How does nonsyndromic craniosynostosis affect on bone width of nasal cavity in children? - Computed tomography study.

Craniosynostosis is caused by premature fusion of one or more cranial sutures, restricting skull, brain and face growth. Nonsyndromic craniosynostosis could disturb the proportions of face. Although morphometric diameters of nasal cavity in healthy children are already known, they have not been established yet in children with nonsyndromic craniosynostosis. The aim our study was to check whether diameters of bone structures of nasal cavity in children with nonsyndromic craniosynostosis measured in CT are within normal range. 249 children aged 0-36 months (96 with clinical diagnosis of nonsyndromic craniosynostosis and 153 in control group) were included into the study. The following diameters were measured on head CT scans: anterior bony width (ABW), bony choanal aperture width (BCAW), right and left posterior bony width (between bone sidewall and nasal cavity septum-RPBW and LPBW). The study group has been divided into 4 categories, depending on child's age. The dimensions measured between bone structures of nasal cavity were statistically significantly lower in comparison to the control group. They did not depend on the sex for ABW, nor on age in groups 7-12 months and < 2 years for BCAW, RPBW and LPBW. The measured dimensions increased with age. In children with nonsyndromic craniosynostosis the diameter of pyriform aperture and bony choanal aperture were lower than in controls, what may be described as fronto-orbital anomalies. Morphometric measurements of anthropometric indicators on CT scans could be used as standards in the clinical identification of craniosynostosis type and may help in planning surgical procedures, particularly in the facial skeleton in children.

Do we have to operate on moderate functional mitral regurgitation during aortic valve replacement for aortic stenosis?

A best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was 'Do we have to operate on moderate functional mitral regurgitation (FMR) during aortic valve replacement (AVR) for aortic stenosis (AS)?' Altogether 325 papers were found using the reported search, of which 9 represented the best evidence to answer the clinical question. The authors, journal, date and country of publication, patient group studied, study type, relevant outcomes and results of these papers are tabulated. The current evidence obtained from these papers revealed that the significant predictors of improvement outcome include lower preoperative mitral regurgitation and lower preoperative left ventricle fractional area change. We also know that persistent atrial fibrillation, enlarged left atrium, increased indexed left ventricular mass, pulmonary hypertension and preoperative peak aortic valve gradient <60 mmHg are predictors of deterioration. Generally, we observed a trend towards improvement or non-progression of FMR following AVR for AS. In the six papers that suggest conservative treatment of FMR, the degree of mitral regurgitation (MR) improved in 45-95%, remained unchanged in 19-38% and deteriorated in 1-14%. In the three papers favoring surgical treatment of MR, the degree of MR improved in 46-69%, stay unchanged in 34-53% and deteriorated in 10%. The current evidence suggests that moderate or less grade of FMR without predictors of deterioration should be treated conservatively and moderate-severe and severe FMR warrants additional surgical procedure. A clearly randomized study, especially in patients with moderate and moderate-severe FMR for AS, seems appropriate to further elucidate surgical strategy.

Portal vein thrombosis in cirrhosis is not associated with intestinal barrier disruption or increased platelet aggregability.

OBJECTIVE: Portal vein thrombosis (PVT) is a common complication of cirrhosis, but its pathogenesis is unclear. We tested the hypotheses that PVT is the result of platelet hyperactivity or intestinal barrier disruption. METHODS: This study included 49 patients with cirrhosis (15 females) of mixed etiology. Based on spiral computed-tomography, the patients were divided into two groups: with PVT (n=16) and without PVT (n=33). Serum biomarkers of intestinal barrier integrity were endotoxins and zonulin, and platelet activity was assessed with multiple electrode aggregometry. RESULTS: The levels of endotoxin (43.5±18.3ng/ml vs. 36.9±7.5ng/ml; P=0.19) and zonulin (56.3±31.1ng/ml vs. 69.3±63.1ng/ml; P=0.69) were not different between the patients with and without PVT. Moreover, endotoxin and zonulin did not correlate with the coagulation and platelet parameters. The platelet aggregability measured with the TRAP and the ADP tests was decreased in PVT patients. In the logistic regression analysis the PVT incidence was related to the levels of D-dimer and bilirubin as well as the TRAP test results. Patients with PVT presented with significantly higher levels of D-dimer (4.45±2.59 vs. 3.03±2.97mg/l; P<0.05) and prothrombin levels (175±98.8µg/ml vs. 115±72.9µg/ml; P<0.05) than patients without thrombosis. PVT could be excluded with a 90% negative predictive value when the D-dimer level was below 1.82mg/l. CONCLUSIONS: Endotoxemia and platelet activity are not determinants of PVT in patients with cirrhosis. The D-dimer measurement has diagnostic significance for PVT in patients with liver cirrhosis.

Coronary artery spasm following on-pump coronary artery bypass grafting with 20 months follow-up.

We report on a 69-year-old woman who demonstrated native coronary artery and grafted vessel spasm following on-pump coronary artery bypass grafting (CABG). Despite intraaortic balloon pump (IABP) insertion, electrocardiogram (ECG) abnormalities did not disappear. Emergency coronary angiography (CAG) was performed. The patient was successfully treated with systemic and intracoronary injection of vasodilator agents. ECG changes disappeared, with normalized and stable hemodynamic function. Intraaortic balloon pump was maintained for 48 h. The patient was discharged in good clinical condition. Coronary artery spasm (CAS) may result in life-threatening arrhythmias, circulatory collapse or death. The etiology of CAS is multifactorial and includes heart manipulation, exogenous vasoconstrictors, stress-related catecholamine release, hypoxia and oxidative stress. Postoperative CAS is most commonly manifested by ST-segment elevation and circulatory collapse without specific causes. The gold standard for revealing CAS is CAG. Infusion of vasodilators combined with IABP is adequate in most instances, but extracorporeal membrane oxygenation has been necessary for more extensive or resistant coronary spasm.