Pneumonia In the name of GOD Hassan Ghobadi MD. Pulmonologist Assistant Professor of Internal Medicine Ardabil University of Medical Science

Pneumonia Definition: Classification: 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 Aspiration Inhalation Contaminated droplets Hematogenous 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 (clinical and radiographic methods ) what is the etiology? 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

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 1-PSI class 1 to class 5 home or hospital 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 Bacilli Enterobacter 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 )

Ventilator-Associated Pneumonia 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).