Surgery - Vascular Flashcards
Which side does the Large Saphenous vein travel down?
Medial
What artery is the dorsalis pedis a branch of?
Anterior Tibial - Opposite to the posterior tibial pulse
Acute Limb Ischaemia Pathophysiology: Causes: Signs: Classification: Investigations: Management: Complications:
Pathophysiology: Sudden decrease in limb perfusion that threatens the viability of the limb
Causes: Embolism eg. AF/post-MI mural thrombus, Thrombosis (clot rupture from adventitia), Trauma eg. compartment syndrome
Signs: 6 Ps, in order:
Pain, Pallor, Pulselessness, Perishingly cold, Paraesthesia, Paralysis
Irreversible = 3 Ms = Mottled skin, muscles that are tender, major necrosis
Classification: Rutherford - 1->3 (2a/b), based on reversibility
Investigations: Doppler ultrasound, Bloods eg. Lactate, Thrombophilia, Group and Save, ECG, CT angiogram
Management: Surgical emergency - 6 hours to irreversible ischaemia
Initial : High flow oxygen, heparin
Surgical: Embolectomy (fogarty catheter), Thrombolysis, Bypass, Thrombectomy (if thrombus caused) + endarterectomy (removal of plaque from wall)
Complications: Ischaemia reperfusion injury, compartment syndrome, K+ release, H+ acidosis, rhabdomyolysis
Chronic limb ischaemia Pathophysiology: Classification: Symptoms: Claudication areas and vessels involved: Risk factors: Investigations: Management: Differentials: Complications:
Pathophysiology: Peripheral arterial disease that results in symptomatic reduction in blood supply to limbs. Typically caused by atherosclerosis.
Classification: Fontaine Classification - 1 - ABPI > 0.9, asymptomatic, 2 - ABPI - 0.6-0.8 Intermittent claudication, 3 - ABPI 0.3-0.6 Rest pain, 4 - ABPI <0.3 Ulceration and Gangrene
Symptoms: Intermittent claudication (cramping pain after walking fixed distance, relieved by rest), Critical limb ischaemia (ischaemic rest pain > 2 weeks duration, presence of ischaemic lesions or ABPI <0.5)
Claudication areas:
- Buttocks - Aorta/Common iliac - Leriche Syndrome (aortic bifurcation, causes ED)
- Thigh - Superficial femoral
Risk factors: Smoking, Diabetes, Hypertension, Hyperlipidaemia
Investigations: Buerger’s test - lift leg to 30 degrees, wait 60 seconds. If goes pale at 20 degrees = severe ischaemia. Rotate over edge of bed and watch if it becomes hyperaemic/gains colour more slowly than other leg. ABPI used to confirm clinical diagnosis.
Management: Conservative in most - smoking, weight loss, increase exercise (induce ischaemia -> angiogenesis top repair)
Medical: Dual antiplatelet (aspirin + clopidogrel), statins, analgesia
Surgical: Angioplasty + stenting OR Endarterectomy (removal of plaque)
Gold standard = saphenous vein graft bypass
Differentials: Neurogenic claudication from spinal stenosis, acute limb ischaemia
Complications:
Why should an ABPI >1.2 be taken with caution?
What ABPI is considered severe?
Calcification and hardening of the arteries can raise ABPI
<0.5 is severe, 0.5-0.8 is moderate
Chronic venous insufficiency Pathophysiology: Causes: Classification (important): Risk factors: Investigations: Management: Complications:
Pathophysiology: Failure of the venous system, characterised by valvular reflux, venous hypertension and obstruction
Causes: Primary causes eg. defects, from congenital/tissue disorders. Secondary causes (causing damage) eg. DVT, post-phlebitis disease, venous outflow obstruction, trauma
Classification: CEAP classification, C1-6: 0 - no disease, 1 - telangiectasia (mini veins), 2 - varicose veins, 3 - oedema, 4a - Haemosiderosis, venous eczema, 4b - Atrophie blanche/Lipodermatosclerosis (leading to wine glass appearance), C5 - ulcers - healed, C6 - ulcers - active
Risk factors: Age, female, pregnancy, previous DVT
Investigations: Duplex USS, ABPI, Foot pulses
Management: Compression stockings if ABPI >0.8, venous stenting
Endovascular: Sclerotherapy (shut down veins)
Surgical: Phlebectomy or Junction ligation
Complications: Ulcers, DVT, Cellulitis, Chronic pain
DVT Virchow's triad: Pre-operative prevention: Causes: Symptoms: Signs: Risk factors: Investigations: Management: Complications:
Virchow’s triad: Venous stasis, endothelial damage, abnormal coagulation
Pre-operative prevention: Compression stockings, Warfarin covered by LMWH
Signs: Calor, dolor, rubor, functio laesa, tumour
Risk factors: Age, FH eg. Factor V leiden, COCP, Sedentary status, malignancy, varicose veins
Investigations: Wells score, CTPA for PE
Management: LMWH and Warfarin together (LMWH until INR = 2-3) - 6 months if caused, lifelong if not caused
Complications: Can lead to post-thrombotic syndrome
Describe the MOA of the following drugs: Unfractionated Heparin: LMWH: Warfarin: DOACs (Direct oral anticoagulants) and NOACs:
UFH: Binds to and activates Antithrombin, which inhibits Factor 10, preventing prothrombin conversion to thrombin (which stops fibrinogen -> fibrin conversion)
LMWH: Activates Antithrombin, which inhibits Factor 10, which inhibits the production of thrombin from prothrombin and so stops production of fibrin from fibrinogen
Warfarin: Vitamin K antagonist (competitively inhibits), reducing clotting factor synthesis
DOACs: Old - Inhibit Factor 10a, involved in the production of the thrombin from prothrombin
New: Directly inhibit thrombin, required for fibrin - fibrinogen production
Varicose Veins Pathophysiology: Causes: Symptoms: Risk factors: Investigations: Management: Complications:
Pathophysiology: Superficial veins that have become dilated and twisted, due to high pressure from valvular reflux. C2 on CEAP.
