PEMICU 1

STATUS EPILEPTIKUS
• Kejang generalisata berulang (sangat sering)
→ tidak terjadi pemulihan kesadaran diantara
episode kejang
• Aktivitas kejang yang berlanjut dalam jangka
waktu panjang

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.
 ETIOLOGI STATUS EPILEPTIKUS
• Lesi primer
– Neurovaskuler : stroke, malformasi arteri-vena,
perdarahan
– Tumor : primer, metastasis
– Infeksi SSP : abses, meningitis, ensefalitis
– Penyakit inflamasi : vaskulitis, acute disseminated
encephalomyelitis
– Trauma kapitis : kontusio, perdarahan
– Epilepsi primer
PERDOSSI. Advanced neurology life
support: student course manual.
Indonesian Neurological Association.
 ETIOLOGI STATUS EPILEPTIKUS
• Lesi non-primer
– Hipoksia / iskemia
– Toksisitas obat / zat : antibiotik, antidepresan,
antipsikotik, bronkodilator, anestesi lokal, obat
imunosupresif, kokain, amfetamin
– Putus obat / zat : barbiturat, benzodiazepin, opioid,
alkohol
– Demam infeksi
– Gangguan metabolik : hiponatremia, hipofosfatemia,
hipoglikemia, gangguan ginjal / hati
PERDOSSI. Advanced neurology life
support: student course manual.
Indonesian Neurological Association.
 PERJALANAN STATUS EPILEPTIKUS
• Fase 1
– ↑ tekanan darah arteri dan aktivitas otonom (↑
glukosa darah, berkeringat, hiperpireksia, salivasi)
• Fase 2 (30 menit setelah fase 1)
– Kegagalan otoregulasi serebral
– ↓ laju darah serebral
– ↑ TIK
– Hipotensi sistemik

PERDOSSI. Advanced neurology life

support: student course manual.
Indonesian Neurological Association.
 SURVEI PRIMER STATUS EPILEPTIKUS
• Hilang kesadaran
• Aktivitas tonik-klonik
• Mulut berbusa
• Lidah tergigit
• Mata bergerak ke atas
• Inkontinensia urin

PERDOSSI. Advanced neurology life

support: student course manual.
Indonesian Neurological Association.
 ANAMNESIS STATUS EPILEPTIKUS
• Riwayat penyakit dahulu
• Deskripsi kejang, keadaan preiktal, iktal, dan
postiktal
• Riwayat penyakit epilepsi
• Faktor risiko epilepsi
• Riwayat hipoglikemia
• Riwayat lesi struktural otak

PERDOSSI. Advanced neurology life

support: student course manual.
Indonesian Neurological Association.
 PEMERIKSAAN FISIK PADA STATUS
EPILEPTIKUS
• Pemeriksaan status neurologis lengkap : GCS,
pupil, tanda rangsang meningeal
• Gejala negatif : koma, letargi, konfusi, afasia,
amnesia
• Gejala positif : otomatisme, mengedip, agitasi

PERDOSSI. Advanced neurology life

support: student course manual.
Indonesian Neurological Association.
 PEMERIKSAAN PENUNJANG PADA
STATUS EPILEPTIKUS
• EEG kontinu 24 jam
• Pencitraan → sesuai indikasi, bila terdapat lesi
fokal di otak
• Pungsi lumbal → sesuai indikasi, bila tidak
terdapat ↑ TIK

PERDOSSI. Advanced neurology life

support: student course manual.
Indonesian Neurological Association.
 DIAGNOSIS BANDING STATUS
EPILEPTIKUS
• Status epileptikus konvulsi / nonkonvulsi
• Keadaan postiktal
• Gangguan pergerakan : mioklonus, tremor, korea, tics,
distonia
• Herniasi otak → postur deserebrasi dan dekortikasi
• Limb shaking TIA
• Gangguan psikiatri : psychogenic nonepileptic seizure,
gangguan konversi, psikotik akut, katatonia
• Gangguan tidur, sinkop

