Lymphedema
Identifieur interne : 005715 ( Istex/Corpus ); précédent : 005714; suivant : 005716Lymphedema
Auteurs : Geza De Takats ; Matthew H. EvoySource :
- Angiology [ 0003-3197 ] ; 1950-02.
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DOI: 10.1177/000331975000100107
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ISTEX:B9543C4B2726D5FA881CA45F0791B3DE7F3CABC9Le document en format XML
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<publisher-name>Sage Publications</publisher-name>
<publisher-loc>Sage CA: Thousand Oaks, CA</publisher-loc>
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<contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>De Takats</surname><given-names>Geza</given-names></name><aff>Department of Surgery, University of Illinois, College of Medicine and St. Luke's Hospital, Chicago</aff></contrib></contrib-group>
<contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Evoy</surname><given-names>Matthew H.</given-names></name><aff>Department of Surgery, University of Illinois, College of Medicine and St. Luke's Hospital, Chicago</aff></contrib></contrib-group>
<pub-date pub-type="ppub"><month>02</month><year>1950</year></pub-date><volume>1</volume><issue>1</issue><fpage>73</fpage><lpage>99</lpage><custom-meta-wrap><custom-meta xlink:type="simple"><meta-name>sagemeta-type</meta-name><meta-value>Journal Article</meta-value></custom-meta><custom-meta xlink:type="simple"><meta-name>search-text</meta-name><meta-value>73 Lymphedema SAGE Publications, Inc.1950DOI: 10.1177/000331975000100107 Geza De Takats Department of Surgery, University of Illinois, College of Medicine and St. Luke's Hospital, Chicago Matthew H. Evoy Department of Surgery, University of Illinois, College of Medicine and St. Luke's Hospital, Chicago The purpose of this communication is to describe a personal experience with 150 cases of lymphedema and describe such principles of its management, which have gradually crystallized during the past twenty years. No attempt will be made to review the literature on the subject, which has been done recently, together with an excellent survey of personal experience by Alien, Barker and Hines ( 1 ) . CLASSIFICATION We have used a simple classification into congenital, traumatic, inflammatory and degenerative types of lymphedema; from the standpoint of the original site of blockage one can observe a peripheral, regional and central type of obstruction, although sooner or later these types become mixed. Finally, indicating our state of ignorance, one may speak of lymphedema of known and unknown etiology, the latter being represented by 31 patients in our series (table 1). THE PERVERTED PHYSIOLOGY OF LYMPHATIC BLOCKADE The mechanism of an ascending lymphangitis producing an enlargement of the regional lymph nodes followed by obstruction of lymphatic channels and lymph glands is clear enough, and one encounters this after erysipelas, after a streptococcus infection of the fingers or toes and frequently after ringworm infection with secondary invasion of bacteria. Conversely, a blockade following extirpation of regional lymph nodes, X-ray therapy of regional lymph nodes or malignant invasion of these nodes will result in a central obstruction with secondary, retrograde changes in the peripheral lymphatics. Retrograde course of malignant cells in cases of uterine cancer or cancer of the breast spreading peripherally is a recognized mode of extension, and there are enough examples in the literature to desist from belaboring this point. We are more interested in some of the early stages in lymphedema, when the change may still be reversible. Throughout our presentation, our emphasis will be on treating the lesion at an early, reversible stage since the results of treatment in the later phases are far from satisfactory. When because of injury, venous stasis, or inflammatory reaction, capillary permeability increases, a protein-rich interstitial fluid appears which has difficulty in being transported away by venous or lymphatic drainage. In early experiments with Zimmermann, one of us (G. d. T.) showed that this exudate, whose protein content we measured, precipitates and forms a fibrinous network in the interstitial tissues (2). Later this "plasma-clot" was found to operate in burns (3), and in immersion limbs (4). This fibrinous exudate is deleterious for two reasons. In the first place, the 74 fibrinous network acts as a scaffolding for further proliferation of fibroblasts and forms a hard, irreversible lymphedema, which is non-absorbable. Clark and Clark (5) found that this exudate contains growth-promoting properties and that fibrinolysis may take place, but results in severe scar-contraction. Secondly, the lymph channels themselves become plugged with the fibrinous exudate and lymphatic thrombosis develops resulting in obliteration of the regional lymphat- ics. While obliterative streptococcus lymphangitis is a generally recognized entity, less attention has been paid to the exotoxin of staphylococcus aureus, which produces necrotizing material and lymphatic blockade (6). Large pools of tissue fluid develop, which are unable to drain and the valvular apparatus of the lymphatic system, which has been studied by Drinker and Yoffey (7), is thrown out of commission. The outer network of the lymphatics, situated in the outer part of the corium, contains very few scattered valves; they end in blind pockets TABLE 1 Ly~nphedema 150 patients in the subcuticular papillae. Many more are found in the deeper lymphatics of the skin, which in turn empty into still larger valved channels, usually accompanying the larger veins. Because the superficial lymphatic system contains such few valves, dyes injected into their system may drift about in any and all directions as governed by gravity or movement of the parts as soon as there is any obstruction, as shown experimentally by Homans, Drinker and Field (8). Clinically, this is manifested by an early lymphatic valvular insufficiency in case of regional obstruction; such lymphedema is readily lessened by massage, elevation, elastic compression. When, however, the lymphatic blockade is in the peripheral lymphatics, and there is a great deal of clotted plasma in the interstitial spaces, the edema is hard, immovable and responds very little to elevation, to bandaging or to massage. The studies of Me-Master and his associates have clarified many of the factors which govern interstitial pressure and interstitial resistance (9). Under conditions of venous obstruction or rapidly forming edema following injury, the pressure of edema fluid may rise to such an extent as to oppose the filtration of fluid from 75 vessels and to increase the formation of lymph. Clinically, there has been considerable confusion in employing measures which increase lymph flow contrasted with measures which improve lymph drainage. The studies of Rlcalaster and his associates (10) carried out with the help of colored streamers have demonstrated that very rapid lymph movement follows the release of venous hyperemia just FIG. 1. Unilateral ly-mphedema in David L., 6 year old bop- without any associated birth- mark or recognizable infection. as much as after violent muscular exercise; there is also excellent now of lyhmp in nephrotic edema with good cardiac action. Pulsatile now in the terminal vascular bed increases the formation and flov- of lymph; conversely, non-pulsatile flow or cardiac edema with failing circulation in motionless limbs result in lymph stasis. Certainly, one must determine in every case whether increasing lymph production will improve or aggravate lymphedema. This question will be discussed under the heading of treatment. 