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656
M Kaneko et al.
Continuous hemodialysis therapy for an extremely low-birthweight infant with hyperammonemia Masatoshi Kaneko, Kei Ogasawara, Hayato Go, Takashi Imamura, Nobuo Momoi and Mitsuaki Hosoya Department of Pediatrics, Fukushima Medical University, Fukushima, Japan Abstract
Hyperammonemia of newborns should be treated promptly, and the outcome depends on the rapid elimination of excessive plasma ammonia. We encountered a case of transient hyperammonemia in an extremely low-birthweight infant whose plasma ammonia decreased sufficiently after continuous hemodialysis therapy. It seems that continuous hemodialysis therapy using the peripheral artery and umbilical vein is useful for hyperammonemia of extremely low-birthweight infants; however, there are several problems to consider due to the immaturity of these infants.
Key words hyperammonemia, low-birthweight infant, hemodialysis.
Hyperammonemia of newborns should be treated promptly, because their outcome depends on the rapid elimination of excessive plasma ammonia. Recently, continuous hemodialysis (CHD) therapy has been suggested for newborns with hyperammonemia. We encountered a case of transient hyperammonemia in an extremely low-birthweight infant (ELBWI), whose plasma ammonia decreased sufficiently after CHD.
Case report At our institution, a cesarean delivery of a male infant was performed because of premature rupture of membranes at 25 weeks of gestation. His birthweight was 716 g, and the Apgar score at 5 min was 9. Results of the blood tests performed at birth were normal, and the chest X-ray showed fine reticular granularity of the parenchyma and air bronchograms. After the diagnosis of respiratory distress syndrome, we started the patient on mechanical ventilation and performed endotracheal instillation of exogenous surfactant. At the age of 1 day, he showed hypotension, metabolic acidosis (arterial blood pH 7.356, pO2 58.1 mm Hg, pCO2 32.2 mm Hg, HCO3 17.6 mEq/L, anion gap 11.4 mEq/L), and hyperammonemia. The level of plasma ammonia was 1640 μg/dL (normal upper limit, 66 μg/dL). The plasma ammonia concentration was no less than 1600 μg/dL in spite of i.v. administration of arginine (250 mg/kg/day) and sodium benzoate (150 mg/kg/day), therefore CHD was started at 26 h old. We inserted an i.v. catheter (SURFLO 24G × 3/4″; TERUMO Medical Corporation, Tokyo, Japan) into the left dorsal pedis artery for blood drainage, and an umbilical vessel catheter (ARGYLE 3.5 FR × 15″; Covidien Group Japan, Tokyo, Japan) for blood return. The blood purifier used was Plasauto iQs21 (Asahi Kasei Medical, Tokyo, Japan); the blood dialysis membrane, PANFLO APF-01D (Asahi Kasei Medical) (Fig. 1); and Correspondence: Masatoshi Kaneko, MD, Department of Pediatrics, Fukushima Medical University, Hikarigaoka 1, Fukushima City, Fukushima 960-1295, Japan. Email: [email protected] Received 3 March 2011; revised 12 February 2013; accepted 19 February 2013. doi: 10.1111/ped.12101
© 2013 The Authors Pediatrics International © 2013 Japan Pediatric Society
the dialysate, Sublood BS (Fuso Pharmaceutical Industries, Osaka, Japan). The circuit was initially primed with 50 mL of packed blood, and CHD was started at a blood flow rate of 4–7 mL/min. Four units/kg of low molecular heparin and 1 mg/ kg/h of nafamostat mesilate were administered in the circuit as anticoagulant drugs, and the activated clotting time (ACT) fluctuated between 156 and 175 s (Fig. 2). His rectal temperature decreased to 35.6°C at 6 h after the dialysis commencement, so we raised the temperature setting of the incubator. Two hours of CHD decreased the plasma ammonia concentration to 862 μg/dL, and 48 h of CHD further decreased it to 320 μg/dL. After verifying that the plasma ammonia concentration did not increase by the discontinuation of CHD, we administered deproteinized milk (S-23: Snow Brand Milk Products, Tokyo, Japan) to the patient from the age of 3 days. We succeeded in replacing it with breast milk at 15 days of age, and we discontinued sodium benzoate and arginine at 16 and 17 days of age, respectively. Although hyperammonemia did not recur even after breast-feeding, the patient died at 19 days of age due to disseminated i.v. coagulation and intraventricular hemorrhage triggered by a bacterial infection (Fig. 3).
