VASCULAR DISEASE AND VASCULAR SURGERY

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VASCULAR DISEASE AND VASCULAR SURGERY

• (OR EVERYTHING YOU EVER WANTED TO KNOW ABOUT
  VASCULAR SURGERY BUT WERE AFRAID TO ASK)
• PGY 1 3
• BASIC SCIENCE LECTURE
• 12/6/07

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VESSEL WALL STRUCTURE

• Tunica intima
• Endothelial cells, subendothelial connective
  tissue (collagen, proteoglycans, elastin,
  glycoproteins), internal elastic lamina
• Tunica media
• Smooth muscle cells, elastic fibers, external
  elastic membrane vaso vasorum
• Tunica adventitia
• Poorly defined layer of connective tissue,
  contains elastic and nerve fibers

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ARTERY TYPES (BLEEDING AND NON-BLEEDING)

• Large or elastic
• Aorta, arch vessels, pulmonary arteries
• Rich in elastin (lost during aging) which helps
  propel blood during diastole
• Medium or muscular
• Rich in nerve fibers, related to autonomic
  regulation of blood flow
• Small
• Loss of elastic membranes, major site of
  autonomic control

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VEINS

• Thin-walled
• Indistinct layers
• Large lumen
• Presence of valves
• Prone to dilation, compression, tumor invasion

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LYMPHATICS

• Very thin-walled
• Lined with endothelium
• Return of extracellular fluid to intravascular
  space
• Some have muscular wall and valves

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VASCULAR ENDOTHELIUM

• Produces vasodilators (PGI2 and PGE2, adenosine,
  and EDRF(nitric oxide))
• Produces vasoconstrictor (endothelin)
• Can sense change in blood velocity and shear and
  respond to maintain consistent flow
• Ability of arteries to dilate in the presence of
  luminal narrowing (lost when plaque is gt40 of
  cross-sectional area)

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RISK FACTORS FOR ATHEROSCLEROSIS

• Age
• Gender
• Family predisposition
• Hyperlipidemia
• Hypertension
• Cigarette smoking
• Diabetes
• Sedentary lifestyle, Type A, stress, obesity

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LIPID METABOLISM

• Chylomicrons
• Dietary TG and cholesterol incorporated with
  lipoproteins within intestinal epithelial cells
• VLDL
• Transports TG synthesized in the liver
• IDL
• Remnants of VLDL hydrolysis
• LDL
• Primary transporter of endogenous cholesterol
• HDL
• Also major transporter of cholesterol

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PATHOGENESIS OF ATHEROSCLEROSIS

• Principal lesion is plaque
• Fibrous cap
• Deeper necrotic core
• May become complicated (calcified, ulcerated,
  rupture leading to embolization, hemorrhage into
  plaque)
• Generally found at ostia and bifurcations
• Reaction to injury hypothesis

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REACTION TO INJURY HYPOTHESIS

• Secondary to irradiation, chemical injury, immune
  complex deposition, hypertension, smoking,
  turbulence, sheer
• Platelets and monocytes adhere
• PDGF produced SMC migrate to the intima and
  proliferate (TGF, FGF)
• Monocytes transform to macrophages which take up
  cholesterol and become foam cells

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ARTERIAL PHYSICS

• Intravascular arterial pressure sum of dynamic
  pressure, hydrostatic pressure, and static
  filling pressure
• Total fluid energy potential energy
  (intravascular pressure gravity) kinetic
  energy (SG of blood velocity)
• i.e. the Bernoulli principle
• Flow (which remains constant) is the product of
  fluid velocity and area (radius squared)

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BLOOD FLOW

• Parabolic profile for laminar flow due to
  cohesive forces throughout arterial tree
• Turbulence results when laminar flow is disrupted
  (Reynolds number gt 2000)
• Shear stress (force to overcome friction between
  fluid layers), viscosity (resistance to blood
  flow hematocrit)
• Boundary layer separation higher flow rates at
  central flow divider of a bifurcation area of
  flow separation created (flow reversal at
  boundary layer) correlates with development of
  atherosclerotic lesions

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ARTERIAL STENOSIS

• Critical stenosis degree of stenosis required
  to produce a reduction in BP or flow (usually
  75-90 reduction in area and 50-70 reduction in
  diameter)
• Energy loss across a lesion depends more on
  degree of stenosis than length of lesion varies
  with flow rate (energy loss is higher with higher
  flowsubcritical lesions may become symptomatic
  during exercise)
• Total resistance in a vessel is additive,
  therefore energy losses across multiple stenoses
  more significant collaterals will develop

