Subdural hematoma

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

ACUTE

acute hematoma

≥10 mm size or midline shift ≥5 mm; with significant neurologic dysfunction; ICP ≥22 mm Hg

1st line – surgery

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1st line –

surgery

Surgery is indicated for an acute subdural hematoma (SDH) that is expanding and/or causing neurologic signs and symptoms. Brain Trauma Foundation guidelines recommend emergency surgical evacuation of the hematoma for patients with any one or more of SDH of >10 mm or a midline shift >5 mm (regardless of Glasgow Coma Scale [GCS] score); a GCS score <9 that has dropped ≥2 points between injury and emergency room (regardless of hematoma width or extent of midline shift); GCS score <9, and one or both of: fixed or asymmetric pupils and/or ICP >22 mmHg (regardless of hematoma width or extent of midline shift).[77]

However, the evidence to underpin the criteria for surgical versus conservative management is weak. In practice, there is a consensus that surgical intervention is indicated for any patient with an acute SDH who is comatose whereas there is substantial variation between neurosurgical centers in the thresholds applied for acute surgical evacuation in non-comatose patients with similar clinical presentations.[37] There is also ongoing debate about the benefits versus risks of emergent surgery for acute SDH in older individuals, with studies reaching conflicting conclusions.[30][79] An evidence review for the UK National Institute for Health and Care Excellence (NICE) guideline on head injury stated that, in practice, neurosurgical intervention is less likely to be offered to adults age ≥75 years due to risks outweighing benefits.[71]

The decision of what type of surgery to perform depends on the radiographic appearance of the hematoma and the surgeon's preference.[116]

Surgical intervention for acute SDH can be a standard trauma craniotomy or a hemicraniectomy and duraplasty if there is significant cerebral swelling or associated contusions. Data from 2023 suggest that patients who underwent standard craniotomy versus decompressive hemicraniectomy for acute SDH had similar functional outcomes and that those with severe, coexisting parenchymal injury may benefit from craniectomy.[117]

In the case of bilateral SDHs, there is no established paradigm for treatment. Decision-making is complicated if significant differences in SDH size/thickness or lateralization of symptoms are present, suggesting that one SDH is asymptomatic.[129] When the two hematomas are equal in size many neurosurgeons treat both sides simultaneously; when the two hematomas are asymmetric many neurosurgeons will treat only the larger or symptomatic one. One study compared patients with bilateral SDHs who were treated either with unilateral surgery or with bilateral surgery. The recurrence rate among patients treated with a unilateral approach was nearly twice as high as that for patients treated with a bilateral approach (21.6% vs. 11.5%); the absence of postoperative drainage and mixed density SDH were independent predictors for retreatment.[66] One study utilizing bilateral middle meningeal artery embolization in combination with bilateral burr hole drainage showed potential for decreased recurrence.[130]

While this would suggest a more aggressive approach to bilateral SDHs, additional studies are required before any guidelines can be established.

Rarely, an epidural hematoma may occur on the contralateral side to the SDH. Although rare, this is potentially life-threatening because the epidural hematoma can rapidly expand when the compressive force of the SDH is relieved by surgical evacuation.[67][68] If it has not been initially recognized, this expansion may not be noticed until after surgery when the surgical drapes are removed and the patient is found to have a blown pupil on the side of the epidural hematoma. Initial recognition is therefore important. Most epidural hematomas are associated with skull fractures coursing through the foramen spinosum where the middle meningeal artery is injured.[57] Any skull fracture involving the foramen spinosum should warn the operating neurosurgeon of this possible situation. The patient can be positioned so that a craniotomy on the contralateral side can quickly be performed.

