01Approach to the Critical Patient/attcp78

Immediate stabilization

›Airway and breathing priorities

›GCS <=8 or inability to protect airway

›Rapid sequence intubation

›Pre-oxygenate to SpO2 >94% before laryngoscopy

›Avoid prolonged apneic periods that worsen hypercapnia

›Oxygenation target

›SpO2 94-99%

›PaO2 >60 mmHg

›Avoid hypoxia; each hypoxic episode doubles secondary injury risk

›Ventilation target after intubation

›PaCO2 35-40 mmHg maintenance

›Avoid PaCO2 <30 mmHg except as brief bridge for herniation

›End-tidal CO2 monitoring with ABG correlation

›Circulation and perfusion priorities

›Cerebral perfusion pressure target

›CPP = MAP - ICP; target CPP 60-70 mmHg

›Avoid SBP <90 mmHg; associated with doubled mortality in TBI

›MAP target >=80 mmHg if ICP unknown and herniation suspected

›Volume resuscitation

›Isotonic saline preferred; avoid hypotonic fluids

›Avoid dextrose solutions that worsen cerebral edema

›Vasopressor if persistent hypotension

›Norepinephrine 0.1-0.3 mcg/kg/min titrated to MAP target

›Arterial line for continuous pressure monitoring

Herniation recognition and escalation

›Herniation warning signs

›Cushing triad

›Hypertension + bradycardia + irregular respirations

›Late and ominous sign of impending brainstem compression

›Unilateral fixed dilated pupil

›Uncal herniation with CN III compression

›Requires immediate intervention within minutes

›Bilateral fixed dilated pupils

›Brainstem compression or terminal herniation

›Poor prognosis; neurosurgery immediately

›Rapid GCS decline >=2 points

›Posturing: decorticate (flexion) or decerebrate (extension)

›Immediate imaging and team activation

›Herniation protocol actions

›Head of bed 30 degrees elevation

›Reduces jugular venous pressure

›Neutral head position to avoid jugular compression

›Hyperosmolar therapy immediately

›Mannitol 20% 1 g/kg IV bolus OR

›Hypertonic saline 23.4% 30 mL IV via central line

›Brief hyperventilation as bridge

›PaCO2 30-35 mmHg during active herniation only

›Not for maintenance; causes cerebral vasoconstriction and ischemia

›Neurosurgery and neurology activation immediately

Monitoring targets

›ICP and CPP monitoring

›ICP target <20-22 mmHg

›Sustained ICP >22 mmHg warrants treatment per Brain Trauma Foundation guidelines

›External ventricular drain is gold standard and allows therapeutic CSF drainage

›CPP target 60-70 mmHg

›Level IIB recommendation Brain Trauma Foundation 2016

›Avoid CPP >70 mmHg due to ARDS risk from aggressive vasopressor use

›Neuromonitoring bundle

›Continuous EEG if seizure risk

›Post-TBI seizure prophylaxis with levetiracetam 7 days

›Non-convulsive status epilepticus elevates ICP

›Pupillometry every hour

›Quantitative pupillometry more reliable than clinical assessment

›Neurological Pupil index (NPi) <3 associated with poor outcome

›Temperature management

›Target normothermia 36-37°C

›Fever increases cerebral metabolic demand and worsens ICP

Consult triggers

›Neurosurgery

›Surgical mass lesion on CT

›Epidural or subdural hematoma with mass effect

›Cerebral abscess or tumor causing herniation

›Hydrocephalus requiring EVD or shunt

›Refractory ICP despite maximal medical therapy

›Neurology

›New papilledema workup

›Suspected IIH or cerebral venous thrombosis

›Seizure management

›Ophthalmology

›Papilledema with visual field loss

›Sixth nerve palsy assessment

02History/hx82

Headache characterization

›ICP headache features

›Morning predominance

›Worsened by recumbency and nocturnal CO2 rise

›Improves upright within 30 minutes

›Valsalva aggravation

›Coughing, straining, bending forward

›Sneezing or holding breath

›Progressive course

›Weeks to months in subacute causes

›Acute severe onset suggests hemorrhage

›Associated symptoms

›Nausea and vomiting

›Projectile vomiting without preceding nausea in posterior fossa lesions

›Persistent vomiting with worsening headache is alarming

›Visual symptoms

›Transient visual obscurations lasting seconds

›Horizontal diplopia from CN VI palsy (false localizing sign)

