MD , MRCP I , CONSULTANT NEONATOLOGY
Weill Cornell Medical College
Assistant Professor Pediatric/Neonatology Weill Cornell Medical college Qatar
Doha, Gulf area | Qatar
Main Specialties: Neonatal-Perinatal Medicine, Pediatrics
Additional Specialties: neonatology
Dr. Khalil Salameh
Dr. Khalil Salameh has over more than 30 years experience in the field of Neonatology encompassing clinical and administrative responsibilities. In the span of these two decades, he is highly involved in research, peer-reviewed journals and abstracts. His most recent research with granted sponsorship from QNRF, where he was a Co-PI. This 3 year research project in collaboration with Cincinnati Children’s Hospital Center was focused to the prevalence and risk factors for low vitamin D status among breastfeeding mother–infant while in an environment with abundant sunshine. These researches had received distinct recognitions and awards for its contribution. In total he has 4 researches and 13 published journals inclusive of the 5 journal articles that were published at international journals this year alone.
He has very keen interest to clinical data and gives great importance to data statistics. He was the Head of Database Committee and HMC representative for Vermont Oxford Network (VON). It is as a database network that collects data from participating NICU’s worldwide, including NICU-AWH, using the data for quality improvement.
Aside from these, he is appointed as Head of Pediatrics at Al Wakra Hospital with 2 years leadership to Obstetric and Gynecology Department. Dr. Khalil is NRP instructor and Assistant professor at Weill Cornell Medical College.
Primary Affiliation: Weill Cornell Medical College - Doha, Gulf area , Qatar
7PubMed Central Citations
Int J Womens Health 2020 4;12:59-70. Epub 2020 Feb 4.
Department of Pediatrics and Neonatology, Al Wakra Hospital, Hamad Medical Corporation, Al Wakra, Qatar.
Download full-text PDF
International Journal of Women’s Health
International Journal of Women’s Health 2020:12 59–70https://www.dovepress.com/ by 22.214.171.124Background: Epidural Analgesia (EA) is the most effective and most commonly used methodfor pain relief during labor. Some researchers have observed an association between EA andincreased neonatal morbidity. But this observation was not consistent in many other studies.Objectives: The primary objective of the study was to examine whether exposure toepidural analgesia increased the risk of NICU admission. The secondary objectives includedthe risks of clinical chorioamnionitis, instrumental delivery, neonatal depression, respiratorydistress, birth trauma, and neonatal seizure during the first 24 hours of life.Methods: This was a retrospective cohort study involving 2360 low-risk nulliparous womenwho delivered at AWH, Qatar, during the two years between January 2016 December and2017. Short-term neonatal outcomes of the mothers who received EA in active labor werecompared with a similar population who did not receive EA. As secondary objectives, laborparameters like maternal temperature elevation, duration of the second stage of labor, andinstrumental delivery were compared.Results: Significantly higher numbers of neonates were admitted to the NICU from the EAgroup (P<0.001, OR 1.89, 95% CI 1.45 to 2.46). They were more likely to have respiratorydistress (P=0.01, OR 1.49, 95% CI 1.07 to 2.07), birth injuries (P=0.02, OR =1.71, 95% CI1.06 to 2.74), admission temperature>37.5 °C (P=0.04, OR 3.40, 95% CI 1.00 to 11.49),need for oxygen on the first day (P=0.04, OR 1.44, 95% CI 1.01 to 2.07) and receiveantibiotics (P<0.001, OR 2.06,95% CI 1.47 to 2.79). There was no difference in the Apgarscore at 1 minute (P=0.12), need of resuscitation at birth (P=0.05), neonatal white cell count(P=0.34), platelet count (P=0.38) and C reactive protein (P=0.84). Mothers who received EAhad a lengthier second stage (P<0.001), temperature elevation >37.5°C (P<0.001, OR 7.40,95% CI 3.93 to 13.69) and instrumental delivery (P<0.001, OR 2.13, 95% CI 1.69 to 2.68).Conclusion: EA increases NICU admission, antibiotic exposure, neonatal birth injuries, needfor positive pressure ventilation at birth, and respiratory distress in the first 24 hours of life.Mothers on epidural analgesia have prolonged second stage of labor, a higher rate of instrumentaldelivery, meconium-stained amniotic fluid, fetal distress, and temperature elevation.Keywords: epidural analgesia, neonatal morbidity, NICU admissionDefinitionsShort term neonatal morbidity-sick conditions of neonates during the early neonatalperiod. For the current study, any morbidity during the first 24 hours of age like theneed for NICU admission, respiratory distress, birth trauma, etc.Chorioamnionitis (intraamniotic infection): Infection of the placenta and theamniotic membranes.Apgar score: the standard code used for coding the condition at birth and theneed for resuscitation in neonates
J Adv Pediatr Child Health. 2019; 2: 004-007. https://doi.org.10.29328/journal.japch.1001004
Journal of Advanced of pediatric and child health
ARCH Women Health Care, Volume 2(4): 4–5, 2019
Archives of Women Health and Care
ARCH Women Health Care, Volume 2(4): 1–5, 2019Archives of Women Health and CareVolume 2 Issue 4 Research OpenARCH Women Health Care, Volume 2(4): 1–5, 2019Research ArticleMicroarray Testing For Symmetrical Intrauterine GrowthRetardationSarfrazul Abedin1, Hakem Nazdaf1 ,Lina Habboub1, Ahmad Tomerak1 and Khalil Salameh1*1Department of pediatrics, Alwakra Hospital Hamad Medical Corporation, Qatar*Corresponding Author: Khalil Salameh, Department of pediatrics, Alwakra Hospital Hamad Medical Corporation, Qatar; Tel: 0097440114258; E-mail: Ksalameh@hamad.qaReceived: August 13, 2019; Accepted: August 22, 2019; Published: August 26, 2019;AbstractBackground: Intrauterine growth restriction (IUGR) is the most common risk factor associated with perinatal mortality after excluding congenitalanomalies 1. IUGR refers to a fetus that has failed to achieve its genetically determined growth potential and affects up to 7–10% of pregnancies 2. Fetalgrowth restriction is associated with an increase in perinatal mortality and morbidity. This is because of a high incidence of intrauterine fetal demise,intrapartum fetal morbidity, and operative deliveries. Neonates affected by IUGR suffer from respiratory difficulties, polycythemia, hypoglycemia,intraventricular hemorrhage, and hypothermia 3,4,5.Objective: 1.Primary objectives: to evaluate the results of Microarray in symmetrical IUGR babies. 2.Secondary objectives: to compare betweenmicroarray positive babies and negative babies regarding: gestation age, weight, Apgar score, need and indications for NICU admission as well aslength of NICU of stay.Result: Between Jan 2016 and December 2017 total 10,695 babis were born. Among that 578 babis were IUGR (501 asymmetric and 77 symmetric IUGR).Total 71 babies were taken in our analysis after excluding 3 down syndrome and 3 babies part of multiple pregnancy. Microarray test had positivefindings in 14/71 (19.7%). There were copy number changes of unknown significance in 8/71 (11.2%)Conclusion: Most of the microarray test results were copy number changes of unknown significane which is comparitvely much higher than reportedprevalence. Microarray positive IUGR had comparable NICU admissions to negative result group but their duration of stay, initial lower apgar scoresand thrombocytopenia was significantly higher. This may be because, even copy number changes has unknown significane, they may have some clinicaleffect which is not known till now and may need further studies and long term follow up for those cases.Keywords: Intrauterine growth restriction (IUGR), Chromosomal microarray analysis (CMA), Neonatal intensive care unit (NICU)Abbreviations and Acronyms: Intrauterine growth restriction(IUGR), Chromosomal microarray analysis (CMA), Copy-numbervariants (CNVs), Toxoplasmosis, rubella, cytomegalovirus, rubella(TORCH), Neonatal intensive care unit (NICU), variant of uncertainsignificance (VUS).IntroductionIntrauterine growth restriction (IUGR) is the most common riskfactor associated with perinatal mortality after excluding