Hypoglycemia is a characteristic condition of early lactation dairy cows and is subsequently depende These are not noted with subclinical hypocalcemia.
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With the initiation of lactation and continued milk production, tremendous adaptations occur in the dairy cow because of the increased need for nutrients to support milk synthesis. Besides the increased need for energy and amino acids for colostrum and afterward for milk synthesis, the requirement for calcium increases two- to three-fold over that required by the dairy cow before calving. Shortly
before calving, a dairy cow deposits 8 to 10 g/d of calcium into her fetus, but when she calves, 20 to 30 g/d are secreted into colostrum and milk. Thus, metabolic adaptations must take place to support the increased need for calcium. If they do not take place soon enough or of sufficient magnitude, the concentration of calcium in the blood drops below a critical threshold and clinical and subclinical hypocalcemia, or milk fever, can result. Role of Calcium
Calcium is vital for skeleton tissue and smooth muscle and nerve function including gastrointestinal motility and skeletal muscle strength. The lowest concentration of blood calcium usually occurs within 12 to 24 hours of calving and generally returns to normal in healthy cows within 2 to 3 days post-calving. Clinical hypocalcemia is the most recognized disease in dairy cattle by dairy farmers, with an incidence rate around 5%. Jersey and Guernsey cattle are more susceptible to the disorder. One reason for this is that Jersey cattle have fewer vitamin D receptors than Holstein cattle. Incidence increases with higher milk production and successive lactation. First-calf heifers rarely develop clinical hypocalcemia because they produce less colostrum and milk and can more rapidly mobilize calcium from bone in their growing skeleton. Reinhardt and co-workers at the National Animal Disease Center in Ames, Iowa, found the prevalence of clinical hypocalcemia was 1% for first-lactation, 4% for second-lactation, 7% for third-lactation, and 10% for fourth-lactation Holstein cows in a study where 1,462 cows were sampled. The concentration of calcium in blood is tightly regulated through control of absorption of dietary calcium and release or uptake of calcium from bone. Two hormones, parathyroid hormone (known as PTH) and 1,25-dihydroxy vitamin D3, control these processes. As the concentration of calcium decreases in the blood, PTH is secreted and acts at the kidney to decrease the excretion of calcium in the urine. This change allows for only small adjustments in the concentration of blood calcium. If greater amounts of calcium are needed, as with the initiation and maintenance of lactation, PTH acts on bone, and calcium is reabsorbed and released into the blood. In addition, PTH acts on the kidney and results in the conversion of a vitamin D metabolite into 1,25-dihydroxy vitamin D3. Then 1,25-dihydroxy vitamin D3 can regulate the absorption of calcium from the small intestine through active transport. In order for PTH to be secreted and effectively bind to its receptor, adequate magnesium and a slightly less alkaline blood pH (known as metabolic acidosis) are needed, thus illustrating the need to provide adequate amounts of magnesium in pre-fresh diets and balance these diets to provide a negative cation-to-anion difference (DCAD) in order to prevent hypocalcemia. Subclinical Hypocalcemia
Dairy cows with subclinical hypocalcemia do not show clinical symptoms but have a low blood concentration of calcium usually within 24 hours after calving. Thus, the only way to know whether dairy cows are experiencing subclinical hypocalcemia is to analyze blood for the concentration of calcium within the first 1 to 2 days after calving. Early clinical symptoms (stage 1: the cow is still able to stand) can include excitability, nervousness, shifting of weight, and shuffling of hind feet. Dairy cows with blood calcium concentrations at or below 8.0 mg/dl (2.0 mmol/l) but not showing clinical signs are considered subclinically hypocalcemic. At this cut-off point, Reinhardt and co-workers in a study with 1,462 dairy cows determined that 50% of mature dairy cows and 25% of first-calf heifers experienced subclinical hypocalcemia. Oetzel at the University of Wisconsin has estimated that the economic cost of subclinical hypocalcemia in a dairy herd is four times the cost of clinical cases, resulting in a substantial impact on profitability of dairy operations. This increased economic cost is attributed to the greater number of cows with subclinical versus clinical hypocalcemia even though a subclinical case costs 40% of a clinical case. Recently, Martinez and co-workers at the University of Florida suggested that this cut-off should be raised to 8.5 mg/dl (2.1 mmol/l) because cows below this concentration were more likely to develop metritis or metabolic disorders. Using this higher criterion, Reinhardt and co-workers’ data indicate that over 65% of mature cows and 51% of first-calf heifers were below this threshold. These data and those from other researchers indicate (1) subclinical hypocalcemia does occur in a large number of dairy cows, but (2) not all fresh cows experience a drop in blood calcium concentration just after calving. Research suggests that subclinical hypocalcemia may be directly associated with other metabolic disorders and may be the primary or secondary cause of decreased performance. Implications of Hypocalcemia on Performance
Hypocalcemia impacts fresh cow health, future milk production, and reproductive performance. Studies also have shown that immune function is compromised in dairy cows with low blood calcium concentrations. Cows with lower blood calcium concentrations within the first day after calving are more likely to have a displaced abomasum, ketosis (and fatty liver), retained placenta and resulting metritis, and mastitis. Some studies have shown a decrease in feed intake and rumination and corresponding higher non-esterified fatty acid (NEFA) concentrations after calving. Cows with high body condition at calving also are more likely to have hypocalcemia. Other studies have failed to show a negative response on feed intake and milk production. Jawor and co-workers at the University of British Columbia showed that cows with subclinical hypocalcemia stood 2.6 hours longer in the 24-hour period before calving and produced 12 pounds more milk during weeks 2, 3, and 4 of lactation. In this study, all third- or greater lactation cows received a preventative calcium therapy after calving regardless of their blood calcium concentration. Prevention of Hypocalcemia
