Peripheral Vascular Conditions Flashcards
Pathogenesis of Atherosclerosis
Normal Artery –> Fatty streak –> Fibrofatty Plaque –> advanced/vulnerable plaque–> aneurysm + rupture/occlusion by thrombus/critical stenosis
Normal artery –> Fibrofatty plaque RFs
At lesion prone areas Endothelial dysfunction Monocyte adhesion/emigration SMC migration to intima SMC proliferation ECM elaboration Lipid accumulation
Fibrofatty Plaque –> Advanced/vulnerable plaque
Cell death/degeneration Inflammation Plaque growth Remodelling of plaque and wall ECM Organization of thrombus Calcification
Advanced/vulnerable plaque –> aneurysm and rupture
Mural thrombosis
Embolization
Wall weakening
Advanced/vulnerable plaque –> occlusion by thrombus
Plaque rupture Plaque erosion Plaque haemorrhage Mural thrombosis Embolization
Advanced/vulnerable plaque –> critical stenosis
Progressive plaque growth
Plaques are made up of
Cells (SMC, macrophages and other WBC)
ECM (collagen, elastin, and PGs)
Lipids
Intermittent claudication
Pain in limb- most often noticed in calf, but may also be felt in buttocks or thighs
Brought on by exertion
Relieved at rest
Recurs on similar effort
Spinal ischaemia
Spinal cord stenosis has similar pain to intermittent claudication
Difference is that just standing doesn’t make it better, they have to sit down
Critical Limb ischaemia
Rest pain (constant pain + opiate analgesia) +/- tissue loss <50mmHg at ankle
PAD epidemiology- in population 55-74 yrs
25% asymptomatic PAD
5%- claudication (23% of claudicants will develop CLI over 10 years)
PAD epidemiology
Correlation of ABPI with increased risk of death
PAD has a greater mortality rate than cerebrovascular/coronary artery disease
3% death per year
Critical limb ischaemia facts
90% require reconstruction/angioplasty
25% amputation rate
50% die within 5 yrs (MI, CVA)
Critical limb ischaemia clinical indicators/examination findings
Sensation
Movement
Pain
Critical limb ischaemia diagnosis
History
Examination
Investigations
Critical limb ischaemia investigations
ABPI (confounders)
Duplex
MRA/CTA
Diagnostic angiogram
Critical limb ischaemia RFs
Smoking Diabetes Hypertension Hypercholesterolaemia Hyperhomocysteinaemia C reactive protein
Claudication timeline- in 100 claudicants-
50 improve
30 remain same
20 deteriorate –> 5 of these have intervention–> 1/2 amputated
Claudication treatment- conservative
Lifestyle modification (exercise) Stop smoking
Claudication treatment- medical
Risk factor optimisation
Claudication treatment- surgical
Endovascular- angioplasty
Open- surgical bypass
Adjuncts
Diabetes control- claudication
Reduce HbA1c by 1% –> 21% reduction in complications
Cholesterol control- claudication
Simvastatin 40mg –> 24% reduction in revascularisation
HDL protective, LDL causes atherosclerosis
Blood pressure control- claudication
HOPE study 26% reduction in events
Anti-platelets- claudication
Aspirin 75mg –> 23% reduction in events
Anti-oxidants and vitamins- claudication
Omega 3 fish oils
Cilostazol (pletal) - claudication
Phosphodiesterase inhibitor
Claudication- angioplasty
Catheter inserted into femoral artery
Balloon/stent positioned
Balloon/stent expanded
Angioplasty risk
Failure to dilate (10-20%) Re-stenosis Surgical salvage (<2%) Amputation (<0.3%) Death (<0.2%) Contrast anaphylaxis Renal dysfunction <24hrs (10%)
Angioplasty benefit
Minimally invasive
Short stay
Quick recovery
Bypass surgery
Preserved for patients with CL (+/- life altering claudication)
Autologous- vein
Synthetic- PTFE/Dacron
Dacron
basic tube used in bypass
PTFE
tube used in bypass- synthetic
Fem- above knee popliteal bypass: 2 yr primary patency
long saphenous vein- 81%
Human umbilical vein- 70%
PTFE- 69%
Fem- above knee popliteal bypass: 5yr primary patency
Long saphenous vein- 73%
Human umbilical vein- 53%
PTFE- 39%
Vein patches- risks
Graft failure (variables) MI Infections Limb loss Death
Vein patches- benefit
Save limb
