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Leg edema and its’ grave consequences

Leg edema and its’ grave consequences

Alain Brassard MD FRCPC

D l i

Alain Brassard MD FRCPC

D l iDermatologist

Professor of Medicine and Dermatology

University of Alberta

Dermatologist

Professor of Medicine and Dermatology

University of Alberta

ObjectivesObjectives

The attendee will be familiarized: with the physiology of oedema

The attendee will be familiarized: with the physiology of oedemap y gy by the fact, when oedema, finding its aetiology and corrective

measures must be prompt on how to recognize soft tissue infections with their

consequences with the insidious, mostly irreversible changes of lymphoedema

p y gy by the fact, when oedema, finding its aetiology and corrective

measures must be prompt on how to recognize soft tissue infections with their

consequences with the insidious, mostly irreversible changes of lymphoedema

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Leg Ulcer EtiologiesLeg Ulcer Etiologies Vascular

Venous

Arterial

Vascular Venous

Arterial

Neuropathic Diabetes

Syringomyelia

Tabes dorsalis

Neuropathic Diabetes

Syringomyelia

Tabes dorsalis

Atherosclerosis

Arteriovenous malformation

Cholesterol embolism

Thromboangiitis obliterans

Vasculitic Small vessel

Atrophie blanche

Behcet ’s syndrome

Hypersensivity vasculitis

Lupus erythematosus

Rheumatoid vasculitis

Scleroderma

Sjogren ’s syndrome

Atherosclerosis

Arteriovenous malformation

Cholesterol embolism

Thromboangiitis obliterans

Vasculitic Small vessel

Atrophie blanche

Behcet ’s syndrome

Hypersensivity vasculitis

Lupus erythematosus

Rheumatoid vasculitis

Scleroderma

Sjogren ’s syndrome

Hematologic Dysproteinemia

Cold agglutinin syndrome

Cryoglobulinemia

Macroglobulinemia

Red blood cell disorders

Hereditary spherocytosis

Polycythemia vera

Sickle cell anemia

Thalassemia

White blood cell disorders (leukemia)

Traumatic

Hematologic Dysproteinemia

Cold agglutinin syndrome

Cryoglobulinemia

Macroglobulinemia

Red blood cell disorders

Hereditary spherocytosis

Polycythemia vera

Sickle cell anemia

Thalassemia

White blood cell disorders (leukemia)

Traumatic Medium and large vessel

Nodular vasculitis

Polyarteritis nodosa

Wegener ’s granulomatosis

Lymphatic (lymphedema)

Medium and large vessel Nodular vasculitis

Polyarteritis nodosa

Wegener ’s granulomatosis

Lymphatic (lymphedema)

Burns

Cold

Facticial

Pressure

Radiation

Burns

Cold

Facticial

Pressure

Radiation

Leg Ulcer EtiologiesLeg Ulcer Etiologies Neoplasic

Epithelioma

Basal cell carcinoma

Neoplasic Epithelioma

Basal cell carcinoma

Infective and infestive Bacterial

Ecthyma, ecthyma gangrenosum Furoncle

Infective and infestive Bacterial

Ecthyma, ecthyma gangrenosum Furoncle

Squamous cell carcinoma

Lymphoma

Cutaneous T cell

Lymphoproliferative

Metastatic tumors

Sarcoma (eg, Kaposi ’s)

Metabolic Diabetic

Gaucher ’s disease

Squamous cell carcinoma

Lymphoma

Cutaneous T cell

Lymphoproliferative

Metastatic tumors

Sarcoma (eg, Kaposi ’s)

Metabolic Diabetic

Gaucher ’s disease

Gram-negative, mycobacterial, spirochetal Septic emboli

Fungal Deep fungal Trichophytic granuloma

Insect bites Protozoal (leishmania)

Miscellaneous Panniculitis

Pancreatic fat necrosis Weber-Christian disease

N bi i li idi di b i

Gram-negative, mycobacterial, spirochetal Septic emboli

Fungal Deep fungal Trichophytic granuloma

Insect bites Protozoal (leishmania)

Miscellaneous Panniculitis

Pancreatic fat necrosis Weber-Christian disease

N bi i li idi di b iGaucher s disease

Gout

Prolidase deficiency

Gaucher s disease

Gout

Prolidase deficiency

Necrobiosis lipoidica diabeticorum Pyoderma gangrenosum Sarcoidosis

Necrobiosis lipoidica diabeticorum Pyoderma gangrenosum Sarcoidosis

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History in leg ulcer patientsHistory in leg ulcer patients

