56 Strategies for the Prevention and Management of Ventilator-associated Pneumonia in a Neurocritical Unit

Mònica Magret ¹, Jordi Rello ²

¹ Critical Care Department. Sant Joan University Hospital, Rovira i Virgili University, Pere Virgili Health Institutm, Reus, Spain

² Critical Care Department. Vall d’Hebron University Hospital, Barcelona, Spain

56.1 Introduction

One of the main causes of morbidity and mortality in the industrialized countries is trauma and traumatic brain injury (TBI). In recent decades its incidence has increased constantly. Severe multiple trauma patients usually require admission to intensive care units (ICU) and most require ventilatory support.

Ventilator-associated pneumonia (VAP) is the most common nosocomial infection in the ICU, with an incidence of 10-30% [1]. In addition, VAP prolongs hospital stay and days on mechanical ventilation and contributes to an increase in mortality. Although mortality attributable to VAP in critically ill patients is still debated, the association between VAP and late mortality has been demonstrated in cohort studies, particularly in patients in whom VAP is caused by virulent pathogens such as Pseudomonas aeruginosa and methicillin-resistant Staphylococcus aureus (MRSA). In patients with VAP, there is an association between increased mortality and morbidity and inappropriate initial antibiotic treatment and delays in initiation of treatment. Early initiation and appropriate antibiotic treatment are important in the management of these patients.

In trauma patients on mechanical ventilation, VAP is a major complication, with an incidence of approximately 40 to 50%. This high incidence may be explained by the decreased level of consciousness, immunosuppression, and the need for emergency tracheal intubation. Although several recent studies have shown that VAP-related mortality in trauma patients is 8-59%, other studies found that VAP did not seem to increase mortality in severe trauma patients.

VAP in trauma patients differs from that in nontrauma patients due to characteristic risk factors and it is frequently associated with specific pathogens in the first week such as methicillin-sensitive Staphylococcus aureus (MSSA) and Haemophilus influenzae. Trauma patients have a different distribution in the incidence of VAP because, unlike nontrauma patients, the incidence of early VAP is 30-40%. According to the American Thoracic Society/Infectious Disease Society of America (ATS/IDSA) guidelines for the management of adults with hospital-acquired, ventilator-associated and healthcare-associated pneumonia, early VAP is defined as occurring within the first four days in the ICU and late VAP when it occurs after five days of admission to the ICU [2].

Brochard et al. recently showed that the beginning of VAP was associated with a higher probability of secondary brain injury, increased intracranial pressure, hypotension, fever and hypoxemia that all lead to a worse outcome [3].

The main objectives of this chapter are to review the risk factors, etiology, antibiotic treatment and prevention of VAP in trauma patients and to determine whether a different approach to such patients is needed.

56.2 Early Ventilatior-associated Pneumonia in Trauma Patients

Trauma patients can aspirate oropharyngeal secretions after brain injury, during resuscitation, and as a result of intubation. Endotracheal intubation is a major risk factor for developing VAP because it increases the risk of aspiration and weakens the bronchial clearance mechanism. The intubation procedure itself significantly increases the risk, as has been demonstrated in patients requiring reintubation [4]. Moreover, a majority of trauma patients require emergency tracheal intubation due to a decreased level of consciousness, cardiorespiratory arrest, psychomotor agitation and for air transport in some cases. Sloane et al. showed that 28% of patients who required prehospital rapid sequence intubation developed VAP and that this incidence was significantly higher than in patients intubated in the emergency department [5]. The cumulative risk of developing VAP is 3% per day of mechanical ventilation primarily within the first week of intubation.

Trauma patients often have a decreased level of consciousness that affects the swallowing reflex. Several studies have shown that the level of consciousness is also an important risk factor that increases the incidence of VAP [6,7]. Our group showed that the incidence of VAP was significantly higher among comatose patients (Glasgow Coma Score [GCS] <9) and the predominant pathogen isolated was MSSA, followed by H. influenzae. These data are consistent with other studies. In another study evaluating the risk factors for developing VAP within the first 48 hours of endotracheal intubation in nontrauma patients, the univariate analysis showed that high-volume aspiration of secretions, sedation, intubation for cardiorespiratory arrest or a decreased level of consciousness, emergency procedure, cardiorespiratory resuscitation, and a GSC <9 were statistically significant factors associated with VAP. But on the multivariate analysis, cardiorespiratory arrest and continuous sedation significantly increased the risk of VAP with an odds ratio (OR) of 5.13 and 4.4, respectively. Calvalcanti et al. showed in a case-control study that severe head and neck trauma, as measured by the Abbreviated Injury Scale (AIS) and Injury Severity Score (ISS), were the only independent risk factors for VAP development [8]. Moreover, they suggested that the need for supine position in patients with cervical fracture could influence this association. An interesting finding was that a GSC <8 was not associated with the development of VAP. Over 60% of patients developed early VAP and the main pathogens were MSSA and H. influenzae.

