Ten days later (about one month after initial examination), the dog was presented for evaluation of acute respiratory distress.
The patient had not been reevaluated since initial hospitalization. On physical examination, the patient was dyspneic and
tachypneic and had pale mucous membranes. Neurologic examination showed that the dog was mentally dull and was ambulatory.
The dog still displayed generalized weakness, but its muscle tone and reflexes seemed slightly improved from one month prior.
Postural reactions were normal, and cranial nerve function was normal.
A CBC and serum chemistry panel were performed (Table 3). A normocytic, normochromic anemia and thrombocytopenia were still present. In addition, elevated AST, alanine transaminase
(ALT), ALP, and gamma-glutamyl transpeptidase (GGT) activities and an elevated total bilirubin concentration were detected.
The serum cholesterol concentration had normalized.
Table 3: Case 1 CBC and serum chemistry profile abnormalities on second examination
Differential diagnoses for the dog's acute respiratory distress included aspiration pneumonia and pulmonary thromboembolism.
In addition, the markedly elevated hepatocellular and cholestatic enzyme activities suggested a degree of acute liver dysfunction,
most likely hypoxic damage. The owner declined diagnostic testing and treatment and elected euthanasia.
A gross necropsy and subsequent histologic evaluation of tissues were performed. The thyroid gland showed evidence of marked
lymphoplasmacytic thyroiditis. Fibrinous thrombi were found in the hepatic sinusoids. The spleen, kidneys, and lungs contained
atherosclerotic vasculature. Additionally, multiple infarcts were found in the vasculature of the lung. Appendicular skeletal
musculature displayed evidence of myofiber necrosis that was consistent with ischemic damage.
The diagnosis was lymphoplasmacytic thyroiditis consistent with hypothyroidism with pulmonary infarcts; atherosclerosis of
the vasculature of the spleen, lungs, and kidneys; and skeletal muscle myofiber necrosis. Although a primary myopathy cannot
be completely excluded, given the atherosclerosis and infarctions found elsewhere, an ischemic myopathy secondary to hypothyroidism
was most likely. In our experience, the marked inflammation of the thyroid gland is a common pathologic finding in dogs with
The brain and spinal cord were unfortunately not examined. However, while speculative, it is probable that the observed neurologic
deficits represented ischemic infarction involving the brain secondary to atherosclerosis given the rest of the necropsy findings.
Ischemic infarction involving the prosencephalon and brainstem may have explained the menace deficit and head tilt, respectively.
Dogs with hypothyroidism have been reported to be hypercoagulable and at risk for thromboembolic events due to atherosclerosis
of the vasculature of the brain.3-7 Similarly, the elevated creatinine kinase activity and thrombocytopenia suggested a possible embolic event manifesting as
ischemic myopathy and consumptive coagulopathy. Recovery was unlikely given the dog's severe respiratory compromise and the
recurrent nature of its disease.