Objectives

Brain Injury due to Cardiac Arrest: Neuropsychological Outcomes and a Model for Early Rehabilitation Management

Kyle Harvison, PhD, LP, ABPP-CN Cindy Kosek, OT

Objectives

• Review of cardiac arrest and associated mechanisms of brain injury

• Overview of therapeutic hypothermia as a neuroprotective strategy post-cardiac arrest

• Overview of neuropsychological outcomes and early non-cardiac rehabilitation needs

• Introduce a model of care focused on these rehabilitation issues

Cardiac Arrest

• Sudden Cardiac Arrest• Not always “heart attack”• Cessation of productive cardiac mechanical activity

– Defined by absence of palpable pulse and spontaneous respiration (Tiainen et al., 2007)

Cardiac Arrest: Causes

– Problems with heart rhythm– Myocardial infarction– Coronary artery disease– Respiratory arrest– Enlarged heart– Valve disease– Congenital heart defect– Coronary artery dissection– Severe physical stress (e.g., blood loss)– Electrocution– Trauma– Fluid buildup– Hypothermia– Overdose– Metabolic disruption– ……

In Cohen and Gunstad (2010), pp. 127-28

Cardiac Arrest: Causes

Electrophysiologically, most common underlying problems are:– Ventricular fibrillation (VF)- Quivering of the

heart’s lower chambersor– Pulseless ventricular tachycardia- Extremely

rapid but ineffective beating of the heart’s lower chambers

Out of Hospital Cardiac Arrest: Annual U.S. Incidence

(Schulman, Hartman, & Geocadin, 2006; Holzer, 2010)

Cardiac Arrest: Management and Survival

• Interventions include cardiopulmonary-cerebral resuscitation, defibrillation, intubation, and heart stimulating drugs, as well as management of underlying causes

• Crucial prognostic factors:– Whether a heart rhythm is detected early– Whether underlying causes of arrest been

identified and treatedYoung (2009)

Post Cardiac-Arrest Syndrome (Holzer, 2010)

• Includes:– Brain Injury– Myocardial Dysfunction– Systemic ischemia– Reperfusion responses– Consequences of disorder that caused CA

How does cardiovascular disease affect the brain?

Primary Secondary

• Cardioembolic stroke• Global cerebral ischemia• Cerebrovascular disease

associated with systemic vascular changes

• Metabolic disruption from injury to other organs

• Psychiatric comorbidities• Medication effects• Adverse postsurgical effects

Cohen (2010), pp. 21-22

Cardiac arrest and Brain Injury: Where?

More vulnerable Less vulnerable

• Cerebral cortex• Cerebellum• Hippocampus• Basal ganglia

• Brainstem• Thalamus/hypothalamus

Geocadin et al. (2008), p. 489

-Memory impairment in out-of-hospital cardiac arrest survivors has been associated with global cerebral atrophy, rather than selective hippocampal damage (Grubb et al., 2000)

Cardiac Arrest and Brain Injury: How? (Holzer, 2010)

• Immediate:– Oxygen and energy stores deplete quickly– Neuronal firing is disrupted– Excessive stimulation kills nerve cells

• Reperfusion injury:– Initial increase in blood flow followed by delayed,

prolonged hypoperfusion– Toxic cell injury due to oxidative stress– Inflammatory response can injure tissue and

disrupt O2 delivery

Cascade of events in Ischemia

Cardiac Arrest: Neurological Prognosis

• Brain damage occurs quickly (seconds to minutes) and is permanent in half or more with conventional treatment (Young, 2009)

• Estimated 12,000 survivors with persistent neuro deficits/year with a prevalence of ~50,000 impaired survivors (Lim et al., 2004)

Cardiac Arrest: Neurological Prognosis

• Early neurological prognosticating often occurs during coma or early stages of confusional state– Focused on likelihood that patient will achieve no

better than vegetative state or severe disability (Young, 2009)

• Some patients may remain comatose for extended periods but still have favorable neurological recovery

• Assessment complicated by interventions (Holzer, 2010)

• Difficult questions of when to withdraw care

Cardiac Arrest: Neuropsychological

Consequences

• Roine, Kajaste, & Kaste (1993) published the first prospective, consecutive, community-based neuropsychological study of non-traumatic out-of-hospital VF cardiac arrest– Part of a larger investigation of nimodipine

treatment to improve cognitive outcome– Occurred in Helsinki between 1986-88

Roine, Kajaste, & Kaste (1993)

