Vascular 2 Flashcards

1
Q

What is the Fontaine Classification?

A
Fontaine: Outlines the progression of chronic limb peripheral arterial disease 
1 - asymptomatic 
2 - intermittent claudication 
3 - ischaemic rest pain 
4 - ulceration/gangrene
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2
Q

What ABPI values suggest PAD?

A

> 1.2: may indicate calcified, stiff arteries. This may be seen with advanced age or PAD
1.0 - 1.2: normal
0.9 - 1.0: acceptable
< 0.9: likely PAD. Values < 0.5 indicate severe disease which should be referred urgently

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3
Q

What does ABPI >1.2 signify?

A

May be a false negative due to calcification giving abnormally stiff vessels
More common in diabetics

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4
Q

What are the causes of ABPI >1.2?

A

Atherosclerosis: by far the most common

Fibromuscular dysplasia: non-inflammatory artery wall thickening

Buerger’s disease (thromboangiitis obliterans): acute inflammation and thrombosis of lower limb arteries/veins, common in young, heavy smokers

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5
Q

What are the symptoms of intermittent claudication?

A

Ischaemic ‘cramping’ muscle pain on walking, relived by rest
Pain reproducible at a similar level - ‘claudication distance’

most commonly in the calf, suggesting femoral disease

Pain in the thigh/buttock suggests ileal disease, which will often be bilateral

Ask about penile function - ‘Leriche syndrome’

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6
Q

What are the signs of intermittent claudication?

A
Absent pulses
Cold, pale legs
Atrophic, hairless and shiny skin 
Buerger's angle: <20 degrees: look for reactive hyperaemia 
arterial ulcers
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7
Q

What is ischaemic rest pain indicative of?

A

Critical lower limb ischaemia

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8
Q

What is the presentation of ischaemic rest pain?

A

Classically occurs at night in the forefoot - due to the decreased effects of gravity and decreased BP

Pain wakes a patient from sleep
They can gain relief by swinging the leg over the side of the bed or walking on a cold floor

History of intermittent claudication and signs of arterial insufficiency in the leg

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9
Q

Why are arterial ulcers more likely to be formed if there is ischaemic rest pain?

A

More likely to form from minor injuries as healing is impaired and infection of these ulcers can lead to rapidly spreading gangrene (more common in those with co-morbid diabetes)

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10
Q

What investigations are done for intermittent claudication/ischaemic rest pain?

A

Bloods: FBC (rule out anaemia: HbA1c, lipids
ABPI is the most important initial investigation

Management depends on ABPI result and level of symptoms

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11
Q

What is the management if ABPI >0.6?

A

Progression from intermittent claudication to critical ischaemia is unlikely, so conservative measures are used

Progression more likely in diabetics, and those with a claudication distance <50m

More aggressive treatment may be considered in these patients

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12
Q

What are the conservative measures for peripheral arterial occlusive disease?

A

Lifestyle changes: stop smoking, exercise to the point of claudication to improve collaterals, weight loss

Raising the heel of shoes (decreased calf work)

Foot care to prevent minor trauma leading to ulceration etc

Optimisation of blood pressure (avoid beta-blockers) and diabetes

Started on anti platelet (clopidogrel and a statin (atorvastatin)

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13
Q

What is the management if ABPI <0.6?

A
Highly symptomatic - leading to a loss of function, or conservative measures ineffective 
PTA
surgical reconstruction
sympathectomy 
amputation
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14
Q

What is PTA?

A

Percutaneous transluminal angioplasty
Balloon inflated in narrowed segment, good for short stenosis
Endoluminal stents may be used to keep the segment patent

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15
Q

What surgical reconstruction procedures are used for peripheral arterial occlusive disease?

A

Bypass grafting may be required in more extensive disease if distal arteries are not diseased, with saphenous vein harvests common

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16
Q

What are the indications for amputation?

A

May relieve intractable pain, and prevent death from septicaemia

Level of amputation must be high enough to ensure healing but above knee amputation has worse rehabilitation than below knee

Gabapentin started pre-op may help phantom limb pain

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17
Q

What is the effect of diabetes on peripheral arterial disease?

A

Diabetics are at a greater risk of developing peripheral arterial disease and presentation can be different due to the presence of peripheral neuropathy, which has three main effects:

sensory neuropathy
autonomic neuropathy
motor neuropathy

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18
Q

How does sensory neuropathy affect peripheral arterial disease?

A

reduces protective reactions to minor injury and reduces awareness of symptoms of infections / ischaemia

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19
Q

How does autonomic neuropathy affect peripheral arterial disease?

