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YR6 Rotations > Surgery - Vascular > Flashcards

Surgery - Vascular Flashcards

1
Q

What is an aortic dissection?

A

Tear in the tunica intima

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2
Q

What is the biggest RF for aortic dissection?

A

HTN

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3
Q

Recall 2 ways in which aortic dissection can be classified and what these entail

A

Stanford classification
Type A: ASCENDING aorta
Type B: DESCENDING aorta

De Bakey classification
Type 1 originates in ASCENDING aorta, EXTENDs to arch + possibly beyond
Type 2: confined to ASCENDING aorta
Type 3: originates in DESCENDING aorta

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4
Q

How should aortic dissection be managed?

A

Aortic root replacement surgery
Bed rest
Beta blockers

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5
Q

What are the main symptoms of aortic dissection?

A

Tearing chest pain, radiates to back
20mmHg BP difference between arms
Possible Horner’s

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6
Q

How should aortic dissection be imaged?

A

Stable: CT CAP
Unstable: TOE/ TTE (transoesophageal echo/ transthoracic echo)

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7
Q

In which type of aortic dissection is surgery not indicated?

A

Descending

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8
Q

What are the 3 subtypes of peripheral artery disease?

A
  1. Intermittent claudication
  2. Critical limb ischaemia
  3. Acute limb-threatening ischaemia
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9
Q

Give 4 features of intermittent claudication

A

Aching/ burning in leg muscles following walking
Typically can walk for predictable distance before Sx start
Usually relieved within mins of stopping
No rest pain

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10
Q

How should a patient with intermittent claudication be assessed?

A

Check femoral, popliteal, posterior tibialis + dorsalis pedis pulses
Check ABPI

1st line Ix: Duplex USS

Magnetic resonance angiography (MRA) should be performed prior to any intervention

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11
Q

What is the usual clinical correlation of each score on ABPI?

A

1: Normal
0.6-0.9: Claudication
0.3-0.5: Rest pain
<0.3: Impending

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12
Q

How can you differentiate between critical and acute limb-threatening limb ischaemia clinically?

A

Onset
CLI = >2w
ALI = <2w

Colour:
CLI = pink
ALI = marble white

Temp:
CLI: warm
ALI: cold

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13
Q

What are the 6 Ps of acute limb ischaemia?

A

Pain
Perishingly cold
Pallor
Pulseless
Paralysis
Paraesthesia

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14
Q

What is the expected ankle arterial pressure in critical limb ischaemia?

A

<40mmHg

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15
Q

What are the causes of limb ischaemia?

A

TRIED to walk:
Thromboangiitis obliterans
Raynaud’s
Injury
Embolism/ thrombosis
Diabetes

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16
Q

How should ischaemic limb be investigated?

A

1st: ABPI
2nd: duplex USS
3rd: MRA/CTA

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17
Q

Describe interpretation of ABPI

A

> 1.2: calcified, stiff arteries. Seen in advanced age, DM or PAD
1.0-1.2: normal
0.9-1.0: acceptable
<0.9: likely PAD
<0.5: severe disease, refer urgently

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18
Q

At what ABPI would you refer to vascular surgeons?

A

<0.8 or >1.3

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19
Q

How should asymptomatic limb ischaemia/ intemittent claudication be managed?

A

Conservative: (WL, quit smoking)

Medical: statin + anti-platelet (Atorvastatin 80mg + Clopidogrel 75mg)
Rarely used: naftidrofuryl oxalate (vasodilator)

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20
Q

What is peripheral arterial disease strongly linked to?

A

Smoking
All should be given help to quit

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21
Q

List 3 co-morbidities that are important to treat in PAD

A

HTN
DM
Obesity

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22
Q

What is the first line intervention recommended for PAD?

A

Exercise training (supervised)

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23
Q

How is severe PAD or critical limb ischaemia managed?

A

Endovascular revascularisation
* percutaneous transluminal angioplasty +/- stent
* endovascular techniques

Surgical revascularisation
* surgical** bypass **with autologous vein or prosthetic material
* endarterectomy
* open surgery

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24
Q

What is angioplasty?

A

Minimally invasive procedure to widen narrowed/ obstructed arteries
Improves blood flow + alleviates Sx of intermittent claudication

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25
Q

When are endovascular revascularisation techniques used in PAD?

