I. What every physician needs to know.

Subdural hematomas (SDH) are intracranial blood collections which form between the dura and arachnoid membranes of the meninges.

Typically, subdural hematoma results from tearing of “bridging veins” draining from the surface of the brain to the dural sinuses. However, 20-30% of SDH develop due to arterial injury, most often at cortical arteries less than 1mm in diameter. Postmortem characteristics are similar in both etiologies. Cerebral damage results from a combination of impaired local blood flow from direct pressure effects, increased intracranial pressure and co-occurring intraparenchymal injuries.

SDH is most commonly precipitated by closed head injury (including falls, motor vehicle accident, and assault). SDH also occasionally results from low CSF pressure following procedures (i.e., lumbar puncture) or neurosurgical interventions. However, SDH may infrequently ‘spontaneously’ develop from arterio-venous malformations, aneurysmal subarachnoid hemorrhages, meningiomas or neoplastic metastases to the dura.

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Antithrombotic agents (i.e., aspirin), coagulopathy (i.e., systemic anticoagulation, liver disease), systemic thrombolysis (i.e., treatment of myocardial infarction), and marked hypertension or vasospasm (i.e., cocaine abuse, atherosclerotic disease) also predispose to spontaneous subdural hematomas. Rarely, SDH occurs without any known predisposing factors.

Subdural hematomas are arbitrarily categorized according to time from onset. Though definitions vary, SDH may be classified as acute (within a few days of onset); subacute (a few days to two weeks from onset); or chronic (more than two weeks since onset).

An acute-on-chronic presentation may develop from re-bleeding at a previous SDH or evolution of a chronic SDH into a hygroma.

II. Diagnostic Confirmation: Are you sure your patient has subdural hematoma?

Imaging of the brain is the gold standard for confirming SDH (see section IIE2).

A. History Part I: Pattern Recognition:

Clinical manifestations of SDH depend on the size, acuity, and time-course of the subdural hematoma. An acute-on-chronic presentation may occur.

Headache is common, especially in chronic SDH. The headache often fluctuates in severity, and may change in intensity with head position. The majority of patients report the headache as:

  • sudden in onset

  • severe

  • associated with nausea or emesis

  • exacerbated by coughing, straining, or exertion

Acute SDH initially manifests with coma in nearly half of cases. However, a significant minority present with a transient “lucid interval” after the acute injury, which is then followed by progressive neurological decline to coma. Posterior fossa SDH may cause ataxia, cranial nerve dysfunction, headache, or nausea. Rapidly increasing acute SDH may cause cerebral infarct or intracranial herniation with resultant Kluver-Bucy syndrome. Ten percent of acute SDH present with seizure.

Chronic and subacute SDH manifest in a more insidious manner, with symptoms which progressively develop over days, to weeks, to months after the initial event. Headache occurs in over 80% of cases. Confusion, cognitive impairment, apathy, and increased somnolence are common. Visual disturbances or focal neurological deficits may also occur. Caregivers may report personality changes or forgetfulness.

Persistent postoperative drowsiness or confusion may be the initial presentation of an undetected chronic SDH, resulting from an associated decreased tolerance to anesthesia and drugs that depress the CNS.

Both acute and subacute SDH may cause increased intracranial pressure, with symptoms of emesis, speech disturbances, papilledema, cranial nerve abnormalities, or seizure.

B. History Part 2: Prevalence:

Predisposing factors for SDH include trauma, cerebral atrophy (i.e., the elderly, chronic alcoholics), systemic anticoagulation or antiplatelet agents, and low cerebrospinal fluid pressure (a.k.a., intracranial hypotension). Both acute and chronic SDH occur more commonly in men than women.

Antecedent closed-head trauma is the most common cause of SDH. The severity of injury needed to produce subdural hematoma decreases with advancing age, so the inciting trauma may be trivialized or forgotten in geriatric patients.

Acute SDH is most common in younger adults following motor vehicle accident, falls or assault. Acute subdural hematoma may also complicate cases of severe organophosphate poisoning.

Chronic SDH is more common in young children or adults older than 40-years old. Nearly 75% of patients are older than 50 years old. About half of all patients with chronic SDH have comorbid alcohol abuse.

Alcohol abuse predisposes to SDH through multiple mechanisms, including accelerated cerebral atrophy, comorbid coagulopathy and thrombocytopenia, and a propensity for falls or other accidents.

