Hypokalemia in Dairy Cattle.
S. F. Peek BVSc. PhD, DACVIM1
T.J. Divers DVM DACVIM DACVECC2
W.C. Rebhun DVM DACVIM DACVO2*
1
Department of Medical Sciences, School of Veterinary Medicine, University of WisconsinMadison, Madison, WI 53706.
2
Department of Clinical Sciences, New York State College of Veterinary Medicine, Cornell
University, Ithaca, NY, 14853.
*Deceased
Primary Author Contact Information;
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
Dairy cattle in early lactation commonly develop hypokalemia secondary to simple
anorexia as well as a variety of forestomach, intestinal and renal disorders, with a clinical
presentation that varies according to the inciting cause, however severe hypokalemia may be
associated with muscle weakness, recumbency and the down cow syndrome.
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.
Physiology of Potassium Homeostasis
Potassium has multifactorial physiologic roles in normal metabolism and homeostasis. It
functions at the cellular level as the principle intracellular cation and plays an important role in
osmotic pressure regulation and water balance1. The balance between intracellular and
extracellular potassium is critical in maintaining the normal resting cell membrane potential and
transmembraneous movement of potassium is pivotal not only for the generation of nerve cell
action potentials but also for restoring the resting nerve cell membrane potential following
depolarization2,3. Potassium movement across myocyte membranes is also critical for contractile
events in skeletal, smooth and cardiac muscle4. The electrophysiologic role of potassium in the
generation of action potentials in cardiac pace maker tissue, the conduction of impulses
throughout the heart and contractile events in the myocardium are of particular clinical relevance
because both hyperkalemia and hypokalemia can have effects on cardiac rhythm and
contractility5,6.
There is no specific endocrine control of potassium homeostasis and as a result cattle are
very heavily dependent upon intake to maintain adequate potassium levels. Due to the high
potassium content of the forage based ruminant diet potassium is normally present in relatively
high concentrations in the intestinal lumen so that absorption occurs principally by passive
diffusion through the lateral intercellular spaces7. Although potassium absorption in ruminants
can occur throughout the intestinal tract the principle sites of absorption are the small intestine
and colon8. As the concentration of dietary potassium on a dry matter basis increases so does the
proportion of dietary potassium that is absorbed 8,9. Potassium excretion is predominantly
through the kidneys and to a lesser degree via obligate losses through the gastrointestinal tract. In
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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.
Acid-Base Issues and Potassium Balance
Transmembraneous movement of potassium is markedly affected by acid base issues and
the pH of the extracellular environment in particular. In broad terms, intracellular movement of
potassium with subsequent hypokalemia is favored by those clinical conditions that promote
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metabolic alkalosis, whilst extracellular movement of potassium and resultant hyperkalemia are
favored by those conditions that are associated with metabolic acidosis.
Insulin, Glucose and Potassium Balance
The balance of intracellular and extracellular potassium may also be affected by
treatment with glucose, glucogenic precursors and insulin. Therapeutic agents that cause
transient hyperglycemia, such as dextrose or propylene glycol will result in insulin production
which promotes intracellular movement of potassium. The repeated treatment of ketotic cows
with 50% dextrose infusions, especially if combined with insulin administration would tend to
promote intracellular potassium movement.
The precise mechanism of insulin-induced hypokalemia is uncertain, but insulin does
increase the activity of membrane bound Na+-K+ ATP-ase resulting in increased potassium
pumping into cells16,17. Furthermore parenteral insulin administration has been associated with
hypokalemic crises in man 18,19. In hypokalemic periodic paralysis in man it is believed that
insulin may potentiate depolarization of skeletal muscle fibers, confining them to a paralyzed
state, by reducing the inward rectifier current responsible for membrane repolarization20.
