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1242| International Journal of Pharmaceutical Research | Oct - Dec 2020 | Vol 12 | Issue 4
Research Article
Hypoxic ischemic encephalopathy and sepsis: A case
study
DR. S P SRINIVAS NAYAK, SHIV DINESH DYARAPOGU, MUNEB AHMED SYED, MOHAMMED SAFI
UR RAHMAN, AMAL TEJ MATTHEW, PURUCHURU AJAY.
Email ID: spnayak843@gmail.com
Received: 16.04.20, Revised: 15.05.20, Accepted: 14.06.20
ABSTRACT
Introduction: Hypoxic ischemic encephalopathy(HIE) is a rare neonatal cerebral hypoxic condition that
occurs when entire brain is deprived of an adequate oxygen supply which can occur due to birth asphyxia. 40-
60% of affected infants die by 2 years of age or have severe disabilities. The incidence of hypoxic ischemic
encephalopathy is estimated to be 1.5 per 1000 live births. The decreased ability of the neonatal brain to
eliminate free radicals and the increased susceptibility to the free radials leads to damage of neuronal tissue
Case report: We found a rare HIE case of 1 day old child who was bought to the hospital with the
complaints of difficulty in breathing and looks dull with a body weight of 2.5kg. The baby delayed crying after
birth, on examination the baby has bluish appearance with irregular respiration and had two episodes of
seizures. The partial pressure of oxygen (spo2) found was 86-98% and heart rate was 126 beats per minute,
Then immediately started treatment was Oxygen inhalation 2litres/min, Intra Venous 10% dextrose and
Normal saline. Brain CT scan was done and in the report focal cephalo hematoma was noted and the patient is
treated with oxygen inhalation, Penicillin injection, Vitamin k, IV fluids, Netilmicin, Phenobarbeton, Ranitidine,
vancomycin and hydrocortisone. The patient was completely stabilized and escorted him back to his house.
Conclusion: The patient was diagnosed by HIE with sepsis as per clinical presentations. The baby was kept in
ICU for five days and managed with anti-epileptics, Vitamin K, Antibiotics and Corticosteroids. The child was
performed with whole body cooling followed by rewarming over 4 hours to maintain desired rectal
temperature. After 5day therapy the child was succesfully stabilized and discharged.
Keywords: Hypoxic Ischemic Enceohalopathy, Sepsis, hypothermia, birth asphyxia, neonatal complication.
INTRODUCTION
Hypoxic ischemic encephalopathy (HIE) is a brain
injury that prevents adequate blood flow to the
infant’s brain occurring as a result of a hypoxic-
ischemic event during the prenatal, intra-partum
or postnatal period [1]. It is a serious birth
complication affecting full term infants: 40–60%
of affected infants die by 2 years of age or have
severe disabilities [2] The incidence of hypoxic
ischemic encephalopathy is estimated to be 1.5
per 1000 live births[3].Risk factors of birth
asphyxia has been divided into ante-partum,
intrapartum and fetal. Risk factors include
increasing or decreasing maternal age,
prolonged rupture of membranes, meconium
stained fluid, multiple births, non-attendance for
antenatal care, low birth weight infants,
malpresentation, augmentation of labour with
oxytocin, ante partum hemorrhage, severe
eclampsia and pre-eclampsia, ante partum and
intrapartum anemia [4],[5].The majority of the
underlying pathologic events of HIE are a result of
impaired cerebral blood flow [7] and oxygen
delivery to the brain.[7]. HIE is graded (i.e., mild,
moderate or severe) by clinical examination
(Sarnat staging or Thompson score) [12,13]. The
clinical HIE grade combined with other measures,
e.g., electroencephalogram (EEG) and
neuroimaging, are used for estimating the
severity and the risk of adverse
neurodevelopmental outcome [14,15,16,17]. For
infants who sustain moderate-to-severe hypoxic
ischemic encephalopathy (HIE) due to perinatal
events, therapeutic hypothermia(TH) is the only
medical intervention with proven
neurodevelopmental benefits when initiated as
early as possible within the first 6 h of life [8,9].