Prevention of hypocalcemia generally occurs through modifications to the pre-fresh or close-up diet. These changes allow for the physiological system which mobilizes calcium to be primed and ready for the increased demand for calcium associated with the synthesis of colostrum and milk. Low calcium diets pre-fresh: Although this practice does reduce the incidence of hypocalcemia, it is difficult to implement on the farm. To be effective, diets must provide less than 20 g of available calcium. These diets often contain very low quality forages that may limit intake, yet low intake pre-fresh is not desired. In some grazing situations (e.g., depending on forage species and pasture fertility), low calcium diets may be possible. Low potassium forages/diets pre-fresh: Incorporating low potassium forages (e.g., corn silage) into diets for pre-fresh dairy cows may decrease the likelihood of clinical hypocalcemia but not the incidence of subclinical hypocalcemia. Changes in the dietary cation-anion difference (DCAD) may not be large enough to cause metabolic acidosis and prevent a subclinical drop in blood calcium concentration when low potassium forages are fed without additional dietary modifications of chlorine and sulfur. The DCAD influences the pH of the blood and the responsiveness of tissues to PTH and the cow’s ability to reabsorb calcium from bone and absorb dietary calcium from the small intestine. Feeding anionic salts for 21 days pre-fresh: Feeding a negative DCAD diet 21 days pre-fresh has been shown to prevent clinical (a five-fold reduction) and subclinical hypocalcemia. Diets should be formulated to result in a dietary DCAD of -10 to -15 mEq/100g dietary dry matter using the most palatable of anionic mineral supplements. Many commercially available anionic mineral or protein-based supplements are available for use in formulating these diets. Before formulating diets, the amount of potassium and sodium provided through forages and other feedstuffs should be kept as low as possible. Close-up diets should be formulated with about 1.0% calcium and 0.35% magnesium to prevent hypocalcemia. Phosphorus concentration of close-up diets should be 0.25% to 0.3% because excess phosphorus (0.4% total diet) increases the risk for hypocalcemia. Urine pH should be used as an indicator of whether DCAD management is effective. However, urine pH does not indicate a reduction in the risk of hypocalcemia. Urine should be collected midstream after cows are fed the anionic salt diet for at least 48 hours. Urine should be free of f***l material. For Holstein cows, urine pH should be between 6.2 and 6.8 (at least less than 7.0) and for Jersey cows between 5.8 and 6.3. If the average urine pH is between 5.0 and 5.5, excessive anions are being fed (coming from both feed and water sources), and the diet needs to be reformulated to prevent a drop in dry matter intake. The verdict is still out on whether it is detrimental, neutral, or perhaps beneficial to provide anionic salts to virgin heifers. Early studies showed a decrease in dry matter intake in heifers fed anionic salts, but other more recent studies have not shown this decrease. Feeding anionic salts to virgin heifers increases feed costs especially with unclear benefits or detriments when supplemented. Anionic salts are usually fed for 21 days prior to calving and are not recommended to be fed for the entire dry period. In herds managed for short dry periods (40 to 45 days dry), feeding and managing dry cows in two separate groups may not be feasible, and feeding anionic salts the entire dry period may be needed to accommodate available facilities and labor. In a recent study by Weich and co-workers at the University of Minnesota, anionic salts were fed 0 (control was no anionic salts pre-fresh), 21, or 42 days before calving. No differences in dry matter intake before or after calving or milk production were seen when anionic salts were supplemented for 21 or 42 days before expected calving date. More studies are needed before extending or reducing the number of days pre-fresh anionic salts are fed in the field. Oral sources of calcium: Calcium supplemented orally (not part of the diet) after calving has shown a positive response for preventing a drop in concentration of blood calcium. Many oral supplements are absorbed within 30 minutes after administration and blood calcium concentration is increased for 4 to 6 hours. Oral supplementation of calcium often is in the form of calcium chloride in gel or paste forms. The calcium chloride in these forms can result in respiratory problems if aspirated, and as such, care must be taken when administering it. More recently, a solid bolus coated with fat containing calcium chloride and calcium sulfate was tested and found effective at increasing the concentration of blood calcium when two doses (one at calving, a second 12 hours post-calving) were given after calving. Coated boluses would help reduce the chances of cows aspirating the product. In another study, these boluses were tested in combination with anionic salts fed pre-calving, but no differences were seen versus providing anionic salts alone. Bottom Line
Prevention of hypocalcemia (low concentration of blood calcium) around calving is an important component when designing transition cow programs for optimum post-calving health, reproduction efficiency, and milk production. Adequate calcium is important for colostrum and milk synthesis, muscle and nerve function, and immunity. Clinical cases of hypocalcemia are easy to diagnose and for dairy managers to understand that feeding and management changes are needed to prevent future cases. On the other hand, subclinical hypocalcemia is not easy to diagnose and may be a contributing factor in herds with a high incidence rate of metabolic disorders. Subclinical hypocalcemia potentially occurs in over 50% of dairy cows, does not present with recognizable symptoms, and can only be diagnosed when blood samples are collected within the first 1 to 2 days post-calving and blood calcium concentration is determined to be below 8.5 md/dl. As with all metabolic disorders, prevention is the key, and the use of anionic salts and other management strategies may help prevent this metabolic disorder.
Prevention of hypocalcemia in cow
Limit calcium intake to less than 100 g/cow/day and phosphorus intake to less than 45g/day for two to three weeks prior to calving. Avoid feeding forages high in calcium such as alfalfa. Grass hays, cereal silages and corn silages are recommended. Work these forages into properly balanced dry cow diets.
Symptom of hypocalcemia in cow
Cows with Stage I hypocalcemia have early signs of milk fever without going down. Symptoms include nervousness, weakness, excitability, and frequent shifting of their weight frequently while standing.
Parturient paresis (milk fever, hypocalcemia, paresis puerperalis, parturient apoplexy) is a disease of adult dairy cows in which acute hypocalcemia causes acute to peracute, afebrile, flaccid paralysis of that occurs most commonly at or soon after parturition. Clinical signs also include changes in mentation and circulatory collapse.
Etiology of Parturient Paresis in Cows
Dairy cows are at considerable risk for hypocalcemia at the onset of lactation, when daily calcium excretion suddenly increases from about 10 g to 30 g per day. This stresses calcium homeostasis and may cause blood calcium concentrations to fall well below the normal lower reference range of approximately 8.5 mg/dL. Blood calcium concentrations typically decrease around the onset of parturition (see Plasma total calcium concentration, parturient paresis, dairy cows ) but recover quickly. Cows with parturient paresis have a more profound decrease in blood calcium concentration—typically below 5.5 mg/dL.
Treating hypocalcemia
Milk fever cases should be treated with 500 milliliters of 23 percent calcium gluconate IV and followed by the administration of two oral calcium bolus given 12 hours apart. It is important to emphasize that oral calcium bolus should not be administered if cows do not respond to the calcium IV treatment.
In milk fever cows, failing to rise after treatment with IV calcium is a signal that normal muscular function has not been reestablished. Cows may choke on the calcium bolus if treatment is given while they are still down. A veterinarian should be consulted and further treatment should be evaluated when milk fever cows do not respond to IV administration of calcium.
Milk Fever
Milk fever, or acute hypocalcemia, occurs when calcium in blood falls below 1.6mmol/L. Symptoms include muscular weakness, subnormal temperature, increased heart rate, sternal recumbancy and loss of consciousness. The primary cause lies in the reduced ability of the animal to mobilize calcium from the bones. Treatment with intravenous or subcutaneous calcium gluconate will usually resolve the problem.
