Clinical Neurosurgery

Cranial Emergencies

Cranial Emergencies

What Do You Need to Know?

  • Acute SDH: surgical evacuation (craniotomy) if thickness >10 mm, midline shift >5 mm, or GCS drop ≥2 points; best outcomes when operated within 4 hours
  • Epidural hematoma: classic lucid interval → rapid deterioration; urgent craniotomy if >15 mm thick, midline shift >5 mm, or GCS <9 with anisocoria
  • Chronic SDH: burr hole drainage (liquefied collection); craniotomy reserved for organized/septated clots
  • Decompressive craniectomy: malignant MCA infarction (DECIMAL/DESTINY/HAMLET — age <60, within 48 h) reduces mortality but increases disability; also for refractory elevated ICP in TBI (RESCUE-ICP)
  • ICP management ladder: stepwise approach from HOB elevation → sedation → osmotherapy → CSF drainage → barbiturate coma → decompressive craniectomy
  • Monroe-Kellie doctrine: fixed cranial vault volume = brain + CSF + blood; increase in one component must be offset by decrease in another or ICP rises
  • Posterior fossa lesions: low threshold for surgical evacuation — small volume changes cause brainstem compression and obstructive hydrocephalus
Subdural Hematoma (SDH)

Classification by Timing

TypeTime from InjuryCT AppearanceClot ConsistencyTypical Surgical Approach
Acute<3 daysHyperdense (bright white) crescentSolid clotCraniotomy
Subacute3–21 daysIsodense (may be missed on CT)Mix of solid + liquidCraniotomy or burr hole
Chronic>21 daysHypodense (dark) crescentLiquefiedBurr hole drainage
  • Mechanism: tearing of bridging veins between cortex and dural sinuses; blood collects between dura and arachnoid
  • Acute SDH: high-velocity injury (falls, MVA, assault); 50–90% mortality in severe cases; often associated with underlying brain contusion
  • Chronic SDH: elderly, anticoagulated, or brain atrophy patients; minor or unrecalled trauma; neomembrane with fragile vessels → recurrent bleeding and gradual enlargement
  • Bilateral SDH: think coagulopathy, anticoagulation, alcohol use, or elderly with atrophy
  • Isodense subacute SDH: easily missed — look for effaced sulci, midline shift without obvious mass, and medial displacement of the gray-white junction

Surgical Indications

Indications for Surgical Evacuation

  • SDH thickness >10 mm
  • Midline shift >5 mm
  • GCS drop ≥2 points from time of injury to hospital arrival
  • ICP >20 mmHg
  • Posterior fossa SDH with any mass effect or neurological deterioration — very low threshold to operate

Surgical Approach

  • Acute SDH → craniotomy: solid clot requires open evacuation and direct hemostasis; large bone flap for adequate exposure
  • Chronic SDH → burr hole drainage: liquefied collection drains easily through 1–2 burr holes; subdural drain left for 24–48 h to prevent re-accumulation
  • Subacute SDH: may require either approach depending on clot consistency (assessed on imaging)
  • Timing: acute SDH should be evacuated within 4 hours of injury for best outcomes (mortality increases significantly with delays beyond 4 h)

Medical (Non-Operative) Management Criteria

  • SDH thickness <10 mm AND midline shift <5 mm
  • Neurologically stable (no GCS decline)
  • ICP <20 mmHg (if monitored)
  • No posterior fossa location
  • Requires serial imaging every 6–12 h initially, then daily
  • Correct coagulopathy; reverse anticoagulation; hold antiplatelets

Board Pearls

  • Acute SDH = craniotomy (solid clot); chronic SDH = burr hole (liquid) — this is a favorite board question
  • Isodense subacute SDH can be invisible on CT — look for unexplained midline shift, effaced sulci, or “missing” cortical ribbon
  • Chronic SDH recurrence rate after burr hole drainage is 10–20%; risk factors include bilateral SDH, coagulopathy, and brain atrophy
  • Posterior fossa SDH has a very low threshold for surgery — small volume changes can cause rapid brainstem compression and death
Epidural Hematoma (EDH)

