NEONATAL EMERGENCIES

Dr Jacinta Shung

A neonate can be regarded as an infant of less than 44 weeks post conceptual age or a
full term that is < 1 month old. For the purposes of this lecture slightly older infants will
be included. Although neonates seldom present for surgery those who do usually have a
multitude of problems. Cognisance must be taken of their unique physiology and
different anatomy

The conditions which may require surgery include:

™ Necrotizing enterocolitis (NEC)
™ Congential diaphragmatic hernia (CDH)
™ Gastroschisis or omphalocoele
™ Pyloric stenosis
™ Bowel atresia
™ Colostomy for anorectal malformation or rectal duplication or Hirshsprung’s disease
™ Malrotation or volvulus of bowel
™ Tracheo‐oesophageal fistula
™ Inguinal hernia – elective or incarcerated/strangulated
™ Congenital lobar emphysema or cystic adenomatous malformation
™ Direct laryngoscopy
™ Choanal atresia
™ Pierre Robin for glossopexy
™ Meningomyelocoeles and VP shunts

Each of these conditions has specific problems as well as problems related to the
neonatal period as a whole.

NECROTIZING ENTEROCOLITIS

This condition is found mainly in sick premature infants. It is the commonest surgical
emergency in neonates. Mortality is 10–30%. A variety of reasons cause reduced
mesenteric blood flow leading to bowel necrosis. There are a number of associated
factors such as birth asphyxia, apnoea, systemic infections, early feeding with high
osmolar feeds, respiratory distress syndrome and umbilical vessel cannulation. Breast
fed infants have a lower incidence of NEC due possibly to the transfer of
immunoglobulins which coat and protect the gut mucosa and the transfer of beneficial
bacteria from the mother. Low birth weight (<1500g) is the commonest cause of NEC.
Management is conservative (NPO, TPN, NGT, antibiotics, abdominal decompression
with a drain, fluid resuscitation) but up to 50% will require surgery.

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Indications for surgery are:
™ Intestinal perforation as evidenced by pneumoperitoneum
™ Haemodynamic instability despite adequate medical resuscitation
™ Severe sepsis
™ Abdominal mass with persistent signs of obstruction
™ Intestinal stricture
™ Increasing abdominal distension with abdominal wall discolouration

Infants who present for surgery are very ill and are usually already intubated and
ventilated. They maybe anaemic, thrombocytopenic (if severe this is a poor prognostic
sign), septic, hypotensive, hypovolaemic, hypoxic and have renal dysfunction.

Special Anaesthetic Points:

™ Blood – Check adult size unit not paediatric unit is in theatre
™ Platelets if needed, platelet set
™ Good IV line, if in doubt insert central line
™ Massive volume requirements in excess of circulating volume
™ Avoid N2O
™ Regional not an option
™ Very sensitive to volatile agents, may need narcotic muscle relaxant technique
™ Will require post‐op ventilation
™ These infants often become severely hyperglycaemic especially in the postoperative
period. This is associated with a poorer outcome.

CONGENITAL DIAPHRAGMATIC HERNIA

CDH is a very common anomaly (1:2500). It can syndromic (isolated) or nonsyndromic

(nonisolated). Diaphragmatic fusion is completed during the 8th to 9th week of gestation.
The majority of CDHs occur through the foramen of Bochdalek (80%) at the
posterolateral aspect of the diaphragm. Herniation can occur through the foramen of
Morgagni (substernal). Bilateral hernias are usually fatal (1%). The primary pathology is
not due to compression of the lungs by herniated viscera. This is a secondary
phenomenon and is preceded by impairment of lung growth. In animals there is a lack of
FGF 10 which is lung fibroblast growth factor that causes branching of the airway and
development of airway smooth muscle. A now banned herbicide, nitrofen, increases the
incidence of CDH. Nitrofen affects the retinoic pathway and a diet deficient in vitamin A,
at least in rats, will induce a CDH. The “dual hit” hypothesis proposes that there are 2
pathologies that result in the morbidity and mortality ie underdevelopment of the lungs
as well as the diaphragmatic defect.

