- Email: [email protected]
Bronchiolitis: A clinical review
The Journal of Emergency
Me&me,
Vol 1, pp 119-I 23, 1983
Prlnted In the USA
Copyright 0 1983 Pergamon Press Ltd
??
Pediatrics
BRONCHIOLITIS:
A CLINICAL
John A. Tercier, Holy
Cross
Hospital,
Calgary,
El Abstract -Broncbiolitis is an acute viral infection primarily caused by respiratory syncytial virus, affecting children under 2 years of age with a peak prior to six months. The clinical picture results from an inflammatory process of the small bronchi and bronchioles. Infants present with tachypnea and wheezing often accompanied by respiratory dktress and hyperlnflation. Supportive care is essential, children respond slowly to hydration and careful observation. Respiratory distress requires hospitalization with treatment including oxygen and ventilator support as indicated. Cl Keywords - bronchiolitis; respiratory syncytial virus; respiratory failure; adenovirus; lower respiratory tract infection
Bronchiolitis is a common acute viral infection affecting the lower respiratory tract primarily in children under 2 years of age. The peak incidence is prior to 6 months with a slight male predilection. It occurs both epidemically and sporadically, urban crowding fostering its epidemic form.’ Respiratory syncytial virus is the most common etiologic agent. Tachypnea and wheezing accompanied by respiratory distress are the most frequent presenting complaints. Although the
REVIEW
MD
Alberta,
Canada
acute morbidity is usually self-limited, the relationship to later reactive airway disease is unresolved at present. In the infant, bronchiolitis is usually preceded by a mild upper respiratory tract infection with serous nasal discharge, rhinorrhea, and a variable low-grade fever of two to three days’ duration. There is a gradual progression of cough, tachypnea, and wheezing, often accompanied by respiratory distress. Despite these findings, children are often remarkably comfortable, although poor feeding and irritability develop. Rarely a rash or conjunctivitis is noted. Severely affected infants show a rapidly progressive course, often deteriorating over a period of hours. Tachypnea in the range of 60 to 80 breaths per minute is present along with air hunger, use of accessory muscles, intercostal and subcostal retractions, flaring of the nasal alae, and cyanosis. The chest is hyperinflated, and diffuse high-pitched expiratory rhonchi and wheezes and an increased expiratory phase of each respiration are present. In the most severe cases, the chest may be quiet because of markedly decreased air movement. Hyperinflation with downward displacement of the diaphragm may result in the liver and spleen being palpable.
B
Clinical Communications features articles on the assessment and management of both adult and childhood emergencies. Clinical Communications/Pediatrics is coordinated by Roger Barkin, MD, of the University of Colorado.
RECEIVED:
8 March 1983;
ACCEPTED:
11 May 1983 119
0736-4679/83 $3.00 + .OO
J. A. Tercier
120
The most critical phase of the illness is the first 48 to 72 hours after the onset of cough and dyspnea. Symptoms last one to three days and then improve, unless the child develops respiratory insufficiency (2% to 5%), with the child tiring and developing signs of severe respiratory failure, hypoxemia, and hypercapnia.2 Chest radiography may be normal in lo%,* show air trapping and hyperexpansion in 50% to 60%) peribronchial thickening or interstitial pneumonia in 50% to 80%) and segmental consolidation or collapse in 10% to 25070.~-~ The white blood cell count and differential are usually within normal limits.2 Viral infection may be demonstrated by immunofluorescent staining of the nasopharyngeal secretions, increases in viral serum antibody titer, or by culture. Many laboratories can perform the fluorescent antibody staining test on the day the patient is seen, providing rapid confirmation of respiratory syncytial virus as the etiologic agent. Mycoplasma can be demonstrated by culture, by increases in cold agglutinins, or by a rise in specific antibody titers.
