neurovascular injuries and closed head injuries Flashcards

(71 cards)

1
Q

head trauma statistics: what gender, age group, mcc, common findings, complications

A

-Men>Women
-Trimodal: Ages 0-4, 15-24, >75 yo
-MC MOI: FALLS, MOTOR VEHICLE ACCIDENT,
pedestrian/bike, projectiles, assaults, sports, abuse
-Common findings: Loss of consciousness, scalp hematoma, vomiting (13%), headache (46%)
-Complications: Post-traumatic seizure (1%), skull fractures , bleeds, concussions

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2
Q

key history questions for head trauma

A

-Was it a High risk MOI: falling >3-5 feet, motor vehicle collision, penetrating trauma
-was there loss of consciousness?
-Confusion
-Seizure
-Severe or worsening headache
-Vomiting
-does pt have known arteriovenous malformation or bleeding disorder?
-Child: Acting normally?

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3
Q

traumatic brain injury: definition and severity scale

A

Definition:
-brain function impairment as a result of external force
-Clinical manifestations are broad: brief confusion, coma, disability, to death

Measure severity using GCS:
- Mild (80% TBIs): GCS 13-15; possible CT using scoring tools
- Moderate: GCS 9-12; head CT
- Severe: GCS < 9; immediate head CT; mortality = 40%

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4
Q

TBI: GCS scoring in relation to what imaging they need -> Canadian head CT rules inclusion and exclusion criteria

A

If GCS under 13: NEED head CT; this is for GCS 13-15 with at least one of the following:
- loss of consciousness
- amnesia to the head injury event
- witnessed disorientation

Exclusion criteria:
- under 16
- pt on blood thinners
- seizures after injury or anticoagulation use

Note:
-HIGH sensitivity 83-100% for clinically important brain injuries
-HIGH sensitivity 100% for injury requiring neurosurgery
-No false negatives for serious injury: serious brain injuries are reliably detected

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5
Q

what is the canadian CT head rule

A

If GCS under 13: NEED head CT; this is for GCS 13-15 with at least one of the following:
- loss of consciousness
- amnesia to the head injury event
- witnessed disorientation

NEED CT if they have anything from below:

High-Risk Criteria (for Neurological Intervention):
- GCS score < 15 at 2 hours post-injury
- Suspected open or depressed skull fracture.
- Signs of basal skull fracture (ex: hemotympanum, raccoon eyes, Battle’s sign, CSF leakage from ears or nose)
- Vomiting 2+ episodes
- Age 65+

Medium-Risk Criteria (for Brain Injury on CT):
If any of the following apply, the patient should
- Amnesia for events before impact lasting 30+ min
- Dangerous mechanism of injury (pedestrian struck by vehicle, occupant ejected from vehicle, fall from a height of >3-5 ft)

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6
Q

TBI: phases

A

Primary phase: at the time of impact
- Due to BLEEDING or DIRECT TRAUMA
-Includes:
-Hematoma (EDH/SDH)
-SAH
-Contusion
-Diffuse axonal injury

Secondary phase: hours/days later
- due to IMPAIRED CEREBRAL BLOOD FLOW -> often the cause of cognitive difficulties
-Causes:
-Edema / ↑ ICP
-Small vessel bleed
-Inflammation
-Physiologic dysfunction
-Often the cause cognitive difficulties

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7
Q

PECARN: pediatric head CT rules

A

Determines which patients DO NOT NEED a CT scan
-PECARN screening tool for pediatric patients: split into under 2 and 2-16 yrs

Note: If GCS<15, AMS, palpable skull fracture/signs of basillar skull fracture they require CT **
- CT in children does cause RISK of BRAIN CANCER

Possible CT:
- LOC
- severe vomiting
- severe headache
- severe mechanism

Severe mechanism definition:
-motor vehicle collision WITH -> Ejection, rollover, vs. pedestrian, death at scene
-High impact object
-Fall >3ft (<2yo) or >5ft (>2yo)

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8
Q

concerning findings in kids

A

Basilar skull fracture:
- HEMOTYMPANUM (1st sign -> do ear exam!!!)
- raccoon eyes (tarsal plate sparing)
- halo sign: indicates CSF mixed with blood; place csf on gauze
- postauricular ecchymosis

orbital fracture:
occipital scalp hematoma (non frontal)
Depressed skull fracture

