Chapter 6:


Student Authors: Lehlohonolo Ntlatlapo and Savannah Verhage

Specialist Advisor: Dr Lesego Ndhlovu

Illustration showing doctor facing a frightened toilet

This chapter covers the following topics:


Diarrhoea is defined by the WHO as≤3 watery stools in 24 hours. Almost every child will have diarrhoea at least once and approximately 1 in 3 hospital admissions in South Africa are due to diarrhoea. It remains a major cause of morbidity and mortality worldwide in children <5 years old. It is the second most common cause of death (after HIV) in South African children of that age group.

Classification, Pathophysiology and Aetiology

In diarrhoea, the excretion of water and electrolytes exceed net absorption. Diarrhoea may be classified according to pathophysiology or duration.

Pathophysiological Classification

Diarrhoea may be classified as:

Classification According to Duration

Diarrhoea may be considered:

Clinical Features

The clinical presentation and course of diarrhoea depends on the aetiology of the diarrhoea and the host (see an image of a child threatened by severe diarrhoea here). The patient may present with:

Table 6.1: Recognising and Classifying Dehydration
Hydration No dehydration Some dehydration (5% dry) Severe dehydration (≤10% dry) Shock (an important danger sign)
Level of consciousness Normal Normal Lethargic Not responding
Eyes Normal Sunken Very sunken Dull
Mucous membranes Moist Dry Very dry Varies
Thirst Drinks normally Thirsty Extremely thirsty Does not want to drink
Skin Normal skin turgor Decreased skin turgor Very decreased skin turgor Mottled and cold
Anterior fontanelle Normal Sunken Very sunken -
Weight loss None <5% 5-10% Varies
Pulse rate Normal Normal Fast Fast/slow
Pulse volume Normal Normal Thready Thready/impalpable
Respiration Normal Deep Fast and deep Irregular and difficult

Note: The most accurate measure of dehydration is loss of weight. One must remember that shock may occur even in the absence of other signs/symptoms of dehydration.


Diarrhoea may be complicated by:


No routine investigations are required, as most children will recover spontaneously within a few days, regardless of the underlying causative organism. However, a urine dipstick and finger-prick glucose should be done on all children admitted to hospital. Investigations may include:


Primary Prevention

Diarrhoea may be prevented by:

Secondary Prevention

This involves the prevention of dehydration and its complications. Acute diarrhoea is usually self-limiting. However, one must always assess the patient for danger signs (not drinking, lethargy, intractable vomiting, convulsions and bloody stools) and give supportive management.

Supportive management includes:

Tertiary Prevention

One’s aim here is to prevent death from dehydration and complications. Thus, tertiary prevention involves appropriately managing the complications that the child has and appropriately managing dehydration and shock (refer to general fluid management in the Feeds and Fluid Management chapter).


Hepatitis is inflammation of the liver which can result in the damage and destruction of hepatocytes.


Common causes of hepatitis include viruses, autoimmune liver disease, and drugs and toxins.

Viral Hepatitis

In viral hepatitis, the damage to the liver is not due to the viral invasion but the immune response to the virus. In neonates the virus is usually vertically transmitted from the mother in the perinatal period. Viral causes of hepatitis include:

Autoimmune Liver Disease

They include:

Drugs and Toxins

Clinical Features

They vary as they depend on the aetiology and the child’s age of the child (infant vs child vs adolescent). Some children may be asymptomatic, while others may present with:

Acute HBV infection is usually symptomatic, while chronic infection is often asymptomatic (children with the latter infection will grow and develop normally). Chronic infection may be associated with polyarteritis nodosa and glomerulonephritis, and can progress to cirrhosis and hepatocellular carcinoma. Most children with chronic HCV infection are asymptomatic, but can develop cirrhosis and hepatocellular carcinoma (especially if there is a hepatitis B co-infection).

Some children may present in acute liver failure i.e. fulminant liver failure without pre-existing liver disease (an uncommon medical emergency). Causes include infection with HAV, HBV, Reye’s syndrome, drugs (e.g. paracetamol, anti-TB drugs) and toxins (e.g. traditional medication).


