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ORIGINAL ARTICLE
Year : 2022  |  Volume : 6  |  Issue : 2  |  Page : 103-107

The Bacteriological and Clinical Outcomes of Ventilator-associated Pneumonia Post-cardiac Surgery in the Pediatric Surgical Intensive Care Unit: A Prospective, Observational Study


1 Department of Cardiac Anaesthesiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research, Mysore, Karnataka, India
2 Department of Anaesthesiology, All India Institute of Medical Sciences (AIIMS), Bathinda, Punjab; Department of Cardiac Anaesthesiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bangalore, Karnataka, India
3 Department of Cardiac Anaesthesiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bangalore, Karnataka, India

Date of Submission12-Dec-2021
Date of Decision03-Feb-2022
Date of Acceptance15-Feb-2022
Date of Web Publication09-May-2022

Correspondence Address:
K S Bharathi
Department of Cardiac Anaesthesiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research, K.R.S. Road, Mysore 570016, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/bjoa.bjoa_174_21

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  Abstract 

Background: Ventilator-associated pneumonia (VAP) is a serious nosocomial infection that threatens pediatric patients who have undergone cardiac surgery. The aim of this study is to analyze the bacteriological profile and antibiotic resistance pattern of the organisms grown from pediatric patients diagnosed as VAP after cardiac surgery and also to study the bacteriological and clinical outcomes of the patients. Patients and Methods: This prospective observational study was conducted in a tertiary care teaching institution in children aged younger than 14 years who had undergone cardiac surgery and were diagnosed to have VAP and on mechanical ventilation (MV). The clinical and the bacteriological profile of patients with VAP, the systemic antibiotics used, the resistance pattern to the antibiotics, and, finally, the bacteriological and clinical outcomes were analyzed. Results: Among the 98 patients with VAP, 55% were early onset (<4 days of MV) and 45% were late onset (>4 days of MV) VAP. Among the most common pathogens causing VAP, Klebsiella and Escherichia coli contributed to 18% each of the total VAP. Twenty percent of VAP were polymicrobial in origin. About 63% of organisms were resistant to Augmentin, and 11% of the organisms were multidrug resistant (MDR). Conclusion: This study not only showed the pattern of early and late onset VAP but also revealed the bacteriological profile and the resistance pattern of the local microbial flora causing VAP, guiding us in a more efficient management of VAP in children.

Keywords: Anti-bacterial agents, cardiac surgical procedures, cross-infection, drug resistance, pediatric


How to cite this article:
Bharathi K, Pruthi G, Lathashree S, Simha PP. The Bacteriological and Clinical Outcomes of Ventilator-associated Pneumonia Post-cardiac Surgery in the Pediatric Surgical Intensive Care Unit: A Prospective, Observational Study. Bali J Anaesthesiol 2022;6:103-7

How to cite this URL:
Bharathi K, Pruthi G, Lathashree S, Simha PP. The Bacteriological and Clinical Outcomes of Ventilator-associated Pneumonia Post-cardiac Surgery in the Pediatric Surgical Intensive Care Unit: A Prospective, Observational Study. Bali J Anaesthesiol [serial online] 2022 [cited 2022 May 26];6:103-7. Available from: https://www.bjoaonline.com/text.asp?2022/6/2/103/344880




  Introduction Top


Ventilator-associated pneumonia (VAP) is the most common complication in the intensive care unit (ICU) in patients who are on mechanical ventilation (MV) for more than 48 h. VAP can complicate the recovery of children who undergo corrective cardiac surgery for congenital heart disease (CHD).[1] It also forms an important predictor of clinical outcome and mortality in these children. The attributable mortality because of VAP in the general population is 33% to 50%.[2],[3]

There are inadequate data regarding the bacteriological and clinical outcomes of VAP in the pediatric population in the post-cardiac surgical ICU (SICU). The etiologic agents of VAP vary widely according to the population of patients in an ICU, the duration of hospital stay, and prior antimicrobial therapy. Despite the advancements in antimicrobial regimes, VAP continues to be an important cause of morbidity and mortality. VAP requires prompt diagnosis and initiation of appropriate antibiotic treatment. Inadequate or inappropriate antibiotic treatment may not only lead to the emergence of multidrug-resistant (MDR) pathogens but also has been associated with higher mortality and morbidity in patients with VAP.

In this study, we have prospectively studied the children who developed VAP post-cardiac surgery in the pediatric SICU. We aimed at ascertaining the causative organisms, antibiotic resistance, and the bacteriological and clinical outcomes of children with VAP.


  Patients and Methods Top


This is a prospective, observational, descriptive study. After approval from the Institutional Ethics committee (SJICR/EC/2016/07 dated 26 February 2016), we conducted a prospective observational study in the 10-bed SICU of a tertiary care teaching hospital from February 2016 to December 2017. A total of 524 pediatric patients underwent cardiac surgery during the study period. Among them, 98 children were diagnosed with VAP after a quantitative culture of endotracheal aspirate (EA) in those with clinical suspicion.