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ANEURYSM PHYSIOLOGY

• Law of Laplace
• Wall tension is proportional to the radius of the
  lumen
• Increase in BP and aneurysm size are proportional
  to wall tensile strength and risk of rupture

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CHRONIC LOWER EXTREMITY ISCHEMIA

• Remains asymptomatic until metabolic demands of
  tissue are not met
• Intermittent claudication
• (claudicoto limp)
• Rest pain
• Ischemic ulceration
• Gangrene

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CLAUDICATION

• Only 5 will progress to amputation if untreated
• lifestyle limiting
• Conservative management well accepted
• Aortoiliac distribution
• Younger pts.
• Less likely to cause symptoms
• Greater disability
• Distal embolization risk

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CLAUDICATION

• Infrainguinal distribution
• Conservative management
• Graft patency better than for limb salvage
• Careful patient selection
• Approach
• H and P (claudication, Leriche syndrome, rest
  pain) (pulses, skin changes) (concomitant medical
  issues)
• Distinguish non-vascular causes
• Non-invasive measurements
• Angiography

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LIMB-THREATENING ISCHEMIA

• Rest pain
• Progresses to limb loss if untreated
• Not relieved by pain meds
• Worse with elevation (night)
• Ankle pressure lt 40mmHg
• Ischemic ulcer
• Results from minor trauma
• Painful
• Dry, punctate, location
• Distinguish from venous ulcers

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LIMB-THREATENING ISCHEMIA

• Gangrene
• Anesthetic tissue
• Dry or wet (need for surgery)
• Acute vs. chronic ischemia
• Embolic vs. thrombotic
• Severity of signs/symptoms and timing determines
  outcome
• Blue toe syndrome
• Sudden onset
• Painful, cyanotic
• Strong pedal pulse present

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NON-INVASIVE TESTING

• Ankle-brachial index
• Bedside test
• gt.85 normal
• .5-.85 claudication
• lt.5 more severe
• Treadmill testing
• 5 min at 2 mph on 12 incline
• Segmental Pressures
• Pulse volume recording (useful in diabetics)
• Duplex imaging (localization, characterization,
  more experienced operator needed)
• MRA/CTA

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TREATMENT

• Aortoiliac disease
• Open
• Aortobifemoral patency 90 _at_ 5yrs
• Axillo-bifemoral patency 70 _at_ 5yrs
• Iliofemoral or fem-fem patency 80 _at_ 5yrs
• Endovascular
• Balloon angioplasty
• Stenting

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TREATMENT

• Fem/pop/tib disease
• Open
• 90/75 1 and 4 yr patency for vein graft
• 80/60 1 and 4 yr patency for PTFE for above
  knee
• 70/40 1 and 4 yr patency for PTFE for below
  knee
• Therefore, preferential use of autogenous vein
• Slightly lower patency rates for tibial bypasses
• Avoid PTFE to tibials

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TREATMENT

• Other options
• Axillo-popliteal bypass
• Profundoplasty
• Primary amputation
• Proximal pedal gangrene
• Chronic renal failure
• BKA vs. AKA

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GRAFT SURVEILLANCE

• Early failure
• Technical
• Inadequate inflow/outflow, conduit
• Unrecognized hypercoaguable state
• 30d to 2 yrs
• Intimal hyperplasia
• Late failure
• Recurrent atherosclerotic disease

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GRAFT SURVEILLANCE

• 20-30 of grafts develop stenoses within 1 yr
• Higher primary assisted patency rates than for
  secondary patency
• Duplex ultrasound
• Absolute velocity
• Ratios
• Change between exams
• ABIs

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ACUTE LOWER EXTREMITY ISCHEMIA

• Six Ps
• Pain
• Parasthesia
• Pulselessness
• Pallor
• Poikilothermy
• Paralysis
• Tissue necrosis may cause acidosis, hyperkalemia,
  and myoglobinuria

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ETIOLOGY

• Embolic
• Exact onset known
• Presence of arrhythmias
• Normal contralateral limb
• Thrombotic
• History of previous symptoms
• Evidence of PAD in opposite limb
• Previous bypass graft

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MANAGEMENT

• Palpation pulses at all levels
• Distal may require thrombolytic therapy
• Determines surgical approach
• Source
• Cardiac (afib, mural thrombus after MI,
  ventricular aneurysms, cardiomyopathy,
  diseased/prosthetic heart valves)
• Non-cardiac (aortic/peripheral aneuryms, ulcers,
  prior cath, venous emboli from PFO) will need
  TEE or angio post-op

