Acute consciousness disorders. Brain death. - PowerPoint Presentation

Slide1

Acute consciousness disorders. Brain death.

Slide2

Consciousness

defined as being awake and aware of both one’s self and one’s surroundings, OR it is

the human

awareness

of both internal and external

stimuli.

Level of consciousness

: is a measurement of a person’s

arousability

and responsiveness to stimuli from the environment.

Slide3

Alert

(Conscious)

- Appearance of wakefulness, awareness of the self and environment.

Lethargy:

mild depression in level of consciousness and can be aroused with little difficulty.

Obtunded

:

More depressed level of consciousness and can not be fully aroused( slow response and

sleepness

).

Stuporous

:

Can not be aroused from a sleep like

state (

only respond by grimacing or drawing away from painful stimuli

).

Coma

:

More depressed level of consciousness and unable to make any purposeful

response.

Slide4

Pathophysiology

Reticular formation is known to play a role in alertness, wakefulness and arousal.

Maintaining alertness requires intact function of the cerebral hemispheres and preservation of arousal mechanisms in the reticular activating

system.

Slide5

CAUSES OF COMA

Diffuse

bilateral hemisphere

damage;

Failure of the ascending reticular activating system;Both.

Slide6

Causes

Slide7

COMA ETHIOLOGYFOCAL- Structural disorders

Trauma

Epidural Hematoma

Lens shaped

Caused by arterial ruptureSkull fracture present in 85% of cases

Slide8

Subdural hematoma

Crescent shaped

Caused by tearing of bridging veins through

dura

and arachnoid

Skull fracture present in 30% of cases

Retinal Hemorrhage in 75% of cases

Slide9

Cerebral Contusion

Can lead to increased ICP

Slide10

Brain tumor

Slide11

Infection

Brain

Abscess

Risc

factors:

chronic sinusitis

chronic

otitis

dental infection

endocarditis

uncorrected

cyanotic congenital heart

disease.

Slide12

Stroke

Hemorrhagic is usually due to aneurysm

Severe headache

Arteriovenous

malformation or cavernous hemangiomaLow flow and less acute symptoms

Slide13

Stroke

Thrombosis or Embolic Stroke

Occlusion of anterior, middle or posterior cerebral artery will NOT cause coma

Infarcts eventually lead to increased ICP

Cerebellar infarcts rarely have comaBasilar Artery infarcts cause rapid coma due to brainstem damage

Slide14

Stroke

Thrombosis or Embolic Stroke

Occlusion of anterior, middle or posterior cerebral artery will NOT cause coma

Infarcts eventually lead to increased ICP

Cerebellar infarcts rarely have comaBasilar Artery infarcts cause rapid coma due to brainstem damage

Slide15

Subarachnoid hemorrhage

Slide16

Nonstructural disorders

Seizures (

eg

,

nonconvulsive status epilepticus) or a postictal state caused by an epileptogenic focus

Slide17

COMA ETHIOLOGYDIFFUSE

Metabolic and endocrine disorders

Diabetic

ketoacidosis

Hepatic encephalopathyHypoxiaHypercapniaHypoglycemia

Hyper- ,

Hyponatremia

Hypercalcemia

Hypothyroidism

Uremia

Wernicke encephalopathy

Slide18

INFECTIONSEncephalitis

Encephalitis – inflammation of the brain parenchyma usually due to viral infection

Herpes simplex viruses – most common devastating cause

Death or permanent neurologic damage in 70% of cases

Affects temporal lobes causing seizures, parenchymal swelling and uncal herniation

Slide19

Meningitis

Bacterial

Most common infection severe enough to cause profound ALOC

Non-bacterial

Slower onset of symptoms

Slide20

Slide21

OTHER DISORDERS

Diffuse axonal injury

Hypertensive encephalopathy

Hyperthermia or hypothermia

TOXINSCarbon monoxide

Slide22

Pathophysiology

Altered consciousness is based on

Increased intracranial pressure

Herniation

Diffuse bilateral lesions

Slide23

Monro-Kellie doctrine:

Monro

-Kellie doctrine or the

Monro

-Kellie hypothesis is the pressure-volume relationship between ICP, volume of CSF, blood, and brain tissue, and cerebral perfusion pressure.

