Hypomagnesemic tetany is a complex metabolic disturbance characterized by hypomagnesemia (plasma tMg <1.5 mg/dL [<0.65 mmol/L]) and a reduced concentration of tMg in the CSF (<1.0 mg/dL [0.4 mmol/L]), which lead to hyperexcitability, muscular spasms, convulsions, respiratory distress, collapse, and death. Adult lactating animals are most susceptible because of the loss of Mg in milk. Hypomagnesemic tetany occurs mainly when animals are grazed on lush grass pastures or green cereal crops but can occur in lactating beef cows fed silage indoors. It is rare in nonlactating cattle but has occurred when undernourished cattle were introduced to green cereal crops.
The disorder 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 wt) and lactation (120 mg/kg milk). This can arise after a reduction in food intake during inclement weather, 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 reduced 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 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 signs of hypomagnesemic tetany until blood calcium concentrations are <0.8 mg/dL (0.35 mmol/L), which commonly occurs in cattle grazing green cereal crops. The hypocalcemia arises from either a reduction 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 reduced 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, 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 convulsions. These convulsive episodes may be repeated at short intervals, and death usually occurs within a few hours. In many instances, animals at pasture are found dead without observed illness, but an indication that the animal had convulsions before death may be seen from marks on the ground. In less severe cases, 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 signs shown depend on which predominates. With hypomagnesemia, tachycardia and loud heart sounds are characteristic signs.
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.
Diagnosis is usually confirmed by response to treatment, followed by confirmation of hypomagnesemia in samples taken before treatment. 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. Urine Mg is usually undetectable in cows with hypomagnesemic tetany. Mg concentrations <1.8 mg/dL (0.75 mmol/L) in the vitreous humour of the eye removed from animals within 24 hr after death are indicative of hypomagnesemic tetany.
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 convulsions. Additional Mg sulfate (200 mL of a 50% 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 2 oz (60 g) of Mg oxide daily; if this is not done, the condition can recur within 36 hr after initial therapy.
Mg must be given daily to animals at risk, because the body has no readily available stores. Daily oral supplements of Mg oxide (2 oz [60 g] to cattle and ⅓ oz [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 yr) 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 wk. 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).
Magnesium absorption efficiency in calves fed milk falls from 87% at 2–3 wk to 32% at 7–8 wk of age. Hypomagnesemic tetany occurs in 2- to 4-mo-old calves being fed milk only, or in younger calves with chronic scours while being fed milk replacer.
Clinical signs are similar to those of hypomagnesemic tetany in adult cattle (see above) and include hyperexcitability, muscular spasms, convulsions, and death.
Hypomagnesemic tetany in calves must be differentiated from acute lead poisoning (see Lead Poisoning), tetanus (see Tetanus in Animals), strychnine poisoning (see Strychnine Poisoning), polioencephalomalacia (see Polioencephalomalacia), and enterotoxemia caused by the toxin of Clostridium perfringens (see Enterotoxemias in Animals). Analysis of bone aids diagnosis—normal bone has a Ca:Mg ratio of 70:1; in hypomagnesemic calves, the ratio may be ≥90:1.
Affected calves require prompt treatment with a 10% solution of Mg sulfate (100 mL, SC) followed by Mg oxide at 10 g/day, PO. Provision of good-quality legume hay and a starter ration from 2 wk of age prevents the disorder.