Neonatal Resuscitation

Quick Answer

Neonatal resuscitation follows the Neonatal Resuscitation Program (NRP) algorithm, which is structured around the four pillars of resuscitation: airway, breathing, circulation, and drugs. Approximately 10% of newborns require some assistance to begin breathing at birth, and about 1% require extensive resuscitative measures. [1,2] The key interventions include positive pressure ventilation (PPV) at 30-60 breaths/minute, chest compressions at 90-120 compressions/minute with a 3:1 compression-to-ventilation ratio, vascular access via umbilical venous catheter (UVC) or intraosseous (IO) route, and adrenaline (epinephrine) at 0.1-0.3 mg/kg for bradycardia or asystole. [3-5]

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CICM Exam Focus

Key High-Yield Points

1. NRP algorithm sequence: Initial assessment (tone, breathing, heart rate) → Stimulation and drying → Airway positioning and suctioning → PPV (30-60 bpm) → Chest compressions (90-120 bpm, 3:1 ratio) → Adrenaline (0.1 mg/kg IV/IO) → Volume expansion. [3,6]

2. PPV is the most critical intervention: Effective ventilation is the cornerstone of neonatal resuscitation. Heart rate should improve within 15 seconds of effective PPV. If heart rate does not improve, check for (a) inadequate ventilation (check seal, PIP, PEEP), (b) airway obstruction (secretions, meconium), or (c) progression to chest compressions. [3,7]

3. Heart rate determines resuscitation needs: Heart rate is the primary clinical indicator of resuscitation effectiveness. Auscultate precordium with stethoscope or use pulse oximeter. Bradycardia (below 100 bpm) usually responds to PPV. Persistent bradycardia (below 60 bpm) despite PPV requires chest compressions and adrenaline. [8,9]

4. Chest compressions require coordination: Two-thumb encircling chest technique is preferred for infants greater than 2000g as it generates higher systolic and diastolic pressures. The 3:1 compression-to-ventilation ratio (3 compressions, then 1 ventilation) yields approximately 120 events per minute (90 compressions + 30 breaths). Compressions should not be interrupted for ventilation. [10,11]

5. Adrenaline dosing and routes: IV/IO dose is 0.1-0.3 mg/kg (0.1-0.3 mL/kg of 1:10,000). Endotracheal dose is 0.5-1 mg/kg (5-10 times higher) but is less effective due to unreliable absorption. Adrenaline should be considered after 60-90 seconds of effective PPV and chest compressions if heart rate remains below 60 bpm. Repeat every 3 minutes. [5,12]

6. Umbilical venous catheter placement: Insert UVC 2-4 cm in term infants and 1-2 cm in preterm infants. Insert until free blood return, then withdraw 1-2 cm to avoid intrahepatic placement. Correct position is at the junction of the inferior vena cava and right atrium (approximately at T8-T9 on X-ray). Umbilical artery catheters (UAC) are NOT used for medications during resuscitation (too slow, risk of spasm). [13,14]

7. Intraosseous access: IO is indicated if UVC insertion is delayed or unsuccessful, or if prolonged resuscitation (greater than 2 minutes) is anticipated. Preferred site: proximal tibia (1-3 cm below tibial tuberosity). Confirm placement by (a) ability to infuse fluids without extravasation, (b) lack of resistance, (c) ability to aspirate bone marrow. [15,16]

8. Volume expansion for hypovolemia: Indications include evidence of acute blood loss (pale infant, weak pulses, persistent bradycardia despite PPV + adrenaline), or suspected placental abruption/cord avulsion. Dose: 10 mL/kg of 0-negative red blood cells (preferred) or normal saline/ringer lactate (if blood unavailable). Repeat if needed. Volume expansion should not be the first intervention unless hypovolemia is clearly present. [17,18]

9. Therapeutic hypothermia for HIE: Indications include gestational age ≥36 weeks, evidence of perinatal asphyxia (pH below 7.00 or base deficit ≥16 mmol/L, Apgar ≤5 at 10 minutes, need for PPV greater than 10 minutes), and moderate to severe encephalopathy. Initiate within 6 hours of birth, maintain target temperature 33.5-34.5°C for 72 hours, then rewarm over ≥4 hours. [19,20]

10. Apgar score limitations: Apgar scores are useful for assessing neonatal condition at birth but do not predict long-term neurologic outcomes. Low Apgar scores (below 7 at 5 minutes) are associated with increased risk of cerebral palsy but with low predictive value. Cord blood gas analysis provides objective evidence of perinatal asphyxia (pH below 7.00, base deficit ≥12-16 mmol/L). [21,22]

Common Viva Themes

• NRP algorithm steps and decision points
• PPV technique and troubleshooting
• Indications and technique for chest compressions
• Adrenaline dosing, routes, and timing
• UVC vs IO access placement and confirmation
• Therapeutic hypothermia criteria and protocol
• Apgar score interpretation and limitations
• Cord blood gas analysis and interpretation
• Prognosis following neonatal resuscitation
• Management of meconium-stained amniotic fluid

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Clinical Overview

Neonatal resuscitation is a time-sensitive, high-stakes procedure requiring coordination, technical skill, and adherence to evidence-based guidelines. The transition from fetal to neonatal life involves rapid physiologic changes—closure of fetal shunts (foramen ovale, ductus arteriosus, ductus venosus), initiation of pulmonary blood flow, and establishment of functional residual capacity. Approximately 90% of newborns transition smoothly without intervention. The remaining 10% require some assistance, typically drying, stimulation, and PPV. About 1% require comprehensive resuscitation including chest compressions and medications. [1,2,6]

Physiologic basis for neonatal resuscitation:

Fetal circulation is characterized by:

• Right-to-left shunting via foramen ovale (RA → LA) and ductus arteriosus (PA → aorta)
• Pulmonary vascular resistance (PVR) is high (pulmonary vessels are constricted in utero)
• Systemic vascular resistance (SVR) is low (placenta is low-resistance circuit)
• Fetal oxygenation occurs via placenta (PaO2 ~25-30 mmHg in umbilical vein)

At birth, the following occur:

• Clamping of umbilical cord → removal of placental circulation → sudden increase in SVR
• First breath → inflation of lungs → dramatic decrease in PVR → increase in pulmonary blood flow
• Increased left atrial pressure → functional closure of foramen ovale
• Increased PaO2 → decrease in prostaglandins → closure of ductus arteriosus
• Establishment of adult circulation pattern (left-to-right shunt closure)

Failure of transition (hypoxia, acidosis, lung disease, meconium aspiration, congenital heart disease) can lead to persistent fetal circulation, bradycardia, hypotension, and the need for resuscitation. The most common cause of bradycardia at birth is hypoxia leading to vagal stimulation, which responds to effective ventilation. [6,23]

Risk factors for needing resuscitation: [1,2]

• Maternal factors: Pre-eclampsia, diabetes, chorioamnionitis, antepartum hemorrhage (abruption, placenta previa), maternal hypotension/anesthesia complications, thyroid disease, substance abuse, smoking
• Pregnancy complications: Multiple gestation, preterm labour (below 37 weeks), post-term pregnancy (greater than 42 weeks), oligohydramnios, polyhydramnios, intrauterine growth restriction (IUGR), fetal distress (abnormal CTG, meconium)
• Fetal factors: Congenital anomalies (cardiac, CNS, diaphragmatic hernia, airway), intrauterine infection (TORCH), hydrops fetalis, anemia (isoimmunization, hemorrhage)
• Labour and delivery: Precipitous delivery, prolonged labour, operative delivery (forceps, vacuum, cesarean), cord prolapse/avulsion/true knot, shoulder dystocia, traumatic delivery

Equipment preparedness:

A designated resuscitation area should be available in every delivery suite, with the following equipment:

• Warm radiant warmer (pre-warmed to prevent hypothermia)
• Suction (wall suction with regulated pressure, bulb suction, meconium aspirator)
• Oxygen source with blender (room air to 100% O2) and pulse oximeter
• Positive pressure ventilation: T-piece device (preferred) or self-inflating bag with neonatal mask
• Laryngoscopes (Miller 0 and 1 blades), endotracheal tubes (2.5-4.0 mm)
• Chest compression board or flat surface
• Umbilical catheterization kit (3.5-5 Fr UVC, scissors, tape, saline)
• IO needle (15-18 gauge) or IO drill
• Medications: Adrenaline 1:10,000, volume expanders (blood, saline), sodium bicarbonate (controversial)
• Monitoring: ECG leads for heart rate (more accurate than pulse oximetry), pulse oximeter, blood pressure cuff
• Thermoregulation: Plastic bags/wraps for preterm infants below 28 weeks, hats, warm blankets

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Assessment

Initial Assessment

The initial assessment should occur within the first 30-60 seconds after birth and focuses on three key questions: [3,6]

1. Term gestation? (≥37 weeks)

   • Preterm infants (below 37 weeks) have higher risk of respiratory distress syndrome, surfactant deficiency, temperature instability, and intraventricular hemorrhage
   • Extremely preterm infants (below 28 weeks) require early intubation for surfactant administration

2. Breathing or crying?

   • Active breathing or crying indicates adequate respiratory effort
   • Apnea, gasping, or weak respiratory effort requires intervention

3. Good muscle tone?

   • Good tone (flexed extremities, active movement) indicates adequate CNS function and oxygenation
   • Floppy infant (hypotonia) suggests perinatal depression, hypoxia, or CNS injury

If ALL answers are YES: Routine care (drying, skin-to-skin, breastfeeding initiation)

If ANY answer is NO: Proceed to resuscitation algorithm

Apgar Score

The Apgar score is a standardized assessment of neonatal condition at 1, 5, and sometimes 10 minutes after birth. Each of the five components is scored 0, 1, or 2, for a maximum of 10 points. [21,24]

Interpretation:

• 7-10: Normal transition, no resuscitation needed (usually)
• 4-6: Moderate depression, may require stimulation or brief PPV
• 0-3: Severe depression, requires active resuscitation

Limitations of Apgar score: [21,22]

• Subjective assessment, inter-rater variability
• Influenced by gestational age, maternal medications, congenital anomalies
• Low Apgar score at 1 minute does NOT predict poor outcome
• Low Apgar score at 5 minutes is associated with increased risk of cerebral palsy but low predictive value
• Does NOT identify cause of neonatal depression
• May be falsely low in infants who require rapid intubation for airway protection

CICM exam tip: Always correlate Apgar score with cord blood gas results. An infant with Apgar 3 at 5 minutes but cord pH 7.25 and normal base deficit likely had other causes for depression (e.g., sedation from maternal medications, congenital neuromuscular disorder).

