01Approach to the Critical Patient/attcp50

Immediate priorities

›Airway and consciousness threats

›GCS 8 or less or inability to protect airway

›Rapid sequence intubation immediately

›Preoxygenate; avoid hypoxia below SpO2 90%

›Avoid succinylcholine if signs of herniation; rocuronium preferred

›Herniation syndrome

›Pupillary asymmetry or fixed dilated pupil

›Cushing triad: hypertension, bradycardia, irregular respirations

›If herniation suspected, hyperosmolar therapy immediately

›Mannitol 1 g/kg IV or hypertonic saline 23.4% 30 mL IV bolus

›Class IIa recommendation; temporizing measure only

›Hemodynamic targets

›Avoid hypotension — MAP goal greater than 80 mmHg

›SBP target 100 to 160 mmHg

›Treat SBP above 160 mmHg to reduce hematoma expansion

›Avoid hyponatremia and hypotonic fluids

›Use isotonic crystalloids only

›Hyponatremia exacerbates cerebral edema

›Normothermia maintenance

›Hyperthermia worsens secondary brain injury

›Antipyretics and cooling measures as needed

Monitoring and escalation

›Neurologic monitoring

›Serial GCS every 30 to 60 minutes in acute phase

›Decline of 2 or more points is a surgical trigger

›Document baseline before sedation

›Pupillary checks every 1 to 2 hours

02History/hx70

Presentation pattern

›Core syndrome

›Headache

›Acute SDH: acute onset headache most common symptom (87% of spontaneous ASDH)

›Chronic SDH: progressive, insidious, often weeks to months after trivial trauma

›Mechanism of injury

›Falls (most common in elderly), motor vehicle collisions, assaults

›Ground-level falls in elderly with brain atrophy

›Trivial or absent trauma in chronic SDH

›Lucid interval

›Initial alertness followed by neurologic decline (talk and deteriorate pattern)

›Classic for expanding acute SDH

›Symptom progression

›Confusion or increasing drowsiness

›Acute: rapid within hours

›Chronic: weeks of cognitive decline or personality change

›Focal neurologic symptoms

›Progressive weakness or hemiparesis

›Speech difficulty or aphasia

›Gait instability (especially chronic SDH)

›Seizures

›Occurs in up to 41% of acute SDH patients

›Status epilepticus possible

›Vomiting

›Repeated vomiting raises posttest probability of intracranial injury to 21% after minor head trauma (JAMA)

