Abdominal surgery

Intussusception

• most common form of intestinal obstruction between infancy and 5 years of age.

• caused by a segment of bowel "telescoping" into a more distal segment

• enlarged Peyer's patches due to a viral infection form the precipitating point.

• presentation:

  • acute abdomen

  • often with the child drawing up its legs

  • bloody or "red current jelly" stools

• diagnosis is confirmed by contrast enema which may actually reduce the intussusception by hydrostatic pressure.

Management

Pre-operative

• Any child with suspected intestinal obstruction should be rehydrated at once since circulatory collapse can occur within a few hours of the onset of symptoms.

• Fluid losses into the bowel, especially in intussusception can be quite significant and are commonly underestimated.

• Infants who present with signs of hypovolaemia should be fluid resuscitated rapidly with colloid, which in may include blood.

• In severe cases 20 ml/kg should be administered as rapidly as possible by syringe with careful assessment of clinical response. Often as much as 30-40 ml/kg, viz. half the circulating volume, may be needed in severe cases.

• Vascular access may be difficult in the under twos and an inter-osseous needle may be required before intravenous access is secured. The haematocrit should be checked prior to surgery, especially if large volumes of colloid have been used in resuscitation.

• Surgery can usually be delayed while gastric decompression; rehydration and correction of electrolyte imbalance take place. However in some circumstances, e.g. intussusception or volvulus, there may be a compromised blood supply to the bowel and delay can increase the chances of and danger from ischaemia, necrosis, perforation and septic shock. Occasionally the metabolic acidosis cannot be corrected until the necrotic segment of bowel has been resected

Anaesthesia

• rapid sequence induction

• extubate fully awake once the protective laryngeal reflexes have returned.

• general principles of anaesthesia for appendicitis are the same as for any acute abdomen.

• may be significant fluid loss and electrolyte disturbances secondary to vomiting in small children.

• Although uncommon in children under 6 months, when it does occur there is a significant mortality from appendicitis mainly due to associated severe dehydration.

• This requires immediate surgery to try and save the affected testis

• Anaesthetic management is the same as for any acute abdomen. However as an orchidopexy on the non-affected testis will also be performed, a caudal extradural block is an ideal form of analgesia.

• Relatively common with an incidence of 1 in 3-400 live births in some populations.

• Risk factors:

  • male (85%)

  • first born

  • family history.

• Hypertrophy of the muscularis layer of the pylorus results in increasing obstruction.

• Presention:

  •  at 3-6 weeks, although the presentation is becoming earlier.

  • vomiting

  • visible gastric peristalsis

• The diagnosis is made on the basis of the history plus palpation of an olive-sized mass in the right hypochondrium and confirmation is by ultrasound scan.

• Dehydration may be severe and cause a low cardiac output and metabolic acidosis and oliguria.

• Repeated vomiting leads to hypochloraemic alkalosis (by loss of gastric HCl) which causes increased renal bicarbonate excretion and thus increases Na⁺ excretion in the proximal renal tubule. However dehydration then results in an increase in Na⁺ reabsorption and thus increased K⁺ loss as a compensatory exchange mechanism. Respiratory compensation for the metabolic alkalosis may result in hypoventilation and even apnoea.

Management

• Pyloric stenosis is a medical, and never a surgical emergency.

• Rehydration with 0.9% saline and correction of the electrolyte abnormalities is paramount. This may take up to 24-48 hours, and sometimes as long as 3-4 days.

• Surgery should be delayed until biochemical values reach:

  • pH 7.3-7.5

  • Na⁺ >132mmol/l

  • Cl^- >90mmol/l

  • K⁺ >3.5mmol/l

  • HCO₃^_ <30mmol/l

• NG tube to empty the stomach and thus reduce the risk of regurgitation and aspiration.

Anaesthesia & post operative care

• Rapid-sequence induction or inhalational induction.

• Extubate when the infant is wide-awake and able to protect its airway.

• Analgesia: intra-operative fentanyl (1-3m g/kg) plus surgical infiltration with 0.25% plain bupivicaine, as well as regular post-operative paracetamol is usually sufficient.

• Oral feeding can usually be commenced within 6-12 hours post-operatively.

• Post-operative respiratory depression is occasionally seen but this is probably related to incomplete pre-operative electrolyte correction and cerebro-spinal alkalosis.

• Incomplete return of gut to abdominal cavity during foetal life resulting in varying degrees of intestinal herniation into the umbilical cord.

• The gut is covered with a thin membrane, although this may be ruptured.

• Often associated with prematurity (30%) and other congenital abnormalities, especially:

  • other GIT malformations (25%)

  • GU anomalies (25%)

  • congenital cardiac disease (10%)

  • Beckwith-Wiedemann syndrome (exomphalos, macroglossia and profound hypoglycaemia.)

Herniation of the intestine through a defect in the lateral abdominal wall, usually on right. It is not covered by a membrane nor associated with other congenital abnormalities.

Management

• Problems include:

  • high heat and fluid losses, fluid requirements may be doubled and there may be significant protein loss from bowel.

  • may be difficult to replace abdominal contents without causing respiratory embarrassment, if this is so then repair of the abdominal wall defect is completed in stages. The exomphalos is gradually reduced over several days, encased in Prolene mesh.

  • increased intra-abdominal pressure after gut replacement may decrease venous return and cause:

    • decreased cardiac output

    • renal failure

    • hepatic impairment

    • lower limb oedema.

  • prolonged post-op ileus is not uncommon and parenteral nutrition may be required for several weeks.

Anaesthesia

• thorough pre-operative fluid resuscitation

• intubation, paralysis and manual ventilation (which facilitates the early detection of excessive reduction in lung compliance due to increased intra-abdominal pressure).

• nitrous oxide should be avoided due to its effects on bowel gas and a combination of air/oxygen plus volatile agent used.

• all IV lines should be in the upper limbs due to the risk of developing lower limb oedema.

• post-op ventilation should continue until the abdominal pressure and distension diminishes.

• usually a disease of the low birth weight premature infant.

• characterised by intestinal mucosal injury secondary to gut ischaemia, which may then proceed to perforation and peritonitis.

• severe fluid and electrolyte disturbances as well as endotoxic shock and coagulopathy follow.

• risk factors include:

  • birth asphyxia

  • respiratory distress

  • shock

• abdominal distension is often profound

• bloody stools and bilious vomiting are common.

• intramural gas seen on an abdominal X-ray confirms the diagnosis.

Management

• These babies are usually already intubated and ventilated on the NICU but special anaesthetic considerations include the correction of:

  • hypovolaemia

  • acidosis

  • coagulopathy

• Nitrous oxide should be avoided

• Beware of interactions of antibiotics such as gentamycin with non-depolarising muscle relaxants.

• Pre-operative fluid losses are usually underestimated and significant volumes (which will usually include blood) may be needed intra-operatively.

• Ventilation should be continued post-operatively on the NICU.