Abdul Gofir

Whisnu Nalendra Tama

Stroke Unit Sardjito Hospital | Department of Neurology
Faculty of Medicine | Universitas Gadjah Mada
 Consciousness
Consciousness is the state of full
awareness of the self and ones
relationship to environment
Consciousness

Content Arousal

(Plum and Posners Diagnosis of Stupor and Coma,2007)

 Anatomi Kesadaran(consciousness)
Hemisfer serebri/
korteks serebri
menentukan
fungsi content
(pengemban)

Ascending
reticular activating
system (ARAS)
Menentukan level
arousal
(penggalak)

Consciousness
interaksi hemisfer serebri dengan ARAS
 Derajat kesadaran :
Ditentukan oleh banyaknya neuron penggalak atau
pengemban yang aktif
Coma
State of reduced alertness and responsiveness
from which patient cannot be aroused
Clinical scoring system for uncosciousness :
Glasgow Coma Scale
Full Outline of Unresponsiveness (FOUR) score
 Pathophysiology
To cause coma,
Extensive and bilateral lesion of the
cerebral hemispheres
Lesions of the brainstem: Upper
pons+mesensephalon, and destroy
both sides of the paramedian
reticulum
(Plum and Posners Diagnosis of Stupor and Coma,2007)
 Lesi yang menyebabkan
perubahan kesadaran

Bilateral
hemispheric
Diencephalic
Upper brainstem

(Plum and Posners Diagnosis of Stupor and Coma,2007)

 Lesi brainstem yang mungkin tidak
menyebabkan penurunan kesadaran

(Plum and Posners Diagnosis of Stupor and Coma,2007)

Pathophysiology
Systemic cause :
brain is diffusely affected
Signs that localize focal brain disfunction
(e.g. Hemiparesis, cranial nerve palsy) are
lacking
CNS cause :
Signs that localize focal brain disfunction are
usually present
Causes of coma
Systemic affecting the CNS disease or trauma
brain diffusely
Encephalopathies Direct CNS trauma (SDH,
Hypoxic EDH, DAI, etc)
Metabolic (hipoglicemia, Vascular disease
hyperosmolar, electrolyte
(e.g. intracerebral hemorrhage,
imbalance, hepatic
large infarct, brainstem infarct)
encephalopathy, renal
failure, etc) Subarachnoid hemorrhage
Toxin CNS infection
Drug reaction Primary/secondary CNS
(Neuroleptic malignant Neoplasm
syndrome) Seizures
Deficiensy state
Sepsis
Etc
 Altered of Consciousness
Abnormal change in level of arousal or altered
content of a patient's thought processes

Change in the level of arousal or alertness

lethargy, stupor, and coma. !!!

Change in content
Relatively simple changes: e.g. speech, calculations,
spelling
More complex changes: emotions, behavior or personality
Examples: confusion, disorientation, hallucinations, poor
comprehension, or verbal expressive difficulty
 Definitions of levels of conciousness (arousal)

Alert (Conscious) - Appearance of wakefulness, awareness of

the self and environment
Somnolence / lethargy / obtundation
Stupor
Coma
 Lethargic
Can be aroused/awakened; then appear to
be in complete possession of her senses;
promptly falls asleep when left alone1
A sleepy patient, responds to being
addressed verbally or light shaking, or
responds verbally to more intense
mechanical stimulation, is said to be
lethargic or obtunded2

1. De Jongs The Neurologic Examination, 6th Ed, 2005.

2. Plum and Posners Diagnosis of Stupor and Coma, 2007.
 Stuporous
Difficult to arouse; slow and inadequate
response, oblivious to what is happening in the
environment, promptly falls back into stuporous1
Best response to deep pain is to attempt to
push the examiners arm away is considered
to be stuporous, with localizing responses2

1. De Jongs The Neurologic Examination, 6th Ed, 2005.

2. Plum and Posners Diagnosis of Stupor and Coma, 2007.
 Coma
complete loss of consciousness & cannot be
aroused)no awareness of herself, no
voluntary movements, no sleep-wake cycles1
nonspecic motor responses (wincing,
restlessness, withdrawal reexes) &
nonlocalizing response. Patients who fail to
respond at all are in the deepest stage of coma2

1. De Jongs The Neurologic Examination, 6th Ed, 2005.

2. Plum and Posners Diagnosis of Stupor and Coma, 2007.
The use of terms other than coma
and stupor to indicate the degree of
impairment of consciousness is
beset with difficulties and more
important is the use of coma scales
(Glasgow Coma Scale)
 HOW TO DIAGNOSE
THE PATIENT WITH UNCONSCIOUSNESS
History taking
Physical examination
Supporting examination
Neurological Examination
Level of consciousness
Brain stem reflex (pupillary, corneal,
Dolls eye, gag, etc)
Respiratory pattern
Assesment of cranial nerve
Assesment of meningeal sign
Assesment of physiologic reflex
Assesment of pathologic reflex
Examination of comatose patients
 History

(Plum and Posners Diagnosis of Stupor and Coma,2007)

 General Physical Exam.

