talk.
As mentioned, the Cor triatriatum Dexter is well documented in the veterinary literature. It is usually diagnosed in young dogs, despite several reported cases relate to dogs. The symptoms most commonly mentioned are ascites and hepatomegaly but also reported exercise intolerance, dyspnea, weakness and syncope.
according to the literature found no increased prevalence by race or sex, however by reviewing existing literature seems usually seen with higher incidence in males and races Chow Chow and Labrador also appear slightly more represented than the rest but is probably not statistically significant.
laboratory findings differ in each case but the hypoproteinemia (probably due to the loss in abdomen) seems to be common to all reported cases. Other findings have been described as elevated ALT and the ALKP , thrombocytosis, microcytic anemia or polycythemia. It is likely that some of these findings are linked to the chronicity of the process, development of liver failure secondary to chronic congestion or low cardiac output.
The presence of erythrocytes schistocytes fragmented or is not a finding reported in the literature, but it is possible that their existence is due to intravascular hemolysis caused by turbulent flow through the intraatrial membrane. Intravascular hemolysis caused by turbulent flow has been described in people with aortic stenosis and pulmonary stenosis but according to Jacobson et al gradient necessary for it to happen this hemolysis must be greater than 50 mmHg while the grandiente found in this case did not exceed 16 mmHg so can not be assured that this is the case.
X-rays may be normal, but often find an increase in the caudal vena cava and / or dilation the right atrium. Sometimes the presence of ascites compressing the chest radiographic interpretation difficult.
Like the chest radiograph, electrocardiogram is usually normal but can be observed pulmonary P wave in lead II.
ascitic fluid analysis revealed a variable content of protein and relatively acellular, often is described as a modified transudate reddish.
echocardiography has now become unnecessary to use angiocardiographic techniques to reach the diagnosis of CTD, but this disease often need for proper display non-standard projections and / or use of contrast solutions. In fact there are reported cases in which echocardiography was inconclusive.
During embryogenesis, the right horn of sinus venosus is gradually incorporated into the right atrium forming the smooth surface of the right atrium. The junction between the right horn of sinus venosus and atrium are named embryonic senoatrial hole that is flanked by the left venous valve and right.
left valve will be part of the septum secundum, while the right tends to regress. Sometimes the right valve of sinus venosus persists valve forming the caudal vena cava (Eustachian valve) and coronary sinus valve (valve Tebesiana).
In humans when the Eustachian valve remains can form a thin veil without hemodynamic consequences known as Chiari rete "or persist as a septum that divides the court in fact two, which is known as cor triatriatum dexter. Intermediate forms also occur.
In human medicine there are six morphologies described for the CTD in response to the blocked vessel but in the cases reported in veterinary found more often obstructed the vena cava and coronary sinus flow. Furthermore, this membrane may appear perforated or imperforate. When presented imperforate anastomosis has been reported from the vena cava caudal to the azygos vein via the vertebral venous circulation.
The CTD is a condition often associated with other congenital malformations in humans, but most of the cases reported so far showed no other abnormalities. Associated malformations have been published in the veterinary literature are: persistent foramen ovale, pericardial agenesis, Ebstein anomaly, septal defect, pulmonary stenosis, stenosis Aortic and persistent left cranial vena cava.
The clinical presentation of CTD is caused by a venous outflow obstruction at posthepatic. The importance of distinguishing the level at which the blockage occurs is that it determines the protein content of ascitic fluid.
The type of obstruction found in the CTD causes a condition known as "Budd-Chiari like syndrome." The Budd-Chiari syndrome was first described in the nineteenth century and refers to a endoflebitis obliterans of the small hepatic veins. Over time was first used to refer to all posthepatic flow obstructions and there has been controversy about its definition.
While, therefore, has become an inconsistent use of the term, Grooters and Smeak propose to use "type Budd-Chiari syndrome" to describe those clinical manifestations caused by a blockage of outflow due to liver mechanical occlusion.
This definition would exclude, therefore, right heart failure or constrictive pericarditis and obstructions that cause functional . It must be noted, moreover, that a the characteristics of congestive right as jugular distension is absent in patients affected by CTD.
CTD A part of other potential causes of "Budd-Chiari like syndrome" are filariasis, right atrial tumors, thrombosis, neoplasia, trauma or scarring of the vena cava flow and abnormalities of hepatic veins.
CTD Treatment is always surgical. Medical treatment, as was our case, is often insufficient to control the ascites and liver congestion.
has also been proposed by catheter intervention for dilatation balloon. Although there have been several cases where this technique has been effective in some cases the membrane may be too fibrous to break with a ball and, on occasion, has been more than one intervention necessary to control symptoms.
also were also described various surgical techniques usually by venous occlusion with or without hypothermia, such as that in this case.
The prognosis of cor triatriatum Dexter is very variable depending on the degree of obstruction, however in cases where cause symptoms on prognosis in the absence of surgical solution is bad because it does not usually respond to medical therapy.
In this case where time to intervention was also continued long observed the presence of cardiac cachexia, probably caused by malabsorption due to intestinal wall edema secondary right heart failure.
