The “DOWNER COW ” Syndrome 2012
The “DOWNER COW”Syndrome
The "downer cow" syndrome is a condition which occurs in cattle usually
following hypocalcemic parturient paresis. If is characterized clinically by
prolonged recumbency even after two successive treatments with calcium .At
necropsy there is traumatic injury to limb muscles and nerves, ischemic necrosis
of limb muscles , myocarditis,and fatty infiltration and degeneration of the liver .
Etiology:
The etiology is not clear but the available evidence and clinical experience
suggest that the disease is complication of hypocalcemic parturient paresis.
Traumatic injuries of the medial thigh muscles and of the tissues around the hip
joint and of the obturator muscles are common in cows which do not recover. The
traumatic injuries may be the result of cows “Spread-eagling” their hindlegs if
they are unsteady during parturition or if they are forced to get up or walk on a
slippery floor immediately before or following parturition .A difficult parturition
due to an oversized calf may result in peripelvic traumatic injury with extensive
edema of the pelvic (Oedema) and vulva, and failure of the cow to get up
following parturition .If these cows develop hypocalcemic parturition paresis , it is
unlikely they will get up following treatment with calcium.
The evidence to support traumatic injury to muscle as an important cause is the
observation of a marked increase in the SGOT levels in cows affected with
hypocalcemic parturient paresis and failure to rise after repeated treatment .The
(SGOT) levels increased markedly between the first and second treatment which
indicated that muscle damaged had occurred and the level were highest in cows
which did not recover. Traumatic injuries to the nerves of the limbs are present in
25% or more of downer cows. In the hindquarters the sciatic and the obturator
nerves are vulnerable to injury by pressure from the calf during parturition.
Pressure injuries on the superficial nerves (radial and peroneal) of the extremities
readily occur in recumbent cows.
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Epidemiology:
The incidence of the downer cow syndrome is distressingly high, particularly
because so many of the affected animals are heavy produces and of great value .It
is impossible to give accurate figures on incidence because of variations in
nomenclature and in the accuracy of diagnoses. For example, some find that all
cases are caused by nerve injury .cases included in this classification by some
veterinarians are classified by others as maternal obstetric paralysis, as obturator
paralysis or as hypophosphatemia. Because it is syndrome lacking in definition
and comprising the residual cases which cannot be otherwise classified, it varies
in size depending largely upon the clinical acuity of the individual veterinarian,
and probably also on varying environmental factors in different area.
Nevertheless, the incidence seems to be increasing, particularly in intensive
farming areas, although this impression could arise from the increased necessity
to affect a cure in valuable animals.
A mail survey of 723 dairy herds in Minnesota revealed an incidence of 21.4/1000
cow years at risk. The overall outcome was that 33% recovered 23% were
slaughtered and 44% died .The herd owners perceived that the downer cows
were high producer (48%) or average producers(46%) with only 6% being low
producers. Approximately 58% occurred within 1 day of parturition and 37%
occurred during the first 100 days of lactation .The incidence was highest (39%)
during three coldest months, December, January and February. In New Zealand,
the prevalence range from 3 to 5% of all dairy cows at calving time.
In a clinical and laboratory survey of 433 periparturient recumbent cows in New
Zealand, 39% recoverd, 30% died and 32% were destroyed. The case fatality rate
was 11% higher in precalving recumbent cows than postcalving cows. The disease
occurs most commonly in the first 2 or 3 days after calving in heavy milk
producers and in many cases occurs concurrently with parturient paresis.
Prolonged recumbency after an overlong delay in the treatment of what was an
uncomplicated hypocalcemic parturient paresis considered to be an important
cause of the downer cow. Prolonged recumbency (more than 4-6 hours) can
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result in ischemic necrosis due to obstruction of the blood supply, especially in a
heavy cow if she lies on one leg for a long period .Cow which develop milk fever
while in a standing tie-stall will often slide into the gutter. Behind the stall with
the result that their hindquarters are subjected to extreme pressure leading to
ischemic necrosis.
