Neuro Emergencies Flashcards

1
Q

What is a good imitator of a stroke?

A
  • hypoglycemia:

give sugar and thiamine - reverse quickly

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2
Q

Why is it ok to have high BP in acute ischemic stroke (220/110)?

A
  • what high BP so brain is still being perfused
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3
Q

Why do we want to keep Na on high end in a stroke?

A
  • to prevent brain cells from swelling
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4
Q

Reversal agents for warfarin?

A
  • FFP and Vit K

FFP works faster

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5
Q

What should you expect if pt presents w/ bradycardia and HTN?

A
  • cushing’s triad - ICP

- need to decrease CP: use mannitol if pt herniating, also give fluids to prevent hypotensive (give hypertonic saline0

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6
Q

PE of AMS?

A
  • ABCs, VS
  • bedside glucose
  • look quickly for immediate life threats:
    hypoglycemia
    hypotension/HTN
    hypoxia
    abnormal resp
    hypo/hyperthermia
  • don’t be afraid to give glucose, thiamine, based on H and P
  • Head to toe exam
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7
Q

DDx for AMS:

AEIOU TIPS?

A
A - alcohol
E - epilepsy; lytes; encephalopathy (HTN, hepatic)
I - insulin (hyper, hypo); intuss (peds)
O - overdose: opiates
U - uremia
T - trauma
I - infection
P - psych; poision
S - shock
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8
Q

Tx of AMS?

A
  • underlying cause
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9
Q

What is status epilepticus?

A
  • considered 5 min or more of convulsions or 2 or more convulsions in a 5 min interval w/o return to preconvulsive neuro baseline
  • traditionally considered to be convulsions longer than 30 min, however don’t halt tx
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10
Q

Etiologies of status epilepticus?

A
  • vascular: stroke, hypoxic encephalopathy
  • toxic: drugs, alcohol w/drawal, meds (isoniazid, TCAs, chemo agents), AED noncompliance
  • metabolic: hyper/hypo-natremia, hypoglycemia,hypocalcemia, liver/renal failure
  • infectious: meningioencephalitis, brain abscess
  • trauma
  • neoplastic
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11
Q

Initial assessment/tx of status epilepticus?

A
  • ABCs: O2, airway, BP: monitor for hypotension
  • labs: CBC, BMP, Ca, Mg, AED levels
  • dx hypoglycemia as cause: D50W amp and thiamine 100 mg IV
  • ***needs to have thiamine given b/f dextrose as 20-40% of seizure pts are alcoholics
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12
Q

First line tx for status epilepticus?

A
  • benzos 1st line:
    ativan 4 mg IV or valium 5 mg IV
  • 2nd line:
    fosphenytoin load 20 mg/kg (up to 150 mg/min)
    valproic acid: load 40 mg/kg, 2nd - 20 mg/kg
    refractory status: phenobarb, pentobarb, versed, propofol - intubate if no response
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13
Q

Post ictal state?

A
  • diff post-ictal state and syncope of another cause
  • usually sleepy and may be confused
  • during possible prior seizure pt has usually been incontinent
  • tongue bitten
  • supportive care
  • w/u why seizure occurred
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14
Q

Cause of acute ischemic stroke?

A
  • caused by sudden loss of blood circ to area of brain resulting in ischemia and corresponding loss of neuro fxn
  • w/in seconds to min of loss of perfusion, an ischemic cascade occurs resulting in central area of irreversible infarction surrounded by an area of potentially reversible ischemic penumbra
  • goal of tx: preserve ischemic penumbra
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15
Q

Hx questions for stroke pt and family?

A
  • time last known well
  • tPA CIs
  • hx of diabetes, seizures?
  • detailed description of sxs:
    onset w/ HA, seizure, syncope, possible ICH
    neck pain, hx of neck trauma, possible vertebral or carotid dissection
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16
Q

PE for ischemic stroke pt?

A
  • level of consciousness
  • eye exam
  • CN
  • motor exam
  • sensory exam
  • reflexes
  • cerebellar exam
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17
Q

W/u of ischemic stroke?

A
  • labs: POCT BG, CBC
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18
Q

Action time needed for AIS tx?

A
  • door to clinician in less than 10 min
  • door to stroke team less than 15 min
  • door to CT initiation less than 25 min
  • door to CT interpretation less than 45 min
  • door to drug (more than 80% compliance) less than 60 min
  • door to stroke unit admission: less than 3 hrs
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19
Q

Characteristics of ACA stroke?

A
  • dysarthria, aphasia
  • unilateral contralateral motor weakness (lower more than upper)
  • LE sensory changes
  • urinary incontinence
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20
Q

Characteristics of MCA stroke?