We included all the children aged 1 day to 14 years who had undergone cardiac surgery and on MV and were diagnosed as VAP. As per the American Thoracic Society Consensus Conference criteria, VAP was defined as follows: the presence of fever greater than 38°C with no other recognized cause, leukopenia (<4,000 white blood cells (WBC)/mm3) or leukocytosis (>12,000 WBC/mm3), purulent tracheal secretions, and new, persistent infiltrate on chest X-ray in patients who had been on mechanical ventilatory support for at least 48 h [4] along with quantitative cultures of EA showing growth. All patients with clinical and radiological signs suggestive of pneumonia on admission were excluded from the study. Early onset ventilator-associated pneumonia was defined as VAP developing during the first four days (within 96 h) of MV, and late-onset ventilator-associated pneumonia was defined as VAP developing five or more days (96 h) after the initiation of MV.

Endotracheal aspirate (≥1 ml) was collected under aseptic precautions whenever the patient was suspected to have developed VAP 48 h after MV in the SICU. The EA was collected using a 22-inch Ramson’s 12 F suction catheter with a mucus extractor, which was gently introduced through the endotracheal tube. The EA sample collected from each patient was immediately taken to the laboratory for processing. The threshold for quantitative cultures of EA was considered as 105 cfu/ml. The growth of any organism below the threshold was assumed to be due to colonization or contamination. Organisms were identified, and the antimicrobial susceptibility tests of the commonly used antibiotics were determined by the Kirby-Bauer disk diffusion method.[5] MDR pathogens were defined as those resistant to three or more classes of antibiotics.

Data were recorded and analyzed by using SPSS version 20.0 software (IBM Corp. Released 2011. IBM SPSS Statistics for Windows, Version 20.0. Armonk, NY: IBM Corp.). The bacteriological outcomes and the clinical outcomes were expressed as percentages.


  Results Top


The study was conducted from February 2016 to December 2017. Among the total 524 pediatric patients who underwent cardiac surgery during the study period, 98 children developed VAP. The age distribution of the study population is depicted in [Table 1]. About 42.8% of the study population was between the age of one and six months. The mean age of the study population is calculated as 14.74 months. Overall, 57% of the patients were male whereas 41% of them were female. Early onset (<4 days of MV) VAP was found in 55% of the subjects.
Table 1: Demographic data

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The study of the bacterial growth of the endotracheal aspirate revealed that 20% of the VAP were because of mixed growth, that is, polymicrobial. Among the most common pathogens causing VAP, Klebsiella and Escherichia coli contributed to 18% each of the total VAP. Psuedomonas was the infecting organism in 15% of cases, whereas Acinetobacter was the infecting organism in 10% of cases. Citrobacter spp caused VAP in 5%, Enterobacter spp in 4%, and non-flagellating gram negative organisms in the remaining 8%. The bacteriological profile of the study population is shown as a pie diagram [Figure 1].
Figure 1: Types of bacterial growth among patients

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The study of the resistance pattern of the pathogens causing VAP to antibiotics revealed that about 63% of them were resistant to Augmentin, followed by 45% to Cefoperazone-sulbactam combination, 41% to ciprofloxacin, 40% to Piperacillin, 24% of the microbes were resistant to Meropenem, 22% to Amikacin, 18% to Cefotaxime, 17% to Ceftriaxone, and 14% to Trimethoprim. About 11% of the organisms were MDR, that is, resistant to more than three classes of antibiotics. Only 4% of the pathogens were resistant to Colistin. The resistance pattern is depicted as a bar diagram in [Figure 2].
Figure 2: Resistance pattern of antibiotics among patients

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When we analyzed the data of the systemic antibiotic use in patients with VAP [Table 2], the patients who received Colistin alone were 27.5% followed by the patients who received Colistin along with Meropenem who were 14.29%. Colistin-amikacin and Colistin-cefoperazone-sulbactam combinations were used in 9% each among the total patients with VAP. Meropenem was used in 8% and Piperacillin-tazobactam in another 8% of patients with VAP. Five percent of the study group received Tigecycline, whereas another 2% received Tigecycline in combination with Colistin. The bacteriological eradication was seen in 74.49% of patients with VAP, whereas recurrence of the causative organism occurred in 6.12% of patients with VAP. In 19.39% of patients with VAP, there was persistent bacterial growth in spite of the treatment.
Table 2: Systemic antibiotics administered

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The majority of the patients recovered clinically from VAP and were discharged from hospital. The death attributable to VAP was 21.43%, whereas 9% of the study population died because of various reasons other than VAP. The average duration of mechanical ventilation was 14.49 days, compared with five days in the case of a patient who did not develop VAP. The mean duration of ICU stay is prolonged to 18 days and the duration of hospital stay to 21 days, causing an increased economic burden.


