Introduction

A neonate is a newborn less than 28 days old, an infant is less than a year, a child is 1–18 years old and an adult is 18 or older. In the UK, those between 13 and 18 are increasingly being managed in adolescent units, where their needs are better met. Many children are treated by general surgeons with a paediatric interest, but surgical problems in infants, major congenital abnormalities and malignant tumours are usually managed in regional centres by specialists. The range of surgical conditions in children differs from adults and varies between age groups, particularly for emergency presentations. Paediatric emergencies are considered here by age group, i.e. newborn (the first few days of life, including premature babies), infants and young children (up to about 2 years) and older children (up to puberty). During puberty, the disorders merge with those of adulthood. Non-emergency and urogenital disorders are less age-specific (see Ch. 51).

Fluid and electrolyte problems

Fluid deficiency and electrolyte imbalances occur rapidly because each compartment has such a small fluid volume and paediatric fluid requirements are relatively greater than adult because the kidneys have less concentrating ability and obligatory urine output is greater. Faecal fluid losses are higher, particularly under 2 years. In severe diarrhoea, dehydration and electrolyte disturbances occur with frightening speed. Signs of fluid depletion are also different from adults. Young fluid-depleted children are often lethargic or drowsy and may even be comatose. The eyes and anterior fontanelle may be sunken but skin turgor is not lost. Tachycardia is usual, but hypotension is a late sign because of compensatory mechanisms. Urine output is likely to be low—normal output should be at least 1 ml per kg body weight per hour.

Blood glucose

Hypoglycaemia readily occurs because a baby’s glycogen stores are meagre; there needs to be a regular supply of glucose by feeding or intravenous infusion. Adrenergic responses to trauma and stress also increase glucose requirements. Hypoglycaemia is likely to occur when a baby is fasted before surgery but not given intravenous dextrose, or when a blood transfusion temporarily replaces i.v. dextrose. All small children undergoing surgery need close monitoring of blood glucose to prevent hypoglycaemic brain damage.

Temperature regulation

Temperature regulation in infants is less robust and hypothermia a real hazard. Infants have a relatively large surface area, poor vasomotor control of skin vessels and are unable to generate heat by shivering. These differences are more marked in premature neonates, who are poorly adapted to life ex utero. A controlled, heated environment is essential for operating on and nursing newborn infants. For those under 1 kg, the temperature is set between 34.5 and 35.5°C, and for those over 3 kg, between 31.5 and 34.5°C. The infant is placed on a heated mattress and all parts of the body kept insulated. Intravenous fluids and skin cleansers are warmed and anaesthetic gases humidified and warmed.

Liver function

Liver function is immature in the newborn. Physiological jaundice caused by high levels of unconjugated bilirubin is common because the immature liver cannot synthesise the enzyme glucuronyl transferase. There is also reduced ability to detoxify analgesic drugs, and many drugs cross the blood–brain barrier more readily and hence are more likely to cause cerebral side-effects. Drugs must often be used in greatly reduced doses after checking a paediatric formulary. A further consequence of liver immaturity is reduced prothrombin production. Prophylactic vitamin K should be given after the baby’s birth, or intravenously in the perioperative period.

Immunity

Infection can be rapidly fatal in small babies, particularly premature and small-for-dates babies likely to have impaired immunological defences. Infection can be minimised by good surgical technique, meticulous haemostasis to avoid haematomas, and prophylactic antibiotics where appropriate. Vigilance for perioperative infection is essential.

Gastrointestinal atresias and stenoses

Atresia is defined as complete obliteration of a segment of the GI tract, which is thus totally obstructed. A web sometimes partially or completely occludes the lumen. A stenosis is an indistensible narrowing causing partial obstruction. These are most common in the oesophagus, the small intestine, and in the colon following necrotising enterocolitis.

Oesophageal and duodenal atresias and anorectal malformations are true embryological abnormalities, often associated with other congenital abnormalities. For example, major cardiac, vertebral or renal abnormalities are found in 40% of babies with oesophageal atresia, and 30% of duodenal atresias are found in infants with trisomy 21. In contrast, small bowel atresias probably result from intrauterine mesenteric vascular accidents or failure of canalisation of the bowel and are rarely associated with other abnormalities.

Midgut malrotation with volvulus

Anorectal abnormalities

The primitive hindgut forms the cloaca in the early embryo and a septum then divides it into an anterior compartment, forming the urinary tract and part of the genital tract, and a posterior compartment forming rectum and upper part of the anal canal. The lower anal canal develops from ectodermal invagination.

