Iron EDTA ingestion and toxicosis in 61 dogs: a multi-center retrospective study of Australian hospital records

Elvany Luswanto¹Claire Rebecca Sharp^1,2*Erin Mooney^3,4Sarah Purcell⁵

• ¹School of Veterinary Medicine, Murdoch University, Murdoch, Australia
• ²Centre for Terrestrial Ecosystem Science and Sustainability, Harry Butler Institute, Murdoch University, Murdoch, Australia
• ³Sydney School of Veterinary Science, Faculty of Science, The University of Sydney, Camperdown, Australia
• ⁴Small Animal Specialist Hospital, North Ryde, Australia
• ⁵Faculty of Science, School of Veterinary Science, The University of Queensland, Gatton, Australia

Introduction: The objective of this retrospective case series was to describe the clinical course and treatment of dogs presenting after iron EDTA ingestion. Methods: Cases were retrieved through an electronic medical records search at three veterinary teaching hospitals and three private referral hospitals in Australia. Non-parametric statistics are reported. Results: 61 dogs met the inclusion criteria. 20 out of 61 dogs (32.8%) had no clinical signs prior to presentation. Vomiting without blood was the most common clinical sign (21), followed by lethargy (16), diarrhea without blood (15), and ataxia/weakness (12). Abdominal pain was the most common physical examination finding (21), followed by dehydration (10). 40 dogs underwent gastrointestinal decontamination. The median pre- and post-chelation serum iron concentrations were 61.3 mol/L (Min-Max 9–356, n = 40), and 14.7 mol/L (5.72-44, n = 22) respectively. 51 dogs were treated as in-patients, where treatments included desferoxamine (43), gastroprotectants (41), antiemetics and/or prokinetics (36), analgesia (24), and hepatoprotectants (4). The most common protocol for desferoxamine was a continuous intravenous infusion at 15 mg/kg/h (n = 27). Two dogs had an anaphylactic reaction to an inadvertent bolus of desferoxamine, while two had allergic reactions possibly related to desferoxamine. Two dogs developed neutropenia, and one developed acute respiratory distress syndrome possibly as a result of desferoxamine treatment. Overall, 91.8 % of dogs survived to discharge. One dog died during hospitalization, experiencing cardiac arrhythmias, shock, and cardiac arrest despite treatment. When considering the stage of iron toxicoses, 16/61 (26.2%) dogs never developed clinical toxicosis, 44 dogs (72.1 %) had evidence of stage 1 clinical signs, 4 dogs (6.6 %) also had evidence of stage 2 clinical signs, and 19 dogs (31.1 %) progressed to stage 3 clinical signs. No dogs had stage 4 clinical signs (delayed gastrointestinal stricture). A single case was euthanized for acute hepatic failure upon re-presentation after initial survival to discharge. Conclusions: Iron EDTA toxicosis has a good prognosis in dogs following prompt treatment, but severe organ damage including hepatic and cardiovascular dysfunction can occur. Additionally, desferoxamine was well tolerated when administered according to published protocols but potentially fatal adverse effects can occur.