Question 62


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Question 62

  1. 1. Question 62 ureterocele A ureterocele is a cystic dilation of the ureter where it inserts into the bladder. An intravesical ureterocele is contained entirely within the bladder. When a portion of the defect extends beyond the bladder (to the urethra or bladder neck), an extravesical ureterocele is present. Typically, the pelvocaliceal system draining into the ureterocele is obstructed. The incidence of ureteroceles in children is estimated between 1 in 5,000 and 1 in 10,000. Ureteroceles are associated with a duplex collecting system in 80% of children; the remainder are associated with a single collecting system. Ureteroceles are four times more common in females than males and occur almost exclusively in Caucasians. A ureterocele is associated most commonly with a complete duplication of the renal collecting system (more common in the left kidney) where the involved ureter is linked to that draining the upper pole moiety. This lesion, which extends beyond the ureterovesical junction, results in ureteral obstruction, with hydroureteral nephrosis of the involved renal unit, usually the upper pole, as described for the infant in the vignette. A ureterocele often results in a mass lesion within the bladder that may be seen on bladder ultrasonography or indirectly as a filling defect of the bladder on voiding cystourethrography (Item C62A). The lower pole of the kidney of a duplex collecting system may drain into an orthotopic site and is associated with vesicoureteral reflux (VUR) in approximately 50% of cases. In addition, VUR is seen in approximately 25% of the kidneys contralateral to the duplex kidney that has a ureterocele. Ureteroceles most commonly are associated with urinary tract infection in infants, although 25% are detected antenatally. Older children present with voiding symptoms or hematuria associated with minimal trauma. Surgical treatment is aimed at relieving the obstruction, preserving the functioning nephron mass, removing nonviable tissue that may result in infection, and treating VUR. Based on patient symptoms, treatments include upper pole nephroureterectomy, endoscopic incision of the ureterocele for relief of obstruction, and clinical observation. Ureteropelvic junction obstruction (Item C62B), ureteral stones (Item C62C), and posterior urethral valves (Item C62D) cause hydronephrosis that involves the entire kidney, not just a portion, as is seen with a ureterocele. In addition, in posterior urethral valves, the hydronephrosis is bilateral. A bladder diverticulum (Item C62E) results in an outpouching of the bladder wall without a filling defect in the bladder. Question 64 hypocalcemia Serum calcium and 1,25 dihydroxyvitamin D concentrations are decreased in children who have chronic kidney disease because of phosphate retention and impaired hydroxylation of 25-hydroxyvitamin D. Physiologic serum calcium concentrations are maintained largely through the use of vitamin D supplements and phosphate binders. As renal function worsens, hypocalcemia can result if vitamin D deficiency or hyperphosphatemia is not addressed or if the use of bicarbonate therapy to treat metabolic acidosis leads to metabolic alkalemia. Metabolic alkalemia increases the binding of calcium to albumin, which decreases the ionized calcium concentration. Decreased ionized calcium can lead to perioral or extremity paresthesias, carpopedal spasm, laryngospasm, and seizures. Children who have hypocalcemia from any cause may be diagnosed mistakenly with croup if they present with tetany-related laryngospasm. Hyperkalemia may lead to muscle weakness and paresthesias and abnormalities in cardiac conduction. Clinical manifestations usually are preceded by conduction abnormalities, which may result in ventricular fibrillation and asystole. Hypermagnesemia generally is not associated with clinical symptoms. Severe hypophosphatemia can cause proximal muscle weakness, cardiac dysfunction, ataxia, seizures, and coma. Hyponatremia is a cause of nausea, vomiting, hypothermia, lethargy, agitation, headache, and seizures. Question 94 low C3 complement value The findings of cola-colored urine, swelling, and hypertension described for the boy in the vignette suggest the diagnosis of acute glomerulonephritis. The "sore throat" 10 days earlier makes acute poststreptococcal glomerulonephritis (APSGN) the most likely diagnosis. The initial assessment of a child in whom ASPGN is suspected must include measurement of blood pressure and serum creatinine to assess disease severity. Both severe hypertension and renal failure can occur as part of a rapidly progressive glomerulonephritis. After initial assessment, the most important diagnostic test is measurement of complement component 3 (C3) to confirm the presence of hypocomplementemia, which occurs in more than 90% of cases. ASPGN is an immune complex-mediated glomerulonephritis that follows an infection by a nephritogenic strain of group A beta-hemolytic Streptococcus of the pharynx or skin. The interval between pharyngitis and the development of APSGN is approximately 1 to 2 weeks. In contrast, the latency period between a skin infection and ASPGN is 3 to 6 weeks. Most patients who have nephritis have a subclinical infection, which is estimated to occur four to five times more frequently than overt disease. APSGN in children is characterized by hematuria (100%), proteinuria (80%), edema (90%), hypertension (70%), and azotemia (33%). Thus, the urinalysis will not be normal. In addition, gross hematuria occurs in approximately 40% of children who have overt disease. As noted previously, the characteristic laboratory feature of ASPGN is hypocomplementemia, which typically
