SAJCH Vol 10, No 3 (2016)

CHILD HEALTH THE SOUTH AFRICAN JOURNAL OF

September 2016

Volume 10

No. 3

• Aetiology and risk factors for neonatal sepsis, Nigeria • Pregnancy-related deaths among adolescents, South Africa • Outcome of children admitted to a general highcare unit, Western Cape • Policies, practices and perceptions regarding children as visitors to public hospitals, KwaZulu-Natal • Clinical presentation of infants hospitalised with pertussis

CHILD HEALTH THE SOUTH AFRICAN JOURNAL OF

EDITOR J M Pettifor FOUNDING EDITOR N P Khumalo

146 Maternal vaccination to prevent pertussis in infants

EDITORIAL BOARD Prof. M Adhikari (University of KwaZuluNatal, Durban) Prof. M Kruger (Stellenbosch University) Prof. H Rode (Red Cross War Memorial Children's Hospital, Cape Town) Prof. L Spitz (Emeritus Nuffield Professor of Paediatric Surgery, London) Prof. A Venter (University of the Free State, Bloemfontein) Dr T Westwood (Red Cross War Memorial Children's Hospital, Cape Town) Prof. D F Wittenberg (University of Pretoria)

HEALTH & MEDICAL PUBLISHING GROUP:

SEPTEMBER 2016

Volume. 10

No. 3

CONTENTS Editorial

Z Dangor, S G Lala

Research

147 Aetiology and risk factors for neonatal sepsis at the Lagos University Teaching Hospital, Idi-Araba, Lagos, Nigeria

E O Shobowale, F T Ogunsola, O O Oduyebo, V I Ezeaka

151 Pregnancy and death: An examination of pregnancy-related deaths among adolescents in South Africa

N de Wet

CEO AND PUBLISHER Hannah Kikaya EXECUTIVE EDITOR Bridget Farham MANAGING EDITORS Ingrid Nye Claudia Naidu TECHNICAL EDITORS Emma Buchanan Paula van der Bijl

156 Outcome of children admitted to a general high-care unit in a regional hospital in the Western Cape, South Africa

NEWS EDITOR Chris Bateman

PRODUCTION MANAGER Emma Jane Couzens

I Kruger, R Gie, J Harvey, M Kruger

161 A review of chronic lung disease in neonates at Charlotte Maxeke Johannesburg Academic Hospital from 1 January 2013 to 31 December 2014

A V Mphaphuli, D E Ballot

166 Pattern and practice of psychoactive substance abuse and risky behaviours among street children in Cameroon

S Cumber, J Tsoka-Gwegweni

171 The existence of policies, practices and perceptions regarding children as visitors to public hospitals in uMgungundlovu, KwaZulu-Natal Province

P Appalsamy, N H McKerrow

176 Clinical presentation of infants hospitalised with pertussis

G Kahl, U M Hallbauer, G Joubert

181 Characteristic of monosymptomatic and non-monosymptomatic childhood nocturnal enuresis in Benin City, Nigeria

N J Iduoriyekemwen, D U Nwaneri

Case Reports

B M Duduyemi, A C Yifieyeh

186 Congenital infantile fibrosarcoma mimicking sacrococcygeal teratoma in a Ghanaian infant: A case report and review of the literature 188 Acute cholecystitis in a child with scarlet fever: A rare association

Y Parvez, S Thomas

190

CPD Questions

CHIEF OPERATING OFFICER Diane Smith | Tel. 012 481 2069 Email: dianes@hmpg.co.za ONLINE SUPPORT Gertrude Fani | Tel. 072 463 2159 Email: publishing@hmpg.co.za FINANCE Tshepiso Mokoena HMPG BOARD OF DIRECTORS Prof. M Lukhele (Chair), Dr M R Abbas, Dr M J Grootboom, Mrs H Kikaya, Prof. E L Mazwai, Dr M Mbokota, Dr G Wolvaardt HEAD OFFICE Block F, Castle Walk Corporate Park, Nossob Street, Erasmuskloof Ext. 3, Pretoria, 0181 EDITORIAL OFFICE Suite 11, Lonsdale Building, Lonsdale Way, Pinelands, 7405 Tel. 021 532 1281 | Cell. 072 635 9825 Email: publishing@hmpg.co.za ISSN 1994-3032

Use of editorial material is subject to the Creative Commons Attribution – Noncommercial Works Licence. http://creativecommons.org/licenses/by-nc/3.0

ublished by Health and Medical Publishing Group, P Suite 11, Lonsdale Building, Lonsdale Way Pinelands 7405 apers for publication should be addressed to the Editor, P via website: www.sajch.org.za Tel: 072 635 9825 E-mail: publishing@hmpg.co.za Cover: Khanyiso, Red Cross War Memorail Children's Hospital Primary School

DTP AND DESIGN Carl Sampson

©Copyright: Health and Medical Publishing Group (Pty) Ltd

EDITORIAL

This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

Maternal vaccination to prevent pertussis in infants Pertussis causes an estimated 16 million cases and 200 000 deaths globally each year, with most of the deaths occurring in infants younger than 2 months of age.[1] Young infants with pertussis may present with severe disease such as pneumonia, apnoea or seizures, and severe illness is more common in HIV-infected and HIV-exposed children than in HIV-uninfected children.[2] The burden of Bordetella pertussis disease is highest in young infants (<3 months of age) and has almost doubled over the last two decades despite the availability of vaccines.[1] The recent increase in incidence of pertussis infection has been facilitated by an increasing pool of susceptible individuals in the community. As fewer adults (including women of child-bearing age) and children have experienced natural pertussis infection, there is less circulating natural immunity among the adult population, and vaccine-mediated immunity after primary childhood vaccination wanes with time. Furthermore, the duration of protection afforded by the newer acellular pertussis vaccine (1 - 3 years) is shorter than that for the whole-cell vaccine (5 - 10 years). As primary vaccination schedules against pertussis begin at 6 weeks of age, the young infant is especially vulnerable to pertussis. The primary administration of pertussis vaccine to infants and the vaccination of close contacts to prevent transmission (‘cocooning’) are measures that will reduce the burden of pertussis, but the protection of young infants from pertussis is most likely achieved through maternal vaccination – a strategy that has been shown as safe and effective.[3] The objective of maternal pertussis vaccination is twofold: it induces or boosts antibody responses in the pregnant woman, which protects the infant through early infancy, and it protects the mother against pertussis infection that may be passed on to her infant postnatally.

The success of maternal vaccination in preventing disease in early infancy is dependent on several factors. Firstly, an immunogenic vaccine is required, to produce sufficient protective antibody levels.

Secondly, efficient transplacental transfer of maternal IgG antibody needs to occur during the third trimester. Thirdly, the half-life of the transferred antibody should be of sufficient duration in the infant. In addition, the protective epitope-specific IgA antibodies in breastmilk may offer some protection.

When a vaccine is administered to a pregnant woman, the safety and immunogenicity of the vaccine to the mother-fetus dyad are major considerations. Although some safety and immunogenicity trials are yet to be reported, the current consensus of opinion is that maternal immunisation with the Tdap (tetanus, diphtheria and acellular pertussis) vaccine is safe. Indeed, maternal vaccination is now recommended to prevent pertussis infection in vulnerable young infants. In the USA and UK, the immunisation of pregnant women with a Tdap or dTaP/IPV (diphtheria, tetanus, acellular pertussis and inactivated poliomyelitis) vaccine has been standard practice since 2012. These recommendations are based primarily on observational and case-control studies that demonstrated the effectiveness of a five-component acellular-pertussis-containing vaccine.[4,5] Although vaccine efficacy is usually demonstrated by controlled double-blind randomised clinical trials, these trials are expensive to perform and often require a very large number of study participants. Nonetheless, the effectiveness of the dTaP/IPV vaccine in preventing pertussis in infancy was greater than 90% even though serological correlates of protection have not been determined.

Even though lower pertussis antibody responses after primary vaccination are noted in infants born to mothers who received Tdap

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vaccine, maternal pertussis immunisation is more beneficial, and recommended for the prevention of severe disease in young infants.

The optimal time to administer Tdap vaccine to the mother is between 27 and 36 weeks of gestation – vaccination during this period induces maximal antibody responses in the mother, so that adequate amounts of IgG1 are transferred to the fetus. Maternal antibody transferred to the young infant has an antibody half-life that provides adequate protection during the first 2 months of life, when the infant is especially vulnerable to pertussis infection. Unlike maternal influenza vaccination, where early vaccination during pregnancy favourably alters maternal and fetal health outcomes, pertussis vaccination can be delayed to the third trimester because the adequate production of protective Tdap antibodies occurs about 2 weeks after vaccination. If the mother is vaccinated before conception of a planned pregnancy, the levels of maternal antibody will decline during the pregnancy and inadequate levels of protective antibody will be transferred to the fetus. Thus, vaccinating the mother during preconception care or immediately after the birth of the newborn will not protect the young infant against pertussis.

South African situation

Maternal vaccination is emerging as a favoured strategy to reduce the burden of neonatal deaths globally. In South Africa (SA), the only form of maternal immunisation presently recommended is vaccination with tetanus toxoid to prevent neonatal tetanus infection. Pertussis infection is common in SA infants,[2] and further studies to determine the efficacy or effectiveness of the acellular pertussis vaccine will almost certainly be needed. In particular, determination of the safety and immunogenicity of vaccination in HIV-infected pregnant women is required. Nonetheless, the introduction of pertussis vaccination into the public maternal immunisation programme is likely to reduce the burden of pertussis disease in early infancy.

Ziyaad Dangor Sanjay G Lala Department of Paediatrics and Child Health, School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa Corresponding author: Z Dangor (ziyaad.dangor@wits.ac.za) 1. Centers for Disease Control and Prevention. Pertussis (Whooping Cough) September 2016. http://www.cdc.gov/pertussis/index.html (accessed 9 September 2016) 2. Muloiwa R, Dube FS, Nicol MP, Zar HJ, Hussey GD. Incidence and diagnosis of pertussis in South African children hospitalized with lower respiratory tract infection. Ped Infect Dis J 2016;35(6):611-616. DOI:10.1097/ INF.0000000000001132 3. Lindsey B, Kampmann B, Jones C. Maternal immunization as a strategy to decrease susceptibility to infection in newborn infants. Curr Opin Infect Dis 2013;26(3):248-253. DOI:10.1097/QCO.0b013e3283607a58 4. Amirthalingam G, Andrews N, Campbell H, et al. Effectiveness of maternal pertussis vaccination in England: An observational study. Lancet 2014;384(9953):1521-1528. DOI:10.1016/S0140-6736(14)60686-3 5. Dabrera G, Amirthalingam G, Andrews N, et al. A case-control study to estimate the effectiveness of maternal pertussis vaccination in protecting newborn infants in England and Wales, 2012-2013. Clin Infec Dis 2015;60(3):333-337.

DOI:10.1093/cid/ciu821 S Afr J Child Health 2016;10(3):146. DOI:10.7196/SAJCH.2016.v10i3.1272

SEPTEMBER 2016 Vol. 10 No. 3

RESEARCH

This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

Aetiology and risk factors for neonatal sepsis at the Lagos University Teaching Hospital, Idi-Araba, Lagos, Nigeria E O Shobowale,1 MBBS, MSc, FMC Path; F T Ogunsola,2 MBBS, MSc, PhD, FMC Path, FWACP; O O Oduyebo,2 MBBS, MSc, FMC Path, FWACP; V I Ezeaka,3 MBBS, FMC Paed, FWACP Department of Medical Microbiology and Parasitology, Babcock University Teaching Hospital, Ogun, Nigeria Department of Medical Microbiology and Parasitology, Lagos University Teaching Hospital, Lagos, Nigeria 3 Department of Paediatrics, Lagos University Teaching Hospital, Lagos, Nigeria 1 2

Corresponding author: E O Shobowale (shoekineh@gmail.com) Background. Neonatal sepsis is a significant cause of morbidity and mortality in developing countries, accounting for a large proportion of neonatal deaths annually. Every year, 4 million neonates die, and one-third of these deaths is attributed directly to neonatal sepsis.

Objectives. To determine the prevalence of neonatal sepsis, characterise and identify causative organisms and identify possible risk factors.

Specific objectives were to determine the aetiological agents responsible for neonatal sepsis at Lagos University Teaching Hospital and also to identify the risk factors responsible for the development of neonatal sepsis.

Methods. Venous blood pairs were collected from clinically septic admitted neonates and inoculated into BACTEC Peds Plus (BD, USA) bottles aerobically in the BACTEC 9050 system. Organisms were identified using the Microbact 12A/E system and biochemicals. A structured questionnaire was used to collect data for risk factors, which were analysed with the SPSS version 17.

Results. Of 250 neonates who were sampled, 85 (34%) had pathogens recovered from their bloodstream, with Klebsiella pneumoniae the predominant organism. Risk factors for sepsis were being delivered outside the hospital (p=0.01), and by frequent changes in antibiotics (p=0.00).

Conclusion. The burden of neonatal sepsis is still high in our environment as evidenced by our isolation rate of 34%. A concerted effort needs to be made to reduce this.

S Afr J Child Health 2016;10(3):147-150. DOI:10.7196/SAJCH.2016.v10i3.965

It is estimated that 20% of all neonates will develop sepsis, and ~1% of them will die of sepsis-related causes. In addition, neonatal deaths account for 43% of all deaths among children under 5 years.[1] In developing countries such as Nigeria, which share 99% of the estimated 4 million neonatal deaths annually, neonatal mortality resulting from neonatal sepsis is estimated to be ~34/1 000 live births, while in developed countries it is ~5/1â&#x20AC;&#x2030;000.[1,2] Neonatal morbidity and mortality are major public health challenges in our local environment, with a huge percentage of deaths in the neonatal period attributable to sepsis. It is estimated that 98.5% of neonatal mortality occurs in developing countries, with neonatal sepsis directly responsible for 26% of neonatal deaths.[1] Neonatal sepsis in itself is potentially treatable and preventable, yet despite considerable advances and improvements in the survival rate of newborns in developed countries, there has not been a concomitant improvement in outcomes recorded in developing countries.[1] Neonatal sepsis is classically divided into early- and late-onset sepsis. Both are associated with different distributions of pathogens.

Early-onset sepsis occurs in the first 7 days of life and is generally acquired from pathogens in the maternal genital tract, whereas late-onset sepsis, which occurs after the 7th day of life, has its origin either in the community or in the healthcare environment.[3] The aetiology of neonatal sepsis varies geographically, with different regions reporting a plethora of prevalent pathogens. Organisms such as Escherichia coli, Klebsiella pneumoniae, Staphylococcus aureus, coagulase-negative staphylococci, Enterococcus spp., Proteus spp., and Pseudomonas aeruginosa have been reported.[3] The objective of the current study was to ascertain and identify the local risk factors responsible for bloodstream infections among neonates at the Lagos University Teaching Hospital (LUTH), and aid in generating baseline data for the prevalent micro-organisms 147

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responsible for neonatal sepsis in our institution, alongside susceptibility and resistance patterns. This also helped to provide relevant information on the practices in our neonatal units that are predisposed to sepsis. These data were used by clinicians to predict susceptibility to antimicrobial agents on an empirical basis while awaiting susceptibility results and the identification of pathogens.

Methods

The study was carried out at the neonatal unit of the LUTH, Idi-Araba, Lagos, Nigeria. The hospital is a 761-bed facility located in an urban cosmopolitan setting. The neonatal unit of the hospital has a total bed space of 73 and is divided into four wards: neonatal unit (NNU), and wards D1, CHER and E4. The sample size was calculated, using the average isolation rate of aerobic bacteria from manual blood culture systems of ~20%.[4] A sample of 250 neonates was determined.[5] The study included neonates delivered within or outside the hospital, who had signs and symptoms of sepsis. Blood samples for culture were collected within 48 hours of admission. These samples included nosocomial sepsis and maternal acquisition. All the neonates recruited into the study were admitted to the hospital and they presented with clinical signs and symptoms of sepsis, including fever, hypothermia, lethargy, bulging fontanelle, irritability, seizures, apnoea and failure to thrive in the first 28 days of life. Sampling was limited to blood cultures for the study, as lumbar punctures for cerebrospinal fluid analysis were performed by the managing team only when indicated. Neonates without clinical signs and symptoms of sepsis and those whose parents withheld consent were excluded from the study.

Two venous blood samples were taken via phlebotomy from the antecubital fossa, forearm or hands of the neonates aseptically, applying universal precautions. The volume of blood withdrawn was 1 - 3 mL. Blood obtained from each neonate was aseptically

SEPTEMBER 2016 Vol. 10 No. 3

RESEARCH Table 1. Demographic characteristics of neonates investigated for sepsis at LUTH Characteristics

n (%) (N=250)

Gender Male

118 (47.2)

Female

132 (52.8)

Age (days) 0-6

151 (60.4)

7 - 28

99 (39.6)

Socioeconomic status* High

18 (7.0)

Middle

50 (19.8)

Low

182 (72.3)

*High socioeconomic status: combined income of >USD5 000 per month; middle socioeconomic status: combined income of USD1 000 - USD5 000 per month; low socioeconomic status: combined income of <USD1 000 per month.

dispensed into the BACTEC Peds Plus (BD, USA) aerobic blood culture bottle, placed in the BACTEC 9050 machine and incubated for a maximum of 5 days. Bottles flagged as positive by the system were removed, Gram stained and sub-cultured onto appropriate media such as blood, chocolate (for Grampositive organisms) and MacConkey agar (for Gram-negative organisms) and iden­ tified using biochemical tests. All isolates were tested for antimicrobial susceptibility with the modified Kirby-Bauer method.

A structured questionnaire was given to patients' relatives/caregivers to complete in order to identify and assess risk factors.

Data obtained from the questionnaires were analysed with Epi Info 3.5.1 software version 2008 (CDC, USA) and SPSS version 21.0 (IBM Corp., USA) by cross-tabulation of risk factors and univariate/multivariate analysis with data from the laboratory results. Analysis was done with the χ2, 95% confidence interval (CI) and odds ratio (OR). Significance set at p<0.05.

Approval was obtained from the Ethics and Research Committee of the LUTH. Informed consent was obtained before the filling in of questionnaires.

Results

There was a predominance of female (n=132, 52.8%) compared with male neonates (n=118, 47.2%), giving a male to female ratio of 1:1.12. The mean age of the neonates was 9.1 days, with most of them <7 days (n=151, 60.4%). The majority of the neonates (n=182, 72.2%) were delivered to parents in the lower socioeconomic strata, with 50 (19.7%) in the mid-strata and the remaining 18 (17%) in the higher socioeconomic strata (Table 1).

148

Table 2. Aetiological agents stratified by age of onset of sepsis n (%)

Organism

Early onset, n (%)

Late onset, n (%)

Acinetobacter baumanii

3 (3.5)

2 (67.0)

1 (33.0)

Acinetobacter iwoffii

1 (1.2)

0 (0.0)

1 (100)

Burkholderia cepacia

6 (7.0)

4 (67.0)

2 (33.0)

Candida albicans

1 (1.2)

0 (0.0)

1 (100)

CONS

10 (11.8)

6 (60.0)

4 (40.0)

Enterococcus spp.

6 (7.0)

3 (50.0)

3 (50.0)

Klebsiella oxytoca

3 (3.5)

3 (100)

0 (0.0)

K. pneumoniae

31 (36.5)

19 (61.3)

12 (38.7)

Proteus vulgaris

4 (4.7)

3 (75.0)

1 (25.0)

S. aureus

16 (18.8)

9 (56.3)

7 (43.7)

Serratia rubidaea

4 (4.7)

1 (25.0)

3 (75.0)

Total

85 (100)

50 (100)

35 (100)

CONS = coagulase-negative staphylococcus.

Table 3. Significant risk factors for sepsis in neonates at LUTH Organism in bloodstream, n (%)

Risk factor

No organism in bloodstream, n (%)

Birth status Inborn

30 (35.3)

74 (44.8)

Outborn

55 (64.7)

91 (55.2)

Change in antibiotics Yes

46 (54.1)

129 (78.2)

No

39 (45.9)

36 (21.8)

Number of switches in antibiotics 0

40 (47.1)

132 (80.0)

>1

45 (52.9)

33 (20.0)

With regard to aetiology, K. pneumoniae (n=31) was the most frequently recovered pathogen in both early-onset (n=19) and late-onset (n=12) sepsis. It was followed by S. aureus (n=16, 9 early onset and 7 late onset).

Coagulase-negative staphylococci were found in 10 neonates, with 6 cases in early-onset and 4 in late-onset sepsis. This was followed

by Enterococcus spp., which accounted for 6 cases spread evenly between early- and late-onset variants. There was also one case of candidaemia in early-onset sepsis (Table 2).

The following were found to be risk factors for sepsis: patients born outside a tertiary hospital tended to be more at risk (p=0.15, OR 0.67, CI 0.39 - 1.15). A change in antibiotic therapy was the second risk factor observed, as those who had any change in antimicrobials were less likely to acquire sepsis (p=0.0001, OR 0.33, 95% CI 0.19 - 0.58). Also, one or more switches in antibiotics was another identified factor (p=0.0024, OR 0.41, CI 0.23 - 0.73) (Table 3).

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p-value

OR

95% CI

0.1475

0.67

0.39 - 1.15

0.0001

0.33

0.19 - 0.58

0.0024

0.41

0.23 - 0.73

The single statistically significant risk factor for early- v. late-onset sepsis was instrumentassisted delivery (p=0.02, OR 3.26, 95% CI 1.19 - 8.97). Babies who had instrumentassisted delivery were 3.26 times more likely to have late-onset sepsis than other neonates with suspected sepsis (Table 4).

Discussion

The findings from our study revealed that Gram-negative organisms were pre­ dominant, as they accounted for 61.1% of organisms recovered, with K. pneumoniae the most frequent Gram-negative pathogen. This finding is in keeping with results obtained by other researchers in previous studies where K. pneumoniae alone was responsible for 30% of cases of neonatal sepsis.[5-7] Klebsiella spp. were also the most frequent cause of sepsis at neonatal intensive care units (NICUs) in other resource-constrained settings.[8] The majority of bloodstream infections due to K. pneumoniae were of early onset

SEPTEMBER 2016 Vol. 10 No. 3

RESEARCH Table 4. Significant risk factor identified for early- and late-onset of sepsis Risk factor

Early onset, n (%)

Late onset, n (%)

Instrumentassisted delivery No

41 (83.7)

22 (61.1)

Yes

8 (16.3)

14 (38.9)

(n=19/31, 61.3%). This is also in line with some previous studies which show this organism to be one of the common causes of early-onset sepsis.[4,9-16] A study from Bangladesh also revealed that Gramnegative organisms were responsible for 73% of episodes of neonatal sepsis, with E. coli identified as the most common cause (30%), followed by Klebsiella spp.

(23%).[12] This highlights the predominance of Gram-negative bacteria in the aetiology of neonatal sepsis; clinicians need to bear this in mind when instituting antimicrobial therapy. However, this pattern is at variance with another study which demonstrated a preponderance of Gram-positive pathogens, highlighting the unique micro-ecological niche of different healthcare facilities.[7] The import of this is that therapeutic regimens should cover both groups of pathogens pending the definitive identification and susceptibility profiles of the agents responsible for sepsis.

A similar pattern was also seen in a study from this centre 11 years ago, which reported K. pneumoniae as the predominant pathogen implicated in neonatal sepsis. The findings from this research show that our microecology, with regard to the predominant pathogens, has not changed, and also indicates that a case needs to be put forward for stringent infection control measures as well as antimicrobial stewardship. S. aureus was the next most common pathogen; this is in line with findings from previous studies that describe it as a frequent cause of sepsis in neonates.[13] However, the isolation rate of 18.8% for S. aureus from this study is less than that obtained by workers at Illorin in Nigeria.[14] It is possible that some of these pathogens may have been transmitted from healthcare personnel or hospital equipment: therefore, continuous and regular training of neonatal unit staff on proper handwashing techniques before and after touching babies will help to reduce the transmission of pathogens in the NICU setting, as this pathogen was recovered from the hands of some healthcare workers.

The following risk factors for neonatal sepsis were identified in the course of the study: delivery outside this teaching hospital, change in antibiotics from the initial regimen and frequent changes in antibiotics. The reasons for these findings could be related to poor levels of antenatal, intrapartum and 149

p-value OR

95% CI

0.02

1.19 - 8.97

3.26

postnatal care, insufficient level of knowledge on the part of attending physicians in those facilities of appropriate antimicrobial use, and delayed detection of neonates at risk of sepsis. Babies delivered outside this tertiary hospital were not more likely to develop sepsis when compared with neonates born at our hospital. However, in order to reduce sepsis rates among our neonates, it is imperative that physicians in our referral centres be trained and retrained on the potential signs of sepsis and that they know what broad-spectrum antimicrobial agents they need to administer based on local susceptibility patterns. Our results also showed that early-onset sepsis was more common than late-onset sepsis, which is compatible with findings from previous studies.[17] A previous study identified the following risk factors for sepsis: lack of antenatal care, maternal colonisation with group B streptococci, preterm labour, low- and very low birth weight, instrumentation and invasive procedures, handling by healthcare workers, prolonged use of antibiotics and resuscitation at birth.[18] Early-onset sepsis was more common than late-onset in our study. This is keeping with previous data that demonstrate a marked propensity for sepsis in the first 7 days of life, given that this is the stage at which neonates are most susceptible to infectious agents.

The performance of invasive procedures, including mechanical ventilation and instru足 ment-assisted delivery, was more common in the early-onset cases owing to this being the stage at which infants are most vulnerable to illnesses and require some form of intervention. It is essential that policies are formulated and strengthened to guide clinicians in the application of safe interventional procedures geared towards reducing the risk of sepsis.

The relatively high rate of early-onset sepsis detected in this study provides a re足servoir of infectious neonates who pose a considerable risk of nosocomial transmission to other neonates. Numerous studies have reported that the most common pathogens isolated in early-onset sepsis include: group B streptococci (which was not found in this study), S. aureus, E. coli (also not seen), Klebsiella spp. and Listeria monocytogenes.[8,19] The data from this study show that the pattern of bacterial isolates in our local SAJCH

centre differ to previously published data and therefore the use of different antibiotic guidelines based on local susceptibility data will be warranted. There is therefore the need to formulate local guidelines that will aid in the rapid identification of atrisk neonates, especially those who have developed sepsis, and develop treatment modules that will help to reduce mortality in our centre. This study has outlined the local risk factors that impact on sepsis in our environment. The identification and use of these factors will help to form a framework for those who may be at risk of acquiring sepsis and help improve outcome in those who are identified early at being at risk of sepsis.

Study limitations

There were challenges in obtaining additional data on risk factors for sepsis, as some of these neonates were referred from other healthcare facilities to the study site and did not come with information on possible risk factors.

Conclusion

Our predominant pathogens were Klebsiella spp. and S. aureus. The burden of neonatal sepsis is still high in our environment, as evidenced by our isolation rate of 34%. The risk factors identified included: delivery outside a tertiary hospital, changes in anti足 biotic therapy and instrument-assisted deli足 very. A concerted effort needs to be made to reduce this scenario.

Recommendations

We recommend that babies presenting with respiratory distress and/or fever are screened immediately for bacterial sepsis. Infection control protocols also need to be instituted and strengthened in both our referral centres and teaching hospitals, with regular neonatal sepsis surveillance.

References 1. Wu JH, Chen CY, Tsao PN, Hsieh WS, Chou HC. Neonatal sepsis: A 6-year analysis in a neonatal care unit in Taiwan, Pediatr Neonatol 2009;50(3):8895. DOI:10.1016/S1875-9572(09)60042-5 2. Black RE, Cousens S, Johnson HL, et al., Global, regional, and national causes of child mortality in 2008: A systematic analysis. Lancet 2010;375(9730):1969-1987. DOI:10.1016/S01406736(10)60549-1 3. Stoll BJ, Hansen NI, Sanchez PJ, et al. Early onset neonatal sepsis: The burden of group B Streptococcal and E. coli disease continues.

Pediatrics 2011;127(5):817-826. DOI:10.1542/ peds.2010-2217 4. Iroegbu KC, Elegba YO, Babaniyi IB. Bacteriological profile of neonatal septicemia in a tertiary hospital in Nigeria. Afr Health Sci 2006;6(3):151-154.

5. Kish L. Survey Sampling. New York: John Wiley, 1965:49-50.

6. Zaidi AK, Hushus WK, Thower D, et al. Hospitalacquired neonatal infections in developing countries. Lancet 2005;365(9465):1175-1183.

DOI:10.1016/S0140-6736(05)71881-X

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RESEARCH 7. Ghotaslou R, GhorashiZ, Nahaei MR. Klebsiella pneumoniae in neonatal sepsis: A 3-year-study in the pediatric hospital of Tabriz, Iran. Jpn J Infect Dis 2007;60(2-3):126-128.

8. Waters D, Jawad I, Ahmad A, et al. Aetiology of community-acquired neonatal sepsis in low and middle income countries. J Glob Health 2011;1(2):154-170.

