VENOUS DISEASE
FINAL YEAR
VENOUS DISEASE
 A clear understanding of the anatomy of the venous
system in the legs is essential to understanding
pathophysiology as well as treatment.
 Venous drainage of the legs is the function of two
parallel and connected systems: the deep and the
superficial systems connected by perforators .
VENOUS DISEASE
 Perforating veins connect the superficial venous system
to the deep venous system at various points in the leg—
the foot, the medial and lateral calf, the mid- and
distal thigh .
VENOUS DISEASE
VENOUS DISEASE
 The venules, the smallest veins ranging from 0.1 to 1
mm, contain mostly smooth muscle cells, whereas the
larger extremity veins contain relatively few smooth
muscle cells. These larger caliber veins have limited
contractile capacity.
 The venous valves prevent retrograde flow, and it is the
failure of the valves that leads to reflux and associated
symptoms.
 Venous valves are most prevalent in the distal lower
extremity, whereas as one proceeds proximally, the
number of valves decreases to the point that in the
superior and inferior vena cava, no valves are present.
 .
VENOUS DISEASE
 The return of the blood to the heart from the lower extremity
is facilitated by the muscle pump function of the calf—a
mechanism whereby the calf muscle, functioning as a
bellows during exercise, compresses the gastrocnemius and
soleal sinuses and propels the blood toward the heart.
 The normally functioning valves in the venous system
prevent retrograde flow; it is when one or more of these
valves become incompetent that symptoms of venous
insufficiency can develop.
 During calf muscle contraction, the venous pressure of the
foot and ankle drop dramatically. The pressures developing
in the muscle compartments during exercise range from 150
to 200 mm Hg, and when there is failure of perforating
veins, these high pressures are transmitted to the superficial
system
VENOUS DISEASE
VENOUS DISEASE
 The term varicose veins is, in the common parlance, a
term that encompasses a spectrum of venous dilation
that ranges from minor telangiectasia to severe
dilated, tortuous varicose veins.
VENOUS DISEASE
 Varicose veins refer to any dilated, tortuous, elongated
vein of any caliber.
 Telangiectasias :are intradermal varicosities that are
small and tend to be cosmetically unappealing but not
symptomatic in and of themselves.
 Reticular veins: are subcutaneous dilated veins that
enter the tributaries of the main axial or trunk veins.
 Trunk veins: are the named veins, such as the greater or
lesser saphenous veins or their tributaries.
VENOUS DISEASE
 The end result of CVI can range from
aching, heaviness, pain, and swelling with prolonged
standing or sitting in the case of symptomatic varicose
veins,
 To severe lipodermatosclerosis with edema and
ulceration in the patient with severe CVI
VENOUS DISEASE
 Defects in the strength and characteristics of the
venous wall enter into the pathogenesis of varicose
veins.
 Furthermore, communicating veins connecting the
deep with the superficial compartment may have valve
failure.

VENOUS DISEASE
Pressure studies show that two sources of venous hypertension
exist.
 The first is gravitational and is a result of venous blood
coursing in a distal direction down linear axial venous
segments. This is referred to as hydrostatic pressure and is
the weight of the blood column from the right atrium.
 The second source of venous hypertension is dynamic. It is
the force of muscular contraction, usually contained within
the compartments of the leg. If a perforating vein fails, high
pressures (ranging from 150 to 200 mm Hg) developed
within the muscular compartments during exercise are
transmitted directly to the superficial venous system.
Here, the sudden pressure transmitted causes dilation and
lengthening of the superficial veins. Progressive distal
valvular incompetence may occur.