Due to the high incidence of early VAP caused by MSSA, several studies assessed the relationship between respiratory tract colonization and VAP. Ewig et al. performed an observational study where they analyzed the patterns of bacterial colonization in mechanically ventilated patients with severe head injury [9]. They noted that the initial colonization of the upper and lower airway was mainly by MSSA, H. influenzae and Streptoccocus pneumoniae. This colonization pattern was an independent risk predictor of subsequent colonization of the tracheobronchial tree. Although initial colonization of the tracheobronchial tree by MSSA, H. influenzae and S. pneumoniae was associated with a higher probability of early VAP, they found no independent risk factor for it. They also showed prior antibiotic use had a protective effect against these pathogens. Subsequently, Sirvent et al. demonstrated that tracheal colonization by MSSA, H. influenzae or S. pneumoniae within the first 24 hours of intubation was an independent risk factor for the development of early VAP in patients with TBI [10]. Bronchard et al. in a prospective observational study in TBI patients showed that nasal bacterial load of MSSA, aspiration before intubation, and use of barbiturates were independent risk factors for early VAP [3]. Recently, Agbaht et al. conducted a retrospective observational study to assess whether trauma influenced the epidemiology of VAP [11]. They found that among patients with early VAP, MSSA was the pathogen most frequently isolated in trauma patients. But in nontrauma patients Streptococcus spp. were the most frequent and significantly associated with early VAP. Moreover, in early VAP with prior antibiotic use, MSSA was significantly more frequent in trauma patients than in nontrauma patients. MRSA was not responsible for early episodes of VAP in trauma patients. Cases of MRSA-related VAP in trauma patients occurred in those with more than 10 days of ICU stay, when the patients had been subjected to the effect of risk factors similar to the other patients.

Other risk factors have been analyzed. Tejada et al. in a prospective cohort study found that continuous enteral feeding, craniotomy, mechanical ventilation for more than 24 hours and the use of positive end-expiratory pressure (PEEP) were independent risk factors for developing VAP in trauma patients [12]. The relationship between continuous enteral feeding and VAP has been documented in other studies. The administration of enteral nutrition with high pH via a nasogastric tube could increase gastric bacterial colonization, as well as volume, pressure and reflux. They suggested that the relationship between the use of PEEP and the development of VAP was due to the use of PEEP among patients with the acute respiratory distress syndrome (ARDS) which predisposes to the development of VAP.

56.3 Late Ventilatior-associated Pneumonia in Trauma Patients

As mentioned, in the study by Rello et al. the risk of developing VAP increased with days of intubation [7]. While cardiorespiratory arrest and continuous sedation were associated with the development of VAP in patients intubated for 48 hours, no association was found in patients intubated for more than 48 hours. In contrast, prior antibiotic use was associated with an increased risk of VAP and the main pathogen associated was P. aeruginosa. Ewig et al. observed that the increase in the colonization of ventilated patients during their stay in the ICU was primarily due to P. aeruginosa and Acinetobacter spp. Multivariate analysis showed that prior antibiotic use was the only risk factor for late VAP [9].

Agbaht et al. in a medical-surgical ICU showed that the pathogens responsible for late VAP were MSSA and nonfermentative Gram-negative bacilli (GNB) [11]. The nonfermentative GNB were significantly more frequent in late VAP than in early VAP. These pathogens were isolated from patients with risk factors such as late VAP and prior antibiotic use. They also observed that late VAP had a different distribution of pathogens in trauma patients where Acinetobacter baumannii was the most frequently isolated compared with nontrauma patients in whom P. aeruginosa was the most common pathogen isolated. MRSA was isolated from patients with more than 10 days of mechanical ventilation. This pathogen was significantly associated with the absence of trauma, late VAP, and prior antibiotic use. The main risk factors for early and late VAP in trauma patients are summarized in Table 56.1 [21].

Table 56.1. Risk factors for the development of early and late ventilator-associated pneumonia.

* Cardiopulmonary arrest or decreased level of consciousness.

56.4 Prevention of Ventilator-associated Pneumonia

There are several different strategies for preventing VAP. These are generally classified into nonpharmacological (Table 56.2) and pharmacological (Table 56.3) strategies. The strategies do not differ according to the type of patient since they should be applied to all patients with endotracheal intubation. Recently, the verification of compliance with a series of measures and the implementation of “care bundles” have emerged as useful integrative strategies to reduce VAP incidence.

Table 56.2. Nonpharmacological strategies for the prevention of ventilator-associated pneumonia.

Table 56.3. Pharmacologic strategies for the prevention of ventilator-associated pneumonia.

56.4.1 Nonpharmacological Strategies for Preventing Ventilator-associated Pneumonia

Nonpharmacological strategies aim to reduce the amount of secretions that reach the lower respiratory tract and include:

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