9. National Neonatology Forum NNPD Network. National Neonatal-perinatal Database: Report for 2002-2003. New Delhi: National Neonatology Forum NNPD Network, 2005.

10. Adejuyigbe EA, Adeodu OO, Ako-Nai KA, Taiwo O, Owa JA. Septicemia in high-risk neonates at a teaching hospital in Ile-ife, Nigeria. East Afr Med J 2001;78(10):540-543.

11. Orrett FA, Shurland SM. Neonatal sepsis and mortality in a regional hospital in Trinidad: Aetiology and risk factors. Ann Trop Paediatr 2001;21(1):20-25.

12. Awaisu A, Sulaiman SA, Ibrahim MI, Saad A. Antibiotics utilization and outcomes of neonatal sepsis among patients admitted to a university teaching hospital in Malaysia. Eastern J Med 2007;12:6-14.

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13. Zaidi AK, Thaver D, Ali SA, Khan TA. Pathogens associated with sepsis in newborns and young infants in developing countries. Paediatr Infect Dis J 2009;28(1):S10-S18. DOI:10.1097/INF.0b013e3181958769 14. Mokuolu AO, Jiya N, Adesiyun OO. Neonatal septicemia in Ilorin: Bacterial pathogens and antibiotic sensitivity pattern. Afr J Med Sci 2002;31(2):127-130.

15. Aftab R, Iqbal I. Bacteriological agents of neonatal sepsis in NICU at Nishtar Hospital Multan. J Coll Physicians Surg Pak 2006;16(3):216-219.

16. Polin RA, Committee on Fetus and Newborn. Managements of neonates with suspected or proven early-onset neonatal sepsis. Pediatrics 2012;129(5):10061015. DOI:10.1542/peds.2012-0541 17. Movahedian AH, Moniri R, Mosayebi Z. Bacterial culture of neonatal sepsis.

Iranian J Publ Health 2006;35(4):84-89.

18. Cohen-Wolkowiez M, Moran C, Benjamin DK, et al. Early and late onset sepsis in late preterm infants. Pediat Inf Dis J 2009;28(12):1052-1056.

19. Gandhi S, Ranjan KP, Ranjan N, Sapre N, Masani M. Incidence of neonatal sepsis in tertiary care hospital: An overview. Int J Med Sci Public Health 2013;2(3):548-552. DOI:10.5455/ijmsph.2013.090320131

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RESEARCH

This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

Pregnancy and death: An examination of pregnancyrelated deaths among adolescents in South Africa N de Wet, PhD Demography and Population Studies Programme, University of the Witwatersrand, Johannesburg, South Africa Corresponding author: Nicole de Wet (nicole.dewet@wits.ac.za) Background. South Africa (SA)’s high adolescent fertility has been extensively studied. A pregnancy outcome that has not received sufficient attention in research is the causes of death among pregnant adolescents.

Objectives. To examine levels and causes of adolescent maternal mortality in SA. Methods. A secondary data analysis of Death Notification Forms from 2006 to 2012 was carried out. SA General Household Surveys from 2006 to 2012 were used to ascertain the number of female adolescents in the population. Frequency distributions and life table techniques were employed.

Results. An estimated 1 164 deaths have been recorded among pregnant adolescents between 2006 and 2012. Adolescent maternal and pregnancy-related mortality is lower than adult maternal and pregnancy-related mortality. The main causes of death among adolescents were hypertension (55.6% of all direct causes), abortion (17.6% of all indirect causes) and injuries (48.9% of all indirect causes). The probability of adolescents dying while pregnant without these causes is practically non-existent (range 0.002 - 0.150%).

Conclusion. Policies and programmes should prioritise these pregnancy-related causes of death in order to further reduce such deaths among adolescents in SA. S Afr J Child Health 2016;10(3):151-155. DOI:10.7196/SAJCH.2016.v10i3.978

Maternal mortality in sub-Saharan Africa (SSA) is higher than in any other region in the world. In countries such as Sierra Leone it is as high as 1 100 per 100 000 live births.[1] The National Committee for Confidential Enquiry into Maternal Deaths in South Africa (SA) reports the current maternal mortality rate at 147.7 deaths per 100 000 live births.[2] Avoidable factors, including patient-related non-compliance (49%) and healthcare and health worker factors (35%), are contributing to maternal mortality.[3] The National Department of Health (NDoH) has made attempts to reduce this, such as the implementation of a programme to reduce child and maternal mortality through strengthening primary healthcare in the country. While progress has been made – maternal mortality has decreased from 299 deaths per 100 000 live births in 2007 to 147.7 in 2013, SA still failed to meets its Millennium Development Goal of 38 deaths per 100 000 live births.[4] In SA, alarmingly high rates of adolescent fertility are a topical issue.[5] Despite teenage pregnancy rates decreasing from 116 per 1 000 women (aged 15 - 19 years) in the 1980s, an astonishing 30% of adolescent females still report ‘ever being pregnant’.[6,7] While research has identified the levels and determinants of adolescent fertility,[8] the issue of adolescent maternal and pregnancy-related deaths has yet to be addressed. Pregnant adolescents face stigmatisation and are unable to afford healthcare,[9] which reduces healthcare accessibility and increases the risk of pregnancy complications and mortality. The extent of this is unknown.

The objective of this article is to determine the level and assess the direct and indirect causes of adolescent maternal mortality in SA. The health and survival of adolescent females is an important development goal of the national government. Adolescents who transition into healthy and productive adults are a key social and labour resource for any country. For this reason, research addressing the levels and causes of adolescent mortality will contribute to reducing deaths and ensure the health and survival of adolescents in the country.

Methods

Maternal death is the death of a woman while pregnant or within 42 days of termination of pregnancy, irrespective of the duration and 151

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site of the pregnancy, from any cause related to or aggravated by the pregnancy or its management but not from accidental or incidental causes.[10] Pregnancy-related death is defined as the death of a woman while pregnant or within 42 days of termination of pregnancy, irrespective of the cause of death.[10] This study examines both maternal deaths (direct maternal causes of death) and pregnancyrelated deaths (all deaths including those from accidental or incidental causes referred to as indirect causes of death) but not those which occurred in the post-natal period (42 days within termination of the pregnancy). The study seeks to answer the question: What are the levels and causes of maternal and pregnancy-related deaths among adolescents in SA? The study was set in SA, where adolescent pregnancies are high and generally adolescent females have higher odds of mortality than adolescent males.[7,11] The study was an analysis of secondary data available in the public domain. All deaths recorded on Death Notification Forms (DNFs) from 2006 to 2012 were analysed.

Adolescent females who were pregnant at the time of their death (n=1 164) were analysed. All completed forms where the deceased was female and pregnancy status was confirmed were included in the study. The percentage of missing cases for pregnancy status ranged from 1.41% to 32.44% over the period. This percentage was checked against direct maternal causes of death (ICD-10 codes O00 - O99) – 8.73% (n=966 of the total 8 433 maternal deaths of females of all ages) were found incomplete. These forms were not included in the analysis. The data were anonymised by Statistics SA before becoming available for public download. The data were not collected by the author and there was no need for institutional review board approval.

Analysis of direct ‘Maternal Conditions’ (ICD-10 codes O00 O99) and indirect causes of death were conducted to quantify the extent to which disease and injuries are contributing to adolescent maternal and pregnancy-related deaths in the country. Direct causes of death include conditions related to the pregnancy, such as maternal haemorrhage, maternal sepsis, gestational hypertension, obstructed labour and abortion. Indirect causes of death include communicable diseases that are not related to maternal or neonatal health, noncommunicable diseases, injuries and causes of death that were coded

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as ill-defined. The latter coding is checked on forms when a definitive cause of death could not be determined. Conventional multiple decrement life table techniques were done to estimate the probability of dying from direct and indirect causes of death among pregnant females in the country. In doing so, the study aimed to estimate the probability that a pregnant female will die from causes of death both related and unrelated to the pregnancy. Population age distribution was taken from the SA General Household Surveys from 2006 to 2012.

MMR / 10 000 births

RESEARCH

Results

152

All Adolescents Adults

2006

2007

2008

2009 Year

2010

2012

2011

Fig. 1. Trends in maternal mortality ratio (MMR) by age of the mother and year of death, 2006 - 2012.

Table 1. Distribution of adolescent maternal mortality by cause of death, 2006 - 2012 Deaths, n (%) PMR, %

Cause of death Direct causes Maternal haemorrhage

3.99

0.000

Maternal sepsis

43 (17.2)

7.45

139 (55.6)

24.09

Obstructed labour

1 (0.4)

0.17

Abortion

44 (17.6)

7.63

Sub-total Communicable (excl. maternal and neonatal)

250 (100)

43.33

82 (25.1)

14.2

0.000

Non-communicable

60 (18.4)

10.4

Injuries

160 (48.9)

27.7

Suicide and self-inflicted

4 (2.5)

0.7

Homicide and violence

10 (6.3)

1.7

Other (transport, accidents, etc.)

146 (91.3)

25.3

Ill-defined

25 (7.7)

4.3

Sub-total Total

p-value

23 (9.2)

Gestational hypertension

Indirect causes

327 (100)

56.7

577

100

A Direct cause of death

The maternal mortality ratio in adolescents (<19 years) and adults (>20 years) was approximated from an analysis of the preg­ nant female’s age and the 1 047 886 live births to adolescents during the period and application of the same proportion to all live births (n=7 320 968) during the study period.[12] The adolescent maternal mortality ratio was 1.11 deaths per 100 000 live births, while the adult maternal mortality ratio was 2.03 deaths per 100 000 live births.

Throughout the period, adolescent maternal mortality rates were consistently lower than those of adult females (Fig. 1). While rates of adolescent and adult maternal mortality appear to have peaked in 2009, these have been consistently declining ever since.

Proportional mortality ratios (PMR) were esti­mated using the total number of female adolescent deaths (n=13 930) and all female deaths (n=41 047) from 2006 to 2012. Hyper­ tension (55.60%) was the leading medical cause of death among adolescent females in SA (Table 1). Hypertension contributed 24.09% PMR to the overall mortality of pregnant adolescent females. In addition, abortion accounted for 17.60% of deaths in pregnant adolescent females over the period.

Further, the PMR for deaths from abortion was 7.63%. Overall, direct causes of death contributed 43.33% PMR of all pregnant adolescent deaths.

All other communicable deaths contri­buted 25.08% of deaths with a PMR of 14.21%.

Injuries contributed almost 50% of all preg­ nant adolescent deaths. More specifically, homicide and violence contributed 6.25% of all deaths, and all other forms of nondisease causes of death (other) have a PMR of 25.30%.

Hypertension is the leading direct cause of maternal mortality for adolescent and adult females, at 13.61 deaths per 100 000 live births overall (Fig. 2. (A)). In addition, hypertension causes more deaths in adol­ escents (13.26 deaths per 100 000 live births) than adult females (11.38 deaths per 100 000 live births) in the country.

Alternatively, there are more adult deaths owing to abortion than adolescent deaths,

26 24 22 20 18 16 14 12 10 8 6 4

Abortion

Adolescent

Obstructed labour

Adult

Hypertension

Total

Maternal sepsis Maternal haemorrhage 0

5

10

15

20

25

30

35

40

45

MMR / 100 000 live births

Fig. 2. (A) MMRs by direct medical cause of death, SA, 2006 - 2012.

with maternal mortality ratios of 7.56 and 4.20, respectively.

In terms of indirect causes of death, communicable causes of death, excluding obstetric (maternal and neonatal) causes, are the highest contributor to overall pregnancySAJCH

related mortality ratios (37.56 deaths per 100 000 live births). However, injuries are the highest indirect cause of death among pregnant adolescent females, at 15.27 deaths per 100 000 live births, compared with the 10.11 adult deaths per 100 000 live births

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RESEARCH B Indirect cause of death

from the same cause (Fig. 2.(B)). Finally, non-communicable diseases are higher among adult females (15.94 deaths per 100 000 live births) than adolescent females (5.73 deaths per 100 000 live births) in the country.

The probability of dying (nqx) and probability of dying if direct and indirect causes were eliminated (nq–ix) from the preg­ nant female population in SA are seen in Table 2.

For young adolescents (10 - 14 years old) the probability of dying in general (nqx) during pregnancy is practically non-existent (0.0001 or 0.01%) and the probability drops even further in the absence of direct (0.002%) and indirect (0.007%) causes of death. The overall probability of dying is higher for older pregnant adolescents at 0.15%; however, when all direct and indirect causes are eliminated, the probability of dying for this age group is practically nonexistent. While the probabilities are higher for older adolescents who are pregnant, at 0.15% overall probability of dying, the probabilities decrease with the elimination of direct and indirect causes. Adult females have consistently higher probabilities of dying during pregnancy, and again in the absence of direct and indirect causes of death, the probability of dying is very low.

Ill-defined Injuries

Adult

Non-communicable

Total

Communicable* 0

153

10

20

30

40

50

60

70

80

MMR / 100 000 live births

Fig. 2. (B) MMRs by indirect medical cuase of death, SA, 2006 - 2012. (*excludes maternal causes.)

Table 2. Probability of dying with and without main direct and indirect cause of death among pregnant women, 2006 - 2012 n

Adolescents Adults

Discussion

The objective of this article was to learn the levels and causes of adolescent maternal mor­ tality in SA. Adolescent maternal mortality rates are lower than adult rates in SA. This is similar to results of a study in Mozambique, which found adolescents to contribute to 22% of all maternal mortality.[13] In other parts of Africa, pregnancy is a leading cause of adolescent female mortality, with rates much higher than in SA and Mozambique.[14] In countries such as Chad, Guinea, Mali and Niger, high prevalence of child marriage and early pregnancy (with about half of adolescents giving birth before the age of 18 years old) is perpetuating adolescent maternal mortality.[15] In SA and Mozambique, child marriage is not nearly as prevalent as elsewhere, and this could explain the reduced contribution of adolescents to overall maternal mortality in these countries.

Of notable importance in SA, however, is the rate of teenage pregnancies, which is high at approximately 11%.[16] The mean age of pregnancy among adolescent females in SA is 18 years.[17] Research has found that older adolescents are at a lower risk of maternal mortality and morbidity; this could explain why adolescent maternal mortality is lower in SA.[18] Further, in a study examining the selfreported sexual behaviours of youth, it was found that termination of pregnancy rates had increased from 5.1% in 2002 to 6.0% in

Adolescent

Age group

n x

Direct

Indirect

10 - 14

0.0001

0.00002

0.00007

15 - 19

0.0015

0.00032

0.00149

20 - 24

0.0039

0.00078

0.00394

25 - 29

0.0058

0.00125

0.00581

30 - 34

0.0061

0.00143

0.00611

35 - 39

0.0043

0.00107

0.00429

40 - 44

0.0019

0.00063

0.00188

45 - 49

0.0009

0.0005

0.00088

50 - 54

0.0008

0.00054

0.00078

55 - 59

0.0002

0.00008

0.0001

2011.[16] This suggests that more adolescent females are utilising abortion services and, since they are surviving to report on it, they are utilising safe services.

Maternal mortality in SA is decreasing over time. This is a unique feature in SSA, with other countries in the region, such as Nigeria, Ethiopia and the Democratic Republic of the Congo, experiencing increasing maternal mortality rates.[19] Healthcare facilities in SA have undergone major reform over the last 20 years, increasing access and affordability for the general population.[20] In the area of obstetric care, the level of antenatal care visits in SA is high, with 97% of the 208 adult females interviewed in a Johannesburg study reporting that they sought care early in their pregnancy.[21] And while access to care could be contributing to reduced maternal mortality, SA’s declining fertility rate offers another possible explanation. The national total fertility rate has declined from 3.2 to 2.6 births between 1996 and 2012.[22,23] However, the declining trend in SA does not signify that the country is on par with more developed countries. The maternal mortality rate in the USA is 29 deaths per 100 000 live births and in Austria it is as low as 4 deaths per 100 000 live births.[24] This comparison proves that SA still has a way to go to further reduce maternal mortality. Despite SAJCH

q

q–ix

the overall improvements in healthcare for pregnant adolescents in SA, incomplete medical histories and discrimination from hospital staff are also known to prevent them from seeking the necessary care.[25,26] A systematic review of causes of maternal mortality found haemorrhage to be the leading cause of death in Africa.[27] In SA though, the current study and another found gestational hypertension to be the leading cause of adolescent and adult maternal death.[28] Risk factors associated with gestational hypertension are poor diet leading to gestational weight gain, pre-existing hyper­ tension and diabetes.[29,30] Specific to this are occurrences of pre-eclampsia among pregnant adolescents. Pre-eclampsia in adol­ escents is particularly dangerous, with a global prevalence of ~1.9% and rates in Africa as high as 5.2%.[31] Adolescents are at higher risk of pre-eclampsia than older females (20 - 29 years), and the known con­sequences include low birth weight and preterm delivery.[31,32] Therefore, among pregnant females, preexisting conditions need to be frequently monitored as potential mortality hazards.

This is offered at prenatal care visits. Yet, one study found that only 41% of pregnant adolescents access this service in SA.[33] A second concerning cause of death affecting pregnant adolescents is abortion.

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RESEARCH The ICD-10 code for an abortion is inclusive of miscarriages, spontaneous abortion as well as termination of pregnancy.[34] While termination of pregnancy (abortion) services have been legal in SA for almost 20 years, there remains a restriction on the accessibility of safe abortions for adolescents. In Africa it was found that 29 abortions per 1 000 women were done in 2003 and 97% of these were unsafe.[35] In SA, race, class, stigma and geographical location are known boundaries to women wishing to seek these services safely. As a result, they resort to quick, unsafe abortions that are not always done by trained service providers and are associated with an increased risk of complications.[36,37] Globally, the proportion of maternal deaths due to unsafe abortions is 13%; the proportion is higher in SSA at 14%.[38] In an effort to address the failings of abortion services in the country, an amendment was made to the SA Termination of Pregnancy Act.[39] A result of this amendment was an increase in the number of facilities offering abortion services, from 31.5% in 2000 to almost 62% in 2003.[40] Since then, definitive and official reports on the number of safe abortions conducted in the country have been moot.[39] It is suggested that due to the cultural and religious significance surrounding pregnancy and termination thereof, conscientious objection by healthcare providers and admission staff at facilities has contributed to irregularity in the access and reporting of services.[41]

Study strengths

Firstly, the pooled data of 7 years of DNFs increased the size of the adolescent maternal deaths sample. This enabled a more robust quantitative and inferential analysis. The combined sample is also larger than any previous hospital-based records used in maternal mortality studies in SA. Secondly, the use of life tables makes it possible to estimate the contribution of specific causes of death to probability of dying by age. By using associated single decrement life tables, this study was able to identify the gains in survival if maternal causes of death were eliminated from the mortality experience of adolescent females. This has important policy and programme implications because it provides empirical proof of the need to reduce direct and indirect causes of maternal mortality. Lastly, this study addressed an issue that has been overlooked in adolescent health research in SA. Adolescent maternal mortality is occurring in the country, and this study has contributed to knowledge through identifying the levels and causes contributing to this occurrence which compromises the future social and economic development of the country.

Study limitations

Outside of hospital data, which is scarce, maternal mortality statistics are difficult to ascertain. DNFs have been used in this study to obtain national estimates of maternal mortality. However, this data source is limited in its capturing of pregnancy status at the time of death, with missing cases reported to be as high as 32.44%. For this reason, the data have been pooled into a single dataset to increase the sample size and provide better estimates. In addition, the data do not account for deaths to females in the postnatal period (up to 42 days after giving birth); therefore the strict definition of maternal mortality, which includes this time period, could not be adhered to in this study. Finally, the data were subject to misclassification of causes of death, which is done at the level of medical practitioner, who completes the forms. In these cases women who died of tuberculosis, for example, could have been classified as ‘maternal sepsis’ owing to the similarity of symptoms of the diseases and the presence of the pregnancy.[42]

Implications of the study

There is a difference in the levels and causes of adolescent and adult maternal mortality in SA. This result is important because it means that the same approach to maternal care that is used for adults should 154

SAJCH

not be used for adolescents. Adolescence is a pivotal developmental stage, whereby adolescents are gaining independence for the first time but are still reliant on care and tutelage. This makes the phase of adolescence markedly different from child- and adulthood. For this reason, age-sensitive approaches should be developed and monitored to address the specific needs of pregnant females at different ages in the country. Further, although rates are not as high for adolescents as for adult women, pregnant adolescents are still dying. In order to combat this, further research into the health-seeking challenges of pregnant adolescents should be conducted. And as not all pregnancies are wanted, resulting in stressful and harmful circumstances, research into the termination of pregnancy practices of adolescents would further assist in the reduction of hypertension and abortion as contributors to adolescent maternal mortality. Should gestational hypertension, abortion, violence and other direct and indirect causes of maternal mortality be removed from the mortality experience of pregnant adolescents, the probability of pregnant adolescents dying practically disappears. As the direct causes are all obstetric and pregnancy related, improved healthcare facilities, including the early and efficient detection of obstetric complications, will improve the survival of adolescents. Continued improvements to healthcare facilities in SA, paying special attention to youth obstetric care, particularly in the area of destigmatising adolescent pregnancy, and subsidising costs should remain a priority. Ensuring that hospitals are appropriately stocked and staffed with specialised care for pregnant adolescents and adults will reduce the number of maternal fatalities.

Indirect causes of death can also be reduced through improving healthcare, but injury and non-communicable disease mortality can even more easily be reduced through behavioural change. The promotion of safe and healthy lifestyle choices through community engagement and education, especially among adolescents, could prevent unwanted pregnancies as well as any complications that may arise from these. In addition, healthy lifestyle choices encourage positive healthy behaviour, such as prenatal care visits. The health and development of pregnant adolescents are hindered by the risk of mortality associated with pregnancy. In recognising that these deaths are avoidable and unnecessary, appropriate measures can be designed and implemented to ensure the survival of adolescent females.

References 1. Jain V, Brown CS, Johnson O. Sierra Leone: The forgotten mortality. Glob Health Action 2015;8. DOI:10.3402/gha.v8.26757 2. National Committee for Confidential Enquiry into Maternal Deaths. Saving Mothers 2011 - 2013: Sixth report on confidential enquiries into maternal deaths in South Africa: Fact sheet. 2015. Pretoria: National Department of Health, 2015.

3. Buga EC, Nethathe GD, Mathivha LR. Obstetric critical care services in South Africa: Opinion. S Afr J Obstet Gynaecol 2015;21(1):4-5. DOI:10.7196/sajog.954 4. Statistics SA. Millennium Development Goals, Country Report 2013. Pretoria: Statistics SA, 2013.

5. Timæus IM, Moultrie TA. Teenage childbearing and educational attainment in South Africa. Stud Fam Plann 2015;46(2):143-160. DOI:10.1111/j.17284465.2015.00021.x 6. Willan S. A Review of Teenage Pregnancy in South Africa. Cape Town: Partners in Sexual Health, 2013.

7. Macleod CI. ‘Adolescence’, Pregnancy and Abortion: Constructing a Threat of Degeneration. Grahamstown, South Africa: Routledge, 2010.

8. Grant MJ, Hallman KK. Pregnancy‐related school dropout and prior school performance in KwaZulu‐Natal, South Africa. Stud Fam Plann 2008;39(4):369382. DOI:10.1111/j.1728-4465.2008.00181.x 9. Ross A, ed. 2015 National Conference on Health Communication, Marketing, and Media (August 11 - 13). In: Your Sexual Health Matters: A Media Campaign Targeting Adolescents. Atlanta, USA: Centers for Disease Control, 2015.

10. Zahr CA, Wardlaw TM. Maternal mortality in 2000: Estimates developed by WHO, UNICEF and UNFPA. Geneva: World Health Organization, 2004.

11. De Wet N, Odimegwu C. Determinants of adolescent mortality in South Africa, 2001 - 2007. J Behav Health 2013;2(3):243-251. DOI:10.5455/jbh.

20130726044607 12. Statistics SA. Recorded Live Births 2012. Pretoria: Statistics SA, 2013.

13. Granja ACL, Machungo F, Gomes A, Bergström S. Adolescent maternal mortality in Mozambique. J Adolesc Health 2001;28(4):303-306. DOI:10.1016/ s1054-139x(00)00205-6

SEPTEMBER 2016 Vol. 10 No. 3

RESEARCH 14. Bhutta ZA, Chopra M, Axelson H, et al. Countdown to 2015 decade report (2000 - 2010): Taking stock of maternal, newborn, and child survival. Lancet 2010;375(9730):2032-2044. DOI:10.1016/s0140-6736(10)60678-2 15. Graczyk K. Adolescent Maternal Mortality: An Overlooked Crisis. Washington, DC: Advocates For Youth, 2007.

16. Jonas K, Crutzen R, van den Borne B, Sewpaul R, Reddy P. Teenage pregnancy rates and associations with other health risk behaviours: A three-wave crosssectional study among South African school-going adolescents. Reprod Health 2016;13(1):1. DOI:10.1186/s12978-016-0170-8 17. Statistics SA. General household survey 2014. In: Africa SS, ed. South Africa General Household Survey 2014. Pretoria: Nesstar, 2015.

18. Althabe F, Moore JL, Gibbons L, et al. Adverse maternal and perinatal outcomes in adolescent pregnancies: The Global Network’s Maternal Newborn Health Registry study. Reprod Health 2015;12(Suppl 2):S8. DOI:10.1186/1742-4755-12-s2-s8 19. Hogan MC, Foreman KJ, Naghavi M, et al. Maternal mortality for 181 countries, 1980 - 2008: A systematic analysis of progress towards Millennium Development Goal 5. Lancet 2010;375(9726):1609-1623. DOI:10.1016/s01406736(10)60518-1 20. Cooper D, Morroni C, Orner P, et al. Ten years of democracy in South Africa: Documenting transformation in reproductive health policy and status. Reprod Health Matters 2004;12(24):70-85. DOI:10.1016/s0968-8080(04)24143-x 21. Solarin I, Black V. 'They told me to come back': Women’s antenatal care booking experience in inner-city Johannesburg. Matern Child Health J 2013;17(2):359367. DOI:10.1007/s10995-012-1019-6 22. Statistics SA. Mid-Year Population Estimates 2015. Pretoria: Statistics SA, 2015.

23. Moultrie TA, Timæus IM. The South African fertility decline: Evidence from two censuses and a demographic and health survey. Popul Stud 2003;57(3):265283. DOI:10.1080/0032472032000137808 24. World Bank. Maternal Mortality Ratios (modeled estimate, per 100,000 live births). Washington, DC: World Bank Group, 2015. http://data.worldbank. org/indicator/SH.STA.MMRT?order=wbapi_data_value_2013+wbapi_data_ value+wbapi_data_value-last&sort=asc (accessed 21 June 2015).

25. Wiemann CM, Rickert VI, Berenson AB, Volk RJ. Are pregnant adolescents stigmatized by pregnancy? J Adolesc Health 2005;36(4):352,e1-e7. DOI:10.1016/ j.jadohealth.2004.06.006 26. Jewkes R, Abrahams N, Mvo Z. Why do nurses abuse patients? Reflections from South African obstetric services. Soc Sci Med 1998;47(11):1781-1795.

DOI:10.1016/s0277-9536(98)00240-8 27. Khan KS, Wojdyla D, Say L, Gülmezoglu AM, van Look PF. WHO analysis of causes of maternal death: A systematic review. Lancet 2006;367(9516):10661074. DOI:10.1016/s0140-6736(06)68397-9

155

SAJCH

28. Soma-Pillay P, Pattinson R, Langa-Mlambo L, Nkosi B, Macdonald A. Maternal near miss and maternal death in the Pretoria Academic Complex, South Africa: A pop­ulation-based study. S Afr Med J 2015;105(7):578-583. DOI:10.7196/ samjnew.8038 29. Swank M, Caughey A, Farinelli C, et al. The impact of change in pregnancy body mass index on the development of gestational hypertensive disorders.

J Perinatol 2014;34(3):181-185. DOI:10.1038/jp.2013.168 30. Wang I-K, Muo C-H, Chang Y-C. Association between hypertensive disorders during pregnancy and end-stage renal disease: A population-based study.

Can Med Assoc J 2013;185(3):207-213. DOI:10.1503/cmaj.120230 31. Ganchimeg T, Ota E, Morisaki N, et al. Pregnancy and childbirth outcomes among adolescent mothers: A World Health Organization multicountry study.

Br J Obstet Gynaecol 2014;121(s1):40-48. DOI:10.1111/1471-0528.12630 32. Eure CR, Lindsay MK, Graves WL. Risk of adverse pregnancy outcomes in young adolescent parturients in an inner-city hospital. Am J Obstet Gynecol 2002;186(5):918-920.

33. McCray TM. An issue of culture: The effects of daily activities on prenatal care utilization patterns in rural South Africa. Soc Sci Med 2004;59(9):18431855. DOI:10.1067/mob.2002.123986 34. American Academy of Professional Coders. ICPD -10 Overview. http://www. aapccom/ICD-10/icd-10aspx (accessed 28 April 2011).