Previous history Deep vein thrombosis

Surgery

Previous history Deep vein thrombosis

SurgerySurgery

Trauma

Personal and family history Diabetes

Obesity

Varicose veins and ulcers

Medications

P l h bi

Surgery

Trauma

Personal and family history Diabetes

Obesity

Varicose veins and ulcers

Medications

P l h bi Personal habits Smoking

Drinking

Personal habits Smoking

Drinking

History in leg ulcer patientsHistory in leg ulcer patients Ulcer

Onset

Localization

D ti

Ulcer Onset

Localization

D ti Duration

Course,previous work-up and treatment,

Recurrence

Associated symptoms Pain

Edema

Anesthesia

Duration

Course,previous work-up and treatment,

Recurrence

Associated symptoms Pain

Edema

Anesthesia

Paresthesia

Intermittent claudication

Exacerbating or relieving factors

Paresthesia

Intermittent claudication

Exacerbating or relieving factors

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Physical examinationPhysical examination

General with emphasis on the following: General with emphasis on the following:Ge e a w t e p as s o t e o ow g: Deep tendon reflex Evidence of peripheral neuropathy Peripheral pulses Joint mobility and difformity

Ulcer characteristics Location

M h l

Ge e a w t e p as s o t e o ow g: Deep tendon reflex Evidence of peripheral neuropathy Peripheral pulses Joint mobility and difformity

Ulcer characteristics Location

M h l Morphology Surrounding skin

Wound assssment Photography Planimetry (Visitrak?)

Morphology Surrounding skin

Wound assssment Photography Planimetry (Visitrak?)

Compression effectsCompression effects

Allows superficial veins to Allows superficial veins to pdrain in the deep system where the calf muscle pump will be more efficient. (improves valvular function)

Increases blood flow in the right direction

Reduces edema

pdrain in the deep system where the calf muscle pump will be more efficient. (improves valvular function)

Increases blood flow in the right direction

Reduces edema

The ideal compression is 30-40mm Hg at the ankle if ABI>0.8.

The ideal compression is 30-40mm Hg at the ankle if ABI>0.8.

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Lymphatic drainageLymphatic drainage

Lymphatic drainageLymphatic drainage

Respond to increased Respond to increasedRespond to increased tissue fluid content by widening their lumina, mediated by the action of anchoring filaments that connect the lymphatic endothelial cells with the

Respond to increased tissue fluid content by widening their lumina, mediated by the action of anchoring filaments that connect the lymphatic endothelial cells with the surrounding interstitium(even up to 2+ mmHg)

Higher pressure lymphedema

surrounding interstitium(even up to 2+ mmHg)

Higher pressure lymphedema

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Lymphatic drainageLymphatic drainage

Return proteins, lipids, and Return proteins, lipids, and p , p ,water from the interstitium to the intravascular space

40-50% of serum proteins are transported by this route each day.

High hydrostatic pressures in arterial capillaries force

p , p ,water from the interstitium to the intravascular space

40-50% of serum proteins are transported by this route each day.

High hydrostatic pressures in arterial capillaries force pproteinaceous fluid into the interstitium, resulting in increased interstitial oncotic pressure that draws in additional water.

pproteinaceous fluid into the interstitium, resulting in increased interstitial oncotic pressure that draws in additional water.

Lymphatic drainageLymphatic drainage

Interstitial fluid normally Interstitial fluid normally ycontributes to the nourishment of tissues.

About 90% of the fluid returns to the circulation via entry into venous capillaries.

The remaining 10% is composed of high-molecular-

ycontributes to the nourishment of tissues.

About 90% of the fluid returns to the circulation via entry into venous capillaries.

The remaining 10% is composed of high-molecular-p gweight proteins and their oncotically associated water, which are too large to readily pass through venous capillary walls.

p gweight proteins and their oncotically associated water, which are too large to readily pass through venous capillary walls.

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Lymphatic drainageLymphatic drainage

This leads to flow into the lymphatic capillaries, where pressures are typically subatmospheric and can accommodate the large size of the proteins and their accompanying water.