Plus – monitoring

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Plus –

monitoring

Treatment recommended for ALL patients in selected patient group

All patients with Glasgow Coma Scale <9 need to have intracranial pressure (ICP) monitoring and should be considered for monitoring of cerebral oxygenation, together with continuous electroencephalographic monitoring for seizures.[55][72][73][74][75][76]

An epileptologist can be consulted for interpretation.[74][75][76]

Consider – anticonvulsant

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Consider –

anticonvulsant

Treatment recommended for SOME patients in selected patient group

The routine use of prophylactic anticonvulsants for patients with acute subdural hematoma (SDH) is controversial and high-quality evidence from randomized controlled trials is needed. Check your local protocol or consult the neurology team for advice. Some guidelines recommend prophylactic anticonvulsants for patients with acute traumatic SDHs for up to 7 days after presentation (in the absence of indication to continue).[49]

Anticonvulsant prophylaxis has been shown to decrease the occurrence of early, post-traumatic seizures.[134][135][136] Levetiracetam and phenytoin are similarly efficacious, and recommended in guidelines.[49][77][137]

However, anticonvulsants carry a notable adverse effect profile and more recent systematic review data and observational studies have not shown any significant reduction in seizure frequency from their use in patients with SDH.[133][138][139][140] On this basis, other commentators argue that there is insufficient evidence to support routine prophylactic use in either acute or chronic SDH and instead recommend limiting the use of anticonvulsants to SDH patients who have clinical or electroencephalogram-based evidence of seizure activity.[30]

In patients with late post-traumatic epilepsy (beyond the first 7 days after injury) or seizures despite anticonvulsant administration, consultation with a neurologist is recommended.

Late posttraumatic epilepsy occurs most commonly in patients with a history of acute SDH and coma >7 days.[141][142]

Primary options

phenytoin: 10-20 mg/kg intravenously as a loading dose (maximum 1000 mg/dose), followed by 4-6 mg/kg/day intravenously/orally given in 2-3 divided doses, adjust dose according to response and serum drug level

levetiracetam: 500-1000 mg intravenously/orally twice daily, adjust dose according to response, maximum 3000 mg/day

Consider – management of antithrombotic therapy

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Consider –

management of antithrombotic therapy

Treatment recommended for SOME patients in selected patient group

When a patient is diagnosed with acute or chronic subdural hematoma (SDH), it is essential to establish whether they are taking any anticoagulation or antiplatelet agents. Tailored management (including possible reversal of) antithrombotic therapy is a key element of initial care for all patients with SDH and of perioperative optimization for those who need neurosurgical intervention.[32][81]

Many patients with severe head injury present with coagulopathy and require normalization of their coagulation profile.[82][83][84] Drug-specific reversal therapy should be initiated for those requiring emergent surgery for life-threatening bleeding.[49] Most patients will need suspension of (and in some cases reversal of) their antithrombotic therapy, although these decisions must be based on judicious weighing of the individual patient’s relative risks of bleeding versus thrombosis.[30][70]

Immediate reversal of anticoagulation is generally recommended if active bleeding is present.[85] Specific anticoagulant reversal recommendations for patients with life-threatening bleeding (all etiologies) are published by the Neurocritical Care Society/Society of Critical Care Medicine, American Heart Association (AHA), and American Society of Hematology.[49][70][86][87]

Patients on oral anticoagulation therapy are estimated to have a 4- to 15-fold increased risk for SDH, leading to a higher likelihood of hematoma expansion, an increased risk of death, and a worse functional outcome unless anticoagulation is quickly reversed.[36] However, decisions around the cessation or reversal of anticoagulation should be individualized. For instance, the risks as well as the benefits of vitamin K antagonist (e.g., warfarin) reversal should be considered in patients with concurrent symptomatic or life-threatening thrombosis, ischemia, heparin-induced thrombocytopenia, or disseminated intravascular coagulation.[70]

Providers managing SDHs should also be aware of direct oral anticoagulants (DOACs) which target either thrombin or factor Xa. Examples of these drugs include dabigatran, rivaroxaban, apixaban, and edoxaban. DOACs have several advantages over warfarin, including less risk of life-threatening hemorrhages, which is why their use is increasing.[70] When treating SDHs in patients on DOACs, providers should be encouraged to consult with their hematology colleagues for potential reversal options.[70][89][90]