35. Sedgh G, Henshaw S, Singh S, Åhman E, Shah IH. Induced abortion: Estimated rates and trends worldwide. Lancet 2007;370(9595):1338-1345.

DOI:10.1016/s0140-6736(07)61575-x 36. Varkey SJ. Abortion services in South Africa: Available yet not accessible to all. Int Fam Plan Perspect 2000;26(2):87-88. DOI:10.2307/2648273 37. Jacobs R, Hornsby N. Why aren’t women getting safe abortions? S Afr Med J 2014;104(12):857-858. DOI:10.7196/samj.9133 38. Ǻhman E, Shah IH. New estimates and trends regarding unsafe abortion mortality. Int J Gynecol Obstet 2011;115(2):121-126. DOI:10.1016/j. ijgo.2011.05.027 39. Hodes R. The culture of illegal abortion in South Africa. J South Afr Stud 2016;42(1):79-93. DOI:10.1080/03057070.2016.1133086 40. Health Systems Trust. ToP Facilities Functioning. Cape Town: Health Systems Trust, 2012. http://www.hst.org.za/news/half-sa-pregnancies-end-abortion (12 August 2015).

41. Harries J, Stinson K, Orner P. Health care providers’ attitudes towards termination of pregnancy: A qualitative study in South Africa. BMC Public Health 2009;9(1):1. DOI:10.1186/1471-2458-9-296 42. Acosta CD, Knight M. Sepsis and maternal mortality. Curr Opin Obstet Gynecol 2013;25(2):109-116. DOI:10.1097/gco.0b013e32835e0e82

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RESEARCH

This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

Outcome of children admitted to a general highcare unit in a regional hospital in the Western Cape, South Africa I Kruger,1 FCPaed (SA); R Gie,1 FCPaed (SA); J Harvey,2 PhD; M Kruger,1 MMed Paed, FCPaed (SA), MPhil, PhD 1 2

Department of Paediatrics and Child Health, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa Centre for Statistical Consultation, Stellenbosch University, Cape Town, South Africa

Corresponding author: I Kruger (immie78@hotmail.co.uk) Background. Critically ill children are often managed in non-tertiary general intensive care units admitting both adults and children, but few data are currently available regarding paediatric outcomes in these general units.

Objective. To determine the outcome of critically ill neonates and children admitted to a general high-care unit in a large regional hospital in the Western Cape, South Africa.

Methods. This was a retrospective descriptive analysis of outcome of all neonatal and paediatric (<13 years of age) patients admitted with non-surgical disease, during a 1-year period, to a general high-care unit at a large regional hospital in Worcester, South Africa. Data included demography, admission time, length of stay, diagnoses, HIV status, therapeutic interventions and outcome. The primary outcome was defined as successful discharge, transfer to a central hospital or death.

Results. There were 185 admissions, with the majority (83%) <12 months of age (median age 3.7 months; range 0 - 151 months) and a male:female ratio of 1.3:1. The majority (70%) were successfully discharged, while 24% were transferred to a tertiary paediatric intensive care unit (PICU) and only 6% died. Causes of death included acute lower respiratory tract infections (33%), acute gastroenteritis (33%), birth asphyxia (16%) and complications of prematurity (16%). Nasal continuous positive airway pressure (p<0.001), ventilation (p<0.001) and HIV infection (p=0.010) were associated with transfer to a PICU in a central hospital or death.

Conclusion. The majority of children (70%) requiring admission to a general high-care unit in a regional hospital were successfully treated and discharged. These good outcomes were only achievable with a good transfer system and supportive tertiary healthcare system.

S Afr J Child Health 2016;10(3):156-160. DOI:10.7196/SAJCH.2016.v10i3.981

Globally, more than 10 million children die annually, and the majority of these deaths occur in sub-Saharan Africa (41%) and southern Asia (34%), where under-5 mortality is attributed mainly to diarrhoea, pneumonia, measles, malaria, HIV/AIDS and malnutrition.[1,2] Neonatal deaths occur due to asphyxia, preterm delivery, sepsis and tetanus.[2] A countryâ&#x20AC;&#x2122;s epidemiological profile and health system largely dictate the implementation and development of public health interventions that will improve childhood survival.[1] Little is known about the need for paediatric high care and critical care in low- and middle-income countries, but published results indicate an inadequate quality of care with high mortality rates.[3] Lack of infrastructure, human resources and expert support leads to children being managed in general wards with low nurse-to-patient ratios, resulting in an increased risk of nosocomial infections and death.[3-6] Paediatric intensive care is defined as a â&#x20AC;&#x2DC;physical space that is designated to manage critically ill children who require comprehensive and intensive healthcareâ&#x20AC;&#x2122;, and should be available to all children irrespective of where they live.[7] Research in developed countries suggests that paediatric intensive care units (PICUs) should be centralised with good retrieval services to ensure safe access. There is no clear guidance regarding the infrastructure of a PICU in a low- or middle-income country where transport services often are weak or non-existent.[8] Transfer of critically ill children poses a challenge in South Africa (SA), and a study from Cape Town revealed a high incidence of transfer-related adverse events in children transferred from non-academic metropolitan hospitals to tertiary care centres.[9] Critically ill children are, therefore, often managed by non-specialist staff in non-tertiary general intensive care units admitting both adults and children, but few data are currently 156

available regarding paediatric outcomes in these general units.[9] This study was done to determine the outcome of neonates and children admitted to a general high-care unit under the care of paediatricians at a large regional hospital in the Western Cape Province, SA.

Methods

The study was conducted at the large regional hospital in Worcester, SA. Worcester Hospital is the regional hospital for the Winelands/ Overberg region of the Western Cape, with ~1 million inhabitants, of whom 1.6% were <1 year of age. The infant mortality and childhood mortality rates at the time of the study were 25.3 and 31.2/1 000 live births, respectively.[10] The hospital has a five-bed general high-care unit. One of these beds is dedicated to paediatric care. The care of neonates and children admitted to the high-care unit takes place under the supervision of a paediatrician, supported by either a paediatric registrar, medical officer or intern depending on the call list. The nursing staff includes six registered nurses trained in adult intensive care and one registered nurse trained in paediatric intensive care. Children and neonates admitted to the general high-care unit can be ventilated for a limited period, and if not weaned within 48 72 hours are transfered to a central PICU. High care is also provided in the neonatal ward but if mechanical ventilation is required, the neonate is transferred to the general high-care unit. There are no other high-care beds in the hospital, therefore all children requiring high or intensive care are admitted to the general high-care unit. This study is a retrospective review of patient records, capturing data for a 12-month period from 1 July 2008 until 30 June 2009. The high-care admissions records were used to determine all neonates and children admitted. The medical record of each patient was retrieved from the

SAJCH SEPTEMBER 2016 Vol. 10 No. 3

RESEARCH hospital records and the data recorded on a case-recording form.

Ethical approval was obtained from the Health Research Ethics Committee at Stellenbosch University (N11/07/209). A waiver of individual consent was granted.

Consent from the hospital management was obtained to access the patient records.

All consecutive admissions of neonates and children meeting the inclusion criteria were included. Inclusion criteria were: all children younger than 13 years of age admitted with a non-surgical condition. Exclusion criteria were: (i) children older than 13 years of age at admission; (ii) children admitted with a surgical condition; and (iii) children directly transferred to tertiary facilities.

Total ICU admissions, N=535

Adult admissions, n=341 Paediatric admissions, n=194

Definitions and outcomes

The three primary outcome measurements were: death, transfer to a central hospital and successful discharge. Death was defined as a death that occurred during the general highcare unit admission. Transfer to dedicated PICUs in central hospitals was defined as a transfer. Successful discharge was defined as discharge from the general high-care unit to a step-down facility, paediatric inpatient ward or home.

Ventilatory support included nasal cont­ inuous positive airway pressure (nCPAP) and/or mechanical ventilation. For the purposes of this study nasal cannula oxygen was not considered an intervention and high-flow nasal oxygen was not used during the study period. Transfusions were defined as infusion of blood, blood products or albumin, while inotropic support referred to intravenous infusion of dopamine, dobutamine, adrenaline or a combination of these drugs. The unit did not have a transfusion policy; transfusions were administered at the clinician’s discretion.

Neonates and children were weighed on admission. If they were too ill to be weighed, their weights were obtained from the most recent weight in the Road to Health Booklet.

Severe malnutrition was defined as a weightfor-age z-score (WAZ) of <–3 SD, while moderate malnutrition was defined as a WAZ of between –3 and –2 SD. The WAZ was determined for each patient’s admission weight. For children 0 - 5 years, the WHO Anthro computer program (version 3.2.2) was used. For children >5 years, the Centre for Health Statistics values were used. To determine the WAZ for premature infants, the Fenton Growth charts were used.[11] These charts reflect actual age instead of completed weeks.

After hours was defined as admission after 17h00, before 08h00 on weekdays and from Friday 17h00 until Monday 08h00 on weekends. Public holidays were regarded as after hours.

157

Children excluded from study, n=9 Incomplete data, n=8 Non-medical admission, n=1

Children included in study, n=185 Fig. 1. Sampling strategy.

3%

2% 3% 3% ALRTI

4%

AGE Complications of prematurity

6% 34%

Other Neonatal complications

7%

AGE/SAM UAO 9%

TB Sepsis SAM with hypotension 29%

Fig. 2. Reasons for admission to ICU. (SAM = severe acute malnutrition.)

Continuous variables were not normally distributed. The descriptive data are pre­ sented as the median with the data range.

To compare continuous variables by group (‘Successful discharge’, ‘Transfer’ or ‘Died’) a Kruskal-Wallis analysis of variance (ANOVA) was used, since data were not normally distributed. In the case of overall significance, post-hoc testing was applied, correcting for multiple comparisons using the Bonferroni approach. Comparisons of nominal variables and group were performed using the χ2 test for association. A significance level of 95% was applied to all analyses.

Results

More than a third (36%, n=194/535) of the admissions to the general high-care unit were paediatric admissions, of whom 22% SAJCH

(n=41/194) were neonates. Of the 194 paed­ iatric admissions, 185 (95%) patient records were analysed. Eight records were excluded owing to incomplete data and one record owing to the patient having a surgical condition (Fig. 1).

The male to female ratio was 1.3:1, and the majority (83%) of the patients were younger than 12 months at the time of admission. The median age was 3.7 (range 0 - 151) months.

The median WAZ was –1.54 SD (range –6.5 SD - 1.88 SD), with 25% (n=46/185) of children severely malnourished (WAZ <–3 SD), and 16% (n=30/185) moderately malnourished (WAZ –2 - –3 SD).

Fig. 2 provides a breakdown of the reasons for admission to the general high-care unit. This reflects only the main reason for admission and not underlying comorbidities.

SEPTEMBER 2016 Vol. 10 No. 3

RESEARCH The majority of admissions were due to acute lower respiratory tract infections (ALRTI) (34%, n=63/185) and acute gastroenteritis (AGE) (29%, n=54/185).

The majority (53%) were directly admitted from the casualty unit, 33% (n=61/185) from inpatient wards, 12% (n=22/185) from other referral healthcare facilities surrounding the hospital and 3 children (<1%) from theatre. The patients admitted directly from theatre included 2 children intubated in theatre due to upper airways obstruction and 1 infant admitted post caesarean section due to respiratory distress. The majority of admissions (62%) occured after hours. The median duration of admission was 1.83 days (range 1 hour - 13.4 days). Ventilatory support was provided to 65% (n=120/185) of patients, of whom 52% (n=62/120) required mechanical ventilation and 48% (n=58/120) nCPAP. Inotropic support was given to 41% (n=75/185) of children and 27% (n=50/185) received blood product transfusions. Thirtyfive (70%) received a blood transfusion, 5 (10%) received fresh frozen plasma and 1 (2%) received an albumin transfusion. Eight (16%) of those transfused received both blood and fresh frozen plasma, while 1 received blood and albumin.

The majority (70%) of patients were suc­ cessfully discharged, while 24% (n=44/185) were transferred to a dedicated PICU at a central/tertiary hospital and 6% (n=12/185) died (Table 1). All deaths occurred in infants <1 year old (median 2.5 months, range newborn to 9.3 months) (Table 1).

Premature infants

Nearly half (49%, n=20/41) of all neonatal admissions were premature babies (<37 com­ pleted weeks’ gestation) with a median gestational age of 29 weeks (range 29 36 weeks) and a median age on admission of 3 days (range 0 - 27 days). The male to female ratio was 2.3:1. The median duration of stay was 1.82 days (range 4 hours - 13.4 days) and 65% were admitted after hours. Forty per cent of premature infants had low birth weight, 45% very low birth weight and 10% had an extremely low birth weight. Sepsis (45%, n=9/20 patients) was the main reason for admission, followed by hyaline membrane disease (30%, n=6/20) and apnoea (25%, n=5/20). Fourteen (70%) premature infants were successfully discharged, 4 (20%) were transferred to a central hospital and 2 babies (10%) died. The 2 deaths that occurred were due to sepsis and pneumonia.

Term infants

Of the neonates admitted, 51% were fullterm with a mean age of 7 days (range newborn - 25 days). Seven of these neonates (33%, n=7/21) were small for gestational age, the rest being normal for gestational age. A 158

Table 1. Outcome of neonates and children admitted to a general high-care unit Age group

Step down/discharge

Referral to tertiary hospital

Death

≤28 days

27

10

4

29 days - 6 months

55

14

7

>6 months - 1 year

28

8

1

>1 year - 5 years

16

11

0

>5 years

3

1

0

Total

129

44

12

% of total admissions

70

24

6

Table 2. Age ranges, nutritional assessment and outcomes of patients admitted to the general high-care unit Data

29 days - 6 months (n=76)

>6 months - 1 year (n=37)

>1 - 5 years (n=27)

>5 years (n=4)

Age (mo), mean

3.1

8.52

22.64

99.86

Male:female ratio

1.71:1

1.05:1

1.25:1

1:3

Duration of stay (days), mean

2.46

2.35

1.75

2.47

WAZ, mean

–2.13

–1.94

–1.76

–1.79

Admissions after hours, n (%)

48 (63)

22 (59)

15 (56)

4 (100)

Death, n (%)

7 (9)

1 (3)

0

0

Transfer out, n (%)

14 (18)

8 (22)

8 (30)

1 (25)

Successful discharge, n (%)

55 (72)

28 (76)

16 (59)

3 (75)

total of 61% of the admissions occurred after hours. The median duration of high-care stay was 1.7 days (range 1.5 hours - 12.3 days).

The majority of patiets (62%, n=13/20) were successfully discharged, while 29% (n=6/21) were transferred to a central hospital and 2 (9%) died. AGE (38%, n=8/21) was the most common cause of admission for full-term babies, followed by sepsis (19%, n=4/21 patients) and birth asphyxia (19%, n=4/21patients). In both neonates who died, the cause of death was birth asphyxia, complicated by pulmonary hypertension.

Older children

The vast majority (77%, n=142/185) of all admissions were children between the ages of 1 month and 1 year; 8 out of the 12 deaths occurred in this age group (Table 2). The median age of this group was 5.6 months (range 1 month - 12.5 years). The majority (62%) were admitted after hours. Most (73%) of these infants were successfully discharged, 20% were transferred to a tertiary facility, and 6% died.

The most common diagnoses for children older than 1 month of age were ALRTI (42%, n=61/144) and AGE (36%, n=52/144) (Fig. 2). In this group, 84% required ventilator SAJCH

support, with 77% requiring nCPAP and 23% mechanical ventilation. In the children with ALRTI, there were 4/61 deaths (7%) and 14/61 were (23%) transferred to a PICU. In addition to these 4 deaths, there were 4 additional deaths, 3 from complicated gastroenteritis. Of these deaths, 85% were admitted after hours.

Children older than 1 year of age accounted for 17% (39/185) of the total admissions, with only 4 children admitted being older than 5 years of age. Of those younger than 5 years, the median age was 15.6 months. Table 2 shows outcomes and nutritional status. No children older than 1 year of age died.

The HIV status of 37% (n=69) of patients was unknown at the time of admission. Five children were known to be HIV-infected on admission and 15% were known to be HIV-exposed. The remainder (n=83, 45%) were unexposed and known to be HIVnegative at the time of admission. The majority of patients older than 1 month of age (n=112/129) were tested for HIV. DNA polymerase chain reaction was performed for 11 patients, and 5 patients were newly diagnosed with HIV. One of the known HIV-infected patients received antiretroviral

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RESEARCH Table 3. Comparing deaths, transfers and successful discharges of neonates and children admitted to a general high-care unit

Male:female ratio

Deaths (n=12)

Transfers (n=44)

Successful discharges (n=119)

2:1

1:1

1.4:1

Age (mo) Mean

2.6

11.9

7.8

Median

2.4

4.06

3.9

Range

0 - 9.2

0 - 12

0 - 9.5

83

45

64

Mean

1.6

1.5

2.9

Median

1.01

1.2

2.0

Range

0.04 - 5

0.08 - 5.1

0.04 - 13.4

Mean

–1.60 SD

–1.40 SD

–1.91 SD

Median

–1.30 SD

–1.49 SD

–1.63 SD

Range

–4.80 - 0.89 SD

–5.20 - 1.88 SD

–6.05 - 1.57 SD

Admissions after hours (%) Duration of stay (days)

WAZ

Interventions (%) 0

8

7

18

1

17

48

52

2

50

32

22

3

25

13

8

ALRTI (%)

33

32

35

AGE (%)

25

23

37

(ARV) therapy at the time of admission.

None of the newly diagnosed HIV-positive children were started on ARV therapy during their admission to the unit. Six of the HIV-positive patients (60%, n=6/10) were successfully discharged, 3 (30%, n=3/10) were transferred and 1 child died (10%, n=1/10).

The majority (62%, 32/52) of patients admitted with AGE were admitted due to hypovolaemic shock not responding to fluid resuscitation. Of these children, 85% required inotropic support. AGE was complicated by severe malnutrition in 13% (n=7/52) of cases, but all these children were successfully discharged despite their poor nutritional states. Three patients admitted with AGE died (n=3/52, 6%) andeight patients (n=8/52, 15%) were transferred to a tertiary facility.

Five patients were admitted with a diag­nosis of TB, of whom four had comorbid disease (respectively HIV, dilated cardiomyopathy, lower airway obstruction and TB meningitis).

One child with complicated pulmonary TB had no complicating comorbid disease.

Three of these patients were transferred and two were successfully discharged. Five patients were admitted due to upper airways 159

obstruction (UAO) and the majority (60%, 3/5) required mechanical ventilation and transfer. Two patients were successfully discharged. There were two patients admitted with acute flaccid paralysis (AFP), of whom one was successfully discharged; the second patient required long-term mechanical ventilation and was transferred. Two patients had acute liver failure due to ingestion of unknown herbal medication. Both of these children were transferred (Table 3).

Of the patients who died, 75% required two or more interventions, compared with 45% of patients transferred to a dedicated PICU and 30% of patients successfully discharged.

Patients requiring nCPAP or mechanical ventilation were more likely to die or require transfer (p=0.0001). A third of the patients received nCPAP, which was associated with either transfer or death (p<0.001). Patients who were diagnosed with HIV infection or patients known to be HIV-positive, had a statistically significant poorer outcome when compared with HIV non-infected children (p=0.01) (Table 3). Only 28% of patients received a transfusion of one or more blood products, but neither the use of blood products (p=0.87), nor the need for inotropic support (p=0.16) was significantly associated SAJCH

with transfer or death. Although AGE and ALRTI were responsible for more than 50% of admissions, there was no statistically significant association between diagnosis and outcome (p=0.17). Complications of prematurity (sepsis, hyaline membrane disease and apnoea) and neonates referred from outside healthcare facilities were not associated with poor outcome (p=0.98 and p=0.38, respectively). There was a trend towards a significant association (p=0.07) between time of admission and outcome in this study, with after-hour admissions tending to have a poorer outcome. The prevalence of severe malnutrition among admissions in this study was 25%, but there was no association between nutritional status and a poor outcome (p=0.56). Although the majority of the patients were younger than 12 months (median age 3.7 months), age was not associated with a poor outcome (p=0.17). In summary, the majority of children requiring access to high-care unit in a regional hospital, were younger than 1 year of age and 70% had a good outcome.

The need for good ventilatory support and being HIV-infected was associated with a poor outcome.

Discussion

In this study we describe the good outcome achieved in children admitted to a general high-care in a regional hospital in the Western Cape. The reported low mortality rate of 6.5% was not solely due to the care in the general high-care unit but also, in large part, due to the fact that there was an effective emergency transport system which allowed for 24% of the children to be transported to a PICU within 100 km of the regional hospital. The study also identified mechanical ventilation and HIV infection as risk factors for transfer to a PICU, which would in future allow for a change in transfer policy resulting in children being transferred earlier for PICU care. The study only included children not requiring surgery. Children with serious trauma and burn wounds were not admitted to the high-care unit but were directly transferred, after resuscitation, to the appropriate tertiary hospital. This policy together with the fact that only minor surgical procedures were performed would have contributed to the low mortality rate.

Age has been reported to be associated with a poor outcome within the PICU.[6] In this study we were not able to demonstrate that age was statistically associated with death or transfer. It should however be noted that 8 (75%) of the deaths occurred in children less than 1 year of age. The two most common causes of death in children <1 year of age were complicated ALRTI and AGE, both potentially treatable conditions.

It was noted that 85% of the children older

SEPTEMBER 2016 Vol. 10 No. 3

RESEARCH than 28 days of age who died were admitted after hours. This might suggest that caregivers did not have easy access to after-hours healthcare facilities, that the emergency transport services did not operate as efficiently after hours, that the healthcare after hours in the regional hospitals is mainly run by junior staff who might underestimate the acuity of disease, or that it is a combination of these reasons. Further research is required to elicit the reason for the poor outcome after hours.

ALRTI, AGE, birth asphyxia and complications of prematurity are reported as the main causes of death in children <5 years of age. This was confirmed in this study, where ALRTI was the leading cause of both admissions and deaths, followed by AGE.[2,11] It is estimated that 20% of infants with birth asphyxia will die within the neonatal period.[12] Only 4 term infants were admitted with birth asphyxia in this study and 2 died. A study limitation is the small sample size and death rate (per 1 000) due to birth asphyxia, which could not be established. Severe malnutrition is reported in 18 - 65% of all paediatric admissions and 15 - 65% of admissions to PICU and has been linked to poor outcome, reporting mortality rates up to 30%.[13] However, differing methodologies used to classify malnutrition make it difficult to compare the incidence and mortality rates between different studies.[13] In this study one of the weaknesses was establishing the exact weight of the neonates and children admitted. This might have resulted in underestimation of the weights of the children, especially those admitted with severe dehydration. Even taking this into account, 25% of the children were considered to be severely malnourished, indicating that their complicated disease was multifactorial. Invasive ventilation has been reported to be associated with a poorer outcome in PICUs, which was similar to our findings (p<0.001).[14] nCPAP has become a common intervention to provide airway support for ALRTI, with up to 10% of children admitted to paediatric intensive care receiving non-invasive airway support.[15] The addition of non-invasive airway support (including nCPAP) is associated with improved outcome without contributing significantly to adverse events.[14] In this study, children receiving nCPAP had an increased rate of transfer to a PICU and death. The use of nCPAP and mechanical ventilation indicates that these children had severe ALRTI resulting in respiratory failure with a high proportion of children requiring transfer to a PICU. This finding illustrates the point that a general high-care unit cannot operate in isolation but requires good emergency transport services and access to PICU beds in a tertiary hospital that is within easy reach. If this were not the case it is postulated that especially the infant mortality rate would have been unacceptably high. On the other hand, 62 (33.5%) neonates and children required ventilation which would not have been possible if they were not admitted to the high-care unit.

This illustrates the importance of having these facilities available in regional hospitals as a minimum to stabilise the neonates and children prior to transfer to a central intensive care unit. The addition of inotropic support to the treatment of patients in our study was not significantly associated with a poorer outcome, which also differs from other studies, where the addition of inotropes to treatment was a risk factor for death during intensive care unit stay.[16] Transfusion of blood products is commonly used (up to 50% of admissions) in critically ill children admitted to PICUs, whereas only 28% of patients in this study received blood product transfusions and there was no association with poor outcome.[17] Limitations of the study include a short study period, small sample size and no objective measurement of the patients’ disease acuity.

Another weakness to take into account is that the outcomes of the patients transferred to a PICU were not determined. This is further

160

compounded by the fact that critically ill patients were also directly transferred from surrounding healthcare facilities to the regional hospital. The outcome of patients referred to tertiary care is not discussed as part of this paper and the reasons for refusal of admission to the unit or to the tertiary referral centre are not included. The data in this study are relatively old, but to our knowledge a study of this kind has not been reported in the interim, illustrating the value of having access to a high-care unit in a regional hospital in SA. A prospective study with routine collection of more comprehensive data, including causes of morbidity and mortality linked to ICD-10 codes, assessments of disease severity and interventions, needs to be performed to provide comprehensive information on the value of admitting neonates and children to a high-care or critical-care unit in a regional hospital.

To our knowledge this is the first study reporting admissions and outcome of neonates and children cared for in a general high-care unit where the care is given by general paediatricians working in a regional hospital in SA. This study suggests that these units in large regional hospitals, with paediatricians supporting their care, may improve child survival in SA if the high care is part of a functional system that includes transport of the severely ill to tertiary facilities with paediatric intensive care facilities. More data are required to support this hypothesis.

References 1. Black RE, Morris SS, Bryce J. Where and why are 10 million children dying every year? Lancet 2003;361(9376):2226-2234. DOI:10.1016/S0140-6736(03)13779-8 2. Jones G, Steketee RW, Black RE, et al. How many child deaths can we prevent this year? Lancet 2003;362(9377):65-71. DOI:10.1016/S0140-6736(03)13811-1 3. Baker T. Critical care in low-income countries. Trop Med Int Health 2009;14(2):143-148. DOI:10.1111/j.1365-3156.2008.02202.x 4. Baker T. Pediatric emergency and critical care in low-income countries.

Paediatr Anaesth 2009;19(1):23-27. DOI:10.1111/j.1460-9592.2008.02868.x 5. Argent A. Critical care in Africa. S Afr J Crit Care 2009;25(1):4.

6. Basnet S, Adhikari N, Koirala J. Challenges in setting up pediatric and neonatal intensive care units in a resource-limited country. Pediatrics 2011;128(4):e986-e992. DOI:10.1542/peds.2010-3657 7. Randolph AG, Gonzales CA, Cortellini L, Yeh TS. Growth of pediatric intensive care units in the United States from 1995 to 2001. J Pediatr 2004;144(6):792798. DOI:10.1016/j.jpeds.2004.03.019 8. Campos-Miño S1, Sasbón JS, von Dessauer B. Pediatric intensive care in Latin America. Med Intensiva 2012;36(1):3-10. DOI:10.1016/j.medin.2011.07.004 9. Hatherill M, Waggie Z, Reynolds L, Argent A. Transport of critically ill children in a resource-limited setting. Intensive Care Med 2003;29(9):1547-1554.

DOI:10.1007/s00134-003-1888-7 10. Groenewald P, Berteler M, Bradshaw D, et al. Western Cape Mortality Profile 2010. Cape Town: South African Medical Research Council, 2013.

11. Fenton TR, Nasser R, Eliaziw M, et al. Validating the weight gain of premature infants between the reference growth curve of fetus and term infants. BMC Pediatr 2013;13:59. DOI:10.1186/1471-2431-13-92 12. Wells, M, Riera-Fanego JF, Luyt DK, Dance M, Lipman J. Poor discriminatory performance of the Pediatric Risk of Mortality (PRISM) score in a South African intensive care unit. Crit Care Med 1996;24(9):1507-1513.

13. Jeena PM, McNally LM, Stobie M, Coovadia HM, Adhikari MA, Petros AJ. Challenges in the provision of ICU services to HIV infected children in resource poor settings: A South African case study. J Med Ethics 2005;31(4):226-230.

DOI:10.1136/jme.2003.004010 14. Tan GH, Tan TH, Goh DY, Yap HK. Risk factors for predicting mortality in a paediatric intensive care unit. Ann Acad Med Singapore 1998;27(6):813-818.

15. Inwald DP, Tasker RC, Peters MJ, Nadel S, Paediatric Intensive Care Society Study Group (PICS-SG). Emergency management of children with severe sepsis in the United Kingdom: The results of the Paediatric Intensive Care Society sepsis audit. Arch Dis Child 2009;94(5):348-353. DOI:10.1136/ adc.2008.153064 16. Ten Berge J, de Gast-Bakker DA, Plötz FB. Circumstances surrounding dying in the paediatric intensive care unit. BMC Pediatr 2006;6:22. DOI:10.1186/1471-2431-6-22 17. Gauvin F, Spinella PC, Lacroix J, et al. Association between length of storage of transfused red blood cells and multiple organ dysfunction syndrome in pediatric intensive care patients. Transfusion 2010;50(9):1902-1913.

