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Pemicu 2 Blok Sistem Saraf & Kejiwaan

Kelompok 17
16 Mei 2017
• Tutor : dr. Triyana Sari
• Ketua : Annisa Kamelia Nasser (405140075)
• Sekretaris : Enrico Chaesan Tanzil (405140122)
• Penulis : Dila Nur Fitriani (405140217)
• Anggota : Risky Suharianto, Tjen (405130134)
Laura Febriana (405130188)
Albert Edo Rahmadi Sinoor (405140023)
Karinnia (405140112)
Egie Madgani Ainul Kamil (405140153)
Vinnie Charlieta Leonardo (405140192)
Muhammad Fahmi Rosyadi (405140220)
Aldora Sindila Febriana (405140240)
Pemicu 2
Seorang laki-laki usia 35 tahun dibawa keluarganya ke UGD RS karena
mengalami penurunan kesadaran. Sejak 1 minggu sebelumnya pasien
mengalami demam tinggi, sudah diberi obat parasetamol tetapi demam
timbul kembali dalam beberapa jam setelah pemberian obat. Pasien juga
mengeluh nyeri kepala berdenyut terutama di bagian belakang kepala yang
dirasakan semakin memberat meskipun sudah minum obat. Satu hari
sebelum masuk RS, pasien terlihat lebih banyak tidur dan sulit untuk
dibangunkan. Apabila dibangunka untuk makan, pasien hanya membuka
mata sesaat dan mengeluarkan kata-kata yang tidak jelas. Pasien bekerja
sebagai supir angkutan umum, mempunyai riwayat merokok dan minum
alkohol. Penggunaan obat-obat terlarang dan seks bebas tidak diketahui oleh
eluarga.
Saat diperiksa di UGD pasien mengalami kejang umum; mata mendelik, terjadi
hipersalivasi, keempat ekstremitak terhentak-hentak. Kejang berlangsung selama 2
menit, sebelum diberikan obat anti kejang, kejang sudah berhenti
Pemeriksaan fisik saat di UGD: (post iktal) tekanan darah 140/90 mmHg, frekuensi
napas 24x/menit, temperature 40 C, frekuensi nadi 76x/menit, GCS :E2M4V2=8.
Pupil bulat isokor diameter 3mm dengan reflex cahaya yang menurun pada ke 2
sisi. Tanda rangsang meningeal: kaku kuduk, Brudzinski I dan II negative. Tidak
ditemukan kelainan pada saraf kranialis lainnya. Saat diberikan rangsang nyeri,
keempat ekstremitas menunjukkan pergerakan yang simetris, tanpa ada 1 sisi
ekstremitas yang tertinggal meskipun secara kuantitatif tidak dapat dinilai.
Pemeriksaan reflek fisiologis masih dalam batas normal, pemeriksaan refleks
patologis positif pada kedua sisi.
Sistem THT: dalam batas normal
Dokter yang merawat melakukan beberapa pemeriksaan laboratorium secara cito
yaitu pemeriksaan glukosa darah, ureum dan elektrolit darah.
Unfamiliar terms
• Kaku kuduk: Pemeriksaan radang meningeal
• Brudzinski: Pemeriksaan radang meningeal
Rumusan Masalah
1. Penyebab nyeri kepala berdenyut pada belakang kepala ?
2. Mengapa setelah diberi PCT demam lagi ?
3. Hubungan lifestyle pasien dengan keluhan ?
4. Penyebab hipersalivasi ?
5. Alasan pemeriksaan lab cito, glukosa, ureum & elektrolit?
6. Makna RP (+) ?
7. Penyebab penurunan reflex cahaya?
8. Penyebab nyeri kepala memberat walau sudah diberi obat?
Curah pendapat
1.-Suplai O2 otak yang menurun
- Nyeri sinus
- Hipertensi
- Vasodilatasi/vasokontriksi pembuluh darah otak
- Peningkatan TIK
2&8. Karena PCT tidak menyembuhkan penyebab
3&5. –Skrining penyebab ekstrakranial/intracranial (penurunan
kesuduran)
-Mengetahui penyebab penurunan kesadaran
-Alkohol  sirosis  gluconeogenesis turun  hipoglokemi
-Merokok  peningkatan CO2 darah  penurunan kesadaran karena
suplai O2 otak
-Merokok  memicu sumbatan pembuluh darah, gangguan jantung
4. Karena rangsang parasimpatis & pasien yang kejang tidak bisa
menelan ludah.
6. Kelainan pada UMN
7. Menandakan adanya gangguan SP
Langkah IV (Mindmap)
• Laki-laki 35 th
-Penurunan kesadaran : GCS = 8 (stupor)
-Nyeri kepala Infeksi & hipertensi
-Lifestyle buruk Sumbatan PD & Sirosis hati
-Kejang umum Infeksi Edema Serebri Ensefalopati hepatik
-Demam ++
-Penurunan reflex cahaya Gangguan UMN
-RP (+)
Penurunan Kesadaran
Learning Issues
1. Fisiologi Kesadaran
2. Macam-macam tingkat kesadaran dan penilaiannya secara
kuantitatif dan kualitatif
3. Klasifikasi etiologi penurunan kesadaran
4. Definisi, etiologi, patofisiologi, gambaran klinik, faktor resiko,
pemeriksaan, tatalaksana, prognosis dari penurunan kesadaran
intrakranial
LI 1 Fisiologi Kesadaran