A
  • contralateral hemiparesis (faces/arms more than legs) and hemianopsia
  • ipsilateral gaze preference
  • aphasia (if dominant hemisphere): Broca’s/wernike’s/global
  • hemi-neglect (if non-dominant hemisphere)
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21
Q

Characteristics of PCA stroke?

A
  • contralateral hemianopsia
  • cortical blindness
  • AMS
  • impaired memory
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22
Q

Initial tx for AIS?

A

ABCDs:

  • airway: intubate for GCS less than 8 or inability to protect airway
  • breathing: O2 if hypoxic, keep PCO2 32-36
  • circulation: maintain adequate CPPl allow permissive HTN (220/110)
  • dextrose: maintain normoglycemia (hyperglycemia worsens neuro outcome)

fever: hyperthermia worsens outcome
- cerebral edema
- seizure control

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23
Q

Thrombolytics used for AIS? indications?

A
  • Altepase (IV tPA): considered in eligible pts tx w/in 3-4.5 hrs of sx onset
  • indications:
    acute neuro deficit expected to result in sig long term disability
  • non-contrast CT w/ no hemorrhage
  • stroke sx onset clearly ID b/t 3-4.5 hrs b/f tPA given
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24
Q

CIs to tPA?

A
  • SBP over 185 or DBP over 110 (labetolol 10 mg q 10 min)
  • CT head w/ ICH or SAH
  • recent intracranial or spinal surgery, head trauma or stroke (more than 3 mos ago)
  • major trauma or surgery w/in 3 months)
  • hx of ICH or aneurysm/vasc. malformation/brain tumor
  • recent active internal bleeding
  • platelets less than 100K, heparin use w/in 48 hrs w/ PTT over 40, INR greater than 1.7
  • known bleeding disorder
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25
Q

Use of mechanical thrombectomy in AIS?

A
  • for pts w/ stroke in large territory vessel of proximal circa
  • composed of direct IA tPA and stent removal of clot if necessary
  • MR clean trial: demostrated that early IA intervention dramatically improved neuro outcome after ischemic stroke w/o increase in sx ICH or 90 day mortality
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26
Q

Diff types of ICH?

A
  • intra-parenchymal (IPH)
  • intra-ventricular (IVH)
  • subarachnoid (SAH)
27
Q

What is a IPH? Signs and sxs?

A
  • hemorrhage w/in brain tissue
  • often clinically silent
  • signs and sxs depend on location of hemorrhage:
    M/c are hemiparesis, aphasia, hemianopsia and hemisensory loss
  • can mimic acute ischemic stroke sxs
28
Q

IPH etiology?

A
  • HTN number 1 cause!!!
  • cerebral amyloid angiopathy
  • anticoag/anti-platelet meds
  • systemic anticoag states (DIC)
  • sympathomimetic drugs (cocaine, MDMA, meth)
  • aneurysms, AVMs, cavernous angiomas
  • brain tumors
29
Q

IVH:

etiology, s/s?

A
  • often result from IPH extending into ventricular system
  • s/s: HA, N/V, progressive deterioration of consciousness, increased ICP, nuchal rigidity
  • increased risk of obstructive hydrocephalus
30
Q

Tx of IPH/IVH?

A
- ABCDs:
intubation if necessary
SBP goal: less than 160
- fluid and lytes:
NS, avoid dextrose, watch for SIADH/cerebral salt washing
-prevent hyperthermia
- seizure ppx 
- correct underlying coag:
FFP, platelet infusion, Vit K
- management of ICP
- recombinant factor VII (NovoSeven): can be beneficial to give w/in 4 hrs, risk of MI and AIS
- surgical evacuation of hemorrhage
31
Q

RFs for SAH?

A
  • aneurysmal rupture accounts for 80% of cases
  • RFs: HTN, smoking, advanced age, cocaine use, alcohol use, CT disorders
  • fatality rate: 50% w/in 2 wks
32
Q

S/S of SAH?

A
  • sudden onset of worse HA of life
  • CN III palsy: down and out gaze, ptosis
  • CV VI palsy: increased ICP: inability to look out
  • retinal hemorrhages
  • AMS
  • nuchal rigidity
33
Q

Tx of SAH?

A
  • ABCDs:
    intubtation of GCS less than 9, tx HTN: goal less than 150, maintain norm–glycemia and euvolemia, normothermia
  • tx of vasospasm:
    nimodipine, Mg gtt and Statin
  • seizure ppx
  • aminocaproic acid bolus/gtt: clotting promoter
  • EVD for obstructive HCP (hydrocephalus)
  • CTA and eventual angiography to ID location of aneurysm
  • angiography w/ endovascular coiling
  • surgical intervention: hemicraniectomy w/ surgical vascular clipping
34
Q

TBI most common in what age group? Diff types?

A
  • leading cause of traumatic death in pts younger than 25
  • primary: at time of impact
  • secondary: develop over time due to inflammatory and neurochemical responses
35
Q

Head trauma hx questions?

