Metabolic acidosis without clinical signs of dehydration in young calves

Metabolic acidosis without clinical signs of dehydration was diagnosed in four calves between nine and 21 days of age. In each calf either coma or depression with weakness and ataxia was observed. Two calves had slow deep respirations. Treatment with intravenous administration of solutions of sodium bicarbonate was accompanied by a rise in blood pH and a return to normal demeanor, ambulation and appetites, allowing these calves to return to their respective herds.     

Comparison of sodium bicarbonate and carbicarb for the treatment of metabolic acidosis in newborn calves

Carbicarb (an equimolar mixture of sodium bicarbonate and sodium carbonate) was compared with sodium bicarbonate alone for the treatment of acidosis in newborn calves: 25 of 49 calves with a blood pH at birth of less than 7-2 and a base deficit of less than -3 mmol/litre were treated intravenously with sodium bicarbonate and 24 were treated with carbicarb. The doses were calculated on the basis of the base deficit in a blood sample taken 10 minutes after birth, and further blood samples were taken immediately after the treatment and 30 and 60 minutes after the treatment for the determination of acid-base status, blood gases and haematological and biochemical variables. Both treatments resulted in a significant increase in blood pH, but there was no difference between them. The mean (sd) blood pH before treatment was 7.09 (0.02) and after treatment it was 7.28 (0.01). There was no increase in the partial pressure of carbon dioxide after treatment with either sodium bicarbonate or carbicarb. Both treatments were associated with an increase in sodium concentration and decreases in the total erythrocyte count, haematocrit and haemoglobin concentration.     

Dietary sodium bicarbonate as a treatment for exertional rhabdomyolysis in a horse

A 3-year-old mare repeatedly had clinical signs of rhabdomyolysis on mild exertion. Serum creatine kinase and aspartate transaminase activities were high at rest. Responses to dietary sodium bicarbonate were tested through 7 alternating periods of supplementation of a basal ration of timothy hay and oats. Physical signs; venous blood pH and gases; blood glucose and lactate; serum electrolytes, enzymes, and creatinine; and urine pH were monitored before and after exercise. Dietary sodium bicarbonate raised resting venous blood pH and bicarbonate slightly and significantly increased urine pH from pH 7.46 to 8.2 (P less than 0.001). An exercise test included 5 minutes at the walk followed by 20 minutes at the trot. The exercise induced gait stiffness, muscle fasciculations, and muscle induration when the diet was not supplemented, but not when it was supplemented with sodium bicarbonate. Myoglobin was present in 16 of 21 urine samples after exercise during nonsupplemented periods, but only in 3 of 28 urine samples during supplemented periods (P less than 0.0001). Bicarbonate supplementation significantly decreased the responses of blood lactic acid, serum creatine kinase, and aspartate transaminase to exercise. Supplementation of the diet was associated with higher venous blood pH and bicarbonate ion concentrations throughout exercise. Dietary sodium bicarbonate apparently mitigated or prevented physical, chemical, and enzymatic characteristics of exertional rhabdomyolysis in this mare, possibly through its enhancement of buffering capacity in muscle tissue fluids.     

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.     

Clinical evaluation of sodium bicarbonate, sodium L-lactate, and sodium acetate for the treatment of acidosis in diarrheic calves

Thirty-six dehydrated diarrheic neonatal calves were used to study the effects of various alkalinizing compounds on acid-base status, the changes in central venous pressure (CVP) in response to rapid IV infusion of large volumes of fluid, and the correlation of acid-base (base deficit) status, using a depression scoring system with physical determinants related to cardiovascular and neurologic function. Calves were allotted randomly to 4 groups (9 calves/group). Over a 4-hour period, each calf was given two 3.6-L volumes (the first 3.6 L given in the first hour) of a polyionic fluid alone (control group) or were given the polyionic fluid with sodium bicarbonate, sodium L-lactate, or sodium acetate added (50 mmol/L). Acid-base status, hematologic examination, and biochemical evaluations were made immediately before infusion of each fluid (at entry) and after 3.6, 4.8, and 7.2 L of fluid had been given. Compared with control values, bicarbonate, lactate, and acetate had significantly greater alkalinizing effects on pH (P less than 0.01) and base deficit (P less than 0.01) after 3.6, 4.8, and 7.2 L of fluid were given. Bicarbonate had the most rapid alkalinizing effect and induced greater changes in base deficit (P less than 0.01) than did acetate or lactate at each of the 3 administered fluid volumes evaluated. Acetate and lactate had similar alkalinizing effects on blood. Rehydration alone did not improve acid-base status. The CVP was elevated in 10 (28%) of the 36 calves after 1 hour of fluid (3.6 L) administration, but significant differences in body weight, PCV, and clinical condition or depression score at entry were not found between calves with elevated CVP and those with normal CVP.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Evaluation of the Total Carbon Dioxide Apparatus and pH Meter for the Determination of Acid-Base Status in Diarrheic and Healthy Calves

