Gastroenterology

Features of gastrointestinal disorders in children are:

• Vomiting, abdominal pain and diarrhoea are common and usually transient; serious causes are uncommon but important to identify

• Worldwide, gastroenteritis is responsible for 1.2 million deaths/year, one of the commonest causes of death in children <5 years old

• The number of children and adolescents developing inflammatory bowel disease is increasing

• In contrast to adults, bowel cancer is extremely rare.

Vomiting

Posseting and regurgitation are terms used to describe the non-forceful return of milk, but differ in degree. Posseting describes the small amounts of milk which often accompany the return of swallowed air (‘wind’), whereas regurgitation describes larger, more frequent losses. Posseting occurs in nearly all babies from time to time, whereas regurgitation may indicate the presence of more significant gastro-oesophageal reflux.

Vomiting is the forceful ejection of gastric contents. It is a common problem in infancy and childhood (Fig. 13.1 and Box 13.1).

Box 13.1 ‘Red Flag’ clinical features in the vomiting child

Bile-stained vomit	Intestinal obstruction
Haematemesis	Oesophagitis, peptic ulceration, oral/nasal bleeding
Projectile vomiting, in first few weeks of life	Pyloric stenosis
Vomiting at the end of paroxysmal coughing	Whooping cough (pertussis)
Abdominal tenderness/abdominal pain on movement	Surgical abdomen
Abdominal distension	Intestinal obstruction, including strangulated inguinal hernia
Hepatosplenomegaly	Chronic liver disease
Blood in the stool	Intussusception, gastroenteritis – salmonella or campylobacter
Severe dehydration, shock	Severe gastroenteritis, systemic infection (urinary tract infection, meningitis), diabetic ketoacidosis
Bulging fontanelle or seizures	Raised intracranial pressure
Failure to thrive	Gasto-oesophageal reflux, coeliac disease and other chronic gastrointestinal conditions

It is usually benign and is often caused by feeding disorders or mild gastro-oesophageal reflux or gastroenteritis. Potentially serious disorders need to be excluded if the vomiting is bilious or prolonged, or if the child is systemically unwell or failing to thrive. In infants, vomiting may be associated with infection outside the gastrointestinal tract, especially in the urinary tract and central nervous system. In intestinal obstruction, the more proximal the obstruction, the more prominent the vomiting and the sooner it becomes bile-stained (unless the obstruction is proximal to the ampulla of Vater). Intestinal obstruction is associated with abdominal distension, more marked in distal obstruction. ‘Red Flag’ clinical features suggesting significant organic pathology are listed in Box 13.1.

Summary

Vomiting in infants

• Common chronic causes are gastro-oesophageal reflux and feeding problems, e.g. force-feeding or overfeeding

• If transient, with other symptoms, e.g. fever, diarrhoea or runny nose and cough, most likely to be gastroenteritis or respiratory tract infection, but consider urine infection and meningitis

• If projectile at 2–7 weeks of age, exclude pyloric stenosis

• If bile stained, exclude intestinal obstruction, especially intussusception, malrotation and a strangulated inguinal hernia. Assess for dehydration and shock.

Gastro-oesophageal reflux

Gastro-oesophageal reflux is the involuntary passage of gastric contents into the oesophagus. It is extremely common in infancy. It is caused by inappropriate relaxation of the lower oesophageal sphincter as a result of functional immaturity. A predominantly fluid diet, a mainly horizontal posture and a short intra-abdominal length of oesophagus all contribute. While common in the first year of life, nearly all symptomatic reflux resolves spontaneously by 12 months of age. This is presumably due to a combination of maturation of the lower oesophageal sphincter, assumption of an upright posture and more solids in the diet.

Most infants with gastro-oesophageal reflux have recurrent regurgitation or vomiting but are putting on weight normally and are otherwise well, although the mess, smell and frequent changes of clothes is frustrating for carers.

Complications are listed in Box 13.2.

