MODULE VASCULAR - UNAIR

MODULE

VASCULAR

NEUROSURGERY SPESIALIST PROGRAME UNIVERSITY of AIRLANGGA

201 6

Aneurysmal SAH +

ICD-10: I 67.1

1. Definition • Aneurysms: cerebrovascular disorders such as weakness cerebral artery or vein wall that causes

(Definition) dilation of local or balooning blood vessel. etiology:

- head trauma

- atherosclerosis or hypertension

- embolism: atrial myxoma

- infection: mycotic aneurysm

- congenital

• If there is rupture of the aneurysm will cause to happen SAH. SAH is bleeding in the subarachnoid cavity.

etiology:

- Trauma: The most frequently

- Spontaneous: aneurysm rupture (75-80%), AVM (4-5%), vasculitis, tumoral bleeding,

cerebral artery dissection, small superficial artery ruptures and infudibulum, blood clotting disorders,

dural

sinus thrombosis, spinal AVM, etc.

2. History - If the aneurysm is small, often asymptomatic.

- term effects because giant aneurysms:

1. brainstem compression: hemiparese

2. cranial neuropathy: double vision, impaired vision, facial pain

3. suppression of the pituitary gland and stalk aneurysm intra-suprasell

Hormonal disorder.

- If the aneurysm rupture causes bleeding SAH:

1. severe headache suddenly (97%), vomiting, syncope, neck pain (meningismus), photophobia, until

loss of consciousness

2.If accompanied ICH, showed the weakness of the limbs, language disorders, seizures, and vision

disorders

3. Low back pain

There is a classification of Hunt and Hest to assess the degree of clinical symptoms in a ruptured aneurysm

Hunt and Hess classification

Level decryption 1

Asymptomatic or mild headache and mild neck stiffness 2

cranial nerve palsy (III, VI) .nyeri moderate to severe head, neck stiffness 3

Mild focal deficit, lethargy, confusion 4

Stupor, hemiparese moderate to severe, deserbrasi 5

Commas in, decerebrate

This classification is used as an indicator of prognosis and management of ruptured aneurysm election.

Grade 1 and 2 operated on immediately after the aneurysm was diagnosed. Grade ≥ 3

postponed surgery until clinical improvement (grade 1 or 2) Exceptions timing of operation in

case of life-threatening ICH.

3. Physical Examination SAH:

- Meningism with pathological reflexes

- Hypertension

- loss of consciousness due to: ICT increases, ICH, hydrocephalus, diffuse ischemia, seizures

- ocular hemorrhage

4. Criteria for Diagnosis clinical

Radilologis

5. Diagnosis of work Unruptured aneurysm (I67.1) ruptured

aneurysm (I60.7) a-SAH (I60)

6. Diagnosis • AVM

• Brain haemorrhage due to hypertension

• Cerebral vein thrombosis

• SAH due to trauma

• intratumoral bleeding

• Pitutiary tumor

• Moyamoya disease

•

Vein of gallen

malformation

7. Investigations Lumbar puncture: most sensitive to SAH (opening pressure increases), xantocrom, cell counts of>

100,000, increased protein, normal or decreased glucose

False positives: traumatic taps

Radiological:

Recommendation Grad e

Reko

No. Examination mend Ref

ation

1 CT

scan

To detect> 90% SAH when the onset of bleeding occurred in

1C 5

24 hours

insensitive to SAH 24-48 hours, preferably 4-7 days

2 MRI Flair most sensitive MRI imaging to detect SAH 2C 6

3 MRA

a sensitivity of 95% for aneurysm size> 35 mm

2A 7

detecting aneurysms 97%. Can describe the shape

4 CTA of the aneurysm 3D crucial for surgical planning 2A 7

1) The gold standard of evaluation eneurisma palsy.

5 Cerebral 1A 7,11

angiogram

Fisher Gr ade

grade

CT scan 1 There does not appear bleeding 2

SAH thickness <1 mm 3

SAH thickness> 1 mm (high risk occurs vasospasm) 4

SAH + IVH / ICH 8. Therapy

Management aneurysm, depends on the rupture or unruptur:

1. Penatalakasanaan ruptured aneurysm

• Management of ruptured aneurysms, pay attention to potential problems in SAH, including:

1. Rebleeding

2. hydrocephalus 3. Delayed Ischemic Neurologic Deficit (dind) due to vasospasm

4. hyponatremia and hypovolemia

5. DVT and pulmonary embolism

6. Seizures

7. Determine the location of the source of bleeding / ruptured aneurysm

Procedures (ICD 9 CM) Grad e

Reko

No. Therapy mend Ref

ation

a) Maintaining CBF • increasing the CPP, improve the rheological,

blood, maintain euvolemia, keep ICP

b) Neuroprotektan: there has been no effective

drugs c) Observation strict in ICU (with

monitor VS), bed rest with head-up sleeping

position 30 °,

d) Diet: NPO (greenberk p 1041)

e) Intravenous fluids (to prevent cerebral salt

wasting): NS + 20 mEq KCl / L ~ 2 ml /

kg / hour. If HCT <40%, 5% albumin

500cc

f) Drugs:

• anticonvulsant prophylaxis

2B 8

• Sedation

1 medical

• analgesia

• Dexametasone, reduce headaches and

neck. Generally given pre-op

• Purgative

1A 9.12

• anti vomiting

• Vasospasm treatment in cases of

hemorrhage SAH:

- calcium channel blockers :

nomidipin (nimotop) 4x60mg dlm 96

hours

after SAH. Tablets and IV equally

effective.

(Grade 1A)

9

- intra arterial vasospasm metal treatments endovasculer

g) Oxygenation: 2 lpm if necessary

h) Blood pressure: TDS keep 120-150mmHg

(Hypertension extreme

Upgrade

unclipped

risks

aneurysm •

rebleeding,

hypotension • ischemia) i) laboratory: DL, electrolytes,

BGA, PTT / APTT, HCT

j) Ragiologis: X-ray thorax serial to

condition stable (evaluation triple treatment H), transcranial doppler.

a) hydrocephalus

1. Acute: • 50% improved spontaneous

• rest with H & H grade IV-V: ventrikulostomi

with ICP 15-25 mmHg. Prevent rapid drop in ICT, increasing the risk of rebleeding.

2. Chronic: controversy

b) Aneurysms: cliping surgery and endovascular

coiling is done to reduce the occurrence of

rebleeding. 1. Endovascular

a) Trombosing aneurysm:

2. Coiling simple

3. The use of intracranial stent-assisted coiling

stenting (stent Leo,

solitair stent, stent enterprise, etc.)

4. Coiling using a compliant balloon

(Hyperform®, hyperglide

balloon, etc.) at the time of installation of coil

2B 10

2 Operations and 5. Flow diverter (pipe line, etc.) in the case of

intervention large size aneurysm (Giant Aneurysm)

b) Trapping preceded Compliant Balloon

1B 2.3

Occlusion Test uses Ballon

c) ligation of the proximal (Hunterian ligation)

for giant aneurysm

2. Surgery

• Clipping: Gold standard. Replacing the clip on the

neck of the aneurysm to seal the relationship

between the aneurysm from circulation without

any other normal blood pembulih clogs.

• Wrapping or coating using a muscle, cotton or

muslin, plastic resins, teflon and fibrin glue

• The combination of difficult cases requires

surgery and endovaskuler. Example: Giant

aneurysm do trapping and surgical bypass

•

proximal ligation

for giant aneurysm

(Hunterian ligation)

•

Coilling (ICD-9: 39.52) Clipping (ICD-9: 39.51)

Older age (> 75 years) young age

Clinical Grade ugly MCA aneurysm

Ruptured aneurysms that are difficult to access Giant aneurysms (diameter> 20mm)

Dg aneurysm morphology: dome-neck ratio Symptoms of an aneurysm mass effect

> 2, neck diameter <5 mm

Aneurysms of the posterior circulation Small aneurysms (diameter 1,5-2mm)

Plavix drug consumption Wide neck aneurysm

Fail in clipping or technically difficult Residual aneurysm coiling post

The timing of surgery:

1) Early (<48-96 hours) • Lower risk of rebleeding • Facilitating vasospasm therapy • lavage clot potential as agents spasmogenik • low mortality • Requirements:

o Good medical condition

o Hunt and Hess grade • 3

o SAH vasospasm potentially thick

o Conditions that would complicate management, ex: TD dud stable, seizures

o SAH thick with future effect

o early Rebleeding

o Indication of imminent rebleeding

2) Late (> 10-14 days post-SAH)

• Clinical condition or age is ugly and old patients

• Ugly neurological condition (Hunt & Hess • 4) • controversy

• Aneurysms are difficult in the clip because of the size and location

• Severe cerebral edema

• active vasospasm

• In the surgical treatment, there are some approach is used based on the location and morphology of the

aneurysm. Among them:

a) Pterional

b) Subfrontal

c) Anterior interhemispheric

d) Transcallosal

e) Transylvian or superior temporal gyrus • MCA aneurysm

f) Subocipital or subtermporal-trantentorial

2. Management unruptur aneurysm

• Indications management on unruptur aneurysm:

a. Symptomatic: that intolerable pain, impaired vision

b. Giant aneurysms in the ring clinoid

c. Aneurysms enlarged on serial imaging

• The choice of therapy in non rupture is non-medical (clipping or coiling)

9. Education • Risk factors for aneurysms

• travel sickness

• complication

• Therapy

• prognosis

10. Prognosis • Prognosis depends on several things:

1. The location and extent of the aneurysm

2. Age

3. The general clinical condition

4. Status of the neurological using Hunt and Hess grade Hunt and Hess 1 and 2 good outcome, grade • 3 ugly outcome, meningaal or permanent paralysis.

