CEREBROVASCULAR DISEASE

(1)

Hendra Samanta, MD, Neurologist,

RSAU dr. Esnawan Antariksa

(2)

Hendra Samanta, MD, Neurologist, Flight Surgeon

1.

TIA (3B)

2.

Infark cerebral (3B)

3.

Hematoma intraserebral (3B)

4.

Perdarahan subarakhnoid (3B)

5.

Enselopati hipertensi

(3)

1. Normal CBF  50-60 cc/100 g/minute

Varies in different regions of the brain

2. CBF 20-30cc/100g/min Loss of electrical activity

3. CBF 10 cc/100g/min Neuronal death

(4)

STROK

E

(5)

PENTING

(6)

1. A stroke is caused by the interruption of the blood supply to the brain, usually because a blood vessel bursts or is blocked by a clot.

This cuts off the supply of oxygen and nutrients, causing damage to the brain tissue (WHO, 2016)

2. A clinical syndrome of rapidly developing clinical signs of focal (or global in case of coma) disturbance of cerebral function, with symptoms lasting twenty - four hours or longer or leading to death with no apparent cause other than of vascular origin (WHO, 1988)

3. TIA (Transient Ischaemic Attack) is defined as signs and symptoms of stroke which resolve within 24 hours, although TIA symptoms normally resolve in a few minutes or hours. If neurological symptoms persist for longer it should be assume that the person has had a stroke (RCP, 2012 ).  42-86 % (history)

(7)



BPJS 2016 Stroke  sebesar 1,43 Trilyun, tahun 2017 naik menjadi 2,18 Trilyun dan tahun 2018 mencapai 2,56 Trilyun rupiah.

http://p2ptm.kemkes.go.id/artikel-sehat/hari-stroke-sedunia-2019-otak-sehat-sdm-unggul



Penyebab kematian pertama di Indonesia (Kemenkes 2014)



Kecacatan (87%)

https://www.who.int/bulletin/volumes/94/9/16-181636/en/

 Waktu perbaikan ( 24 jam - 3 bulan ) (Cerebrovasc Dis. 2011;31(2):185-90. doi:

10.1159/000321869. Epub 2010 Dec 11)

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1. O‘Donnell M, et al. Lancet 2010;376:112-123.

2. Romero JR, et al. Ther Adv Cardiovasc Dis 2008;2(4):287-303.

High blood pressure

(hypertensio n)

Diabetes Atrial fibrillatio

n

Smoking

Heart disease

Obesity High

cholester ol

Lack of exercise

Alcohol intake

Stress

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(14)

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Albers G, et al. Chest 2004;126 (3 Suppl):438S-512S. 25

Haemorrhagic 12%

Other 5%

Cryptogenic

30%

Cardiac embolism

20%

Small vessel disease

“lacunes”

25%

Atherosclerotic cerebrovascular

disease 20%

(26)

(27)

(28)

 Defisit neurologi akut karena kelainan vaskular serta pulih dalam 24 jam.

 300.000-700.000 pasien dicurigai TIA dari riwayat penyakit dahulu

 200.000-500.000 TIA  USA

Gejala Tipikal Gejala Atipikal Kelemahan unilateral dari :

•Wajah

•Lengan

•Tungkai

Perubahan sensasi unilateral Disfasia

Hemianopsia

Kebutaan sesisi (monocular blindness)

Bingung Sinkop

Dizziness / pusing

Kelemahan umum / gejala sensoris

Gangguan penglihatan

bilateral atau kerlipan cahaya Inkontinensia alvi dan atau uri Amnesia

(29)

Riwayat gangguan fungsi tubuh mendadak Memiliki faktor resiko stroke

Tidak ada penyebab lain selain gangguan vascular

(30)

Anamnesis dan Pemeriksaan fisik

Pemeriksaan Penunjang Anamnesis

•Pasien & keluarg

•Faktor resiko

Pemeriksaan Fisik

•Vital sign

•Defisit neurologi

• Bukti tanda dan gejala gangguan pembuluh darah

• Menyingkirkan akibat dari non vaskular

• Mencari faktor resiko yang berhubungan

• Tentukan dan kemungkinan prognosis

(31)

