Hemophilia is a common pediatric hereditary bleeding disorder,including hemophilia A (FⅧ deficiency) and hemophilia B (FⅨ deficiency).Children with hemophilia tend to spontaneous bleeding or bleeding after minor injuries or surgery.In this review,we briefly discussed the preoperative diagnosis and classification of hemophilia,dynamic monitoring of FⅧ or FⅨ,dose of clotting factor and duration of treatment and some other perioperative issues when surgery is needed,to guide hemophilia children's surgery and postoperative rehabilitation.

Objective To investigate the protective effect of astragaloside on cardiomyocyte mitochoddria and inhibition effect on cardiomyocytes apoptosis of the rats with heart failure, and explore the treatment mechanism. Methods Sixty SD rats were randomly divided into control group, model group, astragaloside group, and trimetazidine group. The last three groups were injected subcutaneously with isoproterenol to make the heart failure model. Astragaloside group was given astragaloside 50 mg/(kg?d), and trimetazidine group was given trimetazidine 10 mg/(kg?d) orally for three consecutive weeks. At the end of the experiment, the myocardial tissue specimens of each group were made, inverted fluorescence microscope was utilized for measuring mitochondrial membrane potential (MMP), immunoblotting was utilized for detecting cardiomyocyte telomerase reverse transcriptase (TERT) expression, and flow cytometry was untilized for detecting cardiomyocyte apoptosis. Results The MMP ratio of astragaloside group was 3.226±0.371, significantly higher than the model group and trimetazidine group (P<0.01). The cardiomyocyte apoptosis rate of astragaloside group was 8.91±2.12, significantly lower than the model group and trimetazidine group (P<0.01), and the most obvious expression of TERT was found in astragaloside group. Conclusion Astragaloside can protect damaged mitochondria, promote TERT expression, inhibit cardiomyocyte apoptosis and protect cardiomyocytes.