Communications in Applied Sciences

ISSN 2201-7372

Volume 5, Number 1, 2017, 1-13

A Severe Asphyxiated Newborn: A Case Report

Atiye Fedakâr MD. Pediatrician*

The Departments of Pediatrics, Afiyet Hospital, Ümraniye, İstanbul, Turkey.

Zakir Sakcı MD, Radiology

The Departments of Radiology, Sağlık Bilimleri Üniversitesi Ümraniye Eğitim

Araştırma Hastanesi, Ümraniye, İstanbul, Turkey

__________________________

© Copyright 2017 the authors.

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A Severe Asphyxiated Newborn: A Case Report

Abstract

Perinatal asphyxia is still a major cause of mortality and morbidity despite significant

improvements in neonatal intensive care. The incidence of perinatal asphyxia is 6/1000 in

term infants, and it is the third leading cause of death after prematurity and sepsis.

Perinatal asphyxia is an important cause of permanent damage to the central nervous

system which may result in cerebral palsy and developmental disability later on. It can

also affect renal, gastrointestinal, and hepatic systems and may cause severe non-

reversible sequelae. Therefore, management of asphyxic newborns, appropriate

resuscitation, and planning of follow-up and treatment by an experienced team are

helpful to reduce mortality and morbidity. Herein, we report a severe asphyxiated

newborn in the light of literature review.

Keywords: Perinatal asphyxia, newborn.

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Introduction

Perinatal asphyxia is a clinical process in which hypoxia and ischemia coexist. It

can be defined as the clinical depression table associated with hypoxia, hypercapnia and

acidosis in the newborn and/or fetus depending on the impairment of the functions of

the biological unit consisting of mother, fetus and placenta and the impairment of

postpartum pulmonary gas exchange. According to the clinical findings, it is the clinical

presentation in the newborn which develops due to low Apgar score, acidosis in the cord

blood and hypoxic ischemic encephalopathy (1,2). Although the reported values for the

incidence of perinatal asphyxia are variable due to differences in diagnostic criteria, the

incidence of perinatal asphyxia is reported to be 6/1000 in the literature (3,4). Also,

asphyxia (23%) is the third most common cause of newborn deaths after premature birth

(28%) and sepsis (26%)(5).

Herein, we report a severe asphyxiated newborn in the light of literature review.

Case Report

A 42-year-old mother, in her third pregnancy, gave birth to a male term baby

weighing 2615 g with cesarean section due to fetal distress. His height was 46cm and the

head circumference was 33cm. After birth, his overall condition was very poor, his heart

was not beating, and he was not breathing. There were ecchymosis around the umbilicus

and the chest area. He had respiratory depression and the Apgar score was 0 at the first

min and 2 at the fifth min. Cornea was dull and pupillary light reflex was weak. The

blood pressure was 70/30 mmHg. There was no other abnormal finding. Following

resuscitation and intubation, he was referred to the intensive care unit with the diagnosis

of severe asphyxia. There were two costal fractures on the left side on posterioanterior

chest X-ray. The echogenicity of the bilateral kidney parenchyma found to be increased

in abdominal ultrasound (USG) and cranial sulci were present on cranial USG (Figure-1

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A chest X-ray image of the patient). His personal and familial history were unremarkable.

In the first arterial blood gas analysis; pH was 6.56 mm/Hg, PCO2 was 113 mm/Hg, PO2

was103 mm/Hg, HCO3 was 9.5 mmol/L, BE was -25 mmol/L. In blood count analysis,

leukocyte count was 69.140mm3; platelet count was 65.000 mm3, Htc59%, and Hgb 18g/dL.

