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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
ORIGINAL ARTICLE  
Year : 2021  |  Volume : 32  |  Issue : 2  |  Page : 428-436
Epidemiology of community-acquired acute kidney injury in children as seen in an emergency room of Tertiary Hospital in South-South Nigeria


1 Department of Pediatrics, Federal Medical Centre, Asaba, Delta State, Nigeria
2 Department of Pediatrics, University of Nigeria Teaching Hospital Ituku-Ozalla, Enugu, Enugu State, Nigeria
3 Department of Pediatrics, Imo State University Teaching Hospital, Orlu, Imo State, Nigeria

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Date of Web Publication11-Jan-2022
 

   Abstract 


Acute kidney injury (AKI) is an abrupt or rapid decline in renal function as evidenced by a rapid rise in serum creatinine (SCr) or decrease in urine output. AKI occurs in children. The aim of the study is to document the epidemiology of AKI in our setting. This was a prospective cross-sectional observational study of all the admissions at the children emergency room of Federal Medical Center in Asaba, Delta State. A diagnosis of community-acquired AKI was made using the pRIFLE criteria if there was a 25% decrease in estimated creatinine clearance from the premorbid baseline (if known) or assumed baseline of 100 mL/min/1.73 m2 and/or urine output <0.5 mL/kg/h for >8 h within the 48 h of admission. There were 404 admissions during the period and those with AKI were 58, giving an incidence rate of 14.4 cases per 100 children aged between >1 month and 16 years. The mean age of the subjects with AKI was 35.7 months. Subjects with AKI stages R (risk), I (injury), and F (failure) were, respectively, 44.8%, 39.7%, and 8.6%. The most common causes were acute gastroenteritis (36.2%), complicated malaria (10.3%), and primary renal disease (10.3%). Age group and sickle cell anemia predicted AKI in these subjects. For the outcome of the AKI, two (3.4%) died, while 55 (96.6%) subjects were discharged alive. The level of SCr within 48 h of admission predicted the outcome of AKI. The prevalence of AKI is high, gastroenteritis being the most common etiology.

How to cite this article:
Ezeonwu BU, Abonyi LE, Odetunde OI, Nnodim IJ, Nwafor IO, Ajaegbu OC, Emeagui OD, Okoli NE, Okolo AA. Epidemiology of community-acquired acute kidney injury in children as seen in an emergency room of Tertiary Hospital in South-South Nigeria. Saudi J Kidney Dis Transpl 2021;32:428-36

How to cite this URL:
Ezeonwu BU, Abonyi LE, Odetunde OI, Nnodim IJ, Nwafor IO, Ajaegbu OC, Emeagui OD, Okoli NE, Okolo AA. Epidemiology of community-acquired acute kidney injury in children as seen in an emergency room of Tertiary Hospital in South-South Nigeria. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 Jan 28];32:428-36. Available from: https://www.sjkdt.org/text.asp?2021/32/2/428/335455



   Introduction Top


Acute kidney injury (AKI) is a clinical syndrome characterized by a rapid reduction in renal excretory function due to varied causes.[1] There is an abrupt decline in renal function as evidenced by a rapid rise in serum creatinine (SCr) and/or decrease in urine output.[1] AKI is diagnosed in pediatric population when there is more than 25% decrease in estimated creatinine clearance (eCrCl) based on the modified Schwartz formula and/or urine volume <0.5 mL/kg/h for more than 8 h (pRIFLE definition, [Table 1]).[2] AKI frequently occurs in children[1],[2],[3],[4],[5],[6],[7],[8],[9],[10],[11] and results from common preventable causes presenting at the pediatric emergency room such as sepsis,[3],[4],[6],[10],[11] malaria, hypovolemia,[3],[4],[10],[11] and gastroenteritis.[7] Community-acquired AKI (cAKI) is a type of AKI that is diagnosed on admission or within 48 h of admission.[12] AKI begins well before changes in SCr and is an independent risk factor for pediatric emergency room mortality.[2],[3],[4],[5],[7],[8],[10] Hence, there is a definite need to identify those at risk and monitor them closely.
Table 1: Pediatric-modified (pRIFLE) criteria.

