Our practice has been to obtain serial head CT scans in all patients with traumatic ASDH. Head CT scans are performed at initial arrival, 2-4 hours after arrival, within 7 days after admission, and when symptoms worsen. This protocol has allowed us to follow the progression of traumatic ASDH.

CT sections (consecutive 4.5 mm slices) were obtained in an axial plane parallel to the orbitomeatal line.

The database at our institute included all head traumatic patients admitted over a 7-year period (from 1 January 2005 to 31 July 2011). Initially, 742 ASDH patients were identified, but 113 were excluded because the main lesion was not ASDH. Of the remaining 629 patients, 329 patients underwent emergency surgery after an initial head CT scan, and 31 patients underwent emergency surgery after a second head CT scan (within 4 hours after the initial head CT scan) due to hematoma aggravation or brain swelling. In 41 patients who required emergency surgery, guardians refused surgery or surgery was not possible due to poor general condition. Based on initial or second head CT scans taken within 4 hours after arrival, our guidelines for emergency surgery were; 1) ASDH >10 mm thick or a midline shifting >5 mm with definite neurologic deficit such as an inability of obey commands, an abnormal light reflex, or motor weakness, 2) a comatose status [Glasgow Coma Scale (GCS) <9] with an ASDH <10 mm thick and a midline shifting <5 mm, and 3) aggravation of hematoma or a neurologic symptom within 4 hours of arrival, for example, a GCS decrease of >2 with an increase in hematoma or brain swelling by second head CT.

After excluding 401 patients that required initial surgery, 177 patients of the remaining 228 patients met the inclusion criteria and constituted the study cohort. The inclusion criteria adopted were; 1) initially non-operated ASDH, 2) initially mild neurologic symptoms (GCS ≥10), 3) supratentorial traumatic ASDH, and 4) a time of <4 hours between trauma and arrival. The exclusion criteria were; 1) no definite association between hematoma/edema and neurologic symptoms, such as, diffuse axonal injury, 2) spontaneous ASDH, 3) bilateral ASDH, 4) a history of a cranial operation, 5) an age of <15 years, 6) aggravated or expired patients due to co-morbid condition or complication, and 7) discharge or transfer before recovery.

The patients were divided into four groups according to clinical course. Of the 177 patients, 136 (76.8%) were allocated to the spontaneous resolution group (SRG; spontaneous resolution mainly between 1 week and 4 weeks after onset), 12 (6.8%) to the rapid worsening group (RWG; rapid worsening to the extent of requiring decompression surgery between 4 hours and 7 days after onset), 24 (13.6%) to the subacute worsening group (SWG; an increase in subdural fluid collection or hematoma sufficient to require surgery between 1 week and 4 weeks after onset), and 5 (2.8%) to the delayed worsening group (DWG; delayed aggravation such as hydrocephalus or subdural hygroma at >1 month after onset sufficient to require surgery).

Paramedic field notes, emergency department records, admission notes, progress notes, outpatient notes, and serial head CT scans were reviewed in all patients.

The following data were collected; demographic data including sex and age, mechanism of injury including fall from standing, fall from a height, assault, in-car traffic accident, pedestrian traffic accident, motorcycle accident, or bicycle accident, co-morbid conditions including hypertension, diabetes mellitus, renal disease, ischemic heart disease, liver disease, stroke, cancer, epilepsy, or alcohol abuse, medication history of aspirin, antiplatelet drug, or anticoagulation therapy (e.g., warfarin), GCS scores on admission and at last follow-up, and associated intracranial injuries including cerebral contusion, subarachnoid hemorrhage (SAH), skull fracture, pneumocephalus, epidural hemorrhage (EDH), intraparenchymal hemorrhage (IPH), or intraventricular hemorrhage (IVH). Cerebral contusion was defined as petechial-appearing and ill-defined areas of mixed attenuation on CT scans, and IPH was defined as solid-appearing, discrete, and well-circumscribed hematoma9). SAHs included both cisternal and sulcal SAHs.

