Community Acquired Pneumonia .pdf

COMMUNITY-ACQUIRED PNEUMONIA
(Philippine Clinical Practice Guidelines with 2016 updates)
PGI Roselo S. Alagase
Divine Word Hospital
12/29/18

COMMUNITY ACQUIRED PNEUMONIA
 Lower respiratory tract
infection (pulmonary
parenchyma)
 Acquired in the Community
within 24 hours to less than 2
weeks.
12/29/18

COMMUNITY ACQUIRED PNEUMONIA
 CAP remains the leading cause of death from an infectious disease.
 Third leading cause of morbidity and mortality (CPG 2010)
 Sixth leading cause of death overall and is a major cause of morbidity
and mortality (CPG 2016)
12/29/18

PATHOPHYSIOLOGY
o Infection of pulmonary parenchyma acquired in the community within
24 hours to less than 2 weeks.
o Results from the proliferation of microbial pathogens at the alveolar
level and the host’s response to those pathogens.
o Most common access of microorganisms to the lower respiratory tract is
through aspiration from the oropharynx.

PATHOGENESIS
 3 main mechanisms by which bacteria reaches the lungs:
 Inhalation
 Aspiration
 Hematogenous

MICROBIAL CAUSES OF COMMUNITY-ACQUIREDPNEUMONIA
(By site of care)
OUTPATIENTS NON-ICU ICU
Streptococcus pneumoniae Streptococcus pneumoniae Streptococcus pneumoniae
Mycoplasma pneumoniae M. pneumoniae Staphylococcus aureus
Haemophilus influenzae Chlamydia pneumoniae Legionella spp.
C. pneumoniae H. influenzae Gram-negative bacilli
Respiratory virusesa Legionella spp. H. influenzae
Respiratory viruses
12/29/18

EPIDEMIOLOGY
 More than 5 million CAP cases occur annually in the United States;
80% of the affected patients are treated as outpatients and
20% as inpatients.
 The mortality rate among outpatients is usually ≤1%.
 Hospitalized patients the rate can range from ∼12% to 40%, depending on
whether treatment is provided in or outside of the intensive care unit (ICU).
 CAP results in more than 1.2 million hospitalizations and more than 55,000
deaths annually. 12/29/18

RISK FACTOR
Risk factors for CAP
1. alcoholism,
2. asthma,
3. immunosuppression,
4. institutionalization, and
5. an age of ≥70 years.
Risk factors for pneumococcal
pneumonia
1. Dementia,
2. Seizure
3. Disorders,
4. Heart failure,
5. Cerebrovascular disease,
6. Alcoholism,
7. Tobacco
8. Smoking,
9. Chronic obstructive pulmonary disease
10.HIV infection.
12/29/18

CLINICAL MANIFESTATIONS
 Vary from indolent to fulminant in presentation and from mild to fatal i
n
severity.
 Manifestations of progression and severity include both constitutional
findings and those limited to the lung and associated structures.
 Frequently febrile with tachycardia or may have a history of chills and/or
sweats.
 Cough:
 may be either nonproductive or productive of mucoid,
 purulent, or blood-tinged sputum.

SIGN AND SYMPTOMS
 Fever or hypothermia
 Cough with or without sputum, hemoptysis
 Pleuritic chest pain
 Myalgia, malaise, fatigue
 GI symptoms
 Dyspnea
 Rales, rhonchi, wheezing
 Egophony, bronchial breath sounds
 Dullness to percussion
 Atypical Sx’s in older patients

12/29/18
PE findings
 vary with the degree of pulmonary consolidation and the presence o
r
absence of a significant pleural effusion.
 Inspection : An increased respiratory rate and use of accessory
muscles of respiration are common.
 Palpation : Reveal increased or decreased tactile fremitus,
 Percussion : Can vary from dull to flat, reflecting underlying
consolidated lung and pleural fluid, respectively.
 Auscultation : Crackles, bronchial breath sounds, and possibly a
pleural friction rub may be heard .

