Role of VPL Therapy for Filarial Lymphoedema In India BACK TO MAIN PAGE

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PART I The Background










PART II What we have to say














Lymphoedema has been defined as swelling of the soft tissues caused by abnormal quantity of lymph. This definition can be further expanded to include the after effects of this accumulation i.e., proliferation of connective tissue, a variable degree of round cell infiltration, pigmentation and fibrotic thickening of the dilated lymphatics. In long standing cases this results in a firm enlarged limb with hardened skin and papillomatosis justifying the name ` ELEPHANTIASIS' in severer cases.

Lymphoedema is a common clinical problem. In India, the commonest cause of lymphoedema of the limbs is due to Filariasis a disease that is endemic in many parts of our country (Ahuja, 1976). The magnitude of this problem can be seen from the fact that nearly 200 million (20% of the population)live in the endemic zone and more than 19 million, actually suffer from the disease (Ritu Priya, 1994). As lymphoedema is the commonest clinical manifestation of Filariasis (Ahuja, 1976); there exist a vast number of patients afflicted by this crippling disease. Repeated attacks of fever, lymphangitis and lymphadenitis are accompanied by progressive oedema of the limbs. This is associated with fibrosis and thickening of the skin resulting in the hideous looking limbs often called Elephantiasis; a term coined by the Romans two millennia ago to describe the elephant hide type legs of African tribals. The Konark Temple (~ 1298 A.D.) near Puri in Orissa depicts Elephantiasis and Hydrocele so this disease has been with us for at least that long.

The treatment of this disease is the late stages is very unsatisfactory. The common variety of operations done are borrowed from the West, where the common types of lymphoedema are of the primary idiopathic variety (Kinmonth C., 1957). Their operative technique, evolved mainly for treating primary lymphoedema give very unsatisfactory results, when used in our case who suffer from secondary lymphoedema. Unfortunately very little work has been done in our own country to evolve a system of treatment suitable for our type of cases.

The next few chapters outline some what our assessment and experience of this disease. On the basis of a study we did in AIIMS between 1978-1980, we have evolved a treatment methodology suitable for our type of cases. I believe that it is one possible solution to the problem and should be widely used.




As early as 1500 BC, the laws of Manu stated that a priest should not marry a woman with a family history of tuberculosis, epilepsy, leprosy or elephantiasis. The famous sun temple at Konark near Puri in Orissa (~~1300 A.D.) depicts a couple with hydrocele and elephantiasis. Thus this disease has been with us through the centuries.

Lymphoedema was also known in the Biblical times so much so that it was stated in the Deuteronomy : `It was an act of Providence that for all the wanderings of the Hebrews in the desert, not a single case of swollen dough like feet was noticed.( Deut 8: 4)

Hippocrates ( 460 - 355 BC) used to practise scarification for all kinds of oedema including lymphoedema. he term elephantiasis however originated as a Roman soldier slang for the natives of Libya. This was describing the huge elephant hide type legs and scrotums that they saw during a campaign there.

With the onset of Christianity, medicine underwent a decline. No significant progress was made in all diseases including lymphoedema. The next description of this disease was recorded in Persia through the two great physicians Rhages (865 - 925 A.D.) and Avicenna (980 - 1037 A.D.) naming it as elephantiasis arabicum though some of the lesions were confused with leprosy.

The onset of Renaissance finally uplifted medicine from the Galenic traditions with anatomists like Vesalius (1514 -1564). Using dissected human bodies, they made vivid descriptions of human anatomy, instead of drawing conclusions from animal studies. It was at this time that Gaspare Asselli of Cremona (1581 - 1625) recorded the first complete description of lymphatic ducts. Earlier workers had described Intestinal lacteals as well as the Thoracic duct (Fallopius 1523 -1562, Eustachius 1520 - 1574) but with little knowledge of their function.

When Aselius made the first mention of Intestinal lacteals in 1627, his request to Sir William Harvey for a study of this new circulatory system was met with the reply that the latter could not venture into new fields at his age.

In 1653, Ruttbeck described other lymph vessels ( Courtice 1986). He was complemented by Bartholinus (1615 - 1680). The latter reviewed the works of all the earlier workers and was able to bring out a complete description of the lymphatic system. Malphigi (1628 - 1694) further complemented this work with a description of the lymph nodes.

Further work on the lymphatic system has been done by Hewson (1739 - 1774), Winslow ((1775), Penigzo (1785 - 1867), Mascagni (1752 - 1815) and Hemming (1843 - 1895). Sappey's (1810 - 1896) illustrate manual of lymphatic chains is still a classic and fundamental to any approach to the anatomy of the lymphatic system.

John and William Hunter (1835) gave the first description of the function of the lymphatics i.e. to drain the residual fluid from the interstitial spaces.

Demarquay (1863) first demonstrated microfilaria from hydrocele fluid while Wucherer (1866) found it in chylous urine. Lerois (1872) found it in peripheral blood whereas Bancroft (1876) demonstrated adult worms in the arm of a patient with lymphoedema. Manson (1876) demonstrated microfilaria in the blood and urine of a patient with lymphoedema and established Culex fatigens as the vector.

Ziemann (1924) fed dyes to laboratory animals to visualize the intestinal lacteals on autopsy, while direct injection of contrast into lymph channels was first done by Monteiro (1930) and Zhadnov (1932). Hudack and McMaster (1938) injected dyes into the subcutaneous tissue and demonstrated uptake by the lymph channels. Kinmonth and Taylor directly cannulated these lymph channels to inject contrast and hence initiated lymphangiography.

Dinker (1931) studied the chemical composition of lymph and found the protein content to be 0.69 g%. He also demonstrated the existence of lymphatico -venous communication channels outside the main right and left ducts in the neck.

Kinmonth and Taylor followed this up by demonstrating a direct correlation between degree of lymphoedema and its obstructive element against the lymphatic fluid content.

Kinmonth and Stewart described RIHSA studies in 1958 and demonstrated a slowing of clearance in cases of lymphatic oedema against a quickening in patients with cardiac or renal oedema.

Since then, research in lymph, the lymphatic system and its diseases has broadened into many fields. A new subject concerning this, called Lymph ology, has evolved over the past three decades to encompass the wide range of this branch of medicine.

In the next few chapters, we shall, however, concentrate only on a few aspects of Lymph ology, which concern lymphoedema of the extremities and elephantiasis




The lymphatic system consists of (1) lymph capillaries where lymph is formed and collected (2) lymph vessels which carry the lymph to the regional lymph nodes and then into the (3)larger collecting channels, emptying the lymph into the venous system in the neck via the thoracic duct and the right lymphatic trunk.

Micro anatomy

Lymph capillaries consist of a single layer of epithelial cells which start blindly from glove finger like endings or are arranged as a closed network of tubes (Maccullum, 1903). They do not have any basement membrane, and are surrounded by and loosely adherent to collagen tissue (Rusznayak, Foldi and Szabo, 1967). The intercellular junction of the capillary wall has minute clefts with overlapping of the cells to act as flap valves. A small proportion of these can open widely to accommodate fluid as required being held apart by collagen microfibrils which open up very widely. Essentially the structure is the same as blood capillaries but here the holes are more profuse -from 1% to 6% of the capillary surface area. (Casley Smith, 1976, 1980). Their conductivity can go up 100,000 times during activity, injury and edema.(Casley Smith, 1980). The lymph capillaries can distend two to three times of their size and also constrict to make their lumen invisible (Zhadnov, 1952).

Except the smallest lymphatics all other lymph channels have intima, media and adventitia layers. There is a good amount of smooth muscle in the media. This layer decreases as one goes proximally and is absent in the efferent lymphatics of the nodes (Rusznayak, Foldi and Szabo, 1967).

The lymph vessels have unidirectional valves which allow lymph to flow in a centripetal direction.

These valves are located about a centimetre apart to make the lymph vessels appear like a string of pearls.

The lymphatics of the skin are distributed with a profusion equalling that of the blood capillary system. They form networks which are located in three distinct layers (Forbes, 1938). A superficial plexus, situated in the upper third of the dermis and composed of small vessels of uniform calibre which are devoid of valves, an intermediate plexus vessels of varying calibre, also devoid of valves. Lastly, a deep dermal plexus of vessels varying in size and sometimes quite large in calibre, furnished with valves at the junction of the dermis with the subcutaneous tissue.

The epidermis is devoid of lymphatics. Very little is known about the capillary lymphatic system of the subcutaneous tissue. A plexus situated on the deep fascia plane is sometimes described (Crockett, 1965) but not every one agrees with it.

In the subcutaneous tissue, the valved collecting channels run obliquely or vertically within connective tissue strands linked by horizontal arcades. These empty into the main lymphatic trunks close to the deep fascia (Thompson, 1967).

Muscles in the body have no lymphatic supply, but the lymph trunks have been found next to the perimysiam internum i.e. around the blood vessels (Rusznayak, Foldi and Szabo, 1967).

It is believed that there are no communications between the superficial and deep lymphatics (Kondoleon, 1912). Lewis, (1975), reported that the only communication between the superficial and deep system is at the postero-lateral aspect of the foot. More recently this fact has been utilized for doing contrast studies of the deeper lymphatics. However communications between the superficial and deep lymphatics have been found in pathological studies (Wallace et al, 1964, Jackson, 1966).

Lymphatico-venous Anastomosis

The lymph vessels communicate with the venous system only via the thoracic duct and right lymphatic trunk in the neck. However Rusznayak, Foldi and Szabo (1967), presented data to show that the lymph produced in normal circumstances is much more than the amount which drains out via these channels. Also, ligation of the thoracic duct does not stop dye from reaching the venous system (Drinker & Yoffrey, 1941). Lymphatico-venous anastomoses have been described by various authors (Drinker 1930, Wallace, 1966) and hotly denied by others (Zhadnov, 1952). Thus after critical evaluation of the existing data, Rusznayak, Foldi and Szabo, (1967) concluded that there were no lymphatico-venous anastomosis other than in the neck in normal circumstances. However, some degree of lymph might diffuse into the blood vessels at the lymph node level.

Lymphatic-venous anastomoses have, however been described in pathological states associated with lymphatic obstruction (Wallace, 1964 & Gough, 1966). Whether they arise de-novo or by opening of existing channels is not known.

Lymphatic Drainage of the Lower Extremity

Two distinct set of superficial lymph trunks are developed and these are related to the superficial great and short saphenous veins. The great saphenous lymphatics are readily cannulated over the dorsum of the foot and drain into the superficial inguinal nodes (Thompson, 1967). The thigh, however drains via separate channels from the leg (Ngu, 1964) and some of the thigh lymphatics bypass the superficial inguinal nodes to enter in the lower most lateral Iliac nodes (Jackson, 1967).

The lesser saphenous lymphatics, if cannulated in the posterior calf, flow laterally around the knee and lower thigh to drain the superficial inguinal nodes (Larson et al. 1966). If they are cannulated behind the lateral malleolus, the flow is via the postero-lateral side of the calf into the popliteal lymph node and thence to the deep lymphatics of the thigh (Malek et al, 1959).

Lymphatic Drainage of the Upper Extremity

Three groups of superficial lymph trunks occur in the forearm redial, ulnar and median which accompany the corresponding veins (Danese and Howard, 1955).

The epitrochlear gland belongs to the ulnar group only and may drain via the deep system. The lymphatics from the lower two-thirds of the arm, drain into the axilla but some of the lateral lymphatics of the arm may go via the deltopectoral node into the cephalic vein.




Lymph Formation

The present theory of the formation of lymph was proposed by Starling in 1896. He postulated that blood capillary endothelium is a semi permeable membrane i.e. permeable to water and crystalloids and impermeable to plasma proteins. Hydrodynamic pressure induces ultra filtration in the arterial limb of the capillaries. This slowly diminishes in the subsequent section to become lower than the colloid osmotic pressure of the plasma protein. Since very little protein diffuses out, the pericapillary tissues are practically free of them so that the colloid osmotic pressure acts as a force of absorption in the venous limb of the capillary. Thus filtration ceases and the protein free interstitial fluid is absorbed back. However, protein cannot be absorbed by this manner. These and the corpuscular elements are picked up and transported via the lymphatics, which finally empty into the veins.

Under normal circumstances, force of filtration and reabsorption are equal, but if the former is elevated (e.g. venous congestion) or the latter is decreased (hypoproteinemia), it results in a pathological collection of fluid in the interstitial space and increased lymph flow.

Lymph Absorption

The precise mechanism by which lymphatics are able to drain the protein rich interstitial fluid is not known. Initially it was postulated that the intra lymphatic pressure was lower than the interstitial fluid pressure and this becomes increasingly negative as the lymphatics travel proximally (McMaster, 1947; Rusznayak, Foldi and Szabo, 1967). This simple difference in the pressure gradients was thought to be the mechanism for absorption. However, Casley Smith (1976), observed that the lymphatic capillary pressure was certainly atmospheric or slightly above while the tissue fluid pressure was sub-atmospheric. He theorised that lymph absorption is due to the higher intra capillary colloid pressure. Similar views had been expressed by Ruznayak, Foldi and Szabo (1967).

According to Casley Smith, the mechanism of lymphatic absorption is as follows. The capillary holes held apart by the microfibrils open up and allow the interstitial water and dissolved molecules to enter the lymph capillaries. The slowly diffusing protein macromolecules are also allowed to enter. At rest, there is little flow of lymph, at least in the peripheries. A little movement compresses the lymph capillaries to push up the fluid. Simultaneously the openings (which act as flap valves) are shut by any increase in pressure. Thus massage and movement push up the fluid and relaxation of pressure allows more fluid to enter (Drinker & Yoffrey, 1941). However, this does not end here. Pressure also pushes out some of the fluid and crystalloids back into the tissue spaces to decrease the colloid pressure there as compared to the intra lymphatic colloid pressure (Casley Smith, 1976).

Rusznayak, Foldi and Szabo (1967) state that some water and colloid is reabsorbed by the vascular compartment from the lymph vessel to make lymphatic protein content higher than the tissue protein content. Massage and movement promote the vascular absorption of fluid and allow larger particles to diffuse.

Lymph Flow

This is dependent on (Rusznayak, Foldi & Szabo, 1967).

1. Rate of production.

2. Movement passive and active.

3. Negative intra-thoracic pressure.

4. Cisterna Chyli, which acts as a passive heart.

5. Contraction of smooth muscle of the wall of the lymphatics.

6. Arterial pulsations in the deep lymphatics. (Persons and McMaster, 1938).

Mislin (1976) suggested that the cell at the lymphatic junction called `lymphangion' by him was capable of contraction to help the above mechanism. Other forms of active propulsion by the

lymphatics are also proposed though evidence of an intrinsic lymph pump is still rudimentary (Johnston 1989).

The smooth muscle lining the lymphatics has an automatic tone and undergoes spasm in acute inflammation. The loss of this tone may be one cause of edema in paralysis (Rusznayak, Foldi & Szabo, 1967). Olszewski (1980) has suggested that lymphatic flow is determined, at least in normal lymphatics through a lymphatic pulse carrying upwards.

The normal drainage time of lymph from the foot to the thoracic duct is 5 minutes (Lewis, 1975).

Injection of patent blue V into the dorsal web space may be used as an indicator of lymph flow (Hudack and McMaster, 1937; Larson, 1966).


