Acute Bronchiolitis

Inflammation of the distant bronchioles

Aetiology:

• Viruses- RSV, PIV 3, human metapneumoviruses, adenoviruses (ADV) esp 3,7 and 21,

rhinoviruses, influenza viruses, and enteroviruses in a much lower proportion of cases,

• Bacteria- Mycoplasma pneumoniae and Chlamydia trachomatis

Epidemiologic Risk factors

Age: For anatomical reasons of age-related size of the distal respiratory tree (i.e. the

bronchioles), common among < 2 years at presentation. Indeed, the peak incidence is reportedly

between the second and the 10th month of life

Gender: A male preponderance of cases. Attack rates in males may be 1.5 times greater than in

females.

Breast feeding: Lack of exclusive breast-feeding in first six months of life.

Opportunities for exposure: Early exposure of infants of working mothers to

day-care settings or creche,

in-door crowding and

the presence of older siblings and adults with minor respiratory illnesses

Seasonal factors: In the temperate world, this period is the winter to spring months (but in the

West African subregion, most cases are seen during the rainy season (May-October) or the cold-

but-dry harmattan (November-December) (Johnson et al, 1996).

Others: Racial factors are reportedly unimportant, but black infants were said to be more

vulnerable to parainfluenza type III–associated wheezy illnesses (Welliver et al, 1986). Also,

unlike in pneumonia, malnutrition is an uncommon associated feature of acute viral bronchiolitis

(Johnson, 1993).
Pathology & Pathophysiology:

Viral infection of the infant’s upper respiratory passages usually occurs following inhalation of

infected respiratory droplets, or inoculation of the nostrils or conjunctivae from contaminated

hands.

The spread of the infection to the distal bronchi and bronchioles causes-

mucous hypersecretion,

necrosis of the respiratory epithelium, and

submucosal inflammatory oedema.

There is preservation of submucosal collagen and elastic tissue.

Subsequently, intraluminal plugs of sloughed (epithelial) cellular debris and fibrin are formed.

Characteristically, there is peribronchiolar infiltration by mononuclear cells, and except those

adjoining the inflamed bronchioles, the alveoli are relatively spared.

Several cytokines/chemokines (notably interleukin (IL)-8, macrophage inflammatory protein

[MIP]1-α and regulated on activation normal T-cell expressed and secreted (RANTES)),

interferon-ү and leukotrienes are released due to cellular injury.

The consequent cellular dysregulation initiate, orchestrate and sustain airway inflammation

involving the epithelia of the distal bronchi and the bronchioles.

By virtue of their smaller dimensions, the peripheral airway of infants and toddlers has a greater

propensity for obstruction (and the related increase in airway resistance) from the inflammatory

oedema and intraluminal mucus plugs and epithelial debris.

pressure (by the active contraction of the diaphragm), but with the generation of positive

pressure at expiration, there is dynamic airway compression with the consequent smaller luminal

dimensions.

Air-trapping beyond the site of obstruction causes progressive hyperinflation (ball-valve

obstruction). The consequent increase in the functional residual capacity accounts for the

difficulty and prolongation of the expiratory phase of breathing.

Uneven distribution of resistance and a general decrease in lung compliance result in a

significant increase in the work of breathing.

Progression of the inflammatory events causes complete (check-valve) obstruction in some

bronchioles. The consequent absorption of the trapped air causes multiple but patchy atelectases,

which may be difficult to distinguish from the patchy infiltrates of a complicating

bronchopneumonia on the chest radiograph.

As the resistance to airflow increases, so does the work of breathing, volume of trapped (dead

space) air and the respiratory rate. The tendency for developing fast shallow breathing on a high

functional residual capacity leads to a decreasing amount of inhaled air getting to the alveolar

exchange surfaces. Although the physiological consequence of this is hypercarpnia (elevation of

arterial PCO2), hypoxaemia (low arterial O2) appears earlier, due to the inevitable ventilation

perfusion (V/Q) mismatch associated with the disease. V/Q mismatch is a feature of most

hospitalized cases of acute bronchiolitis, and results from relative hyperperfusion of poorly

ventilated alveoli (occasioned by inflammatory obstruction of the peripheral air-way). That the

low arterial O2 frequently outlasts clinical improvement, underscores the slow resolution of the

initial inflammatory events.

