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Paediatric Anaesthesia
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Neonatal Anaesthesia

Fetal circulation physiology - PVR SVR, PDA-dependent lesions, transition challenges Immature organ systems - Low lung compliance, immature cardiac calcium handling, impaired thermoregulation Pharmacokinetic...

Updated 3 Feb 2026
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Neonatal Anaesthesia

Quick Answer

What is unique about neonatal anaesthesia?

Neonatal anaesthesia requires understanding of developmental physiology, distinct from paediatric and adult practice. Key considerations include:

  1. Fetal circulation physiology - PVR > SVR, PDA-dependent lesions, transition challenges
  2. Immature organ systems - Low lung compliance, immature cardiac calcium handling, impaired thermoregulation
  3. Pharmacokinetic differences - Higher Vd, immature enzyme systems, different receptor expression
  4. Airway considerations - Large tongue, high larynx (C3-C4), narrowest at cricoid
  5. Specific surgical emergencies - CDH, TEF, omphalocele with unique physiological challenges

Clinical Pearl: The neonate is not a "small adult" - expect the unexpected. Cardiovascular collapse can occur rapidly due to limited cardiac reserve.


Clinical Overview

Definition

Neonatal anaesthesia encompasses the perioperative management of infants from birth to 28 days of life. This period represents the most rapid physiological transitions in human development, including the conversion from fetal to neonatal circulation, establishment of pulmonary gas exchange, and adaptation to extrauterine metabolic demands.

The Transition Period

The immediate neonatal period (first 24-72 hours) presents the greatest anaesthetic risk due to ongoing cardiovascular, respiratory, and metabolic transitions.

Cardiovascular Transition

Fetal StateNeonatal StateClinical Implication
PVR > SVRPVR < SVRPVR reduction allows PDA closure; delayed closure causes R→L shunt
Ductus arteriosus openDuctus arteriosus closingCritical for duct-dependent lesions
Foramen ovale openForamen ovale closingAtrial R→L shunt decreases
Right ventricular dominantLeft ventricular dominantCardiac output dependent on left heart
Placental circulationPulmonary circulationPulmonary blood flow increases 10-fold at birth

Critical Concept: Delayed PVR reduction occurs in hypoxia, acidosis, hypothermia, and lung disease - creating potential for persistent pulmonary hypertension of the newborn (PPHN).

Epidemiology

Neonates represent a small but high-risk surgical population:

  • Surgical volume: Approximately 2-3% of all paediatric surgical procedures [1]
  • Mortality: 10-30× higher than older children for similar procedures [2]
  • Prematurity: 30-50% of neonatal surgery performed on premature infants [3]
  • Emergency ratio: 60-70% of neonatal surgery is emergency/emergent [4]

Fetal and Neonatal Physiology

Cardiovascular Physiology

The Fetal Circulation

The fetal circulation is designed for placental gas exchange:

  1. Oxygen delivery: 80% of well-oxygenated blood directed to brain and coronary arteries via preferential streaming

  2. Right-to-left shunting: Essential for bypassing the non-functional lungs

    • Ductus venosus (15% cardiac output)
    • Foramen ovale (30-40% cardiac output)
    • Ductus arteriosus (90% right ventricular output bypasses lungs)
  3. PVR vs SVR: Fetal PVR equals or exceeds SVR, maintaining right-to-left flow

Transition to Neonatal Circulation

First breath and lung expansion:

  • Mechanical stretch and oxygen trigger pulmonary vasodilation
  • NO and prostacyclin release reduce PVR dramatically
  • Pulmonary blood flow increases from 8-10% to 50% of cardiac output [5]

Clamping of umbilical cord:

  • Removes low-resistance placental circulation
  • Increases SVR and left ventricular afterload
  • Promotes functional closure of foramen ovale

Ductus arteriosus closure:

  • Functional closure: 10-15 hours (95% by 72 hours)
  • Anatomical closure: 2-3 weeks
  • Delayed closure occurs with hypoxia, acidosis, prematurity, and prostaglandins

Neonatal Cardiac Function

Key differences from adults:

ParameterNeonateAdult
Resting heart rate120-160 bpm60-80 bpm
Stroke volumeFixed, rate-dependentVariable
Cardiac output300-400 mL/kg/min70-90 mL/kg/min
Contractile reserveLimitedSubstantial
Myocardial compliancePoor (stiff ventricles)Good
Calcium dependenceGreater (immature SR)Less
Response to hypoxiaBradycardia, reduced contractilityTachycardia

Clinical Implication: Neonates cannot increase stroke volume effectively. Bradycardia = ↓ cardiac output = cardiovascular collapse. Always treat bradycardia aggressively.

