Tamer Tadros, Daniel L Traber, et al (The Shriners Burns Institute and The University of Texas Medical Branch, Galveston, Texas)
Angiotensin II Inhibitor DuP753 Attenuates Burn and Endotoxin-Induced Gut Ischemia, Lipid Peroxidation, Mucosal Permeability, and Bacterial Translocation.
Annals of Surgery, April 2000, 231(4), 566-576.
Thermal injuries and endotoxaemia have been shown to induce ischaemia and reperfusion injury to the intestine leading to increased mucosal permeability and bacterial translocation. Angiotensin II is thought to be one of the primary mediations of post burn ischaemia. This study investigates the role of DuP753 (angiotensin inhibitor) in the process of mucosal injury and translocation of bacteria.
In pig models, an ultrasonic flow probe was inserted into the superior mesenteric artery and a catheter into the superior mesenteric vein. The pigs were anaesthetized and were subjected to 40%, third degree burn. DuP753 was administered intravenously immediately after the burns. E.coli lippolysaccharide (LPS) was injected 18 hours after the burn. Systemic and splanchnic hemodynamics were measured and blood gas analyses were done. Plasma conjugated dienes (PCDs) an index of lipid peroxidation were measured every 6 hours. The intestinal permeability was assessed 6 hourly by measuring the lactulose/mannitol excretion ratio. At the end of 42 hours, tissue samples were harvested for bacteriological cultures.
The results showed a significant decrease in mesenteric blood flow 58% of baseline. Treatment with DuP753 prevented this ischaemia and abrogated the postburn endotoxaemia. It also improved mesenteric oxygen supply. PCD levels were also controlled and prevented the mucosal permeability. Bacterial translocation was also considerably reduced.
It is concluded that DuP753 significantly reduces the extent of postburn injury.
M Shoup, L-K He, H Liu et al 1998. (Loyola Univ, Maywood, III):
Cyclooxygenase-2 Inhibitor NS-398 Improves Survival and Restores Leukocyte Counts in Burn Infection (Animal model).
J Trauma: Injury Infect Crit Care 45:215-221,
Cyclooxygenase (COX) plays a central role in the production of prostaglandin E2 (PEG2) from arachidonic acid. Production of (PEG2) may be increased when sepsis develops after trauma, particularly after burns.
There is evidence that PGE2 may play a role in the development of leukopenia during sepsis. Hence, COX inhibitors may be of value.
NS-398 inhibited macrophage PGE2 production, preserved the absolute neutrophil count and improved survival.
MH Desai, R Mlcak, J Richardson et al,1998 (Univ of Texas, Galveston; Shriners Burns Inst, Galveston, Tex);
Reduction in Mortality in Pediatric Patients With Inhalation Injury with Aerosolized Heparin/N-acetylcysteine Therapy.
J Burn Care Rehabil 19:210-212,
Smoke inhalation injury is a major cause of death after burns.The injuries are associated with fibrin cast deposition in the airways as well as progressive carbon dioxide retention resulting from a ball valve effect.
Based on promising results on animal studies, a combination of aerosolized heparin and acetylcysteine was evaluated for the treatment of smoke inhalation injury in children.
The above regime reduced mortality, atelectasis and the need for reintubation. This mode of therapy addresses the pathophysiological mechanics of inhalation injury by reducing free radical ions and inhibiting fibrin cast formation.
A Jonsson, BT Brofeldt, P Nellgard et al (Goteborg Univ, Sweden; Univ of California, Davis, Sacramento), 1998:
Local Anesthetics Improve Dermal Perfusion After Burn Injury (animal expt.)
J Burn Care Rehabil 19:50-56.
Amide local anesthetics inhibit the release of various inflammatory mediators involved in the pathophysiology of burns. At certain concentrations, local anaesthetics can also increase skin perfusion.
The results in the rat model showed that topical (or systemic) administration of local anesthesia can prevent progressive dermal ischaemia after deep partial-thickness burn injury.
A S Unsold, JF Rizzo, S Lessell (Harward Medical School and the Mass. Eye and Ear Infirmary)
Optic Neuropathy after Burns.
Arch.Ophthalmology, Vol.118, Dec.2000, pg.1696-1698.
The authors examined 2 new cases of post-burn optic neuropathy and identified 10 additional cases in medical literature.
Loss of vision was severe and bilateral, with disc oedema present in most cases. Retinal haemorrhages and oedema were observed in some cases. There was a capacity for spontaneous recovery.
Patients with cutaneous scalds and thermal burns may develop bilateral optic neuropathy. The pathogenesis of this visual loss has yet to be established. Various hypothesis, include demyelination caused by a toxin released from burned skin, hypotension leading to ischaemic neuropathy or a combination of aetiological factors in patients having respiratory infections and metabolic complications and receiving multiple medications