Pathophysiology & Clinical Features

  • Source: rupture of the middle meningeal artery (most common; ~85% arterial) — blood collects between dura and inner table of skull
  • Less commonly: dural venous sinuses (especially posterior fossa EDH), diploic veins, or middle meningeal vein
  • Location: temporal bone — thinnest part of the skull; temporal bone fracture crosses the MMA groove
  • CT appearance: biconvex (lenticular) hyperdense collection; does NOT cross suture lines (dura is firmly adherent at sutures)
  • EDH does cross the midline falx (unlike SDH which does not) but does not cross suture lines

Classic Lucid Interval

  • Initial LOC from concussive impact → transient improvement (lucid interval) → rapid deterioration as expanding hematoma causes uncal herniation
  • Present in only ~20–50% of EDH patients — but is a classic board scenario
  • Deterioration: ipsilateral pupil dilation (CN III compression) → contralateral hemiparesis → coma → death
  • Ipsilateral fixed dilated pupil + contralateral hemiparesis = classic uncal herniation sign (Kernohan notch phenomenon may produce ipsilateral hemiparesis — false localizing sign)

Surgical Indications

Indications for Urgent Craniotomy

  • EDH thickness >15 mm
  • Midline shift >5 mm
  • GCS <9 with anisocoria (unequal pupils)
  • Neurological deterioration (any GCS decline)
  • Posterior fossa EDH with any mass effect
  • This is a surgical emergency — one of the most time-critical neurosurgical conditions; outcomes are excellent if evacuated promptly

Conservative (Non-Operative) Criteria

  • Thickness <15 mm
  • Midline shift <5 mm
  • GCS >8 without focal neurological deficit
  • No posterior fossa location
  • Requires close monitoring with serial CT every 6–8 h; neurosurgical standby
  • Must have reliable neurological exam — intubated or sedated patients should not be managed conservatively

Board Pearls

  • EDH = biconvex; SDH = crescent — the single most tested imaging distinction on boards
  • EDH does NOT cross suture lines (dura adherent); SDH does NOT cross the midline falx (stops at dural reflections)
  • The classic lucid interval → rapid deterioration scenario on boards = EDH until proven otherwise
  • EDH has the best prognosis of all traumatic intracranial hemorrhages if treated promptly — underlying brain is often undamaged
  • Kernohan notch: contralateral cerebral peduncle compressed against tentorium → ipsilateral (false-localizing) hemiparesis

Clinical Pearl

Any patient with a temporal bone fracture and declining consciousness — even after an initial period of improvement — should be assumed to have an expanding EDH. Do not wait for imaging if the patient is herniating; proceed with emergent surgical evacuation.

SDH vs. EDH — Comparison Table
FeatureSubdural Hematoma (SDH)Epidural Hematoma (EDH)
SourceBridging veins (venous)Middle meningeal artery (arterial)
LocationBetween dura and arachnoidBetween dura and skull
CT shapeCrescent-shapedBiconvex (lenticular)
Crosses sutures?Yes (spreads freely along subdural space)No (dura adherent at sutures)
Crosses midline?No (blocked by falx)Yes (can cross midline)
Surgical threshold — thickness>10 mm>15 mm
Surgical threshold — midline shift>5 mm>5 mm
Classic presentationElderly, anticoagulated, chronic progressiveYoung, temporal fracture, lucid interval
Surgical approachCraniotomy (acute) or burr hole (chronic)Craniotomy (urgent)
PrognosisPoor in acute (50–90% mortality)Good if treated promptly
Underlying brain injuryOften significant (contusion, DAI)Often minimal (good brain)

Board Pearls

  • Thickness thresholds differ: SDH >10 mm vs. EDH >15 mm — memorize both for boards
  • EDH prognosis is much better than SDH because the underlying brain is usually undamaged in EDH
ICP Management Ladder

Monroe-Kellie Doctrine

  • The cranial vault is a fixed, rigid compartment containing three components: brain parenchyma (~80%), CSF (~10%), and blood (~10%)
  • An increase in the volume of any one component must be compensated by a decrease in another, or ICP rises
  • Initial compensation: CSF displacement into spinal canal + venous blood displacement out of skull → maintains normal ICP
  • Once compensatory reserves are exhausted, small additional volume increases cause exponential ICP rises (steep portion of the compliance curve)
  • Normal ICP: <20 mmHg (7–15 mmHg in adults; <10 mmHg in children)
  • CPP = MAP − ICP; target CPP 60–70 mmHg (Brain Trauma Foundation guidelines)

