Describing the pattern of atypical and typical pneumonia.
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Community Acquired pneumonia DR. D ivygunjan Sahu (PT) Cardiopulmonary P hysical T herapist
DEFINITION OF PNEUMONIA: Pneumonia is defined as inflammation and consolidation of lung tissue due to an infectious agent. A clinical definition of pneumonia is two or more of the following symptoms/physical findings: productive cough, purulent sputum, dyspnea or tachypnea (respiratory rate >20 breaths per minute), rigors or chills, pleuritic chest pain in conjunction with a new opacity on chest radiograph.
CLASSIFICATION Primary Pneumonia: There is no pre-existing abnormality of respiratory system . Secondary Pneumonia: C haracterized by absence of specific pathogenic organism in the sputum but presence of some preexisting abnormality of respiratory system . For e.g Aspiration of pus from any foci , vomitus, or gastric contents. Ineffective coughing as in post-traumatic , post-operative, paralysis of larynx or pharynx. Partial bronchial obstruction.
SECONDARY/ASPIRATION PNEUMONIA OCCUR IN FOLLOWING SETTINGS: Altered Level of Consciousness Alcoholism Seizures Drugs Anesthesia Central nervous system disorders (defective cough/Gag reflex, coma, paralysis) Trauma Dysphagia Esophageal disorders Neurological disorders
CLASSIFICATION ( by mode of acquiring ) NOSOCOMIAL PNEUMONIA Acquired by a patient in the following settings: in a hospital after being admitted for >48 hours or < 7 days after a patient is discharged from hospital. COMMUNITY ACQUIRED PNEUMONIA Pneumonia that develops outside the hospital is considered community-acquired pneumonia (CAP).
COMMUNITY ACQUIRED PNEUMONIA (CAP) Community-acquired pneumonia (CAP) is the prominent cause of mortality and morbidity due to infectious agent. India accounts for 23 per cent of global pneumonia burden with case fatality rates between 14 and 30 per cent. S. pneumoniae was the commonest pathogen implicated (29.2%), followed by A typical pathogens in 25% and Gram-negative bacteria ( K. pneumoniae , P. aeruginosa ) in 22% . Multinational study reveals that viruses are the leading cause of global childhood pneumonia
PREDISPOSING FACTORS (CAP) Old age Cigarette smoking or alcohol Upper Respiratory Tract Infections Pre existing lung disease Recent influenza infection Coticosteriod therapy Antibiotic abuse Immuno-suppresion (AIDS, transplant patient, cancer ) Diabetes - as defective neutrophil function Renal failure- as decreased humoral response
MICROBIOLOGY OF CAP S.NO. BACTERIA VIRUSES FUNGI 1. Streptococcus pneumoniae Influenza A and B viruses Pneumocytis pneumonae 2. Haemophilus influenzae Respiratory syncytial virus(RSV) Coccidioides 3. Staphylococcus aureus Coxsackie virus Blastomycytes 4. MycoplaSma pneumoniae Rhinovirus Aspergillus sp. 5. Legionellaceae Adenovirus Histoplasmosis 6. Pseudomonas enterobacter Coronavirus Cryptococcus
CLASSIFICATION ( by site ) Lobar Pneumonia- Consolidation of whole lobe of lung. Bronchopneumonia- C haracterized first by inflammation of small bronchioles then of alveoli there by resulting in patchy bilateral consolidation of lung. Interstitial Or Atypical Pneumonia Bronchopneumonia
PATHOGENESIS (BACTERIAL): Pathogens Host defence/ Immune response Filteration of pathogens in upper airway Cough reflex Mucociliary clearance Due to one or more of the above mentioned mechanism the organism get the access and reach the alveoli.
FOUR PHASES OF TYPICAL PNEUMONIA 1)Congestion (1-2 days )- Organism after entry from various routes and comes in contact with alveolar walls 2) Red hepatization (2nd-4th day) 3) Gray hepatization (4th-6th day) 4) Resolution (6th day onwards )- The alveolar exudates is then removed and the lung gradually returns to normal.
RED HEPATIZATION (2ND-4TH DAY) Because of this congestion and dilatation there is outpouring of red cells as well as polymorphs and hemorrhage into alveoli T he consistency of the affected lung thus becomes like a liver this stage therefore has been named “red hepatization ”.
