Pa Patient Saf Advis 2012 Sep;9(3):99-105.
The Breadth of Hospital-Acquired Pneumonia: Nonventilated versus Ventilated Patients in Pennsylvania
Critical Care; Infectious Diseases; Nursing; Pulmonary Medicine
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Authors
James Davis, BSN, RN, CCRN, CIC
Senior Infection Prevention Analyst

Edward Finley, BS
Data Analyst
Pennsylvania Patient Safety Authority

Abstract

Considering the evolution of measures designed to prevent nosocomial pneumonia, it makes clinical and financial sense to focus efforts on patients who require mechanical ventilation. Patients at risk for ventilator-associated pneumonia (VAP) are easily identified because they require an endotracheal tube or tracheostomy, require life support, and are commonly admitted to specific areas of the hospital. However, Pennsylvania data reveals that mortality rates for patients with nonventilator-hospital-acquired pneumonia (NV-HAP) are comparable to mortality rates for patients with VAP. Using Pennsylvania data, Pennsylvania Patient Safety Authority analysts have also determined that NV-HAP affects more people than VAP and is as lethal as and more costly than VAP. Furthermore, NV-HAP is a safety issue that is on the rise in patients in the conventional ward, and it is likely to be underreported. Data suggests that if VAP prevention is a focus at a facility, perhaps NV-HAP prevention should also share the spotlight.

Introduction

Hospital-acquired pneumonia (HAP), according to the Centers for Disease Control and Prevention (CDC), “has accounted for approximately 15% of all hospital-associated infections.”1 HAP taxonomy separates event cases into those patients requiring mechanical ventilation and those who do not require ventilator support. A patient receiving mechanical ventilation who is confirmed to have nosocomial pneumonia while on the ventilator is classified as having ventilator-associated pneumonia (VAP). For the purpose of this article, a patient who develops nosocomial pneumonia and is not ventilated is classified as having nonventilator-HAP (NV-HAP). The most recent CDC guideline for preventing HAP identifies that “the primary risk factor for the development of hospital-associated bacterial pneumonia is mechanical ventilation.”1 The CDC guideline stated that some reports showed that “patients receiving continuous mechanical ventilation had 6-21 times the risk of developing hospital-associated pneumonia compared with patients who were not receiving mechanical ventilation.”1 Furthermore, CDC identified that “because of this tremendous risk, in the last two decades, most of the research on hospital-associated pneumonia has been focused on VAP.”1 Literature highlighting incidence and outcome data with regard to NV-HAP is sparse. Esperatti et al. hypothesized that this lack of data “may be caused in part by the dispersion of cases within hospital wards, hindering surveillance.”2

Background

Considering the evolution of measures designed to prevent nosocomial pneumonia, it makes clinical and financial sense to focus efforts on patients who require mechanical ventilation. Patients at risk for VAP are easily identified because they require an endotracheal tube or tracheostomy, require life support, and are commonly admitted to specific areas of the hospital. The intensive care unit (ICU) is one such care area where resources, such as specially trained staff, ventilators, and interventions, could be matched to patient needs.

The CDC provides a surveillance definition for VAP and modules in the National Healthcare Safety Network (NHSN) that enable VAP infection tracking. Standardized surveillance case definitions and a searchable national database provide information for calculating the projected costs of VAP. Therefore, VAP is an identifiable, trackable, fiscally measurable target with evidence-based preventive care bundles that can be applied with focused resources. The Institute for Healthcare Improvement states that “many hospitals have achieved significant reductions in VAP rates in their critical care units, some even reaching zero by taking a comprehensive and multidisciplinary approach to ventilator care.”3 Pennsylvania hospitals have shown impressive VAP rate reductions with the adoption of the adult VAP bundle and innovation by way of developing evidence-based practices in the form of neonatal and pediatric VAP prevention bundles.4 Literature suggests that VAP bundles positively impact VAP infection rates; however, VAP is not the only piece in the nosocomial pneumonia puzzle.

Methods

Pennsylvania state law requires that all healthcare-associated infections are reported through NHSN. Pennsylvania Patient Safety Authority analysts queried NHSN for complete nosocomial pneumonia data sets from calendar years 2009 through 2011, inclusive of the total inpatient population for Pennsylvania acute care facilities. Analysts also extracted data for nosocomial pneumonia that contributed to death during that same time period. Of those cases in which nosocomial pneumonia contributed to death, ventilator status was also extracted. Time series data was aggregated into yearly subtotals and a final total for analysis.

