The Surgery of 'tropical' diseases
From Primary Surgery
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The surgery of neglected infection
As living standards in what are now the industrial countries have improved, many conditions, which once occurred everywhere, are now confined to the tropics. Although they often thought of as being specifically tropical, they are in fact the 'surgery of poverty'. Surgical tuberculosis (Chapter 29), surgical leprosy (Chapter 30), vesicovaginal fistulae (18.18), perforated typhoid ulcers (31.8), and enormous hernias (14.4) are a few of the conditions which were once seen everywhere. There are also a few specifically tropical infections, such as mycetoma (31.3) and filariasis (31.6) which may need surgery. Schistosoma haematobium causes much surgical disease of the urinary tract, but none of the procedures that are possible are sufficiently easy or effective to be mentioned here, apart from a plea for the early diagnosis of the bladder cancer that it may cause (33.31), a note on schistosomal granulomas of the vulva (20.14), and on the occasional usefulness of nephrostomy (23.13).
Tropical ulcers are one of the classical tasks of tropical surgery, so we will start with them.
Tropical ulcers
These were once common over most of the tropics, but as living standards rise they go. There is some disagreement as to what causes them. They are generally said to start as small infected cuts from the sharp grasses of bush paths, which would explain their characteristic distribution (D, in Fig. 31-1). Others consider that they are primarily infective, which would explain why they sometimes occur in small epidemics in the wet season. Tropical ulcers develop through three stages: Stage One. A pustule, or neglected cut, containing Vincent's and fusiformis organisms (both are penicillin-sensitive). This stage is not seen in hospital. Stage Two. Progression of the cut or pustule to form an acutely painful ulcer with a raised, thickened, and slightly undermined edge. This ulcer grows rapidly for several weeks. A bloody discharge covers the grey slough on its floor, the skin around it is dark and swollen, and muscle, bone, and tendon occasionally lie exposed in its base. After about a month, the pain, swelling, and discharge improve, and it either heals, or it goes on to the next stage. Stage Three. It becomes chronic, and resembles any other long-standing indolent ulcer.
In Stage Two, when an ulcer is still less than 5 or 6 cm, penicillin and dressings will usually cure it. But if it is larger than this, the epithelium from its edges will take a long time to grow across it, so it needs grafting—which is something that every health centre should be able to do.
If you first see a patient in Stage Three, his ulcer may have destroyed the whole thickness of his skin; it may have extended through his deep fascia and exposed bone, tendons or a joint. Osteomyelitis is rare, but a reactive periostitis may in time raise an ulcer above the surrounding skin. Sometimes its edge is thickened and everted, and resembles a carcinoma.
TROPICAL ULCERS
DIFFERENTIAL DIAGNOSIS. The site of a tropical ulcer is Its most important diagnostic feature. The differential diagnosis includes: (1) a chronic non-specific ulcer, (2) a squamous cell carcinoma, which resembles a chronic tropical ulcer in that it also has an everted edge (33.19). Also, the following:
Suggesting tuberculosis (unusual)—a ragged, shallow ulcer, with bluish overhanging edges. Its base is less vascular, and more fibrous. It you manage it as a tropical ulcer, it will not improve. If you are in any doubt, biopsy it, and try chemotherapy—a tuberculous ulcer will heal miraculously. Suggesting a Buruli ulcer (restricted areas only)—an otherwise fit child, or young adult, suffering from a huge ulcer with deeply undermined edges, anywhere on his body, and not necessarily on his feet and lower legs (31.2a).
CAUTION! The macroscopic differentiation of a chronic tropical ulcer from a malignant ulcer (33.19) can be difficult when there is no extension into the surrounding tissues. Be sure to do a biopsy before you do any radical surgery.
TREATMENT FOR TROPICAL ULCERS
ACUTE ULCERS. Treat him as an outpatient. Get his ulcer clean with saline soaks. Soak off the dressing each day and change it. Give him a bottle of half-strength saline (tap water and salt, which need not be sterile) and ask him to pour this on the dressing every 2 or 3 hours to keep it moist. Give him penicillin.
When his ulcer is clean, usually within 7 days, and if it is >5 cm in diameter, admit him for split skin grafting (Chapter 57). Smaller ulcers will heal without grafting. Give him penicillin for 3 days perioperatively. This kills any streptococci which might dislodge the graft with their fibrinolysin (57.4).
