The document provides an extensive overview of the lymphatic system, outlining its components, functions, and the pathophysiology of various lymphatic disorders such as lymphoedema and acute lymphangitis. It discusses the physiological roles of lymphatics in fluid balance and immune response, as well as the mechanisms of lymph transport and the impact of underlying conditions on lymphatic health. Additionally, it covers classifications, clinical features, and risk factors associated with lymphatic conditions, including primary and secondary lymphoedema.

1. LYMPHATIC DISORDERS
Dr Karthik K

2. INTRODUCTION
• The lymphatic system comprises
• lymphatic channels,
• lymphoid organs (lymph nodes, spleen,
Peyer’s patches, thymus, tonsils)
• and circulating elements

3. DEVELOPMENT
• In the human embryo lymph sacs develop at 6–7
weeks’ gestation as four cystic spaces, one on
either side of the neck and one in each groin.
• These cisterns enlarge and develop communi-
cations that permit lymph from the lower limbs
and abdomen to drain via the cisterna chyli into
the thoracic duct,
• Cysterna chyli, in turn drains into the left internal
jugular vein at its confluence with the left
subclavian vein.

4. connection to the veins

5. • Lymph from the head and right arm drains via
a separate lymphatic trunk, the right
lymphatic duct, into the right internal jugular
vein.

6. travel along with blood vessels.
1) lymphatic vessels

7. lymphatic capillary
lymphatic trunks
lymphatic collecting vessels
lymphatic ducts
Lymphatic vessels start with
lymphatic capillaries

8. • Lymphatics accompany veins everywhere
• Except in the cortical bony skeleton and
central nervous system, where there is no
lymphatics.
• Although the brain and retina possess
cerebrospinal fluid and aqueous humour,
respectively.

9. PHYSIOLOGY
• The principal function of the lymphatics is the
• Return of protein-rich fluid to the circulation
through the lymphaticovenous junctions in
the jugular area.

10. - collect excess large particles and tissue fluid
lymph

11. • Water, electrolytes, low molecular weight moieties
(polypeptides, cytokines, growth factors) and
macromolecules (fibrinogen, albumin, globulins,
coagulation and fibrinolytic factors) from the
interstitial fluid (ISF) return to the circulation via the
lymphatics.
• Intestinal lymph (chyle) transports cholesterol, long-
chain fatty acids, triglycerides and the fat-soluble
vitamins (A, D, E and K) directly to the circulation,
bypassing the liver.
• Lymphocytes and other immune cells also circulate
within the lymphatic system.

12. Special lymph capillaries --- Lacteals
- collect digested fats ( in chylomicrons)

13. Lymphatics originate within the ISF space from
specialised endothelialised capillaries (initial
lymphatics) or non- endothelialised channels
such as the spaces of Disse in the liver.

14. MICROANATOMY-INITIAL
LYMPHATICS
• Initial lymphatics are :
• blind-ended;
• much larger (50 μm);
• allow the entry of molecules of up to 1000 kDa in size
• because the basement membrane is fenestrated, tenuous
or even absent and the endothelium itself possesses intra-
and intercellular pores;
• they are anchored to interstitial matrix by filaments. In the
resting state, initial lymphatics are collapsed.
• When ISF volume and pressure increases, initial lymphatics
and their pores are held open by these filaments to
facilitate increased drainage.

15. - blind ended vessels
- permeable to proteins even cells

16. TERMINAL LYMPHATICS
•Initial lymphatics drain into terminal (collecting)
lymphatics that possess bicuspid valves and
endothelial cells rich in the contractile protein
actin.
•Larger collecting lymphatics are surrounded by
smooth muscle. Valves partition the lymphatics into
segments (lymphangions) that contract sequentially
to propel lymph into the lymph trunks.

