Lecture III Neonatal Asphyxia & Its Complications

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

birth

• Familiar with the pathogenesis of birth asphyxia

• Hold of Apgar score & ABCDE resuscitation

• Familiar with the complication of severe

asphyxia

Definition

Birth asphyxia is defined as a reduction of

oxygen delivery and an accumulation of carbon

dioxide owing to cessation of blood supply to the

fetus around the time of birth.

This is pathologic condition referred to neonate who have no spontaneous breathing or represented irregular breathing movement after birth. Usually caused by perinatal hypoxia. It is emergency condition and need quickly treatment (resuscitation，复苏).

Etiology

Pathologically, any factors which interfere

with the circulation between maternal and fetal

blood exchange could result in the happens of

perinatal asphyxia. These factors can be

maternal factor, 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

will show a self-defended mechanism which

redistribute blood flow to different organs

called “inter-organs shunt” in order to prevent

some important organs including brain, heart

and adrenal 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

even if hypoxia disappear but the cellular

damages are 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 2Heart rate none <100 > 100Respiration none irregular regularMuscle tone limp reduced normalResponse to none grimaced coughstimulation

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

by suction with syringe（ 注射器）as soon as

possible

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

should be placed to ensure meconium to be

removed

Breathing

1/ ensure face mask covers nose & mouth connect to oxygen bag

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

3/ if no response, intubation & mechanic ventilation（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 IIHypoxic 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 perinatalasphyxia and the most severe condition showed high mortality or remain cerebral complications 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

perinatal 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

mainly symptoms of consciousness

which usually represent in tow types:

Excitation: hyperalert（激惹）, irritable,

hypertonia, tachycardia, tachypnea, seizure,

etc

Depressing: coma, hypotonia, bradycardia,

bradypnea, unresponsibility, etc

Classification—Clinic

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

tone & reflex, no seizure, normal EEG

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

sucking & Moro response, often seizure, EEG+

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

reflex, 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 &

medical treatment, usually:

Mild or moderate cases could be cured completely, but

severe cases represent poor prognosis with high

mortality or cerebral complications such as mental

retardation & cerebral palsy.

Prevention

• Perinatal healthy care

• Prevention of asphyxia

Part IIIIntracranial 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

term ones.

• There are differing etiology and varying prognosis.

With improvement in perinatal care, there have be

considerable 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 & PathologyPressure 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,

lethargy, 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

medications)

Management

Control seizure

Phenobarbital

Diazepam

Chloralhydrate

Management

Decreasing intracranial pressureFurosemide(速尿): 0.5-1mg/kg, iv, q8-12h

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

12h

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

(HIE, 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!