Venous

Disorders

Introduction
The lower limb is the most common site of
venous disorders.
More than 5% of the population have
varicose veins and 1% have, or have had,
venous ulceration.
At any one time, up to 200 000 people in
the UK have active venous ulceration.

ANATOMY

Anatomy

Venous Disorders
To understand:
1) Venous anatomy and the physiology of venous return
2) The pathophysiology of venous disease
3) Superficial thrombophlebitis
4) The clinical significance of varicose veins
5) Deep venous thrombosis
6) Venous insufficiency and venous ulceration and post
thrombotic syndrom

Superficial thrombophlebitis
Inflammation or thrombosis of a superficial veins.
Usually due to septic complication of an
intravascular cannula or other intra vascular
devices that remained in its position for more then
72 hrs.
Pulmonary embolism rarely complicate superficial
thrombophlebitis.

Clinical presentation:
A tender, palpable cord along the course of a
superficial vein , red, warm, indurated vein.
May be a source of fever in the postoperative period.

Superficial thrombophlebitis:
Treatment

1)Remove the infected cannula (Always change the

site of the peripheral intra-venous cannula every 72 hrs
to avoid this complication).
2) Bed rest and elevation of the extremity
3) Local application of heat for relief of pain
4) Support hose worn both during the period of
inflammation and for prophylaxis.
5) NSAID
6) Antibiotics could be prescribed.

Varicose Veins
Definition
Abnormally dilated and tortuous
subcutaneous superficial venous networks
in territory of either long or short saphenous
veins or the perforators.
This is in response to a pathological increase in
the veins intra-luminal pressure & valvular
incompetence of the deep, superficial of
perforator systems.

2) Varicose Veins

2) Varicose Veins
Aetiology:
1) Primary
Cause not known; often familial Probably a weakness of
vein wall that permits valve ring dilatation
2) Secondary
Obstruction to venous outflow:
Repeated pregnancy, fibroids,ovarian cyst ,abdominal
lymphadenopathy, pelvic cancer (cervix, uterus, ovary,
rectum) ,ascites , iliac vein thrombosis, retroperitoneal
fibrosis.
Valve destruction
Deep vein thrombosis
High flow and pressure
Arteriovenous fistula (especially the acquired traumatic
variety)
3) Congenital:
Due to absence of valves: Kippel-Trenaunay syndrome.

2) Varicose Veins
Clinical features:
May either give no symptoms or cause
aching & discomfort in legs.

Often there are no specific symptoms but

the cosmetic appearance is unsatisfactory.

Symptoms of itch and & skin thickening ,

bleeding, phlebitis, lipodermatosclerosis,
eczema , ulceration may be present.

Diagnosis :
1) Clinical (Tourniquet test or Trendelenburg
test).
2) Doppler ultrasound & Duplex imaging
3) Ascending venography ( rarely performed)

2) Varicose Veins
Complications of varicose veins:
1) Venous eczema
2) Venous pigmentations
3) Lipodermatosclerosis
4) Superfecial therombophlebitis
5) Venous ulceration

2) Varicose Veins
Treatment of varicose veins
1) Compression stocking & venotonics administration.
2) Injection sclerotherapy of irritant solution of sodium
tetradecyl (STD).
3) Surgical treatment of varicose veins: The aim of
surgery is two-fold:
Firstly : to disconnect the deep and superficial
systems where there is a direct communication (i.e.
saphenofemoral, saphenopopliteal junction and
above-knee perforators) and followed by sttripping of
the long or short saphenous veins accordingly.
Secondarily :to remove damaged/dilated superficial
varicosities (Multiple phlebectomies with ligation of
the perforators ).

3) Deep vein thrombosis

Definition:
Is thrombosis of a part or all of the deep
venous system in an extremity
Its a serious life threatening condition that
may lead to sudden death in the short term or
to long-term morbidity.
The most frequent location of deep vein
thrombosis is in the lower limbs.
The exact incidence is not well defined but it
may be up to 30% after major surgeries.

3) Deep vein thrombosis

RISK FACTORS
I.Secondary DVT occurring in the setting of a recognized
risk factor.
II. Primary or idiopathic absence of risk factors.
The changes described by Virchow lead to clotting in the
veins:
1) Changes in the vessel wall with damage to the
endothelium due to injury or inflammation, this is
known to happen following previous deep vein
thrombosis.
2) Diminished rate of blood flow in the veins.
In modern medical practice this occurs during and after
operations, and in debilitating conditions such as
strokes and myocardial infarction.

3) Deep vein thrombosis

RISK FACTORS
3) Increased coagulability of the blood. This also occurs
following surgery and in the presence of infection or
systemic malignancy or Thrombophilia due to
deficiencies of anti-thrombin III, protein C, protein S
and factor V Leiden has been shown to lead to
venous thrombosis in young patients, sometimes with
severe or fatal consequences.
Immobility remains one of the most important risk
factors.
Recently, the term 'ethrombosis' has been used to
describe blood clots occurring in people sitting at their
computer for prolonged periods of time.

