Kegawatdaruratan Neurologi

dr. Fidha Rahmayani, M.Sc, Sp.S

 Latar belakang
 Sebagian besar kasus neurologi merupakan
kasus emergensi.
 Morbiditas dan mortalitas yang masih tinggi.
 Penyebab kecacatan tertinggi, misalnya
stroke penyebab kematian ke 3.
 Prevalensi meningkat:
– Trauma kranioserebral  peningkatan
angka kejadian kecelakaan lalulintas
– Kasus infeksi SSP ≈ HIV/AIDS
 Otak merupakan organ tubuh yang
mempunyai tingkat metabolisme yang
tinggi.
 Kemampuan regenerasi jaringan saraf
minimal.
 Golden period sangat singkat.
 Perlu penanganan secara cepat dan tepat
untuk menghindari kerusakan yang lebih
berat atau gangguan fungsi permanen.
 Konsep Dasar Neuroemergensi
 Hal yang sangat mengancam nyawa dan
fungsi neurologi merupakan prioritas utama.
 Kegagalan dalam menegakkan diagnosis
definitif jangan sampai menghalangi
penanganan awal.
 Perolehan riwayat penyakit yang rinci
tidaklah diperlukan untuk memulai evaluasi
dan tindakan emergensi terhadap pasien
dengan gangguan neurologi akut.
 Klasifikasi Neuroemergensi
Kondisi yang terjadi Contoh kelainan
Derajat 1
Benign headache Serangan Migren
Kehilangan penglihatan sesisi (non- Neuritis Optika
vascular)
Brain death SAH derajat V
Derajat 2
Demam & perubahan status mental Ensefalitis arbovirus
Hemianopia homonim akut Perdarahan amiloid angiopati
Derajat 3
Hemiplegia akut Emboli serebral akut
Kehilangan penglihatan sesisi Emboli arteri sentralis retina
(vascular)
Paraparesis akut Kompresi medula spinalis
Hemianopia homonim akut Emboli serebral akut
 Lanjutan…………
Kondisi yang terjadi Contoh kelainan
Derajat 4
Gagal nafas Myasthenia gravis
Neuromuskular
Herniasi serebri Perdarahan serebelum
Kejang menetap Status epilepticus
Sakit kepala “malignant” SAH
Demam & meningismus Meningitis bakterial
Fever & perubahan Ensefalitis Herpes
kesadaran
 Ruang lingkup Neuroemergensi
Semua penyakit saraf atau simptom yang berhubungan dengan
penyakit saraf yang berpotensi/mengancam terjadinya kecacatan
atau kematian bila tidak segera diobati/ diatasi, meliputi:
1. Basic Life Support /Advance Life Support
2. Kesimbangan asam basa dan elektrolit
3. Terapi oksigen
4. Gangguan kesadaran dan Mati Batang Otak
5. Kejang dan status epileptikus
6. Peningkatan Tekanan Intrakranial
7. Stroke
8. Trauma kapitis dan medula spinalis
9. Kegawatan neuromuskular
10. Kegawatan infeksi Sususnan Saraf Pusat
11. Nyeri dan Nyeri kepala emergensi
 Kebutuhan glukosa dan oksigen otak
 Otak memerlukan 6 ml/100gr jar. otak/menit oksigen
untuk subs. nigra
 2 ml/100gr jaringan otak/menit untuk substansia alba
 Kebutuhan glukosa 4.5 - 7 mg/100 gr jar. otak/menit.
 Terbentuk fosfat berenergi tinggi yaitu ATP dan ADP,
melalui citric acid cycle dan rantai transport elektron
mitokhondria
 Dalam keadaan normal tidak terjadi penguraian glukosa
secara anaerobik
 Otak menuntut sekitar 20% dari seluruh output jantung,
yaitu sekitar 800 ml/menit
 Metabolisme Serebral
 Jaringan otak merupakan jaringan dengan
tingkat metabolisme tinggi, meskipun pada
area dengan densitas kapiler yang rendah.
 Fungsi sel otak sangat tergantung pada
ketersediaan O2 & energi (glukosa) yang
kontinyu.
 Tidak ada cadangan O2 dan sumber energi di
otak.

