History
A 12-year-old 22-kg castrated male Staffordshire Bull Terrier was referred to the neurology department for evaluation of sudden-onset vestibular signs. Findings on general physical examination were unremarkable. On neurologic examination, the dog had a right-sided head tilt and positional ventrolateral strabismus of the right eye. The rest of the findings on neurologic examination were clinically normal, and the lesion was localized to the right vestibular system.
Hematology, biochemical analyses, and urinalysis were performed and identified high creatine kinase activity (3,869 U/L; reference range, 67 to 446 U/L) and marginally high cholesterol concentration (6.84 mmol/L; reference range, 3.2 to 6.2 mmol/L). There was also mild lymphopenia (0.95 X 109 cells/L; reference range, 1 to 4.8 X 109 cells/L). The rest of the findings were unremarkable. Noninvasive blood pressure measurements were within reference limits.
Brain MRI findings (images not provided) were consistent with a 6-mm-diameter intra-axial hemorrhagic lesion in the right temporal lobe as well as smaller right-sided ischemic infarcts in the thalamus and the cerebellum. Thoracic and abdominal CT before and after IV administration of iodinated contrast medium was performed immediately following the MRI as a survey test for underlying causes (Figure 1).
Transverse (A) and sagittal reconstruction (B) postcontrast thoracic CT images of a 12-year-old 22-kg castrated male Staffordshire Bull Terrier with sudden-onset vestibular signs and MRI evidence of hemorrhagic and ischemic infarcts in the brain. The images are displayed in a soft tissue window (window width, 400 HU; window level, 40 HU) and a 2.0-mm slice thickness.
Citation: Journal of the American Veterinary Medical Association 259, S1; 10.2460/javma.21.02.0091
Transverse (A) and sagittal reconstruction (B) postcontrast thoracic CT images of a 12-year-old 22-kg castrated male Staffordshire Bull Terrier with sudden-onset vestibular signs and MRI evidence of hemorrhagic and ischemic infarcts in the brain. The images are displayed in a soft tissue window (window width, 400 HU; window level, 40 HU) and a 2.0-mm slice thickness.
Citation: Journal of the American Veterinary Medical Association 259, S1; 10.2460/javma.21.02.0091
Transverse (A) and sagittal reconstruction (B) postcontrast thoracic CT images of a 12-year-old 22-kg castrated male Staffordshire Bull Terrier with sudden-onset vestibular signs and MRI evidence of hemorrhagic and ischemic infarcts in the brain. The images are displayed in a soft tissue window (window width, 400 HU; window level, 40 HU) and a 2.0-mm slice thickness.
Citation: Journal of the American Veterinary Medical Association 259, S1; 10.2460/javma.21.02.0091
Transverse (A) and sagittal reconstruction (B) postcontrast thoracic CT images of a 12-year-old 22-kg castrated male Staffordshire Bull Terrier with sudden-onset vestibular signs and MRI evidence of hemorrhagic and ischemic infarcts in the brain. The images are displayed in a soft tissue window (window width, 400 HU; window level, 40 HU) and a 2.0-mm slice thickness.
Citation: Journal of the American Veterinary Medical Association 259, S1; 10.2460/javma.21.02.0091
Transverse (A) and sagittal reconstruction (B) postcontrast thoracic CT images of a 12-year-old 22-kg castrated male Staffordshire Bull Terrier with sudden-onset vestibular signs and MRI evidence of hemorrhagic and ischemic infarcts in the brain. The images are displayed in a soft tissue window (window width, 400 HU; window level, 40 HU) and a 2.0-mm slice thickness.
Citation: Journal of the American Veterinary Medical Association 259, S1; 10.2460/javma.21.02.0091
Formulate differential diagnoses, then continue reading.
Diagnostic Imaging Findings and Interpretation
Thoracic postcontrast CT images revealed a circumferential, non–contrast-enhancing soft tissue thickening of the wall of the entire aortic arch and thoracic portion of the descending aorta (Figure 2). Aortic wall thickening was variable along its course and irregular, measuring up to 7 mm in thickness. Aortic wall thickening extended into the proximal part of the brachiocephalic trunk, and a small 7-mm-long contrast medium filling defect extended from the thickened aortic wall into the proximal left subclavian artery.