GRAY HEPATIZATION (4TH-6TH DAY) In this stage, the macrophages appear which phagocytose the fragmented polymorphs and other inflammatory debris. The lung now no longer remains congested but still remains firm due to WBCs, lymphocytes, macrophages in this stage of “gray hepatization ”.
Lobar Pneumonia LUL Pneumonia Right Middle Lobe Pneumonia
Bronchopneumonia Air Bronchogram Bronchopneumonia
Complications of Typical Pneumonia 1. Pulmonary fibrosis . 2 . Bronchiectasis 3 . Lung abscess 4 . Empyema 5 . Bacteraemia with abscess in other organs 6. ARDS 7. Haemoptysis
Interstitial Or Atypical Pneumonia Caused by atypical bacteria that do not gram stain. Most of viruses produce this type of pneumonia. Other organisms that cause it: Mycoplasma Legionella Chlamydia Pneumocystis jirovecii Cytomegalovirus
The inflammation is confined to inter-alveolar septa or interstitial spaces between alveoli and radiologically gives appearance of reticulonodular pattern . Various extra-pulmonary manifestations are seen like; Prominent headaches & Ear pain M yalgia Abdominal pain or Diarrhoea Splenomegaly Relative bradycardia Rash (Erythema multiformation in Mycoplasm pnuemonae )
PATHOGENESIS (VIRAL): Viral pneumonia continues to be quite concerning in very young adults and pregnant females. Hospitalization among adults is highest in elderly patients (≥ 65 yr ) and those with preexisting obstructive lung disease. PATHOLOGY: Direct inoculation of viral particle into the lung (e.g., RSV or influenza ) Spread in a contiguous fashion from viral infections near the upper respiratory tract (e.g., measles ) Hematogenous spread from a distant viral infection (e.g., CMV )
CLINICAL MANIFESTATIONS: The common clinical presentation of acute viral respiratory infection includes cough, dyspnea, fever, and pleuritic chest pain . Viral etiologies of lower respiratory infection are less likely to cause sputum production, and if present, tends to be watery or scanty. Clinical signs of viral respiratory illness include fever, rales (crackles) on auscultation, hypoxemia, and tachycardia . Tachycardia or tachypnea out of proportion to the temperature. (Pulse-temperature Dissociation)
Concomitant flu or gastrointestinal symptoms are noted . Patients with viral pneumonia also will present with a normal leukocyte count and bilateral pulmonary infiltrates on chest radiograph . In many moderate to severe cases, hypoxemia occurs from impaired alveolar gas exchange, often necessitating mechanical ventilation.
Atypical/viral pneumonia Progressive disease showing Bilateral patchy opacification with consolidation Complicated Pneumonia with Cavitation
Atypical pneumonia with coexisting COPD Atypical pneumonia in immunocompromised patient HIV
What are the clinical features differ from that of bacterial pneumonia? Symptoms are more than the chest signs and x-ray signs. Viral pneumonia often goes unrecognized because the person may not appear very ill. Characteristic features or constitutional symptoms like fever, cold, aches and pains precedes several days before viral pneumonia occurs than in bacterial pneumonia which is more abrupt in onset . Disease is mild and self limiting and resolves by 7-10 days time . L ess commonly associated with elevated WBC and "left shifts" of the differential than bacterial types of pneumonia.
C-reactive protein - As a reactive phase reactant, the CRP level may be elevated with viral pneumonia, although this is not a specific or sensitive finding. ELISA - rapid antigen tests - ELISA tests allow real-time data for a number of viral pneumonia pathogens. Commonly available ELISA tests include the following: Herpes simplex virus (HSV) Respiratory syncytial virus (RSV) Influenza A and B Cytomegalovirus (CMV)
Chemistry panel - Useful for gauging the degree of dehydration, relative renal dysfunction, and dosing of renal excreted medications. Gene amplification - First and second-generation PCR testing exists and may allow viral pneumonia etiology diagnosis within clinically relevant timing. PCR can detect the nucleic acid of Legionella species, M. pneumoniae , C. pneumoniae , and Mycobacteria.
Viral Cultures- viral cultures are routinely not available for 10 to 15 days, which limits them for acute clinical care decisions. The success of delivering a viable specimen to the lab varies as many of the viruses have very specific transport requirements. The fastidious nature of some viral pathogens limits the validity of a negative culture result.
