PVD Flashcards

1
Q

What is PVD

A

Peripheral arterial disease (PAD) is a major circulatory disorder characterised by arterial obstruction, leading to reduced blood supply and ischaemia in the lower limbs

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2
Q

Epidemiology of PVD

A
  • M>F
  • Prevalence increases with advancing age
  • Commonly caused by atherosclerosis and usually affects the aorta-iliac and infra-inguinal arteries
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3
Q

RFs for PVD

A
  • Diabetes mellitus
  • Hypercholesterolaemia
  • Hypertension
  • Chronic kidney disease
  • Age
  • Male
  • Smoking
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4
Q

What happens when muscle receives less oxygen?

A

becomes ischaemic, the cells release adenosine which affects nearby nerves, causing pain. Lactic acid production may also contribute to pain.

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5
Q

What are the 3 main patters of presentation?

A

intermittent claudication, critical limb ischaemia and acute limb-threatening ischaemia

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6
Q

What is intermittent claudication?

A
  • inadequate increase in skeletal muscle perfusion during exercise
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7
Q

What is acute limb-threatening ischaemia

A

most commonly caused by emboli, usually of cardiac origin, resulting in a sudden decrease in limb perfusion. Emboli tend to lodge at artery bifurcations or in areas where vessels abruptly narrow.

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8
Q

Fontaine classification

A

I - Asymptomatic - low ABPI (<0.9)
II- Intermittent claudication - aching or burning in muscles of leg
IIa- after more than 200m of walking pain
IIb - less than 200m of walking relieved with minutes on rest for II
III - Critical limb ischaemia - rest pain - dangling leg over egde of bed for pain relief - risk of limb losss
IV - Tissue loss: Ulceration or gangrene

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9
Q

Sites of claudication implies sites of disease

A
  • Common iliac:unilateral buttock
  • Common femoral:unilateral thigh
  • Superficial femoral:unilateral calf
  • Aortoiliac (Leriche syndrome)may cause the triad of:
    • Bilateral buttock and thigh claudication
    • Absent or decreased femoral pulses
    • Erectile dysfunction
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10
Q

Primary investigations

A
  • Ankle-brachial pressure index (ABPI): record systolic blood pressure with an appropriately sized cuff in both arms and in the posterior tibial, dorsalis pedis, and, where possible, peroneal arteries
  • Duplex ultrasound:first-line imaging, offering some information on the location and severity of stenosis.
  • Assessment of cardiovascular risk factors: ECG, FBC, U&E, random glucose or HbA1c, serum cholesterol and lipid profiles
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11
Q

Management of intermittent claudication

A
  • Exercise:
    • Can be supervised or unsupervised exercise programme
  • Management of cardiovascular risk factors: smoking cessation, HbA1c control, BP control, diet and weight management, lipid modification (statins), antiplatelet agents (e.g. clopidogrel)
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12
Q

Surgical intervention for intermittent claudication

A
  • Referral to a vascular surgeon is required if quality of life does not improve after a 3-month course of supervised exercise therapy
  • Endovascular procedurese.g. balloon dilatation (angioplasty), stents, and atherectomy
    • Performed on lesions that are deemed to be haemodynamically significant and stenosis has a reasonable likelihood of limiting perfusion to the distal limb
  • Bypass surgery: diverts blood around blocked artery
  • Consideration of naftidrofuryl oxalate: vasodilator
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13
Q

What is critical limb ischaemia

A

Critical limb ischaemia is defined as rest or night pain for greater than 2 weeks, with or without tissue loss such as ulceration.

