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Venous Disease > CVI General Considerations > Flashcards

CVI General Considerations Flashcards

1
Q
A
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2
Q

what conditions contribute to venous pathology?

A

valvular incompetence of the deep or superficial veins

perforator incompetence

venous obstruction

muscle pump dysfunction

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3
Q

what does normal venous pressure do with exercise?

A

resting venous pressure drops with exercise >50%

returns to normal but takes >20sec

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4
Q

What are primary and secondary cause of valve dysfunction?

A

preexisting weakness in vessel or leaflets

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

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5
Q

How does high venous pressure enter the superficial system?

A

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

failure of valves in communicating perforator

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6
Q

What are the most common tributaries with reflux?

A

saphenous
small saphenous
both

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7
Q

What are obstructive causes of reflux?

A

venous thrombosis

destruction of valves from DVT

compression (May-thurner)

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8
Q

What is the genetic inheritance of VV?

A

autosomal dominant with variable penetrance

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9
Q

How does microangiopathy occur?

A

hemo changes in large veins are transmitted to microcirculation

microvalve dysfunction

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10
Q

What are features of microangiopathy?

A

elongation, dilatation, tortuosity of capillary beds

thickening of BM with increased collagen and elastic fibbers

endothelial damage

increased pericapillary edema with ‘halo’ formation

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11
Q

what happens to the capillary once microangiopathy has started?

A

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)

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12
Q

What mechanisms have been postulated for devel of microangiopathy?

A

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)

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13
Q

What are skin changes in CVI?

A

edema

corona phlebectatia

hyper pigmentation from hemosiderin deposition

lipodermatosclerosis with scarring and thickening of the skin

atrophie blanche

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14
Q

what is lipodermatosclerosis?

A

inflammation of the fat under the epidermis

get fat necrosis

causes tapering at ankles

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15
Q

What is atrophie blanche?

A

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

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16
Q

What is the character of the edema associated with CVI?

A

initially pitting
then brawny and resistant to pitting

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17
Q

What is corona phlebectatica?

A

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

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18
Q

What is the Brodie-trendelenburg test?

A

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

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19
Q

What is the C in the CEAP classification?

A

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

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20
Q

What is the E in the CEAP classification?

A

etiology

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

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21
Q

What is the A in the CEAP classification?

A

Anatomic
As superficial
Ad deep
Ap perforator
An no venous location

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22
Q

What is the P in the CEAP classification?

A

Pathophys

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

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23
Q

What is the best test a diagnosing CVI?

A

duplex
phtoplethmysmography

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24
Q

What is the best test a determining severity for CVI?

A

air plethysmography

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25
Q

What is the best test for determining anatomy for CVI?

A

venogram

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26
Q

What is the best test for assessing hem significance?

A

APG
foot pressure

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27
Q

What is the venous filling index?

A

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

28
Q

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

A

NI

DUS
PPG
APG
CTV
MRV

invasive
plebogram
Ambulatory venous P
IVUS

29
Q

What is early treatment recommendation for venous ulcer?

A

compression 30-40
wound care
ablation superficial vein

30
Q

What are exercise recommendations for CVI?

A

regular moderate
vigorous can worsen
leg elevation when resting

31
Q

What are the classes for compression therapy?

A 
class 1--15mmHg 
class 2--20-30mmHg 
class 3 30-40mmHg 
class 4--40-50mmHG 
\>60 unsafe
32
Q

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

A

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

Surgery most cost efficient followed by sclera

33
Q

How does compression work?

A

opposes reflux induced VHTN
improves muscle pump
improved microcirculation

34
Q

What are some adjuncts for compression therapy?

A

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

35
Q

What is the evidence in compression?

A

improves healing times
decreases recurrence

36
Q

What is evidence for compression in C6 dz?

A

ssurgery plus compression ;pwer recurrence then compression alone

37
Q

What is the role of diuretics in CVI?

A

unclear

38
Q

What is the role of zinc in CVI?

A

MA
no benefit

39
Q

What is the role of fibrinolytics in CVI?

A

no proven benefit

40
Q

What is the role of pentoxifylline in CVI?

