VASC - Common Vascular Conditions Flashcards
Acute Limb Ischaemia (ALI)
Aetiology
Clinical Features
Investigations
Complications
1.) Aetiology
- embolisation: original thrombus often from AF, post-MI mural-thrombus, AAA, prosthetic heart valves
- thrombosis-in-situ: ruptured atheroma plaque
- trauma: less common, inc compartment syndrome
2.) Clinical Features - 6Ps: pain, pallor, pulselessness, paraesthesia, perishingly cold, paralysis
- sudden onset of these sx, normal, pulsatile contralateral limb is a sign of embolic occlusion
- potential causes: CLI, AF, recent MI, AAA
- later presentation –> irreversible damage (from 6hrs)
3.) Investigations
- bloods: inc G/S, serum lactate, CK
- ECG, thrombophilia screen (<50 w/o risk factors)
- doppler US (both limbs) –> CT angiography
- CT arteriogram for anatomical location of the occlusion
4.) Complications - reperfusion injury (sudden ↑in capillary permeability -> release of substances lead to:
- hyperkalaemia (K+), acidosis (H+), AKI (myoglobin)
- ↑permeability also leads to compartment syndrome
Management of Acute Limb Ischaemia (ALI)
Rutherford Classifications
Initial and Conservative Management
Surgical Intervention
Long-Term Management
1.) Rutherford Classification - severity
- I-Viable: no immediate threat, audible w/ doppler (US)
- IIA-marginally threatened: salvageable, minimal sensory loss, inaudible in arterial doppler
- IIB-immediately threatened: needs immediate revascularisation, ↑sensory loss, some motor deficit
- III-irreversible: permanent nerve damage, tissue loss, profound sensory/motor deficits, inaudible venous US
2.) Initial and Conservative Management
- high flow oxygen
- IV unfractionated heparin (UFH) infusion
- conservative (1/2a): prolonged course of heparin, regular assessment (monitor APTT and clinical review)
3.) Surgical Intervention - Rutherford 2b
- embolic cause: embolectomy (Fogarty catheter), local intra-arterial thrombolysis, bypass surgery
- thrombotic cause: thrombolysis, angioplasty, bypass
- urgent amputation for irreversible (III), often admit to HDU due to risk of ischaemia reperfusion syndrome
4.) Long-Term Management
- ↓CVD risk: ↓smoking, exercise, weight loss
- anti-platelet or even anti-coagulation therapy
- amputation requires OT/PT and a long term rehabilitation plan
Chronic Limb Ischaemia (Peripheral Arterial Disease)
Aetiology and Risk Factors
Clinical Features
Critical Limb Ischaemia
Investigations
1.) Aetiology - peripheral arterial disease resulting in symptomatic reduced blood supply to the limbs
- often due to atherosclerosis, often lower limbs affected
- occlusion of superficial femoral or popliteal artery
- R.F: smoking, DM, HTN, hyperlipidaemia, ↑age, FH
- HRT in post-menopausal women is protective against PAD but increases the risk of DVT and PE
2.) Clinical Features - depends on the severity (Fontaine classification)
- stage I: asymptomatic, II: intermittent claudication
- III (severe): ischaemic rest pain (often occurs in the foot/toes)
- IV: ulceration or gangrene
- leg pallor on elevation due to reduced perfusion on elevation
- reactive hyperemia: leg becomes redder after a period of reduced perfusion (e.g. elevation) due to ischaemia –> release of vasodilators
- Buerger’s angle <20° indicates severe ischaemia
- Leriche syndrome: buttock/thigh pain w/ ED
- can have erectile dysfunction due to vascular insufficiency
3.) Critical Limb Ischaemia - advanced CLI, definition:
- ischaemic rest pain >2wks, requiring opiate analgesia
- ischaemic lesions or gangrene due to arterial disease
- ABPI < 0.5
- other signs: pallor, pulselessness, cold limbs, hair loss, skin changes, thickened nails
4.) Investigations
- ABPI: ankle:brachial BP index to confirm and quantify
- normal = 0.9-1.2, moderate = 0.5-0.8, severe = 0.4 and below
- >1.2 too high, calcification due to diabetes –> falsely high ABPI
- doppler US –> CT/MR angiography
- cardiovascular risk assessment, thrombophilia screen
Management of Chronic Limb Ischaemia
Medical Management
Revascularization
Complications
1.) Medical Management - CVD risk factor modification
- lifestyle: smoking cessation, weight loss
- optimise diabetes control
- supervised exercise programme: can help with the opening up of collateral vessels around the blockage
- Rx for all patients: atorvastatin 80mg + clopidogrel (OR aspirin)
- 5HT2 antagonist (Naftidrofuryl oxalate)
2.) Revascularization - if supervised exercise has failed to improve symptoms or critical limb ischaemia
- endovascular (stenotic lesion <10cm):
percutaneous transluminal angioplasty +/- stenting
- surgical (long segment >10cm/multifocal):
femoral artery bypass graft or femoral endarterectomy
- below-knee amputations: for widespread gangrene or ischaemic lesions to prevent sepsis