Fisiologi : Human physiology


from cells to systems. 7th ed.
The different pathways are typically
identified depending on specific
neurotransmitters (noradrenalin,
dopamine, acetylcholine, and
glutamate). In particular, ARAS
brainstem nuclei project to the
intralaminar nuclei in the thalamus,
which project diffusely to the cerebral
cortex in order to activate it (Edlow et
al., 2012). Arousal is further mediated
by ARAS connectivity with the
hypothalamus (Ht) (gray arrow), which
participates in the regulation of
autonomic function and circadian sleep-
wake cycles, and with the basal
forebrain (not shown in figure), which
participates in cortical activation and
autonomic integration. This multiplicity
and redundancy of the ascending
wakefulness control system suggests an
adaptive mechanism for the recovery of
consciousness when some components,
but not the entire system, are clinically
disrupted.

https://www.researchgate.net/figure/256983249_fig1_Figure-1-Simplified-representation-of-arousal-control-system-The-ascending-reticular
LI 2 Tingkat Kesadaran Kualitatif dan
Kuantitatif
• Compos mentis
• Apatis
• Delirium
• Somnolen
• Sopor (stupor)
• Semi-coma
• Coma
Glasgow Coma Scale (Kuantitatif)
• Intrepretasi hasil
• 14-15 : Composmentis
• 12-13 : Apatis
• 10-11 : Delirium
• 7-9: Somnolen
• 5-6 : Sopor
• 4 : Semi-coma
• 3 : Coma
Grady Coma Scale

https://www.ncbi.nlm.nih.gov/books/NBK380/
Nilai Agregrat Normal
Nilai Agregrat Normal

Lahir sampai 6 bulan 9

6 bulan sampai 12 bulan 11

1 sampai 2 tahun 12

2 sampai 3 tahun 13

Lebih dari 5 tahun 14

PPMIDAI
LI 3
Klasifikasi
penurunan
kesadaran

Lindsay KW, Bone I, Fuller G, Callander R, Van Gijn J,


Churchill Livingstone. Neurology and neurosurgery
illustrated. Edinburgh [etc.: Churchill
Livingstone/Elsevier; 2015.
Cecil, Russell L., Lee Goldman, MD, and Andrew I Schafer. Goldman's Cecil Medicine. 24th ed. Philadelphia: Elsevier/Saunders, 2012
LI 4 Definisi, etiologi, patofisiologi, gambaran
klinik, faktor resiko, pemeriksaan, tatalaksana,
prognosis dari penurunan kesadaran intrakranial
Hepatic Encephalopathy
• Merupakan komplikasi dari sirosis, portosystemic shunting, hepatitis
kronik aktif atau nekrosis hepatik fulminan karena hepatitis virus
• Penyebab tersering  alkohol
• Onset: akut atau chronic progesif
• Faktor pemicu:
• Perdarahan gastrointestinal
• Infeksi sistemik
• Dehidrasi
• Obat sedasi

