cap dr yuva
TRANSCRIPT
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The New Treatment Paradigm Selecting Appropriate Empiric Antibioti
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Community Acquired Pneumonia (CAP)
Definition an acute infection of the pulmonary parenchyma
that is associated with clinical symptoms
accompanied by the presence of an acute infiltrateon a chest radiograph, or auscultatory findingsconsistent with pneumonia, in a patient not
hospitalized or residing in a long term care facilityfor > 14 days before onset of symptoms.
Bartlett. Clin Infect Dis 2000;31:347-82.
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Pathophysiology
Aspiration of oropharyngeal organisms
Inhalation of infected aerosols Hematogenous spread from extra-pulmonary sites Contiguous spread Direct inoculation
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Pathophysiology
TYPICAL Organisms Streptococcus pneumoniae
Haemophilus influenza
Streptococcus pyogenes Klebsiella pneumoniae
Moraxella catarrhalis
Staph aureus
Enterobacteriaceae/ Gram negative bacilli
Anaerobic organisms (aspiration) Fusobacterium sp. Prevotella sp.
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Pathophysiology
ATYPICAL Organsims Mycoplasma pneumoniae
Chlamydia pneumoniae
Chlaymida sp. Legionella sp. Respiratory viruses Others
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Pathophysiology
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Guidelines for CAP
American Thoracic Society (ATS)Guidelines - Management of Adults with CAP (2001
Infectious Diseases Society of America (IDSA)
Update of Practice Guidelines Management of CAPinImmuno-competent adults (2003)
ATS and IDSA joint effort (we will follow this)
IDSA/ATS Consensus Guidelines on theManagement of CAP in Adults (March 2007)
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CAP The Two Types of Presentations
Classical
Sudden onset of CAP High fever, shaking chills Pleuritic chest pain, SOB Productive cough Rusty sputum, blood tinge
Poor general condition High mortality up to 20% in
patients with bacteremia S.pneumoniae causative
Gradual & insidious onset Low grade fever Dry cough, No blood tinge Good GC Walking CAP Low mortality 1-2%; except
in cases of Legionellosis Mycoplasma, Chlamydiae,Legionella, Ricketessiae,Viruses are causative
Atypical
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CAP Pathogenesis
Inhalation
Aspiration
Hematogenous
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AgeObesity; Exercise is protective
Smoking, PVD Asthma, COPDImmuno-suppression, HIV
Institutionalization, Old age homes etcDementia
CAP Risk Factors for Pneumonia
ID Clinics 1998;12:723. Am J Med 1994;96:313
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Community Acquired Pneumonia (CAP)
Epidemiology4-5 million cases annually~500,000 hospitalizations 20% require admission
~45,000 deathsFewest cases in 18-24 yr groupProbably highest incidence in 65 yrs
Mortality disproportionately high in >65 yrsOver all mortality is 2-30%; Hospitalized Pt mort
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CAP The Pathogens Involved
56%
10%
6%
6%
5%
4%4%
9%S.pneumoniaeH.influenzaChlamydiaLegionella sppS.aureus
MycoplasmaGram Neg bacilliViruses
40-60% - No causative agent identified
2-5% - Two are more agents identified
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Streptococcus pneumonia(Pneumococcus)
Most common cause of CAP About 2/3 of CAP are due to S.pneumoniaeThese are gram positive diplococciTypical symptoms (e.g. malaise, shaking chillsfever, rusty sputum, pleuritic chest pain, cough)Lobar infiltrate on CXRMay be Immuno suppressed host25% will have bacteremia serious effects
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S. aereus CAP Dangerous
This CAP is not common; Multi lobar InvolvemenPost Influenza complication, Class IV or VCompromised host, Co-morbidities, ElderlyCA MRSA A Problem; CA MSSA also occursEmpyema and Necrosis of lung with cavitations
Multiple Pyemic abscesses, Septic ArthritisHypoxemia, Hypoventilation, Hypotension commoVancomycin, Linezolid are the drugs for MRSA
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CAP Age wise Incidence
0
200
400
600
800
1000
1200
1400
65
# of cases
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CAP Age wise Mortality
0
10
20
30
40
50
60
70
80
65
0 0 02
5.7
74.9
# of deaths
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Age > 65Bacteremia (for S. pneumoniae)
S. aureus, MRSA , PseudomonasExtent of radiographic changes
Degree of immuno-suppression Amount of alcohol consumption
CAP Risk Factors for Mortality
ID Clinics 1998;12:723. Am J Med 1994;96:313
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CAP Bacteriology in Hospitalized Pts
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CAP Evaluation of a Patient
Hx. PE, CXR
No Infiltrate
Alternate Dx.
Infiltrate or Clinicalevidence of CAP
Evaluate needfor Admission
PORT &CURB 65
OutPatient
MedicalWard ICU Adm.