›Progressive visual field loss in IIH

›Pulsatile tinnitus

›Unilateral, pulse-synchronous

›Associated with IIH and venous sinus stenosis

Alarm features in history

›Acute high-risk features

›Thunderclap onset

›Worst headache of life instantaneous onset

›Subarachnoid hemorrhage until proven otherwise

›Fever with headache and stiff neck

›Meningitis or encephalitis

›Urgent LP consideration after imaging

›Head trauma

›Mechanism and loss of consciousness duration

›Anticoagulant or antiplatelet use increases hemorrhage risk

›Subacute high-risk features

›Focal neurologic deficits

›Timing of onset relative to headache

›Weakness, speech difficulty, or sensory change

›New seizures

›First seizure with headache warrants neuroimaging

›Postictal focal deficit suggests structural lesion

›Altered consciousness or behavioral change

›Encephalopathy onset timing

›Witness account of confusion or personality change

Etiology-specific history

›Traumatic etiology

›TBI: falls, MVCs, assaults

›Most common acute cause of elevated ICP

›Lucid interval before deterioration suggests epidural hematoma

›Mechanism details

›Direct impact vs deceleration

›Helmet use, restraint use

›IIH history

›Female sex, childbearing age

›Incidence 20 per 100,000 in obese women of childbearing age

›BMI >30 strongest risk factor

›Recent weight gain

›Medication exposures

›Tetracyclines: minocycline, doxycycline

›Retinoids: isotretinoin, vitamin A supplements

›Growth hormone, lithium

›Corticosteroid withdrawal

›Vascular history

›OCP use, pregnancy, postpartum state

›Cerebral venous sinus thrombosis risk

›Headache onset relative to delivery

›Hypercoagulable states

›Known thrombophilia, malignancy

›Prior DVT or PE

Past medical and medication history

›Relevant prior diagnoses

›Prior TBI or neurosurgery

›VP shunt in situ: shunt malfunction most common cause of ICP in shunted patients

›Prior intracranial neoplasm

›Known systemic malignancy

›Metastatic brain lesions common in lung, breast, melanoma

›Leptomeningeal carcinomatosis

›Chronic conditions

›Obesity, sleep apnea, pulmonary hypertension

›Autoimmune: sarcoidosis, lupus (granulomatous meningitis)

