Acute Disturbance of

Consciousness:
Clinical Approach
Luh Ari Indrawati
Division of Clinical Neurophysiology and
Epilepsy
Department of Neurology
FKUI-RSCM

Conscious
ness

Arousal

Arousal (-),
gradation:
Somnolen
Sopor
Coma

Awarenes
s

Arousal (+)
Awareness (-):
Vegetative
state
Dementia

Delirium

Acute altered state of

consciousness

Delirium
Obtundation
Stupor
Coma

Subacute or chronic alteration

of consciousness

Dementia
Abulic
Akinetic mutism
MCS
Vegetative state

Delirium

Other Terms

Scope of this talk

Acute
Alteration of
Consciousness

Anatomy of
Consciousness
Awarene
ss

Arous
al

Requirements to
altered consciousness
Bilateral
dysfunction of
cerebral
hemisphere

Damage ARAS

Metabolically
depress the
brain globally

Epidemiology
Primary reason for the visit: 4% to
10%
25-30% older pts ED

Goals

Recognition

Differentiati
on
various
etiology

Causative
or specific
therapy

Good
outcome

RECOGNITION

Measurements
Measurements
Qualitat
ive
Compos
mentis
Somnolen
Stupor
Coma

Quantitative
GCS

Four
Score

Glasgow Coma Scale

Four Score

Four Score

Four Score

Four Score

DIFFERENTIATION.
ETIOLOGY

Etiology

Supratentor
ial
Rhinencephalic
and subcortical
destructive
lesion
Mass lesion
Tumor
Abscess
etc

Intracranial
lesion

Extracrania
l
metabolic

Infratentori
al

Diffuse,
multifocal

Infarct
Tumor
Abscess
Aneurysm
Demyelination
Inflammatory

Psychiatric

Anoxia,
ischemia
Hypoglycemia
Diffuse
intrinsic brain Nutritional
Hepatic or
disorders
Encephaliti
uremic
encephalopath
s
SAH
y
Pulmonary
NCSE
Primary
disease
Endocrine
neuronal

Clinical Approach:
History Taking
Onset: abrupt, gradual
Details on the immediate events surrounding
the altered consciousness
Accompanying symptoms and signs
Trauma
Preceeding seizure
Underlying medical problem
Psychiatric history
Medications
Toxic exposures

Physical Examination
Vital sign
General Examination
Neurological
examination

Evidence of trauma
Evidence of acute
or chronic systemic
illness
Evidence of drugs
ingestion

Neurological
Examination

Pupillary reaction
Eye movements
Meningeal sign
Cerebral function
Cranial nerves

Cerebellar
Motor
Reflexes
Autonomic
Funduscopy
elevated ICP?

Valuable Signs
Breathing pattern
Pupil diameter and
reactivity
Focal neurological deficit

Breathing Pattern

Pupillary Reactions

Eye movement

Observation
Dolls eyes
movement
DO NOT DO IF
CERVICAL
TRAUMA IS
SUSPECTED

Caloric testing

Ocular Movement

Ocular Movements
Exam Findings
Horizontal gaze
deviation

Localization

Significance

Frontal eye field

Irritative lesion:
contralateral
Paralytic lesion:
ipsilateral

Pons, thalamus

Inversed reaction

Oculocephalic and Vestibuloocular Reflexes

Exam Findings

Localization

Eyes remain fixed with

head turn or cold caloric

Lower brain stem (pons,

medulla)

Common Etiologies
Massive brainstem
injury

Eyes deviate away from Diffuse or bilateral

head turn or toward cold hemispheres, normal
irrigation
brainstem response

Metabolic coma,
elevated ICP without
herniation

Nystagmus with fast

phase away from
irrigated ear

Normal

Psychogenic
unresponsiveness

Neither eye deviates

medially passed midline
with head turn or cold
caloric

Bilateral medial
longitudinal fasciculus

Brainstem stroke lesion

Abnormal corneal
reflexes

CN V, VII, their nucleus,

connections

Peripheral nerve,
brainstem

Oculocephalic and Vestibuloocular Reflexes

Exam Findings

Localization

Common Etiologies

Absent cough or gag

reflex

CN IX, X

Brainstem injury, stroke,

other lesion

Hemipharesis

Corticospinal tracts

Various

Flexor posturing

Thalamus

Extensor posturing

Midbrain, pons

Motor Response

Others
Yawning
Hiccups
Vomiting

Organized at medullary
Lesion in medullary
tegmentum
Lesion in lateral pons or
medulla, nucleus solitary
tract
Others: increased ICP,
other etiology

Localization: Bilateral
Hemisphere

Confusion and stupor precede motor signs

Symmetric motor signs
Preserved pupillary reaction
Asterixis, tremor, myoclonus, seizure

Localization:
Supratentorial

Focal cerebral signs present at the onset

Progress rostral to caudal
Related to anatomic area
Motor sign asymmetric

Localization:
Infratentorial

History of preceeding brainstem dysfunc or sudden onset of coma

Focal brainstem signs precede or accompany onset of coma
Abnormal pupillary and oculomotor
Abnormal respiratory pattern appear at onset

Increased ICP
Signs:
Headache
Projectile vomit
Papiledema
Hypertension
Bradycardia
Bradipneu
Herniation syndrome
Funduscopy:
papiledema

Herniation Syndrome

Uncal Herniation: early

sign

Uncal Herniation: late

sign

Central Transtentorial Herniation: Early

Diencephalic State

Central Transtentorial Herniation: Late

Diencephalic State

Central Transtentorial Herniation: MidbrainUpperpons Stage

Central Transtentorial Herniation: Lower Pons

Upper Medulla Stage

Focal Neurological
Deficit
Think about intracranial
etiology!!!