CLINICAL DIAGNOSIS:
1. CXR : Demonstrable infiltrate
 Establish Diagnosis and presence of complications
(pleural effusion, multilobar disease)
 CXR: classically thought of as the Gold standard
 May show hyper-expansion, Atelectasis or Infiltrates

Normal Pneumonia
CHEST RADIOGRAPH

ETIOLOGIC DIAGNOSIS
2. Gram’s stain and Culture of sputum
 Main purpose of the sputum Gram’s stain is to ensure that a sample i
s
suitable for culture.
 May also identify certain pathogens (e.g., S. pneumoniae, S. aureus, and
gram-negative bacteria) by their characteristic appearance.
 Sensitivity and Specificity of the sputum Gram’s stain and culture are
highly variable.
12/29/18

3. Blood Cultures
 Only 5–14% of cultures of blood from patients hospitalized with CAP are
positive
 The most frequently isolated pathogen is S. pneumoniae.
ETIOLOGIC DIAGNOSIS
12/29/18

4. Urinary antigen tests
 Two commercially available tests detect pneumococcal and Legionella
antigen in urine.
 Legionella urine antigen test (serogroup 1)
Sensitivity 90%, Specificity 99%
 Pneumococcal urine antigen test
Sensitive 80% , Specific >90%
ETIOLOGIC DIAGNOSIS
12/29/18

5. polymerase Chain reaction
 Test amplify a microorganism’s DNA or RNA, are available for a number of
pathogens.
 PCR of nasopharyngeal swabs has become standard for diagnosis of
respiratory viral infection.
 I n addition, PCR can detect the nucleic acid of Legionella species, M.
pneumoniae, C. pneumoniae, and Mycobacteria.
ETIOLOGIC DIAGNOSIS
12/29/18

6. Serology
Four fold rise in specific IgM antibody titer between acute- and
convalescent-phase serum samples is generally considered diagnostic of
infection with the pathogen in question.
 I n the past, serologic tests were used to help identify atypical pathogens
as well as selected unusual organisms such as Coxiella burnetii.
ETIOLOGIC DIAGNOSIS

7.Biomarkers
 Two currently in use are
C-reactive protein (CRP) and
Procalcitonin (PCT)
 CRP may be of use in the identification of worsening disease o
r
treatment failure.
 PCT may play a role in determining the need for antibacterial therapy.
ETIOLOGIC DIAGNOSIS
12/29/18

PHILIPPINE CLINICAL PRACTICE GUIDELINES
12/29/18
On the diagnosis, empiric management, and prevention of
COMMUNITY-ACQUIRED PNEUMONIA (CAP)
IN IMMUNOCOMPETENT ADULTS
2010 CAP CPG with 2016 updates

COMMUNITY-ACQUI
RED PNEUMONI
A
 Lower respiratory tract infection acquired in the community within
24 hoursto lessthan 2 weeks
 COMMONLY PRESENTS WITH
1. An acute cough
2. Abnormal vital signs



Tachypnea (respiratory rate >20 breaths per minute)
Tachycardia (cardiac rate >100/minute), and
Fever (temperature >
37.8ºc)
1. At least one abnormal chest finding
 diminished breath sounds, rhonchi, crackles, or wheeze
12/29/18
Philippine Clinical Practice Guidelines on CAP (2010)

Outlines of the 2010 CPG guideline
 Part I: Clinical Diagnosis
 Part II:Chest Radiography
 Part I
I
I
: Site-of-Care Decisions
 Part IV: Microbiologic Studies
 Part V: Treatment : 2016 CPG updates focuses on treatment of CAP
 Part VI: Prevention
12/29/18

Part One: Clinical Diagnosis

1. Can CAP be diagnosed accurately by
history and physical examination?

2. Isthere any clinical feature that can predict
CAP caused by an atypical pathogen?
12/29/18

Atypical pathogens
 Common cause of CAP in all regions of the world with a global
incidence of 22%
 Mycoplasma pneumoniae, Chlamydophila pneumoniae, and
Legionella
 Main difference: presence of extrapulmonary findings (GI,
cutaneous)

12/29/18
Suspect Legionella in hospitalized CAP because it is the most
important atypical pathogen in termsof severity

Part Two: Chest Radiography
12/29/18

3. What is the value of the chest
radiograph in the diagnosis of CAP?
12/29/18

CXR may not be routinely done in:
 Healthy individuals or those with stable co-morbid conditions, and
 Normal vital signs and physical examination findings, and
 Reliable follow-up can be ensured.
12/29/18

4. What specific views of the chest
radiograph should be requested?
12/29/18

5. Are there characteristic radiographic
features that can predict the likely
etiologic agent from the chest
radiograph?
12/29/18

6. How should a clinician interpret a
radiographic finding of “pneumonitis”?
A radiographic reading of “Pneumonitis” does not always denote an
infectious process.
12/29/18

