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Block 32 GI & Surgery > CT 4.1 Vascular Disease > Flashcards

CT 4.1 Vascular Disease Flashcards

1
Q

what is raynauds

A

episodic vasospasm of the arteries of the extremities resulting in digital ischaemia

can be induced by cold or emotional stress

in 95% of cases is idiopathic

W>M

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2
Q

what are secondary causes of raynaud’s

A

-connective tissue disease: SLE, RA and sjogren’s

  • drugs such as beta blockers, chemo, cocaine
  • buergers, atherosclerosis
  • polycythaemia, leukaemia
  • vibration, frostbite
  • Hep B + C, mycoplasma and parvovirus

_ hypothyroid, pheochromocytoma, carcinoid syndrome

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3
Q

what are the symptoms of raynaud’s

A

pallor of distal fingers
numbness
pain
cyanosis
hyperaemic phase - red and warm fingers

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4
Q

what are clinical features of a connective tissue disorder

A

Abnormal nail-fold capillaries
Suggest underlying disease
Digital ulcers
Infection
Gangrene

Severe ischaemia
AF
Murmur
Malar rash
Hepato-splenomegaly

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5
Q

what investigations can be done for raynauds

A

Full blood count
ESR
Plasma viscosity
Autoimmune screen
Investigating underlying disease
Urea and Electrolytes
Liver and thyroid function tests
Plasma glucose
Urine/protein electrophoresis, Cold agglutinins and fibrinogen levels for hyperviscosity states

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6
Q

what imaging can be used for raynauds

A
  • infrared thermography (cold provocation test)
  • laser doppler flowmetry
  • digital plethysmography
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7
Q

when should you suspect secondary raynauds

A

Onset >30yrs
Asymmetrical, Intense or painful episodes
Features of underlying condition
Digital ulcers
Positive autoimmune tests

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8
Q

what is the management for raynauds

A

Smoking cessation
Maintain body warmth
Minimize stress
Regular exercise
Stop drug if SE

Medical
Calcium channel blockers esp. Nifedipine
Consider antiplatelet
Admit for IV iloprost if conservative and nifedipine not controlling symptoms
Consider immunosuppression for autoimmune associated raynaud’s

Surgical (uncommon)
Digital/thoracoscopic sympathectomy

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9
Q

what are the sub branches of chronic limb ischaemia

A
  • intermittent claudication
  • critical limb ischaemia
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10
Q

what is the pathogenesis of PAD

A

atherosclerosis

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11
Q

what are the steps of atherosclerosis

A

formation of a fatty streak

inflammation and cumulation of foam cell macrophages

fibrosis and progressive luminal narrowing

plaque rupture or ulceration

thrombosis or thromboembolism

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12
Q

what are the risk factors for PAD

A

non modifiable:
age
male sex
family history

modifiable:
smoking
hyperlipidaemia
hypertension
diabetes
sedentary lifestyle

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13
Q

what is intermittent claudication

A

Cramping muscular pain, which is brought on by exertion, relieved by rest and reproducible on walking that distance again.
It is due to inadequate oxygen delivery to the muscles.

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14
Q

what is critical limb ischaemia

A

is when chronic limb ischaemia threatens the loss of a limb.
Defined as ischaemic rest pain for more than 2 weeks, despite analgesia, or the presence of tissue loss (ulcers / gangrene)

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15
Q

what is leriche syndrome

A

aortoiliac occlusion presenting as buttock and thigh claudication + impotence

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16
Q

what is the key feature of critical limb ischaemia

A

pain at rest
pain often felt in toes as it is most distal site

felt at night due to loss of gravity’s help in perfusing the feet so they hang their leg off the bed or sleep in chairs

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17
Q

what is buerger’s test

A

Reported as the angle at which the leg becomes pale when you elevate it against gravity (which healthy limbs don’t do). You then swing the patient’s leg over the side and watch out for a “sunset foot” (arteriolar vasodilatation with foot reperfusion).

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18
Q

what other bedside tests

A

Ankle-brachial pressure index

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19
Q

what bloods for PAD

A

FBC, U&Es, Coagulation profile, lipid profile, HbA1C

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20
Q

what imaging for pad

A

duplex ultrasound

CT Angiogram

MR angiogram

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21
Q

what is percutaneous transluminal angiography

A

An arterial puncture and Seldinger technique places a sheath and catheter within the arterial tree. Injection of contrast gives a “roadmap” of the vessels.
Different wires and catheters can be manipulated to navigate the vessels.
“Digital Subtraction Angiography” (DSA) removes all background structures, such as bone, from the image to allow a more detailed view of the arteries
The “gold-standard’
Radiation dose must be considered
Uses iodinated contrast – risk of causing/ worsening renal impairment
CO2 can sometimes be used as an alternative
Risks of damage to vessels, bleeding, emboli, dissection, pseudoaneurysm
The advantage of PTA is that endovascular procedures - (balloon angioplasty or stenting) - can be performed at the same time

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22
Q

what is the management of intermittent claudication

A

a quarter of IC patients progress to CLI and have a 1-3% risk of amputation

antiplatelet (anticoagulation in some situations). See NICE guidelines

statin (NICE guidelines [Atorvastatin 80mg OD is a good option for most patients])

blood pressure control (NICE & SIGN hypertension guidelines)

