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Flashcards in Neuro Emergencies Deck (64)
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What is a good imitator of a stroke?

- hypoglycemia:
give sugar and thiamine - reverse quickly


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

- what high BP so brain is still being perfused


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

- to prevent brain cells from swelling


Reversal agents for warfarin?

- FFP and Vit K
(FFP works faster)


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

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


PE of AMS?

- ABCs, VS
- bedside glucose
- look quickly for immediate life threats:
abnormal resp
- don't be afraid to give glucose, thiamine, based on H and P
- Head to toe exam


DDx for AMS:

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


Tx of AMS?

- underlying cause


What is status epilepticus?

- 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


Etiologies of status epilepticus?

- 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


Initial assessment/tx of status epilepticus?

- 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


First line tx for status epilepticus?

- 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


Post ictal state?

- 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


Cause of acute ischemic stroke?

- 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


Hx questions for stroke pt and family?

- 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


PE for ischemic stroke pt?

- level of consciousness
- eye exam
- CN
- motor exam
- sensory exam
- reflexes
- cerebellar exam


W/u of ischemic stroke?

- labs: POCT BG, CBC


Action time needed for AIS tx?

- 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


Characteristics of ACA stroke?

- dysarthria, aphasia
- unilateral contralateral motor weakness (lower more than upper)
- LE sensory changes
- urinary incontinence


Characteristics of MCA stroke?

- 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)


Characteristics of PCA stroke?

- contralateral hemianopsia
- cortical blindness
- impaired memory


Initial tx for AIS?

- 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


Thrombolytics used for AIS? indications?

- 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


CIs to tPA?

- 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


Use of mechanical thrombectomy in AIS?

- 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


Diff types of ICH?

- intra-parenchymal (IPH)
- intra-ventricular (IVH)
- subarachnoid (SAH)


What is a IPH? Signs and sxs?

- 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


IPH etiology?

- 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


etiology, s/s?

- 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


Tx of IPH/IVH?

- 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


RFs for SAH?

- 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


S/S of SAH?

- 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
- nuchal rigidity


Tx of SAH?

- 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


TBI most common in what age group? Diff types?

- 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


Head trauma hx questions?

- 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


Initial Assessment of TBI?

- 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


Head injury: PE? Labs?

- rapid primary survey
- VS: cushings triad?
- examining head for signs of outward trauma (penetrating, lacerations, swelling, bruises, abrasions)
- pt should be in c-spine collar
- neuro exam:
level of alertness
look for focal deficits

- labs: CBC, chem, coags, toxicology


How does GCS correlate to injury?

- 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


Guidelines for CT scan in ER?

- 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


Cerebral blood flow and perfusion?

- supplied from internal carotid and vertebral arteries
- drains via cerebral veins and dural sinuses into internal jugular veins
- receives 10-15% of CO
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%


Intracranial compliance - compensatory mech?

- 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


What are causes of increased ICP?

- 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)


S/S of increased ICP?

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


Indicications for ICP monitoring?

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


non-invasive techniques for ICP monitoring?

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


Management of ICP?

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


Tx of fever - in IICP?

- 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


Management of hyperventilation?

- 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


Intubation in IICP?

- 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


Use of mannitol in IICP?

- 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


use of hypertonic saline in IICP?

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


Sedation for management of IICP?

- decreases ICP by reducing metabolic demand
- propofol has good effet since it is easily titratable and has short 1/2 life


When is heavy sedation and paralysis used in IICP?

- 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


Use of craniectomy w/ IICP?

- 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


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



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

- induced hypoventilation


Etiologies of vertigo?

- 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


Dx of vertigo?

- 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


What is a TIA? sxs?

- 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


TIA and CVA correlation?

- 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


TIA w/u?

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


What is myasthenic crisis?

- 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


Acute exacerbations of MS?

- 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


Presentation of Guillian Barre syndrome?

- 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