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Year : 2015  |  Volume : 10  |  Issue : 3  |  Page : 227-234

Pattern, etiological factors and determinants of mortality among sick newborns with seizures in Ilesa, Nigeria

Department of Paediatrics and Child Health, Obafemi Awolowo University, Ile-Ife, Osun, Nigeria

Date of Web Publication18-Sep-2015

Correspondence Address:
Bankole Peter Kuti
Department of Paediatrics and Child Health, Obafemi Awolowo University, Ile-Ife, Osun
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1817-1745.165663

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Background: Neonatal seizures contribute significantly to newborn morbidity and mortality particularly in developing countries including Nigeria. Unfortunately the countries with high incidence of neonatal seizures often lack the facilities to adequately diagnose, monitor and prognosticate the condition. Objective: We set out to determine the factors at presentation that predict death among babies admitted with clinically identifiable seizures. Methods: We prospectively observed consecutive neonatal admissions over a nine month period at the Wesley Guild Hospital, Ilesa, Nigeria. Babies with seizures were identified based on clinical observation. Perinatal history, examination and laboratory findings were compared between babies with seizures who survived and those that died. Multivariate regression analysis was used to determine the predictors of mortality. Results: Over a nine month study period, a total of 340 babies were recruited out of which 55 (16.7 percent) had clinically identifiable seizures. Fifteen (27.3 percent) of the 55 babies with clinically identifiable seizures died; while 20 (7.0 percent) of the 285 babies without seizures died. Clinically identifiable neonatal seizures contributed to 42.9 percent of the overall mortality in the neonatal unit during the study period. The risk factors for mortality among the babies with seizures were clinical seizures in the first 24 hours of life, birth asphyxia co-existing with hyponatraemia and presence of cerebral oedema (P < 0.05). The independent determinant of mortality among babies with clinical seizures was cerebral oedema (OR = 4.025; 95% CI 1.342-26.956; P = 0.019). Conclusion: We conclude that clinically identifiable neonatal seizures contribute significantly to neonatal mortality and presentation within 24 hours of delivery, birth asphyxia and cerebral oedema increased the risk of death in babies with seizures.

Keywords: Death, neonates, predictors, seizures

How to cite this article:
Kuti BP, Oseni SB, Owa JA. Pattern, etiological factors and determinants of mortality among sick newborns with seizures in Ilesa, Nigeria. J Pediatr Neurosci 2015;10:227-34

How to cite this URL:
Kuti BP, Oseni SB, Owa JA. Pattern, etiological factors and determinants of mortality among sick newborns with seizures in Ilesa, Nigeria. J Pediatr Neurosci [serial online] 2015 [cited 2023 Jan 30];10:227-34. Available from: https://www.pediatricneurosciences.com/text.asp?2015/10/3/227/165663

   Introduction Top

Neonatal seizures often indicate the presence of central nervous system dysfunction, and they are one of the most consistent manifestations of acute neonatal encephalopathy. [1],[2] The presence of seizures in sick neonates may be associated with increased risk of long-term neurologic sequelae and/or death. [3],[4] They, therefore, connote signs of poor prognosis particularly in resource-constraint regions where the facilities for adequate management of such babies are not readily available. [5],[6],[7],[8]

The nature and severity of the neurologic process causing neonatal seizures has been reported as a major determinant of outcome .[5],[8],[9],[10] Some babies with neonatal seizures seem to recover without overt sequelae while the others die or survive with neurologic deficit. [5],[6],[7],[8],[10] Facilities for electroencephalography (EEG), viral culture, and brain neuro-imaging useful to adequately characterize the seizure process, decipher the underlying cause, monitor and prognosticate babies are often unavailable in many centers in developing countries. [5],[6],[7],[8] Consequently, the determination of simple, easily recognizable clinical and laboratory factors at the presentation that can predict the death in babies with clinical seizures is of utmost importance. This is particularly relevant in resource-constraint centers to facilitate more aggressive management and close monitoring of such babies at admission to ensure survival. This study, therefore, aims to highlight the pattern, etiological factors and determinants of mortality among ill babies with clinically identifiable seizures at the Wesley Guild Hospital (WGH) Ilesa, Nigeria.