Three simple tests of acid-base status were evaluated for field use. Blood samples were collected from 20 diarrheic and 24 healthy calves less than six weeks of age. One sample was collected anaerobically and immediately analyzed on a blood gas analyzer. The other samples were used for measurement of blood and serum pH using a pH meter and pH paper, and for serum total carbon dioxide (TCO₂) using a TCO₂ apparatus. The TCO₂ apparatus gave the best results and would be useful in the field. TCO₂ apparatus measurements had a high correlation, r=0.91, with blood gas analyzer blood bicarbonate values. Healthy calves have a serum TCO₂ content of 30 mmol/L and bicarbonate requirements for correcting metabolic acidosis in diarrheic calves can be calculated:

Bicarbonate required (mmol) = (30-TCO₂) × Body Weight × 0.6 This can be converted to grams of sodium bicarbonate by dividing by 12.

     

Effects of electrolyte solutions for oral administration on clotting of milk.

The effect of electrolyte solutions commercially formulated for oral administration on clotting of milk was investigated in vitro. Rennet or abomasal fluid was used as the clotting agent. Electrolyte solutions that contained large amounts of bicarbonate or citrate (greater than 40 mEq/L) had marked adverse effects on milk clotting, probably because bicarbonate increased pH and because citrate chelated calcium. Addition of solutions that did not contain alkalinizing agents resulted in normal or enhanced clotting, and enhancement was associated with the presence of acid phosphate salts. Electrolyte solutions that included acetate as the alkalinizing agent did not interfere with milk clotting as long as pH of the final solution was acidic and minimal amounts of citric acid salts were present (less than 10 mEq/L). Acetate-containing electrolyte solutions can be used for oral administration in calves in which alkalinization of blood without interference with milk clotting is desired.     

Correction of metabolic acidosis in diarrheal calves by oral administration of electrolyte solutions with or without bicarbonate

Acid-base balance was evaluated in calves with experimentally induced viral diarrhea. When blood pH decreased to less than 7.200, calves were assigned to treatment groups and fed milk replacer, electrolyte solution without bicarbonate, or electrolyte solution containing bicarbonate. Calves in the electrolyte treatment groups had lower mortality (P less than 0.05), were better hydrated (P less than 0.05), and were less acidotic (P less than 0.05) than calves fed milk replacer. Bicarbonate-containing electrolyte solution restored acid-base balance (P less than 0.05) and corrected depression better (P less than 0.05) than electrolyte solution that did not contain bicarbonate. Both electrolyte solutions were equally good at correcting dehydration.     

Decreased colostral immunoglobulin absorption in calves with postnatal respiratory acidosis

The effect of postnatal acid-base status on the absorption of colostral immunoglobulins by calves was examined in 2 field studies. In study 1, blood pH at 2 and 4 hours after birth was related to serum IgG1 concentration 12 hours after colostrum feeding (P less than 0.05). Decreased IgG1 absorption from colostrum was associated with respiratory, rather than metabolic, acidosis, because blood PCO2 at 2 and 4 hours after birth was negatively related to IgG1 absorption (P less than 0.05), whereas serum bicarbonate concentration was not significantly related to IgG1 absorption. Acidosis was frequently observed in the 30 calves of study 1. At birth, all calves had venous PCO2 value greater than or equal to 60 mm of Hg, 20 of the calves had blood pH less than 7.20, and 8 of the calves had blood bicarbonate concentration less than 24 mEq/L. Blood pH values were considerably improved by 4 hours after birth; only 7 calves had blood pH values less than 7.20. Calves lacking risk factors for acidosis were examined in study 2, and blood pH values at 4 hours after birth ranged from 7.25 to 7.39. Blood pH was unrelated to IgG1 absorption in the calves of study 2. However, blood PCO2 was again found to be negatively related to colostral IgG1 absorption (P less than 0.005). Results indicate that postnatal respiratory acidosis in calves can adversely affect colostral immunoglobulin absorption, despite adequate colostrum intake early in the absorptive period.     