However, even with hypothermia treatment,
approximately 50% of newborn infants with HIE
die or suffer from significant neurological
disabilities. Outcomes are even worse for the
severe type of neonatal HIE [10,11]. The
pathologic events of HIE occur in two phases:
primary energy failure and secondary energy
failure. Primary energy failure occurs as a result
of the initial reduction of cerebral blood flow[18],
The impairment of cerebral blood flow leads to
decreases in oxygen and glucose, which leads to
significantly less energy (adenosine triphosphate
(ATP)) and increased lactate production [19]. The
secondary energy failure phase occurs 6 to 48
hours after the initial injury. The exact
mechanisms of secondary energy failure remain
unclear [20]. During a hypoxic-ischemic state, the
iron that was bound to proteins is released, which
makes the free iron (Fe2+) available to react with
DOI: https://doi.org/10.31838/ijpr/2020.12.04.052
ISSN 0975-2366
S P Srinivas Nayak et al / Hypoxic ischemic encephalopathy and sepsis: A case study
1243| International Journal of Pharmaceutical Research | Oct - Dec 2020 | Vol 12 | Issue 4
peroxides and form free radicals. The decreased
ability of the neonatal brain to eliminate free
radicals and the increased susceptibility to the
free radials leads to damage of neuronal tissue.
[21] The major emerging treatments being
explored include: moderate hypothermia,
erythropoietin, hematopoietic stem cell transplant
from umbilical cord blood, antiepileptic
medications (e.g., topiramate, Phenobarbital),
xenon, docosahexaenoic acid (DHA), and
cannabinoid agonists. Some of these therapies
are being explored in isolation, while other are
being combined with moderate hypothermia or
other treatments in hopes that synergetic effects
will improve outcomes for infants. However, the
exact mechanisms of actions of emerging
treatments remain unknown [2] HIE is one of the
most serious birth complications affecting full
term infants [22] with few preventive treatment
modalities available [23] The hypoxic-ischemic
event can be caused by multiple events, but
ultimately brain injury occurs because of impaired
cerebral blood flow [24] and oxygen delivery to
the brain. [25]
CASE REPORT
A male patient of 1 day old was bought to the
hospital with the following complaints difficulty in
breathing and looks dull with the weight of 2.5kg.
The blood group of the mother was ‘O’ positive
and it was her first pregnancy with normal mode
of delivery. The baby delayed crying after birth,
on examination the baby has bluish appearance
with irregular respiration, The neonatal reflexes
were absent and the capillary filling time 5.6 sec,
no crying and anterior fontanelle was opened
with fixed body posture and had two episodes of
seizures, The partial pressure of oxygen (spo2)
found was 86-98% and heart rate was 126 beats
per minute, Then immediately started treatment
was Oxygen inhalation 2litres/min, Intra Venous
10% dextrose and Normal saline. The lab
investigation showed on the first day was HB -
15.5g%, WBC - 24800 cells /cumm, platelet -1.5
lakhs/cumm, Neutrophils – 80%, lymphocyte -
9%, CRP - 5.20mg/dl which are abnormal mostly
and suspected sepsis.
Other lab data are mentioned below
SEROLOGICAL REPORT
TEST Day 1 Day 2 Reference range
C- reactive protein 5.74 mg/dl 1.48mg/dl <0.60mg/dl
COMPLTE BLOOD PICTURE
TEST RESULTS NORMAL VALUES
Haemoglobin 18% 12.0 -17.0%
RBC 5.0 million/cumm 4.6-6.5%
WBC count 15000 cells/cumm 4000-11000 cells/cumm
Platelet count 70,000 cells/cumm 1.5-4.5 lakhs/cumm
DIFFERENTIAL LEUCOCYTE COUNT
TYPE OF CELL RESULT ADULTS CHILDRENS
Neutrophils 84% 40-75% 20-40%
Lymphocytes 10% 20-45% 40-60%
Monocytes 4% 2-10% 2-10%
Eosinophils 3% 2-6% 01-06%
Basophils 00% 00-01% 00-01%
PERIPHERAL SMEAR EXAMINATION
RBC – Normocytic/normochromic
WBC – Neutrophilc/leucocytosis
PLATELETS – Thrombocytosis
CT BRAIN PLAIN
The study of the brain has been performed 5mm
sections through the posterior fossa and 1mm
sections of the supra temporal compartment
without intravenous contrast injection. Diffuse
mild to moderate soft tissue swelling noted
sparing or bilateral frontal regions a focal
cephalo hematoma noted in the right region and
right occipital regions. Thin linear CSF density
lesion noted in between body or both lateral
ventricles(normal variant).