76 MATERIAL STUDIED A. Congenital lymphedema (fig. 1, 2, 3, 4) The association of this syndrome with other congenital anomalies such as birthmarks, hemangiomas and lymphangiomas and lymphangiectases make it FIG. 2. Congenital lymphatico-vascular anomaly of the right lower extremity. B. S., age 3. There were numerous birthmarks elsewhere in the body. Multiple stage excisions revealed lymph cysts together with vascular dilatation. clear that this is a congenital malformation. In our biopsies and dissections, we are particularly impressed with the presence of lymph cysts, half solid, half fluctuating masses, which may be found in the subcutaneous, but also in subfascial, intramuscular and peritendinous tissues and which may extend into the retroperitoneal space. Quite recently Ehrich and his coworkers (11) were able 77 to show numerous heparinocytes around lymph and blood vessels in a case of scrotal elephantiasis. They could obtain 126 milligrams of purified heparin per kilogram of ,yet tissue. This finding might well explain the frequent absence of clotting in huge lymph pockets and the long lasting lymphorrhea from inguinal wounds. Multiple stage excisions of these masses hare been done; but the extent Fm. 3. Bruce B., 3 year old boy ou whom now- two stages have been completed. The large pocket on the dorsum of the hand could he flittened out by a plastic operation as shown in Fig. 4. of the lesions may frequently prohibit a complete excision. In case of the lower extremities we have seen involvement of the buttocks, of the scrotum and penis, indicating high lymphatic obstruction or extensive local cysts formation. There is no inflammatory component in this lesion and the tissues remain remarkably soft; when a Kondoleun'~ operation is capable of removing the diseased tissue, a fairly useful extremity results. The cosmetic result is never very encouraging. Often amputation is the only possible course (fig. 5). When the congenital anomaly is also hereditary, it is customary to speak of 78 Milroy's disease, but realizing how patients may confuse their parents' thrombophlebitis or cardio-renal edema with something resembling their affliction, great caution must be exercised in diagnosing Milroy's disease. VUe have not encountered a single case in this series. FIG. 4. Bruce B., after first stage of multiple excision. Revised from Kodachrome transparency. Hemihypertrophy of an extremity or of two homolateral extremities may give rise to an erroneous diagnosis of lymphedema. These large, often little used extremities, may show secondary lymph stasis; unilateral lymphedemas following cerebral involvement have been reported by Luhan (12) and others. B. Traumatic lymphedema Every sprain, contusion or laceration which results in injury to cells, change in capillary permeability, and accumulation of tissue fluid, results in an acute lymphedema, which may be then aggravated by such factors as hemorrhage, 79 dependent position, tight bandage, or cast and secondary infection. Every effort should be made in any type of injury, whether mechanical, thermal, chemical, or radiologic, to minimize the early edema, since intractable, irreversible fibrosis may be the result. If the lower extremity is affected, adequate elastic compression should be used, and if immobilization is necessary the extremity should be elevated by placing books or blocks under the foot of the bed. Constricting FIG. 5. DWAYNE L., A 16 YEAR OLD BOY WITH A PsEUDO-CuSHINGS SYNDROME, WHO HAS HAD AN UNSUCCESSFUL KONDOLEON OPERATION Amputation has been advised bandages or casts are notoriously harmful, and one occasionally sees a hard edema of the dorsum of the hand brought about by constriction at the wrists. In case of a fractured metacarpal bone, a soldier had a circular cast applied which was later bivalved. Nevertheless, he developed a massive hard edema over the dorsum of the hand «-without any vasomotor symptoms. The function of the hand was permanently impaired. Traumatic lymphedema is one of the characteristic features of causalgic states (13). Here the stoppage of lymph- now is due to the complete immobility of the 80 injured part, which the patient holds in a fixed and often dependent position (fig. 6). When early pain relief is accomplished by sympathetic block or sympathectomy, the transport of lymph can be reestablished. The late, intractable causalgic hands or feet all suffer from a marked fibrosis of the skin, subcutaneous tissues, muscles, tendon sheaths and joints; there is no need to invoke a special neurotrophic injury: the complete immobility can sufficiently explain it. FIG. 6. CAUSALGIC STATE IN THE CASE OF MARY C. L., 16 YEAR OLD SCHOOLGIRL, WHO HAS HELD HER RIGHT UPPER EXTREMITY IN A FIXED AND DEPENDENT POSITION FOR SEVERAL MONTHS The edema was hard and responded only very slowly to physical treatment. Such hands later become shrunken and atrophic, with a glossy skin and much fibrosis. Injury to the regional lymph nodes in the axilla or groin may lead to lymphedema. The edema of the upper extremity following removal of the breast, is according to the studies of Holman, ::\1cSwain and Beal (14) favored by a combination of infection and radiotherapy; hence the actual clean dissection of the regional nodes does not lead to permanent lymphedema either, because a few nodes are always left intact or because of the well known regenerative powers of lymphatics (15). Infection, however, as will be pointed out later, sets up a descending, obliterative lymphangitis and predisposes to the recurrent acute attack. Roentgen ray is of course capable of obliterating the sinuses of lymph nodes, destroying lymphocytes and closing lymph channels. Not enough use is made, 81 however, of small doses of X-ray (50-80 R. units) in the treatment of acute obstructive lymphadenitis and lymphangitis. This will be discussed further under therapeutic considerations. Following the injury to enlarged lymph nodes, encountered especially in the groin, an extensive lymph now, a lymphorrhea develops, which may last for weeks and months. Such a situation is encountered after vein ligations, embolectomies, aneurysm-operations, and we have two observations to report in this connection. One is, that after a few days of lymphorrhea, a previously swollen extremity loses FIG. 7. INFLAMMATORY LY\II'IIEDEJI_1 IW MARY C., A 45 YEAR OLD HOLSEW'IFE WHOSE EDEMA STARTED WITH A STORMY FEBRILE COURSE WITH CHILLS The leg was never bandaged. Both trichophytosis and trichomonas vaginalis were present. Her general hygiene was poor. Seven years previous to the present picture a modified Kondoleon operation was performed. She had a course of autogenous streptococcus vaccine. Note the raised cutaneous warts, the "pig-skin" of chronic cutaneous lymphedema. Bed rest, mercurial diuretics and well fitting elastic hose permit her to perform her household duties as a mother of nine children. much of the edema only to regain it again when the lymphorrhea stops; secondly, that the lymphorrhea can be very effectively checked by doses of X-ray about 150-200 R. units. C. Inflammatory lymphedema (figs. 7 and 8) By far the largest percentage of lymphedemas are of inflammatory origin. The role of infection in the production of recurrent attacks of acute lymphangitis has been discussed in detail by Ochsner and his associates (16). Elephantiasis is the result of recurrent erysipeloid lymphangitis produced usually by the streptococcus. They were impressed by the importance of reinfection and local tissue sensitivity as dual factors of these recurrent attacks. Attempts to find the organ- 82 isms producing the recurrent attacks have been always made; we have scraped the acutely inflamed skin and examined the scales, we have taken blood cultures at the time of the chill and between attacks, we have injected chill-producing doses (25 million bacteria) of triple typhoid vaccine. Only once was a green-producing streptococcus found in a ten-day blood culture; in another patient, suffering from a chronic thrombophlebitic edema with marked lymph stasis, an acute tonsillitis which yielded streptococcus viridans, provided the source of an autogenous vaccine. In this patient all further attacks stopped for over 5 years, but this has not been true of other patients receiving autogenous vaccines or FIG. 8. SUBCUTANEOUS TISSUE OF MARY C., WHOSE PHOTOGRAPH Is SHOWN IN FIU. 7 Note the irreversible fibrosis, the broken-up elastic fibers which can never function so that even if mobilizable fluid is evacuated, the skin and connective tissue will not contract around it. There is little inflammatory reaction or enlarged lymph spaces in this section. Nothing but excision can remedy such a situation. polyvalent streptococcus antiserum. In fact, the question can be raised, whether or not the staphylococcus aureus is involved in some of these recurrent attacks of obstructive lymphangitis. Especially Menkin (6) has emphasized that the invasive property of a microorganism is determined by the patency of the lymphatic vessels; the staphylococcus aureus produces such blockade and in addition manufactures an exotoxic, necrotizing material, which is thromboplastic and in itself produces lymphatic blockade. One can readily distinguish a reticular and tubular lymphangitis, the former producing the red, raised hot skin or erysipelas, the latter being the red streak which accompanies veins, and is the involvement of collecting lymphatics and finally results in a painful swelling of the regional lymphatics. Such a single attack of tubular or reticular lymphangitis seldom, if 83 ever, leads to persistent lymphedema. It has to recur