MCQ 2007 American academy of Pediatrics

2007 PREP SA on CD-ROM Question: 1 You are precepting a resident who has just evaluated a 4-year-old incompletely immun...

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2007 PREP SA on CD-ROM Question: 1

You are precepting a resident who has just evaluated a 4-year-old incompletely immunized immigrant boy who has classic varicella lesions and a history that is consistent with this diagnosis. Of the following, the MOST accurate statement is that

A. lesions of both varicella and smallpox follow a 7- to 10-day course from eruption to resolution B. lesions of both varicella and smallpox frequently produce deep, pitted scars C. varicella lesions appear in stages or crops; smallpox lesions are uniformly in the same stage of development

D. varicella lesions are concentrated on the face; smallpox lesions are concentrated over bony prominences

E. varicella lesions are transient vesicles; smallpox lesions are persistent pustules until resolution of the illness

Copyright © 2007 by the American Academy of Pediatrics

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2007 PREP SA on CD-ROM Critique: 1

Preferred Response: C

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 (Item C1A). 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) (Item C1B). 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: 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; 2004:23782385 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


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A 15-year-old boy presents with melena and anemia. Endoscopy demonstrates a nodular gastritis of the antrum (Item Q2A) and an ulcer. Biopsies of the antrum demonstrate spiralshaped organisms consistent with Helicobacter pylori (Item Q2B). You prescribe amoxicillin, clarithromycin, and lansoprazole for 2 weeks. At a follow-up visit, the family asks whether the treatment has been successful in eradicating the organism. Of the following, the PREFERRED noninvasive test to evaluate whether the pathogen has been eradicated is

A. fecal Campylobacter-like organisms (CLO) test B. fecal H pylori antigen C. salivary H pylori antibody concentrations D. serum H pylori immunoglobulin G serology E. serum H pylori urease concentrations


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Preferred Response: B

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 (Item C2A), and histology of the gastric mucosa demonstrates the characteristic curved organisms (Item C2B) 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) (Item C2C). 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. 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


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A term newborn is delivered by emergent cesarean section because of intrauterine growth restriction, oligohydramnios, and nonreassuring fetal heart rate monitoring in labor. Delivery room resuscitation includes endotracheal intubation and assisted ventilation with 100% oxygen, chest compressions, intravenous epinephrine, and volume expansion. Apgar scores are 1, 2, and 3 at 1, 5, and 10 minutes, respectively. An umbilical cord arterial blood gas measurement documents a pH of 6.9 and a base deficit of 20 mmol/L. At 12 hours of age, the infant demonstrates tonic-clonic convulsive activity of the arms and legs with a concomitant decrease in heart rate and bedside pulse oximetry saturation. Of the following, the MOST likely cause for this infant's seizure is

A. hypercalcemia B. hypercarbia C. hyperglycemia D. hypomagnesemia E. hypoxia


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Preferred Response: E

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 (50) stings and have been reported to cause renal failure, rhabdomyolysis, diffuse intravascular coagulation, and even seizures. Rapid onset of cutaneous (generalized hives, angioedema, flushing), respiratory (throat tightness, chest tightness, dyspnea, wheezing), or circulatory signs (dizziness, hypotension, syncope) after only a few stings usually represents anaphylaxis, an IgE-mediated reaction. Any individual older than 16 years of age who experiences anaphylaxis after an insect sting should be counseled about the increased risk (30% to 60%) for similar reactions with subsequent insect stings, prescribed self-injectable epinephrine, and considered for allergy consultation. Individuals younger than 16 years of age who experience cutaneous symptoms only (urticaria or angioedema) do not appear to have the same risk with future stings and may be managed conservatively. References: Freeman TM. Clinical practice. Hypersensitivity to hymenoptera stings. N Engl J Med. 2004;351:1978-1984 Sicherer SH, Leung DYM. Insect allergy. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co 2004:786-788


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A 10-year-old child is brought to your office for evaluation of a 1-day history of fever, vomiting, diarrhea, and abdominal pain. His mother states that he has vomited five times, and the emesis has been clear. He has had four episodes of nonbloody diarrhea. He describes his abdominal pain as crampy but cannot localize it to any specific part of his abdomen. He denies any symptoms of dysuria. On physical examination, the child is in no acute distress, his temperature is 99.2°F (37.3°C), heart rate is 102 beats/min, respiratory rate is 26 breaths/min, and blood pressure is 105/70 mm Hg. Results of examination of the head, neck, chest, and heart are normal. His abdomen is soft, and there is no guarding. There is no rebound tenderness. He complains of mild discomfort on deep palpation of his entire abdomen. He has hyperactive bowel sounds on auscultation, and he has no flank tenderness. Of the following, the MOST appropriate next step in the management of this patient is to

A. administer intravenous fluids B. obtain blood for a complete blood count C. obtain serum for electrolyte analysis D. order frontal supine and upright abdomen radiographs E. send the patient home with instructions for supportive care


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The patient described in the vignette has signs and symptoms consistent with viral gastroenteritis. This is a clinical diagnosis that requires no further evaluation in the absence of toxicity, rebound tenderness, distention, or evidence for dehydration, as in this child. Neither a complete blood count nor serum electrolyte determinations are likely to alter management. The boy should be sent home with instructions for supportive care. Most children who have vomiting due to gastroenteritis can maintain sufficient levels of hydration with glucose- and electrolyte-containing solutions. Intravenous hydration is not required unless fluid loss exceeds 10% of body weight or the patient is experiencing more moderate 5% to 10% dehydration in conjunction with persistent vomiting and an inability or unwillingness to take oral fluids. Abdominal radiographs provide limited information for the evaluation of a child who has vomiting and diarrhea, and even in suspected appendicitis, rarely are helpful. Further evaluation for abdominal pain is indicated if information gained from the history and physical examination suggest potential surgical emergencies such as appendicitis (tenderness localized to the right lower quadrant with or without rebound), small bowel obstruction (absent bowel sounds, abdominal distention), perforated viscus (rigid abdomen, distention, fever, toxicity), malrotation (diffuse tenderness, abdominal distention), intussusception (severe crampy abdominal pain alternating regularly with periods of pain relief), or peritonitis (fever, toxicity, diffuse abdominal tenderness). References: Bellemare S, Hartling L, Wiebe N, et al. Oral rehydration versus intravenous therapy for treating dehydration due to gastroenteritis in children: a meta-analysis of randomised controlled trials. BMC Med. 2004;2:11 Available at: http://www.biomedcentral.com/1741-7015/2/11 Fleisher GR. Infectious disease emergencies. In: Fleisher GR, Ludwig S, Henretig FM, eds. Textbook of Pediatric Emergency Medicine. 5th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2006:783-852 Kwok MY, Kim MK, Gorelick MH. Evidence-based approach to the diagnosis of appendicitis in children. Pediatr Emerg Care. 2004;20:690-698 Rothrock SG, Grenn SM, Harding M, et al. Plain abdominal radiography in the detection of acute medical and surgical disease in children: a retrospective analysis. Pediatr Emerg Care. 1991;7:281-285 Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=Pediatr+Emerg+Care[Jour]+AND+281[page]+AND+1991[pdat] Rothrock SG, Pagane J. Acute appendicitis in children: emergency department diagnosis and management. Ann Emerg Med. 2000;36:39-51 Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=Ann+Emerg+Med[Jour]+AND+39[page]+AND+2000[pdat]


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A 1-month-old infant presents with frecklelike macules (Item Q49A) over his face and extremities. The hospital record reveals that he had multiple papules and pustules distributed over his entire body, including palms and soles, at birth. The infant appears to be very healthy and thriving. Of the following, analysis of the pustular contents in the newborn period MOST likely would have revealed

A. eosinophils B. gram-positive cocci C. multinucleated giant cells D. polymorphonuclear leukocytes E. pseudohyphae and budding yeast


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Preferred Response: D

Transient neonatal pustular melanosis (TNPM) is a disorder of unknown cause that begins in utero. At birth, affected infants may exhibit pustules or small hyperpigmented macules (Item C49A) surrounded by a rim of scale, the remnant of the pustule roof. Pustules resolve within several days, but the hyperpigmented macules may persist for 1 to 3 months, as described for the infant in the vignette. TNPM is more common among African-American infants and may be observed on any skin surface, including the palms and soles. A Wright-stained preparation of the pustular contents reveals a predominance of neutrophils. No treatment is necessary for this self-limited condition. A number of neonatal skin conditions are characterized by pustules or vesicles. They may be distinguished from transient neonatal pustular melanosis clinically and by microscopic examination of lesional contents. The vesicles of erythema toxicum (Item C49B) contain eosinophils (Item C49C), the pustules caused by staphylococcal folliculitis (Item C49D) contain gram-positive cocci, the vesicles of herpes simplex virus infection (Item C49E) contain multinucleated giant cells (Item C49F), and the pustules of congenital candidiasis (Item C49G) contain pseudohyphae and budding yeast (Item C49H). References: Eichenfield L, Larralde M. Neonatal skin and skin disorders: congenital erosive and vesicular dermatosis, vesiculopustular and bullous diseases of the newborn. In: Schachner LA, Hansen RC, eds. Pediatric Dermatology. 3rd ed. St. Louis, Mo: Mosby; 2003:232-239 Weston WL, Lane AT, Morelli JG. Skin diseases in newborns: transient skin disease. In: Color Textbook of Pediatric Dermatology. 3rd ed. St. Louis, Mo: Mosby; 2002:299-307


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A 17-year-old boy who has a 5-year history of Crohn disease comes in with a flare of his illness, characterized by fever, diarrhea, and a 15-lb weight loss. He admits he has "forgotten to take his medicines lately." Physical examination demonstrates a very thin patient who has a perianal fistula. Abdominal computed tomography scan demonstrates thickening of the ileum (Item Q50A) and ascending colon. You are trying to decide whether to administer enteral nutrition (through a nasogastric tube) or begin parenteral nutrition. Of the following findings associated with Crohn disease, the BEST indication for instituting parenteral nutrition is

A. abdominal radiograph demonstrating air fluid levels B. active ileitis demonstrated on colonoscopy C. hypophosphatemia D. institution of 6-mercaptopurine therapy E. perianal abscess and fistula


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Preferred Response: A

Crohn disease can cause many complications that require intensive nutritional therapy, including intestinal inflammation, fistulizing disease, and small bowel strictures. In most patients, such problems can be managed with enteral nutrition. Typically, a polymeric or enteral formula is delivered either by nasogastric tube, gastrostomy, or orally. The formula not only provides nutrition, but it may have a beneficial anti-inflammatory effect on the disease itself. Patients who have hypophosphatemia, ileitis, or perianal fistula and those receiving 6-mercaptopurine therapy all could benefit from enteral feedings. Small bowel obstruction, as indicated by air fluid levels on radiography, is a contraindication to enteral feedings. The principle for nourishing a chronically ill child is "if the gut works, use it." If tolerated, enteral nutrition is preferable to parenteral nutrition for many reasons. Enteral nutrition maintains the integrity of the gastrointestinal mucosa, stimulates the recovery of digestive enzymes such as lactase, and stimulates hepatobiliary and pancreatic secretions. Parenteral nutrition, although lifesaving in some circumstances, is associated with an increased risk of bacterial sepsis (from line infections), electrolyte abnormalities, hepatitis, and cholestasis. Currently available commercial formulas allow tube feeding in a variety of circumstances. Hydrolysates and amino acid-based formulas are available for children who have protein allergy, and low-fat formulas can be used for children who have fat malabsorption. Transpyloric tube placement allows enteral feeding while minimizing the risk of aspiration for children at risk for pulmonary aspiration due to reflux. The primary use of parenteral nutrition is in children who have intestinal disorders such as short bowel syndrome, Crohn disease, anatomic obstruction, ileus, pseudo-obstruction, or enteric fistulas. References: Courtney E, Grunko A, McCarthy T. Enteral nutrition. In: Hendricks KM, Duggan C, eds. Manual of Pediatric Nutrition. 4th ed. Hamilton, Ontario, Canada: BC Decker; 2005:252-316 Hyams JS. Inflammatory bowel disease. Pediatr Rev. 2005;26:314-320 Available at: http://pedsinreview.aappublications.org/cgi/content/full/26/9/314


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You are asked to see a term infant in the newborn nursery at 8 hours of age and consider her transfer to the neonatal intensive care unit. The problems and findings reported to you include: poor feeding, emesis, temperature instability (core temperature of 96°F [35.5°C]), hypoglycemia (whole blood glucose concentration of 25 mg/dL [1.4 mmol/L]), and polycythemia (hematocrit of 70% [0.70]). Of the following, the physical finding that is MOST likely to accompany these problems is

A. a tuft of hair over the sacral region B. birthweight of 1,800 g C. café au lait macule on the left leg D. iris coloboma of the right eye E. isolated cleft of the hard palate