Respiratory Physiology

Developmental anatomy:

  • Alveoli: 20-50 million at term (adult: 300 million) - limited surface area
  • Airways: Compliant chest wall, compliant airways, high closing capacity
  • Surfactant: Synthesis begins at 24 weeks, mature at 35 weeks
  • Diaphragm: Type I fibres only 10% (vs 50% in adults), fatigues easily

Mechanical properties:

  • Compliance: Low lung compliance, high chest wall compliance → unstable FRC
  • Work of breathing: 2-3× higher per kg than adults
  • Oxygen consumption: 6-8 mL/kg/min (vs 3-4 mL/kg/min in adults) [6]

Control of breathing:

  • Immature respiratory centre response to hypoxia (initial hyperventilation followed by apnoea)
  • Paradoxical response to CO2 in first weeks of life
  • Periodic breathing and apnoea common, especially in prematurity

Thermoregulation

Brown adipose tissue (BAT):

  • Major site of non-shivering thermogenesis
  • Located between scapulae, neck, and around great vessels
  • Metabolically active, rich in mitochondria with uncoupling protein 1 (UCP1)
  • Consumes O2 and glucose to generate heat

Heat loss mechanisms:

  • Large surface area to volume ratio
  • Thin skin, limited subcutaneous fat
  • Inability to shiver

Critical Temperature: Neonates cannot compensate below 23°C ambient temperature. Hypothermia causes:

  • Increased oxygen consumption (200-300%)
  • Metabolic acidosis
  • Pulmonary vasoconstriction
  • Coagulopathy
  • Impaired drug metabolism

Renal Function

Immature renal handling:

  • GFR: 40-50% of adult values, matures over 2 years
  • Concentrating ability: Limited to 600-700 mOsm/kg (vs 1200 in adults)
  • Sodium handling: Obligate sodium losers (immature tubules)
  • Drug elimination: Reduced clearance of renally-excreted drugs (e.g., morphine, paracetamol)

Hepatic Function

Metabolic limitations:

  • Glycogen stores: Limited; deplete within 6-12 hours
  • Gluconeogenesis: Limited capacity, vulnerable to hypoglycaemia
  • Drug metabolism: Reduced P450 activity, immature glucuronidation
  • Protein synthesis: Low albumin → increased free drug fraction
  • Coagulation: Vitamin K-dependent factors (II, VII, IX, X) low at birth

Pharmacology in Neonates

Key pharmacokinetic differences:

AspectNeonate vs Adult
Volume of distribution↑ Higher (higher TBW, immature protein binding)
Protein binding↓ Lower (low albumin, high bilirubin, free fatty acids)
Metabolism↓ Slower (immature P450, reduced enzyme activity)
Elimination↓ Reduced (low GFR, immature tubular function)
BSA/kg↑ 2.5-3× higher (affects topical/transdermal absorption)

Drug-specific considerations:

DrugNeonatal Consideration
Thiopental↓ Protein binding, ↑ sensitivity, prolonged duration
PropofolRisk of propofol infusion syndrome at lower doses
Volatile agents↓ MAC values (MACneonate ≈ 1.3× adult MAC at term, ↓ in premature)
Suxamethonium↓ Pseudocholinesterase activity, prolonged duration
AtracuriumHofmann elimination less affected; preferred NMBA
Morphine↓ Clearance (50%), ↑ half-life, risk of apnoea
Paracetamol↓ Glucuronidation, ↓ clearance; avoid >60 mg/kg/day

Specific Surgical Conditions

Congenital Diaphragmatic Hernia (CDH)

Pathophysiology

CDH results from failure of the pleuroperitoneal folds to fuse during the 8th week of gestation, allowing abdominal contents to herniate into the thorax.

Lung hypoplasia:

  • Direct compression by herniated viscera
  • Pulmonary hypoplasia (reduced airway generations and alveoli)
  • Type II cell hypoplasia → surfactant deficiency
  • Pulmonary vascular remodeling → PPHN

Hemodynamic consequences:

  • Pulmonary hypoplasia and PPHN → persistent R→L shunting
  • Right ventricular dysfunction
  • Duct-dependent systemic circulation in severe cases

Clinical Presentation

FindingSignificance
Respiratory distress at birthImmediate presentation in 50-60%
Scaphoid abdomenAbsent abdominal contents
Bowel sounds in chestDiagnostic clue
CXR: bowel loops in thorax, mediastinal shiftConfirmatory
Prenatal diagnosis (US)50-60% diagnosed antenatally [7]

Severity markers:

  • Lung-to-head ratio (LHR) on prenatal US: <1.0 = poor prognosis
  • Observed/Expected LHR (O/E LHR): <25% = high mortality
  • Liver position: Intrathoracic liver = worse prognosis [8]

Anaesthetic Management

Preoperative stabilization ("gentle ventilation"):

The key principle is avoiding barotrauma while maintaining oxygenation:

ParameterTarget/Strategy
Peak inspiratory pressure (PIP)<20-25 cmH₂O
PEEP3-5 cmH₂O
Respiratory rate40-60 breaths/min
FiO2Titrate to SpO2 80-95% (avoid hyperoxia)
Permissive hypercapniaPaCO2 45-60 mmHg acceptable

Clinical Pearl: High PIP causes pneumothorax in CDH patients due to compliant hypoplastic lungs. "Gentle ventilation" reduces mortality from 60% to 20-30% [9].

