3st Problem

Emergency Medicine
Block
8st October 2019
Group 15
Group member
Tutor : dr. Alex
Ketua : Caroline Monika
Sekretaris : Louis Rianto
Penulis : Carmelita
• Anggota :
• Claudia
• Denny Bunarsi
• Feni Anglelina
• William Wijaya H. S.
• Ria Nata Sia
• Cindy Marcellina
• Kezia Susanti
Learning Issues
1. Neurology Infection emergencies
2. Neurology Metabolic emergencies
3. Neurology Vascular emergencies
4. Epilepsy and Status Epilepticus
 Mind Map
Meningitis, Status
Epilepsi
Ensefalitis, Kejang Epilepticus
demam, Tetanus Pendarahan
Subaraknoid
Kegawatdaruratan Vaskular
Infeksi
Neurologi Pendarahan
Intrakranial

Hipertensi, DM,
Metabolik
Ensefalopati

Etiologi, Patofisiologi, Tanda & gejala,

PF, PP, Tatalaksana, Komplikasi,
Prognosis
 Diffuse aksonal injury
Epidural Hematoma
Trauma Subarakhnoid hematoma

Intrakranial Subdural Hematoma

Meningitis
Infeksi
Encephalitis
Meningoencephalitis
Penurunan Vaskular
kesadaran Abses
Epilepsi
Keganasan
Hidrocephalus
Lain - lain

Metabolik endokrin
Gangguan respirasi
Ekstrakranial Obat –obatan dan toksin
Gangguan psikiatrik
Gangguan vaskular
Neurology Infection
emergencies
Meningitis
• Ad inflamasi membran sekitar
otak dan medula spinalis
• Bacterial meningitis
• Aseptic meningitis: krn selain
infeksi bakteri misalnya reaksi
obat, rheumatologic
conditions, non bacterial inf.
Spt virus (enterovirus,
echovirus) atau jamur
Sign and Symptoms:
• Triad: fever, neck stifness,
altered conciousness
• Gejala lain: sakit kepala,
demam, nyeri leher, mual,
muntah
• Meningeal sign: nuchal rigidity,
kernig’s sign, brudzinski’s sign
Diagnosis
• Lumbar puncture untuk mengambil CSF
• CT Scan pd mereka yg tdpt perubahan
status mental, new onset seizure,
immunocompromise, focal neurologic sign,
papilledema, jg utk mengetahui
kontraindikasi LP spt massa di otak,
herniasi, brain shift
• Lab: hitung sel dr CSF, kadar glukosa,
protein, pewarnaan gram dan kultur bakteri
• PCR, bacterial antigen testing, ad
pemeriksaan tambahan yg dpt dilakukan
Tinnitali Emergency Medicine Manual 8 th Ed
Management
• Saat bacterial meningitis sdh di diagnosis berikan antibiotik empirik
berdasarkan patogen yg dicurigai
• Pt. usia < 50 berikan cefaosporin gen 3 spt ceftiaxone 2 g IV plus
vankomisin 15 mg/kg IV
• Pt. dg risk inf. Listeria monocytogenes (usia >50 th, hamil, alkoholik,
imunokompromise) berikan ampicillin 2g IV
• Bacterial meningitis: Kortikosteroid dpt menurunkan mortalitas dan
sequele neurologic. Dexamethasone 10 mg IV stp 6 jam utk 4 hr
• Encephalitis: berikan acyclovir 10 mg/kg IV utk HSV infection,
ganciclovir 5 mg/kg IV utk CMV infection
 ENSEFALITIS
• Encephalitis : inflammation of brain Virus
parenchyma that may coexist with
inflammation of the
meninges (meningoencephalitis) or
spinal cord (encephalomyelitis).
• Most frequently :
• Infants (<1 yr)
• Elderly patients (>65 yrs)
•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.

