Vascular Disease Flashcards

1
Q

what causes peripheral vascular disease and where does it usually affect?

A

atherosclerosis

affecting aorta-iliac or infrainguinal arteries

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2
Q

what is the prevalence of peripheral vascular disease and what is the usual consequence of the condition?

A

7% middle aged men
4.5% middle aged women
these patients are more likely to die of MI or stroke rather than losing a leg

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3
Q

what classification system is used to assess chronic limb ischaemia

A

fontaine classification

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4
Q

what are the stages in the fontaine classification of chronic limb ischaemia?

A

I - asymptomatic
II - intermittent claudication
III - rest pain/nocturnal pain
IV - necrosis/ gangrene

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5
Q

what is intermittent claudication?

A

cramping muscular pain, which is brought on by exertion, relieved by rest and is reproducible by walking that distance again

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6
Q

what is aorto-iliac disease?

A

exertional discomfort mainly in the calf which is relieved by rest

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7
Q

what are the signs of peripheral vascular disease?

A

lower limbs are cold with dry skin and lack of hair
pulses may be diminished or absent
ulceration may occur in association with dark discolouration of toes or gangrene
examine abdomen for possible aneurysm

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8
Q

what is the definition of peripheral vascular disease?

A

More correctly known as peripheral arterial disease (PAD), this refers to disease of the peripheral arteries (i.e. not the coronary or brain arteries) which causes narrowing (stenosis) or occlusion and affects the blood supply to the limbs (generally speaking to the lower limbs)

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9
Q

what can peripheral vascular disease a major cause of?

A

acute and chronic limb ischaemia

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10
Q

what is chronic limb ischaemia classified as?

A

intermittent claudication or critical limb ischaemia

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11
Q

when does PAD become critical ischaemia and what action must be taken?

A

when it reaches the level when it threatens the loss of limb

patient generally requires intervention such as open surgery or endovascular revascularisation to salvage the limb

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12
Q

what is the pathogenesis of atherosclerosis?

A
  • formation of fatty streak
  • inflammation and accumulation of foam cell macrophages
  • fibrosis and progressive luminal narrowing
  • plaque rupture or ulceration
  • thrombosis or thromboembolism
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13
Q

what are the non-modifiable risk factors for the development of peripheral vascular disease?

A

age
sex (men more than women)
family history (genetics)
race

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14
Q

what are the modifiable risk factors for the development of peripheral vascular disease?

A
smoking
hyperlipidaemia 
hypertension
diabetes
sedentary lifestyle
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15
Q

what are the aspects of the examination of a patient with PAD?

A
  • inspection-(both legs, pallor, mottling, skin change, loss of hair, ulcers, gangrene)
  • palpation (temp, capillary refill time. pulses)
  • auscultate (femoral bruit)
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16
Q

what is Buerger’s test?

A

before doing this check for back/hip pain.
reported as the angle at which the leg becomes pale when you elevate it against gravity (healthy limbs don’t do this)
swing the patient’s leg over the side and watch for a ‘sunset foot’ (arteriolar vasodilation with foot reperfusion)

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17
Q

what is ankle-brachial pressure index?

A

use hand held doppler and sphygmomanometer.

highest pedal pressure in each limb is divided by the highest brachial pressure

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18
Q

when may ankle bracchial pressure index not be reliable?

A

patients with diabetes or CKD often have calcified arteries making them hard to compress and give falsely high reading.

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19
Q

what are some of the differentials for peripheral vascular disease?

A
  • spinal canal claudication (pulses present)
  • osteoarthritis hip/knee (knee pain at rest)
  • peripheral neuropathy (numbness and tingling)
  • popliteal artery entrapment (young patients may have normal pulses)
  • venous claudication (pain on walking with history of DVT)
  • fibromuscular dysplasia
  • Buerger’s disease (young males, heavy smokers)
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20
Q

What investigations should be performed in a patient with peripheral vascular disease?

A
  • examine pulses

- ABPI-severity of disease

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21
Q

What does an ABPI of 0.5-0.9 suggest?

A

intermittent claudication

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22
Q

what does an ABPI of <0.5 suggest?

A

critical limb ischaemia

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23
Q

what are the types of diagnostic imaging used to detect and assess severity of peripheral vascular disease?

A
  • digital subtraction angiography
  • duplex ultrasound
  • 3D contrast enhanced magnetic resonance angiography
  • computed tomography and angiography
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24
Q

how is digital subtraction angiography used to investigate peripheral vascular disease?

A

arterial map but requires peripheral artery cannulation and exposes patient to iodinated contrast so used immediately before intervention

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25
Q

how is duplex ultrasound using B mode ultrasound and colour doppler used to investigate peripheral vascular disease?

A

accurate anatomical map of the lower limbs with high sensitivity and specificity compared to angiography. operator dependent

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26
Q

how is 3D contrast enhanced magnetic resonance angiography used to investigate peripheral vascular disease?

A

imaging of both legs with simple contrast injection without exposure to ionising radiation
high sensitivity and specificity

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27
Q

how is computed tomography and angiography used to investigate peripheral vascular diseas?

A

effective alternative to MRA but calcification can obscure stenosis
requires ionising contrast media

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28
Q

what is rest pain?

