kuliah kesadaran menurun untar mei 2012 (presentasi)

KESADARAN MENURUN

Hartono Prabowo

Bagian Saraf Universitas TarumanagaraJakarta

10-05-2012

Kesadaran Menurun

Seorang pasien pria 65 th diantar ke UGD oleh tetangga rumahnya oleh karena ditemukan dalam keadaan tidak sadarkan diri. Pada pemeriksaan dengan rangsang nyeri didapatkan kelopak mata sedikit terbuka, kedua lengan fleksi disertai kedua tungkai ekstensi dan pasien terdengar “merintih” kesakitan. TD 140/90 mmHg, S 37.20 C, N 88x/menit dan R 24 x/menit

1. Dari data yang ada dapat disimpulkan GCS (Glasgow Coma Scale) pasien tersebut adalah :

A. E2 M2 V2 = 6B. E2 M3 V2 = 7C. E2 M4 V3 = 9D. E3 M3 V2 = 8

Kesadaran Menurun

B

2. Pemeriksaan penunjang yang perlu dipertimbangkan untuk pasien tersebut adalah sebagai berikut, kecuali :

A. Kadar gula darahB. Analisa gas darahC. Fungsi ginjalD. Kadar Potasium darah

Kesadaran Menurun

D

3. Apabila pada pemeriksaan fisik didapatkan adanya kelemahan ekstremitas kiri, maka pemeriksaan yang harus dipertimbangkan adalah sebagai berikut, kecuali :A. Brain CT-Scan / MRI

B. Kadar glukosa darah

C. Kadar potasium darah

D. Analisa gas darah

Kesadaran Menurun

C

4. Tindakan yang harus dikerjakan pada penderita dengan kesadaran menurun adalah sebagai berikut, kecuali :

A. Tindakan Neuroproteksi

B. Segera berikan Piracetam / citicholine

C. Koreksi kelainan sistemik penyebab penurunan kesadaran

D. Jika perlu segera lakukan reperfusi

Kesadaran Menurun C

Kesadaran

Kesadaran

• William James : “consciousness as awareness of one-self and the environment”.

• Phenomenal consciousness : otak dapat mengenali dan memberikan respons yang sesuai terhadap fenomena – fenomena yang terjadi didalam tubuh dan lingkungan

Definisi kesadaran

Kesadaran diartikan sebagai hasil berbagai fungsi yang kompleks dan berdasar pada alertness/ arousal

dan awareness (mengenali dan merespon dengan adekuat terhadap proses dalam diri dan lingkungan).

awareness

AROUSAL

CO

NS

CIO

US

NE

SS

Bedside :•arousal → eye opening. •External awareness → reproducible command following of “non-reflex”/voluntary movements

Thibaut et al, 2012

Anatomi Kesadaran

Integritas hubungan antara korteks serebri dengan sistem formasio retikularis pada batang otak.

ARAS menyalurkan impuls dari midpons ke rostral melalui tegmentum menuju nukleus intralaminaris (& nukleus

centromedial) thalamus untuk selanjutnya menuju korteks serebri.

12

Anatomi Kesadaran

Laureys et al, 2002

CO

NS

CIO

US

NE

SS

AROUSAL

AWARENESS

LANGUAGE

MOVEMENTSAppropriateLocalizedAbduction

Brainstem reflexes

13Adopted from Laureys, et al, 2007

TWO AWARENESS NETWORK

• awareness (content of consciousness)• arousal (level of consciousness )

Awareness

@ Sensasi

@ Persepsi

@ Fungsi memori

@ Atensi

@ Kognisi

Neurotransmiter pada alertness / arousal

1. Cholinergic (Ach)

2. Monoaminergic a. noradrenergic

b. dopaminergic

c. serotonergic

3. GABA-nergic.

Neuron aminergik pada formasio retikularis

Neurotransmiter Lokasi

Serotonin Nucl. Raphe midbrain, pons, medulla oblongata

Dopamine Tegmentum midbrain.

Norepinephrine Midbrain, pons, medulla oblongata.

Epinephrine Medulla oblongata.

