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Determining lactate concentrations in Korean indigenous calves and evaluating its role as a predictor for acidemia in calf diarrhea

BMC Veterinary Research volume 20, Article number: 373 (2024) Cite this article

Abstract

Background

Calf diarrhea leads to high mortality rates and decreases in growth and productivity, causing negative effects on the livestock industry. Lactate is closely associated with metabolic acidosis in diarrheic calves. However, there have been no reports on lactate concentrations in Korean indigenous (Hanwoo) calves, especially those with diarrhea. This study aimed to determine the reference range of L-lactate and D-lactate concentrations in Hanwoo calves and to better understand the utility of lactate as predictive factors for acidemia in diarrheic calves.

Results

L-lactate and D-lactate concentrations were measured in healthy (n = 44) and diarrheic (n = 93) calves, and blood gas analysis was performed on diarrheic calves. The reference range in healthy calves was 0.2–2.25 mmol/L for L-lactate and 0.42–1.38 mmol/L for D-lactate. Diarrheic calves had higher concentrations of L-lactate and D-lactate than healthy calves. In diarrheic calves, L-lactate and D-lactate each had weak negative correlation with pH (r = − 0.31 and r = − 0.35). In diarrheic calves with hyper-L-lactatemia, the combined concentrations of L-lactate and D-lactate had moderate correlation with pH (r = − 0.51) and anion gap (r = 0.55). Receiver operating characteristic analysis showed D-lactate had fair predictive performance (AUC = 0.74) for severe acidemia, with an optimal cut-off value of > 1.43 mmol/L. The combined concentrations of L-lactate and D-lactate showed fair predictive performance for predicting acidemia (AUC = 0.74) and severe acidemia (AUC = 0.72), with cut-off values of > 6.05 mmol/L and > 5.95 mmol/L.

Conclusions

The determined reference ranges for L-lactate and D-lactate in Hanwoo calves enable the identification of hyper-L-lactatemia and hyper-D-lactatemia. Diarrheic calves exhibited increased lactate concentrations correlated with acid-base parameters. While the concentrations of L-lactate and D-lactate have limitations as single diagnostic biomarkers for predicting acidemia or severe acidemia, their measurement remains important, and L-lactate has the advantage of being measurable at the point-of-care. Assessing lactate concentrations should be considered by clinicians, especially when used alongside other clinical indicators and diagnostic tests. This approach can improve calf diarrhea management, contributing positively to animal welfare and providing economic benefits to farms.

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Background

Lactate is an organic acid produced as the final product of the anaerobic metabolism of pyruvate during glycolysis. It exists in two enantiomeric forms, D-lactate and L-lactate. These forms are generated from pyruvate through the action of lactate dehydrogenase (LDH) and can be converted back to pyruvate. This enzyme is selective in its action, with mammalian cells primarily producing L-lactate. Conversely, bacterial species that ferment carbohydrates (e.g., Lactobacillus spp.) possess both L-LDH and D-LDH enzymes and can produce either D-lactate or L-lactate, or both, depending on the species. Hence, the elevation of L-lactate in most mammals typically reflects anaerobic metabolism, which occurs due to reduced tissue perfusion and hypoxia, whereas the increase in D-lactate is primarily attributed to external factors, commonly arising from bacterial carbohydrate fermentation within the gastrointestinal tract [1,2,3,4].

