Neuro Emergency pada

Stroke
jkt

Dr. Eddy Ario Koentjoro Sp S

Penanganan Stroke Akut harus

Cepat Tepat dan Efisien
Mengurangi

mortalitas, disabilitas, stroke

ulang
Mencegah Komplikasi
Komplikasi Serebral -------Minggu Pertama
Edema Serebri
Komplikasi Non Serebral ----Minggu 2-4

Medical Complication of Stroke

Neurologic

I.
a.
b.

Seizures
Vascular dementia

Infection

II.
a.
b.

Urinary tract infection, urosepsis

Dysphagia, aspiratio pneumonia

Complication of immobility

III.
a.
b.
c.

Falls
Hemiosteoporosis, fractures
Pressure ulcer

Thromboembolism

IV.
a.
b.

Deep vein thrombosis

Pulmonary embolism

Pain

V.
a.
b.

Shoulder pain
Central poststroke pain

Psychological

VI.
a.
b.
c.
d.

Depression
Anxiety
Confusion
Emotional incontinence

Medical Complication of Stroke

VII.
a.
b.
c.
d.
e.
f.

Miscellaneous
Gastrointestinal hemorrhage
Constipation
Cardiac failure, arrythmias
Arthritis
Sleep apnea
Nutritional deficiencies

(Langome et al 2000)

Medical Complication of Stroke

1)

Disorders of immobility
a)
b)
c)
d)
e)

2)

Pain
a)
b)

3)

Deep-vein thrombosis and pulmonary embolus

Hemiosteoporosis and hip fractures
Falls
Pressure sore, skin ulcers
Peripheral nerve injury
Shoulder pain
Central poststroke pain

Incontinence

Komplikasi Neurologik
Timbulnya

edema serebral : memperburuk

daerah penumbra dan menaikan TIK
keadaan darurat/kritis
Proses stroke akut dapat menimbulkan
komplikasi darurat medik :
Perdarahan

gastrointestinal neurologik
Edema pulmoner neurologik
Hyponatremia
Komplikasi cardiac neurologik

EDEMA CEREBRAL PADA STROKE

1.
2.
3.

4.

Sering timbul pada infark cerebri yang

luas
Maximum pada hari ke 7-10 dan
kemudian berkurang
Korelasi dengan effect massa,
pergeseran garis tengah, keadaan klinik
dan outcome
Penyebab kematian utama pada stroke
minggu pertama

Pengobatan Cerebral Edema

1.

2.
3.

Pengobatan pharmakologik cerebral

edema dengan pengobatan zat-zat
osmolar
Pengobatan dengan diuretika
Pengobatan dengan intubasi dan
hyperventilasi

Zat-zat Hyper Osmolar Pada Cerebral

Edema
A.
B.
C.
D.

E.
F.

Glycerol mengurangi dengan efektif cerebral edema

(Rogvi-Hansen & Boysen,1995)
Mengurangi odds of early death sebanyak 42% dan
pada final meta analisis terjadi penurunan 18% saja
Diberikan dalam bentuk larutan 10% glycerol dalam
isotonic saline, 500 cc per 4-6jam, rebound jarang
Mannitol 1-2 gr/bb secara iv yang diberikan selama 30
menit merupakan dosis initial dan jika diperlukan dapat
ditambah 0,25-0,5 gr diberikan selama 30-60 menit
dan dapat di ulang tiap 4-6 jam
Akhir-akhir ini larutan hypertonic saline diberikan
secara bolus dapat mengurangi edema cerebral
Furosemide diberikan tersendiri atau denga kombinasi
manitol. Dapat digunakan sebagai alternatif lain

Zat-Zat Hyper Osmolar pada Cerebral

Edema
G.

H.

Upaya terakhir adalah pasien dimasukkan ke ICU

kemudian di Intubasi, dan dilakukan hyperventilasi
terkontrol dengan sasaran PACO2 dipertahankan 2530 mmHg
Dekompresi dengan kraniotomi dengan segala
resikonya

Intracranial Content
Brain
Blood
CSF
Total

1400 cc
150 cc
150 cc
1700 cc

80%
10%
10%
100%

Intracranial Decompressive Surgery

1)
2)
3)
4)

5)
6)

Age less than 40

Glasgow coma scale score greater than 3 on
initial examination
No extra or intracerebral mass lesion or
infarction on CT
Objective evidence of neurologic deterioration
(change in Glasgow, coma scale score, pupils,
EEG or CBF)
Absence of irreversible neurologic damage
Failure of medical therapies for elevated
intracranial pressure (Gaab et al 1990)