  2. 2. features depressed C3 and normal C4 values. The differential diagnosis of hypocomplementemic glomerulonephritis consists of membranoproliferative glomerulonephritis (MPGN) in a child who has disease limited to the kidney and systemic lupus erythematosus in a child who has multisystem disease. Rarer causes of hypocomplementemic glomerulonephritis include subacute bacterial endocarditis, shunt nephritis (in patients who have ventriculoatrial shunts), and essential mixed cryoglobulinemia. Treatment of ASPGN is typically supportive and aims to reverse the sodium and fluid retention through the use of diuretics accompanied by restriction of sodium and fluid. Vasodilators also may be used for patients who have severe hypertension. Antibiotics can reduce the risk of transmission of the nephritogenic strain of streptococci to close contacts. The key follow-up test is a repeat measurement of C3, which usually normalizes within 8 weeks. Patients in whom depression of C3 persists after 12 weeks may require a renal biopsy to rule out MPGN. The prognosis of ASPGN is excellent. Gross hematuria and hypertension usually resolve within a few weeks and proteinuria within a few months. Microscopic hematuria may persist for 1 to 3 years. A normal urinalysis result is inconsistent with any form of glomerulonephritis, and would, therefore, be highly unlikely in a child who has hypertension and cola-colored urine. A positive urine culture would be unexpected in this clinical scenario. Patients who have hemorrhagic cystitis typically have bright red blood in the urine, often accompanied by clots. Other pertinent parts to the history that are absent in this scenario would be symptoms of dysuria, abdominal pain, frequency, urgency, and possibly fever. Small vessel vasculitides such as Wegener granulomatosis, microscopic polyangiitis, and Churg Strauss disease are less common causes of glomerulonephritis and, therefore, anti-neutrophil cytoplasmic antibody testing is unlikely to be revealing. Another, less likely diagnostic possibility for the child in the vignette is lupus nephritis. However, anti-nuclear antibody should be measured in the setting of acute nephritis to exclude this possibility. Question 110 urinary losses due to tubular damage The symptoms of tingling described for the boy in the vignette may be associated with hypomagnesemia and hypokalemia. Cisplatin is a chemotherapeutic agent that can cause acute losses of magnesium and potassium and chronic losses in some patients that necessitate chronic oral replacement of these electrolytes. Chemotherapeutic agents used to treat pediatric malignancies are associated with a number of untoward complications, including nephrotoxicity. The two classes of drugs that most commonly cause renal toxicity are the platinum drugs (cisplatin and carboplatin) and ifosfamide. The platinum drugs (cisplatin more than carboplatin) cause injury to the late proximal tubule and collecting duct. More specifically, the proximal tubular damage can result in alterations of the brush border and tubular necrosis. The clinical manifestations of this damage are polyuria, electrolyte abnormalities, and azotemia. Inappropriate tubular losses of magnesium, sodium, and potassium are typical and result in the need for aggressive replacement. Prevention of cisplatin-associated nephrotoxicity has been aimed at optimizing hydration before, during, and after the infusion. Mannitol also may be used. Studies have shown that although many of the effects of cisplatin are temporary, altered renal function and magnesium wasting persist in many patients in long-term follow-up. Ifosfamide, which is used to treat many pediatric solid tumors, has been associated with acute and chronic nephrotoxicity. This agent can result in the Fanconi syndrome due to damage to the early portion of the proximal tubule. As a result, glycosuria, phosphaturia, amino aciduria, proteinuria, and altered glomerular filtration rate can be seen. The risks of ifosfamide nephrotoxicity appear to be related to the age of the patient, coexisting nephrotoxins, and nephron mass (with worse outcomes in patients who have prior unilateral nephrectomy). Serum potassium concentrations can be influenced by a number of factors, including dietary intake, intestinal absorption, and urinary excretion. Because potassium is primarily intracellular, in the setting of alkalosis, it shifts intracellularly, and the serum concentrations decrease. Like potassium, magnesium is primarily contained intracellularly. It is absorbed in the ileum, and its extracellular concentrations are regulated in the kidney. When hypomagnesemia and hypokalemia occur together, renal causes should be strongly considered. A metabolic alkalosis may cause the serum potassium to fall, but should have minimal effect on magnesium. Moreover, the patient described in the vignette is not believed to be at risk for an alkalosis. In the setting of normal renal function without ongoing losses, magnesium and potassium concentrations would be expected to be normal, even in the setting of a dietary deficient in these minerals. The patient has only intermittent vomiting and loose stools, making losses from the gastrointestinal tract unlikely. Question 1ophthalmologic examination The child described in the vignette has failure to thrive; symptoms of polyuria and photophobia; signs of apparent mild dehydration; and laboratory findings that include hypokalemia, metabolic acidosis, and hypophosphatemia. Such electrolyte disturbances are characteristic of Fanconi syndrome, a proximal tubulopathy that results in urinary losses of sodium, potassium, bicarbonate, phosphate, amino acids, protein, and glucose.
