Stroke Perawat

7/29/2019 Stroke Perawat

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STROKE

Dodik Tugasworo


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PENYAKIT SARAF

NYERISAKIT KEPALA

MIGREN

VERTIGO

KESEMUTAN

PARKINSON

EPILEPSI

INFEKSI OTAK

GANGGUAN INGATAN

GANGGUAN PERKEMBANGAN ANAK

GANGGUAN GERAK

TUMOR OTAK

GEGAR OTAK

PIKUN BUYUTAN

STROKE


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KENAPA BISA STROKE ?

BAGAIMANA GEJALA STROKE ? BAGAIMANA CARA

PENGOBATANNYA ?

BAGAIMANA PERAWATAN SETELAHSTROKE ?

BAGAIMANA HIDUP DENGAN STROKE

DAN HIDUP DENGAN PENDERITASTROKE ?


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APAKAHSTROKE ?

SUHARTO

GUS DUR

MENDADAK

MENCEMASKAN KESEMBUHAN

MENAKUTKAN KECACATAN

MENGGELISAHKAN KEMATIAN


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STROKE

Penyakit dengan mortalitas tinggi ke 3 di AS (sesudah penyakit jantung & kanker)

(Laporan ke Preseiden, 1964 - 65)

mengenai (insidensi) hampir 400.000/thn (AS,Whisnant, 1971)

membunuh 200.000 orang/tahun (AS, Kurtzke,1980)

INDONESIA & NEG. BERKEMBANG :PREVAL &MORTALITAS MENINGKAT

STROKE adalah MASALAH KESH. MASYARAKAT


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Problems (United State)

160.000 death / years

730.000 new case and recurrent stroke (97)

A new case stroke every minute

Death case stroke every three minute

direct-costs $ 27 billion

indirect-costs $ 13 billion (1996)


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Out Come of Acute Stroke patients

Stroke Unit Dr Kariadi Hospital Semarang 2001

0

50

100

150

Ischaemic Haemorrhagic

Recovery Force discharge Death


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BATASAN STROKE

W.H.O 1986 memberikan batasan sbb ;

Suatu TANDA-TANDA KLINIS yang

BERKEMBANG CEPAT akibatGANGGUAN FUNGSI - OTAK FOKALatau GLOBAL dengan GEJALA GEJALA

yg berlangsung 24 jam atau lebih /menyebabkan KEMATIAN tanpa sebablain selain VASKULER


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STROKE (BRAIN ATTACK)(Adams Jr 2003)

S lurred speech, difficulty understanding others

L

OW

H

E

A

D

egs clumsy or numb

ne side of body affectedeakness

eadache, unusually severe (or facial numbness)

yes: loss of sight (in one eye or both eyes)

rms clumsy or numb AND/OR

izziness


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INCIDENCE OF THE MAIN CAUSES OF STROKE


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Anatomi Otak Kita

Otak kita terdiri atas 2 belahan, otak KIRIdan otak KANAN

Otak kiri berfungsi sebagai pemantau dan

pelaksana the three Rs (Reading, wRitingand aRhithmetic), bersifat logis analistis

Otak kanan pola kognitif yang intuitif holistik,memproses segala informasi secara simultan,memandang problem secara holistis, jauhkedepan, mengenal wajah orang dan melihatsifat sifat secara keseluruhan. Imajinasi,

persepsi visual, orientasi tempat, emosi.


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ANATOMI DAN FUNGSI OTAK

O T A KKUMPULAN

PUSAT-PUSAT

TUGAS BERAT

PERLU MAKANAN YANG CUKUP

DAN TERATUR

TIAP MENIT : 800 CC OKSIGEN

100 MGR GLUKOSA

TERHENTI

30 DETIK

TERHENTI

3 MENIT

TERHENTI

8 MENIT

SEL TERGANGGU

KECACATAN

MENINGGAL

SEL MATI

BERAT :1200 - 1400 GRAM

(2 % BB)


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Gejala dan tanda yang timbul padastroke harus sesuai daerah yang

terkena.