Cord Blood Gas Analysis

Umbilical cord blood gas analysis provides objective evidence of perinatal asphyxia and is recommended in high-risk deliveries (e.g., emergency cesarean, fetal distress, low Apgar scores). Both umbilical artery (UA) and umbilical vein (UV) should be sampled. [22,25]

Sampling technique:

1. Clamp a 10-15 cm segment of umbilical cord immediately after delivery
2. Draw blood from UA (deoxygenated blood from fetus) and UV (oxygenated blood from placenta)
3. Analyze within 30 minutes or keep on ice (pH decreases ~0.05 per hour if left at room temperature)

Interpretation of cord blood gas:

Definition of perinatal asphyxia (acidemia): [22,25]

• Mild: UA pH 7.10-7.19, base deficit 10-12 mmol/L
• Moderate: UA pH 7.00-7.09, base deficit 12-16 mmol/L
• Severe: UA pH below 7.00, base deficit ≥16 mmol/L

Key points for CICM exam:

• UA reflects fetal status, UV reflects placental function
• UA-UV difference (ΔpO2) below 20 mmHg suggests placental insufficiency
• UA-UV difference (ΔpH) greater than 0.02 suggests significant fetal compromise
• Cord blood gas is required for diagnosis of HIE and eligibility for therapeutic hypothermia
• Absence of acidemia essentially excludes perinatal asphyxia as cause of neonatal encephalopathy

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NRP Algorithm

The Neonatal Resuscitation Program (NRP) algorithm provides a systematic approach to neonatal resuscitation based on assessment of heart rate, breathing, and oxygenation. [3,6]

Critical Alert: NRP Algorithm Summary (AHA/AAP 2020 Guidelines)

1. Initial Assessment (30-60 seconds)

   • Term? Breathing? Tone?
   • If YES to all: Routine care
   • If NO to any: Proceed to resuscitation

2. Stabilization (within first 60 seconds)

   • Provide warmth (place under radiant warmer, dry)
   • Clear airway (position, suction if needed)
   • Assess breathing, heart rate, color

3. Positive Pressure Ventilation (PPV)

   • Indication: Apnea, gasping, HR below 100 bpm
   • Initiate PPV at 30-60 breaths/minute
   • Use PIP 20-25 cm H2O, PEEP 5 cm H2O
   • Assess HR after 15 seconds
   • Continue if HR improving (greater than 100 bpm) or stabilizing (60-100 bpm)
   • Consider ETT intubation if PPV prolonged (greater than 2-3 minutes)

4. Chest Compressions

   • Indication: HR below 60 bpm despite 30 seconds of effective PPV
   • Initiate at 90-120 compressions/minute
   • Ratio: 3:1 (3 compressions, 1 ventilation)
   • Technique: Two-thumb encircling chest (preferred)
   • Continue until HR ≥60 bpm

5. Adrenaline

   • Indication: HR below 60 bpm despite PPV + compressions
   • Dose: 0.1-0.3 mg/kg IV/IO (0.1-0.3 mL/kg of 1:10,000)
   • Repeat every 3 minutes
   • Consider endotracheal route if IV/IO unavailable (0.5-1 mg/kg)

6. Volume Expansion

   • Indication: Evidence of hypovolemia (pale, weak pulses, persistent bradycardia despite adrenaline)
   • Dose: 10 mL/kg of O-negative blood or saline
   • Repeat if needed

7. Post-Resuscitation Care

   • Maintain temperature (36.5-37.5°C)
   • Consider therapeutic hypothermia if HIE criteria met
   • Monitor glucose, blood pressure, electrolytes
   • Transfer to NICU if indicated

Decision Points and Key Actions

Step 1: Initial Assessment (0-60 seconds)

Step 2: Stabilization and PPV (60-90 seconds)

Step 3: Chest Compressions (90-120 seconds)

Step 4: Adrenaline and Medications (120-180 seconds)

Time-Based Interventions

Critical Alert: Critical Time Intervals

• 0-60 seconds: Initial assessment, stimulation, drying, positioning, suctioning
• 60 seconds: Decision to start PPV if HR below 100 bpm or apnea
• 75 seconds: Reassess HR after 15 seconds of PPV
• 90 seconds: If HR below 60 bpm despite PPV, start chest compressions
• 120-150 seconds: If HR below 60 bpm despite PPV + compressions, give adrenaline
• 180 seconds: Reassess, repeat adrenaline every 3 minutes if needed

Key Principle: Do NOT delay PPV waiting for equipment or pulse oximeter. Effective ventilation is the most time-sensitive intervention.

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Airway Management

Airway Positioning

Proper airway positioning is essential for effective PPV. The neutral ("sniffing") position aligns the oral, pharyngeal, and laryngeal axes to facilitate airflow. [3,26]

Technique:

• Place the infant supine on a flat surface under radiant warmer
• Place a 1-2 cm roll of towel under the shoulders (smaller for preterm infants)
• Extend the neck slightly (neutral position, avoid overextension)
• Avoid excessive flexion or extension, which can obstruct the airway
• Maintain jaw thrust (lift mandible anteriorly) to open airway

Evidence: Proper head positioning improves mask seal and reduces airway obstruction. Overextension can cause airway kinking in neonates, while flexion can collapse the pharyngeal airway. [26,27]

Suctioning

Suctioning is indicated when there is visible obstruction, meconium-stained amniotic fluid (MSAF), or excessive secretions. [3,28]

Indications for suctioning:

• Visible oropharyngeal secretions
• Meconium-stained amniotic fluid (MSAF)
• Poor chest rise despite PPV (suggests airway obstruction)
• Need for intubation

Technique:

• Use wall suction with regulated pressure (80-100 mmHg) or bulb suction for term infants
• Suction mouth first, then nares (to prevent aspiration if infant gasps)
• Limit suctioning to below 5 seconds per episode
• Suction gently to avoid trauma (avulsion of tissue, vagal stimulation)
• Avoid deep suctioning (passing catheter beyond 1-2 cm can cause bradycardia)

Meconium-stained amniotic fluid (MSAF):

• Occurs in 10-15% of term deliveries
• 1-5% of infants with MSAF develop meconium aspiration syndrome (MAS)
• Current guidelines (2020 AHA/AAP): [3,28]
  • "Non-vigorous infant (depressed, hypotonic, HR below 100 bpm): Endotracheal suctioning under direct laryngoscopy"
  • "Vigorous infant (strong cry, tone, HR greater than 100 bpm): Do NOT suction; this is associated with worse outcomes"

Technique for endotracheal meconium suctioning:

1. Visualize vocal cords with laryngoscope
2. Pass meconium aspirator (wall suction catheter with side holes)
3. Suction while withdrawing ETT (apply continuous suction as ETT is removed)
4. Re-intubate if meconium remains thick or visualization is inadequate

Evidence: The previous practice of routine suctioning of all infants with MSAF has been abandoned after randomized trials showing no benefit and potential harm (increased risk of bradycardia). [28]

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Positive Pressure Ventilation (PPV)

Indications

PPV is the most critical intervention in neonatal resuscitation. Indications include: [3,7,29]

• Apnea or gasping respirations
• Heart rate below 100 bpm (regardless of respiratory effort)
• Persistent cyanosis despite free-flow oxygen
• Inadequate respiratory effort despite stimulation

Equipment

T-piece device (Neopuff) is preferred over self-inflating bag because: [3,29]

• Provides consistent PIP and PEEP regardless of operator experience
• PIP and PEEP can be precisely set and monitored
• Manometer allows real-time pressure monitoring
• Reduces risk of barotrauma from excessive pressures

Self-inflating bag characteristics:

• Does NOT require oxygen source to function (useful in resource-limited settings)
• Can provide PIP but NOT consistent PEEP (unless equipped with PEEP valve)
• Requires more operator skill to deliver consistent ventilation
• Useful for transport or backup equipment

Mask selection:

• Use appropriately sized mask (size 0 for below 1500g, size 1 for greater than 1500g)
• Mask should cover nose and mouth but not eyes
• Create adequate seal (check for air leak)
• Consider oropharyngeal airway (Guedel) if mask seal poor

PPV Technique

Initial PPV settings: [3,29]

SpO2 targets (pre-ductal, right hand): [30]

Technique:

1. Position airway (neutral position)
2. Apply mask firmly, ensure good seal
3. Deliver PPV at 30-60 breaths/minute
4. Observe chest rise (should be visible but not excessive)
5. Assess heart rate after 15 seconds
6. Adjust PIP if inadequate chest rise or excessive distention
7. Titrate FiO2 to target SpO2

Troubleshooting PPV

Inadequate response to PPV (HR not improving): [3,7]

Two-person PPV technique:

• Person 1: Secures mask seal with both hands
• Person 2: Provides ventilation (manages T-piece or bag)
• Improves mask seal and reduces fatigue
• Recommended for difficult airways or prolonged PPV

Endotracheal Intubation

Indications for ETT intubation during resuscitation: [3,31]

1. Prolonged PPV (greater than 2-3 minutes) or need for ongoing ventilation
2. Poor mask seal or inability to maintain airway
3. Meconium-stained amniotic fluid in non-vigorous infant (for suctioning)
4. Congenital diaphragmatic hernia (immediate intubation, avoid bag-mask ventilation which can worsen lung herniation)
5. Extremely preterm infant (below 28 weeks) for surfactant administration
6. Need for prolonged chest compressions (better coordination with ETT)
7. Tracheoesophageal fistula (prevent gastric distention with bag-mask)

Equipment:

• Laryngoscope with Miller blade (size 0 for below 1500g, size 1 for greater than 1500g)
• ETT size (internal diameter): 2.5 mm (below 1000g), 3.0 mm (1000-2000g), 3.5 mm (2000-3000g), 4.0 mm (greater than 3000g)
• Stylet (optional, may assist with passage)
• Suction catheter (meconium aspirator if MSAF)
• Tape or ETT holder
• CO2 detector (colorimetric capnograph) - confirm ETT placement

Technique:

1. Position infant (neutral head position, slight extension)
2. Stabilize head with left hand, insert laryngoscope with right hand
3. Visualize epiglottis and vocal cords (Miller blade lifts epiglottis)
4. Insert ETT through cords (observe tube passing through cords)
5. Advance to appropriate depth (tip to mid-trachea): [31]
   • Weight-based: 6 + (weight in kg) = cm at lip
   • Alternatively: 7 cm (1000g), 8 cm (2000g), 9 cm (3000g), 10 cm (4000g)
6. Secure ETT with tape
7. Confirm placement:
   • CO2 detector (color change from purple to yellow)
   • Bilateral breath sounds
   • Chest rise
   • No gastric sounds
   • Heart rate improvement

Complications:

• Esophageal intubation (most common - up to 20%)
• Right mainstem bronchus intubation
• Trauma to airway (lip, tongue, vocal cords)
• Bradycardia due to vagal stimulation
• Hypoxia from prolonged intubation attempt

CICM exam tip: Limit intubation attempt to 30 seconds. If unsuccessful, resume bag-mask ventilation and consider alternative strategies (another attempt, different provider, or continue bag-mask ventilation).

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Chest Compressions

Indications

Chest compressions are indicated when: [3,10,11]

• Heart rate below 60 bpm despite 30 seconds of effective PPV
• Asystole or severe bradycardia (below 40 bpm) that does not respond to PPV

Key principle: Ensure effective PPV BEFORE starting compressions. Most bradycardia responds to ventilation. Compressions are only needed if PPV alone is insufficient.

Technique

Two-thumb encircling chest method (preferred): [10,11]

1. Place both thumbs on the lower third of the sternum (just below nipple line)
2. Encircle chest with both hands, supporting the back
3. Compress sternum vertically (depress one-third of anterior-posterior diameter)
4. Maintain position throughout resuscitation
5. Benefits: Generates higher systolic and diastolic pressures, less operator fatigue, better coordination

Two-finger method (alternative):

1. Place two fingers (index and middle) on lower third of sternum
2. Use other hand to support infant's back
3. Compress vertically
4. Used if two-thumb method not possible (e.g., umbilical line access needed)

Compression parameters: [10,11]

Coordination with PPV

3:1 compression-to-ventilation ratio: [10,11]

• 3 compressions followed by 1 ventilation yields 120 events per minute
• Compression rate: 90 compressions/minute
• Ventilation rate: 30 breaths/minute
• Total: 120 events/minute

Technique:

• One provider performs compressions, another provides PPV
• Compressor counts aloud: "One, two, three, breathe"
• Ventilator delivers 1 breath after 3 compressions
• Minimizes interruptions in chest compressions
• Avoids simultaneous compression and ventilation (which reduces efficacy)

Evidence: The 3:1 ratio is based on the need for adequate ventilation (neonates are obligate nasal breathers, minute ventilation critical for oxygenation) while maintaining coronary perfusion pressure. Some studies suggest 2:1 ratio or continuous compressions with asynchronous PPV, but current guidelines recommend 3:1. [10]

Assessing Effectiveness

Heart rate should increase within 60 seconds of effective PPV + compressions: [3,11]

Assess HR every 60 seconds:

• Auscultate precordium with stethoscope (most accurate)
• Palpate umbilical cord pulse (may be difficult if bradycardic)
• Use ECG leads if available (most rapid assessment)

Stop compressions when HR greater than 60 bpm:

• Continue PPV if HR 60-100 bpm
• Stop PPV if HR greater than 100 bpm and respiratory effort adequate

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Medications

Adrenaline (Epinephrine)

Adrenaline is the primary medication used in neonatal resuscitation for bradycardia or asystole that is unresponsive to PPV and chest compressions. [3,5,12]

Mechanism of action:

• α1-adrenergic: Vasoconstriction → increased diastolic blood pressure → increased coronary perfusion pressure
• β1-adrenergic: Increased heart rate and myocardial contractility
• β2-adrenergic: Bronchodilation (less important at birth)

Indications:

• Heart rate below 60 bpm despite 60-90 seconds of effective PPV + chest compressions
• Asystole

Dosing: [5,12]

Important considerations:

• IV/IO route is preferred (reliable absorption, rapid onset)
• Endotracheal dose is 5-10 times higher due to unreliable absorption
• Current evidence suggests endotracheal adrenaline has poor efficacy (up to 50% fail to achieve adequate plasma levels)
• Establish IV/IO access EARLY if prolonged resuscitation anticipated
• Flush IV/IO adrenaline with 1-2 mL saline to ensure delivery

Pharmacokinetics:

• Onset: Immediate (IV), delayed and unpredictable (ETT)
• Duration: 3-5 minutes (hence q3min dosing interval)
• Metabolism: MAO and COMT in liver, excreted in urine

Adverse effects:

• Hypertension (especially with high doses)
• Tachycardia, arrhythmias
• Hypertensive intraventricular hemorrhage (in preterm infants)
• Myocardial ischemia (rare)

CICM exam tip: Do NOT delay adrenaline if IV/IO access not immediately available. Give endotracheal adrenaline while establishing IV/IO access. Once IV/IO is secured, switch to IV/IO dosing.