congenitalanomalies . IUGR refers to a fetus that has failed to achieve itsgenetically determined growth potential and affects up to 7–10%of pregnancies . Fetal growth restriction is associated with anincrease in perinatal mortality and morbidity. This is because of a highincidence of intrauterine fetal demise, intrapartum fetal morbidity,and operative deliveries. Neonates affected by IUGR suffer fromrespiratory difficulties, polycythemia, hypoglycemia, intraventricularhemorrhage, and hypothermia [3–5].Intrauterine growth restriction (IUGR) can be either symmetricor asymmetric. Symmetric IUGR is characterized by a similar andproportionate reduction in all auxological parameters, includingweight, length, and cranial and abdominal circumference. Earlygestational growth retardation would be expected to affect the fetusin a symmetric manner, and thus may have permanent neurologicconsequences for the infant. Causes include chromosomal disorders,including trisomy 13, 21 and 18 and some rare genetic syndromes,such as Cornelia de Lange and Silver Russell syndromes andearly congenital infections (rubella, cytomegalovirus, rubella,toxoplasmosis) . Early-onset forms of IUGR represent more severeconditions and more links with perinatal mortalities .Asymmetric IUGR is characterized by a greater reduction inbody weight, when compared to the length and more commonlydue to extrinsic influences that affect the fetus later in gestation,such as preeclampsia, chronic hypertension, and uterine anomalies.Karyotyping is an important investigation for symmetric IURG forchromosomal disorders particularly for babies with abnormal features.Chromosomal microarray analysis (CMA) is a high resolution,whole-genome screening technique that can identify most of thechromosomal imbalances as well as smaller submicroscopic deletionsand duplications that are referred to as copy-number variants (CNVs)and has quicker turnaround time than a karyotype [8–10]. AsKhalil Salameh (2019) Microarray Testing for Symmetrical Intrauterine Growth RetardationARCH Women Health Care, Volume 2(4): 2–5, 2019microarray has a higher diagnostic yield than conventional karyotype,in our institute we are doing microarray instead of a conventionalkaryotype for all symmetrical IUGR.Objectives1. Primary objectives: to evaluate the results of Microarray insymmetrical IUGR babies.2. Secondary objectives: to compare microarray positive babies andnegative babies regarding: gestation age, weight, Apgar score, needand indications for NICU admission as well as the length of NICUof stay.Study MethodologyThis is a retrospective study of symmetrical IUGR babies regardingtheir microarray results. Babies were considered symmetric IUGR iftheir growth parameter is less than 10 centiles of gestation age and sex.Symmetrical IUGR babies (as per growth curves) born in Al Wakrahospital, Qatar between Jan 2016 and December 2017 were includedin this study. Exclusion criteria were Down syndrome babies, Multiplepregnancies and TORCH+ cases.Required maternal and neonatal data were extracted from theelectronic patient records (Cerner) and entered into the data collectionsheet. Maternal data included: age, parity, history of abortions, familyhistory, gestational age, mode of delivery, instrumental use for delivery,meconium stained liquor and fetal deceleration. Newborn dataincluded: weight, sex, Apgar score at 5 minutes, need of resuscitation,cord pH, dysmorphic features or malformations, need for NICUadmission, the reason of admission, duration of NICU stay and labparameters as TORCH, microarray result, leukocyte count, plateletcount, ultrasound and ECHO.Data collection was started after approval from the institutionalreview board and ethical committee. For data analysis, SPSS 18 wasused. Statistical test was applied as appropriate. P value was taken assignificant if less than 0.05.Microarray test methodThe test was done by cytogenetic and molecular cytogeneticlaboratory, Doha, Qatar. Genome-wide oligonucleotide array-basedcomparative genomic hybridization (aCGH) analysis was performedwith the use of Human Genome CGH Microarray kit (OGT). Thearray contains ~40,000–180,000 DNA oligonucleotide probes spacedapproximately 30–37kb apart genome-wide. The probe sequences andlocations were from the human genome build (hg19). The purpose ofthis experiment was to identify any copy number changes (aneuploidy,gain/loss) associated with a chromosomal abnormality. Interpreted asper the database of Genomic Variants (projects.tcag.ca/variation).ResultBetween Jan 2016 and December 2017 total 10,695 babis babieswere born. Among that 578 babis babies were IUGR (501 asymmetricand 77 symmetric IUGR). Total 71 babies were taken in our analysisafter excluding 3 down syndrome and 3 babies part of multiplepregnancies. Microarray test had positive findings in 14/71 (19.7%).There were copy number changes of unknown significance in 8/71(11.2%). In (Table 1) findings are presented. It was abnormal in2/71 cases (2.8%), one 22q11.2 Deletion syndrome consistent withDiGeorge syndrome had left absent kidney but normal ECHO findingand another one trisomy 18 had atrial septal defect and ventricularseptal defect. The latter died on day 18 of life.We had compared maternal outcome in microarray positive resultgroup with negative result group in respect of parity, abortion, motherage, gestation age, delivery mode, instrument used for delivery,meconium stained liquor or fetal deceleration. Findings were notsignificantly different between groups. see (Table 2).When compared some neonatal outcomes between the sametwo groups as sex, birth weight, the need of resuscitation, cord ph.,NICU admissions, findings were not significant either. See Table 2.However apgar score at 5 minutes was statistically significant P 0.008but clinically not significant mean 9.4/ 9.9. Duration of NICU stay wassignificantly high in microarray result positive group P 0.019, meanduration of stay ±SD 18.14 ±10.6 / 8 ±6.28 day. Among blood counts,platelets were significantly low in microarray positive result group P0.045, mean ±SD 148 ±83 / 221±99. TORCH was done in 69/71 caseand it was negative in all.Ultrasound (brain ultrasound done in 13 cases and abdomenultrasound in 13 cases) and ECHO done in 6 cases as clinicallyindicated; findings are presented in (Table 3).DiscussionNeonates affected with Intrauterine growth restriction (IUGR) notonly have high prenatal and postnatal complication but also at highrisk of cerebral palsy, developmental delay and behavioral dysfunction4,5. Increasing evidence points to a link between IUGR and adultmetabolic syndrome [11, 12].As in early-onset symmetric IUGR one cause is chromosomaldisorder. So, karyotyping is one investigation particularly if a baby isfound with abnormal features. As Chromosomal microarray analysis(CMA) is a high resolution, whole-genome screening techniquethat can identify most of the chromosomal imbalances detected byconventional cytogenetic analysis, as well as smaller submicroscopicdeletions and duplications and can be performed on unculturedDNA samples . With accumulating experience during the lastdecade and data demonstrating improved detection of chromosomalabnormalities compared to conventional karyotyping, CMA is provingto be a valuable diagnostic tool in the prenatal setting [8,9]. Somerecommend using CMA for genetic analysis when fetal structuralanomalies and/or stillbirth need to be evaluated and to replace theneed for fetal karyotype in these cases . But CMA analysis willnot detect balanced alterations (reciprocal translocation, inversions,Robertsonian translocations, and balanced insertions).In our study, chromosomal changes were detected by microarraytest in 19.7% (14/71) of symmetric IUGR babies and mostly copynumber changes of unknown significance. In two cases it was abnormal2.8% (2/71), one going with DiGeorge syndrome and another onetrisomy 18. The latter died in the neonatal period. We did not findKhalil Salameh (2019) Microarray Testing for Symmetrical Intrauterine Growth RetardationARCH Women Health Care, Volume 2(4): 3–5, 2019any study in IUGR babies to compare our result. In one study CMVwas used as prenatal test for clinical indications as abnormal findingson fetal ultrasound, positive Down syndrome screening or maternalanxiety concerning advanced maternal age, family history of geneticdisorder or previous child with anomalies; detected 20% (44/220)clinically significant copy number variants (CNV), of which 21 werecommon aneuploidies and 23 had other chromosomal imbalances. In another study to see utility of chromosomal microarray inpredicting neonatal outcomes in the setting of fetal malformations,they found that nineteen (26.8%) had pathogenic CNV and of these,there were 6 neonatal deaths (31.6%) compared to 8 of 49 (16.3%)in normal CMA cases (p . 