Vascular

Question 1

Chronic limb ischaemia (CLI)

Answer 1

PAD, resulting in symptomatic reduction in blood supply to the lower limb. Generally caused by atherosclerosis.

Question 2

CLI risk factors

Answer 2

Smoking 
Hyperlipidaemia
Hypertension 
Male
DM
Increasing age
FHx
Obesity

Question 3

CLI Fontaine classification

Answer 3

Stage 1- Asymptomatic
Stage 2- intermittent claudication (cramping after walked fixed distance- claudication distance)
Stage 3- ischaemic rest pain
Stage 4- ulceration/gangrene/both

Buergers test- Pt supine, raise leg until pale, lower down to reperfuse. If buergers angle less than 20 degrees then severe ischaemia.

Question 4

CLI investigations

Answer 4

ABPI- <0.5 is severe
>0.9 is normal. If >1.2 then consider incorrect reading due to calcification or hardening.

Also conduct CVS assessment as usually have the risk factors.

If <50yrs without RF consider thrombophilia screen.

Question 5

CLI management

Answer 5

Lifestyle
Statin (80mg Atorvastatin)
Anti-platelet therapy
Optimise diabetes control

Enrol in supervised exercise programme.

Consider surgery when supervised exercise and lifestyle failed and RF modification failed.

Surgery options; angioplasty, bypass graft or combination. Also amputation.

Question 6

CLI complications

Answer 6

Sepsis (infected gangrene)
Acute on chronic ischaemia
Amputation
Reduced mobility and QoL

Question 7

Critical limb ischaemia

Answer 7

Complication of CLI;
>2wk of ischaemic rest pain
Gangrene/ischaemic lesions
ABPI<0.5

Differentials; spinal stenosis, acute limb ischaemia

Investigate with a Doppler USS (severity and location). Follow with CT/MRI.

Needs immediate surgical intervention.

Question 8

Acute Limb Ischaemia (ALI)

Answer 8

Sudden full/partial occlusion of the artery, leading to poor functional outcomes/rapid ischaemia.

Caused by embolism (normal contralateral pulse), thrombus from plaque or trauma.

Differentials- critical CLI, acute DVT, SC compression.

Pallor, pulselessness, perishingly cold, paralysis, pain and paraesthesia.

Question 9

ALI Investigations

Answer 9

Bloods (lactate-look at ischaemia, thrombophilia screen if <50yrs without RF, group and save), ECG.
Doppler USS with CT angiography follow up (CT arteriogram if limb salvageable)

Question 10

ALI Management

Answer 10

Surgical emergency-within 6hrs. Embelctomy (if embolic), bypass, intra-arterial thrombolysis, angioplasty.

High flow O2, IV fluids and therapeutic heparin dose.

Conservative- Prolonged heparin, regular assessment.

Question 11

Irreversible Limb Ischaemia

Answer 11

(Mottled, non-blanching, hard woody muscles)- Urgent amputation.

Long term- Reduce CVS RF, start on antiplatelet.

Amputation- Regular physio and occupational health.

Question 12

ALI complications

Answer 12

High mortality
Reperfusion Injury
Compartment syndrome
Damaged muscles releasing K+, H+ and myoglobin (AKI)

Question 13

AAA

Answer 13

Greater than 3mm dilation

RF and aetiology discussed in cardiology.

Question 14

AAA symptoms

Answer 14

Usually asymp.
Ab, loin, back pain.
Pulsatile mass at abdomen

Ruptured may present with shock, syncope, pain, vomiting.

Differential- renal colic

Question 15

AAA Investigations

Answer 15

USS

CT with contrast if >5.5cm

Question 16

AAA Management

Answer 16

Medical- Monitor if <5.5cm.
Reduce CVS risk- BP control, statin, stop smoking, weight loss.

Surgical- Open repair- midline laprotomy.
Endovascular repair- graft via the femoral artery and fixing a stent across the aneurysm.

Endovascular- short hospital stay but increased reintervention.

Question 17

AAA Complications

Answer 17

Rupture (Most common)
Retroperitoneal leak
Embolisation
Aortoduodenal fistula.

Question 18

Ruptured AAA

Answer 18

Increased risk with increased size.
Haemodynamically compromised.
Triad- Flank/back pain, hypotension, pulsatile ab mass.

Manage- Immediate referral and bloods, O2, crossmatch. Stable need CT angiogram to see if endovascular repair appropriate. Unstable need open surgical repair.

Question 19

Deep Venous Insufficiency

Answer 19

DVT+Valvular insufficiency+varicose vein= chronic venous insufficiency.

