Page 721 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

708 SPECIAL THERAPY

frequent cause of hypovolemia and transient hypoten- the severity of azotemia and metabolic acidosis is greatest.
sion. Dialysis-induced hypotension usually responds Clinical signs such as tremors, restlessness, disorientation,
quickly to modest fluid supplementation with either crys- vocalization, amaurosis, seizures, and coma may develop
talloid or colloid solutions as vascular volume refills and during the dialysis session or up to 24 hours after dialysis.
fluid from the extravascular space is mobilized. Adminis- If not recognized and managed properly, the syndrome
tration of small volumes of synthetic colloid solutions may progress to seizures, coma, and death from
often is more effective at maintaining blood pressure, respiratory arrest following herniation of the brainstem
blood volume, and ongoing ultrafiltration with less net or compression of the cerebellum. 34 In dogs, dialysis dis-
fluid administration. Nevertheless, changes in fluid equilibrium syndrome generally is insidious and
removal patterns (i.e., slower ultrafiltration rates and lon- commences with restlessness and vocalization before
ger treatment times) and minute-to-minute monitoring the onset of seizures or coma and affords ample opportu-
of changes in blood volume have mitigated the exacerba- nity to intervene at an early stage. In cats, the develop-
tion of hypotension in the majority of patients. ment of serious or fatal manifestations frequently is
Transcutaneous venous catheters remain the most fea- more acute and without warning.
sible angioaccess for animal dialysis, but they represent Treatment of dialysis disequilibrium syndrome
the most predictable, problematic, and serious source requires immediate attention, slowing or discontinuing
of dialysis-related complications. 59 Dialysis catheter the hemodialysis treatment, and intravenous administra-
thrombosis and cranial vena caval stenosis are still com- tion of hypertonic (20% to 25%) mannitol (0.5 to
mon problems, but earlier and more aggressive use of 1.0 g/kg intravenously) to increase plasma osmolality
thrombolytic agents, selection of less thrombogenic and dissipate the osmotic gradient. Diazepam is used as
catheters, and proactive catheter replacement have dimin- needed to control seizures. For high-risk animals, the
ished the clinical impact of this important complication. intensity of the dialysis treatment should be reduced
There has been no noticeable change in prevalence of purposefully by interspacing periods of dialysis with
dialysis catheter infection over the years. The majority periods of bypass and decreasing the dialysate bicarbonate
of infections reflect exit site or tunnel infections, and to better match that of the patient (see Hemodialysis
the prevalence of catheter-related bacteremia or septice- Prescription for Acute Kidney Injury section). Mannitol
mia is low, especially when considering the hygiene of ani- can be administered prophylactically at 0.5 to 1.0 g/kg
mal patients. Yet, nearly 40% of veterinary dialysis patients intravenously after the initial 20% to 25% of the dialysis
have documented infection at some site including treatment and also at the end of the treatment to reduce
infections of the dialysis catheter, urine, feeding tube exit delayed onset of signs. Mild signs usually dissipate imme-
site, and other site leaving plenty of room for greater diately with mannitol administration, whereas severe
vigilance and improvement in this area. signs may require several doses and 24 to 48 hours of
Dialysis disequilibrium syndrome is a serious neuro- supportive care before resolution. Respiratory arrest from
logic manifestation induced by rapid dialysis of animals cerebral edema and brainstem compression requires
with severe azotemia. Its pathogenesis is not completely ventilatory support until the edema resolves but carries
understoodbutculminateswith cerebraledema, increased a poor prognosis for recovery.
intracranial pressure, and potential herniation of the
brainstem. 34,78,121,125 The disproportionate removal of OUTCOME AND PROGNOSIS
solutes (mostly urea) from ECF relative to intracellular Dogs have been supported on chronic intermittent
fluid in the brain imposes an osmotic pressure causing hemodialysis as long as 1.5 years, but complications
influx of water into brain cells, cerebral edema, and an related to vascular access and anemia management often
increase in intracranial pressure. 78,125,159,160 A possible curtail dialytic support beyond 6 months. Regional avail-
molecular explanation suggests the relative distribution ability and financial and time constraints further limit use
of urea channels is reduced and the distribution of water of hemodialysis for management of either acute or
channels is increased in the brain of uremic animals. These chronic uremia for extended periods of time. For acute
adaptations exacerbate the delayed transference of urea kidney injury, renal recovery is not predicated on dialysis,
from the brain during dialysis, causing increased osmotic but rather the cause, extent of damage, comorbid
accumulation of water. 125 Paradoxical cerebral acidosis diseases, multiple organ involvement, and availability of
caused by rapid correction of severe metabolic acidosis diagnostic and therapeutic services. Overall survival rates
and large transmembrane bicarbonate gradients also of dogs and cats treated with hemodialysis for AKI is 41%
has been suggested to impose osmotic gradients by to 52%, but survival time is highly dependent on the
induction of idiogenic osmoles within the brain, causing cause. 3,59,96,149 The survival rate for AKI of infectious
further brain swelling. 8–12 causes varies between 58% to 100%. 3,59,62,123,149 Hemo-
The risk for dialysis disequilibrium is greatest in cats dynamic and metabolic causes have a reported 40% to
and small dogs during initial dialysis treatments when 72% survival rate. 62,123,149 Only 20% to 40% of patients