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A PROSPECTIVE STUDY OF INCIDENCE, OUTCOME AND RISK FACTORS OF VENTILATOR-ASSOCIATED PNEUMONIA IN

TERTIARY CARE INSTITUTION

DISSERTATION

REGISTRATION NUMBER: 201711706

SUBMITTED IN PARTIAL FULFILMENT OF UNIVERSITY REGULATIONS FOR THE AWARD OF

M.D. DEGREE EXAMINATION BRANCH – I –GENERAL MEDICINE

THE TAMIL NADU Dr. M.G.R. MEDICAL UNIVERSITY CHENNAI, TAMIL NADU

MAY, 2020

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CERTIFICATE FROM THE DEAN

This is to certify that the dissertation entitled “A PROSPECTIVE STUDY OF INCIDENCE, OUTCOME AND RISK FACTORS OF VENTILATOR-ASSOCIATED PNEUMONIA IN TERTIARY CARE INSTITUTION” is the bonafide work of Dr. S.KARTHICK VELAVAN in partial fulfilment of the University regulations of The TamilnaduDr. M.G.R Medical University, Chennai, for the award of degree of Doctor Of Medicine (M.D) Branch- I -General Medicine.

DR.R.BALAJINATHAN M.D DEAN, Kanyakumari Government Medical College,

Asaripallam-Nagercoil-629201

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CERTIFICATE FROM THE HOD

This is to certify that the dissertation entitled “A PROSPECTIVE STUDY OF INCIDENCE, OUTCOME AND RISK FACTORS OF VENTILATOR-ASSOCIATED PNEUMONIA IN TERTIARY CARE INSTITUTION” is the bonafide work of Dr. S. KARTHICK VELAVAN in partial fulfilment of the University regulations of The Tamilnadu Dr. M.G.R Medical University, Chennai, for the award of degree of Doctor Of Medicine (M.D) Branch- I -General Medicine.

Prof.Dr. PRINCE SREE KUMAR PIUS HEAD OF DEPARTMENT, DEPT. OF MEDICINE, Kanyakumari Government Medical College, Asaripallam.

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CERTIFICATE FROM THE GUIDE

This is to certify that the dissertation entitled “A PROSPECTIVE STUDY OF INCIDENCE, OUTCOME AND RISK FACTORS OF VENTILATOR-ASSOCIATED PNEUMONIA IN TERTIARY CARE INSTITUTION” is the bonafide work of Dr.S.KARTHICK VELAVAN in partial fulfilment of the University regulations of The Tamilnadu Dr. M.G.R Medical University, Chennai, for the award of degree of Doctor of Medicine (M.D) Branch- I -General Medicine.

PROF. Dr. P. SANKAR, M.D., DEPT. OF MEDICINE, Kanyakumari Government Medical College, Asaripallam.

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DECLARATION

I, Dr. S.KARTHICK VELAVAN, hereby declare that, I carried out this work entitled “A PROSPECTIVE STUDY OF INCIDENCE, OUTCOME AND RISK FACTORS OF VENTILATOR-ASSOCIATED PNEUMONIA IN TERTIARY CARE INSTITUTION” at Kanyakumari Government Medical College Hospital, Asaripallam, under the guidance of Prof.Dr.

PRINCE SREEKUMAR PIUS M.D., Professor of Medicine, during the period of .I also declare that this bonafide work has not been submitted in part or full by me or any others for any award, degree or diploma to any other University or Board either in India or abroad.

This is submitted to The Tamilnadu Dr. M.G.R Medical University, Chennai, in partial fulfilment of the University rules and regulations for the award of degree of Doctor of Medicine (M.D) Branch- I-General Medicine.

Place: Asaripallam

Date: Dr.S.KARTHICK VELAVAN

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ACKNOWLEDGEMENTS

I would like to express my sincere gratitude to Prof.

Dr.BALAJINATHAN, M.D., Dean, and Kanyakumari Government Medical College, for having permitted me conduct this study and to use the hospital facilities at Kanyakumari Government Medical College Hospital, Asaripallam.

I am greatly indebted to my beloved teacher Prof. Dr. PRINCE SREEKUMAR PIUS, M.D., Professor and Head, Department of Medicine for allowing me to do this study in the Department of Medicine. I also express my sincere thanks to him for giving me proper guidance, protocol and immense help and encouragement in conducting this study.

I express my gratitude to Dr. S. SANKAR M.D., Associate professor, Department of Medicine who immensely helped me in conducting this study.

I express my sincere and heartfelt gratitude to Dr. J. BRINDHA., Dr.

SURESH KUMAR, Assistant professor in the Department of Medicine for her encouragement, kind guidance, constant support and cooperation in evaluating the patients.

I thank the Members, Secretary and Chairman of the Institutional Ethical committee, Kanyakumari Government College hospital, Asaripallam.

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I thank all the paramedical staff and other staff of the Kanyakumari Government Medical College Hospital for all their help and cooperation in conducting this study.

I thank all my colleagues and friends for their constant encouragement and valuable criticism.

I am extremely thankful to all my family members for their continuous support.Above all I thank God Almighty for his immense blessings.

Last, but not least, my profound gratitude to all the patients, to whom I owe everything because this venture would not have been possible without them.

