Lecture III Neonatal Asphyxia & Its

Complications

( 新生儿窒息及其并发症 )

Department of Pediatrics

Soochow University Affiliated Children’s Hospital

Part INeonatal Asphyxia

新生儿窒息

Aim & Claim

• Understand the assessment & care of normal bir

th

• Familiar with the pathogenesis of birth asphyxia

• Hold of Apgar score & ABCDE resuscitation

• Familiar with the complication of severe asphyxi

a

Definition

Birth asphyxia is defined as a reduction of oxy

gen delivery and an accumulation of carbon diox

ide owing to cessation of blood supply to the fetu

s around the time of birth.

This is pathologic condition referred to neonate

who have no spontaneous breathing or represen

ted irregular breathing movement after birth. Usu

ally caused by perinatal hypoxia. It is emergency

condition and need quickly treatment (resuscitati

on ，复苏 ).

Etiology

Pathologically, any factors which interfere wi

th the circulation between maternal and fetal blo

od exchange could result in the happens of perin

atal asphyxia. These factors can be maternal fac

tor, delivery factor and fetal factor.

Etiology—High Risk Factors

• Maternal factor:

hypoxia, anemia, diabetes, hypertension, smoking,

nephritis, heart disease, too old or too young,etc

• Delivery condition:

Abruption of placenta, placenta previa, prolapsed

cord, premature rupture of membranes,etc

• Fetal factor:

Multiple birth, congenital or malformed fetus,etc

Pathophysiology

When fetal asphyxia happens, the body wil

l show a self-defended mechanism which redi

stribute blood flow to different organs called “i

nter-organs shunt” in order to prevent some i

mportant organs including brain, heart and ad

renal from hypoxic damage.

Pathophysiology(I)

Hypoxic cellular damages:

a. Reversible damage(early stage):

Hypoxia may decrease the production of

ATP, and result in the cellular functions . But

these change can be reversible if hypoxia is

reversed in short time.

b. Unreversible damage:

If hypoxia exist in long time enough, the cellular

damage will become unreversible that means eve

n if hypoxia disappear but the cellular damages ar

e not recovers. In other words, the complications

will happen.

Pathophysiology(II)

Asphyxia development:

a. Primary apnea breathing stop but normal muscular tone or hypertonia

（肌张力增高） , tachycardia (quick heart rate), and hypertension

Happens early and shortly, self-defended mechanism ，could not be damage to organ functions if corrected quickly

b. Secondary apnea

Features of severe asphyxia or unsuccessful

resuscitation, usually result in damage of organs

function.

Pathophysiology(III)

Other damages:

a. Persistent pulmonary hypertension (PPHN)

b. Hyper/hypoglycemia

c. Hyperbilirubinemia

Clinic manifestations

Fetal asphyxia

fetal heart rate: tachycardia bradycardia

fetal movement: increase decrease

amniotic fluid: meconium-stained

Clinic manifestations

• Apgar score:

A: appearance(skin color)

P: pulse(heart rate)

G: grimace(reactive ability)

A: activity(muscular tension)

R: respiration

APGAR score

Score 0 1 2

Heart rate none <100 > 100

Respiration none irregular regular

Muscle tone limp reduced normal

Response to none grimaced cough

stimulation

Color of trunk white blue pink

Degree of asphyxia:

Apgar score 8~10: no asphyxia

Apgar score 4~8: mild/cyanosis asphyxia

Apgar score 0~3: severe/pale asphyxia

Clinic manifestations

Complications:CNS: HIE, ICH

RS: MAS, RDS, pulmonary hemorrhage

CVS: heart failure, cardiac shock

GIS: NEC, stress gastric ulcer

Others: hypoglycemia, hypocalcemia （低钙血症） , hyponatremia （低钠血症）

Diagnosis

1/ Evidence of fetal distress

2/ Fetal metabolic acidosis

3/ Abnormal neurological state

4/ Multiorgan involvement

Management

• ABCDE resuscitation

• A (air way)

• B (breathing)

• C (circulation)

• D (drug)

• E (evaluation)