Mineral Deficiency in Cattle
If you run a livestock operation, you know the importance of giving your cattle the nutrition they need for good health. Part of a good nutrition program involves providing the necessary minerals like calcium, phosphorus and potassium, among many others. Growing cattle and pregnant or lactating cows have a particularly high need for minerals, and all cattle require minerals for essential bodily functions and immune support.
Mineral deficiencies in cattle can cause serious health conditions and lead to mortality in some cases. This means cattle will need supplementation if they cannot get the minerals from their pasture or feed.
Glucose concentration is not extensively examined during early lactation period in low-milk-yielding cows as that for high-yielding. Using point-of-care and hand-held glucometers could decrease time and cost of glucose estimation.The current study objectives were (i) to evaluate hypoglycemic status in recently calved low-milk-yielding cows, and (ii) to assess the use of Reflotron as a glucometers for cows. Serum glucose (s-gluc) from recently calved and pregnant cows was estimated using analytical enzymatic method (AnaMeth) to assess the hypoglycemia. Blood glucose (b-gluc), plasma glucose (p-gluc), and s-gluc from recently calved, pregnant, and non-pregnant cows were estimated using devices and method of interest. Passing-Bablok regression and Bland-Altman plot were used to evaluate the agreement between the different methods. Serum glucose was lower, but not statistically significant, in recently calved compared to pregnant cows, and it was significantly greater than the reference value for hypoglycemic cows. No differences were detected between s-gluc and p-gluc using both AnaMeth and Reflo , which were also identical in that estimation. Furthermore, overestimated p-gluc, and both Reflo and significantly overestimated b-gluc in study cows. Hypoglycemia is not evident in recently calved low-milk-yielding cows. Plasma and serum can be used interchangeability for glucose estimation in cows
Cows with a serum calcium concentration below 2.0 mmol/L were considered as hypocalcemic. Although this is a conservative threshold, it is well accepted in research and applied in the field (DeGaris and Lean, 2008; Reinhardt et al., 2011; Wilhelm et al., 2017). Recent studies suggested higher thresholds. It was shown that hypocalcemia using 2.1, 2.2, and 2.3 mmol/L thresholds was associated with a negative health outcome such as displaced abomasum and metritis (Chapinal et al., 2011, 2012; Martinez et al., 2012) or an increased culling risk (Seifi et al., 2011; Roberts et al., 2012). These studies, however, considered a longer risk period postpartum (i.e., of 3 to 7 DIM). Although these epidemiological studies showed an association and also some evidence for a causal relationship between hypocalcemia and an increased risk for infectious diseases (Martinez et al., 2014), one has to be careful when evaluating longer risk periods. It is also plausible that reduced feed intake before clinical signs of disease can affect serum calcium levels as most recently shown by Pinedo et al. (2017) for cows suffering from puerperal metritis. At calving, no difference was present in serum calcium concentration between healthy and metritic cows. On the day of diagnosis (on average 6.1 DIM), however, serum calcium concentration was lower in cows with puerperal metritis (1.57 mmol/L) compared with healthy cows (2.10 mmol/L). To reflect higher thresholds, we calculated the prevalence accordingly. Table 1 shows that a mild increase of the threshold leads to a dramatic increase of animals considered as hypocalcemic. Further evaluations are necessary to define the most appropriate threshold of hypocalcemia within this time period.
In our study, 47.6% of multiparous cows suffered from subclinical hypocalcemia within 48 h after parturition. This finding is in agreement with others (Reinhardt et al., 2011; Gild et al., 2015; Miltenburg, 2015). The inability of the cow to maintain normal serum calcium concentration is caused by a maladaptation of the mineral metabolism in response to an increased demand for calcium. Dairy cows need around 20 g of calcium per day at the end of the dry period. With colostrum production, the demand increases to 30 to 70 g per day depending on milk yield. The mechanisms to decrease urinary calcium excretion, to increase absorption of calcium from the gut, and to upregulate calcium release from bone tissue, however, take about 48 h, which may lead to insufficient calcium supply in this period (Martin-Tereso and Martens, 2014).
Surprisingly, serum calcium concentration of cows that calved at night was higher than serum calcium concentration of cows that calved during the day. The effect, however, was biologically small and without an apparent explanation.
In contrast to multiparous cows, hypocalcemia was rarely found in primiparous cows (5.7%), which is in agreement with a previously described prevalence of 2% for primiparous cows from 7 herds in Canada using the same threshold (Miltenburg, 2015). Overall, there are, however, conflicting reports on the prevalence of hypocalcemia in primiparous cows. Reinhardt et al. (2011) observed a prevalence of 25% from 480 herds in the United States. The reason for this difference remains speculative. The latter report used samples drawn for the 2002 NAHMS study. The understanding of the transition cow biology improved in the last 15 yr and led to the implementation of preventive strategies to control milk fever. As stated in the NAHMS 2002 report (USDA, 2002), 14.3% of heifers and 19.1% of cows were fed anionic salts in their close-up diets. In the more recent NAHMS report, 20.7% of heifers and 27.6% of cows were fed anionic salts (USDA, 2014). This might be an indication of an increased awareness for prevention of milk fever and subclinical hypocalcemia. Furthermore, management practices and production conditions for heifers might have changed in the meantime (e.g., close up feeding, milk yield, feed intake).
A plausible explanation for the higher prevalence of subclinical hypocalcemia in multiparous cows is that these animals have a higher calcium output due to an increased amount of colostrum compared with primiparous cows (Klingbeil, 2015). The calcium output, however, does not explain the increase in prevalence of hypocalcemia within multiparous cows with increasing age as their colostrum yield was not different. The parity-associated increase might be related to a reduced bone remodeling in multiparous cows due to a reduction of the number of active osteoclasts and osteoblasts. These cells must be recruited from progenitor cells in response to parathyroid hormone (PTH) secretion, leading to a delay in calcium mobilization (Goff, 2014).
In a recent study, 51, 54, and 42% of fourth, fifth, and sixth parity cows suffered from subclinical hypocalcemia, respectively (Reinhardt et al., 2011). These results are almost identical to our observations of 52.1, 51.1, and 41.7% for fourth, fifth, and sixth parity cows, respectively. Prevalence of clinical milk fever in our data set (13.4, 15.0, and 21.7% for fourth, fifth, and ≥sixth parity, respectively), however, was higher than described for the United States (10, 8, and 13% for fourth, fifth, and sixth parity, respectively; Reinhardt et al., 2011). We assume that preventive strategies are more common in the United States. In the present study, calcium was supplemented orally (40 herds) or subcutaneously (13 herds) in 46.1% of the collaborating herds. Only 8.7% of the herds used anionic salts to prevent hypocalcemia. In the United States, calcium supplementation also seems to be the most common strategy to prevent hypocalcemia. Based on the recent NAHMS report, 68.9 and 27.6% of the participating herds used calcium products and anionic salts, respectively (USDA, 2014). A trend was observed for large dairy farms (≥500 milking cows) to use calcium supplementation and anionic salts more often than smaller operations.