  3. 3. Although the differential diagnosis for the causes of Fanconi syndrome in the pediatric patient is extensive, the condition often is due to a metabolic disturbance. Causes of Fanconi syndrome include inherited diseases such as glycogen storage disease, hereditary fructose intolerance, tyrosinemia, cytochrome c oxidase deficiency, galactosemia, Lowe syndrome, Wilson disease, Dent disease, and cystinosis. Acquired causes include heavy metal poisoning, ifosfamide, cisplatin, gentamicin, and ingestion of outdated tetracycline. The most common cause of Fanconi syndrome in pediatrics is nephropathic cystinosis. Cystinosis is a lysosomal storage disorder that affects all cells in the body. Cystine normally is a product of protein degradation that is transported out of the lysosome. In cystinosis, cystine accumulates within lysosomes, resulting in cellular dysfunction. This autosomal recessive disorder has an estimated incidence of 1 in 100,000 to 200,000 live births, which translates into approximately 15 new cases diagnosed each year in the United States. The CTNS gene, which is located on chromosome 17p13, encodes for cystinosin, a transporter protein responsible for transporting cystine out of the lysosome. Polyuria, polydipsia, growth failure, rickets, and electrolyte abnormalities manifest in the second half of the first postnatal year in approximately 95% of children who have cystinosis. Cystine accumulation within the proximal tubular cells may result in impaired energy generation and a subsequent defect in solute reabsorption. Cystine accumulation within the cornea results in intense photophobia, as described for the child in the vignette. Patients who have cystinosis also may develop hypothyroidism. Cystinosis may be suspected when cystine crystals are visible within the cornea during slitlamp ophthalmologic examination. The diagnosis is confirmed by the finding of an elevated white blood cell cystine concentration. Treatment includes replacement of electrolyte losses and oral cysteamine therapy. Cysteamine is directed at the transport defect in cystinosis and has been shown to prolong renal survival from 10 years in untreated patients to 23 years when instituted prior to 3 years of age. The practitioner evaluating a child who is failing to thrive should consider electrolyte measurement and renal function tests when no obvious nutritional cause is present. Polyuria, polydipsia, and nocturnal fluid intake (the child awakens from sleep to drink fluid) are suggestive of diabetes insipidus, but specific electrolyte abnormalities can indicate the possibility of Fanconi syndrome. The patient in the vignette is exhibiting failure to thrive, but the electrolyte panel,but the electrolyte panel, which includes a normal chloride value and metabolic acidosis, is inconsistent with that of a patient who has cystic fibrosis (CF). Patients who have CF typically have excessive loss of chloride in their sweat that results in hypochloremia and metabolic alkalosis. Patients who have primary hyperparathyroidism have low phosphorus and slightly low bicarbonate values, but have hypercalcemia. This patient’s normal calcium concentration and hypokalemia are inconsistent with an abnormality of parathyroid hormone secretion. Urine ammonia measurement can be useful in patients who have distal renal tubular acidosis, which is associated with normal anion gap metabolic acidosis, but few of the other electrolyte abnormalities reported for this patient. Urine chloride measurement is useful for those who have Bartter syndrome and Gitelman syndrome, which could explain the hypokalemia and hypomagnesemia, but these conditions are associated with hypochloremic metabolic alkalosis, which is not present in the patient in the vignette. Question 150 vasodilator therapy as an inpatient Hypertension is a major cause of morbidity and mortality in adults, and growing data suggest that it is becoming a greater clinical problem in the pediatric population, particularly adolescents. Although yet to be defined clearly, the lifelong risks for the child who has hypertension or a prehypertensive state are likely to be substantial. Blood pressure is affected by height, weight, sex, and race. A complete medical history, particularly family history and medications (including over-the-counter supplements), and a thorough physical examination are essential to early and accurate diagnosis of hypertension and assessment of its secondary causes, comorbidities, and potential complications. Measurement of the blood pressure is a salient component of the yearly health supervision visit for children beginning at 3 years of age. When the patient is calm and relaxed, blood pressure should be measured in the right arm with the patient seated and the arm resting at the level of the heart. The stethoscope should be placed about 2 cm superior to the cubital fossa, just over the brachial artery. It is extremely important to use the proper size cuff for each patient. The bladder of the cuff (not the