstrable infectious aetiology, lasting for
more than 4 weeks, often associated with malabsorption and
growth faltering.14,15 The cut-off of 4 weeks is arbitrary, however
it endeavours to exclude diarrhoea of infectious aetiology, as
most enteric infections would abate within 1 month.
Pathophysiology of Diarrhoea
In a healthy adult, the gastrointestinal tract handles 8–10 L of
fluid every day, which is an aggregate of salivary, gastric, pancre-
atic and biliary secretions and net secretion by small intestinal
mucosa.16 The small bowel mucosa lined by brush-border colum-
nar epithelial cells is folded into finger-like villi thus enhancing
the surface area available for absorption.17 The cells lining the
villi are mostly absorptive cells; crypt cells are regarded as secre-
tory. Around 99% of fluid entering the midgut is reabsorbed by
the small intestine and only 1.2 L of fluid enters the colon.
Colonic reabsorption recovers another litre of fluid, resulting in
stool volume that rarely exceeds 200 mL/day in healthy
adults.17,18 It is important to note that the colon has a vast
reserve capacity to absorb fluid (~5–15 times the capacity of small
bowel per unit area), thus colonic re-absorptive capacity has to
be exceeded for diarrhoea to manifest.17
It is important to understand the factors that regulate fluid
transport in the gut to fully comprehend the pathogenesis of
diarrhoea.17,19,20
1 Firstly, the most prominent mechanism for reclamation of fluid is
through active transport of ions such as Na+, Cl− and HCO3− across
the enterocyte. These ions are actively transported against an elec-
trochemical gradient via Adenosine triphosphate dependant mem-
brane transporters. Broadly, the movement of Na+ from the
mucosa to the serosa drives fluid absorption, whereas net Cl− ion
movement in the reverse direction drives fluid secretion.
2 Secondly, an intact epithelial barrier function is essential to
prevent the back diffusion of electrolytes and thus water into
the intestinal lumen. The tight junctions which link adjacent
epithelial cells are made up of several proteins such as claudin,
occluding and tricellulin. They are responsible for restricting
passive flow of solutes after secretion or absorption. Reduced
effectiveness of the epithelial barrier alone may be insufficient
to cause significant diarrhoea. However, when coupled with
defective ion transport and fluid accumulation in the lumen, a
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S Shankar and J Rosenbaum
paracellular leak of absorbed solutes back into the lumen com-
promises the efficiency of fluid absorption.
3 Thirdly, net fluid movement depends on normal motility of gut
to allow optimal contact time between absorbable solutes and
a normal epithelium. Rapid transit (toddler’s diarrhoea, irrita-
ble bowel syndrome (IBS) etc) by preventing reabsorption of
normally secreted fluid in the small bowel and slow transit
(chronic intestinal pseudo-obstruction, post-surgery etc.) by
resulting in bacterial overgrowth and bile acid deconjugation
can both cause diarrhoea.
In summary, membrane transport proteins drive transcellular
transport of ions, which sets up an electrochemical gradient to
allow paracellular transport of fluid through tight junctions.
All of the above processes are closely regulated by autocrine,
luminal, paracrine, immunologic, neural and endocrine systems.
A disruption in any or all of the above can result in decreased
absorption of fluid and/or increased secretion of fluid into the
intestinal lumen resulting in diarrhoea.
History
Age of onset and duration
Infection is the most common cause across all age groups. How-
ever, diarrhoea from birth or immediate post-natal period should
prompt evaluation for congenital enteropathies, necrotising
enterocolitis (NEC) or anatomical abnormalities. Presence of con-
sanguinity, polyhydramnios and decreased fetal movements
points to congenital enteropathies. Allergic aetiologies such as
cows milk protein allergy or food protein induced enterocolitis