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Neuro Emergensi
Status epileptikus
Status epileptikus (perdossi, 2007)
• Bangkitan yang berlangsung lebih dari 30
menit, atau adanya dua bangkitan atau lebih
dimana diantara bangkitan-bangkitan tadi
tidak terdapat pemulihan kesadaran.
• Penanganan bangkitan harus dimulai dalam
10 menit pertama setelah bangkitan atau
awitan.
 Status Epileptikus

• Bangkitan > 30 menit

• Atau adanya 2 bangkitan atau lebih
dimana diantaranya tidak terdapat
pemulihan kesadaran

Pedoman Tatalaksana Epilepsi Pokdi Epilepsi Perdossi 2006

 Klasifikasi status epileptikus

1. Status epileptikus konvulsif (bangkitan umum

tonik klonik)
2. Status epileptikus non-konvulsif ( bangkitan
umum bukan tonik klonik
Status epileptikus konvulsif

• Hilangnya kesadaran
• Kejang berulang atau berlanjut
• Gambaran aktifitas iktal secara umum pada
EEG
Status epileptikus konvulsif lanj…

• Kegawatan medis
• Mortalitas dan morbiditas yang tinggi
• High morbidity and mortality
• Pseudostatus
– Pschogenic SE
– Iatrogenic complication: IV BZDs, barbiturates or
anesthetics
– Supresi pernafasan dan hipotensi
Non konvulsif Status Epileptikus
Dapat ditemukan pada 1/3 kasus status
epileptikus
• Dapat dibagi menjadi SE lena, SE
parsial kompleks, SE nonkonvulsif
pada pasien dengan koma, dan SE
pada gangguan belajar
Terapi SE nonkonvulsif

Tipe Terapi pilihan Terapi lain

SE lena Benzodiazepine Volproate IV

IV/Oral

SE parsial kompleks Klobazal oral Lorazepam/phenitoine/

phenobarbital
SE lena atipikal Valproate oral Benzodiazepine ,lamotrigine,
topiramate, methylphenidate,
steroid oral

SE tonik Lamotrigine oral Methylphenidate oral

SE nonkovulsifus Phenytoin IV atau Anestesia dengan thiopentone,

pada pasien koma phenobarbital pentobarbital, propofol atau
midazolam
 Generalized v.s. Partial NCSE

• Generalized
– Ends abruptly without postictal abnormality
• Partial
– Associated with postictal confusion, depression,
or general malaise
Faktor Pencetus Status Epileptikus

• Kelelahan.
• Menderita penyakit lain yang berat.
• Penggunaan obat anti epilepsi yang tidak
sesuai aturan.
• Penggunaan obat-obatan, minum alkohol.
Prinsip Penanganan Status Epileptikus

• Stabilisasi pasien dengan prinsip ABC’s.

• Hentikan bangkitan dan cari etiologi secara
simultan.
• Cegah bangkitan ulang atau atasi penyulit.
• Atasi faktor pencetus.
• >60’  refrakter  rawat ICU.
Algoritma penanganan status epileptikus

NEJM, 1998
Penanganan
SE konvulsif
Perdossi, 2007
 Manajemen Status Epileptikus

Stadium 2 Stadium 3

Stadium 1 Px Neurologis Etiologi

EKG Kejang(+) 
Airway Px darah phenitoin
Breathing Dzpm 10 – 20 mg iv 15-18mg/kg iv
Circulation ( < 2-5 mg/mnt ) (kecp 50mg/mnt)
Koreksi Asidosis Vasopresor kp
( 0 – 10 menit ) 50cc Glukosa 50% Koreksi komplikasi

(1 -60 menit ) (0 – 90 menit )

Pedoman Tatalaksana Epilepsi Pokdi Epilepsi Perdossi 2006

Manajemen Status Epileptikus
Stadium 4

Bila Kejang (+) selama 30 – 60mnt

 ICU  propofol 2mg/kg bolus iv

Atau
Thiopentone 100-250mg bolus iv dlm 20mnt 
Bolus 50mg tiap 2 – 3 mnt
Tappering stlh bangkitan (-)

Pemberian rumatan

(30 – 90 menit )

Pedoman Tatalaksana Epilepsi Pokdi Epilepsi Perdossi 2006

Status epileptikus refrakter
• 80% pasien dengan SE konvulsif terkontrol
dengan pemberian benzodiazepine atau
phenytoin. Bila bangkitan masih berlangsung
disebut sebagai status epileptikus refrakter 
ICU
untuk tindakan anestesi.
Tindakan anestesi untuk status epileptikus (ICU)

