Slide # 23 peripheral blood smear from a dog Cinzia Mastrorilli 1, Elizabeth Welles 1, Lauren Reid 2 1 Department of Pathobiology, 2 Department of Clinical Science College of Veterinary Medicine, Auburn University
Signalment and history 1 year old, castrated male, Shih Tzu rdvm 2 day history of lethargy, vomiting and diarrhea orange colored urine since the night before Resuscitated after cardiopulmonary arrest AUSATH
Physical examination depressed tachycardic tachypneic hypothermic dark red urine collected by cystocentesis
CBC Analyte Patient s values Reference limits Hct (%) 19.9 37-55 MCV (fl) 80.5 60-77 MCHC (g/dl) 30.5 32-36 Reticulocytes (/μl) 263,800 0-60,000 nrbc (/100WBC) 41 / WBC (/μl) 37,290 6,000-17,000 Neutrophils (/μl) 23,490 3,000-11,400 Bands (/μl) 4,475 0-300 Lymphocytes (/μl) 8,580 1,000-4,000 Platelets (/μl) 400,000 164,000-510,000
Blood smear 41 nrbcs/100wbc
Blood smear
Interpretation Anemia, markedly regenerative oxidative damage intravascular hemolysis (ghost RBCs) extravascular hemolysis (removal of eccentrocytes and Heinz body containing RBCs by the spleen) Degree of regeneration hemolysis > 2 days (Reticulocytes 263,800/μL) Inflammatory leukogram hemolytic process tissue necrosis secondary to hypoxia
Abdominal radiographs
Endoscopy Heinz body hemolytic anemia presumptively due to zinc toxicosis
Zinc toxicosis: sources of zinc Acute zinc toxicity reported since mid 1980 due to ingestion of: pennies zinc containing toys skin ointment (zinc oxide and zinc gluconate) galvanized hardware (bolt, nuts, staples, nails) Pennies minted since the mid 1982 contain a zinc wafer core (98%) coated in copper (2%). Zinc content 2.44 mg/penny
Zinc toxicosis: adsorbtion Stomach: Zn + 2HCl ZnCl 2 + H 2 Ionic Zn2+ is more adsorbable than metallic zinc small breed dogs more affected delayed passage through smaller pylorus more time for erosion and adsorption
Zinc toxicosis: clinical signs Local effects: gastrointestinal bleeding (corrosive effect of zinc) Systemic effects: hemolytic anemia acute renal failure pancreatitis
Zinc induced hemolytic anemia direct erythrocyte membrane/organelles damage immune mediated destruction from hapten formation inhibition erythrocyte anti oxidant enzymes: Zn glutathione reductase enzymes of the hexose monophosphate shunt pathway RBCs more susceptible to endogenous/exogenous oxidants Oxidation of Hgb and membrane proteins Heinz bodies
Zinc toxicosis: renal failure Acute renal failure RBC membrane fragments hemoglobinuria Tubular necrosis urine ph < 5.6 Hgb dissociates in ferrihemate toxic heme catabolites cytotoxic to tubular cells NO production vasoconstriction
Zinc toxicosis: renal failure and DIC Renal ischemia/hypoxia DIC Tubular necrosis Coag panel: analyte Patient s values Reference limits PT (sec) 8.3 6.1-10.1 aptt (sec) 55.8 8-14.4 Fibrinogen (mg/dl) 500 100-300 Antithrombin (%) 104 110-150 D-Dimers (ng/ml) >2,000 0-250 Platelets (/μl) 400,000 164,000-510,000
Zinc toxicosis: tubular necrosis Chemistry: analyte Patient s values Reference limits Creatinine 1.3 0.6 1.4 Urea 48 12 26 Serum glucose (mg/dl) 56 76 112 Urinalysis: analyte Patient s values Normal findings Color red yellow Protein (mg/dl) 1920 / Glucose + neg Blood large neg Bilirubin large neg
Zinc toxicosis: diagnosis increased zinc concentration in serum/urine/tissues Reference intervals in serum: 0.7 2 ppm often >10 20 ppm in dogs with zinc toxicosis Trace elements tube (blue royal stopper) www.thomassci.com
Zinc toxicosis: prognosis and therapy Prognosis is good if source of zinc is rapidly removed. The use of chelators such as calcium EDTA can be controversial because of their nephrotoxic potential. Rateofzincdissolutioninthestomachisdependenton thedegreeofacidity antacids are recommended until removal of zinc foreign body can be achieved.
Acknowledgments Dr Welles for the case and supervision Dr Christoferson and Dr Spangler for supervision The Clin Path Ladies for all the slides Beth Landreth for the labels Beth for the endoscopy picture Questions?