Slide24

Brain

parenchyma—1200-1600 ml

Cerebrospinal fluid—100-150 ml

Blood— 100-150 ml

ESF <75 ml

Slide25

Monro-Kellie doctrine:

 sum of volumes of brain, CSF, and intracranial blood is constant.

Because

the overall volume of the cranial vault cannot change, an increase in the volume of one component

(e.g., brain, blood, or cerebrospinal fluid) will elevate pressure and decrease the volume of one of the other elements.

Slide26

Slide27

P

ressure-volume curve

(A)

Increased intracranial

volume

passively displaced

of CSF

into the

spinal subarachnoid space.

As a result, the ICP only modestly

increases during the early stages of the process.

(B)

once

CSF cannot be passively displaced an

d

further,

the ICP

rises more sharply as the space-occupying process continues

to evolve

(B).

Slide28

This relationship between

added volume

to the

intracranial cavity and its matched rise in

ICP

is referred to

as the

intracranial compliance

Slide29

changes

in volume need to be evacuated in order to keep ICP down

since

 

perfusion pressure of the brain = MAP

–

ICP

MAP normal range > 65 mm Hg

ICP -5-15 mm Hg

Slide30

GOALS

Any condition that increases intracranial pressure (ICP) may decrease cerebral perfusion

pressure

Maintain

Cerebral Perfusion Pressure>60 mm HgControl Cerebral Blood Flow

Slide31

CPP= MAP-ICP

CPP- Keep > 60

MAP= SP + 2 DP/3

ICP keep < 20 mmHg

Slide32

Cerebral Blood Flow

Blood Pressure

PaCO2

PaO2

Slide33

C

erebral perfusion

A

relatively

constant

supply

of

blood

to

the

brain

is

ensured

by

cerebral

autoregulation

,

a

physiologic

phenomenon

that

allows

maintenance

of

a

constant

CBF

over

a

wide

range

of

arterial

blood

pressures

.

In

chronic

hypertensives

,

the

autoregulatory

thresholds

are shifted to the right.

Skull= Brain+

Blood

+ CSF

Slide34

Cerebral blood flow

A r

elative

low blood pressure (within

an

autoregulator

range

)

leads

to

cerebral

vasodilation

and a

n

increase

in

cerebral

blood

volume

.

A

relative

blood

pressure

elevation

(

within

an

autoregulator

range

)

leads

to

cerebral

vasoconstriction

and

a

decrease

in

cerebral

blood

volume

.

Such

alterations

in cerebral blood volume can importantly affect the ICP

.

Slide35

Carbon Dioxide

Skull= Brain+

Blood

+ CSF

Slide36

Oxygen

Skull= Brain+

Blood

+ CSF

Slide37

Factors which influence

CBF

and

ICP

Increase

Hyperthermia

Hypercapnia

HTA

Hypoxia

Acidosis

Pain/arousal

Volatil

anestetics

Seizures

PEEP

Decrease

Hypothermia

Hypocapnia

Hyperoxia

Hyperventilation

Alcalosis

Slide38

C

erebral edema

Cerebral

edema

is

defined

as

an

increase

in

brain

water

content

.

1.

vasogenic

edema

2.

cytotoxic

edema

-

cellular

injury

Slide39

Vasogenic

edema

Vasogenic

edema results when increased permeability of capillary endothelial cells permits fluid to escape into the extracellular space

Neurons are not primarily injured

Vasogenic

edema is seen with tumors, intracranial hematomas, infarcts, abscesses, and central nervous system infections

Therapy to decrease the edema may prevent secondary ischemic injury to surrounding brain tissue since neurons are not primarily injured

Steroid therapy may be beneficial for

vasogenic

edema that occurs in the setting of mass lesions

Slide40

Cytotoxic

edema

Cytotoxic edema is caused by intracellular swelling secondary to direct cell injury

It

results

in

the

failure

of

the

adenosine triphosphate

–

dependent

sodium

pump

,

with

resultant

accumulation

of

sodium

and

water

within

the

cells

.