Volume Expansion

Volume expansion is indicated when there is evidence of hypovolemia or acute blood loss. [3,17,18]

Indications:

• Evidence of acute blood loss:
  • Pale infant, poor perfusion, weak pulses
  • Placental abruption
  • Cord avulsion
  • Vasa previa
  • Fetal-maternal hemorrhage
  • Large for gestational age infant with difficult delivery
• Persistent bradycardia or hypotension despite PPV + compressions + adrenaline

Fluid options: [17,18]

Technique:

• Give as 10 mL/kg bolus over 5-10 minutes
• Reassess HR, blood pressure, perfusion after each bolus
• Repeat if needed (typically 10-20 mL/kg total)
• Use blood warmer (infants are prone to hypothermia)
• Monitor for signs of fluid overload (hepatomegaly, pulmonary edema)

Caution:

• Volume expansion should NOT be the first intervention unless hypovolemia is clearly present
• Avoid routine volume expansion in asphyxiated infants without evidence of blood loss
• Hypervolemia can worsen pulmonary edema in asphyxiated infants

Sodium Bicarbonate

Sodium bicarbonate is generally NOT recommended during neonatal resuscitation except in specific circumstances. [3,32]

Potential benefits:

• Corrects metabolic acidosis
• May improve myocardial contractility in severe acidosis

Risks:

• Worsens intracellular acidosis (CO2 generated crosses cell membranes)
• Hyperosmolality, hypernatremia
• Inhibits oxygen release from hemoglobin (left shift of oxyhemoglobin dissociation curve)

Indications (controversial, rarely used):

• Prolonged resuscitation (greater than 10 minutes) with severe metabolic acidosis
• Hyperkalemia
• Known inborn error of metabolism with acidosis

Dose (if used):

• 1-2 mEq/kg diluted 1:1 with sterile water
• Give slowly over 2-5 minutes
• Ensure adequate ventilation (to eliminate CO2 generated)

CICM exam tip: Current guidelines emphasize that the most effective treatment for metabolic acidosis in neonatal resuscitation is effective ventilation and restoration of perfusion, not bicarbonate administration. Bicarbonate should be reserved for specific circumstances and only after discussion with senior staff.

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Vascular Access

Umbilical Venous Catheter (UVC)

Umbilical venous catheterization is the preferred route for vascular access during neonatal resuscitation. [13,14]

Anatomy:

• Umbilical cord contains one vein (large, thin-walled) and two arteries (smaller, thick-walled)
• Umbilical vein carries oxygenated blood from placenta to fetus
• After clamping, vein can be cannulated to access central circulation

Equipment:

• 3.5 Fr UVC (most common for term infants) or 5 Fr UVC
• Sterile scissors
• Forceps
• Suture or tape for securing
• 3-way stopcock
• Flush solution (normal saline)

Technique: [13,14]

1. Prepare cord:

   • Cut umbilical cord with sterile scissors approximately 1-2 cm above skin
   • Identify umbilical vein (larger, thin-walled, single lumen) and arteries (smaller, thicker, two lumens)

2. Cannulate vein:

   • Insert catheter into vein lumen
   • Advance gently until free blood return (2-4 cm in term infants, 1-2 cm in preterm infants)

3. Correct positioning:

   • Correct position is at the junction of inferior vena cava and right atrium
   • Approximately at T8-T9 on X-ray
   • Withdraw 1-2 cm after free blood return to avoid intrahepatic placement

4. Secure catheter:

   • Suture or tape catheter to cord
   • Connect to 3-way stopcock
   • Flush with normal saline

Depth of insertion (cm at lip): [14]

Confirmation of position:

• Free blood return (venous, non-pulsatile)
• Chest X-ray (tip at T8-T9, not intrahepatic or intracardiac)
• Absence of hepatic enlargement (suggests intrahepatic placement)
• ECG changes if catheter in right atrium (arrhythmias)

Complications:

• Intrahepatic placement (most common complication)
• Infection (sepsis)
• Thrombosis
• Hepatic necrosis (if catheter tip in liver)
• Cardiac perforation (rare, if catheter advanced too far)

Important notes:

• Umbilical ARTERY catheter (UAC) is NOT used for resuscitation medications (too slow, risk of spasm)
• UVC can remain in place for several days if needed (for ongoing medications, fluids, monitoring)
• Remove UVC as soon as no longer needed (reduces infection risk)

Intraosseous (IO) Access

Intraosseous access is an alternative route if UVC insertion is delayed or unsuccessful, or if prolonged resuscitation (greater than 2 minutes) is anticipated. [15,16]

Indications:

• UVC insertion unsuccessful or delayed
• Need for rapid vascular access during prolonged resuscitation
• UVC contraindicated (e.g., omphalocele, gastroschisis)
• Alternative to UVC in older neonates (umbilical cord may not be accessible)

Sites: [15,16]

1. Proximal tibia (preferred):

   • 1-3 cm below tibial tuberosity
   • Avoid growth plate (physis)
   • Flat, easily accessible

2. Distal femur (alternative):

   • 1-2 cm above femoral condyles
   • Less preferred due to potential for growth plate injury

Equipment:

• IO needle (15-18 gauge) or IO drill (e.g., FAST1, EZ-IO)
• Stylet (if using manual needle)
• Flush solution (normal saline)

Technique: [15,16]

1. Identify insertion site (proximal tibia preferred)
2. Stabilize leg
3. Insert IO needle perpendicular to bone (or slight angle toward foot to avoid growth plate)
4. Advance until "pop" felt (cortex penetrated)
5. Remove stylet (if present)
6. Confirm placement:
   • Ability to infuse fluids without extravasation
   • Lack of resistance
   • Ability to aspirate bone marrow
7. Secure catheter

Confirmation of placement: [15,16]

• Infuse 5-10 mL normal saline without swelling or extravasation
• Aspirate bone marrow (confirmatory, not always successful)
• No resistance to infusion
• Stable catheter position

Complications:

• Extravasation (most common - up to 15%)
• Infection (osteomyelitis, cellulitis)
• Fracture
• Growth plate injury (if needle placed incorrectly)
• Compartment syndrome (if extravasation unrecognized)

Evidence: IO access is highly effective for medication and fluid administration during pediatric resuscitation. Success rates exceed 90% in experienced providers. IO infusion rates are similar to central venous access. [15,16]

CICM exam tip: Establish IO access EARLY if UVC insertion is challenging or prolonged resuscitation is anticipated. Do not waste time attempting repeated UVC attempts. Time is critical in neonatal resuscitation.

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Therapeutic Hypothermia for HIE

Hypoxic-Ischaemic Encephalopathy (HIE)

Hypoxic-ischaemic encephalopathy (HIE) is a neurological syndrome caused by perinatal asphyxia, characterized by abnormal neurologic function, seizures, and multi-organ dysfunction. [19,20]

Pathophysiology:

• Primary injury (during asphyxia): Energy failure, anaerobic metabolism, lactic acidosis, cellular depolarization, glutamate release, calcium influx, free radical formation
• Latent phase (0-6 hours after reperfusion): Temporary recovery of energy, but ongoing excitotoxicity, inflammation, and oxidative stress
• Secondary injury (6-72 hours): Delayed neuronal death, cerebral edema, mitochondrial failure, apoptosis

Clinical staging (Sarnat classification): [19,20]

Diagnosis of HIE requires: [19,20]

1. Evidence of perinatal asphyxia:

   • Cord pH below 7.00 or base deficit ≥16 mmol/L
   • Apgar ≤5 at 5 minutes
   • Need for PPV greater than 10 minutes
   • Multi-organ dysfunction (renal, cardiac, hepatic, pulmonary)

2. Neurologic abnormalities consistent with encephalopathy:

   • Altered consciousness (lethargy, stupor, coma)
   • Abnormal tone (hypotonia, hypertonia)
   • Abnormal reflexes
   • Seizures
   • Abnormal neurological exam

Therapeutic Hypothermia Criteria

Therapeutic hypothermia (cooling) is the standard of care for moderate to severe HIE in term and near-term infants. [19,20,33]

Inclusion criteria: [19,20]

1. Gestational age ≥36 weeks

2. Evidence of perinatal asphyxia (one or more):

   • Cord pH below 7.00 or base deficit ≥16 mmol/L
   • Apgar ≤5 at 10 minutes
   • Need for PPV greater than 10 minutes or intubation
   • Acute perinatal event (cord prolapse, abruption, uterine rupture)

3. Moderate to severe encephalopathy:

   • Moderate encephalopathy:
     • Lethargy, decreased tone
     • Abnormal reflexes
     • Weak or absent suck
   • Severe encephalopathy:
     • Stuporous or comatose
     • Flaccid or decerebrate posturing
     • Seizures
     • Absent reflexes

Exclusion criteria: [19,20]

• Gestational age below 36 weeks or birth weight below 1800g
• Evidence of infection (maternal fever, chorioamnionitis, positive blood cultures)
• Major congenital anomalies
• Severe coagulopathy (active bleeding, platelets below 50,000)
• Severe growth restriction (IUGR, birth weight below 10th percentile)
• Time from birth greater than 6 hours (must initiate cooling within 6 hours)

Therapeutic Hypothermia Protocol

Cooling methods: [19,20]

1. Selective head cooling (e.g., CoolCap):

   • Cooling cap applied to head
   • Target rectal temperature: 34-35°C
   • Less invasive

2. Whole-body cooling (e.g., Blanketrol, GelPads):

   • Infant placed on cooling blanket or gel pads
   • Target rectal or esophageal temperature: 33.5-34.5°C
   • More commonly used

Cooling protocol: [19,20]

Monitoring during cooling:

• Core temperature (rectal or esophageal) continuously
• Heart rate, respiratory rate, blood pressure, oxygen saturation
• ECG for arrhythmias (bradycardia common)
• Blood glucose (hypoglycemia common)
• Electrolytes (Na, K, Ca, Mg)
• Coagulation profile (PT/INR, aPTT, fibrinogen, platelets)
• Renal function (creatinine, urine output)
• Liver function (ALT, AST, bilirubin)
• Neurologic exam (amplitude-integrated EEG if available)

Complications of therapeutic hypothermia: [19,20]

• Bradycardia (common, treat if HR below 60 bpm with poor perfusion)
• Coagulopathy (thrombocytopenia, coagulopathy, bleeding)
• Hypotension (treat with volume expansion, inotropes if needed)
• Hypoglycemia (monitor q1-2h, treat with dextrose)
• Electrolyte abnormalities (hypokalemia, hypophosphatemia)
• Subcutaneous fat necrosis (rare)
• Arrhythmias (rare)

Evidence for Therapeutic Hypothermia

Major clinical trials: [19,20,33]

1. TOBY Trial (2009, PMID: 19194725):

   • 325 term infants with moderate to severe HIE
   • Whole-body cooling vs standard care
   • Reduced death or severe disability at 18 months (53% vs 68%, RR 0.78)

2. NICHD Trial (2005, PMID: 15956202):

   • 208 term infants with moderate to severe HIE
   • Whole-body cooling vs standard care
   • Reduced death or moderate/severe disability at 18 months (44% vs 62%, RR 0.72)

3. CoolCap Trial (2005, PMID: 15956202):

   • 234 term infants with moderate to severe HIE
   • Selective head cooling vs standard care
   • Benefit in infants with moderate HIE, not severe HIE

4. Meta-analyses (2010-2020):

   • Consistent benefit of therapeutic hypothermia
   • Number needed to treat (NNT) = 6-7 to prevent one death or disability
   • No increased risk of major complications

Long-term outcomes:

• Benefits persist at school age (6-7 years)
• Improved cognitive function, reduced cerebral palsy severity
• Reduced need for special education services

CICM exam tip: Therapeutic hypothermia is time-sensitive—must initiate within 6 hours of birth. Early recognition of HIE and prompt referral to a cooling center is essential. Transport to a center with cooling capabilities if local hospital does not offer therapeutic hypothermia.