DOI:10.1111/j.1537-2995.2010.02661.x Accepted 7 October 2015.

SAJCH SEPTEMBER 2016 Vol. 10 No. 3

RESEARCH

This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

A review of chronic lung disease in neonates at Charlotte Maxeke Johannesburg Academic Hospital from 1 January 2013 to 31 December 2014 A V Mphaphuli, MB BCh, DCH; D E Ballot, MB BCh, FCPaed, PhD Department of Paediatrics and Child Health, University of the Witwatersrand and Charlotte Maxeke Johannesburg Academic Hospital, Johannesburg, South Africa Corresponding author: A V Mphaphuli (mphaphulia@gmail.com) Background. Chronic lung disease (CLD) remains a significant morbidity in preterm babies despite advances in neonatal care. The use of postnatal corticosteroids (PNCSs) to treat CLD remains controversial.

Objectives. To describe the clinical characteristics of babies with CLD at Charlotte Maxeke Johannesburg Academic Hospital (CMJAH) and to explore the use of PNCSs for the prevention and treatment of CLD. Methods. This was a 2-year retrospective review of neonates admitted to CMJAH. Neonates who were in hospital for â&#x2030;Ľ28 days were included. Comparisons were made between neonates with evolving CLD and those with no CLD. Results. A total of 485 neonates were analysed: 237 had evolving CLD and 245 did not have CLD. Overall incidence of evolving CLD was 5%. More neonates with CLD than those without CLD needed resuscitation at birth (48.5% v. 39.8%; p=0.02) and had low 5-minute Apgar scores (17.2% v. 10.6%; p=0.001). Neonates with CLD had increased prevalence of patent ductus arteriosus (30.4% v. 7.7%; p=0.001) and late-onset sepsis (56.5% v. 23.6%; p=0.001). The mortality rate was also higher in CLD babies (10.2 v. 2.4%; p=0.001). Necrotising enterocolitis (NEC) (29.2% v. 8%; p=0.005) and sepsis (83.3% v. 53.8%; p=0.008) were associated with increased mortality. The use of PNCSs was associated with less NEC (3.5% v. 17.2%; p=0.001) and improved survival (95.6% v. 81.7%; p=0.001).

Conclusions. CLD remains a common morbidity in neonates despite advances in neonatal care. The use of PNCSs was shown to have short-term benefits. To get the most out of PNCS use for CLD, further studies need to be conducted to determine the safest type of steroid, safe doses and the duration of treatment.

S Afr J Child Health 2016;10(3):161-165. DOI:10.7196/SAJCH.2016.v10i3.1060

The clinical definition of neonatal chronic lung disease (CLD), also known as bronchopulmonary dysplasia (BPD), has evolved over time. It was first defined by Northway et al.[1] in 1967 as persistent respiratory signs and symptoms along with the need for supplemental oxygen and an abnormal chest X-ray (CXR) at 28 days of age. The definition of CLD was subsequently modified and defines BPD as oxygen dependence at 36 weeks post-menstrual age (PMA) with or without the use of respiratory support and with or without the characteristic radiographical changes.[2] These definitions do not consider gestational age (GA) and do not indicate the level of oxygen dependence, which can range from needing low-flow oxygen to being ventilator dependent. To address this issue, the National Institute of Health (USA) has developed a consensus severity-based definition.

This definition includes all babies born who need more than 21% supplemental oxygen for at least 28 days. CLD is further classified into mild, moderate and severe, depending on the FiO2 needed and the duration of oxygen therapy for preterm babies.[3] Because of the complexity of the definition, some units just consider the need for oxygen on day 28 of life and often refer to this as evolving CLD. The incidence of CLD as defined by the need for oxygen supplementation at 36 weeks PMA is ~30% of premature infants with birth weight (BW) <1 000 g; it is uncommon in infants born at >30 weeksâ&#x20AC;&#x2122; gestation or a weight of >1 250 g.[3] CLD has multifactorial aetiology and remains a major cause of morbidity in premature infants.[1] Contributing factors include infection, exposure to high oxygen levels with the formation of toxic oxygen-free radicals and ventilator-induced lung injury that results in arrested lung development and impaired lung function.[4] Several maternal risk factors, including increasing age, hypertension, lack of antenatal steroid use and chorioamnionitis have been associated with BPD.[4] 161

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The management of CLD includes several preventive and therapeutic strategies that target several pathways and processes involved in the pathogenesis of CLD. Some provide antioxidant protection; others minimise specific aspects of inflammation, reduce elastolytic and proteolytic injury, or regulate growth. In addition, supportive pharmacological treatments that target the development of pulmonary oedema, bronchoconstriction and impaired gas exchange are used. The success of these interventions has been variable.[5] Postnatal corticosteroids (PNCSs) have been extensively studied and have been found to be effective in weaning infants off mechanical ventilation.[6-8] This effect has been proven for dexamethasone, which is the most widely studied PNCS in randomised controlled trials (RCTs). Despite the short-term benefits, dexamethasone has not been shown to reduce the total days of hospitalisation, duration of supplemental oxygen therapy, or incidence of CLD.[6-8] In the era before PNCS treatment, the long-term neurodevelopmental outcome for survivors with CLD was worse than that in similar infants without CLD.[9] However, adverse effects of PNCSs, including hyperglycaemia, gastrointestinal tract (GIT) perforation, hypertension, infection, steroid-induced cardiomyopathy, long-term neurodevelopmental effects and growth retardation complicate the use of PNCSs. The most worrisome long-term effect is increased risk for poor neurological outcome, including cerebral palsy (CP).

Corticosteroids can have direct toxic effects on the developing brain, including neuronal necrosis, interference with healing and inhibition of brain growth.[9,10] A systematic review showed a significantly higher rate of CP after corticosteroid treatment and a non-significant reduction in mortality.[11] A multicentre, double-blinded RCT testing early postnatal dexamethasone therapy for prevention of CLD had to be stopped before completion because of concern about

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RESEARCH serious side-effects such as GIT perforation and periventricular leukomalacia (PVL).[12] The American Academy of Pediatrics (AAP) also recommended that alternative corticosteroids undergo studies and that all infants enrolled in RCTs for PNCSs receive long-term neurodevelopmental follow-up.[13] Owing to concern about the safety of PNCSs, in 2002 the AAP released a policy statement regarding the use of PNCSs for prevention or treatment of CLD, stating that the routine use of dexamethasone could not be recommended.[13] The AAP recommended that dexamethasone use be limited to RCTs with long-term follow-up.

Since the publication of the AAP statement, postnatal use of dexa­ methasone for CLD has reduced; however, the incidence of CLD has not diminished. Some reports have suggested that the incidence and severity of CLD may have actually increased.[14] The data available for PNCS use in CLD are inconclusive and conflicting. As a result, clinicians are advised to use their own clinical judgement to balance potential adverse effects of CLD with the potential adverse effects of PNCS for each individual patient.

The incidence of CLD in very-low-birth-weight (VLBW) babies at Charlotte Maxeke Johannesburg Academic Hospital (CMJAH) is lower than that reported in the Vermont Oxford Network (VON).[15] At CMJAH, babies who are on supplemental O2 for >28 days are given oral prednisolone (OP) for prevention/treatment of CLD. Babies who remain ventilator dependent are given dexamethasone.

Alternative PNCSs include hydrocortisone, nebulised dexa­ methasone and OP.[5] One study looking at the effect of a short course of OP in infants with O2-dependent BPD provided evidence that OP is effective in select patients with BPD.[16] Characteristics of babies with CLD and the use of PNCSs have not been reviewed at CMJAH. This study aimed to describe babies with evolving CLD and to explore the use of PNCSs for evolving CLD at CMJAH. The objectives were to determine the incidence of CLD at CMJAH, to describe clinical and demographic characteristics and survival to discharge in babies with CLD, and to compare these with those of babies without CLD.

Methods

This study was an institution-based retrospective audit conducted in the neonatal unit at CMJAH in Parktown, Gauteng Province, South Africa. Evolving CLD was defined as oxygen use at 28 days of life; the need for supplemental oxygen at 36 weeks PMA was considered as definite CLD (VLBW babies only). Following approval by the Committee for Research in Human Subjects at the University of the Witwatersrand (Medical), a 2-year (1 January 2013 - 30 Dec­ ember 2014) retrospective review of neonatal medical records was performed. Data from the existing CMJAH neonatal database (Research Electronic Data Capture hosted by the University of the Witwatersrand) were used for analysis.[17] The data were collected from clinician-completed hospital records, prospectively on an ongoing basis, for the purpose of clinical audit. All babies admitted to the CMJAH neonatal unit within 72 hours of life (inborn and outborn), with BWs of ≥500 g and who were in hospital for ≥28 days were included. This group was divided into babies with evolving CLD and those without. The neonatal unit at CMJAH has 88 beds, 35 of which are high care, 14 in the paediatric/neonatal intensive care unit, 20 low care and 15 kangaroo mother care. Respiratory support includes early rescue surfactant (SVT), supplemental oxygen via low-flow nasal cannulae (NPO2), nasal continuous positive airway pressure ventilation (NCPAP), intermittent positive-pressure ventilation (IPPV) and high-frequency oscillatory ventilation. Owing to limited resources, ventilatory support in the form of NCPAP was only offered to babies with BW ≥750 g who showed signs of respiratory failure.

Babies with BW ≥900 g who showed signs of respiratory failure on NCPAP or who became apnoeic were offered IPPV. Respiratory failure was defined as O2 saturation <88% on 60% supplemental O2, 162

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respiratory acidosis (pH <7.25 with PaCO2 >60 mmHg) or markedly increased work breathing.

Definitions

Maternal hypertension included both chronic and pregnancyinduced hypertension. Chorioamnionitis was defined as premature and/or prolonged rupture of membranes, fever and foul-smelling liquor in mothers. Resuscitation at birth was defined as the need for bag mask ventilation, chest compressions, or intubation and ventilation. The Ballard score was used to estimate gestational age (GA). Fenton growth charts (2013) were used to assess weight for gestational age.[18] The whole group of neonates was described and then stratified by BW category, namely: • ≥500 - 999 g, extremely low birth weight (ELBW) • ≥1 000 - 1 499 g, very low birth weight (VLBW) • ≥1 500 - 2 499 g, low birth weight (LBW) • ≥2 500 g, normal birth weight (NBW).

Babies were considered to be small for GA if the BW was <10th percentile.[18] The 5-minute Apgar scores were categorised into two groups, namely Apgar score ≤5 and >5. Babies were divided according to GA into two groups, namely <32 weeks and ≥32 weeks. PNCSs were defined as steroids given in an attempt to facilitate weaning of patients off prolonged ventilation or supplemental oxygen. Dexamethasone was given to patients failing to wean off mechanical ventilation. NEC was considered as modified Bell’s stage ≥2.[19] Sepsis was classified as culture-proven bacterial or fungal blood stream sepsis only.

Statistical analysis

The data were assessed for missing information and erroneous or suspicious entries. These entries were verified as far as possible with the original patient records. Information not available from the database was obtained from hospital files drawn from the hospital record archives. The database was then exported to SPSS Statistics version 23.0 (IBM Corp., USA) for analysis.

Babies with evolving CLD

Babies in different weight categories were compared in terms of therapeutic intervention and outcome. Babies who received PNCSs were compared with those who did not, and babies who survived to discharge were compared with those who died. Finally, the CLD group was then compared with the no-CLD group. The data were normally distributed, so continuous variables were described using means and standard deviations (SDs), while frequencies (percentages) were reported for categorical variables. For comparison, χ2 tests were used for categorical variables and independent t-tests for continuous variables. All analyses considered a value of p<0.05 as significant.

Results

There were 485 babies hospitalised for more than 28 days; records were not retrievable for 3 patients. Therefore, 482 patients were included, 237 with evolving CLD and 245 without CLD. The overall incidence of evolving CLD was 5.1%. The incidence in the VLBW babies was 206/1 302 (15.8%) and 31/3 268 (0.94%) in the >1 500 g babies (p<0.0001). The incidence of definite CLD was 98/1 302 (7.5%) in the VLBW babies.

Demographic and birth characteristics are shown in Table 1. There was no difference in the mean (SD) BW between babies with and without CLD (1 017 (101) g v. 1 041 (104) g, p=0.57). Similarly, gestational age was not different between the two groups (CLD 28.2 (1.9) weeks v. no CLD 28.3 (1.9) weeks, p=0.9). There were, however, more babies who were SGA in the no-CLD group than in those with CLD (26.5% v. 12.9%, p=0.03). The percentage of males with CLD was greater (50.2%) than in the no-CLD group (40.8%). There was no significant difference in maternal obstetric and labour-room characteristics between CLD and

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RESEARCH no-CLD babies (Table 1). There were more babies who had 5-minute Apgar scores ≤5 and who needed resuscitation at birth in the CLD group.

Therapeutic interventions, morbidity and outcome are shown in Table 2. Neonates

in the CLD group were more likely to be ventilated and to receive surfactant than those without CLD. The duration of ven­ tilation was significantly longer in babies with CLD compared with those without CLD (15.7 (16.0) days v. 6.1 (2.8) days, p=0.001).

Table 1. Demographic, obstetric and labour room characteristics CLD, n (%)

No CLD, n (%)

χ2

p-value

GA for BW, SGA

30/232 (12.9)

65/243 (26.5)

5.911

0.030

Gender, male

118/235 (50.2)

100/245 (40.8)

5.911

0.016

Black

221/234 (94.4)

237/244 (97.1)

0.038

0.845

Antenatal steroids

93/185 (50.2)

116/219 (52.9)

0.658

0.429

Maternal hypertension

51/206 (24.7)

64/220 (29.0)

1.014

0.328

Chorioamnionitis

7/188 (3.7)

9/223 (4.0)

0.150

0.801

Mode of delivery, CS

133/205 (64.8)

160/241 (66.3)

0.017

0.896

Apgar score at 5 minutes, ≤5

37/214 (17.2)

26/230 (10.6)

85.448

0.001

Resuscitation at birth

100/197 (48.5)

92/231 (39.8)

5.139

0.025

Maternal characteristics

CS = caesarean section.

Table 2. Therapeutic intervention, morbidity and outcome characteristics CLD, n (%)

No CLD, n (%)

χ2

p-value

NCPAP*

120/205 (58.5)

149/237 (62.8)

0.09

0.696

Ventilation

100/233 (42.9)

29/226 (12.8)

15.20

0.001

Postnatal corticosteroids

114/193 (59.0)

13/230 (5.6)

129.07

0.001

Surfactant at anytime

201/232 (86.6)

174/243 (71.6)

16.138

0.001

Therapeutic intervention

Morbidity Necrotising enterocolitis

23/235 (9.4)

14/244 (5.7)

3.323

0.090

Late-onset therapy

133/206 (56.5)

58/245 (23.6)

54.934

0.001

PDA

69/220 (30.4)

19/244 (7.7)

41.508

0.001

Periventricular leukomalacia

3/187 (1.5)

1/131 (0.5)

Mortality

24/236 (10.2)

6/245 (2.4)

12.252

0.001

Need for home oxygen

5/219 (2.2)

0 (0.0)

Outcome

*NCPAP = nasal continuous positive airway pressure ventilation.

Similarly, CLD had an increased duration of NCPAP (5.4 (8.7) days v. 2.9 (6.1) days, p=0.001) and hospitalisation (56.0 (20.7) days v. 42.2 (15.1) days, p=0.001) compared with babies without CLD. However, very few (2.3%) of these neonates with CLD needed home oxygen therapy. Mortality was significantly higher in babies with CLD (10.2% v. 2.4%, p=0.001) and those neonates with CLD were more likely to have a patent ductus arteriosus (PDA) (30.4% v. 7.7%, p=0.001) and late-onset sepsis (LOS) (56.5% v. 23.6%, p=0.001).

The effect of BW in the CLD babies is shown in Table 3. In-hospital mortality (overall 10%) and morbidity in CLD babies was not influenced by BW category. There was, however, a significant difference in the duration of ventilation, with NBW babies staying the longest on the ventilator and VLBW the shortest (31 (21) days v. 12 (12) days). Duration of hospitalisation was longest among the ELBW infants (Table 3).

The use of PNCSs v. no PNCSs in babies with evolving CLD is shown in Table 4.

The overall use of PNCSs was high (55%).

PNCSs were associated with less NEC and a lower mortality; however, the duration of ventilation tended to be longer in babies who received PNCSs. The effect of morbidity and ventilatory support in babies with evolving CLD is shown in Table 5. The incidence of LOS and NEC were significantly higher in the patients who died. The use of early rescue surfactant (SVT) and NCPAP did not improve survival (Table 5), but IPPV was associated with increased mortality: 70.8% v. 39.7% in the non-GLD group.

Discussion

Our study findings showed that evolving CLD in neonates remains a common morbidity in babies at CMJAH, with an overall incidence of 5.1%. The incidence was much higher in the VLBW babies (15.8%). Data from the 2013 and 2014 VON show rates of CLD of between 10.8 and 30.7% among different centres. VON only reports VLBW data; this explains the apparently low incidence of CLD

Table 3. The effect of BW in babies with evolving CLD ELBW, n (%) (n=90)

VLBW, n (%) LBW, n (%) (n=116) (n=21)

NBW, n (%) Total, n (%) (n=10) (N=237)

χ2

p-value

Mortality

10 (11.1)

10 (8.6)

2 (9.5)

2 (20)

24 (10.2)

1.450

0.690

Need for home O2

1/90 (1.1)

3/108 (2.6)

0 (0.0)

1/9 (7.1)

5/219 (2.2)

4.310

0.229

Necrotising enterocolitis

7/89 (7.8)

11 (9.5)

4/20 (20)

2 (20)

24 (10.2)

3.797

0.284

Patent ductus arteriosus

30 (33.3)

38 (32.8)

0

1/5 (7.1)

69/220 (30.4)

5.147

0.161

LOS

59/90 (65.4)

57/116 (49.1)

13/20 (65)

5/10 (35.7)

133/206 (56.5)

6.323

0.970

Duration of hospitalisation (days), mean (SD)

62 (17)

53 (23)

44 (13)

44 (16)

0.001

Duration of ventilation (days), mean (SD)

17 (19)

12 (12)

15 (12)

31 (21)

0.007

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RESEARCH Table 4. The effect of PNCS v. no PNCS use in the evolving CLD PNCS (n=114) Mortality

No PNCS (n=93)

n (%)

n (%)

χ2

p-value

5 (4.4)

17 (18.3)

10.409

0.001

LOS

67 (58.8)

4 (50.5)

1.404

0.148

Necrotising enterocolitis

4 (3.5)

16 (17.2)

11.006

0.001

Patent ductus arteriosus

43 (37.7)

22 (23.7)

4.703

0.350

Home oxygen

3 (2.6)

1 (1.0)

0.530

0.637

NCPAP

104 (91.2)

76 (82.6)

3.430

0.090

Ventilation

43 (38.1)

39 (42.9)

0.484

0.566

Duration of hospitalisation (days), mean (SD)

62 (23.6)

49 (16.2)

0.120

Duration of ventilation (days), mean (SD)

17 (18.1)

10 (10.9)

0.029

Table 5. Morbidity and ventilatory support on survival for babies with evolving CLD Survived, n (%) Died, n (%)

χ2

p-value

Patent ductus arteriosus

62/199 (31.2)

7/22 (31.8)

0.040

1.000

Necrotising enterocolitis

17/212 (8.0)

7/24 (29.2)

10.555

0.005

LOS

114/212 (53.8)

20/24 (83.3)

7.676

0.008

Surfactant

183/209 (87.6)

18/23 (78.3)

1.548

0.206

Ventilation

83/209 (39.7)

17/24 (70.8)

8.510

0.004

NCPAP

178/211 (84.4)

19/24 (79.2)

0.429

0.557

Duration ventilation (days), mean (SD)

15.0 (16.4)

19.1 (13.6)

0.805

Duration of NCPAP (days), mean (SD)

5.0 (8.0)

9.0 (13.2)

0.0001

Duration of hospitalisation (days), mean (SD)

57.3 (20.9)

44.4 (15.1)

0.271

at CMJAH. Although it was not possible to grade the severity of CLD, most babies were not discharged on oxygen, suggesting that there were few with severe disease. More than 50% of neonates with CLD at CMJAH received PNCSs, and the use of PNCSs for CLD was associated with improved survival and less NEC. This is contrary to studies that have shown no significant difference in NEC incidence between PNCS and noPNCS use,[15] and, surprisingly, studies have not shown an association between PNCSs and improved survival.[15] The use of PNCSs at CMJAH was 9.1% of all VLBW infants, which was comparable with that reported in the VON for the same period (2013) at 9.1%.

Our study findings showed that within the group of babies with evolving CLD, BW did not influence survival, reflecting that at CMJAH most babies who die do so within the first week of life or after 28 days of life when BW has less effect on survival. More ELBW babies are being offered ventilatory support now, and those who survive are at higher risk of developing CLD because of severe prematurity. Our study showed that among these CLD patients, there was 164

a significantly increased rate of LOS and PDAs. These findings are in agreement with a study done by Trembath et al.,[20] who outlined the risk factors for CLD. There is much concern surrounding the use of PNCSs, including sepsis and poor neurological outcome (especially PVL and CP). However, there was no significant difference in LOS in the group that received PNCSs compared with those who did not.

Studies have shown an association between use of PNCSs for CLD and PVL.[8,9] The incidence of PVL was very low in the current study and so comparison could not be done.

This study only looked at short-term outcome of neonates with CLD and use of PNCSs. Follow-up to evaluate neurodevelopmental outcome in neonates who received PNCSs is necessary. The use of PNCSs for the prevention and treatment of CLD remains controversial.

This requires investigation with the aim of improving management (prevention and treatment) of CLD in preterm babies.

Study limitations

This was a retrospective analysis from an existing database. Information not routinely SAJCH

collected in the database was not readily available. FiO2 was not recorded, so severity of CLD could not be graded. GA was determined by the attending clinicians and may not be accurate, so the definition of 36 weeks PMA may be inaccurate. LOS was classified as culture-proven bacterial or fungal blood stream sepsis only; endotracheal or induced sputa were not available in the database; therefore, the incidence of sepsis may have been underestimated. The definition of CLD requires that the need for oxygen therapy be for a cumulative ≥28 days and not an acute event. Owing to the retrospective nature of the study, it was not possible to distinguish between babies who had been on O2 for a cumulative 28 days and those who had been acutely placed on O2. The type of steroid administered was not recorded.

Conclusions

CLD remains a common morbidity in VLBW babies despite advances in neonatal care.

More ELBW/VLBW babies are surviving.

The incidence of CLD is not decreasing. The use of PNCSs has shown short-term benefits in terms of its association with improved survival and reduced NEC. Further studies need to be conducted to determine the safest type of steroid, safe doses and duration of treatment to get the most out of PNCS use for CLD. References 1. Northway WH Jr, Rosan RC, Porter DY. Pulmonary disease following respiratory therapy of hyaline-membrane disease: Bronchopulmonary dysplasia. N Engl J Med 1967;276(7):357-368.

DOI:10.1056/NEJM196702162760701 2. Walsh MC, Yao Q, Gettner P, et al. Impact of physiologic definition on bronchopulmonary dysplasia rates. Pediatrics 2004;114(5):1305-1311.

3. Jobe AH, Bancalari E. Bronchopulmonary dysplasia.

Am J Respir Crit Care Med 2001;163(7):1723-1729.

DOI:10.1164/ajrccm.163.7.2011060 4. Klinger G, Sokolover N, Boyko V, et al. Perinatal risk factors for bronchopulmonary dysplasia in a national cohort of very-low-birth weight infants.

Am J Obstet Gynecol 2013;208(2):115.e1-9.

DOI:10.1016/j.ajog.2012.11.026 5. Baveja R, Christou H. Pharmacological strategies in the prevention and management of bronchopulmonary dysplasia. Semin Perinatol 2006;30(4):209-218. DOI:10.1053/j.semperi.2006.

05.008 6. Halliday HL, Ehrenkranz RA, Doyle LW. Early postnatal (<96 hours) corticosteroids for preventing chronic lung disease in preterm infants.

Cochrane Database Syst Rev 2003;(1):CD001146.

7. Halliday HL, Ehrenkranz RA, Doyle LW. Moderately early postnatal (7 - 14 days) corticosteroids for preventing chronic lung disease in preterm infants.

Cochrane Database Syst Rev 2003;(1):CD001144.

DOI:10.1002/14651858.CD001144 8. Halliday HL, Ehrenkranz RA, Doyle LW. Delayed (>3 weeks) postnatal corticosteroids for preventing chronic lung disease in preterm infants.

Cochrane Database Syst Rev 2003;(1):CD001145.

DOI:10.1002/14651858.CD001145 9. Terberg AJ, Pena I, Finello K, Angular T, Hodgman JE. Prediction of neurodevelopmental outcome in infants with and without bronchopulmonary dysplasia. Am J Med Sci 1991;301(6):369-374.

DOI:10.1097/00000441-199106000-00002

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RESEARCH 10. Skidmore MD, Rivers A, Hack M. Increased risk of cerebral palsy among very low birth weight infants with chronic lung disease. Dev Med Child Neurol 1990;32(4):325-331. DOI:10.1111/j.1469-8749.1990.tb16944.x 11. Doyle LW, Halliday HL, Ehrenkranz RA, Davis PG, Sinclair JC. Impact of postnatal systemic corticosteroids on mortality and cerebral palsy in preterm infants: Effect modification by risk for chronic lung disease. Pediatrics 2005;115(3);655-661.

12. Vermont Oxford Network Steroid Study Group. Early postnatal dexamethasone therapy for the prevention of chronic lung disease. Paediatrics 2001;108(3):741-748.

13. Watterberg KL; American Academy of Pediatrics. Committee on Fetus and Newborn. Policy statement - postnatal corticosteroids to prevent or treat bronchopulmonary dysplasia. Pediatrics 2010;126(4):800-808. DOI:10.1542/ peds.2010-1534 14. Yoder BA, Harrison M, Clark RH. Time related changes in steroid use and bronchopulmonary dysplasia in preterm infants. Pediatrics 2009;124(2):673679. DOI:10.1542/peds.2008-2793

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15. Vermont Oxford Network, 2014. http://public.vtoxford.org/ (accessed 28Â September 2015).

16. Bhandari A, Schramm CM, Kimble C, et al. Effect of a short course of prednisolone in infants with oxygen-dependent bronchopulmonary dysplasia.

Pediatrics 2008;121;e344-349. DOI:10.1542/peds.2006-3668 17. Harris PA, Taylor R, Thielke R, et al. Research electronic data capture (REDCap)-A metadata-driven methodology and workflow process for providing translational research informatics support. J Biomed Inform 2009;42(2):377-381. DOI:10.1016/j.jbi.2008.08.010 18. Fenton RT, Kim HJ. A systemic review and meta-analysis to revise the Fenton growth chart for preterm infants. BMC Paediatr 2013;13:59. DOI:10.1186/14712431-13-59 19. Bell MJ, Ternberg JL, Feigin RD, et al. Neonatal necrotizing enterocolitis: Therapeutic decisions based upon clinical staging. Ann Surg 1978;187(1):1-7.

20. Trembath A, Laughon MM. Predictors of bronchopulmonary dysplasia. Clin Perinatol 2012;39(3):585-601. DOI:10.1016/j.clp.2012.06.014

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RESEARCH

This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

Pattern and practice of psychoactive substance abuse and risky behaviours among street children in Cameroon S Cumber, MA, MPH, BA; J Tsoka-Gwegweni, PhD, MPH, MSc, BA, BSc Public Health Medicine, School of Nursing and Public Health, University of KwaZulu-Natal, Durban, South Africa Corresponding author: J Tsoka-Gwegweni (tsokagwegweni@ukzn.ac.za)

Background. Cameroon is among other developing countries reported to be facing an increasing problem of street children involved in drug abuse and other harmful behaviours. Although there are some government efforts to intervene, little is known about the extent of psychoactive substance abuse and the related behaviours among street children in Cameroon. The information is critical to support policy formulation and the implementation of interventions to tackle this problem.

Objective. To document the pattern and practice of psychoactive substance abuse and the related risky behaviours among street children in three cities in Cameroon.

Methods. This study was an analytical cross-sectional survey conducted by the administration of questionnaires to 399 street children who had been homeless for at least a month in three cities of Cameroon during 2015.

Results. All 399 participants reported that they were using some psychoactive substance at the time of the survey. The preferred substances were alcohol (45.9%), tobacco (28.8%), volatiles (11.5%) and cannabis (10.3%). Girls were more predisposed to sex work for survival than boys (p<0.000), with the majority of the participants reporting to have had unprotected sex after using any drug or consuming alcohol (93.98%). In most cases, the pattern and practice of psychoactive substance abuse were higher in the cities of Douala and Yaoundé than in Bamenda. The participants reported that the substances were readily available from street vendors.

