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Year : 2008  |  Volume : 52  |  Issue : 2  |  Page : 148-158 Table of Contents     

Pneumonia in Intensive Care Unit

1 Professor, Department of Anaesthesiology & Critical Care, S.N. Medical College, Jodhpur (Raj.), India
2 Assistant Professor, Department of Anaesthesiology & Critical Care, S.N. Medical College, Jodhpur (Raj.), India

Date of Acceptance28-Feb-2008
Date of Web Publication19-Mar-2010

Correspondence Address:
Vinay Joshi
Q.N.21, MG Hospital Campus, In front of Sanghi Petrol Pump, Station Road, Jodhpur (Raj) 342001
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Source of Support: None, Conflict of Interest: None

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No large data based, or randomized controlled studies are available in reference to pneumonia in ICU especially in adult population, in India. Moreover the types of ICU infrastructure, sterilization& disinfection protocols, empirical antibiotics and antibiotics policy are standardized in the country. Hence this review article has mainly utilized available literature from developed countries. This review article briefly discusses the definition of various pneumonia, epidemiology, causative organism, patho­genesis, risk factors, diagnostic strategies and management modalities. By this article, authors hope that a certain guidelines or standardization of protocols in India will be formulated.

Keywords: Pneumonia; Hospital acquired pneumonia (HAP); Ventilator acquired pneumonia (VAP): Intensive care unit

How to cite this article:
Joshi V, Mohan G. Pneumonia in Intensive Care Unit. Indian J Anaesth 2008;52:148-58

How to cite this URL:
Joshi V, Mohan G. Pneumonia in Intensive Care Unit. Indian J Anaesth [serial online] 2008 [cited 2021 Jan 18];52:148-58. Available from: https://www.ijaweb.org/text.asp?2008/52/2/148/60613

   Introduction Top

In intensive care unit (ICU), a significant number of beds are occupied by the patients suffering from pneu­monia whether it is community or hospital acquired. The important factor is that pneumonia adds significantly to morbidity and mortality. The etiopathogenesis, pre-dis­posing factors, selection of the empirical antibiotics, an­tibiotic protocol in the ICU, diagnostic facility in the ICU, training of paramedical and treating physicians, caus­ative organisms, non adherence to aseptic precautions, lack of monitors and specific ventilators, type of ICU (open or close) are the important factors posing specific challenges in developing countries than in developed countries. Unfortunately, no large randomized, prospec­tive or retrospective literatures on this topic, especially for adults are available in context of India. The guide­lines provided by American Thoracic Society (ATS) [1],[2] are the major source for the content in this article.

Differentiations of different types of pneumonia are important as they differ in terms of predominance of caus­ative organism, selection of antibiotic, and course and prog­nosis of the disease. To be more precise, the pneumonia has been broadly categorized as community acquired pneu­monia (CAP) and hospital acquired pneumonia (HAP).

   Definitions Top

Pneumonia: infection of the lung that is most com­monly caused by bacteria but occasionally caused by viruses, fungi, parasites, and other infectious organisms.

Nosocomial pneumonia (NP) / Hospital acquired pneumonia (HAP): pneumonia that occurs 48 hours or more after admission, which was not incubating at the time of admission.

ICU-acquired pneumonia: pneumonia that arise more than 48 hours after ICU admission.

Ventilator-associated pneumonia (VAP): pneumonia that arises more than 48-72 hours after endotracheal intubation.

Early onset HAP& VAP: occurring within the first 4 days of hospitalization.

Late onset HAP& VAP: at 5 days or more of hospitalization.

Healthcare-associated pneumonia (HACAP): This includes any patient who was hospitalized in an acute care hospital for two or more days within 90 days of the infec­tion; resided in a nursing home or long-term care facility; received recent intravenous antibiotic therapy, chemo­therapy or wound care within the past 30 days of the cur­rent infection; or attended a hospital or hemodialysis clinic.

   Epidemiology Top

The incidence of pneumonia has been reported to be 5-10 cases per 1000 hospital admissions [3],[4],[5] , while in general ICU population incidence has ranged from 8­20% [6] . The risk of pneumonia increases by 6 to 20 folds in mechanically ventilated patients [3],[4],[5] . The risk of pneu­monia increases maximum during first five days. During first 5 days of ventilation, risk increases by 3%/day; during 5-10 days of ventilation it increases by 2%/day and af­ter 10 days of ventilatory support it increases by 1%each day [7] . In a recent PGI Chandigarh study, VAP was found to be 30.7% per 1,000 ventilator days.

   Causative organisms Top

Gram negative bacilli (Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae and Acinetobacter species) are the main culprits for HAP (more than 60%). In patients with diabetes and trauma, Gram positive cocci such as Staphylococus aureus are emerging more common [8] . Anaerobic organism may be responsible following aspiration in non-intubated patient but is rare in VAP [9] .

In VAP, MRSA and K. pneumoniae are more com­mon in non ventilated rather than intubated patients [1] . S. pneumoniae and H. influenzae are frequently found in CAP and in early onset HAP in patients without other risk fac­tors, but are uncommon in late onset HAP. Legionella may be mainly responsible organism in immunocompromised patients. Fungal pathogens as Candida species and Aspergil­lus fumigatus may also occur in immunocompromised and organ transplanted patients. Influenza A is probably the most common viral cause of HAP.

   Pathogenesis Top

In HAP, the major sources of infection are through healthcare devices, environment (air, water, equipment& fomites), and transfer of microorganism from health care provider to the patient [3],[4],[5],[10],[11],[12],[13] .

The major potential reservoirs for organisms in a human body are stomach and sinuses. From these po­tential sites, the bacteria get entry into the trachea via aspiration of oropharyngeal pathogens or via leakage of bacteria around endotracheal tube cuff [14],[15] . From tra­chea, the microbial pathogens migrate to lower respira­tory tract and here organisms are being colonized.

Against the invasion entry or migration of micro­bial pathogen, host defenses in the form of mechanical (ciliated epithelium and formation of mucus favoring expulsion of microorganism), in the form of humoral mechanism (formation of antibody and activation of com­pliment system) or in the form of cellular protection (through polymorphonuclear leucocyte, macrophages, lymphocytes and their cytokines) to expel the microor­ganism out or to kill them or to make them inactive [3],[16]. However if the defense mechanism is weak due to any factor or is insufficient to deal with the number of or­ganisms, infection at lower respiratory tract takes place.

   Risk factors Top

Certain risk factors have been identified which makes the patient more vulnerable for HAP:

   General: H/O smoking, advanced age, male sex Top

Disease: COPD, ARDS, burn, trauma, coma or impaired consciousness, multiple organ failure, longer sur­gical procedure, thoracic or upper abdominal operations, immunosuppression (including systemic corticosteroids,) hypoalbuminemia, high APACHE II score and etc.

Intervention: H2 blockers or antacids, mechanical ventilation more than three days, previous antibiotics, use of paralytic agents or continuous sedation, re-intubations, bronchoscopy, nasogastric tube, ICP monitoring etc.

   Modifiable risk factors Top

The risk of HAP in patients who are intubated and mechanical ventilated, is increased by 6 to 21 fold [10],[16]. Incidence of VAP can be reduced by maintaining endot­racheal cuff pressure at greater than 20 cm H2O and by continuous aspiration of subglottic secretions [15],[17],[18].

Possibly, incidence of HAP can be reduced by lim­iting the use of sedative& paralytic agents that depress cough and other host-protective mechanism and also by use of oral endotracheal& orogastric tubes, rather than nasotracheal& nasogastric tubes [17],[18],[19] . On the other side, incidence of VAP is not affected by frequent changing of ventilatory circuit and also by use of passive humidifi­ers or heat-moisture exchangers [20],[21] .

A significant threefold reduction occurred in the incidence of ICU-acquired HAP in patients treated in the semirecumbent position [22] . Postpyloric feeding as well as strategy of late administration (i.e. day 5 of intu­bation ) of enteral feeding is associated with significant reduction in ICU-acquired HAP [23],[24] .

In a randomized trial of post surgical patients, the use of oral antiseptic chlorhexidine was to be found with significantly reduction in rates of nosocomial infection [25] . Now a days routine prophylactic use of antibiotics as a selective decontamination of the digestive tract (SDD), to reduce HAP, is avoided due to high level of antibiotic resistance 1 . Unnecessary liberal use of allogenic blood products and old stored blood are found to be a risk fac­tor for increased incidence of HAP and in a prospective randomized trial comparing liberal and conservative "trig­gers" to transfusion in ICU patients not exhibiting active bleeding and without underlying cardiac disease demonstrated that awaiting a haemoglobin level of 7.0 g/dl as opposed to a level of 9.0 g/dl before initiating transfu­sion resulted in no adverse effects on outcome [26] .

A large, double blind, randomized trial comparing ranitidine with sucralfate demonstrated a trend towards lower rates of VAP with sucralfate, but clinically signifi­cant gastrointestinal bleeding was 4% higher in the sucralfate group [27] . Aggressive treatment of hypergly­cemia has both theoretical and clinical support, but may not lead to significant benefit in patient with VAP [1] .

A great emphasis should be to ensure effective infection control measure, which includes staff educa­tion, compliance with alcohol-based hand disinfection, and isolation to reduce cross-infection with MDR patho­gens, as these means reduce incidence of HAP by around half [10],[13],[28],[29] . Surveillance of ICU infections, to identify and quantify endemic and new MDR pathogens, and preparation of timely data for infection control and to guide appropriate, antimicrobial therapy in patients with suspected HAP or other nosocomial infections, are rec­ommended (Level II) [1] .

   Diagnosis Top

   Clinical and bacteriological strategy Top

The diagnosis of HAP is suspected if the patient has a radio-graphic infiltrate that is new or progressive, along with fever, purulent sputum, leukocytosis, and de­cline in oxygenation. The diagnostic criteria of a radio­graphic infiltrate and at least one clinical feature (fever, leukocytosis, or purulent tracheal secretions) have high sensitivity but low specificity (especially for VAP)[1] . Combinations of signs and symptoms may increase the specificity. When three clinical variables were used, the sensitivity declined, whereas the use of only one vari­able led to decline in specificity [1] .

All patients should have chest radiography, prefer­ably postero-anterior and lateral if not intubated. The radiography can help to define the severity of pneumo­nia and the presence of complications, such as effusions or cavitations [30] .

The clinical approach is overly sensitive, and it could be difficult to differentiate from other non-infectious conditions like congestive heart failure, atelectasis, pul­monary thromboembolism, pulmonary drug reactions, pulmonary hemorrhage, or ARDS [1] .

The clinical pulmonary infection score (CPIS) scor­ing system grades the severity of pneumonia and this include six features [31] . Each of these six features scores on a scale from 0 to 2, as follows: tracheal secretion: 0= rare, 1= abundant, 2= purulent; radiographic infiltrates: 0= absent, 1= patchy or diffuse 2= localized; fever (°C): 0=≥36.5 and ≤38.4, 1= >38.4 and ≥ 38.9, 2= > 38.9 or < 36; leukocytosis (/mm3): 0 = ≥ 4000 and ≤ 11000, 1= < 4000 or > 11000, 2= < 4000 or > 11000 and > 500 band forms; PaO2/FiO2: 0= >240 or acute respiratory dis­tress syndrome (ARDS), 2= ≤ 240 and no ARDS; mi­crobiology 0= negative, 2= positive.

The absence of a "gold standard" for HAP diagno­sis is a major problem, with which diagnostic results can be compared.

Although an etiologic diagnosis is made from a res­piratory tract culture, colonization of the trachea pre­cedes development of pneumonia in almost all cases of VAP, and thus a positive culture cannot always distin­guish a pathogen from a colonizing organism. However, a sterile culture from the lower respiratory tract of an intubated patient, in the absence of a recent change in antibiotic therapy, is strong evidence that pneumonia is not present, and an extra pulmonary site of infection should be considered (Level II) [1],[32].

Samples of lower respiratory tract secretions should be obtained from all patients with suspected HAP, and should be collected before antibiotic changes. Samples can include an endotracheal aspirate, bronchoalveolar la­vage (BAL) sample, or protected specimen brush (PSB) sample (Level II) [1] . A negative tracheal aspirate (absence of bacteria or inflammatory cells) in a patient without a recent (within 72 hours) change in antibiotics has a strong negative predictive value (94%) for VAP (Level II) [33] .

In a prospective study by Gibot and coworkers used a rapid immunoblot technique on BAL fluid in whom infec­tious pneumonia suspected, and found that levels of soluble triggering receptor expressed on myeloid cells (sTREM-1) were the strongest independent predictor of pneumonia [34] .

Being multifocal nature of VAP, BAL and endot­racheal aspirates can provide more representative samples than the protected specimen brush (PSB), which samples only a single bronchial segment [1] .

Endotracheal aspirates can be cultured quantitatively, and with a threshold of 106cfu/ml or more, the sensitivity of this method for the presence of pneumonia has a mean of 76± 9% and specificity with a mean of 75±28% [35].

Bronchoscopic BAL studies have typically used a diagnostic threshold of 104cfu/ml. A review literature of 23 prospective studies of BAL in suspected VAP showed a sensitivity with a mean of 73± 18%, and a specificity with a mean of 82±19% [36].

Quantitative cultures of PSB samples have used a diagnostic threshold of 103cfu/ml or more. The sensitiv­ity and specificity for PSB have a mean 66±19%) and 90±15%, respectively [36],[37] . PSB appears to be more spe­cific than sensitive for the presence of pneumonia [36] .

If bronchoscopic sampling is not immediately available, non bronchoscopic sampling can reliably obtain lower respi­ratory tract secretions for quantitative cultures, which can be used to guide antibiotic therapy decisions (Level II) [38] .

Semi quantitative cultures of tracheal aspirates cannot be used as reliably as quantitative cultures to define the presence of pneumonia and the need for anti­biotic therapy (Level I). [39]

   Management Top

Approximately 10% of hospitalized patients with CAP require ICU admission. Direct admission to an ICU or high-level monitoring unit is recommended for patients either with any one of the major criteria or 3 of the mi­nor criteria for severe CAP (Level II) as listed in [Table 1] [2] . Summary of the recommended management of HAP as a algorithm is given in [Figure 1] [1] .

   Antibiotic therapy Top

Major points and recommendations for anti­biotic therapy : A major goal of therapy is eradication of the infecting organism, and so, antimicrobials are a mainstay of treatment. Delays in the initiation of appro­priate antibiotic therapy can increase the mortality of VAP and thus, therapy should not be postponed for the purpose of performing diagnostic studies in patients who are clinically unstable (level II) [40],[41].

Recommended empirical antibiotics for community­ acquired pneumonia who admitted to ICU are given in [Table 2] [2] . While, use the algorithm in [Figure 2] for HAP to select an initial empiric therapy based on the absence or presence of risk factors for MDR pathogens [Table 3]& [Table 4] (Level III) [1] .

These risk factors include prolonged duration of hospitalization (5 days or more), admission from a healthcare-related facility, and recent prolonged antibi­otic therapy (Level II) [42] .

A reliable tracheal aspirate Gram stain can be used to direct initial empiric antimicrobial therapy and may increase the diagnostic value of the CPIS (Level II) [43] . Therapy is modified on the basis of the clinical response on Days 2 and 3 [1] .

Choice of specific agents should be dictated by lo­cal microbiology, cost, availability, and formulary restric­tions (Level II) [44],[45] . Patients with healthcare-related pneumonia should be treated for potentially drug-resis­tant organisms, regardless of when during the hospital stay the pneumonia begins (Level II) [46] . Inappropriate therapy (failure of the etiologic pathogen to be sensitive to the administered antibiotic) is major risk factor for excess mortality and length of stay for patients with HAP, and antibiotic-resistant organisms are the pathogens most commonly associated with inappropriate therapy (Level II) [47] .

To achieve adequate therapy, it is necessary not only to use the correct antibiotic, but also the optimal dose and the correct route of administration (oral, intra­venous, or aerosol) to ensure that the antibiotic penetrates to the site of infection, and to use combination therapy if necessary. Most b lactam antibiotics achieve less than 50% of their serum concentration in the lung, whereas fluoroquinolones and linezolid equal or exceed their se­rum concentration in bronchial secretions [48] .

The mechanism of action of certain agents can also affect dosing regimens, efficacy, and toxicity. Some antimicrobials are bactericidal whereas others are bac­teriostatic. Bactericidal agents may act in a concentration dependent fashion (aminoglycosides and quinolones) or in a time dependent fashion (vancomycin and b lactam). Some antibiotics do have postantibiotic effect (PAE), as seen with aminoglycoside and quinolones while b lactam antibiotics lack this effect against gram nega­tive bacilli with the exception of carbapenem [49] .

There is a lot of debate over the use of antibiotics as monotherapy versus combination therapy. A meta­analysis has evaluated all prospective randomized trials of -lactam monotherapy compared with b lactam­aminoglycoside combination regimens in patients with sepsis, of whom at least around 15% patients had either HAP or VAP, showed clinical failure was more com­mon with combination therapy and there was no advan­tage in the therapy of P. aeruginosa infections, compared with monotherapy [50]. In addition, combination therapy did not prevent the emergence of resistance during therapy, but did lead to a significantly higher rate of neph­rotoxicity.

Combination therapy should be used if patients are likely to be infected with MDR pathogens (Level II) [42],[44], though no data documented the superiority of this ap­proach compared with monotherpay, except to enhance the likelihood of initially appropriate empiric therapy (Level I) [50] . If patients receive combination therapy with an aminoglycoside-containing regimen, the aminoglycoside can be stopped after 5-7 days in respond­ing patients (Level III) [51].

Monotherapy should be used and preferred over combination therapy whenever possible because combi­nation therapy is often expensive and exposes patients to unnecessary antibiotics, thereby increasing the risk of MDR pathogens and adverse outcomes [1] . Patients who develop nosocomial pneumonia with no risk factors for drug-resistant organisms are likely to respond to monotherapy with the antibiotics listed in [Table 3]. Monotherapy is also the standard when gram-positive HAP, including MRSA, is documented [1] . Monotherapy with ciprofloxacin has been successful in patients with mild HAP (defined as a CPIS of 6 or less) but is less effective in severe HAP [52] .

To use monotherapy in patients with severe VAP, the ATS committee believed that patients should initially receive combination therapy as described in [Table 4], but therapy could be changed to a single agent if cultures did not shown a resistant pathogen [44] .

Monotherapy with selected agents can be used for patients with severe HAP and VAP in the absence of resistant pathogens (Level I) [53],[54] . Patients in this risk group should initially receive combination therapy until the results of lower respiratory tract cultures are known and confirm that a single agent can be used (Level II).

If P. aeruginosa pneumonia is documented, com­bination therapy is recommended, mainly because of the high frequency of development of resistance on monotherapy [53] . Although combination therapy will not necessary prevent the development of resistance, com­bination therapy is more likely to avoid inappropriate and ineffective treatment of patients. (Level II) [44] .

In case of Acinetobacter species are to be present, the most active agents are the carbapenems, sulbactam, colistin, and polymyxin. There are no data documenting an improved outcome if these organisms are treated with a combination regimen. (Level II) [55] . If ESBL+ Enterbacteriaceae are present, then monotherapy with a third-generation cephalosporin should be avoided. The most active agents are the carbapenems (Level II) [56].

   Duration of therapy Top

If patients receive an initially appropriate antibi­otic regimen, efforts should be made to shorten the du­ration of therapy from the traditional 14 to 21 days to periods as short as 7 days, provided that the etiologic pathogen is not P. aeruginosa, and that the patient has a good clinical response with resolution of clinical features of infection (Level I) [57] . Patients with a low clinical sus­picion of VAP (CPIS of 6 or less) can have antibiotics safely discontinued after 3 days [52] .

Data support the promise that most patients with VAP, who receive appropriate antibiotic therapy, have a good clinical response within first 6 days. Prolonged therapy leads to colonization with antibiotic resistants.

   Aerosolized antibiotics Top

Aerosolized antibiotics have not been proven to have value in the therapy of VAP (Level I) [58] . But may be considered as adjunctive therapy with an inhaled amingolycoside or polymyxin for MDR gram negative pneumonia, especially in patients who are not improving with systemic therapy (Level III) [59] . More studies of this type of therapy are needed.

   Preference of particular antibiotic Top

Linezolide is an alternative to vancomycin for the treatment of MRSA VAP (Level II) and may also be preferred if patients have renal insufficiency or are re­ceiving other nephrotoxic agents, but more data are needed (Level III) [60],[61]

   Antibiotic rotation or restriction or holiday Top

Antibiotic restriction can limit epidemics of infec­tion with specific resistant pathogens. Heterogeneity of antibiotic prescriptions, including formal antibiotic cycling, may be able to reduce the incidence of antibiotic resis­tance. But, the long-term impact of this practice is un­known. (Level II) [62],[63] .

   Continuous versus intermittent infusion Top

Standard administration is by intermittent infusion; however, continuous infusion may be advantageous. Ef­ficacy of drug with bactericidal activity increases with the exposure time that could be well maintained above minimum inhibitory concentration (MIC) by the continu­ous infusion. However, sufficient evidence of its clinical efficacy is limited.

   Supportive therapy Top

Although supportive therapy like chest physio­therapy, postural drainage, humidification and aerosolisation with bronchodilators, mucolytic agents are crucial but with little documentation of efficacy in the management of pneumonia.

   Prognosis Top

Patients with VAP had a longer duration of me­chanical ventilation and longer hospital stay. VAP has its own attributable mortality. The crude mortality rate has ranged from 25-70% in late onset HAP/VAP. The in­creased mortality rates were associated with aerobic gram negative bacteria (Pseudomonas aeruginosa, Acinetobacter species), associated with medical rather than surgical illness, inadequate& ineffective antibiotic therapy and also in patients who had acute respiratory distress syndrome [64],[65].

   References Top

1.American Thoracic Society Documents. Gudelines for the man­agement of adults with hospital-acquired, ventilator-acquired, and healthcare associated pneumonia. Am J Respir Crit Care Med 205; 171:388-416.  Back to cited text no. 1      
2.Mandell LA, Wunderink RG, Anzueto et al. Infectious Dis­eases Society of American/ American Thoracic Society consen­sus guidelines on the management of community-acquired pneu­monia in adults. Clin Infect Dis 2007; 44:27-72.  Back to cited text no. 2      
3.Chastre J, Fagon JY. Ventilator-associated pneumonia. Am J Respir Crit Care Med 2002; 165:867-903.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]  
4.Celis R, Torres A, Gatell JM, Almela M. Rodriguez-Roisin R, Agusti-Vidal A. Nosocomial pneumonia: a multivariate analy­sis of risk and prognosis. Chest 1988; 93:318-324.  Back to cited text no. 4      
5.Torres A. Aznar R, Gatell JM, Jimenez P, Gonzalez J, Ferrer A, Celis R, Rodriguez-Roisin R. Incidence, risk, and prognosis factors of nosocomial pneumonia in mechanically ventialated patients. Am Rev Respir Dis 1990;142:523-528.  Back to cited text no. 5      
6.Richards MJ, Edwards JR, Culver DH, Gaynes RP. Nosoco­mial infections in medical ICUs in the United States: National Nosocomial Infections Surveillance System. Crit Care Med. 1999; 27:887-892.  Back to cited text no. 6      
7.Cook DJ, Walter SD, Cook RJ, Griffith LE, Guyatt GH, Leasa D, Jaeschke RZ, Brun-Buisson C. Incidence of and risk factors for ventilator-associated pneumonia in critically ill patients. Ann Intern Med.1998;129:440.  Back to cited text no. 7      
8.Rello J, Torres A, Ricart M, Valles J, Gonzalez J, Artigas A, Rodriguez-Roisin R. Ventilator-associated pneumonia by Sta­phylococcus aureus: comparision of methicillin-resistant and methicillin-sensitive episodes. Am J Respir Crit Care Med 1994; 150:1545-1549.  Back to cited text no. 8  [PUBMED]    
9.Marik PE, Careau P. The role of anaerobes in patients with ventilator-associated pneumonia and aspiration pneumonia: a prospective study. Chest 1999;115:178-183.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]  
10.Tablan OC, Anderson LJ, Besser R, Bridges C, Hajjeh R. Healthcare Infection Control Practices Advisory Committee, Centers for Disease Control and Prevention. Guidelines for preventioning health-care-associated pneumonia, 2003; recom­mendations of the CDC and the Healthcare Infection Control Practices Advisory Committee. MMWR Recomm Rep 2004;53(RR-3):1-36.  Back to cited text no. 10      
11.Craven DE, Steger KA. Epidemiology of nosocomial pneumonia: new perspectives on an old disease. Chest 1995:108:1S-16S.  Back to cited text no. 11      
12.Pittet D, Hugonnet S, Harbarth S, Mourouga P, Sauvan V, Touveneau S, Perneger TV. Effectiveness of a hospital-wide programme to improve compliance with hand hygiene:Infection control programme. Lancet 2000:356:1307-1312.  Back to cited text no. 12      
13.Kollef MH. The prevention of ventilator-associated pneumo­nia. N Engl J Med. 1999:340:627-634.  Back to cited text no. 13      
14.du Maulin GC, Paterson DG, Hedley-Whyte J, Lisbon A. Aspiration of gastric bacteria in antacid-treated patients: a fre­quent cause of postoperative colonisation of the airway. Lan­cet 1982;1:242-245.  Back to cited text no. 14      
15.Valles J, Artigas A, Rello J, Bonsoms N, Fontanals D, Blanch L, Fernandez R, Baigorri F, Mestre J. Continuous aspiration of subglottic secretions in preventing ventilator-associated pneu­monia, Ann Intern Med 1995;122:179-186.  Back to cited text no. 15      
16.Craven DE, Steger KA. Nosocomial pneumonia in mechani­cally ventilated adult patients:epidemiology and prevention in 1996. Semin Respir Infect 1996;11:32-53.  Back to cited text no. 16  [PUBMED]    
17.Cook D, De Jonghe B, Brochard L, Brun-Buisson C. Influence of airway management on ventilator-associated pneumonia:evidence from randomized trials. JAMA 1998:279:781-787.  Back to cited text no. 17      
18.Rello J. Sonora R, Jubert P, Artigas A, Rue M, Valles J. Pneu­monia in intubated patients: role of respiratory airway care. Am J Respir Crit Care Med 1996:154:111-115.  Back to cited text no. 18      
19.Holzapfel L, Chastang, C, Demingeon G, Bohe J, Piralla B, Coupry A. A randomized study assessing the systematic search for maxillary sinusitis in nasotracheally mechanically venti­lated patients. Influence of nosocomial maxillary sinusitis on the occurrence of ventilator associated pneumonia. Am J Respir Crit Care Med. 1999;159;695-701.  Back to cited text no. 19      
20.Hess D. Prolonged use of heat and moisture exchangers: why do we keep changing things. Crit Care Med 2000;28:1667­1668.  Back to cited text no. 20  [PUBMED]  [FULLTEXT]  
21.Kirton OC, De-Haven B, Morgan J, Morejon O. Civetta J. A prospective randomized comparison of an in-line heat mois­ture exchange filter and heated wire humidifiers: rates of venti­lator-associated early-onset (community-acquired) or late-on­set (hospital-acquired pneumonia and incidence of endotra­cheal tube occlusion. Chest 1997; 112:1055-1059.  Back to cited text no. 21      
22.Drakulovic MB, Torres A, Bauer TT, Nicolas JM, Nogue S, Ferrer M. Supine body position as a risk factor for nosocomial pneumonia in mechanically ventilated patients: a randomised trial. Lancet 1999;354:1851-1858.  Back to cited text no. 22      
23.Heyland DK, Drover GW, MacDonald S, Novak F. Lam M. Effect of postpyloric feeding on gastroesophageal regurgita­tion and pulmonary microaspiration: results of a randomized controlled trial. Crit Care Med 2001;29:1495-1501.  Back to cited text no. 23      
24.Ibrahim EH, Mehringer L, Prentice D, Sherman G, Schaiff R, Fraser V, Kollef MH. Early versus late enteral feeding of me­chanically ventilated patients: results of a clinical trial. J. Parenter Enteral Nutr 2002;26:174-181.  Back to cited text no. 24      
25.De-Reiso AJ II, Ladowski JS, Dillon TA, Justice JW, Peterson AC. Chlorhexidine gluconate 0.12% oral rinse reduces the inci­dence of total nosocomial respiratory infection and nonprophylactic systemic antibiotic use in patients undergo­ing heart surgery. Chest 1996;109:1556-1561.  Back to cited text no. 25      
26.Hebert PC, Wells G, Blachman MA, Marshall J, Martin C, Pagliarello G, Tweeddale M, Schweitzer I, Yetisir E. Transfu­sion Requirements in Critical Care Investigators, Canadian Criti­cal Care Trials Group. A multicenter, randomized. Controlled clinical trial of transfusion requirements in critical care. N. Engl J Med 1999; 340:409-417.  Back to cited text no. 26      
27.Prod'hom G, Leuenberger P, Koerfer J, Blum A, Chiolero R, Schaller MD, Perret C, Spinnler O, Blondel J, Siegrist H. Noso­comial pneumonia in mechanically ventilated patients receiv­ing antacid, ranitidine, or sucralfate as prophylaxis for stress ulcer: a randomized controlled trial. Ann Intern Med 1994: 120:653-662.  Back to cited text no. 27      
28.Bonten MJ. Controversies on diagnosis and prevention of ven­tilator associated pneumonia. Diagn Microbiol Infect Dis 1999, 34:199-204.  Back to cited text no. 28  [PUBMED]  [FULLTEXT]  
29.Weinstein RA. Epidemiology and control of nosocomial infec­tions in adult intensive care units. Am J Med 1991;91:179S-184S.  Back to cited text no. 29  [PUBMED]    
30.Wunderink RG, Woldenberg LS, Zeiss J, Day CM, Ciemins J, Lacher DA. The radiologic diagnosis of autopsy-proven venti­lator-associated pneumonia. Chest 1992;101:458-463.  Back to cited text no. 30  [PUBMED]  [FULLTEXT]  
31.Calandra T, Cohen J. The international sepsis forum consensus conference on definitions of infection in the intensive care unit. Crit Care Med 2005; 33: 1538-1548.  Back to cited text no. 31      
32.Souweline B, Veber B, Bedos JP, Gachot B, Dombret MC, Regnier B, Wolff M. Diagnostic accuracy of protected speci­men brush and bronchoalveolar lavage in nosocomial pneumonia:impact of previous antimicrobial treatments. Crit Care med.1998;26:236-244.  Back to cited text no. 32      
33.Blot F, Raynard B, Chachaty E, Tancrede C, Antoun S, Nitenberg G. Value of Gram Stain examination of lower respiratory tract secretions for early diagnosis of nosocomial pneumonia. Am J Respir Crit Care med 2000; 162:1731-1737.  Back to cited text no. 33      
34.Gibot S, Cravoisy A, Levy B, Bene MC, Faure G, Bollaert PE. Soluble triggering receptor expressed on myeloid cells and the diagnosis of pneumonia. N Engl J Med 2004;350:451-458.  Back to cited text no. 34  [PUBMED]  [FULLTEXT]  
35.Cook D, Mandell L. Endotracheal aspiration in the diagnosis of ventilator-associated pneumonia,. Chest 2000;117:195S-197S.  Back to cited text no. 35  [PUBMED]  [FULLTEXT]  
36.Torres A, El-Ebiary M. Bronchoscopic BAL in the diagnosis of ventilator-associated pneumonia. Chest 2000;117:198S-202S.  Back to cited text no. 36  [PUBMED]  [FULLTEXT]  
37.Marquette CH, Herengt F, Mathieu D, Saulnier F, Courcol R, Ramon P. Diagnosis of pneumonia in mechanically ventilated patients: repeatability of the protected specimen brush. Am Rev Respir Dis 1993; 147:211-214.  Back to cited text no. 37  [PUBMED]    
38.Campbell GD, Blinded invasive diagnostic procedures in ven­tilator-associated pneumonia. Chest 2000;117:207S-211S.  Back to cited text no. 38      
39.Sanchez-Nieto JM. Torres A, Garcia-Cordoba F, El-Ebiary M, Carrillo A, Ruiz J, Nunez ML, Niederman M. Impact of inva­sive and noninvasive quantitative culture sampling on outcome of ventilator-associated pneumonia: a pilot study. Am J Respir Crit Care Med. 1998;157:371-376.  Back to cited text no. 39      
40.Luna CM, Vujacich P, Niederman MS, Vay C, Gherardi C, Matera J, Jolly EC. Impact of BAL data on the therapy and outcome of ventilator associated pneumonia. Chest 1997;111:676-685.  Back to cited text no. 40  [PUBMED]  [FULLTEXT]  
41.Kollef MH, Sherman G, Ward S, Fraser VJ. Inadequate antimi­crobial treatment of infections: a risk factor for hospital mor­tality among critically ill patients. Chest 1999;115:462-474.  Back to cited text no. 41  [PUBMED]  [FULLTEXT]  
42.Trouillet JL, Chastre J, Vuagnat A, Joly-Guillou ML, Combaux D, Dombret MC, Gibert C. Ventilator-associated pneumonia caused by potentially drug-resistant bacteria. Am J Respir Crit Care Med. 1998; 157:531-539.  Back to cited text no. 42      
43.Fartoukh M, Maitre B, Honore S, Cerf C, Zahar JR, Brun­Buisson C. Diagnosing pneumonia during mechanical ventila­tion: the clinical pulmonary infection score revisited. Am J Respir Crit Care Med. 2003;168:173-179.  Back to cited text no. 43      
44.Ibrahim EH, Ward S, Sherman G, Schaiff R, Fraser VJ, Kollef MH. Experience with a clinical guideline for the treatment of ventilator associated pneumonia. Crit Care Med 2001;29:1109-1115.  Back to cited text no. 44  [PUBMED]  [FULLTEXT]  
45.Namias N, Samiian L, Nino D, Shirazi E, O' Neill K, Kett DH, Ginzburg E, Mc-Kenney MG, Sleeman D, Cohn SM. Inci­dence and susceptibility of pathogenic bacteria vary between intensive care units within a single hospital:implications for empiric antibiotic strategies. J. Trauna 2000;49:638-645 [dis­cussion 645-646].  Back to cited text no. 45      