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Malaria, respiratory, and diarrheal diseases are the most common cause of morbidity and mortality in the emergency room of our center.[13] There is every possibility that cAKI occurs in some of these children. Thus, there is an urgent need to look out for AKI and define its etiologies in our setting. In this study, we looked at the epidemiology of AKI in children presenting with pediatric emergency conditions to ascertain the prevalence, etiology, morbidity, and mortality of the disease. Much had not been done on this subject in the subregion. Studies such as this is essential for the formulation of protocols, for the management of children presenting at the emergency department. It will establish baseline patterns of distribution of cAKI and will assist physicians to have a high index of suspicion when handling children with these emergency conditions.


   Subjects and Methods Top


This study was carried out in the Federal Medical Centre (FMC) in Asaba, a tertiary hospital in Delta state of South-South Nigeria. The pediatric department is comprised the children outpatient (CHOP) clinic, the New Born Special Care Unit, the pediatric general ward, and the children’s emergency room (CHER). The CHER has the staff strength of two consultant pediatricians together with two senior and two junior residents who are on rotation, 17 nurses, and other supporting staff.

This was a prospective cross-sectional observational study of all the admissions at the children emergency room of FMC Asaba. There is no operational pediatric intensive care unit in this facility; all critically ill children are managed in CHER until they are stable enough to go home or to be transferred to the children’s ward to complete their treatment. The subjects were children >1 months–16 years, admitted into the CHER of FMC, Asaba. The study was conducted from February 2015 to January 2016. All children admitted into CHER and who had complete requisite data were included in the study. Children who did not have their SCr estimated on 1st day of admission were excluded. The children were stratified into two broad strata; >1 month to <5 years and 5–16 years.

This study was a review of the data of all the subjects recruited by convenience sampling method during the study period. On admission, the requisite data were completed as outlined in the study proforma and entered in the data pool opened in excel worksheet and these were continually updated for each subject throughout the 48 h of their admission in CHER. Urine output was monitored to calculate the urine flow rate per milliliter per kilogram body weight per hour. First blood sample was collected after the first assessment and needed resuscitation of the subjects in CHER, and a second blood sample was collected within 48 h after admission. The blood samples were sent to the laboratory for determination of the 1st and 2nd SCr values, using the Jaffe reaction method. eCrCl was calculated from the two SCr values. cAKI was diagnosed using the pRIFLE (Pediatric Risk, Injury, Failure, Loss, End-Stage Renal Disease) criteria if there was a 25% decrease in the 1st eCrCl (done on admission) based on the modified Schwartz formula, from the known premorbid baseline within the past six months or from an assumed baseline of 100 mL/min/1.73 m2 (if premorbid eCrCl is not known), and/or urine output <0.5 mL/kg/h for >8 h. Subjects with AKI were categorized using the pRIFLE criteria for AKI: R for risk, I for injury, and F for failure.

Subjects who had no AKI as defined above and who showed clinical improvement, completed their treatment, and were discharged home. Subjects with AKI received isotonic crystalloids as initial management for expansion of intravascular volume and other conservative management as contained in the center protocol such as antihypertensives, diuretics, electrolyte correction, and adequate calorie. Dialysis was prescribed in the presence of life-threatening changes in urea (urea >40 mmol/L), anuria persisting after 24 h despite the fluid replacement, and the presence of encephalopathy. Those who had AKI from the first SCr had AKI stages reassessed using their second SCr (48 h after admission) to note resolution, persistence, or worsening of the AKI. The second SCr was also used to diagnose subjects who developed AKI within 48 h of admission.

Ethical issues

Ethical approval was sought and obtained from the ethical committee at FMC Asaba.


