Pediatric Primary Care (53 page)

K.  Education.

1.  Chronicity of problem.

2.  Avoidance of allergens (recent evidence that exposure to cats, dogs in first year of life decreases development of allergies later in childhood).

3.  Medication administration and side effects.

II. APHTHOUS STOMATITIS

A.  Etiology.

1.  Commonly known as canker sores, aphthous stomatitis is recurrence of painful, discrete, shallow ulcers on unattached mucous membranes of mouth.

2.  Considered to be immune-mediated destruction of epithelium, cause is multifactorial, including infection, autoimmune disease, allergies, nutritional deficiencies, and trauma.

3.  Associated risk factors.

a.  Genetic: positive family history.

b.  Deficiencies of iron, vitamin B12, folic acid.

c.  Chronic illness such as IBD, celiac disease, immune suppression, lupus, JRA.

d.  NSAID or ACE inhibitor usage.

e.  Childhood: higher incidence (peak 10-19 years).

B.  Occurrence.

1.  Incidence: up to 20% of population.

2.  Precipitating factors.

a.  Stress/trauma: emotional, physical, hormonal.

b.  Foods: chocolate, nuts, tomatoes.

c.  Malabsorption syndromes.

C.  Clinical manifestations.

1.  Aphthous minor: 80% of cases: 1-5 mm lesions; heal in 5-12 days; no scarring.

2.  Aphthous major: 15% of cases > 1 cm lesions; last 4 weeks; may scar.

3.  Patient complains of single or multiple painful sores in mouth.

4.  Tingling or burning may precede appearance of lesions.

D.  Physical findings.

1.  Painful, yellow, gray, ulcerative lesions with erythematous halo on mucosa.

2.  1-5 ulcerative oval or circular ulcers with an erythematous periphery and pale white/gray or yellow center.

3.  Size: 2-10 mm.

4.  Absence of systemic symptoms (i.e., fever, lymphadenopathy).

E.  Diagnostic tests.

1.  None.

F.  Differential diagnosis.

1.  Infections:

a.  Herpes simplex (rare).

•  Small, irregular vesicles that rupture and leave ulcers.

•  Red at periphery with gray center.

•  Patient often febrile with significant lymphadenopathy.

•  Recurrent herpes infections remain localized to lips, rarely cross mucocutaneous junction.

•  Primary infections sometimes involve oral mucosa.

b.  Coxsackie–hand, foot and mouth disease.

• Sometimes ulcers in the mouth (and will have papules on hands and feet, perhaps buttocks).

2.  Traumatic (injury).

3.  Herpangina–ulcerative pharyngitis (not stomatitis); fever, lymphadenopathy.

4.  Angular cheilitis–erythematous, painful fissures at corners of the mouth. May be caused by lipsucking, sensitivity to agent with which in contact. Treatment is topical with an antibiotic, anti-yeast or low-dose steroid ointment.

G.  Treatment.

1.  Supportive.

a.  Oral analgesics such as acetaminophen or ibuprofen.

b.  Topical anesthetics: especially prior to eating/drinking.

•  Viscous Xylocaine dabbed on lesions with cotton swab.

•  Mouthwashes.

i.   Diphenhydramine elixir: antacid suspension (aluminum and magnesium hydroxide combination): mix 1:1 (parent can do this).

ii.  Pharmacist may add lidocaine 1% for older child to swish and spit.

•  0.1% Triamcinolone (Kenalog) in Orabase: dab on lesions qid.

c.  Avoid acidic, salty foods and drinks.

d.  Good oral hygiene.

•  Rinse mouth frequently with clear water.

•  Offer water to young children frequently, especially after eating or drinking other fluids.

H.  Follow up.

1.  None if healed.

I.  Complications.

1.  Generally none. Young child may refuse to drink.

2.  Referral if persists 3 weeks or no urine output for 12 hours.

J.  Education.

1.  Avoidance of triggers/precipitating factors.

III. CAT-SCRATCH DISEASE

A.  Etiology.

1.  Bacteria
Bartonella henselae
infects humans via cat saliva entering the body through a scratch or bite.

2.  87-99% of patients have had contact with kitten within the last 6 months; 50% have history of scratch.

B.  Occurrence.

1.  More common in children, (younger than 18 years), especially boys.

2.  20,000 cases/year in United States, primarily July-January.

C.  Clinical manifestations.

1.  Typical cat-scratch disease.

a.  Primary skin lesion (papule) appears 3-10 days following inoculation.

b.  Regional lymphadenopathy develops in about 2 weeks, persists sometimes for months. 85% have a single node.

c.  Fever, which may be prolonged (up to 2 weeks) in two-thirds of patients.

d.  10% of nodes may suppurate spontaneously.

e.  Hepatosplenic disease.

2.  Less common clinical manifestations:

a.  Parinaud oculoglandular syndrome.

b.  Neuroretinitis-posterior segment ocular disease.

c.  Encephalopathy.

d.  Radiculopathy.

e.  Facial nerve palsy.

f.  Guillain-Barré syndrome.

g.  Cerebral arteritis.

h.  Transverse myelitis.

i.  Glomerulonephritis.

j.  Thrombocytopenia purpura.

k.  Osteomyelitis.

l.  Arthritis/arthralgia.

m.  Endocarditis.

D.  Physical findings (in typical CSD).

1.  Nonpruritic vesicle or papule(s) over site of inoculation.

2.  Lymphadenopathy of area that drains site of inoculation. Most commonly axillary and epitrochlear nodes, then head, neck, and groin in descending order of frequency.

3.  Skin over affected nodes is warm, taut, tender, indurated.

E.  Diagnostic criteria: (3 of the following 4):

1.  Cat or flea contact regardless of presence of inoculation site.