Survival depends on the degree of lung hypoplasia and pulmonary vascular abnormality.
Severe persistent PHT accounts for 75% of all deaths. One third of all CDHs will have
some other congenital abnormality. Another factor affecting survival is the presence and
severity of congenital heart disease or some other major anomaly. One fifth of infants
will have a cardiac defect, most commonly a patent ductus arteriosus. A small
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percentage will have Cantrell’s Pentalogy viz: 1) cardiac defect usually tetralogy of Fallot;
2) absent pericardium; 3) CDH; 4) sternal cleft; 5) omphalocoele. Infants with CDH and a
cardiac defect have a mortality rate of 73% vs 27% in those without. Fifty percent of
babies with CDH are stillborn or die very soon after birth. The mortality remains high
despite recent advances (40%).

Prenatal diagnosis and imaging studies can give an indication of outcome. This is very
dependent on the competence of the ultrasonographer. Factors that are associated
prenatally with a poor outcome are:
1. diagnosis before 24 weeks
2. liver herniation into the thorax (48% mortality vs 93% survival if not herniated)
3. LHR (lung to head ratio) <0.8 at 24‐26/52 gestation = 100% mortality. LHR >1.4
has no mortality. Measure X‐sectional area of contralateral lung to head
circumference.

Other predictors that are not or not yet as reliable are foetal MRI and echo to measure
lung volumes, LV mass and PA diameters.

CDH is no longer a surgical emergency. Early surgery makes no impact on survival.

Infants are given a “trial of life”. They are stabilized and attempts are made to reduce
pulmonary hypertension by:
1. Oxygenation,
2. “Gentle” ventilation (Pi <25mmHg to try to prevent barotrauma and improve
venous return).
3. Permissive hypercapnia (<60‐65mmHg) even allowing infants to breathe
spontaneously in between pressure limited ventilator breaths*
4. HFOV or HFPPV can be tried if “gentle” ventilation fails ie pH <7.25; pCO2
>60mmHg; O2 saturation <80% and severe respiratory distress*
5. Sedation and analgesia to reduce catecholamine levels
6. Maintenance of temperature
7. Extracorporeal membrane oxygenation (ECMO) if above failed. These patients
however did not do well long term (respiratory, feeding and
neurodevelopmental problems).
8. iNO, pharmacotherapy eg steroids, surfactant have been disappointing
* Boloker’s criteria

Those with severe the pulmonary hypoplasia with congenital heart disease and
persistent pulmonary hypertension have a low survival rate. These infants are not
candidates for surgery.

Postnatal predictors of poor survival include:

1. Severe respiratory distress within 6 hours after birth requiring intubation and
ventilation
2. <1kg
3. <33/52 gestation

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4. Ventilation index >1000 preop and postop (within 2 hrs).
VI = RR x Mean airway pressure (Bohn)
5. Hypercarbia (>40mm Hg), pre‐op and within 2 hours of surgery requiring
aggressive ventilation (ventilatory pressures of >20 H2O and frequencies in excess
of 60b/min) (Bohn).
6. Post surgical pre‐ductal P(A‐a) DO2 >300mm Hg (90% mortality) (Bohn)
Favourable Bohn’s criteria are associated with 86% survival. Neonates who have poor
predictors are not presented for surgery.

“The Honeymoon Period”: This refers to the immediate postoperative period where the
infant seems to improve or stabilize. This is followed by severe pulmonary
hypertension which is unresponsive to treatment.

