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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT  
Year : 2011  |  Volume : 22  |  Issue : 6  |  Page : 1226-1228
Acute urine retention induced by ceftriaxone


Department of Pediatrics Nephrology, Jordan University Hospital, Faculty of Medicine, University of Jordan, Amman, Jordan

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Date of Web Publication8-Nov-2011
 

   Abstract 

Ceftriaxone is known to cause biliary pseudolithiasis and, rarely, nephrolithiasis. When used in neonates receiving intravenous calcium, fatal lung and kidney calcifications occur. There is no satisfactory explanation for the pseudolithiasis, and the mechanism of stone formation remains unknown. Herein, we report a child with acute urinary retention (AUR) secondary to ceftriaxone therapy. The AUR developed on the second hospital day. The urinary excretion of uric acid was elevated. In retrospect, there was a positive paternal family history of gout and stones. A positive family history of gout or stones is a pointer to the possibility of AUR or urolithiasis in patients on treatment with ceftriaxone. If urinary symptoms develop, it is worth checking for crystalluria. This will avoid many unnecessary investigations and procedures.

How to cite this article:
Akl KF, Masri AT, Hjazeen MM. Acute urine retention induced by ceftriaxone. Saudi J Kidney Dis Transpl 2011;22:1226-8

How to cite this URL:
Akl KF, Masri AT, Hjazeen MM. Acute urine retention induced by ceftriaxone. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2019 Nov 12];22:1226-8. Available from: http://www.sjkdt.org/text.asp?2011/22/6/1226/87240

   Introduction Top


Ceftriaxone is a broad-spectrum third-generation cephalosporin widely used in the treatment of pediatric infections. Ceftriaxone is known to induce urinary lithiasis. [1],[2],[3] When used in neonates receiving intravenous calcium, fatal precipitates of calcium ceftriaxone deposit in the lungs and kidneys. [4]

Herein, we report another rare complication, which, to the best of our knowledge, has not been reported in the literature.


   Case Report Top


A 2-year-old boy, who was well until five days prior to admission, developed fever (39°C) for which he received oral and parenteral antibiotics in a private clinic. On the day of admission, he developed headache, decreased activity, hypersomnia without vomiting, skin rash or urinary symptoms. On examination, the patient was febrile (38.5°C) and hypoactive. His weight was 13 kg (50 th percentile) and height was 90 cm (50 th percentile). Rest of the examinations were within normal limits. Laboratory investigations revealed normal complete blood count, serum electrolytes, urea, creatinine and a negative blood culture.

The urine pH was 5. Cerebrospinal fluid (CSF) analysis showed white blood cells 30/mm 3 , 66% polymorphonuclears and 34% lymphocytes, with normal sugar and protein and a negative culture.

The patient was diagnosed as a case of partially treated meningitis and started on ceftriaxone 100 mg/kg/day and vancomycin 65 mg/kg/day. The patient became afebrile and active. On the second hospital day, he developed acute urinary retention (AUR), which was associated with suprapubic pain and tenderness.

There was no previous history of urine catheter insertion. A 24-hour urine collection was performed on the third hospital day while the patient was on intravenous fluids. It showed a total volume of 900 mL, creatinine 17 mg/kg/day, calcium 3.7 mg/kg/day (normal <4 mg/kg/day) and uric acid 21 mg/kg/day (normal for age <13 mg/kg/day). Serum uric acid and an abdominal ultrasound were normal. The same antibiotic regimen was continued for a total of ten days without recurrence of the urine retention. In retrospect, there was a positive paternal family history of gout and kidney stones.


   Discussion Top


AUR, which is defined as the sudden inability to pass any urine, and requiring catheterization, is uncommon in childhood. [5],[6] Our patient developed AUR as a complication of ceftriaxone therapy. Other drugs reported to cause AUR include sympathomimetics, pseudoephedrine [7] and anticholinergics. [8] The purpose of this communication is to report a case of AUR in a child during treatment with ceftriaxone.

Ceftriaxone is a broad-spectrum third-generation cephalosporin that is widely used in pediatrics. It has been associated mainly with biliary pseudolithiasis and, to a lesser extent, urolithiasis. [1],[2],[3] Fatal neo-natal cases occurred when ceftriaxone was given along with intravenous calcium, with deposition of calcium ceftriaxone precipitates in the lungs and kidney. [4] Even though significant biliary clearance (35-45%) occurs, the main route of elimination is by the kidney.