Sumber : Adam’s JG. Emergency medicine. 2nd ed. Saunders-Elsevier: 2013

 Patofisiologi bakteri

Organisme Peradangan
Otak Eksudat
piogenik supuratif

Dinding
Bentuk ruang Bagian tengah
menebal Edema
abses melunak
(kapsul)

2 minggu

Abses Masuk
Pecah Ensefalitis
membesar ventrikulus

Sumber : Perhimpunan dokter spesialis saraf indonesia. Buku ajar neurologi klinis.171-3.
 Patofisiologi virus

Saluran Perbanyak diri

Virus
pernafasan scr lokal

Pertumbuhan
Menyebar ke
dimulai jar Viremia
SSP
ekstraneural

Ensefalitis

Sumber : Perhimpunan dokter spesialis saraf indonesia. Buku ajar neurologi klinis.175-9.
GAMBARAN KLINIK
ENSEFALITIS
ENSEFALITIS BAKTERIAL ENSEFALITIS VIRAL
• Awal  gejala tidak khas seperti infeksi umum 1. Bentuk asimptomatik
• Peningkatan tekanan intrakranial : 2. Bentuk abortif
• Nyeri kepala yg memberat – Nyeri kepala, demam, kaku kuduk ringan
• Muntah 3. Bentuk fulminan
• Tidak nafsu makan – Beberapa jam-hari
• – Pada stadium akut : demam tinggi, nyeri kepala difuse
Demam
hebat, apatis, kaku kuduk, diorientasi, sangat gelisah,
• Penglihatan kabur koma.
• Kejang umum/fokal 4. Bentuk khas ensefalitis
• Kesadaran menurun – Nyeri kepala ringan, demam
• Gejala defisit neurologik : – Tanda radang SSP : kaku kuduk, tanda kernig +, gelisah,
lemah, suka tidur, kesadaran menurun  koma, dpt
• Defisit nervi kraniales, hemiparesis, refleks tendon terjadi kejang fokal/umum, hemiparesis, ggg koordinasi,
meningkat, kaku kuduk, afasia, hemianopia, kelainan kepribadian, disorientasi, ggg bicara, ggg mental.
nistagmus, ataksia

Sumber : Perhimpunan dokter spesialis saraf indonesia. Buku ajar neurologi klinis.175-9.
DIAGNOSIS
• Anamnesis
• PF dan pemeriksaan neurologis
• PP : analisis CSS, foto torax dan tengkorak, EEG, CT-scan, MRI.

Sumber : Perhimpunan dokter spesialis saraf indonesia. Buku ajar neurologi klinis.175-9.
TATALAKSANA
ENSEFALITIS
ENSEFALITIS BAKTERIAL ENSEFALITIS VIRAL
• Ampisillin 3-4g/hari (4x sehari) • Acyclovir IV 10mg/kgbb, setiap 8 jam, selama 10
hari
• Kloramfenikol 1g/hari (4x sehari)
• Acyclovir PO 200mg/kgbb, 5-6x sehari
• Bila ada peningkatan TIK  • Kontrol kadar Hb, jika turun 9%  dosis
deksametason/kortison diturunkan 200mg tiap 8 jam. Turun sampai
• Jika abses berkembang  bedah saraf 7%  pengobatan dihentikan sementara
(kraniotomi dan pengambilan cairan abses • Biopsi korteks
• Tes serologik
• Pasien dalam kondisi koma  cairan parenteral