›Family history

›Intracranial aneurysms

›First-degree relative with SAH doubles risk

›Polycystic kidney disease association

›Coagulopathy or thrombophilia

›Neurofibromatosis or tuberous sclerosis

›CNS tumor predisposition

03Physical Exam/exam71

Vital signs and general

›Hemodynamic and vital sign assessment

›Cushing triad presence

›Hypertension: systolic often >160 mmHg

›Bradycardia: HR typically <60

›Irregular respirations: Cheyne-Stokes or ataxic

›Temperature

›Fever suggests infectious etiology

›Hypothermia in severe hypothalamic dysfunction

›Respiratory rate and pattern

›Hyperventilation from herniation

›Cheyne-Stokes pattern in central herniation

Neurologic examination

›Level of consciousness

›GCS documentation E/V/M

›GCS <=8 defines severe brain injury

›Serial GCS trend more informative than single value

›AVPU scale for rapid triage

›Alert, Voice, Pain, Unresponsive

›Pupillary examination

›Pupil size and reactivity

›Unilateral fixed dilated pupil: uncal herniation CN III compression

›Bilateral fixed dilated: brainstem compression or terminal

›Sensitivity of pupillary dilation for elevated ICP 28%, specificity 86%

›Relative afferent pupillary defect

›Optic nerve or visual pathway injury

›Swinging flashlight test

›Fundoscopy

04Differential Diagnosis/ddx68

Life-threatening causes

›Intracranial hemorrhage

›Epidural hematoma

›ICD-10 S06.4

›Lucid interval followed by rapid deterioration

›Arterial bleed (middle meningeal artery); biconvex lens shape on CT

›Subdural hematoma

›ICD-10 S06.5

›Acute: high-density crescent on CT; crosses suture lines

›Chronic: elderly, low-density; may present with subtle cognitive change

›Subarachnoid hemorrhage

›ICD-10 I60

›Thunderclap headache; star/hyperdense basal cisterns on CT

›CT sensitivity 98% within 6 hours; LP if CT negative

›Intracerebral hemorrhage

›ICD-10 I61

›Focal deficit onset with headache and hypertension

›Anticoagulant reversal priority

›Mass lesions

›Primary or metastatic brain tumor

›ICD-10 C71 primary; C79.31 secondary

›Vasogenic edema surrounding lesion; ring enhancement

›Lung, breast, melanoma most common metastatic sources

›Cerebral abscess

›ICD-10 G06.0

›Ring-enhancing lesion with restricted diffusion on MRI

›Fever and immunocompromise history

›Subdural empyema

05Laboratory Tests/lt67

Core metabolic and hematologic panel

›Complete blood count

›Leukocytosis

›Bacterial infection, abscess, or empyema

›Steroid-induced leukocytosis confounds

›Thrombocytopenia

›Coagulopathy risk with intracranial hemorrhage

›Platelet >100,000 before LP

›Anemia

›Reduced oxygen delivery to brain

›Comprehensive metabolic panel

›Serum sodium

›Hyponatremia causes cerebral edema

›Hypernatremia target with hypertonic saline therapy Na <160 mmol/l

›Renal function

›Mannitol clearance and osmol gap monitoring

›Contrast nephropathy risk assessment

›Glucose

›Hypoglycemia mimics brain injury; correct immediately

›Hyperglycemia worsens outcome in TBI; target 6-10 mmol/l

›Coagulation studies

›PT/INR and aPTT

›Warfarin or coagulopathy reversal need

›Target INR <1.5 before neurosurgical intervention

›Anti-Xa level if LMWH or direct anticoagulant use

›Fibrinogen and TEG if major hemorrhage

Osmolality and osmotherapy monitoring

›Serum osmolality

06Diagnostic Tests/dt105

Scoring Systems

›ICP-related scoring systems

›Glasgow Coma Scale

›Eye: 4 (spontaneous) to 1 (none)

›Verbal: 5 (oriented) to 1 (none)

›Motor: 6 (obeys) to 1 (none)

›Total 3-15; score <=8 defines severe TBI

›Rotterdam CT Score for TBI

›Predicts 6-month mortality after TBI

›Basal cisterns, midline shift, epidural mass, and IVH scored

›Score 1-6; score 6 predicts 97% mortality

›Marshall CT Classification

›Diffuse Injury I-IV and mass lesion categories

›Guides ICP monitoring need and surgical planning

›Modified Rankin Scale

›Functional outcome assessment 0-6

›Used for TBI and stroke outcome tracking

›IIH diagnostic criteria (revised Friedman criteria)

›Criteria requirements

›Papilledema present

›Normal neurologic exam except CN VI palsy

›Normal neuroimaging (no mass, hydrocephalus, meningeal enhancement)

›Normal CSF composition

›Opening pressure >=250 mmH2O in non-obese; >=200 mmH2O may apply in obese

›Monro-Kellie doctrine

›Physiologic framework

›Fixed cranial vault volume

›Volume: brain 80%, blood 10%, CSF 10%

›Initial compensatory buffering then exponential ICP rise

›Explains why small volume changes cause large ICP spikes at plateau

MRI

›MRI brain with contrast

›Indications

›IIH workup (exclude secondary causes)

›Cerebral venous thrombosis

›Posterior fossa lesions (CT limited by bone artifact)

›Meningeal processes and leptomeningeal disease

›Suspected HSV encephalitis

›ICP-specific MRI signs

›Empty sella or partially empty sella

›Flattening of posterior globe (>20% flattening threshold)

›Distended optic nerve sheaths >5.5 mm

›Transverse sinus stenosis or narrowing

›Tonsillar descent below foramen magnum

›Sequences

›DWI/ADC: restricted diffusion in abscess, acute ischemia, herpes

›FLAIR: white matter edema, PRES, contusions

›T1 with gadolinium: ring-enhancing lesion, meningeal enhancement

›T2*: hemorrhage detection (GRE or SWI)

›MRV (MR venography)

›Cerebral venous sinus thrombosis

›Filling defect in dural venous sinus

›Superior sagittal or transverse sinus most common

›Sensitivity 90-100% for major sinus thrombosis

›Transverse sinus stenosis in IIH: stenting emerging option

CT

›Non-contrast CT head

›First-line imaging for acute ICP

›Rapid, widely available, no contrast needed

›Identifies hemorrhage, mass lesion, hydrocephalus, midline shift

›Sensitivity for epidural hematoma >95%

›CT ICP signs

›Basal cistern compression: sensitivity 86%, specificity 61% for ICP >20 mmHg

›Midline shift: sensitivity 81% for elevated ICP

›Midline shift >=10 mm: specificity 89%

›Sulcal effacement, loss of grey-white differentiation

›Contraindications to LP based on CT

›Midline shift or uncal herniation

›Non-communicating hydrocephalus

›Posterior fossa mass

›CT angiography

›Vascular etiology workup

›Aneurysm rupture (SAH)

›AVM, cavernous malformation

›Sensitivity 98-100% for aneurysm >3 mm

›CT venography

›Alternative to MRV for cerebral venous thrombosis

›Can be performed with CT angiography in same contrast run

›CT with contrast

›Ring-enhancing lesion evaluation

›Abscess vs necrotic tumor

›DWI MRI preferred to differentiate

›Toxoplasmosis in HIV-positive patients

Ultrasound

›Optic nerve sheath diameter (ONSD)

›Point-of-care technique

›Linear probe 7.5-10 MHz applied to closed eyelid

›Measure ONSD 3 mm behind posterior globe

›ONSD >5.0 mm (adults) suggests ICP >20 mmHg

›Diagnostic performance

›AUROC 0.94 for ICP >=20 mmHg (meta-analysis)