   Statistical Analysis Top


The data were entered into an excel worksheet and later transferred to and analyzed using IBM SPSS Statistics version 22.0 (IBM Corp., Armonk, NY, USA). Results were expressed in frequency tables. Chi-squared test was used to assess association between categorical variables, while Student’s t-test was used to compare means. Binomial logistic regression was used to determine predictors of AKI and the outcome of AKI in the subjects. For any comparison of variable, P value is significant at <0.05.


   Result Top


There were 404 admissions during the period of the study. Those with cAKI were 58, giving an incidence rate of 14.4 cases per 100 children. The age of the subjects was between >1 month and 16 years (1–192 months) with mean age ± standard deviation of 35.7 ± 45.9 months, [Table 2]. There were 34 (58.6%) males and24 (41.4%) females with male-to-female ratio of 1.4:1. Fifty subjects (86.2%) were under 5 years of age as shown in [Table 2]. A total of 41 (70.7%) subjects with AKI were admitted during the dry season, [Table 2]. AKI stages R, I, and F occurred, respectively, in 28 (44.8%), 25 (39.6%), and 5 (8.6%) of the AKI population on admission [Table 2]. There was only one subject who meet the urine output criteria but also met the SCr criteria. Of the 58 subjects with AKI, 54 (93.1%) had AKI on admission, while only four (6.9%) developed AKI within 48 h of admission. The commonest causes of cAKI were acute gastroenteritis (36.2%), primary renal disease (10.3%), and complicated malaria (10.3%) [Table 3]. Majority of subjects with acute gastroenteritis had moderate-to-severe dehydration. The primary renal diseases encountered were sickle cell nephropathy (with nephrotic syndrome presentation) and posterior urethral valve (PUV). The criteria for complicated malaria in majority of the subjects were cerebral malaria and severe anemia. Single morbidity was diagnosed in 44 (75.9%) subjects while only 14 (24.1%) had recognizable comorbidity [Table 3]. The four subjects who had AKI within 48 h of admission were in pRIFLE stages R (50.0%) and I (50.0%). Within 48 h of admission, six (10.3%) of the subjects who had AKI on admission already had resolution of the AKI, while seven (12.1%) worsened, 10 (17.2%) improved to a milder stage, and 35 (60.4%) persisted at same stage of the AKI. Two (3.4%) subjects with cAKI required RRT: one (1.7%) who had sickle cell nephropathy and refused RRT, while one (1.7%) with sepsis with multiple organ dysfunction on a background of PUV could not access RRT before demise. Fifty-five subjects, (96.6%) were discharged (10 of whom were stabilized and discharged for follow–up, while one discharged against medical advice), and two died giving a mortality rate of AKI as 3.4% [Table 3]. Those subjects who died were all in the F stage of AKI. One of the subjects who died had sepsis with multiple organ dysfunction on a background PUV, while the other death had acute glomerulonephritis with nephrotic range proteinuria. The subject whose parents discharged against medical advice had nephrotic syndrome on a background of sickle cell anemia (SCA).
Table 2: General characteristics of the subjects with community acquired acute kidney injury.

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Table 3: The etiology and outcome of community acquired acute kidney injury in the subjects.

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Other diagnoses in [Table 3] included acute bronchial asthma, kerosene poisoning, burns, malignancies, sepsis, osteomyelitis, abdominal tuberculosis, diabetic ketoacidosis, pharyngotonsillitis, and meningitis. Other comorbidities included sepsis, severe acute malnutrition, uncomplicated malaria, SCA), pharyngotonsillitis, and retroviral disease.

Subjects who had AKI on admission were younger (P = 0.021) and expectedly with much lower eGFR than those who developed AKI within 48 h of admission (P = 0.042) [Table 4]. SCA was the major cause of AKI within 48 h of admission (0.011). As shown in [Table 5], there was a 32% chance that SCA patient will have AKI P = 0.030) and the odds of younger age developing AKI was 8 (P = 0.056). Complicated malaria did not predict AKI. [Table 5] also shows that SCr level within 48 h of admission predicted outcome of AKI with odds ratio of 8 (P = 0.011).
Table 4: Acute kidney injury on admission compared with acute kidney injury within 48 h of admission.

