Ventilator associated pneumonia
Cite this as: BMJ 2012;344:e3325
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I read with interest the recent Clinical Review of Ventilator Associated Pneumonia (VAP) in the BMJ (1).
In the section on Preventing Aspiration, the author highlighted the importance of using the NICE Care Bundle, which includes nursing patients in an inclined position, and using sub-glottic secretion drainage. He then went on to say: "Recently introduced endotracheal tubes feature an ultrathin polyurethane cuff membrane that has narrower longitudinal folds when inflated, which limits microaspiration. A retrospective study reported a reduction in ventilator associated pneumonia rates from 5.3 per 1000 ventilator days to 2.8 per 1000 ventilator days after introduction of these tubes (P=0.0138), although more robust studies are lacking."
This was the only comment on new tube design. I found this rather extraordinary, particularly as the paper quoted as supporting the use of this ultrathin tube was published in 2003 (2)
A silastic tube specifically designed to prevent reflux and the development of VAP has since been developed. The cuff has no creases at any degree of inflation, and is provided with a Tracheal Seal Monitor, which maintains the intracuff pressure at all times at a preset level, usually 20 mm Hg.
The clinical evidence for this tube is becoming significant:
1. A study at Kings Lynn with this system has shown that the VAP rate can be reduced to very low levels (3). In 53 patients there were no episodes of VAP while the tube was in situ. One patient was extubated, and subsequently reintubated with a standard ETT, and went on to develop VAP. This patient is included in the final data set, but the actual VAP rate while the tubes were in situ was zero.
2. Sequential studies in Hull have shown that the VAP rate can be reduced from 30.8% to 6.25% in a general ICU. Prospectively collected data after withdrawal of the silastic tube show that the VAP rate returned to 26% (4,5).
3. A prospective randomised study by Nseir and colleagues in Lille has been the first to show the benefits of continuous cuff pressure monitoring, with significantly decreased microaspiration of gastric contents, measured by the presence of pepsin in tracheal aspirate. The probability of remaining free of VAP over the duration of mechanical ventilation was significantly higher in the intervention group compared to the control group (log-rank test, p = 0.016) (6)
I wrote to the author of your clinical review immediately but have received no reply. I am therefore writing to you, because I do not think that your clinical review stated the current situation accurately.
1. Hunter JO. Clinical Review - Ventilator associated pneumonia. BMJ 2012;344:e3325
2. Dullenkopf A, Gerber A, Weiss M. Fluid leakage past tracheal tube cuffs: evaluation of the new Microcuff endotracheal tube. Intensive Care Med 2003;29:1849-53.
3. Doyle A, Fletcher A, Carter J, Blunt M and Young P. The incidence of ventilator-associated pneumonia using the PneuX System with or without elective endotracheal tube exchange: A pilot study BMC Research Notes 2011, 4:92
4. N.D. Smith, F. Khan, A. Gratrix The Pneux™ Pneumonia Prevention System and the Incidence of Ventilator Associated Pneumonia. Poster 1081, European Society For Intensive Care Medicine, Berlin 2011
5. F.A. Khan, A. Gratrix, P. Gunasekaran, N. Smith. Incidence of ventilator associated pneumonia in a mixed general and neuro Intensive Care Unit in the United Kingdom based on clinical pulmonary infection score (CPIS) Poster 1082, European Society For Intensive Care Medicine, Berlin 2011
6. Nseir S, Zerimech F, Fournier C, Lubret R, Ramon P, Durocher A, Balduyck M. Continuous control of tracheal cuff pressure and microaspiration of gastric contents in critically ill patients Am. J. Respir. Crit. Care Med., on line August 11th 2011
Competing interests: Clinical Advisor to Intavent Direct
Clinical Advisor to Intavent Direct, Bryn-y-Llidiart, Llanrhaeadr-ym-Mochnant, SY10 0BP
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We believe Dr Hunter’s review ‘Ventilator-associated pneumonia’  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) . 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 . 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 . His failure to distinguish selective digestive decontamination (SDD) and selective oropharyngeal decontamination (SOD) from oropharyngeal chlorhexidine rinses may explain the answers . 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.
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
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As the latest edition of the BMJ dropped through my letterbox this week, I carried out the usual cursory scan of the article titles in the top right hand corner. As an advanced Intensive Care Medicine trainee I was immediately interested by the title "Managing ventilator assisted pneumonia". Was this some new therapy or condition I had managed to miss while scouring the critical care literature? Had someone now proven that ventilators could in fact help with pneumonia? Was barotruma, volutrauma and ARDS now a thing of the past with the development of some new mode of ventilation? I quickly flicked to the page in question to discover that there had actually been a typo on the cover and "ventilator associated pneumonia" was the topic of the CME review. Safe in the knowledge that I was not so far behind the times I settled down to read the review which was both thorough and interesting.
Competing interests: None declared
The Western General Hospital, Crewe Road, Edinburgh
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The attributable harm of VAP is a very open question. One longditudinal study of over 4000 patients puts it at 1% (AJRCCM 2011; 184: 1133).
Competing interests: None declared
North Bristol NHS Trust, Frenchay Hospital, Bristol
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