A

severe unremitting pain in the foot which stops a patient sleeping. it is partially relieved by dangling the foot over the end of the bed or standing on cold floor

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29
Q

what is the cause of intermittent claudication?

A

inadequate oxygen delivery to the muscles

angina is intermittent claudication of the cardiac muscle

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30
Q

what is critical limb ischaemia?

A

when chronic limb ischaemia threatens the loss of limb

ischaemic rest pain for more than 2 weeks despite analgesia or the presence of tissue loss (ulcers/gangrene)

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31
Q

what is leriche syndrome?

A

type of perpheral arterial disease

aortoiliac occlusive disease

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32
Q

what is the medical management of peripheral vascular disease?

A
  • risk factor management
  • smoking cessation
  • chiropodist care for those with diabetes mellitus
  • treat hypercholesterolaemia (if over 3.5mmol/L treat with statin)
  • low dose aspirin
  • exercise and avoid obesity
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33
Q

when is surgical vascular intervention usually indicated in claudication?

A
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34
Q

when is percutaneous transluinal angioplasty used for claudication?

A

first option and carried out via catheter inserted into femoral artery

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35
Q

when can arterial stents be used for claudication?

A

used in recurrent iliac disease and drug elating stentsallowing long term latency are being used

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36
Q

how can bypass procedures be performed in treatment of claudication?

A

using dacron, polytetrafluroethlene (PTFE) or autologous veins
bypasses to dital vessels have poorer long term potencies

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37
Q

what surgial treatment needs to be given in a patient with severe ischaemia with unreconstructable arterial disease

A

amputation (70% below knee)

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38
Q

what is the pharmacological management of claudication?

A
  • cilostazol
  • naftidrofury
  • oxpentifylline, inositol nicotinate and cinnarizine
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39
Q

what is the mechanism of action of cilostazol,what is it used to treat and what is a typical dose?

A

phosphodiesterase III inhibitor increases level of cyclic AMP and cause vasodilation and reversible inhibits platelet aggregation

claudication

100mg daily can increase walking distance in patients with short distance claudication

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40
Q

what is the mechanism of action of Naftidrofuryl, what is it used to treat and what dose is typically given?

A

vasodilator agent inhibiting vascular and platelet 5-HT2 receptors reducing lactic acid levels

claudication

1-200mg 3 times a day increase walking distance and improve quality of life

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41
Q

what drugs are not currently recommended for treatment of claudication

A

Oxpentifylline, inositol nicotinate and cinnarizine

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42
Q

what is the risk of amputation in a patient with intermittent claudication?

A

1-3%

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43
Q

what percentage of patients with intermittent claudication will progress to chronic limb ischaemia?

A

20-25%

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44
Q

what treatment should be given to patients with peripheral arterial disease?

A
  • antiplatelet
  • statin (atorvastatin 80mg OD)
  • BP management
  • diabetic control
  • smoking cessation
  • exercise programmes
  • naftidrofuryl
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45
Q

what is the management of critical limb ischaemia?

A
  • refer to vascular surgeon
  • limb revascularisation
  • vascular MDT
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46
Q

what are the options for limb revascularisation?

A
  • open surgical procedure (bypass, endartectomy)
  • andovascular procedure (angioplasty, stenting)
  • hybrid procedure
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47
Q

describe open surgical procedures used to treat critical limb ischaemia?

A
bypass, endarterectomy
autologous vein (eg great saphenous vein) is preferred to prosthetic (dacron/PTFE) graft wherever possible, particularly for below the knee disease
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48
Q

describe endovascular procedure?

A

angioplasty, stenting

technology is moving very quickly, various drug coated balloons, drug eluting stents etc

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49
Q

what is a hybrid approach in management of critical limb ischaemia?

A

combination of both open and endovascular surgical techniques

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50
Q

what is critical limb ischaemia?

A

end of the spectrum of chronic limb ischaemia
usually occurs after history of intermittent claudication but can happen in patients who are immobile without prior intermittent claudication
the limb is at risk

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51
Q

what is the core clinical feature of critical limb ischaemia?

A
  • rest pain
  • pain felt in toes/forefoot as this is the most distal site
  • pain often wakes patient up at night due to loss of gravity in helping foot perfusion
  • patients typically hang their legs over the side of the bed of sleep in chairs
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52
Q

what is percutaneous transluminal angiography/angioplasty?

A
  • an arterial puncture seldinger technique places a sheat and catheter within the arterial tree. injection of contrast gives a ‘roadmap’ of the vessels
  • digital subtraction angiography (removes all backgrounf structures, such as bone)
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53
Q

what are the risks and benefits of using percutaneous transluminal angioplasty?

A
  • gold standard
  • radiation dose must be considered
  • uses iodinated contrast-renal impairment (CO2 as alternative)
  • risk of damage to vessels, bleeding, emboli, dissection, pseudoaneurysm
  • endovascular procedures such as balloon angioplasty or stenting can be performed at the same time
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54
Q

what are the indications for percutaneous transluminal angioplasty and arterial reconstruciton surgery?

A
  • Angina patients
  • Acute myocardial infarction
  • Intermittent claudication that interferes with lifestyle and/or ability to work
  • Non-healing wounds
  • Chronic limb ischaemia
  • Infection/ gangrene
  • These all depend on the extent of disease, how salvageable the limb is (in the case of peripheral arterial disease), how significant the procedure would be to the patient’s quality of life and how fit the patient is to undergo surgery
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55
Q

describe the proces of percutaneous transluminal angioplasty?