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Infants who are small for gestational age (90 days) nasal discharge, congestion, and cough (day or night), as reported for the boy in the vignette. Other symptoms include headache, sore throat, halitosis, intermittent fever, malaise, and poor appetite. The pathogens associated with chronic sinusitis are similar to those of acute disease (eg, Streptococcus pneumoniae, nontypeable Haemophilus influenzae, Moraxella catarrhalis), but Staphylococcus aureus, other streptococci, fungi, and anaerobes play a more prominent role. Complications of chronic sinusitis include orbital cellulitis and central nervous system extension of infection into the cranium (eg, brain abscess, subdural abscess). Due to the lack of data, treatment of patients who have chronic sinusitis is largely empiric. Antibiotic treatment is problematic because of the large amount of beta-lactamase-producing bacteria in the sinuses, the prevalence of methicillin-resistant S aureus, and the unproven efficacy of therapy. Most experts suggest starting a regimen that would treat acute sinusitis for patients who have chronic sinusitis and are being considered for antibiotic therapy. High-dose amoxicillin (75 to 90 mg/kg per day) or amoxicillin-clavulanate is appropriate. Alternative treatments include cephalosporins (eg, cefprozil, cefuroxime axetil, cefpodoxime), clindamycin, and trimethoprim-sulfamethoxazole. The use of decongestants, antihistamines, mucolytics, and intranasal corticosteroids is controversial; most experts suggest that they have no role in the treatment of chronic sinusitis in children. References: Pappas DE, Hendley JO. Sinusitis. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co; 2004:1391-1393 Steele RW. Chronic sinusitis in children. Clin Pediatr (Phila). 2005;44:465-471. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22Clinical+pediatrics%22[Jour]+AND+465[page]+AND+2005[pdat]


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An 11-year-old Caucasian boy who has no significant past medical history presents to the emergency department with a 3-day history of brown urine. He reports no dysuria, urgency, frequency, or abdominal or flank pain. His vital signs reveal: temperature, 99°F (37.2°C); blood pressure, 141/84 mm Hg; heart rate, 92 beats/min; and respiratory rate, 24 breaths/min. Significant findings on physical examination include moderate periorbital and leg edema. His urinalysis reveals moderate blood and 4+ protein. The serum complement 3 (C3) and C4 concentrations are both low. Of the following, the MOST likely cause of his hematuria is

A. immunoglobulin A nephropathy B. membranoproliferative glomerulonephritis C. postinfectious acute glomerulonephritis D. urinary tract infection E. urolithiasis


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Gross hematuria is defined as discolored urine. The precise color may aid in establishing an origin of the “blood.” It is important to recognize that not all patients suspected of having gross hematuria have red blood cells (RBCs) in the urine. Indeed, the urinalysis in some patients who have presumed gross hematuria may lack RBCs, suggesting the presence of myoglobin, hemoglobin, or porphyrins, all of which may discolor the urine. Additionally, some foods (eg, beets), drugs, or additives (red dye) may discolor the urine. A history should be obtained to ascertain a history of renal disease or urinary tract malformation; the duration of gross hematuria; associated symptoms such abdominal, flank, or suprapubic pain (suggesting an infection or renal malformation); fever (suggesting an infection); or the passage of sand, gravel, or stones. The next step in determining the cause of gross hematuria is to obtain a urinalysis to assess for blood, protein, and RBCs. The association of blood and protein in the urine with an elevated blood pressure reported for the boy in the vignette strongly indicates new-onset glomerular disease. The low serum complement values are consistent with acute glomerulonephritis (AGN). Of the options listed, only membranoproliferative GN (MPGN) and postinfectious AGN (PIAGN) result in reduced serum complements, and of these two conditions, the C3 and C4 are reduced only in patients who have MPGN. Although PIAGN is much more common than MPGN, only C3 is low in PIAGN. Patients who have immunoglobulin A nephropathy typically develop recurrent episodes of gross hematuria, but the serum complement values are normal. Patients who have infections may develop gross hematuria, but this is rare and usually is limited to viral cystitis. Finally, gross hematuria is common in patients who have nephrolithiasis, but they usually experience pain and do not develop significant proteinuria or hypocomplementemia. One of the most common causes of gross hematuria in children is hypercalciuria, with or without renal stones. Hypercalciuria usually is idiopathic, but it may be due to causes of hypercalcemia (eg, hyperparathyroidism, malignancy, Addison disease, sarcoidosis, vitamin D therapy) or result from increased urinary excretion of calcium (eg, furosemide therapy, Bartter syndrome, Dent disease [inherited hypercalciuria], distal renal tubular acidosis). Gross hematuria may occur in patients who have sickle cell disease or trait due to intrarenal sickling and sludging. References: Bergstein J, Leiser J, Andreoli S. The clinical significance of asymptomatic gross and microscopic hematuria in children. Arch Pediatr Adolesc Med. 2005;159:353-355. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22Archives+of+pediatrics+%26+adolescent+medicine%22[Jour]+AND+353[page]+AND+20 05[pdat] Feld LG, Waz WR, Perez LM, Joseph DB. Hematuria. An integrated medical and surgical approach. Pediatr Clin North Am. 1997;44:1191-1210. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_ui ds=9326958&query_hl=39&itool=pubmed_docsum Patel HP, Bissler JJ. Hematuria in children. Pediatr Clin North Am. 2001;48:1519-1537. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22Pediatric+clinics+of+North+America%22[Jour]+AND+1519[page]+AND+2001[pdat]


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You are evaluating a 2-year-old boy in your office for recurrent cellulitis of his right thigh. The patient has had three episodes in the last 4 months. According to his mother, all the episodes start with a "red bump" that progressively enlarges and, in most cases, drains spontaneously. He has received two courses of cephalexin in the past, but there was no clinical improvement until the abscess spontaneously drained. On one occasion, an incision and drainage procedure had to be performed. Except for pain with walking, the patient has been afebrile and experienced no other systemic symptoms. On physical examination, you note a 6x6 cm area of induration and erythema on the lateral right thigh that is warm, firm, and tender to palpation. There is no active drainage from the site. Of the following, the MOST appropriate antibiotic for treatment of this patient is

A. amoxicillin B. amoxicillin/clavulanic acid C. clindamycin D. cefdinir E. cephalexin


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The most common etiologic agents associated with skin and soft-tissue infections are Staphylococcus aureus and group A streptococci. The patient described in the vignette has had recurrent episodes of cellulitis and abscess that did not respond to cephalexin, a beta-lactam antibiotic. He most likely has an infection that is caused by a strain of community-acquired methicillin-resistant S aureus. Over the last 5 years, this organism has emerged as the predominant pathogen causing skin and soft-tissue infections nationwide. The pathogen is not susceptible to any of the beta-lactam antibiotics, including amoxicillin, amoxicillin/clavulanic acid, cefdinir, and cephalexin. Clindamycin, trimethoprim/sulfamethoxazole, vancomycin, the tetracyclines, linezolid, and levofloxacin are the drugs of choice for the treatment of infections caused by these organisms. However, because of growing resistance to these drugs, susceptibility testing should be performed, especially when treating staphylococcal infections. Staphylococci that are susceptible to clindamycin but resistant to erythromycin may exhibit inducible clindamycin resistance (resistance develops while the patient is receiving clindamycin therapy), which should be confirmed using a double-disk diffusion test. Regardless of the antibiotic selected, appropriate management of an abscess includes incision and drainage. Clindamycin is a semisynthetic antibiotic that is a member of the lincosamide family of antibiotics whose mechanism of action is binding to the bacterial 50S ribosomal subunit, thereby interfering with protein synthesis. It is considered a bacteriostatic agent but has bactericidal activity against some strains of staphylococci, streptococci, and anaerobes, including Bacteroides fragilis, depending on drug concentration and bacterial growth conditions. It also has demonstrated the ability to inhibit production of staphylococcal exotoxin associated with toxic shock syndromes and to facilitate opsonization and phagocytosis of bacteria, even at low drug concentrations. The drug is well absorbed following oral administration, reaching peak serum concentrations within 1 hour, with intravenous administration resulting in peak concentrations within 20 to 45 minutes. Clindamycin reaches therapeutic concentrations in most body fluids and tissues, including bones and joints; exceptions include cerebrospinal fluid and bile. The drug is metabolized primarily in the liver, with most of the parent drug and its metabolites eliminated in the bile. Clindamycin is active against most gram-positive cocci, most anaerobes, and certain protozoa. Of the aerobic gram-positive cocci, it is active against streptococci (groups A, B, C and G; S bovis; microaerophilic streptococci; and most strains of pneumococci and viridans streptococci), staphylococci (methicillin-sensitive S aureus, certain strains of methicillin-resistant S aureus, and S epidermidis), and Corynebacterium diphtheriae. However, the drug has no activity against enterococci. Among the anaerobes, it is active against most gram-positive cocci (Peptostreptococcus sp), gram-positive nonspore-forming bacilli (Actinomyces sp, Propionibacterium sp), clostridia (excluding C difficile and a significant percentage of some nonperfringens clostridial species), and gram-negative bacilli (Bacteroides, Prevotella, Fusobacterium sp). It also has activity against Chlamydia trachomatis and certain protozoal pathogens (when used in combination with other agents), such as Plasmodium sp, Pneumocystis carinii, Toxoplasma gondii, and Babesia sp. References: Bradley J. Newer antistaphylococcal agents. Curr Opin Pediatr. 2005;17:71-77. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22Current+opinion+in+pediatrics%22[Jour]+AND+71[page]+AND+2005[pdat] Falagas ME, Gorbach SL. Clindamycin and metronidazole. Med Clin North Am. 1995;79:845867. Available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22The+Medical+clinics+of+North+America%22[Jour]+AND+845[page]+AND+1995[pdat] Kasten MJ. Clindamycin, metronidazole, and chloramphenicol. Mayo Clin Proc. 1999;74:825-


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2007 PREP SA on CD-ROM

833. Available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_ui ds=10473362&query_hl=11&itool=pubmed_docsum Marcinak JF, Frank AL. Treatment of community-acquired methicillin-resistant Staphylococcus aureus in children. Curr Opin Infect Dis. 2003;16:265-269. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22Current+opinion+in+infectious+diseases%22[Jour]+AND+265[page]+AND+2003[pdat] Weingarten-Arams J, Adam HM. In brief: clindamycin. Pediatr Rev. 2002;23:149-150. Available at: http://pedsinreview.aappublications.org/cgi/content/full/23/4/149


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You are seeing a 2-month-old male infant who has trisomy 21 for a health supervision visit. The boy's mother expresses concern that the infant has been having "noisy breathing" during the past 2 to 3 weeks. The infant has been exclusively formula-fed and has had no choking or difficulty feeding. According to the mother, the noise, which occurs on inspiration, is louder when the infant is supine and when crying. She has not noticed any rhinorrhea, cough, or other upper respiratory viral illness symptoms. The infant was born via an uneventful vaginal delivery that did not require forceps. Apgar scores were 8 and 9 at 1 and 5 minutes, respectively. On physical examination, the infant, whose physical appearance is consistent with trisomy 21, is resting comfortably. His vital signs are appropriate for age, but you hear an audible noise during inspiration. Of the following, the MOST likely explanation for the infant's respiratory symptoms is

A. laryngomalacia B. subglottic tracheal web C. tracheomalacia D. vascular ring E. vocal cord paralysis


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When evaluating an infant who presents with “noisy breathing,” it is important to obtain a thorough birth history and current medical history, observe breathing patterns in different positions, and auscultate the airway. Secondary evaluation tools include radiography, spirometry, and direct airway visualization. In general, breathing noises can be classified as inspiratory, expiratory, or biphasic. Disorders at the level of and superior to the vocal cords result in a harsh, inspiratory noise called stridor (Item C111A). Lesions inferior to the vocal cords typically result in wheezing, a high-pitched expiratory noise. Laryngomalacia is the most common congenital laryngeal abnormality resulting in stridor. Symptoms may begin shortly after birth, although they typically occur between 1 and 2 months after birth. As with the child described in the vignette, infants are happy, thriving, and not having difficulty during feedings, but stridor usually worsens during supine positioning, increased crying or agitation, or a viral illness. Direct visualization of an omega-shaped epiglottis that prolapses (Item C111B) during inspiration is a hallmark of the condition. Severe cases may require surgical correction, although laryngomalacia usually improves spontaneously by 2 years of age. A laryngeal web results from failure of the embryonic airway to recanalize. Most laryngeal webs occur at the level of the vocal cords and present at birth with stridor. The delayed onset of stridor in the infant in the vignette makes a laryngeal web unlikely. Tracheomalacia (Item C111C) results from defective cartilaginous rings causing flaccidity of the tracheal wall. Both tracheomalacia and laryngomalacia present at similar ages and are exacerbated by crying, viral respiratory infections, and supine positioning. However, infants who have tracheomalacia present with wheezing instead of stridor. Extrinsic compression of the trachea by vascular anomalies such as a vascular ring (Item C111D) can result in recurrent wheezing that is worsened with crying, feeding, or neck flexion. The right-sided aortic arch with left ligamentum arteriosum and the double aortic arch account for most cases. Unilateral or bilateral vocal cord paralysis (Item C111E) can be associated with inspiratory stridor, but often results in a weak cry, coughing, and choking. When vocal cord paralysis is suspected, a thorough search for underlying causes (eg, congenital central lesions, atrial enlargement, birth trauma, traumatic forceps delivery, prior surgical procedures) should be undertaken. References: Bertrand P, Navarro H, Caussade S, Holmgren N, Sanchez I. Airway anomalies in children with Down syndrome: endoscopic findings. Pediatr Pulmonol. 2003;36:137-141. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=Pediatr+Pulmonol[Jour]+AND+137[page]+AND+2003[pdat] Boat TF. Chronic or recurrent respiratory symptoms. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co; 2004:14011404 Paston F, Bye M. In brief: tracheomalacia. Pediatr Rev. 1996;17:328 Vicencio AG, Parikh S. Laryngomalacia and tracheomalacia: common dynamic airway lesions. Pediatr Rev. 2006; 27:e33-35. Available at http://pedsinreview.aappublications.org/cgi/content/full/27/4/e33