Causes: Primary- defect to wall/valve (inc congenital).
Secondary- post damage

Question 20

DVI- RF

Answer 20

Increase Age
Female
Pregnancy
previous DVT
Obesity
Smoking

Question 21

DVI
Differentials
Investigations

Answer 21

Renal, hepatic and cardiac disease.
Doppler USS
Foot pulses and ABPI- compression stocking.

Question 22

DVI- Management

Answer 22

Early identification and management.
Compression stocking, analgaesia.
Surgical less succesfful.

Question 23

DVI- Clinical Features

Answer 23

Swollen legs
Tightness when walking resolved by elevation (v.claudication)
Varicose eczema 
Haemosiderin staining
Thrombophlebitis
Lipodermatosclerosis
Atrophie blanche
Venous ulcers.

Question 24

Varicose veins

Answer 24

Incompetent valves, so blood moves from deep to superficial. Therfero get turtuous dilated superficial veins with venous HTN.

RF: Long standing, obesity, pregnancy, FHx.

Question 25

Varicose veins- Clinical Features

Answer 25

Usually present for cosmetics. Can beocme itchy/achy. | May get skin changes, ulceration, thrombophelbitis etc if left untreated.

Question 26

Varicose veins- Investigations

Answer 26

Duplex USS is gold standard.

Question 27

Varicose veins- Management

Answer 27

Modify RF- reduced standing, lose weight etc. Only give compression stockings if treatment inappropriate since life long commitment. Venous ulcers need 4 layer bandaging. Surgical only if skin changes, recurrent/symptomatic, superficial vein thrombosis, venous leg ulcer.

Question 28

Varicose veins- Surgery types

Answer 28

Thermal ablation Venous ligation and stripping Foam slcerotherapy- Foam leads to inflammation and closing of vein. NB if have DVT at the same time then surgery is contraindicated.

Question 29

Varicose veins- Complications

Answer 29

Untreated will worsen. | Post op complications- haemorrhage, thrombophlebitis, DVT, disease recurrence and nerve damage.

Question 30

Ulcers

Answer 30

Breaks in the skin/mucous membranes. Lower likmb mainly venous, but also arterial and neuropathy related.

Question 31

Venous ulcers- Appearance RF

Answer 31

Shallow, irregular border, granulated base, located at medial malleolus, features of venous insufficiency. Prone to infection, cellulitis related. ``` RF: Increasing age Pre-existing venous incompetence Hx of venous thromboembolism Varicose veins Pregnancy Obesity or physical inactivity Severe leg injury or trauma ```

Question 32

Venous ulcers- Features Investigations

Answer 32

Aching, itching, DVI features i.e. haemosiderin staining. Investigations: Duplex USS. ABPI- is compression suitable. Swab cultures if infection suspected.

Question 33

Venous ulcers- Management

Answer 33

Conservative- Leg elevation, increased exercise, lifestyle changes. Abx if infection. Importantly- Multicomponnet compression bandaging- change 1/2 times per week (Need ABPI>0.6) Ensure area is moist, not dried out by soap, to allow healing. Treat varicose veins to imporve condition.

Question 34

Arterial ulcers- Appearance RF

Answer 34

Reduced BF induced, poor healing. Deep, well defined border, necrotic base. Occur distal to trauma site and at pressure areas. ``` RF: PAD DM Smoking HTN Obestiy Increased age ```

Question 35

Arterial ulcers- Features Investigations

Answer 35

Intermittent claudication or critical LI preceding. Painful and develops over time. Cold limb, absent/reduced pulses, necrotic toes etc. Investigations: ABPI. Locate with duplex USS/CT angiogrpahy/MRI.

Question 36

Arterial ulcers- Management

Answer 36

Need vascular review. Lifestyle changes, CVS modification (statin, anti-P, BP control etc) Angioplasty (+/- stenting) or bypass. If non healing despite good BS- skin graft.

Question 37

Neuropathic ulcers Appearance RF

Answer 37

Due to peripheral neuropathy, therefore repeated stress and injuries. Get painless ulcer at pressure points (secondary to joint deformities in diabetics). Punched out appearnace. RF: DM B12 deficiency Any peripheral neuropathy

Question 38

Neuropathic ulcers Features Investigations

Answer 38

Hx of peripheral neuropathy. Investigations: BG, B12, ABPI. Swab for infection, X-Ray if shows osteomyelitis.