Clinical Neurology 8th Ed


Hepatic Encephalopathy
• Terganggunya mekanisme detoksifikasi hepatoseluler atau
portosystemic shunting PD  akumulasi amonia atau toksin lain di
darah  difusi ke otak  astrocyte & edema otak

Clinical Neurology 8th Ed


Hepatic Encephalopathy
• Tanda & gejala :
• Nausea, anorexia, pe↓ BB
• Somnolen, agitasi, dan koma
• Ocular reflexes are usually brisk
• Nystagmus, tonic downward ocular deviation, disconjugate eye movement
• Asterixis
• Tremor, myoclonus, rigiditad paratonik, spastisitas, decorticate atau
decerebrate posturing, extensor plantas responses
• Focal neurologic signs and focal or generalized seizure

Clinical Neurology 8th Ed


Hepatic Encephalopathy
• Pemeriksaan Lab
• pe↑ bilirubin serum, transaminase, amonia
• pe↑ PT, PTT
• Alkalosis respiratorik
• pe↑ glutamin (paling spesifik)
• EEG
• Diffusely slow with triphasic waves

Clinical Neurology 8th Ed


Hepatic Encephalopathy
• Tatalaksana • Prognosis
• Tangani faktor penyebab • Berhubungan dengan tingkat
• Rifaximin 3 x 200 mg PO keparahan hepatoseluler daripada
• Lactulosa 3-4 x 20-30 g PO atau disfungsi neurologik
Per rektum
• Transplantasi hati

Clinical Neurology 8th Ed


Meningitis
Meningitis is an inflammation of the membranes
(meninges) surrounding your brain and spinal cord.
The swelling from meningitis typically triggers
symptoms such as headache, fever and a stiff neck
• Meningitis bacterial (piogenik) : Neisseria
meningitidis, Haemofilia influenza tipe b,
Streptococcus pneumoniae.
• Meningitis viral www.mayoclinic.com
Meningitis Fungal

www.mayoclinic.com
www.mayoclinic.com
Epidemiologi
• Di negara maju, insidensi meningitis bakterial 5-10 per
100.000 per tahun.
Tiga organisme khusus yg memiliki kejadia khusus :
• Meningitis meningokokal yg dpt terjadi pada epidemi
• Haemophilus influenza umumnya mengenai anak dibawah
5th
• Infeksi pneumokokus lebih sering terjadi pada pasien usia
lanjut dan juga brhubungan dgn alkoholisme
www.mayoclinic.com
Patfis
• Kolonisasi mukosa (infeksi saluran nafas atau traktus GI)
invasi ke ruang intravaskuler multipilkasi menembus
sawar darh otak multiplikasi pd ruang subarakhnoid
inflamasi pleositosis dan gangguan sawar darah otak
• Infeksi dpt mencapai selaput otak melalui hematogen,
perkontinuitatum, implantasilng, aspirasi cairan amnion

www.mayoclinic.com
Sign & symptoms Signs in newborns
• Sudden high fever • Newborns and infants may show
• Stiff neck these signs:
• Severe headache that seems different • High fever
than normal
• Headache with nausea or vomiting • Constant crying
• Confusion or difficulty concentrating • Excessive sleepiness or irritability
• Seizures • Inactivity or sluggishness
• Sleepiness or difficulty waking
• Poor feeding
• Sensitivity to light
• No appetite or thirst • A bulge in the soft spot on top of a
• Skin rash (sometimes, such as in baby's head (fontanel)
meningococcal meningitis) • Stiffness in a baby's body and neck
www.mayoclinic.com
Risk factor
• Skipping vaccinations
• Age. Most cases of viral meningitis occur in children younger than age
5. Bacterial meningitis is common in those under age 20.
• Living in a community setting (spread by the respiratory route, and
spreads quickly through large groups).
• Pregnancy
• Compromised immune system

www.mayoclinic.com
Cecil, Russell L., Lee Goldman, MD, and Andrew I Schafer. Goldman's Cecil Medicine. 24th ed. Philadelphia: Elsevier/Saunders, 2012
Pemeriksaan fisik
• Rangsang meningeal positif (kaku
kuduk, tanda kerning dan tanda
Brudzinski)
• Perubahan tingkat kesadaran
• Kejang, peningkatan intrakranial
dan disfungsi saraf kranial
• Kadang disertai hemiparesis,
demensia dan paralis

CURRENT Diagnosis & Treatment Neurology.


