Overview Penyakit Pembuluh Darah Perifer

Outline

Penyakit Arteri Perifer

 Claudicatio Intermiten
 Chronic Limb Ischemia
 Acute Limb Ischemia
 Buerger Disease
 Raynaud
Penyakit Vena Perifer
 Trombosis Vena Dalam

PENYAKIT ARTERI PERIFER

Peripheral artery occlusive disease or

peripheral arterial disease or peripheral vascular disease
refers to the obstruction or deterioration of arteries other
than those supplying the heart and within the brain.

Patients at Increased Risk of PAD (Table 3)

 Age ≥65 y
 Age 50–64 y, with risk factors for atherosclerosis (e.g.,
diabetes mellitus, history of smoking, hyperlipidemia,
hypertension) or family history of PAD
 Age <50 y, with diabetes mellitus and 1 additional risk factor
for atherosclerosis
 Individuals with known atherosclerotic disease in another
vascular bed (e.g., coronary, carotid, subclavian, renal,
mesenteric artery stenosis, or AAA)

EVALUATION

 History and physical examination

  Testing and Imaging
 Treatment

Characterizing the pain divides PVD into

 Chronic arterial insufficiency

 Acute arterial occlusion

Chronic Arterial Insufficiency

 Asymptomatic to gangrenous tissue loss

 Intermittent claudication: most common presentation

Features of chronic lower limb arterial stenosis or occlusion

 Intermittent claudication
 Rest pain
 Dependent rubor
 Ulceration
 Gangrene
 Arterial pulsation diminished or absent
 Arterial bruit
 Slow capillary refilling

Claudicatio intermittent

• Cramp-like pain felt in the muscles that is:

 brought on by walking;
 not present on taking the first step (unlike
osteoarthritis);
 relieved by standing still (unlike nerve compression from
a lumbar intervertebral disc prolapse or osteoarthritis of
the spine or spinal stenosis)

Clinical Classification of Claudicatio intermiten;

Critical limb ischaemia (CLI)

• Most severe form of PVD

• Acute or chronic presentation

• Chronic CLI is defined as >2 weeks of rest pain, ulcer

or tissue loss and characterized by
 Ankle–brachial index ≤ 0.4
 Ankle systolic pressure ≤ 50 mmHg
 Toe systolic pressure ≤ 30 mmHg

Work up
• Lab tests
• Physiological tests like ankle brachial index
• Imaging :
-Doppler ultrasonography -Duplex ultrasonography
-Angiography -CT angiography
-MR angiography
 Diagnostic Testing for
Suspected PAD

History and physical examination

suggestive of PAD without rest pain, Suspect CLI
nonhealing wound, or gangrene (Figure 2)
(Table 4)

ABI with or without

segmental limb pressures
and waveforms
(Class I)

Noncompressible
Noncompressible arteries
arteries Normal
Normal ABI:
ABI: 1.00–1.40
1.00–1.40 Abnormal
Abnormal ABI:
ABI:
ABI:
ABI: >1.40
>1.40 Borderline
Borderline ABI:
ABI: 0.91–0.99
0.91–0.99 ≤0.90
≤0.90

TBI Exertional
Exertional non–joint
non–joint
(Class I) related
related leg
leg symptoms
symptoms
Exercise ABI
Normal Abnormal (Class IIa)
Yes No
(>0.70) (≤0.70)
Exercise ABI
(Class I) Search for
alternative
Abnormal Normal
diagnosis
Search for (Table 5)
Lifestyle-limiting claudication
alternative
despite GDMT,
diagnosis
revascularization considered
(Table 5)

Continue GDMT Do not perform invasive

Yes No
(Class I) or noninvasive anatomic
Options assessments for
Diagnostic Testing for asymptomatic patients
Anatomic assessment: Suspected CLI (Class III: Harm)
Anatomic assessment:
 Duplex ultrasound
 Invasive angiography
 CTA or MRA
(Class IIa)History and physical examination
(Class I)
suggestive of PAD with rest pain,
Colors correspond
nonhealingto Classorofgangrene
wound, Recommendation in Table 1.
(Table 4)
ABI indicates ankle-brachial index; CLI, critical limb ischemia; CTA,
computed tomography angiography;
Yes No
Search GDMT, guideline-directed
for alternative diagnosis
management and therapy; MRA, magnetic (Tablesresonance
5 and 6) angiography;
PAD, peripheralABI
artery disease; and TBI, toe-brachial index.
(Class I)

Non-compressible
Non-compressible arteries
arteries Normal
Normal ABI:
ABI: 1.00–1.40
1.00–1.40
ABI:
Abnormal ABI: ≤0.90
Abnormal ABI: ≤0.90
ABI: >1.40
>1.40 Borderline
Borderline ABI:
ABI: 0.91–0.99
0.91–0.99
Colors correspond to Class of Recommendation in Table 1.

