Table of Contents
Pneumonia is a respiratory disease that affects the lungs and can be contagious based on the causes. The disease can either be viral or bacterial in nature. However, most studies have concentrated on the bacterial causes considering that the viral causes have not been fully conclusive. According to the Association of for Professionals in Infection Control and Epidemiology, APIC (2009), Pneumonia accounts for between 11 and 15 percent of all hospital acquired infections in the United States. It also accounts for 24 percent of all the infections acquired from the coronary unit and 27 percent for the ones resulting from medial intensive care unit (ICU). One therapy used in the treatment of Pneumonia is the Mechanical ventilations (MV). However, the therapy is not without medical complications and one of them is the Ventilator-associated Pneumonia (VAP). Ventilator-associated pneumonia is understood as a type of pneumonic complications mostly occurring after 48 hours following a tracheotomy or endotracheal intubation on a patient (Kalanuria, Zai, & Mirski, 2014). In this paper, the discussion will revolve around the VAP including its aetiology, pathophysiology, treatment/prevention, and prognosis.
Just like many other medical-related complications, VAP has wide reaching effects, which doubles as disadvantages and they include the following. Patients and families have to foot huge medical and hospitalization bills incurred in the medication and during the hospitalization of the patients (Cason et al., 2007 as cited in O’Keefe-McCarthy, Santiago, & Lau, 2008). Besides the family members, countries suffer from huge economic burdens and especially through the subsidization of the hospital services and medication as well as in the provision of the health insurance covers among the citizens. Also, the patients put under MVs have relatively long stay at the hospital. The situation exacerbates after the patients acquire the VAP since the hospital stay is further stretched. Finally, this medical complication leads to increased mortality and morbidity rates (Klompas et al., 2014).
According to some of the previous studies, the occurrence of the ventilator-associated pneumonia can kick off either early or late after a patient is put under the mechanical ventilation process (O’Keefe-McCarthy, Santiago & Lau, 2008). According to Pruitt and Jacobs 2006 (as cited in O’Keefe-McCarthy, Santiago & Lau, 2008), the early-onset VAP develops between 48 and 96 hrs after the intubation. The most common microorganisms associated with the early-onset VAP includes; Moraxell catarrhalis, and Haemophilus influenza. On the other hand, the late VAP will occur more than 5 days after the mechanical ventilation has been performed on the patient. The common bacteria associated with this category of VAP include; Kebsiella pneumoniae, enterobacter, and Staphylococcus aureus among others (O’Keefe-McCarthy, Santiago, & Lau, 2008). From the above, it is clear that Ventilator-associated pneumonia is classified into two categories, which largely depend on the type of bacteria accessing the lower part of the aero-digestive tract.
It is important to note from the onset, though, that Ventilator-associated pneumonia is a sub-classification of Health acquired pneumonia (APIC, 2009). However, this is only in the instant where a patient has been admitted in the hospital during the mechanical ventilation process. Like many other diseases, the development of VAP is partially contributed to by the presence of a wide range of risk factors. The body should be in a position to fight against diseases though its natural immunity. However, the introduction of foreign objects into the body goes against this principle. VAP arises from mechanical ventilation and, according to O’Keefe-McCarthy, Santiago and Lau (2008); this therapeutic procedure impedes the body and leads to compromised natural immunity of the body to fight against the respiratory infections. In other words, the aspect of introducing a new endotracheal tube deviate the effective cough reflexes, which are very pertinent in protecting the airway against any invasive pathogens. In this case, the endotracheal tube has been considered a major risk factor in the sense that it violates the natural disease resistance mechanisms (Kalanuria, Zai, & Mirski, 2014). It negatively affects the; larynx, glottis, and the cough reflex, which are critical in the respiratory system.
