Nervous System & Special Senses

Intracranial pressure: monitoring and management

Clinical Overview and When to Suspect Elevated ICP

— Severe TBI with GCS ≤8

— Spontaneous ICH, large MCA infarct (malignant edema typically 2–5 days post-stroke)

— Subarachnoid hemorrhage with hydrocephalus

— Fulminant hepatic failure with grade III–IV encephalopathy

— CNS infection (bacterial meningitis, cerebral abscess, cerebral malaria)

— Brain tumor with mass effect, especially pediatric posterior fossa lesions

— Idiopathic intracranial hypertension (IIH) in obese reproductive-age women

— Cerebral venous sinus thrombosis, hypertensive encephalopathy, hyponatremic encephalopathy, DKA cerebral edema in children

— Reduced CPP → ischemia → cytotoxic edema → further ICP rise (vicious cycle)

— Herniation syndromes: uncal, central transtentorial, subfalcine, tonsillar, upward cerebellar

— Cushing reflex (HTN, bradycardia, irregular respirations) is a late, preterminal sign

Board pearl: The Step 3 examinee should recognize ICP as a syndrome requiring simultaneous diagnosis and empiric treatment — do not delay osmotherapy or head-of-bed elevation while awaiting CT in a herniating patient.

CCS pearl: On a CCS case with TBI + unilateral blown pupil, your immediate orders should be: elevate HOB 30°, intubate with RSI, hyperventilate transiently to PaCO₂ 30–35, hypertonic saline or mannitol, STAT non-contrast head CT, and neurosurgery consult — all in the first simulated minutes.

Definition: Intracranial pressure (ICP) >20 mmHg sustained >5 minutes is pathologic; normal adult ICP is 7–15 mmHg supine. Cerebral perfusion pressure (CPP) = MAP − ICP; target CPP 60–70 mmHg in TBI.

Monro-Kellie doctrine: Skull is fixed volume containing brain (~80%), blood (~10%), CSF (~10%). Any volume increase (mass, edema, hemorrhage, hydrocephalus) initially compensated by CSF/venous displacement, then ICP rises exponentially.

When to suspect elevated ICP in the ED:

Pathophysiologic consequences:

Presentation Patterns and Key History

— Worse in morning or with recumbency (overnight CO₂ retention → cerebral vasodilation)

— Worsened by Valsalva, cough, bending, sneezing

— Progressive over days–weeks (mass) vs hyperacute thunderclap (SAH, pituitary apoplexy)

— New headache pattern in patient >50, immunocompromised, or with cancer = red flag

— Transient visual obscurations (seconds-long graying with posture change) → papilledema

— Diplopia from CN VI palsy (false localizing sign due to long intracranial course)

— Enlarging blind spot, peripheral constriction in chronic IIH

— Trauma mechanism, anticoagulant use (warfarin, DOACs, antiplatelets)

— Recent neurosurgery, VP shunt (think shunt malfunction)

— Malignancy history (metastatic edema)

— Pregnancy (eclampsia, CVST), OCP use (CVST, IIH)

— Weight, vitamin A/tetracycline/retinoid exposure (IIH triggers)

— HIV status, TB exposure (opportunistic CNS infection)

Key distinction: A "worst headache of life" with peak intensity <1 minute mandates SAH workup (non-contrast CT, then LP if CT negative beyond 6h), whereas progressive morning headache with vomiting points toward mass-effect physiology requiring contrast MRI.

Classic triad (often incomplete): headache, vomiting, altered mental status. Triad sensitivity is low; absence does not rule out elevated ICP.

Headache features suggesting raised ICP:

Vomiting: Often projectile, classically without preceding nausea, especially in posterior fossa lesions and pediatric patients.

Mental status changes: Earliest sign is often subtle — inattention, drowsiness, behavioral change. Progresses to obtundation and coma as brainstem is compromised.

Visual symptoms:

Seizures: May be presenting feature of tumor, abscess, venous sinus thrombosis, eclampsia.

Focal deficits: Hemiparesis, aphasia, ataxia depending on lesion location.

Pediatric-specific: Bulging fontanelle, increasing head circumference, "setting sun" sign (forced downgaze), irritability, poor feeding, split sutures on plain films.

High-yield history to elicit:

Physical Exam Findings and Hemodynamic Assessment

— Cushing triad (HTN with widened pulse pressure, bradycardia, irregular/Cheyne-Stokes respirations) = impending herniation, brainstem compression. Late finding — act immediately.

— Fever may indicate infection or central hyperthermia

— Hypotension in isolated TBI is rare; if present, look for hemorrhagic source elsewhere (especially in children where intracranial bleeds can cause shock)

— Unilateral fixed/dilated ("blown") pupil → ipsilateral uncal herniation compressing CN III

— Bilateral fixed/dilated → severe brainstem injury or bilateral herniation

— Pinpoint reactive → pontine lesion or opioid (always check)

— Decorticate (flexor) — lesion above red nucleus

— Decerebrate (extensor) — lesion below red nucleus, worse prognosis

— Asymmetric weakness, hyperreflexia, upgoing toes

Step 3 management: A patient with declining GCS and anisocoria gets immediate airway control with RSI (etomidate or ketamine + rocuronium), HOB to 30°, hypertonic saline 3% 250 mL bolus or 23.4% 30 mL via central line, and neurosurgery activation before prolonged imaging — but a non-contrast head CT is still indicated to guide definitive intervention (decompression vs EVD).