• overall mortality of ~ 45%, most improved dg little or no neurological.

• morbidity: paralysis medium - weight ~ 30%, 66% post-clipping does not improve quality of life

• Before surgery: rebleeding is a major cause of morbidity and mortality of ~ 15-20% within the first 2

weeks. • After surgery: vasospasm caused the deaths (7%), and neurological deficit (7%)

11. reviewers were critical 1. Prof. Dr. Abdul Hafid Bajamal, dr., Sp.BS

2. Dr. Agus Turchan, dr., Sp.BS

3. Dr. M. Arifin Parenrengi, dr., Sp.BS

4. Dr. Joni Wahyuhadi, dr., Sp.BS

5. Dr. Eko Agus Subagyo, dr., Sp.BS

6. Dr. Asra Al Fauzi, dr., Sp.BS

7. Wihasto Suyaningtyas, dr., Sp.BS

8. Muhammad Faris, dr., Sp.BS

9. Rahadian Indarto, dr., Sp.BS

10. Fahmi Achmad, dr., Sp.BS

11. Nur Setiawan Suroto, dr., Sp.BS

12. Irwan Barlian Immadoel Haq, dr, Sp.BS

13. Tedy Apriawan, dr., Sp.BS

14. Heri Subianto, dr., Sp.BS

12. Medical Indicators Improvement of neurological status.

13. Bibliography 1. Spetzler RF, Riina HA, Lemole GM Jr: Giant aneurysms. Neurosurgery 49: 902-908, 2001

2. Spetzler RF, RA Hanel: Surgical treatment of complex intracranial aneurysms. Neurosurgery [SHC Suppl 3]:

SHC1289-SHC1299 2008 3. Morris Pearse: Practical Neuroangiography second edition. Lippincott Williams & Wilkins,

2007

4. Spetzler RF, Kalani MYS, Nakaji Peter: Neurovasculer second surgery edition. Thieme, 2015

5. JJ Perry, Stiell IG, Sivilotti ML, Bullard MJ, Emond M, Symington C, Sutherland J, Worster A, Hohl C, Lee JS,

Eisenhauer MA, Mortensen M, Mackey D, Pauls M, Lesiuk H, Wells GA. Sensitivity of computed tomography

performed within six hours of onset of headache for the diagnosis of subarachnoid haemorrhage: prospective

cohort study.BMJ. 2011; 343: d4277

6. Wiesmann M, Mayer TE, Yousry I, Medele R, Hamann GF, Brückmann H. Detection of hyperacute

subarachnoid hemorrhage of the brain by using magnetic resonance imaging.J Neurosurg. 2002; 96 (4): 684.

7. Lu L, Zhang LJ, Poon CS, Wu SY, CS Zhou, Luo S, Wang M, Lu GM. Digital subtraction CT angiography for

detection of intracranial aneurysms: comparison with three-dimensional digital subtraction angiography. Radiology.

2012 February; 262 (2): 605-12. Epub 2011 Dec 5.

8. Marigold R, Günther A, Tiwari D, Kwan J. antiepileptic drugs for the primary and secondary prevention of

seizures after subarachnoid haemorrhage. Cochrane Database Syst Rev. 2013 Jun; 6

9. Dorhout Mees SM, Rinkel GJ, Feigin VL, algra A, van den Bergh WM, Vermeulen M, van Gijn J.

Calcium antagonists for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev. 2007

10. AR Dehdashti, Rilliet B, Rufenacht DA, de Tribolet N. A shunt-dependent hydrocephalus after rupture

of intracranial aneurysms: a prospective study of the influence of the treatment modality. J Neurosurg. 2004;

101 (3): 402.

11. AU Chappell ET, Moure FC, Good MC. Comparison of computed tomographic angiography with digital

subtraction angiography in the diagnosis of cerebral aneurysms: a meta-analysis. Neurosurgery. 2003; 52 (3):

624

12. Abruzzo T, C Moran, Blackman KA, Eskey JK, Lev R, Meyer P, Narayanan S, Prestigiacomo CJ.

Invasive interventional management of post-hemorrhagic cerebral vasospasm in Patients with aneurysmal

subarachnoid hemorrhage.J Neurointenvent surgery. 2012

AVM

ICD-10: I 67.1

1. Definition - Arteriovenous malformation / AVM is a congenital disorder caused by abnormal dilatation of blood

(Definition) vessels of the arterial blood flow is directly related to draining vein without mealui kapier normal tissue.

Not available in nidus of brain parenchymal tissue.

- Often found as a complication of bleeding (risk of spontaneous bleeding occurs 2-4% / year), rare

seizures

- The blood flow in the AVM changed from the low pressure at the time of birth, into the pressure was high -

as an adult so that AVM lesions tend to enlarge. 2. History Symptoms that may arise:

1. ICT symptoms increased because of bleeding (most often): 50%. The peak incidence age of 15-20 years

2. Seizures

3. Effects period, ex: trigeminal neuralgia for CPA AVM

4. Ischemia: steals effect

5. Headache

3. Physical Examination A visible sign

• Signs of ICT increases

• cranial nerve palsy due to the effects of future

• weakness of limbs due to ischemia

• Bruit (especially the dural AVM)

4. Investigation Radiologis:


Reko


ation

1 CT scan

Overview 'flow void', the sensitivity of CT scans will be increased

2B 4

when accompanied by CT angiography

2 MRI

MRI is very sensitive to the identification of the AVM nidus

2A 3

Gold standard diagnosis 1C 4

3 angiography

1) CT scan: good quality detect hemorrhage and calcification 2) MRI: AVM morphology and get rid of DDX 3) angiography: visible Tangle of vessels, feeding artery, draining veins visible

the arterial phase

5. Criteria for Diagnosis 1. Anamnesis according above

2. Clinical examination according above

3. Imaging studies corresponding above

6. Diagnosis

AVM Grading is based on the following classification,

Spetzler Martin AVM grading system

Graded Feature Points

Small size (<3

cm) Medium (3-6 cm) 1

Large (> 6 cm) 2

3

Eloquence of adjacent brain

Non eloquent 0

Eloquent 1

Pattern of venous drainage

superficial only 0

Deep 1

Grading is used as the basis for determining prognosis and selection of treatment

7. Diagnosis • cavernous hemangioma

• Dural arteriovenous fistula

• amyloid angiopathy • cerebral aneurysm • Cerebral venous thrombosis • brain hemorrhage

• Moyamoya disease • Vein of gallen malformation • Tumor

8. Therapy

• There are 4 options AVM management, diperimbangkan diberdasarkan grade Spetzler-Martin. Pembendahan

action is the gold standard, which is indicated in grade 1-3. Multimodality therapy were considered for AVM

with grade III-IV. For grade V-VI konservatif.diutamakan to AVM rupture or rupture of an insane history

kukan action be dah


Reko


ation

1 Operations Surgery is the primary choice 1B 4

• Effective at ~ 20% of cases

2 Radiation

• Stereotactic radiosurgery (SRS) • small size

1B 5

<2.5-3 cm nidus, lies in

Embolization as adjunctive therapy

- embolization using glue (hystoacryl lipiodol or

EVOH (Onyx, etc)

- embolization transvenous (TRENSH) 2B 6

3 Endovascular using EVOH and balloon assisted (compliant

balloon)

The combination of embolization to shrink nidus,

followed by stereotactic

9. Education • Risk factors for AVM

• travel sickness

• complication

• Therapy

• prognosis

10. Prognosis • Prognosis depends on several things:

o In case of spontaneous bleeding, mortality of 30-50%

o The smaller the size, the more deadly because of the risk of further bleeding

big

o Large size associated with morbidity, the risk of further seizures

big

• Based on the grade Spetzler-Martin:

11. Medical Indicators Improvement of neurological status

12. Critical Reviewers 1. Prof. Dr. Abdul Hafid Bajamal, dr., Sp.BS














13. Bibliography 1. Piepgras DG, Sundt TM Jr, Ragoowansi AT, Stevens L. Seizure Outcome in Patients with surgically treated

cerebral arteriovenous malformations. Neurosurg. 1993 January; 78 (1): 5-11.