German farmers favored oral calcium supplementation as a preventive strategy (Table 2). Sound evidence is available about the efficacy of oral calcium supplementation to prevent hypocalcemia (Sampson et al., 2009; Oetzel and Miller, 2012; Blanc et al., 2014; Martinez et al., 2016). Furthermore, economic advantages have been demonstrated (McArt and Oetzel, 2015). Based on a simulation with 1,000 calvings per year, a farm can expect an average net gain ranging from $3,000 to $8,000 after postpartum supplementation of oral calcium to multiparous animals. In the present study, cows in their third or greater lactation were predominantly supplemented with oral calcium products. It is noteworthy, however, that dairy farmers did not consider higher risk for hypocalcemia in older animals as the percentage of supplemented cows was almost the same for cows in lactation 3 (30%) or higher (34%).
Calving ease had no significant effect on serum calcium concentration. Because evidence indicates that primiparous cows have higher serum calcium concentrations, this finding might be confounded as presence of dystocia is more prevalent in primiparous cows (Mee, 2004; USDA, 2010).
Comparing different breeds, serum calcium concentration did not differ among Holstein, Simmental, and Jersey cows. These results must be interpreted with caution, as only 1 and 2 farms kept Jersey and Simmental cows as their dominant breed, respectively.
Serum calcium and magnesium concentration were negatively associated. Cows suffering from hypocalcemia had higher serum magnesium concentration (Figure 2). This seems to be contradictory as magnesium is considered as an important prerequisite for proper PTH-receptor function (Goff, 2014). Renal excretion of magnesium depends on oral magnesium intake and the concentration of PTH (Martin-Tereso and Martens, 2014). In a period of low serum calcium concentration, PTH is secreted into the blood, leading to calcium retention in the kidneys and increased resorption of calcium in the gut via production of 1,25-dihydroxyvitamin D. Our findings are in agreement with a previous assumption, that PTH secretion raises the threshold for renal magnesium excretion, resulting in a higher serum magnesium concentration (Goff, 2008).
In contrast, serum phosphorus concentration was low in cows suffering from hypocalcemia (Figure 3). Mechanisms of phosphorus regulation are not fully understood yet. Also, the role of hypophosphatemia in recumbent cows remains speculative. A 21-mo-long feeding trial with a diet restricted in phosphorus (2.4 g/kg) led to reduced DMI, milk yield, and BW, but did not result in recumbency (Valk and Sebek, 1999). Recently, it has been shown, however, that the presence of PTH in hypocalcemic cows increased phosphorus excretion through urine and saliva (Grünberg, 2014). A reduction of DMI prepartum can also cause insufficient phosphorus uptake through the diet and contribute to phosphorus depletion. Similar to the decrease of calcium around parturition, the major reason for hypophosphatemia is the production of colostrum and milk, as approximately 1 g of phosphorus is excreted in every kilogram of milk (Goff, 1999; Grünberg, 2014).
Study Limitations
The objective of this study was to characterize the cow-level prevalence of clinical and subclinical hypocalcemia in German dairy herds. To achieve this objective, 115 farms of 8 federal states from Germany were enrolled through veterinary practitioners that had been asked to collaborate in this multi-center study. As in many other studies determining prevalences for hyperketonemia (e.g., Ospina et al., 2010; Chapinal et al., 2012; Suthar et al., 2013) or hypocalcemia (Gild et al., 2015; Miltenburg, 2015), the dairy farms enrolled constitute a convenience sample. It is difficult to conclude if the participating dairies are representative for all dairies of the given region. In fact, the selection of herds might have been biased by an underlying interest to participate stimulated by a previous history with the condition at hand. The objective was not to compare within-herd-level prevalences of hypocalcemia because the confidence interval for the prevalence estimate is wide using only 12 samples. Rather, we wanted to categorize herds based on the proportion of positive samples (i.e., blood calcium below threshold) into negative (0 to 2/12), borderline (3 to 5/12), or positive (≥ 6/12). Such classification is appropriate using 12 cows per herd based on the assumptions provided by Oetzel (2004) using a 75% confidence interval and an alarm level of 30% (Figure 1). For practitioners or consultants, this might be an adequate approach to screen a herd for the presence of subclinical hypocalcemia. As obvious from our results, many herds were classified as borderline (44.3%). In such case, we would advise to draw more samples to classify the herd more appropriately. Although the probability to misclassify a herd decreases with increasing sample size, it is the nature of the disease with a very short risk period (0 to 48 h) that limits this approach. In a 1,000 cow dairy, only 5.5 animals are at risk of being sampled for evaluation of hypocalcemia on any given day.
Our study design is not appropriate to give a well-founded statement on blood calcium dynamics postpartum, due to the sampling time of 0 to 48 h postpartum and frequency of sampling (1 sample per cow). Recent studies with a repeated measurement in individual cows (Blanc et al., 2014; Caixeta et al., 2017) are more suitable to illustrate the effect of time of sampling on serum calcium concentration.
Based on our inclusion criteria, small dairy farms (
Periparturient hypocalcemia is a common metabolic disorder in dairy cows that leads to an increased risk of detrimental health and production outcomes and in severe cases can be life threatening. Physiologically, serum calcium concentration in the adult cow is maintained above 2.0 mmol/L (Martin-Tereso and Martens, 2014). Due to the start of colostrum production and consequently increasing calcium demand, the nadir of serum calcium concentration occurs 12 to 24 h after parturition (Kimura et al., 2006; Goff, 2008).
Hypocalcemia is considered as a gateway disease and predisposes the cow to various metabolic and infectious disorders in early lactation (Goff, 2008) such as metritis (Martinez et al., 2012) and mastitis (Curtis et al., 1983). In a study by Martinez et al. (2012), numbers of neutrophils were reduced and their ability to undergo phagocytosis and oxidative burst was impaired in cows affected by hypocalcemia which might in part explain the increased risk for infectious diseases. On a cellular level, suppressed function of immune cells was mediated by reduced cytosolic calcium concentration (Martinez et al., 2014).
