Pedia 3 - Community-Acquired Pneumonia PDF

Book Verbatim High-yield PNEUMONIA § Inflammation in the lung caused by infectious agent Inflammation of the lung parenchyma § Leading infectious cause of death globall...

Book Verbatim High-yield PNEUMONIA § Inflammation in the lung caused by infectious agent Inflammation of the lung parenchyma § Leading infectious cause of death globally among children younger than 5 years old § More the 99% of pneumonia death are in low- and middle- income countries § In develop countries (USA), mortality declined by 97% between 1939 and 1996 à development of vaccines (Measles, pertussis, H. influenza conjugate , PCV) and antibiotics ETIOLOGY Microorganisms Noninfectious causes include: ® Aspiration (of food or gastric acid, foreign bodies, hydrocarbons, and lipoid substances) Lipoid substances kanang maginhale inhale ug vicks; very common in our practice ® Hypersensitivity reactions ® Drug- or radiation-induced pneumonitis Bleomycin The cause in an individual patient is often difficult because direct sampling of lung tissue is invasive Bacterial cultures of sputum or upper respiratory tract samples from children typically do not accurately reflect the cause of lower respiratory tract infection COMMON ETIOLOGIC AGENTS MICROORGANISMS § Streptococcus pneumoniae § most common bacterial pathogen (pneumococcus) in children 3 weeks to 4 years of age § Mycoplasma pneumoniae § Most common bacterial pathogens § Chlamydophila pneumoniae in children ≥ 5 years old § Staphylococcus aureus § Often complicates an illness pneumoniae caused by influenza viruses BOOK NOTES: S. pneumoniae, H. influenzae, and S. aureus – major causes of hospitalization and death from bacterial pneumonia among children in developing countries In children with HIV infection, M. tuberculosis, non-TB mycobacteria, Salmonella, E. coli, P. jiroveci, and CMV, must be considered. Viral pathogens – most common causes of lower respiratory tract infections in infants and children older than 1 month but younger than 5 years of age Respiratory syncytial virus & Rhinoviruses – most commonly identified pathogens, especially in children younger than 2 years of age PATHOGENESIS Lower respiratory tract possesses defense mechanisms against infection, including: ® Mucociliary clearance ® Macrophages and secretory immunoglobulin A Justo, Juliano, Hofeleña, Llanos, Lozano, Maramion Page 1 of 17  ® Clearing of the airways by coughing Recurrent pneumonia – 2 or more episodes in a single year or 3 or Lower respiratory tract in the absence of infection: more episodes ever, with radiographic clearing between occurrences ® Believed sterile but new data shows it contains diverse ® Underlying disorder should be considered microbial communities § Recent conceptual models postulate: ® Pneumonia results from disruption of a complex lower respiratory ecosystem that is the site of dynamic Macrophages fail to destroy interactions between ü potential pneumonia pathogens alveolar bacteria ü resident microbial communities; and ü host immune defenses PMNs with their phagocytic capability are recruited [PATHOGENESIS] Inhalation: contaminated air (bacteria, pulmonary pathogen) Droplets transmitted person-to-person with pharyngeal secretions An inflammatory response (mediated by containing up to 108 bacteria/mL of saliva cytokine release) occurs Bacteria may gain access to the respiratory tract by microaspiration, occurring daily even in normal children Droplet size: determine the level of the respiratory system reached by inhaled bacteria Process continues à results in vascular congestion and Most inhaled bacteria are enveloped in moisture à acquire exuberant edema (pneumococci) aerodynamic and dimensional characteristics à determine destination e.g. particles: Sheets of pneumococci ride waves of edematous fluid from ® 10μ (microns) don’t usually traverse the pharynx alveolus to alveolus (pores of Kohn) bacterial growth and ® 3 - 10μ may lodge in the larger airways; and exudative response à CONSOLIDATION ® 0.5 to 3μ can reach the alveolar surface The lighter it is, the further it is transported peripherally Usually your nebulizing solution is around 0.5 microns that’s why it can be propelled until the distant airways STAGES OF LOBAR PNEUMONIA Medical interventions or anatomic abnormalities can facilitate bacterial transit towards the alveolus Tracheal tube; do a culture first CONGESTION (24 HOURS): Direct extension to the pulmonary parenchyma through a Heavy, red, “baggy” “from blood and bronchopleural fistula à facilitates bacterial access to the alveolar bacteria in alveoli epithelial surfaces Metastatic hematogenous spread from a distant site is also a process for a bacteria to reach the lungs RED HEPATIZATION (DAYS 2 - 4): Bacterium makes initial contact with the alveolar wall and is RBCs, Neutrophils, Fibrin enmeshed in the epithelial lining fluid that contains opsonins Edematous zone of engorgement progresses centrifugally ® immunologic experience of the host, specific immunoglobulin à leaves behind clusters of erythrocytes and purulent G (IgG) antibody exudate consisting of fibrin, PMN leukocytes, and bacteria ® usual outcome of this interaction is ingestion by alveolar macrophages (alveolar type II cells) – e.g. encapsulated bacteria S. pneumoniae An alternative, less common outcome is complement-mediated GRAY HEPATIZATION (DAYS 5- 9): bacterial lysis Active phagocytosis by polymorphonuclear leukocytes à The process is rapid in an animal exposed to a bacterial inoculum, release of bacterial cell wall components and pneumolysin whether aerosolized or instilled onto the alveolar surface, bacteria (enzymatic degradation) à leads to inflammation and remain free for only 30 minutes before being internalized by a cytotoxic effects on all pulmonary cells à result is the macrophage