Accumulation Of Pericardial Effusion Research Articles

Acute cardiac tamponade: A unusual cause of acute kidney injury

Cardiac Tamponade is usually consequence of increased pericardial pressure with accumulation of pericardial effusion. We are reporting a case of acute kidney injury after mitral valve replacement due to acute pericardial effusion with clot. A 38-year-old female presented to CTVS department of our institute with history of palpitations and shortness of breath. On further examination and investigations she was diagnosed with severe mitral stenosis. Mitral valve replacement was done for her. In post operative period she developed cardio renal syndrome due to cardiac tamponade which presented as acute kidney injury. Re-exploration was done and clot was removed. She was shifted to ward after post operative monitoring and extubation.

Pericardial injury with cardiac tamponade and bleeding from the pericardium confirmed using contrast-enhanced computed tomography: a case report

BackgroundSimple pericardial injuries are asymptomatic in many cases and usually do not cause bleeding that leads to cardiac tamponade. In this study, however, we report a case involving a patient with pericardial injury, in whom extravasation in the pericardium was identified using contrast-enhanced computed tomography (CT).Case presentationA 67-year-old man fell from a 3-m-high ladder and was injured and transported to our hospital. No pericardial effusion was observed on focused assessment with sonography for trauma (FAST) or plain CT on arrival, but pericardial effusion was detected on follow-up observation. Thereafter, his circulatory dynamics began to deteriorate. We then performed FAST to identify the bleeding source, but it was difficult to visualize on echocardiography. Thus, contrast-enhanced CT (CECT) was performed and extravasation was confirmed in the pericardium. We believed that the accumulation of pericardial effusion caused cardiac tamponade; hence, we performed emergent thoracotomy. When we released the cardiac tamponade, his circulatory dynamics improved, and we could stabilize the patient’s condition by ligating the bleeding vessel from the pericardium.ConclusionIf visualization is difficult on FAST, like in this case, CECT is useful for identifying the cause of pericardial effusion if circulatory dynamics can be determined. We were able to confirm that extravasation occurred from the pericardium using CECT; hence, we could confirm that pericardial injury caused bleeding and may cause cardiac tamponade. Thus, if cardiac tamponade is suspected, not only damage to the heart itself, but also damage caused by pericardial vascular injury should be considered. Further, if circulatory dynamics are stable, CECT should be performed.

Two cases of primary Sjögren's syndrome with accumulation of pericardial effusion

Two cases of primary Sjögren's syndrome with accumulation of pericardial effusion

Impending cardiac tamponade caused by salt supplement in a hyponatremic patient with chronic kidney disease

We documented a hyponatremic patient who developed imminent cardiac tamponade upon oral salt supplement. A 72-year-old diabetic woman had hemorrhagic stroke; pericardial effusion; and chronic kidney disease, stage IV. She developed hyponatremia (serum sodium level, 125 mmol/L), compatible with the syndrome of inappropriate antidiuretic hormone, and received oral salt supplement 9 g/d for 4 days. Shortness of breathing and increasing heart rate ensued, and the echocardiography found accumulation of pericardial effusion with signs of impending cardiac tamponade. Pig-tail drainage through pericardiocentesis was done, and the vital signs were stabilized. We found the production of pericardial effusion increased from 100 to 220 mL/d after oral salt supplement at 3 g/d was reassumed. We discuss the relationship between serum sodium levels, the dose of salt supplement and the accumulation of pericardial effusion.

