Preethi, J (2010) A Study on Microbial etiology of Ventilator associated Pneumonia. Masters thesis, Madurai Medical College, Madurai.
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Abstract
INTRODUCTION: Pneumonia is an inflammation of the lung that is most often caused by Infection with bacteria, viruses, or other organisms. Occasionally, inhaled Chemicals that irritate the lungs can cause pneumonia. Healthy people can Usually fight off pneumonia infections. However, people who are sick, Including those who are recovering from the flu (influenza) or an upper Respiratory illness, have weakened immune systems that make it easier for Bacteria to grow in their lungs. When air is inhaled through the nose or mouth, it travels down the trachea to The bronchus, where it first enters the lung. From the bronchus, air goes through The bronchi, into the even smaller bronchioles and lastly into the alveoli 2. DEFINING PNEUMONIA BY LOCATION IN THE LUNG Pneumonia may be defined according to its location in the lung: Lobar pneumonia occurs in one part, or lobe, of the lung. Bronchopneumonia tends to be scattered throughout the lung. DEFINING PNEUMONIA BY ORIGIN OF INFECTION COMMUNITY ACQUIRED PNEUMONIA (CAP). People with this type of Pneumonia contracted the infection outside a hospital setting. It is one of the Most common infectious diseases. It often follows a viral respiratory infection, Such as the flu. Commonest organism causing CAP is Streptococcus Pneumoniae. Other pathogens include Haemophilus influenzae, Mycoplasma, And Chlamydia. HOSPITAL ACQUIRED PNEUMONIA.(HAP) Hospital-acquired Pneumonia is an infection of the lungs contracted during a hospital stay. This Type of pneumonia tends to be more serious, because hospital patients already Have weakened defense mechanisms, and the infecting organisms are usually More dangerous than those encountered in the community. Hospital patients are Particularly vulnerable to Gram-negative bacteria and staphylococci. Hospitalacquired Pneumonia is also called nosocomial pneumonia. A subgroup of hospital-acquired pneumonia is Ventilator-Associated Pneumonia (VAP), a highly lethal form contracted by patients on ventilators in Hospitals and long-term nursing facilities. Ventilator associated pneumonia (VAP) is defined as nosocomial pneumonia occurring in a patient after 48 hours Of mechanical ventilation via a tracheal or tracheostomy tube. It is commonly Classified as either early onset (occurring within 96 hours of start of mechanical Ventilation) or late onset (>96 hours after start of mechanical ventilation). It is a Common condition, difficult to diagnose accurately, and expensive to treat. Its Development prolongs a patient’s stay in the intensive care unit (ICU), and is Associated with significant morbidity and mortality. Most cases seem to result From aspiration of pathogenic material that commonly colonises the Oropharyngeal airways of the critically ill. Simple measures to decrease the Incidence of aspiration or reduce the burden of colonisation of the oropharynx May aid in the prevention of ventilator associated pneumonia. A favourable Outcome seems to be more likely if appropriate antibiotics are given in a timely Manner EPIDEMIOLOGY INCIDENCE The incidence of Ventilator associated pneumonia (VAP) was 7% to 70%. Generally, the rates of VAP in surgical ICU were higher than in medical icus, Depending on the differences in the patient population, surgical disorders, the Proportion of patients that needed MV and the duration of ventilation. The risk Of pneumonia increased by the duration of MV and the highest risk was during The first 8–10 days. The need for reintubation, urgent intubation and Documented massive aspiration are also associated with high incidence of VAP. In Korea, the incidence of VAP is 3.5 to 7.1 per 1000 ventilator days. In India Overall rate of VAP of 8.95 per 1000 ventilator days 119 MORTALITY VAP is associated with increases in morbidity and mortality, hospital length of Stay, and costs. The mortality rate attributable to VAP is 27% and has been as High as 43% especially when antibiotic resistant bacteria were responsible. Length of stay in the intensive care unit is increased by 5 to 7 days and hospital