Peripheral vascular disease and Clinical features of acute and chronic arterial stenosis and...

Clinical features of acute and chronic arterial stenosis and

occlusion

Dr Sumer YadavMCh – Plastic and Reconstructive Surgery

sumeryadav2004@gmail.com

What is PVD?Definition:• Also known as PAD or PAOD.

• Occlusive disease of the arteries of the lower extremity.

• Most common cause:o Atherothrombosiso Others: arteritis, aneurysm + embolism.

• Has both ACUTE and CHRONIC

Pathophysiology:• Arterial narrowing Decreased blood flow =

• Pain results from an imbalance between supply and demand of blood flow that fails to satisfy

ongoing metabolic requirements. sumeryadav2004@gmail.com

The Facts:1. The prevalence: >55 years is 10%–25%

2. 70%–80% of affected individuals are asymptomatic

3. Pt’s with PVD alone have the same relative risk of death from cardiovascular causes as those CAD or CVD

1. PVD pt’s = 4X more likely to die within 10 years than pt’s without the disease.

2. The ankle–brachial pressure index (ABPI) is a simple, non-invasive bedside tool for diagnosing PAD — an ABPI <0.9 = diagnostic for PAD

1. Patients with PAD require medical management to prevent future coronary and cerebral vascular events.

1. Prognosis at 1 yr in patient’s with Critical Limb Ischemia (rest pain): • Alive with two limbs — 50%• Amputation — 25%• Cardiovascular mortality 25%

Risk Factors:Typical Patient:• Smoker (2.5-3x)• Diabetic (3-4x)• Hypertension• Hx of Hypercholesterolemia/AF/IHD/CVA • Age ≥ 70 years.

• Age 50 - 69 years with a history of smoking or diabetes.

• Age 40 - 49 with diabetes and at least one other risk factor for atherosclerosis.

• Leg symptoms suggestive of claudication with exertion or ischemic pain at rest.

• Abnormal lower extremity pulse examination.

• Known atherosclerosis at other sites (eg, coronary, carotid, or renal artery disease).

Chronic PVD History:

3. Critical Stenosis = >60%, impending acute ischemic limb:- rest pain- ischemic ulceration- gangrene

2. Other Symptom/Signs:• A burning or aching pain in the feet (especially at night)• Cold skin/feet• Increased occurrence of infection• Non-healing Ulcers• Asymptomatic

1. INTERMITTENT CLAUDICATION• Derived from the Latin word ‘to limp’• “Reproducible pain on exercise which is relieved by rest”• Pain can also be reproduced by elevating the leg • “my legs get sore at night and feel better when I hang them over

the edge of the bed”

Thigh Claudication

60% Upper 2/3 Calf Claudication

Lower 1/3 Calf Claudication

Foot Claudication

30% Buttock & Hip Claudication±Impotence – Leriche’s Syndrome

DDx of Leg Pain1. Vascular

a) DVT (as for risk factors)

b) PVD (claudication)

1. Neurospinala) Disc Disease

b) Spinal Stenosis (Pseudoclaudication)

1. Neuropathica) Diabetes

1. Musculoskeletala) OA (variation with weather + time of day)b) Chronic compartment syndrome

Physical Examination:Examination: What do to:

Inspection

Expose the skin and look for:

• Thick Shiny Skin• Hair Loss • Brittle Nails• Colour Changes (pallor)• Ulcers• Muscle Wasting

Palpation • Temperature (cool, bilateral/unilateral)• Pulses: ?Regular, ?AAA• Capillary Refill• Sensation/Movement

Auscultation • Femoral Bruits

Ankle Brachial Index (ABI)

= Systolic BP in ankle Systolic BP in brachial artery

Buerger’s Test • Elevate the leg to 45° - and look for pallor• Place the leg in a dependent position 90°& look for a red

flushed foot before returning to normal • Pallor at <20° = severe PAD. sumeryadav2004@gmail.com

Pictures:

What does the ABI mean?