(Plum and Posners Diagnosis of Stupor and Coma,2007)

RSST
Level of Consciousness
To arouse the patients :
voice vigorous shaking pain
Locations for pain stimulation

(Plum and Posners Diagnosis of Stupor and Coma,2007)

 Glasgow Coma Scale (GCS)
Best eye Best verbal Best motor
response (E) response (V) response (M)
4 Eyes opening 5 Oriented & converses 6 Obeys commands
spontaneously

3 Eye opening to 4 converse but 5 Localizes to pain

speech disoriented,Confused

2 Eye opening in 3 Inappropriate words 4 Withdraws from pain

response to pain

1 No eye opening 2 Incomprehensible 3 Flexion in response to

sounds pain (decorticate)

1 No verbal response 2 Extension to pain

(decerebrate)
1 No motor response
Full Outline of Unresponsiveness (FOUR) Score
FOUR SCORE & GCS
FOUR SCORE GCS
interrater reliability : interrater reliability :
kappa(w) = 0.82 kappa(w) = 0.82
availability of -
brainstem reflexes
breathing patterns -
recognize different -
stages of herniation
recognizes a locked-in
syndrome
Assess the intubated
patients
Wijdick, et al. Validation of a new coma scale: The FOUR score. Ann.Neurol. 2005 Oct;58(4):585-93
FOUR SCORE : Prediction of
Discharge
The cut-off point of 14 :Poor outcome
sensitivity 0.77 (95% CI, 0.69-0.84) specificity 0.95
(95% CI, 0.90-0.97),
cut-off point of 10 :in-hospital mortality
Sensitivity 0.71 (95% CI, 0.55-0.83)
Specificity 0.93 (95% CI, 0.90-0.96).
The total FOUR score satisfactory
prognostic value for predicting outcome.

The cut-off points for the poor outcome and in-

hospital mortality are 14 and 10, respectively.
Akavipat, et al. Prediction of discharge outcome with the full outline of unresponsiveness (FOUR)
score in neurosurgical patients. Acta Med Okayama. 2011 Jun;65(3):205-10.
 Lateralization
Asymmetry of facial & limb
Eyes deviate to one side
Asymetric pupil size and reaction
Head turning to one side
Asymetric muscle tone
Asymmetric physiologic reflexes
Unilateral pathologic reflexes (e.g. Babinski)
Meningeal Signs:
Kaku kuduk, Brudzinski, kernig
Differential Diagnosis of Coma
by Neurological Examination
Brain stem intact:
(-)lateralizing sign & (-)meningism Diffuse,
metabolic, toxic encephalopathy
()lateralizing sign & (+)meningism Meningitis,
SAH
(+)lateralizing sign & (-) meningism
Supratentorial lesions
Brain stem dysfunction:
Infratentorial lesion (brainstem or cerebellar)
Herniation
 Penurunan Kesadaran

Pemeriksaan neurologis:
Level Kesadaran
Refleks batang otak
Pola pernafasan
Respons motorik
Tanda Lateralisasi
Rangsang meningeal

Lesi Struktural Toxic-metabolic ( Difuse brain disease)

-Defisit neurologis fokal -Pupil reaktif
-Lateralisasi -Tidak ada defisit neurologis fokal
-Abnormal refleks batang otak -Refleks batang otak baik
-TIK Meningkat -TIK tidak meningkat

Supratentorial infratentorial Endogen

Eksogen
IMAGING LABORATORIUM

Intoksikasi Renal, liver, infeksi

Trauma, Perdarahan intrakranial
sistemik,
Stroke, Tumor, Infeksi
EEndokrin., dll
Systemic cause of coma
Diabetic ketoacidosis
Alcoholic ketoacidosis
Hyperosmolar Hyperglicemic State
Etc.
 Diabetic ketoacidosis
Insulin deficiency and couterregulatory hormone excess

