 Hello everyone, I am Dr. Kithi, junior resident from the Department of Radar Diagnosis, Goa Medical College. I will be presenting our tubercular pericarditis. As you know, tuberculosis is one of the oldest and still major cause of mortality and morbidity worldwide. Around 95% of the active TB cases were found in developing countries like Asia, Africa and Latin America. Tubercular pericarditis is rare, but a severe complication. However, it is one of the most common cause of pericarditis in the developing countries. High mortality from the tubercular pericarditis is likely due to the delayed diagnosis in adequate treatment and associated other comorbidities. In this presentation, we have put a case of tubercular constructive pericarditis with a loculated pericardial effusion. High risk 50 year old men with pulmonary coxon treatment since 4 to 5 months were presented with progressive breathlessness and bilateral pedal edema. No history of fever or cough. On physical examination, patient was every way fibrillated with respite rate of 25 with a muffled heart stones and a risked JVP. On laboratory examination, short-race ESR and CFP, however, the total request is concerned no more. The chest x-ray revealed the cardiomegaly, where no pericarditis cavusification noted. On circuitry, performed the echocardiography, the echoshock, decreased ejection fraction with a paradoxical interventricular septal movement with bilateral dilatation. On subsequently, the cardiac MRI was performed, which showed the generalized thickening of the pericardium with the tubular configuration of both the ventricles and the dilated atrium, suggestive of constructive physiology. On loculated, pericardial collection was seen along the left ventricle cavity, which is seen to cause compression on the left ventricle cavity, which resulted in the cardiac temporary. The collection, which also appeared, ISO intends on T1 and T2 and shows peripheral enhancement on post-contrast. Bilateral prelural effusion is also noted and the inferior vena cava was pretty distended. This is the blackboard images and this is the right plate images. On the blackboard images, there is a generalized thickening of the pericardium and the loculated collection, which is seen along the left ventricle cavity, which appears T1 ISO with the muzzle and T2 hyper with the muzzle. On injection of the contrast, fast pass perfusion images shows the enhancement of the myocardium, however, there is no enhancement of the pericardium or the collection is noted. On delayed images, inversion recovery images shows the intense enhancement of the pericardium with the peripheral enhancement of the collection noted. Now, these are the images of the 4-chamber and the 2-chamber. There is generalized thickening of the pericardium with the loculated collection noted along the left ventricle cavity, which is seen to cause poor expansion of the left ventricle cavity and bilateral lateral dilatation. And there is an inter ventricle septum shows the septal bounce on the diastole. Based on what's taken to OTA in the pericardium used there, the OTA finding revealed the pericardium was moderately thickened and densely adhered to the epichardium of heart-causing constriction. A collection of tissues and necrosis are seen along the posterior lateral to the left ventricle cavity, which is also passed out to the left blura. The postpericardium and echocardium are normal biometrical functions with normal ejection function. The pericardium is a two-layer membrane with all 4-chamber, a proximal portion of ascending aorta, pulmonary artery, pulmonary veins, and the superior binaquia. The pericardium consists of outer fibrous and inner serous layer. The serous layer consists of the perital and the visceral layer separated by the small amount of serous fluid. Perital layer lines the inner surface of the fibrous layer and the visceral layer endures the epichardium surface of the heart. The pericardial cavity is the space between the perital and visceral pericardial layer and it typically contains the clear serous fluid produced by the visceral pericardium. Normally the pericardial thickness is less than 2 mm on CT and MR images. Normally pericardium consists of the fibrous tissue, hence it appears low on both T1 and T2 weighted images. The pericardial thickness more than 4 mm or more with the clinical findings of heart failure, highly suggestive of constructive pericardial disease. MR image has reported accuracy of 93% for differential treating between the constructive pericardial and the restrictive cardiomyopathy on the basis of depiction of the thickened pericardium. Pericardial thickening may be limited to the right side of heart or even a small surface or such as right ventricle groove. It is important to remember neither the pericardial calcification or thickening is a diagnostic of constructive pericardial disease unless the patient has the symptom of physiological constriction or restriction. Tubercular involvement of the pericardium can occur via the lymphatics from the paratricial, peribronchial or medecinal lymph nodes or via the hematogenesis spread from the primary tubercular foci. Rarely the contagious spread of the tubercular lung lesion or the hematogenesis spread from the distant skeleton or a genetic urinary can occur. The four stages of the constructive pericardial disease include acute inflammatory pericardial disease, effusive constructive pericardial disease, adhesive constructive pericardial disease and chronic fibrous constructive pericardial disease. Acute inflammatory constructive pericardial disease presents with acute pericardial disease with the marked thickening of the pericardium with associated constructive physiology. Adhesive constructive pericardial disease presents as the fibrous bridge between the paratel and the visceral pericardium. Effusive constructive pericardial disease is a subacute constructive pericardial disease mainly involved in the visceral pericardial disease and with associated chronic pericardial disease. Chronic constructive pericardial disease consists of fibrous changes without associated calcification. Constructive pericardial disease is due to the pericardial fibrosis as a result of inflammatory process. Less compliment pericardial disease imparts the ventricle and the arterial fibrosis. Depending upon the extent of the disease, the free wall of the ventricle chambers have restricted expansion during the dastro. The ventricle capacity of one of the ventricle is strictly related to the filling of the opposite ventricle. The causes of the pericardial disease includes the postcardiac surgery, idiopathic, usually may be due to the viral pericardial disease, post radiation, tuberculosis. In the developing countries, fungal and parasitic, infection, chronic, renal failure, organismal muscular disease, neuroplastic infiltration, and asbestos. Definitive diagnosis is based on the identification of the tubercular bacillus in the pericardial effusion of pericardium. However, the culture may be positive in only 40-50% of the cases and identification of the bacillus in the pericardial bicep may be difficult in the early stages. Imaging can aid an early diagnosis in these cases. The pericardial deponent and the constructive pericardial disease are usually seen in the echocardiography. However, the entire imaging is hindered by anatomical invidation. In our case, the pericardial collection is not seen on the echocardiography. CT can demonstrate the pericardial thickening, acidification, effusion, as well as the presence of the pulmonary and immidational tuberculosis. CT and MRI features of the constructive pericardial disease. In acute inflammatory construct, to your pericardial disease, the pericardial thickness is more than 4 mm and effusion, and the early enhancement of the pericardium is noted. In effusive constructive pericardial disease, the pericardial thickness is more than 4 mm and effusion, and there is a relation between the perital and the visceral pericardium, and the early enhancement of the perital and visceral pericardium is noted. In chronic fibrous constructive pericardial disease, pericardial thickness is more than 4 mm, without pericardial classification, no effusion, and no early enhancement of the pericardium is noted on the contrast images. However, the thickened pericardium shows the delayed enhancement on the inversion sequences. The additive, constructive pericardial disease, which is very rare, the pericardial thickness is more than 4 mm, and then there is a relation between the visceral and perital pericardium, as well as the pericardium and the surrounding mid-strength structure. No early enhancement is noted. Due to constructive pericardial disease, the ventricles chambers may assume tubular configuration or enlargement of one or both atrium, enlargement of the superior and the inferior vena cava. As in images may show the decrease, right and left ventricle ejection, normal sliding of the ventricle over the pericardium, and abnormal septal motion towards the left ventricle in the early diastole, and the increased intraventricular interdependence. Although the tubercular pericardial compresses of 1 to 2% of all the tubercular infection, it is high incidence of the progression to the periconstructive pericardial disease, and the high mortality rate wants the early diagnosis and proper initiation of the anti tubercular treatment and the early surgical intervention if indicated. These are my references. Thank you.