Arterial/Venous Disease

Question 1

HOW DO VEINS WORK?

i) what are perforating veins?
ii) what helps return blood to heart against gravity eg from leg? (2)

Answer 1

i) structures that join deep and superficial veins

ii) muscle pump eg muscle contrac on movement
diaphraghm - increaase in intra-ab pressure, decrease in thoracic preessure pushes blood up to heart

Question 2

VENOUS HYPERTENSION/INSUFFICIENCY

i) what is it?
ii) what pressure is maintained in the veins in the leg?
iii) give four causes
iv) what happens to the legs when the veins fail? what is the area called? what can this cause? (3)
v) do more M or F have venous problems in population studies? what about in clinical studies?

Answer 2

i) valves in veins (usually in arms and legs) dont work properly and cause blood to pool in legs and put pressure on the walls of the veins
ii) incompetent venous valves > maint high venous pressure in the legs
iii) immobility, calf muscle pump fail, deep venous occlusion, obesity

iv) get reflux > blood into ankles by gravity
- area is called Gaiter area
- can result in stasis ulcer, haemosiderin deposition, varicose veins (veins push into skin)

v) population studies M=F, clinical studies F>M

Question 3

VARICOSE VEINS

i) what is it?
ii) what can happen as a result of perforator vein insufficiency (2)
iii) what is perforator disease? how can this be treated? (3)
iv) which veins in the leg often demonstrate reflux? why does this happen

Answer 3

i) vein which has permanently lost its valvular efficiency as a result of continous dilatation under pressure > becomes elongated, tortuous, pouched and thickened
ii) venous reflux > deterioration in varicose veins and dev of ulcers

iii) incompetency of perforator veins (usually stop backflow of blood to superficial veins) > pressure builds up under the skin
- tx with open ligation, sclerotherapy (inject into veins to shrink them), leave alone

iv) lateral plexuses
- some patients have remnants of embryological veins that fill and look varicose

Question 4

PATTERNS OF THIGH REFLUX

i) which vein in the thigh can demonstrate reflux?
ii) what can pudendal vein reflux/incompetency result in?
iii) what can ovarian vein incompetence result in? (3)
iv) what is pelvic congestion syndrome? who does it normally occur in? name three places pain may be felt? what treatment may be most effective
v) what can pelvic congestion syndrome be associated with? what is the equivalent in males?

Answer 4

i) anterior accessory saphenous vein
ii) pudendal vein reflux > incompetenct in retroperitoneal area > cluster of varicosity in the pelvis
iii) ovarian vein incompetence > deep dysparunia, heavy bleeding, unexplained pelvic pain

iv) pelvic congestion syndrome > otherwise unexplained pelvic pain
- occurs in young pre menopausal women
- non cyclical postural back pain, pelvic pain, upper thigh pain
- endovascular therapy is more effective than surgery

v) may be assoc with haemmorhoids
- equiv of varicocele in males

Question 5

CEAP CLASSIFICATION FOR VARICOSE VEINS

i) what is C0?
ii) is C1 treated on the NHS? what are the main reasons for treatment (2) which area is often involved? what may it be secondary to?
iii) what distribution do C2 often have? what does severity depend on?
iv) what is C3 associated with? what should be done prior to definitive treatment? why does this happen?
v) what is associated with C4? how should this be treated? (2)
vi) what is seen in C5? why does this happen? is this treatable on the NHS?
vii) what is seen in C6? why?

Answer 5

i) C0 - no visible venous disease

ii) C1 not usually treated on NHS - mainly treat for cosmetic/QOL
- often involves lateral cutaneous plexus
- may be secondary to underlying superficial or deep vein pathology

iii) often distrib of great saphenous vein
- severity depends on associated complications, not how big the veins are

iv) C3 is assoc with oedema due to venous mechs not strong enough to return blood > pooling
- compression should be done prior to definitive treatment

v) C4 is assoc with skin changes
- treat topically and also treat underlying insufficiency

vi) see a healed ulcer - specific skin area gets high pressure > skin damage
vii) active ulceration > damage to skin due to chronic inflam/venous HTN

Question 6

SYMPTOMS AND COMPLICATIONS OF VARICOSE VEINS

i) name five symptoms? what is the most common?
ii) what complication occurs in 20% of patients with varicose veins? how is this treated?
iii) what should be done if varicose veins bleed? (2)
iv) name two other complications of VV?

