It is estimated that 20% of American women and 7% of American men suffer from venous disease. Venous disease results in symptoms such as aching, fatigue, swelling, and pain in the legs which can interfere with daily living.Cosmetic issues may affect quality of life. At least 20% of patients with venous disease will develop leg ulcers. This presentation outlines the normal anatomy and physiology of venous drainage of the extremities as well as the common venous disorders such as varicose veins and deep vein thrombosis.

1. VENOUS DISORDERS
Professor
Abdulsalam Y Taha
School of Medicine/ University of
Sulaimaniyah/ Sulaimaniyah/ Region
of Kurdistan/ Iraq
https://sulaimaniu.academia.edu/AbdulsalamTaha

2. IMPORTANCE OF VENOUS
DISEASE
It is estimated that
20% of American
women and 7% of
American men
suffer from venous
.disease
Venous disease
results in symptoms
such as aching,
fatigue, swelling,
and pain in the legs
which can interfere
.with daily living

3. IMPORTANCE OF VENOUS
DISEASE
Cosmetic issues may
.affect quality of life
At least 20% of
patients with venous
disease will develop
.leg ulcers

12. Venous Valvular Function

14. SPECTRUM OF VENOUS DISEASE
Telangectasia
Varicose Veins
Lipodermatosclerosis
Superficial Phlebitis
Venous Ulceration

25. Vein Stripping

28. Sapheno-femoral Ligation

29. DEEP VENOUS THROMBOSIS
o Is thrombosis of part or all of the deep venous
system of an extremity.
o It occurs in approximately 500,000 individuals per
year.
o About 10%(50,000) of DVT cases end in death from
pulmonary embolism, usually within a few hrs of the
initial symptoms.
o Postoperative and critically ill patients are at high
risk of developing DVT.
o Incidence: 30% after major abdominal surgery, 38%
after open prostate surgery and 50%-70% after
orthopaedic procedures.
o It is 70 % in medical ICU patients.

30. DVT: SITES
 Lower extremity venous system particularly
the calf veins.
 Pelvic veins.
 Renal veins.
 IVC.
 Ovarian veins.
 Upper extremity and neck veins.
 Right atrium.

31. LOWER EXTREMITY DVT
 Usually starts at the calf vein level and progresses
proximally to involve the popliteal, femoral, or iliac
system.
 80%-90% of pulmonary emboli originate in the calf
veins.
 Treatment of calf vein clots is controversial;
Most recommend a follow up scan in 1 week; if there
is a proximal propagation, anticoagulation is
indicated,
Some physicians believe that all patients with calf
vein thrombosis should receive anticoagulant
therapy.

32. DVT; CLINICAL PRESENTATION
 The classic clinical syndrome includes calf or thigh
pain, oedema, tenderness, and a positive Homans
sign ( calf pain on dorsiflexion of the foot).
 In patients with venographically proven DVT:
a. 50% have the classic clinical findings.
b. 50% have no associated physical findings in the
extremities.
Pulmonary embolism is the presenting symptom in
some patients.

33. DIAGNOSIS OF DVT
 Diagnosis of DVT is made by means of
laboratory tests.
 Duplex ultrasound: has become an accurate
and commonly performed noninvasive
method for diagnosing DVT. In experienced
hands, it is as accurate as venography.
 Duplex refers to the two modes of ultrasound
evaluation used in performing the test
( Doppler ultrasound and B-mode
evaluation).

34. DIAGNOSIS OF DVT
 Doppler ultrasound flow examination has an accuracy rate of
80%-90%.
 It determines:
i. Phasic flow, the variation of flow in the examined vein with
respiration.
ii. Augmentation: which is increased flow in the examined vein
when the more distal muscle mass is squeezed (this
maneuver forces flow proximally when the vein is not
occluded.)
iii. The presence of a difference in ultrasound examination
between the diseased and the normal extremity.

35. DIAGNOSIS OF DVT
 B-mode evaluation: displays the ultrasound beam as
an actual image of the vein being evaluated. A
normal vein will be easily compressible, and the
walls of the vein will actually be seen to coapt.
 Because acute thrombus has a similar echogenicity
to that of blood, compressibility and coaptation of the
walls are thought to be more accurate in detecting
acute DVT than is the visualization of clot in the
lumen.

36. VENOGRAPHY
 This is the traditional diagnostic method for
DVT.
 Radiopaque dye is injected into the pedal
veins, and a tourniquet is loosely applied at
the ankle to direct the flow of dye into the
deep venous system. Inflammation or
thrombosis of the veins occurs in 3% of
patients who undergo venography unless the
vein is flushed with a heparin solution after
infusion.

37. TREATMENT
 Continuous heparin infusion is given for 5-10 days,
followed by administration of warfarin or
subcutaneous administration of heparin for 3-6
months.
 Thrombolytic therapy with urokinase is used if
extensive DVT results in impaired perfusion of the
extremity.
 IVC filter or interruption is used if heparin is
contraindicated or if a pulmonary embolus occurs in
spite of adequate anticoagulation therapy. However,
this treatment only prevents pulmonary embolism
and does not treat the DVT.

