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Also known as: Grass Staggers — Grass Tetany


Hypomagnesaemia is a rare but important cause of sudden death in ruminants.

Adult cattle and sheep have no effective tissue stores of magnesium, so lactating animals are at risk of developing a deficiency. The risk is increased when they are grazing pasture, especially in Spring and Autumn when the absorption of magnesium is influenced by factors including: high levels of potassium, nitrogen and moisture content and low levels of sodium.

70% of magnesium is found in bone and this portion is more labile in young animals making older cows more susceptible to developing the disease.

Magnesium requirements are influenced by production. Therefore rapidly-growing and lactating animals have a higher requirement than non-lactating slow-growing animals. Cows in their third to fifth lactation have an increased risk of developing hypomagnesaemia due to increased production and reduced age-related mobilisation of magnesium from bone.

Ruminants may survive for a few days by using residual magnesium in their soft tissues, but other than this, they cannot store magnesium effectively. A continuous supply of magnesium in the diet is therefore essential to avoid hypomagnesaemia.

Clinical Signs

Acute form in cows

Magnesium plays a critical role in neuromuscular transmission and signs include: depression and dullness, stiffness, excitability, tremors, chewing, hypersalivation, blinking of the third eyelid, ear flapping, collapse, tetanic muscle spasms, coma and death.

Chronic form in cows

In cases with long-standing low levels of magnesium there might be signs of nervousness and irritability, depressed appetite and production and illthrift. Additional stress such as poor weather in winter may precipitate tetany, paresis and death.


Hypomagnesaemia occurs most frequently in heavily lactating ewes 2 to 8 weeks after lambing.

Clinical signs include: tremors of the face and ears, tetanic spasms, fits, recumbency and death.

Lambs may present with a stiff gait and tetany, or in chronic cases show illthrift.


Hypocalcaemia may occur concurrently, as hypomagnesaemia influences calcium metabolism by reducing the secretion of PTH and tissue sensitivity to PTH which is important for calcium absorption.


In acute cases, history and clinical signs provide a strong basis for presumptive diagnosis and response to treatment can support the diagnosis.

On postmortem examination, gross changes, such as petechiationg, are non-specific.

Fluid analysis can be used to confirm the diagnosis:

Blood: magnesium concentrations at which clinical signs appear are usually predictably below 0.5mmol/l.
A blood sample should be taken before treatment of an affected cow in case it does not respond.
Other fluids which provide information on magnesium levels include: CSF, urine and ocular fluids.

Given that ruminants are usually managed in large similarly-fed groups within similar production systems, there is a high risk of subclinical hypomagnesaemia in apparently unaffected individuals in a group where clinical hypomagnesaemia has occurred. Consequently, screening other members of an affected group for evidence of low blood levels of magnesium is the best method of confirming disease and investigating distribution and severity.


Animals with the acute form of the disease require urgent treatment as their condition may deteriorate rapidly and success rates decline with time from the onset of clinical signs.

Usually injections of calcium and magnesium are combined as there is often concurrent hypocalcaemia. They are given in two stages:

  1. Slow intravenous injection of calcium borogluconate and magnesium sulphate
  2. Further subcutaneous injection of a solution containing a higher concentration of magnesium.

Animals may have to be sedated to control the tetany, and affected animals should always be handled quietly and calmly to avoid aggravating the condition.


Prevention of clinical hypomagnesaemia depends upon both reducing risk factors and ensuring daily Mg intake:

Avoid the use of potassium-containing fertilisers including slurry at critical periods, especially when grass is growing rapidly in the spring.

Add magnesium to the feed of at-risk animals at times of greatest risk. Supplements should be mixed with the diet and provided so that every individual receives the necessary dose.

Do not use mineral blocks as individual cows vary widely in their use of licks.

It might be worth considering preventing access of lactating cows to pastures associated with hypomagnesaemia at critical periods. For low risk pastures it might be sufficient to supplement hay to animals following turnout.

Feed concentrates supplemented with magnesium to cows in the parlour and to ewes for 4 to 6 weeks after lambing.

Consider the use of slow-release magnesium boluses in cows.

Add magnesium chloride to the drinking water of cows.

Hypomagnesaemia Learning Resources
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Test your knowledge using flashcard type questions
Cattle Medicine Q&A 08


Scott, P. (2007) Hypomagnesaemia in Beef Cattle Nadis Health Bulletin

Foster, A. (2007) Farm Animal Practice: Magnesium disorders in ruminants In Practice 29:534-539

Scott, P. (1995) Differential diagnosis of common metabolic disorders of sheep In Practice 17:266-269

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