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Subdural hematoma in adults: Management and prognosis

Subdural hematoma in adults: Management and prognosis
Literature review current through: Jan 2024.
This topic last updated: Jul 17, 2023.

INTRODUCTION — Subdural hematoma (SDH) is a form of intracranial hemorrhage characterized by bleeding into the space between the dural and arachnoid membranes surrounding the brain.

The management and prognosis of SDH will be discussed here. A rapid overview summarizes the clinical features, evaluation, and management of SDH in adults (table 1).

Other aspects of SDH are reviewed separately.

(See "Subdural hematoma in adults: Etiology, clinical features, and diagnosis".)

(See "Intracranial subdural hematoma in children: Epidemiology, anatomy, and pathophysiology".)

(See "Intracranial subdural hematoma in children: Clinical features, evaluation, and management".)

Other forms of intracranial hemorrhage are discussed elsewhere.

(See "Intracranial epidural hematoma in adults".)

(See "Aneurysmal subarachnoid hemorrhage: Epidemiology, risk factors, and pathogenesis".)

(See "Nonaneurysmal subarachnoid hemorrhage".)

(See "Perimesencephalic nonaneurysmal subarachnoid hemorrhage".)

(See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis".)

(See "Traumatic brain injury: Epidemiology, classification, and pathophysiology".)

INITIAL MANAGEMENT — SDH can be a neurologic emergency that may cause irreversible brain injury and death caused by hematoma expansion, elevated intracranial pressure (ICP), or brain herniation. Patients with acute or chronic SDH require urgent initial assessment of clinical status to determine the need for surgery and the medical interventions needed to mitigate adverse outcomes (algorithm 1).

Initial assessment and emergency management — The initial assessment of SDH includes airway management for patients with drowsiness or severe bulbar symptoms. Patients with SDH associated with trauma should also undergo a structured primary survey to identify and prioritize management of other injuries. The initial evaluation of adult patients with trauma is discussed in greater detail separately. (See "Initial management of trauma in adults", section on 'Primary evaluation and management'.)

A neurologic examination is performed to determine the severity of initial neurologic deficits and provide a baseline to assess subsequent deterioration. The clinical assessment typically includes the Glasgow Coma Scale (table 2), a simple clinical scale to quantify deficits for patients with brain injury.

Management of antithrombotic medications

Reversing anticoagulation — For most patients with SDH who are taking anticoagulants, we discontinue these medications and give agents to reverse anticoagulant effects. We balance the hemorrhagic risks of anticoagulation with the thrombotic risks of reversal at an individual level. Reversal of anticoagulation is required for patients with acute or chronic SDH prior to surgical intervention. In addition, for most patients with acute SDH who are managed nonoperatively, we reverse anticoagulation to reduce the risk of SDH enlargement.

By contrast, for some patients with a chronic or small acute SDH and no signs of increased ICP who are receiving anticoagulation for a compelling indication such as a mechanical heart valve, the risk-benefit calculation may favor continued anticoagulation with close observation of neurologic status. For such patients, we anticoagulate with heparin during the acute setting whenever possible because it is typically quicker to reverse in the event of hematoma expansion. (See "Anticoagulation for prosthetic heart valves: Management of bleeding and invasive procedures", section on 'Management of bleeding'.)

If reversal of anticoagulation is indicated, the appropriate intervention depends upon the anticoagulant the patient is taking, the time since last dosage, and the urgency with which reversal is needed. Some patients prescribed anticoagulant medications may not require reversal agents if laboratory testing or the time interval since last dose indicates they are effectively not anticoagulated. For other patients with a medication-related coagulopathy:

Warfarin – Four-factor prothrombin complex concentrate (4F PCC) along with intravenous vitamin K is preferred for patients with serious or life-threatening bleeding; the dose of 4F PCC may need to be repeated while awaiting the effects of drug discontinuation (table 3). If a 4F PCC is not available, a three-factor product may be used with recombinant activated factor VII or fresh frozen plasma (FFP). Reversal of anticoagulation in this setting is discussed separately. (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Warfarin'.)

Dabigatran – We use the reversal agent idarucizumab for patients with potentially life-threatening bleeding including SDH. If idarucizumab is not available, an activated PCC such as factor eight inhibitor bypassing agent (FEIBA) can be used (table 4). (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Dabigatran'.)

Direct factor Xa inhibitors (eg, apixaban, edoxaban, rivaroxaban) – We use either andexanet alfa or a 4F PCC to reverse the effects of direct factor Xa inhibitors (table 4). (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Apixaban, edoxaban, and rivaroxaban'.)