Conclusion. The results revealed that the level of psychoactive substance abuse is very high among street children, especially boys, in all three cities. Efforts to prevent and rehabilitate street children from abusing psychoactive substances are required. The government, roleplayers, decision-makers, the ministry of trade and industry and all stakeholders working with street children should consider working together in order to improve the quality of life for street children in Cameroon.

S Afr J Child Health 2016;10(3):166-170. DOI:10.7196/SAJCH.2016.v10i3.1066

Millions of children around the world live on the streets and are being exposed to harmful psychoactive substances. Their right to education, shelter, food, hygiene, healthcare and a loving family has been violated.[1] Street children are defined by the United Nations Children’s Fund (UNICEF) as children in difficult circumstances.[2] However in this study, a street child will be defined as any boy or girl below the age of 18 years, who has taken to the streets (including unoccupied dwellings, wastelands and unfinished buildings) as their habitual abode and source of their livelihood. Although the global estimate of the number of street children is unknown, the existing estimates by UNICEF suggest that there are tens of millions of streetbased children, and ~90% are found in low- and middle-income countries (LMICs).[2,3] Estimates of the prevalence of street children are available in some countries: Ethiopia has over 150 000, Kenya over 300 000, Egypt over 1 million, Bangladesh over 400 000, Latin America over 7 million and Russia has over 16 000 children working on the urban streets.[4,5] Street children are exposed to a number of risks and are more likely to face physical, emotional and sexual abuse, especially at night. There is the risk of unwanted pregnancy, HIV and other sexually transmitted diseases (STDs), from either sexual abuse or from having engaged in risky sexual activities and prostitution.

They often fall sick owing to the harsh cold weather, poor hygiene and sanitation, malnutrition and risk of accidents. Selling or abusing drugs or becoming involved in gang or criminal activities might land them in prison.[4,6-9] Drug use is often characterised by the polydrug use of inexpensive and accessible drugs such as alcohol, tobacco, cannabis and volatiles such as glue, benzene and solvents. These drugs are harmful and even deadly for children below the age of 18 years.[4,10] The long-term effects of solvent abuse include sudden death, 166

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respiratory depression as well as chronic neurological, pulmonary and hepatic toxicity.[3,5] Psychoactive substances are available from roadside traders and sold to minors at a low cost. Although selling drugs to minors is a crime punishable by law in most countries, implementation of the law is often absent. It has been reported that there is a higher prevalence of psychoactive substance abuse among street boys than girls.[11,12] These substances are commonly being consumed by drinking, smoking, sniffing and injecting. Some studies have reported that children abuse these substances to help them cope with the harsh situation on the streets and to give them courage to become involved in risky activities.[13,14] Other studies in Africa have shown that the longer these children are left on the streets, the more frequently they abuse different substances. After a period of time they are more likely to become addicted to these substances.[4,14] Cameroon is one of the many LMICs experiencing an increase in the number of street children living in the major cities.[4,9,13] Government authorities are concerned with the problem of psychoactive substance abuse by these children in Cameroon, yet efforts to implement the intervention process have been slow. Comments from the ministry of children and women affairs state that the ministry has been unable to assess the exact situation and intervene because of insufficient information about the problem.[4,9] The lack of data on the pattern and practice of psychoactive substance abuse and risky behaviours among street children in Cameroon has been the main reason for this study.

Method

An analytical cross-sectional survey of street children aged 12 17 years was conducted from 1 January to 30 March 2015 in the three cities in Cameroon known to have large numbers of street children.

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RESEARCH volatile liquids (11.5%) and cannabis (10.3%) (Fig. 1). When comparing psychoactive substance use by gender, boys reported alcohol (46.9%) and volatiles (11.5%) as their favourite substances, while girls preferred tobacco and cannabis (Fig. 2). The gender differences were not statistically significant (p<0.4699).

n (%)

Variable City Bamenda

125 (31.3)

Douala

137 (34.3)

Yaoundé

137 (34.3)

Gender Boys

320 (80.2)

Girls

79 (19.8)

Age group (years) 12 - 14

89 (22.3)

15 - 17

310 (77.6)

χ2, df=295.5, 4 and p=0.0001 50

45.9

45 40 35 28.8

30 25 20 15

11.5

10.3

10 2.5

5 0 Alcohol

Tobacco

Cannabis

Volatile

Other

Fig. 1. Distribution of preferred psychotic substances used by respondents.

50 45

167

Table 1. Participant characteristics (N=399)

All the participants admitted to having used a psychoactive substance at one point in their life since their being on the streets.

The reasons given for their first use of psychoactive substances were: curiosity (52.6%); peer pressure (27.8%) and emo­ tional problems (19.6%) (Table 2). A similar pattern was observed in each of the three regions. Although clear differences were observed between the overall reasons cited

Results

46.9

χ2, df=3.553, 4 and p=0.4699 41.8

40 32.9

35 Frequency (%)

There were 399 participants who responded to questions on substance abuse in this study.

Of these, 125 (13.4%) were from Bamenda, 137 (34.3%) from Doula and 137 (34.3%) from Yaoundé (Table 1). Approximately fourfifths (80.2%) of the participants were boys.

The mean (standard deviation (SD)) age of study population was 15.4 years (1.1); 310 (77.7%) were 12 - 14 years and 89 (22.3%) were 15 - 17 years (Table 1).

All 399 participants indicated that they were using some type of psychoactive substance at the time of the survey (Table 1). In the study population, the type of psychoactive substance was as follows: alcohol (45.9%) was the most consumed substance, followed by tobacco (28.8%), then

for starting psychoactive substance use, the differences between the regions were not statistically significant (p<0.36). Among

Regional comparisons of the pattern and practice of psychoactive substance use

Frequency (%)

The children were recruited using snowball sampling.[4,9] Informed consent was obtained by the primary researcher using the language in which the children were most comfortable (English, French or a local language). Consent was obtained from all participants in all three cities. Participants had to understand the requirements of the study before signing the consent form. No names were written on the questionnaire and only the authors had access to the data collected. The Catholic Church provided a private, quiet location where the questionnaires were administered with the assistance of six trained research assistants. This was necessary as some of the participants could not read and write.

After the interviews, refreshments were given to the participants and other street children who happened to be around, but no monetary incentive was provided.

Approval to conduct the survey was granted by the University of KwaZulu-Natal Biomedical Research Ethics Committee (ref.: BE331/14) and the Cameroon Bioethics Initiative (ref.: CB1/309/ERCC/CAMBIN).

Questions asked included demographic details, use and names of substances, age at first use of substances, reasons for engaging in the use of the substances, source and person who introduced the child to use substances, the method of ingestion, and involvement in sexual, risky and violent behaviours following use of these substances.

After collection and cleaning, data were captured in a Microsoft Excel spreadsheet (2010; USA) and imported into SPSS statistical package version 19 for windows (IBM Corp., USA) for analysis. Descriptive statistics such as frequency distributions and cross-tabulations were both used to summarise the data. A χ2 test of association was used to assess whether there was any association between region and other categorical variables related to substance use. All the χ2 tests were conducted at 5% significance level.

27.8

30

Male

25

Female

20 13.9

15 9.4

10

12.5 7.6 3.4 3.8

5 0 Alcohol

Tobacco

Cannabis

Fig. 2. Distribution of preferred psychotic substances by gender.

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Volatile

Other

RESEARCH all the participants, the main method of use was smoking (40.9%), followed by drinking (34.3%), chewing (10.5%), sniffing (9.8%) and swallowing (4.5%). There were statistically significant differences (p<0.000) in the main method of using psychoactive substance by region. Drinking, the second overall preferred method of ingesting the substances, was more popular in Yaoundé (40.9%) and Douala (39.4%) and less preferred in Bamenda (Table 2). With regard to the sources of the psychoactive substances, the majority of the participants mentioned that they bought them from roadside petty traders (61.7%) across all the three cities, but more so in Douala compared with Yaoundé and Bamenda. Drug joints seemed to be the least preferred source of substances in Douala and Yaoundé, while bars/clubs were the least preferred supplier of substances in Bamenda (Table 2). There were statistically significant differences in the sources

of the substances between the three cities (p<0.007). Most of the participants were introduced to substance use by their street friends (80%), particularly in Yaoundé and Douala, although some of them were introduced to substance use by their family members (14.4%), a practice commonly observed in Bamenda as opposed to Douala and Yaoundé (Table 2). These sources of influence differed significantly in the three cities (p<0.003).

Pattern of substance abuse and related risky sexual behaviour and violence

Among all 399 participants, 26.8% reported engaging in prostitution after using drugs and/or consuming alcohol, with this pattern similarly observed in all three cities. Also, 55.4% of participants had experienced sexual abuse in the streets after using drugs or

Table 2. Regional comparisons of psychoactive substance (age of first use 12 - 13 years) Total (N=399), n (%)

Bamenda (n=125), n (%)

Douala (n=137), n (%)

Yaoundé (n=137), n (%)

Reasons for first use

p-value 0.36

Curiosity

210 (52.6)

66 (52.8)

76 (55.5)

68 (49.6)

Peer pressure

111 (27.8)

34 (27.2)

31 (22.6)

46 (33.6)

Emotional problem

78 (19.6)

25 (20.0)

30 (21.9)

23 (16.8)

Drinking

137 (34.3)

27 (21.6)

54 (39.4)

56 (40.9)

Smoking

163 (40.9)

47 (37.6)

57 (41.6)

59 (43.1)

Chewing

42 (10.5)

18 (14.4)

13 (9.5)

11 (8.0)

Sniffing

39 (9.8)

25 (20.0)

8 (5.8)

6 (4.4)

Swallowing

18 (4.5)

8 (6.4)

5 (3.7)

5 (3.7)

Drug joints

70 (17.5)

31 (24.8)

18 (13.1)

21 (15.3)

Bars/clubs

83 (20.8)

29 (23.2)

20 (14.6)

34 (24.8)

Roadside petty traders

246 (61.7)

65 (52.0)

99 (72.3)

82 (59.9)

Method of use

0.00

Source of procurement

Persons introducing

0.007

0.003

Street friends

319 (78.0)

86 (68.8)

116 (84.7)

117 (85.4)

Casual acquaintance

37 (9.2)

21 (16.8)

9 (6.6)

7 (5.1)

Family member

43 (10.8)

18 (14.4)

12 (8.8)

13 (9.5)

Table 3. Risky behaviours influenced by substance abuse Behaviour

Total (N=399) Bamenda (n=125) Douala (n=137)

Yaoundé (n=137)

p-value

Ever exchange sex for money after using drugs or consuming alcohol, n (%)

107 (26.8)

32 (26.6)

40 (29.2)

35 (25.6)

0.740

Ever experience sexual abuse in the streets after using drugs or consuming alcohol, n (%)

221 (55.4)

78 (62.4)

66 (48.2)

77 (56.2)

0.117

Ever had unprotected sex after using drugs or consuming alcohol, n (%)

375 (94.0)

119 (95.2)

127 (92.7)

129 (94.2)

0.107

Ever forced a girl to have sex after using drugs or consuming alcohol, n (%)

67 (16.8)

13 (10.4)

38 (27.7)

16 (11.7)

0.000

Used psychoactive substance and had forced sexual intercourse with/(raped) a male/female, n (%)

120 (30.1)

77 (61.6)

27 (19.7)

16 (11.7)

0.000

Used any psychoactive substance but did not use condom during last sexual intercourse, n (%)

306 (76.7)

80 (64.0)

116 (84.7)

110 (80.3)

0.006

Been arrested by the police after using a psychoactive substance, n (%)

225 (56.4)

59 (47.2)

112 (81.8)

54 (39.4)

0.000

168

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RESEARCH consuming alcohol, which was consistent in all three cities (p<0.117) (Table 3). Furthermore, an overall majority of the participants (94.0%) reported that they had unprotected sex (whether abused or not) after using drugs or consuming alcohol. The above practice was witnessed in all three cities with no statistical differences in their frequencies (p<0.107). A considerable proportion of the participants admitted to having been raped/suffered forced sexual intercourse with a boy or girl after using a psychoactive substance (30.0%), with slight differences observed between the regions (Table 3). The majority of the participants (76.7%) reported that they did not use condoms while under the influence of alcohol or drugs. This risky sexual behaviour was more prevalent in Douala (84.7%) and Yaoundé (80.3%) than in Bamenda (64%), showing statistically significant differences (p<0.006). More than 70% of the participants mentioned that they had been involved in a fight after using psychoactive substances, with this behaviour being slightly more pronounced among boys than girls (p<0.495). However, almost 90% of the girls mentioned that they had previously engaged in sex work to survive, compared with only a handful of boys (p<0.000).

Discussion

The study interviewed 399 (320 male and 79 female) street children, all of whom admitted to using psychoactive substances while on the streets. Other studies in Nigeria and India also reported that >70% of street children were abusing psychoactive substances.[2,3] Further studies have showed that more boys than girls abuse psychoactive substances. A reason could be that there are more street boys than girls in urban cities and because boys are more exposed to risky behaviour than girls, particularly in most African countries.[2,6,8] This study found that curiosity, peer pressure and emotional problems were the main reasons for children engaging in psychoactive substance abuse. Similar findings were reported in some African studies.[4,5] Other reasons such as ‘courage and confidence to face and forget the hardships encountered on the streets’, and ‘a coping strategy when feeling sick or depressed’ have also been reported.[3,5] These reasons are not similar to studies of psychoactive substance abuse conducted with non-street children. Children under proper adult supervision are more likely to abuse substances because of peer pressure.[4,7] The majority of street children cited alcohol as the preferred psychoactive substance, followed by tobacco. The most preferred methods of ingesting the substances into their system were by drinking and smoking, and these results were the same across all three regions. A study in Nigeria also produced similar results of abusing mostly alcohol and tobacco.[5] Slightly different results have been reported in another study in Nigeria and in Egypt on street children. Both studies reported a high prevalence in the abuse of other psychoactive substances such as glue, benzene, petrol and paint because of their availability (children buy from supermarkets, retailers and street vendors at a much cheaper price).

They can become addicted to these substances after a certain period of frequent use.[5,11] Significant differences were reported among street/homeless youths in developed countries, where they inject the drugs into their system, placing them at direct risk of several health problems.[1,7] The global differences could also be attributed to the inequality around access and the socioeconomic status of the respective participants in developing and developed countries.

More than 60% of the participants identified roadside petty traders (street vendors) as their main supplier of psychoactive substances, raising questions regarding the regulation of informal trading to minors in Cameroon.[13] Similar negligence in policy implementation is common in most LMICs. Some traders are not even aware that selling psychoactive substances to a minor is a crime punishable by law.[8,9] However, a completely different result was reported in a study in South Africa (SA), where street children have reported seeking assistance from adults to buy them psychoactive substances from 169

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supermarkets and other roadside shops. This is so because it is illegal and punishable by law to sell alcohol, tobacco and other harmful substances to minors, a policy which is generally known by shop owners. However, implementation is not 100% as some traders are more interested in making money than respecting state policies.[6,7] Regional comparisons reveal some unexpected differences between the three cities of Bamenda, Douala and Yaoundé in Cameroon. The percentage of sniffers was high in Bamenda, possibly because of the easy access to sniffers from surrounding villages, and because it is still a culturally accepted practice by the elderly in the community.

Douala had the highest percentage of participants accepting sexual intercourse without condoms and being arrested by the police. This could be because Douala is a city characterised by diverse business enterprises, while Yaoundé is a political capital dominated by administrative activities with high-class dignitaries. In comparison with both cities, Bamenda is a laid-back city known for multicultural activities and political uprising from opposition party leaders.

Results from this study also showed that most of the street children were initiated into abusing psychoactive substances by their peers on the streets. Another study from Cameroon and results from a literature review on street children in Africa also reported similar results.[12,13] It is common knowledge that abuse of these substances is harmful and deadly when ingested into the system, and that risky behaviours by street children can lead to health and social problems.

The association between smoking and tuberculosis/lung cancer is well documented.[14] The abuse of psychoactive substances also puts street children at further risk owing to their frequent involvement in crime, violence, rape, sexual abuse and unprotected sex, which could lead to police arrest, injuries, emotional trauma, unwanted pregnancies, STDs and HIV infections.[1,4] Studies elsewhere have documented the link between HIV/AIDS and substance abuse.[1,14] SA and other countries in sub-Saharan Africa are noted for violence, gender-based violence, rape, sexual abuse and HIV/AIDS.The above behaviours of street children would simply further perpetuate the public health concerns.[4,6,14] However, in SA, the use of a concoction of very harmful drugs (such as rat poison combined with HIV treatment drugs), encourages behaviours such as rape and horrific killings.[6] Some of these dangerous behaviours were sadly revealed in our study, where the majority of participants agreed to have been involved in violence, rape or forced sexual intercourse, sex work and having unprotected sex. Collaboration and immediate interventions by all stakeholders will be the best strategy to help reduce the number of street children in urban cities, thereby protecting them from abusing psychoactive substances. There is a need for formal and health education about the dangers of living on the streets and abusing psychoactive substances.

Early detection through the screening of street children who are addicted to any of the psychoactive substances should be introduced by social workers and other organisations. Because of the complexity of the problem of street children, the involvement of all stakeholders will be necessary for intervention and rehabilitation to be sustainable and affordable. The authors urge the Cameroon government to consider improving the lives of children and families generally in a bid to avoid increasing numbers of children leaving their homes and taking to the streets. All the stakeholders involved with street children should work together and act urgently to address the poverty and challenges these children face while on the streets in urban cities. They should ensure that access to harmful substances is banned for unlicensed traders and enforce strict regulations for street traders selling psychoactive substances in order to stop the trade with minors.

Conclusion

Children living on the streets and engaging in psychoactive substance abuse is a problem in all three cities studied in Cameroon. Initiation into psychoactive substances was by peers, while addiction to any harmful substance was a direct result of the amount of time they have

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RESEARCH been living on the streets. Abuse was more prevalent among boys than girls. Street children mostly use alcohol and tobacco because it is cheap and available from roadside traders. These are important factors that should be taken into consideration when designing public health policies for street children. Immediate intervention and rehabilitation for these children is needed.

References 1. Akinade EA. Risk-taking behavior and substance abuse vis-a-vis HIV transmission in African societies. J Instruct Psychol 2001;28(1):3.

2. Morakinyo J, Odejide AO. A community based study of patterns of psychoactive substance use among street children in a local government area of Nigeria. Drug Alcohol Depend 2003;71(2):109-116. DOI:10.1016/s0376-8716(03)00093-0 3. Seth R, Kotwal A, Ganguly KK. Street and working children of Delhi, India, misusing toluene: An ethnographic exploration. Subst Use Misuse 2005;40(11):1659-1679. DOI:10.1080/10826080500222792 4. Woolf-King SE, Maisto SA. Alcohol use and high-risk sexual behavior in sub-Saharan Africa: A narrative review. Arch Sex Behav 2011;40(1):17-42.

DOI:10.1007/s10508-009-9516-4 5. Morantz G, Cole D, Vreeman R, Ayaya S, Ayuku D, Braitstein P. Child abuse and neglect among orphaned children and youth living in extended families in

170

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sub-Saharan Africa: What have we learned from qualitative inquiry? Vulnerable Child Youth Stud 2003;8(4):338-352. DOI:10.1080/17450128.2013.764476 6. Pluddemann A, Parry C, Cerff P, et al. Monitoring alcohol and drug abuse trends in South Africa. Drug Alcohol Rev 2008;2:185-189.

7. World Health Organization. Management of Substance Abuse. Geneva: WHO, 2008. http://www.who.int/substance_abuse/en/2008 (accessed 12 September 2013).

8. Nada KH, Suliman el DA. Violence, abuse, alcohol and drug use, and sexual behaviors in street children of Greater Cairo and Alexandria, Egypt. AIDS 2010;24(2):S39-S44. DOI:10.1097/01.aids.0000386732.02425.d1 9. Ennew J. Difficult circumstances: Some reflections on street children in Africa.

Africa Insight 1996;26(3):203-210.

10. Elkoussi A, Bakheet S. Volatile substance misuse among street children in Upper Egypt. Subst Use Misuse 2011;46(1):35-39. DOI:10.3109/10826084.2011.580202 11. Nada KH, Suliman el DA. Violence, abuse, alcohol and drug use, and sexual behaviors in street children of Greater Cairo and Alexandria, Egypt. AIDS 2010;24:S39-S44. DOI:10.1097/01.aids.0000386732.02425.d1 12. UNICEF. Street and unsupervised children of Africa, 2003. http://www.unicef. org/Africa/street_children_Report_Eng.pdf (accessed 30 April 2015).

13. Matchinda B. The impact of home background on the decision of children to run away: The case of Yaounde City street children in Cameroon. Child Abuse Negl 1999;23(3):245-255. DOI:10.1016/S0145-2134(98)00130-6 14. Odejide AO. Status of drug use/abuse in Africa: A review. Int J Ment Health Addict 2006;4(2):87-102. DOI:10.1007/s11469-006-9015-y

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RESEARCH

This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

The existence of policies, practices and perceptions regarding children as visitors to public hospitals in uMgungundlovu, KwaZulu-Natal Province P Appalsamy,1 MB ChB, DCH (SA), HIV Dip Man (SA), FC Paed (SA); N H McKerrow,1,2 MB ChB, BA, DCH (SA), FC Paed (SA), MMed (Paeds), PG Dip Int Res Ethics Department of Paediatrics and Child Health, Nelson R Mandela School of Medicine, Faculty of Health Sciences, University of KwaZulu-Natal, Durban, South Africa 2 Department of Health KwaZulu-Natal, Durban, South Africa 1

Corresponding author: P Appalsamy (pranesha_appalsamy@yahoo.com) Background. Current policies and practices regarding child visitors in hospitals in uMgungundlovu, KwaZulu-Natal Province, South Africa, are unknown. Existing literature focuses on provision for child visitors in specialised units in well-resourced countries.

Objective. To identify policies, describe current practices and determine the perceptions of healthcare workers to child visitors.

Methods. Interviews were conducted with 7 nursing managers regarding the existence and content of a hospital visitors’ policy, 12 oper­ ational managers (OMs) to describe ward practices regarding child visitors, and 12 professional nurses and 11 doctors to determine their attitudes towards children as visitors in all four general state hospitals in uMgungundlovu between October 2013 and July 2015.

Results. Five out of seven nursing managers were aware of a visitors’ policy in their hospital. These policies allowed children to visit family or parents in adult wards, but only 2 would allow children to visit a family member and only 1 would allow visits to a friend in the children’s wards. According to the nursing managers, policy was that the visitor must be over 5 years of age to visit in an adult ward while 2 out of 3 nursing managers allowed only children over 12 years of age to visit in children’s wards. Visits must occur during prescribed visiting times and the visitor must be accompanied by an adult. In practice, 7 out of 12 OMs allow child visitors in their wards. Only 2 out of 7 OMs allow unrestricted visitation by children and only to non-infectious patients in children’s wards – this is subject to variable age restrictions in adult wards and an age limit of 12 years in children’s wards. In all wards, visits by children are restricted to prescribed visiting times and conditional on an adult escort. Three out of seven OMs allow 2 visitors only, although most (5 out of 7) allow visits of unlimited duration.

Staff who favoured child visitors were more likely to be younger, male and employed as health professionals for <5 years. More doctors than nurses believed that children should be allowed to visit family and/or friends in hospital. Justifications for not allowing children to visit centred on infection risks and the emotional trauma of visiting a sick loved one. The child, patient and health professional were seen to benefit socially from child visitors, although there are positive and negative emotional consequences for the patient and the child.

Conclusion. Hospitals do make provisions for visitors, but most exclude young children, particularly those who are most vulnerable to the negative consequences of separation from a parent or family member. While policies do exist to guide child visitation in uMgungundlovu, such policies are restrictive, inconsistent and do not necessarily reflect day-to-day practices.

S Afr J Child Health 2016;10(3):171-175. DOI:10.7196/SAJCH.2016v10i3.1098

Disruption of the family unit by hospitalisation can cause major physical and psychological stress for patients and their families, particularly children. Flexible visiting policies are advocated as a positive intervention to help families cope with the stress of illness.

Current surveys, conducted in the adult critical care setting in wellresourced countries, have shown that children are still restricted from visiting.[1] Reasons for such restrictions stem from children disrupting the running of the unit, nurses being unable to cope with their queries and emotions, physicians disapproving of visits and the risk of infection. However, no evidence has been found that visiting children are more prone to infection.[2] Knutssen et al.[3] showed that children actually benefit from visits through increased understanding and involvement in the wellbeing of their family as well as reduced feelings of separation, guilt, fear, helplessness and abandonment.

In South Africa (SA), hospital visiting policies are available to the public online. In Groote Schuur Hospital,[4] a maximum of three visitors are allowed per patient in the general ward and two in the maternity wards and intensive care unit (ICU). Children <12 years old are not permitted to visit unless the patient is the parent or sibling and only if supervised by an accompanying adult.

If a patient’s condition deteriorates, visiting is at the discretion of 171

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the sister in charge and the duration of the visit restricted if it is considered to be detrimental to the patient’s wellbeing. Steve Biko Academic Hospital[5] does not allow children to visit paediatric wards for infection control purposes. Similarly, Inkosi Albert Luthuli Central Hospital[6] does not allow children <12 years in the hospital.

While hospitals allow both adult and paediatric patients to be visited by family and friends, most exclude children as visitors. Existing literature[1-3,7-9] regarding children as visitors to hospitals is limited to ICUs in well-resourced countries. No studies are available on current policies or practices regarding child visitors locally, in SA, or in other resource-limited, non-critical-care settings. This study was undertaken to describe current policies, practices and perceptions of healthcare workers (HCWs) to child visitors in public sector hospitals in the uMgungundlovu district of KwaZulu-Natal (KZN) Province, SA.

Methods

uMgungundlovu comprises 7 municipalities, within which there are 9 state hospitals – 4 are general hospitals, 2 are for TB and 3 are psychiatric hospitals. All four general state hospitals agreed to participate in the study but two private hospitals that were invited to participate declined the invitation. This descriptive study was

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RESEARCH undertaken in the four general state hospitals in uMgungundlovu, including district, reg­ ional and tertiary hospitals in urban, periurban and rural settings. In each hospital, staff who had worked in the relevant ward for at least 3 months were recruited from an adult female, an adult male and a children’s ward. Specialised hospitals and temporary or newly appointed staff in general hospitals were excluded. Three groups of health professionals were interviewed using ques­ tionnaires aimed at determining the following information: (i) nursing managers: regarding the existence and content of a hospital visitor’s policy; (ii) ward operational managers (OMs): to describe practices and the rationale regarding child visitors; and (iii) professional nurses (PNs) and doctors: to determine their attitudes towards children as visitors in their wards. Questionnaires were not piloted prior to administration and hospital visitor policies were not collected to validate the findings. Ethical approval was obtained from the Biomedical Research Ethics Committee of the University of KZN.

Results

Table 1. Visitor policy according to nurse managers Adult nurse manager (n=3)

Paediatric nurse manager (n=4)

Total (N=7)

Policy available

2

3

5

Duration of policy >10 years

1

3

4

Annual

2

2

4

5 years

-

1

1

All patients

2

1

3

Non-infectious

-

2

2

Unrestricted

-

1

1

Restricted

2

2

4

Unrestricted

-

1

1

Restricted

2

2

4

Unlimited

1

1

2

Two only

1

2

3

Parents

1

-

1

Family

1

2

3

Anyone

-

1

1

Any age

-

1

1

>5 years

2

-

2

>12 years

Policy

Frequency of review

Patient Who may be visited

Who is allowed to visit

Visiting times

Number of visitors allowed

A total of 42 participants were interviewed, 39 personally and 3 telephonically, including 7 nurse managers, 12 OMs, 12 PNs and 11 doctors, representing adults’ and children’s wards. Table 1 depicts the responses of nursing managers regarding the existence of a hospital visitors’ policy and details of how long it has existed, how often it is reviewed and the various stipulations pertaining to the patient and visits from children.

Five out of seven nursing managers were aware of a visitors’ policy in their hospital, and the remaining two reported using the infection prevention and control policy instead. When present, most of the visitors’ policies had existed for more than 10 years, were developed within the hospital and were reviewed annually. The policies made provision for visits: • to all patients in adult wards, but 2 out of 3 restricted visits to non-infectious cases in children’s wards • by anyone >5 years of age in adult wards, but only by people >12 years of age in children’s wards • during prescribed visiting times in adult wards, while 1 out of 3 allowed visitors at any time in children’s wards • restricted to 2 visitors at a time in 3 of the 5 policies according to the nursing managers.

• to adult wards if they are >5 years of age, and 2 out of 3 only allowed children >12 years of age to visit in children’s wards • during prescribed visiting times in both wards if accompanied.

The policies allowed child visitors: • to family or parents in an adult ward, but only 2 out of 3 allowed children to visit family members and only 1 out of 3 allowed children who are friends to visit a patient in a children’s ward

Justifications for these restrictions are to: protect children from infection; spare them from emotional trauma; and avoid separation anxiety.