There is a spectrum of congenital anorectal disorders (imperforate anus) that has led to complex classifications. However, clinically, it is sufficient to separate imperforate anus into high or low according to whether the bowel terminates above or below levator ani. In nearly all, there is a fistula from the end of the bowel. When the malformation is low, the fistula opens to skin anterior to the sphincter complex and meconium may emerge from it; because of this, the abnormality may not be immediately recognised (Fig. 50.5). Newborn babies need to be carefully examined to ensure the anus is situated correctly. In high malformations, there is usually a fistula to the urethra in the male or vagina in the female. Patients with a urethral fistula require prophylactic antibiotics to prevent UTIs. Urinary tract malformations and lower vertebral anomalies are commonly associated with anorectal abnormalities and should be sought.

In suspected anorectal abnormalities, the perineum is carefully examined for a fistula. If one is not found, it is worth waiting 24 hours and then examining the perineum under anaesthesia for one. If one is not found, the anomaly is treated as high and a colostomy performed as a first stage.

Treatment depends on the level of the distal pouch. In low lesions, the main pelvic muscle of continence (puborectalis) is well formed and operations via the perineum are often sufficient. An anoplasty or a limited posterior-sagittal ano-rectoplasty (mini-PSARP) is performed, increasing the fistula calibre and importantly, moving the opening into the sphincter complex. High lesions require a preliminary colostomy to allow the baby to empty the bowel and feed, followed by complicated reconstructions later; these involve mobilising the bowel end and reconstructing the sphincter mechanism around it. The essence is accurate apposition and repair of the levator muscles and external anal sphincter. Long-term faecal continence and bowel control is imperfect in many children with either low or high anomalies, and constipation is usually a problem.

Meconium ileus

In meconium ileus, the distal ileum is obstructed by abnormal thick, viscid meconium and mucus plugs. About 95% of babies with this have cystic fibrosis and all babies with meconium ileus must be tested for it. The colon and rectum distal to the obstruction are of very small calibre. This microcolon results from the fact that no bowel contents have passed down it rather than any inherent abnormality (Fig. 50.6).

The condition presents soon after birth with lower intestinal obstruction; the diagnosis is suspected when rectal examination reveals a patent but very narrow rectum. A Gastrografin enema may demonstrate inspissated meconium in the distal ileum and may also break up the material by a detergent-like action, relieving the obstruction. Laparotomy is required for unrelieved obstruction or any with signs of peritonitis. In most cases, the maximally dilated loop of ileum containing the inspissated meconium is resected and a primary anastomosis performed.

Babies with cystic fibrosis have abnormal mucus-secreting glands which cause secondary changes in the lungs, liver, pancreas and small bowel. Pancreatic enzymes which normally liquefy meconium are deficient. Pancreatic enzyme supplements are given to prevent malabsorption and to prevent the equivalent of meconium ileus in older children. Regular physiotherapy is given to help prevent pulmonary complications.

Hirschsprung’s disease (congenital aganglionosis)

Hirschsprung’s disease (Harald Hirschsprung 1830–1916) is a congenital abnormality of distal intestine which affects all of the intramural autonomic nerves and causes functional intestinal obstruction. Ganglion cells are absent from the inter-myenteric and submucosal plexuses, and the parasympathetic and sympathetic nerves are scattered in a disorderly way throughout the layers of the bowel wall. The aganglionosis always involves the rectum, extending into the sigmoid in 80% and reaching the small bowel in 5%. The pathology is continuous without ‘skip’ lesions.

Peristalsis is deficient in the affected bowel and the internal anal sphincter does not relax. The baby therefore has a functional obstruction that usually presents soon after birth with intestinal obstruction; in patients with long-segment disease, it can present in later childhood with constipation and failure to thrive (Fig. 50.7). About 80% of normal babies pass meconium within the first 24 hours but about 80% of babies with Hirschsprung’s disease do not, and this is a diagnostic pointer.