46.Gaynes R. Health-care associated bloodstream infections: a change in thinking. Ann Intern Med. 2002; 137:850-851.  Back to cited text no. 46  [PUBMED]  [FULLTEXT]  
47.Kollef MH. Inadequate antimicrobial treatment: an important determinant of outcome for hospitalized patients. Clin Infect Dis 2000;31: S131-S138.  Back to cited text no. 47  [PUBMED]  [FULLTEXT]  
48.Conte JE Jr, Golden JA, Kipps J. Zurlinden E. Intrapulmo­nary pharmacokinetics of linezolid. Antimicrob Agents Chemother 2002;46:1475-1480.  Back to cited text no. 48      
49.Craig WA. The pharmacology of meropenem, a new carbapenem antibiotic. Clin Infect Dis 1997; 24: S266-S275.  Back to cited text no. 49  [PUBMED]    
50.Paul M, Benuri-Silbiger I, Soares-Weiser K, Liebovici L. - Lactam monotherapy versus -Lactam-aminoglycoside combi­nation therapy for sepsis in immunocompetent patients: sys­tematic review and meta-analysis of randomized trials. BMJ, doi:10.1136/bmj.bmjjournals.com/cgi/reprint/bmj. 38028.520995.63v1.pdf?ck=nck.  Back to cited text no. 50      
51.Gruson D, Hilbert G, Vargas F, et al. Rotation and restricted use of antibiotics in a medical intensive care unit: impact on the incidence of ventilator-associated pneumonia caused by anti­biotic resistant gram negative bacteria. Am J Respir Crit Care Med 2000; 162: 837-843.  Back to cited text no. 51  [PUBMED]  [FULLTEXT]  
52.Singh N, Rogers P, Atwood CW et al. Short course empiric antibi­otic therapy for patients with pulmonary infiltrates in the inten­sive care unit: a proposed solution for indiscriminate antibiotic prescription. Am J Respir Crit Care Med 2000; 162: 505-511.  Back to cited text no. 52      
53.Fink MP, Snydman DR, Niederman MS et al. Severe pneumo­nia study group. Treatment of severe pneumonia in hospital­ized patients: results of a multicenter, randomized double blind trial comparing intravenous ciprofloxacin with imipenem­cilastatin. Antimicrob Agents Chemother 1994; 38: 547-557.  Back to cited text no. 53      
54.Jaccard C, Troillet N, Harbarth S et al. Prospective random­ized comparison of imipenem-cilastatin and piperacillin­tazobactam in nosocomial pneumonia or peritonitis. Antimicrob Agents Chemother 1998; 42:2966-2972.  Back to cited text no. 54      
55.Garnacho-Montero J, Ortiz-Leyba C, Jimenez-Jimenez FJ et al. Treatment of multidrug-resistant Acinetobacter baumannii ventilator-associated pneumonia (VAP) with intravenous colis­tin: a comparison with imipenem-succeptible VAP. Clin Infect Dis 2003;36:1111-1118.  Back to cited text no. 55      
56.Paterson DL, Ko WC, Von Gattberg A, Casellas JM, Mulazimoglu L, Klugman KP, Bonomo RA, Rice LB, Mc Cormack JG, Yu VL. Outcome of cephalosporin treatment for serious infections due to apparently susceptible organisms producing extended-spectrum ?-lactamases: implications for the clinical microbiology laboratory. J Clin Microbiol 2001;39:2206-2212.  Back to cited text no. 56      
57.Chastre J. Wolff M. Fagon JY, Chevret S, Thomas F, Wermert D, Clementi E, Gonzalez J, Jusscrand D. Asfar P, et al, Com­parison of 8 vs 15 days of antibiotic therapy for ventilator­associated pneumonia in adults: a randomized trial. JAMA 2003;290:2588-2598.  Back to cited text no. 57      
58.Brown RB, Kruse JA, Counts GW, Russel JA Christou NV, Sands ML. Endotracheal Tobramycin Study Group. Double­blind study of endotracheal tobramycin in the treatment of gram-negative bacterial pneumonia. Antimicrob Agents Chemother 1990;34:269-272.  Back to cited text no. 58      
59.Hamer DH. Treatment of nosocomial pneumonia and tracheo­bronchitis caused by multidurg-resistant Pseudomonas aeruginosa with aerosolized colistin. Am J Respir Crit Care Med. 2000:162:328-330  Back to cited text no. 59      
60.Wunderink RG, Rello J, Cammarata SK. Cross-Dabrera RV, Kollef MH. Linezolid vs Vancomycin: analysis of two double­blind studies of patients with methicillin-resistant Staphylo­coccus aureus nosocomial pneumonia. Chest 2003; 124:1789­-1797  Back to cited text no. 60      
61.Wunderink RG, Cammarata SK, Oliphant TH, Kollef MH. Continuation of a randomized, double-blind, multicenter study of linezolid versus vancomycin in the treatment of patients with nosocomial pneumonia. Clin Ther 2003;25:980-992.  Back to cited text no. 61      
62.Kollef MH, Ward S, Sherman G et al. Inadequate treatment of nosocomial infection is associated with certain empiric antibi­otic choices. Crit Care Med 2000; 28: 3456-3464.  Back to cited text no. 62      
63.Gruson D, Hilbert G, Vargas F et al. Strategy of antibiotic rotation: long-term effect on incidence and susceptibilities of gram-negative bacilli responsible for ventilator-associated pneu­monia. Crit Care Med 2003;31: 1908-1914.  Back to cited text no. 63      
64.Rello J. Ausina V. Ricart M, Castella J, Prats G. Impact of previous antimicrobial therapy on the etiology and outcome of ventilator associated pneumonia. Chest 1993;104:1230-1235.  Back to cited text no. 64      
65.Heyland DK, Cook DJ, Griffith L, Keenan SP, Brun-Buisson C, Canadian Critical Trials Group. The attributable morbidity and mortality of ventilator-associated pneumonia in the criti­cally ill patient. Am J Respir Crit Care Med 1999;159:1249­-1256.  Back to cited text no. 65      


  [Figure 1], [Figure 2]

  [Table 1], [Table 2], [Table 3], [Table 4]


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