Subdural and Epidural Hematomas

Mechanism of Injury and Vascular Disruption

• Epidural hematoma: Forceful head trauma causes acceleration-deceleration injury with dural separation from the calvarium, rupturing meningeal vessels (most commonly middle meningeal artery in temporal region). Arterial bleeding under systemic pressure creates a high-pressure collection that rapidly expands, causing acute mass effect and transtentorial herniation
• Subdural hematoma: Blunt head trauma causes rotational or linear acceleration forces that shear bridging veins traversing the subdural space. Venous bleeding (lower pressure) accumulates more slowly than epidural collections, but the confined space between dura and arachnoid allows progressive expansion and increased intracranial pressure (ICP)

Cerebral Injury Cascades

• Acute phase (minutes to hours): Direct axonal injury, ionic derangements (calcium influx, potassium efflux), mitochondrial dysfunction, and release of excitatory neurotransmitters trigger neuronal apoptosis. Blood breakdown products (hemoglobin, bilirubin) generate free radicals causing secondary injury
• Inflammatory response (hours to days): Microglial activation, cytokine release (IL-1, TNF-α), blood-brain barrier disruption, and cerebral edema formation. Hematoma expansion occurs in acute SDH due to rebleeding and coagulopathy
• Chronic phase (weeks to months): Membrane formation around chronic SDH with neovascularization and fibrinolytic activity. Osmotic gradients draw fluid into the hematoma cavity, causing gradual expansion and delayed neurologic deterioration

Mass Effect and Herniation

• Hematoma volume, location, and surrounding brain compliance determine ICP elevation. Transtentorial (uncal) herniation from supratentorial masses causes ipsilateral pupillary dilation, contralateral hemiparesis, and brainstem compression
• The Monro-Kellie doctrine (skull is a closed compartment; blood + brain + CSF = fixed volume) explains why expanding hematomas cause exponential ICP elevation

Epidural Hematoma

• Temporal head trauma (most common): Motor vehicle accidents, falls from height, assaults; typically younger patients with dura still adherent to calvarium
• Middle meningeal artery injury: Most frequent arterial source (located in grooves along temporal calvarium); laceration from fracture fragments
• Venous epidural collections: Less common; from dural venous sinus tears, typically with worse prognosis due to increased expansion risk

Subdural Hematoma (Acute, Subacute, Chronic)

• Severe head trauma in younger patients: Motor vehicle accidents, falls, assaults with higher kinetic energy
• Minor head trauma in elderly/anticoagulated patients: Ground-level falls, minor blunt trauma; chronic SDH can develop weeks after trivial injury (patients often cannot recall inciting event)
• Chronic anticoagulation/antiplatelets: Warfarin, direct oral anticoagulants (DOACs), aspirin, clopidogrel significantly increase SDH risk, particularly chronic SDH
• Coagulopathy: Thrombocytopenia, hemophilia, disseminated intravascular coagulation (DIC)
• Chronic liver disease: Impaired synthetic function reduces clotting factors and platelet production
• Chronic alcoholism: Both acute SDH (from falls) and chronic SDH (from coagulopathy and repeated minor trauma)
• Dementia/neurodegenerative disease: Increased fall risk and brain atrophy creating subdural space
• Older age: Cerebral atrophy increases subdural space, making bridging veins vulnerable to shearing

Acute Epidural Hematoma

• Classic "talk and die" syndrome: Initial loss of consciousness → lucid interval (alert and talking) → sudden deterioration with acute mass effect and herniation (pathognomonic but only occurs in ~25% of cases)
• Rapidly progressive neurologic decline: Headache, deteriorating consciousness, seizures (10-25% of cases)
• Ipsilateral dilated pupil: From CN III compression during transtentorial herniation (blown pupil)
• Contralateral hemiparesis: From cerebral peduncle compression
• Altered consciousness: Ranges from minimal symptoms to coma
• Vomiting: From increased ICP

Acute Subdural Hematoma (Within 72 Hours)

• Severe head injury with profound alteration of consciousness: Often immediate coma in severe cases
• Progressive neurologic decline: Unlike EDH, may show gradual rather than sudden deterioration
• Focal neurologic deficits: Ipsilateral or contralateral depending on hematoma location and edema pattern
• Seizures: More common than in EDH (15-20%)
• Associated injuries: Diffuse axonal injury (DAI), cortical contusions, subarachnoid hemorrhage often coexist

Subacute Subdural Hematoma (3-20 Days)

