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No influence of burn size on ventilator-associated pneumonia in burn patients with inhalation injury
burns 38 (2012) 1109–1113
Available online at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/burns
No influence of burn size on ventilator-associated pneumonia in burn patients with inhalation injury Shinsuke Tanizaki a,*, Koichiro Suzuki b a b
The Department of Emergency Medicine, Fukui Prefuctural Hospital, 2-8-1, Yotsui, Fukui 910-8526, Japan The Department of Acute Medicine, Kawasaki Medical School Hospital, Okayama, Japan
article info
abstract
Article history:
Objective: Burn size and inhalation injury are important predictors of mortality following
Accepted 6 August 2012
burn. The important factors for predicting ventilator-associated pneumonia (VAP) following burn remain unclear. The aim of our study was to investigate the effect of burn size on VAP
Keywords:
in burn patients with inhalation injury.
Burn
Methods: We retrospectively studied 52 burn patients with inhalation injury requiring
Inhalation injury
mechanical ventilation admitted to the Department of Acute Medicine, Kawasaki Medical
Ventilator-associated pneumonia
School Hospital, Okayama, Japan, between June 2007 and October 2010. Results: The overall mortality for all patients was 15%. Twenty-six patients (50%) developed VAP. Patients with VAP required longer ICU stay and mechanical ventilation than those without VAP. There was no difference in age, gender, mortality, and TBSA between burn patients with inhalation injury with and Without VAP. VAP rate had no difference with increasing TBSA in burn patients with inhalation injury. Conclusions: Our data indicated that burn size had no relationship with the development of VAP in burn patients with inhalation injury. # 2012 Elsevier Ltd and ISBI. All rights reserved.
1.
Introduction
Until recently, burn size and age of the patient had been accepted as predictors of mortality following burn [1,2]. During the past 2 decades, improvements in burn care have contributed to an increase in survival after burn shock from major thermal injury [3]. Despite advances in the respiratory management of burn patients, pulmonary failure remains one of the most important causes of mortality and morbidity following thermal injury [4,5]. Ventilator-associated pneumonia (VAP), defined as pneumonia occurring more than 48 h after endotracheal intubation and initiation of mechanical ventilation, is one of the leading causes of pulmonary failure in burn patients [6]. Several studies that used multivariate analysis identified many factors responsible for VAP, such as trauma and underlying illness * Corresponding author. Tel.: +81 776 54 5151; fax: +81 776 57 2991. E-mail address: [email protected] (S. Tanizaki). 0305-4179/$36.00 # 2012 Elsevier Ltd and ISBI. All rights reserved. http://dx.doi.org/10.1016/j.burns.2012.08.008
severity [7]. However, the important factors for predicting VAP following burn remain unclear. Burn size and inhalation injury are important predictors of mortality following burn [8]. The aim of our study was to investigate the effect of burn size on VAP in burn patients with inhalation injury.
2.
Methods
We retrospectively studied 52 burn patients with inhalation injury requiring mechanical ventilation admitted to the Department of Acute Medicine, Kawasaki Medical School Hospital, Okayama, Japan, between June 2007 and October 2010. Patients who were ventilated for less than 48 h were considered not to have been ventilated for pulmonary reasons and were excluded from further analysis. Patients who died or were discharged within the first 2 days were also excluded.
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burns 38 (2012) 1109–1113
Data collected included age, gender, TBSA (Total burn surface area), length of stay in the intensive care unit (ICU), duration of mechanical ventilation, outcome. TBSA was defined as the sum of the second-degree burn area and the third-degree burn area. Ventilator-associated pneumonia (VAP) rate was defined as number of patients with VAP per 1000 ventilator-days. Survival was defined as patient discharge from the ICU, either to the patient’s home or to another facility.
2.1.
Burn treatment and supportive intensive care
Fluid resuscitation was performed according to the Parkland formula (Ringer’s lactate solution, 4 ml/kg/TBSA). Diuresis (0.5 ml/kg/h) was used as endpoints [9]. Intubation and mechanical ventilation were initiated if there was evidence of respiratory failure and hypoxemia, reduced level of consciousness, necessity of deep sedation and analgesia for burn care, compromised airway, or circumferential burns of the neck or face. Patients were intubated in the field or the emergency department by emergency physician. Mechanical ventilation included pressure cycled ventilation, positive endexpiratory pressure (PEEP) between 5 and 10 cm H2O, and peak inspiratory pressures of less than 35 cm H2O. The VAP bundles were utilized, including elevation of the head of the bed, daily sedation holidays, daily spontaneous breathing trials, and peptic ulcer disease prophylaxis. The head of the bed was elevated as much as possible while on ventilation. Patients received stress ulcer prophylaxis by sucralfate. If patients presented with gastric or duoduenal ulcer, they were treated with H2 blockers. Tracheostomy was performed before post burn day 7, if necessary. Enteral nutrition was commenced within 24–48 h of admission. The nutritional requirement was empirically estimated according to Curreri or Harris-Benedict equations. Excision and graft of the burn wound was generally initiated within the first 5 days. Burn wounds were treated with closed dressings and daily application of polymyxin B sulfate and fradiomycin sulfate.
