Burns are one of the most common and devastating forms of trauma. Patients with serious thermal injury require immediate specialized care in order to minimize morbidity and mortality. Significant thermal injuries induce a state of immunosuppression that predisposes burn patients to infectious complications. A current summary of the classifications of burn wound infections, including their diagnosis, treatment, and prevention, is given. Early excision of the eschar has substantially decreased the incidence of invasive burn wound infection and secondary sepsis, but most deaths in severely burn-injured patients are still due to burn wound sepsis or complications due to inhalation injury. Burn patients are also at risk for developing sepsis secondary to pneumonia, catheter-related infections, and suppurative thrombophlebitis. The introduction of silver-impregnated devices (e.g., central lines and Foley urinary catheters) may reduce the incidence of nosocomial infections due to prolonged placement of these devices. Improved outcomes for severely burned patients have been attributed to medical advances in fluid resuscitation, nutritional support, pulmonary and burn wound care, and infection control practices.

Burn Wound Infections

Purpose.To review the changing epidemiology of herpes simplex disease and correlate it with the epidemiology of ocular herpes simplex disease.Method.A review of pertinent reports in the world literature about the epidemiology of herpes simplex and specifically about ocular herpes simplex.Results.In

Herpes simplex virus epidemiology and ocular importance.

The pharmacokinetics and pharmacodynamics of drugs are significantly altered in the burn patient, and the burn patient population shows wide inter- and intraindividual variation in drug handling. Burn injury evolves in two phases. The first phase corresponds to the burn shock, which occurs during the first 48 hours after thermal injury. In this phase, hypovolaemia, oedema, hypoalbuminaemia and a low glomerular filtration rate are observed, which result in a slower rate of drug distribution and lower renal clearance. The second phase (beyond 48 hours after injury) is a hyperdynamic state with high blood flow in the kidneys and liver, an increased alpha1-acid-glycoprotein level and loss of the drug with exudate leakage. As a result, protein binding, drug distribution and clearance may be altered. Because of the alteration in these variables, wide intraindividual variation of pharmacokinetic parameters occurs depending upon the time since thermal injury and fluid resuscitation. Interindividual variations may be correlated with the percentage of the body surface area that is burnt, creatinine clearance, albuminaemia or the alpha1-acid-glycoprotein level. A number of important variations in pharmacodynamic parameters have been described, but their mechanisms are poorly understood. From a practical point of view, for the subpopulation of burn patients who eliminate drugs extremely rapidly, higher doses and/or shorter dosing intervals are required to avoid treatment inefficacy. Drug concentration measurements help to take into account interindividual variability. However, adaptation of doses based on Bayesian methods is frequently not possible because the distribution of pharmacokinetic parameters is poorly characterized in this population. Methods based only on individual data or on a surrogate marker for efficacy may be used to optimize the dosing regimen in this population.

Influence of burns on pharmacokinetics and pharmacodynamics of drugs used in the care of burn patients.

There has been a growing interest in micronutrients as a result of their essential role in endogenous antioxidant defense mechanisms and immunity. Critically ill burn and trauma patients are characterized by an increased free radical production, which is proportional to the severity of the injury. In addition, they are at high risk of negative trace element balances, which contribute to the imbalance in endogenous antioxidant capacity and the extension of primary lesions. Although selenium, zinc, and vitamin C and E status are altered in all injured patients, patients with major burns are unique for having copper deficiency. In major burns, high-dose ascorbic acid for 24 hours achieves reduction of resuscitation fluid requirements by endothelial antioxidant mechanisms both in animal models and in 1 human trial. Supplementation trials in trauma and burns including selenium and zinc have shown that early provision of micronutrients improves recovery. Vitamin supplementation trials without selenium have not achieved definitive effects. The human studies show that reinforcing antioxidant defenses early in the course of major injury is rational and that substituting the large initial micronutrient losses of selenium and zinc is safe in trauma, as is the addition of copper in burns. The IV route seems the only way to deliver the doses required to obtain a clinical effect.