Hyperlactatemia refers to an elevation in blood lactate concentration that occurs when lactate production exceeds lactate clearance. Hyperlactatemia can be classified into Types A and B based on the etiology. Type A hyperlactatemia is associated with systemic or local hypoperfusion, impaired oxygen-carrying capacity of hemoglobin, severe tissue hypoxia, and increased oxygen demand. Type B hyperlactatemia occurs secondarily due to mitochondrial dysfunction, drugs altering carbohydrate metabolism, toxins, or pathological conditions [1, 3, 4]. In most clinical situations, the measured enantiomer is L-lactate. In human and veterinary medicine, L-lactate has primarily been reported in critically ill patients. In humans, L-lactate is an indicator of systemic hypoperfusion, tissue hypoxia, prognostic factors, and therapeutic targets. High L-lactate concentrations are associated with a higher mortality rate [5,6,7,8]. Serum lactate was associated with mortality in patients admitted to the emergency department with severe sepsis [5]. In studies using continuous lactate measurements over time in humans, lactate clearance was associated with increased survival, whereas patients who failed to clear lactate (low lactate clearance) had higher mortality [6, 8, 9]. In patients with cardiogenic shock, survivors had greater lactate clearance at 6–8 h and at 24 h compared with non-survivors [8]. In veterinary medicine, L-lactate concentrations in dogs with gastric dilatation-volvulus [10] and dogs with Babesia infection [11] have been identified as reliable prognostic indicators. Studies involving emergency treatment of dogs and cats have also emphasized that the presence and severity of hyper-L-lactatemia aid in identifying animals with high mortality rates [12]. High blood lactate concentrations in equine colic have been shown to be indicators of poor prognosis [13]. In cattle with respiratory diseases, plasma L-lactate has been shown to be a reliable prognostic indicator [14], whereas in calves undergoing surgery for acute abdominal emergencies, early postoperative hyper-L-lactatemia has been reported to assist in identifying patients with high mortality rates [15].

D-lactatemia is uncommon in humans and monogastric animals. It has been reported as a complication of short bowel syndrome following extensive resection of the small intestine in humans [16], and clinical symptoms such as altered mental status, lethargy, ataxia, disorientation, and weakness have been observed in individuals with D-lactic acidosis [17]. Although increased D-lactate concentrations have been observed in dogs infected with parvovirus, there is no correlation with disease severity or acid-base status [18]. D-lactatemia has also been reported in cats with gastrointestinal disorders [19] and endocrine pancreatic insufficiency [20]. In ruminants, physiological conditions can lead to the production and absorption of D-lactate in the gastrointestinal tract. The mechanism of D-lactate production and absorption in the rumen of adult ruminants suffering from acute ruminal acidosis caused by carbohydrate overconsumption is well known [21,22,23,24]. Additionally, D-lactatemia has been reported as a complication of esophageal groove dysfunction (ruminal drinking) and diarrhea in newborn calves [22,23,24]. A study on diarrheic calves showed that D-lactate did not affect prognosis, but could contribute to clinical manifestations associated with metabolic acidosis [25]. D-lactatemia has been associated with impaired posture and behavior, particularly damage to the palpebral reflex [26, 27].

Diarrhea is one of the most important diseases affecting calves and is associated with high morbidity and mortality rates. A study conducted on dairy operations in North America reported that 33.9% of calves experienced at least one episode of illness, with 56% of sick calves showing gastrointestinal symptoms [28]. Another study indicated that over 23% of calves received treatment for neonatal calf diarrhea, with a reported mortality rate of 4.9% for the condition [29]. Research in China reported average morbidity and mortality rates of 14.2% and 3.6%, respectively, for calf diarrhea [30]. In Korea, the calf mortality rate is 10.7%, with over half (53.4%) attributed to gastrointestinal diseases [31]. In addition to the direct losses incurred from calf mortality due to diarrhea, calves affected by diarrhea are known to cause economic losses due to growth retardation, decreased milk production, and increased treatment costs [32,33,34].

Most cases of diarrhea can induce anorexia, fluid loss, dehydration, electrolyte imbalance, and metabolic acidosis, which can be fatal in calves due to dehydration and acidemia. Hemoconcentration, azotemia, hypoglycemia, hyponatremia, hyperkalemia, septicemia, hyper-D-lactatemia, hyper-L-lactatemia, and the development of strong ion metabolic acidosis are well-known complications of neonatal diarrhea. Calf diarrhea commonly presents acutely, underscoring the importance of promptly assessing prognosis, determining appropriate treatment, evaluating acid-base and hydration status, and making timely decisions regarding diagnostic and therapeutic interventions [24, 25, 27, 35,36,37,38].

Moreover, there are currently few reports on lactate concentrations in Korean indigenous cattle; specifically, there are no reports on lactate in diarrheic calves. Therefore, this study aimed to determine lactate concentrations in healthy calves and investigate their alterations in diarrheic calves. Additionally, we analyzed the correlation between lactate concentrations and acid-base parameters and established a cutoff value for blood lactate concentrations predictive of acidemia.