Urolithiasis is reported to occur in 0.6% to 7.8% of patients. [1],[2],[3] In a prospective study by Acun et al, gall bladder and urinary precipitations occurred in 5/35 children. Symptoms included abdominal pain, nausea and vomiting. The gall bladder and urinary precipitations were found after four to nine days and five days of ceftriaxone therapy, respectively. Both resolved spontaneously completely. [3]

The mechanism of formation of biliary pseudolithiasis is poorly understood. Ceftriaxone binds calcium in the biliary tract, forming biliary sludge or stones.

The pathogenesis of nephrolithiasis is unknown. In a prospective study in 284 children, Mohkam et al could not identify the underling metabolic risk factors in stone-forming patients on ceftriaxone therapy. [1] Crystallurias such as hypercalciuria [9] and hyperuricosuria [10] are known risk factors for stone formation. Hyperuricosuria has been associated with recurrent oliguria, the mechanism of which may be due to post-renal obstruction. [11]

In our patient, the mechanism of AUR is unlikely to be due to neurological involvement, which was mild. The child was not taking any drugs that cause AUR. Most likely, it was due to precipitation of ceftriaxone on top of an underlying hyperuricosuria. The positive family history of gout and stones and the finding of elevated urinary uric acid excretion in spite of intravenous fluids lends support to this possibility. The acid urine promotes precipitation of uric acid crystals. The uric acid excretion may have been much higher if it was determined at the onset of urinary retention symptoms and before institution of intravenous fluid therapy. It is also possible that one could easily miss this finding if it was determined at a latter stage. It is prudent to think that children with a genetic predisposition to crystalluria, such as hyperuricosuria, may be more susceptible than others to develop ceftriaxone-associated urinary sludge and stones. This is much more likely to occur in the presence of decreased fluid intake and high fever.

A positive family history of gout or stones is definitely a pointer to the possibility of AUR or urolithiasis in patients on treatment with ceftriaxone. If urinary symptoms develop in children put on ceftriaxone, it is worth checking for crystalluria.

This will avoid many unnecessary investigations and procedures.

 
   References Top

1.Mohkam M, Karimi A, Gharib A, et al. Ceftriaxone associated nephrolithiasis: a prospective study in 284 children. Pediatr Nephrol 2007;2 2(5):690-4.  Back to cited text no. 1
    
2.Avci Z, Koktener A, Uras N, et al. Nephrolithiasis associated with ceftriaxone therapy: a prospective study in 51 children. Arch Dis Child 2004;89(11):1069-72 .  Back to cited text no. 2
    
3.Acun C, Erdem LO, Sogut A, et al. Gallbladder and urinary tract precipitation associated with ceftriaxone therapy in children: a propective study. Ann Trop Paediatr 2004;24(1):25-31.  Back to cited text no. 3
    
4.Monte SV, Prescott WA, Johnson KK, Kuhman L, Paladino JA. Safety of ceftriaxone sodium at extremes of age. Expert Opin Drug Saf 2008;7(5):515-23.  Back to cited text no. 4
    
5.Gatti, JM, Perez-Brayfield M, Kirsch AJ, Smith EA, Massad HC, Broecker BH. Acute urinary retention in children. J Urol 2001;165(3):918-21.  Back to cited text no. 5
    
6.Asgari SA, Mansour Ghanaie M, Simforoosh N, Kajbafzadeh A, Zare A. Acute urinary retention in children . Urol J 2005;2(1):23-7.  Back to cited text no. 6
    
7.Soyer T, Gol IH, Eroglu F, Cetin A. Acute urinary retention due to pseudoephedrine hydrochloride in a 3- year - old child . Turk J Pediatr 2008;50(1):98-100.  Back to cited text no. 7
    
8.Lee AC, So KT. Acute anticholinergic poisoning in children. Hong Kong Med J 2005;11(6): 520-3.  Back to cited text no. 8
    
9.Escribano J, Balaguer A, Pagone F, Feliu A, Roque I, Figuls M. Pharmacological interventions for preventing complications in idiopathic hypercalciuria. Cochrane Database Syst Rev 2009; 1:CD004754 .  Back to cited text no. 9
    
10.La Manna A, Polito C, Marte A, Lovene A, Di Toro R. Hyperuricosuria in children: clinical presentation and natural history. Pediatrics 2001;107(1):86-90 .  Back to cited text no. 10
    
11.Akl K. Hyperuricosuria, an often overlooked cause of recurrent oliguria in children. Saudi J Kidney Dis Transpl 2008;19(4):619-23.  Back to cited text no. 11
    

Top
Correspondence Address:
Kamal F Akl
Associate Professor of Pediatric Nephrology, Jordan University Hospital, Faculty of Medicine, University of Jordan, P.O. Box 831373 Amman 11183
Jordan
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PMID: 22089789

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    Abstract
   Introduction
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    References
 

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