Cacat yang timbul pada strokeumumnya terjadi akibat kerusakan pada

area motorik di otak. Gejala yang timbul pada stroke tidak

selalu nyata, kadang ringan dan

tersamar (misal bahasa, memori, emosi,perilaku, demensia, dsb)


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ARTERIAL TERRITORRIES OF CEREBRAL HEMISPHERES


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ARTERIAL TERRITORRIES OF CEREBRAL HEMISPHERES

LEFT (FRONTAL); RIGHT (HORIZONTAL)

3

21

1

2

3

1 = nucleus lentiformis; 2 = thalamus; 3 = nucleus caudatus

Red =a.cerebri ant. Green =a.cerebri med. Yellow =a.cerebri post. Light blue =a.choroidea ant.Dark green =a.choroidea post. Dark blue =a.commun.post


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ANTERIOR AND POSTERIORVASCULAR SYNDROMES(FELBERG 2003)

Syndrome Localization----------------------------------------------------------------------------------------------------------------- Anterior (carotid) artery syndromesMiddle cerebral artery

Expressive aphasia Dominant posterior frontal lobe Receptive aphasia Dominant superior temporal lobe Weakness of arm and/or leg Contralateral (to weakness) parietal

lobe Loss of lateral visual fields Contralateral parietal lobe

Anterior cerebral artery Weakness of leg Medial (parafalcine) parietal lobe

Posterior (vertebrobasilar) artery syndromesVertigo, nystagmus that changes with the direction Cerebellumof gaze, cranial nerve palsies, retropulsion Hemiparesis, hemisensory loss, of one-half of the Brainstem

body, swallowing difficulty

(motoric)(sensoric)


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COMMON PATTERNS OF NEUROLOGICIMPAIRMENTS IN ACUTE ISCHEMIC STROKE (1)

(Adams 2003)

L. (DOMINANT) HEMISPHERE R. (NONDOMINANT) HEMISPHERE

(major or branch cortical infarction) (Major or branch cortical infarction)

- Aphasia - Left hemiparesis

- Right hemiparesis - Left sided sensory loss

- Right sided sensory loss - Left sided spatial neglect

- Right sided spatial neglect - Left homonymous hemianopia

- Right homonymous hemianopia - Impaired left conjugate gaze

- Impaired right conjugate gaze


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COMMON PATTERNS OF NEUROLOGICIMPAIRMENTS IN ACUTE ISCHEMIC STROKE (2)

(Adams 2003)

DEEP (SUBCORTICAL) HEMISPHERE BRAIN STEMOR BRAINSTEM (LACUNAR STROKE)

- Hemiparesis (pure motor stroke) or - Motor or sensory loss in all

sensory loss (pure sensory stroke). four limbs.- Dysarthria, including dysarthria- - Crossed signs (signs on sameclumsy hand. side of face/other side of

body).- Ataxic-hemiparesis. - Dysconjugate gaze.- No abnormalities of cognition, - Nystagmus ; Ataxia.

language or vision. - Dysarthria; Dysphagia.

CEREBELLUM- Ipsilateral limb ataxia.- Gait ataxia.


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S T R O K E

(GANGGUAN PEREDARAN DARAH OTAK)

DOKTER

SPESIALISSARAF

SEMBUH

SEMPURNA

MENINGGAL

MENYANDANG

CACAT

F A K T O R

R I S I K O

FAKTOR

PENCETUS

TERGANTUNG

PADA KECEPATANBEROBATNYA


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bukan stroke

..

Dokter menyimpulkan : gangguan di otak

stroke

Keluhan pasien :

tentukan jenisnya

SNH atau SHCara : - anamnesis- pemeriksaan klinis neurologi- algoritma dan penilaian dgn skor stroke- pemeriksaan dgn menggunakan alat


26/99Stroke Prevention


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Risk Factors1

Non modifiable Age

Race

Gender

Family history of stroke.


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Risk Factors-2

Modifiable / treatable Hypertension atrial fibrillation

Diabetes mellitus hyperhomocysteinemia Hyperlipidemia hypercoagulability Cigarette smoking oral contraceptive Infection: chlamydia, helicobacter, viruses.

Prior stroke/TIA carotid stenosis Physical inactivity, obesity, sleep apnea/

snoring. Alcohol abuse.