Sepsis and bacterial suppurative meningitis-meningoencephalitis in critically ill neonatal Piedmontese calves: clinical approach and laboratory findings

Sepsis (S) and bacterial suppurative meningitis-meningoencephalitis (M-ME) are common causes of death in bovine neonates. The aim of this prospective study was to evaluate the prevalence of S and M-ME in critically ill neonatal Piedmontese calves. Critically ill animals up to 15 days old referred by practitioners were registered according to their status and subsequently assigned to clinical standardized score. Calves with a clinical score > = 5 were further assessed under a clinical and clinical-pathological protocol to strengthen the suspicion of S and M-ME. Critically ill neonatal calves sent for necropsy were included in the study as well. Fifty-nine calves were investigated, 26 of which referred alive and 33 dead. Ten out of the 26 clinically evaluated calves were classified as suspicious of S on the basis of the clinical and clinical-pathological protocols. S was confirmed by positive bacteriologic culture in 7 cases and in 3 cases on the basis of necroptic lesions. Concomitant suppurative M-ME suspected in 6 of these 10 calves was subsequently confirmed by CSF analysis or histological findings. Of the 33 calves examined only post-mortem, 20 showed pathognomonic findings of S and 14 signs of M-ME. The prevalence of S and M-ME was 46 and 36 %, respectively. Clinical signs of S were confirmed to be vague and overlapping with other diseases. The developed protocol was highly accurate in predicting S in these neonatal calves.     

Infusion of sodium bicarbonate in experimentally induced metabolic acidosis does not provoke cerebrospinal fluid (CSF) acidosis in calves

In a crossover study, 5 calves were made acidotic by intermittent intravenous infusion of isotonic hydrochloric acid (HCl) over approximately 24 h. This was followed by rapid (4 h) or slow (24 h) correction of blood pH with isotonic sodium bicarbonate (NaHCO(3)) to determine if rapid correction of acidemia produced paradoxical cerebrospinal fluid (CSF) acidosis. Infusion of HCl produced a marked metabolic acidosis with respiratory compensation. Venous blood pH (mean ± S(x)) was 7.362 ± 0.021 and 7.116 ± 0.032, partial pressure of carbon dioxide (Pco(2), torr) 48.8 ± 1.3 and 34.8 ± 1.4, and bicarbonate (mmol/L), 27.2 ± 1.27 and 11 ± 0.96; CSF pH was 7.344 ± 0.031 and 7.240 ± 0.039, Pco(2) 42.8 ± 2.9 and 34.5 ± 1.4, and bicarbonate 23.5 ± 0.91 and 14.2 ± 1.09 for the period before the infusion of hydrochloric acid and immediately before the start of sodium bicarbonate correction, respectively. In calves treated with rapid infusion of sodium bicarbonate, correction of venous acidemia was significantly more rapid and increases in Pco(2) and bicarbonate in CSF were also more rapid. However, there was no significant difference in CSF pH. After 4 h of correction, CSF pH was 7.238 ± 0.040 and 7.256 ± 0.050, Pco(2) 44.4 ± 2.2 and 34.2 ± 2.1, and bicarbonate 17.8 ± 1.02 and 14.6 ± 1.4 for rapid and slow correction, respectively. Under the conditions of this experiment, rapid correction of acidemia did not provoke paradoxical CSF acidosis.     

The alkalinizing effects of metabolizable bases in the healthy calf.

The alkalinizing effect of citrate, acetate, propionate, gluconate, L and DL-lactate were compared in healthy neonatal calves. The calves were infused for a 3.5 hour period with 150 mmol/L solutions of the sodium salts of the various bases. Blood pH, base excess, and metabolite concentrations were measured and the responses compared with sodium bicarbonate and sodium chloride infusion. D-gluconate and D-lactate had poor alkalinizing abilities and accumulated in blood during infusion suggesting that they are poorly metabolized by the calf. Acetate, L-lactate and propionate had alkalinizing effects similar to bicarbonate, although those of acetate had a slightly better alkalinizing effect than L-lactate. Acetate was more effectively metabolized because blood acetate concentrations were lower than L-lactate concentrations. There was a tendency for a small improvement in metabolism of acetate and lactate with age. Sodium citrate infusion produced signs of hypocalcemia, presumably because it removed ionized calcium from the circulation. D-gluconate, D-lactate and citrate are unsuitable for use as alkalinizing agents in intravenous fluids. Propionate, acetate and L-lactate are all good alkalinizing agents in healthy calves but will not be as effective in situations where tissue metabolism is impaired.     

