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MD2 Vascular > Venous Disease and Chronic Ulcers > Flashcards

Venous Disease and Chronic Ulcers Flashcards

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1
Q

What is chronic venous disease?

A

Disease where VR is impaired leading to sustained venous HTN

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2
Q

What are the 3 main pathological mechanisms contributing to the development of chronic venous disease?

A

ROC:

Reflux

Obstruction

Calf muscle pump failure

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3
Q

Describe the superficial venous system of the lower limb

A

Greater saphenous vein

Small saphenous vein

Anterior accessory saphenous vein

Vein of Giacomini

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4
Q

Describe the deep venous system of the lower limb

A

Tibial veins

Popliteal vein

Superficial femoral vein

Common femoral vein

External iliac vein

Common iliac vein

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5
Q

What structures join the superficial and deep venous systems?

A

Perforating veins (with unidirectional valves to prevent reflux)

Saphenofemoral junction (SFJ)

Saphenopopliteal junction (SPJ)

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6
Q

What is the prevalence of chronic venous insufficiency in the adult population?

A

10-35%

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7
Q

What % of recognised ulcers have been present for >12 months?

A

50%

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8
Q

Describe the pathophysiology of venous disease

A

Blood flows from superficial to deep veins through unidirectional valves During exercise, a combination of the calf muscle pump, vein patency and valvular competence reduces venous pressure from 90 mmHg to 30 mmHg Failure of any or all of these systems results in chronic venous insufficiency Pathway from venous HTN to ulceration not fully understood and still debated (“white cell trapping” and “fibrin cuff” theories are most popular)

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9
Q

Describe the “white cell trapping” hypothesis of venous disease

A

WBCs are larger and less deformable than RBCs When perfusion pressure is reduced by venous HTN, WBCs plug capillaries and RBCs build up behind WBC activation occurs Endothelial adhesion by WBC releases proteolytic enzymes and oxygen free radicals causing endothelial and tissue damage

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10
Q

Describe the “fibrin cuff” hypothesis of venous disease

A

Increased venous pressure is directly transmitted to capillaries resulting in capillary elongation and increased endothelial permeability Larger molecules such as fibrinogen become deposited into tissues Fibrinogen is converted to fibrin Accumulation of fibrin acts as barrier to oxygen and causes tissue hypoxia leading to ulceration

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11
Q

CEAP classification for chronic venous disease

A

Clinical classification Etiologic classification Anatomic classification Pathophysiologic classification

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12
Q

Categories of clinical classification in CEAP

A

C0: no visible or palpable signs of venous disease C1: telangiectasies or reticular veins C2: varicose veins C3: oedema C4a: pigmentation or eczema C4b: lipodermatosclerosis or atrophie blanche C5: healed venous ulcer C6: active venous ulcer Then can be S: symptomatic or A: asymptomatic

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13
Q

IMAGE

A

Telangiectasies or reticular veins (C1)

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14
Q

IMAGE

A

Lipodermatosclerosis (C4b)

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15
Q

IMAGE

A

Atrophie blanche (C4b)

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16
Q

Symptoms of chronic venous disease

A

Pain (aching, tightness) Skin irritation Calf heaviness Muscle cramps

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17
Q

IMAGE

A

Venous eczema

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18
Q

IMAGE

A

Varicose veins

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19
Q

Categories of etiologic classification in CEAP

A

Ec: congenital Ep: primary Es: secondary (post-thrombotic) En: no venous cause identified

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20
Q

Categories of anatomic classification in CEAP

A

As: superficial veins Ap: perforator veins Ad: deep veins An: no venous location identified

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21
Q

Categories of pathophysiologic classification in CEAP

A

Pr: reflux Po: obstruction Pr,o: reflux and obstruction Pn: no venous pathophysiology identifiable

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22
Q

What is a varicose vein?

A

Elongated, tortuous, dilated vein (thin-walled,, valve deformed, resulting in abnormal blood flow and bulging of the skin)

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23
Q

Distinguish between primary and secondary varicose veins

A

Primary: affecting superficial veins or perforators in the absence of deep incompetence Secondary: associated with deep venous incompetence from recanalisation of previous DVT (i.e. venous obstruction)

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24
Q

What are the only solid predisposing factors for varicose veins?

