Venous disease

Question 1

What is DVT?

Answer 1

Formation of a thrombus within the deep veins (most commonly of the calf or thigh).

Question 2

What is the aetiology of DVT?

Answer 2

VIRCHOW’S TRIAD: venous stasis, vessel wall injury and blood hypercoagulability.

Question 3

What are the risk factors of DVT? (x12)

Answer 3

Oral contraceptive pill, surgery, prolonged immobility, long bone fractures, obesity, pregnancy, dehydration, smoking, polycythaemia, anti-phospholipid syndrome (autoimmune clotting disorder), thrombophilia disorders (such as protein C deficiency), active malignancy.

Question 4

What is the pathophysiology of DVT?

Answer 4

Clots tend to develop just above and behind a venous valve. When propagation of a thrombus occurs, it expands and grows proximally and across the lumen of the vein. This may lead to occlusion. The thrombus may also embolise and cause a PE.

Question 5

What is the epidemiology of DVT: Where is the incidence? Prevalence of complications?

Answer 5

Highest in hospitalised patients. Long-term complications of DVT affect 0.5% of population.

Question 6

What are the symptoms of DVT?

Answer 6

Asymptomatic or lower limb swelling or tenderness. May present with symptoms of PE such as SOB, pleuritic chest pain (worse on breathing), haemoptysis, and tachypnoea.

Question 7

What are the signs of DVT?

Answer 7

• Phlegmasia cerulea dolens from leg oedema and cyanosis from thrombotic occlusion is uncommon
• Signs of PE such as pleural friction rub, pleural effusion, loud P2 and raised JVP

Question 8

What is the Wells Clinical Prediction Score? (x9 measures +1)

Answer 8

Considers likelihood of DVT in patients: Lower limb trauma/surgery/immobilisation, >3 days bedridden, surgery within last 4 weeks, tenderness along deep venous system, entire limb swollen, calf at least 3 cm bigger circumference, pitting oedema, dilated collateral superficial veins (non-varicose), and malignancy each score 1 point. Alternative diagnosis more likely than DVT loses 2 points. If total score is more than 3, probability of DVT is high. Between 1 and 2: probability is moderate.

Question 9

What are the investigations for DVT? (x2 +3)

Answer 9

• Doppler ultrasound is gold standard.
• Bloods: D-dimer are sensitive but not specific.
• ECG, CXR and ABG if there is a suggestion that there might be PE.

Question 10

How is DVT medically managed? (x3 options)

Answer 10

ANTICOAGULATION. There are several treatment options: Rivaroxaban (direct Factor Xa inhibitor) for 3 weeks initially, Apixaban (direct Factor Xa inhibitor) for 1 week initially, or treat patients with a heparin and add warfarin (adjusting dose of warfarin according to target INR). Heparin can be discontinued once INR is above 2 for >24hrs. There are many other options too. Heparin + warfarin is not recommended first-choice.

Question 11

How does management differ depending on location of DVT?

Answer 11

Below-the-knee DVT requires anticoagulation for longer.

Question 12

How are recurrent DVTs treated?

Answer 12

Long-term warfarin/other anticoagulant.

Question 13

What must be tested before starting warfarin?

Answer 13

INR to optimise the therapeutic effect without risking dangerous side-effects such as bleeding. INR 1.1 or below is normal. An INR range of 2-3 is an effective therapeutic range for people on warfarin.

Question 14

What must be tested before starting any heparin?

Answer 14

aPTT and sometimes U&Es (as medication may be contraindicated with renal impairment)

Question 15

How is DVT managed when active anticoagulation is contraindicated and/or high embolization risk?

Answer 15

IVC filter placement to prevent embolus to lungs.

Question 16

How is DVT prevented? (x3)

Answer 16

Compression stockings, mobilisation, prophylactic heparin e.g., LMWH for immobilised hospital patients.

Question 17

What are the complications of DVT? (x3)

Answer 17

PE, damage to vein valves and chronic venous insufficiency (post-thrombotic syndrome), venous infarction (with phlegmasia cerulea dolens; infarct denotes obstruction leading to build-up of pressure, cyanosis and oedema).

Question 18

What is venous insufficiency?

Answer 18

Unable to carry blood back to heart leading to varicose veins, oedema, stasis ulcers and flaking skin.

Question 19

What are the complications associated with DVT management? (x2)

Answer 19

Heparin-induced thrombocytopenia and bleeding.

Question 20

What are varicose veins?

Answer 20

Subcutaneous, permanently dilated superficial veins 3mm or more in diameter when measured in a standing position.

Question 21

What is the aetiology of varicose veins?

Answer 21

Venous valve incompetency leading to increased pressure and distension of veins.

Question 22

What are the risk factors for varicose veins? (x6)

Answer 22

Previous episodes of DVT and genetic predisposition. Old age, female sex (progesterone and oestrogen leads to vein dilation; though severity of disease in men is worse), pregnancy, obesity.

Question 23

What is the pathophysiology of varicose veins? (x3 points)

Answer 23

• Venous flow is dependent on valves and muscle pumping (from walking etc.). Dysfunction of one or both of these mechanisms leads to blood pooling, venous hypertension and insufficiency.
• Compromised valve function leads to abnormal blood flow. It is unclear whether this causes vein dilation, or whether vein dilation predisposes this abnormal flow.
• Varicose veins also demonstrate marked proliferation of collagen matrix and decreased elastin leading to distortion of the muscle fibre layers and dilation.

Question 24

What is the epidemiology of varicose vein: Prevalence? Where? Gender? Ethnicity? Age?

Answer 24

Affects up to 40% of the population. Higher in industrialised countries. More common in women. More prevalent in Hispanics; less in Asians. Increased prevalence with age.