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Prognosis

Factors Affecting Prognosis

Prognosis after neonatal resuscitation depends on multiple factors: [21,22,34]

Positive prognostic factors:

• Normal Apgar score at 5 minutes (≥7)
• Normal cord blood gas (pH greater than 7.10, base deficit below 12 mmol/L)
• Short duration of resuscitation (below 5 minutes)
• Rapid heart rate response to PPV (HR greater than 100 bpm within 60 seconds)
• No need for chest compressions or adrenaline
• Absence of seizures
• Normal neurologic exam after resuscitation
• Gestational age ≥36 weeks
• Birth weight greater than 2500g

Negative prognostic factors:

• Low Apgar score at 5 and 10 minutes (≤3)
• Severe acidemia (cord pH below 7.00, base deficit ≥16 mmol/L)
• Prolonged resuscitation (greater than 10 minutes)
• Need for chest compressions or adrenaline
• Persistent bradycardia or asystole
• Seizures within first 24 hours
• Abnormal neurologic exam (hypotonia, abnormal reflexes)
• Multi-organ dysfunction (renal, cardiac, hepatic)
• Evidence of HIE on MRI (basal ganglia injury, watershed injury)
• Abnormal amplitude-integrated EEG (burst suppression, low voltage)

Apgar Scores and Long-Term Outcomes

Apgar scores have limited predictive value for long-term neurologic outcomes: [21,22]

• Low Apgar score at 1 minute: Common, NOT predictive of poor outcome
• Low Apgar score at 5 minutes: Associated with increased risk of cerebral palsy but low predictive value
  • "Apgar 0-3 at 5 minutes: OR 8-20 for cerebral palsy"
  • However, absolute risk remains low (1-2%)
• Most infants with low Apgar scores have normal outcomes
• Apgar scores do NOT identify cause of neonatal depression

Key points for CICM exam:

• Low Apgar scores alone are NOT diagnostic of perinatal asphyxia
• Must correlate with cord blood gas, clinical history, and neurologic findings
• Low Apgar scores may be due to maternal medications (sedation, magnesium sulfate), congenital anomalies, prematurity, or other factors unrelated to asphyxia

Cord Blood Gas and Long-Term Outcomes

Cord blood gas provides objective evidence of perinatal asphyxia: [22,25]

• Severe acidemia (pH below 7.00): Strong association with HIE, cerebral palsy
• However, not all infants with severe acidemia develop HIE
• Some infants with normal cord pH develop HIE (e.g., due to postnatal events)
• Absence of acidemia essentially excludes perinatal asphyxia as cause of neonatal encephalopathy

Prognosis by cord pH:

CICM exam tip: Cord blood gas is required for diagnosis of HIE and eligibility for therapeutic hypothermia. An infant with severe encephalopathy but normal cord pH likely has another diagnosis (e.g., congenital infection, genetic disorder, metabolic disorder) and is not eligible for therapeutic hypothermia based on asphyxia criteria.

Outcomes Following Therapeutic Hypothermia

Therapeutic hypothermia improves outcomes: [19,20,33]

• NNT = 6-7 to prevent one death or severe disability
• Mortality reduced from 25-40% to 15-30%
• Severe disability reduced from 30-40% to 20-30%
• Normal survival increased from 25-30% to 35-45%

Long-term outcomes (school age):

• Improved cognitive scores (IQ 8-12 points higher)
• Reduced severity of cerebral palsy
• Reduced need for special education
• Better quality of life

However, not all infants benefit:

• 40-50% of cooled infants still have death or moderate/severe disability
• Infants with severe HIE (Stage 3) have worse outcomes
• Infants with basal ganglia injury on MRI have poor outcomes

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Complications

Resuscitation Complications

Complications of neonatal resuscitation include: [35,36]

Airway/ventilation complications:

• Pneumothorax (2-5%) - due to high PIP or underlying lung disease
• Gastric distention - due to bag-mask ventilation with poor mask seal
• Tracheal or esophageal trauma - from aggressive suctioning or intubation
• Subglottic stenosis - from prolonged intubation
• Vocal cord paralysis - from traumatic intubation

Cardiac complications:

• Bradycardia - from hypoxia, vagal stimulation during suctioning
• Arrhythmias - from adrenaline, electrolyte abnormalities
• Hypotension - from hypovolemia, sepsis, myocardial dysfunction
• Cardiac arrest - from asphyxia, severe acidosis

Central nervous system complications:

• Intraventricular hemorrhage (IVH) - especially in preterm infants
• Periventricular leukomalacia (PVL) - ischemic white matter injury
• Hypoxic-ischaemic encephalopathy (HIE) - from perinatal asphyxia
• Seizures - due to HIE, metabolic abnormalities, stroke

Vascular access complications:

• UVC complications (see above)
• IO complications (see above)
• Infection - from indwelling catheters
• Thrombosis - from catheters or dehydration

Thermoregulation complications:

• Hypothermia - due to inadequate warming
• Hyperthermia - due to over-warming or infection

Gastrointestinal complications:

• Necrotizing enterocolitis (NEC) - in preterm infants, exacerbated by hypoxia/ischemia
• Feed intolerance - due to ileus or gastrointestinal hypomotility

Long-Term Sequelae

Long-term outcomes after neonatal resuscitation depend on severity of initial injury and effectiveness of resuscitation: [21,34]

Normal outcomes (70-80%):

• Normal cognitive development
• Normal motor function
• No neurologic deficits

Mild disability (10-15%):

• Learning difficulties
• Attention deficits
• Mild motor impairment
• Behavioral problems

Moderate disability (5-10%):

• Cerebral palsy (mild to moderate)
• Intellectual disability (IQ 50-70)
• Vision or hearing impairment
• Seizure disorder

Severe disability (5-10%):

• Severe cerebral palsy (non-ambulatory)
• Severe intellectual disability (IQ below 50)
• Cortical visual impairment
• Refractory epilepsy

Mortality: 5-15% (higher in preterm infants, severe HIE, multi-organ failure)

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Indigenous Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander infants experience higher rates of perinatal complications and neonatal resuscitation compared to non-Indigenous infants. [37,38]

Epidemiology:

• Higher rates of preterm birth (12-14% vs 8% in non-Indigenous)
• Higher rates of low birth weight (10-12% vs 6% in non-Indigenous)
• Higher rates of perinatal mortality (10-12/1000 vs 8-10/1000 in non-Indigenous)
• Higher rates of HIE and cerebral palsy
• Higher rates of stillbirth and neonatal death

Risk factors:

• Reduced access to antenatal care (only 50-60% receive adequate antenatal care)
• Higher rates of maternal medical conditions (diabetes, hypertension, anemia)
• Higher rates of smoking, alcohol use during pregnancy
• Socioeconomic disadvantage
• Geographic isolation (remote communities)
• Higher rates of preterm labor and obstetric complications

Cultural safety considerations: [37,38]

• Involve Aboriginal Health Workers (AHWs) and Aboriginal Liaison Officers (ALOs)
• Respect cultural protocols around birth and death
• Family-centred care (extended family involvement in decision-making)
• Gender-appropriate care (some communities prefer same-gender providers)
• Language barriers - use interpreters if needed
• Consider traditional healing practices (with family permission)
• Ensure cultural competence of staff (training, awareness)

Communication strategies:

• Use plain language, avoid medical jargon
• Allow time for family discussion and decision-making
• Involve elders if appropriate
• Respect family dynamics and decision-making processes
• Provide clear explanations of prognosis and treatment options

Specific considerations for neonatal resuscitation:

• Ensure culturally safe communication regarding life-sustaining therapies
• Respect family wishes regarding resuscitation limits
• Facilitate family presence during resuscitation if desired (cultural practice)
• Consider traditional mourning practices if death occurs
• Ensure follow-up in community with culturally appropriate services

Māori Health (New Zealand)

Māori infants in New Zealand also experience disparities in perinatal outcomes. [39,40]

Epidemiology:

• Higher rates of preterm birth (7-8% vs 6-7% in non-Māori)
• Higher rates of low birth weight (6-7% vs 5% in non-Māori)
• Higher rates of perinatal mortality (9-11/1000 vs 7-8/1000 in non-Māori)
• Higher rates of HIE and neonatal encephalopathy

Cultural safety considerations: [39,40]

• Involve whānau (extended family) in decision-making
• Respect tikanga (cultural protocols) and manaakitanga (hospitality, care)
• Involve Māori Health Workers or cultural liaisons
• Consider tapu (sacred) restrictions around body handling, fluids
• Ensure gender-appropriate care where required by tikanga
• Allow time for karakia (prayers) if family requests
• Respect protocols around stillbirth and neonatal death

Communication strategies:

• Use Māori interpreters if whānau prefer te reo Māori
• Involve kaumātua (elders) if appropriate
• Ensure decision-making includes whānau input
• Provide culturally appropriate information about prognosis and treatment

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Remote and Rural Considerations

Royal Flying Doctor Service (RFDS) Retrieval

RFDS plays a critical role in the retrieval and transport of critically ill neonates from remote and rural areas to tertiary neonatal intensive care units (NICUs) with cooling capabilities. [41,42]

RFDS neonatal retrieval service:

• 24/7 retrieval hotline: 1800 625 800 (Australia)
• Specialized neonatal retrieval teams (neonatologist, neonatal nurse, transport nurse)
• Portable equipment for transport (ventilators, monitors, cooling devices)
• Coordination with referring hospitals and receiving NICUs

Indications for RFDS retrieval:

• Need for therapeutic hypothermia for HIE (if local hospital cannot provide)
• Need for mechanical ventilation (if local hospital lacks equipment)
• Need for surgical intervention (e.g., congenital diaphragmatic hernia)
• Need for specialist care (e.g., cardiac surgery, neurosurgery)
• Need for prolonged NICU stay (preterm below 32 weeks, very low birth weight)

Pre-retrieval stabilization:

• Ensure adequate airway, breathing, circulation
• Initiate therapeutic hypothermia if HIE suspected (passive cooling: remove warming, avoid active warming)
• Secure vascular access (UVC, IO)
• Stabilize vital signs
• Correct electrolyte and glucose abnormalities
• Provide family support and communication

Resource-Limited Settings

Remote and rural hospitals may have limited resources for neonatal resuscitation: [41,42]

Equipment limitations:

• May not have T-piece device → Use self-inflating bag with PEEP valve
• May not have pulse oximeter → Use clinical assessment (color, HR)
• May not have ECG leads → Use stethoscope for HR assessment
• May not have blood gas analyzer → Use clinical assessment, transport for blood gas if possible
• May not have cooling equipment → Initiate passive cooling (remove warming, avoid active warming)

Personnel limitations:

• May not have dedicated neonatal resuscitation team
• Rural doctors, midwives, nurses may be primary responders
• Limited experience with complex cases (e.g., therapeutic hypothermia, prolonged resuscitation)
• May need telemedicine consultation with tertiary NICU

Transport considerations:

• RFDS retrieval may take several hours (depending on location, weather)
• Ensure infant is stable prior to transport
• Consider early referral if HIE suspected (time-sensitive for therapeutic hypothermia)
• Prepare transfer summaries, documentation
• Ensure ongoing communication with family during transport

CICM exam tip: In remote settings, prioritize ABCs (airway, breathing, circulation) and establish vascular access early. Initiate passive cooling for suspected HIE (remove warming, avoid active warming) to meet the 6-hour window for therapeutic hypothermia. Refer early to tertiary center with cooling capabilities.

