Read Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice Online
Authors: Simon Paterson-Brown MBBS MPhil MS FRCS
Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice (58 page)
Assessment
The diagnosis of peritonitis in the neonate is complicated by a number of factors, including the patient's inability to communicate with the surgeon, as well as several anatomical and physiological differences between neonates and older children/adults. The very thin abdominal wall may develop oedema and erythema as a result of underlying inflammation. Neonates breathe primarily with their diaphragms, so peritonitis results in rapid, shallow respiration, and ultimately will cause elevation in pCO
2
and respiratory failure. Localised peritoneal signs can be elicited by palpation, but the examiner must be gentle, since the signs of involuntary guarding may be very subtle. In addition, the neonate does not have a well-developed omentum, so ability to localise inflammation may be impaired.
Neonates with peritonitis will often develop systemic sepsis, which may differ in its presentation from that in older children and adults. Signs of sepsis in neonates may include lethargy, temperature instability (either fever or hypothermia), increased ventilation requirements, thrombocytopenia, a high or low white blood cell count, and acidosis.
Meconium peritonitis:
This condition occurs when there has been prenatal intestinal perforation, resulting in chemical peritonitis. Prenatally there may be evidence of free fluid or calcification within the abdomen. In some cases, the foetus is able to localise and wall off the perforation, which may result in a meconium cyst. The aetiology of the perforation is often distal obstruction, usually from meconium ileus or intestinal atresia, but in some cases the perforation is idiopathic.
Management of meconium peritonitis involves fluid resuscitation, nasogastric drainage and antibiotics. If there is evidence of associated intestinal obstruction, a contrast enema may be helpful preoperatively. Laparotomy should be performed, with resection of the involved bowel and either stomas or primary anastomosis, depending on the condition of the child and the bowel.
Necrotising enterocolitis:
Necrotising enterocolitis (NEC) is most commonly seen in low-birth-weight and small-for-gestational-age infants.
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The aetiology of NEC is unknown, but a combination of bacterial colonisation, intraluminal substrate and intestinal ischaemia/hypoxia all appear to be important.
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NEC should be suspected in neonates with sepsis, increased abdominal girth, feeding intolerance, abdominal wall discoloration or bloody stools. Abdominal radiograph may show pneumatosis intestinalis, portal venous gas or free intra-abdominal air (
Fig. 12.4
). It is convenient to classify the severity of NEC using the Bell classification (
Table 12.2
), which helps to guide treatment and may assist the surgeon in decision-making about operative intervention.
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Table 12.2
Bell stages of necrotising enterocolitis (NEC)
Reprinted from Bell MJ, Ternberg JL, Feigin RD et al. Neonatal necrotizing enterocolitis. Therapeutic decisions based upon clinical staging. Ann Surg 1978; 187(1):1–7. With permission from Wolters Kluwer Health.
Figure 12.4
Abdominal radiographs of infants with necrotising enterocolitis.
(a)
Pneumatosis intestinalis.
(b)
‘Football sign’ on supine film depicting intra-abdominal free air.
(c)
Free intra-abdominal air on lateral film.
Initial management of NEC includes bowel rest, nasogastric decompression, broad-spectrum antibiotics, parenteral nutrition, and supportive measures to optimise perfusion and oxygenation of the bowel. Persistent clinical deterioration and signs of necrosis or perforation are generally considered indications for operative intervention. Options include bedside peritoneal drainage, or laparotomy with resection of grossly necrotic bowel and either primary anastomosis or stomas, depending on the status of the child and the bowel.
11,
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A recent randomised control trial in neonates less than 1500 g with perforation found no significant difference in outcomes between peritoneal drainage and laparotomy.
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Before laparotomy parents should always be informed of the possibility of a long segment of necrosis requiring massive resection that would leave the child with short-bowel syndrome. Palliative management should then be considered in these infants.
Isolated ileal perforation:
This condition resembles NEC, in that it primarily affects preterm and small-for-gestational-age infants. However, infants with isolated ileal perforation do not have any abnormalities of the intestine other than localised perforation, usually in the distal ileum. It is unclear whether this represents a very localised form of NEC or a distinct entity. Clinically, these infants present with sudden deterioration, sepsis and free air without any evidence of pneumatosis seen on the abdominal radiograph. In general, the same principles of treatment are applied to ileal perforation and NEC.
Incarcerated inguinal hernia
Inguinal hernias are very common throughout childhood. Hernias in children almost always arise from persistence of the processus vaginalis. If the processus contains only fluid, it is known as a hydrocele; the hydrocele is communicating if the processus remains open and non-communicating if the processus has become obliterated proximal to the fluid. Communicating hydroceles should be repaired electively if they have not closed by 1 year of age.
In most cases, inguinal hernias are asymptomatic and can be repaired electively. Incarceration of bowel may result in complete bowel obstruction, and represents a surgical emergency since both the bowel and the testis may become ischaemic. The risk of incarceration is greatest in newborns and is approximately 30% in the first 2 years of life. Premature infants are at highest risk.
Neonates and infants presenting with an incarcerated hernia should be resuscitated if necessary, and an immediate attempt should be made to reduce the hernia. In contrast to the adult with an incarcerated hernia, testicular ischaemia is far more common than intestinal ischaemia, and it is appropriate to be aggressive about reducing the hernia. Multiple attempts and the use of sedation may be necessary. Ice should not be applied to the hernia, since it may induce hypothermia. Surgical repair of an incarcerated hernia in an infant is a formidable undertaking. The sac is often thin and oedematous, and the risks of injury to the cord structures and recurrence of the hernia are very high. Therefore, if a general surgeon is unable to reduce the hernia and a paediatric surgeon is accessible, the patient should be referred immediately.