A

Short segment stenosis <10cm
Aortic iliac disease
High risk patients

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26
Q

When are open surgical techniques used for revacularisation in PAD?

A

Long segment lesions >10cm
Multifocal lesions
Lesions of common femoral artery
Purely infrapopliteal disease

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27
Q

What treatment is reserved for patients with critical limb ischaemia who are unsuitable for angioplasty or bypass surgery?

A

Amputation

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28
Q

Which drugs are licensed for use in PAD?

A

Naftidrofuryl oxalate: vasodiltor, used if poor QoL

Cilostazol: phosphodiesterase III inhibitor with antiplatelet + vasodilator effects (not recommended by NICE)

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29
Q

What are the indications for amputation in critical limb ischaemia?

A

Dead (eg severe PAD/ thromboangiitis obliterans)
Dangerous (sepsis, NF)
Damaged (trauma, burns, frostbite)
Darned nuisance (pain, neurological damage)

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30
Q

What is thromboangiitis obliterans also known as?

A

Buerger’s disease

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31
Q

What is thromboangiitis obliterans?

A

Smoking-related condition that results in thrombosis in small + medium-sized arteries, + less commonly veins
Ends of digits look all necrotic + nasty

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32
Q

Recall 2 classification systems used to classify limb ischaemia

A

Fontaine
Rutherford

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33
Q

What are the 3 stages of venous insufficiency?

A
  • Phlegmasia alba dolens (white leg)
  • Phlegmasia cerulea dolens (blue/ red leg)
  • Gangrene (secondary to acute ischaemia)
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34
Q

How can venous insufficiency be managed?

A

Conservative: compression bandages (ABPI >0.8 required)
Surgical: grafts

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35
Q

What are varicose veins?

A

Dilated, tortuous, superficial veins
Most commonly in
legs.
Often visible + palpable,
Are an indication of superficial lower extremity venous insufficiency.

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36
Q

What causes varicose veins?

A

Valve incompetency in affected vein: results in reflux of blood + increased pressure in vein distally
+/- Weakness/ degeneration of vein wall

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37
Q

List 7 risk factors for varicose veins

A

Age
FH
Female
Obesity
Prolonged standing/ sitting
Hx DVT
Pregnancy

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38
Q

Why is pregnancy a risk factor for varicose veins?

A

Uterus causes compression of pelvic veins

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39
Q

How do deep veins differ to superficial veins subjected to increased pressure?

A

Deep: thick walls, confined by fascia

Superficial: unable to withstand pressure- become dilated + tortuous

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40
Q

What % of varicose veins are primary?

A

95%

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41
Q

List 5 signs/ symptoms of varicose veins

A

Pain/ ache
Itch
Swelling
Discomfort after prolonged standing + relief with elevation
Restless legs + nocturnal leg cramps

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42
Q

List 4 skin changes that may arise as a complication of varicose veins

A

Varicose eczema (aka venous stasis)
Haemosiderin deposition → hyperpigmentation
Lipodermatosclerosis → hard/ tight skin
Atrophie blanche → hypopigmentation

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43
Q

List 5 complications of varicose veins

A

Skin changes
Bleeding
Superficial thrombophlebitis
Venous ulceration
DVT

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44
Q

How should varicose veins be investigated clinically?

A

Cough impulse (should be -ve in varicose pathology)
Tap test: tap proximally + feel for an impulse distally
Tourniquet test

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45
Q

What is the investigations for varicose veins?

A

Venous duplex US: demonstrates retrograde venous flow

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46
Q

How is the tourniquet test for varicose veins performed?

A

Patient supine, elevate legs, milk veins
Apply tourniquet high to compress saphenofemoral junction
Stand patient
Repeat distally until controlled filling

Controlled filling = distal veins do not fill

Uncontrolled filling = distal veins full- meaning there is an incompetent valve below the tourniquet

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47
Q

How can varicose veins be managed?

A

Conservative: WL, avoid prologed standing, compression stockings, emollients

Medical: foam sclerotherapy, endothermal ablation

Surgical: ligation + stripping

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48
Q

What is the MOA of endothermal ablation in VV?

A

Energy from high frequency radiowaves or endovenous lasers to seal off affected veins

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49
Q

What is the MOA of foam sclerotherapy in VV?

A

Injection of irritant foam into vein
Results in an inflammatory response that causes closure of the vein.

