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| ORIGINAL ARTICLE |
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| Year : 2020 | Volume
: 9
| Issue : 1 | Page : 27-31 |
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Clinicoetiological profile of neonatal seizure in a newborn care unit of a tertiary care teaching hospital in Northern India
Bipin K Nair, Jyoti Sharma, Sanjeev Chaudhary
Department of Pediatrics, Dr. Rajender Prasad Govt Medical College, Kangra, Himachal Pradesh, India
| Date of Submission | 13-Jun-2019 |
| Date of Decision | 19-Oct-2019 |
| Date of Acceptance | 22-Dec-2019 |
| Date of Web Publication | 29-Jan-2020 |
Correspondence Address:
Dr. Jyoti Sharma
Department of Pediatrics, Dr. Rajender Prasad Government Medical College, Tanda, Kangra - 176 001, Himachal Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jcn.JCN_70_19
Objective: The aim was to study the clinicoetiological profile of neonatal seizure in a newborn care unit of a tertiary care teaching hospital in Northern India. Materials and Methods: This prospective hospital-based observational study enrolled all term and preterm newborns admitted to the newborn care unit with the first sign of seizure activity occurring within 28 days of life. Results: Out of 75 neonates admitted with neonatal seizure, 49 (65.33%) were male and 26 (34.60%) were female. Majority (52, 69.93%) were term babies. Subtle seizures (39.13%) were most common in both preterm babies (39.13%) and term (53.85%) babies. Age of onset was <24 h of life in 53.33% of the babies. Hypoxic-ischemic encephalopathy (HIE) was the most common cause (52%) of neonatal seizure. Conclusion: The most common cause of neonatal seizure in both preterm and full-term neonates was HIE followed by meningitis. The most common metabolic cause was hypocalcemia. The majority of the patients developed seizures within 24 h of life.
Keywords: Hypoxic-ischemic encephalopathy, neonatal seizure, subtle seizure
How to cite this article:
Nair BK, Sharma J, Chaudhary S. Clinicoetiological profile of neonatal seizure in a newborn care unit of a tertiary care teaching hospital in Northern India. J Clin Neonatol 2020;9:27-31 |
How to cite this URL:
Nair BK, Sharma J, Chaudhary S. Clinicoetiological profile of neonatal seizure in a newborn care unit of a tertiary care teaching hospital in Northern India. J Clin Neonatol [serial online] 2020 [cited 2021 Jan 15];9:27-31. Available from: https://www.jcnonweb.com/text.asp?2020/9/1/27/277227 |
| Introduction | |  |
Neonatal seizures are the most common neurological problem in the newborn.[1] A seizure is defined as paroxysmal electrical discharge from the brain which may manifest as motor, sensory, behavioral, or autonomic dysfunctions.[2] The immature brain seems more prone to seizures than the mature brain. Seizures in the neonatal period are also the most common neurological emergency and are associated with high mortality and morbidity.[3]
The neonatal central nervous system is particularly susceptible to seizures due to a combination of enhanced excitability and low levels of the inhibitory neurotransmitter gamma-aminobutyric acid.[4] Neonatal seizures are clinically significant as they may be suggestive of an underlying disorder or primary epileptic condition. The occurrence of seizure may be the first indication of a neurological disorder, and the time of onset of seizure has a relationship with the etiology of seizures and prognosis.[5]
Neonatal seizures can be divided into epileptic and nonepileptic seizures; neonatal seizures of epileptic origin are generated by hypersynchronous cortical neuronal discharges. There are age-dependent properties of the immature brain that enhance seizure initiation, maintenance of the seizure discharge, and propagation of the seizure discharge. Nonepileptic seizures occur in the absence of electrical seizure activity.[6]
Volpe classified seizures into five clinical types, namely subtle, multifocal clonic, focal clonic, generalized tonic, and myoclonic.[7] Seizures in neonates are different from those seen in older children. The differences are perhaps due to the neuroanatomic and neurophysiologic developmental status of the newborn infant. In the neonatal brain glial proliferation, neuronal migration, the establishment of axonal deposition, dendritic contacts, and myelin deposition are incomplete. For these reasons, clinical presentation differs.[8]
Clinicoetiological profile of neonatal seizure has been found to be varied across different populations. This study aimed to evaluate the clinicoetiological profile of neonatal seizures in newborns admitted at the newborn unit of a tertiary care teaching hospital in Northen India.
