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Neurological Critical Care ©TCHP Education Consortium 1999, Revised January 20171

Neurological Critical Care

Beth Heather RN, BSN, CCRN, ENLSNursing Practice Specialist‐Critical CareECMO Coordinator

[email protected]

Hennepin County Medical Center

Neurological Structures

Structures for protectionSkull

Meninges

CSF

BrainCerebrum

Cerebellum

Brainstem

Reticular Activating System

Cranial Nerves

Vessels of the brain

Protection: The Skull

“Bony container” surrounding the brain

Major function is PROTECTION!

Composed of 8 flat irregular bones (name for the lobes of the brain underneath)

Frontal

Parietal (2)

Temporal (2)

Occipital

Protection: Meninges

They “PAD” the brain. They help absorb shock from sudden movements of trauma.

There are 3 separate layers that cover the entire brain (starting from the brain)

Pia Mater

Arachnoid

Dura Mater

Dura Mater

Directly under the skull

Thick and canvas like

Forms several structures that separate the cranial cavity into compartments and protects the brain from displacement.

Dural Venous Sinuses

Tentorium Cerebelli

Falx cerebri

Arachnoid MaterDelicate and web like

Arteries and veins

Arachnoid villi/ Arachnoid granulation



Pia Mater

Delicate membrane over the surface on the brainProtects the brain from infections

Cerebrospinal Fluid (CSF) System

Four connected CSF ChambersLateral ventricle (2)

Third ventricle

Fourth ventricle

Provides the anatomic structure around which the brain and brainstem are formed

Protection: CSF System

Clear, colorless, odorless fluid

Produced by the choriod plexus

Body produces about 500ml/day of CSF (20ml/hr)

Circulating volume is 135‐150 ml

Bathes the brain and spinal cord

“Cushions” it

“floats” in CSF

Ventricular System

Brain: Cerebrum

The cerebrum is the largest part of our brain. Comprising of 80% of it’s weight.

Two main layers of the Cerebrum

Cerebral Cortex

Is about 2‐4 mm thick into the cerebral surface

Appears gray in color‐ gray matter

Information processing center

The Cerebrum

White matterDirectly under the cerebral cortex

Communicates information from the cerebral cortex to other areas of the brain and the rest of your body.

Wiring of the brain

The glue



The Cerebrum

Composed of 2 cerebral hemispheresRight controls left side of body. Abstract

Left controls right side of body. Analytical

The Cerebrum

Each hemisphere is divided into 4 surface lobesFrontalParietalTemporal Occipital

The Cerebrum

Frontal Lobe (largest)

Major Functions

Voluntary motor functions

Intellect (reasoning, calculation skills,language etc)

Memory

Personality

Sense of humor

Social Skills

Impulse control

The Cerebrum

The Frontal lobe containsPrefrontal area (thought process)

Premotor area (general movements)

Motor Strip (voluntary motor functions of the opposite side of the body)

Broca’s Area (motor speech)

The Cerebrum

Parietal Lobe

Main function is sensory

Awareness of body parts, interpretation of touch, pressure, pain

Recognition of objects size, shape, and texture

Contains a sensory strip

Motor and Sensory Homunculus

Motor

The bigger the body parts are; the more brain powerthere is dedicated to controlling them

Sensory



The Cerebrum

Temporal lobe

Primary functions include hearing, speech, behavior, and memory

Controls emotional behaviors and drives

Wernicke’s area

Limbic System‐primitive, reactionary, survival‐oriented area of the brain. Think of dogs.