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9
Q

Mild TBI (mTBI) vs concussion

A

Mild: 13-15 ± brief LOC (<30min)
-Trauma induced alteration in mental status : GCS 13-15 ± brief LOC (<30min)
-mTBI may lead to significant, debilitating short- and long-term sequelae.
-concussion: the S&S that occur after a mTBI; Trauma-induced brain dysfunction w/o structural injury

-“Mild” is a misnomer -> -Often used interchangeably with “concussion” WRONG
-Moderate TBI: GCS 9-12
-Severe TBI: GCS ≤8

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10
Q

Concussion: MOA

A

Definition: Sequelae of S/S after a mild TBI = Jolting of the head

MOA: Functional not structural injury*
- Shear forces disrupt neural membranes -> K+ efflux out of neuron to the ECF
- increase of Ca 2+ and excitatory amino acids
- followed by further potassium efflux and subsequent SUPPRESSION of neuron activity

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11
Q

concussion MCC and risk factors

A

-MC in elderly = Falls
-MC in young = Motor vehicle accident

Risk factors:
-Previous concussions
-Younger age
-High risk sports (football, ice hockey, lacrosse, rugby, womens soccer)
-Female > male

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12
Q

concussion: early vs late symptoms

A

S/S (Early): within hours
- Confusion and Amnesia = hallmarks!!!!*
-Retrograde amnesia: loss of recall for events immediately before
-Anterograde amnesia: loss of recall for events immediately after
- Headache
- Dizziness
- Nausea/vomitting
- Mental fogging/slowing
- Concentration difficulties
- others: fatigue, lack of awareness of surroundings, unsteadiness

S/S (Late): within hours/days
- Mood or cognitive disturbances
- Sensitivity to light/noise
-Sleep disturbances

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13
Q

Concussion: signs

A

-Incoordination
-No focal neuro deficits

Neuropsychiatric impairments:
-Emotionality out of proportion**
-Memory deficit *
-Vacant stare
-Delayed verbal expression
-Inability to focus
-Disorientation
-Slurred or incoherent speech

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14
Q

Concussion testing and dx:

A

Testing:
-Neuro exam
-Mental status exam
-Standardized assessment of concussion (SAC) or Sport concussion assessment tool (SCAT5)
-Consider CT head NON-contrast based on Canadian CT head or PECARN criteria

Diagnosis:
-Hx of head injury ± brief LOC
-Neurologic symptoms: Confusion/memory loss
-GCS

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15
Q

concussion/MTIBI tx

A

Step 1: initial rest
-Observation for 24 hours
-Physical and cognitive rest 24-48 hours-> Gradual return to activity
-Analgesics for pain
-avoid medications that alter cognition (opioids, tramadol, muscle relaxers, benzos, ETOH, ilicit drugs, aspirin, sleeping pills)
- limit screen time
- don’t drive until cleared by profession
- return to play/sport once cleared by healthcare professional

consider:
-Referral to concussion specialist: Physiatrist, sports medicine, neurologist
-if prolonged symptoms >21 days
-Hx of multiple concussions
-Uncertain diagnosis

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16
Q

concussion: return to play protocol

A
  • any LOC episode -> ER for evaluation
    -Suspected Cervical -spine injury -> immobilize, ER
    -High impact, high risk -> ER
    -Skull fracture findings -> ER
    -Seizure post trauma -> ER
    -Focal neuro signs (weakness, confusion, or imbalance) -> ER

Suspected concussion should be removed from play immediately -> When in doubt, sit them out!”
-Re-evaluation in 1-2 days with specialist
-Clearance by licensed health professional usually requires symptom resolution off meds

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17
Q

concussion injury advice

A

-If you notice any change in behavior, vomiting, worsening headache, double vision or excessive drowsiness, please telephone your doctor or the nearest hospital emergency department immediately.
-!!!!!!!!!Initial rest: Limit physical activity to routine daily activities (avoid exercise, training, sports) and limit activities such as school, work, and screen time to a level that does not worsen symptoms.
-1) Avoid alcohol
-2) Avoid prescription or non-prescription drugs without medical supervision. Specifically:
-a) Avoid sleeping tablets
-b) Do not use aspirin, anti-inflammatory medication or stronger pain medications such as narcotics
-3) Do not drive until cleared by a healthcare professional.
-4) Return to play/sport requires clearance by a healthcare professional

