Ventilator-associated pneumonia (VAP) is a term used to describe pneumonia (lung infection) that develops in a patient who has been on mechanical ventilation for more than 48 hours. Ventilator-associated pneumonia is the second most common hospital-acquired infection among pediatrics and neonatal intensive care unit patients. It accounts for 7% to 32% of healthcare-associated infections and 10% of all pediatric device-related infections reported to the National Healthcare Safety Network (NHSN). Generally, the rate of pneumonia in pediatric intensive care units (PICU) is lower than in adult intensive care units (ICU). In neonates, the rate of ventilator-associated pneumonia is inversely proportional to birth weight. There is limited data on infants and children with VAP, so most of the information is extrapolated from adult studies. 
Children with artificial airways, such as a tracheostomy tube for management of chronic respiratory failure or an endotracheal for acute airway management, are at risk for ventilator-associated pneumonia. It is difficult to diagnose ventilator-associated pneumonia in any patient, and this holds true in young children, particularly in the neonatal ICU population. In 2008, the Centers for Disease Control (CDC) and National Healthcare Safety Network (NHSN) have attempted to provide reproducible criteria for the surveillance of ventilator-associated pneumonia. They have classified it as three types: (1) clinically defined, (2) pneumonia with laboratory findings, and (3) pneumonia in immunocompromised patients. Infants and children are usually classified to the first category.
Tracheitis Versus Ventilator-associated Pneumonia
Ventilator-associated pneumonia is part of a spectrum of upper airway infection after the of an artificial airway with bacteria. For convenience, the infection of an artificial airway after colonization is either diagnosed as tracheitis or ventilator-associated pneumonia.
Tracheitis is the presence of clinical signs of purulent tracheal discharge, fevers, respiratory distress, and the presence of bacteria and white blood cells in the tracheal aspirate without radiological signs of pneumonia.
Ventilator-associated pneumonia includes clinical signs of purulent tracheal discharge, fevers, respiratory distress, and micro-biological signs of the presence of microorganisms along with white blood cells in the tracheal aspirate along with radiological evidence of pneumonia.
Ventilator-associated pneumonia is typically bacterial and from a single organism. However polymicrobial infections are increasing. In a large retrospective review done in the ICU settings of three hospitals, the microbiology was the same across adult and pediatric hospitals. The most common organisms were Staphylococcus aureus (28.4 %), Pseudomonas aeruginosa (25.2 %), and other gram negatives (26.6%). 
Artificial airways become colonized with pathogenic bacteria soon after intubation or tracheostomy, and the major pathogens include both gram-positive and gram-negative bacteria: S. aureus (including MRSA), P. aeruginosa, and Klebsiella and Enterobacter species. Patients in a NICU have a risk of Enterococcus species and group B Streptococcus as well. Other pathogens include the Streptococcus, Enterobacteriaceae, and Acinetobacter species. Anaerobic bacteria are an uncommon cause of Ventilator-associated pneumonia but can play a role in polymicrobial infections, particularly when pneumonia is due to aspiration. Nosocomial viruses and fungi are rare causes of pneumonia in immunocompetent hosts.
In addition, early pneumonia (less than 4 days after admission to the hospital) is most likely from antibiotic-sensitive community-acquired organisms, and late pneumonia (more than 4 days) is more likely due to antibiotic-resistant organisms. However, this distinction is not helpful in children who are frequently admitted to the hospital.
Pediatric patients seem to have a lower risk of ventilator-associated pneumonia than adults, possibly due to fewer comorbidities. According to NHSN, 304 participating hospitals revealed ventilator-associated pneumonia rates of 2.36 to 2.08 per 1000 device-days among neonates weighing less than 750 grams and between 750 and 1,000 grams, respectively.
The estimated incidence of ventilator-associated infection in pediatric ICU ranges from 1.8 to 8.3 per 1000 ventilator days.
