Download 4. Community Acquired Pneumonia

COMMUNITY ACQUIRED PNEUMONIA
Dr Binila Chacko
Associate Professor Medical ICU, CMC Vellore
PENICILLIN
HIPPOCRATES
INTENSIVE CARE
VACCINATION FROM THE 1970s ONWARDS
SIR WILLIAM OSLER
THE BURDEN
Forgotten killer
Most common infectious
cause of death in the world 3.5 million deaths annually
7% of the world’s total
deaths
High burden of deaths,
hospital admission and costs
OVER THE YEARS…
Pre-antibiotic era
100%
Now
Vaccination
Decreased
smoking
75%
50%
25%
0%
Pneumococcus
HOW CAN I
MAKE THIS
VERY
COMMON
TOPIC
INTERESTING
??
WHAT ARE OUR
CHALLENGES TODAY?
TREATMENT
CHALLENGES
WHAT ARE OUR
CHALLENGES TODAY?
• CLINICAL PRESENTATION
• INVESTIGATIONS
• MIMICS
CLINICAL PRESENTATION
•
•
Usual triad is rare
Chest Xray
• An individual radiologist may miss infiltrates in up to
•
15% of cases
Two radiologists reading the same chest radiograph
disagree in 10% of cases.
• Need to be able to identify atypical
presentations
ELDERLY AND
IMMUNOSUPPRESSED
Atypical
More severe symptoms
Higher long term mortality
“Type a quote here.”
–Johnny Appleseed
FEVER+COUGH= PNEUMONIA
CARDIAC
Congestive heart failure with associated viral
NORMAL CHEST XRAY WITH
syndrome
“PNEUMONIA
SYMPTOMS”
IMPORTANCE
OF
PULMONARY
MIMICS
Airway-Acute exacerbation of bronchiectasis
Influenza
Pertussis
Alveolar- Aspiration
pneumonitis,
hypersensitivity
pneumonitis,
crack lung
Over
treatment
Acute
bronchitis
Interstitium
- Fibrosis
COPD/Asthma
exacerbation
Non
resolving
pneumonia
Vessels-Pulmonary infarction/vasculiitis
WHAT’S THE
BUG?
Clinical suspicion
Usual scenario
Special situations
Confirmatory tests
WHAT’S THE
BUG?
Usual scenario
85% of, Streptococcus pneumoniae, Haemophilus
influenzae, and Moraxella catarrhalis.
15% by atypical pathogens - Mycoplasma,
Chlamydia, and Legionella and viruses
DON’T FORGET TO
LOOK AT THE PATIENT
SPECIAL SITUATIONS
Pseudomas aeuruginosa
Advanced structural lung disease
Prior colonisation
MRSA
1.Previous MRSA skin infection/colonisation
2. Close contact with carrier
3. End stage renal disease
4. In dwelling catheters
MDR
HIV/AIDS
Streptococcus pneumoniae
P. jirovecii
CD4(+) cell counts
<200/mm
Fungal
WHAT’S THE
BUG?
Clinical suspicion
Usual scenario
Special situations
Confirmatory tests
IDENTIFYING IS IMPORTANT
• Conscientious effort to determine the causative organism.
• Facilitates rational approach to changing therapy
• Targeted treatment and antibiotic stewardship decreases
costs and complications such as C difficile
ONCE AGAIN FACED WITH
CHALLENGES..
Microbiological diagnosis
in only 40-70%
Widespread antibiotic
(mis) use
India atypical
organisms under
diagnosed
Legionella
pneumophila in over
20% CAP
WHAT TESTS SHOULD WE
DO?
WHAT ARE OUR
CHALLENGES TODAY?
TREATMENT
CHALLENGES
TREATMENT
CHALLENGES
SEVERITY
TREATMENT AND
MONITORING
RESPONSE
NON RESOLVING
PNEUMONIA
Scoring systems
• admission decisions objective
• ?early identification of patients needing
ICU
SMART-COP
Designed to predict ICU admission
SBP
Multi lobar infiltrates
PNEUMONIAAlbumin
SEVERITY INDEX
CURB 65/CRB
PSI
65
Resp rate
Complex
ScoreTachycardia
CURB
≥3 hospitalise
65
Electronic decision support
Less complicated
IDSA-ATS
than PSI
Confusion
Risk categories I to V
Primary
SMART
careCOP
settings
Oxygenation
Lab findings-ABG
pH
as compared with 74% for the PSI and 39% for CURB-65
ADMIT TO ICU?
