Page 702 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Hemodialysis and Extracorporeal Blood Purification 689

solutes to minimize the time-averaged urea BOX 29-2 Clinical Considerations
concentrations mitigates the associated morbidity and
mortality of uremia but does not resolve all uremic symp- Influencing the
tomatology.* It is equally established that additional clas- Hemodialysis
ses of retention solutes including protein-bound, low- Prescription
molecular-weight solutes, secluded solutes, and so called
middle molecules with a molecular weight between 500 1. Patient characteristics (species, size, age, body
Da and 60,000 Da are poorly dialyzed by conventional condition)
high-flux diffusive and hemofiltration techniques, limit- 2. Severity of the azotemia and retained uremic toxins
{
ing the efficacy of extracorporeal techniques. The diffu- 3. Electrolyte and mineral disorders: sodium,
sive removal of urea and small-molecular-weight solutes is potassium, chloride, bicarbonate calcium,
exceptionally efficient in animals because of their small magnesium, and phosphate
size (volume) relative to the surface area and clearance 4. Acid-base imbalances and depleted or deficient
solutes: bicarbonate, calcium, glucose
capabilities of the hemodialyzer. Theoretically, these sol-
5. Exogenous intoxications (e.g., ethylene glycol)
ute and the fluid abnormalities attending uremia could be
6. Hydration status and fluid balance
corrected temporarily during a single hemodialysis ses-
7. Physiologic disturbances: blood pressure, body
sion, but clinical sequelae associated with abrupt temperature, oxygenation, change in body weight,
excursions in the solute and fluid content of the patient mental state
limit the rate and magnitude that they can be altered. 8. Coagulation status
The change in solute concentration (e.g., urea) during 9. Medications, surgical history, and comorbid clinical
dialysis is influenced by the size of the animal and the conditions
interactive parameters defining the dialysis prescription 10. Dialysis treatment history
(see Appendix, Equation 8). The intensity of dialysis
can be adjusted by altering blood flow rate (Q b ), dialysate
flow rate (Q d ), clearance of the hemodialyzer (K d ), rate of
ultrafiltration (UF), or length of the dialysis session (T d ) plasma solids; (5) electrolyte and acid-base abnormalities;
to accommodate the size and therapeutic needs of the (6) oxygenation capacity; and (7) bleeding potential. The
animal. After dialysis, BUN (and other retained uremia prescription is individualized for each patient and every
solutes) increases in proportion to urea generation from dialysis session by selecting dialytic options that best
dietary nitrogen and endogenous protein catabolism (G) achieve the solute removal and ultrafiltration goals of
and inversely with residual renal function (K r ) (see the session without predisposing therapeutic risk. Specific
Figures 29-1 and 29-2). Higher dietary protein intake, factors regulating these processes are prescribed indepen-
increased catabolism, and lower residual renal function dently and are outlined in Box 29-3. Hemodialysis
will produce a steeper increase and higher steady-state prescriptions for animals have been derived empirically
concentration of urea after dialysis unless interrupted as consensus-based guidelines for a diverse array of animal
by an intervening dialysis treatment before achieving a types and clinical conditions. There has been little valida-
steady state (Figure 29-2). The peak predialysis urea, tion or standardization of dialysis therapy based on out-
time-averaged urea concentrations, and the exposure to come assessment. However, animal dialysis has
urea and other uremic toxins will be lower the more fre- advanced over the past 40 years, and dialysis prescriptions
quently and effectively a patient is dialyzed. 46,48,50,64,186 are based on a solid understanding of the physical and
The hemodialysis session is defined by the dialysis physiological principles governing dialysis and clinical
prescription, which is formulated interactively with con- aspects of uremia.
sideration of the physical and clinical condition of the HEMODIALYSIS PRESCRIPTION FOR
patient and the alterations of body fluid volume and com-
position subject to dialytic correction. The prescription ACUTE KIDNEY INJURY (AKI)
must accommodate the physiologic, hematologic, and The rapid accumulation of retained solutes in acute ure-
biochemical status of the patient before dialysis and mia intensifies expression of the clinical signs and meta-
target the desired modifications at the end of the session bolic disturbances compared with the uremia of chronic
(Box 29-2). Patient assessment includes (1) species, kidney disease. Hemodialysis prescriptions are prioritized
breed, weight; (2) degree of azotemia; (3) hemodynamic to resolve hyperkalemia, profound azotemia, fluid imbal-
stability and predisposition to hypotension and ance, metabolic acidosis, and persistent nephrotoxins and
hypovolemia (i.e., body weight, estimated blood volume, to accommodate ongoing therapies (e.g., parenteral feed-
blood pressure, volemic status); (4) hematocrit and total ing). The therapeutic efficiency of hemodialysis must be
applied judiciously to prevent overtreatment when the
*References 48, 49, 56, 57, 106, 120. risks of dialysis disequilibrium syndrome, hypovolemia,
{ References 56, 113, 133, 181, 182, 185. hypotension, and bleeding are high. Consequently,