Clinical history and questions
Various views of a specimen from a 6 year-old bull terrier which was only slightly less vigorous than its peers, until it suddenly went into a decline after taking sides in a dog fight. It was dyspnoeic and staggery and retired to its box and was found dead next morning, its head in a pool of blood stained foam.
- Describe the abnormalities
- What underlying disease process/es could produce these changes?
- Make a differential diagnosis list, in order of priority
- With your preferred diagnosis in mind, what is the pathogenesis of these macroscopic changes?
- Relate the pathology to the clinical signs
An interpretation of Diagnostic Exercise No. 5
(A) and (C): Left ventricle, opened vertically to show the septal cusp of mitral valve (the left auricle off to the left, near the scissor blades, helps identify it as left ventricle). The ventricular myocardium is bulkier than normal, but there seems to be no associated ventricular dilatation. The left atrium, on the other hand, appears rather more voluminous than normal, and its endocardium is distinctly paler than that of the ventricle. There is an irregularity and defect on the right side of the septal cusp of the mitral valve, and in the close view (C), there are small remnants of ruptured chordae tendinae visible beneath an angular flap of cusp remnant. On one edge of the defect there is a small yellowish nodule. In (B) the septal cusp has been bisected to reveal the aortic valve whose cusps are somewhat distorted. Beneath this valve is a thin transverse band-like narrowing of the outflow tract, and the associated endocardium is thickened and irregular. The base of the aorta has a baggy appearance.
Distortion of cardiac valves can be due to developmental or degenerative disorders (endocardiosis), or to inflammation (endocarditis). In endocarditis, platelet/bacterial deposits are usually quite bulky, and there is often a history of fever, malaise and other evidence of chronic bacterial infection. So the clinical history and gross findings are more consistent with a developmental defect followed by secondary degenerative chagnes, culminating in recent rupture of the mitral valve. Neoplasia is not an option.
Congenital sub-aortic stenosis, with secondary valvular endocardiosis, left ventricular hypertrophy, left atrial dilatation and recent valve rupture (the latter probably during the exertion and adrenalin discharge of the dog fight). Possibility of concurrent endocarditis is discounted for the reasons above.
Platelets adhering to the exposed collagen of the chordae and valve would have produced the yellowish nodules in the short interval between rupture and death. Left ventricular hypertension caused by the restriction of left ventricular outflow would have produced the left ventricular hypertrophy (increased work-load) and dilatation of the less muscular atrium. The thickening of the atrial endocardium (so-called fibro-elastosis) is an attempt to limit dilatation. Distortion of the aortic cusps could be partly developmental, partly due to chronic turbulence in the outflow caused by the stenotic band. The same can be said of the dilated base of the aorta.
Pathology and Clinical Signs
This animal had compensated fairly well for its cardiac defect, but the adaptive changes predisposed it to valve rupture during exertion. The mitral rupture caused immediate pulmonary hypertension, with consequent pulmonary oedema and haemorrhage.
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