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An open, prospective, randomized, pilot investigation was implemented to evaluate the pain, cost-effectiveness, ease of use, tolerance, efficacy, and safety of a soft silicone wound contact layer (Mepitel One) vs Bridal Veil and staples used on split thickness skin grafts in the treatment of deep partial or full-thickness thermal burns. Individuals aged between 18 and 70 years with deep partial or full-thickness thermal burns (1-25% TBSA) were randomized into two groups and treated for 14 days or until greater than 95% graft take was achieved, whichever occurred first. Data were obtained and analyzed on pain experienced before, during, and after dressing removal. Secondary considerations included the overall cost (direct), graft take and healing, the ease of product use, overall experience of the dressing, and adverse events. A total of 43 subjects were recruited. There were no significant differences in burn area profiles within the groups. The pain level during dressing removal was significant between the groups (P = .0118) with the removal of Mepitel One being less painful. The staff costs were lower in the group of patients treated with Mepitel One (P = .0064) as reflected in the shorter time required for dressing removal (P = .0005), with Mepitel One taking on average less than a quarter of the time to remove. There was no significant difference in healing between the two groups, with 99.0% of the Mepitel One group and 93.1% of the Bridal Veil and staples group showing greater than 95% graft take at post-op day 7 (+/-1) (P = .2373). Clinicians reported that the soft silicone dressing was easier to use, more conformable, and demonstrated better ability to stay in place, compared with the Bridal Veil and staples regime. Both treatments were well tolerated, with no serious adverse events in either treatment group. Mepitel One was at least as effective in the treatment of patients as the standard care (Bridal Veil and staples). In addition, the group of patients treated with the soft silicone dressing demonstrated decreased pain and lower costs associated with treatment.

Emergence of resistance to vancomycin and the increasing incidence of community-acquired methicillin-resistant Staphylococcus aureus (MRSA) warrant careful initiation of antimicrobial agents after nasal swab polymerase chain recombination (PCR) MRSA positive screen. Current MRSA PCR nasal swab (PCR) screening does not distinguish non-hospital-acquired strains. A retrospective, institutional review board-approved study of collected PCR screenings among 826 burn center admissions over a 23-month period assessed culture results, antimicrobial agents chosen, and patient demographics. Seventy-seven of the 826 were known chronic carriers (n = 11); had MRSA on initial PCR (n = 48); or converted to positive PCR screen on later testing (n = 18). The 48 patients with initial positive PCR were decolonized with mupirocin. MRSA carriers were not decolonized. The 18 patients who became PCR positive were also not decolonized with 10 having positive cultures. The 48 initial PCR nasal swab positive patients represented 5.8% of admissions. Demographic data did not differ among chronic carriers, initial PCR positive patients, nor those converting to PCR positive. Length of stay was shorter for initial PCR positive decolonized patients (P << .05) and they had a 35% of decrease in MRSA infection. All 11 chronic carriers became infected with MRSA; however, five had non-hospital-acquired MRSA and two solely non-hospital-acquired MRSA. For the 48 PCR positive patients, 17 had isolated MRSA and one having exclusively non-hospital-acquired MRSA. Of the 39 patients with isolated MRSA, 20 (43%) non-hospital-acquired MRSA. Non-hospital-acquired MRSA was 43%, however PCR fails to distinguish hospital-acquired MRSA from community-acquired MRSA.

Trimethoprim is well known to cause rashes; however, what is not commonly known is that it causes sudden and profound hyperkalemia in 10 to 20% of treated patients. The uniqueness of burn patients begs the question whether changes known to occur in these patients might also increase this trimethoprim effect. After institutional review board approval, a retrospective study evaluated 224 patients with thermal injury who had been treated with trimethoprim sulfamethoxazole (TMP-SMX), 24 of whom had underlying renal impairment (creatinine clearances50 ml/min) and were excluded, leaving 200 patients for analysis. Three definitions of drug-induced hyperkalemia were used: 1) a ≥ 1 mEq/L rise, 2) a0.8 mEq rise in potassium in24 hours warranting early discontinuation of TMP-SMX, and 3) "marked" hyperkalemia defined as serum potassium of ≥ 5.5 mEq/L within 48 hours. A potassium level before trimethoprim exposure (TxK) and after TxK were collected retrospectively. Demographic data were analyzed with Student's t-test and trimethoprim dose alone, demonstrating a significant difference. Analysis of 200 patients exposed to trimethoprim demonstrated an elevation of potassium (first definition) in 31 patients (15.5%), a rapid change in serum potassium in two patients (second definition), and marked hyperkalemia (5.5 mEq/L) in 13 patients (6.5%). Hyperkalemia never occurred in 166 of 200 patients (82%; before TxK, 3.9 ± 0.4; after TxK, 4.3 ± 0.5 mEq/L). Change in serum potassium among patients with hyperkalemia was 4.0 ± 0.5 mEq/L before TxK and 5.3 ± 0.7 mEq/L after TxK. Twelve published hyperkalemia risk factors were reviewed in these 200 patients and only history of hypertension and need for intubation was more common in those with hyperkalemia. A nearly 20% incidence of hyperkalemia and 6% serious hyperkalemia in burn patients is consistent with reports in patients without burn injury. These data also suggest that the metabolic and hormonal changes associated with burn injury do not increase further the genetically predisposed hyperkalemia resulting from exposure to trimethoprim. These data suggest patients treated with TMP-SMX should have routine serum potassium monitoring before discharge.