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50
Q

Give 5 indications to refer to secondary care for varicose veins

A

Significant/ troublesome LL Sx: pain, discomfort, swelling
Previous bleeding from VV
Skin changes secondary to chronic venous insufficiency: pigmentation + eczema
Superficial thrombophlebitis
Active or healed venous leg ulcer

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51
Q

What investigations should be done in suspected DVT?

A

First do a Well’s score
If >,2 –> USS leg
If 0 or 1 –> D-dimer within 4h –> USS if +ve, other dx if -ve

If DVT is confirmed + unprovoked do a CT AP to identify possible malignancy

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52
Q

How should DVT be managed?

A

DOAC (if renal impairment –> LMWH + warfarin)

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53
Q

Recall the components of the Wells score

A

Mnemonic: DVT SCORES
DVT previous [+1]
Veins - superficial collateral [+1]
Three cm difference in calf diameter [+1]

Static (paralysis/ paresis/ plaster immobilisation) [+1]
Cancer (active within 6 months) [+1]
Oedema (pitting, confined to symptomatic leg) [+1]
Recently bedridden for 3 days [+1]
Entire leg swollen [+1]
Something else equally likely [-2]

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54
Q

What is superficial thrombophlebitis?

A

Thrombus formation in superficial vein + inflammation in surrounding tissue

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55
Q

What is the association to DVT in superficial thrombophlebitis?

A

~20% have underlying DVT at presentation
3-4% progress to DVT if untreated
Risk linked to length of vein affected (>5cm, more likely a/w DVT)

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56
Q

What sites of thrombophelbitis have increased risk of DVT?

A

Where affected superficial vein joins deep veonus system e.g. long saphenous vein (superficial) with the femoral veins (deep)

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57
Q

What is the most common site of superficial thrombophlebitis?

A

Saphenous vein

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58
Q

What are the symptoms of superficial thrombophlebitis?

A

Palpable/ nodular cord
Inflammation
Varicose veins

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59
Q

How should superficial thrombophlebitis be investigated?

A

Doppler USS

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60
Q

How should superficial thrombophlebitis be managed?

A

Compression stockings + NSAIDs PO

If SVT >5cm long/<5cm from SFJ): + Fondaparinux (LMWH)
If anticoagulation CI: saphenofemoral ligation

If recurrent with extensive VV: VV surgery + prophylactic LMWH

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61
Q

What is the cause of venous leg ulcers?

A

Venous HTN, secondary to chronic venous insufficiency (most commonly)
Calf pump dysfunction
Neuromuscular disorders

62
Q

Why do venous ulcers form?

A

Due to capillary fibrin cuff or leucocyte sequestration

63
Q

Give 4 features of venous insufficiency

A

Oedema
Brown pigmentation: haemosiderin deposition
Lipodermatosclerosis: champagne bottle legs
Eczema

64
Q

Give 2 characteristics of venous ulcers

A

Above ankle (medial malleolus)
Painless

65
Q

How does deep venous insufficiency differ from superficial venous insufficiency?

A

Deep: related to previous DVT
Superficial: a/w varicose veins

66
Q

How should venous ulcers be investigated?

A

Doppler USS: presence of reflux
Duplex USS: anatomy + flow
ABPI (to exclude arterial)

67
Q

How should venous ulcers be managed?

A

1st: graded compression stockings
2nd: skin grafting (if not resolved in 12w or area >10cm^2)

68
Q

What are Marjolin’s ulcers? Where do they occur?

A

Squamous cell carcinoma
Occur at sites of chronic inflammation e.g. burns, osteomyelitis after 10-20y
Mainly on LL

69
Q

Describe the appearance of pyoderma gangrenosum

A

Erythematous nodules or pustules which ulcerate
“Margerita pizza”: red base + yellow topping

70
Q

What is pyoderma gangrenosum associated with? Where can it occur?

A

a/w IBD + RhA
Can occur at stoma sites

71
Q

Where do arterial ulcers typically appear?

A

Toes and heel

72
Q

List 5 characteristics of arterial ulcers

A

Deep, punched out appearance
Painful
Areas of gangrene
Cold + no palpable pulses
Low ABPI

73
Q

How should arterial ulcers be managed?

A

Pain Mx
IV prostaglandins
RF modification
Chemical lumbar sympathectomy

74
Q

Where do neuropathic ulcers typically appear?

