Community Acquired Pneumonia, Bronchiectasis and Lung Abscess PDF

COMMUNITY ACQUIRED PNEUMONIA, BRONCHIECTASIS AND LUNG ABSCESS PATHOPHYSIOLOGY IL1 and TNF – Fever COMMUNITY ACQUIRED PNEUMONIA...

COMMUNITY ACQUIRED PNEUMONIA, BRONCHIECTASIS AND LUNG ABSCESS PATHOPHYSIOLOGY IL1 and TNF – Fever COMMUNITY ACQUIRED PNEUMONIA IL8 and GCSF – peripheral leukocytosis and An infection of the pulmonary parenchyma - Increased purulent secretions Remains the leading cause of death worldwide Inflammatory mediators and neutrophils- 6th leading cause of death overall and a major cause of morbidity and mortality - Capillary leak: infiltrate on xray/ rales on auscultation Erythrocytes – hemoptysis Alveolar filling – hypoxemia Increased Respiratory drive in SIRS - Respiratory Alkalosis Dyspnea from - Decreased compliance from capillary leak - Hypoxemia - Increased respiratory drive - Increased secretions - Infection-related bronchospasm PATHOLOGY Edema Phase- bacteria + neutrophil Red Hepatization- rbc Gray Hepatization- neutrophil Resolution- macrophages PNEUMONIA results from the proliferation of microbial pathogens at the alveolar level and the host’s response to those pathogens Access of microorganism to lower respiratory tract: - Aspiration from oropharynx (most common) - Hematogenous spread - Contiguous extension from infected pleural or mediastinal space Mechanical factors are important in host response - hairs and turbinates of the nares - Branching architecture of Tracheobronchial tree - Gag and cough reflex - Normal flora that adheres to mucosal cells of oropharynx Resident alveolar macrophages - Clears and kills pathogen RISK FACTORS FOR CAP Alcoholism DIFFERENTIAL DIAGNOSIS FOR CAP Asthma Acute Bronchitis Immunosuppression Acute exacerbation of chronic bronchitis Institutionalization Heart failure Age of greater than or equal to 70 years old Pulmonary Embolism Hypersensitivity Pneumonitis CLINICAL DIAGNOSIS OF CAP Radiation Pneumonitis Can CAP be diagnosed accurately by history and physical examination? - The accuracy of predicting CAP by physicians’ clinical judgement is between 60-76%. (Grade B), clinical prediction rules combining history and physical ETIOLOGIC DIAGNOSIS examination findings may be utilized to presumptively identify patients with Gram’s stain and Culture – yield is less than or equal to 50% pneumonia. (Grade B) Blood Culture – yield is 5-14% Is there any clinical feature that can predict CAP caused by an atypical pathogen? Urinary Antigen Tests: - There is no clinical feature that can reliably distinguish pneumonia due to a - Legionella Urine Antigen Test: Sensitivity- 70%, specificity 99% typical or an atypical pathogen. (Grade A) - Pneumococcal Urine Antigen Test: Sensitivity 70%, specificity is more than 90% CLINICAL MANIFESTATIONS OF CAP Serology test : fourfold rise in IgM titer between acute and convalescent phase is Fever with tachycardia diagnostic of infection Cough with or without hemoptysis Biomarkers: History of chills and or sweat - CRP – identify worsening disease or treatment failure Short of breath - Procalcitonin – distinguish viral from bacterial infection, to initiate Pleuritic chest pain antibacterial therapy or when to discontinue treatment Gastrointestinal symptoms Fatigue, headache, myalgia, arthralgia CHEST XRAY What is the value of the chest radiograph in the diagnosis of CAP? - The chest x-ray is essential in the diagnosis of CAP, assessing severity, differentiating pneumonia from other conditions, and in prognostication. (Grade A) What specific views of chest radiograph should be requested? - Standing posteroanterior and lateral views of the chest in full inspiration comprise the best radiologic evaluation of a patient suspected of having pneumonia. (Grade A) Are there characteristic radiographic features that can predict the likely etiologic agent from the chest radiograph? - There is no characteristic radiographic feature that can predict the likely etiologic agent in CAP. (Grade B) WHAT MICROBIOLOGIC STUDIES ARE NECESSARY IN CAP? In low-risk CAP, microbiologic studies are optional. (Grade B) In moderate- and high-risk CAP, blood cultures and gram stain and culture with antibiotic sensitivity tests of respiratory