Faktor Resiko Poin

Usia > 60 th

1

Tekanan darah :

Sistolik > 140 / Diastolik > 90 mmHg

1

Klinis TIA

Kelemahan sesisi dengan atau tanpa gangguan bahasa

2

Gangguan bahasa tanpa kelemahan sesisi

1

Durasi

> 60 menit

2

10 – 59 menit

1

Diabetes

1

(32)

Skor Resiko terkena stroke dalam 2

hari (%)

Rekomendasi

0-3 1 Tidak terlalu diperlukan observasi

di RS, kecuali jika ada indikasi lain

( AF)

4-5 4,1 Perlu dipertimbangkan dirawat di

RS

6-7 8,1 Perlu dilakukan observasi di RS

(33)



Terapi antitrombotik



Terapi kardioemboli



Terapi penyakit penyerta

 Hipertensi

 Dislipidemia



Perbaiki pola hidup  pola hidup sehat

(34)



4 %  stroke dalam 2 hari



8 %  stroke dalam 1 bulan



9 %  stroke dalam 90 hari



24-29 %  stroke dalam 5 tahun

(35)



Defenisi sama dengan stroke iskemik



Klasifikasi :

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Nonthrombosis-mediated embolism may originate from septic vegetations, valvular calcified fragments, cardiac tumors (eg, myxoma, papillary fibroelastoma, and sarcoma), fibrocartilaginous material, air, fat, and others.2 Atherosclerotic arteriogenic embolism may originate from any part of the brain-supplying arterial tree, such as the aortic arch and the intracranial and extracranial carotid and vertebrobasilar arteries, but mainly involves those arterial segments that are more prone to develop atherosclerotic plaques, such as the bifurcation of arteries, the origin of an artery from its parent vessel, as well as tortuous arterial segments.

Nonatherosclerotic arteriogenic embolism may originate from dissected cervical arteries, Moya Moya disease, Takayasu arteritis, and others.2 Cardiac chamber embolism may originate from thrombus formed because of left ventricular (LV) dysfunction with preserved or reduced ejection fraction, LV regional wall abnormalities after myocardial infarction, LV noncompaction, atrial septal aneurysm, Chiari network, atrial asystole, sick-sinus syndrome, blood stasis into the atrial appendage, atrial fibrillation (AF), flutter or tachycardias, and others.2 Cardiac embolism because of valvular disease may originate from myxomatous valvulopathy with prolapse, mitral annular calcification, aortic valve disease, calcified aortic valves, and others.2 Non thrombotic cardiac embolism may originate from myxoma, papillary fibroelastoma, sarcoma and other cardiac tumors, fibrocartilaginous material, and others

Rink, Khanna (2010). MicroRNA in ischemic stroke etiology and pathology. Physiol Genomics 43: 521–528, 2011.

(41)

Thrombotic stroke occurs when diseased or damaged cerebral arteries become blocked by the formation of atherosclerotic plaque within the brain. Clinically referred to as focal cerebral thrombosis or cerebral infarction

https://journals.physiology.org/doi/pdf/10.1152/physiolgenomics.00158.201 0

(42)

Berasal dari pembuluh darah besar, arteriol yang menembus dengan penyempitan dan gangguan autoregulasi dari penyakit pembuluh darah kecil serebral. Di hilir, ada parenkim hipoperfusi yang tampak normal pada pencitraan. Dalam kondisi sumbatan pembuluh darah kecil serebral pada pembuluh darah orde kedua, terjadi stroke lakunar. Dalam urutan yang lebih tinggi pembuluh darah dengan penyakit pembuluh darah kecil yang tersumbat, dan terjadi mikroinfark. Area degradasi sawar darah otak dengan penurunan aliran darah otak menghasilkan hiperintensitas materi putih. Sapuan lakunar sejajar dengan pembuluh darah penetrasi, tetapi mereka juga memiliki kecenderungan untuk terbentuk di tepi hiperintensitas pada materi putih. Parenkim hipoperfusi dapat berkembang menjadi stroke lakunar dengan hiperintensitas substansia alba, meskipun gejala sisa penyakit pembuluh darah kecil serebral ini juga dapat membaik seiring waktu, kemungkinan dari adanya keseimbangan perubahan aliran darah fokal pembuluh darah kecil serebral, dan proses perbaikan parenkim