Retain independence
Wound healing
Non surgical treatments in CLI- Prostanoids
Iloporost
Better than placebo for rest pain and ulcer healing
Non surgical treatments in CLI- lumbar sympathectomy
Abolishes arteriolar and capillary construction
Alters pain transmission
Non surgical treatments in CLI- Spinal cord stimulation
Epidural stimulation for intractable ischaemic pain
Non surgical treatments in CLI- gene therapy
Angiogenic growth factors (VEGF, PDGF)
Non surgical treatments in CLI- Stem cell therapy
Endothelial progenitor cells
Aneurysm definition
Localised dilatation of an artery greater than twice normal diameter
Popliteal aneurysm
10% of those with a AAA have a popliteal aneurysm
50% of those with a popliteal aneurysm have an AAA
50% of popliteal aneurysms are bilateral
Abdominal aortic aneurysm epidemiology
Aortic diameter >3cm Growth +-10%/yr 9% prevalence in men over 65 12% incidence in hypertensive men Mortality at rupture 90%
AAA pathology summary
Intimal atherosclerosis
Mural thrombus
Destruction of elastic lamellae
Inflammatory response is due to imbalance (matrix degrading proteinases don’t equal inhibitors (MMP/plasminogen activators))
Autoimmune response, increased cytokines, chemoattractants and peptide growth factors
Altered gene products in AAA formation (in aortic tissue/blood formation)
Increased proteolysis (MMP-1, MMP-9) Increased inflammation- (cytokines, Chlamydia Ag/Ab, Adhesion molecules)
AAA Risk factors
1-5% positive family history Ethnicity- N Europeans > Asians/Africans Smoking- relative risk=2 (and increased expansions) Hypercholesterolaemia Hypertension NOT DIABETES
Types of aneurysm
Saccular aneurysm
Fusiform aneurysm
Ruptured aneurysm
AAA- indication for surgery
AAA>5.5cm diameter
Rapid AAA enlargement (<1cm/yr)
Symptomatic AAA
AAA surgery risk
Mortality (5-10%) Myocardial infarction Multi-organ failure Paraplegia Haemorrhage Infections (wound/graft) Fistulae Hernia
Endovascular AAA repair (EVAR) Pros
2% mortality
Decreased insult
2 day hospital stay
Can be percutaneous
EVAR cons
Cost
surveillance
re-interventions
durability?
Rupture risk in 1 year- aortic diameter <5.5cm
1-2%
Rupture risk in 1 year- aortic diameter 5.5-6.5cm
8%
Rupture risk in 1 year- aortic diameter 6.5-7cm
15-20%
Rupture risk in 1 year- aortic diameter >7cm
30%
Rupture risk in 1 year- aortic diameter 10cm
100%
Most frequent misdiagnoses in patients with AAAs
Miscellaneous 13% Renal colic 23% Diverticulitis 12% GI bleed 13% Acute MI 9% Back pain 9% Motor vehicle accident 7% Sepsis 7% Other GI disorders 7%
AAA screening
Men
Over 65
Single trans- abdominal ultrasound
Varicose veins epidemiology
1/3 population 18-65 Probably genetic link (familial) 90,000 varicose vein procedures/year UK Effect quality of life Surgery improves quality of life
Varicose vein description
Dilated
Tortuous
Incompetent
Refluxing
Varicose vein clinical assessment
history- previous DVT, previous long bone
Examination- bleeding, skin problems
Investigation- patent deep veins, confirm root cause
VV treatment- conservative
Leg elevation
Class 1 compression hosiery
VV treatment- medical
topical relief
VV treatment- surgical
Open ligation + stripping
Foam sclerotherapy
Endovenous solutions
Complications of VVs
Swelling Discomfort Itching Varicose eczema Haemosiderin deposition Lipodermatosclerosis Bleeding Ulceration
VV endovenous treatment
Disposable catheter inserted into vein
Vein warmed and collapses
Catheter withdrawn, closing vein
VV complications of treatment- early
Bleeding Bruising Discomfort Infection DVT/PE
VV complications of treatment- late
Recurrence
Parasthesia
Endovenous technology benefits- improvement over vein stripping
One hour treatment time
Immediate ambulation
Can be performed in physician’s office
Much less expensive
Aortic Dissection
History- cardiac type
Examination- pulses
Diagnosis- CTA
Aortic Dissection RFs
Hypertension
Genetic
Connective tissue
