Rosen & Barkin's 5-Minute Emergency Medicine Consult (392 page)

FOLLOW-UP

• Admission for impetigo alone is rarely necessary
  
• Patients with disease that is widespread, especially widespread bullae, or with larger areas of denuded skin, and dehydration, or refractory to outpatient therapy
  
• Toxic, ill-appearing, or immunocompromised patients require admission, as do neonates suspected of having sepsis
  
• Nephritis may already be present at time patients present for care if presentation is delayed >4–5 days
  
• More typically, nephritis, if seen, occurs 2–4 wk after a streptococcal skin infection
  

• Patients should not be toxic appearing
  
• Patients/caregivers should be able to comply with the recommended treatment regimen
  
• Follow-up for re-evaluation
  

Periorbital edema, leg swelling, or hematuria or proteinuria should suggest poststreptococcal glomerulonephritis and referral to nephrologist

• Follow-up with primary care physician should be arranged to assure resolution without complications
  
• Return for failure of lesions to respond
  
• Return for development of hematuria, periorbital edema, or leg swelling
  

• Treat with systemic antibiotics in the presence of bullous impetigo or if lymphadenopathy is present
  
• Increasing antibiotic resistance continues to limit ability to use historic standard antibiotic protocols
  
• Mupirocin resistance exists, should be suspected in failures to respond and switch to retapamulin
  
• Cultures and sensitivity must be checked for recalcitrant lesions
  
• Relapse, representing reinfection, may occur if other affected family members are not treated at the same time
  

• Darmstadt GL, Osendarp SJ, Ahmed S, et al. Effect of antenatal zinc supplementation on impetigo in infants in Bangladesh.
  Pediatr Infect Dis J.
  2012;31:407–409.
  
• Koning S, van der Wouden JC, Chosidow O, et al. Efficacy and safety of retapamulin ointment as treatment of impetigo: Randomized double-blind multicentre placebo-controlled trial.
  Br J Dermatol.
  2008;158:1077–1082.
  
• Wolfson AB, Hendey GW, Ling LJ, et al., eds.
  Harwood Nuss’ Clinical Practice of Emergency Medicine
  . 5th ed. Philadelphia, PA: Lippincott; 2010.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Cellulitis
  
• Erysipelas
  
• Toxic Epidermal Necrolysis
  

CODES

• 684 Impetigo
  
• 694.3 Impetigo herpetiformis
  
• 704.8 Other specified diseases of hair and hair follicles
  

BASICS

• Defect in the type, amount, and toxicity of metabolites that accumulate due to an inherited abnormal pathway in children; result in a variety of clinical findings; >400 human diseases are caused by inborn errors of metabolism
  
• Epidemiology:
  
  • Incidence:
    
    • Variable: 1:10,000–1:200,000 births
      
• Genetics:
  
  • Common inherited metabolic diseases:
    
    • Amino acid disorders
      
    • Urea cycle defects
      
    • Organic acidemias
      
    • Defects in fatty acid oxidation
      
    • Mitochondrial fatty acid defects and carnitine transport defects
      
    • Mitochondrial disease
      
    • Carbohydrate disorders
      
    • Mucopolysaccharidoses
      
    • Sphingolipidoses
      
    • Peroxisomal disorders
      
    • Protein glycosylation disorders
      
    • Lysosomal disorders
      
    • Rhizomelic chondrodysplasia punctata
      
• Pathophysiology:
  
  • Related to defect in a metabolic pathway
    

Diverse group of disorders involving genetic deficiency of an enzyme of an intermediary metabolite or a membrane transport system.

DIAGNOSIS

• Disorders may present with either a rapid decompensation or a chronic indolent course
  
• Neonates, initial presentation:
  
  • Asymptomatic
    
  • Hypothermia (mitochondrial defects)
    
  • Hypotonia/hypertonia (peroxisomal disorders)
    
  • Apnea (urea cycle defects, organic acidosis)
    
  • Seizures (peroxisomal disorders, glucose transporter defects)
    
  • Coma (numerous)
    
  • Vomiting (numerous)
    
  • Poor feeding, growth (numerous)
    
  • Jaundice (galactosemia, Niemann–Pick C)
    
  • Hypoglycemia (galactosemia, maple syrup urine)
    
  • Dysmorphic features (lysosomal storage disorders, congenital adrenal hyperplasia, Smith–Lemli–Opitz)
    
• Older children, untreated:
  
  • Failure to thrive (urea cycle defects)
    
  • Dehydration (organic acidosis)
    
  • Vomiting (urea cycle defects and others)
    
  • Diarrhea (numerous)
    
  • Food intolerance (lipid defects, amino acid defects)
    
  • Lethargy (urea cycle defects)
    
  • Ataxia (urea cycle defects)
    
  • Seizures (numerous)
    
  • Mental retardation (phenylketonuria and others)
    

Complete history of current and concomitant illness:

• Newborn screening
  
• Dietary
  
• Family
  
• Consanguinity
  
• Other
  

• Abnormal odor
  
• Altered mental status
  
• Tachypnea
  
• Abnormal facies
  
• Cataract
  
• Cardiomyopathy
  
• Hepatomegaly
  
• Splenomegaly
  
• Dermatitis
  
• Jaundice
  

Key is to consider in differential diagnosis:

• Deteriorating neurologic status
  
• Unexplained failure to thrive, with dehydration, persistent vomiting, or acidosis
  
• Shock unresponsive to conventional resuscitative measures
  

• Bedside glucose determination
  
• Electrolytes, BUN/creatinine, glucose
  
• CBC with differential
  
• Calcium level
  
• LFTs, fractionated bilirubin, PTT
  
• Arterial or venous blood gas
  
• Lactate and pyruvate level
  
• Uric acid
  
• Urinalysis
  
• Chemistries, as indicated:
  
  • Ammonia level
    
  • Quantitative serum amino acids
    
  • Urine organic and amino acids
    
• Cultures:
  
  • Blood
    
  • CSF
    

• CT scan of head for altered mental status
  
• CXR
  

Lumbar puncture

• Often misdiagnosed as sepsis, dehydration, failure to thrive, toxic ingestion, or nonaccidental trauma
  
• Infection:
  
  • Sepsis
    
  • Meningitis
    
  • Encephalitis
    
• Metabolic:
  
  • Reye syndrome
    
  • Hepatic encephalopathy
    
  • Hyperinsulinemia
    
  • Hormonal abnormality
    
• Renal:
  
  • Renal failure
    
  • Renal tubular acidosis
    
• Toxic ingestion
  
• CNS mass lesions
  
• Nonaccidental trauma
  

TREATMENT