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Prof. U. Murali.
Venous Ulcer
+
D V T
Learning Objectives
• Outline the etiology & clinical features of Venous ulcer.
• Explain the pathogenesis of venous ulcer.
• Enumerate the complications a well as mention the management aspects of
Venous ulcer.
• Discuss the etiology, clinical features & differential diagnosis of Deep vein
thrombosis.
• Mention the management plan for free and fixed Thrombus lesion.
• Describe the preventives measures in a DVT patient.
• Identify the effects & sequelae of DVT.
Venous Ulcer
Prof. U.Murali.
Venous Ulcer - Introduction
• Venous disease is responsible for
around 85% of all chronic lower
limb ulcers.
• It is a complication of Varicose
veins (or) DVT.
• Furthermore, 15–30% of patients
with ‘venous’ leg ulcers have
concomitant arterial occlusive
disease. This is termed a ‘mixed’
ulcer.
• Mechanism for ulcer formation has
not been fully established.
Venous Ulcer - Etiology
• Ambulatory Venous hypertension
is the prime cause of Venous ulcer
formation.
• Other causes:
– White cell trapping theory
– Fibrin cuff theory
– Abnormal fibroblast activity
– Inhibition of growth factors
• Causes haemosiderin deposition in
the SC plane from lysed RBC’s
↓
• Eczema
↓
• Dermatitis
↓
• Lipodermatosclerosis
↓
• Fibrosis → Anoxia → Ulceration
Valve
incompetence
/ Ch. Venous
hypertension
Defective
micro-
circulation
RBC
diffusion /
lysis
Hemosiderin
deposition
Dermatitis /
capillary
damage
Chronic
Venous
ulceration
Fibrin cuff Theory
Inappropriate
activation
Trapped WBC’s
Proteolytic
enzymes
Cell destruction
& ulceration
White cell trapping Theory
Venous Ulcer – Clinical Features
• Ulcers commonly develops above –
medial malleoli – “Gaiter’s zone”.
• It has a gently sloping edge, and the base
contains granulation tissue with slough
and exudate.
• Ulcers often develop in response to
minor trauma; many patients notice some
itching.
• Mostly they show – Lipodermatosclerosis
- inflammation, thickening, pigmentation, fibrosis
& induration of the calf skin and around ankle.
Venous Ulcer – Complications
• Haemorrhage
• Marjolin’s ulcer (in unstable scar
of long duration)
• Infection
• Talipes equinovarus
• Periostitis is common over the
tibia
• Disability
• Calcification
Venous Ulcer - Investigations
• Blood tests – ESR / CRP / RBC –
Count & Blood sugar.
• Discharge – C / S.
• X-ray of the area to look for
periostitis.
• Biopsy - to rule out Marjolin’s
ulcer.
• Doppler—venous and often
arterial.
• Others – to rule out other causes.
Venous Ulcer – Treatment
• Bisgaard Method:
- Elevation.
- Massage of whole calf.
- Passive & Active exercise.
• Regular cleaning of ulcer.
• Compression Bandage.
• Antibiotics – depending on C/ S.
• Later grafting —SSG.
V U – Treatment – Present concept
• Is to treat the ulcer first by
compression bandage; regular
dressing; skin grafting.
• Once ulcer has healed definitive
procedure for varicose veins is
done - Surgery.
• Studies show that rapidity of
healing of ulcer perse is not
dependent on the surgery for
varicose veins.
Deep Vein Thrombosis
• Venous thrombosis is the formation of a semisolid
coagulum within the venous system and may occur
in the superficial system (superficial vein
thrombosis [SVT] or ‘thrombophlebitis’) or the deep
system (deep vein thrombosis [DVT]) - It is also
called as phlebothrombosis.
• Subsequently, patients are at risk of developing a
post-thrombotic limb and venous ulceration.
• Common site of beginning of thrombus is soleal
veins which later propagate proximally, often
getting detached to cause acute massive pulmonary
embolism.
• H ypercoagulability [abnormal blood]
• S tasis [abnormal flow]
• V ein wall injury [Endothelial damage]
D V T – Causes - THROMBOSIS
• T rauma
• H ormones – OCP’s
• R oad traffic accidents
• O perations – Post –op – 30%
• M alignancy – Spontaneous thrombosis
• B lood Disorders – PV/ Thrombocytosis
• O besity / Old age
• S erious illness – MI / CCF / NS
• I mobilization - (Traveller's thrombosis).