Obat Dosis dewasa

Midazolam 0,01-0,1 mg/kg BB dengan kecepatan pemberian
4mg/menit dilanjutkan dengan pemberian 0,5-0,4
mg kg BB/ jam melalui infus
Thiopenthone 100-250 mg bolus, diberikan dalam 20 detik.
Kemudian dilanjutkan dengan bolus 50 mg setiap
2-3 menit sampai bangkitan teratasi kemudian
dilanjutkan pemberian dalam infus 3-5
mg/kgBB/jam
Pentobarbital 10-20 mg/kgBB dengan kecepatan 25 mg/menit,
kemudian 0,5-1mg/jam

Propofol 2 mg/kgBB kemudian ditingkatkan menjadi 5-

10mg/kgBB/jam
Penanganan epilepsi refrakter

• Terapi bedah
• Stimulasi nervus vagus
• Modifikasi tingkah laku
• Relaksasi
• Mengurangi dosis OAE
 Epilepsy – Surgical Treatment
• A proportion of the pts with intractable epilepsy will
benefit from surgery.
• Epilepsy surgery procedures: Curative (removal of
epileptic focus) and palliative (seizure-related risk
decrease and improvement of the QOL)
• Curative (resective) procedures: Anteromesial temporal
resection, selective amygdalohippocampectomy,
extensive lesionectomy, cortical resection,
hemispherectomy.
• Palliative procedures: Corpus callosotomy and Vagal
nerve stimulation (VNS).
 Guiilain Barre Syndrome (GBS)

Definisi:
GBS atau AIDP atau acute ascending paralysis atau Landry-Guillain-Barre-
Strohl syndrome atau polyneuritis pasca infeksi merupakan suatu kondisi
polineuropati yang akut dan progresif dengan kelemahan otot yang
asenderen dan arefleksia, terjadi akibat proses autoimmune dengan
respon inflamasi pada radiks dan saraf tepi ( poliradikulopati dan
polineuropati ).Keadaan ini berlangsung sangat cepat dalam beberapa
hari sampai beberapa minggu ( David S,2001 )

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33
Clinical Picture of Polyneuropahty (Valenstein, 2000)
Lower before upper extremity; distal first (feet)
Decreased ankle jerks
Stocking, then glove sensory loss
Distal more severe than proximal (Impairment of neurotransmission is more severe in
long nerve, because of the confrontation from greater number of demyelinated
segments (Wilkinson, 1997)

Back
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 GBS=heterogenous syndrome w/ variant
forms
• Think of AIDP as the traditional form as described
previously, accts for 85-90%
• Miller Fisher Syndrome: opthalmoplegia, ataxia, and
areflexia (5%). GQ1b antibody. Only 1/4th w/
extremity weakness
• AMAN: selective involv of motor nerves, DTRs are
preserved, more common in Japan/China, almost all
preceded by Campylobacter infxn
• AMSAN: more severe form of AMAN +sensory
 Mekanisme GBS

•Generally accepted that GBS has an autoimmune pathogenesis

•Involving both cellular and humoral mechanisms
•Cytokines have an important pathogenetic role
•Immune response in GBS may be directed against glycolipid
components of the axolemma and myelin sheath
•Antibodies to peripheral nerve constituents may activate the
complement cascade and macrophages
•Preceding Camplyobacter jejuni infection may initiate an antibody
response due to molecular mimicry between carbohydrate epitopes
present in the axolemma and the bacteria's lipopolysaccharide coat
•The immunologic response initially directed at the bacteria also attack
the myelin sheet because they look alike

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Nobuhiro Yuki, M.D. Guillain Barre Syndrome. N Engl J Med 2012;366:2294-
 Patofisiologi GBS (Seneviratne, 2000)

- Molecular
mimicry
Presence of lymphocyte of small vessels in the
endoneurium and perineurium
- Lymphocyte infiltration of the nerve
- Macrophage mediated segmental demyelinitation

