ECG changes in birth asphyxia and
its correlation with Cardiac troponin-I
Pal P1, Goel M2
1Dr Pankaj Pal, Assistant Professor, Department of Paediatrics, 2Dr
Manjusha Goel, Associate Professor , Department of Paediatrics. Both
are affiliated with Gandhi Medical College, Bhopal, MP.
Address for
correspondence: Dr Pankaj Pal, Email:
roshanchanchlani@gmail.com
Abstract
Introduction:
Cardiac dysfunction is well known in perinatal asphyxia caused by
transit myocardial ischemia. Sometimes cardiac dysfunction may be so
severe that it can cause congestive cardiac failure and shock that
leads to death of newborn. ECG and serum levels of cardiac enzymes can
be used to demonstrate impaired myocardial function. Material and Methods:
It was a case control study conducted in the department of paediatrics,
Gandhi Medical College, Bhopal over a period of 12 months from January
2013 to December 2013. Forty asphyxiated full term neonates were taken
as cases and 20 healthy full term neonates as controls. Forty neonates
with asphyxia admitted to NICU with gestational age >37
completed weeks and with birth weight >2 kg taken as cases and
twenty healthy full term neonates (37 completed wks) unasphyxiated
weighing >2 kg at birth with clear liquor and 1 min Apgar score
>7. Results:
Myocardial dysfunction was present in 90% of the newborns with severe
birth asphyxia and 40% of newborns with moderate birth asphyxia. T wave
changes were seen in 80% neonates with severe asphyxia and 33% neonates
with moderate asphyxia. In present study, cTn I levels in severely
asphyxiated neonates were significantly higher than moderately
asphyxiated neonates and control group neonates (4.6 ng/ml, range 2.1
– 7.8, and 1.8 ng/ml, range 0.2 – 4.8 ng/ml and
0.6ng/ml, range 0.2-1ng/ml respectively). Conclusion: We found
a linear relationship between levels of cardiac troponin-I and birth
asphyxia. Therefore cardiac troponin-I level may be useful in
predicting the mortality and outcome in perinatal asphyxia.
Key words:
Birth Asphyxia, Electrocardiography, Cardiac Troponin I, Neonates
Manuscript received:
1st Apr 2015, Reviewed:12th
Apr 2015
Author Corrected:
6th May 2015, Accepted
for Publication: 20th May 2015
Introduction
In India, the incidence of perinatal asphyxia is as high as 8.4%
(considering the definition of birth asphyxia as Apgar score of
< 7 at 1 min) [1]. Perinatal asphyxia is one of the leading
cause of neonatal mortality (28%) in our country and it is the most
common and important cause of preventable cerebral injury occurring in
the neonatal period [2]. Perinatal asphyxia affects almost all organ
systems of body. In most of the cases multiple organs are involved but
sometimes brain may be the only organ exhibiting dysfunction following
asphyxia.
Perinatal asphyxia leading to hypoxic-ischemic encephalopathy (HIE) is
a common problem causing multi organ dysfunction including myocardial
involvement which can affect the outcome [3]. Sometimes cardiac
dysfunction may be so severe that it can cause congestive cardiac
failure and shock that leads to death newborn. ECG and serum levels of
cardiac enzymes can be used to demonstrate impaired myocardial
function.
Cardiac troponins T and I are the preferred markers for myocardial
injury as they have the highest sensitivities and specificities for the
diagnosis of acute myocardial infarction [4].
Cardiac troponin is a protein released from myocytes when irreversible
myocardial damage occurs. It is highly specific to cardiac tissue and
accurately diagnoses myocardial infarction with a history of ischaemic
pain or ECG changes reflecting ischaemia. Cardiac troponin level is
dependent on infarct size, thus providing an indicator for the
prognosis following an infarction [5].
Studies of cardiac troponin I (cTnI) in newborns are very limited and
less diagnostic because of wide range of serum cTnI I concentrations in
newborns. cTnI concentrations > 1ng/ml in asphyxiated newborns
may be considered significant.
ECG changes have been linked to the myocardial ischemia in newborns
which include generalized T-wave inversion or flattening, ST segment
elevation or depression, abnormal Q wave and bundle branch block.