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0
20
40
60
80
100
Cough Fever Dyspnea Phlegm Chest Pain
P E R C E N T
Diagnosis of Pneumonia
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Diagnostics
Labs CBC
BMP
Imaging CXR
CT scans
Cultures Blood
Sputum
Other tests
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PORT Scoring PSI
Clinical Parameter Scoring
Age in years Example
For Men (Age in yrs) 50
For Women (Age -10) (50-10)
NH Resident 10 points
Co-morbid Illnesses
Neoplasia 30 points
Liver Disease 20 points
CHF 10 points
CVD 10 points
Renal Disease (CKD) 10 points
Clinical Parameter Scoring
Clinical Findings
Altered Sensorium 20 points
Respiratory Rate > 30 20 points
SBP < 90 mm 20 points
Temp < 350 C or > 400 C 15 points
Pulse > 125 per min 10 points
Investigation Findings
Arterial pH < 7.35 30 points
BUN > 30 20 points
Serum Na < 130 20 points
Hematocrit < 30% 10 points
Blood Glucose > 250 10 points
Pa O2 10 points
X Ray e/o Pleural Effusion 10 points
Pneumonia Patient Outcomes
Research Team (PORT)
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Classification of Severity - PORT
Predictors Absent
ClassI
70
ClassII
71 90
ClassIII
91 - 130
Class
IV > 130
Class
V
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PSI: Mortality in Risk Classes
0
5
10
15
20
25
30
I II (130)
P e r c e n t
Score
Fine et al. New Engl J Med 1997; 336(4):243-250
Outpatients Hospitalised
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CAP Management based on PSI Score
PORT Class PSI Score Mortality % Treatment Strategy
Class I No RF 0.1 0.4 Out patient
Class II 70 0.6 0.7 Out patient
Class III 71 - 90 0.9 2.8 Brief hospitalization
Class IV 91 - 130 8.5 9.3 Inpatient
Class V > 130 27 31.1 IP - ICU
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CURB 65 Rule Management of CAP
CURB 65ConfusionBUN > 30RR > 30BP SBP
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Algorithmic Approach
CAP Patient
< 50 YearsNo
Co-morbidity
No CURB
Class I
Only OP
CURB +
OP / IP/ICU
Class II-V
Co-morbidityPresent
50 Years
PORT
Step 1Step 2 Step 3
Step 4
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Who Should be Hospitalized?
Class I and II Usually do not require hospitalizationClass III May require brief hospitalization
Class IV and V Usually do require hospitalization
Severity of CAP with poor prognosis
RR > 30; PaO2/FiO2 < 250, or PO2 < 60 on room air
Need for mechanical ventilation; Multi lobar involvemenHypotension; Need for vasopressors
Oliguria; Altered mental status
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CAP Criteria for ICU AdmissionMajor criteria
Invasive mechanical ventilation requiredSeptic shock with the need of vasopressors
Minor criteria (least 3)
Confusion/disorientationBlood urea nitrogen 20 mg% Respiratory rate 30 / min; Core temperature < 36C Severe hypotension; PaO2/FiO2 ratio 250 Multi-lobar infiltratesWBC < 4000 cells; Platelets
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CHEST X RAY
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Diagnostics: CXR Findings
Infiltrates Pleural effusions Abscess /Cavities
Bulging fissures Atelectasis Air bronchograms
Other findings PTX Pleural thickening/Scarring Pulmonary edema
Lymphadenopathy/Masses
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Diagnostics: CXR Normal CXR
Immunocompromised Dehydrated Early infection
American Journal of Medicine Sept. 2004: 117, 305-11 2706 patients 911 patients with pneumonia and ( )CXR
These patients were older, increased co-morbidities These patients had similar rates of + sputum/blood cultures These patients had a similar mortality
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Diagnostics: CXR
Respiratory Medicine May 2006: 100, 926-32 192 patients with pneumonia Excellent IR for lobes involved, extent of infiltrate, pleura
effusion Poor IR for pattern of infiltrate Minimal relation found between cultured pathogens and
radiologic features of infiltrate on CXR
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Diagnostics: CT scan
CT scan Alternative diagnoses Unresolved cases
Complications suspected Concerning CXR Treatment failure
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In addition to a constellation of suggestive clinical featur
a demonstrable infiltrate by chest radiograph or otherimaging technique, with or without supportingmicrobiological data, is required for the diagnosis ofpneumonia.
Patients with CAP should be investigated for specificpathogens that would significantly alter standard(empirical management decisions, when the presenceof such pathogens is suspected on the basis of clinicaland epidemiologic clues
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CAP Value of Chest Radiograph
Usually needed to establish diagnosis
It is a prognostic indicator To rule out other disorders
May help in etiological diagnosis
J Chr Dis 1984;37:215-25
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Diagnostics: Cultures
Sputum cultures: Recommendations Outpatient
Optional
Inpatient Optional Recommended when result may change therapy
Recommended
ICU admission/Severe CAP Failure of outpatient therapy Cavitary infiltrates (suspect TB) Alcoholism
Severe COPD
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CAP Grams Stain of Sputum
Efficiency of test S. pneumoniae H. influenza
Sensitivity 57 % 82 %
Specificity 97 % 99 %
Positive Predictive Value 95 % 93 %
Negative Predictive Value 71 % 96 %
Good sputum samples is obtained only from 39%83% show only one predominant organism
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RECOMMENDATIONS
Pretreatment Gram stain and culture ofexpectorated sputum should be performedonly with a good-quality specimen.