17. LYMPH TRUNKS
•Terminal lymphatics lead to lymph trunks
•Structure of lymph trunks is similar to that of
veins, namely a single layer of endothelial cells,
lying on a basement membrane overlying a
media comprising smooth muscle cells
•These are innervated with sympathetic,
parasympathetic and sensory nerve endings

18. • About 10% of lymph arising from a limb is
transported in deep lymphatic trunks that
accompany the main neurovascular bundles.
• The majority, however, is conducted against
venous flow from deep to superficial in epifascial
lymph trunks.
• Superficial trunks form lymph bundles of various
sizes, which are located within strips of adipose
tissue, and tend to follow the course of the major
superficial veins.

19. STARLING’S FORCES
•The distribution of fluid and protein between the
vascular system and ISF depends on the balance of
hydrostatic and oncotic pressures between the two
compartments (Starling’s forces).
•Together with the relative impermeability of the
blood capillary membrane to molecules over 70kDa.
In health, there is net capillary filtration, which is
removed by the lymphatic system.

20. TRANSPORT OF PARTICLE
•Particles enter the initial lymphatics through
interendothelial openings and vesicular
transport through intraendothelial pores.
• Large particles are actively phagocytosed by
macrophages and transported through the
lymphatic system intracellularly.

21. MECHANISM OF LYMPH
TRANSPORT
•Resting ISF pressure is negative (-2 to -
6mmH2O),
• whereas lymphatic pressures are positive,
indicating that lymph flows against a small
pressure gradient.
• It is believed that prograde lymphatic flow
depends upon three mechanisms:

22. • 1 transient increases in interstitial pressure
secondary to muscular contraction and
external compression;
• 2 the sequential contraction and relaxation of
lymphan- gions;
• 3 the prevention of reflux because of valves.

23. • Lymphangions are believed to respond to increased lymph
flow in much the same way as the heart responds to
increased venous return, in that they increase their
contractility and stroke volume. Contractility is also
enhanced by noradren aline, serotonin, certain
prostaglandins and thromboxanes, and endothelin-1.
• Pressures of up to 30–50 mmHg have been recorded in
normal lymph trunks and up to 200mmHg in severe
lymphoedema.
• Lymphatics may also modulate their own contractility
through the production of nitric oxide and other local
mediators.

24. • Transport in the thoracic and right lymph
ducts also depends upon intrathoracic
(respiration) and central venous (cardiac
cycle) pressures.
• Therefore, cardiorespiratory disease may
have an adverse effect on lymphatic function.

25. • In summary, in the healthy limb, lymph flow is
largely due to-
• Intrinsic lymphatic contractility, which is
augmented by exercise, limb movement and
external compression.
• However, in lymphoedema, when the
lymphatics are constantly distended with lymph,
these external forces assume a much more
important functional role.

26. ACUTE LYMPHANGITIS
• ACUTE INFLAMMATION OF THE LYMPHATICS
• Acute lymphangitis is an infection, often
caused by Strepto- coccus pyogenes or
Staphylococcus aureus, which spreads to the
draining lymphatics and lymph nodes
(lymphadenitis) where an abscess may form.
Eventually this may progress to bacteraemia
or septicaemia.

28. • The normal signs of infection (rubor, calor,
dolor) are present
• red streak is seen in the skin along the line of
the inflamed lymphatic .
• The part should be rested to reduce lymphatic
drainage and elevated to reduce swelling, and
the patient should be treated with intravenous
antibiotics based upon actual or suspected
sensitivities.

29. TREATMENT
• Rest to the part to reduce lymphatic drainage
• Limb elevation to reduce swelling,
• Intravenous antibiotics based upon actual or
suspected sensitivities.

30. Failure to improve within 48 hrs
• inappropriate antibiotic therapy,
• the presence of undrained pus
• or the presence of an underlying systemic disorder
(malig- nancy, immunodeficiency)
• The lymphatic damage caused by acute
lymphangitis may lead to recurrent attacks of
infection and lymphoedema;
• Patients with lymphoedema are prone to so-called
acute inflammatory episodes.

