inflammation involving the lung parenchyma. Can be broadly classified as either community acquired infections or nosocomial infections.
Pneumonia ETIOLOGI Bacteria Streptococcus pneumoniae (most common) followed by H. influenzae (-) P.aeruginosa, E.coli, Klebsiella pneumoniae, Acinetobacter spp (+) S. aureus Atypical : M. pneumoniae, Legionella, Chlamydia Viruses Influenza, parainfluenza, adenovirus, RSV Fungi Candida, Histoplasma, Cryptococcus, and Aspergillus; Protozoa Pneumocystis carinii (seen in immunocompromised hosts), Nocardia, and Mycobacterium tuberculosis
Pneumonia CLINICAL FEATURES Fever, Pleuritic chest pain Coughing that produces purulent sputum Chills Rigors Dyspnea Malaise Decreased breath sounds and dullness to percussion
The possible causative organism will be suggested by : Clinical presentation and course of the illness Degree of immunocompetency of the patient Presence/absence of underlying lung disease Place of acquisition (hospital or community)
Pneumonia MANAGEMENT Community acquired pneumonia -lactams (eg, amoxicillinclavulanate), macrolides, and fluoroquinolones. Nosocomial pneumonia Low risk 3 rd cephalosporin / fluoroquinolone. High risk antipseudomonal cephalosporin, carbepenem, or fluoroquinolone, along w/ linezolid or vancomycin Pneumococcal vaccine high risk individuals (people with asplenia, older than 65 y.o)
ORAL HEALTH CONSIDERATION Poor oral health status is a risk factor for the development of pneumonia oral intervention to control dental plaque. Bronchiolitis Infection of the lower respiratory tract esp. bronchioles Pathogens : RSV, human metapneumovirus, parainfluenza virus, influenza virus, adenovirus, M. Pneumoniae Pathophysiology - Infection - Inflammatory respone prominent mononuclear infiltrate - Edema, necrosis epithelial cells lining small airways, mucosal thickening, mucus hypersecretion, plugging, bronchospasm
Bronchiolitis CLINICAL AND LABORATORY FINDINGS Infection of the upper respiratory tract Low grade fever, profuse clear rhinorrhea, cough Infection of the lower respiratory tract Tachypnea, retractions, wheezing, cyanosis Chest radiography Peribronchial cuffing, flattening of the diaphragms, hyperinflation, increased lung markings Lab : Mild leukocytosis PMN mostly DIAGNOSIS : history and physical examination, nasopharyngeal cultures DD : asthma, congenital heart disease, cystic fibrosis. Bronchiolitis MANAGEMENT Supportive care O 2 and Hydration must be ensured RSV bronchiolitis with severe disease/ at risk for severe disease Antiviral theraphy with ribavarin aerosol up to 1 week Respiratory failure Mechanical ventilation Prophylaxis of high risk infants Intramuscular monoclonal antibody to RSV F protein, palivizumab
Asthma Chronic inflammatory disorder of the airways Underlying inflammatory process characterized by recurrent & often reversible airflow limitation The etiology is unknown, but allergic sensitivity is seen in most patients Risk factors : Family history of asthma Atopy Respiratory infections Inhaled pollutants Allergens Food sensitivities Other exposures (ex : tobacco smoke) Asthma Clinical Features Intermittent wheezing Coughing Dyspnea Chest tightness Worsen at night & the early morning hours Diagnostic tools: pulmonary function testing/ spirometry & allergen skin testing Diagnosis Suggestive history, physical findings, and the demonstration of reversible airflow limitation. Factors favoring the diagnosis of asthma include : intermittent symptoms with asymptomatic periods Complete / nearly complete reversibility with bronchodilators The absence of digital clubbing History of atopy DD : Chronic rhinitis or sinusitis, CF, gastroesophageal reflux disease, airway narrowing due to compression, and COPD. Management Mild-persistent asthma low dose inhaled corticosteroids Moderate-severe persistent long-acting bronchodilators with inhaled corticosteroids Asthma ORAL HEALTH CONSIDERATION Allergen from dental material and products associated Oral candidiasis antifungal Decreased salivary flow, increased calculus, increased gingivitis, increased periodontal disease, increased incidence of caries maintain OH The patient should be instructed to rinse mouth with water after using inhalers Schedule patients appointment for late morning or later in the day to minimize the risk of an asthmatic attack
O 2 and bronchodilators available in case of an exacerbation of asthma Care should be used in the positioning of suction tips and rubber dam During an acute asthmatic attack discontinue the dental procedure, remove all intraoral devices, place the patient in a comfortable position, make sure the airway is opened, administer a R 2 -agonist and oxygen or epinephrine
Chronic Obstructive Pulmonary Disease Characterized by airflow limitation associated with an abnormal inflammatory response of the lungs to noxious particles or gases. COPD Emphysema Condition characterized by destruction and enlargement of the lung alveoli Chronic Bronchitis Condition with chronic cough and phlegm; and small airways disease, a condition in which small bronchioles are narrowed.