Discussion Few studies have reported transient hyperammonemia in ELBWI. We present here an ELBWI whose plasma ammonia level had successfully decreased due to CHD. Msall et al. suggested that prolonged neonatal hyperammonemic coma was associated with brain damage and impairment of intellectual functions.1 Rajpoot et al. also reported poor prognosis of infants whose ammonia levels exceeded 800 μg/dL for more than 24 h.2 Therefore, both early detection and prompt treatment for hyperammonemia are very important, regardless of the cause. For the treatment of severe hyperammonemia in newborns, especially in low-birthweight infants, peritoneal dialysis or exchange blood transfusion have been performed.3,4 A new adaptation of CHD has recently become popular for infants,5 because CHD leads to significantly higher and more rapid reduction of ammonia levels than does peritoneal dialysis or exchange blood
Continuous hemodialysis for an ELBWI Low molecular heparin
Nafamostat mesilate
Blood drainage (from dorsal pedis artery)
Blood pump
657
Arterial side chamber
Filtration circuit
Blood return (to umbilical vein)
Venous side chamber
Nafamostat mesilate
Fig. 2 The schematic diagram of continuous hemodialysis therapy circuit. To prevent blood clotting in the circuit, anticoagulants (1 mg/ kg/h nafamostat mesilate and 4 units/kg/h of low molecular heparin) were put into the arterial or the venous side.
transfusion.6 However, the use of CHD is difficult in the case of premature infants because of certain technical drawbacks, such as management of the blood access and large extracorporeal circuits relative to an infant’s blood volume.7 For improved ammonia dialysance, sufficient blood flow rate of dialysis is required. Previously, femoral, brachial, or umbilical arteries, and femoral, jugular, or umbilical veins were used for CHD.8,9 In the present case, we used a peripheral artery to draw blood and the umbilical vein to return it. Catheter access was easily established and sufficient flow was obtained. Therefore, CHD, using peripheral artery and umbilical vein, is useful for hyperammonemia of ELBWI. In a previous report, hypothermia was one of the most important complications.10 Hypothermia was, in fact, also observed in our case. Though we raised the temperature of the incubator
Fig. 1 A comparison of membrane size between PANFLO APF01D and APF-10. We used PANFLO APF-01D (left) as the blood dialysis membrane. It is 2.3 cm in diameter, 14 cm in length, 12 mL in capacity, and 0.1 m2 in filtration area: much smaller than the PANFLO APF-10 for adults (right).
Sodium benzonate (150mg/kg/day) Arginine (250mg/kg/day)
Plasma ammonia ( µg/dL)
2000
BM
Proteinless milk (S-23)
CHD
ABPC + CTX
CHD
1500 Nafamostat mesilate gglobulin 1000
FFP PC
500
0
0
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
Age (days)
Fig. 3 Clinical course of the patient. After continuous hemodialysis therapy (CHD), the patient’s ammonia levels fell rapidly. Even though hyperammonemia did not recur after breast-feeding, the patient died from an unrelated bacterial infection at 19 days of age. ABPC, ampicillin hydrate; BM, breast milk; CTX, cefotaxime sodium; FFP, fresh frozen plasma transfusion; PC, concentrated platelet transfusion. © 2013 The Authors Pediatrics International © 2013 Japan Pediatric Society
bs_bs_banner
658
M Kaneko et al.
promptly, we needed approximately 3 h to recover the patient’s body temperature. Afterward, we evaded hypothermia by warming the dialysate. It is necessary to install a heating device within the dialysis circuit before initiation of therapy, especially for ELBWI. It is difficult to determine the degree of heparinization required in CHD in newborns. Bunchman et al. recommended a loading with 10–20 units/kg of heparin followed by a continuous heparin infusion of 10–20 units/kg/h to maintain the ACT between 150 and 200 s in most infants and children. We used a continuous heparin infusion of 4 units/kg/h, which maintained the ACT at approximately 150 s, without clotting in the hemofilter. The effectiveness of heparin will depend on the coagulopathy of the patient, blood flow rate, and vascular access of the patients;11 therefore, the degree of heparinization has to be determined on the basis of the patient’s condition. However, we should have monitored ACT more closely for preventing intracranial hemorrhage and this should be remembered in all cases of ELBWI. We diagnosed this case as transient hyperammonemia due to the following reasons: (i) steep rise of plasma ammonia was seen preceding his mother’s milk; (ii) amino acid analysis of both plasma and urine using tandem mass spectrometry revealed no abnormalities; and (iii) hyperammonemia did not recur even after breast-feeding. Sepsis resulting from skin erosion on his whole body was regarded as the cause of death, though the culture around the umbilical cord was negative.
