Fwd: Bambury lecture on venous and lymphatic disorders of the limb

5,790 views

Published on

---------- Forwarded message ----------
From: Henning L. Stokmo <helangen@gmail.com&gt;
Date: 2009/2/12
Subject: Bambury lecture on venous and lymphatic disorders of the limb
To: ucdgrad09@gmail.com

Published in: Health & Medicine
0 Comments
2 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
5,790
On SlideShare
0
From Embeds
0
Number of Embeds
5
Actions
Shares
0
Downloads
205
Comments
0
Likes
2
Embeds 0
No embeds

No notes for slide

Fwd: Bambury lecture on venous and lymphatic disorders of the limb

  1. 1. Venous and lymphatic disorders of the limb Niamh Bambury Surgical Lecturer 21/10/08
  2. 2. 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.
  3. 3. 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
  4. 4. 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
  5. 5. 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.
  6. 6. 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 +1 Localized tenderness along the distribution of the deep venous system +1 Entire leg swelling +1 Calf swelling >3 cm compared with the asymptomatic leg +1 Pitting edema (greater in the symptomatic leg) +1 Previous DVT documented +1 Collateral superficial veins (nonvaricose) +1 Alternative diagnosis (as likely or greater than that of DVT) +1
  7. 7. Signs and symptoms Edema- principally unilateral, is the most specific symptom Leg pain- pain can occur on dorsiflexion of the foot (Homan’s sign).
  8. 8. 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
  9. 9. Examination • Fever: usually low grade • Colour- reddish purple from venous engorgement and obstruction
  10. 10. 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
  11. 11. 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
  12. 12. 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
  13. 13. 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
  14. 14. 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
  15. 15. 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
  16. 16. 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
  17. 17. 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).
  18. 18. 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.
  19. 19. 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
  20. 20. Sequelae • The original thrombus causes venous valvular incompetence and altered venous return leading to a high incidence of chronic venous insufficiency and postphlebitic syndrome.
  21. 21. Post phlebitic syndrome • characterized by – chronic pain – Swelling – heaviness – Venous ulcers
  22. 22. 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
  23. 23. 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.
  24. 24. 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
  25. 25. 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
  26. 26. 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
  27. 27. Anatomy of the venous system • Superficial Veins • Perforator Veins • Deep veins
  28. 28. 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
  29. 29. 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
  30. 30. 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
  31. 31. Clinical manifestations Lipodermatosclerosis -induration of the dermis and subcutaneous tissue resulting in an inverted champagne bottle appearance
  32. 32. Clinical manifestations • Telangiectasia Dilated intradermal venules greater than 1 mm in diameter
  33. 33. Clinical manifestations • Haemosiderin deposition brownish darkening of the skin, resulting from extravasated blood
  34. 34. Clinical manifestations • Venous ulcers
  35. 35. 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.
  36. 36. 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.
  37. 37. Investigations • Doppler ultrasonography – Useful for both defining the anatomy and outruling DVT as a cause of the symptoms
  38. 38. 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
  39. 39. Management of Varicose veins • Conservative – Management with compression stockings(below or above knee) – Particularly patients unsuitable for theatre
  40. 40. Management of Varicose veins • Surgical management – Stripping and ligation of varicosities • SSV/LSV – Stab phlebectomy – Injection sclerotherapy
  41. 41. 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.
  42. 42. 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.
  43. 43. 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
  44. 44. 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
  45. 45. 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
  46. 46. Milroy’s disease
  47. 47. 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
  48. 48. 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
  49. 49. 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
  50. 50. Management • Skin care • Exercise • Manual lymphatic drainage • Multilayer bandaging • Compression stockings
  51. 51. 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.
  52. 52. 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
  53. 53. Recurrent cellulitis Treating lymphoedema is important as it reduces the swelling improves skin integrity thus preventing bacteria entering the skin and causing cellulitis

×