High-frequency oscillatory ventilation (HFOV):

  • Alternative for failing conventional ventilation
  • Maintains FRC with lower pressure amplitudes
  • Reduces barotrauma

Nitric oxide (iNO):

  • Selective pulmonary vasodilator
  • Dose: 20 ppm
  • Early use in PPHN associated with improved outcomes [10]

ECMO:

  • Salvage therapy for refractory hypoxia
  • Venoarterial or venovenous
  • Criteria: OI >40 for 4 hours or >60 for 1 hour

Surgical repair timing:

  • Delayed repair preferred (48 hours to 7 days)
  • Allows pulmonary vascular reactivity to stabilize
  • Earlier repair only for severe obstruction/strangulation

Anaesthetic technique:

  1. Monitoring:

    • Arterial line (pre- and post-ductal saturation monitoring)
    • Central venous access
    • Temperature monitoring (maintain 36.5-37.5°C)
  2. Induction:

    • Avoid N2O (expands bowel, increases PVR)
    • IV opioids (fentanyl 2-5 mcg/kg) to blunt PVR response
    • Muscle relaxation (rocuronium 0.6-1 mg/kg)
  3. Maintenance:

    • Low-dose volatile (avoid cardiovascular depression)
    • Opioid-based technique preferred
    • Minimize airway pressures
  4. Postoperative:

    • Continue mechanical ventilation 24-72 hours
    • Monitor for rebound PPHN
    • Prepare for ECMO if deterioration

Specific complications:

ComplicationPrevention/Management
PneumothoraxLimit PIP, early chest drain if suspected
PPHN crisisAvoid hypoxia/acidosis, iNO, consider sildenafil
Cardiac failureInotropes, milrinone for RV dysfunction
Reperfusion injuryExpect post-repair deterioration

Tracheo-Oesophageal Fistula (TOF)

Anatomy and Classification

TOF results from failed separation of the foregut into trachea and oesophagus during the 4th week of gestation.

Classification (Gross types):

TypeAnatomyFrequency
A (C)Oesophageal atresia (OA) with distal TEF85%
BOA only, no fistula8%
C (A)OA with proximal TEF1%
DOA with proximal and distal TEF1%
E (H-type)H-type TEF without OA4%
FOesophageal stenosisRare

Memory Aid: Most common = "C" (as in Common) - OA with distal TEF.

Associated Anomalies (VACTERL)

50-60% of TOF patients have associated anomalies [11]:

ComponentFrequencyEvaluation
Vertebral20%Spinal X-ray
Anal atresia15%Clinical exam
Cardiac30-35%ECHO (critical!)
Tracheal10-20%Bronchoscopy
Esophageal (Renal)15%Renal USS
Radial/Renal25%Renal USS
Limb10%Clinical exam

Critical: Cardiac anomalies (especially right-sided aortic arch) alter surgical approach and prognosis.

Pathophysiology

Proximal OA:

  • Accumulation of secretions → aspiration risk
  • Cannot feed orally
  • Requires continuous suctioning

Distal TEF:

  • Gastric distension from air shunting
  • Reflux of gastric contents into lungs
  • Chemical pneumonitis
  • Risk of aspiration pneumonia

Preoperative Management

Suction and positioning:

  • Replogle tube (10-12 Fr) in proximal pouch
  • Continuous low-pressure suction (-20 to -30 cmH₂O)
  • Head-up position (30-45°)
  • Avoid positive pressure ventilation if possible

Timing of surgery:

  • Stable patients: Primary repair within 24-48 hours
  • Unstable: Delayed repair with gastrostomy
  • Absolute indication: Respiratory compromise from gastric distension

Anaesthetic Management

Preoperative assessment:

FactorAssessment
PrematurityGestational age, weight
PneumoniaCXR, work of breathing
Cardiac lesionECHO mandatory
Other VACTERLSpine, renal, limb exam
Gastric distensionClinical assessment

Airway management - THE CRITICAL STEP:

High-Risk Scenario: Intubation can cause gastric overdistension → respiratory failure → cardiac arrest.