The following findings were checked based on initial head CT; side of hematoma (e.g., right or left), dominant location of hematoma (e.g., frontal, temporal, parietal, or occipital), maximum thickness of hematoma, and midline shifting. Midline shifting was defined as distance between the most displaced midline structure and the midline of the skull.

Initial hematoma density was described as homogeneous or mixed. Homogeneous ASDH was defined when Hounsfield units (HUs) were in the range 50 to 100, and mixed ASDH was defined when HUs in the ranges 1 to 40 and 50 to 100 were mixed2). Initial longitudinal proportion of largest hematoma, which was defined as the ratio of hematoma convexity to cerebral hemisphere convexity, was calculated (Fig. 1).

Initial number of CT slices containing hematoma was evaluated. If the longitudinal hematoma size for a particular slice was greater than 75% of the largest hematoma, the slice was considered 1 hematoma slice, if the hematoma size of a slice was approximately 25% to 75% of the largest hematoma, the slice was considered half a hematoma slice, and if the hematoma size of a slice was less than 25% of the largest hematoma, it was not considered a hematoma slice.

In addition, estimated hematoma volume index was evaluated. It was calculated as maximum thickness (mm)×longitudinal proportion×number of CT slices containing hematoma.

Finally, brain atrophy was evaluated. Quantitative atrophy including frontal horn index (FHI) and sylvian fissure ratio (SFR), and qualitative cortical atrophy which was classified as normal, mild, moderate, or severe were measured (Fig. 2)2).

SPSS version 14.0 (SPSS Inc., Chicago, IL, USA) was used to analyze all data. Pearson's chi square test, the independent two samples t-test, the paired samples t-test, one-way analysis of variance (ANOVA), and the bivariate correlation test were used depending on the characteristics of the variables being compared. Multivariate analysis was subsequently performed to identify independent prognostic factors. Statistical significance was accepted for p values of < 0.05.

In the present study, 23.2% of initially non-operated ASDH cases eventually required surgery. In particular, sudden worsening in the subacute phase (that is the SWG) was 13.6%. As mentioned above, in this group, the hematomas shrank transiently, and then, progressed to thick low density subdural fluid collections with marked mass effects. Consideration of this phenomenon is crucial to avoid complacency due to transient ASDH resolution during the acute phase.

As has been previously reported, sex ratio and mechanism of injury were not found to be correlated with clinical course13,22,25). Some have reported a relation between worsening of initially non-operated ASDH and old age12,23). Somewhat surprisingly, although members of the SWG and the DWG tended to be older than members of other groups, no statistical significance was found in the present study, which contradicts previous reports.

Our finding of no difference of initial GCS between the four groups suggests that initial neurologic states and damage intensities were similar in the four study groups. However, based on final GCS scores and mortality ratios, outcomes were significantly poorer in the RWG and the SWG. Interestingly, these findings suggest that initial GCS scores were not predictive of ASDH progression.

In addition, neither the presence of a co-morbid condition including alcohol abuse, nor the use of aspirin and/or an antiplatelet drug appeared to influence the clinical course of ASDH. On the other hand, oral anticoagulants including warfarin worsened clinical course, as has been previously reported13,22,25).

In terms of associated intracranial injuries, two prognostic factors were found to be strongly associated with clinical course, namely, cerebral contusion and SAH. Curiously, cerebral contusion and SAH were common in the RWG, but rare in the SWG. The presence of cerebral contusion or traumatic SAH is perhaps a strong predictor of rapid worsening, which echoes the findings of some other authors5,6,26).

Classically, there are two common types of traumatic ASDH resulted from two distinct pathologies. The first type of ASDH manifests as accumulation into the adjacent subdural space around a parenchymal brain contusion or laceration, and is usually associated with a severe underlying primary brain injury such as cerebral contusion or SAH.

