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GUIDELINES
FOR THE MANAGEMENT
OF
ADULTS WITH COMMUNITY
ACQUIRED PNEUMONIA
(CAP)
BY
Ibrahim Al Sharabi
from the guidelines
of
AMERICAN THORACIC SOCIETY
INTRODUCTION
• CAP remains a common and serious illness, in spite of the
availability of potent new antimicrobials and effective vaccines.
• Sixth leading cause of death and number one infectious death in
USA
• Up to 5.6 million cases of community-acquired pneumonia occur
annually, and as many as 1.1 million of these require
hospitalization.
• The annual cost of treatment was $9.7 billion (1994) ; 92 %
inpatient therapy
• Among patients with CAP who require hospitalization, the
mortality rate averages 12% overall, but increases in specific
populations, such as those with bacteremia(30%of all CAP
cases), and those from nursing home settings, and approaches
40% in those who are most ill and who require admission to the
ICU.
DEFINITION AND
CLASSIFICATION
- Pneumonia means inflammation of the lung substances.
- It can be classified as follow
Primary and secondary
Community-acquired and hospital acquired
Typical and atypical
CLINICAL FEATURES
Presenting symptoms
• Sudden onset of rigors
• Fever, pleuritic chest pain, and
cough productive of purulent
sputum 80 %
• Chest pain 30 %
• Chills 40 - 50 %
• Rigors 15 %
• Most individuals seek medical
care within six days
Physical examination
• Fever 80 %
• Respiratory rate
> 24 /minute 45 - 70 %
• Tachycardia
• Audible rales
• Evidence of
consolidation 30 - 35 %
BOTH THE EPIDEMIOLOGY AND
TREATMENT OF PNEUMONIA HAVE
UNDERGONE CHANGES.
• Pathogen not defined in as many as 50 % patients even with extensive
diagnostic testing
• S. pneumoniae is the leading cause of CAP
• H. influenzae ( type B), S. aureus, and gram (-) bacteria each account for
3 to 10 %
• Staph aureus CAP is usually seen in the elderly and as post-influenza
pneumonia
• P. aeruginosa causes CAP in neutropenia, cystic fibrosis, HIV infection &
bronchiectasis
• N. meningitidis, M. catarrhalis & S. pyogenes can occasionally cause
CAP
• Anaerobic organisms are implicated in aspiration pneumonia and lung
abscess
• MRSA, M. tuberculosis, and certain viral agents are common in
nursing-home patients
• Increasingly common in elderly and those with comorbid illnesses like
COPD, DM, CHF, chronic liver disease and others
• Parallel to the improvement in our antibiotic armamentarium, bacterial
resistance mechanisms have evolved
• Changing resistance patterns among pathogens commonly causing
CAP:
S.pneumonia increasing resistance to tetracyclines and
penicillens.
H.influenzae 30% resistance to penicillens.
Moraxella catarrhalis 90% resistance to penicillens.
• Newly identified and previously unrecognized organisms are emerging
(Atypical pneumonia):
Chlamydia pneumoniae 15% of CAP.
Mycoplasma pneumoniae 20% of CAP.
Legionella pneumophila 5% of CAP.
DIAGNOSTIC TESTING
Chest radiograph to :
Establish the presence of pneumonia.
Evaluate the severity.
Identify coexisting conditions like pleural effusion and
bronchial obstruction.
Identify other diseases as T-B or lung abscesses.
• Arterial blood gas analysis
• CBC count
• Chemistry profile, including renal and LFTs and electrolytes (Na,
glucose, and creatinine)
• HIV serology (15 - 54 yrs )
• Blood culture x 2
IDENTIFY A SPECIFIC ETIOLOGIC
DIAGNOSIS
Sputum Gram stain and culture +/- AFB stain & culture and/or
Legionella test (culture, DFA stain & urine antigen)
Sputum culture.
Serological testing .
Analysis of pleural fluid (if present)
white blood cell, count and differential; protein, glucose, LDH,
and pH;
Gram's stain and acid-fast stain; and culture for bacteria, fungi,
and mycobacteria
However in up to half of all CAP cases a specific etiology can not
be identified even in the presence of extensive diagnostic
testing .
