Approach

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

Correction of coagulopathy

Many patients with severe head injury present with coagulopathy and require normalization of their coagulation profile.[50][51][52]​​​ Most patients on anticoagulation require initial cessation or reversal of their antiplatelet or anticoagulant agent. 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.[53]​ 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.[48]​ All patients require serial prothrombin time, partial thromboplastin time, international normalized ratio (INR), and platelet and fibrinogen levels followed. 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.[54]

Providers managing SDHs should also be aware of newer anticoagulants which target either thrombin or factor Xa. Examples of these direct oral anticoagulants (DOACs) 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.[48]​ When treating SDHs in patients on DOACs, providers should be encouraged to consult with their hematology colleagues for potential reversal options.[48][55][56]​​​ 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), and activated factor VIIa.[57]

Management of elevated intracranial pressure

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 to 70 mmHg and ICP <22 mmHg (in adults).[58]​​ While surgical evacuation would be considered in many patients with an acute SDH and signs of increased ICP, there is a subset of patients with small acute SDHs whose neurologic symptoms are due to other injuries, such as intraparenchymal contusions or diffuse axonal injury. In these patients, surgical evacuation would not be a first-line therapy. 

  • 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.[59] Analgesics and sedation can be useful, as pain and agitation can increase the ICP.[60] Using paralytics in intubated patients can help attenuate the effects of suctioning.[61] 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.[62][63]

  • 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.[6][64][65][66][67][68]​ 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.[69] Some experts also suggest not to exceed a serum osmolality of 320 mOsm/kg if mannitol is to be considered.[70]​ 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.[71]

  • Treatment options for refractory elevated intracranial pressure include maintaining the patient in a pentobarbital coma (requires continuous electroencephalographic [EEG] monitoring),[72] inducing hypothermia by intravascular cooling or topical cooling blankets,[73][74][75] and decompressive hemicraniectomy.[76][77]​​

Acute SDHs

Small SDHs may be associated with other intracranial hematomas requiring either management of elevated ICP or surgical evacuation. Occasionally, small SDHs may cause significant cerebral edema and neurologic deterioration. Management should therefore be based on size and on clinical symptoms/signs. All patients with Glasgow Coma Scale (GCS) score <9 need to have ICP monitoring with ventriculostomy, subarachnoid bolt, or intraparenchymal monitor.[78][79][80]​ Other physiologic 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, or jugular venous bulb monitoring; cerebral perfusion pressure; and continuous EEG monitoring for seizures. An epileptologist can be consulted for interpretation of EEG recordings.[81][82][83]

Conservative management is generally deemed appropriate for acute SDHs that are small, do not cause significant midline shift or cisternal encroachment, and do not cause significant neurologic impairment (beyond headaches). Typically, this includes patients with:[84][85][86]

  • GCS 9 to 15 with SDH <10 mm in width and midline shift <5 mm

  • GCS <9 with a hematoma <10 mm in width and midline shift of <5 mm who have been stable between injury and emergency room and with reactive, symmetric pupils and ICP <22 mmHg.

The decision of what type of surgery to perform depends on the radiographic appearance of the hematoma and the surgeon's preference.[87]​ 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.[88]​ Surgery is typically indicated for:[78]​​​​

  • SDH of >10 mm or a midline shift >5 mm with any GCS

  • GCS <9 that has dropped ≥2 points between injury and emergency room, with SDH of <10 mm and midline shift <5 mm

  • GCS <9, with SDH of <10 mm and midline shift <5 mm, and fixed or asymmetric pupils

  • GCS <9, with SDH of <10 mm and midline shift <5 mm, and ICP >25 mmHg

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

Chronic SDHs

Chronic SDHs may be managed in a variety of ways.

  • Conservative therapy is reserved for hematomas that meet the same criteria as acute hematomas, as described above.

  • Surgical intervention is indicated for hematomas that meet many of the same surgical criteria as acute hematomas, with postoperative recurrence included on the list. Surgical management may be frontotemporoparietal craniotomy, burr hole craniotomy with irrigation, or twist-drill craniotomy with drain placement.[89][90]​ Newer methods of evacuation include subdural evacuating port systems.[91] 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.[90][92] [ Cochrane Clinical Answers logo ] [Evidence B]​​​​ 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.[93][94]​​​ See Emerging treatments.​

Acute-on-chronic hematomas, or hematomas 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.[92] [ 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.[95] Decision-making is complicated if significant differences in SDH size/thickness or lateralization of symptoms are present, suggesting that one SDH is asymptomatic.[95]​ In general, there is no established paradigm for treatment. 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.[45] One study utilizing bilateral middle meningeal artery embolization in combination with bilateral burr hole drainage showed potential for decreased recurrence.[96]​ 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 hematoma

When treating acute SDHs associated with trauma, it is important to recognize the potential for an epidural hematoma on the contralateral side. Although rare, this is a potentially life-threatening situation. A small epidural hematoma contralateral to an acute SDH can rapidly expand when the compressive force of the SDH is relieved by surgical evacuation.[46][47]​ If it has not been initially recognized, expansion of the epidural hematoma 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.

The best approach for treating this situation is initial recognition of a small epidural hematoma contralateral to an acute SDH. Most epidural hematomas are associated with skull fractures coursing through the foramen spinosum where the middle meningeal artery is injured.[38]​ Any skull fracture involving the foramen spinosum should warn the operating neurosurgeon of this possible situation.

When an epidural hematoma is present with a contralateral acute SDH, consideration should be given to the possibility that the epidural hematoma 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 “overshunting” - removal of too much cerebrospinal fluid (CSF) and thereby creating a physiologic pulling force into the subdural space.[97][98]​​​ 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.[99][100]​​ 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. Case reports have also suggested using a combined increasing pressure valve setting in combination with endoscopic third ventriculostomy to simultaneously reduce SDH and allow passive CSF drainage.[101]

Prophylactic antiepileptics

Prophylactic antiepileptics are generally recommended for patients with acute SDHs for up to 7 days after presentation. Antiepileptic prophylaxis has been shown to decrease the occurrence of early, post-traumatic seizures.[102][103][104]​​​​​​ Levetiracetam and phenytoin are similarly efficacious, and recommended in guidelines.[105][106]​​​ In patients with late post-traumatic epilepsy (beyond the first 7 days after injury) or seizures despite antiepileptic 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.[107][108]​​​ For chronic subdural hemorrhages, the rate of new onset seizures has been reported as between 3% and 23%; however, the data on benefit of using prophylactic antiepileptics in this patient group are controversial, and no clear evidence exists on whether routine prophylaxis is indicated.[109]

Antiepileptics are indicated in patients with acute-on-chronic SDH or with a chronic SDH and history of seizures.[110]​ A specialist should be consulted for advice on further management and medication choice. Some have advocated using antiepileptic prophylaxis postoperatively after removing chronic SDHs,[111] although there are no randomized controlled trials concerning the use of routine prophylactic antiepileptics in patients presenting with chronic SDHs.[112]

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