C. History Part 3: Competing diagnoses that can mimic subdural hematomas.

Subdural hematoma (SDH) should be distinguished from:

  • epidural hematoma

  • intraparenchymal bleed

  • mass-occupying infection

  • primary dural neoplasm (i.e., meningioma)

  • neoplastic dural metastases

  • cerebral infarction or ischemia (i.e., stroke, TIA)

  • Parkinson’s disease

  • status epilepticus

  • cerebral contusion

  • post-concussion syndrome

  • hypoglycemia

  • electrolyte abnormalities (i.e., hypernatremia, hyponatremia)

  • uremia

  • hypoxemia and/or hypercapnia

  • drug intoxication

  • other causes of dementia/delirium (i.e., normal pressure hydrocephalus)

History, basic laboratories and radiographic characteristics should be able to distinguish most of these entities. Rarely, neurosurgical intervention may be necessary to confirm the diagnosis.

Subdural hygromas may result from degradation or liquefaction of a previous SDH.

Acute SDH is associated with other intracranial lesions (i.e., intraparenchymal bleed, diffuse axonal injury) in 60% of cases.

D. Physical Examination Findings.

Physical signs of SDH depend on the size, acuity and evolution of the subdural hematoma. An acute-on-chronic presentation may occur.

Acute SDH

Depressed consciousness is nearly universal. Hemiparesis or hemiplegia is also prevalent, occurring in about half of cases. If present, hemiparesis is contralateral to the hematoma 70% of the time. Pupillary abnormalities are common and, when present, are ipsilateral to the acute SDH in 90%. Seizure at time of presentation occasionally occurs.

Chronic SDH

Altered consciousness and amnesia are the most common signs. Motor asymmetry, hyperreflexia, upper-extremity drift, ataxia, aphasia, and gait abnormalities are also prevalent. Findings may be nonspecific and non-localizing (i.e., lethargy), or waxing-and-waning. Papilledema, cranial nerve deficits, and hemianopia are uncommon but highly worrisome signs of impending CNS hernia ion.

Bilateral SDH or coexisting cerebral contusion is common and may cloud localization.

E. What diagnostic tests should be performed?

Urgent cranial imaging (i.e., head computed tomography [CT]) should be done for any patient with recent blunt injury to the head who demonstrates a Glasgow Coma Scale score (GCS) 15 or under, decreased mental status from baseline or focal neurological signs.

Physical exam should also evaluate for concomitant injuries, including basilar skull fracture, spinal trauma, or cephalic lacerations.

Lumbar puncture is relatively contraindicated in SDH due to risk of cerebral herniation.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Initial laboratory tests should evaluate causative and co-morbid consequences of the subdural hematoma.

Complete blood count (CBC) and coagulation profile should be ordered to evaluate for low platelet counts or coagulopathy. Testing for qualitative platelet dysfunction (i.e., von Willebrand factor deficiency, uremia) is useful in appropriate clinical context.

BMP should be evaluated for associated electrolyte abnormalities (i.e., hyponatremia). Evaluate for pituitary dysfunction or central adrenal insufficiency if collaborative signs exist.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

CT is the usual modality of choice. SDH appear as a crescentic collection across the hemispheric convexity. CT appearance provides information about acuity: after initial onset, SDH are hyperdense to brain parenchyma for approximately 1 week; isodense after 2-3 weeks; and then hypodense after 3-4 weeks. Large SDH may deform the brain parenchyma.

Interpretation of head CT may initially fail to recognize an SDH, especially if it is small (<3mm in thickness), bilateral (thus causing symmetric defects) or subacute (thus appearing isodense to brain parenchyma). SDH in older patients may show a “hypernormal CT” (a lack of typical age appropriate atrophy at the sulci and ventricles).

Magnetic resonance imaging (MRI) is notably more sensitive than CT for detecting SDH, though less often used. T1- and T2-weighted MRI should be considered if a high suspicion for SDH remains despite negative head CT. The appearance of SDH on MRI evolves over time akin to the evolution of signal appearance on CT, and thus is also helpful for evaluating the acuity of SDH.

Angiography through magnetic resonance (MRA), computed tomography angiography (CTA), or conventional angiography should be considered when the SDH may be associated with an underlying vascular lesion (i.e., an intracranial aneurysm rupture).

