Surgery - Vascular Flashcards

1
Q

Which side does the Large Saphenous vein travel down?

A

Medial

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2
Q

What artery is the dorsalis pedis a branch of?

A

Anterior Tibial - Opposite to the posterior tibial pulse

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3
Q
Acute Limb Ischaemia
Pathophysiology:
Causes:
Signs:
Classification:
Investigations:
Management:
Complications:
A

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

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4
Q
Chronic limb ischaemia
Pathophysiology:
Classification:
Symptoms:
Claudication areas and vessels involved:
Risk factors:
Investigations:
Management:
Differentials:
Complications:
A

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:

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5
Q

Why should an ABPI >1.2 be taken with caution?

What ABPI is considered severe?

A

Calcification and hardening of the arteries can raise ABPI

<0.5 is severe, 0.5-0.8 is moderate

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6
Q
Chronic venous insufficiency
Pathophysiology:
Causes:
Classification (important):
Risk factors:
Investigations:
Management:
Complications:
A

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

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7
Q
DVT
Virchow's triad:
Pre-operative prevention:
Causes:
Symptoms:
Signs:
Risk factors:
Investigations:
Management:
Complications:
A

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

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8
Q
Describe the MOA of the following drugs:
Unfractionated Heparin:
LMWH:
Warfarin:
DOACs (Direct oral anticoagulants) and NOACs:
A

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

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9
Q
Varicose Veins
Pathophysiology:
Causes:
Symptoms:
Risk factors:
Investigations:
Management:
Complications:
A

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

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10
Q
AAA
Pathophysiology:
Symptoms:
Signs:
Risk factors:
Screening:
Investigations:
Management (non-rupture and rupture):
Complications:
A

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

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11
Q
Venous Ulcers
Description:
Symptoms:
Signs:
Risk factors:
Investigations:
Management:
A

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

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12
Q
Arterial Ulcers
Description:
Symptoms:
Signs:
Risk factors:
Investigations:
Management:
A

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.

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13
Q

Neuropathic Ulcers
Description:
Investigations:
Management:

A

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

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14
Q

What is the name for an ulcer that has become malignant?

A

Marjolin’s ulcer

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15
Q

Describe Buerger’s test

A

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

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