A linear regression analysis of data regarding hospitalized burn patients admitted between July Ist 1978 and June 30th 1979 in the 66 counties of the 6-state region of New England revealed strong associations between calculated burn rates and the following five socioeconomic variables: per capita income, percentage of persons below poverty level, percentage of residences built before 1940, percentage of adults with 16 or more years of education, and percentage of persons moving since 1975 with previous residence in the same county. Greater accuracy in predicting populations at increased risk of bum injury could strengthen the cost-effectiveness of efforts to help persons engaged in planning health care delivery systems, locating the need for specialized bum care facilities, or targeting high-risk population groups for preventive housing inspections or educational intervention.

Locke J.A., MacKay Rossignol A., Burke J.F. Bums, 16: 273-277, 1990.

EFFECT OF ACUTE BURN TRAUMA ON RETICULOENDOTHELIAL SYSTEM PHAGOCYTIC ACTIVITY IN RATS. II: COMPARISON OF UPTAKE OF RADIOLABELLED COLLOID AND BACTERIA.

The purpose of this study was to compare the uptake of radiolabelled colloid or bacteria in normal rats and in rats subjected to acute burns (20% TBSA injury caused by boiling water). In the liver, colloid uptake was unaffected by the trauma, while uptake of the labelled bacteria was reduced. There was a reduction of both colloid and bacteria uptake in the spleen of burned animals, and an increase of both in the lung. The findings are in harmony with the hypothesis that acute bums alter reticuloendothelial system phagocytic activity in the rat towards both inert particles and live bacteria.

Trop M., Schiffrin E.J., Callahan R.J., Strauss H.W., Carter E.A. Burns, 16: 278-280, 1990.

This paper considers the effectiveness of burn prevention campaigns and points out the difficulty of accurate assessment in view of the incompleteness of national and international data. It is also pointed out that any reductions in bum mortality may be due to advances in therapy rather than to the success of burn prevention campaigns. Education may increase knowledge but it does not necessarily lead to changes in behavioural patterns. It is important therefore to consider modem techniques of motivational theory in order to promote public concern and action for individual behavioural change, appropriate legislation and product safety.

Linares A.Z., Linares H.A. Bums, 16: 281-285, 1990.

The present study was designed to assess the effect of bum trauma on immunoglobulin function and to examine if any improvement in function could be caused by the administration of biosynthetic human growth hormone GH (somatropin). Serum concentrations of the immunoglobulin subclasses and their functional activity against pneumococcal polysaccharide and E coli were studied for 15 days in six adult burn patients treated with GH. Six other adult burn patients were, used as concentrations of the major subclasses fell below their normal ranges following trauma but recovered significantly by the I the study. Concentrations of the IgG3

subclasses did not change significantly. The relative proportions of the four subclasses remained unchanged and were comparable to those of normal man. Significantly reduced functional activities were observed in all the subclasses except IgGl. The activities of the major subclasses were correlated with their serum concentrations and when corrected for their concentrations were comparable to those of normal blood donors. Somatropin administration did not cause significant increases in concentrations or activity of the subclasses. It may therefore be concluded that patients with moderately sized burns have a reduced immunoglobulin function resulting from the changes in serum concentration rather than from any qualitative change and that somatropin administration does not usefully improve immunoglobulin function.

controls. The IgGl and IgG2, the burn Ith day of and IgG4

Belcher H.J.C.R., Sheldon J., Riches P. Burns, 16: 286-290, 1990.

Water inhalation as an aerosol from a boiling kettle with or without tincture of benzoin is a fairly common form of adjunct therapy in cases of respiratory tract infection. This form of treatment presents special dangers with small children, who cannot always be prevailed upon to keep still, with the result that the-boiling water is upset, causing scalds. A study of 193 burned infants admitted to a Kuwaiti Bums Unit over a 4-year period revealed I I such cases (5.7%). The scalds increased the morbidity in children who were already suffering from respiratory tract infections. It is recommended that specially designed humidifiers should be used instead for this purpose.

Ebrahim M.K.H., Bang R.L., Lari A.R.A. Burns, 16: 291-293, 1990.

This article lists all the bum care facilities in the Federal Republic of Germany, with addresses, telephone numbers and numbers of beds. There is also a map.

Anonymous Bums, 16: 294-296, 1990.

The sick cell syndrome in burned patients is generally regarded as hypothetical as no complete clinical examples appear to have been reported in the literature. It may however be considered to be a disorder of the sodium/potassium pump which leads to an altered electrolyte exchange through the cellular membrane. Its causes may include anoxia, hypovolaemia, septicaemia and malnourishment. A case is described of a burn patient who suffered from the syndrome twice during his period of hospitalization. The striking features were hyponatraemia despite an increasing sodium intake, reduced natriuria, a trend to hyperkalaemia and unchanged haematological parameters. The syndrome was characterized clinically by confusion and hallucinations, and the problem was solved by treatment of the cause.

Benito Ruiz J., Baena Montilla P., Navarro Monzonis A. Bums, 16: 309-312, 1990.

