SDH & EDH
Subdural & Epidural Hematoma
What You'll Learn
- Anatomy of meningeal layers and spaces — epidural (potential space), subdural (between dura and arachnoid), subarachnoid
- Epidural hematoma: arterial (middle meningeal artery), biconvex/lens-shaped on CT, does NOT cross suture lines, “lucid interval” presentation
- Subdural hematoma: venous (bridging veins), crescent-shaped on CT, crosses suture lines freely, high mortality in acute SDH
- CT density evolution of subdural hematoma: hyperdense (acute) → isodense (subacute) → hypodense (chronic)
- Chronic SDH pathophysiology, risk factors (elderly, atrophy, anticoagulation), and management including MMA embolization
- Herniation syndromes: uncal (CN III palsy, ipsilateral pupil dilation), subfalcine, tonsillar, and Kernohan notch (false localizing sign)
- Surgical indications for both EDH and SDH — thickness, midline shift, and clinical deterioration thresholds
- Special populations: anticoagulated patients, infants (non-accidental trauma), and intracranial hypotension mimicking SDH
HighYield Pearls
- EDH = biconvex/lens-shaped, does NOT cross sutures: middle meningeal artery laceration from temporal bone/pterion fracture → emergent craniotomy + evacuation.
- SDH = crescent-shaped, crosses sutures but NOT dural reflections (falx, tentorium): bridging vein tear; elderly + anticoagulation + alcohol are the classic risk triad.
- Classic “lucid interval” → EDH (brief LOC → lucid → deterioration with ipsilateral blown pupil + contralateral hemiparesis from uncal herniation).
- SDH density evolution: acute (<3 d) hyperdense → subacute (3 d–3 wk) iso-/mixed-density (easy to miss — look for sulcal effacement, midline shift, loss of gray-white) → chronic (>3 wk) hypodense; MRI T1 hyperintense in subacute (methemoglobin).
- Spontaneous SDH + orthostatic headache + bilateral SDHs + pachymeningeal enhancement + brain sag → intracranial hypotension (CSF leak) → epidural blood patch, NOT just evacuation.
- Chronic SDH in elderly can mimic dementia or NPH; consider in any unexplained cognitive decline with falls or anticoagulation.
- Anticoagulant reversal (same as ICH): warfarin → 4F-PCC + vit K; dabigatran → idarucizumab; apixaban/rivaroxaban → andexanet alfa or 4F-PCC. Anticoagulation restart timing is individualized by hematoma stability, surgical status, indication strength, and traumatic vs spontaneous SDH (consider LAA occlusion if high re-bleed risk).
- Middle meningeal artery embolization (MMA emb) reduces chronic SDH recurrence ~50% (EMBOLISE, MAGIC-MT) — key option in recurrent or anticoagulated chronic SDH.
- Infant with multifocal SDH + retinal hemorrhages → non-accidental trauma (shaken baby) — mandatory reporting.
- ICP management: HOB 30°, normothermia/normoglycemia, mannitol or hypertonic saline, controlled hyperventilation as a bridge only; short AED course post-evacuation if seizures.
🔍 Quick ReferenceImaging shape / mechanism · Clinical · Treatment
- Biconvex / lens-shaped hyperdensity, does NOT cross sutures → Epidural hematoma (EDH)
- Crescent / concavo-convex hyperdensity, crosses sutures, stops at falx/tentorium → Subdural hematoma (SDH)
- Temporal bone / pterion fracture with arterial bleed → Middle meningeal artery laceration (EDH)
- Bridging vein tear in elderly with cerebral atrophy → Acute or chronic SDH
- Iso-/mixed-density extra-axial collection with sulcal effacement + midline shift → Subacute SDH (3 d–3 wk)
- T1 hyperintense extra-axial collection on MRI → Subacute SDH (methemoglobin)
- Bilateral SDHs + pachymeningeal enhancement + brain sag → Spontaneous intracranial hypotension
- “Talk and die” / lucid interval → rapid deterioration → EDH with uncal herniation
- Ipsilateral blown pupil + contralateral hemiparesis → Uncal herniation (CN III + cerebral peduncle compression)
- Orthostatic headache (worse upright, better supine) + bilateral SDHs → CSF leak / intracranial hypotension
- Elderly anticoagulated patient with cognitive decline, falls, or gait instability → Chronic SDH mimicking dementia/NPH
- Infant with multifocal SDH + retinal hemorrhages → Non-accidental trauma (shaken baby syndrome)
- Headache + confusion + focal deficit after minor head trauma in alcoholic → SDH (risk: atrophy + coagulopathy)
- Emergent craniotomy + hematoma evacuation + MMA control → Symptomatic EDH
- Craniotomy or burr-hole drainage with subdural drain → Symptomatic / large SDH (drain reduces recurrence)
- Middle meningeal artery embolization (MMA emb) → Recurrent or high-risk chronic SDH (EMBOLISE, MAGIC-MT — ~50% recurrence reduction)
- Epidural blood patch → Spontaneous SDH from intracranial hypotension / CSF leak
- 4F-PCC + vit K / idarucizumab / andexanet alfa → Anticoagulant reversal for warfarin / dabigatran / Xa-inhibitor-associated SDH or EDH
- Observation with serial CT → Small EDH (<30 mL, <15 mm, midline shift <5 mm, GCS >8, no deficit) or small asymptomatic chronic SDH
- Anticoagulation restart timing individualized by hematoma stability, surgical status, indication strength, and traumatic vs spontaneous SDH; LAA occlusion alternative → AF patient post-SDH with high re-bleed risk
- HOB 30°, hypertonic saline or mannitol, controlled hyperventilation as bridge → Elevated ICP from large SDH/EDH
Anatomy of Meningeal Spaces
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
Epidural = arterial (middle meningeal artery), bounded by suture lines. Subdural = venous (bridging veins), crosses sutures but not dural reflections. This anatomic distinction determines CT morphology, clinical course, and management. The key differentiator: EDH is lens-shaped and respects sutures; SDH is crescent-shaped and spreads freely along the convexity.
Epidural Hematoma (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
- The lucid interval is the classic board question presentation for EDH
- Scenario: Young patient with head trauma → initial LOC → “wakes up and appears fine” → rapid deterioration hours later with ipsilateral pupil dilation
- This is an emergency — requires immediate CT and surgical evacuation
- The lucid interval reflects the time between initial concussive injury and the hematoma reaching critical volume to cause herniation
- Do NOT be falsely reassured by neurological improvement after head trauma — always consider EDH
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
EDH = biconvex, does NOT cross suture lines, middle meningeal artery, lucid interval, young patient with temporal bone fracture. The swirl sign on CT indicates active bleeding and demands emergent surgery. Posterior fossa EDH is venous (sinus tear) and has a lower surgical threshold because the posterior fossa has very limited compliance. EDH has the best prognosis of all traumatic intracranial hematomas when treated promptly.
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