2.2.
Diagnosis of inhalation injury
Inhalation injury was diagnosed by clinical presentation and multiple fiberoptic bronchoscopy. Clinical symptoms and signs included carbonaceous sputum and facial burns; for burn injury due to exposure in a confined space, the signs were dyspnea, lacrimation, and singed nasal vibrissae. Positive findings, confirmed by fiberoptic bronchoscopy, included carbon particles in the airways below the vocal cords, mucosal erythema, edema, or ulceration [10]. All 52 patients were underwent multiple fiberoptic bronchoscopy for the diagnosis of inhalation injury.
2.3.
Diagnosis and treatment of VAP
Each patient was evaluated for VAP on the basis of the following criteria, (1) clinical suspicion of VAP, defined by a new and persistent infiltrate on chest radiographs, associated with at one least of following: purulent tracheal secretions, body temperature of 38.5 8C or higher and a leukocyte count above 10,000/ml, and (2) positive quantitative cultures of distal
pulmonary secretion samples of bronchoalveolar lavage fluid obtained by fiberoptic bronchoscopy (significant threshold, >104 colony-forming units/ml), or with a protected specimen brush catheter (significant threshold, >103 colony-forming units/ml) [11,12]. Systemic antibiotics were administered empirically whenever clinical signs of infection developed. If infection by Grampositive cocci was suspected, treatment with vancomycin was administered. Burn patients with gram-negative infection received meropenem or ceftazidime. The initial regimen was converted to a narrow-spectrum therapy according to the findings of the microbiological cultures.
2.4.
Statistical analysis
Univariate analysis of variables was performed by using the chi-square test for categorical data and Student’s t-test for continuous data. Values were reported as mean standard deviation (SD). The statistical analysis, including calculations of means and standard deviations, were performed with SPSS 12.0J software (SPSS Japan Inc., Tokyo, Japan).
3.
Results
The overall mortality was 15.2% (Table 1). Twenty-six patients (50%) developed VAP. The overall VAP rate was 22.4 per 1000 ventilator-days. Patients with VAP required longer mechanical ventilation than those without VAP. The mortality had no difference between burn patients with and without VAP (Table 2). Twenty-one patients (80.8%) developed VAP after 5 days. Of 3 patients intubated in the field, one patient developed VAP (Tables 1 and 2). There was no difference in age, gender, TBSA, the number of operations per patient, and timing of first operation between burn patients with inhalation injury with and without VAP (Table 2). VAP rate had no difference with increasing TBSA in burn patients with inhalation injury (Fig. 1). 6 patients with VAP (19%) and 2 without VAP (7.7%) had multiple organ failure ( p = 0.22). Other complications were
Table 1 – Demographic and clinical characteristics of patients. No. of patients Male gender (%) Age (year) TBSA (%) Partial thickness burn area (%) Full thickness burn area (%) No. of patients intubated in the field The number of operations per patient Timing of first operation (days) ICU length of stay (days) Duration of ventilation (days) VAP (%) VAP rate Mortality (%)
52 36 (69.2) 56.1 16.9 44.5 22.9 22.7 16.4 22.1 8.81 3 (5.7) 2.53 1.42 5.43 1.03 24.6 14.5 22.3 13.7 26 (50) 22.4 8 (15.3)
VAP rate, number of patients with ventilator-associated pneumonias per 1000 ventilator-days.
1111
burns 38 (2012) 1109–1113
Table 2 – Comparison of the patients with and without VAP.
