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8/12/2019 Pathophysiology of Varicose Vein - Chronic Venous Insufficiency
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PATHO-PHYSIOLOGYOF
CHRONIC VENOUSINSUFFICIENCY
DR G MARK MALOUF
SURGEON
SYDNEY AUSTRALIA
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8/12/2019 Pathophysiology of Varicose Vein - Chronic Venous Insufficiency
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8/12/2019 Pathophysiology of Varicose Vein - Chronic Venous Insufficiency
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Four requirements for adequate
venous flowCardiac pump “vis a tergo”
Pressure difference between the legs and
the right heart , assisted by negative
thoracic pressure
Venous pumps Calf muscle pump
Foot pumpCompetent venous valves
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CHRONIC VENOUS DISEASE
THE CLINICAL APPEARANCE we see in
patients with CHRONIC VENOUS
DISEASE represents CHRONIC VENOUSINSUFFICIENCY - CVI
These clinical changes are the result ofPROLONGED HIGH VENOUS PRESSURE
ie CHRONIC VENOUS HYPERTENSION
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CHRONIC VENOUS INSUFFICIENCY
The damage to the MICROCIRCULATION
in patients with CHRONIC VENOUS
HYPERTENSIONIS CALLED
VENOUS HYPERTENSIVE
MICROANGIOPATHY
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CHRONIC VENOUS INSUFFICIENCY
Persistently high venous pressure FROM
WHATEVER CAUSE MAY result in the
SIGNS OF CVI
OEDEMA
PIGMENTATION
VARICOSE ECZEMA
LIPODERMATOSCLEROSIS
ATROPIE BLANCHE
LEG ULCERATION
+/- VISIBLE VARICOSITIES
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CEAP CLASSIFICATION OF VARICOSE
VEINS AND VENOUS DISEASE
CLINICAL C0 C1 C2 C3 C4 C5 C6
ETIOLOGICAL CONGENITAL PRIMARY SECONDARY
ANATOMICAL WHICH VEINS AFFECTED S D P
PATHOPHYSIOLOGICAL REFLUX OBSTRUCTION BOTH
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Grade Description
C 0 No evidence of venous disease
C 1 Superficial spider veins or reticular veins
C 2 Varicose veins
C 3 Ankle / calf oedema of venous origin ( ? not foot
oedema)
C 4a Skin pigmentation in the gaiter area Varicose eczema
4b Atrophie blanche Lipodermatosclerosis
C 5 A healed venous ulcer
C 6 An open venous ulcer
EACH CLASS IS DESIGNATED SYMPTOMATIC S OR
ASYMPTOMATIC A
Clinical Etiological Anatomical
Pathophysiological CEAP
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CAUSES OF PROLONGED HIGH
VENOUSPRESSURE
VENOUS PATHOLOGY
VENOUS REFLUX in SUPERFICIAL or DEEP or
PERFORATING VEINS from Valvular incompetence
VENOUS OBSTRUCTION of DEEP VEINS
COMBINED REFLUX AND OBSTRUCTION
FUNCTIONAL PATHOLOGY
OBESITY
IMMOBILITY
GRAVITY
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VENOUS PATHOLOGY PRODUCING
PROLONGED HIGH VENOUS PRESSURE
VARICOSE VEINS
SFI SPI
VENOUS REFLUX IN SAPHENOUS TRUNKS
AND MAJOR TRIBUTARIES
DEEP VEIN THROMBOSIS
OUTFLOW OBSTRUCTION
DEEP VEIN REFLUX PRIMARY
SECONDARYDEEP VEIN PARTIAL OBSTRUCTION AND REFLUX
PERFORATING VEIN INCOMPETENCE
THIGH CALF
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Valvular Function in V V’s
Healthy Diseased
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8/12/2019 Pathophysiology of Varicose Vein - Chronic Venous Insufficiency
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FUNCTIONAL PATHOLOGY PRODUCING
PROLONGED HIGH VENOUS PRESSURE
OBESITY
IMMOBILITY POOR MOBILITY REDUCES CALF
MUSCLE PUMP AND FOOT PUMP.