Box 13.2 Complications of gastro-oesophageal reflux

• Failure to thrive from severe vomiting

• Oesophagitis – haematemesis, discomfort on feeding or heartburn, iron deficiency anaemia

• Recurrent pulmonary aspiration – recurrent pneumonia, cough or wheeze, apnoea in preterm infants

• Dystonic neck posturing (Sandifer syndrome)

• Apparent life-threatening events (ALTE)

Severe reflux is more common in:

• children with cerebral palsy or other neurodevelopmental disorders, when energetic management, surgical if necessary, may transform the child’s quality of life

• preterm infants, especially if coexistent bronchopulmonary dysplasia

• following surgery for oesophageal atresia or diaphragmatic hernia.

Investigation

Gastro-oesophageal reflux is usually diagnosed clinically and no investigations are required. However, they may be indicated if the history is atypical, complications are present or there is failure to respond to treatment. Investigations include:

• 24-hour oesophageal pH monitoring to quantify the degree of acid reflux (see Case History 13.1).

• 24-hour impedance monitoring. Available in some centres. Weakly acidic or non-acid reflux, which may cause disease, is also measured.

• Endoscopy with oesophageal biopsies to identify oesophagitis and exclude other causes of vomiting.

Contrast studies of the upper gastrointestinal tract may support the diagnosis but are neither sensitive nor specific. They may be required to exclude underlying anatomical abnormalities in the oesophagus, stomach and duodenum, and to identify malrotation.

Case History

13.1 Severe gastro-oesophageal reflux

This infant (Fig. 13.2a) had a history of frequent regurgitation from the first few days of life. He developed two chest infections. Some of the vomits contained altered blood. A 24-hour oesophageal pH study showed severe gastro-oesophageal reflux (Fig. 13.2b,c). Endoscopy showed oesophagitis. He had probably had episodes of aspiration pneumonia. Symptoms resolved on treatment with feed thickeners and omeprazole. His parents also commented on how much better he slept at night. Treatment was reduced from 14 months of age and the symptoms did not recur.

Figure 13.2a A pH sensor has been placed in the lower oesophagus.

Management

Uncomplicated gastro-oesophageal reflux has an excellent prognosis and can be managed by parental reassurance, adding inert thickening agents to feeds (e.g. Nestargel, Carobel) and positioning in a 30° head-up prone position after feeds.

More significant gastro-oesophageal reflux disease is managed with acid suppression with either H₂ receptor antagonists (e.g. ranitidine) or proton pump inhibitors (e.g. omeprazole). These drugs reduce the volume of gastric contents and treat acid-related oesophagitis. Although the evidence for their use is poor, drugs which enhance gastric emptying (e.g. domperidone) may be tried. If the child fails to respond to these measures, other diagnoses such as cow’s milk protein allergy should be considered and further investigations performed.

Surgical management is reserved for children with complications unresponsive to intensive medical treatment or oesophageal stricture. A Nissen fundoplication, in which the fundus of the stomach is wrapped around the intra-abdominal oesophagus, is performed either as an abdominal or laparoscopic procedure.

Summary

Gastro-oesophageal reflux

• Occurs in otherwise normal infants, but risk is increased if neuromuscular problems or surgery to the oesophagus or diaphragm

• Is treated if troublesome with upright positioning, feed thickening, medication and sometimes fundoplication

• Investigations are performed if diagnosis is unclear or complications occur.

Pyloric stenosis

In pyloric stenosis, there is hypertrophy of the pyloric muscle causing gastric outlet obstruction. It presents at between 2 and 7 weeks of age, irrespective of gestational age. It is more common in boys (4 : 1), particularly first-borns, and there may be a family history, especially on the maternal side.

Pyloric stenosis

Clinical features are:

• Vomiting, which increases in frequency and forcefulness over time, ultimately becoming projectile

• Hunger after vomiting until dehydration leads to loss of interest in feeding

• Weight loss if presentation is delayed.

A hypochloraemic metabolic alkalosis with a low plasma sodium and potassium occurs as a result of vomiting stomach contents.

Diagnosis

Unless immediate fluid resuscitation is required, a test feed is performed. The baby is given a milk feed, which will calm the hungry infant, allowing examination. Gastric peristalsis may be seen as a wave moving from left to right across the abdomen (Fig. 13.3a). The pyloric mass, which feels like an olive, is usually palpable in the right upper quadrant (Fig. 13.3b). If the stomach is overdistended with air, it will need to be emptied by a nasogastric tube to allow palpation. Ultrasound examination is helpful (Fig. 13.3c) if the diagnosis is in doubt.