develop chronic respiratory disease characterized by persistent airway obstruction with hyperinflation, wheezing, and recurrent bouts of respiratory infection.13
Complications
Infants with bronchiolitis often have increased rates of ongoing airway problems marked by recurrent coughing attacks, wheezing, and abnormal small airway resistance and arterial PaOz as long as 10 years later.14 Bronchiolitis obliterans is probably a chronic form of bronchiolitis and has been reported following measles, pertussis, and influenza A as well as bronchiolitis, particularly caused by adenovirus infections.7*15 A progressive fibrotic reaction obliterates the bronchioles with nodular masses composed of granulation and fibrous tissue. This causes recurrent atelectasis, pneumonia, and wheezing, often with a fatal outcome.15 If this process involves only one lung, the unilateral hyperlucent lung syndrome develops. On x-ray, the lung appears hyperlucent and of a small or normal size with small pulmonary arteries6 Etiology Acutely, patients, particularly those who were premature, may have apnea. PneuFifty to 70% of cases of bronchiolitis are monia may occur as a complication of due to respiratory syncytial virus (RSV).In6 secondary bacterial infection. Particular atOther causative agents are parainfluenza tention must be focused on assuring adetype 3, rhinovirus, mumps, influenza, my- quate hydration. Mortality rates range from 0.7070to 7% coplasma, and adenovirus types 3, 7, and 21.’ of hospitalized infants.z,12~17*18 The morRSV is a member of the paramyxovirus tality rate is higher with adenoviral infecgroup, appearing in annual epidemics with tions and in infants with underlying proalternating short (7 to 12 months) and long blems such as congenital heart disease or (13 to 16 months) cycles.* Peak occurrence cystic fibrosis. Death is usually due to resis in the winter months. The incubation pe- piratory acidosis, hypoxia, dehydration, riod is four days, and virus excretion con- and apneic spells. tinues for 1 to 3 weeks.* Adenovirus bronchiolitis is more severe than that due to RSV and results in both Pathophysiology high morbidity and high mortality.7*9*11,12 The pathologic lesion is similar to that Bronchiolitis appears to be the result of caused by RSV but extends into the alveo- virus-induced damage to the bronchiolar lar epithelium. Patients have more severe epithelium. A number of factors point to respiratory distress, and as many as 60% I an immune mechanism. Following infec-
Bronchiolitis
121
tion, antibody and complement-fixing anti- infant becomes exhausted and minute ventilation fallsz7 Cor pulmonale occurs rarely body are present in the serum, and neutralizing antibody of the IgA class is secreted owing to increased pulmonary artery presin nasal secretions and co10strum.8~19~11~20sure and right heart failure. The antibody produces an antigen-antibody reaction of the type 1 or type 3 variDifferential Diagnosis eties and may be responsible for the pathologic changes by sensitizing the child.21-23 The incidence of bronchiolitis is highest in There is a great deal of controversy over the the first 2 months of life, when maternally relationship of bronchiolitis to asthma. acquired antibody titers are greatest.*“ Bronchiolitis may be the first episode of Maternal antibodies are not protective. Re- asthma, triggered by RSV or the RSV may selectively infect a population of atopic ininfection may occur as soon as 4 weeks after recovery. The most convincing evi- fants.28.29 Infants with bronchiolitis have dence for a sensitizing role of an antibody been found to have high levels of IgE.30 is in infants who have received killed virus Fifty to 57% of children hospitalized for bronchiolitis have evidence of hyper-reacvaccine against RSV. These infants with tive airway disease later in life.14.3’Bronhigh antibody titers have a much more severe clinical course when they become in- chodilators are not uniformly effective in fected than those infants without prior infants with bronchiolitis, and the disease immunization.24 usually occurs in younger children with a Pathologically there is initially a necrosis clear upper respiratory tract infection as the of the bronchiolar epithelium followed by trigger. a proliferation of flattened or cuboid cells Viral bronchopneumonia is indistinlacking the normal ciliated surface. There guishable from severe bronchiolitis and is an increase in the amount of bronchiomay represent an extension of the same lar secretions, which are handled less effipathologic process. Bacterial pneumonia ciently. The peribronchial tissues are must be differentiated, often on the basis invaded by lymphocytes which migrate in- of presenting signs and symptoms and findto the areas between the epithelial cells.2 ings on chest x-ray. Pertussis should also Ultimately the small bronchi and bronbe considered in the young unimmunized chioles become obstructed with plugs of al- child. veolar debris and fibrin. In severe cases the Noninfectious considerations include alveolar epithelium may be involved.2 The tracheal foreign body, congestive heart failedema and accumulation