In this lengthy review the Author considers methods for the nonoperative debridement of burns. The first steps in this direction date back to the Second World War, when enzymes of bacterial origin, acids, and proteolytic enzymes of bacterial origin were used. Later developments involved the use of sutilains collagenase, other enzymes of plant origin (fig tree enzymes, pineapple), trypsin, blowfly larvae extracts, and vibriolysin. Enzymatic debridement might appear to be an attractive form of treatment, but the results obtained have been extremely variable.
The simultaneous generation of nitric acid (NOİ) and superoxide (O2¯) may lead to the formation of peroxynitrite (ONOO¯). This is a powerful oxidant thought to be involved in the pathogenesis of certain disease states. The study described investigated the possible generation of ONOO¯ in local skin tissues after thermal injury. Male Wistar rats were anaesthetized and subjected to a small abdominal burn of moderate temperature (50 °C, 5-15 min). The animals were then killed either 60 or 180 min post-burn. The skin sites were removed and homogenized. Protein-bound 3-nitrotyrosine (3NT), a biomarker for ONOO¯ in rat skin, was quantified by ELISA. Thermal injury (50 °C, 10 min) caused a significant increase in 3NT and oedema formation when compared with unheated control sites 180 min post-burn. These data are the first to show protein nitration in thermally injured, oedematous skin and suggest that ONOO¯ is generated in burned skin tissues.
In recent years it has been noted that immune-suppression may follow burn injury, with the cellular and humoral immune systems both being affected. This study compares the quantitative differences between cutaneous and electrical burn patients with regard to the partition and levels of the lymphocyte population. Fifteen patients were included in a prospective study. Blood samples were taken 3 and 7 days post-burn (major thermal injury or high-voltage electrical injury). T cell and B cell populations, activated T cells, and natural killer and helper T cells were all suppressed in the two groups of patients. Suppressor T cell levels were elevated in the electrical burn group. The CD 4/CD 8 ratios were therefore more suppressed in the electrical burn group. It is concluded that the lymphocyte population in electrical burn patients, as also contributing factors that play an important role in the development of sepsis, merit further study.
The heat shock response (HSR) has been found to have protective effects in animal models of septic shock and toxaemia. In this study the hypothesis was tested that HSR could be protective in experimental burns. The experiment was performed on 115 adult male Wistar rats, divided into four groups. In the four respective groups, the rats were: anaesthetized and shaved; anaesthetized and heated in a 45 °C water bath; anaesthetized, shaved, and submitted to 26-30% body surface third-degree burns using a brass bar; and anaesthetized, heated, and, one day later, burned. Liver and lung samples were taken from all groups for heat-shock protein 70 detection, which was positive in the heated animals. No animals died in the first and second groups. Heated and burned animals presented significantly decreased mortality after burns compared with unheated burned animals. The eliciting of HSR therefore significantly reduced mortality rates in this experimental burn model.
The purpose of this study was to examine the relationship between the severity of burns and tumour necrosis factor receptor I (TNFRI) and tumour necrosis factor receptor I and II (TFNRII) levels in the acute post-burn period and throughout the following period. Twenty-four burn patients were included in the study (TBSA, 50.2 ± 20.4%). In the immediate post-burn phase, TNFRI and TNFRII levels correlated significantly with TBSA. These levels, immediately after the injury, were significantly higher in the 11 patients who eventually died of their burns than in the 13 patients who survived. The TNF-· levels immediately post-burn did not differ significantly between patients who survived and those who died. TNFRI and TNFRII values in the entire following group also correlated significantly with TBSA. Peak levels were significantly higher in the group that died than in the group that survived. TNF-· levels correlated significantly with TNFRI and TNFRII levels. These levels therefore closely reflected burn severity both in the acute post-burn period and during follow-up. They thus well reflected the severity and outcome of the burns, regardless of the presence or absence of infection.