Surgical problems

Published on 03/06/2015 by admin

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CHAPTER 23 Surgical problems

Mark Davies, Garry Inglis

Bile

Bile may appear in vomitus or in aspirates from gastric tubes. Bilious vomiting should always be considered as potentially serious, especially in a previously well baby when an acute volvulus should be suspected and ruled out.

Generally speaking, the presence of bile that has made its way into the stomach (and is seen in vomitus or gastric tube aspirates) indicates that the gut is obstructed. This obstruction may be complete or partial, and may be anatomical or functional (i.e. with a still patent lumen).

For anatomical causes of obstruction see pages 131–3.

Functional gut obstruction can occur in babies in the following circumstances:

• gastrointestinal perforation (see below)
• necrotising enterocolitis (NEC; see below)
• post-surgical
• any baby that is generally unwell (especially with infection)
• gut immaturity, especially in babies <30–32 weeks gestational age.

Sometimes bile is seen in aspirates when the feeding tube sits at or has passed through the pylorus — this can be confirmed on an abdominal X-ray. In an otherwise well baby, this can be fixed by pulling the tube back so that its tip lies in the body of the stomach.

Determining cause

Significant causes of bile vomiting or bile-stained aspirates need to be distinguished from benign causes (such as a malplaced nasogastric tube or gut immotility due to immaturity) by examining the baby, and doing an abdominal X-ray and a full blood count (FBC) and film examination (and taking a blood culture and starting antibiotics if there is any suspicion of infection).

• Benign causes will usually be found in babies who are otherwise well with a soft, non-distended, non-tender abdomen that is not discoloured, who are passing normal stools.
• Significant causes may be associated with one or more of:

— an unwell baby
— an abnormal abdominal exam — distended, tender or tense, discolouration, mass, absent bowel sounds
— an abnormal abdominal X-ray — evidence of gastrointestinal perforation or necrotising enterocolitis, fluid levels, bowel distension
— an abnormal FBC — signs of infection, thrombocytopaenia.

Gastrointestinal perforation

Extremely preterm infants are prone to gastrointestinal perforation, which can occur in isolation or, more commonly, in association with necrotising enterocolitis (NEC; see below). If intestinal perforation is found, it does not automatically follow that NEC is present. It can be difficult to distinguish the two conditions pre-operatively, and risk factors are similar.

• Clinically the abdomen with perforated bowel and hence free peritoneal gas is almost always ‘smooth’ in appearance. When bowel loops are visible through the abdominal wall, often described as a ‘ropey’ abdomen, free gas is usually not present.
• In a plain supine X-ray of the abdomen, the presence of free gas in the peritoneal cavity (pneumoperitoneum) is demonstrated as a grey outline around the abdominal edge, with the falciform ligament visible in the upper abdomen to the right of the midline. This gas shadow is sometimes called the ‘football’ sign. Remember that the plain abdominal film is not usually taken erect, so don’t waste your time looking for a rim of free gas under the diaphragm. If in doubt, a right-side-up lateral decubitus film may be helpful as the gas may rise above the right lobe of the liver.
• ‘Double-shadowing’ of bowel walls is also indicative of free gas in the abdominal cavity — the Frimann-Dahl sign or Rigler’s sign. Normally only the mucosal surface of the bowel is contrasted by the presence of gas; free gas abutting the serosal surface creates another interface, giving rise to the characteristic double-shadow.
• Suspicion of free gas within the peritoneal cavity should also be raised where an unusually shaped shadow is present — i.e. if the gas shadow does not conform to any anatomical structure.

The management of infants with gastrointestinal perforation should include:

• stopping enteral feeds
• nasogastric tube with regular aspiration
• intravenous fluids
• antibiotics (after blood culture)
• immediate review by a paediatric surgeon; encourage them to do a laparotomy.

Necrotising enterocolitis (NEC)

This inflammatory disorder of the bowel has multifactorial causes. The extremely preterm infant is at greater risk.

There is a wide spectrum of clinical features in NEC. Signs can include feeding intolerance, vomiting, lethargy, temperature instability, abdominal distension, diarrhoea with or without frank blood, abdominal wall erythema and shock.

The Bell criteria are often used to classify the severity of the illness:

• Stage 1 — suspected NEC (generally unwell with feed intolerance and/or non-specific abdominal signs, ±bloody stool, but no pneumatosis)
• Stage 2 — definite NEC (unwell with definite abdominal signs and pneumatosis)
• Stage 3 — advanced NEC (severely ill with shock, marked abdominal signs, and ascites or intestinal perforation).

In general terms, large-bowel NEC is a much more benign illness than small-bowel NEC.

The characteristic radiographic findings are pneumatosis intestinalis and portal venous gas. Pneumatosis intestinalis represents gas in the submucous layer produced by intestinal bacteria.

• There are three patterns of pneumatosis intestinalis:

— the circle of submucous gas in a cross-section of bowel viewed end on;
— a ‘tram-track’ appearance of submucous gas in bowel viewed in longitudinal section; and
— a ‘whorl’ pattern seen when looking through a bowel wall with pneumatosis in it.