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ANTI PLAGIARISM CERTIFICATE

This is to certify that this dissertation work titled “A PROSPECTIVE STUDY OF INCIDENCE, OUTCOME AND RISK FACTORS OF VENTILATOR ASSOCIATED PNEUMONIA IN TERTIARY CARE INSTITUTION” of the candidate Dr. S. KARTHICK VELAVAN with Registration Number 201711706 for the award of M.D in the branch of GENERAL MEDICINE. I personally verified the urkund.com website for the purpose of plagiarism Check. I found that the uploaded thesis file contains from introduction to conclusion pages and result shows 18 percentage of plagiarism in the dissertation.

Guide & Supervisor sign with Seal

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ABBREVIATIONS

ATS - American Thoracic Society BAL - Broncho-alveolar lavage

CAP - Community acquired pneumonia

CDC - Centre for disease control and prevention CFUs/ml - Colony forming units/ milliliter

CNS - Central nervous system

COPD - Chronic obstructive pulmonary disease CPIS - Clinical pulmonary infection score CRF - Chronic renal failure CXR Chest X-ray DM - Diabetes mellitus

DKA - Diabetic ketoacidosis ETA - Endotracheal aspirate GNB - Gram negative bacilli

HIV - Human immunodeficiency virus ICU - Intensive care unit

IHD - Ischemic heart disease NP - Nosocomial pneumonia..

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CONTENTS

S.No CONTENTS PAGE NO

1. ETHICAL COMMITTEE APPROVAL 8

2. ANTI PLAGIARISM RECEIPT 10

3. INTRODUCTION 16

4. AIM OF THE STUDY 18

5. REVIEW OF LITERATURE 19

6. MATERIALS AND METHODS 51

7. OBSERVATION AND RESULTS 56

8. DISCUSSION 86

9. CONCLUSION 93

10. BIBLIOGRAPHY 94

11. PROFORMA 101

12. MASTER CHART 103

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A PROSPECTIVE STUDY OF INCIDENCE,

OUTCOME AND RISK FACTORS OF VENTILATOR- ASSOCIATED PNEUMONIA IN TERTIARY CARE

INSTITUTION

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INTRODUCTION

INTRODUCTION

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Ventilator‐associated pneumonia (VAP) is a nosocomial contamination that arises, More than 48 hours after a patient commences to mechanical ventilation (MV).

It leads to diminished oxygen levels and consequently associated with multiple organ Failure. VAP, in general, makes retrieval of the patient more difficult, who are already seriously ill (1).VAP results after aspiration of stomach contents in addition to spiration or immigration of bacteria‐containing secretions down the endotracheal tube (ETT) starting from the oropharynx into the lungs. The ETT acts as a hindrance to host defenses by deterring the action of cilia,unimpulsive coughing and swallowing by the patient. It moreover inhibits the epiglottis from closing, which would normally Create a physical obstacle by stalling bacterial migration into the lower respiratory Tract. VAP underwrites to almost half of all cases of hospital-acquired pneumonia.

VAP is valued to occur in 9–27 % of all mechanically ventilated patients, with the maximum jeopardy existence in the early course of hospitalization. Ended the years, the attributable risk of death has shrunk and is more recently projected to 9–13 % largely because of enactment of preemptive approaches (Delle Rose et al. 2016).

Approximately 50 % of all antibiotics controlled in ICUs are for treatment of VAP.

Seven Basic Mandatory Measures Three Highly Recommended Measures

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AIMS AND OBJECTIVES

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AIMS AND OBJECTIVES

TO STUDY ABOUT VENTILATOR-ASSOCIATED PNEUMONIA:

INCIDENCE, OUTCOME, RISK FACTORS IN KANYAKUMARI GOVERNMENT MEDICAL COLLEGE HOSPITAL ICU.

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REVIEW OF LITERATURE:

1. Epidemiology & Changing Epidemiology 2. Scenario in India

3. Definition and New Definition 4. Guidelines for Diagnosis 5. Future Directions

6. Summary 7. Pathogenesis 8. Microbiology 9. CPIS Score 10. Treatment 11. Prevention

12. Risk factors of VAP

13. Disinfection and Antisepsis

14. Education and training for health Professionals.

15. Concept of Bundles.

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Epidemiology and changing Epidemiology:

VAP (Ventilator associated pneumonia) is one of the devastating problems encountered in ICU set up (1). VAP is a life threatening illness in ICU patients. It is the second most common infection. Mortality rate varies from 25% to 45 %( 1).

Across the world, no universally accepted criteria for diagnosis created. In India, effect of VAP has been studied by various studies, and found significantly higher in their Hospitals. Rates are about 24/1000 ventilator days. So, we need to create our own hospital based data. Especially in Asian countries, incidence of HAP and VAP are increasing. Incidence of VAP is about 53-58% in India(1) (Delle Rose et al.

2016)). Mortality rates vary from 37.03 to 47.03%. About Ventilator days, it ranges from 8.95 to 9.9 per 1000 ventilator days (1)

SCENARIO IN INDIA:

Incidence of VAP in Indian studies ranges from 30 to 70% (2). Early VAP ranges from 40 to 45%. Majority of VAP are late VAP which has high incidence (55- 60%). In contrasting from western data, Gram negative organisms are the most common etiological agents in both early and late VAP (Kalanuria, Zai, and Mirski 2014). Global scenario of ICU infection different from Indian ICU’s. Indian ICU’s are over whelmed with gram negative infection. Development of Antimicrobial stewardship program based on local epidemiological data and international guidelines is the utmost need of the hour. There is an upswing of multi-drug resistance organisms in ICU’s(3)(Martin-Loeches, Rodriguez, and Torres 2018).