are important differentials in infantile diarrhoea. Coeliac disease
can manifest at any age, but is uncommon in the first
4–6 months of life as adequate gluten exposure is a prerequisite.
Duration of diarrhoea, as discussed earlier, helps define
aetiology. Abrupt onset of diarrhoea lasting for <4 weeks is more
likely to be infectious in origin. Chronic infectious diarrhoea
although uncommon in immunocompetent children, can be sec-
ondary to parasites such as giardia and entamoeba. On the other
hand, in immunocompromised children, bacteria (Yersinia,
Aeromonas, C. difficile, Mycobacterium, Salmonella, Campylobac-
ter), parasites (Crytosporidia, Giardia, Cyclospora, Microsporidia,
Strongyloides), viruses (Norovirus, Rotavirus, CMV) and fungi
(Candida) can all lead to chronic diarrhoea.21 Additionally, his-
tory of recent travel to endemic countries is important to note in
cases of suspected infectious diarrhoea. In the first instance, infec-
tions and coeliac disease should be considered in every child with
chronic diarrhoea (Fig. 1).
Stool characteristics
Eliciting a detailed description of stool and visualising the stool if
able, is vital. Classifying the stools as watery, fatty or bloody
based on history and basic stool tests helps in defining an
approach to evaluating a child with diarrhoea (Figure 1,
Table 1).16,22 Accompanying symptoms such as flatulence,
bloating, relationship of defecation to meals (osmotic) and
fasting; fever, urgency, tenesmus and nocturnal awakening
(inflammatory) offer important clues to underlying aetiology.
Growth failure is a red flag and signifies severity and chronicity.
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S Shankar and J Rosenbaum
Fig 1 Approach to a child with chronic diarrhoea. CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; FBE, full blood examination; FCP, faecal
calprotectin; LFT, liver function test; PCR, polymerase chain reaction; RC, red cells; RFT, renal function test; WC, white cells.
Diet
A detailed dietary history with emphasis on consumption of
fruits, fruit juices and soft drinks which contain high concentra-
tions of fructose or sorbitol and mannitol in an older child is use-
ful. In an infant, a comprehensive feeding history and temporal
correlation of diarrhoea with different aspects of feeding should
be reviewed – breastfed or formula fed, type of formula (cows
milk vs. others), time of introduction of solids and type of solids.
Drugs
Drugs such as magnesium, mycophenolate mofetil and laxative
abuse can result in diarrhoea.
Past history
Past medical and surgical history including exposure to radiation
and bowel resection has to be obtained. An algorithmic approach
to chronic diarrhoea is shown in Figure 1.
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Chronic diarrhoea in children
I Watery diarrhoea implies an osmotic or secretory pro-
cess. 17,22 Although this classification has never been clini-
cally validated and few clinical situations produce pure
secretory or osmotic diarrhoea, it is the most relevant clas-
sification to a clinician as delineating the predominant pro-
cess helps in identifying aetiology and defines diagnostic
approach (Fig. 2).
A Osmotic diarrhoea – Osmotic diarrhoea results from unabsorbed
solutes or nutrients which draw water into the intestinal lumen.
The essential characteristic of osmotic diarrhoea is that it
resolves with fasting or cessation of ingestion of the offending
substance. Osmotic diarrhoea is characterised by explosive,
frothy stools associated with bloating, flatulence and abdominal
distension. Infants can have perianal rash due to the acidic
nature of stool, due to formation of short chain fatty acids from
fermentation of unabsorbed sugar by colonic bacteria.
Usually, stool is iso-osmolar to serum (290mosm) and is
accounted for by major electrolytes (Na+ and K+) in stool.
Osmotic diarrhoea is characterised by an unaccounted gap
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Table 1 List of investigation