Answer 6

i) aching is most common, restless legs, cramps, itching, tingling
ii) phlebitis occ in 20% of pts > treated with anti coagulants
iii) bleeding > elevate leg and press to stop bleeding / treat underlying problem
iv) skin changes and ulceration

Question 7

HISTORY AND EXAMINATION

i) name three signs that may be seen due to venous hypertension complications
ii) what should be tested at the saphenofemoral junction?
iii) what is a tapping test? what is seen if there is an incompetent vein?
iv) what may be heard over the vein if there is reflux? what equipement is used to do this?
v) name four things a duplex ultrasound scan is for?

Answer 7

i) eczema, oedema, ulver, muscle wasting, stiff joints
ii) test control at SF junction > hand on groin > stand up > do veins fill (supine vs standing)
iii) tapping test - tap an incompetent vein > the tap will be transmitted to the vein upstream

iv) reflux = trill or bruit over vein
- auscultate using a hand held doppler

v) duplex US - confirm or establish source of reflux (identifies obstruction), provides a roadmap, assesses deep veins, allows planning of treatment, guides treatment

Question 8

VARICOSE VEIN TREATMENT

i) name three conservative treatments? what should not be used?
ii) name three invasive treatments
iii) what two types of endovenous therapy mau be used? what do these do to the vein?
iv) how does radiofrequency ablation treat VV? name an advantage of this? what is the 5 year success rate
v) name two ways to get rid of residual variscosities

Answer 8

i) leg elevation, weight loss, compression stockings (not great but good alongside other tx), exercise
- dont use TED stockings

ii) surgery, catheter (heat based) therapy, sclerotherapy (inject drug into vein to make it shrink)

iii) laser and radiofrequency
- seal the vein using a laser

iv) heat and seals the vein
- quick recovery time (1-3 days), no groin incision, 85% 5 year sucess rate

v) phlebectomy (remove diseased vein through small incision)
- foam sclerotherapy (inject foam into bv to close it)

Question 9

SCLEROTHERAPY

i) what is it? what type of veins is it usually used for?
ii) what type of veins is foam sclerotherapy used for? name two limitations? what is the max amount of foam that can be injected
iii) name two major complications
iv) name a different type of therapy that may be good for needle phobic patients

Answer 9

i) inject drug into vein to make it shrink - usually used for smaller veins

ii) foam sclerotherapy can be used for bigger/truncal veins
- limitation - size of vein and volume of foam (too much)
- never inject more than 12mls

iii) complications - phlebitis and pigmentation
iv) cyaoacrylate embolisation using glue

Question 10

VENOUS ULCERS

i) what are the three steps that should be used when approaching a venous ulcer? name three underlying problems that may cause them? name three signs of venous insufficiency on the skin
iii) name three things that should be assessed when looking at an ulcer? what imaging technique should be used?
iv) what can be used to assess whether there is an arterial component?
v) what is the mainstay of treatment for active venous ulceration? how does it work? what should be considered before bandaging?

Answer 10

i) accurate assessment > debridement and sensible dressing > compression therapy
- venous problems, mobility, nutritional inssue
- venous insuffic. = skin change, pigmentation, varicose veins

iii) skin damage (need for emoillent), joint stiffness, muscle wasting, pressure damage
- duplex US

iv) ABPI - ankle brachial pressure index (compare highest systolic pressure in the upper limb to the the highest sys pressure at the ankle)

v) compression therapy > diminishes leg vein distention and stasis, oedema and improves overall venous function
- ABPI needs to be >0.6 to bandage

Question 11

DEEP VEIN THROMBOSIS

i) what is virchows triad? name one things that can contribute to each
ii) name four things that are used in diagnosis
iii) why is there increased risk of thrombosis post covid 19?
iv) what is the best management for DVT? name two things that can be done
v) name two drugs that may be given to treat a DVT? how long should compression hoisery be used for?

Answer 11

i) virchows triad - three factors that contribute to thrombosis
- changes to flow (immobikity, perioperative)
- changes to blood coagubility (thrombophilia, severe dehy, malig, sepsis)
- changes to vessel wall (IVDU, trauma eg crush injury)

ii) clinical features (hx, wells score), D dimer, duplex US
iii) likely due tp dorecy endothelial cell infection

iv) prevention - risk assess
- peri op prophylaxis eg TED stockings
- coagubilitu - LMW hepais, good hydration, correct RFs eg COCP and smoking

v) anticoagulate with heparin, DOAC, wafarin
- compression hoisery for 2 wks min

Question 12

THROMBOLYSIS IN DVT

i) how does catheter directed thrombolysis work? what pharma agent may be used
ii) what may be done for a recurrent DVT?