Rectal examination may cause an explosive release of air and meconium. Rectal biopsy is the definitive investigation and should be carried out in all children where a diagnosis of Hirschsprung’s disease is entertained. Contrast radiology may help determine the level of disease, particularly if performed prior to rectal examination, but often unhelpful. Mucosal biopsies show absent ganglion cells in the myenteric plexus and an increase in cholinesterase-positive (parasympathetic) nerves. A severe form of enterocolitis (Hirschsprung’s enterocolitis) may occur in infants where the diagnosis of congenital aganglionosis has been delayed, and death may result from circulatory collapse. This enterocolitis can also occur after definitive surgery. Parents should be warned of the danger of this occurring during a viral illness, which may result in anal sphincter spasm with acute obstruction. The danger of these episodes diminishes as children get older.

Definitive surgery for Hirschsprung’s may be carried out any time after birth but has traditionally been delayed until the baby reaches 10 kg. Initially, a colostomy can be sited in normal bowel to allow the baby to feed and grow, although more often nowadays conservative management is employed with frequent rectal washouts at home by parents after training. Definitive surgery involves removing the entire length of aganglionic bowel and joining normal bowel to rectum at the dentate line. After 4–6 weeks, the patient is readmitted electively for a primary ‘pull-though’ operation, typically performed with laparoscopic assistance.

Vascular ring

This is caused by a persistent double aortic arch or by abnormal configurations of vessels arising from the aortic arch. Either abnormality encircles the trachea and oesophagus causing compression. Symptoms include noisy breathing during the first few weeks and sometimes acute apnoeic events with cyanosis. Sometimes there are persistent respiratory symptoms without frank stridor, often treated as asthma or bronchiolitis. Surgery is necessary in children with severe symptoms. Mild symptoms may improve spontaneously with growth. Oesophageal symptoms include vomiting, choking or dysphagia and tend to occur in older infants and children or even into adulthood.

Congenital pulmonary airway malformations

Congenital pulmonary airway malformation (CPAM), previously known as ‘congenital cystic adenomatoid malformation’ is a rare abnormality of the lower respiratory tract affecting around 1 : 5000 live births. Patients may be discovered antenatally or present with neonatal respiratory distress or may remain asymptomatic until later life. Surgical resection where necessary is definitive treatment.

Congenital lobar emphysema

This usually affects an upper lobe of right or left lung. A weakness in a lobar bronchus allows air to enter the lobe, but bronchial collapse during expiration prevents deflation. Progressive lobar expansion compresses normal lung and leads to deteriorating respiratory function. Surgical excision of the emphysematous lobe is relatively straightforward and curative.

Exomphalos

In exomphalos, the abdominal wall defect may be large (major > 5 cm diameter) or small (minor < 5 cm). Babies may also have congenital cardiac problems, neural tube defects (spina bifida or anencephaly), chromosomal abnormalities or Beckwith–Wiedemann syndrome (gigantism, exomphalos, macroglossia, risk of neonatal hypoglycaemia and predisposition to intra-abdominal tumours, especially Wilms’ tumours).

In exomphalos major, part of the abdominal wall is missing. The defect may be up to 20 cm in diameter and can affect most of the abdominal wall. At birth the bowel is covered with a sac of amnion and peritoneum; this can rupture spontaneously in utero and present as gastroschisis. Rupture after birth is rare in Western countries but may occur in developing countries where exomphalos is likely to be treated conservatively. Rupture allows evisceration of bowel, predisposing to infection and sepsis. Treatment is described below, along with gastroschisis.

Exomphalos minor represents herniation of the umbilical cord. The bowel can be easily reduced and the abdominal wall repaired as a primary procedure. Exomphalos major and exomphalos minor are associated with chromosomal abnormalities and/or other congenital abnormalities and these determine the prognosis. Paradoxically, exomphalos minor is associated with more chromosomal abnormalities.

Gastroschisis

This abdominal wall defect is characterised by bowel herniation through a slit-like defect right of the umbilicus. There are few associated congenital problems, although babies may be small and are often premature. The defect is usually about 3 cm long and the bowel has no covering membrane (Fig. 50.9). A narrow defect may impair the intestinal blood supply in the fetus causing small bowel atresias. Malrotation or non-rotation is usually present. Antenatal exposure to amniotic fluid can cause adhesions and shortened oedematous bowel loops which may lead to intestinal insufficiency.

Ectopia vesicae (bladder exstrophy)

This is a very rare and complex abnormality present at birth, with bladder mucosa exposed on the abdominal wall and penile epispadias in boys. Pubic bones may be widely separated, causing posterior hip joint rotation. Treatment involves closing the defect, aiming to achieve urinary continence without back-pressure on the kidneys. Initially, the exposed bladder mucosa is covered with cling-film or a silicone dressing to prevent damage to the fragile urothelium, followed by early referral to a specialist centre for continuing management. Two main operations are practised in the UK: a soft tissue closure or ‘Kelly’ procedure, or the use of posterior osteotomies to facilitate soft tissue closure.

