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Background and Aims

Assessment of preload responsiveness by dynamic indexes has been recommended to guide fluid therapy in the critical care setting but this strategy has never been tested in neonates. Our aim was to assess respiratory variation in aortic blood flow peak velocity (ΔVpeak) as a predictor of preload responsiveness in mechanically ventilated and hemodynamically unstable neonates.

Methods

Prospective observational diagnostic accuracy study. Consecutive mechanically ventilated and hemodynamically unstable neonates who received a first fluid bolus (10 ml/kg of normal saline over 20 minutes) for suspected hypovolemia were eligible. ΔVpeak and superior vena cava flow (SVCf) were measured at baseline (T0), immediately upon completion of the fluid infusion (T1) and at one hour after fluid administration (T2). Preload responsiveness was defined as an increase in SVCf >10% at T1 (ΔSVCfT1-T0).

Results

Forty-six infants with a median (IQR) gestational age of 30.5 (28-36) weeks were included. Twenty-nine (63%) infants were fluid responders (F-R), and 17 (37%) were fluid non-responders (F-nR). FR had a higher baseline (T0) ΔVpeak than F-NR [9% (8.2-10.8) vs 5.5% (3.7-6.6); p<0.001]. Baseline ΔVpeak was correlated with ΔSVCfT1-T0 (rho=0.841, p<0.001). The area under the ROC curve of ΔVpeak to predict fluid responsiveness was 0.912 (95% CI: 0.82-1). An ΔVpeak cut-off point of 7.8% provided a 90% (95% CI: 71-97) sensitivity, 88% (95% CI: 62-98) specificity, 7.6 (95% CI: 2-28) positive likelihood ratio and 0.11 (95%CI: 0.03-0.34) negative likelihood ratio to predict fluid responsiveness.

Conclusions

ΔVpeak accurately predicted preload responsiveness in hemodynamically unstable neonates under mechanical ventilation.

Background and Aims

Angiogenesis a complex phenomenon, plays a key role in tissue growth . Congenital diaphragmatic hernia (CDH) is a rare acongenital anomaly,associated with lung hypoplasia and abnormal pulmonary vasculature with poor postnatal outcome.

Ante-natal inhibition of arginase activity may improve angiogenesis and lung growth in a CDH rat model.

Methods

Timed pregnant rats randomized into 3 groups: control, nitrofen only (non-treated group), and nitrofen+arginase inhibitor ( (ABH) ((treated group). Pregnant rats were fed 200mg of nitrofen at embryonic day 9.5 to induce CDH. ABH was administered via an osmotic delivery device inserted subcutaneously at day 11.5, at a dose of 5mg/kg/day. At day 21.5 of gestation, fetuses were delivered by cesarean section. Lung and liver tissue obtained from fetuses and arginase activity was confirmed by tissue lysate. Proangiogenic markers; (VEGF, PECAM p-eNOS, TIE/TEK2,) as well as antiangiogenic markers; Arginase I&II and sFlt-1, studied by western blot. Histopathology and vascular density count by CD31 staining.

Results

Arginase inhibition confirmed by low level of arginase activity in lung, liver as well as in serum from pups treated with ABH compared to non-treated group (p<0.05) . Arginase inhibition in CDH pups showed enhanced expression of p-eNOS , VEGF, PECAM and TIE/TEK2 along with a significant decrease in sFlt1, as compared to non-treated pups.(p<0.05). Histopathology show improved vasculature and tissue growth in the treated vs non- treated group.

Conclusions

Arginase inhibition in antenatal period can promote angiogenesis and lung development in CDH rat model. Arginase inhibition may be a promising therapeutic target for future study.

Background and Aims

Prior to first stage palliation, impaired systemic perfusion puts neonates with hypoplastic left heart syndrome (HLHS) at risk for hemodynamic decompensation. The aim of this study was to assess whether decompensation may be preceded by specific patterns in their vital parameters.

Methods

In this retrospective cohort study, all neonates with HLHS admitted to the Pediatric Intensive Care Unit of the University Medical Center Utrecht between 2009-2019 were included. Mortality or the need to delay surgery were chosen as endpoints for hemodynamic decompensation. The course of heart and respiratory rate, oxygen saturation and invasive blood pressure was visualized in the 48 hours prior to clinical interventions (intubation, initiation of inotropic therapy and placement of central venous or arterial catheter) and mixed effects modelling were used to compare between decompensated and non-decompensated patients.

