Annals of Burns and Fire Disasters - vol. X - n. 2 - June 1997

SKIN WOUND ZONE AFTER CHEMICAL INJURY IN EXPERIMENTAL CONDITIONS

Troshev K, Markov D.

Department of Burns and Plastic Surgery, Naval Hospital, Bulgarian Military Medical Academy, Varna, Bulgaria


SUMMARY. There is a significant similarity between wound zones after chemical injuries with NaOH, H2SO4, and HCI and after burn trauma. The morphological differences are not significant either with regard to experimental and control groups or to different causes. This is confirmed by investigations we have conducted on other kinds of wounding. After chemical injury to the skin nonspecific processes occur in the wound zone. There is no difference in their character and dynamics from other skin injuries. Some different metabolic processes may take place, but these were not investigated in the present study. The same diagnostic and therapeutic problems and possibilities exist after chemical injuries as after other kinds of burns.

Introduction

Chemical burns are burns of a special kind, but while there are many research works on electrotrauma few deal with chemical injuries. This is surprising, as there are many skin-destroying substances, such as heavy metals, acids, bases, and salts.
The degree of injury depends on the chemical activity of the substance. We may suppose that the active substance which damages different tissue cells in the wound zone is the same as in all other kinds of skin trauma, although the destructive agents may be different. There are some classic wound descriptions in the literature, but we have no significant data on the wound zone following chemical injury. These circumstances led to the present investigation, the aim of which was to study the morphological changes in the wound zone after chemical trauma.

Materials and methods

The investigation was conducted using 105 Wistar rats (average weight 200 gm). After ether narcosis on a depilated back skin zone of 15 sq cm we used a cotton wad to apply a chemical substance consisting of a 50% solution of HCI, H2SO4 or NaOH for 15 minutes. The wound zone was washed for 15 minutes under water and then dried. Histological preparations were taken after the rats died under narcosis. We used our current laboratory methodics for microscope investigations at the 6th hour and on days 1, 3, 7, 14, 21, and 28. The preparation material always contained part of the necrotic zone and a zone at a distance of 1 cm. The rats were distributed in experimental groups of five animals each. During the experimental period the animals lived in individual cages under standard conditions. As a control group we used the results from the same methods of investigation of the wound zone of skin after nonchemical trauma.

Results

Clinical observations.
Because of the lack of any specific methodology for experimental chemical skin wounds, we were obliged to conduct a preliminary experiment by creating wounds with 100% solutions of HCI, H2S04 or NaOH. After the experiment there was an immediate widening of the zone of about 50%. The difference between the primary and the secondary wound area in the process zone was established on the basis of different skin colours. Independently of water washing, the animals were adynarnic, refused food, and died in the following one or two days. We interpreted this as a result of intoxication and we applied 50% solutions.

Fig. 1 - NaOH. Gravely dystrophic and necrobiotic changes in all tissue cels in the epidermic and dermal layers Fig. 2 - H2SO4. Distrophic changes in epidermal layer and granular formations, wavy line of collagenous fascicles, hyperaemia

Fig. 1 - NaOH. Gravely dystrophic and necrobiotic changes in all tissue cels in the epidermic and dermal layers

Fig. 2 - H2SO4. Distrophic changes in epidermal layer and granular formations, wavy line of collagenous fascicles, hyperaemia

6 hr post-trauma.
There was fragmentation of the fibrillated structures and an increase in the number of mast cells. The level of glycogen in the epidermal and muscle cells decreased. There was haemodynamic collapse when the destroyed tissues enlarged. 24 hr post-trauma. Decrease of haemostasis and gradual non-nalization of capillary lumen. No change in vessels with erythrocyte thrombosis, aggravation of interstitial changes, serious oedema, small cavitations in some cells. Myolysis in some muscle fibres. The keratin is detached from the epidermal and dermal layers. The dystrophic changes in the superficial layers of the epidermal stratum showed necrosis. Germinative layers cells remained cornparatively preserved.

Fig. 3 - NaOH. In addition to the main changes at the 6th hour there is also epidermial inflammation. There are many macrophages among the inflamed cells. Fig. 3 - NaOH. In addition to the main changes at the 6th hour there is also epidermial inflammation. There are many macrophages among the inflamed cells.