• Subtle symptoms: Mild headache, personality change, confusion
• Delayed presentation: May initially seem minor before progressive deterioration
• Hematoma expansion: Up to 25% expand in first week, causing clinical deterioration despite initial stability

Chronic Subdural Hematoma (>20 Days)

• Insidious symptom onset: Often follows trivial head trauma patients don't recall
• Cognitive decline: Dementia-like presentation with memory loss, confusion, personality change ("pseudo-dementia")
• Gait disturbance: Unsteadiness, falls (vicious cycle)
• Headache: May be mild or absent
• Focal deficits: Hemiparesis, speech disturbance (variable)
• Subdural hemorrhage recurrence: Risk of rebleeding into chronic hematoma causing acute decompensation

Imaging (Gold Standard)

• Non-contrast head CT (preferred initial imaging):
• Epidural hematoma: Biconvex (lens-shaped) hyperdense collection that does NOT cross the midline (respects dural attachments); typically temporal location following middle meningeal artery distribution; sharp demarcation from brain
• Acute subdural hematoma (<72 hours): Crescent-shaped (concave toward brain) hyperdense collection that CROSSES suture lines (not confined by dura); may be diffuse over cerebral convexity or loculated; associated cerebral edema, midline shift, sulcal effacement
• Subacute subdural (3-20 days): Isodense to brain, may be subtle; best seen on coronal/sagittal reformats; look for midline shift or sulcal compression
• Chronic subdural (>20 days): Hypodense (CSF density) collection; may appear bilateral and symmetric; fluid level (xanthochromia) may be present; local mass effect less pronounced until rebleeding occurs
• Hemorrhage expansion: Compare serial CTs (at 6 hours and 24 hours in unstable patients); expansion predicts poor outcome

CT Angiography (CTA)

• Identify active extravasation ("spot sign" in acute SDH) as predictor of hematoma expansion
• Evaluate for arterial or venous injuries requiring intervention
• Pseudoaneurysm if vascular injury suspected

MRI with gradient echo or susceptibility-weighted imaging (SWI)

• Superior for detecting chronic SDH and differentiating from other fluid collections
• Useful in subacute phase when CT isodensity makes diagnosis difficult
• Demonstrates associated traumatic axonal injury (DAI) in brainstem, corpus callosum
• Reserved for patients with contraindications to CT or equivocal CT findings

Laboratory Studies

• Prothrombin time (PT), international normalized ratio (INR), activated partial thromboplastin time (aPTT): Assess coagulation status; abnormalities increase SDH risk and may guide reversal therapy
• Platelets: Assess clotting capacity; transfuse if <50,000
• Hemoglobin: Assess baseline; SDH expansion may lower hemoglobin
• Lactate/base deficit: Surrogate markers of injury severity and perfusion in polytrauma
• Troponin: Rule out myocardial injury from trauma or hypoxia

Diagnostic Criteria/Scoring

• Glasgow Coma Scale (GCS): Prognostic value; severe (≤8), moderate (9-12), mild (13-15) TBI
• Rotterdam CT score: Incorporates imaging findings (EDH presence, midline shift, compressed cisternal spaces, traumatic SAH, epidural hematoma) to predict mortality and 6-month outcome
• CRASH score: Combines clinical factors (age, GCS, pupil reactivity, injury severity) to predict mortality

Epidural Hematoma - Urgent Surgical Evacuation

• Indication: Generally all symptomatic EDH require emergent craniotomy/burr hole drainage due to high mortality (10-15% with treatment; >50% without). Surgery is the definitive treatment; medical management alone is insufficient
• Burr holes (two or more): Rapid decompression; less invasive than full craniotomy; allows evacuation and hemostasis
• Craniotomy: For large EDH (>30 mL), thick hematoma, or when burr holes fail to achieve hemostasis
• Middle meningeal artery must be identified and ligated/cauterized to prevent rebleeding
• Timing: Door-to-operating room time <1 hour is target for salvageable cases with GCS >5

Subdural Hematoma - Variable Management Based on Severity

Acute SDH with Mass Effect (Most Require Surgery)

• Craniotomy or burr holes for:
• Thickness >10 mm on any axial slice
• Midline shift >5 mm
• Signs of herniation or GCS ≤8
• Progressive neurologic deterioration
• Pupillary changes or flexor posturing
• Subdural drain placement post-evacuation: Reduces recurrent hematoma (15-20%) and improves drainage
• Surgical technique: Opening dura allows brain expansion, reduces rebleeding risk

Acute SDH Without Mass Effect (Selected Non-Operative Cases)