cuff material) is the most important determinant of cuff size. The bladder width should cover 60% to 70% of the upper arm length. The cuff bladder length should cover 80% to 100% of the circumference of the arm to ensure complete compression of the brachial artery during cuff inflation. A cuff that is too small will result in a falsely elevated reading. A cuff that appears too large will not affect the measurement adversely. Most errors in blood pressure measurement occur in obese or highly muscularized patients when a cuff is used that is too small. Severe hypertension and hypertensive crisis should be managed aggressively. The latter typically results from the ingestion of drugs that cause hypertension, injury, or disease of the kidney or previously unrecognized, progressive hypertension. Symptoms of severe hypertension may include headache, changes in vision, epistaxis, seizure, pulmonary edema with congestive heart failure, and those that may arise from renal failure.
  4. 4. The patient described in the vignette has a significantly elevated blood pressure that involves marked and reproducible systolic and diastolic hypertension. The best management plan is to monitor his blood pressure while the cause is ascertained and treatment begun, which involves admission to the hospital and initial treatment with an intravenous antihypertensive agent. The goal of such therapy is to reduce the blood pressure by 25% or less over the first 8 hours and gradually normalize it over the next 48 hours to avoid complications (eg, cerebrovascular accident). The choice of chronic antihypertensive therapy depends, in part, on the cause of the hypertension, but for immediate short-term management, vasodilators (eg, calcium channel blockers, hydralazine, nitroprusside) are useful. These agents reduce the afterload against which the left ventricle pumps, thereby reducing its work and oxygen consumption. Alternatively, short-acting beta blockers could be used in the acute setting. When using beta blockers, however, the clinician must bear in mind their potential complications, including exacerbation of underlying asthma. Of importance, pharmacologic management of severe hypertension and hypertensive crisis should use medications that can be titrated to effect readily and have a fast onset of action. Diuretics, particularly the thiazide class, often are used as first-line antihypertensive agents for those who have mild or moderate hypertension that can be controlled on an outpatient basis. These may be used in combination with other agents, including but not limited to angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, if adequate control is not obtained with a single agent. The significant hypertension reported for the boy in the vignette requires immediate action; repeating the blood pressure measurement in 1 to 2 weeks is not appropriate. Question 158 repeat urinalysis in 2 weeks The child who has asymptomatic, isolated microscopic hematuria is seen frequently in the ambulatory setting. Results of a urine dipstick test in patients who have hematuria are positive for blood, indicating the presence of hemoglobin or myoglobin. A microscopic evaluation that reveals more than 5 red blood cells/high-power field, as described for the girl in the vignette, confirms the presence of hematuria. Because isolated microscopic hematuria has been found in 4% of children on at least one of four tested samples, evaluation is not recommended unless hematuria is present on at least two of three urine samples. Accordingly, the girl in the vignette should undergo repeat urinalysis in 2 weeks. The prevalence of hematuria in two of three samples is 1% in females and 0.5% in males. Red blood cells in the urine may arise from the kidney (glomerular or nonglomerular), ureter, bladder, or urethra. Persistent hematuria demands evaluation. It is customary to evaluate renal function by measuring blood urea nitrogen and creatinine and to obtain a complete blood count and platelet measurement (looking for thrombocytopenia as a possible a possible cause) and an erythrocyte sedimentation rate (looking for an underlying inflammatory cause of hematuria). In addition, serologic tests, including complement components 3 and 4, antinuclear antibody, and anti-double-stranded DNA, are recommended to look for markers of immune complex-mediated glomerulonephritis, which can be seen with postinfectious nephritis, membranoproliferative glomerulonephritis, and lupus nephritis. Recommended urine studies consist of urinalysis with microscopy, urine protein and creatinine measurement, and urine culture. Measurement of a urine calcium-to-creatinine ratio is advocated by some but is not universally supported. Finally, abdominal computed tomography scan is not indicated in teh evaluation of the patient who has isolated hematuria. This test may be helpful in identifying renal tumors, but these neoplasms usually can be diagnosed by ultrasonography. The absence of symptoms in children who have isolated microscopic