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Pass Medicine > Vascular > Flashcards

Vascular Flashcards

1
Q

At what diameter do we consider someone to have a AAA?

A

> 3cm

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2
Q

What are risk factors for AAA?

A

Most common:
Smoking
HTN
Diabetes

Rarer:
Syphilis
Ehlers Danlos type 1
Marfans

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3
Q

What is the difference between true and false AAAs?

A

True AAA involves all 3 layers of arterial wall

False only involves a siingle layer of fibrous tissue

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4
Q

What demographic is most likely to have a true AAA?

A

Elderly men

As such, screening via US is being offered to all men aged 65

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5
Q

Where does the aneurysm in AAA usually rupture?

A

80% into retroperitoneal space

20% rupture anteriorly

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6
Q

What impacts the risk of rupture with AAA?

A

Size of aneurysm:

2% of 4cm aneurysms will rupture over 5 years compared with 75% of 7cm aneurysms

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7
Q

What are indications for surgery in AAA?

A

> 5.5cm
Symptomatic
Rupture

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8
Q

Outcomes of AAA screening?

A

<3cm - no further action
3-4.4cm - small aneurysm, scan 12 monthly
4.5-5.4 - rescan 3 monthly
>5.5 - refer within 2 weeks to vascular surgery for probable intervention

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9
Q

Management of AAA if <5.5cm?

A

Abdominal US surveillance and optimise risk factors (e.g. smoking, HTN), commence aspirin/statin therapy

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10
Q

Management of AAA if >5.5cm?

A

Elective endovascular repair (EVAR)

This involves placing a stent into the abdominal aorta via the femoral artery to prevent blood collecting in the aneurysm

Open repair (clamping the aorta, then replacing it with a prosthetic graft)

If aneurysm >6.5 must also inform DVLA until repaired (disqual. from driving)

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11
Q

Symptoms of AAA?

A

Abdominal pain
Back/loin pain
Distal embolisation producing limb ischaemia

Signs:
Pulsatile mass felt in abdomen

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12
Q

Other than US, what other imaging would you like in AAA?

A

CT scan with contrast to help plan surgery

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13
Q

Main complication of EVAR?

A

Endovascular leaking (blood leaks out of the graft, allowing for aneurysm to still collect blood)

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14
Q

How to treat ruptured AAA?

A 
High flow O2
IV access
Urgent bloods, crossmatch
Maintain BP <100 (risk of dislodging clot precipitating further bleeding)
Open surgical repair
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15
Q

Where do thoracic aortic aneurysms affect?

A

60% ascending/aortic root
10% aortic arch
40% descending aorta

(This doesn’t add up but.. maybe 2 places affected at once?)

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16
Q

What are thoracic aortic aneurysms due to?

A

Degradation of the tunica media (middle layer of artery/vein)

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17
Q

What are the main causes of thoracic aortic aneurysms?

A

Connective tissue diseases (Marfan’s, Ehler’s danlos)
Bicuspid aortic valve
Trauma
Aortic dissection
Aortic arteritis (e.g. Takayasu arteritis)
Tertiary syphilis

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18
Q

What are the risk factors for thoracic aortic aneurysm?

A 
FHx
HTN
Atherosclerosis
Smoking
High BMI
Male
Age (advanced)
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19
Q

Clinical features of thoracic aortic aneurysm?

A 
Usually asymptomatic
Pain:
Asc. aorta - ant. chest
Aortic arch - neck
Desc. aorta - between scapulae
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20
Q

What do you see on CXR with thoracic aortic aneurysm?

A

Widened mediastinal silhouette and an enlarged aortic knob

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21
Q

What is the imaging of choice in thoracic aortic aneurysm?

A

CT chest with contrast

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22
Q

Management of thoracic aortic aneurysm?

A

Statin + antiplatelet (aspirin)
BP management
Smoking cessation

Surgery:
Usually if >5.5cm

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23
Q

What are the layers of an artery?

A 
Tunica intima (inner)
Tunica media (middle)
Tunica adventitia (outer)
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24
Q

What is an aortic dissection?

A

A tear in the intimal layer of the aortic wall causing blood to flow between and split apart the intima and media

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25
Q

How can we define aortic dissection?

A

Acute <14 days

Chronic >14 days

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26
Q

What are the directions an aortic dissection can progress?

A

Toward the iliac arteries (anterograde dissection)

Toward the aortic valve (retrograde dissection)

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27
Q

What classifications can we use for aortic dissection?

