Thirty-four dogs suffering from severe babesiosis caused by Babesia canis r
ossi were included in this study to evaluate acid-base imbalances with the
quantitative clinical approach proposed by Stewart. All but 3 dogs were sev
erely anemic (hematocrit < 12%). Arterial pH varied from severe acidemia to
alkalemia. Most animals (31 of 34; 91%) had inappropriate hypocapnia with
the partial pressure of CO2 < 10 mm Hg in 12 of 34 dogs (35%). All dogs had
a negative base excess (BE mean of -16.5 mEq/L) and it was below the lower
normal limit in 25. Hypoxemia was present in 3 dogs. Most dogs (28 of 34;
82%) were hyperlactatemic. Seventy percent of dogs (23 of 33) were hypoalbu
minemic. Anion gap (AG) was widely distributed. being high in 15, low in 12
, and normal in 6 of the 33 dogs. The strong ion difference (SID; differenc
e between the sodium and chloride concentrations) was low in 20 of 33 dogs,
chiefly because of hyperchloremia. Dilutional acidosis was present in 23 o
f 34 dogs. Hypoalbuminemic alkalosis was present in all dogs. Increase in u
nmeasured strong anions resulted in a negative BE in all dogs. Concurrent m
etabolic acidosis and respiratory alkalosis was identified in 31 of 34 dogs
. A high AG metabolic acidosis was present in 15 of 33 dogs. The lack of an
AG increase in the remaining dogs was attributed to concurrent hypoalbumin
emia, which is common in this disease. Significant contributors to BE were
the SID, free water abnormalities, and AG (all with P < .01), Mixed metabol
ic and respiratory acid-base imbalances are common in severe canine babesio
sis, and resemble imbalances described in canine endotoxemia and human mala
ria.