   Patients and Methods Top

Study location

The study was conducted at the neonatal unit of the WGH, Ilesa. The WGH is a tertiary unit of the Obafemi Awolowo University Teaching Hospitals Complex (OAUTHC), Ile-Ife. The hospital is one of the main referral centers providing neonatal, general and specialist paediatric health care services to the communities of Osun, Ondo and Ekiti States of South West Nigeria. The newborn ward of the WGH operates a 24-h neonatal service and admits about 600 babies per annum. The ward has facilities for rooming-in of the mothers or care-givers with the sick infants. Ilesa is situated on latitude 7°35΄N and longitude 4°51΄E and is the largest town in Ijesaland, about 200 km North-East of Lagos, the economic nerve center of Nigeria. [11]

Study design

This was a hospital-based, prospective observational study involving the clinical and laboratory data collection.

Study participants

All consecutive neonatal admissions into the unit during the study period were recruited. Babies with clinically observable seizures at presentation and those who develop seizures during the course of their stay in the hospital were noted.


Babies whose mothers/caregivers gave consent to participate in the study were recruited. History obtained at presentation included the age of the babies at the onset of symptoms, birth weight, mode and place of delivery, and the gestational ages of the babies. The babies' gestation ages were estimated from the 1 st day of the last menstrual period of the mother, early (first trimester) ultrasound report, and or by using the new Ballard scoring system done within 48 h of delivery. Babies were classified as small for gestation age (SGA), appropriate for gestation age (AGA) and large for gestational age (LGA) using the method described by Battaglia and Lubchenco. [12] The APGAR scores, if assessed, or history of failure of the baby to cry and breathe normally for a prolonged period after birth were also noted.

Presenting features were also documented; these included the presence of clinically observable seizures. Seizures in this study were diagnosed based on clinical evidence from the history obtained from the parents and or relatives. These include abnormal movements localized or generalized; repetitive, stereotyped and those accompanied by abnormal eye deviations. These abnormal movements should not be suppressible by holding the affected limb or changing baby's position and should not be elicited by stimuli. [13] In addition to the seizures observed by the study, clinicians were included as cases of clinical seizures. Seizure types were described according to Volpe's classification [13] as tonic-clonic, myoclonic, tonic-clonic, and fragmentary at presentation. Other features such as irritability, fever, pallor, cyanosis, and high-pitch cry were also documented.

Other history of interest included maternal age, marital status, and medical history during pregnancy especially history suggestive of diabetes mellitus, hypertension, and febrile illnesses. History of antenatal care, duration of labor, adverse events in labor such as eclampsia, cord accidents, and prolonged rupture of fetal membrane (PROM) were also obtained. The socioeconomic status of the parents was assessed using the method described by Oyedeji. [14] This was based on a rank assessment of the occupation and the highest level of educational qualifications of both parents. Gainfully employed professionals were classified as social class I while the unemployed parents with no formal education were classified as V. [14]

Detailed physical examinations were carried out on all the babies. The weight in grams, taken with (Seca® ) digital infant weighing scale to the nearest gram, the length in centimeters, using an infantometer were measured and recorded. Rectal temperature was taken using a digital clinical thermometer. Findings on systemic examinations were recorded.

Investigations done on the babies included blood glucose, serum electrolytes; plasma ionized calcium and magnesium. Others included full blood count, blood culture, and cerebrospinal fluid (CSF) microscopic culture and sensitivities which were done for all babies with suspected sepsis. Transfontanelle ultrasonography (TFU) was done for all babies with clinically identifiable seizures and on those in which the procedure was indicated by a hospital consultant radiologist using an appropriate probe. The TFU was done only once for each baby at presentation using a real time sector scanner DP-8500 with a high resolution 7.5 MHz transducer, curvilinear probe. The anterior fontanelle which has the widest and the least variable window was used. The scanning was done for both coronal and sagittal sections. The TFU findings were reported as normal without the gross abnormality; with features in keeping with cerebral edema; or intracranial hemorrhage. Intraventricular hemorrhages were classified as either restricted to less than 10.0% of the ventricle as grade 1; those involving 10.0-50.0% of the ventricles as grade 2, grade 3 involved more than 50.0% of the dilated ventricles, while grade 4 involved the brain parenchyma. [15],[16]