Results

Table 1 shows the number of NV-HAP and VAP cases for 2009, 2010, and 2011 from NHSN, with the total for all three years. Also included in the table is the yearly and combined totals for deaths related to either VAP or NV-HAP. Table 1 also depicts the percentage of patients for which NV-HAP or VAP contributed to their deaths. Comparing the data year to year, considering the confidence intervals, there were no statistically significant differences between the two groups. The mortality rates for patients with NV-HAP and VAP were comparable.

Table 1. Pennsylvania Nosocomial Pneumonia and Related Deaths ​ ​ ​ ​ ​ ​


Year
No. of 
NV-HAP Cases
No. of NV-HAP Deaths % of NV-HAP Cases
Contributing to Death
No.
of VAP Cases
No.
of VAP Deaths
% of VAP Cases
Contributing to Death
20091,97636318.4 (95% CI: 16.5 to 20.3)92216317.7 (95% CI: 15.0 to 20.5)
20101,84836619.8 (95% CI: 17.8 to 21.8)73714419.5 (95% CI: 16.3 to 22.7)
20111,77331517.8 (95% CI: 15.8 to 19.7)64012719.8 (95% CI: 16.4 to 23.3)
Total 5,597 1,044 18.7 (95% CI: 17.5 to 19.8) 2,299 434 18.9 (95% CI: 17.1 to 20.7)
Note: NV-HAP refers to nonventilator-hospital-acquired pneumonia and VAP refers to ventilator-associated pneumonia. ​ ​ ​ ​ ​ ​

 
NV-HAP has the potential to be more costly than VAP. Table 2 depicts a comparison of the estimated costs for VAP and NV-HAP cases5 over three years in Pennsylvania.

Table 2. Estimated Costs of NV-HAP and VAP Cases  ​ ​

Year
No. of 
NV-HAP Cases
Cost for 
NV-HAP Cases
No. of 
VAP Cases
Cost for VAP
Cases
20091,976$55,343,808922$34,521,524
20101,848$51,758,784737$27,594,754
20111,773$49,658,184640$23,962,880
Total 5,597 $156,760,776 2,299 $86,079,158
Note: NV-HAP refers to nonventilator-hospital-acquired pneumonia and VAP refers to ventilator-associated pneumonia. The estimated average cost per NV-HAP case is $28,008. The estimated average cost per VAP case is $37,442. Average costs derived from the following study: Kalsekar I, Amsden J, Kothari S, et al. Economic and utilization burden of hospital-acquired pneumonia (HAP): a systematic review and meta-analysis. Chest 2010 Oct;138(4_MeetingAbstracts):739A. ​ ​ ​ ​

 

Discussion

As previously noted,1 the majority of knowledge related to HAP has focused on VAP. VAP is an important subset of HAP; however, if the hypothesis noted by Esperatti et al. is valid, the true incidence of NV-HAP may be underestimated. In a multicenter study of NV-HAP in patients cared for outside of the ICU, Sopena and Sabrià realized that the number of patients with nosocomial pneumonia is increasing in the conventional hospital ward.6 Werarak et al. noted in their study that the differences in outcomes related to NV-HAP and VAP are not significant; however, NV-HAP patients did experience hypoxic episodes more often than patients with VAP.7 Their apparent observation is important given the potential damage repeated hypoxic episodes may have on a patient’s well-being. Because NV-HAP is on the rise in patients cared for in the conventional ward and tends to be underreported, NV-HAP may become more costly if prevention efforts continue to focus largely on VAP.

Etiology of HAP

Major factors that increase the patient’s risk for pneumonia include aspiration, stroke (because of impaired swallowing function or diminished gag reflex), older age, altered level of consciousness (for example, due to medications, substance abuse, or seizure), gastroesophageal reflux disease, and poor oral hygiene.8 For infection to occur, several conditions need to occur in succession. These conditions are referred to as the chain of infection.9 Those conditions needed to complete the chain of infection include the following:

  1. Pathogen in sufficient numbers (dose)
  2. Pathogen of sufficient virulence
  3. Susceptible host
  4. Mode of transmission or transfer of the pathogen from source (reservoir) to host
  5. Portal of entry into the host

Major risk factors for pneumonia understandably allude to the oronasopharynx, oral cavity, and maintenance of functional, chemical, and mechanical safeguards against pathogen invasion. Part of the pathogenesis of HAP involves the oral cavity as a source and reservoir for bacteria that may then cause systemic disease. Li et al. noted that “the teeth are the only nonshedding surfaces in the body, and bacterial levels can reach more than 1011 microorganisms per mg of dental plaque.”10 The presence of subgingival biofilm serves as a continual and enormous bacterial load.10