2. Mohr JP, Parides MK, Stapf C, Moquete E, Moy CS, Overbey JR, Al-Shahi Salman R, Vicaut E, Young

WL,

Houdart E, Cordonnier C, Stefani MA, Hartmann A, von Kummer

R, Biondi A, Berkefeld J, Klijn CJ, Harkness K, Libman R, Barreau X, Moskowitz AJ, ARUBA

international investigators. Medical management with or without interventional therapy for unruptured

brain arteriovenous malformations (ARUBA): a multicentre, non-blinded, randomized trial. Lancet.

2014; 383 (9917): 614.

3. Saleh RS, Singhal A, Lohan D, Duckwiler G, Finn P, Ruehm S Assessment of cerebral arteriovenous

malformations with high temporal and spatial resolution magnetic resonance angiography

contrastenhanced: a review from protocol to clinical application. Top Magn Reson Imaging. 2008 Oct;

19 (5): 251-7.

4. Mohr JP, Kejda-Scharler J, Pile-Spellman J. Diagnosis and treatment of arteriovenous malformations. Curr Neurol

Neurosci Rep. 2013 February; 13 (2): 324.

5. Schäuble B, Cascino GD, Pollock BE, Gorman DA, Weigand S, Cohen-Gadol AA, McClelland RL.

Seizure outcomes after stereotactic radiosurgery for cerebral

arteriovenous malformations.Neurology. 2004; 63 (4): 683.

6. Krings T, Hans FJ, Geibprasert S, Terbrugge K Partial "targeted" embolisation of brain

arteriovenous malformations. Eur Radiol. 2010 November; 20 (11): 2723-31. Epub 2010

June

11.

Carotid Artery Stenosis

I65.2

1. Definition The condition where the narrowing or kontriksi from the carotid artery due to atherosclerosis

(Definition)

2. History - obtained risk factors such as smoking, obesity, dyslipidemia, hypertension, diabetes mellitus

- obtained Transient neurological symptoms ranging from ischemic attack (TIA) to denag stroke

3. Physical Examination General Physical Examination

(Examination by inspection, palpation, percussion and auscultation) a thorough examination to rule out other

causes of epilepsy. At the time of the seizure, the patient should be checked and managed in accordance with

the principle emergency are: secure Airway, Breathing, Circulation

Neurological examination

• The level of awareness Glasgow Coma Scale ( GCS) • Examination of one to twelve cranial nerves • Motor examination thorough

• The sensory examination thorough

• Physiological reflex examination

• Examination of pathological reflexes

4. Criteria for Diagnosis 1. History according above

2. Clinical examination in accordance Issuer

3. Investigations

5. Work Diagnosis Kartis Artery Stenosis (I65,2)

6. Diagnosis - headache

- shingles

-

Transient iskhemic

attack

- Stroke

- retinal occlusion

- neck trauma

- Subarachnoid hemorrhage

- In sexy artery verte bralis

7. Investigations grade

No Inspection Recommendation rekomend Ref

care

- To find out where the anatomy of the

carotid stenosis and its relationship

1 CTA with structures are at bone 1B 1,2,3

surrounding

- To evaluate the carotid artery with

2 MRA

menggunanakn 3D TOF (time of

1B 4,5,6,7,8

flight) or CEMRA (enhnced

contrast MRA)

3 Carotid duplex

- Detect the speed of blood flow in the

1B

9,10,11,1

carotid stenosis 2.13

ultrasound

measuring Peak systolic velocity (PSV),

end-diastolic velocity (EDV), carotid

index (peak Iinternal

carotid artery and the common carotid artery

velocity velocity)

Transcranial

- Evaluate the relationship carotid stenosis

4

with intracerebral arteries leading to the

brain 1B 14,15,16

doppler

parenchyma

5 Cerebral

- Is the gold standard for diagnostic carotid

1A 17,18,19

stenosis

Angigoaphy

8. Therapy grade

No. Therapy Procedures (ICD 9) rekomend Ref

care - Procedures with statins, anti-platelet

1 Medika mentosa therapy of hypertension and diabetes,

2A

20,21,22, 23

healthy lifestyle change

Carotid end - Is a treatment option for carotid

24,25,26,

2 arterectomy

stenosis

1A

27,28

(CEA)

- The choice of therapy for carotid

stenosis if not possible to

done operation.

Using a balloon to dilate continued

permanent carotid stenting.

Carotid Artery

- Used also protective devices against

29,30,31,

3. Angioplasty and 1A

embolism ( embolic 32.33

Stenting (CAS)

Protection Device) can form an umbrella

( umbrella) mounted while in distal

stenosis or balloon catheter that is

placed temporarily at the proximal of

stenosis

9. Education Explanations to patients and families:

• Course of the disease and complications that may occur

• Therapy and actions that will be given along with the advantages and disadvantages

• The procedure for the treatment and the treating physician

10. Prognosis Ad Vitam (Live) : Ad bonam

Ad Sanationam (cured) : Ad Dubia bonam

Ad Fungsionam (function) : Ad Dubia bonam

Prognosis carotid stenosis increases when there is clinical improvement in post-action CEA or CAS



3. Dr. M. Arifin Parenrengi, dr.,

Sp.BS








11. Nur Setiawan Suroto, dr.,

Sp.BS




12. Medical Indicators Carotid artery stenosis management indicators are based on the state of clinical improvement.

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magnetic resonance angiography Compared with digital subtraction angiography. J Vasc Surg

2002; 36: 806.

5. Debrey BC, Yu H, Lynch JK, et al. Diagnostic accuracy of magnetic resonance angiography for

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subsequent ischemic cerebrovascular events: a prospective assessment with MRI - initial

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stroke: building a risk profile for carotid plaque. Stroke 2010; 41: S12.

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and indications. AJR Am J Roentgenol 1992; 158: 29.

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13. Huston J 3rd, James EM, Brown RD Jr, et al. redefined duplex

ultrasonographic criteria for the diagnosis of carotid artery stenosis. Mayo Clin Pro

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15. Wilterdink JL, Feldmann E, Furie KL, et al. Transcranial Doppler ultrasound

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16. Molina CA, Montaner J, Abilleira S, et al. Timing of spontaneous recanalization

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17. Hankey GJ, Warlow CP, RJ Sellar. Cerebral angiographic risk in mild

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18. Wolpert SM, Caplan LR. Current role of cerebral angiography in the

diagnosis of cerebrovascular diseases. AJR Am J Roentgenol 1992; 159:

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19. Kappelle LJ, Eliasziw M, Fox AJ, et al. Importance of intracranial atherosclerotic

Disease in Patients with symptomatic stenosis of the internal carotid artery. The North American

symptomatic carotid endarterectomy Trail. Stroke 1999; 30: 282.

20. Abbott AL. Medical (nonsurgical) intervention alone is now best for prevention

of stroke associated with severe asymptomatic carotid stenosis: results of a systematic review

and analysis. Stroke 2009; 40: e573. 21. Raman G, Moorthy D, Hadar N, et al. Management strategies for

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Carotid Cavernous Fistula

ICD-10: Q28.2

1. Definition An abnormal connection between the carotid artery in the cavernous sinus, which can occur spontaneously

(Definition) or acquired (trauma), CCF grouped by etiology (trauma vs. spontaneous), blood flow velocity (high flow

versus low flow), anatomy (direct vs. dural, internal carotid vs external carotid vs. both)

2. anamnesis

• There is a history of previous trauma

• obtained ptosis

• Obtained their bruit

• Obtained headache

3. Physical examination High flow: - Bruit (80%), usually Traba above eye Boal - Blurred eye sight (25- 59%) - Headache (53- 75%) - Diplopia (50-85%) - Eyeball and orbital pain (35%) - Proptosis (72-87%) - Chemosis and conjunctival injection 955-89%) - Ophthalmoplegic (50-85% N VI palsy, cerebral 67% N III, N IV palsy 49%)

Low flow: - Anterior draining dural, symptoms: khemosis, conjuntival injection, proptosis

- Dural ccf flowing backward to the inferior or superior petrosal sinuses, the symptoms are: painfull

diplopia, N III palsy, cerebral IV N, N VI palsy

Loss of vision is a major problem driaing anterior dural case with a percentage of 33%. The cause of

impaired vision - Increased intraocular pressure sejunder causing venous congestion and glaucoma

- Venous stasis retinopathy - vitreous haemorrhage - proliferative retinopathy - Ischemic optic neuropathy - Exudative retinal detachment - Complications are rare as choroidal effusion and closed angle glaucoma

4. criteria for Diagnosis 1. History according above


3. Imaging studies corresponding Issuer

7. diagnosis Carotid cavernous fistula (ICD-10: Q28,2)

8. Diagnoses 5.

- Intracranial tumors, lymphoma, metastatic

6.