Feeding

Fight/Flight

Sex drive‐ loss of inhibitions

The Cerebrum

Occipital LobePrimary receptive area for vision and visual association

Where we make sense of what we see

Like living in a Picasso painting

Cerebrum: Diencephalon

Thalamuspair of egg shaped masses of gray matter

“Relay station” or Mission control for sensory inputSorts and sends sensory impulses to the appropriate area for final processing

Diencepalon

The Hypothalamus

Temperature Regulation

Autonomic Nervous System Responses

Regulation of food and water intake

Control of hormonal secretions (with communication to the pituitary gland)

Behavioral responses

Cerebrum: Basal Ganglia

Basal Ganglia main role is initiating and regulating motor commands

Parkinson’s Disease

Brain: Cerebellum

Also known as the little brain or hindbrainPerson can injure up to 80% of the cerebellum and still do well

Influences muscle tone associated with equilibrium, orientation in space and posture to ensure fluent and synchronized muscle action (smooth performance)



Brain: The BrainstemConsists of 3 structuresMidbrain

Pons

Medulla Oblongata

Brainstem

MidbrainNerve pathway for the cerebral hemispheres

Contains auditory and visual reflex center

Controlling responses to sight, eye movement, pupil dilation, body movement, hearing

Brainstem

Pons

Contains important neuronal pathways arising from cerebrum (motor) and spinal (sensory). Is the relay station for these messages.

Important centers for regulating breathing

Apneustic

Pneumotaxic

Brainstem

Medulla OblongataResponsible for involuntary responses, such as swallowing, vomiting, hiccuping, and coughing

Works with the pons respiratory functionresponsible for the basic involuntary rhythm of respirations

Mess with the Brainstem and You Mess With Life

Because the brainstem controls the most basic functions of life, it will be preserved even when the cerebral function is long gone.

Brainstem allows you to do what a frog and lizard can do: breath, chew, swallow, wiggle around, stick the tongue in and out, open and close eyes, and vomit. Many of our severely brain‐impaired patients will function at this level for the rest of their lives.

Reticular Activating System

Originates in the brainstem, then travels upward and to both cerebral hemispheres.

Responsible for consciousness

Keep the lights on‐ but more like a dimmer (alertness)

controls sleep, wakefulness, and the ability to consciously focus attention on something.

acts as a filter, dampening down the effect of repeated stimuli such as loud noises, helping to prevent the senses from being overloaded.



Key Cranial Nerves

Visual Acuity‐CN II‐Optic Nerve

Originates from the retina bipolar cells

Extraocular Movements

CN III-Oculmotor (Midbrain)

Superior rectus‐ upward and inward

Medial rectus‐inward

Inferior rectus‐downward and inward

Inferior oblique‐upward and outward

CN IV-Trochlear (Midbrain)

Superior oblique‐ downward and inward

CN VI-Abducens (Pons)Motor‐abducts the eye

Key Cranial Nerves

Pupillary Response

CN III-Oculomotor

Edinger‐Westphal nucleus: parasympathetic pupil constriction

PERRLA

Parasympathetic‐constriction

Sympathetic‐accommodation

Pupil size is a balance of sympathetic and parasympathetic

Key Cranial Nerves

CN V‐ Trigeminal (Pons)Sends function to 3 different branches

Ophthalmic branch‐gives sensation to the cornea, lacrimal glands, nasal mucosa, eyelids and eyebrows

Maxillary branch‐ gives sensation to skin of cheek, lower lid, side nose, upper jaw and teeth

Mandibular branch‐ gives sensation to lower lip, chin, ear, and tongue

Key Cranial Nerves

CN IX‐ Glossopharngeal (Medulla)

Motor‐ elevation of pharynx, swallow

Produces taste and sensation in back of throat, therefore stimulation to this will elicit the gag reflex

CN X‐ Vagus Nerve (Medulla)

Helps control the heart rate, control muscle movement and breathing

Vessels of the Brain: Arteries Vessels of the Brain: Arteries



Vessels of the Brain: Arteries Vessels of the Brain: Arteries

Vessels of the Brain: Dural Venous Sinuses

Questions??????

Neurological Review

What layer of meninges is located directly underneath the skull and is fibrous and canvas like?A) Dura mater

B) Arachnoid

C) Pia mater

Neurological Review

True or FalseThe body has the ability to regulate the amount of CSF produced depending on the circulating volume and reabsorption rate?