Permeability of the blood capillaries is increased at the site of inflammation. This along with an increased hydrostatic pressure (due to arteriolar dilatation) allows large amount of protein rich fluid to diffuse out. So in inflamed edematous tissue, the lymph capillaries and small lymphatics become strongly dilated and filled with protein rich fluid (Drinker and Yoffrey, 1941). In the later stages, a fibrinous network is formed in the inflammatory area which prevents entrance of fluid into the lymphatic channels. There is associated functional spasm (Foldi et al, 1950) of the lymph vessels. Organic occlusion may result from thrombi in the lymphatic circulation (Menkin 1930,1931) leading to lymphatic fixation. Collagen deposition occurs in and around the lymphatics. Thus lymphoedema patients have much thicker lymph vessel walls than normal.(Rada et al,1983; Rada & Tudose,1986)


From Starlings' theory it is clear that insufficiency of lymph flow will give rise to edema. Rusznayak, Foldi and Szabo (1967) categorised the causes of lymphoedema as following.

I Mechanical insufficiency.

i) Organic (anatomical causes)

a) Occlusion of lymphatics.

b) Extirpation of lymphatics or lymph nodes.

ii) Functional (where flow is decreased)

a) Haemodynamic insufficiency

b) Lymphangiospasm

c) Akinetic insufficiency

d) Valvular insufficiency

II Dynamic insufficiency (i.e. when excessive lymph is formed e.g. Cardiac or Renal edema)

III Insufficiency of absorption

a) Change of protein ?

b) Change of interstitial space ?

c) Change of lymph capillaries ?

When lymph flow is blocked, as also in inflammation the residual protein is immediately precipitated into a fibrinous network (Zimmerman and Takats 1931). Fibroblasts wonder into the area leading to a thickening of subcutaneous tissue, multiplication of collagenous elastic fibres and thus result in non pitting edema in late cases.

Garli, Ibba and Fruschelli (1990) have described a fibrillar elastic network around human lymph capillaries which are disrupted in diseases of the same to cause lymphoedema.

Foldi (1977) introduced the term `lymphatic load' (the amount of lymph formed) and lymphatic transport capacity (i.e. cross section of lymph vessels X lymph flow) to explain the insufficiency of lymph flow and lymphoedema. Casley Smith (1976) stated that of all protein that enters the tissue from the vascular system, 1/3rd diffuse back into the vascular system after being lysed by the macrophages into smaller peptides. The remaining 2/3rd is dependent on the lymphatic system for transport.

Drinker, Field and Homan (1934) felt that a block of the lymphatic system is necessary for lymphoedema. Lymphatics are however capable of regeneration so a simple ligation of lymphatics is incapable of producing lymphoedema. Riechert (1926) sectioned all the soft parts of the hind limbs of dogs, except blood vessels and nerves. This resulted in only temporary lymphoedema. Rigvierre and Valet (1937) proved that this recovery was due to regeneration of the lymphatics.

Experimental lymphoedema, was however, produced by Drinker et al (1934). They injected silica powder in a 25% solution of quinine to block the lymphatics. As the residual lymphatics dilated to accommodate the increased load, several sittings were required. In the final stages, the residual lymphatics were found dilated and tortuous with incompetent valves. The protein content of the lymph gradually rose to 5 gram %. The limb size increased painlessly to result in lymphoedema.

Apparently, that was not all, the dogs subsequently had repeated attacks of erysipelas in the involved limb with fever, redness and increase in swelling, which lead on to increased fibrosis and cicatrization, a condition similar to human `elephantiasis'.

These attacks of streptococcal lymphangitis have a major role in the precipitation of clinical lymphoedema as the resulting inflammation causes further obstruction of the lymphatic system (see lymph in inflammation, above). These attacks are, however, commoner in patients with lymphoedema as it was in the experiments on the dogs above. The occurrence and severity may be used as a prognostic factor and index of treatment in the disease and has been used so by many workers (Thompson, 1967; Miller et al, 1973). They occur more in the secondary forms of lymphoedema, notable of filarial origin. (Rusznayak, Foldi & Szabo 1967). Even Milroys disease, lymphangiectiasis, lymphoedema precox etc. run a high risk of recurrent inflammatory attacks (Ehrlich & Young 1925; Rusznayak, Foldi & Szabo 1967).

However, in early cases of filariasis, attacks of lymphangitis are more due to the worm than secondary streptococcal infection (see lymphoedema in filariasis below) (Pani, 1991, Dandapat 1985). In later stages the worm is mostly dead and very few lymphatics remain to allows reinfection. At this stage the above mechanism promotes perpetuation of the disease.

Overfordt et al (1983) have suggested the possibility of a vascular element in the involved limb. They found evidence of decreased muscular blood flow and venous emptying in cases of chronic lymphoedema.

In late case, following recurrent inflammatory attacks, the skin also becomes thickened and may show papillomatosis, exercrecences, verrucal changes, recurrent ulceration and hyperpigmentation, finally ending in a non-pitting fibrotic solid oedema. Most thickening and tissue distension is found in the dermis and subcutaneous tissue. However some increase in the muscle bulk has also been described recently by ultrasound studies. An increase of upto 75% in cases of Primary Lymphoedema and upto 50% in Secondary Lymphoedema. (Doldi et al, 1992). In the same study, average thickness of the dermis was 3-4mm (Normal 1-2mm). The bulk of the increase was however in the subcutaneous tissue varying between 21 -79% of normal.

It is perceived that lymphoedema may be continuing chronic inflammation. Casley Smith, Clodius & Piller (1980), found evidence of the continuous presence of macrophages and increased collagen formation in experimental lymphoedema in dogs.




The following classification has been proposed by Foldi (1971).

1. PRIMARY FORMS (lymphangiography : Malformation of lymph vessels)

1. Congenital a) Familial (Milroys disease)

b) Non familial.

2. Lymphoedema praecox (appears before age 35 but after age 15)

a) Familial

b) Non-familial

3. Lymphoedema tarda (appears after age 35).

2. SECONDARY FORMS (lymphangiography : Dilated, tortuous lymphatics)

1. Neoplastic lymphangitis

2. Obstructive lymphangitis (infection, filariasis, trichophytosis, tuberculosis, etc.)

3. Degenerative lymphangiopathy

4. Lymph node disease

5. Post traumatic lymphangiopathy

6. Surgical resection (block dissection)

7. Roentgen or Radium therapy

8. Causalgia

9. Paralysis


The adults worms in cases of filariasis localise in the lymphatics and causes blockage of the lymphatic trunks to result in lymphoedema (Lewis 1975). The blockage, is however, temporary as the lymphatics drain via collaterals (Evert et al, 1972; Schaker et al, 1972).

Repeated lymphangitis related to release of microfilaria is however common. Macrophage action as well as release of complement and other inflammatory protein result in blockage of a wider group of lymphatics. In endemic areas, massive infection as well as reinfection by the Filaria worm are responsible for lymphoedema. Occurrence of lymphoedema has been correlated with 1)incidence of microfilaraemia, 2) Immunity especially cellular toxicity to the microfilaria and 3) Age which may be dependent on development of immunity. (Sabesan et al,1991; Srividya et al,1991)

In endemic areas, highest cyto-toxicity is found in those individuals who have never manifested the disease with the next highest being in those with high microfilaria(mf) counts (Thommandru et al,1991). Younger patients and those with high mf counts tend to present with more acute symptoms like filarial fever, retroperitoneal lymphangitis and abscesses(Pani et al, 1990). These and persistent oedema in early cases of B. malayi is reversible with Diethyl Carbemazine (DEC).( Pani 1991).

Boseworth and Adam (1975) found a more severe lymphoedema in cats infected with Brugia malayi if the limb was secondarily infected with streptococci. This however resulted in a lower recovery of the live adults worms at necropsy. They suggested that the super added streptococcal lymphangitis may produce increased fibrosis and lymphoedema, and result in the death of the adult worm.

It has long been recognised that patients with filarial lymphoedema do not have microfilaria in their blood (Iyenger, 1956). Brinkman (1976) found that the incidence of microfilaremia decreased with severity of elephantiasis.

According to Dey & Dey (1980), lymphoedema in filariasis is due to associated secondary streptococcal

infection and absorption of allergen from the worm. The symptoms of lymphangitis are due to

1. Mechanical irritation.

2. Liberation of toxic fluid by the female worm during parturition.

3. Absorption of toxic products or allergen by the disintegration of the adult worm.

4. Secondary streptococcal infection.

Thus the essential feature is blockage of all the lymphatics over a distance of a few centimetres at a certain level or even all along the limb. Regeneration can only occur if the block is over a very short length. This is something similar to the silica powder injection experiment by Drinker. My own estimate is that if attacks of lymphangitis are controlled some regeneration will occur in at least 90-95% of cases. Pani (1991) has already reverted recent oedema (R.O.) and a few cases of persistent oedema (P.0.) with D.E.C. Physical methods e.g. VPL, proper skin hygiene and Penicillin prophylaxis can do wonders for P.O. with skin changes.


1. Repeated infection of multiple lymph channels.

2. Endo lymphangitis of the proximal portion obstructing lymph flow.

3. Dilatation of the distal part of the lymphatics and lymph stasis.

4. Infection and

5. Inability to establish adequate collaterals through hypertrophied tissues.

Filarial lymphoedema is also characterized by dilatation and insufficiency of peripheral lymphatics which occurs before the vessels are completely occluded (Rusznayak, Foldi and Szabo,1967). Danese and Howard (1965)believed that recurrent obstruction and lymph stasis resulted in disappearance of lymph channels. Kromosedirdjo and Portono (1977) however correlated acute symptoms in filariasis to the presence of adult worms in the lymph nodes.


Elephantiasis is common in East Africa, where filariasis is not endemic. Price (1975) attributed this to recurrent attacks of lymphangitis and lymphadenitis and lymphadenitis occurring in barefoot young males in areas with a high silica content in the soil.

In the case, described by Price, the lymph nodes showed fibrotic thickening of the capsule and trabeculae, involving the lumen of the sinuses, less towards the hilum. The lymph vessels were dilated and tortuous in `soft' cases and replaced by fibrous tissue in the `hard ' cases.

Primary lymphoedema may be due to absence of lymphatics (aplasia), less number of lymphatics (hypoplasia) as well as obstruction with hyperplasia of the distal lymphatics (Kinmonth, 1957). There is a suggestion that severe primary lymphoedema is associated with obstruction at the level of the pelvic nodes. (Wolfe, 1984).

In the lower extremity affected by venous stasis, long standing chronic ulceration and fibrosis of the subcutaneous tissue results in a rise of intra lymphatic pressure. This results in recurrent lymphangitis and progressive obstruction of the lymph channels. Lymphangiography can show insufficient filling and sometimes even distal dilatation and valvular incompetence (Thompson 1967).

The swollen arm following mastectomy has been the most researched among all types of lymphoedema. Incidence is directly correlated with the degree of node involvement, lymphadenectomy, the use of radiotherapy and the occurrence of seromas and persistent discharge (Kissin et al,1986). Bates, Levick and Mortimer (1993) recently demonstrated that the interstitial protein content of the edematous arm was less than the normal side contrary to expectations.

Post traumatic lymphoedema occurs secondarily to either infection and cellulitis as post inflammatory (above) or if full thickness circumferential skin loss occurs. In case seen by me, attempted coverage of the loss on the anterior side of the thigh by a graft taken from the posterior side had caused distal oedema. Probably the graft was too thick or the donor site got infected.

In the primary (idiopathic) forms, lymphangiographic changes may be of hypoplasia, aplasia or varicosity of the lymph channels (Kinmonth, 1957; Gough,1966). In the secondary forms (except Causalgia and paralysis) the changes are similar to filariasis but the inflammation is generally less severe. In Causalgia and paralysis there is kinetic insufficiency of lymph flow.





Hudack and Mc Master (1933) used various dyes to delineate the lymphatics of the skin. A radio-opaque dye Iotrolan has been used to delineate them radiologically after subcutaneous injection. (Portsch et al. 1988)

Kinmonth (1952) used dyes to delineate the lymphatic trunks during surgery. Later (1952) he injected diodone into the visualised lymph trunks to develop the radiological investigation of lymphanangiography. Present day techniques use ultra-fluid Lipiodol, a fatty based substance as contrast injected via a special slow injector pump (Thompson, 1967).

Kinmonth (1957) divided primary lymphoedema into 3 groups depending on the lymphangiographic appearance of the lymph vessels. These were in the form of

1. Aplasia, where lymph vessels were either not visualised, or they ended blindly

2. Hypoplasia, where the lymph vessels were fewer in number and thinner in appearance as compared to normal.

3. Varicosity, where the lymph vessels were increased in number dilated, tortuous and also exhibited the phenomena of dermal back flow i.e. the phenomena of retrograde filling in the dermal plexus.

In secondary lymphoedema the changes are of dilatation leading on to dermal back flow, varicosity, tortuosity and obliquity (Lewis 1975).

In Filariasis, the initial changes are of secondary lymphoedema but at a later stage they may get fibrosed and decrease in number. Thus Kanetkar (1966) classified these changes into four groups depending on severity of the disease. Grades I and II showed extensive proliferation, varicosities and collaterals which decreased with severity, In later grades the lymph vessels decreased in number but still exhibition dermal back flow. Thus an elephantiatic limb (gr. IV) showed very few lymph channels. Occasionally a figure of 8 shadow may be visualised, suggestive of an adult worm lying coiled up in the lymph node of lymphatics (Kanetkar 1966, Kromosoedirdjo and Portona 1977).


Jepson (1953) injected I-131 labelled radioactive plasma protein in dogs and concluded that this was taken up by the vascular compartment.

He was, however, corrected by Taylor (1948) and others (Ju, 1954) who found that isotope labelled plasma protein, when injected into the subcutaneous tissues, was cleared by the lymphatics and that its clearance was delayed in lymphoedema.

Hollander et al (1956, 1961) utilized I-131 labelled human serum albumin as a marker to measure disappearance of colloid from the subcutaneous tissue. The clearance of this was significantly prolonged in lymphoedema cases while it was accelerated in patients with cardiac on renal edema. This lead them to conclude that lymphatics were the main vessels to remove lymph from the subcutaneous tissues. They suggested that RIHSA clearance could be used as a marker for assessing the lymphatic function in patients suffering from lymphoedema.

Emmet et al (1967) contested the earlier (Taylor 1958) claim that radioactive plasma protein clearance is increased by physical activity. They also stated that protein clearance is decreased in cases of venous edema also possibly because of a raised protein pool.

Since then, RIHSA studies have also been used as markers to demonstrate improvement in lymph flow after treatment (Harvey, 1969; Gorman and Navarre, 1965; Miller et al, 1973). Harvey found improvement of RIHSA clearance in patients after a Thompsons dermal flap operation and subscribed it to increased lymph flow. This has however been contested by Sawhney (1975). Harvey also predicted that patients with a low RIHSA clearance would respond poorly to treatment. He could not, however, correlate severity of disease with RIHSA clearance.

Miller et al found improvement in lymph flow even though their operations were not destined to improve lymph flow (i.e. they were excisional operations).

