Ammonia, NH3

Clinical Chemistry

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Description

Ammonia is generated primarily in the gastrointestinal tract by metabolism of nitrogenous compounds. An excess of ammonia can be toxic to the central nervous system. The Krebs-Henseleit urea cycle provides a means of disposal of ammonia by metabolizing ammonia to urea in the liver. Circulating ammonia concentrations in normal individuals are usually low despite the fact that ammonia is continuously produced from dietary and amino acid metabolism. Ammonia measurement is used to assist in the diagnosis of hepatic encephalopathy. However, the correlation between plasma concentration and the severity of cerebral dysfunction is not always close. Ammonia is increased in fulminant hepatic failure, cirrhosis of the liver, porto-systemic shunts, intestinal haemorrhage, Reyes syndrome and some inherited metabolic diseases. The most significant of the latter are due to defects of the enzymes of the urea cycle and some organic acidaemias. Further investigations include routine, lactate, plasma amino acids, urine organic acids (which includes orotic acid). Discuss with Duty Biochemist.

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Indications

Neurological abnormalities (ataxia, gait disturbance, epilepsy, intellectual impairment, behavioral change including aggression, headaches), cyclical vomiting, protein avoidance, Reye-like syndromes. Investigation of the obtunded patient of any age, especially if respiratory alkalosis. Patients on sodium valproate with any of the above. Liver failure.

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Sample Type

EDTA (purple) tube on ice, to NGH or RHH Lab within 20-30

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Reference Range

Male 16 - 60 umol/LFemale 11 - 51 umol/L

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Turnaround Time

Within 1 hour

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Testing Frequency

24/7.

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Patient Preparation

Avoid haemostasis. Minimise haemolysis at venesection.

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