III. Default Management.

SDH should be considered an emergency situation until proven otherwise. Initial management should focus on medical stabilization, stratifying the severity of patients’ injury, and evaluating the need for emergency neurosurgical intervention.

Initial directed history should assess: mechanism of injury and other potential concurrent injuries; baseline mental status; co-morbidities and past medical history; and advanced directives.

A. Immediate management.

  • Assess GCS score at initial presentation and then periodically

  • Maintain normal oxygen saturation (SAO2 >95%).

  • Initiate rapid sequence intubation for GCS less than 9 or signs of increased intracranial pressure (ICP) with decreasing neurological status

  • Control hypertension with rapid acting agents (i.e., labetalol, nicardipine, hydralazine)

  • Maintain mean arterial pressure (MAP) 100-110mmHg and clinical euvolemia

  • Maintain euglycemic (goal BS 80-150g/dL)

  • Arrange urgent neurosurgical intervention (i.e., in less than 2 to 4 hours) for patients who are comatose or have GCS score below 9, pupillary abnormalities, or intracranial pressure (ICP) at 20mmHg or over.

  • Use mannitol and elevation of the head-of-the-bed to stabilize patients with elevated ICP until definitive surgical intervention can be performed.

  • Acute SDH requires neurosurgical intensive care unit (ICU) level care for close monitoring. Subacute and chronic SDH should be admitted to a monitored setting to evaluate for stability.

  • All SDH patients should receive a neurosurgical consultation.

B. Physical Examination Tips to Guide Management.

Decline in mental status, such as increasing lethargy or new neurological deficits, warrants prompt repeat diagnostic imaging and/or neurosurgical re-evaluation.

GCS, brainstem reflexes, and pupillary symmetry/responsiveness should be assessed and documented at time of initial presentation and then periodically (i.e., at least every 4-6 hours). A GCS score decline of 2 points or less, asymmetric or dilated and fixed pupils or ICP persistently 20mmHg or greater requires emergent surgical decompression.

Seizure, concern for non-convulsive status epilepticus, or signs of increased intracranial pressure or cerebral herniation also merits swift re-evaluation with radiographic imaging.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

  • Platelet counts, coagulation profile and hemoglobin levels should be evaluated upon initial presentation. Abnormalities should be corrected (see below) with subsequent monitoring to ensure normalization.

  • BMP should be periodically evaluated with correction of electrolyte abnormalities.

  • Both hyper- and hypo-glycemia increase mortality and should be corrected and avoided.

  • Maintain normal oxygen saturation (SAO2 >95%). Hyperventilation should be avoided for the first 24-48 hours and should not exceed, reducing PaCO2 to 30mmHg or under.

  • The frequency of lab testing should be titrated to patients’ clinical severity. Coagulation profile, CBC, and basic metabolic panel (BMP) should initially be evaluated multiple times a day for acute SDH or unstable patients, and may be slowly decreased to checks daily or several times a week as patients stabilize.

D. Long-term management.

The majority of acute and subacute SDH will require surgical intervention. The various types of surgical evacuation (i.e., craniotomy, burr hole, twist-drill) have differing profiles of efficacy-to-complication rate and choices are individualized in each case.

Patients with GCS score of 9 or below should undergo placement of ICP monitor. Patients with elevated ICP (ICP ≥20mmHg) or signs of intracranial herniation should be temporized by elevation of the head-of-the-bed to greater than 30˚ and administration of mannitol (1g/kg) while awaiting emergency surgical intervention. Hyperventilation may also be used, though it has been associated with worse clinical outcomes.

In acute SDH, guidelines recommend urgent surgical intervention for patients with:

  • hematoma with radiographic thickness 5mm or greater and associated lethargy, altered mental status, or focal neurological deficit

  • hematoma with radiographic thickness 10mm or greater

  • radiographic CNS midline shift 5mm or greater

  • ICP 20mmHg or greater

  • a 2 point, or greater, decline from initial GCS score

  • asymmetric or fixed and dilated pupils

In chronic SDH, no clear guidelines exist for when surgical evacuation is necessary. In general, surgical intervention should be considered for patient with:

  • hematoma with radiographic thickness 10mm or greater

  • radiographic CNS midline shift 5mm or greater

  • signs of increased ICP

  • objective moderate or severe cognitive impairment (i.e., MMSE)

  • progressive neurological deterioration or signs attributable to the chronic SDH

Medical management alone may be an option for patients with minimal neurological signs (i.e., headache alone without focal neurological signs or significant functional impairment) who do not meet the above criteria. Conservative therapy consists of close observation, with serial reimaging to assess for SDH stability. No medication has clearly been shown to improve rate of recovery from SDH.

