Meningeal Layers (Outer to Inner)

The Three Meninges

• Dura mater: Tough, fibrous outer layer; consists of periosteal layer (adherent to inner skull table) and meningeal layer (inner dura)
• Arachnoid mater: Thin, avascular membrane closely adherent to inner surface of dura
• Pia mater: Delicate membrane intimately adherent to brain surface; follows all sulci and gyri

Epidural Space

• Potential space between inner skull table and periosteal dura — does not normally exist
• Dura firmly adherent to skull, especially at suture lines → epidural collections do NOT cross sutures
• Dura most loosely attached at temporal region → most common site for epidural hematoma
• Middle meningeal artery runs in groove on inner table of temporal bone — temporal bone fracture → arterial rupture → EDH
• Posterior fossa EDH: venous (transverse or sigmoid sinus tear) rather than arterial

Subdural Space

• Potential space between the dural border cell layer (innermost dura) and arachnoid membrane
• Bridging veins traverse this space from cortical surface to dural venous sinuses — vulnerable to shearing injury
• No suture-line adhesions → subdural collections spread freely over the convexity, crossing suture lines
• Limited by dural reflections (falx cerebri, tentorium cerebelli) — SDH does not cross midline or cross the tentorium

Subarachnoid Space

• Between arachnoid and pia — contains CSF, cerebral arteries, and veins
• SAH from aneurysmal rupture or trauma fills this space — distinct entity from SDH/EDH

Epidemiology & Risk Factors

• Incidence: 1–4% of traumatic brain injuries; 5–15% of fatal head injuries
• Age: Predominantly young adults (20–40 years) — rare in elderly (dura firmly adherent to skull) and rare in children <2 years (skull deformable)
• Mechanism: Head trauma with temporal bone fracture in ~85–95% of cases
• Location: Temporal (70–80%), frontal (10%), posterior fossa (5–10%), vertex/parasagittal (rare)
• Male:female ratio: ~4:1

Pathophysiology

• Temporal EDH (most common): Temporal bone fracture → rupture of middle meningeal artery (branch of internal maxillary artery from ECA) → arterial bleeding strips dura from inner skull table
• Middle meningeal artery enters skull through foramen spinosum → runs in groove on inner table of temporal squamous bone
• Posterior fossa EDH: Occipital bone fracture → tear of transverse or sigmoid sinus (venous) or meningeal arteries
• Vertex EDH: Tear of superior sagittal sinus (venous)
• Arterial pressure rapidly dissects dura from skull → rapidly expanding mass lesion
• EDH volume expands quickly due to arterial pressure → rapid rise in ICP → herniation

Clinical Presentation

The “Lucid Interval” (Classic “Talk and Die” Pattern)

• Phase 1: Initial loss of consciousness at time of impact (concussion)
• Phase 2: “Lucid interval” — transient neurological improvement lasting minutes to hours (patient appears well, talks, follows commands)
• Phase 3: Rapid deterioration as hematoma expands → rising ICP → ipsilateral pupil dilation (uncal herniation) → contralateral hemiparesis → coma → death if untreated
• Lucid interval present in only ~20–50% of EDH cases — absence does NOT exclude the diagnosis
• Some patients never lose consciousness initially; others never regain consciousness

Herniation Progression Sequence

• Expanding temporal EDH → medial temporal lobe (uncus) herniates over tentorial edge
• Step 1: Ipsilateral CN III compression → ipsilateral fixed, dilated pupil (parasympathetic fibers on outside of CN III compressed first)
• Step 2: Ipsilateral cerebral peduncle compression → contralateral hemiparesis
• Step 3: Contralateral cerebral peduncle against opposite tentorial edge (Kernohan notch) → ipsilateral hemiparesis (false localizing sign)
• Step 4: Bilateral pupil dilation, bilateral posturing, brainstem compression → respiratory arrest

Imaging

CT Characteristics

• Shape: Biconvex (lens-shaped / lenticular) — blood collects between skull and dura, creating a convex inner margin
• Does NOT cross suture lines — dura is firmly adherent at sutures (pathognomonic distinguishing feature from SDH)
• CAN cross midline if it extends across the vertex (unlike SDH which is limited by falx)
• Density: Hyperdense (60–80 HU) when acute; “swirl sign” (mixed density with hypodense areas) = active bleeding (surgical emergency)
• Location: Most commonly temporal/temporoparietal; adjacent temporal bone fracture in ~85%
• Usually unilateral; bilateral EDH very rare (<5%)