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.
 • 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.
 KOMPLIKASI STATUS EPILEPTIKUS
• Injury
• Peningkatan temperatur
• Asidosis
• Hipotensi
• Gagal ginjal e.c. mioglobinuria
• Ensefalopati epileptik

Ropper AH, Samuels MA, Klein JP. Adams

and victor’s principles of neurology. 10th
ed. New York: McGraw-Hill Education;
 KEJANG DEMAM
• Kejang yang terjadi pada ↑ suhu tubuh (suhu
rektal > 38 oC) e.c. proses ekstrakranial
• 2 – 4% → anak usia 6 bulan – 5 tahun
• Klasifikasi :
Kejang Demam Sederhana Kejang Demam Kompleks
< 15 menit > 15 menit
Kejang umum tonik dan atau Kejang fokal / parsial 1 sisi,
klonik, tanpa gerakan fokal atau kejang umum yang
didahului kejang parsial
Tidak berulang dalam 24 jam Berulang / > 1x dalam 24 jam

Pusponegoro HD, Widodo DP, Ismael S,

editors. Konsensus penatalaksanaan kejang
demam. Jakarta: Unit Kerja Koordinasi
Neurologi Ikatan Dokter Anak Indonesia;
 KEJANG DEMAM
• Kejang lama
– > 15 menit
– Berulang > 2x
– Diantara episode kejang anak tidak sadar
• Kejang berulang
– 2x / > dalam 1 hari
– Diantara episode kejang anak sadar

Pusponegoro HD, Widodo DP, Ismael S,

editors. Konsensus penatalaksanaan kejang
demam. Jakarta: Unit Kerja Koordinasi
Neurologi Ikatan Dokter Anak Indonesia;
KRITERIA LIVINGSTONE UNTUK DIAGNOSIS
KEJANG DEMAM SEDERHANA
1. Usia anak pada saat kejang antara 6 bulan – 4 tahun
2. Kejang berlangsung < 15 menit
3. Kejang bersifat umum
4. Kejang terjadi dalam 16 jam pertama sejak timbulnya
demam
5. Pemeriksaan neurologis normal saat sebelum dan
sesudah kejang
6. Pemeriksaan EEG setelah suhu badan normal
sedikitnya 1 minggu, tidak menunjukkan kelainan
7. Bangkitan kejang dalam 1 tahun tidak > 4x
Setia H.
http://digilib.unimus.ac.id/files/disk1/110/j
tptunimus-gdl-herrysetia-5459-2-babii.pdf
Hirtz DG. Febrile seizures. Pediatrics in
Review. 1997 Jan;18(1):5-9.
 KEJANG DEMAM
Pemeriksaan • Laboratorium → darah tepi, elektrolit, glukosa darah
Penunjang • Cairan serebrospinal (pungsi lumbal) → bayi < 1 tahun
(kemungkinan meningitis)
Tatalaksana • Diazepam IV → (tidak berhasil) → fenitoin IV → (tidak
berhasil) → ICU
• Di rumah → diazepam rektal → (tidak berhasil) →
diulang dalam interval 5 menit → (tidak berhasil) → RS

Pusponegoro HD, Widodo DP, Ismael S,

editors. Konsensus penatalaksanaan kejang
demam. Jakarta: Unit Kerja Koordinasi
Neurologi Ikatan Dokter Anak Indonesia;
 KEJANG DEMAM-EDUKASI ORANG
TUA
• Kejang demam umumnya mempunyai
prognosis baik
• Cara penanganan kejang
• Informasi tentang kemungkinan kejang
kembali
• Pemberian obat untuk mencegah rekurensi +
efek samping yang dapat timbul