Sistem Cholinergic

Jalur cholinergic berperan pada alertness /arousal sebagai komponen ARAS.

Aktivasi thalamus mengurangi tonus inhibisi nukleus retikularis thalamus

fasilitasi transmisi thalamo-

kortikal. Aktivasi struktur medial diencephalon

emosional erousal.

Noradrenergic

brainstem

dorsal thalamus

o locus ceruleus hipothalamus

hipocampus

neokorteks

Brainstem

o Nukleus tegmental lateralis

Med. Spin.

Terman & Bonica, 2001

Schematic diagram of the noradrenergic systemTo neocortex Anterior thalamic

nucleus

Thalamus

Habenula

PAG

N. Iocuscoeruleus(A6)

Trigeminalspinalnucleus

A1

A5

N. Subcoeruleus (A7)

Hippocampus

Amygdata

DLF

ILC

Modifikasi Meliala, 2003

Locus ceruleus medula oblongata.

Nukleus tegmentum lateralis pons dan medula oblongata.

Serotonergic → inhibisi

• Nukleus raphe tegmentum brainstem → proyeksi ke korteks serebri dan sistem limbik termasuk korteks pyriformis, hypothalamus, hippocampus dan diencephalon.

• Defisiensi serotonin (spt. Withdrawal alkohol) →→→ impulsip, over-reaktip,insomnia

(ggn. Siklus tidur).

Cingulate gyrusFronix

Thalamus

Habenula

PAG

N. Iocuscoeruleus

N. RaphePallidus (B1)

N. Central superior (B6. 8)

Hippocampus

Amygdata

Diagram of the origin and projection of the serotonergic system

N. Raphedorsalis (B7)

N. rapheMagnus(B3)

N. rapheObscurus(B2)

Hippocampus

Septum

DLF

VM

Terman & Bonica, 2001Modifikasi Meliala, 2003

Sistem dopaminergic

• Ventral tegmentum brainstem → neostriatal, mesolimbik dan mesokortikal.

o tu. Fungsi kognitip (lihat efek amphetamine dan obat antipsikotik sbg. Dopamine blocker).

o Peranan dalam arousal kecil tetapi dapat meningkatkan responsiveness.

GABA-nergic

• Neuron GABA-nergic tersebar luas pada SSP dengan fungsi pada kesadaran tidak jelas.

• Inhibisi korteks cerebri, thalamus, ganglion basalis, cerebellum dan med. Spinalis.

• Peningkatan GABA-nergic → alertness dan daya konsentrasi menurun

Glutamat dan aspartat.

• Sintesa pada korteks cerebri.

• Eksitatorik.

• Peranan pada kesadaran kecil.

• Lebih berperan pada komunikasi kortiko – kortikal.

A summary diagram of the ascending arousal system

NA : Noradrenaline5-HT : SerotoninDA : DopamineHis : HistamineORX : OrexinMCH : Melanin concentrating hormoneACh : AcetylcholineGABA : Gamma aminobutyric acid

LC : locus coeruleusvPAG : ventral periaqueductal gray matterTMN : Tubero-mammiullary nucleusLH : lateral hypothalamusBF : basal forebrainPPT : pedunculo pontine3

Plum and Posner’s 2007

The cholinergic system, shown in yellow, provides the main input to the relay and reticular nuclei of the thalamus from the upper brainstem. This inhibits the reticular nucleus and activates the thalamic relay nuclei, putting them into transmission mode for relaying sensory information to the cerebral cortex. The cortex is activated simultaneously by a series of direct inputs, shown in red

Kesadaran Menurun


Kesadaran Menurun

Clouding of consciousness

minimally reduced wakefulness or awareness, hyperexcitability and irritability alternating with drowsiness

Delirium Disoriented (first to time, next to place, and then to persons in their environment ), motor restlessness, hallucination → bilateral impairment of cortical function

Obtundation a mild to moderate reduction in alertness, accompanied by a lesser interest in the environment. Such patients have slower psychologic responses to stimulation - increased number of hours of sleep

Stupor condition of deep sleep or similar behavioral unresponsiveness from which the subject can be aroused only with vigorous and continuous stimulation. Even when maximally aroused, the level of cognitive function may be impaired.

