HYPOMAGNESAEMIC TETANY

PRESENTED BY MARIA STEEPHAN

14 BVM 138
 SYNONYMS

 Lactation tetany
 Grass staggers/tetany
 Magnesium deficiency/hypomagnesaemia
 Wheat pasture poisoning/tetany
 Winter tetany
 Spring tetany
 Transit tetany
 Milk tetany
 DEFINITION
 Metabolic disease of cattle, horse, buffalo, sheep
and goat characterised by hyperaethesia, tetany,
incoordination and convulsion as a result of
disturbed magnesium homeostasis.
 May occur as a complex accompanied with varying
degrees of hypocalcaemia, ketosis and
hypophosphatemia
 Voison (1964)- Metabolic disease caused by the
soil
 ‘Disease of civilization’
 CLASSIFICATION
Based on etiology, it can be classified as:
 Lactation tetany
◇Mostly occurs in mares
◇Due to ingestion of excessive green grass and at the
same time lactating profusely
◇Always related with lactation
 Grass staggers/grass tetany
◇Occurs in animals which are maintained on luxuriant
green grass or newly grown green grass which are
deficient in magnesium
 Wheat pasture poisoning/tetany
◇ When excessively fed with wheat
 Milk tetany
◇ Calves which are exclusively fed on milk diet
◇ Also considered as “whole milk tetany”
◇ Milk is deficient in magnesium
 Winter tetany
◇During winter, pastures are not well developed
and remain deficient in magnesium content
◇Animals fed solely on straws may suffer
◇Magnesium levels are lower in cool season grasses
and cereals than in legumes or weeds
◇Bad weather, especially winter storms
 Spring tetany
◇Usually after grazing on pastures of rapidly
growing grass, especially in early spring.
◇Magnesium levels are low when growth is vigorous
 Transit tetany/Transport tetany
◇Occurs after prolonged transport usually in cows
and ewes, in late pregnancy
◇Also recorded in lambs transported to feed lots
◇Characterised by recumbency,alimentary tract
stasis and coma
◇Highly fatal condition
◇Precipitated by heavy feeding before
transportation and deprivation of water and food for
24 hours during transit
◇Sudden exposure to inclement weather may also
cause it
 ETIOLOGY
 Principalcause : Deficiency of magnesium in the
blood stream
 Normal magnesium level : 2.3 mg/dL
 Balancing depends on : Daily intake of Mg in diet
 Main reservoirs : Bones and soft tissues (70% of
body Mg)
 Mobilizationof Mg to the blood circulation varies
with age. Young animals : 30 to 60% ; Adults :
Lesser
 Principal site of absorption : Gut
 In a calf upto age of one month Mg is absorbed
from both small and large intestine but on and
from the middle third of the small intestine
 Mg is excreted through milk in lactating animal
 Also excreted through urine and gut
 FACTORS
 Tetanogenic pasture (↓Ca,Mg,Na; ↑K)
◇ Deificient in Mg- Young green grass, lush grass
pasture, sandy and laterite soils, heavily potassium
rich fertilizer applied soils, light soils, soils with low
pH, soils with fertilizer containing nitrogen or
potassium, cool season grasses, vigorously growing
grasses, high moisture content in grasses
◇Black and brown soils are rich in Mg
◇Potassium interferes with Mg absorption from gut
 Ammonia formation
◇Excessive production of ammonia in the rumen from
protein rich diet
◇Heavy top dressing with ammonia fertilizers lead to
reduce uptake of Mg by plants and thus cause
reduction of availability of ingested Mg
 Starvation

◇Reduction of dry food intake

◇A period of starvation in lactating cow – clinical
tetany
◇Bad weather, transport, unaccustomed pasture
 Water

◇Excessive water in lush greens

 Acids

◇High content of citric acid, transaconite acid and

other organic acids form non ionizable complexes
with Mg and thus reduce its biological efficacy
 Lactation

◇Considerable quantity of Mg (0.12g/litre of milk) is

excreted through milk during lactation
 Chelating agent
◇Chelating agent like alpha-ketobutaric acid
interferes with Mg absorption
 Scour