Stepwise ICP Management

StepInterventionMechanismKey Details
1General measuresOptimize venous drainageHOB 30°; head midline; avoid tight C-collars; treat fever, pain, agitation
2Sedation & analgesiaReduce cerebral metabolic ratePropofol or midazolam + fentanyl; target RASS −2 to −3
3OsmotherapyCreate osmotic gradient → draw water from brainMannitol 0.25–1 g/kg IV (check serum osmolality <320; osmolar gap <20); Hypertonic saline 3–23.4% (no strict upper Na limit; monitor for >160)
4CSF drainageRemove CSF volumeEVD (external ventricular drain); drain intermittently at 10–15 mmHg; gold standard for ICP monitoring + treatment
5Moderate hyperventilationVasoconstriction (lower pCO2)Target pCO2 30–35 mmHg; temporary bridge only; prolonged hyperventilation → cerebral ischemia
6Barbiturate comaMaximal metabolic suppressionPentobarbital; titrate to burst suppression on EEG; major side effects: hypotension, immunosuppression
7Decompressive craniectomyExpand the fixed vault volumeLast resort; large (≥12 cm) bone flap removal; see RESCUE-ICP data below

Osmotherapy — Mannitol vs. Hypertonic Saline

FeatureMannitol (20%)Hypertonic Saline (3–23.4%)
Dose0.25–1 g/kg IV bolus; q4–6h3%: 250 mL bolus; 23.4%: 30 mL via central line
Onset15–30 minMinutes
MonitoringSerum osmolality (<320 mOsm/kg); osmolar gap (<20)Serum Na (usually <160 mEq/L)
AdvantagePeripheral IV access; well-studiedVolume expands (good if hypotensive); no osmolality ceiling
DisadvantageDiuresis → hypovolemia → hypotension; rebound edema23.4% requires central line; risk of central pontine myelinolysis if Na corrected too fast
ContraindicationHypotension, hypovolemiaHypernatremia (Na >160)

Board Pearls

  • CPP = MAP − ICP; target CPP 60–70 mmHg — memorize this formula
  • Mannitol is contraindicated in hypotension (it causes diuresis); use hypertonic saline instead in hypotensive patients — it volume-expands
  • Hyperventilation is only a temporary bridge (30–60 min) while preparing definitive treatment — prolonged use causes cerebral ischemia from vasoconstriction
  • EVD is both a monitoring device AND a therapeutic intervention (CSF drainage) — gold standard for ICP management
  • Monroe-Kellie doctrine: once compliance is exhausted, the ICP-volume curve becomes exponential — small changes in volume cause dramatic ICP spikes

Clinical Pearl

Before attributing elevated ICP to the primary injury, always check for reversible causes: endotracheal tube ties too tight (impedes venous drainage), fever, seizures, pain, agitation, hyponatremia, or the head being below 30°. Correcting these may avoid the need for escalation.

Decompressive Craniectomy

Malignant MCA Infarction

  • Definition: complete MCA territory infarction with progressive edema, midline shift, and impending herniation; typically peaks at 48–72 hours
  • Affects ~10% of ischemic stroke patients; mortality up to 80% with medical management alone
  • CT findings: hypodensity involving >50% of MCA territory, effacement of basal cisterns, midline shift

Landmark Trials

TrialKey Finding
DECIMAL (2007)Surgery within 24 h in patients ≤55 yr → reduced mortality (25% vs. 78%); increased survival with moderate-severe disability
DESTINY (2007)Surgery within 36 h in patients ≤60 yr → significant mortality reduction; stopped early for efficacy
HAMLET (2009)Surgery within 48 h in patients ≤60 yr → reduced mortality; no benefit if performed after 48 h
Pooled analysis (Vahedi 2007)NNT = 2 to prevent death; NNT = 4 for favorable outcome (mRS ≤3); surgery within 48 h, age <60
DESTINY II (2014)Patients >60 yr: reduced mortality (33% vs. 70%) BUT majority survived with severe disability (mRS 4–5); no improvement in favorable outcomes