Vital signs:

GCS: Document E/V/M components. GCS ≤8 = intubate for airway protection. Trend GCS; a 2-point drop is significant.

Pupillary exam:

Fundoscopy: Papilledema (blurred disc margins, elevated disc, loss of venous pulsations). Absence does not exclude acute ICP elevation — papilledema takes hours to days to develop.

Cranial nerves: CN VI palsy as false localizer; CN III palsy with herniation; gaze deviation.

Motor exam and posturing:

Brainstem reflexes: Corneal, gag, cough, oculocephalic ("doll's eyes" — do NOT perform if C-spine not cleared), oculovestibular (cold calorics).

Signs of trauma: Battle sign, raccoon eyes, hemotympanum, CSF oto/rhinorrhea → basilar skull fracture.

Diagnostic Workup — Initial Labs and Imaging

— Detects hemorrhage (epidural, subdural, SAH, ICH), large masses, midline shift, effaced sulci, compressed basal cisterns, hydrocephalus (temporal horn dilation, transependymal flow)

— Quantify midline shift: >5 mm clinically significant

— Loss of gray-white differentiation suggests diffuse edema

— Effacement of basal cisterns is an early imaging sign of raised ICP

— CBC, BMP, glucose, coags (PT/INR, PTT, platelet count)

— Anti-Xa or specific DOAC levels if available and bleeding

— Type and screen

— LFTs (hepatic encephalopathy), ammonia

— Toxicology screen if AMS

— ABG (PaCO₂ guides ventilation; avoid hypoxemia)

— Serum osmolality and sodium (baseline for osmotherapy)

— Troponin (neurogenic stress cardiomyopathy in SAH)

— Optic nerve sheath diameter on ultrasound: >5 mm correlates with ICP >20 mmHg (sensitivity ~90%)

— Transcranial Doppler: pulsatility index >1.2 suggests elevated ICP

Board pearl: In suspected bacterial meningitis with any feature suggesting elevated ICP (papilledema, focal deficit, seizure, GCS <11, immunocompromise, age >60), give empiric antibiotics + dexamethasone first, then CT, then LP. Do not delay antibiotics for imaging.

Non-contrast head CT — first-line, fastest:

CT angiography: When SAH found (aneurysm), suspected dissection, or stroke candidate for thrombectomy.

MRI brain ± contrast: Better for tumor, abscess, early ischemia, posterior fossa lesions, venous sinus thrombosis (MRV), encephalitis.

Initial labs:

ECG: SAH classically produces deep symmetric T-wave inversions ("cerebral T waves"), QT prolongation, U waves.

Lumbar puncture: Contraindicated if focal deficit, papilledema, immunocompromise, or signs of mass effect without prior imaging — risk of herniation. Safe only after CT shows no mass effect.

Bedside adjuncts:

Diagnostic Workup — ICP Monitoring Modalities

— Severe TBI (GCS 3–8 after resuscitation) with abnormal CT

— Severe TBI with normal CT plus two of: age >40, motor posturing, SBP <90 mmHg

— Selected cases of ICH, fulminant hepatic failure, large hemispheric stroke at neurosurgical discretion

— Catheter into lateral ventricle (typically right Kocher's point)

— Advantages: measures ICP and therapeutically drains CSF; can sample CSF; recalibratable

— Disadvantages: highest infection rate (~5–10% ventriculitis), hemorrhage risk ~1–2%, technically difficult with collapsed ventricles

— Zero the transducer at tragus (foramen of Monro)

— Fiberoptic or strain gauge into brain parenchyma

— Easier placement, lower infection risk

— Cannot drain CSF, cannot be recalibrated after insertion (drift over days)

— Normal: P1 (percussion) > P2 (tidal) > P3 (dicrotic)

— Elevated ICP: P2 > P1 ("rounded" waveform) = loss of compliance

— Lundberg A waves (plateau waves, 50–100 mmHg, 5–20 min) = critical, demand intervention

— Lundberg B waves (rhythmic oscillations) suggest cerebrovascular dysregulation

Key distinction: EVD = monitor + therapy (drain CSF); intraparenchymal = monitor only. On boards, the patient with hydrocephalus or who needs CSF diversion gets an EVD, not a bolt.

Step 3 management: Maintain CPP 60–70 mmHg by addressing both numerator (MAP via norepinephrine if needed) and denominator (ICP via tiered therapy). Avoid CPP >70 — increases ARDS risk without outcome benefit.

Indications for invasive ICP monitoring (BTF guidelines):

External ventricular drain (EVD / ventriculostomy) — gold standard:

Intraparenchymal monitor (e.g., Camino, Codman bolt):

Subdural, subarachnoid, epidural bolts: Less accurate, rarely used now.

Waveform analysis:

Adjunctive multimodal monitoring: Brain tissue oxygen (PbtO₂, target >20 mmHg), jugular venous oximetry, cerebral microdialysis, continuous EEG for nonconvulsive seizures.

