Approach

Subdural haematoma (SDH) can be a neurosurgical emergency that, if left untreated, can lead to haematoma expansion, increased intracranial pressure (ICP) or brain herniation. Acute SDH carries a high mortality risk.[4][30]​ Supportive care for an acute trauma-related SDH includes an airway, breathing, circulation, disability (ABCD) approach to assessment.

Neurosurgeons and neurointensivists use many different strategies for managing acute and chronic SDHs. Generally, the most important criteria for determining management of acute SDHs are neurological signs/symptoms and radiographic appearance. Subacute haematomas can be treated in the same way as chronic haematomas; acute-on-chronic haematomas are usually treated in the same way as acute SDHs.

Acute SDH

If a patient has an acute SDH following a traumatic brain injury (TBI), an ABCD approach should be used to ensure rapid assessment of airway, breathing, circulation, and disability.

All patients with Glasgow Coma Scale (GCS) score <9 need to have ICP monitoring with ventriculostomy, subarachnoid bolt, or intraparenchymal monitor.[55][72][73]​​​​ Other physiological parameters can be measured which help guide therapy, including brain oxygenation through monitoring of partial pressures of oxygen in focal brain tissue areas or global cerebral oxygenation with intraparenchymal oximetry monitors, near-infrared spectroscopy, and continuous electroencephalographic (EEG) monitoring for seizures. An epileptologist can be consulted for interpretation of EEG recordings.[74][75][76]

Brain Trauma Foundation guidelines recommend emergency surgical evacuation of the haematoma for patients with any one or more of:[77]​​[78]

  • SDH of >10 mm or a midline shift >5 mm (regardless of GCS score). These features are significant predictors of a poor prognosis and are therefore key factors informing the decision on whether surgical intervention is indicated.

  • A GCS score <9 that has dropped ≥2 points between injury and emergency room (regardless of haematoma width or extent of midline shift).

  • A GCS score <9 and one or both of: fixed or asymmetric pupils and/or ICP >22 mmHg (regardless of haematoma width or extent of midline shift).

Conservative management with ongoing monitoring is generally considered appropriate for patients who have none of the above features.

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 centres in the thresholds applied for acute surgical evacuation in non-comatose patients with similar clinical presentations.[37]

  • The CENTER-TBI study analysis of 1407 patients with trauma-related acute SDH treated in 65 centres in Europe and Israel found there was no clear superiority in functional outcomes (based on GCS scores at 6 months) for centres that tended to prefer acute surgery over initial conservative treatment (with the option for delayed surgery if indicated by ongoing monitoring).[37]

  • Across all 65 centres, 24% of the patients had acute surgical evacuation but this ranged from 5.6% to 51.5% in individual centres, with a twofold higher probability of receiving acute surgery for a clinically similar patient in one centre versus another centre selected at random. Among the 76% who were initially managed conservatively, delayed surgery was needed in 11%.[37]

  • The authors concluded that while the benefit of immediate surgery is well established for a patient with acute SDH who is comatose (i.e., GCS score < 9), it is less clear for patients with a GCS score ≥ 9 and initial conservative treatment can be considered for this group unless a neurosurgeon sees a clear and specific indication for acute surgery.[37]

  • The decision depends on balancing the potential complications of surgery with the risk of irreversible deterioration or death following initial conservative treatment.

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 aged ≥75 years due to risks outweighing benefits.[63]​​

  • One meta-analysis of outcomes following surgical evacuation for acute SDH in patients aged >60 years found that the pooled estimated mortality was 39.8% (95% CI 32.7% to 47.1%) at discharge, based on 10 studies of 739 patients, and 49.3% (95% CI 42.0% to 56.6%) at mean follow-up of 7.1 months, based on 10 studies of 555 patients.[79]​ Severe disability was common among survivors; only 18.8% (95% CI 13.8% to 24.4%) had a GCS score of 4 or 5 at discharge.[79]

  • In one retrospective review, poor outcome for acute SDH surgery (e.g., discharge GCS; recurrence; readmission) was predicted by age over 85 years, but death and complications were not. Those aged greater than 90 years with presentation GCS score <10 all had poor outcomes.[80]

  • However, the CENTER-TBI study reported a non-significant suggestion of benefit from acute surgery versus initial conservative management in patients aged >65 years (adjusted OR 1.18, 95% CI 0.65% to 2.24%).[37]

  • Late (72 hours to 10 days) ICP elevations >25 mmHg.

