Problem 4

STROKE
• Ischemic Stroke
• Hemorrhagic Stroke
Classification by Location

Clinical emergency medicine, Lange. p. 347-52

Clinical emergency medicine, Lange. p. 347-52
STROKE :
RADIOLOGY

Clinical emergency medicine, Lange. p. 347-52

Clinical emergency
medicine, Lange. p.
347-52
Rosen’s emergency medicine, 8th ed. p. 1363-74
Transient Ischemic Attack
• An episode of focal cerebral ischemia that resolves fully and rapidly, usually
within 1 hour
• Investigations :
• Blood tests (complete blood count, prothrombin and partial
thromboplastin time, ESR, treponemal test for syphilis, glucose)
• ECG, Echocardiography
• MRI with diffusion-weighted imaging or CT scan
• MR angiography, CT angiography, or Doppler ultrasonography

Greenberg DA, Aminoff MJ, Simon RP.. Clinical Neurology. 8th ed. USA: McGraw-Hill; 2012.
Kasper DL, Hauser SL, Jameson JL,
Fauci AS, Longo DL, Loscalzo S,
editors. Harrison’s Principles of
Internal Medicine. 19th ed.
McGrawHill; 2015.
Treatment :
• Anticoagulation with heparin
given by continuous
intravenous infusion
followed by warfarin given
orally daily
• Antiplatelet therapy with
aspirin/dipyridamole
• Statins  atorvastatin 80 mg
orally daily
• Carotid endarterectomy
• Carotid artery stenting
• Intracranial artery stenosis

Greenberg DA, Aminoff MJ, Simon RP.. Clinical Neurology. 8th ed. USA: McGraw-Hill; 2012.
Hemorrhagic stroke
• Hemorrhagic stroke - 13 percent of stroke cases.
• It results from a weakened vessel that ruptures and bleeds into the surrounding brain. The blood
accumulates and compresses the surrounding brain tissue. The two types of hemorrhagic strokes
are intracerebral (within the brain) hemorrhage or subarachnoid hemorrhage.
• Hemorrhagic stroke occurs when a weakened blood vessel ruptures. Two types of weakened
blood vessels usually cause hemorrhagic stroke: aneurysms and arteriovenous malformations
(AVMs).
• An aneurysm is a ballooning of a weakened region of a blood vessel. If left untreated, the
aneurysm continues to weaken until it ruptures and bleeds into the brain.
• An arteriovenous malformation (AVM) is a cluster of abnormally formed blood vessels. Any
one of these vessels can rupture, also causing bleeding into the brain.
• Medications used in the treatment of acute stroke include the following:
• Anticonvulsants - To prevent seizure recurrence
• Antihypertensive agents - To reduce BP and other risk factors of heart disease
• Osmotic diuretics - To decrease intracranial pressure in the subarachnoid space
• the AHA/ASA recommendations for treating elevated BP are as follows[3] :
• If systolic BP is over 200 mm Hg or mean arterial pressure (MAP) is over 150 mm
Hg, then consider aggressive reduction of BP with continuous IV infusion; check BP
every 5 minutes
• If systolic BP is over 180 mm Hg or MAP is over 130 mm Hg and intracranial
pressure may be elevated, then consider monitoring intracranial pressure and
reducing BP using intermittent or continuous intravenous medications, while
maintaining a cerebral perfusion pressure of 60 mm Hg or higher
• If systolic BP is over 180 or MAP is over 130 mm Hg and there is no evidence of
elevated intracranial pressure, then consider modest reduction of BP (target MAP of
110 mm Hg or target BP of 160/90 mm Hg) using intermittent or continuous
intravenous medications to control it, and perform clinical reexamination of the
patient every 15 minutes
• In patients presenting with a systolic BP of 150 to 2 20 mm Hg, acute lowering of
systolic BP to 140 mm Hg is probably safe
Hypertensive Encephalopathy
Hypertensive encephalopathy is a true hypertensive emergency
and is a manifestation of diffuse vasogenic cerebral edema. It is
caused by a failure of autoregulation in the brain, with vasospasm,
ischemia, increased vascular permeability, punctate hemorrhages,
and interstitial edema.
The patient generally has severe headache, vomiting, and altered
mental status, which may progress to seizures or coma. Retinal
involvement may cause blurred vision progressing to complete
blindness

Rosen.8ed
Rosen.8ed
nicardipine and labetalol produce an even reduction in
resistance across vascular beds and have become the
agents of choice for patients with hypertensive
encephalopathy.

