Coma and Brain death

How to discriminate?

Dr. Gülay Eren

Change in conscious state

85% due to metabolic and systemic

reasons
15% pure CNS pathologies
Consciousness
 Ascending reticular activating system
(ARAS)
 Direct afferent systems
 (raphe nucleus, locus ceruleus,
parabrachialis)
 Awareness and alertness

Normal awakeness / alertness and sleeping

cycles
depends on

 Excitatory activity from the gray matter of

rostral pons and mesencephalon (ARAS)
 Thalamus IL and CM nuclei
 Antral brain,
 Hypothalamus,
 Cerebral cortex connection
Disorders of consciousness:
definitions

 Coma  Vegetative state

 Stupor  Akinetic mutism

 Lethargia  Hyperkinetic
 Confussion mutism
 Delirium
 Brain death
 Demans
Disorders of consciousness:
definitions
 Coma  Vegetative state
 Stupor  Akinetic mutism
 Lethargia
 Hyperkinetic
 Confüzyon
mutism
 Delirium
 Brain death
Consciousness
Conscious: awake and aware
Somnolan: easily arousable and aware
Stupor: difficultly arousable, decreased
awareness
Coma: not arousable, not aware
Vegetative state: arousable, but not aware
Unconscious patient may be
misdiagnosed

 Vegetative state: sleepness – awakeness

cycle is significant

 Aphasia: motor type is more often

misdiagnosed, but communication with the

patient is distinguishing
What ethiologies?
First:
 Primarily discriminate focal structural CNS

lesions from global metabolic problems

 Physical evaluation together with laboratory,
imaging has to stand with the stabilization and
the treatment of the patient
 O2, at least two large-bore IV line, ECG,
cardiac monitoring to be done immediately
Look for:

 rapid neurologic signs

 any focal (localizing) neurologic

deficit
 Stick blood sugar (hypoglycemia is a
prompt emergency)
 Opioid overdose ?
Ethiology: Systemic reasons causing
global CNS symptoms

Hypoxia
 Wernicke

Hypercapnia
encephalopathy

Hypoglycemia
 Uremic encephalopathy
!!
Hyperglycemia
 Sepsis

Electrolite
 Hepatic encephalopathy
disorders
 Hypertensive
 Hyponatremia !!
encephalopathy
Ethiology: Systemic reasons causing
global CNS symptoms

 Endocrine hypo/  Toxicities

hyperfunction  Drug or alcohol
 Low cardiac output withdrawal
 Diffuse  Drug interactions
hypoperfusion  Serotonin syndrome
 Hypovolemia  Malign neuroleptic
 Anemia syndrome
Ethiology: CNS causes

 CNS trauma
 Intracranial hemorrhage - SAH
 Ischemic stroke
 Space occupying lesion
 CNS infections
 Convulsions (status epilepticus / postictal
period)
 Demans
Evaluation
Physical evaluation
 Vital signs:
 Respiration: hyper- hypoventilation
 BP: hyper- hypotension
 Blood gases: hypoxemia and/or
hypercarbia
 Fever – systemic infections
 Hypothermia?
Physical evaluation
 Consciousness ?
 Pupils ?
 Reaction to stimuli ?
 Any sign of traum?
 Glaskow coma scale (GCS)
Physical evaluation- key points

 If postictal state is considered in a confused

patient: tongue bite ? Convulsion !!!

 Scalp evaluation thoroughly !!!

 often little-unknown traumas are
missed(posttraumatic patient!)

 Coma caused by alcohol overdose ?

18
 Localising clinicical signs

 motor signs

 pupil size and reaction

 eye movements and oculovestibular

response
 respiration pattern
GLASGOW COMA SCALE

Eye
4
 GLASGOW COMA SCALE

Eye
4
4- Spontaneously open
3- opens w verbal stim.
2- opens w noxious stim.
1- not opening
 GLASGOW COMA SCALE

Eye Movement
4 6
4- Spontaneously open
3- opens w verbal stim.
2- opens w noxious stim.
1- not opening
 GLASGOW COMA SCALE

Eye Movement
4 6
4- Spontaneously open
6- obeys
3- opens w verbal stim.
5- localise pain
2- opens w noxious stim.
4-Fleksör Yanıt
1- not opening
3-Dekortike
2-Deserebe
1-Yanıt yok
 GLASGOW COMA SCALE

Eye Movement
4 6
4- Spontaneously open
6- obeys
3- opens w verbal stim.
5- localise pain
2- opens w noxious stim.
4- flexes to pain
1- not opening
3-Dekortike
2-Deserebe
1-Yanıt yok
 GLASGOW KOMA SKALASI

Eye Movement
4 6
4- Spontaneously open
6- obeys
3- opens w verbal stim.
5- localise pain
2- opens w noxious stim.
4- flexes to pain
1- not opening
3- decorticate
2- decerebrate
3-Dekortike
2-Deserebe
1-Yanıt yok
Motor response: Lesion Localization