◇Decreases Mg absorption
 Hyperthyroidism

◇A relation between the both have been erected

but definite proof is awaiting
 Calcitonin

◇Antyhypermagnesemic agent
 PATHOGENESIS

 Magnesium is a co-factor of certain enzymes requiring

thiamine pyrophosphate, an activator of enzyme like
mysinkinase, creatinin kinase, pyruvic acid carboxylase
and is required for the oxidative phosphorylation.
 A decrease in the ratio of magnesium: calcium will
stimulate secretion of acetylcholine esterase (Ach) which
is responsible for tetanic signs like hyperaesthesia,
muscular-tremor, convulsion etc. Magnesium level of CSF
is greatly reduced in grass tetany which therefore suggest
that tetany may result from central effect of brain.
 CLINICAL FINDINGS
A. Acute Tetany   Unusual alertness.
 Sudden caesation to graze.   Severe hyperaesthesia.
 Twitching of the muscles and   Bellowing.
ears.  Opisthotonus.
 Slight disturbances precipitate  Champing of the jaws.
attack.
 Temperature 104-105°F.
 Frothing at the mouth.
 Staggering gait.
 Heart sound increased may be
  Nystagmus.
heard from distance.
 Frothing at the mouth
 Death occurs within half to one
hour.
B. Sub-Acute Tetany
  Onset is gradual
 Wildness of the facial expression.
 Head throwing.
 Spasmodic urination and frequent defaecation. Muscle
tremor and mild tetany of hind limbs.
 Sudden movement, noise may precipitate a violent
convulsion.
 Respond to treatment.
C. Chronic Tetany.
 May not show clinical signs though serum Mg" level is
low
 May show vague syndrome like dullness, un-thriftiness,
indifferent appetite. Chronic tetany may to subacute
form.
D. Parturient Paresis with Hypomagnesaemia.
 It is characterized by paresis, circulatory collapse,
dullness and flaccidity replaced by hyperaesthesia and
tetany.
 DIAGNOSIS AND CLINICAL PATHOLOGY
 Confirmed by response to treatment
 Samples prior to treatment :

◇ Tetany usually occurs when plasma tMg is <1.2

mg/dL (0.5 mmol/L) in cattle and <0.5 mg/dL (0.2 mmol/L)
in sheep.
◇ Urine Mg level collected from live or dead animal
will be <1mg/dl indicates a positive hypomagnesaemia.
Normal value will be 1–20 mg/dl
◇ Serum Mg level is reduced. Normal 1.7-3mg/dl.
Signs occur at 0.5 mg/dl
◇ Potassium level is elevated more than 77 mEq/litre.
 ◇ Mg concentrations <1.8 mg/dL (0.75 mmol/L) in the
vitreous humour of the eye removed from animals within
24 hr after death are indicative of hypomagnesemic
tetany
◇ Serum Aspartate aminotransferase (AST) level and
creatine phosphokinase activity is elevated. These
changes may result as a consequence to muscle damage
 A test has been considered where a pink colour
develops when urine is treated with titian blue.
Commercial available test paper (Akz test paper) can be
used where the urine turns purple with magnesium.
 DIFFERENTIAL DIAGNOSIS
Incoordination, hyperaesthesia and tetany may be confused
with the following:
 Acute lead poisoning: Blindness, history of lead access
 Rabies: Straining, ascending paralysis and absence of tetany
 Nervous form of ketosis: Ketonuria, absence of tetany
 Nitrate poisoning: Absence of hyperaesthesia and
convulsions, coffee coloured urine.
 Strychnine poisoning: Rare in occurrence
 Ergotism: Occur usually in late summer, hypersensitivity to
noise and movement but not to touch.
 LINE OF TREATMENT
 Satisfactory treatment is to administer solution containing
both 'Ca' and 'Mg' salts General recommendation is to use a
combined Ca-Mg preparation IV followed by S/C injection of a
solution of Magnesium salt 
◇Mifex @1 bottle or ½ bottle IV followed by 100-150 ml of
10% magnesium sulphate SC.
The following magnesium salts can be used:
◇Magnesium sulphate 10 to 20% solution @200-300 ml SC
◇Magnesium gluconate-15% solution @200-300 ml SC
◇Magnesium adepate -12% + Ca-gluconate-5% equal volume
about 500 ml (250+250 each)
 Magnesium can be administered as enema, 60 gm of
magnesium sulphate dissolved in 200 ml of water can
be used. The magnesium level rises within 15 minutes.
It can be administered orally (200 to 400 ml of 50%
MgSO4 as drench) 
 A preparation containing 100 gm magnesium oxide
along with 50 gm of calcium carbonate, 100 gm of
dicalcium phosphate and 50 gm of sodium chloride has
been suggested.
 CONTROL
 Feeding of magnesium supplement: Mg should be
supplemented on daily basis magnesium deficient
pastures. This may be achieved by (1) adding Mg salt in
water (2) adding Mg salt in the feeds or concentrates
(3) spraying Mg rich fertilizer top dressing on pasture. It
may be done by spraying 2% Mg sulphate every two
weeks during during danger period
 Provision of shelter: Magnesium level falls in winter and
in inclement weather. Animals should be provided with
comfortable shelter during such period.
 Addition of 3% magnesium oxide in the grain may help
in the prevention of it
 Addition of magnesium oxide @ 60 gm per cow along
with water and molasses has been suggested
 Addition of 5 to 10 kg/200 litre of magnesium sulphate
to drinking water-can be attempted.
 Provision of molasses lick containing other minerals
along with magnesium.
 Use of magnesium releasing intra ruminal bolus. The
bolus remains in the reticulum and there is release of 1
to 1.5 gm per day.
 Protein supplementation as a carrier for magnesium
oxide @ 6% per head per day. Application of
potassium in the pasture should be reduced.
 Stress in any form to be minimized
 Ewes should be provided with 5-7 gm of magnesium
oxide per head per day
 Agronomic practices to increase forage magnesium
content can be explored. 
 Pasture sample should be monitored periodically to
assess the balance between potassium, magnesium
and nitrogen