Risk factors and medications

›Antithrombotic medications

›Warfarin

03Physical Exam/exam58

Vitals and general appearance

›Vital sign patterns

›Cushing triad

›Hypertension with bradycardia: late, ominous, implies herniation

›Irregular respirations

›Hypotension and tachycardia

›Suggests polytrauma or hemorrhagic shock, not SDH alone

›SDH does not cause hypotension in adults

›Temperature

›Hyperthermia worsens secondary brain injury

›Fever may indicate infection or neurogenic hyperthermia

›General appearance

›Decreased arousal or somnolence

›GCS score and baseline comparison

›Agitation

›May represent confusion from raised ICP

Neurologic exam

›Level of consciousness

›GCS scoring

›Eye, verbal, and motor components assessed separately

›GCS 9 or less: coma, immediate escalation

›Serial GCS is essential; decline of 2 or more points is an alarm feature

›Orientation and cognition

›New confusion or memory impairment

›Personality change in chronic SDH

›Pupils

›Size and reactivity bilaterally

›Anisocoria suggests ipsilateral uncal herniation

04Differential Diagnosis/ddx44

Life-threatening diagnoses

›Cannot-miss intracranial conditions

›Epidural hematoma

›ICD-10 S06.4

›Biconvex or lenticular hyperdense collection; does not cross suture lines

›Often associated with temporal bone fracture and middle meningeal artery injury

›Classic lucid interval presentation; often younger patients

›Subarachnoid hemorrhage

›ICD-10 I60

›Thunderclap headache; blood in cisterns, sulci, or sylvian fissure on CT

›Aneurysm rupture is the most common cause

›Ruptured intracranial aneurysm presenting as SDH

›Rare presentation; aneurysm rupture may directly cause subdural collection

›CTA required to exclude when no clear trauma

›Hypertensive intracerebral hemorrhage

›ICD-10 I61

›Intraparenchymal; typical locations: basal ganglia, thalamus, cerebellum

›Ischemic stroke with hemorrhagic transformation

›Acute focal deficits; imaging distinguishes

›Infectious emergencies

›Subdural empyema

›Fever, meningismus, rapid progression

›Ring-enhancing collection with restricted diffusion on MRI

›Neurosurgical emergency requiring drainage

Important mimics

›Structural mimics

›Subdural hygroma

›CSF-density collection (hypodense), often post-traumatic

05Laboratory Tests/lt40

Core labs

›Hematologic workup

›Complete blood count with platelets

›Thrombocytopenia increases bleeding risk and affects reversal strategy

›Leukocytosis may suggest concurrent infection

›Coagulation panel

›PT and INR: warfarin reversal target INR 1.4 or less for neurosurgery

›aPTT: heparin or factor deficiency assessment

›Type and screen

›Required if surgical intervention anticipated

›Crossmatch if intraoperative transfusion likely

›Metabolic panel

›Electrolytes and renal function

›Sodium: hyponatremia exacerbates cerebral edema

›Renal function: critical for DOAC clearance assessment and mannitol monitoring

›Hepatic function panel

›Coagulopathy from liver disease

›Hepatic encephalopathy in differential

Anticoagulation-specific labs

›DOAC-specific testing

›Anti-Xa level for factor Xa inhibitors (apixaban, rivaroxaban)

›Order when timing of last dose is uncertain

›Guides reversal strategy

›Thrombin time or anti-Xa calibrated for dabigatran

›Normal thrombin time excludes clinically relevant dabigatran activity

›Dilute thrombin time (Hemoclot) or ecarin clotting time if available

›Most accurate for dabigatran quantification

›Viscoelastic testing

06Diagnostic Tests/dt93

Scoring Systems

›Head CT decision rules

›Canadian CT Head Rule

›High-risk features: GCS score 15 at 2 hours post-injury, suspected open or depressed skull fracture, signs of basilar skull fracture, vomiting 2 or more episodes, age 65 or older

›Medium-risk features: amnesia before impact 30 minutes or more, dangerous mechanism

›High sensitivity for clinically important TBI

›New Orleans Criteria

›Seven variables: headache, vomiting, age over 60, drug or alcohol intoxication, short-term memory deficit, seizure, clinical evidence of trauma above clavicles

›Any variable positive warrants CT

›Applies to GCS 15 patients only

›SDH severity classification

›Markwalder Grading Scale for chronic SDH

›Grade 0: neurologically normal

›Grade 1: alert and oriented, mild symptoms

›Grade 2: drowsy or disoriented, mild focal deficits

›Grade 3: stuporous, severe focal deficits

›Grade 4: comatose, decerebrate or decorticate posturing

›GCS thresholds

›GCS less than 9: coma; ICP monitoring and surgical consideration

›GCS 13 to 15: mild TBI; may observe with serial exams if small SDH

›Modified Rankin Scale

›Functional outcome assessment pre and post intervention

›0: no symptoms

›5: severe disability

›Used in chronic SDH trial endpoints including Dex-CSDH and Dutch cSDH trials

MRI

›MRI brain indications

›Subacute SDH detection

›Isodense to brain on CT between days 7 to 21; MRI superior for detection

›T1 hyperintensity (methemoglobin) and T2 signal changes distinguish age of blood