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DEFINITION AND NEW DEFINITION:

Ventilator Associated Pneumonia is defined as pneumonia occurring more than 48 hours after patients have been intubated and received mechanical ventilation(2(Hunter 2012)). Diagnosis of VAP requires high clinical suspicion.

Nosocomial Pneumonia occurs more than 48 hours after the patient’s admission to the hospital and when it was not an intubation at the time of hospitalization (3). It affects lung parenchyma.

In Annals ATS supplements, a new consensus surveillance definition and Protocol has been proposed (1). Perhaps the most important charge is that of timing, any Pneumonia in a patient receiving mechanical Ventilation was considered a VAP, even if this occurred within the first 24 hours of admission. Another significant change is the absence of a chest radiograph in the protocol for diagnosis. With the introduction of this more sensitive definition of VAP, the concept was set aside and a new reporting process has begun.

GUIDELINES FOR DIAGNOSIS:

At present time, there is no universally accepted, gold standard diagnostic criteria for VAP(5)(Kalanuria, Zai, and Mirski 2014). About 30% of VAP can be still missed out in clinical diagnosis. So, American Thoracic Society (ATS) and Infectious Diseases Society of America (IDSA) guidelines put forth many interesting criteria.

The European guideline only uses the concept of Clinical Pulmonary Infection Score

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(CPIS)(11). If the CPIS is less, that Clinical presentation will be having low probability for VAP. CPIS more than 6, highly suggestive of VAP. American guidelines accounts only clinical criteria not on CPIS. Fever, purulent secretions, leukocytosis, if present triggers the suspicion grouping of these symptoms predicts the presence of Pneumonia. New onset progressive infiltrate, makes strong suspicion. ATS and IDSA recommend to obtain lower respiratory tract samples for culture and microbiology.

Tracheal aspiration very well used in criteria gives negative predictive value. CPIS takes into account clinical, physiological, microbiological and radiographic evidence makes these into numerical value to predict presence and absence of VAP(4)(Warren et al. 2003)

Many debate the popularity of CPIS score it resulted its sensitivity and specificity is about 65% and 66% respectively. Singh et al and his colleagues demonstrated that CPIS is an effective clinical tool for determining whether to stop on continue antibiotics for longer than 3 days.

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FIGURE 1:CPIS SCORE (14)

FUTURE DIRECTIONS:

Current studies incline towards biological markers and diagnostic algorithm of VAP. Description about soluble Triggering receptor expressed on myeloid cells-1 and Surfactant Protein-D level of Broncho-alveolar lavage fluid and serum pro-calcitonin levels have given a valor to predict VAP. Indispensable about VAP is that to understand more about molecular pathogenesis of Pneumonia. Uncontrollable epithelial cell death is the ultimate initiation for the pathogenesis of Pneumonia, especially on early stages cytotoxins such as alpha hemolysis (HIa). HIa is highly potent in lysing bronchial and alveolar epithelial cells, macrophages and it is official in Pro-inflammatory process

In an animal study, Zou et al discovered expression of a protein named the mortality factor 4 like 1 (mor f 41 I) increased in humans with Pneumonia and it is related to host cell death during inflammation.(16)

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FIGURE 2: DEPICTION OF ENDOTRACHEAL TUBE IN LARYNX.

SUMMARY:

Even though precise incidence and impression of VAP are open to debate, it still presents as vital challenge to caregivers. Exactness of diagnosis and its reproducibility are of much more significant. The drawback in consuming empirical antibiotics for suspicion of VAP is the main cause for antibiotic overuse, emergence of resistance, unnecessary adverse effects and toxicity.(17)

Simple and effective protective measures can be established easily at very low cases. Judicious use of antibiotics and its duration, minimising sedation, proper wearing protocols, hand hygiene and meticulous respiratory care should be maintained. More errensive and overpriced interventions must be kept back for appropriate interventions.18(Karakuzu et al. 2018).

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PATHOGENESIS:

Development of VAP mainly due to the composite relationship between the endotracheal tube and presence of risk factors. Supreme vital risk factor is the existence of endotracheal tube. Damage in the natural defense mechanism which causes micro aspiration around the cuff of endotracheal tube.(19)

The triggering factor in VAP is the aspiration of infected secretions from oropharynx hasty colonization of utmost pathogenic bacteria such as aerobic gram negative bacteria (AGNB) and staphylococcus aureus promptly replace normal flora.(20)

Uninterrupted entry of Bacteria to the lower respiratory tract via. (21) 1) Micro aspiration occurred during intubation.

2) Development of a biofilm laden with bacteria.

3) Pooling and trickling of secretions around the cuff.

4) Weakened mucociliary clearance

Many of the host defense mechanism become ineffective during critical illness which make our immune function in doubt. For mounting an inflammatory response, alveolar macrophages, neutrophils and other elements of humoral immune system must intermingle together. Pneumonia develops due to overwhelming response from host immune system.

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FIGURE 3: SHOWS PATHOGENESIS OF VENTILATOR ASSOCIATED PNEUMONIA.

MICROBIOLOGY:

Origin of type of organism depends upon the duration of mechanical ventilation. Early VAP will be more sensitive to antibiotics. Multi-drug resistant is the reason for late onset VAP, which will be greatest challenge to treat. Still this is not a rule, simply a guide to recruit antibiotic therapy, until further solid information available. The microbiologic flora liable for VAP is diverse from that of the more common community-acquired pneumonia (CAP).(22) In particular, viruses and fungi are unusual causes in public who do not have immune deficiencies.

