pneumonia

PNEUMONIA

INTRODUCTION

A wide variety of problems affect the lower respiratory system. Pneumonia is one of commonest diseases of the lower respiratory system. It is the acute inflammation of the lung parenchyma caused by microbial organism. However despite the new antimicrobial agents , pneumonia is still common and is associated with significant morbidity and mortality.

DEFINITION

Pneumonia is an infection of the pulmonary parenchyma that is caused by microbial agents.

INCIDENCE

Acute respiratory illness accounts for 3.9 million young children dying globally , of these 40% deaths occur in Bangladesh, Nepal, india and Indonesia. About 90% ARI deaths are due to pneumonia. In the developed countries the incidence of pneumonia is low as 3-4 % and in developing countries it si high as 20- 30 %. It is estimated that in India the respiratory infections accounts for 9,87,000 deaths of which 969000were due to acute lower respiratory infections.

ETIOLOGY

Normal defense mechanism Normally the airway distal to the  larynx is sterile because of protective defense mechanisms. These mechanisms include the following :filtration of air, warming and humidification of inspired air, epiglottis closure over the trachea, cough reflex, mucociliary escalator mechanism, secretion of immunoglobulin A and alveolar macrophages.

FACTORS PREDISPOSING TO PNEUMONIA

Pneumonia is occur when the defence mechanisms become incompetent or are overwhelmed by the virulence or quantity of infectious agent.

Ø    Aging – mucociliary mechanism impaired

Ø    Air pollution – mucociliary mechanism impaired

Ø    Altered consciousness: alcoholism, head injury, seizures, anesthesia, drug over dose, stroke [it depresses the cough and epiglottal reflexes which may allow aspiration of oropharyngeal contents into lungs.]

Ø    Altered oropharyngeal flora secondary to antibiotics

Ø    Bed rest and prolonged immobility

Ø    Chronic diseases : chronic lung disease, DM, heart disease, cancer, end stage renal disease.[ increased gram negative organism in the oropharynx]- gram negative bacilli are not normal flora o f respiratory tract

Ø    Debilitating illness

Ø    HIV infection

Ø    Immunosuppressive drugs

Ø    Inhalation or aspiration of noxious substances

Ø    Intestinal and gastric feeding via naso gastric and naso intestinal tubes

Ø    Malnutrition – the functions of lymphocyte and polymorphonuclear leucocyte are altered

Ø    Smoking- mucociliary mechanism impaired

Ø    Tracheal intubation [it interfere with normal cough reflex and mucociliary mechanism   escalator mechanism. It also bypasses the upper  airway in which filtration and humidification of air normally takeplace 

Ø    Upper respiratory tract infection – mucociliary mechanism impaired

ACQUISITION OF ORGANISM

Organisms that cause the pneumonia is reach the lungs by three methods

1.                  Aspiration from the nasopharynx

2.                  Inhalation of microbes present in the air . examples includes mycoplasma pneumonia and fungal pneumonia

3.                  Hematogenous spread from a primary infection else where in the body. An example staphylococcus aureus

TYPES OF PNEUMONIA

Pneumonia can be caused by bacteria, fungi, mycoplasma, viruses, parasites and chemicals . but the clinically effective way to classify the pneumonia a shospital acquired pneumonia and community acquired pneumonia. The classification is important to decide the appropriate treatment for the pneumonia.

ORGANISM ASSOCIATED WITH PNEUMONIA
Community acquired pneumonia	Hospital acquired pneumonia
Ø    Streptococcus pneumonia Ø    Mycoplasma pneumonia Ø    Haemophilus influenza Ø    Respiratory viruses Ø    Chlamydia pneumonia Ø    Legionella pneumonia Ø    Oral anaerobs Ø    Staphylococcus aureuos Ø    Fungi Ø    Enteric aerobic gram negative bacteria	Pseudomonas aeruginosa Enterobacter Ecoli Proteus Klebsiella Staphylococcus aureus Steeptococcus Oral anaerobs

PATHOPHYSIOLOGY

Pneumonia  results from the proliferation of microbial pathogens at the alveolar level and the host's response to those pathogens. Microorganisms gain access to the lower respiratory tract in several ways. The most common is by aspiration from the oropharynx. Small-volume aspiration occurs frequently during sleep (especially in the elderly) and in patients with decreased levels of consciousness. Many pathogens are inhaled as contaminated droplets. Rarely, pneumonia occurs via hematogenous spread (e.g., from tricuspid endocarditis) or by contiguous extension from an infected pleural or mediastinal space.