Length of stay 2- to 3-fold in patients with VAP. Mortality is more likely when VAP is associated with certain microorganisms (Pseudomonas, Acinetobacter), Blood stream infections, and ineffective initial antibiotics. VAP is especially Common in people who have acute respiratory distress syndrome (ARDS). In The Philippines, the crude mortality rate for hospitalized patients with Pneumonia was 42.4%, with a mortality rate attributable to infection of 30.1%. India on HAP that found an overall crude mortality of 67.4% in ICU patients With pneumonia, with 40% of the mortality in these patients attributable to Infection alone 119. Risk factors for ventilator-associated pneumonia Duration of mechanical ventilation Aspiration of gastric contents Chronic obstructive pulmonary disease Histamine type-2 receptor antagonist Nasal intubation and/or sinusitis Use of positive end-expiratory pressure Reintubation Intracranial pressure monitoring and/or depressed consciousness Winter season Daily ventilator circuit changes Thoracic or upper abdominal surgery Age Multiple organ system failure Prior antibiotic administration Supine head positioning (i.e., head of bed not elevated) Duration of hospitalization prior to mechanical ventilation PATHOPHYSIOLOGY Ventilator associated pneumonia (VAP) primarily occurs because the Endotracheal or tracheostomy tube allows free passage of bacteria into the Lower segments of the lung in a person who often has underlying lung or Immune problems. Bacteria travel in small droplets both through the Endotracheal tube and around the cuff. Often, bacteria colonize the Endotracheal or tracheostomy tube and are embolized into the lungs with each Breath. Bacteria may also be brought down into the lungs with procedures such As deep suctioning or bronchoscopy. Whether bacteria also travel from the sinuses or the stomach into the lungs is, As of 2005, controversial. However, spread to the lungs from the blood stream Or the gut is uncommon. Once inside the lungs, bacteria then take advantage of any deficiencies in the Immune system (such as due to malnutrition or chemotherapy) and multiply. A Combination of bacterial damage and consequences of the immune response Lead to disruption of gas exchange with resulting symptoms. 91 Pathogenic mechanisms for infection of the lower Respiratory tract MICROBIOLOGY The microbiologic flora responsible for Ventilator associated pneumonia (VAP) Is different from that of the more common community-acquired pneumonia (CAP). In particular, viruses and fungi are uncommon causes in people who do Not have underlying immune deficiencies. Though any microorganism that Causes CAP can cause VAP, there are several bacteria which are particularly Important causes of VAP because of their resistance to commonly used Antibiotics. These bacteria are referred to as multidrug resistant (MDR). Pseudomonas aeruginosa is the most common MDR Gram-negative Bacterium causing VAP. Pseudomonas has natural resistance to many Antibiotics and has been known to acquire resistance to every antibiotic Except for polymixin B. Resistance is typically acquired through up Regulation or mutation of a variety of efflux pumps which pump Antibiotics out of the cell. Resistance may also occur through loss of an Outer membrane porin channel (oprd) Klebsiella pneumoniae has natural resistance to some beta-lactam Antibiotics such as Ampicillin. Resistance to cephalosporins and Aztreonam may arise through induction of a plasmid-based extended Spectrum beta-lactamase (ESBL) or plasmid-based ampc-type enzyme. Enterobacter, Citrobacter and also Serratia marcescens as a group also Have an inducible ampc gene, which can be induced by exposure to Antibiotics such as cephalosporins. Thus, culture sensitivities may Initially indicate appropriate treatment which fails due to bacterial Response. They may also develop resistance by acquiring plasmids. Stenotrophomonas maltophilia and Acinetobacter often colonizes people Who have endotracheal tubes or tracheostomies but can also cause Pneumonia. They are often resistant to a wide array of antibiotics but are Usually sensitive to co-trimoxazole. Burkholderia cepacia is an important organism in people with cystic Fibrosis is often