hematuria allows the practitioner to defer urgent evaluation because the likelihood of an underlying systemic disease or a disease limited to the urinary tract that warrants urgent attention is low. Similarly, patients who have microscopic hematuria unaccompanied by proteinuria are unlikely to have a significant disruption of the glomerular capillary barrier. On the other hand, if a child is asymptomatic but has hematuria and proteinuria, evaluation should proceed promptly, looking for an underlying renal parenchymal disorder such as glomerulonephritis. Cystoscopy rarely is indicated in pediatrics, and the decision to pursue this invasive evaluation should be made by a pediatric urologist. Question 173 ureteropelvic junction obstruction The differential diagnosis for an infant who has hydronephrosis in the first postnatal year includes ureteropelvic junction (UPJ) obstruction, ureterovesical junction (UVJ) obstruction, single-system ureterocele, vesicoureteral reflux (VUR), and posterior urethral valves (usually causes bilateral hydronephrosis). If hydronephrosis is found on renal/bladder ultrasonography, voiding cystourethrography (VCUG) is undertaken to rule out VUR and assess for a filling defect in the bladder caused by a ureterocele (Item C173A). Following VCUG, a technetium-99m mercaptoacetyltriglycerine (MAG-3) radioisotope scan with furosemide is performed to assess for UPJ obstruction. If UPJ obstruction is present, the radioisotope exhibits delayed washout. During the test, furosemide is infused and may precipitate an episode of renal colic, as reported for the infant in the vignette. If a UPJ obstruction is diagnosed, the practitioner should contact a pediatric nephrologist or urologist to help with further management. A duplex collecting system with a ureterocele is detected by VCUG that reveals a filling defect in the bladder and VUR (in approximately 50% of cases). On ultrasonography, a multicystic dysplastic kidney (MCDK) (Item C173B) exhibits multiple large cysts that do not communicate and a rim of dysplastic renal parenchyma. An MCDK occurs
  5. 5. unilaterally and has no inherent function. Obstructive uropathy from posterior urethral valves is characterized by narrowing of the posterior urethra (Item C173C) and is associated with bilateral hydronephrosis in nearly all cases and VUR in approximately 50% of cases. Nephrolithiasis is defined acalculus within the renal parenchyma. Ultrasonography may reveal a calculus. Only if the calculus moves into the collecting system would hydronephrosis or renal colic following a diuretic renal scan occur. A calculus within the collecting system is known as urolithiasis. Question 209 prescribe a stool softener and regular bowel routine Constipation is defined by infrequent or difficult passage of large or hard fecal material. It occurs commonly in the pediatric population, and its association with urinary tract dysfunction has been well described. Constipation can cause detrusor instability, which can lead to urinary incontinence, large bladder capacity, and dyscoordinated voiding. Urinary retention is common, either from dyscoordinated voiding or from outflow tract obstruction caused by large rectal fecal masses. All of these types of urinary dysfunction can lead to recurrent urinary tract infections. One study of children who had urinary retention found that 13% had functional constipation as the cause of their retention. Another found that approximately 30% of chronically constipated children complained of urinary incontinence, and 11% had urinary tract infection. Treatment of the underlying constipation improved urinary incontinence and prevented recurrent urinary tract infections. The girl described in the vignette is otherwise healthy and growing well, and she has no anatomic urinary tract abnormalities. Accordingly, treatment of her underlying constipation is the next best step in the prevention of recurrent infections. Fecal disimpaction, stool softeners, and regular bowel evacuation using timed toilet sitting are the mainstays of treatment. An evaluation for immunodeficiency is not warranted at this time, but could be considered if her growth parameters were abnormal or if she had additional infections outside of the urinary tract. Renal scintigraphy is used to assess renal anatomy and function and may be warranted in a child who has recurrent urinary tract infections, but it is not helpful in preventing future infections. Anticholinergic therapy, such as oxybutynin, can be helpful if overactive or unstable bladder is suspected, but the girl in the vignette has no symptoms of these conditions. Referral to a pediatric nephrologist may be indicated if evidence of renal dysfunction is present, but treatment of underlying risk factors, such as constipation, should be initiated first. Question 211 blood urea nitrogen, creatinine, and electrolytes Hypertension is a major cause of morbidity and mortality in adults, and growing data suggest that it is becoming a greater clinical problem