In biochemical analysis of blood; Na was 129 mmol/L, blood glucose was 37mg/dL, and

CRP was 3.52mg/dL(reference <0.5). Total urine analysis revealed protein positivity. The

metabolic screening tests were normal. The mortality score was 32.6% according to the

Score for Neonatal Acute Physiology and Perinatal Extension II(SNAPPE-II). The

newborn was internalized with the diagnosis of asphyxia and was connected to the

ventilator in the SIMV mode. For hypoglycemia, 2cc of 10% dextrose was administered

as bolus and 10% maintenance fluid was initiated. When glucose failed to recover, the

fluid was uptitratedto 12.5%. NaHCO3 was also administered for severe metabolic

acidosis. Prophylactic phenobarbital was applied due to asphyxia. Cultures were

obtained due to poor overall status of the patient and low platelet and high leukocyte

counts were detected. Meropenem + vancomycin + intravenous immunoglobulin were

administered. Posterioanterior chest X-ray also revealed an intensive infiltration.

Echocardiography(ECHO) showed pulmonary hypertension+patent foramen ovale.

Sildenafil was planned for pulmonary hypertension;however, it was unable to be

administered, as the gastric content was dirty and contained bile. Ranitidine and

metronidazole were added to the treatment. Hypoglycemia, hyponatremia, and

metabolic acidosis were stabilized after 24 hours. In the biochemical blood analysis on

Day 3, 25OHvitamin D3 was <3ng/mL, Ca was 7.6 mg/dL, total protein was 3.9 mg/dL,

albumin was 2 mg/dL, AST was1999 U/L, ALT was 614 U/L, LDH was 3422 U/L, creatine

kinase was 7070 U/L (reference 24-170),PT time was 45 sec (reference 11-15 s), PT activity

was 16% (reference 70-100), INR was 4.97, urea was 77 mg/dL, and creatinine was 2.73

mg/dL. Diffuse edema was also detected in physical examination.

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Fresh frozen plasma was administered at 10 cc/kg, human albumin was

administered for two days. One-fourth of vitamin D vial was applied intramuscularly.

As the levels of the hepatic enzymes were elevated, phenobarbital was discontinued.

Vancomycin was switched to teicoplanin due to high urea level. In the ECHO performed

on Day 6 postnatally, pulmonary hypertension was recovered. The levels of AST was110

U/L, ALT was 93 U/L, LDH was 1506 U/L. Since platelet count was detected as 31.000mm3

in the blood count, platelet suspension was administered at 10cc/kg for two days.On

postnatal Day 7, repeated cranial USG showed a milimetric calcification in left ventricle

and abdominal USG revealed ascites and Grade1 ectasia. Urea was 109 mg/dL and

creatinine was 2.4 mg/dL.Acute renal failure secondary to severe asphyxia was

considered. The urine output was good. The patient was consulted with pediatric

nephrology. Since the gastric content was clear on the postnatal Day 8, enteral feeding

was started minimally. On the postnatal Day 14, upon severe increase in the distention

of the abdomen, the erect abdominal plain film was obtained and bowel perforation was

detected. The patient was operated urgently by the pediatric surgeons. On the

postoperative Day 2, his overall status deteriorated again and he was taken to operation

twice. Meanwhile, gastric perforation developed (Figures 2-3 The erect abdominal plain

graphy of the patient, the appearance of abdominal distention). The stomach was

repaired by the pediatric surgeon (Figure 4. Postoperative overall status of the patient).

The patient, who started to receive enteral feeding on the postoperative Day 4, was

discharged with cure on the postnatal Day 34. The hepatic enzymes and creatine kinase

were normal on Day 7, the blood count returned to normal on Day 14and renal functions

returned to normal on Day 21. He was followed under mechanical ventilation for 20 days.

Discussion

Perinatal asphyxia is one of the major causes of mortality and morbidity in

newborns, even in developed countries, despite recent developments in neonatal care,

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diagnosis and treatment. According to the estimates of the World Health Organization,

3% of all infants in developing countries are suffering from asphyxia, 23% of them die

due to newborn asphyxia, and in the same number of infants, serious sequelae remain (6).

It is reported that 20% of perinatal asphyxia develops in the antepartum period,

35% in the intrapartum period, 35% in the intrapartum-antepartum period and 10% in

the postnatal period (7).Although 90% of perinatal asphyxia occurs due to intrauterine

and intrapartum events, asphyxia time may not be determined in many cases (6,7).In our

case we attributed the perinatal asphyxia to the advanced maternal age, emergent

cesarean birth due to fetal distress, and the antepartum causes. It has been reported in the

literature that cerebral palsy due to perinatal asphyxia is encountered more in males

(10).Similarly, the Turkish Society of Neonatology reported that three fourth of the babies

who were diagnosed with asphyxia were male (10), as in our case.

