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Different Strokes for Different Folks: Assessment,Interventions, and OutcomesMary Kay Bader Level: Intermediate

Content Description

Patients presenting to the hospital with an acute ischemic

or hemorrhagic stroke must be rapidly identied 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 specic indicators from the JCAHO. Thissession 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.

Learning Outcomes

At the end of this session the attendee will be able to:

Differentiate between the pathophysiology of acute1.

ischemic and hemorrhagic stroke

Relate the evidence based recommendations for2.

primary stroke centers from the ASA/JCAHO as well

as practice protocols for hyperacute ischemic/

hemorrhagic stroke to the acute stroke patient

population

Apply the information presented on stroke3.

management to actual case studies

Summary of Key Points

Introduction: BRAIN ATTACK1.

Denition: abrupt and dramatic developmenta.

of a focal neurologic decit caused by arterialocclusion or hemorrhage

Statistics of strokeb.

Classication of stroke2.

Ischemic strokea.

Hemorrhagic strokeb.

Pathophysiology of Ischemic Stroke3.

Mechanisms of ischemic stroke formationa.

Ischemic stroke-thrombus formationi.

Pathophysiology of occlusion: dense ischemicb.

core of tissue where CBF falls dramatically

surrounded by marginally perfused area known

as the penumbraInterruption of circulation to braini.

Cellular responses to reduced owii.

Cerebral Edema and increased ICPc.

Occurs as a natural evolution of the ischemici.

insult

Minimized if restore perfusionii.

Assess for signs of increased ICP: Decreasediii.

LOC, agitation, worsening of motor exam,

papillary changes/changes in cranial nerve

exam

Even though patient may receive thrombolysis,iv.

does not equate to no edema

Watch the large MCA occulusions forv.

development of malignant MCA syndrome

Blood pressure, blood glucose and temperature -d.

Issues in Stroke Management

BP and Stroke - Ischemic Strokei.

Glucoseii.

Body temperatureiii.

Identity major elements of a primary stroke center4.

including organization, personnel and protocols

Primary Stroke Center Characteristicsa.

Compliance with consensus-based nationali.

standards

Effective use of established clinical practiceii.guidelines to manage and optimize care

An organized approach to performanceiii.

measurement and improvement activities

2008 Frameworkb.

Domainsi.

Stroke Measures 2008ii.

Evidence Based Protocolsc.

Emergency care of patients with ischemic andi.

hemorrhagic stroke

Evidence Based practice protocols5.

Review of the literature and consensus bya.

practitioners: development of evidence basedprotocols; renement of protocols based on ASA/

AHA guidelines for ischemic and hemorrhagic

stroke;

Protocols: Hyperacute Ischemic/Hemorrhagicb.

Stroke Protocol vs. Acute Ischemic Stroke Protocol

Purpose: To rapidly identify and managei.

patients identied with acute ischemic stroke

presenting within 6 hours of symptom onset or

hemorrhagic stroke.

Case Studies: Ischemic vs Hemorrhagic6.

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A A C N 2 0 0 9 N T I & C R I T I C A L C A R E E X P O S I T I O N

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 Scientic 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 SpontaneousIntracerebral 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.

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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

hemorrha e of a vessel feedin the brain

Statistics

750,000 new strokes each year

3rd leading cause of death in US

Anatomy of Cerebral

Vasculature

Anterior circulation

Posterior circulation

Stroke Signs/Symptoms

Classic Signs/symptoms: FAST

Weakness of arm/leg

Difficulty speaking

Headache

Visual problems

Numbness/tingling on one side of body

Stroke Signs/Symptoms

Timing

TIAthe debate continues

Transient appearance of symptoms/signs that

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

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

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

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

Do not medicate with sedation agents unless

monitoring for increased ICP

Prepare for CT

Two Effective Therapies

for Stroke

Thrombolysis

Reduces death and disability

Comprehensive Stroke Care

u sc p nary eamwor re uces mor a y

by more than 25%

Focus

BP

Blood glucose

Temperature

Pathophysiological Issues Related

to Stroke

Blood Pressure

Blood Glucose

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

Do Not treat BP unless...