of cellular debris ure, and cystic fibrosis. result in a critical narrowing of the small airways, producing profound effects on air flow. Treatment Airway resistance is increased in all phases of respiration but more so in expirThe basis of treatment is to support the ation. This produces a ball-valve effect child through the self-limited course of illresulting in air trapping and hyperexpanness and to minimize complications. The sion.25 Atelectasis occurs when trapped air child without respiratory distress or any becomes resorbed. The end results are a de- evidence of apnea, lethargy, or dehydration crease in dynamic compliance and an inwho lives in a reliable environment may crease in mean pulmonary resistance, and usually be discharged home with instructhoracic volume at end expiration.” A tions to parents to encourage the intake of ventilation-perfusion defect results from fluids and to carefully watch the child for underventilation of regions with normal evidence of disease progression. perfusion.26 This produces hypoxemia with In children with moderate to severe discarbon dioxide retention occurring as the tress, hospitalization is warranted. Marked
122
J. A. Tercier
tachypnea, evidence of hypoxia, poor feeding, and dehydration are absolute indications. Premature infants under 6 months of age have an increased incidence of apnea and benefit from observation. Additionally, children living with unreliable caretakers or at great distance from medical facilities will benefit from admission. If the child is in marked respiratory distress and is over 6 months of age, some authors recommend a trial of epinephrine (l:l,OOO) 0.01 ml/kg/dose (maximum: 0.35 ml/dose) subcutaneously. If there is a response, a repeat dose every 20 minutes up to a total of three doses may be administered. Bronchodilator therapy should be initiated if there is a significant response and, although the benefits are controversial, continued for five to ten days. Hydration should be assured. Tachypnea produces a markedly increased water loss and interferes with feeding. It is often necessary to provide 11%to 2 times the normal maintenance requirements. Input, output, and infant weights should be monitored. In the severely ill child with respiratory failures, continuous positive airway pressure (CPAP) should be instituted. Children should have this modality started for increasing respiratory effort, a rising respiratory rate or pulse, decreased responsiveness, decreasing Paoz, or increasing Paco2. The CPAP may be administered using a nasal cannula or endotracheal tube. Thirty to 40% oxygen at 5 cm Hz0 pressure should be used initially. 27Intubation and mechanical ventilation are necessary if CPAP fails or apneic spells are frequent.
Initially the ventilator may be set at a respiratory rate of 30 to 40 per minute, an inspiratory/expiratory ratio of 1: 1, tidal volume of 6 to 10 ml/kg, and an FIO, of 60% to 80% oxygen. The peak inspiratory pressure should not exceed 30 cm of H20, and PEEP may be set at 5 cm H20. Muscle relaxation is rarely needed. Digitalis and diuretics are rarely needed but may be useful if car pulmonale devel0~s.~’Corticosteroids have no proven efficacy. Antibiotics should be used solely for proven bacterial infections.
1. Henderson FW: The etiologic and epidemiologic spectrum of bronchiolitis in pediatric patience. J Pediatr 1979; 95:183. 2. Wohl MEB, Chernick V: Bronchiolitis. Am Rev Respir Dis 1978; 118:759-781. 3. Simpson W, Hacking PM, Court SDM, et al: The radiologic findings in respiratory syncytial virus infections in children. I. Definitions and inter observations in the assessment of abnormalities on the chest xray. Pediatr Radio1 1974; 2:97. 4. Simpson W, Hacking PM, Court SDM, et al: The
radiological findings in respiratory syncytial virus infection in children. II. The correlation of radiological categories with clinical and virological findings. Pediatr Radio1 1974; 2~155. 5. Rice RP, Loda F: A roentgenographic analysis of respiratory syncytial virus pneumonia in infants. Radiology 1966; 87~1021. 6. Hall CB, Douglas RG: Clinically useful method for the isolation of respiratory syncytial virus. J Infect Dis 1975; 1:313. 7. Lang WR, Howden CW, Laws J, Burton JF:
Conclusion Bronchiolitis is a self-limiting viral disease affecting the lower airways and occurring in infants less than 6 months of age. It presents with paroxysmal cough, wheezing, tachypnea, and hyperinflation and may progress to respiratory failure. The main causative agent is the respiratory syncytial virus, but other viruses and mycoplasma are also implicated. The adenovirus is responsible for a particularly severe form of the disease. The pathologic lesion is an inflammation of the small ronchi and bronchioles which may be due to a direct viral insult or an antigen-antibody reaction. The end result is various degrees of respiratory failure. There is a significant mortality rate, and morbidity is primarily in the form of chronic airway disease. Treatment consists of adequate rehydration and support of the respiratory system with oxygen, CPAP, and mechanical ventilation if necessary.