Methods

Animals

Between March and November 2023, 44 calves were selected from farms in Seosan-si, Icheon-si, Geochang-gun, and Yeonggwang-gun, South Korea. These calves were randomly selected from among those that were less than 120 days old and had not shown any clinical symptoms at the time of birth until selection, and their health status was confirmed by an experienced veterinarian. For lactate analysis in diarrheic calves, 93 calves less than 120 days old, who were referred to a veterinary hospital for diarrhea treatment between March and December 2023, were selected. All the calves were the Korean indigenous (Hanwoo) breed. Both sexes were included and raised indoors.

Blood sample collection

Blood samples were taken from the jugular vein of calves by 21 gauge needle and 10 mL syringe (BD Emerald Syringe, Becton Dickinson, Fraga, Spain) and anaerobically collected into five mL serum-separating tubes (Vacuette serum tube, Greiner Bio-One, Kremsmünster, Austria). Blood was collected by a veterinarian before therapeutic intervention. The tubes were transported to the laboratory in a refrigerated state (4–8 °C) and delivery was completed within one hour. The serum-separating tubes were left to stand at room temperature (about 23 °C) for at least one hour, and then the serum was separated by centrifugation at 3000 × g for 10 min. The separated serum was stored in a freezer at − 24 °C.

Laboratory parameters analysis

Blood gases, electrolytes, and chemistry were analyzed in native whole blood immediately after blood collection using an i-STAT device and an EC8 + cartridge (Abbott Point of Care Inc., Abbott Park, IL, USA) [39, 40]. The analyzed parameters were: sodium ions (Na+, mmol/L), potassium ions (K+, mmol/L), chloride ions (Cl−, mmol/L), total carbon dioxide (tCO2, mmol/L), blood urea nitrogen (BUN, mg/dL), glucose (mg/dL), venous pH, partial pressure of carbon dioxide (pCO2, mmHg), bicarbonate ions (HCO3–, mmol/L), base excess of the extracellular fluid (BEecf, mmol/L), and anion gap (mmol/L) levels. In the i-STAT system, electrolytes, pH, and pCO2 are measured at 37 °C through selective electrodes in the cartridge, and HCO3–, tCO2, BEecf, and anion gap are automatically calculated by the analyzer as follows:

$$\text{log}\:{\text{HCO}\text{3}}^{-}=\text{pH}+\text{log}\:\text{p}\text{CO2}-7.608$$
$$\text{tCO2}={\text{HCO3}}^{-}+0.03\text{pCO2}$$
$$\text{BEecf}={\text{HCO3}}^{-}-24.8+16.2\left(\text{pH}-7.4\right)$$
$$\text{Anion}\:\text{gap}=\left({\text{Na}}^{+}+{\text{K}}^{+}\right)-{\text{Cl}}^{-}+\left(\text{tCO2}-1\right)$$

Blood L-lactate concentration was measured using a portable lactate meter (Nova Biomedical, Waltham, MA, USA) immediately after the collection of native whole blood, and serum L-lactate concentration was measured using serum obtained immediately after centrifugation of the blood. L-Lactate measurement is based on an enzymatic amperometric system [41]. Enzymatic amperometry measures the amount of hydrogen peroxide produced by the reaction of L-lactate with a lactate oxidase-containing membrane. Hydrogen peroxide is oxidized and generates an electrical current proportional to the concentration of L-lactate in the sample. The D-lactate concentration was measured using a commercial colorimetric assay kit (D-Lactate Assay kit, ab83429, Abcam, Cambridge, MA, USA). Frozen serum was thawed at room temperature (about 23 °C) for one hour before use. The assay was performed according to the manufacturer’s instructions. It measures reduced nicotinamide adenine dinucleotide (NADH) produced by the oxidation of D-lactate, which is equivalent to the sample D-lactate concentration [42]. The D-lactate measurement was completed within one week from blood collection, except for three samples showing clipping, which were diluted 25-fold and reanalyzed after being stored in frozen serum for 10 months.