Screening for diabetes and ensuring good diabetic control

smoking cessation advice +/- nicotine replacement therapy / further intervention

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23
Q

which vasodilator can be used for IC

A

Naftidrofuryl (a selective 5-HT2 antagonist)

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24
Q

what is the management of CLI

A
  • urgent referral to vascular surgeon as limb is at risk

limb revascularisation is the main course of action :

1) bypass or endarterectomy

2) angioplasty or stenting

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25
what is acute limb ischaemia
sudden decrease in limb perfusion, producing new or worsening symptoms and signs…threatening limb viability. It can occur in people who have had no previous symptoms’
26
what are the thrombotic causes of ALI
rupture of atherosclerotic plaque bypass graft thrombosis cancer + prothrombotic state arteritis infection states of low flow like shock
27
what are the embolic causes of ALI
atheroscleorisis mural thrombus atrial fibrillation thoracic or abdominal aortic aneurysm bacterial endocarditis myxoma
28
what are some rarer causes of ALI
- compartment syndrome - dissection - trauma
29
what are the symptoms of ALI
sudden onset of a painful, numb, weak and cold limb
30
what are the 6 Ps of ALI
pain paraesthesia pallor paralysis pulselessness perishingly cold
31
what are the bedside tests for investigating ALI
handheld doppler ABPI ECG (arrhythmia may precipitate embolic event) bloods: FBc, U+E, coag, group+Save, Creatine kinase(marker of rhabdomyolysis)
32
what classification is used for ALI
Rutherford classification three stages: 1) viable 2) A = marginally 2B immediately 3: irreversible
33
what is the management of ALI
Oxygen, IV fluids and analgesia 5000 units of unfractionated heparin - revascularisation embolectomy or arterial bypass stenting catheter directed thrombolysis or amputation if limb not salvageable
34
what is compartment syndrome
Acute increase in pressure within a compartment which endangers the perfusion of tissues, requiring emergency decompression” Symptoms: Disproportionate ’Crescendo pain’, unresponsive to analgesia
35
what are the 4Ps compartment syndrome
pain on passive movement paraesthesia* pulselessness paralysis* * indicators of severity
36
what are examples of minor amputations
Transmetatarsal (Plus various less common midfoot/ hindfoot/ ankle amputations)
37
what are examples of major amputations
BKA AKA
38
what is the pre-op management for patients undergoing amputation
Optimisation of existing co- morbidities: Diabetes, Cardiovascular, Respiratory Psychological impact considered Social impact considered – home visits etc. if possible
39
what is the post-op management for amputations
Psychological impact considered Risk of infection, ischaemia, prevention of stump trauma, pressure injury Social input and home adaptations Physiotherapy Stump modelling, Prosthesis fitting and ambulation Significant recent improvements in prosthetic technologies In part due to a major drive in research & development after military injuries Phantom limb sensation/ pain
40
what is the official definition of an aneurysm
a permanent focal dilation of an artery with at least a 50% increase in diameter compared to normal
41
facts about AAA
An anteroposterior diameter >3cm in infra-renal abdominal aorta Highest incidence is in Caucasian men aged >65 years: 5% The risk of rupture increases exponentially with increasing size (<1% per annum below 5.5cm)
42
what is the aetiology and risk factors for AAA
Prevalence four to five times higher in males than females Atherosclerosis (degenerative disease) is the predominant cause
43
what are other causes of AAA
infection (“mycotic aneurysm”), connective tissue disorders (Marfans and Ehlers-Danlos), arteritis
44
what are non-modifiable risk factors for AAA
increasing age sex m>f genetics
45
what are modifiable risk factors for AAA
smoking hypercholesterolemia hypertension
46
what is the screening like for AAA
First invitation is at 65yrs of age for men Abdominal USS, measures the anteroposterior (AP) infrarenal aortic diameter If results normal (i.e. aorta diameter < 3cm) → no further scans ‘Small’ AAA (i.e. → aorta diameter 3cm- 4.4cm) → yearly scans ‘Medium’ AAA (i.e. → aorta diameter 4.5- 5.4cm) → scan every 3 months ‘Large’ AAA (i.e. diameter 5.5cm or greater) → referred to Vascular surgeon to discuss further management
47
what are the signs and symptoms of AAA
asymptomatic until rupture Abdominal pain, radiating to back 2) Shock N+V
48
what is the management of triple A
Elective Ultrasound surveillance programme (if diameter <5.5cm), PLUS: Risk factor modification- stop smoking, BP control, antiplatelet, statin Can slow progression, and improve fitness for repair when it becomes necessary CT if diameter 5.5cm or greater Judge suitability for open/ endovascular aneurysm repair (EVAR) At 5.5cm, the risks of rupture generally outweigh the risks of repair All potential elective cases should be discussed in a Vascular MDT meeting Emergency (i.e. ruptured or symptomatic AAA) Urgent CT scan proceed to either open or endovascular repair consider palliation if unfavourable factors for successful outcome
49
what are the treatment options for AAA
1) open repair 2) EVAR (endovascular aneurysm repair)
50
what is chronic venous disease
- superficial venous incompetence - deep venous disease