Background Nebulized antibiotics are used to locally treat colonizations of multi-resistant organisms. Prior systemic nephrotoxic antibiotic use with serum creatinine rises warranted an alternative therapy in 69 ventilator-dependent patients with persisting sputum cultures and need for ventilatory support. Materials and methods Following IRB approval, retrospective patient data were reviewed. Analysis included comparison of these 69 patients (71 treatments) to 142 Gram-negative infected burn patients matched for age and burn size. Results Mean pooled age and burn wound percent for the 71 triplicates ( n = 211 patients) were 55.6 ± 18.3 years and 27.4 ± 22.3% burns. Fifty-seven of 69 (83%) patients had inhalation injuries and 54 of 69 (78%) patients survived. Nebulizations averaged 6.8 ± 3.3 days (range 3–12 days). Serum creatinine rose in 2 patients receiving colistimethate nebulizations, known to cause nephrotoxicity following nebulization. Triplicate comparisons via ANOVA noted prolonged ventilatory support ( F = 13.39; p ≪ 0.05) and length of stay ( F = 6.11; p ≪ 0.5). Variance was attributed to the sicker nebulized patients. Twenty-four inhalation injury-only triplicates further confirmed that nebulized patient subgroup was more ill. Conclusion Short duration antibiotic nebulization may allow higher intra-tracheal antibiotic concentrations and may facilitate weaning from the ventilator by reducing bacterial bioburden.

Vancomycin-resistant Enterococcus faecium and faecalis (VRE) remains a major complication among critically ill patients. A 26-year-old patient with 65% total body surface area burns (TBSA) was infected with several E. faecium strains during his admission that were resistant to vancomycin. Because chloramphenicol was the standard treatment at this time, this drug was initiated until, the organism was identified as E. faecium and reported as susceptible to quinupristin-dalfopristin. Given these data, it was then decided to discontinue the chloramphenicol therapy. Quinupristin-dalfopristin therapy resulted in initial reduction of fever and white blood cell counts that continued over the next 5 days. However, on day 7 of quinupristin-dalfopristin therapy, a return of fever and elevation of the white blood cell count was noted and a repeated E. faecium blood culture demonstrated sudden resistance to quinupristin-dalfopristin (Bauer-Kirby zone size

We sought to evaluate the adverse effect profile of linezolid among thermal injury patients requiring treatment for Enterococcus species or other Gram-positive infection warranting treatment with linezolid. Seventy-six inhalation injury and/or thermal injury patients experiencing 94 exposures to linezolid for 48 hours or longer (range, 2-83 days) were included. We evaluated leukocyte count and platelet count for the time period preceding, during, and after therapy with linezolid based on specified time periods of exposure for evaluation of specific adverse effects. Sixty-three of 76 (83%) patient admissions were complicated by inhalation injury. The average TBSA involvement was 34.4% (range, 0-98%). The onset of thrombocytopenia before linezolid therapy was noted in 21 of 57 patients (36.8%), which was attributable to fluid resuscitation and acute platelet consumption. After they were exposure to linezolid, 12 patients developed thrombocytopenia. Platelet counts recovered in 7 of these 12 patients with continued exposure to linezolid; however, thrombocytopenia persisted for more than 9 days after therapy in 9 patients, of whom 6 patients succumbed to sepsis. On average, thrombocytes increased by 102,000/mm3 during linezolid treatment. Leucopenia was rare in thermal injury patients, and persisting thrombocytopenia in this population was associated with sepsis and mortality. Continuing linezolid therapy after the onset of thrombocytopenia among survivors almost always resulted in recovery from thrombocytopenia.

Among patients exposed to hydrofluoric acid the potentially lethal effect of calcium depletion induced by binding with fluoride ion has not been well reported. Three patients exposed to hydrofluoric acid had acute fluoride poisoning with serum calcium levels equal to or below 4.1 mgm/dl. Treatment included administration of large amounts of calcium, both intravenously and by subsechar injection, to replenish the biologically active calcium and to bind fluoride. This report describes successful treatment of two survivors, apparently the first two, of severe hypocalcemia caused by hydrofluoric acid.