GRAM'S STAIN OF EXPECTORATEDGRAM'S STAIN OF EXPECTORATED
SPUTUMSPUTUM
• Sensitivity and specificity vary widely depending on the
criteria used to define a "positive” stain
• > 25 neutrophils and < 5 squamous epithelial cells per low
power field
• No studies correlate data from sputum Gram stain and
culture to cultures of alveolar material in large numbers of
patients with CAP
• Cytologic screening criteria not evaluated for Legionella,
mycobacteria or viral infections
• Direct staining of sputum may be diagnostic for
Mycobacterium sp., endemic fungi, Legionella sp. (DFA
stain) & P. carinii
PATIENT STRATIFICATION
We divided patients into four groups on the basis of place of
therapy (outpatient, hospital ward, or intensive care unit);
the presence of coexisting cardiopulmonary disease
(COPD, CHF); and the presence of modifying factors that
increase the risk of infection with specific pathogens as
seen below
MODIFYING FACTORS
Penicillin-resistant and drug-resistant pneumococci
Age > 65 yr
β-Lactam therapy within the past 3 mo
Alcoholism
Immune-suppressive illness (including therapy with corticosteroids)
Multiple medical comorbidities
Enteric gram-negatives
Residence in a nursing home
Underlying cardiopulmonary disease
Multiple medical comorbidities
Recent antibiotic therapy
Pseudomonas aeruginosa
Structural lung disease (bronchiectasis)
Corticosteroid therapy (> 10 mg of prednisone per day)
Broad-spectrum antibiotic therapy for >7 d in the past month
Malnutrition
USING THESE FACTORS, THE FOUR
PATIENT GROUPS WERE DEFINED AS THE
FOLLOWING
I - OUTPATIENTS WITH NO HISTORY OF
CARDIOPULMONARY DISEASE, AND NO MODIFYING
FACTORS
ORGANISMS
Streptococcus pneumoniae
Mycoplasma pneumoniae
Chlamydia pneumoniae (alone or
as mixed infection)
Hemophilus influenzae
Respiratory viruses
Miscellaneous
Legionella spp.
Mycobacterium tuberculosis
Endemic fungi
THERAPY
Advanced generation
macrolide:
Clarithromycin (KLACID )
II- OUTPATIENTS WITH CARDIOPULMONARY DISEASE (CHF
OR COPD) AND/OR OTHER MODIFYING FACTORS (RISK
FACTORS FOR DRSP OR GRAM-NEGATIVE BACTERIA)
ORGANISMS
Streptococcus pneumoniae(including DRSP)
Mycoplasma pneumoniae
Chlamydia pneumoniae
Mixed infection
(bacteria plus atypical pathogen or virus)
Hemophilus influenzae
Enteric gram-negatives
Respiratory viruses
Miscellaneous
Moraxella catarrhalis, Legionella spp.,
aspiration (anaerobes), Mycobacterium
tuberculosis, endemic fungi
THERAPY
β-Lactam
(oral cefpodoxime,cefuroxime ,
high-dose amoxicillin,
amoxicillin/clavulanate;
or parenteral ceftriaxone
followed by oral cefpodoxime)
plus
Advanced generation macrolide:
Clarithromycin (KLACID )
or
Antipneumococcal fluoroquinolone
(used alone)
III. INPATIENTS, NOT ADMITTED TO THE ICU, WHO HAVE
THE FOLLOWING
a. Cardiopulmonary disease, and/or other modifying factors (including
being from a nursing home)
ORGANISMS
Streptococcus pneumoniae (Including DRSP)
Hemophilus influenzae
Mycoplasma pneumoniae
Chlamdia pneumoniae
Mixed infection
(bacteria plus atypical pathogen)
Enteric gram-negatives
Aspiration (anaerobes)
Viruses
Legionella spp.
Miscellaneous
M. tuberculosis, endemic fungi,
P. carinii
THERAPY
I.V β -lactam (cefotaxime,
ceftriaxone,
ampicillin/sulbactam, high-dose
ampicillin)
plus
I.V or oral macrolide
(KLACID)
or
I.V antipneumococcal
fluoroquinolone
alone
b. No cardiopulmonary disease, and no other modifying factors
ORGANISMS
S. pneumoniae
H. influenzae
M. pneumoniae
C. pneumoniae
Mixed infection (bacteria
plus atypical pathogen)
Viruses
Legionella spp.
Miscellaneous
M. tuberculosis,
endemic fungi, P. carinii
THERAPY
I.V. clarithromycin(KLACID I.V)
alone
If macrolide allergic or intolerant
Doxycycline
and a β-lactam
or
An antipneumococcal
Fluoroquinolone alone
IV. ICU-ADMITTED PATIENTS WHO HAVE THE FOLLOWING :
a. No risks for Pseudomonas aeruginosa
ORGANISMS
Streptococcus pneumoniae (including DRSP)
Legionella spp.