38. PREVENTION OF DVT
 Simple preventive measures.
i. Leg elevation.
ii. Early mobilization after surgery.
iii. The use of support hose.
iv. Correction of preoperative risk factors.
 Intermittent calf compression.
By means of a pneumatic cuff.
 Unfractionated heparin.
 Low molecular weight heparin.

39. PROPHYLACTIC HEPARIN
 Preoperative and postoperative administration of
prophylactic heparin is effective in preventing DVT.
 In several large series, heparin decreased:
i. Postoperative DVT. There was a 33% incidence in
controls versus a 9% incidence in patients treated
with heparin.
ii. Fatal PE. There was a 7% mortality rate in controls
versus a 1% mortality rate in those treated with
heparin.

40. PROPHYLACTIC HEPARIN
 An intermittent sc dose of 5000 units is given every
8-12 hrs.
 The risk of peri-operative bleeding complication is
slightly increased with heparin prophylaxis ( 6%
versus 4% of controls), but the risk of major
haemorrahge is only about 2%.
 At this dose, heparin activates antithrombin III,
inhibits platelet aggregation, and decreases thrombin
availability.

41. LOW MOLECULAR WEIGHT HEPARIN
 LMWH is thought to cause fewer bleeding
complications than unfractionated heparin because
LMWH has a decreased ability to bind and inhibit
thrombin, yet retains the ability to act as a catalyst in
the inhibition of factor Xa.
 LMWH has a much lower affinity for plasma proteins,
which allows for more predictable anticoagulant
response when used at a fixed dose.
 Several clinical trials have shown that LMWH is just
as effective as traditional heparin for DVT
prophylaxis, with fewer major bleeding complications
(1.9% versus 1%).

42. COMPLICATIONS OF DVT
Phlegmasia alba dolens.
Phlegmasia cerulea dolens.
Postphlebitic syndrome.
Pulmonary embolism.

43. PHLEGMASIA ALBA DOLENS
 It is caused by acute occlusion of the iliac
and femoral veins due to DVT.
 This phlebitis results in a pale cool leg with a
diminished arterial pulse due to spasm.
 Treatment is thrombolytic therapy followed by
heparin administration to prevent progression
to phlegmasia cerulea dolens.

45. PHLEGMASIA CERULEA DOLENS
 This is secondary to acute and nearly total
venous occlusion of the extremity outflow,
including the iliac and femoral veins.
 More common in left leg.
 30% of cases occur in postoperative and
postpartum patients.
 Pelvic malignancy is not infrequent.

46. PHLEGMASIA CERULEA DOLENS
 Physical findings include:
i. cyanosis of the extremity with massive oedema,
severe pain, and absent pulses, followed by venous
gangrene.
ii. Shock may occur as a result of sequestration of a
significant amount of blood in the leg.
Treatment:
i. Thrombolytic therapy followed by heparin
administration.
ii. Thrombectomy occasionally if nonoperative therapy
is unsuccessful.
iii. Bed rest with leg elevation.

47. POSTPHLEBITIC SYNDROME
 This is a common late complication of DVT, often
occurring several yrs after the acute event.
 Clinical presentation: swelling and
ulceration.
i. Chronic valvular incompetence.
ii. Leg oedema.
iii. Local superficial venous hypertension.
iv. Brawny induration from hemoglobin
metabolism.

48. POSTPHLEBITIC SYNDROME
 Patho-physiology:
i. Local superficial venous hypertension leads
to oedema and interstitial exudation of
plasma, cells, and protein ( including RBCs,
WBCs, and fibrinogen).
ii. This oedema and exudation then lead to
brawny induration from Hb metabolism.
Tissue necrosis and skin ulceration result
from poor Oxygen diffusion secondary to
pericapillary protein deposition as well as
WBC release of proteolytic enzymes,
superoxide radicals, and various cytokines.

49. POSTPHLEBITIC SYNDROME
 TREATMENT:
i. Support hose must be worn continually to
prevent superficial venous hypertension
and swelling. If swelling can be prevented;
most ulcers can be prevented.
ii. Ligation of local perforating veins may be
used to lower the venous pressure at the
ulcer if it will not heal.
iii. A change of life style to avoid leg
dependency may improve the ulceration
and reduce the risk of recurrence.

50. COMPLICATIONS OF
ANTICOAGULANT THERAPY
 Major bleeding requiring transfusions occurs in 1%-
2% of patients on anticoagulants.
 Minor bleeding episodes are common in more than
16%.
 Fatal bleeding occurs in 0.1%-1%.
( The risk of bleeding is greater if heparin is
administered intermittently or is given to elderly or
severely hypertensive patients).
PE recurs despite anticoagulant therapy in 1%-8%.
Heparin-induced thrombocytopenia.
Complications of warfarin therapy.

51. WARFARIN
 Warfarin dosage should be carefully
regulated to maintain the international
normalized ratio INR at 2-3 times normal.
 Warfarin interacts with many other drugs,
and its effectiveness can be severely altered
by these drugs and by hepatic disease.