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Transcript
ACUTE RESPIRATORY INFECTIONS OF THE UPPER RESPIRATORY TRACT
IN CHILDREN. ACUTE BRONCHITIS.
1. SIGNIFICANCE
Bronchitis is the most common disease of childhood next to indigestion and diarrhoea. It
is especially prevalent in children who are just starting to mix with other children at
playgroup or nursery school. They have no in-built immunity till then to all the infections
they are likely to contact for the first time. And, so, coughs, colds and bronchitis can
occur with monotonous regularity in this age group, particularly in allergic children
2. PREREQUISITES
The skills listed below will not be taught in this lesson but are necessary to perform physical
examination of the patient practical training. Therefore, before beginning this lesson, one has to
be sure of the ability to:
 Inspect the thorax and its respiratory movements and note rate, rhythm, depth, and effort of
breathing;
 Inspect for retractions of the supraclavicular areas of contractions of the sternomastoid
muscles on respiration;
 Observe shape of child`s chest;
 Palpate the chest for respiratory expansion, tactile fremitus;
 Percuss the chest in the standard areas, comparing one side with the other at each level;
 Auscultate the chest with stethoscope in order to evaluate breath sounds.
3. EDUCATIONAL OBJECTIVES
Student should know:
- theetiology, pathogenesis, clinical manifestation, differencial diagnosis and treatment for
the most common acute respiratory infections of the upper respiratory tract in children, acute
bronchitis and bronchiolitis.
Student should be able:
- to identify the child with the most common acute respiratory infections of the upper
respiratory tract in children, acute bronchitis and bronchiolitis, make correct decisions during
physical examination of the patients, take appropriate actions based on those decisions,
demonstrate skills to develop management and follow up measures.
4. INTERDISCIPLINARY INTEGRATION
Discipline
Normal anatomy,
Physiology
Student should know
Anatomic and physiologic
features of the respiratory system
in children of different age
groups
Biochemistry
Normal ranges for the routine
biochemical blood analysis
Student should be able to
Use knowledge of anatomic and
physiologic features of the
respiratory system in children
for evaluation of clinical
findings
Assess blood biochemistry and
comment on deviations from
normal in a clinical context
Congenital
pulmonary
lymphangiectasia
Children with pulmonary venous obstruction or severe pulmonary
lymphangiectasia present with dyspnea and cyanosis in the newborn
period.
Chest radiographs reveal diffuse, dense, reticular densities with
prominence of Kerley B lines.
If the lung is not completely involved, the spared areas appear
hyperlucent.
Respiration is compromised because of impaired diffusion and decreased
pulmonary compliance.
The diagnosis can be suggested by CT scan and cardiac catheterization;
definitive diagnosis requires lung biopsy (either thoracoscopic or open).
Pathology
Histologic and histochemical
presentation of the respiratory
tract illnesses in children
Pathologic physiology
Pathophysiologic mechanisms of
the respiratory failure
Sampling of sputum, pleural
excudate, blood for bacterial
cultures
Physical examination of the
respiratory system in children.
Correct performance of
pulmonary tests.
Microbiology
Propedeutics of pediatric
diseases
Imaging studies
Intensive care
Indications and methods of
imaging studies in respiratory
tract illnesses
Symptoms and signs of
respiratory failure of different
stages, its etiology, and
principles of intensive care
Use knowledge of histologic and
histochemical presentation of
the respiratory tract illnesses in
children for evaluation of
clinical findings
Recognize symptom and signs
of respiratory failure
Assess microbiologic findings in
clinical context
Perform physical examination of
the respiratory system (gross
inspection, palpation,
percussion, auscultation), Assess
the results of pulmonary tests
Assess radiologic examination
of the chest
Recognize respiratory failure,
assess its severity, provide
emergency care
5. ABSTRACT FOR PRE-WORKSHOP SELF-EDUCATION
Upper respiratory infections, commonly referred to the acronym URI or URTI,
is the illness caused by an acute infection which involves the upper respiratory
tract: nose, sinuses, pharynx or larynx. In the United States, this represents
approximately one billion acute upper respiratory illnesses an
Signs and symptoms
Acute upper respiratory tract infections includes rhinosinusitis (common cold),
sinusitis, pharyngitis/tonsillitis, laryngitis and sometimes bronchitis. Symptoms
of URI's commonly include congestion, cough, running nose, sore throat, fever,
facial pressure and sneezing. Onset of the symptoms usually begins after 1-3 days
after exposure to a microbial pathogen, most commonly a virus. The duration of
the symptoms is typically 7 to 10 days but may persist longer.
It is important to mention that up to 15% of acute pharyngitis cases may be caused
by bacteria, commonly Group A Strep ("Strep Throat"). Generally, patients with
"Strep Throat" start with a sore throat as their first symptom and usually do not
have runny nose or cough or sneezing.
Pain and pressure of the ear caused by a middle ear infection (Otitis media) and the
reddening of they eye caused by Viral Conjunctivitis are often associated with
upper respiratory infections.
Influenza (the flu) is a more systemic illness, which can also involve the upper
respiratory tract, should be recognized as distinct from other causes of URI.
Treatment
Judicious use of antibiotics can decrease unnecessary adverse effects of antibiotics
as well as out-of-pocket costs to the patient. But more important, decreased
antibiotic usage will prevent development of drug resistant bacteria, which is now
a growing problem in the world. International, as well as local US health agencies,
have been strongly encouraging physicians to decrease the prescribing of
antibiotics to treat common upper respiratory tract infections because antibiotic
usage does not significantly reduce recovery time for these viral illnesses . Some
have advocated a delayed antibiotic approach to treating URIswhich seeks to
reduce the consumption of antibiotics while attempting to maintain patient
satisfaction. Most studies show no difference in improvement of symptoms
between those treated with antibiotics right away and those with delayed
prescriptions. Most studies also show no difference in patient satisfaction, patient
complications, symptoms between delayed and no antibiotics. It should be noted
that a strategy of "no antibiotics" results in even less antibiotic use than a strategy
of "delayed antibiotics". Until more effective treatments are available to treat the
common respiratory viruses responsible for the majority of cases, treatment
of URIs with rest, increased fluids, and symptomatic care with over-the-counter
medications will remain the treatment of choice. However, in certain higher risk
patients with underlying lung disease, such as chronic obstructive pulmonary
disease (COPD), evidence does exist to support the treatment of URIs with
antibiotics to shorten the course of illness and decrease treatment failure.