Statistical analysis

Data were analyzed using the SPSS statistical software package (SPSS 21.0; IBM SPSS Statistics, Armonk, NY, USA) and GraphPad Prism 8 (GraphPad Software Inc., San Diego, CA, USA). Descriptive statistics including the mean, median, 95th percentile, minimum value (min), maximum value (max), standard deviation (SD), and confidence interval (CI) of the dataset were calculated. The normality of the data was assessed using the Kolmogorov–Smirnov and Shapiro–Wilk tests. Because most of the data did not follow a normal distribution, non-parametric tests were used, and the Mann–Whitney U test was used to compare laboratory parameters between healthy calves and calves with diarrhea. In the comparison of subgroups classified according to the severity of acidemia, significance was confirmed using the Kruskal–Wallis test. Statistical significance was determined when the P value was < 0.05. Associations between parameters were determined using Spearman’s correlation coefficients. The Spearman correlation coefficient was categorized as very strong (0.90–1.0), strong (0.70–0.89), moderate (0.40–0.69), weak (0.10–0.39), or negligible (0.00–0.09) [43].

Determination of lactate reference range and pH severity prediction cutoff value

The reference range for lactate concentration was determined at the 95th percentile of lactate concentration in healthy calves as the upper limit of the reference interval [44]. Receiver operating characteristic (ROC) analysis was used to predict the presence and severity of acidemia based on lactate concentrations in calves with diarrhea. The prediction performance was confirmed through the calculation of the area under the ROC curve (AUC), and the classification was defined as excellent (0.9–1.0), good (0.8–0.89), fair (0.7–0.79), poor (0.6–0.69), and fail (0.0–0.59) [45, 46]. The lactate concentration with the optimal cutoff value was determined by the Youden’s index [47], and positive predictive values (PPV) and negative predictive values (NPV) were calculated.

Results

Lactate concentrations in healthy and diarrheic calves

The mean (median / min–max) ages of the clinically healthy calves (n = 44) and diarrheic calves (n = 93) were 30.9 (21 / 7–81) and 25.8 (14 / 2–120) days, respectively. Concentration of both L-lactate and D-lactate were higher in the diarrheic calves than in the healthy calves. A comparison of lactate concentrations between healthy and diarrheic calves is presented in Table 1.

Table 1 Comparison of lactate concentrations in healthy calves and diarrheic calves
Full size table

The 5th − 95th percentiles of lactate concentrations (mmol/L) in the blood of healthy calves were L-lactate 0.2–2.25 and D-lactate 0.42–1.38. These values were set as reference ranges for L-lactate and D-lactate concentrations in Hanwoo calves, with values exceeding the upper limits classified as hyper-L-lactatemia or hyper-D-lactatemia.

Alteration of laboratory parameters in diarrheic calves

Diarrheic calves (n = 93) showed hypokalemia in 12/93 (12.9%) cases, normal blood potassium concentration in 64/93 (68.8%), and hyperkalemia in 17/93 (18.3%). Among these, 58/93 (62.4%) calves had acidemia, while 35/93 (37.6%) had normal pH. No alkalemia was observed. The anion gap was normal in 29/93 (31.2%) calves and elevated in 64/93 (68.8%). No reduction in the anion gap was observed. Low BUN was observed in 3/93 (3.2%) calves, normal BUN in 29/93 (31.2%), and azotemia in 61/93 (65.6%). Additionally, 40/93 (43.0%) calves exhibited hyper-L-lactatemia (blood L-lactate > 2.25 mmol/L), and 66/93 (71.0%) had hyper-D-lactatemia (D-lactate > 1.38 mmol/L).

Correlation between lactates and laboratory parameters in diarrheic calves

A weak negative correlation was observed between pH and blood L-lactate (r = − 0.31) as well as D-lactate (r = − 0.35), and a moderate negative correlation was found between the combined concentration of L-lactate and D-lactate (r = − 0.42). Although K+ showed a weak correlation with blood L-lactate (r = − 0.28), no correlation was observed with D-lactate. The correlations between lactate concentrations and acid-base parameters (BEecf, anion gap, tCO2), K+, and BUN are presented in Table 2.

Table 2 Correlation between lactate levels and laboratory parameters in diarrheic calves
Full size table

Alteration of laboratory parameters in hyper-L-lactatemia calves

Significant differences were observed in pH, BEecf, anion gap, and glucose between the subgroups of diarrheic calves with hyper-L-lactatemia and those with normal L-lactate. The hyper-L-lactatemia group showed lower pH and BEecf but higher anion gap and glucose than the normal L-lactate group. Similarly, in the subgroups of diarrheic calves with hyper-D-lactatemia and those with normal D-lactate, significant differences were observed in pH, tCO2, HCO3–, BEecf, and anion gap. The hyper-D-lactatemia group exhibited lower pH, tCO2, HCO3–, and BEecf but higher anion gap than the normal D-lactate group. These differences are presented in Table 3.