Special Anaesthetic Points:

™ Avoid vigorous mask bag ventilation – gastric distension and further compression of
lungs
™ Seldom need blood in theatre if hernia is small but must have an adult unit on
standby
™ Avoid lower extremity IV access as IVC can be compressed with return of viscera to
and closure of abdomen
™ Abdominal approach, seldom need to open chest
™ “Gentle ventilation”: this prevents barotrauma. If this does not work HFOV may have
a role but these infants usually have a poor prognosis.
Ventilator settings: PIP <25 cm H2O; RR <65/min; inspiratory time 0.35s; PEEP <2 cm
H2O; pH >7.25
™ Permissive hypercapnia up to 60mm Hg to avoid barotrauma
™ Keep warm
™ Avoid light anaesthesia
™ Avoid N2O
™ Sudden postoperative deterioration may be due to pneumothorax on contralateral
side
™ Ventilate postop unless very small hernia in a baby who is otherwise coping well
™ Keep MABP >45 mmHg (despite age being < MAP)
™ Inotropic support if required

Long term sequelae:

Most survivors have reasonable pulmonary function despite reduced lung function
parameters. They are often growth retarded and suffer other sequelae:
neurodevelopmental delay; GERD; deafness (ototoxicity of drugs); cardiac complications
– PHT; chronic lung disease.

FETO (foetal endoluminal tracheal occlusion): This has largely been abandoned except
for a few centres where their results are good. The foetal trachea is obstructed with a
balloon to encourage lung growth. It was found that infants with pharyngeal or laryngeal
stenosis and CDH had better outcomes as their lungs were less hypoplastic. The balloon

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must be puncture at 34/52 as prolonged occlusion reduces type II alveolar cells and
reduces the production of surfactant.

GASTROSCHISIS AND OMPHALOCOELE

These conditions result in a defect of the abdominal wall. The differences between the
two conditions are tabulated below.

Gastroschisis Omphalocoele
Caused by occlusion of Caused by failure of gut migration
omphalomesenteric artery from yolk sac into abdomen
Abdominal wall defect lateral to base Herniation of abdominal contents
of umbilical cord, cord remains intact into base of umbilical cord
Bowel is functionally abnormal Bowel is usually normal
No membrane over viscera Viscera within umbilical cord
1:30 000 live births 1:8 000 live births
60% premature 30% premature or LBW
Few associated anomalies or 2/3 have anomalies (NB CVS) or
syndromes associated syndromes eg
Beckworth‐Weidemann,
trisomy13 or 15, Pentalogy of
Cantrell

Successful management of these infants starts immediately after birth. They must be
kept warm, npo, fluid loss is replaced and the abdominal contents protected from
damage (physical, infective or dehydration). The physiological disturbance can range
from minimal to massive fluid and electrolyte derangements. Preop the abdomen is
wrapped in plastic and the abdominal contents kept moist and warm.

Special Anaesthetic Points:

™ Except for the smallest of defects, blood is needed in theatre
™ Do not site IV line in lower extremities
™ Decompress stomach with ngt if none present
™ Avoid N2O
™ Fluid requirements can be enormous especially with gastroschisis
™ Large defects are not closed as the increased intra‐abdominal pressure may decrease
organ perfusion (liver, kidneys, bowel) and affect ventilation. Venous return can also
be compromised. The viscera are placed in a pouch and gradually reduced over a few
days after which the abdomen is closed.
™ Staged closure should be considered if reduction of the viscera causes any of the
following: a CVP rise of more than 4mmHg, intragastric or intravesical pressure rise

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 by more 20mmHg, difficulty with ventilation, mottling of the legs or cessation of
urine output.
™ Monitor glucose if baby has Beckwith‐Weidemann syndrome, may need up
10mg/kg/min.

PYLORIC STENOSIS

Pyloric stenosis is a medical but not a surgical emergency it presents at about 40‐49
weeks post‐conceptual age, males > females. The post‐anaesthetic complication rate
(mainly apnoea) is largely determined by the adequacy of the pre‐operative
resuscitation.

Pathophysiology: Muscular hypertrophy of the gastric outlet causes projectile vomiting.