Pathophysiology

The description incarcerated means a hernia has become acutely irreducible, whereas the term strangulated implies there is also impairment of the blood supply to its contents. Strangulation can follow incarceration but luckily is uncommon in young children, unlike in adults (Fig. 50.10).

Incarcerated inguinal hernia is a common cause of acute surgical admission in boys (and sometimes girls) below the age of 2 years and may occur at any time from birth onwards. There is invariably a congenital patent processus vaginalis, i.e. the hernia is indirect, although an actual hernia may not have been evident before the acute presentation. There is a high incidence of incarceration in premature babies; 40% of hernias in the neonatal period are discovered because they become irreducible but the risk declines as a child becomes older. The high incidence of incarceration in young children is a strong argument for operating upon any hernia in this age group soon after discovery, with the need greatest in the very young.

Clinical features

When a hernia incarcerates it becomes painful, tender and irreducible. Classically, a mother discovers a firm lump in the groin in her crying (usually male) child. He may have vomited but the diagnosis is usually made before intestinal obstruction becomes established. The child is usually well with an obvious, irreducible lump in the groin (Fig. 50.10) sometimes extending into the scrotum. If bowel becomes obstructed, vomiting follows, causing fluid depletion and electrolyte disturbances. The blood supply of the incarcerated segment of intestine may become obstructed (strangulation) causing bowel infarction (Fig. 50.10b). Pressure on the spermatic cord at the external ring may cause testicular vascular obstruction, and rapid treatment is needed to prevent testicular infarction and irreversible damage.

Management

There is usually a painful, acutely tender groin swelling. The child is not systemically unwell and the hernia is neither tender nor red. At this stage, it is very unlikely that bowel has become infarcted. Emergency surgery is best avoided if possible, except in the unwell child with signs of intestinal obstruction, as the friable hernia sac makes surgery difficult and recurrence likely. Treatment involves actively reducing the hernia and performing elective herniotomy 48 hours later when oedema has resolved.

Active reduction is by gentle manipulation with the child sedated with intravenous opiates; it succeeds in about 80% but competent technique and experience are needed. The testis and hernia should be drawn towards the opposite, descended testicle, with the external ring held open with the other hand. This results in narrowing of hernial contents, allowing them to pass back through the ring with a satisfying gurgling. It is often said to be impossible to reduce necrotic bowel in a hernia, but this is untrue so it is important to carefully monitor a child for clinical deterioration after a difficult reduction, including respiratory rate and oxygen saturation. The hernia must be fully reduced; if there is doubt, or if it proves irreducible, urgent surgery should be performed. No child is too small to have surgery provided the team has been trained in paediatric surgery and anaesthesia. Note that failed reduction of an incarcerated hernia is associated with a high rate of testicular atrophy (up to 40%).

Pathophysiology

This common condition of unknown aetiology commonly occurs between 2 weeks and 2 months of age. It presents with a gradual onset of progressive pyloric obstruction over days or even a week or two, with projectile vomiting of milk following feeds. The cause is hypertrophy of mainly circular pyloric muscle, progressively occluding the gastric outlet. It occurs in about 1 in 400 normal babies with a male predominance of 4 : 1. Hereditary factors play a part since it is often found in siblings. It is also common for a parent or other close relative to have had congenital pyloric stenosis, with the risk highest in a male with an affected mother.

Prolonged vomiting results in fluid depletion and characteristic electrolyte disturbances. The loss of hydrochloric acid causes hypochloraemic alkalosis. In severe cases hypokalaemia may occur as a result of renal hydrogen/potassium exchange, in which potassium irons are sacrificed to conserve hydrogen ions. There is usually a paradoxical aciduria as dehydration causes the kidney to conserve plasma tonicity at the expense of hydrogen ions, the loss of which compound the metabolic alkalosis.

Clinical features

Typically, the infant thrives for the first 3 or 4 weeks and then begins to vomit after every feed. This characteristically becomes projectile, i.e. the vomit clears the baby’s chin. The vomitus is not bile-stained, readily distinguishing it from duodenal stenosis or atresia. The child appears well and is eager for further milk. With sustained vomiting, however, the child becomes progressively dehydrated and electrolyte depleted and loses vigour and becomes reluctant to feed. Standard examination often reveals no abdominal abnormality.