A
  • when, where, and how did injury happen?
  • MOI: details
  • if there was LOC at scene
  • EtoH or drugs involved
  • length of time from injury
  • underlying medical problems (diabetes, prev stroke, CVD)
  • allergies and meds
36
Q

Initial Assessment of TBI?

A
  • assess neuro status
  • use GCS: if pt deteriorated during trasport needs immed non-contrast CT and poss. neuro consult
  • if pt stable and nont comatose w. stable VS and no focal neuro findings: can proceed more slowly
  • goal is to prevent brainstem or uncal-herniation and brain edema w/ elevated ICP that causes further brain injury
37
Q

Head injury: PE? Labs?

A
  • rapid primary survey
  • VS: cushings triad?
  • GCS
  • examining head for signs of outward trauma (penetrating, lacerations, swelling, bruises, abrasions)
  • pt should be in c-spine collar
  • neuro exam:
    pupils
    level of alertness
    look for focal deficits
  • labs: CBC, chem, coags, toxicology
38
Q

How does GCS correlate to injury?

A
  • initial GCS correlates to severity of injury
  • avoidance of secondary insults by hypotension and hypoxemia is extermely impt in reducing injury severity
  • GCS less than 8 - intubate
39
Q

Guidelines for CT scan in ER?

A
  • GCS less than 15
  • susp. open or depressed skull fx
  • any sign of basilar skull fx (hemotympanum, raccoon eyes, battle’s sign, CSF leak)
  • 2 or more episodes of vomiting
  • 65 or older
  • amnesia b/f impact of 3 or more min
  • dangerous mech (ejected from vehicle)
  • bleeding diathesis or anticoag use
  • seizure
  • focal neuro sign
  • intoxication
40
Q

Cerebral blood flow and perfusion?

A
  • supplied from internal carotid and vertebral arteries
  • drains via cerebral veins and dural sinuses into internal jugular veins
  • receives 10-15% of CO
  • CPP = MAP - ICP
    normal CPP = 70-90 in adults
    CPP less 50 indicates brain ischemia
  • Monroe-kellie concept: ICP is fxn of volume and compliance of each compartment
  • volume of brian and constituents inside cranium is fixed and can’t be compressed:
    brain vol = 85%
    CSF = 10%
    blood = 5%
41
Q

Intracranial compliance - compensatory mech?

A
  • nonlinear compliance
  • initial compensatory mech:
    displacement of CSF into thecal sac, decrease in cerebral venous blood
  • once compensatory mecahnisms are exhausted - small increases in vol produce large increases in pressure
42
Q

What are causes of increased ICP?

A
  • intracranial mass
  • cerebral edema
  • increased CSF prod (choroid plexus lesion)
  • decreased CSF absorption (adhesions)
  • obsructive hydrocephalus
  • obstruction in venous outflow (venous sinus thrombosis)
  • idiopathic (pseudotumor cerebri)
43
Q

S/S of increased ICP?

A
  • HA
  • vomiting
  • alt consciousness
  • seizures
  • papilledema
  • unequal and/or unreactive pupils
  • cushings triad: bradycardia, HTN and abnorm resp: impending herniation
44
Q

Indicications for ICP monitoring?

A
  • abnorm CT showing mass effect and/or midline shift
  • GCS less than 8
  • high risk for increased ICP (closed head injury)
45
Q

non-invasive techniques for ICP monitoring?

A
  • ocular sonography: measures optic nerve sheath diameter
  • transcranail doppler: measures velocity of blood flow in prox cerebral vasc
  • IOP measurement
  • tympanic membrane displacement
46
Q

Management of ICP?

A
  • optimize cerebral venous outflow:
    promote displacement of CSF from intracranial compartment to spinal compartment
  • elevate head of bed to 30 degrees
  • line placement: subclavian
47
Q

Tx of fever - in IICP?

A
  • elevated metabolic demand results in increased cerebral blood flow and elevated ICP
  • APAP and cooling blankets
  • therapeutic hypothermia can be effective in lowering ICP w/ conventional efforts failed: goal core temp: b/t 32 and 34 C
48
Q

Management of hyperventilation?

A
  • PaCO2 of 35-38
  • hyperventilation to lower PaCO2 levels:
    considered urgent measure but shouldn’t be chronic
  • minimize in pts w/ TBI or acute stroke:
    vasoconstriction causes decrease in cerebral perfusion and can worsen outcome
49
Q

Intubation in IICP?

A
  • hypoxia and hypercapnea can increase ICP: optimal resp management is crucial
  • use PEEP w/ caution: impedes venous return, decreases blood pressure leading to reflex increase in cerebral blood flow
  • pre-medicate w/ lidocaine to prevent IICP surge
50
Q

Use of mannitol in IICP?