Post-surgically, treatment should aim to keep ICP 20mmHg or below, and maintain cerebral perfusion pressure at 60-70mmHg and above. Repeat neuroimaging should be done 24 hours postoperatively, if ICP becomes elevated, or if neurological findings develop or fail to improve. Some experts endorse temporary bed rest with the head-of-the-bed relatively flat because of theoretical benefits for brain re-expansion, but limited trials have not shown clear benefit to this approach.

Prophylactic anticonvulsant (AED) treatment is controversial. In acute SDH, limited data and expert opinions advocate for the administration of phenytoin, valproic acid, or another antiepileptic for 5-7 days after injury to prevent seizure. In chronic SDH, insufficient clinical data exists to evaluate primary anticonvulsant prophylaxis. AED prophylaxis may be more beneficial in SDH patients with associated traumatic brain injury or history of alcohol abuse. Levetiracetam (Keppra) may have a more favorable prophylaxis risk:benefit profile than older anticonvulsants.

Mannitol use to treat cerebral edema without planned surgical intervention is controversial. The use of corticosteroids is also controversial; in studies of traumatic brain injury, the use of glucocorticoids was associated with worse clinical outcomes.

IV. Management with Co-Morbidities


A. Renal Insufficiency.

Uremia causes qualitative platelet dysfunction. Patients with active SDH may benefit from treatment to support platelet function i.e., desmopressin (see IV.J).

Mannitol, if used in patients with signs of elevated intracranial pressure, requires dose adjustment in those with renal insufficiency.

B. Liver Insufficiency.

Coagulopathy associated with hepatic insufficiency should be corrected to ‘normal’ values. FFP, cryoprecipitate, vitamin K, and recombinant Factor VIIa are all useful to offset the coagulation factor deficiencies in hepatic insufficiency (see IV.J).

Hepatic encephalopathy may be difficult to distinguish from symptoms of SDH; maintain a low-threshold for repeat diagnostic imaging in patients with worsening mentation.

C. Systolic and Diastolic Heart Failure

No change in standard management.

D. Coronary Artery Disease or Peripheral Vascular Disease

Patients on anti-aggregation agents (i.e., aspirin, clopidogrel) or anti-coagulation (i.e., artificial heart valves) have both increased risk of SDH as well as risks of complication from reversal of anticoagulation (see also IV.J).

Antiplatelet agents have an uncertain influence on outcomes, length-of-stay, and recurrence of hematoma because of limited and conflicting data. The benefit of reversal of antiplatelet agents is uncertain; both platelet transfusion and/or desmopressin (ddAVP) have been used. Experts advocate the resumption of antiplatelet medications 1 week after surgical evacuation.

Anticoagulation reversal and temporary interruption for patients with SDH is safe, even in those with “high risk” mechanical heart valves. Available data estimates the risk of ischemic stroke within 30 days for SDH patients off anticoagulation and with a CHADS2 greater than 2 or mechanical heart valve as less than 5%.

Sufficient evidence is not available to determine the optimal interval before anticoagulation should be restarted for SDH patients with mechanical heart valves or atrial fibrillation. Expert opinion and limited studies suggest resumption of anticoagulation 1-2 weeks after initial treatment, with serial repeat CT scans over the next 4-6 weeks to monitor for rebleeding. However, some experts advocate interruption of anticoagulation for at least 4-6 weeks in cases where SDH is extensive or managed medically (i.e., without surgical intervention).

E. Diabetes or other Endocrine issues

Both hyper- and hypoglycemia are detrimental to mortality in SDH and should be avoided. Maintain goal blood glucose of 80-150g/dL.

F. Malignancy

No change in standard management.

G. Immunosuppression (HIV, chronic steroids, etc).

No change in standard management.

H. Primary Lung Disease (COPD, Asthma, ILD)

No change in standard management.

