Venous System

Venous blood flows from the

capillaries to the heart .Deep femoral v
.Perforating v
Flow occurs against gravity .Femoral v

Muscular compression of the

veins .Popliteal v

Negative intrathoracic pressure

Calf muscle pump Small saphenous
.v

Low flow, low pressure system Great saphenous

.Perforating v .v

.Image source: Fundamentals of Phlebology: Venous Disease for Clinicians. Illustration by Linda S. Nye. American College of Phlebology 2004
 CEAP Classifications
Clinical Classifications of Venous Insufficiency (CEAP)
Class 0 - No visible or palpable signs of venous disease
Class 1 - Telangiectasias or reticular veins
Class 2 - Varicose veins
Class 3 - Edema
Class 4 - Skin changes
 (4a) Skin changes including pigmentation or venous eczema
 (4b) Skin changes with lipodermatosclerosis

Class 5 - Healed venous ulceration

Class 6 - Active venous ulceration
Diagnosis of VV
History(: symptoms including ache, pain, tightness,
skin irritation, heaviness, muscle cramps, as well as
other complaints attributable to venous dysfunction.
Examination
Duplex scan
Pathophysiology of Venous Insufficiency
 Test for incompetence
Brodie –Trendelenburg test

Empty the
veins & apply
a mid thigh
tourniquet

Let the patient stand

If the veins remain empty, but fill after If the veins fill before removal of
removal of tourniquet, the tourniquet, the incompetence must be
incompetence must be above the below the tourniquet
tourniquet
 :Identification of venous reflux

Coloured Duplex .2
:Ultrasonography

1. Visually demonstrates venous reflux into the

superficial and deep veins.
2. The degree of venous reflux can be assessed.
(Dynamic Study)
3. Can detect incompetent perforators.
Complications
/Stasis Dermatitis
& Varicose eczema
Lipodermatosclerosis
Complications
Thrombophlebitis
Management of Varicose Veins and Venous
Reflux
Conservative treatment (will not solve the problem but will help
:with symptoms)

 elevation
 avoid prolonged sitting/standing
 no leg crossing
 exercise
 weight reduction
 compression stocking therapy
Management

Compression Stocking Therapy

Models of VV managements
Stripping of GSV
Endovascular leaser
Radiofrequency ablation
Sclerotherapy(faom)
Procedure using
the Radiofrequency Ablation Catheter
 CHRONIC VENOUS INSUFFICIENCY
1. PATHOPHYSIOLOGY & EPIDEMIOLOGY
 OCCURS IN 10% OF POPULATION /W DVT
 Stasis of blood in lower extremity-due to prolonged
standing, sitting in one position, pregnancy, and obesity
 INCOMPETENT VALVES IN DEEP VEINS
  VENOUS PRESSURE IMPEDES CAPILLARY
PERFUSION
 PROTEINS LEAK INTO INTERSTITIAL TISSUES
 EDEMA IS CHRONIC  ULCERS & SCARRING
 CHRONIC VENOUS INSUFFICIENCY
Venous Stasis Ulcers
2. SIGNS & SYMPTOMS – INDURATION 
HYPERPIGMENTATION, STASIS DERMATITIS &
ULCERATIONS, EDEMA
3. GOALS: Decrease edema and Promote venous return
4. INTERVENTIONS:
a) COMPRESSION – STOCKINGS OR DRESSINGS
b) ULCERS TREATED WITH TOPICAL AGENTS-Unna,Accuzyme
c) AVOID TRAUMA
d) AVOID SITTING FOR LONG PERIODS
e) EXERCISE TO  MUSCLE ACTIVITY
f) Platelet derivative growth factor ointments-Regranex
g) Apligraf-type of skin graft
Deep Venous Thrombosis
“updates in management”
 The predisposing factors for
DVT
Pregnancy.
Parturition.
Post-partum.
Pills.
Prolonged recumbence in bed.
Prolonged immobilization.
Prolonged pyrexia.
Paraplegia.
Pelvic & orthopedic surgery.
Pelvic & abdominal malignancy.
Patients with morbid obesity.
Polycythemia.
Protein C, protein S, anti thrombin III or factor V gene deficiency.
Past history of DVT.
Clinical Presentation50%
Pain.
Swelling.
Skin (varicosities, temp, cyanosis).
 DD of DVT
Rupture Baker cyst.
Rupture plantaris
tendon.
Cellulitis.
Abscess.
Muscle hematoma.
Rhabdomyolysis.
 Investigations
D-dimer.
Imaging.
 D-Dimer
1. Not needed if there is high probability for DVT.
2. Good negative.
3. Not good positive.
 Imaging
Duplex.
Venography.
CT scan.
MRI/ MRV.
131 labeled fibrinogen scan.
Prevent PE,
Reduce morbidity,
Prevent or minimize the risk of developing the
post-thrombotic syndrome (PTS).
Ideal Treatment Modalities
“step by step”
1. Thrombectomy.
2. Thrombolysis.
3. Parenteral anticoagulation.
4. Oral anticoagulation.
5. GP-Compression therapy.
Thrombectomy
Percutaneous mechanical
thrombectomy (PMT)