MRI

• Not the primary imaging modality for EDH (CT is faster and more practical in trauma)
• Useful for posterior fossa EDH (better than CT for brainstem assessment)
• Signal follows blood product evolution: acute = isointense T1, hypointense T2; subacute = hyperintense T1

Surgical Indications & Management

Indications for Surgical Evacuation

• Hematoma thickness >15 mm
• Midline shift >5 mm
• Any neurological deterioration (decreasing GCS, new pupillary asymmetry, new focal deficit)
• GCS ≤8 with anisocoria (herniation) — requires emergent craniotomy
• Posterior fossa EDH: Lower threshold for surgery due to limited space and risk of brainstem compression → rapid decompression indicated even for smaller collections

Surgical Technique

• Craniotomy (standard of care): Temporal craniotomy with ligation/cauterization of middle meningeal artery
• Emergent burr hole can be performed as temporizing measure if craniotomy not immediately available
• Hematoma evacuation + hemostasis + dural tacking sutures to prevent recurrence

Conservative Management

• Small EDH (<15 mm thickness, <5 mm midline shift) in neurologically intact patient (GCS 15)
• Requires close neurological monitoring and serial imaging
• Any deterioration → immediate surgery

Prognosis

• Excellent prognosis with timely surgical evacuation — mortality <5% when operated before herniation
• Mortality increases dramatically with delayed surgery or herniation at time of operation
• Functional outcome heavily dependent on pre-operative GCS and pupillary status

Epidemiology & Risk Factors

• Most common traumatic intracranial mass lesion — accounts for ~50–60% of traumatic intracranial hematomas
• Bimodal age distribution: Young adults (high-energy trauma — MVC, falls) and elderly (≥65, falls even from standing height)
• Risk factors: Anticoagulation (warfarin, DOACs), antiplatelet therapy, alcoholism, brain atrophy (age-related), coagulopathy, thrombocytopenia
• Mechanism: Usually significant head trauma; in elderly, may occur with trivial or no recalled trauma
• Patients on anticoagulation have a 7–10-fold increased risk of traumatic SDH

Pathophysiology

• Bridging vein rupture: Brain accelerates/decelerates within skull → cortical bridging veins stretched and torn at their dural attachments
• Bridging veins cross the subdural space from cortical surface to superior sagittal sinus (or other dural sinuses)
• Brain atrophy (elderly, alcoholism) → bridging veins are more stretched across a wider subdural space → lower force threshold for rupture
• Venous blood accumulates between dura and arachnoid → spreads freely over the convexity
• Can also result from cortical artery or vein laceration (associated with contusions in high-energy trauma)
• Associated parenchymal injury (contusions, DAI) is common — contributes to worse outcomes compared to EDH

Clinical Presentation

• Presentation depends on rate of accumulation and underlying brain injury
• Hyperacute/severe: Immediate coma, pupillary dilation, posturing — often associated with severe primary brain injury
• Subacute: Progressive headache, confusion, drowsiness, focal deficits developing over hours
• Unlike EDH, the “lucid interval” is uncommon in acute SDH because the underlying brain injury is usually more severe
• Seizures occur in ~10–25%
• Elderly patients: May present with minimal symptoms initially despite large SDH due to brain atrophy providing “extra space”

Imaging

CT Characteristics

• Shape: Crescent-shaped (concavo-convex) — blood layers along the convexity conforming to brain surface
• Crosses suture lines freely (no dural adhesions at sutures in the subdural space)
• Does NOT cross midline (limited by falx cerebri) and does NOT cross the tentorium
• Acute SDH: Hyperdense (50–70 HU) on non-contrast CT
• May extend along the falx (“interhemispheric SDH”) or along the tentorium
• Look for associated findings: midline shift, sulcal effacement, contralateral hydrocephalus, contusions

Management

Surgical Indications

• Hematoma thickness >10 mm
• Midline shift >5 mm
• GCS decrease ≥2 points from time of injury to hospital admission
• ICP >20 mmHg
• Surgical technique: Craniotomy with hematoma evacuation ± decompressive craniectomy
• “Four-hour rule”: Surgery within 4 hours of symptom onset associated with improved outcomes

Anticoagulation Reversal

• Warfarin-related SDH: IV vitamin K + 4-factor PCC (prothrombin complex concentrate) — preferred over FFP for rapid INR reversal; target INR ≤1.4
• Dabigatran: Idarucizumab (Praxbind) — specific reversal agent
• Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban): Andexanet alfa (Andexxa) or 4-factor PCC
• Heparin: Protamine sulfate
• Antiplatelet agents: Platelet transfusion (controversial — PATCH trial showed harm with platelet transfusion in antiplatelet-associated ICH; evidence extrapolated to SDH)
• Timing: Reversal should be initiated immediately — do not wait for coagulation studies to begin reversal in known anticoagulated patients