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An 11-year-old child is brought to the emergency department with massive trauma after a motor vehicle crash. His Glasgow Coma Scale score is 3. Rapid assessment reveals marked bruising of the face and blood from the mouth, nose, and ears. In addition, the child has large areas of bruising and abrasions across the chest, abdomen, and pelvis as well as bright red blood from the urethral meatus and a deformity of the left femur. Among the initial major interventions are insertion of an endotracheal tube and establishment of two large-bore intravenous lines. Of the following, the MOST appropriate next step is to

A. administer broad-spectrum antibiotics to treat his contaminated wounds B. administer tetanus toxoid C. obtain upright abdominal films to assess for ruptured viscus D. order contrast-enhanced magnetic resonance imaging of his head E. place a Foley catheter into his bladder to monitor urine output


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Tetanus toxoid should be administered to all victims of massive trauma who have contaminated wounds and have not received this vaccine within the past 5 years or whose immunization status is not known. For the patient described in the vignette, the widespread areas of abrasion put him at particular risk for tetanus, much like a burn victim. A patient who has blood at the urethral meatus, as described in the vignette, should be assumed to have a urethral injury. Blind placement of a Foley catheter is discouraged because such action may convert a partial urethral tear into a complete transection. Retrograde urethrography should be performed to evaluate for this injury. Upright abdominal films have no role in the evaluation of a patient who has had massive trauma. The cervical, thoracic, and lumbosacral spine must remain immobilized during the initial management of such patients. Optimal radiologic evaluation of the abdomen in major trauma victims is accomplished by computed tomography. Ideally, this should be performed using both intravenous and oral contrast. Computed tomography of the head, not magnetic resonance imaging, is an important part of this patient’s evaluation. Contrast adds no information to the scan, so it should not be administered. Prophylactic antibiotics are not warranted for the patient in the vignette. Even in the case of severe burns, prophylactic antibiotics do not significantly decrease the risk of secondary infections, and they may select for resistant organisms. References: American Academy of Pediatrics. Tetanus. In: Pickering LK, ed. Red Book: 2003 Report of the Committee on Infectious Diseases. 26th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 2003:611-616 Garcia CT. Genitourinary trauma. In: Fleisher GR, Ludwig S, Henretig FM, eds. Textbook of Pediatric Emergency Medicine. Philadelphia, Pa: Lippincott Williams & Wilkins; 2006:1463-1474 American College of Surgeons. Abdominal trauma. In: Advanced Trauma Life Support® Program for Doctors. 6th ed. Chicago, Ill: American College of Surgeons; 1997:157-175


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A 6-week-old infant presents with excessive tearing of the right eye, as evidenced by overflow of tears onto the eyelid and cheek, and frequent appearance of mucoid material. The child exhibits no systemic symptoms. Of the following, the MOST appropriate primary management is

A. administration of systemic antibiotics B. fluorescein staining of the cornea C. instillation of ophthalmic corticosteroid drops D. nasolacrimal massage and cleansing of the lids E. referral to ophthalmology for nasolacrimal duct probing


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Tears enter either the upper or lower punctum at the medial aspect of the eye and drain into the nasolacrimal duct (NLD). Among neonates, obstruction of the NLD frequently occurs at the site where the duct passes through the maxilla into the nose. Some 6% of newborns exhibit obstruction (Item C113A) when the embryonic structures fail to fully canalize. NLD is observed with increased frequency in certain populations, including preterm infants and children who have Down syndrome. Signs of obstruction include pooling or overflowing of tears, which may not be observed until normal tear production develops. Often, there is accumulation of mucoid material at the medial canthus. Stasis of tears in the obstructed NLD results in conditions favorable for bacterial infection. Progression of infection can lead to cellulitis of the overlying soft tissue. Preferred management of the infant described in the vignette is to recommend massage overlying the NLD two to three times daily and cleansing of the lids as necessary. When infection complicates the obstruction of the drainage system, instillation of a topical ophthalmic antibiotic is justified, but systemic antibiotics are not indicated. NLD obstruction typically resolves by 9 to 12 months of age. Persistence of symptoms beyond this time justifies referral to an ophthalmologist for possible probing of the NLD. For the patient in the vignette, the cornea is not involved, and fluorescein staining would not be beneficial. Instillation of a topical ophthalmic corticosteroid is not indicated in the management of this disorder and is associated with significant risks. References: Olitsky SE, Nelson LB. Disorders of the lacrimal system. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co; 2004:2099 Prasad S. Congenital nasolacrimal duct obstruction. Pediatr Rev. 1994:15:88.


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A 16-year-old girl presents to your office with a recent diagnosis of peptic ulcer. The gastroenterologist has prescribed sucralfate. Of the following, the condition that is a relative contraindication to sucralfate treatment is

A. congenital heart disease B. congenital hepatic fibrosis C. diabetes mellitus D. end-stage renal disease E. steroid-dependent asthma


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In 2005, the primary therapy of a gastric or duodenal ulcer involves treatment with a proton pump inhibitor such as omeprazole, lansoprazole, or pantoprazole. If Helicobacter pylori also is present, the pathogen should be eradicated through combination therapy with a proton pump inhibitor (eg, omeprazole, lansoprazole, pantoprazole) and two antibiotics (eg, tetracycline + clarithromycin, amoxicillin + metronidazole, amoxicillin + clarithromycin). At times, other medications, including histamine-2 receptor blockers, antacids, and sucralfate, are used as adjunctive therapy. Histamine-2 blockers reduce acid secretion, antacids neutralize gastric acid, and sucralfate coats the inflamed area and forms a protective barrier. Sucralfate is an aluminum hydroxide complex of sucrose that is effective both for treatment and prevention of peptic ulcers; it is generally less effective as monotherapy compared with either histamine blockers or proton pump inhibitors. It also has been used in a wide variety of other gastrointestinal conditions, including radiation-induced mucositis and proctitis, nonulcer dyspepsia, and bile reflux gastritis. Although the precise mechanism of action of sucralfate is unclear, it is believed to coat the ulcer region, leaving it less susceptible to acid-induced injury. Sucralfate generally is well tolerated, but it may cause constipation and decrease the bioavailability of certain medications (eg, fluoroquinolones, ketoconazole, warfarin). In addition, because it contains aluminum and has been reported to increase plasma aluminum concentrations in patients who have renal failure, it is not recommended for use in such patients. Congenital heart disease, congenital hepatic fibrosis, diabetes mellitus, and steroid-dependent asthma are not contraindications to sucralfate treatment. References: Jacobson K, Chiba N, Chen Y, et al. Gastric acid secretory response in Helicobacter pyloripositive patients with duodenal ulcer disease. Can J Gastroenterol. 2001;15:29-39. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_ui ds=11173324&query_hl=26&itool=pubmed_DocSum Sherrard DJ. Aluminum—much ado about nothing [comment]. N Engl J Med. 1991;324:558-559


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You are making rounds in the neonatal intensive care unit and discussing the complications of necrotizing enterocolitis (NEC) with the residents. Of the following, the MOST likely long-term complication following NEC is

A. encopresis B. failure to thrive C. gastroesophageal reflux disease D. intestinal stricture E. pneumatosis intestinalis


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The diagnosis of neonatal necrotizing enterocolitis (NEC) is based on clinical manifestations (poor feeding, vomiting, gastrointestinal tract bleeding, septic shock); laboratory data and physical findings (thrombocytopenia, abdominal distention); and radiologic evidence of an ileus (paucity of bowel gas), intramural air (intestinal pneumatosis) (Item C115A), portal venous air, or free air in the abdomen indicative of bowel perforation (pneumoperitoneum) (Item C115B). Early radiographic findings may be nonspecific and include dilated loops of intestine and bowel wall thickening consistent with edema. One third of cases lack radiographic findings, and in these, NEC is diagnosed only at surgery or autopsy. Very low-birthweight (14 weeks’ gestation), household members of high-risk patients, and health-care workers. The inactivated intramuscular influenza vaccine may be used in children 6 months of age and older. Children younger than 9 years of age should receive two doses 1 month apart for their initial vaccination, then a single dose each subsequent fall. The live, attenuated, intranasal vaccine is licensed only for use in healthy individuals ages 5 to 49 years. Children 5 to 9 years of age should receive two doses 6 weeks apart for their initial vaccination, then a single dose each year subsequently. Efficacy in the pediatric population is similar for both vaccines, ranging from 70% to 90%. References: Abramson JS, Katz SL, Offit PA, McMillan JA. Reducing the risk of pediatric influenza: prevention strategies help both the young and the old. Contemp Pediatr. 2005;22(suppl 1):1-8 Advanced Studies in Medicine. Prevention of influenza virus infection among children. ASIMCME 2002;2(8):286-323. Available at: http://www.jhasim.com/template.cfm?TEMPLATE=include_program.cfm&ID=38&ZoneID=8&pag


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eName=Volume%202,%20(8) American Academy of Pediatrics. Influenza. In: Pickering LK, ed. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 2006:401-411 Harper SA, Fukuda K, Uyeki TM, Cox NJ, Bridges CB. Prevention and control of influenza. Recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2005;54:1-40. Available at: www.cdc.gov/mmwr/preview/mmwrhtml/rr54e713a1.htm


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A 4-year-old boy presents with a history of chronic upper and lower respiratory tract infections. His weight is 15 kg (25th percentile), height is 97 cm (10th percentile), temperature is 98.1°F (36.8°C), and pulse oximetry is 96% on room air. On physical examination, he coughs intermittently and has mild clubbing. On nasal examination, you note purulent rhinorrhea and nasal polyps (Item Q143A). Auscultation of the heart reveals a regular rate and rhythm, with the point of maximal impulse displaced to the right. Of the following, the MOST likely diagnosis is

A. cystic fibrosis B. human immunodeficiency virus infection C. primary ciliary dyskinesia (Kartagener syndrome) D. severe combined immunodeficiency E. X-linked (Bruton) agammaglobulinemia


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The chronic sinopulmonary infections, nasal polyps, and right-sided heart (dextrocardia) described for the boy in the vignette are virtually diagnostic for primary ciliary dyskinesia (PCD). Approximately 50% of patients who have PCD have situs inversus, a reversal of the visceral organs (Kartagener syndrome). The diagnosis can be confirmed by identification of abnormal cilia orientation or missing dynein arms by electron microscopy. Cystic fibrosis can present similarly to PCD, with chronic sinopulmonary infections, bronchiectasis, nasal polyps, and clubbing, but neither dextrocardia nor situs inversus is a typical finding. Primary immunodeficiencies such as X-linked agammaglobulinemia and severe combined immunodeficiency present with recurrent bacterial and viral infections. Nasal polyps may result from chronic sinusitis, although digital clubbing and dextrocardia are not observed. Clinical manifestations of human immunodeficiency virus infection vary widely. Initial symptoms can include lymphadenopathy, hepatosplenomegaly, failure to thrive, diarrhea, and thrush. Recurrent otitis media, sinusitis, and lymphocytic interstitial pneumonia are common, but bronchiectasis and nasal polyps are rare. References: Chilvers MA, Rutman A, O’Callaghan C. Ciliary beat pattern is associated with specific ultrastructural defects in primary ciliary dyskinesia. J Allergy Clin Immunol. 2003;112:518-524 Haddad GG. Primary ciliary dyskinesia (immotile cilia syndrome). In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co; 2004:1450-1451 Welch JE, Hogan MB, Wilson NW. Ten-year experience using a plastic, disposable curette for the diagnosis of primary ciliary dyskinesia. Ann Allergy Asthma Immunol. 2004;93:189-192


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A 12-year-old child is struck in the right eye by a baseball. He now complains of double vision when he looks to the left. On physical examination, you note marked swelling and bruising circumferentially around the boy's right eye. His pupillary reflexes are normal, he has no blood in the anterior chamber of the eye, and his optic disc margins are sharp. He has dysconjugate gaze to the left but not to the right. His vision is 20/20 out of the left eye and 20/30 out of the right eye. Other findings on his neurologic examination are normal. Of the following, the MOST likely diagnosis is