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Viral Infections Influenza
Epstein - Barr virus
Cytomegalovirus
Hepatitis A, B
HIV
Bacterial Campylobacter jejuni
Infections Mycoplasma Pneumonia
Lyme
Salmonella
Listeria
Shigella
Vaccinations Influenza
Tetanus toxoid
Systemic Illness Sarcoidosis
Systemic lupus erythematosus
Lymphoma
Leukemia
Connective tissue disease
Miscellaneous Surgery
Trauma
Many drugs (only incidental reports
are known and all require
confirmation)
 Background of GBS
• Diagnosis of GBS

– Patient history-- previous illness or vaccination

– Clinical presentation (Physical Exam)
– Laboratory Evaluation
• Increase in protein in CSF
• Electromyography -- nerve conduction block
 Dissosiasi sitoalbumin
Reaksi inflamasi dan edema menimbulkan kompresi.
Terjadi transudasi protein serum ke dalam ruang
subarachnoid dan LCS.
Hal ini menimbulkan kenaikan karakteristik kadar protein
dalam LCS.
Hiperemi dan dilatasi pembuluh darah yang terjadi akibat
inflamasi menyebabkan pasokan protein lebih besar ke
LCS
The course of Guillain-Barré syndrome
(GBS) can be split up into 3 phases
Progressive phase

• This phase lasts typically 2-3 weeks, This point is known

as the 'nadir'.

• GBS patients develop the pain, progressive weakening

and sensory abnormalities that characterise this disease.
The symptoms increase in severity and extent in a very
unpredictable way, depending on how badly affected the
patient is. Cases of mild GBS reach a clinical nadir in a
similar time to those with more severe disease.

• The difference in severity of the syndrome seems to be

determined in this phase. Early treatment shortens the
transition to the recovery phase, and reduces the risk of
permanent physical damage. Treatments focus both on
reducing pain and symptoms
 Plateau phase
• A stable plateau phase, where neither worsening nor
improvement occurs. The attack has ceased, but the
degree of weakness remains unchanged until the
recovery phase begins.
• In this phase, emphasis is laid on supporting the
functions that are weakened or lost. The patient's blood
pressure, cardiac rhythm, respiration, nutritional and fluid
status and general status are monitored carefully.
Immunotherapy treatment begun in the progressive
phase continues.
• The patient is generally very weak and requires lots of
rest, skillful care and physiotherapy.
• The duration of the phase cannot be predicted with any
accuracy.
• It may be a few days or several months.
 Recovery Phase
• Finally, the long-awaited recovery phase begins, with
spontaneous improvement and recovery. The immune
system stops producing the antibodies that destroy myelin,
and the symptoms gradually disappear. Nerve healing
commences.

• Treatment during this phase focuses on physiotherapy, to

build up the patient's muscles, regain muscle movement and
strength, and teach the patient to use the muscles optimally.

• The duration of this phase cannot be predicted. Recovery is

individual, and may be achieved in a few weeks or after
several years. Relapses may occur. Many patients are able
to begin working again after 3-6 months, while others display
slight symptoms for a long time after recovery. The degree of
recovery depends on the severity of the nerve damage that
occurred in the infection phase.
Back
 Kriteria untuk merujuk GBS ke ICU

• Kapasitas vital pulmo <12 mL/kg

• Memburuknya kapasitas vital <18 hingga 20 mL/kg

• Tanda-tanda klinis kelemahan diafragmatika, termasuk

takipneu, diaphoresis dan nafas paradoksikal

• Batuk yang parah, kesulitan menelan, akumulasi sekresi,

pneumonia aspirasi

• Gambaran disautonomik kardiovaskuler mayor (fluktuasi

tekanan darah dan pulsus yang besar; aritmia; blok
jantung, edema paru, ileus dengan risiko rupture visceral)
 Kriteria untuk merujuk GBS ke ICU

• Hipotensi yang dipresipitasi oleh pertukaran

plasma atau pertukaran plasma yang
direncanakan pada pasien dengan ventilator atau
pasien yang tidak stabil

• Sepsis
• Emboli paru

Back
 Komplikasi ICU
• Perawatan di ICU  berminggu2-berbulan2
• Mayoritas sembuh dengan atau tanpa sequele
• Mortalitas 1-8 %

• Lama perawatan di Rumah Sakit disebabkan :