Patients admitted to ICU 48 hours after initial
admission to a general medical service
Higher mortality
No studies have been performed to establish whether initial
admission to the ICU would prevent subsequent
deterioration
SO WHAT ELSE..
PSI and CURB-65 scores
Limited ability to identify patients likely to deteriorate if
admitted to a general ward
IDSA–ATS guidelines minor criteria
IDSA-ATS MINOR CRITERIA
TREATMENT
CHALLENGES
SEVERITY
TREATMENT AND
MONITORING
RESPONSE
NON RESOLVING
PNEUMONIA
TREATMENT AND
MONITORING
RESPONSE
Key therapy-adequate coverage of strept pneumonia
and atypical coverage
IDSA first-line treatment
Either a respiratory fluoroquinolone or combination of
a second-generation or third-generation
cephalosporin and a macrolide
TREATMENT AND
MONITORING
RESPONSE
USE OF FLUOROQUINOLONES IN INDIA
? Induce resistance and mask Tuberculosis
Fluoroquinolones same antibacterial spectrum as
macrolides
Use macrolide combination with beta lactam
Immunomodulatory role
Macrolides interfere with CYP3A4
If on cyclosporine-preferential use of
levo/moxifloxacin.
SPECIAL SITUATIONS
HOW QUICK SHOULD WE BE?
Interval of more than 4 hours to the first antibiotic
dose
Associated with increased in-hospital mortality.
Efforts to decrease the time
Increase in inappropriate antibiotic use and
resistance
Clostridium difficile colitis
Not resulted in decrease in mortality.
TIMING-CURRENT
GUIDELINES
Current IDSA–ATS
guidelines
Encourage treatment as
soon as the diagnosis is
made
Exceptionshock
Decrease in
survival rates of
8% for each hour
of delay.
DURATION OF ANTIBIOTICS
5 to 7 days.
No evidence that prolonged courses lead to better outcomes,
even in severely ill patients
Exception
Legionella 5-10 days of macrolide therapy/2-3 weeks of
quinolones
MONITORING RESPONSE
Clinical
Role of biomarkers
MONITORING RESPONSEROLE OF BIOMARKERS
Biomarkers and antibiotic pre-treatment
Procalcitonin guided antibiotic treatment
So what should we do?
DO WE NEED BIOMARKERS?
Diagnosis and therapeutic decisions in LRTIs
Clinical characteristics not very specific and cannot divide
bacterial from viral LRTI.
Antibiotic universally initiated
Difficult to identify the mimics
ROLE OF BIOMARKERS
Procalcitonin
adjunct to clinical acumen
cannot be used as a sole
marker
not a marker of early infection
Other
biomarkers
role of serial
markers
Co-peptin
CRP
BNP
Recommendation
Adrenomedullin
PCT
and CRP not routine
investigations for the
diagnosis of CAP
monitoring response to
therapy
BIOMARKERS AND
ANTIBIOTIC PRE-TREATMENT
CAPNETZ study
25% of patients pretreated with antibiotics
Copeptin and PCT, but not CRP,
Higher in patients without pre-treatment
More sensitive biomarkers with more dynamic
kinetics that react more promptly to effective therapy
PROCALCITONIN GUIDED
TREATMENT
Effective antibiotic therapy in CAP leads to a
reduction in inflammatory biomarkers
longitudinal measurement of inflammatory
biomarkers is recommended
ProCAP
Significant reduction of antibiotic consumption
Duration of antibiotic therapy reduced by
55%(from 12–5 days) independent of the initial
severity
SO WHAT NOW?
PCT guidance of antibiotic stewardship
Safe, efficient and able to significantly reduce
antibiotic exposure in patients with LRTI
ADJUNCTIVE THERAPY CAP
STEROIDS
ANTI FIBRINOLYTICS
STATINS
STEROIDS SEVERITY
Not recommended given increased risk of
arrhythmias, upper GI bleed, superadded
infections
As always there are studies to advocate use of
steroids
In my practice- Limit to vasopressor dependent
septic shock.