Tiered Management Logic and First-Line Measures

— Head of bed 30°, head midline (avoid jugular venous obstruction)

— Loosen cervical collar/ETT ties

— Treat pain and agitation (fentanyl, propofol)

— Normothermia (treat fever aggressively — acetaminophen, cooling)

— Normoglycemia (target 140–180 mg/dL; avoid hypo- and hyperglycemia)

— Normonatremia to mild hypernatremia (Na 140–150)

— SpO₂ >94%, PaO₂ >60 mmHg

— PaCO₂ 35–40 mmHg (eucapnia); avoid prophylactic hyperventilation

— Treat seizures; consider prophylactic levetiracetam for 7 days post-TBI with cortical injury

— DVT prophylaxis: sequential compression devices immediately; chemical prophylaxis (LMWH) 24–72 h after hemorrhage stable

— Sedation deepening; analgesia optimization

— CSF drainage via EVD (5–10 mL boluses or continuous drainage at 10–15 cm H₂O above tragus)

— Hyperosmolar therapy bolus (hypertonic saline or mannitol)

— Higher-dose hyperosmolar therapy, target Na 150–155

— Mild hyperventilation (PaCO₂ 32–35) as temporizing bridge

— Neuromuscular blockade (cisatracurium) with continuous sedation and train-of-four monitoring

— Optimize CPP with vasopressors

— Decompressive craniectomy

— Barbiturate coma (pentobarbital with continuous EEG to burst suppression)

— Therapeutic hypothermia 32–34°C — controversial; not routinely recommended (Eurotherm, POLAR trials negative)

Board pearl: Steroids are CONTRAINDICATED in TBI (CRASH trial — increased mortality). Steroids ARE indicated for vasogenic edema from brain tumors and abscesses (dexamethasone 10 mg IV load, then 4 mg q6h).

CCS pearl: On the simulated clock, advance time in 15-minute intervals after each intervention to reassess GCS, pupils, and ICP — Step 3 rewards iterative reassessment.

Universal Tier 0 measures (apply to ALL patients with suspected/confirmed elevated ICP):

Tier 1 (when ICP >22 mmHg sustained):

Tier 2:

Tier 3 (refractory ICP):

Pharmacotherapy — Osmotherapy and Sedation

— 3% NaCl: 250–500 mL bolus over 15–30 min, or continuous infusion 30–150 mL/h

— 23.4% NaCl: 30 mL bolus over 10 min via central line only

— Mechanism: osmotic gradient draws water from brain interstitium; also improves CBF and has anti-inflammatory effects

— Target serum Na 145–155 mEq/L; stop if Na >160 or osmolality >320

— Advantages over mannitol: maintains intravascular volume, useful in hypotensive/hypovolemic patients

— Monitor: serum Na q4–6h, chloride (hyperchloremic acidosis), volume status

— 0.25–1 g/kg IV bolus over 15–20 min; may repeat q4–6h

— Mechanism: osmotic diuresis + rheologic effect (reduced blood viscosity, reflex vasoconstriction)

— Onset 15–30 min, duration 4–6 h

— Hold if osmolar gap >20 or serum osm >320

— Causes hypovolemia, hypotension, acute kidney injury (osmotic nephrosis) — avoid in renal failure, hypotension

— Requires Foley catheter and strict I/O

— Propofol 20–80 mcg/kg/min: rapid on/off, decreases CMRO₂, antiseizure; watch for propofol infusion syndrome (PRIS — metabolic acidosis, rhabdomyolysis, cardiac failure) at doses >4 mg/kg/h beyond 48 h

— Fentanyl 25–200 mcg/h: minimal hemodynamic effect

— Midazolam: useful but tachyphylaxis and accumulation

— Dexmedetomidine: avoids respiratory depression, allows neuro exams, but may cause bradycardia/hypotension

— Ketamine: traditionally avoided but recent data suggest safe; useful for hemodynamic stability

— Antiepileptics: levetiracetam 1000 mg load then 500–1500 mg BID

— Antipyretics: scheduled acetaminophen, surface or intravascular cooling

— Vasopressors: norepinephrine to maintain CPP 60–70

Key distinction: Hypotensive/hypovolemic patient with elevated ICP → hypertonic saline (volume-expanding). Euvolemic patient with adequate renal function → either agent acceptable; recent meta-analyses favor HTS for ICP reduction magnitude and duration.

Hypertonic saline (HTS) — increasingly preferred first-line:

Mannitol 20%:

Sedation/analgesia:

Adjuncts:

Procedural and Surgical Management

— Therapeutic for hydrocephalus (SAH, IVH, posterior fossa lesions), allows ICP-guided CSF drainage

— Maintain drain height 10–20 cm above tragus; clamp during transport and neuro exams

— Complications: ventriculitis (start prophylactic cefazolin per protocol; cefazolin/ceftriaxone for established infection adjusted to CSF cultures), catheter tract hemorrhage, malposition

— Removal when ICP normalized for 24–48 h and CSF clears

— DECRA trial: Early bifrontotemporoparietal craniectomy for diffuse TBI reduced ICP but worse functional outcomes — not recommended routinely

— RESCUEicp trial: Last-tier craniectomy for refractory ICP reduced mortality but increased vegetative/severe disability — shared decision-making essential

