Previously Submitted Cases: Dr. Amy Tidwell
Case 1
Patient ID: CTMRSOC
Patient Surname: CTMRSOC
Patient Firstname: CASE1
Accession #: CASE1
Referring MD: TIDWELL
Clinical Information:
6 year old CM Lab
-Owners got dog from rescue pound in Tennessee 4 months ago
-Coughing since; one episode of collapse, initial echo: tricuspid regurgitation, pulmonary hypertension
-Now only coughing, sounds upper airway
-No dyspnea
-Heartworm negative, but past history is unknown
-Current echo: no masses in heart, RVE, no TR so can't measure for pulmonary hypertension
Radiographs: Moderately severe diffuse interstitial pattern and big cranial pulmonary artery
CT and CTA: Large smooth filling defect in lumen of the left pulmonary artery (PA) compatible with thrombus/embolus and bilateral PA enlargement consistent with hypertension; patchy lung opacities; enlarged left PA impinges on left bronchus; possible smaller thrombi/emboli in right pulmonary arteries.
Fortunately, no pathologic followup information is available as the dog is doing fairly well. All labwork to assess for hypercoagulopathy was negative. Thrombi/emboli could be benign or malignant.
This angiogram was performed using a test bolus first to determine time to peak opacification. This permits scanning at the time of maximum contrast enhancement of the vessel of interest.l
Case 2
Patient ID: CTMRSOC
Patient Surname: CTMRSOC
Patient Firstname: CASE2
Accession #: CASE2
Referring MD: TIDWELL
Clinical Information
12 year old SF Cairn Terrier
Seizures, pacing
Has diabetes mellitus, regulated with RX
Glucose normal on presentation; hypertensive, blood pressure 260
CSF tap results were normal
Rx with amlodipine, responded well while in hospital; discharged, but died at home soon thereafter; no post-mortem
MRI Brain: Multifocal bilateral small cavities in the region of the caudate nuclei. Lesions are hyperintense on T2-W spin echo images, hypointense on T1-W spin echo images and have central attenuation with surrounding hyperintensity on FLAIR images. No susceptibility void on T2*-W images. No contrast enhancement. Also, bilateral periventricular T2-hyperintensity in the parietal/occipital lobes on spin echo and FLAIR images and asymmetric ventriculomegaly.
Presumptive diagnosis: Possible lacunar infarcts
Comment: Because of the history of diabetes mellitus and systemic hypertension, and the location of small cavities within the basal ganglia, I believe that the lesions could be compatible with what is described in people as lacunar infarcts. Lacunar infarcts in people are caused by small vessel obstruction and have a predilection for the subcortical nuclei. Hypertension and diabetes are 2 of several predisposing factors. Because I have no pathologic proof and because the imaging features of this disorder have not been published to my knowledge in dogs, this diagnosis should be considered strictly as opinion. If anyone has more to add or disagrees, I would love to hear your views.
Case 3
Patient ID: CTMRSOC
Patient Surname: CTMRSOC
Patient Firstname: CASE3
Accession #: CASE3
Referring MD: TIDWELL
Clinical Information:
-12 year old SF Spitz
-Progressive coughing and gagging for one week. No response to antibiotics
-Pulse OX 87-90%; Elevated liver enzymes
Radiographs:
-Moderate diffuse interstitial pattern.
Ultrasound:
-mottled enlarged liver and masses in spleen
-Rx with oxygen; Improvement in clinical signs, pulse ox, and radiographs
Few days later, dyspneic, cyanotic
CT findings:
Bilateral ventral consolidation; diffuse ground glass opacity with multifocal small patches of consolidation; proximal pulmonary artery enlargement; raised nodules in liver and spleen; hypodense foci that stay hypodense on delayed post-contrast images
Clinical diagnosis:
Acute lung injury(ALI)/acute respiratory distress syndrome (ARDS) or acute interstitial pneumonia (AIP).
Post- mortem: Diffuse alveolar damage (DAD) characterized by moderate diffuse non-uniform alveolar septal thickening; type 2 pneumocyte hyperplasia; alveolar flooding with histiocytes/neutrophils/hemorrhage and fibrin exudates; and fibrosis. Liver: Mild bridging fibrosis and nodular hyperplasia; splenic hyperplasia
Comment: DAD is the pathologic description for the clinical disorders known as ALI, ARDS or AIP. In people, there are subtle clinical and physiologic distinctions between the 3 processes, but this has not been well characterized in dogs. There are 3 phases of these processes: the acute exudative phase, the subacute proliferative phase and the chronic fibrotic phase. Because there was no known underlying stimulus for the lung injury such as septicemia, severe pneumonia or pancreatitis, this dog may best be described as having acute interstitial pneumonia.
Reference: Tomiyama N et al. Acute respiratory distress syndrome and acute interstitial pneumonia: comparison of thin-section CT findings. J Computer Assisted Tomography 2001;25:28-33.