Sage et al (1964) used colloidal 198 Au to study lymph flow and concluded that this was better than RIHSA since some of the RIHSA is drained via the bloodstream. They found a 10-18% clearance in the upper limb, 18-39% in the lower limb. This was however, decreased to 0-3% in obstructive lymphoedema. Colloidal Au is still being used instead of RIHSA (Cordiero 1975) as also Tc99 Sulphur Colloid (Stewart et al, 1985). Technicium 99 labelled albumin (99Tc HSA) is used for the same currently and the procedure is called lympho-scintiscanning. (Kataoka et al, 1991)


Crockett (1956) and Taylor et al (1958) found that patients with idiopathic or obstructive lymphoedema had a raised protein content within the tissue fluid. This ranged from 1-5.5g% with an average of 2.8g%in Taylor's cases. Higher levels were found in more severe cases.

Albumin was the main content, alpha-2- globulins were nearly absent and A/G ratio was higher as compared to edema fluid. The electrophoretic mobility in inflammatory states, was however, similar to serum.


The classical clinical index of severity of lymphoedema is measurement of circumference at fixed points as well as direct measurement through plethysmography. Measurements of the limb volume have been used as an index of adequacy of treatment (Van der Molen, 1977; Thompson 1967; Miller 1973). In a comparison of the two, Casley Smith (1994) that in the upper limb, calculation of the volume through circumference is as accurate as plethysmography but the same is unlikely to be true for the lower limb due to the frequent presence of folds in the latter.

Clodius & Piller (1976) described a tonometer to test the hardness of the subcutaneous tissues in lymphoedema.




Lewis (1975) describes the conservative treatment of lymphoedema to consist of Ace stocking, massage and elevation. Foot care and prevention of infection and ulceration is important. Attacks of lymphangitis should be treated early with appropriate antibiotic therapy. In cases getting repeated attacks, one could justify a long term penicillin prophylaxis similar to the prophylaxis of Rheumatic fever.

Diuretics as treatment for lymphoedema were used previously but fell into disrepute due to the toxicity of mercurial compounds. Stillwell (1958) and later Cattle (1965) tried to introduce the thiazide diuretics as they were less toxic.

Rusznayak, Foldi and Szabo (1967) also favoured the use of diuretics but they are effective only in the early stages and their effect, if any, is short lived (Lewis, 1975; Van der Molen 1977).

Dietary restriction of long chain Triglycerides resulted in improvement in an isolated report of two cases. (Soria et al, 1994).

The biggest focus on lymphoedema treatment worldwide was on drug therapy but now the results are more or less discredited and has shifted to manual massage or what is euphemistically called Combined Physical Therapy (CPT)


Coumarin and the Benzopyrone group of drugs were introduced by Foldi and associates (1970, 1972), for the treatment of lymphoedema. Calnan and Pflugg (1972) clinically tried Venolot, a coumarin-rutin compound and found it effective in cases of primary lymphoedema. Boswork and Casley Smith (1972) suggested a useful role of massage and Coumarin in lymphoedema. Casley Smith et al (1972) proved that Venolot acts by mobilising protein from the tissue fluid. This acted on the macrophages to lyse the residual 2/3rds of protein not lysed by them which had otherwise to be transported in the lymph (Casley Smith 1976, Piller 1976).

In experimental lymphoedema in dogs,12.5 mg per Kg of coumarin and hydroxycoumarin was found to be effective. This is a higher dose than normally prescribed to humans.(Knight, Khajanchi et al 1989). There was a worrisome death of one dog (out of twelve) due to bleeding duodenal ulcer.

Venolot is available as tablets (consisting of 25 mg coumarin + 75 mg sodium rutin sulphate) and injections (25 mg coumarin + 25 mg sodium rutin sulphate/ml). This may act via the macrophages also (Foldi, 1977).

Jamal (1989) treated 169 Filarial patients with 400 mg of Benzopyrones per day and found 25 - 40% reduction. Similar results are described from filarial cases in China. (Casley Smith et al,1993.) They are currently described as slow but effective treatment.(Casley Smith, Morgan & Piller, 1993)

Since they act at the cellular level, they have been described as the best conservative solution to lymphoedema (Clodius and Foldi 1990).


In 1948, Joseph Conrad E., an engineer noted that the conventional elastic stocking used in treatment of venous edema resulted in more of folds of the skin rather than convenience to the patient. Later, he found that standing in a swimming pool decreased edema and made the patient more comfortable. He attributed this to the uniform pressure exerted by water. This lead him to manufacture the Jobst elastic stocking, which took into account all the natural folds and contours of the limb. Later, in 1951, he invented on extremity pump which could drive out fluid from the extremity (Brush et al 1959).

Since then, intermittent pneumatic compression, using a mechanical pump has been found useful in cases of mild to moderate lymphoedema (Brush et al 1955, 1959; Stillwell, 1957; Nelson, 1966). The principle of this pump is as follows :-

The limb is covered by a plastic inflatable encasing connected to an electrically operated air pump. A series of valves are pre-timed to give positive pressure to the encasing for a period of 90-180 seconds. This pressure, which reaches systolic artery pressure, is turned off for a period of 30-60 seconds to restore limb circulation. This causes a massaging action as well.

Wakin et al (1955) used a `massaging' pump which applied pressure in a wave form to the limb but they used lower pressure. The pressure waves would travel centripetally. Zelikovski (1986) reported 37%, 41% & 31% improvement in the dorsum, leg and upper portions respectively with the "Lymphapress".

Nelson (1966) recommended intermittent pneumatic compression for post mastectomy lymphoedema and said that an inflatable arm mitt, made of polythene, could be used to relieve residual swelling of the dorsum after the patient was discharged.

All those workers, however, agreed that it will not work in the hard or fibrotic cases of lymphoedema.

Raines et al (1977) have used a new pump a new pump which gives an earlier rise to peak pressure (5 seconds as opposed to 30 seconds) and found better results. They used xero-radiography to grade the fibrosis (0-III) and found that patients with gr. III fibrosis were not improved.

Raines suggested that the mechanism for the effectiveness of Intermittent Pneumatic External Compression (IPEC) as follows:

IPEC increases interstitial fluid pressure so that water is forced hydrostatically across the capillary bed into the venous system. The resulting increase in venous outflow increases further clearance of water and colloid. Existing lymphatic and collateral flow is also augmented in a similar fashion.

Tissue compressibility or compliance affect the pressure head that can develop in the subcutaneous tissue. Fibrotic or ligneous tissue is less compressible, so in patients with advanced fibrosis, the massaging effect of the pump is not so effective. This results in decreased fluid clearance via the lymphatic collaterals or across the tissue capillary.

He suggested that severe venous obstruction and severe subcutaneous fibrosis (gr. III) are contraindication to IPEC.

However we still do not know why mechanical massage works, though Olszewski (1992) recommends it and Clodius and Foldi (1990) don't.

Most western studies on pneumatic compression have been on primary or post mastectomy oedema. In the latter upto 50% reduction has been described in 18/25 cases by Bunce et al (1994), while Wozniewski (1991) described 50%, 40% and 25% reduction in mild, moderate and severe cases respectively.

Van der Molen (1975) used compression in a different form, using a thick rubber tube around the limb in a centripetal fashion to literally drive out the fluid. He emphasised the use of rubber pads around the ankle to give uniform pressure to the normally depressed areas of the limb. The edema there is harder to treat. His mode of treatment requires medical supervision as the period of compression (as well as distal ischemia) has to be rigidly controlled.

The above has currently been modified to bandaging with help of special elastic bandages. Additional use of exercises, elevation and advice on other ancillary measures such as skin care besides compression therapy preferably with the sequential pump are required. Special clinics for this form of now called `Complex physical therapy' are reporting impressive results. (Bihari and Meleg, 1991; Fritsch and Tomson, 1991; Casley Smith & Casley Smith, 1992). Maximum results are available within the first few days. (Rose, Taylor & Twicross, 1993).

A question mark has arisen regarding the use of high pressures and also the use of unilocular (as apposed to sequential) compression. (Jamal, personal communication; 1995). Miller and Seale (1981) used weights to load the limb. They found that lymph clearance increased till 60 mm Hg and then declined sharply so that after 75 mm Hg there was no flow. We have used high pressures with no problems and think they are the reason for our good results (Gogia, 1981).See chapter XII for further discussions on this topic.

Elastic compression with the help of made to size pressure garments, like the original Jobst stocking (see above) is a must for maintenance life long after IPC or any other form of treatment. It may be useful alone also (Okhuhuma 1992). However addition of pneumatic compression even after six months of elastic compression alone results in further improvement. (Swedborg, 1984). Gartier (1983) immersed the limb in mercury to create a pressure gradient across the affected limb as treatment.


The Chinese have evolved their own method of treatment of lymphoedema. This consists of deep delivery of heat to all the edematous tissue. Previously electric heating or warm bandaging used to be done. Currently microwave therapy is being used. Temperatures of around 39-40 degrees are generated in the muscle and subcutaneous tissue. Elastic dressing is helpful as a conjunct. (Okhuma, 1992).

Chang Tisheng et al (1989) have described upto 75% good or excellent results with upto 3 courses of 15 days each. Each therapy session lasts for around 30 minutes in the specially designed oven. Long term results were however not described.

Olszewski has described this therapy as useful in some cases of post surgical and post inflammatory lymphoedema.


Concentrated lymphocytes derived from the patients own blood were injected into the main limb artery weekly by Nagata et al (1994) with impressive initial results. It is a bit early to comment about long term results but the outlook is promising.




As early as the beginning of the 19th century Lisfranc (Cit. Servelle. 1952) suggested scarification of the skin. Caronochan (Cit. Servelle 1952) ligated the external iliac artery of patients with the belief that edema would decrease by decrease in blood supply.

Jaju from Bharuch Gujarat has advocated this in our filarial cases. Though the complication rate (of Gangrene) is low and the limb shrinks remarkably. Recurrence of 70-80% is the main problem of this one time risky procedure.

Handley (1909) used silk threads to act as drainage wicks, embedding them in the subcutaneous tissue draining from involved to non-involved areas. Later on, drainage tubes, polythene tubes, nylon thread, collodion strips have all been used (Walther, 1911; Ziemann, 1951; Degni,1991). The main problem with these is that these implants, may have to be removed because of persistent infection and discharge. Fibrosis anyway occurs around the thread to disallow drainage. Present day interest, is mainly on the use of monofilament nylon (Gorman and Narvarre, 1965; Degni 1977) and that too as a netting woven all around the limb.

Gillies and Fraser(1935) fashioned a pedicle skin flap to act as a bridge of normal lymphatics to drain the involved area. This has, however, been difficult to emulate, due to the technical difficulties of shaping such a flap without tension which has a normal lymph drainage (Lewis 1975). However patients with circumferential scarring as an obvious site of lymphatic block would be suitable for this procedure.

Goldsmith (1966) created a subcutaneous tunnel in the limb and placed a long, mobilized, length of omentum for his patients. The omentum was supposed to serve as a supply of normal lymphatics. Danese et al (1968) and latter Miller et al (1973) found the omentum to be totally fibrosed 3 months after surgery. However, Nylander and Tjenberg (1968) suggested that improvement was due to the excision of the subcutaneous tissue. There also has been a high complication rate in the form of adhesions, bowel strangulation and wound dehiscence.


Howard (1966) and later Olszewski (1968) anastomosed the lymph nodes to veins and showed lymphangiographic patency after 1 year.

However in a recent review Olszewski (1992) agreed that such shunts inevitably block off in a few months. Dr. Jamal & his team from Madurai have been regular advocates of this procedure for Indian patients. Dandapat (1991) describes it as useful as an isolated procedure for early (grade II) lymphoedema. More about this procedure later.

Direct lymphatic vessel to vein anastomosis have since been started with the advent of microsurgery. (Degni, 1973; Cordeiro, 1974; O'Brien 1977). The result depends on the number of vessels anastomosed and these can be used below the block in cases of obstructive lymphoedema. They are not meant for severe cases or where the lymph vessels are hypoplastic (Cordiero, 1975). This is a tedious procedure and not for the uninitiated. A teflon stent to shorten the procedure has been reported (Shaper, Rutt & Browse, 1992)


Charles (1911) excised all the skin and subcutaneous tissues, until the deep fascia and replaced it by a split skin graft in cases of filariasis. The main problem of this operation is frequent break down of the graft with ulceration; weeping, ugly exercresences, pantalooning of the distal portions, as well as recurrence.

Homans (1938)excised the subcutaneous tissue after raising flaps to close them primarily. This procedure is used even now.

Lanz (1909) believed that the deep fascia had a better lymphatic drainage than the skin, so he excised all the deep fascia, and even trephined the bone to improve lymph drainage of his patients.

Kondoleon excised strips of deep fascia while Sistrunk (1917) modified this procedure to excise subcutaneous tissue as well by raising a flap. However, Berthwhistle and Gregg (1928) reported that the deep fascia regrew in 3 months time. The uptake of lymph is due in these patients to the rich vascular bed of the muscle rather than its lymphatic system. This may be the reason via it seems to act even when both the superficial and the deep systems are effected (A.K. Henri, 1921; Peer, 1955). Thompson (1962) described an operation for lymphoedema which involved transposing a flap of dermis with the epidermis shaved off under the deep fascia. He believed that the dermis which is rich in lymph supply would drain directly into the muscle rather than depend on transmission via the subcutaneous tissue. He later (1967, 1971) emphasised on placing the flap on the direction of lymph flow.

The contraindications to his operation were:

1. Extreme obesity

2. Hyperkeratotic warty skin changes

3. Hypoplastic lymph channels

4. Mild cases (i.e. those requiring only cosmetic relief)

Harvey (1969) found improvement of lymph flow (as measured by RIHSA clearance) after Thompsons operation. Sawhney (1974) could not confirm this and said that results were due to excision of subcutaneous tissue only. In 3 patients, he found RIHSA clearance and leg circumference to revert to the same pre- operative level after a gap of 6 months to 2 years. There is a high incidence of sinus and fistula formation due to necrosis of the embedded flap. (Browse, 1986).

Miller (1973, 1975) uses plain excision of subcutaneous tissue undermining from a 1.1/2 inch thick strip of the skin. He used staged procedure for medial and lateral sides. He emphasised on the preservation of the cutaneous nerves. Good results were shown in 6 patients in a follow up of 2-6 years by RIHSA and clinical studies.

Both Miller and Thompson (1967) emphasised on the use of strict bed rest to decrease edema before and after surgery. Miller suggested suspending the leg from an overhead bed frame using a Thomas splint to provide dependent drainage.

Limited excision of the lymph distended tissues has been demonstrated as easily possible with the help of liposuction. (O'Brein et al, 1989).


In recent review Olszewski (1992) summarised the current state of lymphoedema therapy as follows :

-We are nowhere near a complete cure for lymphoedema.

-Manual and machine massage is effective but how, we do not know.

-Lympho venous anastomosis definitely close over time.

-Microwave hyperthermia is effective in some post surgical and post inflammatory cases.

-Antiphlogistin drugs require a proper control trial.




This study was done under the guidance of Prof N.C. Madan during my post graduation in General Surgery at A.I.I.M.S. New Delhi.

All patients with clinical evidence of lymphoedema who attended the surgical out patients clinics of the All India Institute of Medical Sciences as well as patients directly referred from outside, were studied. A special clinic, called lymphoedema clinic was started for this purpose. The period of the study was January 1979 to December 1980 but a retrospective study of the earlier patients who were undergoing treatment during 1978 were also included in this study. A proforma was drawn up to record all the clinical details, investigations, treatment and especially the longitudinal follow up of these cases. All these pertinent details were carefully recorded on this proforma (Appendix I).