Management

The initial priority is to correct any fluid and electrolyte disturbance with intravenous fluids (0.45% saline and 5% dextrose with potassium supplements). Once hydration and acid–base and electrolytes are normal, definitive treatment by pyloromyotomy can be performed. This involves division of the hypertrophied muscle down to, but not including, the mucosa (Fig. 13.3d). The operation can be performed either as an open procedure via a periumbilical incision or laparoscopically. Postoperatively, the child can usually be fed within 6 h and discharged within 2 days of surgery.

Summary

Pyloric stenosis

• More common in boys and those with a maternal family history

• Signs are: visible gastric peristalsis, palpable abdominal mass on test feed and possible dehydration

• Associated with hyponatraemia, hypokalaemia and hypochloraemic alkalosis

• Diagnosis may be confirmed by ultrasound

• Treated by surgery after rehydration and correction of electrolyte imbalance.

Crying

The time healthy babies cry for is highly variable. In most, it represents the baby’s response to hunger and discomfort. Reassurance and advice on appropriate feeding, wrapping and care will usually suffice.

Some babies cry for prolonged periods in spite of feeding and comforting and this is distressing for all concerned. It can engender a feeling of anxiety, helplessness and depression in the carer, particularly if they are inexperienced or poorly supported. It has also been suggested that the emotional climate within a home may be transmitted to a baby, and that in some instances, tense, anxious or irritable caregivers are more likely to have fretful babies. The complaint that a baby is ‘always crying’ may also be a pointer to potential or actual non-accidental injury.

A significant cause for the crying is identified in a minority of infants. If of sudden onset, it may be due to a urinary tract, middle ear or meningeal infection, to pain from an unrecognised fracture, oesophagitis or torsion of the testis. Severe nappy rash, constipation or coeliac disease may produce a miserable, crying infant. Preterm infants who have spent several weeks in hospital can be difficult to settle, as can infants with a chronic neurological disorder, e.g. cerebral palsy. On the basis of countless reports of parents, eruption of teeth is painful in some infants. However, teething does not cause vomiting, diarrhoea, high fever or seizures.

Infant ‘colic’

The term ‘colic’ is used to describe a common symptom complex which occurs during the first few months of life. Paroxysmal, inconsolable crying or screaming often accompanied by drawing up of the knees and passage of excessive flatus takes place several times a day, particularly in the evening. There is no firm evidence that the cause is gastrointestinal, but this is often suspected. The condition occurs in up to 40% of babies. It typically occurs in the first few weeks of life and resolves by 4 months of age. The condition is benign but it is very frustrating and worrying for parents and may precipitate non-accidental injury in infants already at risk. Support and reassurance should be given. Gripe water is often recommended but is of unproven benefit. If severe and persistent, it may be due to a cow’s milk protein allergy or gastro-oesophageal reflux and an empirical 2-week trial of a whey hydrolysate formula followed by a trial of anti-reflux treatment may be considered.

Acute abdominal pain

Assessment of the child with acute abdominal pain requires considerable skill. The differential diagnosis of acute abdominal pain in children is extremely wide, encompassing non-specific abdominal pain, surgical causes and medical conditions (Fig. 13.4). In nearly half of the children admitted to hospital, the pain resolves undiagnosed. In young children it is essential not to delay the diagnosis and treatment of acute appendicitis, as progression to perforation can be rapid. It is easy to belittle the clinical signs of abdominal tenderness in young children. Of the surgical causes, appendicitis is by far the most common. The testes, hernial orifices and hip joints must always be checked. It is noteworthy that:

• Lower lobe pneumonia may cause pain referred to the abdomen

• Primary peritonitis is seen in patients with ascites from nephrotic syndrome or liver disease

• Diabetic ketoacidosis may cause severe abdominal pain

• Urinary tract infection, including acute pyelonephritis, is a relatively uncommon cause of acute abdominal pain, but must not be missed. It is important to test a urine sample, in order to identify not only diabetes mellitus but also conditions affecting the liver and urinary tract.