Patients with severe CAP, as defined above,
should at least have blood samples drawn forculture, urinary antigen tests for Legionella pneumophila and S. pneumoniae performed,and expectorated sputum samples collectedfor culture.
For intubated patients, an endotrachealaspirate sample should be obtained
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Diagnostics: Cultures Blood Cultures
Yield pathogen 5-15% Blood cultures often do not change management Most commonly isolated organismStreppneumo
High false positive rate Yield of blood cultures decreased by 50% by prior antibio
therapy Optional Recommended
Severe CAP Immunodeficient states (asplenia, liver disease, HIV) Indications for sputum cultures
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Pretreatment blood cultures yielded positive results fa probable pathogen in 5% 14% in large series ofnonselected patients hospitalized with CAP.
The yield of blood cultures is, therefore, relatively lowhen management decisions are analyzed, the impacof positive blood cultures is minor.
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The most common blood culture isolate in all CAP
studies isS. pneumoniae. Because this bacterial organism is always considered t
be then most likely pathogen, positive blood cultureresults have not clearly led to better outcomes orimprovements in antibiotic selection .
Blood cultures are also indicated when patients have ahost defect in the ability to clear bacteremia
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Pathogens Retrieved from Blood Culture
68%
16%
11%5%
S.pneumoniaeEnterobacteriaStaph.aureusOthers
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Procalcitonine and Disease
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0 1 2 3 40.001
0.01
0.1
1
10
100
1000 P
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Mortality of CAP Based on Pathogen
P. aeruginosa - 61.0 %
K. pneumoniae - 35.7 %
S. aureus - 31.8 %Legionella - 14.7 %
S. pneumoniae - 12.0 %
C. pneumoniae - 9.8 %H. influenza - 7.4 %
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Therapy Algorithm CAP
G. Hffken, J. Lorenz, W. Kern, T. Welte, T. Bauer, K. Dalhoff, E. Dietrich, S. Ewig, P. Gastmeier, B. Grabein, E. Halle, M. Kolditz,R. Marre, and H. Sitter. Guidelines of the Paul-Ehrlich-Society of Chemotherapy, the German Respiratory Diseases Society, the
German Infectious Diseases Society and of the Competence Network CAPNETZ for the Management of Lower Respiratory TractInfections and Community-acquired Pneumonia. Pneumologie 64 (3):149-154, 2010.
Diagnosis
Outpatient Care Hospital Admission
Ward ICU
i.v.oral
Pl b ll d S d
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61 Evans GM, Gaisford WF. Lancet 1938;14-19.
Placebo-controlled Study
M th d
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Methods
3 9 g/day of M.& B. 693 2( p - Aminobenzenesulphonamido )pyridine
Gram stain White blood cell count
Clinical data
Evans GM, Gaisford WF. Lancet 1938;14-19.
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Traditional Treatment Paradigm
Conservative start with workhorse antibiotics
Reserve more potent drugs for non-responders
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New Treatment Paradigm
Hit hard and early with appropriate antibiotic(s)
Short Rx. Duration; De-escalate where possible
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Objective 2Objective 1
Avoid emergenceofmultidrug resistantmicroorganisms
Immediate Rx.of patients withserious sepsis
The Therapy Conundrum
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Inappropriate therapy (%)
0
30
50
10
CAP
20
40
HAP HAP on CAP
17
34
45
Kollef, et al. Chest 1999;115:462 474
The Effect of the Traditional Approach
f l
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Dont Wait for Results !