ABI Clinical Correlation

>0.9 Normal Limb

0.5-0.9 Intermittent Claudication

<0.4 Rest Pain

<0.15 Gangrene

CAUTION: Patient’s with Diabetes + Renal Failure:

They have calcified arterial walls which can falsely elevate their ABI.

Investigations:

NON INVASIVE:Duplex Ultrasound normal is triphasic biphasic monophasic absent

BLOOD TESTS:1. Coagulation Studies 2. Fasting Lipids and Fasting Glucose3. HBA1C

WHEN TO IMAGE:1. To image = to intervene2. Pt’s with disabling symptoms where revascularisation is considered3. To accurately depict anatomy of stenosis and plan for PCI or Surgery

ANGIOGRAPHY:

Non-invasive:• CT Angiogram• MR Angiogram

Invasive:• Digital Subtraction Angiography

Gold Standard Intervention at the same time

Tardus et parvus = small amplitude + slow rising pulse sumeryadav2004@gmail.com

CT Angiography Digital Subtraction Angiography

Value of angiographyValue of angiography

Localizes the obstruction

Visualize the arterial tree & distal run-off

Can diagnose an embolus:Sharp cutoff, reversed meniscus or clot silhouette

Treatment:1. RISK FACTOR MODIFICATION:

a) Smoking Cessationb) Rigorous BSL controlc) BP reductiond) Lipid Lowering Therapy

3. MEDICAL MANAGEMENT:a) Antiplatelet therapy e.g.

Aspirin/Clopidogrel b) Phosphodiesterase Inhibitor e.g.

Cilostazol c) Foot Care

2. EXERCISE:a) Claudication exercise rehabilitation

program b) 45-60mins 3x weekly for 12 weeks c) 6 months later +6.5mins walking

time (before pain)

PCI/Surgery:Indications/Considerations:•Poor response to exercise rehabilitation + pharmacologic therapy.•Significantly disabled by claudication, poor QOL•The patient is able to benefit from an improvement in claudication•The individual’s anticipated natural hx and prognosis•Morphology of the lesion (low risk + high probabilty of operation success)

PCI:•Angioplasty and Stenting•Should be offered first to patients with significant comorbidities who are not expected to live more than 1-2 years

Bypass Surgery:•Reverse the saphenous vein for femoro-popliteal bypass•Synthetic prosthesis for aorto-iliac or ilio-femoral bypass•Others = iliac endarterectomy & thrombolysis•Current Cochrane review = not enough evidence for Bypass>PCI

Amputation: Last Resortsumeryadav2004@gmail.com

Some Bypass Options:

Mr. X presents with an acutely painful leg:

You have had a busy day in the ED and the next patient to see is:

Mr. X – a 60 yr old gentleman with a very painful leg.

He tells you that he woke up this morning with an excruciating pain in his left leg and has never felt this pain before.

? Embolism (AF/Recent Infarct/Anuerysm) ? Thrombosis of native vessel or graft

?Trauma

MUST RULE OUT ACUTE LIMB ISCHEMIA

What are the features of an acute ischemic limb?

REMEMBER THE 6 P’S:

1. PAIN

1. PALLOR

1. PULSELESNESS

1. PERISHING COLD (POIKILOTHERMIA)

1. PARASTHESIAS

1. PARALYSIS

Fixed mottling & cyanosis

History & Exam FindingsFurther Hx:• Smokes 20cigs/day for 30 years• 4 months of ‘leg cramps’ in BOTH legs• 2-3 weeks of intermittent chest palpitations Examination:• Inspection:

: below the knee is pale/cool• Palpation:

o Irregularly irregular pulse Capillary return is sluggisho No pulses palpable below L femoral arteryo All pulses palpable but appear reduced in R lego Normal Sensation + Movement bilaterally