Current guidelines suggest that all patients discontinue antiplatelet agents in the acute period postinjury when intracranial hemorrhage is present or suspected.[49][70] The reversal of antiplatelet agent effects in patients with traumatic ICH remains controversial.[49] The American College of Surgeons states that for patients with normal platelet function or documented resistance, reversal therapies are not recommended and routine platelet transfusion is not recommended for use in reversing antiplatelet agent effects.[49] Clinical judgment should be used to determine if patients with TBI on antiplatelet agents who are undergoing surgery or invasive procedures with low platelet counts need platelet transfusions to achieve hemostasis.[49] However, the risk-benefit decision is often particularly complex in patients who are taking dual antiplatelet therapy.[30] Evidence suggesting a significant risk of thrombosis associated with cessation of dual antiplatelet therapy in specific subgroups of patients (e.g., those who have undergone recent placement of drug-eluting stents).[91][92] In such patients, continuation of aspirin monotherapy may be advisable to minimise the risk of cardiac ischemic events.[30] In the specific instance of SDH, practice varies between centers. Advice should be sought from hematology or cardiology colleagues to enable a detailed, personalized risk assessment.[30]

All patients should have serial prothrombin time, partial thromboplastin time, international normalized ratio (INR), and platelet and fibrinogen levels followed. Although anti-Xa assays are available, the AHA notes that these are not widely accessible and often are not able to be run quickly enough in an emergent setting.[93] Evidence from 2019 suggests that targeted reversal utilizing viscoelastic assays, including thromboelastography or rotational thromboelastometry, may provide an overall survival benefit and decrease in recurrent bleeding in the first 6 hours following trauma.[81] Reversal therapy should not be delayed while waiting for laboratory results in emergent situations when the patient is at high risk for bleeding.[49]

Correction of coagulopathy can include vitamin K (useful in patients with warfarin-related prolongation of INR), fresh frozen plasma, platelets (goal platelet count is >100,000/microliter), cryoprecipitate (used in patients with low fibrinogen levels), protamine (used for patients on heparin), recombinant coagulation factor Xa (andexanet alfa) for patients on apixaban or rivaroxaban, and activated factor VIIa.[94]

Consider – intracranial pressure-lowering regimen

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Consider –

intracranial pressure-lowering regimen

Treatment recommended for SOME patients in selected patient group

In patients with increased intracranial pressure (ICP), a standard protocol is used for management. It is important to follow traditional traumatic brain injury principles, including maintaining a cerebral perfusion pressure of 60-70 mmHg.[77]

An ICP <22 mmHg (in adults) is a useful initial threshold for treatment. However, ongoing research suggests this threshold is dependent upon individual patient factors such as injury type and severity.[49] When the risk/benefit of advancing treatment becomes a concern, such as for therapy with significant hazards (e.g., decompressive craniectomy), a treatment range of 20-25 mmHg should be considered.[49][147]

Primary options that can be used to lower ICP include raising the head of the bed to 30°, using the reverse Trendelenberg position if spinal instability or injury is present.[96] Analgesics and sedation can be useful, as pain and agitation can increase the ICP.[97] Using paralytics in intubated patients can help attenuate the effects of suctioning.[98] Hyperventilation to a goal pCO₂ of 30 to 35 mmHg (monitored with serial arterial blood gases) can be beneficial.[100]

Secondary treatment options to lower ICP include hyperosmolar therapy with hypertonic saline in concentrations between 3.0% and 23.4%, and a dosing limit based on an upper serum sodium limit of 155 mmol/L.[7][101][102][103][104][105] There is insufficient evidence to recommend one osmotic agent over another.[77][106] Osmotic diuretics such as mannitol can also be used, but should be avoided if the serum osmolar gap exceeds 18 mOsm/kg to 20 mOsm/kg.[107] Some experts also suggest not to exceed a serum osmolality of 320 mOsm/kg if mannitol is to be considered.[148] Use of hypertonics (saline) or hyperosmolar therapy (mannitol) may be counterproductive due to the risk of expansive hematoma volume, and are used only as a temporizing measure until emergent surgical interventions can be implemented.[108] External ventricular drainage of cerebrospinal fluid can also be considered.[109]