blurring of cellular elements and the loss of cellular When mechanisms fail to destroy alveolar bacteria à PMNS with architecture their phagocytic capability are recruited, and an inflammatory response (mediated by cytokine release) occurs RESOLUTION: of pneumonic consolidation begins when anticapsular antibody appears BOOK NOTES: Viral pneumonia – spread of infection along the airways, accompanied by the direct injury of the respiratory epithelium à PMNS continue to phagocytose the airway obstruction from swelling, abnormal secretions, and cellular pneumococci à monocytic cells clean up debris the debris (zone of resolution) ® Accompanied by: atelectasis, interstitial edema, and hypoxemia ® Also predispose to secondary bacterial infection by disturbing normal host defense mechanisms, altering secretions, and through disruptions in respiratory microbiota Bacterial pneumonia – when respiratory tract organisms colonize the trachea and subsequently gain access to the lungs, but may also result from direct seeding of lung tissue after bacteremia ® Pathologic process varies according to the invading organism Justo, Juliano, Hofeleña, Llanos, Lozano, Maramion Page 2 of 17  § Streptococcus pneumoniae – produces local edema that aids in the proliferation of organisms and their spread à result to focal lobar involvement § Group A streptococcus – lower respiratory tract infection ® More diffuse lung involvement with interstitial pneumonia ® Necrosis of tracheobronchial mucosa ® Formation of large amounts of exudates, edema, and local hemorrhage, with extension into the interalveolar septa ® Involvement of lymphatic vessels with frequent pleural involvement § Staphylococcus aureus pneumonia – manifests as confluent bronchopneumonia ® Often unilateral and characterized by the presence of extensive areas of hemorrhagic necrosis and irregular areas of cavitation of the lung parenchyma ® Results in pneumatoceles, empyema and, at times, bronchopulmonary fistulas M. pneumoniae – attaches to the respiratory epithelium, inhibits ciliary action, and leads to cellular destruction and inflammatory response in the submucosa ® As the infection progresses, sloughed cellular debris, inflammatory cells, and mucus cause airway obstruction with spread of infection occurring along the bronchial tree Underlying Illness in Children with Recurrent Pneumonia A. Recurrent aspirations 2 (10.5%) Gastroesophageal reflux 1 (5.2%) Esophageal stricture 1 (5.2%) (Post op. tracheoesophageal fistula) B. Bronchiectasis 10 (52.6%) Post tubercular 6 (31.6%) Post pneumonia 1 (5.2%) Cause not diagnosed 3 (15.8%) C. Immunodeficiency 1 (5.2%) HIV Infection 1 (5.2%) § As long as the reticular structure of the lung remains intact (i.e., involvement of the interstitium is absent) à complete D. Others 7 (36.8%) parenchymal restoration and healing of the alveolar epithelium Asthma 5 (26.3%) occur after successful treatment. Scarring is minimal. Suspected ciliary dyskinesia 1 (5.2%) § Death from bacterial pneumonia is due to respiratory failure, Foreign body 1 (5.2%) which occurs when the airspaces are filled with edematous fluid or exudate à residual volume of the lung is markedly expanded by this fluid which precludes air exchange at the alveolar level § The clinical picture of sepsis may be concomitant; shock may further complicate end-organ perfusion, and a mixed metabolic and respiratory acidosis therefore typically precedes death The residual volume is reduced when your air sacs are filled with edematous fluid. This is a significant part of the functional residual capacity. Pathogenesis of pneumonia caused by other bacteria may vary: Justo, Juliano, Hofeleña, Llanos, Lozano, Maramion Page 3 of 17  Pathogenesis Direct injury to Colonize trachea PERSISTENT COUGH epithelium-airway obstruction (edema, Direct seeding of lung Congenital Anomalies debris, secretions) tissue after bacteremia Connection of the airway to the esophagus Predispose to Laryngeal cleft secondary bacterial Tracheoesophageal fistula infection Laryngotracheomalacia Clinical Fever lower Sudden high fever Primary laryngotracheomalacia Manifestations Tachypnea, increase Cough, tachypnea, Laryngotracheomalacia secondary to gastroesophageal reflux WOB chest pain, disease, vascular or other compression Cyanosis/lethargy in drowsiness with Bronchopulmonary foregut, malformation infants periods of Congenital mediastinal tumors restlessness Congenital heart disease with pulmonary congestion or vascular Anxiety, delirium airway compression Splinting on the affected side to Infection minimize pleuritic pain Recurrent viral infection (infants and toddlers) Chlamydial infection (infants) GI symptoms – D/V, Whooping cough-like syndrome abdominal (paralytic Bordetella pertussis infection ileus) Chlamydial infection Physical Crackles and wheezing Diminished breath Mycoplasma infection Examination sounds, abdominal Cystic fibrosis (infants and toddlers) breath sounds Granulomatous infection (lower lobe Mycobacterial infection pneumonia) Fungal infection Chest X-Ray Hyperinflation Confluent lobar Bilateral interstitial consolidation Suppurative Lung Disease (Bronchiectasis and Lung Abscess) infiltrates (pneumococcal) Cystic fibrosis Peribronchial cuffing Pleural effusion Foreign body aspiration with secondary suppuration CBC WBC normal or WBC elevated Cilia dyskinesia elevated 15 to 40,000/mm^3 Immunodeficiency 1 year old to 5 years old: ³40 breaths per minute clinical signs and symptoms (E) will accurately diagnose >5 years to 12 years old: ³30 breaths per minute community-acquired pneumonia (O)? >12 years old: ³20 breaths per minute 2. Retractions or Chest indrawing 2. Among infants and children 3 months and 18 years with community- 3. Nasal flaring acquired pneumonia (P), what clinical and ancillary parameters (E) 4. O2 saturation