Hypomagnesemia

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.

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.
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.
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.
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.

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.

Animals showing clinical signs require treatment immediately with combined solutions of calcium and Mg, preferably given slowly IV while monitoring the heart. 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.
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.
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.
Animals with hypomagnesemia are often hypocalcemic as well and should receive therapy containing calcium.
Administer intravenous calcium borogluconate solution containing 5% Mg (500 mL for adult cattle; 50–100 mL for calves and small ruminants).

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