Age (year) Male gender (%) TBSA (%) Partial thickness burn area (%) Full thickness burn area (%) No. of patients intubated in the field The number of operations per patient Timing of first operation (days) ICU length of stay (days) Duration of ventilation (days) Mortality (%)
With VAP (n = 26)
Without VAP (n = 26)
p-Value
51.2 16.9 20 (76.9) 40.1 20.0 20.3 8.46 20.5 12.6 1 (3.8) 2.76 1.24 5.23 0.79 31.1 12.4 28.3 11.3 6 (23.1)
61.2 16.1 16 (61.5) 48.9 25.6 25.1 9.46 21.0 16.8 2 (7.6) 2.31 1.48 5.70 1.18 18.1 14.9 16.2 14.1 2 (7.7)
0.13 0.23 0.34 0.21 0.60 0.55 0.41 0.29 <0.05 <0.05 0.12
Fig. 1 – VAP rate had no difference with increasing TBSA in burn patients with inhalation injury. There was no difference with the number of patients who developed VAP and those who not developed VAP for each TBSA% group.
acute renal failure required dialysis, suppurative thrombophlebitis, stress gastritis, and Acalculous Cholangitis (Table 3). Further, we investigated the pathogens associated with VAP. Staphylococcus aureus was the most common Grampositive bacterial pathogen associated with VAP (16 isolates, 61.5%); all the S. aureus isolates were methicillin resistant. Pseudomonas aeruginosa was the most common gram-negative bacterial pathogen associated with VAP (8 isolates, 30.7%).
Table 3 – Complications of patients.
Multiple organ failure Acute renal failure required dialysis Suppurative thrombophlebitis Stress gastritis Acalculous Cholecystitis
With VAP (n = 26)
Without VAP (n = 26)
p-Value
6 5
2 1
0.22 0.08
1
0
0.31
1 0
0 1
0.31 0.31
4.
Discussions
In summary, the overall incidence of VAP in this study was 50%. Our findings indicated that patients with inhalation injury had undergone a significantly longer duration of mechanical ventilation and increased ICU length of stay. TBSA had no relationship to the development of VAP between burn patients with inhalation injury with and without VAP. The overall incidence of VAP among our burn patients with inhalation injury was 50%. Our pneumonia rate is similar to other published reports that pneumonia occurred in 42–60% of the patients with a combined thermal and inhalation injury [13,14]. Until recently, burn size and age of the patients had been accepted as the predictors of mortality following burn [1,2]. In 1994, Smith reported that burn size was the most accurate predictor of the burn mortality (92.8%) followed by age (88.8%) [1]. Large cutaneous thermal injury can cause increased capillary permeability not only at the injured site but also in remote organ system [15]. The local and systemic cytokine are
1112
burns 38 (2012) 1109–1113
increased after large thermal injury [16]. These changes can be impaired lung physiology and predict nosocomial lung infection. We investigated whether burn severity as assessed by TBSA could be risk factor for VAP in burn patients with inhalation injury. Our data indicated that TBSA, which was an important predictor of mortality following burn, had no relationship with the development of VAP in burn patients with inhalation injury. This finding was in conflict with a previous report that the incidence of pneumonia in inhalation injury patients with at least 20% TBSA burn was significantly higher than the patients with less than 20% TBSA burn [17,18]. About half of these burns were partial thickness and that may explain why burn size does not appear to contribute to VAP risk. Improvements in therapies for treating and managing cutaneous thermal injuries may control the development of VAP in burn patients with inhalation injury. These include topical antimicrobials, enteral nutrition, and early surgery. Our data indicated that there was no difference in age between patients who developed VAP and those who not developed VAP. The impact of age on the development of pneumonia was associated with comorbidities [5]. There were no data about comorbidity. The impact of age on the development of pneumonia in our patients was unclear. Our data indicated that the circumstances of intubation had no relationship with the development of VAP in burn patients with inhalation injury. This finding was in conflict with a previous report that intubation at the initial emergency department appeared to be the risk factors of VAP [19]. A small number of patients intubated in the field may be influence that findings. Despite these advances in burn patients, pulmonary failure remains one of the most important causes of mortality and morbidity following thermal injury [4,5]. Our data indicated there was no difference in mortality between burn patients with inhalation injury with and without VAP. Other factors, such as complications or comorbidities, may influence increased mortality for patients with VAP. Inhalation injury impairs the normal mucociliary clearance of the lung and leads to distal atelectasis, which favors microbial infections [20]. Obstructive cast material occludes the lumen of the airway, resulting in hypoventilation or focal loss of ventilation. Inhalation injury impairs surfactant production by type II pneumocytes and restricts the phagocytic activity of macrophages, while granulocytes get stimulated to release various mediators that alter the integrity of the capillary membrane [21]. All these alterations may explain the development of lower respiratory tract infection, and justify the requirement of a longer period of mechanical ventilation in acute respiratory failure in burn patients with inhalation injury [21,22]. Aggressive use of bronchoscopy is effective in clearing the particulate matter from the airways and decreasing the inflammatory response. Carr reported that aggressive use of bronchoscopy after inhalation injury had a trend toward an improvement in mortality [23]. Multiple bronchoscopies may be contributed to the result that there was no difference in VAP rate compared to patients with smaller TBSA. Most VAP episodes in this study were associated with potentially antibiotic-resistant bacteria (e.g., methicillin