Unfractionated heparin and low molecular weight heparinsProtamine sulfate is used to reverse the effect of heparin agents. The dose depends upon the type of heparin used (unfractionated versus low molecular weight agents), the dose of heparin given, and the time elapsed since that dose. Andexanet alfa may be used for patients taking low molecular weight heparin. (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Unfractionated heparin' and "Reversal of anticoagulation in intracranial hemorrhage", section on 'LMW heparin'.)

Patients on antiplatelets — Antiplatelet medications are typically stopped at the time of diagnosis for most patients with either acute SDH or large or symptomatic chronic SDH to reduce the risk of hematoma enlargement. However, we balance the thrombotic risks of discontinuation with the hemorrhagic risks of continuing antiplatelets at an individual level. We may continue antiplatelet medications during acute monitoring for selected patients at low risk of hematoma expansion and high risk of thrombosis such as those with established atherosclerotic disease or who have undergone intravascular stent placement and who have small or chronic SDH. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk" and "Antithrombotic therapy for elective percutaneous coronary intervention: General use" and "Overview of carotid artery stenting" and "Endovascular techniques for lower extremity revascularization", section on 'Antiplatelet therapy'.)

We do not give platelet transfusion to most patients taking antiplatelet medications who present with SDH. The available data from trials of patients with spontaneous intracerebral hemorrhage suggest that platelet transfusions may be hazardous and should be avoided. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Reverse anticoagulation'.)

We reserve platelet transfusions for those with specific indications, including those with a thrombocytopenia (<100,000/microL) or a known platelet defect. (See "Platelet transfusion: Indications, ordering, and associated risks", section on 'Platelet function disorders'.)

Identifying patients with an indication for surgery — Some patients with SDH require urgent surgical treatment at the time of initial presentation based on severity of imaging findings or clinical exam. Surgery may help to prevent irreversible brain injury and death caused by hematoma expansion, elevated ICP, and brain herniation. The benefits of surgery for patients with SDH are based on the severity of the lesion, the likelihood of subsequent deterioration, and the potential for recovery with surgery [1].

The indications for and timing of surgery and operative approaches for patients with SDH are discussed below. (See 'Surgical indications and approaches' below.)

SURGICAL INDICATIONS AND APPROACHES

Neurosurgical consultation — Neurosurgical consultation may be obtained for most patients with acute or symptomatic chronic SDH. Immediate neurosurgical consultation for urgent surgical evacuation is required for patients with SDH and any of the following clinical and imaging features:

Clinical features

Dilated pupil(s)

Rapid or progressive deterioration (including new drowsiness) on examination

Drop of ≥2 points on Glasgow Coma Scale (GCS) score (table 2)

Cushing triad (bradycardia, respiratory depression, hypertension)

Imaging features

Maximal clot thickness >10 mm

Shift of midline structures >5 mm, measured at the septum pellucidum (image 1)

Hydrocephalus or brainstem compression (image 2)

SDH associated with structural brain lesion (eg, skull fracture, arteriovenous malformation)

For other patients with acute SDH, we monitor nonoperatively with close neurologic examinations and surveillance imaging for clinical or radiographic deterioration. (See 'Nonoperative management' below.)

Acute subdural hematoma — Urgent surgical hematoma evacuation is required for patients with acute SDH and clinical signs attributable to brain herniation or elevated intracranial pressure (ICP) and for such patients who have evidence of neurologic deterioration since the time of injury. We suggest urgent surgical hematoma evacuation for patients with SDH thickness >10 mm or midline shift >5 mm on initial brain scan (algorithm 1). The benefits of surgery for those with an indication based on SDH size alone may be less certain for patients with significant cerebral atrophy and/or with minimal midline shift, patients older than 75 years of age, and those with medical comorbidities that are at elevated surgical risk [2].

For other patients with acute SDH, we monitor nonoperatively with close neurologic examinations and surveillance imaging for clinical or radiographic deterioration. (See 'Nonoperative management' below.)

Guidelines from an expert panel published in 2006 recommended surgical evacuation to reduce the risk of mortality or further morbidity for patients with severe or progressive symptoms and those with large acute SDH [1]. Clinical thresholds for surgery included a drop in the GCS score by ≥2 points from the time of injury to hospital admission and the presence of asymmetric or fixed and dilated pupils [1]. Imaging thresholds for surgery included an SDH clot thickness >10 mm or >5 mm midline shift, regardless of clinical findings. Larger SDH volumes are associated with worse outcomes. In a retrospective study of 174 patients undergoing surgery for SDH, the mortality rate increased with size of clot thickness from 10 percent for patients when SDH <10 mm to 90 percent when SDH >30 mm [3]. In another study of initial nonoperative management of 31 patients with acute SDH, hematoma thickness >10 mm and midline shift >5 mm on initial imaging were associated with subsequent neurologic deterioration and need for surgery [4].