If he is an adult, use local anaesthesia for the donor site (57-4), and ketamine or general anaesthesia if he is a child.
If the granulations are abundant, scrape the base of the ulcer with a scalpel. There is no need to anaesthetize it; there are no nerves in granulation tissue, so this does not hurt, provided you avoid the epithelium. Scraping does not improve the 'take', but it does reduce fibrosis under the graft later, and so makes it more stable.
Control bleeding with hot packs. If possible, apply the graft as a single sheet, which has been meshed to allow the escape of exudate and blood, or, less satisfactorily, apply it as patches or pinch grafts (57.9). If the ulcer is over a joint tendon (uncommon), lay strips of graft across it (57.5).
Keep him in bed for a week to avoid movement, and expose the graft on the 7th day (some surgeons expose it on the 3rd day to inspect it). Then soak off the dressing slowly, to avoid removing the graft at the same time. It may need covering for another week. The donor site should have healed in 10 days.
CHRONIC ULCERS. Split skin grafts do not take well on longstanding fibrotic ulcers, or they may take take initially, and break down later. Ideally, these ulcers need a muscle, or a myocutaneous flap (not described here). Chronic ulcers cause long standing morbidity, and may become malignant, so refer him if you can. If you cannot refer him, you will have to do your best with split skin grafting. You will probably succeed temporarily, but his ulcer will probably recur.
If the base of his ulcer is suitable (57.3), and is not too deeply fibrosed or over bone or tendon, some surgeons would excise and graft it as a single procedure.
Alternatively, and preferably, apply a tourniquet (3.9), and excise the ulcer under ketamine (8.1), or a general anaesthetic. Cut away ail avascular scar tissue, until you reach a raw, bleeding surface; if necessary, use an osteotome to remove any dead bone. Apply hypochlorite, or a dry dressing, to the ulcer bed, cover it with gauze, cotton wool, and a bandage, and release the tourniquet.
Five to twelve days later, when the base of the ulcer is covered with suitable granulation tissue, graft it, as described above.
DIFFICULTIES WITH TROPICAL ULCERS If, after many years, the BASE OF AN ULCER BECOMES HEAPED UP and irregular, and its edges protuberant and rolled, a SQUAMOUS CELL CARCINOMA (epithelioma) has developed, so see Section 33.19. This can happen in three years, or it can take thirty.
Mycobacterium ulcerans infection (Buruli ulcer)
This occurs in restricted areas of the rural tropics near rivers— the Congo in Zaire, the Upper Nile and Lake Kyoga in Uganda, the Nyong in the Cameroons, and in the lowland swamps of Malaysia. It is also occasionally seen in Zambia.
The patient is often a child, and in some areas is likely to be a woman, who presents with a painless, small, well demarcated, indurated swelling, attached to the skin, but not to deeper tissues. It is almost always single and on the limbs, and is often near a joint, although the site is more variable in young children. There is little pain or tenderness, little or no fever, and the regional lymph nodes are not enlarged. The lesion grows, the skin over it desquamates, becomes pigmented, and then breaks down to form a chronic expanding ulcer, with a necrotic base, and edges which may be undermined 5 to 15 cm. Secondary infection occurs, and a foul slough forms. Satellite ulcers may appear, but metastatic spread is rare. Some ulcers remain unchanged for weeks; others cover much of a limb, or the trunk, in a few weeks. Untreated ulcers commonly heal spontaneously, with much scarring and severe contractures.
BURULI ULCER
THE DIAGNOSIS is suggested by the the appearance of the swelling and the ulcer, the absence of lymph node enlargement, and the failure to respond to tropical ulcer therapy (31.2).
SPECIAL TESTS. Look for AAFB in the chronic base of the ulcer, and send material for culture. M ulcerans grows on the media used for M. tuberculosis, but only at 33°C.
THE DIFFERENTIAL DIAGNOSIS in the nodule stage in-eludes: boils, foreign body granulomas, and low-grade fibrosarcomas. In the ulcer stage it includes: tropical, mycotic, parasitic, and malignant ulcers.
CHEMOTHERAPY. M. ulcerans is sensitive in vitro to streptomycin, clofazimine, and rifampicin, but these drugs have little clinical effect. Even so, give them to cover surgery.