A. blow-out fracture B. corneal abrasion C. detached retina D. hyphema E. traumatic iritis


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The findings described for the boy in the vignette are indicative of an internal orbital or “blow-out” fracture, which is defined as a fracture of the orbital floor or orbital wall with an intact orbital rim. This is an uncommon injury before 8 years of age, possibly due to poorly pneumatized sinuses in very young children. Rupture of the orbital wall often is accompanied by extrusion of orbital soft tissue, including periosteum, fat, or muscle. Entrapment of the inferior rectus muscle and, less commonly, the medial rectus muscle is manifested by impaired eye movement. Impaired eye movement results in intermittent diplopia, depending on the direction of eye movement. Surgical reduction is required within 4 to 10 days to prevent necrosis and subsequent fibrosis of the entrapped tissues. A child who has a suspected blow-out fracture should be evaluated by orbital computed tomography (CT) scan; skull films are of limited value. CT scan is especially valuable because it allows for evaluation of both the bony orbit and the globe. Associated injuries include ruptured globe, retrobulbar hemorrhage, and traumatic optic neuropathy, the first two of which can be demonstrated on CT scan. A child in whom a blow-out fracture is confirmed should be examined immediately by an ophthalmologist to determine the need for surgical reduction, assess for associated injuries, and monitor for complications. Corneal abrasion, detached retina, hyphema, and traumatic iritis can occur in conjunction with a blow-out fracture. Corneal abrasion causes severe pain and tearing but does not cause dysconjugate gaze or diplopia. Hyphema (Item C144A) refers to blood in the anterior chamber, which may cause visual impairment but generally not diplopia. Traumatic iritis is characterized by pain and severe photophobia but not diplopia. Detached retina can cause a “curtainlike” deficit in the peripheral vision but does not cause dysconjugate gaze. A detached retina is an ophthalmologic emergency. References: American College of Surgeons. Ocular trauma. In: Advanced Trauma Life Support® Program for Doctors. 6th ed. Chicago, Ill: American College of Surgeons; 1997:411-418 Cruz AA, Eichenberger GCD. Epidemiology and management of orbital fractures. Curr Opin Ophthalmol. 2004;15:416-421. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=Curr+Opin+Ophthalmol[Jour]+AND+416[page]+AND+2004[pdat] Klenk G, Kovacs A. Blow-out fracture of the orbital floor in early childhood. J Craniofac Surg. 2003;14:666-671. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=J+Craniofac+Surg[Jour]+AND+666[page]+AND+2003[pdat] Neuman MI, Eriksson E. Facial trauma. In: Fleisher GR, Ludwig S, Henretig FM, eds. Textbook of Pediatric Emergency Medicine. 5th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2006:1475-1484


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A 14-month-old infant who is breastfed with bottle supplementation presents with early evidence of dental caries (Item Q145A). Of the following, the MOST appropriate practice to disrupt this process is to

A. discontinue bottle feeding B. discontinue bottle feeding except for juices C. encourage brushing teeth with fluoride-containing toothpaste D. switch from formula to whole milk for bottle feeding E. use bottled water to prepare formula


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Nursing infants with erupted dentition and toddlers who are allowed to fall asleep while taking a bottle containing high sugar content liquid such as juices and formula are at risk for the development of nursing bottle caries (Item C145A). Recently, prolonged nocturnal breastfeeding also has been recognized as a contributing factor. Characteristically, the sequence of caries development progresses from maxillary incisors to maxillary molars and subsequently mandibular dentition. Brushing before bedtime and elimination of feeding in bed should greatly decrease the appearance of nursing caries. Bottle feeding should be discontinued for the 14-month-old infant described in the vignette. Continuing juices by bottle would compound the problem. Preparing formula with bottled water would have no impact on the disease process. Changing from formula to whole milk is appropriate for the infant, but nocturnal bottle feeding of whole milk would continue to place the toddler at risk for caries. Brushing teeth is a good practice, but discontinuation of bottle feeding is most important. References: American Academy of Pediatrics. Policy statement: oral health risk assessment timing and establishment of the dental home. Pediatrics. 2003;111:1113-1116. Available at: http://pediatrics.aappublications.org/cgi/content/full/111/5/1113 Tinanoff N. Dental caries. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co; 2004:1209-1211 Zitelli BJ, Davis HW. Caries. In: Atlas of Pediatric Physical Diagnosis. 3rd ed. St. Louis, Mo: Mosby-Wolfe; 1997:613


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During the health supervision visit for a 1-month-old infant, you note mild jaundice, but no fever and clear lungs. Cardiac examination demonstrates a 2/6 systolic murmur at the left sternal border. Abdominal examination demonstrates a firm liver 3 cm below the costal margin and extending past the midline. The alanine aminotransferase is 140 U/L, aspartate aminotransferase is 130 U/L, total bilirubin is 5.5 mg/dL (94.1 mcmol/L), and direct bilirubin is 3.0 mg/dL (51.3 mcmol/L). Of the following, the finding that MOST strongly suggests the need for referral to a surgeon for intraoperative cholangiography is

A. abdominal ultrasonography demonstrating a prominent gallbladder B. brain computed tomography scan demonstrating cerebral calcifications C. echocardiography demonstrating pulmonary artery stenosis D. dimethyl iminodiacetic acid scan demonstrating no tracer in the bowel E. liver biopsy demonstrating periodic acid-Schiff stain-positive globules in the hepatocytes


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In a 1-month-old infant, the liver edge can be palpated below the costal margin. As the infant grows, more of the liver is covered by the ribcage, making it unusual to feel a liver edge in children older than 1 year of age. A preferred approach to assessing liver size in all children involves percussion of the liver span; the dull sound of the liver can be differentiated easily from the more hollow sound of the bowel and chest. Because chest hyperinflation can push the liver down, thus mimicking "hepatomegaly," determination of liver span can help differentiate true enlargement from liver displacement. Hepatomegaly should be suspected when the liver edge extends more than 1 cm below the costal margin, if the liver is hard to palpation, or if there is a prominent left lobe in the epigastrium. The causes of hepatomegaly in the infant and child are diverse and include primary liver disease, infection, malignancy, and storage disorders. For an infant younger than 2 months of age who has direct hyperbilirubinemia and hepatomegaly, such as the infant described in the vignette, the primary responsibility of the physician is to diagnose or rule out extrahepatic biliary atresia. This condition must be differentiated from other anatomic, infectious, and metabolic causes of neonatal cholestasis. Biliary atresia occurs in as many as 30% of infants who have conjugated hyperbilirubinemia. The initial evaluation of an infant who has suspected biliary atresia typically involves exclusion of infectious causes by appropriate cultures and serologies, hepatobiliary ultrasonography to exclude gallstones, and radionuclide scintigraphy. The scintigraphic examination involves injecting an infant with a radionuclide tracer such as dimethyl iminodiacetic acid. A liver that is affected by biliary atresia demonstrates tracer uptake into the liver but no excretion into the bowel (Item C146A). In contrast, a liver affected by cholestasis from other causes but that has a patent biliary system demonstrates delayed uptake in the liver but excretion into the bowel. As a caveat, however, infants who have severe cholestasis may have false-positive test results, in which tracer uptake is so slow that there is no significant excretion into the bowel. If this is the case, additional testing with liver biopsy and intraoperative cholangiography is necessary to exclude biliary atresia. Abdominal ultrasonography demonstrating a prominent gallbladder makes biliary atresia less likely because the gallbladder in biliary atresia is typically shrunken or not visible. Brain calcifications are seen in congenital toxoplasmosis and cytomegalovirus infection, two infectious causes of liver disease. Peripheral pulmonary artery stenosis is characteristic of Alagille syndrome, a genetic cause of intrahepatic bile duct paucity. A liver biopsy with periodic acidSchiff stain-positive granules suggests a storage disorder (glycogen storage disease, alpha-1antitrypsin deficiency) as a cause of the child's hepatomegaly. References: Campbell KM, Bezerra JA. Biliary atresia. In: Walker WA, Goulet O, Kleinman RE, Sherman PM, Shneider BL, Sanderson IR, eds. Pediatric Gastrointestinal Disease. 4th ed. Hamilton, Ontario, Canada: BC Decker; 2005:1122-1138 Wolf AD, Lavine JR. Hepatomegaly in neonates and children. Pediatr Rev. 2000;21:303-310. Available at: http://pedsinreview.aappublications.org/cgi/content/full/21/9/303


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You are evaluating a very low-birthweight (VLBW) preterm infant who experienced polyuria in the first 72 hours after birth. No diuretics have been prescribed, and there is no glycosuria, hematuria, or obvious anasarca on examination. You collect a urine sample to measure electrolytes and creatinine and simultaneously obtain a blood sample to measure serum electrolytes and creatinine. Of the following, the MOST correct statement regarding sodium handling in the VLBW infant is that

A. fractional excretion of sodium is lower than in term infants B. intravenous sodium supplementation is necessary from birth C. phototherapy increases sodium requirements D. sodium excretion increases with gestational age E. water losses generally exceed sodium losses


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The fractional excretion of sodium (FENa) is a measure of renal handling of solute. The equation for calculating the FENa is: FENa = [(Urine Na x Plasma Cr)/(Plasma Na x Urine Cr)] x 100 Example: [(90 x 0.9)/(145 x 120)] x 100 = 0.5 Sodium is reabsorbed in the proximal renal tubule. In the preterm kidney, a number of factors affect the renal handling of sodium. First, the renal blood flow increases throughout gestation in the fetus and in the first week of postnatal life. Second, the glomerular filtration rate increases throughout the first postnatal week. Third, the extracellular fluid compartment, where most of the total body content of sodium is located, is greatest in the most preterm infants. Depending on the degree of prematurity, the functional number of nephrons may be reduced significantly (nephrogenesis is not complete until after 36 weeks’ gestation), and renal efficiency in handling solute load is reduced accordingly because sodium transporter activity in the renal tubules is immature. Additionally, the premature kidney has poor concentrating ability, with maximal urinary concentration of 600 to 800 mOsm/L in the first 2 weeks of postnatal life. This results in a high risk of hypervolemia and hyponatremia (due to dilution) for the preterm infant who is given too much water. However, because of postnatal adjustments in fluid compartments (Item C147A), the addition of sodium to intravenous fluids for the preterm neonate is largely unnecessary in the first 24 to 72 hours after birth. The very low-birthweight (VLBW) newborn described in the vignette has polyuria, generally defined as a urine output of greater than 6 mL/kg per hour. Causes typically include iatrogenic overhydration, diabetes insipidus (genetic or sometimes related to intracranial pathology), hyperglycemia with a corresponding osmotic drag of water and the occurrence of glycosuria, or anatomic renal problems such as an obstruction that has been relieved. Water losses in the VLBW newborn generally exceed solute (sodium) losses, especially in cases of polyuria, and dehydration with elevated serum sodium concentrations may result. As noted previously, sodium excretion (FENa) decreases with increasing gestational age and postnatal age. Accordingly, the FENa is higher in a preterm newborn than in a term infant. Phototherapy increases fluid (water) requirements for the VLBW newborn, but not sodium requirements. Intravenous sodium supplementation is not necessary in most VLBW newborns in the first 24 to 72 hours of postnatal life. References: Chua AN, Sarwal MM. Acute renal failure management in the neonate. NeoReviews. 2005;6:e369-e376. Available at: http://neoreviews.aappublications.org/cgi/content/full/6/8/e369 Dell KM, Davis ID. Fluid and electrolyte management. In: Martin RJ, Fanaroff AA, Walch MC, eds. Fanaroff and Martin’s Neonatal-Perinatal Medicine: Diseases of the Fetus and Infant. 8th ed. Philadelphia, Pa: Mosby-Elsevier; 2006:695-702


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A young mother brings in her toddler immediately after seeing him drink an unknown amount of mineral spirits. He appears tired and has a persistent cough. His respiratory rate is 40 breaths/min, and his lungs are clear bilaterally. There are no other abnormal findings on physical examination. A chest radiograph shows no abnormality. Of the following, the MOST appropriate management option is

A. administration of activated charcoal B. administration of intravenous corticosteroids C. discharge home with follow-up the next day D. gastric lavage E. hospitalization for observation and supportive care