IT REDUCES LYMPHATIC TRANSPORT
GRAVITY PROLONGED STANDING
PROLONGED SITTINGHEIGHT
CVI PATIENTS OFTEN SPEND PROLONGED PERIODS
SITTING IN A CHAIR AND MANY SLEEP PERMANENTLY
IN A CHAIR AND NEVER GO TO BED
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THEORIES TO EXPLAIN HOW HIGH VENOUS
PRESSURE PRODUCES MICROANGIOPATHY
AND THE CLINICAL FINDINGS OF CVI
VENOUS STASIS THEORY
ARTERIO-VENOUS FISTULAE THEORY
DIFFUSION BLOCK THEORY
LEUCOCYTE TRAPPING AND
ACTIVATION THEORY
More modern cellular theories
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CHRONIC VENOUS INSUFFICIENCY
VENOUS STASIS THEORY
1917 HOMANS
BLOOD STASISPOOR NUTRITION
HYPOXIA
TISSUE BREAKDOWN
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CHRONIC VENOUS INSUFFICIENCY
ARTERIO-VENOUS FISTUALE THEORY
1949 PRATT
SHUNT VIA ARTERIOLES
TISSUE HYPOXIA AND BREAKDOWN
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CHRONIC VENOUS INSUFFICIENCY
DIFFUSION BLOCK THEORY
1981-82 BURNAND & BROWSE
WIDENED ENDOTHELIAL GAP JUNCTIONEXTRAVASATION OF FIBRINOGEN
FIBRIN CUFFS DEVELOP
BARRIER TO OXYGEN DIFFUSION ANDNUTRIENT BLOOD FLOW
EPIDERMAL CELL DEATH
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CHRONIC VENOUS INSUFFICIENCY
LEUCOCYTE TRAPPING AND
ACTIVATION THEORY
1988 COLERIDGE SMITH SCURR
CIRCULATING NEUTROPHILS TRAPPED IN VENOUS
MICROCIRCULATION SECONDARY TO HIGH VENOUS
PRESSURE
SLUGGISH CAPILLARY FLOW
HYPOXIA
NEUTROPHIL ACTIVATION
DAMAGE TO ENDOTHELIAL CELLS
EVENTUAL SKIN DAMAGE
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CVI Pathophysiology Sequence of Events
High venous pressure
Extravasation RBCs and 2 macroglobulins &fibrinogen
Degradation & chemotaxis beginning the inflammatoryprocess
Leukocytes attracted especially mast cells and monocytesRelease of Transforming GF 1 - TGF 1
Fibroblast activity is modified by TGF 1
Other cytokines & growth factors released (VEGF &
PDGF)Extracellular matrix changes Soft tissue destruction
Dermal fibrosis and remodeling
Ulceration
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Immunohistochemistry &
Immunoreactivity Studies
TGF 1 is the most potent modulator of
cellular dysfunction in CVI especially of
fibroblastsExpression of intracellular adhesion
molecules ICAM 1 used for diapedesis of
white cellsCascade of inflammatory events
Expression of PDGF & VEGF
Leukocyte recruitment
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Tissue Matrix Changes
Matrix deposition is controlled bymatrix metalloproteinases (MMPs)
Their inhibitors are tissue inhibitors of MMPs= TIMPs
TGF 1 controls matrix deposition and remodelingTGF 1 binds to dermal fibroblasts resulting in
intense dermal fibrosis collagen synthesis
Diminished fibroblast proliferation: senescence
and poor ulcer healingOther matrix proteins Fibronectin
- Galactosidase
Extracellular Matrix Contraction
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CHRONIC VENOUS INSUFFICIENCY
VENOUS MICROCIRCULATION PATHOLOGY
ENDOTHELIAL CELLS THICKER
INTER-ENDOTHELIAL JUNCTIONS WIDER
EXTRACELLULAR MATRIX ALTERED
LEUCOCYTES ARE PARTICIPATINGINTERCELLULAR ADHESION MOLECULES COHESINS
TRANSFORMING GROWTH FACTORS
TGFB1 PDGF VEGF
DERMAL FIBROBLASTS BECOME SENESCENTMATRIX METALLO PROTEINASES
MMPs TIMPS
CYTOKINES VENOUS ULCER WOUND FLUID
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SUMMARY OF CVI PATHO-PHYSIOLOGY
1. VARICOSE VEINS AND VENOUS THROMBOSIS OCCURCOMMONLY AND HAVE A GENETIC COMPONENT MODIFIED BYENVIRONMENTAL AND LIFESTYLE FACTORS
2. THEY PRODUCE CHRONIC VENOUS HYPERTENSION WHICH INSUSCEPTIBLE PATIENTS PRODUCES MICROVASCULAR
PATHOLOGY
3. IN DERMAL CIRCULATION A CASCADE OF INFLAMMATORY
EVENTS OCCURS4. MACROMOLECULES AND RBCs EXTRAVASATE STIMULATING
ONGOING INFLAMMATION CYTOKINES AND GROWTHFACTORS RELEASED LEUCOCYTE MIGRATION INTO
TISSUES
5. INTENSE DERMAL FIBROSIS RESULTS FIBROBLASTPROLIFERATION DIMINISHES – SENESCENCE
MMP-2 SYNTHESIS IMPEDES ULCER HEALING
COMPLEX MULTI-FACTORIAL INTERACTION IN SUSCEPTIBLE PTS
PRODUCING THE CLINICAL FINDINGS OF CVI
Ai f T t t i CVI
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Aims of Treatment in CVI
Patients
Reduce the persistently high venous pressureTreat and eliminate venous reflux
Relieve venous obstruction
Elevate the foot of the bed
Graduated compression stockingsWeight reduction and increased walking
Modify the inflammatory process occurring in the gaiter
area of these legs DAFLON 500Block the release or activation of TGF 1
Modify fibroblast activity Reduce leukocyte attraction
C6 patients: Wound care dressings compression
medications to encourage wound healing
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Practical Points when using stockings in CVI
Below-knee almost always
Patient often unable to apply or remove
strong stockings
Stockings may aggravate venous eczema
due to heat under stocking
Two lower compression stockings easier
to apply than a very strong one
Fitting and education VITAL Who is fitting