Table 2 reflects the responses of the OMs in the wards regarding the existence of a hospital visitors’ policy and their day-to-day practice

172

Child visitors Who may they visit

Who may visit

-

2

2

Prescribed visiting times

2

3

5

Children must be accompanied by an adult

2

3

5

Infection control

2

2

4

Emotional trauma

1

-

1

Separation anxiety

-

1

1

Reasons for not allowing visits

SAJCH

in terms of the stipulations of the policies pertaining to both the patient and child visitor.

Of the 12 OMs, 7 allowed child visitors in their wards. The remainder excluded children to limit their exposure to infections, and in one adult ward out of concern that psychiatric/mentally unstable patients could pose a threat to the children. Only two OMs in adult wards allowed children to visit any category of patient, but the remaining two and all OMs in children’s wards would only allow children to visit non-infectious patients.

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RESEARCH Table 2. Visitor practices according to ward OM Adult ward Paediatric ward Total OM (n=8) OM (n=4) (N=12) Policy Availability of policy

7

3

10

4

3

7

Practice Allow children to visit Reasons if not allowed Infection control

4

3

7

Hazardous

1

3

1

Patient – who may be visited All patients

2

-

2

Non-infectious

2

3

5

-

-

Child visitors – who may be visited Parents

-

Family

4

2

6

Anyone

-

1

1

1

-

1

Who may visit Any age >5 years

1

-

1

>12 years

2

3

5

4

3

7

4

3

7

Visiting times – prescribed Children must be accompanied Number of child visitors Unlimited

2

1

3

Two only

1

2

3

Other

1

-

1

Length of time allowed Limited

1

1

2

Unlimited

3

2

5

Children may visit only family in adult wards but anyone in children’s wards – subject to variable age restrictions in adult wards and an age limit of 12 years in children’s wards. In all wards, visits by children were restricted to prescribed visiting times and under adult supervision.

Three out of 7 OMs allowed two visitors at a time and most (5 out of 7) allowed visits of unlimited duration. More doctors than nurses believed that children should be allowed to visit family and/or friends in hospital (Table 3). More doctors (8 out of 11) would allow children to visit family and/or friends than nurses (5 out of 12). All 4 doctors but only 2 out of 4 PNs in children’s wards would allow child visitors.

A similar pattern was found among staff in the adult ward, although three-quarters of PNs in female wards but none in male wards would allow child visitors. Staff who would allow child visitors tended to be: • younger: 6 out of 8 among 20 - 29-year-olds would allow child visitors, reducing to 2 out of 5 at 40 - 49 years • male: 4 out of 5 would allow child visitors compared with 9 out of 18 of female staff • employed as health professionals for <5 years: 5 out of 6 v. 3 out of 8 of staff employed for 5 - 10 years and 5 out of 9 of those employed for >10 years.

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Table 3 describes the perceptions of PNs and doctors towards the patient being visited by children and explores the reasons for various decisions. More doctors than nurses believed children should be allowed to visit sick family and/or friends. For both cadres this was true for a greater proportion of staff in paediatric than adult wards.

Reasons for restricting children centred on infection risks and the emotional trauma of visiting a sick loved one. Contrary to this, one doctor felt children should only be allowed to visit the terminally ill. Most staff believed that only select patients should be visited, with both nurses and doctors relating this restriction to infection risks and emotional trauma of visiting a sick loved one. Doctors felt that the hospital environment can be hazardous for children and that only terminally ill patients should get preference with regard to child visitors. Staff who would allow all patients to be visited would do so to strengthen family ties (all doctors held this belief) and respect patient’s rights. Nurses felt that the patient should be stable and provisions could be made to facilitate visits to infectious patients. Staff also believed in restricting whom children can visit.

Doctors confined visits to family members, while 2 out of 5 nurses supported visits to friends too. Half of doctors, but only 1 out of 5 nurses, believed children of any age should be allowed to visit. Most nurses would restrict child visitors to those >12 years, while 2 out of 8 doctors suggested maturity rather than age should determine which children can visit. All staff believed child visitors should be restricted to prescribed visiting times and accompanied during visitation. Most staff, especially nurses and those in adult wards, would limit the number of visitors but not the duration of the visit. With regard to consequences of child visitors, HCWs felt that all three cadres, the child, the patient and the health professional, benefitted socially, while there are positive and negative emotional consequences for the patient and child. Reported benefits for the child included the joy of seeing his/her parent/family and reassurance regarding their presence/existence and wellbeing. Benefits for the patient included happiness at seeing their child, strengthening family bonds and speedier recovery. Deleterious consequences for the child centered on infection risks and the emotional trauma of seeing terminally ill patients. Negative effects on the patient focused on emotional upset and possible depression after the child leaves. Furthermore, the parent/caregiver may not want to be seen as physically unfit to the child. Benefits to the HCW focused on improvement of in-patient care, clinical outcomes and recovery time, thereby decreasing their burden of work. The main emotional advantage included having to deal with a patient who does not have anxiety and stress caused by thinking of his/her children at home. Key disadvantages were the disruption child visitors can cause to the ward routine and need for the supervision and control of unruly children. Moreover, HCWs were concerned about the child’s health and safety, and having to deal with a child who reacts negatively to an ill patient.

Discussion

Not all nursing managers in hospitals in uMgungundlovu reported the existence of a hospital visitors’ policy. Available policies defined the category of the patient to be visited, his/her relationship to the visitor, the number and age of child visitors allowed, as well as the times and duration of visits. With regard to child visitor practices, differences were noted among the three cadres of staff, with 7 out of 12 OMs, 5 out of 12 PNs and 8 out of 11 doctors supporting child visitors. This differs from international experience of ICU visiting policies that, despite being specialised units, are less restrictive on child visitors. Quinio et al.[7] found that only 11% of 200 ICUs in France excluded children as visitors, while only 3.9% of ICUs in a UK survey[8] did not permit children. Similarly, in 69 US hospitalbased maternity units, only 5.8% did not allow any children to visit.[9] While only 1 out of the 5 nursing managers (who were aware of a visitor’s policy) indicated that their policy allowed children to visit

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RESEARCH Table 3. Perceptions of PN and doctors regarding child visitors Adult ward

Paediatric ward

Total

PN Doctor (n=8) (n=7)

PN Doctor (n=4) (n=4)

PN Doctor (N=12) (N=11)

3

4

2

4

5

8

4

1

2

-

6

1

Perception Children should be allowed to visit Reasons if not allowed Infection control Emotional trauma

-

1

1

-

1

1

No reason given

1

-

-

-

1

-

Preference to terminally ill only

-

1

-

-

1

-

2

1

1

1

3

2

5

4

2

2

7

6

Patient Who may be visited – all patients Reasons for restrictions Infection control Emotional trauma

1

3

1

-

2

3

Patient dependent

-

1

-

1

-

2

Hazardous environment

-

-

-

1

-

1

Reasons for allowing visit Family bonding

1

-

-

-

1

Patient’s right

1

1

-

-

1

Special provisions

1

-

-

-

1

Patient dependent

-

-

1

1

1

1 1

Child visitors – who may be visited Parents

1

1

-

-

1

1

Family

1

3

1

4

2

7

Anyone

1

-

1

-

2

Who may visit Any age

-

2

1

2

1

4

>5 years

1

1

-

1

1

2

>12 years

2

-

-

-

3

-

Other

-

1

1

1

-

2

Visiting times – prescribed

3

4

2

4

5

8

Must children be accompanied

3

4

2

4

5

8

Number of child visitors Unlimited

-

2

1

1

1

3

2 only

2

1

1

1

3

2

1

1 only

1

1

-

1

Other

-

-

-

1

2

Limited

1

1

1

2

2

3

Unlimited

2

3

1

2

3

5

1

Length of time allowed

without any age limit, this is not common practice. Only 1 out of 7 allowed child vis­ itors of any age, and 5 OMs limited visits to children >12 years. Age restrictions are common, and 12 years is the most common threshold for child visitors. This threshold is 174

applicable in 76.9% of ICUs in Brazil[10] and in 44% of French units that fixed a minimum age limit for visits; the mean age limit was also 12 years.[7] Similarly, some children’s hospitals in the USA only allow child visitors above 12 years old, while others screen for SAJCH

illness before allowing visitation.[11-13] Local restrictions are more severe than those in published reports: 46% of child visitors in French ICUs[7] are allowed to visit without age limits, while 28.9% of US maternity wards[9] allowed open visitation for children during the intrapartum period, rising to 82.6% during the postpartum period. Open visitation was defined as no restrictions based on the child’s age, relationship to the mother or specific visiting hours, and only 5.8% of units physically assessed or observed children for signs of illness prior to visiting.

PNs in our study were more supportive of child visitation in the female than the male wards, possibly indicating preference given to maternal rather than paternal caregivers.

According to the visitors’ policy in our hospitals, 3 out of 5 nursing managers would allow all patients to be visited irrespective of their disease profile. However, only 1 would allow the patient to be visited by anyone – inclusive of both family and friends. In practice, this is reduced to only 2 out of 7 OMs allowing all patients to be visited and 1 out of 7 OMs allowing the patient to be visited by anyone, which demonstrates incongruences between policy and practice.

However, nurses were more likely to allow unrestricted visitation to patients, and 2 out of 5 would allow visits to/both family and friends. This incongruency has been noted elsewhere where restrictive policies exist, but are not always enforced by nursing staff.[9,14] While only one of the staff felt that critically ill patients should get preference for visits by children, this perception is also evident in certain ICUs in the UK where visitation increased in the case of a dying patient.[8] Two out of five nursing managers indicated that their visitors’ policies allowed an unlimited number of visitors. This is endorsed by OMs, although nurses and doctors were more restrictive, with 1 out of 5 nurses and 3 out of 8 doctors allowing an unlimited number of visitors. This differs from many ICU visiting polices that allow just two visitors at a time.[7,8] The literature describes three visiting policies pertaining to time limits. Open visitation allows families to visit at any time in a 24-hour period. Liberalised visiting allows visitors access at a time determined by the staff. Restrictive policies allow a fixed number of visitors at the same time for everyone.[7] In this study, the visitors’ policies prescribed restrictive visiting times that were enforced in adult wards but not in children’s wards, a third of which practise open visitation. The policy is in accordance with ICUs in Europe and the UK that adopt restricted visiting hour policies.[7,8] Many members of staff supported visits of unlimited duration; however, they did specify that children should be accompanied.

Similarly, Ottawa General Hospital[15] in

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RESEARCH Canada allows children under the age of 12 only if accompanied by an adult. In SA, current child visitor policies vary. Groote Schuur Hospital[4] allows children under the age of 12 years to visit only if the patient is a parent or sibling of the child and provided that the child is under adult supervision. Steve Biko Academic Hospital[5] does not allow children to visit in paediatric wards for infection control purposes. Inkosi Albert Luthuli Central Hospital[6] does not allow children <12 years in the hospital.

The focus of available literature is on ICUs in well-resourced settings, which differ from the generalist hospitals included in our study. In exploring the perspectives of HCWs, child visitors were favoured more among the younger, less-experienced male staff.

Years of training, past experience and specific experience within certain patient populations may contribute to the impression of perceived risk or benefit, leading to either restrictive or liberal practices. The most common reason cited for promoting restrictive policies was the protection of the child from infection and emotional distress.[7] Child visitation has been shown to benefit both the child and the patient, particularly when this is a sibling, and children who are allowed to visit the neonatal ICU show less negative behaviour and more knowledge about their ill sibling.[16] In this study, HCWs felt that the child and patient would benefit socially, while acknowledging the positive and negative emotional consequences. These concerns are in keeping with studies that have shown that one of the rationales for restrictive policies is to protect the patient from psychological stress that can be caused by the family.[7]

Study limitations

This was a small descriptive study in one health district in KZN; therefore, caution must be taken in interpreting and generalising the findings. Clearer definitions were required for the advantages and disadvantages of child visitors. Additionally, nursing managers’ responses were not validated with the actual visitor policy for each hospital.

Conclusion

Available literature regarding child visitor policies and practices is based on developed countries, ICU settings and adult patient populations. This is in contrast to the generalist hospitals included in our study, reflecting both adult and children’s wards. Hospitals do make provision for visitors, but most exclude young children who are most vulnerable to the negative consequences of separation from loved ones. Nevertheless, children need and have a right to visit parents and siblings admitted to hospital.

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While policies do exist to guide child visitation in uMgungundlovu, they are restrictive, inconsistent and do not necessarily reflect day-today practices. Furthermore, the difference between practices and the views of different cadres of staff reflects the complexity of the subject.

Attitudes to visiting children must therefore be discussed at all levels and a consensus based on the needs of the patient, child and HCW should be reached.

Recommendation

Liberalised hospital visitor policies that consider the rights of children should be available and implemented uniformly by all cadres of staff.

References 1. Clarke C, Harrison D. The needs of children visiting our adult intensive care units: A review of the literature and recommendations for practice. J Adv Nurs 2001;34(1):61-68. DOI:10.1046/j.1365-2648.2001.3411733.x 2. Knutsson S, Bergbom I. Nurses’ and physicians’ viewpoints regarding children visiting/not visiting adult ICUs. Nurs Crit Care 2007;12(2):64-73. DOI:10.1111/ j.1478-5153.2007.00209.x 3. Knutsson S, Samuelsson IP, Hellström AL, Bergbom I. Children’s experiences of visiting a seriously ill/injured relative on an adult intensive care unit. J Adv Nurs 2008;61(2):154-162. DOI:10.1111/j.1365-2648.2007.04472.x 4. Groote Schuur Hospital. Visiting hours. http://www.gsh.co.za (accessed 22 March 2016).

5. Steve Biko Academic Hospital. http://www.sbah.org.za/index.php/information/ important-information (accessed 22 March 2016).

6. Inkosi Albert Luthuli Central Hospital. Patients/Visitors. http://www.ialch. co.za (accessed 5 February 2016).

7. Quinio P, Savry C, Deghelt A, Guilloux M, Catineau J, de Tinténiac A. A multicenter survey of visiting policies in French intensive care units. Intensive Care Med 2002;28(10):1389-94. DOI:10.1007/s00134-002-1402-7 8. Hunter JD, Goddard C, Rothwell M, Ketharaju S, Cooper H. A survey of intensive care unit visiting policies in the United Kingdom. Anaesthesia 2010;65(11):1101-1105. DOI:10.1111/j.1365-2044.2010.06506 9. Spear HJ. Child visitation policy and practice for maternity units. MCN Am J Matern Child Nurs 2009;34(6):372-377. DOI:10.1097/01.NMC.000363686.

20315.d5 10. Fernando JSR, Renata RLF, Luciano CPA, Guilherme S. Intensive care unit visitation policies in Brazil: A multicenter survey. Rev Bras Ter Intensiva 2014;26(4):339-346. DOI:10.5935/0103-507X.20140052 11. Children’s Hospital Colorado. Visitation policies at Children’s Hospital Colorado. http://www.childrenscolorado.org (accessed 5 February 2016).

12. Boston Children’s Hospital. For patients and families. http://www.childrens­ hospital.org (accessed 5 February 2016).

13. SickKids. Visiting SickKids. http://www.sickkids.on.ca (accessed 5 February 2016).

14. Simon SK, Phillips K, Badalamenti S, Ohlert J, Krumberger J. Current practices regarding visitation policies in critical care units. Am J Crit Care 1997;6(3):210217. DOI:10.109700003246-199501001-00045 15. The Ottawa Hospital. Patients and visitors. http://www.ottawahospital.on.ca (accessed 5 February 2016).

16. Barkmann C, Romer G, Watson M, Schulte-Markwort M. Parental physical illness as a risk for psychosocial maladjustment in children and adolescents: Epidemiological findings from a national survey in Germany. Psychosomatics 2007;48(6):476-481. DOI:10.1179/appi.psy.48.6.476

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RESEARCH

This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

Clinical presentation of infants hospitalised with pertussis G Kahl,1 MB BCh, DCH, MMed (Paed), FC Paed (SA); U M Hallbauer,1 MB BCh, MPraxMed, DCH, MMed (Paed), FC Paed (SA); G Joubert,2 BA, MSc 1 2

Department of Paediatrics and Child Health, Faculty of Health Sciences, University of the Free State, Bloemfontein, South Africa Department of Biostatistics, Faculty of Health Sciences, University of the Free State, Bloemfontein, South Africa

Corresponding author: G Kahl (gkahl11383@yahoo.com) Background. Despite the widespread use of pertussis vaccine, there has been a resurgence of pertussis cases in developed and developing countries. South Africa lacks data regarding clinical presentation and healthcare impact of pertussis.

Objectives. To describe the clinical presentation and healthcare impact in hospitalised infants with confirmed pertussis.

Methods. This was a retrospective cohort study, conducted in Bloemfontein between April 2008 and September 2012. Infants with laboratory-confirmed pertussis (group 1; N=102), were compared with infants with a negative pertussis result (group 2; N=104) and infants with a lower respiratory tract infection of unspecified aetiology (group 3; N=104). The following data were extracted from the clinical records: demographics, presenting symptoms, paediatric intensive care unit (PICU) admission, length of stay in the general ward and PICU, overall hospital stay and outcome.

Results. There were no significant demographic differences between the groups. A larger percentage of infants in group 1 (n=41, 40%) required PICU admission compared with group 2 (n=37, 36%) and group 3 (n=20, 19%). The median PICU stay of group 1 was longer (11 days) compared with group 2 (6 days) and group 3 (5 days). The presence of cough and post-tussive vomiting was significantly higher in group 1 than groups 2 and 3. There was no significant difference in mortality between the groups.

Conclusion. Pertussis results in significant morbidity in infants. Measures to identify and manage this vaccine-preventable disease should be considered at a national level.

S Afr J Child Health 2016;10(3):176-180. DOI:10.7196/SAJCH.2016.v10i3.1115

Pertussis, commonly known as whooping cough, is an acute respiratory illness caused by Bordetella pertussis, a Gram-negative coccobacillus restricted to humans. Although the disease affects all age groups, the disease is most serious in infants (<6 months of age) and in incompletely immunised children.[1] There are ~50 million cases of pertussis and 300 000 pertussis-related deaths annually worldwide according to the World Health Organization (WHO). [2] Data from South Africa (SA) are incomplete. Only patients ill enough to present to hospital are investigated, so available reports are an underestimate of the true number of pertussis cases in SA.[3] Vaccinations have had a major impact on the number of pertussis cases worldwide.[4] The WHO estimates that 687 000 pertussis deaths are prevented annually by global vaccination.[5] Vaccination reduces the severity of clinical disease as well as the duration of coughing, transmission and rate of hospitalisation.[6] Children aged 6 - 24 months who have not received any dose of pertussis vaccine are at a ten-fold risk of hospitalisation compared with those who have been partially or fully immunised.[7] In SA, whole-cell pertussis vaccine (administered as a trivalent vaccine to include tetanus and diphtheria) was replaced by acellular pertussis vaccine in 2009.

The pentavalent vaccine (diphtheria, tetanus, acellular pertussis, inactivated polio vaccine and haemophilus influenza type b (DTaPIPV/Hib) was also introduced as part of the Expanded Programme of Immunisation (EPI).[8] This vaccine is administered at the ages of 6, 10 and 14 weeks, and a booster dose is given at 18 months.

There is no booster for pertussis after 18 months. Infants <18 weeks are still considered to be incompletely vaccinated as they have not yet developed full immunity in response to the pertussis vaccine.[9] According to the EPI, no booster dose is given at school-going age or adolescence. Adolescents and adults play an important role in spreading pertussis to infants.[10] The immunisation of adolescents 176

SAJCH

and adults, especially pregnant women, not only protects them from disease but potentially diminishes its spread to young, vulnerable infants. Some developed countries have introduced preschool and adolescent boosters into their vaccination programmes, as well as maternal third-trimester immunisations.[11] Currently, pertussis is the only vaccine-preventable disease with an increasing incidence globally.[12] Data on the burden of pertussis in developing countries are scarce, particularly in Africa. The morbidity and mortality of pertussis in SA, and the impact that it has on the healthcare system, are unknown. The objective of this study was to describe the clinical presentation of and healthcare impact in infants with pertussis in the public health sector in Bloemfontein, SA. The demographic data, presenting symptoms, HIV and nutritional status, prematurity at birth, length of stay in the general ward and paediatric intensive care unit (PICU) and mortality rate were compared between three groups of patients – those with confirmed pertussis, those tested for pertussis but with a negative result, and those with a lower respiratory tract infection (LRTI) of unspecified aetiology.

Methods

This was a retrospective cohort study. Hospitalised infants <12 mo­nths who were admitted with an LRTI between April 2008 and September 2012 (54 months) were considered for the study. The public sector hospitals were Universitas Hospital (tertiary hospital), Pelonomi Hospital (regional hospital) and National District Hospital (district hospital), which form the academic complex in Bloemfontein.

The data were collected according to three groups: proven pertussis disease, proven negative for pertussis and LRTI of unspecified aetiology. Each study group included patients from Pelonomi Hospital and National District Hospital, where they were initially admitted. If required, intensive care was provided at Pelonomi Hospital and/or

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RESEARCH

In these patients, a nasopharyngeal swab was taken and tested for pertussis using a polymerase chain reaction (PCR) test, specifically targeting the IS481 sequence. Attending doctors requested a pertussis swab at their clinical discretion, but they were also made aware of the suggestive features of pertussis: post-tussive vomiting, apnoea, coughing for more than 2 weeks and a white cell count of more than 20 × 109/L. The swab was taken either on admission or during the hospital stay. The National Health Laboratory Services (NHLS) databank was used to identify all PCR pertussis swabs taken during the specified period in infants <12 months. Only laboratoryconfirmed pertussis-positive cases were included in this group. Of the 117 patients identified by the NHLS with a pertussis PCR-positive result, the medical records of 13 cases could not be traced, and 2 cases were excluded as they did not meet the study criteria (one patient was not admitted, and the other had a pertussis PCR swab done after discharge). A total of 102 patients with proven pertussis disease were thus included in the group (Fig. 1).

and National District Hospital. A total of 929 patients were identified, and 104 were randomly selected to equal the number of patients in groups 1 and 2, using the same random selector as for group 2 (Fig. 1). Group 3 was seen as a control group for groups 1 and 2, and represented infants from the general population with an LRTI with the same background risk of pertussis.

The following demographic and clinical data were obtained from the patients’ hospital records: date of birth (age), gender and whether birth was premature (gestational age <37 weeks), and details of presenting symptoms (presence of cough and duration thereof, post-tussive vomiting, whoop, fever or apnoea). The patients’ HIV and nutritional status was documented. Undernutrition was defined using the WHO charts (2009) and included infants with a weight for length between –2 and –3 z-score or <–3 z-score. The dates of hospital admission and discharge or death were recorded, and if applicable, date of PICU admission and discharge or death. The outcome – survival or death – was also recorded. The data were entered into a study database by the Department of Biostatistics. Results were summarised by frequencies, percentages, means, standard deviations (SDs) and percentiles. The tests used to determine the statistical significance were the Kruskall-Wallis and Mann-Whitney tests for numerical data, and χ2 or Fisher’s exact test for categorical data.

Group 2: proven negative for pertussis

Research ethics committee approval

Universitas Hospital. The period for inclusion of cases was started when the first case had been identified in Bloemfontein (April 2008) until start of the study (September 2012).

Group 1: proven positive for pertussis

This group included infants who had been tested for pertussis but were pertussis PCR negative. The NHLS indicated that 405 cases had a negative PCR pertussis swab result. From this group, 104 cases were randomly selected to equal the number of patients in group 1 (Fig. 1).

This was done prior to the exclusion of two patients who did not meet study criteria in group 1. The random.org online software program (Ireland) was used for this purpose.[13]

Group 3: LRTI of unspecified aetiology

Infants with an LRTI were identified retrospectively using statistics that are kept of all the paediatric admissions to Pelonomi Hospital 929 patients admitted with LRTI <12 months

522 patients – pertussis PCR done (56%)

117 PCR pos.

(22%)

407 patients – no pertussis PCR done (44%)

405 PCR neg.

(78%)

13 files missing

2 patients excluded (did not meet study criteria)

102 pertussis PCR pos. patients GROUP 1

104 pertussis PCR neg. patients GROUP 2

104 randomly selected GROUP 3

Fig. 1. Selection of cases for inclusion in the study.

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SAJCH

The study was approved by the Ethics Committee of the Faculty of Health Sciences of the University of the Free State (ECUFS no.: 216/2012). Written permission to conduct the study was obtained from the Head of Clinical Services of each hospital.

Results

There were no significant differences between the groups with regard to gender, age and gestational age at birth (Table 1). The presence of cough and post-tussive vomiting was significantly higher in the pertussis-positive group compared with the pertussis-negative group and the LRTI group. The median duration of cough was 3 days for all groups (range 1 - 28 days). The presence of apnoea was significantly higher in the pertussis-positive group compared with both the pertussis-negative and LRTI groups. The presence of fever was comparable between all the groups. Only one infant with pertussis had whoop as a presenting symptom (Table 1). A greater proportion of patients in the pertussis-positive group compared with either the pertussis-negative or LRTI group were HIV-positive (n=25 (28.7%); n=20 (20.0%); n=12 (12.1%), respectively). Among the HIV-positive infants (including undernourished, well-nourished and infants born prematurely), the length of stay in the ward, PICU and overall hospital stay were not significantly different between the three groups (Table 2). There was a higher rate of undernutrition in the pertussis-positive group compared with the pertussis-negative or the LRTI groups (n=47 (49.0%); n=34 (33.7%); n=32 (31.7%)). This group included HIV-positive and HIV-negative infants. Among the undernourished infants, the length of stay in the ward, PICU and overall hospital stay were not significantly different between the pertussis-positive, pertussis-negative and LRTI groups (Table 2).

There was no difference in rates of prematurity between the three groups (n=28 (29.2%); n=29 (29.3%); n=29 (29.0%)). The median hospital stay among children born prematurely was longest among the pertussis-positive group and shortest for those with an LRTI of unspecified aetiology (Table 2). Among HIV-negative and wellnourished infants, the length of stay in the ward and PICU was not significantly different between the three groups (Table 3). The hospital stay between the pertussis-positive and pertussis-negative groups was not significantly different (median 8 days v. 7 days, respectively; p=0.19). However, there was a significant difference in hospital stay between the three groups in total, namely between the pertussis-positive (median 8 days) and the LRTI group (median

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RESEARCH Table 1. Baseline data of the pertussis-positive, pertussis-negative and LRTI groups regarding demographic profile and presenting symptoms* Pertussis-positive group (group 1) (N=102)

Pertussis-negative group (group 2) (N=104)

LRTI group (group 3) (N=104)

Group 1 v. 2 p-value*

Group 2 v.

3 p-value*

Group 1 v.

3 p-value*

Overall p-value

13.5 (6 - 24)

12.0 (7 - 26)

-

-

-

0.27

Characteristics Age (weeks), median (IQR) 10.0 (6 - 23) Gender, n (%)

0.07

Male

44 (43.1)

50 (48.1)

61 (58.7)

-

-

-

Female

58 (56.9)

54 (51.9)

43 (41.4)

-

-

-

94 (95.9)

86 (82.7)

89 (85.6)

<0.01

0.57

0.01

Presence of symptoms, n (%) Cough

-

Post-tussive vomiting

40 (42.1)

16 (17.2)

13 (12.9)

<0.01

0.40

<0.01

<0.01

Whoop

1 (1.0)

0 (0)

1 (1.0)

-

-

-

0.77

Fever

42 (43.3)

43 (41.4)

48 (46.2)

-

-

-

0.78

Apnoea

19 (19.0)

13 (12.5)

7 (6.7)

0.20

0.16

0.01

0.03

IQR = interquartile range. *Comparison of the p-values between the groups only given if the overall p-value was significant.

Table 2. Comparison of median length of stay in the ward, PICU and overall hospital stay between the pertussis-positive, pertussisnegative and LRTI groups in HIV-positive and undernourished infants and those with a history of prematurity Pertussis-positive group (group 1)

Pertussis-negative group (group 2)

LRTI group (group 3)

Overall p-value

25/87 (28.7)

20/100 (20.0)

12/99 (12.1)

0.02

Duration of ward stay (days), median (IQR)

(n=25) 9 (6 - 15)

(n=20) 12 (9 - 24)

(n=12) 11 (7.5 - 22.5)

0.31

Duration of PICU stay (days), median (IQR)

(n=12) 11.5 (7 - 16)

(n=8) 5.5 (3.5 – 12)

(n=3) 9 (3 – 33)

0.34

Duration of hospital stay (ward and PICU) (days), median (IQR)

(n=25) 14 (9 - 22)

(n=20) 14 (11.5 - 28.5)

(n=12) 11 (7.5 - 24.5)

0.61

47/96 (49.0)

34/101 (33.7)

32/101 (31.7)

0.02

Duration of ward stay (days), median (IQR)

(n=47) 9 (7 - 16)

(n=34) 8.5 (6 - 21)

(n=32) 7 (5 - 13.5)

0.26

Duration of PICU stay (days), median (IQR)

(n=19) 7 (5 - 13)

(n=15) 7 (4 - 12)

(n=11) 6 (4 - 10)

0.81

Duration of hospital stay (ward and PICU) (days), median (IQR)

(n=47) 12 (8 - 21)

(n=34) 12 (7 - 26)

(n=32) 8.5 (7 - 14.5)

0.13

28/96 (29.2)

29/99 (29.3)

29/100 (29.0)

1.00

Duration of ward stay (days), median (IQR)

(n=28) 8 (4 - 10.5)

(n=29) 8 (6 - 16)

(n=29) 6 (4 - 8)

0.10

Duration of PICU stay (days), median (IQR)

(n=14) 9 (5 - 11)

(n=15) 8 (6 - 13)

(n=8) 4.5 (3 - 9)

0.17

Duration of hospital stay (ward and PICU) (days), median (IQR)

(n=28) 10.5 (8 - 15.5)

(n=29) 13 (8 - 21)

(n=29) 7 (4 - 9)

<0.01

HIV-positive infants (N=87), n (%)*

Undernourished infants, n (%)*

Infants with history of prematurity, n (%)*

*Percentages are calculated for the known totals of each group.

