[Acid-base and potassium balance disorders in neonatal calf diarrhea - Part 1: Pathophysiologic aspects and clinical...

Neonatal diarrhea remains one of the most frequent causes of morbidity, mortality, and economic loss in calves worldwide. The clinical consequences in affected animals are primarily attributable to fluid losses and consecutive dehydration, but also to the occurrence of metabolic acidosis and associated imbalances in potassium homeostasis. In calves with neonatal diarrhea, metabolic acidosis mainly results from the accumulation of strong anions, in particular D-lactate, which arises from bacterial fermentation processes of undigested nutrients within the gastrointestinal tract. Increased blood D-lactate concentrations not only contribute substantially to the development of metabolic acidosis but are also responsible for most of the clinical signs such as depression, weakness, impairment of the ability to stand, and alterations of the palpebral reflex.

Hyperkalemia occurs in up to one-third of severely affected calves despite a negative potassium balance and is linked to dehydration, impaired renal function, and the nature of metabolic acidosis. While D-lactic acidosis is rarely associated with hyperkalemia, the latter is typically accompanied by severe clinical dehydration, muscle weakness, and cardiac conduction abnormalities, thus representing a potentially life-threatening condition.

This review summarizes current pathophysiologic knowledge of these major metabolic disorders in calves with neonatal diarrhea and outlines their clinical relevance for diagnosis and treatment.