Hemophilus influenzae
Enteric gram-negative bacilli
Staphylococcus aureus
Mycoplasma pneumoniae
Respiratory viruses
Miscellaneous
Chlamydia pneumoniae,
M tuberculosis, endemic fungi
THERAPY
I.V β-lactam (cefotaxime,
ceftriaxone) .
plus
I.V macrolide (KLACID)
b. Risks for Pseudomonas aeruginosa
ORGANISMS
P. aeruginosa(22%)
THERAPY
Selected I.V antipseudomonal β-lactam
(cefepime, imipenem, meropenem,
piperacillin/
tazobactam)
plus
I.V antipseudomonal quinolone (ciprofloxacin)
or
Selected IV antipseudomonal β -lactam
(cefepime, imipenem, meropenem,
piperacillin/
tazobactam)
plus
I.V aminoglycoside
plus either
IV macrolide (KLACID)
or I.V nonpseudomonal fluoroquinolone
DECISION TO HOSPITALIZE
• 1. Age over 65 yr1. Age over 65 yr
• 2. Presence of coexisting illnesses or other findings2. Presence of coexisting illnesses or other findings
– a. COPD, bronchiectasis, cystic fibrosis
– b. Diabetes mellitus
– c. Chronic renal failure
– d. Congestive heart failure
– e. Chronic liver disease of any etiology
– f. Previous hospitalization within 1 yr
– g. Suspicion of aspiration (gastric or oropharyngeal secretions)
– h. Altered mental status
– i. Postsplenectomy state
– j. Chronic alcohol abuse or malnutrition
DECISION TO HOSPITALIZE
• 3. Physical findings3. Physical findings
– a. Respiratory rate > 30 breaths/min
– b. DBP 60 mmHg or a SBP 90 mmHg
– c. Temperature >38.3º C (101º F)
– d. Extrapulmonary sites of disease e.g, presence of septic arthritis,
meningitis, etc.
– e. Confusion and/or decreased level of consciousness
DECISION TO HOSPITALIZE
• 4. Laboratory findings4. Laboratory findings
• a. WBC <4,000/mcL or >30,000/mcL or an ANC below 1,000/mcL
• b. Pao2 <60 mmHg or Paco2 of >50 mmHg on room air.
• c. Need for mechanical ventilation.
• d. Serum creatinine >1.2 mg/dl or BUN >20 mg/dl (>7 mmol/L)
• e. Unfavorable chest radiographic findings:
- more than one lobe involvement - presence of a cavity
- rapid radiographic spread z- pleural
effusion
• f. Hct of <30 % or hemoglobin <9 g/dl
• g. Evidence of sepsis or organ dysfunction as manifested by a
metabolic acidosis, an increased PT, an increased PTT, decreased
platelets, fibrin split products > 1:40
• 5. Social considerations5. Social considerations
COMPLICATIONS
• Risk factors include older age, preexisting lung disease, immunodeficiency or
AIDS
• Potential complications include parapneumonic effusion, empyema, necrotizing
pneumonia, and lung abscess
• Parapneumonic effusions caused by PRP are associated with younger age
(approximately two years) and a nearly universal incidence of bacteremia but do
not result in poorer outcome than susceptible strains
• Bacteremia with subsequent seeding of other foci is seen in 25% of cases and
represents the most significant complication. Bacteremic patients were more
likely to die during the first week of illness. Splenectomized patients have an
increased risk of overwhelming sepsis
• Abscesses are usually culture-positive and rapidly responsive to drainage
• Necrotizing pneumonia is culture-negative and responds adversely to
interventional therapy
COMPLICATIONS
DURATION OF THERAPY
The presence of coexisting illness and/or bacteremia, the
severity of illness at the onset of antibiotic therapy, and
the subsequent hospital course should be considered in
determining the duration of antibiotic therapy.
S. pneumoniae pneumonia, and
other bacterial infections,
should be treated for 7 to 10 d
M. pneumoniae
C. pneumoniae
10-14 d
Legionnaire’s disease 10-14 d
Patients chronically treated with
corticosteroids with CAP
14 d or longer
RESPONSE TO THERAPY
On the basis of the clinical response to therapy, patients may
be categorized into three groups
I- Patients with early clinical response should be considered for rapid
switch to oral therapy, followed by prompt hospital discharge.
II- Patients with lack of clinical response which should be defined at
Day 3 of hospitalization
III- Patients with clinical deterioration, which can occur as early as after
24–48 h of therapy
in the second and third categories need an evaluation of host and
pathogen factors, along with a reevaluation of the initial
diagnosis and a search for complications of pneumonia and
pneumonia therapy.
SWITCH TO ORAL THERAPY
Patients should be switched to oral therapy if they meet
four criteria
Improvement in cough and dyspnea.
Fever(<100°F) ) on two occasions 8 h apart.
Functioning gastrointestinal tract with adequate oral
intake.
