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
- TBI severity by GCS: mild 13–15, moderate 9–12, severe ≤8 — severe TBI requires airway protection and neurocritical care; ICP monitoring is recommended for salvageable severe TBI with abnormal head CT, and consider it with normal CT when risk factors (age, motor posturing, hypotension) are present (BTF)
- ICP & CPP targets (BTF): keep ICP <22 mmHg and CPP 60–70 mmHg; CPP = MAP − ICP
- Uncal herniation triad: ipsilateral CN III palsy (down-and-out eye + fixed dilated pupil) + contralateral hemiparesis — surgical emergency
- Kernohan notch phenomenon: ipsilateral hemiparesis from contralateral cerebral peduncle compression against tentorium — false localizing sign in uncal herniation
- Subfalcine herniation: cingulate gyrus under falx → contralateral ACA territory infarct (medial frontal → contralateral leg weakness)
- Cushing’s triad: hypertension + bradycardia + irregular respirations = impending herniation; intubate, hyperosmolar therapy, neurosurgery STAT
- Osmotherapy: mannitol 0.25–1 g/kg IV bolus OR 3% hypertonic saline; target Na 145–155, serum osm 295–320, osm gap <20
- Hyperventilation: brief bridge only (PaCO2 30–32) for impending herniation; sustained hyperventilation causes ischemia — default PaCO2 35–40
- Post-traumatic seizure prophylaxis: levetiracetam or phenytoin for 7 days after severe TBI (BTF); no benefit beyond 7 days for late PTS prevention
- Brain death determination (2023 BD/DNC): coma + absent brainstem reflexes + positive apnea test (PaCO2 ≥60 AND ≥20 above baseline AND pH <7.30); adults require complete neurologic exam plus at least one apnea test; children require two exams and two apnea tests; must exclude hypothermia (<36°C), sedatives, paralytics, and metabolic/electrolyte derangement
- Decompressive craniectomy (DECRA, RESCUE-ICP): reduces mortality in refractory ICP but at cost of severe disability survivors — consent conversation matters
- Secondary insult prevention: avoid SBP <90, SpO2 <90, hyperglycemia, hyperthermia — each single hypotensive episode doubles TBI mortality
Herniation / clinical
- Down-and-out eye + fixed dilated pupil + contralateral hemiparesis → Uncal (transtentorial) herniation with CN III compression
- Ipsilateral hemiparesis with uncal herniation → Kernohan notch phenomenon (false localizing)
- Contralateral leg weakness after mass effect → Subfalcine herniation → ACA territory infarct
- Progressive rostrocaudal deterioration (pupils → posturing → apnea) → Central transtentorial herniation
- Sudden apnea and cardiovascular collapse → Tonsillar herniation through foramen magnum
- Obliterated quadrigeminal cistern + small posterior fossa mass → Upward (reverse) transtentorial herniation
- Hypertension + bradycardia + irregular respirations → Cushing’s triad (impending herniation)
- Lucid interval → rapid deterioration + anisocoria → Epidural hematoma with uncal herniation
ICP / monitoring
- ICP <22 mmHg, CPP 60–70 mmHg → BTF (4th edition) targets in severe TBI
- Papilledema + vomiting + decreased LOC + 6th nerve palsy → Elevated ICP syndrome
- Lundberg A waves (plateau waves >50 mmHg × 5–20 min) → Critical loss of intracranial compliance
- External ventricular drain (EVD) → Gold standard ICP monitor — allows therapeutic CSF drainage
- Apnea test: PaCO2 ≥60 AND ≥20 above baseline AND pH <7.30, no respiratory effort → Positive for brain death (2023 BD/DNC)
- No cerebral blood flow on cerebral angiography / radionuclide perfusion scan / TCD oscillating-reverberating flow / CT angiography → Ancillary brain death confirmation when apnea test cannot be completed (EEG and evoked potentials are NOT recommended ancillary tests in the 2023 guideline)
- Hypothermia <36°C, sedatives, paralytics, severe electrolyte/acid-base derangement → Confounders — do NOT declare brain death
Treatment / pearls
- HOB 30° + normothermia + normocapnia + normonatremia + sedation/analgesia → Tier 1 ICP management
