ABSTRACT
Background: Perinatal asphyxia is an important cause for neonatal morbidity and mortality which affects multiple body organs. Myocardium is one of the organs which could be severely affected and this can leads to compromise of the systemic blood flow. Recently Superior vena cava [SVC] flow is usecl to asses' systemic blood flow
Aim of the work: The aim of this work was to study cardiac output changes using SVC flow in neonates with perinatal hypoxia
Subjects and Methods: This observational prospective study was conducted between March 2015 and August 2[]15 at the Neonatal Intensive Care Unit [NICU] and the normal neonaral ward of Alexandria University Hospital [Al-Shatby] on 30 asphyxiated full term neonates [Group I] and 30 healthy full term neonates [Group Il].Superior yena cava [SVC] flow was measured in the first 3 days of life by Doppler echocardiography using Kluckow and Evans method
Results: Superior yena cava [SVC] flow at 12, 24, 48, 72 hours of Group I was significantly lower than that of Group II. The pattern of change in Superior vena cava[SVC] flow in Group l [asphyxiated] was the slow gradual increase over the period of the study in Superior vena cava [SVC] flow in Group II [normal] is the decrease in mean SVC flow from 91.4 ml/kg/min at Day 1 to 80.8 ml/kg/min at Day 3
Conclusion: In conclusion, the assessment Superior vena cava [SVC] flow changes in the early neonatal period is likely to be of great importance in predicting rnyocardial dysfunction. Developing a functional echocardiography [fEHO] service will provide the important hemodynamic information which is critical in the management of asphyxiated infants
ABSTRACT
In recent years, it is suspected that vascular endothelial cells may have some role in vascular complications noted in thalassemic patients. Activated or injured endothelial cells release their protein constituents mainly thrombomodulin into the circulation. Thrombomodulin is considered the most important indicator of vascular endothelial injury. To study serum thrombomodulin level in children with B-thalassaemia major and its relation to the duration of disease and extent of iron overload. The present study was carried out on 35 patients with fl-thalassaemia major. They were divided according to the age into two groups. Group I: included 15 young children aged less than 10 years. Their mean disease duration was 5.5 years. Group II: included 20 older children and adolescents aged from 10 to 20 years. Their mean disease duration was 15.6 years. Ten apparently healthy children of matching age and sex served as control group. Estimation of serum levels of Thrombomodulin [TM] by ELISA. Echocardiography, two-dimensional, M-mode, and Doppler studies. Cardiomegaly was found in 7 [35%] patients of group II. Pulmonary hypertension was encountered only in 4 [20%] patients of group II. Thromboembolic manifestations [femoral deep vein thrombosis] were found in only 1 [5%] thalassaemic patient in group II. The serum TM level was significantly higher in both groups, in comparison with controls [F=10.36, p<0.001]. No significant difference was found between both thalassaemic groups [t=0.421, p=0.673]. Moreover, no significant difference was found between TM levels in splenectomized and non-splenectomized cases [t=0.62, p=0.541]. TM levels of both thalassemic groups showed no significant correlation with serum ferritin level [r=-0.02, p=0.914]. A significantly higher mean value of right ventricular wall thickness was encountered in group II thalassaemic patient as compared to group I [t=2, 57, P=0.019]. In conclusion, increased serum TM level in our polytransfused thalassaemic patients reflects a state of endothelial cell activation and/or injury in these patients. The statistically significant negative correlation between serum TM level and pulmonary acceleration time [r=-0.45, p=0.047], may point to the possible role of pulmonary vascular endothelium injury as a contributory factor in the pathogenesis of pulmonary hypertension in our thalassaemic patients