Cytotoxic edema is common in patients who have severe cerebral injuries such as traumatic brain injury, diffuse axonal injury, or hypoxic-ischemic injury

Slide41

C

erebral edema

does not directly affect neural

activity

Its main and most severe consequences

are due to

its

mass effect

and

distortion of surrounding brain tissue

,

which can

cause regional ischemia and result in the development

of pressure gradients, leading to

devastating brain tissue

shifts

.

Slide42

B

rain tissue displacement

and

herniations

It

is

important

to

differentiate

mass

effect

and

brain

tissue

displacement

(BTD)

from

intracranial

hypertension

.

T

here

can

be

a

substantial

amount

of

mass

effect

without

an

important

global

elevation

in

ICP,

and

the

mass

effect

alone

can

cause

brain

damage

through

its

regional

effect

on

brain

perfusion

and

/

or

brain

tissue

displacement

(

e.g

.

herniation

).

Slide43

B

rain tissue displacement

and herniations

BTD is a distortion

of brain anatomy, and depression of consciousness is one

common sign associated with such distortion.

However, depressed

consciousness can be a late accompaniment to BTD.

Slide44

B

rain tissue displacement

and herniations

BTD is a distortion

of brain anatomy, and depression of consciousness is one

common sign associated with such distortion.

However, depressed

consciousness can be a late accompaniment to BTD.

Slide45

Cerebral herniation

I

t

is

useful

to

note

the

relationship

between

horizontal brain

displacement

and

depressed

consciousness

.

horizontal

shift

of

the

pineal

(

from

midline

)

:

0

to

3

mm

-

alertness

;

3

to

4

mm

-

drowsiness

;

6

to

8

mm

-

stupor

;

>

8

mm

-

coma

.

Slide46

Herniation Syndromes

Herniation of brain tissue can cause injury by compression or traction on neural and vascular structures

Herniation results when there is a pressure differential between the intracranial compartments, and can occur in three areas of the cranial cavity

Transtentorial

(2)

Subfalcian

(1)

Foramen magnum (3)

Slide47

Herniation Syndromes: Transtentorial

(2)

Most common type

Results from downward displacement of

supratentorial brain tissue into the

infratentorial

compartment, and can be caused by

supratentorial

mass lesions, diffuse brain swelling, focal edema, or acute hydrocephalus.

Can cause compression of the third cranial nerve, the upper brainstem, and the cerebral peduncles, as well as distortion or traction of the superior portion of the basilar artery

Slide48

Herniation Syndromes: Subfalcian

(1)

Occurs when increased pressure in one hemisphere displaces brain tissue under the

falx

cerebri

Can cause compression of the anterior cerebral artery and extensive infarction of the frontal and parietal lobes

Slide49

Herniation Syndromes: Foramen Magnum (3)

Occurs when downward pressure forces the cerebellar tonsils into the foramen magnum, where they compress the medulla oblongata and upper cervical spinal cord

Slide50

Examination of the

c

omatose

p

atient - a

c

linical

a

pproach

Acute

depression

in

level

of

consciousness

is

a

critical

,

lifethreatening

emergency

that

requires

a

systematic

approach

for

evaluation

of

etiology

.

Slide51

Assessment of comatose patient

1. History—through

friend, family or emergency medical personnel

2. General

physical examination3. Neurological assessment—to define the nature of coma

Slide52

HISTORICAL FEATURES

Acute O

nset of coma

may indicate a

:

cerebral vascular etiology

(i.e., subarachnoid hemorrhage, intracerebral hemorrhage, or hemispheric or brain stem stroke),

generalized epileptic activity,

traumatic brain injury,

dru

g

overdose

A

subacute

deterioration may point to

:

systemic illness,

evolving intracranial mass,

a degenerative infectious

paraneoplastic neurologic disorder.

NB.

T

he duration of a comatose state should be documented because it may have predictive value for prognosis in certain causes.

Slide53

General examination

1.