0.16) . In another study done on theutility of chromosomal microarray in anomalous fetuses, AbnormalCMA was not associated with increased odds of perinatal death inthis cohort and fetal; such fetuses are at high risk of perinatal deathirrespective of CMA result .Table 1. microarray test result findings in 14 positive cases. Interpreted as per the database of Genomic Variants (projects.tcag.ca/variation).CASE RESULT MOLECULAR CHANGE CHANGE1 Likely Benign Familial Copy NumberChangearr [hg19] 7q31.1(110,217,966–110,692,136)X1 matloss of the long arm of chromosome7 within cytogenetic band 7q31. The deletedsegment is ~474-kb kilobases (kb) in size.2 familial benign copy number change ofunknown significancearr[hg19] Xq11.2(63,481,708–64,416,909)X3gain of ~935-kb of the long arm of chromosome X, within cytogenetic band Xq11.duplicated region contains OMIM gene ZC4H2, heterozygous deletion, and loss ofmutation in this gene are reported in males with Wieacker-Wolff syndrome.3 copy number change of unknownbiological significancearr [hg19]7q21.22 (88,419,362–89,016,837)X3, arr [hg19]13q21.33(71,030,914–71,903,305)two copy number changes, one is a gain of ~ 1.7 Megabase (Mb) in the long armof chromosome 7 at cytogenetic band 7q21.2 and the second is a loss of ~872kilobases (kb) in the long arm of chromosome 13 at cytogenetic band 13q21. NoOMIM genes reported in these regions.4 Abnormal arr [hg19] 22q11.1q11.2(17,364,612–19,835,391)x1loss of the long arm of chromosome 22 involving the 22q11.2 is known asVelocardiofacial syndrome and DiGeorge syndrome (OMIM #192430)5 copy number change of unknownsignificancearr (hg19)18q12.1(25,278,479–26,575,519)X4gain of the long arm of chromosome 18 involving cytogenetic bands 18q12.The duplicated region is ~1.3 Mb in size and includes the CDH2 gene. Thisgene belongs to cadherin gene family encode proteins that mediate calcium-iondependentadhesion.6 Likely benign copy number change arr [hg19] 15q13.1(29,818,374–30,297,008)X3gain of the long arm of chromosome 15 within cytogenetic band 15q13.1. Theduplicated segment is ~478 kilobases (kb) in size and there is no reported OMIMgene in this region.7 Familial copy number change ofunknown clinical significancearr [hg19] 2p16.3(50,790,968–50,996,447)X1 patloss in the short arm of chromosome 2 within cytogenetic band 2p16.3. The sizeof the deleted segment is ~205 kilobases (kb), which causes partial deletion ofthe NRXN1 gene Heterozygous partial deletions, as well as other mutations anddisruptions, of NRXN1 have been reported in association with susceptibility forneurocognitive disabilities, such as autism spectrum disorders (ASDs)8 copy number change of unknownsignificancearr [hg19] 22q11.1(17,666,611–17,809,359)X1deletion of ~142-kb within cytogenetic band 22q11.1. The loss causes partialdeletion of the CECR1 gene. Mutations in this gene have been reported inPolyarteritis nodosa, childhood-onset, an autosomal recessive condition9 copy number change of unknownsignificancearr [hg19] 7q35(146,079,234–146,570,064)x3duplication of ~491-kb within cytogenetic band 7q35. The copy number changecauses partial duplication CNTNAP2 gene. Disruption of this gene in chromosomalrearrangements has been reported in children with autism. Homozygous mutationsin this gene have been reported in children with seizures10 Copy number change of unknownclinical significancearr [hg19] 11q13.4(73,688,299–73,783,214)X3gain of ~94-kb of the long arm of chromosome 11, within cytogenetic band 11q13.This copy number change causes partial duplication of the OFD14 gene, suspectedto be associated with Orofaciodigital syndrome XIV, an autosomal recessivecondition11 Copy number change of unknownsignificancearr [hg19] 3p26(2,213,357–2,277,767)X1a ~64 kilobases deletion of the short arm of chromosome 3 within cytogenetic band3p26, which causes partial deletion of the CNTN4 gene. Disruption of this genehave been reported in patients with physical features of 3p deletion syndrome12 Copy number change of unknownclinical significancearr [hg19]6q14.3q15(86,371,996–88,176,951)X3gain of ~1.8-Megabases (Mb) in the long arm of chromosome 6 around cytogeneticband 6q14 and q15. The duplicated segment contains multiple genes includingGJB7, HTR1E etc13 Abnormal arr [hg19]18(1–48129895)X3 an extra copy of chromosome 18, known as Edwards syndrome.14 copy number change of unknownsignificancearr [hg19]11q25(133,662,374–134,373,630)X3terminal duplication of ~711-kb of the terminal region of chromosome 11. Theduplicated segment includes OMIM gene JAM3.Khalil Salameh (2019) Microarray Testing for Symmetrical Intrauterine Growth RetardationARCH Women Health Care, Volume 2(4): 4–5, 2019Table 2.Microarray Test doneTotal = 71Positive resultNumber 14 (19.7%)Negative resultNumber 57 (80.2%)Ods Ratio with CI 95% /MD with CI 95%P valueParity Number (%) Nulliparous 6 (43%),multipara 8 (57%)Nulliparous 30 (52%),multipara 27 (48%)1.78 (0.45 to 4.81) 0.512Abortion Number (%) 4 (28.5%) 16 (28%) 1.02 (0.28 to 3.74) 0.97Mother age (year) mean±SD 27.79 ±5.7 range 19–36 29.72 ±4.7 range 20–41 -1.9 (-4.8 to 0.99) 0.192Gestation age (weeks) mean±SD 37.07 ±1.9 range 33–40 36.98 ±1.5 range 33–40 0.08 (-0.86 to 1.04) 0.852Delivery mode Number (%) Vaginal 8 (57%),caesarian 6 (43%)Vaginal 25 (44%),caesarian 32 (56%)1.7 (0.52 to 5.55) 0.372Instrument use Number (%) 1 (7.1%) 5 (8.7%) 0.844Meconium Number (%) 1 (7.1%) 7 (12.2%) 0.54 (0.06 to 4.8) 0.586Deceleration Number (%) 2 (14.2%) 15 (26.3%) 0.46 (0.93 to 2.33) 0.345Sex Number (%) Male 4 (28.5%)female 10 (71.5%)Male 25 (43.8%)female 32 (56.2%)0.51 (0.14 to 1.82) 0.297Weight (gram) mean±SD 2044 ±409 2121 ±332 -77 (-130 to 248) 0.461Apgar at 5 min mean±SD 9.4 ±1.15 9.9 ±0.34 -0.48 (-0.83 to -0.13) 0.008Resuscitation Number (%) 2 (14.2%) 3 (5.2%) 3 (0.45 to 19.5) 0.237Cord pH mean 7.313 7.03 0.28 (-0.66 to 1.2) 0.107NICU admission Number (%) 7 (50%) 31 (54.3%) 0.83 (0.26 to 2.7) 0.768NICU stay (days) mean±SD 18.14 ±10.6 8 ±6.28 10.1 (4.04 to 16.2) 0.019TORCH negative Number (%) 14 (100%) 55 (100%, in 2 cases not done)WBC 1000/cmm mean±SD 10.36 ±4.2 d (one in 8 cases) 12.62 ±5.7 (done in 42 cases) -2.2 (-6.5 to 2.05) 0.244Platelet 100000/cmm mean±SD 148 ±83 (done in 8 cases) 221 ±99 (done in 42 cases) -73.1 (-146 to 0.1) 0.045Platelet <150 x 106 Number (%)<100 x 1064/8 50% d(one in 8 cases)3/4 75%8/42 19% (done in 42 cases)3/8 37%CI – Conficane interval, MD – Mean difference, WBC – white blood cellsTable 3. Ultrasound and ECHO result in microarray positive and negative result cases.ULTRASOUNDBrain Abdomenmicroarray Positive cases Normal 4Flare 1Normal 3Absent one kidney 1Negative cases Normal 7Flare 1Normal 7Abnormal 0ECHOmicroarray Positive cases(done in 2 cases)Normal 1 , VSD &PDA 1Negative cases(done in 4 cases)Normal 2, ASD 1, VSD 1,CMA technique does not require dividing cells, in contrastto conventional karyotyping, which requires cell culture, so hasquicker turnaround time. CMA has a greater resolution thanconventional karyotyping, allowing for the detection of much smaller,submicroscopic deletions, and duplications typically down to a 50- to100-kb level . The disadvantage of CMA is that it looks for genomicimbalance and is not able to detect totally balanced chromosomalrearrangements, such as translocations or inversions. Also, CMA doesnot provide information about the chromosomal mechanism of agenetic imbalance ie change is trisomy or an unbalanced Robertsoniantranslocation which sometimes need to be confirmed by a karyotype.