Coma “Deep sleep / Trance” → unresponsiveness in which the patient lies with eyes closed and cannot be aroused to respond appropriately to stimuli even with vigorous stimulation.

• Plum and Posner’s 2007• Huges. Neurological Emergencies. 4th ed. 2003

28

REDUCING CONSCIOUSNESS TO 2 D

Laureys, 2011

PLUM’S DEFINITION

Coma

(unconsciousness)

is an unarousable/ unresponsiveness condition in which , the patient is not

responsive to all stimuli

Coma is caused by disordered arousal rather than impairment of the awareness

J Neurol Neurosurg Psychiatry 2001;71(suppl I):i13–i17

Gangguan fungsi Formatio Retikularis (ARAS) pada tingkat batang otak.

Gangguan fungsi neuron korteks serebri.

Gangguan fungsi interkoneksi Batang Otak (ARAS) dan korteks serebri.

Kesadaran Menurun

• Kelainan bihemisfer serebri

• Bilateral – difus (infeksi, ggn sistemik spt hipoksia, hipoglikemia, uremia hiponatremia, dll)

• Unilateral → dampak pada midbrain

• Kelainan pada batang otak

• Principles and Practice of Emergency Neurology, 2003• Plum and Posner’s 2007• The Merck Manual for Health Care Professionals, 2008

Kesadaran Menurun

Ekstra – kranial Hipoksia / hipercapnea Hipo/hiperglikemia. Uremia. Hepatik ensefalopati. Gangguan elektrolit

(hipo Natremia). Hipoperfusi. Intoksikasi (CO, dll) Asidosis Drugs

Intra – kranial Trauma. CVD stroke Iskemik /

hemoragik. Infeksi (meningitis /

Ensefalitis. Tekanan Intrakranial ↑ Tumor / brain abscess Kejang / status

konvulsivus


Peningkatan glikolisis anaerobik

ml/100 g/ menit

ELECTRICAL FAILURE

IONIC FAILURE

Dipertahankan denganautoregulasi

Peningkatan ekstraksi O2 untuk pertahankan CMRO2

Penumbra

Depolarisasi anoksik

Oligemia

Nilai normal

Ringan

Moderat

Berat

ISKEMIA

CBF%

100

80

60

40

20

50

40

30

20

10

Cerebral blood flow (CBF)

Endocrinol Metab Clin N Am 35 (2006) 725–751

Hiperglikemia → kesadaran menurun

Hiperglikemia

Ketosis

Asidosis

DKA

Status Hiperglikemia lain :•DM tidak terkontrol•Stress hyperglycemia•HHS

Status ketosis lain :•Ketotic hypoglycemia•Ketosis alkoholik•Ketosis “starvation”•Isoprophyl alcohol•Hiperemesis

Status asidosis metabolik lain :•Laktat asidosis•Asidosis hiperkloremia•Salicylsm•Asidosis uremikum

• Sekresi insulin ↓• Inefektivitas insulin• Pe ↑ hormon kontra insulin

(glucagon, catecholamine, cortisol dan GH)

Hiperglikemia → kesadaran menurun

Hiperglikemia

Ketosis

Asidosis

Osmolaritas ↑Dehidrasi neuron

serebral

pH serebral ↓

Edema serebri

Metabolisme neuron

serebral ↓

Kesadaran ↓

Endocrinol Metab Clin N Am 35 (2006) 725–751

• Suppression / inhibition of insuline release

• Pancreas : secretion of glucagon & pancreatic polypeptide

• Adrenal medulla : secretion of epinephrine & norepinephrine (NE)

• Adrenal cortex : secretion of cortisol

• Sympathetic postganglionic nerve terminal : secretion of NE

• Pituitary gland : secretion of GH

Hipoglikemia (<70 mg/dl)

• Glucogenolysis ↑ • Gluconeogenesis ↑• Lipolysis ↑• Reduces glucose uptake in peripheral tissue