TREATMENT Excise early lesions, if possible with primary closure (unlikely).
If the lesion is ulcerated, control pyogenic infection with antibiotics, and irrigate with saline. Excise all diseased tissue, and graft (57.1). If you fail to remove all diseased tissue, the graft will fail, and healing will be slow, with much scarring.
Mycetoma
Considering the many people who walk barefoot, it is surpising that the saprophytes of the soil so seldom infect the feet. But this does happen occasionally, notably in the Sahel area of Africa, and in parts of South India, Mexico, Brazil, and the Middle East, each area having its own particular species. If a peasant in one of these areas treads on an acacia thorn, or some other sharp object,it may may infect him with filamentous fungus-like bacteria (Streptomyces, Actinomyces,or Nocardia), or the true fungi (the eumycetes, particularly Madurella). These cause a chronic granulomatous swelling, with multiple sinuses that discharge characteristic granules, each of which has arisen in a micro-abscess. The lesion is usually in a patient's foot, but his leg, finger, hand, thigh, trunk, jaw, or head may also be affected, and may be difficult to diagnose.
He is usually a farmer who has a painless swelling on his foot at the site of a thorn prick some months earlier. This grows slowly to form a circumscribed, rubbery or cystic, lobulated mass. If it is on his sole, pressure flattens it into a disc. Sinuses appear, and occasionally discharge granules. As one sinus heals more appear,and become secondarily infected, but this secondary infection does not extend deeply. By the time that five years have elapsed, his whole foot is swollen, and covered with open sinuses and the scars of healed ones. It is still painless, and as he has no systemic symptoms he continues to work. As his foot disintegrates, he takes to a crutch. Spread to his lymph nodes is late and uncommon,and only after about ten years do sinuses start to form in the nodes of his groin.
The primary site of infection is usually in his subcutaneous fat, but it may be in fat which is deep to fascial planes. These form a natural barrier to the spread of infection, so that if it gets under his plantar, or palmar fascia, it may spread between his tendons, along his lumbrical canals, and even through his carpal tunnel, up into his forearm. His bone may be invaded relatively early, still without causing him pain.
Mycetomas never regress spontaneously. Chemotherapy has no effect on the true fungus Madurella, but it is worth trying a long period of dapsone, trimethoprim, and streptomycin on Streptomyces and Nocardia, and trying penicillin on Actinomyces, as described below. Ketoconazole 200 mg once or twice daily with meals (expensive)has also been used. The ultimate treatment is amputation,but perhaps only after 20 years, if necessary accompanied by clearance of the regional nodes. The vascularity of a limb is not impaired, so that you can amputate at a site of election, provided it is through healthy tissue (56.1). Crockett, DJ 'Mycetoma' Tropical Doc tor 1973;3:28-33.
MYCETOMA
DIAGNOSIS. Try to find the granules, because without them all a pathologist can say is that there is a granulomatous infection with multiple micro-abscesses, in the endemic zone in Fig. 31-2.
Streptomyces somaliensis forms yellowish-white medium sized,0.5 to 1 mm, soft, round, smooth granules.
Madurella mycetomi and Leptosphaeria senegalensis, form brown or black, large, 1 to 3 mm, irregular, fissured, aggregated, hard, brittle granules.
Streptomyces pelletieri forms red, minute, 0.3 mm, faceted, aggregated, very hard granules. In the sporadic zone.
Nocardia brasiliensis forms yellowish, minute 0.3 mm, irregular,lobulated, soft granules.
Streptomyces madurae forms white, yellow or pink tinged, large, 1 to 3 mm, soft, lobulated granules.
X-RAYS. Once a patient's periosteum is breached, his tarsal and metatarsal bones are rapidly destroyed. New bone in the walls of abscesses forms buttresses projecting outwards at angles to the shaft of a long bone. The centre of an infected bone has a honeycomb appearance, and a good film shows tiny cystic areas of bone destruction, each the site of a microabscess.
CHEMOTHERAPY FOR MYCETOMA
If you find the granules of Nocardia brasiliensis, try prolonged continuous treatment with dapsone 100 mg twice daily for 2 years or more. Streptomycin 1 g daily by intramuscular injection is also effective. Treatment is so protracted, and the disease so painless, that he is unlikely to co-operate for long. You may be wise to reserve dapsone for lesions of the posterior part of his foot, or in his hand, for which the only alternative is a high amputation.
