Investigations on the association of D-lactate blood concentrations with the outcome of therapy of acidosis, and with posture and demeanour in young calves with diarrhoea

The objective of this prospective study was to elucidate whether amounts of bicarbonate needed for correction of acidosis and normalization of clinical signs are influenced by blood D-lactate concentrations in calves with diarrhoea. In 73 calves up to 3 weeks old with acute diarrhoea and base excess values below -10 mmol/l correction of acidosis was carried out within 3.5-h by intravenous administration of an amount of sodium bicarbonate which was calculated using the formula: HCO (mmol) = body mass (kg) x base deficit (mmol/l) x 0.6 (l/kg). Clinical signs, venous base excess, and plasma D-lactate concentrations were monitored immediately following admission, following correction of acidosis at 4 h and 24 h after admission. The base excess and plasma D-lactate concentrations throughout the study were -17.8 +/- 4.0, -0.4 +/- 0.4, -3.0 +/- 5.5 mmol/l (base excess), and 10.0 +/- 4.9, 9.8 +/- 4.8, 5.4 +/- 3.4 mmol/l (D-lactate) for the three times of examination. Metabolic acidosis was not corrected in more than half of the calves (n = 43) by the calculated amount of bicarbonate, whereas the risk of failure to correct acidosis increases with D-lactate concentrations. The study shows that calves with elevated D-lactate concentrations do not need additional specific therapy, as D-lactate concentrations regularly fall following correction of acidosis and restitution of body fluid volume, for reasons that remain unclear. However, calves with distinct changes in posture and demeanour need higher doses of bicarbonate than calculated with the factor of 0.6 in the formula mentioned above probably because of D-hyperlactataemia.     

Investigations on the influence of serum D-lactate levels on clinical signs in calves with metabolic acidosis

Correlations between the degree of acidosis and clinical signs (changes in posture, behaviour, intensity of suckling reflex) in neonatal diarrhoeic calves have been described in various studies. However, base excess values varied widely in calves exhibiting similar clinical symptoms. The objective of this study was to elucidate whether the clinical picture of acidotic calves with neonatal diarrhoea is influenced more by D-lactate concentration than by degree of acidosis. Eighty calves up to three weeks old that were admitted to the II Medical Animal Clinic with acute diarrhoea and base excess values between -10 and -25 mmol/L were included in the prospective study. Posture, behaviour, suckling and palpebral reflexes, and position of the eyeballs were scored during the initial examination. Base excess and serum D-lactate and urea concentrations were determined in venous blood. In order to quantify the influences of base excess and d-lactate on the clinical parameters, groups of different clinical categories were compared. The results show that variations in behaviour, and in posture can be better explained by elevations of serum D-lactate concentrations than by decreases in base excess. Disturbances of the palpebral reflex appear to be almost completely caused by high levels of D-lactate.     

Significance of respiratory compensation in acidosis in calves

The respiratory component PvCO2 of acid-base-status was observed in n = 36 calves (age: x +/- s = 8.7 +/- 5.0 d) with neonatal diarrhea and an acidosis (venous blood-pH: < 7.30; x +/- s = 7.08 +/- 0.15). In n = 10 (28%) calves with a severe metabolic acidosis (pH: x +/- s = 7.03 +/- 0.12; BE: x +/- s = -22.1 +/- 5.3 mmol/l) the PvCO2 was decreased < 5.3 kPa (x +/- s = 4.5 +/- 0.5 kPa) and showed a distinct respiratory compensation. A PvCO2 between 5.3-6.7 kPa (x +/- s = 6.0 +/- 0.4 kPa) was observed in n = 16 (44%) acidotic calves (pH: x +/- s = 7.11 +/- 0.13; BE: x +/- s = -15.2 +/- 7.4 mmol/l). These n = 26 (72%) calves showed a simple metabolic acidosis which is well known for calves with neonatal diarrhea. The remaining n = 10 (28%) calves showed an increase of the PvCO2 > 6.7 kPa (x +/- s = 8.0 +/- 1.5 kPa). These animals had a mixed respiratory-metabolic acidosis (pH: x +/- s = 7.08 +/- 0.20; BE: x +/- s = -13.9 +/- 10.3 mmol/l), as the decrease of the pH could not be determined by the decreased metabolic component HCO3- of acid-base-status alone. Calves which died during hospitalization and calves with a PvCO2 > 6.7 kPa tended to be younger and showed partially significant lower values for the parameters of oxygen-supply PvO2 and SvO2. Lactate was significantly higher in dying calves but not in calves with a mixed acidosis which on the other hand were more dehydrated. The functional capacity of respiratory compensation of acidotic disorders in the calves studied promised to be almost the same as in dog and man. One reason for the failure of respiratory compensation in some calves could be a more severe hypovolemia. With the use of "venous hypoxemia" (decrease PvO2 and decrease SvO2) the detection of tissue hypoxia was easier than with lactate concentration.     

