Pneumonia PDF

ESGUERRA, HAPITAN, MORAL, MOSTAZA | EBPT 2 1 PNEUMONIA  Strongest predisposing factor: mechanical ventilation or An infection that affects one or both lungs. It causes the air sacs, or a...

ESGUERRA, HAPITAN, MORAL, MOSTAZA | EBPT 2 1 PNEUMONIA  Strongest predisposing factor: mechanical ventilation or An infection that affects one or both lungs. It causes the air sacs, or alveoli, of the intubation lungs to fill up with fluid or pus  Caused by gram-negative aerobic bacilli or S. aureus EPIDEMIOLOGY  Patients with longer lengths of hospital admission or IV  Most common causes of severe sepsis and the leading antibiotic use within the previous 90 days preceding HAP infectious cause of death in children and adults in the United development are more likely to have MDR (multidrug States resistance) organisms. o Mortality rate as high as 50% VENTILATOR ASSOCIATED PNEUMONIA  It occurs throughout the year, with the relative incidence of disease resulting from different etiologic entities varying with the  Subclassified as hospital-acquired pneumonia seasons.  Occurs after 48 or more hours of endotracheal intubation  Occurs in persons of all ages  The risk for developing pneumonia in the hospital increases  Clinical manifestations are most severe in: by 6 to 21 times after a patient is intubated o The very young, the elderly and the chronically ill  Exacerbated by the wide use of acid-suppressing drugs o Such as H2-receptor blocking agents and proton pump ETIOLOGY inhibitors  Caused by variety of viral and bacterial pathogens  More likely to be caused by S. aureus (20%–30%) and  Categorized as either community-acquired or hospital multidrug resistance is more common acquired PATHOGENESIS  Respiratory host defenses comprise innate and adaptive immunity pathways o These defense mechanisms are preserved in healthy individuals and respiratory pathogens are effectively removed before infection occurs.  Immunocompromised individuals lack robust defense mechanisms o Such as those with cystic fibrosis or prolonged neutropenia  Lung infections can also suppress the antibacterial activity of the lung o By impairing alveolar macrophage function and mucociliary clearance, thus setting the stage for secondary bacterial pneumonia.  Any alteration of the normal lung microbiome by infection and/or disease can evolve to pneumonia requiring antimicrobial treatment PATHOPHYSIOLOGY Patients with pneumonia onset outside of the hospital or within 48 hours of hospital admission are considered to have community-acquired pneumonia (CAP). Those with pneumonia onset in the hospital after at least 48 hours of hospitalization are considered to have hospital-acquired pneumonia (HAP). Patients with pneumonia onset following 48 hours of endotracheal intubation are considered to have ventilator-associated pneumonia COMMUNITY ACQUIRED PNEUMONIA  Causative pathogen: Human rhinovirus and influenza  Most prominent bacterial pathogen: S. pneumonia (up to 35% of all acute cases)  Staphylococcus aureus is also an important CAP pathogen in children and less common in adults.  Enteric gram-negative bacteria, including E. coli and K.  Respiratory pathogens enter the lower respiratory tract by pneumoniae one of three routes: o Uncommon, most frequently among patients with o local host defenses chronic illness o aspiration of oropharyngeal contents  Viral pathogens predominate in CAP among pediatric o inflammatory response patients with a prevalence of up to 80% in those less than 2 years of age. LOCAL HOST DEFENSES  H. influenzae type B  Local host defenses of both the upper and lower respiratory o Once a major childhood pathogen tract along with the anatomy of the airways are important o Has become an infrequent cause due to vaccination in preventing infection.  Upper respiratory defenses include the mucociliary HOSPITAL ACQUIRED PNEUMONIA apparatus of the nasopharynx, nasal hair, normal bacterial  Most common in critically ill patient flora, IgA, and complement.  