Different Strokes for Different Folks: Assessment, Interventions, and Outcomes

Mary Kay Bader Level: Intermediate

Content Description
Patients presenting to the hospital with an acute ischemic or hemorrhagic stroke must be rapidly identified so that the hospitals stroke team can be accessed and emergent care provided. From the Emergent phase in the ED to the diagnostic/operative phase in Radiology/OR to the ICU, critical care nurses must be knowledgeable and involved in the care of the acute stroke patient. ICU nurses must be familiar with the national standards for stroke centers devised by the American Stroke Association, evidenced based protocols for assessing, diagnosing, and intervening with stroke patients, and the continuum of care after the patient leaves the ICU including the latest disease specific indicators from the JCAHO. This session will focus on the: a) hyperacute ischemic stroke patient including assessing, intervening with thrombolytics, and managing the critical phase after admission; b) acute ischemic stroke patient admitted to a progressive care stroke unit; and c) hemorrhagic stroke patients including critical interventions in the ED, OR, and ICU, and evidenced based protocols to reduce death/disability associated with this potentially devastating condition.

surrounded by marginally perfused area known as the penumbra i. Interruption of circulation to brain ii. Cellular responses to reduced flow c. Cerebral Edema and increased ICP i. Occurs as a natural evolution of the ischemic insult ii. Minimized if restore perfusion iii. Assess for signs of increased ICP: Decreased LOC, agitation, worsening of motor exam, papillary changes/changes in cranial nerve exam iv. Even though patient may receive thrombolysis, does not equate to no edema v. Watch the large MCA occulusions for development of malignant MCA syndrome d. Blood pressure, blood glucose and temperature Issues in Stroke Management i. BP and Stroke - Ischemic Stroke ii. Glucose iii. Body temperature 4. Identity major elements of a primary stroke center including organization, personnel and protocols a. Primary Stroke Center Characteristics i. Compliance with consensus-based national standards ii. Effective use of established clinical practice guidelines to manage and optimize care iii. An organized approach to performance measurement and improvement activities b. 2008 Framework i. Domains ii. Stroke Measures 2008 c. Evidence Based Protocols i. Emergency care of patients with ischemic and hemorrhagic stroke Evidence Based practice protocols a. Review of the literature and consensus by practitioners: development of evidence based protocols; refinement of protocols based on ASA/ AHA guidelines for ischemic and hemorrhagic stroke; b. Protocols: Hyperacute Ischemic/Hemorrhagic Stroke Protocol vs. Acute Ischemic Stroke Protocol i. Purpose: To rapidly identify and manage patients identified with acute ischemic stroke presenting within 6 hours of symptom onset or hemorrhagic stroke. Case Studies: Ischemic vs Hemorrhagic

Learning Outcomes
At the end of this session the attendee will be able to: 1. Differentiate between the pathophysiology of acute ischemic and hemorrhagic stroke 2. Relate the evidence based recommendations for primary stroke centers from the ASA/JCAHO as well as practice protocols for hyperacute ischemic/ hemorrhagic stroke to the acute stroke patient population 3. Apply the information presented on stroke management to actual case studies

Summary of Key Points

1. Introduction: BRAIN ATTACK a. Definition: abrupt and dramatic development of a focal neurologic deficit caused by arterial occlusion or hemorrhage b. Statistics of stroke Classification of stroke a. Ischemic stroke b. Hemorrhagic stroke Pathophysiology of Ischemic Stroke a. Mechanisms of ischemic stroke formation i. Ischemic stroke-thrombus formation b. Pathophysiology of occlusion: dense ischemic core of tissue where CBF falls dramatically 5.

2.

3.

6.

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Bibliography/Webliography
Adams HP, delZ oppo G, Albers M, , Bhatt D, et al. (2007). Guidelines for the Early Management of Patients With Ischemic Stroke: A Scientific Statement From the Stroke Council of the American Stroke Association. Stroke 38:1655-1711. Broderick, J, Connolly S, Feldmann E, et al. (2007). Guidelines for the Management of Spontaneous Intracerebral hemorrhage in Adults. 2007 Update. A guideline from the American Heart Association, American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Stroke published online May 3, 2007; DOI:10.1161/ STROKEAHA.107.183689. http://stroke.ahajournals.org. Castillo J, Leira R, Garcia MM, Serena J, Blanco M, Davalos A. 2004. Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome. Stroke 35(2):520-6. Hemmen T and Lyden P. (2007). Induced hypothermia for Acute Stroke. Stroke 38:794-799.