Prognosis

• Acute SDH carries the worst prognosis of all traumatic intracranial hematomas
• Mortality: 50–90% depending on GCS at presentation, age, and associated injuries
• Poor prognostic factors: GCS ≤8, age >65, pupillary dilation, coagulopathy, midline shift >10 mm
• Survivors often have significant disability (mRS 4–5)
• Poor outcomes largely driven by underlying parenchymal injury (contusions, DAI), not the SDH itself

Pathophysiology

• Inciting event: Minor or unrecognized head trauma → small subdural hemorrhage from bridging vein tear
• Neomembrane formation: Within days, inflammatory response encapsulates the blood clot → outer and inner neomembranes form along dural and arachnoid surfaces
• Neomembrane neovascularization: New capillaries in the outer membrane are fragile and leaky (immature endothelium, lack of tight junctions)
• Repeated microhemorrhages: Fragile neomembrane capillaries bleed repeatedly → hematoma slowly enlarges over weeks to months
• Inflammatory cascade: VEGF, fibrinolytic factors (tPA, plasmin), and inflammatory cytokines within the hematoma fluid perpetuate membrane leakiness and prevent clot resolution
• Osmotic gradient: Blood product breakdown creates hyperosmolar fluid → draws in additional fluid, further expanding the collection
• This self-perpetuating cycle of microhemorrhage → inflammation → neovascularization → rebleeding explains why chronic SDH is a disease of recurrent hemorrhage, not simply an “old blood clot”

Risk Factors

• Advanced age (>65 years) — single greatest risk factor; brain atrophy stretches bridging veins
• Anticoagulation (warfarin, DOACs) and antiplatelet therapy
• Alcoholism — cerebral atrophy + coagulopathy (liver disease) + frequent falls
• Coagulopathy (hepatic, renal, hematologic)
• CSF shunts (VP shunts) — over-drainage reduces CSF volume → brain sags away from skull → bridging vein stretch
• Intracranial hypotension (spontaneous CSF leak) — same mechanism as CSF over-drainage
• Hemodialysis (heparin use, uremic platelet dysfunction)
• Prior craniotomy or neurosurgery
• Seizure disorder (repeated falls)
• History of trauma reported in only ~50% of cases — trivial or forgotten trauma is common

CT Density Evolution

Clinical Presentation

• Insidious onset over weeks to months — often misdiagnosed as dementia, depression, or stroke
• Headache: Most common symptom (~80%); often bilateral, worse in morning, worse with coughing/straining
• Cognitive decline: Confusion, inattention, memory impairment, personality changes
• Fluctuating mental status: Waxing-waning alertness and orientation — characteristic feature; can mimic delirium or “sundowning”
• Gait difficulty: Unsteadiness, falls; may mimic NPH
• Focal deficits: Contralateral hemiparesis, speech difficulty (if dominant hemisphere)
• Seizures: ~5–10% of chronic SDH patients
• Board scenario: Elderly patient with progressive confusion, gait instability, and headache over weeks → think chronic SDH (especially if on anticoagulation or history of fall)

Management

Surgical Options

• Burr hole drainage: First-line surgical treatment; one or two burr holes with passive drainage or irrigation; can be done under local anesthesia
• Craniotomy: Reserved for organized/septated collections, solid hematoma, or recurrence after burr hole; higher morbidity but more definitive evacuation
• Subdural drain: Closed drainage system placed after burr hole for 24–48 hours — reduces recurrence rate
• Twist-drill craniostomy: Minimally invasive bedside procedure; smaller hole than burr hole; useful in high-surgical-risk patients

Surgical Indications

• Symptomatic patients with neurological deficits attributable to the SDH
• Hematoma thickness >10 mm
• Midline shift >5 mm
• Progressive neurological deterioration
• ICP >20 mmHg

Recurrence

• Recurrence rate after burr hole drainage: 10–30%
• Risk factors for recurrence: Bilateral SDH, continued anticoagulation, coagulopathy, brain atrophy (brain fails to re-expand), residual post-operative collection, diabetes
• Recurrence typically presents 2–6 weeks after initial drainage