›Underlying pathology evaluation

›Dural metastases or tumor as cause of spontaneous SDH

›Cerebral amyloid angiopathy imaging features on gradient echo

›Parenchymal injury assessment

›Diffusion-weighted imaging detects ischemic injury

›Susceptibility-weighted imaging detects microhemorrhages

›MRI sequence selection

›FLAIR: sulcal effacement, white matter changes

›Subacute blood hyperintense on FLAIR

›Gradient echo or susceptibility-weighted imaging

›Hemosiderin deposits; identifies chronic bleeding

›Microbleeds suggesting cerebral amyloid angiopathy

›DWI and ADC

›Subdural empyema: restricted diffusion distinguishes from SDH

›Contrast-enhanced MRI

›Dural enhancement in intracranial hypotension

›Tumor-associated SDH

›MRI limitations

›Availability and time constraints in acute setting

›CT remains first-line for acute SDH evaluation

›MRI reserved for diagnostic uncertainty or subacute presentation

›Contraindications

›Cardiac pacemaker or ferromagnetic implants

›Hemodynamic instability

CT

›Non-contrast CT head

›First-line imaging for all suspected SDH

›ACR Appropriateness Criteria: usually appropriate for head trauma (2021)

›Hyperdense crescent-shaped collection along cerebral convexity in acute SDH

›Density characteristics by age of blood

›Acute less than 3 days: hyperdense (60 to 90 HU)

›Subacute 1 to 3 weeks: isodense to brain parenchyma; most frequently missed

›Chronic greater than 3 weeks: hypodense; mixed density with acute-on-chronic rebleeding

›Key measurements

›Maximum hematoma thickness in mm

›Midline shift in mm

›Thickness greater than 10 mm or shift greater than 5 mm: surgical threshold

›Serial CT imaging

›Repeat CT within 6 hours for conservatively managed acute SDH

›ACR and Brain Trauma Foundation guidance

›Assess for expansion before definitive disposition

›Repeat imaging at 1 to 2 weeks for chronic SDH

›Then 4 to 6 weeks, then as clinically indicated

›Chronic SDH may take months to fully resolve radiographically

›CT angiography

›Indications

›Spontaneous SDH without clear trauma history

›Evaluate for aneurysm, vascular malformation, or dural arteriovenous fistula

›Age under 50 without anticoagulant use and no trauma

›MMA embolization planning

›Pre-procedural vascular mapping for chronic SDH

Ultrasound

›Point-of-care ultrasound

›Optic nerve sheath diameter

›Greater than 5 mm suggests elevated ICP (adjunct, not definitive)

›Rapid bedside assessment when CT delayed

›Sensitivity approximately 74%, specificity 85% for ICP above 20 mmHg

›Transcranial Doppler

›Pulsatility index elevation suggests elevated ICP

›Absent diastolic flow in transtentorial herniation

›Hemodynamic POCUS

›Cardiac assessment in polytrauma

›LV function and pericardial effusion screen

›IVC assessment for fluid responsiveness

›FAST exam

›Polytrauma evaluation for concurrent thoracoabdominal injury

›Free abdominal fluid in high-energy mechanism

07Disposition/dispo41

ICU and neurosurgical admission

›ICU admission criteria

›All acute SDH

›Neurosurgical ICU or equivalent for close neurologic monitoring

›Serial GCS and pupillary checks every 1 to 2 hours

›GCS less than 15 or any new neurologic deficit

›Regardless of hematoma size

›Anticoagulant-associated intracranial hemorrhage on any anticoagulant

›Reversal, monitoring, and surgical availability required

›Inability to perform reliable serial neurologic exams

›Intoxication, sedation, or language barriers

›Neurosurgical step-down unit

›Symptomatic chronic SDH requiring surgical intervention

›Post-operative monitoring

›Stable acute SDH with normal GCS

›Small hematoma with close monitoring and serial CT protocol

Surgical escalation

›Absolute surgical indications

›SDH thickness greater than 10 mm

›Surgical evacuation regardless of GCS per Brain Trauma Foundation

›Midline shift greater than 5 mm

›Surgical evacuation regardless of GCS per Brain Trauma Foundation

›GCS decline of 2 or more points from time of injury to hospital

›Surgery if GCS less than 9

›ICP greater than 20 mmHg refractory to medical management

›Timing of surgery

›Acute SDH: as soon as possible; mortality increases significantly if delayed beyond 4 hours