Other treatment options include maintaining the patient in a pentobarbital coma (requires continuous electroencephalographic monitoring), inducing hypothermia by intravascular cooling or topical cooling blankets, and decompressive hemicraniectomy.[110][111][112][113][114][115]

Consider – adjustment of shunt drainage + other measures as indicated

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Consider –

adjustment of shunt drainage + other measures as indicated

Treatment recommended for SOME patients in selected patient group

Treatment in this situation is initially focused on obstructing additional drainage from the ventriculoperitoneal shunt. If the shunt is programmable, it is recommended that it be adjusted to the highest setting.[131][132] If this setting is not high enough to stop additional drainage or if the shunt is not programmable, the distal end of the shunt can be externalized and connected to a bedside collection system where there is greater control over drainage, including the option to obstruct flow completely.

<10 mm size or midline shift <5 mm; without significant neurologic dysfunction; ICP <22 mmHg

1st line – observation, monitoring, and follow-up imaging

Back

1st line –

observation, monitoring, and follow-up imaging

Conservative management with ongoing monitoring is generally considered appropriate for patients who have none of the indications for surgery outlined by the Brain Trauma Foundation (BTF).[77] BTF guidelines recommend emergency surgical evacuation of the hematoma for patients with any one or more of: subdural hematoma (SDH) of >10 mm or a midline shift >5 mm (regardless of Glasgow Coma Scale [GCS] score); a GCS score <9 that has dropped ≥2 points between injury and emergency room (regardless of hematoma width or extent of midline shift); GCS score <9 and one or both of: fixed or asymmetric pupils and/or ICP >225 mmHg (regardless of hematoma width or extent of midline shift).

However, the evidence to underpin the above criteria for surgical versus conservative management is weak. In practice, there is a consensus that surgical intervention is indicated for any patient with an acute SDH who is comatose whereas there is substantial variation between neurosurgical centers in the thresholds applied for acute surgical evacuation in non-comatose patients with similar clinical presentations.[37] There is also ongoing debate about the benefits versus risks of immediate surgery for acute SDH in older individuals, with studies reaching conflicting conclusions.[30][79] An evidence review for the UK National Institute for Health and Care Excellence (NICE) guideline on head injury stated that, in practice, neurosurgical intervention is less likely to be offered to adults age ≥75 years due to risks outweighing benefits.[71]

All patients with GCS <9 need intracranial pressure monitoring and should be considered for monitoring of cerebral oxygenation, together with continuous electroencephalographic monitoring for seizures.[55][72][73][74][75][76] An epileptologist can be consulted for interpretation.[74][75][76]

Consider – anticonvulsant

Back

Consider –

anticonvulsant

Treatment recommended for SOME patients in selected patient group

The routine use of prophylactic anticonvulsants for patients with acute subdural hematoma (SDH) is controversial and high-quality evidence from randomized controlled trials is needed. Local protocol or the neurology team should be consulted for advice. Some guidelines recommend prophylactic anticonvulsants for patients with acute traumatic SDHs for up to 7 days after presentation (in the absence of indication to continue).[49]

In patients with late post-traumatic epilepsy (beyond the first 7 days after injury) or seizures despite anticonvulsant administration, consultation with a neurologist is recommended.

Late post-traumatic epilepsy occurs most commonly in patients with a history of acute SDH and coma >7 days.[141][142]

Primary options

levetiracetam: 500-1000 mg intravenously/orally twice daily, adjust dose according to response, maximum 3000 mg/day

Consider – management of antithrombotic therapy

Back

Consider –

management of antithrombotic therapy

Treatment recommended for SOME patients in selected patient group

Providers managing SDHs should also be aware of the use of direct oral anticoagulants (DOACs) which target either thrombin or factor Xa. Examples of these drugs include dabigatran, rivaroxaban, apixaban, and edoxaban. DOACs have several advantages over warfarin, including less risk of life-threatening hemorrhages, which is why their use is increasing.[70] When treating SDHs in patients on DOACs, providers should be encouraged to consult with their hematology colleagues for potential reversal options.[70][89][90]

