CHILDHOOD PNUEMONIA

FOR PC-I
Pneumonia
Definition
 Pneumonia inflamation of parenchymal structures of the lung
 Infectious vs non infectious

Epidemology
 Main cause of childhood morbidity and mortality( particularly in less than five years)
 With an estimated 146–159 million new episodes per yr in developing countries
 pneumonia is estimated to cause approximately 4 million deaths among children worldwide.
 developed countries is estimated to be 0.026 episodes per child-year compared to 0.280
episodes per child-year in developing countries.
 up to 10 times higher in developing countries
Etiology
 Streptococcus pneumoniae (pneumococcus) is the most common bacterial
pathogen in children 3 wk to 4 yr of age
 Mycoplasma pneumoniae and - Chlamydophila pneumoniae are the most
frequent pathogens in children 5 yr and older
 other include group A streptococcus (Streptococcus pyogenes ), Staphylococcus
aureus, H. influenzae type b , nontypeable H. influenza and Moraxella
catarrhalis
 Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus
are the major causes of hospitalization and death
 VIRAL CAUSE: Viruses can be detected in 40–80% of children with pneumonia
using molecular diagnostic methods
 Viruses are more commonly identified in children younger than five years
 Respiratory syncytial virus (RSV) is the most common
 Other viral causes include:
 Influenza A and B viruses, Parainfluenza viruses, usually type 3,
Adenovirus, Human metapneumovirus and rhinovirus
 "afebrile pneumonia of infancy" is classically caused by Chlamydia
trachomatis
 other agents, such as CMV, Mycoplasma hominis , and Ureaplasma
urealyticum , also are implicated
 Aspiration pneumonia may be caused by anaerobic oral flora, including:
 Anaerobic streptococci (eg, Peptostreptococcus )
 Fusobacterium spp
 Bacteroides spp
 Prevotella melaninogenica
 Nosocomial bacterial pneumonia is usually caused by gram-negative bacilli or S.
aureus
 In addition, during the winter respiratory viral season, nosocomial pneumonia
caused by RSV, parainfluenza, and influenza viruses
 Risk factors predispose to pneumonia and contribute to increasing severity includes:
 Male sex, with a male-female ratio of 1.25:1 to 2:1
 Lower socioeconomic
 environmental crowding
 secondary infections from school aged family member
 Cigarette smoke(exposure), alcohol
 Congenital heart disease
 Bronchopulmonary dysplasia
 Cystic fibrosis
 Asthma
 Sickle cell disease
 Neuromuscular disorders, especially those associated with a depressed consciousness
 Some gastrointestinal disorders (eg, gastroesophageal reflux, tracheoesophageal fistula)
 Congenital and acquired immunodeficiency disorders
 Unvaccination
PATHOGENESIS  
 Pneumonia occurs because of an impairment of host defenses, invasion by a virulent
organism, and/or invasion by an overwhelming inoculum
 In the typical scenario, pneumonia follows URT illness that permits invasion of the lower
respiratory tract by bacteria
 The agents that cause LRTI are most often transmitted by droplet spread
 Most typical bacterial pneumonias are the result of initial colonization of the
nasopharynx followed by aspiration or inhalation of organisms
 The viral agents that cause pneumonia proliferate and spread by contiguity to involve
lower and more distal portions of the respiratory tract
 Viral infection of the respiratory tract can also predispose to secondary bacterial
infection by
 disturbing normal host defense mechanisms,
 altering secretions, and
 modifying the bacterial flora.
 The lower respiratory tract is normally kept sterile by physiologic
defense mechanisms, including
 mucociliary clearance,
 the properties of normal secretions such as secretory IgA, and
 clearing of the airway by coughing.
 Immunologic defense mechanisms of the lung that limit invasion by
pathogenic organisms include
 macrophages that are present in alveoli and bronchioles,
 secretory IgA, and
 other immunoglobulins.
 invasion of the lower respiratory tract by bacteria, viruses, or other
pathogens that trigger the immune response and produce inflammation.