Technique:

  1. Spontaneous ventilation induction (unless full stomach risk deemed higher than reflux risk)

    • Maintain spontaneous breathing until fistula isolated
    • Use volatile agent (sevoflurane) or gentle IV technique
  2. Intubation:

  • Appropriate-sized ETT (usually uncuffed 3.0-3.5 for term neonate)
    • Position ETT BELOW the fistula (carina or right main bronchus)
    • Verify position with auscultation + EtCO2 waveform
  1. Fistula identification:
    • Surgeon passes catheter through mouth to identify pouch
    • Once identified and ligated, convert to controlled ventilation

Alternative airway strategies:

TechniqueIndication
Fogarty catheterIntubate fistula, inflate balloon to occlude
BronchoscopyRarely, to identify fistula location
Gastrostomy under localHigh-risk, delay definitive repair

Ventilation strategy:

  • Low tidal volumes (avoid gastric distension)
  • Gentle pressures until fistula controlled
  • Hand ventilation preferred for sensitivity

Postoperative care:

  • Extubate if possible at end of procedure
  • If ventilated, careful weaning (risk of anastomotic leak)
  • Avoid positive pressure on fresh anastomosis

Omphalocele and Gastroschisis

Definitions

FeatureOmphaloceleGastroschisis
Defect locationUmbilicus, midlineParaumbilical, usually right
MembranePresent (amnion + peritoneum)Absent - bowel exposed
Defect sizeVariable, often largeUsually <5 cm
Associated anomaliesCommon (50-70%) - cardiac, chromosomalRare (<15%)
PrematurityLess commonCommon (30-50%)
OutcomeDepends on associated anomaliesGenerally good

Pathophysiology

Gastroschisis:

  • Intrauterine exposure of bowel to amniotic fluid
  • Inflammatory peel on bowel surface
  • Bowel dysmotility (functional obstruction)
  • Fluid third-spacing into bowel wall and lumen
  • Hypovolaemia, hypothermia, sepsis risk

Omphalocele:

  • Herniation of abdominal contents through umbilical ring
  • Membrane-covered (temperature protection)
  • Associated with:
    • Beckwith-Wiedemann syndrome (macroglossia, hyperinsulinism, omphalocele)
    • Chromosomal abnormalities (trisomy 13, 18, 21)
    • Cardiac defects (20-30%)

Surgical Approaches

ApproachIndicationTechnique
Primary closureSmall defectImmediate return of contents
Staged closure (Silastic silo)Large defectGradual reduction over 3-7 days
Deferred closureUnstable patientTemporary coverage, delayed repair

Anaesthetic Management

Preoperative resuscitation (critical):

Gastroschisis patients require aggressive resuscitation:

ParameterTarget
Fluid resuscitation1.5-2× maintenance; often 150-200 mL/kg in first 24 hours
Temperature>36.5°C - transport in plastic bag or "bowel bag"
Glucose>2.6 mmol/L
Bowel protectionCover with saline-soaked gauze, plastic wrap
PositionLeft lateral (reduces bowel compression of IVC)

Clinical Pearl: Gastroschisis patients are hypovolaemic due to evaporative losses and third-spacing. Never proceed to OR without adequate resuscitation.

Intraoperative considerations:

Airway:

  • RSI with cricoid pressure (functional obstruction = full stomach)
  • Consider awake intubation if difficult airway (Beckwith-Wiedemann)

Monitoring:

  • Arterial line (frequent ABGs, glucose monitoring)
  • Temperature (forced air warmer + warmed fluids)
  • Urinary catheter (urine output >1 mL/kg/hr)

Ventilation challenges:

  • Increased intra-abdominal pressure after closure
  • Impaired diaphragmatic excursion
  • Reduced FRC, atelectasis
  • Risk of abdominal compartment syndrome

Haemodynamic management:

  • Expect fluid requirements 2-3× normal
  • Inotropes often needed (dopamine 5-10 mcg/kg/min)
  • Vasopressors for low SVR

Closure assessment:

SignImplication
Rising peak airway pressureReduced compliance
HypotensionIVC compression, reduced venous return
OliguriaRenal compression
Lower limb ischaemiaAortic compression
High ventilation pressuresConsider leaving abdomen open

Postoperative:

  • Prolonged ventilation usually required
  • Parenteral nutrition until bowel function returns (7-21 days)
  • Gradual enteral feeding

Airway Management in Neonates

Anatomical Considerations

FeatureImplication
Large head, occiputNatural "sniffing position" - minimal head elevation needed
Large tongueRelative to oral cavity; consider tongue sweep
High larynxC3-C4 (adult C5-C6) - straight blade often preferred
EpiglottisLong, stiff, angled (Ω-shaped) - straight blade lifts epiglottis directly
Vocal cordsAnterior, sloping (low anterior, high posterior)
CricoidNarrowest point (cylindrical airway vs adult funnel)
TracheaShort (4 cm at term) - risk of bronchial intubation

Equipment selection:

AgeETT Size (mm)Insertion Depth (cm)Laryngoscope
<1000 g2.5 uncuffed6-7Miller 0
1000-2500 g3.0 uncuffed7-8Miller 0-1
>2500 g (term)3.0-3.5 uncuffed8-9Miller 1

Depth rule: Weight + 6 cm at lip (approximation for term neonates).