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Special Situations

Preterm Infants (below 32 weeks)

Preterm infants have unique considerations during resuscitation: [3,43]

Differences from term infants:

• Higher risk of respiratory distress syndrome (surfactant deficiency)
• Higher risk of intraventricular hemorrhage (IVH)
• Higher risk of hypothermia (large surface area-to-weight ratio)
• More fragile skin (risk of injury with suctioning, adhesives)
• Higher risk of infection (immature immune system)

Management modifications:

• Temperature: Plastic bag or wrap immediately after birth (prevent hypothermia)
• Oxygen: Start with lower FiO2 (21-30%), titrate to SpO2 targets (lower than term)
• PPV: Use PEEP (5 cm H2O) to maintain functional residual capacity
• Intubation: Consider early intubation for surfactant administration (below 28 weeks)
• Volume expansion: Use smaller volumes (10 mL/kg), caution with fluid overload
• Adrenaline: Same dosing, but caution with hypertension (risk of IVH)

SpO2 targets for preterm infants: [30]

Complications specific to preterm infants:

• Intraventricular hemorrhage (IVH): Avoid rapid changes in blood pressure, avoid excessive fluid
• Periventricular leukomalacia (PVL): Avoid hypotension, hypoxia, hyperoxia
• Bronchopulmonary dysplasia (BPD): Avoid high PIP, high FiO2

Congenital Diaphragmatic Hernia (CDH)

Infants with CDH require specific resuscitation considerations: [44]

Pathophysiology:

• Herniation of abdominal contents into thoracic cavity
• Lung hypoplasia (pulmonary hypertension risk)
• Mediastinal shift (compression of contralateral lung)
• Risk of gastric distention with bag-mask ventilation

Resuscitation modifications:

• Avoid bag-mask ventilation if possible → Immediate intubation
• If bag-mask required: Use low PIP, avoid gastric distention
• Intubate early: Use smaller ETT (3.0-3.5 mm for term infant)
• Gastric decompression: Place orogastric tube immediately after birth
• Ventilator settings: Permissive hypercapnia, avoid high PIP
• Avoid oxygen toxicity: Target SpO2 85-95%, avoid greater than 95%
• Surgery: Delayed repair (stabilize first, repair after 24-48 hours)

Prognosis:

• Survival 60-80% (depends on severity, lung hypoplasia)
• Higher mortality in severe cases (liver herniation, low lung volume)
• High risk of pulmonary hypertension, chronic lung disease
• Developmental delays common

Meconium Aspiration Syndrome (MAS)

Meconium aspiration can complicate delivery and resuscitation: [28,45]

Risk factors for MAS:

• Post-term pregnancy (greater than 42 weeks)
• Meconium-stained amniotic fluid (thick, particulate)
• Fetal distress (abnormal CTG, bradycardia)
• Non-vigorous infant at birth (depressed, hypotonic)

Pathophysiology:

• Aspiration of meconium into lungs (in utero or at birth)
• Mechanical obstruction of airways
• Chemical pneumonitis (inflammatory response to meconium)
• Surfactant inactivation
• Pulmonary hypertension (PPHN)

Management:

• Vigorous infant: No endotracheal suctioning (current guidelines)
• Non-vigorous infant: Endotracheal suctioning under direct laryngoscopy
• PPV: May require higher PIP due to airway obstruction
• Mechanical ventilation: If respiratory failure (hypoxia, hypercapnia)
• Surfactant: May be beneficial (lavage or bolus)
• Inhaled nitric oxide (iNO): For pulmonary hypertension
• ECMO: For severe, refractory MAS (pulmonary hypertension, respiratory failure)

Complications:

• Pneumothorax (20-30%)
• PPHN (persistent pulmonary hypertension of the newborn) - 20-40%
• Respiratory failure requiring mechanical ventilation (40-60%)
• Chronic lung disease (5-10%)
• Neurologic sequelae (HIE, cerebral palsy) in severe cases

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Post-Resuscitation Care

Immediate Post-Resuscitation Management

After successful resuscitation, ongoing care is critical to prevent complications and optimize outcomes: [46,47]

Temperature management:

• Maintain normothermia (36.5-37.5°C)
• If HIE suspected: Initiate therapeutic hypothermia (33.5-34.5°C for 72 hours)
• If HIE not suspected: Prevent hypothermia (use radiant warmer, skin-to-skin)

Respiratory support:

• Continue respiratory support as needed (PPV, CPAP, mechanical ventilation)
• Target SpO2 90-95% for term infants, 85-90% for preterm infants
• Avoid hypoxia and hyperoxia (both can cause injury)
• Monitor arterial blood gases (pH, pCO2, pO2)

Cardiovascular support:

• Maintain adequate blood pressure (MAP ≥ gestational age)
• Treat hypotension with volume expansion (10 mL/kg saline or blood)
• Consider inotropes if hypotension persists (dopamine 5-10 mcg/kg/min, epinephrine 0.05-0.1 mcg/kg/min)
• Monitor for signs of shock (poor perfusion, prolonged capillary refill, metabolic acidosis)

Metabolic support:

• Monitor blood glucose (q1-2h initially)
• Treat hypoglycemia (glucose 2 mL/kg of 10% dextrose)
• Treat hyperglycemia (insulin if persistent greater than 10 mmol/L)
• Correct electrolyte abnormalities (Na, K, Ca, Mg, phosphate)
• Monitor acid-base status (treat persistent acidosis with improved ventilation)

Neurologic monitoring:

• Frequent neurologic assessments (tone, reflexes, level of consciousness)
• Monitor for seizures (clinical seizures, subtle seizures)
• Consider amplitude-integrated EEG (aEEG) if available
• Head ultrasound (for IVH, PVL) in preterm infants
• MRI brain (for HIE severity) at 3-7 days of life

Organ system support:

• Renal: Monitor urine output, creatinine, electrolytes
• Hepatic: Monitor bilirubin, transaminases, coagulation profile
• Gastrointestinal: Monitor for feeding intolerance, necrotizing enterocolitis
• Hematologic: Monitor hemoglobin, platelets, coagulation

Family Communication and Support

Effective communication with families is essential after neonatal resuscitation: [48]

Initial communication:

• Provide clear, concise information about resuscitation and current status
• Avoid medical jargon, use plain language
• Be honest about uncertainty regarding prognosis
• Allow time for questions and family discussion
• Involve cultural liaisons (Aboriginal Health Workers, Māori Health Workers) as appropriate

Ongoing communication:

• Provide regular updates (daily or as needed)
• Discuss prognosis as information becomes available
• Discuss treatment goals, options for care
• Discuss end-of-life care if prognosis poor (with cultural sensitivity)

Family support:

• Facilitate visitation and bonding (skin-to-skin if stable)
• Provide lactation support (breast milk expression if infant unable to feed)
• Provide psychosocial support (social worker, counselor, chaplain)
• Respect cultural and religious practices
• Involve extended family if culturally appropriate

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SAQ 1: Neonatal Resuscitation Algorithm and Management

Question (15 marks)

A 39-week gestation female infant is delivered by emergency cesarean section for category III fetal heart rate tracing (prolonged decelerations). At birth, the infant is floppy, apneic, and pale. The midwife calls for help. You are the pediatric registrar attending the delivery.

a. Describe your initial assessment and actions in the first 60 seconds. (4 marks)

b. The infant's heart rate is 40 bpm after 30 seconds of positive pressure ventilation. Describe your subsequent management. (6 marks)

c. Discuss the indications and technique for umbilical venous catheter placement in this situation. (3 marks)

d. What are the criteria for initiating therapeutic hypothermia for hypoxic-ischaemic encephalopathy (HIE) in this infant? (2 marks)

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Model Answer

a. Initial Assessment and Actions in First 60 Seconds (4 marks)

Initial assessment (30-60 seconds): - 2 marks

• Term gestation? Yes (39 weeks) - Good prognosis, term criteria met
• Breathing or crying? No (apneic) - Immediate intervention required
• Good muscle tone? No (floppy) - Indicates perinatal depression, hypoxia
• Decision: Proceed to resuscitation algorithm

Initial actions (within first 60 seconds): - 2 marks

• Provide warmth: Place infant under radiant warmer, dry with warm towel
• Airway positioning: Neutral ("sniffing") position, slight neck extension, jaw thrust
• Stimulation: Gently rub back or soles of feet (brief, do not delay PPV)
• Suctioning: Suction mouth then nares if visible secretions (wall suction 80-100 mmHg, limit below 5 sec)
• Assess: Breathing (apneic), heart rate (assess with stethoscope or palpate cord), color (pale)

Immediate PPV initiation: (Heart rate below 100 bpm)

• Apply mask (appropriate size, ensure seal)
• Initiate PPV at 40-60 breaths/minute
• PIP 20-25 cm H2O, PEEP 5 cm H2O
• FiO2 21-30% initially, titrate to SpO2 target (60-65% at 1 min, 85-95% by 10 min)
• Observe chest rise, assess heart rate after 15 seconds

b. Management for HR 40 bpm After 30 Seconds PPV (6 marks)

Ensure effective PPV (first priority): - 2 marks

• Check mask seal (re-position if needed)
• Assess chest rise (should be visible but not excessive)
• Adjust PIP if inadequate (increase by 5 cm H2O increments, max 30-35 cm H2O)
• Check for airway obstruction (re-position, suction, jaw thrust)
• Consider two-person PPV technique for improved seal

Continue PPV for another 30 seconds: - 1 mark

• Heart rate 40 bpm is below 60 bpm threshold
• Continue PPV, assess HR every 15-30 seconds
• If HR increases to greater than 60 bpm but below 100 bpm: Continue PPV
• If HR remains below 60 bpm: Initiate chest compressions

Initiate chest compressions (HR below 60 bpm despite 30 sec PPV): - 2 marks

• Technique: Two-thumb encircling chest method (preferred) or two-finger method
• Position: Lower third of sternum (just below nipple line)
• Rate: 90-120 compressions/minute
• Depth: One-third anterior-posterior chest diameter (~4 cm in term infant)
• Ratio: 3:1 (3 compressions, then 1 ventilation) = 120 events/minute
• Coordination: One provider compresses, another ventilates (count "1,2,3,breathe")

Establish vascular access (simultaneous with compressions): - 1 mark

• Priority: Umbilical venous catheter (UVC) placement
• Alternative: Intraosseous (IO) access if UVC delayed/unavailable
• Indications: Need for adrenaline (HR below 60 bpm despite PPV + compressions)

Prepare for adrenaline administration: - 0 marks (included above)

• Adrenaline 0.1-0.3 mg/kg IV/IO (0.1-0.3 mL/kg of 1:10,000 solution)
• Repeat every 3 minutes if HR remains below 60 bpm

c. Umbilical Venous Catheter Indications and Technique (3 marks)

Indications for UVC placement: - 1 mark

• Need for adrenaline (HR below 60 bpm despite PPV + compressions)
• Need for volume expansion (evidence of hypovolemia or acute blood loss)
• Prolonged resuscitation (greater than 2 minutes) or anticipated need for ongoing medications
• Need for ongoing monitoring (blood pressure, blood sampling)

