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LYMPH OEDEMA
ANATOMY AND PHYSIOLOGY
• Function –return of protein rich fluid to the circulation
• Water,electrolytes,low molecular weight moieties
(polypeptides,cytokines ,growth factors )and macromolecules
(fibrinogen ,albumin ,globulins,coagulation and fibrinolytic
factors ) from ISF to circulation
• Intestinal lymph –cholesterol ,long chain fatty
acids,triglycerides and fat soluble vit (A D E K) TO circulation .
DEVOLOPMENT
• Lymph sac -6th to 7th week of gestation as 4 cystic spaces
• Lymph from lower limb and abdomen – cisterna chyli into
thorasic duct –to lt jugular vein
• From head and rt arm –to rt lymphatic duct – to rt jv
• Lymphatics accompany veins every where except –cortical bony
skeleton and CNS
• LYMPHATIC SYSTEM –lymphatic channels,lymphoid organs and
circulating elements
MICROANATOMY &PHYSIOLOGY
• Lymphatic capillaries – terminal lymphatics-lymph trunk
• Lymphatic capillaries –in ISF space ,they are blind ended,much
larger ,anchored by interstitial matrix by filaments
• Terminal lymphatics –bicuspid valves and endothelium rich in
contractile proteins
• Lymph trunks –structurally similar to vein
MECHANISM OF LYMPHFLOW
• Resting ISF pressure is negative and lymph flow against a
positive pressure gradient by :1)transient increase in interstitial
pressure secondary to muscular contraction and external
compression .
• 2)the sequential contraction and relaxation of lymphangiones
• 3)the prevention of reflux because of valves
• In summary in the healthy limb ,lymph flow is largely due to
intrinsic lymphatic contractility ,although this is augmented by
exercise limb movements and external compression .
LYMPHODEMA
• Definition- Lymphoedema may be defined as abnormal limb
swelling caused by the accumulation of increased amounts of
high protein ISF secondary to defective lymphatic drainage in
the presence of (near) normal net capillary filtration.
• At birth, 1 in 6000 people will develop lymphoedema with an
overall prevalence of 0.13–2%
• The severity of unilateral limb lymphoedema can be classified
as:
• mild: 40% excess limb volume.
• moderate: 20–40% excess limb volume;
• severe: >40% excess limb volume.
PATHOPHYSIOLOGY
• The ISF compartment (10–12 litres in a 70-kg man) constitutes
50% of the wet weight of the skin and subcutaneous tissues.
• About 8 litres (protein concentration approximately 20–30 g/L,
similar to ISF) of lymph is produced each day and travels in
afferent lymphatics to lymph nodes.
• in most types of oedema this is because the capillary filtration
rate is pathologically high and overwhelms a normal lymphatic
system, resulting in the accumulation of low-protein oedema
fluid
• In contrast, in true lymphoedema, when the primary problem is in the
lymphatics, capillary filtration is normal and the oedema fluid is
relatively high in protein.
• Lymphoedema results from lymphatic aplasia, hypoplasia,
dysmotility (reduced contractility with or without valvular
insufficiency), obliteration by inflammatory, infective or neoplastic
processes, or surgical extirpation.
• resultant physical and/or functional obstruction leads to lymphatic
hypertension and distension, with further secondary impairment of
contractility and valvular competence. Lymphostasis and
lymphotension lead to the accumulation in the ISF of fluid, proteins,
growth factors and other active peptide moieties,
glycosaminoglycans and particulate matter, including bacteria.
• subdermal fibrosis and dermal thickening and proliferation.
CLASSIFICATION
• 1) Primary lymphoedema: in which the cause is unknown (or at
least uncertain and unproven); it is thought to be caused by
‘congenital lymphatic dysplasia’.
• 2) Secondary: or acquired lymphoedema, in which there is a
clear underlying cause.
• Primary lymphoedema is usually further subdivided on the
basis of the presence of family history, age of onset and
lymphangiographic findings
CLINICAL CLASSIFICATION
SIGNS AND SYMPTOMS
• Unlike other types of oedema, lymphoedema characteristically
involves the foot.
• 1)submalleolar filling
• 2)buffalo hump
• 3)squiring
• 4)stemmers sign
• Initilly pitting
• Later non pitting and fibrosis,dermal thickening and
hyperkeratosis.
• In general, primary lymphoedema progresses more slowly than
secondary lymphoedema. Chronic eczema, fungal infection of
the skin (dermatophytosis) and nails (onychomycosis),
fissuring, verrucae and papillae (warts) are frequently seen in
advanced disease. Ulceration is unusual, except in the presence
of chronic venous insufficiency.
• Lymphangiomas are dilated dermal lymphatics that ‘blister’
onto the skin surface. The fluid is usually clear but may be
blood-stained.