Question 39

Neuropathic ulcers- Management

Answer 39

``` DM foot clinics Good diabetes control Reduced CVS RF Good foot hygiene and appropriate footwear. Necrotic digits may need amputating. ```

Question 40

Charcot's Foot

Answer 40

May get alongside neuropathic ulcers. Loss of joint sensation, therefore increased unnoticed trauma and deformity. Swelling, distortion, pain and loss of function. Loss of transverse arch. Need to reduce weight load on foot.

Question 41

Acutely painful leg

Answer 41

Cold and Pale- Acute limb ischaemia Hot and swollen- DVT (can also be MSK, cellulitis) Trauma- low weight bearing, bony tenderness Neurological- Worse on movement, radiates from back. Need detailed history and examination.

Question 42

Carotid Artery stenosis

Answer 42

Mainly asymptomatic-since dual supply. Can cause TIA or stroke. Ischaemic stroke treat with 300mg aspirin + IV alteplase if within 4.5hrs, haemorrhagic stroke correct anti-coagulation. Investigate stroke wit CT, carotids with duplex USS. Manage stroke/TIA. If stable then remove atheroma. Long term aspirin, statins, HTN control, DM control, lifestyle changes, exercise, smoking cessation.

Question 43

Carotid artery occlusion classification

Answer 43

<50%- Mild 50-69%- Moderate 70-99%- Severe 100%- Total/complete

Question 44

Thoracic Aortic Aneurysm

Answer 44

Usually asymptomatic but can present with pain (ascending-anterior chest, descending-@scapulae, arch-neck). Common in connective tissue disorders or bicuspid valve. RF same as IHD. Investigate with bloods and ECG. Image with CT contrast. Manage medically by reducing CVS RF. Surgical repair is possibility depending on location, likely to recur.

Question 45

``` Acute Mesenteric Ischaemia- Features Causes RF Differentials ```

Answer 45

Ab pain, N+V, disproportionate to the clinical findings. Main cause is embolus, but also thrombus, non occlusive and occlusive causes. RF- Depends on cause. Embolism RF include smoking, HTN, hyperlipidaemia etc. DDx- Symptomatic AAA, bowel perforation, peptic ulcer.

Question 46

Acute Mesenteric Ischaemia- | Investigations

Answer 46

ABG- Raised lactate. Catheter- Monitor output Bloods- FBC, U+E, LFTs, amylase, clotting, G+S. CT with IV contrast- see oedematous bowel, loss of bowel wall enhancement.

Question 47

Acute Mesenteric Ischaemia- | Management

Answer 47

Initially; Fluid resuss, catheter, broad spectrum Abx, analgesics, anti-emetics, needs ITU. Surgical emergency!! Removal of necrosed bowel- will need a stoma following this. More commonly-Revascularisation by thrombo/embolectomy- using radiological intervention.

Question 48

Acute Mesenteric Ischaemia- | Complications

Answer 48

Perforated bowel | Bowel necrosis

Question 49

``` Chronic Mesenteric Ischaemia- Causes Features RF Differentials ```

Answer 49

Atherosclerotic plaque of effecting the CT, SMA or IMA. At least two need to be affected to cause symptoms. Presenting with postprandial pain (since increased demand of blood to colon), weight loss (reduced intake and malabsorption), other existing comorbidities. RF: Smoking, HTN, DM, hypercholesteralaemia. More common in female and >60yrs. DDX: Chronic pancreatitis, GB pathology, peptic ulcer.

Question 50

Chronic Mesenteric Ischaemia- Investigations Management

Answer 50

Blood will be normal, check Ca2+ and Mg2+- ?nutrition. CT angiography investigation of choice. Manage initially with reducing RF i.e. smoking cessation, statins, anti-platelets. Then with either endovascular stent insertion (via femoral/brachial) or open surgery bypass graft.

Question 51

Pseudoaneurysm

Answer 51

Between tunica media and adventitia, due to vessel trauma (IVDU), commonly at femoral artery. Present tender, painful, swollen, erythematous (if infected). Investigate with doppler. Manage small by leaving alone, larger ones can either apply direct compression or US guided thrombin injected into pseudoaneurysm lumen. Can rupture or become infected- sepsis.

Question 52

AAA- Stanford Classification

Answer 52

Type A- Includes DaBakey class I and II as well as the ascending aorta and can include descending aorta and aortic arch. Tear can be anywhere along here. Type B- Includes DaBakey class III and not the ascending aorta.

Question 53

AAA- DaBakey Classification

Answer 53

Class I- Starts at A.aorta and radiates to the arch. (<65) Class II- Confined to ascending aorta. (elderly, HTN) Class III- Starts in D.aorta, distal to subclavian artery. IIIa extends to diaphragm, IIIb to abdominal aorta.

Question 54

Acute Limb Ischaemia- Rutherford Classification

Answer 54

I- Viable, normal. IIa- Marginally threatened, can be salvages, loss of sensory. IIb- Immediately threatened, needs immediate revascularisation. Increased loss of sensory, rest pain and motor loss. III- Irreversible, profound sensory and motor loss.