This leads to flow into the lymphatic capillaries, where pressures are typically subatmospheric and can accommodate the large size of the proteins and their accompanying water.

The proteins then travel as lymph through numerous filtering lymph nodes on their way to join the venous circulation.

The proteins then travel as lymph through numerous filtering lymph nodes on their way to join the venous circulation.

Lymphatic drainageLymphatic drainage

The proteins then travel as The proteins then travel as plymph through numerous filtering lymph nodes on their way to join the venous circulation.

Lymphatic drainage has an essential immunological role.

plymph through numerous filtering lymph nodes on their way to join the venous circulation.

Lymphatic drainage has an essential immunological role.

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Major causes of lymphedemaMajor causes of lymphedema

Pathogenesis could be attributed to Pathogenesis could be attributed togdamage to the lymphatic system by bacterial infections and by venous congestion.

Today we would describe this as a failing lymphatic system due to gross overload.

Also, it is secondary to a lymphatic system that is anatomically either

gdamage to the lymphatic system by bacterial infections and by venous congestion.

Today we would describe this as a failing lymphatic system due to gross overload.

Also, it is secondary to a lymphatic system that is anatomically either y yincompletely formed or disrupted by cancer and its surgical treatment.

Other etiologies includeradiotherapy, filariasis, and paralytic pathology

y yincompletely formed or disrupted by cancer and its surgical treatment.

Other etiologies includeradiotherapy, filariasis, and paralytic pathology

Venous hypertension, major cause of lymphedema

Venous hypertension, major cause of lymphedema

Veins return blood and reabsorb Veins return blood and reabsorb water and low molecular weight substances

If lymphatic are overwhelmed with proteins (increase osmolality), inflammation occur

The increase in the extravascular protein stimulates

water and low molecular weight substances

If lymphatic are overwhelmed with proteins (increase osmolality), inflammation occur

The increase in the extravascular protein stimulates pproliferation of fibroblasts, organization of the fluid, and the development of a nonpittingswelling of the affected extremity

pproliferation of fibroblasts, organization of the fluid, and the development of a nonpittingswelling of the affected extremity

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Infection, the other major cause of lymphedema

Infection, the other major cause of lymphedema

Study of 209 cases of cellulitis: Study of 209 cases of cellulitis: recurrences observed in 17% of pts

Early episodes of cellulitis cause lymphatic inflammation; repeated infection can lead to lymphedema Leg elevation is paramount in

tx of cellulitis Prophylaxis: frequently recurrent

cellulitis in patients with predisposing factors that cannot be

recurrences observed in 17% of pts Early episodes of cellulitis cause

lymphatic inflammation; repeated infection can lead to lymphedema Leg elevation is paramount in

tx of cellulitis Prophylaxis: frequently recurrent

cellulitis in patients with predisposing factors that cannot bepredisposing factors that cannot be alleviated

It is recommended after one episode to wear support stockings especially if Erysipela

Baddour, L.M. Cellulitis and Erysipelas. UpToDate (Nov. 3, 2008).

predisposing factors that cannot be alleviated

It is recommended after one episode to wear support stockings especially if Erysipela

Baddour, L.M. Cellulitis and Erysipelas. UpToDate (Nov. 3, 2008).

Erysipelas: DiagnosisErysipelas: Diagnosis

Bonnetblanc, J.M., Bedane, C. Erysipelas: Bonnetblanc, J.M., Bedane, C. Erysipelas: Baddour, L.M. Cellulitis and Erysipelas. Baddour, L.M. Cellulitis and Erysipelas. Recognition and Management. Am J Clin Dermatol (2003), 4(3): 157-163.Recognition and Management. Am J Clin Dermatol (2003), 4(3): 157-163.

UpToDate (Nov. 3, 2008).UpToDate (Nov. 3, 2008).

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Venous Stasis & Stasis Dermatitis

Venous Stasis & Stasis Dermatitis

Alguire, P.C., Mathes, B.M. Diagnosis of Alguire, P.C., Mathes, B.M. Diagnosis of chronic venous insufficiency. UpToDate(April 15, 2009): 13 pages.

Prominently dilated and tortuous varicose veins associated with moderate hyperpigmentation

chronic venous insufficiency. UpToDate(April 15, 2009): 13 pages.