Common surgical options for acute SDH include craniotomy, craniostomy (eg, burr hole trephination), and decompressive craniectomy [1].

Craniotomy – Craniotomy is often the preferred surgical technique for patients with acute SDH without underlying brain swelling who undergo hematoma evacuation. The procedure involves removal of a small section of skull to expose and drain the SDH. The skull flap is replaced and secured at the end of the procedure. Craniotomy provides better access and more effective drainage of acute SDH than the more limited burr hole craniostomy.

Craniectomy – Decompressive craniectomy involves removal of a section of the skull to permit wide exposure of the underlying dura mater overlying the SDH. This technique facilitates SDH evacuation and can help reduce morbidity from associated or anticipated brain swelling [5]. The removed skull flap is replaced in a delayed fashion.

Craniostomy – Craniostomy involves drilling a small hole through the skull to gain rapid access to SDH and/or to minimize incision size. It may be performed using burr hole trephination or twist drill techniques [6]. Craniostomy is less invasive than craniotomy techniques and can be performed at the bedside for emergency situations. It may also be used to reduce SDH volume in patients with mixed-density (acute-on-chronic) SDH [7].

Surgical technique for SDH evacuation varies by severity of injury, surgeon experience/preference, and available resources. Craniotomy may be preferred to minimize operative time and wound complications while craniectomy may be preferred to reduce risk of morbidity or reoperation from subsequent brain swelling [5]. In a multicenter trial of 462 patients with symptomatic acute SDH who were randomized to craniotomy or craniectomy, the functional outcomes were similar between groups at both 6 and 12 months [8]. However, reoperation within two weeks was more frequent in those assigned to craniotomy (15 versus 7 percent) and wound complications were more common among patients assigned to craniectomy (12 versus 4 percent).

Limited observational data suggest that craniotomy is associated with better outcomes than craniostomy [1]. In a surgical series of 60 patients with SDH, 25 patients underwent craniotomies, 24 were treated with burr holes, 8 had craniotomies with dural grafting, and 3 had decompressive craniectomies [9]. In a subgroup of severely affected patients, patients treated with craniotomy had a lower mortality and greater functional recovery rates than those treated with burr hole surgery. However, these results should be interpreted with caution due to small patient numbers, nonrandomized treatment allocation, and differences between treatment groups [1].

Chronic subdural hematoma — Urgent recommended hematoma evacuation is required for patients with large and symptomatic chronic SDH and the potential for recovery who develop signs attributable to brain herniation or elevated ICP including for such patients with evidence of moderate to severe cognitive impairment or progressive neurologic deterioration attributable to the chronic SDH. We suggest surgical evacuation of chronic SDH for patients with clot thickness >10 mm or midline shift >5 mm on brain scan (algorithm 1).

Nonoperative management is warranted for patients with small chronic SDH that are asymptomatic or causing minimal symptoms. In addition, nonoperative management may be preferred for older patients with chronic SDH not causing elevated ICP or severe symptoms as surgical outcomes may be worse in patients age 75 years or older [2]. (See 'Monitoring' below.)

There are no expert guidelines for the management of symptomatic chronic SDH. Some authors recommend surgery for patients with acute or chronic when SDH thickness is >10 mm or midline shift is >5 mm based on risk of subsequent deterioration and poor outcome [10]. In addition, surgical evacuation of chronic SDH improves outcome for symptomatic patients with evidence of brain herniation or elevated ICP [10].

Surgical evacuation may improve symptoms when chronic SDH causes severe cognitive impairment [11,12]. However, some authors advocate a trial of conservative management for older adult patients with chronic SDH but no evidence of increased ICP, even when the SDH is thought to be causing or contributing to cognitive impairment. In one small series, five patients older than 70 years with persistent SDH four to five weeks after minor head trauma were observed for 30 to 45 days. These patients were symptomatic with headache and decreased cognition on the Mini Mental Status Exam at the outset of the study. Serial head computed tomography (CT) scans revealed complete disappearance or marked reduction in SDH size by 30 to 45 days, and clinical recovery was complete [13].

The benefits of surgical evacuation of chronic SDH need to be balanced with surgical risks and the nonoperative natural history of chronic SDH. Chronic SDH may resolve spontaneously with nonoperative management in many cases, typically over a period of several weeks. In addition, subdural fluid can reaccumulate after surgery for chronic SDH and may lead to repeat surgery, increase risk of seizures, and higher overall treatment costs [14]. (See "Subdural hematoma in adults: Etiology, clinical features, and diagnosis", section on 'Pathophysiology'.)