Sildenafil and steroid therapy effectively improved POEMS syndrome-associated pulmonary arterial hypertension

POEMS syndrome is a rare multi-systemic plasma cell disorder characterized by polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, and skin changes [1]. Pulmonary arterial hypertension (PAH) is one of rare manifestations of POEMS syndrome [1, 2], and steroid therapy is effective in treating POEMS syndrome-associated PAH [3–5]. However, because there is a risk of dosedependent steroid intolerance or insufficient effectiveness in treating POEMS syndrome-associated PAH [5, 6], alternative or adjunctive therapy should be evaluated. In this report, we showed a rare case of POMES syndromeassociated PAH which was successfully treated with sildenafil and relatively low dose of prednisolone. The severity of PAH and effectiveness of therapy were definitively evaluated with right heart catheterization. A 55-year-old man started to suffer from difficulty in walking, and edema in lower extremities from October 2005. He was diagnosed as POEMS syndrome in March 2007 because he met both of 2 major criteria (polyneuropathy and IgG-lambda type monoclonal protein) and 6 of 7 minor criteria (Castleman’s disease, splenomegaly, edema in lower extremities, hypothyroidism, hyperpigmentation, and papilledema) of POEMS syndrome [1]. The vascular endothelial growth factor (VEGF) level was 6630 pg/mL at the time of diagnosis. After improvements of his symptoms with steroid pulse therapy, he was followed up regularly as an outpatient without steroid. Despite relatively low VEGF level of 275 pg/mL, dyspnea and edema in lower extremities exacerbated and transthoracic echocardiography newly revealed possible pulmonary hypertension. He was referred to our institution. This case has also been reported elsewhere from another point of view [7]. PAH was confirmed by right heart catheterization as shown in Table 1. There were no other apparent secondary causes of pulmonary hypertension based on the World Health Organization updated clinical classification of pulmonary hypertension. After recovery from previously reported pulmonary edema [7], sildenafil was started at 20 mg/day and the dose was increased gradually to 60 mg/ day which resulted in improvement of plasma brain natriuretic peptide (BNP) level from 276 to 112 pg/mL [8]. At this point, oral prednisolone (0.4 mg/kg/day) and 2 cycles of intravenous dexamethasone (0.8 mg/kg 9 4 days) administration were added because exacerbation of POEMS syndrome was suspected with accumulation of pericardial effusion. Eventually, 100 mg/day of sildenafil and 0.4 mg/ kg/day of prednisolone administration resulted in dramatic improvement of PAH confirmed by many indexes including right heart catheterization about 3 months after the initiation of sildenafil (Table 1). Until now, steroid therapy has been believed as firstline therapy in treating POEMS syndrome-associated PAH and 1 mg/kg/day prednisolone administration may be We have to inform you that this case has also been reported in Annals of Hematology from another point of view [7]. Especially, laboratory data and part of right heart catheterization findings before the treatment in Table 1 are reproductions from it. However, the concept of this case report is totally different from the other one, and we got reproduction permission from Springer for this submission.

The Syndrome of Cardiac Tamponade with “Small” Pericardial Effusion

Cardiac tamponade is usually a consequence of increased pericardial pressure with accumulation of pericardial effusion. Pericardial effusion may be caused by acute pericarditis, tumor, uremia, hypothyroidism, trauma, cardiac surgery, or other inflammatory/noninflammatory conditions. In this article we describe four scenarios illustrated by case reports where a small or apparently small pericardial effusion may produce cardiac tamponade. The first scenario illustrates how a small pericardial effusion can cause clinically significant cardiac tamponade when it accumulates rapidly. The second scenario exhibits how an apparently small pericardial effusion on transthoracic echocardiogram (TTE) turned out to be a small amount of unclotted blood and an echogenic hematoma. The third scenario details how an apparently small pericardial effusion on TTE was actually a large loculated effusion in an unusual location seen only by transesophageal echocardiogram (TEE). The fourth scenario demonstrates how the combination of a large pleural effusion and a small pericardial effusion can result in cardiac tamponade. The role of echocardiography in the diagnosis and management of these scenarios is discussed here. Although many clinicians depend on the amount of pericardial effusion to suspect cardiac tamponade, it is important to suspect cardiac tamponade when patients have hemodynamic compromise regardless of the amount of pericardial effusion.