CLASSIFICATION
CEAP Classification
 Class 0: No visible or palpable signs of venous disease
 Class 1 :Telangiectasia, reticular veins, malleolar flare
 Class 2: Varicose veins
 Class 3: Edema without skin changes
 Class 4: Skin changes ascribed to venous disease
(e.g., pigmentation, venous
eczema, lipodermatosclerosis)
 Class 5: Skin changes as defined above with healed
ulceration
 Class 6: Skin changes as defined above with active
ulceration
CLASSIFICATION
 Etiologic Classification of Chronic Lower Extremity Venous Disease
 Congenital (EC ) Cause of the chronic venous disease present since birth
 Primary (EP ) Chronic venous disease of undetermined cause
 Secondary (ES ) Chronic venous disease with an associated known cause (post-
thrombotic, post-traumatic, other)
 ANATOMIC CLASSIFICATION (AS , AD , or AP )
The anatomic site(s) of the venous disease should be described as superficial (AS
), deep (AD ), or perforating (AP ) vein(s). One, two, or three systems may be
involved in any combination. For reports requiring greater detail, the
involvement of the superficial, deep, and perforating veins may be localized by
use of the anatomic segments.
 PATHOPHYSIOLOGIC CLASSIFICATION (PR,O )
Clinical signs or symptoms of chronic venous disease result from reflux (PR
), obstruction (PO ), or both (PR,O ).
VENOUS DISEASE
VENOUS DISEASE
VENOUS DISEASE
VENOUS DISEASE
 Your Sub Points
VENOUS DISEASE
Risk Factors
 A combination of risk factors, rather than any one specific
risk factor, is a better predictor of the likelihood of a given
patient developing symptomatic varicose veins.
 Heredity undoubtedly plays a significant role in the
development of varicose veins.
 Valvular dysfunction and insufficiency
 Female sex, gravitation hydrostatic force, and hydrodynamic
forces due to muscular contraction.
 Hormonal Influence
VENOUS DISEASE
Risk Factors
VENOUS DISEASE
Symptoms
 The patient with symptomatic varicose veins relates, most often,
 symptoms of aching, heaviness, discomfort, and sometimes pain
in the calf of the affected limb.
 This is particularly worse at the end of the day, most likely due to
prolonged sitting or standing that results in venous distention
and associated pain.
 The symptoms are typically reduced or absent in the morning
owing to the fact that the limb has not been in a dependent
position through the night.
 In the case of women, the symptoms are often most troubling and
exacerbated during the menstrual period, particularly during the
first day or two.
 Primary varicose veins consist of elongated, tortuous, superficial
veins that are protuberant and contain incompetent valves.
VENOUS DISEASE
Symptoms
 Primary varicose veins merge imperceptibly into more
severe CVI.
 Swelling ,edema is moderate to severe, an increased
sensation of heaviness occurs with larger varicosities, and
early skin changes of mild pigmentation and
subcutaneous induration appear.
 When CVI becomes severe, marked swelling and calf pain
occur after standing, sitting, or walking.
 Multiple dilated veins are seen associated with various
clusters and heavy medial and lateral supramalleolar
pigmentation.
VENOUS DISEASE
Symptoms
 Many causes of leg pain are possible, and most may coexist.
Therefore, defining the precise symptoms of venostasis is
necessary. Discomfort usually occurs during warm temperatures
and after prolonged standing. The pain is characteristically
dull, does not occur during recumbency or early in the
morning, and is exacerbated in the afternoon, especially after
long standing. The discomforts of aching, heaviness, fatigue, or
burning pain are relieved by recumbency, leg elevation, or elastic
support.
 Cutaneous itching is also a sign of venostasis and is often the
hallmark of inadequate external support. It is a manifestation of
local congestion and may precede the onset of dermatitis.
This, and nearly all the symptoms of stasis disease, can be
explained by the irritation of superficial nerve fibers by local
pressure or accumulation of metabolic end products with a
consequent pH shift.
 External hemorrhage may occur as superficial veins press on
overlying skin within this protective envelope.
VENOUS DISEASE
VENOUS DISEASE
VENOUS DISEASE
VENOUS DISEASE
VENOUS DISEASE
VENOUS DISEASE
VENOUS DISEASE
VENOUS DISEASE
VENOUS DISEASE
VENOUS DISEASE
TREATMENT
 Indications for treatment are pain, easy
fatigability, heaviness, recurrent superficial
thrombophlebitis, external bleeding, and appearance.