3.) Complications
- sepsis secondary to infected gangrene
- acute on chronic ischaemia, amputation, ↓QoL
Varicose Veins
Aetiology
Clinical Features
Skin Changes x5
Investigations
Complications
1.) Aetiology - tortuous dilated segments of superficial veins often associated with valvular incompetence
- often at the sapheno-femoral/popliteal junctions
- 98% are primary idiopathic
- secondary causes: DVT, pelvic masses (e.g. pregnancy, tumours), AVM
- risk factors: prolonged standing, obesity, pregnancy, FH
2.) Clinical Features
- cosmetic: unsightly visible veins, skin discolouration
- aching, itching, ulceration, bleeding, DVT
- usually the course of great/short saphenous vein
- CEAP classification used: clinical features, aEtiology, anatomical, pathophysiology
3.) Skin Changes - seen in varicose veins
- superficial thrombophlebitis: tender and hardened veins due to inflammation of superficial veins
- varicose eczema: venous stasis –> eczema changes
- lipodermatosclerosis: hardening and tightening of the skin caused by inflammation of subcutaneous fat
- atrophic blanche: hypopigmented patches of skin due to blood vessel occlusion in the dermal layers of the skin
- haemosiderin deposition: hyperpigmented patches due to haemosiderin deposition from leaky capillaries
4.) Investigation - duplex US
- assess valve incompetence, deep venous incompetence, occlusion (DVT) and stenosis
5.) Complications - untreated worsen overtime
- haemorrhage, thrombophlebitis, DVT, nerve damage
Management of Varicose Veins
Non-Invasive Treatment x3
Surgical Treatment Criteria x4
Surgical Treatment Mehods x3
1.) Non-Invasive Treatment
- lifestyle: ↓prolonged standing, ↑exercise, weight loss
- compression stockings to prevent complications if interventional treatment is not appropriate
- four-layer bandaging for any venous ulceration
2.) Surgical Treatment Criteria
- symptomatic or recurrent varicose veins
- lower limb skin changes: pigmentation, eczema
- superficial vein thrombosis (hard, painful veins)
- venous leg ulcer
3.) Surgical Treatment Methods
- vein ligation, stripping, and avulsion
- foam sclerotherapy: inject an irritating agent into varicosed veins causing the vein to close off
- thermal ablation: close vein off using heat
Deep Venous Insufficiency
Aetiology
Clinical Features
Investigations
Management
1.) Aetiology - failure of deep venous system causing:
- valvular reflux, venous HTN and obstruction
- often caused by DVT or valvular insufficiency
- risk factors: ↑age, female, pregnancy, smoking, obesity, previous DVT or phlebitis, prolonged standing, FH
2.) Clinical Features - chronically swollen lower limbs
- can become aching, pruritic, and painful
- venous claudication: bursting pain and tightness on walking which resolves on leg elevation
- signs: varicose eczema, thrombophlebitis, lipodermatosclerosis,
pedal oedema, venous ulcers,
3.) Investigations
- doppler US assessing for the extent of venous reflux
- routine bloods (exclude diffs), ECHO (?cardiac)
- foot pulses, ABPI
4.) Management
- compression stocking and suitable analgesics
- elevate feet above level of the heart
- surgical management is not too successful
- venous stenting for patients w/ severe sx
Venous Ulcers
Aetiology
Clinical Features
Investigations
Management
1.) Aetiology - venous insufficiency
- venous insufficiency –> venous HTN –> trap WBCs –> inflammatory mediators –> tissue injury, poor healing
- the most common cause of a leg ulcer
- risk factors: ↑age, venous incompetence, pregnancy, obesity, physical inactivity, severe leg injury/trauma
2.) Clinical Features - shallow ulcers with a granulated base (some healing), often located over the MM
- can be painful (particularly worse end of the day)
- other sx: aching, itching, burning sensation
- signs of deep venous insufficiency (+varicose veins)
- prone to infection so can present w/ cellulitis
3.) Investigations - clinical diagnosis
- duplex US for underlying venous insufficiency
- ABPI to assess arterial component
- microbiology swabs for suspected infection
- thrombophilia and vasculitic screen in young patients
4.) Management
- leg elevation, ↑exercise, weight loss, ↑nutrition
- antibiotics for signs of wound infection
- multicomponent compression bandaging (ABPI >0.6), change 1/2x a wk, will take roughly 6 months to heal
- dressing and emollients for surrounding skin health
- treat any varicose veins surgically
Arterial Ulcers
Aetiology
Clinical Fetaures
Investigations
Management
1.) Aetiology - critical limb ischaemia
- reduction in arterial blood flow leading to decreased perfusion of tissues and subsequent poor healing
- no/little healing means there is a necrotic base
- located on distal sites of trauma and pressure areas