Available surgical options for symptomatic chronic SDH include burr hole trephination, craniotomy, and decompressive craniectomy [1]. Endovascular treatment with middle meningeal artery embolization may be used to prevent chronic SDH recurrence or as a primary treatment for symptomatic patients who are at high risk for surgical options. In most cases, burr hold trephination is pursued. When indicated, identification and ligation of the bleeding vessel must be undertaken.

Burr hole and drainage – Burr hole trephination is performed for most patients undergoing surgery for symptomatic chronic SDH to facilitate fluid drainage and reexpansion of underlying brain tissue. One or more burr holes can be placed to allow drainage of the hematoma. A flexible catheter (Jackson–Pratt drain) is usually placed in the subdural space until the drainage subsides [15]. The use of a drain after burr hole placement was found in one trial to reduce SDH recurrence (9 versus 24 percent) and six-month mortality (9 versus 18 percent) without an excess in medical or surgical complications [16]. The optimal time for catheter drainage is uncertain. In a trial of 420 patients with chronic SDH assigned to burr hole drainage for either 24 or 48 hours, outcomes were similar when assessing SDH recurrence (14 versus 13 percent), as well as length of hospital stay, postoperative infections, and mortality [17].

A subdural evacuating port system is a less invasive alternative to craniectomy and burr hole decompression that appears safe and similarly effective in small observational studies [18,19].

Middle meningeal artery embolization – Endovascular middle meningeal artery (MMA) embolization represents a minimally invasive treatment option for the management of chronic SDH [20,21]. MMA embolization may be used as an adjunctive option along with open techniques to decrease the likelihood of hematoma reaccumulation, including for patients with a coagulopathy and those with multiple prior SDH recurrences. It may also be performed as a sole intervention in patients deemed high surgical risk.

A 2021 meta-analysis of 17 retrospective and 3 prospective studies including 1416 patients with chronic SDH, those who had MMA embolization with or without initial surgical evacuation had lower rates of hematoma recurrence than those who had surgical or nonoperative management without MMA (4.8 percent versus 21.5 percent; odds ratio 0.15, 95% CI 0.03-0.75) and similar complication rates [22,23].

Subsequent rescue surgery due to treatment failure after MMA embolization has been reported in 1 to 9 percent of patients in various case series [20,21,24,25]. As an example, in a multicenter series of 138 patients with chronic SDH selected for MMA embolization, more than 70 percent achieved at least 50 percent improvement on imaging and only 7 percent underwent additional subsequent treatment [20]. Predictors of treatment failure include pretreatment anticoagulation and MMA diameter <1.5 mm [25].

Other surgical techniques – A craniotomy with resection of membranes that surround the clot is typically performed in patients with chronic SDH that rebleed after burr hole drainage to prevent reaccumulation of fluid [26-28].

Timing of surgery — Urgent surgical hematoma evacuation (within two to four hours) is required for patients with acute or chronic SDH and signs of brain herniation or elevated ICP and for patients who develop acute neurologic deterioration. We suggest urgent surgical hematoma evacuation for patients with clot thickness >10 mm or midline shift >5 mm on initial brain scan.

Surgery performed within two to four hours after the onset of neurologic deterioration may be associated with a lower mortality than delayed surgery [1,29-32]. Data from observational studies have found mortality rates between 30 and 47 percent with urgent surgery compared with 80 to 90 percent when intervention was delayed beyond four hours [1].

However, other observational studies evaluating the time between injury and surgery have reported no significant relationship with outcome [33-38], and some reports found that early intervention appeared to have a worse outcome than delayed surgery [1,9,35,39]. These data may be confounded by selection bias, since patients who had immediate surgery tended to have more severe injuries and lower initial GCS scores than those in whom intervention was delayed [1].

NONOPERATIVE MANAGEMENT

Monitoring — For all patients with SDH managed nonoperatively, we use serial neurologic examinations and repeat imaging, typically with head computed tomography (CT), to assess for subsequent deterioration and the development of increased intracranial pressure (ICP).

No randomized trials have compared surgery with conservative management for patients with SDH, but limited observational data suggest that patients with acute SDH who are clinically stable and have small hematomas can be managed nonoperatively [4,40,41]. In a series of 65 comatose patients with acute SDH, 15 patients were selected for nonoperative management because they were clinically stable or improved from the time of injury to evaluation, had hematoma thickness <10 mm and midline shift <5 mm on initial head CT, and had no evidence of uncompensated ICP elevation with invasive monitoring [40]. A good functional outcome was achieved in 10 of 15 patients (67 percent) initially managed nonoperatively compared with 13 of 50 patients (26 percent) who initially required with surgery. Only two patients in the nonoperative group had delayed surgical evacuation due to the development of parenchymal hematomas or elevated ICP.