D-lactate production and excretion in diarrheic calves

The origin of D-lactate, the most important acid contributing to metabolic acidosis in the diarrheic calf, is unknown. We hypothesized that because D-lactate is produced only by microbes, gastrointestinal fermentation is the source. The objective of this study was to determine whether D-lactate production occurs in the rumen, colon, or both, and to measure D- and L-lactate concentrations in urine. Fecal, rumen, blood, and urine samples were obtained from 16 diarrheic and 11 healthy calves. Serum electrolyte concentrations were measured in both groups, and blood gas analyses were performed for diarrheic calves. All samples were analyzed for D- and L-lactate by high performance liquid chromatography (HPLC). Diarrheic calves were generally hyperkalemic with high serum anion gap, depressed serum bicarbonate, and low blood pH. L-lactate was markedly higher in rumen contents (22.7 mmol/ L [median]) and feces (8.6 mmol/L) of diarrheic calves than healthy calves (0.5 mmol/L and 5.1 mmol/L, respectively), but not different in serum or urine. Rumen, fecal, serum, and urine D-lactate concentrations were all significantly higher (P < .05) in diarrheic calves (17.0, 25.4, 13.9, and 19.2 mmol/L, respectively) than in healthy calves (0.5, 9.1, 1.4, and 0.5 mmol/L, respectively). Higher D-lactate concentrations in the rumen and feces of diarrheic calves suggests these sites as the source of D-lactate in blood and urine.     

D-Lactic acidosis in calves as a consequence of experimentally induced ruminal acidosis

In order to test the hypothesis that ruminal drinking in calves can lead to D-lactic metabolic acidosis, ruminal acidosis was induced in nine calves by intraruminal application of untreated whole milk via a stomach tube. The amount of the daily force-fed liquid was 3 x 1 l. The experimental design called for an end of intraruminal applications if two or more of the following signs were observed: severe depression, estimated degree of dehydration >10%, absence of sucking reflex, lack of appetite for two consecutive feedings, severe metabolic acidosis with calculated Actual Base Excess (ABE) <-15 mmol/l. The procedure was scheduled to be discontinued on the 17th day of experiment. The onset of ruminal acidification occurred rapidly, and mean pH value fell from 6.70 (+/-0.48) to 4.90 (+/-0.38) after the first application. The following days the pH values varied between 4 and 5. Rumen acidity was characterized biochemically by a significant increase in both isomers of lactic acid. The effects of the intraruminal administration on the calves were detrimental; eight of nine calves showed an acute disease process. According to the pre-established clinical standard, seven of nine calves were removed from the intraruminal feeding schedule. All but one of the calves developed severe systemic acidosis. The increase in anion gap demonstrated the net acid load. In all the calves D-lactate levels were found to show a significant and rapid increase. On the contrary, L-lactate never deviated from physiological levels. These observations confirm that, in young calves as in adult cattle, ruminal acidosis may lead to a clinically manifested D-lactic metabolic acidosis.     