Oozing type of left ventricular rupture via subepicardial aneurysm diagnosed 5 months after myocardial infarction

A 71-year-old man visited our hospital complaining of increasing fatigue and exertional dyspnea. He had had severe epigastric pain for the past 5 months. On admission, chest radiogram showed marked cardiac dilatation and echocardiogram massive pericardial effusion with a small subepicardial aneurysm at the posterior wall of the left ventricle. An urgent pericardiocentesis removed 1300 ml of bloody effusion. The red blood cell count of the pericardial effusion was similar to that of the peripheral blood, and there were no abnormal findings on cytologic and bacteriological examinations. Coronary angiography showed a blunt occlusion of the mid-portion of the circumflex artery. Left ventricular angiogram revealed aneurysmal deformity of the left ventricular posterior wall. These findings suggested that an oozing type of left ventricular rupture via a subepicardial aneurysm had occurred after the onset of myocardial infarction (MI), resulting in massive accumulation of pericardial effusion. The patient is presently doing well without any clinical symptoms 18 months after pericardiocentesis. This is the first case report in which a subepicardial aneurysm with massive pericardial effusion was detected in the chronic stage of MI and successfully managed without surgical repair.

Cardiac damage in dogs infected with T brucei; clinical and electrocardiographic features

ABSTRACTIntravenous infection of dogs with Trypanosoma brucei resulted in an acute disease syndrome, characterised by fever, intense parasitaemia, severe anaemia and rapid weight loss. During the course of infection, evidence of severe cardiac abnormalities developed. Tachycardia and tachypnoea occurred soon after detection of parasitaemia, around day 6, progressing to severe bradycardia and dyspnoea in terminal stages of the disease in week 4. Murmurs of mitral and tricuspid incompetence were heard from day 12 by auscultation of the thoracic cavity. Electrocardiography revealed abnormalities in generation and conduction of electrical impulses, including sinus arrest and atrioventricular blocks, and accumulation of pericardial effusion in terminal stages. Effective treatment with the trypanocidal drug suramin resulted in rapid improvement of one of the dogs. When treatment was unsuccessful, however, chronic myocardial damage developed, with intramyocardial conduction defects, including S‐T segment and T wave changes, and ventricular escape beats. These abnormalities were similar to those reported for human African trypanosomiasis.

Fetal Cardiovascular Effects of Nifedipine in Rats

In this study we clarify the fetal cardiovascular effects of nifedipine. Nifedipine was administered to near-term rats and cardiovascular morphology of the fetus was studied with a rapid whole-body freezing technique. Fetal cardiac failure was estimated by accumulation of pericardial effusion and ventricular dilatation. Dose-response study at 8 h after administration revealed that slight ventricular dilatation occurred with 0.1 mg/kg of nifedipine, and remarkable ventricular dilatation and pericardial fluid accumulation were noted with 10 mg/kg nifedipine. Time-course study with one dose of 10 mg/kg nifedipine revealed early ventricular dilatation at 1 h, peak ventricular dilatation and fluid accumulation at 8 h, and slight effects at 24 h. In conclusion, the cardiodepressive effect of nifedipine in the fetal rat was mild with the therapeutic dose, and its effects increased dose dependently.

Echocardiography in pericardial effusion

Echocardiography has become established as the procedure of choice for the detection, confirmation and serial follow-up of patients with pericardial effusion. In this article the technic and pitfalls of recording, and the criteria and their sensitivity for the diagnosis of pericardial effusion are reviewed. In addition, echographic findings in special instances, such as accumulation of pericardial effusion behind the left artium, the swinging heart syndrome and cardiac tamponade, are discussed.

Pseudocyst of the pericardium developing during maintenance hemodialysis. Report of two cases.

Two cases of pericardial pseudocyst which developed in the course of maintenance hemodialysis are reported. Both patients were usually free of complaints, although there was evidence of the previous pericarditis with recent accumulation of pericardial effusion. As a possible mechanism leading to pericardial pseudocyst formation, distension of a weak area of the thickened pericardium due to an increase in intrapericardial pressure was assumed. Therefore, pericardial pseudocyst is one of the likely complications of patients on maintenance hemodialysis.