3) Deep vein thrombosis

Clinical presentations:
The most significant findings are tenderness in the calf and oedema
at the ankle.
(Homans' sign) Pain in the calf on dorsiflexion of the toes
(It should no longer be used).
Some patients with deep vein thrombosis of the lower limb may have
no symptoms in the leg, but present with severe dyspnoea due to
pulmonary embolism:
Swelling
Pain
Redness or no apparent signs and symptoms
Dilated superficial veins
Calf tenderness
Low-grade pyrexia

50% of the patients are asymptomatic

3) Deep vein thrombosis

Diagnosis:
1) General investigations and screening for Thrombophilia.
2) Doppler ultrasound and duplex imaging is most useful
diagnostic tool have sensitivity a specifity up to 90%.
About 20% of patients with clinical signs and symptoms of
a deep vein thrombosis have normal deep veins.
3) If this is not available, then ascending phlebography should
be undertaken.
4) For diagnosis of pulmonary embolism, enhanced helical
computerised tomography (CT) scanning is considered the
standard test and is replacing isotope imaging studies.

3) Deep vein thrombosis

Differential diagnosis:

Ruptured Baker's cyst,

Superficial thrombophlebitis,
Calf muscle haematomas and
Ruptured plantaris tendon.

All of these diagnoses can be demonstrated on

ultrasonography.
ultrasonography

3) Deep vein thrombosis

Treatment:

1) Intravenous heparin, with the dose adjusted according to the

weight of the patient and controlled by the activated partial
thromboplastin time (APTT) which sould be twice of the control in
first 48 hrs.
The duration of heparin treatment should be at least 5 days.
days
At the same time, the patient should be commenced on warfarin.
warfarin The
aim here is to reduce the risk of a further recurrence of venous
thrombosis.
Warfarin does not remove the clot from blocked veins and the duration
of treatment (usually 3-6 months) is selected to prevent further
episodes of venous thrombosis.
Warfarin dosage is controlled by measuring the international
normalised ratio (INR).
(INR)
The INR should be prolonged to between 2.5 and 3.5 times the control
value.
Patients with recurrent venous thromboembolic problems should be
anticoagulated for life.

3) Deep vein thrombosis

Treatment:

2) Subcutaneous injections of lowmolecular-weight heparin (LMWH) for

the treatment of deep vein thrombosis is
an alternative method of anticoagulation.
The dose is based on the patient's
(100 IU/kg) weight and treatment given
without blood tests to control the dose.

3) Deep vein thrombosis

Treatment:

3) Venous thrombectomy : Occasionally,

massive venous thrombosis in the lower
limb leads to severe impairment in the
blood supply to the limb, leading to
ischaemia and, eventually, gangrene.
This is a surgical emergency and requires
rapid relief of the venous obstruction.

3) Deep vein thrombosis

Treatment:

4) Intra-venous thrombolysis,
thrombolysis achieved
by passing a catheter into the affected
vein and infusing a fbrinolytic drug such
as streptokinase or tissue plasminogen
activator (TPA), is reducing the need
for surgical thrombectomy
nowadays.

3) Deep vein thrombosis

Prevention of deep vein thrombosis:
1) Low risk patents:
patents
Young patients, minor illnesses, operations lasting for less than 30 minutes with no
additional risk factors; needs no specific prophylactic measure.
2) Moderate risk.
Patients over the age of 40 years with debilitating illnesses, undergoing major
surgery but no additional risk factors; these patients have up to 40% change
to develop DVT and about 1% for pulmonary embolism.
embolism They need:

Graduated compression stockings (TED stockings)

Heparin 5000 iu s/c bd or LMWH.
Continued regimen until full mobilisation.

3) High risk:
Patients over the age of 40 years with serious medical conditions, such as stroke
and myocardial infarction, and undergoing major surgery with additional risk
factor, such as a past history of venous thromboembolism, extensive malignant
disease or obesity. These may develop DVT in 40%- 80% of the cases & 10%
will complicate to pulmonary embolism.
They need:

Graduated compression stockings (TED stockings)

Heparin 5000 iu s/c tds or LMWH.
+/- Intra-operative pneumatic calf compression device use.
Continued regimen until full mobilisation.

3) Deep vein thrombosis

Complications of DVT:
1) Systemic complications:
complications pulmonary
embolism, pulmonary hypertension.
2) Local complications :
Post-phlebitic limb,
Phlegmasia alba dolens due to obstruction
of the iliofemoral vein this may progresse to
Phlegmasia cerulea dolence (Venous
gangrene) if not well treated by heparin,
intravenous thrombolysis and even some time
venous thrombectomy.

Phlegmasia Alba Dolens

-

Painful white leg

Proximal deep vein obstruction

Phlegmasia Cerulea Dolens

Triad of painful blue leg with edema
Pain out of proportion to appearance

Deep vein and collateral or superficial vein obstruction

Results in venous congestion (edema) which distinguishes it from
Phlegmasia Alba Dolens