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Downer Cow Syndrome
Downer Cow Syndrome
Department of Medical Sciences, School of Veterinary Medicine, University of WisconsinMadison, Madison, WI 53706.
Department of Clinical Sciences, New York State College of Veterinary Medicine, Cornell
University, Ithaca, NY, 14853.
*Deceased
Dr. S. F. Peek, School of Veterinary Medicine, 2015 Linden Drive West, University of MadisonWisconsin, Madison, WI 53706. Ph. 608 262 6425 Fax. 608 265 8020.
E mail; peeks@svm.vetmed.wisc.edu
Abstract
Hypokalemia in dairy cattle is commonly encountered secondary to anorexia and with a
number of primary diseases of the gastrointestinal tract and renal system such as abomasal
displacements, diarrhea, and acute renal failure. The clinical signs are typically referable to the
primary condition, but with increasingly severe hypokalemia cattle may develop muscle
fasciculations, flaccid paralysis and eventually recumbency. Affected cattle are frequently unable
to support the weight of the body or head and may lie in lateral recumbency or with the head
deviated laterally. Cattle with severe hypokalemia that is associated with weakness and
recumbency are commonly in the first 60 days of lactation and usually have received treatment
for one or more of the common post-parturient diseases of dairy cattle such as ketosis, metritis,
mastitis or abomasal displacements. Chronic, recurrent ketosis appears to be the most common
antecedent condition and the repeated therapeutic use of corticosteroids, particularly those with
mineralocorticoid activity may also be a predisposing factor. As with all other causes of the down
cow syndrome in adult cattle, continued recumbency due to unresolved hypokalemia carries
significant risk for ischemic myopathy and neuropathy. Resolution of mild hypokalemia usually
follows successful treatment of the inciting cause, but specific potassium supplementation is
indicated in cases of moderate to severe hypokalemia with weakness and recumbency. This
article will review the pathogenesis of hypokalemia in dairy cattle and discuss the authors
collective experiences with severe hypokalemia and its treatment.
Focal Point
Key Facts
1. Severe hypokalemia (< 2.3 mEq/L) is a potential cause of significant muscle weakness and
recumbency in lactating cattle.
2. Cattle with recurrent episodes of clinical ketosis in the first month of lactation may be at risk
for the development of severe hypokalemia with muscle weakness and recumbency.
3. Normalization of serum potassium levels is best achieved by a combination of oral and
intravenous potassium supplementation.
4. Intravenous potassium supplementation should not exceed a flow rate of 0.5 mEq K+/kg/hr.
5. Therapeutic use of corticosteroids for ketosis should be in accordance with manufacturers
labeled indications and by the routes and at dosages specified in the product license.
through the kidneys and to a lesser degree via obligate losses through the gastrointestinal tract. In
the lactating dairy cow approximately 13% of the absorbed dietary potassium is secreted in
milk10 . Smaller amounts are lost in sweat and saliva10. More than 95% of the potassium that
enters the proximal nephron in the glomerular filtrate is reabsorbed in the proximal convoluted
tubules such that urinary potassium is predominantly derived from secretion by cells lining the
distal tubules11,12. The rate of potassium secretion is regulated by the amount of sodium in the
lumina of the distal and collecting tubules, the rate of flow of urine through these sections of the
nephron and the aldosterone activity11. Metabolic alkalosis also promotes increased urinary
potassium excretion in humans and rats12 but paradoxically metabolic alkalosis in cattle has been
documented to reduce renal potassium excretion13,14. The rate of potassium secretion is
proportionate to the rate of flow of the tubular fluid such that high volume intravenous fluid
therapy will promote kaluresis and may therefore predispose to hypokalemia, particularly if nonpotassium containing fluids are used. Increased secretion of aldosterone is a normal endocrine
response to increased plasma potassium or decreased plasma sodium and will also result in
increased kaluresis. Hyperaldosteronism has not been documented in cattle but exogenous,
iatrogenic mineralocorticoid excess may be a significant risk factor for the development of
hypokalemia6,15. Use of non-potassium-sparing diuretics such as furosemide would also act to
increase urinary potassium losses.
potassium with subsequent hypokalemia is favored by those clinical conditions that promote
metabolic alkalosis, whilst extracellular movement of potassium and resultant hyperkalemia are
favored by those conditions that are associated with metabolic acidosis.