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Hydrocarbons, such as mineral spirits, kerosene, gasoline, turpentine, and pine oil, are among the most common ingestions in young children. The hydrocarbons that have the lowest viscosity, such as furniture polish, are associated with the highest risk for aspiration. Children who ingest hydrocarbons are at potentially very high risk for complications and should be evaluated carefully. Children who have ingested hydrocarbons may have a slight cough initially, which does not necessarily indicate an aspiration. However, those who exhibit persistent cough, tachypnea, or dyspnea within a few hours are at high risk of aspiration. Some children, including the boy described in the vignette, develop signs of central nervous system involvement, such as irritability or lethargy, which is largely due to hypoxia, not direct toxic effects to the brain. Fever may be present initially but is not an indicator of aspiration pneumonitis. Intestinal symptoms, such as vomiting and abdominal pain, may occur because of mucosal irritation. Children who have confirmed or suspected hydrocarbon ingestion should be evaluated with a chest radiograph, but early radiographs (within 1 hour of ingestion) may appear normal, even in the presence of aspiration. Findings indicative of aspiration include bilateral, patchy opacities (Item C148A), but these findings correlate poorly with clinical manifestations. Blood gas analysis may reveal hypoxemia and should be considered in children who have low pulse oximetry readings. Even children who do not have respiratory symptoms should be observed in the emergency department for 4 to 6 hours before discharge. Hospitalization is indicated for those who have respiratory symptoms, altered mental status, abnormal chest radiographs, or inadequate followup, such as the boy in the vignette. Management is largely supportive. Oxygen should be administered, and intubation with ventilatory support should be performed for those who have impending respiratory failure. Gastric decontamination with lavage is only indicated in cases when the ingested hydrocarbon solution contains other harmful elements, such as camphor, aromatics, heavy metals, or pesticides. Activated charcoal is not effective and should not be administered because it may increase the risk of emesis, thereby further increasing the risk of aspiration. Corticosteroids and antibiotics have not been shown to have a role in the management of hydrocarbon ingestions. Respiratory symptoms of hydrocarbon ingestion typically resolve within 7 days, although chest radiograph abnormalities may be present for weeks. Complications such as pneumatoceles, pneumothorax, empyema, bacterial pneumonia, and respiratory distress syndrome occur in a small number of patients. A few patients may develop chronic pulmonary function abnormalities dues to proliferative alveolar thickening. Another population in which hydrocarbon ingestion is important is adolescents. Adolescents may inhale hydrocarbons chronically and are at risk for long-term symptoms such as peripheral neuropathy and encephalopathy. They are also at risk for sudden cardiac death. References: Lee DC. Hydrocarbons. In: Marx JA, Hockberger RS, Walls RM, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, Mo: Mosby; 2002:2160-2163 McGuigan ME. Poisoning potpourri. Pediatr Rev. 2001;22:295-302. Available at: http://pedsinreview.aappublications.org/cgi/content/full/22/9/295 Tucker JF. Aliphatic hydrocarbons. In: Ford MD, Delaney KA, Ling LJ, Erickson T, eds. Clinical Toxicology. Philadelphia, Pa: WB Saunders Co; 2001:789-793


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A 2-year-old boy who has been followed by your practice since birth presents for a health supervision visit. On careful physical examination, you have difficulty locating the right testis. In reviewing your records, you note that this is a new finding. Of the following, the MOST likely diagnosis is

A. agenesis of the testis B. indirect inguinal hernia C. pseudohermaphroditism D. retractile testis E. undescended testis


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Because the boy described in the vignette has had normal findings on previous testicular examinations, it is likely that the cremasteric reflex is causing retractile testis, preventing examination of the testis on this visit. A warm examination room, warm compresses to the inguinal area, or having the boy sit in the “tailor’s position” (sitting with knees flexed and ankles crossed on the examination table) or squatting may facilitate descent of the normal testis back into the scrotal sac. Retractile testis is not common in early infancy or after puberty. Agenesis of the testis is unlikely because the testes were palpable on previous examinations. Indirect inguinal hernia would be associated with an inguinal mass, but the testis would still be palpable on examination. True undescended testis is the single most common genitourinary problem in boys. Bilateral undescended testes may be associated with chromosomal or endocrine disorders, including pseudohermaphroditism as well as other syndromes and should be evaluated with careful attention to the presence of other malformations or metabolic disturbances. A normal-appearing penis implies intact testicular tissue, but chromosomal and endocrine studies should be performed. An endocrine consultation may be appropriate in an infant who has bilateral undescended testes, but it is not necessary for a child who has a unilateral undescended testis. Failure of the testis to descend along the appropriate track from the abdomen through the inguinal ring and into the scrotal sac may be associated with infertility and up to a 40% increase in the risk for testicular cancer, which would be undetected in the abdominal location. Structural changes in the undescended testis have been documented as early as 2 years of age and diminished sperm production as young as 6 years. Although administration of beta human chorionic gonadotropin has been used infrequently to effect testicular descent, it is not believed to be very effective. Adverse effects include premature closure of the epiphyses and premature onset of secondary sex characteristics (reversible). Laparoscopic orchiopexy of the presumably present unilateral undescended testis is the current treatment of choice and usually is performed at 1 year of age. References: Callaghan P. In brief: undescended testis. Pediatr Rev. 2000;21:395. Available at: http://pedsinreview.aappublications.org/cgi/content/full/21/11/395 Roth DR, Gonzales ET. Disorders of renal development and anomalies of the collecting system, bladder, penis and scrotum. In: McMillan JA, DeAngelis CD, Feigin RD, Warshaw JB, eds. Oski’s Pediatrics: Principles and Practice. 3rd ed. Philadelphia, Pa: Lippincott, Williams & Wilkins; 1999:1555-1556


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A 15-year-old girl is rushed to the emergency department after slipping off a diving board and striking her head on cement. On physical examination, her mental status evaluation results are completely normal. She can abduct her upper extremities at the shoulder, but cannot flex or extend her arms and minimally moves her fingers. She cannot move her limp lower extremities. You order emergent magnetic resonance imaging of the brain and spine. Of the following, the MOST important therapy to implement before the patient is sent for imaging is

A. fosphenytoin 18 phenytoin equivalents/kg intravenously B. dexamethasone 1 mg/kg orally C. low-molecular weight heparin 1 mg/kg subcutaneously D. mannitol 1 g/kg intravenously E. methylprednisolone 30 mg/kg intravenously


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The possibility of occult or overt spinal trauma should be considered with any injury. For any notable body trauma, the cervical and lower spine should be immobilized until spinal trauma has been eliminated as a possibility. Common sites for fracture dislocation spinal cord injuries are C1 through C2, C5 through C6, and T12 through L1 spinal segments. Fracture dislocations of the vertebral column are the most common causes of spinal cord injury, although injury can be as severe as complete cord transection without any visible trauma on radiography. Sudden whiplash (flexion-extension) injuries may contuse (Item C150A) or lacerate the cervical cord. Typical symptoms and signs of spinal trauma include focal pain along the spinal axis or any weakness or sensory loss in the extremities or trunk. “Spinal shock” is characterized by loss of all voluntary movement and sensation inferior to the site of injury. Reflex function in the cord is lost temporarily, resulting in ileus and bladder distention. While the spine is immobilized, the child should undergo a thorough neurologic examination. If there is high index of suspicion for spinal trauma, as for the girl described in the vignette, prompt initiation of methylprednisolone 30 mg/kg administered intravenously over 1 hour, followed by 5.4 mg/kg per hour the next 23 hours, is a protocol that can lead to improved neurologic outcomes. The cervical spine typically is evaluated by radiographs (including lateral, anterior-posterior, and odontoid views), but if there is lingering concern, computed tomography scan or magnetic resonance imaging is warranted. Intravenous dexamethasone is useful for spinal cord compression with tumors, but its efficacy has not been investigated fully for spinal trauma. Anticonvulsants sometimes are administered prophylactically after severe head trauma, but this is controversial. Mannitol is useful only if the patient displays signs of increased intracranial pressure. Low-molecular weight heparin to prevent deep venous thrombosis might be useful if the patient is not expected to regain ambulatory status for several days. References: Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med. 1990;322:1405-1411. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_ui ds=2278545&query_hl=19&itool=pubmed_docsum Haslam RHA. Spinal cord disorders: spinal cord trauma. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co; 2004:2050 Temkin NR, Dikmen SS, Wilensky AJ, Keihm J, Chabal S, Winn HR. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. N Engl J Med. 1990;323:497502. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_ui ds=2115976&query_hl=21&itool=pubmed_docsum


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You care for a 17-year-old boy who is overweight. He has gained 44 lb (20 kg) in the last year, especially in his abdominal area. On examination today, his blood pressure is 158/90 mm Hg using a large, appropriately sized cuff. His mother has a similar body habitus and is being treated for type 2 diabetes mellitus. Of the following, the MOST likely abnormalities to expect in this patient if his present condition continues into adulthood is

A. high triglyceride concentrations, low high-density lipoprotein cholesterol concentrations B. hypoglycemia from insulin sensitivity C. low concentrations of C-reactive protein in the blood D. low fibrinogen concentrations with bleeding diatheses E. low triglyceride concentrations, low low-density lipoprotein cholesterol concentrations


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The metabolic syndrome is a series of clinical and laboratory findings that include truncal obesity, elevated concentrations of serum triglycerides, decreased concentrations of highdensity lipoprotein cholesterol, and an elevation in blood pressure. Sex- and age-specific values exist for each of these values in the adult population. The metabolic syndrome increases the risk for type 2 diabetes and cardiovascular disease. In some recent studies of adult patients, the incidence of the metabolic syndrome was as high as 23%. The metabolic syndrome affects people from all ethnic and cultural backgrounds, but is most prevalent in the Hispanic population. The increasing incidence of the metabolic syndrome in the adult population is likely the result of the growing number of children who develop obesity. The growth in numbers of obese children has paralleled the increased incidence in type 2 diabetes and impaired glucose tolerance. The patient described in the vignette has abdominal obesity, hypertension, and a family history of type 2 diabetes, which places him at risk for the metabolic syndrome and its attendant risks for the development of cardiovascular disease as he ages. The most likely laboratory abnormalities that will be identified with the metabolic syndrome are elevated triglyceride concentrations and decreased concentrations of high-density lipoprotein cholesterol. Insulin resistance, which often is found in metabolic syndrome, may lead to hyperglycemia. C-reactive protein and fibrinogen values often are elevated in patients who have metabolic syndrome. References: Cruz M L, Weigensberg MJ, Huang TT, Ball G, Shaibi GQ, Goran MI. The metabolic syndrome in overweight Hispanic youth and the role of insulin sensitivity. J Clin Endocrinol Metab. 2004;89:108-113. Available at: http://jcem.endojournals.org/cgi/content/full/89/1/108 Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA. 2002;287:356-359. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22JAMA+:++the+journal+of+the+American+Medical+Association%22[Jour]+AND+2002[pdat ]+AND+Ford+E[author]


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A newborn female has loose neck skin (Item Q152A) and nonpitting edema of the lower extremities (Item Q152B). Of the following, the MOST appropriate evaluation for this infant is

A. blood chromosome analysis B. magnetic resonance imaging of the brain C. slitlamp ophthalmologic examination D. ultrasonography of the liver E. voiding cystourethrography


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The finding of loose neck skin (Item C152A), which is suggestive of the presence of a cystic hygroma in fetal life, and nonpitting edema of the lower extremities in a newborn female should raise the suspicion of Turner syndrome (TS). Congenital lymphedema (Item C152B), which occurs in up to 80% of affected females, typically disappears during infancy, leaving only a puffy appearance to the hands and feet, although in some patients it reappears when estrogen therapy is initiated. The redundant posterior neck skin can persist as the pterygium colli, or webbed neck. The clinical diagnosis of TS should be confirmed by peripheral blood chromosome analysis, which will reveal monosomy X, mosaic monosomy X, or the presence of an abnormal X chromosome that contains a deletion. A buccal smear lacks sensitivity and should not be used to make the diagnosis of TS. Affected girls also have short stature, ovarian dysgenesis, a broad chest with wide-spaced nipples (Item C152C), ear anomalies, cubitus valgus, and renal (eg, pelvic kidney, horseshoe kidney) and cardiac (eg, bicuspid aortic valve, coarctation of the aorta) defects. Intelligence typically is normal. Estrogen replacement therapy at the expected time of puberty is required in most cases, and treatment with growth hormone also should be offered. Magnetic resonance imaging of the brain, slitlamp ophthalmologic examination, and ultrasonography of the liver are not routinely indicated. Although renal defects may be present, the most common abnormality is horseshoe kidney, which can be detected by ultrasonography and usually has no clinical effects that would prompt the need for voiding cystourethrography. References: Frias JL, Davenport ML, Committee on Genetics and Section on Endocrinology. Health supervision for children with Turner syndrome. Pediatrics. 2003;111:692-702. Available at: http://pediatrics.aappublications.org/cgi/content/full/111/3/692 Sybert VP, McCauley E. Turner's syndrome. N Engl J Med. 2004;351:1227-1238


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A 16-year-old boy presents for his annual sports physical before wrestling season. He has been participating in a weight lifting program and proudly reports his increased muscle mass and strength. You are concerned that he may be using performance-enhancing substances (eg, creatine). Of the following, the use of creatine is MOST likely to be revealed by

A. abnormal liver enzyme concentrations B. an interview with the patient C. increase in hemoglobin concentration D. presence of gynecomastia E. serum drug screening


