Objective To evaluate COVID-19 pandemic preparedness, available resources, and guidelines for neonatal care delivery among neonatal health care providers in low- and middle-income countries (LMICs) across all continents. Study design Cross-sectional, web-based survey administered between May and June, 2020. Results Of 189 invited participants in 69 LMICs, we received 145 (77%) responses from 58 (84%) countries. The pandemic provides significant challenges to neonatal care, particularly in low-income countries. Respondents noted exacerbations of preexisting shortages in staffing, equipment, and isolation capabilities. In Sub-Saharan Africa, 9/35 (26%) respondents noted increased mortality in non-COVID-19-infected infants. Clinical practices on cord clamping, isolation, and breastfeeding varied widely, often not in line with World Health Organization guidelines. Most respondents noted family access restrictions, and limited shared decision-making. Conclusions Many LMICs face an exacerbation of preexisting resource challenges for neonatal care during the pandemic. Variable approaches to care delivery and deviations from guidelines provide opportunities for international collaborative improvement.

BackgroundIn hydrocephalus an imbalance between production and absorption of cerebrospinal fluid (CSF) results in fluid accumulation, compression and stretching of the brain parenchyma. In addition, changes in CSF composition have a profound influence on the development and function of the brain and together, these can result in severe life-long neurological deficits. Brain damage or degenerative conditions can result in release of proteins expressed predominantly in neurons, astroglia, or oligodendroglia into the brain interstitial fluid, CSF and blood. Determination of such products in the CSF might be of value in diagnosing cause, aetiology and/or assessing the severity of the neurological damage in patients with hydrocephalus. We therefore analysed CSF from human neonates with hydrocephalus for these proteins to provide an insight into the pathophysiology associated with different aetiologies.MethodsCSF was collected during routine lumbar puncture or ventricular tap. Samples were categorized according to age of onset of hydrocephalus and presumed cause (fetal-onset, late-onset, post-haemorrhagic or spina bifida with hydrocephalus). Glial fibrillary acidic protein (GFAP), myelin basic protein (MBP), vimentin and 2′ , 3′-cyclic nucleotide 3′-phosphodiesterase (CNPase) were analysed through Western blotting of hydrocephalic CSF samples (n = 17) and compared with data from CSF of normal infants without neurological deficits (n = 8).ResultsGFAP was significantly raised only in CSF from post-haemorrhagic hydrocephalus while MBP was significantly raised in post-haemorrhagic and in spina bifida with hydrocephalus infants. Vimentin protein was only detected in some CSF samples from infants with late-onset hydrocephalus but not from other conditions. Surprisingly, CNPase was found in all neonatal CSF samples, including normal and hydrocephalic groups, although it was reduced in infants with late onset hydrocephalus compared with normal and other hydrocephalic groups.ConclusionsApart from CNPase, which is an enzyme, the markers investigated are intracellular intermediate filaments and would be present in CSF only if the cells are compromised and the proteins released. Raised GFAP observed in post-haemorrhagic hydrocephalus must reflect damage to astrocytes and ependyma. Raised MBP in post-haemorrhagic and spina bifida with hydrocephalus indicates damage to oligodendrocytes and myelin. Vimentin protein detected in some of the late-onset hydrocephalic samples indicates damage to glial and other progenitors and suggests this condition affects periventricular regions. The presence of CNPase in all CSF samples was unexpected and indicates a possible novel role for this enzyme in brain development/myelination. Less CNPase in some cases of late-onset hydrocephalus could therefore indicate changes in myelination in these infants. This study demonstrates differential glial damage and loss in the developing human neonatal hydrocephalic brain associated with different aetiologies.

BackgroundIn Pakistan, the neonatal mortality rate is 41 per 1,000 live births and birth asphyxia is one of the leading causes of neonatal mortality and morbidity. The goal of this study was to determine whether postnatal magnesium sulfate therapy can improve short-and long-term neurological outcomes in term or near-term neonates with moderate-to-severe birth asphyxia. MethodologyThis prospective double-blind randomized controlled trial was conducted in the Neonatology Department of the Children's Hospital & The Institute of Child Health, Lahore. A total of 62 neonates (31 in each group) were randomized to receive either three doses of magnesium sulfate infusion at 250 mg/kg per dose, 24 hours apart (treatment group), or three doses of injection 10% distilled water infusion at 3 mL/kg, 24 hours apart (placebo group). Both groups received similar supportive care. The neurodevelopmental assessment was done at six months of age using the ShaMaq Developmental Inventory. ResultsDemographic data such as gestational age, mean weight, age at presentation, gender, hypoxic-ischemic encephalopathy grade, mode of delivery, and the presence of seizures at presentation were comparable between both groups. In the magnesium sulfate group, statistically significant results were seen in terms of early seizure control (p = 0.001), early initiation of feed (p = 0.002), and shorter duration of hospital stay (p = 0.003). Moreover, the magnesium sulfate group had lower mortality compared to the control group, though it was not statistically significant (p = 0.390). There was no significant difference in terms of cranial ultrasound findings between the two groups (p = 0.783) at the time of discharge. Regarding the neurodevelopmental delay, there was no significant difference between the magnesium sulfate and control groups (p = 0.535). ConclusionsPostnatal magnesium sulfate treatment improves short-term neurologic outcomes at discharge in term or near-term neonates with moderate-to-severe perinatal asphyxia. However, no difference was noted in the neurodevelopmental outcome at six months.

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Septicemia is an important cause of morbidity and mortality in neonates. Appropriate clinical diagnosis and empirical treatment is crucial as pathogens causing sepsis and their antibiotic susceptibility pattern varies in different settings. Therefore, this study was designed to determine the pattern of organisms causing neonatal sepsis and their antimicrobial resistance profile. One hundred and three blood culture specimens were collected aseptically. The specimens were processed in BACTEC 9120. Antimicrobial resistance profile was determined using Kirby-bauer disc diffusion method. Isolates showing resistance to any of the third generation cephalosporins were further confirmed for the production of ESBL by double disk diffusion method according to CLSI 2009 guidelines. Of 103 blood cultures, 71 (68.9%) were positive. Out of these positive cultures, 62 (87%) cases grew pure growth while 9 (12%) cases had polymicrobial infection. Out of these eighty isolates 30 (37.5%) and 50 (62.5%) were found in early and late onset septicemia, respectively. Thirty (42.2%) neonates died and K. pneumoniae was the main causative agent. The predominant isolates were K. pneumoniae (n=40) and CoNS (n=11). More than 90% of Gram-negative isolates showed resistance against β-lactams, coamoxiclav and amikacin. More than 50% of Gram-positive isolates were resistant to penicillin, macrolides, ciprofloxacin and co-trimoxazole. ESBLs producing K. pneumoniae (n=19), MRCoNS (n=6), MRSA (n=4) have also been found in this study. The study concludes that frequency of organisms was mainly found in late-onset neonatal septicemia. Multidrug resistant and ESBL producing organisms were main contributing factor towards high mortality.