(Stroke, February 2001)


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Diagnosis jenis strok (SI, SH, PSA,PIS)sejak dahulu sulit, seringkali meragukan,

lama sampai diterapkannya CT-Scanningdalam klinik (1972).

DIAGNOSIS JENIS STROK


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ANAMNESIS

Tabel 1. Perbedaan stroke hemoragik dan stroke infark

Mendadak

Istirahat( + )

( - )( - )

Mendadak

Sedang aktif( - )

+++

( + )( + )

+++

-Onset/awitan

-Saat onset-Peringatan

-Nyeri kepala

-Kejang-Muntah

-Penurunankesadaran

Stroke infarkStroke hemoragikGejala (symptom)


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Perbedaan Stroke Hemoragik dan

Stroke Infark berdasarkan anamnesis

Gejala/Simtom Stroke Stroke non

hemoragik hemoragik

Saat onset Sedang aktif Istirahat

Peringatan (warning ) - +

Nyeri kepala +++ +

Kejang + -

Muntah + -

Penurunan kesadaran +++ +


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Tanda (sign) Stroke Hemoragik Stroke Non

Hemoragik

Bradikardi ++ (dari awal) (hari ke-4)

Udem papil Sering + -

Kaku kuduk + -

Tanda Kernig,Brudzinski ++ -

Perbedaan Stroke Hemoragik dan Stroke

Infark berdasarkan tanda-tandanya


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II. STROKE BERDASARKAN PENYEBABNYA

1. STROKE HEMORAGIK = STROKE PERDARAHAN

PERDARAHAN OTAK

KURANG

DARAH

KECACATAN

PUSAT

KESADARAN

KEMATIAN

TIDAK SADAR

PUSAT NAFAS

PUSAT JANTUNG


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2. STROKE NON HEMORAGIK = STROKE SUMBATAN

= SUMBATAN OTAK

DAERAH

MATI

A.

B.

C.

D.

PENEBALAN DINDING

ALIRAN DARAH LAMBAT

DARAH KENTAL

DAERAH PENUMBRA

(DAERAH SETENGAH MATI)

HARUS DISELAMATKAN

KECACATAN

KECACATAN DIKURANGI

SEMAKSIMAL MUNGKIN

FISIOTERAPI

SUMBATAN / EMBOLUS


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Diagnosis Stroke

- Berdasarkan temuan klinis- Pemeriksaan Penunjang

PEMERIKSAAN PENUNJANG

Tujuan : -menegakkan diagnosis

-mencari faktor risiko

-mencari faktor penyulit


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LABORATORIUM

1. DARAH

- Rutin

- Hematokrit

- Masa perdarahan dan pembekuan

- Gula Darah I / II

- Kolesterol total, HDL, LDL- Trigliserid

- Asam urat

- Ureum , Kreatinin

- Elektrolit

- Khusus : - Agregasi trombosit - Homocysteine- APTT - Fibrinogen

- D-dimer - Protein C dan S


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2. LUMBAL PUNGSI

- perdarahan sub arahnoid

3. X- FOTO TORAKS- besar jantung, penyakit paru

4. EKG

- fibrilasi atrium, iskemik/infark jantungEKOKARDIOGRAFI

- sumber emboli di jantung dan aorta proksimal

5. NEUROSONOGRAFI

- stenosis, vaso spasme

6. ANGIOGRAFI SEREBRAL

- AVM, anuerisma


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Pemeriksaan Neuroimajing/neurosonologi (NINS)selain dengan CT Scan & MRI ialah dengan

Angiografi serebral, PET, SPECT, dan sonografidopler (Transcranial Doppler Sonography = TCDS)untuk mendeteksi stenosis vaskular ekstra danintrakranial untuk membantu evaluasi diagnostik,

etiologik, terapetik dan prognostik


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KEUNTUNGAN TCD

EFFEKTIVE

MUDAH DIGUNAKAN

NON-INVASIVE NON-RADIO AKTIVE

PORTABLE

MURAH DAPAT DIULANG DAN AMAN

Report of the American Academy of Neurology (1990)


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KEKURANGAN TCD

POSISI ANATOMI PEMBULUH DARAH BERBEDA, LETAK DARIARTERI SULIT DITEMUKAN

PENYAKIT BILATERAL SIMETRIS, VASOCONSTRICTION ORSTENOSIS PADA REGIO YANG LUAS, DAN ARTERI DISTAL DANARTERI PENETRATING SULIT DIPERIKSA