Switching aftersusceptibility results
p
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Risk assessment approachEarly Antibiotic selectionChange treatment driven by localsurveillanceHit hard and hit early
As short a duration as possibleDe-escalate when and where possible
CAP Treatment Consensus
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OPAT OP Parenteral Antimicrobial Therapy
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Antibiotic Dosage, Route, Frequency and Duration
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Antibiotic Dosage, Route, Frequency and Duration
Doxyclycline 100-200 mg PO/IV BID for 7 to 10 days
Azithromycin 500 mg OD IV 3 days + 500 mg OD PO for 7-10 days
Clarithromycin 250 500 mg BID PO for 7 14 days
Telithromycin 800 mg PO OD for 7 10 days
Levofloxacin 750 mg PO/IV OD for 5 days
Gatifloxacin 400 mg PO or IV OD for 5 to 7 days
Moxifloxacin 400 mg PO or IV OD for 5 to 7 days
Gemifloxacin 320 mg PO OD for 5 7 days
Amoxyclav 2 g of Amoxi +125 mg of Clauv PO BID for 7 to 10 days
Ceftriaxone 2 g IV BID for 3 to 5 days + PO 3G CS
Ertapenum 1 g OD IV or IM for 7 to 14 days
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Empiric Treatment Outpatient
Healthy and no risk factors for DR S.pneumoniae1. Macrolide or DoxycyclinePresence of co-morbidities, use of antimicrobialswithin the previous 3 months, and regions with ahigh rate (>25%) of infection with Macrolideresistant S. pneumoniae1. Respiratory FQ Levoflox, Gemiflox or Moxiflox
2. Beta-lactam (High dose Amoxicillin, Amoxicillin-Clavulanate is preferred; Ceftriaxone, Cefpodoxime,Cefuroxime)plus a Macrolideor Doxycycline
E i i T I i N ICU
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Empiric Treatment Inpatient Non ICU
1. A Respiratory Fluoroquinolone (FQ) Levoor2. A Beta-lactamplus a Macrolide (or Doxycycline)
(Here Beta-lactam agents are 3 GenerationCefotaxime, Ceftriaxone, Amoxiclav)
3. If Penicillin-allergic Respiratory FQ or
Ertapenem is another option
E i i T I i i ICU
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Empiric Treatment: Inpatient in ICU
1. A Beta-lactam (Cefotaxime, Ceftriaxone,
or Ampicillin-Sulbactam)plus
either Azithromycinor Fluoroquinolone2. For penicillin-allergic patients, a respiratory
Fluoroquinolone and Aztreonam
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D ti f Th
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Duration of Therapy
Minimum of 5 days Afebrile for at least 48 to 72 h
No > 1 CAP-associated sign of clinical instability
Longer duration of therapy
If initial therapy was not active against the identified
pathogen or complicated by extra pulmonary infectio
N d t Th S d f D l ! (Cl 4 5)
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New data The Speed of Delay ! (Class 4,5)
0
10
20
30
40
50
60
70
80
90
0.5 1 2 3 4 5 6
Delay in treatment (hours) from hypotension onset
S u r v i v a
l ( % )
Each hour of delay carries7.6% reduction in survival
Kumar, et al. Crit Care Med 2006;34:1589 1596
CAP S f E i i T t t
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CAP Summary of Empiric Treatment
Outpatient Rx any one of the three Macrolide or Doxycycline or FluoroquinolonePatients in General Medical Ward 3rd Generation Cephalosporin + Macrolide Betalactum / B-I + Macrolide or B / B-I + FQ Fluroquinolone alonePatients in ICU 3GC + Macrolide or 3GC + FQ B/B-I + Macrolide or B/B-I + FQ
IDSA guidelines: Clin Infect Dis 2000;31:347-82
CAP T t t S
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CAP Treatment Summary
CAP Class Site of Care Treatment 1 Treatment 2 Treatment 3
Class I OP AZ CLR ER / Doxy
Class II OP FQ B + M B + Doxy
Class III OP + IP FQ IV I V - B + AZ Aztreo + FQ
Class IV Med Ward FQ + AZ B 3G + AZ Etrap + M
Class V ICU B 3G + AZ B 3G + FQ CarbepenumSulbac ,Tazob
Strategies for Prevention of CAP
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Strategies for Prevention of CAP Cessation smoking Influenza Vaccine (Flu shot Oct through Feb)
It offers 90% protection and reduces mortality by 80% Pneumococcal Vaccine (Pneumonia shot)
It protects against 23 types of Pneumococci70% of us have Pneumococci in our RTIt is not 100% protective but reduces mortality Age 19-64 with co morbidity of high for pneumonia Above 65 all must get it even without high risk
Starting first dose of antibiotic with in 4 h & O2 status
Switch to Oral Therapy
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Switch to Oral Therapy
Four criteriaImprovement in cough, dyspnea & clinical sig Afebrile on two occasions 8 h apart
WBC decreasing towards normalFunctioning GI tract with adequate oral intake
If overall clinical picture is otherwise favorabl
hemodynamically stable; can switch to oraltherapy while still febrile.
Management of Poor Responders
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Management of Poor Responders
Consider non-infectious illnessesConsider less common pathogens
Consider serologic testingBroaden antibiotic therapyConsider bronchoscopy
CAP Complications
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CAP Complications
Hypotension and septic shock3-5% Pleural effusion; Clear fluid + pus cells1% Empyema thoracis pus in the pleural space
Lung abscess destruction of lung - CSLDSingle (aspiration) anaerobes,PseudomonasMultiple (metastatic)Staphylococcus aureus
Septicemia Brain abscess, Liver AbscessMultiple Pyemic Abscesses
CAP So How Best to Win the War?
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CAP So How Best to Win the War?