Pusponegoro HD, Widodo DP, Ismael S,

editors. Konsensus penatalaksanaan kejang
demam. Jakarta: Unit Kerja Koordinasi
Neurologi Ikatan Dokter Anak Indonesia;
 KEJANG DEMAM-EDUKASI ORANG
TUA
Penanganan kejang :
• Tetap tenang dan jangan panik
• Kendurkan pakaian ketat di sekitar leher
• Bila tidak sadar → posisi terlentang dengan kepala
miring; Bersihkan muntahan / lendir di mulut / hidung
• Ukur suhu; Pantau dan catat lama dan bentuk kejang
• Tetap bersama pasien
• Diazepam rektal. Stop setelah kejang berhenti
• Bawa ke dokter / RS bila kejang > 5 menit

Pusponegoro HD, Widodo DP, Ismael S,

editors. Konsensus penatalaksanaan kejang
demam. Jakarta: Unit Kerja Koordinasi
Neurologi Ikatan Dokter Anak Indonesia;
 Perdarahan Subaraknoid

Perdarahan antara otak dan jaringan yang melapisi otak

Perdarahan ke dalam ruang subaraknoid dapat bersifat

traumatik atau non-traumatik.
Penyebab traumatik merupakan penyebab tersering.
Pada kasus non traumatik tersering disebabkan oleh
ruptur aneurisma

Simon RP, Greenberg DA, Aminoff MJ. Clinical neurology. 7th

ed. New York: The McGraw-Hill Companies Inc.; 2009.
• Gejala klinis :
- Nyeri kepala seperti tersambar petir (paling buruk
selama hidupnya, “sentinel”), onset mendadak dan
terjadi selama aktivitas.
- Tingkat kesadaran menurun
- Mual, muntah
- Kekakuan leher

• Diagnosis :
- CT Scan
- Pungsi lumbal  Cairan serebrospinal harus
dievaluasi eritrosit dan xantokromia
- Fundus optikus
Simon RP, Greenberg DA, Aminoff MJ. Clinical neurology. 7th
ed. New York: The McGraw-Hill Companies Inc.; 2009.
Subarachnoid Hemorrhage
• Tatalaksana :
- Kontrol tekanan darah
- Tatalaksana nyeri
- Profilaksis serangan kejang
- Kanal kalsium bloker untuk vasospasme

• Komplikasi :
Perdarahan ulang, hidrosefalus, serangan kejang, atau
vasospasme

Simon RP, Greenberg DA, Aminoff MJ. Clinical neurology. 7th

ed. New York: The McGraw-Hill Companies Inc.; 2009.
Diagnostic Algorithm for Subarachnoid Hemorrhage

https://www.ahcmedia.com/articles/125011-is-the-lp-necessary-in-sah-with-new-generation-scanners
 Hematoma Epidural (EH)
• Definisi
Pendarahan pada rongga epidural diantara durameter dan tulang
tengkorak ( antara lapisan periosteal dan lapisan meningeal
durameter )

EH jarang terjadi ( kurang dari 1% kasus trauma kepala )

• Etiology
Rupturnya
A. Arteri meningea media (85%)
B. vena meningea media
C. sinus dura
Dengan atau tanpa disertai fraktur tengkorak.
Pendarahan dari EH dapat menyebabkan kompresi , pergeseran , dan
Peningkatan TIK
• Gejala klinis
1. Mengalami hilang kesadaran singkat setelah trauma kepala , diikuti
Interval Lusid dan kemunduran neurologic.
Ilmu Bedah Saraf Edisi V, 2014
• Diagnosis
Ct scan
Gambaran : Lesi Lentikuler
atau hematoma membentuk
massa bikonveks hyperdense
Lokasi seringkali diregio
temporal atau
temporoparietal.
 Hematoma Subdural Akut
• Akumulasi darah antara duea matter dan araknoid
• Sering terjadi pada trauma berat, pada usia lanjut
pada anak” biasanya karena kekerasan
• Gejala
- nyeri kepala
- mutah , letargi
- hemiparesis
- iregularitas papil disebelah ipsilateral hematoma
- lusid interval

