Surgical Management of Chronic Subdural Hematoma in Adults

Introduction

Chronic subdural hematoma (CSDH) is one of the more commonly encountered pathologies in neurological surgery. Current trends indicate that CSDH are poised to become the most common intracranial diagnosis to require surgical intervention by year 2030, exceeding both primary brain tumors and metastases. The incidence of CSDH is rising due to the combination of an aging population and the increasing use of anticoagulant and antiplatelet medications. In the elderly, CSDH is a significant cause of morbidity and mortality, and has been described as a “sentinel health event” for this age group. Six-month mortality is around 26% and peaks at 32% at 1 year, similar to that of hip fractures. ^, We aim to provide an analysis of the current literature underlying the assessment and management of CSDH in adult patients, to help guide the clinician in providing the best clinical care to optimize outcome.

Epidemiology

The estimated incidence of CSDH ranges from 5 to 14 per 100,000 person-years, with a predilection for the elderly and a male predominance. The incidence is higher for those aged 70 years and above (58 per 100,000 per year). With the population above the age of 65 years predicted to double between 10 and 50 according to the United Nations, the burden of CSDH is expected to follow suit. The mean age at presentation ranges from 36 to 95 years, depending on publications. CSDH predominantly affects males, with an approximately 3:1 male-to-female ratio across all age groups. ^,

Pathogenesis

The development of CSDH requires a predisposing factor of a shrinking volume of brain within the fixed confines of the cranial vault. CSDH arises at the dural border cell layer, a loose cellular layer devoid of intercellular collagen and tight junctions, located between two firm meninges: the dura mater reinforced with abundant intercellular collagen on one side, and the arachnoid mater with cells anchored to a basal membrane and attached together with tight junctions on the other. Traversing veins are increasingly stretched by the shrinking brain until only a minor additional force is sufficient to cause rupture through stretching or shearing. Approximately one-third of patients have no recollection of trauma, suggesting even minor, seemingly inconsequential events can be precipitants of this pathologic condition. The extravasated blood dissects the dural border cell layer, creating a subdural cavity.

There have been several theories proposed on the origin of the CSDH. One theory is that CSDHs develop from traumatic acute subdural hematomas (SDHs), from tearing of the bridging veins or tearing of cortical arteries or veins. However, experience shows that most small acute hematomas reabsorb spontaneously. Another proposed etiology is that it develops from a subdural hygroma, a collection of cerebrospinal fluid in the subdural space caused by splitting of the dural border cell layer. Then, in the subdural space, neovascularization occurs and hemorrhage from these new vessels leads to formation of a CSDH. ^{, ,}

Whatever the initial mechanism, the opening of the dural border cell layer triggers a complex reparative response that is directed toward healing the injured tissue. In young and healthy patients in whom healing is often successfully completed, the subdural hematoma or hygroma will often resolve. However, in elderly patients with impaired coagulation, atrophic brain, and an impaired repair process, injury leads to a localized inflammatory reaction involving dural border cell proliferation, collagen synthesis, and neomembrane formation. With subsequent neovascularization, the formation of fragile capillaries, vascular hyperpermeability, and enzymatic hyperfibrinolysis, there is an increased propensity for microhemorrhages, which can contribute to hematoma development and enlargement. CSDHs are more likely to arise in elderly patients with atrophic brain, impaired coagulation, repeated falls, and conditions resulting in intracranial hypotension, such as ventriculoperitoneal shunt. However, rarer causes of CSDH such as vascular malformations, arachnoid cysts, and neoplasms have been reported. ^,

Radiologic Evaluation

Computed tomography (CT) is the current diagnostic method of choice in the diagnosis of CSDH. The density of a subdural hematoma depends on the interval(s) between the bleeding episode(s) and the time of examination. CSDH are usually seen as a hypodense (<30 Hounsfield units) crescent collection along the convexity, but may have isodense (30 to 60 Hounsfield units) or hyperdense (>60 Hounsfield units) components. Isodense subdural hematomas, which occur 1 to 3 weeks after the acute event, may be difficult to differentiate from normal brain tissue. In those cases, magnetic resonance imaging (MRI) may be helpful in establishing the diagnosis. Features on the CT such as medial displacement of the grey-white matter interface and failure of cortical sulci to reach the inner skull table can suggest the presence of an isodense subdural hematoma. A mixed-density pattern of blood or a fluid level can indicate the presence of blood of various ages and possible rebleeding into a preexisting CSDH or hygroma.

Nomura and colleagues divided subdural hematomas into five types based on CT appearances: hyperdense, isodense, hypodense, mixed-density, and layering types. The authors discussed the relationship between CT classification and the coagulative, fibrinolytic activities of each type of CSDH. They demonstrated that the layering type is characterized by high hyperfibrinolytic activity. The mixed-density type has a lower hyperfibrinolytic activity than the layering type, and the hypodense hematoma has the lowest fibrinolytic activity. Nakaguchi and colleagues grouped subdural hematomas into four types: homogeneous-density (hyperdense, hypodense, isodense), laminar (known as mixed-density), separated (known as layering) including gradation subtype, and trabecular. They showed that the separated type of CSDH had a higher recurrence rate (36%) compared to the laminar (19%) and homogeneous (15%) types. Stanisic and colleagues confirmed the high recurrence rate of the separated (29%) and laminar (27%) types.

As mentioned above, MRI can be helpful in better defining the CSDH and the multicompartmental nature of certain CSDHs especially in the setting of an isodense CSDH.

The MRI signal intensity changes for a subdural hematoma based on the relative age of various blood breakdown products of a layered, multicompartmental SDH. Tsutsumi and colleagues classified CSDHs into five groups according to the intensity of their appearance on T1-weighted MRI: high, mixed high/isointense, isointense, mixed isointense/low, and low. The authors did not demonstrate a correlation between CT classifications and T1-weighted MRI appearances. However, they showed that the recurrence rate of CSDHs that exhibited homogeneous high intensity on T1-weighted images was significantly lower (3.4%) than that in the non–high-intensity groups (11.6%). Tanikawa and colleagues found that subdural hematomas divided into multiple layers by an intrahematomal membrane (as demonstrated on T2-weighted MRI) are more effectively treated with craniotomy than burr-hole craniostomy. However, the need for division of membranous septae remains controversial, and the role of imaging in selecting a surgical technique has not been sufficiently studied.

Twist-Drill Craniostomy

The bedside twist-drill craniostomy was originally developed by Dr. Villiam Cone at Montreal Neurological Institute in the mid-1900s as a substitute for burr holes. Since then, more than 15 publications have reported on the efficacy and safety of the twist-drill craniostomy or modifications of it for the treatment of CSDH. In those studies, the overall morbidity of twist drill craniostomy ranged from 0% to 7.6% and the percentage of patients requiring a subsequent procedure to treat recurrent CSDH ranged from 3% to 76%.