- R.F: same as chronic limb ischaemia
2.) Clinical Features - small deep lesions with well-defined borders and necrotic base, found in distal sites
- hx of intermittent claudication/critical limb ischaemia
- can be painful, develops over a long period of time
- can have other signs of critical limb ischaemia (inc cold limbs and absent pulses)
3.) Investigations
- ABPI for extent of peripheral arterial disease
- imaging: duplex US, CT/MR angiography
4.) Management - same as chronic limb ischaemia
Neuropathic Ulcers
Aetiology
Clinical Features
Investigations
Management
1.) Aetiology - peripheral neuropathy
- ↓sensation –> repetitive stress and unnoticed injuries
- vascular disease will contribute to ↓healing
- risk factors: peripheral neuropathy (inc DM, B12 deficiency), any foot deformity or peripheral vascular disease
2.) Clinical Features
- painless ulcers over pressure points on the limb
- variable in size and depth, warm feet, good pulses
- peripheral neuropathy: burning/tingling in legs, single nerve involvement (mononeuritis e.g. MN palsy)
- Charcot’s Joint: badly disrupted and damaged joint due to reduced sensation, mild pain, joint is typically red, warm and swollen
3.) Investigations
- BG (random BM or HbA1c), serum B12 levels
- testing vibration sensation w/ 128Hz tuning fork
- ABPI +/- duplex for any concurrent arterial disease
- microbiology swab, X-ray if suspected osteomyelitis
4.) Management
- diabetic foot clinics, optimise diabetes control
- maintain good foot hygiene and appropriate footwear
- Abx (flucloxacillin) of signs of infection
- amputation in severe cases (necrosis/infected digits)
Abdominal Aortic Aneurysm
Definition
Aetiology
Clinical Features
Investigations
1.) Definition - permanent dilation of the abdominal aorta > 3cm (or >1.5x expected diameter)
- 90% originate below the renal arteries
2.) Aetiology - degeneration of the tunica media (less elastin and collagen) causing the lumen to dilate
- risk factors: male, ↑age, smoking, hyperlipidaemia, HTN, FH, CT disease (e.g. Marfan’s, Ehler’s Danlos)
- DM is potentially a protective factor for AAA
3.) Clinical Features - asymptomatic until large/rupture
- abdominal pulsatile mass (<50% of cases)
- abdominal pain and nausea (compresses stomach)
- back/loin pain (compresses vertebrae)
- acute limb ischaemia (distal embolisation)
- ruptured AAA: hypotension, pulsatile abdominal mass, flank/back pain
4.) Investigations
- abdominal USS: can detect free peritoneal blood
- screening: single abdo US for all 65yr old men
- CT w/ contrast if >5.5cm for anatomical details
- AXR can only detect AAA if there is calcification
5.) Complications
- rupture (often into retroperitoneal space —> retroperitoneal leak)
- distal embolisation, aorto-duodenal fistula
Management of an AAA
Medical Management
Surgical Intervention
Management of Ruptured AAA
Endovascular Leak
1.) Medical Management
- surveillance: 3-4.4 = yrly US, 4.4-5.5 = 3 monthly US
- ↓CVD risk factors: ↓smoking, improve BP control, weight loss and exercise
- commence statin (primary prevention) and aspirin therapy
2.) Surgical Intervention
- criteria: symptomatic, >5.5cm, expanding >1cm/yr
- can be left to >6cm if patient unfit for surgery
- open or endovascular repair (better short-term outcome but ↑rate of reintervention and rupture)
3.) Management of Ruptured AAA
- A-E assessment, urgent bloods(+lactate, crossmatch 6 units of blood)
- high flow O2, NBM+IV fluids, catheter
- consider activating the massive transfusion protocol
- permissive hypotension: keep BP low (<100 sys) to prevent re-bleeding as first clot made is often the best
- FAST Scan (rapid US looking for fluid) and CT Angio
- treatment is immediate endovascular aneurysm repair
4.) Endovascular Leak - complication of EVAR
- incomplete seal forms around aneurysm causing blood to leak around the prosthetic graft
- often asymptomatic so regular surveillance needed
- aneurysm expansion post-EVAR needs investigation
Acute Mesenteric Ischaemia
Pathophysiology
Clinical Features
Investigations
Management
1.) Pathophysiology - typically caused by an embolism resulting in occlusion of an artery which supplies the small bowel e.g. the SMA
- risk factors: increasing age, AF, endocarditis, malignancy, smoking, hypertension, diabetes
2.) Clinical Features
- sudden onset severe central abdominal pain, out-of-keeping with physical exam findings
- rectal bleeding, diarrhoea, fever
- metabolic acidosis
3.) Investigations
- bloods: FBC (↑WCC,) ↑CRP, ABG (lactic acidosis), LFTs, U+Es, clotting, crossmatch
- CT abdomen
4.) Management
- urgent laparotomy esp w/ signs of advanced ischemia e.g. peritonitis or sepsis
- poor prognosis, especially if surgery delayed
Fourniere’s Gangrene
SMSA’s