Middle Meningeal Artery (MMA) Embolization

• Rationale: The MMA supplies the dural and neomembrane vasculature that perpetuates chronic SDH through microhemorrhages → embolizing the MMA devascularizes the neomembrane and interrupts the rebleeding cycle
• Technique: Endovascular catheterization of MMA via femoral or radial artery access → embolization with particles (PVA), liquid agents (Onyx, NBCA), or coils
• EMBOLISE trial (2024, NEJM): Prospective randomized trial; MMA embolization + standard care vs. standard care alone for symptomatic chronic SDH
• Results: MMA embolization significantly reduced the need for surgical rescue (repeat surgery) and demonstrated lower recurrence rates
• MAGIC-MT trial and other multicenter RCTs: Corroborated findings — MMA embolization reduces SDH recurrence and surgical re-intervention
• Current role: Emerging as adjunctive or primary treatment for chronic SDH, particularly in patients with high recurrence risk; can be performed before or after burr hole drainage
• Safety profile: Low complication rate; potential risks include non-target embolization (facial nerve palsy — petrosal branch of MMA), access-site complications

Medical Management: Dexamethasone

• Rationale: Chronic SDH is an inflammatory process → corticosteroids may reduce inflammation, membrane permeability, and fluid accumulation
• Dex-CSDH trial (2020, NEJM): Randomized trial of dexamethasone vs. placebo for chronic SDH
• Results: Dexamethasone reduced the need for surgery but was associated with increased adverse events (hyperglycemia, infections) and a trend toward worse outcomes and increased mortality at 6 months
• Conclusion: Dexamethasone is NOT routinely recommended for chronic SDH based on current evidence
• Other medications under investigation: atorvastatin, tranexamic acid (TRACS trial), ACE inhibitors — none yet standard of care

SDH in Anticoagulated Patients

• Most rapidly growing demographic for SDH due to aging population and increasing anticoagulation use
• Anticoagulation increases SDH risk 7–10-fold; also increases hematoma expansion risk
• Warfarin: INR >3.0 dramatically increases risk; supratherapeutic INR = highest risk
• DOACs: Lower intracerebral hemorrhage risk than warfarin but still significant SDH risk, especially in elderly
• Management principles:
• • Immediate reversal of anticoagulation (see reversal agents above)
  • Do not wait for coagulation labs to begin reversal
  • Repeat imaging at 6–8 hours to assess for expansion
  • Lower threshold for surgical intervention
  • Restart anticoagulation timing: individualized (typically 7–14 days after stable imaging); multidisciplinary decision involving neurology, neurosurgery, cardiology

SDH in the Elderly

• Incidence increases dramatically with age: ~7–13.5 per 100,000 in those ≥70 years
• Brain atrophy provides “extra space” → larger SDH may accumulate before symptoms appear
• Stretched bridging veins + brain atrophy = lower trauma threshold for SDH
• May present with “failure to thrive,” delirium, falls, or progressive cognitive decline rather than classic headache + focal deficit
• Often misdiagnosed as dementia, UTI-related delirium, stroke, or NPH
• Higher recurrence rates after surgical drainage due to brain’s inability to re-expand to fill the space

SDH in Infants: Non-Accidental Trauma

• Subdural hematomas in infants <2 years are highly suspicious for non-accidental trauma (NAT) / abusive head trauma
• Shaken baby syndrome / abusive head trauma: Violent shaking → acceleration-deceleration forces → bridging vein rupture
• Classic triad: Subdural hematoma + retinal hemorrhages + encephalopathy
• Retinal hemorrhages: Present in ~85% of abusive head trauma; typically bilateral, multilayered, and extending to the periphery (distinguishes from accidental causes)
• Additional findings: Metaphyseal fractures (“bucket-handle” or “corner” fractures), rib fractures at different stages of healing, scalp swelling without clear trauma history
• Interhemispheric SDH (along the falx) is particularly associated with NAT
• Bilateral SDH of different ages (mixed density on CT) suggests repeated episodes of abuse
• Mandatory reporting: Healthcare providers are legally obligated to report suspected child abuse
• Full skeletal survey, ophthalmologic exam, and social work consultation are required

Bilateral Subdural Hematomas

• Bilateral SDH found in ~15–25% of cases
• Common causes: Chronic alcoholism, severe brain atrophy (any cause), anticoagulation, intracranial hypotension, non-accidental trauma (infants)
• CT: May show no midline shift (bilateral masses cancel each other out) — misleadingly “normal” midline on imaging
• Clue: Compressed/effaced sulci bilaterally with normal or slightly compressed ventricles without midline shift
• May require bilateral drainage (staged or simultaneous)