When these barriers are overcome or when the microorganisms are small enough to be inhaled to the alveolar level, resident alveolar macrophages are extremely efficient at clearing and killing pathogens. Macrophages are assisted by local proteins (e.g., surfactant proteins A and D) that have intrinsic opsonizing properties or antibacterial or antiviral activity. Once engulfed by the macrophage, the pathogens—even if they are not killed—are eliminated via either the mucociliary elevator or the lymphatics and no longer represent an infectious challenge. Only when the capacity of the alveolar macrophages to ingest or kill the microorganisms is exceeded does clinical pneumonia become manifest. In that situation, the alveolar macrophages initiate the inflammatory response to bolster lower respiratory tract defenses. The host inflammatory response, rather than the proliferation of microorganisms, triggers the clinical syndrome of  pneumonia. The release of inflammatory mediators, such as interleukin (IL)-1 and tumor necrosis factor (TNF), results in fever. Chemokines, such as IL-8 and granulocyte colony-stimulating factor, stimulate the release of neutrophils and their attraction to the lung, producing both peripheral leukocytosis and increased purulent secretions. Inflammatory mediators released by macrophages and the newly recruited neutrophils create an alveolar capillary leak equivalent to that seen in the acute respiratory distress syndrome (ARDS), although in pneumonia  this leak is localized (at least initially). Even erythrocytes can cross the alveolar-capillary membrane, with consequent hemoptysis. The capillary leak results in a radiographic infiltrate and rales detectable on auscultation, and hypoxemia results from alveolar filling. Moreover, some bacterial pathogens appear to interfere with the hypoxemic vasoconstriction that would normally occur with fluid-filled alveoli, and this interference can result in severe hypoxemia. Increased respiratory drive in the systemic inflammatory response syndrome  leads to respiratory alkalosis. Decreased compliance due to capillary leak, hypoxemia, increased respiratory drive, increased secretions, and occasionally infection-related bronchospasm all lead to dyspnea. If severe enough, the changes in lung mechanics secondary to reductions in lung volume and compliance and the intrapulmonary shunting of blood may cause the patient's death.

PATHOLOGY

Classic pneumonia  evolves through a series of pathologic changes. The initial phase is one of edema, with the presence of a proteinaceous exudate—and often of bacteria—in the alveoli. This phase is rarely evident in clinical or autopsy specimens because it is so rapidly followed by a red hepatization phase. The presence of erythrocytes in the cellular intraalveolar exudate gives this second stage its name, but neutrophil influx is more important from the standpoint of host defense. Bacteria are occasionally seen in pathologic specimens collected during this phase. In the third phase, gray hepatization, no new erythrocytes are extravasating, and those already present have been lysed and degraded. The neutrophil is the predominant cell, fibrin deposition is abundant, and bacteria have disappeared. This phase corresponds with successful containment of the infection and improvement in gas exchange. In the final phase, resolution, the macrophage reappears as the dominant cell type in the alveolar space, and the debris of neutrophils, bacteria, and fibrin has been cleared, as has the inflammatory response.

This pattern has been described best for lobar pneumococcal pneumonia  and may not apply to pneumonias of all etiologies, especially viral or Pneumocystis pneumonia . In VAP, respiratory bronchiolitis may precede the development of a radiologically apparent infiltrate. Because of the microaspiration mechanism, a bronchopneumonia pattern is most common in nosocomial pneumonias, whereas a lobar pattern is more common in bacterial CAP. Despite the radiographic appearance, viral and Pneumocystis pneumonias represent alveolar rather than interstitial processes.

COMMUNITY ACQUIRED PNEUMONIA

Community-acquired pneumonia (CAP) is defined as pneumonia that develops in the outpatient setting or within 48 hours of admission to a hospital

CAP is defined as a lower respiratory tract infection of the lung parenchyma with onset in the community or during the first two days of hospitalization.

Ø    CAP is usually acquired via inhalation or aspiration of pulmonary pathogenic organisms into a lung segment or lobe.Less commonly, CAP results from secondary bacteremia from a distant source, such as Escherichia coli urinary tract infection and/or bacteremia.

Ø    Aspiration pneumonia is the only form of CAP caused by multiple pathogens (eg, aerobic/anaerobic oral organisms).

Ø    The pathogens of the CAP is divided into atypical and typical pathogen. Typical pathogens include typical bacterial pathogens that cause community-acquired pneumonia (CAP) include S pneumoniae , H influenzae, and M catarrhalis. Atypical pneumonias can be divided into those caused by either zoonotic or nonzoonotic atypical pathogens.Zoonotic atypical CAP pathogens -include Chlamydophila (Chlamydia) psittaci(psittacosis), Francisella tularensis (tularemia), and Coxiella burnetii (Q fever).Nonzoonotic atypical CAP pathogens include Legionella species, M pneumoniae,and Chlamydophila (Chlamydia) pneumoniae.

Physical examination

Ø  Physical findings are confined to the lungs in patients with typical bacterial community-acquired pneumonia (CAP).

Ø  Purulent sputum is characteristic of pneumonia caused by typical bacterial CAP pathogens and is not usually a feature of that caused by atypical pathogens, with the exception of Legionnaires disease.

Ø  Blood-tinged sputum may be found in patients with pneumococcal pneumonia, Klebsiella pneumonia, or Legionellapneumonia.

Ø  Rales are heard over the involved lobe or segment. If consolidation is present, an increase in tactile fremitus, bronchial breathing may be present.

Ø  Legionella pneumonia, Q fever, and psittacosis are atypical pneumonias that may present with signs of consolidation. Consolidation is not a feature of pneumonia caused by M pneumoniae or Chlamydophila (Chlamydia) pneumoniae.

Ø  Pleural effusion - Pleural effusion (usually due to H influenzae infection), if large enough, is detectable on physical examination. Patients with pleural effusion have decreased tactile fremitus and dullness on chest percussion.

Ø  Pleural effusion in a patient with CAP and extrapulmonary manifestations should suggest Legionella infection. Pleural effusion with appropriate epidemiologic history findings, such as contact with a rabbit or deer, may suggest tularemia. CAP with a large pleural effusion (serosanguineous) is typical of that caused by group A streptococci.