Acknowledgments We would like to thank Yuki Hasegawa, MD, Hironori Kobayashi, MD, and Yuichi Mushimoto, MD from the Department of Pediatrics, Division of Metabolic Abnormalities Laboratory,
Shimane Medical University for assisting us with tandem mass spectrometry, which was required during the diagnosis of our patient.
References 1 Msall M, Batshaw ML, Suss R, Brusilow SW, Mellits ED. Neurologic outcome in children with inborn errors of urea synthesis. Outcome of urea-cycle enzymopathies. N. Engl. J. Med. 1984; 310: 1500–5. 2 Rajpoot DK, Gargus JJ. Acute hemodialysis for hyperammonemia in small neonates. Pediatr. Nephrol. 2004; 19: 390–5. 3 Ballard RA, Vinocur B, Reynolds JW et al. Transient hyperammonemia of the preterm infant. N. Engl. J. Med. 1978; 299: 920–5. 4 Le Guennec JC, Qureshi IA, Bard H, Siriez JY, Letarte J. Transient hyperammonemia in an early preterm infant. J. Pediatr. 1980; 96: 470–2. 5 Sadwski RH, Harmon WE, Jabs K. Acute hemodialysis of infants weighing less than five kilograms. Kidney Int. 1994; 45: 903– 6. 6 Wong KY, Wong SN, Lam SY, Tam S, Tsoi NS. Ammonia clearance by peritoneal dialysis and continuous arteriovenous hemodiafiltration. Pediatr. Nephrol. 1998; 12: 589–91. 7 Everdell NL, Coulthard MG, Crosier J, Keir MJ. A machine for haemodialysing very small infants. Pediatr. Nephrol. 2005; 20: 636–43. 8 Assadi FK. Treatment of acute renal failure in an infant by continuous arteriovenous hemodialysis. Pediatr. Nephrol. 1998; 2: 320–2. 9 Ronco C, Brendolan A, Bragantini L et al. Treatment of acute renal failure in newborns by continuous arterio-venous hemofiltration. Kidney Int. 1986; 29: 908–15. 10 Jander A, Tkaczyk M, Pagowska KI et al. Continuous veno-venous hemodiafiltration in children after cardiac surgery. Eur. J. Cardiothorac Surg. 2007; 31: 1022–8. 11 Bunchman TE, Donckerwolcke RA. Continuous arterial-venous diahemofiltration and continuous veno-venous diahemofiltration in infants and children. Pediatr. Nephrol. 1994; 8: 96– 102.
Neonatal urethral polyps associated with Beckwith–Wiedemann syndrome Yuko Anzai,1 Shigeki Koshida,1 Takahide Yanagi,1 Kazuyoshi Johnin2 and Yoshihiro Takeuchi1 Departments of 1Pediatrics and 2Urology, Shiga University of Medical Science, Shiga, Japan Abstract
We report the first case of Beckwith–Wiedemann syndrome without urinary obstruction, but with a congenital urethral polyp as a tumor protruding from the external urinary meatus. The present case suggests a possible relation between Beckwith–Wiedemann and the onset of fibroepithelial polyps in the reno-urinary system during the neonatal period.
Key words Beckwith–Wiedemann syndrome, fibroepithelial polyp, neonate, urethral meatus mass, urethral polyp. Correspondence, Yuko Anzai, MD, Nagahama Red Cross Hospital, 14-7 Miyamaecho, Nagahamashi, Shiga 526-8585, Japan. Email: [email protected] Received 4 May 2012; revised 24 October 2012; accepted 19 February 2013. doi: 10.1111/ped.12096
© 2013 The Authors Pediatrics International © 2013 Japan Pediatric Society
Urethral polyps are benign tumors that remain in the bladder and urethra. When infants become older, urethral polyps develop from urinary tract obstruction symptoms caused by hematuria, dysuria, and repeated urinary tract infection. There are no previous reports of congenital urethral polyps in male infants
656
M Kaneko et al.