Some studies are in the support of the above findings. According to a panel of experts from the American Thoraic Society (as cited in Sedwick, Lance-Smith, Reeder, & Nardi, 2012), the introduction and positioning of an endotracheal tube increases the chances of the ventilator-associated Pneuomonia complications from 6 to 20 fold among the patients who have been put under the mechanical ventilation therapy. For VAP to occur, however, the microorganisms must have access to the normal sterile lower part aero-digestive tract (Sedwick, Lance-Smith, Reeder & Nardi, 2012). Sedwick, Lance-Smith, Reeder and Nardi (2012), continues to state that most of the seriously ill patients have depressed levels of consciousness and their weakened gag reflex puts them at a relatively higher risk of the microorganisms having quick access to their lower part of the aero-digestive tract. Although some studies have argued that the development of VAP can be attributed to viral and fungi causes, there are no scientific conclusions. Hence, there some studies are still in progress to ascertain this argument (Deem & Treggari, 2010). In that case, and based on the above discussion, most of VAP cases have been attributed to the bacteria causes. Although, the complication can be either early or late onset, the causes are mainly bacterial-related. The former is caused by antibiotic sensitive bacteria while the latter is mainly as a result of antibiotic resistant pathogens. According to Deem and Treggiari (2010), for the development of the VAP to take place, two processes must take place; bacterial colonisation of the respiratory tract and the aspiration of the contaminated secretions of the lower airway.
VAP is a type of pneumonia and hence, from a broader perspective, some the signs and symptoms may be similar to those of patients suffering from pneumonia. However, most of the patients suffering from the ventilator-associated pneumonia will mainly experience the following signs and symptoms. An important point to note is that the signs may present themselves instantly or may develop gradually. Firstly, the patients are highly likely to experience fever, which implies increased body temperatures beyond the normal body temperature range.
Secondly, there is the presence of chills among the VAP patients. This is a situation where the patients experiences extreme cold and subsequent shivering. Chills are largely evident at the onset of an infection and are as result of rapid changes in muscle contraction and relaxation. Pneumonia is as a result of the pulmonary infection, the reasons as to why most of the patients are likely to experience the chills. Although, a chill may present itself as an individual symptom among the patients, there is strong correlation between chills and fever. In this case, PAV tend to experience both of these two symptoms.
Thirdly, some of the patients may also experience a cough as well as the production of the purulent sputum. A cough partly develops as a result of accumulated foreign irritants and mucus build-up in the trachea. As such, it can be regarded as a common reflex action, whose aim is to clear up the above mentioned accumulations and build ups. On the other hand, sputum production refers to the aspect of coughing out the material that is produced in the respiratory tract.
Fourthly, a shortness of breath is another major symptom among the VAP patients. In fact, shortness of breath has largely been associated with lung and heart diseases and VAP is a complication affecting the respiratory system. This is linked to the above-mentioned symptom, which is as a result of mucus build up and the presence of foreign elements in the trachea that eventually, implicate the normal breathing of the patients.
Fifthly, it is not uncommon for the VAP patients to experience thick mucus. As demonstrated in the previous sections, VAP majorly affects the respiratory tract. The mucus membrane is aligned on the trachea implying that most of the mucus processes take place in the aero-digestive tract. As previously demonstrated, the mechanical ventilation and intubation take place in the respiratory tract. Therefore, the development of VAP, which mainly affects the respiratory tract, will have an impact on the mucus formation and excretion processes.
Finally, some of the patients suffering from VAP complication may experience chest pain symptoms. The primary cause of the chest pain is associated with heart’s muscle problems when the muscle is unable to access enough blood, rich in oxygen. From the preceding sections, it is apparent that the patients of VAP will experience decreased oxygenation. Eventually, the blood will be oxygen deficient (Hypoxemia), thereby triggering the problem of chest pain. Furthermore, lung-related problems have been linked to the causes of chest pain and, hence VAP is not an exceptional.
To this present day, there is no standard diagnostic criterion that has been recommended for VAP and, hence the diagnostic approach to use is still elusive. In fact, some studies have argued that the detection of nosocomial pneumonia, especially VAP, is very difficult to diagnose (Tablan et al., 2003). The traditional methods that have largely been used in the diagnosis criteria of the VAP include; the combined existence of the development of the purulent sputum, coughing, and existence of fever. The cultures of the sputum and some clinical criteria are sensitive for bacterial pathogens. However, some studies have imputed the ability of the above to diagnose VAP, as they are not specific. The culture of the blood has also not been considered effective in testing the presence of VAP (Tablan, 2003).
