Venous and lymphatic disorders of the limb

Niamh Bambury

Surgical Lecturer

21/10/08

Deep Vein Thrombosis

• In conjunction with PE is a leading cause of preventable in-hospital mortality in the United States

• Approximately 1 person in 20 will develop a DVT in the course of his or her lifetime.

DVT

• Virchow’s triad-three broad categories of factors that are thought to contribute to thrombosis– Alterations in normal blood flow (stasis)– Injuries to the vascular endothelium– Alterations in the constitution of blood

Virchow’s Triad

• Stasis– includes turbulence,mitral stenosis and

varicose veins

• Injuries to the vascular endothelium– damage to the veins arising from shear

stress and hypertension

Virchow’s Triad

• Hypercoagulability– deficiency of antithrombin III, nephrotic

syndrome,changes after severe trauma or burns, disseminated cancer, late pregnancy and delivery, race, age, whether the patient is a smoker, and obesity.

Risk FactorsActive cancer (treatment ongoing, or within 6 mo or palliative)

+1

Paralysis or recent plaster immobilization of the lower extremities

+1

Recently bedridden for >3 d or major surgery <4 wk +1Localized tenderness along the distribution of the deep venous system

+1

Entire leg swelling +1Calf swelling >3 cm compared with the asymptomatic leg +1Pitting edema (greater in the symptomatic leg) +1Previous DVT documented +1Collateral superficial veins (nonvaricose) +1Alternative diagnosis (as likely or greater than that of DVT) +1

Signs and symptoms

Edema- principallyunilateral, is themost specific symptom

Leg pain- pain canoccur on dorsiflexionof the foot (Homan’s sign).

Examination

• Tenderness • Warmth or erythema of skin can be

present over the area of thrombosis.• Venous distension and prominence of

the subcutaneous veins• Superficial thrombophlebitis

– a palpable, cordlike, indurated, tender, subcutaneous vein

Examination

• Fever: usually low grade

• Colour- reddishpurple fromvenous engorgementand obstruction

Examination

• Phlegmasia cerulea dolens– ischaemic form of venous occlusion– leg is oedematous, cyanotic, painful, due to

massive ileofemoral venous obstruction

• Phlegmasia alba dolens– massive ileofemoral venous thrombosis and

associated arterial spasm– Painful,pale with poor or even absent distal

pulses– R/O acute arterial occlusion, due to presence of

swelling, petechiae, and distended superficial veins

Examination

• Clinical findings of PE– in about 10% of patients with DVT– DVT may be clinically silent– Presents with chest pain, shortness of

breath of sudden onset

Differential diagnoses

• Cellulitis• Lymphangitis• Superficial thrombophlebitis• Arterial insufficiency• Asymmetric peripheral oedema secondary to CHF, liver

disease, renal failure, or nephrotic syndrome• Extrinsic compression of iliac vein secondary to tumour ,

abscess,haematoma• Postphlebitic syndrome• Varicose veins

Investigations

• FBC• U&E• Inflammatory markers-ESR,CRP• Coagulation markers• D-dimers

– D-dimer fibrin fragments are present in fresh fibrin clot and in fibrin degradation products of cross-linked fibrin

Investigations

• D-dimer level is also elevated in– trauma– recent surgery– hemorrhage – cancer– sepsis

• D-dimer assays should only be used to outrule DVT ie normal d-dimer levels outrule DVT but a high level does not confirm diagnosis due to low specificity

Investigations

• Duplex Ultrasonography– Incompressible vein due to thrombosis– Increased flow is not observed when the

lower extremity is compressed which implies an obstruction (clot) between the transducer and the compressed area.

– DVT may be directly visualized – Doppler flow: Doppler color-flow imaging

can depict absent or abnormal flow in an area where clot might not be visible

Investigations

• Venography– An IV line is placed in a distal foot vein, and

several tourniquets (placed at the ankle and below and above the knee), or reverse Trendelenburg positioning are used to shunt contrast material into the deep venous system.

– The venous system from foot to the pelvis is observed, and detailed images of the entire deep venous system, including the paired tibial veins, iliacs, and IVC can be obtained

Treatment

• IVC filter– mechanical barrier to the flow of emboli

larger than 4 mm– Indications for IVC filter placement include

• DVT with a contraindication to anticoagulation • major bleeding due to anticoagulation therapy• failed anticoagulation (manifest by progressive

DVT or new PE during adequate anticoagulation).

Treatment

• Anticoagulation is the mainstay of the initial treatment for DVT.