Experimentally, enforced recumbency of cattle for 6,9 or 12 hours with one
hindlimb positioned under the body will result in a downer syndrome .Affected
cows are unable to stand and the affected limb is swollen and held rigid similar to
the injured limbs of human patients with compartment /crash syndrome .Serum
electrolyte imbalances or deficits have been suggested as the cause of the
prolonged recumbency following treatment for parturient paresis. persistent
hypophosphatemia is regarded as a common cause in some regions and in some
cases appears to respond to treatment with phosphorus.
Persistent hypocalcemia may occur but is unlikely to be the principal cause
because treatment with calcium salts dose not relive the signs, even temporarily.
However the use of use an insufficient amount of calcium for the treatment of
milk fever in large heavy cows may result in an incomplete response and failure of
the cow to rise. If these cows are not retreated soon enough, ischemic necrosis of
the leg muscles will occur leading to prolonged recumbency even after the cow is
subsequently treated with sufficient calcium.
Along-term low-level hypomagnesemia has been suggested as a cause especially
when it accompanies hypocalcemia. But it is usually manifested by a titanic
hyperesthetic state which is not part of the downer cow syndrome .Hypokalemia
is, with hypophosphatemia ,the most commonly quoted cause, especially in the
so-called “creeper” cows which are bright and alert and crawl about, but are
unable to rise.
One hypothesis is that the hypocalcemic state, or ischemic due to
prolonged,recumbency,may increase the cell membrane permeability of muscle
fiber and allow the loss of potassium from the cell which in turn causes the
myotonia which appears to be the basis of the “downer cow syndrome” This view
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is supported by the observed low serum and muscle potassium levels in downer
cows. Claim are made that potassium salts are successful in treatment ,but they
are highly toxic and opportunities of establishing a response to their use are
limited .A response would be difficult to interpret, anyway , since even a
reduction in food intake can result in a mild hypokalemia .
Howerver, excellent clinical and laboratory evaluation of the downer cow has
demonstrated that there are no differences in the serum biochemistry between
cows which have had hypocalcemic parturient paresis and become downers and
those which do not become downers (uncomplicated hypocalcemic parturient
paresis).
Based on clinical experience and our interpretation of the literature we conclude
that the downer cow syndrome is a complication of hypocalcemic parturient
paresis. Traumatic injury to leg muscle at the time of parturition or when the
cow is unsteady and falls during the first stage of milk fever will result in the
inability of the cow to get up quickly following treatment for milk fever. Another
plausible complication is an overlong delay (4 hours or more) in the treatment of
cows with milk fever which result in ischemic necrosis of the muscles of both the
hindlegs and forelegs. There is now experimental evidence to support the clinical
and epidemiological observation.
Pathogenesis:
Several different primary factors or diseases like parturient hypocalcemia
initially cause recumbency .The recumbency results in pressure damage which
occurs secondarily and is a factor common to all cases .Traumatic injury to limb
muscles and nerves immediately prior to parturition or at the time of parturition
can result in prolonged recumbency and subsequent pressure damage .An
overlong delay in the treatment for hypocalcemic parturient paresis can result in
pressure damage and the subsequent inability to rise after treatment for the
primary disease .
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Regardless of the cause, the prolonged recumbency result in varying degrees of
ischemic necrosis of major muscles of the hindlimbs particularly the
semitendinous and the muscles caudal to the stifle .Prolonged compression of the
muscle leads to tissue anoxia, cell damage and inflammation which causes
swelling which causes a further increase in pressure which limits tissue perfusion
leading to a detrimental cascade of events. The thick fascial boundaries of the
semitendinous muscle prevents expansion which results in pressure induced
compartmental syndrome .Sciatic nerve damage due to pressure also occurs and
may contribute to the downer syndrome. In cows which make efforts to rise but
cannot do so, continued struggling will result in rupture of muscle fibers and
hemorrhage which may make the condition worse.
The prolonged recumbency can result in additional complications sush as acute
mastitis, decubitus ulcers, and traumatic injuries of the limbs.
The phatogenesis of the non-alert downer cow is unknown. Most have had an
initial episode of parturient hypocalcemia but did not respond satisfactorily.