Skin

(for example, rash,

anaemia

, cyanosis, jaundice)

2. Temperature

(fever-infection /hypothermia-drugs/circulatory failure)

3. Blood

pressure (for example,

septic shock, Addison's

disease)

4. Breath (alcohol, other drug intoxication, diabetic ketoacidosis,

fetor

hepaticus

)

5. Cardiovascular

(for example, arrhythmia)

6. Abdomen

(for example,

organomegaly

)

7. Needle marks: Drug overdose (

eg

, of opioids or insulin)

8. A bitten tongue: Seizure

Slide54

N

eurological examination

Assessment

of

Consciousness

Which is etiology?

The

important

neurologic

features

include

respiratory

pattern

,

pupillary

size

and

reactivity

,

eye

position

and

movements

,

corneal

reflexes

,

motor

function

.

Slide55

Assessment of

c

onsciousness

Initially

,

observe

whether

the

patient

appears

asleep

or

wakeful

with

spontaneous

eye

opening

.

In

a

sleeping

patient

,

quantify

how

much

stimulation

is

required

to

arouse

the

patient

.

First step -

ve

rbal

command

Second step -

physical

stimulation

by

shaking

the

patient.

Third step -

noxious

stimulation

can

be

applied

by

digital

pressure

to

the

supraorbital

nerves

or

nailbeds

of

the

fingers

or

toes

.

Slide56

Slide57

Level of conciousness

Glasgow Coma Scale

Best eye response (E)

Best verbal response (V)

Best motor response (M)

4

Eyes opening spontaneously

5

Oriented

6

Obeys commands

3

Eye opening to speech

4

Confused

5

Localizes to pain

2

Eye opening in response to pain

3

Inappropriate words

4

Withdraws from pain

1

No eye opening

2

Incomprehensible sounds

3

Flexion in response to pain

1

None

2

Extension to pain

1

No motor response

Slide58

Respiratory patterns

Slide59

Pupillary responses

Spontaneous eye movements

Oculocephalic

responses

Caloric responses

Corneal responses

Brain stem function

Slide60

Pupils

Size, inequality, reaction to a bright light.

An important general rule: most metabolic

encephalopathies

give small pupils with preserved light reflex.Atropine, and cerebral anoxia tend to dilate the pupils, and opiates will constrict them.

Slide61

Slide62

Ocular

movements

The position of the eyes at rest

Presence of

spontaneous eye movement

The reflex responses to

oculocephalic

and

oculovestibular

maneuvers

In diffuse cerebral disturbance

but intact brainstem function,

slow roving eye

movements

can be observed

Frontal lobe lesion

may cause deviation of the eyes

towards

the side of the lesion

Slide63

Lateral pontine lesion

can cause conjugate deviation to the

opposite

side

Midbrain lesion

Conjugate deviation

downwards

Slide64

Structural brainstem lesion

disconjugate

ocular deviation

Slide65

The oculocephalic

(doll's head) response

rotating the head from side to side and observing the position of the eyes.

If the eyes move

conjugately

in the

opposite direction

to that of head movement, the response is positive and indicates an

intact pons

mediating a normal

vestibulo

-ocular reflex

Slide66

Slide67

Caloric

oculovestibular

responses

These are tested by the instillation of ice-cold water into the external auditory meatus, having confirmed that there is no tympanic rupture.

A normal response in a conscious patient is the development of nystagmus with the quick phase away

from the stimulated side This requires intact

cerebropontine

connections

Slide68

Slide69

Corneal

r

eflex

The

corneal

reflex

is

an

important

protective

mechanism

for

the

cornea

A

fferent

limb

-

via

the

trigeminal

nerve

(CN V),

&

efferent

limb

-

via

the

facial

nerve

(CN VII)

Although

corneal

reflexes

assess

brain

stem

function

Slide70

Motor

f

unction

-

corticospinal tract

Lesions

involving the corticospinal tract generally lead to diminished

contralateral spontaneous activity.

Slide71

Motor function

Particular attention should be directed towards asymmetry of tone or movement.

The plantar responses are usually extensor, but asymmetry is important.