If you find the granules Of Streptomyces somaliensis, try trimethoprim 100 mg, twice a day for many months, or even a year or more.
If you diagnose actinomycosis, caused by such organisms as Actinomyces israeli, try penicillin for 2 or 3 months.
CAUTION! With long-continued treatment, watch carefully for side-effects. Dapsone: neuropathy, allergic dermatitis, anorexia, nausea and vomiting, headache, insomnia, hepatitis, agranulocytosis (all rare). Trimethoprim: vomiting, rashes, erythema multiforme, epidermal necrolysis, eosinophilia, agranulocytosis, granulopenia, purpura, ieucopenia;megaloblastic anaemia. Streptomycin: tinnitus, vertigo and deafness, a widespread fine rash, drug fever, nephrotoxicity (rare), and paraesthesiae of the mouth (very rare).
With all other mycetomas, the only treatment is symptomatic. Short courses of tetracyclines will control secondary infection in the sinuses, and encourage them to heal, but will not eradicate the disease. Curette and drain any low-grade abscesses that form.
SURGERY FOR MYCETOMA
If a lesion is localized, and is confined to a patient's soft tissues, excise it and repair the defect with a split skin graft.
If he has a lesion of his forefoot which involves bone, or which will expose bone on a weight-bearing surface if you remove it, Syme's amputation may be appropriate (56.9).
If he has a lesion of his hindfoot with minor bone involvement,and without severe disorganization of its joints, treatment depends on the organism: (1) If it is Nocardia, as determined by the district he comes from and Fig. 31-2, give him dapsone, and drain the lesions if necessary, but don't amputate. (2) If any other organism is responsible, you will probably have to amputate, but wait until his foot becomes a real nuisance.
If he has a lesion of his hind foot with severe bone and joint destruction, do a below-knee amputation (56.8).
CAUTION! (1) Mycetoma is painless, so don't amputate a limb until he is quite sure that his limb is of no use. (2) Observe him carefully, and make sure he reports any involvement of his inguinal nodes. If he does, amputate immediately, and clear them by block dissection (33.34).
Gross enlargements of parts of the body (elephantiasis)
If a patient has a gross generalized swelling of his leg, arm, or scrotum, or if a woman has a similar swelling of her breast or vulva, the condition is known as elephantiasis. Usually, this is due to long standing lymphatic obstruction. Occasionally, it is due to venous obstruction, but this is seldom gross enough to need surgery. Distinguishing between lymphatic and venous obstruction can be difficult. Oedema due to lymphatic obstruction becomes solid quite rapidly, but early cases may show pitting.Oedema due to venous obstruction becomes solid late, and eventually reaches a stage where it fails to pit.
In most areas, the causes of lymphatic obstruction (lym-phoedema), in decreasing order of frequency are: (1) Tuberculosis. (2) Repeated lymphangitis leading to incompetent valves, usually due to streptococci from wounds. (3) Malignant glands in the groin, or less often the axilla. (4) Kaposi's sarcoma. (5) Block dissection of the glands, usually for carcinoma. (6) Congenital lymphatic hypoplasia, or incompetent lymphatic valves (Milroy's disease). Other causes include chronic fungal infections, and lymphogranuloma inguinale.
Two important causes of lymphatic obstruction are restricted to certain endemic areas: (1) filariasis (commonly due to infection with W. bancrofti and less often to Brugia malayi, or Brugia titnori.). (2) Todoconiosis' (also called non-filarial endemic elephantiasis). Filariasis is restricted by the prevalence of the insect vectors, and podoconiosis by particular characteristics of the soil. Filariasis may involve any of the parts of the body listed above, but usually the legs or scrotum, whereas podoconiosis only involves the legs.
- Mossy foot' is a term used to describe: (1) Commonly, a variety of podoconiosis in which the epithelial hyperplasia is extreme. (2) Rarely, other disease causing multiple excrescences on the feet, notably chromoblastomycosis. Elephantiasis due to advanced podoconiosis (whether it has reached the * mossy foot* stage or not) responds fairly well to surgery. Elephantiasis due to filariasis is difficult to treat surgically. It is a popular misconception that filariasis is the commonest cause of lymphoedema; this is so only in filarial hyperendemic areas.