[15,16] Another disadvantage of CMA is the inability to preciselyinterpret the clinical significance of a previously unreported CNV orto accurately predict the phenotype of some CNVs that are associatedwith variable outcomes 10. CNVs are characterized as benign,clinically significant (ie, pathogenic), and as a variant of uncertainsignificance (VUS). The overall prevalence of VUS is approximately1–2% [17,18,19]. In our study it was in 11.2% symmetric IUGR babieswhich is much higher than reported prevalence. There is no study inIUGR babies to compare our result.When comparing microarray positive cases with microarraynegative cases, most findings were not significant except the durationof NICU stay and platelet count (Table 2). NICU admission was highamong IUGR babies about 50% but comparable in both groups. InKhalil Salameh (2019) Microarray Testing for Symmetrical Intrauterine Growth RetardationARCH Women Health Care, Volume 2(4): 5–5, 2019one study the overall admission rate was 7.2 per 100 births .Leukopenia and thrombocytopenia are known in IURG. In ourstudy thrombocytopenia was present in 24% (12/50) cases. Amongmicroarray positive group it was in 50% (4/8) babies and in 75% ofthem (3/4) count was less than 100 x 106. Among microarray negative,thrombocytopenia was in 19% (8/42) and in 37% of them (3/8) countwas less than 100 x 106. Platelet count is more significantly low inmicroarray test positive group 148/221 x 106 cmm P= 0.045. In ourstudy TORCH was negative in all cases. One case with 22q11.2 Deletionsyndrome had absent one kidney but normal cardiac anatomy. Onecase with trisomy 18 had atrial septal defect and ventricular septaldefect.ConclusionMost of the microarray test results were copy number changesof unknown significance which is comparitively much higher thanreported prevalence. Microarray positive IUGR had comparableNICU admissions to negative result group but their duration of stay,initial lower Apgar scores and thrombocytopenia was significantlyhigher. This may be because even copy number changes have unknownsignificance, they may have some clinical effect which is not known tillnow and may need further studies and long term followup for thosecases.This study has been Approved by Medical Research Center HamadMedical Corporation # MRC-01-18-006References1. Demirci O, Selçuk S, Kumru P, Asoğlu MR, Mahmutoğlu D, et al. (2015) Maternaland fetal risk factors affecting perinatal mortality in early and late fetal growthrestriction. Taiwan J Obstet Gynecol 54: 700–704. [crossref]2. Bernstein IM, Horbar JD, Badger GJ, Ohlsson A, Golan A (2000) Morbidityand mortality among very-low-birth-weight neonates with intrauterine growthrestriction. The Vermont Oxford Network. Am J Obstet Gynecol 182: 198–206.[crossref]3. Brar HS, Rutherford SE (1988) “Classification of intrauterine growth retardation,”.Seminars in Perinatology 12: 2–10.4. Bernstein I, Gabbe SG, Reed KL (2002) Intrauterine growth restriction,” inObstetrics: Normal and Problem Pregnancies. Gabbe SG et al. (Eds.) ChurchillLivingstone, New York, NY, USA, Pg No: 869.5. Soothill PW, Nicolaides KH, Campbell S (1987) Prenatal asphyxia,hyperlacticaemia, hypoglycaemia, and erythroblastosis in growth retarded fetuses.British Medical Journal 294: 1051–1053.6. Nikkila A, Kallen B, Marsal K (2007) Fetal growth and congenital malformations.Ultrasound Obstet Gynecol 29: 289–295.7. Baschat AA, Cosmi E, Bilardo CM, Wolf H, Berg C, et al. (2007) Predictors ofneonatal outcome in early-onset placental dysfunction. Obstet Gynecol 109:253e61.8. Zhu H, Lin S, Huang L (2016) Application of chromosomal microarray analysis inprenatal diagnosis of fetal growth restriction. Prenat Diagn 36: 686.9. Kan AS, Lau ET, Tang WF, Chan SS, Ding SC, et al. (2014) Whole-Genome ArrayCGH Evaluation for Replacing Prenatal Karyotyping in Hong Kong. PLoS ONE9: 87988.10. Lorraine Dugoff, Norton ME, Kuller JA (2016) The use of chromosomal microarrayfor prenatal diagnosis. Am J Obstet Gynecol 215: 2–9.11. Barker DJ, Bull AR, Osmond C, Simmonds SJ (1990) Fetal and placental size andrisk of hypertension in adult life. BMJ 301: 259–262. [crossref]12. Barker DJ, Winter PD, Osmond C, Margetts B, Simmonds SJ (1989) Weight ininfancy and death from ischaemic heart disease. Lancet 2: 577–580. [crossref]13. Jacqueline Parchem, Teresa Sparks, Kristen Gosnell, Mary Norton (2015) Theutility of chromosomal microarray in predicting neonatal outcomes in the setting offetal malformations. American Journal of Obstetrics & Gynecology 212: 174–175.14. Parchem JG, Sparks TN, Gosnell K, Norton ME (2018) Utility of chromosomalmicroarray in anomalous fetuses. Prenatal Diagnosis 38: 140–147.15. Fruhman G, Van den Veyver IB (2010) Applications of array comparative genomichybridization in obstetrics. Obstet Gynecol Clin North Am 37: 71–85.16. South ST, Lee C, Lamb AN, Higgins AW, Kearney HM (2013) Working Groupfor the American College of Medical Genetics and Genomics Laboratory QualityAssurance Committee. ACMG Standards and Guidelines for constitutionalcytogenomic microarray analysis, including postnatal and prenatal applications:revision 2013. Genet Med 15: 901–909.17. Wapner RJ, Martin CL, Levy B, Ballif BC, Eng CM, et al. (2012) Chromosomalmicroarray versus karyotyping for prenatal diagnosis. N Engl J Med 367: 2175–2184. [crossref]18. Hillman SC, McMullan DJ, Hall G (2013) Use of prenatal chromosomal microarray:prospective cohort study and systematic review and metaanalysis. UltrasoundObstet Gynecol 41: 610–620.19. Shaffer LG, Dabell MP, Fisher AJ, Coppinger J, Bandholz AM, et al. (2012)Experience with microarray-based comparative genomic hybridization for prenataldiagnosis in over 5000 pregnancies. Prenat Diagn 32: 976–985. [crossref]20. Harrison WN, Wasserman JR, Goodman DC (2018) Regional Variation in NeonatalIntensive Care Admissions and the Relationship to Bed Supply. J Pediatr 192:73–79.Citation:Abedin S, Nazdaf H, Habboub L, Tomerak A, Salameh KM (2019) MicroarrayTesting For Symmetrical Intrauterine Growth Retardation. ARCH WomenHealth Care Volume 2(4): 1–5.
Nutrients 2019 Jul 17;11(7). Epub 2019 Jul 17.
Sidra Medicine, Doha, Qatar.
In view of continuing reports of high prevalence of severe vitamin D deficiency and low rate of infant vitamin D supplementation, an alternative strategy for prevention of vitamin D deficiency in infants warrants further study. The aim of this randomized controlled trial among 95 exclusively breastfeeding mother-infant pairs with high prevalence of vitamin D deficiency was to compare the effect of six-month post-partum vitamin D maternal supplementation of 6000 IU/day alone with maternal supplementation of 600 IU/day plus infant supplementation of 400 IU/day on the vitamin D status of breastfeeding infants in Doha, Qatar. Serum calcium, parathyroid hormone, maternal urine calcium/creatinine ratio and breast milk vitamin D content were measured. At baseline, the mean serum 25-hydroxyvitamin D (25(OH)D) of mothers on 6000 IU and 600 IU (35.1 vs. 35.7 nmol/L) and in their infants (31.9 vs. 29.6) respectively were low but similar. At the end of the six month supplementation, mothers on 6000 IU achieved higher serum 25(OH)D mean ± SD of 98 ± 35 nmol/L than 52 ± 20 nmol/L in mothers on 600 IU ( < 0.0001). Of mothers on 6000 IU, 96% achieved adequate serum 25(OH)D (?50 nmol/L) compared with 52%in mothers on 600 IU ( < 0.0001). Infants of mothers on 600 IU and also supplemented with 400 IU vitamin D had slightly higher serum 25(OH)D than infants of mothers on 6000 IU alone (109 vs. 92 nmol/L, = 0.03); however, similar percentage of infants in both groups achieved adequate serum 25(OH)D ?50 nmol/L (91% vs. 89%, = 0.75). Mothers on 6000 IU vitamin D/day also had higher human milk vitamin D content. Safety measurements, including serum calcium and urine calcium/creatinine ratios in the mother and serum calcium levels in the infants were similar in both groups. Maternal 6000 IU/day vitamin D supplementation alone safely optimizes maternal vitamin D status, improves milk vitamin D to maintain adequate infant serum 25(OH)D. It thus provides an alternative option to prevent the burden of vitamin D deficiency in exclusively breastfeeding infants in high-risk populations and warrants further study of the effective dose.