›Large frontotemporoparietal craniotomy with or without decompressive craniectomy

08Treatment/t117

Initial stabilization

›Airway and oxygenation

›Maintain SpO2 above 94%

›Supplemental oxygen via nasal cannula or mask

›Intubate if GCS 8 or less or airway compromise

›Avoid hyperventilation except as bridge to surgery

›Target PaCO2 35 to 45 mmHg

›Brief hyperventilation to PaCO2 30 to 35 mmHg only for imminent herniation

›Neuroprotective positioning

›Head of bed elevation to 30 degrees

›Reduces ICP by improving venous drainage

›Neutral head position

›Avoid neck flexion or rotation impeding jugular venous outflow

›Blood pressure management

›SBP target 100 to 160 mmHg

›Avoid hypotension: SBP below 90 mmHg increases mortality

›Treat hypertension above 160 mmHg to reduce expansion risk

›Nicardipine IV infusion for hypertension management

›5 mg/hour IV, titrate by 2.5 mg/hour every 5 to 15 minutes

›Maximum 15 mg/hour

›Labetalol IV alternative

›10 to 20 mg IV bolus every 10 to 20 minutes

›Maximum cumulative 300 mg

Anticoagulation reversal

›Warfarin reversal

›Four-factor prothrombin complex concentrate (4F-PCC)

›INR 2 to 3.9: 25 IU/kg IV

›INR 4 to 6: 35 IU/kg IV

›INR greater than 6: 50 IU/kg IV

›Lower dose 10 to 20 IU/kg if INR below 2.0

›Vitamin K IV concomitantly

›5 to 10 mg IV slow infusion

›Prevents rebound coagulopathy over 12 to 24 hours

›Target INR 1.4 or less prior to surgery

›Factor Xa inhibitor reversal (apixaban, rivaroxaban)

›Four-factor PCC if andexanet alfa unavailable

›25 to 50 IU/kg IV

›Note: andexanet alfa withdrawn from US market (FDA 2026)

›Activated PCC (aPCC, FEIBA) as alternative

›25 to 50 IU/kg IV

›AHA/ASA 2022 guideline supports PCC for factor Xa inhibitor reversal

›Dabigatran reversal

›Idarucizumab 5 g IV

›Two 2.5 g boluses administered consecutively

›Specific reversal agent of choice; AHA/ASA 2022 guideline

›If idarucizumab unavailable

›PCC or aPCC as bridge

›Hemodialysis if renal function allows (dabigatran is dialyzable)

›Antiplatelet reversal

›Routine platelet transfusion not recommended

›Evidence does not support improved outcomes; may be harmful (Lancet Neurology)

›Desmopressin (DDAVP)

›0.3 mcg/kg IV over 30 minutes

›May improve platelet function; useful in aspirin or uremia-related dysfunction

›Class IIb consideration

Intracranial pressure management

›Osmotic therapy

›Mannitol

›0.25 to 1 g/kg IV bolus

›Onset 15 to 30 minutes; duration 1.5 to 6 hours

›Serum osmolality target below 320 mOsm/kg

›Avoid in hypovolemia or renal failure

›Hypertonic saline 3%

›150 to 250 mL IV bolus

›Target serum sodium 145 to 155 mmol/l

›Preferred over mannitol if hypotension present

›Hypertonic saline 23.4%

›30 mL IV bolus via central line for acute herniation

›Fastest osmotic effect for impending herniation

›Sedation and analgesia

›Propofol infusion for ICP management in intubated patients

›5 to 50 mcg/kg/min IV

›Reduces CMRO2 and ICP

›Monitor for propofol infusion syndrome with high doses

›Fentanyl for analgesia

›0.5 to 1 mcg/kg IV PRN

›Avoid pain-related ICP spikes

Seizure prophylaxis and management

›Acute traumatic SDH prophylaxis

›Levetiracetam

›500 to 1000 mg IV loading dose then 500 to 1000 mg IV every 12 hours

›7 days duration per Brain Trauma Foundation guidelines

›Preferred over phenytoin: similar efficacy, fewer adverse effects (Seizure 2017)