Cows with naturally occurring hypocalcemia at parturition had elevated concentrations of NEFA and BHBA as indicators of increased lipomobilization (Martinez et al., 2012). The same group of authors were able to repeat these finding in cows with induced hypocalcemia (Martinez et al., 2014). Induction of hypocalcemia with EDTA infusion caused reduced DMI and decreased plasma concentrations of insulin. These negative effects are supported by other studies showing an increased risk for displaced abomasum (Chapinal et al., 2011; Seifi et al., 2011), increased weight loss in early lactation (Caixeta et al., 2015), and ultimately an increased culling risk (Seifi et al., 2011; Roberts et al., 2012) for cows with hypocalcemia. Furthermore, subclinical hypocalcemia affected reproductive performance such as estrous cyclicity (Ribeiro et al., 2013; Caixeta et al., 2017) and pregnancy rate to first AI (Chapinal et al., 2012).
In a retrospective study including 1,462 cows from 480 dairy farms in 21 states of the United States, the prevalence of hypocalcemia was 25% in first lactation cows and about 50% in multiparous cows (Reinhardt et al., 2011). Clinical milk fever was prevalent in 1, 4, 6, and 10% of first, second, third, and ≥fourth lactation cows, respectively. These results originate from the 2002 National Animal Health Monitoring System (NAHMS) dairy study (USDA, 2002). This study has been used as a reference for the prevalence of hypocalcemia multiple times. But the study was not specifically designed to estimate cow- and herd-level prevalence of hypocalcemia and the currentness of the results are limited.
More recently, different strategies (e.g., oral calcium supplementation, anionic salts) to prevent hypocalcemia have evolved and were implemented in the dairy industry (Martin-Tereso and Martens, 2014). These approaches might affect the prevalence of hypocalcemia. To our knowledge, however, no information is available reporting the actual prevalence of hypocalcemia and associated preventive strategies.
Therefore, the objective of this study was to estimate the prevalence of hypocalcemia on a cow level and the implemented preventive strategies to control for hypocalcemia in commercial German dairy herds.
MATERIALS AND METHODS
The experimental procedures reported herein were conducted with the approval of the Institutional Animal Care and Use Committee of the Freie Universität Berlin.
Study Population
A cross-sectional study was conducted based on a convenience sample of 115 dairy herds from 8 federal states of Germany between February 2015 and August 2016. Inclusion criteria for herds were (1) participation in a federal DHIA testing system, (2) freestall housing with at least 100 milking cows, (3) feeding of a TMR-based diet, and (4) a computerized herd management software. Average herd size was 513 and ranged from 112 to 2,607 lactating cows. The average milk production (305-d ECM, 4.0% fat, 3.4% protein) was 9,231 kg (range 6,257–10,880 kg). Holstein Friesian cows were the dominant breed on 112 farms. Two farms kept Simmental cattle and 1 farm Jersey as the dominant breed.
A sample size calculation was conducted according to Dohoo et al. (2009). We assumed that the prevalence of milk fever tends to be highly clustered within herds because of the effect of herd management (e.g., breed, dry cow nutrition) on the risk of hypocalcemia. Therefore, we selected an intra-cluster correlation coefficient of 0.3. A sample size of 1,388 animals with 12 animals per herd was deemed adequate to estimate the true prevalence of subclinical hypocalcemia on a cow level with 95% confidence and 10% precision.
If a farm provided less than 12 blood samples the farm was excluded from statistical analysis. If a farm supplied more than 12 blood samples, 12 cows were selected, using a random function in Excel (Office 2010, Microsoft Deutschland Ltd., Munich, Germany). A random list was generated separately for each of the farms.
Experimental Procedures
Veterinary practitioners had been invited to participate in the study by an information leaflet sent out by regular mail. Participating practices were informed about the nature and duration of the study and received a package containing serum blood collection systems (S-Monovette 9mL Z, Sarstedt AG and Co, Nürnbrecht, Germany), cryo-vials (Cryvial, Carl Roth GmbH and Co. KG, Karlsruhe, Germany) to store serum at −20°C until analysis, and a written standard operating procedure. This standard operating procedure described which information to record for each cow enrolled and how to examine the cow before blood collection. A case report form for each cow was provided to document time of sampling, ear tag number, time of calving, calving ease (i.e., unassisted calving or assisted calving with at least one person), clinical symptoms of milk fever (i.e., recumbency), and parity. Administration of calcium products, time relative to calving, and route of administration (i.e., subcutaneous, intravenous, oral) of these products was also documented. Sampling 12 cows per herd, veterinarians were asked to include 4 primiparous cows into the cohort. The farm personnel was asked, if other preventive strategies, such as feeding of anionic salts in the close-up group or injection of vitamin D before calving were implemented.
Animals were enrolled by convenience when a veterinarian visited the farm on a given day and an animal met the inclusion criteria of being within 48 h after parturition.
Definition of Hypocalcemia on Cow Level and Herd Level
Normocalcemia was defined as serum calcium concentration greater or equal to 2.0 mmol/L (Reinhardt et al., 2011). Cows not affected clinically but with a serum calcium concentration below 2.0 mmol/L were categorized as subclinical hypocalcemic animals. Recumbent cows with a serum calcium concentration below 2.0 mmol/L were defined as cows suffering from clinical milk fever. Although often used in current literature (Reinhardt et al., 2011; Wilhelm et al., 2017) it was recently shown that 2.0 mmol/L is the most conservative approach as higher thresholds (i.e., 2.1 and 2.2 mmol/L) were also associated with negative health or production outcomes (Chapinal et al., 2011; Seifi et al., 2011; Chapinal et al., 2012; Martinez et al., 2012; Roberts et al., 2012). Therefore, analyses were conducted considering 3 thresholds (i.e., 2.0, 2.1, and 2.2 mmol/L).
Based on the results of the sampled cohort per farm, herds were categorized as negative (≤2 animals per herd with serum calcium concentration below the threshold), borderline (3 to 5 animals per herd with serum calcium concentration below the threshold), or positive (≥6 animals per herd with serum calcium concentration below the threshold) according to Cook et al. (2006). Using a confidence level of 75% and an alarm level of 30%, the sampling of 12 animals per herd is adequate to classify herds into 3 categories Classification of blood calcium concentrations using 75% CI and an alarm level of 30% for test results from 12 cows sampled from a group of 100 cows. This calculation illustrates the association between positive blood samples in the cohort and prevalence of hypocalcemia in the tested herd.
