Therapeutic efficacy of timentin and augmentin versus silvadene in burn wound infections.

Successful closure of thermal injuries, by either skin graft or delayed wound closure, largely depends on the ability to control the number of bacteria in the wound. The purpose of this study was to investigate the efficacy of two new antimicrobial agents, ticarcillin and clavulanate (Timentin) and amoxicillin and clavulanate (Augmentin), in the infected thermal injury. The therapeutic results were compared with the model treated with the standard topical silver sulfadiazine (Silvadene). Seventy-six Sprague-Dawley rats received a 20% full-thickness thermal injury and were then divided into six treatment groups. Three of the groups were inoculated topically with 10(8) Pseudomonas aeruginosa/ml, and three of the groups received topical inoculation of 10(8) Staphylococcus aureus/ml. The groups inoculated with P. aeruginosa received either intraperitoneal Timentin, topical Silvadene, or placebo treatment. The groups inoculated with S. aureus were treated with either enteral Augmentin, topical Silvadene, or placebo. The animals received 10 days of therapy and underwent tissue biopsies on alternate days. Statistical analysis showed that the level of bacteria in the wounds compared with the control group was significantly (p less than 0.05) decreased for both antibiotics tested as measured by quantitative wound biopsies. These studies demonstrate the efficacy of systemic Timentin and Augmentin in the infected thermal injury.

The effect of endogenous skin bacteria on burn wound infection.

Burn wound sepsis can be due to exogenous or endogenous bacteria. When rare organisms cause infection, exogenous sources are implicated. This sets into motion hospital infection control team searches, which are both exhausting and harassing to patients and staff. This study examines the skin bacteria present at admission and the frequency of endogenous infection in burn patients. Sixty-two patients with burns up to 92% of the total body surface area underwent unburned skin bacterial surveillance on admission and at weekly intervals using RODAC contact plates. Burn wounds were biopsied for quantitative and qualitative analyses. Morphologically dissimilar colonies were isolated and identified using standard gram-positive and gram-negative identification strips (Analytab Products, Inc. [API]). On admission, the patients harbored Staphylococcus species, many of which were burn wound sepsis were infected with the same organisms cultured from their unburned skin on admission. A subset of patients (14) grew methicillin-resistant Staphylococcus aureus from their wounds or other sites. A comparison with admission isolates showed identical susceptibilities. These data suggest skin is an endogenous source of infection in the burned patient.

The epidemiology of methicillin-resistant Staphylococcus aureus in a burn center.

The emergence of methicillin-resistant Staphylococcus aureus (MRSA) in a critical care facility creates a multifaceted epidemiological problem in uncovering the source of infection. This study was undertaken to determine the true etiology of MRSA burn wound infections. Patients with a 30% or greater TBSA burn had both burned and unburned skin surface cultured upon admission, using RODAC plates. All other body fluids were cultured when sepsis was suspected. Admission cultures of 14 patients who developed MRSA wound infections were examined for methicillin-resistant organisms. Both admission isolates and infection isolates were compared by antibiogram analysis. Of the 14 patients admitted who developed MRSA infections, 57.1% of these had methicillin-resistant staphylococci present on admission. However, the remaining 42.9% of the patients had methicillin-sensitive, B-lactamase positive staphylococci present on admission. Isolates of group D streptococci resistant to methicillin were isolated in 35.7% of the patients. This data suggests that burn wound infections caused by MRSA very likely arise from the endogenous flora present at the time of injury through conferring the resistant plasmid by conjugational transfer.

Facial and scalp burns from hair activator products.

Review of 1,008 admissions over the past two years to the Detroit Medical Center Burn Unit revealed 227 patients with facial or scalp burns. Of these, 12 patients sustained burns directly as a result of accidentally igniting a hair activator product called "Jheri-Curl." Eleven patients sustained superficial partial-thickness burns and were adequately treated with Dermaide. One had deeper burns requiring split-thickness skin grafting.

Experimental and clinical observations on frostbite.

Experimental ischemia by the classic frostbite rabbit ear model clearly defined the role of thromboxane as a mediator of progressive dermal ischemia in frostbite injuries. The therapeutic groups consisted of the antiprostanoids, methylprednisolone, and aspirin combined with anti-thromboxane agents Aloe vera and methimazole, while the control group received no therapy. Survival was measured by planimetry for all groups. No tissue survival was evident in the frostbite control group. Methimazole treatment allowed 34.3% survival, Aloe vera 28.2% survival, aspirin 22.5% survival, and methylprednisolone 17.5% survival. The data compare the results of a modified frostbite protocol using ibuprofen with therapeutic modalities used by other clinical services. Of 154 patients treated for frostbite from 1982 to 1985, 56 were treated with our frostbite protocol; 98 were treated with other modalities. Of the 56 protocol patients, 18 suffered 1st degree frostbite, 25, 2nd degree frostbite, and 13, 3rd degree frostbite. For all degrees of frostbite, 67.9% healed without tissue loss, 25.0% healed with partial tissue loss, and 7% required amputation (P less than .001). Of the patients not on protocol, 11 suffered 1st degree frostbite, 51, 2nd degree frostbite, and 36, 3rd degree frostbite. Of these, 32.7% healed without tissue loss, 34.6% healed with tissue loss, and 32.7% required amputation. The morbidity of progressive dermal ischemia in frostbite may be decreased by the therapeutic use of inhibitors of the arachidonic acid cascade.

The role of thromboxane in experimental inadvertent intra-arterial drug injections.

Inadvertent intra-arterial injection of drugs produces a well-defined clinical syndrome whose pathophysiology remains unclear. This study was designed to determine the role of the inflammatory mediator, thromboxane, in intra-arterial drug injections. The rabbit ear model, as described by Kinmonth and Sheppard, was used. Five of the experimental groups were treated with specific or nonspecific thromboxane blocking agents and two groups served as controls. Immunohistochemical staining of the control ears showed elevated levels of thromboxane within the first 6 hours postinjury. The specific thromboxane blocking agents, methimazole and Aloe vera, showed almost complete blockade of thromboxane production. The percentage of ear survival was significantly greater in the group treated with topical Aloe vera (p less than 0.05) and even greater survival was achieved in the combined Aloe vera/methimazole group (p less than 0.01). On the basis of these results, we have begun treatment of such injuries with specific and nonspecific thromboxane blocking agents.