resistant to multiple antibiotics. Methicillin-resistant Staphylococcus aureus is an increasing cause of VAP. As many as fifty percent of Staphylococcus aureus isolates in the Intensive care setting are resistant to methicillin. Resistance is conferred By the meca gene. 106 Nosocomial virus and fungal infections are uncommon causes of HAP and VAP In immunocompetent patients. Fungal pathogens causing VAP are Aspergillus Species and Candida albicans. DIAGNOSIS The diagnosis of pneumonia in mechanically ventilated patients is difficult, and Still there is no "gold-standard" diagnostic method. It is usually based on the Combination of clinical, radiological, and microbiological criteria defined by Centers for Disease and Control (CDC) CDC criteria for ventilator associated pneumonia Three or more of the following criteria: Rectal temperature >38°C or <35.5°C Blood leucocytosis (>10.103/mm3) and/or left shift or blood Leukopenia (<3.103/mm3) More than ten leukocytes in Gram stain of tracheal aspirate (in high Power field) Positive culture from endotracheal aspirate New, persistent, or progressive radiographical infiltrate But these criteria have low sensitivity and specificity. The systemic signs fever, Leukocytosis, etc.) Of infection can be seen by any condition in ICU pulmonary Edema, pulmonary infarction, after surgery, trauma, devascularized tissue, open Wounds, etc.). Investigators reported that the clinical diagnosis of VAP is Associated with 30–35% false-negative and 20–25% false-positive Results. And Also, ICU patients do not always have systemic signs of infection due to their Underlying disease (chronic renal failure, immunosuppression, etc.). Radiological infiltration has limited value, mimicking by cardiogenic Pulmonary edema, noncardiogenic pulmonary edema, adult respiratory distress Syndrome(ARDS), atelectasis, pulmonary contusion, which are not uncommon In ICU. The upper respiratory tract of patients is colonized with potential pulmonary Pathogens a few hours after intubation .Consequently, isolation of pathogens From tracheal secretions do not always indicate pulmonary infection. But a Positive Gram's stain may guide the initial antibiotic therapy. However prior Antibiotic and corticosteroid therapy can reduce the sensitivity of this technique CLINICAL PULMONARY INFECTION SCORE (CPIS) This score combine the seven variables (temperature, leukocytes, tracheal Aspirate volume and purulence of tracheal secretions, chest X-ray, oxygenation- Pao2/fio2- and semi quantitative culture of tracheal aspirate) for the diagnosis Of VAP, defined as clinical pulmonary infection score (CPIS) Clinical pulmonary infection score Temperature, °C ≥ 36.5 and ≤ 38.4 0 point ≥ 38.5 and ≤ 38.9 1 point ≥ 39.0 and ≤ 36.0 2 point Blood leucocytosis, mm3 ≥ 4000 and ≤ 11 000 0 point <4000 and >11 000 1 point +band forms ≥ 500 + 1 point Tracheal secretions <14+ of tracheal secretions 0 point ≥ 14+secretions 1 point +purulent sputum +1 point Oxygenation: pao2/fio2, mmhg >240 or ARDS 0 point Chest X-ray No infiltrate 0 point Diffused, or patchy infiltrate 1 point Localized infiltrate 2 point Culture of tracheal aspirate (semi-quantitative: 0- 1-2 or 3+) ≤ 1 or no growth 0 points Pathogenic bacteria cultured >1+ 1 point >1+ and same pathogenic bacteria seen in Gram stain 2 point The score varied from 0 to 12 points and was reported that a CPIS of more than Six was associated with a sensitivity of 93% and a specificity of 100% for the Diagnosis of pneumonia. However, the original scoring system has some Limitations; that it requires 24–48 hours for the results of tracheal aspirate Cultures, and also identifying pulmonary infiltrates progression depends on Intensivist experience. Modified CPIS (calculated at baseline from the first five Clinical variables, and CPIS at 72 hours was based on all variables of the score) That antibiotics were stopped in patients with a persistent low score (<6) after 3 Days of therapy, avoiding unnecessary use of antibiotics, and all patients who Discontinued the therapy improved. The modified CPIS does not perform better When the clinical suspicion of pneumonia is high, so they proposed Incorporating the results of specimens gram stain (by adding two more