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

1. Venous and lymphatic disorders
of the limb
Niamh Bambury
Surgical Lecturer
21/10/08

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. 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. 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. 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. 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. 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. 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. Examination
• Fever: usually
low grade
• Colour- reddish
purple from
venous engorgement
and obstruction

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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. Post phlebitic syndrome
• characterized by
– chronic pain
– Swelling
– heaviness
– Venous ulcers

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. 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. 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. 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. 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. Anatomy of the venous system
• Superficial Veins
• Perforator Veins
• Deep veins

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

32. Clinical manifestations
• Telangiectasia
Dilated intradermal
venules greater
than 1 mm in diameter

33. Clinical manifestations
• Haemosiderin deposition
brownish darkening
of the skin, resulting
from extravasated blood

34. Clinical
manifestations
• Venous ulcers

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. 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. Investigations
• Doppler ultrasonography
– Useful for both defining the anatomy and
outruling DVT as a cause of the symptoms

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. Management of Varicose veins
• Conservative
– Management with compression
stockings(below or above knee)
– Particularly patients unsuitable for theatre

40. Management of Varicose veins
• Surgical management
– Stripping and ligation of varicosities
• SSV/LSV
– Stab phlebectomy
– Injection sclerotherapy

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. 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. 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. 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. 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. Milroy’s disease

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. 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. 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. Management
• Skin care
• Exercise
• Manual lymphatic drainage
• Multilayer bandaging
• Compression stockings

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. 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. Recurrent cellulitis
Treating lymphoedema
is important as it
reduces the swelling
improves skin integrity
thus preventing
bacteria entering
the skin and causing
cellulitis