Page 706 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Hemodialysis and Extracorporeal Blood Purification 693

time. Blood flow can be increased during the bypass The efficacy of sodium profiling has not been validated
intervals to minimize clotting in the extracorporeal circuit in animals but appears beneficial in human patients
without the risk of excessive dialysis. predisposed to hypotension or intradialytic discomfort.*
A modeled dialysate with a sodium concentration of
Dialysate Composition 155 mmol/L for the initial 20% to 25% of the treatment,
Dialysate composition and its temperature and flow rate 150 mmol/L for the next 40% of the treatment, and 140
are active components of the dialysis prescription. Dialy- to 145 mmol/L for the remainder of the treatment has
sate is formulated to maximize elimination of uremia been used for small dogs that are not hypertensive and
toxins, prevent depletion of normal blood solutes, replen- predisposed to hypovolemia. 34,59 For cats, sodium
ish depleted solutes, and minimize physiologic and met- modeling using the respective sodium concentrations of
abolic perturbations during and after the dialysis sessions. 160 mmol/L, 155 mmol/L, and 145 to 150 mmol/L
Conventional dialysate formulations for dogs and cats appears to prevent hypotension in the face of the large
include sodium, approximately 145 mmol/L (dogs), extracorporeal volume required for hemodialysis. The
150 mmol/L (cats); potassium, 0.0 to 3.0 mmol/L, effects of sodium modeling on intravascular volume are
bicarbonate, 25 to 40 mmol/L; chloride, approximately illustrated in Figure 29-7 in which expansion (refilling)
113 mmol/L (dogs), approximately 117 mmol/L (cats); of blood volume coincides with the application of a
calcium, 1.5 mmol/L; magnesium, 1.0 mmol/L; and high-to-low dialysate profile in a dog receiving concurrent
dextrose, 200 mg/dL, which are produced online from ultrafiltration.
standard dialysate concentrates. Dialysate flow conven- Modeling dialysate sodium from isonatremic or
tionally is 500 mL/min but can be decreased to reduce hyponatremic to hypernatremic (dogs: 145 mmol/L
solute clearance during initial treatments or increased for the initial 20% to 25% of the treatment, 150 mmol/L
to maximize the intensity of maintenance treatments. for the next 40% of the treatment, and 155 mmol/L for
For practical purposes, however, there is little additional the remainder of the treatment; cats: 150 mmol/L,
solute clearance until dialysate flow exceeds twice the 155 mmol/L, and 160 mmol/L, respectively) has been
counter current blood flow rate. 78,158 Urea extraction used prophylactically to forestall the neurologic
across the dialyzer is nearly complete at the blood flow manifestations of dialysis disequilibrium in severely azote-
rates used during initial treatments, so it is not practical mic animals. This sodium profile promotes osmotic
(or possible on most delivery systems) to reduce dialysate (sodium) loading of the ECF in the later stages of treat-
flow sufficiently to alter dialysis efficiency. ment when urea disequilibrium can cause osmotic fluid
Rapid solute removal exposes the patient to shifts into the intracellular compartment, exacerbating
nonphysiologic osmotic shifts that can cause osmotic dis- cerebral edema and increased intracranial pressure. This
equilibrium between the vasculature, the interstitium, profile has been derived empirically but appears to offer
and cells. The accompanying shifts of fluid out of the vas- a margin of protection in animals with BUN
culature and interstitium can cause signs of hypovolemia, concentrations greater than 200 mg/dL. Conceptually,
hypotension, cramping, nausea, vomiting, and neuro- this low-to-high dialysate profile could increase the
logic manifestations of dialysis disequilibrium syndrome. osmolality of the ECF by 20 mOsm/kg (approximately
The patient may experience additional hypovolemia, equivalent to the osmotic effects of 60 mg/dL of urea
hypotension, and poor catheter performance when ultra- disequilibrium), promoting an osmotic buffer to lessen
filtration is superimposed on these effects. These signs are fluid shifts into cells (Figure 29-8).
especially likely to develop early in the treatment when Sodium profiling will alter the patient’s sodium
solute removal is the greatest. To offset these physiologic balance if the cumulative sodium transfer is other than
trends, the sodium composition of the dialysate can be neutral. A positive sodium balance is expected with
modeled (or profiled) so that dialysate sodium is adjusted the low-to-high profile and is accepted for initial
systematically during the treatment to counteract solute treatments in patients at risk for dialysis disequilibrium.
disequilibrium, promote vascular refilling, and lessen or Patients may develop untoward complications, including
prevent these adverse signs. 22,60,129,169 Dialysate sodium postdialysis thirst, interdialysis weight gain,
can be programmed to change in stepped or linear hyperkalemia, and hypertension if the profile consistently
adjustments from hypernatremic (155 to 160 mmol/L) promotes sodium accumulation. This can be significant
during the initial stages of the dialysis treatment to during maintenance hemodialysis in animals as
isonatremic or hyponatremic (150 to 140 mmol/L) at documented in human patients. 51 Routine high sodium
the termination of the treatment. During the dialysate profiles have been shown to exaggerate potas-
hypernatremic phase of the profile, the sodium gradient sium rebound and increase interdialytic serum potassium
from dialysate to plasma causes sodium loading and concentrations in human dialysis patients. 45 In dogs
expansion of intravascular volume during this critical time undergoing maintenance hemodialysis, sodium profiling
when the extracorporeal circuit has filled, ultrafiltration
has started, and solute removal is greatest. *References 6, 22, 32, 129, 155, 164, 169, 187.