Sumber : Perhimpunan dokter spesialis saraf indonesia. Buku ajar neurologi klinis.175-9.
 Tetanus.
• Acute disease manifested by skeletal muscle spasm
and autonomic nervous system disturbance.
• Caused by a powerful neurotoxin produced by the
bacterium Clostridium tetani and is completely
preventable by vaccination.
• Tetanus :
• acute onset of hypertonia or painful muscular
contractions (usually of the muscles of the jaw
and neck) and generalized muscle spasms
without other apparent medical cause. (CDC)   be poor.
• Neonatal tetanus : an illness occurring in a child who
has the normal ability to suck and cry in the first 2
days of life but who loses this ability between days 3
and 28 of life and becomes rigid and has spasms.
(WHO)
• Maternal tetanus : tetanus occurring during pregnancy
or within 6 weeks after the conclusion of pregnancy
(whether with birth, miscarriage, or abortion). (WHO)
• Clinical features that are broadly divided into
generalized (including neonatal) and local.
• In the usually mild form of local tetanus,
only isolated areas of the body are affected
and only small areas of local muscle spasm
may be apparent. If the cranial nerves are
involved in localized cephalic tetanus, the
phargyngeal or laryngeal muscles may
spasm, with consequent aspiration or
airway obstruction, and the prognosis may
• In the typical progression of generalized
tetanus, muscles of the face and jaw often
are affected first, presumably because of
the shorter distances toxin must travel up
motor nerves to reach presynaptic
terminals.
Management.
• The entry wound should be identified, cleaned, and
debrided of necrotic material in order to remove
anaerobic foci of infection and prevent further toxin
production.
• Antibiotic :
• Important to establish a secure airway early in
• Metronidazole (400 mg rectally or 500 mg IV every 6 h
for 7 days)  Preferred
severe tetanus.
• Penicillin (100,000–200,000 IU/kg per day), although this
drug theoretically may Antitoxin
• should be given early in an attempt to deactivate any
circulating tetanus toxin and prevent its uptake into the
nervous system.
• Preparations
• human tetanus immune globulin (TIG)
• likely to be associated with anaphylactoid reactions
• Standard therapy is 3000–6000 IU of TIG
• equine antitoxin.
• 10,000–20,000 U of equine antitoxin as a single IM dose
• Spasms are controlled by heavy sedation using
benzodiazepines.
• Chlorpromazine or phenobarbital are
commonly used worldwide, and IV
magnesium sulfate has been used as a muscle
relaxant.
• Problem : doses  Respiratory Depression.
• Patients should be nursed in calm, quiet
environments because light and noise can trigger
spasms.
• Tracheal secretions are increased.
• Cardiovascular stability is improved by increasing
sedation with IV magnesium sulfate (plasma
concentration, 2–4 mmol/L), morphine, or other
sedatives. In addition, drugs acting specifically on
the cardiovascular system (e.g., esmolol, calcium
antagonists, and inotropes) may be required.
Short-acting drugs that allow rapid titration are
preferred;
Prevention. • Prevention of maternal and neonatal
• Tetanus is prevented by good wound care and tetanus
immunization
• Two doses of TT at least 4 weeks apart to
• In neonates, use of safe, clean delivery and cord- the previously unimmunized pregnant
care practices as well as maternal vaccination are woman.
essential.
• Vaccination : • Individuals sustaining tetanus-prone
• Tetanus toxoid (TT) for vaccination is available in wounds should be immunized if their
various preparations:
• single-dose TT
vaccination status is
• TT with high- or low-dose diphtheria toxoid • incomplete
• TT with diphtheria toxoid in combination with whole-
cell/acellular pertussis, Haemophilus influenzae type b, • unknown
hepatitis B, or polio vaccine.
• If their last booster was given >10 years
• The WHO guidelines for tetanus vaccination consist earlier.
of a primary course of three doses in infancy,
• Boosters at 4–7 years of age. • Patients sustaining wounds not classified
• Boosters 12–15 years of age as clean or minor should also undergo
• Booster in adulthood.
passive immunization with TIG.
 Neonatal tetanus
• Neonatal tetanus is defined by the World Health Organization (WHO)
as “an illness occurring in a child who has the normal ability to suck
and cry in the first 2 days of life but who loses this ability between
days 3 and 28 of life and becomes rigid and has spasms.”
• Neonates typically present with inability to suck.
• In neonatal tetanus, the younger the infant is when symptoms occur,
the worse the prognosis.
• In neonates, use of safe, clean delivery and cord-care practices as well
as maternal vaccination are essential.

Harrison, 19th ed
 Treatment for children
• human tetanus immunoglobulin IM
Neonates, children and adults: 500 IU single dose, injected into 2 separate
sites
• metronidazole IV infusion (30 minutes; 60 minutes in neonates) for 7 days
Neonates:
• 0 to 7 days: 15 mg/kg on D1 then, after 24 hours, 7.5 mg/kg every 12 hours
• 8 days to < 1 month (< 2 kg): same doses
• 8 days to < 1 month (≥ 2 kg): 15 mg/kg every 12 hours
Children 1 month and over: 10 mg/kg every 8 hours (max. 1500 mg daily)