Hyperglycemia Lipolyisis and protein breakdown

Osmotic diuresis Ketoacids

Dehydration and
hemoconsentration
Intracelullar dehydration

Shock
Impaired consciousness
Diabetic ketoacidosis
Clinical features :
Polyuria and polydipsia initial symptom
Kusmaul repiration
Tachycardia, hypotension
Fruity/acetone odor on the breath
Alteration of consciousness
Diabetic ketoacidosis
Blood glucose >250mg/dL
Anion gap > 10
Bicarbonate level < 15 mEq/L
pH < 7.3
Ketonemia
Hyperosmolar Hyperglycemic
State
Typically found in debilitated patient with
poor controlled or undiagnosed type II
DM
Other term : hyperosmotic non ketotic
hyperglycemic coma
Hyperosmolar Hyperglycemic
State
Pathophysiology
Physiologic stresses and inadequate water
intake
Insulin resistance or deficiency
Increase hepatic gluconeogenesis and
glycogenolysis
Osmotic diuresis and dehydration
The reasons for the absence of ketoacidosis
is not fully understood
Hyperosmolar Hyperglycemic
State
Usually in elderly and cognitively impaired
patients
Mental status changes - may evolve over
days or weeks
Vital sign abnormality indicate dehydration
Weakness, anorexia, fatique, dyspnea
Poor skin turgor, dry mucous membrane,
sunken eyes
Hyperosmolar Hyperglycemic
State
Serum glucose > 600mg/dL
Osmolality >315 mOsm/kg
Bicarbonate > 15 mEq/L
pH > 7.3
Alcoholic ketoacidosis
Wide anion gap metabolic acidosis
Usually seen in chronic alcoholic
Alcoholic ketoacidosis
symptoms signs
Nausea Tachycardia
Vomiting Tachypnea
Abdominal pain Abdominal tenderness
Shortness of breath Altered mental status
hypotension
Alcoholic ketoacidosis
Diagnostic criteria
Low/normal/slightly increase glucose
level
Drinking ending in nausea, vomiting,
decrease intake
Wide anion gap metabolic acidosis
Positive serum ketone (but absence of
serum keton does not exclude the diagnosis)
INCREASED INTRACRANIAL
PRESSURE
HERNIATION SYNDROME
Uncal Herniation Syndrome
Early N.III stage
Late N.III stage
Midbrain-upper pontine stage
 Early N.III
stage
Penekanan N.III oleh
uncus parasimpatis
N.IIIterganggu

Fungsi N.III lain sering

belum terganggu
 Late N.III
stage
Gangguan fungsi N.III lebih
lanjut

Hemiparese kontralateral,
atau ipsilateral
Midbrain-
upper pons
stage
Central(Transtentorial) Herniation
Syndrome
Early diencephalic stage
Late diencephalic stage
Midbrain-upper pons stage
Pons-upper medulla stage
Early
diencephalic
stage
Late
diencephalic
stage
Midbrain-
upper pons
Stage
Pons-upper
medulla
stage
Dorsal
midbrain
Compression
CheyneStokes respiration:
Hyperpnea (cresendo-decresendo) bergantian dengan
apnea(10-20 detik)
Intact brainstem respiratory reflex
bilateral forebrain impairment (uremia, liver failure), atau
infark bilateral, atau lesi karena adanya massa pada
prosensefalon dengan pergeseran pada diensefalon.
Pada gagal jantung transit dari paru ke reseptor jantung
melambat Cheyne Stokes tanpa adanya kelainan
prosensefalon mengganggu interpretasi
Central neurogenic hyperventilation
Brainstem tegmentum ( upper pons atau batas
pons-mesensefalon)
Pernafasan cepat antara 40-50x/mnt
mostly tumors
PO2, PCO2, Respiratory alkalosis in the
absence of any evidence of pulmonary disease
Eksklusi : stimulating drugs(cth: salicylates),
kondisi yang menstimulasi respirasi (cth:hepatic
failure,sepsis)
Kussmaul breathing
(deep, labored and gasping)
Apneustic breathing
Pause pada akhir inspirasi
Lesi pada bagian bawah Pons
Hilangnya pengaruh pneumotaxic center
dan vagal
Penyerta :deserebrasi; fixed-dilated
pupils; reflek kornea negatif;dolls eye
negatif; negative oculocephalic reflex;
and obliteration of the gag reflex.
Ataxic Respiration
clusters of cyclic irregular breathing
followed by recurrent periods of apnea
Kerusakan : pons bawah atau medulla
Hilangnya pengaruh apneustic center dan
preBotzinger neuron
Biots breathing tipe dari cluster
breathing (ataxic breathing) : klaster
pernafasan yang reguler dipisahkan
dengan periode apnea
 Abnormal breathing patterns in coma
Cheynes - Stokes

Central Neurogenic
Midbrain

Apneustic
Pons

Ataxic Medulla

ARAS
Brainstem Reflexes
Tipe Respons Pupil
Oculocephalic and
Oculovestibular
reflexes in comatose
patients with:
(1) brainstem intact
(doll head eye
phenomenon)
(2) bil. MLF
involvement
(3) and low brainstem
lesion
Motor responses to
noxious stimulation
in acute cerebral
dysfunction.
A = Rt hemisphere
B = Diencephalon
C = Mibrain/Pons
D = Medulla
Tes Klinis MBO (Mati Batang Otak)

1. Koma atau tidak ada respon

2. Tidak ditemukan refleks-refleks batang otak.
3. Apneu komplit yang dikonfirmasi dengan
tes apnea

70
Koma atau tidak ada respon

Tidak ada respon motorik !!

