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Table of Contents
CASE REPORT
Year : 2020  |  Volume : 31  |  Issue : 2  |  Page : 82-84

A case of hyperammonemia in a patient with urinary tract infection and urinary retention


Department of Urology, Showa University, School of Medicine, Tokyo, Japan

Date of Submission24-Sep-2019
Date of Decision10-Nov-2019
Date of Acceptance26-Nov-2019
Date of Web Publication25-Apr-2020

Correspondence Address:
Sat Prasad Nepal
Department of Urology, School of Medicine, Showa University, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555
Japan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/UROS.UROS_70_19

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  Abstract 


Excessive ammonia is harmful to the body. It is mostly hepatic in origin. Hyperammonemia due to urinary tract infection (UTI) is rare. We report a case of hyperammonemia with UTI and urinary retention. A 94-year-old female arrived at our hospital with impaired consciousness that lasted for a day. On arrival, her Glasgow Coma Scale was E1V1M5, blood ammonia was 272 ng/dl, and urinalysis revealed a large number of white and red blood cells. Abdominal computed tomography scan revealed a distended bladder and wall thickness with no hydronephrosis. Urine cultures were positive for urease-producing Corynebacterium, Escherichia coli, and Staphylococcus aureus. The patient was diagnosed with hyperammonemia with UTI and urinary retention. After urinary catheterization, blood ammonia levels normalized, and consciousness improved. We need to consider ammonia toxicity in UTI patients with urine retention presenting with altered consciousness.

Keywords: Ammonia, impaired consciousness, urease producers, urinary tract infection, urine retention


How to cite this article:
Nepal SP, Unoki T, Inoue T, Nakasato T, Naoe M, Ogawa Y, Omizu M, Kato R, Sugishita H, Oshinomi K, Morita J, Maeda Y, Shichijo T. A case of hyperammonemia in a patient with urinary tract infection and urinary retention. Urol Sci 2020;31:82-4

How to cite this URL:
Nepal SP, Unoki T, Inoue T, Nakasato T, Naoe M, Ogawa Y, Omizu M, Kato R, Sugishita H, Oshinomi K, Morita J, Maeda Y, Shichijo T. A case of hyperammonemia in a patient with urinary tract infection and urinary retention. Urol Sci [serial online] 2020 [cited 2020 Sep 23];31:82-4. Available from: http://www.e-urol-sci.com/text.asp?2020/31/2/82/283250




  Introduction Top


High levels of ammonia in blood are lethal, given the toxic effects of ammonia on the brain. Hyperammonemia often originates from hepatic causes. Nonhepatic causes, including urea cycle disorders, portosystemic shunting, medication (sodium valproate, 5-fluorouracil, and salicylates),[1],[2] gastrointestinal hemorrhage, glycine irrigation,[1] and urinary tract infection (UTI) caused by urease-producing organisms, are rare.[1],[2],[3],[4],[5]

Here we present a nonhepatic cause of hyperammonemia due to UTI and urinary retention, which we suspect resulted from urease-producing Corynebacterium, and present its treatment by urinary drainage.


  Case Report Top


A 94-year-old female arrived at our hospital with impaired consciousness that lasted for a day. According to her husband, she did not wake up in the morning and was unable to wake up even after he called on her. She was brought to the hospital soon afterward. With regard to medical history, she has lumbar spinal stenosis in L4 since 2016. On hospital arrival, her Glasgow Coma Scale (GCS) was E1V1M5; pulse rate was 78/min; blood pressure was 158/62 mmHg; SpO2 was 98%; temperature was 37.1°C; and respiratory rate was 18/min. Her pupil reflex was normal, and there were no Babinski signs or meningeal signs. There was bulge in the lower abdominal area, but there were no signs of chronic liver disease. On Foley's catheterization, urine was turbid with hematuria.

Urinalysis revealed 50–99 white blood cells/high power field (HPF) and 20–29 red blood cells/HPF. Complete blood count revealed a white blood cell count of 9700/mm[3], 84.9% neutrophils, and 10.5% monocytes. Elevations were observed for C-reactive protein (4.23 mg/dl), blood pH (pH 7.496), blood ammonia (272 ng/dl), brain natriuretic peptide (324.8 pg/ml), urea nitrogen (38.4 mg/dl), and creatinine kinase (434 IU/L). Liver function and viral serology were normal.

The patient did not exhibit features of cerebral hemorrhage, cerebral infarction, or tumors on head computed tomography (CT). Abdominal CT revealed a large amount of urine in the bladder with no hydronephrosis. The bladder was diffusely thickened, and cystic swelling, which we considered to be an ovarian cyst, was found on the right side of the bladder [Figure 1].
Figure 1: Coronal section of abdomen showing distended urinary bladder with cystic swelling on the right side (arrow), which was suspected to be an ovarian cyst

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The blood sample was taken after catheterization and continuous urinary lavage showed normal levels of ammonia. Consciousness improved the day after hospitalization, with a GCS of E3V5M6. Bladder washing was done till the urine was clear. After 3 days of admission, the catheter was removed, and the patient was able to void.

Urine cultures were positive for urease-producing Corynebacterium species and coagulase-negative Staphylococcus aureus and Escherichia coli. The patient was given oral cefcapene pivoxil hydrochloride hydrate antibiotic for 14 days.