Early antibiotic administration within 4-6 hoursEmpiric antibiotic Rx. as per guidelines (IDSA / ATSPORT PSI scoring and Classification of cases
Early hospitalization in Class IV and VChange Abx. as per pathogen & sensitivity patternDecrease smoking cessation - advice / counseling
Arterial oxygenation assessment in the first 24 hBlood culture collection in the first 24 h prior to AbxPneumococcal & Influenza vaccination; SmokingX
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NOSOCOMIAL PNEUMONIA
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Etiology
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Etiology
Early vs. Late VAP1 Early onset= Pneumonia develops within 96 hours (4 days
of patient s admission to the ICU or intubation formechanical ventilation
Late onset= Pneumonia develops after 96 hours (4 days) opatient s admission to the ICU or intubation for mechanicalventilation
Very early onset= within 48 hours after intubation21 CDC.gov. Guidelines for preventing health-care-associated pneumonia, 2003.
2 Park DR. The microbiology of ventilator-associated pneumonia.
Nosocomial pneumonia
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Nosocomial pneumonia
Mortality and Time of Presentation of HAP
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H o s p
i t a
l M o r t a
l i t y ( % )
0
10
20
30
40
50
None Early Onset Late Onset
Nosocomial Pneumonia
P = .504 P
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Nosocomial Pneumonia
Hence, the importance of focusing on: Accurate diagnosis Appropriate treatment Preventive measures
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Nosocomial Pneumonia
Pathogenesis
Pathogenesis
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Microaspiration may occur in up to 45% of healthy volunteduring sleep
Oropharynx of hospitalized patients is colonized with GNR35-75% of patients depending on the severity and type ofunderlying illness
Multiple factors are associated with higher risk of colonizatwith pathogenic bacteria and higher risk of aspiration
Invasion of the lower respiratory tract by:
Aspiration of oropharyngeal/GI organisms Inhalation of aerosols containing bacteria Hematogenous spread
Oropharyngeal colonization
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Oropharyngeal colonization
Scannapieco et al showed a transition in the colonization odental plaques in patients in the ICU Control=25 subjects presenting to preventive dentistry clin Study group=34 noncardiac patients admitted to medical
ICU at VA hospital (sampled within 12 hours of admissionand every third day)
Scannapieco et al. Colonization of dental plaque by respiratory pathogensin medical intensive care patients
Colonization of oropharynx
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p yMedical ICU (N=34) Dentistry Clinic (N=25)
Species Plaque Mucosa Plaque Mucosa
S. aureus 2 5 0 1
P. aeruginosa 8 7 0 0
K. pneumoniae 2 5 0 0
S. marcescens 3 4 0 0
E. aerogenes 0 0 0 1
E. cloacae 1 1 0 0
E. asburiae 0 0 0 1
P. mirabilis 1 0 0 0
E. coli 0 1 0 0
C. diversus 1 1 0 0 A. calcoaceticus 0 1 0 0
Pasteurella spp. 0 0 1 0
Total 18 24 1 3
Scannapieco et al. Colonization of dental plaque by respiratory pathogensin medical intensive care patients
GI colonization
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GI colonization
Increased gastric pH leads to bacterial overgrowth Reflux can then lead to colonization of oropharynx Use of antacids and H2 blockers associated with GI
colonization
Safdar et al. The pathogenesis of ventilator-associated pneumonia:its relevance to developing effective strategies for prevention
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Nosocomial Pneumonia
Risk Factors
Etiology- select risk factors forh
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pathogensStreptococcus pneumoniae Smoking, COPD, absence of
antibiotic therapy
Haemophilus influenzae Smoking, COPD, absence ofantibiotic therapy
MSSA Younger age, Traumatic coma,Neurosurgery
MRSA COPD, steroid therapy, longerduration of MV, prior antibiotics
Pseudomonas aeruginosa COPD, steroid therapy, longer
duration of MV, prior antibiotics Acinetobacter species ARDS, head trauma,
neurosurgery, gross aspiration,prior cephalosporin therapy
Park DR. The microbiology of ventilator-associated pneumonia.
Nosocomial Pneumonia
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Nosocomial Pneumonia
Risk Factors Host Factors
Extremes of age, severe acute or chronic illnesses,immunosupression, coma, alcoholism, malnutrition, COPD, DM
Factors that enhance colonization of the oropharynx andstomach by pathogenic microorganisms admission to an ICU, administration of antibiotics, chronic lung
disease, endotracheal intubation, etc.
Nosocomial Pneumonia
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Nosocomial Pneumonia
Risk Factors Conditions favoring aspiration or reflux
Supine position, depressed consciousness, endotracheal intubationinsertion of nasogastric tube
Mechanical ventilation Impaired mucociliary function, injury of mucosa favoring bacteri
binding, pooling of secretions in the subglottic area, potentialexposure to contaminated respiratory equipment and contact withcontaminated or colonized hands of HCWs
Factors that impede adequate pulmonary toilet Surgical procedures that involve the head and neck, being
immobilized as a result of trauma or illness, sedation etc.