Download full-text PDF
Progressing Aspects in Pediatrics and Neonatology
DOI: 10.32474/PAPN.2019.02.000128Use Judiciously, or I Will Be Useless” A ClinicalAudit on Use of Antibiotics Within First 72 hrs ofLife in Symptomatic Term Babies With noMaternal Risk for InfectionKhalil Salameh*, Rajesh Pattu Valappil, Abedal khalik Ahmad Khedr and Ahmed Hosny Ahmed TomerakDepartment of Pediatrics, Qatar*Corresponding author: Khalil Salameh, Department of Pediatrics, QatarReceived: December 20, 2018 Published: January 02, 2018BackgroundOver use of antibiotics lead to resistance and unwanted sideeffectsin newborns. Since 1992, professional societies or publichealth agencies have issued several generations of recommendationsfor prevention or management of early-onset neonatal sepsis (EOS)[1-5]. Despite these efforts, recommendations remain inconsistent,clarifications are necessary, local adaptations are common, andcompliance rates are low [6-7]. It is common clinical practiceto discontinue antibiotic treatment of asymptomatic babies ifthe blood cultures are negative at 48 hours [8-10]. But it is verycommon to have prolonged antibiotic courses for more than 48hours due to delayed release of blood culture, high CRP, abnormalCBC or delayed decision by the Physician to stop antibiotics. Ina previous study, McDonald et al.  found this as a commonoccurrence in neonatal intensive care units. The purpose of thisaudit is to rationalize the use of antibiotics in symptomatic termbabies, with no risk for infection.MethodologyThis is a retrospective audit to determine the Use of antibioticsin symptomatic term babies with no maternal risk for infection. Anyfull-term infant who was started on antibiotics after admitting toNICU with various symptoms were included. Preterm babies andbabies with maternal risk for infection (i.e. suspected maternalchorioamnionitis, PROM >18 hrs, GBS bacteriuria in mother) wereexcluded from the audit. Data were collected from January to March2017 and analyzed with descriptive statistics. A re-audit was carriedout between January to March 2018. 35 patients were included inthe first audit and 22 in the second cycle. As a result of the firstaudit cycle following changes in practice were implemented.a) Infants with mild-to-moderate respiratory findings (flaring,grunting, retractions or tachypnea) immediately after birth may bemonitored closely for resolution of transitional behaviors, withoutinitiation of antibiotic treatment unless signs worsen or persist formore than 6 hours without improvement .b) Serial normal diagnostic tests, such as blood counts orC-reactive protein levels, are highly predictive of the absence ofinfection and should be relied upon (in addition to culture results)to minimize the duration of antibiotic exposure. However, isolatedabnormal hematological or acute-phase-reactant measurementsshould not justify continuation of empirical antibiotics for morethan 48 hours in well-appearing infants with negative cultureresults.c) Babies diagnosed as TTN without another differentialdiagnosis, should not be started on antibiotics unless mild tomoderate respiratory signs persist beyond 6 hours. The re-auditevaluated improvement in clinical practice regarding judicious useof antibiotics.Results and ConclusionOverall the unit adhered well to the guidelines and there wasa significant reduction in use of antibiotics in the unit. None of thebabies with mild respiratory distress received Antibiotics before6 hours in the re-audit, where as a significant number (15 babies(42%), with mild respiratory distress that improved in 6 hoursreceived antibiotics during the first audit period. Similarly, in noneof the babies antibiotics were continued for more than 48 hoursfor high CRP. (4 babies initial CRP were high). During the firstDOI: 10.32474/PAPN.2019.02.000128Pr o g A s p i n P e d i a t r i c & N e o n a t V o l u m e 2 - I s s u e 1 Copyrights @ Khalil Salameh, et al.Citation: Khalil S, Rajesh P V, Abedal k Ahmad K, A Hosny A Tomerak. Use Judiciously, or I Will Be Useless” A Clinical Audit on Use ofAntibiotics Within First 72 hrs of Life in Symptomatic Term Babies With no Maternal Risk for Infection. Prog Asp in Pediatric & Neonat2(1)- 2018.PAPN.MS.ID.000128. DOI: 10.32474/PAPN.2019.02.000128.111audit period, 11% of the cases antibiotics were continued beyond48 hours just for high CRP. But when compared to the first audit,more number of babies received antibiotics for cases diagnosed asTTN because the local and international guidelines suggest to startantibiotics in babies with respiratory distress persisting for morethan 6 hours.References1. Committee on Infectious Diseases, Committee on Fetus and Newborn(1992) Guidelines for prevention of group B streptococcal (GBS)infection by chemoprophylaxis. Pediatrics 90(5): 775-778.2. Committee on Technical Bulletins (1993) Group B streptococcalinfections in pregnancy. ACOG Technical Bulletin Number 170. Int JGynaecol Obstet 42(1): 55-59.3. Centers for Disease Control and Prevention (1996) Prevention ofperinatal group B streptococcal disease: a public health perspective.MMWR Recomm Rep 45(RR-7): 1-24.4. Committee on Obstetric Practice (1996) Prevention of early-onsetgroup B streptococcal disease in newborns. ACOG Committee OpinionNumber 173. Int J Gynaecol Obstet 54: 197-205.5. Committee on Infectious Diseases, Committee on Fetus and Newborn(1997) Revised guidelines for prevention of early-onset group Bstreptococcal (GBS) infection. Pediatrics 99(3): 489-496.6. Brady MT, Polin RA (2013) Prevention and management of infantswith suspected or proven neonatal sepsis. Pediatrics 132(1): 166-168.7. Mukhopadhyay S, Dukhovny D, Mao W, Eichenwald EC, PuopoloKM (2014) 2010 perinatal GBS prevention guideline and resourceutilization. Pediatrics 133(2): 196-203.8. Pichichero ME, Todd JK (1979) Detection of neonatal bacteremia. JPediatr 94(6): 958-960.9. Rowley AH, Wald ER (1986) Incubation period necessary to detectbacteremia in neonates. Pediatr Infect Dis J 5(5): 590-591.10. Hurst MK, Yoder BA (1995) Detection of bacteremia in young infants:is 48 hrs adequate? Pediatr Infect Dis J 14(8): 711-713.11. McDonald M, Moloney A, Clarke TA, et al. (1992) Blood cultures andantibiotic use in a neonatal intensive care unit. Ir J Med Sci 161: 163-412. William E Benitz, James L Wynn, Richard A Polin (2015) Reappraisalof Guidelines for Management of Neonates with Suspected Early-OnsetSepsis. J Pediatr 166(4): 1070-1074.This work is licensed under CreativeCommons Attribution 4.0 LicenseTo Submit Your Article Click Here: S u bmit ArticleProgressing Aspects in Pediatricsand NeonatologyAssets of Publishing with us• Global archiving of articles• Immediate, unrestricted online access• Rigorous Peer Review Process• Unique DOI for all articlesDOI: 10.32474/PAPN.2019.02.000128
Vol 1 • I ssue 2 • 2018
Clinical Researc h in Pediatrics
https://asclepiusopen.com/clnical-research-in-pediatrics/volume-1-issue-2/Extremely Post-Term Infant with Adverse Outcome Khalil Salameh, Rajai Al-Bedaywi, Lina Habboub, Naser Abulgasim Elkabir, Ahmad Tomerak Department of Pediatrics, Alwakra Hospital, Hamad Medical Corporation, Al Wakrah, Qatar ABSTRACT Post-term infants are born at a gestational age >42 weeks or 294 days from the 1st day of the last menstrual period. Post-term infants have higher rates of morbidity and mortality than term infants. Risk factors for post-term births include the following: Prim gravida, prior post-term pregnancy, and genetic predisposition as a concordance for post-term pregnancy is higher in monozygotic than dizygotic twin mothers, maternal obesity, older maternal age, and male fetal gender. We are presenting a case of newborn infant delivered at post-term 47 weeks (post conception age) who was born through thick meconium stained liquor delivery showed sever skin peeling. He needed respiratory ventilation since birth and his brain magnetic resonance imaging was abnormal. This report aims to raise awareness among obstetric-gynecology and neonatologists about complications of post maturity and to put a plan to deliver these babies before reaching 42 weeks gestation Key words: BW (Birth weight), CPAP ( continuous positive airway pressure), LSCS (lower section cesarean section), MRI (magnetic resonance imaging), SGA (Small for gestation) CASE REPORT Address for correspondence: Khalil Salameh, Department of Pediatrics, Alwakra Hospital, Hamad Medical Corporation, Al Wakrah, Qatar. Tel.: 0097440114258. E-mail: Ksalameh@hamad.qa © 2018 The Author(s). This open access article is distributed under a Creative Commons Attribution (CC-BY) 4.0 license Salameh, et al.: Extremely post-term infant with adverse outcome 2 Clinical Research in Pediatrics • Vol 1 • Issue 2 • 2018 was unplanned pregnancy so unsure about the date, but mother mentioned that LMP