https://medicalguidelines.msf.org/viewport/CG/english/tetanus-16689919.html
Malaria cerebral
• Cerebral malaria is the most severe neurological complication of infection with Plasmodium
falciparum malaria. It is a clinical syndrome characterized by coma and asexual forms of the
parasite on peripheral blood smears. 
• WHO defines cerebral malaria as a clinical syndrome characterized by coma at least 1 hour after
termination of a seizure or correction of hypoglycemia, asexual forms of Plasmodium
falciparum parasites on peripheral blood smears and no other cause to explain the coma
•  In African children, coma develops suddenly with seizure onset often, following 1-3 days of
fever. A few children develop coma following progressive weakness and prostration. Brain
swelling, intracranial hypertension, retinal changes (hemorrhages, peripheral and macular
whitening, vessel discoloration and or papilledema) and brainstem signs (abnormalities in
posture, pupil size and reaction, ocular movements or abnormal respiratory patterns) are
commonly observed.
• Other systemic complications such as anemia, metabolic acidosis, electrolyte imbalance and
hyperpyrexia or hypoglycemia and shock are commonly present. 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3056312/
Tanda gejala : Pemeriksaan penunjang
1. Tria malaria (menggigil, demam, berkeringat)
2. Penurunan kesadaran
1. Apusan darah  plasmodium falciparum
3. Disertai kejang
aseksual pada penderita yang mengalami
Faktor resiko :
penurunan kesadaran
Tinggal atau pernah berkunjung ke daerah endemic malaria 2. Pemeriksa darah rutin dan gula darah
Riwayat terinfeksi plasmodium falciparum
diagnosis
Pem. Fisik :
4. Penurunan kesadaran yang dapat didahului mengantuk, 3. Ditemukan plasmodium falciparum aseksual
kebingunngan, disorientasi, delirium atau agitasi ( kaku pd darah tepi
kuduk dan ransang meningeal -) , koma.
5. Nistagmus dan deviasi conjugee 4. Coma (e/ demam tinggi , hipoglikemia,
6. Retina pucat, pendarahan retina (jarang), edema papil, syok , ensefalopati uremikum,ensefalopati
dan cotton wood spots hepatikum, sepsis)
7. Lesi upper motor neuron , tonus otot dan refleks
tendon meningkat 5. Demam dengan penurunan kesadaran
8. Babinski + (khusunya jika berkunjung ke daerah
endemik
tatalaksana
Neurology Metabolic
emergencies
HYPERTENSIVE
ENCHEPHALOPHATY
• Hypertensive encephalopathy: reversible acute clinical • Physical Examination:
syndrome triggered by sudden increases in blood pressure • Hypertension crisis: systolic blood pressure> 180 mmHg &
beyond the limit of auto-regulation of the brain. Systolic diastolic> 120 mmHg
blood pressure limit> 180 mmHg & diastolic> 120 mmHg • Papil edema
• Etiology: hypertension, pre-eclampsia or eclampsia, • Impaired vision
neurotoxicity due to cyclosporin A or takrolimus, uremia • Focal neurological deficits
and porphyria.
• Supporting Investigation:
• CT-Scan
• Clinical Manifestations: • MRI
• Severe hypertension syndrome: severe headache, nausea,
vomiting, visual impairment, convulsions, stupor to coma
• The onset of symptoms usually progresses slowly, with a • DD
progression of about 24-48 hours
• Symptoms of diffuse brain disorders • Ischemic stroke
• Severe neurologic manifestations occur when hypertension of • bleeding stroke
maligna or diastolic pressure> 125 mmHg with retinal
hemorrhage, exudates, papillary edema, cardiac and kidney • Epilepsy
disorders • Reversible posterior leukoencephalopathy syndrome
Treatment

Treatment Complication
• Blood pressure reduction: Blood pressure drop target is 25%
reduction in MAP within 1-2 hours / decrease diastolic pressure by • hypertension nephropathy
10-15% or up to 110 mmHg within 30-60 minutes. Blood pressure is
lowered until it reaches normal blood pressure within 24-48 hours • retinopathy hypertension
• Labetalol: 20 mg loading dose loading, followed by 20-80 mg
repeat bolus at 10 min intervals. After that continued with drip drip • intracranial hemorrhage
infusion 1-2 mg / min & titrated according to the desired effect of
hypotension • broad cerebral infarction
• Nicardipin: the recommended dosage is 5mg / hr infusion, which
can be increased by 2.5 mg / hr every five minutes to a maximum
of 15 mg / h, or until the blood target is reached
• Fenoldopam: initial dose of 0.03 mcg / kg / minute IV which can be
gradually raised up to 1.6 mcg / kg / min
NON-FARMAKO THERAPY
• Head Up 30 °
• Oxygenation
Delirium
• Dikarakterisasi dengan
gangguan kesaran,
persepsi, berpikir, memori,
dan kognisi
• Pasien somnolen saat siang
dan agitasi saat malam
• Gejala lain: tremor,
takikardi, sweating,
hipertensi, emotional
outburst, halusinasi
Diagnosis dan Management
• Akut onset atention defisit dan kognitif
abnormalities berfluktuasi epanjang hari dan
memburuk saat malam
• History penggunaan obat
• CT dpt dilakukan bila dicurigai ada lesi
intrakranial, LP dpt dipertimbangkan bila
dicurigai ada meningitis atau SAH

Management:
• Mengatasi penyebab delirium
• Akut episode of agitation: haloperidol 5-10
mg PO atau IM, Lorazepam 0.5-2 mg PO, IM,
atau IV
COMA
• Coma : a sleep-like state in which the
patient makes no purposed response
to the enviroment and from which
he or she cannot be aroused.