— Hemicraniectomy for malignant MCA infarction: Indicated within 48 h in patients ≤60 (DESTINY, DECIMAL, HAMLET trials show mortality benefit and improved mRS); benefit in >60 less clear (DESTINY II — survival ↑ but with severe disability)

— Cranioplasty typically performed 6–12 weeks later

— Epidural hematoma: emergent craniotomy if >30 mL, >15 mm thickness, or midline shift >5 mm

— Subdural: surgical if >10 mm thickness or midline shift >5 mm

— Cerebellar hemorrhage: surgical if >3 cm or brainstem compression/hydrocephalus

— Supratentorial ICH: STICH trials show no clear benefit of routine surgery; consider for lobar hemorrhage with deterioration

Step 3 management: Malignant MCA syndrome in a 55-year-old with declining LOC and >50% MCA territory edema on CT → decompressive hemicraniectomy within 48 hours is the highest-yield answer; medical therapy alone has high mortality.

External ventricular drain (EVD):

Decompressive craniectomy:

Hematoma evacuation:

Aneurysm securing in SAH: Endovascular coiling or surgical clipping within 24–72 h (ISAT trial favors coiling when feasible)

Tumor debulking: Definitive for mass effect; bridge with dexamethasone and osmotherapy

Special Populations — Elderly and Renal/Hepatic Impairment

— Cerebral atrophy creates more compensatory space → mass lesions and chronic subdurals can grow large before symptoms; presentation often delayed and atypical (gait, cognition rather than headache)

— Higher anticoagulant burden (AFib on warfarin/DOACs): reverse aggressively

— Warfarin: 4-factor PCC (preferred over FFP) + vitamin K 10 mg IV

— Dabigatran: idarucizumab 5 g IV

— Factor Xa inhibitors (apixaban, rivaroxaban): andexanet alfa or 4-factor PCC 50 U/kg if andexanet unavailable

— Antiplatelets: platelet transfusion not recommended in spontaneous ICH (PATCH trial showed harm), but consider in surgical candidates

— Decompressive craniectomy benefit attenuated >60 (DESTINY II); discuss goals of care explicitly

— Greater risk of delirium with benzodiazepines — prefer dexmedetomidine, low-dose propofol

— Mannitol contraindicated in oliguric AKI or established renal failure — risk of osmotic nephrosis, volume overload, hyperkalemia

— Hypertonic saline preferred; monitor for hyperchloremic metabolic acidosis (consider sodium acetate–based hypertonic solutions)

— Levetiracetam requires renal dose adjustment (CrCl <50: reduce dose)

— Avoid NSAIDs (renal and bleeding risk)

— Fulminant hepatic failure is a leading cause of cerebral edema in young patients; ammonia >150–200 strongly predicts ICH

— Treat with lactulose, rifaximin, CRRT for ammonia clearance, hypertonic saline (target Na 145–155 prophylactically), mild hypothermia bridge to transplant

— Avoid sedatives metabolized hepatically; use short-acting agents (propofol, fentanyl) cautiously

— Coagulopathy makes invasive ICP monitoring high risk — correct INR with PCC if monitor placement essential

Board pearl: In a cirrhotic with grade IV encephalopathy and bilateral fixed pupils, get a CT and consult transplant emergently — cerebral herniation is the leading cause of death in acute liver failure, and liver transplant reverses the underlying driver.

Elderly (>65):

Renal impairment:

Hepatic impairment:

Special Populations — Pregnancy and Pediatrics

— Eclampsia/PRES: Headache, visual disturbance, seizure in 3rd trimester or postpartum; treat with IV magnesium sulfate (4–6 g load, 2 g/h infusion), labetalol or hydralazine for BP, prompt delivery if antepartum

— Cerebral venous sinus thrombosis risk highest postpartum; treat with anticoagulation (LMWH) even in presence of hemorrhagic infarct

— Pituitary apoplexy (Sheehan's syndrome, adenoma hemorrhage) — sudden headache, visual loss, hypopituitarism; give stress-dose hydrocortisone 100 mg IV, urgent MRI, neurosurgery

— Imaging: non-contrast CT safe; shielded; MRI without gadolinium preferred in 1st trimester

— Mannitol crosses placenta — fetal dehydration risk; use lowest effective dose

— Decompressive surgery not contraindicated when indicated; coordinate with obstetrics

— Sutures unfused (<18 months): bulging fontanelle, split sutures, increasing head circumference — late ICP signs because skull expands

— DKA cerebral edema: 0.5–1% of pediatric DKA cases, ~25% mortality; risk factors include young age, new-onset DM, severe acidosis, low PCO₂, high BUN, bicarbonate administration, rapid fluid resuscitation

— Treat with mannitol 0.5–1 g/kg or 3% saline 5–10 mL/kg, slow rehydration

— Non-accidental trauma: Subdural hematomas of varying ages, retinal hemorrhages, posterior rib fractures — mandatory reporting to child protective services

— Pediatric severe TBI thresholds: ICP >20 mmHg, CPP 40–50 (age-dependent)

— Hypertonic saline preferred over mannitol in pediatric TBI (better evidence)

— Hyperventilation more harmful in children (smaller CBF reserve) — strictly avoid prophylactic use

Key distinction: In pediatric DKA, AMS during treatment = cerebral edema until proven otherwise — treat empirically with hypertonic saline or mannitol while obtaining CT; do not delay.