A

Over plantar surface of metatarsal head + plantar surface of hallux
= sites of pressure

75
Q

Which type of ulcer most commonly leads to amputation in diabetic patients?

A

Plantar neuropathic ulcer

76
Q

How can neuropathic ulcers be managed?

A

Cushioned shoes to reduce callous formation

77
Q

How should popliteal aneurysms be managed?

A

If stable: femoral-distal bypass
If acute: embolectomy +/- femoral-distal bypass

78
Q

In over 50s, what is the normal diameter of the infrarenal aorta?

A

F: 1.5cm
M: 1.7cm

79
Q

List 6 risk factors for AAA

A

Smoking
HTN
COPD
Coronary, cerebrovascular or PAD
Hyperlipidaemia
FH

80
Q

List 3 genetic condition associated with development of AAA

A

Ehlers Danlos
Marfans
Turners

81
Q

What is an abdominal aortic aneurysm?

A

DIlation of the abdominal aorta to >50% of normal diameter/ 3cm, involving all layers of the endothelium

82
Q

What are the 2 types of AAA?

A

Fusiform (equally round)
Saccular (outpouching)

83
Q

What is the process for AAA screening?

A

In males >65y: single abdominal USS
If AAA:
3-4.5cm: f/u scan in 12m
4.5-5.5cm: f/u scan in 3m
>5.5cm: 2ww to vascular

84
Q

Give 2 features suggestive of low rupture risk in AAA. What should ongoing management be?

A

Asymptomatic
Diameter <5.5 cm
USS surveillance + optimise cardiovascular RFs

85
Q

Give 2 features suggestive of high rupture risk in AAA. What should ongoing management be?

A

Symptomatic
Diameter >5.5cm or rapidly enlarging >1cm/ year
2ww referral to vascular surgery
Treat with EVAR or open surgery

86
Q

What operations are used for AAA repair?

A

EVAR
Stent placed in abdominal aorta via femoral artery to prevent blood collecting in the aneurysm

Open replacement
If young (longer recovery time but lower chance of further procedures)

87
Q

Give 1 complication of EVAR

A

Endo-leak: stent fails to exclude blood from the aneurysm
Usually presents w/o Sx on routine f/u

88
Q

What can ruptured AAA present similarly to?

A

Renal colic
Loin to groin pain

89
Q

What are the complications of AAA?

A

Rupture
Embolism (trash foot)
Thrombus
Fistulation

90
Q

How can ruptured AAA present?

A

Catastrophic: sudden collapse
Sub-acute: persistent severe central abdo pain with developing shock

91
Q

What is the mortality rate for ruptured AAA?

92
Q

Give 3 features of ruptured AAA

A

Severe, central abdominal pain radiating to the back
Pulsatile, expansile mass in abdomen
Shock: hypotension + tachycardia, collapse

93
Q

Describe management of ruptured AAA

A

Urgent vascular review
Crossmatch 6 units blood

HD UNstable: clinical dx, send to theatre. If frail consider palliation

HD stable: CT angiogram if dx is in doubt + assess ability of endovascular repair

HD = Haemodynamically

94
Q

What is the 1st line treatment for SVCO?

A

Dexamethosone

95
Q

How should stridor due to SVCO be managed?

A

Intubation –> endovascular stenting

96
Q

What is the gold standard test for peripheral vascular disease?

A

CT arteriogram

97
Q

Briefly describe the Fontaine classification of chronic limb ischaemia

A

Stage 1: asymptomatic
Stage 2: intermittent claudication
Stage 3: Ischaemic rest pain
Stage 4: Ulceration +/- gangrene

98
Q

Recall the 3 ways in which critical limb ischaemia can be defined

A
  1. ABPI <0.5
  2. Presecne of ischaemic lesions/ gangrene objectively attributable to the arterial disease
  3. Ischaemic rest pain for >2w duration
99
Q

What is the key differential for symptoms of limb ischaemia?

A

Spinal stenosis (‘neurogenic claudication’)

100
Q

How can cardiovascular risk factors be managed in patients with chronic limb ischaemia?

A

Lifestyle changes
Statin
Anti-platelet (ideally clopidogrel 75mg)
Optomise diabetes control

101
Q

What can cause varicose veins?

