Download Fluid Therapy - Upstate Veterinary Specialists

FLUID THERAPY
Bernie Hansen DVM MS DACVECC DACVIM (Int. Med)
Associate Professor, NCSU College of Veterinary Medicine
[email protected]
Fluid therapy provides vital support to sick animals, and for many the simple act of rehydration with a
high-sodium fluid like lactated Ringer’s solution vastly improves their potential for recovery. In some
situations, however, a careless approach to fluid therapy stands to do more harm than good. This
presentation will provide an overview of the goals of fluid therapy planning and situations where just
reaching for a bag of LRS stands to do more harm than good.
The 3 classic goals of fluid therapy for support of sick animals are:
1. Repair of existing deficits of water and electrolytes: replace what’s missing
2. Provide for normal ongoing losses until the animal becomes self-sufficient with oral
intake: maintenance needs
3. Replacement of concurrent losses due to ongoing disorders such as vomiting during the
planned fluid therapy period: replace pathological losses as they occur
All 3 goals need to be addressed for most sick animals needing fluid therapy. Therapy should be
planned and executed over 1-24 hours, to be determined by patient needs and your available resources.
At the end of this planned period the physical and laboratory findings are reassessed and the next
treatment period is planned.
Goal 1: Repair of existing deficits
What is required to restore the animal to homeostasis, and how fast do we need to accomplish this?
Typically, we administer fluid therapy to animals that we think are dehydrated or at risk for becoming so.
In addition to water deficits, sick dehydrated animals often have abnormalities of sodium (content more
than concentration), potassium, magnesium, and acid-base balance. Other abnormalities such as
hypoglycemia or hypercalcemia may need correction with fluid therapy; however, these problems are
encountered less often and will not be considered here.
Water deficit is estimated as % dehydration. Dehydration can be classified as iso-, hypo-, or hypertonic
based on the concurrent magnitude of sodium (and other electrolyte) loss, and this determines the basic
IV solution you will use. Potassium and magnesium depletion (with or without low serum concentrations
of those ions) are common in sick, dehydrated animals and replacement needs are estimated based on a
measurement of serum concentrations, evaluation of the underlying disease, and evaluation of clinical
findings consistent with low cellular or extracellular K and Mg depletion. Acid-base evaluation is based on
knowledge of the underlying disease process, physical exam, and measurement of serum TCO2 (or
HCO3) and the Na-Cl difference.
Estimating dehydration is notoriously imprecise.(1) It is generally thought that as the water content of
the skin decreases, it becomes progressively less pliable (elastic) and its turgor (how “full” of fluid/blood it
feels) is reduced. More significant dehydration impairs salivation (but remember that nauseous dogs or
cats may hypersalivate in the face of severe dehydration). Severe dehydration (especially if isotonic)
causes enough loss of fluid & blood from the orbit to cause a sunken appearance of the eyes.
Isotonic Dehydration
The water lost in this class of dehydration is high in sodium (comparable to the concentration found in
extracellular fluid [ECF]). Therefore, this water comes almost exclusively from the ECF compartment; cell
volume is minimally affected but the ECF contracts almost in direct proportion to the volume lost. Thus,
plasma volume sustains a big hit, and many animals develop clinical signs of hypovolemia with only 8 10% dehydration. Other causes of hypovolemia such as hemorrhage or extravasation of plasma do not
cause much dehydration - there is only a small amount of water loss from the body - but has similar
effects on circulation because of the direct impact on blood volume. The dramatic impact of isotonic
dehydration on ECF and plasma volume often gives rise to obvious clinical and laboratory abnormalities,
e.g. an increase in plasma total solids, maximally concentrated urine, and azotemia.
Isotonic dehydration is corrected with replacement fluids. Replacement fluids are characterized by
high sodium content, between 130 and 154 mEq/l, and include Ringer's solution, lactated Ringer's
solution, 0.9% sodium chloride, and several proprietary solutions. Following intravenous administration of
any of these, nearly all of the fluid remains in the ECF. Isotonic dehydration can potentially be corrected
rapidly, and if accompanied by clinically significant hypovolemia that may mean in well under 1 hour. If
hypovolemia is absent or mild, the rate of correction may be more leisurely, but in general one should
strive to complete that goal within 24 hours.