Regenhardt RW, Das AS, Lo EH, Caplan LR. Advances in Understanding the Pathophysiology of Lacunar Stroke: A Review. JAMA Neurology. 2018

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

Criptogenik stroke  penyebab tidak termasuk thrombosis, emboli atau lanukar infark.

Circ Res. 2017;120:527-540.

DOI:10.1161/CIRCRESAHA.116.308447

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Patogenesa Stroke Islemik

Regenhardt RW, Das AS, Lo EH, Caplan LR. Advances in Understanding the Pathophysiology of Lacunar Stroke: A Review. JAMA Neurology. 2018 Oct;75(10):1273-1281. DOI: 10.1001/jamaneurol.2018.1073. PMID: 30167649; PMCID:

PMC7426021.

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Cellular and acellular constituents of the neurovascular unit (NVU). (A) At the level of penetrating arteries, upstream capillaries, endothelial cells (ECs) are surrounded by vascular smooth muscle cells. At this level, cerebral vessels are still surrounded by the pia. The Virchow–Robin space is located between the pia and the glial limitans formed by the astrocytic endfeet. This perivascular space plays an important role in waste removal and in regulation of the interstitial fluid of the brain. (B) At the level of intracerebral capillaries, the NVU is comprised of ECs, pericytes, astrocytes, microglia, and the basement membrane. Both the ECs and surrounding pericytes are unsheathed by a common basement membrane. Pericyte processes encase most of the endothelial surface. Astrocytic endfeet completely surround the capillary wall. Resting microglial have a ramified morphology and are in constant surveillance around brain microvessels. Gap junction channels enable cytoplasmic continuity between astrocytic endfeet, and also exist between pericytes and ECs at peg-socket structures providing quick communication between these cells. Specialized tight junctions between ECs prevent paracellular leakage into the brain parenchyma. (C) The NVU undergoes dramatic structural changes following stroke, affecting cerebrovascular integrity, neuro-vascular coupling and neuronal survival within the peri-infarct territory. Figure prepared with BioRender

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Cara Mengenal Stroke

1

(48)

CVD Classification

(49)

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GEJALA & MANIFESTASI KLINIS 1.Hemiplagia, Hemihipestesi

2.Ggn pendengaran

3.Ggn penglihatan (diplopia) 4.Cadel (disartria)

5.Inkontinensi kandung kemih 6.Ataksia dan pingsan

7.Koma

8.Sulit mengendalikan emosi

(51)



Anamnessa



Defisit neurologi fokal dan global akut



Faktor resiko



Pemeriksaan fisik



Defisit fokal



Defisit global



Pemeriksaan Penunjang

1.

Darah ( Faktor resiko metabolik )

2.

EKG ( faktor resiko jantung )

3.

Rontgen ( faktor resiko )

4.

CT Scan Kepala Non

Kontras ( golden standar )

5.

MRI Kepala Non kontras

6.

CT – MR Angiograpgy

7.

Pemeriksaan lain yang

diperlukan

(52)

Skor Stroke Siriraj

(2,5 x derajat kesadaran) + (2 x muntah) + (2 x nyeri kepala) + (0,1 x tekanan diastolik) – (3 x petanda ateroma) – 12

(53)

Tatalaksana

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Kuriakose, D., & Xiao, Z. (2020). Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives. International journal of molecular sciences, 21(20), 7609. https://doi.org/10.3390/ijms21207609

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Tatalaksana

1. Tatalaksana Umum

a. Stabilkan jalan nafas dan pernapasan b. Stabilitasi hemodinamik (Sirkulasi)

c. Pengendalian peningkatan tekanan intra kranial d. Pengendalian kejang

e. Pengendalian suhu f. Tata laksana cairan g. Nutrisi

h. Pencegahan dan mengatasi komplikasi

i. Penatalaksanaan medik umum lain

(57)

