Urea poisoning
Diagnosis, in ruminants
History (access to, if not ingestion of urea in a quantity to which the affected animal has not been accustomed), clinical signs (dyspnoea, frothing at the nose and mouth, hyperaesthesia and aggression, muscle tremor and incoordination, bloat, evidence of abdominal pain; less acute cases become weak, recumbent and somnolent), necropsy (ammoniacal rumen contents, pulmonary oedema, generalised congestion), estimation of ammonium in blood or aqueous humour.
Pre-existing hepatopathy may facilitate urea poisoning.
Specimens required
Live animal: 1 ml plasma or serum, separated from the blood cells or clot as soon as possible, and chilled or frozen, for ammonium (NH4) analysis. DO NOT USE ammonium heparin tubes.
Dead animal: 1 ml cell-free aqueous humour, frozen within 24 hours of death, for ammonium analysis.
Submitters should separate the serum, plasma or aqueous from any cells as soon as possible by sedimentation or preferably by centrifugation. NSW DPI outsources these tests.
Interpretation, ruminants*
<200 µmol NH4/L serum or plasma at the time of blood collection is normal, but this may increase to 400 µmol within 24 hours unless, in the meantime, the serum or plasma is separated from the blood cells and frozen. The concentration in aqueous humour may increase more rapidly after death.
Hyperammonaemia is typical of, but not definitive for urea poisoning. Typically, cases may have >1000 µmol NH4/L serum, plasma or aqueous humour.
* David Paynter, Regional Laboratory Services, Benalla, Victoria, Australia, pers. comm., 2007.