Diagnosis and Management of Acute Stroke

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Diagnosis and Management of Acute Stroke Briana Witherspoon DNP, ACNP-BC

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Diagnosis and Management of Acute Stroke. Briana Witherspoon DNP, ACNP-BC. Stroke Objectives. Review etiology of strokes Identify likely location/type of stroke based of physical exam Acute management of ischemic stroke Acute management of hemorrhagic stroke. Stroke Fast Facts. - PowerPoint PPT Presentation

Transcript of Diagnosis and Management of Acute Stroke

Page 1: Diagnosis and Management of Acute Stroke

Diagnosis and Management of Acute Stroke

Briana Witherspoon DNP, ACNP-BC

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Stroke Objectives

• Review etiology of strokes• Identify likely location/type of stroke based of

physical exam• Acute management of ischemic stroke• Acute management of hemorrhagic stroke

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Stroke Fast Facts • Affects ~ 800, 000 people per year• Leading cause of disability, cognitive impairment,

and death in the United States• Accounts for 1.7% of national health expenditures.• Estimated U.S. cost for 2012 = $71.5 billion

– Mostly hospital (esp. LOS) & post stroke costs– Appropriate use of IV t-PA s long-term cost– Appropriate billing for AIS w/ thrombolysis ( hospital

reimbursement from $5k to $11.5k)Stroke. 2013;44:2361-2375

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Where We’re Headed• By 2030 ~ 4% of the US population over the

age of 18 is projected to have had a stroke• Between 2012 and 2030, total direct stroke-

related medical costs are expected to increase from $71.55 billion to $183.13 billion

• Total annual costs of stroke are projected to increase to $240.67 billion by 2030, an increase of 129%

Stroke. 2013;44:2361-2375

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Three Stroke TypesIschemicStroke

Clot occludingartery85%

Intracerebral Hemorrhage

Bleedinginto brain

10%

Subarachnoid Hemorrhage

Bleeding around brain5%

www.acponline.org/about_acp/chapters/ok/gordon.ppt

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http://www.phillystroke.org/content/learn_about_stroke/act_fast.asp

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NIHSS• NIHSS (National Institute of Health Stroke Scale)

– Standardized method used by health care professionals to measure the level of impairment caused by a stroke

– Purpose• Main use is as a clinical assessment tool to determine whether

the degree of disability is severe enough to warrant the use of tPA

• Another important use of the NIHSS is in research, where it allows for the objective comparison of efficacy across different stroke treatments and rehabilitation interventions

– Scores are totaled to determine level of severity– Can also serve as a tool to determine if a change in exam has

occurred

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Breaking Down the Scale• 13 item scoring system, 7 minute exam • Integrates neurologic exam components• CN (visual), motor, sensory, cerebellar,

inattention, language, LOC• Maximum score is 42, signifying severe stroke• Minimum score is 0, a normal exam• Scores greater than 15-20 are more severe

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NIHSS cont.• NIHSS Interpretation

Stroke Scale Stroke Severity

0 No Stroke

1-4 Minor Stroke

5-15 Moderate Stroke

15-20 Moderate/Severe Stroke

21-42 Severe Stroke

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NIHSS and Outcome Prediction

• NIHSS below 12-14 will have an 80% good or excellent outcome

• NIHSS above 20-26 will have less than a 20% good or excellent outcome

• Lacunar infarct patients had the best outcomes

Adams HP Neurology 1999;53:126-131Baseline NIH Stroke Scale score strongly predicts outcome after stroke (TOAST)

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Etiology of Ischemic StrokesLARGE VESSEL THROMBOTIC:Virchow’s Triad….• Blood vessel injury

- HTN, Atherosclerosis, Vasculitis• Stasis/turbulent blood flow

- Atherosclerosis, A. fib., Valve disorders• Hypercoagulable state

- Increased number of platelets- Deficiency of anti-coagulation factors - Presence of pro-coagulation factors- Cancer

