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FIRST PROBLEM

A “STORMY” SHIFT
28 SEPTEMBER 2018
-GROUP 14-
PLENARY 1
A “Stormy” Shift

 Group 14
Tutor : dr. Erna & dr. Johan
Leader : Kristo Hadi Audric S. 405150059
Secretary : Nurul Inayah Indah C. 405150051
Writer : Salim, Jessica Greselda 405150153
Members : Sim Wilson Kristianus 405130021
Sanity Savant Suhendar 405140022
Rosemary Febriani 405140042
Gede Raditya Yoga 405140206
Gabriella Jesslyn E. 405150043
Cessy Christy 405150096
Robert Suryajaya H 405150118
Cindy Putri 405150147
PLENARY 1
A “Stormy” Shift

You are an attending emergency department physician when three patients are brought to the Emergency Department
(ED) at the same time.
The first patient, a 22-year-old man is brought to the Emergency Department by his family after seizing. His family
describes the patient body was stiff, his teeth were clenching and eyes were widely open when seizing. The seizure
happened for about 3 times in an hour, each episodes lasted for 2-3 minute between seizure, he appeared lethargy,
drowsy, and difficult to awaken. History of previous seizure is denied. It had been coughing for some times, and
currently also experiences fever and headache for a week. He took paracetamol to treat his fever and headache, but
his symptom only slightly lessened. About a month ago, the patient fell from a motorcycle, but he did not receive any
treatment. He only had several vaccination since birth. His 25 year old cousin is diagnosed with epilepsy 2 years ago
but his symptom is currently under control. On initial examination, the patient appearance soporous, GCS E3M4V2.
blood pressure is 140/90 mmHg, HR 100 beats per minute, RR 28 breaths per minute and temperatur 38,8’C.
The second patient, a 50-year-old man is brought to the emergency department by paramedics after he was found
unconscious with his face down on the bathroom floor by his wife. Traces of vomit were found around his mouth and
clothes. His wife said that while the patient was being transported to emergency department, he had convulsion for 3
times. His wife said his face began to twitch from his right side spread to his right extremities and finally developed
into generalized convulsion. About a week ago, patient start to experience headache, but his pain was getting better
after taking a paracetamol. However, according to his wife, he woke up this morning with stiff neck and severe
headache to the point that he almost could not get up from the bed. He cried the back of his head left like being
tightly constricted and the pain is getting worse when he saw bright light. He has a story of uncontrolled hypertension
for three years. He smokes 1-2 packs of cigarettes a day and sometimes drinks alcohol with his office mates. On initial
examination in the ED, GCS E2M4V2. His blood pressure is 180/100 mmHg, HR is 60 beats per minutes, RR is 20
breaths per minutes and temperature 37,8’C. while performing “doll’s eyes” manuever, there are signs of bilateral
facial nerve paralysis. All meningeal signs are positive.
The third patient, , a 50-year-old man, is brought to the ED by paramedics
after he was assaulted with a blow to the head while walking home. He lost
cosciousness temporarily, but woke up and went home to recover. Several hours
later, his wife called the ambulance because she notices that the patient is
acting confused and has become less responsive progressively. On physical
examination, the patient was noted to have a tense subgaleal hematoma that
is palpable on the right side oh his head. His eyes are closed and he does not
open them to command. His left pupil is 6 mm and sluggishly reactive. His right
pupil is 4 mm and briskly reactive. He localizes to pain with his left upper
extremity and withdraws from pain with his right upper extremity. He
withdraws from pain briskly in lower extremities.

Discuss the cases, asses the patient’s condition, plan the necessary examination
to diagnose and plan proper treatment while considering all possibilities!
Mind Map
Penurunan Kesadaran Kejang

