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U N I T 6
Respiratory Function
person open his or her mouth, and observing the hard
palate for light transmission. Sinus radiographs and com-
puted tomography (CT) scans may be used. CT scans
usually are reserved for diagnosis of chronic rhinosinus-
itis or to exclude complications.
7,8
Magnetic resonance
imaging (MRI) is expensive and usually reserved for
cases of suspected neoplasms or fungal sinusitis.
Treatment.
Treatment of rhinosinusitis depends on the
cause and includes appropriate use of antibiotics, intra-
nasal corticosteroids, mucolytic agents, and symptom
relief measures.
7–12
Antibiotics are usually reserved for
persons with severe or persistent symptoms and specific
findings of bacterial infection. The treatment of acute
rhinosinusitis includes measures to promote adequate
drainage by reducing nasal congestion. The topical
α
-adrenergic decongestants may be used on a short-term
(3 days) basis in older children and adults for this pur-
pose. The use of antihistamines is controversial, par-
ticularly for acute rhinosinusitis, because they can dry
up secretions and thereby decrease drainage. Mucolytic
agents such as guaifenesin may be used to thin secre-
tions. Intranasal corticosteroids reduce inflammation
and edema of the nasal mucosa, nasal turbinates, and
sinus ostia. They may be used as an initial treatment in
persons with acute rhinosinusitis and in those with both
allergies and rhinosinusitis.
7,8
Nonpharmacologic mea-
sures include saline nasal sprays and steam inhalation.
Surgical intervention directed at correcting obstruc-
tion of the ostiomeatal openings may be indicated in
persons with chronic rhinosinusitis that is resistant to
other forms of therapy. Indications for surgical inter-
vention include obstructive nasal polyps and obstructive
nasal deformities.
Complications.
Because of the sinuses’ proximity to
the brain and orbital wall, sinusitis can lead to intracra-
nial and orbital wall complications. Intracranial compli-
cations are seen most commonly with infection of the
frontal and ethmoid sinuses because of their proximity
to the dura and drainage of the veins from the frontal
sinus into the dural sinus. Orbital complications can
range from edema of the eyelids to orbital cellulitis and
subperiosteal abscess formation. Facial swelling over
the involved sinus, abnormal extraocular movements,
protrusion of the eyeball, periorbital edema, or changes
in mental status may indicate intracranial complications
and require immediate medical attention.
Influenza
Influenza is one of the most important causes of acute
upper respiratory tract infection in humans. Until the
advent of acquired immunodeficiency syndrome (AIDS),
influenza was the last uncontrolled, potentially fatal pan-
demic. In the United States, epidemics of influenza typi-
cally occur during the winter months, accounting for over
35,000 deaths annually.
13
Rates of infection are highest
among children, but rates of serious illness and death are
highest among persons who are 65 years of age or older.
Etiology
Influenza is caused by viruses belonging to the Ortho
myxoviridae family, whose members are characterized
by a segmented, single-stranded ribonucleic acid (RNA)
genome.
13–15
There are three distinct types of influenza
viruses, designated A, B, and C. Influenza A and B cause
epidemics. Influenza C does not cause epidemics, but is
responsible for mild upper respiratory infections in chil-
dren and adults.
Influenza A viruses are further categorized into sub-
types based on two glycoproteins studding their lipid
envelope: hemagglutinin (H) and neuraminidase (N)
(Fig. 22-2). Hemagglutinin, for which there are 16 differ-
ent variants (H1 thru H16), allows the virus to anchor to
the surface of epithelial cells in the respiratory tract; and
neuraminidase, of which there are 9 variants (N1 thru
N9), allows for digestion of host secretion and, later,
release of viral particles from host cells.
15
For example,
an influenza virus circulating worldwide in 2013 was
identified as H3N2. Immunity to the surface H and
N antigens reduces the likelihood and severity of infec-
tion with the influenza virus.
Epidemics and pandemics result from the ability of the
influenza virus to develop new subtypes against which
the population is not protected.
13–15
The genetic diver-
sity of influenza A is fostered by its segmented genomic
structure and ability to infect and replicate in humans
and many avian and animal species, including swine.
Epidemics of influenza A occur when minor changes in
the amino acids of the H and N glycoproteins, called
antigenic drift,
generate a new subtype to which the
population is only partially protected by cross-reacting
antibodies. Pandemics occur when a process called an
antigenic shift
causes both the H and N antigens to be
replaced through recombination of the RNA segments
with those of animal viruses, making all individuals sus-
ceptible to the new influenza virus.
As with many viral respiratory tract infections, influ-
enza is more contagious than bacterial respiratory tract
infections. In contrast to the rhinoviruses, transmission
occurs by inhalation of droplet nuclei rather than touch-
ing contaminated objects. Adults are usually considered
infectious from the day before symptom onset to 5 to
10 days after the first symptoms appear.
15
Children can
be infectious for greater than 10 days, and young chil-
dren can shed virus for up to 6 days before their illness
onset. Severely immunocompromised persons can shed
virus for weeks or months.
Pathogenesis
The influenza viruses can cause three types of infections:
an uncomplicated upper respiratory infection (rhinotra-
cheitis), viral pneumonia, and a respiratory viral infec-
tion followed by a bacterial infection. Influenza initially
establishes upper airway infection. In doing this, the
virus first targets and kills mucus-secreting, ciliated, and
other epithelial cells, leaving gaping holes between the
underlying basal cells and allowing extracellular fluid to
escape. This is the reason for the rhinorrhea or “runny
nose” that is characteristic of this phase of the infection.
