diskusi co-ass minggu iv 2016

8/18/2019 Diskusi Co-Ass Minggu IV 2016

http://slidepdf.com/reader/full/diskusi-co-ass-minggu-iv-2016 1/37

Fig. 1.4. One of the most importantbooks in the study of apoplexy. Wepfer was city physician

at Schahausen inSwiterland when he carried outmeticulous examinationson the cerebral blood !essels andbrains of patients whohad suered apoplexy

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$asus 1

• -n )/ laki'laki/ 0 tahun/ datang ke #+" 2S%3() )edan pada pukul 5. wib dengan lemahlengan dan tungkai kanan yang dialami secaratiba'tiba se6ak 1 6am sebelumnya saat os sedang

menonton -,.• "ari anamnese didapati riwayat nyeri kepala 7'8

sebelumnya/ muntah 7'8/ ke6ang 7'8/ demam 7'8/riwayat benturan di kepala 7'8/ bicara celat 798.

Selama : 1 tahun os menderita darah tinggi/namun os tidak berobat secara teratur.

• $eadaan ini tidak pernah dialami pasiensebelumnya.

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"iskusi $asus 1

emiparese "" <<<<<

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$asus 1 = 3em. neurologi

• 3emeriksaan klinis = sensorium &)/

-" 5>11 mmg/ nadi ? x>i reguler/pernafasan x>i/ temp 50/?&.

• Sudut mulut tertarik ke kiri/ mata bisamenutup.

• @engan kanan = tidak ada kontraksi otot

• -ungkai kanan = bisa diangkat dari tempattidur tapi segera ter6atuh kembali

• 2eAeks patologis 7'8

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"iskusi $asus 1

"iagnosa sementara <<

(lasan <<

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)C);C"($(* S# "(* S

SI

• Onset saat istirahat

• %sia lebih tua

• $esadaran umumnyabaik

• -#$ umumnya tdkmeninggi

• $aku kuduk tdkdi6umpai

SH

• Saat aktif

• @ebih muda

• @ebih sering menurun

• @ebih sering meninggi

• ;isa di6umpai

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"iskusi $asus 1

"imana lesi <<

-eritori arteri mana yang

terlibat <<

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The idea of the cortical homunculus

was created by Wilder Penfield.

https://en.wikipedia.org/wiki/Wilder_Penfield

https://en.wikipedia.org/wiki/Wilder_Penfield



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-homas Willis 7101'10DB8



+C(@( "(* -(*"( $@#*#S;C2"(S(2$(* -C2#-O2# (2-C2# G(*+

-C2@#;(-• (. serebri media =

gangguan motorik dan sensorik kontralateral

7wa6ah/ lengan/ dan lebih ringan pada tungkai8

afasia 7bila lesi di hemisfer dominan8neglect 7bila lesi di hemisfer non dominan8

• (. serebri anterior =

gangguan motorik dan sensorik kontralateral7tungkai dan lebih ringan pada lengan8

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+C(@( "(* -(*"( $@#*#S;C2"(S(2$(* -C2#-O2# (2-C2# G(*+

-C2@#;(- 7lan6utan8• (. serebri posterior =

deHsit lapangan pandang kontralateral

afasia dan confusion 7bila pada hemisfer dominan8

• 3enetrating arteries 7lacunar8 =

gangguan motorik atau sensorik kontralateral

7wa6ah/ lengan/ dan tungkai8

;isa di6umpai ataksia atau disartria

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• (. !ertebralis 7atau a. serebelli posteriorinferior8 =

truncal ataxia/ disartria/ disfagia/ gangguansensorik ipsilateral wa6ah dan gangguan sensorikkontralateral dari leher ke bawah

• (. basilaris =

limb ataxia/ disartria/ disfagia/ gangguan motorikdan sensorik 7bisa bilateral8/ pupil asimetris/discon6ugate gae/ gangguan lapangan pandang/respon melambat

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+C(@( "(* -(*"( $@#*#S;C2"(S(2$(* -C2#-O2# (2-C2# G(*+

-C2@#;(- 7lan6utan8



3C2;C"((* S# -rombosisdenganCmboli

-2O);OS#S

• "eHsit neurologik timbul mendadak/ tapiberkembang agak lebih lambat.