Serial clinical examinations

Clinical setting – Patients with an acute or symptomatic chronic SDH should be monitored in an inpatient setting with neurosurgical expertise. Those at risk for respiratory failure with impairment of alertness, coma, or other severe neurologic deficits should be admitted to an intensive care unit.

Other patients with small, asymptomatic chronic SDH that are found incidentally on imaging may be monitored in the ambulatory setting with initial clinical exam and follow-up imaging to document resolution of the hematoma. (See 'Follow-up imaging' below.)

Parameters to monitor – Neurologic examinations should include assessments of alertness, pupillary and other bulbar functions, and sensorimotor functions. For patients with baseline impairment of alertness or weakness, serial testing with Glasgow Coma Scale (GCS) score (table 2) is also performed.

Invasive monitoring of ICP is indicated for patients with SDH due to trauma and those with other risk factors for developing elevated ICP. This is presently separately. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Indications'.)

Monitoring frequency – For patients hospitalized with acute or chronic SDH, serial neurologic examinations should be performed at baseline and every one to two hours for at least the first 24 hours after presentation. The frequency of examinations may be reduced to every four hours for stable patients. A longer interval of initial monitoring or more frequent examinations may be performed for those at higher risk for hematoma expansion.

Risk factors for hematoma expansion include [41-43]:

Older age

History of hypertension

History of ischemic heart disease

Antithrombotic medication exposure

Impaired consciousness on examination

SDH associated with additional intracranial injuries

Larger SDH volume

Presence of intraventricular hemorrhage

The risk of hematoma enlargement and neurologic deterioration may be highest in the first 36 hours after SDH onset [44]. However, SDH expansion or clinical deterioration may occur hours to weeks after injury in patients with SDH. In a study of 31 patients with traumatic SDH who were initially managed nonoperatively, surgery for neurologic deterioration was required in six patients within three days of injury [4].

Follow-up imaging — We suggest that surveillance follow-up head CT be obtained within six to eight hours of the initial scan for all patients hospitalized with acute and symptomatic chronic SDH who are managed nonoperatively [40]. The incidence of hematoma expansion is highest in the initial several hours after onset [42,44]. Hematoma expansion may precede clinical deterioration and patients selected for initial nonoperative management may develop an indication for surgery due to progressive findings on follow-up imaging. (See 'Identifying patients with an indication for surgery' above.)

For patients with stable findings on initial follow-up head CT, subsequent imaging may be performed at transitions of care (eg, prior to hospital discharge) to document stability. In addition, for patients resuming antithrombotic medications that were discontinued during initial management, follow-up head CT is typically obtained prior to resuming antithrombotic medications to document resolution of the hematoma. (See 'Resumption of antithrombotic medications' below.)

Follow-up imaging is also performed for patients with acute or chronic SDH to document resolution after recovery. The timing of imaging varies by size and acuity of the SDH. Resolution of acute bleeding may be found several days up to two weeks from onset, while resolution of chronic SDH may occur several weeks after onset. (See "Subdural hematoma in adults: Etiology, clinical features, and diagnosis", section on 'Imaging features' and "Subdural hematoma in adults: Etiology, clinical features, and diagnosis", section on 'Pathophysiology'.)

Urgent repeat head CT is warranted for all patients with clinical deterioration. (See 'Management of patients who deteriorate' below.)

Management of patients who deteriorate

Urgent repeat imaging to assess for indication for surgery — Urgent repeat imaging with head CT is warranted to assess for progression of the hematoma, brain compression, or hydrocephalus in all patients with SDH who have an acute deterioration in clinical status.

Patients with progression of hematoma – We recommend surgical evacuation when repeat head CT shows progression that meets imaging criteria for surgery. (See 'Surgical indications and approaches' above.)

For patients with clinical deterioration and modest SDH progression on repeat head CT (eg, SDH that is larger than prior study but <10 mm thickness) that does not meet imaging criteria for surgical evacuation, we use clinical status to guide subsequent therapy. (See 'Surgical indications and approaches' above.)

We recommend surgical evacuation for patients with rapid or significant clinical deterioration that is attributable to hematoma expansion (eg, pupillary changes, progressive hemiparesis contralateral to SDH). We also recommend surgical evacuation for patients with evidence of elevated ICP such as new drowsiness, development of the Cushing triad, or a drop of ≥2 points on GCS score (table 2). (See 'Surgical indications and approaches' above.)

For those with minor clinical changes and modest progression on repeat head CT, we may continue close nonoperative monitoring. (See 'Monitoring' above.)