Urinary GGT/creatinine ratio and fractional excretion of electrolytes in diarrhoeic calves

The aim of this study was to monitor renal function in diarrhoeic calves and to determine the effectiveness of an applied fluid therapy. A total of 28 diarrhoeic (n = 18) and healthy (n = 10) Holstein-Friesian calves of different sexes, between 1 and 30 days of age, were used. Blood and urine samples were obtained from diarrhoeic calves before the treatment and then three more times at 24-h intervals during the treatment. From healthy calves, samples were taken only once. Therapy was started by the intravenous administration of 8.4% sodium bicarbonate and 0.9% sodium chloride solutions for the first 24 h, followed by the oral application of a commercial electrolyte solution (sodium chloride 3.5 g, trisodium citrate 2.9 g, potassium chloride 1.5 g and glucose anhydrous 20 g in 1 litre H2O) up to the 48th h of therapy. Before the therapy, the average levels of pH (7.10 +/- 0.12), bicarbonate (HCO3-) (16.48 +/- 3.80 mmol/l), base deficit (-12.65 +/- 5.97 mmo/l) and fractional excretion (FE) of sodium (0.16 +/- 0.11%) and potassium (15.07 +/- 8.56%) were significantly lower while serum urea (17.48 +/- 10.32 mmol/l) and creatinine (Cr) concentrations (169.72 +/- 98.12 micromol/l), haematocrit levels (45.13 +/- 13.60%) and urinary gamma glutamyl transferase (GGT)/Cr ratio (8.6 +/- 4.3 x 1/10(3) U/micromol) were significantly higher in diarrhoeic calves than in healthy calves. Alterations in parameters indicating the presence of renal dysfunction were normalised in the diarrhoeic calves that survived (83.3%). Three calves with severe metabolic acidosis and azotaemia died at the beginning of therapy. It was concluded that the FE of Na and K (FENa, FEK) and urine GGT/Cr ratio may have an important role in assessing renal function in diarrhoeic calves and in evaluating the effectiveness of an applied fluid therapy.     

Anion gap correlates with serum D- and DL-lactate concentration in diarrheic neonatal calves

The objective of this study was to investigate the relationship between serum D- and L-lactate concentrations, and anion gap (AG) in neonatal calves. The association of AG with lactic acidosis in diarrheic calves has only been investigated by measurement of L-lactate in calves with experimentally induced diarrhea. D-lactate has recently been reported to be present in high concentrations in the serum of some diarrheic neonatal calves. The contribution of this acid to AG is not reported. The relationship between AG and L- and D-lactate concentrations was examined in 24 healthy calves and 52 calves with naturally occurring infectious diarrhea with metabolic acidosis. AG was calculated as [Na+ + K+] - [Cl- + HCO3-]. D- and L-lactate were quantified using high-performance liquid chromatography. There was no correlation between L-lactate and AG, contrary to previous reports in the literature. Moderate correlations between D-lactate concentration and AG (r = .74, P < .0001), and between DL-lactate and AG (r = .77), P < .0001) were detected. No differences existed due to the age or sex of the calf. This study indicates that AG provides information on the nature of acidosis in the diarrheic, neonatal calf and reinforces the importance of investigating clinical, in addition to experimental, populations.     

Acidosis and clinical condition in asphyctic calves

In depressed calves (modified APGAR score 4-6) there is at birth an evident combined respiratory-metabolic acidosis (pH = 7.082 +/- 0.175; pCO2 = 73.3 +/- 26.8 mm Hg; BE = -10.6 +/- 7.2 mmol/l). The metabolic adaptation is completed after 6 hours, the respiratory acidosis is present up to 24 hours after delivery. In comparison to normal calves there are significant deviations in pH-values, base excess standard bicarbonate and actual bicarbonate during the whole investigation time. The carbon dioxide tensions of the depressed calves are at birth similar to those of normal calves, but in the following hours they are significantly higher. A definite relationship can be demonstrated between the 1 minute APGAR score and pH-value, base excess, standard bicarbonate and actual bicarbonate. Oxygen tension, oxygen saturation and carbon dioxide do not correlate with the clinical condition.     