I. Gastrointestinal or Nutrition Issues

Nutritional status must be closely monitored in SDH patients, especially those with altered mental status or coma. Supplemental nutrition may be required. However, nasoenteric tube placement should be avoided, if possible, in patients with increased intracranial pressure due to risk of intracranial herniation.

J. Hematologic or Coagulation Issues

Qualitative or quantitative platelet dysfunction can precipitate subdural hematoma. The use of desmopressin (ddAVP) or factor VIII replacement (alphanate) has successfully been used for those with qualitative dysfunction or factor deficiency. Supportive platelet transfusion has also been used, especially in cases of quantitative dysfunction (i.e., idiopathic thrombocytopenic purpura). The optimal goal platelet count is uncertain, but a goal of 50-100 thousand/mL is commonly targeted for active or acute SDH.

Coagulopathy should be corrected in the setting of acute or acute-on-chronic subdural hematoma. This may include giving patients vitamin K, fresh frozen plasma (FFP), or recombinant factor VIIa to reverse the effects of warfarin; protamine to reverse heparin; and factor concentrates or cryoprecipitate to support patients with factor deficiency or hepatic insufficiency. Factor supplementation should also be given for patients with underlying deficiency (i.e., hemophilia). Aminocaproic acid (Amicar) may be a useful augmentation in those with ongoing bleeding.

Antiplatelet agents have an uncertain influence on outcomes, length-of-stay, and recurrence of hematoma because of limited and conflicting data. The benefit of reversal of antiplatelet agents is uncertain; both platelet transfusion and/or desmopressin (ddAVP) have been used. Experts advocate the resumption of antiplatelet medications 1 week after surgical evacuation.

Anticoagulation reversal and temporary interruption for patients with SDH is safe, even in those with “high risk” mechanical heart valves or active atrial fibrillation. Available data estimates the 30-day risk of ischemic stroke for SDH patients off anticoagulation with a CHADS2 score 2 or above or with a mechanical heart valve as less than 5%.

Sufficient evidence is not available to determine the optimal interval before anticoagulation should be restarted for SDH patients with mechanical heart valves or atrial fibrillation. Expert opinion and limited studies suggest resumption of anticoagulation 1-2 weeks after initial treatment, with serial repeat CT scans over the next 4-6 weeks to monitor for rebleeding. However, some experts advocate interruption of anticoagulation for at least 4-6 weeks in cases where SDH is extensive or managed medically (i.e., without surgical intervention).

K. Dementia or Psychiatric Illness/Treatment

Brain atrophy and structural abnormalities are more common in elderly, demented, or psychiatric patients and are risk factors for SDH. Chronic SDH is a reversible cause of dementia and should be treated as such.

V. Transitions of Care

A. Sign-out considerations While Hospitalized.

Include detailed information about the patient’s neurological status, including description of mentation, any neurological deficits present, and most recent GCS score. Include information about advanced directives and code status, if applicable.

Include contact information for appropriate consultants (i.e., neurosurgery) and emergency family contact (i.e., P.O.A., next-of-kin) in case of sudden decline.

Patients should receive urgent reevaluation, including consideration of repeat head imaging, if there is any change in neurological status.

B. Anticipated Length of Stay.

Acute SDH patients most often will require initial ICU level care with subsequent transition to the floor. In chronic SDH, average length of stay is typically 7 to 9 days. Patients who are on chronic anticoagulation or antiplatelet agents often have longer in-patient stays.

C. When is the Patient Ready for Discharge.

Generic criteria for in-patient discharge include stable mental status and neurological exam for greater than 24-48 hours and treatment of underlying co-morbidities, including coagulopathy.

Patients may need evaluation for in-patient rehabilitation or outpatient physical and occupational therapy.

D. Arranging for Clinic Follow-up

Instruct patients and caregivers on symptoms and signs which may indicate recurrent subdural hematoma and require prompt presentation to the emergency room. These include:

  • worsening mentation or increased confusion

  • seizure

  • new neurological defect

  • gait instability

  • fall or other head trauma

1. When should clinic follow up be arranged and with whom.

  • Neurosurgery evaluation, in 1-2 weeks

  • Hematology or primary-care physician

  • Neurology

  • Physical/occupational therapy

2. What tests should be conducted prior to discharge to enable best clinic first visit.

Patients should have repeat diagnostic imaging (i.e., head CT) to evaluate for evolution of the subdural hematoma prior to discharge.