The use of Vitamin C in the prevention and treatment of upper respiratory
infections has been suggested since the initial isolation of vitamin C in
the 1930s. Several studies have failed to demonstrate that vitamin C
supplementation reduces the incidence of colds in the normal healthy population,
indicating that routine large dose prophylaxis with Vitamin C is not beneficial in
widespread community usage. Some evidence exists to indicate that it could be
justified in persons exposed to brief periods of severe physical exercise and/or cold
environments. The evidence does not support the use of Vitamin C at the onset of
colds as effective therapy.
TRACHEITIS
Tracheitis is a bacterial infection of the trachea (wind pipe) capable of producing.
Bacterial tracheitis is most often caused by Staphylococcus aureus and frequently
follows a recent viral upper respiratory infection. It affects mostly young children,
possibly because their small trachea is easily blocked by swelling.
Children may still have a cough from their previous infection but this rapidly
worsens. The child quickly develops stridor, a high pitched, crowing sound with
breathing and increasing breathing difficulty. Fever is generally high and the child
looks very ill. This condition may progress very rapidly.
These children may sound as if they have croup, but the usual croup treatments do
not improve the breathing difficulty.Tracheitis requires hospitalization and,
usually, a breathing tube (endotracheal tube) in order to maintain an open airway.
The infection is treated with an antistaphylococcal medications such as penicillin
or a cephalosporin that covers Staphylococcus. If a different organism is at fault,
the appropriate antibiotic is used.
Pathophysiology
Bacterial tracheitis is a diffuse inflammatory process of the larynx, trachea, and
bronchi with adherent or semiadherentmucopurulent membranes within the
trachea. The major site of disease is at the cricoid cartilage level, the narrowest part
of the trachea. Acute airway obstruction may develop secondary
to subglottic edema and sloughing of epithelial lining or accumulation
of mucopurulent membrane within the trachea. Signs and symptoms are usually
intermediate between those ofepiglottitis and croup.
Bacterial tracheitis may be more common in the pediatric patient because of the
size and shape of the subglottic airway. Thesubglottis is the narrowest portion of
the pediatric airway, assuming a funnel-shaped internal dimension. In this smaller
airway, relatively little edema can significantly reduce the diameter of the pediatric
airway, increasing resistance to airflow and work of breathing. With appropriate
airway support and antibiotics, most patients improve within 5 days.
Although the pathogenesis of bacterial tracheitis is unclear, mucosal damage or
impairment of local immune mechanisms due to a preceding viral infection, an
injury to trachea from recent intubation, or trauma may predispose the airway to
invasive infection with common pyogenic organisms.
History
Symptoms of bacterial tracheitis may be intermediately between those
of epiglottitis and croup. Presentation is either acute orsubacute.
In the classic presentation patients present acutely with fevers, toxic
appearance, stridor, tachypnea, respiratory distress, and high WBC counts. Cough
is frequent and not painful.
In a study by Salamone et al, a significant subset of older children (mean age, 8 y)
did not have severe clinical symptoms.
The prodrome is usually an upper respiratory infection, followed by progression to
higher fever, cough, inspiratory stridor, and a variable degree of respiratory
distress.
Patients may acutely decompensate with worsening respiratory distress due to
airway obstruction from a purulent membrane that has loosened.
Patients have been reported to present with symptoms and signs of
bacterial tracheitis and multiorgan failure due to exotoxin-producing strains of
Staphylococcus aureus or Streptococcus pyogenes in the trachea.
A high index of suspicion for bacterial tracheitis is needed in children with viral
croup–like symptoms who do not respond to standard croup treatment or clinically
worsen.
Causes
 S aureus: Community-associated methicillin-resistant S aureus (CA-MRSA)
has recently emerged as an important agent in the United States; this could
result in a greater frequency of MRSA strains that cause tracheitis.
 S pyogenes,
Streptococcus pneumoniae,
and
other
alpha hemolytic streptococcal species
 Moraxella catarrhalis: Recent reports suggest it is a leading cause of
bacterial tracheitis and associated with increased intubation.
 Haemophilus influenzae type B (Hib): This cause is less common since the
introduction of the Hib vaccine.
 Klebsiella species
 Pseudomonas species
 Anaerobes
 Peptostreptococcus species
 Bacteroides species
 Prevotella species
Other:
 Mycoplasma pneumoniae
 Mycobacterium tuberculosis (endobronchial disease)
Symptoms

increasing deep or barking croup-like cough following a previous upper
respiratory infection
 crowing sound when the child inhales (inspiratory stridor)
 high fever
 very sick-looking child (toxic)
 breathing difficulty, increasing in severity over time
 intercostal retractions (the muscles between the ribs pull in as the child
attempts to breathe)
Signs and tests
 nasopharyngeal culture (shows Staphylococcus aureus or other organisms)
 tracheal culture (shows Staphylococcus aureus or other organisms)
 blood gasses (show decreased oxygen saturation, decreased pO2)
 X-ray of the trachea (shows narrowing of the tracheal airway, but normal
epiglottis)
 purulent (pus-filled) tracheal secretions may be obtained while placing the
breathing tube in the patient
Treatment
Treatment of bacterial tracheitis consists of the following:
Airway
 Maintenance of an adequate airway is of primary importance.
 Avoid agitating the child. If the patient's respiratory status
deteriorates, it is usually because of movement of the membrane,
and bag-valve-mask ventilation should be effective.
 If intubation is required, use an endotracheal tube 0.5-1 size
smaller than expected in order to minimize trauma in the
inflamed subglottic area. Frequent suctioning and high air
humidity is necessary to maintain endotrachealtube patency;
therefore, use the most appropriate-sized tube (without causing
trauma). Most patients (57-100%) require eventual intubation.
Intravenous access and medication
 Once the airway is stabilized, obtain intravenous access for initiation
of antibiotics.
 Antibiotic regimens have traditionally included a third-generation
cephalosporin (eg, cefotaxime, ceftriaxone) and apenicillinaseresistant penicillin (eg, oxacillin, nafcillin). Recently, clindamycin (40
mg/kg/d intravenously [IV], divided every 8 h) is used instead
of penicillinase-resistant penicillin against community acquired–
methicillin-resistant S aureus (CA-MRSA) in places where resistance
rates of CA-MRSA to clindamycin is low.6

Vancomycin (45 mg/kg/d IV, divided every 8 h), with or
without clindamycin, should be started in patients who appear toxic or
have multiorgan involvement or if MRSA is prevalent in the
community.
The child often needs to have an airway or breathing tube placed
(endotracheal tube). Antibiotics are given through a vein, usually a type of
penicillin or one of the cephalosporins. Oxygen is usually given, and the blood
gases are monitored to be sure that the child is breathing adequately.
Surgical Care
 Tracheostomy
 Tracheostomy is rarely necessary unless injury or trauma to the
airway has caused scarring and documented narrowing of the
airway. Tracheostomy is necessary if the patient has
failed extubations despite appropriate medical management or if
intubation is prolonged.
