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The purpose of this study is to determine the incidence of sinusitis in mechanically ventilated burn victims and to examine if the presence of inhalational injury increases the likelihood of developing sinusitis. The authors hypothesize that the incidence of sinusitis will be increased in burn victims who have concomitant inhalational injury. A retrospective chart analysis was performed on all patients who were admitted to the Nathan Speare Regional Burn Treatment Center over a 24-month time frame. Patients who were mechanically ventilated for greater than 24 hours were then selected, resulting in a total of 137 patients for analysis. Multiple variables including number of days on mechanical ventilation, presence of confirmed inhalational injury by bronchoscopy, and method of diagnosis were examined. Of 137 patients, a diagnosis of sinusitis was made in 32 patients (23%). In patients with sinusitis, 87.5% had inhalational injury confirmed with bronchoscopy, compared with only 33.3% of patients without sinusitis (P < .01). Rates of nasotracheal/nasogastric intubation, nasoenteric feeding, and length of mechanical ventilation before sinusitis diagnosis were not significantly different. Patients with sinusitis were found to have suffered inhalational injury at a significantly higher rate than those who did not develop sinusitis. This suggests that inhalational injury is a significant risk factor for developing sinusitis.

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.

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.

We present an interesting case of the first adult reported in the United States to suffer from thermal burns, adult respiratory distress syndrome (ARDS) and to be treated with extracorporeal membrane oxygenation (ECMO) who survived. Our patient is a 26 year old male who sustained thermal burns (12% TBSA) to his face and anterior trunk and broncoscopically demonstrable inhalation injury. He was transported to our regional burn center for burn wound care and ventilatory support. The patient was treated with silver sulfadiazine 1% to his wounds which healed per primam. Because of low oxygen saturation he required increasing FIO2. The following parameters: FIO2= 1, PEEP = 17, minute ventilation of 15.1 1, peak airway pressure of 45 and mean of 27, along with chest X-rays corroborated the severity of ARDS. The patient failed volume control ventilation. A trial of pressure ventilation was attempted but the patient only reached O2 saturation in the low 80s. At this point, the decision was made to transfer the patient to a hospital capable of ECMO treatment. The patient was subsequently treated with veno venous ECMO. Six weeks later the patient was discharged from the hospital off all ventilatory support.