Material
and Methods
It was a case control study conducted in the department of paediatrics,
Gandhi Medical College, Bhopal over a period of 12 months from January
2013 to December 2013.
Sample size
Forty asphyxiated full term neonates were taken as cases and 20 healthy
full term neonates as controls.
Study group
Forty neonates with asphyxia admitted to NICU with gestational age
>37 completed weeks and with birth weight >2 kg.
Inclusion criteria
All cases referred from Sultania Zanana hospital with the diagnosis of
HIE bases on clinical history at birth and Sarnat and Sarnat staging
[6].
Exclusion criteria
1. Newborns with congestive heart disease
2. Newborns with congenital malformations
3. Metabolic disorders
4. Preterm newborn (>37wks)
Control group
Twenty healthy full term neonates (37 completed wks) unasphyxiated
weighing >2 kg at birth with clear liquor and 1 min Apgar
score>7.
Clinical examination
A detailed history was taken and complete physical, neurological and
cardiovascular examination was done on admission and 48-72 hrs.
Electrocardiogram
recording
ECG was recorded around 48-72 hours of age. during ECG recording
calibration factor fixed at 1 standardization that indicate 1 mv equal
to 10mm for the six limb leads and six precordial leads. Recording
speed of paper was 25 mm/sec. The electrocardiogram was recorded using
the ECG machine lead I, II, III, avr, avl and avf were recorded in
direct sequence using neonatal section electrodes. ECG scores were
calculated by using the scoring system developed by R Jedeikin [7].
Method of determining
Cardiac troponin I
The SD bioline troponin I rapid test was used. It is rapid immune
chromatographic assay for the qualitative detection of cTnI in human
blood, serum and heparin plasma as an aid in the diagnosis of
myocardial ischemia. Two ml of whole blood is collected in collection
vial by venupuncture under aseptic precaution and then centrifuge to
get plasma specimen by using dropper. Specimen is taken up to the fill
line, then specimen is added into the sample well of the test device
and result read at 15 minutes.
Results
The present study included 60 subjects of which 40 were cases of
perinatal asphyxia of moderate to severe degree and 20 were healthy
neonates without any evidence of asphyxia as controls. The asphyxiated
cases were further divided into two groups on the basis of severity of
hypoxic ischemic encephalopathy (HIE). Group A (HIE III) had 10 cases
and group B (HIE II) had 30 cases, group C served as controls.
Table No. 1: Distribution
of the newborns into various groups
|
Category
|
Degree
of Asphyxia
|
No.
of Neonates
|
Sex
|
Group
|
|
Male
|
Female
|
|
HIE staging III
|
Severe
|
10(25%)
|
7(70%)
|
3(30%)
|
A
|
|
HIE staging II
|
Moderate
|
30(75%)
|
21(70%)
|
9(30%)
|
B
|
|
Normal
|
Nil
|
20
|
13(65%)
|
7(35%)
|
C
|
Table No 2: Summary of
clinical manifestation as evidence of myocardial dysfunction in birth
asphyxia
|
Myocardial
Dysfunction
|
Group
A(n=10)
|
Group
B(n=30)
|
|
Shock
|
2
|
4
|
|
Respiratory distress
|
4
|
7
|
|
Murmur
|
2
|
1
|
|
CCf
|
1
|
0
|
|
Total
|
9
|
12
|
Myocardial dysfunction was present in nine (9) newborns with severe
birth asphyxia and twelve (12) newborns with moderate birth asphyxia.