Test Remarks/Interpretation

Stool microscopy and culture
Stool Clostridium difficile
toxin26,51
Stool electrolytes
Stool reducing substances
and pH
Stool pancreatic elastase
Faecal calprotectin (FCP)52,53
Stool alpha1-antitrypsin
(α1-AT)54,55
72-h stool fat quantification56
Full blood count
Renal function test
Inflammatory markers
Liver function test
Coeliac serology with IgA
detection57,58
• Presence of white cells and red cells suggests inflammatory diarrhoea
• Presence of fat globules and fatty acid crystals suggests impairment in fat digestion and absorption, respectively
• Presence of ova, cysts or parasites or growth in culture is diagnostic of infectious cause. An extended infectious
screen is necessary in immunocompromised patients
Testing not recommended in children <1 year of age due to high rates of colonisation. Risk factors for CDI include
recurrent antibiotic exposure, hospitalisation, prolonged PPI use and presence of feeding tubes
Important test to differentiate osmotic and secretory diarrhoea
Stool osmotic gap calculation = 290–2 X (Stool Na+ + K+)
Stool osmotic gap >100 mOsm suggestive of osmotic diarrhoea; <50 mOsm suggestive of secretory diarrhoea; 50
and 100 mOsm intermediate
Positive reducing substances and low pH (<5.3) indicates carbohydrate malabsorption (see osmotic diarrhoea)
Pancreatic elastase is resistant to degradation by intestinal proteases. It is low in pancreatic insufficiency, however
can be falsely low due to dilution in high volume diarrhoea
Normal >200 mg/g stool
Calprotectin is a neutrophil-derived cytosolic protein. It gives a non-invasive quantitative measure of neutrophil flux to
the intestine and thus gut inflammation. Laboratory normal value <50 μg/g. This cut-off has high sensitivity but poor
specificity in the diagnosis of IBD. FCP can be elevated in GI infections, juvenile polyps, NSAID use and
gastrointestinal bleeding.
It is important to note that although a cut-off of <50 μg/g is considered normal, calprotectin values have a significant
negative correlation with age with very high FCP levels upto 1500 μg/g observed in healthy infants and wide
variability noted until 4 years of age, thus limiting its use in children younger than 4 years of age
α1-AT is a protein which is neither absorbed nor secreted by the intestine and is normally present in low
concentrations in stool. Protein-losing enteropathy (PLE) can be confirmed by quantifying α1-AT in stool and by
measuring its clearance from plasma. This involves a 72-h stool collection paired with a serum sample to measure
serum α1-AT level. α1-AT clearance is increased in PLE. Normal value <0.9 mg/g stool
Gold standard test to establish steatorrhoea. Normal newborns and infants excrete 15–20% of dietary fat in stool.
Coefficient of fat absorption increases with age and reaches adult values of >95% at over 1 year of age.
Lymphopenia points to possible PLE
Eosinophilia – Cows milk protein allergy, food allergy, eosinophilic gastroenteritis
Thrombocytosis – IBD, iron deficiency anaemia
Anaemia – Iron deficiency, coeliac disease, IBD
Abnormal electrolytes seen in congenital sodium and chloride diarrhoeas. Denotes severity of diarrhoea.
Raised CRP and ESR in inflammatory or infectious diarrhoea
Low albumin secondary to inflammatory diarrhoea and protein losing enteropathy
Raised transaminases – Extra intestinal feature of IBD
Obstructive LFTs – Fatty diarrhoea can be a consequence of cholestasis
Test should be performed on an adequate gluten containing diet. A positive IgA tissue transglutaminase and
endomysial antibody are the most accurate serological tests. Note that in selective IgA deficiency, these tests may
be falsely negative and hence, it is important to measure IgA levels along with coeliac antibodies. An isolated
positive IgG deamidated peptide in an IgA sufficient child is rarely associated with coeliac disease

CDI, Clostridum difficile infection; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; GI, gastrointestinal; IBD, inflammatory bowel disease;
LFT, liver function test; NSAID, Non-steroidal anti inflammatory drug; PLE, protein losing enteropathy; PPI, Proton pump inhibitor.

between the stool electrolytes and the measured stool osmolality
known as osmotic gap (Table 1).23 This gap is caused by poorly
absorbed molecules in the gut lumen which can be as a result of-
1 Reduced nutrient transport
a) Due to mucosal disease resulting in loss of absorptive area –
acute gastroenteritis, post infectious enteropathy, intestinal
resection, short gut etc.
b) Relative or absolute deficiency of specific sugar-splitting
enzymes or transport proteins (Fig. 3) – Acquired or second-
ary deficiency is more common than primary deficiency. The
disaccharidases are expressed on the brush border of the vil-
lous epithelial cells and are lost in an enteropathy of any
cause. Examples of primary or congenital deficiency include
sucrase-isomaltase deficiency, glucose-galactose transport
defect or rarely primary lactase deficiency, all of which result
in early onset osmotic diarrhoea.24
2 Ingestion of poorly absorbed osmotically active substances such
as sorbitol rich fruits (apple, pear, etc), laxatives and drugs
containing magnesium and phosphate can result in osmotic
diarrhoea.

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S Shankar and J Rosenbaum Chronic diarrhoea in children

Fig 2 Approach to watery diarrhoea. SBS, short bowel syndrome; RS, reducing substances; AT, antitrypsin; PLE, protein losing enteropathy; SIBO, small
intestinal bacterial overgrowth; MVID, microvillous inclusion disease; VIP, vasoactive intestinal peptide.