- aneurysms

- Cavernous sinus thrombosis

- Infection

- Tolosa hunt syndrome

- orbital pseudotumor

- vasculitis

- sarcoidosis 9. Examination

Support Recommendation Grad e

Reko


ation

see proptosis, expansion of the cavernous sinus and

superior ophthalmic vein, extraocular muscle dilation

associated with fractures of the skull base. CTA could

1 CT Scan see their CCF especially the proximal region of the 2A 1, 2, 3

cavernous sinus

see proptosis, expansion cavernous sinus and superior

2 MRI

ophthalmic vein, and the widening of the extraocular 1C 4, 5, 6, 7

muscles. Can also see cavernous sinus flow void.

Transcranial Doppler

saw an increase in blood flow velocity and a 1C 4, 8, 9

3 decrease in the index pusatif carotid siphon in

Ultrasound

patients with CCF

TFCA is the gold standard for diagnosis and primary

4

(Trannsfermoral treatment for CCF 1C 10 11

Cerebral

Angiography)

10. Therapy - CCF optimal therapy is to close an abnormal connection between the internal carotid artery to the

cavernous sinus while maintaining patency of the internal carotid artery

- some prosed ur used: Procedures (ICD 9 CM) Grad e

Reko


ation

Using the arterial or venous access. Transarteri embolization is the main option for most cases of particularly high flow CCF.

For the case of low flow CCF, embolization transarteri

12, 13,

difficult because of the small arteries, tortuous

14, 15,

(Grooved) and sometimes

16, 17,

Endovaskuler multpel. The choice combination transarteri and

1 2A 18, 19,

transvenous embolization. Materials used: detachable

20, 21,

ballon, platinum coil,

22, 23,

intracerebral stenting, polyvinyl particles

24

akhohol, Ethylene Vinyl Alcohol / EVOH ( ONYX etc) and-liquid

adhesive used to close the fistula with microcatheters

superselektif.

Transarteri embolization complications include:

- embolan migration into the intracranial circulation,

causing ischemia or cerebral infarction. Therefore,

the use of anticoagulation during the procedure and

the action antiplateletpostaction

decrease rsiko ischemia or infarction

cerebral

- Pseudoaneurisma because of injury in the arterial

wall

Transvenous embolization complications include:

- ischemia or cerebral infarction

- subarachnoid hemorrhage

- ruptured sinus

- extravasation ekstradura therefore

contrast

- cranial nerve parese

Surgery is done if endovaskuler unsuccessful. Her

action includes packing in cavernous sinus fistula for

clogs, sewing or clipping siftula, sealing the fistula

2 Surgery with fascia or glue, or ligation of the internal carotid 2A 12, 15

artery.

17, 25

radiosurgery indicated when

endovaskuler approaches and surgical intervention

aksessibel not pose a high risk of morbidity.

Radiotherapy resulted in obliteration of the dural CCF

stereotactic

around 75-100% despite 1C 26, 27,

3 takes several months. The required dose of 10-40

radiosurgery 28

Gy. Before radiation, determination of lesion size

have to do with the approach endovaskuler (TFCA) to

reduce the radiation dose necessary

,

Manual compression aimed at reducing the flow of

blood to form a thrombus within the cavernous sinus.

4 Manual compression Compression 1C 29, 30,

Vascular

performed for 30 seconds ipsilateral

31

carotid several times daily for 4- 6 weeks.

,

Patients with ocular proptosis lubrican should be

given to avoid exposure keratitis

5

handling 2A 32, 33

ophthalmology Increased intraocular be given obatoba to reduce

intraocular pressure

such as acetazolamide, corticosteroids iv, b

topical blocker





12. prognosis Prognosis depends on:

1. Symptoms of the disease

2. The severity and pathogenesis of the disease

3. The accompanying disease

13. Medical indicators Improvement of neurological status

14. Critical Reviewers 1. Dr. Joni Wahyuhadi, dr., Sp.BS


3. Prof. Dr. Abdul Hafid Bajamal, dr., Sp.BS



6. Eko Agus Subagyo, dr., Sp.BS


8. Asra Al Fauzi, dr., Sp.BS







15. Literature 1. Acierno MD, Trobe JD, Cornblath WT, Gebarski SS. Painful oculomotor palsy the caused by

posteriordraining dural carotid cavernous fistulas. Arch Ophthalmol 1995; 113: 1045.

2. Coskun O, Hamon M, Catroux G, et al. Carotid-cavernous fistulas: diagnosis with spiral

CT angiography. AJNR Am J Neuroradiol 2000; 21: 712.

3. JC Rucker, Biousse V, Newman NJ. Magnetic resonance angiography source images in

carotid cavernous fistulas. Br J Ophthalmol 2004; 88: 311.

4. de Keizer R. Carotid-cavernous and orbital arteriovenous fistulas: ocular features,

diagnostic and hemodynamic considerations in relation to visual impairment and morbidity. Orbit 2003;

22: 121.

5. Hirabuki N, Miura T, Mitomo M, et al. MR imaging of dural arteriovenous malformations

with ocular signs. Neuroradiology 1988; 30: 390.

6. Vattoth S, Cherian J, Pandey T. Magnetic resonance angiographic demonstration of

carotid cavernous fistula using elliptical centric time resolved imaging of contrast

kinetics (EC-TRICKS). Magn Reson Imaging 2007; 25: 1227.

7. YW Chen, Jeng JS, Liu HM, et al. Carotid and transcranial color-coded duplex

sonography in different types of carotid-cavernous fistula. Stroke 2000; 31: 701. 8. Kilic T, Elmaci I, Bayri Y, et al. Value of transcranial Doppler ultrasonography in the

diagnosis and follow-up of carotid-cavernous fistulae. Acta Neurochir (Wien) 2001; 143: 1257.

9. DeBrun GM. Angiographic workup of a carotid cavernous sinus fistula (CCF) or what

information does the interventionalist need for treatment? , Surg Neurol 1995; 44:75.

10. Meyers PM, Halbach VV, Dowd CF, et al. Dural carotid cavernous fistula: definitive

endovascular management and long-term follow-up. Am J Ophthalmol 2002; 134: 85.

11. TK Lin, Chang CN, Wai YY. Spontaneous intracerebral hematoma from occult carotid-

cavernous fistula during pregnancy and puerperal. Case report. J Neurosurg 1992; 76: 714.

12. Lewis AI, Tomsick TA, Tew JM Jr. Management of 100 consecutive direct carotid-cavernous

fistulas: results of treatment with detachable balloons. Neurosurgery 1995; 36: 239.

13. Gupta AK, Purkayastha S, Krishnamoorthy T, et al. Endovascular treatment of direct

carotid cavernous fistulae: a pictorial review. Neuroradiology 2006; 48: 831.

14. Wang W, Li YD, Li MH, et al. Endovascular treatment of post-traumatic direct carotid-

cavernous fistulas: A single-center experience. J Clin Neurosci 2011; 18:24.

15. Ringer AJ, Salud L, Tomsick TA. Carotid cavernous fistulas: anatomy, classification,

and treatment. Neurosurg Clin N Am 2005; 16: 279.

16. Gemmete JJ, Chaudhary N, Pandey A, Ansari S. Treatment of carotid cavernous

fistulas. Curr Treat Options Neurol 2010; 12:43.

17. Phelps CD, Thompson HS, Ossoinig KC. The diagnosis and prognosis of atypical

carotid cavernous fistula (red-eyed shunt syndrome). Am J Ophthalmol 1982; 93: 423.

18. Madan A, Mujic A, Daniels K, et al. Traumatic Carotid artery-cavernous sinus fistula

treated with a covered stent. Report of two cases. J Neurosurg 2006; 104: 969.