These infants can present with:
™ severe dehydration
™ chloride‐ (saline‐) responsive hypochloraemic metabolic alkalosis
™ hyponatraemia (usually mild)
™ hypokalaemia (hypovolaemia → aldosterone release)
™ malnutrition

When the stomach produces acid an equivalent amount of HCO3 – is produced by the
pancreas. As there is a gastric outlet obstruction with pyloric stenosis, the bicarb is not
lost with the acid (HCl) that is vomited. In an attempt to maintain pH, the urine is initially
alkaline. As dehydration worsens the intravascular depletion leads to aldosterone
secretion. Potassium is exchanged for sodium (and along with it water is absorbed),
chloride is absorbed with the sodium to maintain electrical neutrality. The kidneys
exchange even more potassium for hydrogen in an attempt to maintain pH. Continued
chloride loss from the vomiting will cause the kidneys to maximally conserve chloride.
The urinary chloride is low (<20meq/l) as chloride is also exchanged for bicarb. As
dehydration continues, the kidney increases its ability to absorb bicarb proximally and
loses hydrogen distally (under aldosterone control). Additionally the PaCO2 rises in
response to the metabolic alkalosis and enhances renal tubule acid secretion. All this
results in a paradoxically acid urine.

Correction of the metabolic derangement consists of rehydration with normal saline

(NS). If the deficit is mild to moderate (5‐15% ie 50‐150ml/kg), half the deficit is given
over 6‐8 hours. More severe dehydration (>15% ie >150ml/kg) is treated with a bolus of
20ml/kg and then half the deficit over 6‐8 hours. Adequate rehydration can take a few
days in severe cases. The pH, potassium and chloride usually begin to correct with NS
rehydration. Occasionally a large potassium deficit will require replacement before the
alkalosis will respond to NS. Potassium is only administered once urine output is
established. A maximum of 3 meq/l/day is replaced. Hypoglycaemia is a danger as the
hepatic glycogen stores are depleted. Once the infant is rehydrated, maintenance fluid
with potassium supplementation is started.

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Special Anaesthetic Points:
™ If barium swallow performed (seldom done as sonar is preferred), the stomach must
be emptied preop with a large bore orogastric tube and the baby turned from side
to side to ensure adequate removal of barium
™ Once the urine chloride is >20meq/l, resuscitation is adequate and surgery can be
booked
™ An infant that presents with a metabolic acidosis is in imminent danger of collapse.
™ Post‐anaesthetic apnoea will occur if the alkalosis is not improved pre‐operatively.
™ Chloride should be >95meq/l (alkalosis will only reverse when chloride is 105meq/l)
™ pH<7.5
™ Base excess <6mmol/l
™ Serum bicarb <30mmol/l
™ Rapid sequence induction or awake intubation
™ Perfalgan and infiltrate wound with LA for analgesia
™ Monitor for postop apnoea

OBSTRUCTIVE LESIONS

The condition of infants with bowel obstructions will depend on the underlying
pathology and associated anomalies. Except for a well infant for a loop colostomy all
these infants should have blood in theatre or at the very least on standby. The
anaesthetic management will depend on the pathology.

HERNIA REPAIR

Premature infants have a 30% chance of incarceration of an inguinal hernia. The debate
is when to operate. Surgeons would like to operate as soon as possible because of the
risk of incarceration and anaesthesiologists would prefer to delay surgery because of the
risk of post operative apnoea. The timing of surgery should be discussed by both parties
taking into account the infant’s co‐morbid state.

Special Anaesthetic Points:

™ Prematurity
™ Postop apnoea
™ GA vs regional
™ Awake regional vs asleep
™ Caudal vs spinal

TRACHEOESOPHAGEAL FISTULA

1:4 000 live births of whom 25% have CVS anomaly and 25% are prem.

