Chap 55-56 CVI General Considerations

Question 1

what conditions contribute to venous pathology?

Answer 1

valvular incompetence of the deep or superficial veins

perforator incompetence

venous obstruction

muscle pump dysfunction

Question 2

what does normal venous pressure do with exercise?

Answer 2

resting venous pressure drops with exercise >50%

returns to normal but takes >20sec

Question 3

What are primary and secondary cause of valve dysfunction?

Answer 3

preexisting weakness in vessel or leaflets

secondary to direct injury superficial phlebitis
excessive venous distention from hormonal effects or high pressure

Question 4

How does high venous pressure enter the superficial system?

Answer 4

failure of valves located at junctions b/w deep and superficial

failure of valves in communicating perforator

Question 5

What are the most common tributaries with reflux?

Answer 5

saphenous
small saphenous
both

Question 6

What are obstructive causes of reflux?

Answer 6

venous thrombosis

destruction of valves from DVT

compression (May-thurner)

Question 7

What is the genetic inheritance of VV?

Answer 7

autosomal dominant with variable penetrance

Question 8

How does microangiopathy occur?

Answer 8

hemo changes in large veins are transmitted to microcirculation

microvalve dysfunction

Question 9

What are features of microangiopathy?

Answer 9

elongation, dilatation, tortuosity of capillary beds

thickening of BM with increased collagen and elastic fibbers

endothelial damage

increased pericapillary edema with ‘halo’ formation

Question 10

what happens to the capillary once microangiopathy has started?

Answer 10

increase permeability and high venous pressure

accumulation of fluid, macromolecules and extravasated red blood cells in the interstitial

fragmentation and destruction of microlymphatics (impairs drainage)

Question 11

What mechanisms have been postulated for devel of microangiopathy?

Answer 11

fibrin cuff formation (accumulation of fluid in pericapillary sapce)
this impairs fibrinolysis, increase diffusion barrier, inhibit repair process and maintain inflame process

WBC trapping in capillaries with activation of leuks and inflammation

growth factor activation (unavailable for healing)

Question 12

What are skin changes in CVI?

Answer 12

edema

corona phlebectatia

hyper pigmentation from hemosiderin deposition

lipodermatosclerosis with scarring and thickening of the skin

atrophie blanche

Question 13

what is lipodermatosclerosis?

Answer 13

inflammation of the fat under the epidermis

get fat necrosis

causes tapering at ankles

Question 14

What is atrophie blanche?

Answer 14

smooth, ivory-white plaque stippled with telangiectases and is surrounded by hyper-pigmentation

Question 15

What is the character of the edema associated with CVI?

Answer 15

initially pitting

then brawny and resistant to pitting

Question 16

What is corona phlebectatica?

Answer 16

fan shaped appearance of intradermal veins on the ankle (inframalleolar ankle flare)
advanced disease

Question 17

What is the Brodie-trendelenburg test?

Answer 17

distinguish deep and superficial

supine
elevate leg to empty vein
tourniquet over superficial veins
upright

with superficial reflux, release of tourniquet with have rapid filling of superficial veins

with deep reflow the superficial veins will fill despite tourniquet

normal will take >20sec to fill with removal of trouniquet

Question 18

What is the C in the CEAP classification?

Answer 18

clinical
C0 no visible signs
C1 telangiectasia/reticular veins
C2 varicose veins
C3 edema
C4 changes in skin and sub cut
A pigmentation/eczema
B lipodermatosclerosis/atrophie blanche
C5 healed ulcer
C6 active ulcer

Question 19

What is the E in the CEAP classification?

Answer 19

etiology

Ec congenital (KTS)
Ep primary
Es secondary (DVT)
En no venous cause

Question 20

What is the A in the CEAP classification?

Answer 20

Anatomic
As superficial
Ad deep
Ap perforator
An no venous location

Question 21

What is the P in the CEAP classification?

Answer 21

Pathophys

Pr reflux
Po obstruction
Pr,o reflux and obstruction
Pn no venous patho

Question 22

What is the best test a diagnosing CVI?

Answer 22

duplex

phtoplethmysmography

Question 23

What is the best test a determining severity for CVI?

Answer 23

air plethysmography

Question 24

What is the best test for determining anatomy for CVI?

Answer 24

venogram

Question 25

What is the best test for assessing hem significance?

Answer 25

APG

foot pressure

Question 26

What is the venous filling index?

Answer 26

APG
90% of the venous volume divided by the time required to 90% of the venous volume (once upright)
2ml/s normal
>4ml/s abnormal

Question 27

What are invasive/non-invasive methods of measuring CVI?

Answer 27

NI

DUS
PPG
APG
CTV
MRV

invasive
plebogram
Ambulatory venous P
IVUS

Question 28

What is early treatment recommendation for venous ulcer?

Answer 28

compression 30-40
wound care
ablation superficial vein

Question 29

What are exercise recommendations for CVI?

Answer 29

regular moderate
vigorous can worsen
leg elevation when resting

Question 30

What are the classes for compression therapy?

Answer 30

class 1--15mmHg
class 2--20-30mmHg
class 3 30-40mmHg
class 4--40-50mmHG
>60 unsafe

Question 31

What did the REACTIV trial show for C2-3 dz?

Answer 31

2 yr symptom relief, satisfaction, QoL
better with surgery (saph ligation)
sclero better then conservative

Surgery most cost efficient followed by sclera

Question 32

How does compression work?

Answer 32

opposes reflux induced VHTN
improves muscle pump
improved microcirculation

Question 33

What are some adjuncts for compression therapy?

Answer 33

circAid garment
Unna boot
layered elastic and non-elastic compression bandage
IPC (good if edema)

Question 34

What is the evidence in compression?

Answer 34

improves healing times

decreases recurrence

Question 35

What is evidence for compression in C6 dz?

Answer 35

ssurgery plus compression ;pwer recurrence then compression alone

Question 36

What is the role of diuretics in CVI?

Answer 36

unclear

Question 37

What is the role of zinc in CVI?

Answer 37

MA

no benefit

Question 38

What is the role of fibrinolytics in CVI?

Answer 38

no proven benefit

Question 39

What is the role of pentoxifylline in CVI?

Answer 39

evidence of benefit in combo with compression

Question 40

List the tributaries at the saphenofemoral junction.

Answer 40

inferior epigastric
superficial circumflex
lateral accessory saphenous
deep external pudedal
superficial external pudendal
medial accessory saphenous