[The pathogenesis of chronic subdural hematomas and hydromas in children]

Although a chronic hygroma in most cases is residual of incompletely organized old subdural hematoma, both these chronic effusions may lay on different etiological factors and on pathogenetic mechanisms similar in the early stage, then different. The key event common to both the effusions is the neoformation of a subdural mesenchymal membrane (external capsule) with giant sinusoid capillaries. This membrane is due to fibroblastic proliferation of the dura-arachnoid interface layer cells, triggered by subdural bleeding (in cases of hematoma), by phlogistic transudate in meningitis or CSF escape in hydrocephalus or trauma (in cases of hygroma). The different physiopathological activity of the neoformed capsule produces either a hygroma or a hematoma: vascular transudation alone produces the former; hyperfibrinolysis, due to marked plasmin activity, sustaining repetitive microbleeding from the capillaries of the membrane, produces a hematoma. Most of the above data are obtained from adult cases; however, both the chemical composition of the fluid collections and the pathological features of the effusions in infancy are the same as in adulthood. It seems unlike that the enzymatic processes of reparative connective tissue, involving the hemostatic-fibrinolytic balance, be different in the early and late stages of life.