A

Stanford or DeBakey classifications

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28
Q

Risk factors of aortic dissection?

A 
HTN
Atherosclerotic disease
Male
Connective tissue disorders (Ehler's Danlos type 1 or Marfan's)
Bicuspid aortic valve
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29
Q

Clinical features of aortic dissection?

A

Tearing chest pain
Radiates to the back

Signs:
Tachycardia
Hypotension
New aortic regurg. murmur

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30
Q

What investigations would you like for aortic dissection?

A

Baseline bloods - FBC, U+Es, LFTs, troponin, coagulation
Crossmatch of at least 4 units
ABG
ECG

Imaging:
CT angiogram
Transoesophogeal echo

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31
Q

How do we manage aortic dissection?

A

ABCDE + Resus.

Stanford type A:
Managed surgically (replacement of aorta with synth. graft)

Stanford type B:
If uncomplicated, manage medically (beta blockers first line [labetalol], calc. channel blockers second line)

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32
Q

What is Stanford type A and Stanford type B?

A

A involves ascending aorta (includes DeBakey type I + II)

B does not involve ascending aorta (DeBakey type III)

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33
Q

What is chronic limb ischaemia?

A

PAD that results in symptomatic reduced blood supply to the limbs

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34
Q

What causes chronic limb ischaemia?

A

Atherosclerosis

Vasculitis (rarely)

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35
Q

What are the risk factors for chronic limb ischaemia?

A 
Smoking
DM
HTN
Hyperlipidaemia
Increasing age
FHx
Obesity/physical inactivity
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36
Q

What are the 4 stages of chronic limb ischaemia?

A

Stage I - Asymptomatic
Stage II - Intermittent claudication
Stage III - Ischaemic rest pain
Stage IV - Ulceration or gangrene, or both

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37
Q

What is Buerger’s test?

A

The patient lies supine and raises their legs until they go pale. They then slowly lower their legs until the point where their legs regain colour.
The point at which they lose colour is known as Buerger’s angle

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38
Q

What is critical limb ischaemia?

A

An advanced form of chronic limb ischaemia. It can be defined in 3 ways:

Ischaemic rest pain for greater than 2 weeks duration
Presence of ischaemic lesions or gangrene
ABPI less than 0.5

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39
Q

What are the main differentials for limb ischaemia?

A 
Spinal stenosis (neurogenic claudication)
Acute limb ischaemia
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40
Q

What are the features of spinal stenosis?

A

Typically pain from the back radiating down the lateral aspect of the leg. There are often symptoms on initial movement/symptoms that are relieved by sitting rather than standing

Positional pain is the main thing that differentiates this from claudication

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41
Q

How does acute limb ischaemia present?

A

Sudden onset of the 6 P symptoms

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42
Q

How do we manage spinal stenosis?

A

Laminectomy

43
Q

Acute limb ischaemia features?

A

Less than 2 weeks of clinical features

Features include:
Pale
Pulseless
Painful
Paralysed
Paraesthetic
Perishing with cold
44
Q

How do we diagnose chronic limb ischaemia?

A

Clinically

45
Q

How do we confirm the diagnosis/severity of chronic limb ischaemnia?

A 
Ankle-brachial pressure index (ABPI)
Normal >0.9
Mild 0.8-0.9
Moderate 0.5-0.8
Severe <0.5
46
Q

How do we investigate critical limb ischaemia?

A

Doppler ultrasound to investigate the severity and anatomical location of any occlusion
Patients can also maybe have a CT angiography
Also a cardiovascular risk assessment because of the high likelihood of CVS risk factors

47
Q

How do we manage chronic limb ischaemia?

A 
Lifestyle advice (smoking cessation, regular exercise, weight reduction)
Statin therapy (atorvastatin 80mg OD)
Anti-platelet therapy (clopidogrel 75mg OD)
Optimise diabetes control

Surgery

48
Q

How do we manage critical limb ischaemia?

A

Urgent referral for surgery

Angioplasty (with or without stenting)
Bypass grafting (diffuse disease/younger patients)
Amputation

49
Q

What are the complications of chronic limb ischaemia?

A

Sepsis (secondary to infected gangrene)
Acute-on-chronic ischaemia
Amputation
Reduced mobility/QoL

50
Q

What is acute limb ischaemia?

A

Sudden decrease in limb perfusion that threatens the viability of the limb

51
Q

What causes acute limb ischaemia?