sex-eral times, or it must involve a large group of lymph glands before it will do so. Since trichophytosis is of such frequent occurrence in the feet, we believe that this fungus or a secondary invader, a streptococcus, is a frequent source of inflammatory lymphedema. Often this is limited to the dorsum of the foot and can be stopped from ascending by adequate therapy. The recurrent character of flare-ups in infective lymphedema has suggested a possible role of sensitization (16, 17a), and owe have carried out many therapeutic attempts in this direction, which will be described later under therapy. Because of the frequency of pelvic infections and pelvic lymphadenitis in women, because the pelvic or presacral nodes may spread lymphatic blockade in a retrograde fashion to the inguinal ones, and because vaginitis and cervicitis drain to the inguinal lymph glands, we have postulated such a source of lymphatic obstruction in a number of women affected with so called idiopathic non-inflammatory lymphedema. Trichomonas vaginalis, whether through the flagellate itself or with the help of secondary invaders, notably the streptococcus, may produce cervical or pelvic inflammation. It is sufficiently know, that the collecting lymphatics of the cervix form a paracervical plexus; from this plexus three sets of lymphatics emerge: one of these follows the uterine artery in front of the ureter and drains into the external iliac nodes. Another set passes behind the ureter into the hypogastric system, and the third group runs posteriorly to the presacral nodes (fig. 9). Trichomonas can cause vaginitis regardless of bacterial flora, so can monilia. There is a rarity of the parasites above the external os (18), but it is sufficiently known that urethral, rectal involvement, invasion of Bartholin's glands and Skene's glands may occur, and in the male, the prostate may become infected. From Trussell's classical monograph the following facts, pertinent to our present problem, can be assembled (19): 1) Trichomonas vaginalis can produce vaginitis even with a normal vaginal bacterial flora and acidity, but pathogenic organisms and decrease in acidity such as occurs during menstruation facilitate its virulence. 2) Many women harbor this infection in the absence of subjective or objective abnormalities except for a purulent discharge. This may be explained by the avirulence of some of these fungi, but the author has produced data showing that there is immunity as manifested by complement fixation and by micro-agglutination tests. While such methods have hardly any clinical value because of the wide-spread occurrence of this infection, it may explain the regional lymphatic hyperplasia on an immunological basis, the lymph follicles producing antibodies. The results of vaccine therapy of tricho- moniasis has been suggested by some authors (19). One cannot escape the conclusion, that in trichomonas vaginitis occasional lymphatic spread may lead to inguinal adenopathy and for years, we have had our female patients who were lymphedematous, undergo gynecological examination. Case report 1. R. B., a 38 year old white housewife, entered St. Luke's Hospital on January 5, 1947, because of persistent swelling of the right ankle. Three years previously edema developed in the left ankle and lower leg. and this receded in three or four months. The right ankle and lower leg began to swell two months after the edema on the left side had 84 subsided; and this has progressed rather steadily until entrance. Seven months ago an acute inflammatory process developed in the swollen tissues of the right leg, and with this attack the patient had a fever to 101°F. and no chill. Another, similar episode took place two months ago. She had been married for 16 years but had not ever been pregnant. Athlete's FIG. 9. DIAGRAM OF THE LYMPHATIC APPARATUS DRAINING THE INGUINAL, ILIAC AND AORTIC NODES On the left drainage from cervix, vagina and vulva is shown toward the inguinal bottle neck; on the right the lymphatic drainage from the lower extremity is illustrated. Drainage from the parametrium is indicated toward the iliac, sacral and retroperitoneal nodes around the vena cava and aorta. In case of obstructed lymph glands, retrograde and collateral flow of lymph occurs. foot on both sides had been present off and on for eight or ten years and had been treated by home remedies. Very soon after her marriage, a bout of pain was diagnosed as right pelvic inflammatory disease. A leucorrhea of severe degree started 4 years ago, and trichomonas were found. Treatments for this disorder have been futile, although many of the most effective agents have been used. She has to wear a pad constantly. Examination showed a typical right lymphedema extending to the middle third of the lower leg. The edematous tissue was somewhat warm. Temperature was 99.4°F., (and has been that each day for the past 5 days). Gynecological examination showed an extensive trichovaginitis 85 with punctate hemorrhages. Treatment consisted of extensive local treatment of vaginitis by Dr. E. A. Edwards, short bed rest and mercurial diuretics followed by a well fitting elastic hose from toes to groin to be worn constantly during the day. Reexamination two years later showed a marked decrease in edema, although elastic hose has to be worn constantly. The vaginitis has cleared up completely, and there have been no further bouts of fever and chills. While the incidence of trichomonas vaginitis is very high, it is also true that trichophytosis in men is very wide spread and yet only a small percentage of such patients develop lymphatic blockade. Clearing up the original source of infection at least prevents reinfection or further spread; nor is it known, whether the fungus or a secondary invader is responsible for the lymphatic response. The infectious lymphadenopathy, complicated by radiation fibrosis, presents a vexing problem of huge edemas following axillary dissection. The lymph block of the regional lymphatics produces a lateral and retrograde spread of lymphatic blockade in the channels so that gradually the skin lymphatics become involved and exhibit the brawny leathery skin resembling scleroderma. The periphlebitis accompanying venous thrombosis is another frequent form of inflammatory lymphedema and John Homans for many years has emphasized that thrombophlebitic edema is overwhelmingly lymphatic in origin (17b). After some initial doubts, based on animal experiments (2), we fully acknowledge the wisdom and accuracy of his teaching. Also, the so called thrombophlebitic induration with or without ulceration is unquestionably a patchy lymphedema and so often the most disabling consequence of iliofemoral thrombophlebitis. When the perivenous lymphatics and lymph channels become involved as a result of an intravascular thrombosis or an ascending tubular lymphangitis, the adjoining peripheral nerve trunks may get caught in the exudate and a peri- neuritis develops with symptoms of causalgic pain. We have observed this in the form of a saphenous neuritis after femoral thrombosis, after a hand infection with axillary lymphadenopathy followed by severe neuralgia of ulnar distribution and after a cervical lymphadenopathy in which an atypical neuralgia of the face developed. The periadenitis here involved the descending branch of the hypo- glossus, the vagus and the cervical sympathetics. Especially the work of Kiss has emphasized the vicinity of lymph glands to autonomic nerve structures, and the possible functional disturbances derived from this source (20). D. Degenerative lymphedema A glandular metastasis to regional lymph nodes not only blocks the circulation of the lymph but may produce retrograde metastases. We have seen striking examples of this, such as a patch of carcinomatous skin of the heel in cancer of the uterus, the pig skin of upper extremities in axillary metastases from carcinoma of the breast and a lymphedematous penis with skin carcinoma following carcinoma of the bladder. The point should be made that in every case of slowly increasing lymphedema, without obvious congenital, traumatic or inflammatory etiology, the possibility of gland-metastases or primary node involvement, such as Hodgkin's disease or lymphosareoma, should be considered, since again and again a small biopsy will reveal such an origin of lymphatic blockade. 