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

I.
a.

Neurologic
b.

Seizures Vascular dementia

II.
a.

Infection
b.

Urinary tract infection, urosepsis Dysphagia, aspiratio pneumonia

III.
a. b. c.

Complication of immobility
Falls Hemiosteoporosis, fractures Pressure ulcer

IV.
a. b.

Thromboembolism
Deep vein thrombosis Pulmonary embolism

V.
a. b.

Pain
Shoulder pain Central poststroke pain

VI.
a. b. c. d.

Psychological
Depression Anxiety Confusion Emotional incontinence

Medical Complication of Stroke

VII.
a.

Miscellaneous
b.
c. d. e. f.

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)

Deep-vein thrombosis and pulmonary embolus Hemiosteoporosis and hip fractures Falls Pressure sore, skin ulcers Peripheral nerve injury Shoulder pain Central poststroke pain

2)

Pain
a) b)

3)

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

1.

Berupa aritmia dan gangguan repolarisasi transient :

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

2.

Penyebab:

Degenerasi miofibriler otot jantung Di duga karena stress myocard akibat stimulasi symphatetic central

Kejang dan Stroke

1.

2.

Frekuensi 5-10% dalam 2 minggu pertama. Resiko paling tinggi pada perdarahan intracerebral lobar/kortikal Daerah lainnya:
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
Children
Abnormal EEG, esp.epileptiform features Symptomatic cause

Less
Adult
Normal EEG Cryptogenic seizures

Focal onset with secondary generalization Seizure occuring during sleep

COMMON PRESENTATION OF SEIZURES IN THE ICU

SEIZURE TYPE Fokal motor CLINICAL EXPRESSION Face or limb motor seizure, may propagate from distal to proximal, no alteration of sensorium Loss of consciouness, generalized convulsions with tonic phase followed by clonic phase and post-ictal altered sensor sensorium Disturbed sensorium (aura), can br followed by generalized tonic-clonic seizure Disturbed sensorium or loss of consciousness, minimal face or distal limb twitches

Generalized Tonic Clonic

Complex Partial

Non-Consultive Status

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.

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.

2.

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 :

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) Treatment with anti depression : Nortrityline (Lipse et al, 1984) Fluoexetine (Robinson et al 2000) Trazodon (Reading et al, 1986)

Frequency :

Management :

Peripheral Neuropathies in Stroke Patients

Peroneal neuropathy Ulnar neuropathy Median neuropathy Femoral neuropathy Concomitant diabetic neuropathy