SEBAGIAN PENDERITA TIDAK PUNYA WINDOW



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TCD HAS ESTABLISHED VALUE IN :

DETEKSI STENOSIS BERAT (>65%) DI PEMBULUH DASAROTAK

DAPAT MEMBERI GAMBARAN SIRKULASI KOLATERAL DENGAN

MENGETAHUI REGIO PADA STENOSIS BERAT OR SUMBATAN DAPAT EVALUASI DAN MENGIKUTI PASIEN DENGAN

VASOKONSTRIKSI PADA SEMUA KASUS, KHUSUSNYA SETELAHSAH

DETEKSI AVM DAN MELIHAT SUPPLY ARTERI DAN GAMBARAN

ALIRAN DAPAT UNTUK MELIHAT KEMATIAN OTAK

PUSING KRONIS, MIGREN, VERTIGO



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KEGUNAAN TCD :

DETEKSI STENOSIS BERAT (>65%) DI PEMBULUH DASAROTAK

DAPAT MEMBERI GAMBARAN SIRKULASI KOLATERAL DENGANMENGETAHUI REGIO PADA STENOSIS BERAT OR SUMBATAN

DAPAT EVALUASI DAN MENGIKUTI PASIEN DENGANVASOKONSTRIKSI PADA SEMUA KASUS, KHUSUSNYA SETELAHSAH

DETEKSI AVM DAN MELIHAT SUPPLY ARTERI DAN GAMBARAN

ALIRAN DAPAT UNTUK MELIHAT KEMATIAN OTAK

PUSING KRONIS, MIGREN, VERTIGO



51/99

CT Scanning tanpa kontras merupakanpemeriksaan baku emasuntuk menentukan

jenis patologi strok, lokasi dan ekstensi lesi,serta menyingkirkan lesi non vaskular(Konsensus Nasional 1999).

Godfrey HOUNSFIELD (1971) ahli fisika danJames AMBROSE (1972) dokter radiologiInggris, pada 1979 memperoleh anugrahNOBEL untuk penemuan CT Scan, yang

dengan sinar-X diubah impuls listrik,memproyeksi titik-titik tubuh menjadi gambar2 dimensi dengan bantuan komputer


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Pemeriksaan MRI diindikasikan untukdiagnosis jenis lesi patologik strok denganlebih tajam (Konsensus Nasional 1999).

RaYmod DAMADIN (1960), menggunakanMRI dalam riset; atas dasar interaksi

gelombang RADIO dgn inti PROTON dlmMEDAN MAGNIT yg kuat tanpa sinar-X,dgn gambar tajam; dan digunakan di RS

(1980 an)


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KONTRA INDIKASI MRI

Kontra indikasi relatif :

1. Artificial joint2. Middle ear protesis

3. Corpus alienum/benda-benda logam

4. Hamil muda

Kontra indikasi absolut

1. Terhadap penderita dgn alat pemacujantung

2. terhadap pend. dgn hemostatic clip

(cerebral aneurysma.


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KELEBIHAN DAN KEKURANGAN MRI

Kelebihan :

1. Non invasive2. Banyak potongan yg dpt dilakukan secara langsung

3. Dgn akurat sangat tinggi hampir semua jaringan

4. Tdk memakai sinar-X

5. Tdk merusak keshehatan pd penggunaannya yg tepat6. Banyak pekerjaan yg dpt dikerjakan tanpa zat kontras

7. Potongan yg dihasilkan dpt 3 dimensi (aksial, frontal,dan sagital) dan malah banyak potongan dapat dibuathanya dlm datu waktu (dpt membuat > 8 potongansekaligus)


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KELEBIHAN DAN KEKURANGAN MRI

Kekurangan :1.Tdk dpt digunakan u/penderita gawatdarurat/darurat akut, yg non koperatif / anak-anak karena pem ini memerlukan wkt yg lama,

dan alat-alat bantu yg bersifat ferromagnetik tdkdpt masuk ke ruang pemeriksaan (gantry)