Same images as Figure 1. There is a circumferential, non–contrast-enhancing thickening of the aortic wall (white arrowheads) of the entire aortic arch and thoracic portion of the descending aorta, extending into the abdomen. The aortic wall thickening is variable in severity and irregular in outline along its course. The wall thickening extends into the proximal part of the brachiocephalic trunk, and a small, 7-mm-long contrast medium filling defect extends from the thickened aortic wall into the proximal left subclavian artery (white arrow).
Citation: Journal of the American Veterinary Medical Association 259, S1; 10.2460/javma.21.02.0091
Same images as Figure 1. There is a circumferential, non–contrast-enhancing thickening of the aortic wall (white arrowheads) of the entire aortic arch and thoracic portion of the descending aorta, extending into the abdomen. The aortic wall thickening is variable in severity and irregular in outline along its course. The wall thickening extends into the proximal part of the brachiocephalic trunk, and a small, 7-mm-long contrast medium filling defect extends from the thickened aortic wall into the proximal left subclavian artery (white arrow).
Citation: Journal of the American Veterinary Medical Association 259, S1; 10.2460/javma.21.02.0091
Same images as Figure 1. There is a circumferential, non–contrast-enhancing thickening of the aortic wall (white arrowheads) of the entire aortic arch and thoracic portion of the descending aorta, extending into the abdomen. The aortic wall thickening is variable in severity and irregular in outline along its course. The wall thickening extends into the proximal part of the brachiocephalic trunk, and a small, 7-mm-long contrast medium filling defect extends from the thickened aortic wall into the proximal left subclavian artery (white arrow).
Citation: Journal of the American Veterinary Medical Association 259, S1; 10.2460/javma.21.02.0091
Same images as Figure 1. There is a circumferential, non–contrast-enhancing thickening of the aortic wall (white arrowheads) of the entire aortic arch and thoracic portion of the descending aorta, extending into the abdomen. The aortic wall thickening is variable in severity and irregular in outline along its course. The wall thickening extends into the proximal part of the brachiocephalic trunk, and a small, 7-mm-long contrast medium filling defect extends from the thickened aortic wall into the proximal left subclavian artery (white arrow).
Citation: Journal of the American Veterinary Medical Association 259, S1; 10.2460/javma.21.02.0091
Same images as Figure 1. There is a circumferential, non–contrast-enhancing thickening of the aortic wall (white arrowheads) of the entire aortic arch and thoracic portion of the descending aorta, extending into the abdomen. The aortic wall thickening is variable in severity and irregular in outline along its course. The wall thickening extends into the proximal part of the brachiocephalic trunk, and a small, 7-mm-long contrast medium filling defect extends from the thickened aortic wall into the proximal left subclavian artery (white arrow).
Citation: Journal of the American Veterinary Medical Association 259, S1; 10.2460/javma.21.02.0091
Additional findings from the CT (images not provided) included multiple wedge-shaped renal infarcts; lack of contrast medium within the splenic vein and the neighboring portion of the portal vein, attributed to a thrombus; and incidental gallbladder calculi. The diffuse thoracic aortic wall thickening and proximal left subclavian arterial thrombus suggested the presence of an extensive peripheral thrombus, arteritis, or atherosclerosis, with potential underlying causes such as hypothyroidism, hyperadrenocorticism, diabetes mellitus, or a hypercoagulable state.
Treatment and Outcome
Diagnostics for common causes of ischemic and hemorrhagic brain infarction were performed, including tests for Angiostrongylus vasorum infection, hyperadrenocorticism, hypothyroidism, diabetes mellitus, systemic hypertension, protein losing nephropathy (PLN), protein losing enteropathy (PLE), and coagulopathy. Dirofilaria immitis was not on the differential diagnosis list as it is not endemic to the United Kingdom. Angiostrongylus vasorum antigen test (Angio Detect, Idexx Laboratories) result was negative. Concentrations of thyroid-stimulating hormone and thyroxine were within reference limits. Clotting times were within reference limits. Thromboelastography revealed equivocal evidence of hypercoagulability. Further testing, such as concentrations of D-dimers, fibrinogen degradation products, and fibrinogen, was not pursued. In the absence of clinical or biochemical changes consistent with hyperadrenocorticism, diabetes mellitus, PLE, or PLN, further testing for such was not undertaken. Echocardiographic results were unremarkable.