resistant S. aureus, P. aeruginosa). These pathogens are associated with higher rates of attributable hospital mortality. Therefore, knowledge of the local microbiology associated with VAP may allow for predicting antibiotic-resistant bacteria involvement [24]. We updated the bacteriological pattern of our ICU by our own surveillance. We chose vancomycin or antipseudomonal agents for initial empiric therapy, because methicillin resistant S. aureus and P. aeruginosa were the 2 most common pathogens causing VAP in our ICU. There were some potential limitations in this study. First, there were no data about comorbidity, initial PaO2/FiO2 value, and tracheostomy. The timing of tracheostomy in burn patients is controversial. In our institution, early tracheostomy was performed before post burn day 7, if necessary. It was, therefore, unclear how these factors influenced the development of VAP in our patients. Second, diagnostic criteria for the severity of inhalation injury were not established, and there were no data to quantify the severity of inhalation injury. It was unclear how the severity of inhalation injury influenced the development of VAP. Lastly, the accurate diagnosis of VAP remains problematic and there is no accepted gold standard for diagnosis yet. The initial diagnosis of VAP is based on clinical suspicion and the presence of new or progressive radiographic infiltrates. Unfortunately, the accuracy of interpretation of chest radiographs has not been extensively evaluated.
5.
Conclusion
TBSA had no relationship to the development of VAP between burn patients with inhalation injury with and without VAP. Burn size may not be the risk of VAP in burn patients with inhalation injury. Improvements in therapies for treating and managing cutaneous thermal injuries may control the development of VAP in burn patients with inhalation injury.
Conflict of interest statement The authors report this study did not receive any financial and personal relationships with other people or organizations that could inappropriately influence our work. There are no potential conflicts of interest.
references
[1] Smith DL, Cairns BA, Ramadan F, Dalston JS, Fakhry SM, Rutledge R, et al. Effect of inhalation injury, burn size, and age on mortality: a study 1447 consecutive burn patients. J Trauma 1994;37:655–9. [2] Anous MM, Heimbach DM. Causes of death and predictors in burned patients more than 60 years of age. J Trauma 1986;26:135–9. [3] Roberts G, Lloyd M, Parker M, Martin R, Philp B, Shelley O, et al. The Baux score is dead. Long live the Baux score: a 27year retrospective cohort study of mortality at a regional burns service. J Trauma 2012;72:251–6.
burns 38 (2012) 1109–1113
[4] D’Avignon LC, Hogan BK, Murray CK, Loo FL, Hospenthal DR, Cancio LC, et al. Contribution of bacterial and viral infections to attributable mortality in patients with severe burns: an autopsy series. Burns 2010;36:773–9. [5] Pham TN, Kramer CB, Klein MB. Risk factors for the development of pneumonia in older adults with burn injury. J Burn Care Res 2010;31:105–10. [6] Kallinen O, Maisniemi K, Bohling T, Tukiainen E, Koljonen V. Multiple organ failure as a cause of death in patients with severe burns. J Burn Care Res 2012;33:206–11. [7] Chastre J, Fagon JY. Ventilator-associated pneumonia. Am J Respir Crit Care Med 2002;165:867–903. [8] McGwin Jr G, George RL, Cross JM, Rue LW. Improving the ability to predict mortality among burn patients. Burns 2008;34:320–7. [9] Baxter CR. Fluid volume and electrolyte changes of the early postburn period. Clin Plast Surg 1974;1:693–703. [10] Barrow RE, Spies M, Barrow LN, Herndon DN. Influence of demographics and inhalation injury on burn mortality in children. Burns 2004;30:72–7. [11] Chastre J, Wolff M, Fagon JY, Chevret S, Thomas F, Wermert D, et al. Comparison of 8 vs 15 days of antibiotic therapy for ventilator-associated pneumonia in adults: a randomized trial. JAMA 2003;290:2588–98. [12] Horan TC, Gaynes RP. Surveillance of nosocomial infections. In: Mayhall CG, editor. Hospital epidemiology and infection control. 3rd ed., Philadelphia: Lippincott Williams & Wilkins; 2004. p. 1659–702. [13] Rue 3rd LW, Cioffi WG, Mason Jr AD, McManus WF, Pruitt Jr BA. The risk of pneumonia in thermally injured patients requiring ventilatory support. J Burn Care Rehabil 1995;16:262–8. [14] Wurtz R, Karajovic M, Dacumos E, Jovanovic B, Hanumadass M. Nosocomial infections in a burn intensive care unit. Burns 1995;21:181–4.