AACN 2009 NTI & CRITICAL CARE EXPOSITION

Different Strokes for Different Folks: Assessment, Interventions, and Outcomes

Presented by Mary Kay Bader, RN, MSN CCNS, CNRN, CCRN, FAHA Mission Hospital A JCAHO Certified Primary Stroke Center

Disclosures
Mary Kay Bader
Speakers Bureau Integra Neurosciences

Introduction
Definition
Abrupt and dramatic development of a focal neurologic deficit caused by an occlusion or hemorrhage of a vessel feeding the brain g g

Anatomy of Cerebral Vasculature

Anterior circulation Posterior circulation

Statistics
750,000 new strokes each year 3rd leading cause of death in US

Stroke Signs/Symptoms
Classic Signs/symptoms: FAST
Weakness of arm/leg Difficulty speaking Droopy smile Headache Visual problems Numbness/tingling on one side of body

Stroke Signs/Symptoms
Timing
TIAthe debate continues
Transient appearance of symptoms/signs that pp disappear within
15 minutes ??? 24 hours???

Negative MRI demonstrating no signs of ischemia

Stroke
Symptoms/signs do not go away

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Stroke
Ischemic - 80-85% Hemorrhagic - 15-20%
Intracerebral Subarachnoid Hemorrhage
Aneurysm Vascular Malformations

Pathophysiology

Pathophysiology of Ischemic Stroke

Dense core of dead tissue Penumbra Interruption of blood flow

Pathology of Occlusion
Once vessel is occluded
Systemic arterial BP influences CPP and collateral blood flow during ischemia Permanent ischemic cell death ensues after 30 minutes
Continued ischemia (< 50% of baseline CBF) will kill the rest of the vessel territory What can save this area around core?

Collateral Flow
Example MCA occlusion
Leptomeningeal arteries Cross perfusion from internal system
Opposite side Posterior circulation

Pathophysiology of Ischemic Stroke

Cellular Responses to reduced Flow Disturbances in calcium homeostasis Buildup of lactic acidosis Oxygen free radical production

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Pathophysiology of Ischemic Stroke

Three Factors Affecting Outcome
Time dependent Degree of ischemia Collateral circulation

Pathophysiological Issues Related to Stroke

Edema and Increased ICP
Occurs as natural evolution of insult Minimized if restore perfusion Assess for change in neurologic status
Do not medicate with sedation agents unless monitoring for increased ICP Prepare for CT

Two Effective Therapies for Stroke

Thrombolysis
Reduces death and disability

Pathophysiological Issues Related to Stroke

Blood Pressure Blood Glucose Temperature

Comprehensive Stroke Care

M ltidi i li Multidisciplinary t teamwork reduces mortality k d t lit by more than 25% Focus
BP Blood glucose Temperature

Pathophysiology: BP & Stroke

Alteration in cerebral blood flow Brain perfusion dependent on MAP Increases in BP
may be normal homeostatic response usually falls spontaneously within 24 hours to several days

Pathophysiology: BP & Stroke

Treat BP in acute ischemic stroke
No thrombolytics Systolic > 220 mm Hg Diastolic > 120 mm Hg MAP > 130 mm Hg Thrombolytics Systolic > 180-185 mm Hg Diastolic > 100-110 mm Hg

Do Not treat BP unless...

Hill & Hachinski, The Lancet 1998. 352: (suppl III) 10-14. 10-

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Pathophysiology: Serum Glucose & Stroke

Increase in infarct size and edema occur with acute and chronic hyperglycemia Studies showed a correlation between increased morbidity and mortality and serum glucose levels above normal

Pathophysiology: Serum Glucose & Stroke

High serum glucose was an independent risk factor for hemorrhage after treatment with tPA in one study1 Avoid IV glucose solutions Treat hyperglycemia
Maintain blood glucose < 140

Hill & Hachinski, The Lancet 1998. 352: (suppl III) 10-14. 10-

1Demchuck,

Morgenstern, Kochanski et al. Stroke 1998; 29: 273

Pathophysiology: Body Temperature & Stroke

Temperature control
A id h Avoid hyperthermia h i Neuro Populations ++ Stroke

Why develop a stroke center

Improved outcomes associated with stroke centers Increase use of tPA in acute ischemic stroke 1 5% to 10 2% -Lattimore et al 1.5% 10.2% Lattimore

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Why develop a stroke center?