One may order:

Pathophysiology, Diagnosis and Management

Table 6.2: Pathophysiology, Diagnosis and Management of Hepatitis A and B
Pathophysiology It is transmitted by the faecal-oral route and has an incubation period of 15-50 days. The child is most infectious 1-2 weeks before symptom onset. The child may be asymptomatic (young children) or may have a prodrome of nausea, anorexia and malaise. S/he may go on to develop jaundice, dark urine and tender hepatomegaly. Chronic infection does not develop and fulminant infection is very rare. Children may be infected by horizontal, vertical or parenteral transmission. HBV has an incubation period of 2-6 months and a similar prodrome and clinical features to HAV (but the disease is more insidious and there is a longer prodrome). 90% of neonates and 30-40% of infected children become chronic carriers – asymptomatic in the beginning and then develop chronic hepatitis, cirrhosis and HCC.
Diagnosis Current/recent HAV infection is diagnosed if the child is HAV IgM positive (can remain positive for 4-6 months). Previous infection can be diagnosed if the child is HAV IgG positive. Acute HBV infection is diagnosed if the child is HBV IgM, HBsAg and HBeAg positive. Chronic HBV is also diagnosed using the above tests and may be:
  • High-risk (HBeAg-positive. HBeAb-positive, HBV IgG-positive)
  • Low-risk (HBeAg-negative. HBeAb-positive, HBV IgG-positive).
Management The local authorities should be notified (HAV is a notifiable disease). Management includes:
  • Giving supportive care (avoid liver toxic drugs and ensure adequate hydration)
  • Following an appropriate diet (high in calories and low in protein)
  • Encouraging good hand hygiene and in-hospital isolation for 1 week after the onset of jaundice (to prevent transmission)
  • Managing household contacts
The child should be admitted if s/he has any danger signs (prolonged vomiting, dehydration, persistent fever, hypoglycaemia, confusion, intercurrent infection or raised INR).
Treatment of chronic HBV infection includes 𝛼𝛼-interferon, pegylated interferon and nucleotide/-sides (entecavir, tenofovir or lamivudine). Acute infection is usually self-limiting and the patient should just isolate.
Prevention Two doses of the HAV vaccine (0.5 mL IMI) should be administered. The HAV vaccine can also be used as post- or pre-exposure prophylaxis. Otherwise one can give a single dose of pooled human Ig (0.04 mL/kg IM). HBV Ig may be given to:
  • Non-immune children (2 mL IMI given 1-7 days after exposure)
  • Children who have had a high-risk exposure (same as above plus a second dose 1 month later)
  • Infants born to HBsAg-positive mothers (0.5 mL IMI within 12 hours of birth)
The HBV vaccine is part of the routine vaccination programme in SA.

Prevention of other causes of hepatitis:

Note: See the Infectious Diseases chapter for management of other viral causes.


It is defined if the child has a portal pressure <10 mmHg or hepatic venous pressure gradient <4 mmHg. Chronic liver disease results in increased vascular resistance or blood volume within the portal venous system and may be complicated by portal hypertension.


Portal hypertension may be due to a pre-, intra- or post-hepatic cause.

Clinical Features

Portal hypertension should be suspected in any child with significant GI bleeding (acute variceal haemorrhage is the most serious complication) or unexplained splenomegaly. The child may also present with signs of chronic liver disease such as:

Patients with cirrhosis may present with hepatic decompensation and encephalopathy. Pre-hepatic causes may not cause jaundice.


One must look for the underlying aetiology by performing:

  1. Blood tests:
    • FBC
    • Liver enzyme levels
  2. Imaging:
    • Doppler USS e.g. portal vein and splenic vein thrombosis
    • CT angiography (not routinely done but may be ordered depending on the clinical picture)
    • Liver biopsy (not routinely done but may be ordered depending on the clinical picture)
    • Endoscopy (to look for oesophageal varices)


The aim is to treat the underlying aetiology and complications (especially if the child is bleeding). An early referral should be made to a hepatologist or gastroenterologist after the patient has been stabilised.