Simon RP, Greenberg DA, Aminoff MJ. Clinical neurology. 7th

ed. New York: The McGraw-Hill Companies Inc.; 2009.
• Patfis :
Robeknya vena penghubung antara korteks serebri
dan drainase sinus vena  peningkatanTIK

• Diagnosis :
CTscan kepala  kumpulan darah berbentuk bulan
sabit(crescent-shaped) diantara otak dan dura,
sulkus dan penyempitan ventrikel, pergeseran garis
tengah krn vol bekuan yg bsr

Simon RP, Greenberg DA, Aminoff MJ. Clinical neurology. 7th

ed. New York: The McGraw-Hill Companies Inc.; 2009.
• Komplikasi:
Peningkatan TIK, edema otak, perdarahan
rekuren, kejang
• Tatalaksana :
- Meminimalkan cedera otak sekunder
- Bedah kraniotomi

Simon RP, Greenberg DA, Aminoff MJ. Clinical neurology. 7th

ed. New York: The McGraw-Hill Companies Inc.; 2009.
 Subdural
hematoma

Blueprints Neurology-Lippincott Williams & Wilkins (2009)

INTRACEREBRAL HEMATOMA
 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
 Clinical features
• 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.
 HYPERTENSIVE ENCHEPHALOPHATY
• Hypertensive
encephalopathy: reversible
acute clinical syndrome
triggered by sudden
increases in blood pressure
beyond the limit of auto-
regulation of the brain.
Systolic blood pressure
limit> 180 mmHg &
diastolic> 120 mmHg
• Etiology: hypertension, pre-
eclampsia or eclampsia,
neurotoxicity due to
cyclosporin A or takrolimus,
uremia and porphyria.
• Clinical Manifestations:
– Severe hypertension syndrome: severe
headache, nausea, vomiting, visual
impairment, convulsions, stupor to coma
– The onset of symptoms usually progresses
slowly, with a progression of about 24-48
hours
– Symptoms of diffuse brain disorders
– Severe neurologic manifestations occur
when hypertension of maligna or diastolic
pressure> 125 mmHg with retinal
hemorrhage, exudates, papillary edema,
cardiac and kidney disorders
• Physical Examination:
– Hypertension crisis: systolic blood
pressure> 180 mmHg & diastolic> 120
mmHg
– Papil edema
– Impaired vision
– Focal neurological deficits
• Supporting Investigation:
– CT-Scan
– MRI
 HYPERTENSIVE ENCHEPHALOPHATY

DD Complications
• Ischemic stroke • hypertension nephropathy
• bleeding stroke • retinopathy hypertension
• intracranial hemorrhage
• Epilepsy
• broad cerebral infarction
• Reversible posterior
leukoencephalopathy
syndrome
 Treatment
• Blood pressure reduction: Blood pressure drop target is 25% reduction in
MAP within 1-2 hours / decrease diastolic pressure by 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
• Labetalol: 20 mg loading dose loading, followed by 20-80 mg repeat bolus
at 10 min intervals. After that continued with drip drip infusion 1-2 mg /
min & titrated according to the desired effect of hypotension
• 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
 Cerebral Malaria
• Cerebral malaria is a common,
life-threatening complication of P.
falciparum infection
• Parasitized RBCs express malarial
cell surface glycoproteins called
knobs that are sticky → capillary
walls → sludging in the cerebral
microvasculature → localized
ischemia, capillary leak, and
petechial hemorrhages.
• Clinical manifestations : fever,
altered mentation including
obtundation, coma, and
occasionally seizures.
• Treatment :
– Intravenous quinine, quinidine, or
artemisinin (if it is available)
– supportive care, including
mechanical ventilation for
comatose patients and
patients with noncardiogenic
pulmonary edema
– antiepileptics; and correction
of acidosis and hypoglycemia
(associated with quinine use
and cerebral malaria).
 Delirium
Introduction
• 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, confusion may
fluctuate
Clinical Features
• Delirium or acute confusional state
generally develops over days.
• Attention, perception, thinking, and
memory are all altered.
• Alertness is reduced as manifested
by difficulty maintaining attention
and focusing concentration.
• The sleep-wake cycles are often
disrupted, with increased
somnolence during the day and
agitation at night, or “sundowning.”
• Tremor, asterixis, tachycardia,
sweating, hypertension, and
emotional outbursts may be
present. Hallucinations tend to be
visual, although auditory
hallucinations can also occur.
 Etiology