71
Refleks Batang Otak

Pupil
Kornea
Okulosefalik
Respon motorik
pd distribusi
saraf kranialis
Okulo-Vestibular
Gag reflexes

72
Penilaian hilangnya reflek batang otak

Pupil
Tidak ada respon cahaya. Posisi pupil di tengah
dan dilatasi pupil (4 6 mm)
Pergerakan bola mata
Menilai ada tidaknya dolls eye movement.
Penilaian reflek vestibulo-ocular (tes kalori)
dilakukan dengan irigasi air dingin (7 derajat
dibawah suhu tubuh) 50 ml pada tiap telinga
(interval 5 menit).
Pergerakan bola mata

Respons okulosefalik
Dolls Eyes Maneuver
 Pergerakan bola mata

Respons Okulovestibular Cold Caloric Testing

Respons Fasial Sensomotor

Refleks kornea
Menyeringai pada penekanan supraorbital
dan temporomandibular
Penilaian respon motorik dan sensoris

Respon terhadap beberapa rangsangan tidak ada:

reflek kornea, jaw reflex, dan penilaian gerakan otot
wajah pada saat diberikan rangsang nyeri di kuku,
supraorbita, dan temporomandibular.
Reflek muntah dan batuk tidak ada: hilangnya
reflek faring dan trakea. Reflek muntah timbul
dengan stimulasi bagian posterior faring dengan
spatel lidah. Suction trakeal/ bronchial akan
menstimulasi reflek batuk.
Tes Apnea

78
Penilaian tes apnea
Sebelum dilakukan tes apneu perhatikan
syarat yang harus dipenuhi.
Menurut Widjick (1995) tes apnea dapat
dilakukan bila:
Temperatur sentral >36,5C.
Tekanan sistolik >90 mmHg
Euvolemia
pCO2 normal
pO2 normal
Hipotermia

Kondisi hipotermia harus segera dikoreksi.

Bila temperatur sentral (rektal) di bawah
36,5C pasien harus diselimuti, namun di
beberapa literatur kondisi hipotermi dapat
diatasi dengan pemberian cairan dekstrose
5%.
Hipotensi
Pada keadaan hipotensi dapat diberikan maintance
dopamin sampai tekanan sistolik > 90 mmHg.
Untuk dapat memperoleh nilai pCO2 dan pO2 normal
maka dilakukan preoksigenasi dengan oksigen 100%
selama 10-20 menit
Pasang pulse oksimetri dan diskoneksi ventilator
Pada pasien tetap diberikan oksigen 6L/menit ke
dalam trakea (optional tempatkan kanul setinggi
karina)
Pernafasan

Perhatikan gerakan napas (abdominal dan

dada) selama diskoneksi 8-10 menit, ukur pula
pO2 dan pCO2 arterial. Kemudian pasang
kembali ventilator.
Bila tidak terdapat gerakan napas dan pCO2
arterial >60 mmHg, tes apnea dinyatakan positif.
Bila terdapat gerakan napas maka tes apnea
dinyatakan negatif dan tes harus di ulang
Pertimbangan ventilator
Pemasangan kembali ventilator selama tes dilakukan bila TS<90
mmHg atau pulse oksimetri menunjukkan desaturasi oksigen yang
signifikan dan aritmia jantung.

Segera lakukan analisa gas darah.

Bila pCO2 > 60 mmHg atau kenaikkan pCO2 > 20 mmHg dari nilai
awal, maka tes apnea dinyatakan positif. Bila pCO2 < 60 mmHg
atau kenaikkan pCO2 < 20 mmHg nilai awal yang normal maka
hasil tes indeterminat sehingga tes konfirmasi perlu dilakukan.
Pengulangan tes
Tes ulang perlu dilakukan untuk mencegah kesalahan
pengamat dan perubahan tanda-tanda. Interval waktu
berkisar 25 - 24 jam, bergantung rumah sakit atau
rekomendasi yang dianut

Setelah tes apnea dilakukan dan ventilator dipasang

kembali, keluarga pasien, dipanggil untuk mendapat
penjelasan

Keputusan akhir diserahkan kembali kepada keluarga

apakah bantuan ventilator tetap akan dilanjutkan
Confirmatory Testing

Recommended when the proximate

cause of coma is not known or when
confounding clinical conditions limit the
clinical examination
 Confirmatory Testing

EE
G

Normal Electrocerebral Silence

 Confirmatory Testing
Cerebral Angiography

Normal No Intracranial Flow

 Confirmatory Testing
Technetium-99 Isotope Brain Scan
 Confirmatory Testing
MR- Angiography
Confirmatory Testing

Transcranial
Ultrasonography
Terima kasih