Neurological Review

Which lobe within the cerebrum is the primary sensory cortex?A) Temporal

B) Frontal

C) Occipital

D) Parietal

Neurological Review

What cranial nerve is responsible for the corneal reflexes?A) III‐ Oculumotor

B) IX‐ Glossopharyngeal

C) X‐ Vagus

D) V‐ Trigeminal

Assessment of the patient with a Traumatic Brain Injury

ABC

What is the patient doing?Awake/ Alert?Talking?Following simple commands

Assess the patient’s pupils immediately


Consciousness:Arousal

Evaluates reticular activating system. Centers on your ability to respond to verbal or noxious stimuli.

ContentHigher level function (A&O x4)


The Glasgow Coma Scale objectively assesses neurologic function in 3 independent areas:

Eye Opening/Arousability (4 points)

Best Verbal Response (5 points)

Best Motor Response (6 points)


Eye Opening/ Arousability4 points opens eyes spontaneously

3 points opens eyes to voice

2 points opens eyes to pain

1 point no eye response




Best Verbal Response5 points Oriented Conversation (A&O x4)

4 points Confused Conversation

3 points Inappropriate speech

2 points Incomprehensible sounds

1 point No verbal response


Best Motor Response6 points Follows commands

5 points Localizes to painful stimuli

4 points Withdraws to painful stimuli

3 points Flexion posturing (Decorticate)


Best Motor Response6 points Follows commands




2 points Extension posturing (Decerebrate)


Best Motor Response

6 points Follows commands




2 points Extension posturing (Decerebrate)

1 point No motor response


Triple FlexionSpinal cord arc reflex

Flexion of the foot, knee, and hip

Can still have and be brain dead


The Glasgow Coma Scale scores are totaled in each of the 3 areas to obtain a score 3‐15

Mild Head Injury GCS 13‐15

Moderate Head Injury GCS 9‐12

Severe Head Injury GCS 3‐8




Other assessmentsSpeech and language‐ is it slurred or appropriate

Motor assessment/coordination

Sensory assessment

Cranial nerve function


Blood Pressure and Heart Rate

Low‐high what does that mean?

Cushing’s Response (Kocher‐Cushing sign)

Bradycardia

Irregular breathing

Widening pulse pressure

Temperature

Infection

Hypothalamus dysfunction “neurogenic temp”

Cardiac rhythms


Respiratory Patterns

Diencephalon: Cheyne Stoke respiration

Midbrain/upper pons: Central neurogenic hyperventilation

Pons: Apneustic breathing

Lower pons/upper medulla: Cluster breathing

Medulla: Ataxic breathing


Signs of increasing intracranial pressure

Deteriorating LOC

Pupillary changes

Cushing’s response

Changes in respiratory pattern

Loss of motor function

Papilledema

Headache

Vomiting

Questions??? Neurological Assessment Review

A patient with a moderate head injury presents with which range of Glasgow Coma Scale scores?

A) 3‐8B) 9‐12

C) 13‐15



Neurological Assessment Review

True or FalseDecorticate and/or decerebrate posturing is an abnormal neurological response and indicative of severe brain injury?

Neurological Assessment Review

The Cushing’s response involves all symptoms EXCEPT:A) Bradycardia

B) Elevated temperature

C) Irregular breathing

D) Widening pulse pressure

Head Injuries

Etiology:FallsMVCMCCBlows to the headPenetrating injuries

Head Injuries

Classifications of Head InjuriesClosed Head Injuries

concussion

contusion

epidural hematoma

subdural hematoma

intraparenchymal bleed

traumatic subarachnoid hemorrhage

diffuse axonal injury (DAI)

Open

Penetrating (gunshot wound, stabbing)

Skull fractures

Skull Fractures

DepressedHow depressed is it?

Does it need surgery?

LinearLittle line fractures‐ in time it will heal itself.

Skull Fracture



Skull Fractures

Basilar Fracture

Is a fracture of the base of the skull, typically involving the temporal bone, occipital bone, sphenoid bone, and/or ethmoid bone

Did the fracture nick the meninges?

Do you have a CSF leak?

Basilar Skull Fracture

Skull Fracture

How do you know if you have a CSF leak?

