Because published guidelines for surgical decision-making in patients with acute subdural hematomas (ASDHs) are based largely on case series and other weak evidence, management often must be individualized. Nonoperative management is a viable option in many cases. The literature is divided about the effects of anticoagulant and antiplatelet medications on rapid growth of ASDHs and on their likelihood of progression to large chronic subdural hematomas. Close clinical and radiologic follow-up is needed, both acutely to detect rapid expansion of an ASDH, and subacutely to detect formation of a large subacute or chronic subdural hematoma.
Key points
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Although guidelines for surgical decision-making in patients with acute subdural hematomas (ASDHs) are widely available, the evidence supporting these guidelines is weak, and management of these patients must often be individualized.
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Smaller ASDHs in patients in good neurologic condition usually can be successfully managed without surgery.
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Large ASDHs with minimal mass effect in patients with minimal symptoms also may be considered for nonoperative management.
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The literature is divided about the effects of anticoagulant and antiplatelet medications on rapid growth of ASDHs and on their likelihood of progression to large chronic subdural hematomas, but it is reasonable to reverse the effects of these medications promptly.
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Close clinical and radiologic follow-up is needed in these patients, both acutely to detect rapid expansion of an ASDH, and subacutely to detect formation of a large subacute or chronic subdural hematoma.
Introduction
Few emergencies in neurosurgery are as worrisome as a large acute subdural hematoma (ASDH) ( Fig. 1 ). Many of these lesions require immediate evacuation, regardless of the time of day or day of the week. Fortunately for the affected patients, the vast majority of ASDHs are relatively small, thus allowing initial management to consist of nonsurgical observation.
The decision that emergency surgery is not needed is soon followed by an obvious question: what will happen to the ASDH? The ideal scenario is that it will gradually resorb and the patient will be left with no deficits. But the worst-case scenario is rapid and unexpected enlargement of the hematoma, causing the patient to undergo neurologic deterioration and immediate surgical evacuation. Over a more protracted course, another suboptimal outcome is progression of a small ASDH to a large chronic subdural hematoma (CSDH) ( Figs. 2 and 3 ), which may enlarge to such an extent that surgical evacuation becomes necessary ( Fig. 4 ).
Despite the frequency with which neurosurgeons have to make these decisions, and despite the likely increase in incidence of small but potentially worrisome ASDHs as the population ages, becomes more prone to falls, and consumes more antiplatelet and anticoagulant medications, relatively little work has been reported on the natural history of ASDHs. Most published reports are based on retrospective reviews of case series or of large public registries.
Introduction
Few emergencies in neurosurgery are as worrisome as a large acute subdural hematoma (ASDH) ( Fig. 1 ). Many of these lesions require immediate evacuation, regardless of the time of day or day of the week. Fortunately for the affected patients, the vast majority of ASDHs are relatively small, thus allowing initial management to consist of nonsurgical observation.
The decision that emergency surgery is not needed is soon followed by an obvious question: what will happen to the ASDH? The ideal scenario is that it will gradually resorb and the patient will be left with no deficits. But the worst-case scenario is rapid and unexpected enlargement of the hematoma, causing the patient to undergo neurologic deterioration and immediate surgical evacuation. Over a more protracted course, another suboptimal outcome is progression of a small ASDH to a large chronic subdural hematoma (CSDH) ( Figs. 2 and 3 ), which may enlarge to such an extent that surgical evacuation becomes necessary ( Fig. 4 ).
Despite the frequency with which neurosurgeons have to make these decisions, and despite the likely increase in incidence of small but potentially worrisome ASDHs as the population ages, becomes more prone to falls, and consumes more antiplatelet and anticoagulant medications, relatively little work has been reported on the natural history of ASDHs. Most published reports are based on retrospective reviews of case series or of large public registries.
Demographics
Traumatic brain injury (TBI) is a significant cause of mortality and permanent disability across the globe. TBI represents a spectrum of disease processes that ranges from concussion to large intra-axial and extra-axial intracranial hematomas, including ASDH.