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18
Q

concussion recovery time

A

Symptoms often resolve in 72 hours

Most sports related concussion resolve in:
-2 weeks for adults (85%)
-1-3 months for children (70-80%)

The most consistent predictor of prolonged recovery = severity of symptoms immediately after injury

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19
Q

graduated return to play protocol

A

-must be in each stage for 24 hours or longer before you move on
-if you fail a stage -> go back to previous stage

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20
Q

concussion complications

A

1) Post traumatic headaches (25-78%)

2) Post-concussion syndrome
- Similar to concussion except that symptoms last > 3 months (after the brain has healed)

3) Second impact syndrome:
-Fatal brain swelling if a second concussion is sustained before complete recovery from the first concussion

4) Seizures (<5%) – acute symptomatic seizure, not epilepsy
-50% occur within first 24 hours, 25% within first hour
-Increased risk for post traumatic epilepsy

5) Sleep disturbances

6) Chronic traumatic encephalopathy (CTE)

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21
Q

Post-Concussion Syndrome and second impact syndrome

A

Post concussion syndrome:
- typically starts 4 wks after concussion and sx last > 3 months
- sx: Sleep disturbances*, headache, dizziness, cognitive impairment

Second impact syndrome:
- if you get second concussion before complete recovery from 1st -> FATAL brain swelling

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22
Q

arteriovenous malformations (AVMS): defintion, statistics

A

Definition: Direct arterial to venous connections without an intervening capillary network

MC:
- Genetic cause: Hereditary Hemorrhagic Telangiectasia; aka osler-weber-rendu syndrome-> autosomal dominant
- MC location: supratentorial region (90%!!)

Incidence:
- 1-2% of all strokes,
- 3% of strokes in young adults,
- 9% of spontaneous subarachnoid hemorrhages (SAH)

Presentation: bimodal
- childhood
- 30-50
- M>F

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23
Q

AV malformations: presentation

A

Presentations depends on the symptoms produced

-Intracranial Hemorrhage (40-60%): MC intraparenchymal***
-Seizure (10-30%): focal (simple or complex partial) with secondary generalization
-Focal neurologic deficits (caused by mass effect d/t hemorrhage or post-ictal seizure)
-Incidental finding (10-20%)
-Headache (non-specific) - <1%

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24
Q

AV malformations: dx and management

A

Diagnosis
-MRI brain
-CT brain
-+/- CTA or MRA: required for treatment planning and follow up
- suggestive if bruit over eye/mastoid

Acute management:
-Unruptured, no risk factors: OBSERVE! with possible later treatment
-Unruptured, w/ risk factors (low grade 1-2): Microsurgical excision
-Small grade 3 lesions (<3cm diameter): Stereotactic radiosurgery
-Large grade 3 lesions, or grade 4/5/6 (>6cm, high risk surgical morbidity): Conservative medical management
-Seizure prophylaxis not routinely given