Objective
The objective was to study the clinicoetiological profile of neonatal seizures in neonates admitted in the newborn care unit of a tertiary care teaching hospital in Northern India.
| Materials and Methods | | |
It was a prospective observational hospital-based study conducted in the newborn unit of a tertiary care teaching hospital in Northern India. After obtaining the approval of the Institutional Ethical Committee, the study was conducted for 1 year. Parental consent was obtained for every patient enrolled. All term and preterm neonates showing first sign of seizure activity occurring within first 28 days of life and admitted during the study period to the newborn unit of the hospital were enrolled. A detailed antenatal history and baseline characteristics of convulsing neonate including sex, weight, and head circumference were recorded. Clinical details of each seizure episode reported by the mother and subsequently observed by the resident doctors on duty were recorded. Neonatal seizures were classified according to the Volpe's classification.[7]
Complete blood count, sepsis screen, blood glucose, serum (calcium, phosphorus, and alkaline phosphatase) levels were done immediately after a seizure episode. Cerebrospinal fluid study was done in the selected cases to find the etiology. Neurosonogram was done to evaluate any intracranial cause.
Statistical methods
Data were analyzed and presented as frequency and percentages.
| Results | | |
The present study was conducted to evaluate the clinicoetiological profile of neonatal seizures in neonates admitted in the neonatal care unit of a tertiary care teaching hospital in Northern India for 1 year. The study included 75 neonates admitted with neonatal seizures in the newborn care unit. In this study, 65.33% of the neonates were male and 34.66% of the neonates were female. Among all neonates, 62.67% of the neonates were inborn, and 37.33% of the neonates were outborn. Our study showed that 69.33% of the neonates were term and 30.67% of the neonates were preterm, 22.67% with period of gestation (POG) 34–37 weeks, and 8% of the patients had POG <34 weeks [Table 1].
The present study showed that among preterm newborns, majority of the patients (39.13%; n = 9) had subtle type of seizure followed by focal clonic (34.78%; n = 8), generalized tonic (21.74%; n = 5), and multifocal clonic (4.34%; n = 1). Among term babies, majority of the patients (53.85%; n = 28) had subtle type of seizure followed by focal clonic (17.3%; n = 9), generalized tonic (15.38%; n = 8), and multifocal clonic (13.46%; n = 7) [Table 2]. | Table 2: Distribution of newborns according to the type of seizure (n=75)
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Majority of the patients (53.33%) developed seizures within 24 h after birth. About 78.66% of the patients developed seizures within 72 h of birth and 21.33% of the patients developed seizures after 72 h of birth.
There were 6 (8%) newborns with hypocalcemia, 10 (13.33%) with hypoglycemia, 39 (52%) newborns with hypoxic-ischemic encephalopathy (HIE), 5 (6.66%) patients with intracranial bleed (IC bleed), and 15 (20%) patients with meningitis. A detailed presentation is shown in [Table 3].
Among all patients with HIE (n = 39), 35 patients developed seizures within 24 h after birth and 4 patients developed seizures within 24–72 h. Among the patients with meningitis and hypocalcemia, majority developed seizures after 72 h [Table 4].
Among all the 39 patients who had HIE, 64.1% of the patients were outborn and 35.9% patients were inborn. Our analysis showed that intracranial bleeding (ICB) was the cause of seizures in all the patients who were born with extremely low birth weight (<1 kg; n = 1). In very low birth weight neonates (1–1.49 kg; n = 2), meningitis (n = 1) and hypoglycemia (n = 1) were the causes of seizures. In low birth weight neonates (1.5–2.49 kg, n = 23), the most common cause of seizures was hypoglycemia (n = 7), followed by HIE (n = 6) and meningitis [Table 5].