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[15] Ward PA, Till GO. Pathophysiologic events related to thermal injury of skin. J Trauma 1990;30:S75–9. [16] Rodriguez JL, miller CG, Garner WL, Till GO, Guerrero P, Moore NP, et al. Correlation of the local and systemic cytokine response with clinical outcome following thermal injury. J Trauma 1993;34:684–94. [17] Edelman DA, Khan N, Kempf K, White MT. Pneumonia after inhalation injury. J Burn Care Res 2007;28:241–6. [18] Lin CC, Liem AA, Wu CK, Wu YF, Yang JY, Feng CH. Severity score for predicting pneumonia in inhalation injury patients. Burns 2012;38:203–7. [19] Eckert MJ, Wade TE, Davis KA, Luchette FA, Esposito TJ, Poulakidas SJ, et al. Ventilator-associated pneumonia after combined burn and trauma is caused by associated injuries and not the burn wound. J Burn Care Res 2006;27:457–62. [20] Shimazu T, Yukioka T, Ikeuchi H, Mason Jr AD, Wagner PD, Pruitt Jr BA. Ventilation-perfusion alterations after smoke inhalation injury in an ovine model. J Appl Physiol 1996;81:2250–9. [21] Hurst JM, DeHaven CB. Adult respiratory distress syndrome: improved oxygenation during high frequency jet ventilation/continuous positive expiratory pressure. Surgery 1984;96:764–9. [22] Reper P, Wibaux O, Van Laeke P, Vandeenen D, Duinslaeger L, Vanderkelen A. High frequency percussive ventilation and conventional ventilation after smoke inhalation: a randomized study. Burns 2002;28:503–8. [23] Carr JA, Phillips BD, Bowling WM. The utility of bronchoscopy after inhalation injury complicated by pneumonia in burn patients: results from the National Burn Repository. J Burn Care Res 2009;30:967–74. [24] Brusselaers N, Logie D, Vogelaers D, Monstrey S, Blot S. Burns, inhalation injury and ventilator-associated pneumonia: value of routine surveillance cultures. Burns 2012;38:364–70.
Available online at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/burns
No influence of burn size on ventilator-associated pneumonia in burn patients with inhalation injury Shinsuke Tanizaki a,*, Koichiro Suzuki b a b
The Department of Emergency Medicine, Fukui Prefuctural Hospital, 2-8-1, Yotsui, Fukui 910-8526, Japan The Department of Acute Medicine, Kawasaki Medical School Hospital, Okayama, Japan
article info
abstract
Article history:
Objective: Burn size and inhalation injury are important predictors of mortality following
Accepted 6 August 2012
burn. The important factors for predicting ventilator-associated pneumonia (VAP) following burn remain unclear. The aim of our study was to investigate the effect of burn size on VAP
Keywords:
in burn patients with inhalation injury.
Burn
Methods: We retrospectively studied 52 burn patients with inhalation injury requiring
Inhalation injury
mechanical ventilation admitted to the Department of Acute Medicine, Kawasaki Medical
Ventilator-associated pneumonia
School Hospital, Okayama, Japan, between June 2007 and October 2010. Results: The overall mortality for all patients was 15%. Twenty-six patients (50%) developed VAP. Patients with VAP required longer ICU stay and mechanical ventilation than those without VAP. There was no difference in age, gender, mortality, and TBSA between burn patients with inhalation injury with and Without VAP. VAP rate had no difference with increasing TBSA in burn patients with inhalation injury. Conclusions: Our data indicated that burn size had no relationship with the development of VAP in burn patients with inhalation injury. # 2012 Elsevier Ltd and ISBI. All rights reserved.
1.
