ASPHYXIA IN NEONATES

Pokorná P.

Characteristics of the neonatal

period

• Duration of neonatal period (postnatal age)

• Assesment of GA (gestational age)

• The accordance of BW to GA (SGA, NGA, LGA)

• Early postnatal adaptation (maturation, functional adaptation)

ASPHYXIATED – NON ASPHYXIATED NEONATE

CPR – ILCOR guidelines 2010

Risk pregnancy

Evaluation and management after birth

Apgar score:

0 1 2

absent <100 >100

absent slow good,

crying

limp fl of Extr. active

no

response

grimace sneeze

blue,

pale

pink body,

blue ex.

pink

CIRCULATION

RESPIRATION

Score

TONE

REFLEXES

SKIN

Causes of asphyxia

• Prenatal

• Postnatal

• Perinatal

Risk pregnancy

Neonatal

Non - Risk pregnancy

Essential characteristics

• pH≤ 7,0 + BE ≤-12 mmol/l on umbilical cord 1-H blood sample

• Apgar score 0-3 (≥5.min)

• Neurological signs (seizures, HIE =72%)

• MODSF (Martin-Ancel et al. 1995)

MORTALITY RATE : 15-20% → 90% PRENATALLY → 10% of PA → CP

American Academy of Pediatrics, American College of Obstetricians and Gynecologists

(1996)

PERINATAL ASPHYXIA

ASPHYXIA

• A.Definition inicdence 2-9/1000 neonates

• B.Pathophysiology TERM neonates

• C.Clinical presentation: TERM neonates

acute phase MODSF+ HIE (72%)

late phase Cerebral palsy

DIVING REFLEX

LUNG

BOWEL

KIDNEY

SPLEEN

SKIN

MUSCULATURE

BRAIN

MYOCARDADRENAL GLAND

↑↑↑↑ HR, ↑↑↑↑ BP, ↑↑↑↑ CVP

↑↑↑↑ const. CO and const. BRAIN PERFUSION

PERINATAL ASPHYXIA

pH 7.4 7.1 7.0 6.7

RR

HR

BP

CO

CVP

BRAIN

Time 3 5 7 (min)

PERINATAL ASPHYXIA

7.4 7.1 7.0 6.7

Time 3 5 7 (min)PA PA

asphyxia

ischemia

proinflamm.

cells ↑↑↑↑

oxidative

radicals ↑↑↑↑reperfusion apoptosis ↑↑↑↑

MINUTES HOURS – DAYS

THERAPEUTICAL WINDOW

MINUTES – HOURS

PERINATAL ASPHYXIA

ASPHYXIA in TERM

MECHANISMS

• Hypoxic

• Ischemic

• Hypoperfusion

• Reperfusion

• Glutamate release

HIE

ACUTE PHASE HIE 0- 7 days

• Clinical presentation: acute clinical syndrom :

HIE I. 0 H - 48 HYPERALERT

II. 48H - 7 days LETHARGIC

III. >7 days SUPOROUS

LATE PHASE HIE

• Cerebral palsy and PM retardation/ death

Neonatal asphyxia

• 1. Ischemia of cortex, bas. ggl.,

cerebral neuronal necrosis TERM-HIE

• 2. cPVleucomalatia PRETERM

• 3. intraventricular hemorrhage T + P

• 4. Neonatal seizures T+P

• 5. Hydrocephalus

CFM - aEEG

MODSFBrain

HIE

BP

MODSF

Metabolic + ABR

pO2

pCO2

Lactate

Kidney

Brain

RR +/-

HR +/-

BP +/-RDS SpO2,RR

HIE

BP

Abdomen

NEC

infectionHaematology

A- B-C-DA- B-C-D

Diagnosis

• Clinical condition (encephaloapathy)

• Laboratory tests (ABR, S-Na, K, Cl, lactate,

glycemia, haematology)

• Sonography + EEG+MRi

Selected chemistry normal values

• ALT: 3- 54 U/L (< 0,73 ukat/l)

• AST 10 – 65 U/L (< 1,2 ukat/l)

• Bilirubin direct:< 0.6 mg/dL

• Bilirubin total: cord <2.8 mg/dL (<50 -65 umol/l)

• 24 H <8.0 mg/dL

• 48 H <13.0 mg/dL

• 72H <16.0 mg/dL

• 7-30 d <7.0 mg/dL

• Calcium: term 1 week < 7-12 preterm <6-10mg/dL

• Glucose: 40 -1000 mg/dL (1,7 -5,0 mmol/l)

• Creatinin: 0,3-1,0 (0,2-0,4) mg/dL (18-62-106 umol/l)

THERAPY

• 1. Observation

• 2. therapy of MODSF

• 3. therapy of HIE

DRUGS:

a. Anticonvulsants + neruoprotection PHENOBARBITAL, PHENYTOIN, MIDAZOLAM

b. Inotropics

c. Nutrition

d. Sedation, pain control

e. ATB