- Mannitol 0.25–1 g/kg IV bolus → Osmotic diuresis (avoid if hypotensive or osm >320)
- 3% hypertonic saline (target Na 145–155) → Preferred osmotherapy when hypovolemic/hypotensive
- Pentobarbital coma (burst suppression on EEG) → Refractory ICP tier 3 therapy
- Decompressive craniectomy (DECRA, RESCUE-ICP) → Refractory ICP elevation despite maximal medical therapy
- Levetiracetam or phenytoin × 7 days → Early post-traumatic seizure prophylaxis (severe TBI)
- NEXUS criteria / Canadian C-spine rule → Clinical cervical spine clearance in alert trauma patient
- One complete neurologic exam + at least one apnea test by qualified examiner (adults); two exams + two apnea tests (children) → 2023 unified BD/DNC declaration protocol
Subdural Hematoma (SDH)
Classification by Timing
| Type | Time from Injury | CT Appearance | Clot Consistency | Typical Surgical Approach |
|---|
| Acute | <3 days | Hyperdense (bright white) crescent | Solid clot | Craniotomy |
| Subacute | 3–21 days | Isodense (may be missed on CT) | Mix of solid + liquid | Craniotomy or burr hole |
| Chronic | >21 days | Hypodense (dark) crescent | Liquefied | Burr 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
Middle Meningeal Artery (MMA) Embolization for Chronic SDH
Rationale & Mechanism
- Mechanism: devascularizes the neovascular outer membrane of the chronic SDH, removing the fragile vessels that drive recurrent micro-hemorrhage and gradual enlargement
- Delivered via endovascular microcatheter into distal MMA branches; embolic agents include particles (PVA, Embospheres) or liquid embolic (Onyx, n-BCA)
- Used as an adjunct to standard burr-hole drainage (most common application) or as primary therapy for select non-operative chronic SDH
2024 Landmark Randomized Trials
| Trial | Key Finding |
|---|
| EMBOLISE (2024) | MMA embolization after burr-hole drainage for chronic SDH → reduced recurrence/reoperation vs. surgery alone |
| MEMBRANE (2024) | Confirmed reduced recurrence with MMA embolization adjunct to surgical evacuation |
| STEM (2024) | Onyx-based MMA embolization → lower recurrence rate after burr-hole drainage |
| EMPROTECT (2024) | European RCT — MMA embolization reduced recurrence after surgical evacuation of chronic SDH |
Board Pearls
- 2024 RCTs (EMBOLISE, MEMBRANE, STEM, EMPROTECT) established MMA embolization as an effective adjunct to burr-hole drainage for chronic SDH — reduces recurrence
- Mechanism: devascularizes the neovascular outer membrane that drives chronic SDH growth
- Embolic options: particles (PVA, Embospheres) or liquid embolic (Onyx, n-BCA)
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
| Feature | Subdural Hematoma (SDH) | Epidural Hematoma (EDH) |
|---|
| Source | Bridging veins (venous) | Middle meningeal artery (arterial) |
| Location | Between dura and arachnoid | Between dura and skull |
| CT shape | Crescent-shaped | Biconvex (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 presentation | Elderly, anticoagulated, chronic progressive | Young, temporal fracture, lucid interval |
| Surgical approach | Craniotomy (acute) or burr hole (chronic) | Craniotomy (urgent) |
| Prognosis | Poor in acute (50–90% mortality) | Good if treated promptly |
| Underlying brain injury | Often 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
Traumatic Brain Injury — Severity, DAI, Contusions, Penetrating, Skull Fractures
TBI Severity Classification
| Severity | GCS | Typical Features |
|---|
| Mild | GCS 13–15 | Concussion; brief or no LOC; often normal imaging; symptoms usually resolve within weeks |
| Moderate | GCS 9–12 | Prolonged LOC or post-traumatic amnesia; structural injury common on CT; variable outcomes |
| Severe | GCS ≤8 | Coma; intubation typically required; high risk of elevated ICP, herniation, and long-term disability |
Diffuse Axonal Injury (DAI)