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Table 5: Logistic regression analysis.

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   Discussion Top


AKI is increasingly common in seriously ill children. The incidence rate of cAKI in this study was 14.4 per 100 children and remarkably high. This is comparably lower than incidence of 56% documented by Obichukwu et al[8] using the same pRIFLE criteria. This may be because Obichukwu et al[8] used the upper limit of the age-based normative SCr value for all the subjects who had no previously documented eCrCl, whereas this study assumed eCrCl of 100 mL/min/1.73 m2. However, a higher prevalence rate of 51.2% was noted by Anigilaje et al,[11] among same age group, using same criteria probably because this our index study excluded all subjects who had no SCr estimation on admission and most subjects had no comorbidity. Muithya et al,[7] Srinivasa et al[6] and Soler et al[9] also found higher incidence rates of 85.5%, 26.1% and 27.4% respectively which could be explained by their study population of children in PICU, regardless of mechanical ventilator and ionotropic support. In addition, Soler et al[9] assumed a baseline eCrCl of 120 mL/min/1.73 m2 for all their subjects while Muithya et al,[7] and the present study assumed 100 mL/min/1.73 m2. Alkandari et al[5] documented slightly higher incidence of 17.9% most likely because they used AKIN criteria in PICU and age- and gender-based normative values as baseline SCr unlike the present study population comprising children in CHER. In contrast, Evans et al[10] reported a low incidence rate of 10.9% and Olowu et al[4] reported 3.1% and the reason for the disparities could be explained by the fact that Evans et al[10] used KDIGO criteria, while Olowu et al[4] used AKIN criteria which would have excluded stages R and I AKI in their cohorts, while being included in the pRIFLE criteria used in the present study. There was no gender predilection in cAKI noted in this study, which is comparable to the findings by Esezobor et al,[3] Alkandari et al,[5] Srinivasa et al,[6] Soler et al,[9] Evans et al,[10] and Anigilaje et al[11] but not in consonant with Muithya et al[7] who reported female preponderance. The cultural belief that underlines the preference of male to female gender may explain the female preponderance reported by Muithya et al. This male gender preference favors prompt and adequate medical care being offered to them, while the females benefit likewise only when critical. A good number of the children who had AKI in the study were in the F (failure) stage of the AKI unlike the present study. Moreover, this gender bias may no longer be in existence in these communities that harbor this index study population where AKI was reported to affect both genders equally.[7]

Like many other studies on AKI,[3],[4],[5],[6],[7],[8],[9],[10],[11] this our index study corroborates with finding of AKI being more common in younger children. This finding is supported by the fact that the common morbidities seen in CHER where the present study was done are more prevalent in younger children.[12] Gastroenteritis, pneumonia, and malaria which are prevalent in younger children[12] were also reported as the common etiologies of AKI by Muithya et al.[7] Another explanation may be the ongoing functional maturity process in the kidneys of the younger children making them vulnerable to insults irrespective of the degree of the insult. It was also noted that AKI occurred more during the dry season. This is in consonance with the prevalent etiology; AGE has predilection for dry season in the index study area.[13]

Over 90% of the subjects were in the pRIFLE stages of R (Risk) and I (Injury), while only 9.3% were in the F (Failure) stage (90.7 vs. 9.3%). Soler et al[9] documented similar findings of 79.5% versus 20.5%, Obichukwu et al[8] reported 91.7% versus 8.3%, Srinivasa et al[6] reported 89.3% versus 10.7%. This is contrary to the findings by Esezobor et al[3] and Muithya et al[7] where substantial number of the subjects were in the Failure stage, 30% versus 70% and 54% versus 46%, respectively. The subjects studied by Esezobor et al[3] and Muithya et al[7] may have presented late to the hospital.