Pathogenic organisms in the oropharynx may be endogenous or exogenous. Endogenous pathogens may be present secondary to the patient’s dental state, underlying comorbidities, or overgrowth from recent antibiotic use. Exogenous pathogens may be present from the patient’s native environment, the hospital environment, or medical devices (such as suction catheters and endotracheal tubes [ETTs]) and due to inadequate hand hygiene, cross-contamination, or translocation. Poor oral hygiene increases plaque load, which increases the level of enzymes in saliva.10 Furthermore, an increased presence of oral proteolytic enzymes may change the lining of the mouth, increasing attachment and colonization by exogenous or endogenous pathogenic bacteria.11

For a host to be susceptible, immunity needs to be adversely affected. Interrupting the first line of human defense to bacterial invasion may result in significant insult that could easily lead to HAP. Mechanical defenses include an intact, moist, and healthy oral lining and mucosa. Healthy, intact oral epithelial cells not only provide a physical barrier against infection but are capable of mediating a chemical response to the invasion of pathogenic bacteria.12 Functional cilia in the nares and healthy mucosa help limit intrusion of inhaled potential pathogens from entering the airway. The presence of an intact cough and gag reflex also protects the patient from aspiration of oral contents into the lungs. Given the list of major risk factors for HAP, one can easily realize how the innate immune system may be compromised in an at-risk patient. Therefore, patients at risk for HAP are susceptible hosts.

The mode of transmission has been partially explained during the discussion of oral colonization of potential pathogens and biofilm as a constant reservoir. The bacteria are transferred from the oral cavity into the lungs because of lapses in basic host defenses. In VAP cases, the internal and external lumens of the ETT or tracheostomy tube may become covered in biofilm contributing to bacterial transfer as well as aspiration of subglottic secretions containing bacteria derived from oral plaque biofilm. The portal of entry into the host is the oral cavity, the aerodigestive tract, and the ETT or tracheostomy tube, if present, thereby completing the chain to HAP.

Oral Hygiene

During a systematic literature review, Scannapieco et al. noted a 40% decrease in HAP with combined interventions that included mechanical or topical chemical disinfection (or both) or topical oral antibiotic use.13 Paju and Scannapieco state that “institutionalized but non-ventilated patients . . . appear to benefit from improved oral care by showing lower levels of oral bacteria and fewer pneumonia episodes and febrile days.”14 A statistically significant difference (p = 0.044) in oral hygiene index (OHI) scores among individuals with respiratory disease and those with no disease has been noted by Scannapieco et al.15 Furthermore, individuals with median OHI scores are 1.3 times as likely to have respiratory disease, and those with maximum OHI scores are 4.5 times as likely to have respiratory disease.15

The Dental Professional

Healthcare settings depend on teamwork to drive positive patient outcomes; a multidisciplinary approach for planning care is essential for delivering effective complex care. A multidisciplinary approach is also essential for preventing complications associated with exposure to the healthcare setting, such as HAP. Adachi et al. correlated weekly dental cleaning by a hygienist with less fever and fatal pneumonia.16 In a similar study, Abe et al. noted a reduction in influenza infection related to weekly professional dental cleaning.17

Just as a cardiologist is consulted to care for a patient with an underlying heart condition even though a cardiac condition may not be the primary reason for admission, a cardiologist’s expertise is utilized to plan treatment and preventive care. The same line of reasoning holds true for those who practice medical and surgical dentistry and for the registered dental hygienist. The dental professional may be a missing link in the chain of HAP prevention.

NV-HAP Prevention Strategies

Plotting a Course

VAP was discussed as a logical place to start the battle against HAP; however, NV-HAP requires a different approach. The population of patients who may develop NV-HAP could prove to be quite large—are there focal points for implementing preventive measures? To assist the clinician in focusing efforts on care areas, Authority analysts looked to the data. Table 3 provides a view of NV-HAP by NHSN location type for Pennsylvania, by pooled mean and percentiles. This table is presented in a format similar to an NHSN report. The Authority analysts chose to use patient-days as the unit-specific denominator for the development of this analysis. The Authority’s choice of denominator was limited by the constraints of available data. Analysis by patient-days may underestimate the true rate of NV-HAP since this metric potentially lowers rates in regard to extensions of length of stay related to NV-HAP. Authority analysts did not have access to unit-level specific admissions by location type for this analysis, hence the use of patient-days by location type. Rates in Table 3 are reflected as per 1,000 patient-days.

