This document describes a case of perinatal asphyxia in a 22-day old male infant. The infant presented with fever, seizures, and poor feeding for 1-2 days. His birth was uncomplicated but he had delayed crying and cyanosis. Examination found decreased tone and hyperreflexia. Tests showed hypoxic ischemic encephalopathy on brain imaging. He was diagnosed with hypoxic ischemic encephalopathy secondary to birth asphyxia and treated with oxygen, antibiotics, anticonvulsants, and supportive care.

1. Birth Asphyxia/
Perinatal Asphyxia
10/01/2018
1
DR. FARYAL
WAHAB
H.O @Peds ward
7/6/2016

3. HISTORY
A 22 days old male baby Waris Ali, weighing 2kg
and K/C of birth asphyxia delievered via NVD at 38 weeks
of gestation was withC/O
 Fits for 2day
 Fever for 2 day
 Reluctant to feed for 1 day

4. HISTORY OF PRESENTING COMPLAIN:
According to mother of baby, baby was in usual state of
health 2 day back when he developed fever which was high
grade fever every 3 to 4 hour relieved by Panadol drops
started having fits in the morning. Fits were focal and
involved eitherone limb at one time with flickering of eyes
and lasting 5-10 secs occuring every 2 to 3 hrs. There was
no loss of consciousness, fecal or urinary incontinence and
uprolling of eyeballs.There is no history vomiting .Baby is
also reluctant to feed since then.

5. BIRTH HISTORY
 ANTENATAL:
 It was a fullterm pregnancy. neither booked nor planned
 U/S scan was not done
 Mother had no c/o gestational DM, hypertension,fever,rash.
 Mother was anemic
 She has not taken multivitamins and got tetanus toxoid.
 NATAL:
 Motherunderwent NVDof baby at 38 wks of gestation.
 There is no H/O PROM, preeclampsia or any other maternal complication
at birth
of baby.
 POSTNATAL:
 Baby had delayed and weak cry.
 There was peripheral cyanosis.There was no jaundice.
 Mother can not recall any previous fits.

6.  VACCINATION HISTORY:
No BCG vaccination done.
 FEEDING HISTORY:
Baby was kept on Breast feeding since birth. But now
he is reluctant tofeed for 1 day.
 FAMILY HISTORY:
Baby is 3rd baby ,first was a stillbirth and other was
miscarriaged
 SOCIOECONOMIC HISTORY:
 They are poor
 They use unboiled water for drinking.

7.  VITALS
Heartrate: 142/min
Respiratory rate: 48/min
Temprature: 100 F
Anemia: +ve Cyanosis: -ve
jaundice-ve dehydration-ve,
 ANTHROPOMETRIC MEASUREMENTS
Length:
Weight:
53.5cm
2 kg
FOC: 37.5cm
General physical examination

8. Systemic examination
 RESPIRATORY SYSTEM
NVB,equal bilateral airentry
 CVS:
s1+s2+0
 ABDOMEN:
soft, nontender, no liver or spleen palpable, gut sounds audible
 CNS:
Tone :decreased
reflexes hyperactive
Moro reflex absent
rooting and sucking reflexes

9. DIFFERENTIAL
DIAGNOSIS??

10. DIFFERENTIAL DIAGNOSIS
 Hypoxic ischemicencephalopathy
 Meningitis
 Sepsis

11. INVESTIGATIONS
CBC
5/1/18
Hb 9.60
TLC 6200
Neutrophils 45
Lymphocytes 32
Basophils 0
Eosinophils 11
Platelets 371000

14.  CT SCAN brain:
 Extensivewhite matteredema causing effacementof
lateral ventricle.
 Hypodense areas in the temporo-parieto-occipital region
 No hemorrhagic densityidentified
IMPRESSION:
 Ischemic encephalopathy involving parietal,temporal and
occipital regions of cerebral cortex and cerebellar hemisphere.