For the purpose of the present study, birth asphyxia was presumed in home deliveries and those outside the hospital when there was a history that the baby had failed to cry or breathe at birth. [17] This also included babies who had gasped for a long time, had to be stimulated for a prolonged period of time, or when a term baby was unable to suck in the first 24 h of life. [17] The Apgar score was used in all inborn infants; <4 in the 1 st min and <6 at 5 min were regarded as asphyxia. [17]

Hypoglycemia was diagnosed as whole blood glucose <2.2 mmol/L (40 mg/dl) while hyperglycemia was defined as whole blood glucose ≥8.3 mmol/L (150 mg/dl). [18] Hypocalcemia was defined as plasma calcium <2.25 mmol/L while hypomagnesemia was defined as plasma magnesium <0.73 mg/dl. [19] Hyponatremia was defined as serum sodium <130 mmo/l while hypernatremia was defined as serum sodium >150 mmol/L. [20] The venous hematocrit of <45.0% within the 1 st week of life and 35.0% after the 1 st week was regarded as anemia. [21] Diagnosis of sepsis or meningitis were made when the baby had a bacterial growth on blood culture or CSF culture, respectively. [22]

Standard management protocol of the unit was followed which included control of seizures with intravenous (IV) Diazepam 0.3 mg/kg stat, then IV phenobarbitone 20 mg/kg loading dose slowly followed by 3-5 mg/kg/day in two divided doses when indicated. Other anticonvulsants like paraldehyde were also used as necessary. Fluid and calorie balance was maintained in addition to correction of glucose and calcium deficits and the administration of appropriate antibiotics. Other supportive measures such as oxygen therapy and incubator care to maintain thermo-neutral environment were administered as indicated.

The outcome variable for this study was death or survival among the babies with seizures.

Ethical clearance was obtained from the Ethics and Research Committee of the OAUTHC, Ile-Ife. For each baby, an informed written consent was obtained from the parent(s) or guardians.

Data analysis

Data were analyzed using the Statistical Package for Social Sciences (SPSS) for Windows version 17.0 (SPSS Inc., Chicago 2008). Continuous variables were summarized using means and standard deviations (SDs) or median and interquartile range (IQR) for normally and nonnormally distributed variables, respectively. Categorical variables were summarized using percentages and proportions. Differences between the means of continuous variables were compared using Student's t-test (for normally distributed variables), and Mann-Whitney U-test (for nonnormally distributed variables) while categorical variables were compared using Pearson's Chi-square test and Fisher's exact test as appropriate (with Yate's correction where applicable).

Study variables that gave significant results were analyzed using Multivariate logistic regression to determine their independent effect on the outcome (death or survival) variable. Results were interpreted with odds ratios (ORs) at 95% confidence interval (CI). Statistical significance level was established when CI did not embrace unity and P < 0.05.

   Results Top

Over a 9-month period (April 1, 2011, to December 31, 2011), a total of 340 babies were recruited for the study. Fifty-five (16.2%) of the 340 babies had clinically identifiable seizures.

Sociodemographic characteristics of the 55 babies with clinical seizures

Age and sex

0The ages of the 55 babies with clinical seizures at presentation ranged between 12 h and 26 days with a median (IQR) age of 1.6 days (7 h to 7 days). Thirty-nine (70.9%) of the 55 babies were admitted within 72 h of life. The babies with seizures consisted of 41 (74.5%) males and 14 (25.4%) females giving a male to female ratio of 2.9:1 [Table 1].
Table 1: Association between sociodemographic variables and mortality among the babies with seizures

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Gestational age

The estimated gestational ages of the babies with seizures ranged between 26 and 44 weeks with a mean (SD) of 37.5 (3.8) weeks. Forty-five (81.8%) of the babies were delivered at term, 6 (10.9%) were preterm while the remaining (7.3%) babies were post-term.