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25
Cerebral Aneurysm definition and locations
Definition: Thin-walled protrusions from intracranial arteries composed of very thin or absent tunica media - Develops from HTN or normal hemodynamic stress Location: Commonly occurs at junction of communicating arteries and cerebral arteries - MC: Ruptured ”Berry (saccular) aneurysm” (80%) -MC location: Anterior Circulation (Circle of Willis) – 85% -Anterior Comm. + Anterior Cerebral -Posterior Comm. + Internal Carotid Artery (MOST LIKELY TO RUPTURE) -Bifurcation of Middle Cerebral Artery
26
Cerebral aneurysms: risk factors and higher risk of formation
RF: - HTN - smoking - Female (2:1) - ETOH - Family hx aneurysm - Coartion of aortic Conditions with higher risk of formation: - polycystic kidney disease** - Ehlers-Danlos - bicuspid aortic valve
27
posterior communicating artery aneurysm
-CN3 palsy -most likely to rupture: Posterior communicating + internal carotid
28
cerebral aneurysms presentation
INCIDENTAL finding: Asymptomatic until SAH occurs** -Headache -Visual Acuity Loss -Facial Pain May manifest as compression of CN III Palsy (PCA): -Diplopia: sudden onset, binocular, horizontal/vertical/oblique - Ptosis -Eye pain at onset Causes of rupture: - most occur without an identifiable trigger - strenuous activity (exercise, sex, physical work)
29
cerebral aneurysms Dx for unruptured aneurysms and managment
CTA/MRA: - can detect ≥5mm aneurysms** -Cons: Invasive d/t contrast injection, radiation Gold standard: Cerebral angiography* -XR imaging with injected contrast dye -Can detect much smaller aneurysms -Cons: More invasive, higher risk of complications -Not used for screening- no point of it** management - Observation: If <7mm incident finding without prior SAH -Monitoring unruptured aneurysms for growth: CTA/MRA annually for 2-3 years, then spread to every 2-5 years, is clinically and radiographically stable -Surgical clipping -Endovascular coiling (preferred method) **
30
cerebral aneurysm stats with rupture
-33% die before reaching the hospital -20% die in the hospital -30% recover without disability
31
signs of increased ICP
- cushings reflex: increase BP, decreased HR, irregular breathing - headache - n/v
32
epidural hematoma: def, presentation, dx
Def: ARTERIAL bleed between dura and the skull - MCC: trauma - MC: middle meningeal artery from temporal bone fracture Classic presentation: - initial trauma injury with brief LOC - lucid interval for several hours - neurological sx: AMS, coma - VOMITTING - other sx: headache, seizure, confusion, aphasia, hemiparesis Dx: - non contrast CT showing football sign (BICONVENX (lens-shaped, lentiform)* - blood collection that does not cross suture lines of the skull
33
epidural hematoma tx
management: IMMEDIATE hospitalization to REDUCE ICP** -Hyperventilation: Goal pCO2 25-30 mmHg (Temporary measure) -Mannitol: Osmotic diuretic that decreases ICP temporarily NEUROSURGICAL EVALUATION FOR CRANIOTOMY AND HEMATOMA EVACUATION: - surgical evacuation indications: volume > 30 mL, acute and in coma (GCS <8), PUPILLARY changes - if delayed surgical evaluation: BURR HOLE* Observation: - mild sx - volume < 30 mL - clot thickeness < 15mm - no midline shift - no coma - no focal neuro deficits Rarely: brain herniation, stroke, seizures occur
34
subdural hematomas: definition, causes, risk factors
Definition: VENOUS bleed between dura and arachnoid - most often rupture of BRIDGING veins from surface of brain to dural sinuses - MC in elderly Causes: - BLUNT TRAUMA MC - "contre-coup" - shaken baby - AV malformation spontaneous hematoma - neurosurgical procedure complication - non-traumatic causes: ALCOHOLISM, SEIZURES, COAGULOPATHIES Risk factors: - cerebral atrophy - ELDERLY - TBI - M > F
35
subdural hematoma presentation vs epidural
Subdural: elderly pt becomes senile over a month and fell a week ago, seemed ok but now has a headache and acting weird - Headache - vomiting - Confusion - depressed LOC - Seizures - CN palsies -+/- focal neurologic symptoms such as hemiparesis, ipsilateral pupil dilation Epidural presentation: - initial trauma injury with brief LOC - lucid interval for several hours - neurological sx: AMS, coma - VOMITTING - other sx: headache, seizure, confusion, aphasia, hemiparesis