A
  • PTA describes the process of fixing the vessel wall; it involved passing a small plastic tube (with a balloon in a stent at the end of it) through an artery in the leg. It takes about an hour and a half.
  • Once the wire reaches the blockage, the balloon is inflated to expand the vessel. This then expands the stent (which is ultimately like chicken wire) which stays in the vessel to keep it so that blood can flow through it.
  • X-rays will also be taken at the same time to make sure that the blockage is opened; once it is, the plastic tube can be removed
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56
Q

what are the possible risks of percutaneous transluminal angioplasty and arterial reconstruction surgery?

A
  • Haemorrhage
  • Wound infection
  • Nerve injury
  • Thrombosis
  • MI
  • Arrhythmias
  • Leg oedema
  • Pulmonary oedema
  • Bleeding/ clot at the catheter insertion site
  • Restenosis = blockage in blood vessels after procedure
  • There is also risk of rupturing the vessel, though this will be considered and reflected in the type of stent used. Burr stent has little holes in whereas a covered stent has no holes, allowing it to patch up ruptured vessels.
  • Most patients go home the next day.
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57
Q

what are the characteristics of venous ulcers?

A
  • painful-relieved by elevation
  • commonly affect gaiter (perimalleolar) area
  • ulcer is large, shallow, and irregular with exudative and granulating base
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58
Q

what are the associated features of venous ulcers?

A
  • warm skin
  • normal peripheral pulses
  • varicose veins
  • leg oedema
  • haemosiderin pigmentation (leaching of iron from blood into soft tissues)
  • venous eczema
  • lipodermatosclerosis and atrophie blanche
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59
Q

what are the risk factors for developing venous ulcers?

A
  • superficial venous incompetence (varicose veins)
  • previous DVT
  • phlebitis
  • previous fracture, trauma or surgery to leg
  • family history
  • symptoms of venous incompetence including leg pain, itching, swelling, pigmentation, eczema and ulceration
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60
Q

Describe the characteristics of arterial ulcers?

A
  • painful and worse when legs are elevated
  • most commonly affect pressure and trauma sites (pretibial and supra-malleolar) and distal points such as toes
  • lesion is typically small, deep, sharply defined (punched out appearance with time) often with necrotic base
  • represent advanced PAD critical ischaemia
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61
Q

what are the associated features with arterial ulcers?

A
  • cold skin
  • weak or absent peripheral pulses
  • shiny pale skin
  • loss of hair
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62
Q

what are the risk factors associated with developing arterial leg ulcers?

A
  • peripheral arterial disease
  • coronary heart disease
  • history of stroke or transient ischaemic attack
  • diabetes mellitus
  • obesity and immobility
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63
Q

what are mixed ulcers?

A

arterial and venous
shallow, irregular exudative gaiter area ulcers (venous) with smaller punched out deep ulcers on dorsum of the feet (arterial)

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64
Q

what are the characteristics of diabetic ulcers?

A
  • usually foot ulcer rather than leg
  • most commonly affects pressure sites: soles, heels, toes, metatarsal heads
  • painless with absent sensation
  • peripheral neuropathy secondary to diabetes
  • lesion usually punched out, variable size and depth and granulating base
  • many diabetics have coexisting PAD so may be neuroischaemic ulcer
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65
Q

what are the associated features seen in a patent with diabetic ulcers?

A

warm skin
peripheral neuropathy
normal peripheral pulses

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66
Q

what are the causes of venous ulcers?

A
  • Most due to from chronic venous insufficiency (valves incompetent -> reflux -> pooling of blood in lower limb -> sustained venous hypertension)
  • Others due to capillary fibrin cuff or leucocyte sequestration
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67
Q

what are the causes of arterial ulcers?

A

-Due to reduced arterial blood supply to the lower limb -> hypoxia & tissue damage.
Most common cause = atherosclerosis
-Other causes include diabetes (which involves poor quality endothelium & microvascular damage, worsening wound healing), vasculitis, thalassaemia & SCD

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68
Q

generally speaking what are leg ulcers?

A

a breach in epithelial integrity of the skin

  • occur between the knee and malleoli
  • chronic when it has been present for more than 6 weeks
  • > 90% of chronic leg ulcers are vascular
  • chronic venous hypertension is the primary cause of 70% of leg ulcers
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69
Q

what is the prevalence of chronic venous ulceration?

A

0.5%-1%

in patients over 80 it rises to 3%

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70
Q

what is the difference in prevalence in different socioeconomic groups?

A

no difference in prevelance between socioeconomic classes but people in lower social class take longer to heal

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71
Q

how much of NHS budget does leg ulcers make up?

A

2%

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72
Q

what are the investigations involved in recurrent leg ulcers?

A
  • based on underlying aetiology
  • ABPI to exclude arterial disease
  • venous-venous duplex ultrasound to look for venous incompetence
  • arterial-arterial imaging-usually multilevel disesae
  • diabetic-assess sensation-monofilament test. check HBA1C. foot X-rays for osteomyelitis. arterial imaging as for PAD if neuroischaemia
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73
Q

how do you interpret the ABPI score?