19. Gomez F, Escobar W, Gomez AM, et al. Treatment of carotid cavernous fistulas using covered

stents: midterm results in seven Patients. AJNR Am J Neuroradiol 2007; 28: 1762.

20. Morón FE, Klucznik RP, Mawad ME, Strother CM. Endovascular treatment of high-flow

carotid cavernous fistulas by stent-assisted coil placement. AJNR Am J Neuroradiol 2005; 26: 1399.

21. Kocer N, Kizilkilic O, Albayram S, et al. Treatment of iatrogenic internal carotid artery

laceration and carotid cavernous fistula with endovascular stent-graft placement. AJNR Am J

Neuroradiol 2002; 23: 442

22. Li J, ZG Lan, Xie XD, et al. Traumatic carotid-cavernous fistulas treated with covered

stents: experience of 12 cases. World Neurosurg 2010; 73: 514.

23. Marques MC, JG Caldas, Nalli DR, et al. Follow-up of endovascular treatment of direct

carotid cavernous fistulas. Neuroradiology 2010; 52: 1127.

24. Klisch J, Huppertz HJ, Spetzger U, et al. Transvenous treatment of carotid cavernous and dural arteriovenous fistulae: results for 31 Patients and review of the literature. Neurosurgery 2003; 53:

836.

25. O'Leary S, TJ Hodgson, Coley SC, et al. Intracranial dural arteriovenous

malformations: results of stereotactic radiosurgery in 17 Patients. Clin Oncol (R Coll

Radiol) 2002; 14:97.

26. Fiore PM, Latina MA, Shingleton BJ, et al. The dural shunt syndrome. I. Management

of glaucoma. Ophthalmology 1990; 97:56.

27. Tishler RB, Loeffler JS, Lunsford LD, et al. Tolerance of cranial nerves of the

cavernous sinus to radiosurgery. Int J Radiat Oncol Biol Phys 1993; 27: 215.

28. Higashida RT, Hieshima GB, Halbach VV, et al. Closure of carotid cavernous sinus fistulae

by external compression of the carotid artery and jugular vein. Acta Radiol Suppl 1986; 369: 580.

29. Halbach VV, Higashida RT, Hieshima GB, et al. Dural fistulas involving the cavernous

sinus: results of treatment in 30 Patients. Radiology 1987; 163: 437.

30. Kai Y, Hamada J, Morioka M, et al. Treatment of cavernous sinus dural arteriovenous

fistulae by external manual compression of the carotid. Neurosurgery 2007; 60: 253. 31. Luo CB, Teng MM, Yen DH, et al. Endovascular embolization of recurrent traumatic

carotid cavernous fistulas with detachable balloons previously managed. J Trauma 2004; 56: 1214.

32. Halbach VV, Hieshima GB, Higashida RT, Reicher M. Carotid cavernous fistulae:

indications for urgent treatment. AJR Am J Roentgenol 1987; 149: 587.

33. Chen CC, Chang PC, Shy CG, et al. CT angiography and MR angiography in the evaluation

of carotid cavernous sinus fistula prior to embolization: a comparison of techniques. AJNR Am J Neuroradiol

2005; 26: 2349.

DISEASE-MOYA MOYA

ICD-10: I 67.5

1. Definition

Rare vascular disorders, characterized by the progressive narrowing of the blood vessels in the arterial circle at

the

(Definition)

base of the brain ( circle of Willis). Characterized by bilateral stenosis or occlusion of the arteries in the circle of

Willis

so that more prominent collateral circulation.

2. History The symptoms and clinical course varies:

- No symptoms until that result in severe neurologic deficits are temporary.

- Adults are more in line with bleeding;

- cerebral ischemic events are more common in children.

- Children can have hemiparesis, monoparesis, sensory disturbance, involuntary movements,

headache, dizziness, or seizures. Mental retardation or persistent neurological deficit.

- Intraventricular, subarachnoid or intracerebral hemorrhage sudden onset is more common in

adults.


(Examination by inspection, palpation, percussion and auscultation)

• Physical examination was first priority in the evaluation of A ( airways), B

(Breathing), and C ( circulation)


• The level of awareness Glasgow Coma Scale ( GCS)

• Physical examination findings depend on the location and severity of hemorrhage or ischemic.

4. Investigations - CT Scan

- angiography:

- Cerebral angiography is the standard criteria for the diagnosis of Moyamoya disease. The following findings

can support the diagnosis:

- Stenosis or occlusion in the terminal part of the internal carotid artery or the proximal portion or

anterior cerebral artery.

- Abnormal blood vessel tissue around the area occlusive or stenosis.

- Findings were found bilaterally (Although some patients may be at

and then progressive unilateral involvement). Magnetic resonance angiography (MRA) can be

performed.

SPECT (Single photon emission computerized tomography)


Reko


ation

Overview on cortical and subcortical infarcts, found

1 CT scan in early stage MMD Suzuki 1 or 2 2B 4

2 MRI

In contrast T1 or T1 flair obtained picture ' ivy

2A 5

sign '

angiography MRA can memeberikan stenosis picture 1C 6

3 or occlusion of the distal ICA, CTA showed abnormal

collateral vessel or vessels in the basal ganglia

5. Criteria for Diagnosis 1. The history and clinical examination (as per above)

2. CT Scan Head

3. TFCA (angiography)

6. Diagnosis Moya moya disease I67.5

7. Diagnosis The history:

Anterior Circulation Stroke Blood

Basilar Artery Thrombosis

Cavernous Sinus Dyscrasias and

Stroke Syndromes Syndromes

Cerebral Aneurysms Dissection

fibromuscular dysplasia Fabry

Disease Intracranial Hemorrhage

8. Therapy -


Reko


ation

Moyamoya patients are given aspirin to

children or adults who nonsimptomatik or

symptomatic ischemic Moyamoya

2C

1 Medikamentosa 7

Not recommended the use of 1C

anticoagulants old

revascularization

• The superficial temporal artery-middle cerebral

artery (STA-MCA) anastomosis

• EMS (encephalomyosynangiosis)

2 Operations

• Encephaloduroarteriosynangiosis (EDAS) 1C 8

• Encephaloduroarteriomyosynangiosis (Edams)

(ICD-9: 437.5)

• wattle synangiosis

• Omental transplantation





• Require adjuvant treatment for recovery of impaired neurological function, through medical

rehabilitation program

10. Prognosis Prognosis is affected:

- Clinical improvement can be seen after the surgical procedure immediately with the

possibility of 6-12 months will form new blood vessels as supply.

11. Medical Indicators Improvement of neurological status and the underlying disease causes moya-moya


http://emedicine.medscape.com/article/1159900-overview



















2. Library 1.Widow PH, JG Bellew, Veerappan V. Moyamoya disease: case report and literature review. J Am Assoc

osteopath. Oct 2009; 109 (10): 547-53.

2. Mineharu Y, Takenaka K, Yamakawa H, et al. Inheritance pattern of familial Moyamoya disease:

autosomal dominant fashion and genomic imprinting. J Neurol Neurosurg Psychiatry. Sep 2006; 77

(9): 1025-9.

3. Mineharu Y, Liu W, Inoue K, Matsuura N, Inoue S, Takenaka K. Autosomal dominant Moyamoya

disease maps to chromosome 17q25.3. Neurology. Jun 10, 2008; 70 (24 Pt 2): 2357-63.

4. Kim SJ, Heo KG, Shin HY, Bang OY, GM Kim, Chung CS. Association of thyroid autoantibodies with

Moyamoya-type of cerebrovascular disease: a prospective study. Stroke. Jan 2010; 41 (1): 173-6.

5. Kikuta K, Takagi Y, Nozaki K, Hanakawa T, Okada T, Mikuni N, Miki Y, Fushmi Y, Yamamoto A,

Yamada

K, Fukuyama H, Hashimoto N symptomatic microbleeds in Moyamoya disease: T2 * -weighted

gradient-echo magnetic resonance imaging study. J Neurosurg. 2005; 102 (3): 470

6. Roach ES, Golomb MR, Adams R, Biller J, Daniels S, Deveber G, Ferriero D, Jones BV, Kirkham FJ,

Scott

RM, Smith ER, the American Heart Association Stroke Council, Council on Cardiovascular Disease in

the

Young. Management of stroke in infants and children: a scientific statement from a Special Writing

Group

of the American Heart Association Stroke Council and the Council on Cardiovascular Disease in the

Young.Stroke. 2008; 39 (9): 2644.