Usually caused by bacteria  Local host defenses of the lower respiratory tract include o Factors predisposing patients to the development of HAP include high severity of illness, longer duration of hospitalization, supine positioning, cough, mucociliary apparatus of the trachea and bronchi, witnessed aspiration, coma, acute respiratory distress syndrome, patient antibodies (IgA, IgM, and IgG), complement, and alveolar macrophages.  ESGUERRA, HAPITAN, MORAL, MOSTAZA | EBPT 2 2  Mucous lines the cells of the respiratory tract, forming a  Atypical pathogens (Mycoplasma pneumoniae and protective barrier for the cells. This minimizes the ability of Chlamydia pneumoniae), often has a more gradual onset organisms to attach to the cells and initiate the infectious  Patients with atypical pneumonia often have constitutional process. and extrapulmonary symptom  The cilia beat in a uniform fashion upward, moving particles o Often with patchy infiltrates on chest x-ray o Viral: Chest radiographs in patients are often diffuse and interstitial up and out of the lower respiratory tract. o Bacterial: Lobular consolidated infiltrates (Staphylococcal pneumonias ASPIRATION often demonstrate cavitary or necrotizing lesions on imaging)  Aspiration is a fairly common occurrence in adults during sleep. Aspiration of the oropharyngeal or gastric contents may lead to aspiration pneumonia or chemical (acid) pneumonitis.  Risk factors for aspiration include dysphagia, change in oropharyngeal colonization, gastroesophageal reflux (GER), and decreased host defenses INFLAMMATORY RESPONSE  Once breakdown of the local host defenses occurs and DIAGNOSIS OF PNEUMONIA organisms invade the lung tissue, an inflammatory response  Signs and symptoms + physical exam findings suggestive of is generated either by the organisms causing tissue damage a pulmonary infiltrate or by the immune response to the presence of the organisms. o Without abnormal white blood cell (WBC) count or oxygen saturation, can form the basis of a presumed clinical diagnosis of pneumonia.  This inflammatory response either can remain localized in the infected tissue or can become systemic.  Blood cultures and non-invasive sputum cultures are recommended for all adult patients with suspected HAP or  The role of the alveolar macrophages is twofold. First, to VAP. engulf the organisms to contain the infection, and second, to process the antigens for presentation in regional lymph  Cultures are only routinely recommended in patients with nodes in order to generate a specific immune response by more severe CAP o Where knowledge of the causative pathogen and whether the empiric either the cell-mediated or humoral system, or both. antibiotic regimen is active are most important.  The macrophages release cytokines in the area of the infection, which result in increased mucus production, constricting the local vasculature and  Emphasis is placed on determining an etiology in HAP and lymphatic vessels and attraction of other immune cells to the site. VAP due to the high prevalence of MDR organisms and  The increase in mucus is associated with symptoms such as cough and sputum associated risk of ineffective empiric therapy. This allows production. If tumor necrosis factor alpha (TNF-α) and interleukins (ILs)-1 adjustment of initial empiric therapy into optimal, and -6 are released systemically, then the symptoms become more severe and pathogen-specific therapy. can include hypotension, organ dysfunction, and/or a septic or septic-shock clinical presentation  Sputum Gram stain and culture are recommended for hospitalized children CLINICAL PRESENTATION OF PNEUMONIA o Who can produce a sputum sample along with blood cultures in those with moderate/severe CAP. SIGNS AND SYMPTOMS Signs and symptoms are both constitutional (fever, chills and malaise) and  Urinary antigen tests are also available for S. pneumoniae respiratory (cough, increased sputum production and dyspnea) and L. pneumophila, and are recommended in adults with  Abrupt onset of fever, chills, dyspnea, and productive cough severe CAP.  