ventilator - associated pneumonia ( vap ) is defined as a new ( nosocomial ) lower respiratory tract infection diagnosed in mechanically ventilated patients 48 hours ( ' early - onset ' vap ) or 4 days ( ' late - onset ' vap ) after intubation [ 1 - 5 ] . management of early - onset and late - onset vap may differ as the causative factors and likely pathogens will influence treatment strategies , such as antimicrobial therapy . vap is associated with increased mortality and morbidity , prolonged duration of ventilation and hospital stay , and escalated costs of hospitalisation [ 2,3,5 - 9 ] . in resource - rich countries vap is reported to be the second most common nosocomial / hospital - acquired infection in pediatric and neonatal intensive care units , with incidences ranging from 3 to 30% and vap - attributable mortality rates up to 20% . the potential devastating impact of vap is emphasized by the study of abdel gawad and colleagues   where a 50% incidence of vap and 70% mortality with vap means that more than 80% of all the deaths in their unit were due to hospital - acquired infection / vap . defining vap is the easy aspect , making the correct diagnosis ( let alone confirmation ) becomes more challenging , and establishing universally accepted criteria is a distant goal . the clinical pulmonary infection score ( cpis ) , utilized in the study by abdel gawad and colleagues , is based on five clinical parameters - fever , leucocytosis , purulence of secretions , oxygenation , extent of radiographic infiltrates - and strengthened by cultures from the lower respiratory tract ( most often broncho - alveolar lavage ( bal ) ) . it suffers from poor inter - rater agreement and retrograde influence from positive bal results . the current reference standard ( read ' gold standard ' ) comprises the clinical criteria for the diagnosis of vap established by the national nosocomial infection surveillance ( nnis ) system of the centers for disease control and prevention ( cdc ) , which incorporate age - specific criteria . they do not require microbiological confirmation to diagnose pneumonia . the cdc / nnis criteria also suffer from inter - rater inconsistency . additionally , the recurrent question as to whether positive bal cultures reflect true infection or merely bacterial colonization lingers . moreover , many studies show weak concordance between designated diagnostic criteria and clinical diagnosis of vap by ' experts ' . to further muddy the waters , the ' big - brother ' effect of mandatory reporting of health care - associated infections in many countries and penalties for underperformance complicates inter - institutional comparisons by blunting diagnostic accuracy . the pathogenesis of vap is iatrogenic and multifactorial , with major factors being : the endotracheal tube facilitating microbial access to the lung and providing a nidus for growth of biofilm - encased bacteria ; micro - aspiration from oropharynx or gastrointestinal tract ; extension of existing micro - infection ( foci of localized micro - infection causing local bronchiolitis without clinically relevant pneumonia that proceed to develop into macro - bronchopneumonia ) ; blood - borne transmission from other sites ; and inhalation / instillation of contaminants ( for example , aerosols or cross - infected suction catheters ) . endogenous community - acquired pathogens are generally responsible for early - onset and nosocomial microbes residing in oropharyngeal or gastric contents for late - onset vap . abdel gawad and colleagues   confirmed that gastro - oesophageal reflux ( ger ) is common in mechanically ventilated children . the authors demonstrated reflux of alkaline or acidic gastric fluids into the lower half of the oesophagus ( ph probe positioned 5 cm above the gastro - oesophageal sphincter ) , but have not demonstrated gastric fluid in the oropharynx or bronchial tree . neither have they shown changes in ph or gastric pepsin in the bronchial tree to support their inference of gastro - pulmonary spill - over . a high incidence of ger in both vap and non - vap patients , along with small sample size , restricts the association of ger with vap to speculation . a lack of reported data concerning surveillance cultures from the oropharynx and gastro - intestinal tract also curtail support for a gastro - pulmonary route of vap infection . the paucity of these data additionally prevents understanding whether the vap is endogenous or exogenous in origin . the low incidence of bal culture identifying staphylococcus aureus would suggest a low rate of endogenous vap . the high incidence of klebsiella and acinetobacter ( especially if multi - resistant organisms ) implies exogenous infection transmission ( exit ) and/or late - onset vap . the most compelling data are the association of acidic reflux with vap and especially death . this finding is directly contrary to the concept that the acidification of gastric contents inhibits colonization with potentially pathogenic bacteria . if we are to believe that acidic reflux led to gastro - pulmonary acidic rain - out , what were the mechanisms that led to death ? hypotheses include : bronchial mucosal and/or lung parenchymal damage by acid and pepsin ; neutralisation of pulmonary macrophages by gastric acid rain ; enhanced bacterial colonization of denuded aerodigestive tract surfaces by potential pathogens . possibly there is no pulmonary impact from presumed gastric acid rain - out , and most likely exit is the key factor with cross - contamination of intubated patients from an external ( to the patient ) multi - resistant source . certainly the high vap incidence of 50% and accompanying mortality of 70% reported by abdel gawad and colleagues   is troubling . even if it is a matter of death with vap rather than death from vap , the answer to this unit 's problem must lie with the introduction of vap prevention strategies or ' vap bundles ' , concentrating on the basic modifiable risk factors rather than medicinal options and certainly not escalating antibiotic sophistication . vap prevention strategies concentrate on education , minimising invasive mechanical ventilation and reducing airway contamination from endogenous ( oropharynx , gastric , and sputum retention ) and exogenous sources ( exit ) . abdel gawad and colleagues reiterate the brutal reality that the grim reaper remains a close friend of vap . bal : broncho - alveolar lavage ; cdc : centers for disease control and prevention ; exit : exogenous infection transmission ; ger : gastro - oesophageal reflux ; nnis : national nosocomial infection surveillance ; vap : ventilator - associated pneumonia .
ventilator - associated pneumonia ( vap ) is a new ( nosocomial ) lower respiratory tract infection diagnosed in mechanically ventilated patients 48 or more hours after intubation . 
 there is no gold standard for establishing the diagnosis and its pathogenesis is iatrogenic and multifactorial . 
 gastro - oesophageal reflux is common in mechanically ventilated children , but its role in vap remains speculative . 
 vap is associated with increased mortality and morbidity , prolonged duration of ventilation and hospital stay , and escalated costs of hospitalisation . 
 vap ' bundles ' are championed as the antidote .