Answer 12

i) place catheter into clot > infuse drug eg TPA (alteplase) to break it down
ii) put in a stent

Question 13

POST THROMBOTIC SYNDROME

i) what is it?
ii) what % of patients get it after a symptomatic DVT?
iii) what may be seen in young patients?
iv) name three things that can cause it?

Answer 13

i) combination of patient reported symptoms and objective findings such as swelling, skin change following DVT in upper or lower limb
ii) 20-50% patients get it
iii) may see severe pain and ulceration

iv) obstruction of vein at key points, reflux (loss of valve integrity), venous HTN
- get reduced calf perfusion with tissue hypoxia, inc tiss perm > oedema

Question 14

VENOUS INFARCTION

i) what is it?
ii) name three things that may be seen clinically
iii) name three things that must be done? is this an emergency?

Answer 14

i) severe venous insufficiency associated with arterial insuff > build up of pressure
ii) pulses palpable initially, swelling, tenderness, discolouration

iii) elevation of leg, fluid resus, thrombolysis, may beed emergency amputation
- this is a medical emergency

Question 15

AAA

i) what is an aneurysm? what is a AAA?
ii) name three risk factors? name three possible causes? who is offered screening?
iii) name four ways it can present? how may it present if ruptured? (3)
iv) which imaging is used for initial investigation? which scan is then done?

Answer 15

i) aneurysm = abnormal dilatation of a blood vessel by more than 50% of its diameter
- AAA - dilatation of abdominal aorta >3cm

ii) RF - smoking, HTN, hyperlipid, family hx, male gender and increasing age
- possible causes - athero, trauma, infection, connective tissue disease
- Screening is offered to men in 65th year (abdo US scan)

iii) many are asymptomatic/detected incidentally
- presents with abdominal pain, back or loin pain, distal embolisation > limb ischaemia, pulsatile mass felt in abdomen
- if ruptured may present with pain, shock or syncope

iv) initial investigation by US scan
- follow up with CT contrast once USS confirms diagnosis and diameter is 5.5cm

Question 16

AAA TREATMENT AND COMPLICATIONS

i) how is <5.5cm managed? what advice is offered to patients? (3)
ii) when may surgical intervention be offered? what is the patient is unfit for surgery?
iii) name two surgical approaches that can be used? which has improved short term outcomes?
iv) name a surgical complication?
v) what increases the risk of rupture? what is the classic triad of symptoms for rupture? how should it be immed managed? (3)
vi) in what way does shock have to be carefully managed? what is done for rupture if the patient is unstable? if the patient is stable?

Answer 16

i) <5.5cm can be monitored via duplex USS (surgery for smaller diameter has no survival benefit)
* 3-4.4cm - yearly US
* 4.5-5.4 - 3 monthly US
- reduce CV risk factors eg smoking cessation, BP control, statin therapy, weight loss (>6.5 disqualified from driving)

ii) Surgical intervention consider for AAA >5.5cm/expanding >1cm year/symptomatic AAA
* if patient is unfit - may leave until 6cm

iii) open repair (ML laparotomy) > clamp and remove segment > replacce with prosthetic graft
- endovascular - intro graft via femoral artery then stent across the aneurysm
- endovasc has improved short term outcome (decreasing hospital stay and 30 day mortality but higher rate of rupture)

iv) Endovascular leak (from EVAR) - incomplete seal forms around the aneurysm > blood leaks around the graft and can cause rupture

v) Ruptured AAA - increases with diameter of aneurysm and smoking, HTN, female
- classic triad of symptoms for AAA rupture are flank/back pain, hypotension, pulsatile abdo mass (80% rupture posteriorly)
- treat with immediate high flow O2, IV access, urgent bloods and crossmatch

vi) treat shock careful as raising the BP will dislodge a clot > ppt bleeding so keep BP <100
- unstable patient > immediate transfer to theatre for open repair
- stable patient > CT angio to detemine whether EVAR can be done

Question 17

CAROTID ARTERY DISEASE

i) what causes it? are most cases asymp or symptomatic?
ii) how does it begin? name three risk factors? what can predispose?
iii) name two ways it can present? what may be heard on examination? why are most unilateral cases asymptomatic?
iv) what imaging should be done for any patient suspected of isch stroke? what is first line investigation?