7. Monagle P, Chan AK, Goldenberg NA, Ichord RN, Journeycake JM, Nowak-Göttl U, Vesely SK,

American College of Chest PhysiciansAntithrombotic therapy in neonates and children:

antithrombotic

Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians

Evidence-Based Clinical Practice Guidelines.Chest. 2012 February; 141 (2 Suppl): 801S-e737S

8. Fung LW, Thompson D, V. Ganesan Revascularisation Pediatric Surgery for Moyamoya: a review of

the literature. Childs Nerv Syst. 2005; 21 (5): 358

Normal Pressure Hydrocephalus (NPH)

G91.2

3. Definition Condition in which a pathologically enlarged brain ventricles with initial pressure (Opening pressure) in

(Definition) the normal lumbar puncture.

4. History • Classically obtained triad: Dementia

Urinary incontinence

Trouble walking (gait disturbance)

The symptoms appear partially and slowly (gradual) 5. Physical Examination General Physical Examination

(Examination by inspection, palpation, percussion and auscultation) a thorough examination to rule out other

causes of epilepsy. At the time of the seizure, the patient should be checked and managed in accordance with

the principle emergency are: secure Airway, Breathing, Circulation


• The level of awareness Glasgow Coma Scale ( GCS) • Examination of one to twelve cranial nerves • Motor examination thorough

• The sensory examination thorough

• Physiological reflex examination

• Examination of pathological reflexes

• Examination of cognitive function (MMSE)



3. Investigations

7. Work Diagnosis Normal Pressure Hydrocephalus (G91.2)

8. Diagnosis - disease prakinson

- vascular Dementia

- Alzheimer's

- Frontal Lobe Syndrome

- Urinary system disorders

- Tu mor / lesions serebel um

9. Investigations grade

No Inspection Recommendation rekomend Ref

care

- Obtained enlargement in all the

ventricular system WITHOUT any signs

of obstruction or infection

1 CT Scan Head - The presence of periventricular edema 1A 1,2,3,4,5

(Ejection)

- Evan's ratio> 0.3

- Obtained enlargement all the ventricular

2 MRI Head

system

1B 1,2,3,4,5

- An increase in signal in the periventricular

(on FLAIR sequences)

- Evan's ratio> 0.3

- By using isotope

3 Cysternografi

with lumbar puncture. NPH

2B 1,2,3,4,5

enforced when isotopes are lost

from

cysterna in 72 hours

- In Lumbar puncture / lumbar tap test,

issued LCS kemudain much as 3050 cc

Lumbar

of clinical evaluation. Clinical

improvement will provide good results

puncture /

4

when done shunting

1A 1,2,3,4,5

lumbar tap test

- Lumbar tap test can be done up to three

times to see the real clinical improvement

- External LD also issued LCS will however

be maintained within 3-6 days (LCS can

External be issued up to 40

5 Lumbar cc), 1A 1,2,3,4,5

Drainage - Clinical improvement will provide good

results when done shunting

10. Therapy grade

No. Therapy Recommendation rekomend Ref

care

- Programmable VP shunt

provide better results Instead of the VP

shunt with fixed pressure because of

1 Programmable the ability to 1A 1,2,3,4,5

VP shunt modify

and

adjust the ventricular pressure

- VP shunt is used to steamy medium

and low pressure but

2 VP Shunt fixed the risk of 2A 1,2,3,4,5

pressure overshunting very high complication





12. Prognosis Ad Vitam (Live) : Ad bonam

Ad Sanationam (cured) : Ad Dubia bonam

Ad Fungsionam (function) : Ad Dubia bonam

Prognosis NPH operation will increase if there is clinical improvement in pre-operative CSF diversion (with

lumbar tap test or ELD)

13. reviewers were critical

1. Prof. Dr. Abdul Hafid Bajamal, dr.,

Sp.BS

2. Dr. Agus Turchan, dr.,

Sp.BS


4. Dr. Joni Wahyuhadi, dr.,

Sp.BS


6. Dr. Asra Al Fauzi, dr.,

Sp.BS









14. Medical Indicators NPH management indicators based on the state of repair of clinical triad of NPH

15. Bibliography 1. Krauss JK, Halve B. Normal pressure hydrocephalus: survey algorithms on contemporary diagnostic

and therapeutic decision-making in clinical practice. Acta Neurochir (Wien) 2004; 146: 379.

2. Tisell M, Hoglund M, Wikkelsø C. National and regional incidence of surgery for adult hydrocephalus in

Sweden. Acta Neurol Scand 2005; 112: 72.

3. Klassen BT, Ahlskog JE. Normal pressure hydrocephalus: how does the diagnosis Often hold water?

Neurology

2011; 77: 1119.

4. JA Vanneste. Diagnosis and management of normal-pressure hydrocephalus. 4. J Neurol 2000; 247: 5.

5. Petersen RC, Mokri B, Laws ER Jr Surgical treatment of idiopathic hydrocephalus in elderly

patients.Neurology 1985; 35: 307.

6. Black PM, Ojemann RG, Tzouras A. CSF shunts for dementia, incontinence, and gait disturbance. Clin

Neurosurg 1985; 32: 632.

Intracerebral hematoma SPONTANEOUS

ICD-10: I61.0

1. Definition Collection of blood in the brain parenchyma. It can be a little bleeding bleeding-fused, or blood

(Definition) vessel injury is quite large.

2. History • Obtained headache • Obtained neurological disorders (amnesia, loss of consciousness, seizures, etc.) • Obtained risk factors: hypertension, diabetes mellitus



• Physical examination was first priority in the evaluation of A (

airways), B (Breathing), and C ( circulation) other tests

• High blood pressure. Cardiac Disorders. Kidney disorders



• Nerves II-III, VII peripheral nerve lesions • Fundoskopi look for signs of edema pupil, retinal detachment • Motor and sensory, compare the right and left, up and down

• Autonomis



3. The appropriate imaging examination under

5. Work Diagnosis Intracerebral hematoma (ICD 10: I61.0)

6. Diagnosis - trauma

- epileptic fits

- drug intoxication

- P metabolic enyakit

7. Investigations Recommendation Grad

e

No. Examination Reko Ref

mend

care

CT without contrast is widely used

to evaluate the acute ICH, CT scans were able to

1 CT scan

evaluate the location and big hematoma as well 1C 1,2,3

evaluate the extension of the ventricle,

herniation, peripheral edema ,.

2 CTA CTA and MRA can be used to 2A 4.5

screening vascular abnormalities such as

aneurysm, AVM

3 MRI

GRE-T2 sequences to assess bleeding

2A 6

hyperacute, subacute, chronic

4 DSA Screening for vascular disorders such as

1C 9

AVM. aneurysm

X-thoracic images:

• Looking for heart abnormalities CT Scan Head:

• Overview hiperedens shaped biconvex

• May be accompanied by bleeding in the ventricles picture X-photo others by k eperluan

8. Therapy Recommendation Grad

e

No. Therapy Reko Ref

mend

care

When SBP> 200 mmHg or MAP> 150 mmHg

it is recommended to fast reduction of pressure

blood using continuous intravenous OAH

and monitoring every 5 minutes


accompanied by signs of increased ICP then

Blood

OAH administration is intermittent or

1 CPP targets continuously at 61-80 mmHg 1A 7.8

pressure

regulation


without signs of ICT penongkatan

then the target BP is 160/90 use

OAH intravenous intermittent or

continuous observation every 15 minutes

EVD (ICD-9: 2:21)

2 Operative Indications for patients with intraventricular

1B 8

haemmorhage with neurological deficits.

Bilateral EVD can only be performed if bleeding

clogs

monroe foramen. EVD for hydrocephalus due to SAH in patients with loss of consciousness and

proved there was an increase in ICT. Patients with hydrocephalus which do not improve within 24 hours.

Posterior fossa ICH (ICD 9-01.24) diameter> 3 cm with deteriosisasi neurological or brain stem compression and / or hydrocephalus due

to obstruction of the ventricular recommended for evacuation of bleeding (Grade 1B)

Supratentorial ICH (ICD 9-01.24) The volume of> 30cc with a distance of 1 cm from the surface. The next evacuation within 96 hours after the first surgery is not recommended. Surgical intervention is not recommended in patients with full

consciousness or coma in a patient in intermediete level / stupor are candidates operation. Another thing that supports surgery

• new Genesis

• Deteriorisasi progressive neurlogis

• Location of perdaran close to the

surface of the cortex

• The location in the non-dominant hemisphere.

Hematoma small and does not give effect

period ( midlineshift <

0.5 cm), also does not provide clinical symptoms.

Injury diffusely scattered

- Treatment in the room

- Observation GCS, pupil, lateralization, and

physiology vital.

- Optimization of stabilization vital physiology,

maintain solid supply of O 2 to the brain.