was on 16/3/2017, so plan was put by gynecology doctors to do elective LSCS on 24/12/2018, but mother neglected that date. Ultrasound examination done at 35 weeks showed normal fetal growth. AT 47 weeks , she attended the obstetrics and gynecology emergency department with labor pain. She was admitted to the obstetrics ward, and a cardiotocogram showed fetal distress in the form of fetal bradycardia and the liquor was meconium stained., Baby was delivered by vacuum assisted vaginal delivery. With birth weight of 2475-g infant male covered with thick meconium with severe skin peeling [Figures 1 and 2] with Apgar scores of 9/10 at 1 and 5 min, respectively. Cord gas showed arterial PH 7.06 BE −11.3 PCO2 74 and venous PH 7.13 BE −11.8 PCO2 52 . At 5 min, the infant developed respiratory distress needed endotracheal intubation and mechanical ventilation with oxygen of 40%. Then i nfant was transferred to NICU, kept on mechanical ventilation and during that period he got left side pneumothorax needed drainage [Figures 3 and 4], and continue on mechanical ventilation for 2 days, His laboratory result as initial simple blood tests and Metabolic screen test were normal. On day 3, the infant had abnormal non-rhythmic movements of all extremity as convulsion which was aborted with one dose of phenobarbitone. On day 9days of life Brain Magnetic resonance imaging was done and showed mild bilateral symmetric diffusion restriction involving the posterior limb of internal capsule, dorsal midbrain, and dorsal pons. Features were reported as being in favor of metabolic encephalopathy over hypoxic brain injury. During hospital stay infant had feeding difficulty started orogatric tube feed until the 10th day of life when he was discharged on full feed by sucking with follow-up at the high risk baby clinic and pediatric neurology clinic. Figure 1: Staring eye Figure 4: Drained left pneumothorax Figure 3: Left pneumothorax Figure 2: Skin peeling Salameh, et al.: Extremely post-term infant with adverse outcome Clinical Research in Pediatrics • Vol 1 • Issue 2 • 2018 3 DISCUSSION As the optimal intervention is the prevention of post-term births, it has been suggested that induction of labor be routinely performed in mothers who are at 41 weeks’ gestation. Nevertheless, there are settings in which induction of labor at 41 weeks gestation is not an option. For these post-term deliveries, the neonatal management consists of screening and treating complications associated with prolonged pregnancy (e.g., meconium aspiration, perinatal asphyxia, and persistent pulmonary hypertension) and providing routine newborn care. • Before delivery, an assessment of the need for neonatal resuscitation is made based on the GA, anticipated BW, presence of a congenital anomaly or labor complications, mode of delivery (e.g., cesarean delivery), and maternal history. • Immediately after delivery, routine neonatal care is provided which includes drying, clearing the airway of secretions if present, maintaining warmth, and a rapid assessment of the infant’s clinical status based on vigor, including cry, heart rate, and tone, as well as an examination to identify any major congenital anomaly. The need for further intervention is based on this initial evaluation. If the infant does not require additional resuscitation, the infant should be given to the mother for skin-to-skin care and initiation of breastfeeding right after birth. Infants should be fed as quickly as possible after delivery to avoid hypoglycemia. • Further evaluation following transition from the delivery room includes a comprehensive examination to identify any evidence of birth trauma (e.g., perinatal depression, brachial plexus injury, or clavicular fracture), congenital defects, or complications associated with prolonged pregnancy. • Laboratory screening for hypoglycemia and polycythemia should be performed in infants with evidence of poor fetal growth within the first 1–2 h following delivery. • If there are no significant complications that require further intervention, routine newborn care should be provided. Long-term outcome Although data are limited on the long-term outcome of post-term infants, these patients may be at risk for neurodevelopmental complications as follows: Cerebral palsy (CP) Children born post-term appear to have an increased risk of CP compared with those who were born at term. This was illustrated in a population-based follow-up study from Norway which reported that children who were delivered at a GA >42 weeks were more likely to develop CP than children born at 40 weeks’ gestation (relative risk 1.4, 95% confidence interval 1.1–1.8). The prevalence of CP in children with a GA >42 weeks was 1.44/1000 patients. Epilepsy In a cohort Danish study, it appears that prolonged gestation was a risk factor for early epilepsy that occurred within the 1st year of life. However, there was no evidence of an association between post-term delivery and epilepsy beyond 1 year of age. Developmental outcome In an older cohort study from 1977, post-term infants had comparable motor scores on the Bayley Scales of Infant Development at 8 months of age compared with controls, but cognitive scores were lower. Behavioral problems In a study of infants in the Netherlands, the risk of behavioral problems and attention deficit disorder was increased among post-term infants, compared with term counterparts. REFERENCES 1. Mori R, Ota E, Middleton P, Tobe-Gai R, Mahomed K, Bhutta ZA, et al. Zinc supplementation for improving pregnancy and infant outcome. Cochrane Database Syst Rev 2012;7:CD000230. 2. Mannino F. Neonatal complications of postterm gestation. J Reprod Med 1988;33:271-6. 3. Vorherr H. Placental insufficiency in relation to postterm pregnancy and fetal postmaturity. Evaluation of fetoplacental function; Management of the postterm gravida. Am J Obstet Gynecol 1975;123:67-103. 4. Caughey AB, Nicholson JM, Washington AE. First-vs secondtrimester ultrasound: The effect on pregnancy dating and perinatal outcomes. Am J Obstet Gynecol 2008;198:703.e1-5. 5. Haavaldsen C, Sarfraz AA, Samuelsen SO, Eskild A. The impact of maternal age on fetal death: Does length of gestation matter? Am J Obstet Gynecol 2010;203:554.e1-8. 6. Badawi N, Kurinczuk JJ, Keogh JM, Alessandri LM, O’Sullivan F, Burton PR, et al. Antepartum risk factors for newborn encephalopathy: The Western Australian case-control study. BMJ 1998;317:1549-53. 7. Eden RD, Seifert LS, Winegar A, Spellacy WN. Perinatal characteristics of uncomplicated postdate pregnancies. Obstet Gynecol 1987;69:296-9. 8. Heimstad R, Romundstad PR, Eik-Nes SH, Salvesen KA. Outcomes of pregnancy beyond 37 weeks of gestation. Obstet Gynecol 2006;108:500-8. 9. Hernández-Díaz S, Van Marter LJ, Werler MM, Louik C, Mitchell AA. Risk factors for persistent pulmonary hypertension of the newborn. Pediatrics 2007;120:e272-82. 10. Seo IS, Gillim SE, Mirkin LD. Hyaline membranes in postmature infants. Pediatr Pathol 1990;10:539-48. 11. Moster D, Wilcox AJ, Vollset SE, Markestad T, Lie RT. Salameh, et al.: Extremely post-term infant with adverse outcome 4 Clinical Research in Pediatrics • Vol 1 • Issue 2 • 2018 Cerebral palsy among term and postterm births. JAMA 2010;304:976-82. 12. Ehrenstein V, Pedersen L, Holsteen V, Larsen H, Rothman KJ, Sørensen HT, et al. Postterm delivery and risk for epilepsy in childhood. Pediatrics 2007;119:e554-61. How to cite this article: Salameh K, Al-Bedaywi R, Habboub L, Elkabir NA, Tomerak A. Extremely PostTerm Infant with Adverse Outcome. Clin Res Pedi
Khalil Salameh, SF J Pub Health, 2018, 2:5
SciFed Journal of Public Health
Khalil Salameh, SF J Pub Health, 2018, 2:5
*Khalil Salameh, Lina Habboub, Brijroy V, Anvar PV, Samer Alhoyed, Rajai Al-Bedaywi
*Department of Pediatrics, Alwakra Hospital, Hamad Medical Corporation, Al Wakrah, Qatar
NICU: Neonatal Intensive Care Unit;
NPE: Neonatologist Performed Echocardiography;
Tn ECHO: Targeted Neonatal Echo;
CHD: Congenital Heart Disease;
Hs PDA: Haemodynamically Significant Patent Ductus
PPHN: Persistent Pulmonary Hypertension;
RVSP: Right Ventricular Systolic Pressure;
PFO: Patent Foramen Ovale;
IVC: Inferior Venacava;
SVC: Superior Venacava;
iNO: Inhaled Nitric Oxide
Echocardiography is a bedside tool, which is noninvasive,
and gives valuable reproducible information as
long as trained physicians or technicians are available to do it
. Neonatologist performed echo (NPE) or other accepted
terminologies such as targeted neonatal echocardiography
(Tn ECHO) or Functional echocardiography, is the
bedside use of cardiac ultrasound to follow functional and
hemodynamic changes longitudinally in NICU [2, 3]. It is
*Corresponding author: Khalil Salameh, Department of Pediatrics,
Alwakra Hospital, Hamad Medical Corporation, Al Wakrah, Qatar.