Quantitative evaluation of neurological function (i.e., GCS, Mini Mental Status exam, neurocognitive testing) will allow for serial monitoring of functional recovery.

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

Repeat CBC, BMP, coagulation profile, and neuroradiological imaging (i.e., CT scan) should be performed for outpatient follow-up. Applicable drug levels and hepatic function tests should be tested if antiepileptic medications were initiated.

E. Placement Considerations.

After treatment for SDH, patients often require in-patient rehabilitation or long-term care, especially if the subdural hematoma has caused significant functional impairment.

Serial evaluation of the patient’s ability for independence, including their fall risk, should be done throughout their recovery. Formal physical and occupational therapy evaluation should be obtained once patients’ neurological status remains stable for greater than 24 hours

F. Prognosis and Patient Counseling.

Acute SDH carries poor short-term and one-year outcomes. Mortality averages 20% in patients younger than 40 years old; 65% in those 40-80 years old; and exceeds 85% in those older than 80 years old.

In comatose patients, acute SDH is commonly associated with extensive primary brain trauma or delayed brain damage, which increases overall mortality rates to 60%. Initial GCS score 3, or below, indicates near uniform short-term fatality, while initial GCS score 7 or above indicates a low-risk of short-term death. Many survivors do not regain previous levels of functioning, especially if the acute SDH was severe enough to require surgical intervention.

  • In acute SDH, poor prognostic indicators include:

  • initial or post-resuscitation GCS less than 8

  • initial GCS motor score less than 5

  • hypoxia or hypotension

  • injury from motorcycle accidence or antecedent alcohol use

  • elevated or difficult to control ICP

  • unequal pupils

  • nonreactive pupillary response

Goals of care, advanced directives, and organ donation wishes should be discussed for cases or SDH with poor prognostic indicators.

Chronic SDH has an overall 30-day mortality estimate of 3.2-6.5%, with worse outcomes in those older than 60 years old. 80% of patients regain pre-hematoma levels or function after surgical evacuation.

Predictors for inpatient morality in adults with SDH include:

  • Initial GCS score 7 or less

  • Age greater than 80 years old

  • “Acute” subdural formation

  • Need for craniotomy (instead of burr hole) for intervention

Paradoxically, focal neurological signs or midline shift on neuroimaging are not associated with increased hospital mortality.

Post-concussive syndrome with difficulty concentrating, fatigue, and occasional headache may occur after cranial trauma but should improve over time. Patients and caregivers should monitor these symptoms, with medical reevaluation if symptoms worsen or progress.

VI. Patient Safety and Quality Measures


B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

Fall precautions, with use of any indicated DME (i.e., walkers), should be instituted.

Mechanical deep vein thrombosis (DVT) prophylaxis should be used in all patients. Guidelines advocate combining mechanical prophylaxis with pharmaceutical agents (i.e., low-dose UFH or LMWH) starting 12-24 hours postoperatively or when adequate hemostasis has been achieved in patients at high-risk for DVT.

DVT prophylaxis should be used while hospitalized and if prolonged immobilization is anticipated after discharge.

Patients who require ICU level care or intubation may benefit from stress-ulcer prophylaxis. Histamine-receptor antagonist (H2RA) agents (i.e., famotidine, ranitidine) should be considered as proton pump inhibitor (PPi) agents may cause thrombocytopenia.

What's the evidence?

Karnath, B. “Subdural hematoma: Presentation and management in older adults.”. Geriatrics. vol. 58. 2004. pp. 18-23.

Ducruet, AF, Grobelny, BT, Zacharia, BE, Hickman, ZL, DeRosa, PL, Anderson, K, Sussman, E, Carpenter, A, Connolly, ES. “The surgical management of chronic subdural hematoma”. Neurosurg Rev. vol. 35. 2012. pp. 155-69.

Ratilal, BO, Costa, J, Sampaio, C. “Anticonvulsants for preventing seizures in patients with chronic subdural hematoma”. Cochrane Database of Sys Rev. vol. 3. 2005. pp. CD004893

Hanlon, D. “An evidence-based approach to managing the anticoagulated patient in the emergency department”. Emerg Med Pract. vol. 13. 2011. pp. 1-19.

Andrade, A, Hern, HG. “Traumatic hand injuries: the emergency clinician's evidence-based approach”. Emerg Med Pract. vol. 13. 2011. pp. 1-23.

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