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Associated with VACTERL syndrome. They present with excessive salivation, cyanosis
and a ng tube does not enter the stomach. Feeds are stopped and the oesophageal
pouch suctioned. Antibiotics are started if aspiration has occurred.
Classification of TOF (Gross):
Type A: 8% pure oesophageal atresia no involvement of trachea
Type B: <1% oesophageal atresia with fistula connecting proximal pouch to
trachea
Type C: 80% oesophageal atresia with fistula connecting distal pouch to
trachea
Type D: 2% two fistula connecting proximally and distally to trachea
Type E: 4% H‐type, no atresia, fistula to trachea

Prognostic criteria (Spitz):

Group I: Wt >1.5kg no cardiac anomaly survival = 99%
Group II: Wt <1.5kg no cardiac anomaly survival = 82%
Group III: Wt <1.5kg with cardiac anomaly survival = 50%

Investigation:
Bloods, CXR, cardiac echo

Anaesthetic Management:
This is one of the few indications for an awake intubation. However an asleep nasal
intubation is usually performed. Often the exact position of the fistula is not known. The
patient is kept breathing until tube placement is correct. PPV can distend the stomach
through the fistula and make ventilation very difficult. If the fistula is very low the infant
is kept breathing spontaneously for as long as possible. If hypoxia is a problem then IPPV
is started. The stomach may require decompression via a gastrostomy or on occasion
when there is no gastrostomy via the ETT. A gastrostomy can make ventilation difficult
as volume is lost into it. The gastrostomy is then intermittently clamped. Fortunately few
require gastrostomies. The bevel of the ETT can be turned so that it faces anteriorly and
the post wall of the ETT seals off the fistula. Occasionally a fogarty is needed to seal off
the fistula.

Once the ETT is well secured the patient is turned onto the L side with the right arm over
the head. The ECG electrodes and diathermy pad must be positioned out of the surgical
field. A small rolled up swab is placed under the chest to open up the chest. Air entry
must be checked as a R lung intubation will result in no ventilation once the R lung is
collapsed intra‐op. A precordial steth is taped to the L axilla to check for tube placement
intra‐op. A R thoracotomy is performed and the approach is retropleural. It may be
necessary to intermittently inflate the R lung ‐ always warn the surgeon first. Tidal
volume should be kept small. The anastomosis is done over a large bore ngt (Replogle
type). It may be necessary to manipulate the ngt during surgery to locate a very high
fistula. Thorascopic repair can be done. In such cases arterial line placement is desirable
to monitor BP and for sampling of CO2 as ET CO2 is falsely low. CO2 retention is often a
problem. Hypoxia can occur with OLV.
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Inability to ventilate or poor oxygen saturation may be cause by:
™ Kinking of the trachea or ETT by retractor
™ Compression of the R lung
™ Blood or secretions in ETT
™ Contra lateral pneumothorax
™ ETT displaced down R bronchus – no ventilation as R lung collapsed down

Temperature and fluid loss is large with an open procedure. Once the repair is done the
R lung is re‐inflated under vision. The neck is kept flexed (esp while moving) so as not to
stress the anastomosis. The patient is ventilated postop as there has been a period of
OLV and there may also be pneumonia. Other reasons for ventilation include apnoea,
requirement for the patient to remain motionless.

Very rarely is a primary anastomosis not possible because the infant is too small or the
oesophagus too short. One of two approaches can be used. 1) A proximal draining pouch
and a gastrostomy is made and the baby returned for repair at 1 yr of age or 9 kg wt. 2)
The oesophagus is brought out posteriorly through the chest wall! A stitch is placed
through the proximal end and the oesophagus placed on traction until it is long enough
to anastomose (few days).

There is a high incidence of oesophageal stricture and dysmotility. Chronic aspiration is

also a problem. Restrictive and obstructive lung disease is also common.

CONGENITAL LOBAR EMPHYSEMA

Hyperinflation and air trapping occurs in the affected lobe which does not take part in
gas exchange. Compression of the adjacent lung and the mediastinal shift can result in
haemodynamic compromise.