 The lower respiratory tract air spaces fill with white blood cells (WBC),
fluid, and cellular debris.
 This process reduces lung compliance, increases resistance, obstructs
smaller airways, and may result in collapse of distal air spaces, air
trapping, and altered ventilation-perfusion relationships
 The small caliber of airways in young infants makes such patients
particularly susceptible to severe infection
 PATHOLOGY:
 Edema
 Red hepatization phase
 Gray hepatization
 Patterns of pneumonia  — There are five patterns of bacterial pneumonia:
 Lobar pneumonia – involvement of a single lobe or segment of a lobe; this is the
classic pattern of S. pneumoniae pneumonia
 Bronchopneumonia – primary involvement of airways and surrounding interstitium;
this pattern is sometimes seen in Streptococcus pyogenes and Staphylococcus aureus
pneumonia
 Necrotizing pneumonia associated with aspiration pneumonia and pneumonia
resulting from S. pneumoniae , S. pyogenes , and S. aureus )
 Caseating granuloma as in tuberculosis pneumonia)
 Interstitial and peribronchiolar with secondary parenchymal infiltration – this
pattern typically occurs when a severe viral pneumonia is complicated by bacterial
pneumonia
 There are two patterns of viral pneumonia:
 Interstitial pneumonitis
 Parenchymal infection with viral inclusions
Clinical Manifestations
 pneumonias are often preceded by several days of symptoms of an URTI,
typically rhinitis and cough.
 fever is nonspecific and variably present
 temperatures are generally lower for viral than in bacterial pneumonia.
 Fever may be the only sign of occult pneumonia
 Cough may be initial complaint
 chest pain, shortness of breath, difficulty breathing
 Bacterial pneumonia in adults and older children typically begins suddenly with
a shaking chill followed by a high fever, cough, and chest pain
 Other associated symptoms…..
Physical examination
 fever
 Tachypnea is the most consistent clinical manifestation of pneumonia.
 Increased work of breathing accompanied by intercostal, subcostal, and
suprasternal retractions, nasal flaring, and use of accessory muscles is common.
 cyanosis and respiratory fatigue, especially in infants.
 Auscultation of the chest may reveal crackles(crepitations) and wheezing(atypical
bacteria and viruses)
 Consolidation:-Dullness to percussion, Tactile fremitus, Decreased breath sounds,
Bronchial breath sounds, Bronchophony
 Findings suggestive of pleural effusion include chest pain with splinting, dullness to
percussion, distant breath sounds, and a pleural friction rub
 It is often not possible to distinguish viral pneumonia from bacterial
Clinical features of severe pneumonia:
 RR >70 breaths/minute for infants; RR >50 breaths/minute for older children
 Moderate/severe suprasternal, intercostal, or subcostal retractions
 Severe difficulty breathing (≥12 months)
 Grunting
 Nasal flaring
 Apnea
 Significant shortness of breath
 Cyanosis
 Altered mental status
 Hypoxemia
 Not feeding (infants) or signs of dehydration (older children)
Diagnosis
 LABORATORY EVALUATION
 CBC usually is not necessary for children with mild lower respiratory tract infection
 White blood cell (WBC) count <15,000/microL suggests a nonbacterial etiology
 WBC count >15,000/microL is suggestive of pyogenic bacterial disease
 Acute phase reactants, such as the erythrocyte sedimentation rate, C-reactive
protein (CRP), and serum procalcitonin (PCT)
 Clue to distinguish between viral and bacterial etiologies and may be helpful in following
the disease course, response to therapy, and in determining when therapy can be
discontinued
 The definitive diagnosis of a viral infection rests on the - isolation of a virus or
detection of the viral genome or antigen in respiratory tract secretions
 Serology--- viral, for epidemologic
 The definitive diagnosis of a bacterial infection requires isolation of an organism
from the blood, pleural fluid, or lung.