36
subdural hematomas PE and Dx
May have evidence of: - broken basilar skull - +/- CSF oto/rhinorrhea Dx: Non-contrast CT - head showing a concave (crescent shaped) blood collection that DOES cross suture lines   -note: Initial CT scans can often be normal
37
subdural hematoma management
management: immediate hospitalization!! - mild: corticosteroids and reduction of ICP!!!! neurosurgical evaluation for craniotomy and hematoma evacuation: surgical indications - > 5 mm thickness on CT - midline shift - coma (GCS < 8) - progressively decreasing GCS of over 2 points since admission - PUPIL abnormalities - ICP > 20 mmHg Notes: - consider shaken baby syndrome in children - HIGHER mortality due to DELAYED FINDINGS and HIGHER COMORBIDITIES - rare: brain herniation
38
subarachnoid hemorrhage: definition and risk factors
Definition: Arterial bleed between arachnoid and pia mater - MCC: ruptured BERRY aneurysm*, AV malformation -Can be SPONTANEOUS or from TRAUMATIC event -> rupture and bleeding into subarachnoid space -> blood in CSF -> rapid increased ICP - high mortality rate: 42% within 30 days Risk factors: - age: 40-60 - FEMALES >>>>>>>> males - SMOKING - HTN - ETOH, cocaine - first-degree fam hx SAH - AA, connective tissue disorders
39
subarachnoid hemorrhage presentation
- female 40-60s - Acute, sudden “thunderclap” headache described as “worst headache of my life” * -Meningeal signs: Nuchal rigidity, photophobia -Vomiting -Confusion, AMS -+/- brief LOC Focal signs based on location: -PCA aneurysm: CN III - oculomotor nerve paralysis (ipsilateral ptosis, eye pointed down/out, mydriasis, loss of light reflex) -Anterior or middle cerebral: numbness, muscle weakness -Brocas area: slurred speech -Wernicke’s area: difficulty understanding speech
40
subarachnoid hemorrhage: dx
Dx: - non contrast CT: blood within basal cisterns - if you are highly suspicious with negative CT -> LP* - LP: gold standard; xanthochromia (yellow CSF from broken down RBCs); increased RBCs in all vials -CTA/MRA/Digital subtraction cerebral angiography vs. Cerebral angiogram (definitive) -EKG: Increased QRS, QT intervals, Decreased PR intervals, U waves, dysrhymias
41
subarachnoid hemorrhage complications and management
complications: -Re-rupture (30%)* -Vasospasm (50%)* -Hydrocephalus, SIADH, HTN, cerebral ischemia, elevated ICP, seizures, cardiac abnormalities Management: immediate hospitalization to prevent complications - lower SBP <140 mmHg: labetolol - prevent vasospasm: CCB nimodipine - seizure prophylaxis: phenytoin/phenobarbital** - Surgery: craniotomy and clipping/coiling** -Supportive care: bedrest, stool softeners, analgesia, IV fluids, VTE prophylaxis, decrease ICP
42
intracerebral hemorrhage (ICH): def, MCC, other causes
Definition: blood accumulation in the intraparenchymal space -> compression of blood vessels and tissue -> HYPOXIA -> hypoxemia MCC: HTN - leads to atherosclerosis of large arteries, subclinical microbleeds, microaneurysms (Charcot-Bouchard aneurysms) - BASAL GANGLIA, THALAMUS, pons, and cerebellum are most often affected Other causes: -Cerebral amyloid angiopathy: Deposition of amyloid into blood vessel walls makes them weak and prone to rupture* -AVMs* -Post-traumatic -Coagulopathies -Sickle cell disease
43
intracerebral hemorrhage risk factors
- MALE - Black, Asian - Heavy alcohol use - amphetamines, cocaine - anti-thrombotic medications - previous cerebrovascular incident Very poor prognosis
44
intracerebral hemorrhage presentation and sx based on location of bleed