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In recent studies, the most common organism associated with VAP is Pseudomonas (43.24%) followed by klebsiella (18.91%). Mortality rate is high in pseudomonas group (62.5%). These information are from north Indian studies. In other studies, about 15-25% are pseudomonas group.Common pathogens presently related with VAP:(23)

A] Early onset VAP

1) Gram positive cocci

 Streptococcus pneumoniae

 Methicillin sensitive Staphylococcus aureus (MSSA) 2) Gram negative bacilli

 Escherichia coli

 Klebsiella species

 Serratiamarcescens

B] Late onset VAP:

1) Gram positive cocci

 Methicillin resistant Staphylococcus aureus (MRSA) 2) Gram negative bacilli

 Enterobacteriaceae family

 Pseudomonas aeruginosa

 Acinetobacter Baumanni

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Pathogens causing VAP, according to Kalanuria et al.(24) 1. Pseudomonas (24.4%)

2. S. aureus (20.4%, > 50% MRSA)

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3. Enterobacteriaceae (14.1%)

4. Streptococcus species

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5. Hemophilusspecies(9.8%)

6.Acinetobacter species (7.9%)

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7. Neisseria species (2.6%)

8. Stenotrophomonamaltophilia (1.7%)

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9. Coagulase negative staphylococcus (1.4%)

10. Others 4.7% - includes Corynebacterium, Moraxella, Enterococcus fungi.

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FIGURE: 4 COMMON ORGANISMS ASSOCIATED WITH VAP (25)

FIGURE 5: COLONY COUNTER

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CPISScore :

(26)

Deficiency in making the diagnosis is the major offender, in the pitiable outcome of VAP. X-Ray changes in suspected VAP could also exist in conditions like acute respiratory distress syndrome, pulmonary edema, atelectasis and pulmonary infarction.

Nonspecific symptoms and signs such as fever and leukocytosis can be seen in many conditions even though microbiology assists in diagnosis, it does not warrant us.

The clinical pulmonary infection scoring (CPIs) initially projected by PUGIN et al which has better sensitivity (72%) and specificity (80%). CPIs proceeds with clinical, microbiological and radiographic evidence to allow arithmetic value, which may foretell the presence or absence of VAP. Score ranges from 0 to 12 score. More than 6 shows a parallel relationship with presence of VAP.

Singh and colleagues defined CPIS as current clinical tool to approach to define VAP and whether to continue (or) to stop antibiotics for more than 3 days.

Antimicrobial resistance interior amid patients who discontinued antibiotics matched with the patients who got standard care.(27)

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CDC criteria for ventilator associated pneumonia. (28)

Three or more of the following criteria:

 Rectal temperature >38°C or <35.5°C

 Blood leukocytosis (>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 AND

 New, persistent, or progressive radio graphical infiltrate

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FIGURE 6: THIS PICTURE SHOWS X RAY ON THE 1ST DAY AND 3RD DAY OF PATIENTS IN ICU AFFECTED BY VAP

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TREATMENT:

Since VAP is accompanied with high morbidity, diagnosis is essential for speedy treatment in all doubted critically ill patients. Even though bacteriological sampling is vital, it should not significantly interrupt the starting of treatment.

Initiation of early antibiotic is the determining factor of outcome.

Plump for suitable antibiotic depends on duration of mechanical ventilation.

Late onset VAP (>4 days) entails broad spectrum antibiotics limited range of antibiotics used for early onset VAP(<4 days). A simplified local antibiogram for each hospital and each ICU which is built on local bacteriological patterns, will be critical and essential for mitigation of antibiotic therapy.(28)

High rate of resistance to monotherapy witnessed with Pseudomonas aeruginosa. So, combination therapy is always recommended. Even with best therapy, if no comeback is seen, it will be judicious to reconsider the diagnosis (swoboda et al).

In two surgical ICUs, there has been prescription of antibiotics without pneumonia.

Initial effective therapy for VAP is accompanied with reduced mortality. Luna et al, established that insufficient therapy during the initial 48 hours, even though delivery of suitable therapy after BAL results was associated with a mortality rate of 91% VAP should be well thought of with CPIs score >6.(29)

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FIGURE 7 : TREATMENT OF VAP

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FIGURE 7: ALGORITHM REGARDING TREATMENT OF VAP

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PREVENTION :

(29)

There are several recommended measures for the prevention of VAP.Since Endotracheal tube is a substantial risk factor for the progression of VAP, the chief preventive measure is to minimize the duration alternate to ET intubation should be used.

Nursing care play a main role. It acts as a first line defense in averting to bacterial colonization in oropharynx. Execution of proper hand washing technique for 10seconds should be implemented before and later contacting the patients.

Oral sanitization can lessen the number of bacteria within the patients of oral cavity. Chlorhexidine oral wash can be used twice a day.

Practically, all patients getting mechanical ventilation are given stress ulcer prophylaxis. Stress rises gastric PH which in turn proliferates pathogen and lead to bacterial colonization and aspiration.

Slime may become stagnant in airways and grow become a medium for bacterial growth. So, endotracheal suctioning is compulsory to avoid contamination of airways.

Rotating patients every 2 hours escalates pulmonary drainage and cuts the progression of VAP. Specialty couches capable of incessant lateral rotation reduce the frequency of VAP, however does not reduce the mortality and length of stay.

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It is appropriate to change the ventilator circuit only when noticeably soiled. It is inconclusive that, usage of heat as well as moisture exchangers does not play any role in the incidence of VAP.

Raising the head end by 30 to 45 degrees avoids the gastric reflux and also prevents aspiration. Semi-recumbent position is well preferred.