The tendon reflexes are less useful.

The motor response to painful stimuli should be assessed carefully (part of GCS)

Slide72

Painful stimuli

: supraorbital nerve pressure and nail-bed pressure

Patients may localize or exhibit a variety of responses,

asymmetry

is important

Slide73

Posturing

bilateral mid-brain or

pontine

lesions

upper brain stem lesion

D

ecerebrate

rigidity -

consists

of

opisthotonos

, clenching of the jaws, and stiff extension of the limbs, with internal rotation of the arms and plantar flexion of the

feet.

Slide74

Posturing

Decorticate rigidity

, with arm

in

flexion and adduction and leg(s) extended, signifies lesions at a higher level, in cerebral white matter or

internal capsule and thalamus, also upper midbrain.

Slide75

Neurological investigations

CT imaging

Magnetic resonance

imaging

The electroencephalographyLP

Slide76

Laboratory Procedures

Blood and urine ("toxic screen").

Accurate means are available for measuring the blood concentrations of

phenytoin

and other anticonvulsants, opiates, diazepines, barbiturates, alcohol, and a wide range of other toxic substances.

Proteinuria

for 2 or 3 days after a subarachnoid hemorrhage or with high fever.

Urine of high specific gravity,

glycosuria

, and

acetonuria

occur almost invariably in diabetic coma; but transient

glycosuria

and hyperglycemia may result from a massive cerebral lesion

Slide77

Management of Intracranial Pressure

C

ontroling

agravating factors

Control of BP

Patient

positioning

Control of temperature

Sedation for ensure efficient ventilation with

hyperventlation

Positive end-expiratory pressure (PEEP)

Control of seizures

Slide78

Management Strategies in elevated ICP

Control of blood component

Control of CSF

Control of volume of brain

Skull=

Brain

+

Blood

+

CSF

Slide79

Management of Intracranial Pressure

M

echanical

ventilation to ensure efficient oxygenation

Skull= Brain+

Blood

+ CSF

Slide80

ICP control

Goal:

ICP

≤ 20 mm

Hgcerebral perfusion pressure - 50 to 70 mm Hg.

elevate

the head of the bed to 30°

keep

the patient’s head in a midline position.

Slide81

Sedation

control

agitation, excessive muscular activity (

eg

, due to delirium), or pain. Propofol is often used in adults Benzodiazepines (midazolam, lorazepam)

Slide82

Hyperventilation

causes

hypocapnia

, which causes vasoconstriction, thus decreasing cerebral blood flow globally.

Reduction in Pco2 from 40 to 30 mm Hg can reduce ICP about 30%. ICP decreases for

only about 30 min and is used

as

a temporary measure until other treatments take effect.

Slide83

Osmotic diuretics

Goal:

Serum osmolality

-

295 to 320 mOsm/kg. Osmotic diuretics-mannitol-3% saline

solution

Skull=

Brain

+ Blood+ CSF

Slide84

Loop diuretics:

Furosemide

Diuretics

exert their effect through:

an

osmotic

gradient

caused

by

a

mild

diuresis

,

reduction

in

CSF

formation

,

reduction

in

brain

water

.

Slide85

Corticosteroids

helpful

for patients with a brain tumor or brain

abscess

ineffective for patients with head trauma, cerebral hemorrhage, ischemic stroke, or hypoxic brain damage after cardiac arrest.

Slide86

BP control

hypertension

(> 180/95 mm Hg

)

Nicardipine, labetalol

Slide87

Management: CSF Drainage

In cases of uncontrolled intracranial hypertension, an intracranial drain can be placed to remove CSF and monitor ICP

As the ICP increases, the compliance of the brain decreases, and small changes in volume (

eg

, the removal of as little as 1 mL of CSF) can significantly reduce ICP Skull= Brain+ Blood+

CSF

Slide88

Pentobarbital coma

reduce

cerebral blood flow and metabolic demands

.

adverse effects – Hypotension, arrhythmias, myocardial depression, and impaired uptake or release of glutamate.