Airway

1/ open by placing the head in the neutral position

2/ clean up completely amniotic fluid from the airway b

y suction with syringe （ 注射器） as soon as possib

le

3/ if meconium-stained, tracheal catheter （气管插管）

should be placed to ensure meconium to be remove

d

Breathing

1/ ensure face mask covers nose & mouth con

nect to oxygen bag

2/ establish respiration of 30-40/min with chest

wall movement

3/ if no response, intubation & mechanic ventil

ation （通气） is necessary

Circulation

1/ if heart rate <60/bpm, start external cardiac compression with fingers

2/ ratio 3:1 ( 90 compressions to 30

bpm)

Drugs

1/ if profound bradycardia （心动过缓） , give adrenaline（肾上腺素） (1:10000, 0.1-0.3ml/kg) by endotracheal（气管内） tube or umbilical vein

2/ if no response, intravenous fluid (saline, albumin, plasma, blood) with 10ml/kg

3/ if acidosis, give 5% sodium bicarbonate (SB) with 3-5ml/kg

4/ if bradypnea, consider using naloxone （纳洛酮） (0.1mg/kg)

Evaluation

Evaluate the result of resuscitation to

determine if more rescue necessary:

– If not good, repeat the resuscitation

– If good, transmit baby to NICU

Remember

In the whole resuscitation,

the most important step is A ---

clean up completely the airway

Part II Hypoxic Ischemic

Encephalopathy (HIE)

( 新生儿缺氧缺血性脑病 )

Aim & Claim

• Familiar with the severity of HIE

• Familiar with the management of HIE

Definition

The brain damage after perinatal asphy

xia and the most severe condition showed

high mortality or remain cerebral complicati

ons such as mental retardation & cerebral

palsy.

Clinically, more term babies suffered

from this disease than premature

babies.

Pathologically, more premature

babies suffered from this disease

than term babies.

Etiology & Pathology

• Etiology

The most and direct cause of HIE is perina

tal asphyxia.

• Pathology

Pathophysiology

• Cerebral blood flow

early stage: normal (intraorgans shunt)

then slow down (selective vulnerability)

finally ischemia

• Cerebral metabolism

Clinic Manifestation

The clinic features of HIE are mainl

y symptoms of consciousness which u

sually represent in tow types:

Excitation: hyperalert （激惹） , irritable, hyperto

nia, tachycardia, tachypnea, seizure, etc

Depressing: coma, hypotonia, bradycardia, brad

ypnea, unresponsibility, etc

Classification—Clinic

• Mild(stage I): hyperalert, irritable, normal muscular to

ne & reflex, no seizure, normal EEG

• Moderate(stage II): lethargy, hypotonia, weak suckin

g & Moro response, often seizure, EEG+

• Severe(stage III): coma, absent muscular tone & refl

ex, persistent seizure, EEG++

Classification—CT

• Stage I(normal): no hypodensity （低密度）

• Stage II(mild): local or patchy hypodensity

• Stage III(moderate): hypodensity in tow area of brain or more,

usually no hemorrhage

• Stage IV(severe): extensive & generalized hypodensity, usually

combined with brain hemorrhage

轻度：散在或局限性低密度改变，在 2 个脑叶以内

中度 ： 低密度改变超过 2 个脑叶，灰白质对比模糊

中度不伴出血中度不伴出血

中度伴出血中度伴出血

重度 ： 弥漫性低密度改变， 灰白质界限消失，脑室受压。 中、重度 HIE 常伴 ICH 。

颅内出血

Management(I)

Generalized treatment:

– Ventilation: CPAP, CMV, HFOV

– Circulation: Dopamine( 多巴胺） /Dobutamine （多巴酚丁胺）

– Energy: normal glucose

– Fluid: restriction < 60-80ml/kg/d

Management(II)

Control of seizures:

– Phenobarbital( 苯巴比妥 ):

loading dose 15-20mg/kg, iv

maintenance dose 3-5mg/kg, iv

– Diazepam( 安定 ): 0.1-0.3mg/kg, iv

– Chloralhydrate( 水合氯醛 ): 50mg/kg, E

Management(III)

Cerebral edema & high pressure

– Furosemide( 速尿 ): 1mg/kg, iv, q4-12h

– Mannitol( 甘露醇 ): 0.5g/kg, iv, q8-12h

– Albumin( 白蛋白 ): 0.5-1.0g/kg, iv

Prognosis

Depend on the severity of brain damage & m

edical treatment, usually:

Mild or moderate cases could be cured completely, but s

evere cases represent poor prognosis with high mortality

or cerebral complications such as mental retardation & c

erebral palsy.