Presentation: -Slow onset, gradually worsening within a few hours, increased ICP -Fever, AMS, HA, N/V - anisocoria: UNEQUAL pupil sizes * Symptoms: depend on location of bleed -Basal ganglia = Loss of contralateral sensory, motor functions, honomymous hemianopsia -Thalamus = Contralateral loss of sensory, motor functions, homonymous hemianopsia, aphasia if dominant side / neglect if non-dominant side, small pupils -Lobar = honomymous hemianopsia, seizures, contralateral leg paresis if frontal -Pons = coma within few minutes, quadraplegia miosis, deafness, speaking difficulties when awake -Cerebellum = ataxia, same side face weakness, occipital headache, neck stiffness, loss of face/body sensory functioning -ACA, MCA = numbness, weakness -PCA = Impaired vision -Broca’s area = Slurred speech -Wernicke’s area = Difficulty understanding speech
45
intracerebral hemorrhage (ICH) dx and management
Dx: -!CT head non-contrast will show hyperdense blood acutely -CTA should be done to evaluate for vascular causes of hemorrhage -+/- CT venography if suspicious of cerebral vein thrombosis with hemorrhagic conversion Management: medical emergency-> BRAIN HERNIATION -Goal in early management: place an ICP monitoring device -Anticoagulation reversal -Antipyretics for fever -Osmotic diuresis (mannitol): reduce ICP -Nicardipine: BP control -Phenytoin or levetiracetam for seizure prophylaxis*
46
all intracranial bleeds: what do you need to do
1) Get labs: -CMP, CBC -PT/PTT, INR, fibrinogen -Anti-Xa activity for patient on apixiban/rivaroxaban -Tox screen if warranted -Pregnancy test if warranted -ABG/VBG if intubated 2) Anticoagulation reversal 3) Control BP -Preferred agent: Nicardipine or clevidipine -Do not drop below 130mmHg as this may cause harm -If b/w 150-220 –> reduce to 130-150 -If >220 –> reduce to 140-180 4) neurosurgical consult
47
anticoagulation reversal agents
for all intracranial bleeds -Warfarin –> Vitamin K, PCC, FFP -Antiplatelets –> DDAVP, cryoprecipitate -New DOACS –> Praxbind (Idearucimab) for Dabigatran (Pradaxa), KCentra (Four factor PCC) for most others (fondaparinux, rivaroxaban, Eliquis) -Heparin –> Protamine -Thrombolytics (e.g. TPA) –> TXA, Cryo, FFFP
48
all intracranial bleeds: BP control what value
-Preferred agent: Nicardipine or clevidipine -Do not drop below 130mmHg as this may cause harm -If b/w 150-220 –> reduce to 130-150 -If >220 –> reduce to 140-180 SAH: goal of SBP <140 mmHg - use labetolol
49
cerebral vein thrombosis (CVT)
rare - but serious blood clot that forms in cerebral veins or dural sinuses ethiology: -Prothrombotic states: pregnancy, post-partum, OCPs, thrombophilia (protein C and S deficiency, Factor V Leiden mutation) -Chronic inflammatory disease: SLE, IBD, malignancy, vasculitis -Local inflammation: Mastoiditis, otitis media, sinusitis presentation: - headache 90%* -benign intracranial hypertension, SAH, focal neuro deficit, seizures, meningoencephalitis, stroke (hemorrhagic conversion) CT/MR venogram
50
increased intracranial pressure (ICP): normal values and pathologic; Monroe-Kellie doctrine
-Normal ICP <15 mmHg (adults), 9-12 mmHg (children) -Pathologic: >20mmHg for both Monroe-Kellie doctrine: Cranial cavity is a fixed space w fixed proportions: - Brain (1400ml) - Blood (150ml) - CSF (150ml) -Increase in a component = ↑ ICP -To decrease ICP, must decrease either brain, blood, or CSF
51
Major causes of ↑ ICP
-Intracranial mass! (tumor, hematoma)* -Cerebral edema! (HIE, TBI, infarct)* -Obstructive hydrocephalus* -Idiopathic Intracranial HTN (IIH, pseudotumor cerebri) * -↑ CSF production (choroid plexus papilloma) -↓ CSF absorption (arachnoid granulation adhesion from bacterial meningitis) -Obstructive venous outflow
52
where is csf produced and reabsorped
CSF is produced by choroid plexus and reabsorbed by the arachnoid granulations
53
sx of increased ICP
Adults: -± Head trauma -HEADACHE (80%) -AMS -N/V -Visual changes Infants/Children: -Macrocephaly (big for age) -Bulging anterior fontanelles -Irritability (1st sign) -Nausea, vomiting -Lethargy, poor feeding, lack of interest
54
signs of increased ICP
- Papilledema (4-9%)* - Cushing reflex: bradycardia, HTN, irregular breathing ** -CN VI palsy -Periorbital bruising -Children more likely to get abnormal gait or poor coordination -Herniation: Decorticate or decerebrate posturing, Change in GCS Absent: Hypotension, Hypoxemia, Hypothermia
55
3 main consequences of increased ICP