• Results from a disturbance in the

function of either the brainstem
reticular activating system above
the mid pons or of both cerebral
hemispheres
Sumber : Ginsberg L, et al. Neurology. Edisi ke-8. page : 45.
Sumber : Aminof MJ, et al. Clinical neurology. 9th edition. 2012; page 48.
Neurology Vascular
emergencies
 Pendarahan Subaraknoid
• Definisi: masuknya darah ke ruang subaraknoid
(antara piameter dg memb araknoid)
• Etiologi:
• Nontrauma:
• Aneurisma (tersering)
• Angioma
• Neoplasma
• Cortical thrombosis
• Infeksi
• Vaskulitis
• Trauma: sering krn fraktur basis cranium → aneurisma
a. Carotid interna
http://www.strokecenter.org/patients/about-stroke/subarachn

https://emedicine.medscape.com/article/1164341-overview
 • Gejala prodromal: muncul 10 – 20 hari sebelumnya, tjd krn adanya
• Faktor risiko pembentukan aneurisma:
• Atherosclerosis
• Hypertension
• Advancing age
• Smoking
• Hemodynamic stress
• Heavy alcohol consumption
• Tanda dan gejala: tergantung dr derajat perdarahan dan lokasi lesi
• Herediter
• Patofisiologi:
Stres hemodinamik (aliran darah dan turbulensi) →
pembentukan pouching kecil → ukuran bertambah besar
→ tunika media yg elastis digantikan o/ jar ikat
→ ruptur → ekstravasasi darah
→ pe↑ tek intrakranial
→ kompensasi → vasokonstriksi PD kranial &
pengeluaran mediator inflamasi →
iskemik sekunder
→ menekan jar otak sekitar → injury
→ terbentuk massa → menghambat aliran darah dr
distal
https://emedicine.medscape.com/article/1164341-overview
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5288992/
kebocoran, emboli atau massa aneurisma yg menekan jar sekitar
• Headache (48%)
• Dizziness (10%)
• Orbital pain (7%)
• Diplopia (4%)
• Visual loss (4%)
• Sudden and explosive headache (paling sering)
• Loss of consciousness: krn penurunan perfusi darah ke otak
• Seizure (6-16%)
• Jk aneurism terbentuk di:
• posterior communicating artery → bisa tjd disfungsi pupil
• middle cerebral artery → Motor neurologic deficits (10 – 15%)
• ophthalmic artery → monocular vision loss krn penekanan ke
optic nerve ipsilateral
• Dapat ada gej sakit kepala ringan beberapa minggu sebelumnya krn
adanya kebocoran darah ke subarachnoid space
• mild to moderate blood pressure (BP) elevation → mjd labil stl tek
intrakranial meningkat
• Takikardi
• Peningkatan suhu jk disertai dg meningits
• Pemeriksaan penunjang:
• Lab: CT scan:
• CBC: evaluation of possible infection or hematologic • Grade 1 - No subarachnoid blood seen on CT scan
abnormality
• Grade 2 - Diffuse or vertical layers of SAH less than 1 mm thick
• PT & aPTT: evaluation of possible coagulopathy
• Grade 3 - Diffuse clot and/or vertical layer greater than 1 mm
• Blood typing: prepare for possible intraoperative transfusions
thick
• Cardiac enzymes: possible myocardial ischemia
• Grade 4 - Intracerebral or intraventricular clot with diffuse or
• Radiologi: no subarachnoid blood
• CT scan: first choice (paling sensitif), dapat mendeteksi
perdarahan yg baru terjadi
• Cerebral angiography
• CTA (CT angiography)
• MRI:
• performed if no lesion is found on angiography
• Not sensitive for SAH within the first 48 hours
• monitoring the status of small, unruptured aneurysms
• Pungsi lumbar:
• Jk gejala klinis menunjukkan SAH tapi hasil imaging negatif
• Paling baik dilakukan 12 jam stl munculnya gejala
• Melihat adanya eritrosit dan cek xantochromia (CSF berwarna
kuning/pink stl sentrifugasi ak. Pecahnya eritrosit shg pigmen
heme dikeluarkan)