Rust-colored sputum or hemoptysis o These tests have a high specificity (90%–99%) but lower sensitivity (50%–80%).  Pleuritic chest pain  UAT can detect pathogen antigen days (S. pneumoniae) to weeks  Dyspnea (L. pneumophila) after initiation of antibiotic therapy.  Urinary antigen tests - These tests are more rapid than traditional PHYSICAL EXAMINATION microbiological methods  Tachypnea and tachycardia MANAGEMENT OF PNEUMONIA  Dullness to percussion  Increased tactile fremitus, whisper pectoriloquy, and TREATMENT GOALS egophony  Eradication of the offending organism o Through selection of the appropriate antibiotic(s) and subsequent  Chest wall retractions and grunting respirations complete clinical cure  Diminished breath sounds over affected area  Minimization of the unintended consequences of therapy  Inspiratory crackles during lung expansion o Including toxicities and selection for secondary infections such a Clostridioides difficile or antibiotic-resistant pathogens, and minimizing CHEST RADIOGRAPH costs through outpatient and oral therapy when the patient’s severity of  Dense lobar or segmental infiltrate illness and clinical considerations permit. LABORATORY TESTS GENERAL APPROACH TO TREATMENT  Leukocytosis with predominance of polymorphonuclear cells  Antimicrobial treatment o It is the provision of the right antimicrobial or lack thereof when  Low oxygen saturation on arterial blood gas or pulse infection is not present, at the right time, at the right dose, for the right oximetry duration. o It is the balance between providing therapy to cover likely pathogens and unnecessary drug toxicity, secondary infection, or antibiotic resistance.  ESGUERRA, HAPITAN, MORAL, MOSTAZA | EBPT 2 3  Continual monitoring of patient clinical status and diagnostic data o This is to support the decision to either continue therapy, narrow or alter and discontinue therapy if infection is ruled out.  CURB-65 and CRB-65 o Most commonly used severity assessment CURB-65 1 point for each criterion present:  Confusion  Uremia (BUN >20mg/dL or 7.1 mmol/L)  Respiratory rate ≥30 breaths/min  Blood pressure (systolic: 7 days within the past month) use of broad-spectrum antibiotic therapy  Severe underlying bronchopulmonary disease  Malnutrition  Chronic use of steroids >15 mg/day for at least 2weeks ETIOLOGY REGIMEN COMMENTS Potential Pathogens: S. pneumoniae, H. No risk for P. aeruginosa: (Ceftriaxone 2g IV Empiric therapy for MRSA among influenzae, C. pneumoniae, M. q24h OR Ertapenem 1g IV q24h) PLUS hospitalized patients with severe CAP is pneumoniae, M. catarrhalis; Enteric (Azithromycin 500mg IV daily OR Levofloxacin indicated in any of the following Gram (-) bacilli; L. pneumophila, 750mg IV daily) conditions: Anaerobes (among those with risk of Risk for P. aeruginosa: (Piperacillin-  requirement for intensive care unit aspiration), S. aureus, P. aeruginosa tazobactam 4.5g IV q6h OR Cefepime 2g IV  necrotizing or cavitary infiltrates q8-12h OR Meropenem 1g IV q8h) PLUS  Empyema Azithromycin 500mg IV daily PLUS (Gentamicin  ESGUERRA, HAPITAN, MORAL, MOSTAZA | EBPT 2 8 5-7mg/kg IV daily OR Amikacin 15mg/kg IV Treatment should be modified according daily) OR (Piperacillin-tazobactam 4.5g IV q6h to culture/sensitivity results once OR Cefepime 2g IV q8-12h OR Meropenem 1g available. Use of Linezolid or Clindamycin IV q8h) PLUS (Levofloxacin 750mg IV daily OR monotherapy for Ciprofloxacin 400mg IV q8-12h) MRSA bacteremia, even if associated with If MRSA pneumonia is suspected, ADD a pulmonary source, is not recommended. Vancomycin 25-30mg/kg loading dose then 15-20mg/kg IV q8-12h OR Linezolid 600mg IV q12h Duration: 7-10 days may be adequate. A longer duration of up to 28 days may be given for S. aureus or P. aeruginosa if with concomitant bacteremia. DIRECTED ANTIMICROBIAL THERAPY FOR COMMON PNEUMONIA PATHOGENS IN ADULT  S. pneumonia – is the most common bacterial cause of CAP, primarily depends on penicillin susceptibility.  