›Sensitivity 90%, specificity 84% at 5.0 mm threshold

›Bilateral measurements averaged; bilateral elevation more specific

›Limitations

›Cannot provide continuous ICP monitoring

›Operator-dependent measurement variability

›Confounded by optic nerve pathology and proptosis

›Transcranial Doppler (TCD)

›Pulsatility index measurement

›PI = (Vsystolic - Vdiastolic) / Vmean

›PI >1.19 associated with ICP >20 mmHg

›Poor diagnostic performance: AUROC 0.55-0.72; not recommended as sole tool

›Middle cerebral artery waveform

›Absent diastolic flow or flow reversal suggests critically elevated ICP

›Cerebral circulatory arrest pattern in brain death evaluation

›FAST and extended FAST

›Trauma setting

›Pneumothorax evaluation (tension pneumothorax elevates ICP indirectly via hypoxia)

›Hemopericardium affecting MAP and CPP

07Disposition/dispo44

ICU admission criteria

›ICU-level care triggers

›Neurologic criteria

›GCS <=8 or declining neurologic exam

›Cushing triad or herniation signs present

›Invasive ICP monitoring in situ or planned

›Post-operative neurosurgical patients

›Physiologic criteria

›Refractory ICP requiring osmotherapy or ventilator management

›Hemodynamic instability affecting CPP

›Need for continuous sedation or barbiturate coma

›Seizure requiring continuous EEG monitoring

›Neurosurgery consultation triggers

›Surgical indications

›Epidural hematoma >30 mL or >5 mm thickness or >15 mm shift

›Acute subdural hematoma >10 mm thickness or >5 mm midline shift

›Hydrocephalus requiring EVD

›Posterior fossa hematoma with compression or hydrocephalus

›Refractory ICP for decompressive craniectomy consideration

Step-down and floor admission

›Intermediate care criteria

›New papilledema requiring urgent workup

›Neuroimaging, LP, ophthalmology consult

›Visual field assessment within 24 hours

›New IIH with visual field loss

›Acetazolamide initiation

›Ophthalmology follow-up mandatory

›Cerebral venous thrombosis

08Treatment/t132

Immediate first-tier interventions

›Head positioning

›Head of bed 30 degrees elevation

›Reduces venous outflow resistance and ICP

›Neutral head position; avoid neck rotation or flexion

›Level positioning if hypotensive to maintain CPP

›Hyperosmolar therapy

›Mannitol 20%

›Dose: 0.25-1 g/kg IV bolus over 15-30 minutes

›Onset: 15-30 minutes; duration 4-6 hours

›Mechanism: osmotic dehydration and plasma expansion

›Hold if serum osmolality >320 mOsm/l

›Hold if hemodynamically unstable (osmotic diuresis worsens hypotension)

›Class IIA recommendation Brain Trauma Foundation 2016

›Hypertonic saline 3%

›Dose: 2-5 mL/kg IV bolus over 10-20 minutes

›Alternative: 150-250 mL bolus in adults

›Preferred over mannitol if hypotension present

›Target serum sodium <160 mmol/l

›Hypertonic saline 23.4%

›Dose: 30 mL IV via central line only

›Reserved for refractory ICP or active herniation

›Rapid onset within 5-10 minutes

›Monitor for central pontine myelinolysis with rapid correction

›CSF drainage

›External ventricular drain

›Gold standard diagnostic and therapeutic

›Intermittent drainage to keep ICP <20 mmHg

›Continuous monitoring with intermittent drainage protocol

›Risk: infection rate 2-22% increasing with duration

Ventilatory management

›Controlled ventilation targets

›Normocapnia maintenance

›PaCO2 35-40 mmHg target

›Avoid hypercapnia: cerebral vasodilation increases ICP

›Monitor with end-tidal CO2 correlated to ABG

›Therapeutic hyperventilation (bridge only)

›PaCO2 30-35 mmHg during acute herniation

›Duration limited to minutes to hours maximum

›Prophylactic hyperventilation to PaCO2 <30 mmHg contraindicated

›Risk: cerebral ischemia from excessive vasoconstriction

›PEEP management

›Moderate PEEP (5-8 cmH2O) generally well tolerated

›High PEEP (>10 cmH2O) may impair venous drainage

›Titrate to balance oxygenation and ICP

Sedation and analgesia

›Sedation protocol

›Propofol infusion

›Dose: 5-50 mcg/kg/min continuous infusion

›Reduces cerebral metabolic rate of oxygen (CMRO2)