Fig 3 Schematic diagram representing

mechanisms involved in carbohydrate mal-
absorption.24 (a) Lactase deficiency.
(b) Glucose-galactose malabsorption due
to genetic defect in SGLT1. (c) Fructose
malabsorption due to dose-dependent
overload of transporters. (d) Sucrose mal-
absorption due to genetic defect in
sucrose-isomaltase activity.

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Chronic diarrhoea in children
B Secretory diarrhoea – Secretory diarrhoea results from disor-
dered electrolyte transport. It is due to net secretion of anions
(chloride or bicarbonate) or potassium or net inhibition of
sodium absorption.25 The mechanisms of secretory diarrhoea
are the following22:
1 Exogenous secretagogues – Infections such as cholera,
Escherichia coli and rotaviral gastroenteritis are the commonest
causes of secretory diarrhoea. Enterotoxin produced by Vibrio
cholerae is the prototype of secretagogue resulting in large vol-
ume secretory diarrhoea.
2 Endogenous secretagogues – A rare but often considered cause
of secretory diarrhoea, is due to neuro-endocrine tumours such
as VIPoma (vasointestinal peptide), carcinoid tumour etc. Pep-
tides produced by these tumours are potent stimulants
resulting in secretory diarrhoea.
3 Absence of ion transporter – Rare congenital syndromes
(e.g. congenital chloride diarrhoea, congenital sodium diar-
rhoea) are caused by the absence of a specific transport
molecule.
4 Loss of intestinal surface area – Extensive gut resections
resulting in substantial loss of surface area results in diarrhoea
which has both secretory and osmotic components.
II Bloody or Inflammatory diarrhoea (Fig. 4) is characterised by
presence of blood and mucus in stool. Bloody diarrhoea when
associated with abdominal pain, urgency and tenesmus often
indicates colitis. Gastrointestinal (GI) infections remain the
most common cause of acute bloody diarrhoea. It is impor-
tant to have a high index of suspicion for C. difficile infection
and test accordingly (Table 1).26 Once infections are ruled
out, aetiology varies depending on the age of presentation.
An older child with persistent bloody diarrhoea with negative
stool infectious screen needs to be investigated for inflamma-
tory bowel disease. Bloody diarrhoea in a neonate or infant is
concerning for NEC, cows milk protein allergy, very early
onset IBD, primary immunodeficiency disorders and rarely
autoimmune enteropathy.
III Fatty diarrhoea or steatorrhoea (Fig. 5) implies defective diges-
tion or absorption of fat.27,28 Stools are described as oily, foul
smelling, pale, bulky and difficult-to-flush. Occasionally a his-
tory of leakage of oil per rectum may be forthcoming. In the
evaluation of fatty diarrhoea, it is important to distinguish
between maldigestion (inadequate luminal breakdown of tri-
glycerides) and malabsorption (inadequate mucosal transport
of products of fat breakdown).
1 Maldigestion – Exocrine pancreatic insufficiency (Cystic fibro-
sis, Shwachman diamond syndrome, chronic pancreatitis) and
inadequate bile acid pool (cholestatic disorders, small intestinal
bacterial overgrowth (SIBO), ileal resection, drugs).
2 Malabsorption – Mucosal disease (coeliac disease, Crohn’s dis-
ease, mesenteric ischaemia, bowel resection) and defects in
lipid transport and metabolism (primary or secondary
lymphangiectasias, abetalipoproteinemia, chylomicron reten-
