PATHOPHYSIOLOGICAL ASPECTS OF NEONATAL CALF DIARRHEA

Pathophysiological changes in calves affected with neonatal diarrhea are primarily characterized by the hypotonic dehydration due to increased faecal losses of electrolytes and fluid. Although the sympathic-adrenergic system and the renin-angiotensin-aldosterone system are activated, a hypovolemic shock may progressively develop with a decreased cardiac output and a reduction of blood pressure resulting in a circulatory hypoxia. Disturbances of macro- and microcirculation, intestinal bicarbonate losses and reduced renal excretion of protons induce a metabolic acidosis. Especially in young calves (< 1 week of age), blood lactate levels rise caused by an increased lactate production combined with a decreased lactate utilization. Calves with diarrhea are confronted with a massive energy deficit due to decreased intestinal absorption and a reduction of oxidative phosphorylization and gluconeogenesis. Hypoglycemia is found frequently in critically ill calves. In moribund calves hypothermia is a common symptom indicating an adaptive mechanism to reduce energy expenditure. Hyperkalemia in calves with severe diarrhea is related to the metabolic acidosis and caused mainly by a shift of potassium from the intracellular to the extracellular compartment. Despite hyperkalemia, the calf is in a potassium deficit. Septicemia seems to play a minor role in most of the calves with diarrhea. The kev element of therapy in severely ill calves is the rapid intravenous restoration of salt and water depletion.