A
  • > 1.3: generally indicates calcified, stiff arteries. May be seen with advanced age, diabetes, or chronic kidney disease
  • 0.9 – 1.29: normal
  • 0.8 – 0.9: borderline-often requires additional tests such as exercise ABPI (treadmill)
  • <0.8: PAD likely
  • <0.5: indicates severe PAD and should be referred urgently
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74
Q

what is the management for diabetic face ulcers?

A
  • Need an MDT approach
  • Podiatry and orthotists – debridement, offloading/pressure relieving footwear
  • Diabetology – management of diabetes
  • Vascular surgeon – improving perfusion, controlling infection soft tissue, osteomyelitis
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75
Q

what is the management for mixed venous/arterial ulcers?

A

Initially cautious modified strength compression with close observation (revascularization if necessary)

76
Q

what is the management for arterial ulcers?

A

vascular reconstruction

77
Q

what is the management for venous ulcers?

A
If ABPI >0.8 apply compression bandaging or class 2-3 compression hosiery 
If venous duplex shows superficial venous incompetence, offer treatment
78
Q

what affects the prognosis of diabetic foot ulcers?

A

Depends on multiple factors including coexisting PAD, diabetic control, compliance with offloading, infection

79
Q

what is the prognosis for mixed arterial/venous ulcers?

A

2/3 healed at 6 months using modified compression therapy

Revascularisation was performed in only 10% of these patients

80
Q

what is the prognosis for arterial ulcers?

A

Ulceration due to severe arterial disease has a healing rate of less than ½
This is despite aggressive policy of revscularisation as these patients are often unfit or unsuitable for arterial intervention

81
Q

what is the prognosis for venous ulcers?

A

Healing rates from between 1/3 to ¾ at 6 months

Upto 20% of chronic venous ulcers may remain unhealed after 1 year, despite compression bandaging

82
Q

what is the role of dulpex ultrasound?

A
  • A combination of B-mode and doppler ultrasound, enabling analysis of arterial flow and the pulse waveform.
  • Remember “Poiseuille’s law” - a decrease in the radius of a vessel results in an increase in flow rate to maintain the same pressure
  • Changes in flow velocities and doppler waveform can be used to accurately estimate the degree of arterial stenosis
  • Non-invasive, good for imaging limbs, carotids
83
Q

what is acute limb ishcaemia?

A

quickly developing or sudden decrease in limb perfusion, producing new or worsening symptoms and sings that threaten limb viability. The incidence rate is 1 in 12,000 per year

84
Q

what are the symptoms of acute limb ischaemia?

A
  • sudden onset of painful, numb, weak, cold limb
  • Presentation may differ between thrombosis and embolism yet it doesn’t effect clinical management
  • Atherosclerosis is predominant underlying cause and can manifest in thrombotic and embolic presentations
85
Q

what are the signs of acute limb ischaemia?

A

6 Ps

Pain
Paresthesia
Paralysis 
Pallor 
Pulselessness 
Perishingly cold 
Pistol shot (sudden onset)
86
Q

what is a sign of progression of ischaemia?

A

Skin mottling and calf tenderness

87
Q

what are the late signs of ischaemia?

A

Fixed mottling and loss of sensorimotor function

88
Q

what are the thrombotic mechanisms leading to acute limb ischaemia?

A
rupture of atherosclerotic plaque
bypass graft thrombosis 
prothrombotic eg malignancy
arteritis 
infection
states of low flow eg shock
89
Q

what are the embolic causes of acute limb ischaemia?

A
atherosclerosis 
mural thrombus 
atrial fibrillation
abdominal aortic aneurysm 
bacterial endocarditis
cardiac tumour
90
Q

what are the rare causes of acute limb ischaemia?

A

compartment syndrome
dissection
trauma

91
Q

what is the prognosis for acute limb ischaemia?

A

Poor prognosis especially if delayed diagnosis

30 day mortality is upto 30% (mainly due to cardiac disease)

92
Q

how quickly is treatment needed in a patient with acute limb ischaemia?

A

Once the patient is in acute limb ischaemia, it is only a matter of hours (approx. 6-12) before the tissue supplied by that artery dies.

93
Q

what determines the type and urgency of acute limb ischaemia?

A

Pulses – arterial pulses can be palpated; arterial and venous can be assessed by Doppler

Sensation – testing neuropathy in the lower limb

Motor function – can the patient move his/ her toes? indicates if there is blood supply to the region

94
Q

what classification system is used to assess acute limb ischaemia and what are the categories?

A

rutherford classification
I = viable
II = threatened (IIa = marginally. IIb = immediately)
III = irreversible

95
Q

what is the prognosis for acute limb ischaemia category I?

A

not immediately threatened

96
Q

what is the prognosis for acute limb ischaemia category IIa?

A

salvageable if promptly treated

97
Q

what is the prognosis for acute limb ischaemia category IIb?

A

salvageable with immediate revascularisation

98
Q

what is the prognosis for acute limb ischaemia category III?

A

major tissue loss or permanent nerve damage inevitable

99
Q

what are the findings and doppler signals found for category I acute limb ischaemia?

A

no sensory loss
no muscle weakness
audible artery
audible vein

100
Q

what are the findings and doppler signals found for category IIa acute limb ischaemia?

A

minimal sensory loss
no muscle weakness
often inaudible artery
audible vein

101
Q

what are the findings and doppler signals found for category IIb acute limb ischaemia?