 Pulmonary toilet is potentially better with tracheostomy.
 Consultations
 Otorhinolaryngology - For endoscopic procedures and acute
airway management
 Pediatric intensivist - Necessary because of potential for
acute decompensation
Medication
Antibiotic agents
Empiric antimicrobial therapy in bacterial tracheitis must be comprehensive and
should cover all likely pathogens in the context of the clinical setting.
Expectations (prognosis)
Full recovery is expected if the patient can be brought to a medical facility in time.
 fairway obstruction with cardiorespiratory arrest and possibly death — the
breathing stops, then the heartbeat stops
 toxic shock syndrome (only if the organism is Staphylococcus)
Rhinitis
Rhinitis (pron.: /raɪˈnaɪtɪs/) is a medical term for irritation and inflammation of
the mucous membrane inside the nose. Common symptoms of rhinitis are a stuffy
nose, runny nose, and post-nasal drip. The most common kind of rhinitis is allergic
rhinitis, which is usually triggered by airborne allergens such as pollen and dander.
Allergic rhinitis may cause additional symptoms, such as sneezing and nasal
itching, coughing, headache, fatigue, malaise, and cognitive impairment. The
allergens may also affect the eyes, causing watery, reddened or itchy eyes and
puffiness around the eyes.
Rhinitis is very common. Allergic rhinitis is more common in some countries than
others; in the United States, about 10%-30% of adults are affected annually.
In rhinitis, the inflammation of the mucous membrane is caused by viruses,
bacteria, irritants or allergens. The inflammation results in the generation of large
amounts of mucus, commonly producing a runny nose, as well as a stuffy nose and
post-nasal drip. In the case of allergic rhinitis, the inflammation is caused by
the degranulation of mast cells in the nose. When mast cellsdegranulate, they
release histamine and other chemicals, starting an inflammatory process that can
cause symptoms outside the nose, such as fatigue and malaise.
Types
Rhinitis is categorized into three types: (i) infective rhinitis includes acute and
chronic bacterial infections; (ii) nonallergic(vasomotor) rhinitis includes
autonomic, hormonal, drug-induced, atrophic, and gustatory rhinitis, as well as
rhinitismedicamentosa; (iii) allergic rhinitis, triggered by pollen, mold, animal
dander, dust and other similar inhaled allergens.
Infectious
Rhinitis is commonly caused by a viral or bacterial infection, including the
common cold, which is caused by Rhinoviruses andCoronaviruses, or bacterial
sinusitis. Symptoms of the common cold include rhinorrhea, sore throat
(pharyngitis), cough, congestion, and slight headache.
Vasomotor rhinitis
Non-allergic rhinitis refers to runny nose that is not due to allergy. Non-allergic
rhinitis can be classified as either non-inflammatory or inflammatory rhinitis. One
very common type of non-inflammatory, non-allergic rhinitis that is sometimes
confused with allergy is called vasomotor rhinitis, in which certain nonspecific
stimuli, including changes in environment (temperature, humidity, barometric
pressure, or weather); airborne irritants (odors, fumes); dietary factors (spicy food,
alcohol); sexual arousal; and emotional factors. There is still much to be learned
about this entity, but it is thought that these non-allergic triggers cause dilation of
the blood vessels in the lining of the nose, which results in swelling, and drainage.
Vasomotor rhinitis can coexist with allergic rhinitis, and this is called "mixed
rhinitis." (Middleton's Allergy Principles and Practice, seventh edition.) The
pathology of vasomotor rhinitis appears to involve neurogenic inflammation and is
as yet not very well understood. Vasomotor rhinitis appears to be significantly
more common in women than men, leading some researchers to believe that
hormones play a role. In general, age of onset occurs after 20 years of age, in
contrast to allergic rhinitis which can be developed at any age. Individuals
suffering from vasomotor rhinitis typically experience symptoms year-round,
though symptoms may be exacerbated in the spring and autumn when rapid
weather changes are more common. An estimated 17 million United States citizens
have vasomotor rhinitis. The antihistamines azelastine and olopatadine, applied as
nasal sprays, may both be effective for vasomotor rhinitis. Fluticasone propionate
or budesonide (both are steroids) in nostril spray form may also be used for
symptomatic treatment.
Allergic
Pollen grains from a variety of common plants can cause hay fever
Allergic rhinitis or hay fever may follow when an allergen such as pollen or dust
is inhaled by an individual with a sensitized immune system, triggering antibody
production. These antibodies mostly bind to mast cells, which contain histamine.
When the mast cells are stimulated by pollen and dust, histamine (and other
chemicals) are released. This
causes
itching,
swelling,
and
mucus
production. Symptoms vary in severity between individuals. Very sensitive
individuals can experience hives or other rashes. Particulate matter in polluted air
and chemicals such as chlorine and detergents, which can normally be tolerated,
can greatly aggravate the condition.
Characteristic physical findings in individuals who have allergic rhinitis
include conjunctival swelling and erythema, eyelid swelling, lower eyelid venous
stasis, lateral crease on the nose, swollen nasal turbinates, and middle ear effusion.
Even if a person has negative skin-prick, intradermal and blood tests for allergies,
they may still have allergic rhinitis, from a local allergy in the nose. This is called
local allergic rhinitis. Many people who were previously diagnosed
with nonallergicrhinitis may actually have local allergic rhinitis.
detergents, which can normally be tolerated, can greatly aggravate allergic rhinitis.
The physician John Bostock first described hay fever in 1819 as a disease.
The characteristic symptoms of allergic rhinitis are: rhinorrhea (excess nasal
secretion), itching, and nasal congestion and obstruction. Characteristic physical
findings include conjunctival swelling and erythema, eyelid swelling, lower eyelid
venous stasis, swollen nasal turbinates, and middle ear effusion.
Other physical signs include folds in the skin below the lower eyelid known
as Dennie–Morgan folds, and rings under the eyes, known in patients with allergic
rhinitis as "allergic shiners". There can also be behavioural signs; in order to
relieve the irritation or flow of mucus, patients may wipe or rub their nose with the
palm of their hand in an upward motion: an action known as the "nasal salute" or
the "allergic salute".
Management
The goal of rhinitis treatment is to prevent or reduce the symptoms caused by the
inflammation of affected tissues. Measures which are effective include avoiding
the allergen. Intranasal corticosteroids are the preferred treatment if medications
are required with other options used only if these are not effective. Mite proof
covers, air filters, and withholding certain foods in childhood do not have evidence
supporting their effectiveness.