In practice, the exact diagnosis of the grosser forms of oedema leading to elephantiasis is not absolutely essential, because the practical methods of surgical treatment are similar in all of them—excision and grafting.
ELEPHANTIASIS
This is the patient with gross enlargement of some part of his body.
LYMPHATIC OR VENOUS OBSTRUCTION? Lymphatic obstruction is much more likely.
Suggesting lymphatic obstruction—a slow onset, pitting except in late stages, when there is much secondary fibrosis, hyperkeratosis of the epidermis, which may be extreme ('mossy foot').
Suggesting venous obstruction—a rapid onset, some obvious cause for the obstruction, pitting on pressure, often ulceration of the skin, rarely gangrene.
INVESTIGATIONS. If he comes from an area where W. bancrofti is endemic, examine several nocturnal blood smears. There are no bone changes, so an X-ray is normal. Lymphangiograms are unlikely to be helpful.
THE DIFFERENTIAL DIAGNOSIS includes the common medical causes of peripheral oedema (heart failure, nephritis, and cirrhosis of the liver, etc.). In these the swelling is usually equal in both legs. In the surgical causes, particularly podoconiosis, it is usually unequal.
Suggesting bancroftian filariasis—scrotal involement, oedema which starts at the most dependent part for each site and moves upwards—below the malleoli for the leg, the fundus for the scrotum, the foreskin for the penis, and the dorsum of the hand for the arm. Elephantiasis of the scrotum with few changes in its skin.
Suggesting podoconiosis —a bare-footed patient from a podoconiosis area; worse on one leg than the other; below-knee swellings most marked distally. Symptoms are the first evidence of disease (in filariasis they are the last), and include burning of the lower legs at night, with persistent itching of the 1st and 2nd toe clefts, and plantar oedema of the forefoot. No filaria in the blood, and a chronic warty thickening of the lower legs ('mossy foot').
Suggesting chronic non-specific infection—some source for it, such as a tropical ulcer (if the swelling is in the lower leg). Acute recurrent attacks of lymphangitis. Enlargement of the nodes draining the swollen area only: these may be large and firm, or small and fibrotic. Lines of hyperpigmentation on the skin indicating previous lymphangitis (not easy to find, so look carefully; and seldom visible on a dark skin). A lymph node biopsy showing fibrosis and non-specific inflammatory changes.
Suggesting tuberculosis—chronic enlargement of many superficial nodes—inguinal, axillary, and cervical; a history of prolonged illness in the past, with fever and enlarged nodes, some of which discharged for long periods; multiple sinuses, or the scars that follow their healing. Lymphogranuloma also produces sinuses, but these are usually confined to the superior group of nodes, over the medial part of the inguinal ligament. Scars over the lower end of the vertical chain are more likely to be caused by tuberculosis. Involvement of an entire leg from toes to groin, or an entire arm or a woman's breast. A positive lymph node biopsy confirms the diagnosis; if tuberculosis is no longer active only non-specific fibrosis may be seen.
The site involved also influences the probable cause. Breast and arm, or vulva—tuberculosis. Scrotum—bancroftian filariasis. Lower leg—filariasis, podoconiosis.
CHEMOTHERAPY If you are in doubt, try the appropriate specific treatment for tuberculosis or filariasis. Lymphoedema due to tuberculosis nearly always settles with chemotherapy, unless it is diagnosed very Late. Antibiotics are unlikely to influence chronic non-specific inflammation.
Podoconiosis (non-filarial endemic elephantiasis of the lower legs)
Podoconiosis ('dust in the feet') presents as bilateral asymmetrical swelling of the feet and lower legs. It is seen in susceptible families of bare-footed farmers in well-defined fertile volcanic highland zones of Africa, Central and South America, and Indonesia, and also in the lowlands irrigated by rivers from these highlands. It is due to the absorption of silica particles from the soil, through the feet of someone from a susceptible family. This causes the patient's lymphatics to fibrose, and obstruct, and his femoral nodes to enlarge. This in turn makes his legs and feet swell, and progress through stages which are described as 'water bag', 'rubbery', and 'wooden'. Finally, his leg becomes hyperkeratotic, 'mossy', and nodular. Lymph may ooze through his skin, which may be secondarily infected by fungi or bacteria. The disease may progress steadily, or there may be a succession of acute episodes which resolve incompletely. Villagers in endemic areas are often able to recognize the early stages.
