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Also known as: '''''Grass staggers — Grass tetany'''''
==Introduction==
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 hypomagnesiaemia.
==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.
===Sheep===
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===
'''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.
==Diagnosis==
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 predictable, usually 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.
==Treatment and prevention==
===Treatment===
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:
#'''Slow''' intravenous injection of '''calcium borogluconate''' and '''magnesium sulphate'''
#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.
===Control===
Prevention of clinical hypomagnesaemia depends upon both reducing risk factors and ensuring daily 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.
==References==
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
[[Category:Vascular Fluid]]
[[Category:Vascular Fluid]]
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