- komplikasi intubasi atau trakeostomi,
- pneumonia
- ISK
- Flebitis
- Perdarahan gastrointestinal,
- Emboli paru
Back
- Depressi psikologis
 Intubation
• Generally, intubation is required whenever the vital
capacity falls to 15 ml/kg
• Endotracheal intubation is complicated in patients
with GBS because of
– Dysautonomia
• Can result in marked hypotension, arrhythmias, and sudden
death due to various drugs and to airway manipulation
– Hyperkalemia
• Further potentiated by succinylcholine, which can cause
arrhythmias and cardiac arrest
 Indication for intubation (Lawn 2001)
• 1. Force Vital Capasity <15 ml/kg.
• 2. Oropharyngeal paresis with aspiration
• 3. Declining FVC over 6 hrs
• 4. Clinical signs of respiratory failure at FVC 15
ml/kg.
• (minimal insp press < 30 cm H2O, minimal eksp
press < 40 cm H2O)
Back
 Critical Care of GBS
• Patients with suspected GBS should be hospitalized,
regardless of how mild their disorder appears initially
– Rapid deterioration occurring over a brief period of time can
occur
• ICU admissions occurs in ~ 30% of GBS patients who are
hospitalized
• Patients must be assessed and monitored to avoid the
major life-threatening complications of GBS
– Respiratory failure
– Dysautonomia
– Venous thromboembolism
 Respiratory Failure
• The most serious complication and most common
• Weakness of the respiratory muscles, particularly the
diaphragm, is most often responsible
– Other factors include weakness of various bulbar-innervated
muscles and pulmonary complications, (atelectasis,
pneumonia, and pulmonary embolism)
• Assessment of respiratory function
– Arterial blood gas analysis
– Bedside spirometry: peak expiratory flow, maximum
inspiratory/expiratory pressures
– Vital capacity measurements (most useful)
 Fisiologi Gagal Nafas Neuromuskuler
Akut dan Subakut

• Kapasitas vital turun expiratory flow

rate turun  batuk tidak kuat  sulit
membersihkan sekresi paru

• Penurunan kapasitas paru lbh lanjut 

kolaps alveoli  shunting vaskuler
pulmoner  penurunan PaO2
Critical Care of GBS
 Dysautonomia
• Occurs more frequently and more severely
in GBS patients with respiratory failure and
severe motor deficits
• Difficult complications to manage include
– Severe paroxysmal hypertension
– Orthostatic hypotension
– Various cardiac arrhythmias
Disautonomi
 Venous Thromboembolism
• Pulmonary embolism occurs in about 5% of
patients immobilized with GBS
– Typically after the 2nd week of immobilization
• In one series, it was responsible for ~ 28% of
deaths
• Preventive measures include
– Subcutaneous heparin--switched to Coumadin if long-
term anticoagulation necessary
– Intermittent calf pneumatic compression devices
 Perubahan EKG dan Aritmia

• Perubahan segmen ST-T

• Abnormalitas gel T

• Peningkatan CPK pada 1/3 kasus (perlu

disingkirkan adanya iskemi)
• Frekuensi denyut jantung menurun,
beberapa pasien mengalami takikardia
• Aritmia banyak disebabkan oleh :
hipoksia, iskemia jantung atau emboli paru

• Winer & Hughes  penurunan denyut

jantung & hipertensi berat  aritmia yang
serius

• Blok jantung komplit, bradikardia, asistole

 pacu jantung
 SIADH
• Hiponatremia
• Therapi penambahan volume intravaskuler dan
natrium

Hipotensi

• Sering karena tirah baring yang lama

• Dehidrasi
• Ventilator tekanan positif
• Suction, Stimulasi vagal
• Therapi cairan atau vasopressor (fenilefrin)
 Hipertensi

• Kematian mendadak, perdarahan subarachnoid, kejang,

edema paru, ensefalopati hipertensi
• MAP > 125  Tx. Inj Labetolol iv, esmolol atau infus
nitroprusside
• Beta adrenergik, Ca Channel Blocker  hipotensi yang
berlebihan

Gagal Nafas

• Kelemahan otot diafragma

• Sebelum ada tx imun  1/3 kasus memerlukan ventilator
 Other Complications
• Neurogenic bladder / Urinary tract infections
• Gastrointestinal disorders
– Bleeding secondary to stress ulcers and erosive gastritis
– Ileus and fecal impaction
• Hyponatremia
– Usually in ventilated patients
– Due to inappropriate release of antidiuretic hormone
– Responds to fluid restriction
• Complications of protracted paralysis
• Non-life-threatening complications
– Pain and psychological trauma
Back
 Plasmapharesis

