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24 Januari 2009

Peripheral Vascular Disease

A non-invasive perspective

AZHARI GANI

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Peripheral artery disease and cerebrovasculardisease are artherosclerotic disease involving

the the vascular tree of the particular organs Majority are asymptomatic Prevalence are increasing:

Ageing population

Co morbidities cigarette, DM, HPT,

Hyperlipidemia

Better screening

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Claudication intermittent is a sensation of aching,burning, heaviness, or tightness in the muscles of thelegs that usually begins after walking a certaindistance, walking up a hill, or climbing stairs, and goes

away after resting for a few minutes. Buttock, thigh, or calf pain with exertion

(claudication) No symptomsdiagnosed by abnormal ABI test

Erectile dysfunction Uncommon Pain in legs and feet at rest Sore (ulcer) on leg that does not heal Arm pain with exertion (PAD of arms) Different blood pressures in the right and left arms

of more than 15 points (PAD of arms)

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painful joints (arthritis),

tingling or a pinsand- needles sensation(neuropathy),

pain running down the back of the thighs

due to arthritis of the spine (sciatica orspinal stenosis).

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PVD prevalence 16% in men > 60 years20% in men > 80 years

13% in women > 60 years

Incidence of 3 vessel higher in patients withPVD (63%) than those without PVD (11%)

Schroll M, J Chr Dis 1981

Sukhija R, Am J Cardiol 2003

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Persons with PVD at increased risk for allcause mortality (RR 3.1), cardiovascular

mortality (RR 5.9) and cardiovascular events.

Marked reduction in QOL, similar to CCF andother chronic diseases

Criqui MH, NEJM 1992

Jaff M, PCR 2003

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PVD is a notably underdiagnosed andundertreated health condition. Offering a

screening program is an excellent approachfor providing services. PVD screeningprograms can tap new patient markets,increase referrals and ultimately boost directand indirect revenue

Medicare contribution margin is 30% forPVD, comparable to cardiac services

Vesey J, Health Care Strategic Mx 2003

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Supraaortic arteries carotids, vertebral,subclavian

Renal arteries Aorta abdominal and thoracic Lower limbs iliacs, femoral, infrageniculate Others areas

Intracranial

Penile

Coeliac, mesenteric

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Duplex USG is one of the most importanttechniques in evaluating PVD

Combination of B mode, colour and pulsedDoppler is the way- accurate and simple

Sensitivity and specificity of close to > 95% Newer tissue Doppler, harmonic imaging,

contrast enhancement and 3D imaging yet toplay role in daily practice CT and MRI has a role but impractical for

screening

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More than 80% of ischaemic events are dueto arteriosclerosis affecting the extracranialarteries, mostly at the bifurcation/prox ICA

Duplex examination most important Most vascular surgeons rely on USG alone

prior to CEA

Carotid artery stenting still limited tosymptomatic patients with >50% stenosisand asymptomatic with >80% stenosis withhigh risk

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Diagnosis of arterial occlusion usually made onbasis of history and physical examination

ABI plays a major role in screening Duplex scanning of arteries can identify specific

segment for study with high accuracy Image however less accessible in the deeper

vessels, pelvic area, adductor canal and

infrageniculate arteries. Lower sensitivity for detecting second order

stenosis, or stenosis distal to severe occlusions

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Meluzin et al Eur J Echo 2003

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Simple test to screen for arterial occlusion ABI : ratio of the leg pressure to the arm

pressure (ankle blood pressure divided by armblood pressure)

ABI > 0.9 normal0.7-0.89 mild disease0.41-0.69 moderate< 0.4 severe

Unreliable in calcified vessels, diabetics. Segmental blood pressure recordings might be

measured to further pinpoint area of occlusion Plethysmography and exercise component may

be added

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USG proves to be useful in terms of safety,low cost and high sensitivity

Several Doppler criteria from few groups:e.g. Renal aorta ratio > 3.5 signifies 60-99%stenosis, velocity >180cm/s

Neumeyer M, Hershey Med Dept

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Colour and CW Doppler from inflow, graftand outflow artery

Doppler signals are triphasic and changes to

biphasic can be significant Graft velocity of < 45 cm/s signifies a

potential graft failure Peak stenotic and prestenotic systolic

velocities will estimate narrowing : 2:1 ratio : >50% 4:1 ratio : >75%

> 400cm/s : > 75%

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Venous Thrombo-embolisms (VTE) isserious medical problem

Prevalence of VTE is high VTE usually undiagnosed Many physicians still unrecognized VTE Heart failure is one of the high risk for

VTE The best treatment VTE is prophylaxis

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1Cohen AT. Presented at the 5th Annual Congress of the European Federation of Internal Medicine; 2005.2Eurostat statistics on health and safety 2001. Available from: http://epp.eurostat.cec.eu.int.

