Chap 55-56 CVI General Considerations Flashcards
what conditions contribute to venous pathology?
valvular incompetence of the deep or superficial veins
perforator incompetence
venous obstruction
muscle pump dysfunction
what does normal venous pressure do with exercise?
resting venous pressure drops with exercise >50%
returns to normal but takes >20sec
What are primary and secondary cause of valve dysfunction?
preexisting weakness in vessel or leaflets
secondary to direct injury superficial phlebitis
excessive venous distention from hormonal effects or high pressure
How does high venous pressure enter the superficial system?
failure of valves located at junctions b/w deep and superficial
failure of valves in communicating perforator
What are the most common tributaries with reflux?
saphenous
small saphenous
both
What are obstructive causes of reflux?
venous thrombosis
destruction of valves from DVT
compression (May-thurner)
What is the genetic inheritance of VV?
autosomal dominant with variable penetrance
How does microangiopathy occur?
hemo changes in large veins are transmitted to microcirculation
microvalve dysfunction
What are features of microangiopathy?
elongation, dilatation, tortuosity of capillary beds
thickening of BM with increased collagen and elastic fibbers
endothelial damage
increased pericapillary edema with ‘halo’ formation
what happens to the capillary once microangiopathy has started?
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)
What mechanisms have been postulated for devel of microangiopathy?
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)
What are skin changes in CVI?
edema
corona phlebectatia
hyper pigmentation from hemosiderin deposition
lipodermatosclerosis with scarring and thickening of the skin
atrophie blanche
what is lipodermatosclerosis?
inflammation of the fat under the epidermis
get fat necrosis
causes tapering at ankles
What is atrophie blanche?
smooth, ivory-white plaque stippled with telangiectases and is surrounded by hyper-pigmentation
What is the character of the edema associated with CVI?
initially pitting
then brawny and resistant to pitting
What is corona phlebectatica?
fan shaped appearance of intradermal veins on the ankle (inframalleolar ankle flare)
advanced disease
What is the Brodie-trendelenburg test?
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
What is the C in the CEAP classification?
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
What is the E in the CEAP classification?
etiology
Ec congenital (KTS)
Ep primary
Es secondary (DVT)
En no venous cause
What is the A in the CEAP classification?
Anatomic As superficial Ad deep Ap perforator An no venous location
What is the P in the CEAP classification?
Pathophys
Pr reflux
Po obstruction
Pr,o reflux and obstruction
Pn no venous patho
What is the best test a diagnosing CVI?
duplex
phtoplethmysmography
What is the best test a determining severity for CVI?
air plethysmography
What is the best test for determining anatomy for CVI?
venogram
What is the best test for assessing hem significance?
APG
foot pressure
What is the venous filling index?
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
What are invasive/non-invasive methods of measuring CVI?
NI
DUS PPG APG CTV MRV
invasive
plebogram
Ambulatory venous P
IVUS
What is early treatment recommendation for venous ulcer?
compression 30-40
wound care
ablation superficial vein
What are exercise recommendations for CVI?
regular moderate
vigorous can worsen
leg elevation when resting
What are the classes for compression therapy?
class 1--15mmHg class 2--20-30mmHg class 3 30-40mmHg class 4--40-50mmHG >60 unsafe
What did the REACTIV trial show for C2-3 dz?
2 yr symptom relief, satisfaction, QoL
better with surgery (saph ligation)
sclero better then conservative
Surgery most cost efficient followed by sclera
How does compression work?
opposes reflux induced VHTN
improves muscle pump
improved microcirculation
What are some adjuncts for compression therapy?
circAid garment
Unna boot
layered elastic and non-elastic compression bandage
IPC (good if edema)
What is the evidence in compression?
improves healing times
decreases recurrence
What is evidence for compression in C6 dz?
ssurgery plus compression ;pwer recurrence then compression alone
What is the role of diuretics in CVI?
unclear
What is the role of zinc in CVI?
MA
no benefit
What is the role of fibrinolytics in CVI?
no proven benefit
What is the role of pentoxifylline in CVI?
evidence of benefit in combo with compression
List the tributaries at the saphenofemoral junction.
inferior epigastric superficial circumflex lateral accessory saphenous deep external pudedal superficial external pudendal medial accessory saphenous