• Follow-up assessments at 3 and 12 months • Of 155 who met entry criteria, 70 (45%) were

alive at 3 months and 59 (38%) at 12 months

• Descriptives:– Average age = 65 (range 36-85)– Approximately 70% were men– Average WAIS VIQs ~100

Roine, Kajaste, & Kaste (1993): Summary

• Moderate to severe deficits (i.e. < 2nd percentile) present in 60% at 3 months and 48% at 12 months

• Findings generally stable between 3 and 12 months, but 23% improved and 8% declined (of those who survived)

• Most common cognitive impairment was delayed memory, with visuoconstruction, psychomotor function, PIQ, and arithmetic also being commonly affected

• Depression evident in 35% at 3 months and 31% at 12 months

Cardiac Arrest: Neuropsychological Consequences

• Subsequent studies (Grubb et al., 1996; Suave’ et al., 1996 ; van Alem et al, 2004) have demonstrated cognitive deficits in 28-50% of survivors at intervals ranging 6 -12 months

• Most common pattern is combination of memory, psychomotor, and executive deficits (Lim et al., 2004)

• Mayo study (Mateen et al., 2011) of survivors at 8 years found primarily memory difficulties but the group (n=47) retained strong verbal IQ, normal MMSE and high rates of functional independence

2002, Volume 346 (8)

Mild Therapeutic Hypothermia to Improve the Neurologic Outcome after Cardiac ArrestThe Hypothermia after Cardiac Arrest Study Group

Treatment of Comatose Survivors of Out-of-Hospital Cardiac Arrest with Induced Hypothermia

Stephen A. Bernard, M.B., B.S., Timothy W. Gray, M.B., B.S., Michael D. Buist, M.B., B.S., Bruce M. Jones, M.B., B.S., William Silvester, M.B., B.S., Geoff Gutteridge, M.B., B.S., and Karen Smith, B.Sc.

“Favorable” Neurological Outcome and Cerebral Performance Category

• CPC1= Good outcome: conscious, alert, able to work, possible mild neurologic or psychologic deficit

• CPC2= Moderate disability: conscious, sufficient cerebral function for independent activities of daily life. Able to work in sheltered environment.

• CPC3 = Severe cerebral disability, functionally dependent; includes severe dementia states

• CPC4 = Coma or vegetative state• CPC5 = Brain death

Safar P. Resuscitation after Brain Ischemia, in Grenvik A and Safar P Eds: Brain Failure and Resuscitation, Churchill Livingstone, New York, 1981; 155-184.

Rates of favorable neurological recovery in survivors after therapeutic

hypothermia (TH)

Hypothermia

Normothermia

Discharged to home or rehab facility (Bernard et al., 2002)

21/43 (49%) 9/34 (26%)

Cerebral Performance Category 1 or 2 @ 6 Months (HACA, 2002)

75/136 (55%)

54/137 (39%)

“…hypothermia provides protection against numerous deleterious biochemical mechanisms” Safar & Kochanek (2002)

TH Protocol

• Cooling initiated ASAP, typically within at least 4 hours of return of spontaneous circulation

• Target core body temperature is 33-36 degrees Celsius• Hypothermia continued for 24 hours• Followed by passive rewarming• Broader care includes ventilation, hemodynamic support,

cardiovascular intervention, dialysis, infection management, glucose management, etc…

Cooling Methods

• Include:– Surface cooling

• Pre-cooled pads• Water-circulating pads

– Core cooling• Cold IV fluids• Catheter based endovascular delivery of cool

saline

TH Mechanisms of Action (Hopkins, 2008, Holzer, 2010)

• Reduced brain metabolism• Decreased levels of excitatory substances• Attenuated oxidative stress• Decreased inflammation• Better regulated cerebral microcirculation• Decreased cell death

• Could also have beneficial effects on non-CNS aspects of post-CA syndrome

• Therapeutic hypothermia after cardiac arrest.An advisory statement by the Advanced Life Support Task Force of the International

Liaison Committee on ResuscitationResuscitation 57 (2003) 231-235

• Unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32-34 dgs. C for 12-24 hrs. when the initial rhythm was VF.

• Such cooling may also be beneficial for other rhythms or in-hospital cardiac arrest.

