Transcript Is this pneumonia?

In the name of GOD
Pneumonia
Hassan Ghobadi MD. Pulmonologist
Assistant Professor of Internal Medicine
Ardabil University of Medical Science
Pneumonia
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Definition:
Pneumonia is an infection of the pulmonary parenchyma
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Classification:
Community-acquired (CAP),
Health care – associated pneumonia (HCAP)
Hospital-acquired (HAP)
Ventilator-associated (VAP)
Pneumonia
Over the last decade or two, however, patients
presenting to the hospital have often been found to be
infected with multi drug-resistant (MDR) pathogens
previously associated with hospital-acquired pneumonia
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Widespread use of potent oral antibiotics
Earlier transfer of patients out of acute-care hospitals to
their homes
Increased use of outpatient IV antibiotic therapy
General aging of the population
More extensive immunomodulatory therapies
Pathogens in HCAP
Host Defenses
 Mucociliary
clearance
 Local antibacterial factors
 Gag reflex
 Cough mechanism
 Normal flora
 Mucosal barriers
 Alveolar macrophages
 Intrinsic opsonizing properties
Pathophysiology
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Proliferation of microbial pathogens at the alveolar level .
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when the capacity of the alveolar macrophages to ingest or kill the
microorganisms is exceeded does clinical pneumonia become
manifest.
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The host inflammatory response, rather than the proliferation of
microorganisms, triggers the clinical syndrome of pneumonia
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The release of inflammatory mediators, such as interleukin (IL) 1 and
tumor necrosis factor (TNF), results in fever
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Chemokines, such as IL-8 and granulocyte colony-stimulating factor,
stimulate the release of neutrophils
Pathophysiology
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Newly recruited neutrophils create an alveolar capillary leak
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The capillary leak results in a radiographic infiltrate and rales
detectable on auscultation
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Hypoxemia results from alveolar filling
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Increased respiratory drive in the systemic inflammatory response
syndrome (SIRS) leads to respiratory alkalosis
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Reductions in lung volume and compliance and the intrapulmonary
shunting of blood may cause the patient's death.
Access of microorganisms to the
lower respiratory tract
Aspiration
 Inhalation
 Contaminated droplets
 Hematogenous spread
 Contiguous extension
 Reactivation of occult infection
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Aspiration
The most common route is by aspiration from
the oropharynx.
Small-volume aspiration occurs frequently
during sleep.
Patients with decreased levels of
consciousness are at risk of aspiration.
The gag reflex and the cough mechanism
offer critical protection from aspiration.
Pathology
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The initial phase is one of edema, in clinical or autopsy
specimens it is so rapidly followed by
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Red hepatization phase (The presence of erythrocytes in the cellular
intraalveolar exudate )
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Gray hepatization (no new erythrocytes are extravasating, and those
already present have been lysed and degraded ) The neutrophil is the
predominant cell, fibrin deposition is abundant, and bacteria
have disappeared
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Resolution, the macrophage is the dominant cell type in the
alveolar space, and the debris of neutrophils, bacteria, and
fibrin has been cleared
Etiology
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Streptococcus pneumonia is the most common pathogen.
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Typical bacterial pathogens includes :
S. pneumoniae, Haemophilus influenzae,
and (in selected patients) S. aureus and gram-negative bacilli
such as Klebsiella pneumoniae and Pseudomonas aeruginosa
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Atypical organisms include :
Mycoplasma pneumoniae, Chlamydophila pneumoniae, and
Legionella spp. as well as respiratory viruses such as influenza
viruses, adenoviruses, and respiratory syncytial viruses (RSVs).
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The atypical organisms cannot be cultured on standard media,
nor can they be seen on Gram's stain
Etiology
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Bacteria, fungi, protozoa and viruses (responsible in
up to 18% of cases of CAP)
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Etiology of pneumonia usually cannot be determined
on the basis of clinical presentation.
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Treatment directed at a specific pathogen is not
superior to empirical therapy.
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Identification of an unexpected pathogen allows
narrowing of the initial empirical regimen.
Microbial Causes of CAP
Microbial Causes of CAP
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Anaerobes play a significant role only when an episode of
aspiration has occurred
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The combination of
(1) An unprotected airway (e.g., in patients with alcohol or
drug overdose or a seizure disorder) and
(2) significant gingivitis constitutes the major risk factor
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Anaerobic pneumonias are often complicated by abscess
formation and significant empyemas or parapneumonic
effusions.