Birth weight

The mean (SD) birth weight of the babies was 3000 (600) g, this ranged between 1400 and 4000 g. Thirteen (23.6%) of the 55 babies were low birth weight babies while 40 (72.7%) were normal weight babies. The rest (5.5%) were macrosomic babies. Forty-two (76.4%), 9 (16.4%) and 4 (7.2%) were AGA, SGA and LGA, respectively [Table 1].

Maternal age

The maternal ages of the babies ranged between 17 and 48 years with a mean (SD) of 28.0 (6.4) years. Five (9.1%) of the mothers were teenagers [Table 2].
Table 2: Association between maternal variables and mortality among babies with seizures

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Parental socioeconomic status

Majority (58.2%) of the parents whose babies had clinical seizure were from middle socioeconomic class III, 16 (29.1%) were from low socioeconomic class, while only 7 (12.7%) of the parents were from high social class [Table 2].

Modes of delivery

The majority (78.2%) of the babies were delivered per vaginam, only 12 (21.80%) were delivered via caesarian section.

Places of delivery

Forty-nine (89.1%) of the babies were delivered outside the WGH (outborns). This included private maternity homes/hospitals in 22 (40.0%), 22 (40.0%) in churches (mission homes), 1 (1.8%) in general hospitals, and the remaining 4 (7.3%) were delivered in their homes or homes of traditional birth attendants. The 6 babies (10.6%) with seizures delivered at the WGH were rushed in for emergency cesarian section following prolonged labor at the peripheral centers.

Adverse perinatal events

Twelve (21.8%) of the 55 babies with seizures and meningitis were born to mothers with adverse perinatal events such as preeclampsia, PROM, and cord accidents [Table 2].

   Presenting Clinical Features of the Babies with Clinical Seizures Top

The leading clinical features observed in the babies at presentation were respiratory distress (43.6%), poor sucking (36.4%), irritability (36.4%), and jaundice (34.5%). The other presenting features are highlighted in [Table 3].
Table 3: Association between presenting features and mortality among babies with seizures

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   Examination Findings in the Babies with Clinical Seizures Top

Weight at admission

The weights of the babies at admission ranged between 1500 and 400 g with a mean (SD) weight of 2665 (800) g.

Length of the babies at admission

The lengths of the babies range between 40.0 and 54.0 cm with a mean (SD) of 49.4 (2.6) cm.

Temperature at presentation

The rectal temperature at presentation ranged between 35.5°C and 39.8°C with a mean (SD) of 37.4 (1.0)°C. Five (9.1%) of the 55 babies had hypothermia at presentation, 10 (18.2%) had a fever while the remaining 40 babies (72.7%) had normal temperature [Table 3].

The types of clinically observable seizures among the babies

Thirty-seven (67.3%) of the 55 babies with seizures had early onset seizures while the remaining 18 (32.7%) had late onset seizures. Forty-eight (87.3%) of the babies presented with seizures at admission, while 7 (12.7%) developed seizures within 24 h of admission. [Figure 1] shows the seizure types observed among the 55 babies. Generalized tonic and fragmentary seizures were the predominant types of seizures observed in 24 (43.6%) and 13 (23.6%) babies respectively. Myoclonic seizures were the least represented occurring in 2 (3.6%) babies. Of the six preterm babies with clinical seizures, 4 (66.7%) had a fragmentary type, while the remaining 2 (33.3%) had generalized tonic seizures.
Figure 1: Distribution of the seizure types observed among the 55 babies with clinical seizures

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   Laboratory Findings among the Babies with Clinical Seizures Top


The hematocrit of the babies at admission ranged between 35.0% and 60.0% with a mean (SD) of 49.6 (8.3%). Eighteen (32.7%) babies had anemia at presentation while the remaining 37 (67.3%) had normal hematocrit [Table 4].
Table 4: Association between abnormal laboratory parameters, diagnosis and mortality

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Blood glucose

The mean (SD) blood glucose of the babies was 4.4 (2.2) mmol/L. This ranged between 0.8 mmol/L and 9.4 mmol/L. Fifteen (27.3%) had hypoglycemia at presentation while 5 (9.1%) had hyperglycemia. The remaining 35 (63.6%) had normal blood sugar at presentation.