E-mail: Ksalameh@hamad.qa; Tel: 0097440114258
Received December 10, 2018; Accepted December 12, 2018; Published
Citation: Khalil Salameh (2018) Neonatal Echocardiography in a Level
II NICU – 1st Experience from Qatar. SF J Pub Health 2:5.
Copyright: © 2018 Khalil Salameh. This is an open-access article
distributed under the terms of the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any
medium, provided the original author and source are credited.
NICU at Al Wakra hospital in Qatar is a level II B NICU with a target population of babies born more than
30 weeks and weight more than 1.25 kg. Critically ill babies and babies outside the scope of service, if are born in AL
Wakra hospital, these babies are stabilized and later transferred to Women’s hospital. The main reason for this difficult
arrangement has been done due to lack of subspecialty services including pediatric cardiology in AL Wakra hospital.
Neonates with suspected CHD and hemodynamic instability with suspected pulmonary artery hypertension were also
transferred to Women’s hospital at Doha. Stable neonates with cardiac murmur detected during post natal check up
often faced, delayed diagnosis, delayed discharge and most cases were referred to cardiology in Hamad General
hospital at Doha. Since neonatologist performed echo has become a standard of practice in many advanced NICUs
from early 2000, NICU at Al Wakra hospital has adopted this practice from 2015. Here we report a 3 years experience
of neonatologist-performed echo as an audit report.
Volume 2 · Issue 4 · 1000029
SciFed Journal of Public Health
Introduction IHPS is a common cause of gastric outlet obstruction in infants. The cardinal features of IHPS are non-bilious projectile vomiting and visible peristalsis in the left upper abdominal quadrant. Bilious vomiting in this condition is rarely reported and may create confusions in diagnosis . This is a report of a 30 days old infant with IHPS presenting with bilious vomiting and is intended to raise awareness and enhance index of suspicion
Khalil Salameh, SF J Emer Med, 2017, 1:1
SciFed Journal of Emergency Medicine
Abstract Cleone Pardoe, Mohamed Omer, Hala Elkuni EL Mohamed, Merva Yahya, *Khalil Salameh *Department of pediatrics, Alwakra Hospital Hamad Medical Corporation, Qatar *Corresponding author: Khalil Salameh, Department of pediatrics, Alwakra Hospital Hamad Medical Corporation, Qatar. E-mail: Ksalameh@ hamad.qa Received December 06, 2017; Accepted December 07, 2017; Published December 26, 2017 Citation: Khalil Salameh (2017) A Case Report of Acute Cardiac Failure in a Child: An Atypical Presentation Acute Rheumatic Fever; A Challenging Diagnosis. SF J Emer Med 1:1. Copyright: © 2017 Khalil Salameh. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Acute rheumatic fever (ARF) is recognized as a diagnostic challenge and can present with a wide variety of symptoms. The Revised Jones criteria (RJC) (2015) aids the diagnostic process by identifying key major and minor features (Table 1), however non-conforming cases continue to arise. Consequent misdiagnosis results in over and under recognition of ARF and risks inappropriate management. A significant complication of ARF is rheumatic heart disease; a cause of significant morbidity worldwide. An awareness of unusual cases aids clinical judgement and can help make difficult diagnoses. We present the case of a nine-year-old Malaysian boy who presented acutely in congestive cardiac failure. He had features consistent with the RJC including carditis, increasing erythrocyte sedimentation rate (ESR), elevated anti-streptolysin O titer (ASOT) and electrocardiogram (ECG) changes. Despite this, he did not fulfil the RJC as ECG findings are non-diagnostic in the presence of carditis. In addition, a raised ASOT lacks significance in areas with a high prevalence of streptococcal infection if the RJC are not met such as in this case. Consequently, due to the atypical nature of the presentation and isolated cardiac features, an alternative diagnosis of rheumatic heart disease was considered. We discuss the diagnostic challenges of ARF and RHD faced in this case
Summary Antenatal Bartter syndrome is a rare condition that can present with different clinical features. These features include early onset maternal polyhydramnios, failure to thrive, prematurity and nephrocalcinosis. We are presenting this 20-day-old girl who had an antenatal history of polyhydramnios. She developed persistent non-bilious vomiting that was associated with constipation soon after birth. She presented with failure to thrive and features suggestive of intestinal obstruction. On the initial evaluation, she was noted to have hypokalaemic, hyponatraemic metabolic alkalosis. The initial work-up was done to exclude surgical and renal causes of her presentation, and the diagnosis was confirmed by gene analysis to be type III—classic Bartter syndrome. She was closely monitored for her growth and development with the appropriate salt replacement therapy.
Pediatric Health, Medicine and Therapeutics
Abstract: Omental infarction (OI) is a rare cause of acute abdominal pain occurring in 0.1% of children, which is typically diagnosed during surgery for suspected appendicitis. We present the case of a 7-year-old Pakistani girl. She presented with acute, severe, progressive, right-sided abdominal pain, which was present for 12 hours before presentation. No constitutional symptoms such as fever, anorexia, nausea or vomiting were present. Clinical examination revealed an adequately growing child following the 50th centile. She had severe generalized abdominal tenderness with rebound tenderness and guarding, mainly on the right lower abdominal quadrant, with all other system examinations normal. She had mildly increased inflammatory markers, and her initial abdominal ultrasound scan result was within normal limits. She had laparoscopic surgery following a diagnosis of suspected acute appendicitis; however, an intraoperative diagnosis of OI was made. This was later confirmed by histopathology. This case report highlights the importance of including OI in the differential diagnosis list of acute abdominal pain in children, in addition to the importance of computed tomography (CT) as the gold standard tool to aid diagnosis. In the presence of typical symptoms and signs of OI, a CT scan can assist and guide the management of similar cases. This course of action is suggested for the reason that OI typically runs a self-limited course and conservative care may be the most appropriate recommended course of action. Consequently, unnecessary operations could be avoided due to the diagnosis confirmation of studying images. Keywords: omentum, infarction, abdominal pain, child Introduction Omentum
Salameh, et al., Neonat Pediatr Med 2017, 3:1
Journal of Neonatal and Pediatric Medicine Salameh, et al., Neonat Pediatr Med 2017, 3:1
Neonatal purpura fulminans is a clinical entity characterised by echymotic skin lesions, consumptive coagulopathy and widespread micro and macro vascular thrombosis. This can be hereditary or secondary to acquired causes. Clinical presentation of hereditary Protein C deficiency can be solely limited to localised echymotic skin lesions in the early stage, with wide spread vascular thrombosis ensuing eventually, in the absence of timely Protein C replacement. A case of a neonate presenting with localised scalp ecchymosis at birth, that soon progressed to skin necrosis and renal vein thrombosis is discussed. The report aims to raise awareness among neonatologists regarding the need to consider this rare condition with potentially devastating consequences, while evaluating bruise-like skin lesions in neonates.