Indications — Malignant MCA Infarction

  • Age <60 years (strongest evidence)
  • Surgery within 48 hours of symptom onset (before maximal edema)
  • Infarction >50% of MCA territory on imaging
  • Clinical deterioration (decreasing consciousness) despite medical management
  • Key counseling point: reduces mortality but increases the proportion surviving with moderate-severe disability (mRS 4)
  • Age >60: discuss with family — survival benefit exists but most survivors are severely disabled (DESTINY II)

Refractory ICP in Traumatic Brain Injury

  • Indication: ICP >20–25 mmHg refractory to maximum medical therapy (full ICP ladder exhausted)
  • RESCUE-ICP trial (2016): decompressive craniectomy vs. continued medical management in TBI patients with refractory ICP >25 mmHg

RESCUE-ICP Results

  • Surgery reduced mortality (26.9% vs. 48.9%)
  • Surgery reduced ICP effectively
  • BUT: increased the rate of vegetative state (8.5% vs. 2.1%) and severe disability
  • At 12 months: more patients in surgery group had favorable outcomes (mRS 1–4) when vegetative state and death were grouped as unfavorable
  • Bottom line: craniectomy is a life-saving procedure but must be weighed against quality-of-life outcomes; shared decision-making essential

Surgical Technique

  • Bone flap must be large — at least 12 cm (anteroposterior diameter) for unilateral craniectomy
  • Small craniectomies are harmful — brain herniates through the defect, causing venous infarction at bone edges
  • Unilateral: standard for MCA infarction or unilateral TBI
  • Bifrontal: for diffuse bifrontal edema or bilateral pathology
  • Duraplasty (opening and expanding the dura) is performed to maximize volume expansion
  • Cranioplasty (bone flap replacement) typically performed 6–12 weeks later once edema has resolved; bone stored frozen or synthetic implant used

Board Pearls

  • DECIMAL/DESTINY/HAMLET: decompressive craniectomy for malignant MCA infarction reduces mortality (NNT = 2) but increases moderate-severe disability — age <60, within 48 h
  • DESTINY II: age >60 patients — mortality drops but most survivors are severely disabled (mRS 4–5)
  • RESCUE-ICP: craniectomy for refractory ICP in TBI lowers mortality but increases vegetative state — classic boards trade-off question
  • Bone flap must be ≥12 cm — small craniectomies cause brain herniation through the defect and are worse than no surgery
  • Cranioplasty (“syndrome of the trephined”): some patients deteriorate neurologically after craniectomy and improve after bone flap replacement — due to atmospheric pressure on exposed brain
Burr Holes — Indications & Technique

Indications for Burr Holes

  • Chronic subdural hematoma drainage — most common indication; 1–2 burr holes with subdural drain placement
  • Emergent ventricular access: external ventricular drain (EVD) placement for acute hydrocephalus or ICP monitoring
  • Brain biopsy: stereotactic needle biopsy through a burr hole for deep-seated or eloquent-area lesions
  • Subdural empyema drainage
  • ICP monitor placement: intraparenchymal bolt or fiberoptic monitor

Twist Drill vs. Burr Hole vs. Craniotomy

ProcedureHole SizeCommon IndicationsAdvantagesLimitations
Twist drill<5 mmBedside chronic SDH drainage; ICP bolt placementCan be done at bedside; minimal equipment; local anesthesiaSmall access; cannot evacuate solid clots; higher recurrence for SDH
Burr hole10–15 mmChronic SDH; EVD; brain biopsyGood drainage; lower recurrence than twist drill; OR or bedsideCannot evacuate organized clots; limited visualization
CraniotomyLarge bone flapAcute SDH; EDH; tumor; organized chronic SDHFull visualization; hemostasis; can address underlying pathologyRequires general anesthesia; longer operative time; higher morbidity

