A 22 day old male baby was brought to the hospital with complaints of fever for 2 days, fits for 2 days, and reluctance to feed for 1 day. The baby's birth history included delivery via normal vaginal delivery at 38 weeks gestation with delayed and weak crying, peripheral cyanosis, and no jaundice. On examination, the baby had decreased tone and hyperactive reflexes. Investigations revealed ischemic encephalopathy involving multiple regions of the brain. The baby was diagnosed with hypoxic ischemic encephalopathy secondary to birth asphyxia and treated accordingly.

2. 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

3. 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
continuous and low grade with spikes of high grade fever
every 3 to 4 hour 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.

4. 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.

5.  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.

6.  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

7. 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

8. DIFFERENTIAL
DIAGNOSIS??

9. DIFFERENTIAL DIAGNOSIS
 Hypoxic ischemicencephalopathy
 Meningitis
 Sepsis

10. INVESTIGATIONS
CBC
5/1/18
Hb 12.60
MCV 101.5
MCH 36.8
MCHC 35.2
HCT 38.9
TLC 6200
Neutrophils 45
Lymphocytes 32
Basophils 0
Eosinophils 11
Platelets 371000

13.  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.

15. FINAL DIAGNOSIS
HYPOXIC ISCHEMIC
ENCEPHALOPATHY SECONDARYTO
BIRTH ASPHYXIA

16. TREATMENT
 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

17. Birth Asphyxia/
Perinatal Asphyxia
10/01/2018
17
DR. FARYAL
WAHAB
H.O @Peds ward
7/6/2016

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.

27. Diagnosis
 Before birth
 After birth

29. 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).

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

31. 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.

32. 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

35. THANK YOU