A

sensory loss in more than toes
mild to moderate muscle weakness
usually inaudible artery
audible vein

102
Q

what are the findings and doppler signals found for category III acute limb ischaemia?

A

profound anesthesia
profound paralysis
inaudible artery
inaudible vein

103
Q

what are the emergency investigations of a patient with acute limb ischaemia?

A
  • Full cardiovascular examination
  • Assess sensory and motor function of leg
  • Assess for muscle tenderness=late sign

Bedside tests

  • Handheld doppler to detect arterial and venous flow
  • ABPI (if tolerated but may be too painful)
  • ECG-arrythmia may precipitate embolic event. These patients are often critically unwell

Bloods

  • FBC
  • U&E
  • Coag
  • Group and save
  • Creatine kinase (marker of rhabdomyolysis)
104
Q

what are the initial medical measures that should be taken in a patient with acute limb ischaemia?

A

oxygen, IV fluids and analgesia

5000 units of unfractionated heparin (+/- heparin infusion if not immediately going to theatre

105
Q

what are the interventions for patient with acute limb ischaemia?

A

Revascularisation
-Open surgery: embolectomy or arterial bypass

-Endovascular
——PTA/stenting
——Catheter directed thrombolysis (Less invasive, however contraindicated in many patients,
Trauma, recent GI bleed, stroke within 2 months)

-Amputation if the limb isn’t salvageable (Palliation may be more appropriate if end of live care and a frail patient)

106
Q

what is chronic limb ischaemia?

A

Also known as critical limb ischaemia, it’s advanced peripheral vascular disease.
Arterial obstruction is so severe that blood flow to the extremities is insufficient at rest.
‘The [unstable angina to NSTEMI] of the lower limb’

107
Q

what are the characteristics of chronic limb ischaemia?

A

Pain at rest – burning sensation, tends to be in the skin of the fore foot, raising it makes it worse, hanging it off the side of the bed/ sleeping in a chair makes it better; indicates ischaemia of the skin & underlying tissue

Arterial ulceration – marker of reduced blood supply to the lower limb; can be a result of trauma/ thrombosis (acute) as well as atherosclerosis (most common)

Gangrene – sign of tissue necrosis

Buerger’s test – assesses whether peripheral arterial pressure is high enough to overcome the effects of gravity. In patiens with chronic limb ischaemia, it isn’t enough -> ischaemia -> pain

The poorer the arterial supply, the smaller the angle required to raise the legs to the point of ischaemia.

108
Q

what is gangrene?

A
cell necrosis; can be dry or wet (there isn’t a pathological difference; wet would be caused by spreading infection)
Dark red = deoxygenated blood
Swollen
Dry
Black toes; tissue death

Known as ‘sunset foot’; such a poor blood supply that unless you do something, that leg will be lost (name comes from the concept of the sun going down)

109
Q

what are the NICE guidelines for the management of peripheral arterial disease?

A

Assessment by vascular multidisciplinary team before making treatment decisions

Pain management – paracetamol & either weak or strong opioids depending on severity of pain in the patient. Where opioids are prescribed, laxatives and antiemetics may also be required.

Imaging – for if revascularisation is being considered

Major amputation – where the limb has no salvageable blood supply/ the patient isn’t fit for revascularisation surgery.

110
Q

what palliative support is given to patients with intractable limb ischaemia?

A

Explanation of the causes of their symptoms and severity of disease
Explanation of the risks of limb loss and cardiovascular events associated with peripheral arterial disease
Encouraging improvement of modifiable risk factors (the same ones for CVD)
Information on how the patient can access support for dealing with depression and anxiety

111
Q

what is the reason for most amputations in the NHS?

A

treat complications of PAD or diabetes

112
Q

what are the indications for limb amputation?

A

Trauma and military injuries-most common cause worldwide especially in young men
Neoplasm
Venous ulcers
Congenital deformity
Chronic pain
Neurological injury causing non-functional limb

113
Q

what are minor amputations?

A

Transmetatarsal (plus various less common midfoot/hindfoot/ankle amputations)

114
Q

what are major amputations?

A

below knee amputation

above knee amputations

115
Q

what is the pre-op management needed in a patient before amputation?

A

Select appropriate level of amputation

  • Try to salvage as much of limb as possible whilst also eliminating problem, enabling good healing and long-term function
  • Ambulating with above knee prosthesis requires significantly greater energy expenditure than that required for below knee (which is best for patients rehabilitation)

Optimisation of existing co-morbidities: diabetes, cardiovascular, respiratory

Psychological impact considered

Social impact considered-home visits etc

116
Q

what is the post op management for a patient after amputation?

A

Psychological impact considered

Risk of infection, ischaemia, prevention of stump trauma, pressure injury

Social input and home adaptations

Physiotherapy

Phantom limb sensation/pain

Stump modelling, prosthesis fitting and ambulation
Significant recent improvements in prosthetic technologies
In part due to a major drive in research and development after military injuries

117
Q

what is the prognosis in patients following amputation?

A

Major amputation typically reflects ‘end stage’ PAD
For UK vascular patients, in hospital mortality is 6.7% for BKA and nearly double (12.4%) for AKA
Following major amputation, patients with PAD have a 31% 5 year survival rate
Amputees may develop pathologies as a result of unnatural gait through the use of prosthetics (eg hip arthritis)
Risk of sedentary lifestyle, many elderly PAD patients fail to be fully ambulant

118
Q

how does blood in deep veins return to the heart?