Seven states have mandated stroke center systems:
Florida, Massachusetts, New Jersey, Maryland, Michigan, New Mexico, and Texas

Stroke Care: PSC vs CSC

PSC
Personnel, programs, expertise, and infrastructure to care for patients with uncomplicated stroke
Use tPA and admit to stroke units

CSC
Cares for patients with complicated types of strokes, ICH, SAH, and those pts who need interventional tx, surgery and a Neuro ICU

AHA/ASA scientific statement

recommends the creation of acute stroke Centers and recommend certification by a governing body (Level 1B)

Achieving Success: The Nuts and Bolts

Creation of Evidence Based protocols
Review of literature and consensus by practitioners Development of evidence based protocols Refinement of protocols based on ASA/AHA guidelines for ischemic and hemorrhagic stroke

Evidence Based Protocols

Consensus by practitioners
Develop EBP protocols
BP management Hyperglycemia Fever Fe er ASA within 48 hours of admit Prevention of complications
Aspiration DVT UTI

Evidence Based Protocols

Consensus by practitioners
Develop EBP protocols
Designate acute stroke unit Neurology involvement A Fib management Lipid profile Discharge: antithrombotics, stroke ed, smoking cessation, and rehab consult Establish measurable stroke goals

Evidence Based Protocols

Hyperacute Ischemic/Hemorrhagic
Purpose: rapidly identify and manage patients identified with acute ischemic stroke presenting within 6 hours of symptom onset (ischemic) or hemorrhagic stroke Purpose: provide evidence based protocol to minimize complications and facilitate recovery in patients unable to receive tPA

Acute Ischemic Stroke protocol

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Evidence Based Protocols

Designation of patient and activation of stroke team Initial team interventions
Assess: Primary/secondary survey NIHSS

Evidence Based Protocols

Initial team interventions
Tests
Labs, chest-x-ray, 12 lead

ED MD consult with 10 minutes Notification of neurologist within 15 minutes To CT scan within 25 minutes/interpret by 45 minutes

Evidence Based Protocol Medical Management

Goal: reestablish perfusion Rule out stroke mimics Interventions

Ischemic Stroke Management g

Job 1: R/O Stroke Mimics

Intracranial hemorrhage Post-seizure (Todds) Paralysis Hypoglycemia Complicated migraine Brain tumor/metastasis Brain abscess or encephalitis Conversion disorder or malingering

Job 2: Treatment Decisions

Acute

Treatment Options Ischemic

Within 180 minutes tPA unless contraindicated IV (typical dose 60-90 mg total) 60 90 given in ED then admit to ICU IV/IA give 2/3 of dose IV then to angio suite Within 6 hours of presentation IA tPA with typical dose 5-8 mg Merci retrieval device Within 8 hours of presentation Merci retrieval device

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Job 3: Consider Intravenous tPA

Results of NINDS trial
patients receiving tPA within 3 hours of symptoms onset had better outcomes at 3 months than those treated with placebo increase risk of intracerebral hemorrhage in patients treated with tPA NIH stroke score > 201 Brain edema or mass effect on CT1

Intravenous tPA Time Window < 3 hours

1NINDS

Study Group. Stroke 1997. 28: 2109-2118.