Continuous hemodialysis therapy for an extremely low-birthweight infant with hyperammonemia Masatoshi Kaneko, Kei Ogasawara, Hayato Go, Takashi Imamura, Nobuo Momoi and Mitsuaki Hosoya Department of Pediatrics, Fukushima Medical University, Fukushima, Japan Abstract
Hyperammonemia of newborns should be treated promptly, and the outcome depends on the rapid elimination of excessive plasma ammonia. We encountered a case of transient hyperammonemia in an extremely low-birthweight infant whose plasma ammonia decreased sufficiently after continuous hemodialysis therapy. It seems that continuous hemodialysis therapy using the peripheral artery and umbilical vein is useful for hyperammonemia of extremely low-birthweight infants; however, there are several problems to consider due to the immaturity of these infants.
Key words hyperammonemia, low-birthweight infant, hemodialysis.
Hyperammonemia of newborns should be treated promptly, because their outcome depends on the rapid elimination of excessive plasma ammonia. Recently, continuous hemodialysis (CHD) therapy has been suggested for newborns with hyperammonemia. We encountered a case of transient hyperammonemia in an extremely low-birthweight infant (ELBWI), whose plasma ammonia decreased sufficiently after CHD.
Case report At our institution, a cesarean delivery of a male infant was performed because of premature rupture of membranes at 25 weeks of gestation. His birthweight was 716 g, and the Apgar score at 5 min was 9. Results of the blood tests performed at birth were normal, and the chest X-ray showed fine reticular granularity of the parenchyma and air bronchograms. After the diagnosis of respiratory distress syndrome, we started the patient on mechanical ventilation and performed endotracheal instillation of exogenous surfactant. At the age of 1 day, he showed hypotension, metabolic acidosis (arterial blood pH 7.356, pO2 58.1 mm Hg, pCO2 32.2 mm Hg, HCO3 17.6 mEq/L, anion gap 11.4 mEq/L), and hyperammonemia. The level of plasma ammonia was 1640 μg/dL (normal upper limit, 66 μg/dL). The plasma ammonia concentration was no less than 1600 μg/dL in spite of i.v. administration of arginine (250 mg/kg/day) and sodium benzoate (150 mg/kg/day), therefore CHD was started at 26 h old. We inserted an i.v. catheter (SURFLO 24G × 3/4″; TERUMO Medical Corporation, Tokyo, Japan) into the left dorsal pedis artery for blood drainage, and an umbilical vessel catheter (ARGYLE 3.5 FR × 15″; Covidien Group Japan, Tokyo, Japan) for blood return. The blood purifier used was Plasauto iQs21 (Asahi Kasei Medical, Tokyo, Japan); the blood dialysis membrane, PANFLO APF-01D (Asahi Kasei Medical) (Fig. 1); and Correspondence: Masatoshi Kaneko, MD, Department of Pediatrics, Fukushima Medical University, Hikarigaoka 1, Fukushima City, Fukushima 960-1295, Japan. Email: [email protected] Received 3 March 2011; revised 12 February 2013; accepted 19 February 2013. doi: 10.1111/ped.12101
© 2013 The Authors Pediatrics International © 2013 Japan Pediatric Society
the dialysate, Sublood BS (Fuso Pharmaceutical Industries, Osaka, Japan). The circuit was initially primed with 50 mL of packed blood, and CHD was started at a blood flow rate of 4–7 mL/min. Four units/kg of low molecular heparin and 1 mg/ kg/h of nafamostat mesilate were administered in the circuit as anticoagulant drugs, and the activated clotting time (ACT) fluctuated between 156 and 175 s (Fig. 2). His rectal temperature decreased to 35.6°C at 6 h after the dialysis commencement, so we raised the temperature setting of the incubator. Two hours of CHD decreased the plasma ammonia concentration to 862 μg/dL, and 48 h of CHD further decreased it to 320 μg/dL. After verifying that the plasma ammonia concentration did not increase by the discontinuation of CHD, we administered deproteinized milk (S-23: Snow Brand Milk Products, Tokyo, Japan) to the patient from the age of 3 days. We succeeded in replacing it with breast milk at 15 days of age, and we discontinued sodium benzoate and arginine at 16 and 17 days of age, respectively. Although hyperammonemia did not recur even after breast-feeding, the patient died at 19 days of age due to disseminated i.v. coagulation and intraventricular hemorrhage triggered by a bacterial infection (Fig. 3).
