Peripheral Vascular Disease Flashcards
When does PVD arise?
Significant narrowing of arteries distal to arch of aorta
Types of PVD
(3)
- Peripheral Vascular Disease
- Chronic Arterial Insufficiency
- Chronic Vascular Disease
(3) mechanisms contributing to the development of PVD
- atherosclerosis
- vasospasm (e.g. Raynaud’s)
- inflammation/vasculitis
Risk factors for PVD
- smoking
- DM
- Hypertension
- Hyperlipidaemia
- Fx
- Sedentary lifestyle
The difference between Atherosclerosis and Acute Limb Ischemia
- Atherosclerosis: Toxins accumulate in tunica intima -> this narrows the lumen of the tube (so we cannot ‚just pull it out’)
- Acute limb ischaemia: there is a physical blockage (embolism) blocking the outflow
Clinical presentation re progression of PVD
- Asymptomatic
- Intermittent claudication
- Critical limb ischaemia (end stage of PVD)
*if we leave claudication stage alone -> it will perhaps stay like that till the end of life
*if we leave critical limb ischaemia alone -> amputation always needed
What’ s pathophysiology of claudication?
In claudication, as there is increased demand for oxygen and glucose to exercising muscle -> blockage would not allow enough blood to pass through -> anaerobic respiration -> lactic acid - > pain
*Cramps at certain distance
Does intermittent claudication result in amputation?
- Intermittent claudication does not generally threaten the limb (amputation not usually required)
- will impact on the life
- it is a red alarm for vascular disease -> MI, strokes etc common
(20-30% with intermittent claudication will be dead in 5 years - as other arteries e.g. in the brain are also affected)
What artery is most commonly involved in intermittent claudication?
Distal femoral a. -> claudication in the calf muscle area
(located just above the knee)
What questions to include in the history from a patient with suspected PVD?
- duration
- distance before the pain occurs
- time taken for pain to go away at rest
- trophic changes: colour changes, nail malformations, hair loss
- infections/healing
- medication
- occupation
- smoking
- FHx
- other risk factors (e.g. HTN, hyperlipidaemia, sedementary lifestyle)
Values and interpretation of ABPI - symptoms that occur with them
- 1 or more -> symptoms free
- 0.95 - 0.5 -> intermittent claudication
- 0.5 - 0.3 -> rest pain (critical ischaemia)
- <0.2 -> gangrane and ulceration (critical ischaemia)
Non-operative management of PVD
- Lifestyle: quit smoking, exercise (1 hr a day for 6 months), weight loss
- Statins - even if cholesterol is low; for secondary prevention
- Antiplatelet agents: Aspirin or Clopidogrel
- BP control: target <140/90
- Glycaemic control
Is surgery usually indicated in case of claudication?
Vascular surgery is very risky, perhaps not provided for people with claudication -> usually for people at risk of amputation due to risks vs benefits -> therefore more focus on non-operative
How do we approach ‘exercise’ advice in Mx of PVD?
- Exercise is not just an advice to exercise
- it is a formal and supervised programme under direction of specialist nurses -> it trains the muscle to get used to slightly anaerobic situations and that will make them to work more without pain
What about smoking and PVD?
Stop smoking -> as smoking will stop co-lateral circulation from forming -> and we want colateral
circulation!
(It has been proved that stop smoking and exercise would double walking distance in 6 months)
Pathophysiology of development of ‘critical limb ischaemia’
- pain even at rest - leg has an inadequate blood flow
- Tissue may start to die - ulcers (punched out, deep)
- Gangrene or necrosis - starts with toe
*Pain felt in early stages (just when they switch from claudication to ‘rest pain’) ->
felt in the toes (as further away from main
arterial supply)
What’s a warning sign for critical limb ischaemia?
patient waking up at night with toes or heel pain
Why does pain in critical limb ischaemia come initially at night?
- legs are up (so patient may hang the legs on the side of bed as gravity helps the blood to get to peripheries) -> some patients need to use morphine daily as pain is horrible
- cardiac output will slow town
- temperature drops by 0.5 degree -> peripheral vasoconstriction
How to assess the severity of PVD (questions about pain) (4)
Assessment - severity:
- Can they walk? -> if yes, either no PVD or asymptomatic
- Can they walk but pain comes while exercise ? -> claudication
- Pain at night -> critical ischaemia
- Pain all the time -> tissue loss
Can the leg appearance and cap refill be normal in the claudicant patient?
Yes, this is possible due to collateral circulation
How to perform ‘Burger’s test’? (what happens and why)
Burger’s test
- lifting patient foot up in the air -> foot will go white
- Sit patient with the legs down (side of the bed) ->
Toxins from anaerobic respiration (when foot was up) will vasodilate vessels in the foot & foot
goes really red ‘sunset foot’
Examples of trophic changes in PVD
- no hair at all
- veins will collapse down and imprint of filled vein left after that ‘venous scattering’
- swelling is typical if people have rest pain because that means a patient will sit all day with their foot hanging down
- shiny foot - skin starts to die off, nails unhealthy/malformation, ulcers form
What is the diagnostic Ix for PVD?
- Hx and Examination - KEY (as can diagnose, predict severity by these)
- scans - to plan surgical treatment ; not needed to diagnose PVD
* this is because the pattern of blocked arteries does not match superficial manifestations
What scan is a ‘gold standard’ for PVD?
CTA (CT angiography) - gold standard (CT of the whole body) with a dye injected into the vein and timed -> to highlight arterial tree
*good to look at arteries from the knee up as they are bigger; also dye will be white but Ca++ may be white as well, and plaques are filled with Ca so cannot be sure if it’s a plaque or dye)