EVD Placement

  • Landmark: Kocher point — 11 cm posterior to nasion (or 1 cm anterior to coronal suture), 3 cm lateral to midline
  • Trajectory: aim toward the medial canthus of the ipsilateral eye in the coronal plane and the tragus of the ipsilateral ear in the sagittal plane → targets the frontal horn of the lateral ventricle
  • Typical depth: 5–7 cm from the cortical surface
  • Usually placed on the right side (non-dominant hemisphere in right-handed patients)
  • Complications: infection (ventriculitis; ~5–10%), hemorrhage (~5%), malposition, overdrainage

Board Pearls

  • Kocher point: 11 cm posterior to nasion, 3 cm lateral to midline — classic anatomy question for EVD placement
  • Chronic SDH: twist drill and burr hole are both effective; burr hole has lower recurrence; craniotomy reserved for organized or septated collections
  • Twist drill craniostomy can be performed at the bedside under local anesthesia in critically ill patients who cannot tolerate OR transport
Special Considerations

Posterior Fossa Emergencies

  • The posterior fossa is a small, non-compliant space — even small hematomas or infarctions cause rapid brainstem compression and obstructive hydrocephalus
  • Cerebellar hemorrhage >3 cm or with brainstem compression or hydrocephalus → surgical evacuation (suboccipital craniectomy)
  • Cerebellar infarction with edema: suboccipital decompressive craniectomy if deteriorating despite medical management
  • Posterior fossa EDH: very low surgical threshold; rapid deterioration from brainstem compression; often venous (transverse/sigmoid sinus)
  • EVD placement for acute obstructive hydrocephalus — but beware of upward herniation if CSF drained too rapidly without addressing the posterior fossa mass

Anticoagulation Reversal Before Surgery

AnticoagulantReversal AgentKey Points
Warfarin4-factor PCC (KCentra) + IV vitamin KPCC works in minutes; vitamin K takes 6–12 h; target INR <1.4
DabigatranIdarucizumab (Praxbind)Monoclonal antibody fragment; immediate reversal; 5 g IV
Rivaroxaban / ApixabanAndexanet alfa (Andexxa) or 4F-PCCAndexanet: recombinant factor Xa decoy; expensive; PCC commonly used as alternative
HeparinProtamine sulfate1 mg protamine per 100 units heparin; risk of anaphylaxis
AntiplateletsPlatelet transfusion (controversial)PATCH trial: platelet transfusion was harmful in spontaneous ICH; consider only for surgical patients

Herniation Syndromes — Quick Reference

TypeStructure DisplacedKey Findings
Uncal (transtentorial)Medial temporal lobe through tentorial notchIpsilateral CN III palsy (fixed dilated pupil) → contralateral hemiparesis → Duret hemorrhages in brainstem
Central (descending)Bilateral diencephalon downwardProgressive rostral-to-caudal deterioration: diencephalic → midbrain → pontine → medullary stages
Subfalcine (cingulate)Cingulate gyrus under falxACA compression → contralateral leg weakness; can compress foramen of Monro → hydrocephalus
TonsillarCerebellar tonsils through foramen magnumMedullary compression → respiratory arrest, bradycardia — rapidly fatal
Upward (ascending)Cerebellum upward through tentorial notchMidbrain compression; can occur with posterior fossa EVD drainage

Board Pearls

  • Cerebellar hemorrhage >3 cm = surgical evacuation — classic board-tested threshold
  • Posterior fossa EVD without addressing the mass lesion risks upward herniation
  • Uncal herniation: ipsilateral CN III palsy (parasympathetic fibers on the outside of CN III are compressed first → pupil dilation before ptosis/ophthalmoplegia)
  • Duret hemorrhages: secondary brainstem hemorrhages from stretching of perforating vessels during transtentorial herniation — a sign of irreversible brainstem damage
  • PATCH trial showed platelet transfusion is harmful in spontaneous ICH on antiplatelet therapy — high-yield board knowledge

Clinical Pearl

In the acute setting, a rapidly dilating pupil on one side with contralateral motor posturing is the most urgent clinical sign of uncal herniation. Administer IV mannitol or 23.4% hypertonic saline immediately as a temporizing measure while arranging emergent CT and neurosurgical evaluation. Do not delay osmotherapy waiting for imaging confirmation.