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Creatine and other substances such as anabolic steroids, androstenedione, growth hormone, and erythropoietin have been used by athletes because of their performance-enhancing reputations. Most adolescent users of performance-enhancing substances (PESs) seek to improve their athletic performance, although some use these agents to enhance their physical appearance by developing a more muscular body. All athletes, whether in organized sports or individual training programs (eg, weight lifting), should be asked about the use of PESs. The diagnosis of PES use is aided by a high index of suspicion and a history that includes the recognition of signs of use and adverse effects. Creatine enhances the ability of muscles to maintain power in short maximal exercise efforts. Creatine cannot work without strength training; those who lift weights achieve a greater benefit compared with those who do not lift. Adverse effects include muscle cramping and gastrointestinal symptoms of vomiting and diarrhea. The use of creatine is not recommended for adolescent athletes because its safety has not been established. The use of creatine and other PESs is most likely to be revealed by an interview with an adolescent. There is no specific assay to identify creatine use. Creatine has not been reported to cause abnormal liver enzyme concentrations, increased hemoglobin concentrations, or gynecomastia. The lifetime prevalence of illegal steroid use among high school students in the United States has been reported to be as high as 6%. Users of anabolic steroids anticipate gains in muscle mass and strength. Deepening of the voice and hirsutism in a female and gynecomastia and a high voice in a male should heighten the clinician’s suspicion for the use of anabolic steroids. Virilization in the female also may result in hair loss. Hypogonadism or a decrease in testicular size associated with oligospermia/azoospermia and decreased sexual function/desire may occur in male users. Acne, often severe, can be observed in both male and female abusers. Other adverse effects associated with anabolic steroid abuse include hypertension, hyperaggressiveness, mood swings, psychosis, and mania. Depression can occur during withdrawal. Prepubertal abusers of anabolic steroids are at risk for premature closure of their epiphyseal growth plates. Nonspecific evidence of anabolic steroid use may be found in laboratory study results, including elevated liver enzyme concentrations and decreased highdensity and increased low-density lipoprotein cholesterol levels. Laboratory evidence of orally administered steroids can be present in the urine for days to weeks; injected steroids can be present for 6 months or longer. Androstenedione has received considerable attention in the media and is purported to increase muscle mass and strength. As a precursor to testosterone, use theoretically can induce premature puberty or the premature closure of growth plates and cause other adverse effects that have been attributed to anabolic steroid use. Assays (urine screens confirmed by gas chromatography) included in some mandatory drug screens of collegiate athletes are available to detect androstenedione by specialized laboratories. Growth hormone (GH) use theoretically increases protein anabolism and lipolysis; thus, it has a particular lure for bodybuilders. The anticipated signs of GH abuse are clinical findings consistent with acromegaly. These findings include coarsening of facial features, growth of facial bones (including the mandible, with increased separation of teeth), increase in head circumference, broadening of the nose, enlargement of the tongue, and thickness of fingers and toes. GH abuse may be associated with adverse behavior changes, hypertension, diabetes, cardiovascular disease, and peripheral neuropathy. There is no readily available, reliable test or metabolic marker to detect the use of exogenous GH. Erythropoietin increases red blood cell mass and improves oxygen delivery to skeletal muscle, thereby improving exercise endurance. Specialized laboratory testing can identify the use of natural and recombinant erythropoietin. The increased red blood cell mass also increases blood viscosity and may cause vascular occlusions. References: Coupey SM. Specific drugs. In: Schydlower M, ed. Substance Abuse: A Guide for Health Professionals. 2nd ed. Elk Grove Village, Ill: American Academy of Pediatrics; 2002:191-276


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Greydanus DE, Patel DR. Sports doping in the adolescent athlete: the hope, hype, and hyperbole. Pediatr Clin North Am. 2002;49:829-855. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22Pediatric+clinics+of+North+America%22[Jour]+AND+829[page]+AND+2002[pdat] Hergenroeder AC, Neinstein LS. Guidelines in sports medicine. In: Neinstein LS, ed. Adolescent Health Care A Practice Guide. 4th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2002:380438 Koch JJ. Performance-enhancing substances and their use among adolescent athletes. Pediatr Rev. 2002;23:310-317. Available at: http://pedsinreview.aappublications.org/cgi/content/full/23/9/310


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A 14-year-old boy has a body mass index that is greater than the 95th percentile for age and an accelerating weight curve. His blood pressure is 135/85 mm Hg. His mother has type 2 diabetes that developed during her first pregnancy, and several paternal relatives also have type 2 diabetes. The family emigrated from the Caribbean when he was a toddler. He has dark velvety thickening (Item Q154A) of the skin on his neck and under his arms. Of the following, the findings that are MOST supportive of a diagnosis of metabolic syndrome in this young man are

A. acanthosis nigricans, hypertension, obesity B. acanthosis nigricans and maternal history of diabetes C. acanthosis nigricans, obesity D. hypertension, obesity E. obesity and maternal history of diabetes


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The constellation of findings that lead to the diagnosis of metabolic syndrome in adults varies, depending upon the criteria used, although hypertension and obesity are common to all definitions. The latest criteria from the International Diabetes Federation include ethnicity-specific waist circumference criteria or a body mass index greater than 30 kg/M2 plus two of the following: •Fasting triglyceride concentration greater than 150 mg/dL (1.7 mmol/L) or treatment for this finding •High-density lipoprotein cholesterol concentration less than 40 mg/dL (1.03 mmol/L) in men and 50 mg/dL (1.29 mmol/L) in women •Hypertension manifested by systolic blood pressure of 130 mm Hg or greater and diastolic pressure of 85 mm Hg or greater or previously treated hypertension •Fasting plasma glucose value of 100 mg/dL (5.5 mmol/L) or greater or previously diagnosed type 2 diabetes Definitions in childhood are not established, but usually consist of similar criteria adjusted to age-appropriate values greater than the 85th percentile for blood pressure, weight, and waist circumference. A recent review of the criteria for the diagnosis of metabolic syndrome concludes that “metabolic syndrome” may not be an entity in adults that is greater in severity than the sum of its components. Acanthosis nigricans is not included as a criterion for the diagnosis of metabolic syndrome, although it often is found. Maternal or family history of diabetes frequently is found and increases the risk of type 2 diabetes in the child, but it is not one of the criteria for the diagnosis of metabolic syndrome. References: Boney CM, Verma A, Tucker R, Vohr BR. Metabolic syndrome in childhood: association with birth weight, maternal obesity, and gestational diabetes mellitus. Pediatrics. 2005;115:e290-e296. Available at: http://pediatrics.aappublications.org/cgi/content/full/115/3/e290 Ford ES. Prevalence of the metabolic syndrome defined by the International Diabetes Federation among adults in the U.S. Diabetes Care. 2005;28:2745-2749. Available at: http://care.diabetesjournals.org/cgi/content/full/28/11/2745 Hirschler V, Aranda C, Calcagno Mde L, Maccalini G, Jadzinsky M. Can waist circumference identify children with the metabolic syndrome? Arch Pediatr Adolesc Med. 2005;159:740-744. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22Archives+of+pediatrics+%26+adolescent+medicine%22[Jour]+AND+740[page]+AND+20 05[pdat] Janssen I, Katzmarzyk PT, Srinivasan SR, et al. Combined influence of body mass index and waist circumference on coronary artery disease risk factors among children and adolescents. Pediatrics. 2005;115:1623-1630. Available at: http://pediatrics.aappublications.org/cgi/content/full/115/6/1623 Kahn R, Buse J, Ferrannini E, Stern M; American Diabetes Association; European Association for the Study of Diabetes. The metabolic syndrome: time for a critical appraisal: joint statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care. 2005;28:2289-2304. Available at: http://care.diabetesjournals.org/cgi/content/full/28/9/2289


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Ten S, Maclaren N. Insulin resistance syndrome in children. J Clin Endocrinol Metab. 2004;89:2526-2539. Available at: http://jcem.endojournals.org/cgi/content/full/89/6/2526


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You are evaluating a 10-year-old boy who has behavior problems. He hits his younger brother, talks back to his parents, and refuses to perform his assigned household chores. He does well in school, but is oppositional in the classroom. His parents ask what they can do to improve his behavior. Of the following, your BEST response is that

A. he needs cognitive testing B. he should be referred for individual counseling C. medication is the preferred first-line treatment D. school-based behavior programs are preferred to home-based programs E. the parents should be trained in behavior modification techniques


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Behavior modification is a general category of therapy that refers to principles and techniques based on learning theory and used to change behavior. Behavioral techniques are used to either strengthen or maintain desired behaviors or to decrease or eliminate undesired behaviors. For example, parental praise or token economies are examples of techniques used to reinforce behavior, and time-out is a technique used to decrease or eliminate a behavior. The child described in the vignette has oppositional behavior that may respond to behavioral management. He is doing well in school and, therefore, probably does not need cognitive testing. Individual counseling may be used as an adjunct, but he is more likely to respond to consistent behavior management. Behavioral approaches should be tried before using medication to control behavior. The behavioral plan should be instituted both at home and in school, with communication between teacher and parents to maintain consistency. References: Boris NW, Dalton R. Disruptive behavioral disorders. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co; 2004:88-90 Vitulano LA. Child and adolescent behavior therapy. In: Lewis M, ed. Child and Adolescent Psychiatry: A Comprehensive Textbook. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2002:998-1014


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A 14-month-old girl is brought to the emergency department with a 12-hour history of fever and rash. Her mother became frightened when it was difficult to arouse the girl after her nap. Findings on physical examination include a temperature of 104°F (40°C), a heart rate of 164 beats/min, a respiratory rate of 42 breaths/min, and a blood pressure of 75/45 mm Hg. There are petechiae and purpura (Item Q156A) on the chest, arms, and legs. As you are establishing intravenous access and drawing blood for initial laboratory evaluations, you request an immediate dose of antibiotics. Of the following, the MOST appropriate therapy is

A. ceftriaxone B. penicillin C. vancomycin D. vancomycin plus ceftriaxone E. vancomycin plus gentamicin


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The findings reported for the patient in the vignette suggest that she has sepsis due to Neisseria meningitidis, but nearly all pathogenic bacteria can cause petechiae and purpura. When treating patients who have potentially life-threatening infections, the initial choice of antimicrobial agents should be broad enough to cover the endemic pathogenic bacteria in the local community. Once a bacterial pathogen is isolated and susceptibility data are known, the antimicrobial therapy can be simplified. The treatment of sepsis varies with age of the patient. Vancomycin and ceftriaxone represent the best choice for most patients older than 3 months who have potentially life-threatening infections. Vancomycin provides coverage for penicillin- and cephalosporin-resistant Streptococcus pneumoniae, Staphylococcus aureus, and Enterococcus, and ceftriaxone is effective against N meningitidis, most S pneumoniae, and other gram-negative organisms such as Haemophilus influenzae. Single agents (eg, ceftriaxone, penicillin, vancomycin) do not provide enough coverage in a critically ill patient. Vancomycin and gentamicin provide broad coverage, but gentamicin is not active against H influenzae and does not penetrate the central nervous system as effectively as ceftriaxone. For most neonates, ampicillin in addition to cefotaxime or gentamicin is an appropriate choice. Many experts suggest that if central nervous system disease has not or cannot be ruled out, cefotaxime is preferable because the cephalosporins penetrate the central nervous system better than the aminoglycosides. Vancomycin rarely is included in the treatment of neonates who have community-acquired sepsis. Certain situations may call for the addition of acyclovir. Patients between 1 and 3 months of age are more problematic. It is during this age that a crossover can occur from pathogens commonly seen in the neonatal period (eg, group B Streptococcus, Escherichia coli, Listeria monocytogenes, Enterococcus) to those usually encountered in children older than 3 months of age (eg, S pneumoniae, N meningitidis, S aureus). Clinicians should understand the common bacterial pathogens and their resistance patterns in their community when making antibiotic choices. If there is concern for methicillinresistant S aureus or penicillin- or cephalosporin-resistant S pneumoniae, vancomycin should be part of the empiric regimen. References: Stormorken A, Powell KR. Sepsis and shock. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co; 2004:846-850 American Academy of Pediatrics. Meningococcal 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; 2006:452-460 Durbin WJ. Pneumococcal infections. Pediatr Rev. 2004;25:418-424. Available at: http://pedsinreview.aappublications.org/cgi/content/full/25/12/418


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You are evaluating a newborn boy who has lax abdominal musculature (Item Q157A) and bilateral undescended testes. Other findings on physical examination are normal. Of the following, the MOST likely urologic abnormality in this boy is