Ø  Empyema -  Empyema is most often associated with Klebsiella, group A streptococci, and S pneumoniae.

Diagnostic findings

PORT (Pneumonia Patient Outcomes Research Team) Sevearity Index.

Identifying the level of risk – this tool may be used as a supplement to clinical judgement

Pneumonia Severity Index PSI

Patient characteristic	Points
Demographic factors Age –males Age –females Nursing home resident	Age in years Age in years  minus 10 +10
Comorbid disease Neoplastic diseases Liver disease Heart failure Cerebrovascular disease Renal disease	+30 +20 +10 +10 +10
Physical examination findings Altered mental status Respiratory rate >=30 breaths /minute Systolic BP<90 mm of Hg Temp <95  or >104 degree F Pulse >125 beats /minute	+20 +20 +20 +15 +10
Lab results Ph <7.35 BUN >10.7mmol/L Sodium <130meq/L Glucose >13.9 mmol/L Hematocrit <30% Pao2<60mm of Hg Pleural effusion	+30 +20 +20 +10 +10 +10 +10

Scoring the risk level

Based on PSI score patients risk level is identified and site to treat is indicated.

Risk	Risk class	Based on	Recommended Treatment site
Low Low Low Moderate High	I II III IV V	None 70 or fewer points 71-90 91-130 >130	Out patient Out patient Out patient Inpatient Inpatient

Ø  Agglutinin level - Low-titer cold agglutinin elevations occur in various viral and neoplastic illnesses. Of patients with Mycoplasma pneumonia, 75% develop transient elevations of cold agglutinins 1-2 weeks into the illness.

Ø  Direct fluorescent antibody testing - In a patient with suspected Legionella pneumonia, direct fluorescent antibody (DFA) testing of the sputum can assist in diagnosis if obtained early and before antimicrobial treatment. Antimicrobial treatment rapidly decreases the sputum yield of DFA testing.

Ø  Immunoglobulin studies - Obtain immunoglobulin M (IgM) and immunoglobulin G (IgG) titers for C pneumoniae and M pneumoniae if they are a diagnostic possibility. An increase in the IgG titer for either organism suggests past exposure and does not indicate acute infection. An increase in the IgM titer for either pathogen allows the diagnosis in a patient with CAP.

If Chlamydophila (Chlamydia) pneumoniae infection is suspected, obtain specific pneumonia IgM and IgG titers

Ø  Peripheral smear - Impaired splenic function is determined by demonstrating Howell-Jolly bodies or "pitted red blood cells" in the peripheral smear. The number of Howell-Jolly bodies is inversely proportional to splenic function.

Ø  Urinary antigen test - In patients with CAP who produce no sputum, a positive urinary antigen test for S pneumoniae, if suspected, confirms the diagnosis of pneumococcal CAP.

Ø  Chest radiography and CT scanning -Obtain chest radiographs in all patients with suspected community-acquired pneumonia (CAP) to exclude conditions that mimic CAP and to confirm the presence of an infiltrate compatible with the presentation of CAP. Viral pneumonias display few or no infiltrates on chest radiography, but when infiltrates are present, they are almost always bilateral, perihilar, symmetric, and interstitial. Bacterial pneumonias have a predominantly focal segmental or lobar distribution. In contrast, typical or atypical pathogens produce a lobar or segmental pattern on chest radiography, with or without consolidation or pleural effusion.

Community-acquired, methicillin-resistant S aureus (CA-MRSA) CAP presents as a fulminant CAP with rapid cavitation and necrotizing pneumonia caused by CA-MRSA. Aspiration pneumonitis may develop cavitation 1 week after aspiration. Signs of cavitation are absent on the initial chest radiograph in patients with CAP due to aspiration. Serial chest radiography can be used to observe the progression of CAP. Rapidly progressive, asymmetric infiltrates suggest the possibility of Legionnaires disease.

To rule out bronchogenic carcinoma CT scanning is used.

Ø  FNA,TTA, bronchoscopy - Transthoracic fine-needle aspiration (FNA) of the infiltrate can be performed and is most useful in determining the cause of noninfectious-associated infiltrates that are not responding to antibiotic treatment. Bronchscopy with bronchoalveolar lavage is used also as diagnostic procedure.

Ø  Histologic findings -Lung sections with typical bacterial pneumonias show the progression from red hepatization to white hepatization during the resolution process. The lung is repaired after bacterial pneumonia is complete and the infectious process resolves.

Treatment

There is no optimal therapy for community-acquired pneumonia (CAP). CAP may be treated with monotherapy or combination therapy.

The main antibiotics used for the treatment of community acquired pneumonia include