SP Nayak et al / Hypoxic ischemic encephalopathy and sepsis: A case study
1244| International Journal of Pharmaceutical Research | Oct - Dec 2020 | Vol 12 | Issue 4
DRUGS PRESCRIBED
DAY 1
S.No DRUG DOSE FREQUENCY ROUTE OF ADMINISTRATION
1 OXYGEN INHALATION 2litres/minute SOS Inhalation
2 INJ.PIPERACILLIN 250mg TID IV
3 VITAMIN K 2mg Single dose IV
4 IVF:10%
DEXTROSE+POLYBION
35ml
35ml QID IV
DAY 2
S. No DRUG DOSE FREQUENCY ROUTE OF ADMINISTRATION
1. OXYGEN INHALATION 2litres/minute SOS Inhalation
2 INJ.PIPERACILLIN 250mg TID IV
3. INJ.NETILMICIN 9mg BD IV
4 INJ.PHENOBARBITONE 40mg START IV
5 INJ.PHENOBARBITONE 7mg BD IV
6 INJ.RANITIDINE 0.2ml BD IV
7 VITAMIN K 3mg OD IV
8 IVF:ISOLATE P+
POLYBION+CALCIUM
GLUCONATE 30ml
- QID IV
DAY 3
S. No DRUG DOSE FREQUENCY ROUTE OF ADMINISTRATION
1. OXYGEN INHALATION 2litres/minute SOS INHALATION
2 INJ.PIPERACILLIN 250mg TID IV
3. INJ.NETILMICIN 9mg BD IV
4 INJ.PHENOBARBITONE 7mg BD IV
5 INJ.RANITIDINE 0.2ml BD IV
6 VITAMIN K 3mg IV
DAY 4
S. No DRUG DOSE FREQUENCY ROUTE OF ADMINISTRATION
1. OXYGEN INHALATION 2litres/minute SOS Inhalaton
2 INJ.PIPERACILLIN 250mg TID Iv
3. INJ.NETILMICIN 9mg BD IV
4 INJ.PHENOBARBITONE 7mg BD IV
5 INJ.RANITIDINE 0.2ml BD IV
6 VITAMIN K 3mg OD IV
7 INJ.MEROPENAM 50mg BD IV
8 VANCOMYCIN 50mg BD IV
9 INJ.HYDROCORTISONE 12.5mg BD IV
DAY 5
S.no DRUG DOSE FREQUENCY ROUTE OF ADMINISTRATION
1. OXYGEN INHALATION 2litres/minute SOS Inhalation
2 INJ.PIPERACILLIN 250mg TID IV
3 SYRUP.PHENOBARBITONE 1.5ml BD Oral
4 INJ.RANTAC 0.2ml BD IV
5 VITAMIN K 3mg OD IV
6 INJ.MEROPENAM 50mg BD IV
7 VANCOMYCIN 50mg BD IV
8 INJ.HYDROCORTISONE 12.5mg BD IV
SP Nayak et al / Hypoxic ischemic encephalopathy and sepsis: A case study
1245| International Journal of Pharmaceutical Research | Oct - Dec 2020 | Vol 12 | Issue 4
On day 4 started with 10ml reyles tube feed and
increased to 20ml on day 5 and changed Inj.
Phenobarbitone to syrup 1.5ml BD and continued
with same treatment further.
DISCUSSION
A male child of 1 day old was brought to the
hospital and the child was diagnosed with HIA
and Sepsis. Immediately treatment was started
and patients serological reports were taken where
C reactive protein found was very high, complete
blood picture is taken and abnormal data was
found in them as well.
Brain CT scan was done and in the report focal
cephalo hematoma was noted and the patient is
treated with oxygen inhalation, Penicillin injection,
Vitamin k, IV fluids, Netilmicin, Phenobarbeton,
Ranitidine, vancomycin and hydrocortisone. The
patient was completely stabilized and escorted
him back to his house.
CONCLUSION
HIE is a brain injury that prevents adequate blood
flow to the infant’s brain occurring as a result of a
hypoxic-ischemic events in early childhood. The
studied case had complaints of difficulty in
breathing, cyanosis, episodes of seizures,
neonatal reflexes were absentand no crying after
birth. The patient was diagnosed by HIE with
sepsis as per clinical presentations. The baby was
kept in ICU for five days and managed with anti-
epileptics, Vitamin K, Antibiotics and
Corticosteroids. The child was performed with
whole body cooling followed by rewarming over
4 hours to maintain desired rectal temperature.