A

pressure generated by calf muscles

119
Q

how much of venous return from the legs is via the deep veins?

A

80%

120
Q

describe the normal physiology of valves in the legs?

A

Blood collected from superficial venous capillaries is directed upward and inward via one-way valves into superficial veins
These in turn drain via junctions and perforator veins, which pass through muscular fascia into deeper veins
Valves prevent retrograde flow (reflux)

121
Q

what contributes to pathology of the lower limb

A

Complex interplay of factors results in venous incompetence
Unlike deep veins which are thicker walled and confined by fascia, superficial veins cannot withstand high pressure and eventually become dilated and tortuous
The pathological processes are incompletely understood but appear to be inflammatory

122
Q

what is the epidemiology of venous disease of the lower limb?

A

Superficial venous incompetence is common
Prevalence = 30%
Men = women in most epidemiological studies (more women present with symptoms
35000 varicose vein interventions per year in NHS(80% of these are done in women

123
Q

what are the risk factors for venous disease of the lower limb?

A

Obesity
Increasing age
Family history/genetics
Pregnancy (hormonal factors increase laxity of venous walls and valves

124
Q

what are the symptoms of venous disease of the lower limb?

A

Significant cause of morbidity
Itching, aching discomfort and heaviness of the legs
Leg swelling
“Restless” legs
Symptoms typically worse after prolonged standing / towards end of day
Bleeding varicosities (typically after minor trauma)
(Cosmetic concerns)

125
Q

what aggrevating factors may lead to venous disease of the lower limb?

A

occupation: prolonged standing, lifting e.g. factory production lines etc
pregnancy
hormonal changes – endogenous or exogenous
menstruation

126
Q

how can you identify varicose veins on examination?

A

Varicose veins will typically empty when lying down or with application of pressure, and then refill when pressure is released or patient stands up

127
Q

describe great saphenous vein varicosities?

A

Great saphenous vein varicosities may run the whole length of the leg and are generally distributed medially

128
Q

describe varicosities of small saphenous veins?

A

Varicosities of the small saphenous vein are seen below the knee and are distributed posterolaterally

129
Q

what skin changes would be suggestive of advanced venous insuficiency?

A

(healed) ulcers, lipodermatosclerosis, haemosiderin pigmentation, telangiectasia or eczema / atrophie blanche.

130
Q

what is the CEAP classification system?

A
The C.E.A.P. Classification for venous disease is a method of objectively classifying patients according to the severity of their presentation. 
CEAP stands for:
Clinical
aEtiologic,
Anatomic
Pathophysiologic
131
Q

describe the C part of the CEAP classification system?

A

C0: No visible or palpable signs of venous disease
C1: Telangiectasia or reticular veins
C2: Varicose veins
C3: Oedema
C4a: Eczema or Pigmentation (haemosiderin)
C4b: Lipodermatosclerosis or atrophie blanche
C5: Healed venous ulcer
C6: Active venous ulcer

132
Q

when should patients with venous disease of the lower limb be referred to vascular service?

A

Symptomatic varicose veins (primary or recurrent).
Lower-limb skin changes, such as pigmentation or eczema, thought to be caused by chronic venous insufficiency.
Superficial vein thrombosis (characterised by the appearance of hard, painful veins) and suspected venous incompetence.
A venous ulcer (a break in the skin below the knee that has not healed within 2 weeks).
A healed venous leg ulcer.

133
Q

what investigations would be performed in a patient with lower limb venous disease?

A
Duplex ultrasound (combination of Doppler and B-mode ultrasound) is the gold standard, with a high sensitivity and specificity
Assessment of all deep &amp; superficial veins, junctions &amp; perforators &amp; assessment of blood flow/ reflux
134
Q

what are the treatment options for patients with venous disease of the lower limb?

A

endovenous thermal ablation

ultrasound guided foam sclerotherapy

conventional surgery such as junctional ligation, stripping and avulsions

135
Q

describe endovenous thermal ablation in the treatment of venous disease of the lower limb?

A

ablation (laser or radiofrequency) involves sealing the lumen of the incompetent vein by delivering thermal energy via a catheter under ultrasound guidance
This is the NEW gold-standard treatment
Should be offered as 1st-line treatment

136
Q

describe ultrasound guided foam sclerotherapy in the treatment of venous disease of the lower limb?

A

This is recommended if endothermal ablation is unsuitable. It involves injection of a sclerosant chemical into the veins.
Offered as 2nd line treatment to patients unsuitable for Thermal Ablation

137
Q

describe the role of conventional surgery in the treatment of venous disease of the lower limb?

A

This is the OLD gold-standard treatment

3rd-line option if the above treatments not feasible

138
Q

what is the mechanism of action of endovenous thermal ablation?

A

Thermal injury to venous endothelium
Luminal obliteration
Contraction & fibrosis

139
Q

what are the features of endovenous thermal ablation?

A

Performed in NHS since 2004
Daycase procedure
Walk-in, walk-out
Local anaesthetic
Fewer complications compared to conventional surgery
Lower recurrence rates compared to conventional surgery

140
Q

describe the process of ultrasound guided foam sclerotherapy?