Risk factors for MDR pa
thogens
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Risk factors for MDR pathogens
1.Receipt of antibiotics within the preceding 90 days2.Current hospitalization of 5 days3.Admission from a healthcare-related facility (eg, long-term car
facility, dialysis unit)4.High frequency of antibiotic resistance in the community or in
specific hospital unit5.Presence of risk factors for HCAP including: hospitalization fo
days or more in the preceding 90 days; residence in an extendecare facility; home infusion therapy; chronic dialysis; home wcare; and a family member with an MDR pathogen
6 Immunosuppressive disease and/or therapy
Risk Factors Of VAP In Patienti i M h i l V til ti
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receiving Mechanical Ventilation
Age >70 years Chronic lung disease Depressed consciousness Large volume aspiration
Chest surgery Frequent ventilator circuit changes The presence of an intracranial pressure monitor or nasogastric tube H-2 blocker or antacid therapy
Transport from the ICU for diagnostic or therapeutic procedures Previous antibiotic exposure, particularly to third generation cephalosporins Reintubation Hospitalization during the fall or winter season
Mechanical ventilation for ARDS
Nosocomial Pneumonia
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Etiologic Agents S.aureus Enterobacteriaceae P.aeruginosa Acinetobacter sp. Polymicrobial Anaerobic bacteria
Legionella sp. Aspergillus sp. Viral
Pathogens Associated With HAP
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N o s o c o m
i a l P n e u m o n
i a ( % )
0
5
10
15
20
25
30
35
40
PA OSSA ORSA ES SM
P = .003
P = .043
P = .408
P = .985 P = .144
Patho gen
Early-onset NP Late-onset NP
PA = P aerug ino saOSSA = Oxacillin-sensitive
S aureusORSA = Oxacillin-resistant
S aureus
ES = Enterobac te r species
SM = S marcescens
Pathogens Associated With HAP
Ibrahim, et al. Chest. 2000;117:1434-1442.
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Nosocomial pneumonia
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Bronchoscopically Directed Techniques for diagnosis of VAPand Quantitative cultures Bronchoscopy with BAL/bronchial brushings (10,000 to 100,000 CFU
and less than 1% of squamous cells)
Protected specimen brush method (>10 CFU/ml)
Protected BAL with a balloon tipped catheter (>5% of neutrophils ormacrophages with intracellular organisms on a Wright-Giemsa stain)
Nosocomial Pneumonia
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Differential diagnosis ARDS Pulmonary edema Pulmonary embolism Atelectasis Alveolar hemorrhage Lung contusion
Nosocomial Pneumonia
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Duration of antimicrobial treatment
Optimal duration of treatment has not been established
Most experts recommend 14-21 days of treatment
Recent data support shorter treatment regimens (8 days)
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Treatment of Nosocomial Pneumonia
0369
12151821242730
3336394245
Mortality RecurInfec
P.aerug Abx FreeDays
8days15 days
Nosocomial Pneumonia
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Preventive Measures Incentive spirometry Promote early ambulation Avoid CNS depressants Decrease duration of immunosupression Infection control measures Educate and train personnel
Nosocomial Pneumonia
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Preventive Measures Avoid prolonged nasal intubation Suction secretions Semi-recumbent position( 30-45 head elevation) Do not change ventilator circuits routinely more often tha
every 48 hours Drain and discard tubing condensate
Use sterile water for respiratory humidifying devices Subglottic secretions drainage
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117Craven, et al. Chest. 1995;108:s1-s 16.
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Role of gastric pH(2)
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Sucralfate : lower median gastric pH (P < 0.001) and less freqgastric colonization (P = 0.015)
84% late-onset GNB pneumonia have gastric colonization witsame bacteria before pneumonia developed
CONCLUSION: Stress ulcer prophylaxis with sucralfate reducesthe risk for late-onset pneumonia in ventilated patients comparedwith antacid or ranitidine
Decontamination of the digestivetract
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tract
preventing oropharyngeal and gastric colonization with aerobiGNB and Candida spp, without disrupting the anaerobic flora
locally administered nonabsorbable antibiotic (eg,polymyxin) andan aminoglycoside or fluoroquinolone + amphotericin B ornystatin.
One RCS showed decrease in pneumonia due to GNB
Decontamination of the digestivetract (2)
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tract (2)
A large prospective randomized trial of ICU in the Netherlandt934) :
SDD group lower mortality both in the ICU and duringhospitalization(mortality :15 vs 23% ICU, 24 vs 31 % hospital)
The preventative effects of SDD for HAP have been considerablylower in ICUs with high rates of endemic MDR pathogens
Patient positioning
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Several studies supine position vs semirecumbent predisposed to microaspiration of gastric contents
lower incidence of both clinically suspected and microbiologicconfirmed HAP in semirecumbent versus supine patients
No difference in mortality
Suggest : place intubated patients in the semirecumbent positiounless contraindicated.