Hypertonic Dehydration
Volume depletion is mild in this form of dehydration because the water loss occurs by evaporation or
as dilute urine in diabetes insipidus and contains very little electrolyte. Thus, the water is lost in
proportion from each body water compartment, and since plasma water accounts for just 1/12 of total
body water loss from that compartment is minimal and this form of dehydration will not produce significant
hypovolemia. Normal dogs and cats in a thermoneutral environment can survive up to 24-37 days
without food or water and up to 3 (dogs) – 20 (cats) weeks without water when fed a 10.5% moisture
diet.(2) Death appears to be due not to hypovolemic shock, but rather due to deranged cell function as a
consequence of water loss.
Animals with hypertonic dehydration require water to restore normal hydration and osmolality. If pure
water loss alone was responsible the best treatment is a bowl of water; if parenteral rehydration is
necessary then 5% dextrose in water is the way to provide pure water in a temporarily isotonic form. If a
‘mixed’ form of dehydration is present and substantial ECF was also lost, begin with a replacement
solution (e.g., LRS or 0.9% saline) to expand the ECF compartment first, then follow with the dextrose
solution. If the hypernatremia is chronic (>2 days), you must replace water and decrease serum [Na+]
slowly, with a maximum reduction of serum [Na+] of about 2 mEq Na+/L/hour for 6 hours, followed by a
rate not to exceed about 1/2 mEq/l/hour. Acute reduction of serum [Na+] by >15 mEq/l will cause
significant clinical signs of water intoxication (cerebral edema) including "drowsiness", irritability, inactivity,
stupor, exaggerated startle response, hyperventilation, seizures, and coma leading to death. For a review
of treatment of hypernatremia in dogs see reference (3).
Hypotonic Dehydration
This form of dehydration is most often seen in animals with GI fluid losses high in sodium and
potassium that are partially restored by drinking water. Consequently, these animals present with
variable dehydration (due to water loss), hypovolemia (due to sodium loss) and hyponatremia (due to
hypovolemia-induced release of ADH). With the exception of hypoadrenocorticism and some animals
with marked colitis, severe hyponatremia is uncommon in animals because most affected individuals
usually don’t drink enough or are vomiting. Dogs with very low cardiac output – usually due to dilated
cardiomyopathy – that require high doses of diuretics may become hyponatremic with or without
dehydration as their low output stimulates thirst and release of ADH at a lower threshold of osmolality.
The severity of dehydration and hyponatremia is variable, depending on the animal’s ability to drink
and the magnitude of hypovolemia, respectively. The degree of hypovolemia is proportional to severity of
sodium loss and contraction of ECF. Neurologic signs are more likely to be seen with rapid development
due to diarrhea, and are rare in hyponatremia secondary to circulatory failure. Persistent hyponatremia in
a treated heart failure patient is a poor prognostic sign.
Serum (ECF) sodium concentration is determined by the relationship between total body sodium
content and total body water content. Hyponatremia may occur in animals that are normally-, under-, or
overhydrated. If the hyponatremia is due to water retention secondary to heart failure, the treatment is
usually to improve circulation, NOT to administer sodium!! Administration of sodium to a hyponatremic
heart failure patient will cause congestion if the animal’s blood volume is already increased. Compared to
animals with isotonic dehydration, dehydrated hyponatremic animals without congestive heart failure
need proportionally more Na than water. If the animal is capable of excreting free water, this may be
accomplished by treating with any replacement solution.
Chronic (> 1-2 days) hyponatremia should be corrected slowly. Experimentally (in rabbits) it is safe to
increase serum [Na+] by 12 mEq/L over the first 24 hours, then half that rate until correction is complete.
For acute symptomatic hyponatremia you can treat more rapidly but it is probably not necessary to
increase serum [Na+] by more than 6 - 8 mEq/l as this will have major impact on cerebral edema. For a
review of management of hyponatremia see reference (4).
Most animals with a combination of isotonic dehydration and some other problem will benefit from
rapid treatment of any hypovolemia first. For example, a dog with heat stroke and these abnormalities
would benefit from resuscitation with a replacement solution to rapidly restore ECF volume, even though
it also has hypernatremia. The remaining water deficit may be completely restored more slowly
afterwards.
