Pediatric Examination and Board Review (95 page)

16.
Which of the following is the main etiology of dental caries?

(A)
Streptococcus pyogenes

(B)
Streptococcus viridans

(C)
Streptococcus mutans

(D)
Streptococcus pneumoniae

(E)
Enterococcus
species

ANSWERS

1.
(A)
The duration of epistaxis that should prompt further workup is 30 minutes. Most nosebleeds can be stopped sooner, if proper technique is used: blowing the nose first, tilting the head forward, followed by firm and constant pressure just below the bridge of the nose for a minimum of 5 minutes. Children younger than 2 years should be evaluated further because epistaxis in this age group is rare, and because most epistaxis in children is secondary to self-inflicted trauma (vigorous nose rubbing or picking).

2.
(C)
Nasopharyngeal angiofibromas occur in children and 30- to 40-year-old adults but have a peak incidence in adolescent boys. They present with nasal obstruction and recurrent epistaxis. A CT of the relevant structures can define the extent of the tumor. Surgical excision is the usual treatment.

3.
(B)
Nasal polyps are benign pedunculated tumors of the nasal mucosa that are associated with multiple chronic diseases. Presentation includes nasal obstruction, hyponasal speech, rhinorrhea, and mouth breathing (see
Figure 58-1
).

FIGURE 58-1.
Endoscopic view of nasal polyp obstructing the posterior nasal airway. A small residual air passage (A) is seen between the polyp and the nasal septum. (Reproduced, with permission, from Brunicardi FC, Andersen DK, Billiar TR, et al. Schwartz’s Principles of Surgery, 9th ed. New York: McGraw-Hill; 2010: Fig. 18-3.)

4.
(E)
Approximately 30% of children with cystic fibrosis (CF) develop nasal polyps. In any child younger than 12 years old in whom nasal polyps are diagnosed, regardless of other risk factors, sweat testing for CF should be performed. All the other diseases listed are associated with nasal polyps, including the Samter triad of aspirin sensitivity, nasal polyps, and asthma.

5.
(E)
Besides surgical removal, steroids are the most successful treatment for nasal polyps. Intranasal steroids should be tried first, and systemic steroids are an alternative depending on the severity of disease. Neither antihistamines nor decongestants will shrink a polyp, although they may provide symptomatic relief from associated illnesses, such as allergic rhinitis.

6.
(C)
The nasal turbinates in a patient with allergic rhinitis are usually pale or blue and edematous; erythematous turbinates are more commonly seen with infectious causes of nasal discharge. The “allergic salute” (rubbing the nose upward) causes a longterm crease across the bridge, which is indicative of chronic allergic rhinitis. “Allergic shiners” are dark circles under the eyes, caused by chronic lid edema and resolution, in addition to subcutaneous venodilation. Postnasal drip eventually leads to a cobblestoned appearance in the posterior pharynx and often a nighttime cough.

7.
(D)
Allergic rhinitis is associated with otitis media with effusion, not otitis externa.

8.
(A)
The prevalence of allergic rhinitis peaks in late childhood. The incidence of allergic rhinitis is increasing, especially in affluent societies. Risk factors include high socioeconomic status, high IgE in childhood, family history of atopy, heavy indoor allergen concentrations, mothers who smoke near their children in the first year of life, and early introduction of solids in infancy. This last risk factor has led to the recommendation by the American Academy of Pediatrics that solid food not be started until infants are 6 months old.

9.
(D)
Intranasal steroids have the greatest effect against nasal congestion with allergic rhinitis. First-generation antihistamines are sedating and have limited use for daytime control of symptoms in children. Second-generation antihistamines, leukotriene inhibitors, and avoidance of allergens will provide good control of symptoms, whereas decongestants are short term and will give no lasting benefit. Allergen injections are considered the last resort for symptom control in children.

10.
(D)
Cleft lip with or without associated cleft palate is present in 1 in 750 white births; cleft palate alone is present in 1 in 2500 white births. It is more common in males and can be inherited dominantly in Van der Woude syndrome. It has the highest incidence ethnically in Asians and the lowest in African Americans. Conductive hearing loss is commonly associated with cleft palate but not sensorineural hearing loss (see
Figure 58-2
).

11.
(D)
From birth, a team of services should be alerted and develop a management plan for the child with the family. These would likely include, but are not limited to, a pediatrician, an otolaryngologist, a pediatric dentist, a speech therapist, a geneticist, a social worker, and/or a psychologist.

12.
(C)
CATCH-22 syndrome includes cardiac, abnormalities, abnormal facies, thymic hypoplasia, cleft palate, and hypocalcemia. TAR syndrome is thrombocytopenia and absent radii. Waardenburg syndrome, or partial albinism, includes acrocephaly, facial dysmorphism (not cleft lip or palate), ocular problems, deafness, and abnormal dentition.

13.
(A)
Ankyloglossia, or “tongue tie,” is an abnormally short lingual frenulum (see
Figure 58-3
). In most children, the frenulum grows with them and does not cause any difficulties. In some, feeding trouble ensues in early infancy because of restricted extension of the tongue. These children should see a general pediatric surgeon early on and be counseled regarding surgical correction, especially if they are failing to gain weight appropriately. In others, speech difficulties arise later on. Most speechdelayed children still do not require surgery but will benefit from speech therapy.

FIGURE 58-2.
Anatomy of cleft palate.
(A)
Normal anatomy; note the sling formed by the two sides of the levator palatini muscle.
(B)
Cleft palate; the levator muscle is oriented longitudinally, somewhat parallel with the cleft margin. (Reproduced, with permission, from Lalwani AK. Current Diagnosis & Treatment in Otolaryngology: Head & Neck Surgery, 2nd ed. New York: McGraw-Hill; 2008: Fig. 19-7.)

FIGURE 58-3.
Ankyloglossia (tongue-tie). (Reproduced, with permission, from Hay Jr WW, Levin MJ, Sondheimer JM, et al. Current Diagnosis & Treatment: Pediatrics, 19th ed. New York: McGraw-Hill; 2009: Fig. 16-4.)

14.
(E)
Most often children start eruption of their primary teeth at 6 months and continue until 22 months. Primary eruption can be as early as 4 months but more often occurs after 6 months.

15.
(E)
Dental caries are common chronic diseases of childhood (see
Figure 58-4
). Caused by bacterial overgrowth and stagnation in the oral cavity, caries can be prevented by several means, including all of the given choices. Fluoride-containing toothpaste is generally recommended starting at 2 years of age, at a time when children can begin to spit out the paste after use (the danger is an overdose of fluoride if too much is used at an early age and the child swallows it all). Sucrose is the most likely carbohydrate involved in caries formation and is contained in sweetened drinks that children often start drinking at a young age.

FIGURE 58-4.
Dental caries. (Reproduced, with permission, from South-Paul JE, Matheny SC, Lewis EL. Current Diagnosis & Treatment in Family Medicine, 2nd ed. New York: McGraw-Hill; 2008: Fig. 45-5.)

16.
(C)

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