R. Friesen1; A.P. Sarraff-Lopes1; A.L.P.D. Fam1; L.G.A. Capriglione1; J. Werner2
Congenital laryngeal paralysis is characterized by total or partial lost of laryngeal muscle fibers innervation that promote abduction and adduction of arytenoid cartilage and focal folds. The congenital form is quite uncommon when compared to the acquired form and have been described in a great number of dog breeds, including Labradors with age varying between two to twelve-month-old. Gender predilection was not demonstrated. Clinical signs vary based on the severity of the paralysis and include inspiratory dyspnea, audible stridor, exercise intolerance, change in bark and central or peripheral neuropathy. Diagnosis is based upon the clinical signs, laryngoscopy and histopathological findings, which is characterized by laryngeal recurrent nerve degeneration and atrophy of dorsal cricoarytenoid muscles. The aim of this work is report a case of a 2-month old Labrador bitch with sings of subacute inspiratory dyspnea, audible stridor, orthopneic position and bark changing. Thoracic radiography revealed mild alveolar infiltrate, blood and blood gas analysis no significant alteration were seen. Laryngoscopy with superficial sedation revealed bilateral paralysis of arytenoid cartilages, confirming the diagnosis of laryngeal paralysis. Surgical repositioning of arytenoid cartilage was recommended but the owner decided for euthanasia. Histopathological findings revealed important atrophy of laryngeal muscle fibers with severe edema and mononuclear cells infiltration between the fibers. No pathological alteration was seen in peripheral laryngeal nerves but there was pulmonary edema. The congenital form of the disease is uncommonly described, except in Dalmatians and Rottweilers. The extensive atrophy of dorsal muscle fibers of cricoarytenoid observed in this case leads to bilateral paralysis of arytenoid cartilages and suggest possible involvement of laryngeal recurrent nerve. The denervation of this muscle fibers results in failure of inspiratory adduction of arytenoid cartilages and vocal folds leading to the clinical signs. The exact inciting mechanism of pulmonary edema in the dogs with congenital laryngeal paralysis is not completely understood, but is proposed that hypoxia leads to increase pulmonary permeability resulting in edema. The treatment of choice is surgical repositioning of arytenoid cartilages. The prognosis to dogs with polyneuropathies and pulmonary involvement is bad. In the reported case, factors related to bilateral paralysis of arytenoid cartilage and pulmonary edema lead to unfavorable prognosis.