31. LYMPHOEDEMA
•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.

32. SYMPTOMS
• Swelling, clothing or jewellery becoming tighter
• Constant dull ache, even severe pain
• Burning and bursting sensations
• General tiredness and debility
• Sensitivity to heat
• ‘Pins and needles’
• Cramp
• Skin problems, including flakiness, weeping, excoriation and
• breakdown
• Immobility, leading to obesity and muscle wasting
• Backache and joint problems
• Athlete’s foot
• Acute infective episodes

33. CLASSIFICATION
• The severity of unilateral limb lymphoedema
can be classified as:
–
● mild: <20% excess limb volume;
–
● moderate: 20–40% excess limb volume;
–
● severe: >40% excess limb volume.

34. PATHOPHYSIOLOGY
•The ISF compartment (10–12 litres in a 70-kg man)
constitutes 50% of the wet weight of the skin and
subcutaneous tissues and.
•For oedema to be clinically detectable, its volume
has to double.
• 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.

35. • There, the volume is halved and the protein
concentration doubled, resulting in 4 litres of
lymph re-entering the venous circulation each
day via efferent lymphatics.
• All oedema is lymphoedema which results
from an inability of the lymphatic system to
clear the ISF compartment.

36. • Lymphoedema results from-
• Lymphatic aplasia,
• Hypoplasia,
• Dysmotility (reduced contractility with or
without valvular insufficiency),
• Obliteration by inflammatory, infective or
neo- plastic processes, or surgical extirpation.

37. CLASSIFICATION
•Two main types of lymphoedema are
recognised:
•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.

38. PRIMARY
• Primary lymphoedema
• Congenital (onset <2 years old): sporadic; familial (Nonne–Milroy’s disease)
• Praecox (onset 2–35 years old): sporadic; familial (Letessier–Meige’s disease)
• Tarda (onset after 35 years old)
• Secondary lymphoedema
• Parasitic infection (filariasis)
• Fungal infection (tinea pedis)
• Exposure to foreign body material (silica particles)
• Primary lymphatic malignancy
• Metastatic spread to lymph nodes
• Radiotherapy to lymph nodes
• Surgical excision of lymph nodes
• Trauma (particularly degloving injuries)
• Superficial thrombophlebitis
• Deep venous thrombosis

39. • Clinical classification of lymphoedema.
• Grade (Brunner)
• Clinical features
• Subclinical (latent)
• There is excess interstitial fluid and histological abnormalities in
lymphatics and lymph nodes, but no clinically apparent lymphoedema
• I
• Oedema pits on pressure and swelling largely or completely disappears on
elevation and bed rest
• II
• Oedema does not pit and does not significantly reduce upon elevation,
positive Stemmer’s sign
• III
• Oedema is associated with irreversible skin changes, i.e. fibrosis, papillae

40. RISK FACTORS
•Number of factors are thought to predispose
an individual to its development and predict
progression, severity and outcome of the
condition

41. UPPER LIMB
• Surgery with axillary lymph node dissection like breast
surgery.
• Scar formation,fibrosis andradiodermatitis.
• Radiotherapy to breast and axilla.
• Drain ,wound complication and infection.
• Cording(axillary web syndrome)
• Seroma formation
• Advanced cancer
• Obesity

42. LOWER LIMB
• Surgery with inguinal lymph node dissection.
• Post-op pelvic radiotherapy.
• Rec.soft tissue infection.
• Obesity.
• Varicose vein stripping and vein harvesting
• Advanced cancer.
• Pelvic or abdominal tm
• Orthopaedic surgery.

43. SYMPTOMS AND SIGNS
•The diagnosis of primary or secondary lymph-
oedema can be made and the condition can be
differentiated from other causes of a swollen
limb on the basis of history and examination
without recourse to complex investigation

44. • Unlike other types of oedema, lymphoedema
characteristically involves the foot .
• The contour of the ankle is lost through infilling
of the submalleolar depressions,
• A‘buffalo hump’ forms on the dorsum of the
foot,
• Toes appear ‘square’ because of confinement of
footwear
• The skin on the dorsum of the toes cannot be
pinched because of subcutaneous fibrosis
(Stemmer’s sign)

45. • Lymphoedema usually spreads proximally to
knee level and less commonly affects the
whole leg .
• In the early stages,
• lymphoedema will ‘pit’ and the patient will
report that the swelling is down in the
morning.