The important clinical details were history, examination followed by limb volume and measurement of circumference at prefixed points. Besides routine investigation and nocturnal smear, lymphangiography and RIHSA uptake was done in select cases. Photographs and careful record keeping was the essence of our study.

Treatment was through IPEC therapy using the JOBST pump with additional use of Esmarch bandage in resistant cases. The exact method is described as part of my recommendations (Chapter XII) and need not be repeated here.

Our results are presented in the accompanying tables and graphs.


We had 132 patients who attended our lymphoedema clinic. 120 were clinically evaluated for cause. These results are tabulated Tables I-III as well as figure 1-4.

Andhra Pradesh

3 2.3%


27 20.5%


41 31.1%


9 6.8%


6 4.6%

Madhya Prapesh 

3 2.3%

East U.P.

19 13.9%

West U.P.

15 11.4%

Others (Incl. Afghanistan/Rajasthan 2 each, Nepal/Burma/Guj/H.P./Orissa 1Each) 

9 6.8% 


132 100.0% 

Most of the patients had received some form of treatment elsewhere, before being referred to us. This consist-ed of crepe bandage, leg elevation and many courses of Hetrazan in the filarial as well as in most of the non-filarial patients also. four of these 120 patients had undergone previous surgery outside which was Charle's operation in three patients and Homan's operation in one.

All the 55 patients with filarial lymphoedema gave history of attacks of lymphangitis and fever ranging for 1-2 per year to 3-4 per month. Attacks of lymphangitis had occurred in 16 out of 27 cases of primary lymphoedema. These episodes of lymphangitis were much less common with other causative diagnoses. The occurrence of attacks of lymphangitis pre and post therapy is given in Table III.


90 out of 132 patients underwent compression treatment. Of these 90 patients 42 were of filarial origin. The remaining 28 patients who did not undertake compression included:

1. Those considered too mild to be treated (9 patients).

2. Those prescribed compression but could not undergo therapy. Either they could not stay in Delhi or were given a later date-only 8 patients could be treated at a time- and did not turn up (15 patients).

3. These treated by other modes of therapy (venolot-3, Anti-tumour therapy -1) An additional 14 patients left therapy midway before our protocol could be completed so they were not included in this study.



East Uttar Pradesh


West Uttar Pradesh
















Compression was given for a period ranging from 4 days to 3 months (average 25 days). Esmarch bandaging was required for 26 patients all with initial moderate to severe lymphoedema.


Subjective :-

Though pain by itself was an uncommon symptom; the decrease in limb size resulted in a greater feeling of well being. Walking was made easier. Attacks of lymphangitis occurred during therapy in 8 out of 90 patients (9%). These patients were taken off IPEC fora while and given a course of antibiotics (Penicillin or erythromycin). Compression was restarted after fever and other symptoms had subsided. Four of these eight patients who developed fever during compression had more then one attack and in 2 patients, there were recurrent attacks. These decreased spontaneously by the end of therapy in one patient. In the other patient (I.O.) however, prophylactic long acting Benzathine Penicillin was given once every three weeks with which the frequency of attacks decreased to zero. He has now under-gone surgery and has had no recurrence of problem for over a year.

The pre and post therapy occurrence of attacks of lymphangitis is given in Table IV. As can be seen the improvement is to some extent dependent on the pre-therapy state, but the diminution in occurrence of the attacks of lymphangitis is striking in the patients whose follow-up is available (25 in number). In none of the patients did the frequency of attacks increase in number.

Change in the Skin

Most of our cases of chronic lymphoedema had significant secondary skin changes in the involved limbs. The changes noticed were thickening, rough and course skin, verrucal changes, papillomatosis and some times frank nodularity. Effect of compression therapy on these changes were carefully observed and it was seen that these verrucal changes and the papillomatosis improved considerably but they generally did not disappear altogether. Although Xeroradiography, skin fold thickness or the tonometry of the tissue were not measured, it was seen that the skin became softer gradually and the oedema that was not pitting to start with, now became pitting. Thus the skin could be lifted up and pinched, something which could not be done before therapy. This was considered by us to be a significant change as we could now predict that the limb was responding and would improve rapidly with further treatment. If the limb did not soften initially, we could start compression with the Esmarch bandage incorporating very high pressure, to accelerate the process. In at least 2 patients (E.C. & I.C.) this was the turning point of the treatment.

Classifying the limb into grades I to III according to the degree of subcutaneous fibrosis, table V shows the pre and post therapy condition of the limb of 90 such patients. As can be seen, none of the limbs became harder or of a worse grade than they were previously. In five of our ninety patients, the skin eventually became soft after a prolonged course of compression treatment.

Prev grade

Total (F)






33 (9)






40 (17)






17 (16)






90 (42)





Esmarch bandaging, tied at pressures well above the arterial pressure of the limb was required more for the higher grades of edema. That was on the dorsum and the toes which were generally `harder' than the leg and also more difficult to manage.

If the limb became soft but excess skin folds were left, the patient was considered an ideal candidate for surgery.

Improvement in the limb circumference - leg

Measurements of the limb before, during and after the treatment, were done very carefully and along the same reference points (Appendix I) so as to be clearly comparative. It was seen in the lower limb that decrease in limb circumference at a point was dependent on the initial difference from the normal or uninvolved limb. Improvement was best observed at points 3-4 where an average 5.1 cm decrease was found (in 75 patients with lymphoedema involving the leg).
  Of these 75 patients in 4 cases the decrease was striking and the limb decreased by more than 20 cm representing 75% reduction in the limb size in these cases. The average percentage decrease was 65% of the possible decrease in circumference. The average decrease at reference points 1-2 was 4.49 cm and on the dorsum (reference points A-3), the circumference decrease was 3.52cm.

It was observed that the swelling around the ankle was most difficult to reduce and this did not improve even after adding special foam padding around these area.

Filarial Lymphoedema

























Non Filarial Secondary Lymphoedema



















Primary Lymphoedema













OVERALL TOTAL (No Severe in Primary Lymphoedema)


The thigh showed improvement (Reference 9-14) in all 14 patients who had swelling but the surprising fact was that 3 patients showed decrease in circumference at points 13-16 (2 cm average decrease) despite the fact that the encasing used for compression did not reach these points.

Improvement in limb circumference - Arm.

Two patients had therapy for both arm and leg. Thus results of 17 patients with involvement of upper extremities are available. The nature of lymphoedema in these cases was mainly post-mastectomy or primary lymphoedema. two patients had history and finding suggestive of filariasis (1 patient had concomitant leg edema). Best improvement was seen just above the wrist (points 1-2) an average of 2.5 cm for 11 patients with a maximum decrease of 5.5 cm. Verrucal and skin changes were less of a problem in these patients, most patients being grade I or 0.


This was done in 16 patients pre and post therapy. At a height of 60 cm, the average limb volume was between 10-14 litres in the severe cases and between 5-7 litres in the mild cases. The changes in limb volume decreased between 0.5-4 litres after compression. Representing a 30-80% decrease of that possible after comparing normal and involved sides (av. 65%). Table VII shows limb volume, pre and post therapy, including post surgery limb volume in cases who underwent surgery.


16 patients underwent Radio-Iodine clearance studies. Overall the RIHSA clearance studies showed that prior to start of treatment there was significant delay in the clearance of the diseased side in 14 of the 16 cases. The delay (measured as the difference between the biological T &frac12; of the two sides) varied from &frac12; hr. to 16 hours with an average of 3 hrs. The T &frac12; was between 3.1/2 to 26 hrs. (av. 10 hrs.) on the involved side and between 3

to 10 hrs. (av. 7 hrs.) on the uninvolved side. The difference of clearance between the two sides is significant (P.< 0.05).

The results of RIHSA clearance as well as therapy in these 16 patients is shown in Table VII. Figs. V, VI & VII show the representative graphs of 3 patients who had RIHSA clearance pre and post therapy. The clearance was improved in 1 patient and remained the same in the second patient in comparison to the contralateral limb.


A few representative pre IPEC, post IPEC as well as post surgery photographs are given.

As the photographs were taken under strictly similar and comparative conditions, at all stages of treatment, these served an important evaluable parameter of improvement. Representative photographs are shown in Figs. VIII to XV confirming the good results achieved.


Surgery was done in 12 patients. The aim was to remove the excess skin, diseased subcutaneous tissue and the smoothen out the folds. A detailed study and follow up data of these patients is given in Table VII. Three patients out of 7 who had surgery on the foot had flap loss on the dorsum of the foot which required split skin grafting This did not make any difference to the final result. Another three patients out of 12 who were operated on the leg had a minor flap loss on the leg which was treated conservatively. 2 patients had a chronic lymphatic fistula which closed spontaneously over 3-4 months. The post op. hospital stay was between 2 weeks to 2 months (av. 23 days.)


Follow up of non operated cases for 1 year is available for 13 cases. The occurrence of attacks of lymphangitis dropped strikingly as shown previously. Recurrence of edema upto 30% of the original decrease was seen in 9 patients (69%). This edema was of a lower grade than before. Subjective improvement was present in all these 13 patients. Recurrence was related to lack of care in using an elastic stocking which got torn or was found uncomfortable due to sweating etc. These patients required further compression therapy albeit of a far shorter duration. Another stocking was prescribed and they could be sent home much improved.


Tables VIII, IX & X show the overall results of compression in our patients. These are all immediate post therapy. As can be seen the best results were obtainable in patients with filarial edema.

The criteria for classifying response to be excellent were:

1) More then 75% possible improvement in leg circumference.

2) Limb volume decreased by more than 75% possible.

3) Subjective well being.

4) Decrease in number of attacks of lymphangitis to less than one year.

5) Significant softening of the skin texture.

Improvement was classified as good if :

1) Relief of limb swelling between 50-75% by measurement of limb circumference and limb volume.

2) Softening of skin texture upto grade I.

3) Rest same as above.

Improvement was classified as fair if :

1)Relief of limb swelling between 25-50% by measurement of limb volume and circumference.

2)Change in grade to at least 1 degree below the previous one (i.e. gr II to gr I).

3)Decrease in attacks of lymphangitis.

Improvement was classified as poor if:

1) Less than 25% improvement in edema.

2) No change in limb grade.

3) No decrease in attacks of lymphangitis.

For a better classification of the type of improvement we got, we had further classified the initial stage of lymphoedema into mild, moderate and severe.

The criteria for calling it severe were (any one or more of three).

1) Gr. III skin changes.

2) Attacks of lymphangitis greater than 1/month.

3) Limb circumference more than twice the uninvolved side.

The criteria for calling it moderate lymphoedema were

1) Gr. II skin changes

2) Limb circumference more than 50% of the uninvolved side.

3) Attacks of lymphangitis 2 or more per year.

The criteria for calling it mild lymphoedema were

1) All cases not considered moderate or severe.

Patients with very mild edema i.e. less than 10-20% increase in limb circumference did not receive treatment with IPEC and hence were not considered here.


* 132 patients of lymphoedema were seen in our clinic between January 1978 to December 1980.

* 120 patients were etiologically evaluated of which 55 were of filarial origin.

* 90 patients were treated with Intermittent External Pneumatic Compression of which there was an excellent response in 35 (39%) good response in 44 (49%) while 3 (3%) responded poorly.

* 12 patients of these 90 required a simple operation to neaten residual skin folds. There was a 50% minor complication rate but no significant morbidity or mortality.




I would like to quote verbatim here from what I wrote at the end of my thesis: ROLE OF PNEUMATIC COMPRESSION IN THE INDIAN SET UP

`The Jobst Institute, IPEC pump can easily be manufactured in India as it consists of an oscillating timer connected to the valves of an electrically operated pneumatic pump. The elastic stocking, however is expensive but is necessary to prevent recurrence. Recurrences are present, but they are mild and can be adequately treated by further compression.'

`Thus this pump can be a useful adjunct to the National Filariasis Control Programme (Parks 1979) since no prevention programme can succeed without promising cure for the disease. These pumps can be kept in various PHCs (Primary Health Centres) or sub centres in endemic areas. Compression can be given to the local people who are afflicted by this dreaded disease which causes more morbidity than mortality. It requires a great sacrifice for people to leave their homes to get themselves treated. Local PHC level treatment is possible. A doctor only needs to initially evaluate these patients and review occasionally in between as the procedure is painless and free of complication except for exacerbation of occasional attacks of lymphangitis. Use of the Esmarch bandage, however requires trained supervision and thus patients with severe disease can undergo this treatment only in a hospital under expert medical care. Such patients with severe disease would generally require surgery which can be done at any small surgical centre after compression treatment. The surgical treatment prescribed by us cannot be surpassed for its simplicity. Any general surgeon with no experience of plastic surgery can perform this operation.'

`Thus we suggest that its about time we took care of patients with the wide spread malady of filarial lymphoedema, suggest a suitable simplified methodology of treatment for doing so which can easily be used on a mass scale. '

What I wrote had always been at the back of my mind. The real trigger to start came when effective pressure garments became available. This gave me the stimulus to start making the machine.

Initially Mr.Vimal Seth and Mr.Sunil Sharma were involved in the project. Progress was slow but by early '93 our first prototype was ready. One patient agreed to undergo the daily therapy sessions. Usual teething problems occurred. The most difficult was when the encasing just ripped open from the zipper end. Despite all the hurdles she was reasonably satisfied. But for us it was back to the drawing board.

By now we were getting quite a few inquiries about our machine and the method of treatment.Mr. Atul Kumar had included information about our venture in his famous Doordarshan programme Turning Point. He told us about DEBEL i.e.Defence Bio Engineering and Electro medical laboratory a DRDO unit located at Bangalore.

Just one letter to Dr.A.P.J.Abdul Kalam and to Dr.T. Lazar Mathew and the encasing was ready through their good office-so much so that the letter to Dr.Kalam was written on 16th Nov. and our sample garment was being demonstrated in Cuttack on 26th December for ASICON '94.

We still have a long way to go. This machine works is what is being felt by my patients. The biggest test of whether this will work on a larger scale -will many more doctors with their own beliefs take up this treatment methodology and get the good results that I am claiming is the final proof of the pudding.

This idea was presented by Dr. N.C.Madan in 1983 at the 7th International Conference of Plastic Surgery in Canada. Since then occasional reports of it have appeared. Dr. Jamal & his team have simultaneously been working on Nodo Venous Shunts. They have formulated a wonderful regime which is as follows :

A Nodo Venous shunt is done under local anaesthesia. The limb deflates. Fluid gets absorbed but excess skin is left behind. This excess skin is then removed surgically by exactly the same method as what Dr. Madan advocated. Only it is much faster. However currently with the use of continuous compression (18 to 22 hours per day), we can obtain similar results with compression alone.

In a debate on the pros & cons of both the methods i.e. of Dr.Madan & Dr.Jamal whether prior reduction of fluid should be through Pneumatic Compression (VPL) or Lympho Venous Anastomosis(L.V.A.) the consensus was that both are applicable However since L,V.A. requires specialists with experience of this procedure while V.P.L. just depends on the availability of the machine the later is more applicable on a wider scale in our country. No one denies that looking at the vastness of the problem both should run concurrently.

It is the viability of this V.P.L. method that we can send this machine to each patient or his locality. Not all of them will require surgery so every local practitioner can install the machine to treat his patients. Recurrence is there with both the methods, but with V.P.L. the beauty lies in the repeatability. Besides it is non invasive, painless and would expectedly have a higher patient acceptability.

