46 - Pathophysiology of Chronic Subdural Hematomas

Abstract

Chronic subdural hematoma (CSDH) most commonly develops in patients with craniocerebral disproportion as a result of multiple possible underlying conditions. Platelet-vessel and coagulation disorders increase the risk. Minor trauma causes shearing in the dural border cell layer that may injure cortical veins bridging to the dura, where their walls are thinnest as they pass through the dural border cell layer. Injury and possible acute bleeding essentially create a cut through the dural border cell layer. The response is similar to the cutaneous wound-healing response. There is an inflammatory response to injury with proliferation of the mesenchyme-derived dural border cells. A layer of granulation tissue forms adjacent to the dura (the outer membrane), which is characterized by inflammation and angiogenesis with thin-walled sinusoidal blood vessels, inflammatory cells, fibroblasts, and myofibroblasts. A thin inner membrane encapsulates the hematoma but does not proliferate considerably, probably because it is derived embryologically from neuroectoderm and does not possess vascularity. The hematoma initially clots, but then fibrinolysis and hemolysis occurs. The enclosed CSDH cavity likely prevents clearance of fibrinolytic enzymes, inflammatory cytokines, and angiogenic factors, leading to a cycle of inflammation, fibrinolysis, angiogenesis, and rebleeding. As with cutaneous wounds, healing can occur, but this depends on the balance of factors promoting healing, such as intact coagulation, removal of some of the CSDH fluid by surgery, and resolution of craniocerebral disproportion versus ongoing inflammation, bleeding, and lack of brain reexpansion.