46. • This represents a reversible component to the
swelling, which can be controlled.
• Failure to do so allows fibrosis, dermal thickening and
hyperkeratosis to occur.
• 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 insufficienc

47. LYMPHANGIOMA
• Lymphangiomas are dilated dermal lymphatics
that ‘blister’ onto the skin surface.
• The fluid is usually clear but may be blood-
stained.
• In the long term, lymphangiomas thrombose
and fibrose, forming hard nodules that may
raise concerns about malignancy.

48. • If lymphangiomas are <5 cm across, they are
termed lymphangioma circumscriptum,
• If they are more widespread, they are termed
lymphangioma diffusum.
• If they form a reticulate pattern of ridges then
it has been termed lymphoedema ab igne.

49. •Lymphangiomas frequently weep (lym-
phorrhoea, chylorrhoea), causing skin
maceration, and they act as a portal for
infection.
• Protein-losing diarrhoea, chylous ascites,
chylothorax, chyluria and discharge from
lymphangiomas suggest lymphangectasia
(megalymphatics) and chylous reflux.

50. • Ulceration, non-healing bruises and raised
purple-red nodules should lead to suspicion of
malignancy. Lymphangio- sarcoma was
originally described in postmastectomy
oedema (Stewart–
Treves’syndrome)andaffectsaround0.5%ofpati
ents at a mean onset of 10 years.

51. LYMPANGIOSARCOMA
• Lymphangiosarcoma can develop in any long-
standing lymphoedema, but usually takes
longer to manifest (20 years).
• It presents as single or multiple bluish/red
skin and subcutaneous nodules that spread to
form satellite lesions, which may then become
confluent.

52. MALIGNANCY ASSOCIATED WITH
LYMPHOEDEMA
• Lymphangiosarcoma
• Kaposi’s sarcoma
• Squamous cell carcinoma
• Liposarcoma
• Malignant melanoma
• Malignant fibrous histiocytoma
• Basal cell carcinoma
• Lymphoma

53. PRIMARY LYMPHOEDEMA
•Aetiology –due to
An inherited abnormality of the lymphatic
system, sometimes termed ‘congenital
lymphatic dysplasia’

54. • Primary lymphoedema may occur in the
presence of a (near-)normal lymphatic system.
• Bacterial and/or
• Fungal infections,
• Insect bites,
• Barefoot walking (silica),
• Deep venous thrombosis (DVT) or
• Episodes of superficial thrombo- phlebitis.

55. • Primary lymphoedema is much more common
in the legs than the arms.
• This may be because of gravity and a bipedal
posture, the fact that the lymphatic system of
the leg is less well developed,
• The increased susceptibility of the leg to
trauma and/or infection.

56. • Classification
• Primary lymphoedema is usually classified on
the basis of
• apparent genetic susceptibility,
• age of onset or
• lymphangiographic findings.

57. • Genetic susceptibility
• Primary lymphoedema can be familial or
sporadic. In familial cases the genetic mutations
can be inherited in an autosomal dominant,
recessive or x-linked pattern.

58. AGE
•Lymphoedema congenita (onset at or within 2
years of birth) is more common in males and is
more likely to be bilateral and involve the whole
leg.
•Lymphoedema praecox (onset from 2 to 35 years)
is three times more common in females, has a peak
incidence shortly after menarche, is three times
more likely to be unilateral than bilateral and
usually only extends to the knee.

59. • Lymphoedema tarda develops, by definition,
after the age of 35 years and is often
associated with obesity, with lymph nodes
being replaced with fibrofatty tissue. The cause
is unknown.
• Lymphoedema developing for the first time
after 50 years should prompt a thorough
search for underlying (pelvic, genitalia)
malignancy.

60. SECONDARY LYMPHOEDEMA
•This is the most common form of lymphoedema.
Causes including- infection,
-inflammation,
-neoplasia and
- trauma
•

61. FILARIASIS
•This is the most common cause of lymphoedema
worldwide, affecting up to 100 million individuals.
• It is particularly prevalent in Africa, India and
South America where 5–10% of the population may
be affected.
•The viviparous nematode Wuche- ria bancrofti,
whose only host is man, is responsible for 90% of
cases and is spread by the mosquito.
• The disease is associated with poor sanitation.

