<b>Introduction: </b> Noninvasive ventilation (NIV) has been developed to reduce complications associated with invasive ventilation (IV). Failure of NIV and delay in endotracheal intubation can increase patients’ morbidity and mortality. Thus early determination of patients who are unlikely to benefit from NIV is crucial for their management. We aimed in this study to identify the early predictors of success of NIV in children with acute respiratory failure (ARF).<br /> <b>Material and methods: </b> Fifty patients with ARF who fulfilled the study selection criteria were ventilated non-invasively and were assessed initially for their severity of critical illness by the Pediatric Logistic Organ Dysfunction (PELOD) score. Clinical, gasometric, respiratory mechanics and oxygenation indices were assessed at 0, 30 and 60 min and 4 and 24 h from the start of NIV. The success group was identified by reduction in respiratory effort, reduction in oxygen demand, improvement in gasometric parameters, and avoidance of intubation.<br /> <b>Results</b>: Sixty-two percent of patients had successful NIV. Neither type of ARF nor patients’ demographics affected the outcome of NIV. The success rate was 80% among patients with mild to moderate acute respiratory distress syndrome (ARDS), 20% with severe ARDS, and 71.8% in patients with bronchopneumonia. Multivariate analysis revealed that baseline PELOD score of less than 14.5 ±2.7, SpO2/FiO2 ratio more than 208 ±57, oxygenation index (OI) 7 ±3.4 and mean airway pressure (MAP) 8.6 ±1.3 are independent predictors for success of NIV.<br /> <b>Conclusions</b>: The NIV is a promising respiratory support modality in pediatric ARF. Baseline degree of critical illness and saturation oxygenation indices together with MAP change after the 1st h from the NIV trial represented the best predictors of success of the trial in the current study.

Background:The incidence of stroke in young adults is around 10%. The majority is due to known risk factors (dyslipidemia, smoking, hypertension, diabetes mellitus, heart disease, etc). Nevertheless, in around 30% no identifiable cause is found, despite extensive diagnostic work up. Protein S is a vitamin K-dependent glycoprotein, which serves as a natural coagulation inhibitor by acting as a cofactor to Protein C, in order to deactivate factor V and VIII. Hereditary protein S deficiency is an independent risk factor for venous thromboembolism. However, whether it is a risk factor for arterial thrombotic events remains unclear. Aims: To identify whether hereditary protein S deficiency could be a risk factor for stroke in adults, aged below 59, without cardiovascular risk factors. Methods: We evaluated patients with a diagnosis of ischaemic stroke who were referred to the Haemostasis and Thrombosis Clinic during the last 8 years. Only patients less than 59 years old, without any known risk factors for stroke were included in the study: 83 patients in total, 29 men and 54 women. The mean age was 42,8 years (range 17-59). They were all subjected to the specific blood tests of our thrombophilia panel, which included APA testing (lupus anticoagulant (LA), anticardiolipin antibody (ACL) and anti-b2 glycoprotein 1 (anti-b2GPI), antithrombin III levels, free protein S and C levels, serum homocysteine levels. They also had vasculitis screening done. Furthermore, they underwent transesophageal echocardiogram, Holter monitoring and carotid duplex scan. Results: In most cases (31/83, 37.3%) antiphospholipid syndrome was identified. Decreased levels of protein S were found in 9 (10.8%) without any other abnormal tests. One patient (1.2%) had low levels of protein C. From the group of the patients with low levels of protein S, 8 were female with mean age 47,8 (range 30-58) and 1 was male, 47 years old. The mean value of protein S was 35,2% (range 6-54%) (normal range 60-140%). The abnormal blood tests were confirmed on repeat testing a few months later. Patent foramen ovale was found in 8 patients (9.6%) and carotid dissection in 3 (3.6%). Two patients were diagnosed with chronic atrial fibrillation and 4 patients with vasculitis. High levels of serum homocysteine >200 mmol/L were found in only one patient. In 12 patients (14,4%), no cause could be identified. Summary/Conclusion: As expected, the most frequent cause for ischaemic stroke identified was antiphospholipid syndrome. Low levels of protein S was the second cause. The role of protein S deficiency in patients with ischaemic stroke remains controversial. Although a wide prospective study is needed, we believe that it is essential to identify those patients early. As they have a relatively high life expectancy, it is crucial to avoid recurrent thrombotic events in the future, which will have significant impact on their quality of life. Therefore we suggest that protein S should be part of the screening tests in every patient with stroke.

negative results of the all examined patients. However, due to low Se it's impossible to narrow the quantity of patients with the APS possibility. On the mix-stage we observed the low Se and high Sp of index of circulating anticoagulant (ICA) all the tests (c 2 >44,74; P < 0,001). On the confirmatory stage Se for LA ratio of all the test was 61,5% -74,4% and Sp LA ratio -95,4% -98,4% (c 2 >87,42; P < 0,001). Ac of all the tests was >87,8% Summary/Conclusion: Coagulation tests of the first stage have a high diagnostic reliability due to considerable Sp and Ac. Low Se does not give a considerable certainty of anticoagulant absence if the coagulation time is within the norm. On the second stage with ICA >15,0% LA can be suspected with high probability, but the low Se does not allow us to confidently differentiate the deficiency of clotting factor from the presence of pathological inhibitors. The highest significant diagnostic efficacy was found in the confirmatory stage.