Sites: LUL >> RML>RUL

DDx: pneumothorax or CDH or congenital cystic adenomatous malformation (CCAM)
Age: <6 mo
Management: lobectomy

Anaesthetic Management
Will depend on the degree of compromise. Induction is the critical phase as a crying
struggling infant will increase air trapping. Spontaneous ventilation is maintained and
gentle PPV (low pressure and long expiratory time) applied only if absolutely necessary.
N2O is absolutely C/I. Once the chest is opened IPPV can be started. The surgeon must
be present at induction in the event that the lobe suddenly expands and requires urgent
decompression. Decompression under ketamine and LA can be undertaken in very
compromised infants. Anaesthesia is then induced and lobectomy preformed. There is
no place for palliation with repeated decompression (needle or ICD).

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DIRECT LARYNGOSCOPY

Neonates who require DL usually have stridor or marked respiratory distress due to
some form of obstruction. A neonate with stridor may have bilateral choanal atresia or
stenosis. Laryngomalacia is the commonest cause of stridor in the neonatal period. The
loudness of the stridor is also not always an indication of the severity of the obstruction.
Quietening stridor and laboured breathing makes the situation more urgent.

The timing of the stridor in the respiratory cycle may indicate the level of the
obstruction. Inspiratory stridor usually indicates supraglottic obstruction. This is caused
by the collapse of nonrigid soft tissues above the glottis by the negative pressure
generated during inspiration. Expiratory stridor may indicate an obstruction at the
trachea or distal airways.
Biphasic stridor indicates a glottic or subglottic (at or above the cricoid ring) obstruction.
Improvement in the prone position may indicate laryngomalacia or a vascular ring.

Atropine is given to dry secretions, counteract the vagal response to airway

instrumentation and also to help maintain cardiac output should there be a bradycardia
from deep halothane anaesthesia.

Where appropriate good topicalization of the airway with lignocaine will help smooth
the examination.

The patient with an obstructed airway should breathe spontaneously and muscle
relaxants used only once ventilation is possible after the airway has been secured. There
is the question of which volatile agent should be used, halothane vs sevoflurane. The
case for sevoflurane is that it allows for a more rapid less irritant induction and it is more
cardiac stable. Proponents for halothane prefer its greater potency which allows for a
deeper level of anaesthesia and also as it more fat soluble its offset is slower which
allows for a longer time to instrument the airway. Halothane also causes less upper
airway obstruction in paediatric patients than sevoflurane. The downside is its cardiac
depressant effects and potential dysrhythmogenic properties in the presence of
hypercapnia. N2O should be avoided. A deep level of anaesthesia may take a long time
to establish because of the obstruction.

All anaesthetic agents decrease upper airway muscle activity. This results in varying
degrees of upper airway collapse. Some agents affect muscle tone even at small doses
eg isoflurane whereas other drugs do so in a dose dependent manner eg propofol.
Propofol decreases both central respiratory output to upper airway dilator muscles as
well as decreasing upper airway reflexes. In infants upper airway patency is very
dependent on central neural control. Propofol depresses this mechanism more than it
does in older children. Thus infants are very susceptible to upper airway obstruction if
propofol is administered.

Once anaesthesia is induced obstruction may worsen as a result of loss of muscle tone.
Application of CPAP may help to splint the airway open eg laryngomalacia. Pharyngeal
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obstruction will not be relieved by an LMA if there is an anatomical problem / mass in
the pharynx. Anaesthesia must be deep before laryngoscopy is performed.

CHOANAL ATRESIA

These infants are pink when they cry and dusky when quiet. A suction catheter will not
pass through the nostrils. An oral airway is strapped in place and an orogastric tube is
placed for feeding. These babies cannot suck without becoming hypoxic (obligate nose
breathers). This is not a surgical emergency. Care should be taken to ensure that the
pharynx is kept well suctioned and that feeding tubes are correctly placed. These
neonates may be syndromic eg CHARGE association (coloboma, heart anomaly, choanal
atresia, mental and growth retardation, genital anomlies, ear anomalies). Post op
ventilation will be required. The neonate is intubated with an oral RAE ETT. No throat
pack is inserted. ETT’s are placed in the nostrils after the passage is opened up. The ends
of the ETT are pulled out orally, stitched together and pulled up into the posterior nasal
space. The ETTs are cut off at the nose and stay sutures secured to the cheek with
plaster. The infant will return either for decannulation or redilatation.