Hemispheric Lesions

Upper Mesencephalon injury

Upper Pontine injury

İstanbul, Kasım 2011

 GLASGOW COMA SCALE

Eye Movement Verbal

4 6 5
4- Spontaneously open
6- obeys
3- opens w verbal stim.
5- localise pain
2- opens w noxious stim.
4- flexes to pain
1- not opening
3- decorticate
2- decerebrate
1- no response
3-Dekortike
2-Deserebe
1-Yanıt yok
 GLASGOW COMA SCALE

Eye Movement Verbal

4 6 5
4- spontaneously open
6- obeys 5- oriented
3- opens w verbal stim.
5- localise pain 4- disoriented
2- opens w noxious stim.
4- flexes to pain 3- inappropriate resp.
1- not opening
3- decorticate 2- mumbling
2- decerebrate 1- no response
1- no response
3-Dekortike
2-Deserebe
1-Yanıt yok
Pupils

Metabolic ensephalopathy:
small, reactive

diensephalic: prethectal:
small, reactive large, fixed

III CN (unchal):
dilated, fixed

mesansephalic: pons:
İstanbul, Kasım 2011
mildly dilated, fixed pinpoint
 Pupils

 Midriatic, nonreactive to light

 Atropin, skopolamin, glutetimid,e barbiturate

 Hypoxia

 Hypothermia

 Deeply myotic pupil

 Opioid intoxication
Eye movements

 Hemispheric lesions:
 horizontal conjugated eye movements
 “rovling” eye movements
Eye movements
 Upper brain stem;

 Vertical conjugated eye motion

 Convergance retraction nistagmus
 3.CN nuclear or fasicular lesion
 Pons;
 Horizontal conjugated vision
 Ocular bobbing
 Skew deviation
 6.CN lesions
Oculocephalic Reflex
Head up at 30 degrees: head turned to
both sides while observing eye
movements (normal: eye movement to
opposite side)

Unconscious but
Brain stem intact
Vestibulo-ocular reflex
Vestibulo-ocular reflex

Cold water Cold water

Unconscious but
Brain stem intact
Breathing in coma

İstanbul, Kasım 2011

Coma - Treatment

Laboratory tests :
 Correct Hypoglycemia
 esp in DM and chronic alcoholism etiology
is usually hypoglycemia
 Electrolytes (Na)
 Hyponatremia mostly, sometimes in cancer
patients calsium metabolism disorders

38
BRAIN DEATH
Brain Death
 Clinical definition:

“irreversible loss of all brain

functions”
 physiopathologically intracerebral
perfusion is stopped
Brain Death = «litherally» DEATH

Death due to circulatory

arrest
First cardiac death
(thus: neurological death)

DEATH

Neurologically dead=
Brain death
(first neurologic death)
Who is said to be ‘brain dead’?

Only patients in the ICU under

mechanical ventilation with
acute cerebral lesion
Brain injury – cerebral hemorrhage
stroke – brain tumor
Anoxia – cerebral infection
Causes
 in adults:
* Massive head trauma
* Cardiopulmonary arrest
* Intracerebral hemorrahage /SAH
* Diffuse ischemic stroke and herniation
* Fulminant hepatic encephalopathy
Causes
 in children:
* Traumatic brain injury
* Bacterial menenjitis
* Asfixia
* Suffocation
in order to say ‘Brain death’, you have
to exclude

 Severe electrolyte, acid-base and

endocrinologic disorder
 Body temperature < 32oC
 Hypotension
 Drug intoxications (esp: barbiturates)
Reversible causes of coma
Metabolic or Drugs Others
Endocrine
Adrenal IV anesthetics Brain stem
insufficiency encephalitis
Hyperglycemia / Neuromuscular Hypothermia
ketoacidosis blockers
Hyponatremia Tricyclic Shock
antidepressants
Hypoglycemia Anticholinergics Guillaine Barre
Syndrome
Uremia Bretylium Food toxicities

Hypercalsemia Locked-in
6 Şubat 2009 YBU – Kursu syndrome
Clinical diagnosis of Brain
death
 Coma and unresponsiveness
 responsive (spontaneously / against
stimuli)
 decerebrate, decorticate posture ( - )
 spinal cord reflexes (primitive R. ±)
 Loss of brain stem functions
Response to noxious
stimuli Decorticated Posture: Hemispheric/Diencphephalic

Decerebrated Posture: mesencephlon/ pons

 Reflexes in Brain death

 Tendon reflexes are segmental spinal reflexes

 In brain death there can be areflexia during spinal

shock period
 Later some abnormal reflexes can occur due to
spinal cord viability under region of lesion
 There is no impact of extremity reflexes in case of
brain death
 Spinal reflexes in brain death
Brain infarction 1

