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Perinatal Asphyxia, Trauma & Neonatal
Resuscitation
Dr. Cheung Kam LauConsultant Paediatrician, PWH
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Educational objectives
To understand the critical adaptation after birth
Definition of perinatal asphyxia
Pathophysiology of hypoxaemia/ischaemia in
causing organ damages
Principles of newborn resuscitation, including MSL
Common birth trauma
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3Critical transition from fetal to extra-uterine life
Birth is a stressful process
Changes in circulatory system closure of
R-> L shunt, Ductus venosis, PFO, PDA
Onset of breathing in AIR and adaptation of respiratory system
Any cause of maladaptation may lead to persistent fetal
circulation and hypoxaemia
Adaptative capacity is lower in preterm infants
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Newborn lungs are different
Fluid filled at birth (35 mL/kg)
Large proportion may be unaerated at birth
Transition of high pulmonary pressure
Limited absorptive surface
Existence of R to L shunts
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Definition of perinatal asphyxia
An event or condition during the perinatal period that is
likely to severely reduce oxygen delivery and lead to
acidosis
And
A failure of function of at least two organs (may include
lung, heart, liver, brain, kidneys and hematological)
consistent with the effects of acute asphyxia
Committee Expert Panel on Perinatal Morbidity
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Damages from hypoxia & ischaemia, occurred before / during delivery
Obstetrician’s role in identify compromised fetuses
High risk pregnancies should be referred to tertiary centres equipped with neonatal ICU to cut down mortality & morbidity
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Hypoxia / ischaemia -> anaerobic respiration -> lactic acidaemia Together with Hypercapnia -> mixed metabolic and respiratory acidosis
Compensatory mechanism : Body try to preserve perfusion by shunting of blood flow to vital organs e.g. Brain, Heart , kidney
Decompensation of autoregulation -> irreversible damage
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Incidence of perinatal asphyxia
HIE : 0.3 and 1.8% (various reports) In 1995 in Australia the incidence of antepartum
fetal death was 3.5/1000 live births the incidence of intrapartum fetal death was
1.0/1000 the incidence of neonatal death was 3.2/1000 Apgar scores of 1-3 at 1 minute were recorded in
2.8% and at 5 minutes in 0.3% of live births in Australia in 1995(exclude Victoria)
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9Intra-partum monitoring to identify
fetal distress
cardiotocography/oxy-cardiotocography
fetal blood pH estimation
detection of MSL
* Poor correlation with fetal outcome & CP risk
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Risk factors1. Hypertensive disease of pregnancy or pre-
eclampsia,
2. Intrauterine growth restriction,
3. Placental abruption,
4. Fetal anaemia (eg rhesus incompatibility),
5. Post maturity,
6. Unphysiological labour (eg induction), and
7. Malpresentation including cord prolapse.
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11Detection of at risk infants1. Fetal movement counting (typical sensitivity 12 to 50%,
specificity 91 to 97%), 2. Non-stress testing (typical sensitivity 14 to 59%, specificity 79
to 97%), 3. Fetal biophysical profile (typical positive likelihood ratio 2.5 to
27.4, negative likelihood ratio 0.2 to 0.9), 4. Abnormal fetal heart rate (FHR) recording (typical sensitivity
70%, specificity 80%), 5. Fetal scalp pH (decreases sensitivity to 31% and increases
specificity to 93% + FHR monitoring). In addition, the following clinical factors may be associated with a low Apgar score:
6. Reduction of liquor volume 7. Meconium staining of the liquor5.
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But, overall
Only about half of the infants needing resuscitation
are predicted by antenatal history or signs during
labour
That means half of the babies who cannot stand the stress
of labour are not predicted before delivery
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Preparation for delivery - Personnel Personnel capable of initiating resuscitation should
attend every delivery More than 1 experienced person should attend an
anticipated high-risk delivery Severely depressed infants - need 1 to ventilate & 1 to
monitor HR +/- chest compression A team of 3 or more is highly desirable during
resuscitation including medications A separate team should be present for each infant of a
multiple gestation
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14Anticipation of Resuscitation Need
Antepartum risk factors
Maternal diabetes
Pregnancy-induced hypertension
Chronic hypertension
Chronic maternal illness
Cardiovascular
Thyroid
Neurological
Pulmonary
Renal
Anemia or isoimmunization
Previous fetal or neonatal death
Bleeding in second or third trimester
Maternal infection
Polyhydramnios
Oligohydramnios
Premature rupture of membranes
Post-term gestation
Multiple gestation
Size-dates discrepancy
Drug therapy, eg,
Lithium carbonate
Magnesium
Adrenergic-blocking drugs
Maternal substance abuse
Fetal malformation
Diminished fetal activity
No prenatal care
Age <16 or >35 years
Intrapartum risk factors
Emergency cesarean section
Forceps or vacuum-assisted delivery
Breech or other abnormal presentation
Premature labor
Precipitous labor
Chorioamnionitis
Prolonged rupture of membranes (>18 hours before delivery)
Prolonged labor (>24 hours)
Prolonged second stage of labor (>2 hours)
Fetal bradycardia
Non-reassuring fetal heart rate patterns
Use of general anesthesia
Uterine tetany
Narcotics administered to mother within 4 hours of delivery
Meconium-stained amniotic fluid
Prolapsed cord
Abruptio placentae
Placenta previa
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Management at birth1. Wipe dry
2. Keep warm
3. Position
4. Oral/nasal suction
5. Examine for gross congenital anomaly
6. If HR > 80/min, observe
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Evaluation, Decision, Action Cycle
Action Evaluation Decision Action
No respiration
Adequate respiration
Tactile stimulation
Need to ventilate
Make additional evaluation
PPV
Check heart rate
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Initiate IPPV with bag and mask if:
Inadequate respiratory efforts at 1 min.
Use opening inspiratory pressure 30-40 cm H2O
for higher FRC for initial breathes
Maintain pressure for 1 sec.
Inflation bag volume > 500ml
Rate – 40-60 /min
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18Effective Bag-Mask Ventilation Is an Essential BLS Skill
Effective Bag-Mask Ventilation Is an Essential BLS Skill
Use only the amount of force and tidal volume needed to make the chest rise
Avoid excessive volume or pressure
Increased inspiratory time may reduce gastric inflation
Cricoid pressure may reduce gastric inflation
Cricoid cartilage
Occluded esophagus
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Indications for intubation
Prolonged PPV is required Face Mask ventilation is not effective Tracheal suctioning is required Diaphragmatic hernia is suspected When chest compression is performed Tracheal medication is required +/- Preterm infant less than 1000g
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20Endotracheal intubation if:
HR < 80/min or poor response to above
Inspiratory pressure up to 40 - 50 cmH2O
Safe to use 100% O2
Cardiac Massage if:
HR < 60.min Hand-round-the-chest method better than 2 fingers
compression Three compressions for every lung inflation
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21Two Thumb–Encircling Hands Technique Preferred
for Infant 2-Rescuer CPR by HCPTwo Thumb–Encircling Hands Technique Preferred
for Infant 2-Rescuer CPR by HCP
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22Drugs:
Adrenaline (1:10,000)
0.1 - 0.2 ml/kg/dose IT/IV
Sodium Bicarbonate (4.2%)
1 - 2 mmol/ kg IV
Naloxone
0.1 mg/kg IT/ IV/ IM
* Make sure of adequate ventilation before NaCO3
* No resp. depression from high dose Naloxone
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Neonatal Resuscitation Program -AAP
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MSL babies -Joint protocol from AAP,
NRP, AHA, ARC, ERC, Heart & Stroke