1) Decreased cerebral perfusion pressure (CPP): ISCHEMIA - CPP = MAP - ICP; normal CPP = 60-100 - as↑ ICP, ↓ CPP -> reduced cerebral blood flow -> ischemia 2) HERNIATION: -↑ ICP -> brain shifts to other spaces of the skull -> brain tissue herniation -Ischemia or death 3) Cushing’s reflex: -HTN: as ↑ ICP ,↓ CPP -> compensatory activation of the sympathetic nervous system to ↑ Systolic BP - Bradycardia: aortic arch baroreceptors activate the parasympathetic nervous system -> bradycardia -↑ Pressure on brain stem -> dysfunction of respiratory drive -> irregular breathing
56
ICP dx
Non-contrast CT head = initial step -Look for causes: acute obstructive hydrocephalus, edema, or space-occupying lesions such as intracranial hematoma, masses -Consider repeat CT if clinical deterioration -> Not everything shows on a CT scan* Signs of ↑ ICP on CT scan: -Midline shift -Effacement of the ventricles, basal cisterns and other CSF spaces (loss of visibility) -Brain herniation (uncal, tonsillar) -Edema: Loss of grey-white matter differentiation LP opening pressure of >20cm is indicative of ↑ ICP -Always image first r/o space occupying lesion… sudden and rapid decrease of ICP from the LP can trigger a brain herniation
57
ICP monitoring
CPP (cerebral perfusion pressure) = MAP – ICP -Generally ICP>20mmHg is considered elevated Intraventricular catheter = gold standard with external ventricular drain (EVD)**** - allows for continuous ICP monitoring and is therapeutic for drainage -Complications: infection (20%), hemorrhage (2%) -Other monitoring devices: intraparenchymal, subarachnoid, epidural -------- -ICH (regardless of cause) is considered a medical emergency due to danger of brain herniation -Goal in early management: place an ICP monitoring device
58
ICP management
resuscitation efforts: - head of bed at 30 degrees* - therapeutic hyperventilation: goal of pCO2 of 26-30 mmHg -> induces vasoconstriction and reduce cerebral blood flow aggressively treat fever: acetaminophen, mechanical cooling hyperosmolar therapy (in emergencies) - mannitol: osmotic diuretics - mechanical ventilation - AVOID free water solutions that can worsen edema like D5W, half NS; USE ISOTONIC fluids (0.9% NS)** other tx: -Furosemide: sometimes given as adjunct therapy to potentiate effects; Can worsen dehydration and hypokalemia -Decompressive Craniectomy (last line)
59
Mannitol (osmotic diuretic)
Use: -Reduces brain volume by drawing free water out of tissue and into circulation -Excreted by kidneys -> volume depletion, hypotension + hypernatremia -Caution in patients with renal insufficiency IV Mannitol: - initial dose: 1 g/kg bolus, re-dose 0.25-0.5 g/kg PRN q 6-8 h -Effects peak at 1 hour and last 4-24 hours, can have “rebound” increase in ICP after it wears off -Monitor: serum Na, osmolality, renal function -Side effects: hyperosmolarity, hypovolemia, hypo-K, hyper-Na, renal failure
60
uncal herniation
B -Innermost temporal lobe is compressed and moves towards the brainstem, causing pressure on CN III -Classic presentation of uncal herniation: -!Ipsilateral fixed dilated pupil + contralateral hemiplegia + cushing reflex
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idiopathic intracranial HTN (IIH)
-Idiopathic increased intracranial pressure with no known cause Classic presentation: OVERWEIGHT FEMALE of childbearing age, with worsening headache, worse with straining, and vision changes - Exam reveals papilledema - Imaging normal -Other symptoms: N/V, pulsatile tinnitus, vision loss, NECK STIFFNESS, back pain, retrobulbar pain -Other signs: Papilledema (hallmark), 6th nerve palsy, visual field loss Treatment: -Weight loss -Acetazolamide -Consider CSF shunt
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hydrocephalus definition and two types
Excessive amount of CSF within cerebral ventricles and/or subarachnoid spaces = Ventricular dilation and increased ICP Two Types: 1) Obstructive (Non-Communicating) - CSF accumulation due to structural blockage of flow within ventricles - MCC in children 2) Absorptive (Communicating) - CSF accumulation due to impaired absorption; rarely excessive CSF production - normal pressure hydrocephalus