Serum calcium

The mean (SD) serum calcium of the babies was 2.1 (0.3) mmol/L with a range between 1.66 and 2.55 mmol/L. Thirty-six (65.5%) of the babies with clinical seizures had hypocalcemia at presentation.

Serum magnesium

The serum magnesium of the babies ranged from 0.5 to 1.2 mmol/L with a mean (SD) value of 0.7 (0.2) mmol/L. Seventeen (30.9%) of the babies had hypomagnesemia at presentation. Some babies (27.3%) however, had both hypocalcemia and hypomagnesemia [Table 4].

Serum sodium

About one-third of the babies with clinical seizures had low serum sodium at presentation. The serum sodium of the babies ranged between 115 and 149 mmol/L with a mean (SD) of 135 (6.3) mmol/L.

Blood culture

Blood culture was positive in 8 (14.5%) of 55 babies with seizures. The bacterial isolates from the eight positive blood cultures were Staphylococcus aureus in 4 (50.0%),  Escherichia More Details coli in 2 (25.0%), Klebsiella spp. in 1 (11.3%), and coagulase negative Staphylococcus (CONS) 1 (3.8%).

The overall sensitivity patterns of the isolates to the commonly used antibiotics in the unit were as follows: Ciprofloxacin (95.0%); cefuroxime (89.5%); ceftriaxone (72.0%); ceftadixime (70.0%); ampicillin (30.5%) and gentamicin (30.5%) Gram-positive.

Cerebrospinal fluid analysis

Forty-nine (89.1%) of the 55 babies with seizures had lumbar puncture for CSF analysis. Three (5.5%) of the babies with seizure had pyogenic meningitis.

The isolates from the CSF of the babies with seizures and meningitis were E. coli in 2 (66.7%) and Klebsiella spp. in 1 (33.3%). Six babies with seizures did not have a lumbar puncture done because four of the babies were not clinically stable for the procedure before they died and lumbar puncture was not successful in the two other babies.

The overall antibiotics sensitivities patterns were ciprofloxacin (100.0%), ceftriaxone (95.0%), cefuroxime (95.0%), ceftazidime (89.5%), ampicillin (25.0%), and gentamicin (25.0%).

Transfontanelle ultrasonography

Fifty-two (94.5%) of the 55 babies with clinical seizures had TFU done. The three babies whose transfontanelle ultrasound was not done, were clinically unstable throughout admission before death.

Of the 52 babies that had TFU done, 36 (69.2%) had normal scan reports while four (7.7%) of the babies who were also preterm babies had scan report of grade 1 intraventricular hemorrhage [Figure 2].
Figure 2: Findings on transfontanelle ultrasound of the babies with seizures

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Diagnosis made in the babies with clinical seizures

Birth asphyxia and hypocalcaemia were the leading diagnoses made in the babies with clinically identifiable seizures observed in 54.5% and 65.5% of the babies, respectively [Table 4]. Many of the babies had multiple diagnoses as birth asphyxia was often associated with metabolic abnormalities such as hypoglycemia, hypocalcaemia, and hypomagnesemia [Table 4].

   Outcome of Hospitalization Top

Admission outcomes

Of the 55 babies with clinical seizures, two babies (3.6%) were discharged against medical advice, 38 (69.1%) babies were discharged home while 15 (27.3%) babies died. The mortality in the unit among babies without seizures during the study period was 20 (7.0%) out of 285 babies.

Fifteen (42.9%) babies among the 35 total mortality during the study period had seizures. Mortality rate was significantly higher among babies with seizures compared to those without seizures (28.3% vs. 7.0%; χ?2 = 20.496; df = 1; P < 0.001).

Duration of hospital stay

The mean hospital stay of the babies with seizures was 8.5 (7.0) days, median (IQR) 8.3 (4.5-16.0) days. This ranged from 2 h to 21 days.

