Fluid therapy was initiated with a 20 ml/kg bolus of lactated Ringer’s
solution (Baxter Healthcare Corporation), given over 15 minutes,
improving Doppler blood pressure to 110 mm Hg. Maropitant (Cerenia;
Zoetis Inc) was also administered for the reported vomiting (1 mg/kg, IV
q24). The dog was then admitted to the ICU for overnight care on a
continuous infusion of lactated Ringer’s solution (Baxter Healthcare
Corporation) at 120 ml/kg/d to encourage diuresis, monitoring of
temperature, pulse, and respiration, and every 2-hour monitoring of
blood pressure. The first systolic blood pressure obtained in the ICU
was 70 mm Hg. An additional 10 ml/kg lactated Ringer’s solution fluid
bolus was administered, with minimal effect as a recheck blood pressure
was 80 mm Hg.
The consulting veterinarian at the poison control center (Pet Poison
Helpline, SafetyCall International, LLC) was not confident that the
reported amlodipine ingestion was likely to have caused all of the
clinical signs given the timeline, but recommended monitoring
electrolytes and blood pressure, fluid therapy at 120 ml/kg/day, and
administering IV calcium as either bolus or CRI in case of persistent
hypotension or bradycardia, with atropine also recommended for
bradycardia.
Due to the persistent hypotension, continuous telemetry (Fukuda Denshi
USA, Inc.) was initiated, and a 9.3 mg/kg bolus of 10% calcium
gluconate (Fresenius Kabi) was administered over 10 minutes, followed by
a continuous rate infusion (CRI) at 2.3 mg/kg/hr. Contemporaneously, a
venous blood gas was obtained, revealing worsening hyponatremia,
hyperkalemia, and azotemia (Table 1, hour 4). To address the
hyperkalemia, the dog received 0.2 U/kg regular insulin (Humulin-R, Eli
Lilly and Co.) IM, and the replacement fluid was changed to 0.9% sodium
chloride (Vetivex; Dechra Pharmaceuticals) for the hyponatremia. Therapy
with a 20% intralipid emulsion (ILE) (Clinoclipid; Baxter Healthcare
Corporation) was initiated with a 1.5 ml/kg bolus followed by a 15 ml/kg
infusion over 1 hour. Worsening respiratory rate and effort were noted,
and the dog was placed in a climate-controlled oxygen cage (ICU 2100;
Snyder Mfg. Co.) with an FiO2 of 40%. After initiation of intravenous
calcium therapy, repeated blood pressure monitoring overnight ranged
from 90-105 mm Hg, and the dog’s demeanor was improved, eating small
amounts of food and tolerating short walks. Similarly, a blood gas 4
hours after insulin showed improved hyperkalemia and hypocalcemia (Table
1, hour 10).
On the morning of the second day of hospitalization, the dog was
subjectively overhydrated with serous nasal discharge and subcutaneous
edema, tachypnea at 100 breaths/min with increased respiratory effort. A
point-of-care ultrasound revealed moderate bilateral pleural effusion,
severe bilateral B-lines (3+ in all fields), subjectively decreased
cardiac contractility, and scant ascites. Weight had increased to 16.2
kg. In response to the hypervolemia, fluid therapy was discontinued. The
dog was sedated with 0.1 mg/kg butorphanol (Torbugesic; Zoetis Inc) IV,
a right-sided thoracocentesis was performed removing approximately 200
mL or 13 mL/kg of a straw-colored effusion, and furosemide (Salix; Merck
Animal Health) was administered at 2 mg/kg IV. A chemistry panel about
that time revealed azotemia, hyponatremia, hyperkalemia, hypochloremia,
decreased bicarbonate, hyperphosphatemia, and an elevated anion gap
(Table 2). A baseline cortisol was elevated at 16.1 ug/dL. In response
to the hyperkalemia, terbutaline (Fresenius Kabi) was administered at
0.01 mg/kg IV. In response to the fluid intolerance, azotemia, and
concern for poor cardiac output, the decision was made to initiate
hyperinsulinemia-euglycemia therapy (HIET) approximately 16 hours after
presentation, as detailed in Table 3. A central venous catheter (MILA
International, Inc.) was placed using the modified Seldinger technique
as well as a continuous interstitial glucose monitor (FreeStyle Libre 2,
Abbott) to allow for monitoring of interstitial glucose. Insulin
(Humulin-R, Eli Lilly and Co.) was initially initiated at 0.1 U/kg/hr
during placement of the central venous catheter and incrementally
increased to 0.5 U/kg/hr over 12 hours. Supplemental dextrose was
provided with a 5% solution of dextrose (50% dextrose, VetOne) in
0.9% saline (Vetivex; Dechra Pharmaceuticals) at 16 ml/kg/d, which was
incrementally increased to a 15% solution over the next 12 hours. A 0.5
ml/kg bolus of 50% dextrose (VetOne) diluted 1:1 with 0.9% saline
(Vetivex; Dechra Pharmaceuticals) was administered 6 hours after
initiation of HIET in response to a blood sugar of 54 mg/dL. Repeated
blood gas analysis after initiation of HIET showed improvement in
azotemia and hyperkalemia (Table 1, hour 18). 10 hours after initiation
of HIET, the dog developed recurrent hypotension at 60 mm Hg, and a
norepinephrine (Levophed; Hospira, Inc.) CRI was started at a range of
0.1-0.5 µg/kg/min to maintain a systolic blood pressure of at least 90
mm Hg while increasing insulin and dextrose concentrations. Supplemental
oxygen was increased to an FiO2 of 60% and 3 additional furosemide
(Salix; Merck Animal Health) doses of 1, 1, and 2 mg/kg were
administered overnight in response to worsening tachypnea. Serial
point-of-care ultrasound every 4 hours after starting HIET revealed
subjectively improved cardiac contractility with no evidence of
worsening of pleural or abdominal effusion, but the B-lines were
persistent.
TABLE 2. Serial biochemical analysis.