62. • The parasite enters lymphatics from the blood
and lodges in lymph nodes, where it causes
fibrosis and obstruction, due partly to direct
physical damage and partly to the immune
response of the host.
• Proximal lymphatics become grossly dilated
with adult parasites.

63. Elephantiasis
– blockage by
parasitic worms

64. • The degree of oedema is often massive, in which
case it is termed elephantiasis
• Immature parasites (microfilariae) enter the
blood at night and can be identified on a blood
smear, in a centrifuged specimen of urine or in
lymph itself.
• A complement fixation test is also available and is
positive in present or past infection.
• Eosinophilia is usually present.

65. FEATURES OF FILARIASIS
• ACUTE-Fever,headache,Malaise,Inguinal and
axillary lymphadenitis, Lympangitis, Cellulitis,
abscess formation and ulceration,
Funiculoepididymo-orchitis
• CHRONIC-Lymphoedema of legs ,arms and
breast, Hydrocoele, Abdominal lymphatic
varices-chyluria, Lymphuria

66. TREATMENT
• Diethylcarbamazine destroys the parasites but
does not reverse the lymphatic changes,
although there may be some regression over
time.
• Once the infection has been cleared,
treatment is as for primary lymphoedema

67. ENDEMIC ELEPHANTIASIS
•(podoconiosis)
•This is common in the tropics and affects more than 500
000 people in Africa.
• The barefoot cultivation of soil composed of alkaline
volcanic rocks leads to destruction of the peripheral
lymphatics by particles of silica, which can be seen in
macro- phages in draining lymph nodes.
• Plantar oedema develops in childhood and rapidly
spreads proximally.
•The condition is prevented and its progression is slowed
by the wearing of shoes.

68. BACTERIAL INFECTION
•Lymphangitis and lymphadenitis can cause
lymphatic destruction that predisposes to
lymphoedema complicated by further acute
inflammatory episodes. Interestingly.
• Lymphatic and lymph node destruction by
tuberculosis is also a well-recognised cause of
lymph- oedema, especially in resource-poor
countries.

69. MALIGNANCY &TREATMENT
•Treatment (surgery, radiotherapy) for breast carcinoma
is the most common cause of lymphoedema in resource-
rich countries, but is decreasing in incidence as surgery
becomes more conservative .
•Lymphoma may present with lymphoedema, as may
malignancy of the pelvic organs and external genitalia.
• Kaposi’s sarcoma, developing in the course of human
immunodeficiency virus (HIV)-related illness, may cause
lymphatic obstruction and is a growing cause of lymph-
oedema in certain parts of the world.

70. TRAUMA
•It is not unusual for patients to develop chronic localised
or generalised swelling following trauma.
• The aetiology is often multifactorial and includes disuse,
venous thrombosis and lymphatic injury or destruction.
•Degloving injuries and burns are particularly likely to
disrupt dermal lymphatics.
•Tenosynovitis can also be associated with localised
subcutaneous lymphoedema, which can be a cause of
troublesome persistent swelling following ankle and wrist
‘sprains’ and repetitive strain injury.

71. MISCELLANEOUS
•Rheumatoid and psoriatic arthritis (chronic
inflammation and lymph node fibrosis),
• contact dermatitis,
•snake and insect bites and
•retroperitoneal fibrosis are all rare but well-
documented causes of lymphoedema.
• Pretibial myxoedema is due to the obliteration of
initial lymphatics by mucin.

72. • Conditions mimicking lymphoedema
• Factitious lymphoedema
This is caused by application of a tourniquet (a
‘rut’ and sharp cut-off is seen on examination)
or ‘hysterical’ disuse in patients with
psychological and psychiatric problems.

73. • Immobility
Generalized or localized immobility of any cause
leads to chronic limb swelling that can be
misdiagnosed as lymphedema
ex: the elderly person who spends all day (and
sometimes all night) sitting in a chair (armchair
legs)
the hemiplegic stroke patient and the young
patient with multiple sclerosis.