Acute appendicitis

Acute appendicitis is the commonest cause of abdominal pain in childhood requiring surgical intervention (Fig. 13.5). Although it may occur at any age, it is very uncommon in children <3 years old. The clinical features of acute uncomplicated appendicitis are:

Figure 13.5 Appendicitis at operation showing a perforated acutely inflamed appendix covered in fibrin.

• Symptoms

– Anorexia

– Vomiting (usually only a few times)

– Abdominal pain, initially central and colicky (appendicular midgut colic), but then localising to the right iliac fossa (from localised peritoneal inflammation)

• Signs

– Flushed face with oral fetor

– Low-grade fever 37.2–38°C

– Abdominal pain aggravated by movement, e.g. on walking, coughing, jumping, bumps on the road during a car journey

– Persistent tenderness with guarding in the right iliac fossa (McBurney’s point).

In preschool children:

• The diagnosis is more difficult, particularly early in the disease

• Faecoliths are more common and can be seen on a plain abdominal X-ray

• Perforation may be rapid, as the omentum is less well developed and fails to surround the appendix, and the signs are easy to underestimate at this age.

With a retrocaecal appendix, localised guarding may be absent, and in a pelvic appendix there may be few abdominal signs.

Appendicitis is a progressive condition and so repeated observation and clinical review every few hours are key to making the correct diagnosis, avoiding delay on the one hand and unnecessary laparotomy on the other.

No laboratory investigation or imaging is consistently helpful in making the diagnosis. A neutrophilia is not always present on a full blood count. White blood cells or organisms in the urine are not uncommon in appendicitis as the inflamed appendix may be adjacent to the ureter or bladder. Although ultrasound is no substitute for regular clinical review, it may support the clinical diagnosis (thickened, non-compressible appendix with increased blood flow); demonstrate associated complications such as abscess, perforation or appendix mass; and exclude other pathology causing the symptoms. In some centres, laparoscopy is available to see whether or not the appendix is inflamed.

Appendicectomy is straightforward in uncomplicated appendicitis. Complicated appendicitis includes the presence of an appendix mass, an abscess or perforation. If there is generalised guarding consistent with perforation, fluid resuscitation and intravenous antibiotics are given prior to laparotomy. If there is a palpable mass in the right iliac fossa and there are no signs of generalised peritonitis, it may be reasonable to elect for conservative management with intravenous antibiotics, with appendicectomy being performed after several weeks. If symptoms progress, laparotomy is indicated.

Non-specific abdominal pain and mesenteric adenitis

Non-specific abdominal pain (NSAP) is abdominal pain which resolves in 24–48 h. The pain is less severe than in appendicitis, and tenderness in the right iliac fossa is variable. It is often accompanied by an upper respiratory tract infection with cervical lymphadenopathy. In some of these children, the abdominal signs do not resolve and an appendicectomy is performed. The diagnosis of mesenteric adenitis can only be made definitively in those children in whom large mesenteric nodes are seen at laparotomy or laparoscopy and whose appendix is normal.

Summary

Acute abdominal pain in older children and adolescents

• Exclude medical causes, in particular lower lobe pneumonia, diabetic ketoacidosis, hepatitis, pyelonephritis

• Check for strangulated inguinal hernia or torsion of the testis in boys

• On palpating the abdomen in children with acute appendicitis, guarding and rebound tenderness are often absent or unimpressive, but pain from peritoneal inflammation may be demonstrated on coughing, walking or jumping

• To distinguish between acute appendicitis and non-specific abdominal pain may require close monitoring and repeated evaluation in hospital.

Intussusception

Intussusception describes the invagination of proximal bowel into a distal segment. It most commonly involves ileum passing into the caecum through the ileocaecal valve (Fig. 13.6a). Intussusception is the commonest cause of intestinal obstruction in infants after the neonatal period. Although it may occur at any age, the peak age of presentation is between 3 months and 2 years. The most serious complication is stretching and constriction of the mesentery resulting in venous obstruction, causing engorgement and bleeding from the bowel mucosa, fluid loss and subsequently bowel perforation, peritonitis and gut necrosis. Prompt diagnosis, immediate fluid resuscitation and urgent reduction of the intussusception are essential to avoid complications.

Intussusception