Blood Sampling and Laboratory Analyses
Blood samples were taken from the coccygeal vessels using a serum blood collection system. Samples were kept at room temperature and allowed to clot. Within 5 h of blood collection, samples were centrifuged to harvest serum, which was frozen at −20°C. Analysis of blood samples was carried out by a commercial laboratory (Synlab Services GmbH, Augsburg, Germany). Total serum calcium, magnesium, and phosphorus concentration was analyzed using photometry (AU680, Beckman Coulter, Krefeld, Germany). The interassay coefficient of variation was 1.03% (Ca 2.37 mmol/L; n = 16), 1.06% (Mg = 0.99 mmol/L; n = 16), and 2.43% (P = 0.83 mmol/L; n = 16) for calcium, magnesium, and phosphorus, respectively. The intraassay coefficient of variation was 1.19% (Ca 2.40 mmol/L; n = 10), 0.88% (Mg = 0.99 mmol/L; n = 10), and 1.03% (P = 0.85 mmol/L; n = 10) for calcium, magnesium, and phosphorus, respectively.
Statistical Analyses
Individual cow data were transferred to Microsoft Excel (Office 2013, Microsoft Deutschland Ltd.). Statistical analyses were performed using SPSS for Windows (version 22.0, SPSS Inc., IBM, Ehningen, Germany). The association of lactation number and the type of hypocalcemia or the type of individual preventive strategy was analyzed using cross tabulations and χ2 tests.
For evaluation of the association between serum calcium concentration and time of calving, ease of calving, and time interval from calving to sampling, we used the GENLINMIXED procedure of SPSS. Cow was the experimental unit and herd was considered as a random effect. According to the model-building strategies described by Dohoo et al. (2009), each parameter considered for the mixed model should be separately analyzed in a univariate model, including the parameter as a fixed factor (i.e., categorical parameter) or covariate (i.e., continuous parameter). Only parameters resulting in univariate models with P ≤ 0.2 should be included in the final mixed model. The initial model contained the following explanatory variables as fixed effects: parity (1, 2, 3, ≥4), breed (Holstein, Jersey, or Simmental), time of calving (daytime from 0600 to 1759 h vs. nighttime 1800 to 0559 h), calving ease (unassisted calving vs. assisted calving), and time interval from calving to sampling (continuous; 0 to 48 h).
The concentration of calcium was related to the concentration of phosphorus or magnesium using a linear regression model and the LINEAR REGRESSION procedure from SPSS: yi = a + bXi, where yi is the dependent variable (magnesium or phosphorous concentration), Xi is the independent variable (calcium concentration), b is the slope of the regression line, and a is the intercept. R2 describes the coefficient of determination, which is the relative proportion of variance in yi that can be explained
Overall, blood samples were drawn from 1,709 animals at 0 to 48 h after calving from 125 farms. Ten farms with 54 animals were excluded from analysis because they provided less than 12 samples per farm. Another 275 animals were randomly excluded because 60 farms provided more than 12 samples per farm.
Data of 1,380 animals were available for final analyses. Of those, 228 (16.5%), 355 (25.7%), 332 (24.1%), and 465 (33.7%) were in first, second, third, and ≥fourth lactation, respectively.
Based on a calcium threshold of 2.0 mmol/L and clinical signs, the prevalence of subclinical hypocalcemia and clinical milk fever was 40.7% (561/1,380) and 7.2% (99/1,380), respectively. Considering higher thresholds of 2.1 and 2.2 mmol/L, prevalence of subclinical hypocalcemia increased to 53.0% (732/1380) and 67.5% (931/1380), respectively The prevalence of hypocalcemia increased with parity. None of the cows in first lactation was suffering from clinical milk fever. Prevalence of clinical milk fever was 1.4% (5/355), 5.7% (19/332), and 16.1% (75/465) for second, third, and ≥fourth parity cows, respectively
Table 1. Prevalence (no./total; % in parentheses) of subclinical hypocalcemia and milk fever 0 to 48 h after parturition in dairy cows stratified by parity considering 3 thresholds for blood calcium
Type of hypocalcemia Lactation 1 Lactation 2 Lactation 3 Lactation ≥4
Subclinical
Threshold 2.0 mmol/L 13/228a 103/355b 164/332c 281/465d
(5.7) (29.0) (49.4) (60.4)
Threshold 2.1 mmol/L 32/228a 158/355b 211/332c 331/465d
(14.0) (44.5) (63.6) (71.2)
Threshold 2.2 mmol/L 83/228a 222/355b 256/332c 370/465bc
(36.4) (62.5) (77.1) (79.6)
Clinical 0/228a 5/355a 19/332b 75/465c
(0.0) (1.4) (5.7) (16.1)
a–d
Values with different superscripts within rows differ, P < 0.05.
A significant effect of parity (P < 0.001) was observed on serum calcium concentration. Cows in first, second, third, or ≥fourth lactation had a serum calcium concentration of 2.213 mmol/L (95% CI: 2.054–2.372), 2.102 mmol/L (95% CI: 1.942–2.262), 1.997 mmol/L (95% CI: 1.837–2.158), and 1.891 mmol/L (95% CI: 1.735–2.046), respectively. Serum calcium concentration of cows that calved at night was 0.087 mmol/L higher compared with cows that calved during the day (95% CI: 0.044–0.130; P = 0.001). No significant effect of breed (P = 0.811), time from calving to sampling (P = 0.288), or calving ease (P = 0.902) was observed on serum calcium concentration.
A negative association of serum calcium and serum magnesium concentration was observed (y = −0.208x + 1.454; R2 = 0.151; P < 0.001; In contrast, there was a positive association of serum calcium and serum phosphorus concentration (y = 0.900x − 0.229; R2 = 0.335; P < 0.001; Association between serum calcium and serum magnesium concentration for all cows (n = 1,380, y = −0.208x + 1.454; R2 = 0.151; P < 0.001).
Association between serum calcium and serum phosphorus concentration for all cows (n = 1,380, y = 0.900x – 0.229; R2 = 0.335; P < 0.001).
Prevention of hypocalcemia on a cow level was more prevalent in multiparous cows compared with primiparous cows. Oral calcium supplementation was implemented in 13.8, 24.1, and 26.0% in second, third, and ≥fourth parity cows (Table 2) and most prevalent for prevention of hypocalcemia at the cow-level (n = 255; Table 2). Subcutaneous calcium injection or prepartum vitamin D application played a minor role and was on the herd level always combined with another preventive strategy (Table 2). In 34.8% (40/115), 6.1% (7/115), and 2.6% (3/115) of the herds, oral calcium supplementation, anionic salts, or a combination of both was used to control hypocalcemia on a herd level, respectively. Most of the herds (65/115) did not implement a control strategy for hypocalcemia.