Microbial Causes of CAP
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It is usually impossible to predict
the pathogen in a case of CAP
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It is important to consider
epidemiologic and risk factors that
might suggest certain pathogens
Epidemiology
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80% of the CAP cases are treated on an outpatient basis, and ~20%
are treated in the hospital
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The incidence rates are highest at the extremes of age
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The risk factors for CAP in general and for pneumococcal pneumonia
in particular have implications for treatment regimens
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Risk factors for CAP include alcoholism, immunosuppression,
institutionalization, asthma, and an age of >70 years
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Risk factors for pneumococcal pneumonia include dementia, seizure
disorders, heart failure, cerebrovascular disease, alcoholism, tobacco
smoking, chronic obstructive pulmonary disease, and HIV infection
Epidemiology
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CA-MRSA infection is more likely in Native Americans,
homeless youths, men who have sex with men, military
recruits, children in day-care centers, and athletes such
as wrestlers.
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P. aeruginosa may also infect these patients as well as
those with severe structural lung disease.
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Risk factors for Legionella infection include diabetes,
hematologic malignancy, cancer, severe renal disease,
HIV infection, smoking, male gender, and a recent hotel
stay or ship cruise .
Epidemiologic Factors
Clinical Manifestations
SYMPTOMS :
Fever & Chill & Sweats
 Tachycardia
 Cough (nonproductive or productive )
 Blood-tinged sputum (Hemotysis)
 Short of breath
 Pleuritic chest pain
 nausea, vomiting, and diarrhea (up to 20%)
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fatigue, headache, myalgias, and arthralgias
Clinical Manifestations
SIGNS :
Inspection : Use of accessory muscles of
respiration,
 Palpation : Increased or decreased tactile
fremitus,
 Percussion : Dull to flat ( consolidated lung
and pleural fluid ),
 Auscultation : Crackles, bronchial breath
sounds,
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Diagnosis
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Is this pneumonia?
(clinical and radiographic methods )
 what is the etiology?
( laboratory techniques )
Differential diagnosis
Acute bronchitis
 Acute exacerbations of COPD
 Chronic bronchitis
 Heart failure
 Pulmonary embolism
 Radiation pneumonitis
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Diagnosis
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The main purpose of the sputum Gram's stain is to ensure
that a sample is suitable for culture
Gram's staining may also help to identify certain pathogens
To be adequate for culture, a sputum sample must have >25
neutrophils and <10 squamous epithelial cells per low-power
field
For patients admitted to the ICU and intubated, a deepsuction aspirate or bronchoalveolar lavage sample should
be sent to the microbiology laboratory as soon as possible
For suspected tuberculosis or fungal infection, specific stains
are available
Cultures of pleural fluid obtained from effusions >1 cm in
height on a lateral decubitus CXR
Diagnosis
Blood Cultures: Only ~5–14% of cultures of
blood from patients hospitalized with CAP are
positive .
Antigen Tests: Detect pneumococcal and
Legionella antigens in urine The sensitivity 90%
and specificity 99% ,
Serology: A fourfold rise in specific IgM antibody
titer,
Imaging
Imaging
Abscess-staph
Pneumonia-lingula
Treatment
2- CURB-65 criteria
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Confusion (C);
Urea >7 mmol/L (U);
Respiratory rate 30/min (R);
SBP < 90 mmHg or DBP < 60 mmHg (B);
Age > 65 years ,
Patients With a score of 2 should be admitted to the hospital .
Patients With a score of >3 may require admission to an ICU.
Treatment
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Site of Care
home or hospital
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1-PSI
Points are given for 20 variables, including
age, coexisting illness, and abnormal
physical and laboratory findings
class 1 to class 5
Patients in classes 4 and 5 should be
admitted to the hospital
Treatment
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pneumococcal resistance to penicillin associated with reduced
susceptibility to other drugs, such as macrolides,
tetracyclines, and trimethoprim-sulfamethoxazole (TMP-SMX)
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For strains of S. pneumoniae with intermediate levels of
resistance, higher doses of the drug should be used
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Risk factors for drug-resistant pneumococcal infection include
recent antimicrobial therapy, an age of <2 years or >65 years,
attendance at day-care centers, recent hospitalization, and HIV
infection .
Treatment
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CAP due to MRSA
resistance to all beta-lactam drugs
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Gram-Negative Bacilli
Enterobacter spp. are resistant to cephalosporins
the drugs of choice are fluoroquinolones or
carbapenems
Empirical Treatment (CAP)
Empirical Treatment (CAP)
Treatment
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The duration of treatment for CAP : 10–14 days
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with fluoroquinolones and telithromycin a 5-day course is
sufficient for otherwise uncomplicated CAP
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A longer course for patients with bacteremia, metastatic
infection, or infection with P. aeruginosa or CA-MRSA
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Longer-term therapy should also be considered if initial
treatment was ineffective and in most cases of severe CAP
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Patients with severe CAP who remain hypotensive despite fluid
resuscitation may have adrenal insufficiency
Failure to Improve
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Respond to therapy should be reevaluated at about day 3
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(1) Is this a noninfectious condition?