• S ome deficiencies – Protein C / S /
antithrombin III
• Pelvic veins – Int. iliac veins
• Leg veins – Soleus / Femoral / I FV
• Upper limb – Axillary vein
Sites
D V T – Clinical Features
• Mostly asymptomatic – 60%
• Fever – common & earliest symptom
• Pain & swelling – calf & thigh /
Bilateral – 30%
• Leg – tender, warm, pale or bluish
with stretched & shiny skin
• Signs related to D V T –
Homan’s / Mose’s / Nehof’s sign
• Inverted champagne bottle sign
• F O – Pulmonary embolism
D V T – Differential Diagnosis
• Ruptured Baker’s cyst
• Ruptured plantaris tendon
• Calf muscle haematoma
• Cellulitis leg
• Superficial thrombophlebitis
• Thrombosed popliteal
aneurysm
D V T – Investigations
• Venous doppler with Duplex scan – It
shows non-compressible vein / S & S.
• Ascending Venogram, Impedence
plethysmography & Radioactive
• D-Dimer test – For FDP.
• CBP + Platelet count.
• CT – scan – pulm. artery
• Ventilation Perfusion scan }
• C T P Angiogram }
D V T – Treatment
General
•Rest
•Elevation of limb
•Crepe Bandaging
Fixed Thrombus
•LMWH x 7 days
•Warfarin x 3-6mths
[INR – 2 – 3]
Free Thrombus
•Fibrinolysins
- Streptokinase
- Urokinase
• Venous Thrombectomy –
(Using Fogarty catheter)
•Intra-caval filters
•Open thrombectomy
D V T – Prevention
Categorize - Patient
• Low risk – Young
patients - Minor surgery
< 30 minutes
• Moderate risk – > 40
years - Major surgery
• High risk – Major abd,
pelvic, ortho surgery / pts
with existing cardiac dis.,
pre. h/o DVT, PE
Mechanical
•Elevation &
Ambulation
•Elastic compression
•External pneumatic
compression
Pharmacological
• Earlier - Un-fractioned
heparin – IV / SC
•LMWH – SC – O/D
D V T – Effects & Sequalae
• Pulmonary embolism—15%
• Infection; venous gangrene
• Partial re-canalisation, chronic
venous hypertension around the
ankle region causing venous
ulcers— chronic venous insufficiency-CVI
• Recurrent DVT—30%
• Propagation of thrombus
proximally—20-30%
D V T - TYPES
• DVT – Femoral vein –
“White Leg”
• DVT – Iliac & pelvic
veins – “Blue Leg”
Phlegmasia Alba Dolens Phlegmasia Caerulea Dolens • White Leg - It is DVT of femoral
vein (deep femoral vein
commonly) causing painful
congestion and oedema of leg,
with lymphangitis, which
further increases the oedema
and worsens the situation….
• Blue Leg - It is extensive
DVT of iliac and pelvic
veins causing blue leg with
either venous gangrene (or)
areas of infarction.
SCORES - D V T / PE
References
To Summarize
• Etiopathogenesis & Clinical features of venous ulcer.
• Complications & Investigations of venous ulcer.
• Various treatment options for venous ulcer.
• Causes, Pathogenesis & Clinical features of DVT.
• D/D & Sequalae of DVT.
• Investigative methods & the various treatment options of
DVT.
• Prophylactic methods against DVT.
Question Time
• Enumerate 5 complications of venous ulcer.
• Explain the pathogenesis of venous ulcer.
• Mention the treatment options for venous ulcer.
• List 5 causes of DVT.
• Write 5 D/D for DVT.
• Outline the various treatment options of DVT.
• Enlist 4 sequalae of deep vein thrombosis.
• Write the prophylactic measures against DVT.
Treatment of choice for a patient presenting with
venous ulcer and incompetent perforators is –
• A) Stripping of varicose vein.
• B) Subfascial ligation of perforators.
• C) Saphenofemoral ligation.
• D) Conservative treatment.
Virchow’s triad consists of all the
following, EXCEPT –
• A) Hypercoagulability.
• B) Endothelial injury.
• C) Increased turbulence of blood flow.
• D) Increased platelet count.
The most important component in the conservative
management of venous ulcers of the leg is –
• A) Topical antibiotics.
• B) Regular debridement.
• C) Compression dressings.
• D) Topical steroids.
A patient had retrograde pelvic thrombophlebitis
and it progressed to bilateral iliofemoral occlusion
and now the presentation is –
• A) Red leg.
• B) White leg.
• C) Purple leg.
• D) Blue leg.
The main cause of venous ulcerations is –
• A) Superficial thrombophlebitis.
• B) White cell trapping theory.
• C) Ambulatory venous hypertension.
• D) Fibrin cuff theory.
The duration of heparin therapy in deep vein
thrombosis is –
• A) 1 week.
• B) 7 – 10 days.
• C) 15 – 20 days.
• D) 1 month.
The patient falls in high-risk group for DVT and
pulmonary embolism after –
• A) Major burns.
• B) Major surgery < 40 years.
• C) Major medical illness / cancer.
• D) Major orthopedic surgery / fracture pelvis.