 Blood culture results are positive in only 10% of children with pneumococcal
pneumonia, increases to 30 to 40 percent in patients with a parapneumonic
effusion or empyema
 Sputum cultures: ‘’>25 neutrophils and <10 squamous epithelial cells per low-
power field’’
 Pleural fluid cultures
 Cold agglutinins at titers >1: 64 are found in the blood in ≈50% of patients with
M. pneumoniae infections
 Acute infection caused by M. pneumoniae can be diagnosed on the basis of a
positive PCR test result or seroconversion in an IgG assay
 Invasive procedures may be necessary to obtain lower respiratory tract
specimens for culture
 RADIOLOGIC EVALUATION  — The presence of an infiltrate on chest radiograph is
often used to define pneumonia
 Indications include:
 Severe disease
 Confirmation of the diagnosis when clinical findings are inconclusive
 Exclusion of alternate explanations for respiratory distress
 Assessment of complications, particularly in children whose pneumonia is prolonged
and unresponsive to antimicrobial therapy
 Exclusion of pneumonia in young children (3 to 36 months) with fever >39ºC and
leukocytosis (≥20,000 white blood cell [WBC]/microL) and older children (<10 years)
with fever >38ºC, cough, and leukocytosis (≥15,000 WBC/microL)
 Radiographic findings are poor indicators of the etiologic diagnosis and must be
used in conjunction with other clinical features
Treatment
 Treatment of suspected bacterial pneumonia is based on the presumptive
cause and the age and clinical appearance of the child.
 For mildly ill children who do not require hospitalization, amoxicillin is
recommended
 Therapeutic alternatives include
- cefuroxime axetil and
- amoxicillin/clavulanate.
 For school-aged children and in children in whom infection with M.
pneumoniae or C. pneumoniae is suggested, a macrolide antibiotic such as
azithromycin is an appropriate choice.
 In adolescents, a respiratory fluoroquinolone (levofloxacin, moxifloxacin,
gemifloxacin) may be considered as an alternative
 The empiric treatment of suspected bacterial pneumonia in a hospitalized child
requires an approach based on the clinical manifestations at the time of
presentation.
 Parenteral cefotaxime or ceftriaxone is the mainstay of therapy when bacterial
pneumonia is suggested.
 If clinical features suggest staphylococcal pneumonia (pneumatoceles,
empyema), initial antimicrobial therapy should also include vancomycin or
clindamycin.
 Supportive care includes ensuring adequate antipyresis, analgesia, respiratory
support, and hydration
 If viral pneumonia is suspected, it is reasonable to withhold antibiotic therapy,
especially for those patients who are mildly ill
 Up to 30% of patients with known viral infection may have coexisting bacterial
pathogens
 DISCHARGE CRITERIA includes:
I. Improvement of vital signs
II. Ability to maintain adequate fluid and nutrition orally
III. Ability to maintain oxygen saturation ≥90 percent in room air
IV. Improvement in respiratory distress
V. Overall clinical improvement including level of activity, appetite, and decreased fever for at
least 12 to 24 hours
VI. Stable and/or baseline mental status
VII. Parents’ ability to administer and child’s ability to comply with home antibiotic regimen
VIII. Safe and compliant home environment

 The respiratory status will improve within 48 to 72 hours

 fevers may persist for several days after initiation of appropriate therapy
 They continue to cough for several weeks and have moderate dyspnea on exertion for two to
three months
Prognosis
 Typically, patients with uncomplicated community-acquired bacterial
pneumonia show response to therapy within 48-96 hr of initiation of antibiotics
 Radiographic evidence of improvement lags substantially behind clinical
improvement
 A repeat chest radiograph is the 1st step in determining the reason for delay in
response to treatment
 Mortality from community-acquired pneumonia in developed nations is rare,