(2) If this is an infection, is the correct pathogen being targeted?
( e.g., M. tuberculosis or a fungus )
(3) Is this a superinfection with a new nosocomial pathogen?
(4) If this is an infection, is the complicated pneumonia
(e.g., a lung abscess or empyema )
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Noninfectious conditions can mimic pneumonia, including
pulmonary edema, pulmonary embolism, lung carcinoma,
radiation and hypersensitivity pneumonitis, and connective
tissue disease involving the lungs
Complications
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Respiratory failure
Shock and multiorgan failure
Bleeding diatheses
Exacerbation of comorbid illnesses
Lung abscess
Complicated pleural effusion
If the fluid has a pH of <7, a glucose level of <2.2 m mol/L,
and a LDH concentration of >1000 U/L or if bacteria are
seen or cultured, then the fluid should be drained; a chest
tube is required.( complicated para pneumonic effusion )
Follow-Up & Prevention
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Fever usually resolve within 2 days.
 Leukocytosis usually resolve within 4 days.
 Physical findings may persist longer.
 CXR abnormality resolve with in 4–12 Weeks.
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The main preventive measure is vaccination.
( for influenza and pneumococcal vaccines )
VAP
Ventilator-Associated
Pneumonia
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The pathogens and treatment strategies for VAP are more similar to
those for HAP than to those for pure CAP
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Etiologic agents of VAP include both MDR and non-MDR bacterial
pathogens
Microbiologic Causes of VAP
Prevention Strategies for VAP
Prevention Strategies for VAP
Clinical Manifestations of VAP
Are the same as other forms of pneumonia
Fever
 Leukocytosis
 Increase in respiratory secretions
 Pulmonary consolidation on physical examination
 New or changing radiographic infiltrate
 Tachypnea, tachycardia,
 Worsening oxygenation,
 Increased minute ventilation.
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Diagnosis of VAP
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No single set of criteria is reliably diagnostic of
pneumonia in a ventilated patient
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The differential diagnosis of VAP includes:
atypical pulmonary edema, pulmonary contusion
and/or hemorrhage, hypersensitivity pneumonitis,
ARDS, and pulmonary embolism , antibioticassociated diarrhea, sinusitis, urinary tract
infection, pancreatitis, and drug fever.
The recent IDSA/ATS guidelines for HCAP suggest
that either approach is clinically valid.
Diagnosis of VAP
Quantitative-Culture Approach
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Discriminate between colonization and true infection
The diagnostic threshold is 106 cfu/mL
The PSB method has a threshold of 103 cfu/mL
With sensitive microorganisms, a single antibiotic dose can reduce
colony counts
After > 3 days of consistent antibiotic therapy for another infection
prior to suspicion of pneumonia, the accuracy of diagnostic tests for
pneumonia is unaffected.
Colony counts above the diagnostic threshold during antibiotic
therapy suggest that the current antibiotics are ineffective
Diagnosis of VAP
The Clinical Pulmonary Infection Score (CPIS)
VAP Treatment
Frequent use of beta-lactam drugs, especially
cephalosporins, is the major risk factor for
infection with MRSA and ESBL-positive strains.
 Treatment should be started once diagnostic
specimens have been obtained
 A negative tracheal-aspirate culture or growth
below the threshold for quantitative cultures
strongly suggests that antibiotics should be
discontinued
 Combination therapy with a beta-lactam and an
aminoglycoside for Pseudomonas infection
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Empirical Antibiotic Treatment (VAP)
Empirical Antibiotic Treatment (VAP)
Prevention (VAP)
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Avoid endotracheal intubation or at least to
minimize its duration
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Minimizing the amount of microaspiration
around the ET cuff
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Simply elevating the head of the bed (at least
30° but preferably 45°) decreases VAP rates
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Emphasis on the avoidance of agents that raise
gastric pH
Hospital-Acquired Pneumonia
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HAP is similar to VAP
The main differences are in the higher frequency
of non-MDR pathogens and the better underlying
host immunity
The lower frequency of MDR pathogens
As in the management of CAP, specific therapy
targeting anaerobes probably is not indicated
unless gross aspiration is a concern.
Blood cultures are infrequently positive (<15% of
cases).