Type of prophylaxis (no./total; % in parentheses) to prevent hypocalcemia in 1,380 cows of 115 dairy herds considering parity
Type of prophylaxis Lactation 1 Lactation 2 Lactation 3 Lactation ≥4
Oral calcium 5/228a 49/355b 80/332c 121/465c
(2.2) (13.8) (24.1) (26.0)
Subcutaneous calcium 0/228a 7/355ab 14/332b 23/465b
(0.0) (2.0) (4.2) (4.9)
Vitamin D prepartum 0/228ab 0/355b 7/332ac 15/465c
(0.0) (0.0) (2.1) (3.2)
Overall 5/228 56/355 101/332 159/465
(2.2) (15.8) (30.4) (34.2)
a–c
Values with different superscripts within rows differ, P < 0.05.
Only 12.2% of the 115 herds enrolled were classified as negative based on the alarm levels set by Cook et al. (2006).
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Glucose concentration is not extensively examined during early lactation period in low-milk-yielding cows as that for high-yielding. Using point-of-care and hand-held glucometers could decrease time and cost of glucose estimation.The current study objectives were (i) to evaluate hypoglycemic status in recently calved low-milk-yielding cows, and (ii) to assess the use of Reflotron as a glucometers for cows. Serum glucose (s-gluc) from recently calved and pregnant cows was estimated using analytical enzymatic method (AnaMeth) to assess the hypoglycemia. Blood glucose (b-gluc), plasma glucose (p-gluc), and s-gluc from recently calved, pregnant, and non-pregnant cows were estimated using devices and method of interest. Passing-Bablok regression and Bland-Altman plot were used to evaluate the agreement between the different methods. Serum glucose was lower, but not statistically significant, in recently calved compared to pregnant cows, and it was significantly greater than the reference value for hypoglycemic cows. No differences were detected between s-gluc and p-gluc using both AnaMeth and Reflo , which were also identical in that estimation. Furthermore, overestimated p-gluc, and both Reflo and significantly overestimated b-gluc in study cows. Hypoglycemia is not evident in recently calved low-milk-yielding cows. Plasma and serum can be used interchangeability for glucose estimation in cows
Cows with a serum calcium concentration below 2.0 mmol/L were considered as hypocalcemic. Although this is a conservative threshold, it is well accepted in research and applied in the field (DeGaris and Lean, 2008; Reinhardt et al., 2011; Wilhelm et al., 2017). Recent studies suggested higher thresholds. It was shown that hypocalcemia using 2.1, 2.2, and 2.3 mmol/L thresholds was associated with a negative health outcome such as displaced abomasum and metritis (Chapinal et al., 2011, 2012; Martinez et al., 2012) or an increased culling risk (Seifi et al., 2011; Roberts et al., 2012). These studies, however, considered a longer risk period postpartum (i.e., of 3 to 7 DIM). Although these epidemiological studies showed an association and also some evidence for a causal relationship between hypocalcemia and an increased risk for infectious diseases (Martinez et al., 2014), one has to be careful when evaluating longer risk periods. It is also plausible that reduced feed intake before clinical signs of disease can affect serum calcium levels as most recently shown by Pinedo et al. (2017) for cows suffering from puerperal metritis. At calving, no difference was present in serum calcium concentration between healthy and metritic cows. On the day of diagnosis (on average 6.1 DIM), however, serum calcium concentration was lower in cows with puerperal metritis (1.57 mmol/L) compared with healthy cows (2.10 mmol/L). To reflect higher thresholds, we calculated the prevalence accordingly. Table 1 shows that a mild increase of the threshold leads to a dramatic increase of animals considered as hypocalcemic. Further evaluations are necessary to define the most appropriate threshold of hypocalcemia within this time period. In our study, 47.6% of multiparous cows suffered from subclinical hypocalcemia within 48 h after parturition. This finding is in agreement with others (Reinhardt et al., 2011; Gild et al., 2015; Miltenburg, 2015). The inability of the cow to maintain normal serum
Periparturient hypocalcemia is a common metabolic disorder in dairy cows that leads to an increased risk of detrimental health and production outcomes and in severe cases can be life threatening. Physiologically, serum calcium concentration in the adult cow is maintained above 2.0 mmol/L (Martin-Tereso and Martens, 2014). Due to the start of colostrum production and consequently increasing calcium demand, the nadir of serum calcium concentration occurs 12 to 24 h after parturition (Kimura et al., 2006; Goff, 2008). Hypocalcemia is considered as a gateway disease and predisposes the cow to various metabolic and infectious disorders in early lactation (Goff, 2008) such as metritis (Martinez et al., 2012) and mastitis (Curtis et al., 1983). In a study by Martinez et al. (2012), numbers of neutrophils were reduced and their ability to undergo phagocytosis and oxidative burst was impaired in cows affected by hypocalcemia which might in part explain the increased risk for infectious diseases. On a cellular level, suppressed function of immune cells was mediated by reduced cytosolic calcium concentration (Martinez et al., 2014). Cows with naturally occurring hypocalcemia at parturition had elevated concentrations of NEFA and BHBA as indicators of increased lipomobilization (Martinez et al., 2012). The same group of authors were able to repeat these finding in cows with induced hypocalcemia (Martinez et al., 2014). Induction of hypocalcemia with EDTA infusion caused reduced DMI and decreased plasma concentrations of insulin. These negative effects are supported by other studies showing an increased risk for displaced abomasum (Chapinal et al., 2011; Seifi et al., 2011), increased weight loss in early lactation (Caixeta et al., 2015), and ultimately an increased culling risk (Seifi et al., 2011; Roberts et al., 2012) for cows with hypocalcemia. Furthermore, subclinical hypocalcemia affected reproductive performance such as estrous cyclicity (Ribeiro et al., 2013; Caixeta et
Hypocalcemia around calving is considered a gateway disease that can lead to health disorders and decreased milk production. The objective of this cross-sectional study was to evaluate the prevalence of clinical and subclinical hypocalcemia 0 to 48 h after calving. Blood samples were drawn from 12 animals of each dairy farm (n = 115) and analyzed for serum calcium, magnesium, and phosphorus concentration. Cows not affected clinically but with a serum calcium concentration below 2.0 mmol/L were characterized as subclinical hypocalcemic animals. Recumbent cows with a serum calcium concentration below 2.0 mmol/L were defined as cows suffering from clinical milk fever. Herds were classified into negative (0 to 2/12), borderline (3 to 5/12), and positive (≥6/12) according to the number of animals with hypocalcemia. Strategies to control hypocalcemia were documented. Prevalence of clinical milk fever was 1.4, 5.7, and 16.1% for second, third, and ≥fourth parity cows, respectively. None of the cows in first lactation were suffering from clinical milk fever. Based on the threshold of 2.0 mmol/L, 5.7, 29.0, 49.4, and 60.4% of cows in first, second, third, and ≥fourth lactation were suffering from subclinical hypocalcemia, respectively. Fourteen, 51, and 50 herds were classified as negative, borderline, and positive, respectively. A positive association was observed between serum calcium and serum phosphorus concentration. Serum calcium and magnesium concentration were negatively associated. Only 50 of 115 farms had a control strategy implemented to avoid hypocalcemia. Most common was the use of oral calcium products (40/115 herds), followed by feeding of anionic salts in the close-up diet (10/115 herds). These results indicate that the prevalence of clinical and subclinical hypocalcemia in German dairy herds was high and that an active control strategy was not implemented on all farms. The negative association between calcium and magnesium warrants further research reg
