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.     

Metabolic acidosis in diarrheic calves: the importance of alkalinizing agents in therapy

Metabolic acidosis is one of the prime factors responsible for the death of many diarrheic calves. This article begins with a general discussion about the recognition of metabolic acidosis. The remaining sections detail the utilization of certain subjective and objective methods to assess the severity of acidosis as well as the approach to treatment of this metabolic condition.     

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.     

Effect of suckling an isotonic solution of sodium acetate, sodium bicarbonate, or sodium chloride on abomasal emptying rate and luminal pH in calves

OBJECTIVES: To compare abomasal emptying rates in calves after suckling milk replacer or 3 common orally administered electrolyte solution components. ANIMALS: 5 male calves < 35 days of age. PROCEDURES: Calves with a cannula fitted in the abomasal body were fed 2 L of milk replacer with or without parenteral administration of atropine (0.01 mg/kg, i.v., then 0.02 mg/ kg, s.c., q 30 min) or isotonic (150 mM) solutions of sodium acetate, NaHCO(3), or NaCl in a randomized crossover design. Abomasal emptying rates were determined via scintigraphy, acetaminophen absorption, ultrasonography, and change in abomasal luminal pH. RESULTS: Scintigraphic half-emptying time, time of maximal plasma acetaminophen concentration, ultrasonographic half-emptying time, and pH return time indicated similar abomasal emptying rates following suckling of isotonic sodium acetate, NaHCO(3), and NaCl solutions, whereas the emptying rate of milk replacer was significantly slower. Mean maximal abomasal luminal pH was highest following suckling of NaHCO(3) (pH(max)=7.85) and lowest following suckling of NaCl (pH(max)=4.52); sodium acetate (pH(max)=6.59) and milk replacer (pH(max)=5.84) yielded intermediate pH values. CONCLUSIONS AND CLINICAL RELEVANCE: Isotonic solutions of sodium acetate, NaHCO(3), and NaCl were rapidly emptied from the abomasum but varied markedly in their ability to alkalinize the abomasum. Sodium bicarbonate-containing orally administered electrolyte solution might increase the frequency of infection or severity of clinical disease in diarrheic calves treated for dehydration by causing prolonged abomasal alkalinization.     

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.     

Severity and nature of acidosis in diarrheic calves over and under one week of age

A prospective study of the severity of dehydration and acidosis was carried out in 42 calves under 35 days of age presented for treatment of neonatal diarrhea. Clinically the mean level of dehydration was 8 to 10%. The plasma volume was 65% of that in the hydrated calf but the calves only gained 6.5% in weight during therapy.

Calves under eight days of age often had a lactic acidosis. Blood pH was 7.118±0.026 (mean ± 1 standard error), bicarbonate concentration 18.8±1.3 mmol/L, base deficit 11.4±1.7 mmol/L and lactate of 3.6± 0.06 mmol/L. Calves over eight days usually had a nonlactic acidosis. Blood pH was 7.042±0.021, bicarbonate 10.8±1.0 mmol/L, base deficit 19.5±1.2 mmol/L and lactate 1.2±0.3 mmol/L. These values were all significantly different from those in younger calves.

Over all calves there was a poor correlation between the severity of acidosis and dehydration(r=0.05). The severity of lactic acidosis was related to the severity of dehydration. Mean bicarbonate requirements to correct acidosis were calculated to be 200 mmol(17 g of sodium bicarbonate)and 450 mmol(37 g of sodium bicarbonate)in calves under and over eight days of age respectively. Both groups of calves required a mean volume of 4L of fluid to correct dehydration.

     

A retrospective study of the relationship between clinical signs and severity of acidosis in diarrheic calves

A retrospective study of 123 calves under two months of age with signs of diarrhea was performed to investigate the relationships among the calf's demeanor, dehydration, rectal temperature, and base deficit. The severity of dehydration, hypothermia, and metabolic acidosis were associated with level of depression. Clinical signs and age of calf could be used to predict the severity of acidosis. Acidosis was more severe in calves over eight days of age and also increased in severity with the degree of depression. The most severe metabolic acidosis was seen in calves over eight days of age presented in sternal or lateral recumbency; the base deficit in these groups was 16.3 ± 8.3 (means ± 1SD) and 20.3 ± 10.1 mmol/L respectively, and on average these calves require 2.4 and 3.0 L respectively of 1.3% sodium bicarbonate solution to correct the acidosis.     

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.     

Evaluation of isotonic sodium bicarbonate solution for alkalizing effects in conscious calves

After intravenous (i.v.) infusion of various volumes of 1.35%-isotonic sodium bicarbonate solution (ISB), acid-base equilibrium, blood pressure, plasma volume and biochemical parameters in healthy Holstein calves were studied. Four calves each were randomly assigned to the low-dose (LD; i.v. infusion of 5 ml/kg ISB), middle-dose (MD; i.v. infusion of 10 ml/kg ISB) and the high-dose groups (HD; i.v. infusion of 15 ml/kg ISB). Administration volumes of ISB in the LD, MD and HD groups were decided based on the first half volumes of 5, 10 and 15 mEq of base requirement by the acceptable equation. Systemic, pulmonary artery and central venous pressures, cardiac output and plasma osmotic pressure were not changed by ISB infusion and remained constant throughout the experiment for all groups. There was good correlation (r(2) = 0.950) between relative changes in base excess and infused volume of bicarbonate (y=2.491x). The coefficient of distribution for bicarbonate ions was calculated to be 0.401 (=1/2.491). Therefore, it is suggested that a value of 0.4 would be most appropriate when calculating the base requirements in calves. Therefore, the first half volumes of ISB correcting base deficits of 5, 10 and 15 mEq in calves were estimated to be 6, 12 and 18 ml/kg, respectively. On the basis of the findings in this study, ISB may be used to correct metabolic acidosis without altering the plasma osmotic pressure, hemodynamic status and respiratory function in the calves.     