• Submucosal gas is sometimes absorbed into the portal venous system and travels to the liver, where it can be evident on a plain radiograph. It can also be detected with real-time ultrasound.
• Other radiographic signs to look for in NEC are generalised or local distension from ileus, separation of bowel loops by extra intraperitoneal fluid, and pneumoperitoneum from perforation (see section on intestinal perforation).

Treatment of NEC consists of:

• stopping enteral feeds
• nasogastric tube with regular aspiration
• intravenous fluids
• antibiotics (after blood culture) — traditionally ampicillin, gentamicin and metronidazole
• frequent clinical review
• surgical intervention — evidence of perforation or ischaemic bowel (e.g. a persistent dilated loop) is an absolute indication for this.

Gut obstruction — anatomical causes

Gut obstructions are usually anatomical and congenital. The presenting features of gut obstruction will depend on the anatomical level of the obstruction. In general: the higher the obstruction, the earlier is the presentation; and the lower the obstruction, the more impressive is the abdominal distension.

Some obstructions (e.g. oesophageal atresia, imperforate anus, duodenal atresia) are often associated with other congenital anomalies or may occur as part of recognised syndromes (e.g. VATER, CHARGE, Down syndrome). Many anatomical obstructions, particularly those in the mid to lower small bowel, are thought to result from in-utero vascular events. Also, the presence of one gut atresia makes a second atresia more likely in the same baby. Always examine the baby carefully for associated anomalies.

Oesophageal atresia

Oesophageal obstructions often present with difficulty feeding and the baby is frequently described as being excessively ‘mucusy’.

• If oesophageal atresia is suspected, insert a large (8–10FG) tube into the oesophageal pouch. The tube will stop at around 10 cm from the mouth. A narrow tube may coil in the upper oesophageal pouch without resistance being felt, which can falsely lead to the assumption that the oesophagus is patent. Always obtain a chest and abdominal X-ray.
• Some like to perform an air oesophagogram to demonstrate the oesophageal pouch: inject 20 mL of air quickly as the X-ray exposure is made.
• The presence of gas in the stomach indicates that a distal tracheo-oesophageal fistula is present.
• Mechanical ventilation may result in distension of the stomach via the fistula, which can result in gastric rupture.

— Ventilate as gently as possible and request an early paediatric surgical review.
— Insert a large-bore catheter (e.g. a Replogle tube) for continuous suction, nurse prone and give parenteral fluids.
— Almost all infants will have residual problems with gastro-oesophageal reflux and oesophageal dysmotility.

Proximal bowel obstruction

Proximal intestinal obstructions present with early onset of vomiting and distension of the upper abdomen. The vomiting may be bile-stained or non-bile-stained, depending on whether the obstruction is distal or proximal to the ampulla of Vater.

Pyloric stenosis

Pyloric stenosis is uncommon in neonates. It causes non-bile-stained ‘projectile’ vomiting.

• If suspected, examine for a palpable pyloric tumour and visible upper abdominal peristaltic waves.
• Ultrasound examination can be used to measure the length and thickness of the pyloric muscle.
• Intravenous fluids may be needed.
• Check arterial blood gas (ABG) and electrolytes.

Duodenal atresia

Duodenal atresia presents soon after birth with persistent vomiting, which is usually bile-stained.

• Insert a nasogastric tube and aspirate — there will usually be a large volume of fluid.
• Give intravenous fluids. Monitor electrolytes.
• On a plain supine radiograph there will be a J-shaped shadow, representative of gas in a distended stomach and duodenum, with absence of gas more distally. The typical ‘double bubble’ is demonstrated on an erect film.
• Paediatric surgical intervention is required.

Jejunal/ileal atresia

Distal small-bowel atresia presents later than duodenal atresia. Bile-stained vomiting and abdominal distension are typical. With more distal obstructions, fluid and electrolyte disturbance at presentation is more likely.

Malrotation

Malrotation with volvulus can present from soon after birth to several months later. Features include bile-stained vomiting and variable abdominal distension. If the mesenteric vascular supply is compromised the infant can rapidly progress to peritonitis and shock, with gangrene of the bowel.

• This is a medical emergency that must be recognised and treated urgently to avoid potentially catastrophic ischaemic bowel injury.
• A plain abdominal radiograph may show a dilated stomach and proximal duodenum. The appearance of a malrotation with volvulus can be indistinguishable from that of duodenal atresia. However, the latter can be excluded by the appearance of gas more distal to the obstruction.
• An upper gastrointestinal contrast study can be useful in defining the nature of the obstruction, but do not allow this to delay a paediatric surgeon seeing the baby.
• Start intravenous fluids and antibiotics. Many will require parenteral nutrition.

Baby of mother with polyhydramnios

The cause of polyhydramnios is usually not known. It can be associated with maternal conditions such as diabetes or pre-eclampsia.