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TREATMENT

• Approx. 6 hrs before irreversible tissue loss
  (variable depending on situation)
• Start anticoagulation
• Thrombolysis unless contraindicated (active
  bleeding, recent stroke, recent surgery, GI
  bleed, pregnancy, uncontrolled HTN)
• Surgery (embolectomy/thrombectomy) and
  intraoperative lysis

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COMPARTMENT SYNDROME

• Especially after prolonged period of ischemia
• Physical exam unreliable
• Measure compartment pressures (gt30mmHg)
• Signs of neurologic compromise

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MESENTERIC ISCHEMIA

• Acute
• Embolic, thrombotic (history of chronic
  symptoms), non-occlusive, venous thrombosis
• Most common site for embolus at middle colic,
  just distal to jejunal branches
• Need high index of suspicion
• Sudden onset, bowel evacuation, GI bleeding,
  unremarkable exam
• May need angio could be therapeutic
• Heparinize, resuscitate, operate

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MESENTERIC ISCHEMIA

• Chronic
• Usually 2 or more vessels have significant
  stenosis (multiple collateral pathways)
• Post-prandial pain
• Concomitant PAD
• Food fear
• Weight loss
• Chronic abd. Pain
• Diarrhea
• Angio to work up
• Surgery or endovascular approach to treat

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RENAL ARTERY STENOSIS

• Renovascular hypertension
• 5-10 of all HTN
• Especially diastolic and spiking episodes
• 70 athersclerotic at the ostium
• Renin- vs. volume- dependent
• Fibromuscular dyplasia
• Most common is medial fibrodysplasia
• More common in women
• Often bilateral
• Treat (surgery or endo) symptomatic lesions and
  those gt80

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AORTIC ANEURYSMS

• 13TH leading cause of death
• 15,000 deaths per year
• Focal dilation of gt50 usual diameter
• 4-6x more common in men
• 95 infrarenal
• 50 involve the iliacs
• 12 have TAAs
• Risks CAD, HTN, PAD, smoking, COPD
• 15-20 of 1st degree relatives affected
• May have connective tissue disorder

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AORTIC ANEURYSMS

• Pathophysiology unknown (hemodynamic, immune,
  inflammatory mechanisms suggested)
• Most are asymtomatic
• Discovered on PE or radiologic exam
• Occasionally cause duodenal compression ( with
  early satiety), hydronephrosis, iliocaval
  compression, back pain
• Severe abd. or back pain with rupture

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AAA MANAGEMENT

• If ruptured, diagnose on PE or CT, then proceed
  to open repair or EVAR
• If elective, then U/S or CTA
• MRI expensive, not as widely available
• Angiography invasive, doesnt assess size, but
  can be useful selectively
• Risk of rupture lt5cm 4 annually, 5-7cm 7,
  gt7cm 20
• Autopsy studiessmaller AAAs do rupture

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AAA MANAGEMENT

• Major periop mortality is due to CAD
• Open vs. EVAR
• Complications
• Sigmoid colon ischemia
• Lower extremity ischemia
• Retrograde ejaculation
• Spinal cord ischemia
• Anastomotic pseudoaneurysm
• Graft infection, aorto-enteric fistula

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PERIPHERAL ANEURYSMS

• Popliteal most common site
• 50 chance of having a contralateral aneurysm
• 30 chance of having AAA
• Repair at 2cm or 1.5x normal diameter
• Thrombosis, rupture, and distal embolization
• Femoral thrombose and rupture
• 70 contralateral
• 85 have AAA (only 3 with AAA have femoral)
• 40 have popliteal aneurysm
• Fix at 2x normal diameter

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SPLANCHNIC ARTERY ANEURYSMS

• Splenic most common (60)
• 4x more frequent in women
• Found on plain films (calcified)
• Repair when 2cm or even smaller in women of
  child-bearing age (90 found during pregnancy
  will rupture 75/95 mortality
• Splenectomy if at the hilum
• Embolization newer treatment
• Hepatic (20)
• More common in men
• Common hepatic can be ligated

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VENOUS DISORDERS

• DVT
• Phlegmasia cerulea dolens
• Phlegmasia alba dolens
• Pulmonary embolism
• Varicose veins
• Chronic venous insufficiency

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QUESTIONS??