Table 3. Distribution of NV-HAP Cases (based on aggregate data for Pennsylvania for 2009, 2010, and 2011) ​ ​ ​ ​ ​ ​ ​ ​ ​
Unit Type* No. of
Locations
No. of NV-HAP Cases Patient-Days Pooled Mean†,‡ Percentile‡,§ ​ ​ ​ ​


    
10%

25%
(Median)
50%

75%

90%
Critical Care         
Neurologic31140,5120.272  0.247  
Cardiothoracic33216930,9910.2320.0620.1330.2100.3630.484
Surgery16154670,5090.2300.0400.1210.2100.3300.459
Trauma11107515,2520.2080.1530.1830.2070.2860.319
Medical/surgical1378484,480,6560.1890.0000.0510.1230.2490.449
Neurosurgical885454,8380.187  0.139  
Cardiac29131927,2860.1410.0000.0380.1090.1950.330
Medical311901,364,3970.1390.0160.0560.0990.2460.347
Burn4782,4430.085  0.082  
Respiratory2465,6370.061  0.080  
Cardiothoracic pediatric38180,9150.044  0.000  
Nursery24251,049,2290.0240.0000.0000.0000.0220.071
Medical/surgical pediatric67343,1640.020  0.004  
Ward         
Genitourinary312124,9720.096  0.110  
Neurologic939410,2190.095  0.078  
Pulmonary432359,7030.089  0.071  
Neurosurgical827354,4100.076  0.075  
Surgical483124,209,2990.0740.0000.0370.0690.1130.168
Vascular surgery2570,2310.071  0.060  
Medical/surgical152167323,904,0850.0700.0000.0180.0520.0960.158
Medical585078,064,4120.0630.0000.0190.0350.0700.116
Orthopedic501332,145,5120.0620.0000.0000.0440.0930.186
Gynecology83157,1760.019  0.000  
Gerontology22118,3330.017  0.023  
Behavioral110908,258,6520.0110.0000.0000.0000.0150.075
Medical pediatric45472,1000.011  0.002  
Orthopedic pediatric3195,9760.010  0.000  
Nursery79101,362,6090.0070.0000.0000.0000.0000.000
Behavioral health pediatric122302,4010.0070.0000.0000.0000.0000.007
Postpartum63121,944,6650.0060.0000.0000.0000.0000.026
Rehabilitation pediatric51176,5510.006  0.069  
Medical/surgical pediatric445959,5430.0050.0000.0000.0000.0000.000
Behavioral health adolescent112417,4120.0050.0000.0000.0000.0000.014
Labor & delivery/postpartum434837,2940.0050.0000.0000.0000.0000.000
Labor & delivery221426,1760.0020.0000.0000.0000.0000.000
Rehabilitation821635,649,4930.0290.0000.0000.0200.0620.128
Specialty Care Area
Bone marrow transplant533291,8570.113  0.133  
Hematology/oncology161721,905,1410.0900.0000.0250.0630.1100.192
Solid organ transplant1224,6450.081  0.081  
Hematology/oncology pediatric413297,8270.044  0.024  
Solid organ transplant pediatric1183,5590.012  0.012  
Step-Down Unit
Adult733795,332,9980.0710.0000.0100.0460.1020.156
Nursery2312484,8250.0250.0000.0000.0000.0440.114
Pediatric42190,2710.011  0.010  
Long-Term Acute Care
 281172,688,8120.0440.0000.0000.0200.0730.122

Note: NV-HAP refers to nonventilator-hospital-acquired pneumonia. Locations that are not represented reported no events.
*Units are based on National Healthcare Safety Network classifications.
† Pooled mean = total infections ÷ total patient-days x 1000
‡ Per 1000 patient-days
§ For locations that have less than 10 units, reporting percentile distributions have not been calculated.

 

Targeted Intervention

After a patient population or unit is identified at the facility level, proven interventions and lessons derived from VAP prevention activities can be applied to the NV-HAP patient. Selected interventions from the literature that may be applicable to the NV-HAP population are reflected in the Figure.

Figure. Selected Interventions to Prevent Nonventilator-Hospital-Acquired Pneumonia

Figure. Selected Interventions to Prevent Nonventilator-Hospital-Acquired Pneumonia

Conclusion

The chain of infection that perpetuates HAP can be broken with appropriate interventions. In the case of VAP, the majority of interventions are aimed at reducing the risk for aspiration, decolonizing the oral cavity, maintaining the aerodigestive tract, and protecting the mouth. Furthermore, if oral hygiene is compromised, the oral cavity and nasopharyngeal tract will serve as a constant reservoir of pathogens.