Thank you
Venous Ulcer and Deep Vein Thrombosis - Causes & Management
Venous Ulcer and Deep Vein Thrombosis - Causes & Management
Venous Ulcer and Deep Vein Thrombosis - Causes & Management
Venous Ulcer and Deep Vein Thrombosis - Causes & Management
Venous Ulcer and Deep Vein Thrombosis - Causes & Management

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Venous Ulcer and Deep Vein Thrombosis - Causes & Management

  • 1. Prof. U. Murali. Venous Ulcer + D V T
  • 2. Learning Objectives • Outline the etiology & clinical features of Venous ulcer. • Explain the pathogenesis of venous ulcer. • Enumerate the complications a well as mention the management aspects of Venous ulcer. • Discuss the etiology, clinical features & differential diagnosis of Deep vein thrombosis. • Mention the management plan for free and fixed Thrombus lesion. • Describe the preventives measures in a DVT patient. • Identify the effects & sequelae of DVT.
  • 4. Venous Ulcer - Introduction • Venous disease is responsible for around 85% of all chronic lower limb ulcers. • It is a complication of Varicose veins (or) DVT. • Furthermore, 15–30% of patients with ‘venous’ leg ulcers have concomitant arterial occlusive disease. This is termed a ‘mixed’ ulcer. • Mechanism for ulcer formation has not been fully established.
  • 5. Venous Ulcer - Etiology • Ambulatory Venous hypertension is the prime cause of Venous ulcer formation. • Other causes: – White cell trapping theory – Fibrin cuff theory – Abnormal fibroblast activity – Inhibition of growth factors • Causes haemosiderin deposition in the SC plane from lysed RBC’s ↓ • Eczema ↓ • Dermatitis ↓ • Lipodermatosclerosis ↓ • Fibrosis → Anoxia → Ulceration
  • 6. Valve incompetence / Ch. Venous hypertension Defective micro- circulation RBC diffusion / lysis Hemosiderin deposition Dermatitis / capillary damage Chronic Venous ulceration Fibrin cuff Theory Inappropriate activation Trapped WBC’s Proteolytic enzymes Cell destruction & ulceration White cell trapping Theory
  • 7.
  • 8.
  • 9. Venous Ulcer – Clinical Features • Ulcers commonly develops above – medial malleoli – “Gaiter’s zone”. • It has a gently sloping edge, and the base contains granulation tissue with slough and exudate. • Ulcers often develop in response to minor trauma; many patients notice some itching. • Mostly they show – Lipodermatosclerosis - inflammation, thickening, pigmentation, fibrosis & induration of the calf skin and around ankle.
  • 10. Venous Ulcer – Complications • Haemorrhage • Marjolin’s ulcer (in unstable scar of long duration) • Infection • Talipes equinovarus • Periostitis is common over the tibia • Disability • Calcification
  • 11. Venous Ulcer - Investigations • Blood tests – ESR / CRP / RBC – Count & Blood sugar. • Discharge – C / S. • X-ray of the area to look for periostitis. • Biopsy - to rule out Marjolin’s ulcer. • Doppler—venous and often arterial. • Others – to rule out other causes.
  • 12. Venous Ulcer – Treatment • Bisgaard Method: - Elevation. - Massage of whole calf. - Passive & Active exercise. • Regular cleaning of ulcer. • Compression Bandage. • Antibiotics – depending on C/ S. • Later grafting —SSG.
  • 13.
  • 14. V U – Treatment – Present concept • Is to treat the ulcer first by compression bandage; regular dressing; skin grafting. • Once ulcer has healed definitive procedure for varicose veins is done - Surgery. • Studies show that rapidity of healing of ulcer perse is not dependent on the surgery for varicose veins.
  • 15.
  • 16. Deep Vein Thrombosis • Venous thrombosis is the formation of a semisolid coagulum within the venous system and may occur in the superficial system (superficial vein thrombosis [SVT] or ‘thrombophlebitis’) or the deep system (deep vein thrombosis [DVT]) - It is also called as phlebothrombosis. • Subsequently, patients are at risk of developing a post-thrombotic limb and venous ulceration. • Common site of beginning of thrombus is soleal veins which later propagate proximally, often getting detached to cause acute massive pulmonary embolism.
  • 17.