51
how is the venous system of the legs arranged
80% of venous return to the heart is via deep veins. superficial veins are connected to deep veins via perforating veins pressure needed is achieved via the calf muscles
52
what is the pathology of varicose veins
tends to affect the superficial veins which are less thicker walled and not confined by fascia so cannot withstand high pressure and over time wall becomes damaged due to leaky valves, inflammation, or venous hypertension. therefore the veins become dilated and tortuous
53
what is the prevalence of varicose veins
30% of adult pop M = F but more females present
54
what are the risk factors for developing varicose veins
obesity increasing age family history / genetics pregnancy hormonal factors
55
what are the symptoms of varicose veins
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) Aggravating factors may include: occupation: prolonged standing, lifting e.g. factory production lines etc pregnancy hormonal changes – endogenous or exogenous menstruation
56
what skin signs suggest advanced venous insufficiency
(healed) ulcers, lipodermatosclerosis, haemosiderin pigmentation, telangiectasia or eczema / atrophie blanche. change may occur around typical site near medial malleolus
57
what classification system is used for varicose veins
CEAP clinical etiologic anatomic pathophysiologic ranges from C0 to C6
58
what is the management of varicose veins
- if bleeding refer immediately to vascular seervices - referral also required if there are symotomatic, there are skin changes or healed ulcers or signs of superficial vein thrombosis
59
what are the investigations for VVeins
duplex ultrasound
60
what are the treatment options for V veins
Endovenous thermal ablation (laser or radiofrequency) involves sealing the lumen of the incompetent vein by delivering thermal energy via a catheter under ultrasound guidance Ultrasound-guided foam sclerotherapy - This is recommended if endothermal ablation is unsuitable. It involves injection of a sclerosant chemical into the veins. Conventional surgery: (junctional ligation, stripping and avulsions)
61
what are the causes of chronic leg ulceration
venous 70% mixed 15% arterial 5% other 10% Chronic venous hypertension is thought to be the primary cause of around 70% of leg ulcers, and a contributory cause in a further 15%
62
epidemiology and socio-economics of leg ulcers
1% prevalence lower SES tend to take longer to heal 2% of NHS budget
63
venous ulcers
v painful (releived on elevation) mostly affect medial merimalleolar area ulcer is large, shallow and irregular with exudates Associated features: warm skin normal peripheral pulses varicose veins leg oedema haemosiderin pigmentation (leaching of iron from blood into the soft tissues) venous eczema lipodermatosclerosis and atrophie blanche
64
what are the risk factors for venous ulcers
Superficial venous incompetence (e.g. Varicose veins) Previous deep vein thrombosis in the affected leg Phlebitis in the affected leg Previous fracture, trauma, or surgery to leg Family history of venous disease.
65
arterial ulcers
painful (worse when leg is elevated) mostly affects pressure and trauma sites (pretibial and supra-malleolar) and distal points such as toes lesion is small, deep and well defined (punched out appearance often with necrotic base) Associated features: cold skin, weak or absent peripheral pulses, shiny pale skin, loss of hair Represent advanced PAD – Critical Ischaemia
66
what are the RFs for arterial ulcers
Peripheral arterial disease. Coronary heart disease. History of stroke or transient ischaemic attack. Diabetes mellitus. Obesity and immobility.
67
diabetic ulcers
usually foot ulcers rather than leg Most commonly affects pressure sites: soles, heels, toes, metatarsal heads Often painless with abnormal or absent sensation Underlying pathology is peripheral neuropathy secondary to diabetes lesion is punched out Associated features: warm skin, peripheral neuropathy, normal peripheral pulses Be aware that many diabetic patients will have coexisting PAD, in which case it may be a neuroischaemic ulcer
68
investigations for leg ulcers
ABPI (rule out significant arterial disease venous duplex ultrasound arterial imaging diabetic: monofilament, HBA1c and foot x-rays
69
what does a ABPI of >1.3 suggest
generally indicates calcified, stiff arteries. This may be seen with advanced age, diabetes or chronic kidney disease
70
ABPI of 0.9 to 1.29 suggests
normal
71
ABPI of 0.8 - 0.9 suggest
borderline often require additional tests, e.g. exercise ABPI (treadmill)
72
ABPI of <0.8 suggests what
PAD very likely
73
ABPI of <0.5 suggest what
severe PAD and should be referred urgently
74
management of venous ulcers
: If ABPI >0.8 apply compression bandaging or Class 2-3 compression hosiery
75
management of arterial ulcers
vascular reconstruction
76
management of mixed ulcers
: Initially cautious modified-strength compression with close observation (+ revascularisation if necessary, but may not be needed)
77
management of diabetic ulcers
A complex group of patients, requiring an MDT approach to include:- Podiatry & orthotists: debridement, offloading/pressure relieving footwear Diabetology: management of diabetes Vascular surgeon: improving perfusion, controlling infection soft tissue, osteomyelitis

Block 32 GI & Surgery (13 decks)

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