• Lymphangioma circumscriptum ,diffusum,lymphoedema ab
igne
• Ulceration, non-healing bruises and raised purple-red nodules
should lead to suspicion of malignancy
D/D
• 1)non –lymphatic or non vascular-genral ds process,local ds
state ,gigantism,drugs ,trauma ,obesity
• 2)venous –dvt ,post thrombotic syndrome ,vv
• 3)arterial –a v malformations ,aneurysms
• Primary lymph oedema
SECONDARY
CONDITIONS MIMICKING LYMPHOEDEMA
• 1)Factitious lymphoedema
• 2) Immobility
• 3)lipodema
INVESTIGATION
• 1)routine tests
• 2) Lymphangiography and isotope lymphoscintigraphy-Direct
lymphangiography remains the ‘gold standard’ for showing
structural abnormalities of larger lymphatics and nodes ,but
obsolete now
• Isotope lymphoscintigraphy now the primary diagnostic
technique in cases of clinical uncertainty. Radioactive
technetium-labelled protein or colloid particles
• The technique provides a qualitative measure of lymphatic
function rather than quantitative function or anatomical detail.
• 3)Computed tomography-single axial slice through mid calf
section shows a coarse, non-enhancing, reticular ‘honeycomb’
pattern in an enlarged subcutaneous compartment
• 4)MRI
• 5) Ultrasound
• 6) Lympho-fluoroscopies
• 7) Pathological examination
• 8) Limb volume measurement-is a useful tool to determine
severity of lymphoedema, guide management and assess
response to treatment.
MANAGEMENT OF LYMPHOEDEMA
• delivered by a multiprofessional team comprising physical
therapists, nurses, orthotists, physicians (dermatologists,
oncologists, palliative care specialists), surgeons and social
service professionals.
• 1) Relief of pain
• 2) Control of swelling-Physical therapy for lymphoedema,
comprising bed rest, elevation, bandaging, compression
garments, massage and exercises,now it is DLT(decongestive
lymphoedema therapy ).COMPRISES short intensive &long
maintenance phase
• Intesive –MLD &MLLB&exercise
• 2)SKIN CARE -
• 3) Exercise- slow, rhythmic isotonic movements (e.g.
swimming) and massage will increase venous and lymphatic
return through the production of movement between skin and
underlying tissues (essential to the filling of initial lymphatics)
and augmentation of the muscle pumps
• 4)DRUGS-benzopyrones especially flavonoids grp.
• 5)SURGERY- Only a small minority of patients with
lymphoedema benefit from surgery. Operations fall into three
categories: bypass procedures, liposuction and reduction
procedures.
• 1) Bypass procedures:
The rare patient with proximal ilioinguinal lymphatic obstruction
and normal distal lymphatic channels might benefit, at least in
theory, from lymphatic bypass.
Procedures are: 1) omental pedicle, 2)the skin bridge (Gillies),
3)anastomosing lymph nodes to veins (Neilubowicz) and the4)
ileal mucosal patch (Kinmonth).
Recently direct lymphaticovenular anastomosis (LVA) has been
carried out on vessels of 0.3–0.8mm diameter using super-
microsurgical techniques. But has some benefit in early stage
cases
• 2) Liposuction: Liposuction has been used in the treament of
chronic lymphoedema. It is usually reserved for patients who
have progressed to non-pitting oedema. Case series reported
thus far have shown promising results with more than 100%
reduction in limb oedema volume, which can be maintained by
ongoing use of compression hosiery for at least 1 year. While
liposuction appears to be safe, results of long-term efficacy
and effects on the incidence of future lymphoedema
complications (e.g. infection) are awaited.
• 3) Limb reduction procedures: These are indicated when a limb
is so swollen that it interferes with mobility and livelihood.
These operations are not ‘cosmetic’ in the sense that they do
not create a normally-shaped leg.there are 4 procedures are
noted
• A) SISTRUNK :A wedge of skin and subcutaneous tissue is
excised and the wound closed primarily. This is most
commonly carried out to reduce the girth of the thigh.
• B HOMANS First, skin flaps are elevated, and then
subcutaneous tissue is excised from beneath the flaps, which
are then trimmed to size to accommodate the reduced girth of
the limb and closed primarily. This is the most satisfactory
operation for the calf :
• C) THOMPSON: This is a modification of the Homans’ procedure
aimed to create new lymphatic connections between the
superficial and deep systems.