Management of antithrombotic therapy

When a patient is diagnosed with acute or chronic 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 peri-operative optimisation for those who need neurosurgical intervention.[32][81]​​

Many patients with severe head injury present with coagulopathy and require normalisation of their coagulation profile.[82][83][84]​​​​​ 

Drug-specific reversal therapy should be initiated for those requiring urgent 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][85]​​​​ Immediate reversal of anticoagulation is generally recommended if active bleeding is present.[86]​ Specific anticoagulant reversal recommendations for patients with life-threatening bleeding (all aetiologies) are published by the Neurocritical Care Society/Society of Critical Care Medicine, American Heart Association (AHA), and American Society of Hematology.[49][85]​​[87][88]​​

  • Antithrombotic therapy is a risk factor for acute and chronic SDH.[11][15][16][34][35]​ Patients on oral anticoagulation therapy are estimated to have a 4- to 15-fold increased risk for SDH, leading to a higher likelihood of haematoma expansion, an increased risk of death, and a worse functional outcome unless anticoagulation is quickly reversed.[36][89]

  • Use of antithrombotic therapy is particularly common among older patients who present with chronic SDH, in whom there are often indications for anticoagulation and/or antiplatelet agents (e.g., atrial fibrillation, mechanical heart valves).[30]

  • Evidence is scarce to inform decisions around the cessation of antithrombotic therapy and reversal of anticoagulation in patients with intracranial bleeding.[30]​ Decisions around the cessation or reversal of anticoagulation should be individualised.

  • 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, ischaemia, heparin-induced thrombocytopenia, or disseminated intravascular coagulation.[85]

  • 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 haemorrhages, which is why their use is increasing.[85]​ When treating SDHs in patients on DOACs, providers are encouraged to consult with their haematology colleagues for potential reversal options.[85][90][91]

  • Current guidelines suggest that all patients discontinue antiplatelet agents in the acute period post injury when intracranial haemorrhage (ICH) is present or suspected.[49][85]​​​ The reversal of antiplatelet agent effects in patients with traumatic intracranial haemorrhage remains controversial.[49]​ The American College of Surgeons (ACS) 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 haemostasis.[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).[92][93]​​​ In such patients, continuation of aspirin monotherapy may be advisable to minimise the risk of cardiac ischaemic events.[30]​ In the specific instance of SDH, practice varies between centres. Advice should be sought from haematology or cardiology colleagues to enable a detailed, personalised risk assessment.[30]

  • For patients with chronic SDH without acute bleeding, there are very few data available to guide the decision on whether to suspend or continue anticoagulation.[30]​ In practice, if a patient with a chronic SDH has no signs of raised ICP and will be managed conservatively, the risk-benefit balance may sometimes be in favour of continuing anticoagulation therapy, depending on the strength of the specific indication for its use. Specialist advice is needed to make these nuanced decisions.

All patients with acute SDH who are on antithrombotic therapy require serial prothrombin time, partial thromboplastin time, international normalised 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 urgent setting.[94]​ Evidence from 2019 suggests that targeted reversal utilising 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 urgent 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 x 10⁹/L; >100,000/microlitre), 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.[95]

Restarting antithrombotic therapy

  • The ACS recommends restarting anticoagulation no later than 14-90 days after TBI, depending on patient-specific risk for thrombosis and bleeding.[49]

  • Clinical practice varies significantly but most clinicians consider it safe to restart anticoagulation in the majority of patients after a 2-week break, although it may need to be sooner in individuals with a very strong indication for anticoagulation (e.g., a recent venous thromboembolism or a metallic heart valve).[30]​​[59]​​[96]​​ Safe restart of anticoagulant therapy may also occur significantly sooner if traumatic intracranial bleeding is less significant and/or stable on repeat CT imaging.[49][88]

  • Antiplatelet agents may be restarted as early as 4 days after injury, based on assessment of patient-specific risk for thrombosis and bleeding.[49]​ Risks for acute and delayed ICH after restarting antiplatelet agents must be weighed against the morbidity of thrombotic complications that can have significant clinical consequences.[49]

Management of raised intracranial pressure

In patients with increased 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 of 22 mmHg (in adults) is a useful initial threshold for treatment.[49]

  • An ICP of 22 mmHg 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]

  • 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.[97] Analgesics and sedation can be useful, as pain and agitation can increase the ICP.[98] Using paralytics in intubated patients can help to attenuate the effects of suctioning.[99] Hyperventilation to a goal pCO₂ of 30 to 35 mmHg (monitored with serial arterial blood gases) can be beneficial in reducing ICP, but is only recommended as a temporary measure as prolonged use can be associated with cerebral vessel constriction and decreased blood flow.[100][101]

