An extreme extension contracture of wrist with dorsal contracture of fingers 15 years after burn injury is described. Shortening of extensor tendons, secondary lengthening of flexor tendons, contracted wrist joint capsule, unusual dislocation of carpals, dorsal dislocation of metacarpophalangeal joints of fingers, and provision of sufficient amount of good-quality skin were some of the issues that had to be addressed in treatment. The contracture was released, the carpals and metacarpophalangeal joint dislocations were corrected and fixed with K wires, and the resulting defect was covered with a sheet split-thickness skin graft. An exercise program was designed that consisted of isotonic, isokinetic, and isometric resistance exercises and passive, active, and active-assistive range of motion exercises. These exercises were pursued with the intention of increasing dynamic strength, endurance, and overall functional recovery of the flexor muscles by exploiting the immature nature of early scar tissue. The resultant enhanced flexor muscle power from exercises along with the dynamic splint helped in lengthening of extensor tendons, wrist joint capsule, and split-thickness skin graft. It also helped in resisting the recontracting tendency, with further recovery of good range of wrist and fingers movements, obviating the need of tendon-lengthening surgery and flap coverage. One and half years of follow up didn't show any sign of recontracture, and the patient was able to perform his routine activities. Postburn wrist contractures of such magnitude have been seldom described. Emphasis is put on simple contracture release and a postoperative exercise program.

Adolescent↗

PubMedDate not supplied

Postburn galactorrhea with refractory hypertrophic scars: role of obesity under scrutiny.

Postburn galactorrhea, although relatively uncommon, is a complex problem to treat. Three of 25 female premenopausal patients who were admitted during the years 1995 to 2001 with more than 40% TBSA burns developed this problem. All three patients were obese according to body mass index and other clinical criteria. It was observed that the additional disturbance of equilibrium of hypothalamus because of burn injury, which is already disturbed as per se in obese patients, precipitates sustained release of prolactin, leading to galactorrhea. Hyperinsulinemia because of obesity and associated reactive metabolic response of burn trauma contribute to the stimulation of prolactin secretion and sustained hyperprolactinemia. Interestingly, our patients who developed postburn galactorrhea also developed refractory hypertrophic scars not readily amenable to preventive and conservative therapeutic treatment methods. The responsible factor for its development can be a rise in prolactin levels with interplay of other hormones, such as melanocyte-stimulating hormone (MSH), from the anterior pituitary. Repeated serum prolactin measurements and early control of rising levels during the burn treatment, particularly in obese patients, are recommended. Early and vigorous measures to prevent scar hypertrophy also are advocated. In our study, we failed to correlate chest wall burns with galactorrhea.

Adult↗