Macam-macam Macam-macam
Penurunan Kesadaran Kejang

Primary Survey

Diagnosis PP Secondary Survey

Komplikasi dan prognosis


Learning Issues
1. MM Macam-macam Penurunan Kesadaran Berdasarkan Penyebab Neurologis
2. MM Tanda dan Gejala Penurunan Kesadaran pada Primary Survey dan Ciri Khas masing-
masing Penyebab dari Tanda dan Gejala (kasus neurologis)
3. MM Pemeriksaan Penunjang dan Interpretasi untuk Diagnosis Penurunan Kesadaran
(neurologis)
4. MM Tatalaksana Umum dan Spesifik sesuai Penyebab
5. MM Komplikasi dan Prognosis Penurunan Kesadaran
6. MM Primary Survey pada Kasus Cedera Kepala (Epidural hematom, Subdural Hematom,
Subarachnoid Hemorrage, Spinal cord Injury)
7. MM Pemeriksaan Penunjang untuk Diagnosis dan Tatalaksana Pasien dengan Cedera
Kepala
8. MM Komplikasi dan Prognosis Cedera Kepala
9. MM Penyebab Kejang secara Neurologis
10. MM Tanda dan Gejala Kejang pada Anak dan Dewasa untuk Primary Survey dan Ciri Khas
setiap Penyebab Kejang
11. MM Pemeriksaan Penunjang dan Interpretasi dalam mendiagnosis Kejang pada Dewasa
dan Anak
12. MM Tatalaksana Kejang dan Status Epileptikus pada Dewasa dan Anak
13. MM Hubungan Kronologis pada Kasus ini secara Patofisiologi
Penurunan Kesadaran
- Stroke dan TIA
- Infeksi : Meningitis dan ensefalitis
- Ensefalopati
- Malaria
PENURUNAN KESADARAN

Penilaian Penurunan
Kesadaran :
1. Kuantitatif (ex:GCS)
2. Kualitatif

Howlett WP. Coma and transient loss of consciousness. In: Howlett WP. Neurology in africa.
Norway: University of Bergen; 2012.
Rosen’s Emergency medicine : Concepts and Clinical Practice. 8 th ed.Philadelphia, Elsevier;2014.
Stroke and TIA
 Type of Stroke  Based on time:
 Transient Ischemic Attack
(TIA)
 Recover in <24h
 Stroke in Evolution
 Develops in 1-2d
 Reversible Ischemic
Neurological Deficits
(RIND)
 Recover in <3w
 Iskemik:  Complete stroke
 Trombotik  Symptoms till >3w
 embolik

Advanced Neurology Life Support


(ANLS)
Gejala Stroke

Gejala Stroke Deteksi dini dan Diagnosis Stroke


 Kelumpuhan mendadak wajah atau
anggota badan (pada umumnya sesisi
 Facial drop
hemiparesis)  Arm drift
 Gangguan bicara/komunikasi mendadak
( disartria atau afasia)  Slurred speech
Gangguan sensibilitas (kebas atau
 Time

kesemutan)
 Gangguan status mental (kesadaran Diagnosis :
menurun)
 Gangguan penglihatan (buta satu, dua  Anamnesis
mata atau sesisi)
 PF
 Gangguan keseimbangan (vertigo,
ataksia )  PP(Gold standart: CT
 Gangguan daya ingat (amnesia,dll) scan)
https://www.healthcentral.com/article/what-is-a-
stroke Advanced Neurology Life Support (ANLS)
Disartria
Disfagia
Tonus nasofaring
stroke
turun
Kesadaran menurun
Sekresi berlebih

Hipoksemia Obstruksi
hiperkarbia jalan napas

Managemen Umum :
• Stabilisasi jalan nafas dan pernafasan
• Stabilisasi hemodinamik
• Mencegah peninggian tekanan intrakranial•
• Pengendalian kejang
• Pengendalian suhu tubuh
Advanced Neurology Life Support (ANLS)
Manajemen
 A: bebaskan jalan napas Cegah Peningkatan TIK
 Triple manuver
 Tinggikan posisi kepala
 Pasang pipa orofaring
 Suction(hati2 peninggian TIK)
30⁰
 Pertimbangkan intubasi atau pasang LMA  Leher dalam posisi lurus
bila SKG ≤8
 Hindari cairan hipotonik
 B: Nilai oksigenasiTarget O2 Sat > 95%.
 Terapi oksigen.  Hindari demam
 C: Stroke  datang terlambat  kalo  Jaga normovolemia
dehidrasi :
 Lakukan rehidrasi IV 50 –150 cc/jam  Rapid sequence intubation