HOSPITAL DISCHARGE
In the absence of any unstable coexisting illnesses, or other life-
threatening complications, the patient should be discharged home
the same day that clinical stability occurs and oral therapy is
initiated. In-hospital observation on oral therapy is not necessary,
and only adds to cost and length of stay, without any measurable
clinical benefit
EVALUATING THE NONRESPONDING
PATIENT
Bronchoscopy is usually not needed, and patience is
necessary to observe the full course of radiographic clearing of
community-acquired pneumonia . However, bronchoscopy
should be considered in patients below the age of 55 yr, who
have multilobar disease and are nonsmokers. If bronchoscopy
is performed, the goal is to identify unusual organisms or drug-
resistant pathogens, but the clinician could also obtain this
information by collecting lower respiratory tract secretions
(sputum or endotracheal aspirate) for culture. Cultures should
be sent to evaluate for drug-resistant and unusual pathogens,
including tuberculosis.
EVALUATING THE NONRESPONDING
PATIENT
In addition to sampling lower respiratory tract secretions, other
tests should be considered. Computed tomography may reveal
unsuspected collections of pleural fluid, multiple lung nodules,
or cavitation within a lung infiltrate. Lung scanning, spiral CT
scanning, and/or pulmonary angiography should be considered
if the patient is at risk for pulmonary embolus with infarction.
While the routine use of serologic testing is not useful in the
initial evaluation of patients with community-acquired
pneumonia, serologic tests for Legionella sp., Myco-plasma
pneumoniae, viral agents, endemic fungi, and other unusual
pathogens should be considered at this point.
EVALUATING THE NONRESPONDING
PATIENT
• Legionella urinary antigen testing should also be considered.
This test is positive in more than half of all patients with proven
Legionellapneumophila infection, and more than 80% of patients
with Legionella pneumophila serogroup 1 infection (81, 82).
• If this extensive diagnostic evaluation has not been useful,
and if the patient is seriously ill, open lung biopsy of an involved
area of lung should be considered.
TREATMENT OF COMMUNITY-
AQUIRED PNEUMONIA KEY POINTS
• CAP is frequently a mixed infection of typical and
atypical bacteria.
• The clinical features of CAP can not be reliably
used to identify the causative agent of
pneumonia with adequate sensitivity and
specifity .therefore empiric therapy is usually
required.
• The initial side of care decision is perhaps the
single most important clinical decision made by
physicians during the entire course of CAP.
TREATMENT OF COMMUNITY-
AQUIRED PNEUMONIA KEY POINTS
• When multiple risk factors co-exist, intensely
supervised care should be strongly considered.
• A significant number of treatment failures have
been documented for S. pneumoniae resistant to
many drugs. Be prepared for possible treatment
failure.
TREATMENT OF COMMUNITY-
AQUIRED PNEUMONIA KEY POINTS
• Viral and pneumococcal infections predominant
in the under age 5 population. Above age 5,
atypicals begin to dominate with increasing age,
but S. pneumoniae still represent 25-35% of the
cases.
• In order to minimize the development of resistant
to this valuable agents, antipneumococcal
fluoroquinolones should not be used in patients
under the age of 18 and should be avoided in
adults when alternatives exists.
WHY KLACID XL ?
• Erythromycin was introduced in 1952 and has
remained the prototype of the macrolides.
• The limitations of erythromycin include variable
absorption, instability in gastric acid, poor
tissues penetration, short elimination half life, GI
irritation, and a narrow spectrum of activity.
• Modifications of the macrolide structure are
designed to improve the chemical, biological and
pharmacokinetic properties of erythromycin.
• Clarithromycin (KLACID) is a14-membered
macrolide known as 6-O-methyl-erythromycin
which overcomes all of the above limitations.
PERFECT SPECTRUM
• KLACID XL covers almost the whole
spectrum of important pathogens in RTIs
(Typical as S.pneumoniae ,H.influenzae,
moraxella catarrhalis, S.aureus and
atypical as
C.pneumoniae,M.pneumoniae,L.pneumop
hila) with bactericidal activities. Therefore
KLACID XL is the ideal antibiotic to be
used empirically in the treatment of CAP.