A. hydronephrosis B. renal cysts C. ureterocele D. ureteropelvic junction obstruction E. vesicoureteral reflux


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Prune belly (Eagle-Barrett) syndrome (PBS) is a relatively uncommon condition resulting from poorly developed abdominal musculature. Affected children may have a variety of urinary tract anomalies, including undescended testes, hydronephrosis, posterior urethral valves (PUV), and bladder dysfunction. The lax abdominal musculature (Item C157A) and bilateral undescended testes described for the boy in the vignette suggest the diagnosis of PBS. Abdominal ultrasonography and voiding cystourethrography are indicated in all children who have PBS to study the entire urinary tract. Hydronephrosis is a common anomaly associated with PBS. The hydronephrosis usually is obstructive and due to PUV or vesicoureteral reflux and ureteropelvic junction obstruction. Renal cysts are very uncommon, and ureteroceles are seen only occasionally in children who have PBS. Some affected children may have nonobstructive hydronephrosis. The best test to differentiate obstructive from nonobstructive hydronephrosis is renal scintigraphy. In obstructive hydronephrosis, the tracer cannot escape the kidney, but in most kidneys with nonobstructive hydronephrosis, some amount of the tracer exits the kidney. The renal outcome for children who have PBS is generally poor. Meticulous attention must be paid to the prevention of urinary tract infections (UTIs). Thus, it is imperative to institute antibiotic prophylaxis if obstruction is present, and in some cases of moderate-to-severe hydronephrosis with obstruction, early surgical repair is recommended. Urinary diversion via a vesicostomy or Mitrofanoff procedure (using the appendix to connect the bladder to the abdomen, with exit near the umbilicus) may be indicated to prevent urinary stasis and UTIs. Unfortunately, renal growth usually is compromised because of multiple abnormalities within the urinary tract, and most children who have PBS develop renal insufficiency. References: Denes FT, Arap MA, Giron AM, Silva FA, Arap S. Comprehensive surgical treatment of prune belly syndrome: 17 years' experience with 32 patients. Urology. 2004;64:789-793. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22Urology%22[Jour]+AND+789[page]+AND+2004[pdat] Jennings RW. Prune belly syndrome. Semin Pediatr Surg. 2000;9:115-120. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22Seminars+in+pediatric+surgery%22[Jour]+AND+115[page]+AND+2000[pdat] Strand WR. Initial management of complex pediatric disorders: prunebelly syndrome, posterior urethral valves. Urol Clin North Am. 2004;31:399-415. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22The+Urologic+clinics+of+North+America%22[Jour]+AND+399[page]+AND+2004[pdat]


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A 15-year-old boy was camping with friends 1 week ago. Over the last 4 days, he has developed fever, worsening headache, increasing sleepiness, and combativeness. You suspect arboviral meningoencephalitis. Of the following, the MOST frequently used method to confirm the diagnosis is

A. detection of myelin basic protein in the cerebrospinal fluid (CSF) B. detection of viral antigen in brain biopsy tissue C. detection of viral nucleic acid in the CSF by polymerase chain reaction D. isolation of the virus by culture of the CSF E. measurement of acute and convalescent antibody titers in serum or CSF


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Arboviruses are an important cause of encephalitis in the United States during the late spring and summer months. These agents are transmitted by the bites of mosquitos, ticks, or sandflies. Examples of arboviral encephalitis encountered in North America include St. Louis encephalitis, La Crosse encephalitis, Western and Eastern equine encephalitis, California encephalitis, West Nile encephalitis, and Colorado tick fever. The diagnosis should be suspected in any child who presents with symptoms of fever, irritability or change in mental status, and headache. Cerebrospinal fluid (CSF) shows pleocytosis (usually 106 seconds •Aspartate aminotransferase concentration of 3,086 U/L •Alanine aminotransferase concentration of 456 U/L •Total bilirubin of 4.4 mg/dL (75.2 mcmol/L) The chest radiograph demonstrated diffuse interstitial infiltrates bilaterally (Item Q204A). The patient did poorly over the next 3 days and died despite aggressive management in a pediatric intensive care unit. Of the following, the MOST likely cause of this patient's death is

A. adenovirus B. Escherichia coli C. group B Streptococcus D. herpes simplex virus E. Listeria monocytogenes


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Neonates presenting with shocklike symptoms during the first 7 to 10 days after birth are a diagnostic challenge. The differential diagnosis includes five major categories: 1) bacterial sepsis, 2) inborn errors of metabolism, 3) ductal-dependent complex congenital heart disease, 4) nonaccidental trauma, and 5) viral sepsis. Clinicians must make rapid treatment decisions based on history and physical examination. The fever, hepatosplenomegaly, leukopenia, and abnormal findings on chest radiography reported for the patient in the vignette suggest infection as the most likely cause of the infant’s illness. Group B Streptococcus, Escherichia coli, and Listeria monocytogenes are causes of neonatal septic shock, but the interstitial pulmonary involvement and hepatitis reported in this case make a virus more likely. Although adenoviral infection can have this type of presentation, the most likely viral pathogen is herpes simplex. Neonatal infections with the herpes simplex virus (HSV) may be due to either HSV type 1 (25%) or HSV type 2 (75%). Approximately 80% of mothers of affected infants have no signs or symptoms of HSV infection prior to delivery. The virus commonly is transmitted to the infant from the mother because of the large amount of virus present and the prolonged shedding. If the primary infection affects only the cervix, the mother is usually asymptomatic. The infants become colonized with HSV at delivery and usually present with active disease between 5 and 10 days after birth. Neonatal disease may present as: 1) disease localized to the skin, eye, or mouth (SEM); 2) disseminated disease involving the liver, lungs, adrenal glands, central nervous system, and skin; and 3) localized central nervous system disease. In disseminated disease, approximately 20% of neonates never develop skin lesions. Therefore, the lack of skin lesions does not eliminate HSV as a potential pathogen for a sick infant. The diagnosis of neonatal HSV can be confirmed with: 1) viral cultures of skin lesions, the nasopharynx, or cerebrospinal fluid; 2) direct fluorescent antibody staining of vesicle scrapings; or 3) DNA detection by polymerase chain reaction test of the cerebrospinal fluid. The Tzanck preparation can be helpful but only indicates the presence of a DNA virus and is not specific for HSV. All neonatal HSV infections should be treated with intravenous acyclovir. The dosage is 60 mg/kg per day in three divided doses given intravenously for 14 days for SEM disease and for at least 21 days for disseminated or central nervous system disease. References: Kimberlin DW, Lin CY, Jacobs RF, et al. Natural history of neonatal herpes simplex virus infections in the acyclovir era. Pediatrics. 2001;108:223-229. Available at: http://pediatrics.aappublications.org/cgi/content/full/108/2/223 Waggoner-Fountain LA, Grossman LB. Herpes simplex virus. Pediatr Rev. 2004;25:86-93. Available at: http://pedsinreview.aappublications.org/cgi/content/full/25/3/86


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A 10-year-old girl presents to the emergency department with a 1-day history of brown urine. She reports no dysuria, urgency, frequency, or abdominal or flank pain. Her vital signs include: temperature, 98.8°F (37.1°C); blood pressure, 165/97 mm Hg; heart rate, 84 beats/min; and respiratory rate, 20 breaths/min. On physical examination, moderate periorbital edema is evident, but there are no other abnormalities. Urinalysis reveals moderate blood and 4+ protein. The serum complement 3 (C3) concentration is low, and the C4 concentration is normal. Of the following, the MOST likely cause of this girl's hematuria is

A. focal segmental glomerulosclerosis B. immunoglobulin A nephropathy C. lupus nephritis D. membranoproliferative glomerulonephritis E. postinfectious acute glomerulonephritis


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The girl in the vignette has painless gross hematuria without fever. Fever would suggest possible infection, and abdominal pain would hint at infection, stone, or renal malformation (tumor, cyst). She has an elevated blood pressure and periorbital edema, which may be due to hypoalbuminemia or fluid retention. Her urinalysis shows blood and protein. The most significant clue to the cause of her renal disease is her low serum complement 3 (C3) concentration and normal C4 concentration. She has strong evidence of nephritis (gross hematuria, hypertension, periorbital edema), decreased C3, and normal C4 values, which are consistent with postinfectious acute glomerulonephritis (PIAGN). If both the C3 and C4 values were low, the nephritis more likely would be membranoproliferative GN or lupus nephritis. Children who have either focal segmental glomerulosclerosis or immunoglobulin A nephropathy may develop gross hematuria, hypertension, edema, and nephritis, but because of the pathogenesis of these diseases, the serum complement values would be normal. PIAGN is a common but generally self-limited renal disease that usually occurs in childhood. Among the several known pathogenetic organisms associated with PIAGN, the most common is group A beta-hemolytic Streptococcus. Most children who have PIAGN recover complete renal function and exhibit normalization of C3 levels by 6 weeks, although some continue to exhibit hematuria and/or proteinuria for prolonged periods after initial presentation. Some also have hypertension, primarily due to salt and water retention, for up to 3 months. Occasionally, the disease may assume a rapidly progressive course, resulting in acute renal failure and the need for treatment with high-dose intravenous corticosteroids and possibly intravenous cyclophosphamide or dialysis if renal failure persists. In these patients, the renal outcome is guarded. References: Berrios X, Lagomarsino E, Solar E, Sandoval G, Guzman B, Riedel I. Post-streptococcal acute glomerulonephritis in Chile--20 years of experience. Pediatr Nephrol. 2004;19:306-312. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_ui ds=14689289&query_hl=61&itool=pubmed_docsum Kasahara T, Hayakawa H, Okubo S, et al. Prognosis of acute poststreptococcal glomerulonephritis (APSGN) is excellent in children, when adequately diagnosed. Pediatr Int. 2001;43:364-367. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22Pediatrics+international+:+official+journal+of+the+Japan+Pediatric+Society%22[Jour]+AN D+364[page]+AND+2001[pdat] Pinto SW, Sesso R, Vasconcelos E, Watanabe YJ, Pansute AM. Follow-up of patients with epidemic poststreptococcal glomerulonephritis. Am J Kidney Dis. 2001;38:249-255. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=am+j+kidney+dis[Jour]+AND+249[page]+AND+2001[pdat]


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A 5-month-old female infant presents with a 1-day history of fever to 102ºF (38.9ºC), emesis, and multiple episodes of greenish diarrhea with streaks of blood. Her mother states that the infant is less active, sleepier, and has no interest in feeding. Physical examination reveals a listless infant who has a sunken anterior fontanelle, dry mucous membranes with decreased skin turgor, and skin irritation in the diaper area. Of the following, the MOST likely cause of this patient's gastroenteritis is

A. astrovirus B. Escherichia coli C. Norwalk virus D. rotavirus E. Salmonella sp


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Diarrheal diseases in children younger than 5 years of age remain one of the leading causes of morbidity and mortality in developing countries and are important causes of morbidity in developed countries. In the United States, children 5 years of age and younger have between 35 and 40 million episodes of diarrhea annually, resulting in about 170,000 hospitalizations and 300 deaths due to complications. Item C206A shows the most common viral and bacterial diarrheal pathogens in children by age group. Most of the infectious organisms that cause diarrhea are spread via the fecal-oral route. Organisms such as Shigella, Giardia, and Campylobacter also may be transmitted by person-toperson contact because of their low infective inoculum dose. Foodborne diseases affect all age groups. Common causes include: E coli 0157:H7 (EHEC) associated with ingestion of undercooked meat, Salmonella and Campylobacter associated with contaminated poultry products and unpasteurized milk, Yersinia enterocolitica associated with contaminated pork products, and Norwalk virus associated with the consumption of raw seafood. Water also has been documented as a vehicle of transmission for Giardia lamblia, Campylobacter, Cryptosporidium, and Norwalk virus. Child care centers serve as important reservoirs for transmission of infectious diarrheal agents, with the peak incidence of diarrhea occurring in children younger than 3 years of age who are not toilet trained. Rotavirus (seen most commonly in children younger than 12 months of age), Shigella, and Giardia have been associated with outbreaks in child care centers. The child described in the vignette has diarrhea caused by rotavirus, the most common cause of viral diarrheal disease in infants and toddlers. Norwalk virus and E coli are not common causes of diarrhea in young infants. Astrovirus is a cause of diarrhea in children younger than 4 years of age, but most of the infections are asymptomatic. Salmonella sp also may cause diarrhea in infants, but it is much less common than a viral etiology, especially in developed countries. References: American Academy of Pediatrics. Escherichia coli diarrhea (including hemolytic-uremic syndrome). In: Pickering LK, ed. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 2006:291-296 American Academy of Pediatrics. Rotavirus 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; 2006:572-574 Ramaswamy K, Jacobson K. Infectious diarrhea in children. Gastroenterol Clin North Am. 2001;30:611-624. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22Gastroenterology+clinics+of+North+America%22[Jour]+AND+611[page]+AND+2001[pda t] Thielman NM, Guerrant RL. Clinical practice. Acute infectious diarrhea. N Engl J Med. 2004;350:38-47


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A mother brings in her 2-year-old boy for food avoidance education after he was seen in the emergency department last week for anaphylaxis following peanut ingestion. This is the third anaphylactic episode after peanut ingestion since he was diagnosed with a peanut food allergy at age 1 year. At that time, he was evaluated by a pediatric allergist and determined to have positive skin tests and an elevated serum immunoglobulin (Ig) E to peanut antigen, consistent with an IgE-mediated allergy. The mother is frustrated and would like advice regarding peanut food allergy. Of the following, the BEST advice at this time is to