Prominently dilated and tortuous varicose veins associated with moderate hyperpigmentation

Venous Stasis & Stasis Dermatitis

Venous Stasis & Stasis Dermatitis

Alguire, P.C., Mathes, B.M. Epidemiology and clinical manifestations of chronic venous disease. Alguire, P.C., Mathes, B.M. Epidemiology and clinical manifestations of chronic venous disease. UpToDate (May 22, 2009): 48 pages.UpToDate (May 22, 2009): 48 pages.

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Compare…Compare…

Erysipelas Erysipelas Venous Stasis & Stasis Venous Stasis & StasisErysipelasErysipelas Venous Stasis & Stasis DermatitisVenous Stasis & Stasis Dermatitis

Venous Eczema vs. CellulitisVenous Eczema vs. Cellulitis

Eczema: Crusting or Eczema: Crusting or Cellulitis: skin is smooth Cellulitis: skin is smoothEczema: Crusting or scaling

Small blisters (vesicles) are common in eczema; break down → serous fluid released, dries to form crusts which

Eczema: Crusting or scaling

Small blisters (vesicles) are common in eczema; break down → serous fluid released, dries to form crusts which

Cellulitis: skin is smooth and shiny

Blister formation is uncommon in cellulitis if blisters do develop they

are large and herald the onset of skin necrosis

Cellulitis: skin is smooth and shiny

Blister formation is uncommon in cellulitis if blisters do develop they

are large and herald the onset of skin necrosisform crusts which

coalesceform crusts which coalesce

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Clinical signs of chronic oedemaClinical signs of chronic oedema

Venous Eczema vs. CellulitisVenous Eczema vs. Cellulitis

Eczema: No fever Eczema: No fever Cellulitis: Fever possible Cellulitis: Fever possible

Itching

History of varicose veins or DVT

On exam: erythematous, inflamed skin, nontender, +vesicles, +crusting

Lesions on other parts of the

Itching

History of varicose veins or DVT

On exam: erythematous, inflamed skin, nontender, +vesicles, +crusting

Lesions on other parts of the

Pain to area History possibly of trauma On exam: erythematous,

inflamed skin, tender, few large bullae, no crusting

No lesions elsewhere (unilateral)

Pain to area History possibly of trauma On exam: erythematous,

inflamed skin, tender, few large bullae, no crusting

No lesions elsewhere (unilateral)

Lesions on other parts of the body, particularly other leg (bilateral)

Lesions on other parts of the body, particularly other leg (bilateral)

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Venous EczemaVenous Eczema

Nazarko, L. Diagnosis and Treatment of Venous Eczema. British Journal of Community Nursing Nazarko, L. Diagnosis and Treatment of Venous Eczema. British Journal of Community Nursing(2008), 14(5): 188-194.(2008), 14(5): 188-194.

Clinical signs of chronic oedemaClinical signs of chronic oedema

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LymphoedemaLymphoedema

Elephantiasis Elephantiasis The overlying skin becomes thi k d d di l th

The overlying skin becomes thi k d d di l th

pverrucosa nostra

pverrucosa nostra

thickened and displays the typical peau d'orange (orange skin) appearance of congested dermal lymphatics.

thickened and displays the typical peau d'orange (orange skin) appearance of congested dermal lymphatics.

LymphoedemaLymphoedema

Elephantiasis Elephantiasis C d i h i di id l i hC d i h i di id l i h

pverrucosa nostra

pverrucosa nostra

Compared with individuals with upper extremity lymphedema, individuals with lower extremity lymphedema experienced more frequent and more severe symptoms (p<.001), infection episodes (p<.001), and infection-related hospitalizations (p<.001)

Compared with individuals with upper extremity lymphedema, individuals with lower extremity lymphedema experienced more frequent and more severe symptoms (p<.001), infection episodes (p<.001), and infection-related hospitalizations (p<.001)

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Lymphoedema-ElephantiasisLymphoedema-Elephantiasis

Clinical Factors with influence on healing a VLU

Clinical Factors with influence on healing a VLU

1. Factors with no influence on ulcer healing (sex, age, previous operations, 1. Factors with no influence on ulcer healing (sex, age, previous operations, g ( g p pulcer recurrence).

2. Favorable prognostic factors for ulcer healing (ulceration surface <20 cm2, time since ulcer onset <12 months, reduction in calf circumference 3 cm during the first 50 days of treatment, and emergence of new skin islets on more than 10% of ulcer surface).

