Coma-Delirium in ICU/CCM Board review

8/10/2019 Coma-Delirium in ICU/CCM Board review

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John F. McConville, M.D.

Associate Professor

University of Chicago


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Objectives:

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Global cerebral dysfunction in the ICU

Very frequent in ICU

Increases risk of death

Cerebral injury vs. complication of

systemic disease


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Blood flow and the brain

Cerebral perfusion pressure

Cerebralbloodflow


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9A BA

CA /A

Audience Response Question


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Coma and Delirium

Acute brain dysfunction

- chronic cognitive impairment

Disorders of consciousness

- wakefulness and awareness

- hierarchical relationship


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Consciousness

Wakefulness = arousal, alertness

reticular activating system (RAS)

localized in pons/midbrain

diffuse in cerebral hemispheres


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Consciousness: wakefulness

RAS to cerebral cortex


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Consciousness

Awareness

sum of all functions mediated at a

cerebral cortical level including

cognitive and affective responses


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Impaired consciousness

Term Awake Aware Sleep/wake Motor fx

Brain death

Coma

Vegetative

Minimally

conscious

Akinetic

mutism

Locked-in

No

No

No

Partial

Partial

Yes

Absent

Absent

Yes

Yes

Yes

YesAdapted from Stevens. Crit Care Med 2006;34:31

Absent

Absent

Present

Present

Present

Present

Absent

No purpose

No purpose

Intermittent

purpose

Very little

Absent


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Impaired consciousness


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Coma

Absence of wakefulness/awareness!1 hr

No eye opening

No purposeful movements/speech

No purposeful response to painful stimuli

Sleep-wake cycle is absent

TRANSITIONAL STATE


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Coma: prevalence

Mechanical ventilation15-20% coma

JAMA 2004;291:1753AJRCCM 2000; 161: 1450

S/p cardiac arrest80-90% coma

JAMA 2004;291:870

Sepsis16% coma

JAMA 1996;275:470


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Glasgow coma scaleEye opening

SpontaneouslyTo speech

To pain

Never

Points

43

2

1

Best verbal

Oriented

Confused

InappropriateGarbled

None

Points

5

4

32

1

Best motor

Obeys

Localizes pain

WithdrawalAbnormal flexion

Extension

None

Points

6

5

43

2

1


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Full Outline of UnResponsiveness score

Wijdicks. Ann Neurol 2005;58: 585

Eye response4 = eyelids open, tracks to command3 = eyelids open but not tracking

2 = eyelids closed, open to loud voice

1 = eyelids closed but open to pain

0 = eyelids remain closed with pain

Motor response4 = thumbs-up, fist, or peace sign

3 = localizing to pain

2 = flexion response to pain1 = extension response to pain

0 = no response to pain

Brainstem reflexes4 = pupil/corneal reflexes present3 = one pupil wide and fixed

2 = pupil or corneal reflexes absent

1 = pupil/corneal reflexes absent

0 = absent pupil/corneal/cough reflex

Respiration4 = no ETT, regular breathing pattern

3 = no ETT, CheyneStokes pattern

2 = no ETT, irregular breathing1 = breathes above ventilator rate

0 = breathes at MV rate or apnea


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Young. NEJM. 2009;361:605-611.

Outcome scales


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Coma: etiology

Toxic-metabolic:most common- drug overdose *

- toxins

- sepsis- hypoxia, hypercapnia

- hypothermia

- electrolyte/glucose disorders

- hepatic and renal dysfunction


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Coma: etiology

Primary cerebral

- trauma *- hypoxic-ischemic encephalopathy *

- hemorrhage, malignancy or infection

- diffuse hemispheric injury

- one hemisphere w/ midbrain effect

- brainstem lesion

- hydrocephalous

- severe intracranial hypertension


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Coma: immediate steps

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Treat, if indicated


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Coma: quick exam

Assess level of consciousness

voice

eyes

pain


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Coma: quick exam

Coma exam: proximity of RAS to pupillary


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Coma exam: proximity of RAS to pupillaryresponse neurons

C i it f RAS t CN l i


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Coma exam: proximity of RAS to CN nuclei

C ill


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Coma exam: pupillary responses

Plum and Posners diagnosis of stupor and coma, 4thed


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Coma: diagnostic testing

Stevens. Crit Care Med 2006;34:31

- Chemistry panel, ABG, glucose, CBC,toxicology screen, liver/thyroid function tests

- Computed tomography (CT)

toxic-metabolic and hypoxic-ischemic

- Magnetic resonance imaging (MRI)

- Lumbar puncture

- Electroencephalography (EEG)


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Stevens. Crit Care Med 2006;34:31


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Correlation of Midline Shift and Level of

Consciousness

Degree of Shift at the Pineal Level

2.5 - 4 mm: Somnolent

5.0 8 mm: Stuporous

> 8 mm: Comatose

Ropper AH. NEJM 1986;314:914


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Audience Response Question


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Coma: Prognosis

Etiology matters

- toxic/metabolic > structural lesion

- trauma > anoxic injury

Anoxic injuries!

bad outcome if:- absent pupil/corneal @ 24 hrs

- no w/d to pain @ 72 hrs

- no motor response @ 24 or 72 hrs

Booth. JAMA 2004;291:870

Predictors of outcomes after hypothermia

more data needed


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Coma: Prognosis

NEJM. 1994;330:1572.

