Publications by authors named "Arturson G"

The body's reaction to thermal injury is much more than an initial, local inflammatory response. The burn wound is a continuous, severe threat against the rest of the body due to invasion of infectious agents, antigen challenge and repeated additional trauma caused by wound cleaning and excision. The inflammatory mediators which control blood supply and microvascular permeability in the wound have been extensively studied and are largely understood.

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Management of burns.

J Wound Care

March 1993

A review of the priorities of care during the acute management of burnt patients.

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Separation techniques for obtaining pure and biologically active swine C3 have been improved in this study. Using these procedures and through the further characterization of porcine C3, the possibilities for developing more specific techniques for the analysis of the complement system in swine have been improved. Plasma was initially treated with protease inhibitors, polyethylene glycol (PEG)-fractionation, plasminogen-depletion and a rapid chromatographic desalting step.

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Because it is difficult to estimate the extent of deep tissue injury clinically, angiography was carried out in 28 patients with signs of damage from current flow through the body. Eight of the arteriograms showed normal extremities, 6 showed changes of small arteries, and 38 showed injury to the main arteries. In the latter group there were 24 total arterial occlusions, narrow irregular lumens in 10, and 4 had occlusion and distal refilling.

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This investigation was undertaken to determine the splanchnic exchange of 3-methylhistidine (3MH) in infection. Hepatic vein, femoral vein, and radial artery catheterizations were performed in 12 febrile patients with infections of varying severity. Differences in arteriovenous 3MH, analyzed by high-performance liquid chromatography, were multiplied by the plasma flows, determined by a dye dilution technique.

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A comprehensive pathophysiologic model has been designed to describe the fluid shifts and hemodynamics in connection with fluid therapy for patients who have had trauma. The model is used to simulate treatment of a patient with burn injury, and these results are compared with measured physiologic and biochemical variables. Various formulas for resuscitation of patients with thermal injuries are also simulated to illustrate the potential use of the "patient simulator" for designing fluid resuscitation programs.

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Following thermal injury many subsystems of the human body interact closely. The effects both of the pathological event in one subsystem and the subsequent therapy are masked or compensated by changes in other homeostatic subsystems. Not until the capacity of the homeostatic subsystems and/or the therapy is inadequate will the effects become obvious.

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Computer-based 'patient simulators' are of a potential value in diagnosis, monitoring and therapy of the severely ill patient with trauma. An extensive pathophysiological model is described and documented in full detail. The model makes it possible to calculate and predict clinically important state variables on the basis of fluid input and fluid losses.

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During the early morning of Monday, 19 November 1984, one of the largest disasters in industrial history occurred in the Mexico City Area, causing the greatest rescue effort to assist population in an emergency ever undertaken. The tragic catastrophe started in a large LPG (Liquid Petroleum Gas) storage and distribution centre in San Juan Ixhuatepec, 20 km north of Mexico City. The facilities, owned by the Pemex State Oil Company, consisted of six spherical storage tanks (four with a volume of 1600 m3 and two with a volume of 2400 m3) and 48 horizontal cylindrical bullet tanks of different sizes.

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Heat loss during anaesthesia and surgery is a common problem. In patients with restricted cardio-pulmonary reserves this may endanger the postoperative outcome. In order to compare thermal balance we studied 25 men undergoing transurethral resection of the prostate (TURP), using either general anaesthesia (G.

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A standardized, reproducible burn model on rat paw was used and the effect of prompt local cooling on the oedema formation was measured using a newly developed non-invasive method. A transient reduction in oedema formation was observed lasting for a longer period of time with decreasing temperature down to 0 degrees C and increasing cooling time up to 120 min. The decrease in oedema formation was followed by an increase towards or above the amount of oedema in untreated scald injury.

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A highly standardized, reproducible burn model on rat hind paws with objective measurement of oedema volume was used to study the post-burn oedema formation in leucocyte-free rats as compared to a matched group of normal rats. No difference in oedema volume could be detected during the first 4 h post-burn. Thus the mechanical effect of sticking leucocytes in the injured area or leucocyte derived substances do not seem to play any significant role in the early local oedema formation which we postulate is entirely mediated by local events.

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A highly standardized, reproducible burn model on rat hind paw as well as a method to measure oedema volume non-invasively is described. Along with a review of the literature on earlier methods to measure post-burn oedema we present a statistical evaluation of the present model with notes on its applicability in various experimental settings.

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Burns wound sepsis is not only the most common but also the most severe complication following extensive thermal injury. One conceivable explanation of this problem is a reduced capacity of the polymorphonuclear neutrophil leucocytes of these patients to combat the invading microbes. Fifty patients (42 male and 8 female) with deep dermal burns, covering 20-90 per cent of the total body surface area, were investigated from immediately after the injury until death or until healing of the wounds.

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The potential usefulness of computer-based 'patient-simulators' in burn care is discussed and illustrated in the special case of oedema formation in three patients with severe thermal injuries. The present model was derived from a model by Wiederhielm (1978), and modified to be applicable to thermal injuries. The model seems to describe accurately the oedema formation as well as the distribution and composition of local and general oedema.

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A 40% total body scald burn was produced in mature rats. An immediate decrease of the metabolic rate was followed by a hypermetabolic response similar to that described in human beings following thermal injury. The amounts of adenine nucleotides and hexosemonophosphates were monitored in three types of cells: erythrocytes (which lack mitochondria), skeletal muscle cells (which to a certain extent can rely on an increased glycolysis for their increased energy supply) and liver cells (which are sensitive to hypoxia and have a great need of energy in the post-traumatic period).

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Fifty patients with high-tension electrical injuries referred for primary treatment to the Burn Center at the University of Uppsala, Sweden during the period 1969 to 1982, have been investigated with special regard to the resuscitation and early complications from internal organs. Seven patients (14%) died, five of them prior to 1974, one in cardiac infarction and four in renal failure. Two died after 1974, one in cardiac infarction and the other in severe shock (98% burn).

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The effects of the topical application and the intraperitoneal administration of epidermal growth factor (EGF) on the healing of epidermal wounds, and of partial-thickness scalds in rats and of corneal wounds in rabbits were evaluated. The parameters measured were the daily percentage body weight change, time to complete healing of the wounds, the evaporative water loss from the wound surface and the rate of new formation of epithelial cell layers on the epidermal and corneal wounds. Wounded animals treated with 0.

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