Empirical Antibiotic Treatment of Community-Acquired pneumonia

Outpatients  Previously healthy and no antibiotics in past 3 months A macrolide [clarithromycin (500 mg PO bid) or azithromycin (500 mg PO once, then 250 mg qd)] or   Doxycycline (100 mg PO bid) Comorbidities or antibiotics in past 3 months: select an alternative from a different class A respiratory fluoroquinolone [moxifloxacin (400 mg PO qd), gemifloxacin (320 mg PO qd), levofloxacin (750 mg PO qd)] or  A β-lactam [preferred: high-dose amoxicillin (1 g tid) or amoxicillin/clavulanate (2 g bid); alternatives: ceftriaxone (1–2 g IV qd), cefpodoxime (200 mg PO bid), cefuroxime (500 mg PO bid)] plus a macrolidea  In regions with a high rate of "high-level" pneumococcal macrolide resistance,b consider alternatives listed above for patients with comorbidities.  Inpatients, Non-ICU  A respiratory fluoroquinolone [moxifloxacin (400 mg PO or IV qd), gemifloxacin (320 mg PO qd), levofloxacin (750 mg PO or IV qd)] A β-lactam [cefotaxime (1–2 g IV q8h), ceftriaxone (1–2 g IV qd), ampicillin (1–2 g IV q4–6h), ertapenem (1 g IV qd in selected patients)] plus a macrolided [oral clarithromycin or azithromycin (as listed above for previously healthy patients) or IV azithromycin (1 g once, then 500 mg qd)] Inpatients, ICU  A β-lactame [cefotaxime (1–2 g IV q8h), ceftriaxone (2 g IV qd), ampicillin-sulbactam (2 g IV q8h)] plus   Azithromycin or a fluoroquinolone (as listed above for inpatients, non-ICU) Special Concerns  If Pseudomonas is a consideration  An antipneumococcal, antipseudomonal β-lactam [piperacillin/tazobactam (4.5 g IV q6h), cefepime (1–2 g IV q12h), imipenem (500 mg IV q6h), meropenem (1 g IV q8h)] plus either ciprofloxacin (400 mg IV q12h) or levofloxacin (750 mg IV qd) The above β-lactams plus an aminoglycoside [amikacin (15 mg/kg qd) or tobramycin (1.7 mg/kg qd) and azithromycin] The above β-lactamsfplus an aminoglycoside plus an antipneumococcal fluoroquinolone If CA-MRSA is a consideration Add linezolid (600 mg IV q12h) or vancomycin (1 g IV q12h).

Macrolides Erythromycin Azithromycin Clarithromycin

Respiratory fluroquinolones Moxifloxacin Levofloxacin

β-lactem high dose amoxicillin amoxicillin/clavulinate cefpodoxime cefprozil cefuroxime

Antopseudomonal agents Piperacillin Imipenem/cilastatin Meropenem Cefepime Piperacillin /tazobactum

Vaccination

Pneumococcal vaccines prevent pneumococcal bacteremia but not necessarily pneumococcal pneumonia. Two pneumococcal vaccines are approved in the United States. Prevnar 13, a pneumococcal 13-valent conjugate vaccine is approved for children aged 6 weeks to 5 years and adults aged 50 years or older. The 23-valent vaccine (Pneumovax 23) is approved for adults aged 50 years or older and persons aged 2 years or older who are at increased risk for pneumococcal disease.

MYCOPLASMA PNEUMONIA

It is a common cause of community acquired pneumonia and the disease usually has a prolonged onset.

Etiology

The causative agent of mycoplasmal pneumonia is M pneumoniae, a bacterium lacking a cell wall, which belongs to the class Mollicutes, the smallest known free-living microorganisms. Because the organism can be excreted from the respiratory tract for several weeks after the acute infection, isolation of the organism may not indicate acute infection.

Pathophysiology

The organism responsible for mycoplasmal pneumonia, M pneumoniae, is a pleomorphic organism that, unlike bacteria, lacks a cell wall, and unlike viruses, does not need a host cell for replication. The prolonged paroxysmal cough seen in this disease is thought to be due to the inhibition of ciliary movement. M pneumoniae has a remarkable gliding motility and specialized filamentous tips end that allows it to burrow between cilia within the respiratory epithelium, eventually causing sloughing of the respiratory epithelial cell.

The organism has 2 properties that seem to correlate well with its pathogenicity in humans. The first is a selective affinity for respiratory epithelial cells, and the second is the ability to produce hydrogen peroxide, which is thought to be responsible for much of the initial cell disruption in the respiratory tract and for damage to erythrocyte membranes.

The pathogenicity of M pneumoniae has been linked to the activation of inflammatory mediators , including cytokines.

Diagnosis

Ø  History and physical examination

·         Fever

·         Malaise

·         Persistent, slowly worsening dry cough

·         Headache

·         Chills, not rigors

·         Scratchy sore throat

·         Sore chest and tracheal tenderness result of protracted cough

·         Pleuritic  chest pain

·         Physical examinations

·         Most cases of pneumonia due to M.pneumoniae resolve after several weeks although a dry cough can be present for as long as a month

·         A nontoxic general appearance

·         Erythematous tympanic membrane or bullous myringitis in patients older than 2 years an uncommon but unique sign

·         Mild pharyngeal infection with minimal or no cervical adenopathy

·         Normal lung findings with early infection but rhonchi, rales and or wheezes several days later

·         Various examthems including erythema multiforme and Stevens Johnson syndrome

Ø  Sputum culture

Sputum Gram stains and cultures are usually not helpful because M pneumoniaelacks a cell wall and cannot be stained. M pneumoniae is difficult to culture, requires special culture media , and needs 7-21 days to grow.

Ø  Polymerized chain reaction

Polymerase chain reaction (PCR) has been shown to accurately diagnose atypical pneumonia and is becoming the criterion standard confirmatory test for M pneumoniae.

Ø  DNA probe test

A radiolabeled DNA probe detects M pneumoniae ribosomal RNA in respiratory secretions with 90% sensitivity.  