Prevention

• Perinatal healthy care

• Prevention of asphyxia

Part III

Intracranial Hemorrhage (ICH)( 颅内出血 )

Aim & Claim

• Familiar with the etiology of ICH

• Familiar with the characterastic of all types

of ICH

Introduction

The intracranial hemorrhage (ICH) is

one of the most common and dangerous

disease with very high mortality &

disability rate in alive cases.

• The morbidity is higher in premature infants than in te

rm ones.

• There are differing etiology and varying prognosis. Wi

th improvement in perinatal care, there have be consi

derable improvement in survival recently.

Etiology & Pathology

Vessels factor Pressure factor

ICH

Injury factor Other factors

(Vit K deficiency, maternal medication, thrombopenia, etc)

Etiology & PathologyVessels factors

• Premature vessels of neonate especially in

preterm babies is vulnerable to damage

Etiology & Pathology Pressure factor

Any change of blood pressure could

interfere with the cerebral circulation

and break the blood vessels

Etiology & PathologyInjury factor

• Any injury during the delivery may

break the blood vessels

Etiology & PathologyOther factors

• Deficiency of vitamin K

• Maternal bleeding or thrombocytopenia （血小板减少

症）

• Maternal medications

Classification of ICH

• Periventricular-intraventricular hemorrhage(PVH-

IVH)

• Primary subarachoid hemorrhage (SAH)

• Intraperenchymal hemorrhage (IPH)

• Subdural hemorrhage (SDH)

• intracerebellar hemorrhage (ICH)

PVH-IVH

• Premature infant, especially VLBW

• Onset early, <72 h

• Depressing symptoms: apnea, hypotonia, let

hargy, no crying, coma

SAH

• Usually have history of birth injury

• Excitation symptom

• Seizure appear in 2nd day

• Bloody cerebral spinal fluid

• Hydrocephalus （脑积水）

IPH

• Usually term baby

• Caused by hypertension

• Poor prognosis

SDH

• Usually huge baby

• Often have injury history

• Onset early: <24h

ICH

• Premature below 32 weeks GA

• Nonspecific features

• Affected vital signs

• Frequent apnea & bradycardia

• Poor prognosis

Diagnosis

History:

asphyxia

birth injury

premature, etc

Symptoms & signs:

excitation or depressing

Radiological evidence:

hyperdencity （高密度） (white) on CT or

MRI

Management

General management: keep quiet,

keep normal glucose (5mmol/L)

maintain normal blood-gas analysis

maintain the balance of vital signs & fluid/energy

Management

• Hemostasis( 止血 )

– vitamin K, plasma or blood transfusion,

– hemostatic (bleeding stopping medicatio

ns)

Management

Control seizure

Phenobarbital

Diazepam

Chloralhydrate

Management

Decreasing intracranial pressure

Furosemide( 速尿 ): 0.5-1mg/kg, iv, q8-12h

Dexmethasone( 地塞米松 ):0.5-1.0 1mg/kg, iv, q8-1

2h

Albumin( 白蛋白 ): 0.5-1.0g/kg, iv

Mannitol( 甘露醇 ): 0.5g/kg, iv, q8-12h

Management

Treatment of hydrocephalus

serial lumbar punctures

surgery operation

Prognosis

• Related to the severity of bleeding

and locations. High mortality and

instabilities.

Prevention

Prenatal care

Prevention of asphyxia & birth injury

Summery

Neonatal asphyxia and its complication (HI

E, ICH) are the most dangerous conditions

clinically with high mortality and incidence

of poor neurological outcome

Questions

• What is APGAR score ?

• What is the composition of ABCDE

resuscitation ?

Thank you for your

cooperation!