points When gram stains were positive) to modified CPIS to increase the sensitivity of The score and the physicians' diagnostic accuracy. Qualitative cultures of tracheal aspirate (TA) is not a specific diagnostic Method because of the lower respiratory tract colonization and a high Percentage of false-positive results .However, investigators reported that Quantitative cultures of TA have equal diagnostic accuracy to the other invasive Techniques . Although, quantitative cultures of TA is non-invasive, inexpensive And a simple method, it has some risks, that if the cut-off value ≥ 106 cfu/ml is Used, sensitivity will be low and some patients with VAP may not be identified Or when the cut-off value ≥ 105 cfu/ml is used, unnecessary antibiotic treatment Will be given because of low specificity. 96 INVASIVE TECHNIQUES FOR THE DIAGNOSIS OF VAP 1. Protected-specimen brush (PSB) 2. Bronchoalveolar lavage (BAL) 3. Blood or pleural fluid In PSB, 0.001 ml of secretions are collected and the presence of >103 cfu/ml Bacteria have 80–90% sensitivity and 95% specificity for the diagnosis of VAP. In BAL, larger proportion of lung can be sampled and the diagnostic threshold Is >104 cfu/ml. The sensitivity and specificity of BAL are 86–100% and 95– 100%, respectively .102 The disadvantages of these invasive techniques are; A) Prior antibiotic use may decrease the sensitivity and accuracy of these Methods. B) These techniques are based on quantitative culture and results of these Cultures require 24–48 hours, and, therefore miss early cases, and also Give no information about appropriate initial antibiotic therapy. C) These invasive tests may worsen the patient's status (cardiac Arrhythmias, hypoxemia, bleeding, etc.). D) Increase the costs of caring. E) It has not been proven that the use of these invasive techniques lead to A decrease in patients' mortality. The spread of microorganism to blood or pleural space is <10%, so blood and Pleural effusion cultures have low sensitivity and specificity. Blood cultures in Patients with VAP are useful if there is suspicion of another probable infectious Condition, but the isolation of a microorganism in the blood does not confirm That microorganism as the pathogen causing Ventilator Associated Pneumonia. Therefore, two sets of blood samples for culture and tapping pleural effusions >10 mm should be performed in patients suspected Ventilator Associated Pneumonia. Microbiological testing should be always performed to decide the appropriate Initial empirical antibiotic therapy. Clinicians can choose optimal diagnostic Test for specific patients in their clinical setting.98 MANAGEMENT OF VENTILATOR ASSOCIATED PNEUMONIA Early recognition and appropriate management of ventilator-Associated Pneumonia reduces the incidence of complications such as acute lung injury, Multiple organ dysfunction and respiratory decompensation. Empirical therapy Should be started as a matter of urgency if infection is identified. Unnecessary Delay in antibiotic therapy leads to adverse outcomes, particularly if the patient Is septic .However, antibiotic therapy for non-infective syndromes is also Detrimental. It is important to balance the risks and benefits of treatment and This is a matter for individual clinical judgement. Antibiotic rationale Empirical therapy will usually take into account: Time of onset of illness (<5 vs. 5 days after admission) and therefor e Probable pathogens Previous antibiotic administration (rates of Pseudomonas aeruginosa or Acinetobacter spp. Infection increase significantly in patients treated With antibiotics within 10 days before the onset of pneumonia) Severity and speed of progression of the illness Local pathogens and resistance patterns Other patient-related factors such as renal or hepatic impairment. Therapy should be broad-spectrum, and have high activity against the probable Pathogens. In patients previously untreated with antibiotics the predominant Pathogens are Gram-positive cocci in ‘early’ infections and aerobic Gramnegative Bacilli in ‘late’ infections. There are some data to suggest that Monotherapy may be as effective as combination therapy in severe ventilatorassociated Pneumonia.130 However, there is considerable