 Pilih cairan isotonik, jangan berikan cairan


hipotonik karena akan
menyebabkan/memperberat edema otak
 Bila TIK ↑, hati-hati kelebihan cairan.
 Pantau elektrolit setiap hari dan segera
terapi bila ada kelainan. Advanced Neurology Life Support (ANLS)
Source : American Heart
Association (AHA)
ENCHEPHALOPATHY
 enchephalopathy is a term for any disease of the brain that alters brain
function or structure
 enchephalopathy may be caused by :
(1) infectious agent (2) metabolic or mitochondrial dysfunction (3) brain tumor or
increased pressure in the skull (4)prolonged exposure to toxic elements (5) chronic
progressive trauma (6) poor nutrition (7) lack of oxygen or blood flow to the brain

Diagnosis :
Sign and Symptoms
 Anamnesis
- myoclonus
- nystagmus  Medical examination:
- tremor - Vital sign
- muscle atrophy and - neurological
weakness
- seizures - head to toe
- loss of ability to - metabolic sign
swallow or speak  Lab : blood test
 CT or MRI scan
 EEG

https://www.ninds.nih.gov/Disorders/All-Disorders/Encephalopathy-Information-Page#disorders-r3
CLASSIFICATION
 CHRONIC TRAUMATIC
ENCHEPHALOPATHY  HYPOXIC ISCHEMIC ENCEPHALOPATHY
multiple trauma and injuries -> lead
to nerve damage in the brain brain damage cause doesn’t get enough
 GLYCINE ENCEPHALOPATHY
oxygen
genetic -> abnormally high levels of  TOXIC-METABOLIC ENCHEPHALOPATHY
glycine (amino acid) in the brain
medication or chemichal in body off
 HASHIMOTO’S ENCEPHALOPATHY
their normal balance
autoimmune condition -> immune
system attack thyroid gland  INFECTIOUS ENCHEPHALOPATHY
 HEPATIC ENCHEPHALOPATHY as enchephalitis and meningitis
liver disease -> toxin that should be
remove is build in blood and reach  UREMIC ENCEPHALOPATHY
brain uremic toxin in blood
 HYPERTENSIVE ENCEPHALOPATHY
 WERNICK ENCEPHALOPATHY
severely high blood pressure
untreated for too long vitamin B1 deficiency

https://www.ninds.nih.gov/Disorders/All-Disorders/Encephalopathy-Information-Page#disorders-r3
https://www.ninds.nih.gov/Disorders/All-Disorders/Encephalopathy-Information-Page#disorders-r3
Management and Prognosis

Management Prognosis
 A : air patency
- Non devinitive : head tilt, chin lift
Some enchephalopaties
- Devinitive : endotracheal tube, nasotracheal
may be easily reversible,
tube while others can progress
 B: oxygen supplementation
- nasal canal, RM (reservoir mask), ventilator
and cause permanent
 C: circulation (provide suitable infusion)
structural changes in the
- ringer lactate preferred for non hepatic cause brain and even death; the
- nasal saline outlook depends on the
- add manitol for any indication of brain edema
- dextrose (glucose level)
underlying cause of
 D: GCS
enchephalopathy and its
 E: provide warmth blanket potential for treatment

https://www.ninds.nih.gov/Disorders/All-Disorders/Encephalopathy-Information-Page#disorders-r3
Meningitis and Encephalitis

 Meningitis : Inflammation of the membrane surrounding the brain


and spinal cord ; (Common  Bacterial: Encapsulated
microorganisms).
 Aseptic Meningitis  caused by drug rx, rheumatologic,
nonbacterial infection (Enteroviruses and Echoviruses)
 Triad of Meningitis  Fever, Neck Stiffness, and Altered Mental
Status.
 Physical Findings : Meningeal signs such as nuchal rigidity, Kernig’s
sign, and Brudzinski’s sign
 Encephalitis : infection of the brain parenchyma that causes
inflammation within the CNS and is often caused by viral infection
(Mostly caused by HSV).
 clinical features : altered mental status, cognitive deficits, psychiatric
symptoms, or seizures
Tintinalli’s Emergency Medicine Manual 8th Edition 2018
Meningitis and Encephalitis
Diagnosis and Differential

 Lumbar Puncture (LP)