After 5day therapy the child was succesfully
stabilized and discharged.
ETHICAL CLEARANCE AND CONFLICT OF
INTEREST
No conflict of interest is existed as the study is
performed in the department of pediatric in Vijay
Marie secondary care Hospital in Khairtabad,
Hyderabad, India which has memorandum of
understanding between the institute and the
hospital.
Data is taken from the patients with informed
consent and no patient name, guardian,
photographs were included without consent.
Neither human beings nor animal blood sample
was used and no direct intervention is done in the
case study, it is a part of case collection in the
hospitals and patient councilling was performed
and along with consent quires were made to
ensure the knowledge of the case study.
Research and ethics board/ institutional review
board has screened the unethical procedures and
permitted to carry the prospective observational
study in paediatric department
SOURCE OF FUNDING
No source of funding involved in the study. The
total expenses of study and publication was bared
by the authors individually.
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Hypoxic ischemic encephalopathy and sepsis: A case study

  • 1. 1242| International Journal of Pharmaceutical Research | Oct - Dec 2020 | Vol 12 | Issue 4 Research Article Hypoxic ischemic encephalopathy and sepsis: A case study DR. S P SRINIVAS NAYAK, SHIV DINESH DYARAPOGU, MUNEB AHMED SYED, MOHAMMED SAFI UR RAHMAN, AMAL TEJ MATTHEW, PURUCHURU AJAY. Email ID: spnayak843@gmail.com Received: 16.04.20, Revised: 15.05.20, Accepted: 14.06.20 ABSTRACT Introduction: Hypoxic ischemic encephalopathy(HIE) is a rare neonatal cerebral hypoxic condition that occurs when entire brain is deprived of an adequate oxygen supply which can occur due to birth asphyxia. 40- 60% of affected infants die by 2 years of age or have severe disabilities. The incidence of hypoxic ischemic encephalopathy is estimated to be 1.5 per 1000 live births. The decreased ability of the neonatal brain to eliminate free radicals and the increased susceptibility to the free radials leads to damage of neuronal tissue Case report: We found a rare HIE case of 1 day old child who was bought to the hospital with the complaints of difficulty in breathing and looks dull with a body weight of 2.5kg. The baby delayed crying after birth, on examination the baby has bluish appearance with irregular respiration and had two episodes of seizures. The partial pressure of oxygen (spo2) found was 86-98% and heart rate was 126 beats per minute, Then immediately started treatment was Oxygen inhalation 2litres/min, Intra Venous 10% dextrose and Normal saline. Brain CT scan was done and in the report focal cephalo hematoma was noted and the patient is treated with oxygen inhalation, Penicillin injection, Vitamin k, IV fluids, Netilmicin, Phenobarbeton, Ranitidine, vancomycin and hydrocortisone. The patient was completely stabilized and escorted him back to his house. Conclusion: The patient was diagnosed by HIE with sepsis as per clinical presentations. The baby was kept in ICU for five days and managed with anti-epileptics, Vitamin K, Antibiotics and Corticosteroids. The child was performed with whole body cooling followed by rewarming over 4 hours to maintain desired rectal temperature. After 5day therapy the child was succesfully stabilized and discharged. Keywords: Hypoxic Ischemic Enceohalopathy, Sepsis, hypothermia, birth asphyxia, neonatal complication. INTRODUCTION Hypoxic ischemic encephalopathy (HIE) is a brain injury that prevents adequate blood flow to the infant’s brain occurring as a result of a hypoxic- ischemic event during the prenatal, intra-partum or postnatal period [1]. It is a serious birth complication affecting full term infants: 40–60% of affected infants die by 2 years of age or have severe disabilities [2] The incidence of hypoxic ischemic encephalopathy is estimated to be 1.5 per 1000 live births[3].Risk factors of birth asphyxia has been divided into ante-partum, intrapartum and fetal. Risk factors include increasing or decreasing maternal age, prolonged rupture of membranes, meconium stained fluid, multiple births, non-attendance for antenatal care, low birth weight infants, malpresentation, augmentation of labour with oxytocin, ante partum hemorrhage, severe eclampsia and pre-eclampsia, ante partum and intrapartum anemia [4],[5].The majority of the underlying pathologic events of HIE are a result of impaired cerebral blood flow [7] and oxygen delivery to the brain.