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Etiology Of Ischemic Stroke:

LARGE VESSEL EMBOLIC:• The Heart

– Valve diseases, A. Fib, Dilated cardiomyopathy, Myxoma

• Arterial Circulation (artery to artery emboli)– Atherosclerosis of carotid, Arterial dissection, Vasculitis

• The Venous Circulation – PFO w/R to L shunt, Emboli

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Determining the Location• Large Vessel:

– Look for cortical signs

• Small Vessel:– No cortical signs on exam

• Posterior Circulation:– Crossed signs– Cranial nerve findings

• Watershed:– Look at watershed and borderzone areas– Hypo-perfusion

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Cortical SignsRIGHT BRAIN: LEFT BRAIN:

- Right gaze preference - Left gaze preference

- Neglect - Aphasia

• If present, think LARGE VESSEL stroke

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Large Vessel Stroke Syndromes• MCA:

– Arm>leg weakness– LMCA cognitive: Aphasia– RMCA cognitive: Neglect,, topographical difficulty, apraxia,

constructional impairment

• ACA: – Leg>arm weakness, grasp– Cognitive: muteness, perseveration, abulia, disinhibition

• PCA: – Hemianopia– Cognitive: memory loss/confusion, alexia

• Cerebellum: – Ipsilateral ataxia

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Aphasia• Broca’s

– Expressive aphasia– Left posterior inferior

frontal gyrus

• Wernicke’s– Receptive aphasia– Posterior part of the superior temporal gyrus– Located on the dominant side (left) of the brain

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Case 1 • 74 year old African American female with sudden

onset of left-sided weakness

• She was at church when she noted left facial droop

• History of HTN and atrial fibrillation

• Meds: Losartan

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Case 1• BP- 172/89, P– 104, T- 98.0, RR– 22, O2- 94%

• General exam: Unremarkable except irregular rate and rhythm

• NEURO EXAM:- Speech dysarthric but language intact- Right gaze preference- Left facial droop- Left- sided hemiplegia- Neglect

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Case 1

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Case 1

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Case 1• Right MCA infarct, most likely cardioembolic from atrial fibrillation

• Patient underwent mechanical thrombectomy with intra-arterial verapamil, clot removal successful

• Excellent recovery – patient was discharged 48 hours later on Coumadin

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Determining the Location• Large Vessel:

– Look for cortical signs

• Small Vessel:– No cortical signs on exam

• Posterior Circulation:– Crossed signs– Cranial nerve findings

• Watershed:– Look for watershed pattern – S/S of Hypo-perfusion

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Etiology of Stroke

SMALL VESSEL (Lacunes <1.5cm)•Risk Factors

– HTN– HLD– DM– Tobacco Use– Sleep apnea

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Case 2

• 85 year old male who woke up with left face, arm, and leg numbness

• History of HTN, DM, and tobacco use

• Meds: Insulin, aspirin

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Case 2• BP- 168/96, P– 92

• General exam: Unremarkable, RRR

• NEURO EXAM:- Decreased sensation on left face, arm, and leg

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Case 2

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Case 2

• Right thalamic lacunar infarct• Not a candidate for intervention (WHY?)• Discharged to rehab 72 hours after admission

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Determining the Location• Large Vessel:

– Look for cortical signs

• Small Vessel:– No cortical signs on exam

• Posterior Circulation:– Crossed signs– Cranial nerve findings

• Watershed:– Look at watershed and borderzone areas– Hypo-perfusion

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Brainstem Stroke Syndromes

• Rarely presents with an isolated symptom

• Usually a combination of cranial nerve abnormalities, and crossed motor/sensory findings such as:

– Double vision– Facial numbness and/or weakness– Slurred speech– Difficulty swallowing– Ataxia– Vertigo– Nausea and vomiting– Hoarseness

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Case 3• 55 year old male with acute onset of right sided numbness

and tingling, left sided face pain and numbness, gait imbalance, nausea/vomiting, vertigo, swallowing difficulties, and hoarse speech