Cerebral contusions are focal lesions of subpial hemorrhage and swelling, and sometimes are referred to as lacerations when overlying pia mater is compromised. Generally, contusions are caused by direct or indirect impact, and common in regions that contact bony surfaces in the cranial vault, such as, the frontal base or temporal pole. Occasionally, contusions can cause significant mass effects due to progressive surrounding edema or progression to an IPH during the acute phase (within 1 week of injury). Contusions also represent a significant source of secondary injury to adjacent tissue via the release of neurotransmitters and local biochemical changes32).

Traumatic SAH has cisternal (basal cisterns, interhemispheric spaces, and Sylvian fissures) or sulcal (cortical convexity) distributions, and results from relatively severe injury to the brain; high angular acceleration of considerable duration is necessary to produce sufficient strain to rupture of superficial vessels in subarachnoid spaces. Post-traumatic vasospasm can also occur early (within 5 days), and induce focal or diffuse cerebral edema32).

Accordingly, the presence of combined contusion or SAH with ASDH indicates the first type of ASDH associated with substantial impact and more severe brain parenchymal injury, and can worsen the course of the ASDH during the acute phase (within 1 week after onset) by the above-mentioned mechanisms. In fact, in the present study, presences of cerebral contusion or SAH were found to be significantly related, and correlated with severity of initial injury as estimated by initial GCS scores.

Unlike the first type of ASDH, the second type of ASDH is caused by inertial forces (acceleration or deceleration) that tear surface bridging vessels entering dural sinuses, and accumulates diffusely and thickly over the cerebral convexity. In general, the absence of combined contusion or SAH indicates this second type of ASDH associated with less severe brain parhenchymal injury. Primary brain damage may be less severe for this etiology, and a lucid interval may occur with subsequent subacute deterioration. In other words, because hematoma is diffuse and thick, and sometimes venous bleeding is continuous, hematoma resolution is relatively slow and may even be aggravated during the subacute phase (1 week and 4 weeks after onset)32).

Regarding hematoma locations in the four groups, a parietal location was found to be indicative of a poorer ASDH course. In particular, parietal area is prone to subdural bleeding because it contains more cortical vessels entering dural sinuses. In addition, because the subdural space extends over a more widespread field in the parietal area than in other brain areas, the compressive effect that suppresses hematoma accumulation is weakest. Accordingly, in the parietal area, it is easier to accumulate thick hematoma, and subsequently, more difficult to resolve spontaneously.

From the viewpoint of hematoma density, mixed density was more common in the RWG and the SWG, whereas homogeneous density was more common in the SRG.

There are several suspected causes for mixed density. First, mixed hematoma density could be due to hyperacute hematoma produced by ongoing active bleeding or the onset of coagulopathy complicating the management of these lesions10). Head CT scans demonstrate areas of high density corresponding to clotted hematoma, a mixed with areas of relatively low density, corresponding to liquid blood10). This mixed density ASDH can exhibit deterioration in the acute phase (within 1 week after onset), due to rapid arterial hematoma accumulation, or in the subacute phase (1 to 4 weeks after onset), due to slow and steady venous hematoma accumulation20).

Second, mixed hematoma density could also be due to cerebrospinal fluid (CSF) mixed hematoma. In this situation, the arachnoid membrane is frequently torn, which causes a mixture of CSF and blood to accumulate in the subdural space. Head CT scans reveal an expansive lesion with a low density area in the hematoma. This CSF mixture may exhibit rapid resolution within 24 hours due to dilution of the hematoma by CSF1,14,15). On the other hand, steady CSF leakage from the subarachnoid space can cause worsening due to CSF accumulation during the subacute phase (1 to 4 weeks after onset).

The third cause of mixed hematoma density is acute-on-chronic SDH, which appears as a hyperdense layer of clot with expansive, irregular blurred margin or lumps in liquefied chronic hematoma18,23). Acute trauma on the patients with chronic SDH may develop acute subdural bleeding within chronic SDH. Generally, acute-on-chronic SDH tends to occur in elderly patients with brain atrophy18,30). In the present study, we speculate that the majority of mixed density ASDHs were acute-on-chronic SDHs, because mixed density ASDH was found to be strongly correlated with old age or brain atrophy. Since the potential subdural space is substantial and the bleeder is usually a venous capillary, symptoms can be mild despite thick hematoma18). Furthermore, since chronic SDH is usually associated with excessive activation of the coagulation and fibrinolytic systems, acute bleeding into the hematoma cavity may not produce a solid clot and its spontaneous resolution may be difficult24). As a result, acute-on-chronic SDH can cause subacute worsening (1 to 4 weeks after onset) due to disturbance of hematoma resolution.