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hydrocephalus: MCC of congenital hydrocephalus and MCC of acquired
-MCC of congenital hydrocephalus : myelomeningocele (15-25%) -MCC of acquired hydrocephalus: hemorrhage
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hydrocephalus: risk factors
Low birth weight prematurity maternal DM male sex low socioeconomic status race/ethnicity
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hydrocephalus: sx and singsn
Symptoms -HEADACHE: early morning, worse with cough/micturition/defecation/recumbency* -Irritability, Lethargy , weakness -Altered mental status / behavioral changes* -Nausea, vomiting -Diplopia, abnormal eye movements Signs: -Head circumference in children: full anterior fontanelles, frontal bossing, prominent scalp veins -Developmental delays in children -Spasticity -“Setting sun” sign - papilledema -Sacral dimpling *
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hydrocephalus dx and management
Dx: - first line: CT head - Fundoscopy – papilledema -Lumbar puncture will have ↑ opening pressure - Not usually necessary management: Asymptotic: Watchful waiting, serial head measurements, serial US, monitor development if Symptomatic, acute, rapid, progressive: - VP shunt* -Endoscopic third ventriculostomy (for non-communicating) -Temporary: External ventricular drain (EVD) -Avoid rapid aspiration of CSF… aim for 1-2mL/min for 2-3 minutes at a time - Goal ICP <20 mm Hg
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normal pressure hydrocephalus (NPH) def and risk factors
Definition: Pathologically enlarged ventricular size with normal CSF opening pressures (ICP normal) -A form of COMMUNICATING hydrocephalus caused by structural blockage of the CSF within the ventricular system (e.g. stenosis of aqueduct of Sylvius) - wet, whacky, wobbly Risk factors: -Idiopathic NPH increases in prevalence with age, MC >60*
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normal pressure hydrocephalus proposed ethiologies and secondary NPH
Proposed Etiologies: -Congenital/Chronic -Cerebrovascular Disease -Decreased CSF Absorption -Increased Central Venous Pressure -Neurodegenerative Disorders (dementia) Secondary NPH: Symptomatic NPH due to “pressure effect” on brain -MOA: Impaired CSF resorption - accumulation within ventricular system - local “pressure effect” on periventricular white matter -MCC: intraventricular (IVH) or subarachnoid hemorrhage (SAH) ******** - other MCC: 2/2 aneurysm or trauma, or prior acute/ongoing chronic meningitis
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NPH classic triad “wet, whacky, wobbly”
Gait Disturbance - Magnetic, glued foot gait: small wide based steps - Difficulty with ambulation: reduced ability to walk Cognitive Disturbance: - Dementia that develops over months-years - early: impaired executive function -Apathy, depression, psychomotor slowing, decreased attention and concentration Urinary Incontinence: - early: Urgency - Slow gait makes it hard to reach bathroom - late: lack of concern due to frontal lobe impairment
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normal pressure hydrocephalus (NPH): sx and dx
Sx: -Normally have NO ICP symptoms (other than wet, whacky, wobbly) -No headache, N/V, vision loss, papilledema Dx: -Lumbar puncture: Normal opening pressure** -Check labs for other causes of AMS: Include B12, TSH -MRI brain : Ventriculomegaly (hallmark) without obstruction*** -Diagnosis of exclusion Confirmatory tests: -Remove 30-50mL CSF via LP, then test gait ~60 minutes after, if improvement of gait, would benefit from VP shunt
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how do you confirm normal pressure hydrocephalus and what is tx?
Confirmatory tests: -Remove 30-50mL CSF via LP, then test gait ~60 minutes after, if improvement of gait, would benefit from VP shunt Treatment: VP shunt ! ----- Dx: -Lumbar puncture: Normal opening pressure** -Check labs for other causes of AMS: Include B12, TSH -MRI brain : Ventriculomegaly (hallmark) without obstruction*** -Diagnosis of exclusion