 CT Scan
 the goal for imaging in this circumstances is to identify
possible contraindications to LP such as occult mass or signs of
brain shift or herniation.
 Laboratory studies  complete blood count (CBC),
serum glucose and electrolytes, blood urea nitrogen
(BUN) and creatinine
 MRI
 Differential Diagnosis : SAH, meningeal neoplasms,
brain abscess, cerebral toxoplasmosis and other systemic
or bacterial infections

Tintinalli’s Emergency Medicine Manual 8th Edition 2018


Tintinalli’s Emergency Medicine Manual 8th Edition 2018
Meningitis and Encephalitis
Emergency Department Care and Disposition

1. Empiric AB therapy
2. Adults < 50 yrs old  3rd gen cephalosporin such as
ceftriaxone 2 g IV + vancomycin 15 mg/kg IV. Patients at
risk for Listeria monocytogenes  should additionally
receive ampicillin 2 g IV.
3. Consider additional dexamethasone 10 mg IV every 6
hrs for 4 days in adults or 0,15 mg/kg IV every 6 hrs for 4
days in children 3 months and older.
4. Suspected Encephalitis : acyclovir 10 mg/kg IV to cover
for possible HSV or Herpes Zoster virus infections. CMV
encephalitis can be treated w/ Ganciclovir 5 mg/kg IV

Tintinalli’s Emergency Medicine Manual 8th Edition 2018


Meningitis • Lumbal Pungsi
• 50 - 500 white cells /mm³
• polymorphonuclear leukocytes dan

Tuberkulosis •
lymphocytes
protein CSF meningkat antara 100
and 200 mg/ dL
• Ziehl Neelsen
 Etiologi : Mycobacterium tuberculosis dan
• Kultur Bakteri
Mycobacterium bovis, Mycobacterium avian,
Mycobacterium kansasii, and Mycobacterium fortuitum. • PCR
• CT scan dan MRI
 Patogenesis : bakteri  meninges and subpial regions
 tubercles disertai ruptur satu atau lebih tubercles
dan discharge bacteria  subarachnoid space.
 Tanda dan gejala :
 subfebris, malaise, headache (> 50 % kasus)
 lethargy, confusion, and stiff neck (75% kasus) + Kernig
and Brudzinski
 Pada bayi dan anak apathy, hyperirritability,
vomiting, and seizures merupakan symptom yang
sering ditunjukan ; kaku kuduk bisa didapatkan +/-
 Gejala nervus kranialis ( ocular palsies, facial palsies
atau deafness ) dan papilledema juga dapat
ditemukan (20 % kasus)
 TALAK : isoniazid (INH), rifampin (RMP), ethambutol
(EMB), dan pyrazinamide (PZA).

Munir B. Neurologi dasar. Jakarta: Sagung Seto, 2015.


SEVERE (COMPLICATED) MALARIA
 usually due toP. falciparum  - When cerebral malaria is
coma with or without seizures suspected, meningitis or
(“cerebral malaria”),
prostration, severe anemia, encephalitis must be either
acidosis, hypoglyce- mia, acute excluded or treated, and the
renal failure, acute respiratory clinician must decide whether a
distress syndrome, pulmonary lumbar puncture is safe.
edema, jaundice, intravascular
hemolysis, shock, and - At lumbar puncture, the
disseminated intravascular opening pressure is usually
coagulation. raised in children and normal
 Complications of malaria can in adults. The fluid is normal in
develop rapidly in untreated P. appearance and on routine
falciparum infection or may
supervene early in the course tests.
of treatment. - In a child with coma and
parasitemia, the presence of a
recently identified retinopathy
(Figure 158-1) greatly
strengthens confidence that
malaria is the cause of the
Tintinalli’s Emergency Medicine Manual 8th Edition 2018 syndrome.
DIAGNOSIS
- Clues to the diagnosis of
P. falciparum infection
include the presence of
small ring forms with
double-chromatin dots
within the erythrocyte,
 THICK BLOOD FILM
 THIN BLOOD FILM

Tintinalli’s Emergency Medicine Manual 8th Edition 2018


TREATMENT

Supportive Management Initial resuscitation may require oxygen for hypoxia, fluid
replacement, IV glucose for hypoglycemia, blood transfusion for severe anemia or for
disseminated intravascular coagulation, and occasionally intubation for severe respiratory
distress or suspected raised intracranial pressure with altered mental status.
Trauma Kepala
• Subdural Hematom
• Epidural Hematom
• Subarachnoid Hemorrage
• Intracerebral hematom
• Trauma Spinal Cord
http://r1.emsworld.com/files/base/image/EMSR/2009/04/16x9/640x360/1242402277713_10320436.jpg
The ED algorithm for early diagnosis and emergent intervention.