Current guidelines suggest that all patients discontinue antiplatelet agents in the acute period postinjury when intracranial hemorrhage (ICH) is present or suspected.[49][70] The reversal of antiplatelet agent effects in patients with traumatic ICH remains controversial.[49] The American College of Surgeons states that for patients with normal platelet function or documented resistance, reversal therapies are not recommended and routine platelet transfusion is not recommended for use in reversing antiplatelet agent effects.[49] Clinical judgment should be used to determine if patients with TBI on antiplatelet agents who are undergoing surgery or invasive procedures with low platelet counts need platelet transfusions to achieve hemostasis.[49] However, the risk-benefit decision is often particularly complex in patients who are taking dual antiplatelet therapy.[30] Evidence suggesting a significant risk of thrombosis associated with cessation of dual antiplatelet therapy in specific subgroups of patients (e.g., those who have undergone recent placement of drug-eluting stents).[91][92] In such patients, continuation of aspirin monotherapy may be advisable to minimize the risk of cardiac ischemic events.[30] In the specific instance of SDH, practice varies between centers. Advice should be sought from hematology or cardiology colleagues to enable a detailed, personalized risk assessment.[30]

Consider – intracranial pressure-lowering regimen

Back

Consider –

intracranial pressure-lowering regimen

Treatment recommended for SOME patients in selected patient group

Secondary treatment options to lower ICP include hyperosmolar therapy with hypertonic saline in concentrations between 3.0% and 23.4%, and a dosing limit based on an upper serum sodium limit of 155 mmol/L.[7][101][102][103][104][105] There is insufficient evidence to recommend one osmotic agent over another.[77][106] Osmotic diuretics such as mannitol can also be used, but should be avoided if the serum osmolar gap exceeds 18 mOsm/kg to 20 mOsm/kg.[107] Use of hypertonics (saline) or hyperosmolar therapy (mannitol) may be counterproductive due to the risk of expansive hematoma volume, and are used only as a temporizing measure until emergent surgical interventions can be implemented.[108] External ventricular drainage of cerebrospinal fluid can also be considered.[109]

Consider – adjustment of shunt drainage + other measures as indicated

Back

Consider –

adjustment of shunt drainage + other measures as indicated

Treatment recommended for SOME patients in selected patient group

Subdural hematoma (SDHs) can occur in patients with a ventriculoperitoneal shunt, often due to “overshunting” - removal of too much cerebrospinal fluid (CSF) and thereby creating a physiologic pulling force into the subdural space.[43][44] In this situation, expansion of the SDH increases pressure inside the brain, which is subsequently relieved through additional shunting of CSF from the ventricular system. With additional CSF drainage, the ventricular system becomes smaller and the SDH continues to expand. Treatment in this situation is initially focused on obstructing additional drainage from the ventriculoperitoneal shunt. If the shunt is programmable, it is recommended that it be adjusted to the highest setting.[131][132] If this setting is not high enough to stop additional drainage or if the shunt is not programmable, the distal end of the shunt can be externalized and connected to a bedside collection system where there is greater control over drainage, including the option to obstruct flow completely.

ONGOING

chronic hematoma

1st line – conservative management or surgery

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1st line –

conservative management or surgery

The choice between conservative management or surgery for chronic subdural hematoma (SDH) is typically based on hematoma size, extent of midline shift, severity of neurologic dysfunction and degree of raised intracranial pressure. The degree of surgical risk and potential for recovery may also be considered.

There are several surgical treatment options for symptomatic chronic SDHs.[123] There is no high-quality evidence available to show whether one technique is superior to others.[59] Options include frontotemporoparietal craniotomy, burr hole craniotomy with irrigation, or twist-drill craniotomy with drain placement.[118][123] Newer methods of evacuation include subdural evacuating port systems.[124] Recurrent SDHs that have a fluid consistency may be treated with a subdural-peritoneal shunt. The use of a subdural drain or subdural evacuation port system (SEPS) decreases recurrence rates and mortality without increasing complications.[123][125][126] [ ]

Trials have shown that SEPS placement in combination with middle meningeal artery embolization reduces size, decreases length of stay, decreases seizure burden, and has minimal perioperative morbidity.[127][128] See Emerging treatments.