Steroids
Intranasal corticosteroids are used to control symptoms associated with
sneezing, rhinorrhea, itching and nasal congestion. It is an excellent choice for
perennial rhinitis. Steroid nasal sprays are effective and safe, and may be effective
without oral antihistamines. They take several days to act and so need be taken
continually for several weeks as their therapeutic effect builds up with time.
Systemic steroids such as prednisone are effective at reducing nasal inflammation,
but their use is limited by their short duration of effect and the side effects of
prolonged steroid therapy.
Other
Other measures that may be used second line include: antihistamines,
decongestants, cromolyn, leukotriene receptor antagonists,
and nonpharmacologic therapies such as nasal irrigation.
Antihistamine drugs can have undesirable side-effects, most notably drowsiness.
First generation antihistamine drugs such asdiphenhydramine cause drowsiness,
but not second- and third-generation antihistamines such
as cetirizine and loratadine.
Antihistamine drugs can be taken orally to control symptoms such as
sneezing, rhinorrhea, itching and conjunctivitis. It is best to take the medication
before exposure, especially for seasonal allergic rhinitis. Ophthalmic
antihistamines (such as ketotifen) are used for conjunctivitis; intranasal forms are
used for sneezing, rhinorrhea and nasal pruritus.
Pseudoephedrine is also indicated for vasomotor rhinitis. It is only used when
nasal congestion is present and can be used with antihistamines. In the United
States, oral decongestants containing pseudoephedrine must be purchased behind
the pharmacy counter by law to combat the making of methamphetamine.
Topical decongestants: may also be helpful in reducing symptoms such as nasal
congestion, but should not be used for long periods as stopping them after
protracted use can lead to a rebound nasal congestion (Rhinitis medicamentosa).
For nocturnal symptoms, intranasal corticosteroids can be combined with
nightly oxymetazoline, an adrenergic alpha-agonist, without risk of
rhinitis medicamentosa.
Desensitization
Common cold
The common cold (also known as nasopharyngitis, rhinopharyngitis, acute coryza,
or a cold) is a viral infectious disease of the upper respiratory tract which affects
primarily the nose. Symptoms include coughing, sore throat, runny nose, and fever
which usually resolve in seven to ten days, with some symptoms lasting up to three
weeks. Well over 200 viruses are implicated in the cause of the common cold; the
rhinoviruses are the most common.
Upper respiratory tract infections are loosely divided by the areas they affect, with
the common cold primarily affecting the nose, the throat (pharyngitis), and the
sinuses (sinusitis). Symptoms are mostly due to the body's immune response to the
infection rather than to tissue destruction by the viruses themselves. The primary
method of prevention is by hand washing with some evidence to support the
effectiveness of wearing face masks.
No cure for the common cold exists, but the symptoms can be treated. It is the
most frequent infectious disease in humans with the average adult contracting two
to three colds a year and the average child contracting between six and
twelve. Theseinfections have been with humanity since antiquity.
Signs and symptoms
The typical symptoms of a cold include cough, runny nose, nasal congestion and a
sore throat, sometimes accompanied by muscle ache, fatigue, headache, and loss of
appetite. A sore throat is present in about 40% of the cases and a cough in about
50%, while muscle ache occurs in about half. In adults, a fever is generally not
present but it is common in infants and young children. The cough is usually mild
compared to that accompanying influenza. While a cough and a fever indicate a
higher likelihood of influenza in adults, a great deal of similarity exists between
these two conditions. A number of the viruses that cause the common cold may
also result in asymptomatic infections. The color of the sputum or nasal secretion
may vary from clear to yellow to green and does not predict the class of agent
causing the infection.
Progression
A cold usually begins with fatigue, a feeling of being chilled, sneezing and a
headache, followed in a couple of days by a runny nose and cough. Symptoms may
begin within 16 hours of exposure and typically peak two to four days after onset.
They usually resolve in seven to ten days but some can last for up to three weeks.
In children, the cough lasts for more than ten days in 35–40% of the cases and
continues for more than 25 days in 10%.
Cause:Viruses
The common cold is a viral infection of the upper respiratory tract. The most
commonly implicated virus is a rhinovirus (30–80%), a type of picornavirus with
99
known
serotypes.
Others
include: coronavirus (10–15%),
human parainfluenza viruses,
human
respiratory syncytial virus,
adenoviruses, enteroviruses, and metapneumovirus. Frequently more than one
virus is present. In total over 200 different viral types are associated with colds.
Transmission
The common cold virus is typically transmitted via airborne droplets (aerosols),
direct contact with infected nasal secretions, orfomites (contaminated objects).
Which of these routes is of primary importance has not been determined. The
viruses may survive for prolonged periods in the environment and can be picked up
by people's hands and subsequently carried to their eyes or nose where infection
occurs. Transmission is common in daycare and at school due to the close
proximity of many children with little immunity and frequently poor hygiene.
These infections are then brought home to other members of the family. There is
no evidence that recirculated air during commercial flight is a method of
transmission. However, people sitting in close proximity appear at greater risk.
Rhinovirus-caused colds are most infectious during the first three days of
symptoms; they are much less infectious afterwards.
Weather
The traditional folk theory is that a cold can be "caught" by prolonged exposure to
cold weather such as rain or winter conditions, which is how the disease got its
name. The role of body cooling as a risk factor for the common cold is
controversial. Some of the viruses that cause the common colds are seasonal,
occurring more frequently during cold or wet weather. Some believe this to be due
primarily to increased time spent indoors in close proximity; specifically children
returning to school. However, it may also be related to changes in the respiratory
system that result in greater susceptibility. Low humidity increases viral
transmission rates potentially due to dry air allowing small viral droplets to
disperse farther and stay in the air longer.
Other
Herd immunity, generated from previous exposure to cold viruses, plays an
important role in limiting viral spread, as seen with younger populations that have
greater rates of respiratory infections. Poor immune function is also a risk factor
for disease. Insufficient sleep and malnutrition have been associated with a greater
risk of developing infection following rhinovirus exposure; this is believed to be
due to their effects on immune function.
Pathophysiology
The common cold is a disease of the upper respiratory tract.
The symptoms of the common cold are believed to be primarily related to the
immune response to the virus. The mechanism of this immune response is virus
specific. For example, the rhinovirus is typically acquired by direct contact; it
binds to human ICAM-1 receptors through unknown mechanisms to trigger the
release of inflammatory mediators. These inflammatory mediators then produce
the symptoms. It does not generally cause damage to the nasal epithelium. The
respiratory syncytialvirus (RSV) on the other hand is contracted by both direct
contact and air born droplets. It then replicates in the nose and throat before
frequently spreading to the lower respiratory tract. RSV does cause epithelium
damage. Human parainfluenzavirus typically results in inflammation of the nose,
throat, and bronchi. In young children when it affects the trachea it may produce
the symptoms of croup due to the small size of their airway.