4 hrs

CLINICAL DIABETES. Volume 24, Number 3, 2006•

• Suppression / inhibition of insuline release• Pancreas : secretion of glucagon & pancreatic polypeptide• Adrenal medulla : secretion of epinephrine & norepinephrine (NE)• Adrenal cortex : secretion of cortisol• Sympathetic postganglionic nerve terminal : secretion of NE• Pituitary gland : secretion of GH

Hipoglikemia (<70 mg/dl)

• Glucogenolysis ↑ • Gluconeogenesis ↑• Lipolysis ↑• Reduces glucose uptake in peripheral tissue

4 hrs


Autonomic symptoms

Brain neuronal glucose

deprivation symptoms

Neurogenic (ANS) symptoms Neuroglycopenic symptoms

Shakiness (limbung) Abnormal mentation

Trembling (gemetar) Irritability

Anxiety (cemas) Confusion

Nervousness (gelisah) Difficulty in thinking

Palpitasion Dissiculty speaking

Clamminess (tangan basah/lembab)

Ataxia

Sweating (berkeringat dingin) Paresthesia

Dry mouth Headaches

Hunger Stupor

Pallor (pucat) Coma

Pupil dilation Death (if untreated)

Hipoglikemia


Ensefalopati Hepatikum

Ggn fungsi hati

Ammonia darah ↑

Uptake ammonia otak ↑

Metab Ammonia dalam Astrosit →

glutamin ↑

Permeabilitas BBB ↑ tanpa kerusakan membran basal

Edema serebri

TIK ↑ CBF ↓


Kesadaran ↓

Hiponatremia Hipernatremia


Ensefalopati hiper / hipo-Natremia

Obat-obat berpengaruh pada kesadaran

• Sedativa

• Barbiturates

• Tranquilisers

• Alkohol

• Opiates

• Anticholinergics

• Lithium

• Psikotropika

• Paraldehyde

Kesadaran ↓


• Diagnosis dan ABC koma harus simultan

• Ukur kadar Glucose darah segera → hipoglikemia?

• Pada kasus trauma dengan kesadaran menurun → imobilisasi leher sampai dapat dibuktikan tidak ada kelainan pada vertebra servikalis

Evaluasi penderita kesadaran menurun

The Merck Manual for Health Care Professionals, 2008The Merck Manual for Health Care Professionals, 2008

Evaluasi penderita kesadaran menurun

• Riwayat penyakit • Pemeriksaan fisik umum• Pemeriksaan neurologis termasuk (pemeriksaan

mata) • Pemeriksaan Laboratorium (darah, urin dan jika

perlu AGD ) • Neuroimaging (Brain CTScan / MRI, Ro-Thorax)• Ukur tekanan intrakranial (jika perlu dan mungkin) • Bila diagnosa tidak jelas → LP / EEG

Pemeriksaan fisik

• Keadaan umum• Tanda vital• Pola pernafasan dan “odor” spesifik• Jantung / paru / abdomen• Pupils• RBO (Refleks batang otak)• Reaksi terhadap rangsang nyeri• Fungsi traktus piramidalis• Tanda rangsang meningeal • Tanda TIK ↑

Observasi umum

• Gerakan menelan “brain function is still intact”• Asterixis dan “multifocal myoclonus” → ggn

metabolik (uremia, ensefalopati hepatikum, encephalopati hipoksik, intoksikasi obat) →ggn fungsi otak difus

• Psychogenic ? → tonus otot / refleks fisiologis / refleks batang otak normal (lateralisasi / refleks patologis negatip)


Penilaian kesadaran

Kwalitatip

CMSomnolen

SoporSoporokoma

Koma

KwantitatipGCS

(Glasgow Coma Scale)

Skala lain penilaian kesadaran•Innsbruck Coma Scale•Edinburgh-2 Coma Scale•Reaction Level Scale•Coma Recovery Scale Revised•FOUR Score (Full Outline of Unresponsiveness)•AVPU•ACDU

Metoda rangsang nyeri pada kesadaran menurun


Verbal response Oriented to person, place, and date = 5 Converses but is disoriented = 4 Says inappropriate words = 3 Says incomprehensible sounds = 2 No response = 1

Glasgow Coma ScaleEye opening Spontaneous = 4 To speech = 3 To painful stimulation = 2 No response = 1

Motor response Follows commands = 6 Makes localizing movements to pain = 5 Makes withdrawal movements to pain = 4 Flexor (decorticate) posturing to pain = 3 Extensor (decerebrate) posturing to pain = 2 No response = 1


STEREOTYPED MOTOR RESPONSE

Flaccidity without movement → the lower brain stem is not affecting movement

Flaccidity without movement → the lower brain stem is not affecting movement

Decorticate → hemispheric damage with preservation of motor centers in the upper portion of the brain stem (eg, rubrospinal tract).

