The Henderson-Hasselbalch equation and Stewart's strong ion model are currently used to describe mammalian acid-base equilibria. Anomalies exist when the Henderson-Hasselbalch equation is applied to plasma, whereas the strong ion model does not provide a practical method for determining the total plasma concentration of nonvolatile weak acids ([Atot]) and the effective dissociation constant for plasma weak acids (Ka). A simplified strong ion model, which was developed from the assumption that plasma ions act as strong ions, volatile buffer ions (HCO-3), or nonvolatile buffer ions, indicates that plasma pH is determined by five independent variables: PCO2, strong ion difference, concentration of individual nonvolatile plasma buffers (albumin, globulin, and phosphate), ionic strength, and temperature. The simplified strong ion model conveys on a fundamental level the mechanism for change in acid-base status, explains many of the anomalies when the Henderson-Hasselbalch equation is applied to plasma, is conceptually and algebraically simpler than Stewart's strong ion model, and provides a practical in vitro method for determining [Atot] and Ka of plasma. Application of the simplified strong ion model to CO2-tonometered horse plasma produced values for [Atot] (15.0 +/- 3.1 meq/l) and Ka (2.22 +/- 0.32 x 10(-7) eq/l) that were significantly different from the values commonly assumed for human plasma ([Atot] = 20.0 meq/l, Ka = 3.0 x 10(-7) eq/l). Moreover, application of the experimentally determined values for [Atot] and Ka to published data for the horse (known PCO2, strong ion difference, and plasma protein concentration) predicted plasma pH more accurately than the values for [Atot] and Ka commonly assumed for human plasma. Species-specific values for [Atot] and Ka should be experimentally determined when the simplified strong ion model (or strong ion model) is used to describe acid-base equilibria.

Measurements of both PLL:PL and A:PL are recommended in dogs with patellar luxation, and surgical correction should be considered in those with abnormal values.

The traditional approach for clinically assessing acid-base status uses the Henderson-Hasselbalch equation to categorize 4 primary acid-base disturbances: respiratory acidosis (increased PCO2), respiratory alkalosis (decreased PCO2), metabolic acidosis (decreased extracellular base excess or actual HCO3- concentration), and metabolic alkalosis (increased extracellular base excess or actual HCO3- concentration). The anion gap is calculated to detect unidentified anions in plasma. This approach works well clinically and is recommended for use whenever serum total protein, albumin, and phosphate concentrations are approximately normal. However, because the Henderson-Hasselbalch approach is more descriptive than mechanistic, when these concentrations are markedly abnormal the Henderson-Hasselbalch equation frequently provides erroneous information as to the cause of an acid-base disturbance. The new quantitive physicochemical approach to evaluating acid-base balance uses the simplified strong ion model to categorize 6 primary acid-base disturbances: respiratory acidosis (increased PCO2), respiratory alkalosis (decreased PCO2), strong ion acidosis (decreased strong ion difference), strong ion alkalosis (increased strong ion difference), nonvolatile buffer ion acidosis (increased plasma concentrations of albumin, globulins, or phosphate), and nonvolatile buffer ion alkalosis (decreased plasma concentrations of albumin, globulins, or phosphate). The strong ion gap is calculated to detect unidentified anions in plasma. The simplified strong ion approach works well clinically and is recommended for use whenever serum total protein, albumin, or phosphate concentrations are markedly abnormal. The simplified strong ion approach is mechanistic and is therefore well suited for describing the cause of any acid-base disturbance.