Table 3 Laboratory parameters in hyper-L-lactatemia and hyper-D-lactatemia subgroups
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Correlation between lactate concentrations and laboratory parameters in hyper-L-lactatemia calves

In the hyper-L-lactatemia group, moderate correlations were observed between blood L-lactate and pH (r = − 0.42), and anion gap (r = 0.50), accompanied by a weak negative correlation with BEecf (r = − 0.32). D-lactate exhibited weak negative correlations with pH (r = − 0.36) and BEecf (r = − 0.36), but no significant correlation with anion gap was observed. The combined concentration of L-lactate and D-lactate showed moderate negative correlations with pH (r = − 0.51) and BEecf (r = − 0.47) and a moderate positive correlation with anion gap (r = − 0.55). The correlations between lactate and acid-base parameters in the hyper-L-lactatemia group are presented in Table 4. Scatterplots depicting the relationship between lactate concentrations and acid-base parameters are presented in Fig. 1. Notably, in the subgroup of calves with hyper-L-lactatemia, the correlation between lactate and other acid-base parameters appeared to be stronger than in the entire group of diarrheic calves.

Table 4 Correlation between lactate levels and acid-base parameters in the hyper-L-lactatemia calves
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Fig. 1
figure 1

Scatterplots depicting the correlation between lactate and laboratory parameters in diarrheic calves. Dashed lines represent linear regression slopes for the entire group of diarrheic calves. a, b, c: Scatterplots depicting the correlation between blood L-lactate concentrations and pH, BEecf, and anion gap. d, e, f: Scatterplots depicting the correlation between serum D-lactate concentrations and pH, BEecf, and anion gap. g, h, i: Scatterplots depicting the correlation between the combined concentrations of serum L-lactate and D-lactate and pH, BEecf, and anion gap. j, k: Scatterplots depicting the correlation between the combined concentrations of serum L-lactate and D-lactate and K+and BUN. Abbreviations: BEecf: base excess of the extracellular fluid; BUN: blood urea nitrogen

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Laboratory parameters according to the severity of acidemia

Diarrheic calves were grouped by venous blood pH as follows: very severe (pH < 7.0), severe (7.0 ≤ pH < 7.2), moderate (7.2 ≤ pH < 7.3), and mild acidemia (7.3 ≤ pH < 7.35) and normal pH (pH ≥ 7.35) [35, 48, 49]. As the severity of acidemia increased, lactate concentrations also increased. Moreover, parameters reflecting the acid-base balance, such as decreased BEecf, tCO2, and HCO3–, exhibited changes corresponding to decreased pH. K+ and anion gap increased, whereas pCO2 decreased. The classifications based on the severity of acidemia and the laboratory parameters in each group are presented in Table 5.

Table 5 Classification and laboratory parameters based on the severity of acidosis in diarrheic calves
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Evaluation of lactate as a predictor for acidemia and severe acidemia

ROC curve analysis was conducted to determine whether lactate concentration could predict the presence of acidemia (pH < 7.35) and severe acidemia (pH < 7.2) in diarrheic calves.

Blood L-lactate exhibited poor predictive performance for both acidemia (AUC 0.69) and severe acidemia (AUC 0.65). For acidemia, the optimal cutoff value was > 2.8 mmol/L, with a sensitivity of 46.6%, specificity of 88.6%, PPV of 87.1%, and NPV of 50.0%. For severe acidemia, the optimal cutoff value was > 2.65 mmol/L, with a sensitivity of 65.2%, specificity of 74.3%, PPV of 45.5%, and NPV of 86.7%.

Serum D-lactate also showed poor predictive performance for acidemia (AUC 0.67), but fair predictive performance for severe acidemia (AUC 0.74). For acidemia, the optimal cutoff value was > 2.23 mmol/L, with a sensitivity of 39.7%, specificity of 91.4%, PPV of 88.5%, and NPV of 47.8%. For severe acidemia, the optimal cutoff value was > 1.43 mmol/L, with a sensitivity of 100%, specificity of 41.4%, PPV of 35.9%, and NPV of 100%.