Decerebrate → the upper brain stem motor centers damage → only the lower brain stem centers (eg, vestibulospinal tract, reticulospinal tract), which facilitate extension, are responding to sensory stimuli.


Pola pernafasan dikaitkan lokasi lesi

Cheyne Stokes lesi pada hemisfer serebri / batang otak bagian atas

Central neurogenic hyperventilaion

= 40-70/m (Kussmaul/ Biot ) lesi pada tegmentum serebri / bagian atas pons


Apneustic lesi pada Pons (bilateral)

Ataksik lesi pada bagian dorsomedial formatio reticularis dan medula oblongata

Apnea lesi pada bagian Ventrolateral Medulla (bilateral)

Cheyne Stokes lesi pada hemisfer serebri / batang otak bagian atas

Central neurogenic hyperventilaion lesi pada tegmentum serebri / bagian atas pons

Apneustic lesi pada Pons (bilateral)Ataksik lesi pada bagian dorsomedial formatio reticularis dan medula oblongata Apnea lesi pada bagian Ventrolateral Medulla (bilateral)

Pola pernafasan dikaitkan lokasi lesi


Lesion Location

Eyes PositionLight

ReflexesPUPIL SIZE

EYES PICTURE

Hemisphere

Conjugate deviation to destructive lesion side

Normal Normal

Thalamus See to the nose Negative Small

Pons Medial eyes (Doll’s eyes)

Negative Small

Cerebellum Medial eyes Normal Big

The PupilsThe Pupils


Kelainan pupil dikaitkan lokasi lesiKelainan pupil dikaitkan lokasi lesi


Refleks Batang Otak (RBO)

Pupil reflexesDoll’s eye

phenomenon

Corneal reflexes

Vomiting reflexes

Oculovestibular reflexes/

cold-water calories testing• Principles and Practice of Emergency Neurology, 2003• Plum and Posner’s 2007• The Merck Manual for Health Care Professionals, 2008

PYRAMIDAL -TRACT LESIONS

Motoric UMN paresis /paralysis

• Physiol Reflexes increase

• Pathol Reflexes (+)

• Muscle Tonus increase

Right Hemiparesis(lesion of left internal capsule)

Crossed Paresis(left midbrain lesion causing left oculomotor nerve palsy

and right hemiparesis

Crossed Paresis(lesion at the level of the

pyramidal decussation causing paresis of right arm

and left leg

Right Left

Intrakranial Herniasi


Tanda-Tanda awal herniasi unkus


Tanda-Tanda lanjut herniasi unkus


Tanda-Tanda awal herniasi sentral / trantentorial


Tanda-Tanda lanjut herniasi sentral / trantentorial


Tanda-Tanda herniasi sentral / trantentorial (midbrain-upper pons)


Tanda-Tanda herniasi sentral / trantentorial (lower pons – med. oblongata)


DIAGNOSTIC TOOLS

Adopted from Laureys, 2011

Adopted from Laureys, 2011

Bruno et al, 2011

Vegetative State / Coma Vigil / Apallic State

• Responsiveness and awareness negatip → fungsi kognitip (-)

• Akibat disfungsi hemisfer serebri dengan batang otak dan diensefalon normal

• Refleks Otonom, refleks motorik dan siklus tidur normal

• > 1 bulan• Principles and Practice of Emergency Neurology, 2003• Plum and Posner’s 2007• The Merck Manual for Health Care Professionals, 2008

• Etiologi : tu pasca hipoksia (ensefalopati) / trauma • Prognosis : dubia • Terapi : Suportip• Harapan hidup : 2 – 5 tahun• C.o.d : infeksi (paru / ISK)

Multi organ failure

Vegetative State / Coma Vigil / Apallic State


The locked-in syndrome describes a state in which the patient is de-efferented, resulting in paralysis of all four

limbs and the lower cranial nerves.