If one looks at the way health care is administered in this country :

- Most males go to work in the daytime and have time to go to the doctor only late in the evening. Females generally have time after the husband has gone to work. If the person requires hospitalisation one or two people and sometimes the whole family accompanies him to the city at great cost and sacrifice from their work. Thus our population can spare time for 3-4 hours per day for treatment for months on end. Hospitalisation they try to avoid unless there is no alternative.

In this scenario too, V.P.L. scores over L.V.A.. Besides it is theoretically possible to prepare the limb for surgery or pressure garment faster if continuous therapy is used as shown by other workers. Whether it will give results as good as ours, only time will tell.




What is the basic concept of pneumatic compression :

The limb is enclosed in an inflatable encasing which is then pressurised with compressed air. The air flow to the encasing is controlled through a series of valves which are controlled through timing devices. The encasing is pressurised for 150 -180 seconds and then, to restore circulation, this pressure is dropped to zero for 45 - 60 seconds.

Current machines available abroad are more user friendly in the form that the timers for switching the pressure on and off are preset at 90 seconds on and 30 seconds off.

We had used a machine with four outlets with adjustable timers for each of the outlets so that each patient could receive the exact pressure that he would require. Also the machine could give pressures upto 150 mm of mercury which again could be individualized for each patient.

Recently our request to the company for a similar machine was met with the response that currently those models are obsolete. Also they no longer recommend pressures higher than 60 -80 mm Hg for pneumatic compression. In fact none of the machines available abroad provide pressures higher than 100 mm Hg. However we never had any reason to regret the use of pressures that current European and American manufacturers are shunning from. None of our patients have had any problem pertaining to the same. On the other hand, we have frequently adding Esmarch bandage therapy in addition to the above, which means that pressures of upto 250 mm Hg are certainly not harmful.

Thus the basic design of the machine consists of an air source supplying the required pressure of upto 160 mm Hg. A timer switched this air source on and off along the circuit we had to incorporate a pressure control device which could decrease the pressure if required. A gauge to indicate the transmitted pressure was the only other part besides the usual switches and tubes etc.

The Encasing has many specifications :

a) It should be appropriate to the size of the limb.

b) All the material used should withstand the required pressures including the base material, the seal, the zip, as well as the stitching thread.

c) Design of the encasing -Our initial leg samples had a 90o turn at the ankle. We were thoroughly unsatisfied with this design because of many reasons 1) Fitting a proper zipper which could turn 90o was difficult and 2) Pressure transmission to the ankle and dorsum could not be possible.

The solution was to decrease the angle of turning at the ankle to 60o and leave an open ended zip all along. This has worked very well.

Inserts One will get patients and limbs of various sizes. Manufacture of even one design meeting the above specifications is a labourious process and economy of scale matters.

Too small an encasing will not work as it cannot be completely zipped up. Too big an encasing cannot transmit the requisite pressure. So a system of inserts have been devised. These are attached to a standard sized encasing to maintain flexibility as well as uniformity. (see diagram)

There are 6 standard encasings for the leg and 3 for the arm. However among our millions of patients the range of limb problems is very large. One particular encasing will work less effectively if too loose and not at all if too tight to be completely zipped up the leg.

The other problem is that after the onset of therapy the limb starts thinning and changing shape. A previously effective encasing becomes less effective than a tighter one.

It was then decided to use a range of inserts which are zipped in between the ends of a normal encasing using the principal of open ended zips. However inserts have one basic problem. They can be zipped up only all along the limb. The problem of localised collections of fluid is found in around 50-60% cases of massive gr III edema. So frequently one faces the problem of the encasing not fitting at a small segment of the limb only. The best solution for this is to use an Esmarch Bandage over this localised area for a few days till it decreases enough in size to allow fitting of the encasing.

The insert is of the same length as the main encasing with open ended zip on either side. It is zipped up on the front side of the main encasing. Two or three sizes would be required for Indian patients.

The average normal Indian mid calf circumference is 25cm(dia 8cm) and thigh is 50cm(dia 16.5).

In lymphoedematous conditions, calf circumference may vary between 35-40cm (dia-12cm) to up to 85cm(dia 27cm).

A normal encasing has a circumference of 55cm i.e. a diameter of 17.5cm. Whatever the outer diameter of the inflated encasing- to maintain complete pressure transmission its inner diameter should be capable of reaching zero. Although this encasing works well in the smaller limbs, larger limbs will require bigger encasings. Inserts are useful here as the basic encasing design then does not require to be changed.

Also as the limb circumference improves, one an progressively keep using a smaller encasing by simply using a thinner insert. The goal being to use no inserts towards the end of therapy. Upto three insert sizes will be required for our patients with widths of 5, 10 and 15 cms at the calf level. These have to be gradually tapered, widening as one goes to the thigh.




As stated above, we have never had to regret using upto 160 mm Hg pressure while current machines available abroad have stopped their manufacture. Probably they have run into problems due to litigation etc. from sufferers of Post mastectomy or venous oedema. Higher pressures are not recommended for these patients. However we should not lose sight of the fact that our patients suffer from Filarial lymphoedema and they require pressures much higher than the above.

The results of Miller (1981) after compressive loading suggested that more than 75 mm Hg pressure may actually be harmful as lymph flow thereafter is nil. Most clinicians have a similar experience as even a tight crepe bandage can result in distal edema. While not denying this premise, what we have to re- emphasize is that a) this is seen in otherwise normal tissue, b) the lymph accumulates slowly and certainly not over the two or three minutes. c) The slow rise and fall of pressure during IPC ensures that higher pressures occur only for a very short time and d) There is a subtle difference between use of pressure directly (as in Miller's test) and circumferentially at least in a limb which has fibrosed skin and subcutaneous tissue. e) Nutritive circulation of the tissues in lymphoedema is normal or even may be enhanced (Solti et el, 1986). Another reason why they can with stand higher pressures.

If we go back to the pathogenesis of lymphoedema, the main components in this condition are tissue fluid and fibrosis. Pneumatic compression works through pushing excess fluid back into the vascular compartment though the exact route of transport is uncertain. What makes our patients different from other lymphoedematous conditions is in the amount of fibrosis. It is this fibrosis which acts as a pressure block and absorber.

Most of the fibrosis is in the dermis and this is what results in the secondary changes of verrucae, warty outgrowths and papillomatosis etc. Fluid is more in the deeper areas i.e. the subcutaneous tissue and the deeper dermis. Due to the circular arrangement of the skin in the extremity the fibrosis in the same is also arranged circularly. Fibrosis is unaffected by pressure and a circular arrangement of the fibrosis presents something like an arch effect (see diagram). Though the exact differential of pressure across this arch is a matter of conjecture due to the absence of a proper measuring technique, that it exists is virtually certain.

One has to titrate the exact dose of pressure to the individuals requirements according to the benefit and the tolerance. Pain should not be allowed to occur. In a really fibrotic limb, one will see the appearance of pitting even though initially one had not expected any results. Even if we do not as long as it is not done in active infection, no harm is caused by such a trial.

Venous oedema has a higher fluid component while post mastectomy oedema presents very early to the clinician. Thus fibrosis in both these conditions is very low. Thus higher pressures are not easily tolerated by these patients. We should not withhold the benefits of higher pressures for this reason as our cases are different and do require high pressures.

We have also the results that others have just not shown. Every where lymphoedema is quoted to be not treatable if it is severe, and mild cases do not require any more compression than can be provided by a simple pressure garment. We have found that higher pressures are required for these very severe cases if at all to prepare the limb for surgery. The key is to push out all the fluid component of the swelling and excise the fibrotic excess skin.

Excess fluid is the reason for post operative infection and the consequent ill effects. Squeezing out the same results in better postoperative results besides shortening the preoperative preparation time of suspending the leg for three to four weeks from a roof bar. Not to mention the inconvenience of the same. A high pressure stocking is a must as a follow up.

Sequential pressure through the "Lymphapress" (Zelikovski, 1984) has been quoted as a better replacement to Van der Molen's therapy (Gruffaz, 1981) but Zelikovski's own results have been quoted at 37% improvement of volume at the ankle; 41% for the leg and 31% above. Our results are much better with a much cheaper and simpler machine.

We still do not know however that how does it work. Here I am reproducing the comments of Mr. Jay Choudhary of the Deptt. of Biomedical Engineering, IIT Delhi, who has done lot of work on cellular and tissue energy levels.

"With Compression, Boyle,s law comes into play. For gases as well as liquids, the volume is inversely proportional to external pressure. Thus at twice the atmospheric pressure a gas occupies half the volume. Compression of the limb causes decrease in the free gas volume inside the limb along with a proportionately less decrease in the liquid volume. This disturbed or new equation causes alteration of intra lymphatic osmotic pressure and interstitial tissue fluid pressure. Accordingly higher pressures result in faster decrease of limb volume. Probably graded rise of pressure every 30 seconds would be better."

"The alteration of the colloid osmotic pressure is due to something called the Donnan effect which graphically defines that rise in pressure has a sine wave effect on protein concentration. Change in the protein concentration causes accompanying leaking out or absorption of H2 O."

"Pumping by lymphatic system is the basic cause of negative tissue fluid pressure. When available fluid (as leaking from the blood capillaries) is very slight, then the lymphatic capillaries can actually pump a slight intermittent negative pressure, reflecting the average negative pressure observed in loose tissues."


"In many places in our body, connective tissue is absent. Here tissues can glide over each other but they are held together with the help of the vacuum like state of negative interstitial tissue fluid pressure which is partially vacuum. When pressure is applied, tissues regain this negative pressure which may have been lost due to fluid accumulation."

"External compression causes pressure on the tissues. This pressure rise causes increase in available energy in the tissues due to decrease in volume. Thus pressure results in rise of localised temperature. [t1-t2 : t2-t1 = +^t]. Rise in temperature causes increase of biological entropy i.e. the relation between various molecules like proteins, Na+, Mg+, fats etc."

"Entropy change may be defined as amount of heat absorbed isothermally and reversibly divided by the absolute temperature.

^S = q/T

where ^S = change in entropy

T=Absolute temperature

& q = amount of extra heat available due to pressure.

Every system tends to minimize free energy via entropy.
 Gibbs Free Energy G = H - TS

Where H = Heat Content

T = Absolute temperature

& S = Entropy

.:. ^G = ^H - T^S
 Thus decrease in free energy of a particular system is a measure of the useful or network during the change."
 "Increase of tissue temperature and available tissue heat releases pyrogens from the WBCs. This activates the macrophages to eat up extracellular fluid protein and restore the negative tissue pressure status."




The elastic socking was invented by Joseph Conrad. E. in 1948 (Brock, 1960). The role this has to play is that it enhances the action of the natural pumps of the body. Activity of the calf and thigh muscles create a massage effect on the lymphatics. The subcutaneous and dermal lymphatics are ordinarily unaffected by the `massaging' action unless external support is given by crepe bandage or elastic stocking.

Though the crepe bandage is cheap and easily available in India, it is hard to apply correctly and especially difficult to maintain in position. Dr. Dasmahapatra (Personal Communication) maintains that a properly applied crepe bandage for six months is the only treatment for elephantiasis besides routine measures. He admitted that self training of the patient was essential (and not always successful) regarding proper usage.

Dr. Tambwekar and his team from Bombay are using an elastic bandage which is cheap and fairly effective. A proper velcro grip has been ingeniously designed for fixation at the proper level. Training is however required for proper use which most patients do acquire over a period of time.

Having no experience in this regard we have discarded crepe bandage almost completely. The only good ones, made by Johnson & Johnson are not exactly cheap. The headache of training remains. After all it has to be worn several times a day for months on end. Too tight even in one turn can be disastrous causing distal edema and pain, while too loose is ineffective and very uncomfortable. The only place we still use it is in between VIPEL therapy sessions, utilizing there flexibility of fine tuning it each day to the patient's current limb size. Even there the cheaper stockings are a better substitute.

The elastic stocking, though expensive, once made to proper size is easy to retain in place after an easy application. Pressures used for lymphoedema are around 60 mm Hg which rise to 120 mm Hg during muscular activity. (Van Der Molen, 1975). Such pressures do not affect the circulation because they are absorbed by the fibrous subcutaneous tissue and dermis. There is a similar arch effect involved as described for the pump (see Chapter XII).

Residual or persistent oedema greater than grade I will not be helped by the stocking alone as they require higher pressures than available through the stocking.

Excessive folds in the skin work against proper pressure transmission by the stocking and they should be properly trimmed by surgery before using the stocking which, obviously should be made to the patient's final reduced size.

The original JOBST stocking supplied to us was made out of lycra, the wonder stretch fabric (from DuPont) which is used for skin tights. This is a woven porous fabric which is easily worn and removed.

The main problems faced in our situation for this fabric were:

a) High cost as well as the cumbersome procedures for arranging foreign exchange in those days.

b) Delayed delivery almost six weeks used to elapse before any hopes for delivery.

c) This wonder material was not exactly suited for our Indian weather.

We have shifted to micronised cotton (MICRA) which has the same properties of stretchability and skin hugging characteristics. In addition it is absorbent and is thus more skin friendly. Being thicker it lasts longer. It also has the advantage of being stretchable in both the directions which helps in preventing wrinkles around folds and especially on the anterior side of the ankle if it is well designed. The last point has so far been a very sore point mitigating against continuous use. The previous material was stretchable only transversely, resulting in uneven pressure transmission.

Indian patients are barefoot most of the time so the thick material makes it fairly cheap due its long life. Initial cost roughly is the twice of the cheapest cotton based stockings. Although the basic material is imported, stitching is done locally. Thus it is far cheaper than the original stocking and can be made available faster to the patient.

A tape to allow easy measurements and subsequent customized stitching has been made.

The garment should be worn throughout the working hours and removed only for therapy, bathing etc as well as while resting. During rest hours the leg should be kept elevated and daily exercises are must. A pair is recommended so that daily washing and cleaning of the garment can be done. A special foot mitten made of silk is provided to facilitate easy wearing.

Due to its tight feel, it is not exactly comfortable, so the patient has to be explained accordingly.




Some what similar to what we did is what I am recommending. This can be done individually or through a special clinic. The latter will be preferable in endemic areas or referral centres.

Detailed history and examination are done on the patients very first visit to the clinic emphasising on reaching a clinical diagnosis. The lymphoedema can be classified as filarial in origin after considering the following points :

1. Geographical history.

2. Previous diagnosis and treatment.

3. Occurrence and severity of attacks of lymphangitis.

4. Age of onset.

5. Absence of any other cause for lymphoedema.

The diagnoses are made along established criteria given by Kinmonth (1960).

The patients weight, height, site and severity of lymphoedema along with associated skin changes is noticed. The limb is then clinically categorised into grades I to III according to the amount of secondary changes as well as clinical assessment of tissue resistance.

Thus grade I is 1) significantly pitting edema 2) no associated skin changes.

Grade II lymphoedema is 1) mildly pitting edema 2) a little scarring, verrucal changes and papillomatosis restricted to the toes and distal part of foot.

Grade III lymphoedema is the term used for 1) non-pitting edema, which cannot be pinched up with 2) marked pigmentation, scarring as well as papillomatosis, exercrescences and verrucae.

Associated conditions like hydrocele, epidydmo-orchitis, lymphadenitis, congenital diseases etc. are recorded.

The occurrence of attacks of lymphangitis are noted separately as a prognostic factor to judge adequacy of treatment.