One must avoid morbidity and mortality after a bleeding episode. Management of the patient with an acute variceal haemorrhage may include:


It is the involuntary passage of gastric contents into the oesophagus and is a normal physiological process. Episodes occur in the distal oesophagus, last <3 mins and are asymptomatic. Secretions contain food, drink, saliva, and gastric, pancreatic and biliary secretions. See also an image related to Reflux Gastro-Oesophagien here.


GOR is usually due to transient relaxation of the lower oesophageal sphincter (LOS). Less commonly it may be due to low LOS tone (chalasia). When the refluxed material passes into the mouth, this is termed regurgitation. Regurgitation is common in infancy (present in 60% of infants at 3 months old; resolved in 90% of infants by 1 year old). GOR and regurgitation are often not pathological, but complications may arise in a few children.

Clinical Features and Complications

GOR disease (GORD) is diagnosed when there are complications of GOR. There are no clinical features that are diagnostic of GORD but the following clinical features suggest the diagnosis:


One may order the following investigations:

One must, therefore, exclude other causes of chronic respiratory disease that may mimic GORD and assess the patient for signs of raised intracranial pressure, GI obstruction (e.g. projectile vomiting, abdominal distension) and urinary tract infection.


GOR does not require treatment, however GORD does.

Management of Functional Regurgitation

It will include:

Management of GORD

Young infants with severe malnutrition or respiratory complications should be given = transpyloric (NGT) feeds and PPIs for acid-related complications. H2-receptor antagonists may also help acutely (if the patient presents with gastritis), however they should not be chronically used. Surgery may be performed if there is no response to optimal medical treatment



Constipation is the infrequent or irregular passage of unduly hard stools.

Faecal loading is the build-up of faeces due to ineffective or incomplete evacuation of stool. Encopresis is an apparently wilful passage of normal consistency stool into underclothes or other places. (Refer to child psychiatry.)

Soiling is involuntary leakage of small amounts of soft or watery stool secondary to faecal loading and rectal dysfunction.


Causes may be grouped according to the age of the child.

Other causes of constipation include coeliac disease and drugs. See related image here.

Clinical Features

The child may have


They may include:

Other tests that are not routinely done (but may be performed depending on the suspected aetiology) include:


Immediate Management

The parents and child should be counselled on constipation and the importance of behavioural and dietary changes. The colon can then be cleared with repeated phosphate-containing enemas (for disimpaction) or a balanced electrolyte polyethylene glycol (PEG) solution.

Klean Prep® (15-25 mL/kg/hour) may also be given and an enema done (within the first hour of starting Klean Prep®. The solution should be continued until the rectum is clear and the abdomen is soft (~6-8 hours). However, the patient should be observed for aspiration.

Maintenance Therapy

It may need to be continued for months or years and may include


Constipation may be prevented with:


Jaundice is the yellow discolouration of the skin and mucous membranes and is a sign of hyperbilirubinaemia.

Pathophysiology, Classification and Aetiology

Unconjugated Hyperbilirubinaemia

It may be further subclassified as:

Conjugated Hyperbilirubinaemia

It is diagnosed if the conjugated bilirubin level is >34mmol/L or >15% of the total bilirubin level. Causes include:

Clinical Features

The child may present with:

Jaundice which develops within the first 24 hours of life is likely to be pathological and requires further investigation. Jaundice which develops after day 3 of life also needs close monitoring and investigation.


They should include:


It is important to diagnose and manage jaundice appropriately as it can result in kernicterus if left untreated. Generally, management includes:

Management of Early-Onset Jaundice

Jaundice which develops within the first 24 hours of life is most likely due to haemolytic disease of the neonate (ABO or Rh incompatibility). Management, therefore, includes:

The following tests should also be done:

Rarely, one may need to test for glucose-6-phosphate-dehydrogenase (G6PD) deficiency and do Hb electrophoresis.

Management of Late-Onset Jaundice

If the jaundice develops >24 hours after birth and the unconjugated bilirubin is above the normal limit, one must:


It is enlargement of both the spleen and the liver.


Causes of hepatosplenomegaly include:

Clinical Features

The child may present with:


Investigations should only be performed as indicated. They may include:


One must treat the cause. Thus, the patient should be referred to the relevant paediatric specialist depending on the cause or a hepatologist if the cause is unknown.