https://emedicine.medscape.com/article/1164341-overview
Tatalaksana • Vasospasm:
• Nimodipine:
• Calcium channel blocker
• Menghambat vasospasme: menghambat Ca
• Monitoring: masuk ke sel otot polos & mencegah
• Cardiac monitoring pelepasan substansi dr platelet dan sel
endotel
• Pulse oximetry • Bersifat neuroprotektif: menghambat
masuknya Ca ke neuron yg rusak
• Blood pressure • Dapat mencegah dan mjd terapi pada delayed
• Urine output dg foley catheter ischaemic
• Dosis 60mg tiap 4 jam selama 3 minggu
• Terapi: • Magnesium: calcium antagonis
• Hipovolemik: isotonic crystalloid for • Statin: meningkatkan pembentukan NO →
vasodilator
volume replacement
• Surgery: pemasangan clip pd aneurisma
• Bari antihipertensi jk MAP >130mmHg yg ruptur
• Peningkatan tek intrakranial (ICP):
• Osmotic agents (manitol)
• Loop diuretic

https://emedicine.medscape.com/article/1164341-overview
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5288992/
 Prognosis dan DD DD: • Migraine
• Aseptic Headache
• The Hunt and Hess grading system is as follows: Meningitis • Transient
• Grade 0 - Unruptured aneurysm Ischemic Attack
• Cluster Headache
• Grade I - Asymptomatic or mild headache and slight nuchal
rigidity • Encephalitis • Komplikasi:
• Grade Ia - Fixed neurological deficit without acute • First Adult • Hydrocephalus
meningeal/brain reaction Seizure • Rebleeding
• Grade II - Cranial nerve palsy, moderate to severe headache, • Hypertensive • Vasospasm
nuchal rigidity Emergencies in • Seizures
• Grade III - Mild focal deficit, lethargy, or confusion Emergency
• Grade IV - Stupor, moderate to severe hemiparesis, early Medicine • Cardiac
dysfunction
decerebrate rigidity • Intracranial
• Grade V - Deep coma, decerebrate rigidity, moribund Hemorrhage
appearance • Ischemic Stroke
• Semakin rendah grading, prognosis semakin baik in Emergency
• Grade I – III prognosis cukup baik, bisa segera dioperasi Medicine
• Grade IV – V prognosis buruk, harus stabilisasi kondisi sampai min
grade III utk bisa dioperasi • Meningitis
https://emedicine.medscape.com/article/1164341-overview
Hematom Intraserebral
• Clinical features:
• Risk Factors
• Long standing hypertension
• Arteriovenous malformations
• Arterial aneurysm
• Anticoagulant therapy
• Use of sympathomimetic drugs
(cocaine and phenylpropanolamine)
• Intracranial tumors
• Amyloid angiopathy in the elderly
• In intracerebral hemorrhage, headache,
nausea, and vomiting often precede the
neurologic deficit
• In hypertensive intracerebral hemorrhage,
bleeding is usually localized to the
putamen, thalamus, pons, or cerebellum
(in decreasing order of frequency)
• Cerebellar hemorrhage is commonly
associated with dizziness, vomiting,
marked truncal ataxia, gaze palsies, and
depressed level of consciousness
 Diagnosis
• CT is optimal for demonstrating hemorrhage extension
into the ventricles, whereas MRI is superior for
demonstrating underlying structural lesions
• Cerebral angiography may be useful in selected patients
in stable condition who do not require urgent surgery,
particularly those in whom no obvious cause of bleeding
is identified and those younger than 45 years of age
without hypertension
• including a complete blood count, electrolyte levels,
creatinine level, glucose level, electrocardiogram, chest
radiograph, coagulation studies, and blood type and
screen
Treatment
• Maintain close attention to the patient’s airway, monitoring of
neurologic status, management of hyperthermia with antipyretics,
administration of antiepileptic medications if seizures occur,
aggressive management of hyperglycemia (>160 milligrams/dL), blood
pressure management, and reversal of coagulopathy (if present)
• Elevated intracranial pressure  raising the head of the bed 30
degrees and providing appropriate analgesia and sedation.
Epilepsy and Status
Epilepticus
 Kejang Demam
• Kejang yang terjadi pada anak setelah
Klasifikasi Kejang Demam
usia 1 bulan yang terkait dengan Simple Febrile Seizure Complex Febrile Seizure
demam & tidak disebabkan oleh
infeksi dari SSP, tanpa ada riwayat • Singkat (<15 menit), • Dengan salah satu ciri:
kejang neonatal sebelumnya atau berhenti sendiri • Kejang lama >15
kejang unprovoked sebelumnya, dan • Bentuk umum tonik menit
tidak memenuhi kriteria untuk kejang &/klonik, tanpa • Kejang fokal/parsial
gerakan fokal satu sisi, atau kejang
simtomatik akut. (ILAE) • Tidak berulang dalam umum didahului
• Bangkitan kejang yang terjadi pada 24 jam kejang parsial
kenaikan suhu tubuh (suhu rektal • Tidak menyebabkan • Berulang atau >1X
>380C) yang disebabkan oleh suatu pe↓ IQ, epilepsi, dalam 24 jam
proses ekstrakranial tanpa adanya kematian
proses infeksi intrakranial
Buku ajar neurologi. Sagung Seto, 2017.
FEBRILE
SEIZURE