Hill & Hachinski, The Lancet 1998. 352: (suppl III) 10Hill & Hachinski, The Lancet 1998. 352: (supp l III) 10--14.14.

Pathophysiology:

BP & Stroke Treat BP in acute ischemic stroke

No thrombolytics

Systolic > 220 mm Hg

MAP > 130 mm Hg

Thrombolytics

Systolic > 180-185 mm Hg

Diastolic > 100-110 mm Hg

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Pathophysiology:

Serum Glucose & Stroke

Increase in infarct size and edema occurwith acute and chronic hyperglycemia

Studies showed a correlation between

serum glucose levels above normal

Hill & Hachinski, The Lancet 1998. 352: (suppl III) 10Hill & Hachinski, The Lancet 1998. 352: (suppl III) 10--14.14.

Pathophysiology:

Serum Glucose & Stroke

High serum glucose was an independentrisk factor for hemorrhage after treatment

with tPA in one study11

Treat hyperglycemia

Maintain blood glucose < 140

11Demchuck, Morgenstern, Kochanski et al. Stroke 1998; 29: 273Demchuck, Morgenstern, Kochanski et al. Stroke 1998; 29: 273

Pathophysiology:

Body Temperature & Stroke

Temperature controlAvoid hyperthermia

Neuro Populations ++

Stroke

Why develop a stroke center

Improved outcomes associated with

stroke centers

Increase use of tPA in acute ischemic

. . -

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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

AHA/ASA scientific statement

recommends the creation ofacute stroke Centers

and recommend certification by a governing body

(Level 1B)

Stroke Care: PSC vs CSC

PSC

Personnel, programs, expertise, andinfrastructure to care for patients with

uncomplicated stroke

CSC

Cares for patients with complicated types

of strokes, ICH, SAH, and those pts who

need interventional tx, surgery and a Neuro

ICU

Achieving Success:

The Nuts and Bolts

Creation of Evidence Based protocols

Review of literature and consensus by

practitioners

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

ever

ASA within 48 hours of admit

Prevention of complications

Aspiration

DVT

UTI


Consensus by practitioners

Develop EBP protocols

Designate acute stroke unit

Neurolo involvement

A Fib management

Lipid profile

Discharge: antithrombotics, stroke

ed, smoking cessation, and rehab

consult

Establish measurable stroke goals


Hyperacute Ischemic/Hemorrhagic

Purpose: rapidly identify and managepatients identified with acute ischemicstroke presenting within 6 hours of

symptom onset (ischemic) orhemorrhagic stroke

Acute Ischemic Stroke protocol

Purpose: provide evidence basedprotocol to minimize complicationsand facilitate recovery in patientsunable to receive tPA

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Designation of patient and

activation of stroke team

Initial team interventions

survey

NIHSS


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

Interventions

Ischemic Stroke

Mana ement

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 Treatment Options Ischemic

Acute

Within 180 minutes tPA unlesscontraindicated

IV t ical dose 60-90 m totalgiven in ED then admit to ICU

IV/IA give 2/3 of dose IV then toangio 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

1NINDS Study Group. Stroke 1997. 28: 2109-2118.

Intravenous tPA

Time Window

< 3 hours

IV tPA:

Nursing Management

Start 2nd IV for thrombolytics

Reassess neuro status using

NIHSS 15 min

Weigh patient or assess likelyweight

Avoid invasive tubes: foley/NG

Infusion Guidelines tPA

Preparation of IV tPA drip

0.9 mg/kg

10% IV bolus over 1-2 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

Maintain systolic BP < 180-185 mm Hg< -

Use labetalol or nicardipine

No invasive tubes for 24 hours

Do not give ASA, heparin, warfarin, ticlid, lovenox,

plavix, aggrenox, fragmin, orantithrombotic/antiplatelet

Keep NPO until swallow assessmentdone


Check blood glucose levels q 4 hours x 2 If elevated > 140 mg/dl, contact MD for

intensive insulin therapy vs sliding scale

Maintain temperature 36-37 degrees

Watch for peak edema 48-72 hours

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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 OptionsIntraarterial tPA