Table No 3: Summary of
ECG changes in birth asphyxia
|
Group
|
Abnormal
Q
wave
|
Abnormal
T
wave
|
Abnormal
ST segment
|
Prolonged
QRS
|
Bundle
branch block
|
|
Asphyxiated
|
0
|
18
|
6
|
1
|
1
|
|
Control
|
0
|
9
|
0
|
0
|
0
|
Table No 4: Jedeikins
grading versus HIE cross tabulation
|
Jedkeins
grading
|
HIE
grading
|
Total
|
|
II
|
III
|
|
I
|
3
|
0
|
3
|
|
II
|
7
|
4
|
11
|
|
III
|
1
|
4
|
5
|
|
IV
|
0
|
1
|
1
|
|
Normal
|
19
|
1
|
20
|
|
Total
|
30
|
10
|
40
|
In present study, cTn I levels in severely asphyxiated neonates were
significantly higher than moderately asphyxiated neonates and control
group neonates (4.6 ng/ml, range 2.1 – 7.8, and 1.8 ng/ml,
range 0.2 – 4.8 ng/ml and 0.6ng/ml, range 0.2-1ng/ml
respectively, P value <0.005)
Discussion
In our study, CVS was the most common organ system to suffer from
dysfunction (52.5%). Similarly in a study conducted by P.S. Rajkumar et
al. in 2005, cardiovascular dysfunction was seen in 70% cases [8]. P.
Shah et al. also studied 130 newborns with birth asphyxia and reported
cardiovascular dysfunction in 62% cases [9].
Electrocardiographic
Evaluation
In the present study no significant abnormality of heart rate and
rhythm was observed in asphyxiated babies. T wave changes were seen in
80% neonates with severe asphyxia and 33% neonates with moderate
asphyxia. Thus the overall incidence was 45% in asphyxiated babies.
Control group had grade I ECG changes in 45% cases. Mean axis was 128,
which is within normal limit. Prolonged QRS duration was seen in one
severely asphyxiated baby. The incidence of RBBB was 10% in severely
asphyxiated babies. No one in the study group showed LBBB. Q wave was
normal in all cases. Abnormal ST segment was seen in 50% neonates with
severe asphyxia and 33% neonates with moderate asphyxia.
Thus the overall incidence was 15%, so according to Jedkeins criteria
grade I ECG changes were present in 3 (7.5%) cases, grade II in 11
(27.5%), grade III in 5 (12.5%) and grade IV in 1 (2.5%) cases.
I Barberi et al. reported grade II ECG changes in 100% cases with
moderate asphyxia, grade II in 38.5%, grade III in 38.5% and grade IV
in 23% cases with severe asphyxia. Control group had 41% cases with
grade I changes that were similar to our present study [10]
Esra Kanik et al. also reported ECG changes in asphyxiated neonates
where ECG changes increased with severity of asphyxia [11].
Cardiac Troponin I (cTn I)
In present study, cTn I levels in severely asphyxiated neonates were
significantly higher than moderately asphyxiated neonates and control
group neonates (4.6 ng/ml, range 2.1 – 7.8, and 1.8 ng/ml,
range 0.2 – 4.8 ng/ml and 0.6ng/ml, range 0.2-1ng/ml
respectively, P value <0.005). Gulcan turker et al. reported
that infants with hypoxia had significantly higher cord blood cTnI
levels than normal newborns and in non survivors cord blood cTn I
levels were significantly higher than survivors (5.9 ng/ml, range 2.1
– 12.8, and 1.6 ng/ml, range 0.4 – 5.8 ng/ml
respectively) [12].
Esra Kanik et al. studied that serum cTn I level was significantly
higher in newborns with birth asphyxia [11]. Danicle Trevisanoto et al.
concluded that in asphyxiated neonates, cTn I concentrations were
higher with respect to healthy neonates, suggesting the presence of
myocardial damage in this group of high risk infants, cTn I did not
correlate with traditional marker of asphyxia [13].
Conclusion
It has been well established that troponin-T is elevated in myocardial
ischemia in perinatal asphyxia. Cardiac troponin-I is specific and
sensitive in the diagnosis of cardiac dysfunction in perinatal
asphyxia. Mean cardiac troponin-I level in cases with cardiac
dysfunction was found significantly higher in cases with severe
asphyxia. We found a linear relationship between levels of cardiac
troponin-I and birth asphyxia. Therefore cardiac troponin-I level may
be useful in predicting the mortality and outcome in perinatal
asphyxia.
Funding:
Nil, Conflict of
interest: None initiated.
Permission from IRB:
Yes
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How to cite this article?
Pal P, Goel M. ECG changes in birth asphyxia and its correlation with
Cardiac troponin-I. Int J Med Res Rev 2015;3(4):400-403. doi:
10.17511/ijmrr.2015.i4.075.