calgaryguide.ucalgary.ca
Prognosis
1. Kecacatan atau kelainan neurologis
• Kelainan neurologis dapat terjadi pada kasus kejang lama atau kejang berulang, baik umum maupun fokal.
• Suatu studi melaporkan terdapat gangguan recognition memory pada anak yang mengalami kejang lama.
2. Faktor risiko terjadinya epilepsi
• Terdapat kelainan neurologis atau perkembangan yang jelas sebelum kejang demam pertama
• Kejang demam kompleks
• Riwayat epilepsi pada orangtua atau saudara kandung
• Kejang demam sederhana yang berulang 4 episode atau lebih dalam satu tahun.
3. Kematian
4. Kemungkinan berulangnya kejang demam
• Faktor risiko berulangnya kejang demam adalah:
• Riwayat kejang demam atau epilepsi dalam keluarga
• Usia kurang dari 12 bulan
• Suhu tubuh kurang dari 39 derajat Celsius saat kejang
• Interval waktu yang singkat antara awitan demam dengan terjadinya kejang.
• Apabila kejang demam pertama merupakan kejang demam kompleks.
• Ket: Bila seluruh faktor tersebut di atas ada, kemungkinan berulangnya kejang demam adalah 80%, sedangkan bila
tidak terdapat faktor tersebut kemungkinan berulangnya kejang demam hanya 10-15%. Kemungkinan berulangnya
kejang demam paling besar pada tahun pertama.
 KEJANG EPILEPSI

• Kejang : suatu kelainan yang • Epilepsi : kumpulan kelainan

ditandai dengan adanya gejala yang ditandai dengan kejang
neurologis sementara sebagai rekuren, merupakan suatu
hasil dari abnormalitas aktifitas penyebab umum dari hilangnya
elektrikal pada korteks serebral. kesadaran secara episodik.

Sumber : Clinical neurology lange-8 th ed

Sumber : Ropper AH, Samuels MA, Klein JP. Adams and Victor’s Principles of Neurology. 10 th Ed.2014;345-6.
Anamnesis

Acuan Panduan Praktik Klinis Neurologi. Perdosi.2016.

 Kriteria diagnosis & DD
PF • SE konvulsif
Bangkitan dengan durasi > 5 menit, atau
bangkitan berulang 2 klai atau lebih tanpa
pulihnya kesadaran diantara bangkitan
• SE non konvulsif
Bangkitan epileptik berupa perubahan
kesadaran maupun perilaku tanpa disertai
manifestasi motorik yang jelas namun
didapatkan aktivitas bangkitan elektrografik
pada perekaman EEG, dapat didahului oleh
status epileptikus konvulsivus

• DD: sinkop, bangkitan non epileptik

psikogenik, aritmia jantung, sindroma
hiperventilasi atau serangan panik
Acuan Panduan Praktik Klinis Neurologi. Perdosi.2016.
 Tatalaksana

Stadium 1 • Diazepam 10 mg IV bolus lambat dalam 5 menit, • Berikan oksigen

(0-10 stop jika kejang berhenti, jika masih kejang dapat • Periksa fungsi kardiorespirasi
menit) diulang 1x lagi atau Midazolam 0,1 mg/kgBB IM • Pasang infus
• Pertahankan patensi jalan napas dan resusitasi

