Re: Ventilator associated pneumonia
15 June 2012
We believe Dr Hunter’s review ‘Ventilator-associated pneumonia’ [1] to be a classical example of raising the right questions but giving the wrong answers. Three examples justify our statement.
Dr Hunter states the principal risk factor for pneumonia is an endotracheal tube. We would argue the severity of underlying disease is the major determinant of developing pneumonia in patients requiring treatment in the intensive care unit (ICU) [2]. Our statement ‘the sicker the patient, the higher the pneumonia rate’ is supported by the following. Incidence of hospital acquired pneumonia is approximately 5-12 per 1,000 admissions. Pneumonia rate is 7% in patients requiring ICU treatment without endotracheal intubation, and 12% in those requiring it. The pneumonia rate is lower with non-invasive ventilation (1.58 per 1,000 ventilator days), compared with invasive ventilation (5.44 per 1,000 ventilator days). Patients receiving non-invasive ventilation were less ill than those endotracheally intubated. A recent ICU study on prevalence of infection showed the pneumonia rate was related to disease severity.
Dr Hunter states the pathogens associated with pneumonia depend on case mix, underlying co-morbidity, hospital, and type of ICU. Would it not be more instructive to write that critical illness impacts body flora promoting a shift from (i) normal to abnormal flora, and (ii) low to high grade oropharyngeal carriage (i.e., oropharyngeal overgrowth). Five bacterial species are part of ‘normal’ flora as they are carried by healthy individuals: Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis carried in the throat, Escherichia coli carried in the gut, Streptococcus aureus carried in throat and gut. Candida albicans, not a bacterium, is a ‘normal’ potential pathogen present in throat and gut of healthy individuals. There are nine ‘abnormal’ bacteria carried by individuals who suffer underlying diseases; eight aerobic Gram-negative bacilli (AGNB): Kelbsiella, Enterobacter, Proteus, Morganella, Serratia, Acinetobacter and Pseudomonas species. The ninth ‘abnormal’ bacterium is methicillin-resistant Staphylococcus aureus (MRSA). ‘Abnormal’ bacteria are carried in throat and gut. Johanson demonstrated the main factor associated with carriage of AGNB in the oropharynx was illness severity. Chang using nasal surveillance cultures, showed that in patients with cirrhosis severity of liver disease was associated with MRSA carriage. Overgrowth is defined as ≥105 potential pathogens including ‘normal’ bacteria and yeasts and AGNB per mL of saliva or faeces. Overgrowth is a risk factor for developing a clinically important outcome such as infection and resistance [3]. Critical illness related carriage in overgrowth concentration (CIRCO) is common on admission: primary endogenous infections are the most common infections in the ICU (55%). They are caused by both ‘normal’ and ‘abnormal’ potential pathogens and generally occur, during the first week of ICU treatment. CIRCO often develops during ICU treatment. Secondary endogenous infections are invariably caused by the nine ‘abnormal’ bacteria, accounting for one third of ICU-infections. This type of infection generally occurs after one week of ICU-treatment. Gut overgrowth is the issue in endogenous infections but is not involved in exogenous infections, i.e., without previous carriage. Exogenous infections (15%) are invariably caused by ‘abnormal’ bacteria, and may occur any time during ICU-treatment.
Dr Hunter suggests the three main ways of preventing pneumonia are to reduce colonisation of the aerodigestive tract with pathogenic bacteria, prevent aspiration, and limit duration of mechanical ventilation. Only decontamination protocols have been shown to provide a survival benefit [4]. His failure to distinguish selective digestive decontamination (SDD) and selective oropharyngeal decontamination (SOD) from oropharyngeal chlorhexidine rinses may explain the answers [5]. SDD is an antimicrobial prophylaxis against infections of lower airways and bloodstream. SOD and oropharyngeal chlorhexidine rinses are modified SDD manoeuvres to prevent lower airway infections using antimicrobials and antiseptics, respectively. The former employs parenteral and enteral antimicrobial agents. Parenteral cefotaxime is intended to control oropharyngeal overgrowth of ‘normal’ bacteria. Enteral antimicrobials amphotericin or nystatin, polymyxin, and tobramycin are applied into the oropharynx (a sticky gel) and into the gut (a suspension) to control oropharyngeal and gut overgrowth of Candida species and AGNB. The parenteral antibiotic and the gut component of the enteral antimicrobials are omitted in SOD and oropharyngeal chlorhexidine rinsing. Hygiene and regular throat surveillance cultures are mandatory with all three manoeuvres. A rectal surveillance culture is part of the full SDD protocol.
How to explain a review giving the wrong answers to the right questions? Screening of the references reveals a biased search towards US literature; the external peer reviewers did not detect his bias.
References
1. Hunter JD. Ventilator associated pneumonia. BMJ 2012; 344: e3325
2. Zandstra DF, Petros AJ, Silvestri L, van Saene HKF. Critical illness related pneumonia rather than ventilator-associated pneumonia (VAP) Respir Care 2012; 57: 329-331.
3. van Saene HKF, Damjanovic V, Murray AE, de la Cal MA. How to classify infections in intensive care units – the carrier state, a criterion whose time has come? J Hosp Infect 1996; 33: 1-12.
4. Laupland KB, Fisman DN. Selective digestive tract decontamination: a tough pill to swallow. Can J Infect Dis Med Microbiol 2009; 20: 9-11.
5. Silvestri L, Petros AJ, Roos D, Zandstra DF, Taylor N, van Saene HKF. Selective digestive decontamination, selective oropharyngeal decontamination, and oropharyngeal chlorhexidine: three different manoeuvres. Surg Infect 2012; 13: doi: 10.1089/sur.2011.098
Competing interests: None declared
University of Liverpool, Daulby Street, Liverpool, L69 3GA