86 Case report ,~. In the case of Mr. J. S., who developed a unilateral edema following an injection treatment of hemorrhoids, a diagnosis of thrombophlebitis was made by several physicians in a large city on the Pacific Coast. When seen by me, 2 months later, in May 1940, he exhibited a large firm lymphedema of the right lower extremity with palpable firm lymph glands in the groin and no evidence of venous stasis. X-ray of the spine revealed metastatic bony lesions in the spine. He died in less than a year from the onset of the lymphedema from an inoperable carcinoma of the rectum. Large lymphedemas as a result of retroperitoneal glandular metastases from uterine, prostatic, or vesical cancers are comparatively frequent; it is well to realize that the blockade is higher than the groin and that Roentgen ray therapy should be directed to the paravertebral and preaortic glands. Case report 3. A young woman of 25, cashier at the Palmer House, had been told that her unilateral edema was due to prolonged standing. The edema was rather soft but included the gluteal fold and buttocks; she had hard inguinal lymph nodes but no other palpable lymphatic enlargement. Biopsy showed Hodgkin's disease; she later developed intermittent cervical and axillary glandular enlargements with fever and died 6 months after the initial symptom of unilateral lymphedema of the left lower extremity. E. Atypical mixed forms Bartender's legs. The combination of prolonged standing, chronic alcoholism, avitaminosis, poor nutritional status with hypoproteinemia and increased capillary fragility produces swollen, rather intractable lesions to which skin infections, dermatitis, ulceration and lymphadenitis add a lymphatic component. Such men stand 12 to 18 hours daily and can hardly be rehabilitated without change in occupation. Causalgic edema, to which we have referred under the traumatic group differs from it because of the considerable vasomotor element (early vasodilatation, late vasoconstriction) and the complete voluntary fixation in which these extremities are held. While in the early weeks the edema readily yields to appropriate treatment, the late fibrosis, the contracture of synovial membranes, tendon sheaths and ligaments is an irreversible process. Recurrent (allergic?) lymphedema. Following the work of Matas (21), Thomp- son (22), Naide (23), and Ochsner (16), we have studied a considerable number of patients with Dr. J. H. Jesser, an allergist associated with our vascular clinic. We have tested a number of patients with intracutaneous tests with fungi, streptococci and autogenous vaccines but neither the diagnostic or therapeutic attempts yielded any practical results. Bret Ratner (24) has recently postulated that the terminal arterioles may be the shock organ in allergic states, that the wheal formation is the result of arteriolar spasm followed by increased permeability. We have not seen, however, any evidence of increased whealing in clinical cases of lymphedema, although they were tested with histamine flares. However, sensitization phenomena such as dermatitis due to the use of sulfa drugs and urticaria due to penicillin are often localized in the lymphedematous extremity; one can readily explain this by the concentration of allergens in areas with poor lymphatic drainage. Peripheral lymph gland being the site of antibody formation, the efferent 87 lymph channels pour out lymphocytes in large quantities on certain stimuli. Ehrich (25) showed that triple typhoid vaccine may raise the efferent lymphocyte count from 15,000 to 60,000 per cubic millimeter, together with enlargement of lymph glands. Later a regression of lymphoid tissue was observed. The immunologic aspect of inflammatory lymphedema permeates the entire field of pathogenesis, even if the therapeutic attempts have so far been of little promise. TREATMENT The objectives of treatment can be readily summarized as follows: 1) mobilization of edema fluid as soon as possible, 2) prevention of reaccumulation of fluid in the dependent position, and 3) removal of irreversibly damaged fibrous tissue together with non-draining pools of stagnant lymph. Obviously, the success or failure of these procedures will depend on the early or late stage of the disease in which treatment is undertaken, and whether or not the process of lymph blockade can be arrested, whether it is progressive or recurrent. A. Treatment of acute lymphedema In the acute stage of lymphedema, be it traumatic, inflammatory or allergic in origin, the following measures have been of value to minimize permanent damage. 1 ) Elevation of the affected extremity. In case of the upper extremity, this is hung down from a Balkan frame, care being exerted not to constrict the wrist or hand in hanging it through a sling. In case of the lower extremity the bed is lifted on two chairs or 10 to 12 inch shock-blocks. Pillows under the feet and lower legs produce angulation at the knee and groin and do not drain veins and lymphatics adequately. 2) Frequent active moment or at least muscular contractions are urged, whether the limb is in a splint or wrapped in foments; only in acute spreading lymphangitis is complete rest enforced. 3) Adequate elastic compression of the edematous part is accomplished with elastic bandages or glycerin-gelatin boots. This will reduce tissue pressure, collapse superficial veins and lymphatics and enhance deep venous and lymphatic circulation. 4) ltTercuriat diuresis, preceded by acidifying drugs, such as ammonium chloride or ammonium nitrate, has been found by one of us to rapidly decrease thrombophlebitic edema (26). In the light of our present knowledge, this is overwhelmingly a lymphedema. It is important not to dehydrate the patient to an extent that his clotting mechanism is disturbed, and therefore one or two intravenous injections of mercuhydrin should suffice. We have seen extensive vascular thrombosis from prolonged intensive dehydration. 5) Sympathetic block. Ochsner and De Bakey (27) have recently revie`~-ed and extended their concept of postphlebitic sequelae. In this excellent survey they maintain that not only the acute, but 90 per cent of the chronic thrombophlebitic edemas are maintained by vasospasm. V'e fully agree, that chronic thrombophlebitic edemas respond sometimes surprisingly well to one or two sympathetic blocks with procaine; we shall discuss this observation in the treatment of the 88 late cases. In acute lymphedema, however, no matter of what origin, sympathetic blocks have only been used when there is evidence of a cold, cyanotic extremity with diminished pulsations and diffuse, poorly localizable, agonizing vascular pain. In such patients the effect of paravertebral block is truly dramatic. The majority of our patients, however, have a warm, throbbing extremity with increased oscillations or plethysmographic tracings, and the percentage of the paravertebral blocks which we have performed is small in this series. 6) Heparin therapy. For some time we have felt, that the marked diminution of periphlebitic, i.e. lymphatic edema which one observes on administering heparin in the acute phase, must be due to the effect of the anticoagulant on the extravascular formation of fibrin. With Zimmermann, one of us (G. de T.), showed in 1931 (2), that in acute thrombophlebitic edema, produced experimentally in animals, a massive fibrinous exudate appeared in the muscles and other soft tissues. We also measured the protein content of this fluid, which obviously was clotted plasma. Heparin then, as pointed out by Loewe and his associates (28), may well act on this extravasated plasma and facilitate its uptake into lymphatics; it also, if administered early enough, should militate against thrombosis of the lymph channels and in lymph glands whose sinusoids often contain fibrin. It would be difficult to explain the often spectacular diminution of acute periphlebitic, lymphatic edema any other way, unless heparin operated through release of vasospasm. Such an action has recently been suggested on coronary vessels by Gilbert and Nalefski (29) for certain types of heparin and is now under investigation on our service. Our method of administration of heparin is as follows: with the help of a priming, intravenous dose of 3 to 5 cubic centimeters of 1 per cent aqueous heparin the capillary clotting time is raised from 3 to between 8 and 12 minutes within an hour; this elevation can be maintained by intramuscular injections of 10 per cent heparin (30), given every 6 to 8 hours in amounts of 100 to 200 milligrams, depending on the patient's response to heparin (31). Four to five days of this regime should suffice, provided the patient can be mobilized. Should he be bed-ridden for a longer time, this type of administration can be maintained for as long as desired. Few patients show sensitization phenomena to heparin, sometimes of an alarming nature, and only in these is dicumarol given. Elsewhere (32) we have marshalled our objections to dicumarol which consist briefly in 1) incidence of hemorrhage at so called "safe" prothrombin levels, 2) poor correlation between prothrombin levels and occurrence of hemorrhage and thrombosis, 3) lack of standardized prothrombin times, which even if reliable, reflect only one aspect of the clotting mechanism. For this reason, dicumarol is only exceptionally used at the moment. 