A raíz del vídeo de acceso yugular derecho para la resolución del síndrome de la vena vana producido por la filariosis nos han preguntado como se diagnostica dicho síndrome en perros con filariosis y que diferencia existe entre síndrome de la vena cava y una filariosis muy avanzada.
Vamos a empezar denominando para así poder entender mejor which is the Vena Cava Syndrome.
syndrome is a cluster of symptoms caused in this case by the accumulation of Dirofilaria immitis parasites (in the Canary Islands) in the right atrium, right ventricle and vena cava.
filariasis
Although initially classified into 3 stages according to their severity, vena cava syndrome is considered by some authors as grade 4, and by others as a complication of grade 3. Occurs mainly in endemic areas of the parasite, such as Gran Canaria, usually in spring and summer. Epidemiology tells us that young males are usually who have received a high parasite load in the previous year which more often suffer from this disease. But it also looks pretty in adult dogs have not taken preventive.
normal
By vena cava syndrome occurs when the adult filaria "migrate" from the pulmonary artery to right ventricle. Although migration is defined as active movement of the parasite and although this is able to move, in the case of this migration, there is no active movement by the parasite, but for reasons not yet well understood (it is believed that pulmonary hypotension, pulmonary hypoperfusion ) falls into the right ventricle. Once adults come to the right ventricle to right atrium step is simple with the support of the structures that make up the right atrioventricular valve (tricuspid).
The syndrome is caused by the presence of these parasites in the middle of the hole that forms the tricuspid valve, which prevents the proper functioning of this and causes a very severe tricuspid regurgitation. This prevents blood regurgitation during systole is sent to the pulmonary circuit. If we add that in dogs with heartworm disease there is usually a state associated with pulmonary hypertension, have resulted in a decrease in the blood supply to the circuit left heart, and therefore a decrease in the outflow of the left ventricle. Manifesting at this time signs of low cardiac output (dition femoral pulse deficit, pre-renal failure, exercise intolerance, syncope).
Parasites preventing closure of the tricuspid valve regurgitation and high are quickly presented show no signs of congestive right heart failure due to accumulation of blood in the input circuit to the right atrium.
Another condition associated with this syndrome and which undoubtedly worse life expectancy eritrolisis patient is produced with the consequent hemoglobinuria. Although there are still doubts as to its cause, was thought to be caused by the passage of red blood cells in adults housed in the tricuspid valve. These red blood cells must pass through an area of \u200b\u200bhigh pressure (remember that the tricuspid valve is full of adult parasites obliterated and passing it between systole and diastole) and lysed. This analysis can also lead to disseminated intravascular coagulation (DIC), by activation of the coagulation cascade from ruptured erythrocytes.
Interestingly syndrome in full, including lysis of erythrocytes with hemoglobinuria, IDC and ICC the right have been reproduced in experimental dogs after inoculating large numbers of strands of silicon in right cavities.
Now, what will observe outward signs?, Mainly signs of low cardiac output as well explained in the pathogenesis of this syndrome. Ie dition hypokinetic femoral pulse.
ICC also evidence of right, ascites, portal hypertension. Auscultation
diastolic murmur and diastolic gallop, the presence of parasites between the leaflets of the tricuspid.
course echocardiography is the diagnostic tool, and you can see examples of a patient in our veterinary center (here video1) and ( here Video2). In both you can see how the interior volume of both right ventricle and atrium are invaded by numerous parasites. These are found across the tricuspid valve orifice preventing the closure of this and causing regurgitation previously described.
Alexis J. Santana González. DVM. Col829.
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