6 days; p<0.01), and between the pertussis-negative (median 7 days) and LRTI group (median 6 days; p=0.01). Forty-one patients (40%) with confirmed pertussis were admitted to PICU compared with 37 (36%) patients in the pertussis-negative group (p=0.49) and 20 (19%) patients in the LRTI group (p<0.01; p=0.01 between pertussisnegative and LRTI groups). Median PICU stay was significantly longer in the confirmed pertussis group compared with both the pertussisnegative group (p=0.02) and the LRTI group (p=0.01). The length 178

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of general ward stay was longer in both the confirmed pertussis and pertussis-negative groups compared with the LRTI group. Overall median hospital (PICU plus general ward) stay was significantly longer in the pertussis-positive group compared with both the pertussis-negative (p=0.05) and LRTI groups (p<0.01) (Table 4).

There was no statistically significant difference in mortality between the three groups. In both the confirmed pertussis group and the LRTI group, seven patients died (6.8% and 6.7%, respectively), and three

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RESEARCH

Discussion

Pertussis is associated with considerable morbidity and some mortality, and the recent resurgence of pertussis in developed and developing countries has necessitated the need to evaluate its impact in SA. Scant data are available from SA regarding the morbidity and healthcare burden of pertussis. The data from this study show that 40% of infants with proven pertussis required PICU admission, compared with only 19% of infants with an LRTI of unspecified origin, and 36% of infants who tested negative for pertussis. The death rate was not significantly different between the three groups but was generally very high. The high rates of PICU admission and mortality rates may be a reflection that two of the hospitals (Pelonomi and Universitas) are secondary- or tertiarylevel hospitals that include infants who were too ill to be managed at peripheral hospitals.

The length of stay in PICU for confirmed pertussis patients was also far greater than for the pertussis-negative and LRTI groups.

General ward stay and overall hospital stay

were also significantly prolonged in the group with confirmed pertussis. However, general ward stay and overall hospital stay were also longer in the pertussis-negative group compared with the LRTI group. Perhaps some infants in the pertussis-negative group were tested for pertussis because they had already been admitted in hospital for a long time and were not responding to treatment, and other diagnoses were being explored.

In addition, group 2 may have included false-negative cases. A greater proportion of infants with proven pertussis were immune compromised (HIV-positive or undernourished) than infants of either the pertussis-negative or the LRTI of unknown aetiology groups. This may indicate a greater

predisposition to acquiring pertussis infection due to compromised immunity.

Infants with proven pertussis who were HIV-positive or undernourished did not have a significantly longer length of stay in the ward, PICU or overall hospital stay compared with infants who tested negative for pertussis or had an LRTI of unknown aetiology. Possibly this is because children who are immune compromised often have other concurrent disease processes or opportunistic infections requiring them to stay in hospital for a longer period. Among HIV-negative and well-nourished children, the overall hospital stay was significantly longer in the pertussis-positive group compared with the LRTI group, and in

18

14 Admissions / month (n)

patients died in the pertussis-negative group (2.9%). In the confirmed pertussis group, six of the seven patients (85.7%) who died were <6 months of age, and five of the seven (71.4%) were <3 months old. More patients were diagnosed with pertussis in the months between January and April of each year.

There was also a marked rise in incidence of pertussis in the year 2011 (Fig. 2).

11

7

4

0 Apr 08 Aug 08 Dec 08 Apr 09 Aug 09 Dec 09 Apr 10 Aug 10 Dec 10 Apr 11 Aug 11 Dec 11 Apr 12 Aug 12

Fig. 2. Pertussis cases in infants per month between April 2008 and September 2012.

Table 3. Comparison of median length of stay in the ward, PICU and overall hospital stay between the pertussis-positive, pertussisnegative and LRTI groups in HIV-negative and well-nourished infants Pertussis-positive group (group 1)

Pertussis-negative group (group 2)

LRTI group (group 3)

Overall p-value

HIV-negative and well-nourished infants, n

35

54

64

Duration of ward stay (days), median (IQR)

(n=35) 6 (3 - 10)

(n=54) 6 (4 - 8)

(n=64) 5 (4 - 7)

0.39

Duration of PICU stay (days), median (IQR)

(n=12) 9 (6 - 11)

(n=16) 5 (3.5 - 10)

(n=5) 4 (3 - 8)

0.17

Duration of hospital stay (ward and PICU) (days), median (IQR)

(n=35) 8 (6 - 13)

(n=54) 7 (5 - 10)

(n=64) 6 (4 - 8)

<0.05

Table 4. Comparison of median length of stay in the ward, PICU and overall hospital admission between the confirmed pertussispositive, pertussis-negative and LRTI (unspecified aetiology) groups Pertussis-positive group (group 1) (N=102)

Pertussis-negative group (group 2) (N=104)

LRTI group (unspecified aetiology) (group 3) (N=104)

Duration of ward stay (days), median (IQR)

(n=102) 8 (5 - 13)

(n=104) 7 (5 - 11)

Duration of PICU stay (days), median (IQR)

(n=41) 11 (6 -14)

Duration of hospital stay (ward and PICU) (days), median (IQR)

(n=102) 11 (7 - 20)

179

p-value group 1 v. 2

p-value group 2 v. 3

p-value group 1 v. 3

(n=104) 6 (4 - 8)

0.47

0.01

<0.01

(n=37) 6 (4 - 11)

(n=20) 5 (3.5 - 9.5)

0.02

0.61

0.01

(n=104) 8 (6 - 14.5)

(n=104) 7 (4 - 9)

0.05

<0.01

<0.01

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RESEARCH the pertussis-negative group compared with the LRTI group. This reflects that infants affected by pertussis without conditions that contribute to immune compromise are more affected than infants with LRTI of unknown aetiology. The pertussis-negative group may include false-negative infants, and in addition, these infants may have been tested for pertussis because they had been admitted to hospital for a long time and were not improving on treatment, and other diagnoses were being considered. Confirmation of pertussis can be difficult in hospitals with minimal access to laboratories, and considering pertussis on clinical grounds is important. In this study, the presence of cough was the most common symptom, followed by post-tussive vomiting and apnoea. Few infants presented with a fever or whoop. The duration of cough in infants with pertussis in this study was very variable, and if only infants with a cough for >2 weeks had been tested for pertussis, as the WHO definition required,[14] many pertussis diagnoses may have been missed. It is therefore important to consider pertussis in infants with a short duration of cough. Bearing in mind the severity of pertussis in infants <18 weeks who are incompletely immunised, prevention of, rather than treating, the disease should be a priority. In SA, replacing the current tetanus and diphtheria (Td) vaccine scheduled at the age of 6 years with DTaP, as well as immunisation of adolescents and pregnant women, could be a feasible intervention, as is being done in many countries.[10] Early diagnosis and early appropriate treatment with an antibiotic (macrolide) are important, as these reduce the period of communicability of pertussis, and may also reduce the duration and severity of symptoms,[15] and in turn reduce the length of hospital stay. Close contacts at risk of acquiring severe disease should receive a course of a macrolide as well, as secondary disease is estimated to occur in up to 80% of household contacts.[16] The patients who tested positive in this study, as well as their mothers, were treated for 7 days with a macrolide (erythromycin or clarithromycin).

Study limitations

There were several limitations to this study. The technique for collection of the PCR pertussis swab in infants suspected of having pertussis was not predefined, and poor collection technique may have resulted in false-negative results. In addition, not all infants who were admitted to one of the hospitals were tested for pertussis, as testing was only done on clinical suspicion and therefore infants with pertussis may have been missed. Another limitation was that the pertussis immunisation details could not be included nor accurately documented in the analysis record, as this was often not available from the parent or caregiver. Vaccination could have been compared among the three groups. The infants tested for pertussis were generally more ill than the infants with an LRTI of unknown aetiology; the pertussis-positive group may therefore represent a sicker group of pertussis cases, and other less severe cases may not have been tested, with the potential for selection bias.

Conclusion

Pertussis has re-emerged as a serious illness with a significant morbidity and some mortality, even in high-income countries. Not

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many data about pertussis are available in SA. Health resources are often scarce, and more information needs to be available regarding pertussis in order to target specific prevention strategies and treatment policies. This study has provided an indication of the impact that pertussis has on healthcare, namely prolonged PICU and overall hospital stay. Coughing for <2 weeks does not exclude a diagnosis of pertussis. Whoop is rare in infants with pertussis.

HIV infection, undernutrition and prematurity at birth do not worsen the clinical presentation of pertussis. Further research into the epidemiology of pertussis in SA is needed in order to inform national control strategies and vaccination policies. This study from one region of SA provides some insight into the healthcare burden of pertussis.

Acknowledgements. Prof. G Hussey reviewed the draft manuscript and provided valuable suggestions.

References

1. Gordon M, Davies HD, Gold R. Clinical and microbiological features of children presenting with pertussis to a Canadian pediatric hospital during an elevenyear period. Pediatr Infect Dis J 1994;13(7):617-622. DOI:10.1097/00006454199407000-00007 2. World Health Organization. WHO-recommended surveillance standard of pertussis. http:/apps.who.int/immunization-monitoring/en/globalsummary/ diseaseselect.cfm (accessed 12 February 2014).

3. Archer B, Lowman W, Kularatne R, et al. Laboratory-confirmed pertussis in the public health sector, 2008 - 2011. National Health Laboratory Service, National Institute for Communicable Diseases 2011;9(4):81-83.

4. Cherry JD. Epidemic pertussis in 2012 – the resurgence of a vaccine-preventable disease. N Engl J Med 2012;367(9):785-787. DOI:10.1056/NEJMp1209051 5. World Health Organization. Vaccines and diseases. Pertussis. http://www.who. int/immunization/diseases/pertussis/en (accessed 12 February 2014).

6. Baptista PN, Magalhaes V, Rodrigues LC, et al. Pertussis vaccine effectiveness in reducing clinical disease, transmissibility and proportion of cases with a positive culture after household exposure in Brazil. Pediatr Infect Dis J 2006;25(9):844-846. DOI:10.1097/01.inf.0000232642.25495.95 7. Stojanov S, Liese J, Belohradsky BH. Hospitalization and complications in children under 2 years of age with Bordetella pertussis infection. Infection 2000;28(2):106-110. DOI:10.1007/s150100050056 8. Baker L. The face of South Africa’s Expanded Programme on Immunisation (EPI) schedule. S Afr Pharm J 2010;77(1):18-21.

9. Greenberg DP, von König CH, Heininger U. Health burden of pertussis in infants and children. Pediatr Infect Dis J 2005;24(5):S39-43. DOI:10.1097/01. inf.0000160911.65632.e1 10. Pan American Health Organization. Control of diphtheria, pertussis, haemophilus influenzae type b, and hepatitis B: Field guide. Washington DC: Pan American Health Organization, World Health Organization, 2005.

11. Ward JI, Cherry JD, Chang SJ, et al. Efficacy of an acellular pertussis vaccine among adolescents and adults. N Engl J Med 2005;353(15):1555-1563.

DOI:10.1056/NEJMoa050824 12. Black S. Epidemiology of pertussis. Pediatr Infect Dis J 1997;16(4):85-89.

DOI:10.1097/00006454-199704001-00003 13. Mads Haahr, School of Computer Science and Statistics at Trinity College, Dublin. http://www.random.org/sequences (accessed 15 March 2013).

14. World Health Organization. WHO-recommended surveillance standard of pertussis. www.who.int/.../monitoring_surveillance/burden/vpd/surveillance_ type/passive/pertussis_standards/en (accessed 11 February 2011).

15. Tiwari T, Murphy TV, Moran J, National Immunization Program CDC. Recommended antimicrobial agents for the treatment and post exposure prophylaxis of pertussis: 2005 CDC Guidelines. MMWR Recomm Rep 2005;54(RR-14):1-16.

16. Schellekens J, Wirsing von König C, Gardner P. Pertussis sources of infection and routes of transmission in the vaccination era. Ped Infect Dis J 2005;24(5):S19-S24. DOI:10.1097/01.inf.0000160909.24879.e6.

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RESEARCH

This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

Characteristic of monosymptomatic and nonmonosymptomatic childhood nocturnal enuresis in Benin City, Nigeria N J Iduoriyekemwen,1 MBBS, FWACP; D U Nwaneri,2 MBBS, MPH, FMCPaed 1 2

Department of Child Health, University of Benin/University of Benin Teaching Hospital, Benin City, Nigeria Institute of Child Health, University of Benin/University of Benin Teaching Hospital, Benin City, Nigeria

Corresponding author: N J Iduoriyekemwen (nosaiduos2006@yahoo.com)

Background. In recent years, nocturnal enuresis (NE) has been classified into monosymptomatic nocturnal enuresis (MNE) and nonmonosymptomatic nocturnal enuresis (NMNE) on the basis of the absence or presence of daytime voiding symptoms. Identifying clinical features that differentiate MNE from NMNE would aid in quick diagnosis, which would foster the introduction of early and appropriate therapeutic care options.

Objective. To identify distinguishing characteristics of MNE and NMNE in Nigerian children.

Methods. The parents of children in public primary and secondary schools in Egor local government area, Edo State, were interviewed using a semi-structured questionnaire.

Results. The total studied population included 1 221 parent/child pairs. Of the children studied, 228 were enuretic. There were 149 (65.4%) MNE and 79 (34.6%) NMNE children. Enuretic children with a history of multiple wetting per night or whose parents observed difficulty awakening them from sleep were significantly more likely to be in the NMNE group.

Conclusion. MNE is twice as common as NMNE and the main distinguishing features between the two groups of enuretic children are multiple wetting at night and difficulty awakening the child from sleep. These were significantly more commonly observed among the NMNE group of children.

S Afr J Child Health 2016;10(3):181-185. DOI:10.7196/SAJCH.2016.v10i3.1140

Nocturnal enuresis (NE), also known as bed-wetting, is the inter­ mittent involuntary passage of urine during sleep in a child 5 years and older.[1] It is a very common problem of childhood, affecting children of all races worldwide.[2] Although bed-wetting does not cause any physical harm to the child, it is a cause of great psychological distress to the family and to the enuretic child.[3,4] Several studies worldwide have classified children with either primary or secondary NE based on whether the child has never been dry at night (primary NE (PNE)) or has been dry for at least 6 months (secondary NE (SNE)).[5-7] The majority of studies on enuresis have been on PNE, which has been reported as the most common type of NE.[5-9] However, recently NE has also been further classified into monosymptomatic NE (MNE) and non-monosymptomatic NE (NMNE) on the basis of the absence or presence of daytime voiding symptoms.[1,10] This classification of NE is essential because children with NE who have daytime voiding or lower urinary tract symptoms are pathogenetically and clinically different from those who bed-wet at night only. In addition, children with MNE and NMNE require different modalities for management.

Most of the studies in Nigeria on NE have been on the determination of the prevalence of NE in primary school children.[11-14] There is no study that has classified enuretic children using the recent classification (MNE and NMNE), indicating that children with daytime voiding and/or lower urinary tract symptoms are usually missed both in terms of diagnosis and treatment modalities.

This study was conducted in order to identify distinguishing characteristics of MNE and NMNE enuresis in Nigerian children using children residing in Egor local government area (LGA), Benin City.

Benin City, a predominantly urban setting with nine political wards, of which two are rural. The main occupation of the inhabitants includes farming, trading and the civil service. There are 17 public primary and 12 secondary schools (government-owned schools).

Subjects were parent/child pairs of the public primary and secondary schools in Egor (LGA), Edo State. The population was chosen because children in public schools derive from different social classes, ensuring a good representation of all social classes.

A pre-tested, self-administered questionnaire was used. It was distributed to all the parents by their children. The completed questionnaires were returned the following day. The information captured included parent demography (mother’s age, mother’s level of education and occupation, father’s level of education and occupation, marital status and family size). Social class of the child’s family was determined by the method described by Olusanya et al.[15] Information on the child’s demographic characteristics was also obtained (age, gender and birth order). In addition, information was sought regarding the child’s enuretic characteristics, namely: • the presence of NE • onset of NE • presence of daytime voiding symptoms • frequency of enuresis • history of multiple voidings per night • predominant night period when wetting usually occurs • family history of enuresis • relationship of the individual with a positive history of enuresis to the child.

Methods

Only children with a history of bed-wetting since birth were recruited. Children were classified as NMNE when there was no history of daytime symptoms (voiding frequency, voiding urgency or daytime wetting). If they had daytime symptoms and nocturnal

This descriptive, cross-sectional survey was carried out from April to August 2014 during the third-term of the school year. The study location was Egor LGA in Edo State, which is one of the five LGAs in 181

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RESEARCH wetting, they were classified as NMNE. The severity of bed-wetting was based on the frequency of nocturnal bed-wetting. If a child bed-wet only once a week or one to two times a month, she or he was classified as having mild NE; if bed-wetting occurred twice or more in a week, it was classified as moderate NE; and if the child wet every night it was classified as severe NE. Family size was defined as small if the number of children residing in the home was equal to or less than five and large if the number was greater than five.

Data obtained were entered into IBM Statistical Package for Social Sciences (SPSS) version 20.0 (USA) and were analysed using the same software. Quantitative variables were summarised using means and standard deviations (SDs), and comparisons of pro­ portions were done accordingly. The sig­ nificance of association between variables was tested using χ2 and Fisher’s exact tests where appropriate, while independent t-test was used for comparison of means. The level of significance of each test was set at p<0.05.

Ethical considerations

An ethical certificate for this study was obtained from the Research and Ethics Committee of the College of Medical Sci­ ence, University of Benin, and permission was sought from the Ministry of Education and the headpersons of each primary school and the principal of each secondary school.

Written informed consent forms were given to each child to deliver to their parents at the first visit to the schools. Parents who returned a signed informed consent were recruited in the study. All the children of both the primary and secondary schools in the LGA whose parents gave written informed consent were recruited for this study.

Results

A total of 1 800 questionnaires were dis­ tributed to the parents of the students, of which 1 574 were returned, giving a response rate 87.4%. However, only 1 221 questionnaire were correctly completed; therefore the total studied population was 1 221 parent/child pairs. The mean (SD) age of the 1 221 children analysed was 12.1 (1.9) years, median 12 (range 5 - 17) years. Most of the children (84.6%) were under 10 years of age and were female (64.0%). Of the 1 221 children analysed in the study, 228 were enuretic. The mean age of these children was 11.4 (2.4) years and the modal age was 14 years. The mean age of the enuretic children was significantly younger than that of non-enuretic children (p<0.0001).

The proportion of children with enuresis (47%) was highest in the 5 - 9-year-old age group, falling to 7% in the 15 - 17-yearolds. Age was significantly associated with 182

Table 1. Sociodemographic characteristics of the enuretic children compared with NE children Characteristics

Enuretic children (N=228), n (%)

NE children (N=993), n (%)

Age (yr), mean (SD)

11.4 (2.4)

12.3 (1.8)

Total

p-value <0.001

Age group (yr) 5-9

38 (47.5)

42 (53.2)

80

10 - 14

182 (17.6)

851 (86.0)

1 033

15 - 17

8 (7.4)

100 (92.6)

108

Male

85 (23.9)

355 (76.1)

440

Female

143 (18.3)

638 (81.7)

781

<0.001

Gender 0.70

Socioeconomic class Upper

13 (16.0)

68 (83.9)

81

Middle

133 (20.0)

532 (80.0)

665

Lower

82 (17.3)

393 (82.7)

475

0.41

Table 2. Sociodemographic characteristics of the MNE and NMNE children Characteristics

MNE children N=149, n (%)

NMNE children N=79, n (%)

Age (yr), mean (SD)

11.5 (2.)4

11.2 (2.3)

Total

p-value 0.36

Age (yr) 5-9

23 (62.1)

14 (37.9)

37

10 - 14

119 (65.0)

64 (35.0)

183

15 - 17

7 (87.5)

1 (12.5)

8

Gender

0.20

Male

51 (60.0)

34 (40.0)

85

Female

98 (68.5)

45 (31.5)

143

Upper

12 (92.3)

1 (7.7)

13

Middle

88 (66.2)

45 (33.8)

133

Lower

49 (59.7)

33 (40.2)

82

Socioeconomic class

0.07

enuresis (p<0.001). There were slightly more enuretic male children (23.9%) than enuretic female children (18.3%), however this was not statistically significant (p=0.70). The prevalence of enuresis was no different between the three socioeconomic classes (Table 1).

A total of 149 (65.4%) of the 228 enuretic children were MNE, while 79 (34.6%) were NMNE. Therefore, the proportion of MNE to NMNE children was 1.8:1. There was no significant difference between the two groups of enuretic children in terms of their age (p=0.39), gender (p=0.20) and socioeconomic class (p=0.07) (Table 2). The proportion of male and female children with MNE and NMNE was similar, and there was no statistical difference in proportions of children with the two types of NE between the socioeconomic classes.

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0.39

Table 3 shows the characteristics of the MNE and NMNE children. Children whose parents observed difficulty waking their children from sleep were significantly more likely to have NMNE than the MNE (p=0.006).

Similarly, enuretic children with history of multiple wetting per night were significantly more likely to have NMNE than MNE (p=0.005). However, there was no statistical significant difference between MNE and NMNE children in terms of the child’s birth order, family size, family history of enuresis, severity of enuresis and predominant period of the night that wetting occurs (e.g. wetting soon after falling asleep or wetting occurring more towards morning).

Parental sociodemographic characteristics were also not significantly different in the two groups of enuretic children (Table 4) except for marital status of the parents. The proportions

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RESEARCH Table 3. Characteristics of the MNE and NMNE children MNE children NMNE children (N=149), n (%) (N=79), n (%)

Characteristics Child’s birth order

p-value 0.930

1st

35 (23.5)

19 (24.1)

2nd

33 (22.1)

17 (21.5)

3rd

25 (16.8)

10 (12.7)

4th

23 (15.4)

14 (17.7)

5th

9 (6.0)

5 (6.3)

>5th

16 (10.7)

6 (7.6)

No response

8 (5.4)

8 (10.1)

Family size

Discussion

0.190

Small: <5 children

29 (19.5)

22 (27.8)

Large: >5 children

116 (77.9)

57 (72.2)

No response

4 (2.7)

0 (0)

Family history of enuresis

0.130

Yes

72 (48.3)

47 (59.5)

No

77 (51.7)

32 (40.5)

Relationship of individual with family history

0.620

Father

8 (5.4)

3 (3.8)

Mother

7 (4.7)

6 (7.6)

Brother

23 (15.4)

16 (20.3)

Sister

13 (8.7)

12 (15.2)

Uncle

19 (12.8)

9 (11.4)

Other

3 (2.0)

1 (1.3)

No response

76 (51.0)

32 (40.5)

Severity of enuresis

0.130

Mild

56 (37.6)

18 (22.8)

Moderate

26 (17.4)

17 (21.5)

Severe

52 (34.9)

31 (39.2)

No response

15 (10.1)

13 (16.5)

Difficulty in waking child from sleep

0.006

Yes

45 (30.2)

39 (49.4)

No

104 (69.8)

40 (50.6)

40 (26.8) 109 (73.2)

36 (47.6) 43 (54.4)

Wetting multiple times at night

0.005

Yes No Wetting soon after falling asleep

0.760

Yes

42 (28.2)

24 (30.4)

No

107 (71.3)

55 (69.6)

Yes

35 (23.5)

19 (24.1)

No

114 (76.5)

60 (75.9)

Wetting more towards morning

1.000

of unmarried parents were significantly greater in the NMNE group of children, compared with MNE children (p=0.002).

The association between the child’s age group and other characteristics was deter­ 183

mined for each of the groups of enuretic children. Among the MNE children, the child’s age group was significantly associated with severity of bed-wetting (p=0.013), family history of enuresis (p=0.04), father’s SAJCH

educational level (p=0.014) and marital status of parents (p=0.028). However, among the NME children, no association was observed between child’s age group and other characteristics.

Although NE has been extensively studied in relation to the onset of bed-wetting (primary and secondary bed-wetting),[5–9] very few studies have been conducted in terms of the absence or presence of daytime voiding symptoms,[16,17] which means there is a dearth of data for comparison. In a large population study on MNE and NMNE by Butler and Heron,[16] the proportion of MNE children to NMNE children was documented as 2:1, a figure similar to that found in the present study.

This observation, therefore, supports the notion that MNE is twice as common as NMNE. The main distinguishing features between children with MNE and NMNE observed in this study were that children with NMNE were more likely to bedwet multiple times per night and were more difficult to rouse from sleep. There is a dearth of studies on distinguishing MNE from NMNE, therefore precluding comparison. The presence of lower urinary tract dysfunction in children with NMNE may explain why they tend to bed-wet multiple times per night compared with children with MNE. In a study by Naseri and Hiradfar,[17] bladder dysfunctions – overactive bladder, detrusor hyperactivity conditions which predispose to multiple wetting – were detected by urodynamic studies, and they were reported to be more common in children with NMNE. Difficulty in rousing child from sleep, which is one of the three well-established pathophysiological factors of MNE,[2,18] was not observed in our study to be exclusive to the MNE group of children. This, therefore, justifies the need for extensive interview of any child with NE to reveal if they have daytime voiding symptoms or lower urinary tract symptoms, as investigative evaluation for the children with NMNE is mandatory. Parental marital status was the only other distinguishing factor observed in this study. The observation that in the homes where the parents were unmarried (divorced, separated, etc.) NMNE was more common compared with MNE, may imply that family dysfunction is an important associated factor in NMNE and in secondary enuresis. Dysfunctional or split families are an identifiable stressful environmental factor, which predisposes children to greater risk of developmental and behavioural problems.[19] The import of this is the inclusion of psychotherapy for both child and family as relevant adjuvant

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RESEARCH Table 4. Characteristics of the parents of the monosymptomatic and nonmonosymptomatic enuretic children Characteristics

MNE children (N=149) n (%)

NMNE children (N=79), n (%)

Mother’s age (yr)

p-value 0.700

20 - 29

11 (7.4)

3 (3.8)

30 - 39

61 (40.9)

33 (41.8)

40 - 49

44 (29.5)

27 (34.2)

50 - 59

15 (10.1)

7 (8.9)

>60

1 (0.7)

2 (2.5)

No response

17 (11.4)

7 (8.9)

Primary

38 (25.5)

19 (24.1)

Secondary

42 (28.2)

28 (35.4)

Tertiary

39 (26.2)

13 (16.5)

No response

30 (20.1)

19 (24.1)

Mother’s educational status

0.220

Father’s educational status

0.270

Primary

23 (15.4)

10 (12.7)

Secondary

42 (28.2)

28 (35.4)

Tertiary

48 (32.2)

18 (22.8)

No response

36 (24.2)

23 (29.1)

Marital status

0.002

Married

126 (84.6)

62 (78.5)

Unmarried

4 (2.7)

12 (15.2)

No response

19 (12.9)

5 (6.3)

therapeutic option in management of children with NMNE. Although there were no observed differ­ ences between the two enuretic groups of children in terms of sociodemographic characteristics, the following trends were observed in this study.

The mean ages of children with MNE and NMNE were similar. This finding is in consonance with the works of Naseri and Hiradfar,[17] who also studied a similar age range as in this study. Of note, however, is that the mean (SD) ages of the children in the study by Naseri and Hiradfar[17] were lower in both groups of children (8.66 (2.2) years in those with MNE and 8.2 (2.5) years in those with NMNE) when compared with 11.5 (2.4) years for the children with MNE and 11.2 (2.3) years for those with NMNE observed in the present study.

These differences may be explained by the fact that a larger proportion of children in this study were >10 years, while in the study

by Naseri and Hiradfar[17] the majority of the children were <10 years old.

The observed trend from several other studies that the prevalence of NE decreases with increasing age[5-9,20-22] was also observed in this study, even among the NMNE group of children. The reason why the MNE 184

group of children did not show this trend is difficult to explain. The widely documented finding that NE is more common in males than females[5-9,20-22] was also observed in this study; however, when comparing the MNE and NMNE group of enuretic children, this difference in gender was not observed.