• The anticoagulant effect of heparin is due to to its activation of antithrombin III. Antithrombin III, inactivates thrombin and inhibits the activity of activated factor X in the coagulation process.

• Heparin prevents extension of the thrombus and has been shown to significantly reduce the incidence of fatal and nonfatal pulmonary emboli as well as recurrent thrombosis.

Treatment

• Warfarin therapy is used initially with heparin for 4-5 days until the INR is therapeutically elevated to 2-3.

• This overlap is due to an initial transient hypercoagulable state induced by warfarin. This effect is related to the differential half-lives of protein C, protein S, and the vitamin K–dependent clotting factors II, VII, IX, and X.

• Long-term anticoagulation is indicated for patients with recurrent venous thrombosis and/or persistent or irreversible risk factors

Sequelae

• The original thrombus causes venous valvular incompetence and altered venous return leading to a high incidence of chronic venous insufficiency and postphlebitic syndrome.

Post phlebitic syndrome

• characterized by – chronic pain– Swelling– heaviness – Venous ulcers

Chronic Venous Insuffiency

• Two mechanisms prevent venous hypertension.– bicuspid valves in the veins prevent backflow of

blood and venous pooling. DVTs commonly occur at these valves, causing irreversible damage to the valve.

– calf muscles decrease venous pressures by approximately 70% in the lower extremities when exercising. With rest, pressures return to normal in approximately 30 seconds. In diseased veins, movement decreases venous pressures by only 20%. When ambulation is stopped, pressure in the vein lumen increases slowly, returning to normal over a period of minutes

Chronic Venous insuffiency

• Leg veins cannot pump enough oxygen-poor blood back to the heart. This is due to damaged or "incompetent" valves

• Sequelae– Varicose veins -a sign of venous hypertension,

the most common result of CVI.– Leg discomfort: exercise and prolonged

standing results in the characteristic ache due to venous hypertension in the muscles.

Chronic Venous Insuffiency

– Venous ulcers: esp. at the medial malleolus, where venous pressure is maximal due to the presence of large perforating veins

– Leg edema: white blood cells damage the capillary basement leading to leg edema

– Lipodermatosclerosis: These characteristic skin changes in the lower extremities include capillary proliferation, fat necrosis, and fibrosis of skin and subcutaneous tissues leading to an ‘inverted champagne bottle’ appearance. Skin becomes reddish or brown because of the deposition of hemosiderin from red blood cells

Varicose Veins

• Represent underlying chronic venous insufficiency with ensuing venous hypertension. This venous hypertension leads to a broad spectrum of clinical manifestations, ranging from symptoms to cutaneous findings like varicose veins, reticular veins, telangiectasia, swelling, skin discoloration, and ulceration

Varicose Veins

• Primary varicose veins – incompetent venous valves that

result in venous hypertension. 

• Secondary varicose veins– Secondary to deep venous thrombosis

and its sequelae or congenital anatomic abnormalities

Anatomy of the venous system

• Superficial Veins

• Perforator Veins

• Deep veins

Anatomy

The superficial system communicates with the deep system at– Perforator veins: These veins transverse the

deep fascia of the lower extremity. – Saphenofemoral junction -located

proximally at the groin where the GSV meets the femoral vein

– Saphenopopliteal junction -behind the knee where the SSV joins with the popliteal vein   

Pathophysiology

• In healthy veins, the flow of venous blood is through the superficial system into the deep and up the leg into the IVC and toward the heart  

• One-way venous valves are found in both systems and the perforating veins.

• Incompetence in any of these valves can lead to a disruption of the flow of blood toward the heart and result in venous hypertension

Pathophysiology

• The calf pump mechanism helps to empty the deep venous system, but if perforating vein valves fail, then the pressure generated is transmitted to the superficial system resulting in varicose veins

Clinical manifestations

Lipodermatosclerosis-induration of the dermis and subcutaneous tissue resulting in an inverted champagne bottle appearance

Clinical manifestations

• Telangiectasia

Dilated intradermal venules greater than 1 mm in diameter

Clinical manifestations

• Haemosiderin depositionbrownish darkeningof the skin, resulting from extravasated blood

Clinical manifestations

• Venous ulcers

Investigations

• Trendelenburg test– distinguish patients with reflux at the SFJ from

those with incompetent deep venous valves. – The leg is elevated until the congested

superficial veins have all collapsed. Direct pressure is used to occlude the GSV just below the SFJ. The patient stands with the occlusion still in place. If the distal superficial varicosities remain empty or fills very slowly, the principal entry point of high pressure into the superficial system is at the SFJ. Rapid filling despite manual occlusion means that some other reflux pathway is involved.  

