Quiz 2: Key Concepts in Ischemic Stroke Management and Related Neurological Definitions

what is the most common type of stroke?

a. ischemic

b. hemorrhagic

a. ischemic

1 multiple choice option

what is the most common risk factor for ischemic stroke?

- HTN

- DM

- dyslipidemia

- tobacco use

- physical inactivity

how are ischemic strokes treated?

assess ABCs & vital signs

- stabilize the patient

- determine last known well

- obtain point of care glucose

- NIH stroke scale

- prepare to transfer

- stat CT of head w/o contrast to r/o intracranial hemorrhage (brain bleed)

- if no evidence of bleed is seen, stat CT angiography of head/neck to help determine location of obstruction

- tPA (door to needle time is < 60 mins)

- thrombectomy prn

- admit to ICU & neuro will follow

during ischemic stroke work-up, what is the purpose of doing a stat CT of head w/o contrast?

to r/o intracranial hemorrhage

during ischemic stroke work-up, what is the purpose of doing a stat CT angiography of head/neck?

done if no evidence of intracranial hemorrhage is seen on CT of head, to determine location of obstruction

what is the door-to-needle time for tPA in acute ischemic stroke?

< 60 mins

why is treatment of ischemic stroke time sensitive?

TIME IS BRAIN!

- for optimal recovery, tx should be performed w/i 3-4.5 hrs for thrombolytic therapy & w/i 24 hrs for thrombectomy

for ischemic stroke, thrombolytic therapy should be performed within _________ hrs for optimal recovery

3-4.5 hrs

3 multiple choice options

for ischemic stroke, thrombectomy should be performed within _________ hrs for optimal recovery

24 hrs

3 multiple choice options

what is a transient ischemic attack (TIA)?

s/s of a stroke that last minutes w/ resolution

how are TIAs treated?

full workup for stroke

- consider short term DAPT (aspirin & clopidogrel)

what is the number one cause of intraparenchymal hemorrhage (IPH)?

HTN

how can you differentiate between acute ischemic stroke & IPH?

they present similar, but IPH will have more altered mental status

- CT of head will definitively differentiate

how are acute IPHs treated?

all the same initial treatments of stroke (ABCs, bedside glucose, NIH stroke score)

- stabilize & prepare to transfer

- reverse anticoagulants if taking

* give PCC & Vit K IV for goal INR < 1.4 if taking warfarin

* give PCC if taking a NOAC (rivaroxaban, apixaban, or dabigatran)

- control BP (systolic <160 w/ IV beta blockers or CCB)

- seizure prophylaxis

- neurosurgical consult

- admit to ICU for monitoring

- CT angiography 4-6 hrs from initial CT of head to document stability (no more bleeding)

for IPH treatment, when should you give prothrombin complex concentrate (PCC)?

- w/ Vit K IV if taking warfarin

- if taking a NOAC (rivaroxaban, apixaban, or dabigatran)

when giving PCC + Vit K IV for reversal of warfarin in IPH treatment, what is the INR goal?

< 1.4

when giving a BB or CCB for BP control in IPH treatment, what is the BP goal?

systolic < 160

during IPH treatment, CT angiography should be repeated _______ hrs from initial CT of head to document that there is no more bleed

4-6 hrs

3 multiple choice options

what is the secondary prevention of stroke treatment?

if unable to be treated w/ tPA (outside of 3-4.5 hr window), they are to receive 325mg aspirin po if not currently on any anticoagulants; otherwise, aspirin is initiated 24 hrs post-tPA

- mgmt of modifiable risk factors (managing BP, lipids, blood glucose, encouraging healthy diet & exercise)

- high intensity statin

- appropriate anticoagulation

- patient education regarding signs of stroke & when to call 911

s/s of subarachnoid hemorrhage (SAH)

worst headache of their life (thunderclap headache)

- syncopal episodes

- N/V

- confusion or irritability

- possible nuchal rigidity &/or positive brudzinski sign

worst HA of life (thunderclap HA) =

SAH

what are SAHs caused by?

most commonly trauma, but could also be a ruptured aneurysm

how is a SAH diagnosed?

stat CT of head w/o contrast

- if not seen on CT, but suspicion is high then LP is indicated

- gold standard to detect cause = cerebral angiogram

what is the goal standard imaging to detect the cause of a SAH?

cerebral angiogram

3 multiple choice options

LP finding consistent w/ SAH:

RBCs w/ xanthochromia

what are the characteristics of myasthenia gravis?

- generalized symmetrical weakness (especially proximal limb weakness, neck muscles, diaphragm, & eye muscles)

- dysphagia

- dysarthria

- facial weakness

- nasal tone voice

- repetition exacerbates weakness

- reflexes & sensory exam are normal

s/s of guillain barre syndrome (GBS)

usually preceded by an infection or other immune stimulation

- rapidly progressive bilateral weakness

- classically starting distally (ascending weakness), but can start proximally

- paraparesis

- possible cranial nerve involvement

- ataxia &/or dysautonomia

- reduced or absent reflexes

how is GBS treated?

HOSPITALIZE

- intravenous immunoglobulin (IVIG) &/or plasma exchange

- supportive care: anticoagulation, monitor autonomic function, mechanical ventilation, swallow eval & nutritional support, pain mgmt (gabapentin or carbamazepine), &/or PT

myasthenia or GBS?

- generalized, symmetrical proximal weakness

- repetition exacerbates weakness

- reflexes & sensory exam are normal

myasthenia gravis

1 multiple choice option

myasthenia or GBS?

- preceded by an infection

- rapidly progressive, symmetrical distal weakness

- reflexes & sensory exam are reduced or absent

gullian barre syndrome (GBS)

1 multiple choice option