debate about the merits of monotherapy in these Patients largely because of some limitations in the data, particularly the range Of infections included in the trials, the sample sizes and the use of sub-optimal Doses of Aminoglycosides. Combination therapy has the advantage of giving Cover against a broader-spectrum of organisms and some combinations have a Synergistic mechanism of action which reduces the potential for resistance Developing during treatment, e.g. An Aminoglycosides with a beta-lactam. Pseudomonas aeruginosa has been associated with resistance developing during The course of treatment and therefore if pseudomonas involvement is suspected, Vigorous anti-pseudomonas therapy is indicated.35 Empirical therapy Given that there is minimal margin for error in seriously ill patients, it would be Prudent to use empirical combination therapy. Factors to be considered Include: Previous antibiotic therapy Known prevalence and resistance patterns Patient condition. If a satisfactory clinical response is observed with combination therapy after –4 Days, monotherapy can be considered and the Aminoglycosides withdrawn. The Optimal treatment duration has not been established in ventilator-associated Pneumonia. Most studies report treatment durations of 7–10 days, although Shorter courses may be effective.26 PREVENTION OF VENTILATOR ASSOCIATED PNEUMONIA The following measures to reduce Ventilator Associated Pneumonia: Strict infection control policies Alcohol-based hand disinfection Collection of timely microbiologic surveillance data on Multidrug- resistant pathogens Monitoring and early removal of invasive devices Programs to reduce antibiotic prescribing practices Continuous aspiration of subglottic secretions Detection of pneumonia and deescalation of drug treatment Use of oral rather than nasal endotracheal tubes Maintenance of endotracheal cuff pressure > 20 cm H20 Limited use of sedative and paralytic agents Positioning of the patient Semi recumbent positioning (30 to 45 degrees) is recommended To reduce the risk of aspiration. Proper care should be taken when turning the patient or the bed Rail is raised to avoid inadvertently flushing the condensate that Collects on the ventilator circuit into the lower airway or to inline Medication nebulizers. Intensive insulin therapy to maintain normal blood glucose level Emphasis on bleeding prophylaxis; use of H2 antagonists or sucralfate Avoidance of intubation by using noninvasive ventilation wherever Possible, particularly in patients with chronic obstructive pulmonary Disease and cardiogenic pulmonary edema Avoidance of blood transfusion Adequate nurse-to-patient ratios Staff education 40 Though various Indian and International studies on epidemiology of Ventilator Associated Pneumonia are available, no such study has been carried out in Madurai. Since Government Rajaji Hospital, (GRH) Madurai is the largest Tertiary care hospital attached to Madurai Medical College catering to the needs Of lakhs of people from southern districts of Tamilnadu, the present study was Carried out among patients admitted at Intensive Respiratory Care Unit, Government Rajaji Hospital in Ventilators and the data were analysed with Reference to objectives. Efforts have been made to diagnose ventilator associated pneumonia by Collecting blood, bronchoscopic and non bronchoscopic sampling, from Patients satisfying CDC criteria of Ventilator Associated Pneumonia and Processing them by various microbiological techniques like Gram stain, Isolation of microbes using quantitative culture methods and antimicrobial Susceptibility testing.. In addition, fungal culture was also performed. The Results were analysed sample wise and also technique wise and epidemiological Factors of Ventilator Associated Pneumonia were studied.
| Item Type: | Thesis (Masters) |
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| Uncontrolled Keywords: | Microbial Etiology ; Ventilator Associated Pneumonia. |
| Subjects: | MEDICAL > Microbiology |
| Depositing User: | Subramani R |
| Date Deposited: | 19 Aug 2017 02:21 |
| Last Modified: | 19 Aug 2017 02:21 |
| URI: | http://repository-tnmgrmu.ac.in/id/eprint/1472 |
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