• Thin SDH (<10 mm thickness, <5 mm midline shift, minimal sulcal effacement): May be managed conservatively with ICU monitoring, serial imaging
• Requirements for non-operative management: GCS ≥9, stable neuro exams, no pupillary abnormalities, close monitoring capability, reliable follow-up
• Serial CT scans: At 6, 24 hours, then daily or PRN for deterioration; 25% progress and require surgery
• Escalation to surgery if: Hematoma expansion >2 mm, midline shift develops, neurologic deterioration, pupil changes

Medical Management (Adjunctive, Not Primary Treatment)

• Reversal of anticoagulation (critical for SDH prevention of expansion):
• Warfarin: Fresh frozen plasma (FFP) 10-15 mL/kg OR prothrombin complex concentrate (PCC) 25-50 units/kg (preferred; faster, less volume); target INR <1.5; add vitamin K 10 mg IV slowly (requires 12-24 hours to fully work)
• DOAC (apixaban, rivaroxaban, edoxaban): Idarucizumab (Praxbind) 5 g IV for dabigatran (reversal in minutes); Andexanet alfa for apixaban/rivaroxaban (expensive; limited data); PCC 25-50 units/kg as alternative (less specific); activated charcoal if ingestion <2 hours
• Antiplatelet agents (aspirin, clopidogrel): No reversal agent; platelet transfusion if life-threatening bleeding; desmopressin may help
• Goal: Stop anticoagulation and reverse existing coagulopathy to prevent expansion

• Seizure prophylaxis: Levetiracetam (Keppra) 500 mg IV BID (preferred; no drug interactions) or fosphenytoin 750 mg IV loading dose, then 100 mg IV TID (Dilantin less favored in modern practice due to interactions, toxicity); continue 7 days post-SDH given increased seizure risk

• Hemostasis optimization:
• Platelet transfusion if <50,000/μL (goal >100,000 if bleeding)
• Tranexamic acid (TXA) 1 g IV loading then 1 g IV q6h (within 3 hours of injury): Reduces bleeding by inhibiting fibrinolysis; should be considered in bleeding SDH but does not replace surgical evacuation

• ICP management (for GCS ≤8 or signs of herniation):
• Head of bed 30 degrees, midline head position, avoid neck compression
• Hyperosmolar therapy:
• Hypertonic saline (3% or 23.4%): 3% at 250 mL bolus (osmolality goal 320 mOsm/L); preferred in hypotension
• Mannitol 0.25-1 g/kg IV q4-6h (osmolality goal 320 mOsm/L); use with caution if renal failure or hypotension
• Sedation/analgesia: Propofol or midazolam to reduce cerebral metabolism and ICP (hypotension monitoring essential)
• Mechanical ventilation: Target PaCO₂ 35-40 mmHg (avoid severe hyperventilation which causes cerebral vasoconstriction); maintain PaO₂ >100 mmHg
• Temperature management: Avoid hyperthermia (increased mortality); hypothermia not proven beneficial; target normothermia
• Glucose control: Maintain 140-180 mg/dL (avoid both hypoglycemia and hyperglycemia)

• DVT/PE prophylaxis: Sequential compression devices immediately (chemical prophylaxis delayed until no active bleeding risk); enoxaparin or unfractionated heparin subcutaneous when bleeding controlled (typically 24-48 hours post-evacuation); if contraindicated (active bleeding), use mechanical prophylaxis or IVC filter if very high VTE risk

Chronic Subdural Hematoma - Burr Holes ± Twist Drill

• Symptomatic chronic SDH: Burr hole evacuation under local or general anesthesia; standard treatment
• Two burr holes (anterior and posterior): Allows complete evacuation and subdural drain placement
• Twist drill aspiration (smaller procedure): Percutaneous needle aspiration for thin collections (<10 mm), elderly with severe comorbidities; higher recurrence rate (20-30%); consider if operative risk prohibitive
• Subdural drain post-evacuation: Reduces recurrence to 5-10% (vs 20-30% without drainage)
• Drain duration: 24-48 hours typical; remove when drainage minimal (<20-30 mL/day)
• Outcomes: 80-90% improvement in neurologic symptoms; mortality <5%

Non-Pharmacological Measures

• Activity restriction: Bed rest initially; progressive mobilization post-operatively
• Fall prevention: Especially critical in chronic SDH patients at risk for rebleeding

Emergent complications (immediate neurosurgical consultation)

