Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4466_Библиотеки_им_академика_М_И_Перельмана

In general, CST occurs in previously healthy children, most commonly in the pres­ence of or after mastoiditis (characterized by postauricular pain, swelling, erythema, or tenderness) and head/neck infections such as sinusitis, dehydration, and iron de­ciency anemia. Other risk factors predisposing children to CST are inammatory bowel disease, congenital heart diseases, cancer, autoimmune disorders, chronic kidney disease, nephrotic syndrome, systemic lupus erythematosus, and other chronic diseases [2, 3]. Local stasis that may occur in cerebral blood ow and condi­tions that may cause it (such as head trauma, CNS tumors, and intracranial surgery) may predispose to CST and/or aggravate the existing CST condition [3]. In addi­tion, hereditary causes of thrombophilia such as antithrombin deciency, protein C and protein S deciency, factor V Leiden mutation, and homocysteinemia resulting from methylenetetrahydrofolate reductase (MTHFR) gene mutation are prothrom­botic genetic conditions. Acquired nephrotic syndrome and antiphospholipid anti­bodies are other causes that may be risk factors in etiology, which tend to cause thrombosis in general, and are also the risk factors for CST, although not detected in every patient. Approximately 10–20% of children with CST may develop a recur­rent thrombotic venous event in the future, of which at least half develop as sys­temic rather than cerebral venous thrombosis [3].