Causes:
Symptoms: Cosmetics, Ache, Heavy legs, Restless legs, Swelling, Pruritus, Venous Eczema, Ulcers
Risk factors: Pregnancy, COCP, Obesity, FH, DVT
Investigations: Duplex USS, Pelvic USS for intra-abdominal mass causing obstruction, Coag screen for thrombophilia
Management: Compression hosiery, foam sclerotherapy, endovenous ablation with a laser
Complications: Thrombophlebitis, Venous eczema, venous ulcers, venous gangrene, DVT
AAA Pathophysiology: Symptoms: Signs: Risk factors: Screening: Investigations: Management (non-rupture and rupture): Complications:
Pathophysiology: Permanent pathological dilatation of the aorta with a diameter of 50% or more. Diameter of 3cm or more is most common threshold. Caused by degeneration of the tunica medial of the arterial wall due to atherosclerotic plaques. Foam cells (lipids), calcification, thrombosis causes layer damage. Elastin and collagen are degraded in the media.
Symptoms: Most are asymptomatic and infrarenal (L1-L4) and retroperitoneal, allowing bleeding to be tamponaded.
Rupture = Abdominal pain that radiates to back and shoulder blades.
Signs: Pulsatile abdominal mass, hypotension, Cullen’s and Grey Turner’s.
Risk factors: Male, 60-70, Smoking, Hypertension, Atherosclerosis, FH, Connective tissue disorder
Screening: Once, at 65 years old, abdominal USS scan
Investigations: Physical examination, USS, CT with contrast after USS if above 5.5cm
Management:
Non-Rupture:
Conservative:eg. smoking cessation, hypertension control, frequent USS scans. Surgical (>5.5cm or symptomatic): Endovascular aneurysm repair (EVAR) or Open repair
Rupture: Fluid resuscitate to 90 systolic, cross match, high flow oxygen, pain management, call vascular surgeons, bedside USS/urgent CT
Venous Ulcers Description: Symptoms: Signs: Risk factors: Investigations: Management:
Description: Shallow, irregular border, granulating base, usually on the gaiter region or medial malleolus
Symptoms: Painful, worse on standing
Signs: Normal peripheral pulses, warm skin, haemosiderin deposit/oedema likely
Investigations: USS doppler, normal ABPI should be seen, swab, check peripheral pulses, which should be normal
Management: Leg elevation, increased exercise, compression bandages
Arterial Ulcers Description: Symptoms: Signs: Risk factors: Investigations: Management:
Description: Punched out, deep, regular round border, irregular base and poor healing with necrosis. Located in poor circulation area - not specifically. Develop slowly.
Symptoms: Very painful, especially at night, critical limb ischaemia.
Signs: Cold skin, absent pulses, loss of hair.
Risk factors:
Investigations: ABPI < 0.8.
Management: Vascular review, statin + anti-platelet. Angioplasty + bypass grafts.
Neuropathic Ulcers
Description:
Investigations:
Management:
Description: Deep, painless ulcers at pressure points eg. base of foot. Associated with Charcot’s rocker bottom foot.
Investigations: Blood sugars + Serum B12, swab, X-ray for osteomyelitis, touch test for neuropathy
Management: Diabetic foot clinic, diabetic control, wound debridement
What is the name for an ulcer that has become malignant?
Marjolin’s ulcer
Describe Buerger’s test
Lift legs to 20 degrees - if pale, severe ischaemia
Lift legs to 45 degrees, wait 60 seconds
Swing legs round, assess how fast colour recovers and look for “sunset sign” - hyperaemia