and most children with pneumonia do not experience long-term pulmonary
sequelae
 Some data suggest that up to 45% of children have symptoms of asthma 5 yr
after hospitalization for pneumonia
Causes of slowly resolving pneumonia:
(1) complications, such as empyema;
(2) bacterial resistance;
(3) nonbacterial etiologies such as viruses and aspiration of foreign bodies or
food;
(4) bronchial obstruction from endobronchial lesions, foreign body, or mucous
plugs;
(5) pre-existing diseases such as immunodeficiencies, ciliary dyskinesia, cystic
fibrosis, pulmonary sequestration, or cystic adenomatoid malformation; and
(6) other noninfectious causes
Complications
 Complications of pneumonia are usually the result of :
a. direct spread of bacterial infection within the thoracic cavity (pleural effusion,
empyema, pericarditis) or
b. bacteremia and hematologic spread (Meningitis, suppurative arthritis, and osteomyelitis)

 S. aureus, S. pneumoniae, and S. pyogenes are the most common causes of

parapneumonic effusions and of empyema

 PREVENTION
 Adequate nutrition
 Vaccination
 Vitamin A supplementation
Parapneumonic Effusion and Empyema
DEFINITIONS
 Empyema
 Empyema is defined as pus within the pleural space.
 In its development, pleural fluid passes through stages of increasing host-defense
activity and bacterial invasion.
 Not all infected pleural effusions progress to empyema
 Parapneumonic Effusion
 Any pleural effusion associated with bacterial pneumonia, lung abscess or
bronchiectasis is a PPE
 Complicated Parapneumonic Effusion
 Complicated PPEs are conditions that do not resolve without therapeutic
thoracentesis or tube throracostomy. Some of these are purulent (empyemas),
while others have non-purulent pleural fluid
PATHOGENESIS
 There are three distinct pathophysiological stages in PPE, reflecting the changing
physiology within the pleural space.
 The distinctions between the stages are not sharply demarcated.
 There are different characteristics of pleural fluid seen during the different stages of PPE
1, Exudative Stage
 This stage is characterized by accumulation of sterile fluid within the pleural space.
 This is in response to inflammation induced by bacterial infection within the lung
parenchyma and the pleural membranes.
 The pleural fluid at this stage is a combination of interstitial tissue fluid and the
microvascular exudate, characterized by low Lactate Dehydrogenase (LDH), normal
glucose levels, and is not infected.
 If appropriate antibiotic therapy is instituted, the effusion is likely to resolve and
intercostal drainage is not required
2, Fibrinopurulent Stage
 The fibrinopurulent stage occurs in response to bacterial invasion, usually as a
consequence of inadequate or inappropriate therapy.
 Early on, there is increase in pleural fluid which contains polymorphs, bacteria and
cellular debris.
 Later, there is formation of fibrin clots and fibrinous septae due to clotting factors from
the serum entering the pleural space.
 This results in a heavily loculated pleural space that may be resistant to drainage with a
single intercostal tube.
 As infection progresses, the pleural fluid pH and glucose levels reduce and LDH level goes
up.
 Pus is formed by the lysis of bacteria and inflammatory cells
3, Organizational Stage
 The last stage is characterized by fibroblast proliferation and deposition of
fibrous tissue on both the visceral and the parietal pleural membranes—the
inelastic “pleural peel”.
 This results in restriction of lung expansion and impairment of gas exchange.
 If untreated, there is potential for chronic infection resulting in penetration of
fluid into the chest wall (empyema necessitans) or into the lung, resulting in a
bronchopleural fistula.
 The further course after organization is variable, some individuals undergo
spontaneous healing with resolution of pleural thickening, others are left with
“pleural peel”
BACTERIOLOGY
 the most commonly isolated organisms;
 Strep. pneumoniae,
 Strep. hemolyticus,
 Staph. aureus.