Laboratory:
CBC
Glucose
Electrolytes (Na, K, Cl,
Ca, Mg)
Blood gas analysis
Renal function
Liver function
Urine
Hemostasis panel
Thyroid
Cortisol
Drug ad toxin screen
Serum osmolality
Lactate

Anoxia, ischemia
Hypoglycemia
Nutritional
Hepatic or uremic
CSF analysis
encephalopathy
Pulmonary disease
Endocrine disorder
Drugs
Acid-base imbalance
Electrolyte imb
Septic

Other Additional
Examination

ECG
EEG NCSE?
Brain imaging
Evoked potential prognosis

Brain Imaging
Exclude intracranial etiology
Usually not specific in metabolic
etiology, except:
Posterior reversible encephalopathy
syndrome
Metronidazole encephalopathy

CT or MRI?
Contrast or non-contrast

Goals of Management
Stabilized ABC
Empirical therapy
Exploration
Specific therapy
Prevent 2nd injury

Management Sequences

Initial Management
Control agitation

Hocker S, Rabinstein
AA. Management
of the patient with
diminished
responsiveness.
Neurol Clin 30 (2012)

Management of
Increased ICP
Head elevation 30 degree
Moderate hyperventilation
(PCO2 target 30-35 mmHg)
Sedation and analgesia
Control hypertension
Treat fever
Cytotoxic: mannitol,
hypertonic saline (3%,
23%)
Vasogenic: steroid
(dexamethasone)
Obstructive: drainage

Management of Status
Epilepticus
Prehospital
Hospital

Luh Ari Indrawati, FKUI,

RSCM

Stabilizatio
n
ABC

Airway
patency
O2
supplementa
tion
IV access
SaO2
Vital sign
monitor
ECG

Seizure
terminati
on

Stabilization ABC
Exploration of etiology, management of
complications, treatment of underlying diseases
Seizure termination

1 st line
Benzodiazepine
Diazepam
rectal 10-20
mg repeat 15
mnt if
needed
Midazolam
im

1 st line
Benzodiazep
ine
Diazepa
m iv
Lorazepa
m iv 2-4
mg
Midazola
m im

2nd line
Phenytoin iv
Fosphenytoin
iv
Phenobarbit
al iv
Valproic
acid iv / oral
Levetiraceta
m iv /oral
Lacosamide

ICU
3rd line
Pentobarbital
iv
Thiopental iv
Midazolam
iv
Propofol iv

4th line
Ketamine
Inhalation
anesthetic
agents
Topiramate

Convulsive seizure stop

EEG monitoring for detection of electrographic seizure

Prognosis: Outcome of Coma by

Etiology

HIE
Toxicmetabolic
Cerebrovasc
ular
Total

Death
(%)

PVS (%)

58
47

20
6

Good
Recovery
(%)
8
25

74

61

12

10

Case 1
Female, 48 years old. Proggresive verbal memory
disturbance. Mild headache
Last 5 days, vomit several times per day, nausea,
difficult intake
1 day before admission she was appeared drowsy
Decreased consciouness since 2 hours before hospital
admission. Headache was increased before. Once
general tonic clonic seizure after decreased
consciousness but no further decreased cons after
that
No medication
No other medical problem

Case 1
Phy Ex:
Somnolen, confused. BP: 100/70, HR 110 /mnt RR 20/mnt T
37.2oC, GCS E3M5V4, SaO2 98% without oxygen,
supplementation. Breathing pattern eupnea
General ex:
Eye: roving eye movement
Skin: decreased turgor

Neurology status:

Pupil 4 mm/4mm isochor, direct and indirect reflex +/+ fast

Meningeal sign: none
Cranial nerves: none
Motoric: no lateralization
Physiological reflexes: +2 symmetric
Pathological reflexes: none
Sensory: can not be assesed
Funduscopy: no papiledema

Laboratory
Blood glucose 110
CBC: Hb 13, Ht 50, leu 8700, Tr
180000
Na 125, K 3.4, Cl 100
ALT 30, AST 35
Ur 60, Cr 1.6
Blood gas analysis: pH 7.35/ pCO2
34/ pO2 95/ HCO3 3/ SaO2 98%

Brain MRI

Possibilities?

Normal

Normal

Nonconvulsive status
epilepticus!!!
Think about

THANK
YOU