However, according to Tablan et al., (2003), some methods of diagnosing pneumonia, which extends to VAP, were proposed back in the year 1992 by a group of investigators. These were considered the standard diagnosis methods for detecting this medical complication. The methods incorporated the aspect of carrying out the bronchoscopic techniques on the patient (Tablan et al., 2003). However, with time more researches have been conducted and have established that using bronchoscopic methods can lead to more complications considering that they are invasive in nature.
According to the Infectious Diseases Society of America (AIDS) and the American Thoracic Society (ATS), the diagnosis of VAP can be made possible through the extraction of some samples from the lower aero-digestive tract, which can then be used for culture and microbiology. According to AIDS and ATS, the samples can be either qualitative or quantitative.
Additionally, based on the guidelines proposed by the Infectious Society of American and the American Thoracic society, the tracheal aspirates can be used for the negative predictive value (Kalanuria, Zai, & Mirski, 2014). Johnson et al., (as cited in Kalanuria, Zai, & Mirski, 2014), offered the description of the clinical diagnosis for VAP as described below. According to authors the psychological, microbiological, clinical, and radiographic evidence are taken into account by the clinical pulmonary infection score (CPIS), which let a numerical value to help predict the existence of the ventilator-associated pneumonia (Munro & Ruggiero, 2014). The score range is between 0 and 12, and the score value of more than 6 indicates a strong correlation with the incidence of ventilator-associated pneumonia. However, despite the existence and application of the CPIS, there are debates revolving around its diagnostic validity (Kalanuria, Zai, & Mirski, 2014). The inter-observer variability in CPIS remains significant regardless of its straightforward computation.
This denotes the aspect of using medical imaging in the detection, such as the X-rays of the chest in the diagnosis process. Previous studies have imputed the possibility of the normal chest radiograph in the diagnosis of the presence of VAP (Munro & Ruggiero, 2014). Some of these studies have argued that the asymmetric pulmonary infiltrates that are consistent with the ventilator-associated pneumonia can result from among other causes such as drug reaction, chemical penumonitis, and pulmonary embolism among others. The total radiographic specificity of a pulmonary opacity consistent with pneumonia stands at between 27 and 35 percent. However, medical researchers are convinced that the high specificity degrees present in some of the radiograph findings can be very critical and effective in the diagnosis of the pneumonia, especially in the case where it is present. Although the radiographic diagnosis criterion has been considered to have specificity percentage of 96, radiographic abnormalities are common (Munro & Ruggiero, 2014).
The clinical criteria for the diagnosis of the Ventilator-associated pneumonia require the mandatory use of the portable chest radiograph. However, the use of this approach is considered to present specificity and sensitivity challenges. Studies have, additionally, cited low-quality of the films, obtained from the chest X-rays as presenting another compromise to diagnosing the presence of VAP. What is evident is that the clinical criterion in the diagnosis of VAP has limited diagnostic accuracy. The development of purulent tracheobronchial secretions, leukoytosis, and chest radiograph predicate the presence of suspected Ventilated-associated pneumonia (Kalanuria, Zai, & Mirski, 2014). However, the clinical diagnosis criterion for pneumonia has been limited in the diagnosis of the Ventilator Associated Pneumonia relative to its appropriateness in the diagnosis of community acquired pneumonia. Previous studies have stated that; more diagnostic symptoms have to be used in the combination of the above mentioned three. They further establish that the elimination of one of the above-mentioned clinical variables will reduce the sensitivity and the use of a single variable declines it further. Further, such studies have argued that symptoms such as fever, leukoytosis, and tachycardia, which are common symptoms of VAP, do not qualify as the final specific diagnostic criteria considering that they are present in other medical conditions (Munro & Ruggiero, 2014). Additionally, patients receiving mechanical ventilations are likely to exhibit purulent tracheal bronchial secretions, which in such a case are not caused by the presence of pneumonia. The sensitivity of VAP among the above discussed cluster of patients is more challenging for those patients suffering from Acute Respiratory Disease Sydrome (ARDS) (Center for Disease Control and Prevention, 2014). According to the clinical VAP diagnosis approach, the diagnosis of the nosocomial tracheobronchotis is only validated if there is the presence of leukocytosis, fever, and purulent sptum that has a positive sputum culture. However, in such a case scenario, there has to be the absence of any new lung infliltrate. Nosocomial tracheobronchial has largely been associated with the longer ICU stay and extended time on the ventilator for the patients undergoing the mechanical ventilation. In the case of the clinical criteria diagnosis criterion, the CPIS is largely recommended as compared to the direct therapy. Although it is sensitive, the chest radiography is typically nonspecific. On the other hand, the clinical diagnosis criterion has been used alongside other features in the diagnosis of the ventilator-associated pneumonia. To this point, CPIS has been considered helpful in the diagnosis of VAP. Unfortunately, it has moderate performance and a considerably high degree of inter-observer variability, which compromises its reliability in VAP diagnosis.