Antioxidant Micronutrients in Major Trauma and Burns: Evidence and Practice

Infections by herpes simplex virus (HSV) types I and II are diverse and quite frequent. After primary infection, the virus establishes a life-long latency in the sensory ganglia and recrudescences may occur at an unpredictable rate. Recurrent labial and genital herpes infections represent the majority of clinical manifestations of HSV infections. Their management is currently well established using evidence-based medicine data. Primary labial herpes is generally not treated with antivirals in otherwise healthy children, although intravenous aciclovir may be offered in severe primary infections, particularly in the immunocompromised patient. The decision whether or not to treat recurrent labial herpes should be evaluated individually and depends on the frequency and severity of relapses, the impairment of the quality of life, and the cost of therapy. Patients with mild disease may benefit from topical therapy, and those with severe and frequent recurrences may be considered for intermittent or long-term oral antiviral therapy. Primary genital herpes is treated with oral or intravenous antivirals, depending on the severity of the infection and associated symptoms. Recurrent genital herpes can be managed with episodic short courses of oral antivirals in patients whose recurrences are moderate to severe and rare, and have a clear prodrome. Patients with >5 episodes/year, severe recurrences or unrecognisable prodromes may be best managed with long-term suppressive antiviral prophylaxis. HSV is also responsible for a variety of other clinical manifestations, including herpetic whitlow, neonatal infection, disseminated and atypical cutaneous infections, traumatic herpes, eczema herpeticum, and HSV— associated erythema multiforme. HSV infection may also represent a complication following cosmetic procedures of the oro-facial region, surgical and dental interventions, sun exposure and burns. Precise treatment guidelines for these HSV infections are not firmly established.

Treatment of mucocutaneous presentations of herpes simplex virus infections.

Herpes simplex virus infection in burned patients: Epidemiology of 11 cases

Assessment of vitamin and trace elementsupplementation in severely burned patients undergoing long-term parenteral and enteral nutrition

Pharmacocinétique de l'amikacine chez le brûlé de gravité moyenne.

Influence of chlorhexidine on the flora of burns

Introduction: Le traitement des intoxications cyanhydriques est base sur l'administration precoce de fortes doses de cyanocobalamine qui entrainent une coloration rouge des teguments genant l'evaluation de la profondeur des brulures. Seul le dosage permet d'affirmer cette intoxication mais son delai d'obtention est toujours > a 24h. Or, il a ete ecrit qu'un taux de lactates >10 mM 1 ou un trou anionique eleve pouvaient predire l'existence d'une intoxication par le cyanure. Objectifs: Rechercher une correlation entre ces parametres et le taux de cyanure lors de l'admission. Materiel et methodes: Nous avons mesure chez 42 brules (8 F et 34 H, âge 38 ans ± 19, surface brulee 38% ± 26) les taux d'ions cyanure, de lactate, les parametres de l'equilibre acido-basique, l'HbCO et calcule le trou anionique. Resultats: 40 % des patients ont des taux non significatifs d'ions cyanure, 56 % presentent une intoxication moderee (cyanure 139 ug 1 ± 79, trou anionique 15 mM 1 ± 4, lactates 3,1 mM 1 ± 1,1) et 5% une intoxication grave (6-39 ug 1 ± 71, trou anionique 16 mM 1 ± 6, lactates 4,8 mM 1 ± 0,1). Il n'est retrouve aucune correlation significative. Discussion: L'existence d'un delai de plusieurs heures entre la realisation des prelevements sanguins specifiques et la prise en charge therapeutique expliquent probablement que nous ne retrouvions pas les correlations proposees dans la litterature.

Le taux des lactates plasmatiques et le calcul du trou anionique ne sont pas prédictifs d'une intoxication cyanhydrique au cours des brûlures par incendie

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