7) Roentgen therapy. Since 1933, when one of us with Zimmermann, Gault and Halpern (33) described the disappearance of experimentally produced thrombophlebitic edema following radiation, we have exposed a group of patients suffering from acute lymphatic or periphlebitic obstruction to small doses of Roentgen ray; recently a report was made of 100 patients subjected to such therapy (34). It is sufficiently known, that Roentgen ray hastens the absorption 89 of inflammatory exudates and that it produces dissolution of ly mphocytes both with small and large doses, the small dose only acting in the presence of an intact pituitary-adrenal mechanism (35). While many other mechanisms have been postulated to operate in the treatment of inflammatory reactions by Roentgen rays, the presence of lymphopenia, and the rise in immune globulin as a result of lymphocyte dissolution is well established, and this is of great interest in connection with lymphedema. The radiation of isthmic points, such as the popliteal, inguinal and paravertebral spaces, produces not only a diminution in the size of the lymph glands, but possibly a rise in antibodies against the offending organism. The selection of cases for this type of therapy will be discussed below. The general rule, that the more acute the inflammation, the smaller should be the dose, must be strictly observed. We have observed severe febrile reactions from 150 to 200 r given by zealous residents; from 50 to 80 r seems to be the optimal for most acute and subacute cases of lymphangitis and lymphadenitis. Most patients require 1 to 3 treatments of each area, using 20 K.V., 20 M.A., F.S.D. 50 centimeters and medium Thoraeus filter. The H.V.L. is 1.9 millimeter copper (34). Selection of cases for different forms of treatment. Certainly, elevation of limbs, active movement and elastic compression are indicated in all cases, early or late. Mercurial diuresis was used frequently in our early experience, but recently, we have restricted its use to patients in whom other methods of rapid release of edema are not indicated or impossible. We still employ it in chronic lymphedemas preparatory to the fitting of an elastic hose. Anticoagulant therapy is employed in all lymphatic obstructions which accompany iliofemoral thrombophlebitis. Sympathetic block as mentioned above is only used in the vasospastic group but in the chronic cases especially if accompanied by a causalgic type of pain, its use has been of great value. Roentgen therapy has been employed in patients showing lymphangitic streaks, hyperplasia of lymph glands, and in lymphorrhea following operations on lymphedematous extremities. B. Treatment of chronic lymphedema Inspection of the fibrotic subcutaneous fat, the lacunar spaces filled with tissue fluid which undulates to and fro with gravity, palpation of the thickened deep fascia which barricades the lymph-soaked tissue from the muscle spaces, and the histological study of soft tissues and lymph glands make it clear, that one is dealing with an irreversible process, and that the object of treatment can only be either an arrest of the disease so that further deterioration is prevented or the removal of as much of this tissue as possible without sacrificing the function of the limb. Again elevation of the foot of the bed during the night and adequate support are helpful. The elastic bandage or the elastic hose made to order from toes to groin will not decrease the edema; they may hold the edema, which has been reduced over night by elevation, by a few days of bed rest, by mercurial diuretics or by sympathetic block. In massive edemas, it is ,vise to start with one of these procedures. Also, for years we have prescribed a low-salt diet with a daily water 90 restriction to 1500 cubic centimeters. Certainly, excessive fluid intake, especially in the pretzel-beer consuming group, demonstrably increases lymphedema. (See FIG. 10. CONGENITAL LYMPHEDEMA I1 TI-IE CASE OF DOLORES L., OF THE RIGHT LOWER EXTREMITY, WHICH CONTAINED A :0:"LMBER OF LARGE LYMPH CYSTS This picture was obtained one year after operation. Neo elastic support has been necessary under Bartender's Legs.) In chronic lymphedemas due to malignant invasion of inguinal, pelvic and periaortic lymph glands, deep X-ray therapy frequently gave temporary relief fro:n pain and decreased the edema. 91 C. The surgical treatment of lymphedema In order to accept a surgical indication in the treatment of lymphedema, the lesion must be chronic, stationary or progressive and the cosmetic appearance not be a reason for operation li'hcn the extremity is painfully heavy, when the FIG. 11. KONDOLEON OPERATION IN THE CASE OF Mns. K. E. The lateral aspect of the left and the medial aspect of the right lower extremity have been operated on a w-eek apart. Stitches have just been removed. Glycerin-gelatin casts are applied for 3-4 months before the operations on the contra-lateral sides. wearing of shoes becomes difficult, when ulceration or draining cutaneous lymph cysts appear, a radical excision is indicated (fig. 10); hut minor edemas are better left alone, since the cosmetic result leaves much to be desired. For many years we have used the modification of the Iiondoleon operation as described by Sistrunk and by Homans (fig. 11), --\Iace-,-'s two stage procedure (36) was employed twice and complete dermatome grafts laid on bare muscle in one instance. In addition, Dr. William C. Beck (3r`~ tried some plastic tube 92 drainage on our service and reports good results in 60 per cent of the patients.' In one instance the discovery of multiple congenital lymph cysts in the retroperitoneal fossa lead to their puncture and drainage into the loose paravertebral tissue with marked diminution of the edema in the lower extremity. We have not found it necessary to visualize the dilated channels according to Servelle's method (38), but our procedure is actually identical with his, namely a total resection of the aponeurosis from the knee to ankle and foot, occasionally to the groin with maintenance of skin flaps, whose venous return, as pointed out by Homans, is jealously guarded. We have adequate follow-up records of 28 patients on whom radical excision of the subcutaneous lymphatic spaces, together with the fibrotic aponeurosis, was done. The following table summarizes our results (table 2). Generally speaking, the congenital lymphedemas, operated on early between the ages of 6-10 years, have done better than the inflammatory ones. While we TABLE 2 The surgical treatment of lymphedema 28 patients followed from 1-25 years Satisfactory: disease arrested, limb has excellent function, with no economic handicap. Doubtful: some return of edema, recurrent inflammation, reoperation contemplated or in progress. Poor: progress of the disease, ulcerations, limb a severe handicap to the patient. originally felt, that the recurrent streptococcus infections constitute a contraindication to operation, more recent experience, especially in one patient whose recurrent episodes stopped after surgical excision, makes us feel, that the removal of the infectious focus, the trigger for sensitization, may be a worth while procedure; naturally, preliminary bed rest and preoperative and postoperative penicillin therapy are important against activating a dormant infection. We have never used the sulfa drugs in the prophylaxis of recurrent infection for fear of increasing sensitivity phenomena. Case report 4. Mrs. S. B., a 31 year old married woman, consulted us the first time in January 1947, complaining of repeated attacks of chills, rash and fever. The right ankle began to swell 9 years ago when she was pregnant. This pregnancy was followed by an abortion and ever since that time there has been a gradual increase in the size of the right lower extremity. She also knows of ringworm infection of both feet. On examination, there was a typical, hard edema of the right leg and thigh, with enlarged glands in the groin. Dr. Eugene A. Edwards found no pelvic infection but some cystic ovaries. Biopsy of the inguinal lymph gland revealed dense fibrous tissue with practically no lymphatic tissue. She was given 1 William C. Beck: Personal communication. 