• Transtentorial (uncal) herniation: expanding supratentorial clot displaces the uncus over the tentorial edge, compressing CN III (peripheral parasympathetic fibers first) and the cerebral peduncle. Signaled by a fixed, dilated ipsilateral pupil, contralateral hemiparesis, and decreasing GCS — a surgical emergency, not an imaging-and-observe situation.
• Kernohan notch phenomenon: the contralateral peduncle is crushed against the opposite tentorial edge, producing hemiparesis ipsilateral to the clot — a classic false localizing sign; the pupil, not the motor exam, localizes the side.
• Cushing reflex and tonsillar herniation: hypertension, bradycardia, and irregular respiration signal near-terminal ICP elevation with brainstem compression. Treat as impending herniation — head-of-bed elevation with midline head position, brief controlled hyperventilation only as a bridge, hyperosmolar therapy (mannitol or hypertonic saline), and emergent surgical decompression — following the herniation-rescue algorithm of the Neurocritical Care Society's Emergency Neurological Life Support and ACS TQIP best-practice guidance. Brain Trauma Foundation severe TBI guidance is the reference for treating sustained ICP above roughly 22 mmHg, not for the specific osmotherapy agent.
• Hematoma expansion / delayed EDH: arterial rebleeding or loss of tamponade after decompression; a drop of ≥2 GCS points, a new focal deficit, or any pupillary change should prompt immediate repeat non-contrast CT (a practical bedside trigger rather than a validated threshold).

Complications of the injury itself

• Post-traumatic seizures and epilepsy: cortical irritation by iron and glutamate; early seizures are more frequent with acute SDH given underlying contusion. Brain Trauma Foundation guidance supports short-course prophylaxis to reduce early post-traumatic seizures only — it does not prevent late epilepsy.
• Malignant cerebral edema / secondary ischemic injury: loss of autoregulation with hypotension or hypoxia; even a single episode of systolic hypotension or hypoxemia markedly worsens outcome.
• Hyponatremia (SIADH or cerebral salt wasting): distinguished by volume status; abrupt sodium drop worsens edema.
• Communicating hydrocephalus: blood degradation products obstruct arachnoid granulations; presents late with gait apraxia, incontinence, cognitive decline.

Treatment-related complications

• Recurrence of chronic SDH: neomembrane neovascularization and ongoing fibrinolysis; recurrence is reduced by subdural drain placement, and middle meningeal artery embolization is increasingly used as an adjunct.
• Tension pneumocephalus: air trapped after burr hole drainage causing Mount Fuji sign and acute deterioration — emergency.
• Subdural empyema, wound infection, seizure from cortical injury after craniotomy.
• Hyperosmolar therapy harms: mannitol-induced hypovolemia and acute kidney injury; hypertonic saline causing hypernatremia and volume overload.
• Reversal-related thrombosis and VTE: PCC and prolonged immobility with delayed chemoprophylaxis.

• Shape is the answer: biconvex/lens-shaped = epidural, stops at suture lines because the dura is fused there, but can cross the midline and tentorium. Crescent-shaped = subdural, crosses suture lines but cannot cross the falx or tentorium. Stated once more because stems reverse it: sutures limit EDH; dural reflections limit SDH.
• The lucid interval is EDH, not SDH: brief loss of consciousness from concussion → alert talk-and-die interval → rapid decline as arterial blood outpaces compensatory CSF and venous displacement (Monro-Kellie). Only a minority of EDH patients show it, so its absence does not exclude EDH.
• The single association tested: temporal-bone fracture at the pterion lacerating the middle meningeal artery (a branch of the maxillary artery, from the external carotid). For SDH, the association is bridging vein shearing.
• Single best next step, almost always: non-contrast head CT, then emergent neurosurgical consultation. Lumbar puncture is contraindicated with a mass lesion — herniation risk. Do not order MRI first in the unstable trauma patient.
• The elderly/alcoholic distractor: weeks of progressive confusion, gait unsteadiness, and headache after a fall the patient cannot recall is chronic SDH, not dementia, delirium, or normal pressure hydrocephalus. Brain atrophy stretches bridging veins and enlarges the subdural space — the same atrophy allows a large clot with surprisingly little midline shift.
• The isodense trap: a subacute SDH (roughly 1–3 weeks old) can be isodense to cortex and look like a "normal" CT. Look for effaced sulci, loss of gray–white interdigitation, and a shifted midline; bilateral isodense collections may offset each other with no shift at all.
• Bilateral SDH plus retinal hemorrhages in an infant should prompt evaluation for abusive head trauma with mandatory reporting, per AAP guidance — retinal hemorrhages are not typical of accidental short falls.
• Reverse the anticoagulant, then operate: identify and reverse warfarin or DOAC therapy urgently; anticoagulation does not delay a needed evacuation.