Answer 17

i) build up of atherosclerotic plaque in one or both common internal carotid arteries > stenosis or occlusion
- majority is asymptomatic > responsible for 15% ischaemic strokes

ii) atheroma starts with a fatty streak > accum a lipid core > fibrous cap
- turbulent flow at the bifurcation of the carotid artery predisposes
- RFs - age >65, smoking, HTN, hypercholesterol, obesity, diabetes, hx/FH of CV disease

iii) Often asymptomatic
- may present as a focal neuro deficit as either TIA or stroke
- TIA - lasts less than 24hrs before full resolution
- stroke - lasts for more than 24hrs before full resolution
- may hear a carotid bruit in the neck (<50% of the time)
- likely asymp if unilateral due to collateral supply from contralateral internal carotid and vertebral arteries in COW

iv) any patient suspected of ischaemic stroke > do urgent non contrast CT head to look for evidence of infarction (can it be treated with thrombolysis?)
- first line investigation is carotid US doppler

Question 18

CAROTID ARTERY DISEASE TREATMENT

i) what is the acute management for all patients with suspected stroke? (2) what other assessment can be done?
ii) what should be given if ischaemic stroke? (2) what should be done if haemmorhagic? when may a thrombectomy be implicated?
iii) what does CV risk management for all patients with known stroke/TIA consist of? (5) who may they be referred to?
iv) which procedure should patients be refered for if acute non disabling stroke/TIA and have carotid stenosis? what does this procedure involve?
v) what are the main risks of carotid endarterectomy?

Answer 18

i) all pts with suspected stroke should be treated with high flow oxygen and optimise blood glucose
- swallowing screen assessment

ii) if ischaemic stroke > IV alteplase within 4.5hrs and 300mg aspirin
- if haemmorhagic > correction of coagulopathy and refer to neurosurgery
- thombectomy in patients with acute ischaemic stroke and confised occluion of proximal anterior circulation

iii) all patients with known stroke or TIA should be started in CV risk management: Anti plat (aspirin for 2 weeks then clopidogrel), statin, manage HTN and diabetes, smoking cessation, exericse and weight loss
- SALT referral for dysphagia, dysphasia

iv) Carotid endarterectomy
- involves removing the atheroma and associated damaged intima > reduces risk of future strokes/TIAs
- cut into affected artery wall, remove plaque and intima then stitch to repair artery > restore blood flow -

v) main risks are stroke, nerve damage to hypoglossal, glossopharyngeal or vagus, MI, local bleeding, infection
* seen as superior to carotid stenting

Question 19

PERIPHERAL/VISCERAL ANEURYSMS

i) what is an aneurysm? what is the most commonly affected vessel for aneurysms? name three RFs
ii) what is the most common location for pseudoaneurysms? why? name another thing that can cause them here
iii) which peripheral site are they most commonly found in? how may the limb look? what associated symptom may there be?
iv) where do visceral artery anuerysms most commonly occur? how do they present if not ruptured (2) how do they present if ruptured?
v) what are 50% of hepatic artery anurysms due to? how may they present? how may the patient appear if there is biliary obstruction?
vi) name three symptoms of a renal artery aneurysm

Answer 19

i) aneurysm = persistent, abnormal dilatation of an artery above 1.5x normal diameter
- abdo aorta is most commonly affected vessel but can also affect periph and visceral
- RFs - smoking, HTN, hyperlipidaemia, family history

ii) femoral artery - typically pseudoaneurysms
- due to percutaneous vascular intervention
- patient self injecting > groin

iii) popliteal artery (most common site) - usually symptomatic
- acute limb ischaemia
- intermittent claudication
- may be found incidentally

iv) visceral artery aneurysms - most commonly in the splenic artery
- present with vague epigastric/LUQ pain
- severe abdo paina and haemodynamic compromise if ruptured

v) hepatic artery present usually asymp
- assoc with percutaneous instrumentation in 50% cases
- can present with vague RUQ pain or epigastric pain
- may get jaundice if biliary obstruction

vi) renal artery
- haematuria, resistant hypertension, loin pain

Question 20

PERIPHERAL/VISC ANEURYSMS INVESTIGATIONS AND TX

i) what scan is done on the popliteal artery? name another reason it may be swelled? which imaging may be used for anatomical and patency assess?
ii) which scan is used for femoral artery? what is the mainstay scan for splenic/hepatic/renal artery?
iii) why should all popliteal aneurysms be treated? at what size should treatment be considered? how may they be repaired? (2)
iv) what is the mainstay tx for femoral aneurysms? what is first line for splenic/hepatic? what can be done if the patient is les stable?
v) what is the mainstay tx for renal artery? what can be done if it affects the main renal artery?