Introduction
Until recently, burn size and age of the patient had been accepted as predictors of mortality following burn [1,2]. During the past 2 decades, improvements in burn care have contributed to an increase in survival after burn shock from major thermal injury [3]. Despite advances in the respiratory management of burn patients, pulmonary failure remains one of the most important causes of mortality and morbidity following thermal injury [4,5]. Ventilator-associated pneumonia (VAP), defined as pneumonia occurring more than 48 h after endotracheal intubation and initiation of mechanical ventilation, is one of the leading causes of pulmonary failure in burn patients [6]. Several studies that used multivariate analysis identified many factors responsible for VAP, such as trauma and underlying illness * Corresponding author. Tel.: +81 776 54 5151; fax: +81 776 57 2991. E-mail address: [email protected] (S. Tanizaki). 0305-4179/$36.00 # 2012 Elsevier Ltd and ISBI. All rights reserved. http://dx.doi.org/10.1016/j.burns.2012.08.008
severity [7]. However, the important factors for predicting VAP following burn remain unclear. Burn size and inhalation injury are important predictors of mortality following burn [8]. The aim of our study was to investigate the effect of burn size on VAP in burn patients with inhalation injury.
2.
Methods
We retrospectively studied 52 burn patients with inhalation injury requiring mechanical ventilation admitted to the Department of Acute Medicine, Kawasaki Medical School Hospital, Okayama, Japan, between June 2007 and October 2010. Patients who were ventilated for less than 48 h were considered not to have been ventilated for pulmonary reasons and were excluded from further analysis. Patients who died or were discharged within the first 2 days were also excluded.
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burns 38 (2012) 1109–1113
Data collected included age, gender, TBSA (Total burn surface area), length of stay in the intensive care unit (ICU), duration of mechanical ventilation, outcome. TBSA was defined as the sum of the second-degree burn area and the third-degree burn area. Ventilator-associated pneumonia (VAP) rate was defined as number of patients with VAP per 1000 ventilator-days. Survival was defined as patient discharge from the ICU, either to the patient’s home or to another facility.
2.1.
Burn treatment and supportive intensive care
Fluid resuscitation was performed according to the Parkland formula (Ringer’s lactate solution, 4 ml/kg/TBSA). Diuresis (0.5 ml/kg/h) was used as endpoints [9]. Intubation and mechanical ventilation were initiated if there was evidence of respiratory failure and hypoxemia, reduced level of consciousness, necessity of deep sedation and analgesia for burn care, compromised airway, or circumferential burns of the neck or face. Patients were intubated in the field or the emergency department by emergency physician. Mechanical ventilation included pressure cycled ventilation, positive endexpiratory pressure (PEEP) between 5 and 10 cm H2O, and peak inspiratory pressures of less than 35 cm H2O. The VAP bundles were utilized, including elevation of the head of the bed, daily sedation holidays, daily spontaneous breathing trials, and peptic ulcer disease prophylaxis. The head of the bed was elevated as much as possible while on ventilation. Patients received stress ulcer prophylaxis by sucralfate. If patients presented with gastric or duoduenal ulcer, they were treated with H2 blockers. Tracheostomy was performed before post burn day 7, if necessary. Enteral nutrition was commenced within 24–48 h of admission. The nutritional requirement was empirically estimated according to Curreri or Harris-Benedict equations. Excision and graft of the burn wound was generally initiated within the first 5 days. Burn wounds were treated with closed dressings and daily application of polymyxin B sulfate and fradiomycin sulfate.
2.2.
Diagnosis of inhalation injury
Inhalation injury was diagnosed by clinical presentation and multiple fiberoptic bronchoscopy. Clinical symptoms and signs included carbonaceous sputum and facial burns; for burn injury due to exposure in a confined space, the signs were dyspnea, lacrimation, and singed nasal vibrissae. Positive findings, confirmed by fiberoptic bronchoscopy, included carbon particles in the airways below the vocal cords, mucosal erythema, edema, or ulceration [10]. All 52 patients were underwent multiple fiberoptic bronchoscopy for the diagnosis of inhalation injury.
2.3.
Diagnosis and treatment of VAP
Each patient was evaluated for VAP on the basis of the following criteria, (1) clinical suspicion of VAP, defined by a new and persistent infiltrate on chest radiographs, associated with at one least of following: purulent tracheal secretions, body temperature of 38.5 8C or higher and a leukocyte count above 10,000/ml, and (2) positive quantitative cultures of distal
pulmonary secretion samples of bronchoalveolar lavage fluid obtained by fiberoptic bronchoscopy (significant threshold, >104 colony-forming units/ml), or with a protected specimen brush catheter (significant threshold, >103 colony-forming units/ml) [11,12]. Systemic antibiotics were administered empirically whenever clinical signs of infection developed. If infection by Grampositive cocci was suspected, treatment with vancomycin was administered. Burn patients with gram-negative infection received meropenem or ceftazidime. The initial regimen was converted to a narrow-spectrum therapy according to the findings of the microbiological cultures.
