Case summary
A 15-year-old female spayed Siamese cat presented for amlodipine toxicosis. Two months prior, the cat was treated by her primary veterinarian for a urinary tract infection and diagnosed with hypertension. She was started on telmisartan 6.5mg PO q24h (Semintra, Boehringer Ingelheim Vetmedica, Inc., St. Joseph, MO) and transitioned onto amlodipine 2 weeks prior to hospitalization. For the 5 days leading up to presentation the cat received 2.5mg instead of 0.625mg per os every 24 hours. The cat had known pre-existing renal disease which was managed with a prescription diet and stool softener (Miralax, Bayer Healthcare LLC, Whippany, NJ; 1/8tsp per os ever 12 hours).
The cat presented to the authors’ hospital for decreased appetite and water intake for 24 hours and lethargy for several days. The owner reported a single episode of vomiting the night before. Amlodipine was last given that morning. Upon presentation (day one), the cat was dehydrated with a prolonged skin tent and weak femoral pulses. She had a decreased axillary temperature (35.5°C; 38.1-39.2°C)8and borderline bradycardia (160 beats per minute). She was weakly ambulatory and quiet. Systolic blood pressure (SBP) as measured by Doppler ultrasonography (Doppler flow detector model 811-B, Parks Medical Electronics) was low at 70mmHg (110-132mHg)9. An intravenous (IV) catheter was placed, and a minimum database was performed, which identified mild anemia and hyperproteinemia (see Table 1). Spot blood glucose (sBG), (AlphaTRAK 2, Abbott Animal Health, Abbott Park, IL) was high at 14.37mmol;/L (259mg/dl; RI [3.72-9.32mmol/L])10. A venous blood gas (vBG; RAPIDPoint 500 System, Siemens Healthineers, Malvern, PA) revealed a metabolic acidosis with hyperlactatemia (see Table 1). A chemistry panel (Catalyst One, IDEXX Laboratories Inc, Westbrook, ME) revealed azotemia and hyperamylasemia (see Table 2). A 10ml/kg IV crystalloid bolus of LRS (Lactated Ringer’s Solution; Dechra Veterinary Products, Overland Park, KS) was administered. Systolic BP improved to 92mmHg. A 90mg/kg calcium gluconate (Calcium Gluconate Injection USP 100mg per mL, HF Acquisition Co LLC, DBA HealthFirst) bolus diluted 1:1 with NaCl 0.9% (0.9% Sodium Chloride Injection USP, B.Braun Medical, Irvine, CA) was given intravenously over 20 minutes. The cat was started on intravenous fluid therapy with NaCl 0.9% and was administered maropitant citrate (Cerenia 10mg/ml, Zoetis Inc, Kalamazoo, MI; 1 mg/kg IV q24h).
The following morning (day 2), the cat was transferred to the Critical Care service. Systolic blood pressure was 80mmHg and rectal temperature was 32.9°C (38.1-39.2°C)8. Repeat bloodwork revealed persistent hyperglycemia with a sBG of 23.87mmol/L (430mg/dl; RI [3.72-9.32])10. Serum ketones were negative (Precision Xtra, Abbott Animal Health, Abbott Park, IL). A vBG showed a worsening metabolic acidosis with improving hyperlactatemia (see Table 1). A CBC (Procyte Dx Hematology Analyzer, IDEXX Laboratories Inc, Westbrook, ME) showed a non-regenerative anemia and neutrophilia (see Table 2). One unit (1U) regular insulin (HumulinR, Lilly USA LLC, Indianapolis, IN) was administered IV. Two further doses (90mg/kg and 150mg/kg respectively) of calcium gluconate diluted 1:1 with NaCl 0.9% were given IV. Bradycardia worsened to 90 beats per minute and a single dose of atropine sulfate (Atropine Sulfate Injection 1/120 Grain, Med-Pharmex, Pomona, CA) 0.04mg/kg IV was given with no effect. A calcium gluconate continuous rate infusion (CRI) was started at 0.05mcg/kg/h. Bradycardia persisted and an electrocardiogram (cECG; MD9000vet, Meditech Equipment Co., Ltd) identified intermittent absence of P-waves. A point-of-care thoracic ultrasound showed scant pleural effusion and markedly decreased cardiac contractility. Intravenous fluid therapy was discontinued and a dobutamine CRI (2.5-3.75mcg/kg/min; DOBUTamine Injection USP, Hospira Inc., Lake Forrest IL) was started; calcium gluconate was discontinued. Intralipid emulsion therapy (ILE; Intralipid 20% Baxter Healthcare Corporation, Deerfield, IL) was administered: 0.5mls/kg IV bolus followed by 0.25mls/kg/min for 1 hour. Hypothermia worsened to 33.2°C (38.1-39.2°C)8 despite heat support and the cat’s mentation deteriorated to dull. Serial vBGs showed a worsening metabolic acidosis and hypokalemia (see Table 1). Crystalloid fluid therapy was restarted at a rate of 5 ml/hr with potassium supplementation (Potassium Chloride injection 2mEq/ml, Hospira Inc Lake Forest, IL) at 80 meq/L. High-dose insulin/euglycemia therapy (HIET) was initiated with a bolus of 1U/kg IV regular insulin and a bolus of 1g/kg dextrose (50% dextrose injection, USP 25g/50ml Hospira Inc., Lake Forest IL) IV followed by a regular insulin CRI at 1U/kg/h for the first hour with a rate decrease to 0.5 U/kg/h as of the second hour. A 5% dextrose CRI was administered concurrently. Within 5-10 minutes of starting HIET, there was a notable improvement in the patient’s blood pressure, heart rate and temperature. After 2 hours of therapy, blood pressure was 112 mmHg, heart rate was 140 beats per minute with normal sinus rhythm, and temperature was 36.7°C. Serum potassium increased (see Table 1) and potassium supplementation was decreased from 80 to 60mEq/L. Hypoglycemia (BG <3.72mmol/L) was identified five times during HIET; and was treated with intermittent dextrose boluses (0.5 g/kg IV) and an increase in dextrose supplementation to 7.5%. Insulin therapy was discontinued after approximately 3 hours due to persistent hypoglycemia. At that time the cat was ambulatory and interactive. Point-of-care ultrasound showed a marked improvement in cardiac contractility. Overnight dextrose supplementation was decreased then discontinued as euglycemia was maintained. Crystalloid fluids were continued at 5 mls/hr with 60 mEq KCl/L supplementation. Temperature normalized and heat support was discontinued. Heart rate remained > 150 beats per minute and blood pressure remained between 90 mmHg and 132 mmHg on a dobutamine CRI at 3.75mcg/kg/min.
Early the next day (Day 3), the cat became hypotensive with a decrease in SBP to 80 mmHg. A CRI of norepinephrine (Levophed TM, Norepinephrine Bitartrate Injection USP, Hospira Inc., Lake Forest, IL) was started at 0.1mcg/kg/min and titrated up to 0.2mcg/kg/min. Mild respiratory effort was noted and oxygen therapy at FiO2 0.4 (Snyder MFG.CO Intensive Care Unit) was provided. Point-of-care ultrasound revealed an increase in the volume of pleural effusion. Based on progression of clinical signs and financial constraints, the owners elected humane euthanasia.