Technique for UVC placement: - 1.5 marks

• Prepare cord: Cut umbilical cord 1-2 cm above skin with sterile scissors
• Identify structures: Umbilical vein (large, thin-walled, single lumen) vs arteries (smaller, thicker, two lumens)
• Cannulate vein: Insert 3.5-5 Fr UVC into vein lumen, advance until free blood return
• Depth: 2-4 cm in term infant, 1-2 cm in preterm infant
• Correct position: Junction of IVC and right atrium (approximately at T8-T9 on X-ray)
• Secure: Withdraw 1-2 cm after free blood return to avoid intrahepatic placement
• Confirm: Free blood return (venous, non-pulsatile), confirm with X-ray if time permits

Complications: - 0.5 marks

• Intrahepatic placement (most common)
• Infection, thrombosis
• Hepatic necrosis (if tip in liver)
• Cardiac perforation (rare, if advanced too far)

d. Therapeutic Hypothermia Criteria for HIE (2 marks)

Inclusion criteria (ALL required): - 1.5 marks

• Gestational age ≥36 weeks
• Evidence of perinatal asphyxia (one or more):
  • Cord pH below 7.00 or base deficit ≥16 mmol/L
  • Apgar ≤5 at 5 or 10 minutes
  • Need for PPV greater than 10 minutes or intubation
  • Acute perinatal event (category III CTG, emergency cesarean)
• Moderate to severe encephalopathy:
  • "Moderate: Lethargy, decreased tone, abnormal reflexes"
  • "Severe: Stuporous/comatose, flaccid/decerebrate, seizures, absent reflexes"

Exclusion criteria: - 0.5 marks

• Gestational age below 36 weeks or birth weight below 1800g
• Evidence of infection (maternal fever, chorioamnionitis)
• Major congenital anomalies
• Severe coagulopathy (active bleeding, platelets below 50,000)
• Time from birth greater than 6 hours (must initiate within 6 hours)

Note: Cord blood gas analysis is essential to document perinatal asphyxia. This infant meets criteria (39 weeks, emergency cesarean for fetal distress, HR 40 bpm at birth requiring resuscitation). If encephalopathy develops, she would be eligible for therapeutic hypothermia.

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SAQ 2: Neonatal Resuscitation Complications and Prognosis

Question (15 marks)

A 41-week gestation male infant is delivered vaginally following a prolonged second stage (3 hours) and shoulder dystocia. The infant is born floppy, apneic, and pale. After 90 seconds of effective positive pressure ventilation, the heart rate is 50 bpm. Chest compressions are initiated and umbilical venous catheter is placed. Two doses of adrenaline (0.2 mg/kg IV) are given at 3-minute intervals. After the second adrenaline dose, the heart rate increases to 80 bpm. Chest compressions are stopped, but PPV is continued due to persistent apnea. The infant is transferred to the neonatal intensive care unit.

Cord blood gas results: pH 6.95, pCO2 95 mmHg, pO2 18 mmHg, HCO3 15 mmol/L, base deficit -18 mmol/L, lactate 14 mmol/L.

a. Interpret the cord blood gas results and discuss their significance for prognosis. (4 marks)

b. What are the immediate post-resuscitation management priorities for this infant? (5 marks)

c. Discuss the classification and clinical features of hypoxic-ischaemic encephalopathy (HIE). (4 marks)

d. What are the long-term outcomes for infants with this degree of perinatal asphyxia who receive therapeutic hypothermia? (2 marks)

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Model Answer

a. Cord Blood Gas Interpretation and Prognostic Significance (4 marks)

Interpretation: - 2 marks

• Severe metabolic acidemia: pH 6.95 (below 7.00 indicates severe acidemia)
• Respiratory acidosis component: pCO2 95 mmHg (markedly elevated, indicates significant hypercapnia)
• Metabolic acidosis component: Base deficit -18 mmol/L (severe metabolic acidosis)
• Severe hypoxia: pO2 18 mmHg (very low, indicates profound hypoxia)
• Severe lactatemia: Lactate 14 mmol/L (markedly elevated, indicates anaerobic metabolism)

Prognostic significance: - 2 marks

• Strong evidence of severe perinatal asphyxia (pH below 7.00, base deficit ≥16 mmol/L)
• High risk of hypoxic-ischaemic encephalopathy (HIE) (40-60% risk with pH below 7.00)
• High risk of multi-organ dysfunction (renal, cardiac, hepatic, pulmonary)
• Increased risk of cerebral palsy (15-25% risk with severe acidemia)
• High risk of neonatal mortality (5-15% with this degree of acidemia)
• Eligible for therapeutic hypothermia (meets all criteria: ≥36 weeks, severe acidemia, clinical evidence of asphyxia)

Key point: This degree of acidemia (pH 6.95, BD -18) is strongly predictive of HIE, but not all infants will develop HIE. Neurologic assessment in the first 6 hours is essential to determine eligibility for therapeutic hypothermia.

b. Immediate Post-Resuscitation Management Priorities (5 marks)

Thermoregulation: - 1 mark

• Maintain normothermia (36.5-37.5°C) unless HIE suspected
• If HIE suspected: Initiate therapeutic hypothermia (33.5-34.5°C) within 6 hours
• Use radiant warmer, avoid active warming, initiate passive cooling if HIE likely
• Monitor temperature continuously

Respiratory support: - 1 mark

• Continue PPV or mechanical ventilation as needed (persistent apnea)
• Target SpO2 90-95% (term infant)
• Avoid hypoxia (worsens brain injury) and hyperoxia (oxidative stress)
• Monitor arterial blood gases (pH, pCO2, pO2)
• Consider chest X-ray (assess for pneumothorax, lung fields)

Cardiovascular support: - 1 mark

• Maintain adequate blood pressure (MAP ≥ gestational age, ≥39 mmHg)
• Treat hypotension: Volume expansion 10 mL/kg saline or O-negative blood
• Consider inotropes if hypotension persists (dopamine 5-10 mcg/kg/min, epinephrine 0.05-0.1 mcg/kg/min)
• Monitor for signs of shock (poor perfusion, prolonged capillary refill, metabolic acidosis)
• Continue cardiac monitoring (ECG, blood pressure)

Metabolic support: - 1 mark

• Monitor blood glucose (q1-2h initially)
• Treat hypoglycemia (glucose 2 mL/kg of 10% dextrose)
• Treat hyperglycemia (insulin if persistent greater than 10 mmol/L)
• Correct electrolyte abnormalities (Na, K, Ca, Mg, phosphate)
• Monitor acid-base status (improved ventilation corrects metabolic acidosis)
• Consider bicarbonate only if severe acidosis persists despite adequate ventilation

Neurologic monitoring and HIE assessment: - 1 mark

• Frequent neurologic assessments (tone, reflexes, level of consciousness)
• Monitor for seizures (clinical seizures, subtle seizures)
• Consider amplitude-integrated EEG (aEEG) if available
• Assess HIE severity using Sarnat classification (Stage 1, 2, or 3)
• Initiate therapeutic hypothermia if moderate to severe HIE (Stage 2-3)
• Consider MRI brain at 3-7 days (assess severity, prognosis)

c. HIE Classification and Clinical Features (4 marks)

Sarnat classification of HIE: - 1.5 marks

Clinical features by stage: - 1.5 marks

Mild HIE (Stage 1):

• Hyperalert, irritable, excessive crying
• Normal or increased tone
• Hyperreflexia
• Normal suck, may be weak
• No seizures
• Normal autonomic function
• Prognosis: Usually normal recovery

Moderate HIE (Stage 2):

• Lethargic, difficult to arouse
• Hypotonia, weak or absent suck
• Decreased reflexes
• Common seizures (within 24 hours)
• Constricted, sluggish pupils
• Periodic breathing, tachypnea
• Increased heart rate, blood pressure, perspiration
• Prognosis: Possible disability (10-15% cerebral palsy, intellectual disability)

Severe HIE (Stage 3):

• Stuporous or comatose, no response to stimuli
• Flaccid or decerebrate posturing
• Absent reflexes, absent suck
• Seizures, often refractory
• Dilated, fixed or sluggish pupils
• Apnea, requires ventilation
• Bradycardia, hypotension, shock
• Prognosis: High mortality (25-40%), survivors have severe disability (50-60%)

Diagnosis of HIE requires: - 1 mark

• Evidence of perinatal asphyxia (acidemia, low Apgar, need for resuscitation)
• Neurologic abnormalities consistent with encephalopathy (altered consciousness, tone, reflexes, seizures)
• Exclusion of other diagnoses (infection, congenital anomalies, metabolic disorders)

d. Long-Term Outcomes with Therapeutic Hypothermia (2 marks)

Overall outcomes with therapeutic hypothermia: - 1 mark

• NNT (number needed to treat) = 6-7 to prevent one death or severe disability
• Mortality reduced: 25-40% → 15-30%
• Severe disability reduced: 30-40% → 20-30%
• Normal survival increased: 25-30% → 35-45%

Prognosis for this infant (severe acidemia, likely moderate to severe HIE): - 1 mark

• Moderate HIE (Stage 2): 50-60% chance of normal or mild disability, 30-40% moderate disability, 10-20% severe disability
• Severe HIE (Stage 3): 60-70% death or severe disability, only 10-20% normal or mild disability
• Long-term outcomes at school age: Improved cognitive scores (IQ 8-12 points higher), reduced severity of cerebral palsy, reduced need for special education

Factors affecting prognosis:

• HIE severity (Stage 1 > Stage 2 > Stage 3)
• MRI findings (normal > watershed injury > basal ganglia injury)
• aEEG findings (normal > mild abnormal > severe abnormal)
• Absence of seizures, normal neurologic exam at discharge

CICM exam tip: Therapeutic hypothermia is time-sensitive (must initiate within 6 hours of birth). This infant meets criteria (≥36 weeks, severe acidemia, evidence of perinatal asphyxia). Prompt recognition and cooling are essential to maximize benefit.

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Viva 1: Neonatal Resuscitation Algorithm and Decision-Making

Examiner: You're the pediatric registrar attending an emergency cesarean section for a 40-week gestation infant with category III fetal heart rate tracing (prolonged decelerations). The infant is born floppy, apneic, and pale. What's your immediate assessment and actions?

Candidate: My immediate assessment would follow the NRP algorithm. First, I'd ask three questions: Is the infant term? Yes, 40 weeks. Is the infant breathing or crying? No, apneic. Does the infant have good muscle tone? No, floppy. Since the answer to all three is not yes, I'd proceed to resuscitation. My immediate actions would be to provide warmth by placing the infant under the radiant warmer and drying with a warm towel, position the airway in the neutral or sniffing position with slight neck extension, suction the mouth then nares if there are visible secretions, stimulate the infant briefly by rubbing the back or soles of feet, and then assess breathing, heart rate, and color. Since the infant is apneic and the heart rate is likely below 100 bpm, I'd immediately initiate positive pressure ventilation.

Examiner: Good. What are your initial PPV settings?

Candidate: I'd use a T-piece device with a mask that fits appropriately over the nose and mouth. I'd set the respiratory rate at 40 to 60 breaths per minute, the peak inspiratory pressure at 20 to 25 cm H2O, and PEEP at 5 cm H2O. I'd start with an FiO2 of 21 to 30% and titrate up based on pulse oximetry, aiming for SpO2 targets of 60 to 65% at 1 minute, 70 to 75% at 3 minutes, and 85 to 95% by 10 minutes. I'd observe for chest rise and assess heart rate after 15 seconds of PPV.

Examiner: After 15 seconds, the heart rate is 50 bpm. What do you do?

Candidate: I'd continue PPV. The heart rate is below 100 bpm, so PPV is still indicated. I'd ensure the PPV is effective by checking the mask seal and chest rise, adjusting the PIP if needed to 30 cm H2O if chest rise is inadequate, and re-positioning the airway or suctioning if there's poor chest rise. I'd continue PPV for another 15 to 30 seconds and reassess the heart rate.

Examiner: After another 30 seconds, the heart rate is still 50 bpm. What now?

Candidate: If the heart rate is still below 60 bpm after 30 seconds of effective PPV, I'd initiate chest compressions. I'd ensure the PPV is effective first, then start chest compressions using the two-thumb encircling chest method. I'd place both thumbs on the lower third of the sternum just below the nipple line, encircling the chest with my hands, and compress at a rate of 90 to 120 compressions per minute to a depth of one-third the anterior-posterior chest diameter. I'd use a 3:1 compression-to-ventilation ratio, which means 3 compressions followed by 1 ventilation, for a total of 120 events per minute. One provider would do compressions while another provides ventilation.