For patients with clinical deterioration that is not attributable to hematoma expansion or elevated ICP, we pursue additional testing to identify the source. As an example, a patient with new isolated aphasia in the setting of a right hemisphere SDH that progressed from 4 mm to 6 mm maximal thickness may require additional testing for seizure or ischemic stroke. (See 'Testing for other causes of deterioration when repeat imaging is stable' below.)

Patients with elevated intracranial pressure – Patients with SDH may develop elevated ICP requiring urgent intervention. For patients managed nonoperatively with an ICP monitor, we recommend urgent surgical evacuation if the ICP is persistently >20 mmHg.

Definitive therapy for elevated ICP is usually hematoma evacuation; medical resuscitation used as a temporizing measure for patients awaiting surgery includes head elevation, hyperventilation, and osmotic diuresis with intravenous mannitol or hypertonic saline. The management of elevated ICP is reviewed elsewhere. (See "Evaluation and management of elevated intracranial pressure in adults".)

Testing for other causes of deterioration when repeat imaging is stable — Patients with SDH are at risk of clinical deterioration due to neurologic events other than hematoma expansion or elevated ICP. Additional testing is warranted for patients with SDH and evidence of clinical deterioration not accounted for by findings on repeat head CT. Specific testing is determined by clinical features and patient risk factors.

Seizures – SDH may cause seizures due to compression of underlying cerebral cortex. Seizures may accompany acute SDH in the setting of mild or severe traumatic brain injury. (See "Posttraumatic seizures and epilepsy".)

Patients with a persistent impairment in alertness not due to elevated ICP, those with fluctuating changes in neurologic examination, and those with witnessed convulsions warrant evaluation for seizures with electroencephalography.

Ischemic stroke – SDH may be complicated by ischemic stroke in patients with thromboembolic risk factors such as atrial fibrillation due to the reversal of anticoagulation to manage the SDH. In addition, ischemic stroke may infrequently occur in nonambulatory patients in the setting of embolization of a deep venous thrombosis. (See "Atrial septal abnormalities (PFO, ASD, and ASA) and risk of cerebral emboli in adults", section on 'Paradoxical emboli'.)

Ischemic stroke should be suspected in at-risk patients with SDH who have a sudden clinical deterioration consistent with ischemic stroke (table 5) and stable head CT. Brain magnetic resonance imaging (MRI) is the preferred imaging modality because acute ischemic stroke may not be visible on initial repeat head CT. The treatment of acute ischemic stroke is discussed separately. (See "Initial assessment and management of acute stroke".)

Acute toxic-metabolic encephalopathy – Patients with SDH may develop delirium due several causes including preexisting medical conditions, pain, or medications. The evaluation of patients with delirium is discussed separately. (See "Diagnosis of delirium and confusional states".)

Evaluation for underlying causes — Some patients with spontaneous SDH not associated with trauma or other obvious cause may warrant brain and/or vascular imaging and other testing to identify possible secondary causes. The evaluation of underlying causes of SDH is discussed separately. (See "Subdural hematoma in adults: Etiology, clinical features, and diagnosis", section on 'Evaluation for underlying causes'.)

Prevention and management of medical complications — Patients with acute or chronic SDH are at risk for medical complications due to immobility or direct effects of the SDH. These complications can be associated with worse outcomes based on data from patients with intracerebral hemorrhage [45].

Seizure prophylaxis and management – Patients with SDH are at risk for seizure or status epilepticus [46]. We do not routinely start antiseizure medicine prophylaxis for patients who have not had a seizure. In systematic reviews and observational studies, the seizure rate appears similar whether or not patients with SDH receive antiseizure medication prophylaxis [46-49].

For patients with impairment of consciousness not attributed to mass effect from the SDH, we evaluate for other causes of symptoms. This includes electroencephalography to assess for nonconvulsive seizures or status epilepticus. (See 'Evaluation for underlying causes' above.)

Antiseizure medications are typically reserved for patients with SDH who have clinical or electrographic seizures. The choice of initial antiseizure medication is guided by medical comorbidities, drug interactions, side effect drug profile, and contraindications (table 6). (See "Evaluation and management of the first seizure in adults".)

Prevention of venous thromboembolism – Patients hospitalized with an acute illness and those with a neurologic condition that impairs mobility are at risk for venous thromboembolism. Intermittent pneumatic compression should be started on the first day of hospital admission for patients with SDH and impaired mobility. We add chemical prophylaxis for most patients one to four days after SDH stability is documented. An exception would be some patients being evaluated for urgent surgery for whom chemical prophylaxis may be temporarily withheld. (See "Prevention of venous thromboembolic disease in acutely ill hospitalized medical adults".)