Metabolic profile of newborn calves and levels of immunoglobulins in the first days of life

After examination of the clinical state of 128 new-born calves, blood was collected from their vena jugularis for the determination of blood actual pH value, concentration of lactic acid, pCO2, base excess, buffer base and standard acid bicarbonate. The course and difficulty of parturition exerted a significant influence on the vitality of the calves and on the studied parameters of acid-base state. In the normally born calves, compared with those after dystocia, the following values were obtained: pH 7.20 +/- 0.03 : 7.11 +/- 0.07, pCO2 = 8.4 +/- 0.9 : 10.0 +/- 1.1 kPa, base excess -2.30 +/- 2.10 : 5.80 +/- 4.60 mmol/l, buffer base 43.0 +/- 2.4 : 39.5 +/- 6.5 mmol/l, standard acid bicarbonate 22.3 +/- 1.8 : 19.6 +/- 4.1 mmol/l and lactic acid concentration 5.6 +/- 2.0 : 10.7 +/- 5.1 mmol/l. The differences were statistically significant (P less than 0.05) and statistically highly significant (P less than 0.01). The continual study of the blood actual pH value and lactic acid concentration in the calves in the first 24 hours of life showed that with the same trend of changes in calves after dystocia the initial values were less favourable and that their normalization lasted longer. Attention is drawn to the importance of dystocia for the rise of respiratory metabolic acidosis and its effect on the vitality of newborn calves, and/or on their survival. The discussion deals with the importance of immunoglobulin levels in calves in the first days after birth for their further development. The determination of antibody content in colostral serum from the first milking in 33 and 29 cows on two farms showed great drawbacks in quality. A satisfactory level of IgG was found only in 36.36% and 58.62% of the cows, and a satisfactory level of IgM only in 12.12% and 24.13% of the studied cows. The determination of immunoglobulin content in their calves two to three days from birth (33 + 33 animals) showed normoglobulinemia only in 24.24% and 15.15% of cases. In 33 and 29 cows on two farms the colostrum serum from the first milking had an average content of immunoglobulins of class G amounting to 27.99 +/- 20.25 mg/ml and 36.95 +/- 21.62 mg/ml, and class M amounting to 3.64 +/- 1.25 and 2.04 +/- 1.42 mg/ml. Three days from birth, their calves had an IgG content of 4.25 +/- 2.57 mg/ml and 3.99 +/- 1.86 mg/ml and an IgM content of 0.30 +/- 0.20 and 6.38 +/- 0.25 mg/ml.     

Lactobacillus GG does not affect D-lactic acidosis in diarrheic calves, in a clinical setting

D-lactate, produced by gastrointestinal fermentation, is a major contributor to metabolic acidosis in diarrheic calves. Lactobacillus rhamnosus GG survives gastrointestinal transit in the neonatal calf and does not produce D-lactate. To determine whether this probiotic reduces gastrointestinal D-lactate production or severity of diarrhea or both, 48 calves (mean, 11 days old; range, 2-30 days) admitted to the clinic for treatment of diarrhea were randomly allocated to 2 groups. The experimental group was given Lactobacillus rhamnosus GG (1 x 10(11) cfu/d) PO, dissolved in milk or oral electrolyte solution, in addition to clinic treatment protocols; the other group served as a control. Serum and fecal samples were obtained at admission and at 24 and 48 hours after initial administration of Lactobacillus rhamnosus GG. All samples were analyzed for D- and L-lactate by using high-pressure liquid chromatography. Feces were also analyzed for pathogens, Lactobacillus rhamnosus GG recovery, and dry matter. D-lactic acidemia (>3 mmol/L) was present in 37/48 calves at admission. Lactobacillus rhamnosus GG was recovered in the feces of 13 experimental calves and 0 control calves 24 hours after administration. No difference in serum or fecal D- or L-lactate between the groups was detected at any time point. After therapy, D-lactic acidosis was absent at 48 hours in all but 1 calf. No relation between fecal pathogen (viral, bacterial, or protozoal) and degree of D-lactic acidosis was observed. The reduction in mortality and greater fecal dry matter in Lactobacillus rhamnosus GG-treated calves was not statistically significant.     