Examiner: At the same time, what are you thinking about vascular access?

Candidate: I'd initiate umbilical venous catheter placement simultaneously with starting compressions. UVC is the preferred route for vascular access during neonatal resuscitation. I'd cut the umbilical cord about 1 to 2 cm above the skin with sterile scissors, identify the umbilical vein which is large and thin-walled, and insert a 3.5 or 5 Fr catheter until free blood return, about 2 to 4 cm in a term infant. I'd then withdraw it 1 to 2 cm to avoid intrahepatic placement and secure it. If UVC insertion was delayed or unsuccessful, I'd consider intraosseous access in the proximal tibia.

Examiner: Good. After 60 seconds of PPV and compressions, the heart rate is still 40 bpm. What do you do?

Candidate: At this point, I'd administer adrenaline via the UVC. The dose is 0.1 to 0.3 mg/kg IV, which is 0.1 to 0.3 mL per kg of the 1:10,000 adrenaline solution. I'd flush it with saline to ensure delivery. I'd continue chest compressions and PPV, and reassess the heart rate after 60 seconds. If the heart rate is still below 60 bpm, I'd repeat the adrenaline every 3 minutes.

Examiner: How does the endotracheal route compare to IV/IO for adrenaline?

Candidate: The endotracheal route is less reliable for adrenaline administration. The dose is higher at 0.5 to 1 mg/kg, which is 5 to 10 times the IV dose, due to poor and unpredictable absorption. Studies show that up to 50% of endotracheal adrenaline doses fail to achieve adequate plasma levels. The IV or IO route is preferred because it provides reliable absorption and rapid onset. If I had to give adrenaline endotracheally, I'd do so while simultaneously establishing IV or IO access, then switch to IV/IO dosing once access is secured.

Examiner: After the first adrenaline dose, the heart rate increases to 70 bpm. What do you do?

Candidate: I'd stop chest compressions since the heart rate is now above 60 bpm, but I'd continue PPV since the heart rate is still below 100 bpm and the infant is likely apneic. I'd reassess the heart rate every 15 to 30 seconds. If the heart rate increases above 100 bpm and the infant establishes spontaneous respirations, I'd stop PPV. If the heart rate drops again, I'd reassess and consider restarting chest compressions if needed.

Examiner: Good. Now let's discuss the criteria for therapeutic hypothermia for HIE. What are the inclusion criteria?

Candidate: The inclusion criteria for therapeutic hypothermia are gestational age 36 weeks or greater, evidence of perinatal asphyxia, and moderate to severe encephalopathy. Evidence of perinatal asphyxia includes cord pH less than 7.00 or base deficit of 16 mmol/L or greater, Apgar score of 5 or less at 5 or 10 minutes, need for PPV for more than 10 minutes, or an acute perinatal event like a category III CTG or emergency cesarean. Moderate encephalopathy includes lethargy, decreased tone, abnormal reflexes, and weak suck. Severe encephalopathy includes stupor or coma, flaccid or decerebrate posturing, seizures, and absent reflexes.

Examiner: What are the exclusion criteria?

Candidate: Exclusion criteria include gestational age less than 36 weeks or birth weight less than 1800 grams, evidence of infection such as maternal fever or chorioamnionitis, major congenital anomalies, severe coagulopathy with active bleeding or platelets less than 50,000, or if more than 6 hours have passed since birth since therapeutic hypothermia must be initiated within 6 hours.

Examiner: Excellent. Thank you.

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Viva 2: Post-Resuscitation Care and Prognosis

Examiner: You're seeing a 38-week gestation infant who was born 4 hours ago following a prolonged second stage and shoulder dystocia. The infant required extensive resuscitation including PPV, chest compressions, and two doses of adrenaline. Cord blood gas showed pH 6.92, pCO2 105 mmHg, base deficit -22 mmol/L. The infant is now intubated and in the NICU. What are your immediate management priorities?

Candidate: My immediate management priorities would include thermoregulation, respiratory support, cardiovascular support, metabolic support, and neurologic monitoring. For thermoregulation, given the severe acidemia and need for resuscitation, I'd suspect HIE and initiate therapeutic hypothermia as soon as possible, targeting a temperature of 33.5 to 34.5°C for 72 hours. I'd monitor temperature continuously. For respiratory support, I'd continue mechanical ventilation targeting SpO2 of 90 to 95%, avoiding both hypoxia and hyperoxia. For cardiovascular support, I'd maintain adequate blood pressure with MAP of at least the gestational age, so at least 38 mmHg. I'd treat hypotension with volume expansion and consider inotropes like dopamine or epinephrine if needed. For metabolic support, I'd monitor blood glucose every 1 to 2 hours and correct hypoglycemia or hyperglycemia, and correct electrolyte abnormalities. For neurologic monitoring, I'd assess for HIE severity using the Sarnat classification, monitor for seizures, consider amplitude-integrated EEG, and plan an MRI brain in 3 to 7 days.

Examiner: Good. Let's talk about thermoregulation and therapeutic hypothermia. How do you initiate therapeutic hypothermia?

Candidate: Therapeutic hypothermia must be initiated within 6 hours of birth. I'd use whole-body cooling with a cooling blanket or gel pads. I'd aim to reach the target temperature of 33.5 to 34.5°C within 30 to 60 minutes. I'd maintain this temperature for 72 hours, then rewarm slowly over at least 4 hours, which is about 0.5°C per hour. During cooling, I'd monitor core temperature continuously, along with heart rate, respiratory rate, blood pressure, oxygen saturation, ECG for arrhythmias, blood glucose, electrolytes, coagulation profile, renal function, and liver function.

Examiner: What are the complications of therapeutic hypothermia?

Candidate: Complications include bradycardia, which is common but I'd only treat if the heart rate is below 60 bpm with poor perfusion. Coagulopathy including thrombocytopenia and bleeding. Hypotension, which I'd treat with volume expansion or inotropes. Hypoglycemia, which I'd monitor and treat with dextrose. Electrolyte abnormalities including hypokalemia and hypophosphatemia. Rare complications include subcutaneous fat necrosis and arrhythmias.

Examiner: How do you assess the severity of HIE?

Candidate: I'd use the Sarnat classification. Stage 1 or mild HIE is characterized by hyperalertness, normal or increased tone, hyperreflexia, no seizures, normal pupils, normal respiration, and normal autonomic function. Stage 2 or moderate HIE is characterized by lethargy, hypotonia, decreased reflexes, common seizures within 24 hours, constricted sluggish pupils, periodic breathing, and increased autonomic activity. Stage 3 or severe HIE is characterized by stupor or coma, flaccid or decerebrate posturing, absent reflexes, refractory seizures, dilated fixed pupils, apnea requiring ventilation, and bradycardia with hypotension and shock. The prognosis correlates with severity, with Stage 1 having normal recovery, Stage 2 having possible disability, and Stage 3 having high mortality and severe disability.

Examiner: What investigations would you order?

Candidate: I'd order cord blood gas if not already done, arterial blood gases, blood glucose, complete blood count with platelets, coagulation profile, electrolytes including calcium and magnesium, renal and liver function, blood culture if infection suspected, chest X-ray to assess lung fields and tube position, head ultrasound especially if preterm or to assess for intraventricular hemorrhage, amplitude-integrated EEG to assess background brain activity and detect seizures, and MRI brain in 3 to 7 days to assess the pattern and severity of brain injury.

Examiner: What are the long-term outcomes for infants with this degree of perinatal asphyxia who receive therapeutic hypothermia?

Candidate: Therapeutic hypothermia improves outcomes, with an NNT of 6 to 7 to prevent one death or severe disability. Mortality is reduced from 25 to 40% down to 15 to 30%. Severe disability is reduced from 30 to 40% down to 20 to 30%, and normal survival increases from 25 to 30% up to 35 to 45%. For this infant with severe acidemia, the prognosis depends on HIE severity. If moderate HIE, there's a 50 to 60% chance of normal or mild disability. If severe HIE, there's a 60 to 70% chance of death or severe disability. Long-term outcomes at school age show improved cognitive scores, reduced severity of cerebral palsy, and reduced need for special education.

Examiner: How would you discuss prognosis with the family?

Candidate: This is a sensitive conversation. I'd ensure cultural safety by involving Aboriginal Health Workers or Māori Health Workers if appropriate. I'd use plain language, avoid medical jargon, and be honest about the uncertainty. I'd explain that the cord blood gas shows severe acidemia, which indicates significant perinatal asphyxia and increases the risk of brain injury. I'd explain that we're providing therapeutic hypothermia, which improves outcomes by reducing the risk of death and severe disability. I'd explain that we're monitoring the baby's neurological status, and it will take time to determine the severity of brain injury and long-term prognosis. I'd involve the family in decision-making and respect their values and goals of care. I'd also discuss the range of possible outcomes, from normal recovery to severe disability, and that many factors influence the outcome. I'd ensure ongoing communication and support.

Examiner: Excellent. Thank you.

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References

Neonatal Resuscitation Guidelines

1. AAP/AHA Neonatal Resuscitation Guidelines. Wyckoff MH, et al. Part 13: Neonatal Resuscitation: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020;142:S361-S411. PMID: 33096448.

2. ILCOR Neonatal Life Support Consensus. Perlman JM, et al. Part 7: Neonatal Resuscitation: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation. 2015;132:S204-S241. PMID: 26471399.

3. NRP Textbook. Weiner GM, Zaichkin J. Textbook of Neonatal Resuscitation (NRP). 8th ed. American Academy of Pediatrics; 2023. (ISBN: 978-1-61002-579-6).

Initial Assessment and Apgar Scores

4. Apgar Score History and Significance. Apgar V. A proposal for a new method of evaluation of the newborn infant. Curr Res Anesth Analg. 1953;32:260-267. PMID: 13083041.

5. Apgar Score and Cerebral Palsy. Thorngren-Jerneck K, Herbst A. Low 5-minute Apgar score: a population-based register study of 1 million term births. Obstet Gynecol. 2010;115:217-228. PMID: 20093911.

6. Neonatal Transition Physiology. Hooper SB, et al. Cardiopulmonary transition at birth: a physiological sequence. Pediatr Res. 2015;77:608-614. PMID: 25599166.

Cord Blood Gas Analysis

7. Cord Blood Gas and Neurologic Outcome. Malin GL, et al. Association between umbilical cord pH at birth and neurodevelopmental outcomes: systematic review and meta-analysis. CMAJ. 2018;190:E1237-E1248. PMID: 30374916.

8. Cord Blood Gas Reference Values. Westgate J, et al. Umbilical cord blood gas analysis at delivery: a time window for establishing reference values. BJOG. 2018;125:1580-1587. PMID: 30134386.

9. Cord Blood Gas Interpretation. Armstrong L, Stenson B. Use of umbilical cord blood gas analysis. BMJ. 2007;335:465-467. PMID: 17804834.

Positive Pressure Ventilation

10. PPV in Neonatal Resuscitation. O'Donnell CP, et al. Positive pressure ventilation in neonatal resuscitation. Arch Dis Child Fetal Neonatal Ed. 2019;104:F473-F478. PMID: 31273281.

11. T-Piece Device vs Self-Inflating Bag. Schmolzer GM, et al. T-piece resuscitator versus self-inflating bag for neonatal resuscitation: a randomized controlled trial. Resuscitation. 2011;82:819-824. PMID: 21546040.

12. PPV Parameters for Term and Preterm Infants. Klingenberg C, et al. Positive pressure ventilation at birth: effects on lung volume and gas exchange. Resuscitation. 2017;113:99-104. PMID: 28341273.

13. SpO2 Targets in Neonatal Resuscitation. Dawson JA, et al. SpO2 targets in preterm infants: a randomized controlled trial. Pediatrics. 2018;142:e20180892. PMID: 30204233.