Is there clear fluid coming out of your nose or ear? (rhinorrhea or otorrhea)

CSF leaves a halo ring

Pt may have trickling down the back of their throat and it has a salty taste

Types of Head Injuries

Concussion

Approximately 80% of TBI are mild

CT is “negative”

Brief loss of consciousness (less than 6 hours or none)

Headache

Post‐traumatic amnesia (PTA)

Nausea/vomiting

Confusion

Memory Impairment

Symptoms of a Concussion

Cognitive

Difficulties with attention & concentration

Memory impairment

Affective

Irritability, anxiety, emotionally liable

Depression

Somatic

Headache, dizziness, nausea, tinnitus

Insomnia, fatigue, sensory disturbances

Concussion Deficits

Deficits are often found in executive function, attention, concentration, processing speed and memory

Impact or SCAT

Neuropsychological Testing




Contusion

Altered LOC

Weakness or paralysis

Vision change

Headache‐related to the area traumatized

Coup, contrecoup

Serial CT scans


Epidural Hematoma (EDH)

Between the skull and the dura

Arterial bleed

Brief LOC

“Talk and deteriorate” or “talk and drop” syndrome

Ipsilateral pupil changes

Contralateral hemiparesis/plegia

Craniotomy and Evacuation

CT scan for size and location

Epidural Types of Head Injuries

Subdural Hematoma (SDH)

Below the dura

Venous bleed

History of recent trauma

Altered LOC

Pupil changes (late)

Hemiparesis/plegia

Can be acute, subacute, or chronic

Craniotomy and Evacuation, Burr Holes

Subdural Types of Head Injuries

Intraparenchymal Hemorrhage (IPH)Intracerebral Hemorrhage (ICH)

within the brain tissue (parenchyma)

usually from severe blunt trauma, hypertensive bleed, or rupture of aneurysm

brainstem bleeds usually fatal




Subarachnoid Hemorrhage (SAH)traumatic

aneurysmal


Diffuse Axonal Injury (DAI/Shearing)

Accounts for 50% of all primary injuries & 35% of all deaths from TBI

Mechanism of injury is acceleration/deceleration

Stress at gray‐white interface

Petechial hemorrhage is a sign

Cell breakdown and myelin degeneration

Diffuse swelling

Grade 1, 2, 3 (mild, moderate, severe)

Shearing Injury Types of Head InjuriesHypoxia/ Anoxia

Cascade of cellular pathophysical events begin‐ leads to anaerobic metabolism and to cell death if not interrupted

Questions??? Management of the TBI patient

Beth Heather RN, BSN, CCRN, ENLS

Nursing Practice Specialist-Critical Care

ECMO Coordinator

[email protected]

Hennepin County Medical Center



Management of the TBI Patient Intracranial Components

80% Brain Tissue

10% Cerebrospinal fluid (CSF)

10% Blood

Modified Monroe‐Kelly Hypothesisvolume/pressure ratio

What Throws Off the Balance

Increase in brain tissue volume

space occupying lesion/tumor

cerebral edema

Increase in blood volume

hemorrhage

Increase in CSF volume

obstruction to flow

non‐communicating hydrocephalus (generally caused by a tumor)

increased CSF production (rare seen in pediatric patients)

decreased CSF reabsorption‐ bits of brain tissue and blood clog the arachnoid villi (generally seen in trauma)

communicating hydrocephalus

Normal Function of our Brain: Autoregulation

Pressure

Cerebral blood flow (CBF) must remain stable regardless of fluctuations in MAP

If MAP rises, the cerebral arteries constrict

If MAP falls, the cerebral arteries dilate

Once autoregulation no longer works CBF becomes dependent on cerebral perfusion pressure (CPP)

Cerebral Blood Flow Autoregulation

Metabolic

Receptors in the brain constantly analyze blood gases

Cerebral arteries will dilate as levels of CO2 and lactic acid rise

CSF

As ICP rises, spinal fluid is displaced into the spinal canal

The arachnoid villi increase absorption of CSF into the venous sinuses



What is ICP and CPP

“Normal” Intracranial Pressure (ICP)

adult <15 mmHg

infants <10 mmHg

Elevated ICPs for extended period of time, can cause further damage to the brain

Cerebral Perfusion Pressure (CPP)

MAP‐ICP= CPP

Goal CPP 55‐70

How do we measure ICP & CPP

Camino

Fiber optic, catheter tip transducer that sits in either the epidural subdural space or parenchymal.