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Subglottic drainage
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Hi-Lo EVAC tube(CASS)
Continuous aspiration of subglotticsecretions (CASS)
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secretions (CASS)
Kollef et al. A randomized clinical trial of continuous aspiration ofSubglottic secretions in cardiac surgery patients
Subglottic drainage (2)
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Lessen risk of aspiration
5 studies (896 intubated pt) The use of CASS reduced theincidence of VAP by nearly half - risk ratio 0.51 (95% CI 0.37-0.71).
The effect of CASS in limiting VAP was most pronounced ampatients expected to require >72 hours of mechanical ventilati
Via the tube
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1) Ventilator circuit changes2) Condensate3) Silver-lined ET tubes
Ventilator circuit management
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Craven and colleagues showed that ventilator circuitchange every 24 hours compared to 48 hoursincreased VAP incidence
Several later studies showed that circuit changescould be used safely for greater than 48 hours
Kollef et al. Mechanical ventilation with or without 7-day circuit changes
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Condensate management
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Heat-moisture exchanger Theoretical advantage=prevents bacterial colonization of tubing Studies= Mixed results Disadvantage=increases dead space and resistance to breathing
Heated wire to elevate temp of inspired air Advantage=Decreases condensate formation Disadvantage=Blockage of ET tube by dried secretions
CDC.gov. Guidelines for preventing health-care-associated pneumonia, 2003.
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Safety isues of nebulisers in home Safety isues of using nebulisers in in patients and icu Developing guidelines regarding adequate care and
proper usage of nebulisers. Change of tubings and masks.
Silver-lined ET tube
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Broad-spectrum antimicrobial activity in vitro Reduces bacterial adhesion to devices in vitro Blocks biofilm formation on the device in animal
models Dog model- decreased severity of lung colonization
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1) Baseline2) Wh VAP i li i ll
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2) When VAP is clinicallysuspected
3) 3 days later
Am J Respir Crit Care Med2000;162:505
CPIS>6 suggests of pneumonia
Noninfectious causes of fever andl i filt t i VAP
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pulmonary infiltrates in VAP
Chemical aspiration without infection (Aspiration pneumoniti Atelectasis
Pulmonary embolism ARDS Pulmonary hemorrhage
Lung contusion Infiltrative tumor Radiation pneumonitis Drug reaction
Diagnosis
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Imaging
Gram's stain and culture Bronchoscopy
Gram's stain and culture
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unreliable due to contamination with bacteria colonizing theoropharynx The presence ofmany polymorphonuclear leukocytes (and few
epithelial cells) and bacteria, which are morphologically consistenwith bacteria found on culture, improve the predictive power
In addition, the lack of isolation of a pathogen (eg, MRSA orPseudomonas) from a well-collected and adequate expectoratesputum sample can be used to narrow the antimicrobial regime
Blood cultures are extremely helpful when positive, but the yilow
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Bronchoscopy
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Protected brush specimen (PBS)
Using a threshold of>103
colony forming units (CFU)/mL sensitivity : 64 to 100 % specificity : 60 to 100 %
Bronchoalveolar lavage (BAL)
Quantitative cultures using a threshold of>104 CFU/mL sensitivity : 72 - 100 % specificity : 69 - 100 %
At least 4 studies concluded that bronchoscopically directed techniques werenot more accurate for diagnosis of VAP than clinical and X-ray criteria,combined with cultures of tracheal aspirate
Therefore no old standard criteria exist
Initial Antibiotic Therapy
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Inappropriate therapy is a major risk factor for excessmortality and length of stay in patients with HAP, andantibiotic resistant organisms are the pathogens mostcommonly associated with inappropriate therapy.
In selecting empiric therapy for patients who have
recently received an antibiotic use an agent from adifferent antibiotic class , since recent therapy increasesthe probability of inappropriate therapy and canpredispose to resistance to that same class of
antibiotics .
Initial Antibiotic Therapy
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Initial antibiotic therapy should be given promptly sincedelays in administration may add to excess mortality inVAP.
Initial empiric therapy is more likely to be appropriate ifa protocol for antibiotic selection is developedbutadapted to local patterns of antibiotic resistance, witheach ICU collecting this information, and updating it on aregular basis.
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144 TABLE 3. INITIAL EMPIRIC ANTIBIOTIC THERAPY FOR HAP OR VAP IN PATIENTSWITH NO KNOWN RISK FACTORS FOR MDR PATHOGENS, EARLY ONSET, ANDANY DISEASE SEVERITY
Potential Pathogen Recommended Antibiotic*
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Potential Pathogen Recommended Antibiotic
Streptococcus pneumoniae Ceftriaxone
Haemophilus influenzae or
Levofloxacin, moxifloxacin, or ciprofloxacin
Methicillin-sensitive Staphylococcus aureus or
Antibiotic-sensitive enteric gram-negative bacilliEscherichia coli Ampicillin/sulbactam
Klebsiella pneumoniae or
Enterobacter species Ertapenem
Proteus species
Serratia marcescens
* See Table 5 for proper initial doses of antibiotics.