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
forage-based rations because higher levels of potassium can be antagonistic to magnesium
3
absorption and predispose to hypomagnesemia10,21,22. Dry cow rations that are high in potassium
will also increase the dietary cation-anion difference (DCAD) from its target range of –50 to 150 mEq/kg dry matter, thereby increasing the risk of milk fever at parturition23. Lactating dairy
cattle require higher levels of dietary potassium, specifically between 0.8 and 1% to
counterbalance potassium secretion in milk21. Heat stress and high production are factors that
have been documented to increase dietary potassium requirements21,24 . Diets that are high in
grains carry a greater risk for inadequate dietary potassium because grains rarely contain greater
than 0.5% potassium21. By comparison forages typically contain between 1% and 4% potassium
and are a therefore a more significant source of dietary potassium. Frequent application of liquid
cow manure, which is a rich source of potassium, may significantly increase the potassium
content of pastures. Increased urinary excretion of potassium as an adaptation to a relatively high
dietary potassium load in dairy cattle may actually predispose to the development of
hypokalemia particularly following marked or protracted anorexia14.
The obligate requirement for potassium in lactating dairy cows and the absence of any
endocrine control of potassium homeostasis underscores the relevance of simple anorexia to the
development of hypokalemia. Profound or protracted anorexia, particularly if accompanied by
other conditions that either increase potassium loss (diarrhea, increased renal excretion) or
promote intracellular movement of potassium (metabolic alkalosis, hyperglycemia, insulin
administration) may result in hypokalemia that is severe enough to be associated with muscle
weakness and recumbency.
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Hypokalemia – General Pathophysiology and Clinical Signs
Hypokalemia may result from whole body potassium depletion, a redistribution of
extracellular and intracellular potassium, diminished potassium intake or increased potassium
excretion in urine and feces. Due to the lack of endocrine control of potassium homeostasis cattle
are very heavily dependent upon dietary intake to maintain adequate potassium levels. The added
potassium loss from secretion in milk in the lactating dairy cow exacerbates potassium depletion
in those conditions such as ketosis that diminish appetite more than milk production. Although
serum or plasma potassium measurement is a notoriously poor indicator of total body potassium
status, hypokalemia has been associated with neuromuscular weakness in cats and cattle15,18,25. In
cattle the normal range for serum potassium is 3.9-5.8 mEq/L but clinical signs of neuromuscular
weakness and muscle flaccidity in association with hypokalemia are generally not observed until
serum potassium falls below 2.3 mEq/L15,25. Mild to moderate hypokalemia (2.3 – 3.8 mEq/L)
may be associated with more subtle clinical signs such as muscle fasciculations, but is frequently
asymptomatic.
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
5
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 acid-base disturbances26. Experimental induction of metabolic alkalosis and mild
to moderate hypokalemia in mature cattle is associated with the development of atrial
fibrillation27. Atrial fibrillation was documented in 4 of 10 cattle with severe hypokalemia and
recumbency in a report by Sielman et al.15
Gastrointestinal Disease and Hypokalemia
Several of the commonly encountered conditions of the bovine forestomachs are
associated with mild to moderate hypokalemia. The development of hypokalemia in association
with left or right abomasal displacement, abomasal volvulus or any other condition that restricts
abomasal pyloric outflow is multifactorial28,29. Potassium becomes not only sequestered within
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
6
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: Johne’s 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.
Renal Disease and Hypokalemia
Although clinically significant renal disease is uncommonly encountered in dairy
practice, mild to moderate hypokalemia frequently accompanies renal failure in cattle33.
Metabolic alkalosis is the commonest acid-base disturbance associated with renal failure in cattle
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.
Severe Hypokalemia, Muscle Weakness and Recumbency
In 1997, Sielman et al., documented an association between severe hypokalemia,
weakness and recumbency in adult dairy cattle that had received the corticosteroid
7
isofluprednone acetatea,15. All 10 cattle in that report were less than 30 days in milk and had
received the drug as part of therapy for moderate to severe ketosis15. Serum potassium
measurement at admission varied between 1.4 mEq/l and 2.3 mEq/L. Based upon our own
experiences, the prevalence of severe hypokalemia and muscle weakness in early lactation may
currently be underestimated and is not necessarily confined to those cattle that have received
repeated doses of this drug. However, the repeated use of isofluprednone, in excess of the
manufacturer’s current recommendations, should be avoided. We have observed severe
hypokalemia and muscle weakness profound enough to cause recumbency in both first calf
heifers and adult dairy cattle during the first 60 days of lactation34. Chronic, recurrent ketosis
appears to be the most common antecedent condition, although we have observed one herd in
which a cluster of cases occurred in conjunction with repeated intramammary infusion of
isofluprednone acetate for clinical mastitis. Severe hypokalemia has also been documented as a
potential cause of muscle weakness in cattle of varying ages, independent of corticosteroid
administration25.