Limited information is available to assist in the ante-mortem prediction of tumor type and grade for dogs with primary brain tumors. The objective of the current study was to identify magnetic resonance imaging (MRI) criteria related to the histopathological type and grade of gliomas in dogs. A convenience sample utilizing client-owned dogs (n=31) with gliomas was used. Medical records of dogs with intracranial lesions admitted to two veterinary referral hospitals were reviewed and cases with a complete brain MRI and definitive histopathological diagnosis were retrieved for analysis. Each MRI was independently interpreted by five investigators who were provided with standardized grading instructions and remained blinded to the histopathological diagnosis. Mild to no contrast enhancement, an absence of cystic structures (single or multiple), and a tumor location other than the thalamo-capsular region were independently associated with grade II tumors compared to higher grade tumors. In comparison to oligodendrogliomas, astrocytomas were independently associated with the presence of moderate to extensive peri-tumoral edema, a lack of ventricular distortion, and an isointense or hyperintense T1W-signal. When clinical and MRI features indicate that a glioma is most likely, certain MRI criteria can be used to inform the level of suspicion for low tumor grade, particularly poor contrast enhancement. Information obtained from the MRI of such dogs can also assist in predicting an astrocytoma or an oligodendroglioma, but no single imaging characteristic allows for a particular tumor type to be ruled out.

Acid-base abnormalities are frequently present in sick calves. The mechanism for an acid-base disturbance can be characterized using the strong ion approach, which requires accurate values for the total concentration of plasma nonvolatile buffers (A tot ) and the effective dissociation constant for plasma weak acids (K a ). The aims of this study were to experimentally determine A tot , K a , and net protein charge values for calf plasma and to apply these values quantitatively to data from sick calves to determine underlying mechanisms for the observed acid-base disturbance. Plasma was harvested from 9 healthy Holstein-Friesian calves and concentrations of quantitatively important strong ions (Na ϩ , K ϩ , Ca 2ϩ , Mg 2ϩ , Cl Ϫ , L-lactate) and nonvolatile buffer ions (total protein, albumin, phosphate) were determined. Plasma was tonometered with CO 2 at 37ЊC, and plasma PCO 2 and pH measured over a range of 15-159 mm Hg and 6.93-7.79, respectively. Strong ion difference (SID) was calculated from the measured strong ion concentrations, and nonlinear regression was used to estimate values for A tot and K a from the measured pH and PCO 2 and calculated SID. The estimated A tot and K a values were then validated using data from 2 in vivo studies. Mean (Ϯ SD) values for calf plasma were A tot ϭ 0.343 mmol/g of total protein or 0.622 mmol/g of albumin; K a ϭ (0.84 Ϯ 0.41) ϫ 10 Ϫ7 ; pK a ϭ 7.08. The net protein charge of calf plasma was 10.5 mEq/L, equivalent to 0.19 mEq/g of total protein or 0.34 mEq/g of albumin. Application of the strong ion approach to acid-base disturbances in 231 sick calves with or without diarrhea indicated that acidemia was due predominantly to a strong ion acidosis in response to hyponatremia accompanied by normochloremia or hyperchloremia and the presence of unidentified strong anions. These results confirm current recommendations that treatment of acidemia in sick calves with or without diarrhea should focus on intravenous or PO administration of a fluid containing sodium and a high effective SID.Key words: Calf diarrhea; D-lactic acidosis; Hyponatremia; Metabolic acidosis.A cidemia and metabolic acidosis occur commonly in sick calves with or without diarrhea. Metabolic acidosis in diarrheic calves was originally attributed to fecal bonate loss as well as the presence of unidentified organic acids in plasma and a decrease in glomerular filtration rate in response to severe dehydration.1-4 These proposed mechanisms for development of metabolic acidosis were based, in part, on the presence of hyper-L-lactatemia in diarrheic calves, 1,2,5,6 hyper-L-lactatemia and extensive loss of bicarbonate in the watery stool of humans with cholera, 7 and from (personal communication) of a high fecal bicarbonate concentration (40 mEq/L) in 4 calves with experimentally induced enterotoxigenic Escherichia coli diarrhea.c However, metabolic acidosis in diarrheic calves is probably predominantly due to causes other than fecal bicarbonate loss because diarrheic calves have measured mean daily fecal losses of s...