StrokeACNP Bootcamp 2012

Briana Witherspoon, MSN, ACNP-BC, CCRN, CNRN

Stroke Objectives

• Review Ischemic Stroke Algorithm• Identifying location of ischemic stroke• Acute management of an ischemic stroke• Acute management of hemorrhagic stroke

Stroke Algorithm

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

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

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

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)

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

Etiology Of 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, Fat, air, or septic emboli

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

Cortical SignsRIGHT BRAIN: LEFT BRAIN:

- Right gaze preference - Left gaze preference

- Neglect - Aphasia

• If present, think LARGE VESSEL stroke

Large Vessel Stroke Syndromes• MCA:

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

apraxia, constructional impairment

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

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

• Cerebellum: – Ipsilateral ataxia

Circle of Willis

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

Case 1 • 71 year old female with sudden onset of left-sided

weakness

• She was out with her sisters when she suddenly slumped her head and appeared to have a left facial droop

• History of HTN and atrial fibrillation

• Meds: Losartan

Case 1• BP- 142/83, 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- DTR's are symmetric, Left toe up

Case 1

Case 1

Case 1

Case 1

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

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

Etiology of StrokeSMALL VESSEL (Lacunes <1.5cm)•Risk Factors

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

Case 2 • 65 year old male with acute onset of left face, arm, and leg

numbness

• History of HTN, DM, and tobacco use

• Meds: Insulin, aspirin

Case 2• BP- 168/96, P– 92

• General exam: Unremarkable, RRR

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

Case 2

Case 2

• Right thalamic lacunar infarct

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

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

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

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

Case 3

Case 3

Case 3 • Brainstem Stroke

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

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

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

Case 4

Case 4

Case 4

Case 4

Case 4

Case 4

Case 4

Case 4• 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

Intracranial Hemorrhages

Causes of ICH • Traumatic• Spontaneous

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

Causes of ICH

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

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

downward• AMS (stupor, coma)

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

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

Cerebral Hemorrhage

JPG

Management

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

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

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)

tPaFast Facts

• Tissue plasminogen activator

• “clot buster”• IV tpa window 3 hours• IA tpa window 4.5 hours

Contraindications• Hemorrhage• SBP > 185 or DBP > 110, or

aggressive treatment (IV medication) necessary to achieve these limits

• Surgery, trauma or stroke within last 3 months

• Coagulopathy• Seizure at onset of symptoms• NIHSS <4, >21• Age?

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

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)

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

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

Hypothermia• “ Although strong experimental and clinical

evidence indicates that induced hypothermia can protect the brain in the presence of hypoxia or ischemia, including cardiac arrest, data about the utility of induced hypothermia for patients with acute stroke are not yet available”.

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

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

Questions?