- Circulation: impartial liquid NaCl-glucose

3 Non-operative infusion, prevented the occurrence of

overhydration, when it stabilized gradually

replace fluids / EN / pipe stomach.

- Haemorrhagic stroke patients with lesions

that do not require the evacuation and

patients with impaired blood gas analysis

was treated in a respirator.

- Maintain cerebral perfusion, head of

the head-up position about 30 •• to

avoid neck flexion.

- Bladder catheter is required to record the

production of urine, prevent urinary

retention, preventing the bed was wet (thus

reducing the risk of pressure sores).

- Hypertonic fluids (mannitol 20%), when

looked edema or injury that is not operable

on CT Scan. Mannitol can be administered

as a bolus of 0.5 to 1 g / kg. BB in certain

circumstances, or repeated small doses, for

example, (4-6) x 100 cc of mannitol 20% in

24 hours. Gradual discontinuation.

- Analgesic, anti-inflammatory, antipiretika:

mefenamic acid, paracetamol 500 mg 3-4

times daily or Na diklofenac 2-3 times daily

or 50 mg in adults.

- Antisida and or antagonists H 2

- Antiepileptikum







10. Prognosis Prognosis is affected:

- Age (<50 years)

- initial GCS

- The distance between the incident and surgery

- cerebral edema

- location hematoma

- factors extracranial

11. reviewers were critical

1. Prof. Dr. Abdul Hafid Bajamal, dr.,

Sp.BS











12. Irwan Barlian Immadoel Haq, dr,

Sp.BS



12. Medical Indicators Improvement of neurological

status.

13. Bibliography 1. Rordorf, G, McDonald, C. 2013.Spontaneous Intracerebral Hemorrhage: Pathogenesis, Clinical Features, and

Diagnosis. Wolters Kluwe.

2. Rordorf, G, McDonald, C. 2014.Spontaneous Intracerebral Hemorrhage: Treatment and Prognosis.

Wolters Kluwe

3. Ohwaki K, Yano E, Nagashima H, Hirata M, Nakagomi T, Tamura A. Blood pressure

management in acute intracerebral hemorrhage: relationship between elevated blood pressure

and hematoma enlargement. Stroke. 2004; 35 (6): 1364.

4. Alberico RA, Patel M, Casey S, Jacobs B, Maguire W, Decker. Evaluation of the circle of Willis with

three-dimensional CT angiography in Patients with suspected intracranial aneurysms. AJNR Am J Neuroradiol.

1995; 16 (8): 1571.

5. GK Wong, Siu DY, Abrigo JM, Poon WS, Tsang FC, XL Zhu, Yu SC, Ahuja AT. Computed

tomographic angiography and Venography for young or nonhypertensive Patients with acute

spontaneous intracerebral hemorrhage. Stroke. 2011; 42 (1): 211.

6. Fiebach JB, Schellinger PD, Gass A, Kucinski T, Siebler M, Villringer A, Olkers P, Hirsch JG, Heiland

S, Wilde P, Jansen O, Rother J, Hacke W, Sartor K, Kompetenznetzwerk Schlaganfall B5Stroke

magnetic resonance imaging is accurate in hyperacute intracerebral hemorrhage: a multicenter study on

the validity of stroke imaging. Stroke. 2004; 35 (2): 502

7. Morgenstern LB, JC 3rd Hemphill, Anderson C, Becker K, Broderick JP, Connolly ES Jr, Greenberg SM,

Huang JN, MacDonald RL, MesséSR, Mitchell PH, Selim M, Tamargo RJ, the American Heart

Association Stroke Council and the Council on cardiovascular Nursing. Stroke. 2010; 41 (9): 2108

8. Broderick J, Connolly S, Feldmann E, Hanley D, Kase C, Krieger D, Mayberg M, L Morgenstern,

Ogilvy CS, Vespa P, Zuccarello M, American Heart Association, American Stroke Association Stroke

Council, High Blood Pressure Research Council Quality of Care and Outcomes in Research

Interdisciplinary Working Group. Guidelines for the management of spontaneous intracerebral

hemorrhage in adults: 2007 update: a guideline from the American Heart Association / American

Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care

and Outcomes in Research Interdisciplinary Working Group.Stroke. 2007; 38 (6): 2001

9. Cloft HJ, Joseph GJ, Dion JE. Risk of cerebral angiography in Patients with subarachnoid hemorrhage, cerebral aneurysm, and arteriovenous malformation: a meta-analysis. Stroke

1999; 30: 317.

http://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-aneurysmal-subarachnoid-hemorrhage/abstract/49



STROKE infarction ICD-10: I63.0

1. Definition

Focal neurological deficits caused by a blockage in the blood vessels of the brain.

(Definition)

2. History Focal neurological deficit

Asymmetrical face, loss of speech, paralyzed half of the body. Old

occurrence Fainting Headache Seizures Decreased consciousness

Alloanamnesis when an unconscious patient

medication history

History DM pain, heart disease, epilepsy, certain drugs

3. PemeriksaanFisikk PemeriksaanFisikUmum

• Pemeriksaanfisikpertama times diutamakanpadaevaluasi

• A ( airways) prevent the tongue falling menghalangai airway. stridor ?,

• B ( breathing), evaluation of normal breath sounds. There ronkhi, whezing, signs of effusion

• C ( circulation) blood pressure, pulse rate content, regularity, perfusion to peripheral tissues. Evaluation

of additional sound heart.

• The skin should be evaluated to determine if there are signs that lead to endocarditis, cholesterol

embolism, ecchymosis purpura, or signs of action for invasive procedures

PemeriksaanNeurologis


• Nerves II-III,

• Especially cranial nerves VII nerve lesions of peripheral / central

• Fundoskopi look for signs of edema pupil, retinal detachment

• Motor and sensory, bandingkankanandankiri, lower atasdan whether there Hempiparesis

• Autonomis

4. Criteria for Diagnosis Focal neurologic deficits

The discovery of the ischemic area / infarction on CT scan and / or MRI

5. Work Diagnosis Stroke infarction (I63.0)

6. Diagnosis hypoglycemia

Hyperglycemia

7. Investigations • Are required to do a CT scan and / or MRI in all patients with either acute ischemic

stroke or hemoragic

• CTA / MRA

• DSA


No. Examination

Reko

Ref

mend

care

In hyperakut phase CT scan can be used to exclude a

bleeding stroke. The sensitivity of the non-contrast CT in

1 CT scan- CTA- CT stroke infarction increased after 24 hours of onset of the 2A 6

perfusion attack.

MRI sequences T1 and T2 DWI, PWI, GRE can

2 MRI diagnose acute ischemic stroke. DWI superior in

1B 7

diagnosing acute ischemic stroke within 12 hours of

onset

MRA for detecting vascular stenosis or

2B 8

3 MR Angiography occlusion.

• Also conducted inspection • Complete blood • GDA • BGA • SE • BUN / SK • ECG

• cardiac enzymes • FH and INR • LFT

• toxicology screening • Unexpected pregnancy test in women hami • Thorax photo • EEG

8. Therapy 1. If the patient has no risk to occur peningktan ICT, aspiration, or a suspicious

condition suggested Kardipulmonary flat head 0-15 degrees

2. In patients with suspected signs of increased ICP, decreased kesadran,

aspirations, decompensation cordis, or desatuari it is advisable head up 30

degrees.


Reko


ation

1. Suggested alteplase intravenously at onset

less than 3 hours (Grade 1B), Anti-thrombotic

(eg aspirin) may be administered within 48

hours of onset of the case (Grade 1A)

2. The second attack prevention of stroke in

1 rtPA patients with a history of stroke or TIA

1A 9

noncardioembolic, lacunar infarction

recommended use

antiplatelet drug clopidogrel (Grade 1)

3. The use of aspirin in patients with GIT

bleeding recommended 50100 mg / day

for prevention

second stroke (Grade 1B)

4. Not recommended use

the combination of aspirin and clopidogrel in patients

with stroke or TIA noncardioembolik (Grade 1A)

The provision of anti-hypertensive medication given at

systole> 220 or diastolic> 120 atauterdapat indication is

unclear (CHD, heart failure, aortic dissection, hypertensive

2 OAH encephalopathy, GGA, or pre-eclampsia / eclampsia). 1C 10

Target blood pressure reduction is 15% of the initial tension

3 Endovasculer

Mechanical thrombectomy procedure with 1A 11

stent retriever (solitaire, etc.)

3. Antipyretic also recommended be administered to patients fever usually occurs in the

acute phase of ischemic stroke

4.