123
Bronchopneumonia with serious sequelae in children with evidence of adenovirus type 21 infection. Br Med J 1969; 1:73. 8. Scott R, Gardener PS: The local antibody response to respiratory syncytial virus infection in the respiratory tract. J Hyg (Camb) 1974; 72~111. 9. Gold R, Wilt JC, Adhikari PK, Gardner PS: Adenoviral pneumonia and its complications in infancy and childhood. J Can Assoc Radio1 1969; 20:218.
10. Holdaway D, Romer AC, Gardner PS: The diagnosis and management of bronchiolitis. Pediatrics 1967; 39~924.
11. Phelan PD, Williams HE, Freeman M: The disturbance of ventilation in acute viral bronchiolitis. Aust Paediatr J 1968; 4:96. 12. Heycock JB, Noble TC: 1230 cases of acute bronchiolitis in infancy. Br Med J 1962; ii:879.
13. Chernick V, Macpherson RI: Respiratory syncytial and adenovirus infections of the lower respiratory tract in infancy. Ciin Notes Respir Dis 1971; 10:3. 14. Kattan M, Keen TG, Lapierre JG, Levison H, Bryan AC, Reilly BJ: Pulmonary function abnormalities in symptom free children after bronchiolitis.
20. Glezen WP, Denny FW: Epidemiology of acute lower respiratory disease in children. N Engl J Med 1973; 288:498. 21. Chanock RM, Kapikian AZ, Mills J, Kim HW,
Parrott RH: Influence of immunologic factors in respiratory syncytial virus disease. Arch Environ Health 1970; 211347. 22. Iamprecht CI, Krause HE, Mufson MA: Role of
maternal antibody in pneumonia and bronchiolitis due to respiratory syncytial virus. J Infect Dis 1976; 134:211. 23. Downham M, Scott R, Sims DG, Webb J, Gardner PS: Breast feeding protects against respiratory syncytial virus infections. Br Med J 1976; 2:274. 24. Kapikian AZ, Mitchell RH, Chanock RM, Shvedoff RA, Stewart CE: An epidemiologic study of altered clinical reactivity to respiratory syncytial virus infection in children previously vaccinated with an inactivated RS virus vaccine. Am J Epidemiol 1968; 89:405. 25. Wohl MEB, Stigol LC, Mead J: Resistance of the
26.
Pediatrics 1977; 59:683.
15. Azizirad H, Polgar C, Borns PF, Chatten J: Bronchiolitis obliterans. Clin Pediatr 1975; 14:572. 16. Kattan M: Long term sequelae of respiratory illness in infancy and childhood. Ped Clin North Am
27.
28.
1979; 26:525. 17. Elderkin FM, Gardner PS, Turk DC, et al: Aetiol-
ogy and management of bronchiolitis and pneumonia in childhood. Br Med J 1965; ii:722. 18. Gardner PS: Diagnosis of bronchiolitis: How etiologic, pathologic, and clinical diagnosis can be made in a correlated fashion. Pediatr Res 1977; 11:254. 19. Parrot RH, Kim HW, Arrobio JO, Hodes DS, Murphy BR, Brandt CD, Camargo E, Chanock RM: Epidemiology of respiratory syncytial virus infection in Washington DC. Am .I Epidemiol 1973; 98:216.