Rosen.8ed
Rosen.8ed
Rosen.8ed
Meningitis
• Meningitis is a clinical syndrome characterized by inflammation of the meninges.
• The classic triad of bacterial meningitis consists of the following:
• Fever
• Headache
• Neck stiffness
• Other symptoms can include nausea, vomiting, photalgia (photophobia),
sleepiness, confusion, irritability, delirium, and coma. Patients with viral
meningitis may have a history of preceding systemic symptoms (eg, myalgias,
fatigue, or anorexia).
• The examination should evaluate the following:
• Focal neurologic signs
• Signs of meningeal irritation
• Systemic and extracranial findings
• Level of consciousness
• In chronic meningitis, it is essential to perform careful general, systemic,
and neurologic examinations, looking especially for the following:
• Lymphadenopathy
• Papilledema
• Meningismus
• Cranial nerve palsies
• Other focal neurological signs
• The diagnostic challenges in patients with clinical findings of
meningitis are as follows:
• Early identification and treatment of patients with acute bacterial meningitis
• Assessing whether a treatable CNS infection is present in those with
suspected subacute or chronic meningitis
• Identifying the causative organism
• Blood studies that may be useful include the following:
• Complete blood count (CBC) with differential
• Serum electrolytes
• Serum glucose (which is compared with the CSF glucose)
• Blood urea nitrogen (BUN) or creatinine and liver profile
• Initial measures include the following:
• Shock or hypotension – Crystalloids
• Altered mental status – Seizure precautions and treatment (if necessary), along with
airway protection (if warranted)
• Stable with normal vital signs – Oxygen, IV access, and rapid transport to the
emergency department (ED)
• Treatment of bacterial meningitis includes the following:
• Prompt initiation of empiric antibacterial therapy as appropriate for patient age and
condition
• After identification of the pathogen and determination of susceptibilities, targeted
antibiotic therapy as appropriate for patient age and condition
• Steroid (typically, dexamethasone) therapy
• In certain patients, consideration of intrathecal antibiotics
• The following systemic complications of acute bacterial meningitis
must be treated:
• Hypotension or shock
• Hypoxemia
• Hyponatremia
• Cardiac arrhythmias and ischemia
• Stroke
• Exacerbation of chronic diseases
• Fungal meningitis - Cryptococcal (amphotericin B, flucytosine,
fluconazole),Coccidioides immitis (fluconazole, amphotericin B,
itraconazole),Histoplasma capsulatum (liposomal amphotericin B,
itraconazole), orCandida (amphotericin plus 5-flucytosine)
• Tuberculous meningitis (isoniazid, rifampin, pyrazinamide,
ethambutol, streptomycin)
• Parasitic meningitis (amebic [ Naegleria fowleri] or acanthamebic) -
Variable regimens
• Lyme meningitis (ceftriaxone; alternatively, penicillin G, doxycycline,
chloramphenicol)
Ensefalitis viral
• Virus herpes simpleks adl penyebab tersering ensefalitis • Immunoassay Ag virus & PCR u/ amplifikasi DNA
sporadik virus
• Invasi virus pd otak dpt menyebabkan reaksi inflamasi • EEG menunjukkan kelainan dng bukti disfungsi otak
limfositik dng nekrosis neuron & sel glia difus. Gambaran khas : kompleks periodik yg dpt
terjadi pd regio temporalis
• Gambaran klinis :
• Nyeri kepala • Tatalaksana :
• Demam • Acyclovir 10mg/kgBB IV tiap 8 jam selama 14 hari
• Pada kecurigaan adanya CMV diberi gancyclovir
• ↓ tingkat kesadaran dlm berberapa jam atau hari
• Dpt terjadi kejang & tanda neurologis fokal yg • Terapi suportif : antikonvulsan u/ kejang &
mungkin menunjukkan disfungsi hemisfer serebri deksametason atau manitol u/ edema serebri
atau batang otak
• Tanda hemisferik (disfasia, hemiparesis)
• Pemeriksaan penunjang :
• CT scan & MRI otak dpt menyingkirkan
kemungkinan lesi massa & menunjukkan edema
otak
• Terjadi ↑ tekanan cairan serebrospinal biasanya
disertai dng limfositosis, ↑ protein, & kadar
glukosa yg normal
Lecture notes neurology. 8th ed. 2007
Kejang Demam
• Bangkitan kejang yg terjadi pada kenaikan suhu tubuh • Kejang berbentuk umum tonik & atau klonik,
(suhu rektal di atas 380 C) yang disebabkan oleh suatu tanpa gerakan fokal
proses ekstrakranium • Kejang tidak berulang dalam waktu 24 jam
• Kejang biasanya singkat, berhenti sendiri, kejang timbul • Kejang demam sederhana merupakan 80% di
dalam 24 jam setelah ↑ suhu badan akibat infeksi antara seluruh kejang demam
diluar susunan saraf • Kejang demam kompleks (Complex febrile seizure)
• Bangkitan kejang dpt berbentuk tonik klonik,tonik, • Kejang lama > 15 menit
klonik, fokal atau atonik • Kejang fokal atau parsial satu sisi, atau kejang
• Faktor Risiko : umum didahului kejang parsial
• Riwayat kejang demam dalam keluarga • Berulang atau lebih dari 1 kali dalam 24 jam
• Pemulangan neonatus >28 hari
• Keterlambatan perkembangan
• Temperatur tinggi
• Klasifikasi :
• Kejang demam sederhana (Simple febrile seizure)
• Berlangsung singkat, <15 menit, & umumnya
akan berhenti sendiri