Therapies not recommended or of uncertain benefit

Statin medications – Limited data suggest that low-dose statin medications may reduce hematoma size for patients with chronic SDH. In a systematic review that identified 156 patients with chronic SDH from three observational studies, atorvastatin 20 mg daily for one to six months was associated with reduced hematoma volume and low rates of recurrence [50]. In a trial of 196 patients with chronic SDH from China, those assigned atorvastatin 20 mg daily had better outcomes at eight weeks than those assigned to placebo, including greater reduction in SDH volumes (29 versus 17 mL) and lower rates of surgery for hematoma enlargement or deterioration (11 versus 24 percent; hazard ratio 0.47, 95% CI 0.24-0.92) [51]. Additional studies are needed to better identify the role of statin medications in the nonoperative management of patients with chronic SDH.

Tranexamic acid – The role of tranexamic acid (TXA) in the nonoperative management of patients with SDH is uncertain. TXA is an antifibrinolytic agent used in some patients with chronic SDH to reduce the rate of rebleeding after surgery or to promote resorption [52]. In a systematic review of 105 patients from four studies, only low-quality evidence was identified showing that tranexamic acid was associated with reduction in hematoma volume [53]. Data were limited by small numbers and variability in patient characteristics. In addition, TXA was used as an adjunctive therapy to surgical evacuation in most cases. In an observational study of 27 patients with chronic SDH managed nonoperatively including TXA for a mean of 65 days, resolution occurred in all patients and no complications were reported [54]. Additional trial data are needed to clarify the role of TXA for patients with chronic SDH.

Glucocorticoids – We avoid glucocorticoid therapy for patients with SDH. In a trial of 748 patients with symptomatic chronic SDH, those assigned to a two-week course of dexamethasone were less likely to achieve a good functional outcome at six months than those assigned to placebo (84 versus 90 percent) [55]. Glucocorticoid therapy has also been associated with increased acute mortality following head injury. This issue is discussed separately. (See "Management of acute moderate and severe traumatic brain injury", section on 'Glucocorticoids'.)

PROGNOSIS AND LONG-TERM MANAGEMENT — The prognosis of SDH depends on severity of SDH and associated medical comorbidities. In a study that included 746 procedures of patients with SDH who underwent surgery between 2005 and 2012, the 30-day mortality rate was 17 percent [56]. In another study assessing outcome of patients undergoing surgery for acute SDH that included 462 patients (median age 49 years old), mortality at six months was 31 percent [8]. The estimated mortality rate for patients with more severe injuries who require surgery for SDH is as high as 60 percent in some small studies [1,3,9,29,33,40]. For patients who presented with coma prior to surgical evacuation, mortality rates were 57 to 68 percent [1,34,57].

Risk factors for poor outcome — Age greater than 60 years and severe neurologic impairment are important prognostic indicators in patients with acute SDH [9,34]. Clinical features associated with poor outcome after SDH include the following:

Older age [34,56]

Lower Glasgow Coma Scale score [9,39]

Coma at presentation [56,57]

Coagulopathy [1,56,58]

In addition, several studies have identified head computed tomography (CT) findings that correlate with poor outcome after acute SDH, including the following:

Hematoma thickness [3,35]

Hematoma volume [36]

Presence and/or degree of midline brain shift [3,34-36]

Reduced patency of the basal cisterns [35]

Coexisting intraparenchymal injury [33,58]

Arterial source to SDH [59,60]

However, some studies have not confirmed these relationships [61].

Risk of recurrence — Recurrence of an acute SDH after initial resolution is uncommon and usually associated with an underlying fixed bleeding source such as a dural arteriovenous malformation, metastases, liver failure, hematological malignancies, or intracranial hypotension [62-65]. The risk of recurrence may be higher in patients with spontaneous SDH than those with a clear precipitant such as trauma.

Recurrence of chronic SDH has been described in 5 up to 30 percent of patients [66-68]. Older age, thicker hematoma width, and bilateral presentation have been linked to higher rates of recurrence [68-73]. Ongoing antiplatelet and anticoagulant therapy may also increase the risk of recurrent SDH, although this has not been consistently found [72,74,75]. The use of postoperative drainage is associated with a lower risk of secondary recurrence.

Resumption of antithrombotic medications — The decision to resume anticoagulant or antiplatelet medications that were discontinued during initial SDH management should be individualized balancing the strength of the specific indication for therapy with the risk of SDH recurrence.

We suggest resuming antiplatelet therapy after SDH resolution for most patients with a specific indication for such therapy. In one study of 2939 patients with SDH, the risk of subsequent arterial ischemic events was elevated in the first four weeks after SDH (hazard ratio 3.6, 95% CI 1.9-5.5), driven largely by patients with strong indications for antithrombotic therapy [76]. Accordingly, the risk-benefit analysis might favor resumption of antiplatelet therapy in a patient with active coronary or vascular disease, particularly after a SDH related to a traumatic injury that was not likely to recur.