The microbiologic diagnosis criterion has been considered the most appropriate approach in the diagnosis of ventilator-associated pneumonia. This method makes use of invasive techniques, which require the aspect of obtaining samples such as B-PSB, NB-BAL, and B-BAL. The samples are later on evaluated through the use of Gram stain, which uses quantitative cultures (Marti & Ewig, 2011). Based on previous findings, there can also be the use of less invasive suctioning of the trachea (Marti & Ewig, 2011). This way, there is the yielding of valuable ETAs that are later accessed by the bacterial culture and Gram stain, either semi-quantitatively or quantitatively. Gram stain has been considered reliable in the sense that it provides rapid information on the quality of the specificity as well as the number and morphology of the infecting pathogens. The presence of any offending bacteria is made possible by the morphology of that particular bacterium. Also, the presence of a myriad of squamous epithelial cells indicates the presence of oral contamination of the particular specimen (Kalanuria, Zai, & Mirski, 2014). The infections leading to the emergence of the ventilator-associated pneumonia are suspected in the case where the Gram stain is contaminated or colonized by relatively too many bacteria and polymorphonuclear cells (Marti & Ewig, 2011).
However, there is a strong negative predictive value for the presence of VAP in the case where Gram stain of the ETA or sputum has no inflammatory cells and there is non-existence of bacteria. This is primarily because, the fever detected as being the cause of the VAP may have been as a result of another medical conditions. The invasive techniques, B-PSB (10^3 cfu/ml), NB-BAL (10^4 cfu/ml), and B-BAL (10^4 cfu/ml) have presented the standardization criteria in the diagnosis of VAP (Kalanuria, Zai, & Mirski, 2014). Any quantitative cultures, with values ranking below the above stipulated thresholds, imply a colonization or contamination by other exceptions. Most of the laboratory tests make use of the semi-quantitative techniques and there is no single quantitative technique that can be used in the diagnosis of an infection. Most of the laboratory tests make use of the threshold of > (greater or equal to) 10^5 cfu/ml. Any growth of pathogens below the pre-stated threshold is mostly associated with colonization (Kalanuria, Zai, & Mirski, 2014).
Previous studies have established that the interplay between risk factors and the presence of the endotracheal tube largely contribute to the development of the Ventilator associated pneumonia (Kalanuria, Zai, & Mirski, 2014). As demonstrated in the preceding sections, the onset and development of the ventilator-associated pneumonia is triggered by the invasion of the lung parenchyma and the lower sections of aero-digestive tract by microorganisms. The pathogenesis of VAP, whether nosocomial or ICU acquired, is highly characterized by the invasion and colonization of the oral cavity by aero-digestive pathogens that access the lower sections of the respiratory tract. Most of the patients admitted in the intensive care units often suffer from critical medical conditions and their overall bodies’ natural immunity, to fight against any potential infections, is compromised. One of the factors that have been attributed to the eruption of pneumonia is the inability of the host patient’s inability to fight against any invading microbial pathogens. The reduced state of the immune system has been linked with the interplay of a myriad of multilevel factors.
Ventilator- associated pneumonia accounts for approximately 30 percent of the all the ICU-related infections. VAP has the probability of increasing the hospital stay among the affected patients and may also negatively affect the overall outcome (Klompas, 2014). According to Deem and Treggiari (2010), an argument can be made that relative to the ventilator, the endotracheal tube predisposes the high susceptibility to VAP among the ICU patients. The positioning and regular maintenance of the tube through the glottis increases the chances of developing the VAP (Hess, et al., 2003).
