NR 602 WEEK 2 QUIZ ANSWERS
Restrictive Processes
Restrictive disease is less common in pediatric patients and is characterized by decreased lung compliance with relatively normal flow rates.
Examples of causative factors include neuromuscular weakness, lobar pneumonia, pleural effusion or masses, severe pectus excavatum, or
abdominal distention. Key findings of restrictive lung disease are rapid respiratory rate and decreased tidal volume/capacity ( Carter and
Marshall, 2011).
Defense Systems
The respiratory defense system includes mechanical and biologic processes. Mechanical defenses include:
• Filtering of particles
• Warming and humidifying of inspired air
• Clearing of airway through mucociliary and coughing actions
• Spasm and breathing changes
Approximately 75% of inspired air is warmed as it passes through the nose, paranasal sinuses, pharynx, larynx, and upper portion of the
trachea. Final warming and humidifying of the airstream take place in the trachea and large bronchi. Heat and moisture are removed during
the expiratory phase of respiration. The nose has a large surface area on which particles larger than 5 mm are trapped and filtered to prevent
them from entering the lower airways. The trachea and bronchioles are lined with various defensive cells and mucus glands. Goblet cells
secrete the mucous layer that lies on the tip of cilia. Particles entering the conducting airway are quickly cleared by the mucociliary defenses.
Coughing is a reflex mechanism that has three phases: (1) inspiratory, (2) compressive, and (3) expiratory. Through forceful expiration FBs
and other materials can be removed from the airways; coughing propels particles. Young infants and children cannot effectively expectorate
mucus, so they swallow it. Loss of the cough reflex leads to aspiration and pneumonia. Temporary breathing cessation, reflex shallow
breathing, laryngospasm, and even bronchospasm are compensatory efforts aimed at stopping foreign matter from further entry into the lower
respiratory tract. 797However, these respiratory efforts offer limited protection and have significant drawbacks.
Biologic processes that protect the respiratory system include:
• Phagocytosis
• Absorption of noxious gases in the vasculature of the upper airway
• Absorption of particles by the lymph system
Phagocytosis, aided by the secretory IgA plus interferon, lysozyme, and lactoferrin, is the principal antimicrobial defense. Particles
reaching the alveoli can be phagocytized by alveolar macrophages and polymorphonuclear (PMN) cells, cleared from the lung by the
mucociliary system, or carried by lymphocytes into regional nodes or the blood. These particles can take days to months to clear.
The respiratory defense system is at risk for compromise from numerous environmental factors. Damage to epithelial cells is caused by a
variety of substances and gases, such as sulfur, nitrogen dioxide, ozone, chlorine, ammonia, and cigarette smoke. Hypothermia, hyperthermia,
morphine, codeine, and hypothyroidism can adversely alter mucociliary defenses. Dry air from mouth breathing during periods of nasal
obstruction, tracheostomy placement, or inadequately humidified oxygen therapy results in dryness of the mucous membrane and slowing of
the cilia beat. Cold air is also irritating to the lower airways.
Phagocytic ability is also reduced by many substances, including ethanol ingestion and cigarette smoke. Hypoxemia, starvation, chilling,
corticosteroids, increased oxygen, narcotics, and some anesthetic gases also impair phagocytosis. Recent acute viral infections can reduce
antibacterial killing capacity. Damage from infection and chemical irritants may or may not be reversible.
Recurrent respiratory infections in children merit investigation for immunodeficiency or other underlying diseases, such as primary ciliary
dyskinesia or CF. The mnemonic SPUR (Bush, 2009) can help determine which children need further workup:
Severe infection
Persistent infection and poor recovery
Unusual organisms
Recurrent infection
Immunodeficiencies should be considered if the child has four or more new ear infections in a year, two or more serious sinus infections,
two or more pneumonias in a year, persistent oral candidiasis, failure to thrive, two or more deep seeded skin abscesses, 2 or more months on
antibiotics without improvement, and/or the need for intravenous (IV) antibiotics to clear infections. Also consider immunodeficiencies if
there is a family history of immunodeficiency or two or more deep skin infections (Modell et al, 2014).
Assessment of the Respiratory System
The history provides valuable information about the causes, progression, and potential complications of a child's respiratory condition. The
physical examination and diagnostic testing allow the provider to determine the extent of respiratory distress.
History
,History of the present illness can be assessed using the mnemonic PQRST:
• Promoting, preventing, precipitating, palliating factors
• Contacts: Are any family members or close contacts (e.g., day care, school) ill with similar signs and symptoms?
