L6: DISEASE OF VEIN 2) Deep Venous System

ANATOMY • The deep veins run beneath the deep

 Venous drainage of the legs is divided into fascia of the lower limbs
two parallel and connected systems: the • The deep veins accompany and share the
deep and the superficial systems name of the major arteries in the lower
connected by perforators limb
• The artery and vein are located within the
1) Superficial Venous System same vascular sheath – arterial pulsations
• The superficial veins run in the aid venous return
subcutaneous tissues and eventually a) The foot and leg
drain into the deep veins. o Main venous structure of foot is
• 2 major superficial veins: the great the dorsal venous arch which
saphenous vein and the small saphenous mostly drains into the superficial
vein veins
• The great saphenous vein is formed by o Some veins from the arch
the dorsal venous arch of the foot, and penetrate deep into the leg,
the dorsal vein of the great toe forming the anterior tibial vein
• It ascends up the medial side of the leg, o The plantar digital veins in the
passing anteriorly to the medial malleolus foot empty into a network of
at the ankle metatarsal veins that comprise
• It then crosses and ascends medially, the deep plantar venous arch
passing posteriorly to the medial condyle o This continues into the medial and
at the knee lateral plantar veins that then
• As the vein moves up the leg, it receives drain into the posterior tibial and
tributaries from other small superficial fibular veins
veins o The dorsalis pedis veins on the
• The great saphenous vein terminates by dorsum of the foot form the
draining into the femoral vein paired anterior tibial veins at the
immediately inferior to the inguinal ankle
ligament after entering the fossa ovalis o The paired posterior tibial veins,
• The small saphenous vein is formed by adjacent to and flanking the
the dorsal venous arch of the foot, and posterior tibial artery, run under
the dorsal vein of the little toe the fascia of the deep posterior
• It moves up the posterior side of the leg, compartment. These veins enter
passing posteriorly to the lateral the soleus and join the popliteal
malleolus, along the lateral border of the vein, after joining with the paired
calcaneal tendon peroneal and anterior tibial veins
• It moves between the two heads of the o There are large venous sinuses
gastrocnemius muscle and empties into within the soleus muscle—the
the popliteal vein in the popliteal fossa soleal sinuses—that empty into
the posterior tibial and peroneal
veins
o On the posterior surface of the
knee, the anterior tibial, posterior
tibial and fibular veins unite to
form the popliteal vein
o The popliteal vein enters the thigh
via the adductor canal in the
adductor magnus
 b) The thigh Venous Function
o Once the popliteal vein enters the  The venules contain mostly smooth
thigh, it is termed the femoral muscle cells whereas the larger extremity
vein veins contain relatively few smooth
o It is situated anteriorly, muscle cells
accompanying the femoral artery  These larger caliber veins have limited
o The deep vein of the thigh contractile capacity
(profunda femoris vein) drains  The venous valves prevent retrograde
blood from the thigh muscles via flow
the perforating veins  Failure of the valves leads to reflux and
o It then empties into the distal associated symptoms
section of the femoral vein  Venous valves are most prevalent in the
o The femoral vein leaves the thigh distal lower extremity
by running underneath the  As one proceeds proximally, the number
inguinal ligament, at which point of valves decreases to the point that in
it is known as the external iliac the superior and inferior vena cava, no
vein valves are present
 The return of the blood to the heart from
c) The gluteal region the lower extremity is facilitated by the
o The gluteal region is drained by muscle pump function of the calf
inferior and superior gluteal veins  During calf muscle contraction, the
o These empty into the internal iliac venous pressure of the foot and ankle
vein 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

Varicose Veins
 The term varicose veins is a term that
encompasses a spectrum of venous
dilation that ranges from minor
telangiectasia to severe dilated, tortuous
varicose veins
3) Perforating veins  Varicose veins refer to any dilated,
o Perforating veins connect the tortuous, elongated vein of any caliber
superficial venous system to the  Telangiectasias are intradermal
deep venous system at various varicosities that are small and tend to be
points in the leg—the foot, the cosmetically unappealing but not
medial and lateral calf, the mid- symptomatic in and of themselves
and distal thigh
 Reticular veins are subcutaneous dilated  The result is passive venous dilation,
veins that enter the tributaries of the which, in many instances, causes valvular
main axial or trunk veins dysfunction

