Download as pdf or txt
Download as pdf or txt
You are on page 1of 5

Sadam D.

Hasan, BVMS, MSc, PhD


Scientific degree (Lect.), Department of Internal and Preventive Medicine
College of Veterinary Medicine, University of Mosul, Mosul, Iraq
https://orcid.org/ 0000-0002-3010-501x
https://www.researchgate.net/profile/ Sadam Hasan
Metabolic Disease | Part I | 5th year 2019

Metabolic Disease
Hypomagnesemia

*Tetany associated with a marked decrease in serum magnesium concentration is a common


occurrence in ruminants. The syndrome associated with hypomagnesemia is relatively
constant, irrespective of the cause, but the group of diseases in which it occurs has been
divided into:
• Hypomagnesemic tetany of calves, which appears to result specifically from a deficiency
of magnesium in the diet transport tetany
• a group of hypomagnesemia in ruminants characterized by lactation tetany, in which there
may be a partial dietary deficiency of magnesium but in which nutritional or metabolic
factors reduce the availability, or increase the body’s loss of the element so that serum
magnesium levels fall below a critical point.

magnesium homeostasis
•Magnesium (Mg) homeostasis is not under direct hormonal control but is mainly
determined by absorption from the GI tract; excretion by the kidneys; and the varying
requirements of the body for pregnancy, lactation, and growth.
•Magnesium ions are by no means efficiently absorbed from the gastrointestinal tract and
only 7 to 25% is absorbed under usual dietary conditions.
•Plasma magnesium, just like calcium, is also found in ionised form, protein-bound and in
complexes, with the ionized magnesium being the most active form.
•Mg is a constituent of bones (approximately 60 to 70% of the total body magnesium is
present in the skeleton), 30-40% is distributed in the soft tissues and only about 1% can
be found in the extracellular space. Therefore, plasma Mg does not provide an indication
of intracellular or bone Mg stores.

Roles of magnesium
•The magnesium ion is essential for normal bone metabolism, normal nerve function and
muscle irritability. Magnesium also plays an essential part in the coenzyme system which
links normal carbohydrate metabolism with phosphate metabolism and the provision of
energy for muscle contraction.
•Magnesium within the cell acts as a counter ion for the energy-rich ATP and nuclear acids.
Magnesium is a cofactor in >300 enzymatic reactions.
•Thus, one should keep in mind that ATP metabolism, muscle contraction and relaxation,
normal neurological function and release of neurotransmitters are all magnesium
dependent.
•It is also important to note that magnesium contributes to the regulation of vascular tone,
heart rhythm, platelet-activated thrombosis and bone formation

Internal and preventive medicince | Metabolic disease | Dr. Sadam D. hasan Page | 1
•Extracellular Mg is involved in the regulation of membrane channels as well as in
excitation-contraction coupling in skeletal muscle. Low ionic Mg concentrations
accelerate the transmission of nerve impulses
•In muscle contraction, for example, magnesium stimulates calcium re-uptake.
•Magnesium further modulates insulin signal transduction and cell proliferation and is
important for cell adhesion and transmembrane transport including transport of potassium
and calcium ions
•The normal level of magnesium in plasma for cows is in the range of 0.75-1.00 mmol/l or
1.8-2.4 mg/dl.
•Milk contains about 0.12-0.15 g magnesium /kg and a high yielding cow may lose around
3-4 g through milk per day.
•Colostrum contains about 0.4 g magnesium/kg ,Because the amount of magnesium in the
extra cellular fluid equals the amount excreted in 17 kg of milk (0.15 g/kg 4% milk; milk
production in high lactating animals can quickly deplete the extracellular pool of
magnesium, resulting in hypomagnesaemia if not rapidly replaced.

Hypomagnesemic tetany
(lactation tetany, grass tetany, grass staggers, wheat pasture poisoning)

Hypomagnesemic tetany is a complex metabolic disturbance characterized by


hypomagnesemia (plasma Mg <1.5 mg/dL [<0.65 mmol/L]) and a reduction in the
concentration of Mg in the CSF (<1.0 mg/dL [0.5 mmol/L]), which lead to
hyperexcitability, muscular spasms, convulsions, respiratory distress, collapse, and death.

