Hospital-acquired Pneumonia and Ventilator-associated Pneumonia

Recent Advances in Epidemiology and Management

François Barbier; Antoine Andremont; Michel Wolff; Lila Bouadma

Disclosures

Curr Opin Pulm Med. 2013;19(3):216-228. 

In This Article

Recent Advances in the Diagnosis of Hospital-acquired Pneumonia and Ventilator-associated Pneumonia

The diagnosis of HAP/VAP is challenging and conventional strategies have been extensively reviewed in recent guidelines.[1,8–10] However, two current research areas warrant developments. First, several biomarkers have been evaluated as complementary diagnostic tools during the past years.[81,82] Studies on BALF concentrations of the soluble triggered receptor expressed on myeloid cells 1 (sTREM-1) yielded conflicting results.[83–86] C-reactive protein may lack sensitivity in ICU patients.[87,88] The diagnostic values of BALF concentrations of interleukin-1β, interleukin-8, granulocyte colony-stimulating factor and macrophage inflammatory protein-1[alpha] could be discriminative but require validation on larger cohorts,[89] as do BALF levels of plasminogen activation inhibitor 1 (PAI-1).[90] By contrast, BALF levels of Clara cell protein 10 yield poor diagnostic accuracy.[91] The usefulness of plasma levels of Clara cell protein 16 (CC-16), soluble receptor for advanced glycation end products (sRAGE) and surfactant protein D (SP-D) is unclear.[92] Copeptin,[93,94] midregional atrial natriuretic factor (MR-ANF)[95,96] and adrenomedullin[97] were evaluated as prognostic rather than diagnostic biomarkers in pneumonia. To date, the literature does not support a clinical role for these biomarkers, including procalcitonin (PCT), in predicting VAP. However, using serum PCT concentration to customize antibiotic-treatment duration in patients with VAP has been evaluated in five studies, all showing less antibiotic consumption when a PCT-based algorithm was applied, with no detrimental impact on outcomes. Consequently, in patients treated for a VAP whose serum PCT concentration is less than 0.5 ng/ml or decreased by more than 80% (compared with the peak concentration), antibiotic discontinuation may be considered at day 3 after initiation.[87,88,98,99,100,101,102]

Conventional bacteriological methods imply an incompressible delay of 48–72 h for complete antimicrobial susceptibility testing of pneumonia-causative pathogens. Therefore, the on-going development of rapid molecular methods raises comprehensible hopes for optimizing the choice of initial drugs and avoiding the overprescription of very broad-spectrum molecules in this situation.[103] Such tools should reliably identify both the most common pathogens and their most frequent resistance genotypes within a time ranging from 2 to 6 h. Real-time PCR, in-situ DNA hybridization and mass spectrometry are currently the leading investigation methods.[104] Several systems are already commercialized for direct analysis of clinical samples such as blood cultures and swabs (most notably for MRSA screening). However, and despite promising preliminary results,[103,104,105] no system has been validated so far for direct application on BALF or tracheal aspirates in suspected VAP/HAP. Oversensitivity and quantification of bacterial loads may represent important issues. Indeed, genetic material from more than 15 distinct pathogens (including bacteria, virus and fungi) can be detected in BALF from ICU patients, most of them being not reliably considered as causative for the current pneumonia episode.[106]

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