It is pertinent to document that 93.1% of the subjects already developed AKI on presentation, this is similar to the findings of Esezobor et al[3] who reported 80% and Olowu et al[4] found 72.8%. This could be due to the poor health-seeking habit prevalent in our community and worsened by the out-of-pocket payment obtainnable in low-income countries such as ours which propagates late presentation of sick children to the hospital. Although the course of AKI in this index study showed that majority had persisted in the same pRIFLE stage by 48 h on admission, they were mostly at R (Risk) stage.

The most common etiologies of AKI in this study were acute gastroenteritis, malaria, and primary renal disease. Similarly, Muithya et al[7] found gastroenteritis, pneumonia, and malaria as the most common cause of AKI in their subjects, Evans et al[10] reported malaria and sepsis, Anigilaje et al[11] found sepsis, acute glomerulonephritis, diarrheal dehydration, severe falciparum malaria, and hemolytic-uremic syndrome, and Esezobor et al[3] reported sepsis and primary renal disease. In other studies, Srinivasa et al[6] reported nephrotoxics and infections (notably dengue fever, sepsis and pneumonia) and Olowu et al[4] reportednephrotoxics as the leading cause of AKI in their subjects. Like in the present study where the common etiologies of AKI are similar to the pattern of morbidity in the CHER of their facility,[13] the etiologies documented by other studies[3],[4],[6],[7],[10],[11] are likely to be the morbidity pattern seen in their study site.

Although the renal replacement therapy (RRT) rate is low, one of the subjects who needed RRT could not access it because of late presentation and financial constraint. These factors among others have been regular causes of inaccessibility of RRT in our environment. The mortality rate of 3.4% was comparably lower than those of other studies[3],[4],[7],[9],[11] and involved only those in F (Failure) stage. The characteristics of the study population may explain in part the disparity in mortality rates, for instance, Soler et al[9] documented 12.3% in children admitted in PICU unlike the present study. The preponderance of subjects in F (Failure) stage can explain the high mortality rates documented by Esezobor et al[3] (28.4%) unlike the present study whose subjects were mainly in the R (Risk) stage and pRIFLE stage predicted outcome. This could also explain the low RRT need in the present study of 3.4 % compared to over 30% reported by Esezobor et al.[3] The absence of comorbidity in most of the subject could explain the low percentage of subjects in F (Failure) stage, the low RRT rate and the low mortality. The mortality rate of 13.1% documented by Obichukwu et al,[8] 21.4% by Muithya et al,[7] 30.2% by Anigilaje et al[11] and 36.7% by Olowu et al[4] could be attributed to the presence of comorbidities in their subjects among other factors.

SCA crisis was a strong predictor of AKI as noted in this study. Santoch et al[14] and Baddam et al,[15] both in the USA noted incidence of AKI in subjects admitted for SCA crisis as 40% and 17%, respectively. The occurrence of AKI in SCA crisis has been attributed to vasoocclusion and the use of non-steroidal anti-inflammatory drugs during painful crisis.[14]

We encountered some limitations during the course of this study. During some of the periods of health workers industrial actions, only skeletal services were rendered and thus, many subjects did not have the requisite laboratory information for analysis. Due to the prevalent out-of-pocket payment for medical services in our country, most subjects could not pay for the relevant investigations on admission including blood chemistry (which is contained in the emergency protocol, researchers paid for the second SCr only).

In future, much more elaborate fully funded study should be planned for so that all children admitted in CHER should have all the requisite laboratory work up and be followed up for the required 7 days for AKI. The follow up should also be extended to monitor for long-term complication such as chronic kidney disease.


   Conclusion Top


The prevalence of AKI is on the increase, but is treatable and modifiable causes such as gastroenteritis, malaria, and primary renal disease being the most common etiologies.


   Acknowledgment Top


We are grateful to all parents and children who participated in this study. We all appreciate the residents and doctor interns who assisted in collecting the specimens. Furthermore, the nurses and supporting staff in CHER.

Conflict of interest: None declared.