COMPLICATIONS OF VIRAL PNEUMONIA: Concomitant bacterial infection, resulting in an abscess, empyema, and or pleural effusion Sepsis with secondary multiple organ failure ( Hepatitis, Pericarditis, Myocaritis ) Acute respiratory failure Cardiovascular collapse, MI Acute respiratory distress syndrome Pyrexia due to drug hypersentivity
SPUTUM GRAM STAIN AND CULTURE Main purpose of the sputum Gram’s stain is to ensure that a sample is suitable for culture. A lso identify certain pathogens (e.g., S. pneumoniae , S. aureus , and gram-negative bacteria) by their characteristic appearance. May be contaminated with resident flora of the upper airways, thus leading to false positive results. Not sensitive in patients who have taken antibiotics previously or unable to expectorate. Sensitivity and Specificity of the sputum Gram’s stain and culture are highly variable.
OTHER TESTS CBC- neutrophilic , luekocytosis UREA AND ELECTROLYTE- urea > 7mmol/L, hyponatremia LFT- raised bilirubin, hypoalbuminemia BLOOD CULTURE (chronic liver disease, leukopenia, host unable to clear bacterimia ) COLD AGGLUTININS- mycoplasmas ABG- hypoxemia PCR- mycoplasma, other atypical organism PCT- to determine the need of antibacterial therapy HIV
URINARY ANTIGEN TESTS: Two commercially available tests detect pneumococcal and Legionella antigen in urine. Legionella urine antigen test (Sensitivity 90%, Specificity 99%) Pneumococcal urine antigen test (Sensitive 80% , Specific >90 %)
INVASIVE TESTS Bronchoscopy Thoracoscopy P leural aspiration Percutaneous aspiration/biopsy Biopsies obtained during influenza infection reveal a wide range of pathologies, including alveolar edema and exudate, interstitial inflammatory infiltration , and ulceration of bronchial mucosa to type II cell metaplasia.
ROLE OF CT SCAN Lobar pneumonia R ight unilateral involvement constituted by consolidation with air- bronchogram , mainly in the upper lobe in an atypical pneumonia patient.
Acute interstitial Pneumonia Bronchopneumonia in the middle lobe and in both lower lobes
1 2 3 4 5 WHEN TO DISCHARGE THE PATIENT? HOW MUCH TESTING IS REQUIRED TO CONFIRM THE DIAGNOSIS? ONCE PNEUMONIA IS DIAGNOSED 4 DECISIONS HAS TO BE MADE: WHICH ANTIBIOTICS TO PRESCRIBE? WHERE THE PATIENTS SHOULD BE TREATED?
MARKERS OF SEVERITY IN PNEUMONIA AT INITIAL ASSESSMENT: Altered mental state/confusion Tachypnoea ≥30 breaths/min Hypotension, systolic <90mmHg, diastolic <60mmHg or need for vasopressors. Arterial hypoxaemia Pao <60mmHg or Pao2:Fio2ratio< 250mmHg on oxygen or need for >35% Fio2 to keep Sao2>90% Arterial hypercarbia Paco2>50mmHg or consideration of the need for mechanical ventilation. Chest radiograph shows more than one lobe involved or rapid progression. Evidence of renal insufficiency serum urea ≥7mmol/L Low urine output <20mL/h
CURB-65 RULE SEVERITY OF ILLNESS SCORING SYSTEM FOR CAP
ANTIBIOTIC prescription through CURB-65
Although CURB 65 can detect high risk patients but it has a major limitations of overestimating the risks in patients >65 and it lacks formal assessment of hypoxemia. Therefore, should be used with Pneumonia Severity Index (PSI) or SMART COP in case of discrepancies. SMART COP is a severity score method designed to identify individuals who require intensive respiratory or vasopressor support (IRVS) support due to pneumonia.