Prevention of the occurrence of complications therapy

- IMA

- Heart failure

- disfagi

- aspiration Pneumonia

- UTI

- DVT

- malnutrition

- Dehidarsi

- decubitus ulcers

- contractures

Initiation of antithrombotic drugs regularly take

9. Education nonsteroidal anti lipid

Once the acute phase has passed can begin management decrease blood terkanan Lifestyle

changes Exercise, not smoking, healthy diet

10. Prognosis Konsis patients who are good with adequate treatment at the onset of less than 4 hours gave a

good prognosis.


2. Dr. Agus Turchan, dr.,

Sp.BS




6. Dr. Asra Al Fauzi, dr.,

Sp.BS


8. Muhammad Faris, dr.,

Sp.BS







12. Medical Indicators Repair common neurological status / focal

13. Bibliography 1. Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early management of Patients with acute

ischemic stroke: a guideline for healthcare professionals from the American Heart Association / American

Stroke Association. Stroke 2013; 44: 870.

2. Adams HP Jr, del Zoppo G, Alberts MJ, et al. Guidelines for the early management of adults with

ischemic stroke: a guideline from the American Heart Association / American Stroke Association

Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and

the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research

Interdisciplinary Working Groups: the American Academy of Neurology affirms the value of this

guideline as an educational tool for neurologists. Stroke 2007; 38: 1655.

3. The National Institute for Health and Clinical Excellence. Stroke: The diagnosis and acute

management of stroke and transient ischemic attacks. Royal College of Physicians, London, 2008.

http://www.nice.org.uk/CG068 (Accessed on February 01, 2011).

4. Burns JD, Green DM, Metivier K, DeFusco C. Intensive care management of acute ischemic stroke.

Emerg Med Clin North Am 2012; 30: 713

5. Lansberg MG, MJ O'Donnell, Khatri P, Lang ES, Nguyen-Huynh MN, NE Schwartz, Sonnenberg FA,

Schulman S, Vandvik PO, Spencer FA, Alonso-Coello P, Guyatt GH, Akl EA, the American College of

Chest Physicians. Antithrombotic and thrombolytic therapy for ischemic stroke: antithrombotic Therapy

and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical

Practice Guidelines. Chest. 2012; 141 (2 Suppl): e601S.

6. Wardlaw JM, Seymour J, J Cairns, Keir S, Lewis S, Sandercock P. Immediate computed

tomography scanning of acute stroke is cost-effective and improves quality of life. Stroke 2004;

35 (11): 2477.

7. Schellinger PD, Bryan RN, Caplan LR, Detre JA, Edelman RR, Jaigobin C, Kidwell CS, Mohr JP,

Sloan M, Sorensen AG, Warach S, Therapeutics and Technology Assessment Subcommittee of the

American Academy of Neurology Evidence-based guidelines : The role of diffusion and perfusion

MRI for the diagnosis of acute ischemic stroke: report of the Therapeutics and Technology

Assessment Subcommittee of the American Academy of Neurology.

8. Latchaw RE, Alberts MJ, Lev MH, JJ Connors, Harbaugh RE, Higashida RT, R Hobson, Kidwell CS,

Koroshetz WJ, Mathews V, Villablanca P, Warach S, Walters B, the American Heart Association

Council on Cardiovascular Radiology and Intervention stroke Council, and the Interdisciplinary

Council on Peripheral Vascular Disease Recommendations for imaging of acute ischemic stroke: a

scientific statement from the American Heart Association. Stroke. 2009; 40 (11): 364

9. Lansberg MG, MJ O'Donnell, Khatri P, Lang ES, Nguyen-Huynh MN, NE Schwartz, Sonnenberg FA,

Schulman S, Vandvik PO, Spencer FA, Alonso-Coello P, Guyatt GH, Ak. Antithrombotic and

thrombolytic therapy for ischemic stroke: antithrombotic Therapy and Prevention of Thrombosis,

9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines Chest.

2012; 141 (2 Suppl): e601S

10. Jauch EC, Saver JL, Adams HP Jr, Bruno A, JJ Connors, Demaerschalk BM, Khatri P,

PW McMullan Jr., Qureshi AI, Rosenfield K, Scott PA, Summers DR, Wang DZ, Wintermark M,

Yonas H, the American Heart Association Stroke Council, Council on Cardiovascular Nursing,

Council on Peripheral Vascular Disease, Council on Clinical Cardiology. Guidelines for the early

management of Patients with acute ischemic stroke: a guideline for healthcare professionals from the

American Heart Association / American Stroke Association.Stroke. 2013; 44 (3): 870.

11. Saver JL et al. Stent-Retriever thrombectomy after intravenous t-PA vs. t-PA

Alone in Stroke. N Engl J Med 2015; 372: 2285-2295

Dural arteriovenous fistula

ICD-10: I67.1

1. Definition Dural arteriovenous fistula (DAVf) is a pathological condition which found their fistulae (relations) between the

(Definition) branches of the dural arteries with veins or the dural venous sinuses

2. History - Patients with DAVf may have no symptoms at all

- Symptoms in patients DAVf fistula usually occurs depending on the location can be: vision disturbances,

ophtlamoplegi, diplopia, atupun bleeding.

- Patients may experience symptoms of hearing voices bruit, tinnitus, diplopia, proptosis up with severe

symptoms are neurological deficits



• Physical examination was first priority in the evaluation of A ( airways), B

(Breathing), and C (

circulation)

• Auscultation of the orbit, lateral orbital, supra-orbital, mastoid, and other areas in accordance

sinus venosus



• meningeal sign

• Motor and sensory, compare the right and left, up and down

• Autonomis

4. Criteria for Diagnosis 1. The history and clinical examination (as per above)

2. Investigations (according to the above)

5. Work Diagnosis Dural arteriovenous fistula I67.1

6. Diagnosis - dural AVM

- Intracranial tumors

7. Investigations No. Examination Information Grade of References

Recommendat

ion

1. CT Scan Head Nonkontras head CT scan 1A 1,2,3,4

should be performed before an

invasive examination to rule

out the presence of bleeding

2. CTA CT angiography is 1A 1,2,3,4

necessary to know the

anatomy of intracranial

pembuluhdarah

3. MRI DAVf MRI showed cortical 1B 1,2,3,4

venous dilation in the

absence

parenchymal nidus,

in addition to the MRI

also showed

thickening of the dura layer,

parenkimal arterial hypertrophy,

dilation of the vein, turtous veins,

venous thrombosis

4 Angiography (Trans-Femoral Angiography is the gold 1A 1,2,3,4

Cerebral angiography) standard for DVAf.

Angiography is for

identification purpose

arterial feeders, locations

fistula, and the pattern and

direction of venous drainage

8. Therapy No. Therapy Information Grade of References

Recommendat

ion

1. endovascular Therapy endovaskuler on 1A 1,2,3,4

DAVf is the first line, it can

be through some

kind

method well

transarterial, transvenous or

combination

use:

- embolization particles

-

Injection glue ( n-

buthylcyanoacrylate or

Ethylenvenyl

Alcohol / EVOH) through a

vein or artery s

- coiling through venou

s

to close the fistula ( packing

transvenous)

- Carotid artery stenting

2. Operation Operations carried out in 1A 1,2,3,4

(surgery) some cases, such as the

fossa skull anterior DAVf

3. Radiation therapy Radiation therapy is done by 2B 1,2,3,4

sterotaktik, and usually most

effective when combined

with endovascular or surgery

is not optimal.







10. Prognosis Prognosis is influenced by the degree of symptoms and the degree of neurological

dysfunction

11. Medical Indicators Repair and improvement of clinical status radiology















15. Bibliography 1. Van Dijk JM, terBrugge KG, Willinsky RA, Wallace MC. Clinical Course of Cranial

Dural arteriovenous fistulas With Long-Term persitent Cortical Venous Reflux.

Stroke 2002; 33: 1233-1236

2. Borden JA, Wu JK, Shucart WA. A proposed classification for spinal and cranial

dural arteriovenous fistulous malformations and implications for treatment.

1995. J Neurosurg; 82 (2): 166-79.

3. Lawton MT, Chun J, Wilson CB, Halbach VV. Ethmoidal dural arteriovenous

fistulae: An assessment of surgical and endovascular management.

Neurosurgery. 1999; 45: 805-11. 4. awaguchi S, Sakaki T, Morimoto T, Hoshida T, Nakase H. Surgery for dural

arteriovenous fistula in the superior sagittal sinus and transverse sinus. J Clin Neurosci. 2000; 7: 47-9

5. Ito J, Imamura H, Kobayashi K, Tsuchida T, Sato S. Dural arteriovenous malformations of the base

of the anterior cranial fossa. Neuroradiology. 1983; 24: 149-54.

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