Balanced distribution
• Pneumonia caused by pneumococci
leads to bacteremia in about 30% of
the patients. Only with sufficient
serum antibiotic levels the
circulating micro-organisms can be
eliminated
Concentration of different antibiotics in
serum ,soft tissues and macrophages
Antibiotic Serum level Extracellular
levels
Conc. in
macrophages
clarithromycin + + + + + +
Roxithromycin + + + +
Azithromycin + + + + + +
Β-lactams + + + + ▬
EXCELLENT SAFETY PROFILE
0
0.02
0.04
0.06
0.08
0.1
0.12
0.14
0.16
6% 15%
KLACID
Amoxicillin/clavulanate
• Significantly less GI upset than amoxicillin/clavulanate
EXCELLENT PATIENT COMPLIANCE
• KLACID XL improves patients compliance so reducing
the risk of resistance
0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1
OD TID
NO FOOD INTERACTION
• Misadministration rate
0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1
0% 89% 94%
KLACID
Azithromycin
Roxythromycin

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Guidelines for the management of adults with community acquired pneumonia

  • 1. GUIDELINES FOR THE MANAGEMENT OF ADULTS WITH COMMUNITY ACQUIRED PNEUMONIA (CAP) BY Ibrahim Al Sharabi from the guidelines of AMERICAN THORACIC SOCIETY
  • 2. INTRODUCTION • CAP remains a common and serious illness, in spite of the availability of potent new antimicrobials and effective vaccines. • Sixth leading cause of death and number one infectious death in USA • Up to 5.6 million cases of community-acquired pneumonia occur annually, and as many as 1.1 million of these require hospitalization. • The annual cost of treatment was $9.7 billion (1994) ; 92 % inpatient therapy • Among patients with CAP who require hospitalization, the mortality rate averages 12% overall, but increases in specific populations, such as those with bacteremia(30%of all CAP cases), and those from nursing home settings, and approaches 40% in those who are most ill and who require admission to the ICU.
  • 3. DEFINITION AND CLASSIFICATION - Pneumonia means inflammation of the lung substances. - It can be classified as follow Primary and secondary Community-acquired and hospital acquired Typical and atypical
  • 4. CLINICAL FEATURES Presenting symptoms • Sudden onset of rigors • Fever, pleuritic chest pain, and cough productive of purulent sputum 80 % • Chest pain 30 % • Chills 40 - 50 % • Rigors 15 % • Most individuals seek medical care within six days Physical examination • Fever 80 % • Respiratory rate > 24 /minute 45 - 70 % • Tachycardia • Audible rales • Evidence of consolidation 30 - 35 %
  • 5. BOTH THE EPIDEMIOLOGY AND TREATMENT OF PNEUMONIA HAVE UNDERGONE CHANGES. • Pathogen not defined in as many as 50 % patients even with extensive diagnostic testing • S. pneumoniae is the leading cause of CAP • H. influenzae ( type B), S. aureus, and gram (-) bacteria each account for 3 to 10 % • Staph aureus CAP is usually seen in the elderly and as post-influenza pneumonia • P. aeruginosa causes CAP in neutropenia, cystic fibrosis, HIV infection & bronchiectasis • N. meningitidis, M. catarrhalis & S. pyogenes can occasionally cause CAP • Anaerobic organisms are implicated in aspiration pneumonia and lung abscess
  • 6. • MRSA, M. tuberculosis, and certain viral agents are common in nursing-home patients • Increasingly common in elderly and those with comorbid illnesses like COPD, DM, CHF, chronic liver disease and others • Parallel to the improvement in our antibiotic armamentarium, bacterial resistance mechanisms have evolved • Changing resistance patterns among pathogens commonly causing CAP: S.pneumonia increasing resistance to tetracyclines and penicillens. H.influenzae 30% resistance to penicillens. Moraxella catarrhalis 90% resistance to penicillens. • Newly identified and previously unrecognized organisms are emerging (Atypical pneumonia): Chlamydia pneumoniae 15% of CAP. Mycoplasma pneumoniae 20% of CAP. Legionella pneumophila 5% of CAP.
  • 8. Chest radiograph to : Establish the presence of pneumonia. Evaluate the severity. Identify coexisting conditions like pleural effusion and bronchial obstruction. Identify other diseases as T-B or lung abscesses. • Arterial blood gas analysis • CBC count • Chemistry profile, including renal and LFTs and electrolytes (Na, glucose, and creatinine) • HIV serology (15 - 54 yrs ) • Blood culture x 2
  • 9. IDENTIFY A SPECIFIC ETIOLOGIC DIAGNOSIS Sputum Gram stain and culture +/- AFB stain & culture and/or Legionella test (culture, DFA stain & urine antigen) Sputum culture. Serological testing . Analysis of pleural fluid (if present) white blood cell, count and differential; protein, glucose, LDH, and pH; Gram's stain and acid-fast stain; and culture for bacteria, fungi, and mycobacteria However in up to half of all CAP cases a specific etiology can not be identified even in the presence of extensive diagnostic testing .