Consider – anticonvulsant

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Consider –

anticonvulsant

Treatment recommended for SOME patients in selected patient group

Anticonvulsants are indicated in patients with acute-on-chronic subdural hematoma (SDH) or with chronic SDH and history of seizures.[144] A specialist should be consulted for advice on further management and choice of drug.

The data on benefit of using prophylactic anticonvulsants in patients with chronic SDH is controversial, and no clear evidence exists to support routine prophylactic use of anticonvulsants.[143] Some have advocated using anticonvulsant prophylaxis postoperatively after removing chronic SDHs, although there are no randomized controlled trials concerning the use of routine prophylactic anticonvulsants in patients presenting with chronic SDHs.[145][146]

Primary options

levetiracetam: 500-1000 mg intravenously/orally twice daily, adjust dose according to response, maximum 3000 mg/day

Consider – management of antithrombotic therapy

Back

Consider –

management of antithrombotic therapy

Treatment recommended for SOME patients in selected patient group

Immediate reversal of anticoagulation is generally recommended if active bleeding is present.[85] Specific anticoagulant reversal recommendations for patients with life-threatening bleeding (all etiologies) are published by the Neurocritical Care Society/Society of Critical Care Medicine, American Heart Association, and American Society of Hematology.[49][70][86][87]

Providers managing SDHs should also be aware of direct oral anticoagulants (DOACs) which target either thrombin or factor Xa. Examples of these drugs include dabigatran, rivaroxaban, apixaban, and edoxaban. DOACs have several advantages over warfarin, including less risk of life-threatening hemorrhages, which is why their use is increasing.[70] When treating SDHs in patients on DOACs, providers should consult with their hematology colleagues for potential reversal options.[70][89][90]

Current guidelines suggest that all patients discontinue antiplatelet agents in the acute period postinjury when intracranial hemorrhage is present or suspected.[49][70] The reversal of antiplatelet agent effects in patients with traumatic ICH remains controversial.[49] The American College of Surgeons states that for patients with normal platelet function or documented resistance, reversal therapies are not recommended and routine platelet transfusion is not recommended for use in reversing antiplatelet agent effects.[49] Clinical judgment should be used to determine if patients with TBI on antiplatelet agents who are undergoing surgery or invasive procedures with low platelet counts need platelet transfusions to achieve hemostasis.[49] However, the risk-benefit decision is often particularly complex in patients who are taking dual antiplatelet therapy.[30] Evidence suggesting a significant risk of thrombosis associated with cessation of dual antiplatelet therapy in specific subgroups of patients (e.g., those who have undergone recent placement of drug-eluting stents).[91][92] In such patients, continuation of aspirin monotherapy may be advisable to minimize the risk of cardiac ischemic events.[30] In the specific instance of SDH, practice varies between centers. Advice should be sought from hematology or cardiology colleagues to enable a detailed, personalized risk assessment.[30]

Consider – adjustment of shunt drainage + other measures as indicated

Back

Consider –

adjustment of shunt drainage + other measures as indicated

Treatment recommended for SOME patients in selected patient group

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Subdural hematoma

Treatment algorithm

acute hematoma

surgery

monitoring

anticonvulsant

Primary options

management of antithrombotic therapy

intracranial pressure-lowering regimen

adjustment of shunt drainage + other measures as indicated

observation, monitoring, and follow-up imaging

anticonvulsant

Primary options

management of antithrombotic therapy

intracranial pressure-lowering regimen

adjustment of shunt drainage + other measures as indicated

chronic hematoma

conservative management or surgery

anticonvulsant

Primary options

management of antithrombotic therapy

adjustment of shunt drainage + other measures as indicated