Vigilant use of narcotics is essential as limits deep breathing and weakens oxygenation. Cautious use of Narcotics reduces the aspiration.

Drugs that augment gastric motility can be used in order to avoid gastric over distension thereby preventing VAP.

Meticulous suctioning of Endotracheal tube prevent the pooling of secretions in oropharynx, thereby avoids aspiration retaining adequate cuff pressure, no less than 20cm H2O and constant suctioning shrinks the incidence of VAP.

Using silver nitrate inhibits the formation of formation of biofilm thereby snooping the capacity of bacteria to line the endotracheal tube.

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FIGURE 8: THIS FIGURE SHOWS HOW TO PREVENT VAP(30)

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RISK FACTORS FOR VAP:

(31)

1. Intubation

2. Use of H2 blockers --changes the acidity – favours bacterial colonization.

3. Reintubation 4. Undue sedation 5. Old age

6. APACHE 11 score >16

7. Acute (or) chronic lung Disease 8. Enteral feeding

9. GCS>9 10. Smoker 11. Trauma

12. Ventilator circuit

13. Inadequate Hand washing 14. Improper use of gloves.

15. Indecorous use of persons protective.

16. Immunosuppression.

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FIGURE 9: PATHOGENESIS OF VAP(37)

DISINFECTION AND ANTISEPSIS :

(32)

Even though environmental contamination ensues with multidrug resistant organisms, major tool of organisms colonized in ICU patient. Dwindling this reservoir could reduce the risk of transmission and this might reinforce the ability of patients to repel against colonization using chlorhexidine baths shared with nasal mupirocin has been related with lessened acquisition rate of MRSA and also declined MRSA associated nosocomial infections.

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Various bedside measures should be implemented under the supervision of infection control team multidisciplinary approach giving importance to these priories gives a good quality of care.(38)

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FIGURE 10: THIS FIGURE SHOWS ROUTES OF COLONISATION

1. Recommendations with proper written guidelines to the staff and ICU physicians regarding ICU care. (33)

1. Surgical swab used for skin cleaning.

2. Apart from haircutting, shaving is preferred.

3. Before insertion, alcohol-based solution with chlorhexidine gluconate should be used.

4. Sterile gown, caps, drapes and mask should be used.

5. For central vein prefer subclavian vein and for short lines prefer wrist vein.

6. Promotion of drag gauze based dressing, with replacement of the dressing within 72 hours.

7. Specific lines for blood product liquid emulsion replace after use can within 72 hours.

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8. Use of antiseptic impregnated pads after hand disinfection by opening a hub.

9. If there is any source of infection, remove the catheter immediately.

Individual Components of the Ventilator-Associated Pneumonia Prevention Measure

 Selective decontamination of the digestive tract or selective 2. Oropharyngeal decontamination.

1. Strict hand hygiene with alcohol solutions before airwayManagement.

2. Continuous aspiration of subglottic secretions.

3. Control and maintenance of cuff pressure.

4. Short course (2-3 doses) of systemic antibiotics during intubation 5. Of patients with previous decreased consciousness.

6. Oral hygiene with chlorhexidine.

7. Semi recumbent positioning. Avoidance of 0° supine positioning If possible.

8. Promoting procedures and protocols that safely avoid 9. Reduce duration of mechanical ventilation.

10. Avoidance of elective changes of ventilator circuits, humidifiers, a. And endotracheal tubes.

11. Two educational modules about ventilator-associated pneumonia prevention and patient safety with their corresponding examinations are freely accessible online

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12. Continuously monitored for ICUs successfully completing the tests.

Coordinators in each unit have access to this 13. Registry and report to the regional coordinators.

14. Protocols for noninvasive mechanical ventilation in acute exacerbations of chronic obstructive pulmonary disease, for weaning or sedation promoting lower

15. Infusion doses or its daily interruption should be available.

FIGURE 11: THIS SHOWS BRONCHOALVEOLAR LAVAGE PROCEDURE

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EDUCATION AND TRAINING OF HEALTH PROFESSIONALS:

Proper education and training of health professionals with a well-organized system and proper implementation will have a dramatic impact in reduction of VAP.

Finest methods for improving practices will entail the integration of experience medical knowledge, patient’s preferences (34). Energetic participation by enthusiastic clinicians in the development of guidelines must have an increased utilization of resources. Self-study education modules on nursing care will have drastic reduction in pneumonia, duration of mechanical ventilation and costs of the disease.

CONCEPT OF BUNDLES (35)

Bundle comprises of a small set of preventive actions with proven effectiveness which guarantees more effective prevention compared to other implementation.

Institute of health care approved certain preventive measures for VAP.

1. Increase the height of bed 30 to 45degrees.

2. Day to day regular interruption of sedation to assess the readiness to extubate.

3. Proper oral care with chlorhexidine.

4. Peptic ulcer prophylaxis.

5. Deep vein thrombosis prophylaxis.

Still studies are required to assess a bundle that includes trials and proper Recommendations by the freshest guidelines. In order to estimate the effect on patients clinical outcomes and VAP incidence when executed together.

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MATERIALS AND METHODOLOGY

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MATERIALS AND METHODOLOGY STUDY DESIGN

A PROSPECTIVE STUDY OF INCIDENCE, OUTCOME AND RISK FACTORS OF VENTILATOR-ASSOCIATED PNEUMONIA IN TERTIARY CARE INSTITUTION

LOCATION

Conducted at

DEPARTMENT OF MEDICINE

Kanyakumari Government Medical College, Nagercoil, Tamilnadu.

