Page 117 - Clinical Small Animal Internal Medicine

11 Hypoadrenocorticism in Dogs and Cats 85

Therapy while monitoring the ECG. Rapid administration may
VetBooks.ir Acute Management cause additional arrhythmias, such as shortened Q‐T
interval and more severe bradycardia.
Patients with hypoadrenocorticism fall along a contin-
Intravenous regular insulin helps drive the potassium
uum of disease. While some patients present in hypov- intracellularly. Dosages of 0.2–0.5 U/kg regular insulin
olemic shock with severe hyperkalemia, most are less are administered, followed by 2 g of dextrose (diluted to
critical, but require intravenous fluids and other sup- 25% in an isotonic crystalloid) per unit of insulin admin-
portive therapy. The most severe cases (true Addisonian istered. Dextrose should then be added to the intrave-
crises) will be discussed in this section. nous fluids (e.g., 0.9% saline or LRS) to produce a
The initial goal of treatment of Addisonian crisis is
to correct hypovolemia, hyperkalemia and associated 1.25–2.5% dextrose solution, and blood glucose should
be monitored. Generally, 5% dextrose alone (D5W)
arrhythmias, hypoglycemia, and acidosis. Aggressive should not be given, as it becomes hypotonic and enters
intravenous fluid resuscitation is the top priority. In the interstitial space once the dextrose is metabolized.
addition to correcting hypovolemia, it also helps treat Hypoglycemia is uncommon, but should be treated
hyperkalemia, hyponatremia, hypochloremia, and aci- with an IV dose of 1 mL/kg of 25–50% dextrose in a 1:1
dosis. One‐third of a shock bolus of crystalloids is solution of dextrose and 0.9% saline. Maintenance fluids
given initially, and response is assessed based on heart should then be supplemented with dextrose to make a
rate, pulse quality/blood pressure, capillary refill time, 1.25–5% dextrose solution.
and mental status. Additional fluids are then given as Glucocorticoid deficiency is responsible for the hypo-
necessary. glycemia, gastrointestinal signs, and general debility of
Historically, 0.9% NaCl has been recommended as the
fluid of choice, since it contains sodium and chloride patients in crisis, and may also contribute to hypoten-
sion. Supplementation should be instituted after the
but no potassium. However, Normosol‐R®, Plasma‐Lyte life‐threatening issues (hypovolemia, hyperkalemia,
A®, and/or lactated Ringer’s solution (LRS) are preferred and hypoglycemia) have been initially addressed.
by some clinicians, since they are more alkalinizing Dexamethasone sodium phosphate (0.25 mg/kg IV) is
than saline, thus correcting acidosis more efficiently. recommended, since it does not cross‐react with the
Although they contain a small amount of potassium, cortisol assay. Since it has approximately eight times
these crystalloids still allow for correction of hyper- the glucocorticoid activity of prednisone, this is equiva-
kalemia via dilution and increased renal perfusion. lent to 2 mg/kg of prednisone, or 10 times the physio-
Hydroxyethyl starch can also be used in conjunction logic dose. Higher doses previously recommended
with crystalloids for more rapid fluid resuscitation, at a (such as 2 mg/kg) are excessive and unnecessary.
dosage of 5–10 mL/kg. Hydrocortisone sodium succinate (0.5 mg/kg/h), corti-
Sodium concentration should not be increased by more
than 0.5 mEq/kg/h, as myelinolysis may occur with more sol acetate (1 mg/kg), and prednisolone sodium succi-
nate (2 mg/kg) can also be used. However, since they
rapid correction. Thus, hypertonic saline should not be cross‐react with the cortisol assay, they should not be
used to treat an Addisonian crisis. Normosol‐R, Plasma‐ given until after the ACTH stimulation test.
Lyte A, and LRS all have lower sodium concentrations Additional supportive therapy is provided as necessary.
than 0.9% saline (140 mEq/L, 140 mEq/L, 130 mEq/L, and Dogs with gastrointestinal signs are given gastroprotect-
154 mEq/L, respectively). Their use is sometimes pre- ants, including proton pump inhibitors (omeprazole or
ferred in patients with severe hyponatremia, as they are pantoprazole, which can be given IV) and sucralfate. Due
less likely to increase the serum sodium concentration as to potential bacterial translocation from the GI tract,
rapidly as 0.9% saline. dogs with significant GI signs may be given prophylactic
Hyperkalemia is often the most life‐threatening conse-
quence of HOAC, and must be addressed immediately. antibiotics (such as ampicillin), but this is controversial.
Packed red cell or whole blood transfusion is occasionally
Mild to moderate hyperkalemia usually responds to fluid necessary in dogs with severe GI blood loss.
therapy alone. However, severe hyperkalemia (>9 mEq/L) Frequent reassessment of patients is necessary follow-
and/or hyperkalemia accompanied by life‐threatening ing initial stabilization. Fluid rates should be adjusted to
arrhythmias (severe bradycardia, absent P‐waves, idio- correct dehydration and azotemia. The ECG should be
ventricular rhythm) require specific therapy. reassessed until arrhythmias resolve. Electrolyte concen-
Calcium gluconate is given for its cardioprotective
effects, allowing time for fluids and other therapies to trations should be rechecked following initial stabiliza-
tion, and then every 6–12 hours until potassium and
take effect. However, it does not directly decrease the sodium concentrations normalize.
potassium concentration. A dosage of 0.5–1.5 mL/kg of Intravenous fluids are continued until the dog is
10% calcium gluconate is given slowly over 15 minutes,
able to eat and maintain hydration on its own, and