Impression?60yo male with a L Acute Ischemic limb on the background of heavy

smoking, untreated AF and symptomatic PVD.sumeryadav2004@gmail.com

What will you do now?1. CALL THE VASCULAR REGISTRAR

2. ORDER INVESTIGATIONSa) FBEb) Coagulation Studiesc) Group and Holdd) 12 Lead ECGe) Chest XR

3. INITATE ACUTE MANAGEMENT:a) Analgesiab) Commence IV heparinc) Call Radiology for Angiography if limb still viabled) Discuss with registrar:

i) Thrombotic cause ?cathetar induced thrombolysisii) Embolic cause ?embolectomyiii) All other measures not possible Bypass/Amputation

Simple measures to improve existing perfusion:

• Keep the foot dependant

• Avoid pressure over the heel

• Avoid extremes of temperature (cold induces vasospasm)

• Maximum tissue oxygenation (oxygen inhalation)

• Correct hypotension

Mr. X’s Complication- Angiogram is done in radiology- Shows acute thrombosis of L popliteal artery- Cathetar induced urokinase and heparin infusion is started

…. 3-4 hours later

-Severe calf pain in the reperfused limb-All pulses are present -Leg is swollen, tense and +++ tender

REPERFUSION INJURY!-Restored blood flow can lead to unwanted local + systemic effects

1) Washout =oMetabolic AcidosisoHyperkalemiaoARF (myoglobinuria)oNon-cardiac APO

2) Compartment Syndrome = oMay need fasciotomy

Learning Outcomes1. Risk factors for PVD

2. Recognise signs and symptoms of chronic ischemia of the lower limbs

3. Differential diagnosis for leg pain

4. Examine a chronic ischemic limb

5. Understand medical/surgical of management of PVD

6. Recognise an acute ischemic limb

7. Know it is important to call the vascular registrar ASAP

8. Know what investigations to order in the ED

9. Be aware of the manifestations of reperfusion injury sumeryadav2004@gmail.com

ACUTE ARTERIAL OCCLUSION

• “ The operation was a success but the patient died”

• High Morbidity and Mortality – Emergent operations in high risk patients – 20% mortality reported (Dale, JVS 1984) – Endovascular approaches may lower peri-

procedural mortality while preserving outcomes sumeryadav2004@gmail.com

Evolution of Atherosclerosis

• Areas of low wall shear stress • Increased endothelial permeability • Sub-endothelial lipid and macrophage

accumulation • Foam cells • Formation of Fatty Streak • Fibrin deposition and stabilizing fibrous cap

Evolution of Atherosclerosis

• Rupture of Fibrous Cap • • Pro-thrombotic core Exposed to lumen • • Acute thrombosis • • Embolization of plaque materials and

thrombus

Thromboembolism

• Embolus- greek “embolos” means projectile • Mortality of 10-25% • Mean age increasing – 70 years – Rhumatic disease to atherosclerotic disease • Classified by size or content – Macroemboli and microemboli – Thrombus, fibrinoplatelet clumps, cholesterol

Macroemboli

• Cardiac Emboli – Heart source 80-90% of thrombus macroemboli – MI, A.fib, Mitral valve, Valvular prost hesis –

Multiple emboli 10% cases – TEE • Views left atrial appendage, valves, aortic root

• not highly sensitivesumeryadav2004@gmail.com

Thromboembolism

• 75% of emboli involve axial limb vasculature • Femoral and Polilteal – >50% of emboli • Branch sites • Areas of stenosis

Thromboembolism

Thromboembolism Non-cardiac sources • Aneurysmal (popliteal > abdominal) • Paradoxical – Follows PE with PFO • Thoracic outlet syndrome• Cryptogenic –5-10% • Atheroemboli (artery to artery)

Atheromatous Embolization

• Shaggy Aorta – Thoracic or abdominal • Spontaneous • Iatrogenic – 45% of all atheroemboli • “Blue toe syndrome” – Sudden – Painful – cyanotic – palpable pulses • livedo reticularis

