Parturient paresis in pregnant and lactating ewes and does is a disturbance of metabolism characterized by acute-onset hypocalcemia and rapid development of hyperexcitability and ataxia, progressing to depression, recumbency, coma, and death. Unlike parturient paresis in dairy cattle, which primarily occurs within a few days of calving, the condition in ewes and does usually occurs before and less commonly after parturition. This condition may be underdiagnosed in some situations.
Parturient paresis is caused by 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 wk before to 10 wk after parturition; however, the greatest demand for calcium because of mineralization of the fetal skeleton occurs 1–3 wk prepartum, particularly when multiple fetuses are present in utero. Whenever an abrupt decrease in calcium intake occurs, the body requires 24–72 hr to activate the metabolic machinery necessary to mobilize stored calcium. Mobilization of stored calcium can be inadequate to meet the 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 little 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.
Clinical Findings and Diagnosis:
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, but severe outbreaks may involve up to 30% of the flock. The onset is sudden and often follows—within 24 hr—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 Transport Tetany in Ruminants ). In early hypocalcemia in sheep, the most commonly noted signs are stiff gait, ataxia, salivation, constipation, and depressed rumen motility, progressing to hyposensitivity, 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-lying position, with the hindlegs extended behind. Goats have a similar presentation, although muscle tremors are more commonly seen than in sheep.
A working diagnosis is based on the history and clinical signs. In outbreaks occurring before parturition, pregnancy toxemia (see Pregnancy Toxemia in Sheep and Goats Pregnancy Toxemia in Sheep and Goats Pregnancy toxemia, the most common metabolic disorder of pregnant small ruminants, occurs during the final stage of gestation as the result of inappropriate metabolism of carbohydrates and fats... read more ) is the main differential diagnosis. These diseases also occur concurrently. A tentative diagnosis of acute hypocalcemia is supported by a dramatic and usually lasting response to slow IV administration of calcium. Diagnosis can be confirmed by testing serum calcium levels before treatment. Urine ketone or serum β-hydroxybutyrate levels should always be evaluated at the same time. Hypocalcemia is often classified as total serum calcium levels <2 mmol/L or, if expressed as ionized calcium, <1.1 mmol/L. Normal values are reported as 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, such as occurs with Johne’s disease and clinical GI parasitism, may have low total serum calcium and normal ionized calcium.
Treatment and Prevention:
Treatment should be initiated immediately, usually administered as calcium 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 SC administration of a calcium solution helps to prevent relapse. During treatment, the heart should be monitored, and therapy slowed or 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 min. Dietary modifications to increase the calcium:phosphorus ratio (>1.5:1) and ensure total calcium in the diet meets NRC requirements (see Table: Calcium Requirements of a Meat Ewe and Dairy Doe During Gestation and Lactation Calcium Requirements of a Meat Ewe and Dairy Doe During Gestation and Lactation ), 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.