Answer 20

i) Popliteal artery > US duplex scan > differentiate between other causes of swelling eg bakers cyst
- CT angio or MR angio to allow good anatomical assessment of aneurysm and asses distal artery patency

ii) Femoral artery > US duplex scan before CT or MR angio for further anatomical imaging and surgical planning
- Splenic/hepatic/renal artery mainstay is CT/MR angiography
* USS for monitoring on thin patients

iii) Popliteal aneurysm - high risk of embolic events therefore treat regardless of size
- asymp but >2.5cm then consider treatment
- embolectomy or thrombolysis if no patent tibial vessel seen
- endovascular repair > stent insert across aneurysm (need normal calibre artery above and below for the stent to seal in)
- surigcal repair - ligation of aneurysm or resection with a bypass graft

iv) Femoral - mainstay of treatment is open surgical repair
- Splenic/hepatic - first line management is endovascular repair - embolisation/covered stent grafts once patient is haemodynaically stable
- may do open repair if patient is less stable

v) Renal artery > endovascular repair is mainstay of treatment > insert a stent if aneurysm affects main renal artery
- if aneurysm is in the hilum then endovascular repair with coils and covered stent graft may be used

Question 21

ACUTE LIMB ISCHAEMIA

i) what is it? what is the most common cause? name two other cause? what are the 6Ps? (symptoms/signs)
ii) which blood marker can look at level of ischaemia? what is gold standard imaging?
iii) what would cause it to be a surgical emergency? how should this be managed? (3)
iv) how may a patient be managed conservatively? what will management be if embolic cause? if thrombotic cause? if irreversible limb ischaemia?
v) name three complications

Answer 21

i) sudden decrease in limb perfusion which threatens viability of the limb
- caused by embolisation (most common)
- thrombosis in situ (atheroma rupture and form plaque), trauma are other causes
- 6 Ps - pain, pallor, paraesthesia, perishingly cold, pulseless, paralysis

ii) serum lactate to look at the level of ischaemia
- CT angiography is gold standard

iii) surgical emergency if complete occlusion > irreversible tissue damage if not treated in 6 hours
- start on high flow O2 and ensure IV acess
- heparin bolus followed by heparin infusion

iv) conservative management = prolonged course of heparin (monitor APTT)
- if embolic cause do embolectomy, thrombolysis or bypass surgery
- if thrombotic cause do local thrombolysis, angioplasty, bypass
- if limb ischaemia is irreversible then amputate

v) reperfusion injury - sudden increase in cap permeability
- compartment syndrome
- release of substances from damaged muscle cells eg K+ > hyperkal, H+ > acidosis, myoglobin > AKI

Question 22

CHRONIC LIMB ISCHAEMIA

i) what is it? what is it typically caused by? name another cause? name three RFs? what assessment do all patients need?
ii) what is critical limb iscahemia? what type of diagnosis is it? how is it characterised? name two things that may be seen? how may limbs appear? name three other assoc features
iii) what do chronic limb isch features depend on? what is an early sign? what classification is used? what is buergers test?
iv) what is ABPI? what level is critical?
v) which two imaging techniques may be used to investigate?

Answer 22

i) symptomatic reduced blood supply to the limbs typically caused by atherosclerosis
- can also be caused by vasculitis
- RFs - smoking, DM, HTN, hyperlipidaemia
* all patients need a CV risk assess

ii) critical limb ischaemia = advanced form of chronic limb ischaemia
- diagnosis is clinical
- ischaemic rest pain >2 weeks that requires opiates
- may see ischaemic lesions/gangrene
- pale and cold limbs > weak/absent pulses
- limb hair loss/skin damage/thick nails

iii) clinical features depend on severity
- intermittent claudication is an early sign (cramping after walking a fixed distance with rest relief)
- use fontaine classification - I = asymp and IV = ulcer/gangrene
- Buergers test - lay supine > raise legs > angle at which limb goes pale is buerger angle (<20 is severe ischaemia)

iv) ABPI (ankle brachial pressure index) - systolic pressure recorded at brachial and ankle - <0.5 is critical

v) doppler US for anatomical location
- CT/MRI angiography

Question 23

TREATMENT OF CHRONIC LIMB ISCHAEMIA

i) name three medical managements
ii) name three surgical managements? what is done if disease is diffuse or patient is young? what is done if unsuitable for revasc?
iii) name three complocations? what is 5 year mortality?