  • 10. GRAM'S STAIN OF EXPECTORATEDGRAM'S STAIN OF EXPECTORATED SPUTUMSPUTUM • Sensitivity and specificity vary widely depending on the criteria used to define a "positive” stain • > 25 neutrophils and < 5 squamous epithelial cells per low power field • No studies correlate data from sputum Gram stain and culture to cultures of alveolar material in large numbers of patients with CAP • Cytologic screening criteria not evaluated for Legionella, mycobacteria or viral infections • Direct staining of sputum may be diagnostic for Mycobacterium sp., endemic fungi, Legionella sp. (DFA stain) & P. carinii
  • 11. PATIENT STRATIFICATION We divided patients into four groups on the basis of place of therapy (outpatient, hospital ward, or intensive care unit); the presence of coexisting cardiopulmonary disease (COPD, CHF); and the presence of modifying factors that increase the risk of infection with specific pathogens as seen below
  • 12. MODIFYING FACTORS Penicillin-resistant and drug-resistant pneumococci Age > 65 yr β-Lactam therapy within the past 3 mo Alcoholism Immune-suppressive illness (including therapy with corticosteroids) Multiple medical comorbidities Enteric gram-negatives Residence in a nursing home Underlying cardiopulmonary disease Multiple medical comorbidities Recent antibiotic therapy Pseudomonas aeruginosa Structural lung disease (bronchiectasis) Corticosteroid therapy (> 10 mg of prednisone per day) Broad-spectrum antibiotic therapy for >7 d in the past month Malnutrition
  • 13. USING THESE FACTORS, THE FOUR PATIENT GROUPS WERE DEFINED AS THE FOLLOWING
  • 14. I - OUTPATIENTS WITH NO HISTORY OF CARDIOPULMONARY DISEASE, AND NO MODIFYING FACTORS ORGANISMS Streptococcus pneumoniae Mycoplasma pneumoniae Chlamydia pneumoniae (alone or as mixed infection) Hemophilus influenzae Respiratory viruses Miscellaneous Legionella spp. Mycobacterium tuberculosis Endemic fungi THERAPY Advanced generation macrolide: Clarithromycin (KLACID )
  • 15. II- OUTPATIENTS WITH CARDIOPULMONARY DISEASE (CHF OR COPD) AND/OR OTHER MODIFYING FACTORS (RISK FACTORS FOR DRSP OR GRAM-NEGATIVE BACTERIA) ORGANISMS Streptococcus pneumoniae(including DRSP) Mycoplasma pneumoniae Chlamydia pneumoniae Mixed infection (bacteria plus atypical pathogen or virus) Hemophilus influenzae Enteric gram-negatives Respiratory viruses Miscellaneous Moraxella catarrhalis, Legionella spp., aspiration (anaerobes), Mycobacterium tuberculosis, endemic fungi THERAPY β-Lactam (oral cefpodoxime,cefuroxime , high-dose amoxicillin, amoxicillin/clavulanate; or parenteral ceftriaxone followed by oral cefpodoxime) plus Advanced generation macrolide: Clarithromycin (KLACID ) or Antipneumococcal fluoroquinolone (used alone)
  • 16. III. INPATIENTS, NOT ADMITTED TO THE ICU, WHO HAVE THE FOLLOWING a. Cardiopulmonary disease, and/or other modifying factors (including being from a nursing home) ORGANISMS Streptococcus pneumoniae (Including DRSP) Hemophilus influenzae Mycoplasma pneumoniae Chlamdia pneumoniae Mixed infection (bacteria plus atypical pathogen) Enteric gram-negatives Aspiration (anaerobes) Viruses Legionella spp. Miscellaneous M. tuberculosis, endemic fungi, P. carinii THERAPY I.V β -lactam (cefotaxime, ceftriaxone, ampicillin/sulbactam, high-dose ampicillin) plus I.V or oral macrolide (KLACID) or I.V antipneumococcal fluoroquinolone alone
  • 17. b. No cardiopulmonary disease, and no other modifying factors ORGANISMS S. pneumoniae H. influenzae M. pneumoniae C. pneumoniae Mixed infection (bacteria plus atypical pathogen) Viruses Legionella spp. Miscellaneous M. tuberculosis, endemic fungi, P. carinii THERAPY I.V. clarithromycin(KLACID I.V) alone If macrolide allergic or intolerant Doxycycline and a β-lactam or An antipneumococcal Fluoroquinolone alone
  • 18. IV. ICU-ADMITTED PATIENTS WHO HAVE THE FOLLOWING : a. No risks for Pseudomonas aeruginosa ORGANISMS Streptococcus pneumoniae (including DRSP) Legionella spp. Hemophilus influenzae Enteric gram-negative bacilli Staphylococcus aureus Mycoplasma pneumoniae Respiratory viruses Miscellaneous Chlamydia pneumoniae, M tuberculosis, endemic fungi THERAPY I.V β-lactam (cefotaxime, ceftriaxone) . plus I.V macrolide (KLACID)