Goal 2: Replacing normal ongoing losses (maintenance therapy)
Two-thirds of lean body weight in adult mammals is water. Of this, roughly 2/3 is present as cellular
water, and 1/3 is extracellular fluid (ECF). 1/4 of the extracellular water, or about 50 cc per kg of lean
body weight, is plasma. The single most important determinant of plasma volume is the ECF
compartment volume, as plasma volume remains a relatively constant fraction (1/4) of that compartment.
The ECF compartment size is controlled by manipulation of the total body sodium content. As the body’s
content of sodium is increased or decreased, osmoregulation and thirst adjust water balance to maintain
osmolality in the normal range.
Maintenance calculations are based on requirements to maintain homeostasis in a normal animal is
resting in a cage at room temperature with no activity and no oral food or water. The requirement for
water and electrolytes is based on the animal’s mass and is not affected by health problems – therefore it
is always the same and may be obtained from a table or chart.
The easiest way to administer water and electrolytes needed for maintaining the animal’s physiology is
to use a commercial maintenance solution. These products have approximately 30-40 mEq/l of sodium,
13-16 mEq/l of potassium, and variable amounts of bicarbonate precursor, calcium, magnesium, and
other electrolytes. Although the sodium content is still higher than necessary, these fluids are reliably too
low in potassium and need to be supplemented to ~28 mEq/l (or higher, if the fluid administration rate is
calibrated for a lethargic/quiet animal). If the solution contains 28 mEq/l of potassium, and is
administered at a high maintenance rate for water, this will deliver 0.05 - 0.1 mEq/kg/hour of potassium to
the patient, meeting its maintenance needs for that electrolyte.
This goal is where you can get into trouble with high sodium fluids like LRS. Veterinarians often use
replacement solutions (for example, lactated Ringer’s solution [LRS]) to provide maintenance water. This
provides the patient with around 15 x maintenance for sodium – in fact, one liter of LRS solution provides
the amount of sodium present in 5 kg of dry dog food formulated to A.A.F.C.O. standards. Inappropriate
use of replacement solutions in animals with heart disease, systemic inflammation, or other causes of
congestion may be a fatal mistake. Many critically ill patients – often immobile and inflamed - are prone
to edema and will readily retain excessive sodium and water administered for maintenance. Always think
about whether the patient can tolerate the high sodium load it will receive if you use replacement
solutions to provide maintenance water!!!
Goal 3: Replacement of ongoing losses
This goal is necessary if an animal continues to lose fluids during the planned period of fluid therapy.
Common examples of ongoing fluid loss in hospitalized animals include drainage of wounds, vomiting,
diarrhea, polyuria, hyperventilation, or increased evaporation from damaged skin. Electrolyte losses may
be high (e.g., sodium loss to wound drainage, potassium losses to vomiting) or low (e.g., evaporation
through the respiratory tract). These losses need to be replaced over the course of the planned treatment
period to avoid falling behind.
The rate of ongoing water losses is estimated from history initially, then by observation of the animal
once in the hospital. Daily (or even 2-3 times daily) body weights, on a single, accurate scale, are the
most important method to follow changes in body water. If you estimate fluid volumes by looking at the
puddle on the cage floor, be sure to estimate in terms of kitchen measures:
1 tsp. = 5 ml
1 Tbls. = 15 ml 1 cup = 240 ml 1 pint = 480 ml
Ongoing isotonic fluid loss should be replaced with replacement solutions. Patients with effusions
associated with hypoproteinemia may also benefit from treatment with plasma, albumin solutions, or
synthetic colloids to maintain the colloid oncotic pressure of plasma. Hypotonic fluid loss, resulting in
hypertonic dehydration of the patient, is usually seen in dogs with high insensible losses due to
hyperventilation +/- hyperthermia. This is best replaced with IV fluids low in sodium and other
electrolytes, for example 5% dextrose in water or a commercial maintenance solution. Hypertonic fluid
loss is not seen clinically in companion animals (or in any mammal, I think!) To replace ongoing losses,
first guesstimate how much water the animal will lose during the planning period (6 - 24 hours). The fluid
type (high or low sodium) is determined by the nature of the losses.