Iatrogenic hypocalcaemia during parenteral fluid therapy of diarrhoeic calves

Acid-base balance and electrolyte concentrations, including ionised calcium, were monitored during intravenous fluid therapy of 11 collapsed diarrhoeic suckler calves aged five to 10 days. Six healthy calves of similar age and type were used to provide control data. All the diarrhoeic calves were severely acidotic (TCO2<12 mmol/litre). Isotonic sodium bicarbonate (1-3 per cent) was administered until the metabolic acidosis was half corrected, as indicated by the TCO2 increasing to 17 to 24 mmol/litre when the infusion was changed to an extracellular volume replacement fluid containing 144 mmol/litre Na+, 35 mmol/litre HCO3-, 4 mmol/litre K+ and 113 mmol/litre Cl- which was administered until the calf was discharged. Milk feeding was started as soon as the calf had a suck reflex. The treatment was successful in 10 calves. At admission the diarrhoeic calves were hypocalcaemic compared with the control calves, but their ionised calcium was significantly higher, with significantly less calcium being protein bound. Treatment with isotonic sodium bicarbonate resulted in a significant improvement in acid-base balance, but both total and ionised calcium decreased significantly, the decrease in ionised calcium being proportionately greater owing partly to a significant increase in the protein binding of calcium. The mean total, bound and ionised calcium concentrations were all significantly lower in the treated calves after they had received isotonic sodium bicarbonate than in the control calves. Further treatment with replacement fluid had no significant effect on any of the parameters apart from pCO2 which increased significantly. Milk feeding had no significant effect on plasma calcium concentrations. The calves' mean ionised calcium concentration was significantly lower at the end of the treatment than before it, but there was no difference in the mean total and bound calcium concentrations. The calves' mean plasma potassium and magnesium concentrations decreased significantly during the course of the treatment.     

Relationships between acid-base balance, serum composition and colostrum absorption in newborn calves

Twenty-seven newborn Holstein bull calves were bottle-fed 2 litres of pooled colostrum which had been stored at -20 degrees C. Blood gas analysis before feeding showed a partially compensated respiratory acidosis in most of the calves, although they all appeared to be clinically normal. Mean venous blood pH was 7.346, carbon dioxide tension (PCO2) was 57.5 mmHg (7.6 kPa), bicarbonate was 30.6 mmol/l and base excess was 3.82 mmol/l. Mean serum IgG1 increased to 8.1 g/l after feeding colostrum. Several significant positive correlations were observed between post-absorptive serum protein, IgG1, IgM, gamma-glutamyltransferase (gamma GT) and D-xylose. Calves with either low serum albumin, high serum CK or low serum gamma GT before feeding tended to have less absorption of colostral protein. It was concluded that reduced absorption of IgG1 from colostrum is associated with hypercapnia in apparently healthy newborn calves.     

The prevalence and clinical relevance of hyperkalaemia in calves with neonatal diarrhoea