  Discussion Top


Out of the 98 VAP cases, 55% were categorized under early onset VAP and 45% under late-onset VAP, which was in concordance with other studies.[6],[7] The rates of polymicrobial infection vary widely. In our study, only 20% of cultures were polymicrobial, which is less compared with other published reports.[8],[9],[10] In this study, the most common microorganisms isolated from VAP cases were Gram-negative bacilli. No Gram-positive infections were recorded, indicating the efficient infection control protocols used in the ICU possibly reducing their growth, which is similar to a Saudi Arabian study.[11]

The most common organisms isolated in this study are Klebsiella and Escherichia coli, both of which contribute 18% each of the total VAP. Pseudomonas was the infecting organism in 15%. This is in contrast to other studies,[12],[13] where the most common causative pathogens were Pseudomonas aeruginosa and Acinetobacter spp, indicating the importance of conducting the surveillance studies to know about the local microbial flora. Acinetobacter also remains one of the core pathogens causing deadly VAP. Chittawatanarat et al.[14] also reported Gram-negative organisms as the major pathogens (94.7%), with the most common organisms being Acinetobacter baumanii, K. pneumoniae, and P. aeruginosa with a significant case fatality rate.

The antibiotic resistance pattern plays a key role in the outcome of the patients. The high rates of microbial resistance reported in the different studies are an important cause of concern to the medical fraternity. In this study, most of the organisms are resistant to the commonly used antibiotics such as Augmentin (63%), Cefaperazone-sulbactam (45%), and Ciprofloxacin (41%). Chittawatanarat et al.[14] reported antibiotic resistance in 49.3% of the Gram-negative bacteria and in 62.5% of the Gram-positive cocci.

Several other studies also demonstrated resistance to multiple antibiotics by the pathogens causing VAP, similar to the results of this study.[15],[16],[17] A meta-analysis reported that in patients who have undergone cardiac surgery, gram-negative bacteria, particularly Pseudomonas aeruginosa, is the major cause of VAP.[18] They also recommended third- or fourth-generation cephalosporins as the preferred antimicrobial regimen (e.g., cefoperazone, ceftazidime, or cefepime).

This study highlights the burden of MDR pathogens in VAP in postoperative pediatric cardiac patients. Knowledge of the susceptibility pattern of the local pathogens will guide us in the de-escalation strategy of antimicrobial treatment depending on the microbiological data.

This study also shows that VAP has caused an increase in the number of days on MV (14.49 days), as against the patients without VAP (five days). Fischer et al.[1] performed a prospective cohort study and attributed the delay of extubation to VAP among neonates and children undergoing repair of congenital heart disease. The same is also proven by other studies,[19],[20] where there is a significant prolongation of duration of MV and ICU stay in patients with VAP.

The duration of ICU stay, as evidenced in our study, is an average 18 days. In his nine-month prospective cohort study conducted in an academic tertiary care center, Elward et al.[21] revealed that patients with VAP had a mean ICU length of stay of 27 days versus six days for uninfected patients. In that same study, the mortality rates with and without VAP were 20% and7%, respectively. This is similar to the mortality attributed to VAP in our study (21.43%). However, Gupta et al.[20] reported a much higher (46.67%) mortality rate.

The study emphasizes the need for timely local surveillance data. This study suggests that most cases of VAP in our setting are caused by MDR Gram-negative bacteria. However, the limitation of this study is that it is a single-center study and hence the results cannot be extrapolated to other institutes, as various factors and bacteriological agents causing VAP may vary from institution to institution.

Conclusion

This study concludes that postoperative pediatric cardiac patients are at a risk of developing VAP. The quantitative culture of EA is a useful test for the early diagnosis of VAP and provides specific knowledge of the causative organisms. MDR Gram-negative bacteria account for a large proportion of the pathogens. The antibiotic susceptibility pattern of these isolates helps the clinicians to choose the appropriate antimicrobial agents for prophylactic as well as therapeutic purposes.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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Joseph NM, Sistla S, Dutta TK, Badhe AD, Parija SC. Ventilator-associated pneumonia in a tertiary care hospital in India: Incidence and risk factors. Eur J Inter Med 2010:21:360-8.  Back to cited text no. 9
    
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Balkhy HH, El-Saed A, Maghraby R, Al-Dorzi HM, Khan R, Rishu AH, et al. Drug-resistant ventilator associated pneumonia in a tertiary care hospital in Saudi Arabia. Ann Thorac Med 2014;9:104-11.  Back to cited text no. 11
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Chittawatanarat K, Jaipakdee W, Chotirosniramit N, Chandacham K, Jirapongcharoenlap T. Microbiology, resistance patterns, and risk factors of mortality in ventilator-associated bacterial pneumonia in a northern Thai tertiary-care university based general surgical intensive care unit. Infect Drug Resist 2014;7:203-10.  Back to cited text no. 14
    
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Hudson CM, Bent ZW, Meagher RJ, Williams KP. Resistance determinants and mobile genetic elements of an Ndm-1-encoding klebsiella pneumoniae strain. PLOS One 2014;9:e99209.  Back to cited text no. 15
    
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