PNEUMONIA SEVERITY INDEX (PSI)
SMART COP IRVS is Intensive respiratory or vassopresor support
I nitial Empiric Antimicrobial Therapy for CAP: Without comorbidities use Macrolide or Amoxycillin If co- morbity present use combination : Amoxycillin + Macrolide Fluroquinolone should be avoided as it mask the tuberculosis or develop resistance . I n patient with no risk factors for pseudomonas: I/V Amoxiclav or I/V Cefotaxime or I/V Ceftriaxone + Macrolide
IF PSEUDOMONAS PRESENT : Cefoperazone Sulbactam Piperacillin Tazobactam Cefepime Meropenem Imipenem ± Aminoglycoside Or Fluroquinolone (after ruling out TB)
IF MRSA IS SUSPECTED Multiple patchy consolidation Cavitation Pneumatoceles Pneumothorax Effusion Vancomycin or Linezolid or Teicoplanin
ORGANISM DIRECTED SENSITIVE DRUGS: For klebsiella , legionella, actinomycosis : Gentamycin , Azithromycin, ceftriaxone. Rifampicin can be given in legionella. For actinomycosis use Benzyle penicillin. In severe cases piperacillin plus tazobactam / Meropenem . Clindamycin in aspiration pneumonia .
FUNGAL First give test of Amphotericin B as follows: 1 mg in 20 ml of D5W over 30 minutes to 1 hour; monitor vital signs every 30 minutes for next 2 hours . I f no adverse reaction occurs then do as follows .. It should NEVER be mixed with Normal Saline or Half Normal Saline as it will precipitate . Flush I.V. line with 5% dextrose injection before and after infusion. Pretreat with antihistamines, antipyretics, or corticosteroids, as prescribed .
VIRAL Acyclovir the duration of intravenous therapy with Acyclovir is usually 5 days. The doses recommended above (5 or 10mg/ kgBW ) should be given every 12 hours . Adults: 5 mg/kg infused at a constant rate over at least 1 hour, every 8 hours for 7 days in adult patients with normal renal function. O ral dose 800mg 4 hrly x7-10days.
SUPPORTIVE CARE (CORNERSTONE) T he treatment of viral pneumonia revolved around supportive care: Supplemental oxygen when indicated Airway augmentation as appropriate Monitoring and replacement of any fluid deficits Symptomatic control of temperature and cough Rest to reduce oxygen demand Treatment of any comorbidities and/or concomitant bacterial pneumonia
What should be done for patients who are not improving after 72hrs of empiric antibiotic therapy? The lack of response to seemingly appropriate treatment in a patient with CAP should lead to a complete reappraisal, rather than simply to selection of alternative antibiotics . The clinical history , physical examination and the results of all available investigations should be reviewed . T he patient should be reassessed for possible resistance to the antibiotics being given and rule other atypical organisms. Treatment should then be revised according to culture result.
When we should deescalate Antibiotics? De-escalation of initial empiric broad spectrum antibiotic or combination parenteral therapy to a single narrow spectrum parenteral or oral agents based on available laboratory data is recommended when: T he patient is clinically improving (normal RR, less cough), Improving white blood cell count, no bacteremia Is hemodynamically stable and Has a functioning gastrointestinal tract.
POOR PROGNOSTIC CRITERIA Neurological, male sex>65yrs, Rapidly progressive radiographic abnormalities during therapy . Staphylococcus aureus , Gram-negative bacilli (including Pseudomonas aeruginosa ), aspiration organisms. S evere acute respiratory syndrome. Drug resistant pneumococci. Delay in initial antibiotic therapy (> 4-6 hours) Initial therapy with inappropriate antibiotic therapy Failure to have a clinical response to empirical therapy within 72 hours
DISCHARGE CRITERIA Temperature < 37.5 HR < 100 bpm RR < 24 b pm SBP > 90 O2 saturation at room air ≥ 90 % Ability to maintain oral intake without aid Normal mental status Do not discharge patients with CAP if in the past 24 hours they haven’t had 2 or more of the above findings. Delay discharge if temperature > 37.5 in the last 24 hours
ANTIBIOTIC RESISTANCE B acterial AMR was directly responsible for 1.27 million global deaths in 2019 and contributed to 4.95 million deaths. The misuse and overuse of antimicrobials are the main drivers in the development of drug-resistant pathogens.
PREVENTION Annual Pneumococcal vaccination (PPV23) contains capsular material from 23 pneumococcal serotypes; In PCV13 capsular polysaccharide from 13 of the most frequent pneumococcal pathogens affecting children is linked to an immunogenic protein. PCV13 produces T cell–dependent antigens that result in long-term immunologic memory . High risk groups whom vaccinated is important is elderly, COPD, chronic kidney diseases, Asplenia or patients on long term glucocoticoides .