tion disease, etc.). Lymphangiectasias are associated with a pro-
tein losing enteropathy with hypoalbuminemia, lymphopenia
and hypogammaglobulinemia.
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In maldigestion, stools are fatty but not very loose as the fat is
intact, whereas diarrhoea secondary to malabsorption can be
voluminous due to the cathartic action of free fatty acids in the
small bowel lumen.
SIBO is a condition characterised by excessive growth of micro-
organisms in the small intestine.53 It can result in both osmotic
and fatty diarrhoea due to carbohydrate fermentation by bacteria
leading to excess gas and water production and bacterial
deconjugation of bile acids, respectively. Symptoms include non-
specific GI disturbances such as flatulence, belching, abdominal
pain and distension. Risk factors for SIBO include use of proton
pump inhibitors,54 impaired intestinal motility55 and short gut
syndrome.56
Gold standard for diagnosis of SIBO is invasive and requires
duodenal/jejunal aspirate culture demonstrating >105 CFU/mL of
bacteria.57 Non-invasive tests include glucose and lactulose
breath hydrogen (H2) and methane (CH4) tests. An increase in
H2 of ≥20 ppm over baseline within the first 90 min of the test
with either lactulose or glucose, or when there is an increase in
CH4 of ≥10 ppm at any time point of the test is suggestive of
SIBO.50 Principle of BHT is based on orocaecal transit time (usu-
ally 90 min) and normal production of intraluminal gas by
colonic bacteria.29 Early peak in hydrogen or methane produc-
tion before 90 min is abnormal and indicates fermentation of glu-
cose/lactulose by bacteria in the small bowel suggestive of SIBO.
Functional Diarrhoea and Irritable Bowel
Syndrome
In the absence of red flags (Fig. 1), functional diarrhoea (previously
called toddler’s diarrhoea or chronic nonspecific diarrhoea) and
IBS with diarrhoea (IBS-D) are important benign entities to recog-
nise in children, as it is the leading cause of chronic diarrhoea in
an otherwise well child (Tables 2 and 3).51,52
According to the previous Rome III criteria, 2.4% of infants
<1 year and 6.4% of toddlers aged 1–3 years in USA presented
with functional diarrhoea. Stools typically contain mucus and/or
visible undigested food. There is no defect in small bowel trans-
port of water or electrolytes in children with functional diar-
rhoea. Dietary factors such as overfeeding, excessive fruit juice or
carbohydrate consumption with low fat intake, and excessive sor-
bitol intake have been reported. Functional diarrhoea and IBS-D
are partly due to disordered intestinal motility. Disturbances in
motility such as failure of interruption of migrating motor com-
plexes by food have been noted in functional diarrhoea.
On the other hand, patients with functional constipation can
present with overflow incontinence which can be mistaken for
diarrhoea.
Some studies have shown a high prevalence of positive BHT in
children with IBS like symptoms thus suggesting an association
between IBS and SIBO37,38 however it is unclear if IBS precedes
SIBO or vice versa.39 Children with symptoms of IBS-D may war-
rant evaluation and treatment for SIBO.
Management of Chronic Diarrhoea
Principles of management of chronic diarrhoea in children
involve accurate and timely diagnosis and specific treatment of
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Fig 4 Approach to inflammatory/bloody