One hundred and twenty-four calves with neonatal diarrhoea were investigated in order to assess the prevalence of hyperkalaemia and the associated clinical signs. Hyperkalaemia (potassium concentration >5.8 mmol/L) was recognized in 42 (34%) calves and was more closely associated with dehydration than with decreases in base excess or venous blood pH. In 75 calves with normal blood concentrations of D-lactate (i.e. ?3.96 mmol/L), K concentrations were moderately correlated with base excess values (r = ?0.48, P < 0.001). In contrast, no significant correlation was observed in 49 calves with elevated D-lactate. Only three hyperkalaemic calves had bradycardia and a weak positive correlation was found between heart rate and K concentrations (r = 0.22, P = 0.014). Ten of the 124 calves had cardiac arrhythmia and of these seven had hyperkalaemia indicating that cardiac arrhythmia had a low sensitivity (17%) but a high specificity (96%) as a predictor of hyperkalaemia.In a subset of 34 calves with base excess values ??5 mmol/L and D-lactate concentrations <5 mmol/L (of which 22 had hyperkalaemia), changes in posture/ability to stand could be mainly explained by elevations of K concentrations (P < 0.001) and to a lesser extent by increases in L-lactate concentrations (P = 0.024). Skeletal muscle weakness due to hyperkalaemia alongside hypovolaemia may produce a clinical picture that is similar to that in calves with marked D-lactic acidosis. However, since reductions in the strength of the palpebral reflex are closely correlated with D-lactate concentrations, a prompt palpebral reflex can assist the clinical prediction of hyperkalaemia in calves presenting with a distinct impairment in their ability to stand (specificity 99%, sensitivity 29%).     

Bile acid concentrations in serum, bile and feces of healthy calves and calves with diarrhea

On 32 calves (age 3 to 14 days) with spontaneously occurring diarrhoea, the following investigations were carried out: Regular examination of serum bile acid concentrations, collection of the entire faeces with determination of bile acid concentrations, as well as microbiological examinations. Six clinically healthy calves served as control group. In addition, bile acids in bile were determined in 16 other calves of the same age group and in 6 beef bulls. There was no significant influence of daytime or feed intake on serum bile acid concentration in diarrhoeic or healthy calves. Possibly due to the low concentrations of bile acids in the bile of young calves (4.8 +/- 3.7 mmol/l, compared to 57 +/- 13 mmol/l in the bulls), the concentrations in faeces were also rather low (control group 623 +/- 92, calves with diarrhoea 318 +/- 277, after diarrhoea. 794 +/- 935 mumol/kg). Most of it was cholic acid, whereas only traces of desoxycholic acid were found. In spite of the comparatively low concentrations of fecal bile acids, the diarrhoeic calves excreted larger amounts of bile acids than the healthy calves (12.7 +/- 13.5 vs. 1.4 +/- 0.8 mumol/kg), but this was independent of the type of enteropathogen or pathogen combinations which were detected. There were no indications for a direct influence of the diarrhoea by bile acids. However, through enteral bile acid losses, profuse diarrhoea lasting several days can cause a reduction in the total bile acid pool.     

Effect of intravenous infusion of isotonic sodium bicarbonate solution on acidemic calves with diarrhea

The effect of 1.35% isotonic sodium bicarbonate solution (ISB) administered intravenously on acid-base equilibrium was examined in 18 acidemic Japanese black beef calves with spontaneous diarrhea. The infusion volumes of ISB were decided based on the first half volumes of base needed. In 72.2% (13/18) of calves, improvement of acidemia was detected. There was good correlation (r=0.693, p<0.01) between infused volume of ISB and changes in base excess (y=1.097x + 4.762). Infusion volumes of ISB were 7.5, 10.2, 12.9 and 15.7 ml/kg, respectively, enough to correcting the first half of 5, 10, 15 and 20 mEq/l of base deficit in acidemic calves. Our finding suggested that ISB could be used to correct metabolic acidosis without altering electrolyte concentrations in calves.     