For patients with TBI in general, outcomes have improved somewhat over the past decades because of better organization of emergency medical systems, greater speed and quality of computed tomography (CT) scanning, and refinements in general critical care practices.
However, mortality and outcome in patients with ASDH have not seen as much improvement. Mortality has been reported to range from 50% to 90% or even higher in some series that include patients receiving anticoagulant therapies. Associated intracranial and extracranial injuries are common and may contribute to increased morbidity and mortality. Overall outcomes may worsen in coming years as the population ages.
Specific types of acute subdural hematoma
The natural history of a subdural hematoma (SDH) is influenced by whether it is traumatic or nontraumatic in origin ( Table 1 ). A retrospective cohort study based on several statewide administrative claims databases analyzed more than 27,000 patients with conservatively managed SDH. This study included both traumatic SDH, identified by such International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) discharge codes as 852.2x or 852.3x, and nontraumatic SDH, coded as 432.1. Approximately 71% of all cases were traumatic SDHs, and 29% were nontraumatic. This latter group had higher rates of subsequent SDH-related hospitalization, surgery, and death. The overall readmission rate within 90 days for SDH was approximately 1 in 8.
| Type | Causes |
|---|---|
| Trauma | Motor vehicle collisions, falls, assaults, accidents |
| Coagulopathy or medical anticoagulation | Warfarin, heparin, hemophilia, liver disease, thrombocytopenia |
| Nontraumatic hemorrhage | Cerebral aneurysm, arteriovenous malformation, tumor (especially meningioma or dural metastasis) |
| Postsurgical | Craniotomy, CSF shunting |
| Intracranial hypotension | Lumbar puncture, lumbar CSF leak, lumboperitoneal shunt, spinal epidural anesthesia |
| Inflicted injury | Usually pediatric age group; also can be seen in the elderly |
| Spontaneous or unknown | Rare |
Parafalcine and Tentorial Acute Subdural Hematoma
Certain subtypes of traumatic ASDH and certain patient characteristics taken together may portend a benign course. Howard and colleagues found that isolated thin parafalcine and tentorial ASDHs in younger patients with mild TBI (Glasgow Coma Scale [GCS] score 13–15) did not enlarge, even when patients were taking antiplatelet or anticoagulant agents, or both. They suggested that such patients could be managed on a standard medical/surgical ward and did not require observation in an intensive care unit or intermediate care unit. However, only 65 patients met inclusion criteria for their study, which represented 8% of all patients admitted to their Level I trauma center with an ICD-9 code for SDH after closed head injury.
Posterior Fossa Acute Subdural Hematoma
Although rare, traumatic posterior fossa ASDHs are often associated with poor outcome. In a retrospective analysis of their experience with 10 patients, Takeuchi and colleagues reported a 90% poor outcome rate and a 50% mortality rate in patients with posterior fossa ASDH. Half of their patients exhibited coagulopathy. Their review of the literature revealed that posterior fossa SDHs were associated with occipital impacts and fractures, low GCS score, additional intracranial lesions (especially supratentorial lesions and intracerebellar hematomas), a significant rate of lesion evolution within the first 2 postinjury days, and high rates of poor outcome and mortality. Similarly, Oliveira de Amorim and colleagues retrospectively identified 4 cases of traumatic posterior fossa ASDH from their own institution and added an additional 57 cases from the literature. More than half the patients had an initial GCS score below 8, and unfavorable outcomes were recorded in 63%.
Nontraumatic Acute Subdural Hematoma
Numerous nontraumatic conditions may cause ASDH, either as a result of direct bleeding into the subdural space or as an extension of an intraparenchymal hematoma into the subdural space. These conditions include (1) ruptured intracranial aneurysm, (2) ruptured cortical artery, (3) hypertensive cerebral hemorrhage, (4) neoplasm, (5) hematologic disorder, (6) anticoagulant or thrombolytic therapy, (7) cerebral amyloid angiopathy, (8) dural arteriovenous fistula, and (9) acquired immune deficiency syndrome ( Table 2 ).
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