http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
Kejang Demam
• Kriteria diagnosis : • Tatalaksana :
• Timbul 24 jam stelah ↑ suhu badan • Kejang  dirumah (diazepam per rektal)  beri
• Pemeriksaan saraf sebelum & sesudah kejang obat ↓ panas
normal • Di RS : diazepam IV, kecepatan 0,5-1 mg/menit (3-
• Pemeriksaan EEG yg dibuat sedikitnya 1 mnggu 5mnt)  kejang (fenitonin bolus IV 10-20
setelah suhu normal tidak memperlihatkan mg/kgBB)
kelainan • Diazepam rektal 0,5 mg/kgBB
• Frekuensi serangan kejang dalam 1 tahun tidak > • BB < 10 kg : 5 mg
dari 4 kali • BB > 10 kg : 10 mg
• Pada anak yg kejang & menderita demam, harus • Diazepam IV 0,3 -0,5 mg/kgBB
disingkirkan kemungkinan infeksi susunan saraf
pusat sentral & selaputnya
• Pemeriksaan penunjang :
• Pemeriksaan lab : u/ mengetahui sumber infeksi
penyebab demam, atau keadaan lain misalnya
gastroenteritis dehidrasi disertai demam
• Pemeriksaan lab : darah perifer, elektrolit dan gula
darah