• Risk factors: PVD, HTN, elderly, CAD, recent arterial manipulation

• Emboli consist of thrombus, platelet fibrin material or cholesterol crystals

• Lodge in arteries 100 –200 micron diameter

• Affect variety of end organs – extremities, pelvis ,GI, kidney, brain • Work-up: – TEE ascending aorta, CT Angio, Angiography • Laboratory: CRP elevated, eosinophilia • Warfarin may destablize fibrin cap and trigger

emboli.sumeryadav2004@gmail.com

• Reported incidence of 0.5-1.5% following catherter manipulation

– Advance/remove catheters over guidewire – Brachial access? – controversial • Limited Sx– Anti-coagulation/ observation • Temporal delay up to 8 weeks before renal

symptoms sumeryadav2004@gmail.com

Atheromatous Embolization Therapy

• Prevention and supportive care – Statins, prostacyclin analogs (iloprost)

• Elimination of embolic source and reestablishing blood flow to heal lesions

• Surgical options: endaterectomy or resection and graft placement – Abdominal Aorta – Aorta-bi-fem bypass – Ligation of external iliac and extra-anatomic bypass if high risk • Endovascular therapy – Angioplasty & stenting - higher rate of recurrence – Athrectomy – no datasumeryadav2004@gmail.com

Acute Thrombosis

• Graft thrombosis (80%)

– intimal hyperlasia at distal anastamosis (prosthetic)

– Retained valve cusp – Stenosis at previous site of injury

• Native artery • Intra-plaque hemmorhage • Hypovolemia • Cardiac failure • hypercoagable state • Trauma • Arteritis, popliteal entrapment, adventitial cystic disease

Acute ThrombosisHeparin Induced Thrombosis • White Clot Syndrome • Heparin dependent IgG anti-body against platelet factor

• 3-10 days following heparin contact • Dx: thrombosis with > 50% decrease in Platelet count • Tx: Direct throbin inhibiors: Agartroban & Hirudin

– Avoid all heparin products • Morbity and Mortality: 7.4-61% and 1.1-23%sumeryadav2004@gmail.com

Other causes of Thrombosis

– Anti-thrombin III Defiency – Protein C & S Defiency – Factor V Leiden – Prothrombin 20210 Polymorphism – Hyper-homocystinemia – Lupus Anti-coagulant (anti phospho-lipid

syndrome)sumeryadav2004@gmail.com

“The Cold Leg”

• Clinical Diagnosis – Avoid Delay – Anti-coagulate immediately – Pulse exam – 6 P’s (pain, pallor, pulselessness,

parathesias, paralysis,poiklothermia) • Acute –vs- Acute on chronic – Collateral circulation preserves tissue – Traditional 4-6 hr rule may not apply

Diagnostic Evaluation• SVS/ISCVS Classification • – “Rutherford Criteria” • • Class I: Viable – Pain, No paralysis or sensory loss • • Class 2: Threatened but salvageable • • 2A: some sensory loss, No paralysis >No immediate threat • • 2B: Sensory and Motor loss > needs immediate treatment • • Class 3: Non-viable – Profound neurologic deficit, absent capillary

flow,skin marbling, absent arterial& venous signal

Therapeutic Options

– Class 1 or 2A • Anti-coagulation, angiography and elective

revascularzation – Class 2B • Early angiographic evaluation and intervention • Exception: suspected common femoral emboli – Class3 • Amputation

Diagnostic Evaluation• Modalities – Non-invasive: • Waveforms • CTA / MRA : avoid nephrotoxity – Contrast Angiography • Gold Standard

Thrombotic –vs- Embolic• Thrombotic – History • Claudication, PVD • Bypass graft – Physical • Hair loss, shiny skin

• Bi-lateral Disease – Angiographic

• Diffuse disease • mid vessel occlusion – PVD confuses diagnosis

Thrombotic –vs- Embolic

• Embolic – History

• Cardiac events

• Acute onset • Hx of emboli – Physical • Normal contralateral exam

– Angiographic

• meniscus Cut-off in normal vessel • Bifurcations affected Determination of etiology possible in 85% of cases