7. What is the significance of an initial
“normal” chest radiograph in a patient
suspected to have CAP?
12/29/18

8. Should a chest radiograph be
repeated routinely?
12/29/18

Repeat CXR
 Low-risk CAP recovering satisfactorily –not needed
 CAP not clinically improving or shows progressive disease –should
be repeated as needed based on clinician’sjudgement
 6 weeks after hospital discharge
 New radiographic baseline
 Exclude malignancy
12/29/18

9. What is the role of chest CTscan in
CAP?
12/29/18

Part Three: Site-of-Care Decisions
12/29/18

10. Which patients will need hospital
admission?
12/29/18

12/29/18

Part Four: Microbiologic Studies
12/29/18

11. What microbiologic studies are
necessary in CAP?
12/29/18

Microbiologic Studies
 Definite etiology
 Pathogen isisolated from normally sterile or uncontaminated
specimens (blood, pleural fluid or secretions obtained from
transtracheal or transthoracic aspiration)
 Probable etiology
 Pathogensdemonstrated by smear or isolated from cultures in
moderate to heavy quantity from respiratory secretions (e.g.,
expectorated sputum, bronchoscopic aspirate, quantitatively
cultured bronchoalveolar lavage fluid or brush catheter
specimen)
12/29/18

 Sputum culture
 May be contaminated with resident flora of the upper airways,
thusleading to false positive results
 Not sensitive in patientswho have taken previous antibiotics,
unable to expectorate and in those with delays in the
processing
 S.pneumoniae was isolated in 64%(29/45) of patients with
presumed pneumococcal pneumonia based on the finding of
Gram-positive diplococci compared to 6%(2/31) of patients
without Gram-positive diplococci
Philippine Clinical Practice Guidelines on CAP (2010) 12/29/18

ATYPICALPATHOGENS
 Group of pathogens(M. pneumoniae, C. pneumoniae and L.
pneumophila)
 Do not grow on routine culture isolation in the laboratory
 It isrecommended that the presence of L. pneumophila be
documented through
 Urine antigen test (UAT) or
 Direct fluorescent antigen test (DFA) of respiratory secretions

Emerging Etiologies (Human Pandemic
Influenza A [H1N1] 2009, SARS)
 Rapid influenza diagnostic tests (RIDTs)in respiratory clinical
specimenshave low overall sensitivity in detecting H1N1 (40-69%)
 If the presence of H1N1 issuspected in patientswith moderate
and high risk pneumonia, a definitive determination with rRT-PCR
should be conducted (95.4 –100%).

Part Five: Treatment
12/29/18

12. When should antibiotics be initiated for the
empiric treatment of CAP ?
Patient should receive initial therapy as soon as possible after
the diagnosis is established
Reduced in hospital mortality when antimicrobial therapy was
initiated within the first four hours of admission and diagnosis of
CAP.

13. What initial antibiotics are recommended for
the empiric treatment of CAP ?
For low risk CAP without comorbid illness AMOXICILLIN remains the
standard choice ( use of extended macrolides may also be considered)
For low risk CAP with stable comorbid illness, B-Lactam with B-
lactamse inhibitor combinations (BLIC) or second generation cephalosporin
with or without extended macrolides are recommended
For patients who have completed first line treament (BLIC or 2nd
generation cephalosporin) with no response , an extensive work up(sputum
Gram stain and culture) should be done to identify the factors for failure of
response

For moderate risk CAP a combination of
•an IV non-antipseudomonal B-Lactam with
•either an extended macrolide or a repiratory fluoroquinolone
For high risk CAP without risk for P
. aeruginosa a combination of
•IV non-antipseudomonal B-lactam (BLIC, cephalosporin or carbapenem) with
• either an IV extended macrolide or an IV respiratory fluoroquinolone

For high risk CAP with risk for P
. aeruginosa , a combination of
•an IV antipneumococcal ,antipseudomonal B-lactam ( BLIC, cephalosporin or
carbapene with
•an extended macrolide and aminoglycoside
OR a combination of
•an IV antipneumococcal, antipseudomonal B-Lactam and
• an IV ciprofloxacin or high dose IV levofloxacin

