Grass Tetany – A Complicated Disorder with An Easy Prevention

May 12, 2022

By Dr. Jeff Lehmkuhler

Classic “grass tetany” is a rapidly progressing and potentially fatal disorder caused by low magnesium level in the blood, also known as “hypomagnesemia”. It is usually seen in older, lactating beef cows when grazing young, succulent grass in early spring, particularly during cool and rainy weather. Other common names for this disorder, including spring tetany, grass staggers, wheat pasture poisoning, and lactation tetany, reflect the season of the year, symptoms seen, types of forage, or physiology of the animals most often involved.

Magnesium is an essential mineral as its presence is vital for many enzymes of major metabolic pathways, in normal nerve conduction and muscle contraction, and in bone mineral formation. Approximately 60-70% of total magnesium in the body is bound up in the bones. Grass tetany occurs when the magnesium (Mg) level in blood decreases rapidly, resulting in less than adequate Mg reaching the cerebrospinal fluid surrounding the brain and spinal cord. Without Mg present in spinal fluid, there is uncontrolled activation of the nerves supplying muscles throughout the body. This causes constant overstimulation and contraction of muscles, appearing first as nervousness then muscle stiffness and rigidity (“tetany”), that can progress to convulsions then death.

Maintenance of normal blood magnesium depends on daily absorption of enough Mg from the rumen to meet the amount required for milk production, soft tissue and bone growth, fetal development during pregnancy, and the small amount lost in feces. Any excess dietary Mg is excreted by the kidneys in the urine (see Figure 1). Hypomagnesemia results when magnesium absorption is less than the daily Mg lost. Cattle have no effective tissue Mg reservoir so a shortage cannot be compensated for by removal from bones or increasing Mg²⁺ ion absorption from other sites in the body. In addition, Mg is not under direct hormonal control to keep it in balance as with other major minerals. Although a simple lack of Mg intake in the diet can happen as in cases of starvation or if off feed, deficiencies are most often due to interference with Mg absorption in the rumen. Absorption basically depends on 1) the amount of soluble Mg²⁺ ions available (“in solution”) in the rumen fluid and 2) the performance of the transport mechanisms that move Mg²⁺ ions across the rumen wall to the bloodstream.

Known factors negatively affecting Mg absorption include:
1. High potassium (K⁺) in rumen fluid. High K⁺ is consistently cited as the most important factor in development of hypomagnesemia. The movement of magnesium across the rumen wall depends on an active transport mechanism (or “pump”) driven by an electrical potential created at the cell membrane. High potassium along with low sodium conditions alters the ion gradient required for active transport. If this active transport mechanism fails due to high K⁺, there is a secondary pathway, but it requires a much higher rumen magnesium concentration (4X higher) to enable Mg²⁺ ions to override the pump and passively flow down a concentration gradient to the blood.

High K⁺ levels in rumen fluid (Figure 2) are expected in any of the following situations: 1) cattle naturally high in K 2) cattle graze pastures fertilized with excessive potash or when high nitrogen fertilizer is added when soil phosphorous is low; 3) when cows are deficient in sodium (salt) and 4) when the diet changes suddenly from hay/dry feed to lush pasture. Small grain forages, including wheat, oats and rye, ryegrass and cool season perennial pastures in spring are often high in potassium (K⁺) and nitrogen (N⁺) ions and low in magnesium (Mg²⁺) and sodium (Na⁺) ions; these forage factors collectively reduce absorption of dietary magnesium.

2. Sudden increase in rumen ammonia. Lush grass is often high in soluble nitrogen and rumen degradable protein which allows for an increase in rumen ammonia levels. A rapid change from low-nitrogen to a high-nitrogen diet and rapid increase of ruminal ammonium ions (NH4+) impairs ruminal Mg²⁺ absorption, although the effect is transient and lasts for just a few days.

3. Insoluble Form of Magnesium. Magnesium must be present in soluble form (ionized) to be absorbed through the rumen wall. Solubility declines as the rumen fluid pH rises above 6.5. Grazing beef cattle often have higher rumen pH due to buffers present in saliva and slower production of volatile fatty acids from forage fermentation compared to grain diets. In addition, Mg²⁺ ion binders within forages, such as unsaturated fatty acids, can form insoluble Mg²⁺ salts reducing availability for absorption in the rumen.

4. Lack of dietary energy (fermentable carbohydrates)- In rumen fluid, a lack of fermentable carbohydrates results in fewer short-chain fatty acids (SCFA), a higher rumen pH, and an increase in ammonia concentration which decreases Mg²⁺ ion absorption. This is an important factor in development of winter tetany, an underlying form of hypomagnesemia that most often occurs when feeding harvested forages high in K⁺ but low in Mg²⁺, calcium (Ca²⁺), sodium (Na⁺) and energy throughout the winter. Cattle will have borderline low Mg and Ca blood levels but do not show tetany symptoms until triggered by a stressor such as severe weather, a new feed or environment, or after shipping. The stress hormone adrenaline rapidly shifts Mg²⁺ ions to the inside of cells, making it unavailable to the spinal fluid of the animal. If blood calcium is concurrently low, Mg levels in the spinal fluid decline even more quickly.