2.4.
Statistical analysis
Univariate analysis of variables was performed by using the chi-square test for categorical data and Student’s t-test for continuous data. Values were reported as mean standard deviation (SD). The statistical analysis, including calculations of means and standard deviations, were performed with SPSS 12.0J software (SPSS Japan Inc., Tokyo, Japan).
3.
Results
The overall mortality was 15.2% (Table 1). Twenty-six patients (50%) developed VAP. The overall VAP rate was 22.4 per 1000 ventilator-days. Patients with VAP required longer mechanical ventilation than those without VAP. The mortality had no difference between burn patients with and without VAP (Table 2). Twenty-one patients (80.8%) developed VAP after 5 days. Of 3 patients intubated in the field, one patient developed VAP (Tables 1 and 2). There was no difference in age, gender, TBSA, the number of operations per patient, and timing of first operation between burn patients with inhalation injury with and without VAP (Table 2). VAP rate had no difference with increasing TBSA in burn patients with inhalation injury (Fig. 1). 6 patients with VAP (19%) and 2 without VAP (7.7%) had multiple organ failure ( p = 0.22). Other complications were
Table 1 – Demographic and clinical characteristics of patients. No. of patients Male gender (%) Age (year) TBSA (%) Partial thickness burn area (%) Full thickness burn area (%) No. of patients intubated in the field The number of operations per patient Timing of first operation (days) ICU length of stay (days) Duration of ventilation (days) VAP (%) VAP rate Mortality (%)
52 36 (69.2) 56.1 16.9 44.5 22.9 22.7 16.4 22.1 8.81 3 (5.7) 2.53 1.42 5.43 1.03 24.6 14.5 22.3 13.7 26 (50) 22.4 8 (15.3)
VAP rate, number of patients with ventilator-associated pneumonias per 1000 ventilator-days.
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burns 38 (2012) 1109–1113
Table 2 – Comparison of the patients with and without VAP.
Age (year) Male gender (%) TBSA (%) Partial thickness burn area (%) Full thickness burn area (%) No. of patients intubated in the field The number of operations per patient Timing of first operation (days) ICU length of stay (days) Duration of ventilation (days) Mortality (%)
With VAP (n = 26)
Without VAP (n = 26)
p-Value
51.2 16.9 20 (76.9) 40.1 20.0 20.3 8.46 20.5 12.6 1 (3.8) 2.76 1.24 5.23 0.79 31.1 12.4 28.3 11.3 6 (23.1)
61.2 16.1 16 (61.5) 48.9 25.6 25.1 9.46 21.0 16.8 2 (7.6) 2.31 1.48 5.70 1.18 18.1 14.9 16.2 14.1 2 (7.7)
0.13 0.23 0.34 0.21 0.60 0.55 0.41 0.29 <0.05 <0.05 0.12
Fig. 1 – VAP rate had no difference with increasing TBSA in burn patients with inhalation injury. There was no difference with the number of patients who developed VAP and those who not developed VAP for each TBSA% group.
acute renal failure required dialysis, suppurative thrombophlebitis, stress gastritis, and Acalculous Cholangitis (Table 3). Further, we investigated the pathogens associated with VAP. Staphylococcus aureus was the most common Grampositive bacterial pathogen associated with VAP (16 isolates, 61.5%); all the S. aureus isolates were methicillin resistant. Pseudomonas aeruginosa was the most common gram-negative bacterial pathogen associated with VAP (8 isolates, 30.7%).
Table 3 – Complications of patients.
Multiple organ failure Acute renal failure required dialysis Suppurative thrombophlebitis Stress gastritis Acalculous Cholecystitis
With VAP (n = 26)
Without VAP (n = 26)
p-Value
6 5
2 1
0.22 0.08
1
0
0.31
1 0
0 1
0.31 0.31
4.