Empiric antimicrobial therapy for CAP with usual recommended
dosages in 50-60kg adults with normal liver and renal functions
Risk stratification Potentential pathogens Empiric Therapy
Low -risk CAP
Stable vital signs
•RR<30/minute
•PR<125/min
•SBP>90mmhg
•DBP>60mmhg
•Temp>36c or 40c
No altered mental state of acute onset
No suspected aspiration
No or stable comorbid conditions
Chest xray
• localized infiltrates
•No evidence of pleural effusion
Streptococcus pneumoniae
Haemophilus influenzae
Chlamydophila pneumoniae
Mycoplasma pneumoniae
Moraxella catarrhalis
Enteric gram negative bacilli (among those
with co-morbid illness)
Without co -morbid illness
Amoxicillin 1gm TID or, extended
macrolides
Azithromycin 500mg OD or clarithromycin
500mg BID
With stable comorbid illness
B-lactam / B- lactamase inhibitor
combination (BLIC) OR, 2nd gen oral
cephalosporin +/- extended macrolides
Co- amoxiclav 1gm BID OR,
Sultamicillin 750mg BID OR,
Cefuroxime axetil 500mg BID +/-
Azithromycin 500mg OD OR
Clarithromycin 500mg BID

MODERATE RISK CAP
Unstable vital sign
•RR > 30/minute
•PR > 125/min
•Temp < 36c or > 40c
•SBP < 90mmhg
•DBP < 60mmhg
Altered mental state of acute onset
Suspected aspiration
Unstable / Decompensated comorbid condition
•Uncontrolled diabetes mellitus
•Active malignancies
•Neurologic disease in evolution
•Congestive heart failure Class (CHF) II-IV
•Unstable coronary artery disease
•Renal failure on dialysis
•Uncompesated COPD
•Decompensated liver disease
Enteric gram- negative bacilli
Legionella pneumophila
Anaerobes (among those with risk of
aspiration)
IV non-antipseudomonal B-lactam (BLIC, cephalosporin) +
extended macrolides or respiratory fluoroquinolones (PO)
Ampicillin-sulbactam 1.5gm q6h IV OR Cefuroxime 1.5gm
q8h IV OR Ceftriaxone 2gm OD +
Azithromycin 500 OD PO OR Clarithromycin 500mg BID PO
OR Levofloxcin 500mg OD PO OR Moxifloxacin 400mg OD
PO
If aspiration pneumonia is suspected and a regimen
containing ampicillin-sulbactam and /or moxifloxacin is used
there is no need to add another antibiotic for additional
anaerobic coverage. If another combination is used may add
clindamycin to the regimen to cover microaerophilic
streptococci
Clindamyicn 600mg q8h IV OR Ampicillin Sulbactam 3g q6hr
IV OR
Moxifloxacin 400mg OD PO
Empiric antimicrobial therapy for CAP

High risk CAP
Any of the clinical feature of moderate risk CAP
plus any of the following
•Severe sepsis and septic shock OR
•need for mechanical ventilation
Enteric gram negative bacilli
Anaerobes (among those with risk of aspiration)
Staphylococcus aureus
Pseudomas aeruginosa
No risk for P.aeruginosa
IV non- antipseudomonal B-lactam + I V extended
macrolides
or IV respiratory fluoroquinlones
Ceftriaxone 2gm OD OR Ertapenem 1gm OD +
Azithromycin dihydrate 500mg OD IV OR
Levofloxacin 500mg OD IV OR Moxifloxacin 400mg
OD IV

High risk CAP
Any of the clinical feature of moderate risk CAP
plus any of the following
•Severe sepsis and septic shock OR
•need for mechanical ventilation
Enteric gram negative bacilli
Anaerobes (among those with risk of aspiration)
Staphylococcus aureus
Pseudomas aeruginosa
Risk for P.aeruginosa
IV antipneumococcal antipseudomonal B-latam
(BLIC, Cephalosporin or carbapenem) + IV
extended macrolides + aminoglycoside
Piperacillin-Tazobactam 4.5gm q6hr OR
Cefepime 2 gm q8-12hr OR Meropenem 1gm
q8h + Azithromycin dihydrate 500mg OD IV+
Gentamicin 3mg/kg OD OR amikacin 15mg/kg
OD OR IV antipneumococcal antipseudomonal B-
lactam (BLIC, cephalosporin or carbapenem) +IV
ciprofloxacin /high dose levofloxacin
Piperacillin-tazobactam 4.5gm q6hr OR Cefepime
2gm q8-12hr OR meropenem 1gm q8h+
levofloxain 750mg OD iv or ciprofloxacin 400mg
q8-12hr IV
If MRSA pneumonia is suspected add
Vancomycin 15mg/kg q8-12hr OR Linezolid
600mg q12hr IV OR
Clindamycin 600mg qq8hr IV