Cyrus K Dastur, and Wengui Yu


Stroke Vasc Neurol 2017;svn-
2016-000047

Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to
http://www.bmj.com/company/products-services/rights-and-licensing/
SPINAL
CORD
INJURY
Kejang
• Epilepsi/Status Epileptikus
• Kejang Demam
• Kejang Tetanus
Seizure
• Seizures are disorders characterized by temporary neurologic signs or symptoms
resulting from abnormal, paroxysmal, and hypersynchronous electrical neuronal
activity in the cerebral cortex

Vojvodic M, Young A, editors. Toronto notes 2014. Toronto:


Toronto Notes for Medical Students Inc.; 2014.

Clinical Neurology
Lange 9th ed
Antiepileptic drugs

Adams and Victor’s Principles of Neurology 10th ed


Adams and Victor’s Principles of Neurology 10th ed
STATUS EPILEPTIKUS
Adalah suatu kondisi kegawatdaruratan berupa 2) Lesi non-primer
kejang yag berlangsung lebih dari 30 menit atau 2  Hipoksia / iskemia
atau lebih kejang berturut-turut tanpa pulihnya  Toksisitas obat / zat : antibiotik,
kesadaran diantara kejang yang dapat antidepresan, antipsikotik,
berlangsung lebih dari 30 menit bronkodilator, anestesi lokal,
obat imunosupresif, kokain,
amfetamin
 Etiologi  Putus obat / zat : barbiturat,
1) Lesi primer benzodiazepin, opioid, alkohol
 Neurovaskuler : stroke, malformasi  Demam infeksi
arteri-vena, perdarahan  Gangguan metabolik :
 Tumor : primer, metastasis hiponatremia, hipofosfatemia,
hipoglikemia, gangguan ginjal /
 Infeksi SSP : abses, meningitis, hati
ensefalitis
 Penyakit inflamasi : vaskulitis, acute
disseminated encephalomyelitis
 Trauma kapitis : kontusio, perdarahan
 Epilepsi primer PERDOSSI. Advanced neurology life support: student course manual. Indonesian Neurological
Association.
Penilaian awal
• Periksa fungsi kardiorespirasi → pastikan ventilasi adekuat,
oksigenasi baik, tekanan darah baik, EKG
• Intubasi bila diperlukan (berdasarkan saturasi oksigen dan
usaha napas)
• Cek glukosa darah kapiler
• Intravenous line

• Ambil darah → pemeriksaan glukosa, BUN, elektrolit, obat-


obatan, zat toksik
• Infus normosalin dan pemberian glukosa bolus (50 ml IV) /
dekstrose 50% → dengan tiamin 100 mg IV bila malnutrisi dan
alkoholisme merupakan faktor potensial (cegah ensefalopati
Wernicke)

Ropper AH, Samuels MA, Klein JP. Adams and victor’s principles of neurology. 10th ed. New York: McGraw-Hill Education; 2014.
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.
PERDOSSI. Advanced neurology life support: student course manual. Indonesian Neurological Association.
• Diazepam IV, dosis 0,2 mg/kg, kecepatan 2 – 4 mg/menit, selama 1 – 2
menit atau sampai kejang berhenti atau dosis total 10 – 20 mg
ATAU
• Lorazepam IV, dosis 0,1 mg/kg, kecepatan tidak lebih dari 2 mg/menit
(luar negeri lebih dipilih ini → durasi kerja hingga 24 jam, depresi napas
dan hipotensi lebih ringan)
• Aktivitas kejang tidak berhenti dalam
10 menit
• Kejang intermiten berlangsung 20
menit / >

• Fenitoin IV, loading dose 15 – 20 mg/kg, kecepatan 25 – 50 mg/menit (> 50


mg/menit risiko hipotensi dan blok jantung). Larutkan dalam normosalin.
Monitor tekanan darah dan EKG (risiko hipotensi, aritmia, pemanjangan QT)
ATAU
• Fosfenitoin IV, dosis 20 mg/kg, kecepatan 150 mg/menit