A

evidence of benefit in combo with compression

41
Q

List the tributaries at the saphenofemoral junction.

A

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

42
Q

What are compression indications?

A

symptomatic VV (20-30)
healing ulcers
against as primary for VV for those who are candidates for SV ablation

43
Q

What is recommendation for surgery?

A

EVLT > surgery

44
Q

What are recommendation for treatment of incompetent GSV?

A

high ligation and inversion stripping to level of knee

45
Q

What perforators are the most important? what are they?

A

medial perforators

medial thigh
posteromedial
popliteal fossa
medial gastroc
post tib
medial ankle
medial foot
parartibial

46
Q

What are surgical techniques for reflux?

A

high ligation of the GSV
divide tributaries
resect 5-10cm portion of gsv

GSV stripping

47
Q

Name the six tributaries of the saphenofemoral junction.

A

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

48
Q

What are adjuncts for stripping?

A

US guidance
Tumescent anesthesia
compressive dressing and elevation
leg elevation before and after
proximal tourniquet (massive varices)

49
Q

What were the results of the ESCHAR trial?

A

RCT C5-6
No difference in healing, recurrence reduce with sx at one year 12 vs 28
Sx better QoL (LT no diff)
EVLT less peri-procedural morbidity

50
Q

When to consider Sx >EVLT in environment where EVLT is recommended over sx?

A

sperficial saphenous tributary
GSV dilation/aneurysm
Chrinic thrombophleb
excessive tortuosity
acute superficial thrombosis
economic

51
Q

How does sclerotherapy work?

A

sclerosants destroy endothelium
veins transformed into fibrous cord

52
Q

What are different sclerosants?

A

Hypertonic salin
Sclerodex
Chromated glycerin
Nonchromated glycerin
Polidocanol
Sodium tetradecyl sulfate

53
Q

What are indications for EVLT?

A

saphenous
VV
perforating veins
reticular VV
telangiectasia
residual

54
Q

What are CI for EVLT?

A

known allergy
acute DVT/PE
local infection
r-l shunt for sclerosant

relative
pregnancy
breast feeding
severe PAD

55
Q

What are compression indications?

A

symptomatic VV (20-30)
healing ulcers
against as primary for VV for those who are candidates for SV ablation

56
Q

What is recommendation for surgery?

A

EVLT > surgery

57
Q

What are recommendation for treatment of incompetent GSV?

A

high ligation and inversion stripping to level of knee

58
Q

What perforators are the most important? what are they?

A

medial perforators

medial thigh
posteromedial
popliteal fossa
medial gastroc
post tib
medial ankle
medial foot
parartibial

59
Q

What are surgical techniques for reflux?

A

high ligation of the GSV
divide tributaries
resect 5-10cm portion of gsv

GSV stripping

60
Q

Name the six tributaries of the saphenofemoral junction.

A

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

61
Q

What are adjuncts for stripping?

A

US guidance
Tumescent anesthesia
compressive dressing and elevation
leg elevation before and after
proximal tourniquet (massive varices)

62
Q

What were the results of the ESCHAR trial?

A

RCT C5-6
No difference in healing, recurrence reduce with sx at one year 12 vs 28
Sx better QoL (LT no diff)
EVLT less peri-procedural morbidity

63
Q

When to consider Sx >EVLT in environment where EVLT is recommended over sx?

A

sperficial saphenous tributary
GSV dilation/aneurysm
Chrinic thrombophleb
excessive tortuosity
acute superficial thrombosis
economic

64
Q

How does sclerotherapy work?

A

sclerosants destroy endothelium
veins transformed into fibrous cord

65
Q

What are different sclerosants?

A

Hypertonic salin
Sclerodex
Chromated glycerin
Nonchromated glycerin
Polidocanol
Sodium tetradecyl sulfate

66
Q

What are indications for EVLT?

A

saphenous
VV
perforating veins
reticular VV
telangiectasia
residual

67
Q

What are CI for EVLT?

A

known allergy
acute DVT/PE
local infection
r-l shunt for sclerosant

relative
pregnancy
breast feeding
severe PAD

Venous Disease (6 decks)

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