93 continuous elastic compression, and salve and powder for the ringworm infection. In September 1947, the patient had another acute attack, together with sore throat. The throat culture yielded a green-producing streptococcus and an autogenous vaccine was prepared. Dr. Jesser, our allergist, outlined the dosage and subcutaneous injections for her at home, . FIG. 12. PLEXIFOR~1 XEL"RO:.IA ON THE RIGHT L()W ER LEG IN A 12 YEAR OLD BOY There is considerable lymphedema associated with this condition. While the biopsy revealed no malignant cells, a hemipelvectomy may have to be done to arrest the spread of the lesion. which she took. After doubling the dose to 0.2 cc. she had a severe reaction, local and general. In October 1947, a marked sensitivity to two types of molds was found, but no further vaccines were prepared. In March 1948 the swelling persisted but there was no new attack. However, in July 1948, another attack occurred, which was rapidly aborted with penicillin. At the time a Kondoleon operation wars suggested, which was performed elsewhere. Reexamination in July 1949 yielded marked diminution of edema since the first stage of the operation. She was pleased with the result and was planning to continue with the second stage at a later date. 94 In the congenital group, some patients were seen in their early infancy, and we have generally urged multiple stage operations, starting after the age of 2 years, certainly an arbitrary period. Many of these lesions are associated with hemangiomas, plexiform neuromas (fig. 12) or even unilateral hemihypertrophies. If there is "an increased rate of growth of the affected extremityian]epiphyseal FIG. 13. CONGENITAL VASCULAR ANOMALY WITH LYMPHEDEMA AND HEMIHYPERTROPHY IN A 16 YEAR OLD BOY, WHOSE CASE' HAS BEEN FOLLOWED FOR 10 YEARS An epiphyseal arrest has been done which successfully equalizes the 2 extremities arrest must be made at a time (fig. 13) calculated from Phemister's tables (39). However, a true isolated lymphedema does not show an increased rate of growth, and when this is present, a vascular anomaly is to be suspected. In the congenital group, multiple stage excisions of huge tissue-spaces together with visible granular lymphoid tissue is successful, but in some cases the lesion extends into the subfascial spaces and is frankly inoperable. It is likely that some of these children will come to amputation at a later date. None of the traumatic cases were operated on and none of the malignant ones, except that exarticulation of the shoulder 95 was performed in a huge intractably painful lymphedema hollowing a radical mastectomy for cancer of the breast. The majority of patients, subjected to some modification of the Iiondoleon operation, were of the inflammatory type or of unknown etiology. We suspect that the latter are frequently caused by a slowly ascending obliterative lymphangitis, starting at the ankle; but some of them show popliteal or inguinal lymphatic hyperplasia, when first seen, and biopsies of lymph glands-generally speaking-are disappointing. With the exception of one young woman w-ho FIG. 14. INGUINAL BIOPSY OF A LYMPH ~ODE TAKEN FRO.NI J;. 1',., A .~l ~EAR OLD WOMAN WITH BILATERAL PROGRESSIVE IjYMPHEDEMA Multiple strains and 3 miscarriages are in her past history. This biopsy was taken in 1944; five years later she w-as subjected to a radical excision of the subcutaneous tissue and fascia. Note the active lymph follicles and the marked periadenitis, which prevents entrance and exit to the lymph glands. Sympathectomy was advised elsewhere. presented a unilateral, slowly increasing lymphedema of one lower extremity, and in whom the inguinal biopsy revealed Hodgkin's disease, and a middle aged undernourished colored man, in whom a tuberculous lymphadenitis was found, all other inguinal biopsies were reported as non-specific lymphadenitides. Closer study of this group indicates that out of 15 biopsies only one was reported as normal; in all cases the predominant tissue alteration is fibrosis, and the fibrous process may be periglandular, constricting a normal appearing node (fig. 14), infiltrative, replacing the lymphoid tissue (fig. 15) or occlusive with the fibrin filling the sinusoids but the lymphatic nodes w-ell presented (fig. 16). It is highly unlikely that these forms represent different types of infection. They are different stages or different intensities of the lymphatic hyperplasia as a result of the 96 FIG. 15. BIOPSY OF INGUINAL LYMPH NODE IN THE CASE OF ISABEL E., A 42 YEAR OLD WHITE FEMALE WHO HAD A UNILATERAL LYMPHEDEMA OF TEN YEARS DURATION, SAID TO HAVE STARTED AFTER A TOOTH EXTRACTION Note the almost complete disappearance of lymphoid tissue, replaced by fibrous and hyaline masses. This lymph gland is certainly and permanently out of function. Enlarged lymph spaces are seen on the left side of the other section. FIG. 16. THIS IS A BIOPSY TAKE-N FROM JANE D., 3 35 YEAR OLD HOUSEWIFE Leucorrhea since the age of 14. Progressive unilateral edema for 3 years. Sprained left ankle shortly before onset. Note that the lymphatic nodules are intact, surrounded by a marginal zone of small lymphocytes; in the center of the field some macrophages are seen and complete replacement fibrosis. Note the enlarged lymph spaces. 97 infective or allergenic stimulus. From a therapeutic standpoint, we are most interested in the plugging up of sinusoids, since if these were freed early by dissolution of lymphocytes and fibrinolysis, better lymphatic drainage could be expected. This we have tried to accomplish by heparinization and by emptying of the sinusoids with Roentgen therapy and minimal doses of triple typhoid vaccine in smaller than fever-producing doses. SUMMARY This study is based on 150 personally observed cases, of whom 28 were classified congenital, 11 traumatic, 58 inflammatory, 22 degenerative (malignant) and 31 of unknown origin. There were 35 males to 115 females. Xo cases of thrombophlebitic edema are included in this series although a lymphatic component is present in this group to greater or lesser degree. This simple classification is of value in understanding the mechanism of this insidious malady. With increasing knowledge, the number of cases of unknown origin should gradually fall into one of these groups. From the standpoint of therapy, the acute, chronic and slowly progressive stages are important, since the acute lymphedema if treated early and intensively yields readily to therapy and leaves the least amount of irreversible edema and fibrosis. Attention has been called to the beneficial effects of elevation, elastic compression, mercurial diuresis, heparinization and sympathetic blocks, each having their proper place, used alone or in combination with each other. To decompress the swollen lymph glands and clear their sinusoids from debris and fibrin deposits Roentgen therapy and small doses of typhoid vaccine have been employed. In the chronic, late cases which cannot be controlled by conservative measures, excision of the diseased tissues has been performed; the cosmetic results are not striking, but out of 28 cases followed from one to twenty-five years, 17 had satisfactory, 5 had doubtful and six had poor results. BIBLIOGRAPHY Allen, E.V., Barker, N.W. AND Hines, E.A.: Peripheral Vascular Diseases. W. B. Saunders and Co., Philadelphia and London , 1946, p. 680. Zimmermann, L.H. AND De Takats , G.: The mechanism of thrombophlebitic edema. Arch. Surg., 23: 937, 1931. Glenn, W.W., Peterson, D.K. AND Drinker, L.K.: The flow of lymph from burned tissue with particular reference to the effects of fibrin-formation upon lymph drainage and composition. Surgery, 12: 685, 1942. White, J.C. AND Warren, S.: Causes of pain in feet after prolonged immersion. War Med. , 5: 6, 1944. Clark, E.R. AND Clark, E.L.: Growth and behavior of epidermis, as observed microscopically in the living, in chambers, introduced in the rabbit's ear. Anat. Rec., 88: 426, 1944. Menkin, V.: Dynamics of Inflammation. McMillan & Co., New York 1940. Drinker, L.H. AND Yoffey, J.M.: Lymphatics, Lymph and Lymphoid Tissue. Harvard University Press. Cambridge, Mass. 1941. Homans, J., Drinker, L.K. AND Field, M.E.: Elephantiasis and the clinical implication of its experimental reproduction in animals. Ann. Surg., 100: 812, 1934. McMaster, P.D. : Conditions in skin, influencing interstitial fluid movement, lymph formation and lymph flow. Ann. N. Y. Acad. Science, 46: 743-787 (Sept.) 1946. 