According to Kalanuria, Zai, and Mirski, (2014), bacteria can access the lower respiratory tract in four major ways. Firstly, they can do this by impairing the mucociliary clearance of secretions and the placement of the endotracheal tube has been found to increase this risk considering that it depresses the epiglottic reflexes and also prevents the mucociliary clearance of secretions (Kalanuria, Zai, & Mirski, 2014). In such cases, the bacteria will travel around the cuff or through the tube in small quantities. What follows is the embolization of the bacteria into the lungs after every other breath. Secondly, the bacteria can pool and trickle secretions around the cuff, through the micro-aspirations of secretions. Most of the aspirations, among the patient subjects, happen during the night. Risk factors are higher among the hospitalized and ICU patients and especially the ones who have undergone the mechanical ventilation process (Hess, 2003). This is mostly among the patients who have an underlying disease as well as the patients who have been put under sedative drugs, which are common in the Intensive care units. Studies have established that most cases of micro aspirations are linked to high volume-low pressure inflated ETT cuffs (Huff, 2003). Thirdly, the access can be accelerated during the instances when the intubation is being performed. Aspiration and oropharyngeal secretions are bound to occur during the intubation process (Deem & Treggiari, 2010). Finally, the bacteria access can be triggered by the development of a biofilm lumen in the tube. According to Deem and Treggiari (2010), there is a strong concordance between tracheal-suction samples, obtained from VAP patients, and the biofilm. Further, the study establishes that the biofilm creates a good environment for the proliferation of the bacteria while at the same time acting as a resistant to antibiotics. Eventually, the increase of the bacteria in the aero-digestive tract leads to its colonization. Consequently, the excess secretions, presence of aspirated oesophageal as well as the pools and leaks have relatively high potential of infiltrating the lungs, thereby, causing the Pneumonia and, in this case, the Ventilator Associated Pneumonia (Kalanuria, Zai, & Mirski, 2014).
According to O’Keefe-McCarthy, Santiago and Lau (2010), the risk factors linked to the ventilator-associated pneumonia include the ones that can increase the possible aspiration and oral secretions as well as those that impair a patient’s defence system. Additionally, according to Ablan et al., (2003), the potential risk factors associated with the nosocomial bacteria related pneumonia have been researched in several studies. According to these authors, the risk factors can be categorized into four major groups despite the fact that the populations that were used in the studies varied slightly. These risk factors include the following; firstly, the factors that promotes the colonization of the oropharynx by microorganisms. Secondly, other risk factors include the conditions that favour the aspirations into the reflux or the aero-digestive tract from the gastrointestinal tract. Thirdly, the conditions that require the prolonged dependence on the mechanical ventilatory support and which have potential exposure to respiratory devices that are contaminated or are in constant contact with colonized hands, especially in the case of the healthcare personnel. In this line, there should be more education on ventilator-associated pneumonia (AARC, 2003). Finally, there is a cluster of other factors such as extreme underlying conditions, malnutrition, and the ones that are age-related (Ablan et al., 2003). The risk factors can be either modifiable or non-modifiable. The modifiable risk factors are the ones that can be prevented and are amenable to change since they are within human control, for instance physical inactivity and discharge from the ICU. On the other hand, the non-modifiable risk factors are the ones that are beyond human control and there is nothing that can be done to alter or reduce them, for instance age and sex.
As regards VAP, the modifiable risk factors include the following discussed. One of the risk factors associated with the ventilator-associated pneumonia is the issue of colonized hands among the healthcare personnel. The issue of “unclean” hands is not uncommon as a lead risk factor to nosocomial and ICU acquired infections. The use of combined interventions is appropriate in the prevention of VAP. For instance, there is a need to use enough staffing, alcohol-based hand sterilizations, and education-based infection-control interventions so as to reduce the VAP incidence levels (APIC, 2009).
Secondly, increased aspiration of microorganisms, which are rich in colonizing flora bacteria, into the lower parts of the aero-digestive tract promote the incidence of VAP. Through the use of subglottic secretions, there is a high probability of reducing the incidence of Ventilator associated pneumonia.