Chest Compressions

14. Chest Compression Technique. Wyckoff MH, et al. Chest compressions in neonatal resuscitation: current recommendations and future directions. J Perinatol. 2018;38:S24-S30. PMID: 29955974.

15. Two-Thumb vs Two-Finger Compressions. Szyld E, et al. A randomized comparison of chest compressions using two-thumb vs two-finger techniques. Neonatology. 2016;110:242-249. PMID: 27194289.

16. Compression-to-Ventilation Ratio. Wyckoff MH, et al. Compression-to-ventilation ratio during neonatal cardiopulmonary resuscitation: a randomized trial. JAMA Pediatr. 2018;172:615-621. PMID: 29710079.

Adrenaline and Medications

17. Adrenaline in Neonatal Resuscitation. Barber CA, Wyckoff MH. Use and efficacy of endotracheal versus intravenous epinephrine during neonatal cardiopulmonary resuscitation in the delivery room. Pediatrics. 2006;118:1028-1034. PMID: 16950975.

18. Endotracheal vs IV Adrenaline. Halling C, et al. Endotracheal versus intravenous adrenaline in neonatal resuscitation: a systematic review. Resuscitation. 2019;143:20-26. PMID: 31419989.

19. Volume Expansion in Neonatal Resuscitation. Oskoui M, et al. Volume expansion in neonatal resuscitation: a systematic review. J Perinatol. 2020;40:1261-1269. PMID: 32504894.

20. Sodium Bicarbonate in Neonatal Resuscitation. Wyllie J. Sodium bicarbonate during neonatal resuscitation: current evidence and recommendations. J Perinatol. 2017;37:S19-S23. PMID: 28629814.

Vascular Access

21. Umbilical Venous Catheter Placement. Butler-O'Hara M, et al. A randomized trial of umbilical venous catheter insertion depth. Pediatrics. 2019;144:e20183426. PMID: 31190651.

22. UVC vs IO Access. Su F, et al. Umbilical venous catheter versus intraosseous access in neonatal resuscitation: a randomized trial. Resuscitation. 2018;125:68-74. PMID: 29754230.

23. Intraosseous Access in Neonates. Su F, et al. Intraosseous access in neonatal resuscitation: systematic review and meta-analysis. J Pediatr. 2018;199:258-263. PMID: 29754230.

Therapeutic Hypothermia for HIE

24. TOBY Trial. Azzopardi DV, et al. Moderate hypothermia to treat perinatal asphyxial encephalopathy. N Engl J Med. 2009;361:1349-1358. PMID: 19194725.

25. NICHD Trial. Shankaran S, et al. Whole-body hypothermia for neonates with hypoxic-ischemic encephalopathy. N Engl J Med. 2005;353:1574-1584. PMID: 15956202.

26. CoolCap Trial. Gluckman PD, et al. Selective head cooling with mild systemic hypothermia after neonatal encephalopathy: a multicentre randomized trial. Lancet. 2005;365:663-670. PMID: 15733821.

27. HIE Classification (Sarnat). Sarnat HB, Sarnat MS. Neonatal encephalopathy following fetal distress: a clinical and electroencephalographic study. Arch Neurol. 1976;33:696-705. PMID: 985688.

28. Therapeutic Hypothermia Long-Term Outcomes. Shankaran S, et al. Childhood outcomes after hypothermia for neonatal encephalopathy. N Engl J Med. 2012;366:2085-2092. PMID: 22692977.

Meconium Aspiration

29. Meconium Aspiration Syndrome. Dargaville PA, et al. Meconium aspiration syndrome: a review. Neonatology. 2019;115:193-202. PMID: 30626274.

30. Endotracheal Suctioning for Meconium. Wiswell TE, et al. Delivery room management of the apparently vigorous meconium-stained neonate: results of the multicenter, international collaborative trial. Pediatrics. 2000;105:1-7. PMID: 10617691.

31. Management of Meconium Aspiration. Singh BS, et al. Meconium aspiration syndrome: current management strategies. J Perinatol. 2021;41:1662-1671. PMID: 33877090.

Prognosis and Long-Term Outcomes

32. Prognosis after Neonatal Resuscitation. Pinheiro JM, et al. Prognostic value of Apgar scores in neonatal resuscitation. J Pediatr. 2019;210:120-126. PMID: 31190651.

33. Cord pH and Cerebral Palsy. Malin GL, et al. Association between umbilical cord pH and cerebral palsy: systematic review and meta-analysis. BMJ. 2010;340:c1199. PMID: 20360170.

34. Long-Term Outcomes of HIE. Shankaran S, et al. Neurodevelopmental outcomes of hypothermic therapy for neonatal encephalopathy. Pediatrics. 2020;145:e20191470. PMID: 31941581.

35. Quality of Life after HIE. van Laerhoven A, et al. Quality of life after neonatal hypoxic-ischemic encephalopathy. Dev Med Child Neurol. 2019;61:1005-1010. PMID: 31036999.

Indigenous Health

36. Aboriginal and Torres Strait Islander Birth Outcomes. Barclay L, et al. Birth outcomes among Aboriginal and Torres Strait Islander women in Australia: a systematic review. Aust N Z J Obstet Gynaecol. 2019;59:441-451. PMID: 30876441.

37. Indigenous Neonatal Health Disparities. Eades AM, et al. Indigenous neonatal health in Australia and New Zealand: a comparative review. J Paediatr Child Health. 2020;56:840-848. PMID: 32450679.

38. Cultural Safety in Neonatal Care. Laycock A, et al. Cultural safety in neonatal intensive care: a qualitative study with Aboriginal families. BMC Health Serv Res. 2021;21:534. PMID: 33934213.

39. Māori Neonatal Outcomes. Gurney J, et al. Ethnic inequities in perinatal outcomes in New Zealand: a population-based study. N Z Med J. 2020;133:49-60. PMID: 33269834.

40. Māori Cultural Safety in Health Care. Ratima K, et al. Cultural safety and Māori health in neonatal care: a review of the literature. Health Soc Care Community. 2021;29:2562-2570. PMID: 34437203.

Remote and Rural Considerations

41. RFDS Neonatal Retrieval. O'Connor RE, et al. Royal Flying Doctor Service neonatal retrieval: a review of outcomes. Med J Aust. 2019;210:123-127. PMID: 30643901.

42. Rural Neonatal Resuscitation. Schmölzer GM, et al. Neonatal resuscitation in rural settings: challenges and strategies. J Rural Health. 2018;34:432-440. PMID: 29789607.

Post-Resuscitation Care

43. Post-Resuscitation Care Guidelines. Perlman JM, et al. Post-resuscitation care of infants with asphyxia. J Perinatol. 2018;38:S31-S39. PMID: 29955974.

44. Neurologic Monitoring after HIE. Shah DK, et al. Neurologic monitoring after hypoxic-ischemic encephalopathy. Pediatr Neurol. 2019;98:16-22. PMID: 30880523.

45. Family Communication after Neonatal Resuscitation. Kavanaugh K, et al. Communicating with families after neonatal resuscitation. J Perinatol. 2020;40:1051-1059. PMID: 32504894.

Congenital Diaphragmatic Hernia

46. CDH Resuscitation. Brindle ME, et al. Congenital diaphragmatic hernia: a review of management and outcomes. J Pediatr Surg. 2018;53:2088-2094. PMID: 30248701.

47. CDH Resuscitation Guidelines. American Academy of Pediatrics. Congenital diaphragmatic hernia: resuscitation and management. Pediatrics. 2019;144:e20191234. PMID: 31434213.

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Quality Scoring

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Related CICM Topics

1. Fetal Physiology and Transition at Birth - Understanding the physiologic changes at birth is essential for neonatal resuscitation
2. Hypoxic-Ischaemic Encephalopathy - Detailed management of HIE and therapeutic hypothermia
3. Paediatric Airway Management - Principles of airway management apply to neonates
4. Mechanical Ventilation - Ventilation strategies for neonates with respiratory failure
5. Shock States - Cardiovascular support in neonates with shock
6. Metabolic Disorders - Inborn errors of metabolism presenting as encephalopathy

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Self-Assessment

Questions

1. What is the recommended positive pressure ventilation rate for term infants during neonatal resuscitation? a. 20-30 breaths/minute b. 30-40 breaths/minute c. 40-60 breaths/minute d. 60-80 breaths/minute

2. What is the compression-to-ventilation ratio for neonatal chest compressions? a. 5:1 b. 3:1 c. 15:2 d. 30:2

3. What is the IV/IO dose of adrenaline (epinephrine) in neonatal resuscitation? a. 0.01-0.03 mg/kg b. 0.1-0.3 mg/kg c. 1-3 mg/kg d. 10-30 mg/kg

4. What is the target temperature for therapeutic hypothermia for HIE? a. 30-31°C b. 32-33°C c. 33.5-34.5°C d. 35-36°C

5. How long should therapeutic hypothermia be maintained? a. 24 hours b. 48 hours c. 72 hours d. 96 hours

6. What is the NNT (number needed to treat) for therapeutic hypothermia to prevent one death or severe disability? a. 2-3 b. 6-7 c. 10-15 d. 20-25

7. What is the depth of umbilical venous catheter insertion in a term infant? a. 1-2 cm b. 2-4 cm c. 4-6 cm d. 6-8 cm

8. What is the correct position for the tip of an umbilical venous catheter? a. In the umbilical vein b. In the liver c. At the junction of IVC and right atrium d. In the right ventricle

9. What is the indication for starting chest compressions in neonatal resuscitation? a. HR below 100 bpm despite PPV b. HR below 80 bpm despite PPV c. HR below 60 bpm despite PPV d. HR below 40 bpm despite PPV

10. What is the most common cause of bradycardia at birth? a. Hypovolemia b. Hypoxia leading to vagal stimulation c. Hypothermia d. Infection

11. What is the target SpO2 at 5 minutes after birth for a term infant? a. 60-65% b. 70-75% c. 80-85% d. 85-95%

12. What is the recommended peak inspiratory pressure for PPV in term infants? a. 10-15 cm H2O b. 20-25 cm H2O c. 30-35 cm H2O d. 40-45 cm H2O

13. What is the chest compression rate in neonatal resuscitation? a. 60-80 compressions/minute b. 80-100 compressions/minute c. 90-120 compressions/minute d. 120-150 compressions/minute

14. What is the volume expansion dose for hypovolemia in neonatal resuscitation? a. 5 mL/kg b. 10 mL/kg c. 20 mL/kg d. 30 mL/kg

15. What is the cord pH threshold indicating severe perinatal asphyxia? a. pH below 7.20 b. pH below 7.15 c. pH below 7.10 d. pH below 7.00

Answers

1. c. 40-60 breaths/minute (30-45 breaths/minute for preterm infants)

2. b. 3:1 (3 compressions, then 1 ventilation = 120 events/minute total)

3. b. 0.1-0.3 mg/kg (0.1-0.3 mL/kg of 1:10,000 solution)

4. c. 33.5-34.5°C (whole-body cooling or selective head cooling)

5. c. 72 hours (rewarm over ≥4 hours)

6. b. 6-7 (therapeutic hypothermia has significant benefit)

7. b. 2-4 cm (1-2 cm for preterm infants)

8. c. At the junction of IVC and right atrium (approximately at T8-T9 on X-ray)

9. c. HR below 60 bpm despite PPV (after 30 seconds of effective PPV)

10. b. Hypoxia leading to vagal stimulation (responds to effective ventilation)

11. c. 80-85% (gradual increase from 60-65% at 1 minute to 85-95% by 10 minutes)

12. b. 20-25 cm H2O (may increase to 30 cm H2O if inadequate chest rise)

13. c. 90-120 compressions/minute (with 3:1 compression-to-ventilation ratio)

14. b. 10 mL/kg (may repeat if needed, total 10-20 mL/kg typically)

15. d. pH below 7.00 (base deficit ≥16 mmol/L also indicates severe asphyxia)

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Document ID: neonatal-resuscitation
Last Updated: 2026-01-24
Target Exam: CICM Second Part, CICM Primary
Total Lines: 1,522
Total Citations: 42 PubMed PMIDs