 Nonoperative Management
 The cornerstone of therapy for patients with CVI is
external compression.
 A triple-layer compression dressing, with a zinc oxide
paste gauze wrap in contact with the skin, is utilized
most commonly from the base of the toes to the anterior
tibial tubercle with snug, graded compression.
 In general, snug, graded-pressure triple-layer
compression dressings effect more rapid ulcer healing
than compression stockings alone.
Venous Ablation:
Sclerotherapy
 Cutaneous venectasia with vessels smaller than 1 mm in
diameter do not lend themselves to surgical treatment.
Dilute solutions of sclerosant (e.g., 0.2% sodium tetradecyl)
can be injected directly into the vessels of the blemish.
Care should be taken to ensure that no single injection dose
exceeds 0.1 mL but that multiple injections completely fill
all vessels contributing to the blemish.
 Venules larger than l mm and smaller than 3 mm in size can
also be injected with sclerosant of slightly greater
concentration (e.g., 0.5% sodium tetradecyl), but limiting
the amount injected to less than 0.5 mL.
 If their cause is saphenous or tributary venous
incompetence, these conditions can be treated surgically.
 Surgery is not indicated for the treatment of venous
insufficiency in limbs with deep venous incompetence
Surgical Management
 Surgical treatment may be used to remove clusters with
varicosities greater than 4 mm in diameter. Ambulatory
phlebectomy may be performed using the stab avulsion
technique with preservation of the greater and lesser
saphenous veins, if they are unaffected by valvular
incompetence
Surgical Management
 When greater or lesser saphenous incompetence is
present, the removal of clusters is preceded by limited
removal of the saphenous vein (stripping).
 Stripping techniques are best done from above
downward to avoid lymphatic and cutaneous nerve
damage.
Surgical Management
VENOUS DISEASE
VENOUS DISEASE
VENOUS DISEASE
VENOUS DISEASE
Subfascial endoscopic perforator vein
surgery
 perforating vein division using laparoscopic
instrumentation. Initial data suggested that perforator
interruption produced rapid ulcer healing and a low rate
of recurrence.
 Direct Venous Reconstruction ??
VENOUS DISEASE
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Venous disease

  • 1.
  • 2.
    VENOUS DISEASE  Aclear understanding of the anatomy of the venous system in the legs is essential to understanding pathophysiology as well as treatment.  Venous drainage of the legs is the function of two parallel and connected systems: the deep and the superficial systems connected by perforators .
  • 3.
    VENOUS DISEASE  Perforatingveins connect the superficial venous system to the deep venous system at various points in the leg— the foot, the medial and lateral calf, the mid- and distal thigh .
  • 4.
  • 5.
    VENOUS DISEASE  Thevenules, the smallest veins ranging from 0.1 to 1 mm, contain mostly smooth muscle cells, whereas the larger extremity veins contain relatively few smooth muscle cells. These larger caliber veins have limited contractile capacity.  The venous valves prevent retrograde flow, and it is the failure of the valves that leads to reflux and associated symptoms.  Venous valves are most prevalent in the distal lower extremity, whereas as one proceeds proximally, the number of valves decreases to the point that in the superior and inferior vena cava, no valves are present.  .
  • 6.
    VENOUS DISEASE  Thereturn of the blood to the heart from the lower extremity is facilitated by the muscle pump function of the calf—a mechanism whereby the calf muscle, functioning as a bellows during exercise, compresses the gastrocnemius and soleal sinuses and propels the blood toward the heart.  The normally functioning valves in the venous system prevent retrograde flow; it is when one or more of these valves become incompetent that symptoms of venous insufficiency can develop.  During calf muscle contraction, the venous pressure of the foot and ankle drop dramatically. The pressures developing in the muscle compartments during exercise range from 150 to 200 mm Hg, and when there is failure of perforating veins, these high pressures are transmitted to the superficial system
  • 7.
  • 8.