LANGE 2ND edition
Farmako Non farmako
• Heparinisasi • Terapi cairan untuk menghindari
• Antikonvulsan syok hipovolemik. IV NaCl 0,9%
20ml/kg dalam 5-10menit
• Sblm hasil kultur keluar : beri
• Koreksi elektrolit
AB empiris (cefotaxime atau
ceftriaxon) • Menurunkan TIK
• Deksametason (10mg setiap
6jam selama 4hri) untuk
menekan sitokin infamasi

CURRENT Diagnosis & Treatment Neurology.


LANGE 2ND edition
Prognosis dan gejala sisa meningitis
• Angka kematian
• 5% pada H. influenzae; meningokokal meningitis,
• 15% pada pneumokokal meningitis
• 40-75% pada neonatus
• Cranial nerve palsies
• Ggg pendengaran
• Ggg lainnya biasa menghilang dlm bbrp mgg-bln

Ropper AH, Samuels MA, Klein JP. Adams and Victor’s principles of neurology. 10th ed. 2014. New York: McGraw-Hill education. P. 707-8..
http://www.aafp.org/afp/2010/1215/p1491.pdf
Complications
• Altered consciousness or even coma
• hearing loss, epilepsy, hemiplegia, neuropsychological impairment,
developmental and learning disabilities
• Shock or disseminated intravascular coagulation, frequently is
associated with meningococcal meningitis
• Apnea and respiratory failure may occur with any bacterial meningitis,
especially in infants

https://cdn.intechopen.com/pdfs-wm/34319.pdf
Coma
• The patient make no response to the environment
• Results from disturbance in brainstem reticular activating system
above the mid pons or of both cerebral hemispheres

Clinical Neurology 8th Ed


Emergency management
• Ensure adequacy of airway, ventilation and circulation
• Insert IV catheter and withdraw blood for serum glucose, renal
function tests, PT, PTT, and CBC
• 25g Dextrose IV for hypoglycemic coma and 100 mg thiamine iv.
Naloxone 0.4-1.2 IV
• If caused by intoxication of benzodiazepine  Flumazenil 1-10 mg IV
• Withdraw arterial blood for pH and blood gas analysis

Clinical Neurology 8th Ed


Netter, Frank H., et al. Netter's Neurology. 2nd ed. Philadelphia, PA: Elsevier Saunders, 2012
Etiology
• Sudden onset of coma suggests vascular origin, especially brainstem
stroke or subarachnoid hemorrhage
• Rapid progression from hemispheric signs  intracerebral
hemorrhage (minutes-hours)
• Days-weeks  tumor, abscess, or chronic subdural hematoma
• Metabolic or infection  agitated delirium  coma
Netter, Frank H., et al. Netter's Neurology. 2nd ed. Philadelphia, PA: Elsevier Saunders, 2012
Netter, Frank H., et al. Netter's Neurology. 2nd ed. Philadelphia, PA: Elsevier Saunders, 2012
Physical examination
• Bloodpressure ( hypertension ) ( Hypertensive encephalopathy)
• Temperature (Hypothermia)(Wernicke encephalopathy, hepatic
encephalopathy, intoxication of ethanol or drugs, myxedema)
• Hyperthermia (heat stroke, status epilepticus, anticholinergic drug
intoxication