Etiology:
*Magnesium concentrations is determined by balance between dietary intake of magnesium,
loss in feces and milk, and the modulating effect of magnesium homeostasis by the
kidney.
* Low Dietary intake of Mg.
* Renal excretion regulation.
* There are large stores of magnesium in the body, especially in bone. These are available to
the young calf but mobilization decreases with age and in the adult ruminant there is little
mobilization in response to short-term deficits of magnesium.
* Lactation: Increased requirement for magnesium is almost always associated with the loss
of magnesium in the milk during lactation.
*Low pasture Ma. The recommended minimal 'safe' concentration of magnesium in pastures
is 2 g/kg DM.

Factors influencing absorption of magnesium:


1- magnesium concentration, is influenced by the Na:K ratio in the rumen, which is
determined by the dietary and salivary concentrations of sodium and potassium. Young
rapidly growing grass is low in sodium and high in potassium which lead to impairment
of magnesium absorption
2-Saliva normally has a high Na:K ratio but where there is a deficit of sodium in the diet, a
proportion of sodium in saliva may be replaced with potassium under the influence of
aldosterone, which further negatively influences the uptake of magnesium.

Internal and preventive medicince | Metabolic disease | Dr. Sadam D. hasan Page | 2
3-Young grass fertilized with nitrogenous fertilizers has an increased crude protein which is
readily fermentable and leads to increased ammonia concentrations. A sudden rise in
ruminal concentrations of ammonia impairs magnesium absorption in the rumen.
4-magnesium absorption is depressed in ruminal acidosis.
5- hypomagnesemia can have effect on calcium homeostasis as Hypomagnesemia reduces
the production and secretion of parathyroid hormone and reduces hydroxylation of
vitamin D in the liver, therefore hypomagnesemia can increase susceptibility to milk
fever and downer cow syndrome .thus Mg, therapy must added to milk fever treatment.

Epidemiology and Risk Factors:


*Lactation tetany in dairy and beef cattle turned out to graze on lush, grass-dominant pasture
after winter housing is common in northern Europe, the United Kingdom, and the
northern parts of North America. Grass tetany also occurs in Australia and New Zealand,
where the cows are not housed in winter but have access to a phenomenal flush of pasture
growth in the spring. This also commonly occurs in beef cattle in all countries.
*most cases occur during the first 2 weeks after the cattle are turned out to spring pasture.
*Pasture that has been heavily top dressed with fertilizers rich in nitrogen and potash is
potentially the most dangerous.
*In regions where there is an autumn flush of pasture, a high incidence of hypomagnesemic
tetany may occur in the autumn or early winter.
*Cattle in the first 2 months of lactation and 4-7 years of age are most susceptible, which
probably reflects an increased risk due to a higher loss of magnesium in milk.
*Wheat pasture poisoning is a misnomer because it can occur with grazing of any small-
grain cereal pasture.
*the morbidity rate is highly variable, reaching as high as 12% in individual herds and up to
2% in particular areas. The incidence varies from year to year depending largely on
climatic conditions and management practices.
*Hypomagnesemia is a problem on grass dominant pastures.
* Application of potash and nitrogenous fertilizers to pastures will decrease the
concentration of calcium and magnesium in plants. and also interfere with absorption
from intestine.
*a period of starvation in lactating cows and ewes is sufficient to produce a marked
hypomagnesemia, and the fall may be sufficiently great to cause clinical tetany. A period
of bad weather, yarding, transport, or movement to new pastures or the introduction to
unpalatable pastures may provide such a period of partial starvation.
*.Diarrhea is commonly associated with lactation tetany on spring pasture and, by
decreasing the alimentary sojourn, may also reduce magnesium absorption.
*serum magnesium levels has also been observed. Reduced levels occur in adult cattle and
sheep exposed to cold, wet, windy weather with little sunshine and no access to shelter or
supplementary feed.

Pathogenesis:
*Normal serum Mg. value is 1.7-3mg/dl (0.4 mmol/L) and sings start when the level of Mg.
become below1mg/dl(0.7 to 1.2 mmol/L)
*Magnesium has many influences on impulse transmission at the neuromuscular system,
including effects on the release of acetylcholine, on the sensitivity of the motor end plate,

Internal and preventive medicince | Metabolic disease | Dr. Sadam D. hasan Page | 3
on the threshold of the muscle membrane and on activation of the cholinesterase system,
those were result in tetanic sings but the concurrent hypocalcemia may have a
contributory effect.
*it has also been established that magnesium concentrations in the cerebrospinal fluid (CSF)
are more predictive of clinical disease than those in serum.