IV tPA: Nursing Management

Start 2nd IV for thrombolytics Reassess neuro status using NIHSS q 15 min Weigh patient or assess likely weight Avoid invasive tubes: foley/NG

Infusion Guidelines tPA

Preparation of IV tPA drip
0.9 mg/kg 10% IV bolus over 1-2 minutes 90% IV over 60 minutes

Administration of tPA
Monitor VS: Q 15 min x 2 hrs, Q 30 min x 6 hrs, then Q 1 hour x 16 hours Treat BP accordingly

ICU Phase Interventions

Monitor neuro checks/VS
every 15 minutes x 2 hours, every 30 minutes x 6 hours then every hour Use labetalol or nicardipine

ICU Phase Interventions

Check blood glucose levels q 4 hours x 2
If elevated > 140 mg/dl, contact MD for intensive insulin therapy vs sliding scale

Maintain systolic BP < 180-185 mm Hg or diastolic BP < 100-110 mm Hg 100 110 No invasive tubes for 24 hours Do not give

Maintain temperature 36-37 degrees p g Watch for peak edema 48-72 hours

Keep NPO until swallow assessment done

ASA, heparin, warfarin, ticlid, lovenox, plavix, aggrenox, fragmin, or antithrombotic/antiplatelet

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ICU Phase Interventions

TED hose/compression boots Check orthostatic vital signs Aggressive pulmonary toilet Skin/mobility issues Consult PT/OT/ST/Rehab and physiatrist

Job 4: Consider Interventional Options

Intraarterial tPA Merci Retrieval Time Window < 6 hours

Intraarterial Thrombolytics
Time window is < 6 hours Requires cerebral angiogram and trained interventional neuroradiologist
Prepare patient for cerebral angiography Femoral site and insertion of catheter Technique for superselective catheter placement into clot

Job 4: Consider Interventional Options

Intraarterial tPA Merci Retrieval Time Window < 6 hours

BP control: Systolic >180/Diastolic > 100

Intraarterial Thrombolytics
Time window is < 6 hours Requires cerebral angiogram and trained interventional neuroradiologist
P Prepare patient for cerebral angiography ti t f b l i h Femoral site and insertion of catheter Technique for superselective catheter placement into clot

Job 5: No tPA
Optimize Systems!! Prevent Complications!!

BP control: Systolic >180/Diastolic > 100

AACN 2009 NTI & CRITICAL CARE EXPOSITION

No tPA: Admit to Stroke Unit

Supportive therapy of patient if tPA not administered or is admitted 6 hours or more after onset of symptoms
Admit to designated Stroke Unit
Monitored bed, 1:3 staff ratio B/P management for ischemic stroke: treat SBP >220 or DBP >120.
DO NOT USE SL NIFEDIPINE

No tPA: Admit to Stroke Unit

Administer 325 mm ASA within 12 hours of admission per rectum if NPO or orally is swallow evaluation complete and patient safe to swallow Implement measures to prevent complications:
DVT prophylaxis, aspiration precautions, reduce blood glucose, treat fever

Consult OT/PT/ST and physiatrist within 24 hours of arrival

No tPA: Admit to ICU

Unable to control BP with labetalol, mechanical ventilation, malignant MCA syndrome, or brain stem stroke
Evaluate BP and treat as follow per MD order:
T t if SBP >220 or DBP > 120 Treat Labetalol or nicardipine

Hemorrhagic Stroke Management g

Monitor neuro check/vital signs hourly Reduce risk of complication: aspiration, DVT; treat hyperglycemia and fevers Give ASA/Antithrombotic medication within 48 hours of admit Consult OT/PT/ST and physiatrist on day after admission

Etiology ICH
Systemic hypertension

Intracerebral Hemorrhage

56-81% of all cases Aka Charcot-Bouchard microaneurysms S ll perforating Small f ti branches of lenticulostriate arteries 46% of hypertensive patients > 66 years of age

Brain tumors
Usually malignant

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Etiology ICH
Systemic hemorrhagic disorders Cerebral amyloid angiopathy
Pathological deposits of beta amyloid protein within walls of small meningeal and cortical vessels (esp. white matter) Common in > 70 years of age

Epidemiology
10-20% of all strokes 30 day mortality 43% Incidence varies
Increases with age Race
African-Americans 32 per 100,000 Caucasians 15 per 100,000

Anticoagulants Venous infarction Vasculitis Drug abuse: cocaine, amphetamines

Prevention
Non-modifiable Modifiable
Hypertension Age, gender and race

Pathophysiology
Rupture of vessel from pressure, pathological changes to vessels, congenital weakness Changes in tissue
release toxins from hematoma local decrease in perfusion cellular changes

Tx of mild to moderate HTN reduces by 36-48% Tx of isolated systolic HTN in elderly by 50%