  • 18. • H ypercoagulability [abnormal blood] • S tasis [abnormal flow] • V ein wall injury [Endothelial damage]
  • 19. D V T – Causes - THROMBOSIS • T rauma • H ormones – OCP’s • R oad traffic accidents • O perations – Post –op – 30% • M alignancy – Spontaneous thrombosis • B lood Disorders – PV/ Thrombocytosis • O besity / Old age • S erious illness – MI / CCF / NS • I mobilization - (Traveller's thrombosis). • S ome deficiencies – Protein C / S / antithrombin III • Pelvic veins – Int. iliac veins • Leg veins – Soleus / Femoral / I FV • Upper limb – Axillary vein Sites
  • 20. D V T – Clinical Features • Mostly asymptomatic – 60% • Fever – common & earliest symptom • Pain & swelling – calf & thigh / Bilateral – 30% • Leg – tender, warm, pale or bluish with stretched & shiny skin • Signs related to D V T – Homan’s / Mose’s / Nehof’s sign • Inverted champagne bottle sign • F O – Pulmonary embolism
  • 21. D V T – Differential Diagnosis • Ruptured Baker’s cyst • Ruptured plantaris tendon • Calf muscle haematoma • Cellulitis leg • Superficial thrombophlebitis • Thrombosed popliteal aneurysm
  • 22. D V T – Investigations • Venous doppler with Duplex scan – It shows non-compressible vein / S & S. • Ascending Venogram, Impedence plethysmography & Radioactive • D-Dimer test – For FDP. • CBP + Platelet count. • CT – scan – pulm. artery • Ventilation Perfusion scan } • C T P Angiogram }
  • 23. D V T – Treatment General •Rest •Elevation of limb •Crepe Bandaging Fixed Thrombus •LMWH x 7 days •Warfarin x 3-6mths [INR – 2 – 3] Free Thrombus •Fibrinolysins - Streptokinase - Urokinase • Venous Thrombectomy – (Using Fogarty catheter) •Intra-caval filters •Open thrombectomy
  • 24. D V T – Prevention Categorize - Patient • Low risk – Young patients - Minor surgery < 30 minutes • Moderate risk – > 40 years - Major surgery • High risk – Major abd, pelvic, ortho surgery / pts with existing cardiac dis., pre. h/o DVT, PE Mechanical •Elevation & Ambulation •Elastic compression •External pneumatic compression Pharmacological • Earlier - Un-fractioned heparin – IV / SC •LMWH – SC – O/D
  • 25.
  • 26.
  • 27. D V T – Effects & Sequalae • Pulmonary embolism—15% • Infection; venous gangrene • Partial re-canalisation, chronic venous hypertension around the ankle region causing venous ulcers— chronic venous insufficiency-CVI • Recurrent DVT—30% • Propagation of thrombus proximally—20-30%
  • 28. D V T - TYPES • DVT – Femoral vein – “White Leg” • DVT – Iliac & pelvic veins – “Blue Leg” Phlegmasia Alba Dolens Phlegmasia Caerulea Dolens • White Leg - It is DVT of femoral vein (deep femoral vein commonly) causing painful congestion and oedema of leg, with lymphangitis, which further increases the oedema and worsens the situation…. • Blue Leg - It is extensive DVT of iliac and pelvic veins causing blue leg with either venous gangrene (or) areas of infarction.
  • 29. SCORES - D V T / PE
  • 31. To Summarize • Etiopathogenesis & Clinical features of venous ulcer. • Complications & Investigations of venous ulcer. • Various treatment options for venous ulcer. • Causes, Pathogenesis & Clinical features of DVT. • D/D & Sequalae of DVT. • Investigative methods & the various treatment options of DVT. • Prophylactic methods against DVT.
  • 32. Question Time • Enumerate 5 complications of venous ulcer. • Explain the pathogenesis of venous ulcer. • Mention the treatment options for venous ulcer. • List 5 causes of DVT. • Write 5 D/D for DVT. • Outline the various treatment options of DVT. • Enlist 4 sequalae of deep vein thrombosis. • Write the prophylactic measures against DVT.
  • 33. Treatment of choice for a patient presenting with venous ulcer and incompetent perforators is – • A) Stripping of varicose vein. • B) Subfascial ligation of perforators. • C) Saphenofemoral ligation. • D) Conservative treatment.
  • 34. Virchow’s triad consists of all the following, EXCEPT – • A) Hypercoagulability. • B) Endothelial injury. • C) Increased turbulence of blood flow. • D) Increased platelet count.
  • 35. The most important component in the conservative management of venous ulcers of the leg is – • A) Topical antibiotics. • B) Regular debridement. • C) Compression dressings. • D) Topical steroids.
  • 36. A patient had retrograde pelvic thrombophlebitis and it progressed to bilateral iliofemoral occlusion and now the presentation is – • A) Red leg. • B) White leg. • C) Purple leg. • D) Blue leg.
  • 37. The main cause of venous ulcerations is – • A) Superficial thrombophlebitis. • B) White cell trapping theory. • C) Ambulatory venous hypertension. • D) Fibrin cuff theory.
  • 38. The duration of heparin therapy in deep vein thrombosis is – • A) 1 week. • B) 7 – 10 days. • C) 15 – 20 days. • D) 1 month.
  • 39. The patient falls in high-risk group for DVT and pulmonary embolism after – • A) Major burns. • B) Major surgery < 40 years. • C) Major medical illness / cancer. • D) Major orthopedic surgery / fracture pelvis.