*Order based on expert consensus.

†TBI with waveforms, if not already performed.
ABI indicates ankle-brachial index; CLI, critical limb ischemia; CTA, computed
tomography angiography; MRA, magnetic resonance angiography; TcPO 2,
transcutaneous oxygen pressure; and TBI, toe-brachial index.

Ankle Brachial Index (ABI)

Manajemen

 Antiplatelet : Aspirin/Clopidogrel (IA)

 Statin (IA)
 Antihypertensive (IA)
 Smoking cessation (IA)
 Glycemic control (IA)
 Cilostazol (IA)
 Acute limb ischemia

Etiology of acute limb ischemia

 Acute arterial embolism:

Of a relatively health arterial tree

 Acute arterial thrombosis:

Of a previously diseased arterial tree

 Acute traumatic ischemia:

 Example of acute arterial embolus

“Saddle” Embolus of right iliac

artery
 Diagnosis and Management
of ALI

Acutely cold, painful leg

Suspected ALI

Clinical evaluation, including: symptoms,

motor and sensory assessment, arterial
and venous Doppler signals
(Class I)

Audible arterial Inaudible arterial Inaudible arterial

Audible venous Audible venous Inaudible venous

Revascularization (urgent) Category I: Category III:

AND Viable limb Motor function Irreversible Primary
anticoagulation, Normal motor function assessment Complete loss of motor function amputation
unless contraindicated No sensory loss Complete sensory loss (Class I)
(Class I) Intact capillary refill Absent capillary refill

Intact Impaired

Category IIa: Category IIb:

Marginally threatened Immediately threatened
Slow-to-intact capillary refill Slow-to-absent capillary refill
Sensory loss limited to toes if present Sensory loss more than toes and with rest pain
No muscle weakness Mild or moderate muscle weakness

Salvageable if Salvageable if
treated promptly treated emergently

Revascularization (emergency) Revascularization (emergency)

AND AND
Anticoagulation, unless contraindicated Anticoagulation, unless contraindicated
(Class I) (Class I)

Colors correspond to Class of Recommendation in Table 1.

ALI indicates acute limb ischemia.

Embolism Trombosis
 obvious cardiac source § No obvious cardiac source
 No hx of cluadication § Abnormal pulses in contralateral limb
 Normal pulses in § Angiogram : diffuse atherosclerotic
contralateral limb § Well developed collateral
Angiogram: minimal
atherosclerotic Few
collateral
 Thromboangiitis Obliterans (Buerger’s Disease)

§ Adalah vaskulitis (proses inflamasi & trombotik)

mempengaruhi pembuluh darah perifer (arteri & vena),
terutama sekali di ekstremitas

§ Penyebabnya tidak diketahui namun hampir selalu

ditemukan pada laki - laki usia kurang dari 40 tahun &
perokok berat

• Non-atherosclerotic vascular disease characterized by :

• absence or minimal presence of atheromas,

• segmental recurring and progressive vascular inflammation,
• vasoocclusive phenomenon and
• thrombosis of small and medium arteries and veins of hands
and feet.
• Lack of unanimous diagnostic criteria: is a disease of exclusion
 OLIN Diagnosis Criteria

• Age younger than 45 years

• Current or recent history of tobacco use
• Presence of distal extremity ischemia (indicated by
claudication, rest pain, ischemic ulcers, gangrene)
documented by non invasive vascular testing
• Exclusion of autoimmune dis, hypercoagulable states and
diabetes
• Exclusion of proximal source of emboli by ECHO and
arteriography
• Consistent arteriographic findings in the clinically involved and
non
• involved limbs

Color duplex ultrasonography in TAO

• Occlusion of distal calf orpedal arteries
• Occlusion of forearm, palmar arch ordigital arteries
• Normal appearing arteries proximal tolesion
• Serpigineous or corkscrew collaterals atthe site of occlusion
• Intact vesselwall in the level ofthrombotic occlusion often
free of calcification
 Treatment of Buerger’s disease

• Tobacco cessation : Only proven preventing guideline

• Explanation advice
• Drugs
• Surgery

Explanation advice

• Adjustment of lifestyle Exercise and diet

• Care of feet Heel raise
• Analgesics and position

Drugs
• Prostaglandins: prostacyclin or PGI2 (iloprost) 40 times
antiplatelet and vasodilator effect as compared to PGE1
• Intra-arterial thrombolytic therapy
• Intra-arterial streptokinase (bolus 10,000 U f/b 5000 units
per hour
• Trental (pentoxyfiline)
• Praxiline: niftidrofuryl oxalate
• Aspirin