Status epileptikus berlanjut

Ropper AH, Samuels MA, Klein JP. Adams and victor’s principles of neurology. 10th ed. New York: McGraw-Hill Education; 2014.
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.
PERDOSSI. Advanced neurology life support: student course manual. Indonesian Neurological Association.
• Intubasi bila belum dilakukan
• Fenobarbital IV, dosis 20 mg/kg,
kecepatan perlahan (10 mg/menit)
Status epileptikus refrakter
• Dibawa ke ICU
• Induksi koma dengan barbiturat (pentobarbital), midazolam,
atau propofol
• Pentobarbital, dosis awal 5 – 10 mg/kg/jam → dosis
pemeliharaan 0,5 – 2 mg/kg/jam
• Midazolam, loading dose 0,2 mg/kg → 0,1 – 0,4 mg/kg/jam
• Propofol, bolus 2 mg/kg → IV drip 2 – 10 mg/kg/jam
• Pertahankan pemberian fenitoin dan fenobarbital
• Monitor EEG

Ropper AH, Samuels MA, Klein JP. Adams and victor’s principles of neurology. 10th ed. New York: McGraw-Hill Education; 2014.
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.
PERDOSSI. Advanced neurology life support: student course manual. Indonesian Neurological Association.
https://emergencymedicinecases.com/emergency-management-of-pediatric-seizures/
KOMPLIKASI STATUS EPILEPTIKUS

Komplikasi Diagnosis Banding


Status epileptikus konvulsi /
 Injury 
nonkonvulsi
Keadaan postiktal
 Peningkatan temperatur 

 Gangguan pergerakan : mioklonus,


 Asidosis tremor, korea, tics, distonia
 Herniasi otak → postur deserebrasi
 Hipotensi dan dekortikasi
 Limb shaking TIA
 Gagal ginjal e.c.  Gangguan psikiatri : psychogenic
nonepileptic seizure, gangguan
mioglobinuria konversi, psikotik akut, katatonia
Gangguan tidur, sinkop
 Ensefalopati epileptik 

Ropper AH, Samuels MA, Klein JP. Adams and victor’s principles of PERDOSSI. Advanced neurology life support:
neurology. 10th ed. New York: McGraw-Hill Education; 2014.
student course manual. Indonesian Neurological Association.
Kejang Demam

Definisi
 Bangkitan kejang yang terjadi pada
kenaikan suhu tubuh >38 derajat
celcius karena suatu proses
ekstrakranium
 Terjadi tanpa adanya infeksi
intrakranial dan gangguan
metabolik
 Kejang dengan demam pada anak
yang pernah mengalami kejang
tanpa demam sebelumnya tidak
termasuk dalam kriteria ini
 Terjadi pada anak usia 6 bulan-5
tahun
(IDAI)
Kejang Demam
Klasifikasi : Diagnosis Kejang Demam
1. KEJANG DEMAM SEDERHANA  Umur 6bln-4th
 Singkat, <15 mnt  sebentar, <15 mnt
 Berhenti sendiri  Kejang umum
 Kejang tonik dan/atau klonik, tanpa
 Timbul dalam 16 jam pertama
fokal
setelah demam
 Tidak berulang dlm 24 jam
 Px neurologis sblm dan sesudah
demam  normal
2. KEJANG DEMAM KOMPLEKS
 Px EEG 1 minggu stlh suhu normal 
 Lama, >15 mnt tdk ada kelainan
 Kejang fokal atau kejang umum yg  Frek bangkitan kejang dalam 1 thn
didahului parsial
<4x
 Berulang >1x dalam 24 jam

Gejala
 Singkat
 Kejang klinik atau tonik-klonik bilateral
 Sering berhenti sendiri  anak tidak memberi reaksi apapun sejenak  bbrp detik atau
menit: sadar kembali
 Peningkatan suhu tubuh mendadak hingga >38 derajat celcius (IDAI)
Bila setelah
pemberian
diazepam rektal
kejang belum
berhenti, dapat
diulang lagi dengan
cara dan dosis yang
sama dengan
interval waktu 5
menit.