- Mechanism: rotational/shear forces stretch axons at tissue interfaces; classic in high-velocity deceleration (MVA)
- Distribution: gray-white matter junction, corpus callosum (splenium most common), dorsolateral brainstem (rostral midbrain, upper pons)
- Imaging: CT often underestimates; SWI / T2* GRE MRI shows microhemorrhages; FLAIR shows non-hemorrhagic axonal injury
- Clinical: immediate coma disproportionate to CT findings; poor prognosis if brainstem involvement; recovery often prolonged and incomplete
Cerebral Contusions
- Coup: contusion at the site of direct impact
- Contrecoup: contusion at the brain surface opposite the impact — typically larger than the coup lesion
- Predilection: frontal poles, anterior temporal lobes, orbitofrontal cortex (brain striking rough inner skull surfaces)
- Risk of expansion: contusions characteristically blossom over 24–72 h — mandate serial CT (typically at 6 h and 24 h) and close neuro checks
- Surgical evacuation considered for >20–50 mL volume with mass effect, GCS decline, or refractory ICP elevation
Penetrating Brain Injury
- High mortality — gunshot wounds to the head carry >90% mortality when bihemispheric or trans-ventricular
- Aggressive ICP management as per standard ICP ladder; early operative debridement of accessible necrotic tissue and removal of accessible fragments (deep fragments often left to avoid additional injury)
- Broad-spectrum antibiotics for prophylaxis against intracranial infection (organisms from skin, hair, projectile contamination)
- AED prophylaxis: recommended for all penetrating TBI (higher seizure risk than blunt TBI, where guidelines recommend only 7-day prophylaxis with levetiracetam or phenytoin)
Basilar Skull Fracture — Clinical Signs
- Battle sign: mastoid ecchymosis (posterior to the ear) — petrous/mastoid temporal bone fracture
- Raccoon eyes: bilateral periorbital ecchymosis — anterior cranial fossa fracture
- Hemotympanum: blood behind the tympanic membrane — petrous temporal fracture
- CSF rhinorrhea: cribriform plate fracture; CSF leaks through the nose
- CSF otorrhea: petrous temporal fracture with tympanic membrane disruption
- Halo sign: drop of bloody fluid on filter paper shows central blood with a clear (CSF) ring — quick bedside screen
- β2-transferrin assay: gold-standard laboratory confirmation of CSF leak (specific to CSF and perilymph)
Board Pearls
- TBI severity by GCS: mild 13–15 / moderate 9–12 / severe ≤8 — memorize cutoffs
- DAI classically involves gray-white junction, corpus callosum, and dorsolateral brainstem — SWI/T2* is the most sensitive sequence; brainstem involvement portends poor outcome
- Contusions blossom — obtain serial CT at 6 h and 24 h regardless of initial appearance
- Penetrating brain injury: antibiotics + AED prophylaxis are standard (differs from blunt TBI 7-day prophylaxis only)
- Battle sign + raccoon eyes + hemotympanum + CSF rhinorrhea/otorrhea = basilar skull fracture quartet; confirm CSF with halo sign at bedside and β2-transferrin in the lab
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: 7–15 mmHg in adults (<10 mmHg in children); treatment threshold >20–22 mmHg per Brain Trauma Foundation 4th edition
- CPP = MAP − ICP; target CPP 60–70 mmHg (Brain Trauma Foundation guidelines)
Stepwise ICP Management
| Step | Intervention | Mechanism | Key Details |
|---|
| 1 | General measures | Optimize venous drainage | HOB 30°; head midline; avoid tight C-collars; treat fever, pain, agitation |
| 2 | Sedation & analgesia | Reduce cerebral metabolic rate | Propofol or midazolam + fentanyl; target deeper sedation (RASS −4 to −5) for ICP control; titrate to suppression of agitation, ventilator dyssynchrony, and ICP response |
| 3 | Osmotherapy | Create osmotic gradient → draw water from brain | Mannitol 0.25–1 g/kg IV (check serum osmolality <320; osmolar gap <20); Hypertonic saline 3% (250 mL bolus) or 23.4% (30 mL via central line); target Na 145–155 mEq/L; AVOID Na >160 mEq/L |