Discussions
In summary, the overall incidence of VAP in this study was 50%. Our findings indicated that patients with inhalation injury had undergone a significantly longer duration of mechanical ventilation and increased ICU length of stay. TBSA had no relationship to the development of VAP between burn patients with inhalation injury with and without VAP. The overall incidence of VAP among our burn patients with inhalation injury was 50%. Our pneumonia rate is similar to other published reports that pneumonia occurred in 42–60% of the patients with a combined thermal and inhalation injury [13,14]. Until recently, burn size and age of the patients had been accepted as the predictors of mortality following burn [1,2]. In 1994, Smith reported that burn size was the most accurate predictor of the burn mortality (92.8%) followed by age (88.8%) [1]. Large cutaneous thermal injury can cause increased capillary permeability not only at the injured site but also in remote organ system [15]. The local and systemic cytokine are
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increased after large thermal injury [16]. These changes can be impaired lung physiology and predict nosocomial lung infection. We investigated whether burn severity as assessed by TBSA could be risk factor for VAP in burn patients with inhalation injury. Our data indicated that TBSA, which was an important predictor of mortality following burn, had no relationship with the development of VAP in burn patients with inhalation injury. This finding was in conflict with a previous report that the incidence of pneumonia in inhalation injury patients with at least 20% TBSA burn was significantly higher than the patients with less than 20% TBSA burn [17,18]. About half of these burns were partial thickness and that may explain why burn size does not appear to contribute to VAP risk. Improvements in therapies for treating and managing cutaneous thermal injuries may control the development of VAP in burn patients with inhalation injury. These include topical antimicrobials, enteral nutrition, and early surgery. Our data indicated that there was no difference in age between patients who developed VAP and those who not developed VAP. The impact of age on the development of pneumonia was associated with comorbidities [5]. There were no data about comorbidity. The impact of age on the development of pneumonia in our patients was unclear. Our data indicated that the circumstances of intubation had no relationship with the development of VAP in burn patients with inhalation injury. This finding was in conflict with a previous report that intubation at the initial emergency department appeared to be the risk factors of VAP [19]. A small number of patients intubated in the field may be influence that findings. Despite these advances in burn patients, pulmonary failure remains one of the most important causes of mortality and morbidity following thermal injury [4,5]. Our data indicated there was no difference in mortality between burn patients with inhalation injury with and without VAP. Other factors, such as complications or comorbidities, may influence increased mortality for patients with VAP. Inhalation injury impairs the normal mucociliary clearance of the lung and leads to distal atelectasis, which favors microbial infections [20]. Obstructive cast material occludes the lumen of the airway, resulting in hypoventilation or focal loss of ventilation. Inhalation injury impairs surfactant production by type II pneumocytes and restricts the phagocytic activity of macrophages, while granulocytes get stimulated to release various mediators that alter the integrity of the capillary membrane [21]. All these alterations may explain the development of lower respiratory tract infection, and justify the requirement of a longer period of mechanical ventilation in acute respiratory failure in burn patients with inhalation injury [21,22]. Aggressive use of bronchoscopy is effective in clearing the particulate matter from the airways and decreasing the inflammatory response. Carr reported that aggressive use of bronchoscopy after inhalation injury had a trend toward an improvement in mortality [23]. Multiple bronchoscopies may be contributed to the result that there was no difference in VAP rate compared to patients with smaller TBSA. Most VAP episodes in this study were associated with potentially antibiotic-resistant bacteria (e.g., methicillin
resistant S. aureus, P. aeruginosa). These pathogens are associated with higher rates of attributable hospital mortality. Therefore, knowledge of the local microbiology associated with VAP may allow for predicting antibiotic-resistant bacteria involvement [24]. We updated the bacteriological pattern of our ICU by our own surveillance. We chose vancomycin or antipseudomonal agents for initial empiric therapy, because methicillin resistant S. aureus and P. aeruginosa were the 2 most common pathogens causing VAP in our ICU. There were some potential limitations in this study. First, there were no data about comorbidity, initial PaO2/FiO2 value, and tracheostomy. The timing of tracheostomy in burn patients is controversial. In our institution, early tracheostomy was performed before post burn day 7, if necessary. It was, therefore, unclear how these factors influenced the development of VAP in our patients. Second, diagnostic criteria for the severity of inhalation injury were not established, and there were no data to quantify the severity of inhalation injury. It was unclear how the severity of inhalation injury influenced the development of VAP. Lastly, the accurate diagnosis of VAP remains problematic and there is no accepted gold standard for diagnosis yet. The initial diagnosis of VAP is based on clinical suspicion and the presence of new or progressive radiographic infiltrates. Unfortunately, the accuracy of interpretation of chest radiographs has not been extensively evaluated.
5.
Conclusion
TBSA had no relationship to the development of VAP between burn patients with inhalation injury with and without VAP. Burn size may not be the risk of VAP in burn patients with inhalation injury. Improvements in therapies for treating and managing cutaneous thermal injuries may control the development of VAP in burn patients with inhalation injury.
Conflict of interest statement The authors report this study did not receive any financial and personal relationships with other people or organizations that could inappropriately influence our work. There are no potential conflicts of interest.
references
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