c) Clinical features
 Patients will typically present initially
with cosmetic issues, presenting with
unsightly visible veins or discolouration
of the skin
 Worsening varicose veins may then
cause heaviness, aching or itching in the
calf or affected limb
 Subsequent complications if left untreated
can include skin changes, ulceration,
 Trunk veins are the named veins, such as thrombophlebitis, or bleeding (often
the greater or lesser saphenous veins or presenting post-trauma)
their tributaries.  On examination, varicosities will be
 The end result of CVI can range from present in the course of
aching, heaviness, pain, and swelling with the great and/or short saphenous veins
prolonged standing or sitting in the case  They can also present with clinical
of symptomatic varicose veins, to severe features of venous insufficiency, such as
lipodermatosclerosis with edema and ulceration, varicose eczema, or
ulceration in the patient with severe CVI haemosiderin deposition
 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
a) Risk Factors often most troubling and exacerbated
 Heredity undoubtedly plays a significant during the menstrual period, particularly
role in the development of varicose veins during the first day or two
 Valvular dysfunction and insufficiency  Primary varicose veins consist of
 Female sex, gravitation hydrostatic force, elongated, tortuous, superficial veins that
and hydrodynamic forces due to muscular are protuberant and contain incompetent
contraction valves
 Obesity  When CVI becomes severe, marked
 Prolonged standing swelling and calf pain occur after
 Pregnancy standing, sitting, or walking
 Multiple dilated veins are seen associated
b) Hormonal Influence with various clusters and heavy medial
 Venous function is undoubtedly and lateral supramalleolar pigmentation
influenced by hormonal changes  Many causes of leg pain are possible, and
 In particular, progesterone causing most may coexist
relaxation of smooth muscle fibers  Therefore, defining the precise symptoms
 This effect directly influences venous of venostasis is necessary
function  The pain is characteristically dull, does not
occur during recumbency or early in the
 morning, and is exacerbated in the e) Classification
afternoon, especially after long standing  The C-E-A-P classification is a recent
 The discomforts of aching, heaviness, scoring system that stratifies venous
fatigue, or burning pain are relieved by disease based on clinical presentation,
recumbency, leg elevation, or elastic etiology, anatomy, and pathophysiology
support  C: Clinical signs (grade 0–6, supplemented
 Cutaneous itching is also a sign of by “A” for asymptomatic and “S” for
venostasis and is often the hallmark of symptomatic presentation
inadequate external support  E: Etiologic classification (congenital,
 It is a manifestation of primary, secondary)
local congestion and may  A: Anatomic distribution (superficial,
precede the onset of deep, or perforator, alone or in
dermatitis combination)
 External hemorrhage  P: Pathophysiologic dysfunction (reflux or
may occur as superficial obstruction, alone or in combination)
veins press on overlying
skin I. Clinical Classification of Chronic Lower
Extremity Venous Disease
d) Pathogenesis  Class 0: No visible or palpable signs of
 They arise from incompetent valves, venous disease
which permit blood flow from the deep  Class 1: Telangiectasia, reticular veins,
venous system to the superficial venous malleolar flare
system (at the sapheno-femoral junction  Class 2: Varicose veins
and sapheno-popliteal junction, but other  Class 3: Edema without skin changes
perforating veins exist)  Class 4: Skin changes ascribed to venous
 This results in venous disease (e.g., pigmentation, venous
hypertension and dilatation of the eczema, lipodermatosclerosis)
superficial venous system  Class 5: Skin changes as defined above
 Changes occur at the cellular level with healed ulceration
 In the distal liposclerotic area, capillary  Class 6: Skin changes as defined above
proliferation is seen, and extensive with active ulceration
capillary permeability occurs as a result of
the widening of interendothelial cell pores II. Etiologic Classification of Chronic Lower
 Transcapillary leakage of osmotically Extremity Venous Disease
active particles, the principal one being  Congenital (EC): Cause of the chronic
fibrinogen, occurs venous disease present since birth
 The extravascular fibrin remains to  Primary (EP) Chronic venous disease of
prevent the normal exchange of oxygen undetermined cause
and nutrients in the surrounding cells  Secondary (ES): Chronic venous disease
 However, little proof exists for an actual with an associated known cause (post-
abnormality in the delivery of oxygen to thrombotic, post-traumatic, other)
the tissues (Fibrin cuffs theory)
 Another factor is the proteolytic enzymes III. Anatomic Classification (AS, AD, AP)
from the extravasated leukocytes  The anatomic site(s) of the venous disease
(Leukocyte entrapment theory) 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
IV. Pathophysiologic Classification (PR, O)
 Clinical signs or symptoms of chronic
venous disease result from reflux (PR),
obstruction (PO), or both (PR, O)

f) Diagnostic evaluation
 Clinical examination of the patient in good
light provides nearly all the information
necessary
 Visual examination can be supplemented  Venous Ablation: Sclerotherapy
by noting a downward-going impulse on
coughing
 Tapping the venous column of blood also
demonstrates pressure transmission
through the static column to incompetent
distal veins
 The modified Perthes test for deep
venous occlusion
 Brodie-Trendelenburg test, and multiple
torniquet test of axial reflux  Cutaneous venectasia with vessels
 These tests have been replaced by in- smaller than 1 mm in diameter do not
office use of the continuous wave, lend themselves to surgical treatment
handheld Doppler instrument  Dilute solutions of sclerosant (e.g., 0.2%
supplemented by duplex evaluation sodium tetradecyl) can be injected directly
 The handheld Doppler instrument can into the vessels of the blemish
confirm an impression of saphenous  Care should be taken to ensure that no
reflux and incompetent valves of single injection dose exceeds 0.1 mL but
perforators that multiple injections completely fill all
 Duplex technology more precisely defines vessels contributing to the blemish
which veins are refluxing by imaging the  Venules larger than l mm and smaller than
superficial and deep veins 3 mm in size can also be injected with
sclerosant of slightly greater
g) Treatment concentration (e.g., 0.5% sodium
 Indications for treatment are pain, easy tetradecyl), but limiting the amount
fatigability, heaviness, recurrent injected to less than 0.5 mL.
superficial thrombophlebitis, external
 If their cause is saphenous or tributary
bleeding, and appearance venous incompetence, these conditions
can be treated surgically
h) Nonoperative management  Surgery is not indicated for the treatment
 The cornerstone of therapy for patients
of venous insufficiency in limbs with deep
with CVI is external compression venous incompetence
 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
i) 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

 Direct Venous Reconstruction NOT

indicated as treatment because venous
system is a low-pressure system and
blood remains stagnant (stasis) so clotting
will occur rapidly after surgery hence it
has a very high failure rate

 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

 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