The neurologic status of the patient gradually improved without treatment, and further work-up was not pursued by the owner. The patient was examined 7 days after the initial presentation, and the owners reported that the dog had improved but remained lethargic and occasionally ataxic. Forty-nine days after the dog was initially presented to the hospital, the owners reported deterioration and elected euthanasia with postmortem examination for the dog. Histopathology of the aorta was consistent with severe, diffuse, chronic, proliferative, fibrous endarteritis. There was a segmental, chronic thrombus within the brachiocephalic trunk and the left subclavian artery. The kidneys showed multifocal, severe, chronic membranous glomerulonephritis with acute and chronic infarcts and fibrin thrombi. The spleen contained a subacute infarct with rare fibrin thrombi. The brain contained multiple subacute intra-axial hemorrhages that affected both the white and gray matter in the frontal and parietal lobes.
Comments
Diffuse thoracic aortic wall thickening is rarely seen in dogs, and endarteritis has not been previously described on CT. Spirocercosis can cause thoracic aortic wall thickening but is more likely to cause aneurysms, thrombosis, and mineralization of the aortic wall and is not endemic in the United Kingdom.1,2 There have been reports3,4 of abdominal aortic wall thickening due to various causes including infectious and noninfectious inflammatory conditions. The postmortem report suggested that the cause of the severe thickening of the aortic wall in the dog of the present report was endarteritis and fibrosis. There were also changes suggestive of severe, chronic glomerulonephritis and multiple acute and chronic infarcts. The histological findings were highly suggestive of longstanding hypertension, of which, renal disease can be a cause or consequence. These findings are interesting because the renal values on the biochemical analyses and the blood pressure measurements for this dog were all within reference limits. Urinalysis was also not suggestive of PLN. In cases of chronic kidney disease, mineralization of tissues such as the alveoli and stomach mucosa are often found on postmortem examination, and this was not found in this case. Hypertension in domestic animals has usually been associated with dissections and aneurysms as opposed to aortic wall thickenings.5 In this case, imaging both helped with the initial diagnosis of cerebral infarcts and ruled out neoplasia from the list of differential diagnoses. The thrombi and thoracic aortic wall thickening were unlikely to be found with other diagnostic tests. These findings, along with the renal infarcts and infarctions in the brain, provide further evidence toward a possible hypercoagulable state that could have been caused by primary glomerular disease, by primary arteritis, or by another inflammatory process. For the dog of the present report, the primary cause of the disease process was not clearly ascertained. Although PLNs have been found to be the most common cause of aortic thrombi, there are multiple other causes and often no cause is identified.6 The findings for the dog of the present report suggested that arteritis and vessel fibrosis should be added to the list of differential diagnoses to be considered in dogs and cats with circumferential, non–contrast-enhancing soft tissue thickening of the wall of the thoracic aorta.
References
- 1. ↑
Kirberger RM, Stander N, Cassel N, Pazzi P, Mukorera V, Christie J. Computed tomographic and radiographic characteristics of aortic lesions in 42 dogs with spirocercosis. Vet Radiol Ultrasound. 2013;54:212–222.
- 2. ↑
Kirberger RM, Zambelli A. Imaging diagnosis—aortic thromboembolism associated with spirocercosis in a dog. Vet Radiol Ultrasound. 2007;48:418–420.
- 3. ↑
Specchi S, d’Anjou MA. Diagnostic imaging for the assessment of acquired abdominal vascular diseases in small animals: a pictorial review. Vet Radiol Ultrasound. 2019;60:613–632.
- 4. ↑
Morabito S, Specchi S, Auriemma E, Ferro S, Kuhnert P, Zini E. Computed tomographic and ultrasonographic findings of abdominal arterial pseudoaneurysms caused by systemic mycosis in dogs. J Small Anim Prac. 2020;61:300–307.
- 5. ↑
Scollan K, Sisson D. Multi-detector computed tomography of an aortic dissection in a cat. J Vet Cardiol. 2014;16(1):67–72.
- 6. ↑
Williams TPE, Scott Shaw MS, Porter A, Berkwitt L. Aortic thrombosis in dogs. J Vet Emerg Crit Care (San Antonio). 2017;27(1):9–22.