A

98% are primary idiopathic

Secondary causes include:
Pelvic masses (eg malignancy, fibroids)
AV malformations eg Klippel-Trenaunay Syndrome

102
Q

What are the 4 major risk factors for developing varicose veins?

A

Prolonged standing
Obesity
FH
Pregnancy

103
Q

Recall 3 signs of venous insufficiency

A

Ulceration
Varicose eczema
Haemosiderin deposition

104
Q

What is a saphena varix?

A

Dilatation of saphenous vein at the saphenofemoral junction in the groin.
Displays a cough impulse- commonly mistaken for a femoral hernia.

105
Q

Briefly describe the classification system for varicose veins

A

CEAR system -
C0-6 is based on clinical features with C1 being telangiectasias + C6 being an active venous ulcer
E = aEtiology (Ep = primary, Es = secondary, Ec = congenital)
Anatomical (s = superficial, d = deep, p = perforating)
R = reflux/obstruction?

106
Q

What is the gold standard test for varicose veins?

A

Duplex ultrasound

107
Q

How should venous ulcers be managed?

A

4-layer bandaging to produce graduated compression - aims to move blood distal –> proximal

108
Q

Recall 3 options for treating varicose veins

A
  1. Venous ligation, stripping + avulsion: tying off responsible vein + stripping it away
  2. Foam sclerotherapy: injection of a sclerosing agent causes inflammation which causes the vein to close off
  3. Thermal ablation: heating from the inside to cause irreversible damage which closes it off
109
Q

Recall 5 signs of deep venous insufficiency

A

Varicose eczema (dry + scaly skin)
Thrombophlebitis
Haemosiderin skin staining
Lipodermatosclerosis
Atrophie blanche

110
Q

What is venous stenting and what is it used for?

A

Metal mesh stent expanded in occluded vein

Patients with severe post thrombotic syndrome with an occluded iliac vein may be suitable for deep venous stenting

111
Q

What are the 3 main groups of causes of acute limb ischaemia?

A
  1. Embolisation
  2. Thrombus in sit (eg due to local atheroma)
  3. Trauma (less common) eg compartment syndrome
112
Q

What are the 6 Ps of acute limb ischaemia?

A
  • Pain
  • Pallor
  • Pulselessness
  • Paresthesia
  • Perishingly cold
  • Paralysis
113
Q

What classification system is used to classify acute limb ischaemia?

A

Rutherford

114
Q

How should suspected acute limb ischaemia be investigated?

A

Handheld Doppler USS (at bedside, 1st line)
ABPI (doesn’t guide acute Mx)

115
Q

Give 4 features of acute limb ischaemia suggestive of thrombus

A

Pre-existing claudication with sudden deterioration
No obvious source of emboli
Reduced/ absent pulses in contralateral limb
Evidence widespread vascular disease e.g. MI, stroke, TIA

116
Q

Give 5 features of acute limb ischaemia suggestive of embolus

A

Sudden onset painful leg <24h
No hx claudication
Clinically obvious source of embolus e.g.** AF**, recent MI
No evidence PVD (normal pulses in contralateral limb)
vidence of proximal aneurysm e.g. abdominal or popliteal

117
Q

Within what time frame will complete arterial occlusion in the lower limb lead to irreversible tissue damage?

118
Q

How should acute limb ischaemia be managed?

A

Initial: O2, IV access, heparin infusion, analgesia + vascular review

Ongoing:

  • Low Rutherford: conservative Mx via heparin
  • High Rutherford: surgical input
119
Q

Give 2 endovascular interventions for acute limb ischaemia

A

Percutaneous catheter-directed thrombolytic therapy
Percutaneous mechanical thrombus extraction

120
Q

List 3 surgical interventions for acute limb ischaemia

A

Surgical thromboembolectomy
Endarterectomy
Bypass surgery

121
Q

How should irreversible acute limb ischaemia be managed?

A

Urgent amputation

122
Q

What is the mortality rate of acute limb ischaemia?

123
Q

What is reperfusion injury?

A

Important complication of acute limb ischaemia treatment

Sudden increase in capillary permeability can result in:

  • Compartment syndrome
  • Release of substances from the damaged muscle cells, such as:
    • K+ ions causing hyperkalaemia
    • H+ ions causing acidosis
    • Myoglobin, resulting in significant AKI
124
Q

What is Leriche’s syndrome?

