2. EPIDEMIOLOGY AND ETIOLOGY
ā¢ Acute viral infection
ā¢ Prevelent in children
ā¢ Peaks during the winter months
ā¢ more common in males than in females
3. EPIDEMIOLOGY AND ETIOLOGY
ā¢ Respiratory syncytial virus (RSV) is the most
common cause ā 70%
ā¢ Parainfluenza viruses type 3 (10%ā15%)
ā¢ Type 1 (5%ā10%)
ā¢ type 2 (1%ā5%) are the second most common
pathogens
ā¢ MPV
4. CP
ā¢ Prodrome with irritability, restlessness, and
mild fever
ā¢ Cough and coryza
ā¢ Noisy breathing, and increased respiratory
rate as symptoms progress
5. CP
ā¢ As a result of limited oral intake because of
coughing combined with fever, vomiting, and
diarrhea, infants frequently are dehydrated
ā¢ The increased work of breathing an tachypnea
most likely further increases fluid loss. In most
cases, this clinical picture persists between 3
and 7 days
6. CP
ā¢ Although the hospital course of bronchiolitic
children often is variable, substantial clinical
improvement usually is observed within the
first 2 days, with gradual improvement and
complete resolution requiring 4 to 8 weeks
7. Physical examination
ā¢ Tachycardia and increased respiratory rate
ā¢ Wheezing
ā¢ Mild conjunctivitis in one third of patients
ā¢ Otitis media in 5%ā10% of patients
8. Physical examination
ā¢ The proliferation of commercial enzyme-linked
immunosorbent assays and fluorescent
antibody staining techniques of
nasopharyngeal secretions has increased the
ability to identify viral antigens within several
hours
11. Bronchodilator therapy
ā¢ Nebulized epinephrine seems to be more
efficacious than salbutamol in hospitalized
patients with bronchiolitis
ā¢ Corticosteroids have failed to reveal any
therapeutic benefit (or harmful effect) when
administered to bronchiolitic infants
12. Anti-viral therapy
ā¢ Most experts recommend reserving use of
ribavirin for severely ill patients, especially
those with chronic lung disease (particularly
bronchopulmonary dysplasia), congenital
heart disease, prematurity, and
immunodeficiency
13. Ribavirin
ā¢ Use of the drug requires special equipment
(small-particle aerosol generator) and
specially trained personnel for administration
via oxygen
ā¢ Special care must be taken to avoid drug
particle deposition and the resulting clogging
of respiratory tubing and valves in mechanical
ventilators
14. Prophylaxis Need
ā¢ In infants with underlying pulmonary or
cardiovascular disease, prophylaxis against
RSV may be warranted
15. Prophylaxis
ā¢ When administered monthly during the RSV
season, both RSV immune globulin and
Palivizumab (a monoclonal antibody for RSV) may
decrease the number of RSV episodes and the
need for hospitalization
ā¢ Between the two, palivizumab appears to be
preferred, given its ease of administration, lack of
administration-related adverse effects, and
noninterference with select immunizations
17. What is it?
ā¢ Pneumonia: "inflammation of the lungsā
ā¢ Pneumon: lung
ā¢ Probably by influence of pnein: to breathe
ā¢ Also known: Pneumonitis
18. Introduction
ā¢ Pneumonia is an infection of the pulmonary
parenchyma
ā¢ Despite being the cause of significant
morbidity and mortality, pneumonia is often
misdiagnosed, mistreated, and
underestimated
19. Introduction
ā¢ Pneumonia is defined as acute inflammation of
the lung parenchyma distal to the terminal
bronchioles
ā¢ The terms āpneumoniaā and āpneumonitisā are
often used synonymously for inflammation of the
lungs
ā¢ āconsolidationā (meaning solidification) is the
term used for gross and radiologic appearance of
the lungs in pneumonia
20. Classification: Microbial Involvement
1. Infectious pneumonia ā this can be further
categorized according to the causative
microorganisms
2. Non-infectious pneumonia ā this is caused
by a number of mechanisms that trigger
inflammation
25. Noninfectious Pneumonia
ā¢ Chemical pneumonia: Inhalation of toxic
gases or fumes
ā¢ Aspiration pneumonia:
ā¢ This is chemical or infectious pneumonia that
is a result of the following entering the lung :
ā Gastric (stomach) contents
ā Aspirated fluids
27. Setting of Infection
A. Community Acquired Pneumonia (CAP)
B. Hospital Care Associated Pneumonia (HCAP)
1. Hospital-acquired pneumonia (HAP)
2. Ventilator-associated pneumonia (VAP).
28.