Comparison of the measurement of total carbon dioxide and strong ion difference for the evaluation of metabolic acidosis in diarrhoeic calves

Eighty-four calves with diarrhoea were treated with fluids and 13 apparently healthy calves of similar ages were sampled as controls. Their total blood carbon dioxide (TCO2) was measured with a Harleco apparatus and 31 of the calves were treated with oral fluids and 53 with parenteral fluids. The oral fluid contained 118 mmol/litre Na+, 25 mmol/litre K+, 110 mmol/litre glucose, 108 mmol/litre bicarbonate (HCO3- as citrate), 43 mmol/litre Cl-, 4 mmol/litre Ca++, 4 mmol/litre Mg++ and 20 mmol/litre glycine, and the parenteral fluid contained 144 mmol/litre Na+, 4 mmol/litre K+, 35 mmol/litre HCO3- and 113 mmol/litre Cl-. Both treatments resulted in significant improvements in acid-base status as demonstrated by an increase in TCO2, and the treatment was successful in 27 of the 31 calves receiving oral fluids and in 45 of the 53 calves receiving parenteral fluids. Thirty-seven of the calves treated parenterally were very severely acidotic (TCO2 <8 mmol/litre) initially and they received an additional 400 mmol HCO3- added to the first 5 litres of infusion. Treatment was successful in 33 of these calves. The decision to administer additional bicarbonate was made on the basis of their acid-base status as measured with a Harleco apparatus. The strong ion difference (Na++K+-Cl-) (SID) of the calves was calculated retrospectively. There was a significant correlation between the SID and TCO2 of the calves treated with oral fluids but not among the control calves or the calves treated parenterally. Furthermore, measurements of the change in SID during therapy gave little indication of the change in acid-base status as measured by the Harleco apparatus, with the SID decreasing (suggesting a worsening of acid-base status) in 16 calves in which the TCO2 increased (suggesting an improvement in acid-base status). There was a significant correlation between the change in SID and the change in TCO2 during treatment in the calves receiving oral fluids but not in the calves treated parenterally.     

Suspected renal tubular acidosis in two dogs

Clinical signs of hyperventilation, muscle weakness and lethargy were recognised in a one-year-old female Bichon Frise and a three-year-old male Poodle. One dog was also hyperexcitable and pyrexic. The diagnosis of renal tubular acidosis was confirmed by demonstrating the tendency to an elevated urine pH, a low blood pH and low blood bicarbonate level, and by eliminating other causes of metabolic acidosis. Both dogs were treated with oral sodium bicarbonate resulting in improvement in their clinical condition and a return to near normal blood pH and bicarbonate levels.     

Suspected renal tubular acidosis in two dogs

Clinical signs of hyperventilation, muscle weakness and lethargy were recognised in a one-year-old female Bichon Frise and a three-year-old male Poodle. One dog was also hyperexcitable and pyrexic. The diagnosis of renal tubular acidosis was confirmed by demonstrating the tendency to an elevated urine pH, a low blood pH and low blood bicarbonate level, and by eliminating other causes of metabolic acidosis. Both dogs were treated with oral sodium bicarbonate resulting in improvement in their clinical condition and a return to near normal blood pH and bicarbonate levels.     

Blood bactericidal assay (Pasteurella haemolytica) comparison of morbidity in marketed feeder calves

An in vitro bactericidal assay that used bovine heparinized blood was investigated for its usefulness in detecting differences in the bactericidal immunity of calves against Pasteurella haemolytica serotype 1 (Ph1). Greater than 90% of killing occurred within 30 minutes. The substitution of fetal calf serum for autologous calf plasma caused loss of bactericidal activity of the blood. Decomplemented calf serum also was low in bactericidal activity. The blood bactericidal assay appears to be opsonin antibody-dependent and complement-dependent. The coefficient of variation (CV) that can be expected with this assay was established by use of a group of 8 calves; within-day CV maximum was 0.9, and between-day CV maximum was 2.1. The blood bactericidal assay was used to evaluate 30 calves under typical market stress from 4 farms in eastern Tennessee. All calves had decreased bactericidal activity, as they moved into a feedyard in Texas. The bactericidal activity was reduced among sick calves, based on the severity of clinical signs. Morbidity was highest during the first 14 days in the feedlot. During this period, healthy calves had a decreased bactericidal index (BI) of 4 points, and calves with clinical signs of bovine respiratory tract disease for 3 days had a decreased BI of 8 points. The average reduction in the BI of calves with clinical signs of bovine respiratory tract disease for 6 or more days was 14 points.     

