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The role of lymphoscintigraphy, performed with 99mTc-labeled antimony sulfur colloid, in the diagnosis of lymphedema and as a test for selection of patients for microvascular operation was evaluated in 32 patients with primary and secondary lymphedema and four patients with other causes of leg edema. Lymphoscintigraphy clearly demonstrated if edema was of lymphatic origin. Five different image patterns were identified; abnormal image patterns could not be predicted from clinical history or physical findings. Quantitative evaluation of removal of the radioactive colloid from the injection site and appearance in lymph node sites and liver was of limited usefulness. Nine patients underwent various surgical procedures before or after lymphoscintigraphy. Lympho-venous anastomoses were possible only in patients who had patent lymph channels visible on lymphoscintigrams. Based on initial experience, lymphoscintigraphy seems to be useful to select patients for microvascular operation.

The microcirculation of adipose tissue is poorly understood either because of the absence of histological documents or because they fail to explain pathological conditions. However, disturbances of blood flow and parietal lesions of the microvessels are the basis for these disorders. Although we speak of disturbances of the vascular control mechanisms, these mechanisms are poorly understood and although we speak of arteriovenous short-circuits, the existence of these lesions has not been proven. In fact, classically, the circulation in the dermis and hypodermis is assured by a meshwork of arterioles, venules and capillaries, but biopsies of lateral and anterior regions of the thigh have demonstrated "block devices" in the walls of small arteries and arterioles which are able to regulate the rate of blood flow towards the capillary bed. Following contraction of these devices, the vascular lumen dilates, ensuring free circulation and when they relax, the lumen closes, resulting in decreased or no blood flow. These smooth muscle devices within the arterial wall resemble small cushions in the small arteries and more or less pedunculated polyps in the arterioles, either simple or fissured in the form of an elephant's trunk with a safety valve effect, arranged either in a single column or in two columns face to face. This provides evidence for the particularly disturbed vasculo-tissue inter-relations observed in venous insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Twelve patients with primary lymphedema of the lower limb were examined with computed tomography (CT). A characteristic "honeycomb" pattern of the subcutaneous compartment was seen in 10 of these patients. CT scans in nine other patients with swollen leg secondary to chronic venous disease or lipedema did not show this characteristic pattern. CT may be helpful in the differential diagnosis of a swollen leg, thus obviating venography or lymphangiography.

Patients with lipoedema of the typus rusticanus Moncorps show a skin elasticity deficit of the skin of the calf. This is partly due to the derma oedema in the skin of these patients and seems partly to be due to an intrinsic connective tissue defect in the skin of such patients. The auteurs put forward the hypothesis that also present calf muscle pump dysfunction in these patients is the result of a connective tissue defect of the fascia of the muscular compartment, as an expression of a more generalized connective tissue defect.

Two cases of lipedema are presented. They illustrate this clinical syndrome which occurs almost exclusively in women and presents as grossly enlarged legs, thighs and buttocks. The etiology remains uncertain. Although infrequently diagnosed, lipedema is not rare. We report success treating such patients with properly measured and fitted compression garments.

Lipedema of the legs is a symmetrical thickening of upper and lower leg and topically accentuated fat pads. The back of the foot is usually free of swelling. Pathogenetically it is a disturbance of the distribution pattern of subcutaneous fat tissue. Epidemiologically, the subjects affected are women, starting from puberty. Weight reduction programs do not influence the real deformations. If this abnormal fat tissue is infiltrated by angiological diseases, these manifest themselves in modified form. In particular, all the symptoms are more painful. In arterial ischemic syndromes that taut skin is susceptible to necrosis at atypical locations. For reconstruction of trunk arteries it is advisable to bypass larger bulges for better wound nealing. Venous strips should be peeled out away from fat pads and venous-bridges very carefully to protect the tissue. Acute and chronic phlebothrombosis lead to unusual and asymmetrical forms of swelling. The venous ulcer lies directly beneath a fat-muff in the gaiter region. Since they are hard to compress, free skin transplants should be considered early in the course of development. Surgery of varicose veins calls for most careful technique to ensure wound healing. From the lymphological viewpoint there are clinically and lymphographically mixed forms of lymphedema with lipedema.