Tatalaksana

1. Tatalaksana Spesifik

a. Trombolisis intravena

b. Terapi neurovaskular / endovskular

c. Pemberian antikoagulan sebagai pencegahan sekunder d. Pemberia antiagregasi trombosit

e. Tatalaksana spesifik lain dan neuroproteksi

2. Neurorehabilitasi / neurorestorasi pasca stroke

3. Edukasi

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Stroke – treatment pathway

58

Effective EMS systems can minimise delays in pre-hospital dispatch, assessment, and transport, and increase the number of stroke patients reaching the hospital and receiving thrombolytic therapy

within the approved time window Rapid patient

recognition and reaction

to stroke warning signs

Rapid emergency

medical services (EMS)

dispatch

Rapid EMS system transport and

hospital pre-notification

Delivery direct to imaging

Rapid in- hospital diagnosis and

treatment

Patient EMS Transport CT/MRI Treatment

Adapted from: Jauch E, et al. Stroke 2013;44:870-947. Wojner-Alexandrov AW. Stroke 2005;36:1512-1518.

Deng YZ, et al. Neurology 2006;66:306-312.

!

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Benefit and Risk of Stroke Thrombolysis

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(61)

Areas of ischaemia following middle cerebral artery occlusion before (left) and after (right) reperfusion

An untreated patient loses approximately 1.9 million neurons every minute in the

ischaemic area¹

Reperfusion offers the potential

to reduce the extent of ischaemic injury³ Penumbra

(salvageable brain area)²

Adapted from:

1. Saver J. Stroke 2006;37:263-266.

2. González RG. Am J Neuroradiol 2006;27:728-735.

3. Donnan G, Davis S. Lancet 2002;1:417-425.

Ischaemic core (brain tissue destined to

die)²

(62)

The penumbra is moderately ischaemic

tissue that may remain

salvageable for several hours if reperfusion

takes place

^1,2

Thrombolysis needs to be given as early as possible to prevent the conversion of potentially viable brain tissue in the penumbra from

becoming completely ischaemic and dying

1. Saver J. Stroke 2006;37:263-266.

2. Moustafa RR, Baron JC. Br J Pharmacol 2008;153:S44-S54.

Cerebral blood flow pattern after middle cerebral artery Cerebral blood flow pattern after middle cerebral artery occlusion

occlusion

Onset of stroke:

death of brain cells within minutes¹

Infarct Penumbra

(63)

The area of infarct

represents severe

ischaemia

²

1. Saver J. Stroke 2006;37:263-266.

occlusion

6 hours after stroke onset Infarct

Penumbra

(64)

The area of infarct

represents severe

ischaemia

²

1. Saver J. Stroke 2006;37:263-266.

occlusion

24 hours after stroke onset Infarct

Penumbra

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Contraindications for rt-PA The ASPECTS score

A score of zero indicates diffuse ischaemic damage

A score of ten indicates a normal CT scan Clinical studies¹ have demonstrated that patients with an ASPECTS score of >7 were most likely to benefit from treatment

Those with an ASPECTS score of <5 were unlikely to see any improved outcome and were exposed to a significantly higher risk of haemorrhage following thrombolysis

NIHSS score

Score Stroke Severity

0 No Stroke Symptoms

1-4 Minor Stroke

5-15 Moderate Stroke

16-20 Moderate to Severe Stroke

21-42 Severe Stroke

Minor neurological deficit or symptoms rapidly improving before start of infusion

Severe stroke as assessed

clinically (e.g. NIHSS >25) and/or by appropriate imaging

techniques

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1. NINDS rt-PA Stroke Study Group. N Engl J Med 1995;333:1581-1587.