98 McMaster, P.D. AND Pearsons, R.J.: The effect of pulse on the spread of substances through tissues. J. Exp. Med., 68: 377, 1938. Grossman, R.D. AND Blalock, A.: The effect of pulse upon flow of lymph. Proc. Soc. Biol. & Med., 41: 140, 1939. Ehrich, W.E. , Seifter, J., Alourn, H.E. AND Begany, A.J.: Heparin and heparinocytes in elephantiasis scroti. Proc. Soc. Exp. Biol. and Med., 70: 1, 1949. Luhan, J.A.: Hemiedema in cases of hemiplegia. Arch. Neurol. and Psychiatr ., 36: 42, 1936. De Takats, G. : Causalgic states in peace and war. J. A. M. A., 128: 699-704, 1945. Holman, C., Mcswain, B. AND Beal, J.M.: Swelling of the upper extremity following radical mastectomy. Surgery, 15: 757, 1944. Reichert, F.D. : The regeneration of the lymphatics. Ann. Surg., 13: 871, 1926. Ochsner, A. , Longacre, A.B. AND Murray, S.D.: Progressive lymphedema associated with recurrent erysipeloid infection. Surgery, 8: 383, 1940. Homans, J.: Lymphedema of limbs. Arch. Surg., 40: 232, 1940. B) The operative treatment of phlegmasia alba dolens. A preliminary report. New Engl. J. of Med., 204: 1025, 1931. Pattyson, R.A. : Trichomonas vaginalis vaginitis. N. Y. State J. of Med., 37: 4k, 1937. Trussell, R.E. : Trichomonas Vaginalis and Trichomoniasis. Charles C. Thomas, Springfield, Illinois , 1947. Kiss, F. AND Zadory, E.: Experimentell-morphologische Analyse der Rami Communicantes. Anat. Anzeiger, 91: 14, 1941. Matas, R.: The surgical treatment of elephantiasis and elephantoid states dependent upon chronic obstruction of the lymphatic and venous channel. Am. J. Trop. Dis., 1: 60, 1913. Thompson, K.W. : Studies on the relationship of dermatomycosis to ulceration and gangrene of the extremities. Yale J. of Biol. and Med., 16: 665, 1935. Naide, M.: Allergic lesions following thrombophlebitis. Arch. Int. Med. , 80: 388-396, 1947. Ratner, B.: Allergy, Anaphylaxis and Immune Therapy. Williams & Wilkins, Baltimore, Maryland, 1943 . Ehrich, Wm E. : The role of lymphocytes in the circulation of lymph in lymph. Ann. N. Y. Acad. of Sciences, 46: 823, 1946. De Takats, G.: The management of acute thrombophlebitic edema. J. A. M. A., 100: 34-37, 1933. Ochsner, A. AND De Bakey, M.: Postphlebitic sequelae. J. A. M. A., 139: 423, 1949. Loewe, L., Hirsch, E. AND Grayzel, D.M.: The action of heparin on experimental venous thrombosis. Surg., 22: 746, 1947. Gilbert, N.C. AND Nalefski, L.A.: The effect of heparin and dicumarol in increasing the coronary flow volume. J. Lab. and Clin. Med. , 34: 6, 797-805, 1949. Stats, D. AND Neuhof, H.: Concentrated aqueous heparin. A new form of intramuscular administration. Am. J. of Med. Sci., 214: 2, 1947. De Takats, G.: Heparin tolerance. A test of the patient's clotting mechanism. Surg., Gyn. & Obst., 77: 31, 1943. De Takats, G.: The present status of anticoagulant therapy in surgery. J.A.M.A., in press. Zimmermann, L.H., Gault, J.T., Halpern , S.S. AND De Takats , G.: The effect of salyrgan and x-ray on the rate of disappearance of thrombophlebitic edema . J. Lab. & Clin. Med., 19: 243, 1933. Snead, L.R. , Lasner, J., Jenkinson , E.L. AND De Takats , G.: Roentgen therapy of thrombophlebitis. J. A. M. A., 141: 967, 1949 . White, A. AND Dougherty, T.F.: Significance of the effect of x-ray on lymphoid tissue. Fed. Proc. Am. Soc. Biol. Chem., 4: 109, 1945. 99 Macey, H.B.: A surgical procedure for lymphedema of the extremities. J. Bone & Joint Surg., 30 (A): 339, 1948. Guthrie, D. AND Gagnon, G.: The prevention and treatment of postoperative lymphedema in the arm . Ann. Surg., 123: 5, 1946. Servelle, M. : La lymphangectomie superficielle totale. Traitement chirurgical de l'elephantiasis . Revue de Chir., 66: 294, 1947. Phemister, D.B. : Operative arrest of longitudinal growth of bones in the treatment of deformities. J. Bone & Joint Surg., 15: 1, 1933.</meta-value></custom-meta></custom-meta-wrap></article-meta></front><back><notes>
<p>1 William C. Beck: Personal communication.</p>
</notes><ref-list>
<ref>
<citation citation-type="book" xlink:type="simple">
<name name-style="western"><surname>Allen, E.V.</surname></name>, <name name-style="western"><surname>Barker, N.W.</surname></name> AND <name name-style="western"><surname>Hines, E.A.</surname></name>: <source>Peripheral Vascular Diseases</source>. <publisher-name>W. B. Saunders and Co.</publisher-name>, <publisher-loc>Philadelphia</publisher-loc> and <publisher-loc>London</publisher-loc> , <year>1946</year>, p. <fpage>680</fpage>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Zimmermann, L.H.</surname></name> AND <name name-style="western"><surname>De Takats , G.</surname></name>: <article-title>The mechanism of thrombophlebitic edema</article-title>. <source>Arch. Surg.</source>, <volume>23</volume>: <fpage>937</fpage>, <year>1931</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Glenn, W.W.</surname></name>, <name name-style="western"><surname>Peterson, D.K.</surname></name> AND <name name-style="western"><surname>Drinker, L.K.</surname></name>: <article-title>The flow of lymph from burned tissue with particular reference to the effects of fibrin-formation upon lymph drainage and composition</article-title>. <source>Surgery</source>, <volume>12</volume>: <fpage>685</fpage>, <year>1942</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>White, J.C.</surname></name> AND <name name-style="western"><surname>Warren, S.</surname></name>: <article-title>Causes of pain in feet after prolonged immersion. War</article-title>
<source>Med.</source> , <volume>5</volume>: <fpage>6</fpage>, <year>1944</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Clark, E.R.</surname></name> AND <name name-style="western"><surname>Clark, E.L.</surname></name>: <article-title>Growth and behavior of epidermis, as observed microscopically in the living, in chambers, introduced in the rabbit's ear</article-title>. <source>Anat. Rec.</source>, <volume>88</volume>: <fpage>426</fpage>, <year>1944</year>.</citation>
</ref>
<ref>
<citation citation-type="book" xlink:type="simple">
<name name-style="western"><surname>Menkin, V.</surname></name>: <source>Dynamics of Inflammation</source>. <publisher-name>McMillan & Co</publisher-name>., <publisher-loc>New York</publisher-loc>
<year>1940</year>.</citation>
</ref>
<ref>
<citation citation-type="book" xlink:type="simple">
<name name-style="western"><surname>Drinker, L.H.</surname></name> AND <name name-style="western"><surname>Yoffey, J.M.</surname></name>: <source>Lymphatics, Lymph and Lymphoid Tissue</source>. <publisher-name>Harvard University Press</publisher-name>. <publisher-loc>Cambridge, Mass.</publisher-loc>
<year>1941</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Homans, J.</surname></name>, <name name-style="western"><surname>Drinker, L.K.</surname></name> AND <name name-style="western"><surname>Field, M.E.</surname></name>: <article-title>Elephantiasis and the clinical implication of its experimental reproduction in animals</article-title>. <source>Ann. Surg.</source>, <volume>100</volume>: <fpage>812</fpage>, <year>1934</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>McMaster, P.D.</surname></name> : <article-title>Conditions in skin, influencing interstitial fluid movement, lymph formation and lymph flow</article-title>. <source>Ann. N. Y. Acad. Science</source>, <volume>46</volume>: <fpage>743</fpage>-<lpage>787</lpage> (Sept.) <year>1946</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>McMaster, P.D.</surname></name> AND <name name-style="western"><surname>Pearsons, R.J.</surname></name>: <article-title>The effect of pulse on the spread of substances through tissues</article-title>. <source>J. Exp. Med.</source>, <volume>68</volume>: <fpage>377</fpage>, <year>1938</year>. <name name-style="western"><surname>Grossman, R.D.</surname></name> AND <name name-style="western"><surname>Blalock, A.</surname></name>: <article-title>The effect of pulse upon flow of lymph</article-title>. <source>Proc. Soc. Biol. & Med.</source>, <volume>41</volume>: <fpage>140</fpage>, <year>1939</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Ehrich, W.E.</surname></name> , <name name-style="western"><surname>Seifter, J.</surname></name>, <name name-style="western"><surname>Alourn, H.E.</surname></name> AND <name name-style="western"><surname>Begany, A.J.</surname></name>: <article-title>Heparin and heparinocytes in elephantiasis scroti</article-title>. <source>Proc. Soc. Exp. Biol. and Med.</source>, <volume>70</volume>: <fpage>1</fpage>, <year>1949</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Luhan, J.A.</surname></name>: <article-title>Hemiedema in cases of hemiplegia</article-title>. <source>Arch. Neurol. and Psychiatr</source> ., <volume>36</volume>: <fpage>42</fpage>, <year>1936</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>De Takats, G.</surname></name> : <article-title>Causalgic states in peace and war</article-title>. <source>J. A. M. A.</source>, <volume>128</volume>: <fpage>699</fpage>-<lpage>704</lpage>, <year>1945</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Holman, C.</surname></name>, <name name-style="western"><surname>Mcswain, B.</surname></name> AND <name name-style="western"><surname>Beal, J.M.</surname></name>: <article-title>Swelling of the upper extremity following radical mastectomy</article-title>. <source>Surgery</source>, <volume>15</volume>: <fpage>757</fpage>, <year>1944</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Reichert, F.D.</surname></name> : <article-title>The regeneration of the lymphatics</article-title>. <source>Ann. Surg.</source>, <volume>13</volume>: <fpage>871</fpage>, <year>1926</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Ochsner, A.</surname></name> , <name name-style="western"><surname>Longacre, A.B.</surname></name> AND <name name-style="western"><surname>Murray, S.D.</surname></name>: <article-title>Progressive lymphedema associated with recurrent erysipeloid infection</article-title>. <source>Surgery</source>, <volume>8</volume>: <fpage>383</fpage>, <year>1940</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Homans, J.</surname></name>: <article-title>Lymphedema of limbs</article-title>. <source>Arch. Surg.,</source>