diarrhoea. AIE, autoimmune enteropathy;
IBD, inflammatory bowel disease; NEC,
necrotising enterocolitis; PID, primary
immunodeficiency; VEO-IBD, very early
onset IBD.

Fig 5 Approach to fatty diarrhoea. AT, antitrypsin; BHT, breath hydrogen test; CF, cystic fibrosis; SDS, Shwachman Diamond syndrome; SIBO, small intesti-
nal bacterial overgrowth.

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Chronic diarrhoea in children
Table 2 Rome IV diagnostic criteria for functional diarrhoea35
Must include all of the following
1 Daily painless, recurrent passage of 4 or more large, unformed
stools
2 Symptoms last more than 4 weeks
3 Onset between 6 and 60 months of age
4 No failure to thrive if caloric intake is adequate
Table 3 Rome IV diagnostic criteria for irritable bowel syndrome36
Must include all of the following
1 Abdominal pain at least 4 days per month associated with one or
more of the following
a. Related to defecation
b. A change in frequency of stool
c. A change in form (appearance) of stool
2 In children with constipation, the pain does not resolve with
resolution of the constipation
3 After appropriate evaluation, the symptoms cannot be fully
explained by another medical condition
Criteria fulfilled for at least 2 months before diagnosis
underlying cause. In patients presenting with dehydration, elec-
trolyte abnormalities or oedema, fluid resuscitation and electro-
lyte correction should be initiated as necessary. Nutritional
rehabilitation is the most important aspect of managing a child
with chronic diarrhoea. Enteral supplementation is always prefer-
able to parenteral nutrition but the latter becomes necessary in
children with significant failure to thrive.
Diet modification
In osmotic diarrhoea, dietary modification is based on the defi-
cient enzyme or transport protein (low glucose-galactose diet
in glucose-galactose malabsorption, lactose-free diet in lactase
deficiency, low sucrose diet in sucrose-isomaltase deficiency,
low fructose diet in fructose malabsorption etc).24 In suspected
cows milk protein allergy, depending on severity, treatment
ranges from strict maternal dietary exclusion of dairy in
breastfed infants to commencing an extensively hydrolysed
protein-based or amino-acid based formula.40 Diet based on
medium chain triglycerides is recommended in patients with
lymphangiectasia.41 A strict gluten-free diet is the treatment
for coeliac disease
It is important to review the ongoing need for elimination or
special diets in conditions expected to resolve with time. To
ensure patients receive adequate calories and micronutrients,
periodic review with an experienced paediatric dietician is
advisable.
In functional diarrhoea, management includes dietary advice
and reassurance to care giver.33Diet low in fermentable oligosac-
charides, disaccharides, monosaccharides and polyols can be used
in management of patients with IBS-D.34
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Drug therapy
Specific drug therapies depend on underlying aetiology. Antimi-
crobials for infections, rifaximin for SIBO, immunomodulators for
IBD and autoimmune enteropathy, pancreatic enzyme replace-
ment therapy in patients with pancreatic insufficiency, bile acid
sequestrants in bile acid diarrhoea and octreotide or somatostatin
analogues in lymphangiectasias and secretory diarrhoeas due to
VIPomas and other neuro-endocrine tumours.42,43 Although pro-
biotics have proven efficacy in treatment of acute infectious diar-
rhoea and prevention of antibiotic-associated diarrhoea and
C. difficile associated diarrhoea, there is insufficient evidence to
recommend probiotics in the management of chronic diarrhoea
secondary to IBS in children.44
Empiric therapy
This becomes necessary when testing does not reveal a specific
diagnosis or when no specific treatment is available. Loperamide,
an anti-motility opioid agonist with minimal penetration across
the blood brain barrier thus less potential for abuse, is useful in
patients with short gut syndrome to reduce stool losses.45 Bile
acid sequestrants such as cholestyramine have been used empiri-
cally with varying efficacy.46 Racecadotril, an enkephalinase
inhibitor which is an anti-secretory agent has proven efficacy in
acute diarrhoea in children, but data in chronic diarrhoea is lac-
king.12,47 Tricyclic antidepressants were more effective than pla-
cebo in the treatment of IBS.48 Soluble fibre supplements such as
psyllium, partially hydrolyzed guar gum and corn fibre have been
studied in randomised control trials and found to be better than
placebo in the treatment of IBS.49 However, recommendations
do not suggest routine use of fibre in the management of paediat-
ric IBS.44
Behavioural therapy
Cognitive behavioural therapy and hypnotherapy has been used
in children and adolescents with IBS for symptom control and
optimising symptom-coping skills.44
Parenteral nutrition and intestinal transplantation
Long term parenteral nutrition (PN) is necessary in the manage-
ment of children with functional (chronic intestinal pseudo-
obstruction, microvillous inclusion disease, tufting enteropathy,
etc.) and anatomical (gastroschisis, NEC, intestinal atresia, etc.)
short bowel syndrome who fail to achieve enteral autonomy with
resultant intestinal failure. Intestinal transplantation remains a
viable treatment option for those who have complications of
long-term PN or are unable to receive PN for survival.58 Cur-
rently, paediatric intestinal transplant service in Australia is
offered solely by the Victorian Liver transplant Unit and is
awaiting recognition as a nationally funded centre.
What’s New?
Funding and research in diarrhoeal diseases are rightly focussed
on preventative strategies such as vaccine development,
improved sanitation and provision of safe drinking water and
Journal of Paediatrics and Child Health 56 (2020) 1029–1038
S Shankar and J Rosenbaum
essential medicines. Simultaneously, there have been advances in
diagnostics for both infectious and non-infectious diarrhoea with
advent of PCR-based testing and next generation sequencing.
Whole exome and genome sequencing are continuing to expand
our knowledge of early onset inflammatory bowel disease and
congenital enteropathies.15 This has accelerated our understand-
ing of gut immunology, improved our ability to prognosticate
and offer specific therapies. There are new drugs including anti-
secretory drugs, small molecules and new biologics for IBD
emerging in the pipeline.25 The ever-increasing literature on gut
microbiome and its role in chronic disease, both GI and non-GI is
promising, but not ready for prime time yet.
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