SOAP Pedi – Impetigo

Source: Manual of Ambulatory Pediatrics 2010

SOAP Note – Impetigo 

IMPETIGO
A purulent infection of the skin characterized by honey-colored, crusted lesions or bullae surrounded by a narrow margin of erythema.

I. Etiology

A. Most common causative organism: S. aureus
B. Earlier research suggested that most crusted impetigo was streptococcal in origin. It now appears that most crusted and bullous impetigo is caused by S. aureus.
C. Streptococcal impetigo is always crusted. Bullous impetigo is virtually never streptococcal.
D. Secondary impetigo (superimposed on a preexisting condition, such as atopic dermatitis) is nearly always staphylococcal.

II. Incidence

A. Primary bacterial skin infection in children seen in all age groups
B. Predisposing factors include poor hygiene and antecedent lesions, such as chickenpox, scabies, insect bites, atopic dermatitis, or trauma.

III. Incubation period:

1 to 3 days

IV. Communicability:

A. Very contagious through person to person contact.
B. Less than 48 hours once therapy is initiated; weeks to months if untreated

V. Subjective data

A. Sores

1. Mainly on the head (particularly around the nares and mouth) and extremities; may occur anywhere on body
2. Begin as macules, which develop into vesicles and then become pustular

B. Pruritus, which may spread the infection
C. Often a history of minor trauma (e.g., insect bites, scratches, scabies, or herpes simplex) providing entry to the organism
D. History of exposure to impetigo

VI. Objective data

A. Nonbullous

1. Lesion appears as clear vesicle on an erythematous base and rapidly becomes pustular. Pustule ruptures, enlarges, and spreads. The characteristic honey-colored adherent crust is formed. Satellite lesions are common.
2. Inspect entire body; lesions may be multiple.
3. Check for regional adenopathy.
4. Lesions commonly perioral or perinasal following URI.

B. Bullous

1. Lesions are rapidly formed; fragile bullae surrounded by a thin margin of erythema, filled with clear fluid, which progresses to cloudy fluid prior to rupture. These bullae heal centrally, leaving a crusted arcuate or annular formation. Recently ruptured bullae have an erythematous, shiny base. Older lesions are dry and not erythematous.
2. Inspect entire body.
3. Check for regional adenopathy.

VII. Assessment

A. Diagnosis

1. Usually made by clinical picture of oozing vesicles and honey colored adherent crusts
2. Routine culturing of lesions not indicated but recommended if lesions are extensive or severe

B. Differential diagnosis (all of the following may become secondarily impetiginized)

1. Herpes simplex
2. Contact dermatitis
3. Eczema
4. Seborrhea
5. Fungal infection

VIII. Plan

A. Local treatment may be adequate when only one or two lesions are present.

1. Remove crusts by gentle washing with warm water and an antiseptic soap or cleaner, such as Betadine.
2. Bactroban ointment (prescription required): Apply 3 times a day.
3. Follow-up with a telephone check in 24 hours. If other lesions have appeared or clearing has not begun, institute systemic treatment.

B. Systemic treatment for multiple lesions, widely separated lesions (e.g., one on the face and one on the buttocks), or lesions that are not showing rapid response to local therapy: Administer one of the following:

1. Dicloxacillin: Less than 40 kg, 12.5 to 25 mg/kg/d in 4 divided doses for 10 days; more than 40 kg, up to 250 mg 4 times a day
or
2. Keflex: 25 to 50 mg/kg/d in 2 divided doses for 10 days (usual dose for child over 40 kg, 250 mg every 12 hours)
or
3. Augmentin: Under 40 kg, 45 mg/kg/d every 12 hours (oral suspension or chewables only); over 40 kg, 500 mg every 12 hours (dosed according to adult recommendations)

C. Recurrent impetigo may be secondary to colonization of S. aureus in nares or groin. Mupirocin applied tid to nares is effective in eliminating carrier state in approximately 90% of patients.
D. Note: Macrolide antibiotics, including erythromycin and clarithromycin, may be used in patients allergic to penicillin but are generally not recommended as first-line therapy because of emerging antimicrobial resistance to these drugs.

IX. Education

A. Continue medication for 10 full days; do not stop because lesions have cleared.
B. Spread occurs cutaneously as well as systemically.
C. Bullous impetigo is more likely to spread.
D. Incubation period is 1 to 3 days.
E. Not communicable after 48 hours on antibiotic therapy
F. Use separate towel, washcloth, and so forth to prevent spread.
G. Wash linen and clothing in hot water.
H. Keep fingernails short to minimize spread caused by scratching.
I. Check contacts and other family members.
J. Child should not return to school until lesions are clear or he or she has been on antibiotics for 48 hours.
K. Transmitted by direct and sometimes indirect contact.
L. Athletes, particularly wrestlers, should not participate for 24–48 hours once treatment has been initiated.

X. Follow-up

A. Call office if no improvement is noted within 24 hours after treatment is started.
B. Call immediately if dark-colored urine, decreased urinary output, or edema is noted.
C. Return in 3 days if not markedly improved.

XI. Complications:

Acute glomerulonephritis, the most important complication, occurs with nephritogenic strains of streptococci. There is no conclusive evidence that early, vigorous treatment will prevent glomerulonephritis.

XII. Consultation/referral

A. Signs or symptoms of acute glomerulonephritis
B. No response to treatment after 4 to 5 days
C. Bullous impetigo in newborn or infant