Pediatrics Questions Bank

References:

• American Academy of Pediatrics. Smallpox (variola). In: Pickering LK, ed. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 2006: 591-595
• Cieslak J, Henretig FM. Biologic and chemical terrorism. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co; 2004:2378-2385
• Myers MG, Stanberry LR, Sevard JF. Varicella-zoster virus. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co; 2004:1057-1062
• Paller AS, Mancini AJ. Viral diseases of the skin. In: Hurwitz Clinical Pediatric Dermatology. 3rd
  ed. Philadelphia, Pa: Elsevier Inc; 2006: 397-423

Historically, the disease most often confused with severe varicella was smallpox. Smallpox, caused by the variola virus, a member of the orthopoxvirus family, has an incubation period of 7 to 17 days. During the incubation period, virus replicates in the upper respiratory tract.

A primary viremia ensues, during which the liver and spleen are seeded. A secondary viremia follows, the skin is seeded, and the classic eruption appears. Initial symptoms of smallpox may include fever as high as 104°F (40°C), generalized malaise, severe headache, vomiting, and backache. Characteristic skin findings appear 1 to 2 days after the onset of fever.

The rash begins on the face and then spreads to involve the extremities and trunk. Initially, lesions are erythematous macules; they evolve into papules, vesicles, and firm pustules . Crusts form at 8 or 9 days and persist for 3 to 4 weeks. As crusts separate, patients often are left with significant scars or depigmentation.

Aspects of smallpox that differentiate it from severe varicella are that the majority of lesions are observed on the face and extremities (with lesser numbers on the trunk) and that all lesions are in a similar stage of development. In contrast, the lesions of varicella erupt initially on the trunk and later appear on the face and extremities. Lesions are erythematous papules that evolve to form superficial vesicles, pustules, and crusts.

In varicella (unlike smallpox), lesions are observed in varying stages of development (ie, as older lesions crust, new lesions appear). By 7 to 10 days after infection, all lesions have crusted. Permanent scars are rare, occurring only when lesions have been secondarily infected with bacteria.

References:

• Allan WC. The clinical spectrum and prediction of outcome in hypoxic-ischemic encephalopathy. NeoReviews. 2002;3:e108-e115. Available at: http://neoreviews.aappublications.org/cgi/content/full/3/6/e108
• Hahn JS, Olson DM. Etiology of neonatal seizures. NeoReviews. 2004;5:e327-e335. Available at: http://neoreviews.aappublications.org/cgi/content/full/5/8/e327
• Riviello JJ, Jr. Pharmacology review: drug therapy for neonatal seizures: part 2. NeoReviews. 2004;5:e262-e268. Available at: http://neoreviews.aappublications.org/cgi/content/full/5/6/e262
• Thureen PJ, Anderson MS, Hay WW, Jr. The small-for-gestational age infant. NeoReviews. 2001;2:e139-e149. Available at: http://neoreviews.aappublications.org/cgi/content/full/2/6/e139
• Wu YW, Backstrand KH, Zhao S, Fullerton HJ, Johnston SC. Declining diagnosis of birth asphyxia in California: 1991-2000. Pediatrics. 2004;114:1584-1590. Available at: http://pediatrics.aappublications.org/cgi/content/full/114/6/1584

Seizures are the most frequent sign of central nervous system injury in the newborn.

When seizures occur in a newborn who has depressed neuromotor tone, reflexes, and cardiopulmonary function at birth that requires assisted ventilation, perinatal asphyxia is likely.

In this event, Apgar scores typically are depressed to less than 3 at 5 or more minutes after birth, and there is a severely acidotic umbilical cord arterial pH (<7.0), with evidence of metabolic acidemia.

Poor tolerance of labor and asphyxia are more common in fetuses that have experienced intrauterine growth restriction.

Because the infant in the vignette has the previously described features, hypoxic-ischemic encephalopathy (HIE) must be considered as a cause for the seizures.

HIE is the most common cause of seizures occurring in the first 24 hours of postnatal life and accounts for up to 67% of early neonatal seizures.

Other causes of neonatal seizure include intracranial hemorrhage, cerebrovascular accidents (stroke), or hemorrhagic infarction (10% to 15%); intracranial malformation (<10%); transient hypoglycemia or hypocalcemia (<10%); drug withdrawal (<5%); and inborn errors of metabolism (<5%).

When seizures occur beyond the first 24 hours after birth, especially in the absence of any history of fetal or neonatal asphyxia, the evaluation should focus on potential causes other than HIE. An additional cause for later seizures is infection (meningitis, encephalitis).

Asphyxia may result in hypocalcemia and hypoglycemia; hyperglycemia and hypercalcemia are not associated with HIE and do not typically cause seizures.

Hypomagnesemia may accompany hypocalcemia in the infant of a diabetic mother, but it is not common following asphyxia and is not associated with neonatal seizures.

Hypercarbia may occur in the depressed newborn who has inadequate ventilation, but it is not associated with seizures unless there is corresponding hypoxia.

References:

• American Academy of Pediatrics. Helicobacter pylori infections. In: Pickering LK, ed. Red Book:2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 2006:321-322
• Gold BD, Colletti RB, Abbott M, et al. Helicobacter pylori infection in children: recommendations for diagnosis and treatment. J Pediatr Gastroenterol Nutr. 2000;31:490-497. Available at: http://www.jpgn.org/pt/re/jpgn/fulltext.00005176-200011000-00007.htm

Helicobacter pylori infection is a known risk factor for gastritis and duodenal ulcers in children and adults. Rarely, and primarily in older adulthood, H pylori also is associated with a gastric lymphoma of the mucosal-associated lymphoid tissue (MALToma). The “gold standard” for the diagnosis of H pylori infection of the stomach is endoscopy with biopsy. Endoscopy may show a nodular gastritis of the antrum, and histology of the gastric mucosa demonstrates the characteristic curved organisms in the gastric glands.

Because endoscopy is invasive, other surrogate markers of infection have been identified. Of the options offered, the H pylori fecal antigen is the best to document eradication in a previously treated host. Patients colonized with H pylori have detectable antigen in their stool that disappears upon eradication of the organism. H pylori immunoglobulin G serology (serum antibody) is a useful marker for epidemiologic studies of past or current infection, but its sensitivity and positive predictive value in children is suboptimal. The same is true for salivary antibody. Accordingly, a positive antibody screen should be confirmed by a second test (either fecal antigen, urea breath test, or endoscopy). The Campylobacter-like organisms (CLO) test is performed on a duodenal biopsy. In the CLO test, the duodenal biopsy specimen is placed in a test tube containing chemical reagents. The H pylori bacteria convert urea to ammonia and carbon dioxide via their urease enzyme, and the alkalinity of the ammonia can be detected using an indicator dye. The CLO test cannot be performed on feces. Serum urease concentrations are not helpful in identifying H pylori, which is a mucosal bacterium.

Diagnosis, treatment, and eradication of H pylori are well summarized in the American Academy of Pediatrics Red Book and in the North American Society for Pediatric Gastroenterology practice guideline. Patients who have documented ulcers should be tested for H pylori and the organism eradicated if found, but it is unclear if asymptomatic children colonized with H pylori need to be treated. Therapy is given for 14 days and should include a proton pump inhibitor (eg, omeprazole, lansoprazole, pantoprazole) and two antibiotics (eg, tetracycline + clarithromycin, amoxicillin + metronidazole, amoxicillin + clarithromycin). Treatment failures are common, either because of resistant bacteria or because of poor compliance with the regimen. Therefore, testing for eradication of the organism (either by fecal antigen, urease breath test, or endoscopy) should be performed more than 1 month after therapy has been completed.