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Clinical features of acute and chronic arterial stenosis and
occlusion
Dr Sumer YadavMCh – Plastic and Reconstructive Surgery
Dr Sumer YadavMCh – Plastic and Reconstructive Surgery
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
• Pain results from an imbalance between supply and demand of blood flow that fails to satisfy
ongoing metabolic requirements. [email protected]
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. [email protected]
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 [email protected]
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 [email protected]
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 [email protected]
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 [email protected]
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 [email protected]
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 [email protected]
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
Atheromatous Embolization
• 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
Atheromatous Embolization
• 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
Atheromatous Embolization
• 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 [email protected]
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 [email protected]
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
4
• 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%[email protected]
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)[email protected]
“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 [email protected]
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 [email protected]
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 [email protected]
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