2. 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 .
3. 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 .
5. 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.
.
6. 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
8. 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.
9. 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.
10. 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
11. 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.
12. 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.
13. 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
14. 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 ).
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
21. 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.
22. 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.
23. 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.
34. 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.
35. 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
36. 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
37. 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.
42. 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 ??