›Propofol infusion syndrome risk at doses >80 mcg/kg/min >48 hours

›Monitor triglycerides and lactate

›Midazolam

›Dose: 0.02-0.1 mg/kg/hr continuous infusion

›Alternative if propofol not tolerated

›Accumulates in renal failure

›Fentanyl

›Dose: 25-100 mcg/hr continuous infusion

›Minimizes pain-related ICP spikes during suctioning

›Minimal effect on ICP at analgesic doses

›Neuromuscular blockade

›Cisatracurium or vecuronium for refractory ICP spikes

›Reserved for severe ICP surges uncontrolled by sedation

›Impairs neurologic monitoring; use with continuous EEG

›Dose: cisatracurium 0.1-0.2 mg/kg bolus; 1-3 mcg/kg/min infusion

Second-tier therapies

›Barbiturate therapy

›Pentobarbital

›Load: 10 mg/kg IV over 30 minutes; then 5 mg/kg/hr x3 hours

›Maintenance: 1-4 mg/kg/hr titrated to burst suppression on EEG

›Burst suppression target: 5-10 second suppression intervals

›Requires continuous EEG monitoring and hemodynamic support

›Risk: hypotension requiring vasopressors; cardiac depression

›Last-tier for refractory ICP only

›Therapeutic hypothermia

›Target temperature 32-33°C

›Reduces CMRO2 by 6-7% per degree Celsius reduction

›Reduces ICP 1-10 mmHg

›Duration 48-72 hours; controlled rewarming 0.25°C/hour

›Risk: coagulopathy, arrhythmia, infection, electrolyte shifts

Cause-specific treatments

›Vasogenic edema (tumor, abscess)

›Dexamethasone

›Dose: 10 mg IV loading dose; then 4 mg IV every 6 hours

›Highly effective for tumor-associated vasogenic edema

›NOT effective for cytotoxic edema (TBI, ischemic stroke)

›Onset 6-12 hours; not for acute herniation management

›Risk: hyperglycemia, immunosuppression

›Idiopathic intracranial hypertension

›Acetazolamide

›Dose: 500-1000 mg BID orally; titrate to 4 g/day maximum

›Mechanism: reduces CSF production by inhibiting carbonic anhydrase

›Onset weeks; monitor potassium (causes hypokalemia)

›Level A evidence for IIH (IIHTT trial)

›Weight loss

›Target 5-10% body weight reduction

›Even modest loss significantly lowers opening pressure

›Low-calorie diet 425-1200 kcal/day studied in IIHTT trial

›Therapeutic LP

›Remove CSF to closing pressure 20 cmH2O

›Acute visual threat indication

›Temporary measure; ICP recurs within hours to days

›Surgical options for refractory IIH

›Optic nerve sheath fenestration: protects vision from disc edema

›VP or LP shunt: continuous CSF diversion

›Venous sinus stenting: if transverse sinus stenosis documented

›Cerebral venous thrombosis

›Anticoagulation

›Heparin IV or LMWH even if hemorrhagic venous infarction present

›AHA/ASA Class I recommendation based on meta-analysis

›Transition to warfarin or DOAC after 3-6 months

›Endovascular thrombectomy

›Consider if deteriorating despite anticoagulation

›Seizure prophylaxis

›Levetiracetam

›Dose: 500-1500 mg IV BID

›Standard for post-TBI prophylaxis x7 days

›Level IIA Brain Trauma Foundation

›Preferred over phenytoin (fewer drug interactions, no monitoring)

Surgical interventions

›Decompressive craniectomy

›Indications

›Refractory ICP >20 mmHg despite maximal medical therapy

›Large hemispheric infarction (malignant MCA syndrome)

›Cochrane 2019: reduces mortality but increases survival with disability

›DECRA trial: early craniectomy improved ICP but not outcomes at 6 months

›Surgical technique consideration

›Unilateral (hemi-craniectomy) vs bilateral depending on pathology

›Durotomy essential component

›Mass lesion evacuation

›Surgical indications for hemorrhage

›Epidural hematoma >30 mL or causing neurologic deterioration

›Acute subdural >10 mm or >5 mm shift with worsening GCS

›Cerebellar hematoma >3 cm or causing brainstem compression

›Aspiration or drainage for abscess

›Stereotactic aspiration for accessible deep lesions

›Open craniotomy for multiloculated or superficial lesions

›Combined with targeted antibiotics 4-8 weeks

09Special Populations/sp118

Pregnancy

›Physiologic considerations in pregnancy

›Hemodynamic changes

›Increased blood volume 40-50% by third trimester

›Reduced MAP due to systemic vasodilation

›CPP calculation affected by lower baseline MAP

›CSF pressure changes

›Slightly elevated CSF pressure in third trimester

›IIH risk increased in pregnancy and postpartum

›Hormone fluctuations implicated in ICP elevation

›IIH in pregnancy

›Risk profile

›Most common in first trimester

›Weight gain in pregnancy exacerbates IIH

›Visual loss is primary risk requiring urgent treatment

›Treatment modifications

›Acetazolamide: limited data; avoid first trimester

›Category C; weigh visual threat vs teratogenicity

›Serial LP preferred for acute management in pregnancy

›Weight management counseling

›Imaging considerations

›MRI preferred over CT for fetal radiation exposure

›No contrast gadolinium unless essential (Category C)

