Split skin grafts heal over a living dermal replica

Split skin grafts heal over a living dermal replica

180 Bums (1993) 19, (Z), 18(r181 in Grecrf Britain Printed Abstracts CLINICAL STUDIES Split skin grafts heal over a living dermal replica Excised...

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180

Bums (1993) 19, (Z), 18(r181

in Grecrf Britain Printed

Abstracts CLINICAL

STUDIES

Split skin grafts heal over a living dermal replica Excised human bum wounds were covered with a derrnal tissue replica consisting of fibroblasts incorporated into a poly galactin acid Vicryl mesh beneath an outer covering of meshed expanded split thickness skin grafts. The ‘take’ of the skin grafts was not significantly different between the control and dermal tissue replica sites. The mesh intersticies over the control and experimental sites were equally well covered with the epithelium. Wound biopsy sites showed no evidence of rejection of the cultured allogeneic fibroblasts and minimal inflammatory reaction to the Vicryl fibres. Evidence of continuous basement membrane formation at the junction between the epidermis and the dermal tissue replica was seen by 14 days beneath the healed epithelium in the intersticies. The Vicryl fibres were slowly hydrolysed in the wound area. Elastic fibres were not seen in any of the healed wounds. Hansbrough J. F., Dore C. and Hansbrough W. B. (1992) Clinical trials of a living dermal tissue replacement placed beneath meshed split thickness skin grafts on excised bum wounds. 1. Bum Care Rehbil. 13,(S). 519-529.

Cytokine responses following bums Studies in 31 patients with partial or full skin thickness bums covering between 10 and 95 rjer cent TBSA indicated that early after bum injury there is a correspondence of interleukin-1 beta (IL-@) and tumour necrosis factor alpha (TNFc() with certain host responses but these correlations disappear during the ensuing weeks. In general IL-@ and TNFc( appear to be poor indicators of prognosis in burned patients; however the observed association between mortality and low levels of IL-@ supports the suggestion that this cytokine is an essential mediator for host defences. Cannon J. G., Friedberg J. S., Gelfand J. A. et al. (1992) Circulating interleukin-IB and tumor necrosis factor g concentrations after bum injury in humans. Crif. Care Med. 20, (lo), 1414-1419.

Wound size-related haemostatic changes Fibrinolytic activation, coagulation and contact factors were analysed sequentially in 47 male and 13 female patients with bums covering a wide range of severity. Haemostatic marker levels on admission that correlated with the severity of injury were tissue plasminogen activator, plasminogen activator inhibitor, D-dimer, plasminogen, proteins C and S, antithrombin III, thrombin antithrombin complex, kallikrein, kinin, C,, esterase inhibitor and the clotting and antigen components of Factor VII. Subsequently thrombogenicity was increased because of a decrease in antithrombin III and the C and S proteins. Fibrinolysis activation occurred via a marked increase in plasminogen activator and a decrease in plasminogen activator inhibitor. C, esterase 0 1993 Butterworth-Heinemann 0305-4179/93/020180-02

Ltd

inhibitor levels were depressed in all patients and may have contributed to the postbum fluid sequestration. Kowal-Vem A., Gamelli R. L., and Walenga J. M. (1992) The effect of bum wound size on hemostasis. A correlation of the hemostatic changes to the clinical state. 1. Truum 33, (I), 50-57.

Inhalation injury-induced mortality A retrospective review of two groups of patients (n = 49 and 43) with matched ages and sex, all of whom had thermal and inhalation injuries but who were treated 10 years apart, indicated that in spite of newer methods of treatment, and a statistically significant decrease in the severity of the thermal injury between 1977-8 and 1987-8, there had been no change in the mortality rate of the two groups. Apparently the newer methods of treatment have not decreased the inhalation injury-induced mortality rate. Sobel J. B., Goldfarb I. W., Slater H. et al. (1992) Inhalation injury: a decade without progress. J. Bum Cure Rehabil. 13, (s), 573-57s.

ANIMAL

STUDIES

Vitamin C and microvascular permeability Hourly lymph flow rates and plasma and lymph total protein concentrations were measured in 24 dog hind paws, one of each pair of paws having been burned. Half the dogs received 14 mg vitamin C (ascorbic acid) per kg body weight per hour for at least 6 h after burning. Non-burned paws showed no significant differences in lymph flow rates or total protein flux. The lymph flow rates increased by seven fold in the nontreatment group but only three-fold in the treatment group. The hourly total protein flux increased by 15.fold in the non-treatment group but only five-fold in the treatment group. Apparently treatment with vitamin C reduced the early microvascular leakage of fluid and protein following burns. Matsuda T., Tanaka H., Hanumadass M. et al. (1992) Effects of high-dose vitamin C administration on postbum microvascular fluid and protein flux. 1. Bctm Cure Rehabil. 13, (5), 560-566.

Exotoxin A from Pseudomonas aeruginosa impedes wound healing Studies on 90 rats with granulating skin wounds showed that the harmful effects on wound healing (as measured by the rate of contraction) of I? aeruginosa organisms at concentrations of more than 10.~colony forming units per gram of tissue is the result of the exotoxin A production by the cells rather than the presence of the cells per se. Topical application of adequate amounts of the antitoxin to exotoxin A restored the healing process to normal rates.