DIAGNOSA BANDING PENURUNAN KESADARAN MANAJEMEN
Dipresentasikan oleh Jofizal Jannis | Neurologist| National Brain Centre
pada PIT VI IDI Kota Bogor | 10 Nopember 2013
2. Kesadaran adalah : is the body’s state of
arousal or awareness of self and environment
Koma : keadaan tidak sadar total terhadap
diri dan lingkungan meski di stimulasi dengan
kuat.
Diantara sadar dan koma terdapat variasi
status gangguan kesadaran.
Klinis dapat ditentukan dengan bedside.
3. OBJEKTIF
• Dokter mampu melakukan
stabilisasi, diagnosis, mengatasi
dan evaluasi pasien koma.
• Dokter dapat mengatur prioritas
pendekatan secara berurutan
5. Objektif Sekunder
• Dokter mengenal perbedaan koma
struktural dan metabolik toksik
• Dokter mengerti dan mengenal
• Koma
• TTIK
• Sindrom Herniasi
• Tanda lesi massa supratentorial
• Tanda lesi massa infra tentorial
6. Dua (2) komponen kesadaran :
formasio retikularis dan hemisfer serebral
Formasio retikularis : a diffuse collection of
neurons that extends throughout the brainstem
(terpusat pons. Dari mes, pons dan m.o).
Reticular Activating System : a diffuse collection
of neuron in the reticular formation, plays an
essential role in keeping the concious brain.
ARAS : Blocking jaras asending antara formatio
reticular dan korteks serebri menyebabkan tidak
sadar
15. Kesadaran (arousal)
• Asending RAS, dari sisi bawah pons ke
pons ke talamus ventromedial
• Sel yang berasal dari sistem ini menduduki
area paramedian di brainstem
Korteks serebral
TALAMUS
HJPOTALAMUS
RAS
26. Vegetative state (coma vigil, apallic syndrome)
Pasien tertolong dari koma, tapi berkembang
keadaan persistent unresponsif, tapi sleep–
wake cycles kembali.
• Setelah cedera kepala berat, fungsi brainstem
kenbali mengalami sleep–wake
cycles, membuka mata respons terhadap
stimuli verbal dan kontrol pernafasan normal.
•
29. Locked in syndrome
• Pasien awake and alert, tapi tidak
sanggup bergerak atau bicara
• Lesi Pontine mempengaruhi pergerakan
mata ke lateral dan kontrol gerak.
• Lesi sering spare vertical eye movements
and blinking.
30. Psikogenik unresponsif
• Pasien, walau tampak tidak sadar, biasa
menunjukkan beberapa respons stimuli
eksternal
• Refleks kornea menyebabkan kontraksi otot
orbikularis okuli
• Ditandai oleh resistensi gerak pasif tungkai
dan tanda penyakit organik tidak ada
35. Abnormalitas pernafasan dapat
membantu lokalisasi tetapi tidak selalu
dalam konteks tanda lain seperti
hiperpnea refleks sentral (midbrainhipotalamus)
Apneustik, kluster, ataksik,(pons bawah)
Hilangnya pernafasan otomatis (medula)
36. Abnormalitas
Penafasan
Deskripsi
Lokalisasi
Cheyne – Stokes
Pola pernafasan kresendo
dekresendo diiluti oleh apnue atau
hipobnea, menetap selama tidur
Bihemisfer (unilateral /
bilateral), atau brainstem
Cluster
Ireguler pernafasan diikuti periode
apnue yang lamanya bervariasi
Bihemisfer /pons
Ataxic or irregular
Kecepatan pernafasan yang tidak
teratur irama dan amplitudo diputus
oleh apnue
Tidak terlokalisasi atau
medula dorsomedial
Apneustic
Inspirasi panjang dengan 2-3 detik
berhenti kemudian ekspirasi.