The profound weakness associated with severe hypokalemia in adult cattle produces a
flaccid paralysis quite reminiscent of botulism. Affected cattle are often unable to support
themselves in sternal recumbency and consequently lie laterally (Figures 1 and 2). The authors
have dealt with several instances were more than one animal on a farm has been affected and
initial diagnostics have been directed towards a primary neurologic or neuromuscular cause of
weakness and recumbency such as botulism or listeriosis. The report by Sielman et al., also
described severe weakness and an inability to support the weight of the head. These authors were
able to demonstrate histologic lesions in non-weight bearing muscles that were consistent with
8
hypokalemic myopathy in cats and humans, including myofiber vacuolation and multifocal
myonecrosis with macrophage infiltration15,18. We have also documented similar histologic
lesions in muscle tissue obtained from the diaphragm and intercostal musculature in severely
hypokalemic cattle (Figure 3).
There are a number of factors that might contribute to the development of severe
hypokalemia in cattle with recurrent ketosis. Reduced potassium intake and intracellular shifting
of potassium due to metabolic alkalosis will be simple consequences of repeated bouts of
anorexia due to ketosis. Repeated treatment with dextrose containing preparations and other
hyperglycemic agents such as glucocorticoids will induce recurrent, transient hyperglycemia and
subsequent insulin release further driving potassium intracellularly as well as promoting
kaluresis due to hyperglycemic osmotic diuresis. Parenteral insulin administration, as a
component of therapy for ketosis, would also promote hypokalemia and was documented in 2 of
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.
9
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 individual’s
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
volume (0.3 in an adult). The refractoriness to conventional intravenous supplementation in
severe cases of hypokalemia associated with profound muscle weakness or recumbency may be
related to whole body potassium depletion but a categorical reason for this is uncertain at this
time.
In cases of severe hypokalemia (< 2.3 mEq/L) potassium supplementation should ideally
include both intravenous and oral administration, although for practitioners oral supplementation
is frequently the chosen route. It should be remembered that kaluresis will be a consequence of
diuresis with all intravenous fluids and so proprietary or homemade preparations should always
contain supplemental potassium. Intravenous potassium can be administered in the form of
10
supplemental potassium chloride added to polyionic fluids. The final concentration of potassium
to be administered intravenously should vary with the severity of the hypokalemia, but is
typically in the range of 30 to 100 mEq/L, at flow rates of between 2 and 4 L/hr. However, in all
cases of supplemental intravenous potassium administration practitioners are cautioned not to
exceed a maximum infusion rate of 0.5 mEq/kg/hr, in order to avoid potential pathologic cardiac
arrhythmias. It is the opinion of the authors that oral supplementation either alone or in
combination with intravenous potassium supplementation more rapidly restores normokalemia
than exclusively intravenous supplementation. Similar observations have been made by Sielman
et al. 15 and Sattler et al. 25. Due to the poor palatability of potassium salts and the low likelihood
of adequate voluntary intake, oral supplementation is best done by orogastric tube. We suggest
between 125 and 500 grams of potassium chloride in 15-20 litres of water twice daily.
Recommendations would be not to exceed 500 grams (0.5 lb) of potassium chloride orally twice
daily, due to the risks of inducing severe osmotic diarrhea at higher doses. The restoration of
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.
11
a
Isofluprednone acetate: Predef® 2X, Pharmacia and Upjohn, Kalamazoo, MI, USA.
12
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