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.