Rotational devices (Trerotola

device & Amplatz thrombectomy
device).
Oscillating device (Trellis).
Rheolytic device (AngioJet).
Ultrasound assisted devices
(EKOS).
 Amplatz thrombectomy device
It employs a high velocity rotating helix to
macerate up the thrombus.
 Trellis
It employs an oscillating rather than rotating sinusoidal
nitinol wire between proximal and distal balloons while at the same time
infusing thrombolytic agents in the segment 'isolated' by the balloon.
 AngioJet
It generates a high-pressure saline jet to create a
pressure gradient resulting in rheolytic
thrombectomy with aspiration of the softened
thrombus into the catheter.
 EKOS
Ultrasound assisted devices, contains
multiple ultrasound transducers that emit high frequency, low energy
ultrasound waves in a radial fashion to enhance the penetration of
thrombolysis by exposing plasminogen receptor sites.
 Less hemolytic effect than saline pressure thrombectomy
 Less endothelial damage than rotational thrombectomy devices.
 The disadvantage is that it is not a single session technique, employing typical
16–25 h for treatment of a possible iliofemoral DVT.
Thrombolysis
CDT
Parenteral Anticoagulation
 Advantages of LMWH Over
Standard Unfractionated Heparin
Superior or equivalent efficacy
Superior safety (Anti II to Anti X)
No laboratory monitoring***
Superior bioavailability & half life
Subcutaneous once- or twice-daily dosing
Less phlebotomy (no monitoring/no intravenous line)
 Less thrombocytopenia
Oral Anticoagulation
New oral anticoagulants
A. Rivaroxaban (Xarelto)
B. Dabigatran (Pradaxa)
C. Apixaban (Eliquis)
 CAUSIS OF SUPERFICIAL
THROMBOPHLEBITIS
Venipunctures and infusions of hyperosmolar
solutions and drugs.
Cannula for longer than 24–48 hours often leads to
thrombosis.
Some systemic diseases such as thromboangiitis
obliterans (Buerger’s disease) and malignancy,
especially of the pancreas,can lead to a flitting
thrombophlebitis (thrombophlebitis migrans)
Coagulation disorders such as polycythaemia
CLINICAL PRESENTATION
of SVT are a firm,
 tender,
 erythematous fibrous cord
 usually in the area of a previous varicose or normal-
appearing vein
 VENOUS TUMOURS AND MALFORMATION
These malformations are common, often affecting
the skin but also extending into the
deep tissues, including bones and
joints
MRA.CT angio are good Dg tools.
Treatment options include surgical
excision or sclerotherapy.
Neither of these is entirely curative
because it is difficult to
remove all of the angiomatous tissue
 ENTRAPMENT OF VEINS
The axillary vein and
the popliteal vein are
the two veins that are
most commonly
compressed. The
former is compressed
at the thoracic outlet
between the first rib
and the clavicle,
 Klippel–Trenaunay syndrome

This is a combined anomaly of a

cutaneous naevus, persistent
vestigial veins with varicose veins, and
soft tissue and bone hypertrophy.
The condition is a mesodermal
abnormality
associated obstruction of the
lymphatics.
conservatively with elastic
compression