A. perform an oral challenge to determine the maximum peanut amount tolerated by the patient B. recommend that the patient avoid hot-pressed peanut oil C. recommend strict avoidance of all legumes (eg, peanuts, beans, soy) D. recommend strict avoidance of peanuts and tree nuts E. start daily antihistamine prophylaxis for accidental peanut ingestion


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Peanut (Arachis hypogaea) allergy is one of the most common food allergies in the United States. The initial approach to peanut food allergy is strict avoidance of all peanut food products and rapid administration of intramuscular epinephrine if a severe allergic reaction occurs. Although tree nuts are not related to the legume family (ie, peanuts, soy, beans), patients who have peanut food allergies should be counseled to avoid tree nuts for two reasons. First, approximately 25% to 50% of patients who are allergic to peanuts also are allergic to tree nuts. Second, tree nut foods may contain trace amounts of peanut because these foods frequently are processed in the same factory. Interestingly, children who have peanut food allergy rarely (approximately 5%) react to soy. Also, sunflower oil is tolerated in peanut-allergic patients. However, patients should be counseled to avoid unrefined (eg, cold-pressed, crude) and some gourmet peanut oils that may contain significant amounts of residual peanut protein. Studies have demonstrated that refined peanut oil (eg, hot-pressed) does not contain significant residual proteins that bind immunoglobulin (Ig) E from sera in peanut-allergic patients. Oral challenges typically are reserved to rule out unlikely foods that may cause a reaction or to determine if a person has outgrown a food allergy based on either history (eg, no longer experiencing a reaction after accidental ingestion), skin testing (eg, negative skin testing result), or serum IgE testing (eg, a peanut IgE 60,000 mcM/L). Of the following, the MOST likely cause of this child's acidosis is

A. inborn error of metabolism B. lactic acidosis C. type I (distal renal tubular) acidosis D. type II (proximal renal tubular) acidosis E. type IV renal tubular acidosis


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The infant described in the vignette presents with failure to thrive, and measurement of his serum electrolytes reveals a normal anion gap and hyperchloremic metabolic acidosis. The key element in his presentation is the urine pH, which is 7.5, indicating that it is highly alkaline. In proximal renal tubular acidosis (RTA), as the urine leaves the proximal tubule, the relative inability to reabsorb bicarbonate results in a very alkaline pH of the tubular fluid. However, the distal tubule in patients who have proximal RTA is healthy, and it extrudes high quantities of acid, dropping the tubular pH to a lower value (=6.0). In contrast, because the distal nephron represents the last real opportunity for the kidney to regulate acid-base balance, children who have distal RTA cannot adequately compensate for the lack of acid extrusion, resulting in very alkaline urine. The urine ammonium value in the child in the vignette is very low at 12,000 mcM/L (normal >60,000 mcM/L), which is consistent with reduced acid (as part of ammonium) secretion and strongly predictive of distal RTA. RTA is a common cause of metabolic acidosis in childhood. There are two primary types of RTA: proximal or type II and distal or type I. Type IV RTA, also called hyperkalemic RTA, is uncommon and will be discussed only briefly. A review of basic renal physiology in the maintenance of acid-base balance is necessary to understand RTA. The primary responsibility of the proximal tubule in the preservation of normal acid-base homeostasis is to reabsorb filtered bicarbonate. It achieves this goal by reabsorbing water and carbon dioxide from the renal (apical membrane) tubule into the cell and then converting them to hydrogen and bicarbonate within the cell. Hydrogen is extruded back into the tubule, and bicarbonate is reabsorbed at the other end (basolateral membrane) of the cell. Thus, the reabsorption of base (bicarbonate) is linked with the expulsion of acid (hydrogen). In contrast, the primary role of the distal tubule is to secrete acid, either as free hydrogen ion, as part of ammonium (ammonia plus hydrogen), or linked to phosphorous. The distal nephron does play a role in bicarbonate reabsorption, but its primary role is to secrete acid. Because children who have proximal (type II) RTA have difficulty reabsorbing bicarbonate, the serum bicarbonate concentration falls, resulting in acidosis. In distal (type I) RTA, the distal tubule struggles to secrete acid. This excess acid must be buffered in the blood, principally by bicarbonate, which also results in a decline in the serum bicarbonate or acidosis. In distal RTA, there may be concomitant proximal tubule disturbances. The level of the serum bicarbonate in either proximal or distal RTA may vary, depending on the extent of the deficit. To maintain electroneutrality in RTA, the loss of bicarbonate is compensated by the retention of chloride, also a negatively charged ion. Thus, the anion gap ([sodium]-[chloride + bicarbonate]) is maintained at 10 to 16. In other types of acidosis, such as lactic acidosis, the excess accumulation of acid does not induce an increase in chloride absorption and, thus, the anion gap is elevated. Given the normal anion gap, this child cannot have either an inborn error of metabolism or lactic acidosis, which typically results in a high (>16) anion gap. Additionally, the normal serum potassium value effectively eliminates type IV RTA as a cause of the acidosis because the lack of aldosterone or renal resistance to aldosterone in this condition induces acidosis and hyperkalemia. References: Adedoyin O, Gottlieb B, Frank R, et al. Evaluation of failure to thrive: diagnostic yield of testing for renal tubular acidosis. Pediatrics. 2003;112:e463-e466. Available at: http://pediatrics.aappublications.org/cgi/content/full/112/6/e463 Roth KS, Chan JC. Renal tubular acidosis: a new look at an old problem. Clin Pediatr (Phila). 2001;40:533-543. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22Clinical+pediatrics%22[Jour]+AND+533[page]+AND+2001[pdat] Watanabe T. Proximal renal tubular dysfunction in primary distal renal tubular acidosis. Pediatr Nephrol. 2005;20:86-88. Abstract available at:


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http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_ui ds=15549407&query_hl=72&itool=pubmed_docsum


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You are asked to evaluate two children, ages 3 and 9 years, on the pediatric hematologyoncology inpatient unit who have developed fever, cough, increased work of breathing, and nodular lesions on their chest radiographs. The children are isolated in private rooms and have different nurses and doctors caring for them. The children's rooms are located adjacent to an area where a new playroom is being constructed. Of the following, the MOST likely pathogen causing these patients' pneumonia is

A. Aspergillus sp B. Candida parapsilosis C. Legionella pneumophila D. Pseudomonas aeruginosa E. respiratory syncytial virus


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Transmission-based precautions in the hospital are designed for patients documented or suspected to be colonized or infected with pathogens spread by the airborne, droplet, or contact routes. Such patients require additional precautions beyond standard precautions to interrupt transmission or spread of disease. Airborne transmission occurs by dissemination of airborne droplet nuclei (small-particle residue of evaporated droplets containing microorganisms that remain suspended in the air for long periods), dust particles containing the infectious agent, or fungal spores. Microorganisms spread by the airborne route can be dispersed widely by air currents (eg, ventilation systems, particularly during times of construction) and may be inhaled by or deposited on a susceptible host within the same room or a long distance from the source patient, depending on environmental factors. Therefore, special air handling and ventilation are required to prevent airborne transmission. Spores of filamentous fungi, such as Aspergillus, represent a considerable environmental hazard, especially to severely immunosuppressed patients, such as the children described in the vignette. Other microorganisms transmitted by airborne droplet nuclei include Mycobacterium tuberculosis, measles virus, varicella virus, and disseminated zoster. Specific recommendations in airborne precautions include: the use of private rooms; negative air-pressure ventilation with externally exhausted or HEPA-filtered air, if recirculated; and wearing of respiratory protective devices in cases of suspected or proven tuberculosis. Droplet transmission occurs when droplets containing microorganisms generated from infected persons, primarily during coughing, sneezing, and talking, are propelled a short distance and deposited on the host’s conjunctivae, nasal mucosa, or mouth. Because these relatively large droplets do not remain suspended in the air, special air handling and ventilation are not required to prevent transmission. Contact transmission is the most frequent route of transmission of nosocomial infections and can occur by direct or indirect contact with the infected or colonized surface. Candida parapsilosis, Legionella pneumophila, and Pseudomonas aeruginosa are not transmitted by the airborne route, and only standard precautions are needed to prevent spread. Respiratory syncytial virus is transmitted by direct or close contact with contaminated secretions, and limiting its spread in the hospital only requires contact precautions. References: American Academy of Pediatrics. Infection control for hospitalized children. In: Pickering LK, ed. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 2006:153-164 Edmond M. Isolation. Infect Control Hosp Epidemiol. 1997;18:58-64. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?orig_db=PubMed&db=PubMed&cmd=Search&ter m=%22Infection+control+and+hospital+epidemiology+:+the+official+journal+of+the+Society+of+H ospital+Epidemiologists+of+America%22[Jour]+AND+58[page]+AND+1997[pdat] Garner JS. The Hospital Infection Control Practices Advisory Committee. Guideline for isolation precautions in hospitals. Infect Control Hosp Epidemiol. 1996;17:53-80


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A 10-year-old boy presents to the emergency department with a severe asthma exacerbation that requires intubation and admission to the intensive care unit. The child's parents state that this is the third hospital admission for asthma since he was diagnosed at age 6 years. The parents are worried about the severity of their son's asthma flares and would like to know the underlying risk factors for fatal asthma. His current medications include an oral antihistamine, an inhaled corticosteroid, and an as-needed beta-2 agonist. Of the following, the risk factor MOST associated with fatal and near-fatal asthma is

A. coexisting allergic rhinitis B. female sex C. high socioeconomic status D. inhaled corticosteroid use E. poor perception of symptoms


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In the past 30 years, asthma-related case-fatality rates in industrialized countries have varied from 1.5 to 8.5 per 100,000 persons. Patients who have severe disease are believed to be at greatest risk, but those who have mild disease may have near-fatal or fatal asthma attacks. Identified risk factors for near-fatal and fatal asthma attacks include marked circadian variation in lung function, male sex, psychosocial disturbances, frequent visits to the emergency department, hospitalization for asthma within the past year, poor perception of hypoxia or airway obstruction, use of two or more beta-agonist inhalers per month, low socioeconomic status coupled with a low educational level, and previous life-threatening asthma attacks. Neither increased inhaled corticosteroid use nor allergic rhinitis has been linked to near-fatal or fatal asthma attacks. References: Guill MF. Asthma update: clinical aspects and management. Pediatr Rev. 2004;25:335-344. Available at: http://pedsinreview.aappublications.org/cgi/content/full/25/10/335 Liu AH, Spahn JD, Leung DYM. Childhood asthma. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co 2004:760-774


page 535


A 17-year-old boy is brought to the emergency department after he drove his car head-on into another motor vehicle. He was not restrained and was ejected from the vehicle. On physical examination, he has a Glasgow Coma Scale score of 5 and severe head trauma with an open scalp wound that is actively bleeding. He is breathing spontaneously, but a portion of the right side of his chest seems to move paradoxically, moving in with inspiration and out with expiration. On auscultation, he has decreased breath sounds on the affected side. Of the following, the MOST likely cause for his chest examination abnormalities is

A. flail chest B. hemothorax C. lung contusion with splinting D. open pneumothorax E. tension pneumothorax


page 536



The boy described in the vignette has a flail chest, a condition that occurs after blunt trauma fractures two or more ribs in two or more places, interrupting the continuity of this segment of the chest wall with the rest of the thoracic cage. The injury typically results in paradoxic motion of the chest wall, as demonstrated by the patient in the vignette. Negative intrapleural pressure during the inspiratory phase of breathing causes the segment to be pulled down into the chest cavity with chest expansion, and positive intrapleural pressure during the expiratory phase causes the segment to bulge out from the thoracic cage with chest wall relaxation. Flail chest can lead to respiratory insufficiency due to splinting from pain or to airway edema from an underlying pulmonary contusion. At the scene of the injury, the patient should be placed with the injured segment down, allowing better expansion and ventilation of the unaffected side. A patient who has flail chest and is in respiratory distress should undergo endotracheal intubation and be supported with positive pressure ventilation. This protects the airway and provides optimal expansion and splinting of the affected segment. Most patients who have flail chest do not require intubation and can be managed with analgesics and aggressive pulmonary physiotherapy. Hemothorax refers to the accumulation of blood in the pleural space. An open pneumothorax is characterized by a penetrating injury to the thoracic wall that permits air to move in and out of the thoracic cavity with each breath. A tension pneumothorax (Item C256A) is caused by an air leak within the lung in the absence of a penetrating injury to the thoracic wall. This causes an increasing amount of air under increasing pressure within the pleural space, leading to collapse of the ipsilateral lung. A patient who has splinting due to lung contusion limits ipsilateral chest wall movement during both phases of respiration to decrease pain. Any of these conditions can be present in conjunction with a flail chest, but only flail chest causes paradoxic motion of a segment of the thoracic wall. References: American College of Surgeons. Thoracic trauma. In: Advanced Trauma Life Support® Program for Doctors. Chicago, Ill: American College of Surgeons; 1997:125-141 Kadish HA. Thoracic trauma. In: Fleisher GR, Ludwig S, Henretig FM, eds. Textbook of Pediatric Emergency Medicine. 5th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2006:1433-1452


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