Clinical Science Session Penurunan Kesadaran
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KESADARANKeadaan dimana mencerminkan integrasi
secara optimal antara respon stimulasi aferen dan eferen.
Kesadaran adalah kesiagaan seseorang terhadap diri dan sekitarnya.
Kesadaran merupakan fungsi utama susunan saraf pusat.
Untuk mempertahankan fungsi kesadaran yang baik, perlu suatu interaksi yang konstan dan efektif antara hemisfer serebri yang intak dan formasio retikularis di batang otak.
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Kesadaran mempunyai 2 aspek :derajat kesadaran(LOC)kualitas kesadaran(COC)
Derajat kesadaran atau tinggi rendahnya kesadaran mencerminkan tingkat kemampuan sadar seseorang dan merupakan manifestasi aktifitas fungsional ARAS terhadap stimulus somatosensorik.
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Reticular activating system
AS dibentuk oleh beberapa sirkuit neuronalMenghubungkan batang otak menuju cortex
cerebri Beberapa area yang termasuk RAS :
Midbrain Reticular FormationMesencephalic Nucleus (mesencephalon)Thalamic Intralaminar nucleus (centromedian
nucleus)Dorsal HypothalamusTegmentum
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Fungsi RAS
Sebagai pusat kesadaran (mengatur transisi tidur-bangun)
Kewaspadaan
Kesadaran diatur oleh aktifitas elektrik otak ayng dipengaruhi oleh neurotransmiter (cholinergic & adrenergic) dan neuron mesengger nitric oxide(NO)
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Derajat Kesadaran
Menurut GCSComposmentis (15)Somnolent (12-14)Sopor (8-11)Koma (3-7)
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Pendahuluan Penurunan kesadaran adalah keadaan dimana penderita tidak sadar dalam arti tidak terjaga / tidak terbangun secara utuh sehingga tidak mampu memberikan respons yang normal terhadap stimulus.
Kesadaran secara sederhana dapat dikatakan sebagai keadaan dimana seseorang mengenal / mengetahui tentang dirinya maupun lingkungannya.
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KOMAKoma merupakan penurunan kesadaran yang
paling rendah atau keadaan ‘unarousable unresponsiveness’, yaitu keadaan dimana dengan semua rangsangan, penderita tidak dapat dibangunkan.
Koma bukanlah suatu penyakit, melainkan suatu keadaan klinik yang disebabkan oleh berbagai faktor serta membutuhkan tindakan penanganan yang cepat dan tepat.
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ETIOLOGIS : Sirkulasi – gangguan pembuluh darah otak
(perdarahan maupun infark)E : Ensefalitis – akibat infeksi baik oleh bakteri,
virus, jamur, dllM : Metabolik – akibat gangguan metabolik yang
menekan/mengganggu kinerja otak. (gangguan hepar, uremia, hipoglikemia, koma diabetikum, dsb).
E : Elektrolit – gangguan keseimbangan elektrolit (seperti kalium, natrium).
N : Neoplasma – tumor baik primer ataupun sekunder yang menyebabkan penekanan intracranial.
I : Intoksikasi – keracunan.T : Trauma – kecelakaan.E : Epilepsi.
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Etiologi penurunan LOC
Intra-cranial Extra-cranial
Diffuse
Meningitis, Encephalitis
Focal
Stroke, Tumour, Abscess
Hepar
Renal
Lungs
Diabetes
Intoxication
Lumbal puncture
CT-Scan
Laboratory
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Klasifikasi
Koma dibagi menjadi 2 yaitu :1.Koma kortikal bihemisferik Bila metabolisme neuron otak tergangguDapat terjadi apabila kekurangan oksigen
dan glukosaYang dapat membangkitkan koma metabolik
antara lain:HipoventilasiAnoksia iskemik.Hipoksia atau iskemia difus akut.Gangguan metabolisme karbohidrat, dll.
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2. Koma diensefalik.Koma akibat gangguan fungsi atau lesi
struktural formation retikularis di daerah mesensefalon dan diensefalon.