Pregnancy:

Pediatrics:

Shaken baby/abusive head trauma: Triad of subdural hemorrhage, retinal hemorrhage, encephalopathy

Complications and Adverse Outcomes

— Uncal (transtentorial): Ipsilateral CN III palsy (blown pupil), contralateral hemiparesis, then ipsilateral hemiparesis from Kernohan's notch phenomenon (false localizing sign)

— Central transtentorial: Progressive rostral-to-caudal deterioration; small reactive pupils → fixed midposition → decerebrate posturing

— Subfalcine (cingulate): Midline shift, ACA territory infarct (contralateral leg weakness)

— Tonsillar: Cerebellar tonsils through foramen magnum → medullary compression, apnea, cardiovascular collapse, sudden death

— Upward cerebellar: From posterior fossa mass post-EVD placement (decompresses supratentorial only)

— Diabetes insipidus — high urine output, hypernatremia, dilute urine; treat with desmopressin and free water

— SIADH — hyponatremia; fluid restrict (caution: avoid hypovolemia in SAH)

— Cerebral salt wasting — hyponatremia with volume depletion; treat with hypertonic saline and salt tablets

— Distinguishing SIADH vs CSW = volume status (euvolemic vs hypovolemic)

Board pearl: A SAH patient day 5–7 with hyponatremia and orthostasis = cerebral salt wasting; fluid-restricting them (as you would for SIADH) will worsen vasospasm and cause infarction. Give hypertonic saline + fludrocortisone.

Herniation syndromes:

Cerebral ischemia and infarction: From sustained low CPP or direct vascular compression (PCA in uncal herniation → occipital infarct, ACA in subfalcine)

Seizures: Both cause and consequence of elevated ICP; nonconvulsive status epilepticus underdiagnosed — get continuous EEG in unexplained coma

Neurogenic pulmonary edema: Sympathetic surge → capillary leak; treat with ICP control, supportive ventilation, avoid excessive PEEP (can raise ICP slightly but oxygenation takes priority)

Cardiac: Neurogenic stunned myocardium, takotsubo, arrhythmias (especially with SAH)

Endocrine:

Long-term: Cognitive impairment, post-concussive syndrome, depression, post-traumatic epilepsy, hydrocephalus (may develop weeks-months later)

ICU-related: VAP, DVT/PE, pressure injuries, ICU-acquired weakness, delirium

When to Escalate Care — ICU, Consult, and Triage

— Any structural lesion with mass effect or midline shift

— Acute hydrocephalus requiring EVD

— Depressed skull fracture, open fracture, penetrating injury

— Spontaneous ICH with deterioration or cerebellar hemorrhage >3 cm

— SAH (vascular neurosurgery + endovascular)

— Refractory ICP for craniectomy consideration

— Status epilepticus, suspected NCSE

— Stroke with potential thrombectomy

— CVST, autoimmune/infectious encephalitis

— Goals-of-care discussions in devastating brain injury

— GCS ≤8 or rapidly declining

— Intubated for neuro indication

— Requiring osmotherapy, vasopressors for CPP, or invasive ICP monitoring

— Status epilepticus

— Hemodynamic instability with intracranial pathology

— Capability for 24/7 neurosurgery, neuro-interventional, neuro-ICU

— Use telestroke or telemedicine for initial guidance if local resources limited

— Stabilize first (airway, BP, osmotherapy bolus) before transfer

— Front-load CT, CTA, labs, IV access, weight

— Mobilize blood bank for reversal agents

— Early prognosis discussions; avoid premature withdrawal in first 72 h post-TBI (especially if hypothermic, sedated, or recently arrested)

— Document GCS pre-sedation/paralytic

Step 3 management: In a community ED with a herniating patient and no neurosurgery, your sequence is: intubate, hypertonic saline bolus, mannitol if HTS unavailable, mild hyperventilation as temporizing bridge, reverse anticoagulation, then arrange emergent transfer with continuous monitoring and physician-accompanied transport.

Immediate neurosurgical consultation:

Neurology/Neurocritical care consultation:

ICU admission criteria:

Transfer to comprehensive stroke center / Level 1 trauma center:

Code stroke/code neuro activation:

Family communication:

Key Differentials — Same-Category (Intracranial) Causes

— Epidural hematoma: lucid interval, biconvex lens-shaped, middle meningeal artery, typically arterial

— Acute subdural hematoma: crescent-shaped, crosses sutures not midline, bridging veins, often elderly/anticoagulated

— Chronic subdural: weeks-months post minor trauma, hypodense or mixed-density crescent

— Subarachnoid hemorrhage (traumatic vs aneurysmal)

— Diffuse axonal injury: minimal CT findings, MRI shows punctate hemorrhages at gray-white junction

— Cerebral contusion: coup/contrecoup, may expand over 24–72 h

— Aneurysmal SAH: thunderclap headache, basal cistern blood, CTA aneurysm

— Spontaneous ICH: hypertensive (basal ganglia, thalamus, pons, cerebellum); amyloid angiopathy (lobar, elderly); AVM, cavernoma

— Cerebral venous sinus thrombosis: peripartum, OCP, thrombophilia; "delta sign"

