ACUTE ARTERIAL
OCCLUSION
Vascular Surgery Conference
Michael Lebow, MD
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
Etiology of Arterial Occlusion
• Overview
– Atherosclerosis
– Thrombotic occlusion
– Embolic occlusion
– Treatment Options
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
•
• Necrosis
• Inflammatory environment
• Destabilization of fibrious 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 prosthesis
– Multiple emboli 10% cases
– TEE
• Views left atrial appendage,
valves, aortic root
• not highly sensitive
Thromboembolism
• 75% of emboli involve
axial limb vasculature
• Femoral and Polilteal
– >50% of emboli
• Branch sites
• Areas of stenosis
Thromboembolism
Non-cardiac sources
• Aneurysmal (popliteal > abdominal)
• Paradoxical
– Follows PE with PFO
• TOS
• 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 my destablize
fibrin cap and trigger
emboli.
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
Atheromatous Embolization
Therapy
• Prevention and supportive care
– Statins, prostacyclin analogs (iloprost), ASA, Plavix
• 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 data
Acute Thrombosis
• Graft thrombosis • Native artery
(80%) • Intra-plaque
hemmorhage
– intimal hyperlasia at
• Hypovolemia
distal anastamosis
• Cardiac failure
(prosthetic)
• hypercoagable state
– Retained valve cusp • Trauma
– Stenosis at previous • Arteritis, popliteal
site of injury entrapment, adventitial
cystic disease
Acute Thrombosis
• Heparin 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%
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)
“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:
• Segmental pressure
drop of 30mmhg
• Waveforms
• CTA / MRA : avoid
nephrotoxity
– Center dependent
– Wave of the future?
– Contrast Angiography
• Gold Standard
Thrombotic –vs- Embolic
• Thrombotic • Embolic
– History – History
• Claudication, PVD • Cardiac events
• Acute onset
• Bypass graft
• Hx of emboli
– Physical
– Physical
• Hair loss, shiny skin
• Normal contralateral exam
• Bi-lateral Dz • A.fib
– Angiographic – Angiographic
• Diffuse disease • meniscus Cut-off in
• mid vessel occlusion normal vessel
– PVD confuses diagnosis • 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
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
Treatment : Thrombosis
Separate graft thrombosis into early and Late groups
Early thrombosis Late thrombosis
• Technical defect – Duration & degree of ischemia
• Repairable – Lytic Thearpy (clas1-2a)
• Avoid lytic Tx • Good 1st approach
• 14 days vein • Unmasks lesion
• 30 days graft (valve/stenosis)
• Explore both anastamosis • F/u endo or open repair
• On-table Angio – Open surgery (2b)
• Twists, kniks,stenosis • Thrombectomy/patch
• Re-bypass
Embolectomy
• Fogarty embolectomy
catheter
– Intoduced 1961
• Adherent clot catheter
• Graft thrombectomy
catheter
• Thru-lumen catheter
– Selective 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 • Distal embolectomy
– 49% success rate from – Retrograde/antegrade
femoral approach
via ankle incisions
– Blind passage selects
peroneal 90% – Frequent Rethrombosis
– may expose tibial-
– Thrombolytic Tx
peroneal trunk & guide
catheter viable alternative
– Idrectly cannulate
distal vessels
Embolectomy
• Completion angiography
– 35% incdence of retained thrombus
– IVUS more sensitive then angio
• Failure requires
– Thrombolytic thearpy
– revascularization
Thrombolytic Therapy
Advantages Risks
• Opens collaterals & • Hemmorhage
microcirculation
• Stroke
• Avoids sudden
reperfusion • Renal failure
• Reveals underlying • Distal emboli
stenosis transiently worsen
• Prevent endothelial ischemia
damage from balloons
Surgery –vs- Thrombolysis
• STILE Trial
• Surgery vs Thrombolytics for Ischemia of Lower
Extremity
– 393 pts with non-embolic occlusion
– Surgery vs r-TPA or r-UK
• Thrombolytics : improved amputation free survival and
shorter hospital stay (0-14 days)
• Surgery: revascularization more effective for ischemia of >
14 days duration
Ann Surg 1994, 220:251
Surgery –vs- Thrombolysis
TOPAS Trial
• 2 phase
• 544 patients
• r-UK vs Surgery
• Need for surgery
Reduced 55%
• Similar amputation
and mortality rates
NEJM 338, 4/16/98
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 gtt
– Fibrinogen levels
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 Tx
Reperfusion Syndrome
• Ischemic-reperfusion syndrome
– Local: 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