A

A lack of sweating leads to development of dry, fissured skin allowing entry of bacteria

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20
Q

How does motor neuropathy affect peripheral arterial disease?

A

Wasting of the small muscles of the foot - leading to loss of the arches and development of abnormal pressure areas in the feet

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21
Q

What is the difference between peripheral neuropathy and ischaemic rest pain?

A

Stabbing pains in feet
red and warm feet - STRONG pulses

Unlikely to be relieved by swing foot over bed/walking on a cold floor

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22
Q

How are diabetics with peripheral arterial disease likely to present

A

Can be severely ischaemic, but painleess

More likely to present with ulceration, due to the combination of sensory, autonomic and motor neuropathy combined with poor arterial supply to heal ulcers

This can rapidly progress to gangrene

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23
Q

What is gangrene?

A

Dead tissue, normally colonised by bacteria

Wet gangrene: infected with proliferating organisms
Dry gangrene: colonised, but organisms are not proliferating

Presents in the toes first, progressing proximally to line where there is adequate oxygenation

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24
Q

What is the appearance of gangrene?

A

Blue-purple in colour, with progressive blacking of tissues and numbness

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25
Q

What is the presentation of gangrene in diabetics?

A

In diabetics, usually presents earlier - affecting smaller areas e.g. a single toe, or ischaemic area of the heel

This is due to the more extensive atherosclerotic changes of smaller vessels seen in diabetes

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26
Q

Which area is most usually affected by intermittent claudication?

A

Calf - as it is the femoral Artery that most commonly becomes atheromatous

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27
Q

Why does intermittent claudication occur?

A

At rest, the oxygen requirement of muscles is met by the collateral system of the profonda femoris (deep femoral artery that joins the popliteal artery just below the knee)

Exercise produces a demand that cannot be met and the calf muscles become ischaemic

By resting, the collateral system can once again supply enough blood for the pain to be relieved

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28
Q

What are the ddx of intermittent claudication?

A

Spinal stenosis

venous claudication

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29
Q

What is the cause of spinal stenosis?

A

Spinal osteophyte formation

symptoms are due to lumbar nerve roots / cauda equina compression

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30
Q

What are the features of spinal stenosis?

A

features similar to intermittent claudication, but pain is relieved by sitting down or flexing the spine rather than standing still
Symptoms vary day to day
associated with numbness/tingling and pulses will be present

Diagnosis confirmed with MRI

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31
Q

What is the cause of venous claudication?

A

Obstruction of the venous outflow of the leg (ileofemoral occlusion)
Pain comes on gradually from the moment walking starts
Pain affects the whole leg, and is bursting in nature
leg elevation can relieve the pain

There are signs of venous disease and often a history of DVT

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32
Q

What are the other causes of leg pain?

A
intermittent claudication
spinal stenosis 
venous claudication
musculoskeletal (OA/RA) 
peripheral neuropaty 
popliteal artery entrapment - young patients with normal pulses
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33
Q

What proportion of leg ulcers are venous?

A

85%

many also have an arterial element

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34
Q

what is the cause of venous leg ulcers?

A

occur due to venous hypertension and oedema causing subcutaneous hypoxia

an episode of minor trauma then precedes development of an ulcer as the skin is poorly nourished and cannot heal

Secondary infections common

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35
Q

What is the cause of an arterial ulcer?

A

10% ulcers are entirely the consequence of arterial disease

occur after an episode of minor trauma, with inadequate healing due to poor arterial supply

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36
Q

Arterial vs venous ulcer: history

A

arterial: IC, IHD, HTN, DM
venous: DVT, varicosities, obesity

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37
Q

Arterial vs venous ulcer: pain

A

arterial: very painful
venous: rare

38
Q

Arterial vs venous ulcer: site

A

arterial: lateral malleolus, also toes/heels
venonus: medial malleolus and gaiter area

39
Q

Arterial vs venous ulcer: progression

A

arterial: rapidly increasing but painful so present small
venous: slowly increasing but can become very large

40
Q

Arterial vs venous ulcer: oedema

A

arterial: uncommon
venous: common

41
Q

Arterial vs venous ulcer: skin appearance

A

arterial: shiny, hairless, atrophic nails
cool and pale

venous: signs of venous insufficiency, red and warm

42
Q

Arterial vs venous ulcer: ulcer appearance

A

arterial: small and punched out
venous: shallow with a flat margin

43
Q

How do diabetic ulcers occur?

A

occur due to the three neuropathy processes described above, which are compounded by arterial disease and infection

Usually occur on the foot with a classic unbalanced looking foot with ulcers on the pressure area

44
Q

How are ulcer causes initially investigated?