2. Sementara pemeriksaan berlangsung ada suaragaduh

3. Biaya pemeriksaan dan pemeliharaan lebih tinggidari biaya pemeriksaan radiologi lainnya.


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PENANGANAN STROKE


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PENANGANAN STROKE

5 B

Penanganan Stroke Akut

Penanganan Faktor risiko

Penanganan Komplikasi

Rehabilitasi

Penanganan Post Stroke


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5 "NO" OF MEIER RUGE FOR ACUTE


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5 NO OF MEIER RUGE FOR ACUTE

ISCHEMIC STROKE THERAPY (1990)

1. No antihypertensives *,

2. No diuretics,

3. No dexamethasone,

4. No glucose infusion,

5. No anticoagulant 4 hours after onset ofstroke.

* Except aortic dissection, acute myocardial infarction,heart failure, acute renal failure, hypertensiveencephalopathy, thrombolytic therapy (T 185/110mm Hg) (Brott 2000).

APPROACH TO ACUTE ISCHEMIC STROKE


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APPROACH TO ACUTE ISCHEMIC STROKEMANAGEMENT (5 P): (Felberg 2003)

PARENCHYMA: Management of the ischemic cascade neuroprotectiveagents. Until now none is approved by the FDA.

PIPES (BLOOD VESSEL) :1. Antitrombotic

1.1 Anti-platelet ASA 160-300 mg (IST 1997, CAST 1997)1.2 Anti-coagulantia (LMWH no benefit) (Hommel 1998, TOAST 1998,

Adams1999)

2. Trombolytic2.1 Trombolysis IV rtPA (FDA 1996) (time window 3 hrs).2.2 Trombolysis IA (1998) (prourokinase) time window 6 hrs.

PERFUSION: Induced hypertension ? ; Crystalloid/colloid solution

(Pentastarch?) in cardiac output 10% improved outcome;Bed position < 300 angle. PENUMBRA: Management of the ischemic penumbra neuroprotectors ? PREVENTING COMPLICATION: Control of fever; glycemic control; DVTprecautions; aspiration precaution; avoid indwelling catheters; bowelregimen; early mobilization.


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The first 30 minutes.

Rapidly stabilize the patient, insert anIV- line. No glucose.

Make a quick but thorough neurologicalassessment: stroke or non stroke?

Withdraw blood for the most urgenttests: blood glucose, CBC, electrolytes.

Sent the patient for brain-scan.

CDP-choline?


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Common stroke mimics.

Hypoglycemia

Post-ictal state

Drug overdose

Encephalopathies with focal signs Hyponatremia

Subdural hematoma/empyema

Concussion with neck injury Facial nerve palsy!

Migraineous accompaniment.


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The next hour.

CT-scan reveals no ICH, blood tests andhistory no contra-indication forthrombolytic therapy: r-tPA. Followguidelines scrupulously! May inducehemorrhagic transformation of infarct.

Pentoxyfilline, nimodipine or piracetam ?

Cerebrolysin ?European Stroke Conference2001.

CDP-choline?

LMWH in selected cases.


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.r-tPA induced bleeding. - 7%

74-year old.

2 hours after onset

BP 155/70 Normal platelets, etc.

.t-PA administered

Stuporous after 9 hrs. Re-CT bleeding


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The first 24 hours.

Observe the patient closely for any signs ofdeterioration. Repeat brain scan ifnecessary.

Do not lower blood pressure except in thepresence of impending cardiacdecompensation.

Perform additional laboratory tests the nextday. Do not forget albumin, repeat everyfew days.

Special tests may be needed to help


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Intravenous Pentoxyfilline.

Can be given directly, as a bolus.

Better if given at a constant rate, with a non-glucose fluid.

Dosage may be individualized for each patient.

Duration: 5-7 days, followed by oral medication.

Handschu et al: most German hospitals useeither Pentoxyfilline or piracetam for acuteischemic stroke!

Stroke, 2001


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Reperfusion injury.

In the presence of disruption of theBBB, reperfusion may induce cerebral

edema and hemorrhage.After a prolonged period of occlusion

leading to cellular injury: reperfusion

may result in increased production offree radicals, gene expression andinflammatory events augmentation

of cellular damage.


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LMWH.

Usually not used as monotherapy.

Personal preference: give together with

another drug to selected strokepatients.