Perdarahan Gastro-Intestinal pada Stroke

Sering

terjadi pada akut stroke

Akibat stimulasi central simpatetik, pada infark cerebri
lebih sering terjadi hyperasiditas lambung
Pada perdarahan intracerebral lebih sering terjadi
perdarahan lambung
Pada keadaan koma/kesadaran menurun,
pemasangan tube nasogastrik diharuskan untuk
mengeluarkan cairan lambung dan mencegah
aspirasi cairan
Pengobatan
Pada keadaan hyper asiditas dilakukan spooling
cairan lambung yang periodic dan ditambahkan
cairan yang bersifat basa untuk mengikat asam
lambung
Perdarahan lambung diatasi dengan puasa dengan
pemberian obat-obatan yang memblokade sekresi
asam ( H receptor Antagonis)

Neurogenic Pulmonary Edema

Akibat stimulasi sympatetik sentral

Lesi di Hypotalamus, Nukleus Tractus
Solitarius dan Medulla Oblongata

Bentuk Klinik :

A.
B.

Bentuk Klasik timbul Menit - Jam setelah

Insult
Delayed Form timbul 12-72 Jam Post
Insult

Gambaran Klinik Neurogenic Pulmonary

Edema
1.
2.
3.
4.

Berupa dyspnea, nyeri dada, dan

hemoptisis ringan
Pemeriksaan menunjukkan tachypnea,
tachycardia dan rhonchi Basah difus
Thoraks foto : Gambaran Edema paru
Umumnya menghilang spontan atau
dicegah dengan ganglion blocker (misal :
Dobutamin)

Hyponatremia
1.

2.

Syndrome of inapropriate secretion of

antidiuretic hormone (SADH):
Hyponatermia urine, Hypernatremia dan
Hypervolumia Restriksi cairan
(Scwartz, 1957)
Cerebral Salt Wasting Syndrome (CSW) :
Hypernatremia, urine hypernatermia, dan
Hypovolumia -----Salt & fluid
Replacement (Peters, 1950)

Komplikasi Cardiak Pada Stroke

Berupa aritmia dan gangguan repolarisasi
transient :

1.

AV Block
Supra ventrikular tachycardi
Sinus bradicardi
Paroksisma ventricular tachycardi
AV disosiasi
Ritme nodal

Penyebab:

2.

Degenerasi miofibriler otot jantung

Di duga karena stress myocard akibat stimulasi
symphatetic central

Kejang dan Stroke

Frekuensi 5-10% dalam 2 minggu
pertama. Resiko paling tinggi pada
perdarahan intracerebral lobar/kortikal
Daerah lainnya:

1.

2.

Stroke di daerah teritori karotis

Stroke yang luas dengan defisit neurologik
yang menetap

(Olsen et al 1987, Giroud et al 1994, Killpatrick et al 1990)

Neurological Pathology

Neurovascular
Thrombo - emboli ischemic Stroke
Vascular malformations
Hemorrhagic states resulting from the above
Tumor
Primary
Metastatic
CTN infection
Absces
Meningitis
Encephalitis
Inflammtory disease
Vasculitis

Acute disseminated encephalomyelitis

Trauma
Contusion
Hemorraghe
Primary epilepsy
Primary inherited CNS metabolic disturbance

Risk factor for recurrence

after an initial seizure
Greater

Less

Children

Adult

Abnormal EEG, esp.epileptiform

features

Normal EEG

Symptomatic cause

Cryptogenic seizures

Focal onset with secondary

generalization
Seizure occuring during sleep

COMMON PRESENTATION OF SEIZURES IN

THE ICU
SEIZURE TYPE

CLINICAL EXPRESSION

Fokal motor

Face or limb motor seizure, may propagate

from distal to proximal, no alteration of
sensorium

Generalized Tonic Clonic

Loss of consciouness, generalized

convulsions with tonic phase followed by
clonic phase and post-ictal altered sensor
sensorium

Complex Partial

Disturbed sensorium (aura), can br followed

by generalized tonic-clonic seizure

Non-Consultive Status

Disturbed sensorium or loss of

consciousness, minimal face or distal limb
twitches

Proposed Duration of Status Epilepticus

30 minutes - EFA Working Group on SE
1991
20 minutes - Bleck
10 minutes - Treiman et al
1998
5 minutes - Lowenstein
1983

TREATMENT OF ICU SEIZURES

1.

2.

Brief single seizures (<60 scc)

Observer Ensure adequate O2 saturation and vital signs. Eliminate

etiology.

Consider chronic therapy : phenytoin 15-20mg / kg or

fosphenytoin15-20 mg/kg phenytoin equivalents (PE) loading dose
and 300-400 mg/day. Goal serum level 10-20 mcg/ml or free level 1-2
mcg/ml.

Phenytoin intolerant patients: IV/PO valproic acid, 15-20 mg/kg load,

maintenance 600-3000 mg/day or PO carbamezapine 600-1200
mg/day.

Seizure precautions - padding bed rails, increased observation.