3. Indicators of slow healing (ulceration surface >20 cm2, time since ulcer onset >12 months, BMI 33kg/m2, walking distance shorter than 200 meters during the day, history of surgical wound debridement, 50% of wound covered

g ( g p pulcer recurrence).

2. Favorable prognostic factors for ulcer healing (ulceration surface <20 cm2, time since ulcer onset <12 months, reduction in calf circumference 3 cm during the first 50 days of treatment, and emergence of new skin islets on more than 10% of ulcer surface).

3. Indicators of slow healing (ulceration surface >20 cm2, time since ulcer onset >12 months, BMI 33kg/m2, walking distance shorter than 200 meters during the day, history of surgical wound debridement, 50% of wound covered g y, y g ,with fibrin, depth of the wound >2 cm).

4. Risk factors associated with non-healing (Calf-Ankle Circumference ratio (CAC) ratio <1.3, fixed ankle joint, and reduced ROM)

J Vasc Surg 2009;49:1242-7

g y, y g ,with fibrin, depth of the wound >2 cm).

4. Risk factors associated with non-healing (Calf-Ankle Circumference ratio (CAC) ratio <1.3, fixed ankle joint, and reduced ROM)

J Vasc Surg 2009;49:1242-7

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Surprises on varicose veinsSurprises on varicose veins

40% of VLU due to superficial 40% of VLU due to superficial40% of VLU due to superficial reflux do not have visible varicose veins

25% of patients with telangiectasias have underlying long or short saphenous incompetence

25% of patients with superficial thrombophlebitis have a DVT

40% of VLU due to superficial reflux do not have visible varicose veins

25% of patients with telangiectasias have underlying long or short saphenous incompetence

25% of patients with superficial thrombophlebitis have a DVT

Surprises with the arterial examSurprises with the arterial exam

37% i h d l bl37% i h d l bl 37% with good palpable pulses have abnormal ABPI

25% with no palpable pulses have normal ABPI

37% with good palpable pulses have abnormal ABPI

25% with no palpable pulses have normal ABPI

Pedal pulses only indicate a BP >80mmHg

Pedal pulses only indicate a BP >80mmHg

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BasicsBasics

A= Arterial supply A= Arterial supply A= Arterial supply

B= Bacterial Burden

C= Compression

D= Debridment

E Ed t l E l t di i

A= Arterial supply

B= Bacterial Burden

C= Compression

D= Debridment

E Ed t l E l t di i E= Edema control, Evaluate diagnosis E= Edema control, Evaluate diagnosis

Question 2Question 2

Gait changes does not influence the calf Gait changes does not influence the calf Gait changes does not influence the calf pump function? True

False

Gait changes does not influence the calf pump function? True

False

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True: Gait changes and painTrue: Gait changes and pain

Can occur in up to 72% of VLU patients Can occur in up to 72% of VLU patients Can occur in up to 72% of VLU patients

Can induce avoidance of contracting the calf muscle in fear of pain

Can lead to calf muscle atrophy

Exercise should be as important as

Can occur in up to 72% of VLU patients

Can induce avoidance of contracting the calf muscle in fear of pain

Can lead to calf muscle atrophy

Exercise should be as important as Exercise should be as important as compression in the management of VLU Exercise should be as important as

compression in the management of VLU

CompressionCompression

Laplace’s law compression

P = TN(constant)CL

P = pression under the bandage

T = tension within the bandage

N = number of layer

C = circumference of thelimb

L = bandage’s with

dégressive

L = bandage s with

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Pascal’s LawPascal’s Law

Current breakthrough research has demonstrated Current breakthrough research has demonstrated Current breakthrough research has demonstrated that Pascal’s Law provides a better understanding of the effects of compression.

Pascal’s Law states that when pressure is applied on a fluid (a muscle or muscle group) in a closed container (fascia and compression bandage), the

Current breakthrough research has demonstrated that Pascal’s Law provides a better understanding of the effects of compression.

Pascal’s Law states that when pressure is applied on a fluid (a muscle or muscle group) in a closed container (fascia and compression bandage), thecontainer (fascia and compression bandage), the pressure is transmitted equally and undiminished in all directions throughout the fluid.

container (fascia and compression bandage), the pressure is transmitted equally and undiminished in all directions throughout the fluid.