Elevation, elastic stockings, and long leather boots help in the earlier stages, but once the 'wooden' stage has developed, the only treatment is surgical. If you see a patient early, persuade him to wear boots or shoes which will minimize further progression. The main preventive measure is wearing fully protective shoes from childhood. Sandals, or shoes with many open spaces on their uppers, may not protect.
Podoconiosis is disfiguring, and may make the patient a social outcast, so treatment is important. Unfortunately, by the time you see him, his lymphatics will probably be incurably blocked, so that medical treatment is unlikely to be effective. Surgically, you can: (1) Compress the leg of a 'soft' case in a decompression machine (if you have one), excise the folds of superfluous skin and subcutaneous tissue that are left after decompression, and then bring his skin edges together. (2) Excise the thickened tissue of a 'hard case', and graft the bare area. (3) Excise individual nodules. Or you can combine these procedures. Surgery is said to be simple and beneficial, but opinions differ.
Pn< v; EW, The pre-elephantiasic stage of nori-filarial elephantiasis oF the lower legs: podocornosis': Tropical Doctor 1984; 14:115-119
Pi x LvV, Mai uX- : M-; ii • eitden lie (i torvfilanal) eiopnant;as s of the lower legs' Fropical Doctor 1975,5-70-75
PODOCONIOSIS
EARLY DIAGNOSIS. After a long day's work in the fields, or a long walk, one of a patient's feet becomes swollen, and feels tense. His lymph nodes are enlarged and firm. For the differential diagnosis see the previous section. Try to recognize the following early stages:
'Burning leg' He has a burning sensation in his lower leg, from in front of his medial malleolus to behind the medial condyle of his knee, sometimes extending upwards into his thigh. His femoral nodes may be tender. Pain is usually worst at night, and is relieved by uncovering his leg. Each episode usually affects the same leg, and the second leg does not usually become involved untii the first one shows clear signs of disease. Although the burning area of the leg may be tender, few patients seek help at this stage.
'Itchy foot' is a persistent localized itching, usually on the dorsum at the base of the first or second toe clefts, or below the middle malleolus. Thickening of the skin (pachydermia), from constant scratching, may bring him to the clinic. When his toes start swelling, the itchy area precedes the upper level of the swelling, and indicates progression of the disease.
'Splayed forefoot' is a widening of his forefoot, and separation of his toes, which gives his foot a spatula-like appearance, on one or both sides (B, in Fig. 31-3). It is due to deep oedema between his metatarsal heads. His skin is unusually resistant to being lifted by your fingers.
Plantar oedema is asymmetrical (unlike cardiac or renal oedema). Press with your thumb on his sole over the head of his first metatarsal. Test for it when he has recovered from any temporary physiological oedema, which may be the result of walking a long way to the clinic. You may see mild lymphatic oozing, tiny blebs of lymph, or an an unusual number of flies attracted to it.
A pachydermic forefoot shows an excessive deposit of keratin on the dorsum at the base of the first or second toe cleft. The clefts themselves usually remain normal, even in advanced disease.
Increased skin markings at the base of the first toe cleft and running longitudinally rather than laterally (as is normal). Compressing them, as in D, Fig. 31-3, shows them more clearly.
'Block toes' lack their normal curves, and look wooden and rigid, as if they were nailed on the forefoot (A).
EARLY TREATMENT. Advise him like this: "(1) Raise the foot of your bed to the height which relieves the discomfort; a hammock is suitable. (2) Put on ankle-length elastic socks before rising in the morning; or apply wide (10 cm) one-way stretch elastic bandages; crepe bandages are inadequate. (3) Protect the skin of your feet from the soil, preferably in shoes. (4) Choose another occupation which does not involve contact with the soil (difficult). (5) Move to a non-endemic area (even more difficult)'. Meanwhile, treat whatever other conditions he has (parasites, anaemia, etc.).
CAUTION! Don't try to remove his femoral nodes.
EXCISION OF FOOT NODULES. Excise them for aesthetic reasons, or to make wearing shoes easier. They have no sensory nerves, so you can remove them without anaesthesia, which is useful, because they are so thickly indurated that infiltration may be impossible.