Start early, continue for 5-7 days.

Avoid LMWH if:- systolic blood pressure > 180 mmHg.

- very large infarctor even a tiny

bleed.


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LMWH.

Usually not used as monotherapy.

Personal preference: give together with

another drug to selected strokepatients.

Start early, continue for 5-7 days.

Avoid LMWH if:- systolic blood pressure > 180 mmHg.

- very large infarctor even a tiny

bleed.


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The next three days.

Watch out for brain edema!

Repeat all necessary tests as often as

necessary, including CT. Keep the patients energy metabolism

and electrolytes in an optimal condition.

Treat fever aggressively!

In case something goes


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In case something goeswrong.

Most common complications of acutestroke:

Cerebral edema Fever

Electrolytes imbalance

Malnutrition.

Convulsions

DVT.


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Cerebral edema.

May develop acutely, usually after secondday.

Strict attention to fluid balance, avoid theuse of hypotonic solutions, such as 5%glucose.

Use mannitol with caution.Albumin, 25% solution, helpful, especially if

serum albumin < 3.6 g/dl.

Surgical help in case everything else fails.


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Fever. May be annoying and is bad for recovery.

Prevention is better than cure: meticulous

attention to good nursing practice. Try to determine exact cause and eradicate it.

Use suitable antibiotics as necessary.

Use water bed! If possible treat the patient in an air-conditioned

room.

Fever is bad for stroke


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Fever is bad for stroke

patients! Increases the release of excitotoxic

transmitters

Increases production of free radicals Induces more damage to BBB

Increases post-ischemic depolarization in

thepenumbra.

Harmful to the recovery of cellular

metabolism.


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Electrolyte imbalance.

Bad for recovery, may be life-threatening!

Repeat electrolyte test as often asneeded.

Treat promptly, do not rely on clinical

judgment alone! Enlist the help of a good internist.

Proceed with caution, do not over-

treat.


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Malnutrition.

Remember to feed the patient!

Fluid infusions alone is not enough.

Starvation is very bad for the patient.

A well balanced diet is important to thepatients recovery.

Laboratory tests may help to determinethe patients nutritional status.


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Convulsions.

Occur in approximately 10-20% ofstroke patients, especially those withlarge infarct.

Use parenteral dilantin except if contra-indicated.

Oral route is too slow!

Control drug level and possible sideeffects.

Routine administration of an

anticonvulsant is not recommended.


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Deep vein thrombosis.

Not frequent in Indonesia.

Can be prevented by early mobilization.

Use of LMWH or heparin may beindicated.

Often overlooked unless inspected

daily!Inspect the patients leg, daily!

Increased level of


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Increased level ofHomocysteine.

Harmful effects due to impairment ofendothelial

function through production of hydrogen

peroxide and consumption of NO to form

nitrosohomocysteine.

Aggravates atherosclerosis and coagulation. Provokes neuropathy, retinopathy,

nephropathy

and cerebral vasospasm in SAH


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Homocysteine-2

Deficiency of folic acid, vitamin B-12, B-6,

genetic defects of certain enzymes:

methionine- synthetase,methylenetetrahydrofolate-reductase (folicacid), and cystathione -synthetase (B6).

Indication to treat when homocysteine levels

> 14 mol/L. (folic acid + vitamins B-6 + B-12).

New data: hyper-homocysteinemia may just

be a result of the ischemic event. (Stroke,

BLOOD PRESSURE MANAGEMENT


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IN ICH(Broderick 1999)

- If SBP > 230 mm Hg or DBP > 140 mm Hg on 2 readings5 minutes apart nitroprusside 0.5-10 g/kg/min.

- If SBP is 180-230 mm Hg, DBP 105-140 mm Hg, or meanarterial BP 130 mm Hg on 2 readings 20 minutes apart labetolol, esmolol, enalapril, or other smaller dosesof titrabble IV medications eg diltiazem, lisinopril, orverapamil.

- If SBP is < 180 mm Hg and DBP < 105 mm Hg, deferantihypertensive therapy.

- If ICP monitoring is available, cerebral perfusionpressure should be kept at > 70 mm Hg.

Labetolol: 5-100 mg/h by intermittent bolus doses of 10-40 mg or continuous drip (2-8mg/min).