For isolates considered susceptible to intravenous penicillin by the Clinical & Laboratory Standards Institute - CLSI (MIC ≤ 2 mg/L), a narrow-spectrum penicillin such as penicillin, ampicillin, or amoxicillin is preferred. Alternatively, a cephalosporin antibiotic may be used, or in the case of a severe β-lactam allergy, either a macrolide or anti-pneumococcal fluoroquinolone.  For penicillin-resistant strains, a third-generation cephalosporin or fluoroquinolone is preferred. High-dose amoxicillin (3 g/day) may be used for penicillin-intermediate strains (MIC = 4 mg/L)  ESGUERRA, HAPITAN, MORAL, MOSTAZA | EBPT 2 9 HOSPITAL ACQUIRED PNEUMONIA dicloxacillin, is preferred by the community-acquired  The vast majority of HAP cases are caused by gram- pneumonia guidelines for methicillin-susceptible strains. negative bacilli, predominantly P. aeruginosa and the  Cefazolin is an alternative for methicillin-susceptible strains Enterobacteriaceae, or S. aureus. As such, all empiric HAP with fewer clinical data in pneumonia. regimens should consist of at least one antibiotic with  Clindamycin or vancomycin may also be used, although coverage against these pathogens, usually an these agents are not preferred for treatment of MSSA antipseudomonal, antistaphylococcal β-lactam (such as infections. piperacillin/tazobactam or cefepime) or an  Vancomycin or Linezolid - treatment of choice for MRSA antipseudomonal, antistaphylococcal fluoroquinolone (such pneumonia. as levofloxacin).  Additional alternatives for MRSA pneumonia include  Patients contracting the pneumonia in a hospital or hospital quinupristin-dalfopristin, ceftaroline, sulfamethoxazole - unit with an MRSA prevalence of 20% or greater should trimethoprim, and clindamycin. also receive MRSA coverage with either vancomycin or o Clinical evidence for these alternative options remains limited. linezolid. 6 Patients with MDR HAP risk factors, such as DIRECTED THERAPY FOR IMPORTANT GRAM-NEGATIVE receipt of IV antibiotics in the past 90 days or structural lung PATHOGENS disease, should also receive MRSA coverage in addition to a second antipseudomonal agent to cover for MDR gram-  H. influenzae –is the most common gram-negative cause of negative bacilli. CAP. Non-β-lactamase-producing strains - ampicillin (IV) or  An empiric antibiotic regimen containing dual pseudomonal amoxicillin (oral).  The choice of directed therapy is dependent on whether the strain is β- and MRSA coverage is also indicated in patients at high risk lactamase producing. of mortality, such as those requiring mechanical ventilation  Non- β-lactamase - producing strains - ampicillin (IV) or as a result of their pneumonia and those in septic shock. This approach is taken to maximize the likelihood of early amoxicillin (oral). effective therapy in those patients where the consequences  Β-lactamase - producing strains - third-generation of delayed appropriate therapy in the event the pathogen cephalosporin is the treatment of choice is resistant to the empiric regimen are greatest.  Alternative therapy for H. influenzae includes Fluoroquinolone, doxycycline, azithromycin, or VENTILATOR- ACQUIRED PNEUMONIA clarithromycin.  Empiric antibiotic regimens for patients with VAP are similar o Azithromycin is generally preferred to clarithromycin. A larger to patients with HAP proportion of H. influenzae strains are susceptible to azithromycin relative to clarithromycin and azithromycin has a more favourable drug  In patients with no MDR VAP risk factors, who contracted interaction profile VAP in a unit with a low prevalence of both MRSA (less than  P.aeruginosa is a notoriously antibiotic-resistant pathogen 10%–20%) and of gram negative bacilli resistance (