The combined concentration of serum L-lactate and D-lactate exhibited fair predictive performance for predicting both acidemia and severe acidemia. For acidemia, the AUC was 0.74, with an optimal cutoff value of > 6.05 mmol/L, sensitivity of 52.5%, specificity of 81.3%, PPV of 84.2%, and NPV of 47.3%. For severe acidemia, the AUC was 0.72, with an optimal cutoff value of > 5.95 mmol/L, sensitivity of 73.9%, specificity of 67.1%, PPV of 42.5%, and NPV of 88.7%.

The results of the ROC analysis, including the optimal cutoff values, sensitivity, specificity, PPV, and NPV at these cutoff values, are presented in Table 6.

Table 6 Results of ROC analysis for acidosis prediction
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Discussion

In diarrheic calves, the prevalence rates of hyper-L-lactatemia and hyper-D-lactatemia were 43% and 71%, respectively. However, because this study was conducted on diarrheic calves for which treatment was requested by farmers, meaning cases may have been preselected to some extent as severe. Therefore, the prevalence may have been overestimated. Additionally, since this study specifically focused on Korean indigenous (Hanwoo) calves under 120 days old, and there are limitations to generalizing the results to other species, bovine breeds, or age groups.

Lactate measurements provide valuable information on metabolic acidosis in diarrheic calves. In our results, the reference ranges for lactate concentration in Hanwoo calves were L-lactate 0.3–2.25 mmol/L and D-lactate 0.42–1.38 mmol/L. The previously reported reference range for L-lactate was 0.6–2.2 mmol/L [48], similar to our results. However, there was a difference in the reference range of D-lactate concentration, which was previously reported as < 3.96 mmol/L [42]. D-lactate is produced by carbohydrate fermentation by intestinal microorganisms, which can vary due to dietary, genetic, and other factors [50, 51]. This may explain the differences observed in the reference ranges of serum D-lactate concentration.

In this study, diarrheic calves showed an increase in L-lactate and D-lactate concentrations. Consistent with previous research, hyper-L-lactatemia and hyper-d-lactatemia were a commonly observed complication in diarrheic calves. Diarrhea in calves can lead to fluid loss, resulting in dehydration and decreased tissue perfusion, which may manifest as an elevation in blood L-lactate concentration. When calves are infected with organisms that cause villous atrophy, they experience digestive disorders and impaired nutrient absorption, leading to an increase in unabsorbed carbohydrates and bacterial overgrowth in the gastrointestinal tract, subsequently increasing D-lactate production. Consequently, an increase in blood D-lactate concentration may occur. Since ruminal milk accumulation (ruminal drinking) due to dysfunction of the esophageal groove reflex is commonly concurrent in diarrheic calves, an elevation in D-lactate concentration might be expected. Additionally, along with increased production, a decrease in hepatic and/or renal function due to concurrent hypoperfusion associated with diarrhea could result in reduced removal of blood lactate [22,23,24, 52]. In our study, some diarrheic calves did not show an increase in blood lactate concentration, which could indicate mild diarrhea or dehydration. Furthermore, serum D-lactate concentrations are lower in diarrheic calves without ruminal acidosis than in those with ruminal acidosis [25]. Experimental studies have also shown that, while metabolic acidosis occurs in experimentally induced osmotic diarrhea, hyper-L-lactatemia and hyper-D-lactatemia do not occur [53].

Diarrhea typically results in the loss of fluids and electrolytes from the gastrointestinal tract. In diarrheic calves, increased BUN concentrations were observed. This may reflect a decrease in the glomerular filtration rate (pre-renal azotemia) due to fluid loss associated with diarrhea. However, since other potential causes of elevated BUN were not evaluated, complete exclusion of renal and postrenal azotemia cannot be guaranteed. An increased BUN in diarrheic calves has been reported as a predictor of poor prognosis [54]. Despite the net loss of K+ due to diarrhea, hyperkalemia can still occur. This indicates that the movement of K+ from the intracellular to the extracellular compartments buffers the metabolic acidosis caused by diarrhea. This is further exacerbated by the dysfunction of Na+/K+ ATPase, which distributes K+ between intracellular and extracellular spaces, and impaired renal excretion of K+ due to decreased blood volume [27]. Similarly, in our study, normal blood K+ concentration, hyperkalemia, and hypokalemia were observed in diarrheic calves.