Direct arterial surgery

• Revascularization surgery rarely feasible
• Arterialization of veins by creating AV fistula
between artery proximal to site of block and
adjacent vein
 Raynaud’s phenomenon
• Excessively reduced blood flow in response to cold or
emotional stress, causing discoloration of the fingers, toes,
and occasionally other areas
• Raynaud's disease (also known as primary Raynaud's
phenomenon), where the cause is unknown
• Raynaud's syndrome (secondary Raynaud's phenomenon),
caused by a known primary disease, most commonly
connective tissue disorders such as SLE, Sjogrens disease,
Rheumatoid arthritis, Multiple sclerosis
• Hyperactivation of sympathetic nervous system causing
extreme vasoconstriction of the peripheral blood vessels,
leading to tissue hypoxia

Clinical Manifestations

• Usually bilateral –(both arms or feet are affected)

• Pallor, coldness, numbness, cutaneous cyanosis and pain
• With longstanding or prolonged Raynaud’s disease –
ulcerations can develop on the fingertips and toes
 Management

• Aimed at prevention
 Person is advised to protect against exposure to cold
 Quit smoking
• Drug therapy – calcium channel blockers, vascular smooth
muscle relaxants, vasodilators – to promote circulation and
reduce pain
• Botox
• Sympathectomy to relieve symptoms in the early stage of
advanced ischemia
• If ulceration/gangrene occur, the area may need to be
amputated

TROMBOSIS VENA DALAM

formation of a blood clot in

one of the deep veins of
the body, usually in the leg
 Etiology and risk factors

3 main factors contribute in development of DVT

 Stasis
 Endothelial injury
 Hypercoagulability

a. Venous stasis
 prolonged bed rest (4 days or more)
 a cast on the leg
 limb paralysis from stroke or spinal cord injury
 extended travel in a vehicle
 heart failure

b. Hypercoagulability
 Surgery and trauma - responsible for up to 40% of all
thromboembolic disease
 Malignancy
 Increased estrogen (due to a fall in protein ‘S) Increased
estrogen occurs during
 all stages of pregnancy
 the first three months postpartum,
 after elective abortion, and
 during treatment with oral contraceptive pills

c. Inherited disorders of coagulation

 deficiencies of protein ‘S’,
 protein ‘C’ and
 antithrombin III.
 Acquired disorders of coagulation
§ nephrotic syndrome results in urinary loss of
antithrombin III, this diagnosis should be considered
in children presenting with thromboembolic disease
Antiphospholipid antibodies accelerate coagulation and
include the lupus anticoagulant and anticardiolipin antibodies

Inflammatory processes, such as

 systemic lupus erythematosus (SLE),

 sickle cell disease, and
 inflammatory bowel disease (IBD),
also predispose to thrombosis, presumably due to
hypercoagulability

Symptoms:

 Dull pain, heaviness, oedema and warm limb

 With extensive DVT:-massive oedema, cyanosis, dilated
superficial collateral veins and low grade fever.
 With ilio-femoral DVT:-
 Phlegmasia cerulea dolens (cyanosed limb due to obstructed
vein)
 Phlegmasia alba dolens (pale, pulseless cold limb due to
concurrent arterial spasm)
AND THESE TWO UPPER CASES ARE LIMB THREATENING
CONDITION!!

Phlegmasia cerulea dolens Venous gangrene

SIGN

§ HOMAN'S sign (tenderness during passive

dorsiflexion of foot). And it was contraindicated
because of it’s role in thrombus deattachment and
thus emobilization

§ Hotness, cyanosis, oedema (non-pitting)

DVT Clinical Prediction

 Algorithm

Diagnostic Studies

-Clinical examination alone is able to confirm only 20-30%

of cases of DVT

- Blood Tests

 the D-dimer - have predictive value for DVT

 INR - useful for guiding the management of patients
with known DVT who are on warfarin (Coumadin)

D-dimer

 D-dimer is a specific degradation product of cross-linked

fibrin.
 Concurrent production and breakdown of clot characterize
thrombosis, patients with thromboembolic disease have
elevated levels of D-dimer
 Ultrasonography
§ color-flow Duplex scanning is the imaging test of
choice for patients with suspected DVT
l inexpensive,
l noninvasive,
l widely available
Ultrasound can also distinguish other causes of leg swelling,
such as tumor, popliteal cyst, abscess, aneurysm, or
hematoma.

clinical limitations
 reader dependent
 Duplex scans are less likely to detect non-occluding thrombi.
 During the second half of pregnancy, ultrasound becomes
less specific, because the gravid uterus compresses the
inferior vena cava, thereby changing Doppler flow in the
lower extremities

The finding are:

§ Acute DVT:

 Absence of spontaneous flow.

 Loss of flow variation with respiration.
 Failure to increase the flow after distal augmentation.
 Not visible thrombi (anechoic thrombi).

§ Chronic DVT:

 Not well established

 Narrow vein
 Patent collateral
 Visible thrombi
Color duplex scan of DVT

The only disadvantage of duplex study is that, it is highly

operator dependant!!!