• Prevention: Do you give your child any medications or supplements (include any herbs, botanicals, or vitamins) to try to prevent a
cold? What are your hand washing practices? Do you encourage fluids when your child has a URI? Are the child's immunizations up
to date?
• Progression: Are the respiratory signs or symptoms increasing in severity, lessening, or about the same? Is the child easily fatigued,
less active, having trouble sleeping, or working harder to breathe?
• Treatment: Have any OTC, prescription drugs, herbs, supplements, or botanicals been used? Have any other treatment modalities been
used, including folk cures or home remedies?
• Quality or quantity
• How severe are the symptoms? Is the illness interfering with school attendance or play? Are breathing problems affecting the child's
ability to sleep and eat?
• Region or radiation
• Does the child complain of chest pain?
• Severity, setting, simultaneous symptoms or similar illnesses in the past
• Key signs and symptoms: Has the child had symptoms or signs of a daytime or nighttime cough, fever, vomiting, malaise, rhinorrhea,
sore throat, lesions in the mouth, retractions, cyanosis, dyspnea, or increased respiratory effort? Table 32-1 lists key characteristics
and causes of cough.
TABLE 32-1
Key Characteristics of Cough, Common Causes, and Questions to Ask in a Pediatric History
Key Characteristics to
Description and Questions to Ask
Consider
Age factor Infants have a weak, nonproductive cough.
Staccato-like (Chlamydia trachomatis in infants); barking or brassy (croup, tracheomalacia, habit cough); paroxysmal or
inspiratory whoop (pertussis or parapertussis); honking (psychogenic).
Quality Is the cough wet or dry?
Acute (most causes are infectious and last less than 2 weeks), subacute (cough lasts from 2 to 4
weeks); recurrent (associated with allergies and asthma), or chronic (lasting greater than 4 to 8 weeks [e.g., CF, asthma]).
Duration Is the cough continuous or intermittent?
Productivity Mucus producing or nonproductive?
Timing During the day, night (associated with asthma), or both?
Effect on parent and Are parents frustrated with the cough? Is it causing them to lose sleep and work time? Are they concerned that the child may
child have something serious?
Associated symptoms Fever: May indicate bacterial infection (pneumonia).
, Key Characteristics to
Description and Questions to Ask
Consider
Rhinorrhea, sneezing, wheezing, atopic dermatitis: Associated with asthma and allergic rhinitis.
Malaise, sneezing, watery nasal discharge, mild sore throat, no or low fever, not ill appearing: Typical of URI.
Tachypnea: Pneumonia or bronchiolitis in infants (infants may not have a cough).
Exposure to infection or Has the child been out of the country (tuberculosis)? Is there a member of the household being treated for “bronchitis” or
travel another cough illness?
Causes
Congenital anomalies Tracheoesophageal fistula, vascular ring, laryngeal cleft, vocal cord paralysis, pulmonary malformations,
tracheobronchomalacia, congenital heart disease
Infectious agent Viral (RSV, adenovirus, parainfluenza, HIV, metapneumovirus, human bocavirus), bacterial (tuberculosis,
pertussis, Streptococcus pneumoniae), fungal, and atypical bacteria (C. and M. pneumoniae)
Allergic condition Allergic rhinitis, asthma
Other FB aspiration, gastroesophageal reflux, psychogenic cough, environmental triggers (air pollution, tobacco smoke, wood
smoke, glue sniffing, volatile chemicals), CF, drug induced, tumor, congestive heart failure
CF, Cystic fibrosis; FB, foreign body; HIV, human immunodeficiency virus; RSV, respiratory syncytial virus; URI, upper respiratory infection.
Adapted from Chang AB: Cough, Pediatr Clin North Am 56(1):19–31, 2009; Cherry JD: Croup (laryngitis, laryngotracheitis, spasmodic croup,
laryngotracheobronchitis, bacterial tracheitis, and laryngotracheobronchopneumonitis). In Cherry J, Kaplan S, Demmler-Harrison G, et al, editors: Feigin
& Cherry's textbook of pediatric infectious diseases, ed 6, vol 1, Philadelphia, 2009, Saunders/Elsevier, pp 254–268.
• Associated symptoms: Has there been a decrease in appetite or feeding? Any rashes, headaches, or abdominal pain?
• Similar illnesses in the past: Does the child have a history of respiratory tract infections, allergies, or asthma? How many similar
infections has the child had (e.g., croup, pneumonia, rhinosinusitis, streptococcal tonsillopharyngitis, or frequent colds)?
• Temporal factors
• When did the illness begin?
• Was the onset acute or insidious or proceeded by the common cold?