The typical clinical scenario is that of an infant or toddler below 2 years, presenting with an

initial coryzal illness during the vulnerable wet season (rainy season or winter), frequently in

close temporal association with (a preceding exposure to) an older contact with an

undifferentiated upper respiratory illness.

This initial prodrome of clear rhinorrhoea, nasal congestion, excessive sneezing and cough is

associated with a mild fever lasting for 1 – 7 days.

The definitive disease is heralded by a sudden onset of wheezy breathlessness, episodic or

paroxysmal cough, irritability, poor feeding, and (especially in tropical environment where

malaria may coexist) an exacerbation of the initial pyrexia.

Cough and wheezing may be minimal in the neonates/younger infants in whom apnoea is a more

frequent presenting feature.

Those requiring admission will usually present with severe symptoms within the first 3-4 days of

the definitive stage.

Examination-

• Fast breathing for the age, chest retraction, and tachycardia are near-constant findings;

• an occasional child may present with grunting and/or cyanosis.

• Auscultatory rhonchi (typically expiratory and polyphonic) and fine inspiratory

crepitations may be associated with (non-auscultatory) wheezing, which is usually

suggested by the prolonged expiration (“visible wheeze”).

• the temperature may range from 38.0 – 400C.

• Irritability (or sometimes lethargy), cyanosis, features of “increased work of breathing”

• A palpable liver is consequent on the hyperinflation, as is splenomegaly.

cases), or complications like a bacterial pneumonia (usually associated with unusual

bacterial agentsref) dehydration or metabolic acidosis.

The natural course

• An initial 48-72 hours of a frightening severity of the respiratory distress with the

attendant highest risk of precipitous respiratory/metabolic decompensation causing a fatal

outcome in a few(< 1%).

• In the majority of affected children, there is a gradual resolution of the respiratory

distress, an improvement in the paroxysms of cough, fever, appetite and other features

over the subsequent 1-2 weeks.

Risk factors of severe disease or death

• underlying congenital heart disease (especially the cyanotic types),

• underlying congenital or acquired chronic respiratory illness (e.g. laryngo- or

tracheomalacia, bronchopulmonary dysplasia),

• a neonatal age.

• Adenovirus aetiology may result in obliterative bronchiolitis (a chronic lung disease)

and rarely unilateral hyperluscent lung syndrome (Swyer-James syndrome).

• Prematurity

Investigations:

• Clinical premise.

• Radiological investigations-The chest radiograph provides useful anatomic clues of the

disease extent/complications. A postero-anterior chest X-ray shows peribronchial

diaphragmatic domes as well as a “relative microcardia” (because of the hyperinflation).

Increased bronchovascular markings as well as interstitial streaks radiating from the hilar

are frequent findings. The lateral radiograph is likely to corroborate hyperinflation with

an increase anteroposterior diameter of the chest. Patchy or segmental shadows may

suggest either atelectasis, and or superimposed bacterial consolidation.

• Microbiological- Nasopharyngeal aspirate or nasopharyngeal swab

o immunofluorescence (IF) studies or

o polymerase chain reaction analysis

o Viral cultures

o Serological diagnosis (using paired sera obtained 10-14 days apart) serves little

therapeutic purpose for the individual case, but may be useful in confirming

epidemics.

o A superimposed bacterial pneumonia (usually Staphylococcus aureus or S.

epidermidis in severe cases requiring hospitalization) may be occasionally

confirmed with a blood culture

• Other investigations-

o Blood gas/acid base aberrations include metabolic acidosis, and less commonly

respiratory alkalosis, initial (arterial) hypoxaemia and with the subsequent CO2

retention, acute respiratory acidosis.

o Pulse oximetry

o The haematological findings - non-specific, and may be normal without the

typical viral leucopaenia with relative lymphocytosis. Furthermore, the presence

to suggest the advent of a superimposed bacterial pneumonia.