Diagnosis

Persistent vomiting leads to hospital admission, where the child’s response to feeding is observed. Diagnosis is made by carrying out a test feed, i.e. feeding the baby and palpating the abdomen at the same time. It is important to decompress the stomach first by nasogastric tube, as a dilated stomach often displaces the pylorus to lie under the liver edge. If pyloric stenosis is present, a firm mass about 2 cm in diameter (often described as olive-like) is usually palpable deeply below the liver and disappears after the feed. The condition can be detected by ultrasound, but requires a skilled operator. If the diagnosis remains in doubt, an upper gastrointestinal contrast study can reveal the typical narrow pylorus and little contrast in the duodenum.

Treatment

The natural history without surgery is for the hypertrophy to gradually resolve over several months. However, most children would die from electrolyte disturbances or malnutrition before this happened. Treatment is surgical, by Ramstedt’s pyloromyotomy—Figure 50.11—described in 1912 (Conrad Ramstedt, 1867–1963). However GA in an unprepared neonate with alkalosis and an immature respiratory drive would often result in prolonged postoperative ventilation and all its attendant risks. Operation should be performed only on a stable baby after correcting dehydration responsible for the metabolic alkalosis. The stomach should be emptied by nasogastric aspiration and washed out with normal saline to prevent further vomiting.

In the classical operation, operation is via an incision lateral to the umbilicus. Nowadays the procedure is carried out via a periumbilical incision or laparoscopically. The hypertrophied pyloric muscle is incised longitudinally and then split without breaching the mucosa (Fig. 50.11). Postoperative recovery is rapid, with full-strength milk feeding started immediately afterwards. Babies typically tolerate sufficient feeds to be discharged within 24 h. Babies with a prolonged preoperative course may develop gastritis, which may itself lead to postoperative vomiting; this may be helped by ranitidine.

Pathophysiology

Intussusception is an acquired disorder most common between the ages of 6 weeks and 2 years. There appears to be a seasonal increase in the spring and autumn. Up to 40% of children with intussusception have adenovirus infection, commoner at these times of year. Intussusception arises when a proximal segment of bowel becomes telescoped or prolapsed into the bowel immediately distal to it (Fig. 50.12). The lead point (intussusceptum) is commonly a thickening of bowel wall caused by non-specific or viral hypertrophy of Peyer’s lymphatic patches. The invaginated segment progressively elongates as it is propelled distally by peristalsis. Ileocolic intussusception is the usual variety and it commonly extends well into the transverse colon and sometimes even prolapses from the anus.

Intussusception presents with severe colicky abdominal pain. If untreated, the affected segment may undergo venous infarction over a period of hours or days. Pathology other than Peyer’s patch hypertrophy may initiate intussusception, and should be suspected in a child presenting outside the usual age range or if it recurs after radiological reduction. Ten per cent of patients have an anatomical abnormality termed a pathological lead point (PLP). In older children or adults, the initiating factor may be a bowel wall tumour or polyp. Meckel’s diverticulum or even a lymphoma may also present in this manner. Children with Henoch–Schönlein purpura (characterised by a purpuric rash on the extensor surface of the legs and buttocks and microscopic haematuria) may sometimes develop ileo-ileal intussusception.

Clinical features

Intussusception classically presents with bouts of severe colicky abdominal pain lasting for minutes during which the child is doubled up and screaming. Episodes are separated by periods when the child appears entirely well. Within the first few hours, the child often passes a small amount of jelly-like blood per rectum described as redcurrant jelly stool, which is almost pathognomonic when the other clinical features are present. Vomiting begins later, consistent with distal small bowel obstruction, but there may be profound fluid depletion even without complete obstruction. Some children with intussusception may be very drowsy, only partly explained by fluid depletion.

Diagnosis should generally be made on clinical grounds. A sausage-shaped mass is often found in the upper right quadrant with a scaphoid (hollowed) appearance in the right iliac fossa (Dance’s sign). The rectum is empty but may contain a little blood. Ultrasound may detect an intussusception and in skilled hands has a high sensitivity and specificity, but a normal result does not exclude it. An air enema and plain X-ray is quick to carry out and reliably demonstrates the condition provided it has reached the colon. Intussusception is potentially life-threatening so a definitive diagnosis must be made urgently with a view to treatment, even in children who appear initially well.