A

Genetics Previous DVT

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25
How much risk does genetics confer for varicose veins?
If both parents affected, risk is 90% If one parent affected, risk is 25% for males and 62% for females
26
Describe the clinical presentation of varicose veins
Cosmetic issues (e.g. telangiectasia, reticular veins, varices) Pain (general leg ache or heaviness) Swelling (early on causes ankle pitting oedema, later may become indurated) Thrombophlebitis Bleeding Skin changes (varicose eczema, pigmentation, lipodermatosclerosis, atrophie blanche) Ulceration
27
Thrombophlebitis
28
How can venous claudication be distinguished from arterial claudication?
Arterial: resolves with rest Venous: does not resolve with rest but requires elevation for 10-20 mins
29
"Inverted champagne bottle" is the common descriptor for this skin change seen in venous disease
Lipodermatosclerosis
30
What Ix should be performed in the setting of varicose veins?
Venous duplex Descending venography
31
Descending venography method
Dye injected and XRs taken
32
Describe the principles of conservative management for varicose veins
Elevation Avoid standing still (activate calf muscle pump) Dressings for ulceration Graduated compression stockings
33
Classes of graduated compression stockings
1: 45 mmHg
34
Options for varicose vein therapy
Conservative Sclerotherapy Open surgery Endovenous laser therapy (EVLT) Radiofrequency ablation (RFA)
35
What different kinds of sclerotherapy are there? What is the difference between the two?
UGS (usually for larger veins) Microsclerotherapy (for smaller veins)
36
What different options are their for surgical management of varicose veins?
SFL (saphenofemoral ligation) SPL (saphenopopliteal ligation) GSV strip Stab phlebectomy (removing varicose veins on surface of legs; tiny punctures are made and veins are removed through these)
37
How is EVLT performed?
Endovenous laser treatment treats varicose veins using an optical fiber that is inserted into the vein to be treated, and laser light, normally in the infrared portion of the spectrum, shines into the interior of the vein; this causes the vein to contract, and the optical fiber is slowly withdrawn
38
How is RFA performed?
Under ultrasound guidance, a radiofrequency catheter is inserted into the abnormal vein and the vessel treated with radio-energy, resulting in closure of the involved vein Usually used to treat the greater saphenous, small saphenous and perforator veins
39
What are the 3 most common kinds of ulcer?
Ischaemic Neuropathic Stasis/venous NB Ulcers may be of mixed aetiology (arterial/venous, neuroischaemic)
40
List 4 other types of ulcer
Infective Neoplastic Systemic disease Traumatic
41
List 3 types of infective ulcers
Syphilis Mycobacterium Osteomyelitis
42
List 5 types of neoplastic ulcers
SCC BCC Melanoma Metastatic Kaposi's sarcoma
43
List 4 features on Hx of ischaemic ulcers
Painful ulcer Hx of claudication or rest pain CV RFs Previous peripheral vascular surgery
44
What is the typical location of an ischaemic ulcer?
Distal periphery, over dorsum of foot or pretibia
45
What is the typical appearance of an ischaemic ulcer?
Punched out edges Ulcer base: poorly developed grey granulation tissue Surrounding skin is pale or mottled with no signs of inflammation Little bleeding when debrided
46
List 5 signs of chronic arterial insufficiency
Atrophic nails/skin Venous guttering Slow capillary return Absent pulses Beurger's +ive
47
List 2 features on Hx of a neuropathic ulcer
Painless Hx of DM or other causes of neuropathy
48
What is the typical location of neuropathic ulcer?
Deep, on pressure points or calluses
49
Give 6 examples of pressure points on the feet
Plantar surface of MTP joints "Bunion" or "bunionette" areas Dorsum of IP joints Base of 5th metatarsal MM or LM Callused posterior rim of heel pad
50
List 4 signs of neuropathy
Hypoaesthesia Proprioception 2-point discrimination Vibratory perception
51
Describe 3 features of distorted foot architecture
Hyperextension of MTP joints Hyperflexion of IP joints Charcot's deformity ("rocker-bottom" appearance)
52
List 4 features on Hx of a venous ulcer
Hx of venous insufficiency (varicose veins, superficial thrombophlebitis or DVT, variceal bleeding) Previous venous surgery
53
Describe the typical location of a venous ulcer
Over gaiter area (commonly medial malleolus)
54
Describe the typical appearance of a venous ulcer
Larger and irregular edge Shallow Moist granulating base Surrounded by zone of inflammation and stasis dermatitis
55
List 6 signs associated with venous insufficiency
Varicose veins Pitting oedema Varicose eczema Pigmentation Lipodermatosclerosis Atrophie blanche
56
Compare the 3 main types of ulcer by their most common site
Arterial: distal at toe tips, pressure areas Venous: gaiter area Neuropathic: dorsum of PIP/DIP, plantar surface MTP, MM or LM, heel, other calloused areas
57
Compare the 3 main types of ulcer by size/shape/depth
Arterial: small deep Venous: large, irregular, shallow Neuropathic: variable
58
Compare the 3 main types of ulcer by their base
Arterial: pale and sloughy Venous: granulating Neuropathic: granulating
59
Compare the 3 main types of ulcer by their edges
Arterial: punched out Venous: sloping and shallow Neuropathic: punched out
60
What initial investigations should be performed in the case of an ulcer?
Basic bloods: FBE, UEC, CRP, glucose, HbA1c, vasculitic screen, ESR, thrombophilic screen Swab M/C/S XR +/- bone scan +/- MRI Duplex (arterial or venous) CTA DSA Biopsy
61
List 6 principles of treatment for ulcers
Bed rest Elevation or dependency IV Abx Dressings Debridement/split skin graft Treat underlying aetiology (revascularisation, compression stockings/varicose vein surgery, pressure offloading footwear/total contact cast)
62
What kind of ulcer? Why?
Arterial
63
What kind of ulcer? Why?
Neuropathic
64
What kind of ulcer? Why?
Venous
65
Spot diagnosis
Venous eczema
66
Spot diagnosis
Atrophie blanche Scarring after skin injury with poor perfusion
67
Spot diagnosis
Lipodermatosclerosis

MD2 Vascular (3 decks)

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