• Onset sewaktu istirahat > bangun tidur.

C);O@# =

• "eHsit neurologik timbul mendadak dan sekaligus

mencapai puncak.• Onset sewaktu aktif.

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"iskusi $asus 1

3emeriksaan penun6ang <<<

$apan dilakukan <<

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$asus 1 = 3em penun6ang

• &- scan kepala = tidak tampak adanyainfark/ hematom maupun lesi lainnyadi otak/

$ok bisa <<<

@angkah selan6utnya <<

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• +old standard = &- scan kepala

• $apan dilakukan <<<<<

• -idak ada ketentuan yang pasti• #nfark secara radiologis !isible I 4E 6am



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-C2(3# -2O);O@#S#S JJJ

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The penumbra is the zone of reversibleischemia around the core of irreversible

infarction.



penumbra core

1 hour 2 hour 3-4hour

4-6hour

Corepenumbra

= ~ 1 :1

~ 2-3 :1

~ 4-5 :1

? 10-20 :1

DS-2O$C #S$C)#$ F$'%S% 1B

S(,C -C 3C*%);2( JJJJ



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3enatalaksanaan

• (nti hipertensi <<

• (nti platelet <<

• (nti koagulan <<• &iticholin <<

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1. (cute therapy and optimiation ofneurological status

• )aintenance of cerebral perfusion eu!olemia/ support ;3/ bed Aat

• "o not treat hypertension acutely/ unless =

1. was treated by -3(. end organ damage 7 &F/ )&#/ C/

dissecting aortic aneurysm etc8

5. S;3I mmg or ";3 I 1 mmg

• %se short'acting agent = labetalol/nicardipine

• +oal = ;3 reduction 1'1BK

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1. (cute therapy and optimiation ofneurological status

• (ntiplatelet = aspirin eecti!e for acutetreatment

• (nticoagulant = not eecti!e for acute

treatment/ only for secondary pre!ention in(F and cardioembolic stroke

*e!er start anticoagulant without brainimaging

• yperglycemia = treat glucose aggressi!ely

• yperthermia = treat aggressi!ely withacetaminophen and cooling blanket

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. Ctiological work'up for secondarypre!ention

• Screening for arterial stenosis>obstruction )2(/ carotid ultrasound/ -&"/ "S(/ &-(

• &ardiac e!aluation C$+/ echocardiogram

• 2ecurrent stroke risk factors screening =L monitor ;3

L obtain fasting lipid panel

L screen for diabetes

L screen for hyperhomocysteinemia

L smoking cessation

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5 3 ti f l i l



5. 3re!ention of neurologicaldeterioration or medical

complications

• ",- prophylaxis

• (spiration precautions

• +astrointestinal ulcer prophylaxis• -ake out indwelling urinary catheter

as soon as possible

• )onitor platelet counts if on heparin

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4. 3re!ention of neurological deterioration ormedical complications = "rug therapy in the Hrst

D hours =

1. (ntiplatelet = L aspirin E1'5B mg O"

L clopidogrel DBmg O"

L aspirin B mg 9 dypiridamole mg O"

. ",- prophylaxis = heparin/ @)W/ compression stocking

5. (nticoagulant for cardioembolic stroke = heparin/coumadin/

*O(& 7dabigatran/ ri!aroxaban8

4. #nsulin to treat hyperglycemia

B. (cetaminophen to treat hypertermia

0. Statins = target @"@ M 1 mgK

D. (ntihypertensi!e = (&C#/ (2;/ diuretics/ beta blockers/

&a'channnel blockers

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diskusi co-ass minggu iv 2016

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