A

Triad of symptoms due to atherosclerosis of abdominal aorta/ iliac arteries:

  1. Claudication of the buttocks and thighs
  2. Atrophy of the musculature of the legs
  3. Impotence (due to paralysis of the L1 nerve)
125
Q

How do symptoms of peripheral vascular disease differ in femoral and iliac stenosis?

A

Iliac stenosis = buttock pain

Femoral stenosis = calf pain

126
Q

How does the anatomy of the collateral circulation of arterial inflow impact vacular disorders of the upper limb?

A

In region of subclavian + axillary arteries, collateral vessels passing around the shoulder joint may provide pathways for flow if main vessels are stenotic or occluded

If increased metabolic demand, collateral flow is not sufficient + vertebral arteries may have diminished flow- diminished flow to brain + neuro sequalae e.g. syncope

127
Q

Where do most upper limb emboli lodge?

A

50% Brachial artery
30% Axillary artery

128
Q

What are the symptoms caused by axillary/ brachial emboli?

A

Sudden onset:
Pain
Pallow
Paresis
Pulselessness
Paraesthesia

129
Q

What are the sources of axillary/ brachial emboli?

A

Left atrium with cardiac arrhythmia (mainly AF)
Mural thrombus

130
Q

Other than embolus, what may cardiac arrhythmias result in?

A

Impaired consciousness

131
Q

What is the most common cause of arterial occlusion?

132
Q

What is a rare cause of arterial occlusion?

A

Trauma resulting in vascular changes + long term occlusion

133
Q

Give 4 features of arterial occlusion

A

Claudication
Ulceration
Gangrene
Proximally sited lesions: subclavian steal syndrome

134
Q

What causes subclavian steal syndrome?

A

Proximal stenotic lesiono of subclavian artery
Results in retrograde flow through vertebral/ internal thoracic arteries
Decreases cerebral blood flow leading to syncope

135
Q

5 RFs for subclavian steal syndrome

A

Age
HTN
Hyperlipidaemia
Smoking
DM

Offending lesions tend to be atherosclerotic

136
Q

What are the investigations for subclavian steal syndrome?

A

Duplex USS: retrograde flow in affected vertebral artery
CT angiography: definitive- identifies occlusive lesion

137
Q

7 S/S caused by subclavian steal syndrome

A

Vertigo
Diplopia
Dysphagia
Dysarthria
Visual loss
Syncope
Arm claudication

138
Q

What does the progressive nature of arterial occlusion allow?

A

Development of collaterals
Acute ischaemia may occur as a result of acute thrombosis

139
Q

What is a cervical rib?

A

Supernumery fibrous band arising frfom 7th cervical vertebra
Incidence: 1 in 500

140
Q

What can the presence of a cervical rib cause?

A

Thoracic outlet obstruction

141
Q

What is Takayasu’s arteritis? What does it typically cause?

A

Large vessel granulomatous vasculitis
Results in intimal thickening: occlusion of aorta

142
Q

Epidemiology of Takayasu’s arteritis

A

Young: 10-40y
Females
Asian

143
Q

Give 6 S/S of Takayasu’s arteritis

A

Systemic features e.g. malaise
Unequal BP in upper limbs
Carotid bruit + tenderness
Absent/ weak peripheral pulses
Upper + lower limb claudication
Aortic regurg (~20%)

144
Q

Ix for Takayasu’s arteritis

A

MR or CT angiography

145
Q

Mx for Takayasu’s arteritis

A

Prednisolone PO

146
Q

What is Coarctation of the aorta?

A

Congenital narrowing of descending aorta at site of ductus arteriosus insertion
M > F despite a/w Turners

147
Q

List 4 associations to coarctation of the aorta

A

Turner’s syndrome
Bicuspid aortic valve
Berry aneurysms
Neurofibromatosis

148
Q

How does coarctation of the aorta present in infants and adults?

A

Infants: heart failure
Adults: HTN

149
Q

Give 4 clinical signs of coarctation of the aorta

A

Radio-femoral delay
Mid systolic murmur, max. over back
Apical click from aortic valve
Notching of inferior border of ribs (due to collateral vessels)

150
Q

How may patients with coarctation of the aorta present?

A

Sx of arterial insufficiency e.g. syncope + claudication

151
Q

Mx of coarctation of the aorta

A

Angioplasty or surgical resection

YR6 Rotations (22 decks)

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