   Determinants of Mortality among Babies with Seizures Top

Sociodemographic factors in relation to mortality among babies with clinical seizures are presented in [Table 1]. Significantly higher proportions of babies who had seizures within the first 24 h of life died, as 10 (45.5%) of the 22 babies who had seizures within the first 24 h of life compared to 5 (16.1%) of the remaining 31 babies who had seizures after 24 h of life died (χ?2 = 5.456; P = 0.020 df = 1). There was, however, no significant association between the other sociodemographic factors including sex, place of residence as well as birth weight and gestational age of the babies with seizures and mortality [Table 1]. Likewise no significant difference in the mean maternal ages between the mortality cases and those who survived (29.2 [7.2] years vs. 27.6 [6.1] years; t = 0.82; P = 0.418). Also, parity of the mother and parental socioeconomic class were not significantly associated with mortality or survival among babies with seizures [Table 2].

Perinatal events, clinical features and seizure types at presentation in relation to mortality

Adverse perinatal events in pregnancy and place/modes of delivery of mothers whose babies had seizures were not significantly associated with mortality or survival [Table 2]. Also, the clinical features at presentation including the seizure types were not significantly associated with mortality or survival among hospitalized babies with clinical seizures [Table 3].

Abnormal laboratory parameters, diagnosis with mortality

Significantly more babies with seizures who had birth asphyxia co-existing with hyponatremia died compared to those without these diagnoses (66.7% vs. 16.3%; χ?2 = 7.942; P = 0.005; df = 1) Also cerebral edema in babies with seizures was more often associated with mortality (58.3% vs. 18.6%; χ?2 = 5.114; P = 0.024; df = 1) [Table 4].

Birth asphyxia, hypoglycemia, hypocalcemia, sepsis, and meningitis were not significantly associated with mortality in babies with seizures compared to those without these diagnoses (P > 0.05) [Table 4].

Predictors of mortality among babies with seizures

The study variables that were found to be significantly associated with mortality among babies with clinical seizures using univariate analysis [Table 1],[Table 2],[Table 3] and [Table 4] were subjected to further analysis using multivariate regression analysis. Only the presence of cerebral edema at presentation (OR = 4.025; 95% CI: 1.342-26.952; P = 0.019) was found to be the independent predictor of mortality among babies with clinical seizures [Table 5].
Table 5: Independent predictor of mortality among babies with seizures using multiple regression analysis

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   Discussion Top

The present study has shown that clinically identifiable neonatal seizures are a major cause of morbidity and mortality among newborns admitted to the neonatal unit of the WGH, Ilesa. It has also highlighted the determinants of mortality among babies with clinical seizures. In the present study, approximately one out of every 6 (16.2%) admitted babies had clinically identifiable seizures. This prevalence is similar to reported prevalence of 19.2% by Digra and Gupta [23] among the hospitalized neonates in India. However, it is higher than earlier reported prevalence of 0.35% from Benin, [6] 0.75% from Jos, [8] 4.0% from Calabar [7] all in Nigeria. The high prevalence of clinical neonatal seizures (16.2%) observed in the present study and other recent studies in Nigeria [5],[10] compared to the studies in the 1980s and 1990s [6],[7],[8] may be a reflection of increasingly poor state of perinatal care in Nigeria. [24],[25] The available standard obstetric and neonatal facilities in Nigeria may probably dwarf by increasing the population. [24],[25] In addition, the failure of pregnant women to embrace the available orthodox health care facilities and their preference for unorthodox and traditional care may contribute to increasing newborn morbidity [24],[25] hence the higher prevalence of newborn seizures found in this study.

Newborns with clinical seizures in the present study were 4 times more likely to die compared to those without seizures. In addition, clinically identifiable neonatal seizures contributed to more than 40.0% of the overall neonatal mortality observed during the study period. The significant contribution of seizures to neonatal morbidity and mortality has also been reported by other workers in Nigeria [5],[6],[7],[8] and outside the country. [3],[4] These findings were comparable to a mortality rate of 25.0% observed by Nunes et al.[9] in Brasil, which like the present study was 3-4 times more than those without seizures. Higher mortality rates of 43.8% and 43.6% were, however, reported from Osogbo [10] and Sagamu, [5] respectively. Mortality rates are dependent on the nature and severity of underlying etiologies hence the variations reported in mortality rates across centers.

