Untersuchungen zum Einfluss des D-Laktatblutspiegels auf Azidose, Körperhaltung und Verhalten bei Kälbern mit Neugeborenendurchfall

Some calves with neonatal diarrhea and distinctly disturbed general
condition have elevated blood levels of D-lactate and respond
poorly to the usual correction of acidosis. This observation led to
this prospective study with the objective to elucidate whether
calves with elevated D-lactate levels require higher doses of
sodium bicarbonate and more frequent treatments than calves with
normal D-lactate levels. Among the calves admitted to the clinic
between September, 2002, and March, 2003, 73 calves with an age of
up to 3 weeks were included in this study. Further selection
criteria were diarrhea (according to the history or upon
admission), and metabolic acidosis with a base excess below -10
mmol/l. Exclusion criteria were hypoglycemia, hyperkalemia,
evidence of myodystrophy, severe bronchopneumonia, and navel ill
requiring surgical intervention. Within the period of investigation
(24 hours) the calves received a standardized therapy but no
anti-inflammatory drugs and no oral rehydration solutions. Dosage
of sodium bicarbonate was calculated using the formula body weight
x base deficit x 0.6 and administered in a volume of 2.5 liters
within 3.5 hours. During the subsequent 20 hours the calves
received infusions of 0.9 % sodium chloride in volumes
corresponding to the estimated fluid loss. Blood samples were taken
before the infusion and after four and 24 hours and assayed for
D-lactate concentration and base excess; additionally, behavior and
posture of the calves were recorded. Voluntary milk intake at the
first regular feeding after the end of the investigation was also
recorded. Approximately 85 % of the calves had elevated D-lactate
levels. Significant correlations between D-lactate levels and both
behavior and posture were found, allowing for a relatively reliable
diagnosis of hyper-D-lactatemia on the basis of clinical signs.
Posture and behavior seemed to be more strongly influenced by
D-lactate than by degree of acidosis. No correlations were found
between either D-lactate level or base excess, and milk intake.
Mean D-lactate concentration decreased very little after the first
four hours, whereas a distinct drop was observed after the
subsequent 20 hours. A possible explanation for this finding is
that metabolism of D-lactate increases after the normalization of
blood pH. Significant correlations between D-lactate levels and
base excess after the sodium bicarbonate infusion indicate that
calves with elevated D-lactate levels have received to little
buffer. Furthermore significant correlations between D-lactate
levels and base excess after 24 hours indicate that those calves,
which still had elevated D-lactate levels after this period of
time, in most cases required a repeated treatment with buffer.
Conclusion: Calves with clinical evidence of D-lactate acidosis
require higher doses of buffer and possibly repeated treatments.