Clinical efficacy of intravenous hypertonic saline solution or hypertonic bicarbonate solution in the treatment of inappetent calves with neonatal diarrhea

BACKGROUND: The clinical efficacy of IV administered hypertonic saline solution and hypertonic bicarbonate solution (HBS) in the treatment of inappetent diarrheic calves has not been compared yet. HYPOTHESIS: HBS is more advantageous than hypertonic saline in the treatment of calves with severe metabolic acidosis. ANIMALS: Twenty-eight dehydrated, inappetent calves with neonatal diarrhea. METHODS: In 2 consecutive clinical studies, calves were initially treated with saline (5.85%; 5 mL/kg body weight [BW] over 4 minutes; study I: N = 16) or bicarbonate solution (8.4%; 10 mL/kg BW over 8 minutes; study II: N = 12), respectively, followed by oral administration of 3 L isotonic electrolyte solution 5 minutes after injection. Clinical and laboratory variables were monitored for 72 hours. RESULTS: Treatment failed in 6 calves of study I and in 1 calf of study II as indicated by a deterioration of the general condition. All treatment failures had more severe metabolic acidosis compared with successfully treated calves before treatment. In the latter, rehydration was completed within 18 hours after injection; metabolic acidosis was corrected within 24 hours (study I) and 6 hours (study II) after injection. CONCLUSIONS AND CLINICAL IMPORTANCE: Diarrheic calves with slight metabolic acidosis (base excess [BE] >-10 mM) can be treated successfully with hypertonic saline. HBS is appropriate in calves without respiratory problems with more severe metabolic acidosis (BE up to -20 mM). Intensive care of the calves is required to ensure a sufficient oral fluid intake after the initial IV treatment.     

Qualification of the Stewart variables for the assessment of the acid-base status in healthy dogs and dogs with different diseases

Peter Stewart criticized the traditional theory of the acid-base status by Henderson-Hasselbalch as too simple and incomplete. He developed a new model with 3 independent variables: (1) pCO2, (2) SID (strong ion difference) and (3) Atot (Acid total). In healthy and ill dogs the diagnostic usefulness of both acid-base models were compared. This study included n=58 healthy dogs and 3 clinical cases of sick dogs.The age of the healthy dogs was 5.0 (2.0-7.0) years (= median (1.-3. quartil)).The 3 clinical cases included (1) a dog with septic shock, (2) with acute renal insufficiency, and (3) with hypovolaemic shock due to gastric torsion.Venous blood was taken of all dogs and the acid-base parameters were determined within < or =30 minutes. Electrolytes and albumin were determined in blood serum and used for calculation of the Stewart variables. Limits of reference intervals (x+/-1.96 - s) were determined for the healthy dogs yielding pCO2 = 3.6-6.5 kPa, [SID3] = 33.1-50.9 mmol/l resp. [SID4] = 31.8-49.6 mmol/l and [Al = 8.5-13.1 mmol/l. In Case 1 the Henderson-Hasselbalch parameters demonstrated the presence of a strong metabolic acidosis with mild respiratory influence (pH, [HCO3-], [BE] and PCO2 at upper range of normal). Analysis of the Stewart variables [SID3] resp. [SID4] revealed an electrolyte imbalance with [Cl-] and [lactate-] as the reason for metabolic acidosis. Case 2 showed a metabolic acidosis with respiratory compensation (pH, [HCO3-], [BE] and PCO2). Analysis of the Stewart variables with [SID3] resp. [SID4 caused by [K+], [Na+] and [lactate-]demonstrated the acidotic metabolism due to a renal malfunction. Case 3 had a metabolic acidosis (pH-value in the lower range) caused by electrolyte imbalances ([SID4]. The Stewart variables allow a better understanding of the causes of acid-base-disturbances in animals with implications for successful therapy via infusion.     