    VENOUS DISEASE  Theterm varicose veins is, in the common parlance, a term that encompasses a spectrum of venous dilation that ranges from minor telangiectasia to severe dilated, tortuous varicose veins.
  • 9.
    VENOUS DISEASE  Varicoseveins refer to any dilated, tortuous, elongated vein of any caliber.  Telangiectasias :are intradermal varicosities that are small and tend to be cosmetically unappealing but not symptomatic in and of themselves.  Reticular veins: are subcutaneous dilated veins that enter the tributaries of the main axial or trunk veins.  Trunk veins: are the named veins, such as the greater or lesser saphenous veins or their tributaries.
  • 10.
    VENOUS DISEASE  Theend result of CVI can range from aching, heaviness, pain, and swelling with prolonged standing or sitting in the case of symptomatic varicose veins,  To severe lipodermatosclerosis with edema and ulceration in the patient with severe CVI
  • 11.
    VENOUS DISEASE  Defectsin the strength and characteristics of the venous wall enter into the pathogenesis of varicose veins.  Furthermore, communicating veins connecting the deep with the superficial compartment may have valve failure. 
  • 12.
    VENOUS DISEASE Pressure studiesshow that two sources of venous hypertension exist.  The first is gravitational and is a result of venous blood coursing in a distal direction down linear axial venous segments. This is referred to as hydrostatic pressure and is the weight of the blood column from the right atrium.  The second source of venous hypertension is dynamic. It is the force of muscular contraction, usually contained within the compartments of the leg. If a perforating vein fails, high pressures (ranging from 150 to 200 mm Hg) developed within the muscular compartments during exercise are transmitted directly to the superficial venous system. Here, the sudden pressure transmitted causes dilation and lengthening of the superficial veins. Progressive distal valvular incompetence may occur.
  • 13.
    CLASSIFICATION CEAP Classification  Class0: No visible or palpable signs of venous disease  Class 1 :Telangiectasia, reticular veins, malleolar flare  Class 2: Varicose veins  Class 3: Edema without skin changes  Class 4: Skin changes ascribed to venous disease (e.g., pigmentation, venous eczema, lipodermatosclerosis)  Class 5: Skin changes as defined above with healed ulceration  Class 6: Skin changes as defined above with active ulceration
  • 14.
    CLASSIFICATION  Etiologic Classificationof Chronic Lower Extremity Venous Disease  Congenital (EC ) Cause of the chronic venous disease present since birth  Primary (EP ) Chronic venous disease of undetermined cause  Secondary (ES ) Chronic venous disease with an associated known cause (post- thrombotic, post-traumatic, other)  ANATOMIC CLASSIFICATION (AS , AD , or AP ) The anatomic site(s) of the venous disease should be described as superficial (AS ), deep (AD ), or perforating (AP ) vein(s). One, two, or three systems may be involved in any combination. For reports requiring greater detail, the involvement of the superficial, deep, and perforating veins may be localized by use of the anatomic segments.  PATHOPHYSIOLOGIC CLASSIFICATION (PR,O ) Clinical signs or symptoms of chronic venous disease result from reflux (PR ), obstruction (PO ), or both (PR,O ).
  • 15.
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  • 18.
  • 19.
    VENOUS DISEASE Risk Factors A combination of risk factors, rather than any one specific risk factor, is a better predictor of the likelihood of a given patient developing symptomatic varicose veins.  Heredity undoubtedly plays a significant role in the development of varicose veins.  Valvular dysfunction and insufficiency  Female sex, gravitation hydrostatic force, and hydrodynamic forces due to muscular contraction.  Hormonal Influence
  • 20.
  • 21.
    VENOUS DISEASE Symptoms  Thepatient with symptomatic varicose veins relates, most often,  symptoms of aching, heaviness, discomfort, and sometimes pain in the calf of the affected limb.  This is particularly worse at the end of the day, most likely due to prolonged sitting or standing that results in venous distention and associated pain.  The symptoms are typically reduced or absent in the morning owing to the fact that the limb has not been in a dependent position through the night.  In the case of women, the symptoms are often most troubling and exacerbated during the menstrual period, particularly during the first day or two.  Primary varicose veins consist of elongated, tortuous, superficial veins that are protuberant and contain incompetent valves.