— Hemorrhagic transformation of ischemic stroke

— Hypertensive encephalopathy / PRES: posterior white matter, vasogenic edema

— Primary brain tumor (GBM, meningioma)

— Metastases (lung, breast, melanoma, renal, colon)

— Brain abscess: ring-enhancing with restricted diffusion (distinguishes from tumor)

— Bacterial meningitis ± ventriculitis

— Viral encephalitis (HSV — temporal lobe)

— Cerebral malaria, neurocysticercosis, toxoplasmosis (HIV)

— Obstructive hydrocephalus (tumor, blood, congenital aqueductal stenosis)

— Communicating hydrocephalus (post-SAH, post-meningitis)

— Shunt malfunction in patient with VP shunt

— Idiopathic intracranial hypertension

Key distinction: Ring-enhancing lesion with restricted diffusion on DWI = abscess (pus); ring-enhancing lesion with central necrosis without restriction = high-grade tumor. Empiric antibiotics + neurosurgery for abscess; biopsy + oncology for tumor.

Traumatic:

Vascular non-traumatic:

Mass lesions:

Infectious:

CSF dynamics:

Key Differentials — Other-Category (Mimics and Systemic) Causes

— Hepatic encephalopathy (hyperammonemia)

— Uremic encephalopathy

— Severe hyponatremia (<120) or rapid sodium shift → osmotic demyelination

— Hyperglycemic crises (HHS, DKA)

— Hypoglycemia

— Thyroid storm or myxedema coma

— Adrenal crisis

— Opioids (pinpoint pupils, respiratory depression — treat with naloxone)

— Benzodiazepines, alcohol, sedative-hypnotics

— CO poisoning, cyanide

— Heavy metals

— Methanol, ethylene glycol (anion gap acidosis, osmolar gap)

— Sepsis-associated encephalopathy

— Severe pneumonia/ARDS with hypoxic encephalopathy

— Catatonia

— Conversion disorder

— Severe depression with psychomotor slowing

— Postictal state

— Migraine with aura (especially basilar)

— Transient global amnesia

— Wernicke encephalopathy (thiamine deficiency — give thiamine 500 mg IV TID before glucose in malnourished/alcoholic patients)

— Autoimmune encephalitis (anti-NMDA, limbic) — subacute, psychiatric features, seizures

— Massive PE with cerebral hypoperfusion

— Cardiac arrest with anoxic brain injury → diffuse cerebral edema 24–72 h later

— Fat embolism (long-bone fracture: petechiae, hypoxemia, AMS)

Board pearl: A young patient with subacute psychiatric symptoms, orofacial dyskinesias, autonomic instability, and seizures → think anti-NMDA receptor encephalitis; check anti-NMDAR antibodies in CSF, look for ovarian teratoma, treat with steroids/IVIG/plasmapheresis and tumor removal. Not all "elevated ICP" pictures are structural.

Toxic-metabolic encephalopathy (mimics ICP elevation with AMS):

Toxic ingestions:

Infectious systemic:

Psychiatric:

Neurologic mimics:

Cardiac/embolic:

Secondary Prevention, Discharge Medications, and Long-Term Plan

— Generally restart 4–8 weeks after ICH if indication strong (mechanical valve, recurrent VTE, high CHA₂DS₂-VASc)

— For AFib: consider left atrial appendage closure (Watchman) as alternative

— Shared decision-making documented

— Long-term target SBP <130 (SPRINT, secondary prevention of ICH)

— First-line: thiazide + ACEi/ARB ± CCB

— Post-TBI: levetiracetam or phenytoin × 7 days reduces early seizures; does not prevent late epilepsy

— Continue antiepileptics if seizure occurred; reassess at 6–12 months with EEG

— Weight loss (5–10% body weight often diagnostic and therapeutic)

— Acetazolamide 500 mg BID titrated up; topiramate alternative

— Avoid triggers: tetracyclines, retinoids, excess vitamin A, lithium

— Optic nerve sheath fenestration or CSF shunting for visual loss

— Venous sinus stenting in selected cases with transverse sinus stenosis

— Educate on shunt malfunction symptoms (headache, vomiting, lethargy)

— Avoid contact sports per neurosurgeon

— Shunt series imaging at any concern

Step 3 management: After lobar ICH in a 75-year-old with AFib and probable amyloid angiopathy, do not restart anticoagulation — recurrence risk exceeds embolic risk; refer for LAA closure and continue rate control.

Anticoagulation reinitiation after intracranial hemorrhage:

Blood pressure control:

Seizure prophylaxis:

IIH long-term:

Shunt patients:

Stroke secondary prevention: Antiplatelet (aspirin or clopidogrel), high-intensity statin, BP/glucose control, lifestyle

Tumor patients: Oncology follow-up, radiation/chemotherapy planning, taper dexamethasone to lowest effective dose (PCP prophylaxis with TMP-SMX if dex >20 mg/day equivalent for >4 weeks)

Driving restrictions: State-specific; typically no driving for 3–12 months after seizure; document and counsel

Follow-Up, Monitoring Parameters, and Rehabilitation

— Serial neuro exams q1–2h initially, then q4h

— Daily sodium, glucose, renal function while on osmotherapy

— Continuous EEG if persistent AMS or known seizures

— Repeat CT 6–24 h after initial hemorrhage to assess expansion

— TCD daily in SAH to monitor for vasospasm (days 4–14)