2. Product Information Actilyse 2017

Contraindications fall under the following broad categories^{1, 2}

Severity Increased

bleeding risk

Onset of

symptoms more than 4.5 hours

ago

Unstable patient Aged

<18 & >80 years

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Keluaran

(70)

(71)

Stroke Hemoragik

– Salah satu jenis stroke karena pecahnya pembuluh darah intraserebral

– Di Indonesia angka nya 33 %.

(72)

(73)

– Patofisiologi

1.Hipertensive vascular change

2.Cerebral amyloid angiopathy

3.Molecular pathophysiology

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Giuseppe Faraco. Hypertension. Hypertension, Volume: 62, Issue: 5,

(75)

Cerebral amyloid angiopathy Patofisiologi

Gatti, L., Tinelli, F., Scelzo, E., Arioli, F., Di Fede, G., Obici, L., Pantoni, L., Giaccone, G., Caroppo, P., Parati, E. A., & Bersano, A. (2020). Understanding the Pathophysiology of Cerebral Amyloid Angiopathy. International journal of molecular sciences, 21(10), 3435. https://doi.org/10.3390/ijms21103435

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Faktor Resiko Stroke Hemoragik

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Gejala Klinis Stroke Hemoragik

1. Gajala peningkatan tekanan intra kranial 2. Sakit kepala

3. Mual dan muntah (50 %) 4. Kejang (10-50 %)

5. Penurunanan kesadaran

6. Defisit neurologi fokal

(78)

Tatalaksana

1. Tatalaksana Umum

a. Stabilkan jalan nafas dan pernapasan b. Stabilitasi hemodinamik (Sirkulasi)

c. Pengendalian peningkatan tekanan intra kranial d. Pengendalian kejang

e. Pengendalian suhu f. Tata laksana cairan g. Nutrisi

h. Pencegahan dan mengatasi komplikasi

i. Penatalaksanaan khusus

(79)

Tatalaksana

1. Tatalaksana Khusus

a. Perawatan stroke unit b. Koreksi koagulopati

c. Kendalikan tekanan darah

d. Pertahankan tekanan perfusi serebral e. Tatalaksana bedah

f. Pemberian obat antiepilepsi

g. Pencegahan perdarahan intraserebral berulang

h. Lakukan rehabilitasi medis.

(80)

Tatalaksana TIK meningkat

– Elevasi kepala 30 derajat

– Hindari penekanan vena jugularis – Hindari hipertermia

– Pemberian osmoterapi (manitol)

– Intubasi untuk menjaga normoventilasi – Hindari gelisah

– Operasi

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PERDARAHAN SUBARAKNOID

– Merupakan ekstravasasi darah menuju ruang subaraknoid dan pial – Perdarahan dapat berdistribusi ke sistem ventrikel, sisterrna dan

fissura.

– Insiden 10,5 / 100.000

– Perempuan 1,6 x lebih tinggi dari laki laki – Kulit hitam 2,1 x lebih tinggi

– 50 %  dari aneurisma

(82)

PERDARAHAN SUBARAKNOID

– Etiologi

• Aneurisma  85 %

• Perdarahan perimesensefalik non aneurisma  10 %

(83)

Patofisiologi

Aneurisma Intrakranial

•Dinding arteri intrakranial lebih tipis  aneurisma (tidak ada lamina elastika eksterna dan tipisnya tunika media)

•Tekanan pulsasi tinggi maksimal di titik percabangan di proksimal arteri

(84)

Klinis SAH

1. Sakit kepala

2. Penurunan kesadaran 3. Kejang

4. Kaku kuduk

5. Perdarahan subhialoid 6. Demam

7. Hipertensi

8. Defisit neurologi fokal

(85)

Diagnosis

• CT Scan kepala non kontras

• MRI

• Lumbl Fungsi

• CT Angiografi

• MR Angiografi

• DSA (Digital substraction angiography)

(86)

Tatalaksana

Tatalaksana umum

•Kendalikan hipertensi

•Kendalikan tekanan intra kranial

(87)

Tatalaksana komplikasi

• Rebleeding

• vasospasme

(88)

