Abstract
Although several studies on ammonia poisoning have been carried out, there is a lack of information on acid-base balance status in ammonia-poisoned cattle. Twelve crossbred steers received intraruminally 0.5 g of urea per kg of body weight in order to induce a clinical picture of ammonia poisoning. Blood samples were collected throughout the trials in order to determine the blood ammonia, lactate, and perform blood gas analysis. All cattle presented aclassical clinical picture of ammonia poisoning, with a blood ammonia concentration rising progressively from the beginning until reaching higher values at 180 min (27 ± 3 to 1719 ± 101 µmol L-1), with a similar pattern occurring with blood L-lactate levels (1.7 ± 0.3 to 26.0 ± 1.7 mmol L-1). The higher the blood ammonia concentration the higher the blood L-lactate levels (r = 0.86). All animals developed metabolic acidosis, as blood pH lowered to 7.24 ± 0.03. The steers tried to compensate the metabolic acidosis mainly through the use of blood buffers and respiratory adjustments by lowering the pCO2 levels in the blood to 32.8 ± 2.0 mm Hg.
Highlights
The occurrence of outbreaks of ammonia poisoning is getting more often as the use of urea is increasing among cattlemen as a protein replacer to cattle raised under extensive management on subtropical or tropical environment, mainly during the dry season (Kitamura et al, 2003)
The clinical picture is acute with a quick development and most often the clinical signs are characterized by restlessness, dullness, weakness, muscle tremors, profuse salivation, rumen atony, bloat, dyspnea, incoordination, vocalization, lung edema, tonicclonic convulsions, and death by heart failure that may occur within 30 minutes (Froslie, 1977; Antonelli et al, 2004; Radostits et al, 2007; Kitamura et al, 2010a)
There is no consensus between researchers about the effects on acidbase status in ammonia-poisoned animals as different authors described the effects as a metabolic alkalosis, a metabolic acidosis, and a respiratory acidosis (Rash et al, 1968; Roller et al, 1982)
Summary
The occurrence of outbreaks of ammonia poisoning is getting more often as the use of urea is increasing among cattlemen as a protein replacer to cattle raised under extensive management on subtropical or tropical environment, mainly during the dry season (Kitamura et al, 2003). The supplementation of urea to ruminants is generally safe, acute ammonia poisoning due to urea ingestion resulting in the death of animals are often reported by veterinarians and cattlemen (Ortolani et al, 2000). Ammonia poisoning may occur mainly when ruminants not adapted to urea consume large quantities of it, or when feeds are inappropriately mixed with urea. Establishing the acid-base status will not assure the success of the treatment but might help when handling with severe cases of ammonia poisoning that would require a correction of the acid-base balance in addition to conventional treatment (Ortolani et al, 2000). There is no consensus between researchers about the effects on acidbase status in ammonia-poisoned animals as different authors described the effects as a metabolic alkalosis, a metabolic acidosis, and a respiratory acidosis (Rash et al, 1968; Roller et al, 1982)
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