Int Angiol 2010;29;431-5

Compression mechanismCompression mechanism

Passive Compression Passive Compression Active Compression Active Compression Passive Compression (support)

Passive Compression (support)

Active Compression (elastic)

Active Compression (elastic)

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Pressure-variation according to compression type

Pressure-variation according to compression type

Effect of Higher stiffness compression

Effect of Higher stiffness compression

Int Angiol 2010;29;431-5

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Ideal Compression?Ideal Compression?

Can vary according to height weight and Can vary according to height weight and Can vary according to height, weight and venous insufficiency severity

An external compression of 35-40mm Hg is necessary to prevent capillary leakage in venous hypertension

Can vary according to height, weight and venous insufficiency severity

An external compression of 35-40mm Hg is necessary to prevent capillary leakage in venous hypertension

Blair, S.D. & Al B.M.J. 297: 1159-1161, 1988. Blair, S.D. & Al B.M.J. 297: 1159-1161, 1988.

Poor patient compliance and sub-optimal compression technique are very likely the principal causes for

Poor patient compliance and sub-optimal compression technique are very likely the principal causes fortechnique are very likely the principal causes for

therapeutic failure in chronic venous disease.

Erickson CA & Al J Vasc Surg 1995;22:629-636.

technique are very likely the principal causes for therapeutic failure in chronic venous disease.

Erickson CA & Al J Vasc Surg 1995;22:629-636.

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Compression and arterial diseaseCompression and arterial disease

Edema impedes the oxygenization of the Edema impedes the oxygenization of the Edema impedes the oxygenization of the skin.

In arterial occlusive disease, a reduction of swelling by a careful intermittent compression regime may improve the

Edema impedes the oxygenization of the skin.

In arterial occlusive disease, a reduction of swelling by a careful intermittent compression regime may improve the condition.condition.

Elastic stockingsElastic stockings

Elastic stockings Pressure (mmHg) Indicationsg ( g)

Class 1 20-30 Simple varicoseMild edemaTiredness

Class 2 30-40 Moderate edemaSevere varicoseModerate venoushypertension

Class 3 40-50 Lymphoedema

Class 4 50-60 Severe lymphoedemaElephantiasis

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Lymphedema treatmentLymphedema treatment

The first treatment for patients with lymphedema is The first treatment for patients with lymphedema is p y psymptomatic, using decongestive physiotherapy, which includes manual lymphatic drainage and compression bandage combined with a physical exercise protocol and pneumatic compression garments (50-60 mm Hg),although these procedures are not recommended in children because of their low tolerance.

p y psymptomatic, using decongestive physiotherapy, which includes manual lymphatic drainage and compression bandage combined with a physical exercise protocol and pneumatic compression garments (50-60 mm Hg),although these procedures are not recommended in children because of their low tolerance.low tolerance.

Other essential measures include skin care to prevent infections and a dietary regimen to control weight.

low tolerance. Other essential measures include skin care to

prevent infections and a dietary regimen to control weight.

Inelastic Systems:Inelastic Systems:

Cannot tolerate elastic systems Cannot tolerate elastic systems Cannot tolerate elastic systems

Controls edema

Reusable, allows showering

Variable compliance

L h f d l i

Cannot tolerate elastic systems

Controls edema

Reusable, allows showering

Variable compliance

L h f d l i Less chance of secondary lesions Less chance of secondary lesions

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Question 5Question 5

This recent onset This recent onset This recent onset eruption in a VLU patient could be: A) Allergic contact

dermatitis

B) Psoriasis

This recent onset eruption in a VLU patient could be: A) Allergic contact

dermatitis

B) Psoriasis

C) Cellulitis

D) Esysipela

E) Burn

C) Cellulitis

D) Esysipela

E) Burn

Contact Allergens in Leg ulcer treatment

Contact Allergens in Leg ulcer treatment

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ObjectivesObjectives

The attendee will be familiarized: with the physiology of oedema

The attendee will be familiarized: with the physiology of oedemap y gy by the fact, when oedema, finding its aetiology and corrective

measures must be prompt on how to recognize soft tissue infections with their

consequences with the insidious, mostly irreversible changes of lymphoedema

p y gy by the fact, when oedema, finding its aetiology and corrective

measures must be prompt on how to recognize soft tissue infections with their

consequences with the insidious, mostly irreversible changes of lymphoedema