Mencegah vasospasme

• Nimodipin

• Trombolisis setelah clipping

• Aspirasi dan ligasi

• Drainase lcs

• Statin

• Triple H

• Angioplasti balon transmural

• Infus vasodilator

(89)

Pemicu ruptur aneurisma

• Pemicu ruptur aneurisma

– Aktifitas fisik (2-20%)

– Hubungan seksual (0-11%) – Manuver valsava (4-20%) – Stress (1-2%)

– Merokok (odds rasio 7) – Alkohol (odds rasio 4,3)

(90)

Komplikasi

• Hidrosefalus

• Hiponatremia

• kejang

(91)

(92)

(93)

(94)

(95)

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(97)

(98)

Derajat Defisit Neurologi

(99)

(100)

ENSEPALOPATI HIPERTENSI

• Merupakan istilah yang dipakai untuk menyatakan suatu perubahan kesadaran dan defisit neurologi lainnya yang diakibatkan oleh suatu hipertensi krisis.

• 15 % pasien dengan krisis hipertensi menjadi ensepalopati hipertensi

Kim, Syed. Hypetension Encephalopathy: A case of a male who bit off his finger. Cureus 9(6) . 2017

(101)

Hipertensi

(102)

Term

Malignant hypertension:

Severe BP  >200/120 mm Hg  advanced bilateral retinopathy (hemorrhages, cotton wool spots, papilledema).

Hypertensive encephalopathy:

Severe BP elevation  lethargy, seizures, cortical blindness and coma in the absence of other explanations.

Hypertensive thrombotic microangiopathy:

Severe BP elevation  hemolysis and thrombocytopenia in the

absence of other causes and improvement with BP-lowering therapy.

Other

presentations of hypertensive emergencies include severe BP elevation  cerebral hemorrhage, acute stroke, acute coronary

syndrome, cardiogenic pulmonary edema, aortic

aneurysm/dissection, and severe preeclampsia and eclampsia

.

(103)

Etiologi Malignan Hipertensi

1. Krisis / hipertensi maligna 2. Secondary malignant

hypertension

3. Chronic kidney disease

4. Chronic glomerulonephritisa 5. Chronic pyelonephritisa

6. Analgesic nephropathya 7. Immunoglobulin A

nephropathya

8. Acute glomerulonephritis 9. Radiation nephritis

10.Ask-Upmark kidney

11.Renovascular hypertensiona

https://abdominalkey.com/malignant-hypertension-and-other-hypertensive-crises/

12. Oral contraceptives

13. Renal cholesterol embolization 14. Scleroderma renal crisis

15. Antiphospholipid

(anticardiolipin) antibody syndrome

16. Chronic lead poisoning 17. Endocrine hypertension 18. Pheochromocytoma

19. Aldosterone-producing adenoma 20. Cushing syndrome

21. Congenital adrenal hyperplasia 22. Most common underlying

etiologies^.

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(105)

Patogenesa

(106)

Klinis

• Penurunan kesadaran

• Defisit neurologi fokal  stroke

• Cortical blindness

William, Mancia, Rosei, et l. 2018 ESC/ESH Guidelines for the management of arterial hypertension. European Heart Journal (2018) 00, 1–98

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Diagnosa

• Anamnesa : Riwayat Hipertensi

• Pemeriksaan Fisik : Tekanan darah (Krisis)

• Pemeriksaan penunjang :

– Fundus kopi

– CT Scan Kepala – MRI kepala

Unger et al. Clinical Practice Guidelines. 2020 International Society of Hypertension Global. Hypertensionn Practice Guidelines. Journal of Hypertension. https://www.ahajournals.org/journal/hyp

(108)

Manajemen

Unger et al. Clinical Practice Guidelines. 2020 International Society of Hypertension Global. Hypertensionn Practice Guidelines. Journal of Hypertension. https://www.ahajournals.org/journal/hyp

(109)

Komplikasi Terjadi kerusakan Target Organ

1.Renal Failure, 2.Retinopathy,

3.Myocardial Infarction, 4.Stroke.

Potter T, Schaefer TJ. Hypertensive Encephalopathy. [Updated 2021 Aug 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554499/

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