Secara anatomi koma diensefalik dibagi menjadi 2 :
a.koma akibat lesi supratentorial. b.Koma akibat lesi infratentorial.
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a. Koma Supratentorialterjadi karena kompresi terjadi pada diensefalon, msensefalon, pons, dan medulla oblongata.Proses dapat berupa :- TTIK di supratentorial (ICH,EDH,SDH)- Proses kompresi pada bagian lateral fossa
kranii media (kompresi di ventral CN III)- sindrom kompresi rostrokaudal terhadap batang otak
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a. Koma supratentorial.Proses kompresi supratentorial
Lama kelamaanmendesak hemisferium kearah foramen magnum
batang otak bagian depan (diensefalon) mengalami distorsi dan penekanan
Saraf-saraf otak mengalami penarikan dan menjadi lumpuh dan substansia retikularis mengalami
gangguan
kelumpuhan saraf otak yang disertai gangguan penurunan derajat kesadaran.
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b. Koma infratentorial.2 macam proses patologik dalam ruang infratentorial (fossa kranii posterior)
1.Proses diluar batang otak atau serebelum mendesak sistem retikularis.Contoh :-abses serebelum- pendarahan serebelum
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2. Proses di dalam batang otak secara langsung mendesak dan merusak sistem retikularis dan batang otak.Contoh:-infark/pendarahan batang otak- tumor batang otak- trauma batang otak
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Manifestasi Klinis
Supratentorial koma
Didahului dengan defisit neurologis fokal berdasar pada lokasi lesi > penurunan LOC
Kompresi dimulai secara rostrokaudal :
Diencephalon
Midbrain
Pons
Medulla oblongata
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Diencephalon Stage
Somnolence; stupor; restless
Regular respiration
Small reactive pupil
Positive occulocephalic reflex
Positive and bilatelar patologic reflex
Hypertonic ; rigidity
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Midbrain - Pons Stage
Stupor coma
Hyperthermia
Hyperventilation
Dilating pupil
Negative Doll’s eye phenomen
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Pons – Medulla oblongata Stage
Shallow, slow, and irregular respiration
Dilated pupil and negative corneal reflex
Negative occulo-cephalic reflex (Doll’s eye)
Flaccid position
Irregular pulse
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Infratentorial Coma
Irregular respiration, blood pressure, heart rate
Impaired occular movement
Alternating hemiparesis
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Toxic-Metabolic Coma
Paling banyak disebabkan oleh:Hypoxia :
Normal : 3.3 mL / 100 gm brain / minuteKoma jika < 2 mL / 100 gm brain / minute
HypoglycaemiaNormal : 2/3 of blood levelKoma jika < 10 mg/dL
ToxinHepatic comaUremic coma
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Metabolic Coma
Impaired LOC or COC precedes neurologic deficits
Symmetric and bilateral neurologic deficitsRespiratory pattern – CSR (Cheyne-Stokes respiration) [ impairement of bilateral cortex and diencephalon]
Isocor pupil with normal light reflex
Involuntary movementMyoclonusTremor , flaping
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Pemeriksaan
Tujuan :
Mengetahui penyebab :
primer / structural
metabolik / functional
Mengetahui lokasi lesi
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Anamnesa
Onset : tiba-tiba, progressive
Riwayat trauma
Riwayat penyakit(hipertensi, DM, gangguan faal hati, ginjal)
Nyeri Kepala
Muntah-muntah
Medikasi (Narkotika)
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Physical Examination
Tanda vitalTekanan DarahRespirasiNadiSuhu
GCSHead-to-toe
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GLASGOW COMA SCALE
Best Motor Best Verbal Eye Response Response Opening
6 - Obeys commands 5 - Oriented 4 - Spontaneous
5 - Localizes pain 4 - Confused 3 - To speech
4 - Withdraws to pain 3 - Inappropriate words 2 - To pain
3 - Abnormal flexion 2 - Incomprehensible 1 - None
2 - Abnormal extension 1 - None
1 - None
TOTAL (3-15): _____
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•Peradagan Meningeal Kaku kuduk Laseque / Kernig Brudzinki I, II, III
•Cranial Nerve(CN) : CN I – CN XII
•Pupil :Midryasis :Lesi pada midbrainPin point :Lesi pada ponsAnisokor :Penekanan pada CN III, Herniasi Otak
Pemeriksaan Neurologis
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•Pergerakan Bola Mata : Kerusakan CN III, IV, VIOccular Bobbing : Lesi pada ponsRoving Eye Movement: Lesi pada supranuclear
area
•INGAT: Refleks pupil pada metabolik koma adalah NORMAL.