foundation of CanadaPediatrics 1999;103(4):1-13
meconium aspirator
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Poor response to resuscitation:
1. Shock
2. Metabolic acidosis
3. Anatomical problems:
- Pneumothorax
- Diaphragmatic Hernia
- Lung hypoplasia
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Discontinuation of Resuscitation
No response after 15 minNo response after 15 min
Resuscitation of newborn after 10 min of asystole is very unlikely to result in survival or survival without severe disability ( Class IIb) Davis DJ, Pediatrics 1993
Jain L, J Pediatr 1991
Yeo CL J Paediatr Child Health 1994
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Apgar Score Subjective and observer dependent depend on color, respiration, tone, reflexes, and heart
rate with resuscitation, baby usually reversed in the
sequence : HR, reflexes, color, respiration, and tone AS 0-3 at 5 min is defined as significantly low, with
higher mortality and CNS morbidity low extended AS at 10, 15 minutes more predictive of
death and CP risk
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28Reappraisal of Apgar Score after 50 years Brian M Casey et al NEngJMed 2001;344(7):467-471
Retrospective cohort study of 151,891 LB >26 weeks Compare AS & cord pH in predicting NN death (28 D) For 26-36 wks, AS at 5 min 0-3, NNMR 315/1000 Vs 5/1000
if AS at 5 min is 7-10 For babies born at /after 37wks, if AS at 5 min 0-3, NNMR
244 Vs 0.2 /1000 LB Risk of NND in term infants born with AS 0-3 at 5 min is 8X
the risk of term infants born with cord pH <=7.0 Apgar Score remain relevant in predicting neonatal survival
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Acute organ damages after perinatal asphyxia
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Complications of perinatal asphyxia
Respiratory
Cardiovascular
Neurological
Renal
Metabolic
Haematological
Gastro-intestinal
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31Respiratory complications
Pulmonary complications including respiratory distress and
persistent pulmonary hypertension of the neonate (25%)
Meconium aspiration syndrome
Air leaks-pneumothorax, pneumomediastinum, pneumo-
pericardium, pneumoperitoneum
Haemorrhagic pulmonary oedema
Persistent fetal circulation*/PPHN
Amniotic fluid aspiration
“Shock lung” - decreased surfactant synthesis
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32PPHN - caused by
1. Pulmonary arterial constriction by acidosis & hypoxia
2. Prenatal remodeling of musculature in pulmonary arteries
3. Release of vasoactive mediators e.g.leukotrienes constricting the pulmonary vessels
4. Pulmonary thrombo-embolic formationJ Clin Invest 1966; 45:399
J Pediatr 1981; 98:962
N Eng J Med 1983; 309:77
J Pediatr 1985; 106:806
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Cardiogenic shock after asphyxia
Hypoxic cardiomyopathy (Echo or ECG abnormality) (25%),
History of fetal distress, documented by fetal pH & low AS
Clinical finding resemble RDS
Cardiomegaly, ECG changes of myocardial ischaemia, decreased
myocardial contractility
Hepatomegaly, elevated CVP
Severe lactic acidosis
Responds to inotropic agents
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Inotropic Agents:
Dopamine 2 - 10 ug/kg/min
Dobutamine 5 - 20 ug/kg/min
Adrenaline 0.1 - 1 ug/kg/min
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35RenalOliguria (< 1 ml/kg/hr for > 24 hrs.) - 40%Elevated urinary beta-2-microglobulin - 57%Elevated Creatinine (> 90 micromol/L) - 17%
CNSHIE (including seizures) - 31%Abn cerebral USS - 26%
CVSAbn Echocardiogram - 25%Abn ECG - 11%
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Renal complications
Renal compromise with oliguria and elevated
creatinine (40%)
Cloudy swelling & hydropic degeneration of tubules
Infarction of nephron or cortico-medullary necrosis
Renal venous thrombosis
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37Metabolic complications
Fluid imbalance-renal dysfunction, SiAdH
Hypoglycaemia
Hypocalcaemia
Hypomagnesaemia
Hyperphosphataemia
Hyperammonaemia-semi-comatose
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Haematological complication
Disseminated intravascular coagulation
Gastro-intestinal complications
Stress gastric ulcers
Necrotising enterocolitis
Liver failure
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Clinical staging of post-asphyxial encephalopathy
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Sarnat staging : Grade I (Mild)
Irritable, hyperalert, mild hypotonia, poor sucking, uninhibited reflexes, sympathetic overactivity
* recover within 48 hrs.