 In children, bacteriology is slightly different than in adults H. influenzae
being the most commonly isolated aerobe, the anaerobes being much less
frequent
 Of hospital-acquired cases, the commonest aerobe;
 Staphylococcus
 Gram negative organisms and
 Streptococcus
 CLINICAL FEATURES AND DIAGNOSIS
 Patients with aerobic pleural infection usually present with features of
pneumonia with an acute febrile illness, cough, purulent sputum and dyspnea.
 Pleuritic chest pain (due to parietal pleural involvement) is present in around 60%
of patients.
 Absence of pain does not exclude the diagnosis of pleural infection.
 Anaerobic infections present often in an indolent manner with weight loss,
 anorexia and malaise There are no clinical criteria that could distinguish between
pneumonia with or without PPE.
 Therefore, PPE should be considered while evaluating all patients with
pneumonia, particularly those who are unresponsive to antimicrobial therapy.
 Radiological Investigations
 Chest radiograph (PA view) can detect significant effusion and is often the only required
imaging for its detection.
 Effusion may be free or loculated, may show evidence of air-fluid level.
 Empyema may give the appearance of pleural mass or tumor within the lung, when the
collection occurs within a fissure.
 In resource limited settings, blunting of the costophrenic angle on a lateral chest
radiograph or obscuration of the dome of the diaphragm are considered sufficient to detect
the presence of pleural fluid.
 Decubitus views may complement the information obtained from the erect chest
radiographs
 In the lateral decubitus film, the amount of fluid can be roughly quantitated by measuring
the distance between the chest wall and the lower part of the adjacent lung.
 If the length is less than 10 mm, the effusion is deemed to be too small to be clinically
significant. Such effusions resolve with antibiotics alone.
 Computed Tomography (CT) scan of the chest is used to detect and
quantitate minimal effusion.
 CT evidence of pleural thickening is present in 80-100% of the empyemas, so, its
presence would favor this diagnosis,
 “Split pleura sign” on contrast CT enhancement of visceral and parietal pleura
differentiates empyema from a peripherally situated lung abscess
 Ultrasonography is an excellent method to assess pleural effusion.
 It can also help to quantify the amount of effusion by assessing the depth of fluid.
 It can also be used at the bedside for example in the Intensive Care Units (ICUs).
 Empyema results in dense echogenicity and loculations which are detectable on
ultrasonogram.
 It is also helpful in ensuring successful pleural fluid aspiration in as high as 97% of
the cases
Thoracocentesis
 It is recommended that diagnostic pleural aspiration should be performed in
all patients with PPE.
 The exception to this rule is a small pleural effusion (<10 mm on a lateral
decubitus chest radiograph), which may resolve with antibiotics alone.
 When the effusion is small and does not completely cover the dome of the
diaphragm in a chest radiograph (P-A view), it is safer to perform an
ultrasoundguided aspiration.
 The presence of frank pus on thoracentesis is diagnostic of empyema, no
further tests are needed to confirm the diagnosis.
 If not, the pleural fluid should be sent for microbiological and biochemical
studies.
 Pus from empyema is also sent for microbiological cultures to aid in the
choice of antibiotics.
 PLEURAL FLUID ANALYSIS
 After gross examination, the pleural fluid is tested for proteins, LDH,
glucose and pH.
 Another sample is sent for microbiological studies—Gram stain, aerobic
cultures, mycobacterial and fungal cultures, as deemed necessary.
 Poor prognostic and other factors that distinguished complicated from
incomplicated PPE could be summarized as:
 pH less than or equal to 7.2,
 pleural fluid glucose less than or equal to 60 mg/dL and
 pleural fluid LDH greater than or equal to 3 times upper limit for
serum.
TREATMENT
 Antibiotic therapy and drainage of fluid collection constitute the
cornerstone of management.
 Antibiotic Treatment
 All patients suspected of having pleural infection need treatment with
antibiotics.