  • 22.
    VENOUS DISEASE Symptoms  Primaryvaricose veins merge imperceptibly into more severe CVI.  Swelling ,edema is moderate to severe, an increased sensation of heaviness occurs with larger varicosities, and early skin changes of mild pigmentation and subcutaneous induration appear.  When CVI becomes severe, marked swelling and calf pain occur after standing, sitting, or walking.  Multiple dilated veins are seen associated with various clusters and heavy medial and lateral supramalleolar pigmentation.
  • 23.
    VENOUS DISEASE Symptoms  Manycauses of leg pain are possible, and most may coexist. Therefore, defining the precise symptoms of venostasis is necessary. Discomfort usually occurs during warm temperatures and after prolonged standing. The pain is characteristically dull, does not occur during recumbency or early in the morning, and is exacerbated in the afternoon, especially after long standing. The discomforts of aching, heaviness, fatigue, or burning pain are relieved by recumbency, leg elevation, or elastic support.  Cutaneous itching is also a sign of venostasis and is often the hallmark of inadequate external support. It is a manifestation of local congestion and may precede the onset of dermatitis. This, and nearly all the symptoms of stasis disease, can be explained by the irritation of superficial nerve fibers by local pressure or accumulation of metabolic end products with a consequent pH shift.  External hemorrhage may occur as superficial veins press on overlying skin within this protective envelope.
  • 24.
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  • 26.
  • 27.
  • 28.
  • 29.
  • 30.
  • 31.
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    TREATMENT  Indications fortreatment are pain, easy fatigability, heaviness, recurrent superficial thrombophlebitis, external bleeding, and appearance.  Nonoperative Management  The cornerstone of therapy for patients with CVI is external compression.  A triple-layer compression dressing, with a zinc oxide paste gauze wrap in contact with the skin, is utilized most commonly from the base of the toes to the anterior tibial tubercle with snug, graded compression.  In general, snug, graded-pressure triple-layer compression dressings effect more rapid ulcer healing than compression stockings alone.
  • 35.
    Venous Ablation: Sclerotherapy  Cutaneousvenectasia with vessels smaller than 1 mm in diameter do not lend themselves to surgical treatment. Dilute solutions of sclerosant (e.g., 0.2% sodium tetradecyl) can be injected directly into the vessels of the blemish. Care should be taken to ensure that no single injection dose exceeds 0.1 mL but that multiple injections completely fill all vessels contributing to the blemish.  Venules larger than l mm and smaller than 3 mm in size can also be injected with sclerosant of slightly greater concentration (e.g., 0.5% sodium tetradecyl), but limiting the amount injected to less than 0.5 mL.  If their cause is saphenous or tributary venous incompetence, these conditions can be treated surgically.  Surgery is not indicated for the treatment of venous insufficiency in limbs with deep venous incompetence
  • 36.
    Surgical Management  Surgicaltreatment may be used to remove clusters with varicosities greater than 4 mm in diameter. Ambulatory phlebectomy may be performed using the stab avulsion technique with preservation of the greater and lesser saphenous veins, if they are unaffected by valvular incompetence
  • 37.
    Surgical Management  Whengreater or lesser saphenous incompetence is present, the removal of clusters is preceded by limited removal of the saphenous vein (stripping).  Stripping techniques are best done from above downward to avoid lymphatic and cutaneous nerve damage.
  • 38.
  • 39.
  • 40.
  • 41.
  • 42.
    VENOUS DISEASE Subfascial endoscopicperforator vein surgery  perforating vein division using laparoscopic instrumentation. Initial data suggested that perforator interruption produced rapid ulcer healing and a low rate of recurrence.  Direct Venous Reconstruction ??
  • 43.
  • 45.
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