Thirdly, the incidence of VAP is triggered by the bacteria formation during the intubation process and is also largely dependent on the longevity of the mechanical ventilator in the body. The ventilators should be avoided at all costs (Klompas, 2014). There could also be the use of alternative strategies and application of non-invasive methods, Non-invasive positive pressure ventilation, so as to reduce the incidence of the disease.
Fourthly, some studies have cited the formation of the biofilm as one the risk factors that increases the incindence of VAP (Klompas, 2014). The bacterial biofilm is formed on the inner side of the endotracheal tube. Eventually, the accumulation of these bacteria results in resistance to antibiotics. Additionally, they lead to the humoral and cellular defenses and have been attributed to increased recurrence rates of infections. Some of the bacteria that have been linked to the formation of the biofilm include among others the pseudomonas (Klompas, 2014). What follows is the mechanical dislodge of the bacteria through the bronchoscope, airway, and the suction catheters in the trachea. Eventually, this increases the incidence rate of VAP. This incidence rate can be corrected by making use of antimicrobial agents in coating all the intravascular catheters such as in the case with the intubation and mechanical ventilation performed in the respiratory tract. Consequently, this will help mitigate a large number of infections that are device-associated.
Finally, the presence of the Oropharyngeal colonization has linked to VAP incidence. This is caused by the p. Aeruginosa and entric gram-negative bacteria. The Oropharyngeal colonization is positively correlated with the time of admission as well as the length of stay in the ICU (Wunderink & Rello, 2011). In this case, the intonation of the Oropharyngeal colonization can be achieved through the optimal use of the appropriate chlorhexidine therapy and antibiotics.
A number of strategies have been proposed as mechanisms to helping prevent the incidence of VAP. Most of the VAP prevention strategies focus on the contamination of equipment used, the colonization of the respiratory tract, and aspiration (APIC, 2009). According to Kalanuria, Zai and Mirski (2014), there are five VAP bundles that can be used in the mitigation and improvement of the VAP outcome. Firstly, there is the need to have a daily sedation assessment as well as spontaneous breathing tests, accompanied with possible and effective extubation. Secondly, there is a need to have a deep venous thrombosis prophylaxis. Thirdly, there is a need to avoid the supine head positioning by ensuring the appropriate head elevation. Fourthly, there is a need to use chlorhexidine as a daily oral care (Health Protection Scotland, 2012). Finally, the healthcare personnel should consider the concept of stress ulcer prophylaxis (Sedwick, Lance-Smith, Reeder, & Nardi, 2012). According to O’Keefe-McCarthy, Santiago and Lau (2008), the collective implementation of all the VAP bundles achieves better outcome as compared to the individual application. Eventually, this reduces the incidence of VAP. In connection to the above, there is a need to adopt the following prevention strategies if success is to be achieved.
The first prevention to use is extubation. From the above-discussed risk factors, it is clear that one potential to the increased incidence rates is the time span of the endotracheal tube (APIC, 2009). This is also captured in the five “VAP Bundles”. In this connection, therefore, there is a need to perform daily tests on patients’ weaning to mitigate the higher chances of VAP incidence (O’Keefe-McCarthy, Santiago & Lau, 2009). The second prevention strategy can be obtained from the “VAP Bundles”, which require the proper position of a patient’s head. There is a need to ensure a semirecumbent head positioning for the ventilated patients (APIC, 2009; Deem & Treggiari, 2010). The third highly ranked prevention strategy is to ensure minimized or zero instrumentation of the aero-digestive tract. In other words, the healthcare personnel should try as much to avoid the use of endotrachea tube, which eventually increases the rates of bacteria colonization (APIC, 2009; Deem & Treggiari, 2010). In this connection, APIC 2009, cites the issue of hand hygiene as being a contributor risk factor to VAP incidence. The fourth prevention strategy is the decontamination of the f the oropharynx with topical chlorhexi-dine, which has been cited by APIC, (2009) as well as Deem and Treggiari (2010). This concept is also captured in the VAP bundles. The fifth prevention strategy can be adopted from the article by Deem and Treggiari (2010), who proposes the use of modified designs of the endotracheal tube so as to reduce the issue of biofilm formations. The sixth VAP prevention strategy stems from VAP bundles and has been stressed by Dickinson and Zalewski (2016), and regards the use of antiseptic agents such as chlorhexidine in the daily mouth care. Other proposed prevention approaches include mobility and nutrition, which pertain to reduced time length of bed rest and enteral feeding respectively (APIC, 2009).