Esmolol: 500 g/kg as a load, maintenance use, 50-200 g/kg/min. Hydralazine: 10-20 mg Q 4-6 h

Enalapril: 0.625-1.2 mg Q 6 h as needed.

MANAGEMENT OF ICP( d i k 999)


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(Broderick 1999)

Osmotherapy:- Mannitol 20% (0.25-0.5 g/kg every 4 h), for only 5 d.

- Furosemide (10 mg Q 2-8 h) simultaneously with mannitol.

- Serum osmolality 310 mOsm/L, measured 2 X daily.

No steroidHyperventilation:

- Reduction of pCO2 to 35-30 mm Hg, by raising ventilation rateat constant tidal volume (12-14 mL/kg), lowers ICP 25%-30%.

Muscle relaxants:- Neuromuscular paralysis in combination with adequatesedation can reduce elevated ICP.

- Vecuronium or pancuronium, with only minor histamineliberation and ganglion-blocking effects are preferred.

RECOMMENDATIONS FOR SURGICALTREATMENT OF ICH


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TREATMENT OF ICH (Broderick 1999)

NON SURGICAL CANDIDATES1. Small hemorrhages ( 3 cm who are neurologicallydeteriorating or who have brainstem compression and

hydrocepahalus from ventricular obstruction.2. ICH with structural lesion eg aneurysm, AVM, or

cavernous angioma.

3. Young patients with a moderate or large lobar

hemorrhage who are clinically deteriorating.

MANAGEMENT OF SAH (1)


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1. BEDREST + tranquilizers + head position horizontal.

2. PREVENTION OF REBLEEDING- Antihypertensive medications (controversial)- Antifibrinolytics:

- Tranexamic acid 6 X 1gr (7-14 days) 40% in rebleeding offset by 43% in focal ischemic deficits (Kassell 1984).- Tranexamic acid + nimodipine ischemic deficits (van Gijn 1992).- Carotid ligation (indeterminate value)- Intraluminal coils & balloons (experimental)

3. PREVENTION OF VASOSPASM- Hypertension/hypervolemia/hemodilition (experimental)- Calcium ch.antagonists : Nimodipine 6 X 60 mg p.o./infuse 1-2 mg/hr for 5-

14 ds.- Intracisternal fibrinolysis +antioxidant+ antiinflammatory agents

uncertain value- Transluminal angioplasty in whom conventional therapy has failed.

MANAGEMENT OF SAH (2)


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4. HYDROCEPHALUS

- Acute (obstructive) hydrocephalus

ventriculostomy.- Chronic (communicating) hydrocephalus temporary/permanent CSF diversion.

5. PREVENTION OF HYPONATREMIA- Intravascular administration of isotonic fluids.- Monitoring CVP, pulmonary capillary wedge pressure, fluid balance & body weight.- Volume contraction should be corrected by increasing the volume of fluids.

6. PREVENTION OF SEIZURES- Prophylactic anticonvulsants is recommended.- Longterm anticonvulsants not routinely recommended.

7. SURGICAL INDICATION- RUPTURED ANEURYSMSWFNS grade 1-3 (good-intermediate grade) surgery strongly indicated.

- UNRUPTURED ANEURYSMSSurgery recommended

- ASYMPTOMATIC ANEURYSMS> 1 cm operate; < 1 cm do not operate (consensus).


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STROKpenyakit gawat dan akutEmergency :

Diagnosa yang tepat dan segera sangat

menentukan TERAPI yang cepat & terarahMorbiditas dan Mortalitas dapat

diturunkan

The Ideal Stroke team


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The Ideal Stroke team.

The team should consist of:

neurologists with special interest in stroke

neuro-radiologists, well-trained to do angiograms +

Doppler evaluation of vessels supplying the brain A neurosurgeon, with special training in vascular surgery.

Well-trained team of nursing personnel, physiotherapists.

Other related specialists: social worker, psychiatrists.

A well-run hospital with lab and imaging facilities,

available 24 hours a day, seven days a week.

Yin Yang


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Yin Yang

Th k T i k ih!


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Thank you Terima kasih!

Stroke Perawat

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Transcript of Stroke Perawat