INTERMITTENT COMPRESSION AND THE EXCISION OF REDUNDANT TISSUE. Start by reducing the size of the swellings with the intermittent compression machine in A, Fig. 31-4.
Have blood cross-matched. With a tourniquet applied (essential), make an incision from the upper level of the loose skin behind his medial malleolus, along the medial side of the dorsum of his foot, and then lateraly across the dorsum. Excise the loose skin. If bringing the skin edges together is difficult, graft the raw area (D, 31-4). Advise him to wear stockings and boots (E).
EXCISION ALONE. See also Charles' operation in Section 31.6.
The surgery of filariasis
Wuchereria bancrofti and Brugia malayi, or W. timori behave in a similar, but not identical, way. The acute lesions they cause may mimic other diseases, so, if yours is an endemic area, keep the possibility of filariasis in mind. The first two stages are common, but filarial elephantiasis is not.
The acute stage starts within a few months of infection, as fever, lymphadenopathy, erythema, and epididymitis, usually without microfilariae in the blood. Secondary infection may occur.
The subacute stage is characterized by fever and enlarged tender lymph nodes, which persist and are accompanied by lymphangitis. The inguinal, epitrochlear, and axillary nodes are commonly involved. Lymphangitis presents as a shiny area, radiating distally from the involved lymph nodes, usually down the front or medial aspect of the thigh, or round the anterior axillary fold towards the oreast. Attacks may be repeated every few months. The lesions may also be infected secondarily, so that both the affected lymph nodes and the areas of lymphangitis may suppurate to form abscesses.
A patient's spermatic cord is often infected, and also his testes and epididymes, so that he has painful recurrent attacks of funiculo-epididymo-orchitis, which may be followed by suppuration in his scrotum.
Synovitis and arthritis also occur.
The chronic stage is the result of lymphatic obstruction, commonly in the retroperitoneum. This can cause:
(I) Lymphoedema, which may progress to gross hypertrophy Slis subcutaneous tissues (elephantiasis). This may involve his lower limbs and scrotum (common), or the arm, breast, or abdominal wall (less common), or the axillary or inguinal nodes (rare). No known treatment will reverse these changes. There is little you can do surgically except to excise the swellings; when you have done so, they may recur in a few years, or even a few months. Charles' operation is described; its immediate results may be acceptable, but its final results may be worse than before, and are said not to stand up to the wear and tear of village life. The surgery of elephantiasis is unsatisfactory, the account we give of Charles' operation is the classical one, and we were unable to find any recent 'experts'.
(2) Hydroceles, which are common in areas of Bancroftian filariasis (23.23). Treat these as usual.
(3) Lymphatic varices (uncommon). These are soft cystic swellings in his axilla, neck, or groin.
(4) Chyluria (not uncommon, 23.30), due to rupture of dilated lymphatics into his urinary tract.
Banjara BR 'Surgery for massive lymphoedema of the legs'. The Proceedings of the Association of Surgeons of East Africa 1982;5:79-81.
de Souza LJ, 'Rarer surgical aspects of filariasis'. East African Medical Journal 1964;41:413-8.
FILARIASIS
SPECIAL TESTS. (1) The microfilariae of W. bancrofti are usually present in blood films taken between 10 pm and 2 am. R malayi may be semiperiodic, or nonperiodic. Take fresh blood into an anticoagulant, and look for motile microfilaria under a coverslip. (2) Puncture an enlarged node, or lymphatic varix, with a needle, and look for filariae in the small volume of fluid you aspirate.
VARIOUS FILARIAL SYNDROMES See elsewhere for hydroceles (23.23) and chyluria (23.30).
If the patient's inguinal or axillary nodes are involved (rare), treat him medically and don't operate, or a troublesome fistula discharging lymph may result.
If his spermatic cord is involved ("endemic funiculitis'), don t mistake this for a strangulated hernia (14.6), or torsion of the testis (23.24).
If he complains of a painful swelling Mike a bag of worms'above his testis, one possibility is a varicoele, and another is a lymphocele of the cord (E. Fig. 31-5). At operation you may see distended lymphatics, not distended veins.
If the swelling in his cord is like a hen's egg, it may be an