Investigations

• Perthes manoeuver: – a tourniquet is placed over the proximal part of

the leg to compress any superficial varicose veins while leaving deep veins unaffected.

– The patient performs toe-stands to activate the calf-muscle pump which normally causes varicose veins to be emptied.

– if obstruction of the deep system exists, then activation of the calf-muscle pump causes a paradoxical congestion of the superficial venous system and engorgement of varicose veins resulting in a positive test. 

Investigations

• Doppler ultrasonography– Useful for both defining the anatomy and

outruling DVT as a cause of the symptoms

Indications for surgery

• Cosmesis• Symptoms-swelling pain cramps• Recurrent superficial thrombophlebitis• Bleeding• Eczema• Ulceration• Contraindications inc,lude previous DVT where there

is loss of patency of the deep system and the patient is relying on superficial system for venous return

Management of Varicose veins

• Conservative– Management with compression

stockings(below or above knee)– Particularly patients unsuitable for theatre

Management of Varicose veins

• Surgical management– Stripping and ligation of varicosities

• SSV/LSV

– Stab phlebectomy– Injection sclerotherapy

Stripping and Ligation

• Incision at Saphenofemoral junction in groin crease 2 cm below inguinal ligament

• Tributaries of long saphenous are ligated and divided

• LSV is divided at the junction• Stripper is introduced into the LSVand fed down

vein to below the knee• LSV is then stripped• Multiple phlebectomies performed.

Endovenous laser therapy

• A laser fiber produces endoluminal heat that destroys the vascular endothelium

• advance a long catheter along the entire length of the truncal varicosity (usually the GSV) to be ablated. A bare laser fiber is passed through the catheter until the end protrudes from the tip of the catheter by approximately 2 cm, and the laser fiber tip is positioned at the SFJ.  

Endovenous laser therapy

• Firm pressure is applied to collapse the vein

• laser is fired generating heat, leading to irreversible endothelial damage and thrombosis. The fiber and catheter are withdrawn approximately 2 mm, and the laser is fired again. This process is repeated along the entire course of the vessel

Lymphatic disorders

• Lymphoedema - excessive accumulation of interstitial fluid as a result of defective lymphatic dainage.

• Primary– Idiopathic– Female predominance– 1/3 patients have a family history

Classification of primary lymphoedema

• Milroy’s disease– Occurs soon after birth

• Lymphoedema praecox– Presents before the age of 35

• Lymphoedema tarda– Presents after the age of 35

Milroy’s disease

Secondary Lymphoedema

• Neoplastic causes– Infiltration of lymph nodes– Pelvic masses

• Surgery eg. during vein harvesting or varicose vein surgery

• Radiotherapy- nodal fibrosis leads to obstruction of the lymphatic vessels esp post excision of sarcoma

Clinical manifestations

• Oedema that resists pitting• Kaposi-Stemmer's sign is

pathognomonic of lymphoedema– the inability to pinch or pick up a fold of skin

at the base of the second toe because of its thickness

• Dilatation of the upper dermal lymphatics and subsequent fibrosis

• Skin creases become pronounced and hyperkeratosis develops

Investigations

• NB- exclude neoplastic causes in the pelvis

• Lymphoscintigraphy – inject a radio-labeled protein exclusively

cleared by lymphatics, into the dermis/subcutis.

– Measurement of uptake and transit through the lymphatics permits analysis of lymph drainage

– can distinguish between different mechanisms of lymphatic failure

Management

• Skin care

• Exercise

• Manual lymphatic drainage

• Multilayer bandaging

• Compression stockings

Management

External Compression enhances the muscle-pump effect.– Multilayer Lymphoedema Bandaging

• system of strong nonelastic bandages providing a rigid casing for the muscles to work against.

• also provide low-grade pressure at rest and so allow refilling of initial lymphatics.

Management

– Compression Garment• suited to motivated patients with good dexterity,

intact skin, minimal pitting edema or limb distortion• Used also in patients post multilayer lymphoedema

bandaging– Manual lymphatic drainage (MLD) massage

• technique designed to relocate lymph fluid from the lymphedematous region to unaffected areas that may drain freely.

• Tissue movement must be gentle if it is to stimulate lymph flow without increasing blood flow

Recurrent cellulitis

Treating lymphoedemais important as itreduces the swellingimproves skin integritythus preventingbacteria enteringthe skin and causing cellulitis