A
Injection of the vein with a sclerosant chemical foam
Mechanism of action:
Chemical injury to venous endothelium
→ Luminal obliteration
→  Contraction &amp; fibrosis
141
Q

what are the features of ultrasound guided foam sclerotherapy?

A

Daycase procedure, very well tolerated
Walk-in, walk-out
Local anaesthetic
Higher risk of DVT than surgery or EVTA
Can cause transient migraine/ visual aura (bubbles in circulation)
Higher failure and recurrence rates than EVTA / surgery

142
Q

describe avulsion of varicosities?

A

Avulsion of the varicosities through 2mm stab incisions
Features:
General anaesthetic procedure
Daycase if patient fit, may require overnight stay
Risks include wound infection, DVT/PE,
Recurrence approx 35% at 5 years
Low patient satisfaction
Often delayed return to work/ normal activities

143
Q

what is the prognosis for patients with venous disease of the lower limb?

A

Untreated, superficial venous incompetence tends to progress over time
Patients with significant reflux are prone to develop venous skin changes and / or ulceration.
The rate of progression from untreated C2 to higher disease severity is not well studied, but is probably around 5% per year
Many elderly patients with venous ulceration have had prior uncomplicated varicose veins for 10-20 years
Rate of clinical recurrence of treated varicose veins at 3-5 years is approximately 20% (not necessarily symptomatic)
Studies suggest a 90-98% occlusion with endothermal ablation after 2 years.

144
Q

what is an aneurysm?

A

a permanent, focal dilation of an artery with at least a 50% increase in diameter compared to normal

145
Q

describe the features of abdominal aortic aneurysm?

A

Anteroposterior diameter >3cm in intra-renal abdominal aorta
Highest incidence is in Caucasian men aged >65 years 5%
The risk of rupture increase exponentially with increasing size (<1% per annum below 5.5cm)
There is a screening programme in place in the UK NHS: the NAAASP
If aneurysm detected, surveillance scans offered, with frequency based on size and rate of growth of aneurysm
AAA may be found incidentally on imaging abdomen for other reasons
Should be referred to vascular service and follow same pathways

146
Q

what is the prevalence of AAA?

A

Prevalence four to five times higher in males than females so not cost-effective to screen women

147
Q

what is the aetiology of AAA?

A

Atherosclerosis is the predominant cause
Rare causes include infection (‘mycotic aneurysm’), connective tissue disorders (marfans and ehlers-danlos), arteritis
Diabetes appears to have a relative protective effect against development and progression but unknown why

148
Q

what are the non modifiable risk factors for AAA?

A

age
sex
family history

149
Q

what are the modifiable risk factors for AAA?

A

smoking
hypercholesterolaemia
hypertension

150
Q

What is NAAASP?

A

national abdominal aortic aneurysm screening programme

151
Q

who is invited to take part in NAAASP?

A

men over the age of 65

152
Q

what does NAAASP measure?

A

Abdominal USS, measures the AP infrarenal aortic diameter

153
Q

what should normal aortic diameter measure?

A

<3cm

no further action taken

154
Q

what does a small AAA measure and what further action should be taken?

A

3cm-4.4cm

yearly scans

155
Q

what does a medium AAA measure and what further action should be taken?

A

4.5cm-5.4cm

scan every 3 months

156
Q

what does a large AAA measure and what further action should be taken?

A

5.5cm or greater

refer to vascular surgeon

157
Q

what are the signs and symptoms of AAA?

A

Generally asymptomatic until rupture
Some patients may report back or hip pain if large or rapidly expanding AAA
May compress surrounding structures-vague GI symptoms, DVT
Embolism of thrombus or atherosclerotic debris from the aneurysm sac may cause -> acute ishaemia of lower limb

158
Q

what are the common features of AAA rupture?

A

Abdominal pain, radiating to back
Shock
Have low threshold for suspecting it as it can be mistaken for other conditions eg renal colic, sciatica, pancreatitis and is fatal without repair

159
Q

what is the elective management for aortic aneurysm?

A

Ultrasound surveillance programme (if diameter <5.5cm)

PLUS:
CT if diameter 5.5cm or greater
Judge suitability for open/endovascular aneurysm repair (EVAR)
At 5.5cm, the risks of rupture generally outweigh risks of repair

Risk factor modification-
Stop smoking, BP control, antiplatelet, statin
Can slow progression and improve fitness for repair when it becomes necessary

160
Q

what is the emergency management for aortic aneurysm?

A

-Ruptured or symptomatic AAA
-Urgent CT scan
Proceed to either open or endovascular reapin
Consider palliation if unfavorable factors for successful outcome

161
Q

what is the prognosis for aortic aneursym with elective repair?

A

In hospital postoperative morality for open repair->2.9%
In hospital postoperative mortality for EVAR->0.4%
Pros and cons of both options, individualized to patient

162
Q

what is the prognosis for aortic aneurysm with emergency repair?

A

IMPROVE trial-suspected AAA were randomized to either repair or EVAR. It showed that there was no statistically significant difference between groups. 30 day mortality for open repair=37.4% and for EVAR=35.4%

163
Q

what is Raynaud’s pnenomenon?

A

episodic vasospasm of the arteries of the extremities resulting in digital ischaemia that can be induced by cold or emotional stress

164
Q

what is the most common type of Raynaud’s?