• History of CAD s/p CABG, DM2, HTN, HLD, OSA

• Meds: Aspirin, plavix, insulin, lipitor, metoprolol, lisinopril

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Case 3• NEURO EXAM: BP- 194/102, P– 105

• General exam: Unremarkable, RRR

• NEURO EXAM:- Decreased sensation on left face- Decreased sensation on right body- Left ataxia on FNF, and unsteady gait- Voice hoarse- Nystagmus

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Case 3

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Case 3

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Case 3

• Brainstem Stroke• Received IV tPa• Post-tPa symptoms greatly improved

regained sensation, ataxia resolved• Discharged home with out patient PT/OT

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Determining the Location• Large Vessel:

– Look for cortical signs

• Small Vessel:– No cortical signs on exam

• Posterior Circulation:– Crossed signs– Cranial nerve findings

• Watershed:– Look for the watershed pattern– Think about reasons of hypo-perfusion

• Hypotension• Stenosed vessel, etc

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Case 4• 56 year old female who upon waking post-op after elective

surgery was found to have L sided weakness and neglect

• History of HTN

• Meds - Lisinopril

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Case 4• BP- 132/74, P– 84

• General exam: Unremarkable, RRR

• NEURO EXAM:- Left face, arm, and leg weakness- Neglect- DTR’s brisk on the left, toe up on left

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• Right hemisphere watershed infarct secondary to hypoperfusion in the setting of Right ICA stenosis

• On review of anesthesia records, blood pressure dropped to 82/54 during the procedure

• Patient was discharged to in-patient rehab

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Intracranial Hemorrhages

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Etiology of ICH

• Traumatic• Spontaneous

– Hypertensive– Amyloid angiopathy– Aneurysmal rupture– Arteriovenous malformation rupture– Bleeding into tumor– Cocaine and amphetamine use

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Causes of ICH

http://spinwarp.ucsd.edu/neuroweb/Text/non-trauma-ER.htm

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Hypertensive ICH• Spontaneous rupture of a small artery deep in the brain• Typical sites

– Basal Ganglia– Cerebellum– Pons

• Typical clinical presentation– Patient typically awake and often stressed, then abrupt

onset of symptoms with acute decompensation

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Ganglionic Bleed • Contralateral hemiparesis• Hemisensory loss• Homonymous hemianopia• Conjugate deviation of eyes toward the side of the bleed or

downward• AMS (stupor, coma)

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Cerebellar Hemorrhage• Vomiting (more common in ICH than SAH or Ischemic CVA)• Ataxia• Eye deviation toward the opposite side of the bleed • Small sluggish pupils• AMS

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Cerebellar Hemorrhage

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Pontine Hemorrhage• Pin-point but reactive pupils• Abrupt onset of coma• Decerebrate posturing or flaccidity • Ataxic breathing pattern

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Pontine Hemorrhage

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Subarachnoid Hemorrhage• “Worst headache of my life”• AMS• Photophobia• Nuchal rigidity • Seizures• Nausea and vomiting

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Subarachnoid Hemorrhage

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Management

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Airway • Most likely related to decreased level of consciousness (LOC),

dysarthria, dysphagia• GCS < 8 - INTUBATE• Avoid Hyperventilation or Hypoventilation• NPO until swallow assessment completed- high aspiration risk • Begin mobilization as soon as clinically safe• Keep HOB greater than 30 degrees

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Stroke Algorithm

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ImagingCT scan• Non- contrast CTH remains

the gold standard as it is superior for showing IVH and ICH

• CT with contrast may help identify aneurysms, AVMs, or tumors but is not required to determine whether or not the patient is a tPa candidate

MRI• Superior for showing

underlying structural lesions• Contraindications

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Acute (4 hours)Infarction

Subtle blurring of gray-white junction & sulcal effacement

Subacute (4 days) Infarction

Obvious dark changes & “mass effect” (e.g.,

ventricle compression)