Deaths caused of VTE: 543,4541

Exceed combined deaths due to:

AIDS 5,8602

breast cancer 86,8312

prostate cancer 63,6362

transport accidents 53,5992

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Within 5 years of DVT, 80% of patients

developed become Post Phlebotic Syndrome

(varicose veins, ulceration veins)

30-70% of patients with DVT (VTE) have

Asymptomatic Pulmonal Embolisms

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GRIP- VTE SURVEY

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1Geerts WH, et al. Chest. 2004;126:338S-400S.2Leizorovicz A, et al. Circulation. 2004;110(24 Suppl 1):IV13-9. (%)

17

20

50

50

0 10 20 30 40 50 60

Internal medicine

General surgery

Acute ischemic stroke

Orthopedic surgery

Prevalence of VTE is High

DVT prevalence in stroke patients is one of the highest inhospitalized patients (no prophylaxis)

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70% of deaths due to PEoccur in medical patients

In 5,000 autopsies, VTEwas discovered in 43%of patients

PE causes 10% of hospital

deaths

70%

Medical30%

Surgical

Inpatient VTE, %

Adapted from: Diebold J, Lohrs U. Pathol Res Pract. 1991;187:260-266.

5,039 Hospitalized Patients

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VTE mostly Undiagnosed

Less than half of all casesoffatal PE are detected

prior to death 1

Approximately 80% of DVT

are clinically silent 2,3

1. Goldhaber SZ, et al. American Journal of Medicine1982;73:822-826.

2. Lethen H, et al. American Journal of Cardiology1997;80:1066-1069.

3. Sandler DA, et al. J. Royal Soc. Med.1989; 82:203-205.

20 %

Often goes undetected until

too late

80 %

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General medical patients 10-26% [Cade 1982, Belch et al., 1981]

Stroke 11- 75% [Nicolaides et al.,1997]

Myocardial infarction (MI) 17-34% [Nicolaides et al., 1997]

Spinal cord injury 6 -100% [Nicolaides et al. , 1997]

Congestive heart failure 20- 40% (Anderson et al., 1950]

Medical intensive care 25- 42% [Cade, 1982, Dekker et al., 1991,

Hirsh et al., 1995]

The Acute illness Hospitalized medical Patients

frequency of VTE in the absence of prophylaxis

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MECHANISME VTEIN HEART FAILURE

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Venous stasis(Immobilization)

Vascular lesion (surgical,trauma, inflammation)

Hypercoagulability.(Deficiency of Protein C,

Protein S, AT III)

Rudolf Ludwig Karl Virchow (1821-1902)"Father of Pathology

Thrombogenesis

http://upload.wikimedia.org/wikipedia/commons/8/80/Rudolf_Virchow.jpg

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Chest 2002;122;1440-1456

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Lopez, J. A. et al. Hematology 2004;2004:439-456

Model for venous thrombosis

Endothelial activation

Stasis (eg., RVF)-infection (TNF-)

(Vessel injury)

Monocytes stimulation toproduce TF

-Cancer

-IBD

-infection (TNF-)

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Venous thrombosis:

Stasis leads to the development of a

thrombus composed of red cells and fibrin

Slow, turbulent blood flow in valve cusps

result in areas of local stasis

Prandoni P, et al.Haematologica1997; 82:423428.

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Venous thrombosis:

Deep vein thrombosis

Thrombus growth results inproximal progression along the

vein

Pulmonary embolism

Damage to veins (PTS)

Prandoni P, et al.Haematologica1997; 82:423428.

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Symptoms : pain, redness and swelling of the leg, usually unilateral

Within 5 years of DVT, 80% of patients develop post phlebitic syndrome, which manifestin chronic leg discomfort and swelling, varicose veins, skin discoloration and ulceration insevere cases.