Penuntun neurologi, Soemarmo Markam

http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
Tetanus
• Disebabkan oleh neurotoksin clostridium tetani • Disfungsi otonom demam, tekanan darah tdk
(anaerobik gram positif bacillus) stabil, diaphoresis & aritmia
• Portal of entry luka trauma, surgikal, injeksi, skin • Pemeriksaan laboratorium : CSF analisis
ulcer, luka bakar, & plasenta yg terinfeksi
• Diagnosis : mengobservasi tanda-tanda spesifik gejala
• Jaringan nekrosis & supurasi  bakteri masuk tetanus
produksi toksin (tetanospasmin) dibawa oleh • DD : neuroleptik-induced dystonia, meningitis, dental
terminal N.periferke atas spinal cord/batang abses, status epileptikus, pendarahan subarachnoid,
otaktetanospasmin menghambat inhibitor hipokalemik tetani, sedative or opiate withdrawal &
interneuron discharge motor neuron >>  disfungsi rabies
otonomik
• Tanda & gejala :
• Masa inkubasi 7-21 hari
• Gejala awal : trismus, kaku pada leher & otot
paraspinal
• Kekakuan bisa menyebar ke ekstremitas, otot muka
(rizuz sardonicus)
• Paraspinal rigidity  opisthotonus
• Otot pharingeal spasmedisfagia
• Otot laryngeal & pernapasan spasme asifiksia
Tetanus
• Prognosis : pernapasan): diberikan ventilator (endotrcheal
• Berlanjut sampai 2 minggu setelah pemberian intubasi & trakeostomi)
antitoksin • Benzodiazepine (vecuronium 6-8 mg/jam) :
• Tetanus yg parah  membutuhkan wkt bbrp mengontrol spasme & sedasi (spasme parah)
minggu utk penyembuhan • Magnesium sulfat
• Angka kematian 25% • Labetalol 0,25 – 1 mg/menit  utk HT
• Komplikasi : • Verapamil  takikardi
• Patah tulang • Pencegahan :
• Dehidrasi • Imunisasi DPT bulan ke 2,4,6 & 15 bulan dan 4-6
• Pneumonia tahun
• Emboli pulmonal • Booster imunisasi tiap 10 tahun
• Treatment : • Imunisasi pasif dgn human tetanus Imunoglobulin
• ICU direkomendasi utk luka yg beresiko infeksi tetanus
• Lukanya di bersihkan setelah pemberian HTIG (luka yg terkontaminasi tanah, feses, saliva)
(human tetanus immune globulin) 3000-6000 unit
diberikan pada satu ekstremitas & tetanus toksoid
pada bagian ekstremitas yg lain
• Metronidazole 2g/hr selama 7-10 hari
• pasien dgn tetanus spasme (gangguan
Tetanus Neonatorum
• Tanda & gejala : spontan  resusitasi, & jika belum berhasil dirujuk
• Terjadi pada usia 3-14 hari ke RS yg punya fasilitas NICU
• Bayi rewel • Jika ada, beri human tetanus immunoglobulin 500
• Kesulitan menyusu IU IM atau tetanus antitoksin 5 000 IU IM
• Tetanus toksoid 0.5 mL IM diberikan pada tempat
• Mulut mencucu/trismus
yg berbeda dng tempat pemberian antitoksin
• Otot-otot mengalami kekakuan
• Penisilin prokain 50 000 IU/kgBB/hari IM dosis
• Kejang tunggal atau Metronidazol IV selama 10 hari
• Tatalaksana : • Jika tjd kemerahan &/atau pembengkakan pd kulit
• Pasang jalur IV & beri cairan dng dosis rumatan sekitar pangkal tali pusat, atau keluar nanah dari
• Beri diazepam 10 mg/kgBB/hari IV dalam 24 jam permukaan tali pusat, atau bau busuk dari area tali
atau bolus IV tiap 3 jam (0.5 mL/x pemberian), pusat, berikan pengobatan untuk infeksi lokal tali
maks 40 mg/kgBB/hari pusat
• Jika jalur IV tdk terpasang, berikan diazepam mll
rektum
• Jika frekuensi napas < 20 x/menit, obat dihentikan,
meskipun bayi masih alami spasme
• Jika bayi alami henti napas selama spasme atau
sianosis sentral setelah spasme, beri O₂ dng
kecepatan aliran sedang. Jika belum bernapas
WHO, Buku Saku Pelayanan Kesehatan Anak di Rumah Sakit, 2009
Koma
• Hilangnya kemampuan pasien u/ memberi respon yg
dpt dimengerti thd rangsangan dr luar atau thd