LOCK-IN SYNDROME

• Plum and Posner’s 2007• Demerti, 2010

Locked-in syndrome can be caused by stroke at the level of the basilar artery suppling denying blood to the Pons,

among other causes..

Unlike persistent vegetative state, in which the upper portions of the brain are damaged and the lower portions are spared, locked-in syndrome is caused by damage to specific portions of the lower brain and brainstem with no damage to the upper brain.

Agranoff, 2007

LOCK-IN SYNDROME

• Plum and Posner’s 2007• Demerti, 2010

http://en.wikipedia.org/wiki/File:Gray760.png

Brain death

• Kebutuhan penggunaan ventilator jangka panjang.

• Kemungkinan terjadinya pemberian harapan yang tidak tepat kepada keluarga penderita.

Diagnosa Brain death perlu ditegakkan

•1959 (Mollaret & Goulon) → Irreversible coma

•1971 (Mohandas & Chou) → a critical component of severe brain damage

•1979 (Model Brain Death Act / US)→ Irreversible cessation of

• circulatory and respiratory function

• All function of brain


• Death :– Irreversible end of

life.

– Irreversible cessation of heartbeat and respiration.

• Brain Death :– Death of the brain

without cessation of the heart beat.


Brain death

• Harvard Committee (1968).

• The Minnesota Criteria (1971).

• President’s Commission for the study of Ethical Problem in Medicine and Biomedical and Behavioral Research, USA (1981).

• UK criteria (1995).

• AAN 1995.

Brain Death is defined as the irreversible loss of the capacity for consciousness combined with the

irreversible loss of all brainstem functions including the capacity to breathe.


Kriteria MBO (Brain death)

Brain Death Eelco F.M. Wijdicks, M.D.

N Engl J Med, Vol. 344, No. 16 April 19, 2001

• Koma (GCS 3).• Pupil dilatasi

maksimal.

Ventilator

Refleks Batang Otak

• Refleks okulosefalik.• Refleks pupil /

cahaya.• Refleks kornea.• Test irigasi• Refleks batuk /

muntah.• Test Sulfas Atropin. • Test apneu

Singkirkan :– Gangguan

keseimbangan asam-basa dan elektrolit.

– Hipothermia berat ( < 32o C).

– Hipotensi.– Intoksikasi ……

neuromuscular inhibitor.

NEGATIP

Should never be diagnosed hurriedly in the emergency room.

Brain Death (Eelco, 2001)

Evaluasi : 2 x

< 2 mo 48 hrs

2 mo – 1 y 24 hrs

1 – 18 y Facultative.

> 18 y Facultative

Should never be diagnosed hurriedly in the emergency room

Guidelines for determination of death JAMA 246:333,393. 1978

Pemeriksaan tambahan Dx – Brain deathEelco, 2001

Pemeriksaan Keterangan

Cerebral angiography Absence of intra-cerebral filling of the intracranial arteries at the entry into the skull.

EEG electro-cerebral silence

Transcranial Doppler (TCD).

Small systolic peaks in early systole with retrograde (reverberating, oscillation) or absent flow during diastole

Cerebral Scintigraphy

Atropine test Vagal component of 10th nerve

Jugular bulb oxygen saturation

SSEP / BAEP

• Kesadaran menurun merupakan keadaan emergensi • Kesadaran menurun dapat disebabkan oleh berbagai

kelainan baik intra maupun ekstrakranial. • Diagnosis yang cepat dan tepat merupakan tantangan

utama guna penatalaksanaan yang edekuat. • Diagnosis dapat ditegakkan dengan pemeriksaan

fisik, neurologis dan dengan bantuan pemeriksaan penunjang yang sesuai.

Kesimpulan

kuliah kesadaran menurun untar mei 2012 (presentasi)

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