Answer 23

i) Medical management = lifestyle change, statin, anti plat therapy

ii) Surgical management
- angioplasty +/- stent
- bypass graft if diffuse disease or young
- amputation if unsuitable for revascularisation

iii) Sepsis secondary to infected gangrene
- acute on chronic ischaemia
- loss of mobility and QOL
- 5 year mortality is 50%

Question 24

AORTIC DISSECTION PATHOPHYS AND SIGNS

i) what is it? after how many days does a dx go from acute to chronic? in which two patient groups is it more common? what is peak age of onset?
ii) where may anterograde dissection progress to? where may retrograde dissection progress to?
iii) which classification is used? what is Group A and group B? name another classification used?
iv) name four risk factors
v) how does it classically present? what may be heard on auscultation? why may there be hypotension?
vi) name three signs of end organ damage

Answer 24

i) Tear in the intimal layer of the aortic wall > blood flows between intima and media and splits it apart
- acute = dx <14days and chronic = dx >14 days
- more common in men and patients with connective tissue disorders
- peak onset of 50-70yrs

ii) can progress distal or proximally or both
- Anterograde dissection > iliac arteries
- Retrograde dissection > aotic valve at root of the aorta

iii) Stanford classification
- Group A - involves asc aorta and can propagate to aortic arch/desc aorta
- Group B - dissections dont involve the ascending aorta
- can also use De Bakey classification
* I - orig in asc aorta > at least aortic arch
II - confined to asc aorta
III - orig distal to subclavian and desc aorta

iv) RFs > HTN, atherosclerosis, male gender, connective tissue disorders, bicuspid aortic valve

v) Classic presentation is of tearing chest pain radiating to the back
- tachycardia
- hypotension secondary to hypovol from blood loss or cardiogenic from severe aortic regurg/tamponade
- may hear new aortic regurg murmur

vi) signs of end organ hypoperfusion (reduced urine output, paraplegia, low limb ischaemia, abdo pain, lessening conciousness)

Question 25

AORTIC DISSECTION TX

i) name four baseline bloods that should be done? how many units should be cross matched? what is first line imaging? what other imaging can be useful
ii) what two things should be done as part of urgent initial asses? how does fluid resus need to be approached? what medication should all patients be put on life long?
iii) how are type A sx managed? how should type B be sx managed? in what situation should type B have surgical mx? which has worse prognosis?
iv) which type can usually be managed medically? what should be given first line? what do you want to achieve - why? is endocascular repair recommended?

Answer 25

i) baseline bloods - FBC, UE, LFT, troponin, coag screen
- Cross match of at least 4 units
- CT angio is first line - allows classification, anatomy of dissection and assists surgical planning
- transoesophageal echo can be useful

ii) urgent initial assessment > start high flow O2 and gain IV access
- be cautious with fluid resus > sufficient for cerebral perfusion only (if uncomplicated target systolic should be <110)
- all patients need lifelong anti hypertensive therapy and surveillance imaging due to high risk of further dissection/complications

iii) Type A should be managed surgically (involving asc aorta) - worse prognosis than type B
- transfer to cardiothoracic centre and remove asc aorta > replace with a synthetic graft
- additional branches of aortic arch may require reinplantation into the graft if dissection is long and inv desc/abdo aorta
- only manage type B surgically if there are certain complications eg ruputre, ischaemia, uncontrolled HTN

iv) Medical management - Type B (not involving asc aorta) can usually be managed medically - gold standard
- first line is to manage the hypertension with IV beta blockers (labetalol) or CCB
- want to rapidly lower systolic pressure, pulse pressure and pulse rate to minimise stress of the dissection and stop further propagation
- endovascular repair is not reccomended due to risk of retrograde dissection