Reduction/cessation of drug use Anticoagulant use: Keep INR < 3

Intracranial Pressure
Normal range
Children 0-10 mm Hg Adolescents/Adults 0-15 mm Hg g

Pathophysiological Issues Related to Hemorrhagic Stroke Edema and Increased ICP

Concern: Is the brain receiving enough blood flow to maintain cerebral oxygenation

Abnormal ranges
Infant/Child
moderate > 15 mm Hg severe > 20 mm Hg

New technology to monitor brain tissue oxygen

Adolescent/Adults
moderate 20-40 severe > 40 mm Hg

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Brain Tissue Oxygen (Pbt02)

Normal: 20-40 mm Hg Risk of death increases
< 15 mm Hg for 30 minutes < 10 mm H f 10 minutes Hg for i t

Pathophysiology: Interventions and PbtO2

Decreasing PbtO2
Hypoxia Low Hemoglobin g Decreasing PaCO2 Increased ICP Decreased MAP Increasing temperature Systemic Causes
Pulmonary Cardiac/Hemodynamic

Increasing PbtO2
Increasing FIO2 Increasing Hemoglobin g g Increasing PaCO2 Draining CSF Decreasing ICP Increasing MAP Decreasing temperature Barbiturates

PbtO2 < 5 mm Hg
high mortality

PbtO2 < 2mm Hg - neuronal death

Assessment
Subjective
Sudden onset of focal deficit Severe headache Nausea and vomiting g Decrease LOC Motor deficits if large hemorrhage Sensory deficit CN abnormalities

Medical Management
Dependent on multiple factors
Age Pre-morbid condition Location and size of ICH Patients advance directive
No aggressive life support = institute palliative care Aggressive interventions Get the neurosurgeon involved!

Objective

Medical Management
Aggressive Management Options
Surgical Non-surgical Pharmacologic
Factor VIIa
Phase III failed to show decrease in mortality

Medical Management
CT demonstrates hemorrhage
ICH deep bleed
Medical team factors location of clot/age/ g advanced directive If family wants Tx- go to OR for ICP and will treat medically

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Medical Management
CT demonstrates hemorrhage
ICH Cerebellum
Usually present with severe g y headache, nuchal rigidity, n/v, balance problems, coordinationto posturing and coma Emergently treated OR

Medical Management
Non-operative management
Maintain airway, ventilation, and circulatory support Supportive therapy for systems Ventriculostomy/LICOX

Hemorrhagic Stroke Protocol

Assess oxygenation/ventilation
If decreased LOC, unable to maintain patent airway, motor score < 5, PaCO2 > 45
RSI Watch administration of paralyticalways must follow with IV sedation/analgesia Keep PaCO2 > 35 do not hyperventilate Keep 100% FIO2 Pulse oximetry, capnography, and watch vent alarms

Hemorrhagic Stroke Protocol

Circulation
Start 2 IV lines BP must be kept < Systolic 150 mm Hg
Treat with IV labetalol or Nicardipine Place arterial line for close monitoring

Place foley Administer Mannitol or Hypertonic saline if posturing/blown pupil

Hemorrhagic Stroke Protocol

Provide other meds
Phosphenytoin 18mg/kg loading dose followed by 100 mg IV q 8 hours Propofol if intubated and need to decrease ICP or provide sedation
10-50 mcg/kg/min

Nursing Management of ICH

Goal: preserve life, prevent further neurologic deterioration & maintain normal body functions ABC A-B-C
Maintain patent airway, oxygenate, & titrate PaCO2 to balance ICP/oxygenation IV, check blood glucose, & assess BP, heart rate and rhythm

MS 1 4 mg IV for pain

Frequent repeat neurologic checks

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Nursing Management of ICH

Nursing Management of ICH

Circulation Do not dehydrate Hypertonic saline or Osmotic diuretics for inc. ICP Watch CPP = MAP - ICP
replace fluids optimize Titrate CPP to maintain PbtO2 and ICP in normal ranges euvolemic

BP management

Keep Systolic BP < 150 mm Hg in first hours then titrate to maintain perfusion Use
Labetalol Nicardipine