29. 30.
total respiratory system in healthy infants and infants with bronchiolitis. Pediatrics 1969; 43:495. Reynolds EOR: Recovery from bronchiolitis as judged by arterial blood gas tension measurements. J Pediatr 1963; 63:1182. Beastley JM: Continuous positive airway pressure in bronchiolitis. Br Med J 1981; 283:1506-1508. Lang I: Atopy predisposing to acute bronchiolitis during an epidemic of respiratory syncytial virus. Br Med J 1982; 284: 1070. Ellis EF: Relationship between the allergic state and susceptibility to infectious airway disease. Pediatr Res 1977; 11~227, Foucard T, Berg T, Johansson SGO, Wahren B: Virus serology and serum IgE levels in children with asthmatoid bronchitis. Acta Paediatr Stand
1971; 60:621. 31. Gurwitz D, Midorff C, Levison H: Increased in-
cidence of bronchial reactivity in children with a history of bronchiolitis. J Pediatr 1981; 98:551.
Me&me,
Vol 1, pp 119-I 23, 1983
Prlnted In the USA
Copyright 0 1983 Pergamon Press Ltd
??
Pediatrics
BRONCHIOLITIS:
A CLINICAL
John A. Tercier, Holy
Cross
Hospital,
Calgary,
El Abstract -Broncbiolitis is an acute viral infection primarily caused by respiratory syncytial virus, affecting children under 2 years of age with a peak prior to six months. The clinical picture results from an inflammatory process of the small bronchi and bronchioles. Infants present with tachypnea and wheezing often accompanied by respiratory dktress and hyperlnflation. Supportive care is essential, children respond slowly to hydration and careful observation. Respiratory distress requires hospitalization with treatment including oxygen and ventilator support as indicated. Cl Keywords - bronchiolitis; respiratory syncytial virus; respiratory failure; adenovirus; lower respiratory tract infection
Bronchiolitis is a common acute viral infection affecting the lower respiratory tract primarily in children under 2 years of age. The peak incidence is prior to 6 months with a slight male predilection. It occurs both epidemically and sporadically, urban crowding fostering its epidemic form.’ Respiratory syncytial virus is the most common etiologic agent. Tachypnea and wheezing accompanied by respiratory distress are the most frequent presenting complaints. Although the
REVIEW
MD
Alberta,
Canada
acute morbidity is usually self-limited, the relationship to later reactive airway disease is unresolved at present. In the infant, bronchiolitis is usually preceded by a mild upper respiratory tract infection with serous nasal discharge, rhinorrhea, and a variable low-grade fever of two to three days’ duration. There is a gradual progression of cough, tachypnea, and wheezing, often accompanied by respiratory distress. Despite these findings, children are often remarkably comfortable, although poor feeding and irritability develop. Rarely a rash or conjunctivitis is noted. Severely affected infants show a rapidly progressive course, often deteriorating over a period of hours. Tachypnea in the range of 60 to 80 breaths per minute is present along with air hunger, use of accessory muscles, intercostal and subcostal retractions, flaring of the nasal alae, and cyanosis. The chest is hyperinflated, and diffuse high-pitched expiratory rhonchi and wheezes and an increased expiratory phase of each respiration are present. In the most severe cases, the chest may be quiet because of markedly decreased air movement. Hyperinflation with downward displacement of the diaphragm may result in the liver and spleen being palpable.
B
Clinical Communications features articles on the assessment and management of both adult and childhood emergencies. Clinical Communications/Pediatrics is coordinated by Roger Barkin, MD, of the University of Colorado.
RECEIVED:
8 March 1983;
ACCEPTED:
11 May 1983 119
0736-4679/83 $3.00 + .OO
J. A. Tercier
120
The most critical phase of the illness is the first 48 to 72 hours after the onset of cough and dyspnea. Symptoms last one to three days and then improve, unless the child develops respiratory insufficiency (2% to 5%), with the child tiring and developing signs of severe respiratory failure, hypoxemia, and hypercapnia.2 Chest radiography may be normal in lo%,* show air trapping and hyperexpansion in 50% to 60%) peribronchial thickening or interstitial pneumonia in 50% to 80%) and segmental consolidation or collapse in 10% to 25070.~-~ The white blood cell count and differential are usually within normal limits.2 Viral infection may be demonstrated by immunofluorescent staining of the nasopharyngeal secretions, increases in viral serum antibody titer, or by culture. Many laboratories can perform the fluorescent antibody staining test on the day the patient is seen, providing rapid confirmation of respiratory syncytial virus as the etiologic agent. Mycoplasma can be demonstrated by culture, by increases in cold agglutinins, or by a rise in specific antibody titers.