Discussion Few studies have reported transient hyperammonemia in ELBWI. We present here an ELBWI whose plasma ammonia level had successfully decreased due to CHD. Msall et al. suggested that prolonged neonatal hyperammonemic coma was associated with brain damage and impairment of intellectual functions.1 Rajpoot et al. also reported poor prognosis of infants whose ammonia levels exceeded 800 μg/dL for more than 24 h.2 Therefore, both early detection and prompt treatment for hyperammonemia are very important, regardless of the cause. For the treatment of severe hyperammonemia in newborns, especially in low-birthweight infants, peritoneal dialysis or exchange blood transfusion have been performed.3,4 A new adaptation of CHD has recently become popular for infants,5 because CHD leads to significantly higher and more rapid reduction of ammonia levels than does peritoneal dialysis or exchange blood
Continuous hemodialysis for an ELBWI Low molecular heparin
Nafamostat mesilate
Blood drainage (from dorsal pedis artery)
Blood pump
657
Arterial side chamber
Filtration circuit
Blood return (to umbilical vein)
Venous side chamber
Nafamostat mesilate
Fig. 2 The schematic diagram of continuous hemodialysis therapy circuit. To prevent blood clotting in the circuit, anticoagulants (1 mg/ kg/h nafamostat mesilate and 4 units/kg/h of low molecular heparin) were put into the arterial or the venous side.
transfusion.6 However, the use of CHD is difficult in the case of premature infants because of certain technical drawbacks, such as management of the blood access and large extracorporeal circuits relative to an infant’s blood volume.7 For improved ammonia dialysance, sufficient blood flow rate of dialysis is required. Previously, femoral, brachial, or umbilical arteries, and femoral, jugular, or umbilical veins were used for CHD.8,9 In the present case, we used a peripheral artery to draw blood and the umbilical vein to return it. Catheter access was easily established and sufficient flow was obtained. Therefore, CHD, using peripheral artery and umbilical vein, is useful for hyperammonemia of ELBWI. In a previous report, hypothermia was one of the most important complications.10 Hypothermia was, in fact, also observed in our case. Though we raised the temperature of the incubator
Fig. 1 A comparison of membrane size between PANFLO APF01D and APF-10. We used PANFLO APF-01D (left) as the blood dialysis membrane. It is 2.3 cm in diameter, 14 cm in length, 12 mL in capacity, and 0.1 m2 in filtration area: much smaller than the PANFLO APF-10 for adults (right).
Sodium benzonate (150mg/kg/day) Arginine (250mg/kg/day)
Plasma ammonia ( µg/dL)
2000
BM
Proteinless milk (S-23)
CHD
ABPC + CTX
CHD
1500 Nafamostat mesilate gglobulin 1000
FFP PC
500
0
0
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
Age (days)
Fig. 3 Clinical course of the patient. After continuous hemodialysis therapy (CHD), the patient’s ammonia levels fell rapidly. Even though hyperammonemia did not recur after breast-feeding, the patient died from an unrelated bacterial infection at 19 days of age. ABPC, ampicillin hydrate; BM, breast milk; CTX, cefotaxime sodium; FFP, fresh frozen plasma transfusion; PC, concentrated platelet transfusion. © 2013 The Authors Pediatrics International © 2013 Japan Pediatric Society
bs_bs_banner
658
M Kaneko et al.
promptly, we needed approximately 3 h to recover the patient’s body temperature. Afterward, we evaded hypothermia by warming the dialysate. It is necessary to install a heating device within the dialysis circuit before initiation of therapy, especially for ELBWI. It is difficult to determine the degree of heparinization required in CHD in newborns. Bunchman et al. recommended a loading with 10–20 units/kg of heparin followed by a continuous heparin infusion of 10–20 units/kg/h to maintain the ACT between 150 and 200 s in most infants and children. We used a continuous heparin infusion of 4 units/kg/h, which maintained the ACT at approximately 150 s, without clotting in the hemofilter. The effectiveness of heparin will depend on the coagulopathy of the patient, blood flow rate, and vascular access of the patients;11 therefore, the degree of heparinization has to be determined on the basis of the patient’s condition. However, we should have monitored ACT more closely for preventing intracranial hemorrhage and this should be remembered in all cases of ELBWI. We diagnosed this case as transient hyperammonemia due to the following reasons: (i) steep rise of plasma ammonia was seen preceding his mother’s milk; (ii) amino acid analysis of both plasma and urine using tandem mass spectrometry revealed no abnormalities; and (iii) hyperammonemia did not recur even after breast-feeding. Sepsis resulting from skin erosion on his whole body was regarded as the cause of death, though the culture around the umbilical cord was negative.