Merci Retrieval

Time Window

< 6 hours

Intraarterial Thrombolytics

Time window is < 6 hours

Requires cerebral angiogram and trainedinterventional neuroradiologist Prepare patient for cerebral angiography

Femoral site and insertion of catheter

Technique for superselective catheterplacement into clot

BP control: Systolic >180/Diastolic > 100

Job 4: Consider

Interventional OptionsIntraarterial tPA

Merci Retrieval

Time Window

< 6 hours

Intraarterial Thrombolytics

Time window is < 6 hours

Requires cerebral angiogram and

trained interventional neuroradiologist

repare pa en or cere ra ang ograp y Femoral site and insertion of catheter

Technique for superselective catheter

placement into clot

BP control: Systolic >180/Diastolic >

100

Job 5: No tPA

Prevent

Complications!!

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No tPA: Admit to Stroke Unit

Supportive therapy of patient if tPA notadministered or is admitted 6 hours or

more after onset of symptoms

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 12hours of admission per rectum if NPO

or orally is swallow evaluation

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 MCAsyndrome, or brain stem stroke Evaluate BP and treat as follow per MD

order:

rea > or >

Labetalol or nicardipine

Monitor neuro check/vital signs hourly

Reduce risk of complication: aspiration,DVT; treat hyperglycemia and fevers

Give ASA/Antithrombotic medication within48 hours of admit

Consult OT/PT/ST and physiatrist on dayafter admission

Hemorrhagic Stroke

Mana ement

Intracerebral

Etiology ICH

Systemic hypertension

56-81% of all cases

Aka Charcot-Bouchard

microaneurysms

ma per ora ngbranches 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

Anticoagulants

Venous infarction

Vasculitis

Drug abuse: cocaine, amphetamines

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

Prevention

Non-modifiable

Age, gender and race

Modifiable

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

Pathophysiology

Rupture of vessel from pressure,

pathological changes to vessels,

congenital weakness

release toxins from hematoma

local decrease in perfusion

cellular changes

Intracranial Pressure

Normal range Children 0-10 mm Hg

Adolescents/Adults 0-15 mm Hg

Abnormal ranges

Infant/Child moderate > 15 mm Hg

severe > 20 mm Hg

Adolescent/Adults moderate 20-40

severe > 40 mm Hg

Pathophysiological Issues Related to

Hemorrhagic Stroke

Edema and Increased ICP

Concern: Is the brain receiving

cerebral oxygenation

New technology to monitor brain

tissue oxygen

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Brain Tissue Oxygen (Pbt02)

Normal: 20-40 mm Hg Risk of death increases

< 15 mm Hg for 30 minutes

< mm g or m nu es

PbtO2 < 5 mm Hg

high mortality

PbtO2 < 2mm Hg - neuronal death

Pathophysiology:

Interventions and PbtO2

Decreasing PbtO2

Hypoxia

Low Hemo lobin

Increasing PbtO2

Increasing FIO2

Increasin Hemo lobin

Decreasing PaCO2

Increased ICP

Decreased MAP

Increasing temperature

Systemic Causes

Pulmonary

Cardiac/Hemodynamic

Increasing PaCO2

Draining CSF

Decreasing ICP

Increasing MAP

Decreasing temperature

Barbiturates

Assessment

Subjective Sudden onset of focal deficit

Severe headache

Nausea and vomiting

Decrease LOC

Objective Motor deficits if large hemorrhage

Sensory deficit

CN abnormalities

Medical Management

Dependent on multiple factors

Age

Pre-morbid condition

Patients advance directive

No aggressive life support = institute palliative care

Aggressive interventions Get the neurosurgeon

involved!