Dead

PVS

Recover

consciousness

Anoxic injury Trauma


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Coma: Poor Prognosis

Myoclonus

- persistent, bilat face, limbs, axial

EEG

- burst suppression

Imaging

- less predictive than clinical exam

Biomarkers: neuron specific enolase

- sensitive but lack predictive value


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EEG: burst suppression


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Somatosensory evoked potentials

Bilateral absence predicts poor outcome

< 1% chance of awakening

Robinson Crit Care Med 2003;31:960


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Coma: Treatment

NEJM 2002;346:549-56


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Good outcome: 49% 26% p=0.046

Coma: Treatment

Bernard. NEJM 2002;346:557-563


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Determination of death

Medical and legal definitions are clear:cardiac death = brain death

Clinical diagnosis requires:

-known (and adequate) cause

-lack of consciousness

- no motor response to noxious stimuli

- no brainstem reflexes

- no respiratory drive


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Clinical diagnosis requires exclusion of:

- hypotension, hypoxemia, sedatives

- muscle relaxants, severe endocrine

problems

Confirmatory testing required in 10%

Transcranial doppler ultrasound

Apnea test requires 20 mmHg increase in

CO2 without hypoxemia or respiratory effort

Determination of death


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Delirium

Acute confused state

Impaired attention and

disorganized thinking

Fluctuates

Develops over hours to days Often missed


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Delirium

Prevalence of 20-80% in ICU cohort studies

Subtypes based on activity

Hyper- v. hypo- v. mixed

Agitation, hallucinations NOT always present

Bergeron. Intensive Care Medicine. 2001; 27: 859

McNicoll. J Am Geriatr Soc. 2003; 51: 591

Ely. JAMA. 2001;286: 2703

A it ti i t l t


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Agitation is not always present

Delirium subtype

%ptsinage

category

Peterson. J Am Geriatr Soc 2006;54:479

Delirium risk factors


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Delirium risk factors

Host Acute illness IatrogenicElderly

Comorbidities

Dementia

Hearing/vision

Neurologic

disease

EtOH or

smoking

Severe sepsis

ARDS

MODS

Drug overdose

Illicit drug use

Nosocomial infect

Metabolic

Sedative meds

Analgesic meds

Restraints

TPN/malnutrition

Sleep deprivation

Anemia

Adapted from Principles of Critical Care 2005. Chapter 62


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Delirium: scoring systems

Confusion assessment method for

ICU (CAM-ICU)

ICU delirium screening checklist

Delirium detection score

Ely. JAMA 2001;286:2703Bergeron. Inten Care Med. 2001;27: 859Otter. Neurocrit Care. 2005;2: 150

CAM ICU


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Ely. JAMA 2001;286:2703

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CAM - ICU

Attention Screening Exam

auditory

visual

Someone who is attentive is NOT delirious


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D li i i d t


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Delirium = increased costs

ICU cost Hospital cost

Media

ncost

Milbrandt. Crit Care Med 2004;32:955

Delirium: treatment


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Delirium: treatment

Rule out life-threatening issues first

- shock, hypoxia, metabolic

Primary prevention

- not extensively studied in ICU

Pharmacologic Tx as last resort

Delirium: treatment


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Delirium: treatment

Common sense treatments

sleep/wake cycles

early mobilization

remove unnecessary hardware

scheduled pain management

Reorientation family involvement

Delirium: treatment


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Delirium: treatment

Haloperidol

small case series

side effects

Atypical antipsychotics

Risperidone, Ziprasidone,

Quetiapine, Olanzapine

Delirium: treatment


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Benzodiazepines

prevention in EtOH or sedative withdrawalcan also exacerbate delirium

Delirium: treatment

Pandharipande, Anesthesiology. 2006; 104(1):21-26.

Delirium: treatment


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Delirium: treatment

Pandharipande. JAMA. 2007;298:2644Riker. JAMA. 2009;301:489Reade. Critical Care. 2009;13:75

Rubino. Interact Cardiovasc Thorac Surg. 2010; 10:58

"-2 agonists

dexmedetomidine and clonidine

Dex RCTs:

105 pts vs. lorazepam: DCFD 7 v 3 d, p= 0.01375 pts vs. midazolam: delirium & MV

20 pts vs. haldoperidol: time to liberation

Clonidine:30 pts vs. placebo: severe delirium, MV, ICU LOS

D li i T W k ! A d ?


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Delirium Tx: Wake up! And move? Intervention Patients

Daily passive ROM and PT/OT

Control Patients

Usual care Both groups received protocol-directed

SBT, sedation, nutrition and glucose control

Intervention!shorter duration ofdelirium2 vs. 4 days


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Coma patients have alterations consciousness

(wakefulness and awareness)

Physical exam findings best predict outcome

after anoxic injury

Sedation and delirium assessments should be

coupled

Non-pharmacologic interventions can reduce

delirium prevalence

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E(0",+2(0- Booth. JAMA 2004;291:870

- Principles of Critical Care 2005. Chapter 62 and 67

- Stevens. Crit Care Med 2006;34:31

- Ely. JAMA 2001;286:2703

- Milbrandt. Crit Care Med 2005;33:226

- Riker. JAMA. 2009;301:489

- Ely. JAMA 2004;291:1753

- Plum and Posners Diagnosis of stupor and coma


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Coma-Delirium in ICU/CCM Board review