Tintinalli’s Emergency Medicine pg 1157

 Diagnosis
• The acute onset of attention
deficits and cognitive
abnormalities fluctuating in
severity throughout the day and
worsening at night is virtually
diagnostic of delirium.
• Check for drug interactions.
• Assess for an underlying process
 pneumonia or urinary tract
infection.
• Ancillary testing : serum
electrolyte levels, hepatic and
renal studies, urinalysis, CBC, and
a chest radiograph.
• Order a head CT if a mass lesion
such as subdural hematoma is
suspected
• Performing a lumbar puncture if
meningitis or subarachnoid
hemorrhage is considered.
• One key tool for detecting
delirium is the mental status
examination and other cognitive
screening instruments
• The Quick Confusion Scale has
been tested in ED patients
• Depression may resemble
hypoactive delirium, with
withdrawal, slowed speech, and
poor results on cognitive testing
present in both conditions.
• Patients with depression are
oriented and able to perform
commands.
 Diagnosis

Tintinalli’s Emergency Medicine pg 1157

 Treatment
• Direct treatment at the underlying cause.
• 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
 Coma
• Coma is a state of reduced alertness and responsiveness from
which the patient cannot be aroused.
• The Glasgow Coma Scale is a widely used clinical scoring
system for alterations in consciousness.