INFLUENZA VACCINATION Natural infection with viral causes of pneumonia does not induce long-term protective immunity due to an evolutionary advantage allowing viruses to evade host immune defenses via antigenic shift and drift thus vaccination is important. Two forms of influenza vaccine are available: I ntramuscular inactivated vaccine and Intranasal live-attenuated cold-adapted vaccine.
Cigarette smoking, both active and passive, is a recognized independent risk factor for CAP. Smoking, tobacco should be stopped . Patient can opt for Pulmonary Rehabilitation for speedy recovery. PATIENT EDUCATION
Vibration, percussion and forced expiration 01 Nutritional counseling & low intensity endurance training. 02 For decreasing general debility: Single nostril breathing and Lung strengthening exercises 03 For increasing the immunity & preventing re-infection (UARS & LRTI) P U LM O N A R Y R E H A B For Airway clearances (Acute condition):
NEWER ADJUVANT Phage therapy is important for treatment of drug-resistant pathogens as compared to antibiotics in this modern era. As phage has evolved to more narrowly target bacterial strains or species leaving the microbiome . This specificity makes phage therapy an attractive alternative for managing infections . Variation in intracellular targets of the type II DNA topoisomerases acquired by recombination with the fluoroquinolones have shown resistance against streptococcus strain.
Case1: Atypical pneumonia with comorbidities. A 66yrs old female patient came in the OPD with the history of high grade fever 102F, tachycardia ( 141bpm ), tachypnea-33bpm , dyspnea and cough with expectoration. CURB score-3 ESR (98mm/ hr ) & CRP was elevated. Mild Anaemia & leucocytosis (15600cumm) in the CBC. RFT implicated high levels of creatinine (3.4mg/dl), urea (143mg/dl ) & hypoalbuminea in LFT. Elevated NT- ProBNP (12593pg/ml) called for ECHO which concluded mild to moderate MR with good LV function . Sputum reported Moraxella Catrehhalis in the examination.
Along with supportive care and diuretic therapy, meropenam and clolistin has been started. First Xray when she arrived. After 2 days, patient was stable along with improved lab reports and was shifted to ward.
Case2: A complicated Pneumonia with pleural effusion A 45yr old smoker patient came to the emergency department with tachycardia (134bpm), dyspnea , moderate left sided chest pain with complain of high grade fever since 5 days & cough with expectorations. CBC reported leucocytosis (20,200/ cumm ) with leucopenia (7%). LFT & RFT was normal. Sputum test excluded TB, fungal aliments and confirmed the presence of plenty of gram negative bacteria . Echo revealed normal findings.
Xray showed consolidated left lung with pleural effusion . Cytology of pleural aspirate was negative for malignant cells and dominantly present with polymorphs . The patient was initiated with piperacilin-tazobctum , amikacin and deescalated with cefuroxime & azithromycin according to the lab reports. Once the vitals signs were stable he was discharged with oral antibiotics, nebulisation & nutritional supplements.
Case3: Viral Pneumonia in a young alcoholic male. A 28yrs old alcoholic male patient came in the OPD with the history of 7days high grade fever 102F, mild abdominal discomfort, tachycardia (121bpm), tachypnea-32bpm, dyspnea and cough with expectoration. ESR, CRP was elevated, ECG confirmed sinus tachycardia, no signs of leucocytosis but borderline thrombocytopenia, & lymphopenia in the CBC. Blood sugars & RFT was within normal, and there was slightly elevated liver enzymes, ABG report revealed hypoximea (PaO2 63mmhg) and Sputum was sent for examination but report was inconclusive. The patient was managed with supportive care and the need for hydration along with antibiotics ( pepar , amikacin ). Nebulisation with hyperneb to aid expectoration & salbutamol was advised.
X ray showed bilateral infiltrates and patient was sent for CT after RT-PCR and Influenza profile came normal. CT denoted bilateral patchy opacities thus ?viral Pneumonitis. The patient was managed well by antibiotics, pulmonary rehab, oxygenation & nebulisation. As the lungs get cleared and breathing was easier ( RR-25,HR-95, Spo2 95% on Room air ) the patient was discharged after 4 days.
CONCLUSION Initial management in the primary care depends on clinical assessment while the hospitalized patients require combination of clinical scores, chest radiography and various microbiological and biomarker assays. This comprehensive diagnostic approach together with additional sampling and molecular tests in selected high-risk patients should be practiced. Inappropriate therapy in CAP in hospitalized patients lengthens hospital stay and increases cost and mortality.