Management

Treatment needs to be prompt and active. Intravenous access should be secured early as deterioration may be imminent. Fluid resuscitation is vital even before attempting to diagnose or reduce an intussusception in an often isolated radiology department. Patients are usually given a fluid bolus of 20ml/kg of suitable crystalloid and an empirical broad-spectrum antibiotic therapy before transfer to the radiology department. The intussusception can usually be reduced using an air enema with carefully controlled pressure, performed under X-ray screening (Fig. 50.12b). Reported rates of successful reduction are as high as 90%. Radiological reduction is inappropriate if the child is unwell; in these, rapid resuscitation should be followed by laparotomy. At operation, the intussusception is reduced by gentle manipulation. Resection with primary bowel anastomosis becomes necessary if the intestine is ischaemic or if it proves impossible to completely reduce without causing major trauma to the bowel (see Fig. 50.12c).

Differential diagnosis (Box 50.2)

From childhood to adolescence, acute abdominal pain is a common cause of surgical admission. Appendicitis is usually suspected (see Ch. 26). Major differential diagnoses are acute non-specific abdominal pain (common), closely followed by mesenteric adenitis (Box 50.2). Mesenteric adenitis sometimes causes a higher fever than appendicitis and signs and symptoms usually settle within 24 hours; there is often a recent history of viral upper respiratory tract infection, and enlarged cervical lymph nodes may be palpable.

Less commonly, acute abdominal pain in this age group is caused by extra-abdominal causes such as:

Principles of management

If acute appendicitis is diagnosed when the child is first seen, operation should be performed after necessary resuscitation and giving empirical antibiotics. More commonly, the diagnosis is uncertain. In these children, urinary tract infection should be excluded by dip stick testing and the child should be re-examined at intervals and a worsening or improving trend soon becomes apparent.

Acute appendicitis (see also Ch. 26)

Acute appendicitis is uncommon in children less than 2 years of age. Anorexia is usual, although this may be absent in adolescent males, and vomiting often starts after the onset of pain. Children with appendicitis find that movement exacerbates pain. If asked to hop or jump, some children bluntly refuse, and others complain of pain. An inflamed pelvic appendix may cause secondary inflammation of rectum or bladder, causing diarrhoea or urinary symptoms. Pus cells may be found in the urine.

A full general examination must include an ear and throat assessment, chest examination, testicular examination and a search for rashes and neck stiffness. Otitis media, pharyngeal inflammation, basal pneumonia, testicular torsion or even meningitis can cause abdominal pain in children. Mesenteric adenitis can mimic appendicitis; a high fever and widespread lymphadenopathy suggest this diagnosis.

On examination the child’s breath may be foul (foetor oris) and there may be signs of dehydration or shock. The child may be pyrexial but a temperature of more than 38.5°C suggests a cause other than appendicitis, unless there is generalised peritonitis. The abdomen is often tender in the right iliac fossa with localised guarding—the cardinal feature of appendicitis. Appendiceal perforation can lead to generalised peritonitis, with guarding over the whole abdomen. Unlike adults, children often present with peritonitis, and children under the age of 5 usually have a perforation or a gangrenous appendix at operation.

A definitive diagnosis of appendicitis often cannot be made initially. Investigations are of little help other than to exclude urinary tract infection and the child may find them frightening. The white blood count and CRP are unhelpful as these are raised in other inflammatory conditions. Ultrasound has some positive predictive value but cannot exclude appendicitis, and a CT scan involves a substantial radiation burden, particularly in small children, and is not normally performed. Laparoscopy gives a precise diagnosis, but requires general anaesthesia; the procedure is better avoided if the appendix is not inflamed, as most children would agree.

In the equivocal case, the best way to diagnose appendicitis is active observation. The child is admitted and allowed to eat (because fasting ameliorates the physical signs and delays diagnosis). The child is examined every 2 hours or so, preferably by the same doctor, including abdominal palpation. By the second or third examination it is usually clear whether physical signs are getting better or worse. This approach may be used in family practice and during surgical admission. It reduces psychological trauma and the rate of unnecessary operations and ensures appendicitis is not missed until peritonitis has become all too obvious. The argument that this risks perforation, pelvic infection and infertility in girls is not borne out by fact. Active observation can select out those children with acute non-specific pain without detectable pathology and who need no active treatment, least of all surgical invasion of their peritoneal cavity.