Among the babies with seizures, the risk factors for mortality observed in this study included cerebral edema, co-existence of birth asphyxia and hyponatremia and occurrence of clinical seizures in the first 24 h of life. The occurrence of clinical seizures within 24 h of delivery is a pointer to adverse perinatal events usually from delivery not attended to at all or attended to by unskilled personnel often outside the hospital. [24],[25] Patronage of home delivery or delivery outside the health facilities may be informed by poverty, ignorance, religious, and cultural beliefs as observed by Adelaja, [24] which support the finding in the present study that low socio-economic status was a risk factor for mortality among the babies with clinical seizures.

Co-existence of asphyxia with hyponatremia was observed in the present study to be a risk factor for mortality among the babies with clinical seizures. Co-existence of metabolic problems with asphyxia was also observed by Ogunlesi et al.[5] in Sagamu. The presence of hyponatremia in the babies with asphyxia may be the sequelae of syndrome of inappropriate anti-diuretic hormone secretion which is a recognized complication of perinatal asphyxia. [17],[26],[27] It may also be due to the failure of the ATPase-dependent membrane Na + /K + pump (sick cell syndrome) leading to a net influx of sodium and water intracellularly and cellular damage and death. [26],[27] Cellular death leads to the release of intracellular enzymes and substances which further damage more cells, hence the poorer prognosis observed among this group of babies. This implies that newborn admitted with seizures should be closely monitored for cerebral edema and electrolyte derangement particularly serum sodium, in order to improve their chances of survival.

We recognize the limitation that the diagnosis of seizures in this study were based on only clinical observations because of nonavailability of neonatal EEG, which could have better characterized the seizures. Also, the diagnosis of intracranial hemorhages in this study was based only on transfontanelle ultrasound findings. Magnetic resonance imaging and computerized tomography scans which give better resolution of intracranial lesions would have helped to better diagnose intracranial bleedings. Viral studies and screening for viral causes of neonatal seizures were not also done. Nevertheless, we were able to highlight the major determinants of mortality in newborn seizures in a resource-constrained developing country.

   Conclusion Top

Clinically identifiable newborn seizures are in no doubt a major contributor to neonatal morbidity and mortality. Babies with seizures noticed within the 1 st day of life, those with birth asphyxia in association with hyponatremia and the presence of cerebral edema increased the risk of death in these babies.


The authors hereby acknowledge the contributions of all the clinicians and nurses at the neonatal unit of the Wesley Guild Hospital, Ilesa for their assistance in the management of the babies.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