* 99% favourable outcome on FU
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Grade II (Moderate)Lethargic, seizures, marked abnormalities of
tone, hypotonia, suppressed primitive reflexesRequires tube feeding
* recover within one week
* 75% favourable outcome on long term FU
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Grade III (Severe)
Comatose, prolonged seizures, severe hypotonia, suppressed brain-stem function
Failure to maintain spontaneous respiration
* recover > one week
* 22% favourable outcome on long term FU
91% sensitive in predicting future neurological outcome Fenichel, Arch Neurol 1983; 40:261
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43Treatment for hypoxic ischaemic encephalopathy (HIE)
Goals
1. Correct hypoxic state
2. Restore tissue perfusion
3. Minimize delayed organ injuries
Intensive monitoring is the key
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Birth Trauma
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Introduction
Risk factors instrumentation prolonged labour maternal pelvic anomalies maternal short stature abnormal presentations macrosomia big head prematurity oligohydramnios
In modern obstetric care, birth trauma is usually mild while severe trauma is uncommonly seen
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Head and neck injuries
associated with fetal monitoring cephalhaematoma subaponeurotic haemorrhage caput succedaneum vacuum caput skull fracture facial / mandibular fracture ocular injuries ear injuries sternocleidomastoid muscle injuries
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Cephalhaematoma Subperiosteal collection of blood delineated by suture lines usually not visible until a few hours after birth anaemia, hypotension, jaundice in severe cases infection esp. after needle aspiration or drainage investigation for coagulopathy conservative treatment calcify with an organised rim by the end of second week resolve spontaneously within 1 to 2 months
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Subaponeurotic haemorrhage spread across the whole calvarium may bleed insidiously or rapidly haemorrhagic shock and death
Caput succedaneum head moulding oedematous subcutaneous swelling of the scalp poorly defined margin may extend across midline and sutures resolve over a few days
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Vacuum caput
vacuum extractor resolve within days rarely abrasions and lacerations may lead to
infections
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Skull fractures
linear or depressed brain contusion or disruption of blood vessels linear fracture most often asymptomatic may lie beneath a cephalhaematoma most severe form as seizure, hypotension or even
death depressed fracture may range from inward
depression of the outer bony layer without true fracture to complete disruption of bone
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Skull fracture
Diagnosed by X-ray CT scan may show intracranial haemorrhage or
oedema linear fracture should heal without treatment depressed fracture needs surgical intervention
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Sternocleidomastoid muscle injury
Torticollis and palpable mass head tilted to the affected side chin pointed to the other side muscle or fascia disruption haematoma and fibrous formation lead to shortening
of the muscle physiotherapy with passive stretching complete recovery
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Facial nerve
Compression by forceps blade pressure from maternal pelvis asymmetric crying facies inability to close the eye, smooth forehead,
absent nasolabial fold supportive treatment prognosis good
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Brachial plexus
Erb’s palsy C5 and C6– shoulder dystocia or neck traction during
breech delivery– shoulder adducted and internally rotated, elbow
extended– forearm pronated, wrist flexed– Moro, biceps, and radial reflexes are absent– finger movement and grasp reflex normal
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Brachial plexus
X-ray upper arm to rule out fracture usually transient, recovery within few
months physiotherapy with passive movement prognosis is poor if recovery not occur
beyond 6 months neuroplasty and tendon transfer may help
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Brachial plexus
Klumpke’s palsy– breech delivery with the arm extended over the
head– rare– intrinsic muscle of hand affected
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Fracture clavicle
Most common orthopaedic problem Pseudo-paralysis on the affected side crepitus and palpable bony irregularities greenstick fracture may be asymptomatic callus formation 7-10 days no treatment required
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Long bone fractures
Humeral and femoral shafts localised swelling and pain on manipulation splinting healing and callus formation 2-4 weeks
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Soft tissue injuries
Petechiae and ecchymosis– common– differentiate from bleeding disorder and
infection– resolve spontaneously
laceration and abrasion– fetal monitoring– cut wound in caesarian section
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Soft tissue injuries
Subcutaneous fat necrosis– caused by pressure during delivery
– irregularly shaped, hard, non-pitting, subcutaneous plaque
– usually on the cheeks, arms, back, buttocks, and thighs may calcified but complete resolution