Spinal cord without any upper Spinal shock

central control
2
Spinal functions
heal

3
Hyperexcitability
Spinal man
 Brainstem reflexes
Painful stimulus
Oculocephalic
Cornea Oculovestibular

Pupil response Tracheal

VI VII

V VIII

III X
II XI
 Brain stem functions are lost

Brain Stem (Mesencephalon, Pons, Medulla oblangata)

Evaluate functions of reflex pathways

Brain stem functions

 Pupils size and reaction to light

 Eye movements
 Oculocephalic reflex
 Oculovestibular reflex
Brain stem functions
 Facial sensorial and motor responses
 Cornea reflex
 “face grimacing” against painful
stimulus
 Gag and cough reflex
 Apne test
Pupils

 2. ve 3. cranial nerves

 Light unresponsive, fixed, dilated (4-9 mm)

 Mistaken evaluations due to:

 Drug toxicities (narcotics)
 After CPR (adrenalin - atropin)
 Severe face injuries
Eye movements

Oculocephalic reflex
Not in cervical trauma
Head moved 90o vertically and horizontally

Normally Eyes move in opposite to head

direction
Brain
death Eyes immobile in orbita
YBU – Kursu
Eye movements : Oculocephalic

Unconscious
Brain stem injured
Eye movements :
Oculovestibular reflex
or Caloric test

3, 6 ve 8. cranial nerves

Tympanic membrane has to be intact and

external ear canal open
Caloric test: iced water (50ml)

Both ear canals washed with 50 ml iced water.

1min to wait after washing
 5min wait for the second ear
Eye movements :
Oculovestibular reflex

Normally Eyes move towards the washed

ear.
Brain Eyes immobile in orbita
death
Eye movements :
Oculovestibular reflex

Cold water Cold water

Unconscious
Brain stem injured
Facial sensorial motor responses

 cornea reflex ( - )

 mandibular reflex ( - )

 face grimacing ( - )
Gag and cough reflex

 No gag against posterior pharengial

stimulus
 No coughing with tracheal aspiration

YBU – Kursu
Apnea test
 Most important brain stem reflex is respiration
response
 Prerequisites for the test ;
 Nearly normal body temp
 Systolic blood pres > 90 mmHg
 No hypovolemia
 PCO2 and PO2 levels normal
 PCO2; 30 - 40 mmHg
 PO2 > 200 mmHg (with 10-30 min of ispiration of
100% O2 )
Problems with apnea test

Inability to provide the prerequisite conditions

During apnea test hypoxia, hypotension and

arrhythmia can be limiting
Previous severe lung problems can be challanging
*Hypoxemia
*Chronic hypercarbia
 APNEA TEST
130 78 23 130

NO Respiratory drive of patient 98

PaCO2 > 60mmHg

100% Oxygen
 Apnea test algorythm
Gerekli
Optimize
ön koşulları
conditions
sağla Replace from
Mekanik mechanic ventilator
ventilatörden ayır
 Apnea test algorythm

Optimize conditions Replace from mechanic ventilator

observe respiration for place cannula over carina to

8 minutes give O2 (%100 O2 6lt/min)
 Apnea test algorythm
Optimize conditions Replace from mechanic ventilator

observe respiration for place cannula over carina to

8 minutes give O2 (%100 O2 6lt/min)

Patient
breaths
 Apnea test algorythm
Optimize conditions Replace from mechanic ventilator

observe respiration for place cannula over carina to

8 minutes give O2 (%100 O2 6lt/min)

APNEA

NO PCO2 > 60
Hypotension
Desaturation
Cardiac Aritmia
 Apnea test algorythm
Optimize conditions Replace from mechanic ventilator

observe respiration for place cannula over carina to

8 minutes give O2 (%100 O2 6lt/min)

APNEA

NO
PCO2 < 60
Hypotension
Desaturation
Cardiac Aritmia
 Apnea test algorythm
Optimize conditions Replace from mechanic ventilator

observe respiration for place cannula over carina to

8 minutes give O2 (%100 O2 6lt/min)

Hypotension
Desaturation
APNEA Cardiac Aritmia

occurs

PCO2 < 60
 Apnea test algorythm
Optimize conditions Replace from mechanic ventilator

observe respiration for place cannula over carina to

8 minutes give O2 (%100 O2 6lt/min)
Hypotension
Desaturation
APNEA Cardiac Aritmia

occurs

PCO2 > 60
Complications of Apnea test
 Hypotension
 Acidosis
 Cardiac arrhythmia
 Hypoxemia
Adjunctive tests to support diagnosis
of Brain Death

 Transcranial Doppler Ultrasonography

 EEG
 BT Angiography / MRA
 Cerebral angiography
 SPECT