Tintinalli’s Emergency Medicine pg 1159

 DD

Tintinalli’s Emergency Medicine pg 1159

 Clinical Features
Coma from Supratentorial
Toxic Metabolic Coma Lesions
• The diffuse CNS dysfunction is • Coma caused by lesions of
reflected by the lack of focal
physical examination findings the hemispheres, or
that point to a specific region supratentorial masses, may
of brain dysfunction present with progressive
• A notable exception is severe hemiparesis or asymmetric
sedative poisoning as from
barbiturates; the pupils may muscle tone and reflexes.
be large, extraocular
movements absent, muscles
flaccid, and the patient apneic,
which simulates the
appearance of brain death.
 Clinical Features
Coma from Infratentorial Lesions
• An expanding lesion, such as
cerebellar hemorrhage or
infarction, may cause abrupt
coma, abnormal extensor
posturing, loss of pupillary
reflexes, and loss of
extraocular movements.
• Infratentorial cause of coma is
pontine hemorrhage, which
may present with the unique
signs of pinpoint-sized pupils.
Pseudocoma
• Pseudocoma or psychogenic
coma is occasionally
encountered and may
present a perplexing clinical
problem.
• Pupillary responses,
extraocular movements,
muscle tone, and reflexes
are shown to be intact on
careful examination.
 Diagnosis
• Address airway, breathing, and circulation immediately.
• Consider reversible causes of coma, such as
hypoglycemia or opiate overdose. Access all available
historical sources (EMS personnel, caregivers, family,
witnesses, medical records) to aid in diagnosis.
• Abrupt coma suggests abrupt CNS failure with possible
causes such as catastrophic stroke or seizures.
• A slowly progressive onset of coma may suggest a
progressive CNS lesion such as tumor or subdural
hematoma.
• Metabolic causes, such as hyperglycemia, may also
develop over several days.
 Treatment
Antidotes
• Rapid point-of-care glucose
determination can identify
the need for dextrose.
• Naloxone, the opiate
antagonist, is useful in coma
because typical signs of
opiate overdose may be
absent.
Increased Intracranial Pressure
• Mannitol (0.5 to 1.0 gram/kg IV)
can decrease intravascular volume
and brain water and may
transiently reduce ICP
• In cases of brain edema associated
with tumor, dexamethasone, 10
milligrams IV, reduces edema over
several hours.
• Hyperventilation with reduction of
partial pressure of arterial carbon
dioxide can reduce cere- bral blood
volume and transiently lower ICP
 current recommendations are to
avoid excessive hyperventilation
(partial pressure of arterial carbon
dioxide ≤35 mm Hg) during the first
24 hours after brain injury.
 Seizure
• Seizures are episodes of
abnormal neuronal excitation and
are generally a manifestation of
an underlying process.
• Seizures are classified based on
cause (primary or secondary)
– Primary  unprovoked and
not linked to an inciting
event.
– Secondary  trauma, illness,
intoxications and poisonings,
metabolic disturbances, and
cerebral tumors.
• Generalized seizure  abnormal
neuronal activity in both cerebral
hemispheres  alteration in the
level of consciousness.
– Divided into: tonic-clonic,
absence, atonic, and myoclonic.
• Focal seizures  involve one
cerebral hemisphere, thereby
preserving consciousness, although
these seizures may progress and
cause an altered sensorium.
• Some seizures are impossible to
classify because of inadequate or
inaccurate description of the ictal
activity
 Seizure
• Convulsive seizures  • Status epilepticus has
characterized by been classically defined as
uncontrolled, rhythmic at least 30 minutes of
motor movements and persistent seizures or a
can affect part or all of series of recurrent
the body. seizures without
• Nonconvulsive seizures intervening return to full
may manifest consciousness
automatisms, confusion,
altered mental status,
abnormal behavior, or
coma.
 BACTERIAL MENINGITIS
Definition Etiology
• The inflammatory process • Streptococcus pneumonia
of meninges (the lining of (50%)
the brain), especially • Neisseria meningitides
arachnoids & pia mater (25%)
involves the invasion of • Listeria monocytogenes
bacteria into the • Staphylococcus
subarakhnoid space • E.coli
• Klebsiella
• Enterobacter &
Pseudomonas aeruginosa
 Treatment
1. Non farmako
– Fluid therapy: fluid bolus through intravenous or intraosseus NaCl
0.9% 20 ml / kg in 5-10 min
– Electrolyte correction: usually hyponatremia -> intracranial increase
– Decreases intracranial pressure: raises the head by 30 ° and
hyperventilates u / defends PaCO2 ranges from 27-30 mmHg
2. Farmako
– Antibotics: third generation cephalosporins, such as ceftriaxone /
cefotaxim. When resistant to cephalosporin, plus vancomysin. The
duration of administration for 10-14 days is given parenteral scr
– Anti-inflammatory: dexamethasone 10 mg every 6 hours for 4 days
– Osmotic diuresis: Manitol 20% & urea
– Heparinication
– Anticonvulsants
 Fungal Meningitis
• Develops in much the same way as bacterial • Common CNS complications of fungal
meningitis, although this has been meningitis include
incompletely studied. – abscesses,
• Etiology and mechanisms of infection – increased ICP,
– Pulmonary exposure followed by – neurological defcits,
hematogenous spread
– seizures,
– Immune system defects or
– bone invasion, and
immunosuppressive medications compromise
host defense mechanisms – fluid collections.

– Iatrogenic injection with contaminated • The mortality rate is high but variable and is
methylprednisolone related to the timeliness of diagnosis,
underlying illness, and therapeutic regimens
 Comparison of Meningitis

