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T O day' S Ve T erinary Prac T ice | September/October 2016 | tvpjournal.com cO n S ider Thi S c a S e Peer r eviewed 94 bradycardia; tall, tented T waves; prolonged Q r S intervals; prolonged P r intervals; absent P waves; and deviation of the ST segment. INITIAL DIAGNOSIS Electrolyte Abnormalities Lucky's sodium:potassium ratio was 16:1, which is most often seen in veterinary patients as a result of hypoadrenocorticism and mineralocorticoid deficiency. The hyperkalemia can potentially be life-threatening, resulting in severe arrhythmias. The hypoglycemia can result in clinical signs of weakness, tremors, vomiting, seizures, collapse, and death. Prompt treatment of the electrolyte abnormalities and hypoglycemia in this patient was imperative. Dehydration & Hypovolemic Shock This patient had both dehydration and hypovolemic shock. While the patient was only mildly bradycardiac, this was likely an inappropriate response to hypovolemia secondary to a life- threatening hyperkalemia. The presence of both dehydration and hypovolemia are likely due to both glucocorticoid and mineralocorticoid deficiencies. Differential Diagnosis d ifferential diagnosis—in addition to glucocorticoid/ mineralocorticoid deficiencies—includes underlying metabolic conditions (eg, ascites, pericardial effusion, severe metabolic acidosis), gastrointestinal disease (eg, whipworm infection), acute kidney injury ( a K i ), neoplasia, trauma (eg, uroabdomen, rhabdomyolysis), and sepsis. 1-6 INITIAL THERAPY Therapy for Electrolyte Abnormalities h yperkalemia decreases resting potential, which makes it less negative and initially results in more hyperexcitable cells. 7 To increase the normal threshold membrane potential, thereby normalizing the difference between the 2 potentials, a bolus of 50 mg/kg 10% calcium gluconate, delivered slowly over 15 minutes, was administered to Lucky. 7 a lternatively, use of sodium bicarbonate or insulin:dextrose can be considered. a lthough calcium gluconate has the most rapid stabilizing effect in hyperkalemic patients, it does not address the hyperkalemia itself. Both sodium bicarbonate and insulin therapy result in a transient lowering of serum potassium, promoting its translocation from the extracellular to the intracellular fluid compartment (Figure 2). Lucky received continuous ec G monitoring during calcium gluconate administration and until she was more cardiovascularly stable. i t is important to remember that calcium gluconate does not directly affect potassium levels. Therapy for Dehydration & Hypovolemic Shock Lucky received an initial i V bolus of 0.5 g/kg dextrose (10 mL of 50% dextrose diluted in 20 mL of 0.9% saline) over 2 to 3 minutes to address the hypoglycemia. a n additional bolus of 400 mL (20 mL/kg) of warmed lactated r inger's solution was administered over 15 minutes. Ongoing Fluid Therapy 1. Replacement fluids: Lucky's estimated dehydration was 5%. To correct this deficit over the next 8 hours, Lucky needed to receive Figure 1. e lectrocardiogram showing sinoventricular rhythm, with absent P waves and widened Q r S complexes. Courtesy Gordon Peddle, VMD, Diplomate ACVIM (Cardiology) Table 2. l aboratory r esults val UE r E s U lt r EFE r E nc E rang E Packed cell volume (%) 35 33.6–58.7 t otal solids (g/dL) 6.1 5–8.3 Blood glucose (mg/dL) 42 74–145 Blood urea nitrogen (mg/dL) 50–80 8–30 s odium (mEq/L) 136 141–159 Potassium (mEq/L) 8.2 3.4–5.6 c hlorine (mEq/L) 104 100–121 i onized calcium (mmol/L) 1.49 1.3–1.46 l actate (mmol/L) 3.5 0.99–4.77