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Parturient Paresis in Cows

(Milk fever, Hypocalcemia)


Andrew J. Allen

, DVM, PhD, DACVIM-LAIM, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University

Last full review/revision Jun 2015 | Content last modified Jun 2016
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Parturient paresis is an acute to peracute, afebrile, flaccid paralysis of mature dairy cows that occurs most commonly at or soon after parturition. It is manifest by changes in mentation, generalized paresis, and circulatory collapse.


Dairy cows will secrete 20–30 g of calcium in the production of colostrum and milk in the early stages of lactation. This secretion of calcium causes serum calcium levels to decline from a normal of 8.5–10 mg/dL to <7.5 mg/dL. The sudden decrease in serum calcium levels causes hyperexcitability of the nervous system and reduced strength of muscle contractions, resulting in both tetany and paresis. Parturient paresis may be seen in cows of any age but is most common in high-producing dairy cows entering their third or later lactations. Incidence is higher in Channel Island breeds.

Clinical Findings and Diagnosis:

Parturient paresis usually occurs within 72 hr of parturition. It can contribute to dystocia, uterine prolapse, retained fetal membranes, metritis, abomasal displacement, and mastitis.

Parturient paresis has three discernible stages. During stage 1, animals are ambulatory but show signs of hypersensitivity and excitability. Cows may be mildly ataxic, have fine tremors over the flanks and triceps, and display ear twitching and head bobbing. Cows may appear restless, shuffling their rear feet and bellowing. If calcium therapy is not instituted, cows will likely progress to the second, more severe stage.

Cows in stage 2 are unable to stand but can maintain sternal recumbency. Cows are obtunded, anorectic, and have a dry muzzle, subnormal body temperature, and cold extremities. Auscultation reveals tachycardia and decreased intensity of heart sounds. Peripheral pulses are weak. Smooth muscle paralysis leads to GI stasis, which can manifest as bloat, failure to defecate, and loss of anal sphincter tone. An inability to urinate may manifest as a distended bladder on rectal examination. Cows often tuck their heads into their flanks, or if the head is extended, an S-shaped curve to the neck may be noted.

In stage 3, cows lose consciousness progressively to the point of coma. They are unable to maintain sternal recumbency, have complete muscle flaccidity, are unresponsive to stimuli, and can suffer severe bloat. As cardiac output worsens, heart rate can approach 120 bpm, and peripheral pulses may be undetectable. If untreated, cows in stage 3 may survive only a few hours.

Differential diagnoses include toxic mastitis, toxic metritis, other systemic toxic conditions, traumatic injury (eg, stifle injury, coxofemoral luxation, fractured pelvis, spinal compression), calving paralysis syndrome (damage to the L6 lumbar roots of sciatic and obturator nerves), or compartment syndrome. Some of these diseases, in addition to aspiration pneumonia, may also occur concurrently with parturient paresis or as complications. (Also see Bovine Secondary Recumbency Bovine Secondary Recumbency .)


Treatment is directed toward restoring normal serum calcium levels as soon as possible to avoid muscle and nerve damage and recumbency. Recommended treatment is 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 wt. Most solutions are available in single-dose, 500-mL bottles that contain 8–11 g of calcium. In large, heavily lactating cows, a second bottle given SC may be helpful, because it is thought to provide a prolonged release of calcium into the circulation. SC calcium alone may not be adequately absorbed because of poor peripheral perfusion and should not be the sole route of therapy. No matter what route is used, strict asepsis should be used to lessen the chance of infection at the injection site. Solutions containing formaldehyde or >25 g dextrose/500 mL are irritating if given SC. Many solutions contain phosphorus and magnesium in addition to calcium. Although administration of phosphorus and magnesium is not usually necessary in uncomplicated parturient paresis, detrimental effects of their use have not been reported. Magnesium may protect against myocardial irritation caused by the administration of calcium. Magnesium is also necessary for appropriate parathyroid hormone (PTH) secretion and activity in response to hypocalcemia. Most products available to veterinarians contain phosphite salts as the source of phosphorus. However, phosphorus found in blood and tissues of cattle is primarily in the form of the phosphate anion. Because no pathway exists for the conversion of phosphite to the usable phosphate form, it is unlikely these solutions are of any benefit in addressing hypophosphatemia.

Calcium is cardiotoxic; therefore, calcium-containing solutions should be administered slowly (10–20 min) while cardiac auscultation is performed. If severe dysrhythmias or bradycardia develop, administration should be stopped until the heart rhythm has returned to normal. Endotoxic animals are especially prone to dysrhythmias caused by IV calcium therapy.

Administration of oral calcium avoids the risks of cardiotoxic adverse effects and may be useful in mild cases of parturient paresis; however, it is not recommended as the sole approach for clinical milk fever cases. Products containing calcium chloride are effective but can be caustic to oral and pharyngeal tissues, especially if used repeatedly. Calcium propionate in propylene glycol gel or powdered calcium propionate (0.5 kg dissolved in 8–16 L water administered as a drench) is effective, less injurious to tissues, avoids the potential for metabolic acidosis caused by calcium chloride, and supplies the gluconeogenic precursor propionate. Oral administration of 50 g of soluble calcium results in ~4 g of calcium being absorbed into the circulation.

Regardless of the source of oral calcium, it is important to note that cows with hypocalcemia often have poor swallowing and gag reflexes. Care must be exercised during administration of calcium-containing solutions to avoid aspiration pneumonia. Gels containing calcium chloride should not be administered to cows unable to swallow.