This is in contrast to the works of Naseri and Hiradfar[17] and Bakker et al.,[23] who reported that among the MNE group, males were recorded more than females but the reverse was observed among the NMNE group. The difference is difficult to explain, because even in a study on lower urinary tract symptoms in children who do not bedwet, the daytime voiding symptoms were also reported to be more common in girls than boys.[19] Of note is that some studies on MNE reported that the sex difference is only observed until the age of 10 years, and thereafter the frequency is the same for both boys and girls.[24] This may be the reason for the findings in this study, as the majority of the children were older than 10 years.

The limitation of this study was that the children could not be evaluated radiologically owing to financial constraints. Radiological assessment would have aided in diagnosing the specific lower urinary tract dysfunction the children with NMNE had. In addition, SAJCH

daytime voiding symptoms used to define NMNE were only ascertained by history; a 48-hour frequency and volume chart was not used to confirm.

Conclusions

MNE is twice as common as NMNE, and the main distinguishing features between the two groups of enuretic children are multiple wetting at night and difficulty in waking up a child from sleep, which was significantly observed among the NMNE group of chil­ dren. We therefore recommend that while evaluating patients, the presence of these factors (multiple wetting at night and difficult sleep arousal) should alert the physician to probe for the presence of lower urinary symptoms or daytime voiding symptoms.

This would help reduce missed opportunities in the diagnosis of children with NMNE. Acknowledgements. The authors thank Mr Moses Adekunle Abiodun who assisted in data collection, Miss Itohan Ibhawa for data entry into Microsoft Excel and the management of the selected schools for providing the enabling environment for this study.

References 1. Austin PF, Bauer SB, Bower W, et al. The standardization of terminology of lower tract function in children and adolescent: Update report from the Standardization Committee of the International Children’s Continence Society. J Urol 2014;191(6):1863-1865. DOI:10.1016/j. juro.2014.01.110 2. Wright A. Evidence-based assessment and management of childhood enuresis. Paediatr Child Health 2008;18(12):561-567. DOI:10.1016/j. paed.2008.09.006 3. Fritz G, Rockney R, Bernet W, et al. Practice parameter for the assessment and treatment of children and adolescents with enuresis. J Am Acad Child Adolesc Psychiatry 2004;43:(12):1540-1550.

DOI:10.1097/01.chi.0000142196.41215.cc 4. Joinson C, Heron J, Emond A, Butler R. Psychological problems in children with bedwetting and combined (day and night) wetting: A UK population-based study. J Paediatr Psychol 2007;32(5):605-616. DOI:10.1093/jpepsy/jsl039 5. Chang P, Chen WJ, Tsai WY, Chiu YN. An epidemiological study of nocturnal enuresis in Taiwanese children. BJU Int 2001;87(7):678-681.

DOI:10.1046/j.1464-410x.2001.02161.x 6. Hazza I, Tarawneh H. Primary nocturnal enuresis among school children in Jordan. Saudi J Kidney Dis Transpl 2002;13(4):478-480.

7. Kanaheswari Y. Epidemiology of children nocturnal enuresis in Malaysia. J Paediatr Child Health 2003;39(2):118-123. DOI:10.1046/j.14401754.2003.00105.x 8. Yeung CK, Sreedhar B, Sihoe JD, Sit FK, Lau J. Differences in characteristics of nocturnal enuresis between children and adolescents: A critical appraisal from a large epidemiological study. BJU Int 2006;97(5):1069-1073. DOI:10.1111/j.1464410X.2006.06074.x 9. Ozden C, Ozdal O, Altinova S, Oguzulgen I, Urgancioglu G, Memis A. Prevalence and associated factors of enuresis in Turkish children.

Int Braz J Urol 2007;33(2):216-222.

10. Djurhuus JC. Definitions of subtypes of enuresis.

Scand J Urol Nephrol Suppl 1999;202:5-7.

11. Osungbade KO, Oshiname FO. Prevalence and perception of nocturnal enuresis in children of a rural community in southwestern Nigeria. Trop Doct 2003;33(4):234-236.

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RESEARCH 12. Etuk IS, Ikpeme O, Essiet GA. Nocturnal enuresis and its treatment among primary school children in Calabar Nigeria. Niger J Paediatr 2011;38(2):7881.

13. Paul NI, Alikor EA, Anochie IC. Prevalence of enuresis among primary school children in Port Harcourt. Niger J Paediatr 2012;39(1):18-21.

14. Chinawa JM, Obu HA, Manyike PC, Odetunde OI. Nocturnal enuresis among school-age children in south-eastern Nigeria: A concealed social malaise. Int J Trop Dis Health 2014;4(6):683-695.

15. Olusanya O, Okpere E, Ezimokai M. The importance of social class in voluntary fertility control in a developing country. West Afr J Med 1985;4:205-212.

16. Butler R, Heron J. Exploring the difference between mono- and polysymptomatic nocturnal enuresis. Scand J Urol Nephrol 2006;40(4):313-319.

17. Naseri M, Hiradfar M. Monosymptomatic and non-monosymptomatic nocturnal enuresis: A clinical evaluation. Arch Iran Med 2012;15(11):702706.

18. Tryggve N. Nocturnal enuresis â&#x20AC;&#x201C; theoretical background and practical guidelines. Pediatr Nephrol 2011;26(8):1207-1214. DOI:10.1007/s00467-0111762-8

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19. Vaz GT, Vasconcelos MM, Oliveira EA, et al. Prevalence of lower urinary tract symptoms in school children. Pediatr Nephrol 2012;27(4):597-603.

DOI:10.1007/s00467-011-2028-1 20. Shan S, Ahmed A, Rehman SU, Rehman G. Prevalence and risk factors of monosymptomatic nocturnal enuresis in Pakistani children. Khyber J Med Sci 2011;3(1):16-20.

21. Abu Merhi B, Hammoud A, Ziade F, Kamel R, Rajab M. Mono-symptomatic nocturnal enuresis in Lebanese children: Prevalence, relation with obesity, and psychological effect. Clin Med Insights Pediatr 2014;8:5-9. DOI:10.4137/ CMPed.S13068 22. Iduoriyekemwen NJ, Ibadin MO, Abiodun PO. Survey of childhood enuresis in the Ehor community, the Edo State, Nigeria. Saudi J Kidney Dis Transpl 2006;17(2):177-182.

23. Bakker E, van Sprundel M, van der Auwera JC, van Gool JD, Wyndaele JJ. Voiding habits and wetting in a population of 4 332 Belgian school children aged between 10-14 years. Scand J Urol Nephrol 2002;36(5):354-362.

24. Meneses R. Monosymptomatic nocturnal enuresis. J Pediatr (Rio J) 2001;77(3):161-168.

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CASE REPORT

This open access article is distributed under Creative Commons licence CC-BY-NC 4.0.

Congenital infantile fibrosarcoma mimicking sacrococcygeal teratoma in a Ghanaian infant: A case report and review of the literature B M Duduyemi,1 MB ChB, MSc, FMC Path; A C Yifieyeh,2 MBBS, FWACS 1 2

Department of Pathology, School of Medical Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana Directorate of Surgery, Komfo Anokye Teaching Hospital, Kumasi, Ghana

Corresponding author: B M Duduyemi (tundeduduyemi@gmail.com)

Congenital infantile fibrosarcoma (CIFS) is a rare tumour of childhood accounting for less than 1% of malignant tumours in children.

Reports from sub-Saharan Africa are particularly rare and the occurrence in the sacral region mimicking a sacrococcygeal teratoma has not been reported in Africa to the best of our knowledge. The poor predilection of the tumour for distant metastases may contribute to its above average prognosis, but the rarity of systemic antenatal detection of congenital conditions in most parts of Africa may mitigate this good fortune. We report the very rare case of a 9-month-old female infant who presented with a progressively increasing painless sacral mass from birth which was thought to be a sacrococcygeal teratoma clinically but histopathological assessment revealed a CIFS. S Afr J Child Health 2016;10(3):186-187. DOI:10.7196/SAJCH.2016.v10i3.955

Congenital infantile fibrosarcoma (CIFS) is a rare tumour of childhood.

It accounts for <1% of malignant tumours in children.[1] The varied pattern of presentation of this cancer can be deduced from the occasional case reports that have emanated from almost every continent.[2-5] Reports from sub-Saharan Africa are particularly rare. CIFS occurrence in the sacrococcygeal region mimicking a sacrococcygeal teratoma has been reported,[3] and such presentation is generally uncommon. The poor predilection of the tumour for distant metastases may contribute to its above-average prognosis, but the rarity of systemic antenatal detection of congenital conditions in most parts of Africa may mitigate this good fortune.[2,6] We report the case of a 9-month-old female infant thought to have a sacrococcygeal teratoma. Pathological examination of the surgical specimen revealed a CIFS.

Case report

A 9-month-old female infant was brought to our outpatient depart­ ment by a distraught mother. The infant was born with a painless sacral mass, which had been progressively increasing in size. Her mother had sought help from faith healers and traditionalists, which accounted for the late presentation. There were no associated local or systemic symptoms. There was no history of maternal illness during pregnancy nor was there use of unprescribed medications. Physical examination revealed a healthy-looking female infant who was not pale, no pedal oedema or significant lymphadenopathy. There was a 25 × 20 cm mass of mixed consistency overlying the sacral region, extending to both gluteal regions and partially surrounding the anus (Fig. 1). Anal sphincteric tone was found to be slightly reduced on digital rectal examination. A tentative diagnosis of sacrococcygeal teratoma was made.

Sacral X-rays were normal. Ultrasonography confirmed the heterogeneous nature of the mass and ruled out any intra-abdominal extension. Serum alpha-fetoprotein levels were not elevated. The mass was excised via a standard Chevron incision. There was significant infiltration of both gluteal and sphincteric muscles precluding complete excision. The tip of the coccyx was excised in continuity with the mass. Grossly, we received ulcerated soft tissue measuring 12 × 9 × 7 cm covered by an eclipse of skin with cut section showing greyish-white and haemorrhagic areas. Microscopic 186

SAJCH

assessment of the sacrococcygeal mass showed a hypercellular tumour composed of plump spindle cells with elongated nuclei and abundant eosinophilic cytoplasm arranged in storiform and herringbone patterns in areas. There was rare abnormal mitosis and the margins of resection were involved. These features were in keeping with CIFS (Fig. 2).

Postoperatively there was superficial surgical site infection, which was managed with povidone iodine dressings. Chemotherapy (vincristine and actinomycin D) was commenced after histopathological diagnosis.

The patient’s condition has been generally stable for the past 6 months and she is periodically followed up.

Discussion

CIFS has been reported as congenital in a few cases.[1,5] In our case, the mother reported that her daughter was born with a sacral mass. The tumour is a fibroblastic soft-tissue sarcoma with a low-to-intermediate malignant potential.[5,7-15] An incidence of five per million infants has been reported, with males more commonly affected.[1,5,16] CIFS can occur in any part of the body and has been found in unusual parts of the body;[17,18] however, the extremities, namely the head, neck and trunk, in that order, are the most frequently affected locations.[1,4] The lesions in the trunk are usually more aggressive and recurrence rates are high, especially when the excision is incomplete. Presentation in the sacral region has been reported by Al-Salem;[3] this is the only recorded occurrence in this location. Our patient presented in a similar fashion and we understandably made a misdiagnosis of sacrococcygeal teratoma. Sacrococcygeal teratomas present at birth as sacrococcygeal masses.[11] Our curiosity was, however, aroused by normal serum alpha-fetoprotein levels. This tumour marker, although not diagnostic of sacrococcygeal teratomas, is elevated in many cases.[12] The margins of resection were involved, which would have been avoided if a biopsy was taken. We admit that an atypical mass of this nature would have been biopsied for histology before definitive treatment. Because the imaging features of CIFS are non-specific, this diagnosis was not entertained following ultrasonography of the sacral mass.[9] Infiltration of surrounding structures by the tumour is well documented. This usually limits extensive resection that would otherwise leave the patient mutilated.[4,15] This was our experience, as both gluteal and sphincteric muscles were involved. Coccygectomy in this patient

SEPTEMBER 2016 Vol. 10 No. 3

CASE REPORT

Fig. 1. A soft non-tender tissue mass on the sacrococcygeal area of the infant.

was in keeping with the general principle of reducing the risk of recurrence since we had assumed it was a sacrococcygeal teratoma.[13] Although cytogenetic analysis of CIFS has been shown to be useful in confirming diagnosis, revealing the fusion transcript ETV6-NTRK3, such studies are not routine in our centre. The biological behaviour of the tumour and its chemosensitivity have been attributed to this defect, which itself is the result of a recurrent chromosomal translocation t (12;15) (p13; q25).[1,2,5,7] This is a translocation between the ETS-related transcription regulator (12p13) and tyrosine kinase cell surface receptor (15q25).

Neo-adjuvant chemotherapy is the current treatment approach, which makes surgery less mutilating. Vincristine and actinomycin D are the most frequently employed agents.[1,2,4] CIFS has been successfully treated with chemotherapy alone.[4,5] Two percent of patients in the series reported by Orbach et al.[4] and 2 of the 11 in that by Lohl et al.[2] received radiotherapy in addition to surgery and chemotherapy. Our patient received vincristine and actinomycin D chemotherapy. The risk of recurrence is generally high, especially in fibrosarcoma of the trunk, and therefore our patient is periodically followed up after chemotherapy. Differential diagnoses to be entertained in masses located in this abnormal area in our patient should include, but not be limited to, embryonal rhabdomyosarcoma, neurofibroma and schwannoma.

Conclusion

CIFS can mimic a sacrococcygeal teratoma. The possibility of this diagnosis should be entertained especially if the serum alphafetoprotein levels are not elevated. Radiological imaging may not help with differentiation. In our opinion, a core biopsy in such instances may help determine the appropriate therapeutic approach, as CIFS is chemosensitive. Neo-adjuvant chemotherapy would allow for complete resection without sacrificing vital structures. With the reported excellent survival rates of >80%, the outlook for our patient is good.[4,5] References 1. Tarik E, Lamiae R, Abdelouahed A, Tarik M, Hassan G, Anouar DM. Unusual case of congenital/infantile fibrosarcoma in a new born. Afr J Paediatr Surg 2013;10(2):185-187. DOI:10.4103/0189-6725.115052 2. Loh ML, Ahn P, Perez-Atayde AR, Gebhardt MC, Shamberger RC, Grier HE. Treatment of infantile fibrosarcoma with chemotherapy and surgery: Results from the Dana-Faber Cancer Institute and Children’s Hospital, Boston. J Pediatr Hematol Oncol 2002;24(9):722-726. DOI:10.1097/00043426-200212000-00008

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A

B

C

D

Fig. 2. Microscopy of the sacrococcygeal mass showing hypercellular tumour composed of plump spindle cells with elongated nuclei and abundant eosinophilic cytoplasm arranged in storiform and herring-bone pattern in areas. There is rare abnormal mitosis. (A, B, C and D are H&E stains at × 40, 100, 200 and 400, respectively.)

3. Al-Salem AH. Congenital infantile fibrosarcoma masquerading as sacro­ coccygeal teratoma. J Pediatr Surg 2011;46(11):2177-2180. DOI:10.1016/j. jpedsurg.2011.08.011 4. Orbach D, Rey A, Cecchetto G, et al. Infantile fibrosarcorma: Management based on the European experience. J Clin Oncol 2010;28(2):318-323.

DOI:10.1200/JCO.2009.21.9972 5. Minard-Colin V, Orbach D, Martelli H, Bodemer C, Oberlin O. Soft tissue tumours in infants. Arch Pediatr 2009;16(7):1039-1048. DOI:10.1016/j. arcped.2009.03.005 6. Carrera JM. Obstetric ultrasounds in Africa: Is it necessary to promote their appropriate use? Donald School J Ultrasound Obstet Gynaecol 2011;5(3):289296. DOI:10.5005/jp-journals-10009-1205 7. McMahon E, Sorensen PH, Davis JH, Rogers PC, Schultz KR. Non-resectable congenital tumours with ETV6-NTRK3 gene fusion are highly responsive to chemotherapy. Med Pediatr Oncol 2003;40(5):288-292. DOI:10.1002/ mpo.10272 8. Mukai M, Sameshima H, Kodama Y, et al. Congenital infantile fibrosarcoma in a very low-birth-weight infant. J Pediatr Surg 2012;47(4):1-4. DOI:10.1016/j. jpedsurg.2011.11.052 9. Ainsworth KE, Chavhan GB, Gupta AA, Hopyan S, Taylor G. Congenital infantile fibrosarcoma: Review of imaging features. Paediatr Radiol 2014;44(9):1124-1129. DOI:10.1007/s00247-014-2957-5 10. Akyuz C, Kupeli S, Varan A, et al. Infantile fibrosarcoma: Retrospective analysis of eleven patients. Tumori 2011;97(2):166-169. DOI:10.1700/667.7778 11. Rescorlar FJ, Sawin RS, Coran AG, Dillon PW, Azizkhan RG. Long-term outcome for infants and children with sacrococcygeal teratoma: A report from the Children’s Cancer Group. J Paediatr Surg 1998;33(2):171-176.

12. Huddart SN, Mann JR, Robinson K, et al. Sacrococcygeal teratomas: The UK Children’s Cancer Study Group’s experience. I. Neonatal. Paediatr Surg Int 2003;19(1-2):47-51.

13. Hashish A, Fayad H, El-attar A, et al. Sacrococcygeal teratoma: Management and outcomes. Ann Paediatr Surgery 2009;5(2):119-125.

14. Kraneburg UM, Rinsky LA, Chisholm KM, Khosla RK. Emergency surgical treatment of an ulcerative and haemorrhagic congenital/infantile fibrosarcoma of the lower leg: Case report and literature review. J Pediatr Orthop B 2013;22(3):228-232. DOI:10.1097/BPB.0b013e3283536908.

15. Ferrari A, Orbach D, Sultan I, Casanova M, Bisogno G. Neonatal soft tissue sarcomas.

Semin Fetal Neonatal Med 2012;17(4):231-238. DOI:10.1016/j.siny.2012.05.003 16. Ries LAG, Smith MA, Gurney JG, et al. Cancer Incidence and survival Among Children and Adolescents: United States SEER Program 1975-1995, National Cancer Institute, SEER Program. NIH Pub. No. 99-4649. Bethesda, USA: National Institues of Health, 1999.

17. Steelman C, Katzensteen H, Parsham D, et al. Unusual presentation of congenital infantile fibrosarcoma in seven infants with molecular genetic analysis. Fetal Pediatr Pathol 2011;30(5):329-337. DOI:10.3109/15513815.2011.587497 18. Kagon B, Shehata B, Katzensteen H, et al. Primary congenital infantile fibrosarcoma of the heart: The first confirmed case. Ann Thorac Surg 2011;91(4):166-169. DOI:10.1016/j.athoracsur.2010.08.070

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CASE REPORT

This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

Acute cholecystitis in a child with scarlet fever: A rare association Y Parvez, MBBS, MD, MRCPCH, MRCPS, DCH (UK); S Thomas, MBBS, MD Department of Pediatrics, Dubai Hospital, United Arab Emirates Corresponding author: Y Parvez (dryparvez@gmail.com)

Group A streptococcal infection is common in children; however, scarlet fever is now considered rare except for isolated outbreaks. One of the rarest complications of scarlet fever is acute cholecystitis – very few cases have been reported in the literature. A 5-year-old boy was admitted with scarlet fever complicated by acute cholecystitis. Clinical examination along with ultrasound of the abdomen confirmed the diagnosis of acute cholecystitis associated with scarlet fever. The patient was managed conservatively with broad-spectrum antibiotics and was discharged home successfully. Acute cholecystitis should be suspected as a rare complication of scarlet fever presenting with an acute abdomen.

S Afr J Child Health 2016;10(3):188-189. DOI:10.7196/SAJCH.2016.v10i3.1088

Scarlet fever is a syndrome characterised by exudative pharyngitis, fever and bright-red exanthem. It is caused by toxin-producing Group A β-haemolytic streptococcus. Otitis media, bronchopneumonia, meningitis, renal failure and hepatitis are some of the complications described in the literature. Acute cholecystitis is the rarest complication of scarlet fever – very few cases have been reported so far. We report a classic case to highlight this important complication and its management. A 5-year-old, previously healthy boy was admitted to our hospital with complaints of high-grade fever and scarlatiniform rash of 3 days’ duration. On examination, the child was mildly icteric with a strawberry tongue, exudative pharyngitis and circumoral pallor. Besides the typical rash suggestive of scarlet fever, other systemic examination was unremarkable. His initial laboratory work-up showed: leukocytosis (14 300 cells/µL) with neutrophilia (76%); C-reactive protein (CRP) 57 mg/L; total bilirubin 3.8 mg/dL; direct bilirubin 1.6 mg/dL; alanine transaminse (ALT) 161 IU/L; aspartate transaminase (AST) 104 IU/L; gamma glutamyl transpeptidase (GGT) 24 IU/L; alkaline phosphatase (ALP) 355 IU/L; albumin 3.8 g/dL; prothombin time (PT) 12.9 s; activated partial thromboplastin time (APTT) 36.2 s; international normalised ratio (INR) 1.1; urine and stool examinations were normal. Serial antistreptolysin O titres showed a rising trend, eventually rising to 540 IU/µL from 220 IU/µL. Anti-DNase B blood test was not done owing to the unavailability of kit in the laboratory. The child’s throat culture was positive for Group A β-haemolytic streptococcus.

He was started on intravenous cefuroxime along with oral chlorpheniramine and emollients for local application. Two days after admission, the child developed abdominal pain in the right upper quadrant, associated with mild fever. On examination there was tenderness in the right upper quadrant of his abdomen. His amylase was 35 IU/L, lipase 22.6 IU/L, full blood count 16 800/µL (neutrophils 65%) and CRP 74 mg/L. Virology studies including Epstein-Barr virus (EBV, hepatitis A, B and C, cytomegalovirus (CMV) and HIV were normal. Urgent ultrasound of the abdomen was done, showing a mildly distended gallbladder with wall thickening and intraluminal sludge, likely representing acalculous cholecystitis (Fig. 1). The child was examined by a paediatric surgeon who advised management with intravenous cefuroxime, fluids and analgesics. His abdominal pain and fever gradually settled and he became asymptomatic after 10 days of treatment. The investigations that were repeated before discharge showed: white blood cell count 9 400 cells/µL (neutrophils 52%, lymphocytes 47%, Hb 10.4 g/dL); CRP 10 mg/L; total bilirubin 1.8 mg/dL; direct bilirubin 0.2 mg/dL; 188

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Fig. 1. Ultrasound scan of the abdomen showing distended gallbladder with mucosal thickening with intraluminal biliary sludge.

ALT 32 IU/L; AST 28 IU/L; GGT 15 IU/L; ALP 355 IU/L; albumin 3.9 g/dL; PT 12.2 s, APTT 34.3 s; INR 1. His blood, urine and stool cultures were negative. The ultrasound was repeated 2 weeks after discharge and it was normal. The child is being followed up and he is doing fine with no complications.

Discussion

Group A streptococci are extracellular, Gram-positive pathogens responsible for pharyngitis, impetigo, scarlet fever, rheumatic fever and acute glomerulonephritis. Scarlet fever, which is rare nowadays owing to frequent antibiotic prescriptions in children, is caused by a toxin-producing Group A β-haemolytic streptococcus found in sec­retions from the nose, throat, ears and skin.[1] The characteristic clinical features are exudative pharyngitis, fever and bright red exanthema. Otitis media, pneumonia, septicaemia, osteomyelitis, rheumatic fever and acute glomerulonephritis are the common complications associated with scarlet fever. However, hepatitis and vasculitis are other rare complications described in the literature.[2-4] Acute cholecystitis as a complication of typhoid and various viral infections such as Epstein-Barr virus, CMV and hepatitis A and B has been well described in the existing literature; however, the association of scarlet fever with acute cholecystitis has rarely been

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CASE REPORT reported and its pathogenesis is not clear.[5-7] It has been postulated that the streptococcus enters the gall bladder through the mucous mem­brane of the stomach by way of lymphatic channel producing toxin and lymphocytic infiltration responsible for the lesion in the gallbladder as well in the liver.[8] Patients with acute cholecystitis due to scarlet fever usually present with fever, right upper abdominal pain, vomiting and jaundice. The diagnosis is based on clinical manifestation, laboratory investigations (leukocytosis, abnormal liver function tests) and ultrasonographic findings (gallbladder distension, gall bladder wall thickness (>3.5 mm), non-shadowing echogenic materials or sludge, and pericholecystic fluid collections); however, these may sometimes be ambiguous and confusing in children.[8] The management is usually non-operative although cholecystectomy may be required.[7,8]

Conclusion

Scarlet fever is usually a benign disease, but may develop serious complications. Acute cholecystitis should be suspected in a child presenting with an acute abdomen associated with scarlet fever. Urgent

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ultrasound of the abdomen, along with laboratory investigations, is warranted to diagnose acute cholecystitis.

References

1. Cunningham MW. Pathogenesis of group A streptococcal infections. Clin Microbiol Rev 2000;13(3):470-511.

2. Gidaris D, Zafeiriou D, Mavridis P, Gombakis N. Scarlet fever and hepatitis: A case report. Hippokratia 2008;12(3):186-187.

3. Reddy UP, Albini TA, Banta JT, Davis JL. Post-streptococcal vasculitis. Ocul Immunol Inflamm 2008;16(1):35-36. DOI:10.1080/09273940701799163 4. Sandrini J, Beucher AB, Kouatchet A, Lavigne C. [Scarlet fever with multisystem organ failure and hypertrophic gastritis]. Rev Med Interne 2009;30(5):456-459.

DOI:10.1016/j.revmed.2008.07.010 5. Gora-Gebka M, Liberek A, Bako W, et al. Acute acalculous cholecystitis of viral etiology–a rare condition in children? J Pediatr Surg 2008;43(1):e25-27.

DOI:10.1016/j.jpedsurg.2007.10.073 6. Gnassingbé K, Katakoa G, Kanassoua KK, et al. Acute cholecystitis from typhic origin in children. Afr J Paediatr Surg 2013;10(2):108-111. DOI:10.4103/0189-6725.115033 7. Yasuda H, Takada T, Kawarada Y, et al. Unusual cases of acute cholecystitis and cholangitis: Tokyo Guidelines. J Hepatobiliary Pancreat Surg 2007;14(1):98113. DOI:10.1007/s00534-006-1162-9 8. Imamoğlu M, Sarihan H, Sari A, Ahmetoğlu A. Acute acalculous cholecystitis in children: Diagnosis and treatment. J Pediatr Surg 2002;37(1):36.

DOI:10.1053/jpsu.2002.29423

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CPD September 2016 CPD questionnaires must be completed online at www.mpconsulting.co.za

True (T) or False (F): Regarding neonatal sepsis 1. In developing countries, neonatal sepsis accounts for ~40% of deaths in under-5 children.

2. Early neonatal sepsis is defined as sepsis occurring within the first 7 days of life in full-term infants.

Regarding maternal mortality rates 3. In South Africa (SA), the maternal mortality rate is estimated to be ~150 per 10 000 live births.

4. Adolescent maternal mortality in SA is higher than that of adult maternal mortality.

Regarding the utilisation of high-care beds in the Western Cape 5. Acute lower respiratory tract infection is the most common cause for admission of children <5 years of age to a high-care facility in the Western Cape.

6. Approximately a quarter of admitted children required transfer to a paediatric intensive care unit.

Regarding chronic lung disease in neonates 7. Bronchopulmonary dysplasia is defined as oxygen dependence at 40 weeks’ gestation.

8. Chronic lung disease is common in neonates born at <1 250 g and <30 weeks’ gestation.

Regarding substance abuse among street children 9. Cannabis is the most common substance abused by street children in Cameroon.

10. Condoms were used in the majority of the sexual encounters of street children.

Regarding visiting regulations at hospitals in SA 11. There is a uniform set of regulations governing visiting and visitors’ hours in SA hospitals.

12. Children under the age of 12 years are excluded from visiting at a number of hospitals.

Regarding infants with pertussis 13. The median age of infants admitted with pertussis was <12 weeks.

14. Post-tussive vomiting occurred in the majority of infants.

15. The antibiotic of choice is a macrolide.

Regarding nocturnal enuresis in children 16. The majority of children with nocturnal enuresis do not have symptoms during the day.

Regarding congenital infantile fibrosarcoma 17. Congenital infantile fibrosarcoma is a common tumour in the sacrococcygeal region of infants.

18. It may be confused with a sacrococcygeal teratoma.

Regarding scarlet fever causing acute cholecystitis 19. Scarlet fever is caused by Group A β haemolytic streptococcus.

20. Acute glomerulonephritis and rheumatic fever are caused by Group B streptococci.

A maximum of 3 CEUs will be awarded per correctly completed test.

CPD questionnaires must be completed online via www.mpconsulting.co.za. After submission you can check the answers and print your certificate. Accreditation number: MDB015/177/02/2016 (Clinical)

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