A routine haemogram and urine check up is done in all patients. Certain other investigations done are as follows :-


As measurements of the limb under treatment are of paramount importance in this study, a system has been devised to evaluate the limb circumference by serial measurements at fixed points. These points are placed at 4.5 to 6 cm distance and are given reference numbers. Thus the ankle is point 1. measured across the heel. Distally, foot points are referred to as A,B,C & D, each being 4.5 cm apart. Proximal to the ankle i.e. along the leg itself, similar points at 6cm distance were designated 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, etc., going superiorly. The tape used for measurements of the stocking does adequately.

Using a tailor's measuring tape, the limb circumference is measured along these fixed points and recorded on the proforma in a chart form (Appendix I). The limb circumference is measured prior to treatment and thereafter every week or fortnight, these are repeated at these points to assess progress. Improvement can then be suitably quantitated in all cases. Circumference of the uninvolved limb is also measured to index severity of disease as well as to assess the goal for therapy.

These measurements are also used for follow up after surgery and compression treatment.


A large acrylic glass or G.I. sheet tank is constructed measuring roughly 30 x 30 x 80 cm in the inner surface. The top of this tank is left open. Nozzle outlets are placed at heights of 70 or 75 cms., which can be closed at will. This tank should also have a lower outlet nozzle which is normally kept closed so that the tank can be emptied if not in use.

Place this tank in a secure tiled enclosure to avoid inadvertent tilting and spillage while in use. Also this enclosure should have enough standing space to facilitate introduction of the limb.

The tank is initially partly filled with water. The patients are asked to stand with the involved limb placed in the tank, ensuring that his toes, metatarsal heads and heel all touch the floor of the tank equally with the knee fully extended. Excess water is allowed to run out via the 70 cm outlet or more is filled up as required. After the water level stabilizes at 70 cms, the limb is with drawn after closing the outlet nozzle. The fall in water level is measured after the water level is stable. The limb volume thus represents 30 x 30 x A1 c.c., A1 being the fall in water level. This limb volume is measured volume up to a 70 cm height of the limb and can not be used for comparison between different patients. This is used to assess results of therapy and as such is serially monitored after V.P.L. therapy, surgery and during follow up.


Test for filariasis & for other diseases are done as routinely prescribed. Nocturnal smear preferably using some concentration technique (W.H.O. Tech. Rep Series 542) is important as filariasis should be treated in all cases with active disease.


Clinical photographs of the healthy and the diseased limbs before, during and after the treatment, are taken. This is one of the most important modes of recording the progress, meticulous care is taken while taking the photographs. The distance of the camera and the exposures should always be identical as well as the views taken. This includes one straight view and one lateral view of the legs. In all cases, name of the patient and the date of the photograph is displayed on the limbs.


The following are expensive tests useful only for research centres.


Radio iodinated human serum albumin (obtained from BARC, Trombay)

is used. (Tc99 labelled albumin may also be used). The former incorporates I-131 as a tracer and is used to asses the lymphatic function (Hollander, 1968). The half life of I-131 is 192 hours. The activity of the RIHSA depends on its aging. An average of 10-15 micro-curies of RIHSA is injected subcutaneously (0.2-0.3 ml suitably diluted to requirements) in the 1st web space of each affected limb as well as the contralateral limb.

After the injection, the limb is placed under a gamma camera counter (Phillips India Ltd.) readings are taken at the point of maximum activity as measured with the I-131 10 cm diameter sensor. Background radiation is subtracted. The point of maximum activity is marked with gentian violet and readings repeated hourly for both the limbs at the point of maximum intensity marked previously. These are recorded till the counts dropped to below 50% of the first 3 readings.

The readings are tabulated on a semi-logarithmic graph against time and the slope and the biological T &frac12; of each limb calculated from the graph. RIHSA clearance is measured in both the involved and normal limbs before and after the treatment.

Lympho-scintiscanning is somewhat similar only a different dye is used (Tc99 labelled sulphur colloid). This can be traced into the lymph nodes to obtain photographic evidence.


Lymphangiography need to be done only in selected cases where the diagnosis is in some doubt. If planning a Lympho -Venous anastomosis in a primary lymphoedema patient, it is essential.

However ultra fluid lipiodol has to be imported at great cost and the slow injection syringe is not easily available. So this procedure has fallen into disuse. However injectors can be borrowed from Thalassaemia centres where it is used it for Desferrioxime. It is not mandatory in filarial cases where the block is invariably beyond the groin. B. malayi infestation some of whom may have a lower level block are found in only 2% of our cases.


Contrast Medium

Oily Lipiodol ultrafluid. (Glands and lymphatic vessels opacified.) Vol. used=7ml max per side-leg, 4ml-arm).

Water Soluble Hypaque 45, or equivalent. Only lymphatic vessels are opacified.) Vol.used =10 ml.

Equipment 1.McCarthy disposable lymphogram needles (30G).

2.Motor-driven or gravity pump injector.

Patient preparation

1. Leg must be elevated for 24 hours prior to the procedure, and severe cases may require a compression bandage so that the lymphatics may be cannulated more easily.

2. Children under 10 may require a general anaesthetic.

3. The patient micturates prior to the procedure.

4. It should be explained to the patient that the urine may be blue for a few days after the procedure.

Prelim X-rays 1.PA Chest 2.Supine abdomen

Position Supine


1. 2ml of 1% Lignocaine is mixed with 2ml of Patent Blue dye. Of this 0.5 is injected in the medial 2 web spaces of each side.

2. The feet are exercised for half an hour until the lymphatics are visible on the dorsum.

3.Under sterile precautions the skin over the lymphatic is anaesthetized and incised transversely. The lymphatic is isolated with ties.

4.The McCarthy cannula is flushed with saline to exclude air and to check patency.

5.Cannulate the lymphatic.

6.Aspirate to check for venous cannulation.

7.Make a trial injection of water soluble contrast and check for characteristic pain of lymphatic injection. Also inject saline to exclude extravasation.

8.Perform the same procedure on the opposite side and start injection at the rate of 2 ml per minute. Stop for pain (due to extravasation or dermal back flow).

9.Terminate the procedure once the maximum dose is reached or the dye reaches L3 level.

10.Remove the needles close the skin and take X-rays as required under fluoroscopic control.



All the patient clinical details and investigations are carefully recorded in a special proforma. After this the patient is started on a course of V.P.L. Therapy.

This is through electrically operated device which supplies compressed air at desired pressures to a special limb encasing made of a special polymer. Pressures used varied from case to case being guided by the solidity and firmness of the edematous leg. Generally these varied from 90 to 160 mm. The pressure is maintained for 60 to 180 seconds and then released for period of 30-60 seconds. The cycle is regulated by a special electronic circuit.

Before starting therapy a careful clinical examination is done by the physician in charge. The skin condition, grading of lymphoedema and the presence of secondary infection are used as guidelines to prescribe ancillary treatment (e.g. anti -fungal) as well as the type of therapy. Thus higher grades of lymphoedema would require higher initial starting pressures. Antibiotics would be required pre-therapy in most instances.

Other systemic diseases especially those contributing to oedema should be specifically sought for. Diuretics will be required in these cases. Patients with very large limbs have lost upto 2 Kgs of weight after the very first therapy session. This is secondary to redistribution of fluid to the body and thence excreted through the kidneys. A patient with Congestive failure or Renal problems may go into pulmonary oedema if one is not careful.

Generally the compression therapy is given for 3-4 hours daily. The treatment should be supervised by a trained technician. This is best done in the outpatient department or physiotherapy clinic. Since these patients will be there for 3-4 hours at a stretch, an effort should be made to keep them occupied by doing something useful. General atmosphere can be brightened up by music or television. A sincere effort should be made to inculcate a sense of team spirit and unity, if many patients are undergoing treatment simultaneously.

Results of this treatment are monitored regularly and carefully recorded in the prescribed proforma. Clinical assessment, limb volume and photographs are recorded. Measurements as described above are extremely important. All these should be done by the same person each time preferably the trained technician.

If any of the cases develop acute lymphangitis during this therapy, then compression is discontinued for a while, till the attack has subsided. Treatment of acute lymphangitis consists of rest and antibiotics, mostly penicillin or rarely doxycycline. Lincomycin injections o.d. for three to five days are a reasonable alternative (watch for diarrhoea). D.E.C. may be used in R.O. (Lymphoedema of recent origin).

At the end of each days compression therapy session; an elastic crepe bandage or temporary stocking is carefully applied before letting the patient go home. For the former he should be instructed and trained to reapply it in the event of this becoming loose. Instructions to elevate the leg during the night should also he given along with centripetal massage.

Esmarch Bandage therapy may be done to further the improvement once this is found less than effective.


Initial work up should include ruling out other contributing causes like cardiac disease, hypertension, renal disease etc. If found treat these first. Diuretics are essential if any suspicion of such a cause occurs. Also some effort should be made to classify lymphoedema & treat the cause if possible.

* Measure the circumference of the limb volume with the help of plethysmography.

* Take initial photographs. These should be taken at a fixed distance in two standard front and lateral views of each limb. Additional side/back views for a special problem may also be taken. Affix an identifying sticking label mentioning the patients name and date of photograph on the patients limb.

* Measure and record the skin condition and attacks of lymphangitis etc.

* Proper record should be kept and updated weekly. (A few samples proforma and limb marking tape are supplied with the machine).

Start treatment using the minimum recommended pressure and timings. Initial pressure settings should be 60-80 mm Hg for arm and 80-100 mm Hg for leg. Timer settings are 90-120 seconds for On and 30 to 45 seconds for Off timer. After the initial diuretic phase these are increased gradually as tolerated.

Normally patients will experience a diuresis even in the absence of diuretics. This is due to reabsorption of the lymph into the body and subsequent excretion into kidneys. Cardiac or renal patients have a chance of decompensation during this time-for them use even lower pressure and timer settings and give diuretics in addition. 3-4 hourly daily sittings with the V.P.L. system are conducted. The patients may use a temporary stocking or crepe bandage between therapy sessions. Before and at the end of each session, the limb should be examined for fungal infection and cuts between the skin folds. Appropriate anti fungal treatment will be required.

Try to individualize the encasing for each patient. Wash it a minimum once a week. Use only when fully dry. Keep the air Inlet nozzle closed while washing. do not iron or steam press, wash in lukewarm water with a standard detergent. Hand wash only. Rinse dry by hanging. After washing the same encasing can be used for another patient.

After the initial few sittings, the diuresis will slowly revert to normal. One will feel a softening of the skin texture and the skin will start lifting up in folds. This will be maximum in the area with the maximum diameter. As this occurs reset the timers and pressure upwards.

Once it is felt that the limb is not improving further with V.P.L. at maximum pressure, one can now start using ESMARCH BANDAGE sessions.

This is done as follows.

An assistant holds up the limb. A 6" Esmarch bandage is encircled on the toes and forefoot. After 2 rounds to ensure snugness, this is carried proximally in a spiral manner using a projection of approx. 2" (or 1/3rd width of the bandage beyond the previous spiral). This is carried around the ankle similarly. However one figure of 8 round may be used on the ankle if the bandage tends to slip into a constricting fold anteriorly.

The spiral is continued superiorly till the thigh or at least one full width above the swollen area using two or three lengths of the bandage as necessary. Pressures generated should be roughly between 200-250 mm of mercury. This is kept for 2-3 minutes and then removed and reapplied quickly in the same manner. The second application is kept on till about 15-20 minutes. It is removed earlier if the patient complains of pain. It is repeated on a daily basis till there is no fluid component in the limb.

This above procedure is done only under strict medical supervision and not to be done if the patient has loss of sensation or during attacks of lymphangitis.

Within a few weeks the limb will be near normal. The limb will then be ready for fitting the stocking.

Measurements are taken and a 50-60 mm Hg pressure stocking is fitted. A pair will required for each limb to allow washing etc. One has to wear it continuously for rest of life.

Lympho Nodo Venous Anastomosis


* Pre op patent blue violet injection in the web space of foot helps localisation of draining node.

* Anaesthesia-local

* Magnifying Loupe 2-4X preferred.

* Horizontal or vertical incision centring on the sapheno- femoral junction


1. Identify the saphenous vein and mobilize over 6-8 cm

2. Check for competence of sepheno- femoral valve by milking up blood after clamping the distal end and checking for regurgitation. If the valve is incompetent search for suitable portion of vein distal to a valve or abandon procedure.

3. Identify suitable moderate sized lymph node in the neighbourhood of the vein. Make a transverse section without mobilization. Discard the superficial portion. Ensure flow of lymph across the cut end .

4. Now section the saphenous vein at a point suitable for anastomosis. Ligate distal end. Rotate the proximal end and tailor it close to the node without tension or kinks.

5.Anastomose vessel wall to the lymph node capsule with 6-0 prolene burying the node in the vein .

6. Close skin.

POST OP :- Keep limb elevated. VPL therapy will help faster reduction of edema. Within 4-7 days limb will be ready for excisional surgery or stocking.


After it is ensured that the maximum improvement has been achieved, the patient is prescribed a custom made elastic leg support. For this the leg is carefully measured and a custom mode elastic stocking ensuring a minimum pressure of 40-60 mm Hg is ordered. Every patient is advised to wear these continuously and to replace them as necessary. For this a regular follow up has to be maintained. After this is obtained therapy for 2-3 days is desirable to facilitate a proper fit.


Selected patients, who had severe lymphoedema initially, will require surgery after the edema has decreased leaving behind folds of excess skin, Our surgery consisted only of excision of excess of skin with a wide panniculus of subcutaneous tissue, serving only to neaten the folds. The surgical technique we used almost then was as follows :-

General or spinal anaesthesia. Cleaning was done with savlon, iodine and spirit and the limb draped. The proposed excision of skin is marked with Gentian Violet. All cases were operated under a properly applied tourniquet, which was maintained for 60-to 90 minutes.

Carefully planned long elliptical incisions were made over the diseased areas with the aim of excising the excess skin and subcutaneous tissues. The location of these incisions were varied according to the needs of each extremity.

Enough skin was left behind to allow primary closure. Flaps were raised on each side, carefully varying the thickness of these flaps. Thus they were quite thin near the incision but became thicker as they were raised further laterally. The flaps were raised over the deep fascia in some and under the deep fascia in others. Excess of skin and subcutaneous tissue was excised from over the toes, feet and the leg. Haemostasis was done and the skin sutured after leaving corrugated red rubber drains. (Romovac would be more preferable in the current age). After the limb was firmly bandaged with crepe bandages, it was elevated and then the tourniquet was released. The limb was kept bandaged and elevated for 5 days and thereafter the patient was gradually mobilized. Drains were removed after 48 hours.

A second stage procedure was adopted if the anticipated excision required more than 90 minutes of tourniquet time. Further excision was done on the other side of the limb. This was however needed in only very few cases in our series:

There is very little to add to the above procedure. However a few interesting innovations are given below.

(1). Continuous compression therapy (over 18 hours per day following admission) softens the limb in less than a week in most instances. This obviates the need for a prior lympho - venous shunt.

(2). Use of a Steinman pin and stirrup (see photo) to elevate the limb through out the procedure. This is passed pre operatively through the calcaneum. It makes the pre op cleaning, Esmarch Bandage application and surgery much easier. (We just lift up the leg with the help of a bandage -see photo.)