While the term cellulitis is incorrect, it is commonly used and deserves a nosological classification. "Cellulitis is a dermohypodermosis and an oedemato-sclerous panniculopathy- It is indeed a true histangiography in which the fibroblastic reaction predominates over capillaro-veinular changes. Adipocytes of exaggerated size interpenetrate into micro- and later into macronodules marked off by more or less structured conjunctive fibrilla, thereby making treatment difficult.

Systemic causes of leg edema include idiopathic cyclic edema, heart failure, cirrhosis, nephrosis and other hypoproteinemic states. Lymphedema may be primary, or secondary to neoplasm, lymphangitis, retroperitoneal fibrosis and, rarely (in the U.S.), filariasis. Thrombophlebitis and chronic venous insufficiency are not uncommon causes. Finally, infection, ischemia, lipedema, vascular anomalies, tumors and trauma can be responsible for the swollen leg.

To the Editor.— I do not believe that Stallworth et al (228:1656, 1974) have proven their case for a definite clinical entity of "lipedema" in the patients described.The plasma lipid values seem high, but are of no significance unless the controls were patients of comparable sex, age, and mean weight; this is not stated. The origin of tissue lipid values would similarly have to be a group of middle-aged, overweight patients with fat legs but no symptoms, to make their figures valid.I have seen and treated many patients with a clinical picture identical with that described in their paper. Many of these patients have clinical evidence of past phlebitis; others do not. Both groups have episodes of painful, lumpy swellings in their legs, that may be accompanied by redness, heat, and tenderness in the affected areas. This picture frequently takes many weeks to resolve and may leave some ...

A 22 yr old woman with bilateral symmetrical enlargement of her lower extremities since the age of 11 is reported. A diagnosis of lipedema of the legs was made on the basis of history, physical examination, biopsy and phlebography. Lipedema of the legs should be included in the differential diagnosis of symmetrical nonpitting edematous lower extremities. According to Allen and Hines, the characteristic points to be made for a diagnosis of lipedema of the legs included the following: almost exclusively seen in women; always bilateral and symmetrical with minimal involvement of the feet; minimal to absent pitting edems; all parts of the limbs are involved simultaneously; persistent enlargement despite elevation of the extremities. 16% of their patients gave a family history of the disorder; 40% complained of pain in the lower extremities; and approximately half of the patients were obese. The age of onset was variable, from childhood to the sixth or seventh decade. There was no racial preponderance. No patient gave a history compatible with progressive lipodystrophy. Treatment included diet, diuretics, tight stockings, rest and elevation, and massage, but was unsatisfactory in most cases.

Lipoedema was first described by Allen and Hines (1940), and it is characterised by fat legs and orthostatic edema. Generalised obesity may be presend or absent, the mean weight of five illustrative patients in their paper ws 154.5 lbs. Allen and his co-workers (1951) then reported 119 cases of lipoedema at the Mayo Clinic from 1937 to 1946. The condition affects women almost exclusively. Hines (1952) states that the diagnosis of lipoedema can be made easily from observation: (1) The characteristic symmetrical distribution of fat in the lower half of the body, excepting the feet, and (2) the oedema of varying degrees in the more dependent portions of the legs. The condition is briefly mentioned by Martin et al. (1956). The condition is often confused with vascular diseases affecting lower extremities, and lymphoedema (Wold et al., 1951). Furthermore, these workers consider that lipoedema can be distinguished from lipodystrophy progressiva by the extensive loss of subcutaneous fat in the upper half of the body associated with deposition of fat in the buttocks and lower extremities (Whittle, 1944). Two patients are presented with lipoedema, associated with diabetes mellitus. The possibility that lipoedema may be a variatn of lipodystrophy progressive is discussed.