Nursing Management of ICH

Assess neuro status closely
Monitor LOC closely-watch for neuro changes esp. during peak edema 2-5 days Assess motor status-check strength and note status check increase in tone Cranial nerves-especially III, IV, VI; V & VII; and IX & X Sensory status changes

Nursing Management of ICH

Provide enteral nutrition Establish bowel program Foley care Range of motion DVT prevention Good skin care Family involvement PT/OT/ST & Rehab consult

Aneurysmal Subarachnoid Hemorrhage

Subarachnoid Hemorrhage

Sacular outpouching of a cerebral artery which ruptures into the subarachnoid space 25,000 cases each year 30 day mortality 40-50% Age Females>males

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Aneurysm
Diseases
Congenital Trauma Polycystic kidney disease Connective tissue disease

Grading SAH
Hunt and Hess Scale
Grade 0: unruptured Grade 1: SAH unsymptomatic/minimal headache h d h Grade 2: Severe headache, meningismus, 3rd cranial nerve deficit Grade 3: Drowsy with minimal deficit Grade 4: Stuporous, hemiparesis Grade 5: Coma, extensor posturing

Ehler Danlos Syndrome

Smoking

Patient Presentation
Worst headache of their life Photophobia and stiff neck Cranial nerve deficit Motor weakness to posturing Decrease LOC to coma
That can change in a second!

Pathophysiology: Rebleeding
Lethal complication - 11% risk 2nd leading cause of increased morbidity and mortality I Increases with conservative therapy ith ti th Fatal in up to 70% of patients Greatest risk is first 24 hours

Medical Management Reduce Rebleeding

Reduce risk by controlling BP
Keep systolic BP < 150 mmHg

Pathophysiology: Vasospasm
Narrowing of cerebral arteries around the Circle of Willis
causes an increase in velocities of arteries decreases blood delivery to cerebral tissue

Occlusion of Aneurysm y
Operative Neurointerventional therapies: Intraluminal Coils

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Vasospasm
Signs/symptoms
In the awake pt.
Global: headache & increasing lethargy Localizing: hemiparesis, aphasia in dominant hemisphere, loss of spatial awareness (nondominant hemisphere)

Medical Management Vasospasm

Vasospasm
Nimodipine Keep BP 160-180 mm Hg p g Triple H Therapy
PCWP 14-16 mmHg

Monitoring in the awake pt.

TCDs, CBF, Oxygen monitoring (INVOS or LICOX), and Cerebral Angiogram

CT scan to r/o infarct or bleed Angiogram

Intraarterial verapamil Cerebral angioplasty

Medical Management
CT demonstrates hemorrhage
SAH
Present with worse headache of their life, photophobia, nuchal rigidity, n/v, motor weaknessto weakness to posturing/coma Emergently treated CT angio or Angio

Nursing Management of Aneurysm: Preop

Assess neuro status for subtle changes Watch for arrhythmias Watch for neurogenic pulmonary edema Assist with care activities Limit visitors Support systems Private room-keep lights low

Medical Interventions
Postop A-B-C ICP control

Nursing Management of Aneurysm Postop

Maintain airway, breathing, circulation
based on severity of SAH & pt. status BP 140 systolic first 24 hours BP 160-180 systolic after 24 hours 160 180 Triple H: hypertensive, hypervolemic, hemodilutional therapy Balance with ICP problems

FIO2 and CO2 tit ti orders (> 35) d titration d CPP, ICP drainage, Mannitol/Hypertonic Saline Barbiturates

Orders TCDs Nimodipine

Drain CSF Magnesium drip Statins

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Nursing Management of Aneurysm Postop

Assess neuro status post-op closely Support body systems: nutrition, skin, mobility, DVT prevention, bowel and bladder support WATCH FOR SIGNS OF VASOSPASM
large clots > 3 x 5 mm in basal cisterns Symptomatic vs. angiographic

Nursing Management of Aneurysm Postop

Vasospasm: greatest risk 4-14 days post bleed
Prevention is the key

Monitor
TCD and other technologies Clinical exam Onset of hyponatremia

Nursing Management of Aneurysm Postop

If vasospasm occurs:
Cerebral angiography Injection of verapamil

P Prepare pt. and f il t d family

Informed consent Monitoring of pt. after procedure

Conclusion

AACN 2009 NTI & CRITICAL CARE EXPOSITION