— Acute inpatient rehab (IRF) if can tolerate ≥3 h therapy/day and functional gain expected

— Subacute rehab/SNF for lower-intensity needs

— Long-term acute care (LTAC) for vent-dependent

— Home with outpatient therapy for mild deficits

— Neurosurgery: 2 weeks post-discharge for wound check, then 6–12 weeks for imaging

— Neurology: 4–6 weeks for ongoing seizure/cognitive management

— PCP: within 1–2 weeks for medication reconciliation, BP, mood screen

— Repeat MRI for tumors per oncology; angiography for AVMs/aneurysms

— PT (mobility, balance, gait)

— OT (ADLs, cognitive-functional integration)

— Speech-language pathology (aphasia, dysphagia, cognitive-communication)

— Neuropsychology testing at 3–6 months

— Vision rehab for visual field cuts

— Post-concussion syndrome education; gradual return to school/work/sport (graduated return-to-play protocols)

— Mood disorders: screen for depression (PHQ-9), anxiety, PTSD at every visit

— Caregiver support and burnout assessment

— Driving evaluation before return

— Sleep hygiene; treat sleep apnea (worsens ICP and cognition)

Board pearl: A second-impact concussion before the first has resolved can cause catastrophic cerebral edema and death — adolescent athletes must be symptom-free and off all medications before progressing through graduated return-to-play stages.

Inpatient monitoring (post-acute phase):

Discharge planning:

Follow-up cadence:

Rehabilitation domains:

Counseling:

Monitoring for late hydrocephalus: Especially after SAH — new gait disturbance, urinary incontinence, cognitive decline = NPH triad; assess with imaging and high-volume LP

Ethical, Legal, and Patient Safety Considerations

— Established irreversible cause, normothermia, no confounding sedation/paralytics/severe metabolic derangement

— Coma, absent brainstem reflexes (pupillary, corneal, oculocephalic, oculovestibular, gag, cough)

— Apnea test: PaCO₂ rise ≥20 mmHg above baseline (or >60) without respiratory effort

— Ancillary tests (EEG, cerebral angiography, nuclear flow) when apnea test cannot be completed

— Two examinations per institutional policy; document carefully

— In US, brain death = legal death (Uniform Determination of Death Act); family consent not required to declare, though communication is essential

— Approach via organ procurement organization (OPO), not primary team — avoid conflict of interest

— Donation after circulatory death (DCD) protocols for non-brain-dead but withdrawing patients

— Avoid premature prognostication in first 72 h post-arrest or severe TBI (self-fulfilling prophecy bias)

— Use validated tools (IMPACT, CRASH for TBI; ICH score) but acknowledge uncertainty

— Surrogate decision-making hierarchy per state law

— Document substituted judgment vs best-interest standard

— Emergency exception: implied consent for life-saving intervention in incapacitated patient without surrogate

— Advance directive review at every transition of care

— Transitions of care: Medication reconciliation critical — antiepileptic doses, taper of dexamethasone, anticoagulation status must be explicitly communicated to receiving team and PCP

— Fall prevention post-discharge (gait instability, antiepileptic side effects)

— Read-back of critical neuro exam changes during handoff

— Suspected child abuse (shaken baby/AHT) → CPS, even on suspicion

— Suspected elder abuse → APS

— Gunshot wounds and certain assault injuries → law enforcement per state law

— Seizure disorder reporting to DMV varies by state

Step 3 management: When a TBI patient progresses to brain death, the OPO, not the ICU team, approaches the family about donation — this firewall preserves trust and is the tested correct answer.

Brain death determination (death by neurologic criteria):

Organ donation:

Goals of care and withdrawal of life-sustaining treatment:

Informed consent edge cases:

Patient safety:

Mandatory reporting:

High-Yield Associations and Rapid-Fire Clinical Facts

— Blown pupil = uncal herniation, CN III compression

— Bilateral fixed midposition = central herniation

— Pinpoint reactive = pons or opioid

— Setting sun sign = pediatric hydrocephalus

— Don't give steroids in TBI (CRASH)

— Don't routinely hyperventilate prophylactically

— Don't transfuse platelets in spontaneous ICH on antiplatelets (PATCH)

— Don't LP a patient with focal deficits or papilledema before imaging

— Don't restart anticoagulation early after lobar ICH with amyloid angiopathy

— HOB 30°, normocapnia, normothermia, normoglycemia, normonatremia (target high-normal)

— Reverse anticoagulation immediately

— Antibiotics + dex BEFORE LP in suspected meningitis with red flags

— Decompressive hemicraniectomy <48 h for malignant MCA in patients ≤60

— Hypertonic saline preferred in hypovolemia/hyponatremia; mannitol fine if euvolemic and normal renal function

Board pearl: The single most useful bedside intervention in suspected ICP elevation is HOB elevation to 30° with neutral head position — costs nothing, no contraindications, and improves cerebral venous outflow immediately.