12/29/18
Pneumonia Risk Score (CURB-65)
Predicts Mortality In CAP
C Confusion of new onset
U Urea (BUN) > 7mmol/L (19mg/dl)
R Respiratory rate > 30 breaths per minute
B Blood pressure <90/60 mmhg
65 Age > 65 years old
Interpretation:
0-1: Treat as outpatient
2: Admit patient
>3 : Consider ICU admission

14. How can response to initial therapy be assessed?

Temperature, respiratory rate, heart rate, blood pressure, sensorium, oxygen saturation and
inspired oxygen concentration should be monitored to assess response to therapy.
 Response to therapy is expected within 24-72 hrs of initiating treatment .
 Failure to improve after 72 hrs of treatment is an indication to repeat chest radiograph
 Follow up cultures of blood and sputum are not indicated for patients who are responding to
treatment.

15. When should de-escalation of empiric antibiotic
therapy be done ?
 De-escalation of initial empiric broad spectrm antibiotic or combination
parenteral therapy to a single narrow spectrum parenteral or oral
agents based on avaialble laboratory data is recommended
•
•
•
Once the patient is clinically improving ,
Is hemodynamically stable and
Has a functioning gastrointestinal tract.

Indications for streamlining of antibiotic therapy
1. Resolution of fever for >24hrs
2. Less cough and resolution of respiratory distress (normalization of
respiratory rate)
3. Improving white blood cell count, no bacteremia.
4. Etiologic agent is not a high risk (virulent/ resistant) pathogen e.g. Legionella
S. aureus or Gram-negative enteric bacilli
5. No instable comorbid condition or life threatning complication such as
myocardial infarction, congestive heart failure, complete heart block, new
atrial fibrillation, SVT etc.
6. No sign of organ dysfunction such as hypotension , acute mental changes ,
BUN to creatinine ratio of >10:1 , hypoxemia and metabolic acidosis
7. Patient is clinically hydrated , taking oral fluids and is able to take oral
medications.

16. Which oral antibiotics are recommended for de-escalation or
switch therapy from parenteral antibiotics?
 The choice of oral antibiotics following initial parenteral therapy i
s
based on available culture results, antimicrobial spectrum ,
efficacy , safety and cost.
 In general when switching to oral antibiotics, either the same agent
as the parenteral antibiotic or an antibiotic from the same drug
class should be used

Antibiotic dosage of oral agents for streamlining or
switch therapy
Antibiotic Dosage
Amoxicillin -clavulanic acid 625 mg TID or 1gm BID
Azithromycin 500mg OD
Cefixime 200mg BID
Cefuroxime axetil 500mg BID
Cefpodoxime proxetil 200mgw BID
Levofloxacin 500-750mg OD
Moxifloxacin 400mg OD
Sultamicillin 750mg BID

17. How long is the duration of treatment for CAP?

Low risk uncomplicated bacterial pneumonia : 5 to 7 days
 Moderate risk bacterial pneumonia : 7-10 days
 For moderate risk and high risk CAP or for those with suspected or confirmed
Gram- negative, S. aureus or P.aruginosa pneumonia, treatment should be
prolonged to 28 days if with associated bacteremia.
 Mycoplasma : 10 to 14 days
 Chlamydophila pneumonia and Legionella pneumonia : 4 to 21 days

Duration Of Antibiotics Use Based On Etiology
Etiologic agent Duration of therapy (days)
Most bacterial pneumonias except enteric Gram -negative
pathogens S.aureus (MSSA and MRSA) , and P.aeruginosa
5-7 days
3-5 (azalides) for S.pneumniae
Enteric gram negative pathogens S.aureus (MSSA and
MRSA), and P.aeruginosa
MSSA community acquired pneumonia
a. non bacteremic - 7-14days
b. bacterimic -longer up to 21 days
MRSA community acquired pneumonia
a. non-bacteremic -7-21 days
b. bacterimic -longer up to 28days
Pseudomonas aeruginosa
a. non-bacteremic -14-21days
b. bacetrimic-longer up to 28days
Mycoplasma and Chlamydophila 10-14 days
Legionella 14-21 ; 10 azalides

18. What should be done for patients who are not
improving after 72hrs of empiric antibiotic therapy?
 The lack of response to seemingly appropriate treatment in a patient with CAP should
lead to a complete reappraisal, rather than simply to selection of alternative antibiotics.
 The clinical history , physical examination and the results of all available investigations
should be reviewed.the patient should be reassessed for possibl resistance to the
antibitics being given or for the presence of other pathogens such as M. tuberculosis ,
virsuses , parasites or fungi .
 Treatment should then be revised according to culture result.

