Subdural hemorrhage (SDH) is an accumulation of blood between arachnoid & inner dural layers of meninges [1]. According to their clinical onset, SDH can be classified into acute (<72 hours), subacute (72 hours to 3 weeks) & chronic (≥3 weeks) [2].

Chronic subdural hematoma (CSDH) is defined as a predominantly hypodense or isodense crescentic collection along the cerebral convexity on cranial computed tomography (CT) [1]. Intraoperatively, it can be defined as an SDH surrounded by a thin capsule (hematoma membrane) and consisting of dark reddish liquefied blood at operation [3]. It can be caused by traumatic stretching & tearing of cortical bridging veins that cross subdural space & drain into dura or dural sinus, coagulopathy, subdural dissection of parenchymal hematomas & rupture of vascular anomaly into subdural space [1,4].

CSDH is a common neurosurgical disease among elderly, but can also occur in infants. It is associated with substantial morbidity and mortality. Multiple etiological concepts has been proposed, such as trauma, inflammation and aging [4-7]. Furthermore, several studies had been published regarding its incidence. In Awaji, Japan and it is reported an overall incidence of 13.1 per 43 100,000 persons per year from 1986 to 1988 [4]. In Finnish CSDH cohort study (1990-2015), the overall incidence of CSDH among 80 years and older doubled from 8.2 to 17.6/100,000/year [8]. In infants, it is 16.5 per 100.000 [9]. From 2005 to 2007, a national registry in Japan revealed an incidence rate of 20.6 per 100,000 per year. Among United States veteran population between 2000 and 2012, the incidence of CSDH is 79.4 per 100,000/year. Global population of people aged 80 and older is expected to be more than triple between 2015 and 2050 [10,11]. Consequently, there will be a growing burden related to CSDH.

The dura mater is separated from the arachnoid by a thin layer of dural border cells. The dural border cell layer contains flattened, elongated cells connected by desmosomes with amorphous extracellular matrix and limited extracellular fibers which makes this cell layer a natural cleavage plane easily separated. Walls of veins traversing from cortex to the dura (bridging veins of dura to venous sinuses) are as thin as 10 µm when passing through the dural border cell layer. These veins are predisposed to tearing when traversing from potentially mobile brain to the fixed points in dural sinuses (Fig. 1) [1,4].

CSDHs are encapsulated, flattened structures. It developed by proliferation from cells of the dura and probably of dural border cell layer with ingrowth of dural capillaries. It contains numerous thin-walled sinusoidal blood vessels, fibroblasts, mast cells, eosinophils, and myofibroblasts. The inner membrane is a thin (30 to 300 µm), relatively avascular layer of cells that adheres to the residual dural border cells and arachnoid cells. CSDHs also contain fluid ranging from yellow to dark brown [3,4,7].

In the past, pathophysiological concepts suggested that CSDH is secondary to degradation of subdural collections of blood and its products exerting merely a mass effect on the underlying brain. Development of CSDH also requires a predisposing factor of a shrinking volume within the cranial vault [5]. Nowadays, pathophysiologic cycle of CSDH formation and expansion involves traumatic and inflammatory components that promote formation of membranes with permeable neo-vessels, in which molecular & angiogenic factors involved (Fig. 2) [7,10,11].

After initial development phase of an acute subdural hematoma, clotted blood can liquefy and cellular components of the hemorrhage can disintegrate, leaving serous fluid in the subdural space. This serous fluid is often intermixed with clotted blood. Its resolution relies on neuroparenchymal counterpressure. Reorganization and formation of vascular membranes that encapsulate the CSDH can further prevent reabsorption. Clotting cascade dysfunction can result in defective clot formation and hemorrhage recurrence, with elevated levels of tissue plasminogen activators which exacerbates this problem [12].

More specifically, subclinical traumatic injury can split open the dural border cell layer which leads to a reactive inflammatory cascade and the release of angiogenic factors leading to formation of an inflammatory membrane and fragile neo-vessels that cause continuous exudation of fluid and blood over time. As the hematoma expands, it raises intracranial pressure, and compresses nearby brain parenchyma, variable clinical manifestations may result, including headache, nausea or vomiting, mental status change, seizure, weakness, sensory disturbance, gait abnormality, and coma. CSDH has also been known as the ‘great immitator’ because of its heterogenous presentation [6,11].