develop chronic respiratory disease characterized by persistent airway obstruction with hyperinflation, wheezing, and recurrent bouts of respiratory infection.13
Complications
Infants with bronchiolitis often have increased rates of ongoing airway problems marked by recurrent coughing attacks, wheezing, and abnormal small airway resistance and arterial PaOz as long as 10 years later.14 Bronchiolitis obliterans is probably a chronic form of bronchiolitis and has been reported following measles, pertussis, and influenza A as well as bronchiolitis, particularly caused by adenovirus infections.7*15 A progressive fibrotic reaction obliterates the bronchioles with nodular masses composed of granulation and fibrous tissue. This causes recurrent atelectasis, pneumonia, and wheezing, often with a fatal outcome.15 If this process involves only one lung, the unilateral hyperlucent lung syndrome develops. On x-ray, the lung appears hyperlucent and of a small or normal size with small pulmonary arteries6 Etiology Acutely, patients, particularly those who were premature, may have apnea. PneuFifty to 70% of cases of bronchiolitis are monia may occur as a complication of due to respiratory syncytial virus (RSV).In6 secondary bacterial infection. Particular atOther causative agents are parainfluenza tention must be focused on assuring adetype 3, rhinovirus, mumps, influenza, my- quate hydration. Mortality rates range from 0.7070to 7% coplasma, and adenovirus types 3, 7, and 21.’ of hospitalized infants.z,12~17*18 The morRSV is a member of the paramyxovirus tality rate is higher with adenoviral infecgroup, appearing in annual epidemics with tions and in infants with underlying proalternating short (7 to 12 months) and long blems such as congenital heart disease or (13 to 16 months) cycles.* Peak occurrence cystic fibrosis. Death is usually due to resis in the winter months. The incubation pe- piratory acidosis, hypoxia, dehydration, riod is four days, and virus excretion con- and apneic spells. tinues for 1 to 3 weeks.* Adenovirus bronchiolitis is more severe than that due to RSV and results in both Pathophysiology high morbidity and high mortality.7*9*11,12 The pathologic lesion is similar to that Bronchiolitis appears to be the result of caused by RSV but extends into the alveo- virus-induced damage to the bronchiolar lar epithelium. Patients have more severe epithelium. A number of factors point to respiratory distress, and as many as 60% I an immune mechanism. Following infec-
Bronchiolitis
121
tion, antibody and complement-fixing anti- infant becomes exhausted and minute ventilation fallsz7 Cor pulmonale occurs rarely body are present in the serum, and neutralizing antibody of the IgA class is secreted owing to increased pulmonary artery presin nasal secretions and co10strum.8~19~11~20sure and right heart failure. The antibody produces an antigen-antibody reaction of the type 1 or type 3 variDifferential Diagnosis eties and may be responsible for the pathologic changes by sensitizing the child.21-23 The incidence of bronchiolitis is highest in There is a great deal of controversy over the the first 2 months of life, when maternally relationship of bronchiolitis to asthma. acquired antibody titers are greatest.*“ Bronchiolitis may be the first episode of Maternal antibodies are not protective. Re- asthma, triggered by RSV or the RSV may selectively infect a population of atopic ininfection may occur as soon as 4 weeks after recovery. The most convincing evi- fants.28.29 Infants with bronchiolitis have dence for a sensitizing role of an antibody been found to have high levels of IgE.30 is in infants who have received killed virus Fifty to 57% of children hospitalized for bronchiolitis have evidence of hyper-reacvaccine against RSV. These infants with tive airway disease later in life.14.3’Bronhigh antibody titers have a much more severe clinical course when they become in- chodilators are not uniformly effective in fected than those infants without prior infants with bronchiolitis, and the disease immunization.24 usually occurs in younger children with a Pathologically there is initially a necrosis clear upper respiratory tract infection as the