  Discussion Top


Excessive ammonia is toxic to the body. When the urea cycle cannot compensate for excessive ammonia production, other regions of the body, such as skeletal muscle, kidneys, and the brain, attempt to protect against ammonia by forming glutamine, but only in a limited capacity.[1],[6] In the brain, astrocytes form glutamine in order to counteract ammonia toxicity, leading to increased osmolarity and swelling. Moreover, interleukin 1, interleukin 6, tumor necrosis factor, and interferon are released by astrocytes, leading to further damage.[1],[6] The Krebs cycle is also disturbed, which results in lactate accumulation. The reduction in glutamate receptor expression in astrocytes leads to excessive accumulation of glutamate, which can cause seizures. These factors collectively damage astrocytes, cause cerebral edema, and increase intracranial pressure and cerebral herniation.[1],[6]

Liver disease was ruled out since the patient showed no signs of chronic liver disease and had normal liver function test results, normal hepatitis viral serology, and no portal vein shunts on CT. Urea cycle disorders were also unlikely, given her age and immediate normalization of blood ammonia levels on catheterization. She had no history of being treated with valproate or surgery which could have caused increased ammonia levels. Thus, we suspect UTI by urease-producing Corynebacterium to be the cause.

Urease producers form ammonia and carbon dioxide from urea.[2],[4],[5],[7],[8],[9],[10] Urease producers (Proteus species, Pseudomonas aeruginosa, Klebsiella species, Morganella morganii, and Corynebacterium species) form urease, which converts urea to ammonia and carbon dioxide, causing alkaline urine.[2],[4],[5],[7],[8],[9],[10] Ammonia is in equilibrium with ammonium ions. Due to an increase in pH, ammonia's concentration rises and passes through the bladder cell membrane due to its electrical neutrality and lipid solubility.[2],[4] In the systemic circulation, ammonia is converted back to ammonium ions. Most of the venous supply of the bladder bypasses the portal circulation and drains directly into the systemic circulation. Therefore, the high levels of ammonia produced by bacteria in our case were detected in blood and led to encephalopathy.

Corynebacterium species (the causative organisms in our case) are Gram-positive, catalase-positive, aerobic, or facultative anaerobic organisms. They occur in soil, water, plants and food products.[11]

While we suspect that urease-producing bacteria caused hyperammonemia in our case, some studies have shown that hyperammonemia can be caused by nonurease-producing bacteria (E. coli,[7],[8]Enterococcus faecalis,[8]Streptococcus faecalis)[12] as well.

To treat excessive ammonia, intracranial hypertension must first be managed, as it can lead to cerebral edema and cerebral herniation.[6] Various methods exist to reduce ammonia, including protein intake restriction and elimination of ammonia by sodium phenylacetate, sodium benzoate, antibiotics, and in extreme circumstances, dialysis.[2],[3],[6],[7],[12] In our case, relieving urinary retention by bladder catheterization led to prompt normalization of blood ammonia levels. We suspect our patient to have urinary distention because of the neurogenic bladder due to aging.


  Conclusion Top


We present a case of hyperammonemia with UTI and urinary retention, which we suspect was caused by urease-producing Corynebacterium. Our findings highlight the importance of considering ammonia excess when UTI patients with urine retention have encephalopathy.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understand that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Walker V. Severe hyperammonaemia in adults not explained by liver disease. Ann Clin Biochem 2012;49:214-28.  Back to cited text no. 1
    
2.
Albersen M, Joniau S, van Poppel H, Cuyle PJ, Knockaert DC, Meersseman W. Urea-splitting urinary tract infection contributing to hyperammonemic encephalopathy. Nat Clin Pract Urol 2007;4:455-8.  Back to cited text no. 2
    
3.
Cheang HK, Rangecroft L, Plant ND, Morris AA. Hyperammonaemia due to klebsiella infection in a neuropathic bladder. Pediatr Nephrol 1998;12:658-9.  Back to cited text no. 3
    
4.
Miyauchi, R., Matsuda, Y. and Tokuda, Y. Urinary Tract Infection as a Cause of Hyperammonemic Encephalopathy. General Medicine 2015;16:95-8. doi:10.14442/general.16.95.  Back to cited text no. 4
    
5.
Samtoy B, DeBeukelaer MM. Ammonia encephalopathy secondary to urinary tract infection with Proteus mirabilis. Pediatrics 1980;65:294-7.  Back to cited text no. 5
    
6.
Clay AS, Hainline BE. Hyperammonemia in the ICU. Chest 2007;132:1368-78.  Back to cited text no. 6
    
7.
Kenzaka T, Kato K, Kitao A, Kosami K, Minami K, Yahata S, et al. Hyperammonemia in urinary tract infections. PLoS One 2015;10:e0136220.  Back to cited text no. 7
    
8.
Cordano C, Traverso E, Calabrò V, Borzone C, Stara S, Marchese R, et al. Recurring hyperammonemic encephalopathy induced by bacteria usually not producing urease. BMC Res Notes 2014;7:324.  Back to cited text no. 8
    
9.
Burne RA, Chen YY. Bacterial ureases in infectious diseases. Microbes Infect 2000;2:533-42.  Back to cited text no. 9
    
10.
De Jonghe B, Janier V, Abderrahim N, Hillion D, Lacherade JC, Outin H. Urinary tract infection and coma. Lancet 2002;360:996.  Back to cited text no. 10
    
11.
Yassin AF, Kroppenstedt RM, Ludwig W. Corynebacterium glaucum sp. nov. Int J Syst Evol Microbiol 2003;53:705-9.  Back to cited text no. 11
    
12.
Oliver RM, Talbot S, Raman GV. Hyperammonaemic coma in ureterosigmoid urinary diversion. Postgrad Med J 1989;65:502-4.  Back to cited text no. 12
    


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