[7]. HIE is graded (i.e., mild, moderate or severe) by clinical examination (Sarnat staging or Thompson score) [12,13]. The clinical HIE grade combined with other measures, e.g., electroencephalogram (EEG) and neuroimaging, are used for estimating the severity and the risk of adverse neurodevelopmental outcome [14,15,16,17]. For infants who sustain moderate-to-severe hypoxic ischemic encephalopathy (HIE) due to perinatal events, therapeutic hypothermia(TH) is the only medical intervention with proven neurodevelopmental benefits when initiated as early as possible within the first 6 h of life [8,9]. However, even with hypothermia treatment, approximately 50% of newborn infants with HIE die or suffer from significant neurological disabilities. Outcomes are even worse for the severe type of neonatal HIE [10,11]. The pathologic events of HIE occur in two phases: primary energy failure and secondary energy failure. Primary energy failure occurs as a result of the initial reduction of cerebral blood flow[18], The impairment of cerebral blood flow leads to decreases in oxygen and glucose, which leads to significantly less energy (adenosine triphosphate (ATP)) and increased lactate production [19]. The secondary energy failure phase occurs 6 to 48 hours after the initial injury. The exact mechanisms of secondary energy failure remain unclear [20]. During a hypoxic-ischemic state, the iron that was bound to proteins is released, which makes the free iron (Fe2+) available to react with DOI: https://doi.org/10.31838/ijpr/2020.12.04.052 ISSN 0975-2366
  • 2. S P Srinivas Nayak et al / Hypoxic ischemic encephalopathy and sepsis: A case study 1243| International Journal of Pharmaceutical Research | Oct - Dec 2020 | Vol 12 | Issue 4 peroxides and form free radicals. The decreased ability of the neonatal brain to eliminate free radicals and the increased susceptibility to the free radials leads to damage of neuronal tissue. [21] The major emerging treatments being explored include: moderate hypothermia, erythropoietin, hematopoietic stem cell transplant from umbilical cord blood, antiepileptic medications (e.g., topiramate, Phenobarbital), xenon, docosahexaenoic acid (DHA), and cannabinoid agonists. Some of these therapies are being explored in isolation, while other are being combined with moderate hypothermia or other treatments in hopes that synergetic effects will improve outcomes for infants. However, the exact mechanisms of actions of emerging treatments remain unknown [2] HIE is one of the most serious birth complications affecting full term infants [22] with few preventive treatment modalities available [23] The hypoxic-ischemic event can be caused by multiple events, but ultimately brain injury occurs because of impaired cerebral blood flow [24] and oxygen delivery to the brain. [25] CASE REPORT A male patient of 1 day old was bought to the hospital with the following complaints difficulty in breathing and looks dull with the weight of 2.5kg. The blood group of the mother was ‘O’ positive and it was her first pregnancy with normal mode of delivery. The baby delayed crying after birth, on examination the baby has bluish appearance with irregular respiration, The neonatal reflexes were absent and the capillary filling time 5.6 sec, no crying and anterior fontanelle was opened with fixed body posture and had two episodes of seizures, The partial pressure of oxygen (spo2) found was 86-98% and heart rate was 126 beats per minute, Then immediately started treatment was Oxygen inhalation 2litres/min, Intra Venous 10% dextrose and Normal saline. The lab investigation showed on the first day was HB - 15.5g%, WBC - 24800 cells /cumm, platelet -1.5 lakhs/cumm, Neutrophils – 80%, lymphocyte - 9%, CRP - 5.20mg/dl which are abnormal mostly and suspected sepsis. Other lab data are mentioned below SEROLOGICAL REPORT TEST Day 1 Day 2 Reference range C- reactive protein 5.74 mg/dl 1.48mg/dl <0.60mg/dl COMPLTE BLOOD PICTURE TEST RESULTS NORMAL VALUES Haemoglobin 18% 12.0 -17.0% RBC 5.0 million/cumm 4.6-6.5% WBC count 15000 cells/cumm 4000-11000 cells/cumm Platelet count 70,000 cells/cumm 1.5-4.5 lakhs/cumm DIFFERENTIAL LEUCOCYTE COUNT TYPE OF CELL RESULT ADULTS CHILDRENS Neutrophils 84% 40-75% 20-40% Lymphocytes 10% 20-45% 40-60% Monocytes 4% 2-10% 2-10% Eosinophils 3% 2-6% 01-06% Basophils 00% 00-01% 00-01% PERIPHERAL SMEAR EXAMINATION RBC – Normocytic/normochromic WBC – Neutrophilc/leucocytosis PLATELETS – Thrombocytosis CT BRAIN PLAIN The study of the brain has been performed 5mm sections through the posterior fossa and 1mm sections of the supra temporal compartment without intravenous contrast injection. Diffuse mild to moderate soft tissue swelling noted sparing or bilateral frontal regions a focal cephalo hematoma noted in the right region and right occipital regions. Thin linear CSF density lesion noted in between body or both lateral ventricles(normal variant).