of the bronchiolar epithelium followed by trigger. a proliferation of flattened or cuboid cells Viral bronchopneumonia is indistinlacking the normal ciliated surface. There guishable from severe bronchiolitis and is an increase in the amount of bronchiomay represent an extension of the same lar secretions, which are handled less effipathologic process. Bacterial pneumonia ciently. The peribronchial tissues are must be differentiated, often on the basis invaded by lymphocytes which migrate in- of presenting signs and symptoms and findto the areas between the epithelial cells.2 ings on chest x-ray. Pertussis should also Ultimately the small bronchi and bronbe considered in the young unimmunized chioles become obstructed with plugs of al- child. veolar debris and fibrin. In severe cases the Noninfectious considerations include alveolar epithelium may be involved.2 The tracheal foreign body, congestive heart failedema and accumulation of cellular debris ure, and cystic fibrosis. result in a critical narrowing of the small airways, producing profound effects on air flow. Treatment Airway resistance is increased in all phases of respiration but more so in expirThe basis of treatment is to support the ation. This produces a ball-valve effect child through the self-limited course of illresulting in air trapping and hyperexpanness and to minimize complications. The sion.25 Atelectasis occurs when trapped air child without respiratory distress or any becomes resorbed. The end results are a de- evidence of apnea, lethargy, or dehydration crease in dynamic compliance and an inwho lives in a reliable environment may crease in mean pulmonary resistance, and usually be discharged home with instructhoracic volume at end expiration.” A tions to parents to encourage the intake of ventilation-perfusion defect results from fluids and to carefully watch the child for underventilation of regions with normal evidence of disease progression. perfusion.26 This produces hypoxemia with In children with moderate to severe discarbon dioxide retention occurring as the tress, hospitalization is warranted. Marked
122
J. A. Tercier
tachypnea, evidence of hypoxia, poor feeding, and dehydration are absolute indications. Premature infants under 6 months of age have an increased incidence of apnea and benefit from observation. Additionally, children living with unreliable caretakers or at great distance from medical facilities will benefit from admission. If the child is in marked respiratory distress and is over 6 months of age, some authors recommend a trial of epinephrine (l:l,OOO) 0.01 ml/kg/dose (maximum: 0.35 ml/dose) subcutaneously. If there is a response, a repeat dose every 20 minutes up to a total of three doses may be administered. Bronchodilator therapy should be initiated if there is a significant response and, although the benefits are controversial, continued for five to ten days. Hydration should be assured. Tachypnea produces a markedly increased water loss and interferes with feeding. It is often necessary to provide 11%to 2 times the normal maintenance requirements. Input, output, and infant weights should be monitored. In the severely ill child with respiratory failures, continuous positive airway pressure (CPAP) should be instituted. Children should have this modality started for increasing respiratory effort, a rising respiratory rate or pulse, decreased responsiveness, decreasing Paoz, or increasing Paco2. The CPAP may be administered using a nasal cannula or endotracheal tube. Thirty to 40% oxygen at 5 cm Hz0 pressure should be used initially. 27Intubation and mechanical ventilation are necessary if CPAP fails or apneic spells are frequent.
Initially the ventilator may be set at a respiratory rate of 30 to 40 per minute, an inspiratory/expiratory ratio of 1: 1, tidal volume of 6 to 10 ml/kg, and an FIO, of 60% to 80% oxygen. The peak inspiratory pressure should not exceed 30 cm of H20, and PEEP may be set at 5 cm H20. Muscle relaxation is rarely needed. Digitalis and diuretics are rarely needed but may be useful if car pulmonale devel0~s.~’Corticosteroids have no proven efficacy. Antibiotics should be used solely for proven bacterial infections.