Intubation Technique

Positioning:

  • Supine, slight head extension (but avoid overextension in neonates)
  • Roll under shoulders if needed
  • Neck in neutral position

Technique:

  1. Preoxygenate (100% O2 for 2-3 minutes if stable)
  2. Gentle laryngoscopy with straight blade (Miller)
  3. Lift epiglottis directly (do not sweep into vallecula)
  4. Insert ETT to appropriate depth
  5. Confirm position with auscultation + EtCO2
  6. Secure with tape/holder

Difficult airway:

  • Consider video laryngoscopy
  • Laryngeal mask airway (size 1) as rescue
  • Needle cricothyroidotomy (14G cannula) if failed

Ventilation Strategies

Hand ventilation:

  • Preferred for neonates (detect compliance changes)
  • Low tidal volumes (4-6 mL/kg)
  • Rapid rates (30-40/min)
  • PEEP 3-5 cmH₂O

Mechanical ventilation:

  • Pressure-controlled mode often preferred
  • Avoid high pressures (>20-25 cmH₂O)
  • Monitor for air leaks

Vascular Access

Peripheral Access

SiteConsiderations
Upper limbPreferred for long lines; avoid if planning arterial line
Lower limbAvoid in CDH, omphalocele (IVC compression risk)
ScalpUseful temporary access; risk of scalp necrosis
External jugularShort-term use; difficult to secure

Central Access

Umbilical venous catheter (UVC):

  • Preferred emergency access in delivery room
  • Tip position: IVC-RA junction (T8-T9)
  • Can be used for monitoring (CVP) and drug administration
  • Remove by day 5-7 (infection risk)

Umbilical arterial catheter (UAC):

  • "High" position: T6-T9 (above coeliac, mesenteric)
  • "Low" position: L3-L4 (below renal arteries, above aortic bifurcation)
  • Monitoring: BP, ABGs, continuous PaO2
  • Complications: Thrombosis, embolisation, vasospasm

Peripherally inserted central catheter (PICC):

  • Long-term access
  • Basilic or saphenous veins
  • Tip in SVC or IVC
  • Ultrasound guidance recommended

Fluid and Electrolyte Management

Fluid Requirements

AgeFluid Requirement (mL/kg/day)
Day 160-80
Day 280-100
Day 3100-120
Day 4-7120-150
Week 2+150-180

Note: Premature infants have higher requirements (up to 200 mL/kg/day).

Composition

ComponentRequirement
Glucose4-6 mg/kg/min (prevents hypoglycaemia)
Sodium2-4 mmol/kg/day (obligate sodium losers)
Potassium1-2 mmol/kg/day (after first 24 hours, if urinating)
Calcium1-2 mmol/kg/day (especially in prematurity)

Common Electrolyte Abnormalities

AbnormalityCauseManagement
HypoglycaemiaLimited glycogen, hyperinsulinism (BWS)10% dextrose bolus 2 mL/kg, then increase concentration
HyperglycaemiaSteroid use, prematurityReduce glucose concentration, insulin if >12 mmol/L
HyponatraemiaExcess free water, SIADHRestrict fluids; rarely need hypertonic saline
HyperkalaemiaRenal failure, tissue breakdownCalcium gluconate, insulin/glucose, salbutamol
HypocalcaemiaPrematurity, maternal diabetes, blood transfusionCalcium gluconate 1-2 mL/kg (slow IV)

Monitoring

Essential Monitoring

ParameterRationale
ECGHeart rate, rhythm, ischaemia
Pulse oximetrySpO2; consider pre- and post-ductal
EtCO2Ventilation adequacy
TemperatureCore temperature (oesophageal/rectal)
Blood pressureNIBP or arterial line
Urine outputRenal perfusion (target >1 mL/kg/hr)
Blood glucoseFrequent monitoring (target 2.6-7 mmol/L)

Arterial Blood Gas Targets

ParameterTarget
pH7.30-7.40
PaO250-80 mmHg (premature), 60-100 mmHg (term)
PaCO240-55 mmHg (permissive hypercapnia acceptable)
Base excess-5 to 0
Lactate<2 mmol/L (rising lactate = poor perfusion)
Glucose2.6-7 mmol/L

Indigenous Health Considerations

Aboriginal and Torres Strait Islander Neonatal Health

Health disparities:

Aboriginal and Torres Strait Islander neonates experience significant health inequities compared to non-Indigenous Australian neonates:

  • Preterm birth rate: 1.5-1.8× higher than non-Indigenous infants [12]
  • Low birth weight: 2× higher incidence [13]
  • Perinatal mortality: 1.5× higher rate [14]
  • Congenital anomalies: Higher rates of some conditions, including renal and cardiac defects

Contributing factors:

FactorImpact
Maternal healthHigher rates of diabetes, hypertension, smoking in pregnancy
Access to careGeographic isolation, transport barriers, late presentation
Socioeconomic factorsPoverty, overcrowding, limited education
Cultural factorsCultural safety in healthcare, institutional racism
Remote locationLimited specialist services, need for retrieval

Cultural safety in neonatal care:

When caring for Aboriginal neonates:

  1. Family-centered care:

    • Recognise importance of extended family (kinship systems)
    • Involve family in decision-making
    • Respect cultural protocols around birth and death
  2. Communication:

    • Use interpreters or Aboriginal Liaison Officers when needed
    • Avoid medical jargon; check understanding
    • Be aware that English may be second, third, or fourth language
  3. Traditional practices:

    • Some communities have specific practices around umbilical cord and placenta
    • Respect these where medically safe
  4. Discharge planning:

    • Consider remote location and ability to access follow-up
    • Liaise with primary health care and community services
    • Ensure culturally appropriate education for families

Māori Neonatal Health (Aotearoa New Zealand)

Health outcomes:

Māori neonates in New Zealand face similar disparities:

  • Preterm birth: 1.4× higher than European infants [15]
  • Perinatal mortality: 1.4× higher rate [16]
  • Sudden unexpected death in infancy (SUDI): 5× higher rate [17]

Whānau-centred care:

The concept of whānau (extended family) is central to Māori health:

  • Involve whānau in all care decisions
  • Recognise whakapapa (genealogy) and intergenerational connections
  • Respect tikanga (customs) and kawa (protocols)
  • Māori Health Workers can facilitate culturally safe care

Te Tiriti o Waitangi considerations:

Healthcare in New Zealand is guided by Te Tiriti principles:

  • Partnership: Working together with Māori
  • Protection: Safeguarding Māori health interests
  • Participation: Ensuring Māori involvement in healthcare

Rural and Remote Considerations

Challenges in remote Australia:

ChallengeImplication for Neonatal Anaesthesia
Geographic distanceStabilisation at regional hospital before transfer
Transport timeRisk of clinical deterioration during retrieval
Limited resourcesMay lack ECMO, cardiac surgery capabilities
Weather dependenceRFDS flights may be delayed
Indigenous populationHigher proportion requiring care

Stabilisation and retrieval:

  • Use of RFDS or state-based retrieval services (NETS, PIPER)
  • Telemedicine support from tertiary centres
  • Training of rural practitioners in neonatal stabilisation
  • Consider delayed surgery until transfer completed

ANZCA Professional Standards and Guidelines

Relevant ANZCA Documents

DocumentRelevance to Neonatal Anaesthesia
PS08Anaesthesia for the unwell adult/child (applies to neonates)
PS09Anaesthesia for emergency surgery
PS15Anaesthesia and sedation outside the operating room
PS18Guidelines for transport of critically ill patients
PS28Guidelines for the management of major blood loss
PS46Statement on paediatric anaesthesia

PS46 - Specific recommendations for paediatric/neonatal anaesthesia:

  1. Qualified personnel:

    • Dedicated paediatric anaesthesia training
    • Maintenance of paediatric skills
    • Paediatric life support certification
  2. Equipment:

    • Appropriate-sized airway equipment
    • Vascular access devices
    • Monitoring suitable for paediatric patients
  3. Environment:

    • Temperature control
    • Access to paediatric ICU
    • Blood product availability
  4. Resuscitation:

    • Equipment for neonatal resuscitation
    • Protocols for difficult airway

Paediatric-Specific Equipment

Airway equipment checklist:

EquipmentSizes Available
ETT (uncuffed)2.5, 3.0, 3.5, 4.0 mm
Laryngoscope bladesMiller 0, 1; Macintosh 1
LMASize 1, 1.5
Suction catheters6, 8, 10 Fr
StyletPaediatric
Meconium aspiratorAvailable

Monitoring:

EquipmentSpecification
Pulse oximeterPaediatric probes (limb/wrap)
NIBP cuffNeonatal sizes (3-6 cm width)
TemperatureOesophageal/rectal probes
CO2 detectorPaediatric (low flow)

Vascular access:

EquipmentUse
UVC kitUmbilical venous catheterisation
UAC kitUmbilical arterial catheterisation
24-26G cannulaPeripheral IV
3.5-5 Fr PICCCentral access

Drug Dosing in Neonates

DrugDoseComments
Induction
Propofol2-3 mg/kgSlow injection, risk of hypotension
Thiopental3-5 mg/kgReduced dose due to low protein binding
Ketamine1-2 mg/kgPreserves respiratory drive
Analgesia
Fentanyl2-5 mcg/kgReduced clearance
Morphine0.05-0.1 mg/kgRisk of apnoea
Paracetamol7.5-10 mg/kgMax 30 mg/kg/day (premature)
Muscle relaxants
Suxamethonium2 mg/kg↑ Duration due to low pseudocholinesterase
Atracurium0.5 mg/kgHofmann elimination - organ-independent
Rocuronium0.6 mg/kgStandard intubation
Emergency drugs
Atropine20 mcg/kgMinimum dose 100 mcg
Adrenaline0.01-0.1 mg/kg (IV)1:10,000 concentration
Sodium bicarbonate1-2 mmol/kgSlow IV, dilute if possible
Calcium gluconate1-2 mL/kgSlow IV, especially with blood
Dextrose 10%2-4 mL/kgHypoglycaemia treatment
Inotropes
Adrenaline0.05-0.5 mcg/kg/minFirst-line for cardiac arrest
Dopamine5-20 mcg/kg/minRenal dose 2-5, inotropic 5-10
Dobutamine5-20 mcg/kg/minPrimarily inotropic
Milrinone0.25-0.75 mcg/kg/minAfterload reduction, PPHN