A

Embolisation
Thrombosis in situ
Trauma (including compartment syndrome)

52
Q

If someone presents without any risk factors for PVD and is younger than 50, what tests should be done?

A

Thrombophilia screen

Homocysteine (high levels can cause disease)

53
Q

If one leg is completely fine (pulses etc.) but the other is showing signs of acute limb ischaemia, what is the likely cause?

A

Embolic occlusion

54
Q

What should you establish in your history if patient presents with acute limb ischaemia?

A

Potential causes of embolisation (chronic limb ischaemia, AF, MI, AAA, peripheral aneurysms)

55
Q

How do you investigate suspected acute limb ischaemia?

A

Bloods, including serum lactate
Thrombophilia screen
ECG

Doppler ultrasound (both limbs)
CT angiography
56
Q

How concerned are we about acute limb ischaemia?

A

Surgical emergency - complete art. occlusion can cause irreversible tissue damage within 6 hours

57
Q

What is the initial management of acute limb ischaemia?

A

Refer to senior surgical
High flow O2
IV access
Heparin bolus/treatment dose

58
Q

When do we offer conservative management in acute limb ischaemia?

A

Rutherford 1 and 2a

59
Q

What is the conservative management of acute limb ischaemia?

A

Prolonged course of heparin

Regular APTT monitoring and clinical review

60
Q

When do we surgical intervention in acute limb ischaemia?

A

Rutherford 2b

61
Q

How do we treat acute limb ischaemia surgically?

A

If embolic:
Embolectomy
Thrombolysis
Bypass surgery

If thrombotic:
Thrombolysis
Angioplasty
Bypass surgery

62
Q

What indicates amputation in acute limb ischaemia?

A

Irreversible limb ischaemia (mottled non-blanching appearance with hard woody muscles)

63
Q

What indicates a need for amputation in acute limb ischaemia?

A

Irreversible limb ischaemia (mottled non-blanching appearance with hard woody muscles)

64
Q

What is the long term management for patients who have had an acute limb ischaemia?

A

Managing the cardiovascular mortality risk:
Smoking cessation
Weight loss
Increase in exercise

Often started on an antiplatelet such as aspirin or clopidogrel as well

65
Q

What is an important complication of acute limb ischaemia?

A 
Reperfusion injury resulting in:
Compartment syndrome
Release of substances from the damaged muscle cells, e.g. -
K+ ions
H+ ions
Myoglobin (resulting in AKI)
66
Q

What is chronic mesenteric ischaemia?

A

Reduced blood supply to the bowel which gradually deteriorates over time as a result of atherosclerosis in the coeliac trunk, SMA or IMA

67
Q

What are the clinical features of chronic mesenteric ischaemia?

A 
Postprandial pain (10 mins-4 hours after eating)
Weight loss (decreased calorie intake/malabsorption)
Concurrent vascular comorbidities
68
Q

What is the diagnostic test of choice in chronic mesenteric ischaemia?

A

CT angiography

69
Q

How do we manage chronic mesenteric ischaemia?

A

Modify risk factors
Anti-platelet/statin
Endovascular/open procedures (angioplasty + stenting/endarctectomy or bypass)

70
Q

What are the complications of chronic mesenteric ischaemia?

A

Bowel infarction

Malabsorption

71
Q

What is acute mesenteric ischaemia?

A

Sudden decrease in blood supply to the bowel, resultiing in bowel ischaemia and if not promptly treated, gangrene and death

72
Q

What are the causes of acute mesenteric ischaemia?

A

Thrombus in situ (25%)
Embolism (50%)
Non-occlusive cause (20%)
Venous occlusion and congestion (10%)

73
Q

What are the clinical features of acute mesenteric ischaemia?

A

Generalised abdominal pain, out of proportion to clinical findings
Nausea, vomiting (75%)

74
Q

Investigations for acute mesenteric ischaemia?

A

ABG - serum lactate/acidosis
Routine blood tests

Imaging:
CT scan with IV contrast

75
Q

What will acute mesenteric ischaemia show on CT scan?

A

Arterial bowel ischaemia will show:
Oedematous bowel (secondary to ischaemia + vasodilation)
Loss of bowel wall enhancement
Pneumatosis

76
Q

Management of acute mesenteric ischaemia?

A 
Resuscitation
Senior involvement
Broad spectrum abx
Catheter + fluid balance chart
Excision of necrotic or non-viable bowel
Revascularisation of the bowel
77
Q

What are the complications of acute mesenteric ischaemia?