  • 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][102][103][104][105][106]​​​ There is insufficient evidence to recommend one osmotic agent over another.[77][107]​ 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.[108] Use of hypertonics (saline) or hyperosmolar therapy (mannitol) may be counterproductive due to the risk of expansive haematoma volume, and are used only as a temporising measure until urgent surgical interventions can be implemented.[109]​ External ventricular drainage of cerebrospinal fluid can also be considered.[110]

  • Treatment options for refractory elevated intracranial pressure include maintaining the patient in a pentobarbital coma (requires continuous EEG monitoring), inducing hypothermia by intravascular cooling or topical cooling blankets, and decompressive hemicraniectomy.[111][112][113][114]​​[115][116]​​​​

Surgical technique for acute SDH

The decision of what type of surgery to perform depends on the radiographic appearance of the haematoma and the surgeon's preference.[117]​ 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.[118]​

Evidence suggests similar functional outcomes for craniotomy and primary decompressive craniectomy.[110]

  • The RESCUE-ASDH trial of 450 patients with acute SDH in 11 countries involved intraoperative randomisation to craniotomy or decompressive craniectomy. Results published in 2023 showed similar disability and quality-of-life outcomes at 6- and-12 month follow-up.[119] Those undergoing craniotomy were significantly more likely to require further cranial surgery within 2 weeks (14.6% vs. 6.9% of the craniectomy group) but wound complications were threefold more common in those who had craniectomy (12.2% vs. 3.9% of the craniotomy group).[119]

  • Observational cohort data from the multi-centre CENTER-TBI study, covering 336 patients with acute SDH requiring surgical evacuation, also concluded that there were no significant differences in functional outcomes between centres that preferred primary decompressive craniectomy versus those that favoured craniotomy.[37]

  • The leaders of both studies concluded that primary decompressive craniectomy should be reserved for patients in whom immediate replacement of the bone flap is not possible due to intraoperative swelling and should not be used pre-emptively for acute SDH.[37][119]​​

Secondary decompressive craniectomy

A small proportion of patients will have refractory intracranial hypertension following craniotomy for surgical evacuation of an acute SDH.[110]​ Secondary decompression involves the removal of the bone flap later in the patient's course - typically to treat the elevation of ICP refractory to other treatments.[120]​ In this scenario, the evidence base is complex and the decision to proceed with secondary decompressive craniectomy versus ongoing medical management must be individualised based on the patient’s potential for benefits versus risk of complications.[110]​ In practice, the presence of pre-existing comorbidities is a significant factor determining the most appropriate treatment for older people with acute SDH, since this is a major driver of poor outcomes even with surgery.[30][37]​​

Brain Trauma Foundation guidelines recommend consideration of secondary decompressive craniectomy for late (within 10 days of admission) refractory ICP elevation to improve mortality and favourable outcomes.[120][121]​​ Secondary decompressive craniectomy performed for early (within the first 72 hours of care) refractory ICP elevation is not recommended to improve favourable outcomes and medical management is advised instead.[120][122]​ This recommendation was based on findings from two high-quality studies:[120]

  • The DECRA trial randomised 155 patients with severe, diffuse TBI and early refractory intracranial hypertension (within the first 72 hours of care) to either decompressive craniectomy or intensive medical therapy. It found that decompressive craniectomy did not improve survival or neurological outcomes compared with medical management but it did increase the risk of vegetative survival.[122]

  • The RESCUEicp trial randomised 408 patients with TBI and late refractory intracranial hypertension (within 10 days) to secondary decompressive craniectomy or ongoing medical care. It found that decompressive craniectomy was associated with a significant mortality reduction.[121]​ Two-year follow-up data also showed better functional improvement over 6 to 24 months for the group who had decompressive craniectomy compared with those who have standard medical management.[123]

Chronic SDH

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

Chronic SDHs may be surgically managed in a variety of ways. There is no high-quality evidence available to show whether one technique is superior to others.[59]

  • Surgical management may be frontotemporoparietal craniotomy, burr hole craniotomy with irrigation, or twist-drill craniotomy with drain placement.[119][124]​​ Newer methods of evacuation include subdural evacuating port systems.[125] 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.[124][126][127]​​ [ Cochrane Clinical Answers logo ] [Evidence B]​​​​​ Trials have shown that SEPS placement in combination with middle meningeal artery embolisation reduces size, decreases length of stay, decreases seizure burden, and has minimal peri-operative morbidity.[128][129]​​​​ See Emerging treatments.​

