VENTILATOR ASSOCIATED INJURIES,COMPLICATIONS AND INFECTIONS

1
VENTILATOR ASSOCIATED INJURIES,COMPLICATIONS AND
INFECTIONS
www.anaesthesia.co.in anaesthesia.co.in_at_gmail.c
om

• 
  ModeratorDr.B.Kaur
• 
  SpeakerDr.Ashish

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Ventilator-associated lung injury

• Components
• BAROTRAUMA
• VOLUTRAUMA
• ATELECTOTRAUMA
• BIOTRAUMA
• OXYGEN TOXIC EFFECTS

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Barotrauma

• Barotrauma - rupture of alveolus with subsequent
  entry of air into pleural space (pneumothorax)
  and/or tracking or air along the vascular bundle
  to mediastinum (pneumomediastinum).
• Large tidal volumes and elevated peak inspiratory
  and plateau pressures are risk factors.

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Barotrauma

• Studies in patients with ARDS demonstrated that
  severity of underlying lung pathology is a better
  predictor of barotrauma than observed peak
  inspiratory pressure.

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Barotrauma

• The IE ratio can be adjusted by increasing
  inspiratory flow rate, by decreasing tidal
  volume, and by decreasing ventilatory rate.
• Attention to IE ratio is important to prevent
  barotrauma in patients with obstructive airway
  disease (eg, asthma, chronic obstructive
  pulmonary disease).

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Volutrauma

• Volutrauma - local overdistention of normal
  alveoli.
• Volutrauma has gained recognition over last 2
  decades d/t importance of lung protection
  ventilation with low tidal volumes of 68 mL/kg.

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Volutrauma

• When a mechanical ventilation breath is forced
  into patient - positive pressure tends to follow
  path of least resistance to normal or relatively
  normal alveoli, potentially causing
  overdistention.
• This overdistention l/t inflammatory cascade that
  augments or perpetuates the initial lung injury,
  causing additional damage to previously
  unaffected alveoli.

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Volutrauma

• The increased local inflammation lowers the
  patient's potential to recover from ARDS.
• The inflammatory cascade occurs locally and may
  augment the systemic inflammatory response as
  well.

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Volutrauma

• Another aspect of volutrauma associated with
  positive ventilation is the shear force
  associated with the opening and closing effects
  on collapsible alveoli.
• This has also been linked to worsening the local
  inflammatory cascade.

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Volutrauma

• PEEP prevents alveoli from totally collapsing at
  the end of exhalation and may be beneficial in
  preventing this type of injury.

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ATLECTOTRAUMA

• Lung injury a/w repeated recruitment and collapse
• Preventable by using level of PEEP greater then
  lower inflection point of pressure-volume curve.
• Also k/a low volume or low end expiratory volume
  injury

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BIOTRAUMA

• Pulmonary and systemic inflammation caused by
  release of mediators from lungs subjected to
  injurious mechanical ventiltion.
• Mechanism MECHANOTRANSDUCTION-physical forces
  are detected by cells and converted into
  biochemical signals
• Injurious ventilatory strategy are as/w release
  of proinflammatory mediators like thromboxane B2,
  platelet activating factor and several cytokines.

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Oxygen toxicity

• Oxygen toxicity is a function of increased FIO2
  and its duration of use.
• Oxygen toxicity is due to production of oxygen
  free radicals, such as superoxide anion, hydroxyl
  radical, and hydrogen peroxide.

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Oxygen toxicity

• Oxygen toxicity can cause a variety of
  complications ranging from mild
  tracheobronchitis, absorptive atelectasis, and
  hypercarbia to diffuse alveolar damage .

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Oxygen toxicity

• No consensus has been established for the level
  of FIO2 required to cause oxygen toxicity
• Use the lowest FIO2 that accomplishes the needed
  oxygenation.

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Oxygen toxicity

• It is adviced to attain an FIO2 of 60 or less
  within the first 24 hours of mechanical
  ventilation.
• If necessary, PEEP should be considered a means
  to improve oxygenation while a safe FIO2 is
  maintained.

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Lung Protective Strategy

• ARDSNet Study - GOALS
• PaO2 55-80 mmhg
• T.V 6 ml/Kg IBW
• RR up to 35 to maintain a pH gt 7.30,
• if lt7.15 then HCO3
• Plateau Pressure lt 30 cm H2O

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How to set PEEP

• Use PEEP FIO2 table from ARDSnet study
• FiO2 .3 .4 .4 .5 .5 .6 .7 .7 .7 .8
  .9 .9 .9 1.0
• PEEP 5 5 8 8 10 10 10 12 14 14 14 16
  18 18-24
• This table is designed to be appropriate for the
  average patient, but sometimes PEEP needs to be
  individualized

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Ventilator associated pneumonia

• Ventilator-associated pneumonia (VAP) is
  pneumonia that develops 48 hours or longer after
  mechanical ventilation is given by means of an
  Endotracheal tube or Tracheostomy.

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Ventilator associated pneumonia

• Ventilator-associated pneumonia remain important
  causes of morbidity and mortality despite
• advances in antibiotics therapy,
• better supportive care modalities,
• and use of a wide-range of preventive measures

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Ventilator associated pneumonia

• The exact incidence of VAP is 6 to 20 fold
  greater than in Non-Ventilated patients.
• VAP is associated with a higher crude mortality
  than other hospital-acquired infections (Level
  II).

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How does the lung get infected ?

• Sources of pathogens for VAP include
• The environment (air, water, equipment,), and
• Transfer of microorganisms between the patient
  and staff or other patients (Level II)
• A number of host- and treatment-related factors,
• Severity of the patients underlying disease,
• Prior surgery,
• Exposure to antibiotics
• Exposure to invasive respiratory devices and
  equipment. (Level II).

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How does the lung get infected ?

• Aspiration of
• oropharyngeal pathogens, or
• leakage of secretions around the endotracheal
  tube
• are the primary routes of bacterial entry into
  the lower respiratory tract (Level II)

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How does the lung get infected ?

• Hematogenous spread from infected intravenous
  Catheters.
• Bacterial translocation from the gastrointestinal
  tract lumen are uncommon pathogenic mechanisms
  (Level II)

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How does the lung get infected ?

• Infected bio-film in the endotracheal tube, with
  subsequent embolization to distal airways, may be
  important in the pathogenesis of VAP (Level III)
• The sinuses may be potential reservoirs of
  nosocomial pathogens but their contribution is
  controversial, (Level II)

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Early Late VAP

• Early
• lt 3 days of mechanical ventilation
• Typically community acquired agents
• Strep. Pneumoniae
• Other Streptococci
• MSSA

• Late
• gt 3 days from initiation of ventilation
• Gram negatives
• Pseudomonas
• Acinetobacter
• Klebsiella
• MRSA

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Early vs late VAP

• Time of onset of pneumonia is an important
  variable for the outcomes in patients with VAP .
• Early-onset VAP, usually carry a better
  prognosis, and are more likely to be caused by
  antibiotic-sensitive bacteria.
• Late-onset VAP are likely to be caused by
  multi-drug resistant (MDR) pathogens, and are
  associated with increased patient mortality and
  morbidity.

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Clinical presentation of VAP

• Usually suspected when a patient on mechanical
  ventilation develops
• new pulmonary infiltrates
• fever,
• leucocytosis
• purulent secretions.
• Additional indicators maybe
• increased Respiratory Rate,
• increased minute ventilation,
• decreased oxygenation,
• or need of higher ventilatory support.

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Diagnosis of VAP

• Diagnosis is DIFFICULT because the clinical signs
  and x-ray features are non specific.
• ONLY 50 OF PATIENTS WITH ALL ABOVE FINDINGS WILL
  HAVE VAP.

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CLINICAL PULMONARY INFECTION SCORE (CPIS)

• Points are given for 7 variables
• Temperature
• WBC Count
• PaO2/FiO2
• Chest X-ray
• Quality of tracheal secretions
• Progression of infiltrate
• Culture of aspirate
• Score gt6 is considered suggestive of VAP.
• BUT, recent studies have consistently shown low
  specificity and sensitivity of CPIS.

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How Do We Diagnose? 2-1-2

• Radiographic evidence x 2 consecutive days
• New, progressive or persistent infiltrate
• Consolidation, opacity, or cavitation
• At least 1 of the following
• Fever (gt 38 degrees C) with no other recognized
  cause
• Leukopenia (lt 4,000 WBC/mm3) or leukocytosis (gt
  12,000 WBC/mm3)
• At least 2 of the following
• New onset of purulent sputum or change in
  character of secretions
• New onset or worsening cough, dyspnea, or
  tachypnea
• Rales or bronchial breath sounds
• Worsening gas exchange (? sats, PF ratio lt 240,
  ? O2 req.)

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MICROBIOLOGY OF LOWER RESPIRATORY TRACT

• 2 TYPES OF METHODS
• A BRONCHOSCOPIC METHODS
• i) BAL (broncho-alveolar lavage)
• ii) PSB (protected specimen brush)
• B NON BRONCHOSCOPIC (blind) METHODS
• i) TRACHEO-BRONCHIAL ASPIRATION
  
  
• ii) mini- BAL

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BRONCHOSCOPIC METHODS

• BAL(Bronchoalveolar lavage)
• Involves infusion aspiration of saline through
  a flexible fiberoptic bronchoscope that is wedged
  in a bronchial segment.
• use atleast 140 ml saline to maximize yield
• gt 10 4 CFU/ml are taken as positive.
• PSB( Protected specimen brush)
• Minimises contamination during bronchoscopy,
  because the brush is contained in a protective
  sheath.
• gt 10 3 CFU/ml are taken as positive.

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BAL vs PSB

• PSB is 90 sensitive and 95 specific.
• BAL is 80 sensitive and 85 specific.

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NON-BRONCHOSCOPIC METHODS

• TRACHEOBRONCHIAL ASPIRATION
• blind method
• basically it is the suction of ET secretions
• gt 10 5 CFU/ml are taken as positive.
• Mini BAL
• blind method
• catheter is advanced till resistance is met, then
  saline is instilled, followed by aspiration of
  sample.

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BRONCHOSPIC vs BLIND TECHNIQUES

• Evidence suggests that Bronchoscopic sampling and
  culture methods tend to have higher specificity,
  but the overall diagnostic accuracy is
  comparable.
• Bronchoscopic methods have failed to show
  improvement in
• mortality,
• length of hospital stay, and
• duration of mechanical ventilation when compared
  to blind methods.
• It may, however, lead to a narrower antibiotic
  regimen.

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• The present CONSENSUS is-
• PROVIDED EMPIRICAL ANTIBIOTICS ARE STARTED AT THE
  TIME OF SUSPICION OF VAP,
• EITHER OF THE TWO METHODS CAN BE USED FOR THE
  DIAGNOSIS.

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Controversy Use of Selective decontamination
of digestive tract

• SDD use of prophylactic iv and oral antibiotics
  to sterilize the gut
• In low resistance settings, efficacy of SDD is
  convincing.
• In conditions of high antibiotic resistance (like
  in most Indian ICUs), SDD cant be recommended for
  prevention of VAP.

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Modifiable Risk Factors

• General prophylaxis.
• Effective infection control measures
• staff education,
• compliance with hand disinfection,
• and isolation to reduce cross-infection with MDR
  pathogens should be used routinely (Level I)

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Modifiable Risk Factors

• 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 VAP, are recommended (Level II)

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Intubation and mechanical ventilation.

• Intubation and reintubation should be avoided, if
  possible as it increases the risk of VAP (Level
  I)
• Noninvasive ventilation should be used whenever
  possible in selected patients with respiratory
  failure (Level I).
• Continuous aspiration of subglottic secretions
  can reduce the risk of early-onset VAP, and
  should be used, if available (Level I)

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Intubation and mechanical ventilation.

• Heatmoisture exchangers decrease ventilator
  circuit colonization, but do not reduce the
  incidence of VAP.(Level I)
• Orotracheal intubation and orogastric tubes are
  preferred over nasotracheal intubation and
  nasogastric tubes to prevent nosocomial sinusitis
  and to reduce the risk of VAP, (Level II)

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Intubation and mechanical ventilation.

• The endotracheal tube cuff pressure should be
  maintained at greater than 20 cm H2O to prevent
  leakage of bacterial pathogens around the cuff
  into the lower respiratory tract (Level II)
• Contaminated condensate should be carefully
  emptied from ventilator circuits and condensate
  should be prevented from entering the
  endotracheal tube(Level II)

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Intubation and Mechanical Ventilation.

• Reduced duration of intubation and mechanical
  ventilation may prevent VAP and can be achieved
  by protocols to improve the use of sedation and
  to accelerate weaning (Level II)
• Maintaining adequate staffing levels in the ICU
  can reduce length of stay, improve infection
  control practices, and reduce duration of
  mechanical ventilation (Level II)

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Enteral feeding.

• Enteral nutrition is preferred over parenteral
  nutrition to reduce the risk of complications
  related to central intravenous catheters and to
  prevent reflux villous atrophy of the intestinal
  mucosa that may increase the risk of bacterial
  translocation (Level I)

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Body position

• Patients should be kept in the semi-recumbent
  position 3045. (Level I)

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HOB Elevation gt 30 Degrees on all Mechanically
Ventilated Patients

• Contraindications
• Hypotension MAP lt70
• Tachycardia gt150
• CI lt2.0
• Central line procedure
• Posterior circulation strokes
• Cervical spine instability use reverse
  trendelenburg
• Some femoral lines ie IABP no higher than 30
  degrees use reverse trendelenburg
• Increased ICP, No higher than 30 degrees avoid
  hip flexion
• Proning

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Modulation of colonization Oral
antiseptics and antibiotics.

• In prior administration of systemic antibiotics
  there should be increased suspicion of infection
  with MDR pathogens (Level II)
• Prophylactic administration of systemic
  antibiotics for 24 hours at the time of
  Intubation is not recommended. (Level I)

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Modulation of colonization Oral
antiseptics and antibiotics.

• Modulation of oro-pharyngeal colonization by the
  use of oral chlorhexidine. Its routine use is not
  recommended (Level I)
• Use daily interruption or lightening of sedation
  to avoid constant heavy sedation (Level II)

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Stress bleeding prophylaxis, transfusion, and
hyperglycemia.

• There is trend toward reduced VAP with
  sucralfate, but if stress bleeding prophylaxis is
  needed either H2 antagonists or sucralfate is
  acceptable (Level I)
• Transfusion of red blood cell and other
  allogeneic blood products should follow a
  restricted transfusion trigger policy (Level I)
• Intensive insulin therapy is recommended to
  maintain serum glucose levels between 80 and 110
  mg/dl in ICU patients to reduce nosocomial blood
  stream infections, duration of mechanical
  ventilation, ICU stay, morbidity, and mortality
  (Level I)

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Recommendations for Diagnosis

• Tracheal colonization is common in intubated
  patients, but in the absence of clinical findings
  is not a sign of infection, and does not require
  therapy or diagnostic evaluation (Level II)
• All patients with suspected VAP should have blood
  cultures collected, recognizing that a positive
  result can indicate the presence of either
  pneumonia or extrapulmonary infection (Level II)
• Samples of lower respiratory tract secretions
  should be obtained from all patients with
  suspected VAP, and should be collected before
  antibiotic changes. (Level II)

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Recommendations for Diagnosis

• For patients with ARDS, it is difficult to
  demonstrate deterioration of radiographic images.
• At least one of the three clinical criteria or
  hemodynamic instability or deterioration of blood
  gases, should lead to more diagnostic testing
  (Level II)

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Recommendations for the clinical strategy.

• A reliable tracheal aspirate Gram stain can be
  used to direct initial empiric antimicrobial
  therapy. (Level II)
• 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 and should lead to a search for alternative
  sources of fever (Level II)
• The presence of a new or progressive radiographic
  infiltrate plus at least two of three clinical
  features (fever, leukocytosis, and purulent
  secretions) represent the most accurate clinical
  criteria for starting empiric antibiotic therapy
  (Level II)
• Re-evaluation of the decision to use antibiotics
  based on the results lower respiratory tract
  cultures by Day 3 or sooner, is necessary (Level
  II)

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Recommendations for initial antibiotic therapy.

• Select an initial empiric therapy based on the
  absence or presence of risk factors for MDR
  pathogens (Level III). These risk factors include
  
• prolonged duration of hospitalization (gt5 days)
• admission from a healthcare-related facility
• recent prolonged antibiotic therapy (Level II)
• Inappropriate therapy is a major risk factor for
  excess mortality and length of stay for patients
  with VAP.(Level II).

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• In patients who have recently received an
  antibiotic, an effort should be made to use an
  agent from a different antibiotic class (Level
  III).
• Initial empiric therapy should be adapted to
  local patterns of antibiotic resistance, with
  each ICU collecting this information and updating
  it on a regular basis (Level II).

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Recommendations for Optimal Antibiotic Therapy

• Aerosolized antibiotics have not been proven to
  have value in the therapy of VAP (Level I) .
• Combination therapy should be used if patients
  are likely to be infected with MDR pathogens
  (Level II).
• Combination therapy has enhanced likelihood of
  initially appropriate empiric therapy (Level I).
• If patients receive combination therapy with an
  aminoglycoside- containing regimen, the
  aminoglycoside can be stopped after 57 days in
  responding patients (Level III)

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Recommendations for Optimal Antibiotic Therapy

• 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).

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Recommendations for selected MDR pathogens.

• If Acinetobacter are 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)
• If Enterobacteriaceae are isolated, then
  monotherapy with a third-generation cephalosporin
  should be avoided. The most active agents are the
  carbapenems (Level II).
• Linezolid is an alternative to vancomycin for the
  treatment of MRSA VAP.(Level III).

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Recommendations for Assessing Response to Therapy

• An assessment of clinical parameters should
  define the response to therapy. (Level II)
• Unless the patient is rapidly deteriorating give
  48 -72 Hrs for the therapy to work. (Level III).
• Nonresponse to therapy is usually evident by Day
  3, (Level II).
• A responding patient should have de-escalation of
  antibiotics, on the basis of culture data (Level
  II).

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Recommendations for Assessing Response to Therapy

• The non-responding patient should be evaluated
  for
• noninfectious mimics of pneumonia,
• unsuspected or drug-resistant organisms,
• Extra-pulmonary sites of infection, and
• complications of pneumonia and its therapy.
• Diagnostic testing should be directed to
  whichever of these causes is likely (Level III).

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Four major principles underlie the management of
VAP.

• Avoid untreated or inadequately treated VAP.
• Recognize the variability of bacteriology from
• one hospital to another,
• specific sites within the hospital, and
• from one time period to another,
• and use this information to select
  antibiotic treatment.
• Avoid the overuse of antibiotics by focusing on
  accurate diagnosis.
• Apply prevention strategies aimed at modifiable
  risk factors.

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Things that DO NOT prevent VAP

• Chest physiotherapy
• Early tracheostomy.
• Change of ventilatory circuits
• Change of HME filters
• In line suctioning
• Prophylactic antibiotics

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Thank you.
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