In the name of GOD

Pneumonia

Hassan Ghobadi MD. PulmonologistAssistant Professor of Internal MedicineArdabil University of Medical Science

Pneumonia

Definition: Pneumonia is an infection of the pulmonary parenchyma

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

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 Proliferation of microbial pathogens at the alveolar level .

when the capacity of the alveolar macrophages to ingest or kill the microorganisms is exceeded does clinical pneumonia become manifest.

The host inflammatory response, rather than the proliferation of microorganisms, triggers the clinical syndrome of pneumonia

The release of inflammatory mediators, such as interleukin (IL) 1 and tumor necrosis factor (TNF), results in fever

Chemokines, such as IL-8 and granulocyte colony-stimulating factor, stimulate the release of neutrophils

Pathophysiology

Newly recruited neutrophils create an alveolar capillary leak

The capillary leak results in a radiographic infiltrate and rales detectable on auscultation

Hypoxemia results from alveolar filling

Increased respiratory drive in the systemic inflammatory response syndrome (SIRS) leads to respiratory alkalosis

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

AspirationInhalationContaminated dropletsHematogenous spread Contiguous extension Reactivation of occult infection

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

The initial phase is one of edema, in clinical or autopsy specimens it is so rapidly followed by

Red hepatization phase (The presence of erythrocytes in the cellular intraalveolar exudate )

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

Resolution, the macrophage is the dominant cell type in the alveolar space, and the debris of neutrophils, bacteria, and fibrin has been cleared

Etiology Streptococcus pneumonia is the most common pathogen.

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

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).

The atypical organisms cannot be cultured on standard media, nor can they be seen on Gram's stain

Etiology

Bacteria, fungi, protozoa and viruses (responsible in up to 18% of cases of CAP)

Etiology of pneumonia usually cannot be determined on the basis of clinical presentation.

Treatment directed at a specific pathogen is not superior to empirical therapy.

Identification of an unexpected pathogen allows narrowing of the initial empirical regimen.

Microbial Causes of CAP

Microbial Causes of CAP

Anaerobes play a significant role only when an episode of aspiration has occurred

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

Anaerobic pneumonias are often complicated by abscess formation and significant empyemas or parapneumonic effusions.

Microbial Causes of CAP

It is usually impossible to predict the pathogen in a case of CAP

It is important to consider epidemiologic and risk factors that might suggest certain pathogens

Epidemiology

80% of the CAP cases are treated on an outpatient basis, and ~20% are treated in the hospital

The incidence rates are highest at the extremes of age

The risk factors for CAP in general and for pneumococcal pneumonia in particular have implications for treatment regimens

Risk factors for CAP include alcoholism, immunosuppression, institutionalization, asthma, and an age of >70 years

Risk factors for pneumococcal pneumonia include dementia, seizure disorders, heart failure, cerebrovascular disease, alcoholism, tobacco smoking, chronic obstructive pulmonary disease, and HIV infection

Epidemiology

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.

P. aeruginosa may also infect these patients as well as those with severe structural lung disease.

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%)

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,

Diagnosis

Is this pneumonia?

(clinical and radiographic methods )

what is the etiology?

( laboratory techniques )

Differential diagnosis

Acute bronchitisAcute exacerbations of COPD Chronic bronchitisHeart failurePulmonary embolismRadiation pneumonitis

Diagnosis

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 deep-suction 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

1- Confusion (C); 2- Urea >7 mmol/L (U); 3- Respiratory rate 30/min (R); 4- SBP < 90 mmHg or DBP < 60 mmHg (B); 5- 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

Site of Care home or hospital

o 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

pneumococcal resistance to penicillin associated with reduced susceptibility to other drugs, such as macrolides,

tetracyclines, and trimethoprim-sulfamethoxazole (TMP-SMX)

For strains of S. pneumoniae with intermediate levels of resistance, higher doses of the drug should be used

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

CAP due to MRSA resistance to all beta-lactam drugs

Gram-Negative BacilliEnterobacter spp. are resistant to cephalosporins

the drugs of choice are fluoroquinolones or carbapenems

Empirical Treatment (CAP)

Empirical Treatment (CAP)

Treatment

The duration of treatment for CAP : 10–14 days with fluoroquinolones and telithromycin a 5-day course is

sufficient for otherwise uncomplicated CAP

A longer course for patients with bacteremia, metastatic infection, or infection with P. aeruginosa or CA-MRSA

Longer-term therapy should also be considered if initial treatment was ineffective and in most cases of severe CAP

Patients with severe CAP who remain hypotensive despite fluid resuscitation may have adrenal insufficiency

Failure to Improve

Respond to therapy should be reevaluated at about day 3

(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 )

Noninfectious conditions can mimic pneumonia, including pulmonary edema, pulmonary embolism, lung carcinoma, radiation and hypersensitivity pneumonitis,

and connective tissue disease involving the lungs

Complications

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

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.

The main preventive measure is vaccination.

( for influenza and pneumococcal vaccines )

VAP

Ventilator-Associated Pneumonia

The pathogens and treatment strategies for VAP are more similar to those for HAP than to those for pure CAP

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.

Diagnosis of VAP

No single set of criteria is reliably diagnostic of pneumonia in a ventilated patient

The differential diagnosis of VAP includes: atypical pulmonary edema, pulmonary contusion and/or hemorrhage, hypersensitivity pneumonitis, ARDS, and pulmonary embolism , antibiotic-associated 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

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

Empirical Antibiotic Treatment (VAP)

Empirical Antibiotic Treatment (VAP)

Prevention (VAP)

Avoid endotracheal intubation or at least to minimize its duration

Minimizing the amount of microaspiration around the ET cuff

Simply elevating the head of the bed (at least 30° but preferably 45°) decreases VAP rates

Emphasis on the avoidance of agents that raise gastric pH

Hospital-Acquired Pneumonia

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).