A

95% of cases are primary

no cause

165
Q

who is usually affected by primary (idiopathic) Raynauds?

A

women 20s-30s

166
Q

who is mainly affected by secondary Raynaud’s?

A

secondary to other conditions. 5% of causes. Incidence of 2-3% over 10 years. In older age occurs in similar number of males and females. Many causes and associations

167
Q

what is the aetiology of secondary Raynaud’s phenomenon?

A

Older age group, men and women are affected equally

Associated with connective tissue disease especially scleroderma (also SLE, RA, siogens syndrome)

Drugs eg amphetamines, cocaine, beta blockers, chemotherapy, COCP

Vascular occlusive disease eg Buerger’s, atherosclerosis, thromboembolic

Haematological eg polycythemia, leaukaemia, protein C, S or antithrombin III deficiency

Environmental/occupational eg vibration, frostbite, ulnar aneurysm

Anatomical eg thoracic outlet syndrome, carpal tunnel

Infections eg Hep B & C (cryoglobulinaemia), mycoplasma (cold agglutins), parovirus B19

Endocrine eg hypothyroidism, phaeochromocytoma, carcinoid syndrome

168
Q

what are the symptoms of Raynaud’s?

A
  • Pallor of distal part of fingers
  • Numbness
  • Pain
  • Blue finger (cyanosis)
  • Hyperaemic phase-red and warm fingers
-Associated symptoms (related to underlying causes) (Migraines 
Joint/muscle pain
Weight loss 
Dry eyes etc (sicca syndrome)
Gastro-oesophageal reflux 
Rashes)
169
Q

what are the signs of Raynaud’s phenomenom?

A

Clinical features of connective tissue disorder:

Digital ulcers
Infection
Gangrene 
Severe ischemia 
AF 
Murmur 
Malar rash 
Hepato-splenomegaly
Abnormal nail-fold capillaries
Suggest underlying disease

General and focused examination of the hands
Blanching then cyanosis
Hyperaemiacan occur after cyanosis

170
Q

what investigations would be carried out in a patient with Raynaud’s?

A
Bloods: 
Full blood count
ESR
Plasma viscosity 
Autoimmune screen
Investigating  underlying disease 
Urea and electrolytes 
Liver and thyroid function tests 
Plasma glucose
Urine/protein eletrophoresis, cold agglutin's and fibrinogen levels for hyperviscosity states
171
Q

what imaging may be used in a patient with Raynaud’s?

A
Infrared thermography (cold provocation test)
Laser doppler flowmetry
Digital plethysmography
172
Q

how can you make a diagnosis of Raynaud’s?

A

Clear demarcated digital pallor
At least one colour change eg cyanosis/erythema
Identified cold/emotion triggers
Exclude cervical rib/thoracic outlet syndrome

173
Q

when should you suspect Raynaud’s

A
Onset >30yrs
Asymmetrical, intense of painful episodes
Features of underlying condition 
Digital ulcers
Positive autoimmune tests
174
Q

what is the prognosis for Raynaud’s?

A

Don’t go onto develop digital ulceration and can be managed with conservative medical strategies
Remission rates highly variable
Incidence of tissue loss in those with Raynaud’s secondary to systemic sclerosis-17%

175
Q

what general measures are used in management of Raynaud’s?

A
Smoking cessation
Maintain body warmth 
Minimise stress
Regular exercise
Stop drug if SE
176
Q

what medical measures are used in treatment of Raynaud’s?

A

Calcium channel blocker (nifedipine)

Consider antiplatelet

Admit for IV iloprost if conservative and nifedipine not controlling symptoms

Consider immunosuppression for autoimmune associated Raynaud’s

177
Q

what surgery may be used in treatment of Raynaud’s?

A

(uncommon)

Digital/thoracoscopic sympathectomy

178
Q

what is compartment syndrome?

A

Acute increase in pressure within a compartment which endangers the perfusion of tissues, requiring emergency decompression

179
Q

what are the symptoms of compartment syndrome?

A

disproportionate ‘crescendo pain’ unresponsive to analgesia

180
Q

what is the aetiology of compartment syndrome?

A

Reperfusion injury post revasculisation in acute limb ischaemia
Other causes include fractures, crash injuries and burns

181
Q

what is the pathophysiology of compartment syndrome?

A

Ischaemia-reperfusion injury
Release of free radicals, K+, Ca2+, toxins etc
Vascular leakage causing tissue swelling within fixed fascial compartment
Decreased perfusion pressure

182
Q

what are the signs of compartment syndrome?

A

Pain on passive movement
Parasthesia
Pulselessness (late)
Paralysis (late)

183
Q

what investigations would be performed if suspect compartment syndrome?

A

Should be a clinical diagnosis
If there is diagnostic uncertainty
Compartment pressures
pH

184
Q

what is the management of compartment syndrome?

A

Urgent fasciotomy
Optimise medical condition
Remove constrictive dressings

185
Q

what is the prognosis if compartment syndrome goes undiagnosed?

A
Poor if undiagnosed
Necrosis
Ischaemic contracture
Neuro deficit
Rhabdomyolysis 
AKI
Amputation
186
Q

what is the prognosis of compartment syndrome post fasciotomy?

A

Chronic pain
Swelling
Recurrent ulceration