Vascular Flashcards
Chronic limb ischaemia (CLI)
PAD, resulting in symptomatic reduction in blood supply to the lower limb. Generally caused by atherosclerosis.
CLI risk factors
Smoking Hyperlipidaemia Hypertension Male DM Increasing age FHx Obesity
CLI Fontaine classification
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.
CLI investigations
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.
CLI management
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.
CLI complications
Sepsis (infected gangrene)
Acute on chronic ischaemia
Amputation
Reduced mobility and QoL
Critical limb ischaemia
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.
Acute Limb Ischaemia (ALI)
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.
ALI Investigations
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)
ALI Management
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.
Irreversible Limb Ischaemia
(Mottled, non-blanching, hard woody muscles)- Urgent amputation.
Long term- Reduce CVS RF, start on antiplatelet.
Amputation- Regular physio and occupational health.
ALI complications
High mortality
Reperfusion Injury
Compartment syndrome
Damaged muscles releasing K+, H+ and myoglobin (AKI)
AAA
Greater than 3mm dilation
RF and aetiology discussed in cardiology.
AAA symptoms
Usually asymp.
Ab, loin, back pain.
Pulsatile mass at abdomen
Ruptured may present with shock, syncope, pain, vomiting.
Differential- renal colic
AAA Investigations
USS
CT with contrast if >5.5cm
AAA Management
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.
AAA Complications
Rupture (Most common)
Retroperitoneal leak
Embolisation
Aortoduodenal fistula.
Ruptured AAA
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.
Deep Venous Insufficiency
DVT+Valvular insufficiency+varicose vein= chronic venous insufficiency.
Causes: Primary- defect to wall/valve (inc congenital).
Secondary- post damage
DVI- RF
Increase Age Female Pregnancy previous DVT Obesity Smoking
DVI
Differentials
Investigations
Renal, hepatic and cardiac disease.
Doppler USS
Foot pulses and ABPI- compression stocking.
DVI- Management
Early identification and management.
Compression stocking, analgaesia.
Surgical less succesfful.
DVI- Clinical Features
Swollen legs Tightness when walking resolved by elevation (v.claudication) Varicose eczema Haemosiderin staining Thrombophlebitis Lipodermatosclerosis Atrophie blanche Venous ulcers.
Varicose veins
Incompetent valves, so blood moves from deep to superficial. Therfero get turtuous dilated superficial veins with venous HTN.
RF: Long standing, obesity, pregnancy, FHx.
Varicose veins- Clinical Features
Usually present for cosmetics. Can beocme itchy/achy.
May get skin changes, ulceration, thrombophelbitis etc if left untreated.
Varicose veins- Investigations
Duplex USS is gold standard.
Varicose veins- Management
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.
Varicose veins- Surgery types
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.
Varicose veins- Complications
Untreated will worsen.
Post op complications- haemorrhage, thrombophlebitis, DVT, disease recurrence and nerve damage.
Ulcers
Breaks in the skin/mucous membranes. Lower likmb mainly venous, but also arterial and neuropathy related.
Venous ulcers-
Appearance
RF
Shallow, irregular border, granulated base, located at medial malleolus, featuresof venous insufficiency.
Prone to infection, cellulitis related.
RF: Increasing age Pre-existingvenous incompetence Hx of venous thromboembolism Varicose veins Pregnancy Obesityorphysical inactivity Severeleg injuryor trauma
Venous ulcers-
Features
Investigations
Aching, itching, DVI features i.e. haemosiderin staining.
Investigations: Duplex USS. ABPI- is compression suitable.
Swab cultures if infection suspected.
Venous ulcers- Management
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.
Arterial ulcers-
Appearance
RF
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
Arterial ulcers-
Features
Investigations
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.
Arterial ulcers- Management
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.
Neuropathic ulcers
Appearance
RF
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
Neuropathic ulcers
Features
Investigations
Hx of peripheral neuropathy.
Investigations: BG, B12, ABPI. Swab for infection, X-Ray if shows osteomyelitis.
Neuropathic ulcers- Management
DM foot clinics Good diabetes control Reduced CVS RF Good foot hygiene and appropriate footwear. Necrotic digits may need amputating.
Charcot’s Foot
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.
Acutely painful leg
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.
Carotid Artery stenosis
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.
Carotid artery occlusion classification
<50%- Mild
50-69%- Moderate
70-99%- Severe
100%- Total/complete
Thoracic Aortic Aneurysm
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.
Acute Mesenteric Ischaemia- Features Causes RF Differentials
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.
Acute Mesenteric Ischaemia-
Investigations
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.
Acute Mesenteric Ischaemia-
Management
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.
Acute Mesenteric Ischaemia-
Complications
Perforated bowel
Bowel necrosis
Chronic Mesenteric Ischaemia- Causes Features RF Differentials
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.
Chronic Mesenteric Ischaemia-
Investigations
Management
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.
Pseudoaneurysm
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.
AAA- Stanford Classification
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.
AAA- DaBakey Classification
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.
Acute Limb Ischaemia- Rutherford Classification
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.