Diagnosis
The distinction between different viral upper respiratory tract infections is loosely
based on the location of symptoms with the common cold affecting primarily the
nose, pharyngitis the throat, and bronchitis the lungs. There however can be
significant overlap and multiple areas can be affected. The common cold is
frequently defined as nasal inflammation with varying amount of throat
inflammation. Self-diagnosis is frequent. Isolation of the actual viral agent
involved is rarely performed, and it is generally not possible to identify the virus
type through symptoms.
Prevention
Physical measures to prevent the spread of cold viruses have been deemed the
only potentially effective measures for prevention. These measures include
primarily hand washing and face masks; in the health care environment, gowns and
disposable gloves are also used. Efforts such as quarantine are not possible as the
disease is so widespread and symptoms are non-specific. Vaccination has proved
difficult as there are so many viruses involved and they change rapidly. Creation of
a broadly effective vaccine is thus highly improbable.
Regular hand washing appears to be effective at reducing the transmission of cold
viruses
especially
among
children.
Whether
the
addition
of antivirals or antibacterials to normal hand washing provides greater benefit is
unknown. Wearing face masks when around people who are infected may be
beneficial; however, there is insufficient evidence for maintaining a greater social
distance. Zinc supplementation may be effective at decreasing the rate of
colds.[36] Routine vitamin C supplementation does not reduce the risk or severity
of the common cold, though it may reduce its duration.
Management
There are currently no medications or herbal remedies which have been
conclusively demonstrated to shorten the duration of infection. Treatment thus
comprises symptomatic relief. Getting plenty of rest, drinking fluids to maintain
hydration, and gargling with warm salt water, are reasonable conservative
measures. Much of the benefit from treatment is however attributed to the placebo
effect.
Symptomatic
Treatments that help alleviate symptoms include simple analgesics and
antipyretics such as ibuprofen and acetaminophen/paracetamol. Evidence does not
show that cough medicines are any more effective than simple analgesics and they
are not recommended for use in children due to a lack of evidence supporting
effectiveness and the potential for harm. In 2009, Canada restricted the use of overthe-counter cough and cold medication in children six years and under due to
concerns regarding risks and unproven benefits. In adults there is insufficient
evidence to support the use of cough medications in adults. The misuse
of dextromethorphan (an over-the-counter cough medicine) has led to its ban in a
number of countries.
In adults the symptoms of a runny nose can be reduced by first-generation
antihistamines; however, they are associated with adverse effects such as
drowsiness. Other decongestants such as pseudoephedrine are also effective in this
population.Ipratropium nasal spray may reduce the symptoms of a runny nose but
there is little effect on stuffiness. Second-generation antihistamines however do not
appear to be effective.
Due to lack of studies, it is not known whether increased fluid intake improves
symptoms or shortens respiratory illness and a similar lack of data exists for the
use of heated humidified air. One study has found chest vapor rub to be effective at
providing some symptomatic relief of nocturnal cough, congestion, and sleep
difficulty.
Antibiotics and antivirals
Antibiotics have no effect against viral infections and thus have no effect against
the viruses that cause the common cold. Due to their side effects they cause overall
harm; however, they are still frequently prescribed. Some of the reasons that
antibiotics are so commonly prescribed include: people's expectations for them,
physicians' desire to do something, and the difficulty in excluding complications
that may be amenable to antibiotics. There are no effective antiviral drugs for the
common cold even though some preliminary research has shown benefit.
Alternative treatments
While there are many alternative treatments used for the common cold, there is
insufficient scientific evidence to support the use of most. As of 2010 there is
insufficient evidence to recommend for or against either honey or nasal irrigation.
Studies suggested that zinc, if taken within 24 hours of the onset of symptoms,
reduces the duration and severity of the common cold in healthy people. Due to
wide differences between the studies, further research may be needed to determine
how and when zinc may be effective. Vitamin C's effect on the common cold while
extensively researched is disappointing, except in limited circumstances,
specifically, individuals exercising vigorously in cold environments. Evidence
about
the
usefulness
of echinaceais
inconsistent.
Different
types
of echinacea supplements may vary in their effectiveness. It is unknown if garlic is
effective.[64] A single trial of vitamin D did not find benefit.
Prognosis
The common cold is generally mild and self-limiting with most symptoms
generally improving in a week. Severe complications, if they occur, are usually in
the very old, the very young or those who are immunosuppressed. Secondary
bacterial infections may occur resulting in sinusitis, pharyngitis, or an ear
infection. It is estimated that sinusitis occurs in 8% and an ear infection in 30% of
cases.
Epidemiology
The common cold is the most common human disease and all peoples globally are
affected. Adults typically have two to five infections annually and children may
have six to ten colds a year (and up to twelve colds a year for school children).
Rates of symptomatic infections increase in the elderly due to a worsening immune
system.
Research
A number of antivirals have been tested for effectiveness in the common cold;
however as of 2009 none have been both found effective and licensed for use.
Researchersfrom University of Maryland, CollegePark and University of Wisconsi
n–Madison have mapped the genome for all known virus strains that cause the
common cold
ACUTE BRONCHITIS
CLINICAL MANIFESTATIONS.
Acute bronchitis is commonly preceded by a viral upper respiratory tract infection.
It is more common in the winter when respiratory viral syndromes predominate.
The tracheobronchial epithelium is invaded by the infectious agent, leading to
activation of inflammatory cells and release of cytokines. Constitutional
symptoms, such as fever and malaise, follow. The tracheobronchial epithelium
may become significantly damaged or hypersensitized, leading to a protracted
cough lasting 1–3 wk.
The child 1st presents with nonspecific upper respiratory infectious symptoms,
such as rhinitis. Three to 4 days later, a frequent, dry, hacking cough develops,
which may or may not be productive. After several days, the sputum may become
purulent, indicating leukocyte migration but not necessarily bacterial infection.
Many children swallow their sputum, and this may produce emesis. Chest pain
may be a prominent complaint in older children, exacerbated by coughing. The
mucus gradually thins, usually within 5–10 days, and then the cough gradually
abates. The entire episode usually lasts about 2 wk and seldom longer than 3 wk.
Findings on physical examination vary with age of the patient and stage of the
disease. Early findings are absent or are low-grade fever and upper respiratory
signs such as nasopharyngitis, conjunctivitis, and rhinitis. Auscultation of the chest
may be unremarkable at this early phase. As the syndrome progresses and cough
worsens, breath sounds become coarse, with coarse and fine crackles and scattered
high-pitched wheezing. Chest radiographs are normal or may have increased
bronchial markings.