Measure Normal Viral meningitis Bacterial meningitis

Opening pressure (mmH2O) < 180 < 180 > 180
Protein (mg/dL) < 40 Normal or < 100 > 100-200
Glucose (nmol/L) > 2.5 > 2.5 < 2.2
CSF glucose > 0.6 > 0.6 < 0.4
WBC count/mm3 <5 < 1,000 > 1,000
WBC differential 70% lymphocytes MNLs Mainly PMNLs
30% monocytes
Gram stain (%) None NA 75-90
Positive culture (%) None NA More than 70
PCR NA Enterovirus, HSV, VZV, EBV, Test for N meningitidis, S
etc pneumoniae, H. Influenzae
 ENCEPHALITIS
DEFINITION ETIOLOGY EPIDEMIOLOGY PATHOPHYSIOLOGY
Inflammation The most • Virus is the most • The virus enters the
of brain tissue frequently are common cause, Central Nervous
caused by : especially herpes System via two
virus • Herpes virus. routes:
• VZV • Approximately 1. Hematogen
• CMV 30-50% of cases 2. Dissemination
• EBV still not known of retrograde
• HHV6 the exact cause neurons
• Adenovirus • The virus
infecting
parenchyma
brain and nerve
cell cells,
and also the Blood
vessels.
 CLINICAL MANIFESTASION
• Acute Flu-like syndrome + high fever
• Severe headache
• Nausea, vomiting
• Seizures Decreased consciousness
(hallucinations, agitation, changes in
personality, behavioral abnormalities,
and psychotic conditions.
DIAGNOSE
• Anamnesis to determine
etiology
• History may be affected by
smallpox, parotitis, testicular
pain due to pancreatitis caused
by mumps virus.
• Travel history to the tropics.
 Physical Examination Supporting Investigation DD

• Giving the airway, • Cerebrospinal fluid (CSF) 1. Cerebral abscess

measuring the degree examination: 2. Subdural
of consciousness (GCS, • Increased protein empyema
quantitative scale) and concentration 3. Meningoencepha
infection complication • Glucose is normal litis
therapy. • CSF pleocytosis (> 5 4. Toxoplasmosis
• Skin examination of cells) 5. Subdural
purpuric rash • CSF PCR is the ultimate hematoma
(mengococcal) and diagnostic test !!! 6. Tuberculosis.
exanthema. • Examination of HSV CSF
• In HIV patients antibodies.
leukoplakia can be • Neuroimaging examination:
found, sarcoma • CT SCAN head plus
caposis. contrast
• MRI head plus contrast
(> sensitive)
• EEG check
 TREATMENT PROGNOSE
COMMON SPECIALLY • Morbidity rate is still
• Oxygen via mask • Acyclovir 10 mg / kg (3 high.
(NRBM) times daily) IV for 14- • Prognosis factors when
• Sufficient fluids 21 days. age> 60 years and GCS
• Sufficient nutritional • Or Gansiclovir, <6:
needs foscarnet, cidofovir • Neuropsychiatric,
• Symptomatic therapy can also be given. • Impairment of
(anti-pain, febrifuge, memory(69%)
anti-seizure and • personalized
others) change (45%)
• Treatment of • dysphagia (41%)
complications • epilepsy (25%)
(mannitol or
dexamethasone to
reduce ICT)
• Prevents deep vein
thrombosis and
pulmonary embolism
 Treatment

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121461/table/T1/
 Tetanus
• Tetanos – a greek word – to
strech
• A Neurological disease
characterised by increased
muscle tone & spasms.
• Caused by CLOSTRIDIUM TETANI
• An anaerobic, motile, gram
positive rod that forms oval,
colourless, terminal spores –
tennis racket or drumstick shape.
• It is found in soil, animal faeces &
occasionally human faeces
Mode of transmission
• Infection is acquired by contamination
of wounds with tetanus spores.
• Range of injuries & accidents – trivial
pin prick, skin abrasion, puncture
wounds, burns, human bites, animal
bites & stings, unsterile surgery, IUD,
bowel surgery, dental extractions,
injections, unsterile division of umbilical
cord, otitis media, chr.skin ulcers, eye
infections, gangrene
• NOT TRANSMITTED FROM PERSON TO
PERSON
• Types=
– Generalized
– Neonatal
– local
– cephalic
 Clinical features
• May begin from 2 days to several weeks after the
injury – USUALLY 1 WEEK