›Non-contrast MRI safe at all gestational ages

›CT head if maternal life-threatening emergency

›Fetal dose <0.1 mGy from cranial CT; acceptable for acute emergency

›Drug safety in pregnancy

›Mannitol: use with caution

›Theoretical fetal dehydration risk

›Acceptable for life-threatening maternal herniation

›Dexamethasone: generally safe

›May accelerate fetal lung maturity if preterm

›Avoid: prophylactic phenytoin (teratogenic)

›Anticoagulation for CVT: LMWH preferred; warfarin and DOACs avoided

›Cerebral venous thrombosis post-partum

›Highest risk in first 4 weeks postpartum

›Headache with or without focal deficits

›MRV diagnostic

›LMWH therapeutic anticoagulation

Geriatric

›Age-related physiologic changes

›Brain atrophy effects

›Greater subdural space allows large blood collections before symptoms

›Chronic subdural hematoma may present insidiously

›Baseline cognitive impairment complicates GCS interpretation

›Cerebrovascular compliance

›Reduced cerebrovascular autoregulation reserve

›Narrower therapeutic range for CPP targets

›Cerebral small vessel disease increases vulnerability to secondary injury

›Fall risk and hemorrhage patterns

›Anticoagulant use prevalence

›Warfarin, apixaban, rivaroxaban common in elderly

›Reversal: vitamin K + 4-factor PCC for warfarin; andexanet for anti-Xa agents

›Target INR <1.5 before surgical intervention

›Subdural hematoma

›Most common traumatic intracranial injury in elderly

›Bridging vein vulnerability increased with brain atrophy

›Bilateral in 20-25% of chronic cases

›Medication considerations

›Acetazolamide in geriatric patients

›Increased risk of hypokalemia and metabolic acidosis

›Monitor electrolytes frequently

›Dose reduce with renal impairment

›Mannitol caution

›Pre-existing renal impairment common; monitor creatinine

›Dehydration risk from osmotic diuresis

›Corticosteroids

›Increased risk of hyperglycemia and infection

›Careful monitoring for delirium

›Frailty and goals of care

›Poor prognosis indicators

›Age >70 with GCS <6 and bi-hemispheric injury

›Early goals of care discussion with family

›Aggressive intervention decision-making

›Decompressive craniectomy in elderly: survival with disability risk high

›Individualized based on premorbid function and patient wishes

Pediatrics

›Age-specific normal ICP values

›Normal ICP by age

›Neonates: 1.5-6 mmHg

›Infants: 1.5-6 mmHg; open fontanelle partially buffers

›Children 3-7 years: 3-7 mmHg

›Older children/adolescents: 5-15 mmHg (similar to adults)

›Treatment threshold

›ICP >20 mmHg warrants treatment in all pediatric ages

›CPP target 40-50 mmHg in younger children; 50-60 mmHg in adolescents

›Clinical presentation differences

›Infants

›Bulging anterior fontanelle (palpable sign of elevated ICP)

›Irritability, poor feeding, high-pitched cry

›Sunsetting sign: downward gaze palsy in infants

›Head circumference increase with chronic elevation

›Children

›Headache and vomiting common; may not communicate well

›Behavioral changes and school performance decline

›Sixth nerve palsy as false localizing sign (same as adults)

›Pediatric TBI considerations

›Abusive head trauma (AHT)

›Subdural hematoma in infants without adequate trauma history

›Retinal hemorrhages on fundoscopy

›American Academy of Pediatrics technical report 2025

›Mandatory reporting obligation

›Management differences

›ICP monitoring threshold: GCS <=8 with salvageable injury

›Hypertonic saline preferred over mannitol in pediatric TBI

›Avoid prophylactic hypothermia: COOLKIDS trial showed harm

›Pediatric IIH

›Age-specific features

›Pre-pubertal: equal sex distribution; obesity less common

›Post-pubertal: female predominance, obesity similar to adults

›More commonly associated with systemic illness or medications

›Treatment

›Acetazolamide: dose 25 mg/kg/day divided BID to max 100 mg/kg/day

›Weight management in obese adolescents

›Serial LP for acute visual threat

›Hydrocephalus in children

›VP shunt malfunction

›Most common complication of treated pediatric hydrocephalus

›Classic triad: headache, vomiting, altered consciousness

›Shunt series X-ray and CT head

›Neurosurgical emergency if shunt valve failure confirmed

10Background/b113

Epidemiology

›Incidence and prevalence

›Traumatic brain injury (most common acute cause)