Question 26

AORTIC DISSECTION COMPLICATIONS

i) what do complications depend on?
ii) name four complications?
iii) what can retrograde dissections result in?
iv) which type can be chronic and continue to leak even when a stent in placed? what can this result in?
v) what % of patient die before reaching hospital? name three things that improve prognosis

Answer 26

i) Complications depend on site and spread of the dissection into aortic branches and damage of end organs
ii) aortic rupture. aortic regurg, myocardial ischaemia, cardiac tamponade, stroke ot paraplegia
iii) retrograde dissections can result in prolapse of the aortic valve > bleed into pericardium > cardiac tamponade
iv) type B can be chronic > continued leakage into the dissection even if a stent is placed > aneurysm

v) mortality is high - over 20% die before reaching hospital
- early dx, intervention and BP control significantly improves prognosis

Question 27

DEEP VENOUS INSUFFICIENCY

i) what is it commonly caused by? (2) what happens in the venous system?
ii) name two primary causes? name three secondary causes? how is it different to varicose veins? name three risk factors
iii) how do the lower limbs appear? how may patients with previous DVT present?
iv) what is venous claudication? what is lipdermatosclerosis? what is atrophie blanche? name two other features
v) where are venous ulcers commonly found?

Answer 27

i) commonly caused by either DVT or valvular insufficiency
- happens as a result of failure of the venous system - valvular reflux, venous hypertension and obstruction

ii) Primary causes - underlying defect to vein wall/valves (congenital and CT defects)
- Secondary causes - defect second to damage - post thrombotic disease, post phlebitic disease, venous outflow obstruc and trauma
- similar pathophys to VV but affects deep venous system instead of superficial
- RFs - increasing age, female gender, pregnancy, long periods of standing, prev DVT/phlebitis, obesity and smoking

iii) Chronically swollen lower limbs - aching, pruritic and painful
- patients with a previous DVT may present with symptoms of post thrombotic syndrome eg heaviness, cramps, pruritic, pretibial oedema and ulceration
- venous claudication - bursting pain and tightness on walking that resolves on leg elevation
- lipodermatosclerosis - tapering of leg above the ankle (inverted champagne bottle)
- atrophie blanche (loc round white atropic lesions surrounded by dilated capillaries)
- may also see varicose eczema (dry scaly skin), thrombophelbitis, haemosidering skin staining, varying levels of pedal oedema

v) venous ulcers typically found over the medial malleolus

Question 28

DEEP VENOUS INSUFFICIENCY TX AND COMPLICATIONS

i) what is the primary investigation? name three things it can assess
ii) name two things that should be documented? which one determines suitability for compression therapy?
iii) name three ways to conservatively manage? what should be done for a venous ulcer?
iv) name two surgical appraoches to management? are these succesful?
v) name four complications

Answer 28

i) Primary investigation is doppler US to assess extent of venous reflux, sites of stenosis and pres of DVT/varicose vein
ii) document foot pulses and document ABPI - req to determine suitability for compression therapy

iii) conservative = compression stockings, analgesia
- elevate feet above the level of the heart can reduce symptoms and disease progression
- if venous ulcer - start full compression treatment eg 4 layer bandage

iv) Surgical - less successful
- valvuloplasty but little evidence of effectiveness
- deep venous stenting - reserved for patients with severe symptoms > balloon > venous stent

v) swelling
* recurrent cellulitis
* chronic pain
* ulceration

Question 29

LEG SWELLING

i) name four things that can cause bilateral and four things that can cause unilateral swelling? what is lymphoedema?
ii) what causes primary leg swelling? name a familial syndrome that can cause it? does it affect M or F more?
iii) name four secondary causes of leg swelling? (FIIT)
iv) what imaging should be done?
v) name four things that can be done to conservatively manage? what surgery may be done?