A

Consider diabetes / vasculitic causes

Perform ABPI / Duplex USS (can show arterial and venous disease

45
Q

What are the conservative measures for ulcers?

A

Lifestyle changes in ?arterial disease

avoid prolonged standing in suspected venous disease, tightly control DM

46
Q

What is the management if ?venous disease and ABPI >0.8?

A

4-layer compression bandaging is the gold standard initial treatment
Leg elevation important to help decrease the venous hypertension
Once healed, long term compression stockings advised

If duple shows superficial disease only - treatment of varicose veins may resolve the venous outflow issues, to allow ulcer healing

47
Q

What is the manamgent if ABPI <0.8?

A

Refer to GP for CV risk modification

Refer to vascular surgery for investigation of arterial disease

48
Q

What is the management for mixed arterial/venous ulcers?

A

Arterial problem should be surgically corrected, and then compression can occur
Arterial ulcers are signs of critical limb ischaemia and thus are treated surgically if the patient is fit

Only swab if there is signs of infection

Biopsy if the ulcer looks atypical!

49
Q

What are the sx of chronic small bowel ischaemia?

A

Severe post-prandial colic: (gut claudication)
PR bleeding
Weight loss
Malabsorption

50
Q

How is small bowel ischaemia visualised?

A

Angiography - treated with angioplasty

51
Q

What are the sx of large bowel ischaemia?

A
Presents with ischaemic colitis 
Left sided abdominal pain
Bloody diarrhoea 
Pyrexia,
tachycardia
leucocytosis 

Can progress to gangrenous colitis with peritonitis an shock

52
Q

What are the investigations for large bowel ischaemia?

A

Barium enema /AXR: thumb printing

MR angiography: diagnostic

53
Q

What is the management of large bowel ischaemia?

A

Conservative: most recover with fluids and antibiotics

Percutaneous transluminal angioplasty and stenting for severe cases

54
Q

What are the causes of renal artery stenosis?

A

80% due to atherosclerosis

10% due to fibromuscular dysplasia

55
Q

What is the presentation of renal artery stenosis?

A

Resistant HTN
Worsening renal function after ACEis (if bilateral)
Sudden onset pulmonary oedema (with normal LV function)
renal bruits on examination

56
Q

How is renal artery stenosis diagnosed?

A

Renal USS: small affected kidney, Doppler showing disturbance in renal flow
CT/MR angiography can then confirm diagnosis
Renal angiography gold standard

57
Q

What is the treatment of renal artery stenosis?

A

Medical: ACEi with statins and anti-platelets
Contraindicated in bilateral disase

surgical management: angioplasty and stenting
thought to be equally effective as medical management

58
Q

What are the causes of acute arterial occlusion?

A

Embolus (40%)
Thrombus (40%)
Trauma (including during angioplasty

59
Q

What is Virchow’s triad?

What is the meaning?

A

thrombus is Predisposed to by Virchow’s triad:

Endothelial dysfunction: trauma, inflammation or atheroma

Changes in blood flow: stasis or slow blood flow

Changes in blood coagulability: inflammatory response / congenital causes

60
Q

What is embolic occlusion?

A

Occlusion of a vessel by a mass of material transported in the blood stream, most commonly fragments of thrombus (thromboemboli)

61
Q

Where might thromboemboli arise from?

A

Left atrium in AF
left ventricle post MI
heart valves in endocarditis
mural thrombi from an AAA

62
Q

What are the clinical features of the acutely ischaemic limb?

A
Six Ps: 
Pulseless
Pallor 
Painful
Perishingly cold
Paralysis 
Paraesthesia 

(final two indicate a threatened limb, as well as pain on passive movement or squeezing the calf)

63
Q

What are the indications of a ‘non viable limb’

A

Fixed staining (colour changes that are non-blanching of the leftest) and rigid muscles

64
Q

What is the maximum time to re-establish flow in an acutely ischaemic limb?

A

6 Hours

65
Q

What is the management of the acutely ischaemic limb?

A

A-E
IV heparin as soon as the diagnosis is made, to prevent propagation of the clot

Assessment of the limb - If block seems to be resolving, collateral circulation may negate the need for surgery/thrombolysis may be used

Urgent CT angiogram - can help differentiate between thrombotic/embolic causes

Embolus management - open embolectomy
interval investigation to the underlying cause

thrombosis management - thrombolysis to restore patency
interval angioplasty to treat underling disease

66
Q

How is an open embolectomy performed?

A

Using a Fogarty catheter

local thrombolysis if the clot has propagated beyond the original embolus

67
Q

What is the management if the leg is not thought to be viable?

A

AMPUTATION

68
Q

What are the important things to observe for post-operatively?