›TBI incidence approximately 200-300 per 100,000 per year globally

›Leading cause of death and disability under age 45

›Falls most common mechanism in elderly; MVCs in young adults

›Mortality for severe TBI (GCS <=8) approximately 30-40%

›Idiopathic intracranial hypertension

›Overall incidence 1-3 per 100,000 per year

›Incidence in obese women of childbearing age: 20 per 100,000 per year

›Prevalence increasing with rising obesity rates globally

›Female:male ratio 8:1 in reproductive years

›Cerebral venous sinus thrombosis

›Incidence 1.5-3 per 100,000 per year

›Female predominance; OCP most common modifiable risk factor

›Mortality 5-10%; significant neurologic morbidity in survivors

›Mortality and morbidity by etiology

›Epidural hematoma

›Mortality 5-10% with prompt surgical intervention

›Without treatment: near 100% mortality from herniation

›Subdural hematoma

›Acute: mortality 40-60% in elderly with GCS <=8

›Chronic: good prognosis with drainage; recurrence 10-20%

›Raised ICP in meningitis

›Bacterial meningitis: mortality 20-30% even with treatment

›Associated herniation risk with LP without prior CT

Pathophysiology

›Monro-Kellie doctrine and compensatory mechanisms

›Fixed intracranial volume

›Total cranial volume approximately 1700 mL (adult)

›Brain parenchyma 1400 mL, CSF 150 mL, blood 150 mL

›Any added volume must displace brain, blood, or CSF

›Initial compensation

›CSF displacement into spinal subarachnoid space

›Venous blood displacement from dural sinuses

›Compliance curve: flat initially then exponential rise

›Decompensation

›Compensatory reserve exhausted; exponential ICP rise

›Small additional volume causes catastrophic ICP spikes

›Cerebral autoregulation

›Normal autoregulation

›Maintains CBF 50 mL/100 g/min over MAP range 50-150 mmHg

›Myogenic and metabolic mechanisms

›Impaired in TBI and malignant hypertension

›CPP and ICP relationship

›CPP = MAP - ICP

›Critical closing pressure: CPP <40 mmHg causes ischemia

›Pressure reactivity index (PRx) monitors autoregulation status

›Cerebral edema types

›Vasogenic edema

›Blood-brain barrier disruption; protein-rich fluid

›Tumor, abscess, inflammation around lesion

›Responds to corticosteroids

›Cytotoxic edema

›Intracellular swelling from Na/K pump failure

›Ischemic stroke, severe TBI, hypoxic injury

›Does NOT respond to corticosteroids

›Osmotic therapy (hypertonic saline) partially effective

›Interstitial edema

›Transependymal CSF absorption in obstructive hydrocephalus

›Periventricular white matter signal on MRI

›Herniation syndromes

›Uncal herniation

›Temporal lobe uncus displaces over tentorium

›CN III compression: ipsilateral fixed dilated pupil

›PCA compression: contralateral visual field loss

›Ipsilateral hemiparesis from Kernohan notch (contralateral peduncle compression)

›Central transtentorial herniation

›Bilateral downward displacement

›Diencephalon and midbrain compression

›Cheyne-Stokes breathing progressing to central hyperventilation

›Tonsillar herniation

›Cerebellar tonsils through foramen magnum

›Medullary compression: respiratory and cardiac arrest

›Most deadly herniation pattern

Therapeutic Considerations

›Evidence base for osmotherapy

›Mannitol vs hypertonic saline

›Cochrane 2020: HTS likely superior to mannitol for ICP reduction in TBI

›No significant mortality difference between agents

›HTS preferred if hemodynamically unstable

›Equimolar doses show similar ICP-lowering efficacy

›Osmotherapy monitoring

›Serum osmolality every 4-6 hours during active treatment

›Serum sodium every 4-6 hours with HTS

›Renal function daily with mannitol; nephrotoxic with prolonged use

›ICP monitoring evidence

›BEST-TRIP trial

›Randomized controlled trial of ICP monitoring in TBI (2012)

›ICP monitoring vs imaging-clinical examination protocol

›No mortality difference at 6 months

›ICP monitoring remains standard in severe TBI in resource-rich settings

›EVD vs intraparenchymal monitor

›EVD gold standard: allows CSF drainage and calibration

›Intraparenchymal bolt: lower infection risk, no drainage

›Brain Trauma Foundation: Level IIB recommendation for monitoring

›Medications that elevate ICP (to avoid or discontinue)

›Strongly associated medications

›Tetracyclines: minocycline, doxycycline (drug-induced IIH)

›Retinoids: isotretinoin, vitamin A excess

›Recombinant growth hormone

›Lithium

›Moderately associated

›Corticosteroid withdrawal (rebound ICP elevation)