Surveillance for Ventilator-Associated Events (VAE) and VAP, and the Rationale for the VAE/VAP Surveillance Definition Algorithm
Due to the challenges experienced in the accurate diagnosis of VAP, the National Healthcare Safety Network (NHSN) came up with new surveillance approach, VAE that includes VAP. VAE is an acronym to Ventilator-Associated-Events. According to the Center for Disease Control and Prevention (2014), VAEs constitutes the combination of objective criteria, which are commonly referred to as the 3-tiers. These include; “deterioration in respiratory status after a period of stability or improvement on the ventilator, evidence of infection or inflammation, and laboratory evidence of respiratory infection” (Center for Disease Control and Prevention, 2014, p. 18).
The surveillance definition algorithm of VAE, as proposed by the NHSN, has a definition rationale that utilizes the following five steps. The first step focuses on the Ventilator-Associated Events (VAE) Surveillance Algorithm. It concentrates on the patient stability improvement while in the ventilator, oxygenation, temperature variations, antimicrobial agents, purulent respiratory secretions, and positive cultures. The second stage revolves around issues on the Ventilator-Associated Condition (VAC). It focuses on the baseline improvement of a patient stability on the ventilator. This should be “defined by more than or equal to 2 calendar days of stable daily decreasing minimums*FiO2 or PEEP values” (Center for Disease Control and Prevention, 2014, p. 18). Different indicators of worsening oxygenation must also be assessed on a daily basis. In the third step, the focus is on the Infection-related Ventilator-Associated Complications (IVAC), which requires the patient to have met the VAC criteria. Worsening oxygenation criteria, temperature variations, and antimicrobial agents must be taken into consideration during this stage. The fourth step focuses on the Possible Ventilator-Associated Pneumonia (VAP), which necessitates the client to meet both the VAC and IVAC criteria. Additionally, factors relating to worsening oxygenation and purulent respiratory must be taken into account. Alternatively, positive cultures can be used in the place of the purulent respiratory. The final step relates to the Probable Ventilator-Associated Pneumonia (VAP) and requires the patient to have met the VAC and IVAC criteria. Additionally, there has to be the assessment of the worsening oxygenation criteria as well as one of a host of other factors such as the positive fleural fluid culture; positive lung histopathology; positive diagnostic test for aero digestive tract secretions; or positive culture of, lung tissue and protected specimen brush among others.
As opposed to the traditionally used VAP diagnostic approaches, which lack accuracy, the new VAE surveillance algorithm definition is able to address the diagnosis issues. The suspected patient is put under the five different stages that take into account all the possible criteria used in the diagnosis process.
Previous studies have demonstrated that VAP has continued to be major medical complication increasing the morbidity and mortality rates among the critically ill patients (Stevens, 2014). Major developments are being made regarding this disease including coming up with appropriate diagnostic methods such as the one adopted by the NHSN, VAE/VAP surveillance definition. Eventually, this implies that treatment will be offered on evidence-based diagnosis that goes beyond the traditional and inaccurate VAP diagnosis such the clinical, radiology, and microbiologic approaches. Besides the increased mortality rates, there are high costs incurred among the VAP patients to cover for the mechanical ventilation and intubation. Additionally, the patients are likely to suffer from lung-induced injuries as well discomfort especially in cases where there is delayed removal of the mechanical ventilator. Fourthly, there could be medical negligence during the mechanical ventilation and intubation process and this may lead to ventilatory muscle fatigue. Finally, there is likelihood of extended length of hospital and ICU stay among the patients suffering from ventilator-associated pneumonia (Stevens, 2014).