| 4 | CSF drainage | Remove CSF volume | EVD (external ventricular drain); drain intermittently at 10–15 mmHg; gold standard for ICP monitoring + treatment |
| 5 | Moderate hyperventilation | Vasoconstriction (lower pCO2) | Target pCO2 30–35 mmHg; temporary bridge only; prolonged hyperventilation → cerebral ischemia |
| 6 | Barbiturate coma | Maximal metabolic suppression | Pentobarbital; titrate to burst suppression on EEG; major side effects: hypotension, immunosuppression |
| 7 | Decompressive craniectomy | Expand the fixed vault volume | Last resort; large (≥12 cm) bone flap removal; see RESCUE-ICP data below |
Osmotherapy — Mannitol vs. Hypertonic Saline
| Feature | Mannitol (20%) | Hypertonic Saline (3–23.4%) |
|---|
| Dose | 0.25–1 g/kg IV bolus; q4–6h | 3%: 250 mL bolus; 23.4%: 30 mL via central line |
| Onset | 15–30 min | Minutes |
| Monitoring | Serum osmolality (<320 mOsm/kg); osmolar gap (<20) | Serum Na: target 145–155 mEq/L; AVOID Na >160 mEq/L |
| Advantage | Peripheral IV access; well-studied | Volume expands (good if hypotensive); no osmolality ceiling |
| Disadvantage | Diuresis → hypovolemia → hypotension; rebound edema | 23.4% requires central line; risk of central pontine myelinolysis if Na corrected too fast |
| Contraindication | Hypotension, hypovolemia | Hypernatremia (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
| Trial | Key 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 for survival (mRS ≤4); 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 >22 mmHg (Brain Trauma Foundation 4th edition threshold) refractory to maximal 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 6 and 12 months (GOS-E): surgery group had more upper-severe-disability-or-better outcomes; benefit driven by mortality reduction, with increased vegetative state and lower severe disability
- 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 (NNT = 2 for survival, mRS ≤4; NNT = 4 for favorable outcome, mRS ≤3) 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
| Procedure | Hole Size | Common Indications | Advantages | Limitations |
|---|
| Twist drill | <5 mm | Bedside chronic SDH drainage; ICP bolt placement | Can be done at bedside; minimal equipment; local anesthesia | Small access; cannot evacuate solid clots; higher recurrence for SDH |
| Burr hole | 10–15 mm | Chronic SDH; EVD; brain biopsy | Good drainage; lower recurrence than twist drill; OR or bedside | Cannot evacuate organized clots; limited visualization |
| Craniotomy | Large bone flap | Acute SDH; EDH; tumor; organized chronic SDH | Full visualization; hemostasis; can address underlying pathology | Requires 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
Brainstem Breathing Patterns — Rostro-Caudal Localization
| Pattern | Description | Localization |
|---|
| Cheyne-Stokes respirations | Crescendo-decrescendo hyperpnea alternating with central apneas (~30–120 s cycles) | Bilateral hemispheric / diencephalic dysfunction; also CHF, high altitude, opiates |
| Central neurogenic hyperventilation | Sustained rapid (40–70/min) regular deep breathing despite low PaCO2 | Midbrain / upper pontine tegmentum |
| Apneustic breathing | Prolonged inspiratory hold ("cramping") with brief expiration | Mid-to-lower pons (pneumotaxic / apneustic centers) |
| Cluster (Biot) breathing | Groups of irregular breaths separated by apneas | Lower pons / upper medulla |
| Ataxic breathing | Completely irregular, arrhythmic rate and depth | Medulla (dorsal respiratory group); pre-terminal pattern |
| Agonal gasping | Slow, deep, irregular gasps | Brainstem failure — heralds imminent respiratory arrest |
- Rostro-caudal progression: Cheyne-Stokes → central hyperventilation → apneustic → cluster/Biot → ataxic → apnea — mirrors the herniation track from forebrain to medulla.
- In a comatose patient: ataxic breathing is a true emergency — intubate before respiratory arrest.