  • 19. b. Risks for Pseudomonas aeruginosa ORGANISMS P. aeruginosa(22%) THERAPY Selected I.V antipseudomonal β-lactam (cefepime, imipenem, meropenem, piperacillin/ tazobactam) plus I.V antipseudomonal quinolone (ciprofloxacin) or Selected IV antipseudomonal β -lactam (cefepime, imipenem, meropenem, piperacillin/ tazobactam) plus I.V aminoglycoside plus either IV macrolide (KLACID) or I.V nonpseudomonal fluoroquinolone
  • 20. DECISION TO HOSPITALIZE • 1. Age over 65 yr1. Age over 65 yr • 2. Presence of coexisting illnesses or other findings2. Presence of coexisting illnesses or other findings – a. COPD, bronchiectasis, cystic fibrosis – b. Diabetes mellitus – c. Chronic renal failure – d. Congestive heart failure – e. Chronic liver disease of any etiology – f. Previous hospitalization within 1 yr – g. Suspicion of aspiration (gastric or oropharyngeal secretions) – h. Altered mental status – i. Postsplenectomy state – j. Chronic alcohol abuse or malnutrition
  • 21. DECISION TO HOSPITALIZE • 3. Physical findings3. Physical findings – a. Respiratory rate > 30 breaths/min – b. DBP 60 mmHg or a SBP 90 mmHg – c. Temperature >38.3º C (101º F) – d. Extrapulmonary sites of disease e.g, presence of septic arthritis, meningitis, etc. – e. Confusion and/or decreased level of consciousness
  • 22. DECISION TO HOSPITALIZE • 4. Laboratory findings4. Laboratory findings • a. WBC <4,000/mcL or >30,000/mcL or an ANC below 1,000/mcL • b. Pao2 <60 mmHg or Paco2 of >50 mmHg on room air. • c. Need for mechanical ventilation. • d. Serum creatinine >1.2 mg/dl or BUN >20 mg/dl (>7 mmol/L) • e. Unfavorable chest radiographic findings: - more than one lobe involvement - presence of a cavity - rapid radiographic spread z- pleural effusion • f. Hct of <30 % or hemoglobin <9 g/dl • g. Evidence of sepsis or organ dysfunction as manifested by a metabolic acidosis, an increased PT, an increased PTT, decreased platelets, fibrin split products > 1:40 • 5. Social considerations5. Social considerations
  • 23. COMPLICATIONS • Risk factors include older age, preexisting lung disease, immunodeficiency or AIDS • Potential complications include parapneumonic effusion, empyema, necrotizing pneumonia, and lung abscess • Parapneumonic effusions caused by PRP are associated with younger age (approximately two years) and a nearly universal incidence of bacteremia but do not result in poorer outcome than susceptible strains • Bacteremia with subsequent seeding of other foci is seen in 25% of cases and represents the most significant complication. Bacteremic patients were more likely to die during the first week of illness. Splenectomized patients have an increased risk of overwhelming sepsis • Abscesses are usually culture-positive and rapidly responsive to drainage • Necrotizing pneumonia is culture-negative and responds adversely to interventional therapy
  • 25. DURATION OF THERAPY The presence of coexisting illness and/or bacteremia, the severity of illness at the onset of antibiotic therapy, and the subsequent hospital course should be considered in determining the duration of antibiotic therapy. S. pneumoniae pneumonia, and other bacterial infections, should be treated for 7 to 10 d M. pneumoniae C. pneumoniae 10-14 d Legionnaire’s disease 10-14 d Patients chronically treated with corticosteroids with CAP 14 d or longer
  • 26. RESPONSE TO THERAPY On the basis of the clinical response to therapy, patients may be categorized into three groups I- Patients with early clinical response should be considered for rapid switch to oral therapy, followed by prompt hospital discharge. II- Patients with lack of clinical response which should be defined at Day 3 of hospitalization III- Patients with clinical deterioration, which can occur as early as after 24–48 h of therapy in the second and third categories need an evaluation of host and pathogen factors, along with a reevaluation of the initial diagnosis and a search for complications of pneumonia and pneumonia therapy.
  • 27. SWITCH TO ORAL THERAPY Patients should be switched to oral therapy if they meet four criteria Improvement in cough and dyspnea. Fever(<100°F) ) on two occasions 8 h apart. Functioning gastrointestinal tract with adequate oral intake.
