Traumatic subdural effusion evolves into chronic subdural hematoma: Two stages of the same inflammatory reaction?

Summary

Traumatic subdural effusion (TSE) is one of the main associated complications of brain trauma. About half of the asymptomatic TSEs ultimately evolve into chronic subdural hematomas (CSDHs), most of which will be inevitably treated by surgical evacuation. With the emergence of subdural hydroma (SDH), rupture of bridge-veins, bleeding of the hydroma wall, hyperfunction of fibrinolysis and increasing protein content in the hydroma are some of the traditionally cited explanations of the pathogenesis of TSE evolving into CSHD. 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. Compared with peripheral venous blood, inflammatory cytokines were elevated in TSE and CSDH demonstrated by a number of investigators. Neoformation of capillaries, vascular hyper-permeability, serum protein exudation and other characteristics of aseptic inflammatory reaction were observed. Meanwhile, steroid was applied to treat CSDH in several groups, which was generally used as an effective anti-inflammatory agent. Based on systemic thinking, we hypothesize that TSE and CSDH are different stages, with different appearances, of the same inflammatory reaction. The evolution from TSE into CSDH and propagation of CSDH seem to be the results of local aseptic inflammation. Our hypothesis holds potential as a target for therapeutic intervention.

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.