1

Perinatal Asphyxia, Trauma & Neonatal

Resuscitation

Dr. Cheung Kam LauConsultant Paediatrician, PWH

2

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

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

4

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

5

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

6

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

8

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)

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.

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

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

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

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

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

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

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

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

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

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

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

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

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

Birth Trauma

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

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

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

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

Vacuum caput

vacuum extractor resolve within days rarely abrasions and lacerations may lead to

infections

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

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

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

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

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

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

Brachial plexus

Klumpke’s palsy– breech delivery with the arm extended over the

head– rare– intrinsic muscle of hand affected

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

Long bone fractures

Humeral and femoral shafts localised swelling and pain on manipulation splinting healing and callus formation 2-4 weeks

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

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