Treatment Options• Multiple options available – Conventional surgery • embolectomy • endarterectomy

• revascularization – Thrombolytic therapy – Percutanious mechanical thrombectomy • Native vessel thrombosis often require more elaborate

operations sumeryadav2004@gmail.com

Treatment Fundamentals

• Early recognition and anti-coagulation

– Minimizes distal propagation and recurrent emboli • Modality of Tx depends on: – Presumed etiology – Location/morphology of lesion – Viability of extremity – Physiologic state of patient – Available vein conduit for bypass grafting

Embolectomy

• Fogarty embolectomy catheter – Intoduced 1961 • Thru-lumen catheter – Selecti ve placement over wire – Administer: lytics, contrast

Embolectomy

Surgical Therapy • Iliac and femoral embolectomy – Common femoral approach

– Transverse arteriotomy proximal profunda origin – Collateral circulation may increase backbleeding

– Examine thrombus

Embolectomy• Popliteal embolectomy – 49% success rate from femoral approach

– Blind passage selects peroneal 90%

– may expose tibialperoneal trunk & guide catheter

– Idrectly cannulate distal vessels

• Distal embolectomy – Retrograde/antegrade via ankle incisions – Frequent Rethrombosis – Thrombolytic Tx viable alternative

Embolectomy

• Completion angiography – 35% incdence of retained thrombus

• Failure requires – Thrombolytic thearpy – revascularization

Thrombolytic Therapy• Advantages • Opens collaterals & microcirculation • Avoids sudden reperfusion • Reveals underlying stenosis

• Prevent endothelial damage from balloons Risks • Hemmorhage • Stroke • Renal failure • Distal emboli

transiently worsen ischemia

Indications for Thrombolysis• Category 1-2a limbs should be considered – Class 2b : Two schools of thought 1)“Delay in definitive Tx” 2)“Thrombolytics extend window of opportunity” • Clots <14days most responsive– But even chronic thrombus can be lysed• Large clot burden– Better response to lytic tx than surgery– Requires longer duration of thrombolytics

Technique of Thrombolysis

• Guide Wire Traversal Test (GTT) – Abilty to traverse lesion best predictor of

success – Use 0.035 in angled glide wire – “knuckling-over” indicates sub-intimal plane – Attempt pro-grade, Anti-grade, lytic bolus

Technique of Thrombolysis

• Catheter directed delivery 1) Lace clot via catheter with side holes 2) Pulse-Spray technique (mechanical component)

• Urokinase and TPA equally effective • 4 hr treatment followed by angiogram – 4000IU/min x4hr,

2000Iu/M=min x 48h – r-UK (TOPAS Trial) – no improvement after 4hr >> surgery

– Continue Heparin tt

– Fibrinogen levelssumeryadav2004@gmail.com

Mechanical Thrombectomy

• Percutaneous aspiration embolectomy – Viable alternative in selected patents

– Varity of devises – Combines diagnostic and therapeutic procedure

– Removes non-lysable debris – Effective in distal vessels

– Risk distal embolization • Combine with lytic T x

Reperfusion SyndromeLocal: endothelial damage, capillary permeability,

Transudative swelling, cellular damage • Compartment Syndrome • Tx: Fasciotomy

Systemic: Lactic Acidosis, Hyperkalemia, Myoglobin, Inflammatory Cytokines

• Cardiopulmonary complications

Renal Tubular necrosis • Myoglobin precipitates • Tx: Volume, Urinary alklinization

SUMMARY

• Thrombotic and embolic occlusions are separate processes with different presentations and treatments

• Treatment pathways in AAO are complex and vary depending on clinical situation

• Catheter-based treatments preserve outcomes with less overall morbidity

Thanks sumeryadav2004@gmail.com

Peripheral vascular disease and Clinical features of acute and chronic arterial stenosis and...

Health & Medicine

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