Differential Diagnoses:

• bronchial asthma.

• pertussis,

• foreign body or food aspiration,

• gastroesophageal reflux, Microscopy of nasopharyngeal secretions for alveolar

macrophages and/or pH studies

• upper airway obstructive lesions like adenoidal hypertrophy, and croup.

• congestive cardiac failure.

Treatment:

the management is essentially supportive care.

In hospitalized cases, the goals comprise

1. supporting the child to mitigate the consequences of airway obstruction and the related

mismatch of ventilation and lung perfusion,

2. ascertain the presence of (and hence initiate appropriate measures) complications,

3. and protecting other children at risk.

The important elements of the supportive care in acute bronchiolitis which can be categorized

under these three goals include:

Oxygen therapy- Humidified oxygen at a concentration of 30-40% will suffice.

Amelioration of Fever and Control of Environmental Temperature: Fever, chilling and the

related shivering/rigors can all increase the oxygen requirements of the child with bronchiolitis
and hence enhance an earlier advent of hypoxaemia and respiratory failure. These possibilities

constitutes the rationale behind the use of antipyretics (especially paracetamol), and indeed,

providing a thermoneutral environment like the incubator or a radiant warmer for the affected

infant,

Provision of Additional fluid and Feeds- Besides a judicious fluid supplementation, there is an

equally important need to provide additional calories via frequent small volume, and preferably

calorie-dense nutrients. The breast – fed infant will obviously need to be offered more frequently

than before the illness.

Antimicrobial/Antibiotic Therapy: Except in the occasional case with a mycoplasmal aetiology

(in which a macrolide agent like erythromycin may be beneficial), specific antimicrobial agents

are rarely required in the majority of cases of this predominantly viral disease.

Ribavirin for RSV bronchiolitis is reportedly associated with a more rapid viral shedding and an

overall clinical improvement. These correlate well with an equally more rapid improvement in

oxygen saturation. The drug is administered as small particle aerosol via an oxygen hood, or a

ventilator as a 3-5 day course, comprising 12-20 hour duration of treatment per day is sufficient

to achieve the desired result. If available, ribavirin therapy is recommended for mortality-prone

infants with bronchiolitis.

The use of antibiotics or antibacterial chemotherapy should be individualized for those with

superimposed bacterial pneumonia, based on a combination of clinical and radiographic

parameters. The choice of an antibacterial agent must take cognizance of Staphylococcus species

in addition to the usual agents associated with community-acquired pneumonia.

Others:

Trial of Bronchodilators:
Nasal Decongestion: The potential benefit of nasal decongestion in infants with bronchiolitis

lies in the fact that most infants are obligate nasal breathers. Nasal decongestion will not only

ameliorate the respiratory distress, but enhance oral intake of fluids and calories. Intermittent

gentle suctioning of the nostrils and the nasopharynx (with or without saline nasal drops) using a

suctioning machine in hospitalized infants and parent-assisted mouth to nose clearing of

secretions in ambulatory cases are useful adjunctive treatment measures.

Prevention:

Immunisation:

• periodic passive immunoprophylaxis with palivisumab before or during the peak

season, has proved an effective preventative tool in children with high-risk disease

• intravenous polyclonal RSV-hyperimmune immunoglobulin (RespiGAM) may serve

a similar purpose, though avoid in infants with underlying congental cyanotic heart

disease.

Protecting other Children / Preventing Child-to-Child transmission:.

• inter-contact hand-washing is required to minimize the risk of child-to-child

spread of the virus especially in nurseries and emergency rooms.

• excusing children and staff with acute respiratory illness from attendance, at least

during the active phase.