ROLE OF CT
Role of CT with a negative Chest Xray unclear
Centrilobular nodules non-bacterial pneumonia
Airspace nodules - bacterial pneumonia
(specificity90%) when located in the outer lung
areas.
Diagnosing complications such as lung abscess
and empyema
TREATMENT
CHALLENGES
SEVERITY
TREATMENT AND
MONITORING
RESPONSE
NON RESOLVING
PNEUMONIA
TREATMENT FAILURE
Radiological
failure
?Correct
bug
must consider the slow resolvers
- only
30% show
resolution
APPROACH
TO THIS
SITUATION
Thinkelderly
Complications
CHEST
severe pneumonia CT
- can
take up to 10 weeks
rates ofBRONCHOSCOPY
resolution with different organisms
Thinkdifferent
Resistance
LUNG BIOPSY
Mycoplasma, moraxella,
chlamydia, non -bacteremic
strept pneumoniae- fast resolvers
Think Mimics
Legionella, bacteremic strept pneumoniae, staph
aureusupto 5 months
Rule out
tuberculosis
NON RESOLVING
PNEUMONIA
PREMATURE DECLARATION
OF VICTORY
Late 1960s-Surgeon General William H. Stewart
declared, “It is time to close the book on
infectious disease.”
ON THE RISEPNEUMOCOCCAL
RESISTANCE
Between 1998 and 2009,SENTRY Program
Striking falls (P < 0.05)
in susceptibility rates for
IN INDIA
1940
1970s
susceptible
pneumococci
Amoxycillin/clavulinate
93.8IBIS
to 82.7%
LANCET
1999Intermediate
resistance
penicillin in only four (1.3%) isolates;
Penicillin
94.7 toto84.1%,
Resistance
to
co-trimoxazole
and
chloramphenicol
was
seen
56%
and
1977-78-outbreaks
of87.5%
resistance in South Africa
Ceftriaxone 97.4 to
17% isolates, respectively.
Macrolide (erythromycin) 82.2 to 60.8%
Clindamycin 96.2 to 79.1%,
SO WHAT ARE OUR
OPTIONS?
Ceftaroline
Fifth-generation parenteral cephalosporin
• DEFINITION
OF of
RESISTANCE
(MIC)
HAS CHANGED
Broad spectrum
Gram-positive and
Gram-negative
pathogens, and is the first approved cephalosporin with invitro activity
againstDEFINITIONS,
MRSA.The efficacy
safety of IN
• USING
EARLIER
NOand
CHANGE
intravenous ceftaroline (600 mg twice daily)
OUTCOME OF EXTRA-MENINGEAL INFECTIONS
Ceftobiprole
Ketolides
• POSSIBLE
THAT
WERE
The ketolides
are a DRUG
subclassLEVELS
of macrolides,
which were
SUFFICIENT
TO OVERCOME
RESISTANCE
designed specifically
to overcome macrolide-resistant
respiratory pathogens.
Cethromycin
WHAT ARE OUR
CHALLENGES TODAY?
TREATMENT
CHALLENGES
VACCINATION
Pneumococcal vaccination
Children
Adults > 65 years
Risk factors
Influenza vaccination
Large cohort studies have shown reduced risk
of influenza infections and mortality in elderly
patients
VACCINATION INDIA VERSUS
WEST
RISK
AREAS
OFOF
MDR
UNCERTAINTY
ORGANISMS
Role of broad spectrum antibiotics in patients with risk factors of
MDR organisms
Incidence of MDR pathogens generally is not significantly
increased unless three or more risk factors are present.
AREAS OF UNCERTAINTY
MRSA is an exception: the presence of one
MRSA-specific risk factor
prior MRSA infection or colonization
long-term hemodialysis
TAKE HOME POINTS
DIAGNOSTIC CHALLENGES
Diagnostic clues in special situations
TREATMENT CHALLENGES
Resistance is increasing in the out patient and hospital settings
Antibiotic stewardship should look to optimise outcomes and employ tactics to minimise
resistance
Non resolving pneumonia- AFB Testing, CT Chest, bronchoscopy +/- biopsy
PREVENTION
Role of vaccination