HACA Trial Neuropsychological Outcome (Tiainen et al., 2007)

• 27 TH and 18 Normothermia (NT) at 3 months post

• Most CPC 1 or 2• Most living at home but only 25-33% back to work

• Psychometric testing focused on memory, executive, and psychomotor speed

• No significant group differences

HACA Trial Neuropsychological Outcome (Tiainen et al., 2007)

TH (n = 27)n(%)

NT (n = 18)n (%)

Intact or subtle deficits (0-2/8 tests impaired*)

18 (67) 8 (44)

Moderate impairment (3-4/8 tests impaired*)

5 (19) 5 (28)

Severe impairment (5-8/8 tests impaired*)

4 (15) 5 (28)-”The use of therapeutic hypothermia was not associated with cognitive decline…”

*<1.5 SDs

Post TH outcomes: Study 2(Cronberg et al., 2009)

• Prospective study of all patients with CA treated with hypothermia at intensive care units at two university hospitals and one regional hospital in Sweden

• 43/48 survivors agreed to follow-up at ~7 months• Cognitive, mood, and quality of life measurement• Encouraging findings but let’s consider from a rehab

lens


• “mild cognitive impairment is common”

Cognitive Outcomes (Cronberg et al., 2009)

WNLn (%)

Mildn (%)

Moderaten (%)

Severen (%)

Self Reported Global Deterioration (n = 43)

19 (44.2) 20 (46.5) 3 (7) 1 (2.3)

Frontal Lobe Assessment Battery (n = 40)

25 (62.5) 5 (12.5) 10 (25) 0(0)

Rivermead BMT (n = 39)

8 (20.5) 18 (46.2) 11 (28.2) 2 (5.1)

Cognistat Memory (n = 42)

15? (35.7) 17? (40.5) 4 (9.5) 6 (14.3)



• But moderate memory and executive impairment not uncommon



• “high level of functioning as reflected in the CPC categories”

• Indeed, but meaning what? Also, moderate memory and executive impairment not uncommon

• CPC insensitivity




• “quality of life is good”


• CPC insensitivity.

• QofL <90% with 1/4 below 70%; plus 14% depressed and 22% can’t sleep





• “Overt neurological findings are uncommon”


• CPC insensitivity.

• QofL <90% with 1/4 below 70%; plus 14% depressed and 22% can’t sleep

• But ~25% showed motor difficulties causing difficulties in handling daily routines





• “Overt neurological findings are uncommon”

• “Clearly the outcome following TH-treated CA is dichotomized into survival with good neurological outcome or death”

• Indeed, but meaning what? Also, moderate memory and executive impairment not uncommon

• So what? We knew that. • But most reported QofL <90% with

1/4 below 70%; plus 14% depressed and 22% can’t sleep

• But ~25% showed motor difficulties causing difficulties in handling daily routines

• Clearly it’s not that simple!

Post TH outcomes: Study 3( Torgersen et al., 2010)

• 24 CA survivors post TH with CPC 1 or 2; seen at 13–28 month follow up in university hospitals in Sweden

• 52% showed deficits in memory and executive functioning on the CANTAB

• Group level QoL consistent with population norms; QoL not correlated with cognitive outcomes

• Mild cognitive deficits are common in OHCA survivors with a high functional status treated with TH but do not affect HRQOL. (p. 7).

• Problems include small sample and poorly validated test which samples limited domains

Post TH outcomes: Study 4( Fugate et al., 2013)

• Prospective study from Mayo of OOH CA survivors post TH (n=56); short post-CA coma

• Followed at 20 months using a telephone-based interview of cognitive status– 91% living independently– 40% cognitively impaired, primarily weak delayed recall– 79% of those employed at time of CA had returned to

work– Long time to ROSC did not preclude good outcome (avg

20 mins in both groups)

Post TH outcomes: Study 5( Larsson et al., 2014)

• Quality of life and mood outcomes in 26 survivors post CA at discharge, one month and six months

• Changes in reporting of low QofL from 73% at discharge to 50% at one month and 41% by six months

• Physical problems most common complaint affecting QofL

• Correlation with depressive symptoms; rates of clinically significant depressive symptoms 11% or lower

Conclusions from literature

• Cardiac arrest causes heterogeneous brain damage via global ischemia; injury continues through reperfusion

• Usually fatal, but survival improving with community resources and improved treatments

• TH associated with “favorable neurological outcome,” relatively speaking

• Memory, psychomotor, and executive problems common but functional status often essentially normal

• Quality of life improves over about first six months; longer-term outcome less clear

• Need better operationalized definition of “impairment”

Next Steps

• From ICU to Discharge…..– The need for a program at ANW was identified by a

previous patient• Therapeutic Hypothermia work group was established

(Goal: no patient will slip through the cracks)

