Ventilator-associated pneumonia

Ventilator-associated pneumonia
Classification and external resources
ICD-10 J95.851
ICD-9-CM 997.31

Ventilator-associated pneumonia (VAP) is a type of lung infection that occurs in people who are on breathing machines in hospitals. As such, VAP typically affects critically ill persons that are in an intensive care unit (ICU).[1] VAP is a major source of increased illness and death. Persons with VAP have increased lengths of ICU hospitalization and have up to a 20-30% death rate.[2] The diagnosis of VAP varies among hospitals and providers but usually requires a new infiltrate on chest x-ray plus two or more other factors. These factors include temperature of >38 °C or <36 °C, a white blood cell count of >12 × 109/ml, purulent secretions from the airways in the lung, and/or reduction in gas exchange.[1][3]

Signs and symptoms

People who are on mechanical ventilation are often sedated and are rarely able to communicate. As such, many of the typical symptoms of pneumonia will either be absent or unable to be obtained. The most important signs are fever or low body temperature, new purulent sputum, and hypoxemia (decreasing amounts of oxygen in the blood).

Cause

Risk factors

Risk factors for VAP include underlying heart or lung disease, neurologic disease, and trauma, as well as modifiable risk factors such as whether the head of the bed is flat (increased risk) or raised, whether the patient had an aspiration event before intubation, and prior antibiotic exposure.[2] Patients who are in the ICU for head trauma or other severe neurologic illness, as well as patients who are in the ICU for blunt or penetrating trauma, are at especially high risk of developing VAP.[1] Further, patients hospitalized for blunt trauma are at a higher risk of developing VAP compared to patients with penetrating trauma.[1]

Microbiology

The microbiologic flora responsible for VAP is different from that of the more common community-acquired pneumonia (CAP). In particular, viruses and fungi are uncommon causes in people who do not have underlying immune deficiencies. Though any microorganism that causes CAP can cause VAP, there are several bacteria which are particularly important causes of VAP because of their resistance to commonly used antibiotics. These bacteria are referred to as multidrug resistant (MDR).

The development of molecular diagnostic techniques is changing the understanding of the microbiology of VAP, with an increasing appreciation of the role of hard to culture bacteria and the change in the lung microbiome.[4] A recent finding has highlighted the presence of Mycoplasma in the lavage of patients with VAP, a finding which was largely absent from ventilated patients without VAP and healthy controls.[5] Interestingly the Mycoplasma species most commonly identified, Mycoplasma salivarium, was able to impair the antibacterial functions of monocytes and macrophages.[5]

Pathophysiology

It is thought by many, that VAP primarily occurs because the endotracheal or tracheostomy tube allows free passage of bacteria into the lower segments of the lung in a person who often has underlying lung or immune problems. Bacteria travel in small droplets both through the endotracheal tube and around the cuff. Often, bacteria colonize the endotracheal or tracheostomy tube and are embolized into the lungs with each breath. Bacteria may also be brought down into the lungs with procedures such as deep suctioning or bronchoscopy. Another possibility is that the bacteria already exist in the mucus lining the bronchial tree, and are just kept in check by the body's first line of defenses. Ciliary action of the cells lining the trachea drive the mucus superiorly, leading to a build-up of fluids around the inflated cuff where there is little to no airway clearance. The bacteria can then colonize easily without disturbance and then rise in numbers enough to become infective. The droplets that are driven into the airstream and into the lung fields are lofted by way of Bernoulli's principle. There is also a condition called oxidative damage that occurs when concentrations of pure oxygen come into prolonged contact with cells and this damages the cilia of the cells, thus inhibiting their action as part of the body's first line of defense.

Whether bacteria also travel from the sinuses or the stomach into the lungs is, as of 2005, controversial. However, spread to the lungs from the blood stream or the gut is uncommon.

Once inside the lungs, bacteria then take advantage of any deficiencies in the immune system (such as due to malnutrition or chemotherapy) and multiply. Patients with VAP demonstrate impaired function of key immune cells, including the neutrophil, both in the blood and in the alveolar space,[6] with this impairment being driven by pro-inflammatory molecules such as C5a.[7] These defects in immune function appear to be casually linked to the development of VAP, as they are seen before clinical infection develops.[8] A combination of bacterial damage and consequences of the immune response lead to disruption of gas exchange with resulting symptoms.

