Hypomagnesemic Tetany in Cattle and Sheep

Hypomagnesemic tetany occurs after a decrease in plasma Mg concentration when absorption of dietary Mg is unable to meet the requirements for maintenance (3 mg/kg body weight) and lactation (120 mg/kg milk). This can arise after a decrease in food intake during inclement weather, during transport, or when cows graze short-grass dominant pastures containing < 0.2% Mg on a dry-matter basis. Low herbage availability (< 1,000 kg dry matter/hectare) results in liveweight losses during lactation, and plasma Mg decreases because insufficient Mg is obtained from body tissues mobilized during loss of liveweight to support lactation.

Mg absorption from the rumen may be decreased when potassium and nitrogen intakes are high and sodium and phosphorus intakes are low. Soils naturally high in potassium and those fertilized with potash and nitrogen (eg, via poultry manure) are high-risk areas for hypomagnesemic tetany. The more complex mineral interactions are likely to be involved in herds in which hypomagnesemic tetany occurs in first- and second-calving cows as well as in older cows.

Cows often do not develop clinical signs of hypomagnesemic tetany until blood calcium concentrations are also reduced, to < 0.8 mg/dL (0.35 mmol/L), which commonly occurs in cattle grazing green cereal crops. The hypocalcemia arises from either a decrease in calcium intake or absorption, or both. Lush grass pastures and green cereal crops may predispose cattle to metabolic alkalosis (urine pH >8.5) with a decreased available pool of ionized calcium and magnesium, thereby increasing the risk of hypocalcemia and hypomagnesemia. Urine Mg concentrations are a useful guide to Mg status and are undetectable in cows with hypomagnesemia.

In the most acute form of hypomagnesemic tetany, affected cows, which may appear to be grazing normally, suddenly throw up their heads, bellow, gallop in a blind frenzy, fall, and exhibit severe paddling seizures with chomping of the jaws, frothy salivation, fluttering of the eyelids, and nystagmus. Seizures may recur at short intervals, and death usually occurs within a few hours. In many instances, animals at pasture are found dead without observed illness; however, an indication that the animal had seizures before death may be evident from marks on the ground.

In less severe cases, twitching of the muscles of the face, flank, and shoulder may occur. The cow is obviously ill at ease, walks stiffly, is hypersensitive to touch and sound, urinates frequently, and may progress to the acute convulsive stage after a period as long as 2–3 days. This period may be shortened if the cow is transported or driven to a fresh pasture. When animals have hypocalcemia and hypomagnesemia, the clinical signs depend on which predominates. With hypomagnesemia, tachycardia (approaching 150 beats/minute) and loud heart sounds (audible without a stethoscope) are characteristic clinical signs. Elevated rectal temperatures can occur (up to 40.5°C or 105°F) due to excessive muscular activity.

Clinical signs of hypomagnesemic tetany in sheep occur when hypomagnesemia (plasma tMg < 0.5 mg/dL [0.2 mmol/L]) occurs concomitantly with hypocalcemia (plasma tCa < 8 mg/dL [2.0 mmol/L]). The disease in lactating ewes occurs under essentially the same conditions and has the same clinical signs as in cattle.

• Presumptive diagnosis: typical clinical signs and response to treatment

• Definitive diagnosis: low total or ionized serum or urine magnesium concentrations (antemortem), or low CSF or vitreous humor concentrations (postmortem)

Diagnosis is usually confirmed by response to treatment, followed by confirmation of hypomagnesemia in samples taken before treatment. The reference range for tMg in cattle is 1.8–2.4 mg/dL (0.75–1 mmol/L) and in sheep is 2.2–2.8 mg/dL (0.9–1.15 mmol/L). Tetany usually occurs when plasma tMg is < 1.2 mg/dL (0.5 mmol/L) in cattle and < 0.5 mg/dL (0.2 mmol/L) in sheep. There is often concurrent hypocalcemia. Urine Mg is usually undetectable in cows with hypomagnesemic tetany.

Mg concentrations from dead animals may be normal due to muscle damage and leakage from intracellular pools. Mg concentrations < 1 mg/dL (0.4 mmol/L) from the CSF within 12 hours of death or from the vitreous humor of the eye within 24–48 hours after death are indicative of hypomagnesemic tetany, provided environmental temperatures have remained below 23°C.

• Clinical signs of hypomagnesemia require emergency parenteral treatment with ongoing treatment paramount

• Preventative oral magnesium supplementation should be immediately initiated to prevent additional cases of tetany and possible deaths in affected herds

Animals showing clinical signs require treatment immediately with combined solutions of calcium and Mg, preferably given slowly IV while monitoring the heart ( see Parturient Paresis in Cows). The response to treatment is slower in animals with hypomagnesemic tetany than in animals with hypocalcemia alone, because of the time it takes to restore Mg in the CSF. The animal should not be stimulated during treatment, because this could trigger fatal seizures. An adult cow requires 1.5–2.25 g of elemental Mg. As Mg sulfate is only 9.7% elemental Mg, this is equivalent to 15–22.5 g of Mg sulfate solution or 30–45 ml of a 50% Mg sulfate solution. Other commercial intravenous formulations contain Mg as chloride, borogluconate, or hypophosphite solutions. A common treatment regime is to administer 400 ml of 40% calcium borogluconate plus 50 ml of 25% magnesium sulfate by slow IV injection. Additional Mg sulfate (120 to 400 mL of a 25% solution/cow) can be given SC. After treatment, cows should be left to respond without stimulation and then moved off the tetany-prone pasture, if possible. Animals must be provided with hay treated with 60 g of Mg oxide daily; if this is not done, the condition can recur within 36 hours after initial treatment.

Mg must be given daily to animals at risk, because the body has no readily available stores. Daily oral supplements of Mg oxide (60 g to cattle and 10 g to sheep) should be given in the danger period. Most Mg salts are unpalatable and must be combined with other palatable ingredients such as molasses, concentrates, or hay. Feeding hay alone may be all that is required to prevent hypomagnesemic tetany in herds in which only old cows (>6 years) are affected.

If slow-release intraruminal Mg devices are administered, the animals also should be provided with hay. Fertilizers containing Mg effectively increase herbage Mg only on certain soil types. Herbage may be dusted with powdered Mg oxide (500 g/cow) or sprayed with a 2% solution of Mg sulfate at intervals of 1–2 weeks. If rainfall exceeds 40–50 mm within 2–3 days of dusting, the herbage will require another dusting.

Out-wintered stock should be protected from wind and cold and provided with supplementary food. Sheep and cattle should have access to hay, particularly when grazing either green cereal crops or pastures fertilized with potassium or nitrogen (or both).