Conclusively, the above discussion has established that ventilator-associated pneumonia accounts for a large number of mortality and morbidity rates in the United States. Early onset VAP is acquired within the first 48-96 hours after mechanical ventilation or intubation. On the other hand, late onset VAP sets in several days after the mechanical ventilation or intubation. This medical complication has several negative implications, which doubles as disadvantages. The primary cause of VAP is mechanical ventilation and intubation. Traditionally, there has been no accurate diagnosis for VAP and the medical fraternity has relied on the radiology, clinical, and microbiological criteria. There are four different mechanisms through which the development of the ICU acquired VAP can occur. However, there are some modifiable risk factors that can help mitigate the incidence of VAP, if properly controlled. These are the risk factors that are within the control of the patients and the healthcare providers. Eventually, these risk factors have some connection with some of the VAP prevention strategies that can be used in the mitigation or total elimination of the disease’s incidence. The lack of reliable and accurate VAP diagnosis criteria has necessitated the development of a new diagnosis approach, ventilator-associated events (VAE). The new criterion follows a surveillance definition algorithm that incorporates five steps and three tiers. The adoption of the new diagnosis criterion helps incorporates different VAP-related symptoms, thereby ensuring diagnosis specificity. Huge costs, injuries on the respiratory tract, increased mortality rates, and elongated hospital stays are some of the outcomes of VAP.
AARC. (2003). Care of the ventilator circuit and its relation to ventilator-associated pneumonia. AARC Evidence-Based Clinical Practice Guidelines, 48(9), 869-879.
APIC. (2009). Guide to the elimination of ventilator-associated pneumonia. K Street, NW: APIC.
Center for Disease Control and Prevention. (2014). Ventilator-Associated-Event. Device Associted Module, 10, 1-46.
Deem, S & Treggiari, M. M. (2010). New endotracheal tubes designed to prevent ventilator associated pneumonia : Do they make a difference?. Respiratory Care, 55(8), 1046-1055.
Dickinson, S & Zalewski, C. A. (2016). Oral care during mechanical ventilation-critical for VAP prevention. Society of Critical Care Medicine, 1-4.
Health Protection Scotland (2012). What are the key prevention and control recommendations to inform a minimising ventilator associated pneumonia (VAP) quality improvement tool?, National Services Scotland, 1-12.
Hess, D. R., Kallstrom, T. J., Mottram, C. D., Myers, R., Sorenson, H. M., & Vines, D. L. (2003). AARC evidence-based clinical practice guidelines: Care of the ventilator circuit and its relation-associated pneumonia. Respiratory Care, 48(9), 869-879.
Kalanuria, A. A., Zai, W., & Mirski, M. (2014). Ventilator-associated pneumonia in ICU. Critical Care, 1-8.
Klompas, et al. (2014). Strategies to prevent ventilation-associated pneumonia in acute care hosptials: 2014 update. Infection Control and Hospital Epidemiology, 35(8), 1-23.
Marti, A. T., & Ewig, S. (2011). Nosocomial and ventilator-associated pneumonia. Sheffield: European Respiratory Society.
Munro, N & Ruggiero, M. (2014). Ventilator associated pneumonia bundle. American Association of Critical-Care Nurses, 25(2), 163-175.
O’Keefe-McCarthy, S., Santiago C., & Lau, G. (2008). Ventilator-associated pneumonia bundled strategies: An evidence-based practice. World Views on Evidence-Based Nursing, 5(4), 193-204.
Tablan, O. C., Anderson, L. J., Besser, R. Bridges, C., & Hajjeh, R. (2003). Recommendations of CDC and the healthcare infection control practices advisory Committee. Guidelines to Preventing Healthcare Associated Pneumonia, 1-179.
Sedwick, M. B., Lance-Smith, M., Reeder, S. J., & Nardi, J. (2012). Using evidence-based practice to prevent ventilator-associated pneumonia. Critical Care Nurse, 32(4), 41-51.
Stevens, J. P., Silva, G., Gillis, J., Novack, V., Talmor, D., Klompas, M., & Howell, M. D. (2014). Automated surveillance for ventilator-associated pneumonia. CHEST, 146(6), 1612-1618.
Wunderink, R. G., & Rello, J. (2001). Ventilator-Associated Pneumonia. Boston, MA: Springer US.