specimens should be done in laboratories with quality assurance. (Grade A) When possible, tests to document the presence of legionella pneumophila are recommended for hospitalized CAP. (Grade B) Invasive procedures (i.E., Transtracheal, transthoracic biopsy, Bronchoalveolar lavage, protected brush specimen) to obtain specimens for special microbiologic studies for atypical pathogens (e.g., Mycobacteria and other microorganisms that will not grow on routine culture) are options for non-resolving pneumonia, immunocompromised patients, and patients in whom no adequate respiratory specimens can be sent despite sputum induction and routine diagnostic testing. (Grade B) TREATMENT BY CAP RISK CATEGORIES WHICH PATIENTS WILL NEED HOSPITAL ADMISSION? Low Risk CAP Streptococcus pneumoniae Without co-morbid illness: Haemophilus influenzae Amoxicillin 1 gm TID OR Chlamydophila pneumoniae Extended macrolides: A management-oriented risk stratification of CAP based on the patient’s clinical Mycoplasma pneumoniae Azithromycin 500 mg OD OR presentation or condition, status of any co-morbid condition, and chest x-ray findings Moraxella catarrhalis Enteric Clarithromycin 500 mg Gram-negative bacilli (among BID should be utilized in the decision to determine the site of care for patients. (Grade A) those with co-morbid illness) With stable co-morbid illness: Patients with low-risk CAP are considered suitable for outpatient care in the absence β-lactam/β-lactamase of contraindications. (Grade A) inhibitor combination (BLIC)b OR 2nd gen oral cephalosporins Patients with moderate- and high-risk CAP need to be hospitalized for closer +/- extended macrolides monitoring and/or parenteral therapy. (Grade A) Co-amoxiclav 1 gm BID O Sultamicillin 750 mg BID OR Cefuroxime axetil 500 mg BID +/- Azithromycin 500 mg OD OR Clarithromycin 500 mg BID  DURATION OF ANTIBIOTIC USE BASED ON ETIOLOGY Moderate Risk CAP Streptococcus pneumoniae IV non-antipseudomonal Haemophilus influenzae β-lactams (BLIC, cephalosporin) ETIOLOGIC AGENT DURATION OF THERAPY (DAYS) Chlamydophila pneumoniae + extended macrolides or Mycoplasma pneumoniae respiratory fluoroquinolones Moraxella catarrhalis Enteric (PO) Most bacterial pneumonias except enteric Gram- 5-7 days Gram-negative bacilli Ampicillin-Sulbactam 1.5 gm q6h negative pathogens S. aureus (MSSA and MRSA), 3-5 (azalides) for S. pneumoniae Legionella pneumophila IV OR Cefotaxime 1-2g q8h IV and P. aeruginosa Anaerobes (among those with OR Ceftriaxone 1- 2 g OD risk of aspiration) + Azithromycin 500mg OD PO Enteric Gram-negative pathogens, S. aureus (MSSA MSSA community-acquired pneumonia OR Clarithromycin 500 mg BID and MRSA), and P. aeruginosa a. non-bacteremic - 7-14 days PO OR Levofloxacin 500 mg OD b. bacteremic - longer up to 21 days PO OR Moxifloxacin 400 mg OD MRSA community-acquired pneumonia PO a. non-bacteremic - 7-21 days b. bacteremic - longer up to 28 days High Risk CAP Streptococcus pneumoniae No risk for P. aeruginosa: Pseudomonas aeruginosa Haemophilus influenzae IV non-antipseudomonal a. non-bacteremic - 14-21 days Chlamydophila pneumoniae β-lactam b. bacteremic - longer up to 28 days Mycoplasma pneumoniae + IV extended macrolides or IV Moraxella catarrhalis Enteric respiratory fuoroquinolones Mycoplasma and Chlamydophila 10 - 14 days Gram-negative bacilli Ceftriaxone 2 gm OD OR Legionella pneumophila Ertapenem 1 gm OD Legionella 14-21; 10 (azalides) Anaerobes (among those with + Azithromycin dihydrate risk of aspiration) 500mgODIVOR Levofloxacin 500 Staphylococcus aureus mg OD IV OR Moxifoxacin 400 Pseudomonas aeruginosa mg OD IV RECOMMENDED HOSPITAL DISCHARGE CRITERIA During the 24 hours before discharge, the patient should have the following characteristics (unless High Risk CASP Risk for P. aeruginosa : IV antipneumococcal this represents the baseline status): IV antipneumococcal f antipseudomonal β-lactam antipseudomonal β-lactam (BLIC, cephalosporin or 1. Temperature of 36-37.5oC (BLIC, cephalosporin or carbapenem) carbapenem) + IV extended + IV ciprofloxacin / high dose macrolides + aminoglycosides levofloxacin 2. Pulse < 100/min Piperacillin-tazobactam 4.5 gm Piperacillin-tazobactam 4.5 gm q6h OR Cefepime 2 gm q8-12h q6h OR Cefepime 2 gms