Ø  Eosinophil Cationic protein

the role of eosinophil cationic protein (ECP) has been studied in M pneumoniaeinfection and asthma, in which ECP levels have been found to be increased.This protein may play a role in damage to the respiratory epithelium and accelerated hypersensitivity in the respiratory system.

Treatment

Antibiotic therapy

 In the treatment of mycoplasmal pneumonia, antimicrobials against M pneumoniae are bacteriostatic, not bactericidal. Tetracycline and erythromycin compounds are very effective, and the second generation  tetracyclines (doxycycline) and macrolides are the drugs of choice. Penicillins and cephalosporins are ineffective, because the organism lacks a cell wall.

Azithromycin

Azithromycin is a macrolide antibiotic that is very effective against M pneumoniae and may be the most common agent used to treat M pneumoniae given its ease of administration.

Doxicycline

Doxycycline is a tetracycline antibiotic that is used to treat susceptible  bacterial infections of both gram-positive and gram-negative organisms, as well as infections caused by mycoplasma

Levofloxacin

Levofloxacin is a fluoroquinolone antibiotic that can be used to treat Mycoplasma infections. It works by inhibiting the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription.

HOSPITAL ACQUIRED /VENTILATOR ASSOCIATED /HEALTH CARE ASSOCIATED PNEUMONIA

HAP is pneumonia occurring 48 hours or longer after hospital admission and not intubation at the time of hospitalization.

VAP refers to pneumonia that occurs more than 48-72 hours after endotracheal intubation

HCAP includes any patient with a new onset pneumonia who1)was hospitalized in an acute care hospital for 2 or more days within 90 days of infection 2)resided in a long term care facility 3) received recent IV antibiotics therapy , chemotherapy, or wound care, within the past 30 days of the current infection or 4) attended a hospital or hemodialysis clinic .

Clinical features

The clinical manifestations are generally the same in VAP as in all other forms of pneumonia : fever, leukocytosis, increase in respiratory secretions, and pulmonary consolidation on physical examination, along with a new or changing radiographic infiltrate. Other clinical features may include tachypnea, tachycardia, worsening oxygenation, and increased minute ventilation

Pathogenic Mechanisms and Corresponding Prevention Strategies for Ventilator-Associated pneumonia

Pathogenic Mechanism Prevention Strategy Oropharyngeal colonization with pathogenic bacteria   Elimination of normal flora Avoidance of prolonged antibiotic courses   Large-volume oropharyngeal aspiration around time of intubation Short course of prophylactic antibiotics for comatose patients   Gastroesophageal reflux Postpyloric enteral feeding; avoidance of high gastric residuals, prokinetic agents    Bacterial overgrowth of stomach Prophylactic agents that raise gastric pH; selective decontamination of digestive tract with nonabsorbable antibiotics Cross-infection from other colonized patients Hand washing, especially with alcohol-based hand rub; intensive infection control education; isolation; proper cleaning of reusable equipment  Large-volume aspiration Endotracheal intubation; avoidance of sedation; decompression of small-bowel obstruction Microaspiration around endotracheal tube   Endotracheal intubation Noninvasive ventilation   Prolonged duration of ventilation Daily awakening from sedation,weaning protocols   Abnormal swallowing function Early percutaneous tracheostomy   Secretions pooled above endotracheal tube Head of bed elevated; continuous aspiration of subglottic secretions with specialized endotracheal tube; avoidance of reintubation; minimization of sedation and patient transport  Altered lower respiratory host defenses Tight glycemic control; lowering of hemoglobin transfusion threshold; specialized enteral feeding formula

Diagnosis

Clinical Pulmonary Infection Score (CPIS)

Criterion Score Fever (°C)   38.5 but 38.9 1   >39 or <36 2 Leukocytosis   <4000 or >11,000/L 1   Bands >50% 1 (additional) Oxygenation (mmHg)   PaO2/FIO2 <250 and no ARDS   2 Chest radiograph   Localized infiltrate 2   Patchy or diffuse infiltrate 1   Progression of infiltrate (no ARDS or CHF) 2 Tracheal aspirate   Moderate or heavy growth 1   Same morphology on Gram's stain 1 (additional) Maximal scorea  12

Treatment

Many studies have demonstrated higher mortality rates with inappropriate than with appropriate empirical antibiotic therapy. The key to appropriate antibiotic management of VAP is an appreciation of the patterns of resistance of the most likely pathogens in any given patient.

Empirical Antibiotic Treatment of Health Care–Associated pneumonia

Patients without Risk Factors for MDR Pathogens  Ceftriaxone (2 g IV q24h) or  Moxifloxacin (400 mg IV q24h), ciprofloxacin (400 mg IV q8h), or levofloxacin (750 mg IV q24h) or  Ampicillin/sulbactam (3 g IV q6h) or  Ertapenem (1 g IV q24h) Patients with Risk Factors for MDR Pathogens  1. A β-lactam:     Ceftazidime (2 g IV q8h) or cefepime (2 g IV q8–12h) or     Piperacillin/tazobactam (4.5 g IV q6h), imipenem (500 mg IV q6h or 1 g IV q8h), or meropenem (1 g IV q8h) plus 2. A second agent active against gram-negative bacterial pathogens:     Gentamicin or tobramycin (7 mg/kg IV q24h) or amikacin (20 mg/kg IV q24h) or     Ciprofloxacin (400 mg IV q8h) or levofloxacin (750 mg IV q24h) plus 3. An agent active against gram-positive bacteria pathogens:     Linezolid (600 mg IV q12h) or    Vancomycin (15 mg/kg, up to 1 g IV, q12h)