Scher MS. Brain disorders of the fetus and neonate. In: Klaus MH, Fanaroff AA, editors. Care of the High-risk Neonates. 5 th ed. Philadelphia: WB Saunders Company; 2001. p. 481-527.  Back to cited text no. 1
Sheth RD, Kao A. Neonatal Seizures. (9 screens). Available from: . [Last updated on 2013 Jan 16; Last accessed on 2013 Feb 06].  Back to cited text no. 2
Scher MS, Aso K, Beggarly ME, Hamid MY, Steppe DA, Painter MJ. Electrographic seizures in preterm and full-term neonates : c0 linical correlates, associated brain lesions, and risk for neurologic sequelae. Pediatrics 1993;91:128-34.  Back to cited text no. 3
Volpe JJ. Neonatal seizures. In: Volpe JJ, Fletcher J, Hund R, editors. Neurology of the Newborn. 4 th ed. Philadelphia: WB Saunders; 2001. p. 178-214.  Back to cited text no. 4
Ogunlesi T, Adekambi F, Fetuga B, Ogunfowora O, Ogundeji M. Risk factors for mortality in neonatal seizures in a Nigerian newborn unit. SAJCH 2007;1:64-7.  Back to cited text no. 5
Omene JA, Longe AC, Okolo AA. Seizures in the Nigerian neonate : p0 erinatal factors. Int J Gynaecol Obstet 1981;19:295-9.  Back to cited text no. 6
Asindi AA, Antia-Obong OE, Ibia EO, Udo JJ. Neonatal seizures in Nigerian infants. Afr J Med Med Sci 1995;24:243-8.  Back to cited text no. 7
Airede KI. Neonatal seizures and a 2-year neurological outcome. J Trop Pediatr 1991;37:313-7.  Back to cited text no. 8
Nunes ML, Martins MP, Barea BM, Wainberg RC, Costa JC. Neurological outcome of newborns with neonatal seizures : a0 cohort study in a tertiary university hospital. Arq Neuropsiquiatr 2008;66:168-74.  Back to cited text no. 9
Adebami OJ. Pattern of neonatal seizures in Osogbo, South-Western Nigeria. SAJCH 2010;4:46-9.  Back to cited text no. 10
Ilesa in Osun State, Nigeria. Available from: http://www.en.wikipedia.org/wiki/Ilesa. [Last updated on 2012 Jun 08; Last accessed on 2012 Jun 15].  Back to cited text no. 11
Battaglia FC, Lubchenco LO. A practical classification of newborn infants by weight and gestational age. J Pediatr 1967;71:159-63.  Back to cited text no. 12
Volpe JJ. Neonatal seizures : c0 urrent concepts and revised classification. Pediatrics 1989;84:422-8.  Back to cited text no. 13
Oyedeji GA. Socioeconomic and cultural background of hospitalized children in Ilesa. Niger J Paediatr 1985;13:111-18.  Back to cited text no. 14
Volpe JJ. Neonatal intracranial hemorrhage. Pathophysiology, neuropathology, and clinical features. Clin Perinatol 1977;4:77-102.  Back to cited text no. 15
Stoll BJ, Kliegman RM. Intracranial-intraventricular haemorrhage and periventricular leukomalacia. In: Behrman RE, Kliegman RM, Jenson HB, editors. Nelson Textbook of Pediatrics. 17 th ed. Philadelphia: WB Saunders; 2004. p. 562-4.  Back to cited text no. 16
Costello AM, Manandhar OS. Perinatal asphyxia in less developed countries. Arch Dis Child 1994;71:1-3.  Back to cited text no. 17
Jain A, Aggarwal R, Jeevasanker M, Agarwal R, Deorari AK, Paul VK. Hypoglycemia in the newborn. Indian J Pediatr 2008;75:63-7.  Back to cited text no. 18
Lynch BJ, Rust RS. Natural history and outcome of neonatal hypocalcemic and hypomagnesemic seizures. Pediatr Neurol 1994;11:23-7.  Back to cited text no. 19
Larry AG. Pathophysiology of body fluids and fluid therapy. In: Berman RE, Kliegman RM, Jenson HB, editors. Nelson Textbook of Pediatrics. 17 th ed. Philadelphia: WB Saunders; 2004. p. 210-3.  Back to cited text no. 20
Emodi I. The anaemias. In: Azubuike JC, Nkagineme KE, editors. Paediatrics and Child Health in a Tropical Region. 2 nd ed. Owerri, Nigeria: African Educational Series; 2007. p. 355-63.  Back to cited text no. 21
Feigin RD, McCracken GH Jr, Klein JO. Diagnosis and management of meningitis. Pediatr Infect Dis J 1992;11:785-814.  Back to cited text no. 22
Digra SK, Gupta A. Prevalence of seizures in hospitalized neonates. JK Sci 2007;9:27-9.  Back to cited text no. 23
Adelaja LM. A Survey of home delivery and newborn care practices among women in a suburban area of Western Nigeria. ISRN Obstet Gynecol 2011;2011:983542.  Back to cited text no. 24
UNICEF. 2009 State of the World′s Children. New York: United Nations Children′s Fund; 2009. Available from: http://www.unicef.org. [Last accessed on 2014 Feb 21].  Back to cited text no. 25
Zanelli SA, Stanley DP, Kauffman DA. Hypoxic-ischemic encephalopathy. (7 screens). Available from: http://www.emedicine.medscape.com/article/973501-overview. [Last updated on 2012 Nov19; Last accessed on 2013 Feb 06].  Back to cited text no. 26
Volpe JJ. Hypoxic-ischemic encephalopathy. In: Volpe JJ, Fletcher J, Hund R, editors. Neurology of the Newborn. 5 th ed. Philadelphia: WB Saunders; 2008. p. 6-9.  Back to cited text no. 27


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