Within 1 or 2 days affected cows have a preference for lateral recumbency and
exhibit expiratory moaning .They represent about 2% of all causes of milk fever.
Clinical Finding:
The “Downer Cow “syndrome may occur independently, or follow apparent
recovery after treatment for parturient paresis, except for the continued
recumbency which, in effect, constitutes the disease. In the typical case, affected
cow either make no effort or are unable to rise following treatment for parturient
paresis .About 30% of cows treated for parturient paresis will not rise for up to 24
hours following treatment. Those which are unable to rise after 24 hours and
after two treatments can be classified as downers. They are usually bright and
alert and although the appetite is reduced, the cow eats and drinks moderately
well. The temperature is normal and the heart rate may be normal or elevated to
80-100/min. Tachycardia and arrhythmia occur in some cows especially
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immediately following the administration of calcium intravenously and sudden
death has occurred. Respirations are usually unaffected. Defecation and urination
are normal and proteinuria is common. Marked proteinuria may indicate
extensive muscle damage.
Some affected cows may make no effort to rise but most will make frequent
attempt to rise but are unable completely to extend their hindlegs and to lift their
hindquarters more than a few centimeters off the ground. These frequent
attempts to rise result in the cow “Crawling” or creeping along the ground with
both hindlegs in a partially flexed position and displaced posteriorly- the frogleg
attitude. On a non-slippery surface some cows are able to stand with some cows
are able to stand with some assistance by lifting on the tail head or with the use
of hip slings. Those cows which do not make an effort to rise usually cannot stand
with assistance and if supported with hip slings will usually make no effort to bear
weight with either the hindlegs or the forelegs. In some cows the signs may be
more marked and include particularly a tendency to be in lateral recumbency with
the head drawn back.
When lifted and supported ,these cows appear almost normal but ,when they are
left alone ,they always revert to the position of lateral recumbency within a short
time .still more severe cases show hyperesthesia and some tetany of the limbs
but only when lying in lateral recumbency . These more severe cases do not
usually eat or drink. These have been described as non-alert downer’s and are
thought to have brain damage. Complications in the downer cow syndrome are
common and often result in death or the need for euthanasia .Coliform mastitis,
decubitus ulceration, especially over the prominences of the hock and elbow
joint, and traumatic injuries around the tuber coxae caused by the hip slings are
common .when these complication occur in the early stage of the disease they
commonly interfere with any progress being made become the center of concern.
The course of the disease is variable and dependent on the nature and extent of
the lesions and the quality of the care and comfort which is provided for the cow
during the first few days. About the 50% of downer cows will get up within 4 days
or less if cared for properly .the prognoses is poor for those which are still
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recumbent after 7 days, although some affected cows have been down for 10-14
days and subsequently stood up and recoverd.Death may occurs in 48-72 hours
following the onset and is usually associated with myocarditis.
Treatment:
Many treatments including the injections of magnesium salts, phosphates,
corticosteroids, stimulant tonics and vitamin E and selenium have been used
without consistent success. Attempts at slinging are usually unsuccessful unless
the cow is partially able to get up on her own. The use of solutions containing
potassium, calcium, magnesium and phosphorus has been recommended but
there is no scientific evidence that these electrolytes, in addition to what was
probably given to the cow already, are indicated of any beneficial value. Fluid
therapy by the oral or parentral route is indicated for cows which may not be
drinking a normal amount of water.
The most important aspect of treatment is to provide the most comfortable
bedding possible and to turn the cow from side to side several times daily to
minimize the degree of ischemio-necrosis and para-analgsia which results from
prolonged recumbency.
There is a need to develop a field technique for the provision of physiotherapy in
the form of muscle massage to restore the normal muscle activity in the affected
limbs. With conscientious care and the provision of good bedding, most cows will
attempt to rise in a few days a cows and can stand normally a day or two later.
Sand is an ideal from of bedding which facilitates standing when downer cows
attempt to stand. If affected cows are left on a slippery ground surface, they will
not make an effort to rise and will become progressively worse.
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