Supportive therapy

Supportive measures include the following (some were mentioned previously):

·         Analgesia and antipyretics

·         Chest physiotherapy

·         Intravenous fluids (and, conversely, diuretics) if indicated

·         Monitoring – Pulse oximetry with or without cardiac monitoring, as indicated

·         Oxygen supplementation

·         Positioning of the patient to minimize aspiration risk

·         Respiratory therapy, including treatment with bronchodilators and N –acetylcysteine

·         Suctioning and bronchial hygiene – Pulmonary toilet may include active suction of secretions, chest physiotherapy, positioning to promote dependent drainage, and incentive spirometry to enhance elimination of purulent sputum and to avoid atelectasis.

·         Ventilation with low tidal volumes (6 mL/kg of ideal body weight) in patients requiring mechanical ventilation secondary to bilateral pneumonia or acute respiratory distress syndrome (ARDS)^[16]

·         Systemic support may include proper hydration, nutrition, and mobilization to create a positive host milieu to fight infection and speed recovery. Early mobilization of patients, with encouragement to sit, stand, and walk when tolerated, speeds recovery.

ASPIRATION PNEUMONIA

It refers to the sequelae occurring from abnormal entry of secretions or substances in to the lower air way. It usually follows aspiration of material from the mouth or stomach in to the trachea and subsequently the lungs.

                          Three types of material cause 3 different pneumonic syndromes. Aspiration of gastric acid causes chemical pneumonia, which has also been called aspiration pneumonitis (Mendelson's syndrome)—although the former is an infectious process and the latter is a chemical injury, and both are managed differently. Aspiration of bacteria from oral and pharyngeal areas causes bacterial pneumonia, and aspiration of oil (eg, mineral oil or vegetable oil) causes exogenous lipoid pneumonia, a rare form of pneumonia. In addition, aspiration of a foreign body may cause an acute respiratory emergency and, in some cases, may predispose the patient to bacterial pneumonia.

Factors that predisposes to aspiration pneumonia

Conditions associated with altered or reduced consciousness, including any condition that reduces a patient's gag reflex, ability to maintain an airway, or both, increases the risk of aspiration pneumonia or pneumonitis. Such conditions are as follows:

·         Alcoholism

·         Drug overdose

·         Seizures

·         Stroke

·         Head trauma

·         General anesthesia

·         Intracranial mass lesion

Esophageal conditions associated with aspiration pneumonia include the following:

·         Dysphagia: Oropharyngeal dysphagia has been found in the majority of elderly patients  

·         Esophageal strictures

·         Esophageal neoplasm

·         Esophageal diverticula

·         Tracheoesophageal fistula

·         Gastroesophageal reflux disease

Neurologic disorders also predispose to aspiration pneumonia, such as the following:

·         Multiple sclerosis

·         Dementia

·         Parkinson disease

·         Myasthenia gravis

·         Pseudobulbar palsy

Aspiration pneumonia is also associated with the following mechanical conditions:

·         Nasogastric tube

·         Endotracheal intubation

·         Tracheostomy

·         Upper gastrointestinal endoscopy

·         Bronchoscopy

·         Gastrostomy or postpyloric feeding tubes

Chemical pneumonia

Chemical pneumonia is an unusual type of lung irritation. In chemical pneumonia, inflammation of lung tissueis from poisons or toxins. Only a small percentage of pneumonias are caused by chemicals.

The acidity of gastric contents results in chemical burns to the tracheobronchial tree involved in the aspiration. If the pH of the aspirated fluid is less than 2.5 and the volume of aspirate is greater than 0.3 mL/kg of body weight (20-25 mL in adults), it has a greater potential for causing chemical pneumonia. The initial chemical burn is followed by an inflammatory cellular reaction fueled by the release of potent cytokines, particularly tumor necrosis factor (TNF)–alpha and interleukin (IL)–8.

Factors that increase the severity of chemical pneumonia

·         Type and strength of chemical

·         Exposure environment: indoor, outdoor, heat, cold

·         Length of exposure: seconds, minutes, hours

·         Form of chemical: gas, vapor, particulate, liquid

·         Protective measures used to avoid exposure to chemicals

·         Prior medical condition

·         Age of the person

Signs and symptoms

·         Burning of the nose, eyes, lips, mouth, and throat

·         Dry cough

·         Wet cough producing clear, yellow, or green mucus

·         Cough producing blood or frothy pink matter in saliva

·         Nausea or abdominal pain

·         Chest pain

·         Shortness of breath

·         Painful breathing or pleuritis 

·         Headache

·         Flu symptoms

·         Weakness or a general ill feeling

·         Delirium or disorientation

Signs

·         Rapid pulse

·         Oral, nasal, or skin burns

·         Pale or cyanotic skin and lips

·         Heavy sweating

·         Altered thinking and reasoning skills

·         Unconsciousness

·         Swelling of eyes or tongue

·         Hoarse or muffled voice

·         Chemical odors on other areas of the body

·         Frothy spit from a cough

·         Fever

Bacterial pneumonia

Bacterial pneumonia most commonly occurs in individuals with chronically impaired airway defense mechanisms, such as gag reflex, coughing, ciliary movement, and immune mechanisms, all of which aid in removing infectious material from the lower airways.

