Parturient Paresis in Sheep and Goats

Parturient paresis is due to a decrease in calcium intake under conditions of increased calcium requirements, usually during late gestation. This results in a low serum calcium concentration, particularly in animals pregnant with multiple fetuses. Some cases are complicated by concurrent pregnancy toxemia. Ewes that are both hypocalcemic and hyperketonemic may not be able to produce endogenous glucose as readily as ewes that are only hyperketonemic, leading to the risk of more severe disease developing when both conditions are present.

Parturient paresis can occur at any time from 6 weeks before to 10 weeks after parturition; however, the greatest demand for calcium because of mineralization of the fetal skeleton occurs 1–3 weeks prepartum, particularly when multiple fetuses are present in utero.

Whenever an abrupt decrease in calcium intake occurs, the body requires 24–72 hours to activate the metabolic mechanisms necessary to mobilize stored calcium. Mobilization of stored calcium can be inadequate to meet an animal’s needs in older ewes and does, in animals with chronic calcium deficiency, and when diets are calcium deficient.

Examples of forages with low calcium levels include cereal hays or pasture, poor-quality grassy hays and pasture, and corn silage. Most grains also contain minimal calcium but additionally have high levels of phosphorus, causing an inverse calcium:phosphorus ratio, increasing dietary risk. Vitamin D deficiency, which occurs in housed ruminants during winter months, also depresses calcium absorption from the GI tract.

• Parturient paresis occurs more often around parturition and can be aggravated by stressful situations

• Under field conditions, a response to calcium administration would support diagnosis of parturient paresis

• A definitive diagnosis can be made only by assessment of calcium concentration in blood (<2 mmol/L)

Characteristically, parturient paresis occurs in outbreaks, with most cases occurring in the last few weeks of gestation, although it is not uncommon for individual animals to be affected. Usually, <5% of animals are affected; however, severe outbreaks may involve up to 30% of the flock.

Onset is sudden and often follows—within 24 hours—an abrupt change of feed, a sudden change in weather, or short periods of fasting imposed by circumstances such as shearing or transportation (also see Transport Tetany in Ruminants).

In early hypocalcemia in sheep, the most commonly noted clinical signs are stiff gait, ataxia, salivation, constipation, and depressed rumen motility, progressing to bloat, recumbency, loss of anal reflex and, if untreated, death. Tachycardia may be present; heart sounds are quieter than normal. Often when recumbent, ewes are in a sternal frog-type position, with the hindlegs extended caudally. Goats have a similar presentation, although muscle tremors are more common than in sheep.

A working diagnosis is based on history and clinical signs. In outbreaks occurring before parturition, pregnancy toxemia is the main differential diagnosis. These diseases may also occur concurrently. A tentative diagnosis of acute hypocalcemia is supported by an immediate, dramatic, and usually lasting response to slow IV administration of calcium.

Diagnosis can be confirmed by testing serum calcium concentration before treatment. Urine ketone or serum beta-hydroxybutyrate concentrations should always be evaluated at the same time. Hypocalcemia is often classified as total serum calcium concentration <2 mmol/L or, if expressed as ionized calcium, <1.1 mmol/L. Normal values for serum calcium concentration are reportedly 2.8–3.2 mmol/L for sheep and 2.2–3.05 mmol/L for goats. (To convert from mmol/L to mg/dL, divide the value by 0.25.) Animals with low serum albumin concentration, such as occurs with Johne’s disease and clinical gastrointestinal parasitism, may have low total serum calcium and normal ionized calcium concentration.

• Treatment is IV administration of calcium, which leads to rapid alleviation of clinical signs

• Prevention is based on provision of adequate dietary calcium throughout gestation

Treatment of parturient paresis should be initiated immediately, usually administered ascalcium borogluconate, IV (50–150 mL of a 23% solution). Calcium-containing products that also contain phosphorus and magnesium, as well as dextrose, likely have additional therapeutic value. Oral or subcutaneous administration of a calcium solution helps to prevent relapse. Before administration, calcium solution should be heated to 35 to 40°C. Intravenous administration must be performed slowly, over 5 to 7 minutes.

During treatment, the heart should be monitored, and treatment stopped if arrhythmias occur. For ease of IV administration, it may be preferred to increase the volume of the product by adding 50–150 mL of a 23% calcium borogluconate or gluconate solution to 1 L of a 5% dextrose solution and administering this volume over 10 minutes. Calcium solutions are irritating, so when administration is subcutaneous, the total volume should be divided to 2 or 3 equal quantities and administered to different parts of the body. Calcium administration can be repeated after 24 hours.

Dietary modifications to increase the calcium:phosphorus ratio (>1.5:1) and ensure total calcium in the diet meets National Research Council requirements ( see Table: Periparturient Calcium Requirements of a Meat Ewe and Dairy Doe), as well as vitamin D levels, may help to prevent further cases in pregnant animals. Sudden dietary changes or other stressors should be avoided during late gestation, and risk factors for pregnancy toxemia investigated.