  • 3. SP Nayak et al / Hypoxic ischemic encephalopathy and sepsis: A case study 1244| International Journal of Pharmaceutical Research | Oct - Dec 2020 | Vol 12 | Issue 4 DRUGS PRESCRIBED DAY 1 S.No DRUG DOSE FREQUENCY ROUTE OF ADMINISTRATION 1 OXYGEN INHALATION 2litres/minute SOS Inhalation 2 INJ.PIPERACILLIN 250mg TID IV 3 VITAMIN K 2mg Single dose IV 4 IVF:10% DEXTROSE+POLYBION 35ml 35ml QID IV DAY 2 S. No DRUG DOSE FREQUENCY ROUTE OF ADMINISTRATION 1. OXYGEN INHALATION 2litres/minute SOS Inhalation 2 INJ.PIPERACILLIN 250mg TID IV 3. INJ.NETILMICIN 9mg BD IV 4 INJ.PHENOBARBITONE 40mg START IV 5 INJ.PHENOBARBITONE 7mg BD IV 6 INJ.RANITIDINE 0.2ml BD IV 7 VITAMIN K 3mg OD IV 8 IVF:ISOLATE P+ POLYBION+CALCIUM GLUCONATE 30ml - QID IV DAY 3 S. No DRUG DOSE FREQUENCY ROUTE OF ADMINISTRATION 1. OXYGEN INHALATION 2litres/minute SOS INHALATION 2 INJ.PIPERACILLIN 250mg TID IV 3. INJ.NETILMICIN 9mg BD IV 4 INJ.PHENOBARBITONE 7mg BD IV 5 INJ.RANITIDINE 0.2ml BD IV 6 VITAMIN K 3mg IV DAY 4 S. No DRUG DOSE FREQUENCY ROUTE OF ADMINISTRATION 1. OXYGEN INHALATION 2litres/minute SOS Inhalaton 2 INJ.PIPERACILLIN 250mg TID Iv 3. INJ.NETILMICIN 9mg BD IV 4 INJ.PHENOBARBITONE 7mg BD IV 5 INJ.RANITIDINE 0.2ml BD IV 6 VITAMIN K 3mg OD IV 7 INJ.MEROPENAM 50mg BD IV 8 VANCOMYCIN 50mg BD IV 9 INJ.HYDROCORTISONE 12.5mg BD IV DAY 5 S.no DRUG DOSE FREQUENCY ROUTE OF ADMINISTRATION 1. OXYGEN INHALATION 2litres/minute SOS Inhalation 2 INJ.PIPERACILLIN 250mg TID IV 3 SYRUP.PHENOBARBITONE 1.5ml BD Oral 4 INJ.RANTAC 0.2ml BD IV 5 VITAMIN K 3mg OD IV 6 INJ.MEROPENAM 50mg BD IV 7 VANCOMYCIN 50mg BD IV 8 INJ.HYDROCORTISONE 12.5mg BD IV
  • 4. SP Nayak et al / Hypoxic ischemic encephalopathy and sepsis: A case study 1245| International Journal of Pharmaceutical Research | Oct - Dec 2020 | Vol 12 | Issue 4 On day 4 started with 10ml reyles tube feed and increased to 20ml on day 5 and changed Inj. Phenobarbitone to syrup 1.5ml BD and continued with same treatment further. DISCUSSION A male child of 1 day old was brought to the hospital and the child was diagnosed with HIA and Sepsis. Immediately treatment was started and patients serological reports were taken where C reactive protein found was very high, complete blood picture is taken and abnormal data was found in them as well. Brain CT scan was done and in the report focal cephalo hematoma was noted and the patient is treated with oxygen inhalation, Penicillin injection, Vitamin k, IV fluids, Netilmicin, Phenobarbeton, Ranitidine, vancomycin and hydrocortisone. The patient was completely stabilized and escorted him back to his house. CONCLUSION HIE is a brain injury that prevents adequate blood flow to the infant’s brain occurring as a result of a hypoxic-ischemic events in early childhood. The studied case had complaints of difficulty in breathing, cyanosis, episodes of seizures, neonatal reflexes were absentand no crying after birth. The patient was diagnosed by HIE with sepsis as per clinical presentations. The baby was kept in ICU for five days and managed with anti- epileptics, Vitamin K, Antibiotics and Corticosteroids. The child was performed with whole body cooling followed by rewarming over 4 hours to maintain desired rectal temperature. After 5day therapy the child was succesfully stabilized and