Traumatic subdural effusion evolves into chronic subdural hematoma: Two stages of the same inflammatory reaction?
Introduction
Traumatic subdural effusion (TSE), also called as subdural fluid collection or subdural hydroma (SDH), is described in the literature as a common complication of blunt head trauma occurring in a reported 6–21.6% of all closed head injury [1], [2], [3]. Most TSE resolves when the brain is well expanded. However, a few TSEs become chronic subdural hematomas (CSDHs), which are encapsulated collections of old blood, mostly or totally liquefied and located between the dura matter and arachnoid. 16.7–32.8% of all TSEs developed into CSDHs, especially in the aged [3], [4], [5]. And nearly 50% of patients with asymptomatic or minimally symptomatic subdural fluid collection may develop a CSDH [6]. The main clinical manifestations of CSDH include headache, dizziness, nausea, hemiplegia, and abnormal mentality. With the disease progress becoming life-threatening, most CSDHs will be inevitably treated by surgical evacuation. Burr hole craniotomy and twist drill craniotomy with a closed system drainage are generally applied as effective surgical alternatives [7]. As the genesis and development of a CSDH is concerned, neoformation of a subdural membrane, abnormal vascular permeability, defective local hemostasis (hyperfibrinolysis) and chronic rebleeding are traditional explanations [8]. In recent years the involvement of inflammation has been investigated by researchers [9], [10], [11], [12], [13], [14].
Despite intensive research and subsequent advances in surgical techniques of CSDH, a single treatment with measurable clinical impact on the evolution interruption has yet to be investigated. There is an interval between TSE and evolution of CSDH, 101.5 days in average [5] or 22–100 days after head injury [4]. What can we choose to interrupt the evolution, but not just observing the development? On the other hand, some CSDH patients with co-morbidity or surgical contraindication have to choose conservative treatments. Therefore, the pathophysiology of the evolution from TSE to CSDH and propagation of CSDH have to be deeply analyzed.
Section snippets
The role of inflammation in the evolution from TSE into CSDH
There is a rich history of research in the area of TSE and CSDH with a number of inflammatory cytokines and indications of local inflammation identified in their pathogenesis. Interleukin (IL)-6 and IL-8 in both CSDH and TSE groups were much higher than those in the blood of both groups, and the levels in CSDH patients were significantly higher (10 times) than in TSE patients. But the blood levels of tumor necrosis factor (TNF)-α, IL-1β, IL-6 and IL-8 in both groups were almost normal [9]. The
The hypothesis
We therefore hypothesize that TSE and CSDH are two stages of the same inflammatory reaction. The evolution from TSE into CSDH and propagation of CSDH seem to be the results of local inflammation. Besides the similar inflammatory reaction in TSE and CSDH, both of them have similar clinical manifestations and prognoses, displaying as liquid, space occupying lesions which cause pressure in the underlying brain [20], ultimately resolved or progressed to be treated by surgical intervention. The
Implication of hypothesis
Aside from careful observation or surgical evacuation, TSE and CSDH can be treated by anti-inflammatory agents. Administration of methylprednisolone acetate into the subdural cavity in an infant with subdural fluid collection was observed [23]. Steroids can be an alternative treatment of CSDH, particularly in patients with co-morbidity [24], [25] and in elderly or alcoholic patients [26], with no significant complication from steroid therapy. Effect of platelet-activating factor receptor
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