(3). Double application of Esmarch Bandage tourniquet As the first application drives out residual fluid it tends to loose out, so reapply within 5 minutes to prevent troublesome venous ooze.

(4). Prior planning to include horizontal incisions at the level of the folds and joints can avoid dog ears. Cosmetic appearances will be better.


Limb volume, measurements and photographs are done and post operatively as well as after therapy. These are repeated at 3,6 and 12 month periods and yearly thereafter.




Recurrences are approx. 20-30% per year and generally related to disuse of stocking. For each recurrence a short course of VPL (approx. 3-4 days) with fresh measurement and stocking will suffice.

Recurrence may also be related to attacks of lymphangitis. Mostly attacks of lymphangitis decrease remarkably with VPL therapy

Why this is so is not known but can be speculated. Lymphangitis is related to 2 main factors (a) the release of microfilaria and associated toxins either directly or as a consequence of allergy (b) Secondary bacterial infection mostly of streptococcal origin Most attacks of lymphangitis in the early phase of disease are due to the former and hence the finding that Recent Oedema (R.O.) can be reversed with D.E.C. In the later phase however the worm is mostly dead and reinfection cannot occur as very few lymphatics remain. The excess lymphatic fluid however is a potent culture medium and secondary bacterial infection is then the main cause of lymphangitis. VPL squeezes out this excess fluid. Thus diminution of an important host factor contributes to decrease in the attack of lymphangitis.

The above mentioned factors may be the reason why patients tolerate excisional surgery better after V.P.L. therapy. As also after Lympho venous anastomosis. Less infection means less flap loss, and its ill effects of delayed healing, lymphatic ooze etc.

Another factor contributing to a possible decrease in streptococcal lymphangitis attacks after V.P.L. therapy may be the opening up of natural Lympho venous shunts, but this is as yet unproved. RIHSA (Radio Iodine Human Serum Albumin) clearance studies at AIIMS were done which showed improvement in only one out of two cases it was done in. The number of cases done are too few to draw a definite conclusion.

Surgical Lympho venous shunting either by Nodo venous or lymphatico venous shunting are other means of decreasing the fluid element in the limb. Most workers have reported dramatic falls in limb circumference and volume within 7 - 14 days (as compared to 6 - 8 weeks with VPL) after Lympho venous anastomosis alone. Continuous (i.e.16 - 20 hours per day) therapy with pneumatic compression is described to give results as fast. (Zelikovski 1986).

Addition of VPL after Lympho Venous anastomosis shortens recovery time even further. With this however the problem of recurrence remains.

Although no precise comparative figures are available as yet preliminary reports do suggest that recurrence rates may be less after VPL alone than after LVA alone. The main problem with LVA is that of blockage which is inevitable within months. As soon as blockage occurs, limb will start re-accumulating lymph and patient will develop lymphoedema. And once you have used up a vein the chances of creating another shunt are bleak.

Sridhar (Personal communication) treated one such patient with such a recurrence after L.V.A. by rotating a tensor fascia lata myocutaneous flap. Over two year later a similar recurrence occurred.

With VPL mostly temporary shunts are created during the therapy session but probably some internal permanent shunt are also created by the bodies' own recovery mechanism. These permanent shunts are something like vascular collateral channels. Which help in long term decrease in recurrence.

Attacks of lymphangitis decrease definitely. They may be due to the emphasis on skin hygiene during the prolonged therapy session.

A contributing factor to decrease in attacks may be the opening up of permanent internal shunts. The important host factor of increased tissue fluid which is a good culture medicine is decreased after treatment. Whatever the reason, decrease in lymphangitis attacks does decrease chances of recurrence. A vicious cycle of lymphoedema - recurrent lymphangitis - further blockage and further lymphoedema is there by not only broken but probably reversed. Absence of infection allows the body's repair mechanisms in remaking collaterals.

It is well proved that a simple transverse section of the lymphatics at a single level does not produce lymphoedema (Riechart). Inflammation alone can and does (Drinker).

In Filariasis recurrent lymphangitis contributes to lymphoedema. If further attacks are stopped (by D. E. C.), lymphoedema progression is stopped and can even be reversed, (S. P. Pani) In late cases these are no worms and probably no suitable lymphatics for them. Here secondary streptococcal infection is the main culprit in promoting further lymphoedema, filariasis, secondary skin changes etc.

Control of this secondary infection by proper hygiene, reduction in tissue fluid and in selected cases Penicillin Prophylaxis does stop further progress and probably allows collaterals to form.


There are 6 standard encasings for the leg and 3 for the arm. However among our millions of patients the range of limb problems is very large. One particular encasing will work less effectively if too loose and not at all if too tight to be completely zipped up the leg.

The other problem is that after the onset of therapy the limb starts thinning and changing shape. a previously effective encasing becomes less effective than a tighter one.

It was then decided to use a range of inserts which are zipped in between the ends of a normal encasing using the principal of open ended zips. However inserts have one basic problem. They can be zipped up only all along the limb. The problem of localised collections of fluid is found in around 50-60% cases of massive gr III edema. So frequently one faces the problem of the encasing not fitting at a small segment of the limb only. The best solution for this is to use an Esmarch Bandage over this localised area for a few days till it decreases enough in size to allow fitting of the encasing.




So far we can claim at best that VPL is providing a possible answer where there was none previously. Obviously not all will be satisfied with therapy. The clue lies in predicting who will benefit and to what extent. A pre informed patient is always more likely to be satisfied with new forms of therapy.

Dr. Dasmahapatra is the senior most name in surgery in Orissa. He is among the first FRCS ever to come back to our country around the time of Independence. He has accumulated a wealth of experience in managing Filariasis and its dreaded manifestations.

When I first met him to introduce him to my work on this machine I was careful to rather drink in his words rather than possibly talk about something which might be old hat for him. And here is his assessment in brief :

"There are two forms of elephantiasis : the fluid type and the fibrotic type. The fluid type is the one which is more prone to problems but this one has got a possible cure in the form of massage and compression besides the routine thorough cleanup of the leg ( for him compression meant continuous use of a proper crepe bandage applied by the patient or his relative after personally supervised training. This was required for upto six months or more.) The fibrotic type requires surgery."

Although, he used to do Charles' procedure and had been quoted in Bailey & Love's surgery textbook for the same, he was not happy with operating. Routine pre-op preparation for him meant suspending the leg from an overhead beam for three weeks to reduce the fluid component.

Was I glad for listening to him and looking back I realise that I am recommending on the basis of his words. A few visits to other endemic areas have added to my limited experience.

Getting the right results depends on the amount of fluid component found in the limb. It is quiet possible clinically to judge how much improvement is possible in any individual. The key is to check the amount of pitting present which decreases somewhat proportionally to the amount of fibrosis along with other features discussed below. Both components are present in each and every case, so the presence of fibrosis perse does not automatically rule out the amount of fluid present in addition. What one would be interested in is the total amount as well of the proportion of the easily treatable component.

Some features to make our job easier are given hereby :

Age : As fibrosis follows lymphangitis attacks we would expect older patients to have a more solid oedema. However the fibrosis in the younger patients is more resistant as the associated inflammatory fluid is absorbed faster. Attacks of lymphangitis block the lymphatics more and more with each attack thus tendency towards fluid accumulation is more in the old. microfilaraemia disappears by age 35 probably due to acquired immunity, so there is no need for DEC.

Sex : Females invariably have a more solid oedema than males. The reason for this need to be looked into but a few features we found obvious were : a) The hygiene level in females is much better than the males. This makes them less prone to attacks of lymphangitis. b) Females wear sarees and hence their legs and ankles are covered most of the time. This decreases the incidence of mosquito and other insect bites. This also decreases the incidence of skin allergies and boils.

Occupation : The highest incidence of elephantiasis even in the endemic areas would be in the highly religious temple towns. We have visited only two namely Puri in Orissa and Baidyanatham Deoghar in Bihar. The number of Pandas (temple pujaris) afflicted with the disease has only to be seen to be believed. This is due to being barefoot almost all the time and the general lack of hygiene in the holiest of the holi places of our Hindu culture.

These temples were constructed centuries ago and are not meant to cater to the needs of today's population. In Deoghar, the main temple is roughly 15 X 15 feet with only one 5 feet wide common entrance cum exit. When I visited this Sanctum Sanctorum where the main Shivling is placed I was told to remove my watch and spectacles etc. as they would surely have broken in the rush. On the way I stepped over many broken pieces of khullar (clay glasses used to carry water to bathe the Shivling). The Pandas have to do this several times everyday. Flower petals, prasadum, leaves to carry the prasad, khullars are used and then thrown on the ground by thousands of our pilgrims everyday in these towns which have no drainage system and worse no waste disposal system. On top of that is the need to walk barefoot over these things. Minor injuries and subsequent infection is inevitable.

In Deoghar, in the monsoon month of Ashad (End July), there is a festival for which pilgrims carry the Ganga water from over a 100 km distance barefoot to finally bathe the Shivling. Some of them do not walk but glide their body like a snake a large part of this distance. This is the peak livelihood time with crowds and unhygienic conditions too at the peak.

All in all one can clearly say that Elephantiasis is an occupational hazard for Pandas and some of our serious pilgrims.

On the other hand, in Kerala (as well as other parts of South India), it is the Muslim clergy who have to work in unhygienic conditions and hence they suffer more from this disease.

Coming to the type of disease, in these pts, mostly Elephantiasis is due to lack of personal hygiene and secondary bacterial infection. Thus the fluid component is far higher. Some of the worst looking limbs will be found in these patients. On the contrary, they also have a good prognosis as long as they change to a more hygienic and safer lifestyle.

History : A fair number with treatable oedema will tell the doctor that the swelling is least on waking up in the morning.

Attacks of lymphangitis : We had found that decrease in the attacks of lymphangitis occurs after proper compression therapy. This has been found to be a good prognostic index (Thompson ).

For us a person with attacks of lymphangitis is ideally suited for therapy.

General Hygiene : General cleanliness is a must for successful treatment by any method. A good bath with soap and water is the best. The skin should be dried properly being careful to remove residual soap from inside the folds - this promotes persistent wetness and secondary fungal infection, and dust a suitable anti fungal powder.

Condition of the skin : Papillomatosis and other changes are more frequent following inflammatory attacks and hence indicate treatability. Pitting even minimal on deep pressure is the best indicator of significant fluid component. General hygiene as well as fungal infection, secondary ulcers, weeping areas have to be looked into and treated properly before initiating compression therapy.

During treatment, a clinical grading varying from mild to severe is the best guide to amount of starting pressure required. Thus if there is little pitting with secondary changes would mean higher starting pressures of above 100 mm Hg, while significant pitting and no secondary changes would mean 50 mm Hg starting pressure. Average starting pressure should be around 70 - 80 mm Hg.

The presence of cuts and ulcers as well as secondary fungal infection has to be looked into and treated vigorously. Compression therapy should be withheld till these are adequately treated. In fact the presence of secondary infection is an indication for Lympho venous anastomosis for the same reason.

Lymphoedema Grading : A person with a bigger swelling would improve much more than earlier grades of the disease. After trying out many modalities of treatment and facing the consequent disappointment, he would be more easily satisfied. Also once he sees an initial reduction in the swelling he would take much more care in following the doctors advice on maintenance.

The reverse would apply to persons with early disease as he would not be satisfied till the leg is back to the original size. Not that any patient should be refused treatment, but a careful appraisal of an individual's aspirations and hopes is a must. Simultaneously he has to be given a realistic estimate as to how much reduction is likely and what all he should do especially the stocking to maintain the reduction. Mild oedema is mostly of recent origin (R.O.) and is hence reversible but we are talking of intractable cases.

Some patients may refuse treatment on finding the improvement to be too modest as per the doctors estimate but the patient who undergoes it is more likely to be ultimately satisfied. A satisfied patient is the best advertisement for any doctor.

Folds : The presence of folds means results are likely to be better though there is a high likelihood of surgery.

Site of Oedema : Dorsum and ankles are the most intractable and do not improve well with VPL. This is due to the lack of proper pressure transmission and also maybe excessive fibrosis especially for the dorsum. Van der Molen used to apply ankle pads (made of rubber) before compressing. The other answer can be surgery or liposuction of the resistant dorsal oedema.

In the upper extremity though better results are reported for the distal areas than proximally (Mridha & Odman, 1989). Our results have not matched these.




About 140 million people all over the world have filariasis. Two thirds of them live in China, India and Indonesia. In India filariasis is endemic in the coastal belts of India as well as the Eastern plains of the Indo-Gangetic plain. An estimated 18 million people are microfilaria carriers and 14 million manifest clinically.


Filariasis in India is caused by the helminths Wuchereria bancrofti and Brugia malayi. Macaques and leaf monkeys are reservoirs in some parts of the world. Acute infection is caused by the microfilariae, which are the larval forms and are transmitted by mosquitoes of various species. Chronic filarial lymphoedema is caused by the adult worms which deposit in, and block the lymphatics. Collateral lymphatic channels develop. Experimental evidence suggests that unless there is associated inflammation, simple lymphatic occlusion may not cause lymphoedema. occluded lymph vessels are greatly prone to attacks of lymphangitis followed by edema and fibrosis block all becomes thickened and hard with excrescences to end in the condition known as elephantiasis .

Lymphoedema and elephantiasis are common in the lower limb, and in decreasing order, the genitalia the upper extremity, breast and other areas.

The commonest manifestation of filariasis is, however, hydrocele. Lymphatic blockage of and around the cysterna chyli may result in retrograde flow and consequent leakage of chyle through the pelvi-calyceal system (Chyluria), the intestines (Chylous diarrhoea), the skin -- generally around the groin (Chylorrhagia), the mediastinum (Chylothorax), and the peritoneum (Chylous ascites).

The male : female ratio is 10:1. This may be because females, by their mode of dress, are more covered than males. About 50% of the patients are in their 3rd or 4th decades of life, though no age is exempt. Most patients are from the lower socioeconomic groups. The incubation period from mosquito bite to clinical manifestation may be as short as 4 weeks but is generally 8-16 months, or even longer. Attacks last 3-15 days and repeated occurrences are common.

Asymptomatic Infection may occur, and may last for life..

Acute Manifestations of lymphatic filariasis are episodic attacks of lymphadenitis and lymphangitis (fever, pain in the affected part, tender red streaks) along with fever and malaise. Over 90% of cases with chronic manifestations will give a history of acute attacks. Occasionally the adult worms and their associated granulomatous reaction present as lumps in the subcutaneous tissue, breasts or testicles.



Clinical manifestation Incidence

Chronic lymphadenitis 10 %

Chronic epididymo-orchitis 6 %

Chronic arthritis 1 %

Lymphoedema (Limbs 3%,

Scrotum 2% Penis 1%) 6 %

Hydrocele (Bilateral in 38 %) 48 %

Chyluria 2 %

Elephantiasis 19 %

Scrotum 11 %

Penis 5 %

Upper Limb 2 %

Lower Limb 4 %

Breast 1 %

Vulva 2 %

Other rare forms : chylous ascites, chylothorax, chylous diarrhoea.

Bancroftian Filariasis presents more often with involvement of the male genitalia causing funiculitis, epidydimitis and orchitis. An occasional differential diagnosis of strangulated hernia may be made especially if an acute hydrocele is noted.

Involvement of deep retroperitoneal nodes may present as acute abdomen. Sterile filarial abscesses may occur, especially in the medial upper thigh or behind the lower half of the rectus abdominis. They usually lie deep to the fascia and incision reveals communicating pockets.