kebutuhan dr dalam
• Ps tdk dpt dibangunkan, matanya tertutup & tdk
menjawab thd rangsangan suara maupun nyeri
• Etiologi :
• Kelainan struktur intrakranial (koma diensefalik)
• Lesi supratentorial
• Herniasi uncal atau sentral transtentorial
yg menyebabkan penekanan bag otak ke
arah bawah & tjdnya gagal fungsi rostro-
caudal batang otak
• Lesi infratentorial
• Herniasi otak ke atas (transtentorial) atau
ke bawah (melalui foramen magnum)
• Penyebab lesi bs stroke, trauma
perdarahan, abses cerebri, trabekuloma,
dll
• Kelainan bihemisferik (koma metabolik)
• Hipoglikemia, krisis hiperglikemik, gangguan
elektrolit, kejang/status epileptikus,
intoksikasi, endokrinopati, infeksi CNS,
penggunaan dosis obat berlebihan
• Manajemen koma :
• Menentukan tidak adanya respons :
• Observasi : mata tertutup, immobilitas,
ekspresi wajah berkurang
• Penilaian respons u/ tingkat rangsangan :
rangsangan verbal, taktil & nyeri
• Menilai jalan napas, pernafasan & sirkulasi.
Penanganan mengikuti modul ABC (airway,
breathing, & circulation)
• Pemeriksaan bg kepala, leher, dada, abdomen, &
ekstremitas. Cervical spine di immobilisasi jika
curiga tjd trauma
• Pemeriksaan GDS : jika < 70mg/dL, diberikan
dextrose 50% 25 mL bersama thiamine 100 mg IV
Koma
• Jika curiga adanya toxidrome opiod (rw narkoba, • Respons motorik :
koma, bradipnea, konstriksi pupil), diberikan • Pergerakan spontan : lihat adanya suatu
naloxone 0.4-0.8 mg IV & diulang jika perlu asimetri
• Pemeriksaan neurologis pd ps tidak sadar meliputi • Pemeriksaan tonus otot
3 bagian : • Induksi pergerakan melalui :
• Tingkat kesadaran : GCS  kesadaran penuh • Perintah verbal
skor 15, koma skor 3
• Rangsang nyeri
• Pemeriksaan batang otak
• Pupil : pastikan bentuk, ukuran, & reaksi • Pernafasan : pola pernafasan yg abnormal dpt
pupil thd rangsang cahaya membantu menentukan lokalisasi dr koma
• Refleks kornea : menandakan intaknya • Tes laboratorium :
batang otak pons • Kimia darah
• Refleks okulosefalik (doll’s eye), respons yg • Darah lengkap
intak tjd pergerakan bola mata • BGA (Arterial Blood Gas)
berlawanan dr arah pemutaran kepala
• Tingkat alkohol dalam darah
• Refleks okulovestibular (kalori dingin)
• Urinalisis, kultur darah, kultur urin
• Refleks muntah : dpt dilakukan dng
memanipulasi endotracheal tube
• Refleks batuk
Delirium
• Delirium, acute confusional state, acute cognitive impairment, acute encephalopathy, altered mental status, and
other synonyms all refer to a transient disorder with impairment of attention and cognition.
• The patient has difficulty focusing, shifting, or sustaining attention.
• Pathologic mechanisms producing delirium are complex and are thought to involve widespread neuronal or
neurotransmitter dysfunction. There are four general causes :
• Primary intracranial disease
• Systemic diseases secondarily affecting the CNS
• Exogenous toxins
• Drug withdrawal
• Environmental manipulations such as adequate lighting, psychosocial support, and mobilization may be helpful in
enhancing the patient’s ability to interpret the surroundings correctly.
• Haloperidol is a frequent initial choice at a dose of 5 to 10 milligrams PO, IM, or IV with reduced dosing of 1 to 2
milligrams in the elderly. Repeat at 20- to 30-minute intervals as needed.
• Benzodiazepines such as lorazepam, 0.5 to 2.0 milligrams PO, IM, or IV, may be used in combination with
haloperidol in doses of 1 to 2 milligrams, with the dose varying widely depending on the age and size of the
patient and the degree of agitation