Plasmapheresis, or Plasma Exchange (PE) is a

mechanical process that involves the exchange of plasma
and removal of disease-causing antibodies from the
patients blood. It appears to reduce both the duration and
severity of the disease.
The method resembles dialysis slightly.
PE is proven more beneficial when started within seven
days after disease onset rather than later, but was still
beneficial in patients treated up to 30 days after disease
onset
 Plasmapharesis
The GBS patient is connected to a machine, that slowly removes
small amounts of blood from the body, treats it and returns it to the
body.
Red and white blood corpuscles are separated from the liquid part of
the blood, the plasma, that contains the unwanted antibodies.
The plasma with antibodies is discarded, fresh plasma is added to the
blood corpuscles and returned to the body.
The fresh GBS-antibody-free plasma is taken from the blood of blood
donors, or other fluids are used.
The procedure is repeated over 4-6 days during the first week of the
disease, with 250 ml plasma/kg body weight used as replacement,
after which sufficient antibodies have been removed. The subsequent
treatments usually take a day, once every 4-8 weeks.
 Mekanisme plasmaparesis

• The mechanism of plasmapheresis is the removal of

immunoglobulins and antibodies from the serum by
removing the blood from the body, separating cells
from the plasma, and replacing the cells in fresh
frozen plasma, albumin, or saline.
Adult Dose
3-5 exchanges of 50 mL/kg of plasma over 1-2 week
via central venous catheter suggested
• Pertukaran plasma lbh baik dilakukan sedini
mungkin

• Risiko dan komplikasi tidak berbeda dg kelompok

kontrol

• 10% pasien yg membaik setelah beberapa kali

pertukaran plasma dapat memburuk lagi dlm 1-2
minggu setelah pertukaran plasma terakhir
- murni dari dekompensasi respirasi
- emboli paru
- pneumonia
- sepsis
- relaps
• Kebanyakan membaik dg beberapa kali
pertukaran palsma kedua

• Perlu dihindari pertukaran plasma pd :

- infark myokard 6 bln sebelumnya
- aritmia yang baru terjadi
- hipotensi
 IVIG

• IVIG sama efektifnya dengan pertukaran plasma pd

GBS

• Penggunaanya lbh mudah

• 0,4 g/kgBB perhari selama 5 hari

• Efek samping yg mungkin timbul :

anafilaksis, respon imun vaskuler pd vena, infark
myokard, gagal jantung kongestif, meningitis
aseptic, sakit kepala berat.
Mekanisme kerja IG (Abe, 1996)

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 Mekanisme IVIg
• IVIG is derived from fractionated purified human
plasma from a large pool of multiple donors. The
product is treated with solvents and detergents to
inactivate any blood-borne virus.

• IVIG may work via several mechanisms including

- blocking macrophage receptors,
- inhibiting antibody production,
- inhibiting complement binding,
- neutralizing pathologic antibodies.
 IVIg Side Effect

• Chills / fever / myalgia ( flu like )

• Diaphoreses / flushing
• Hypotension
• Fluid overload
• Nausea / vomiting
• Headache / aseptic meningitis
• Renal insufficiency
• Allergic reaction ( Hives, macular rash )
• Anaphilaxis
• Hepatitis C
• Neutropenia
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75
 Corticosteroid

Effective in other acute and chronic autoimmune disoders,

have no effect in patients with acute GBS. However, when
used in combination with IVIg in relapsed disease or chronic
demyelinating polyneuropathy, they may help to inhibit
cellular activity and suppress inflamation (Hartung H.,1995)
The dose of methylprednisolone was 500 mg daily for 5 days
( David S,.2001 )