Currently, NV-HAP bundles are lacking in the peer-reviewed literature. Focusing care on reservoirs and the portal of entry may be the most realistic approach for preventing NV-HAP at this time. Improving oral hygiene and collaborating with a dental professional may prove essential in preventing NV-HAP (and VAP). NV-HAP in Pennsylvania may potentially have a greater impact than VAP. If VAP prevention is a focus at a facility, perhaps the prevention of NV-HAP—which has the potential to affect more patients, be more costly, and be as lethal as VAP—deserves to share the spotlight.

Notes

  1. Tablan OC, Anderson LJ, Besser R, et al. Guidelines for preventing health-care-associated pneumonia, 2003. Recommendations of CDC and the Healthcare Infection Control Practices Advisory Committee [online]. 2003 [cited 2012 Mar 30]. http://www.cdc.gov/hicpac/pdf/guidelines/HApneu2003guidelines.pdf.
  2. Esperatti M, Ferrer M, Theessen A, et al. Nosocomial pneumonia in the intensive care unit acquired by mechanically ventilated versus nonventilated patients. Am J Respir Crit Care Med 2010 Dec;182(12):1533-9.
  3. Institute for Healthcare Improvement (IHI). Prevent ventilator-associated pneumonia [website]. [cited 2012 Mar 30]. Cambridge (MA): IHI. http://www.ihi.org/explore/VAP/Pages/default.aspx.
  4. Successful reduction of ventilator-associated pneumonia. Pa Patient Saf Advis [online] 2009 Jun [cited 2012 Mar 30]. http://patientsafetyauthority.org/ADVISORIES/AdvisoryLibrary/2009/Jun6(2)/Pages/63.aspx.
  5. Kalsekar I, Amsden J, Kothari S, et al. Economic and utilization burden of hospital-acquired pneumonia (HAP): a systematic review and meta-analysis. Chest 2010 Oct;138(4_MeetingAbstracts):739A.
  6. Sopena N, Sabrià M. Neunos 2000 Study Group. Multicenter study of hospital-acquired pneumonia in non-ICU patients. Chest 2005 Jan;127(1):213-9.
  7. Werarak P, Kiratisin P, Thamlikitkul V. Hospital-acquired pneumonia and ventilator-associated pneumonia in adults at Siriraj Hospital: etiology, clinical outcomes, and impact of antimicrobial resistance. J Med Assoc Thai 2010 Jan;93 Suppl 1:S126-38.
  8. Shigemitsu H, Afshar K. Aspiration pneumonias: under-diagnosed and under-treated. Curr Opin Pulm Med 2007;13(3):192-8. Also available at http://www.medscape.com/viewarticle/556082_print.
  9. Sehulster LM, Chinn RYW, Arduino MJ, et al. Guidelines for environmental infection control in health-care facilities. Recommendations of CDC and the Healthcare Infection Control Practices Advisory Committee (HICPAC) [online]. 2003 [cited 2012 April 4]. http://www.cdc.gov/hicpac/pdf/guidelines/eic_in_HCF_03.pdf.
  10. Li X, Kolltveit KM, Tronstad L, et al. Systemic diseases caused by oral infection. Clin Microbiol Rev 2000 Oct;13(4):547-58. Also available at http://cmr.asm.org/content/13/4/547.full.
  11. Childs WC 3rd, Gibbions RJ. Selective modulation of bacterial attachment to oral epithelial cells by enzyme activities associated with poor oral hygiene. J Periodontal Res 1990 May;25(3):172-8.
  12. Sugawara S, Uehara A, Tamai R, et al. Innate immune responses in oral mucosa. J Endotoxin Res 2002 Dec;8(6):465-8.
  13. Scannapieco FA, Bush RB, Paju S. Associations between periodontal disease and risk for nosocomial bacterial pneumonia and chronic obstructive pulmonary disease. A systematic review. Ann Periodontol 2003 Dec;8(1):54-69.
  14. Paju S, Scannapieco FA. Oral biofilms, periodontitis, and pulmonary infections. Oral Dis 2007 Nov;13(6):508-12.
  15. Scannapieco FA, Papandonatos GD, Dunford RG. Associations between oral conditions and respiratory disease in a national sample survey population. Ann Periodontol 1998 Jul;3(1):251-6.
  16. Adachi M, Ishihara K, Abe S, et al. Effect of professional oral health care on the elderly living in nursing homes. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002 Aug;94(2):191-5.
  17. Abe S, Ishihara K, Adachi M, et al. Professional oral care reduces influenza infection in elderly. Arch Gerontol Geriatr 2006 Sep-Oct;43(2):157-64.
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