16. FINAL DIAGNOSIS
HYPOXIC ISCHEMIC
ENCEPHALOPATHY SECONDARYTO
BIRTH ASPHYXIA

17. TREATMENT
 Oxygen inhalation continuous 1litre
 Ptwas kept NPO initially ,then motherfeed was given 2cc 2hrlyvia
N/G
 Inj 10% D/S150cc/kg/day
i.e 450cc in 24 hrs
 Inj cefotaxime 150mg/kg/day
i.e 225 mg iv B.D
 Inj amikacin 15mg/kg/day
i.e 22 mg iv B.D
 Tab phenobarbitone 30 mg
¼ + ¼
 Inj diazepam 0.3mg/kg ivsos
 Neb with N/S 6hrly

18. Few usually used terms
18
• Anoxia:
– Complete lack of oxygen.
• Hypoxia:
– Decreased availability of oxygen
• Hypoxemia:
– Decreased arterial concentration of oxygen.
• Ischemia:
– Insufficient blood flow to cells or organ resulting in interrupted
metabolism and death of the cell or organ affected.

19. Perinatal Asphyxia (PA)
19
 Asphyxia (greek word) meaning PULSELESS
‘‘It is defined as failure to establish breathing at birth’’
Perinatal asphyxia, neonatal asphyxia,
or birth asphyxia is the medical condition resulting
from deprivation of oxygen to a newborn infant that
causes physical harm,mainly to the brain. cause
metabolic acidosis, neonatal encephalopathy, and
multiorgan system dysfunction.

20. Why it is important???
20

21. Causes of neonatal death
(n=258)
21
Not
established
14.7%
Others
10.7% Birth asphyxia
20.9%
Infection
33.2%
Prematurity
15.2%
Congenital
malformation
5.4%
Others: Hypothermia, RD, Jn, Pulm. Haemorrhage, Seizure etc. ICMR 2006

22. ETIOLOGY
90%Antepartum /intrapartum, 10% Postpartum
FACTORS
Maternal:
- Hypertension-preeclampsia or eclampsia
- Diabetes
- anemia,, malnutrition
- Hypoxia-Pulmonary/Cardiac diseases
5

23. FACTORS
Maternal……:
Hypotension
infections
Prolonged and difficult 2nd stage of labour
Placental: Infarction/fibrosis/abruption
CordAccidents:
Prolapse

24. FACTORS
Fetal:
• Infection - intrauterine
• Anemia - Feto-fetal or feto maternal
transfusion
• IUGR/ Postmaturity - Meconium aspiration
tracheal plug by blood mucus
• Cong malformations - choanal
atresia, laryngeal web,D. hernia, TEF,ICH
• Hydrops fetalis

25. Physiology of Asphyxia
7/6/2016 25
When babies become asphyxiated (either in utero or
after delivery), they undergo a well defined sequence
of events, ie primary apnea followed by secondary
apnea.

26. Systemic manifestation
oBrain(28%) HIE ,ICH
oHeart(25%)myocardial damage,TR,CCF
oLungs(23%) meconium aspiration,pul:
haemorrhage,pneumothorax pneumonia.
oKidney (50%)hematuria, ARF.
oGIT :Necrotizing enterocolitis.

27. Diagnosis
 Before birth
 After birth

30. Hypoxic Ischemic
Encephalopathy
• Hypoxic-ischemic encephalopathy, is
characterized by clinical and laboratory
evidence of acute or subacute brain injury
due to asphyxia. The primary causes of this
condition are systemic hypoxemia and/or
reduced cerebral blood flow (CBF).

31. • 25-30% of survivors have permanent damage like
CP and MR.
• 15-20% with HIE die

32. Fetal response to asphyxiaillustrating the initial redistributionof blood
flow to vital organs. With prolonged asphyxial insult and failure of
compensatory mechanisms, cerebral blood flow falls, leading to ischemic
braininjury.

33. Pathophysiology of hypoxic-ischemic brain injury in the developing brain. During the
initial phase of energy failure, glutamate mediated excitotoxicity andNa+/K+ATPase
failure lead to necrotic cel death. After transient recovery of cerebral energy
metabolism, a secondary phase of apoptotic neuronaldeathoccurs.(ROS = Reactive

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