This analysis showed that 50% of the hypocalcemic patients, 10% of the hypoglycemic patients, and 33.33% of the patients with meningitis had faulty feeding in the form of delayed feeding and feeding with cow's milk. Our analysis showed that 8% of the patients had hypothyroidism in mothers, 4% had pregnancy-induced hypertension (PIH), 1.33% had antepartam hemorrhage (APH), and premature rupture of membranes (PROM).
Among hypocalcemic patients (n = 6), 50% of the patients had multifocal clonic seizures, followed by focal clonic (33.33%) seizures. About 40% of the hypoglycemic patients had focal clonic seizures followed by subtle seizures (30%). Subtle seizures were the most common seizure type in patients with HIE (69.23%), followed by generalized tonic (15.38%) and focal clonic (12.82%). Forty percent of the patients with IC bleed had generalized tonic seizures. The most common type of seizure in patients with meningitis was subtle (40%), followed by focal clonic (33.33%). Neurosonogram findings were abnormal in 9 patients. In 9.33% of the patients, neurosonogram could not be done. Our study showed that 60% of the patients with IC bleed had a period of gestation <34 weeks and 20% of the patients were between 34 and 37 weeks.
Our study showed that death was the outcome of 15 patients. Among the expired patients, the causes of seizures were HIE, meningitis, and IC bleed in 60%, 26.67%, and 13.33% of the patients, respectively [Table 6].
| Discussion | | |
The present study aimed to evaluate the clinicoetiological profile of neonatal seizures in neonates admitted in the newborn care unit of a tertiary care teaching hospital in Northern India.
In our study, male patients were more in number with inborn neonates outnumbering the outborn newborns. Al-Naddawi et al. have shown that the male-to-female ratio was 1.2:1.[9] Das and Debbarma have found that the male-to-female ratio was 1.7:1.[10] In our culture, the male preponderance may be caused by social beliefs such that male babies are cared better by their parents and brought to the hospital even with minor complaints, but female babies are usually neglected and are managed at home even if they are very sick.
In this study, neonatal seizure occurred more in term neonates than in preterms. Previous investigators have reported a higher incidence of seizures ranging from 91% to 95% in full-term newborns.[11],[12]
In our study, the predominant seizure pattern was subtle seizures both in term neonates (53.8%) and preterm neonates (39%).
Taksande et al. studied the incidence, etiological factors, day of onset, clinical types, and various biochemical abnormalities in neonatal seizures. The authors reported that in term babies, 77 neonates had seizures, of which 24 (31.1%) had subtle seizures, 36 (46.7%) had clonic seizures, 15 (19.4%) had tonic seizures, and 2 (2.5%) had myoclonic seizures.[13]
Shah et al. reported that subtle (39.6%) was the most common type of seizure followed by tonic (31.4%).[14] Similar findings have also been reported in other studies.[15],[16]
The most common cause of seizures in both preterm and full-term newborns was HIE followed by meningitis. Among metabolic abnormalities that caused seizures, hypoglycemia was the most common one. ICB was also found to be the cause of seizures in few newborns.
Holanda and Melo have reported that HIE was the cause of seizures in 54% of the newborns and hypocalcemia was the most common metabolic abnormality (15%).[15] Kumar et al. reported that perinatal asphyxia was the most common cause of neonatal seizures in both preterm (39.02%) and term (48.98%) babies and 23.34% of the newborns had seizures associated with hypoglycemia.[16]
Sabzehei et al. found that the major diagnoses in neonates with seizures were HIE (34.3%), infections (24.4%), intracranial hemorrhage (6.9%), hypoglycemia (5.9%), and hypocalcemia (2.9%).[17]
Our study showed that infections were the cause of seizures in some newborns in number which were consistent with previously reported studies.[18],[19] Similarly, intracranial hemorrhage was observed in number of newborns with seizures which was comparable to previous studies.[19],[20]
Majority of patients developed seizures within 72 h after birth. Among all patients with HIE, the first seizure episode occurred in majority within 24 h of life. Among the patients with meningitis and hypocalcemia, majority developed seizures after 72 h.