Nutritional Issues
Dietary potassium requirements for dairy cattle vary according to the stage of lactation
but are higher than the recommended levels for beef cattle. Potassium levels in the dry period
should not exceed 0.65 % of the total ration on a dry matter basis, particularly if cattle are fed
The clinical signs of neuromuscular weakness are largely the result of changes in cell
membrane potential. Decreased extracellular potassium results in an increase in resting
cell membrane potential, thereby increasing the difference between the resting and
threshold membrane potentials. Consequently cell membranes become less excitable
and demonstrate prolonged repolarization1,3,4. Prolongation of repolarization in cardiac
muscle can result in electrocardiographic abnormalities such as ST segment depression,
decreased T wave amplitude and prolongation of the PT interval5. Although
hypokalemia may be associated with cardiac arrhythmias such as atrial fibrillation, the
electrophysiologic implications for the heart of hypokalemia tend not to be as clinically
severe as the potentially fatal bradyarrhythmias observed with hyperkalemia26. Atrial
fibrillation is the most common arrythmia in cattle and is frequently observed in dairy
cattle with primary gastrointestinal conditions that promote mixed electrolyte and acidbase disturbances26. Experimental induction of metabolic alkalosis and mild to moderate
hypokalemia in mature cattle is associated with the development of atrial fibrillation 27.
Atrial fibrillation was documented in 4 of 10 cattle with severe hypokalemia and
recumbency in a report by Sielman et al.15
the abomasum but is also shifted intracellulary throughout the body due to the metabolic
alkalosis that attends simple abomasal displacement and early abomasal volvulus29. In severe
right sided abomasal volvulus, ischemic damage to the torsed organ, combined with marked
systemic hypovolemia may produce metabolic acidosis that will promote extracellular movement
of potassium and a tendency towards normalization of serum potassium30. However, even in
advanced abomasal/omasal volvulus cattle usually continue to demonstrate measurable
hypokalemia31,32.
Increased potassium loss is feature of acute diarrhea in all species, such that mild to
moderate hypokalemia should be anticipated in dairy cattle with a variety of causes of acute
enteritis such as Salmonellosis, bovine viral diarrhea virus infection, and winter dysentery.
Experience would suggest that normokalemia may be preserved in mild or chronic cases of
enteritis (eg: Johnes disease) where cows are able to counteract increased fecal potassium loss
by maintaining adequate dietary intake. In contrast, it is worth noting that severe hyperkalemia is
a common finding in association with neonatal enteritis in calves, when hypovolemic shock and
secretory diarrhea combine to produce a profound metabolic acidosis. This association is
noteworthy due to the pathologic effects of marked hyperkalemia on cardiac function and the
potential for fatal bradyarrhythmias.
and tends to potentiate the hypokalemia 14,32,33. It is likely that the metabolic alkalosis observed
during renal failure in cattle occurs due to a combination of sequestration of abomasal secretions
as well as failure of the diseased kidneys to excrete the large volume of salivary bicarbonate
imposed by the ruminant diet 14. Reduced dietary potassium intake associated with organ failure
will exacerbate hypokalemia with advanced renal disease.
the 10 cases reported by Sielman et al.15 Increased renal potassium loss due to the
mineralocortocoid effects of exogenously administered corticosteroids is another potential
contributory factor to the development of clinically significant hypokalemia in the chronically
ketotic cow. Although the specific mineralocorticoid activity of isoflupredone acetate is not
documented, it has been shown to possess as potent a mineralocorticoid effect as aldosterone
both in vivo and in vitro in an adrenalectomized rat model35,36. By comparison, dexamethasone is
considered to have minimal mineralocorticoid effect. Furthermore isofluprednone acetate therapy
has been associated with hypokalemic myopathy in humans35.
Treatment of Hypokalemia
Specific potassium supplementation in cases of mild hypokalemia accompanying
uncomplicated primary conditions such as left sided abomasal displacement is generally
unnecessary. Restoration of normokalemia will follow prompt correction of the inciting primary
disease. However, in a hospital setting, or with conditions such as abomasal volvulus where the
patient may have multiple electrolyte, acid base and hypovolemic deficits, large volume
intravenous fluid therapy with potassium supplementation may be warranted. However, in the
authors experience traditional formulae for calculating the amount of supplemental potassium
required to restore normokalemia in a severely hypokalemic cow tend to significantly
underestimate the amount of potassium required for clinical improvement and resolution of the
hypokalemia. These formulae are based upon calculating the difference between an individuals
measured serum or plasma potassium and the normal reference range and multiplying this deficit
first by the bodyweight (in kgs) and then by a factor that corrects for extracellular fluid space
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normokalemia in cows with severe (< 2.3 mEq/L) hypokalemia can be challenging and may
require several days of aggressive potassium supplementation15. Case management may be
complicated by recumbency and the subsequent potential for ischemic myopathy and peripheral
nerve injury. The implications of recumbency of even a relatively short period of time accentuate
the need for aggressive recognition and treatment of correctable electrolyte and mineral
abnormalities and attention to management factors that avoid further injury and maximize the
chances of recovery. Subsequently, oral potassium supplementation to at risk animals,
particularly those showing signs of early hypokalemia including muscle fasciculations and
weakness is recommended.
Isofluprednone acetate: Predef 2X, Pharmacia and Upjohn, Kalamazoo, MI, USA.
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