The Apgar score is often used to determine the clinical condition of the newborn

at birth. The prolonged duration of the low Apgar score is associated with mortality and

the increased likelihood of neurological morbidity in the surviving newborns (8). In term

infants, if the Apgar score is between 0 and 3 in the 1st minute and it does not improve

at 20 minutes, then the mortality increases from 5.6 to 59% (11,12). The Apgar score of

our patient was 0 at the first min and 2 at the fifth min.

In perinatal asphyxia, blood flow is rearranged so as to provide more oxygen

support to vital organs such as the brain and heart. In this case, there may be damage to

the organs such as the kidney, liver and intestine which are already affected by hypoxia.

In the literature, the additional organ involvement is reported as central nervous system

(72%), pulmonary (71-86%), cardiac (43 to 78%), renal (46 to 72%), liver (80 to 85%),

hematological (32 to 54%), and gastrointestinal tract (29%) following the asphyxia

(13.14,15).

In a study conducted by Star et al. (16) with 205 cases, the kidney was identified as

the mostly affected organ with 40.5%. In the study of Shah et al. (14), they reported that

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the hepatic involvement was 85%, pulmonary involvement was 86% and renal

involvement was 70%. In our case, the central nervous system being in the first place,

pulmonary, cardiac, renal and gastrointestinal systems were affected. The most severely

affected system was the gastrointestinal system in which postnatal both intestinal and

gastric perforation developed secondary to mesenteric ischemia on Day 14 of asphyxia.

The intestinal and gastric perforations were repaired by the pediatric surgeon.

The effect of perinatal asphyxia on bone marrow can be seen as thrombocytopenia.

Thrombocytopenia may continue up to 12 hours to three days, particularly after brain

damage. It may cause intracranial hemorrhage (8). In our case, thrombocyte count was

65.000 mm3 on the first day and thrombocyte count was 31.000 mm3 on the third day.

Therefore, platelet suspension was administered at a dose of 10cc/kg for two days. Since

the PT time was long, fresh frozen plasma was administered for two days to prevent

possible bleeding complications.

As a result of renal system involvement secondary to asphyxia, the levels of

creatinine and urea may increase, oliguria-anuria may occur, fluid retention and

hyponatremia due to inappropriate release of anti-diuretic hormone may develop. It is

reported in the literature that as a result of liver dysfunction, the liver enzymes such as

ALT, AST, LDH, particularly in the first 3-4 days may elevate, hypoglycemia may occur

and there may be prolongation of coagulation studies (8,17).

Adequate ventilation, heat, perfusion, supply of glucose, calcium and acid-base

balance are the gold standard in treatment. One of the major causes of neurological

damage in asphyxiated neonates is the timing of postnatal ventilation and perfusion. For

this reason, it is very important to monitor the oxygen and carbon dioxide levels and keep

them within the normal limits (11).

In our case, right after the resuscitation and intubation, cardiac and respiratory

support was commenced. Hypoglycemia, hyponatremia and metabolic acidosis

improved after 24 hours. The infection was taken under control with the appropriate

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antibiotic treatment. Hepatic enzymes and creatine kinase levels were normal on Day 7

and renal functions returned to normal on Day 20.

In conclusion, perinatal asphyxia may develop in intrauterine period, during birth

or in the postnatal period. Recognition of risky cases, their referral to perinatal centers,

adequate antenatal care in pregnancy, foresightful approach of the experienced health

personnel to the newborn with asphyxia, appropriate and adequate resuscitation are

crucial in terms of reducing mortality and morbidity.

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Figure-1 A chest X-ray image of the patient

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(Figures 2-3 The erect abdominal plain graphy of the patient, the appearance of

abdominal distention

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Figure 4. Postoperative overall status of the patient

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