Clinical findings
For convenience, lactation tetany is described in acute, subacute, and chronic forms.

Acute form
*The animal may be grazing at the time and suddenly stop grazing.
*uncomfortable twitching of the muscles and ears , severe hyperesthesia and slight
disturbances precipitate attacks of continuous bellowing, frenzied galloping, and
occasionally aggression.
* The gait becomes staggering and the animal falls with obvious tetany of the limbs, which
is rapidly followed by clonic convulsions lasting for about a minute.
*During the convulsive episodes there is:
Opisthotonos, Nystagmus, Champing of the jaws, Frothing at the mouth, Pricking of the
ears, and Retraction of the eyelids.
* The temperature rises to 40-40.5°C, after severe muscle exertion, the pulse and respiratory
rates are also high.
*Death usually occurs within 5 to 60 minutes, and the mortality rate is high because many
die before treatment can be provided.

Sub-acute :
*the onset is more gradual over a period of 3-4 days, there is slight inappetance ,and
exaggerated limb movements.
*wildness of the facial expression, and exaggerated limb movements.
* refuse to move with spasmodic urination and frequent defecation and decrease milk
production.
* Muscle tremor and mild tetany of the hind legs
* straddling gait may be accompanied by retraction of the head and trismus
*recover spontaneously within a few days or progress to a stage of recumbency.

Chronic form:
* Many animals in affected herds have low serum magnesium levels but do not show
clinical signs and There may be sudden death.
*few animals may show signs of dullness, unthriftiness, decrease appetite paresis and a milk
fever-like syndrome.

►Clinical signs of hypomagnesemic tetany in sheep occur when hypomagnesemia (plasma


Mg <0.5 mg/dL [0.2 mmol/L]) occurs concomitantly with hypocalcemia (plasma Ca<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.

Internal and preventive medicince | Metabolic disease | Dr. Sadam D. hasan Page | 4
Diagnosis:
Diagnosis is usually confirmed by response to treatment, followed by confirmation of
hypomagnesemia in samples taken prior to treatment. Clinical pathology:
*estimation of serum Mg level, risk for tetany is not present until the level falls to below 1.2
mg/ dL (0.49 mmol/L).
*Total serum calcium concentrations are often reduced to 5 to 8 mg/dL (1.25 to 2.00
mmol/L)
*In acute tetany, serum potassium concentrations are usually dangerously high and may
contribute to the high death rate.
*Estimation of Magnesium concentrations in CSF can be used as a diagnostic procedure.
*vitreous humor magnesium concentrations less than 0.55 mmol/L for cattle and less than
0.65 mmol/L for sheep up to 48 hours after death indicate the presence of
hypomagnesemia
* The occurrence of low urine magnesium levels is good evidence of hypomagnesemia.

Necropsy findings
There are no specific necropsy findings

Differential diagnosis:
Cattle
• Acute lead poisoning • Rabies • Nervous ketosis • Bovine spongiform encephalopathy
Sheep
• Hypocalcemia

Treatment:
*Slow I.V administration of preparations containing magnesium or magnesium and calcium
are used.
combined calcium-magnesium preparation 500 mL of a solution containing 25% calcium
borogluconate and 5% magnesium hypophosphite for cattle,50 mL for sheep lV followed
by a SC injection of a concentrated solution of a magnesium salt.
or magnesium sulfate 200-300 mL of a 20% solution injected half IV and half SC.
*A combination of 12% magnesium adipate and 5% calcium gluconate at a dose rate of 500
mL is also used.
Note: The rapid IV injection of magnesium may induce cardiac dysrhythmia, or medullary
depression which may be severe enough to cause respiratory failure.
*lV chloral hydrate may be administered to reduce the severity of convulsions during
treatment with magnesium.

Control
*Where possible, animals at high risk should be moved to low-risk pastures during the grass
tetany season.
*A requirement as high as 3.0 g/kg DM diet may be required for lactating cows on spring
pasture
* blocked minerals containing magnesium or foliar dressing of magnesium may be adequate
delivery systems where there is a high stocking density of cattle.

Internal and preventive medicince | Metabolic disease | Dr. Sadam D. hasan Page | 5

You might also like