Collaborating departments

Department of Anesthesia, Department of surgery

Kanyakumari government medical college,Nagercoil,Tamilnadu

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MATERIALS AND METHODOLOGY

• Prospective interventional study . The study to be conducted over a period of 1 years.

• A total of 100 patients who are kept on mechanical ventilator are randomly selected.

SELECTION CRITERIA

INCLUSION CRITERIA Both sexes-age >15 years On mechanical ventilator >48 h.

EXCLUSION CRITERIA:

Those died or developed pneumonia within 48 h .

Those who are admitted with pneumonia at the time of admission.

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SAMPLING

• SAMPLE SIZE:

4PQ d2 Q-1-P

P- EXPECTED PREVALANCE OR PROPORTION d-precision

SAMPLE SIZE: 84

Observations are analyzed statistically using SPSS statistical package- version23

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INVESTIGATIONS

• Routine investigations

• Special investigations-culture of tracheal tube, blood and urine

• Serum cholinesterase levels when needed, were performed

• ABG

• Sputum-collected from the tip of the suction catheter and transported to the laboratory in a sterile tube.

• Patients were monitored from the date of inclusion in the study to the final outcome in the ICU.

• VAP was diagnosed on clinical grounds based on the modified CPIS system

• VAP group-classified into two groups 1. Early-onset type(within 48–96 h) 2. Late-onset type (>96 h).

• Once the clinical suspicion was established, empirical antibiotic therapy was initiated based on guidelines prescribed by the American Thoracic Society

• Patients were routinely screened by arterial blood gas (ABG) analysis every 12 hourly and appropriate steps were taken to correct any change.

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RESULTS

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RESULTS

In our study, total patients around 80,out of which males 59 (73.8%), females 21 (26.3%)

TABLE SHOWS TOTAL ALIVE VS DEAD PATIENTS Crosstab

Methods

Total

EL EM

Alive_Dead

Alive

Count 7 24 31

% of Total 8.8% 30.0% 38.8%

Dead

Count 7 42 49

% of Total 8.8% 52.5% 61.3%

Total

Count 14 66 80

% of Total 17.5% 82.5% 100.0%

ABOVE FIGURE SHOWS ALIVE VS DEAD DISTRIBUTION IN MALE AND FEMALE PATIENTS.

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MALE VS FEMALE GENDER COMPARISON OF MORTALITY

TABLE 1: SHOWS GENDER DISTRIBUTION

Crosstab

Gender

Total

F M

Alive Dead

Alive

Count 10 21 31

% of Total 12.5% 26.3% 38.8%

Dead

Count 11 38 49

% of Total 13.8% 47.5% 61.3%

Total

Count 21 59 80

% of Total 26.3% 73.8% 100.0%

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FIGURE 1: SHOWS MALE GENDER DISTRIBUTION

In our study total male patients around 59, alive patients at the end were 21(36%). Dead patients were around 38(64%).

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FIGURE 2 : SHOWS FEMALE GENDER DISTRIBUTION

In our study, female patients alive are 10(48%) and dead 11(52%).

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ELECTIVE Vs EMERGENCY

TABLE 2 : SHOWS :ELECTIVE VS EMERGENCY INTUBATON COMPARISON

Methods

Total

EL EM

Alive Dead

Alive

Count 7 24 31

% of Total 8.8% 30.0% 38.8%

Dead

Count 7 42 49

% of Total 8.8% 52.5% 61.3%

Total

Count 14 66 80

% of Total 17.5% 82.5% 100.0%

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FIGURE 3; SHOWS DEAD VS ALIVE DISTRIBUTION IN ELECTIVE AND EMERGENCY GROUP.

In our study, more death occurred in emergency intubation group (61%) alive patients are about (38%).

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FIGURE 4: ALIVE VS DEAD IN EMERGENCY INTUBATION PATIENTS

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TABLE 3 : AGE DISTRIBUTION

S.no Age Distribution No of patients

1 <18 1

2 18-30 5

3 31-40 7

4 41-50 10

5 51-60 25

6 61-70 22

7 >70 10

In our study, most of the VAP Patients are around the age group,50 to 60 years old, next comes 60 to 70 age group.

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FIGURE 5:AGE DISTRIBUTION AMONG VAP PATIENTS

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GRAPH 1 : SHOWS AGE WISE DISTRIBUTION

Around 49%, were 50 to70 years.34% were in 30 to 50 years.

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TABLE 4: TREATMENT METHODS VS VAP

VAP

Treatment Methods

Total Fisher Exact test(sig)

EM EL

Early onset 38(48%) 4(5%) 42(53%)

P=0.07

Late onset 28(35%) 10(13%) 38(48%)

Total 66(83%) 14(17%) 80(100%)

IN OUR STUDY, Early onset VAP is more commonly seen in emergency around 38(48%) patients and in elective patients around 4(5%) patients developed early onset VAP.

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FIGURE 6: SHOWS EARLY ONSET VS LATE ONSET VAP

Late onset VAP developed around 28 patients (35%) in emergency intubated patients. In electively patients, around 10 patients (13%) developed late onset VAP.

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TABLE 4: OUTCOME VS ONSET OF VAP

VAP

Outcome

Total

Fisher Exact test(sig)

Alive Death

Early onset 15(19%) 27(34%) 42(53%)

P=0.360 Late onset 16(20%) 22(28%) 38(48%)

Total 31(39%) 49(61%) 80(100%)

In our study, Early onset VAP is around 27 patients (34%) are dead. 15 patients were alive (19%). Upto 42 patients (53%) were affected by early onset VAP. IN OUR STUDY patients 38 patients(48%) were affected by late onset VAP. In which,22 patients (28%) were dead. 16 patients (20%) were alive.

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FIGURE 5: TREATMENT OUTCOME VS ONSET OF VAP

In our study, most common organism is pseudomonas(45%),MRSA(21%), A.Baumani(10%).

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TABLE 5: ONSET OF VAP VS ORGANISM

Organism

Total A.BAU E.COLI KLEB MRSA POLYM

IC PSEUD

Alive_

Dead

Alive

Count 4 2 1 7 2 15 31

% of

Total 5.0% 2.5% 1.3% 8.8% 2.5% 18.8% 38.8%

Dead

Count 4 4 4 10 6 21 49

% of

Total 5.0% 5.0% 5.0% 12.5% 7.5% 26.3% 61.3%

Total

Count 8 6 5 17 8 36 80

% of

Total 10.0% 7.5% 6.3% 21.3% 10.0% 45.0% 100.0%

FIGURE 6: DISTRIBUTION OF ORGANISM

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PIE CHART SHOWS DISTRIBUTION OF ORGANISMS

From our study, distribution of organisms in order, 1. Pseudomonas (36 patients) 45%

2. MRSA(17 patients) 21.3%

3. Aceinobacterbaumani(8 patients)10%

4. Polymicrobial(8 patients)10%

5. E.coli(6 patients)7.5%

6. Klebsiella (5 patients)6.3%

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ORGANISMS DISTRIBUTION AMONG VAP GROUP

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FIGURE 7: ONSET OF VAP VS ORGANISM

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FIGURE 8. : SHOWS ONSET OF VAP VS ORGANISM ISOLATED

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TABLE 6: ONSET OF VAP VS CPIS SCORE

S.no Onset of VAP CPIS score Sig

1 Early Onset 8.214±1.16

P=0.41

2 Late Onset 8.447±1.75

FIGURE 9: ONSET OF VAP VS CPIS SCORE

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FIGURE 10 :SHOWS :DISTRIBUTION OF CPIS SCORE AMONG VAP PATIENTS

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TABLE 7: ONSET OF VAP VS CAUSES

Causes Onset Fisher Exact

Test Early Onset Late Onset

ALP POIS 3 0

P= 0.212

BS STROK 1 0

CAD 0 1

CAD/CCF 0 1

CAD/DCM 1 1

CAD/DKA 1 0

CAD/PE 0 2

CAD/PTB 0 1

CCF 2 0

CKD 2 1

CKD/PE 2 1

CLD/HE 1 0

COPD 1 5

COPD/AE 0 1

COPD/DCM 0 1

CVA 1 4

DCLD 1 0

HE 0 2

ICH 1 0

ME/SEPSI 0 1

OLEANDER 1 0

OPC 8 8

PARAQUAT 3 0

PE 5 2

PE/CKD 1 1

REC CVA 0 1

RF 0 1

SEPSIS 4 2

SEPTIC S 0 1

STATUS E 1 0

STROKE 1 0

UK POISO 1 0

Total 42 38

THE ABOVE TABLE SHOWS ONSET OF VAP AND ITS CAUSES.

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FIGURE 11: CAUSES OF INTUBATION IN ICU AND ITS ASSOCIATION WITH VAP.

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TABLE 8: ONSET OF VAP VS COMORBITIES

VAP

Organism

Total

Fisher Exact test(sig)

CAD CKD/HT CLD COPD DM DM/

CVA DM/HT DM/HT/

CAD HT NO

Early onset

2 4 1

0

12 1 1

0

4 17 42

P=0.551 (2.5%) (5%) (1.3%) (15%) (1.3%) (1.3%) (5%) (21.3%) (52.5%)

Late onset

6 2 1 1 7

0

2 1 2 16 38

(7.5%) (2.5%) (1.3%) (1.3%) (8.8%) (2.5%) (1.3%) (2.5%) (20%) (47.5%)

Total

8 6 2 1 19 1 3 1 6 33 80

(10%) (7.5%) (2.5%) (1.3%) (23.8%) (1.3%) (3.8%) (1.3%) (7.5%) (33%) (100%)

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FIGURE 9 : ONSET OF VAP VS COMORBITIES

FIGURE 10: SHOWS DEVELOPMENT OF VAP AND ITS CO MORBIDITIES

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FIGURE 11: DIABETES DISTRIBUTION AMONG VAP PATIENTS

ABOVE FIGURE SHOWS DISTRIBUTION OF DIABETES IN VAP

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FIGURE 12: HYPERTENSION DISTRIBUTION AMONG VAP PATIENTS

FIGURE 13: CAD DISTRIBUTION AMONG VAP PATIENTS

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FIGURE 14:CO-MORBIDITIES DISTRIBUTION AMONG VAP:

FIGURE 15: SHOWS DAYS OF ILLNESS VS VAP PATIENTS

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DISCUSSION

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DISCUSSION

Nosocomial infections denote a major health problem in our society. It causes surplus morbidity, mortality, personal distress, and cost. Ventilator associated

pneumonia is considered to be one of the most worrisome problem in every ICU set up. Nosocomial pneumonia is a particularly common problem in intubated patients getting mechanical ventilation in ICU.

Noticeable effort has been taken to develop and improve preventive measures to reduce the incidence of VAP. The preventive strategy is based on modifiable risk factors. Aim to reduce the risk of VAP by several pharmacological and non-

pharmacological measures available. Endotracheal intubation and prevention of micro aspiration of pathogens to the lower airways will be the ultimate measure, that should be taken.

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1) INCIDENCE:

80 patients were analyzed in our study group. Compared with our hospital admissions in icu set up, the overall incidence of VAP in Kanyakumari government medical college ICU. According to this study around 30% is the incidence of VAP.

The prevalence of VAP may differ from 6 to 52 cases per 100 patients depending on the population studied. In an ICU on any given day about 10% of patients will develop pneumonia, VAP in the majority of cases.

2) AGE DISTRIBUTION:

In our study ,males affected were 59 patients .Around 31 were female patients.

In our study ,Most of the VAP Patients are around the age group,50 to 60 years old, next comes 60 to 70 age group. The higher incidence of VAP in the middle age group can be attributed to more number of patients getting admitted and undergoing

mechanical ventilation in this age group.

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3) SEX DISTRIBUTION:

In our hospital among patients who developed VAP two thirds Were males (73%) and one third were females (26%). This is because of increased number of male patients being admitted. Also male gender as such is a risk factor for the development of VAP. 64% male patients were dead. Male patients with VAP were in a higher risk of going to complications

.

4) TYPES OF VAP:

Early onset VAP is pneumonia follows after 2 days of mechanical ventilation.

While late onset VAP arises 4 days after intubation. Among the 80 patients studied 42(53%) had early onset VAP and 38(48%) had late onset VAP. Among those 42 who developed early onset VAP 27(34%) expired. In late onset group 22(28%) were expired. The probability of getting VAP increases with the duration of mechanical ventilation. It has been found that the risk for VAP increased from 5% in patients receiving one day of respiratory assistance to 68.8% in patients receiving more than 30 days. In our study early onset VAP ,is more severe and has high mortality compared to late onset VAP.

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5) ELECTIVE VERSUS EMERGENCY INTUBATION:

In our study 66 patients underwent emergency intubation and 14 patients with Elective intubation. Out of which emergency intubation has high mortality rate around 61%. The method of intubation has significant association with the development of onset of VAP and mortality.

6) MICROBIOLOGICAL PROFILE:

From our study, distribution of organisms in order ,Pseudomonas (36 patients) 45% , MRSA (17 patients) 21.3%, Aceinobacter baumani (8 patients) 10%, Polymicrobial (8 patients) 10%, E.coli (6 patients) 7.5%, Klebsiella (5 patients) 6.3%.

7) CPIS AND ITS CORRELATION WITH VAP:

The Clinical Pulmonary Infection Score(CPIS) comprises of clinical, microbiological and radiographic evidence to allow a numerical value to determine the presence or absence of VAP. Scores vary between 0 and 12. CPIS score more than 6 is reliable with diagnosis of VAP. In our study about 53% of patients have scores 6 to 8 and 32% patients have score more than 10. Higher the CPIS score has high risk of mortality .significant association between the CPIS score and mortality rate has been found.

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8) DURATION OF MECHANICAL VENTILATION FOLLOWING DEVELOPMENT OF VAP:

The risk for development of VAP is maximum for the duration of initial five Days of mechanical ventilation and the average duration between intubation And VAP development is 3.3 days. The incidence of VAP is straight away related to the duration of mechanical ventilation. The risk falls to 2% per day after 5 to 10 days of mechanical ventilation and then to 1% per day thereafter.

There is a significant association that patients had to be on Mechanical ventilation for prolonged periods following development of VAP have increased mortality. Late onset VAP have seen to have increased mortality, morbidity, stay in hospital and increased cost utilization.

9) OUTCOME RELATED TO VAP:

In our study, more death occurred in emergency intubation group (61%) alive patients are about 38%.In our study total male patients around 59,alive patients at the end were 21(36%). Dead patients were around 38(64%). In our study ,female patients alive are 10(48%) and dead 11(52%). In our study, more death occurred in emergency intubation group (61%) alive patients are about 38%.

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OUTCOME:

In our study, total patients around 80, out of which males 59(73.8%), females21 (26.3%) In our study total male patients around 59, alive patients at the end were 21(36%). Dead patients were around 38(64%). In our study, female patients alive are 10(48%) and dead 11(52%). In our study, more death occurred in emergency intubation group (61%) alive patients are about (38%). Recovery is perhaps credited to better nursing care. Appropriate antibiotic coverage is needed for adequate period.

The major clinical conditions intubated in ICU were OPC poisoning. The related conditions which are considered as significant risk factors were Diabetes mellitus (20%), CAD(17%),HT(16%). About 45% of patients have co- morbid which plays a vital role in the development of VAP. Consolidation was mostly seen in lower lobe of right lung. Majority of the VAP episodes were of late onset type .

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CONCLUSION

The observations based on our study are:

● VAP occurs commonly in ICU set up. It is concomitant with significant Morbidity in critically ill patients.

● The incidence of VAP is directly proportional to the duration of mechanical ventilation.

● Aspiration is a foremost precipitating factor for developing VAP and diabetes mellitus carries an important risk factor in its causation.

● There is a high incidence of MDR organisms in patients with VAP contrasting from community acquired pneumonia.

● The major aims of VAP management are early, appropriate antibiotics in adequate doses followed by de-escalation based on Microbiological culture results and clinical response of the patient.

● Pseudomonas is the most common organism isolated from in our set up.so we will use antibiotics covering these group.

● Age, sex ,onset of VAP , involvement of organism ,have a significant association with the mortality in VAP.

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References

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