Urea toxicity

Urea toxicity
Included in ruminant rations @ 3% of total concentration or 1% of total ration as a source of NPN. As a fertilizer and as a substitute for salts in melting of snow and ice in residential areas.
Sources:
Ø Excess in urea - molasses mixtures. (Salty in taste, hence animals relish)
Ø Improper mixing
Ø Spilling or improper storage of urea
Urea is acted upon by urease present in plants releasing ammonium ion, as the alkaline pH increases this is converted to ammonia. Ammonia is absorbed into the blood, enters CNS and inhibits citric acid cycle.
Only cattle are affected the reason is - urease in plants and alkaline pH of rumen. Monogastrics have acidic pH; even young ruminants whose rumen is not fully developed also are not susceptible. Degree of adaptation is important: Animal accustomed to ingestion of urea can ingest 1g/kg/day but in unaccustomed animals 0.3 - 0.5 g /kg/day may be toxic.
High body temperature, absence of water, rapid ingestion by starved / fasted animals, fibrous diet and feeds rich in urease all increase toxicity.
Physiological detoxification mechanism
In liver ammonia is converted into urea by urea cycle or incorporated into glutamic acid in the synthesis of glutamine. When the liberation of ammonia is more and the normal detoxification mechanisms fail, then ammonia crosses BBB, enters CNS (-) citric acid cycle causing decreased energy production, decreased cellular respiration, anoxia - convulsions that are tonic and elicitable like strychnine. (Ammonia decreases postsynaptic inhibition of cortical and spinal motoneurons, also seen in O.C. poisoning). Urine output also decreases. Death could be due to ventricular fibrillation / cardiac stoppage due to hyperkalemia. / respiratory paralysis
Signs: GI & CNS signs are prominent.
CNS signs:
Restlessness, dull / excited, hyperaesthesia, tremors, twitching and spasms of muscles progressing from head to tail, terminally tonic seizures with opisthotonus condition. Convulsions are elicitable by external stimuli and between the convulsions animal is rigid. In coordination and stumbling in the terminal stage.
Fever due to convulsive activity (Hot ears and skin) laboured breathing, (lung edema, fever), cardiac arrhythmias (direct effects of ammonia), frothing at the mouth, cyanosis. GI signs: Salivation, colic, atony, bloat (figure)
(tooth grinding, groaning, kicking at the abdomen, rolling on the ground, looking towards the abdomen - all colicky signs.) Absence of diarrhoea and aspiration of ruminal contents.
Diagnosis: history of, characteristic GI & CNS signs.
Severe colic (absence of diarrhoea), salivation, dyspnoea, strychnine like convulsions. Odour of ammonia in rumen. Ammonia is dissolved in ruminal liquor so collect ruminal liquor and freeze. Blood is refrigerated – if left at room temperature

ammonia increases in biologic samples due to decomposition. Suspected feed / molasses also should be frozen.
Differential diagnosis:
Caustic substances / arsenic - cause severe colic & bloody diarrhoea whereas in urea there is no diarrhoea.
OP compounds - atropinization is effective, in urea atropinization is ineffective.
Rx: In early stages
Cold water: acetic acid is helpful
In adult cow 19-38 L of cold water and 3.8 L of 5% vinegar (dil. acetic acid) are employed but after relieving bloat through puncture of rumen.

This treatment reduces alkaline pH (responsible for hydrolysis) and also dilutes ruminal contents therefore prevents further absorption of ammonia.
Rumenotomy or Gastric lavage is aimed at removing the ruminal liquor.