1. Henderson FW: The etiologic and epidemiologic spectrum of bronchiolitis in pediatric patience. J Pediatr 1979; 95:183. 2. Wohl MEB, Chernick V: Bronchiolitis. Am Rev Respir Dis 1978; 118:759-781. 3. Simpson W, Hacking PM, Court SDM, et al: The radiologic findings in respiratory syncytial virus infections in children. I. Definitions and inter observations in the assessment of abnormalities on the chest xray. Pediatr Radio1 1974; 2:97. 4. Simpson W, Hacking PM, Court SDM, et al: The
radiological findings in respiratory syncytial virus infection in children. II. The correlation of radiological categories with clinical and virological findings. Pediatr Radio1 1974; 2~155. 5. Rice RP, Loda F: A roentgenographic analysis of respiratory syncytial virus pneumonia in infants. Radiology 1966; 87~1021. 6. Hall CB, Douglas RG: Clinically useful method for the isolation of respiratory syncytial virus. J Infect Dis 1975; 1:313. 7. Lang WR, Howden CW, Laws J, Burton JF:
Conclusion Bronchiolitis is a self-limiting viral disease affecting the lower airways and occurring in infants less than 6 months of age. It presents with paroxysmal cough, wheezing, tachypnea, and hyperinflation and may progress to respiratory failure. The main causative agent is the respiratory syncytial virus, but other viruses and mycoplasma are also implicated. The adenovirus is responsible for a particularly severe form of the disease. The pathologic lesion is an inflammation of the small ronchi and bronchioles which may be due to a direct viral insult or an antigen-antibody reaction. The end result is various degrees of respiratory failure. There is a significant mortality rate, and morbidity is primarily in the form of chronic airway disease. Treatment consists of adequate rehydration and support of the respiratory system with oxygen, CPAP, and mechanical ventilation if necessary.
123
Bronchopneumonia with serious sequelae in children with evidence of adenovirus type 21 infection. Br Med J 1969; 1:73. 8. Scott R, Gardener PS: The local antibody response to respiratory syncytial virus infection in the respiratory tract. J Hyg (Camb) 1974; 72~111. 9. Gold R, Wilt JC, Adhikari PK, Gardner PS: Adenoviral pneumonia and its complications in infancy and childhood. J Can Assoc Radio1 1969; 20:218.
10. Holdaway D, Romer AC, Gardner PS: The diagnosis and management of bronchiolitis. Pediatrics 1967; 39~924.
11. Phelan PD, Williams HE, Freeman M: The disturbance of ventilation in acute viral bronchiolitis. Aust Paediatr J 1968; 4:96. 12. Heycock JB, Noble TC: 1230 cases of acute bronchiolitis in infancy. Br Med J 1962; ii:879.
13. Chernick V, Macpherson RI: Respiratory syncytial and adenovirus infections of the lower respiratory tract in infancy. Ciin Notes Respir Dis 1971; 10:3. 14. Kattan M, Keen TG, Lapierre JG, Levison H, Bryan AC, Reilly BJ: Pulmonary function abnormalities in symptom free children after bronchiolitis.
20. Glezen WP, Denny FW: Epidemiology of acute lower respiratory disease in children. N Engl J Med 1973; 288:498. 21. Chanock RM, Kapikian AZ, Mills J, Kim HW,
Parrott RH: Influence of immunologic factors in respiratory syncytial virus disease. Arch Environ Health 1970; 211347. 22. Iamprecht CI, Krause HE, Mufson MA: Role of
maternal antibody in pneumonia and bronchiolitis due to respiratory syncytial virus. J Infect Dis 1976; 134:211. 23. Downham M, Scott R, Sims DG, Webb J, Gardner PS: Breast feeding protects against respiratory syncytial virus infections. Br Med J 1976; 2:274. 24. Kapikian AZ, Mitchell RH, Chanock RM, Shvedoff RA, Stewart CE: An epidemiologic study of altered clinical reactivity to respiratory syncytial virus infection in children previously vaccinated with an inactivated RS virus vaccine. Am J Epidemiol 1968; 89:405. 25. Wohl MEB, Stigol LC, Mead J: Resistance of the
26.
Pediatrics 1977; 59:683.
15. Azizirad H, Polgar C, Borns PF, Chatten J: Bronchiolitis obliterans. Clin Pediatr 1975; 14:572. 16. Kattan M: Long term sequelae of respiratory illness in infancy and childhood. Ped Clin North Am
27.
28.
1979; 26:525. 17. Elderkin FM, Gardner PS, Turk DC, et al: Aetiol-
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