Diagnosis

Diagnosis of ventilator-associated pneumonia is difficult and is not standardized.[9] The criteria used for diagnosis of VAP varies by institution, but tends to be a combination of several of the following radiographic, clinical sign, and laboratory evidence:[10]

  1. Temperature greater than 38C or less than 36C[10]
  2. White blood cell count greater than 12,000/mm3 or less than 4,000/mm3[10]
  3. Purulent secretions, increased secretions, or change in secretions[10]
  4. Positive tracheal cultures or bronchoalvelolar lavage cultures[10]
  5. Some sign of respiratory distress, such as shortness of breath, rapid breathing, abnormal breathing sounds when listening with stethoscope[10]
  6. Increased need for oxygen on the ventilator[10]
  7. Chest X-Rays: at least two serial xrays showing sustained or worsening shadowing (infiltrates or consolidations)[10]
  8. Positive cultures that were obtained directly from the lung environment, such as from the trachea or bronchioles[10]

As an example, some institutions may require one clinical symptoms such as shortness of breath, one clinical sign such as fever, plus evidence on chest xray and in tracheal cultures.[10]

There is no gold standard for getting cultures or other evidence of bacterial, viral, or fungal culprit. One strategy collects cultures from the trachea of people with symptoms of VAP. Another is more invasive and advocates a bronchoscopy plus bronchoalveolar lavage (BAL) for people with symptoms of VAP. Both strategies also require a new or enlarging infiltrate on chest x-ray as well as clinical signs/symptoms such as fever and shortness of breath.

Blood cultures may reveal the microorganisms causing VAP, but are often not helpful as they are positive in only 25% of clinical VAP cases.[11] Even in cases with positive blood cultures, the bacteremia may be from a source other than the lung infection.[11]

Prevention

Prevention of VAP involves limiting exposure to resistant bacteria, discontinuing mechanical ventilation as soon as possible, and a variety of strategies to limit infection while intubated. Resistant bacteria are spread in much the same ways as any communicable disease. Proper hand washing, sterile technique for invasive procedures, and isolation of individuals with known resistant organisms are all mandatory for effective infection control. A variety of aggressive weaning protocols to limit the amount of time a person spends intubated have been proposed. One important aspect is limiting the amount of sedation that a ventilated person receives.

Other recommendations for preventing VAP include raising the head of the bed to at least 30 degrees. Antiseptic mouthwashes such as chlorhexidine may also reduce the incidence of VAP, although the evidence is mainly restricted to those who have undergone cardiac surgery.[12]

American and Canadian guidelines strongly recommend the use of supraglottic secretion drainage (SSD) Special tracheal tubes with an incorporated suction lumen as the EVAC tracheal tube form Covidien / Mallinckrodt can be used for that reason. New cuff technology based on polyurethane material in combination with subglottic drainage (SealGuard Evac tracheal tube from Covidien/Mallinckrodt)showed significant delay in early and late onset of VAP.[13]

A recent clinical trial indicates that the use of silver-coated endotracheal tubes may also reduce the incidence of VAP.[14] There is tentative evidence that the use of probiotics may reduced the likelihood of getting VAP, however it is unclear if probiotics have an impact on ICU or in-hospital death.[15]

Treatment

Treatment of VAP should be matched to known causative bacteria. However, when VAP is first suspected, the bacteria causing infection is typically not known and broad-spectrum antibiotics are given (empiric therapy) until the particular bacterium and its sensitivities are determined. Empiric antibiotics should take into account both the risk factors a particular individual has for resistant bacteria as well as the local prevalence of resistant microorganisms. If a person has previously had episodes of pneumonia, information may be available about prior causative bacteria. The choice of initial therapy is therefore entirely dependent on knowledge of local flora and will vary from hospital to hospital.

Risk factors for infection with an MDR strain include ventilation for more than five days, recent hospitalization (last 90 days), residence in a nursing home, treatment in a hemodialysis clinic, and prior antibiotic use (last 90 days).