Blood gas and acid-base analysis of arterial blood in 57 newborn calves

The pH, partial pressure of oxygen (pO(2)), partial pressure of carbon dioxide (pCO(2)), concentration of bicarbonate (HCO(3)(-)), base excess and oxygen saturation (SO(2)) were measured in venous and arterial blood from 57 newborn calves from 55 dams. Blood samples were collected immediately after birth and 30 minutes, four, 12 and 24 hours later from a jugular vein and a caudal auricular artery. The mean (sd) pO(2) and SO(2) of arterial blood increased from 45.31 (16.02) mmHg and 64.16 (20.82) per cent at birth to a maximum of 71.89 (8.32) mmHg and 92.81 (2.32) per cent 12 hours after birth, respectively. During the same period, the arterial pCO(2) decreased from 57.31 (4.98) mmHg to 43.74 (4.75) mmHg. The correlation coefficients for arterial and venous blood were r=0.86 for pH, r=0.85 for base excess and r=0.76 for HCO(3)(-). The calves with a venous blood pH of less than 7.2 immediately after birth had significantly lower base excess and HCO(3)(-) concentrations for 30 minutes after birth than the calves with a venous blood pH of 7.2 or higher. In contrast, the arterial pO(2) was higher in the calves with a blood pH of less than 7.2 than in those with a higher pH for 30 minutes after birth.     

Abdominal distension in collapsed diarrhoeic calves: biochemical findings and treatment.

Thirty-seven of 53 diarrhoeic calves hospitalised for intravenous fluid therapy were classified as very severely acidotic (total carbon dioxide less than 8 mmol/litre) by using a Harleco apparatus. All the calves were given intravenously 10 to 20 litres of electrolyte solution which contained 144 mmol/litre sodium, 4 mmol/litre potassium, 113 mmol/litre chloride and 35 mmol/litre bicarbonate, and in addition the 37 very severely acidotic calves received 400 ml of 1M sodium bicarbonate in the first 5 litres of fluid administered. Sixteen of the 37 very severely acidotic calves had a distended right flank, suggesting the presence of a dilated fluid-filled viscus. Neither their history nor other clinical signs were useful predictors of the distension. The distended calves had significantly higher plasma concentrations of sodium and chloride, and significantly lower plasma creatinine concentrations than the calves which were not distended. Treatment was successful in all the 21 non-distended calves but four of the distended calves died despite treatment. The resolution of the distension in the successfully treated calves, coincided with a significant increase in plasma bicarbonate concentration and the passage of large amounts of malodorous mucoid faeces.     

The comparative effectiveness of three commercial oral solutions in correcting fluid, electrolyte and acid-base disturbances caused by calf diarrhoea.

Three commercial oral rehydration solutions (Effydral ('E'), Lectade ('L') and Lectade Plus ('LP')) were evaluated in young calves with diarrhoea following the administration of E. coli. Twenty calves with non-fatal diarrhoea were included in each group and examined for electrolytes, acidosis (pH, PCO2 and TCO2), PCV and selected biochemical parameters. Faecal consistency and clinical state were also assessed. Eight calves were examined for plasma and ECF volume. Calves were treated with the appropriate ORS only for 2 days and with ORS plus milk substitute for a further 2 days. No other treatments were given. Solutions E, L and LP were chosen specifically to test the hypothesis that their ability to repair extracellular volume would depend on their sodium content (E > L > LP) and their ability to correct metabolic acidosis would reflect their content of bicarbonate precursor (E > LP > L). Both hypotheses were confirmed as was the fact that the higher sodium content of E helps it to repair ECF volume without predisposing to hypernatraemia. The importance of correcting hyponatraemia as well as ECF volume is emphasized. Direct measurement of such changes proved much more sensitive than traditional clinical parameters such as weight loss, skin elasticity, etc. Although this study was not designed to examine mortality, it is noted that nine treated calves died, none in the E-treated group.