A
  • MC used osmotic diuretic
  • draws free water out of brain and into circ.
  • dose: 20% soln given as 1 g/kg bolus, repeat dosign q 6-8 hrs as needed
  • can be given through peripheral line
  • good option if also interested in lowering BP
  • monitoring parameters: serum Na+, serum osmolality and renal fxn
51
Q

use of hypertonic saline in IICP?

A
  • varying vol and tonicity either as bolus or infusion:
    3%
    23% (ICU or actively herniating pts only)
  • admin via central line preferred, but 3% ok peripherally
  • goal keep serum Na+ less than 155
52
Q

Sedation for management of IICP?

A
  • decreases ICP by reducing metabolic demand

- propofol has good effet since it is easily titratable and has short 1/2 life

53
Q

When is heavy sedation and paralysis used in IICP?

A
  • used in refractory IICP
  • common regimen includes morphine and lorazepam and analgesia/sedation and cisatracurium or vecuronium for paralysis
  • can’t closely monitor neuro exam
54
Q

Use of craniectomy w/ IICP?

A
  • bypasses monroe-kellie doctrine
  • used alone will lower ICP by 15%
  • craniectomy including removal of dura will lower ICP up to 70%
  • complications: herniation through bony defect, spinal fluid leak, infection, epidural and subdural hematoma
55
Q

A pt presents w/ R sided hemianopsia and memory loss. This is indicative of an ischemic stroke of what vessel?

A
  • PCA
56
Q

Which of the following is not an effective measure of decreasing elevated ICP?

A
  • induced hypoventilation
57
Q

Etiologies of vertigo?

A
  • central: migrainous, brainstem ischemia, cerebellar infarction and hemorrhage, MS
  • somatic: panic attack, weak, dizzy, nearly fainting pt
  • peripheral: BPPV, vestibular neuritis, herpes zoster oticus, meniere’s, labyrinthitis, perilymphatic fistula, acoustic neuroma, aminoglycoside toxicity, otitis media
58
Q

Dx of vertigo?

A
  • N/V more severe w/ peripheral causes
  • gait disturbances more pronounced w/ central etiologies
  • generally central last hours-days, while peripheral are recurrent and last for a few min to 2-3 hrs
  • impt: get good hx, thorough PE looking for nystagmus and focal neuro signs, look at RFs for more serious central disease
59
Q

What is a TIA? sxs?

A
  • sxs last 5-20 min, rarely longer than an hour, w/o evidence of acute infarction
  • if neuro defects last 4 hrs or longer pts often have infarcts on MRI
  • sxs:
    hemiparesis, hemiparesthesia
    dysarthria, dysphasia, dysplopia, circumoral numbness, imbalance, monocular blindness
60
Q

TIA and CVA correlation?

A
  • among pts who present to ER w/ TIA - 5% will have CVA in 2 days and 25% will have recurrent event in 3 months
  • urgently IDing cause of pt’s first stroke or TIA is crucial in determining proper tx to prevent 2nd. Since often neuro s/s subtle and timing inexact usually get CT or MRI to r/o infarct
61
Q

TIA w/u?

A
  • depends on susp area affected:
    -low flow:
    int carotid - duplex US or transcranial doppler,
    MCA: MRA or CT angio
    vertebrobasilar: CT angio
    -Embolic:
    echo, cardiac monitoring: afib
    -lacunar: r/o others, dx of exclusion
62
Q

What is myasthenic crisis?

A
  • myasthenia gravis: disorder of neuromuscular transmission affecting ocular, bulbar and limb and resp muscles
  • crisis: occurs when there is severe enough weakness to necessitate intubation
  • severe bulbar weakness produces dysphagia and aspiration that often complicates resp failure
  • often pt experiences generalized weakness as a warning
  • intubation should be done if pt at risk for aspiration, in obvious resp failure
  • tx: plasmapharesis or IVIG
63
Q

Acute exacerbations of MS?

A
  • result in fxnlly disabling sxs w/ objective neuro impairment (loss of vision, motor and/or cerebellar sxs)
  • tx w/ high dose IV glucocorticoids
  • sometimes MS causes seizures: benzos
64
Q

Presentation of Guillian Barre syndrome?

A
  • symmetric ascending muscle weakness
  • usually starts in proximal legs
  • progress to severe resp muscle weakness - vent support if progress quickly
  • may have paresthesias of hands/feet
  • severe back pain
  • dysautonia: tachy, urinary retention, HTN/hypotension, brady, ileus, loss of ability to sweat
    dx: LP: marked elevation of CSF protein w/ normal WBC
  • EMG an nerve conduction, serum - glycolipid abs to gangliosides
  • tx: close monitoring for resp failure, close CV monitoring of rhythm, pulse and BP
    fluids for hypotension, admission to ICU for further stabilization and tx