This syndrome caused by aspiration can occur in the community or in the hospital (ie, nosocomial). In both situations, anaerobic organisms alone or in combination with aerobic and/or microaerophilic organisms play a role. In anaerobic pneumonia, the pathogenesis is related to the large volume of aspirated anaerobes (eg, as in persons with poor dentition, poor oral care, and periodontal disease) and to host factors (eg, as in alcoholism) that suppress cough, mucociliary clearance, and phagocytic efficiency, both of which increase the bacterial burden of oropharyngeal secretions.

Nosocomial bacterial pneumonia caused by aspiration is common, and the major pathogens involved are hospital-acquired florae through oropharyngeal colonization (eg, enteric gram-negative bacteria, staphylococci). Colonization of gram-negative organisms in the oropharynx, sedation, and intubation of the patient's airways are important pathogenetic factors in nosocomial pneumonia.

Clinical presentation

 The presentation of bacterial aspiration pneumonia is similar to that of community-acquired pneumonia (CAP) and may include nonspecific symptoms including headache, nausea/vomiting, anorexia, weight loss. The onset of illness may be subacute or insidious, with the symptoms manifesting in days to weeks when anaerobic organisms are the pathogens.

Diagnostic features

Ø  ABG and mixed venous analysis

ABG analysis is used to assess oxygenation and pH status and adds information to guiding oxygen supplementation. The results demonstrate acute hypoxemia in patients with chemical pneumonia and normal to low partial pressure of carbon dioxide with respiratory alkalosis. The lactate level (often included with blood gases) can be used as an early marker of severe sepsis or septic shock.

Ø  Basic metabolic panel

Serum electrolyte, blood urea nitrogen (BUN), and creatinine levels can be used to assess fluid status and the need for intravenous hydration. This is especially important in patients who present with fever, vomiting, or diarrhea who may have significant fluid loss.

Serum BUN and creatinine levels can also be used to assess renal function in order to appropriately dose antibiotics. In addition, these values can be used to assess end-organ damage in patients who present with sepsis or septic shock.

The complete blood cell (CBC) count may reveal an elevated white blood cell (WBC) count, increased neutrophils, anemia, and thrombocytosis in patients with bacterial pneumonia caused by anaerobic bacteria. Elevated WBC count and increased neutrophils may also be present in patients with chemical pneumonia

                                                                                                                                                            Next Section: Sputum Gram Stain, 

Ø  Sputu m gram staining microscopy and culture

Ø  Blood cultures

Use blood cultures as a baseline screening for bacteremia

Ø  Chest radiography

Chest radiographic findings in patients with chemical pneumonia are characterized by the presence of infiltrates, predominantly the alveolar type, in one or both lower lobes, or diffuse simulation of the appearance of pulmonary edema. Volume loss in any lobar area suggests obstruction (eg, by aspirated food particles or other foreign bodies) in the bronchus.

Chest radiographic findings in patients with anaerobic bacterial pneumonia typically demonstrate an infiltrate with or without cavitation in one of the dependent segments of the lungs (ie, posterior segments of the upper lobes, superior segments of the lower lobes). Lucency within the infiltrate suggests a necrotizing pneumonia. Air-fluid levels within a circumscribed infiltrate (density) indicate a lung abscess or a bronchopleural fistula. Costophrenic angle blunting and the presence of a meniscus are signs of a parapneumonic pleural effusion.

Treatment

Prehospital management

Prehospital care should focus on stabilizing the patient's airway, breathing, and circulation. In patients found with signs of gastric aspiration (ie, vomitus) suctioning of the upper airway may remove a significant amount of aspirate or potential aspirate.

Intubation should be considered in any patient who is unable to protect his or her airway. The ability of paramedics to provide this intervention depends on the level of their training. In addition, emergency  intubation may choose to intubate patients with poor gag reflex before aspiration.

Other measures include the following:

·         Oxygen supplementation

·         Cardiac monitoring and pulse oximetry

·         Intravenous (IV) catheter placement and IV fluids, as indicated

Emergency department

Ø  Emergency department care should start with stabilizing the patient's airway, breathing, and circulation. Oropharyngeal/tracheal suctioning may be indicated to further remove aspirate.

Ø  Reassess the need for intubation on a frequent basis depending on the patient’s oxygenation, the patient's mental status, signs of increased work of breathing, or impending respiratory failure.

Ø  Continue supplemental oxygenation as needed, as well as continue cardiac monitoring and pulse oximetry and provide continued supportive care with intravenous fluids and electrolyte replacement.

Inpatient management

Patients with aspiration pneumonia, both chemical pneumonia (chemical pneumonia) and bacterial pneumonia (bacterial pneumonia), need inpatient care for several reasons, including the acuity of illness, host factors, and the uncertain course and prognosis of aspiration pneumonia.

Admit patients with severe hemodynamic compromise and/or persistent respiratory distress to the intensive care unit (ICU). Intubated and ventilated patients must be transferred to a hospital with an ICU, as well as patients with signs or symptoms indicating severe sepsis or septic shock.

If the patient's respiratory status is stabilized, admit the patient to a general-care floor.

Antibiotic therapy

Ø  In patients without a toxic appearance, the antibiotic chosen should cover typical community-acquired pathogens. Ceftriaxone plus azithromycin, levofloxacin, ormoxifloxacin are appropriate choices.