Results

Of 46 patients, nine (20%) decompensated of whom five (11%) died prior to surgery. Figure 1 shows the course of vital parameters in one non-decompensated and three decompensated patients. Decompensated infants showed statistically significant differences in the course of heart rate (p=0.007) and respiratory rate (p<0.001) prior to inotropic therapy and heart rate (p=0.012) and respiratory rate (p=0.030) prior to placement of a catheter.

Conclusions

Subtle but significant differences exist in the course of vital parameters between decompensated and non-decompensated neonates with HLHS prior to first stage palliation. Implementation of reference values of these vital parameters for this critical population in monitoring and patient data management systems might support clinicians in recognizing decompensation early on.

Background and Aims

Bronchiolitis is the most common lower respiratory tract infection in children. Extrapulmonary manifestations have been studied in the past, however, scarce data are available regarding global cardiac function. The aim of this study was to assess cardiac function in patients with bronchiolitis and to analyze whether a correlation between cardiac dysfunction and adverse clinical outcomes exists.

Methods

This was a prospective cohort study of infants less than 12 months hospitalized with diagnosis of bronchiolitis. At admission, patients were classify using a clinical score (BROSJOD), an echocardiography was performed and NT-proBNP plasma levels were obtained in those children requiring blood draws. Severity was established based on the need for positive pressure respiratory support (PPRS). Echocardiographic data were compared with healthy age-matched controls (n=25).

Results

181 patients were included, (median age 2 [1-4] months). 72 required PPRS.

When compared to controls, PPRS patients showed RV systolic dysfunction measured by TAPSE(p=0.002) as well as indicators of left ventricle (LV) diastolic dysfunction: trans mitral E and Tissue Doppler Index mitral a’ waves(p=0.02 and p=0.005, respectively).

NT-proBNP was measured in 47 patients. PPRS patients had higher values than milder cases (p=0.007).

A NT-Pro BNP value greater than 753pg/dL, a TAPSE <11.5mm, and ≥8 BROSJOD score at admission were considered cut-off points with the greatest discriminatory power to predict the need for PPRS.

Conclusions

In addition to the expected RV systolic dysfunction, patients with severe bronchiolitis have altered LV diastolic function. NT-Pro BNP and TAPSE values, and BROSJOD score at admission had strong discriminatory power to detect poor outcomes.

Background and Aims

Extracorporeal-cardiopulmonary-resuscitation (ECPR) improves survival after in-hospital cardiac arrest. However, functional outcome remains poor. We aimed to characterize ECPR outcomes and develop an accurate model to predict functional outcome at discharge and 6 months, using a validated organ-dysfunction score and, for the first time in pediatrics, a detailed granular neuroimaging score.

Methods

All cardiac ECPR events between 2011-2019 were reviewed. The primary outcome measure was the Functional-Status-Score(FSS) at discharge. Organ-dysfunction was graded using the Pediatric-Logistic-Organ-Dysfunction-Score-2(PELOD-2); neuroimaging was graded using the modified-Alberta-Stroke-Program-Early-Computed-Tomography-Score(ASPECTS)/DWI-ASPECTS. Multivariable logistic regression was used to model FSS≥19 (severe functional impairment) at discharge and at 6 months.

Results

Of the 214 patients who underwent cardiac-ECPR, 182 were included (median age 148 days, IQR 14–827). Seventy-one (39%) had single-ventricle physiology. Neuroimaging was performed in 110 patients: 52 (47%) had hypoxic-ischemic injury, 45 (41%) hemorrhage. Median ECMO duration was 4days (IQR 2-8). Nighty-five patients (52%) either died or exhibited severe functional impairment at discharge. The most accurate predictive model (AUC=0.931) identified FSS at admission, single-ventricle physiology, ECMO duration, mean PELOD-2 in the 0-28 days, and worst mASPECTS/DWI-ASPECTS as independent predictors of poor functional outcome at discharge. The same model predicted severe functional impairment at 6months with an AUC=0.924.

Conclusions

Mortality and functional impairment following ECPR in children remain high. It is possible to model the functional outcome at discharge and at 6months with high accuracy using granular data for organ-dysfunction and brain injury in the 28days following the event. This represents a valuable tool to help physicians defining prognosis and to identify modifiable factors.