Hypocalcemic cows typically respond to IV calcium therapy immediately. Tremors are seen as neuromuscular function returns. Improved cardiac output results in stronger heart sounds and decreased heart rate. Return of smooth muscle function results in eructation, defecation, and urination once the cow rises. Approximately 75% of cows stand within 2 hr of treatment. Animals not responding by 4–8 hr should be reevaluated and retreated if necessary. Of cows that respond initially, 25%–30% relapse within 24–48 hr and require additional therapy. Incomplete milking has been advised to reduce the incidence of relapse. Historically, udder inflation has been used to reduce the secretion of milk and loss of calcium; however, the risk of introducing bacteria into the mammary gland is high.


Historically, prevention of parturient paresis has been approached by feeding low-calcium diets during the dry period. The negative calcium balance results in a minor decline in blood calcium concentrations. This stimulates PTH secretion, which in turn stimulates bone resorption and renal production of 1,25 dihydroxyvitamin D. Increased 1,25 dihydroxyvitamin D increases bone calcium release and increases the efficiency of intestinal calcium absorption. Although mobilization of calcium is enhanced, it is now known that feeding low-calcium diets is not as effective as initially believed. Furthermore, on most dairy farms today, it is difficult to formulate diets low enough in calcium (<20 g absorbed calcium/cow/day), although the use of dietary straw and calcium-binding agents such as zeolite or vegetable oil may make this approach more useful.

Alternative methods to prevent hypocalcemia include delayed or incomplete milking after calving, which maintains pressure within the udder and decreases milk production; however, this practice may aggravate latent mammary infections and increase incidence of mastitis. Prophylactic treatment of susceptible cows at calving may help reduce parturient paresis. Cows are administered either SC calcium on the day of calving or oral calcium gels at calving and 12 hr later.

Most recently, the prevention of parturient paresis has been revolutionized by use of the dietary cation-anion difference (DCAD), a method that decreases the blood pH of cows during the late prepartum and early postpartum period. This method is more effective and more practical than lowering prepartum calcium in the diet. The DCAD approach is based on the finding that most dairy cows are in a state of metabolic alkalosis due to the high potassium content of their diets. This state of metabolic alkalosis with increased blood pH predisposes cows to hypocalcemia by altering the conformation of the PTH receptor, resulting in tissues less sensitive to PTH. Lack of PTH responsiveness prevents effective use of bone calcium, prevents activation of osteoclastic bone resorption, reduces renal reabsorption of calcium from the glomerulus, and inhibits renal conversion to its active form.

An important strategy to decrease blood pH in periparturient cattle is to reduce the potassium content of the diet. It is essential to include corn silage as a major portion of the dry cow’s diet, because it tends to have the lowest content potassium of available forages. Alfalfa is another forage source that may prove beneficial in maintaining proper blood pH. In the past, including alfalfa in a dry cow ration was not considered ideal because of the high calcium content. However, it has since been determined that calcium has little effect on the alkalinity of cow’s blood. Withholding potassium fertilizers on fields used to grow dry cow forages is another way to decrease potassium levels in hay fed to dry cows. Alternatively, readily absorbable anions can be added to the diet to increase the total negative charges in the blood, allowing more H+ to exist, decreasing the pH of the blood. Anionic salts to consider include calcium chloride, magnesium chloride, magnesium sulfate, calcium sulfate, ammonium sulfate, and ammonium chloride. Research evaluating the acidifying activity of different anionic salts has resulted in the following equation that describes the ion balance in rations:

DCAD = (Na+ + K+) – (Cl- + S-2)

The target value for close-up dry cow rations is -15 to +15 mEq/100 g dry matter. Sodium and potassium should be provided as close to the required levels as possible (0.1% dietary dry matter sodium, and 1% dietary dry matter potassium). Chloride should be added to the ration to offset the effects of low levels of potassium on blood alkalinity. In general, providing ~0.5% less dietary chloride than the concentration of potassium being fed will result in appropriate acidification. Urine pH provides an inexpensive and relatively accurate estimate of blood pH in dairy cattle. Mean urine pH ranges from ~6–6.5 are optimal to manage DCAD and prevent milk fever. Urine should be measured >24 hr after addition of an anionic diet in pre-fresh cows.

An important drawback to feeding anionic salts is poor palatability, which can be overcome by using a mixture of anionic salts within a moist, palatable ration such as corn silage, brewer’s grain, distiller’s grain, or molasses. Although sulfate salts are more palatable than chloride salts, they are less effective in acidifying the blood. Dietary sulfur should be >0.22% dry matter to support rumen microbial amino acid synthesis but <0.4% dry matter to avoid neurologic signs associated with sulfur toxicity. If dry matter intake drops >1 kg/day in a group of pre-fresh dry cows fed an acidifying diet, the dose of anions should be decreased to the point that dry matter intake is restored.

Administration of vitamin D3 and its metabolites effectively prevents parturient paresis. Large doses of vitamin D (20–30 million U/day), given in the feed for 5–7 days before parturition, reduces the incidence. However, if administration is stopped >4 days before calving, the cow is more susceptible. Dosing for periods longer than those recommended should be avoided because of potential toxicity. A single injection (IV or SC) of 10 million IU of crystalline vitamin D given 8 days before calving is an effective preventive. The dose is repeated if the cow does not calve on the due date. Newer compounds used (where available and approved) in lieu of vitamin D and less likely to cause hypervitaminosis include 25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, and 1α-hydroxycholecalciferol. After calving, a diet high in calcium is required. Administering large doses of calcium in gel form (PO) is commonly practiced. Doses of 150 g of calcium gel are given 1 day before, the day of, and 1 day after calving.

Use of synthetic bovine PTH may prove to be superior to administration of vitamin D metabolites. Vitamin D metabolites enhance GI calcium absorption, whereas PTH enhances GI calcium absorption and stimulates bone resorption. PTH is administered either IV 60 hr before parturition, or IM 6 days before parturition. Drawbacks to the use of PTH include increased labor requirements for administration, as well as the availability of such compounds.

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