Pediatr Ther 2017, 7:1 DOI: 10.4172/2161-0665.1000307
Pediatrics & Therapeutics
Abstract The diagnosis of incomplete or atypical Kawasaki disease (KD) is challenging. Children presenting with febrile illnesses may have few of the classical diagnostic criteria, yet develop clinical, laboratory and echocardiographic findings compatible with the condition. Early recognition and prompt treatment of KD is essential for better outcomes. This is particularly the case for infants who are at a greater risk of developing complications such as coronary artery aneurysms. This may be partly attributed to late diagnosis or initiation of therapy. This report discusses the case of a febrile infant with atypical Kawasaki disease presenting with aseptic meningitis and coronary artery aneurysm. The case highlights the importance of considering atypical Kawasaki disease in any infant with prolonged fever (more than seven days), following exclusion of infectious causes and in the absence of classical diagnostic criteria.
Salamah et al., Neonat Pediatr Med 2016, 2:2
Journal of Neonatal and Pediatric Medicine
Background: An unknown number of children who attend an Emergency Department may have a serious underlying, systemic infection as a cause of their fever. Blood culture (BC) remains the gold standard approach to establish the diagnosis and presence of pathogens in a child with a suspected, serious bacterial infection. This study investigated the proportion of positive blood cultures and the correlation with basic laboratory investigations (Creactive protein, white blood cell count, and absolute neutrophil count), prescription of antibiotics in patients visiting a pediatric emergency department in a primary hospital Methods: A retrospective study in Qatar- Al Wakra Hospital- Pediatric Emergency Department, over one year. Patients younger than 3 months of age and patients with any form of immune deficiency were excluded. Results: A total of 828 patients (median age 3.55 years) with fever (>38°C) or a history of fever (>38°C). 121 (14.6%) were later admitted to the pediatric ward; 10 (1.2%) to the pediatric intensive care unit and 4 (0.4%) to pediatric surgery. In total, positive blood culture was present in 20 (2.42%) children. Of these 20,4 (20%) were admitted to the pediatric ward, and 9 (45%) were observed in the hospital for less than 24 hrs and 7 (35.0%) were sent back home after a clinical assessment and the results of the initial laboratory tests. The referrals of patients with negative blood culture were similar. There were no differences in the mean value of absolute neutrophil counts or CRP measurement between patients exhibiting positive or negative BC. Conclusion: The incidence of a positive BC in routine care of febrile patients in an emergency department setting is low, 2.42%. There were no significant differences in associated clinical laboratory results (WBC, CRP or ANC) or admission to hospital wards between the groups with positive or negative BC.
Journal of Neonatal Biology
Abstract Aim: To assess the usefulness of postnatal renal ultrasound in newborns with isolated external ear anomalies in the presence of a normal renal ultrasound on the routine surveillance prenatal ultrasound. Study design: 80 consecutive patients with isolated minor ear anomalies were collected retrospectively starting from December 2008 till February 2011; the prevalence of renal anomalies detected in postnatal ultrasound in those patients was compared with that detected in prenatal ultrasound. Results: Our study included only 64 patients with isolated minor ear anomalies who have prenatal and postnatal ultrasound while 16 patients were excluded (14 patients with no recorded data regarding the prenatal ultrasound, one patient with associated imperforate anus and another patient with unilateral undescended testes). Out of the 64 patients, only one patient was reported to have unilateral pyelactasis in prenatal ultrasound but was reported to be normal on postnatal ultrasound. Otherwise all prenatal renal ultrasound findings were normal on both the prenatal and postnatal renal ultrasound findings. Conclusion: There is no difference in the detection of renal anomalies between postnatal renal ultrasound in infants with isolated minor ear anomalies compared with that found on routine prenatal ultrasound. *Corresponding author: Khalil Mohamad Salameh, Hamad Medical Corporation, Doha, Qatar, Tel: 0097440114258; E-mail: firstname.lastname@example.org Received December 07, 2016; Accepted December 27, 2016; Published December 31, 2016 Citation: Salameh KM, Fadl SAA, Badr SSHA, Kamel HA, Habboub LH (2016) A Comparative Study between Pre-Natal and Post-Natal Screening Ultrasound in Detection of Renal Anomalies in Neonates with Isolated Minor Ear Anomalies. J Neonatal Biol 5: 242. doi:10.4172/2167-0897.1000242 Copyright: © 2016 Salameh KM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Characteristics
Int J Womens Health 2016 23;8:529-535. Epub 2016 Sep 23.
Global Health Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Download full-text PDF
BMC Pediatr 2015 Aug 28;15:104. Epub 2015 Aug 28.
Pharmacy Department, Al Wakra Hospital, Al Wakra, Qatar.
Download full-text PDF
J Pak Med Assoc 2013 May;63(5):598-603
Department of Medical Statistics & Epidemiology, Hamad Medical Corporation, Hamad General Hospital, Qatar.
Download full-text PDF
J Clin Neonatol 2012 Oct;1(4):195-201
Department of Pediatrics, NICU, Women's Hospital, Hamad Medical Corporation, Doha, Qatar ; Department of Pediatrics, Weill Cornell Medical College, Doha, Qatar.
Download full-text PDF
ISRN Obstet Gynecol 2012 8;2012:540495. Epub 2012 Sep 8.
Department of Epidemiology and Medical Statistices, Hamad General Hospital, Hamad Medical Corporation, Qatar ; Department Evidence for Population Health Unit, School of Epidemiology and Health Sciences, The University of Manchester, Manchester, UK ; Departments of Public Health and Medical Education, Weill Cornell Medical College, P.O. Box 3050, Doha, Qatar.
Download full-text PDF
J Clin Neonatol 2012 Jan;1(1):25-8
Department of Pediatrics, NICU Women's Hospital, Hamad Medical Corporation, Doha, Qatar.
Download full-text PDF
Int J Womens Health 2010 Sep 17;2:311-8. Epub 2010 Sep 17.
Women's Hospital, Hamad Medical Corporation, Doha, Qatar.
Download full-text PDF
Journal of Perinatology (2009) 29, 765–770
Journal of Perinatology
Objective: This study was designed to analyze the trends and differences in perinatal and neonatal mortality rates in the State of Qatar over a period of 30 years (1977 to 2007), to examine the causes of neonatal deaths and compare them with some regional Gulf states and developed world countries. Study Design: This is a retrospective study conducted in the Women’s Hospital, Hamad Medical Corporation, State of Qatar from 1977 to 2007. Method: The study included all perinatal and neonatal deaths for the period 1977 to 2007, which were monitored through registers of the Neonatal Intensive Care Unit (NICU), Women’s hospital. Cause of death was determined using information from hospital records, including discharge certificates. There is a national database in the Department of Preventive Medicine that records all deaths through death certificates. The missing information for the early years was collected from this database. All causes of deaths were classified in accordance with criteria based on the International Classification of Disease tenth revision (ICD-10). Result: There was a notable peak in neonatal (14.1), early neonatal (12.5) and perinatal (24.7) mortality rates in 1977. There was a second peak in neonatal (12.1) and late neonatal (7.5) mortality rates in 2000. Over a period of three decades (1977 to 2007), there was a significant decline in mortality rates (P<0.0001). By 2007, the neonatal mortality rate had decreased from 14.1 to 5.1; the early neonatal mortality rate had a dramatic fall from 12.5 to 2.3; and perinatal mortality came down from 24.7 to 10.3. There was no notable reduction in the late neonatal mortality rate in 2007 (2.8) compared with that in 1980 (3.0). The still-birth (8), neonatal (5), early neonatal (2.3) and perinatal (10.3) mortality rates in Qatar were very close to the rates found in developed countries, but lower than the rates in Bahrain and Saudi Arabia. Similar to developed countries, prematurity was the leading cause of neonatal death in Qatar (42.6%), followed by congenital anomalies (28%). Conclusion: This study revealed that there was a sharp significant decline in neonatal and perinatal mortality rates during the study period in Qatar. The stillbirth, neonatal and perinatal mortality rates in Qatar are comparable with those in some of the developed countries and were lower than those in some of the Gulf countries. The proportion of underweight live births was found constant during the study period. Prematurity was the leading cause of neonatal death, followed by congenital anomalies. Journal of Perinatology (2009) 29, 765–770; doi:10.1038/jp.2009.89; published online 30 July 2009
Am J Physiol 1975 Dec;229(6):1510-3
Download full-text PDF