PIERRE ROBIN SYNDROME

These neonates can present an extreme airway challenges. They have mandibular
hypoplasia, micrognathia and glossoptosis. Most do not require surgery however a tiny
minority will require airway management in the form of either glossopexy,
tracheostomy or mandibular distraction. The prone position may the only position
where the airway is patent. They may of course also require intubation for some other
neonatal emergency.

Special Anaesthetic Points:

™ Vagal hyperreflexia
™ At risk for aspiration because of reflux or swallowing difficulties
™ Cardiac anomalies
™ Apnoea (central or obstructive)
™ Facemask seal difficult
™ Insertion of oral airway difficult
™ Laryngoscopy very difficult
™ Subglottic stenosis
™ Airway control may need
ƒ Nasopharyngeal airway
ƒ LMA
ƒ Intubation with Miller blade using right paraglossal approach and a bougie
– needs practise
ƒ Intubation with FOB – most places do not have a 2.2mm FOB
™ Needs ICU or high care postop to monitor airway

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MENINGOMYELOCOELE REPAIR

Although this is not a true emergency it is a semi‐elective emergency as closure is

required to minimize the risk of infection. The procedure is done within the first few
days of life. A VP shunt may be done at the time or a few days after the initial surgery if
ICP rises (more often than not).

Special anaesthetic points:

™ Have blood in theatre unless it is a tiny defect. Large skin flaps are undermined to
allow for closure and this bleeds profusely.
™ The body may need to be raised or the head turned sideways to allow for intubation.
™ Good venous access with extension sets
™ Procedure is done in the prone position. Pad or free up pressure points, check ETT is
secured and not kinked, check ventilation.
™ Hypothermia is a problem

ISSUES TO CONSIDER IN NEONATAL ANAESTHESIA

POST–OPERATIVE APNOEA

Former preterm infants who present for surgery are at risk for post‐op apnoea (POA).
The postconceptual age (PCA) as well as the postgestational age is important. Exprems
of 48/52 PCA have a 5% chance of POA. This decreases to <1% at 55/52 PCA. Infants at
higher risk are the exprems who are very young, those with Hb<10g/dl, those with a
history of apnoea or respiratory problems. All exprems younger than 48/52 should be
monitored for at least 12 hours after surgery or after any apnoeic episode. An infant
who was very premature and had a stormy postgestational course should probably be
considered at risk until 60/52 PCA.

Intra‐operative factors that increase the risk of POA include:

™ GA. Although POA has been described in infants undergoing regional anaesthesia
™ Hypothermia, hypoxia, hypoglycaemia, hypocalcaemia, acidosis and hypercarbia
™ High ventilatory pressures
™ Sedative agents

These at risk infants are not candidates for day stay anaesthesia or for admission to
hospitals that do not have neonatal ICU facilities. Although the use of aminophylline or
caffeine to prevent POA is widely practised it is not universally accepted. The use of
these agents do not abolish POA completely and monitoring for 12 hours is still required.
A full term infant who has any respiratory episode after surgery should be regarded as at
risk and also monitored for 12 hours.

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RETINOPATHY OF PREMATURITY

Retinopathy of prematurity (ROP) is not related entirely to hyperoxia as infants who

have never been exposed to supplemental oxygen have developed ROP. The at risk
group is the sick LBW baby who has been exposed to oxygen for an extended period of
time. ROP is rare in infants born after 30/52 PCA. There are many causes for ROP
including candida sepsis, blood transfusions and hypoxia. The retina only matures at 42
to 44 weeks postconception. It has been suggested that elective surgery be delayed until
after 44/52 PCA or if surgery cannot be delayed then to maintain oxygen saturations
between 93 and 95% to prevent hyperoxia. Despite these concerns oxygen must not be
withheld if the child is at risk for hypoxia.

