Joseph Beninson

Lipedema — The Non-Lymphatic Masquerader

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 di agnosed, lipedema is not rare. We report success treating such patients with properly measured and fitted compression garments.

A universally applicable clinical classification of lymphedema.

A simple classification of lymphedema is presented that is based solely on clinical obser vation. It is suggested that the universal use of such a classification would facilitate the collection of meaningful epidemiologic data and would make possible understandable comparisons of the effectiveness of various treatment modalities.

Elephantiasis Nostras—A Case Report

Elephantiasis nostras, the result of chronic lymphedema, is character ized by marked edema of the affected extremity with a thickened, verru cous, pebbly appearance of the skin. The pathogenesis is thought to be re lated to fibroblast proliferation fol lowing impaired lymphatic drainage, leading to fibrosis and further re striction of lymph drainage with pro gressive edema. A case report of a patient with massive chronic lymphe dema of her feet is presented.

Necrobiosis Lipoidica: Treatment with Porcine Dressings, Split-thickness Skin Grafts and Pressure Garments A case report and review of treatment modalities

A 39-year old nondiabetic female had severely ulcerated necrobiosis li poidica of the legs which was refractory to medical management for 2½ years. Surgical management with porcine grafting followed by autologous split-thick ness skin grafts successfully healed these ulcerations. With the use of custom- fitted contoured pads and pressure gradient stockings, the grafts have remained intact for 21/2 years, and there has been significant improvement of the nonul cerated plaques.

Cause of primary congenital lymphedema.

at birth), praecox (pubertal onset), and tarda (midlife onset). Congenital lymphedema is a rare form and the most severe of the three, having the highest penetrance which makes it easy to determine which family members are affected. This determination is essential for a genome-wide search, a largely automated, rapid method of locating a locus with a suitable large multigeneration family. DNA samples from large cooperative volunteer American families were used to map the congenital lymphedema locus. Heterogeneity is evident in other congenital onset families in

Successful embolization of multiple AV foot lesions : a case history

A 39-year-old white female with multiple arteriovenous malformations of the left foot had had surgical ligation on her left dorsalis pedis artery at age 12 with no clinical improvement. She was placed into a leotard at age 16 and was able to function but would tire very easily and her left foot was twice the size of her right one. In May 1988, she had four large feeder vessels off the posterior tibial artery and two off the anterior tibial artery embolized by use of 1,000 microns PVA particles, occlusive spring coils, and detachable balloons. Her foot shrunk and is now smaller than her normal right foot; she does not tire, and she now wears a knee length stocking to help prevent other channels from opening.

Successful Treatment of Elephantiasis Nostras of the Lip

Department of Dermatology, Henry Ford Hospital, Detroit, Michigan. Elephantiasis nostras designates recurrent episodes of inflammation of the involved parts with or without constitutional involvement. Sir John Hutchinson’ in 1883 first described solid edema of the face following repeated attacks of erysipelas and its dependence upon lymphatic obstruction. Sabouraud,2 in five cases reported in 1893, was able by scarifying the skin during erysipelatous attacks to culture the blood and serum and demonstrate pure cultures of streptococci. Between attacks all cultures remained sterile. Elliott3 in 1917 reported 3 cases of solid edema of the face in which all were secondary to nasal infections. From cultures taken from the nasal mucosa in

Lymphedema: Patho-Physiologic and Clinical Concepts

Kinmonth et al reported that primary lymphedema is due to hyperplasia (55%), varicose lymphatics (24%) or aplasia (14%) of the lymphatics. This author also reported these varieties of primary lymphedema albeit in different percentages, in his studies (2, 3). Secondary lymphedema in the main follows surgical ablation, obliterative or obstructive disease states or traumatic interruption of a significant number of lymphatic channels. In some instances this occurs with a slight decrease of the channels of the affected part in a patient who clinically had no evidence of

Hereditary congenital lymphedema-Milroy's: A report of 30 cases in a family

Hereditary congenital lymphedema is a rare disorder. A family with 30 occurrences of this condition in three generations consisting of 58 persons is described. This case is unusual in that all 11 children of clinically normal parents are affected. The etiology of hereditary congenital lymphedema is a hypoplasia or aplasia of lymphatic tissue. Mechanical pumping and adequate pressure gradient prostheses have been a successful treatment. The authors reviewed the world literature and cited the explanations that were offered for lymphedema. Various treatments used in the past and present are included.

The Support of the Venous Circulation

venous insufficiency in all of its manifestations. When the first hominid raised his legs from the supine position or grasped, wrapped or otherwise tried to counterbalance this hydrostatic loss, support of the venous circulation was initiated. The exact sequence of events leading to the modalities used today would be impossible to amass and too multitudinous to enumerate; however, in this instance, I should like to honor an engineer who before his demise succeeded not only in helping himself but making it feasible for us to help patients with this and other vascular problems in the most effective way known to me as of this writing.