  • 28. HOSPITAL DISCHARGE In the absence of any unstable coexisting illnesses, or other life- threatening complications, the patient should be discharged home the same day that clinical stability occurs and oral therapy is initiated. In-hospital observation on oral therapy is not necessary, and only adds to cost and length of stay, without any measurable clinical benefit
  • 29. EVALUATING THE NONRESPONDING PATIENT Bronchoscopy is usually not needed, and patience is necessary to observe the full course of radiographic clearing of community-acquired pneumonia . However, bronchoscopy should be considered in patients below the age of 55 yr, who have multilobar disease and are nonsmokers. If bronchoscopy is performed, the goal is to identify unusual organisms or drug- resistant pathogens, but the clinician could also obtain this information by collecting lower respiratory tract secretions (sputum or endotracheal aspirate) for culture. Cultures should be sent to evaluate for drug-resistant and unusual pathogens, including tuberculosis.
  • 30. EVALUATING THE NONRESPONDING PATIENT In addition to sampling lower respiratory tract secretions, other tests should be considered. Computed tomography may reveal unsuspected collections of pleural fluid, multiple lung nodules, or cavitation within a lung infiltrate. Lung scanning, spiral CT scanning, and/or pulmonary angiography should be considered if the patient is at risk for pulmonary embolus with infarction. While the routine use of serologic testing is not useful in the initial evaluation of patients with community-acquired pneumonia, serologic tests for Legionella sp., Myco-plasma pneumoniae, viral agents, endemic fungi, and other unusual pathogens should be considered at this point.
  • 31. EVALUATING THE NONRESPONDING PATIENT • Legionella urinary antigen testing should also be considered. This test is positive in more than half of all patients with proven Legionellapneumophila infection, and more than 80% of patients with Legionella pneumophila serogroup 1 infection (81, 82). • If this extensive diagnostic evaluation has not been useful, and if the patient is seriously ill, open lung biopsy of an involved area of lung should be considered.
  • 32. TREATMENT OF COMMUNITY- AQUIRED PNEUMONIA KEY POINTS • CAP is frequently a mixed infection of typical and atypical bacteria. • The clinical features of CAP can not be reliably used to identify the causative agent of pneumonia with adequate sensitivity and specifity .therefore empiric therapy is usually required. • The initial side of care decision is perhaps the single most important clinical decision made by physicians during the entire course of CAP.
  • 33. TREATMENT OF COMMUNITY- AQUIRED PNEUMONIA KEY POINTS • When multiple risk factors co-exist, intensely supervised care should be strongly considered. • A significant number of treatment failures have been documented for S. pneumoniae resistant to many drugs. Be prepared for possible treatment failure.
  • 34. TREATMENT OF COMMUNITY- AQUIRED PNEUMONIA KEY POINTS • Viral and pneumococcal infections predominant in the under age 5 population. Above age 5, atypicals begin to dominate with increasing age, but S. pneumoniae still represent 25-35% of the cases. • In order to minimize the development of resistant to this valuable agents, antipneumococcal fluoroquinolones should not be used in patients under the age of 18 and should be avoided in adults when alternatives exists.
  • 35. WHY KLACID XL ? • Erythromycin was introduced in 1952 and has remained the prototype of the macrolides. • The limitations of erythromycin include variable absorption, instability in gastric acid, poor tissues penetration, short elimination half life, GI irritation, and a narrow spectrum of activity. • Modifications of the macrolide structure are designed to improve the chemical, biological and pharmacokinetic properties of erythromycin. • Clarithromycin (KLACID) is a14-membered macrolide known as 6-O-methyl-erythromycin which overcomes all of the above limitations.
  • 36. PERFECT SPECTRUM • KLACID XL covers almost the whole spectrum of important pathogens in RTIs (Typical as S.pneumoniae ,H.influenzae, moraxella catarrhalis, S.aureus and atypical as C.pneumoniae,M.pneumoniae,L.pneumop hila) with bactericidal activities. Therefore KLACID XL is the ideal antibiotic to be used empirically in the treatment of CAP.
  • 37. Balanced distribution • Pneumonia caused by pneumococci leads to bacteremia in about 30% of the patients. Only with sufficient serum antibiotic levels the circulating micro-organisms can be eliminated
  • 38.
  • 39. Concentration of different antibiotics in serum ,soft tissues and macrophages Antibiotic Serum level Extracellular levels Conc. in macrophages clarithromycin + + + + + + Roxithromycin + + + + Azithromycin + + + + + + Β-lactams + + + + ▬
  • 40. EXCELLENT SAFETY PROFILE 0 0.02 0.04 0.06 0.08 0.1 0.12 0.14 0.16 6% 15% KLACID Amoxicillin/clavulanate • Significantly less GI upset than amoxicillin/clavulanate
  • 41. EXCELLENT PATIENT COMPLIANCE • KLACID XL improves patients compliance so reducing the risk of resistance 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 OD TID
  • 42. NO FOOD INTERACTION • Misadministration rate 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 0% 89% 94% KLACID Azithromycin Roxythromycin