Miocardiopatía aguda en un perro con crisis addisoniana: a propósito de un caso clínico

espanolUn Bearded Collie, hembra de 10 anos de edad es atendida de urgencia por cuadro clinico evolutivo de vomito, letargia y debilidad progresiva. Al examen fisico, la paciente presenta depresion, bradicardia severa e hipotension. El resultado de las pruebas diagnosticas confirma la presencia de azotemia, hiperpotasemia, hiponatremia asi como de hipocortisolemia pre y post estimulacion con ACTH. El diagnostico es de crisis addisoniana por lo que se instaura tratamiento con fluidos cristaloides isotonicos y bolos de gluconato de calcio 10%, dextrosa 40% e insulina regular con el objetivo de corregir los signos de cardiotoxicidad asociada a la hiperpotasemia. La condicion de la paciente mejora parcialmente, y la terapia con corticoides se inicia de inmediato con la aplicacion de dexametasona intravenosa y fludrocortisona por via oral, transcurridas doce horas tras la admision. El dia 2, la actitud de la paciente mejora, pero persiste la bradicardia sinusal y presenta disnea de aparicion aguda. El analisis de gases confirma la presencia de hipoxemia severa e hiperlactatemia. Las concentraciones en sangre de troponina cardiaca, concentraciones seriadas de lactato y relaciones de lactato/piruvato en conjuncion con los hallazgos radiologicos, asi como las medidas cardiacas realizadas en la ecocardiografia de urgencia, confirman la presencia de insuficiencia cardiaca congestiva secundaria a dano miocardico agudo. La paciente responde favorablemente a la administracion de tratamiento de soporte y oxigenoterapia por lo que, a pesar de la hiperlactatemia persistente, es dada de alta transcurridos seis dias de su admision. En la actualidad la paciente no presenta signo alguno de enfermedad cardiaca y el hipoadrenocorticismo se encuentra bajo control con tratamiento corticoide de substitucion. EnglishA 10-year-old spayed female Bearded Collie was presented to the emergency service for evaluation of several days’ history of vomiting, lethargy, and progressive weakness. On presentation, the dog was obtunded, bradycardic, and hypotensive. Results of diagnostic work-up such as complete blood cell count, biochemistry panel (pre-renal azotemia, severe hyperkalemia, and hyponatremia), urinalysis, basal cortisol, and ACTH stimulation test were all consistent with an acute adrenal (Addisonian) crisis. The dog was initially treated with isotonic crystalloids and several bolus of calcium gluconate 10%, dextrose 40%, and regular insulin to correct the cardiotoxicity signs associated to the hyperkalemia. The patient’s condition improved partially and corticoid therapy was started immediately: dexamethasone IV initially and fludrocortisone PO 12h post-admission. On Day 2, the patient’s attitude was better and the electrolyte imbalance was completely corrected, but sinus bradycardia persisted and severe respiratory distress appeared, with arterial blood gas analysis revealing severe hypoxemia and hyperlactatemia. Blood concentrations of cardiac troponin, serial concentrations of lactate and lactate/pyruvate ratios in conjunction with findings on thoracic X-rays and several cardiac measures performed on emergency echocardiography confirmed the presence of congestive heart failure secondary to acute myocardial damage. Despite persistent hyperlactatemia, the patient’s condition improved clinically and was finally discharged 6 days after admission. Currently the patient has no signs of cardiac disease and Addison’s disease is under control with corticosteroid treatment.