Prolonged or > 1 seizure

Ensure adequate oxygen saturation, vital signs

IV benzodiazepine - lorazepam 1-2 mg, diazepam 10-20 mg or
midazolam 2-5 mg with concurrent loading dose phenytoin or
fosphenytoin (PE) 15-20 mg/kg and maintenance as above.
Phenytoin intolerant : Valproic acid 15-20 mg/kg, maintenance 400600 mg q6hr
Similar seizure precautions.

TREATMENT OF ICU SEIZURES

3.

Recurrent or refractory seizures > 5 min 0r > 2 discrete seizures

without recovery of coenynsciousness

Consider as status epilepticus

Maintain airway, preserve ventilation and oxygenation, endotracheal
intubation if indicated to protect airway.
Measure blood glucose. IV glucose only if less 10-60 mg/100 dl.
Immediate benzodiazepines-IV, lorazepam 5-10mg, diazepam 20-40 mg, or
midazolam 5-20 mg over 5 min.
Phenytoin loading dose 20 mg/kg at 50 mg/min or fosphenytoin 20 mg/kg
PE at 150 mg/min.
Continuous EEG, if available.
If Seizures continue phenytoin or fosphenytoin (additional 5-10mg/Kg or 510mg/Kg PE)
If seizures continue : pharmacological EEG seizures supression, burst
supression if necessary- profapol 2 mg/Kg and 150-200mcg/Kg/min
infusion or thiopental 4 mg/Kg and 0,3-0,4 mg/Kg/min
Hemodynamic support : fluids, pressors, inotropes
Once EEG supressed, complete loading of anticonvulsant, add aditional
benzodiazepine if necessary, and consider wearing infusion agent several
hrs after optimal anticonvulsant levels obtained through serum levels
measurement
If seizures persist, consider prolonged barbiturate or anesthetic coma with
pentobarbital 12 mg/Kg at 0,2-0,1 mg/Kg/min followed by an infusion of
0,25-2,0 mg/Kg/hr for continued EEG supression

THROMBOE STRMBOLISME PADA STROKE

Bentuk Klinik :
A.
Thrombosis vena dalam
B.
Emboli pulmunal

Frekuensi terjadi pada 10-20% kasus stroke akut, penyebab 510% kematian (kelly, 2001)

Faktor penting lain : Hypertensi, Obesitas, dan merokok

Resiko tinggi pada stroke dengan imobilitas berat.

Diagnosa dengan :
1. CT Scan paru dengan spiral CT
2. Pemeriksaan baku emas : Angiografi pulmoner

Pengobatan dengan
1. Heparin 5000 unit 2x sehari selama 1-2 minggu
Dilanjutkan dengan oral anti kuagulan selama 6 bulan.
2. Low moleculer weight heparin diberikan beberapa minggu
kemudian di teruskan dengan oral anti kuagulan selam 6
bulan.

Medical Treatment for Central

Poststroke Pain

First-line
Amitriptyline
Lamotrigine

Alternative and adjunctive options

Lidocaine, intravenous
Other tricyclic antidepressants : nortriptyline, desipramine,
maprotiline
Other anticonvulsants valproate, carbamazepine, phenytoin
Mexiletine
Naloxone
Baclofen
Supported by controlled clinical trials data

Factors Contributing to Poststroke

Urinary Incontinence
Premorbid conditions
a)
b)
c)

Peripheral neuropathy (eg, diabetic

dysautonomia)
Changes in the urinary tract (eg, prostatic
hypertrophy)
Medications : anticholinergic drugs
(precipitate retention), alpha-adrenergic
blockers (worsen urethral sphincter
weakness), diuretics (detrusor contraction
by causing rapid bladder filling)

Acute Stroke-related dificits

a)

b)
c)

Impairment of neurologic micturition

control mechanism, causing a
hyperreflexic bladder
Acute bladder hypotonia at the time of
stroke
Lapse in diabetic control, leading to
glycosuria

Depression After Stroke

Symptoms :

Frequency :

Sadness, anxiety, tension, less of interest, sleep disturbance

with early morning awakening , apetite and weight loss, difficulty
in concentrating and thingking, and thoughts of death (at least 5
symptoms should be present)
40-50% acute stroke patients sufferd from major depression
(burville et al, 1995)
Major post stroke depression is asociated with left cortical lesion
(mainly frontal) and sub cortical lesion (mainly basal ganglia)

Management :

Treatment with anti depression :

Nortrityline (Lipse et al, 1984)
Fluoexetine (Robinson et al 2000)
Trazodon (Reading et al, 1986)

Peripheral Neuropathies in Stroke

Patients
Peroneal

neuropathy
Ulnar neuropathy
Median neuropathy
Femoral neuropathy
Concomitant diabetic neuropathy