Not surprisingly, midline shifting, hematoma thickness, and number of CT slices containing hematoma were found to be predictors of worsening. Initial midline shifting may be resulted from thick hematoma or diffuse cerebral edema. Relationships between such factors and subsequent worsening suggest thin hematomas are in general stable, whereas thick hematomas are at risk of progression. We were somewhat surprised to find that longitudinal proportion of hematoma and estimated hematoma volume index were not predictive of progression. These results suggest that degrees of longitudinal spread and hematoma volume are not associated with clinical course.

Brain atrophy was severe in the SWG and the DWG, but mild in the SRG and the RWG. Some authors believe that the space created by premorbid cerebral atrophy contributes to the development of subacute fluid collection, delayed subdural hygroma, or delayed hydrocephalus12,23,27). In other words, subacute fluid collection, delayed subdural hygroma, or delayed hydrocephalus could be presented as a compensatory increase in subdural space in intracranial hypotension caused by cortical atrophy4,11,16,17,31).

On the other hand, the absence of brain atrophy could suppress the accumulation of hematoma or fluid collection as in the SRG, or paradoxically cause acute brain compression due to cerebral edema or hematoma because of the restricted free subdural space as in the RWG.

Several conditions have been proposed for the spontaneous resolution of ASDH15,21,29). In the present study, the factors for spontaneous resolution include no anticoagulant medication, homogeneous density, mild midline shifting (1.7±2.0 mm), thin hematoma (5.2±2.7 mm), fewer CT slices containing hematoma (14±4.7), and the absence of brain atrophy.

Rapid (within 1 week after onset) worsening of ASDH is often encountered clinically, and in the present study, the risk factors for rapid worsening were anticoagulation therapy, associated intracranial injury including cerebral contusion or SAH, a parietal location, mixed density, severe midline shifting (3.8±2.4 mm), thick hematoma (6.8±2.0 mm), many hematoma slices (16.8±5.1), and the absence of brain atrophy. In summary, we postulate three potential mechanisms for rapid worsening; 1) the rapid accumulation of ASDH due to cortical vessel rupture (i.e., hyperacute mixed density SDH), 2) the rapid aggravation of ASDH due to coagulopathy, 3) the rapid aggravation of brain swelling due to combined cerebral contusion or SAH.

Several previous studies have addressed subacute (1 to 4 weeks after onset) worsening of non-operated ASDH12,19,23). In the present study, the factors found to predict subacute worsening were anticoagulation therapy, the absence of combined cerebral contusion or SAH, a parietal location, mixed density, severe midline shifting (3.8±2.2 mm), thick hematoma (9.0±3.8 mm), many hematoma slices (19.3±3.3), and brain atrophy. In summary, we postulate two possible mechanisms for subacute worsening; 1) delayed resolution of hematoma in conditions such as acute-on-chronic SDH or thick ASDH, 2) subacute CSF accumulation in the subdural space in conditions such as CSF mixed ASDH or brain atrophy.

Delayed (more than 1 month after onset) complications such as hydrocephalus and subdural hygroma were reported by some authors4,11,16,17,31). In the present study, the only factors found to predict delayed worsening was brain atrophy.

This study has several limitations that warrant consideration. Foremost, its retrospective nature is intrinsically prone to patient-selection bias. In addition, we only examined ASDH found in the acute traumatic period (within 4 hours after trauma), and therefore, our findings cannot be applied to ASDH arising many hours or even days after injury. In fact, a considerable portion of traumatic ASDHs develop after several hours and are often associated with coagulopathy28).