Answer 29

i) Bilateral = ↑ Venous Pressure
• RHF
• Venous insufficiency → stasis • Drugs: e.g. nifedipine
• ↓ Oncotic Pressure
• Nephrotic syndrome
• Hepatic failure
• Protein losing enteropathy
• Lymphoedema
• Myxoedema
• Hyper- / hypo-thyroidism
- Unilateral = Venous insufficiency, DVT, Infection or inflammation, Lymphoedema
- Lymphoedema = collection of interstitial fluid due to blockage or absence of lymphatics

ii) congenital absence of lymphatics > may or may not be familial
- Milroy’s Syndrome = familial AD subtype of congenital lymphoedema
- F>M

iii) Fibrosis: e.g. post-radiotherapy Infiltration, Ca: prostate, lymphoma, Filariasis: Wuchereria bancrofti, Infection: TB, Trauma: block dissection of lymphatics
iv) doppler US

v) conservative - Skin care, Compression stocking, Physio, Treat or prevent comorbid infections
- Surgical: debulking operation (rarely done)

Question 30

DIABETIC FOOT

i) name three things that can happen in a diabetic foot? what % req amputation? name two things that result from uncontrolled diabetes that can cause diabetic foot?
ii) what is charcot foot? name four symptoms of diabetic foot? name three deformities that increase risk of ulceration? name two signs of peripheral artery disease that can acuse diabetic foot?
iii) what imaging can be used to assess deep soft tissue collections? what needs to be done before starting abx?
iv) what surgical approach is taken? name a drug that needs to be given? what supportive care can be done? name two other things that help management?

Answer 30

i) infection, ulceration, destruction of foot tissue (1.5% require amputation)
* uncontrolled diabetes contributes to neuropathy > loss of sensation and peripheral artery disease > foot ulcers

ii) charcot foot = progressive destruc of bones, joints and soft tssue caused by neuropathy, abnormal foot loading, micro trauma and metabolic abnorms
- symptoms: ulceration on feet, gangrene, fungal infection, cracks, skin fissures, deformed nails, macerated web spaces, calluses
- deformity such as hammer toe, claw toe, pes cavus > inc risk of ulceration
- PAD > intermittent claudication/rest pain, absent pedal pulses

iii) US to asses pressence of deep soft tissue fluid collections and osteomyelitis
- swab area to identify bacteria > prior to starting abx

iv) surgery > local debridement, admin of culture specific abx and offload of foot in a brace or cast
regular foot examination
* aggressive abx if implicated
* good glycaemic control to prevent neuropathy
* patient education
* footwear appropriate

Question 31

PERIPHERAL ARTERIAL DISEASE

i) what happens in leg arteries? how quickly does this happen? name five RFs? name three causes in the aorta
ii) name four symptoms that may be seen in leg disease? name four symptoms of aortic disease?
iii) what measurement is important to take? what imaging can be done on legs? (2) what imaging can be done on aorta?
iv) name four lifestyle factors that can be modified in management? what happens in endovascular repair? what happens in open repair? what other surgical approach can be used?

Answer 31

i) chronic disease where plaque builds up in arteries to legs > occ gradually
- RF common in >65yrs, smoking, HTN, high choles, hypertryglycerides, DM, kidney fail, obesity
- can also occur in aorta caused by athero, aortic dissection, congenital (coarctation), swelling from inflam conditions

ii) may be asymptomatic, fatigue or cramping of muscles while walking (claudication) in calf, thigh, hip, buttock - goes away with rest, pain in toes or feet at rest, open wound on toes or feet (often at pressure point)
- symptoms of aortic disease > dizzy, faint, erectile dysfunc, HTN, pain/fatigue/numb arms and legs, stroke, TIA, abdo pain > weight loss

iii) ABPI
* angiogram to determine where the plaque is > CT or MRI or catheter directed
- aortic > duplex US, ABPI, CTA or MRA

iv) manage RF, lifestyle change and medication = smoking cessation, control BP and cholesterol, diabetes and weight loss > can all improve symptoms
- may need balloon angioplasty, stent placement or surgical bypass - endovascular repair > stent into damage area of aorta
- open repair > endarctectomy, prostethic graft
- surgical bypass > detour around the blockage

Question 32

ARTERIOVENOUS FISTULA

i) what is it? what does this cause to happen? what is it used for? where is it often created
ii) what imaging may be done first? how long does it take to develop before it can be used?
iii) what happens if it doesnt mature? name two other approaches that can be used

Answer 32

i) Connection made between an artery and a vein > causes extra pressure and blood flow into the vein to make it large and strong > allows for use in haemodialysis
- often created in forearm

ii) do vessel mapping test using doppler US before surgery > select best vessels
- 2-3 months to develop before it can be used

iii) if an AV fistula doesnt mature then an AV graft can be used > looped plastic tube that conn artery to vein (more likely to have probs with infection and clotting)
- use the vein to remove and return blood during haemodialysis
- venous catheter > tube into vein but only good for short term use