Upper GI bleeding (UGIB) is GI bleeding which is proximal to the ligament of Treitz (the junction of the duodenum and jejunum) i.e. oesophagus, stomach or duodenum. These patients often present with haematemesis and/or melena.

Lower GIGI bleeding (LGIB) is bleeding which is distal to the ligament of Treitz i.e. small bowel or colon. These patients usually present with haematochezia.


The causes of GI bleeding vary depending on the child’s age.

Table 6.3: Causes of UGIB and LGIB
Age Group Cause of UGIB Cause of LGIB
Age Group Cause of UGIB Cause of LGIB
  • Swallowed maternal blood i.e. not true bleeding
  • Vitamin K deficiency/ haemorrhagic disease of the neonate
  • Vascular malformations
  • Stress gastritis or ulcers associated with critical illness
  • Coagulopathy
  • Cow’s milk protein intolerance
  • Gastric or duodenal ulcers
  • GI duplication cyst
  • Swallowed maternal blood (not true bleeding)
  • Anorectal fissures
  • Necrotising enterocolitis
  • Malrotation with midgut volvulus
  • Hirschsprung’s disease with enterocolitis
  • Coagulopathy
  • Brisk UGIB
  • Vascular malformations
Infants and toddlers
  • Mallory-Weiss syndrome
  • Oesophageal or GI foreign body
  • Oesophagitis
  • Peptic ulcers and gastritis
  • Bleeding oesophageal varices or gastric varices
  • Arterial bleeding (rare)
  • Meckel’s diverticulum
  • Intussusception
  • Anal fissures (especially around the time of the introduction of solid food or cow’s milk)
  • Milk- or soy protein-induced colitis (allergic colitis)
  • Infectious colitis
  • Lymphonodular hyperplasia
  • GI duplication cyst
  • Coagulopathy
  • Eosinophilic GI disease
  • Infantile and very early-onset inflammatory bowel disease (IBD)
Pre-school going age
  • Anal fissures
  • Intussusception
  • Meckel’s diverticulum
  • Other causes e.g. infectious colitis, haemolytic uraemic syndrome, IgA vasculitis, Henoch-Schonlein purpura, juvenile polyps, very early-onset IBD, solitary ulcer syndrome
School going age
  • Anal fissures
  • Juvenile polyps
  • Infectious colitis (Salmonella sp, Shigella sp, Campylobacter sp, E.coli, Clostridium difficile are the most common)
  • Inflammatory bowel disease
  • Meckel’s diverticulum
  • Solitary rectal ulcer syndrome
  • IgA vasculitis (Henoch-Schonlein purpura
  • Haemorrhoids

Clinical Features

The child may present with:


When a patient presents with GI bleeding, one must ask the following questions

  1. Is the patient haemodynamically stable or is resuscitation indicated?
  2. Is it blood?
  3. Is the blood from the upper GIT (dark red/black) or lower GIT (bright red)?
  4. What are the most likely causes of the bleed?

The patient should then be assessed based on:


Emergency Management

A gastroenterologist and general surgeon should be immediately called for any patient with severe acute UGIB. The patient should then be resuscitated and stabilised:

Follow-up visits should be scheduled, especially for first-time bleeders.

Routine Management

Patients who have had a UGIB:

The cause of the lower GI bleed should be identified and treated. See also a figure on Deployed Sengstaken-Blakemore Tube in the Patient with an UGIB here.


These disorders are the most common causes of chronic (>2 months) abdominal pain in children and adolescents.


The pathophysiology is poorly understood but it is thought to involve an interplay between enteric and CNS regulatory factors. These disorders may be associated with:

Diagnosis, Classification and Clinical Features

The diagnosis is made in the child with chronic abdominal pain, no danger signs, normal examination and stool which is negative for occult blood. Certain recognisable patterns of symptoms may be used to classify the FAP:


It should be managed in a primary care setting. The goal of treatment is a return to normal function rather than complete elimination of pain. However, a referral may be made if the pain cannot be managed at a primary care level.

Management is individualised and depends on the child’s and family behaviours, triggers and symptoms. Regardless of the subtype of FAP, the management includes: