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Executive Summary(4)
A shorter duration of ABx therapy (7 to 8 days):
recommended for
- uncomplicated HAP, VAP, or HCAP
- with initially appropriate therapy
- a good clinical response
- with no evidence of infection with nonfermenting gram-negative bacilli
Introduction(1)
HAP: pneumonia occurs  48 hrs after admission
( not intubated at admission)
VAP: pneumonia occurs48-72 hrs after intubation
HCAP: pneumonia occurs including those
- hospitalized in an acute care hospital for  2 days
within 90 days
- received recent IV antibiotic therapy, chemotherapy, or
wound care within the past 30 days
- resided in a nursing home or long-term care facility
- attended a hospital or hemodialysis clinic
Introduction(2)
4 major principles to manage HAP, VAP, HCAP:
Avoid untreated or inadequately treatment;
because failure to initiate prompt appropriate and
adequate therapy   increased mortality
Avoid the overuse of antibiotics by focusing on
accurate diagnosis, tailoring therapy to the results
of LRTCs, and shortening duration of therapy to
the minimal effective period
Introduction(2)
4 major principles to manage HAP, VAP, HCAP:
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 alter the selection of an
appropriate antibiotic treatment regimen for any
specific clinical setting
Apply prevention strategies aimed at modifiable
risk factors
Epidemiology (1)
Time of onset of pneumonia: an important
epidemiologic variable and risk factor for specific
pathogens and outcomes
Early-onset HAP and VAP(  4 days):
usually better prognosis, more likely to be caused
by antibioticsensitive bacteria
(Level II)
Epidemiology (2)
Late-onset HAP and VAP ( 5 days ): usually with
increased mortality and morbidity, more likely to
be caused by multidrug-resistant (MDR)
pathogens (Level II)
Early-onset HAP with prior ABx or prior
hospitalization within the past 90 days: are at
greater risk for colonization and infection with
MDR pathogens treat as late-onset HAP or
VAP (Level II)
Epidemiology (3)
Epidemiology (4)
HAP/VAP Pts:  risk for colonization and
infection with MDR pathogens (Level II)
Incidence of HAP/VAP: difficult to define exactly
(overlap with tracheobronchitis) (Level III)
The exact incidence of HAP: usually between
5~15/1,000 admissions (Level II)
The exact incidence of VAP: 6~20-fold greater
than in non-ventilated patients (Level II)
Epidemiology (5)
Causes of most cases of HAP, VAP, and HCAP:
Bacteria, usually polymicrobial; especially high
rate in patients with ARDS (Level I)
Common bacteria: (Level II)
- Aerobic GNB: P. aeruginosa, K. pneumoniae, and
Acinetobacter species
- Aerobic GPC, such as S. aureus ( much MRSA)
- Anaerobes: uncommon .
Epidemiology (6)
Rates of L. pneumophila: vary between hospitals,
occurs commonly in serogroup1; with colonized
water supply and ongoing construction (Level II)
Nosocomial virus and fungal infections:
uncommon in immunocompetent patients (Level I)
Outbreaks of influenza: occurred sporadically and
risk of infection reduced with widespread
effective infection control, vaccination, and use
of antiinfluenza agents (Level I)
Epidemiology (7)
Prevalence of MDR pathogens: varies by patient
population, hospital, and type of ICU; need for
local surveillance data (Level II)
MDR pathogens: (Level II)
more commonly isolated from patients
- with severe, chronic underlying disease
- with risk factors for HCAP
- with late-onset HAP or VAP
Pathogenesis (1)
Sources of pathogens: (Level II)
- healthcare devices
- the environment (air, water, equipment, and fomites)
- transfer of microorganisms between patients and staffs
Host- and treatment-related colonization factors:
important pathogenesis: (Level II)
- the severity of underlying disease
- prior surgery
- exposure to antibiotics
- other medications
- exposure to invasive respiratory devices and equipment
Pathogenesis (2)
Primary routes of bacterial entry: (Level II)
- aspiration of oropharyngeal pathogens
- leakage of secretions
which containing bacteria around tube cuff
Uncommon pathogenic mechanisms (Level II)
- inhalation or direct inoculation of pathogens
- hematogenous spread from infected intravenous
catheters
- bacterial translocation from GI tract
Pathogenesis (3)
Infected biofilm in the endotracheal tube, with
subsequent embolization to distal airways, may be
important in the pathogenesis of VAP (Level III)
Stomach and sinuses: potential reservoirs of
pathogens, contribute to bacterial colonization of
the oropharynx, but their contribution is
controversial (Level II)
Modifiable Risk Factors (1)
General prophylaxis.
Effective infection control measures: (Level I)
-staff education
-alcohol-based hand disinfection
-isolation: cross-infection with MDR pathogens
Surveillance of ICU infections: (Level II)
to identify and quantify endemic and new MDR
pathogens, and preparation of timely data for
infection control
Modifiable Risk Factors (2)
Intubation and mechanical ventilation
Avoid intubation and reintubation (risk of VAP)
(Level I)
Noninvasive ventilation should be used whenever
possible in selected patients (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 ( direct causality has
not been proved) (Level II)
Modifiable Risk Factors (3)
Intubation and mechanical ventilation
Continuous aspiration of subglottic secretions:
risk of early-onset VAP (Level I)
Cuff pressure  20 cm H2O to prevent leakage of
bacterial pathogens (Level II)
Clear contaminated condensate from ventilator
circuits and prevent to enter either the
endotracheal tube or inline medication nebulizers
(Level II)
Modifiable Risk Factors (4)
Intubation and mechanical ventilation
Passive humidifiers or heat–moisture exchangers:
circuit colonization, but not consistently
incidence of VAP not a pneumonia prevention
tool (Level I)
duration of intubation and MV: may prevent VAP,
achieved by the use of sedation and to accelerate
weaning (Level II)
Modifiable Risk Factors (5)
Aspiration, body position, and enteral feeding.
Kept in the semirecumbent position (30–45) rather
than supine to prevent aspiration, especially
when receiving enteral feeding (Level I)
Enteral nutrition: preferred over parenteral
nutrition (Level I)
-  risk of complications related to CVP
- prevent reflux villous atrophy of intestinal mucosa
( whichrisk of bacterial translocation)
Modifiable Risk Factors (6)
Modulation of colonization:oral antiseptics and ABx
Routine prophylaxis of HAP with oral antibiotics
with or without systemic antibiotics:
-incidence of VAP
-has helped contain outbreaks of MDR bacteria (Level I)
Not recommended especially in patients who may
be colonized with MDR pathogens (Level II)
Onset of infection with prior systemic ABx
suspicious infection with MDR pathogens
(Level II)
Modifiable Risk Factors (7)
Modulation of colonization:oral antiseptics and ABx
Prophylactic systemic ABx for 24 hrs at the time of
intubation: demonstrated to prevent HAP in patients
with closed head injury, but not recommended a
routine until more data become available (Level I)
Modulation of oropharyngeal colonization by the
use of oral chlorhexidine: has prevented HAP in
CABG, but not recommended a routine until more
data become available (Level I)
Modifiable Risk Factors (8)
Modulation of colonization:oral antiseptics and ABx
Use daily interruption or lightening of sedation to
avoid constant heavy sedation and try to avoid
paralytic agents, both of which can depress cough
and thereby  risk of HAP (Level II)
Modifiable Risk Factors (9)
Stress bleeding prophylaxis, transfusion
Sucralfate: VAP, but slightly rate of significant
gastric bleeding compared with H2 antagonists.