74. INVESTIGATION
Routine’ tests
•These include a full blood count, urea and electrolytes, creatinine,
liver function tests, thyroid function tests, plasma total protein and
albumin, fasting glucose, C-reactive protein, urine dipstick including
observation for chyluria, blood smear for microfilariae, chest
radiograph and ultrasound.
Lymphangiography and isotope lymphoscintigraphy
Computed tomography
Ultrasound
•Ultrasound can provide useful information about venous function
including DVT and venous abnormalities.
MRI

75. Malignancies associated with lymphoedema
• Lymphangiosarcoma (Stewart–Treves’ syndrome)
• Kaposi’s sarcoma (human immunodeficiency virus)
• Squamous cell carcinoma
• Liposarcoma
• Malignant melanoma
• Malignant fibrous histiocytoma
• Basal cell carcinoma
• Lymphoma

76. Pathological examination
•In cases in which malignancy is suspected,
samples of lymph nodes may be obtained by
fine-needle aspiration, needle core biopsy or
surgical excision. Skin biopsy will confirm the
diagnosis of lymphangiosarcoma.

77. Limb volume measurement
•limb volume measurement is a useful tool to determine severity of
lymphoedema, guide management and assess response to treatment.
•Limb volume is typically measured at diagnosis, following intensive
treatment and at follow-up.
•In unilateral limb swelling the affected side can be compared to the
contralateral unaffected limb.
•In bilateral swelling the volume of both limbs is tracked with time.
•Measurements are recorded in millilitres or expressed as a
percentage of the normal limb.
•Water plethysmography (water displacement) is the ‘gold standard’
method, but is limited by practicalities of measurement and hygiene
issues.
•Other options include circumferential limb measurements and
perometry (infrared light beams measure the outline of the limb to
calculate volume).

78. MANAGEMENT
The identification, education and treatment of
such ‘at-risk’ patients can slow down, even
prevent, the onset of disease.
In patients with established lymphoedema, the
three goals of treatment are to relieve pain,
reduce swelling and prevent the development of
complications.

79. RELIEF OF PAIN
• Treatment involves the considered use of
o non-opioid and opioid analgesics,
o Corticosteroids
o tricyclic antidepressants
o muscle relaxants
o Antiepileptics
o nerve blocks
o physiotherapy and adjuvant anticancer therapies
(chemo-, radio- and hormonal therapy)
o as well as measures to reduce swelling, if possible.
• In patients with non- cancer related lymphoedema, the
best way to reduce pain is to control swelling and
prevent the development of complications.

80. CONTROLL OF SWELLING
• Physical therapy for lymphoedema,
comprising bed rest, elevation, bandaging,
compression garments, massage and exercise
• The current preferred term is decongestive
lymphoedema therapy (DLT), which comprises
two phases. The first is a short intensive
period of therapist-led care and the second is
a maintenance phase in which the patient
uses a self-care regime

81. SKIN CARE
The limb should be washed daily; the use of bath
oil, e.g. Balneum, is recommended as a
moisturiser and the limb must be carefully dried
afterwards.
A hair drier on low heat is more effective and
hygienic, and less traumatic, than a towel.
If the skin is in good condition daily application of
a bland emollient, e.g. aqueous cream, is
recommended .

82. SKIN CARE
• Protect hands when washing up or gardening,
wear a thimble when sewing.
• Never walk barefoot & wear protective footwear
outside.
• Use an electric razor.
• Never let the skin become macerated.
• Treat cuts and grazes promptly.
• Use insect repellent and treat insect bite
promptly.
• Protect the affected skin from sun.

83. MANUAL LYMPHATIC DRAINAGE
•Several different techniques of MLD have been
described and all aim to evacuate fluid and protein
from the interstitial space and stimulate
lymphangion contraction, with decongestion of
impaired lymphatic pathways and development of
collateral routes.
• The therapist should perform MLD daily;
• Patient (and/or carer) should be trained to
perform a simpler, modified form of massage
termed simple lymphatic drainage (SLD).