Acknowledgments We would like to thank Yuki Hasegawa, MD, Hironori Kobayashi, MD, and Yuichi Mushimoto, MD from the Department of Pediatrics, Division of Metabolic Abnormalities Laboratory,
Shimane Medical University for assisting us with tandem mass spectrometry, which was required during the diagnosis of our patient.
References 1 Msall M, Batshaw ML, Suss R, Brusilow SW, Mellits ED. Neurologic outcome in children with inborn errors of urea synthesis. Outcome of urea-cycle enzymopathies. N. Engl. J. Med. 1984; 310: 1500–5. 2 Rajpoot DK, Gargus JJ. Acute hemodialysis for hyperammonemia in small neonates. Pediatr. Nephrol. 2004; 19: 390–5. 3 Ballard RA, Vinocur B, Reynolds JW et al. Transient hyperammonemia of the preterm infant. N. Engl. J. Med. 1978; 299: 920–5. 4 Le Guennec JC, Qureshi IA, Bard H, Siriez JY, Letarte J. Transient hyperammonemia in an early preterm infant. J. Pediatr. 1980; 96: 470–2. 5 Sadwski RH, Harmon WE, Jabs K. Acute hemodialysis of infants weighing less than five kilograms. Kidney Int. 1994; 45: 903– 6. 6 Wong KY, Wong SN, Lam SY, Tam S, Tsoi NS. Ammonia clearance by peritoneal dialysis and continuous arteriovenous hemodiafiltration. Pediatr. Nephrol. 1998; 12: 589–91. 7 Everdell NL, Coulthard MG, Crosier J, Keir MJ. A machine for haemodialysing very small infants. Pediatr. Nephrol. 2005; 20: 636–43. 8 Assadi FK. Treatment of acute renal failure in an infant by continuous arteriovenous hemodialysis. Pediatr. Nephrol. 1998; 2: 320–2. 9 Ronco C, Brendolan A, Bragantini L et al. Treatment of acute renal failure in newborns by continuous arterio-venous hemofiltration. Kidney Int. 1986; 29: 908–15. 10 Jander A, Tkaczyk M, Pagowska KI et al. Continuous veno-venous hemodiafiltration in children after cardiac surgery. Eur. J. Cardiothorac Surg. 2007; 31: 1022–8. 11 Bunchman TE, Donckerwolcke RA. Continuous arterial-venous diahemofiltration and continuous veno-venous diahemofiltration in infants and children. Pediatr. Nephrol. 1994; 8: 96– 102.
Neonatal urethral polyps associated with Beckwith–Wiedemann syndrome Yuko Anzai,1 Shigeki Koshida,1 Takahide Yanagi,1 Kazuyoshi Johnin2 and Yoshihiro Takeuchi1 Departments of 1Pediatrics and 2Urology, Shiga University of Medical Science, Shiga, Japan Abstract
We report the first case of Beckwith–Wiedemann syndrome without urinary obstruction, but with a congenital urethral polyp as a tumor protruding from the external urinary meatus. The present case suggests a possible relation between Beckwith–Wiedemann and the onset of fibroepithelial polyps in the reno-urinary system during the neonatal period.
Key words Beckwith–Wiedemann syndrome, fibroepithelial polyp, neonate, urethral meatus mass, urethral polyp. Correspondence, Yuko Anzai, MD, Nagahama Red Cross Hospital, 14-7 Miyamaecho, Nagahamashi, Shiga 526-8585, Japan. Email: [email protected] Received 4 May 2012; revised 24 October 2012; accepted 19 February 2013. doi: 10.1111/ped.12096
© 2013 The Authors Pediatrics International © 2013 Japan Pediatric Society
Urethral polyps are benign tumors that remain in the bladder and urethra. When infants become older, urethral polyps develop from urinary tract obstruction symptoms caused by hematuria, dysuria, and repeated urinary tract infection. There are no previous reports of congenital urethral polyps in male infants