Potassium and Magnesium supplementation
Many disorders that cause dehydration also cause concurrent depletion of body potassium and
magnesium, and measurement of their serum concentrations should always be performed to assess
patients at risk. However, since nearly all body stores of these electrolytes are intracellular their serum
concentrations may not accurately reflect patient need. Unfortunately, there is no simple method to
accurately determine K/Mg requirements in depleted animals, and serum concentration is usually the only
available means of laboratory assessment. Although significant body losses of K/Mg will usually cause
hypokalemia/hypomagnesemia, some animals have normal, low or high serum concentrations in the face
of severe total body losses.
Signs of potassium depletion include muscle weakness and electrocardiogram (ECG) changes.
Skeletal muscle weakness manifests as locomotor difficulties in dogs and cats, and weakness of the neck
(ventroflexion) in cats. Smooth muscle weakness may contribute to intestinal ileus. Although this may
not be clinically apparent, animals with diarrhea associated with ileus (e.g. parvoviral enteritis) should be
monitored and treated aggressively for hypokalemia to prevent aggravation of ileus. Chronic potassium
depletion may cause myopathy (with elevated serum CK concentration) and kidney injury.
The electrocardiogram is a useful way to evaluate the physiological impact of potassium depletion and
hypokalemia on the body. The ECG may show abnormalities including arrhythmias (atrial and ventricular
premature depolarizations) or prolongation of the Q-T interval to values greater than 0.25 second.
Finding those changes should prompt more aggressive supplementation even if serum [K] is only mildly
decreased; for example a dog with only moderate hypokalemia (serum [K+] = 3.0 - 3.5 mEq/L) with
arrhythmias or a long Q-T interval should usually be treated more aggressively than might be predicted
from the serum measurement alone. Remember that acid - base disturbances will also affect serum [K]:
Non-gap (hyperchloremic) metabolic acidosis will increase serum [K], and metabolic alkalosis will
decrease it relative to total body stores.
The amount of potassium required to maintain potassium homeostasis in a normal animal that is given
IV maintenance water and no food is approximately 0.05 (large dogs) – 0.1 (small dogs and cats)
mEq/kg/hour If potassium depletion is present, or if ongoing losses include potassium, extra potassium
should be given.
There is no easy-to-use accurate technique to determine potassium deficit. However, a relatively
simple approach to potassium administration may be used. Consider that the amount of IV potassium
required by a normal dog or cat to maintain a positive K balance is approximately 0.05 - 0.1 mEq/kg/hour
(use the low end for large animals, the higher end for small animals). If added to a bag of fluid designed
to provide water at a high maintenance rate ((140 x Wt^.73) per 24 hours), the final concentration is
roughly 24-28 mEq/l. On the high end of administration rates, the routine safe maximal rate of K
administration to a K-depleted animal with normal renal function is about 0.5 mEq/kg/hour. Thus, the total
potassium administration rate required for all 3 of our goals (deficit repair, replacement of ongoing losses,
and maintenance) is usually 0.05 - 0.5 mEq/kg/hour. Animals with mild deficits and/or small ongoing loss
may be treated with around 0.15 - 0.2 mEq/kg/hour; for moderate depletion or loss rates use 0.2 - 0.3
mEq/kg/hour, and for more severe problems use 0.3 - 0.5 mEq/kg/hr. At these higher administration
rates, the serum potassium concentration should be checked at least every 24 hours.
Magnesium depletion is caused by much the same disorders that cause potassium depletion, and
serum concentration of magnesium also has a loose relationship to total body stores. The empiric rate of
magnesium repletion in intravenous fluid therapy is 10% of the rate of potassium; therefore the amount
needed for routine maintenance of homeostasis in a dog or cat held off food is 0.005 – 0.01 mEq/kg/hour,
and the maximum rate of administration is .05 mEq/kg/hour. Animals with azotemia should not be given
magnesium unless hypomagnesemia is confirmed with an assay, as many of those animals have
hypermagnesemia until the azotemia resolves.