in the pediatric population, particularly adolescents. Although yet to be defined clearly, the lifelong risks for the child who has hypertension or a prehypertensive state are likely to be substantial. Blood pressure is affected by height, weight, sex, and race. A complete medical history, particularly family history and medications (including over-the-counter supplements), and a thorough physical examination are essential to early and accurate diagnosis of hypertension and assessment of secondary causes, comorbidities, and potential complications. Specific questions in the history should seek to identify clinical findings that might suggest an underlying systemic disorder, including the presence of gross hematuria, swelling or edema, shortness of breath, or rashes. The past medical history should focus on prior hospitalizations, previous trauma, and urinary tract infections. The family history should evaluate for hypertension, diabetes, obesity, stroke, and renal disease. In addition, the history should explore the possibility of medications or drugs (prescribed, illicit, or over-the-counter) that can be associated with hypertension. An example of the latter may be the use of pseudoephedrine as a nasal decongestant. Additionally, some families and adolescents use dietary supplements, vitamins, herbal remedies, and homeopathic preparations. Some of these "supplements" may be associated with sympathomimetic or hypertensive effects. The laboratory and diagnostic evaluation of the child who has hypertension should be guided by findings on the history and physical examination. For the pediatric patient who has confirmed hypertension, a screening panel of electrolytes, blood urea nitrogen, and creatinine as well as urinalysis and culture are indicated. Such blood tests are obtained to rule out renal disease. A urinary drug screen is indicated if the history or patient behavior suggests a possible contribution by illicit substances, drugs, or supplements that can be associated with hypertension. The child described in the vignette is overweight, but he has no historical or physical examination findings suggestive of the use of illicit substances, drugs, or supplements. Echocardiography also is not necessary at this stage of diagnosis because there is no evidence of congenital heart disease such as coarctation or end-organ involvement. Pediatric patients who have comorbid factors such as diabetes or systemic lupus erythematosus should undergo echocardiography as part of their hypertension evaluations. Radionuclide imaging of the kidneys involves exposure to ionizing radiation and typically is reserved for children of this age whose blood pressures are more than 5 mm Hg greater than the 99th percentile. Although renal vascular ultrasonography does not involve ionizing radiation, it also generally is reserved for young children whose blood pressures are beyond the 95th percentile and older children and adolescents whose blood pressures exceed the 99th percentile.
  6. 6. Question 218 Escherichia coli Escherichia coli is the causative organism in 80% to 90% of first-time urinary tract infections (UTIs) in children. Other pathogens include Klebsiella pneumonia, Proteus sp, Enterococcus sp, and Staphyloccus saprophyticus. Pseudomonas also can be a pathogen in immunocompromised patients or those who have received repeated courses of antibiotics for recurrent infections. The clinician must assess the patient for a UTI based on signs, symptoms, and urinalysis findings. Organisms such as E coli, K pneumoniae, and Proteus sp can reduce dietary nitrate to nitrite, so a positive urine dipstick test for nitrite, as reported for the girl in the vignette, is virtually diagnostic of gram-negative bacteruria. If the test result is negative in an older child in whom a UTI is suspected, the infection may be caused by a gram- positive organism such as Enterococcus sp or S saprophyticus. Of note, the nitrite test is much less helpful in infants. Conversion of nitrate to nitrite may take up to 4 hours. Because infants and young children have small bladder volumes and urinate frequently, there may be insufficient time for nitrites to be formed and, therefore, the nitrite test may be negative even in the presence of a UTI caused by a gram-negative organism. Urine pH also may be useful in diagnosing UTIs. Urease-producing organisms (eg, Proteus mirabilis, some strains of S saprophyticus) degrade urea into ammonia, resulting in an elevated urine pH (8.0 to 8.5). The girl described in the vignette has symptoms of a lower UTI. Options for therapy include trimethoprim- sulfamethoxazole (if local resistance patterns indicate low levels of E coli resistance) or a third-generation cephalosporin (eg, cefixime, cefdinir). These antibiotics also may be used for outpatient management of acute pyelonephritis. For hospitalized patients, a third-generation cephalosporin such as ceftriaxone or cefotaxime provides adequate coverage. An alternative regimen is ampicillin plus gentamicin.