• Remember
– The shorter incubation period lead to more severe attack
and worsen the prognosis
Clinical Features (Generalized Tetanus)
• Most common • Risus Sardonicus : Spasm of facial
• Increased muscle tone & muscles ( frontalis & angle of mouth
generalized spasms muscles ) producing grinning facies
• Median time of onset after • Opisthotonus : Painful spasms of neck,
injury – 7 days trunk and extremity. producing
• Pt 1st notices increased tone in characteristic bowing and arching of
masseter ( back
Trismus, lock jaw ) • Some pts develop paroxysmal, violent,
• Dysphagia painful, generalized muscle spasms –
• Stiffness / pain in neck, cyanosis .
shoulder, back muscles appear • Spasms occur repetitively & may be
concurrently / or soon spontaneous / provoked by slightest
thereafter stimulation.
• Rigid abd & stiff prox.limb
muscles . • Constant threat during gen.spasm is
reduced ventilation, apnea /
• Hands, feet spared. laryngospasm.
Generalized Tetanus Risus Sardonicus
 Tetanus
Neonatal Tetanus
• Usually fatal if untreated
• Children born to
inadequately immunized
mothers, after unsterile
treatment of umbilical
stump
• During first 2 weeks of life.
• Poor feeding ,rigidity
and spasms
Local Tetanus
• Uncommon form
• Manifestations are restricted to
muscles near the wound.
• Cramping and twisting in skeletal
muscles surrounding the wound – local
rigidity
• Prognosis – excellent
Cephalic Tetanus
• A rare form of local tetanus
• Follows head injury / ear infection
• Involves one / more facial cranial nerves
• Trismus and localised paralysis ,usually
facial nerve, often unilateral.
• Incubation period : few days
• Mortality : high
 Tetanus
Diagnosis
• Based entirely on clinical findings
• Examine all cases with wound infection
& muscle stiffness
• C.tetani can be isolated from wounds of
pts without tetanus & freq cannot be
isolated from wounds of those with
tetanus
• Electromyograms – continous discharge
of motor units, shortening / absence of
silent interval seen after AP.
• Muscle enzymes – raised
• Serum Anti toxin levels >= 0.1 IU/ml –
protective & makes tetanus unlikely .
DD
• Cond producing trismus :
alveolar abscess, strychnine
poisoning, dystonic drug
reactions, hypocalemic
tetany
• Meningitis/encephalitis
• Marked increased tone in
central muscles , with
superimposed generalized
spasms & relative sparing of
hands & feet – sugg tetanus
 Treatment – general measures
• Goal is to eliminate the source of toxin,
neutralize the unbound toxin & prevent
muscle spasm & providing support - resp
support
• Admit in a quiet room in ICU
• Continuous careful observation &
cardiopulmonary monitoring
• Minimize stimulation
• Protect airway
• Explore wounds – debridement
 Treatment
NEUTRALIZE TOXIN :
• Inj.Human Tetanus Immunoglobulin 3000 – 6000 units IM, usually in
divided doses as volume is large.

ANTIBIOTIC THERAPY :
• Although of unproven value , antibiotics adm to eradicate
vegetative cells – the source of toxin
• IV Penicillin 10 -12 million units daily for 10 days
• IV Metronidazole 500mg Q 6 hrly for 7 days
• Allergic to Penicillin : consider Clindamycin & Erythromycin

MANAGEMENT OF AUTONOMIC DYSFUNCTION

• Labetalol
• Continuous infusion of esmolol
• Clonidine / verapamil
 Control of Spasms
• Nurse in a quiet dark room
• Avoid noise & other stimuli
• IV Diazepam / Lorazepam / Midazolam
• Barbiturates & Chlorpromazine –2nd line drugs
• Continued spasms : intubate & ventilate
• Propofol, dantrolene, intrathecal baclofen,
succinylcholine & magnesium sulfate can be tried