NOSOCOMIAL PNEUMONIA

CHAPTER 96 NOSOCOMIAL PNEUMONIA



The two broad classes of pneumonia are nosocomial and community-acquired pneumonia. Nosocomial pneumonia is often referred to as hospital-acquired pneumonia (HAP), defined as pneumonia occurring 48 hours or more after admission that was not incubating at the time of admission. Postoperative pneumonia is essentially HAP, except in a patient who has undergone a surgical procedure. Finally, ventilator-associated pneumonia (VAP) refers to pneumonia occurring 48 hours or more after initiating mechanical ventilation via endotracheal intubation or tracheostomy.


Our goals in this chapter are to review the incidence of nosocomial pneumonia in the trauma patient, risk factors contributing to pneumonia, proven prevention strategies, the specifics of diagnosis, appropriate management of pneumonia once diagnosed, and associated morbidity and mortality relevant to the trauma population such as the relationship between prophylactic antibiotics, tube thoracostomy, and pneumonia.



INCIDENCE/MORBIDITY AND MORTALITY


Nosocomial infections cause significant mortality and morbidity in the critical care setting. HAP is the most common infection in the intensive care unit (ICU), causing between 25% and 48% of all nosocomial infections. Pneumonia is the leading cause of death due to hospital-acquired infections, with an estimated associated mortality ranging from 20% to 50%. The majority of nosocomial pneumonia episodes, 80%–90%, are associated with mechanical ventilation. While VAP makes up 90% of all infections in intubated patients, the overall reported incidence of VAP varies, with rates between 6% and 52%. The incidence varies due to differences in the definition of VAP in studies as well as differences in patient populations. There is, for example, a lower incidence in respiratory and medical ICUs (4.2 and 7.4 cases per 1000 ventilator days, respectively) as compared to trauma, neurosurgical, and burn units (15–16.3 cases per 1000 ventilator days). Although there is approximately a 1% cumulative risk per day of mechanical ventilation, the risk is highest in the first 5 days (approximately 3% per day), and steadily decreases after that. A number of studies place nosocomial pneumonia’s risk ratio for death around 2.0. Developing pneumonia increases the overall hospital stay by approximately 9–11.5 days, and for critically ill patients, increases the ICU stay by 4–6 days. In addition to prolonging hospital and ICU stays, pneumonia increases hospital cost by requiring more antibiotics, chest radiographs, and days of mechanical ventilation, with all its associated care. The attributable cost of a single episode of HAP is estimated to be between $12,000 and $16,000.



RISK FACTORS AND PREVENTIVE MEASURES



Nonmodifiable versus Modifiable Risk Factors


While the greatest risk factor for VAP is the duration of mechanical ventilation, there are many other independent predictors, including modifiable and nonmodifiable risk factors (Table 1).


Table 1 Risk Factors for Ventilator-Associated Pneumonia









Nonmodifiable Factors Modifiable Factors Affording Prevention Strategies


































ICU, Intensive care unit.


These risk factors are directly related to the pathogenesis of VAP. As the lower respiratory tract is sterile under basal conditions, the introduction of pathogens into the lungs and the impairment of traditional host defenses are necessary to cause infection. There is growing evidence that aspiration of pathogens colonizing or contaminating the oropharynx or gastrointestinal tract results in lower respiratory tract infection. Colonization of the endotracheal tube itself also may lead to alveolar infection during suctioning or bronchoscopy. Other less frequent sources include bacteremia and hematogenous spread or inhalation of infected aerosols.



Mechanical Ventilation


Mechanical ventilation is the greatest risk factor for HAP and is associated with a 6- to 20-fold increase in the risk of lung infection. Intubation itself increases the risk of pneumonia due to the potential for direct inoculation of pathogens into the lungs during the procedure. Therefore, intubation should be avoided, with noninvasive positive-pressure ventilation being the preferred alternative to mechanical ventilation, when clinically feasible. A prospective survey of those who underwent mechanical ventilation versus noninvasive ventilation showed that even after adjusting for the severity of illness using the Simplified Acute Physiology Score (SAPS II), both the risk of VAP as well as the risk of nosocomial infections in general were reduced. Other invasive procedures such as tracheostomy, bronchoscopy, placement of a nasogastric (NG) tube, and chest tube thoracostomy also increase the risk. Thoracic trauma and chest operations lead to a disproportionately higher incidence of VAP, likely due to direct inoculation of pathogens, as well as infection due to chest tube placement.