RR L L

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Multimodal ImagingMultimodal CT• Typically includes non-

contrast CT, perfusion CT, and CTA

• Two types of perfusion CT– Whole brain perfusion CT– Dynamic perfusion CT

Multimodal MRI• Standard MRI sequences

( T1 weighted, T2 weighted, and proton density) are relatively insensitive to changes in cerebral ischemia

• Multimodal adds diffuse-weighted imaging (DWI) and PWI (perfusion- weighted imaging)

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tPaFast Facts• Tissue plasminogen

activator• “clot buster”• IV tpa window 3 hours• IA tpa window 4.5 hours • Disability risk 30% despite

~5% symptomatic ICH risk

Contraindications• Hemorrhage• SBP > 185 or DBP > 110• Recent surgery, trauma or

stroke • Coagulopathy• Seizure at onset of symptoms• NIHSS >21 • Age?• Glucose < 50

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Mechanical Thrombolysis• Often used in adjunct with tPa• MERCI (Mechanical Embolus Removal in

Cerebral Ischemia) Retrieval System is a corkscrew-like apparatus designed to remove clots from vessels

• PENUMBRA system aspirates the clot

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Blood Pressure Management•BP Management

– The goal is to maintain cerebral perfusion!!– CPP = MAP – ICP (needs to be at least 70)– Higher BP goals with Ischemic stroke– Lower BP goals with Hemorrhagic stroke (avoid hemorrhagic

expansion, especially in AVMs and aneurysms)

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BP-AIS Relationship• BP increase is due to

arterial occlusion (i.e., an effort to perfuse penumbra)

• Failure to recanalize (w/ or w/o thrombolytic therapy) results in high BP and poor neuro outcomes

• Lowering BP starves penumbra, worsens outcomes

Penumbra

Core

Clot in Artery

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Save the Penumbra!!

CEREBRALBLOODFLOW(ml/100g/min)

CBF< 8

CBF8-18

TIME (hours)1 2 3

20

15

10

5

PENUMBRA

CORE

Neuronal dysfunctio

n

Neuronal death

Normal function

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Supportive Therapy

• Glucose Management– Infarction size and edema increase with acute and chronic

hyperglycemia– Hyperglycemia is an independent risk factor for hemorrhage

when stroke is treated with t-PA• Antiepileptic Drugs

– Seizures are common after hemorrhagic CVAs– ICH related seizures are generally non-convulsive and are

associated to with higher NIHSS scores, a midline shift, and tend to predict poorer outcomes

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Hyperthermia

• Treat fevers!– Evidence shows that fevers > 37.5 C that persists

for > 24 hrs correlates with ventricular extension and is found in 83% of patients with poor outcomes

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References• Adams, H., del Zappo, G., Alberts, M., Bhatt, D., Brass, L., Furlan, A., Grubb, R., &

Higashida, R. (2007). Guidelines for the early management of adults with ischemic stroke. Stroke, 38, 1655-1711.

• Bradley G Walter, Daroff B Robert, Fenichel M Gerald, Jancovic, Joseph; Neurology in clinical practice, principles of diagnosis and

management. Philadelphia Elsevier, 2004.

• Castillo, J., Leira, R., Garcia, M., Serena, J., Blanco, M. Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor

stroke outcome. Stroke. 2004: 35: 520-526.• Goals for Management of Patients With Suspected Stroke Algorithm.

http://circ.ahajournals.org/content/112/24_suppl/IV-111/F1.expansion.html. Accessed May 8, 2012

• Gordon, D. L. (n.d.). Update in stroke management . Retrieved from www.acponline.org/about_acp/chapters/ok/gordon.ppt

• Hesselink, J. Imaging of cerebral hemorrhages and AV malformations. http://spinwarp.ucsd.edu/neuroweb/Text/br-740.htm. accessed May 10, 2012.

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