Effects of hypertonic sodium bicarbonate solution on electrolyte concentrations and enzyme activities in newborn calves with respiratory and metabolic acidosis

OBJECTIVE: To determine concentrations of electrolytes, total bilirubin, urea, creatinine, and hemoglobin; activities of some enzymes; and Hct and number of leukocytes and erythrocytes of newborn calves in relation to the degree of acidosis and treatment with a hypertonic sodium bicarbonate (NaHCO(3)) solution. ANIMALS: 20 acidotic newborn calves with a blood pH < 7.2 and 22 newborn control calves with a blood pH > or = 7.2. PROCEDURES: Approximately 10 minutes after birth, acidotic calves were treated by IV administration of 5% NaHCO(3) solution. The amount of hypertonic solution infused was dependent on the severity of the acidosis. RESULTS: Treatment resulted in a significant increase in the mean +/- SEM base excess from -8.4 +/- 1.2 mmol/L immediately after birth to 0.3 +/- 1.1 mmol/L 120 minutes later. During the same period, sodium concentration significantly increased from 145.3 +/- 0.8 mmol/L to 147.8 +/- 0.7 mmol/L. Mean chloride concentration before NaHCO(3) administration was significantly lower in the acidotic calves (99.6 +/- 1.1 mmol/L) than in the control calves (104.1 +/- 0.9 mmol/L). Calcium concentration in acidotic calves decreased significantly from before to after treatment. Concentrations of potassium, magnesium, and inorganic phosphorus were not affected by treatment. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of hypertonic NaHCO(3) solution to acidotic neonatal calves did not have any adverse effects on plasma concentrations of several commonly measured electrolytes or enzyme activities. The treatment volume used was smaller, compared with that for an isotonic solution, which makes it more practical for use in field settings.     

Effect of acute acidemia on blood biochemical variables in healthy ponies

L-Lactic acid and D,L-lactic acid infusion in ponies resulted in metabolic acidosis with high anion gap (AG). Increased AG was explained entirely by increased blood L- and D-lactate concentrations. Hydrochloric acid infusion caused metabolic acidosis with decreased AG. Saline (NaCl) infusion caused mild metabolic acidosis, with no significant change in AG. Plasma K+ concentration was decreased by all types of infusions, with a maximum of 0.50, 0.25, 0.40, 0.50 mmol/L below baseline at the end of infusion in the L-lactic acid-, D,L-lactic acid-, HCl-, and NaCl-infused ponies, respectively. Only hydrochloric acid had a tendency to increase plasma K+ concentration. Hypophosphatemia developed in NaCl- and HCl-infused ponies, but not in the D,L-lactic acid-infused ponies. Serum inorganic phosphate concentration in L-lactic acid-infused ponies increased initially, but was significantly (P less than 0.05) lower than values in the other ponies at 4 hours after onset of infusion. In ponies, the effect of acidemia on plasma K+ and serum inorganic phosphate concentrations was similar to that reported for other species. Changes were small in magnitude and depended on the nature of the acid anion. Results indicate that large changes in plasma K+ and serum inorganic phosphate concentrations during acidosis are probably not a direct result of acidemia.     

Evaluation of acid-base disturbances in calf diarrhoea

The severity of acid-base disturbances in diarrhoeic calves was investigated and a simple, inexpensive method of monitoring them was evaluated. The Harleco apparatus measures the 'total carbon dioxide' in a blood sample, mostly generated from the bicarbonate present, and any abnormalities are mainly due to metabolic acidosis or alkalosis. Its performance was tested against a standard blood gas analyser by comparing the results obtained by both methods with nearly 2000 blood samples from healthy or diarrhoeic calves. After technical modifications, the technique gave excellent precision and accuracy for the clinical evaluation of acid-base balance, using venous whole blood. The samples were very stable, especially at 0 degrees C, but also at room temperature. The normal range (mean +/- 1.96 sd) for total carbon dioxide in whole blood from calves was 21 to 28 mmol/litre. For samples corresponding to mild, moderate or severe acidosis, 79 per cent were correctly classified by the Harleco apparatus and only 0.1 per cent were beyond the adjacent degree of severity. After four days of diarrhoea, the calves which later died had twice the deficit in plasma bicarbonate of those which survived. As death approached, the deficit was almost three times that in surviving calves and the blood pH shortly before death was as low as 6.79 +/- 0.08. The Harleco apparatus was less successful with alkalotic samples, but metabolic alkalosis is less common and usually less severe.