Tekmentum lateral dari pons
bawah
Central neurogenetic
hiperventilation
Hiperventilasi terus terusan
kecepatan pernafasana tidak
melebihi 40 kali/menit
Bihemisfer pons dan midbrain
41. Pendekatan DD
Unresponsif
ABCs
Glucosa, ABG, Lytes, Mg, Ca,
Tox, ammonia
Y
IV D50, narcan,
Brainstem
at tanda
Fokal
Y
CT
N
Unconscious
N
Disfungsi otak difus
Metabolik / infeksi
Lesi fokal
Tumor, ICH/SAH/ infark
Pseudo-Coma
Psikogenik, Lo
oked-in,
NM paralysis
LP± CT
42. Koma
Intubasi –ventilasi/stabilisasi tekanan darah
Sindrom
Neurologi
Pencitraan
otak
CT otak
CT otak
Abnormal
Hasil
Penyebab
Stroke
TBI
Bedah Evakuasi
Kraniektomi
Rx ICP
Abnormal
Normal
Massa
Tumor
Pilihan
pengobatan
Intrinsik batang otak
Jaringan Otak dan
pergeseran batang otak
Basilar
embolus
arteri
ICH
TBI
Massa
Trombolisis
Pengambilan
bekuan
Perawatan
medik
Perawatan
medik
Biopsi
Infeksi
43. Resusitasi, memakai ABC Neurologi
N
A
B
C
D
–
–
–
–
–
Neck
Airway
Breathing
Circulation
Diabetes
Drug
E
F
G
H
I
–
–
–
–
–
Epilepsi
Fever
GCS
Herniation
Investigate
48. Level lesithin pada trauma kapitis
- Secara eksperimental
- Pada sisi cedera :
3 hari pertama cedera terjadi
penurunan lecithin
- Pada sisi lain tidak terjadi perubahan
49. FARMAKODINAMIK SITIKHOLIN
Bekerja langsung pada SSP
Mengaktifkan for. retikularis di Batang Otak
sehingga menurunkan ambang rangsang reaksi
arousal untuk membantu membangkitkan
kesadaran
Mengaktifkan fungsi pyramidal dan ekspiramidal
yang tersisa
Menurunkan ambang rangsang evoke muscular
discharge shg merangsang aktivitas system
piramidal yang berkaitan dg fungsi motorik
50. Efek sitikholin pada CDP Kholin sinthetase endogen
dan penggunaan FFA
CDP Kholin (sitikholin)
Sistidin
kholin
FOSFATIDIL KHOLIN
MEMBRAN SEL
FFA
Sistidin
CTP
kholin
FOSFORIL KHOLIN
DYACYL GLYCEROL + SITIKHOLIN
51. Mekanisme kerja citikholin
Sebagai derivate asam nukleat melakukan
biosintesis lecithin dan stabilisasi membran sel
Memperbaiki aktivitas membrane ATP ase
Mengaktifkan kembali metabolisme serebral
Memperbaiki sirkulasi serebral secara selektif
Pembentukan neurotransmitter
Mencegah akumulasi asam lemak toksik shg
mencegah luas infark dan kerusakan jaringan
52. Terapeutik Window citikholin 24 – 48 jam
Citikholin mempunyai efek neuroproteksi
Mengurangi lesi pada membran saraf
dengan cara meningkatkan sintesis
fosfolipid dan mengurangi kadar asam
lemak bebas
Beberapa studi membuktikan bahwa
citikholin mempunyai.terapeutik window
24 – 48 jam
53. Treatment of acute cerebral
infarction with a choline precursor in
a multicenter
A multicenter double-blind placebo-controlled study of cytidine 5'diphosphocholine (CDP-choline) was conducted to evaluate possible
clinical benefits of the drug in patients with acute, moderate to
severe cerebral infarction. The patients included also suffered from
moderate to mild disturbances of consciousness, and all were admitted
within 14 days of the ictus. Patients were allocated randomly to treatment
with either CDP-choline (1,000 mg/day i.v. once daily for 14 days) or with
placebo (physiological saline). One hundred thirty-three patients received
CDP-choline treatment, and 139 received placebo. The group treated with
CDP-choline showed significant improvements in level of consciousness
compared with the placebo-treated group, and CDP-choline was an
entirely safe treatment. (Stroke 1988; 19:211-216)
54. Oral Citicoline in Acute Ischemic Stroke
An Individual Patient Data Pooling
Analysis of Clinical Trials
Treatment with oral citicoline within the
first 24 hours after onset in patients with
moderate to severe stroke increases the
probability of complete recovery at 3
months. (Stroke. 2002;33:2850-2857.)
55. Citicoline Preclinical and
Clinical Update 2009–2010
Abstract—Citicoline is a neuroprotectant
and neurorestorative drug that is used in the
treatment of acute ischemic stroke in some
countries. The research with this compound
continues. In this review, we focus on the
latest publications or communications or
both and on the major ongoing experimental
and clinical projects involving citicoline in
stroke recovery. (Stroke. 2011;42[suppl
1]:S36-S39.)
56. Citicoline in the treatment of acute ischaemic
stroke:
an international, randomised, multicentre,
placebo-controlled study (ICTUS trial)
Results 2298 patients were enrolled into the study from Nov 26,
2006, to Oct 27, 2011. 37 centres in Spain, 11 in Portugal, and 11 in
Germany recruited patients. Of the 2298 patients who gave
informed consent and underwent randomisation, 1148 were
assigned to citicoline and 1150 to placebo. The trial was stopped
for futility at the third interim analysis on the basis of complete
data from 2078 patients. The fi nal randomised analysis was based
on data for 2298 patients: 1148 in citicoline group and 1150 in
placebo group. Global recovery was similar in both groups
(odds ratio 1ÅE03, 95% CI 0ÅE86–1ÅE25; p=0ÅE364). No
significant diff erences were reported in the safety variables nor in
the rate of adverse events.
57. The Role of Citicoline in Neuroprotection
and Neurorepair in
Ischemic Stroke
Advances in acute stroke therapy resulting from thrombolytic treatment,
endovascular procedures, and stroke units have improved significantly
stroke survival and prognosis; however, for the large majority of
patients lacking access to advanced therapies stroke mortality and
residual morbidity remain high and many patients become
incapacitated by motor and cognitive deficits, with loss of independence
in activities of daily living. Citicoline has therapeutic effects at several
stages of the ischemic cascade in acute ischemic stroke and has
demonstrated efficiency in a multiplicity of animal models of acute
stroke. Long-term treatment with citicoline is safe and effective,
improving post-stroke cognitive decline and enhancing patients’
functional recovery. Prolonged citicoline administration at optimal doses
has been demonstrated to be remarkably well tolerated and to enhance
endogenous mechanisms of neurogenesis and neurorepair contributing
to physical therapy and rehabilitation.