 While it is ideal to prescribe antibiotics based on the results of pleural
and/or blood cultures
 Cultures do not always grow pathogens, but may remain negative in up to
42% of the cases
 When cultures are negative, antibiotics should cover community acquired or
hospital acquired pathogens as the case may be, anaerobes should be
covered too
 Most physicians continue antibiotic treatment for at least 3 weeks, with
atleast 1 week of intravenous antibiotics
 Drainage
 There is consensus of opinion regarding the need of pleural space drainage under the
following circumstances:
 Frank pus or turbid/cloudy fluid within the pleural space
 Presence of organisms identified by gram stain or culture from (non-purulent) effusion
 Effusion fluid with a pH less than 7.2
 Large uncomplicated effusions for relief of dyspnea
 It is practice to remove the drainage tube, when the drainage is less than 50 ml;
provided the fluid is clear and non-turbid
 Intrapleural Fibrinolytics
 Over the years, streptokinase, streptodornase, urokinase and tPA have been used to
break fibrin adhesions and facilitate drainage
 schedule for instillation of streptokinase is 250 000 units (once or twice daily for 3
days) and for urokinase, 100 000 units (once daily for 3 days).
 Surgical Treatment
 Medical therapy fails in up to 30% of patients with Empyema
 Patients who do not improve clinically and radiologically after 7 days of standard
treatment, can derive benefit from surgical interventions.
 The Video-Assisted Thoracic Surgery (VATS) is the possible next step in the
treatment of empyema when tube drainage has failed
 The outcome of thoracotomy and decortication is generally good, with success rates
of up to 95% in this highly selected group, with significant associated complications
 Decortication is likely the only treatment option in cases of chronic empyema with
persistent sepsis and pleural fibrosis
RECURRENT PNEUMONIA
 Recurrent pneumonia is defined as 2 or more episodes in a single year
or 3 or more episodes ever, with radiographic clearing between
occurrences.
 An underlying disorder should be considered if a child experiences
recurrent pneumonia
I. HEREDITARY DISORDERS– cystic fibrosis, sickle cell anemia
II. DISORDERS OF IMMUNITY like HIV or primary immunodeficiency
III. DISORDERS OF CILIA
IV. ANATOMIC DISORDERS including TEF, GERD, foreign body and aspiration
BRONCHIOLITIS
FOR C-I
BRONCHIOLITIS

ETHIOLOGY
 Acute bronchiolitis is predominantly a viral disease.
 RSV is responsible for >50% of cases
 Other agents include rhinovirus (2nd common), parainfluenza,
adenovirus, and Mycoplasma.
 two or more viruses are detected in approximately one-third of young
children hospitalized with bronchiolitis
 Emerging pathogens include human metapneumovirus and human
bocavirus
 There is no evidence of a bacterial cause for bronchiolitis
EPIDEMOLOGY
 Bronchiolitis is more common in boys, in those who have not been breast-fed,
and in those who live in crowded conditions.
 occurs in children <2 years of age
 Risk is higher for infants with young mothers or mothers who smoked during
pregnancy.
 Older family members are a common source of infection; they might only
experience minor upper respiratory symptoms (colds).
 Host anatomic and immunologic factors and the nature of the viral pathogen
play a significant role in the severity of the clinical syndrome and the nature
of the viral pathogen
 PATHOGENESIS
 Bronchiolitis occurs when viruses infect the terminal bronchiolar epithelial
cells, causing direct damage and inflammation in the small bronchi and
bronchioles
 It is characterized by bronchiolar obstruction with edema, mucus, and
cellular debris.
 Even minor bronchiolar wall thickening significantly affects airflow because
resistance is inversely proportional to the 4th power of the radius of the
bronchiolar passage.
 Resistance in the small air passages is increased during both inspiration and
exhalation, but because the radius of an airway is smaller during expiration
 the resultant respiratory obstruction leads to early air trapping and
overinflation.