The principal objective of the clinician is to exclude pneumonia, which is more
likely caused by bacterial agents requiring antibiotic therapy. In adults, absence of
abnormality of vital signs (tachycardia, tachypnea, fever) and a normal physical
examination of the chest reduce the likelihood of pneumonia.
DIFFERENTIAL DIAGNOSIS.
Persistent or recurrent symptoms should lead the clinician to consider entities other than
acute bronchitis. Many entities manifest with cough as a prominent symptom ( Table
388-3 ).
TABLE 388-3 -- Disorders with Cough as a Prominent Finding
CATEGORY
DIAGNOSES
Inflammatory
Asthma
Chronic pulmonary processes
Bronchopulmonary dysplasia/chronic lung disease
Postinfectious bronchiectasis
Cystic fibrosis
Tracheo- or bronchomalacia
Ciliary abnormalities
Other chronic disease/congenital
disorders
Laryngeal cleft
Swallowing disorders
Gastroesophageal reflux
Airway compression (such as a vascular ring or
hemangioma)
Congenital heart disease
Infectious/immune disorders
Immunodeficiency
Tuberculosis
Allergy
Sinusitis
Tonsillitis or adenoiditis
Chlamydia, Ureaplasma (infants)
Bordetella pertussis
Mycoplasma pneumoniae
Acquired
Foreign body aspiration, tracheal or esophageal
TREATMENT.There is no specific therapy for acute bronchitis. The disease is selflimited, and antibiotics, although frequently prescribed, do not hasten improvement.
Frequent shifts in position may facilitate pulmonary drainage in infants. Older children
are sometimes more comfortable with humidity, but this does not shorten the disease
course. Cough suppressants may produce symptomatic relief but may also increase the
risk of suppuration and inspissated secretions and, therefore, should be used judiciously.
Antihistamines dry secretions and are not helpful; expectorants are likewise not
indicated.
ACUTE BRONCHIOLITIS AND INFLAMMATION OF THE AIRWAY.
Infection can cause obstruction to flow by internal narrowing of the airways.
Acute bronchiolitis is predominantly a viral disease. Respiratory syncytial virus
(RSV) is responsible for >50% of cases (see Chapter 257 ). Other agents include
parainfluenza (see Chapter 256 ), adenovirus, Mycoplasma, and, occasionally,
other viruses. Human metapneumovirus (see Chapter 258 ) is an important primary
cause of viral respiratory infection or it can occur as a co-infection with RSV.
There is no evidence of a bacterial cause for bronchiolitis, although bacterial
pneumonia is sometimes confused clinically with bronchiolitis and bronchiolitis is
rarely followed by bacterial superinfection.
Approximately 50,000–80,000 of hospitalizations annually among children <1 yr
old are attributable to RSV infection, with 200–500 deaths per yr in the United
States. Increasing rates of hospitalization may reflect increased attendance of
infants in daycare centers, changes in criteria for hospital admission, and/or
improved survival of premature infants and others at risk for severe RSVassociated disease.
Bronchiolitis is more common in males, in those who have not been breast-fed, and
in those who live in crowded conditions. Older family members are a common
source of infection; they may only experience minor respiratory symptoms. The
clinical manifestations of lower respiratory tract illness (LRTI) seen in young
infants may be minimal in older patients, in whom bronchiolar edema is better
tolerated.
Not all infected infants develop LRTI. Host anatomic and immunologic factors
seem to play a significant role in the severity of the clinical syndrome. Infants with
pre-existent smaller airways and diminished lung function have a more severe
course. In addition, RSV infection incites a complex immune response.
Eosinophils degranulate and release eosinophil cationic protein, which is cytotoxic
to airway epithelium. Immunoglobulin E (IgE) antibody release may also be
related to wheezing. Other mediators invoked in the pathogenesis of airway
inflammation include chemokines such as interleukin 8 (IL-8), macrophage
inflammatory protein (MIP) 1α, and RANTES (regulated on activation, normal
Tcell expressed and secreted). RSV-infected infants who wheeze express higher
levels of interferon-γ in the airway as well as leukotrienes. RSV co-infection with
metapneumovirus can be more severe than monoinfection.
Acute bronchiolitis 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 bron chiolar 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, there will be resorption of
trapped distal air, 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 may
develop.
Chronic infectious causes of wheezing should be considered in those infants who
seem to fall out of the range of a normal clinical course. Cystic fibrosis is one such
entity; suspicion increases in a patient with persistent respiratory symptoms, digital
clubbing, malabsorption, failure to thrive, electrolyte abnormalities, or a resistance
to bronchodilator treatment (see Chapter 400 ).
Allergy and asthma are important causes of wheezing and probably generate the
most questions by the parents of a wheezing infant. Asthma is characterized by
airway inflammation, bronchial hyperreactivity, and reversibility of obstruction
(see Chapter 143 ). Three identified patterns of infant wheezing are: the transient
early wheezer, 19.9% of the general population, had wheezing at least once with a
lower respiratory infection before the age of 3 yr but never wheezed again; the
persistent wheezer, 13.7% of the general population, had wheezing episodes before
3 yr and was still wheezing at 6 yr of age; and the late onset wheezer, 15% of the
general population, had no wheezing by 3 yr but was wheezing by 6 yr. The other
½ of the children had never wheezed by 6 yr. Of all the infants who wheezed
before 3 yr old, almost 60% stopped wheezing by 6 yr. Risk factors for persistent
wheezing included maternal asthma, maternal smoking, persistent rhinitis (apart
from acute upper respiratory tract infections), and eczema at <1 yr of age.
OTHER CAUSES.
Congenital malformations of the respiratory tract cause wheezing in early infancy.
These findings can be diffuse or focal and can be from an external compression or
an intrinsic abnormality. External vascular compression includes a vascular ring,
in which the trachea and esophagus are surrounded completely by vascular
structures, or a vascular sling, in which the trachea and esophagus are not
completely encircled (see Chapter 432 ). Cardiovascular causes of wheezing
include dilated chambers of the heart including massive cardiomegaly, left atrial
enlargement, and dilated pulmonary arteries. Pulmonary edema caused by heart
failure can also cause wheezing by lymphatic and bronchial vessel engorgement
that leads to obstruction and edema of the bronchioles and further obstruction (see
Chapter 442 ).
Foreign body aspiration (see Chapter 384 ) can cause acute or chronic wheezing. It
is estimated that 78% of those who die from foreign body aspiration are between 2
mo and 4 yr old. Even in young infants, a foreign body can be ingested if given to
the infant by another person such as an older sibling. Infants who have atypical
histories or misleading clinical and radiologic findings may be misdiagnosed with
asthma or another obstructive disorder as inflammation and granulation develop
around the foreign body. Esophageal foreign body can transmit pressure to the
membranous trachea, causing compromise of the airway lumen.
