Venous disease Flashcards

1
Q

What is DVT?

A

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

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2
Q

What is the aetiology of DVT?

A

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

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3
Q

What are the risk factors of DVT? (x12)

A

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.

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4
Q

What is the pathophysiology of DVT?

A

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.

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5
Q

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

A

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

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6
Q

What are the symptoms of DVT?

A

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.

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7
Q

What are the signs of DVT?

A
  • 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
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8
Q

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

A

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.

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9
Q

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

A
  • 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.
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10
Q

How is DVT medically managed? (x3 options)

A

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.

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11
Q

How does management differ depending on location of DVT?

A

Below-the-knee DVT requires anticoagulation for longer.

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12
Q

How are recurrent DVTs treated?

A

Long-term warfarin/other anticoagulant.

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13
Q

What must be tested before starting warfarin?

A

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.

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14
Q

What must be tested before starting any heparin?

A

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

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15
Q

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

A

IVC filter placement to prevent embolus to lungs.

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16
Q

How is DVT prevented? (x3)

A

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

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17
Q

What are the complications of DVT? (x3)

A

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).

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18
Q

What is venous insufficiency?

A

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

19
Q

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

A

Heparin-induced thrombocytopenia and bleeding.

20
Q

What are varicose veins?

A

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

21
Q

What is the aetiology of varicose veins?

A

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

22
Q

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

A

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.

23
Q

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

A
  • 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.
24
Q

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

A

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.

25
Q

What are the symptoms of varicose veins? (x5)

A
  • Dilated tortuous veins
  • Leg fatigue and aching with prolonged standing
  • Leg cramps
  • Restless legs
  • Itching
26
Q

What are the signs of varicose veins? (x5)

A
  • 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
27
Q

What are the investigations for varicose veins?

A

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

28
Q

What are differentials for varicose veins?

A

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

29
Q

How are varicose veins treated? (x5)

A
  • 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.
30
Q

What are the complications of varicose veins? (x6)

A

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.

31
Q

What is the prognosis of varicose veins?

A

Recurrence is likely.

32
Q

What are venous ulcers?

A

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

33
Q

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

A

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

34
Q

What are risk factors of venous ulcers? (x8)

A

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

35
Q

What is the pathophysiology of venous ulcers?

A
  • 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.
36
Q

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

A
  • 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).
37
Q

What are the investigations for venous ulcer?

A

Based on examination and assessed with a clinical severity score.

38
Q

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

A
  • 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
39
Q

How are venous ulcers conservatively managed? (x4)

A

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

40
Q

How may venous ulcers be medically managed? (x2)

A

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

41
Q

How may venous ulcers be surgically managed? (x2)

A

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.

42
Q

What are the complications of venous ulcers?

A

Infection leading to cellulitis, or gangrene.

43
Q

What is the difference between cellulitis and gangrene?

A

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.

44
Q

What is the prognosis of venous ulcers?

A

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