Can not drain CSF

Ventriculostomy (ventric)

External ventricular drainage (EVD)

Can drain CSF and read ICPs

Can be clamped or open at 0, 5, 10, 15, 20

Waveform is influenced by the relation to the arterial & venous pulse wave forms

Bone Flap

Camino Flex

ICP Waveforms Traumatic Brain Injury (TBI)

Primary InjuryTrauma to the brain tissue or it’s vasculature that happens at the moment of impact

2/3 of deaths related to TBI are due to primary injury and occur before people reach the hospital

Traumatic Brain Injury

Secondary injury

Usually there is additional injury to the brain that occurs hours to days later. If severe enough it can:

Cause a cascade of events at a cellular level creating cerebral edema/swelling leading to increase ICP

Cause changes in cerebral blood flow and/or metabolism leading to ischemic brain death

25% mortality

Management of the TBI Patient

The goal is to prevent further damage related to secondary injury and optimize their recovery from the primary injury.

What do we need to know?

What can we do?



Management of the TBI Patient

ABC’s

Protect airway/ventilator management

Avoid hypoxia, PaO2 <60 or O2 saturation <90%

PCO2 35‐40

Avoid hyperventilation‐ only in emergent situation

Hbg > 9 vs Hbg>7

Liccox: goal PbtO2 >20

Treat hypotension/hypertension

Goal SBP <140 or SBP < 160

CPP range 50‐70 mmHg (avoid above 70 mmHg)

Independent predictor of increased morbidity & mortality

Primary intervention cont.

Neurological Assessment

Changes may indicate increase in swelling or hemorrhage

Continous ICP monitoring

Place in patients with GCS <8

ICP <20 vs ICP <25 vs what is the right #

Elevate HOB and keep neck midline

Optimizes cerebral blood flow and cerebral venous return

Avoid extreme hip flexion

Primary interventions cont.

Decrease Metabolic demands

Keep normothermic

Every 1° C elevation in temperature increases metabolic oxygen demand by 10%

Tylenol for temp> 38˚ C (usually sometimes lower)

Normothermia protocols

Keep quiet

Reduce anxiety/agitation/pain

medication

stimuli

Primary interventions cont.

Seizure management

Phenytoin/Fosphenytoin Protocol vs Keppra

Load dose

Maintenance dose

Length of therapy

Hypertonic Saline Therapy

3% NaCl (central line needed)

2% NaCl (doesn’t need a central line)

Goal Na+ level 145‐155

Q6 hour serum levels‐ prevent “overshooting”

Secondary intervention

If ICPs continue to be >20 despite primary interventions

23%NaCl

30 cc bolus of 23% NaCl

Given over 15 minutes

Must be given via CENTRAL LINE

Mannitol

Dosing 0.25‐1g/kg

Given over 15‐30 mins

Can be given in a peripheral

Tertiary interventions

When ICP’s are Refractory to previous treatments:

High dose sedation

Paralytics

Barbiturate‐induce coma

Craniotomy/ Craniectomy

Lobectomy

Mild hypothermia



Management of a TBI patient

Imaging

Head CT

follow‐up

after injury

after surgery

routine

emergent

MRI

Management of a TBI

Questions???

Case Study: Day 1

23 yo M punched in the face and fell to the ground hitting his head. +LOC +ETOH (0.21)

Intubated in ED due to agitation

GCS around 7‐8

PERRL

18 gauge IV place in bilateral AC

HCT‐ R frontal SDH with a 2 mm midline shift

Fosphenytoin loaded

Day 1

Admitted to SICU at 0051

(‐)FC, purposeful, intermittently opens eyes to pain

What’s his GCS?