• setelah 2 kali
pemberian
diazepam
rektal masih
tetap kejang,
dianjurkan ke
rumah sakit.
• Di rumah sakit
dapat
diberikan
diazepam
intravena
dengan dosis
0,3-0,5
mg/kg.
Bila kejang telah
berhenti,
pemberian obat
selanjutnya
tergantung
dari jenis kejang
demam apakah
kejang demam
sederhana
atau kompleks
dan faktor
risikonya.
Konsensus Penatalaksanaan Kejang Demam IDAI 2006
http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
TREATMENT
 Tetanus is diagnosed clinically.
TETANUS NEONATORUM
 Penyakit sistem saraf
yg berlangsung akut
dengan karakteristik
spasme tonik persisten
& eksaserbasi singkat.
 Terjadi pada bayi
yang baru lahir &
terjadi pada bayi
yang baru lahir tanpa
adanya protektif
imunitas pasif.

http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/tetanus.pdf
TETANUS NEONATORUM
 Penyebab kematian ke-2 DIAGNOSIS
setelah asfiksia neonatorum.
 Anamnesa
 Berhubungan dengan aspek
pelayanan kesehatan neonatal  Riwayat persalinan yg
: kurang higenis
 Pelayanan persalinan  Perawatan tali pusat yg
(bersih, aman, khususnya tidak higienis
perawatan tali pusat  Bayi sadar + sering kaku
 Komplikasi : spasme otot (spasme)  jika
diafragma tersentuh
 Bayi malas minum
 Pemeriksaan :
 Pemeriksaan darah rutin
 Pungsi umbal
Sumber : IDAI.Pedoman pelayanan medis.2009;315-8.
TETANUS NEONATORUM
 TREATMENT
 Diazepam 10mg/kg/hari,
IV, 24 jam
 Bolus IV tiap 3-6 jam (0.1-
0.2 mg/kg/hari) max 40
mg/hari.
 Bayi
 Human tetanus Ig 500 U IM
atau antitoksin tetanus
 Lini 1 : metronidazol 30
mg/kg/hari, tiap 6 jam,
PO, 7-10hari
 Ibu
 Imunisasi tetanus toksoid
0.5ml

IDAI. Buku ajar neonatologi Edisi pertama. Kejang pada neonatus;226-249


Nelson. Pediatric. 20th ed
Conclusion and Suggestions
 Patient 1 : seizing. Beetween seezing -> patient
apperead lethargic -> DD: seizure, status Epilepticus.
Patient had been coughing and currently also
experiences fever and headache -> DD : Meningitis TB
 Patient 2 : unconscious, have experience headche, stiff
neck and all meningeal sign are (+), history of
uncontrolled hypertension -> Suspect Meningitis, DD:
ensefalitis, HT ensefalopati, stroke/TIA
 Patient 3 : Subgaleal hematom, history of head trauma
(+) -> DD : Trauma Capitis
Do primary survey for all patients!!! After all patients are
stable, do secondary survey and give spesific treatment
References
 Advanced Neurology Life Support (ANLS)
 Clinical Neurology Lange 9th ed
 Tintinalli’s Emergency Medicine Manual 8th Edition 2018
 Ropper AH, Samuels MA, Klein JP. Adams and victor’s principles of neurology. 10th
ed. New York: McGraw-Hill Education; 2014.
 PERDOSSI. Advanced neurology life support: student course manual. Indonesian
Neurological Association.
 Rosen’s Emergency medicine : Concepts and Clinical Practice. 8th ed.Philadelphia,
Elsevier;2014.
 Konsensus Penatalaksanaan Kejang Demam IDAI 2006
 http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-
2012.pdf
 IDAI. Buku ajar neonatologi Edisi pertama. Kejang pada neonatus;226-249
 Nelson. Pediatric. 20th ed
 http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/tetanus.pdf
 https://emergencymedicinecases.com/emergency-management-of-pediatric-
seizures/
 Cyrus K Dastur, and Wengui Yu Stroke Vasc Neurology 2017;svn-2016-000047
 http://r1.emsworld.com/files/base/image/EMSR/2009/04/16x9/640x360/12424022777
13_10320436.jpg

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