Assessment Content

Short Answer Questions (SAQs)

SAQ 1: CDH Pathophysiology and Management (20 marks)

Question:

A term neonate with antenatally diagnosed left-sided congenital diaphragmatic hernia is born and immediately develops respiratory distress. Describe the pathophysiology of CDH and outline the principles of perioperative management for this infant. (20 marks)

Model Answer:

Pathophysiology (10 marks):

Lung hypoplasia (4 marks):

  • Failure of pleuroperitoneal fold fusion at 8 weeks gestation [1]
  • Herniation of abdominal contents into thorax causing direct lung compression
  • Reduced airway branching and alveolar development
  • Surfactant deficiency from Type II pneumocyte hypoplasia

Pulmonary hypertension (4 marks):

  • Abnormal pulmonary vascular development with thickened arteriolar walls
  • Increased PVR causing right-to-left shunting through PDA and foramen ovale
  • Hypoxia and acidosis perpetuate pulmonary vasoconstriction [2]
  • Risk of PPHN crisis with hypoxia, acidosis, cold stress

Cardiac dysfunction (2 marks):

  • Right ventricular pressure overload and dysfunction
  • Left ventricular compression by mediastinal shift
  • Duct-dependent systemic circulation in severe cases

Perioperative Management (10 marks):

Preoperative stabilisation (4 marks):

  • Gentle ventilation: PIP <20-25 cmH₂O, avoid hyperventilation
  • Permissive hypercapnia (PaCO2 45-60 mmHg acceptable)
  • Maintain SpO2 80-95% (avoid hyperoxia)
  • Consider HFOV and iNO (20 ppm) for refractory hypoxia
  • Delay surgery 48 hours to 7 days to allow stabilisation

Intraoperative management (3 marks):

  • Avoid N2O (expands bowel, increases PVR)
  • Pre- and post-ductal arterial line monitoring
  • Opioid-based anaesthetic to blunt PVR response
  • Minimise airway pressures
  • Prepare for haemodynamic instability during reduction

Postoperative care (3 marks):

  • Continue mechanical ventilation 24-72 hours minimum
  • Monitor for rebound PPHN
  • Inotropic support (milrinone for RV dysfunction)
  • ECMO available for refractory failure (OI >40)

SAQ 2: TOF Intraoperative Management (20 marks)

Question:

A 2-day-old infant with tracheo-oesophageal fistula (Gross Type C) is scheduled for repair. Describe the specific anaesthetic considerations and the technique for safe airway management in this patient. (20 marks)

Model Answer:

Preoperative Considerations (6 marks):

Assessment (3 marks):

  • Evaluate for VACTERL association (cardiac ECHO mandatory, spine/renal imaging)
  • Assess for pneumonia/aspiration (CXR, clinical examination)
  • Determine timing (primary repair vs gastrostomy first)
  • Continuous Replogle tube suction with head-up positioning

Resuscitation (3 marks):

  • Optimise respiratory status before surgery
  • Avoid positive pressure ventilation preoperatively if possible
  • Correct fluid and electrolyte abnormalities
  • Crossmatch blood

Airway Management (10 marks):

Induction strategy (4 marks):

  • Maintain spontaneous ventilation if possible (awake intubation or gentle inhalational)
  • High risk of gastric distension from positive pressure through fistula
  • Have surgeon present and prepared to identify fistula rapidly

Intubation technique (4 marks):

  • Size 3.0-3.5 uncuffed ETT for term neonate
  • Position ETT tip BELOW the fistula (at carina or right main bronchus)
  • Verify with equal breath sounds and EtCO2 waveform
  • Once fistula identified and controlled by surgeon, convert to controlled ventilation

Alternative strategies (2 marks):

  • Fogarty catheter through fistula with balloon occlusion
  • Emergency gastrostomy if respiratory failure
  • Bronchoscopy rarely to identify anatomy

Intraoperative Considerations (4 marks):

  • Low tidal volumes until fistula controlled (avoid gastric distension)
  • Hand ventilation for sensitivity to compliance changes
  • Avoid hyperoxia/hyperventilation if pulmonary hypertension
  • Extubate at end if possible; if ventilated, avoid positive pressure on anastomosis

SAQ 3: Neonatal Pharmacology (20 marks)

Question: Explain the key pharmacokinetic and pharmacodynamic differences between neonates and adults that impact anaesthetic drug administration, using specific examples. (20 marks)

