Volume Overload, Prevention, Identification, and Management
EVECC 2022 Congress
Alessio Vigani, DVM, PhD, DACVECC, DACVAA
University of Zurich, Zürich, Switzerland

Overzealous fluid administration is undoubtedly one of the most common drug overdose: why?

  • Fluids are not properly considered as “drugs,” so there is a more naïve tendency among clinicians to use them compared to other medications.
  • Important questions to answer before administering IV fluids to prevent overload:
  • Why do we give fluids to a specific patient? Often even this question does not find a reasonable answer when IV fluids are given (i.e., administering maintenance IV fluids to a patient in ICU that is eating and drinking).
  • Which therapeutic goal do we want to reach?
  • Which is the real need of fluids of the patient? Has the patient the ability to handle a possible excess of administered fluids?

In the critically ill patient the homeostatic balance is impaired, therefore, many organic functions of volume regulation (cardiovascular, renal, endocrine) are impaired. This predisposes such patients to the risks of overzealous fluid administration. Importantly the critically ill patient doesn’t need to be explicitly azotemic or in congestive heart failure to retain fluids in excess and consequently develop volume overload.

Fluid plan

  • Fluid resuscitation (hypovolemia)
  • Fluid replacement (restore ECF from dehydration, excessive ongoing fluid losses)
  • Fluid maintenance (= actual patient needs, depending from metabolic rate and physiologic losses)

Approach

  • Goal: why do we give fluids?
  • Type: which is the right fluid for that patient?
  • Rate/timing
  • Considerations/limits

Example: Addisonian crisis: hypovolemic shock → prerenal azotemia → AKI

Goals

Correct hypovolemia, restore circulation and perfusion, restore GFR (fluid responsive AKI) TYPE: iso-osmotic crystalloid solution

Rate

Fluid resuscitation boluses to restore circulation and perfusion, followed by fluid replacement to correct dehydration and replace ongoing losses considerations: prevent rapid correction of hyponatremia.

Where do fluids distribute in the body? It depends on the type of fluid.

  • Isosmolar replacement solutions with plasma osmolarity (Na fluid = Na plasma) = isotonic crystalloids (balanced or not balanced), are compartmentalized to the extracellular space fluid (ECF) volume. ECF (1/3 of total body water): isotonic fluids tend to stay in ECF and not cross the cell membrane in absence of a concentration gradient of solutes.
  • Maintenance fluid solutions are characterized by lower Na concentration than plasma. Administering this type of fluids represents then a source of free water which can cross the cell membrane based on electrochemical gradient between ECF and ICF.

Fluid Maintenance

Requirements of fluid correlates to energy metabolism:

  • Dog 1 ml water/1 kcal of resting fed energy requirement.
  • Cat 0.7 ml water/1 kcal of resting fed energy requirement.

Overestimation of fluid needs can be due to misinterpretation of dehydration signs.

Common dogmas are:

  • 5% dehydration: dry mucous membranes.
  • 6–8% dehydration: decreased skin elasticity, sunken eye, dry mucous membranes.

The correlation between clinical signs and the degree of fluid deficit in a patient is extremely weak and unreliable. As a general reminder 5% dehydration in an adult human being represents a 3.5 liters fluid deficit. Keeping this in mind may be helpful when we estimate the fluid deficit of small animal patients. It may make it easier to realize that it is extremely unlikely that a cat or a dog would become 5% dehydrated just because he/she had vomited a couple of times over the previous 12 hours.

Positive fluid balance → increase in mortality.

A strong correlation between iatrogenic positive fluid balance and worsening of outcome has been largely demonstrated in multiple clinical conditions. The most obvious conditions for which a positive fluid balance represents a negative prognostic factor are heart failure and pulmonary diseases. The same strong correlation, however, between fluid overload and negative outcome has been demonstrated also for postoperative patients undergoing gastrointestinal surgery, for septic patients, as well as for AKI. IV fluids represent a mainstay therapy in renal patients. A patient presenting with evidence of AKI often is treated with IV fluids to determine fluid responsiveness of the initial azotemia. If the form of AKI is fluid-responsive (i.e., Addisonian crisis), the restoration of renal perfusion by IV fluids will promote an improvement of GFR with improvement/resolution of the azotemia within hours. If the patient, however, has a non-fluid responsive AKI, the administration of IV fluids will not induce any significant improvement of GFR. In these patients, especially the oligo/anuric ones any excess of fluid will induce an increase in total body water. Insisting with fluid administration then will expand the extracellular compartment inducing edema formation.

Administration of excessive fluids → redistribution in ECF → ECF enlarges and increases intracapsular pressure → causing renal edema (the kidney are not compliant organs due to the presence of renal capsule) → GFR is regulated by a pressure gradient, that is neutralized in course of edema → anuria

Mean glomerular capillary pressure 45 mm Hg - Intracapsular pressure 10 mm Hg = Mean hydrostatic pressure gradient 35 mm Hg - Mean colloid pressure 25 mm Hg = Mean pressure driving UF 10 mm Hg → production of urine

If intracapsular pressure increases up to 20 mm Hg (renal edema) → mean pressure driving ultrafiltration 0 mm Hg = anuria

Careful evaluation of daily body weight changes of hospitalized patients still represents the best tool to reliably identify changes in the patient’s fluid balance. In high-risk patients, body weight should actually be checked multiple times daily to even better prevent the risk of excess fluid accumulation. The development of obvious subcutaneous edema is unfortunately a late consequence of fluid overload and once it is present normally reflects a massive expansion of the extracellular space volume also of the viscera and parenchymal organs.

Once volume overload is present, homeostatic organic and hormonal compensatory mechanisms become impaired and the patient may become unable to spontaneously eliminate the excess fluid. Discontinuation of fluid administration, diuretic therapy, and in extreme cases extracorporeal fluid removal represent the therapeutic interventions necessary to restore the physiologic fluid status.

References

References are available upon request.

 

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Alessio Vigani, DVM, PhD, DACVECC, DACVAA
University of Zurich
Zürich, Switzerland


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