›Phenytoin alternative if levetiracetam unavailable

›20 mg/kg IV loading at maximum 50 mg/min

›Maintenance 5 to 7 mg/kg/day in divided doses

›Monitor QTc and blood pressure during loading

›Chronic SDH seizure prophylaxis not clearly beneficial

›Journal of Neurosurgery 2020 cohort study: no benefit demonstrated

›Acute seizure management

›Lorazepam IV first line for active seizure

›4 mg IV bolus; repeat once if no response in 5 minutes

›Levetiracetam IV second line

›60 mg/kg IV (maximum 4500 mg) over 10 minutes

›Continuous EEG monitoring if not awakening as expected after seizure treatment

Surgical management

›Acute SDH surgery

›Craniotomy for surgical evacuation

›Large frontotemporoparietal craniotomy

›Decompressive craniectomy when significant cerebral edema or infarction

›Timing: as soon as possible; mortality increases significantly if delayed beyond 4 hours

›Conservative management for acute SDH

›Small SDH with minimal mass effect and GCS 13 to 15

›Serial neurologic exams and repeat CT within 6 hours

›ICU or step-down monitoring

›Chronic SDH surgery

›Burr-hole drainage standard of care

›With subdural drain placement; reduces recurrence (RR 0.46; Neurosurgery 2022)

›Irrigation during burr-hole drainage non-inferior when omitted (FINISH trial, Lancet 2024)

›Drain left in place 24 to 48 hours post-operatively

›Dexamethasone not recommended as primary treatment

›Dex-CSDH trial (NEJM 2020): fewer favorable outcomes and more adverse events than placebo in surgical patients

›Dutch cSDH trial (NEJM 2023): dexamethasone inferior to surgery

›Middle meningeal artery embolization

›Adjunctive therapy for chronic SDH

›SNIS 2026: Class I Level A recommendation as adjunct to surgical drainage to decrease recurrence

›EMBOLISE trial (NEJM 2024): reduced recurrence with liquid embolic agents

›EMMA-Can trial (JAMA 2026): confirmed reduced recurrence

›EMPROTECT trial (JAMA 2025): microparticles did not reach statistical significance

›Standalone MMA embolization

›Reasonable option in high-risk surgical patients who cannot undergo craniotomy

›SNIS 2026 guideline endorsement

09Special Populations/sp57

Pregnancy

›Pregnancy-specific considerations

›Rare presentation; consider eclampsia and venous sinus thrombosis in differential

›HELLP syndrome may cause coagulopathy

›Cerebral venous sinus thrombosis may present with SDH or hemorrhagic infarct

›Imaging approach

›Non-contrast CT head when maternal indication is clear

›Fetal radiation exposure is low from head CT; maternal benefit outweighs risk

›MRI without gadolinium preferred when time permits

›Anticoagulation reversal in pregnancy

›PCC and vitamin K acceptable; discuss with maternal-fetal medicine

›DDAVP 0.3 mcg/kg IV for antiplatelet reversal

›Obstetric consultation

›Maternal-fetal medicine involvement for all cases

›Fetal monitoring if viable gestation

›Surgical management

›Craniotomy generally safe in pregnancy; coordinate positioning and anesthesia

›Avoid prolonged hypotension or hypoxia; risk of fetal compromise

Geriatric

›Older adult features

›Atypical presentation common

›Subacute or chronic course masquerading as dementia or depression

›Afebrile despite significant injury

›Falls may be the presenting event rather than the cause

›Traumatic SDH incidence tripled in elderly since 1990

›Incidence of chronic SDH 2 to 21 per 100,000; projected to become most common cranial neurosurgical condition by 2030