Stress bleeding prophylaxis: H2 antagonists or
sucralfate is acceptable (Level I)
Transfusion of RBC with a restricted policy;
leukocyte-depleted RBC transfusions can  HAP in
selected patient populations (Level I)
Modifiable Risk Factors (9)
Hyperglycemia
Intensive insulin therapy: recommended to maintain
BS between 80 and 110 mg/dl in ICU patients
- nosocomial blood stream infections
- duration of mechanical ventilation
-  ICU stay
-  morbidity
-  mortality
(Level I)
Diagnose (1)
Diagnosis (2)
Ccomprehensive medical history, PE, CXR,
severity of HAP, exclude other potential infection,
specific conditions that can influence the likely
etiologic pathogens (Level II)
Tracheal colonization: does not require therapy or
diagnostic evaluation in the absence of clinical
findings or sign of infection (Level II)
Diagnosis (3)
Blood cultures: All patients should collect; A
positive result indicate pneumonia or extrapulmonary infection (Level II)
Sample collection: Protected specimen brush
samples- specificity>sensitivity; Endotracheal
aspirate, BAL-sensitivity>specificity (Level II)
Diagnostic threshold of quantitative culture:
PSB 103 cfu/ml; BAL 104~105 cfu/ml;
tracheal aspirates 106 cfu/ml
Diagnosis (4)
A sterile culture without a new antibiotic in the
past 72 hours: virtually rules out the presence of
bacterial pneumonia (NPV 94%), but viral or
Legionella infection is still possible (Level II)
Semiquantitative cultures of tracheal aspirates
cannot be reliably as quantitative cultures to
define the presence of pneumonia and the need for
antibiotic therapy (Level I)
Diagnosis (5)
Bronchoscopic bacteriologic strategy:  14-day
mortality, compared with a clinical strategy in
VAP (Level I) should not postpone diagnostic
studies in clinically unstable (Level II)
Treatment (1)
Treatment (2)
Treatment (3)
Penicillin-resistant S. pneumoniae and multidrug-resistant S. pneumoniae:
frequency; levofloxacin or moxifloxacin are preferred to ciprofloxacin and the
role of other new quinolones, such as gatifloxacin, has not been established
Treatment (4)
•ESBL strain: such as K.
pneumoniae or
Acinetobacter:
carbepenem is a
reliable choice.
• L. pneumophila:
combination antibiotic
regimen should include
macolide (azithromycin)
or a fluoroquinolone
(e.g., ciprofloxacin or
levofloxacin)
• MRSA risk factors are
present or there is a
high incidence locally:
Vancomycin or linezolid
Treatment (5)
Trough levels: for gentamicin and tobramycin  1 g/ml; and for amikacin 
4–5 g/ml; for vancomycin: 15–20 g/ml.
Treatment (6)
Initial IV form; a switch to oral/enteral therapy;
Highly bioavailable agents, such as quinolones
and linezolid, may be easily switched to oral
therapy (Level II)
Aerosolized antibiotics have not been proven to
have value in the therapy of VAP (Level I)
However, they may be considered as adjunctive
therapy in MDR gram-negatives pathogens, not
responding to systemic therapy (Level III)
Treatment (7)
Combination therapy: for possible MDR
pathogens (Level II); No documented superiority
compared with monotherapy, except to enhance
likelihood of initially appropriate empiric (Level I)
Combination with aminoglycoside: stopped after
5–7 days in responding patients (Level III)
Monotherapy: Only in the absence of resistant
pathogens (Level I)
Treatment (8)
If initially appropriate ABx: efforts to shorten
duration from the traditional 14~21 to 7 days,
except P. aeruginosa, and with good clinical
response & resolution of clinical features (Level I)
In P. aeruginosa pneumonia: combination
recommended (  resistance on monotherapy);
combination will not necessarily prevent the
development of resistance, but avoid inappropriate
and ineffective tx (Level II)
Treatment (9)
In Acinetobacter species: the most active agents
are the carbapenems, sulbactam, colistin, and
polymyxin; no data documenting an improved
outcome with combination regimen (Level II)
In ESBL Enterobacteriaceae: monotherapy with
a third-generation cephalosporin should be
avoided. The most active agents are carbapenems
(Level II)
Treatment (10)
Adjunctive inhaled aminoglycoside or polymyxin:
should be considered for MDR gram-negative
pneumonia, especially not improving with
systemic therapy (Level III)
Linezolid: an alternative to vancomycin for
MRSA (Level II), preferred in renal insufficiency
or receiving other nephrotoxic agents, but more
data are needed (Level III).
Treatment (11)
Antibiotic restriction: limit epidemic infection
with specific resistant pathogens
Heterogeneity of antibiotic prescriptions:
including formal antibiotic cycling
  overall frequency of antibiotic resistance
long-term impact of this practice: unknown
(Level II)
Response (1)
Serial assessment of clinical parameters to define
the response to initial empiric therapy (Level II)
Clinical improvement: takes 48–72 hours don’t
change therapy during this time; unless rapid
clinical decline (Level III)
Non-response: evident by Day 3, using an
assessment of clinical parameters (Level II)
Response (2)
Response (3)
In responding patient: de-escalation of antibiotics,
narrowing therapy to the most focused regimen
on the basis of culture data (Level II)
In nonresponding patient: evaluate for
-noninfectious mimics of pneumonia
-drug-resistant organisms
-extrapulmonary sites of infection
-complications of pneumonia and its therapy. (Level III)