If the hernia is reduced, repair should be undertaken 24–48 hours later, allowing some of the oedema to settle, but hopefully before re-incarceration.
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Gastroschisis is characterised by an abdominal wall defect to the right of the umbilicus, through which most of the intestinal tract protrudes.
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Omphalocele (also called exomphalos) is characterised by herniation of bowel with or without solid organs, into the umbilical cord. Gastroschisis tends to be an isolated anomaly, whereas omphalocele is often associated with chromosomal, cardiac, renal, limb and facial anomalies.
If the diagnosis is made prenatally, delivery should occur at a centre with paediatric surgical support. Resuscitation and nasogastric decompression should begin in the delivery room. The bowel or sac should be wrapped in warm, saline-soaked, sterile gauze and covered with sterile plastic wrap to minimise heat and evaporative fluid loss.
Repair of both conditions should be undertaken by an experienced paediatric surgeon. Options include primary closure, or staged closure using a Silastic® silo that allows the bowel to be reduced gradually into the abdomen over 1–6 days.
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Hypertrophic pyloric stenosis
Hypertrophic pyloric stenosis (HPS) is an acquired condition in which the pylorus becomes abnormally thickened, causing gastric outlet obstruction. This occurs in infants during the first 2–12 weeks of life and is characterised by projectile, non-bilious vomiting usually occurring after feeds. HPS occurs in approximately 1:400 children, with a significant male predominance.
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Diagnosis is suspected based on a history of progressive, forceful, non-bilious vomiting in a child of the appropriate age. Physical examination usually reveals some level of dehydration. The presence of a palpable ‘olive’ in the epigastrium has a 99% positive predictive value for the disease.
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Vomiting of gastric contents leads to depletion of sodium, potassium and hydrochloric acid, resulting in the typical hypochloraemic, hypokalaemic metabolic alkalosis. The kidneys attempt to conserve sodium at the expense of hydrogen ions, often leading to paradoxical aciduria.
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The level of dehydration can be estimated by clinical examination, urine output, and serum chloride and bicarbonate levels. If the pyloric olive is not palpable, the diagnosis can be confirmed by ultrasound (pyloric length > 16 mm and single wall thickness > 3 mm). If an experienced sonographer is not available, the diagnosis can be made using a barium swallow (
Fig. 12.5
).
Figure 12.5
Images of hypertrophic pyloric stenosis.
(a)
Abdominal ultrasound.
(b)
Upper gastrointestinal contrast study.
Surgery should be deferred until the infant is fully resuscitated. This is accomplished by using normal saline or Ringer's lactate with potassium. Most children should receive a bolus of 20 mL/kg, and then an infusion consisting of 1.5 times the maintenance requirement (i.e. 6 mL/kg/h for this age group) until the urine output and electrolytes have been normalised.
Surgical management of HPS consists of extramucosal longitudinal splitting of the pyloric muscle. The original procedure described by Ramstedt in 1912 was performed through a transverse right upper quadrant incision. This technique has been modified in many institutions to utilise circumumbilical incisions and, more recently, laparoscopic techniques.
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Following pyloromyotomy, many infants will experience continued vomiting for 24–48 hours, although the majority will eventually tolerate feeds and be discharged. Postoperative complications are rare but include wound infection, duodenal or gastric perforation and incomplete pyloromyotomy.
Intussusception, or ‘telescoping of the bowel’, occurs when one portion of bowel invaginates into a more distant portion. This results in venous congestion, bowel wall oedema, intestinal obstruction and ultimately full-thickness necrosis of the intussusceptum. The peak incidence of intussusception is seen at 6–9 months of age.
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The majority are ileocolic with hyperplastic lymphoid tissue in Peyer's patches acting as a lead point.
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These are often referred to as ‘idiopathic’. Asymptomatic small-bowel to small-bowel intussusception may be seen incidentally on abdominal ultrasound, or sometimes may be associated with Henoch–Schonlein purpura or cystic fibrosis. Less than 5% of intussuceptions are due to a pathological lead point such as a Meckel diverticulum, polyp or small-bowel tumour such as lymphoma or leiomyoma. Intussusception occurring outside of the usual age range, or those that recur, should raise suspicion for a pathological lead point.
Few children with ileocolic intussusception will demonstrate the classic triad of intermittent severe abdominal pain with drawing up of the legs, palpable abdominal mass and ‘redcurrant jelly’ stool. Physicians must therefore have a high index of suspicion due to the variability of symptoms. Patients may present with irritability, lethargy, abdominal pain, vomiting, diarrhoea or constipation, haematochezia, fever, dehydration or shock. Management should initially focus on diagnosis and resuscitation.
Following fluid resuscitation, imaging should be performed to confirm the diagnosis of intussusception. Abdominal radiograph may show air-fluid levels and distention of the small bowel and there may be a characteristic lack of air in the right lower quadrant. Ultrasonography has a high sensitivity and is currently the investigation of choice.
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Traditionally, the treatment of intussusception has been barium enema. More recently, pneumatic reduction using air or CO
2
has been associated with an 80–95% success rate.
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If the intussusception is partially but not completely reduced it is worth trying again a few hours later, since some of the oedema may have been eliminated by the first attempt and a second attempt may be associated with a 50% chance of success.
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Pneumatic pressures of 60–100 mmHg are recommended.
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Surgical intervention is reserved for those patients who fail hydrostatic or pneumatic reduction, or who have signs of infarcted or perforated bowel such as peritonitis or free air on abdominal radiograph at the time of presentation. At laparotomy, the intussusception is manually reduced if possible. If the intussusception is not reducible, the bowel appears necrotic or a pathological lead point is identified, a segmental resection should be performed with primary anastamosis. Recently some authors have documented excellent results using a laparoscopic approach to this condition.
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