• In most instances where there is an underlying fetal cause it should be fairly obvious clinically once the baby is born. As you examine the baby, think of why he/she might have had reduced fetal swallowing or increased urine output.
• The most commonly identified cause is upper gastrointestinal obstruction (especially oesophageal or duodenal atresia — see above). Can you pass a feeding tube into the stomach?
• Central nervous system defects (e.g. anencephaly, neuromuscular disorders affecting swallowing) should be quite obvious, as should abdominal wall defects, severe skeletal dysplasias and chromosomal abnormalities.
• Examine the infant for evidence of respiratory tract abnormalities (e.g. congenital cyst-adenomatoid malformation), congenital diaphragmatic hernia or cardiac anomalies.
• Polyhydramnios may be associated with hydrops fetalis. In multiple gestation, consider twin–twin transfusion syndrome.
• Monitor urine output to check for polyuric renal disorders.

Delayed passage of meconium

The normal time to passage of meconium increases with decreasing gestational age (GA).

• At term, first passage of meconium should occur by 48 hours.
• Below 32 weeks GA, up to half may not pass meconium until beyond 48 hours, and some may take up to 10 days.

Common causes of delayed passage of meconium include anorectal malformations, Hirschsprung disease and meconium ileus. All can present also with vomiting and abdominal distension.

Diagnosis

Always examine the perineum and anus carefully.

• The finding of meconium in the nappy does not exclude anal atresia, as it is often associated with a recto-perineal, recto-vesical or recto-vaginal fistula. An ‘anal’ dimple, usually more anterior than normal, can be mistaken for an anus but the diagnosis of this condition need not be difficult.

— If imperforate anus is present, abdominal X-ray will often show dilated bowel with or without gas in the rectum, depending on the length of the atretic segment.
— Keep ‘nil by mouth’ and give intravenous fluids.
— Check for associated anomalies.
— Seek specialist neonatal and paediatric surgical advice.

• The diagnosis of Hirschsprung disease may be more difficult. These infants usually have delayed passage of meconium with or without vomiting and abdominal distension. In milder cases there may be a history of recurrent constipation.

— If suspected, get an abdominal X-ray, which may show dilated loops of bowel but is generally non-specific. Likewise, a lower bowel contrast study is also generally not specific for any particular diagnosis. However, if contrast material is still present on a late film (24 hours after the contrast study), it makes Hirschsprung disease the most likely diagnosis, as normal bowel motility would usually evacuate the contrast material quickly after such a study.
— The typical appearance of a narrowed distal segment with more proximal dilatation may not become apparent in the neonatal period. Rectal suction biopsy is usually performed to confirm absence of ganglion cells prior to more definitive repair — seek paediatric surgical advice.
— If the baby is unwell, stop feeds, check electrolytes, give intravenous fluids and give antibiotics.

• Meconium ileus is suggested by the delayed passage of (thick, inspissated) meconium, with or without abdominal distension and vomiting.

— The abdominal X-ray often shows dilated loops of bowel but with an absence or paucity of gas in the right iliac fossa due to the presence of the inspissated meconium, which can appear granular.
— A contrast enema may show a microcolon, indicating that the colon has not had any solid contents in it for a long time, and may be effective in relieving the obstruction.
— Complicated meconium ileus (e.g. volvulus, atresia, perforation) will require surgical intervention.

Gastroschisis

The major risks to the infant with gastroschisis are compromised circulation to the gut, gut obstruction, loss of heat and water from the exposed bowel, and infection.

Therefore, the important aspects of the immediate management of a baby born with gastroschisis are:

• Manage any respiratory problems as for babies without gastroschisis — some surgeons would prefer that you avoid nasal continuous positive airway pressure (CPAP).
• Make sure that the external bowel is not twisted on itself (usually occurs at the abdominal wall defect).
• Support the gut so that the external bowel is not being stretched.
• Cover the bowel — either put baby in a ‘bowel bag’ up to the chest, or cover with polyethylene kitchen-wrap/cling-wrap.
• Insert a nasogastric tube, leave on free drainage and aspirate every 15 minutes.
• Intravenous antibiotics (metronidazole, gentamicin, penicillin).
• Maintenance intravenous fluids.

Call a paediatric surgeon prior to delivery if the diagnosis was made antenatally, otherwise call them as soon as you can after the baby is stabilised.

The sooner the gut is reduced, the better.

Congenital diaphragmatic hernia (CDH)

The diagnosis is usually known before birth. If not, it should be suspected immediately after birth in a baby who requires resuscitation with initial respiratory distress, rapid deterioration (cyanosis, bradycardia, pallor), poor response to resuscitation, right-sided heart sounds (if a left CDH) and a scaphoid abdomen.

Immediate management should include:

• Intubation and ventilation.
• Insert a gastric tube to empty stomach of air (and keep empty).
• Surfactant.
• Sedation (morphine and midazolam).
• Admit to the intensive care nursery.
• Ongoing ventilation is managed as for pulmonary hypertension (see p 60).
• Surgery to close the diaphragm and relocate the abdominal contents should be delayed for a few days until the baby is stable.

The primary problem in CDH is the pulmonary hypoplasia. In babies with a left-sided hernia (∼85%), there is gross hypoplasia of the left lung and significant hypoplasia of the right lung — surgery will not cure this. The hypoplastic lungs have a reduced number of poorly formed peripheral air spaces and abnormal pulmonary vasculature: this results in poor ventilation and severely restricted pulmonary blood flow.

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