Chronic Obstructive Pulmonary Disease Risk Factors Environmental exposures Tobacco smoke Heavy exposure to occupational dusts and chemicals (vapors, irritants, fumes) Indoor/outdoor pollution Host factors Hereditary deficiency in the enzyme 1-antitrypsin PATHOPHYSIOLOGY
Chronic inflammation throughout the airways, parenchyma, and pulmonary vasculature; oxidative stress; imbalance of proteases and antiproteases in the lung Mucus hypersecretion, ciliary dysfunction, airflow limitation, pulmonary hyperinflation, gas exchange abnormalities, pulmonary hypertension, cor pulmonale ` CLINICAL AND LABORATORY FINDINGS Dyspnea, cough, and sputum production Physical findings : diffuse wheezing, respiratory distress, tachypnea Chest radiography : increase lung compliance, flattened diaphragms, hyperexpansion, increase AP diameter Spirometry : airflow limitation, with decreases in the FEV 1 and the FEV 1 /FVC ratio Complete pulmonary function : increase in residual volume and total lung capacity, decrease pulmonary diffusion capacity
Chronic Obstructive Pulmonary Disease Diagnostic The history and physical findings Cough, dyspnea, and sputum production and/or a history of exposure to risk factors Complete pulmonary function tests O 2 status with pulse oximetry A determination of arterial blood gases Chest radiography Management Avoidance of risk factors Bronchodilators Severe COPD corticosteroids Chronic respiratory failure long term oxygen therapy Exacerbations of COPD oral broad spectrum antibiotics Chronic Obstructive Pulmonary Disease Cystic Fibrosis Multiple genetic disorder that is characterized by chronic airways obstruction and infection and by exocrine pancreatic insufficiency GI function, nutrition, growth, maturation Caused by numerous mutations in the gene that encodes CFTR that helps regulate ion flux at epithelial surfaces Pulmonary complications are major factors affecting life expectancy in CF patients Cystic Fibrosis PATHOPHYSIOLOGY Defect in the CFTR gene Defective chloride transport system in exocrine glands Mucus productions occurs without sufficient water transport into the lumen The resultant mucus inspissation in the affected glands and organs In the airways viscid secretions impair mucociliary clearence and promote airway obstruction and bacterial colonization Cystic Fibrosis Management Antibiotics Bronchodilators Antiinflammatory agents slow the decline of lung function Proper nutrition and exercise except those with severe lung disease and hypoxemia Clinical and Laboratory Findings Thickened secretion in multiple organ systems malabsorption & intestinal obstruction Viscid mucus in lungs airway obstruction, infection, and bronchiectasis Sweat testing >60 mEq/L chloride (+) Nasal epithelial bioelectric abnormalities Oral Health Considerations Tongue, buccal mucosa, dental plaque, saliva serve as reservoir of colonization P. aeruginosa bacterial pathogen for CF Improved OH reduce level of pathogens in mouth and lung infection, minimize exacerbation Pulmonary Embolism Result of an exogenous / endogenous material traveling to the lung Blockage of a pulmonary arterial vessel The embolus may originate anywhere usually lower extrimities Other substances : neoplastic cells, air bubbles, carbon dioxide, IV catheters, fat droplets Risk factors : - Prolonged immobilization - Lower extremity trauma - History of deep vein thromboses - Use of estrogen containing oral contraceptives Pathophysiology
PE Blockage of pulmonary arterial vessels Ventilation- perfusion mismatch Pulmonary Embolism CLINICAL AND LABORATORY FINDINGS Dyspnea Chest pain, fever, diaphoresis, cough, hemoptysis, syncope Lower extremity deep venous thrombosis, tachypnea, crackles, rub on lung auscultation, heart murmur Acute PE : Hypoxemia Measurements of arterial blood gases : PaO 2 and PaCO 2
, pH
Pulmonary Embolism History and physical findings CT scan Pulmonary arteriography Diagnosis Heparin Systemic thrombolytic therapy hemodynamically unstable Pulmonary embolectomy unable to receive thrombolytic therapy Oxygen , intubation, mechanical ventilation massive PE Placement of an inferior vena cava filter recurrent disease Management Patients with PE is being managed with oral anticoagulants Dental care PT 20 s /international normalized ratio of 2.5 Any dental care should be coordinated with their primary medical care provider Oral Health Considerations Pulmonary Neoplasm Squamous Cell Carcinomas Derives from bronchial epithelial cells metaplasia Slow growing neoplasm that invades the bronchi airway obstruction Small Cell Carcinomas Highest assocation with smoking Derive from neuroendocrine cells in the airway and metastasize rapidly Adenocarcinomas Glandular origin and develop in a peripheral distribution Grow more rapidly than SCC and tend to invade pleura Large cell carcinomas Anaplastic and giant cell tumors Poorly differentiated, resemble neither SCC nor adenocarcinoma
PATHOPHYSIOLOGY Prolonged injury (ex. : smoking) Metaplasia of the respiratory epithelium Dysplastic with the loss of differentiating features Neoplastic change occurs locally ;invasive carcinoma usually follows after
CLINICAL AND LABORATORY FINDINGS Chronic nonproductive cough Sputum production may occur obstructive lesions Variably : Hemoptysis, dyspnea Metastatic and paraneoplastic effects depend on site involved and size of tumor
Pulmonary Neoplasm Pulmonary Neoplasm Diagnosis History and physical examination Diagnosis depends on : the type of lung cancer Site and size Presence of metastasis Clinical status of the patient CT scan Sputum, pleural fluid cytology, excisional biopsy, transthoracic needle aspiration, bronchoscopy Management Complete surgical resection of localized lung cancer Treatment based on the stage of the disease and patient clinical status Early stage Surgically managed Locally advanced disease Chemotherapy Radiotherapy Advanced disease Supportive care and/chemotherapy