Question 25

What are the symptoms of varicose veins? (x5)

Answer 25

• Dilated tortuous veins
• Leg fatigue and aching with prolonged standing
• Leg cramps
• Restless legs
• Itching

Question 26

What are the signs of varicose veins? (x5)

Answer 26

• Corona phlebectatica: fine vein branches that suggest venous insufficiency
• Haemosiderin deposition (stores iron) and is a sign of venous hypertension. It increases risk of ulceration and looks like yellow/brown/black staining with bruise-like appearance.
• Lipodermatosclerosis is a sign of venous hypertension and indicates risk of ulceration. It is a complication of haemosiderin causing inflammation and soft tissue damage leading to redness and skin tightness of mostly ankles (giving inverted champagne bottle appearance).
• Ankle swelling
• Varicose ulcers – from chronic venous insufficiency

Question 27

What are the investigations for varicose veins?

Answer 27

Duplex USS to assess for reflux flow of blood by evaluating time taking for valve closure. May also indicate underlying venous insufficiency.

Question 28

What are differentials for varicose veins?

Answer 28

Telangiectasias (dilated venules that resemble spider veins) and reticular veins (dilated intradermal veins – shown in photo).

Question 29

How are varicose veins treated? (x5)

Answer 29

• Treatment option depends on how patients present and what complications they have:
• Compression therapy with bandages or stockings
• Phlebectomy: removal of varicose veins by multiple 2-3 mm incisions in the skin overlying the veins. Veins are grasped and extracted.
• Foam sclerotherapy: injection of foamed solution such as sodium tetradecyl sulphate into small veins followed by compression. The solution skrinks the veins.
• Endovenous (within a vein) thermal ablation: radiofrequency ablation causes closure of vein; laser ablation causes thrombosis and destruction of vein.
• Open surgery: stripping and ligation of vein.

Question 30

What are the complications of varicose veins? (x6)

Answer 30

Chronic venous insufficiency, haemorrhage (from erosion of varices), venous ulceration (from dilation and venous hypertension. May also be contributed by perforator incompetence), venous eczema (from insufficiency – thin, brown skin with irritation), lipodermatosclerosis, haemosiderin deposition.

Question 31

What is the prognosis of varicose veins?

Answer 31

Recurrence is likely.

Question 32

What are venous ulcers?

Answer 32

Wounds that usually occur on the legs due to improper functioning of venous valves.

Question 33

What is the aetiology of venous ulcers? (x2 (x3))

Answer 33

Chronic venous insufficiency (from DVT, phlebitis, perforator valve incompetence) or congestive heart failure.

Question 34

What are risk factors of venous ulcers? (x8)

Answer 34

Varicose veins, DVT, older age, female, family history, obesity, pregnancy, smoking.

Question 35

What is the pathophysiology of venous ulcers?

Answer 35

• Venous insufficiency leads to stasis which leads to venous hypertension. When this occurs, the pressure gradient between the arterial and venous system in the legs means that blood is not pumped as effectively into that area.
• Venous hypertension also results in venous dilation and protein exudate into the ECM. This prevents wound healing and leads to oedema.
• Venous insufficiency also results in WBC accumulation releasing inflammatory factors and reactive oxygen species, further contributing to wound formation
• Ultimately, hypertension leads to subcutaneous tissue breakdown and ulcer formation.

Question 36

What are the symptoms and signs of venous ulcers? (x6)

Answer 36

• Shallow, wet (from exudate) lesion with irregular sloping edges, usually on medial side of leg of medial malleoulus
• Moderate pain which improves on elevation (unlike arterial ulcers)
• Oedema
• Atrophie blanche – localised loss of skin pigmentation due to death of erythrocytes and scarring
• Lipodermatosclerosis
• Increased pigmentation in lower legs is an early sign (sign of venous insufficiency).

Question 37

What are the investigations for venous ulcer?

Answer 37

Based on examination and assessed with a clinical severity score.

Question 38

!!! How can a venous ulcer be differentiated from arterial ulcer? (x5)

Answer 38

• Venous develops medial side of leg, typically around medial malleolus, whereas arterial ulcer on lateral side of leg
• Venous is shallow with irregular sloping edges, whereas arterial ulcer has ‘punched out’ appearance
• Venous are ‘wet with moderate exudate, whereas arterial are ‘dry’ and scabbed
• Surrounding skin of venous ulcer is oedematous and may be evidence of varicose veins, whereas arterial is pale and cold.
• Arterial more painful on elevation

Question 39

How are venous ulcers conservatively managed? (x4)

Answer 39

Elevation of foot, elastic compression, mobility. Dress with honey and resin salve to promote skin to regrow across ulcer.

Question 40

How may venous ulcers be medically managed? (x2)

Answer 40

Pentoxifylline and sulodexide can be used to reduce platelet aggregation and reduce inflammation – this improves healing. Antibiotics used if infective.

Question 41

How may venous ulcers be surgically managed? (x2)

Answer 41

Skin grafts and artificial skin to cover ulcers. Artificial skin can excrete growth factors to help healing. May also use endovenous laser/radiofrequency ablation and foam sclerotherapy.

Question 42

What are the complications of venous ulcers?

Answer 42

Infection leading to cellulitis, or gangrene.

Question 43

What is the difference between cellulitis and gangrene?

Answer 43

Cellulitis is bacterial infection of dermis and subcutaneous fat leading to redness and tenderness. Gangrene is more severe – tissue death caused by lack of blood supply or infection.

Question 44

What is the prognosis of venous ulcers?

Answer 44

Recurrence likely – 48% 5-year recurrence. Ablatio reduces recurrence rates.