Gastroesophageal reflux (see Chapter 320.1 ) can cause wheezing with or without
direct aspiration into the tracheobronchial tree. Without aspiration, the reflux is
thought to trigger a vagal or neural reflex, causing increased airway resistance and
airway reactivity. Aspiration from gastroesophageal reflux or from the direct
aspiration from oral liquids can also cause wheezing.Trauma and tumors are much
more rare causes of wheezing in infants. Trauma of any type to the
tracheobronchial tree can cause an obstruction to airflow. Accidental or
nonaccidental aspirations, burns, or scalds of the tracheobronchial tree can cause
inflammation of the airways and subsequent wheezing. Any space-occupying
lesion either in the lung itself or extrinsic to the lung can cause tracheobronchial
compression and obstruction to airflow.
CLINICAL MANIFESTATIONS
HISTORY AND PHYSICAL EXAMINATION.
Initial history of a wheezing infant should include accounts of the recent event
including onset, duration, and associated factors ( Table 388-2 ). Birth history
includes weeks of gestation, neonatal intensive care unit admission, history of
intubation or oxygen requirement, maternal complications including infection,
herpes simplex virus (HSV) status, HIV status, and prenatal smoke exposure. Past
medical history includes any co-morbid conditions including syndromes or
associations. Family history of cystic fibrosis, immunodeficiencies, asthma in a
1st-degree relative, or any other recurrent respiratory conditions in children should
be obtained. Social history should include an environmental history including any
smokers at home, inside or out, daycare exposure, number of siblings, occupation
of inhabitants of the home, pets, tuberculosis exposure, and concerns regarding
home environment (i.e. dust mites, construction dust, heating and cooling
techniques, mold, cockroaches).
TABLE 388-2 -- Pertinent Medical History in the Wheezing Infant
Did the onset of symptoms begin at birth or thereafter?
Is the infant a noisy breather and when is it most prominent?
Is there a history of cough apart from wheezing?
Was there an earlier lower respiratory tract infection?
Have there been any emergency department visits, hospitalizations, or
intensive care unit admissions for respiratory distress?
Is there a history of eczema?
Does the infant cough after crying or cough at night?
How is the infant growing and developing?
Is there associated failure to thrive?
Is there failure to thrive without feeding difficulties?
Is there a history of electrolyte abnormalities?
Are there signs of intestinal malabsorption including frequent, greasy, or
oily stools?
Is there a maternal history of genital herpes simplex virus (HSV) infection?
What was the gestational age at delivery?
Was the patient intubated as a neonate?
Does the infant bottle-feed in the bed or the crib, especially in a propped
position?
Are there any feeding difficulties including choking, gagging, arching, or
vomiting with feeds?
Any new food exposure?
Is there a toddler in the home or lapse in supervision in which foreign body
aspiration could have occurred?
Change in caregivers or chance of nonaccidental trauma?
On physical examination, evaluation of the patient's vital signs with special
attention to the respiratory rate and the pulse oximetry reading for oxygen
saturation is an important initial step. There should also be a thorough review of
the patient's growth chart for signs of failure to thrive. Wheezing produces an
expiratory whistling sound that can be polyphonic or monophonic in nature.
Prolonged expiratory time may be present. Biphasic wheezing can occur if there is
a central, large airway obstruction. The lack of audible wheezing is not reassuring
if the infant shows other signs of respiratory distress because complete obstruction
to airflow can eliminate the turbulence, which causes the sound to resonate.
Aeration should be noted and a trial of a bronchodilator may be warranted to
evaluate for any change in wheezing after treatment. Listening to breath sounds
over the neck will help differentiate upper airway from lower airway sounds. The
absence or presence of stridor should be noted and appreciated on inspiration.
Signs of respiratory distress include tachypnea, increased respiratory effort, nasal
flaring, tracheal tugging, subcostal and intercostal retractions, and excess use of
accessory muscles. In the upper airway, signs of atopy, including boggy turbinates
and posterior oropharynx cobblestoning, can be evaluated in older infants. It is also
useful to evaluate the skin of the patient for eczema and any significant
hemangiomas; midline lesions may be associated with an intrathoracic lesion.
Digital clubbing should be noted (see Chapter 371 ).
Acute bronchiolitis is usually preceded by exposure to an older contact with a
minor respiratory syndrome within the previous wk. 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),
although the temperature may range from subnormal to markedly elevated.
Gradually, respiratory distress ensues, with paroxysmal wheezy cough, dyspnea,
and irritability. The infant is often tachypneic, which may interfere with feeding.
The child does not usually have other systemic complaints, such as diarrhea or
vomiting. Apnea may be more prominent than wheezing early in the course of the
disease, particularly with very young infants (<2 mo old) or former premature
infants.
The physical examination is characterized most prominently by wheezing. The
degree of tachypnea does not always correlate with the degree of hypoxemia or
hypercarbia, so the use of pulse oximetry and noninvasive carbon dioxide
determination is essential. Work of breathing may be markedly increased, with
nasal flaring and retractions. Auscultation may 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 may permit palpation of the liver and
spleen.
DIAGNOSTIC EVALUATION.
Initial evaluation is dependent on likely etiology; a baseline chest radiograph,
including posteroanterior and lateral films, is warranted in many cases and for any
infant in acute respiratory distress. Focal infiltrates are most often found in
wheezing infants who have a pulse oximetry reading <93%, grunting, decreased
breath sounds, prolonged inspiratory to expiratory ratio, and crackles. The chest
radiograph may also be useful for evaluation of hyperinflation (common in
bronchiolitis and viral pneumonia), signs of chronic disease such as bronchiectasis,
or a space-occupying lesion causing airway compression. A trial of bronchodilator
may be diagnostic as well as therapeutic because these medications can reverse
conditions such as bronchiolitis (occasionally) and asthma but will not affect a
fixed obstruction. Bronchodilators may potentially worsen a case of wheezing
caused by tracheal or bronchial malacia. A sweat test to evaluate for cystic fibrosis
and evaluation of baseline immune status are reasonable in infants with recurrent
wheezing or complicated courses. Further evaluation such as upper gastrointestinal
(GI) contrast x-rays, chest CT, bronchoscopy, infant pulmonary function testing,
video swallow study, and pH probe can be considered second-tier diagnostic
procedures in complicated patients.
In acute bronchiolitis, chest radiography reveals hyperinflated lungs with patchy
atelectasis. The white blood cell and differential counts are usually normal. Viral
testing (usually rapid immunofluorescence, polymerase chain reaction, or viral
culture) is helpful if the diagnosis is uncertain or for epidemiologic purposes. The
diagnosis is clinical, particularly in a previously healthy infant presenting with a
first-time wheezing episode during a community outbreak. Because concurrent
bacterial infection (sepsis, pneumonia, meningitis) is highly unlikely, confirmation
of viral bronchiolitis may obviate the need for a sepsis evaluation in a febrile infant
and assist with respiratory precautions and isolation if the patient requires
hospitalization.