Other theories why CSDHs can enlarge over time: (1) Self-perpetuating cycle of recurrent hemorrhage, fibrinolysis, inflammation, and angiogenesis. (i) Extravasated blood undergoes platelet activation, which causes the release of platelet-derived growth factor and clotting, which causes the release of thrombin and fibrinogen; (ii) Recurrent cycles of bleeding will start new cycles of clotting-fibrinolysis-inflammation-angiogenesis cycle that overlap with other ongoing phases; (iii) Hemolysis of blood will cause the cycle of recurrent CSDH. (2) Difference in osmolarity between CSF, blood and CSDH fluid cause the CSDH to enlarge by imbibing CSF. But this concept is not supported by studies [4].

Mainstay in diagnosing CSDH is CT Scan. It is a rapid & cost-effective modality. It is well suited for identifying hematoma site, thickness, midline displacement and presence of subdural clots [6]. CSDH can be identified on CT scan as a crescent-shaped mass, and based on density, it can be classified as hyperdense (>60 Hounsfield unit [HU]), isodense (30-60 HU), or hypodense (8-30 HU) mass [4,7]. With time, the hematoma becomes less dense. It is due to hemoglobin in CSDH fluid. CSDH is often more hypodense in the early stage, isodense or of high density in the mature stage, of mixed density in the progressive stage, and of low density in the resolving phase (Fig. 3) [4,12].

Based on its internal architecture and density, CSDHs can be classified into 4 types: (1) Homogeneous type was defined as a hematoma with homogeneous density (low-high=hypo, iso & hyperdense) [3]. (i) Outer and inner membranes develop around the subdural space. As the hematoma matures, blood vessels derived from the middle-meningeal artery (MMA) extend into hematoma membrane, causing vascular congestion. Arterial pressure stresses the walls of the sinusoidal microcapillaries, resulting in minor, but persistent, subdural bleeding episodes [3,4]; (ii) Risk for enlargement and recurrence is 10% to 15% [4]. (2) Laminar type was defined as a subtype of homogeneous type that had a thin high-density layer along inner membrane [3]. (i) High-density laminar structure running along the inner membrane is considered to consist of fresh blood from the hematoma membrane [3]; (ii) Higher risk for enlargement [4]. (3) Layered Separated type is a hematoma containing 2 components of different densities with a clear boundary (distinct boundary) lying between, where a lower density component located above a higher density component [3,6]. (i) As the hematoma matures, fibrinolysis occurs. Hematoma separates into 2 components, such that a thin component becomes mixed with a thick component of the liquefied hematoma and normal head motion cannot homogenize these components. It increases in volume and compress & congest surrounding brain [3]. (4) Layered Gradation type is a hematoma with indistinct boundary, in which the low and high density being mingled at the border, this was called the “gradation” type and was considered to be a subtype of the separated type. Mild head movement causes homogenization of hematoma. Therefore, the hematoma is not completely separated [3,6]. (5) Trabecular (multilocular) type is a hematoma with inhomogeneous contents and a high-density septum running between inner and outer membrane on a low-density to isodense (mixed density) background (high-density septa created by fibrosis) usually with low-intensity or isointense background [3]. (i) Interstitial hematoma matrix changes from an isodense to a low-density signal on CT scans, and on surgical inspection (from a dark reddish to xanthochromic translucent liquefied hematoma) which diminishes in volume over time; (ii) Low risk for growth and recurrence [4].

After surgery, bed rest is adviced to reduce recurrent rates by promoting brain expansion, early mobilization is thought to decrease medical complications associated with immobility, specifically venous thromboembolism and hospital-acquired infection. There is no difference in recurrent rates but increased medical complicated in delayed mobilization (after 3 days) compared with early mobilization (on 1st postoperative day) [6]. Patients with impaired mobility should receive physiotherapy assistance, thromboprophylaxis (thromboembolism deterrent stockings, low molecular weight heparin after drain removal) [11].

Patients can be discharged when mobile or returning to baseline function. Early postop CT scans are not performed unless clinically indicated (symptomatic) [4].

CSDH is a common neurosurgical problem in elderly. In the future, the burden of this disease will become heavier. Knowledge about pathophysiology of this disease is changing over time, and so do the modalities of treatment, with their own indications, advantages and disadvantages. Nowadays, BHC is the most common procedure performed because of its efficacy. MMA embolization has also play a part in reducing recurrence rate after surgery.