29. Epidemiology
ā¢ One of the most common disease
ā¢ May lead to death
ā¢ It occurs in persons of all ages, although the
clinical manifestations are most severe in the
very young, the elderly, and the chronically ill
30. PATHOGENESIS
ā¢ The microorganisms gain entry into the lungs by
one of the following four routes:
1. Inhalation of the microbes present in the air
2. Aspiration of organisms from the nasopharynx
or oropharynx
3. Haematogenous spread from a distant focus of
infection
4. Direct spread from an adjoining site of infection
31. Failure of defence mechanism
1. Altered consciousness
2. Depressed cough and glottic reflexes
3. Impaired mucociliary transport
4. Impaired alveolar macrophage function
5. Endobronchial obstruction
6. Leucocyte dysfunctions
32. Pathologic stages
ā¢ Laennecās original description divides lobar
pneumonia into 4 sequential pathologic
phases
ā¢ Stage of congestion (initial phase)
ā¢ Red hepatisation (early consolidation)
ā¢ Grey hepatisation (late consolidation)
ā¢ Resolution
33. CP
ā¢ Abrupt onset of fever, chills, dyspnea, and
productive cough
ā¢ Rust-colored sputum or hemoptysis
ā¢ Pleuritic chest pain
34. Physical examination
ā¢ Tachypnea and tachycardia
ā¢ Dullness to percussion
ā¢ Increased tactile fremitus
ā¢ Inspiratory crackles during lung expansion
ā¢ Chest radiograph
36. General treatment approach
ā¢ Oxygen or, in severe cases, mechanical
ventilation and fluid resuscitation should be
provided as necessary
ā¢ humidified oxygen for hypoxemia,
administration of bronchodilators (albuterol)
when bronchospasm is present, and chest
physiotherapy
37. General treatment approach
ā¢ Additional therapeutic adjuncts include
adequate hydration (intravenously if
necessary), optimal nutritional support, and
control of fever
ā¢ Selection of an appropriate antimicrobial must
be made based on the patientās probable or
documented microbiology, distribution in the
respiratory tract, side effects, and cost
38. Antibiotic Concentrations
ā¢ Antibiotic concentrations in respiratory
secretions in excess of the pathogen MIC are
necessary for successful treatment of
pulmonary Lower Respiratory Tract Infections
infections
39. Antibiotic Concentrations
ā¢ The aminoglycosides are large polar molecules that
diffuse poorly into tissue and respiratory secretions;
however, with increasing concentrations obtained
with once-daily dosing, increased target-tissue
concentrations would be expected with increasing
individual doses
ā¢ Substantial clinical experience supports this practice
for treating pulmonary infections with certain
antibiotics (e.g., concentration-dependent
antimicrobials)
40. Selection of Antimicrobial Agents
ā¢ Treatment of bacterial pneumonia, like the
treatment of most infectious diseases, initially
involves the empirical use of a relatively
broad-spectrum antibiotic
ā¢ Followed by Definite Therapy
41. Factors for predicting pathogen
ā¢ Patient age
ā¢ Previous and current medication history
ā¢ Underlying disease
ā¢ Major organ function
ā¢ Present clinical status
ā¢ Multiple Antibiotic alternatives available
42.
43.
44.
45. Community-Acquired Pneumonia
ā¢ The bacterial causes are relatively constant, even
across geographic areas and patient populations
ā¢ Unfortunately, pathogen resistance to standard
antimicrobials is increasing (e.g., penicillin-
resistant pneumococci), necessitating careful
attention by the clinician to local and regional
bacterial susceptibility patterns
46. Community-Acquired Pneumonia
ā¢ Thus, whenever possible, initial therapy
should be based on presumed antibacterial
susceptibility and consist of older, less-
expensive agents, with newer and more
expensive antibiotics reserved for
unresponsive illness or special circumstances
47. Starting of Antimicrobials
ā¢ Antimicrobial therapy should be initiated in
hospitalized patients with acute pneumonia
within 8 hours of admission
ā¢ Because an increase in mortality has been
demonstrated when therapy was delayed
beyond 8 hours of admission.
48. Nosocomial Pneumonia
ā¢ Ironically, some Ī²-lactam antibiotics, which
were developed to treat multiple-antibioticā
resistant hospitalacquired organisms, can
themselves induce broad-spectrum bacterial
Ī²- lactamases and thereby lead to even
greater problems with resistance
49. Nosocomial Pneumonia
ā¢ Newer antibiotics developed for treatment of
resistant, hospital-acquired pathogens are
costly, so their use must be moderated to
some extent in an era where capitated
hospital costs and mandated budget cuts will
not tolerate careless antibiotic use.
50. Severe Acute Respiratory Syndrome
ā¢ Treatment of SARS involves primarily supportive
care and procedures to prevent transmission to
othersOwing to the uncertainty associated with
the diagnosis of SARS, empirical therapy with
broad-spectrum antibiotics should be used
ā¢ To date, fluoroquinolones (e.g., moxifloxacin,
levofloxacin) or macrolides/azalides (e.g.,
erythromycin, clarithromycin, azithromycin)
typically have been used
51. Severe Acute Respiratory Syndrome
ā¢ Although its efficacy is unproven, ribavirin also
has been used to treat patients
ā¢ Owing to the potential benefit of
corticosteroids in the presence of progressive
pulmonary disease, methylprednisolone has
been used in doses ranging from 80 to 500
mg/day
52. Avian Influenza
ā¢ Treatment of avian influenza is primarily supportive, with
the majority of patients requiring aggressive oxygen
therapy and intensive care monitoring
ā¢ Due to observed resistance with amantadine, the
neuraminidase inhibitors are the recommended treatment
of avian influenza, with oseltamivir being the preferred
agent
ā¢ For optimal efficacy, treatment should be initiated within
48 hours of the first sign of infection. Of note, there is
concern regarding oseltamivir, with a resistant A/H5N1
isolate identified in Vietnam