A

Reperfusion injury

Compartment syndrome

69
Q

What is a reperfusion injury?

A

inflammation and oxidative damage when blood flow is restored to a tissue after a long period of anoxia
Can lead to oedema and comportment syndrome

70
Q

Embolus vs thrombosis onset?

A

embolus - sudden onset, very severe symptoms due to lack of collaterals

Thrombosis - insidious onset, less severe symptoms as advanced collateral

71
Q

Embolus vs thrombosis source?

A

embolus: normally identifiable, e.g. AF/AAA
thrombosis: no obvious course

72
Q

Embolus vs thrombosis pulses?

A

Embolus: previously normal, normal contralateral pulses

thrombosis: long-standing decreased pulses bilaterally

73
Q

Embolus vs thrombosis history

A

embolus: no history of arterial disease
thrombosis: previous history of IC, stroke, MI etc

74
Q

What investigations are used in suspected arterial bleeds?

A

Angiography or contrast CT

75
Q

What is the management of transection?

A

Haemorrhage can normally be arrested by applying pressure to gauze swabs

If there is significant ischaemia, vascular grafting/repair may be needed

If the main artery and vein have been severed, the vein will always be repaired first to allow venous drainage before repairing the artery

76
Q

What is an arterio-venous fistula?

A

acquired communication between an artery and vein

77
Q

What are the causes of an AVF?

A

penetrating trauma: most common
erosion of aneurysm into a neighbouring vein
iatrogenic: patients on haemodialysis

78
Q

Describe how a AVF occurs

A

there Is shunting from the high pressure arterial side to the Low pressure venous side

increased flow leads to dilation, thickening and tortuosity of the vein ( ‘arterialisation’ ) and the turbulent flow gives a palpable thrill

79
Q

What is the effect of an AVF on peripheral venous and arterial pressures?

A

Peripheral venous pressures are increased, leading to swelling, varicosities and sometimes venous ulceration in the limb

Peripheral arterial resistance decreases, thus the heart responds by increasing stroke volume, eventually leading to left ventricular dilation and heart failure

80
Q

What might patients with AVF (non iatrogenic) complain of?

A

limb heaviness, aggravated with dependency and relieved by elecation

Pain also common

81
Q

What examination findings will there be if pt has an AVF?

A

Oedema and prominent veins with an audible murmur or palpable thrill (can be pulsatile)
rarely - signs of CCF if the communication is very large

Blood gas will show higher oxygen sats distal to the AVF and also there will be consumptive coagulopathies due to the changes in blood flow activating the clotting cascade

Duplex USS / Contrast CT can confirm

82
Q

What is the management of AVF?

A

surgery / interventional measures

83
Q

What is Raynaud’s phenomenon?

A

General term describing episodic digital vasospasm in the absence of an identifiable associated disorder

84
Q

What is Raynaud’s syndrome?

A

Raynaud’s phenomenon occurring secondary to another condition

85
Q

What are the secondary cause of Raynaud’s syndrome?

A

Connective tissue disorders: systemic sclerosis, mixed connective tissue disease, SLE, Sjogren’s syndrome, polyarteritis nods

Macrovascular disease: atherosclerosis, thoracic outlet syndrome, Buerger’s disease

Occupational trauma: vibration white finger, repeated extreme cold or chemical exposure

Drugs: beta blockers, cytotoxic drugs

Others: malignancy, AVF

86
Q

How does Raynaud’s phenomenon occur?

A

Cold exposure or emotional stress

87
Q

What are the three phases of Raynaud’s phenomenon?

A

Pallor: due to digital artery spasm
Cyanosis: due to accumulation of deoxygenated blood
Rubor: erythema due to reactive hyperaemia

As the fingers return to normal, there may be numbness, a burning sensation and severe pain

Attacks are usually <45 mins in duration but can last for hours with very severe cases involving tissue infarction and loss of digits

88
Q

What are the features suggesting a secondary cause of Raynaud’s?

A

Dilated nail fold capillary loops (seen with an ophthalmoscope)
Presentation in early childhood, or over the age of 30
Asymmetrical distribution
Male sex

89
Q

What baseline investigations should be done for raynauds?

A
FBC: polycythaemia, malignancy 
U+Es: renal impairment / dehydration 
Coagulation: hepatic dysfunction 
Glucose: DM
TFTs 
ANA/RF/APA: autoimmune screen if suspecting secondary cause
90
Q

What is the management of Raynaud’s?

A

Keep extremities warm (heated gloves etc)
Stop smoking and stop exacerbating drugs e.g. B-blocker/OCP

Medical: nifedipine
losartan/prazosin/fluoxetine first line

Sympathectomy may help those with severe disease but may be short lived