Brugia malayi infestations present similarly but involve mainly the thigh and leg lymphatics. In general lymphadenitis with a characteristic retrograde lymphangitis is described. The affected lymphatics are tender, cord like with associated transient lymphoedema of the foot and ankle. The axilla and upper limb are occasionally involved similarly. At any time, involvement of more than one limb is uncommon.

Chronic manifestations of filariasis generally occur after repeated acute attacks over a period of 10-15 years. The subcutaneous tissue and the dermis are thickened, and there are warty outgrowths of the skin, fissures, ulcers, and secondary fungal infection.

Lymphatic blockage at a more proximal level occasionally causes retrograde lymph flow and pathologic dilatation of the lymph vessels. This may result in chyluria, chylothorax, lymphorrhagia and chylorrhagia. In most endemic areas a hydrocele is the most common feature of filariasis. In areas of high endemicity, 40% of hydroceles are filarial; In other areas this incidence may be 5% or less. The hydrocele fluid itself is amber in colour and the sediment shows a predominance of vacuolated mesothelial cells, fibrin, old blood clots, cholesterol clefts and calcium dust. Presence of these is diagnostic of filarial origin even in the absence of microfilaria.

Lymphoedema is initially transient in the acute stages; it has been classified as recent edema and persistent edema. The latter has further been subclassified as persistent edema with skin changes (elephantiasis) and persistent edema without skin changes. The legs, scrotum, arms, penis, vulva and breast are affected usually in that order of decreasing frequency.

Differential diagnosis. For the chronic stages, lymphatic blockage due to tumour, irradiation or surgery will need to be excluded. Deep venous obstruction may also present with similar swelling of the limb. In this, cyanosis or pain are prominent features and skin changes and non-pitting edema occur very late in the clinical course. Endemic non-filarial elephantiasis is described among people who walk barefoot in highland areas of Africa, where alkaline red clay soils of volcanic origin are present. This is probably due to the irritant effect of minerals especially aluminium and ferromangnese silicates present in volcanic clay. These penetrate the skin and are absorbed by the lymphatics, finally damaging the vascular endothelium of regional nodes and lymphatics. The edema starts characteristically from the plantar areas with initial hyperkeratosis of the toes.


Investigations for microfilaria in the acute stages are helpful. A nocturnal periodicity is characteristic of microfilaria of most W. bancrofti and B. malayi strains: during day time, they live mainly in the pulmonary capillaries. Microfilariae may also be looked for in hydrocele fluid and chyle besides in nocturnal blood samples. In chronic disease, examination of night blood is positive in about 20% of cases. On provocative testing the positivity doubles.

In chronic stages limb circumference at several prefixed points, and limb volume may serve as markers for assessing treatment. The latter is done by checking water displacement and comparing with the normal side. Other studies like protein studies of edema fluid, lymphangiography, and radio iodine human serum albumin (RIHSA) clearance studies are meant for research centres. In the last one, RIHSA is injected in the subcutaneous tissue and the clearance of radioactivity is measured against time. Since RIHSA will disappear from the limb only through lymph, this study is an indicator of lymph flow.

Serology: Enzyme-linked immunosorbent assay (ELISA) has a reported accuracy of over 90%. Immunodiagnosis for lymphatic filariasis may be useful for

(1) Diagnosis of a Microfilaraemia states, i.e. persistent infections, elephantiasis where other causes may be suspected (above), tropical pulmonary eosinophilia and filarial granuloma.

(2) Defining the etiology of potentially filaria related syndromes, i.e. arthritis, tenosynovitis, cardiomyopathy etc.

(3) For epidemiological situations and in assessing the worm burden and effects of treatment.

A major drawback of Immuno diagnosis tests, which include enzyme-linked immunosorbent assay (ELISA), radioimmunoassay (RIA), and skin tests is that there is cross reactivity with other helminthic infections and there is difficulty in distinguishing recent and previous infection. Some tests are expensive.

Biopsy of lymph nodes may show the adult calcified worm in about a third of cases; the remainder will show nonspecific changes.

Examination of hydrocele fluid shows microfilariae in about a fifth of filarial hydroceles. Over half of cases will show chyle.

Dye injections : Injection of patent blue dye into the dorsal web space will demonstrate a fine network of intradermal lymphatics, Massage and foot movements help to delineate the larger and deeper lymphatics.

Lymphangiography helps confirm the diagnosis, and to decide upon the type of surgery. It is essential if Lympho venous anastomosis is planned. After visualising the lymphatics on the dorsum of the foot by patent blue Injection, an incision is made and a single subcutaneous lymphatic cannulated. Slow Injection with a special injector pump of 7 cc of radio-opaque (ultra fluid lipiodol) dye into this dorsal lymph vessel will delineate the lymph vessels in the limb and later the trunk up to the neck. In filariasis, lymphangiography shows dilatation of lymph vessels leading on to dermal back flow, varicosity, tortuosity, and obliquity. there is increase in the number of collaterals in the initial phases which later decrease in number. Towards the fibrotic or so called elephantiatic stage, very few lymph channel will be seen. Occasionally lymphangiography shows a figure of eight shadow of an adult worm.


Drug therapy

Diethyl carbamazine (DEC) is the mainstay of acute filarial infection. This is a white powder, freely soluble in water and has a slightly unpleasant sweetish taste. In mass trials it has been added to common salt and has not been found to be affected by cooking. DEC kills the adult worm and has no effect on microfilariae in vitro. However in vivo some micro filariacidal action also takes place. This is dependent on cellular and humeral immunity. DEC does cause a rapid disappearance of microfilaria from nocturnal blood smears, through microfilariae in hydrocele fluid are not affected. In the acute stages DEC causes a decrease in frequency or even disappearance if acute attacks of lymphangitis. Repeated courses are however necessary as not all adult worms are killed and reinfection is common.

In recent edema, regression of edema is well described (70%) while in persistent edema, especially without skin changes, some regression may occur (30-50%). Complete regression has been described for early lymphoedema, hydrocele and chyluria. Antibiotics, Anti-inflammatory and antipyretic drugs, and anti-histaminic are generally also given in the acute stages. Primary foci of infection like dental caries or fungal infection of skin folds should be treated. Long term benzathine penicillin has been prescribed for a few with frequent relapses.

Administration of DEC tablets.Bancroftian filariasis 6mg/kg/day over 3 divided doses after meals for 12 days. Repeated courses may be necessary. These may be monthly or longer. Even shorter courses ,given by health care workers without diagnosis, i.e. presumptive treatment may be beneficial.

Brugian filariasis : 3-6 mg/kg/ day up to a total of 18-72 mg/kg. Repeated courses may be needed.

DEC medicated salts: These are given over a long period adding DEC 1-4g/kg of salt. Over 18 million people have been treated safely in China and also Lakshwadweep islands in India. This is a safe, cheap and effective treatment; in one study the microfilaria rate was lowered from 4% to 0.4%. Certain populations do not accept the change in taste of the salt.

Other drugs like levamisole and mebendazole are, in the doses required for filaricidal effects, too toxic or expensive compared to DEC. Ivermectin, flubendazole and centperazine are under trial and may be useful. Ivermectin is being regularly used now a days. Diuretics, leg elevation, massage & bandaging may help to decrease the swelling in recent and early persistent edema. Diuretics may have some effect, mostly presumptive.

Coumarin rutin salts have a direct albeit slow action in decreasing oedema. They act through the macrophages to increase breakdown of protein.

Intermittent Pneumatic External Compression (IPC) or V.P.L.

In this the limb is enclosed in an inflatable encasing which is inflated through an air compression pump to upto 150 mm Hg pressure. Compression of the limb drives out the edema fluid. The pressure is then released after a period of 150-180 seconds. The circulation is thereby restored for a rest period of 15-60 seconds. After this the entire cycle is repeated continuously over 4-6 hours. This is a very comfortable procedure, entirely painless. One can even do it at home. Treatment over 10-15 days is enough to treat persistent edema without skin changes. Follow up requires continuous wearing of pressurised elastic stockings. Repeat courses may be given if necessary. Two types of IPEC machines are available, the Lymphapress (single encasing) type and the Flowtron which uses multiple encasings with individuals tubes and pumps to produce a wave like effect massaging the fluid proximally. The latter is more effective though its extra cost does not justify this benefit. A longer treatment course may be required if the former is used.

Interestingly some patients specially those with cardiac/renal problems treated with VPL massage and tourniquet etc develop edema in the contralateral limb concurrently with control of the affected side. This is more common if higher pressures are used. Probably fluid as well as protein enter the vascular channels which holds the reabsorbed fluid back in the kidneys. It is suspected that diuretics help to decrease the total volume load in the body. Some people use them routinely with or without VPL. Sub-clinical lymphatic obstruction also contributes to fluid accumulation in the contralateral limb.

In persistent edema with skin changes VPL over 4-8 weeks is known to soften the limb converting the hard keratotic skin to pliable folds which are more easily amenable to surgery. This technique gives excellent results (Table II).

Where the VPL pump is not available, similar treatment can be administered by manually compressing the limb by tight rubber (Esmarch) bandages. Spirally applied from below upwards (like in the use of a tourniquet for surgery), these are kept in place for 15-20 minutes or till bursting pain occurs. This treatment is not recommended without medical supervision as it may be painful and has complication not very different to tourniquet application. Use of a custom built stocking (Fig. II) is essential after this treatment.

Heat Treatment

The Chinese have devised a new method of treatment of lymphoedema by alternatively heating and cooling the leg in an oven. This method is reported to be very effective though cumbersome. Use of a microwave oven has been found to be better.

Surgical Treatment

Hydrocele is treated by traditional procedures like excision/ eversion. Excision of overlying elephantiasis skin is frequently necessary. Thorough cleaning of the skin is recommended along with peri-operative antibiotic cover as the infection rate is excessive.

Surgery for lymphoedema of the limb can be classified into 2 main types drainage procedures and excisional procedures. Drainage procedures are essentially designed to improved lymph flows by either (1) bypassing the block e.g. Lympho venous anastomosis or (2)creating additional lymph channels e.g. omental transposition. Excisional procedures are debulking procedures where the extra large limb volume is trimmed. The different named procedures differ amongst each other as to the site and type of incision and how final skin cover is given as well as in the staging of the various operations. eg in Homan's procedure the entire circumference of the leg is cleared in 2-4 stages. Other operations have tried to combine the two.

DRAINAGE PROCEDURES : Insertion of silk threads (to act as wicks) and many other materials like colloid strips &polythene tubes were tried without success. Recently monofilament nylon netting has been tried. Pedicle flaps acting as a bridge of normal lymphatic tissue may be useful in post traumatic lymphoedema caused by post traumatic scarring. Goldsmith (1965) used the omentum suitably lengthened to travel across the limb as a means to provide lymphatic drainage.

Lympho venous anastomoses : All the above type of operations have fallen into disrepute. Newer drainage procedures are lympho-nodo-venous anastomosis and direct micro vascular lymphatico venous anastomosis. Both of these especially the latter have been found useful in persistent edema without skin changes. In the former, the cut face of a lymph node (with its lymphatics intact) is inserted into a neighbouring vein, stitching the capsule into the vessel wall. The vein rather than the lymph node is mobilised. (See Box on pg 42)

Direct lymphatico venous anastomoses are technically more difficult, and the operating microscope is required. The lymphatics should not be too enlarged to prevent reflux of blood. Eight to ten anastomosis are required in one or two sittings. These are inserted using small nicks in the vein. A long needle is used to pick up the lymphatic. This is then held up and then pushed into the adjacent incision.

Monofilament nylon netting : Gormann and Navarre ( See Diagram)

Gillies and Fraser (1935) fashioned a pedicle skin flap to act as a bridge of normal lymphatics to drain the involved area. This however has been difficult to emulate due to the technical difficulties of shaping such a flap without tension. Localised circumferentially scarring of the limb with secondary distal lymphoedema is an occasional indication. e.g. a flap across this scar. Use of omentum : Goldsmith (1966) created a subcutaneous tunnel in the limb and placed a long mobilized length of omentum to serve as a source of normal lymphatics. Danese (1968) and later Miller et al (1973) found the omentum totally fibrosed 3 months after surgery. Nylander & Tjenberg (1968) say that the only benefit that ensued because of the excision of subcutaneous tissue. Bowel adhesions, obstruction, strangulation etc. are associated complications.

EXCISIONAL PROCEDURES : The essence of these is excision of all or part of the involved skin and subcutaneous tissue. Cover is either by skin graft or by raising flaps. Complication of surgery include lymphorrhea, hemorrhage, and lymphangitis. In most cases they are temporary and controlled with conservative therapy.

The excision is carried right down to the deep fascia of the leg. The foot and toes are treated similarly, excising a large ellipse of skin. Even with maximum care, there is a 30-50% incidence of flap necrosis resulting in an average hospital stay of 4-6 weeks.

In the Charles procedure the entire skin is excised in one from the calf after grafts has been harvested from non warty areas of the portion to be excised. This same skin graft is now placed directly on the deep fascia. A pressure bandage is given along with a plaster of Paris slab. Immediate post operative results are good if the graft takes, but continued discharge weeping and excoriation are frequent post operative dorsum as it has too many tendons and very sparse deep fascia. Pantalooning of this portion are later complications.

Variations to the above have been devised in attempts to drain the superficial lymphatic system to the deep system by excising the entire deep fascia (Lanz) or strips of deep fascia with little increase in success.

Thompson (1962) implanted the de- epitheliaized dermal flaps behind the deep fascia in attempt to promote direct drainage. He reported an improvement in RIHSA clearance, which is an indicator of lymph flow. Sawhney (1974) later discounted his findings and attributed his results to excision alone.

Authors Recommendation : Simple excision of the skin and subcutaneous tissue, with direct closure after raising minimal thick flaps. Pre-op preparation is by a course of VPL or Esmarch Bandage compression. Liposuction for small folds or persistent dorsum swelling after VPL.


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Code No. : .............


Date : .............

Name : .................................

S/D/W/of : ................................

Caste : ...... Sex : ..... Age ....

Occupation : ..............................

Place of Survey: ......................

Address :

House No. : ..................

Village : ..................

Distt. : ..................

State : ..................

Referred by :


Clinical History :


Direct Questioning :

1. Duration of onset:

2. Age at onset : ..........

3. History of rec. lymphangitis : YES / NO

4. History of rec. lymphadenitis : YES / NO

5. Freq. of attacks : <1/yr 1-3/yr 3-12/yr 1/month

6. History of Chyluria : YES / NO

7. Number of Children : Male :

Female :

Still births (if any) :

Family History :


Previous treatment :




General Physical Exam : Weight :

Height :

Systemic Exam.


Specific Examination :

Edema : Parts involved : Extent of Pitting : Non Pitting

Mildly Pitting

Significant Pitting

Condition of the skin of the involved parts

Genitalia : Hydrocele :

Enlargement of testis :

Epididymis :

Scrotum :

Labia majora :

Penis :

Breasts :


Regional Lymph Nodes :



1. HAEMOGRAM : HB : TLC : DLC : ESR : other

2. URINE :






Blood Film| | | | | | Counting

Chamber | | | | | | Membrane | | | Conc- | | | entration







9. PHOTOGRAPHS 1st. visit 2nd 3rd Date

reel/film no.

Serial Wt. Record