Medical Management

Aggressive Management Options

Surgical

Non-surgical

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/

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

headache, nuchal rigidity, n/v,

balance problems, coordinationto

posturing and coma

Emergently treated OR

Medical Management

Non-operative management Maintain airway, ventilation, and circulatorysupport

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


Circulation

Start 2 IV lines

BP must be ke t < S stolic 150 mm H

Treat with IV labetalol or Nicardipine

Place arterial line for close monitoring

Place foley

Administer Mannitol or Hypertonic saline if

posturing/blown pupil


Provide other meds

Phosphenytoin 18mg/kg loading dose

followed by 100 mg IV q 8 hours

ICP or provide sedation

10-50 mcg/kg/min

MS 1 4 mg IV for pain

Frequent repeat neurologic checks

Nursing Management of ICH

Goal: preserve life, prevent further

neurologic deterioration & maintain normal

body functions

- - Maintain patent airway, oxygenate, & titrate

PaCO2 to balance ICP/oxygenation

IV, check blood glucose, & assess BP, heart

rate and rhythm

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BP managementKeep Systolic BP < 150 mm Hg infirst hours then titrate to maintain

erfusion

Use Labetalol

Nicardipine


Circulation- Do not dehydrate

euvolemic

Hypertonic saline or Osmotic diuretics for inc.

replace fluids

Watch CPP = MAP - ICP optimize

Titrate CPP to maintain PbtO2 and ICP in normalranges

Assess neuro status closely

Monitor LOC closely-watch for neuro

changes esp. during peak edema 2-5 days

-


increase in tone

Cranial nerves-especially III, IV, VI; V & VII;

and IX & X

Sensory status changes

Provide enteral nutrition

Establish bowel program

Foley care


Range of motion

DVT prevention

Good skin care

Family involvement

PT/OT/ST & Rehab consult

Subarachnoid

Aneurysmal 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

Ehler Danlos Syndrome

Smoking

Grading SAH

Hunt and Hess Scale Grade 0: unruptured

Grade 1: SAH unsymptomatic/minimal

ea ac e

Grade 2: Severe headache, meningismus,

3rd cranial nerve deficit

Grade 3: Drowsy with minimal deficit

Grade 4: Stuporous, hemiparesis

Grade 5: Coma, extensor posturing

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

ncreases w conserva ve erapy

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

Occlusion of Aneurysm

Operative

Neurointerventional therapies: Intraluminal

Coils

Pathophysiology:

Vasospasm

Narrowing of cerebral arteries around the

Circle of Willis

causes an increase in velocities of arteries

decreases blood delivery to cerebral tissue

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Vasospasm

Signs/symptoms In the awake pt. Global: headache & increasing lethargy

Localizin : hemi aresis a hasia indominant,

hemisphere, loss of spatial awareness (non-

dominant hemisphere)

Monitoring in the awake pt.

TCDs, CBF, Oxygen monitoring (INVOS or

LICOX), and Cerebral Angiogram

Medical Management

Vasospasm

Vasospasm

Nimodipine

Kee BP 160-180 mm H

Triple H Therapy

PCWP 14-16 mmHg

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

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

an ra on or ers > CPP, ICP drainage, Mannitol/Hypertonic Saline

Barbiturates

Orders TCDs

Nimodipine

Nursing Management of Aneurysm

Postop

Maintain airway, breathing, circulation based on severity of SAH & pt. status

BP 140 systolic first 24 hours

- Triple H: hypertensive, hypervolemic,

hemodilutional therapy

Balance with ICP problems

Drain CSF

Magnesium drip

Statins

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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


Postop

Vasospasm: greatest risk 4-14 days postbleed

Prevention is the key

TCD and other technologies

Clinical exam

Onset of hyponatremia


Postop

If vasospasm occurs:

Cerebral angiography

Injection of verapamil

repare p . an am y

Informed consent

Monitoring of pt. after procedure

Conclusion

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