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Neonatal Asphyxia
Neonatal Asphyxia
Neonatal Asphyxia
2. Obstetric Factor:
◦ Placenta Previa
◦ Cord prolaps
◦ PROM
◦ Polyhidramnion
◦ Placenta insuffeciency
◦ Chorioamnionitis
B. Inpartum Conditions
1. Abnormal plasentation
2. Pricipitate or prolonged delivery
3. Difficult delivery
4. Post term delivery
5. Forceps or vacum delivery
9
All O2 difuse across the palcental membrane
from the mother’s blood to the baby blood
Only a small fraction of the fetal blodood
passed through the fetal lungs
Alveoli is filled with fluid
The blood vessels in the fetal lungs are
markedly constricted
Most of the blood flow through the ductus
arteriosus into the aorta
After Birth:
+ Noconnection to the placenta
+ A baby get oxygen from the lung
1. The fluid in the alveoli is absorbed into the lungs
tissue and replace by air
2. The umbilical arteri and vein clamped increases
systemic blood presure
3. O2 ↑ in the alveoli relaxation of blood vessel in
the
lungs
4. The ductus arteriosus begin to constrict more
blood flow trough the lungs O2 ↑ to tissues
1. Cardiac output is maintenaned early, but
changes radically
2. Selective vasocontrictor to gut, kidneys,
muscles, skin
3. Pulmonary blood flow ↓ by hypoxia and
asidosis
4. Respiration center is depressed
5. Severe stage of asphyxia O2 ↓ to the heart
& brain - myocardial function ↓
O2 ↓↓ to the vital organ
- brain injury
Score
Sign 0 1 2
Heart Rate Absent < 100/ m ≥ 100/ m
Respiratons - Slow, irregular Good, crying
Muscle tone Limp Some flexion Active motion
Reflex irritability No response Grimace Cough,
sneeze,cry
Colour Blue or pale Pink body, blue Completely pink
extremitas
Grade II HIE
- Lethargy
- Poor feeding, depressed gag reflex
- Hypotonia
- Low heart rate and pupillary constriction indicating
parasympathetic stimulation
- 50 – 70 % neonates display seizures usually in the first 24 hour
after birth
Grade III HIE :
Neurological abnormality progressing :
- Coma
- Flacidity
- Absent reflexes
- Pupil : fixed, slight reactive
- Apnea, bradycardia, hypotension
- Seizzure are uncomon but if present they are
intractable
- Acute tubular necrosis : oliguria,
hematuria, polyuria
- Cardiomyopathy : hypotension
- Persistent pulmonary hypertension :
tachypnea, hypoxemia
- Hepatic necrosis : ↑ ammonia, jaundice,
- ↑ AST/ ALT
- NEC : distention, bloody stools
- Adrenal insufficiency : ↓ glucose, ↓ Na,
BP ↓
- Inappropiate secretion of ADH : oliguria, ↓ Na
1. Prevention in the best management
2. Timing is very crucial and a few minute of
delay can lead to death or life long suffering
from handicap
3. Maintain oxygenation and acid base balance
4. Start mechanical ventilation if necessary
5. Monitor and maintain body temperature
6. Correct and maintain caloric, fluid, electrolyte
and glucose levels ( D 10 % at 60 cc/kg/day )
7. Correct hypovolemia (whole blood)
8. Avoid fluid overload, hypertension, hyperviscocity
9. Administer phenobarbital for treatment of
seizzurnes
- Administer phenobabital 20 mg/kg iv over 5
minute
- can be increased in dose 5 mg/kg every 5 minute
until seizurnes are controlled or until maximum
dose 40 mg/kb is reached
10. No other therapeutic interventions have been
proven helpful ie. Corticosteroids, prophylactic
phenobarbital, furosemite, manitol, etc