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 ICH with neurologic deterioration, brainstem compression, obstructive hydrocephalus, or cerebellar ICH volume ≥15 mL (the classic >3 cm heuristic) → immediate surgical evacuation, with or without EVD (suboccipital craniectomy) per 2022 AHA/ASA
- 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
| Anticoagulant | Reversal Agent | Key Points |
|---|
| Warfarin | 4-factor PCC (KCentra) + IV vitamin K | PCC works in minutes; vitamin K takes 6–12 h; target INR <1.4 |
| Dabigatran | Idarucizumab (Praxbind) | Monoclonal antibody fragment; immediate reversal; 5 g IV |
| Rivaroxaban / Apixaban | Andexanet alfa (Andexxa) or 4F-PCC | Andexanet: recombinant factor Xa decoy; expensive; PCC commonly used as alternative |
| Heparin | Protamine sulfate | 1 mg protamine per 100 units heparin; risk of anaphylaxis |
| Antiplatelets | Platelet transfusion (controversial) | PATCH excluded patients undergoing surgery within 24 h; in surgical/neurosurgical candidates, platelet transfusion is still commonly given despite lack of trial evidence |
Herniation Syndromes — Quick Reference
| Type | Structure Displaced | Key Findings |
|---|
| Uncal (transtentorial) | Medial temporal lobe through tentorial notch | Ipsilateral CN III palsy (fixed dilated pupil) → contralateral hemiparesis → Duret hemorrhages in brainstem |
| Central (descending) | Bilateral diencephalon downward | Progressive rostral-to-caudal deterioration: diencephalic → midbrain → pontine → medullary stages |
| Subfalcine (cingulate) | Cingulate gyrus under falx | ACA compression → contralateral leg weakness; can compress foramen of Monro → hydrocephalus |
| Tonsillar | Cerebellar tonsils through foramen magnum | Medullary compression → respiratory arrest, bradycardia — rapidly fatal |
| Upward (ascending) | Cerebellum upward through tentorial notch | Midbrain compression; can occur with posterior fossa EVD drainage |
Board Pearls
- Cerebellar ICH with neurologic deterioration, brainstem compression, obstructive hydrocephalus, or volume ≥15 mL (classic >3 cm heuristic) = surgical evacuation per 2022 AHA/ASA — 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.
Brain Death Determination — 2023 Greer Guidelines
- 2023 unified pediatric and adult guidelines (Greer DM et al., JAMA 2023) — first consensus document covering both populations in a single framework
- Diagnosis = irreversible cessation of all brain function, including the brainstem (“brain death / death by neurologic criteria”, BD/DNC)
Prerequisites
- Known cause of irreversible brain injury (imaging, history, mechanism must support catastrophic, irreversible injury)
- Exclusion of confounders that can mimic brain death:
- Hypothermia: core temperature must be ≥36°C
- Severe acid–base, electrolyte, or endocrine derangements corrected
- Drug intoxication / sedative effect excluded (allow adequate clearance time)
- Neuromuscular blockade excluded (train-of-four if recently administered)
- Adequate hemodynamics (SBP/MAP sufficient to support cerebral perfusion during testing)
Clinical Examination
- Coma — no response to noxious stimulation above the foramen magnum
- Absent brainstem reflexes:
- Pupillary light reflex (mid-position, non-reactive pupils)
- Corneal reflex
- Oculocephalic (“doll's eyes”) and oculovestibular (cold caloric) reflexes
- Gag reflex
- Cough reflex (tracheal suctioning)
Apnea Test
- Pre-oxygenate with 100% FiO2; establish normocapnia and normoxia baseline
- Disconnect from ventilator (provide passive O2); observe for any spontaneous respiratory effort
- PaCO2 must reach ≥60 mmHg AND rise ≥20 mmHg above baseline AND pH must fall below 7.30 without spontaneous respirations to be diagnostic of apnea
- Abort the test for significant hypoxemia, hypotension, or cardiac arrhythmia → proceed to ancillary testing
Ancillary Tests
- Used when the apnea test cannot be safely completed or clinical exam components are confounded:
- Cerebral angiography: no intracranial flow above the carotid siphon/circle of Willis (gold-standard)
- Nuclear medicine cerebral perfusion (radionuclide angiography) scan: no isotope uptake (“empty light bulb / hollow skull” sign)
- CT angiography: absent intracranial arterial opacification (validated cerebral blood flow study)
- Transcranial Doppler (TCD): reverberating or absent flow patterns
- EEG and evoked potentials are NOT recommended as ancillary tests in the 2023 guideline — they do not assess brainstem function
Board Pearls
- Greer 2023 (JAMA): first unified adult + pediatric BD/DNC guideline — one framework; adults = complete neuro exam + at least one apnea test; children = two exams + two apnea tests
- Apnea test diagnostic threshold: PaCO2 ≥60 mmHg absolute AND ≥20 mmHg above baseline AND pH <7.30 without respiratory effort
- Core temperature must be ≥36°C before exam (older ≥32°C threshold is outdated)
- Ancillary tests are only used when the apnea test cannot be safely completed or exam components are confounded; restricted to cerebral blood flow studies (cerebral angiography, radionuclide perfusion, CT angiography, or TCD)
- EEG and evoked potentials are NOT recommended ancillary tests in the 2023 guideline because they do not assess brainstem function
- Gold-standard ancillary test = cerebral angiography showing absent intracranial flow
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