Possible empirical therapy combinations include (but are not limited to):

Therapy is typically changed once the causative bacteria are known and continued until symptoms resolve (often 7 to 14 days). For patients with VAP not caused by nonfermenting Gram-negative bacilli (like Acinetobacter, Pseudomonas aeruginosa) the available evidence seems to support the use of short-course antimicrobial treatments (< or =10 days).[16]

People who do not have risk factors for MDR organisms may be treated differently depending on local knowledge of prevalent bacteria. Appropriate antibiotics may include ceftriaxone, ciprofloxacin, levofloxacin, or ampicillin/sulbactam.

As of 2005, there is ongoing research into inhaled antibiotics as an adjunct to conventional therapy. Tobramycin and polymyxin B are commonly used in certain centres but there is no clinical evidence to support their use.

Epidemiology

Between 8 and 28% of patients receiving mechanical ventilation are affected by VAP.[17] VAP can develop at any time during ventilation, but occurs most often in the first week of mechanical ventilation.[18] There is some evidence for gender differences in the course of VAP: men have been found to get VAP more often, but women are more likely to die after contracting VAP.[19]

Prognosis

VAP occurring early after intubation typically involves fewer resistant organisms and is thus associated with a more favorable outcome. Because respiratory failure requiring mechanical ventilation is itself associated with a high mortality, determination of the exact contribution of VAP to mortality has been difficult. As of 2006, estimates range from 33% to 50% death in patients who develop VAP. Mortality is more likely when VAP is associated with certain microorganisms (Pseudomonas, Acinetobacter), blood stream infections, and ineffective initial antibiotics. VAP is especially common in people who have acute respiratory distress syndrome (ARDS).