discharged. ETHICAL CLEARANCE AND CONFLICT OF INTEREST No conflict of interest is existed as the study is performed in the department of pediatric in Vijay Marie secondary care Hospital in Khairtabad, Hyderabad, India which has memorandum of understanding between the institute and the hospital. Data is taken from the patients with informed consent and no patient name, guardian, photographs were included without consent. Neither human beings nor animal blood sample was used and no direct intervention is done in the case study, it is a part of case collection in the hospitals and patient councilling was performed and along with consent quires were made to ensure the knowledge of the case study. Research and ethics board/ institutional review board has screened the unethical procedures and permitted to carry the prospective observational study in paediatric department SOURCE OF FUNDING No source of funding involved in the study. The total expenses of study and publication was bared by the authors individually. REFERENCES 1. Long M, Brandon DH. (2007) Induced hypothermia for neonates with hypoxic-ischemic encephalopathy. Journal of Obstetrics Gynecology Neonatal Nursing ;36:293–298. 2. Kimberly A. Allen, et al. (2011)Hypoxic Ischemic Encephalopathy: Pathophysiology and Experimental Treatments NIA PA Author manuscript, Newborn Infant Nurs Rev.11(3): 125–133. 3. Kurinczuk JJ, White-Koning M, Badawi N. (2010) Epidemiology of neonatal encephalopathy and hypoxic-ischaemic encephalopathy. Early Hum Dev. 86(6):3329–38.4. 4. KayeD. (2003) Antenatal and intrapartum risk factors for birth asphyxia among emergency obstetric referrals in Mulago Hospital, Kampala, Uganda. East Afr Med J, 80 (3): 140-143. 5. Majeed R, Memon Y, Majeed F, Shaikh NP, Rajar UD.(2007) Risk factors of birth asphyxia. J Ayub Med Coll Abbottabad, 19 (3): 67-71. 6. Shalak L, Perlman JM. (2004) Hypoxic-ischemic brain injury in the term infant-current concepts. Early Hum Dev.80:125–141. [PubMed] [Google Scholar]. 7. Shankaran S, Laptook AR, Ehrenkranz RA, Tyson JE, McDonald SA, Donovan EF, et al. (2005) National Institute of Child Health and Human Development Neonatal Research Network. Whole-body hypothermia for neonates with hypoxic-ischemic encephalopathy. N Engl J Med. Oct;353(15):1574–84. 8. Simbruner G, Mittal RA, Rohlmann F, et al (2010) Systemic hypothermia after neonatal encephalopathy: outcomes of neo.nEURO.network RCT. Pediatrics. 126(4):e771–8. 9. Gluckman PD, Wyatt JS, Azzopardi D, Ballard R, Edwards AD, Ferriero DM, et al. (2005) Selective head cooling with mild systemic hypothermia after neonatal encephalopathy: multicentre randomised trial. Lancet. 365(9460):663–70. 10. Azzopardi DV, Strohm B, Edwards AD, Dyet L, Halliday HL, Juszczak E, et al. (2009) Moderate hypothermia to treat perinatal asphyxial encephalopathy. N Engl J Med;361: 1349–1358. 11. Shankaran S, Laptook AR, Ehrenkranz RA, Tyson JE, McDonald SA, Donovan EF, et al. (2005) Whole-body hypothermia for neonates with hypoxic-ischemic encephalopathy. N Engl J Med,353: 1574–1584. pmid:16221780. 12. Sarnat HB, Sarnat MS. (1976) Neonatal encephalopathy following fetal distress. A clinical and electroencephalographic study. Arch Neurol.33(10):696–705.
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