Many patients will benefit from resuming anticoagulation when the thromboembolic risk is higher than the risk of recurrent SDH. The specific risks and benefits should be weighed for individual patients. As examples:

Anticoagulation may be resumed for selected patients with a traumatic SDH and atrial fibrillation with an elevated risk of thromboembolism after follow-up head CT shows resolution of the hematoma. (See "Atrial fibrillation in adults: Selection of candidates for anticoagulation".)

Anticoagulation may be resumed for selected patients with a spontaneous SDH and a history of deep venous thrombosis and a high recurrence risk after follow-up head CT shows resolution of the hematoma. (See "Selecting adult patients with lower extremity deep venous thrombosis and pulmonary embolism for indefinite anticoagulation", section on 'High recurrence risk'.)

Anticoagulation may be withheld for selected patients with SDH and a high risk of recurrence, such as those with SDH due to a secondary source such as an unsecured arteriovenous malformation that has bled or cerebral amyloid angiopathy. (See "Brain arteriovenous malformations", section on 'Ruptured AVMs' and "Cerebral amyloid angiopathy", section on 'Managing anticoagulant and antiplatelet medications'.)

Limited data suggest anticoagulation can be safely resumed following SDH in properly selected patients. In a meta-analysis of observational studies of the postoperative course of patients with chronic SDH, hemorrhagic complications were similar among those who resumed or discontinued anticoagulation [77]. However, the subsequent thromboembolic rate was lower among patients who resumed anticoagulation (3 versus 7 percent). In an analysis of 98 patients with chronic SDH who underwent surgical evacuation, the subsequent SDH recurrence rate was similar among those who started long-term anticoagulation and propensity score-matched patients who did not [78].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Stroke in adults".)

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Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Subdural hematoma and epidural hematoma (The Basics)")

SUMMARY AND RECOMMENDATIONS

Initial management – Subdural hematoma (SDH) can be a neurologic emergency that may cause irreversible brain injury and death caused by hematoma expansion, elevated intracranial pressure (ICP), and brain herniation. Patients with SDH require urgent assessment of clinical status, the management of any antithrombotic medications, and evaluation of the need for immediate surgery (table 1). (See 'Initial management' above.)

Surgical management – Urgent surgical hematoma evacuation is required for patients with SDH and signs attributable to brain herniation or elevated ICP and for those with clinical deterioration due to hematoma expansion (algorithm 1). (See 'Surgical indications and approaches' above.)

We also suggest surgical hematoma evacuation for patients with clot thickness >10 mm or midline shift >5 mm on initial brain scan especially if there is neurologic deterioration (Grade 2C). For other patients, we monitor nonoperatively with close neurologic monitoring for clinical or radiographic deterioration.

Nonoperative management for all others – Nonoperative management of SDH may be appropriate for patients who are clinically stable and have small hematomas with no signs of brain herniation (ie, midline shift <5 mm) or elevated ICP. Patients with SDH managed nonoperatively are closely monitored to assess for subsequent deterioration (algorithm 1). (See 'Nonoperative management' above.)

Monitoring – Neurologic examinations should be performed at baseline and every one to two hours for at least the first 24 hours. Examinations include assessments of alertness, pupillary and other bulbar functions, sensorimotor functions, and Glasgow Coma Scale scoring (table 2). (See 'Monitoring' above.)

Repeat imaging – Surveillance follow-up imaging with head computed tomography (CT) should be obtained within six to eight hours of the initial scan for all patients with SDH. Urgent repeat head CT is warranted for all patients who have an acute deterioration in clinical status. (See 'Follow-up imaging' above and 'Urgent repeat imaging to assess for indication for surgery' above.)

Patients who deteriorate – Surgical evacuation is indicated when clinical deterioration is due to significant progression of the hematoma. Testing for other causes is warranted for patients with SDH and evidence of clinical deterioration not accounted for by findings on repeat head CT. (See 'Management of patients who deteriorate' above.)

Resumption of antithrombotic medications – The decision should be individualized balancing the strength of the specific indication for therapy with the risk of SDH recurrence. Many patients will benefit from resuming anticoagulation when the thromboembolic risk is higher than the risk of recurrent SDH. (See 'Resumption of antithrombotic medications' above.)

Prognosis – The 30-day mortality rate in patients with SDH who underwent surgery is approximately 17 percent but may be higher in patients who present with clinical features such as older age, preexisting coagulopathy, severe deficits on exam, and imaging features such as larger SDH volume, brain compression, or coexisting intraparenchymal injury. (See 'Risk factors for poor outcome' above.)

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