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14
Q

RFs for critical limb ischaemia

A
  • Family history of vascular disease
  • Smoking
  • Sedentary lifestyle
  • Age
  • PVD
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15
Q

Signs of critical limb ischaemia

A
  • Non-healing ulcer or wound with shiny, hairless skin
  • Gangrene
  • Absent or diminished pulses in the legs or feet
  • Reactive hyperaemia:
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16
Q

Symptoms of critical limb ischaemia

A
  • Pain: a history of ‘aching’ intermittent leg claudication for 2 or more weeks
    • Restornight pain must be present
    • Patients often hang their legs out of bed at night to relieve the pain
  • Evidence of aortoiliac disease(Leriche syndrome)
  • Cool peripheries
17
Q

Primary investigations of critical limb ischaemia

A
  • Ankle-brachial pressure index (ABPI):significant collateral vessels may form in chronic limb ischaemia, resulting in ABPI results that are more difficult to interpret
    • >1.4= abnormally calcified vessels; false-negative often due to diabetes
    • 0.9-1.2= normal; does not exclude the diagnosis if clinically suspected
    • 0.5-0.9= claudication; mild to moderate arterial disease
    • <0.5= rest pain, ulceration, gangrene (critical limb ischaemia)
  • Duplex ultrasound:first-line imaging, offering information on the location and severity of stenosis
18
Q

Conservative management of critical limb ischaemia - only 20% of patients

A
  • Multidisciplinary team (MDT) referral: all patients should be referred to a vascular MDT unless inappropriate, such as palliative patients
  • Analgesia: paracetamol with either a weak or strong opioid (depending on pain level)
  • Supervised exercise programme:
19
Q

Revascularisation for critical limb ischaemia - 65%

A
  • Endovascular intervention:angioplasty or stenting is offered to 40% of patients and should be offered forshortocclusions
  • Bypass surgery:offered to 25% of patients; preferred forlongocclusions
  • Amputation:considered if revascularisation has been unsuccessful or is inappropriate
20
Q

Complications of critical limb ischaemia

A
  • Permanent limb weakness or pain:revascularise expediently to avoid this complication
  • Acute-on-chronic limb ischaemia: patients with longstanding peripheral arterial disease may develop acute limb ischaemia
  • Gangrene:occurs in the non-viable leg and usually requires amputation
21
Q

What is acute limb ischaemia

A

sudden decrease in perfusion due to arterial occlusion, and can result in rapid ischaemia

22
Q

RFs for acute limb ischaemia

A

Modifiable RFs - diabetes, smoking, HT, sedentary lifestyle
Non modifiable - FH of CA or PVD, Age older than 40

23
Q

Most common form of ALI?

A
  • Emboli followed by thrombosis
  • Emboli causes - AF, MI, Valvular vegetation
  • Most common site of emobolisation is femoral artery
24
Q

What is first to be affected in ALI

A

Nerves are the first to be affected, with irreversible damage after 6 hours. Muscles are more tolerant, with irreversible damage after 6-10 hours, whilst the skin is the last to show necrosis.

25
Q

6 Ps of ALI

A
  • Pain
  • Pallor
  • Pulselessness
  • Paresthesia
  • Perishingly cold
  • Paralysis
26
Q

Investigations for ALI

A
  • Contrast-enhanced CT angiogram:the most important pre-operative investigation to determine the precise vasculature -GS
  • Duplex ultrasound:first-line imaging, offering some information on the location and severity of stenosis
  • Ankle-brachial pressure index (ABPI)
27
Q

Rutherford classification

A
  • I: Viable/ Sensory present Motor present Arterial doppler present
  • IIA : Threatened/ Partial sensory loss (toes) Motor present Often absent flow Arterial doppler
  • IIIB: Threatened/ Partial loss (more than toes) Partial motor paralysis Often absent arterial doppler flow
  • III: Irreversible/ Profound loss of everything
28
Q

Initial management for ALI

A

IV unfractionated heparin (UFH): UFH has a shorter half-life than low-molecular-weight heparin (LMWH), making it an effective, more reversible pre-operative anticoagulant

29
Q

Definitive treatment for ALI

A

I - revascularise within 6-24 hours - catheter directed thrombolysis
IIA - Revasc within 6 hours - catheter directed thrombolysis or percutaneous thromboelectomy
IIB - Revasc within 6 hours - percutaneous or open thromboelectomy
III - amputation, palliation