 
   References Top

1.
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute kidney injury. Kidney Int Suppl 2012;2:1-138.  Back to cited text no. 1
    
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Akcan-Arikan A, Zappitelli M, Loftis LL, Washburn KK, Jefferson LS, Goldstein SL. Modified RIFLE criteria in critically ill children with acute kidney injury. Kidney Int 2007;71: 1028-35.  Back to cited text no. 2
    
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Esezobor CI, Ladapo TA, Osinaike B, Lesi FE. Paediatric acute kidney injury in a tertiary hospital in Nigeria: Prevalence, causes and mortality rate. PLoS One 2012;7:e51229.  Back to cited text no. 3
    
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Olowu WA, Adefehinti O, Bisiriyu AL. Hospital-acquired acute kidney injury in critically ill children and adolescents. Saudi J Kidney Dis Transpl 2012;23:68-77.  Back to cited text no. 4
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Alkandari O, Eddington KA, Hyder A, et al. Acute kidney injury is an independent risk factor for pediatric intensive care unit mortality, longer length of stay and prolonged mechanical ventilation in critically ill children: A two-center retrospective cohort study. Crit Care 2011;15:R146.  Back to cited text no. 5
    
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Srinivasa S, Reshmavathi V. Incidence and etiology of acute kidney injury in children admitted to PICU using PRIFLE criteria. Curr Pediatr Res 2016;20:1-6.  Back to cited text no. 6
    
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Muithya C, Admani B, Were F. Prevalence of acute kidney injury in critically ill children at tertiary hospital in Kenya. Afr J Paed Nephrol 2015;2:6-12.  Back to cited text no. 7
    
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Obichukwu CC, Odetunde OI, Chinawa JM, Okafor HU, Adiele DK, Ibe BC. Community-acquired acute kidney injury in critically Ill children as seen in the emergency unit of a tertiary hospital in Enugu, Southeast Nigeria. Niger J Clin Pract 2017;20:746-53.  Back to cited text no. 8
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Soler YA, Nieves-Plaza M, Prieto M, García-De Jesús R, Suárez-Rivera M. Pediatric risk, injury, failure, loss, end-stage renal disease score identifies acute kidney injury and predicts mortality in critically ill children: A prospective study. Pediatr Crit Care Med 2013;14:e189-95.  Back to cited text no. 9
    
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Evans RDR, Docherty M, Seeley A, et al. Incidence, etiology, and outcomes of community-acquired acute kidney injury in pediatric admissions in malawi. Perit Dial Int 2018;38:405-12.  Back to cited text no. 10
    
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Anigilaje EA, Adebayo AI, Ocheni SA. Acute kidney injury in children: A study of etiology, clinical profile, and short-term outcomes at the University of Abuja Teaching Hospital, Gwagwalada, Abuja, Nigeria. Saudi J Kidney Dis Transpl 2019;30:421-39.  Back to cited text no. 11
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Holmes J, Geen J, Phillips B, Williams JD, Phillips AO; Welsh AKI Steering Group. Community acquired acute kidney injury: Findings from a large population cohort. QJM 2017;110:741-6.  Back to cited text no. 12
    
13.
Ezeonwu B, Chima O, Oguonu T, Ikefuna A, Nwafor I. Morbidity and mortality pattern of childhood illnesses seen at the children emergency unit of Federal Medical Center, Asaba, Nigeria. Ann Med Health Sci Res 2014;4:S239-44.  Back to cited text no. 13
    
14.
Santosh LS, Maya V, Ariel R, et al. HMOX1 and acute kidney injury in sickle cell anemia. Blood 2017;130 Suppl 1:686.  Back to cited text no. 14
    
15.
Baddam S, Aban I, Hilliard T, Howard T, Askenazi D, Lebensburger JD. Acute kidney injury during a paediatric sickle cell vasoocclusive pain crisis. Pediatr Nephrol 2017;32: 1451-6.  Back to cited text no. 15
    

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Correspondence Address:
Bertilla Uzoma Ezeonwu
Department of Pediatrics, Federal Medical Centre, Asaba, Delta State
Nigeria
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DOI: 10.4103/1319-2442.335455

PMID: 35017337

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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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