There are few mechanisms suggested for development of ventilator-associated pneumonia: (1) most commonly it is thought to be a progression from colonization of the upper airway, leading to tracheal colonization, then tracheitis, and finally pneumonia. This depends on the number, type, and virulence of the bacteria as well as natural host defenses such as mechanical factors and humoral and cellular immunity. Mechanical defenses, such as ciliary motion and mucus secretion, can be altered in an intubated patient. Artificial airway inhibits gag reflex and ciliary functions and provides a substrate for growth of biofilm which acts as a reservoir for pathogens. This biofilm can be dislodged and delivered to the lower respiratory tract through mechanical suctioning or high-pressure airflow, leading to pneumonia in a susceptible host. Bacteria overgrowth can be secondary to proton-pump inhibitors and histamine type 2 receptor antagonists for stress ulcer prophylaxis, which neutralized gastric pH and promotes colonization of the upper gastrointestinal tract. In a supine patient with likely depressed mental status (possibly secondary to sedation), the risk of aspiration is high.
Diagnosis of ventilator-associated pneumonia can be difficult. It requires a combination of clinical, radiographic, and microbiologic data. The longer the length of intubation, the higher the likelihood of ventilator-associated pneumonia. Ventilator-associated pneumonia is suspected in the setting of fever, change in auscultation exam, a change in the chest x-ray, and an increasing requirement for respiratory support. However, auscultation is hindered by sounds of the ventilation system itself, especially with high-frequency ventilation. Many neonates have chest x-ray findings that interfere with the early detection of new infiltrates.
Clinical findings include fever, leukocytosis or leukopenia, purulent secretions, and worsening gas exchange. Chest X-ray with new or worsening pulmonary infiltrates, cavitation, air bronchograms, or pneumatoceles is a requirement. Microbiologic data are important, both for diagnosis and for guiding treatment. Samples of lower respiratory tract secretions are often obtained and sent for culture as well as blood cultures in all patients suspected of ventilator-associated pneumonia. However, many experts recommend against taking a culture from intubated patients as most are colonized after 48 hours, and the culture is of little clinical use.
In adults, specimens are obtained via bronchoscopy, lung biopsy, lung aspiration, protected specimen brushing (PSB), or transtracheal aspiration rather than by aspiration of tracheal content through an endotracheal tube. However, use of bronchoscopic bronchoalveolar lavage (BAL) or PSB to obtain secretions of the lower respiratory tract for quantitative bacterial culture is limited in children due to technical difficulties and potential for complication. This problem is even more challenging in NICU patients.
Obtaining a microbiological specimen from neonates is often impossible, so the CDC has come up with purely clinical criteria for the diagnosis of ventilator-associated pneumonia among infants less than one year of age. These include
Once ventilator-associated pneumonia is suspected and appropriate culture samples are sent, empirical therapy will be based on the duration of intubation and hospitalization, prior or current antibiotic therapy, the severity of clinical disease, and knowledge of local pathogen’s susceptibility patterns. Initial broad-spectrum therapy with coverage of gram-negative bacilli, including P. aeruginosa, and possibly methicillin-resistant S. aureus is generally appropriate. Treatment is then narrowed based on subsequent culture data and clinical and radiographic findings.
Treatment duration has not been evaluated in children. In adults, uncomplicated cases may be treated with 7 to 10 days of therapy. For complicated cases or those with necrotizing pneumonia, at least 14 days of therapy should be administered. Courses less than 7 days may be appropriate for children with ventilator-associated tracheitis without evidence of pneumonia.
Pediatric infectious disease and pediatric pulmonology consultations should be considered in such cases.
Ventilator-associated pneumonia is usually managed by an interprofessional team that includes an intensivist, pulmonologist, respiratory therapy, ICU nurse, dietitian, pharmacist, and thoracic surgeon. The key with VAP is to reduce the risk by enforcing preventive techniques in patient care. All the modifiable risk factors should be addressed such as endotracheal and tracheostomy suctioning, use of gastric acid modifying agents, enteral nutrition, hand washing and single use of equipment. The supine position should be avoided, and one should minimize transport of the patient in and out of the ICU. The cuff pressure of the endotracheal tube should be at 20 mmHg or above, to help prevent passage of oropharyngeal contents into the lower airways. The pharmacist should ensure that the right antibiotics are selected and that there is a recycling of the medications to avoid the development of resistant organisms. The patient must be fed enterally whenever possible. Finally, there should be protocols for weaning and early extubation in order to avoid VAP. (Level V)
In general, VAP is associated with a higher mortality when the patient has numerous comorbidities. However, younger patients with no additional organ involvement do tend to have a good prognosis without any major sequelae. Higher mortality rates have been reported in older patients, diabetics, those with COPD, smokers and poor functional status. (Level V)
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