• D) CHARLES: This operation was initially designed for filariasis
and involved excision of all of the skin and subcutaneous
tissues down to the deep fascia, with coverage using split-skin
grafts (Figure 58.13). This leaves a very unsatisfactory cosmetic
result and graft failure is not uncommon. However, it does
enable the surgeon to reduce greatly the girth of a massively
swollen
THANK YOU

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Lymph odema.pptx

  • 2. ANATOMY AND PHYSIOLOGY • Function –return of protein rich fluid to the circulation • Water,electrolytes,low molecular weight moieties (polypeptides,cytokines ,growth factors )and macromolecules (fibrinogen ,albumin ,globulins,coagulation and fibrinolytic factors ) from ISF to circulation • Intestinal lymph –cholesterol ,long chain fatty acids,triglycerides and fat soluble vit (A D E K) TO circulation .
  • 3. DEVOLOPMENT • Lymph sac -6th to 7th week of gestation as 4 cystic spaces • Lymph from lower limb and abdomen – cisterna chyli into thorasic duct –to lt jugular vein • From head and rt arm –to rt lymphatic duct – to rt jv • Lymphatics accompany veins every where except –cortical bony skeleton and CNS • LYMPHATIC SYSTEM –lymphatic channels,lymphoid organs and circulating elements
  • 4. MICROANATOMY &PHYSIOLOGY • Lymphatic capillaries – terminal lymphatics-lymph trunk • Lymphatic capillaries –in ISF space ,they are blind ended,much larger ,anchored by interstitial matrix by filaments • Terminal lymphatics –bicuspid valves and endothelium rich in contractile proteins • Lymph trunks –structurally similar to vein
  • 5. MECHANISM OF LYMPHFLOW • Resting ISF pressure is negative and lymph flow against a positive pressure gradient by :1)transient increase in interstitial pressure secondary to muscular contraction and external compression . • 2)the sequential contraction and relaxation of lymphangiones • 3)the prevention of reflux because of valves • In summary in the healthy limb ,lymph flow is largely due to intrinsic lymphatic contractility ,although this is augmented by exercise limb movements and external compression .
  • 6. LYMPHODEMA • Definition- Lymphoedema may be defined as abnormal limb swelling caused by the accumulation of increased amounts of high protein ISF secondary to defective lymphatic drainage in the presence of (near) normal net capillary filtration. • At birth, 1 in 6000 people will develop lymphoedema with an overall prevalence of 0.13–2%
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  • 8. • The severity of unilateral limb lymphoedema can be classified as: • mild: 40% excess limb volume. • moderate: 20–40% excess limb volume; • severe: >40% excess limb volume.
  • 9. PATHOPHYSIOLOGY • The ISF compartment (10–12 litres in a 70-kg man) constitutes 50% of the wet weight of the skin and subcutaneous tissues. • About 8 litres (protein concentration approximately 20–30 g/L, similar to ISF) of lymph is produced each day and travels in afferent lymphatics to lymph nodes. • in most types of oedema this is because the capillary filtration rate is pathologically high and overwhelms a normal lymphatic system, resulting in the accumulation of low-protein oedema fluid
  • 10. • In contrast, in true lymphoedema, when the primary problem is in the lymphatics, capillary filtration is normal and the oedema fluid is relatively high in protein. • Lymphoedema results from lymphatic aplasia, hypoplasia, dysmotility (reduced contractility with or without valvular insufficiency), obliteration by inflammatory, infective or neoplastic processes, or surgical extirpation. • resultant physical and/or functional obstruction leads to lymphatic hypertension and distension, with further secondary impairment of contractility and valvular competence. Lymphostasis and lymphotension lead to the accumulation in the ISF of fluid, proteins, growth factors and other active peptide moieties, glycosaminoglycans and particulate matter, including bacteria. • subdermal fibrosis and dermal thickening and proliferation.
  • 11. CLASSIFICATION • 1) Primary lymphoedema: in which the cause is unknown (or at least uncertain and unproven); it is thought to be caused by ‘congenital lymphatic dysplasia’. • 2) Secondary: or acquired lymphoedema, in which there is a clear underlying cause.
  • 12. • Primary lymphoedema is usually further subdivided on the basis of the presence of family history, age of onset and lymphangiographic findings
  • 14. SIGNS AND SYMPTOMS • Unlike other types of oedema, lymphoedema characteristically involves the foot.
  • 15. • 1)submalleolar filling • 2)buffalo hump • 3)squiring • 4)stemmers sign
  • 16. • Initilly pitting • Later non pitting and fibrosis,dermal thickening and hyperkeratosis. • In general, primary lymphoedema progresses more slowly than secondary lymphoedema. Chronic eczema, fungal infection of the skin (dermatophytosis) and nails (onychomycosis), fissuring, verrucae and papillae (warts) are frequently seen in advanced disease. Ulceration is unusual, except in the presence of chronic venous insufficiency.