q8-12h 3. Respiratory rate between 16-24/minute OR Meropenem 1 gm q8h OR Meropenem 1 gm q8h + Azithromycin dihydrate + Levofloxacin 750 mg OD IV OR 4. Systolic BP >90 mmHg 500mgODIV Ciprofloxacin 400 mg q8-12h IV + Gentamicin 3mg/kg OD OR Amikacin 15 mg/kg OD OR If MRSA pneumonia is 5. Blood oxygen saturation >90% suspected, add Vancomycin 15 mg/kg q8-12 h 6. Functioning gastrointestinal tract OR Linezolid 600 mg q12h IV OR Clindamycin 600 mg q8h IV PREVENTION HOW CAN RESPONSE TO INITIAL THERAPY BE ASSESSED? HOW CAN CAP BE PREVENTED? Temperature, respiratory rate, heart rate, blood pressure, sensorium, oxygen - Influenza vaccination is recommended for the prevention of CAP. saturation and inspired oxygen concentration should be monitored to assess response (Grade A) to therapy. - Pneumococcal vaccination is recommended for the prevention of Response to therapy is expected within 24-72 hours of initiating treatment. Failure to invasive pneumococcal disease in adults. (Grade A) improve after 72 hours of treatment is an indication to repeat the chest radiograph. - Smoking cessation is recommended for all persons with CAP who Follow-up cultures of blood and sputum are not indicated for patients who are smoke. (Grade A) responding to treatment.  persistent productive cough with ongoing production of thick, tenacious sputum BRONCHIECTASIS Physical findings : - crackles and wheezing on lung auscultation, refers to an irreversible airway dilation - some patients exhibit clubbing of the digits - involves the lung in either a focal or a diffuse manner PFT – mild to moderate airflow obstruction categorized as cylindrical or tubular (the most common form), varicose, or cystic Acute exacerbations: can arise from infectious or noninfectious causes - increase in sputum volume and purulence clues to the underlying etiology are often provided by the pattern of lung involvement Diagnosis: - Focal bronchiectasis refers to bronchiectatic changes in a localized area of - X-ray - tram tracks indicating dilated airways consistent with bronchiectasis the lung (low sensitivity) - Diffuse bronchiectasis is characterized by widespread bronchiectatic - Chest CT scan - imaging modality of choice-confirming diagnosis of changes throughout the lung bronchiectasis (more specific) - often arises from an underlying systemic or infectious disease process Tram tracks; signet ring sign; lack of bronchial tapering; bronchial wall thickening in dilated airways, inspissated secretions or cysts emanating from bronchial wall CATEGORIES OF BRONCHIECTASIS ON CHEST CT SCAN Treatment of infectious bronchiectasis is directed at - control of active infection and - improvements in secretion clearance and - bronchial hygiene so as to decrease the microbial load within the airways and minimize the risk of repeated infections PREVENTION Reversal of an underlying immunodeficient state (By administration of gamma globulin for immunoglobulin-deficient patients) and vaccination of patients with chronic respiratory conditions ( Influenza and pneumococcal vaccines) can decrease the risk of recurrent infections Smoking cessation counselling for those who continue to smoke LUNG ABSCESS In secondary lung abscesses, antibiotic coverage should be directed at the identified Lung abscesses are pus-containing necrotic lesions of the lung parenchyma that result pathogen, and a prolonged course (until resolution of the abscess is documented) is from aspiration of bacteria- laden secretions and show an air- fluid level often required Lung abscesses are usually characterized as either primary (~80%) or secondary Primary lung abscesses usually arise from aspiration, are often caused principally by anaerobic bacteria, and occur in the absence of an underlying pulmonary or systemic condition Secondary lung abscesses arise in the setting of an underlying condition, SUMMARY - postobstructive process ( A bronchial foreign body or tumor) or - a systemic process (HIV infection or another immunocompromising Pneumonia is an infection of the pulmonary parenchyma and remains the condition) leading cause of death worldwide. Lung abscesses can also be characterized as Pneumonia results from the proliferation of microbial pathogens at the - acute (