›Lancet Neurology 2025 review on TBI in older adults

›Unique management considerations

10Background/b83

Epidemiology

›Incidence and demographics

›Chronic SDH incidence

›2 to 21 per 100,000 population per year

›Incidence tripled in elderly since 1990

›Projected to become most common cranial neurosurgical condition by 2030 (Neurology 2025)

›Acute SDH

›Most common focal brain lesion in traumatic brain injury

›Mortality 40 to 60% in comatose patients

›Spontaneous (non-traumatic) SDH accounts for approximately 5% of acute cases

›Age distribution

›Two peaks: young adults from high-energy trauma, and elderly from falls

›Age greater than 65 is the single most significant risk factor

›Outcomes and mortality

›Acute SDH prognosis

›GCS at presentation and age are strongest outcome predictors

›Early surgery improves outcomes; delay beyond 4 hours significantly worsens mortality

›Chronic SDH functional recovery

›57 to 75% achieve good functional recovery after treatment

›Recurrence rate 10 to 20% after surgical evacuation

›MMA embolization reduces recurrence rate

›Post-traumatic epilepsy

›Cumulative 2-year incidence up to 40% after SDH

›Seizures in up to 41% of acute SDH during hospitalization

Pathophysiology

›Mechanisms of acute SDH

›Bridging vein rupture

›Bridging veins traverse subdural space from cortex to dural sinuses

›Acceleration-deceleration forces stretch and tear these veins

›Brain atrophy increases vein length and vulnerability

›Arterial sources

›Cortical artery laceration from penetrating trauma or contusion

›Spontaneous SDH: aneurysm rupture or vascular malformation (rare)

›Mechanisms of chronic SDH

›Outer membrane formation

›Dural border cell layer is the origin of the outer SDH membrane

›Neovascularization creates fragile vessels prone to rebleeding

›Inflammatory cytokines drive osmotic gradient and fluid accumulation

›Self-perpetuating expansion

›Fibrinolytic activity within the hematoma prevents clot organization

›Repeated microhemorrhages from fragile neomembranes

›Middle meningeal artery supplies the outer membrane via dural branches (basis for MMA embolization)

›Pathophysiology of injury

›Primary brain injury

›Direct compression of cortex and white matter

›Mass effect and distortion of brainstem

›Secondary brain injury

›Raised ICP reduces cerebral perfusion pressure

›Ischemia from compromised CBF

›Edema propagation around hematoma

›Herniation syndromes

›Uncal herniation: temporal lobe pushed over tentorium, compresses CN III

›Transtentorial herniation: brainstem compression causing Cushing triad

›Subfalcine herniation: cingulate gyrus crosses under falx

Therapeutic Considerations

›Anticoagulation restart after SDH

›Timing is individualized and requires neurosurgical guidance

›Typical range: 1 to 4 weeks post-injury or surgery

›High-risk cardiac indications (mechanical valve, AF with high stroke risk) may prompt earlier restart

›Risk-benefit discussion with patient and caregivers

›Thromboembolism risk from anticoagulation interruption vs rebleeding risk

›Bridging anticoagulation generally avoided

›LMWH bridging may increase rebleeding in first weeks

›MMA embolization evidence base

›Mechanism: devascularizes the outer membrane to halt expansion and rebleeding

›Liquid embolic agents (Onyx, PHIL) preferred based on EMBOLISE trial

›Microparticles (EMPROTECT trial, JAMA 2025) did not reach statistical significance

›Patient selection

›Adjunct to burr-hole drainage: SNIS 2026 Class I Level A recommendation

›Standalone therapy: high-risk surgical patients who are poor operative candidates