Stadium 2 • Monitor pasien • Berikan glukosa (D50% 50 ml) dan/atau thiamin

(0-30 • Pertimbangkan kemungkinan kondisi non epileptik 250 mg iv bila ada kecurigaan penyalahgunaan
menit) • Pemeriksaan emergensi laboratorium alkohol atau defisiensi nutrisi
• Terapi asifosis bila terdapat asidosis bera

Stadium 3 • Pastikan etiologi • Phenytoin iv dosis 15-18 mg/kg dengan kecepatan

(0-60 • Siapakan untuk rujuk ke ICU pemberian 50 mg /menit dan /atau bolu
menit) • Identifikasi dan terapi komplikasi medias ynag Phenobarbital 10-15 mg/kg iv dengan kecepatan
terjadi pemberian 100mg/menit
• Vasopressor bila diperlukan

Stadium 4 • Pindah ke ICU

(30-90 • Anestesi umum dengan dalah satu obat dibwah ini:
menit) • Propofol 1-2 mg /kgBB bolus, dilanjutkan 2-10 mg/kg/jam dititrasi naik sampai SE terkontrol
• Midazolam 0,1-0,2 mg/kg bolus, dilajutkan 0,05-0,5 mg/kg/jam dititrasi naik sampai SE terkontrol
• Thiopental sodium 3-5mg/kg bolus, dilanjutkan 3-5 mg/kg/jam dititrasi naik sampai terkontrol
• Perawatan intensif dan monitor EEG
• Monitor TIK bila perlu
• Berikan antiepilepsi rumatan jangka panjang

Acuan Panduan Praktik Klinis Neurologi. Perdosi.2016.

TATALAKSANA

Drislane FW et al. Neurology. Blueprints. 3 rd ed Philadelphia: Lippincot:

Williams & Wilkins, 2009.
 Pra Rumah Sakit Rumah Sakit
Stabilisasi ABC
Stabilisasi Terminasi
ABC bangkitan Ekplorasi etiologi, manajemen komplikasi, tatalaksana
penyebab
Sesuai Terminasi bangkitan
kemampuan
Lini kedua
penolong
Lini pertama -Fenitoin iv Lini ketiga:
Lini pertama
Benzodiazepin: -Fosfenitoin iv -phenobarbital
Benzodiazepin:
-Fenobarbital iv iv
-Diazepam -Midozolam im
rektal -asam valproat -Tiopebtal iv
-Diazepam iv iv
-midazolam -Midazolam iv
-Lorazepam iv -levetricetam iv
intranasal, -Propofol iv
intrabukal Topiramat oral

Bangkitan konvulsif berhenti

Monitoring EEG untuk mendeteksi
Aninditha A, Wiratman W. Buku ajar neurologi. Buku 1. Jakarta: Departemen
Neurologi FKUI, 2017
bangkitan elektrografik
Kesimpulan dan saran kasus
pemicu
Kesimpulan
Kami telah mempelajari mengenai kagawatdaruratan neurologi
akibat infeksi, kelainan metabolic, kelainan vascular serta epilepsy
dan status epileptikus.

Saran
Pasien dianjurkan untuk melakukan pemeriksaan penunjang lebih
lanjut untuk mengetahui penyebab keluhannya dan dokter
melakukan tatalaksana awal sesuai penyebab keluhan pasien.
 DAFTAR PUSTAKA
• Ropper AH, Samuels MA, Klein JP. Adams and victor’s principles of neurology. 10th ed. New York: McGraw-
Hill Education; 2014.
• Simon RP, Greenberg DA, Aminoff MJ. Clinical neurology. 7th ed. New York: The McGraw-Hill Companies
Inc.; 2009.
• Drislane FW, Benatar M, Chang BS, Acosta J, Tarulli A, Caplan LR. Blueprints neurology. 3rd ed.
Philadelphia: Lippincott Williams & Wilkins; 2009.
• Vojvodic M, Young A, editors. Toronto notes 2014. Toronto: Toronto Notes for Medical Students Inc.; 2014.
• Stafstrom CE. The pathophysiology of epileptic seizures: a primer for pediatricians. Pediatrics in Review.
1998 Oct;19(10):342-51.
• PERDOSSI. Advanced neurology life support: student course manual. Indonesian Neurological Association.
• Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors. Harrison’s principle of internal
medicine. 18th ed. USA: The McGraw-Hill Medical; 2012.
• Pusponegoro HD, Widodo DP, Ismael S, editors. Konsensus penatalaksanaan kejang demam. Jakarta: Unit
Kerja Koordinasi Neurologi Ikatan Dokter Anak Indonesia; 2006.