Acute-on-chronic haematomas, or haematomas that fail to evacuate after drain placement, are treated with either burr hole craniotomy with irrigation or standard frontotemporoparietal craniotomy with or without intraoperative drain placement. Drain placement has been shown to lower recurrence rates.[126][127]​​ [ Cochrane Clinical Answers logo ] [Evidence B]

Bilateral SDHs

Treatment of bilateral SDHs is more complex than treatment of unilateral SDHs, and there is a significantly higher recurrence rate associated with treatment of chronic bilateral SDHs.[130] ​Decision-making is complicated if significant differences in SDH size/thickness or lateralisation of symptoms are present, suggesting that one SDH is asymptomatic.[130]​

  • In general, there is no established paradigm for treatment. When the two haematomas are equal in size many neurosurgeons treat both sides simultaneously; when the two haematomas 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 post-operative drainage and mixed density SDH were independent predictors for re-treatment.[68] One study utilising bilateral middle meningeal artery embolisation in combination with bilateral burr hole drainage showed potential for decreased recurrence.[131]​ While this would suggest using a more aggressive approach to treat bilateral SDHs, additional studies are required before any guidelines can be established.

Unilateral SDH with contralateral epidural haematoma

When treating acute SDHs associated with trauma, it is important to recognise the potential for an epidural haematoma on the contralateral side. Although rare, this is a potentially life-threatening situation. A small epidural haematoma contralateral to an acute SDH can rapidly expand when the compressive force of the SDH is relieved by surgical evacuation.[69][70]​​ If it has not been initially recognised, expansion of the epidural haematoma 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 haematoma.

The best approach for treating this situation is initial recognition of a small epidural haematoma contralateral to an acute SDH. Most epidural haematomas 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.

When an epidural haematoma is present with a contralateral acute SDH, consideration should be given to the possibility that the epidural haematoma may expand after evacuating the SDH. In this situation the patient can be positioned so that a craniotomy on the contralateral side can quickly be performed.

SDH with associated ventriculoperitoneal shunt

SDHs can occur in patients with a ventriculoperitoneal shunt, often due to 'over shunting' - removal of too much cerebrospinal fluid (CSF) and thereby creating a physiological 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 a programmable shunt, it is recommended that the shunt be adjusted to the highest setting.[132][133]​​​

  • 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 externalised and connected to a bedside collection system where there is greater control over drainage, including the option to obstruct flow completely.

Prophylactic anticonvulsants

The routine use of prophylactic anticonvulsants for patients with acute SDH is controversial and high-quality evidence from randomised controlled trials (RCTs) is needed. Local protocol or the neurology team should be consulted for advice.

  • Patients with trauma-induced and non-trauma-related SDH are at increased risk of seizures.[134]

  • 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]

  • Seizure prophylaxis may be continued beyond 7 days if seizure activity (clinical or EEG) occurs beyond 24 hours or if the patient was previously receiving drug treatment for a known seizure disorder.[49]

  • Anticonvulsant prophylaxis has been shown to decrease the occurrence of early, post-traumatic seizures.[135][136][137]​​​​​​​ Levetiracetam and phenytoin are similarly efficacious, and recommended in guidelines.​​​​​​​​[49]​​[138][138]

  • However, anticonvulsants carry a notable adverse effect profile and subsequent systematic review data and observational studies have not shown any significant reduction in seizure frequency from their use in patients with SDH.[134][139]​​[140][141]​​​ 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 EEG-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 post-traumatic epilepsy occurs most commonly in patients with a history of acute SDH and coma for >7 days.[142][143]​​​​​ 

For chronic subdural haemorrhages, the rate of new onset seizures has been reported as between 3% and 23%; however, the data on benefit of using prophylactic anticonvulsants in this patient group are controversial, and no clear evidence exists to support routine prophylactic use of anticonvulsants in this setting.[144]

Anticonvulsants are indicated in patients with acute-on-chronic SDH or with a chronic SDH and history of seizures.[145]​ A specialist should be consulted for advice on further management and treatment choice. Some have advocated using anticonvulsant prophylaxis post-operatively after removing chronic SDHs, although there are no RCTs concerning the use of routine prophylactic anticonvulsants in patients presenting with chronic SDHs.[146][147]

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