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MOTOR SYSTEM
•Respons terhadap rangsangan•Decortikasi : Hyperextensi > Flexi tangan dan kaki > Lesi supratentorial•Deserebrasi : Ekstensi tangan dan kaki > Lesi pada midbrain•Kekakuan otak difus : lesi pada batang otak / lesi berada di daerah distal ponto-medullar area
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Pemeriksaan Penunjang
LABORATORIUM
Darah : Hb, Leukosit,Ht, Thrombosit, GDS,
Ureum, Kreatinine, SGOT, SGPT, Elektrolit.
Foto Thorax
MRI/CT-Scan
EKG (apabila perlu)
Angiography (apabila perlu)
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MANAGEMENT
UMUM
• Perbaiki jalan nafas
• Perbaiki kerusakan cardiovaskular
• Perbaiki gangguan elektrolit
• Perbaiki gizi
• Terapi antiedema (atas indikasi)
• Terapi antibiotika(atas indikasi)
• kateter
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MANAGEMENT
KHUSUSApabila causa telah terdiagnosa :Contoh:
Stroke PIS : Suportif, Tindakan bisa diperlukanMeningitis : Antibiotik yang tepatEpilepsi: AntiepilepsiUremic Coma : DialysisOverdosis Opiat : Nalokson
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• Edema Otak
• SIADH (Syndrome of Inappropriate
Antidiuretic Hormone Secretion)
• Infeksi
• Dehidrasi
KOMPLIKASI
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Koma e.c gangguan struktural: burukInsufisiensi Batang Otak : buruk (mati batang otak)Tanda-tanda prognosis buruk : Pupil Reflex dan Pergerakan bola mata negatif :
kematian 95%
Korneal Reflex negatif Atonia tungkai Refleks visual, pendengaran, dan somatosensori
negatif
PROGNOSIS
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Eye movements seen in the comatose patient include:
roving eye movements —Description: slow random predominantly horizontal conjugate eye movements (though there may be a degree of exophoria) similar to those seen in deep sleep.Likely cause: metabolic encephalopathy (may be absent in deep coma), bilateral supranuclear lesions
ocular bobbing —Description: Rapid, conjugate, downward movement; slow return to primary positionLikely cause: Pontine strokes; other structural, metabolic, or toxic disorders
ocular dipping —Description: Slow downward movement; rapid return to primary positionLikely cause: Unreliable for localization; follows hypoxic-ischemic insult or metabolic disorder
reverse ocular bobbing —Description: Rapid upward movement; slow return to primary positionLikely cause: Unreliable for localization; may occur with metabolic disorders
reverse ocular dipping —Description: Slow upward movement; rapid return to primary positionLikely cause: Unreliable for localization; pontine infarction and with AIDS
ping-pong gaze —Description: Horizontal conjugate deviation of the eyes, alternating every few secondsLikely cause: metabolic encephalopathy, bilateral cerebral hemispheric dysfunction; toxic ingestion
periodic alternating gaze deviation —Description: Horizontal conjugate deviation of the eyes, alternating every 2 minutesLikely cause: Hepatic encephalopathy; disorders causing periodic alternating nystagmus and unconsciousness or vegetative state
vertical myoclonus —Description: vertical pendular oscillations (2–3 Hz)Likely cause: Pontine strokes
horizontal myoclonus —Description: rapid horizontal pendular oscillations; the eyes appear to be shaking.Likely cause: Serotonin toxicity
monocular eye movements —Description: Small, intermittent, rapid monocular horizontal, vertical, or torsional movementsLikely cause: Pontine or midbrain destructive lesions, perhaps with coexistent seizures