Venous Insufficiency and Ulceration Flashcards Preview

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Flashcards in Venous Insufficiency and Ulceration Deck (23):
1

What is chronic venous insufficiency?

Chronic elevation of deep venous pressure (venous HTN) and blood pooling in lower extremities.

2

Aetiology of chronic venous insufficiency?

-Calf muscle pump dysfunction and valvular incompetence (phlebitis, varicosities or DVT)
-Venous obstruction
-AV fistulas, venous malformations

3

What are the clinical features of chronic venous insufficiency?

-Pain, LL oedema (relieved with elevation)
-Pruritus, haemosiderin deposits
-Stasis dermatitis, subcutaneous fibrosis
-Ulceration: shallow, above medial malleolus, weeping, painless, irregular outline
-Signs of DVT/varicose veins / thrombophlebitis

4

Ix in chronic venous insufficiency?

-ambulatory venous pressure measurement
-Doppler U/S
-photoplethysmography

5

Conservative Mx chronic venous insufficiency?

-Compression stockings, elevation, avoid prolonged standing
-Ulcers: zinc oxide wraps, split thickness skin grafts, ABx, debridement

6

Surgical Mx chronic venous insufficiency?

-Surgical ligation of perforators in ulcer region, greater saphenous stripping
-venous bypass if short segment obstruction

7

Pathophysiology of venous chronic venous disease?

-Blood flow superficial -> deep through unidirectional valves
-Exercise: calf muscle pump + vein patency + competent valves decrease venous pressure 90>30mmHg.
-Failure of any of these results in chronic venous insufficiency

8

What are the two theories of venous hypertension causing venous ulceration?

1. White cell trapping hypothesis
2. Fibrin cuff hypothesis

9

What is the white cell trapping hypothesis of venous ulceration?

-WBCs larger, less bendy than RBCs
-When perfusion pressure decreased by venous hypertension, WBC plug capillaries -> RBCs congest behind
-WBCs activated --> adhere to endothelium --> release of proteolytic enzymes and ROS
-Endothelial and tissue damage

10

What is the fibrin cuff hypothesis of venous disease causing venous ulceration?

-increased venous pressure transmitted to capillaries==> capillary elongation and increased endothelial permeability
-fibrinogen deposited into tissues ==> fibrin
-accumulation of fibrin barrier to oxygen ==> tissue hypoxia ==> ulceration

11

How is severity of venous disease classified?

CEAP
C: clinical (i.e. severity of AFx)
E: etiology
A: anatomic classification
P: pathophysiologic classification

12

What are the major types of leg ulcers?

1. Ischaemic
2. Neuropathic (DM, EtOH, spinal cord lesions)
3. Stasis / venous

13

CFx ischaemic leg ulcers?

-Painful ulcer
-Hx claudication
-CV RFx
-previous peripheral vascular surgery

14

Location of ischaemic leg ulcers?

-Distal periphery: dorsum of foot / pretibia

15

Appearance of ischaemic leg ulcer?

-Puched out edges
-Ulcer base: poorly developed grey granulation tissue
-Surrounding skin pale / mottled with no sigs of inflammation
-Little bleeding with debridement

16

Signs of chronic arterial insufficiency?

-Atrophic nails / skin
-venous guttering
-slow capillary return
-Absent pulses
-Beurger's +ve

17

CFx neuropathic ulcers?

-Painless
-Hx diabetes / other causes of neuropathy

18

Signs of neuropathy (a/w neuropathic ulcers)?

-Hypoaesthesia
-Proprioception decreased
-2 point discrimination diminished
-Vibratory perception decreased

19

Location of neuropathic ulcers?

-Plantar surface of MTPs
-"Bunion" areas
-Dorsum of IP joints
-Base of 5th MT
-MM or LM
-Callused posterior rim of heel pad

20

CFx venous ulcers?

-Hx venous insufficiency (VVs, thrombophlebitis, DVT)
-Previous venous surgery

21

Appearance venous ulcers?

-Large, irregular area
-Shallow
-Location: over gaiter area (common = medial malleolus)
-Moist, granulating base
-Surrounded by zone of inflammation and stasis dermatitis

22

Ix in ulcer workup?

-FBE
-UEC
-CRP
-BSL + HbA1C
-Vasculitic screen
-ESR
-Thrombophilic screen
-Swab MCS
-Xray/bone scan / MRI
-Duplex (art / venous)
-CTA
-Biopsy

23

Treatment ulcers?

-Bed rest
-Elevation or dependency
-IV ABx
-Dressings
-Debridement / split skin graft
-Treat underlying aetiology (revascularisation, compression stockings, pressure offloading footwear)