The frequency of penicillin -resistant S. pneumoniae and multidrug-resistant S. pneumoniae is increasing; levofloxacin ormoxifloxacin are preferred to ciprofloxacin and the role of other new quinolones, such as gatifloxacin, has not been established.
TABLE 4. INITIAL EMPIRIC ANTIBIOTIC THERAPY FOR HAP OR VAP IN PATIENTS WITHLATE-ONSET DISEASE OR RISK FACTORS FOR MDR PATHOGENS, AND ANY DISEASESEVERITY
Potential Pathogen Combination Antibiotic Therapy*
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Pathogens listed in Table 3 and Antipseudomonal cephalosporin
MDR pathogens (cefepime, ceftazidime)
Pseudomonas aeruginosa orKlebsiella pneumoniae (ESBL) Antipseudomonal carbepenem
Acinetobacter species (imipenem or meropenem) or
Lactam/-lactamase inhibitor(piperacillin tazobactam)
plus Antipseudomonal fluoroquinolone (ciprofloxacin or levofloxacin)
or Aminoglycoside
(amikacin, gentamicin, or tobramycin)
plus
Methicillin-resistant Staphylococcus aureus (MRSA) Linezolid or vancomycin
Legionella pneumophila * Initial antibiotic therapy should be adjusted or streamlined on the basis of microbiologic data and clinical response to therapy. If an ESBL strain, such as K. pneumoniae , or an Acinetobacter species is suspected, a carbepenem is a reliable choice. If L. pneumophila is suspected, thecombination antibiotic regimen should include a macolide (e.g., azithromycin) or a fluoroquinolone (e.g., ciprofloxacin or levofloxacin) should be used ratherthan an aminoglycoside. If MRSA risk factors are present or there is a high incidence locally.
Optimal Antibiotic Therapy
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Empiric therapy of patients with severe HAP or VAP requires theuse of antibiotics at optimal doses to assure maximum efficacy.
Initial therapy should be administered to all patientsintravenously, with a switch to oral/enteral therapy in selectedpatients with a good clinical response and a functioning intestinaltract. Highly bioavailable agents, such as the quinolones andlinezolid, may be easily switched to oral therapy in such patients.
Aerosolized antibiotics have not been proven to have value inthe therapy of VAP.
Optimal Antibiotic TherapyCombination therapy should be used if patients are likely to be
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infected with MDR pathogens. No data have documented thesuperiority of this approach to monotherapy, except to enhance thelikelihood of initially appropriate empiric therapy.
If patients receive combination therapy with an aminoglycosidecontaining regimen, the aminoglycoside can be stopped after 5-7days in responding patients.
Monotherapy with selected agents can be used for patients with
severe HAP and VAP in the absence of resistant pathogens.Patients in this risk group should initially receive combination therapyuntil the results of lower respiratory tract cultures are known andconfirm that a single agent can be used.
Optimal Antibiotic Therapy
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MRSA pneumonias:
- prolonged intubation periods- prior use of antibiotics
Pseudomonas aeruginosa pneumonias:- structural pulmonary disease
- 1 week of prior hospitalization- prolonged periods of intubation (>5 days) - prior exposure to antibiotics
A. Baumannii VAP:- neurosurgery- ARDS- head trauma- large-volume pulmonary aspiration.
Combinationpiperacillin/tazobactam + ciprofloxacin ,
oramikacin + imipenem, meropenem or anantipseudomonal cephalosporin.
carbapenems, sulbactam,tigecycline, colistin
linezolid
Duration of antimicrobial treatment
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Optimal duration of treatment has not beenestablished
Most experts recommend 14-21 days of treatment
Recent data support shorter treatment regimens (8days)
Comparison of 8 vs.15 days of antibiotics for VAP
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Prospective, randomized, double blind clinical trial51 French ICUs401 patients with VAP (quantitative culture results)
Clinical effectiveness comparable, with the possibleexception of VAP caused by non fermenting GNR
JAMA 290 No 19, November 2003
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Non resolving pneumonia
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Non resolving pneumonia is a clinicalsyndrome in which focal infiltrates beginwith some clinical association of acutepulmonary infection and despite a minimum
of 10 days of antibiotic therapy patientseither dont improve or worsen orradiographic opacities fail to resolve within12 week
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Normal CXR & Pneumonic Consolidation
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Lobar Pneumonia S.pneumoniae
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CXR PA and Lateral Views
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157
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Lobar Pneumonia
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Special forms of Consolidation
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Special Forms of Pneumonia
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Special Forms of Pneumonia
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Complications of Pneumonia
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Mycoplasma Pneumonia
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Chlamydia Trachomatis
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Rare Types of Pneumonia
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