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Predictors of poor prognosis
1. Axonal degeneration/CMAP<20%
2. Recent C. jejuni infection
3. GM1 antibodies
4. Rapid onset < 7 days.
7. Delay in treatment
8. Requiring intubation
9. Older age >60 yrs.
(Proone,2002)
Faktor Prognosis
(Lyu, dkk, 1997)
Nyeri kepala emergensi
Seorang pria 25 tahun datang ke poli dengan
keluhan nyeri kepala sebelah sejak 2 hari yang
lalu. Nyeri terasa berdenyut dan terasa
memberat dengan aktifitas sehari-hari. Pasien
mengatakan bahwa sebelum serangan muncul,
pasien mengeluhkan mata berkunang-kunang
dan kadang disertai dengan melihat adanya
kilatan cahaya.
Pada pemeriksaan didapatkan tanda vital: TD:
120/80mmHg, HR: 94x/m, RR: 21x/m, T:36,20 C.
Pada pemeriksaan fisik tidak didapatkan kelainan.
Seorang pria berusia 40 tahun dibawa ke IGD
dengan keluhan tiba-tiba mengeluh sakit kepala
hebat, sakit kepala paling hebat seumur hidup,
disertai muntah dan pandangan kabur.
Tanda-tanda vital pasien saat diperiksa adalah
tekanan darah 180/100 mmHg, frekuensi nadi 100
kali/menit, suhu 37 oC, dan frekuensi pernapasan
25 kali/menit.
Pada pemeriksaan didapatkan tanda-tanda kaku
kuduk. Pemeriksaan CT Scan menunjukkan adanya
gambaran hiperdens di daerah sisterna suprasellar
Sub-Arachnoid Hemorrhage
PEMERIKSAAN FISIK

 Vital sign
(suhu, tensi, nadi, respirasi
 cari etiologi nyeri:
neurologis dan nonneurologis
terutama diseputar kepala
 Red Flags in the Evaluation of Acute Headaches in Adults

Red flag Differential diagnosis Possible work-up

Headache beginning Temporal arteritis, mass lesion Erythrocyte sedimentation rate,
neuroimaging
after 50 years of age
Sudden onset of SAH, hemorrhage into a mass lesion or Neuroimaging; lumbar puncture if
neuroimaging is negative*
headache vascular malformation, mass lesion
Headaches increasing in Mass lesion, subdural hematoma, medication Neuroimaging, drug
frequency and severity overuse screen
New-onset headache in a Meningitis (chronic or carcinomatous), brain Neuroimaging; lumbar puncture if
patient with risk factors for neuroimaging is negative*
HIV infection or cancer abscess (including toxoplasmosis), metastasis
Headache with signs of Meningitis, encephalitis, systemic infection, Neuroimaging, lumbar
systemic illness (fever, stiff
neck, rash) collagen vascular disease puncture,¥ serology
Focal neurologic signs or Mass lesion, vascular malformation, stroke, Neuroimaging, collagen vascular
symptoms of disease (other evaluation (including
than typical aura) collagen vascular disease antiphospholipid antibodies)

Papilledema Mass lesion, pseudotumor cerebri, meningitis Neuroimaging, lumbar

puncture¥
Headache subsequent Intracranial hemorrhage, subdural hematoma, Neuroimaging of brain, skull
to head trauma epidural hematoma, post-traumatic headache and, possibly, cervical spine

American Family Physician, 2001

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NYERI KEPALA YG PERLU PERHATIAN

1) Perjalanan penyakit sub-akut progresif

2) Onset usia tua ( > 50 tahun )
3) NK disertai tanda-tanda:
- mual/muntah tanpa peny.sistemik
- memberat pada dini hari
- memberat dengan perubahan posisi
- disertai kejang, kelemahan, pe kesadaran,
tanda neurologis abnormal

(Dodick, 1997)
 Neuroimaging Studies in Headache Sufferers

Neuroimaging may be important for headache patients who

have
• Abnormal unexplained neurological exam
• Rapidly increasing frequency and/or severity of headaches
• Change in headache clinical features
• First or “worst” headache ever experienced
• Headache with extremely abrupt onset
• New-onset headache after age 50
• Headache refractory to aggressive treatment
• Dizziness, numbness, or tingling

(Frishberg B, et al.,2000; Evans RW, et al.; 2001)

 CT Scan dan MRI pada Nyeri kepala

• Gambaran jelas pd proses desak ruang

intrakranial  tumor otak, hematoma
intraserebral, infark otak, abses otak,
hidrosefalus, EDH, SDH & SAH
• Cluster headache, tension headache 
normal
• Migren  normal / kadang edema cerebri
 CNS Imaging in Headache
• The definitive diagnosis of migraine does not
require negative imaging study

• AAN practice parameter - imaging studies are

not indicated if the following hold:
– no red flags in the headache history
– normal neurological examination with regards to
causation of the headache pain