Holanda and Melo reported that majority of term neonates developed seizures early (within 48 h), while most of the preterm neonates developed seizures after 72 h.[15] Taksande et al. concluded that the most common cause of seizure in term babies was birth asphyxia, with majority presenting to them within the first 72 h.[13] The onset of seizures was reported in the first 72 h of life in 42.6% of the neonates.[9] Das and Debbarma have reported that 80% of the cases had the onset of seizures within the first 3 days, the highest number being on the 1st day of life.[10] These findings were consistent with previously reported studies.
The incidence of HIE was more in outborn patients due to the lack of skilled health personnel and facilities in the periphery.
Maternal risk factors observed in our analysis were hypothyroidism, PIH, APH, and PROM. Alyasiri reported that 9.8% of the neonates were born to mother who had a history of preeclampsia, 4.9% of the neonates had mothers with a history of diabetes mellitus, chorioamnionitis was observed in 2.5% of the neonates, and APH in 3.3% of the neonates.[11]
In this study, in newborns with low birth weight, the most common cause of seizures was hypoglycemia followed by HIE and meningitis.
Das et al. reported that hypoglycemia was more common in low birth weight babies (55%).[10] Kumar et al. reported that hypoglycemia was more common in low birth weight newborns.[16] Bhatt et al. found that hypoglycemia was more frequent in low birth weight babies, most of them being small for gestational age.[21]
Our analysis showed that half the number of hypocalcemic patients, almost one-third of the patients of meningitis, and some patients of hypoglycemia had faulty feeding in the form of delayed feeding or feeding cow milk. Shah et al. have reported that prematurity and poor feeding in the early neonatal age caused hypoglycemia.[14]
Our study showed that multifocal clonic seizures pattern was the predominant one in hypocalcemic newborns, whereas the focal seizures were the most common in hypoglycemic patients. Subtle seizures were the most common seizures in patients of HIE, and generalized tonic seizures were the most common in patients with IC bleed. The most common type of seizure pattern in patients with meningitis was subtle seizures.
Das and Debbarma have reported that subtle seizures were most commonly associated with birth asphyxia and preterm babies, followed by clonic seizures. Tonic seizures were present in 34% of the cases and were associated with meningitis and birth asphyxia.[10]
Taksande et al. found that in birth asphyxia, the most common type of seizures was a subtle seizure, followed by focal clonic and multifocal clonic.[13]
In our study, IC bleed occurred more in preterm newborns <34 weeks of gestation.
Al-Naddawi et al. have concluded that IC bleed occurred mainly in preterm infants and was a major cause of death.[9] Vasudevan and Levene have reported that in preterm neonates, IC bleed and infections caused most of the seizures.[22] Our study findings were consistent with the above-mentioned studies.
Causes of seizures among expired patients in our study in descending order were HIE, meningitis, and IC bleed.
Tekgul et al. concluded that association between seizure etiology and the outcome remained strong, with cerebral dysgenesis and global hypoxia-ischemia associated with poor outcome.[23] Shah et al. have suggested that cases of HIE were associated with higher mortality as compared to cases with metabolic seizures.[14] The mortality rate in the cohort has been previously reported as 15%, with HIE being the most common cause.[24]
Alasiri et al. concluded that the neonatal HIE and infection were the two most common diagnoses associated with neonatal seizure that carry increased mortality rate and neurological sequelae.[11]
| Conclusion | | |
The present study concluded that the most common cause of neonatal seizure in both preterm and full-term newborns was HIE followed by meningitis. The most common metabolic cause was hypoglycemia. IC bleed was a major cause of seizures in preterm neonates. The most common type of seizure was subtle in both preterm and term neonates. The majority of the patients developed seizures within 24 h, of which HIE being the most common cause.