The classic grass tetany cow is most often found dead with disturbed soil around her hooves due to paddling and seizures before death. The interval between first symptoms and death may be as few as 4-8 hours. However, if noticed in the beginning stage, the earliest signs are twitching of the ears, facial muscles, shoulder, and flank and a stiff gait. The affected cow separates from the herd and may show a variety of symptoms including excitement, teeth grinding, aggression, galloping, bellowing, staggering and may appear blind. As the fall in magnesium progresses, sustained muscle spasms eventually cause the cow to stagger and fall, legs outstretched, stiff and paddling. Convulsions and seizures follow with the head arched back and the legs paddling. The heart rate may reach 150 beats per minute (approximately twice the normal rate) and can often be heard without the use of a stethoscope.

Respiratory rates of 60 breaths per minute (normal is 10-30 breaths per minute) and a rectal temperature as high as 105°F may result from the excessive muscle activity. Animals may get up and repeat these convulsive episodes several times before death. The diagnosis is made based on history, symptoms, and low magnesium concentration measured in the blood, urine or cerebrospinal fluid prior to death. After death, postmortem samples of spinal fluid that test below 1 mg/dL of magnesium or vitreous humor, fluid within the eye, below 1.34 mg/dL are reliable indicators of grass tetany if collected within 1-2 days after death.

Cattle exhibiting symptoms of grass tetany need immediate veterinary treatment; preferably 1.5-2.25 grams of magnesium intravenously for an adult cow. If unable to treat in the vein, a 10% magnesium sulfate solution given SQ or as an enema is a useful alternative therapy until a veterinarian arrives. Response to therapy depends on the length of time between onset of symptoms and treatment. Cattle that do recover take at least an hour to return to normal. Many of these cows will relapse and require additional Mg treatment within 12 hours. Administering oral magnesium gel or drenching with magnesium oxide or magnesium sulfate once the animal has regained good swallowing reflexes will reduce the rate of relapse. A magnesium sulfate enema can be administered because the large intestine can absorb Mg rapidly. If grass tetany has occurred within a herd, an effort should be made to immediately increase the intake of magnesium to other members of the herd to prevent further losses.

Prevention of grass tetany is based on maintaining consistent intake of soluble magnesium to be absorbed in the rumen of susceptible cattle when conditions for grass tetany exist.

Highly susceptible groups include lactating cows or cows in late pregnancy, especially 2-3 weeks prior to spring grass. These groups should be provided supplementary dietary sources of magnesium, commonly magnesium oxide. The average beef cow reaches peak lactation at 6-8 weeks post-partum which is her highest demand for magnesium.
UK Beef IRM mineral recommendations for free choice supplements for grazing beef cattle include 4 oz/head/day of a 12% magnesium trace mineral mix and all from magnesium oxide (no dolomitic limestone or magnesium mica). This will provide approximately 13 grams of magnesium which is approximately 50% of the daily requirement for lactating beef cows. These complete mineral mixtures also supply additional sodium in the form of salt to aid in combatting high potassium intakes that can interfere with the active transport of magnesium.
For cooked molasses products with a recommended intake of approximately 1 pound per day, the guaranteed analysis for Mg²⁺ should be approximately 4%. Read the label to ensure adequate Mg²⁺ levels; know recommended intake and monitor consumption.
Mineral consumption should be monitored because intake is generally inadequate if using poor quality mineral products since magnesium oxide is not palatable.
High magnesium mineral may be discontinued in late spring once the grass is more mature, the water content of the forage is decreased, and daily temperatures reach at or above 60°F.
Provide the required amount of salt in the diet. A deficiency of sodium triggers the release of the hormone aldosterone that conserves sodium in saliva and rumen fluid and replaces it with potassium. Adding the correct level of sodium to the diet is important but too much sodium increases urination and loss of magnesium in the urine. Research has shown that the negative effects of high potassium cannot be overcome by the addition of large quantities of salt.
The ionophores monensin and lasalocid significantly increase Mg absorption. Both ionophores lower ruminal K⁺ concentrations and help maintain Mg transport.
If feeding grain is an option, mixing 5# Magnesium Oxide (MgOx) to 50# Dried Distillers Grains (DDG) and feeding the mix at 1#/head/day will provide 22 grams Mg daily. MgOx is often sold as a “laxative powder”.
If the water source is a tank, soluble Mg²⁺ salts can be added, such as magnesium acetate, magnesium chloride and magnesium sulfate (Epsom salts) at a rate of 3 g/L water.
Delay turn-out to spring grass until plants are 4 to 6 inches tall. Mg²⁺ is more available in mature plants.
Graze the less susceptible animals (heifers, dry cows, stocker cattle) on the higher risk pastures since the threat of disease is lower in non-lactating cattle.
Limit grazing to 2-3 hours per day and provide free-choice access to hay while cattle are grazing lush pastures. Dry forages can provide additional Mg²⁺ and Ca²⁺and slow passage through the rumen, increasing the time available for absorption.

In the long term, prevention of disease is based on instituting management changes that decrease K⁺ and increase Mg²⁺ and Ca²⁺ in the forage.

One approach is to incorporate more legumes into pasture mixes, as legumes have higher Mg²⁺ and Ca²⁺ than do immature grasses, resulting in a better balance across the pasture.
Soil test and apply fertilizer based on soil test results and use no more potassium than recommended. When potassium is applied to forages in the early spring, plants take up more potassium than needed, called “luxury consumption”. High soil potassium also inhibits Mg²⁺ uptake by forages. The resulting high potassium forage blocks the uptake of Mg²⁺ in the rumen.
Use caution if applying broiler house litter for fertilizer as this has been associated with an increased risk of grass tetany due to the high K⁺ and N⁺ content.

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