Clinical Neurology 8th Ed


Acute Encephalitis
Definitio Encephalitis  inflammation of brain parenchyma that may coexist with
n inflammation of the meninges (meningoencephalitis) or spinal
cord (encephalomyelitis).
Epid Most frequently  infants (<1 yr) & elderly patients (>65 yrs)
Etiology Virus
•Herpes family viruses  HSV, HHV-6, VZV, CMV
•Arboviruses la crosse virus, st. Louis virus, WNV, western equine
virus, eastern equine virus
•Enteroviruses
Bacteria
•Pyogenic bacteria  syphilis, leptospirosis, brucellosis, tuberculosis,
and listeriosis
Fungal
•Encephalitis is a presenting manifestation  cryptococcosis,
histoplasmosis, blastomycosis, / coccidiomycosis.
• Adam’s JG. Emergency medicine. 2nd ed. Saunders-Elsevier: 2013
• Beckham JD, Tyler KL. Encephalitis. In: Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases,
Updated Edition. 8rd ed. Saunders-Elsevier: 2015
Pathophysiology
• The pattern of brain involvement depends on the specific pathogen,
the immunological state of the host, and a range of environmental
factors
• In viral encephalitis the virus initially gains entry and replicates in local
or regional tissue, such as the GI tract, skin, urogenital system, or
respiratory system
• dissemination to the CNS occurs by haematogenous routes
(enterovirus, arboviruses, HSV, HIV, mumps) or via retrograde axonal
transport as with the herpes virus, the rabies virus, or variant scrapie-
isoform prion proteins.
http://bestpractice.bmj.com/best-
practice/monograph/436/basics/pathophy
siology.html
Treatment
Acyclovir 10mg/kg IV @8h (child and adult)
• 20 mg/kg IV @8h (neonatus)

Tunkel, A., Glaser, C., Bloch, K., Sejvar, J., Marra, C., Roos, K., Hartman, B., Kaplan, S., Scheld, W. and
Whitley, R. (2008). The Management of Encephalitis: Clinical Practice Guidelines by the Infectious
Diseases Society of America. Clinical Infectious Diseases, 47(3), pp.303-327
Tunkel, A., Glaser, C., Bloch, K., Sejvar, J., Marra, C., Roos, K., Hartman, B., Kaplan, S., Scheld, W. and
Whitley, R. (2008). The Management of Encephalitis: Clinical Practice Guidelines by the Infectious
Diseases Society of America. Clinical Infectious Diseases, 47(3), pp.303-327
Brainstem Death

Etiology :

• May follow global insult such as hypoxia / direct insult (trauma) or


focal ischemia
• Most common : traumatic brain injury, cerebral tumours, meningitis
& hypoxic brain injury

Waldman C, Soni N, Rhodes A. Oxford desk reference critical


care. New York; Oxford University Press: 2008.
Process of confirming death
Pre-conditions
(certain condition before neurological testing)

• The cause of the coma


• Patient must be deeply comatose, apnoeic & dependent on mechanical ventilation
• Patient unresponsive with reversible causes of brainstem depressed excluded

Waldman C, Soni N, Rhodes A. Oxford desk reference critical


care. New York; Oxford University Press: 2008.
Process of confirming death
Establishing the irreversible loss of brainstem reflex

• Pupils are fixed without direct / consensual response to light


• Corneal reflex is absent
• No motor response within the cranial nerve distribution to a painful stimulus
• The oculovestibular (caloric) reflex is absent
• No gag reflex / cough reflex in response to a suction catheter being passed into
the pharynx / down the ETT to stimulate the carina

Waldman C, Soni N, Rhodes A. Oxford desk reference critical


care. New York; Oxford University Press: 2008.
Process of confirming death
Apnoea Testing
The responsiveness of respiratory to hypercsrbia

Timing of testing : at least 6h after the onset of apnoeic coma, if hypoxic injury
following cardiac arrest  min. 24h after the restoration of circulation

Conduct of testing : test performed by 2 medical practitioners (one should be an


ICU consultant)

Waldman C, Soni N, Rhodes A. Oxford desk reference critical


care. New York; Oxford University Press: 2008.
Netter, Frank H., et al. Netter's Neurology. 2nd ed. Philadelphia, PA: Elsevier Saunders, 2012
Kesimpulan & Saran
• Kesimpulan : Kami telah mempelajari definisi, klasifikasi,
patofisiologi, etiologi, tanda & gejala, pemeriksaan fisik, neurologis,
penunjang, DD, tatalaksana, komplikasi & prognosis dari penurunan
kesadaran intracranial
• Saran : Disarankan untuk diberikan terapi awal sebelum diagnosa
pasti karena infeksi pada otak merupakan hal yang emergensi dan
dilakukan pemeriksaan lebih lanjut.