Venous Disorders

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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.

transcript

VENOUS DISORDERS

Professor

Abdulsalam Y Taha

School of Medicine/ University ofSulaimaniyah/ Sulaimaniyah/ Region

of Kurdistan/ Iraqhttps://sulaimaniu.academia.edu/AbdulsalamTaha

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.

IMPORTANCE OF VENOUS DISEASE

Cosmetic issues may affect quality of life.

At least 20% of patients with venous disease will develop leg ulcers.

Venous Valvular Function

SPECTRUM OF VENOUS DISEASE

Telangectasia

Varicose Veins

Lipodermatosclerosis

Superficial Phlebitis

Venous Ulceration

Vein Stripping

Sapheno-femoral Ligation

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.

DVT: SITES

Lower extremity venous system particularly the calf veins.

Pelvic veins. Renal veins. IVC. Ovarian veins. Upper extremity and neck veins. Right atrium.

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.

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.

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).

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.

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.

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.

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.

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.

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.

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.

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%).

COMPLICATIONS OF DVT

Phlegmasia alba dolens.Phlegmasia cerulea dolens.Postphlebitic syndrome.Pulmonary embolism.

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.

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.

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.

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.

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.

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.

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.

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.