References

  1. 1 2 3 4 Michetti, CP; Fakhry, SM; Ferguson, PL; Cook, A; Moore, FO; Gross, R; AAST Ventilator-Associated Pneumonia, Investigators (May 2012). "Ventilator-associated pneumonia rates at major trauma centers compared with a national benchmark: a multi-institutional study of the AAST.". The journal of trauma and acute care surgery 72 (5): 1165–73. doi:10.1097/TA.0b013e31824d10fa. PMID 22673241.
  2. 1 2 Cook, D (2000). "Ventilator associated pneumonia: perspectives on the burden of illness.". IntensiveCare Medicine. 26 Suppl 1: S31–7. doi:10.1007/s001340051116. PMID 10786956.
  3. ↑ Koenig Steven M., Truwit Jonathon D. (October 2006). "Ventilator-Associated Pneumonia: Diagnosis, Treatment, and Prevention". Clin Microbiol Rev. 19 (4): 637–657. doi:10.1128/cmr.00051-05.
  4. ↑ "Lung Bacterial Population Diversity in CAP, VAP and Health using 16S rDNA Sequencing". ResearchGate. Retrieved 2016-04-19.
  5. 1 2 Nolan, T. J.; Gadsby, N. J.; Hellyer, T. P.; Templeton, K. E.; McMullan, R.; McKenna, J. P.; Rennie, J.; Robb, C. T.; Walsh, T. S. (2016-04-12). "Low-pathogenicity Mycoplasma spp. alter human monocyte and macrophage function and are highly prevalent among patients with ventilator-acquired pneumonia". Thorax: thoraxjnl–2015–208050. doi:10.1136/thoraxjnl-2015-208050. ISSN 1468-3296. PMID 27071419.
  6. ↑ Conway Morris, Andrew; Kefala, Kallirroi; Wilkinson, Thomas S.; Dhaliwal, Kevin; Farrell, Lesley; Walsh, Tim; Mackenzie, Simon J.; Reid, Hamish; Davidson, Donald J. (2009-07-01). "C5a Mediates Peripheral Blood Neutrophil Dysfunction in Critically Ill Patients". American Journal of Respiratory and Critical Care Medicine 180 (1): 19–28. doi:10.1164/rccm.200812-1928OC. ISSN 1073-449X. PMC: 2948533. PMID 19324972.
  7. ↑ Morris, Andrew Conway; Brittan, Mairi; Wilkinson, Thomas S.; McAuley, Danny F.; Antonelli, Jean; McCulloch, Corrienne; Barr, Laura C.; McDonald, Neil A.; Dhaliwal, Kev (2011-05-12). "C5a-mediated neutrophil dysfunction is RhoA-dependent and predicts infection in critically ill patients". Blood 117 (19): 5178–5188. doi:10.1182/blood-2010-08-304667. ISSN 0006-4971. PMID 21292772.
  8. ↑ Morris, A. Conway; Anderson, N.; Brittan, M.; Wilkinson, T. S.; McAuley, D. F.; Antonelli, J.; McCulloch, C.; Barr, L. C.; Dhaliwal, K. (2013-11-01). "Combined dysfunctions of immune cells predict nosocomial infection in critically ill patients". British Journal of Anaesthesia 111 (5): 778–787. doi:10.1093/bja/aet205. ISSN 0007-0912. PMID 23756248.
  9. ↑ Marino, Paul L. (2014). Marino's the ICU book (Fourth ed.). ISBN 1451121180.
  10. 1 2 3 4 5 6 7 8 9 10 "Pneumonia (Ventilator-associated [VAP] and non-ventilator-associated Pneumonia [PNEU]) Event". http://www.cdc.gov/nhsn/pdfs/pscmanual/6pscvapcurrent.pdf. Centers for Disease Control and Prevention. January 2015. External link in |website= (help);
  11. 1 2 Gast, Paul L. Marino ; with contributions from Kenneth M. Sutin ; illustrations & page layout by Patricia (2009). The little ICU book of facts and formulas. Philadelphia: Wolter Kluwer Health/Lippincott Williams & Wilkins. ISBN 0781778239.
  12. ↑ Klompas M, Speck K, Howell MD, Greene LR, Berenholtz SM; Speck; Howell; Greene; Berenholtz (2014). "Reappraisal of routine oral care with chlorhexidine gluconate for patients receiving mechanical ventilation - systematic review and meta-analysis". JAMA Intern Med 174 (5): 751–61. doi:10.1001/jamainternmed.2014.359. PMID 24663255.
  13. ↑ Lorente L, Lecuona M, Jiménez A, Mora ML, Sierra A; Lecuona; Jiménez; Mora; Sierra (2007). "Influence of an endotracheal tube with polyurethane cuff and subglottic secretion drainage on pneumonia". Am. J. Respir. Crit. Care Med. 176 (11): 1079–83. doi:10.1164/rccm.200705-761OC. PMID 17872488.
  14. ↑ Kollef MH, Afessa B, Anzueto A, et al. (August 2008). "Silver-coated endotracheal tubes and incidence of ventilator-associated pneumonia: the NASCENT randomized trial". JAMA 300 (7): 805–13. doi:10.1001/jama.300.7.805. PMID 18714060.
  15. ↑ Bo, L; Li, J; Tao, T; Bai, Y; Ye, X; Hotchkiss, RS; Kollef, MH; Crooks, NH; Deng, X (Oct 25, 2014). "Probiotics for preventing ventilator-associated pneumonia". The Cochrane database of systematic reviews 10: CD009066. doi:10.1002/14651858.CD009066.pub2. PMID 25344083.
  16. ↑ Grammatikos AP, Siempos II, Michalopoulos A, Falagas ME; Siempos; Michalopoulos; Falagas (December 2008). "Optimal duration of the antimicrobial treatment of ventilator-acquired pneumonia". Expert Rev Anti Infect Ther 6 (6): 861–6. doi:10.1586/14787210.6.6.861. PMID 19053899.
  17. ↑ Chastre J, Fagon JY; Fagon (April 2002). "Ventilator-associated pneumonia". Am. J. Respir. Crit. Care Med. 165 (7): 867–903. doi:10.1164/ajrccm.165.7.2105078. PMID 11934711.
  18. ↑ Cook, D (2000). "Ventilator associated pneumonia: perspectives on the burden of illness.". Intensive Care Medicine. 26 Suppl 1: S31–7. doi:10.1007/s001340051116. PMID 10786956.
  19. ↑ Sharpe, JP; Magnotti, LJ; Weinberg, JA; Brocker, JA; Schroeppel, TJ; Zarzaur, BL; Fabian, TC; Croce, MA (July 2014). "Gender disparity in ventilator-associated pneumonia following trauma: identifying risk factors for mortality.". The journal of trauma and acute care surgery 77 (1): 161–5. doi:10.1097/TA.0000000000000251. PMID 24977772.

Additional reading

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