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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
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
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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
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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
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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)
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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.
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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
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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?
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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
Assessment of the patient with a Traumatic Brain Injury
Consciousness:Arousal
Evaluates reticular activating system. Centers on your ability to respond to verbal or noxious stimuli.
ContentHigher level function (A&O x4)
Assessment of the patient with a Traumatic Brain Injury
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)
Assessment of the patient with a Traumatic Brain Injury
Eye Opening/ Arousability4 points opens eyes spontaneously
3 points opens eyes to voice
2 points opens eyes to pain
1 point no eye response
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Assessment of the patient with a Traumatic Brain Injury
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
Assessment of the patient with a Traumatic Brain Injury
Best Motor Response6 points Follows commands
5 points Localizes to painful stimuli
4 points Withdraws to painful stimuli
3 points Flexion posturing (Decorticate)
Assessment of the patient with a Traumatic Brain Injury
Best Motor Response6 points Follows commands
5 points Localizes to painful stimuli
4 points Withdraws to painful stimuli
3 points Flexion posturing (Decorticate)
2 points Extension posturing (Decerebrate)
Assessment of the patient with a Traumatic Brain Injury
Best Motor Response
6 points Follows commands
5 points Localizes to painful stimuli
4 points Withdraws to painful stimuli
3 points Flexion posturing (Decorticate)
2 points Extension posturing (Decerebrate)
1 point No motor response
Assessment of the patient with a Traumatic Brain Injury
Triple FlexionSpinal cord arc reflex
Flexion of the foot, knee, and hip
Can still have and be brain dead
Assessment of the patient with a Traumatic Brain Injury
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
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Assessment of the patient with a Traumatic Brain Injury
Other assessmentsSpeech and language‐ is it slurred or appropriate
Motor assessment/coordination
Sensory assessment
Cranial nerve function
Assessment of the patient with a Traumatic Brain Injury
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
Assessment of the patient with a Traumatic Brain Injury
Respiratory Patterns
Diencephalon: Cheyne Stoke respiration
Midbrain/upper pons: Central neurogenic hyperventilation
Pons: Apneustic breathing
Lower pons/upper medulla: Cluster breathing
Medulla: Ataxic breathing
Assessment of the patient with a Traumatic Brain Injury
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
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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
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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
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Types of Head Injuries
Contusion
Altered LOC
Weakness or paralysis
Vision change
Headache‐related to the area traumatized
Coup, contrecoup
Serial CT scans
Types of Head Injuries
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
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Types of Head Injuries
Subarachnoid Hemorrhage (SAH)traumatic
aneurysmal
Types of Head Injuries
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
Hennepin County Medical Center
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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
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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?
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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
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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
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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
23% NaCl given, ICP after 10
Ventric open @ 0
Day 5
0000ICP 21, Na+ 151, PERRL
23% NaCl given, ICP after 8
Switch propofol gtt to ativan gtt @ 14 mg/hr & Fentanyl 200 mcg/hr
0600ICP 22, Na+ 153, PERRL
23% NaCl given, ICP after 11
Ativan gtt @ 18 mg/hr
0800ICP 22, PERRL
23% NaCl given, ICP after 15
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.
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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
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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
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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.
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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.
Images have been removed from the PowerPoint slides in this handout due to copyright restrictions.
Neurological Critical Care ©TCHP Education Consortium 1999, Revised January 201724
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