In a trauma or surgical unit, the majority of patients are mechanically ventilated secondary to the need for surgery. However, all efforts to decrease sedation and wean the patient to extubation postoperatively should be made. The risk of reintubation and emergency intubation should be minimized, as these events are also associated with increased risk of VAP.


Subglottic secretions are also potential sources of infection. A recent meta-analysis showed that continuous aspiration of subglottic secretions resulted in a 50% decrease in incidence of VAP. This was particularly beneficial in those who were mechanically ventilated for longer than 72 hours. If mechanical ventilation is necessary, this technique should be utilized. Besides this, the ventilator circuit can also become contaminated due to patient secretions. Many prospective randomized trials have shown that the incidence of VAP is not associated with the frequency of ventilator circuit changes. However, care should be taken to frequently clean the circuit and prevent aspiration of accumulated secretions. The endotracheal tube cuff pressure should also be greater than 20 mm H2O to prevent tracking of bacterial pathogens around the cuff and into the lower respiratory tract.





Aspiration


Due to the association between VAP and aspiration, factors involved in increased risk of aspiration such as continuous sedation, a low Glasgow Coma Scale, use of paralytic agents, and a supine position have all been shown to increase the risk of VAP. All efforts should be made to reduce the aspiration of gastric and oropharyngeal contents. One randomized trial was stopped ahead of schedule when it was apparent that the supine position results in increased aspiration and increased incidence of VAP compared to the semirecumbent position. Therefore, patients should be semirecumbent with the head of the bed raised to an angle of 30–45 degrees whenever possible. Continuous lateral rotation of ICU patients has also shown a protective effect and is another possibility. Transporting patients out of the ICU for procedures also leads to increased risk of VAP. This is potentially due to the fact that they are supine during transport. Thus, patients should be kept semirecumbent during transport whenever possible.


While it has been postulated that enteral nutrition would result in increased risk of VAP compared to parenteral nutrition due to aspiration, the evidence goes against that hypothesis, with VAP odds ratios of 2.65 and 3.27, respectively. As parenteral feeding is associated with many other risks like bacteremia as a complication of intravascular lines, and bacterial overgrowth and translocation, enteral feeding is preferred. As enteral feeding in the supine position maximizes risk, with a 50% incidence of VAP, feeding in the semirecumbent position is preferable. Other hypotheses include a benefit to smaller nasogastric tubes as well as a benefit to postpyloric or small intestine feeding. However, neither of those techniques has been proven to decrease the risk of VAP.



Gastrointestinal Tract Bacterial Overgrowth


Given their associated predisposition to bacterial overgrowth in the gastrointestinal tract, antacids and histamine type-2 antagonists are also associated with increased risk of VAP. There have been multiple trials comparing various stress ulcer prophylaxis agents. While there have been controversial results on the effect of sucralfate on VAP, the latest large randomized trial showed that while sucralfate resulted in a significantly lower rate of VAP compared to ranitidine and antacids, it is associated with a higher incidence of gastrointestinal bleeding. Therefore, sucralfate is recommended in all patients except those with risk factors for gastrointestinal bleeding.


Selective decontamination of the digestive tract (SDD) may be effective in reducing incidence of VAP. It attempts to reduce oropharyngeal and gastric colonization with aerobic Gram-negative bacilli and Candida species, without affecting anaerobic flora. Most regimens include a combination of an aminoglycoside, amphotericin B, or nystatin, and a nonabsorbable antibiotic like polymyxin. Systemic cefuroxime was also added in a few trials. Multiple randomized controlled trials have shown that SDD results in reduced incidence of VAP, decreased hospital mortality, and a decrease in antibiotic-resistant microorganism infections as well. However, these preventive effects were inversely related to study quality, and were much less pronounced in hospitals with high levels of antibiotic resistance. Therefore, SDD is not recommended for routine use, particularly for patients with risk factors for resistant pathogens.


It has been postulated that the intravenous antibiotic component of SDD is the main cause of improved survival, and current randomized trials are evaluating the effect of prophylactic IV antibiotics around the time of intubation. Intravenous cefuroxime reduced the incidence of early-onset hospital-acquired pneumonia in one recent trial. Intravenous antibiotics are currently not recommended for routine use, pending results from further trials.




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Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on NOSOCOMIAL PNEUMONIA

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