Flashcards in Vascular disease Deck (28):
Name the ABI cut offs that suggest critical limb ischaemia, claudication and significant arterial lower limb disease respectively?
ABI less than 0.9 indicates PVD- arterial insufficiency
ABI 0.4-0.9 associated with claudication
ABI less than 0.4 indicates critical limb ischaemia
what is the main pathophysiology of PVD?
what drugs are used to manage claudication?
cliostazol- a peripheral vasodilating drug and aspirin/clopidogrel (an anti platelet drug)
what is the overall management of PVD? include medical management, lifestyle changes and surgical treatment options.
1. Cliostazol- a peripheral vasodilating drug is used for intermittent claudication
2. Anti-platelet drug like clopidegrel or aspirin for atherosclerosis
3. Consider Ace inhibitor for CV risk factor management
4. Regular supervised exercise
5. Management of other cardiovascular risk factors such DM, dyslipidaemia and HT
6. Cessation of smoking
Last resort if the above management is ineffective or progression to critical limb ischaemia is surgical intervention such as bypass, stenting, and endarterectomy.
what are some symptoms a patient may have that indicate critical limb ischaemia?
1. rest pain
2. Ischaemic ulceration
3. Gangrenous toes
Describe Buerger's test.
lift the lower limbs at approx. 45 degrees for 30-60 secs until pallor is established, then hang legs dependently over the edge of the bed at 90 degrees. Arterial insufficiency will cause the legs to return colour slowly, and then become hyperaemic. The lower the angle at which the legs become pale with lifting, the more severe the arterial disease is.
how might you ask a patient about rest pain?
Ask if they have ever woken up with severe pain in their legs at night, and were required to hang their legs out bed to relieve the pain. Ask if their sleep has been disturbed due to the problem. Ask if they have ever had to sleep in a chair so that their legs are hanging down.
what are some other systems you need to screen for when you are presented with a patient who has PVD?
screen for CV risk factors, ask if there was a previous MI or TIA or stroke in patient's history. Ask about AF, chest pain, breathlessness etc
what is the normal physiology of venous return in the lower limbs?
When you walk, the calf muscles contract around the deep veins.
When this happens the valves snap close and you should have an augmented backflow of blood back to the right atrium.
When the calf muscles relax, the veins should be able to fill again, and move from superficial to deep
what is the white cell trapping hypothesis in venous insufficiency? Describe process that may lead to incompetent valves.
One way valves are present in the perforating veins leading to the deep veins. These valves can become incompetent though infection, direct trauma/damage by DVT or if they already have congenital defects.
Once incompetent, venous hypertension may occur as there is less blood returning to the heart and more blood pooling in the venous system.
Increased venous stasis can cause WBC trapping in capillaries, leading to WBC activation. Factors released by WBC further damage the valves.
what are the risk factors for venous insufficiency?
1. Hx of DVT- damages the valves
2. Pregnancy- hormones damage the valves
3. Obesity/sedentary lifestyle- reduces calf muscle action
and 4. Smoking
how might we determine the incompetent valve on physical examination?
tredenlenberg test. Place a torniquet or your finger on the saphenofemoral junction in the groin. Get the patient to stand up and look for filling of veins distal to the occlude saphenofemoral junction. If there is still rapid filling then the incompetent valve is distal to the saphenofemoral junction
what causes lipodermatosclerosis?
Chronic venous insufficiency leads to fat necrosis and ulceration in the distal part of the leg, and also swelling in the proximal part of the leg. This results in inverted champagne bottles looking legs.
what causes dark pigmentation in venous stained legs?
define an aneurysm.
Focal dilatation of the artery; 1.25 greater diameter than adjacent normal artery. Dilation due to weakness in elastin and collagen in the adventitia and media.
what is the natural history of an aneurysm?
Natural history= gradual expansion and then it gets to a certain size and bursts.
what are the risk factors for an abdominal aortic aneurysm?
and Being male (60 years +)
what is the general management of an UNRUPTURED AAA?
continued monitoring until the aneurysm reaches 5.5 cm in diameter. control of BP
what are the surgical options for a ruptured AAA?
2 options; open AAA surgery with grafts or an endovascular stent option
what are the risk factors for aortic dissection?
• Marfan's or other connective tissue disorder
• Familial thorax aneurysm
• Chest trauma
Iatrogenic + previous aortic surgeries
what are type A and type B aortic dissections?
The Stanford classification specifies two types, as follows:
• Type A - The ascending aorta is involved (DeBakey types I and II)
• Type B - The descending aorta is involved (DeBakey type III)
This system also helps delineate treatment. Type A dissections usually must be treated surgically, whereas type B dissections are managed medically under most conditions
outline management for type A aortic dissection.
Type A dissections require emergency surgery to replace the ascending aorta- surgical management
outline management for type B aortic dissection
Medical management to reduce MAP:
1. beta blockers
2. calcium channel blockers
Surgical repair sometimes required
what is a pseudo aneurysm? what is its other name?
False aneurysm. this is usually the result of trauma to an artery (e.g. from catheterisation) which then causes blood to leak out. The blood runs alongside the vessel, trapped by the adventitia. This makes it more susceptible to rupture than a true aneurysm, in which there is focal dilation of all three layers of the wall.
what sort of blood abnormality can be associated with chug strauss syndrome?
What are the two types of varicose veins?
1. primary- Superficial valve or perforating veins incompetence
2. secondary- due to recanalisation from previous DVT. Deep valves incompetence.
what are the 3 components of venous insufficiency?
vein not patent
calf muscle pump failure