Time to Attain Full Enteral Feeds Among Preterm Fetal Growth Restricted Neonates With Absent/Reversed End-Diastolic Flow.

OBJECTIVES: To determine the difference in time to attainment of full enteral feeds between fetal growth restricted (FGR) preterm neonates with and without absent/reversed end-diastolic flow (AREDF). Secondary objectives were to compare the short-term outcomes including the incidence of necrotizing enterocolitis (NEC) and feed intolerance between the two groups and to determine the factors affecting the time to attainment of full enteral feeds (FEF) among preterm FGR neonates. METHODS: A prospective cohort study was conducted among consecutive preterm FGR neonates delivered at 28-36 weeks gestation admitted in level III NICU. An umbilical artery doppler ultrasound was performed antenatally for all participants to detect AREDF. FGR neonates with AREDF were taken as the study group and those without AREDF were taken as the comparison group. Time to attain FEF was defined as time taken to establish enteral feeds of 150 ml/kg/day and tolerating it for the next 3 consecutive days. Delayed attainment of FEF was taken as ≥10 days needed to attain FEF. RESULTS: The median (IQR) time to attainment of full feeds was longer among neonates with AREDF compared to those without AREDF [12 (8, 16.5) vs 8 (5, 10) days; P < 0.001]. Neonates with AREDF had more feed intolerance [RR, 95% CI = 1.51 (1.13 - 2.02); P = 0.004], higher mortality [RR, 95% CI = 2.5 (1.02 - 6.2); P = 0.036], prolonged time to regain birth weight [15 (11.5, 19) days, P = 0.035], longer NICU stay [10 (7, 15), P < 0.001] and longer hospital stay [33 (23, 49), P < 0.001]. Also, neonates with AREDF had more hypoglycemia [RR, 95% CI=2.15 (1.2-3.7); P = 0.004], hypoxic ischemic encephalopathy [RR, 95% CI 5.05 (1.13 - 22.4); P = 0.016], hypothyroidism [RR, 95% CI= 8.08 (1.02 - 63.4), P = 0.016], cholestasis (P = 0.007), prolonged parenteral nutrition requirement [10 (7, 15) days, P < 0.001] and oxygen requirement [4.5 (2, 8) days, P < 0.001]. Multivariable logistic regression showed, AREDF [aOR 95% CI 2.91 (1.49 - 5.68), P = 0.002], lower gestational age [aOR 95% CI 0.724 (0.604 - 0.867), P < 0.001] and thrombocytopenia at birth [aOR 95% CI 2.625 (1.342 - 5.136), P = 0.005] are significant predictors of delayed attainment of full feeds among preterm FGR neonates. CONCLUSION: Preterm FGR neonates with AREDF are slower to attain FEF, have more feed intolerance, higher mortality, need longer time to regain birth weight, prolonged NICU stay and hospital stay. AREDF, lower gestation, sepsis and thrombocytopenia at birth are significant predictors of delayed full feed attainment among preterm FGR neonates. It is essential to devise strategies to reduce morbidity and mortality among this group of preterm neonates.

Outcomes of neonatal critical congenital heart disease: results of a prospective registry-based study from South India.

OBJECTIVES: Congenital heart disease (CHD) is now a leading contributor of infant and neonatal mortality in many low/middle-income countries including India. We established a prospective neonatal heart disease registry in Kerala to understand presentation of CHD, proportion of newborns with critical defects who receive timely intervention, outcomes at 1 month, predictors of mortality and barriers to timely management. METHODS: The congenital heart disease registry for newborns (≤28 days) in Kerala (CHRONIK) was a prospective hospital-based registry involving 47 hospitals from 1 June 2018 to 31 May 2019. All CHDs, except small shunts with a high likelihood of spontaneous closure, were included. Data on demographics, complete diagnosis, details of antenatal and postnatal screening, mode of transport and distance travelled and need for surgical or percutaneous interventions and survival were collected. RESULTS: Of the 1474 neonates with CHD identified, 418 (27%) had critical CHD, 22% of whom died at 1 month. Median age at diagnosis of critical CHD was 1 (0-22) day. Pulse oximeter screening identified 72% of critical CHD and 14% were diagnosed prenatally. Only 8% of neonates with duct-dependent lesions were transported on prostaglandin. Preoperative mortality accounted for 86% all deaths. On multivariable analysis, only birth weight (OR 2.7; 95% CI 2.1 to 6.5; p<0.0005) and duct-dependent systemic circulation (OR 6.43; 95% CI 5 to 21.8, p<0.0005) were predictive of mortality. CONCLUSIONS: While systematic screening, especially pulse oximetry screening, enabled early identification and prompt management of a significant proportion of neonates with critical CHD, important health system challenges like low use of prostaglandin need to be overcome to minimise preoperative mortality.

Cardiac Troponin-T as a Marker of Myocardial Dysfunction in Term Neonates with Perinatal Asphyxia.

OBJECTIVES: To describe the diagnostic test properties of Cardiac Troponin-T (cTnT) in predicting myocardial dysfunction in asphyxiated term neonates by taking echocardiography as the gold standard and to establish the optimum cut-off values of cTnT for myocardial dysfunction, shock, severe hypoxic ischemic encephalopathy (HIE) and mortality by receiver operator characteristic (ROC) curve analysis. METHODS: This was a prospective study based on diagnostic test evaluation. The study included 120 term asphyxiated neonates in a tertiary care neonatal intensive care unit (NICU) in Southern India from June 2011 through June 2015. All the neonates were clinically evaluated. Venous blood was taken at 4 h of life for cTnT estimation. Echocardiography was done within 24 h of birth. RESULTS: The mean cTnT level of asphyxiated term neonates was 0.207±0.289 ng/ml (mean ± SD). Asphyxiated neonates with myocardial dysfunction had higher cTnT levels (0.277±0.231) as compared to those without myocardial dysfunction (0.061±0.036, p = 0.0001). Using ROC curve, the cut-off cTnT values for myocardial dysfunction was 0.1145 ng/ml with sensitivity 92.4% and specificity 94.1%. Cardiac Troponin-T levels were significantly higher among asphyxiated neonates with shock (0.378±0.348, p = 0.0001) and the levels also correlated positively with increasing grades of HIE. The cut-off cTnT value for mortality was 0.2505 ng/ml with sensitivity 83.9% and specificity 96.6%. CONCLUSIONS: In asphyxiated term neonates, early cTnT elevation is a marker for predicting myocardial dysfunction and elevated cTnT levels had high sensitivity and specificity. There was significant relation with increasing cTnT values and increasing grades of HIE.

Klippel-Trenaunay syndrome and gestational trophoblastic neoplasm.

BACKGROUND: Klippel-Trenaunay syndrome is a non-heritable venous malformation with bone and soft tissue hypertrophy and cutaneous nevi. CASE CHARACTERISTICS: Neonate with Klippel Trenaunay syndrome born to a mother with past history of Gestational trophoblastic neoplasm. OBSERVATION: Antenatally, a fetal vascular malformation was identified ultrasonologically at 29 weeks gestation. Acute myeloid leukemia was diagnosed in mother at 33 weeks gestation. MESSAGE: A rare association of Klippel Trenaunay syndrome and gestational trophoblastic neoplasm with the possible role of either hyperglycosylated Human Chorionic Gonadotropin or chemotherapy as a link is highlighted.

Guillain-Barre syndrome following dengue fever.

Guillain-Barre syndrome is a post infectious polyradiculoneuropathy. It is equally prevalent in both the adult and the pediatric populations. Guillain-Barre syndrome following dengue fever is not a classically described entity and has not been reported in children.