Ø  In patients with a toxic appearance or who were recently hospitalized, although community-acquired pathogens are still the most common, gram-negative bacteria including Pseudomonas aeruginosa and Klebsiella pneumoniae as well as methicillin-resistant Staphylococcus aureus (MRSA) must be covered.Piperacillin/tazobactam or imipenem/cilastatin plus vancomycin would be appropriate.

Ø  Telavancin is indicated for hospital-acquired pneumonia, including ventilator-associated bacterial pneumonia caused by susceptible isolates ofStaphylococcus aureus, including methicillin-susceptible and resistant isolates, when alternative treatments are not suitable.

Ø  The presence of chronic aspiration risks, putriddischarge, indolent hospital course, and necrotizing pneumonia should raise the suspicion for anaerobic bacteria involvement and prompt consideration of adding clindamycin to the antibiotic regimen.

Ø  Treatment of individuals with chemical pneumonia should include maintenance of the airways and clearance of secretions with tracheal suctioning

Ø  Oxygen supplementation

Ø  Mechanical ventilation if the patient is unable to maintain adequate oxygenation, early use of positive end-expiratory pressure (PEEP)

Ø  Administration of intravenous (IV) fluids.

Corticosteroid

Historically corticosteroids have been used in the treatment of aspiration pneumonitis, but randomized control studies have been unable to demonstrate a benefit to using high-dose corticosteroids.

Post discharge management

Patients who recover from chemical pneumonia generally do not require additional outpatient care, except for adherence to measures to prevent further aspiration episodes.

Unlike chemical pneumonia, anaerobic bacterial infections require prolonged antibiotic treatment; therefore, outpatient treatment is necessary. Patients can be discharged from the hospital after clinical improvement and stability (eg, no fever, no leucocytosis, resolution of hypoxemia) and radiographic improvement (eg, decreased infiltrate or cavity size, no pleural effusion).

In cases with lung abscess, oral antibiotic therapy (ie, clindamycin) is continued for several weeks

Prevention of aspiration pneumonia

Ø  Position patients with altered consciousness in a semirecumbent position with the head of the bed at a 30-45° angle. This reduces the risk of aspiration leading to pneumonia.

Ø  For patients with known swallowing dysfunction (eg, dysphagia and/or a poor gag reflex), helpful compensatory techniques to reduce aspiration include a soft diet reducing the bite size, keeping the chin tucked and the head turned, and repeated swallowing.

Ø  Use of nonparticulate antacids and histamine 2 (H2) blockers to reduce gastric acidity has been a common practice; however, this is very questionable, because gastric acid suppression and consequent loss of the acid barrier to bacteria is associated with a higher rate of pneumonia.

Ø  Use antiemetics to reduce lower esophageal sphincter pressure. Before starting enteral tube feeding, confirm the tip location radiographically. Check residual gastric volume regularly. For those on bolus tube, feeding residual should not exceed 150 mL before the next bolus feed.

Ø  Avoid oversedating patients.

Prognosis

The mortality rate for aspiration pneumonitis complicated by empyema is approximately 20%; the mortality for uncomplicated pneumonitis is approximately 5%. An animal model study demonstrated that mice with aspiration pneumonitis were more susceptible to subsequent respiratory infection with certain pathogens.

NURSING CARE PLAN

Nursing Interventions:

In effective airway clearance related to inflammation, accumulation of secretion
monitor  respiratory status every 2 hours, assess the increase in respiratory status and abnormal breath sounds.

1.      Perform percussion, vibration and postural drainage every 4-6 hours.

2.      Give oxygen therapy  according to the program.

3.      Help patients cough up secretions / suctioning.

4.      Give a comfortable position that allows the patient to breathe.

5.      Create a comfortable environment so that patients can sleep.

6.      Monitor blood gas analysis to assess respiratory status.

7.      Give drink enough.

8.      Provide sputum for culture /sensitivity test.

9.      Collaboration of antibiotics and other drugs according to the program.

2. Impaired gas exchange related to changes in alveolar capillary membrane.

Goal: Patients showed improved ventilation, optimal gas exchange and tissue oxygenation adequately.

Nursing Interventions:

1.      Observation of level of consciousness, respiratory status, cyanosis signs every 2 hours.

2.      Give Fowler position / semi-Fowler.

3.      Give oxygen according to the program.

4.      Monitor blood gas analysis.

5.      Create an environment that is quiet and patient comfort.

6.      Prevent the occurrence of fatigue in patients.

3. Fluid Volume Deficit related to inadequate oral intake, fever, tachypnoea.

Goal: Patient will maintain normal body fluids

Nursing Interventions:

1.      Record intake and out put of fluids. Encourage the mother to continue giving fluids orally and avoid the condensed milk / drink cold or cough inducing.

2.      Monitor fluid balance in the mucous membranes, skin turgor, rapid pulse, decreased consciousness, vital signs.

3.      Keep drip infusion accuracy according to the program.

4.      Perform oral hygeine

5.      Activity intolerance related to decreased blood oxygen levels.

Goal :
Patients can do activities based on conditions.

Interventions :

·         Assess the patient's physical tolerance.

·         Assist patients in activities of daily activities.

·         Provide age-appropriate games that patients with activities that do not spend a lot of energy, match the activity with the condition.

·         Give oxygenation by program.

·         Give the energy needs.