HYPOTHERMIA

Neonates are at significant risk for hypothermia not only during surgery but pre‐
operatively as well. The neonate who is difficult to drip often becomes very cold (34°C!)
if active measures are not taken to keep the child warm. These include warming the
theatre, only exposing the area being worked on, wrapping the other areas and actively
warming the baby. During surgery a wet baby will become hypothermic. We try to
“waterproof” the non operated on area by sealing it off with plastic and waterproof
plaster. The surface area of an infant’s head is 20 % of BSA so keeping the head wrapped
(eg stockinette hat) will help to reduce heat loss.

Hypothermia can worsen pulmonary hypertension by increasing oxygen consumption

and worsening hypoxia. Other problems associated with hypothermia include
prolongation of action of drugs, apnoea, decreased surfactant production and raised
SVR.

Critical Temperature: ambient temperature below which an unclothed,

unanaesthetized patient cannot maintain temperature.
Neutral temperature: temperature at which O2 consumption is minimal

Temperature Premature Term Adult

Critical temp (°C) 28 23 1
Neutral temp (°C) 34 32 28

INTRAVENTRICULAR HAEMORRHAGE

Premature infants are at risk for intraventricular haemorrhages. It is unknown whether

anaesthetic practices can contribute towards these bleeds. As the outcome of infants

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with large bleeds is poor, it is prudent to avoid factors which may cause these bleeds.
Risk factors include:
™ Awake intubation. It has been argued that the rise in anterior fontanelle pressure
during crying is comparable to that during awake intubation.
™ Any sudden severe hypertension eg awake neonatal circumcision; no analgesia in a
premature infant who also has a coagulation defect.
™ Large increases in osmolarity eg rapid bolus of hypertonic sodium bicarbonate or
dextrose water with concentrations >10%.
™ Large fluctuations in oxygen tension

POTENTIAL CARDIAC SHUNTS

All neonates who present for surgery are at risk for paradoxical air emboli as the
foramen ovale maybe functionally but not anatomically closed. Half of all 5 year olds will
have a probe patent foramen ovale. Infants with congenital intracardiac shunts are at
particularly high risk. Care must be taken when connecting IV lines, flushing and injecting
of drugs to avoid injection of air bubbles. A bubble trap should be used with high risk
patients especially if a fluid warmer is used.

ANALGESIA

All babies feel pain even the premature ones. The expression of and assessment of pain
maybe difficult in this age group. This is however no excuse not to give analgesia. Local
anaesthetic infiltration and regional techniques are very useful.
Paracetamol:. The PO or PR dose is reduced to a maximum of 60 mg/kg/day for 5 days or
less; loading dose of 20mg/kg and maintenance dose of 15mg/kg six to eight hourly.
Intravenous paracetamol has been shown to be safe and effective in neonates. Clear
dosing guidelines are not available but preliminary data suggest the following to be safe
(Stockholm protocol):

PCA (weeks) Dose Interval

28‐32 7.5mg/kg 8 hourly
33‐36 7.5mg/kg 6 hourly
≥ 37 10‐15mg/kg 6 hourly

Opiates can be used but respiratory depression is a real risk. Adequate postop
monitoring and resuscitation facilities are needed if neonates are given opiates.

Neonatal Emergencies 14
Dr J Shung
2009 Part II Refresher Course
OXYGEN TOXICITY

Hyperoxia has been shown to be dangerous in neonates. Oxygen causes tissue damage
by the formation of reactive oxygen intermediates that cause lipid peroxidation, DNA
damage and protein sulfhydryl oxidation. Excess oxygen can cause neuronal death;
pulmonary oedema and atelectasis; bronchopulmonary dysplasia; apnoea in neonates;
ROP; survival was poorer after resuscitation with 100% oxygen versus room air. Oxygen
saturation in neonates should be kept between 85 and 95%. Having said all this oxygen
should not be withheld in a hypoxic patient.

Neonatal Emergencies 15
Dr J Shung
2009 Part II Refresher Course