<volume>40</volume>: <fpage>232</fpage>, <year>1940</year>. B) <article-title>The operative treatment of phlegmasia alba dolens. A preliminary report</article-title>. <source>New Engl. J. of Med.</source>, <volume>204</volume>: <fpage>1025</fpage>, <year>1931</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Pattyson, R.A.</surname></name> : <article-title>Trichomonas vaginalis vaginitis</article-title>. <source>N. Y. State J. of Med.</source>, <volume>37</volume>: <fpage>4k</fpage>, <year>1937</year>.</citation>
</ref>
<ref>
<citation citation-type="book" xlink:type="simple">
<name name-style="western"><surname>Trussell, R.E.</surname></name> : <source>Trichomonas Vaginalis and Trichomoniasis</source>. <publisher-name>Charles C. Thomas</publisher-name>, <publisher-loc>Springfield, Illinois</publisher-loc> , <year>1947</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Kiss, F.</surname></name> AND <name name-style="western"><surname>Zadory, E.</surname></name>: <article-title>Experimentell-morphologische Analyse der Rami Communicantes</article-title>. <source>Anat. Anzeiger</source>, <volume>91</volume>: <fpage>14</fpage>, <year>1941</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Matas, R.</surname></name>: <article-title>The surgical treatment of elephantiasis and elephantoid states dependent upon chronic obstruction of the lymphatic and venous channel</article-title>. <source>Am. J. Trop. Dis.</source>, <volume>1</volume>: <fpage>60</fpage>, <year>1913</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Thompson, K.W.</surname></name> : <article-title>Studies on the relationship of dermatomycosis to ulceration and gangrene of the extremities. Yale J. of Biol. and</article-title>
<source>Med.</source>, <volume>16</volume>: <fpage>665</fpage>, <year>1935</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Naide, M.</surname></name>: <article-title>Allergic lesions following thrombophlebitis</article-title>. <source>Arch. Int. Med.</source> , <volume>80</volume>: <fpage>388</fpage>-<lpage>396</lpage>, <year>1947</year>.</citation>
</ref>
<ref>
<citation citation-type="book" xlink:type="simple">
<name name-style="western"><surname>Ratner, B.</surname></name>: <source>Allergy, Anaphylaxis and Immune Therapy</source>. <publisher-name>Williams & Wilkins</publisher-name>, <publisher-loc>Baltimore, Maryland</publisher-loc>, <year>1943</year> .</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Ehrich, Wm E.</surname></name> : <article-title>The role of lymphocytes in the circulation of lymph in lymph</article-title>. <source>Ann. N. Y. Acad. of Sciences,</source>
<volume>46</volume>: <fpage>823</fpage>, <year>1946</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>De Takats, G.</surname></name>: <article-title>The management of acute thrombophlebitic edema</article-title>. <source>J. A. M. A.</source>, <volume>100</volume>: <fpage>34</fpage>-<lpage>37</lpage>, <year>1933</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Ochsner, A.</surname></name> AND <name name-style="western"><surname>De Bakey, M.</surname></name>: <article-title>Postphlebitic sequelae</article-title>. <source>J. A. M. A.</source>, <volume>139</volume>: <fpage>423</fpage>, <year>1949</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Loewe, L.</surname></name>, <name name-style="western"><surname>Hirsch, E.</surname></name> AND <name name-style="western"><surname>Grayzel, D.M.</surname></name>: <article-title>The action of heparin on experimental venous thrombosis</article-title>. <source>Surg.</source>, <volume>22</volume>: <fpage>746</fpage>, <year>1947</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Gilbert, N.C.</surname></name> AND <name name-style="western"><surname>Nalefski, L.A.</surname></name>: <article-title>The effect of heparin and dicumarol in increasing the coronary flow</article-title> volume. <source>J. Lab. and Clin. Med.</source> , <volume>34</volume>: <fpage>6</fpage>, <fpage>797</fpage>-<lpage>805</lpage>, <year>1949</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Stats, D.</surname></name> AND <name name-style="western"><surname>Neuhof, H.</surname></name>: <article-title>Concentrated aqueous heparin. A new form of intramuscular administration. Am</article-title>. <source>J. of Med. Sci.</source>, <volume>214</volume>: <fpage>2</fpage>, <year>1947</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>De Takats, G.</surname></name>: <article-title>Heparin tolerance. A test of the patient's clotting mechanism</article-title>. <source>Surg., Gyn. & Obst.</source>, <volume>77</volume>: <fpage>31</fpage>, <year>1943</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>De Takats, G.</surname></name>: <article-title>The present status of anticoagulant therapy in surgery</article-title>. <source>J.A.M.A.</source>, in press.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Zimmermann, L.H.</surname></name>, <name name-style="western"><surname>Gault, J.T.</surname></name>, <name name-style="western"><surname>Halpern , S.S.</surname></name> AND <name name-style="western"><surname>De Takats , G.</surname></name>: <article-title>The effect of salyrgan and x-ray on the rate of disappearance of thrombophlebitic edema</article-title> . <source>J. Lab. & Clin. Med.</source>, <volume>19</volume>: <fpage>243</fpage>, <year>1933</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Snead, L.R.</surname></name> , <name name-style="western"><surname>Lasner, J.</surname></name>, <name name-style="western"><surname>Jenkinson , E.L.</surname></name> AND <name name-style="western"><surname>De Takats , G.</surname></name>: <article-title>Roentgen therapy of thrombophlebitis</article-title>. <source>J. A. M. A.</source>, <volume>141</volume>: <fpage>967</fpage>, <year>1949</year> .</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>White, A.</surname></name> AND <name name-style="western"><surname>Dougherty, T.F.</surname></name>: <article-title>Significance of the effect of x-ray on lymphoid tissue. Fed. Proc. Am</article-title>. <source>Soc. Biol. Chem.</source>, <volume>4</volume>: <fpage>109</fpage>, <year>1945</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Macey, H.B.</surname></name>: <article-title>A surgical procedure for lymphedema of the extremities</article-title>. <source>J. Bone & Joint Surg.</source>, <volume>30</volume> (A): <fpage>339</fpage>, <year>1948</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Guthrie, D.</surname></name> AND <name name-style="western"><surname>Gagnon, G.</surname></name>: <article-title>The prevention and treatment of postoperative lymphedema in the arm</article-title> . <source>Ann. Surg.</source>, <volume>123</volume>: <fpage>5</fpage>, <year>1946</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Servelle, M.</surname></name> : <article-title>La lymphangectomie superficielle totale. Traitement chirurgical de l'elephantiasis</article-title> . <source>Revue de Chir.</source>, <volume>66</volume>: <fpage>294</fpage>, <year>1947</year>.</citation>
</ref>
<ref>
<citation citation-type="journal" xlink:type="simple">
<name name-style="western"><surname>Phemister, D.B.</surname></name> : <article-title>Operative arrest of longitudinal growth of bones in the treatment of deformities</article-title>. <source>J. Bone & Joint Surg.</source>, <volume>15</volume>: <fpage>1</fpage>, <year>1933</year>.</citation>
</ref>
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