Effects of intravenous sodium bicarbonate and sodium acetate on equine acid-base status

Changes in blood gases, pH, and plasma electrolyte concentrations in response to intravenously infused sodium bicarbonate (NaHCO₃) and sodium acetate (NaCH₃CO₂) solutions (1.34 mEq/mL) in 5 light breed mares were investigated. Jugular venous blood samples were collected before and after completion of the infusions in 20-minute intervals for 200 minutes. Infusion of sodium bicarbonate and sodium acetate caused significant (P < .00l) increases in blood pH and bicarbonate ion concentration that persisted throughout the collection period. The elevation in blood pH and bicarbonate ion concentrations was greater (P < .01) for sodium bicarbonate than for sodium acetate immediately after the completion of the infusions but was not different (P > .05) thereafter. There were significant reductions (P < .01) in plasma-ionized calcium and potassium after infusion of both sodium bicarbonate and sodium acetate. This study found that significant metabolic alkalosis in horses and corresponding shifts in electrolyte concentrations can be induced by intravenous infusion of solutions of either sodium bicarbonate or sodium acetate, and they persist for at least 3 hours. These data show that the short-term elevation in pH and bicarbonate ion concentration is momentarily higher after infusion of sodium bicarbonate. This is likely due to the direct infusion of bicarbonate ions in the sodium bicarbonate treatment, such that further metabolism is not required to be effective. However, the longer-term alkalosis did not differ between isomolar solutions of sodium bicarbonate and sodium acetate.     

A comparison of three oral electrolyte solutions in the treatment of diarrheic calves

Thirty-six diarrheic calves infected with rota- and coronaviruses were randomly allocated to one of three oral electrolyte treatments: Ion-Aid (Syntex Agribusiness), Life-Guard (Norden Inc), or Revibe (Langford Inc). The calves were also allowed voluntary access to milk which was offered at the rate of 5% of body weight per feeding in two feedings daily. There were significant differences in recovery rate among calves treated with the different electrolytes. Only 33% of Ion-Aid-treated calves recovered; Revibe- and Life-Guard-treated calves had high recovery rates of 92% and 83%, respectively. The much higher recovery rates with Life-Guard and Revibe were attributed to the presence of an alkalizing agent in these preparations. Life-Guard uses bicarbonate to counteract acidosis and there was some evidence that this may have interfered with milk digestion. Revibe uses acetate; this was effectively metabolized within the calves' tissues and produced alkalization without interference with milk digestion.     

Effects of sodium acetate, bicarbonate and lactate on acid-base status in anaesthetized dogs

Equal doses of sodium acetate, bicarbonate and lactate (6.6 mEq/L) infused intravenously over 30 min into three groups of halothane-anaesthetized dogs caused changes in acid-base status. Arterial carbon dioxide tension (PaCO2), pHa, base excess (BE) and standard bicarbonate (SB) increased. Sodium bicarbonate caused the most rapid and greatest changes. The bicarbonate group was significantly different (P less than 0.05) from the other groups at 15 and 30 min after the start of infusion for pHa, BE and SB. The greater effects of bicarbonate are due to its production of alkalinization without a requirement for metabolism; acetate and lactate require oxidation to be effective. The acetate and bicarbonate groups were not statistically different at 45 min after the onset of drug infusion, but both had significantly higher SB and BE mean values than the lactate group. All measurements made after 45 min revealed no significant differences among groups. Thus, after the earlier differences noted above, the three alkalinizers caused similar effects on acid-base status. PaCO2 was elevated in all groups, but there were no differences among groups. Cardiovascular effects caused by infusion of the three drugs were minimal.     

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.     

Clinical application of 2.16% hypertonic saline solution to correct the blood sodium concentration in diarrheic calves with hyponatremia

The aim of this study was to examine whether 2.16% hypertonic saline solution (HSS) is useful for the treatment of diarrheic calves with hyponatremia. Eleven of 13 female Holstein calves exhibiting moderate diarrhea and hyponatremia received 1,250 ml of 2.16% HSS over 15 min regardless of body weight. The remaining two calves that were unable to stand and had severe hyponatremia received 2,500 ml of 2.16% HSS intravenously over 30 min. As a result, hyponatremia in all diarrheic calves was significantly improved by the administration of 2.16% HSS from 122.2 ± 7.0 mEq/l at pre to 134.8 ± 3.7 mEq/l at post, which was above the threshold of 132 mEq/l for hyponatremia. Therefore, 2.16% HSS may be useful for hyponatremia in calves with diarrhea.     

Fluid therapy for diarrheic calves. What, how, and how much

The pathophysiologic consequences of neonatal diarrhea in calves are presented. A brief discussion of intestinal function, nutrient absorption, and osmolar effects follows. A rationale for appropriate fluid therapy is presented, and comparison of some currently marketed products are made.