After day 1: Fluid Therapy after Deficit Repair Has Been Accomplished
Once the initial planned period of therapy (first 2-24 hours to accomplish deficit repair) is complete, the
animal is re-weighed and re-evaluated. If body weight has increased to the predicted value (initial weight
plus weight of deficit fluids) and the animal appears normally hydrated, the repair of water deficit may be
complete. Subsequent fluid therapy requires only replacement of any ongoing losses and provision of
maintenance needs. Parenteral administration of fluids should continue until the animal is capable of
meeting its maintenance and (ongoing loss) needs by ingestion. Once this condition is met, parenteral
fluids may be tapered while observing the animal and then discontinued.
If upon reevaluation an animal receiving parenteral fluids does not weigh what was expected, the
clinician must decide the reason why based on all available clues:
Interpretation of Body Weight Changes after Fluid Therapy
Body Weight
Possible Interpretation
As Predicted
All estimates of dehydration, ongoing losses, and maintenance needs
for that period where accurate
As Predicted
The animal is still dehydrated and the ongoing losses were as
expected
As Predicted
The animal is overhydrated and incapable of excreting the excess
because of renal disease
< Predicted
The animal was not as dehydrated as initially estimated and excreted
the excess fluids you administered
< Predicted
The animal had higher than expected ongoing losses and is still
dehydrated
> Predicted
The animal was more dehydrated than estimated and had lower
ongoing losses than predicted, allowing it to retain some of the ongoing
loss fluid
> Predicted
The animal is overhydrated and is incapable of excreting the excess
because of renal impairment
DRUG DOSE AND SPECIALTY APPS
Veterinary Information Network
VIN desktop drug dilution calculator
https://www.vin.com/Members/login/login.aspx?ReturnUrl=/members/cms/document/def
ault.aspx?id=5315915&pid=&catid=&said=1
VIN mobile app free water deficit calculator
https://beta.vin.com/Members/login/login.aspx?ReturnUrl=/Members/Calculators/jsCalcs
/freewaterCalc_iOS.html
VIN mobile app CRI calculator
https://beta.vin.com/Members/login/login.aspx?ReturnUrl=/Members/Calculators/jsCalcs
/criCalc_iOS.html
Veterinary Anesthesia & Analgesia Support Group (VASG)
Drug delivery calculators for IV fluids, syringe pumps, and special analgesia applications
http://www.vasg.org/drug_delivery_calculators.htm
Cardiology Care Network
Cardiac drug CRI calculator for fluids or syringe pumps (and oral meds)
http://www.cardiologycarenetwork.com/
North Carolina State University College of Veterinary Medicine
Drug CRI calculator for syringe pump
http://www.ncstatevets.org/veterinarians/
Fluid therapy calculators
Abbott Animal Health
Old school poster on 24-hour fluid administration rate
http://www.abbottanimalhealth.com/docs/FLU041_R3_How_Much_Fluid_Should_I_Give_poster.pdf
Abbott fluid therapy calculator mobile device app
https://play.google.com/store/apps/details?id=air.com.abbott.AbbottAnimalHealth_IVFlu
idVolumeCalculator&hl=en
(Not a calculator but a cool fluid therapy educational resource)
http://www.abbottanimalhealthce.com/
Dechra animal health (UK)
Onling/downloadable calculator program for desktop
http://www.dechra.co.uk/therapy-areas/companion-animal/fluid-therapy
North Carolina State University College of Veterinary Medicine
Fluid therapy calculator
http://www.ncstatevets.org/veterinarians/
Reference List
(1) Hansen B, DeFrancesco T. Relationship between hydration estimate and body weight change after
fluid therapy in critically ill dogs and cats. J Vet Emerg Crit Care 2002;12(4):235-43.
(2) Prentiss PG, Wolf AV, Eddy HA. Hydropenia in cat and dog. Ability of the cat to meet its water
requirements soley from a diet of fish or meat. Am J Physiol 1959;196(3):626-32.
(3) Goldkamp C, Schaer M. Hypernatremia in dogs. Compend Contin Educ Vet 2007 Mar;29(3):148,
150, 152-48, 150, 161.
(4) James KM, Lunn KF. Normal and abnormal water balance: hyponatremia and hypernatremia.
Compendium Continuing Education for Veterinarian 2007;29(10):589-608.