, • How long has it lasted? How has it changed over time?
• Family history
• Do others in the family have a history of allergies or asthma?
798
• Is there any family history of immunodeficiency, ear-nose-throat, or respiratory problems?
• Does anyone in the family have genetic diseases, such as CF or alpha 1-antitrypsin deficiency?
• Are other family members ill?
• Review of systems
• Note any infections, constitutional diseases, or congenital problems that might have a respiratory component.
• Environment
• Does anyone in the family or in the day care setting smoke? Does the child live or attend school in an urban or industrial area subject to
air pollution (e.g., near a major highway, industrial plant, or bus terminal)? Has the child or a family contact traveled recently and
where?
Physical Examination
When determining respiratory distress, think about the total presentation and not just individual isolated findings. Consider the anxiety level,
respiratory rate and rhythm, use of accessory muscles, color, breath sounds, grunting, and pulse oximetry results. Information pertinent to the
physical examination of a child with suspected respiratory disease includes the following:
• Measurement of vital signs and observation of general appearance:
• A normal respiratory rate is age dependent and, if elevated, is a key indicator of lower respiratory involvement.
• The level of anxiety, nasal flaring, and position of comfort are useful indicators of respiratory distress. 799Changes in skin color may
be subtle or obvious, depending on the level of deoxygenation. Grunting is a sign of small airway disease.
• Inspection of:
• Nose: Look for rhinorrhea—clear, mucoid, mucopurulent; FBs, erosion, polyps, lesions, bleeding, septal position, and color of the
mucous membrane.
• Throat, pharynx, and tonsils: Look for lesions, vesicles, exudate, enlargement of any structure, or other abnormalities. If epiglottitis is a
consideration, do not inspect the mouth or attempt to elicit a gag reflex (see discussion later in this chapter).
• Chest: Look at the depth, ease, symmetry, and rhythm of respiration. These are key indicators of lower respiratory tract involvement.
The use of accessory muscles and the presence of retractions should be noted. A prolonged expiratory phase is associated with
respiratory obstruction in the lower airways.
• Palpation or percussion of:
• Chest: Percuss for signs of dullness or hyperresonance caused by consolidation, fluid, or air trapping.
• Auscultation of the chest:
• Upper tract: Pathology frequently causes noisy breathing, snoring, stridor, and musical or wheezing tracheal breath sounds and can be a
source of referred breath sounds (Bohadana et al, 2014).
• Lower tract: Pathology is suggested by fine crackles, coarse crackles, rhonchus, pleural friction rub, wheezing, and bronchial breath
sounds (Bohadana et al, 2014).
Upper Respiratory Tract
The upper respiratory tract includes the nostrils, nasopharynx, larynx, upper part of the trachea, eustachian
tubes, and sinuses. Air is warmed and humidified as it travels through the nasal passages, and coarse nasal
hairs filter out particles. The nasal passages are lined with lysozymes, secretory immunoglobulin A (IgA), and
immunoglobulin G (IgG) in nasal mucosa to defend against microbial invasion. The nasal mucosa is continuous
and similar to the sinus mucosa except that the nasal mucosa is thicker with more glands. A blanket of mucus
covers the surface epithelium of the nasal and sinus mucosa.
The mucosal lining of the sinuses is composed of pseudostratified, ciliated columnar epithelium interspersed
with mucus producing goblet cells (Rose et al, 2013). The mucociliary action of the paranasal epithelium moves
secretions from the sinuses to the nasal cavity. The frontal, maxillary, and anterior parts of the ethmoid sinuses
drain to the middle meatus of the nose, whereas the sphenoid and posterior parts of the ethmoid sinuses drain
to the superior meatus of the nose. Secretions need to be able to move through patent ostia into the nose. The
quality of secretions and normally functioning cilia are key factors in the movement of secretions into the nose.
Inflammation of nasal mucosa frequently causes edema and disruption of the sinus secretions. If there is
significant swelling of the ostia due to a URI or allergic inflammation, or mechanical or local obstruction, ostial
obstruction results and obstruction of the sinus secretions occurs. Cilia movement and mucus flow allow the
sinuses to be free of pathogens.
The maxillary sinuses are present by the second trimester of gestation but are not fully pneumatized until a
child is about 4 years old. Ethmoid sinuses develop by the fourth month of gestation and form the thin lateral
walls of the orbit of the eye. They are pneumatized at birth and can be visualized on plain radiographs when
the child is 1 to 2 years old. The sphenoid sinuses start to form in the first 2 years of life but remain
rudimentary until age 6, which is when they become visible on radiographs. By 12 years old, they reach their