Differential diagnoses: Toxic mastitis Toxic metritis Other systemic toxic conditions Traumatic injury (stifle injury, coxofemoral luxation, fractured pelvis, spinal compression) Calving paralysis syndrome (damage to the L6 lumbar roots of sciatic and obturator nerves) Compartment syndrome: condition characterized by insufficient blood supply due to increased pressure to tissues that results in pain, decreased ability to move or numbness Treatment Treatment Options IV injection of a calcium gluconate salt, although SC and IP routes are also used. A general rule for dosing is 1 g calcium/45 kg (100 lb) body weight. Calcium is cardiotoxic, so calcium-containing solutions should be administered slowly (10-20 min.) while cardiac auscultation is performed. Oral calcium avoids the risks of cardiotoxic adverse effects and may be useful in mild cases of parturient paresis. Prevention Diet modifications to face the increased calcium demand1: Low calcium diets: To be effective, diets must provide less than 20 g of available calcium. Low potassium forages/diets: Decrease the likelihood of clinical hypocalcemia but not the incidence of subclinical hypocalcemia. Feeding anionic salts for 21 days: Prevent clinical (a five-fold reduction) and subclinical hypocalcemia. Many commercially available anionic mineral- or protein-based supplements are available for use in formulating these diets. Oral sources of calcium: In the form of calcium chloride in gel or paste forms, many oral supplements are absorbed within 30 minutes after administration and blood calcium concentration is increased for four to six hours.
HypocalcemiaSHARE Sudden Decrease in Serum Calcium Levels That Occurs in the Production of Colostrum and Milk in Early Stages of Lactation Also known as milk fever or parturient paresis Can be clinical or subclinical Cows with subclinical do not show clinical symptoms The only way to detect subclinical hypocalcemia is to analyze blood for the concentration of calcium within the first one to two days after calving Clinical Signs Three Stages Stage 1: Signs of hypersensitivity and excitability Mildly ataxic Fine tremors over the flanks and triceps Ear twitching and head bobbing If calcium therapy is not instituted, cows will likely progress to the second, more severe stage. Stage 2: Unable to stand but can maintain sternal recumbency Anorexia, confusion, dry muzzle, subnormal body temperature and cold extremities Auscultation reveals low heart rate and decreased intensity of heart sounds; peripheral pulses are weak, and smooth muscle paralysis leads to GI stasis Inability to urinate Cows often tuck their heads into their flanks – if the head is extended, one may see an S-shaped curve to the neck. Stage 3: Progressive loss of consciousness to the point of coma Unable to maintain sternal recumbency, complete muscle flaccidity, unresponsive to stimuli and severe bloat Heart rate approaching 120 bpm and undetectable peripheral pulses If untreated, cows in stage 3 may only survive a few hours.
Calcium levels are controlled by a pair of parathyroid glands. These two tiny glands are embedded in the thyroid gland, which sits just below the larynx, or "voice box," overlying the windpipe. The parathyroid glands are responsible for monitoring the level of calcium in the blood. When calcium levels are too low, the glands release a hormone called parathyroid hormone (PTH), which acts to return calcium levels to normal. Why is having low calcium bad for my pet? Low calcium levels are associated with a number of serious disorders including antifreeze poisoning, inflammation of the pancreas, kidney failure, and parathyroid gland failure. In nursing female dogs, heavy milk production can lead to hypocalcemia (milk fever) and may result in seizures. Pets with abnormally low calcium levels often show signs of muscle twitching, loss of appetite, weakness, and listlessness. In severe cases, pets may have convulsions or seizures. How is calcium measured? Two forms of calcium are found the blood, called total calcium and ionized calcium (also called free calcium). Total calcium. The test for total calcium is simple, rapid, and relatively inexpensive, and it is typically used as a preliminary test to measure calcium levels. However, total calcium can appear falsely decreased due to low levels of albumin (a blood protein that carries calcium around in the blood stream), as well as delayed testing (i.e., sample left standing on the counter for too long before testing). If preliminary testing reveals hypocalcemia, then measuring ionized calcium is often recommended to confirm the finding. Ionized calcium. This is the definitive test for measuring blood calcium levels. It is an excellent test, but is more difficult to perform than total calcium, and requires patient preparation and special sample handling of the sample. It also tends to be more expensive and often takes longer to get results back from the laboratory. What further testing is required if my pet has low total calc
Hypocalcaemia / Milk fever Hypocalcaemia, or milk fever, occurs in cattle, sheep and goats. It is most common in high producing or dairy-cross cows and in milking goats. Clinical signs develop when serum calcium levels fall below a critical level (hypocalcaemia). Affected animals are initially excited or agitated with muscle tremors, then go down and are unable to rise. Conditions when hypocalcaemia is likely to occur property history of hypocalcaemia in cows greater than five years old, in does greater than four 4 years old and in ewes late pregnancy and also after calving in dairy cows high producing and dairy-cross cows cows with a history of hypocalcaemia alkaline diets high in sodium and potassium, and low in sulphate and chloride low calcium intake after calving and high intake before low roughage intake heavy grain feeding of sheep fat cows with a fat score of 3.5 or greater. Identification and diagnosis Clinical signs that would lead you to suspect hypocalcaemia include: tetany, unable to rise, dry muzzle ewes cast after handling, often with hind legs behind response to treatment with calcium borogluconate blood samples can also be collected to determine serum calcium levels Prevention An integrated approach to prevent hypocalcaemia should consider the following: avoiding over-fattening cows ensuring constant access to feed during calving avoiding grazing high-risk pastures as per grass tetany feeding hay before calving. Using the Health Cost Benefit Calculator to determine the cost-benefit of the this option keeping calcium intake to less than 50g/day before calving feeding as much calcium as possible after calving. Clover-dominant pasture is one way to do this avoiding handling of heavily pregnant ewes lowering the herd/flock age structure as older cows, does and ewes are higher risk.
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