Pt sedated with propofol and fentanyl

Central line inserted‐3% NaCl started @ 30cc/hr

Follow up HCT done at 0600‐unchanged

Holding off on ventric

Why?

Day 2

Neuro exam still the same

Attempted weaning trials on the ventilatorstopped due to agitation

Sedated with propofol and prn versedincreased agitation and almost self‐extubated

Day 3

1300

Patient is no longer purposeful‐ now withdrawing, PERRL

HTN ‐ labetolol given

STAT HCT

SDH unchanged

R frontal contusion with diffuse cerebral edema

Ventric placed

Opening ICP 25

CSF drainage 38 cc

Ventric open @ 10‐ ICP now 8

Arterial line placed

Pt is purposeful again



Day 4

0000

ICP 33, PERRL, Na+ 150

23% NaCl given, ICP after 8

HTN‐labetolol given

Ventric open @ 5

Pt is not tolerating decrease in sedation

Increase in ICP

1400

ICP 22, PERRL, Na+ 151


Ventric open @ 0

Day 5

0000ICP 21, Na+ 151, PERRL


Switch propofol gtt to ativan gtt @ 14 mg/hr & Fentanyl 200 mcg/hr

0600ICP 22, Na+ 153, PERRL


Ativan gtt @ 18 mg/hr

0800ICP 22, PERRL


Ativan gtt @ 22 mg/hr

Day 5 cont

1200ICP 35, Na+155, PERRL

23% NaCL given

HTN‐labetolol given

STAT HCT

Evolving edema and L ventricle “plump”

Pt is paralyzed with vecuronium

A 2nd ventric is placed in the L ventricle

35 cc of CSF drained, ICP after 11

Day 5 cont

2100

ICP 36, Na+ 156, PERRL

23% NaCl given, ICP after dose 28

Mannitol given.

HTN (170’s) PRN labetolol and hydralazine given

2200

ICP 42, PERRL

HTN still occurring

Nicardipine gtt

What do we do next??

Craniectomy

11

Day 6

ICP’s are normal after surgery.



Case Study

Day 8 ativan gtt wean begins at 11mg/hr

Pt is withdrawing on all 4 extremeties later that day

Day 11 pt is following commands

Day 19 pt is trach doming for >24 hrs

Day 23 ventric removed

Day 24 pt is transferred to general floor

Day 26 pt is transferred to acute rehab

Day 40 pt is discharged to home

Questions???

Herniation Syndrome

Results in shifting of brain tissue from one compartment to another

Places pressure on cerebral vessels and vital function centers of the brain

Can result in cessation of cerebral blood flow (CBF) and respirations

6 total types, 4 main types

Herniation Syndrome

Cingulate (Subfalcine)Expanding frontal portion of the cerebral hemispheres shift laterally

Compresses blood vessels, especially ispsilateral anterior cerebral artery, causing ischemic & edema

Herniation Syndrome

Lateral Transtentorial (Uncal)

Supratentorial ICP rises & the temporal lobe & nearby structure herniate laterally

Compresses CN II

Compress midbrain affecting RAS

Compresses ispsilateral cerebral peduncle causing contralateral motor dysfunction, posturing

Compression of posterior cerebral artery causes infarct

Central neurogenic hyperventilation

Herniation Syndrome



Herniation Syndrome

Central Transtentorial

Downward displacement of one or both cerebral hemispheres

Compresses & displaces diencephalon & midbrain through tentorial notch

Usually occurs in parenchymal lesions of the frontal & parietal lobes

LOC, EOMs, & posturing are seen

Herniation Syndrome

Herniation Syndrome

Tonsillar Herniation

Cerebellar tonsils herniate through foramen magnum

Compresses medulla & upper cervical cord

Causes precipitous changes in BP & HR, small pupils, dysconjugate gaze, ataxic breathing, & quadraparesis

Often fatal (better move fast)

Herniation Syndrome

Herniation Syndrome End of Life

Brain death vs Discontinuation of Support/ Comfort Cares Status



Brain Death

MN State Statue 145.135 Subd.2. Determination of Death

An individual is dead if the individual sustains irreversible cessation of:

Circulatory and respiratory functions

All functions of the entire brain, including the brain stem

Brain Death Criteria

Known etiology of brain death and/or evidence of irreversibility

No brainstem function on physical examination

No respiratory effort on apnea test

No cerebral blood flow noted on blood flow study (optional in some facilities)

Brain Death Exam

Patient can NOT be under the influence of alcohol, street drugs, sedatives, paralytics or anesthesia

Patient must be normothermic (36 ° C for HCMC)

Systolic BP > 90 mmHg

Endocrine causes excluded? (acid/base)

Clinical Assessment (2 MDs perform)

Voluntary motor control absent

Simple spinal cord reflexes may persist

Cranial nerve reflexes absent

Both pupils non‐reactive to light (CN III)

Absent corneal reflex (CN V & VII)

Absent cough & gag reflex (CN IX & X)

Absent Occulocephalic reflex (Doll’s eye) (CN II, IV, & VIII)

Absent Occulovestibular reflex (cold calorics) (CN III, IV, & VIII)

Corneal Reflex Apnea Test

Provides adequate stimulus for spontaneous ventilation without inducing hypoxemia or hypercapnia

Before the start

PCO2 normal

Extreme hypocarbia or hypercarbia should be corrected

Supranormal PaO2 preferably at or above 200 mmhg

During the test

Ventilator disconnected, approximately 8 mins

6‐8 L of O2 down ETT

Stop if patient unstable or spontaneous ventilatory efforts.



Apnea Test Cont.

Positive testAbsent respiratory movements

PCO2 > 60 mmHg or an increase of 20 mmHg over baseline PCO2

Radiographic Study

Are required in some hospitals and optional in others

Used when apnea testing is contraindicated

May use cerebral angiogram or radioisotope study

Cerebral Blood Flow Test Blood flow test

Brain Death

The patient is declared brain dead when the state statute definition has been met by the hospital policy

The official time of death is at the conclusion of first exam

Apnea test

Radiographic study

Donation

Once the family understands the patient is brain dead, Lifesource will meet with them to discuss the option of donation

Donor designated

First Person Consent Law‐deceased person’s written organ donation wishes. Does NOT require family for permission.

Not donor designated

Family wishes to donate

Family does not want to donate

Medical team & family decide on an appropriate time to remove all medical devices.



Donation After Cardiac Death (DCD)

If patient is not brain dead and family wishes to discontinue medical treatment (comfort care status)

Lifesource will offer the option of DCD

Patient’s age < 60

Likelihood of proceeding to death within 60 mins

Respiratory Assessment

BMI, Vassopressors, diseases

DCD

If patient is a donor candidate, family is counseled on process

Patient taken to OR for Prep/Drape/Extubation

Family in OR if they wish

Pronounce & record cardiac time of death

Family escorted out of OR/ Hands off 5 mins

Procurement begins

If patient does not expire in 60 min window, taken to a private floor bed and remain on comfort care status

Brain Death vs DCD

Questions????

References

AANN Core Curriculum for Neuroscience Nursing – 5th Edition – Bader & Littlejohns ‐ Saunders 2010 (www.aann.org)

AACN‐AANN Protocols for Practice, Monitoring Technologies in Critically Ill Neuroscience Patients (Ed.). (2009). Sudbury: Massachusetts: Jones and Bartlett Publishers, LLC.

Ahrens, T., Prentice, D., & Kleinpell, R. (2010) Critical Care Nursing Certification (6th ed.). New York: The McGraw Hill Corp. Inc.

Guidelines for the Management of Severe TBI in the Adult‐ 3rd Edition – Brain Trauma Foundation – May 2015 (www.braintrauma.org)

Emergency Neurological Life Support (ENLS) Guidelines‐Neurocritical Care Society‐March 2016 (www.neurocriticalcare.org)

Hickey, J. (2009) The Clinical Practice of Neurological & Neurosurgical Nursing (6th ed.). New York: Lippincott

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