›Limitation of current evidence

›Optimal patient selection, timing, and embolic agent still under investigation

›ICP monitoring thresholds

›Target ICP below 22 mmHg

›Based on BEST-TRIP trial and Brain Trauma Foundation guidelines

›CPP target 60 to 70 mmHg

›Lower CPP targets in elderly with chronic hypertension may be needed

›Multimodality monitoring where available

›Brain tissue oxygen monitoring, jugular oximetry as adjuncts

›Classification systems

›Acute SDH less than 3 days

›Hyperdense on CT; most commonly traumatic

›Subacute SDH 3 to 21 days

›Isodense; easily missed; MRI superior

›Chronic SDH greater than 21 days

›Hypodense; may have mixed density with acute-on-chronic pattern

11Patient Discharge Instructions/pdi48

copy discharge instructions

›Subdural hematoma home care instructions

›Activity restrictions

›No contact sports or high-risk physical activity until cleared by neurosurgeon

›Avoid heavy lifting or straining

›No driving until medically cleared (typically at least 4 to 6 weeks)

›Medications

›Take medications exactly as prescribed

›Do not restart blood thinners until told to do so by your neurosurgeon or stroke neurologist

›Do not take aspirin, ibuprofen, naproxen, or other anti-inflammatory medications without approval

›Alcohol

›Avoid alcohol completely during recovery

›Alcohol increases fall risk and can worsen bleeding

›Fall prevention

›Remove trip hazards at home (loose rugs, clutter)

›Use handrails on stairs

›Wear proper footwear

›Consider a walker or cane if balance is impaired

›Warning signs to return to ER immediately

›Neurologic red flags

›Worsening headache or new severe headache

›Increasing confusion, excessive drowsiness, or difficulty waking

›New or worsening weakness or numbness on one side of the body

›Difficulty speaking or understanding speech

›Vision changes

›Other urgent symptoms

›Seizure of any kind

›Repeated vomiting

12References/r30

Guidelines and key sources

›Neurosurgical and TBI guidelines

›Brain Trauma Foundation: Management of Acute Subdural Hematomas (Bullock et al., Neurosurgery 2006)

›Surgical indications: thickness greater than 10 mm or shift greater than 5 mm

›American College of Surgeons Best Practices in the Management of Traumatic Brain Injury (2024)

›Anticoagulation reversal, seizure prophylaxis, and ICP management protocols

›ACR Appropriateness Criteria for Head Trauma 2021 Update (Shih et al., JACR 2021)

›Imaging recommendations including CT and MRI indications

›SNIS Guidelines on MMA Embolization for Chronic SDH (Mascitelli et al., J Neurointerv Surg 2026)

›Class I Level A recommendation for MMA embolization as adjunct to surgery

›Stroke and hemorrhage guidelines

›AHA/ASA 2022 Guideline for Spontaneous Intracerebral Hemorrhage (Greenberg et al., Stroke 2022)

›Anticoagulation reversal strategies and blood pressure targets

›AHA/ASA 2024 Performance and Quality Measures for ICH (Ruff et al., Stroke 2024)

›Key trials

›Dex-CSDH Trial (Hutchinson et al., NEJM 2020): dexamethasone inferior to placebo in surgical chronic SDH

›Trial stopped early; fewer favorable outcomes and more adverse events with dexamethasone

›Dutch cSDH Trial (Miah et al., NEJM 2023): dexamethasone inferior to surgery for chronic SDH

›FINISH Trial (Raj et al., Lancet 2024): irrigation non-inferior to no irrigation in burr-hole drainage

›EMBOLISE Trial (Davies et al., NEJM 2024): MMA embolization reduced chronic SDH recurrence

›EMMA-Can Trial (Shankar et al., JAMA 2026): confirmed MMA embolization reduces recurrence

›EMPROTECT Trial (Shotar et al., JAMA 2025): microparticle MMA embolization did not reach significance

›Epidemiology and risk

›Gaist et al. JAMA 2017: antithrombotic drug use and SDH risk; warfarin OR 3-4; combination therapy OR approximately 8

›Rivier et al. JAMA Neurology 2024: cerebral amyloid angiopathy as independent risk factor for nontraumatic SDH

›Henry et al. Neurosurgery 2022: systematic review of 103,645 chronic SDH cases; drain placement reduces recurrence RR 0.46

›van Essen et al. Lancet Neurology 2022 and JAMA Network Open 2025: surgery versus conservative treatment for acute SDH

›Coding standards

Evidence & Review