84. MULTILAYER LYMPHOEDEMA BANDAGING
compression garments
•Elastic bandages provide compression, produce a
sustained high resting pressure and ‘follow in’ as limb
swelling reduces.
•However, the sub-bandage pressure does not alter
greatly.
• By contrast, short-stretch bandages exert support
through the production of a semi-rigid casing where
the resting pressure is low.
• Whether the aim is to provide support or
compression, the pressure exerted must be
graduated (100% ankle/foot, 70% knee, 50% mid-
thigh, 40% groin).

85. Effects of multilayer lymphoedema bandaging
•Reduces oedema
•Restores shape to the affected area
•Reduces skin changes (hyperkeratosis,
papillomatosis)
•Eliminates lymphorrhoea
•Supports inelastic skin
•Softens subcutaneous tissues

86. EXERCISE
•Lymph formation is directly proportional
to arterial inflow and 40% of lymph is
formed within skeletal muscle.
• Vigorous exercise, especially if it is
anaerobic and isometric, will tend to
exacerbate lymphoedema and patients
should be advised to avoid prolonged
static activities, for example carrying heavy
shopping bags or prolonged standing

87. Exercise
•In contrast, 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
• Exercise also helps to maintain joint mobility
•Patients who are unable to move their limbs
benefit from passive exercises
•When at rest, the lymphoedematous limb should
be positioned with the foot/hand above the level of
the heart
•A pillow under the mattress or block under bed

88. DRUGS
• Pts experiencing recurrent lymphangitis or
cellulitis may require long term prophylactic
treatment with antimicrobial agents such as
penicillin,cephalexinor erythromycin.
• Filariasis has been treated with anthelmintic
agents diethylcarbamazine and albendazole.

89. SURGERY
• Only a small minority of patients with
lymphoedema benefit from surgery.
Operations fall into three categories: bypass
procedures, liposuction and reduction
procedures.

90. BY-PASS PROCEDURE
• A number of methods have been described,
• including the omental pedicle,
• the skin bridge (Gillies),
• anastomosing lymph nodes to veins (Neilubowicz)
and the
• ileal mucosal patch (Kinmonth).
• More recently, direct lymphaticovenular
anastomosis (LVA) has been carried out on vessels
of 0.3–0.8mm diameter using super-microsurgical
techniques.

92. Liposuction
• Liposuction has been used in the treatment of
chronic lymphedema. It is usually reserved for
patients who have progressed to non-pitting
edema.
• Shown promising results with more than 100%
reduction in limb edema volume, which can
be maintained by use of compression hosiery.

93. 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 and are usually associated with significant
scarring.
•Four operations have been described.

94. 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.

97. 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.
• 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 limb.

101. CHYLOTHORAX
Chylous ascites and chylothorax
•These are associated with megalymphatics.
•Usually accompanied by lymphoedema and
lymphangioma.
•However, some patients develop chylous
ascites and/or chylothorax .

102. CHYLUREA
•Filariasis is the most common cause, with chyluria occurring
in 1–2% of cases 10–20 years after initial infestation.
• It usually presents as painless passage of milky white urine,
particularly after a fatty meal.
•The chyle may clot, leading to renal colic, and
hypoproteinaemia may result.
•Chyluria may also be caused by ascariasis, malaria, tumour
and tuberculosis.
• Intravenous urography and/or lymphangiography will often
demonstrate the lymphourinary fistula.

103. TREATMENT
• Treatment includes a low-fat and high-
protein diet,
• Increased oral fluids to prevent clot colic
• Laparotomy and ligation of the dilated
lymphatics.
• Sclerose the lymphatics either directly or via
instrumentation of the bladder, ureter and
renal pelvis.

104. LYMPHOCOELE
•Lymphocoele is a localised collection of lymph
without a distinct epithelial lining. It results from
leakage of lymph into the soft tissues or body cavity
secondary to surgical disruption of lymphatic
vessels.
•Clinically, lymphocoele presents as a non-tender,
non-pulsatile mobile lump and can be
differentiated from a seroma or a localised
postoperative oedema by the presence of lymph-
rich fluid.