 If obstruction becomes complete, trapped distal air will be resorbed and
the child will develop atelectasis
 Hypoxemia is a consequence of ventilation-perfusion mismatch early in the
course.
 With severe obstructive disease and tiring of respiratory effort,
hypercapnia can develop
 RISK FACTORS FOR SEVERE DISEASE  — Risk factors for severe or complicated
bronchiolitis include:
A. Prematurity (gestational age <37 weeks)
B. Age less than 12 weeks
C. Chronic pulmonary disease, particularly bronchopulmonary dysplasia
D. Congenital and anatomic defects of the airways
E. Congenital heart disease
F. Immunodeficiency
G. Neurologic disease
 Clinical Manifestations
 Acute bronchiolitis is usually preceded by exposure to an older contact with a
minor respiratory syndrome within the previous week.
 The infant 1st develops a mild upper respiratory tract infection with sneezing
and clear rhinorrhea.
 This may be accompanied by diminished appetite and fever of 38.5-39?C (101-
102?F)
 Gradually, respiratory distress ensues, with paroxysmal wheezy cough, dyspnea,
and irritability.
 peak on days five to seven and then gradually resolve
 The infant is often tachypneic, which can interfere with feeding.
 The child does not usually have other systemic complaints, such as diarrhea or
vomiting.
 Apnea may be more prominent early in the course of the disease,
particularly with very young infants (<2 mo old) or premature infants
 The physical examination is often dominated by wheezing.
 Severely affected patients may appear cyanotic and have poor peripheral
perfusion
 increased work of breathing (subcostal, intercostal, and supraclavicular
retractions; nasal flaring; and expiratory grunting).
 Auscultation might reveal fine crackles or overt wheezes, with prolongation
of the expiratory phase of breathing.
 Barely audible breath sounds suggest very severe disease with nearly
complete bronchiolar obstruction.
 Hyperinflation of the lungs can permit palpation of the liver and spleen
 Other findings may include mild conjunctivitis, pharyngitis, and acute otitis
media
 The diagnosis of acute bronchiolitis is clinical
 Radiographs are not routinely indicated in the evaluation of infants
and children with bronchiolitis.
 Hyperinflation with patchy atelectasis.
 The white blood cell and differential counts are usually normal.
 Viral testing (polymerase chain reaction, rapid immunofluorescence,
or viral culture) is helpful if the diagnosis is uncertain or for
epidemiologic purposes.
 Treatment
 Infants with respiratory distress (hypoxia, inability to take oral
feedings, extreme tachypnea) should be hospitalized;
 The mainstay of treatment is supportive.
 Hypoxemic children should receive cool humidified oxygen intubation
if necessary.
 Sedatives are to be avoided because they can depress respiratory
drive.
 The infant may be fed through a nasogastric tube or put on
maintenance if severe distress
 Frequent suctioning of nasal and oral secretions often provides relief
of distress or cyanosis.
 Bronchodilators can produce modest short-term improvement in clinical
features.
 A trial dose of inhaled bronchodilator may be reasonable, with further
therapy predicated on response in the individual patient.
 Corticosteroids are not recommended in previously healthy infants with RSV.
 Ribavirin, an antiviral agent administered by aerosol, has been used for
infants with congenital heart disease or chronic lung disease.
 Prognosis
 Infants with acute bronchiolitis are at highest risk for further respiratory
compromise in the 1st 48-72 hr after onset of cough and dyspnea; the child
may be desperately ill with air hunger, apnea, and respiratory acidosis.
 The case fatality rate is <1%, with death attributable to apnea, respiratory
arrest, or severe dehydration.
 After this critical period, symptoms can persist.
 The median duration of symptoms in ambulatory patients is ∼14 days; 10%
may be symptomatic for 3 wk
 There is a higher incidence of wheezing and asthma in children with a history
of bronchiolitis unexplained by family history or other atopic syndromes.
END