TREATMENT
Treatment of an infant with wheezing depends on the underlying etiology.
Response to bronchodilators is unpredictable, regardless of cause, but suggests a
component of bronchial hyperreactivity. It is appropriate to administer albuterol
aerosol and objectively observe the response. For infants <3 yr of age, it is
acceptable to continue to administer inhaled medications through an MDI with
mask and spacer if a therapeutic benefit is demonstrated. Therapy should be
continued in all patients with asthma exacerbations from a viral illness.
The use of ipratropium bromide in this population is controversial, but it appears to
be somewhat effective as an adjunct therapy. It is also useful in infants with
significant tracheal and bronchial malacia who may be made worse by β-2 agonists
such as albuterol because of the subsequent decrease in smooth muscle tone.
A trial of inhaled steroids may be warranted in a patient who has responded to
multiple courses of oral steroids, has moderate to severe wheezing, or a significant
history of atopy including food allergy or eczema. Inhaled steroids are appropriate
for maintenance therapy in patients with known reactive airways but are
controversial when used for episodic or acute illnesses.
Oral steroids are generally reserved for atopic wheezing infants thought to have
asthma that is refractory to other medications. Their use in first-time wheezing
infants or those infants that do not warrant hospitalization is controversial.
Infants with acute bronchiolitis who are experiencing respiratory distress should be
hospitalized; the mainstay of treatment is supportive. If hypoxemic, the child
should receive cool humidified oxygen. Sedatives are to be avoided because they
may depress respiratory drive. The infant is sometimes more comfortable if sitting
with head and chest elevated at a 30-degree angle with neck extended. The risk of
aspiration of oral feedings may be high in infants with bronchiolitis, owing to
tachypnea and the increased work of breathing. The infant may be fed through a
nasogastric tube. If there is any risk for further respiratory decompensation
potentially necessitating tracheal intubation, however, the infant should not be fed
orally but be maintained with parenteral fluids. Frequent suctioning of nasal and
oral secretions often provides relief of distress or cyanosis. Oxygen is indicated in
all infants with hypoxia.
A number of agents have been proposed as adjunctive therapies for bronchiolitis.
Bronchodilators produce modest short-term improvement in clinical features, but
the statistical improvement in clinical scoring systems seen with them is not
always clinically significant. Several studies have included both infants with 1sttime wheezing and those with recurrent wheezing, complicating interpretation of
the data. Nebulized epinephrine may be more effective than β-agonists. A trial
dose of inhaled bronchodilator may be reasonable, with further therapy predicated
on response in the individual patient. Corticosteroids, whether parenteral, oral, or
inhaled, have been used for bronchiolitis despite conflicting and often negative
studies. Differences of diagnostic criteria, measures of effect, timing and route of
administration, and severity of illness complicate these studies. 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. There is no convincing evidence of a positive
impact on clinically important outcomes such as mortality and duration of
hospitalization. Antibiotics have no value unless there is secondary bacterial
pneumonia. Likewise, there is no support for RSV immunoglobulin administration
during acute episodes of RSV bronchiolitis.
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, uncompensated respiratory acidosis,
or severe dehydration. After this critical period, symptoms may persist. The
median duration of symptoms in ambulatory patients is ≈12 days. Infants with
conditions such as congenital heart disease, bronchopulmonary dysplasia, and
immunodeficiency often have more severe disease, with higher morbidity and
mortality. There is a higher incidence of wheezing and asthma in children with a
history of bronchiolitis unexplained by family history or other atopic syndromes. It
is unclear whether bronchiolitis incites an immune response that manifests as
asthma later or whether those infants have an inherent predilection for asthma that
is merely unmasked by their episode of RSV. Approximately 60% of infants who
wheeze will stop wheezing.
PREVENTION
Reduction in the severity and incidence of acute bronchiolitis due to RSV is
possible through the administration of pooled hyperimmune RSV intravenous
immunoglobulin (RSV-IVIG, RespiGam) and palivizumab (Synagis), an
intramuscular monoclonal antibody to the RSV F protein, before and during RSV
season. Palivizumab is recommended for infants <2 yr of age with chronic lung
disease (bronchopulmonary dysplasia) or prematurity. Meticulous handwashing is
the best measure to prevent nosocomial transmission.
6. MATERIALS FOR METHODOLOGICAL BACKGROUND OF THE WORKSHOP
6.1. Quiz
1. What is the diagnosis and differential diagnosis for the most common
acute respiratory infections of the upper respiratory tract in children?
2. What is the etiology of acute bronchitis?
3. What is the diagnosis and differential diagnosis for acute bronchitis?
4. What is the treatment approach for acute bronchitis?
5. What is the diagnosis and differential diagnosis for bronchiolitis?
6. What are the complications for bronchiolitis?
7. What is the treatment for bronchiolitis?
8. What is follow-up in bronchiolitis ?
6.2. Multi-choice questions
1. Acute bronchitis is more frequent in:
A.
The first year of life
B.
Newborn period
C.
Preschool age*
D.
School age
E.
Teenagers
6.3. The case report
On admission to the hospital, the physicianobserved the child aged 8 months
with fever, rhinirrhea and cough. On physical examination he revealed hoarseness,
tachypnea with usually shallow respirations, tachycardia, nasal flaring, retractions
and hyperinflation, wheeze, increased expiratory phase .
1. What is the diagnosis?
2. What is the plan of investigations?
3. What is the treatment plan?
Suggested reading
1. Nelson Textbook of Pediatrics, 2-Volume Set, 20th ed. by Kliegman R.M.,
Bonita M.D. Stanton MD, Geme J.S., Nina F Schor MD / Elsevier Inc.,
2016. P. 2057-2061.
2. Daniel Bernstein, Steven P. Shelov. Pediatrics for medical students. - USA:
Lippinkot Williams & Wilkins. – 2008. - 650 p.
3. Janette B. Benson. Diseases and Disorders in Infancy and Early Childhood /
Janette B. Benson Marshall M. Haith. - Academic Press, 2009 - 424 p.
Additional reading
1. Lecture:Bronchitis. Upperrespiratorytractinfections
2. Pediatric Skills /Jean W. Solomon, Jane Clifford O`Brien/ . USA: Mosby. 2011. - 630 p.
3. www.bookfinder.com/author/american-academy-of-pediatrics
4. www.emedicine.medscape.com
5. http://www.nlm.nih.gov/medlineplus/medlineplus.html