  • 17. • Lymphangiomas are dilated dermal lymphatics that ‘blister’ onto the skin surface. The fluid is usually clear but may be blood-stained. • Lymphangioma circumscriptum ,diffusum,lymphoedema ab igne • Ulceration, non-healing bruises and raised purple-red nodules should lead to suspicion of malignancy
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  • 19. D/D • 1)non –lymphatic or non vascular-genral ds process,local ds state ,gigantism,drugs ,trauma ,obesity • 2)venous –dvt ,post thrombotic syndrome ,vv • 3)arterial –a v malformations ,aneurysms
  • 22. CONDITIONS MIMICKING LYMPHOEDEMA • 1)Factitious lymphoedema • 2) Immobility • 3)lipodema
  • 23. INVESTIGATION • 1)routine tests • 2) Lymphangiography and isotope lymphoscintigraphy-Direct lymphangiography remains the ‘gold standard’ for showing structural abnormalities of larger lymphatics and nodes ,but obsolete now • Isotope lymphoscintigraphy now the primary diagnostic technique in cases of clinical uncertainty. Radioactive technetium-labelled protein or colloid particles • The technique provides a qualitative measure of lymphatic function rather than quantitative function or anatomical detail.
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  • 25. • 3)Computed tomography-single axial slice through mid calf section shows a coarse, non-enhancing, reticular ‘honeycomb’ pattern in an enlarged subcutaneous compartment • 4)MRI • 5) Ultrasound • 6) Lympho-fluoroscopies • 7) Pathological examination • 8) Limb volume measurement-is a useful tool to determine severity of lymphoedema, guide management and assess response to treatment.
  • 26. MANAGEMENT OF LYMPHOEDEMA • delivered by a multiprofessional team comprising physical therapists, nurses, orthotists, physicians (dermatologists, oncologists, palliative care specialists), surgeons and social service professionals. • 1) Relief of pain • 2) Control of swelling-Physical therapy for lymphoedema, comprising bed rest, elevation, bandaging, compression garments, massage and exercises,now it is DLT(decongestive lymphoedema therapy ).COMPRISES short intensive &long maintenance phase
  • 27. • Intesive –MLD &MLLB&exercise • 2)SKIN CARE -
  • 28. • 3) Exercise- slow, rhythmic isotonic movements (e.g. swimming) and massage will increase venous and lymphatic return through the production of movement between skin and underlying tissues (essential to the filling of initial lymphatics) and augmentation of the muscle pumps • 4)DRUGS-benzopyrones especially flavonoids grp. • 5)SURGERY- Only a small minority of patients with lymphoedema benefit from surgery. Operations fall into three categories: bypass procedures, liposuction and reduction procedures.
  • 29. • 1) Bypass procedures: The rare patient with proximal ilioinguinal lymphatic obstruction and normal distal lymphatic channels might benefit, at least in theory, from lymphatic bypass. Procedures are: 1) omental pedicle, 2)the skin bridge (Gillies), 3)anastomosing lymph nodes to veins (Neilubowicz) and the4) ileal mucosal patch (Kinmonth). Recently direct lymphaticovenular anastomosis (LVA) has been carried out on vessels of 0.3–0.8mm diameter using super- microsurgical techniques. But has some benefit in early stage cases
  • 30. • 2) Liposuction: Liposuction has been used in the treament of chronic lymphoedema. It is usually reserved for patients who have progressed to non-pitting oedema. Case series reported thus far have shown promising results with more than 100% reduction in limb oedema volume, which can be maintained by ongoing use of compression hosiery for at least 1 year. While liposuction appears to be safe, results of long-term efficacy and effects on the incidence of future lymphoedema complications (e.g. infection) are awaited.
  • 31. • 3) Limb reduction procedures: These are indicated when a limb is so swollen that it interferes with mobility and livelihood. These operations are not ‘cosmetic’ in the sense that they do not create a normally-shaped leg.there are 4 procedures are noted • A) SISTRUNK :A wedge of skin and subcutaneous tissue is excised and the wound closed primarily. This is most commonly carried out to reduce the girth of the thigh. • B HOMANS First, skin flaps are elevated, and then subcutaneous tissue is excised from beneath the flaps, which are then trimmed to size to accommodate the reduced girth of the limb and closed primarily. This is the most satisfactory operation for the calf :
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  • 33. • C) THOMPSON: This is a modification of the Homans’ procedure aimed to create new lymphatic connections between the superficial and deep systems. • D) CHARLES: This operation was initially designed for filariasis and involved excision of all of the skin and subcutaneous tissues down to the deep fascia, with coverage using split-skin grafts (Figure 58.13). This leaves a very unsatisfactory cosmetic result and graft failure is not uncommon. However, it does enable the surgeon to reduce greatly the girth of a massively swollen
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