Cushing reflex = HTN + bradycardia + irregular respirations = late herniation

Lundberg A waves = plateau waves >50 mmHg, sustained — emergency

Monro-Kellie doctrine = fixed cranial volume; small initial changes compensated, then steep exponential rise

CPP = MAP − ICP; target 60–70 in adults

Eyes:

Imaging signs of raised ICP: Effaced basal cisterns, loss of gray-white differentiation, midline shift, sulcal effacement, transependymal CSF flow

Optic nerve sheath diameter >5 mm on US = elevated ICP

Don't:

Do:

IIH: Obese reproductive-age woman, papilledema, normal MRI/MRV, opening pressure >25 cm H₂O, treat with weight loss + acetazolamide

CSW vs SIADH: Volume status differentiates — hypovolemic = CSW (treat with salt + volume); euvolemic = SIADH (fluid restrict)

Cerebellar hemorrhage >3 cm = surgical emergency (suboccipital decompression)

Pediatric DKA + AMS during treatment = cerebral edema → mannitol or 3% saline

Acute liver failure + ammonia >200 = high herniation risk → prophylactic Na 145–155

Board Question Stem Patterns

Key distinction: Stems mentioning anticoagulant use require reversal as the next step before any procedure; stems with papilledema or focal deficits require CT before LP; stems with GCS ≤8 require intubation before transport or extended imaging.

Stem 1: 24M unrestrained driver, GCS 6, R pupil 6 mm nonreactive, BP 180/95, HR 50. → Intubate, HOB 30°, hypertonic saline, STAT CT, emergent neurosurgery for likely epidural/subdural with uncal herniation.

Stem 2: 62F sudden "worst headache of life," vomiting, neck stiffness, photophobia. CT shows blood in basal cisterns. → SAH; CTA for aneurysm, nimodipine 60 mg PO q4h × 21 days (vasospasm prevention), BP control <160, neurosurgery for coiling/clipping within 24 h.

Stem 3: 28F obese, daily headaches worse on waking, transient visual obscurations, papilledema, normal MRI, LP opening pressure 32 cm H₂O. → IIH; acetazolamide, weight loss, ophthalmology follow-up for visual fields, optic nerve fenestration if vision threatened.

Stem 4: 8-year-old in DKA on insulin drip × 6 h, becomes lethargic with severe headache. → Cerebral edema; mannitol 0.5–1 g/kg or 3% saline 5 mL/kg, slow rehydration, CT after stabilization.

Stem 5: 75F on warfarin (INR 3.2), fell, now obtunded with L hemiparesis. CT shows R acute subdural with 8 mm shift. → 4-factor PCC + vitamin K 10 mg IV, neurosurgery for evacuation, ICU.

Stem 6: Postpartum day 5, severe headache, seizure, focal deficit, MRV shows superior sagittal sinus thrombosis. → CVST; LMWH anticoagulation despite hemorrhagic infarction, treat seizures.

Stem 7: 55M severe TBI, ICP 28 sustained despite sedation and HOB elevation; CT no surgical lesion. → Hypertonic saline bolus, deepen sedation, CSF drain via EVD, escalate to neuromuscular blockade and consider decompressive craniectomy.

Stem 8: SAH day 6, hyponatremia 128, orthostatic, urine Na 80. → Cerebral salt wasting; hypertonic saline + fludrocortisone, NOT fluid restriction.

Stem 9: Cirrhotic with grade IV encephalopathy, ammonia 280, fixed pupils. → Acute liver failure with cerebral edema; lactulose, CRRT, hypertonic saline, transplant evaluation, intubate.

Stem 10: Bacterial meningitis suspected, papilledema present. → Blood cultures, dexamethasone + empiric ceftriaxone/vancomycin/ampicillin (age-dependent) FIRST, then CT, then LP if safe.

One-Line Recap

Elevated intracranial pressure is a time-critical syndrome where the goal is to maintain cerebral perfusion (CPP 60–70 mmHg) while reducing intracranial volume through a tiered approach — universal measures, osmotherapy, CSF drainage, and surgical decompression — guided by neurologic exam and, when indicated, invasive ICP monitoring, with treatment often started empirically before definitive imaging in herniating patients.

Board pearl: If you remember only one algorithm for Step 3: Airway (intubate if GCS ≤8), Breathing (PaCO₂ 35–40, SpO₂ >94%), Circulation (MAP for CPP 60–70), Disability (HOB 30°, hypertonic saline/mannitol, CT, neurosurgery), Expose and reverse (anticoagulants, hypothermia if accidental, seizures). Then reassess every 15 minutes.

Recognition: Headache + vomiting + AMS, with late Cushing triad and pupillary changes signaling herniation; don't wait for the full picture to act.

Universal measures first: HOB 30°, neutral head, normocapnia, normothermia, normoglycemia, treat pain/agitation, target Na 140–150 — these cost nothing and start immediately.

Tiered escalation: Sedation → osmotherapy (hypertonic saline preferred when hypovolemic; mannitol acceptable when euvolemic with normal renal function) → CSF drainage via EVD → neuromuscular blockade → decompressive craniectomy or barbiturate coma for refractory cases.

Etiology drives definitive therapy: Reverse anticoagulation in hemorrhage, evacuate surgical lesions, secure aneurysms, treat infections (antibiotics before LP if papilledema), hemicraniectomy <48 h for malignant MCA in patients ≤60, and never give steroids in TBI but do give dexamethasone for tumor/abscess edema.