Model Answer:

Pharmacokinetic Differences (10 marks):

Absorption and distribution (4 marks):

  • Higher volume of distribution (higher TBW, 75% vs 60% in adults)
  • Lower protein binding (low albumin, high free bilirubin and fatty acids displace drugs)
  • Increased free fraction of highly protein-bound drugs (thiopental, bupivacaine)
  • Larger relative BSA increases transdermal absorption risk

Metabolism (3 marks):

  • Immature hepatic enzyme systems (P450 activity 30-50% of adult)
  • Reduced glucuronidation (morphine, paracetamol) causing prolonged effect
  • Reduced pseudocholinesterase activity (suxamethonium lasts 2× longer)

Elimination (3 marks):

  • Low GFR (40-50% of adult values)
  • Immature tubular function
  • Prolonged clearance of renally-excreted drugs (morphine, aminoglycosides)

Pharmacodynamic Differences (6 marks):

CNS sensitivity (2 marks):

  • ↑ Sensitivity to anaesthetic agents (immature BBB, higher cerebral blood flow)
  • MAC values different (volatile MAC higher in neonates than infants, then decreases)

Cardiovascular effects (2 marks):

  • Greater myocardial depression from negative inotropes (immature calcium handling)
  • Bradycardia more profound with vagal stimulation (dominant parasympathetic tone)

Respiratory effects (2 marks):

  • Greater respiratory depression from opioids (immature respiratory centre)
  • Risk of apnoea with minimal stimulation

Clinical Examples (4 marks):

  • Morphine: ↓ clearance (50% of adult), ↓ glucuronidation, ↑ half-life → apnoea risk
  • Suxamethonium: ↓ pseudocholinesterase → 2× prolonged block
  • Paracetamol: ↓ glucuronidation → max dose 60 mg/kg/day (vs 90 in adults)
  • Volatile agents: MACneonate ≈ 1.3× MACadult at term, lower in premature infants

Viva Voce Scenarios

Viva 1: CDH Management (15 marks)

Scenario: You are the anaesthetic fellow covering the paediatric list. A term neonate with antenatally diagnosed left CDH is born and immediately transferred to the neonatal unit with severe respiratory distress.

Examiner Questions:

Q1: "What are the key pathophysiological features of CDH that make this infant high-risk?" (5 marks)

Model Answer:

  • Lung hypoplasia: Reduced alveolar and airway development from compression
  • Pulmonary hypertension: Abnormal vasculature with medial hypertrophy, increased PVR
  • Right-to-left shunting: Through PDA and foramen ovale
  • Cardiac dysfunction: RV pressure overload, left heart compression from mediastinal shift
  • Surfactant deficiency: Type II cell hypoplasia

Q2: "The neonatologist calls for urgent surgery. What is your response?" (5 marks)

Model Answer:

  • Surgery is NOT urgent - delay is preferred (48 hours to 7 days)
  • Stabilisation takes priority: gentle ventilation (PIP <20-25), permissive hypercapnia
  • Avoid N2O, avoid hyperoxia
  • Consider HFOV or iNO if failing
  • Emergency only for obstruction/strangulation

Q3: "What monitoring and access do you need for surgery?" (5 marks)

Model Answer:

  • Arterial line: Pre-ductal (right radial) and post-ductal for differential saturations
  • Central venous access: UVC or femoral for drugs and monitoring
  • Temperature: Core monitoring, forced air warmer
  • Urinary catheter for output monitoring
  • ABG monitoring for acidosis/hypoxia

Viva 2: TOF Airway Crisis (15 marks)

Scenario: A 1-day-old infant with TOF is undergoing repair. During induction, the surgeon is delayed. You have induced anaesthesia and are hand-ventilating, but the infant's oxygen saturation is falling and you notice increasing resistance to ventilation.

Examiner Questions:

Q1: "What is your immediate concern and differential diagnosis?" (5 marks)

Model Answer:

  • Gastric overdistension from positive pressure through fistula
  • Right main bronchus intubation
  • Pneumothorax (common in neonates)
  • Aspiration
  • Equipment disconnection/malfunction

Q2: "What are your immediate management steps?" (5 marks)

Model Answer:

  • Stop positive pressure ventilation immediately
  • Release cricoid pressure, allow spontaneous breathing if possible
  • Decompress stomach with orogastric tube
  • Check ETT position (withdraw slightly if right main bronchus)
  • Call surgeon urgently to identify and control fistula
  • Prepare for emergency gastrostomy if needed

Q3: "How would you prevent this situation?" (5 marks)

Model Answer:

  • Maintain spontaneous ventilation until fistula controlled
  • Have surgeon present and prepared before induction
  • Position ETT below fistula (at carina) - may need to accept right main intubation temporarily
  • Use gentle hand ventilation with low pressures
  • Consider awake intubation in high-risk cases

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