Spontaneous Intracranial Hypotension Mimicking SDH

• Spontaneous intracranial hypotension (SIH): Spontaneous CSF leak → low CSF volume → brain sags → stretches bridging veins → SDH
• Orthostatic headache is the hallmark feature (worse upright, better supine) — but may be absent in chronic cases
• MRI findings of SIH: Diffuse pachymeningeal (dural) enhancement, subdural collections (often bilateral), brain sagging (low-lying cerebellar tonsils, effacement of prepontine cistern, “slumping” midbrain)
• Key diagnostic clue: Bilateral subdural collections + diffuse dural enhancement on MRI → think SIH before considering surgery
• Treatment: Conservative (bed rest, hydration, caffeine) → epidural blood patch (EBP) → targeted fibrin glue patching or surgical repair of CSF leak if refractory
• Critical: Draining the SDH in SIH without addressing the underlying CSF leak can worsen brain sagging and lead to clinical deterioration

Uncal (Transtentorial) Herniation

• Most clinically important herniation syndrome in the context of SDH/EDH
• Mechanism: Expanding supratentorial mass (SDH, EDH) pushes medial temporal lobe (uncus) over the tentorial edge
• Step 1 — CN III compression: Ipsilateral pupil dilation (parasympathetic fibers on outer surface of CN III are compressed first) → ptosis, “down and out” gaze
• Step 2 — Ipsilateral cerebral peduncle: Contralateral hemiparesis (corticospinal tract compressed)
• Step 3 — PCA compression: Ipsilateral PCA compressed against tentorial edge → occipital infarction → contralateral homonymous hemianopia
• Step 4 — Brainstem compression: Midbrain distortion → progressive decrease in consciousness → bilateral posturing → cardiorespiratory arrest
• Hutchinson pupil: A fixed, dilated pupil ipsilateral to the hematoma is an ominous sign of active uncal herniation — demands immediate intervention

Kernohan Notch Phenomenon

• False localizing sign: Contralateral cerebral peduncle is compressed against the opposite tentorial edge by the herniating uncus
• Results in ipsilateral hemiparesis (motor deficit on the SAME side as the hematoma)
• Board trap: Patient with EDH/SDH presents with motor deficit ipsilateral to the hematoma — Kernohan notch phenomenon, NOT a contralateral lesion
• The ipsilateral dilated pupil (CN III) still correctly lateralizes the hematoma — the motor deficit is misleading

Subfalcine Herniation

• Mechanism: Cingulate gyrus herniates under the falx cerebri to the contralateral side
• ACA (pericallosal artery) compression: → Contralateral (or bilateral) leg weakness (ACA territory infarction)
• Most common type of herniation overall; often seen with midline shift on CT
• Can compress the foramen of Monro → obstructive hydrocephalus (ipsilateral lateral ventricle dilation)

Tonsillar (Downward Cerebellar) Herniation

• Mechanism: Cerebellar tonsils herniate through the foramen magnum
• Brainstem (medulla) compression: Cardiorespiratory arrest, Cushing triad (hypertension + bradycardia + irregular respirations)
• Can occur with posterior fossa EDH or large supratentorial masses causing global downward shift
• Cushing triad (Cushing reflex): A late and ominous sign of critically elevated ICP — indicates imminent brainstem herniation

Upward (Ascending Transtentorial) Herniation

• Mechanism: Posterior fossa mass compresses cerebellum/brainstem upward through the tentorial notch
• Compression of superior cerebellar arteries, aqueduct obstruction → acute hydrocephalus
• Associated with posterior fossa EDH or large cerebellar hematoma

EDH Prognosis Details

• Excellent outcomes when evacuated before herniation — many patients make full recovery
• Pre-operative GCS is the strongest predictor of outcome
• GCS 15 at time of surgery: >95% good outcome
• GCS ≤8 with bilateral fixed pupils: Mortality >75%
• Posterior fossa EDH: Higher mortality than supratentorial EDH due to limited space and rapid brainstem compression

Acute SDH Prognosis Details

• Mortality remains 50–60% even with surgery in many series
• Functional independence (GOS 4–5) achieved in only 20–30% of survivors
• Surgery within 4 hours improves outcomes but does not overcome the burden of severe primary brain injury
• Age >65 independently doubles mortality risk
• Anticoagulation-associated acute SDH has even higher mortality

Chronic SDH Prognosis Details

• Surgical mortality is low (~1–5%); most deaths related to medical comorbidities in elderly patients
• ~70–85% of patients return to baseline neurological function after successful drainage
• Recurrence (10–30%) is the main challenge; MMA embolization is reducing recurrence rates
• Persistent cognitive deficits may occur, especially if diagnosis was delayed