Day 3 post-trauma.
Autolysis of dead cells and structures in the epidermal and dermal layers. Inflammation persisted. The number of leucocytes and macrophages increased, and no erythrocyte thrombosis could be seen. The inflammatory reaction spread over the wound zone and the superficial muscle layer. Moderate signs of regeneration of the epidermal cells and hair follicles could be seen. NaOH. We can see epidermal necrosis and homogenization of the dermal tissues and inflammatory subdermal infiltrates.

Fig. 4 - H2SO4. Dystrpphic and necrobiotic changes in the cells. Inflammation and subdermal oedema. Inflammation infiltrates of histiocyte and macrophage character.

Fig. 4 - H2SO4. Dystrpphic and necrobiotic changes in the cells. Inflammation and subdermal oedema. Inflammation infiltrates of histiocyte and macrophage character.

Day 7 post-trauma.
The number of inflamed cells decreased. Hyperaen-lia disappeared and significant regeneration processes could be observed, especially at the basic layer in the epidermis and hair follicles. The number of leucocytes and fibrocytes in the dermal layer increased, and histiocytes and fibroblasts could also be seen. Granulation tissues spread subdermally and the regenerated epithelium expanded subdermally to the necrotic zone. Germinative and lymphoid cells predominated. The number of segmented neutrophils decreased. Collagenous fibres precipitated and homogenized.

Fig. 5 - H2SO4. Dystrophic changes, inflammatory oedema and inflamed cells can be seen.

Fig. 5 - H2SO4. Dystrophic changes, inflammatory oedema and inflamed cells can be seen.

Day 14 post-trauma.
Complete regeneration of cover epithelium in the necrotic zone and differentiation of all the cell layers. The process in the hair follicles was slower, while in the sebaceous and sweat glands it was still starting. The homogenization and fragmentation of collagenous fibres in the dermal layer state was unchanged. In the granulation tissue there was an increase in the number of fibroblasts and fibrocytes, and a decrease in the number of capillary vessels. Precollagenous and collagenous filaments appeared and inflammation was still active in the deep layers, mainly presented by lymphoid cells and plasmocytes, macrophages, and histiocytes.

Fig. 6 - NaOH. Initial proliferation of young granulated tissues.

Fig. 6 - NaOH. Initial proliferation of young granulated tissues.

Day 21 post-trauma.
NaOH. The covering of epithelium proliferated at the wound edge. In the superficial necrotic layer there was precipitated calcium. There was also considerable proliferation of fibroblasts and fibrocytes with fibroaenesis and young blood vessels. HS04. The regeneration process was strengthened.hillammation in the granulated tissue was moderate. HCI. No differences from H2SO4

Fig. 7 - NaOH. Granulation tissue with expressed fibrogenesis under the scar

Fig. 7 - NaOH. Granulation tissue with expressed fibrogenesis under the scar

Day 28 post-trauma.
There was no scar on the wound surface. In all tissues there were proliferation, differentiation, and maturation. H2SO4. The wound was covered with fibrin. There was great proliferation at the edge of the wound epithelium. Granulation in the bed of the wound and regeneration processes in the skin adnexa were observed.HCl. No differences from H2SO4 group.


BIBLIOGRAPHY.

  1. Shindarski B.: Chemical burns. In "Burntrauma", Medical Academy, Sofia, 1989.
  2. Simko S.: "Osetrovanie popalenych", Osveta, Martin, 1985.

 

This paper was received on 6 June 1994.

Address correspondence to: Prof. Konstantin Troshev, M.D., Ph.D
44 Alexander Batenberg Str.
9000 Varna, Bulgaria.

 

G. WHITAKER INTERNATIONAL BURNS PRIZE
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Under the patronage of the Authorities of the Sicilian Region for 1998

By law n. 57 of June 14th 1983 the Sicilian Regional Assembly authorized the President of the Region to grant the Giuseppe Whitaker Foundation, a non-profit-making organization under the patronage of the Accademia dei Lincei with seat in Palermo, an annual contribution for the establishment of the G. Whitaker International Burns Prize aimed at recognizing the activity of the most qualified experts from all countries in the field of burns pathology and treatment. The amount of the prize is fixed at twenty million Italian Lire. The prize will be awarded every year by the month of June in Palermo at the seat of the G. Whitaker Foundation.
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Anyone who considers himself/herself to be qualified to compete for the award may send by January 31st 1998 a detailed curriculum vitae to: Michele Masellis M.D., Secretary-Member of the Scientific Committee G. Whitaker Foundation, Via Dante 167, 90141 Palermo, Italy.




 

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