Two approaches have been used to assess acid-base imbalance: the Henderson-Hasselbalch approach and, more recently, a physicochemical approach. The former focuses on indicators of the metabolic components of acid-base balance, emphasizing plasma HCO3– and extracellular excess base concentrations. The quantitative physicochemical approach highlights the importance of strong electrolytes (Na+, K+, and Cl–), unmeasured strong anions (including L-lactate and D-lactate), pCO2, and total plasma protein concentration [55,56,57]. Traditionally, metabolic acidosis has been commonly observed in neonatal calves with diarrhea, which is attributed to the intestinal loss of HCO3– and an increase in L-lactate concentration due to dehydration and associated tissue hypoperfusion. Metabolic acidosis in diarrheic calves is typically accompanied by an increase in the anion gap, indicating the presence of unmeasured anions. However, the increase in the anion gap cannot be solely explained by the elevation in blood L-lactate concentration. Subsequent studies found that unmeasured strong anions such as D-lactate play an important role in the pathogenesis of metabolic acidosis in diarrheic calves. Furthermore, recent research has shown that hyperphosphatemic acidosis commonly occurs in dehydrated neonatal diarrheic calves and that hyperphosphatemia is an important predictor of venous blood pH [23,24,25, 35, 52, 57]. Similarly, in this study, 58/93 (62.4%) diarrheic calves exhibited acidemia, which is characterized by an elevated anion gap metabolic acidosis. Among them, 28/58 (48.3%) had a mixed form of respiratory acidosis with elevated pCO2. In diarrheic calves, lactate concentrations showed a weak correlation with acid-base parameters, and in calves with hyper-L-lactatemia, these correlations were slightly stronger. Among these, the combined concentration of L-lactate and D-lactate exhibited the highest correlation, which was a moderate correlation.

In this study, ROC analysis results indicate suboptimal AUC values. Specifically, the AUC for predicting acidemia using L-lactate was 0.69, and for severe acidemia, it was 0.65. D-lactate also showed limited predictive performance, with an AUC of 0.67 for acidemia and 0.74 for severe acidemia. Although the combined concentration of L-lactate and D-lactate exhibited acceptable predictive performance with AUCs of 0.74 and 0.72, these values remain below the generally accepted cutpoint (AUC ≥ 0.80) for reliable diagnostic performance [45]. This suggests limited diagnostic accuracy for acidemia or severe acidemia in diarrheic calves when these biomarkers are used alone.

Measurement of pH using a blood gas analyzer is an accurate method for evaluating acidemia, and portable blood gas analyzers can be used to assess the blood gas and acid-base status. However, these analyzers are expensive and not commonly used in most practices. Other less expensive methods for the determination of acid-base status use a portable pH meter or the Harleco-System to determine the tCO2 concentration, but these methods are not widely used in bovine clinical practice [52]. In most bovine clinical practices, the assessment and diagnosis of metabolic acidosis are based on clinical signs. Measurement of L-lactate can be performed using a portable lactate analyzer, which enables rapid assessment with a small amount of whole blood, providing results at the point-of-care. Moreover, this method is cost-effective, and the validation of the portable lactate analyser test results in cattle has been reported. However, there is no simple analytical method for measuring D-lactate in clinical practice, and it has primarily been used in experimental studies and teaching hospitals [46, 58].

Correcting metabolic acidosis is a key objective for calves with diarrhea. Acute metabolic acidosis can affect multiple organ systems, with the cardiovascular system being the most severely affected, leading to decreased cardiac contractility and output. Additionally, adverse effects, such as impaired leukocyte function, suppression of lymphocyte function, insulin resistance, and stimulation of apoptosis, may occur. Generally, severe acidemia due to metabolic acidosis in critically ill calves is defined as a blood pH < 7.2 and is associated with poor clinical outcomes and high mortality rates [35, 44, 59]. According to a retrospective study involving 1400 calves with diarrhea, the mortality rate was 28% in calves with a pH < 7.00, while the mortality rate was 57% in calves with a pH < 6.80, indicating that jugular venous blood pH < 6.85 can predict non-survival in critically ill neonatal calves [35]. In the treatment of acute metabolic acidosis, base therapy is considered when the whole blood pH is < 7.10 in the presence of lactic acidosis, or when there is evidence of hemodynamic compromise with a pH < 7.20 [44, 59]. In the management of diarrhea in calves, base administration is indicated for severe acidemia with a pH < 7.20, with isotonic sodium bicarbonate being preferred, whereas lactated Ringer’s solution and acetated Ringer’s solution may be used for correction of less severe metabolic acidosis [36, 37, 52].