A

Bowel necrosis
Perforation
Mortality rate of 50%

78
Q

What do you need to rule out in hyperhidrosis?

A 
Secondary causes:
Pregnancy/menopause
Anxiety
Infection
Malignancy
Endocrine disorders
Medications
79
Q

What causes deep venous insuffiency?

A

DVT/Valvular insufficiency

Caused by failure of the venous system

80
Q

Risk factors for deep venous insufficiency?

A 
Female gender
Pregnancy
Increasing age
Previous DVT/phlebitis
Obesity
Smoking
81
Q

Clinical features of deep venous insufficiency

A 
Chronically swollen lower limbs
Pruritic, painful and aching lower limbs
Varicose eczema
Thrombophlebitis
Haemosiderin skin staining
Lipodermatosclerosis
Atrophie blanche
82
Q

How do we investigate deep venous insufficiency?

A

Doppler ultrasound scan
Routine blood tests to assess other aetiologies
Documentation of foot pulses/ABPI to assess viability of compression therapy

83
Q

How do we manage deep venous insufficiency?

A

Conservative:
Compression stockings
Analgesia

Surgical:
If post DVT/thrombotic type syndrome you can do venous stenting

84
Q

Complications of DVI?

A 
Swelling
Recurrent cellulitis
Chronic pain
Ulceration
DVT
85
Q

What are varicose veins?

A

Tortuous dilated segments of veins associated with valvular incompetence

86
Q

What are the four major risk factors for development of varicose veins?

A

Prolonged standing
Obesity
Pregnancy
Family history

87
Q

Clinical features of varicose veins

A

Unsightly veins
Pain/aching/swelling/itching

Variscosities in the course of the great/short saphenous veins
Features of venous insufficiency

88
Q

What classification do we use for varicose veins?

A

CEAP classification

89
Q

Investigations for varicose veins?

A

Duplex ultrasound

90
Q

Conservative management of varicose veins

A

Education - avoid prolonged standing, weight loss, increase exercise
Compression stockings* (if interventional treatment is not appropriate)

91
Q

Surgical treatment of varicose veins

A

Vein ligation, stripping and avulsion
Foam sclerotherapy
Thermal ablation

92
Q

Complications of varicose veins

A 
Surgical complications:
Haemorrhage
Thrombophlebitis
DVT
Disease recurrence
Nerve damage
93
Q

What type of ulcer is most common?

A

Venous (80%)

Remaining 20% are arterial and neuropathic

94
Q

Features of a venous ulcer

A 
Painful
Shallow
Irregular border
Granulating base
Gaiter region of legs
Varicose eczema
Thrombophlebitis
Haemosiderin skin staining
Lipodermatosclerosis
Atrophie blanche
95
Q

Investigations in venous ulcers

A

Usually a clinical diagnosis
Can confirm underlying venous insufficiency with duplex ultrasound
ABPI to assess for any arterial component
Swab cultures if suspecting infection

96
Q

Management of venous ulcers

A 
Conservative:
Leg elevation
Increased exercise
Lifestyle changes
Weight reduction
*Multicomponent compression bandaging

If varicose veins also present, endovenous techniques or open surgery

97
Q

Features of an arterial ulcer

A 
Small deep lesions
Well defined borders
Necrotic base
Pressure areas/sites of trauma
Usually a history of intermittent claudication/critical limb ischaemia
Painful
Cold
Absent pulses
98
Q

Investigating arterial ulcers

A 
ABPI:
>0.9 normal
0.8-0.9 mild
0.5-0.8 moderate
<0.5 severe
99
Q

Management of arterial ulcers

A

Conservative:
Lifestyle changes

Medical:
Aspirin/clopidogrel

Surgical:
Angioplasty
Bypass grafting

100
Q

Neuropathic ulcer features

A 
Painless ulcers at pressure points
History of peripheral neuropathy
Burning/tingling in the legs
Wasting of muscles
Punched out appearance
Glove/stocking distribution
Pulses present
101
Q

Investigations for a neuropathic ulcer

A

Blood glucose levels
Serum B12 levels
ABPI +/- duplex (for concurrent arterial disease)
Check the extent of peripheral neuropathy with touch test/vibration test

102
Q

Management of neuropathic ulcer

A

Diabetic foot clinic

Manage diabetes

103
Q

What is Charcot’s foot?

A

A neuroarthropathy whereby a loss of joint sensation results in continual unnoticed trauma/deformity occurring
Can predispose patients to neuropathic ulcer formation

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