DOPPLER USG, VENOGRAPHY

REMEMBER : 80-90% DVT ARE ASYMPTOMATIC (CLINACALLY SILENT)

MANY PHYSICIANS UNREGCONIZED VTE

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P U L M O N A R Y E M B O L I S M S

A S Y M P T O M A T I C

80-90% 10-20%V T E

C H F

V T E

S Y M P T O M A T I C

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Practice guidelines

ACCP 2008

- LDUH* or LMWH recommended in general

medical patients with clinical risk factors for VTE

(including cancer, bed rest, CHF, severe

lung disease) (Grade 1A)

International Consensus Statement 2001

- LMWH OD recommended for hospitalized patients

with chronic respiratory disease or CHF (Grade A)

*LDUH: UFH 5,000 U SC BID or TID

1. Albers GW, et al. Chest. 2008;133:71-109

2. Nicolaides AN. Int Angiol, 2001; 20: 1-37

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PRIME1 86% UFH 5000 IU tid

Enoxaparin 40 mg od

THE-PRINCE2 19% UFH 5000 IU tid

Enoxaparin 40 mg od

Hillbom, et al3 43% UFH 5000 IU tid

Enoxaparin 40 mg od

1.4

0.2

Trial RRR Thromboprophylaxis Patients with VTE (%)

10.4

8.4

34.7

19.7

1Lechler E, et al. Haemostasis. 1996;26 Suppl 2:49-56.2

Kleber FX, et al.Am Heart J. 2003;145:614-21.3Hillbom M, et al.Acta Neurol Scand. 2002;106:84-92.

P< 0.001 for

equivalence

P= 0.015 forequivalence

P= 0.044

LMWH vs UFH

tid = three times daily.

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Safety end point

Enoxaparin UFH Fisher's exact(n= 332), (n= 333), test (2-tailed)

n (%) n (%) P value

Patients with bleeding complications 5 (1.5) 12 (3.6) NS

With minor bleeding 4 (1.2) 11 (3.3) NS

With major bleeding 1 (0.3) 1 (0.3) NS

Patients with injection site hematoma* 24 (7.2) 42 (12.6) 0.02686

Death 9 (2.7) 15 (4.5) NS

Patients with Aes 152 (45.8) 179 (53.8) 0.04382

With possible/ probable drug relation 7 (2.1) 30 (9.0) 0.00013

With withdrawal due to Aes 12 (3.6) 24 (7.2) NS

Patients with raised levels of ALAT 75 (22.6) 111 (33.3) 0.00245

Patients with raised levels of ASAT 46 (13.9) 70 (21.0) 0.01851

Aes = adverse event; ALAT=Alanine aminotransferase; ASAT= aspartate aminotransferase*>5 cm diameter at injection site

CONSENSUS RECOMMENDATIONS IN

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CONSENSUS RECOMMENDATIONS IN

ACUTE HEART FAILURE

Consensus body

Subcutaneous UFH

LMWH+

Recommendationgrade**

ACCP Consensus Statement5

Recommendation

1 A

International Union

of Angiology*

Subcutaneous UFHHigh dose LMWH+

A

*Recommendations are for medical patients with disease-related and/or additional

patient-related risk factors+Enoxaparin (40 mg once-daily) is the only low molecular weight heparin licensed

for the prevention of venous thromboembolism in hospitalised, acutely ill patients

with heart failure NYHA Class III/IV

**Grade of recommendation based on scientifically sound clinical trials in which the

results are clear cut

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100 100 100

53

68

3441

4540

22 25

13

0

20

40

60

80

100

120

Acute heart

failure

Acute non-

infectious

respiratory

disease

Respiratory

infection

Infection

(non-

respiratory)

Ischaemic

stroke

Active

Malignancy

At risk of VTE At risk of VTE and receiving ACCP prophylaxis

VTE risk and ACCP prophylaxis use in medical patientswith 6 key diagnoses

Medicalpatients

(%)

Bergmann J-F, et al. XXIII World Congress of the IUA. June 2008;Athens, Greece.

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Non invasive service in PVD is essential in

screening and ensuring the livelihood of the

peripheral intervention team

Adequate training of personnel is available andaccredited

Good relationship with the vascular surgeons,

interventional radiologists, cardiologist to ensure

a healthy practice which benefits the patient Patients immobilized with critically ill condition

including congestive heart failure (30%) are at

risk of venous thrombo-embolism.