19. What should be done for patients who are not
improving after 72hrs of empiric antibiotic therapy?
 Follow up chest radiograph is recommended
•
• investigate for other conditions such as pneumothorax, cavitation and extension to previously
univolved lobes , pleural effusion , pulmonary edema and ARDS , for an underlying mass,
bronchiectasis , loculation, pulmonary abscesses
a CT scan would provide more information
 Obtaining additional specimens for microbiologic testing should be considered

12/29/18
Reasons for lack of response to treatment of CAP
 Correct organism but inappropriate antibiotic choices or dose.
 Resistance of oraganism to selected antibiotics
 Wrong dose (e.g. in apatient whois morbidly obese or has fluid overload)
 Antibiotics not administered
 Correct organism and correct antibiotic but infection is loculated (e.g. most
commonly empyema)
 Obstruction (e.g lung cancer , foreign body)
 Incorrect identification of causative organism
 No identification of causative organism and empirical therapy directe toward wrong
organism
 Non-infectious cause
 Drug induced fever
 Presence of an unrecognized concurrent infection

12/29/18
20. When can a hospitalized patient with CAP be
discharged ?
 In the absence of any unstable coexisting illness or other life
threatening complication , the patient may be discharged once clinically
stable and oral therapy is initiated.
 A repeat chest radiograph prior to hospital discharge is not needed in
a patient who is clinically improving.
 A repeat chest radiograph is recommended during a follow up visit
approximately 4 to 6 weeks after hospital discharge to establish a new
radiograph baseline and to exclude the possibility of malignancy
associated with CAP, particularly in older smokers.

Recommended hospital discharge criteria
During the 24 hours before discharge , the patient should have the following
characteristics (unless this represents the baseline status):
1. Temperature of 36 -37.5c
2. Pulse <100/min
3. Respiratory rate between 16-24/minute
4. Systolic BP>90mmHg
5. Bloodoxygen saturation >90%
6. Functioning gastrointestinal tract

21. What other information should be explained and
discussed with the patient ?


Explain to patients with CAP that after starting treatment their symptoms are expected to
steadily improve , although the rate of improvement will vary with the severity of the
pneumonia.
Most people can expect that by:
 1week :fever should have resolved
 4weeks :chest pain and sputum production should have substantailly reduced
 6weeks: cough and breathlessness should have substantially reduced
 3months : most symptoms should have resolved but fatigue may still be present
 6months :most people will feel back to normal.

PROGNOSIS
 Prognosis depends on the
• Patient’s age,
• Comorbidities, and
• Site of treatment (inpatient or outpatient).
 Young patients without comorbidity do well and usually recover fully
after ~2 weeks.
 Older patients and those with comorbid conditions can take several
weeks longer to recover fully.

PartSix: P
revention
12/29/18

PREVENTION
The main preventive measure is vaccination
• PPV23 contains capsular material from 23 pneumococcal serotypes;
• In PCV13 capsular polysaccharide from 13 of the most frequent
pneumococcal pathogens affecting children is linked to an immunogenic
protein.
• PCV13 produces T cell–dependent antigens that result in long-term
immunologic memory.

PREVENTION
 Administration of PCV13 vaccine to children has
• Led to an overall decrease in the prevalence of antimicrobial-resistant
pneumococci and
• In the incidence of invasive pneumococcal disease among both children and
adults.
 PCV13 now is also recommended for the elderly and for younger
immunocompromised patients.

PREVENTION
 Two forms of influenza vaccine are available:
intramuscular inactivated vaccine and
intranasal live-attenuated cold-adapted vaccine.
 The latter is contraindicated in immunocompromised patients.

Smoking Cessation
 Cigarette smoking, both active and passive, is a recognized
independent risk factor for CAP.
 It is the major avoidable risk factor for acute pneumonia in adults.
 Smoking cessation isrecommended for all patientswith CAP who
are current smokers.

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