Slide89

Management: Hypothermia

Controlled hypothermia has been shown to help reduce ICP in some patients with refractory intracranial hypertension and may improve outcome

Slide90

H

ypothermia

L

imits

hypoperfusion

brain

injury

Reduce ICP

I

mprove

CPP

C

oagulopathy

P

neumonia

C

ardiac arrhythmia

Shevering

Slide91

Decompressive craniotomy

Craniotomy with

duraplasty

can be done to provide room for brain swelling. prevents deaths, but overall functional outcome may not improve much.

Slide92

CHRONIC ALTERATION OF NEUROLOGICAL STATE

Slide93

Vegetative

Locked-in

Locked-in syndrome is caused by damage to specific portions of the lower brain and

brainstem

, with no damage to the upper brain.

upper portions of the brain are damaged and the lower portions are spared

Slide94

Locked in syndrome

patient is aware but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for the eyes

Slide95

VEGETATIVE STATE

unresponsiveness to ext. stimuli

open eyelids when feeding

experiences sleep- wake cycle

grinding teeth

sheding

tears

dont

require life supportive device

brain stem is intact so vegetative functions occur

absence of cognitive functions

Slide96

Akinetic

mutism

Is a severe form of neurological injury, in which a person is

unspeaking

(mute) &

unmoving

(

akinetic

).

A person with

akinetic

mutism has "sleep-waking cycles but, when apparently awake, with eyes open, lies mute, immobile and unresponsive.“

Akinetic

mutism is often due to damage to the frontal lobes of the brain.

Slide97

BRAIN DEATH

is irreversible end of brain activities due to total necrosis of neurons due to loss of O2

Slide98

Brain death

Complete unresponsiveness to all modes of stimulation, respiratory arrest, and absence of all EEG activity for 24 h.

The central considerations in the diagnosis of brain death are

(1) absence of cerebral functions;

(2) absence of brainstem functions, including spontaneous respiration

(3) irreversibility of the state such as drug overdose.

Slide99

Brain Death

I. The clinical evaluation

A. Establish irreversible cause of coma.

The cause of coma can usually be established by history, examination, neuroimaging, and laboratory tests.

Exclude the presence of a CNS-depressant drug, no recent administration of neuromuscular blocking agentsThere should be no severe electrolyte, acid-base, or endocrine disturbance. Achieve normal core temperature.

Slide100

B. Achieve normal systolic blood pressure.

C. Perform 2 neurologic examinations

Slide101

The clinical evaluation (neurologic assessment).

A. Coma.

B. Absence of brainstem reflexes.

Absence of

pupillary response to a bright light is documented in both eyes.Absence of ocular movements using oculocephalic testing and oculovestibular

reflex testing.

Absence of corneal reflex.

Absence of facial muscle movement to a noxious stimulus.

Absence of the pharyngeal and tracheal reflexes.

Slide102

Apnea Test

Absence of a Respiratory Drive.

Absence of a breathing drive is tested with a CO

2

challenge. Disconnect the patient from the ventilator.Preserve oxygenationIf respiratory movements are absent and arterial PO

2

is 60 mm Hg the apnea test result is positive.

Slide103

Common confirmatory tests in Brain Death

Cerebral angiography

No

intracerebral

filling at the level of the carotid or vertebral artery entry to the skullElectroencephalography

no electroencephalographic reactivity to intense

somatosensory

or audiovisual stimuli

Transcranial

Doppler

ultrasonography

lack of diastolic or reverberating flow, small systolic peaks in early systole, and a lack of flow found by the investigator who previously demonstrated normal velocities

Slide104

Brain death – social problem

In recent years, the success rate of

organ transplantation

has

increased dramatically, and transplantation has become standard

therapy for patients with end-stage kidney, heart, and

liver disease.

Unfortunately,

thousands

of critically ill patients

will not receive needed organs due to a lack of understanding

of the concepts and criteria for the declaration of death.

Slide105

Brain death – social problem

We

are wasting a rare and precious resource because health professionals,

as well as the public, have been

misinformed

about

definitions and procedures necessary to declare death in the

setting of

massive, irreversible brain damage

.