Rehabilitation Approach

• Our challenges:– Don’t let relief of survival overshadow need to focus on

rehab-relevant adverse outcomes

– Select array of tests with validity and reliability in this population, acceptably easy to administer, broad yet focused• Screening model: find survivors with any cognitive

dysfunction after Cool-it knowing:– would over-identify dysfunction – not all dysfunction identified would necessarily be due to

effects of CA-related global cerebral ischemia

Work Group Outcomes for Rehabilitation

• Routine orders sets now include:– Therapies– PM&R consult– Neuropsych consult

• Discharge conference– Team and patient

• Routine order for Outpt follow up– Neuropsych and OT

ICU

Typical Patient Profile• Multiple lines

• Impulsive

• Emerging Alertness

• Amnesia around the event

• Decreased Fine Motor Control

• Family Relief of survival

Therapy Roles:• PT:

– Early mobilization

OT:– Family Education– Early ADL’s– Min-stim protocol

SLP:- Swallow screen

Social Work: - Family connection

Telemetry Unit

Typical Patient Profile• Most lines removed

• Impaired Balance persists

• Impulsivity

• Decreased Attention

• Impaired short term memory

• Decreased Insight

Therapy RolesPT:• Progress Mobility

OT:– Functional Cognition– Assess high risk ADL’s

SLP /Neuropsych – Formal Cognitive Testing

PM&R Consult

Cardiac Rehab– Trains in CPR– Outpatient referral

Patient Education:

Other Defaulted Consults

• Social work– Will follow patients from admission to discharge– Will coordinate Discharge Planning meeting

• Case management– Will actively follow patients at time of transfer– Will coordinate required After Discharge appointments

• Spiritual care• Smoking cessation (if appropriate)• Hospitalist/Cardiologist

– Manages non-cardiac or cardiac issues

Day of Discharge

Patient Profile

• Up and moving independently

• Varying levels of insight

• Anxious and focused on discharge home

Day of Discharge Cont.

Discharge Conference

– Patient & Family

– Case Manager

– Social Worker

– Therapies

– MD Providers

– Physiatrist

– Neuropsych

• Discharge Recommendations– ADLs/mobility

– Supervision

– Driving

– Working

– Out patient therapies

– Cardiac Rehab

Outpatient Follow-up

• Brain Injury Case Manager Phone Follow Up• 4-6 weeks s/p discharge

• Clinic Follow up:• Neuropsychological Re-assessment• Occupational Therapy

Case Manager Phone Follow Up

– Confirm dates/ times of follow up appointment

– Notify Cardiology

– Checks on patient’s current status:• Assistance with personal cares• Living situation• Return to work?• Return to driving?• Any other concerns/ questions

Day of Follow Up

• Neuropsychology Re-assessment• Neuropsychologist reviews the findings• Neuropsychologist updates OT on outcome• OT meets with patient

3 primary Roles of OT

1. Strategy identification in any areas of inefficiency identified by neuropsychologist

2. Education on core concepts 3. Provide assessment information to care

team to assist with interdisciplinary recommendations in the area of higher level IADL’s

Core Educational Concepts

• Multi-factor Model• 6 Things that need to be Managed for Best

Cognitive Health

Multi-factor Model

Brain impairment combines in some fashion with personal and situational factors to influence performance, social interactions and coping with failures and other stresses.

• When individuals have had a cardiac event, their disability is determined by:– Brain impairment– The effects of problematic factors, both personal and situational

• Montgomery, 1995

Multi Factor Model

Personal Factors:– Fatigue– Arousal/Tension– Physical symptoms (i.e. headaches, nausea)– Negative thoughts

Situational Factors– External environmental distracters– Multi-task demands– Information processing demandsMontgomery 1995

6 Key Areas That Need To Be Managed For Cognitive Health

1. Good Nutrition Stay hydrated

Eat consistently

Let Dr. know if nausea or appetite are a problem

Use supplements

Get easy to prepare foods

Use external prompts


2. Good Sleep Get up and go to bed at a set time

No caffeine after 2:00 pm

No TV in the bedroom

Relaxation prior to sleep

Medications may be helpful

Be mindful of napping

6 Key Areas That Need To Be Managed For Cognitive Health:

3. Physical Exercise Resume some level of

exercise Take breaks Begin slowly and build

4. Stress Reduction Develop relaxation skills. Schedule relaxation time

into your day


5. Brain Engagement It matters It needs to challenge you It needs to be fun The list is endless…..just do

something each day!

6. Social Engagement Need connections and interaction Support groups Consistent contact with family and

friends

Case study

Conclusions

• As CA survival rates are improving, neuropsychological outcomes are of increasing importance

• Patients likely leave hospital below baseline, but improvements may be made over several months or more

• Roles for both cardiac and neuro-rehab

Objectives

Documents

Transcript of Objectives