›Antihypertensives to avoid in elevated ICP

›Nifedipine, chlorpromazine, reserpine

›Risk: cerebral vasodilation raising ICP and decreasing CPP

›Emerging and adjunctive therapies

›Albumin infusion

›SAFE trial: albumin associated with higher mortality in TBI vs saline; avoided

›Progesterone

›Phase III trials (ProTECT III, SyNAPSe) showed no benefit in TBI

›Tranexamic acid

›CRASH-3 trial: reduces head injury death if given within 3 hours of injury

›Dose: 1 g IV over 10 minutes; then 1 g over 8 hours

›Benefits greatest in mild-moderate TBI (GCS 9-15)

11Patient Discharge Instructions/pdi36

copy discharge instructions

›Discharge instructions for increased intracranial pressure

›What you were treated for

›You were assessed for increased pressure inside your skull (intracranial pressure)

›This can be caused by conditions such as idiopathic intracranial hypertension, headache disorders, or other conditions affecting the brain

›Your tests today showed your condition is safe for discharge with close follow-up

›Medications prescribed

›Take all prescribed medications exactly as directed

›If prescribed acetazolamide, take with food to reduce stomach upset

›Do not stop any medications without speaking to your doctor first

›Diet and lifestyle

›If overweight, weight loss is one of the most effective treatments for idiopathic intracranial hypertension

›Avoid vitamin A supplements, cod liver oil, and liver in large amounts

›Avoid tetracycline-class antibiotics unless prescribed and discussed with your specialist

›Limit sodium intake if on hypertonic saline or diuretic therapy

›Activity restrictions

›Avoid heavy lifting, straining, or any activity that causes head pressure

›No diving or activities causing rapid pressure changes without medical clearance

›Do not drive until cleared by your doctor if you had vision changes or seizures

›Monitoring your vision

›Check vision daily; any sudden vision loss requires immediate ER return

›Cover one eye at a time to detect monocular vision loss

›Transient flickering of vision lasting seconds is a warning sign; notify your doctor

›Return to emergency immediately if

›Red flag symptoms requiring immediate return

›Worst headache of your life or headache that starts suddenly like a thunderclap

›New or worsening vision loss or double vision

›Vomiting that you cannot control

12References/r28

Guidelines and key sources

›Brain Trauma Foundation guidelines

›Carney N, Totten AM, et al. Guidelines for the Management of Severe Traumatic Brain Injury, 4th Edition. Brain Trauma Foundation, 2016

›ICP treatment threshold >22 mmHg (Level IIB)

›CPP target 60-70 mmHg (Level IIB)

›Osmotherapy recommendations for mannitol and HTS

›Manley GT, Albert MW, Brophy GM, et al. Best Practices in the Management of Traumatic Brain Injury. American College of Surgeons, 2024

›Lulla A, Lumba-Brown A, Totten AM, et al. Prehospital Guidelines for the Management of TBI, 3rd Edition. Prehospital Emergency Care, 2023

›Key clinical trials and systematic reviews

›Stocchetti N, Maas AI. Traumatic Intracranial Hypertension. N Engl J Med, 2014

›Comprehensive review of ICP pathophysiology and management

›Chen H, Song Z, Dennis JA. Hypertonic Saline vs Other ICP-Lowering Agents for Acute TBI. Cochrane Database Syst Rev, 2020

›HTS likely superior to mannitol for ICP reduction

›Sahuquillo J, Dennis JA. Decompressive Craniectomy for High ICP in Closed TBI. Cochrane Database Syst Rev, 2019

›Reduces mortality but increases survival with disability

›Fernando SM, Tran A, Cheng W, et al. Diagnosis of Elevated ICP in Critically Ill Adults: Systematic Review and Meta-Analysis. BMJ, 2019

›Diagnostic and non-invasive monitoring

›Olaru C, Langberg S, McCoin NS. Clinical Presentation, Causes, and Diagnostic Evaluation of Increased ICP in the ED. West J Emerg Med, 2024

›CT basal cistern compression sensitivity 86%, specificity 61%

›ONSD AUROC 0.94 for ICP >=20 mmHg

›Sallam A, Alkhatip MA, Kamel MG, et al. Diagnostic Accuracy of Noninvasive Methods to Measure ICP. Anesth Analg, 2021

›D'Antona L, Asif H, Craven CL, et al. Brain MRI and Ophthalmic Biomarkers of Intracranial Pressure. Neurology, 2021

›IIH and special topics

›Horton JC. Idiopathic Intracranial Hypertension. N Engl J Med, 2025

›Comprehensive review of IIH epidemiology, pathophysiology, and treatment

›Saposnik G, Bushnell C, Coutinho JM, et al. Diagnosis and Management of Cerebral Venous Thrombosis. AHA Scientific Statement, Stroke, 2024

›Tan MG, Worley B, Kim WB, et al. Drug-Induced Intracranial Hypertension: Systematic Review. Am J Clin Dermatol, 2020

›Narang SK, Haney S, Duhaime AC, et al. Abusive Head Trauma in Infants and Children: Technical Report. Pediatrics, 2025

Evidence & Review