In patients with inhalation injury (from which about one third of all patients treated at Burns Centres suffer) the frequent occurrence of respiratory insufficiency and the high incidence of bronchopneumonia, together with its early onset, emphasize the importance of early accurate diagnosis. A predictor of inhalation injury based on the readily available clinical variables of injury in a closed space, presence of facial burns, total extent of body surface burned, and age was therefore derived, by a stepwise logistic regression. Early diagnosis is best achieved by endoscopic bronchoscopy and 133 xenon ventilation perfusion scan. This method permits timely application of high-frequency ventilation that appears to reduce the incidence of pneumonia and to decrease mortality. Some pharmacological agents also assist in improving the deleterious alterations in the vasculature.

Pruitt B.A. Jr., Cioffi W.G., Shimazu T., lkeuchi H., Mason A.D. Supplement to The Journal of Trauma, 30, 12: S63-S69, 1990.

The immune consequences of thermal injury and their causes are reviewed in four distinct categories: nutritional factors, gut-derived factors, complement degradation products, and wound-derived immunosuppre.ssive polypeptides. After ample discussion it is concluded that early aggressive enteral nutrition with specially formulated diets is the easiest and by far the most effective way of preventing immune defects and preventing infection. Recent investigations have also shown a beneficial effect on the immune function of H2 receptor blockade, xanthine oxidase inhibitors, inhibitors of free oxygen radical generation, and prostaglandin inhibitors. Inhibitor of prostaglandin function has some adverse as well as beneficial effects. The use of protease inhibitors can also improve resistance to infection.

Alexander J.W. Supplement to The Journal of Trauma, 30, 12: S70-S75, 1990.

Acute thermal injury of the skin (second-degree, 25% TBS) causes a series of pathophysiological events that lead to distant and local tissue/organ injury. The distant effects include intravascular haemolysis and acute lung injury, due to complement activation and intravascular stimulation of neutrophils, causing oxygen radical production, itself resulting in injury of red cells and pulmonary vascular endothelial cells. Locally, at the burn site, the gradual increase in vascular permeability is linked to complement activation and histamine release, leading to interaction of histamine with xanthine oxidase, which in turn enhances the enzyme's catalytic activity. The increased vascular permeability can be much attenuated by the use of inhibitors of xanthine oxidase, the inhibitor of histamine release (cromolyn), catalase, an iron chelator (deferoxamine), or scavengers of the hydroxyl radical. In the rat model studied here, neutrophils appeared to play little if any role in dermal vascular injury. The studies suggest that the pathophysiological events subsequent to local thermal trauma are complex and involve various mediator pathways.

Ward P.A., Till G.O. Supplement to The Journal of Trauma, 30, 12: S75-S79, 1990.

NEUTROPHIL DISORDERS IN BURN INJURY:

The bacterial infection following burn injury has led to numerous studies characterizing neutrophil function in such conditions. The studies provide a picture of intravascular complement activation, neutrophil-C5a inteactions, and consequent disordered cellular function. Neutrophil dysfunction includes suppressed random and C5a-directed migration and hyperresponsiveness to oxidative stimuli. The histological and functional involvement of neutrophils in ARDS and some other organ failure states remains unexplained. It would appear from circumstantial and extrapolated information that macrophage-lineage cells function as regulators of neutrophil function within matrix environments in burn injury. Burned patients sometimes present elevated endotoxin levels, and this would support the theory of endotoxin-stimulated monocytes/ macrophages inducing a) neutrophil migration into connective tissue matrices (LTB4 and IL-8), b) prolonged oxidant production (TNF-alpha, GM-CSF), and c) neutrophil release of regulatory substances from neutrophils (G-CSF). A variety of experimental approaches for the testing of this hypothesis are suggested by this information.

Solomkin J.S. Supplement to The Journal of Trauma, 30, 12: S80-S85, 1990.

It is becoming clear that T cells play a modulatory role in wound healing although the full range of their effects is still not fully delineated. The evidence for T-cell participation in wound healing has been obtained by various methods described in this paper. T lymphocytes have been demonstrated both in vitro and in vivo to possess the capacity to regulate essential steps in the process of wound healing. T cells do not appear to be required for the initiation of the healing process, but while healing can progress in the absence of T lymphocytes, an intact cellular immune response is essential for a normal outcome.

Barbul A., Regan M.C. Supplement to The Journal of Trauma, 30, 12: S97-S100, 1990.

DEVELOPMENT AND POTENTIAL USE OF ANTIBODY DIRECTED AGAINST LIPOPOLYSACCHARIDE FOR THE TREATMENT OF GRAM-NEGATIVE BACTERIAL SEPSIS

Despite routine therapeutic methods antimicrobial agents, haemodynamic monitoring and fluid resuscitation, and metabolic support - Grainnegative bacterial sepsis is still a major cause of death in hospitalized patients. As there is considerable evidence to suggest that Gram-negative bacterial lipopolysaccharide (endotoxin, LPS) is responsible for many of the direct and host mediator-induced deleterious effects, recent research has concentrated on the development and use of anti-LPS antibody preparations in order to improve prospects of survival. Antibody preparations (both poly- and monoclonal) directed against the common deep core/lipid A region of LPS are cross-reactive in vitro and cross-protective in vivo against a wide range of challenge organisms and LPS, and from preliminary clinical trials it would appear that mortality can be reduced. The precise endotoxin epitope against which antibody should be directed in order to maximize protection has not however been established. This method is likely to become a standard form of adjunctive therapy before very long for the treatment of Gram-negative bacterial sepsis.

Dunn D.L.

Supplement to The Journal of Trauma, 30, 12: S100-S106, 1990.