Conclusions

The reference ranges for blood L-lactate and serum D-lactate in Hanwoo calves were determined to be 0.3–2.25 mmol/L and 0.42–1.38 mmol/L, respectively. Diarrheic calves exhibited increased lactate concentrations correlated with acid-base parameters. The concentrations of L-lactate and D-lactate have limitations as single diagnostic biomarkers for predicting acidemia or severe acidemia, their measurement remains important. Calf diarrhea is mostly acute, and correcting metabolic acidosis in diarrheic calves is an important goal. Considering this, measuring lactate concentrations can be a crucial consideration for clinicians when making decisions alongside other clinical indicators and diagnostic tests. Such an approach offers the potential to aid in the successful management of calf diarrhea, ultimately contributing positively to animal welfare and the economic benefits of farms.

Abbreviations: BEecf, base excess of the extracellular fluid; BUN, blood urea nitrogen.

Data availability

The datasets used and/or analyzed in the current study are available from the corresponding author upon reasonable request.

Abbreviations

AUC:

area under the receiver operating characteristic curve

BEecf:

base excess of the extracellular fluid

BUN:

blood urea nitrogen

CI:

confidence interval

Cl– :

chloride ions

HCO3 – :

bicarbonate ions

K+ :

potassium ions

LDH:

lactate dehydrogenase

max:

maximum value

min:

minimum value

NADH:

nicotinamide adenine dinucleotide

Na+ :

sodium ions

NPV:

negative predictive value

pCO2 :

partial pressure of carbon dioxide

PPV:

positive predictive value

ROC:

receiver operating characteristic

SD:

standard deviation

tCO2 :

total carbon dioxide

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Acknowledgements

The authors wish to thank all farmers, herders, and veterinarians for their valuable assistance in handling calves and collecting blood samples.

Funding

This study was supported by the Korea Institute of Planning and Evaluation for Technology in Food, Agriculture, and Forestry (IPET) (grant No. RS-2024-00402276). This research was partially supported by ‘regional innovation mega project’ program through the Korea Innovation Foundation funded by Ministry of Science and ICT (Project Number: 2023-DD-UP-0031).

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Authors and Affiliations

  1. Department of Veterinary Internal Medicine, College of Veterinary Medicine, Jeonbuk National University, 79 Gobong-ro, Iksan, 54596, Republic of Korea

    Youngwoo Jung, Ji-Yeong Ku, Byoungsoo Kim, Youngjun Kim, Kwang-Man Park, Jonghun Baek & Jinho Park

  2. Hanwoo (Korean Indigenous Cattle) Genetic Improvement Center, National Agricultural Cooperative Federation, Seosan, Republic of Korea

    Youngjun Kim

  3. Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju, 52828, Republic of Korea

    DoHyeon Yu

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Contributions

YJ, J-YK, DHY, and JP contributed to the design of this study. J-YK, BK, YK, K-MP, and JB performed the experiments and collected the data. YJ, J-YK, BK, YK, K-MP, and JB interpreted and analyzed the data. J-YK prepared figures. YJ wrote the initial drafts of the manuscript. DHY and JP supervised, wrote, and edited the manuscript, and reviewed the final submission. All the authors have read and agreed to the final version of the manuscript.

Corresponding authors

Correspondence to DoHyeon Yu or Jinho Park.

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Ethics approval and consent to participate

The present study was approved by the Institutional Animal Care and Use Committee of the National Institute of Animal Science, Republic of Korea (JBNU IACUC No. NON2023-123). Informed consent for blood sample collection was obtained from all owners.

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Not applicable.

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The authors declare no competing interests.

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Jung, Y., Ku, JY., Kim, B. et al. Determining lactate concentrations in Korean indigenous calves and evaluating its role as a predictor for acidemia in calf diarrhea. BMC Vet Res 20, 373 (2024). https://doi.org/10.1186/s12917-024-04235-0

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BMC Veterinary Research

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