Acknowledgment
All the residents posted in the newborn care unit during the study period
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Silverstein FS, Jensen FE. Neonatal seizures. Ann Neurol 2007;62:112-20.  |
| 2. | Mikati M, Kliegman R, Behrman R, Stanton B. Nelson Textbook of Paediatrics. 19 th ed. Philadelphia: WB Saunders; 2011 |
| 3. | Bartha AI, Shen J, Katz KH, Mischel RE, Yap KR, Ivacko JA, et al. Neonatal seizures: Multicenter variability in current treatment practices. Pediatr Neurol 2007;37:85-90. |
| 4. | Rennie JM. Neonatal seizures. Eur J Pediatr 1997;156:83-7. |
| 5. | Sankar MJ, Agarwal R, Aggarwal R, Deorari AK, Paul VK. Seizures in the newborn. Indian J Pediatr 2008;75:149-55. |
| 6. | Holmes GL. Epilepsy in the developing brain: Lessons from the laboratory and clinic. Epilepsia 1997;38:12-30. |
| 7. | Volpe J. Neonatal Seizures. N Engl J Med 1973;289:413-6. |
| 8. | Rose AL, Lombroso CT. A study of clinical, pathological, and electroencephalographic features in 137 full-term babies with a long-term follow-up. Pediatrics 1970;45:404-25. |
| 9. | Al-Naddawi M, Hameed N, Kadum J, Al-Dabbas N. Clinical types and possible etiologies of neonatal seizures: A hospital based study. J Fac Med Baghdad 2011;53:1-5. |
| 10. | Das D, Debbarma SK. A Study on Clinico-Biochemical Profile of Neonatal Seizure. J Neurol Res 2016;6:95-101. |
| 11. | Alyasiri AA. Etiology and short outcome of neonatal seizures in Babylon gynecology and pediatrics teaching hospital. Med Res Chron Med Res Chronicles 2015;2:30-40. |
| 12. | AlMarzoki J. Clinco-biochemical profile of neonatal seizures. QMJ 2010;6:163-4. |
| 13. | Taksande A, Vilhekar K, Jain M, Lakra M. Clinico-biochemical profile of neonatal seizures. Pediatric Oncall J 2005;2. |
| 14. | Shah FU, Jehanzeb M, Khan MA. Etiological study of seizures in neonates. Khyber Med Univ J 2013;5:9-12. |
| 15. | Holanda MR, Melo AN. Comparative clinical study of preterm and full-term newborn neonatal seizures. Arq Neuropsiquiatr 2006;64:45-50. Erratum in: Khyber Med Univ J. 2013;5:9-12. |
| 16. | Kumar A, Gupta A, Talukdar B. Clinico-etiological and EEG profile of neonatal seizures. Indian J Pediatr 2007;74:33-7. |
| 17. | Sabzehei MK, Basiri B, Bazmamoun H. The Etiology, Clinical Type, and Short Outcome of Seizures in NewbornsHospitalized in Besat Hospital/Hamadan/Iran. Iran J Child Neurol 2014;8:24-8. |
| 18. | Aziz A, Gattoo I, Aziz M, Rasool G. Clinical and etiological profile of neonatal seizures – A tertiary care hospital based study – ScopeMed. Int J Res Med 2015;3:2198-203. |
| 19. | Faiz N, Malik M, Azam M, Afzal U. Title of the topic etiological profile of neonatal seizure. Ann Pak Inst Med Sci 2009;5:77-86. |
| 20. | Rehman Malik A, Iqbal Quddusi A, Naila. Neonatal seizures, experience at Children Hospital and Institute of Child Health Multan. Pak J Med Sci 2013;29:1128-31. |
| 21. | Bhatt S, Raju N, Phanse S. Clinico-etiological and EEG profile of neonatal seizures. Indian J Clin Pract 2013;29:1128-31. |
| 22. | Vasudevan C, Levene M. Epidemiology and aetiology of neonatal seizures. Semin Fetal Neonatal Med 2013;18:185-91. |
| 23. | Tekgul H, Gauvreau K, Soul J, Murphy L, Robertson R, Stewart J, et al. The current etiologic profile and neurodevelopmental outcome of seizures in term newborn infants. Pediatrics 2006;117:1270-80. |
| 24. | Ghanshyambhai P, Sharma D, Patel A, Shastri S. To study the incidence, etiology and EEG profile of neonatal seizures: A prospective observational study from India. J Matern Neonatal Med 2015;125:1-5. |
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]
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