Massive pericardial effusion in a hypothyroid child

A child with Down's syndrome and long standing severe hypothyroidism had a massive pericardial effusion without cardiac tamponade. The effusion completely resolved with medical treatment without pericardiocentesis.     

Massive haemorrhagic pericardial effusion in beta-thalassaemia major

The case of a child with beta-thalassaemia major who developeda massive haemorrhagic pericardial effusion is reported andin whom the clinical picture completely resolved after pericardiocentesis.Possible causes are discussed and the role of echocardiographyin the follow-up of thalassaemic patients is emphasized.     

Massive pericardial effusion with left-to-right intracardiac shunt

We describe a 31-year-old man with Down's syndrome who presented with severe chronic hypothyroidism and a massive pericardial effusion. Following partial aspiration of this effusion, he rapidly deteriorated and died. Findings at autopsy revealed him to have an atrioventricular septal defect with shunting at the atrial level. We postulate that, by releasing extrinsic pressure on his right heart by the aspiration, there was sudden shunting of blood from left-to-right, resulting in hypotension, shock, and subsequent death. We highlight the difficulties in management of such a case, and suggest alternative strategies.     

Massive pericardial effusion secondary to Hashimoto's disease

Although relatively rare, hypothyroidism remains a significant cause of moderate to severe pericardial effusion. Pericardial effusion secondary to hypothyroidism does not usually cause symptoms since it tends to regress slowly and ultimately disappear several months after the patient has reverted to the euthyroid state. Thus, hypothyroidism must be ruled out in patients with an unexplained pericardial effusion, both to improve prognosis and to avoid unnecessary pericardiocentesis. Even when they have a massive pericardial effusion, patients should receive the standard treatment for hypothyroidism. We herein describe a 79-year-old woman with a massive pericardial effusion associated with hypothyroidism who showed a good response to standard levothyroxine replacement therapy after 5months.     

Massive pericardial effusion in a patient with scleroderma with special reference to concentration of alpha-hANP in plasma and pericardial effusion

A 41-year-old woman was admitted to our hospital because of scleroderma and combined valvular disease (mitral stenosis, aortic regurgitation, tricuspid regurgitation) associated with massive pericardial effusion. Plasma atrial natriuretic peptide (alpha-hANP) level was 130 pg/ml on admission, and increased temporarily with a decrease of pericardial effusion, without significant of changes of pulmonary capillary wedge pressure, pulmonary arterial pressure, right ventricular pressure nor right atrial pressure. These findings suggest that one of the mechanisms of alpha-hANP secretion, a stretch receptor mechanism, is interfered by the massive pericardial effusion. There was no relationship between atrial pressures and plasma alpha-hANP levels in this case. alpha-hANP concentration in pericardial effusion (486 pg/ml) was four to five folds higher than the plasma alpha-hANP levels.     

Massive intractable pericardial effusion in a patient with systemic lupus erythematosus treated successfully with pericardial fenestration alone

Systemic lupus erythematosus (SLE) is often complicated by pericarditis with effusion, which generally responds well to glucocorticoid. We report herein a Japanese patient with SLE who showed a sign of cardiac tamponade and severe chest and back pain because of massive intractable pericardial effusion. Pulse glucocorticoid and pulse cyclophosphamide gained marginal effects. Pericardial effusion accumulated again soon after ultrasound-guided pericardiocentesis and drainage. Pericardial fenestration performed surgically as a last resort, for draining pericardial fluid into the pleural space, was very effective, and only a much smaller amount of fluid was observed in the space thereafter in comparison with the volume before the surgery. Pathological examination of the retrieved pericardium unfolded intense hyperplasia of small vessels and capillaries. Levels of IL-6 and TNF-alpha in pericardial effusion were extremely higher than those in serum. Pericardial effusion with extensive capillary hyperplasia in SLE would be resistant to medical treatment and require surgical fenestration.     

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 atrium, the swinging heart syndrome and cardiac tamponade, are discussed.     

Copious pericardial and pleural effusion of hypothyroid origin. Report of a case and review of the literature

The authors report the case of a female of 57 years presenting hypothyroidism with pericardial tamponade followed by development of copious pleural extravasation. The present observation and those reported in the literature are used to evoke the characteristics of copious pericardial and pleural extravasation during hypothyroidism. The authors emphasize the importance of cardiac echography during myxedema. A few exceptional observations aside, extravasation is reduced by supplementary hormone therapy.     

Electrocardiographic voltage in pericardial effusion.

The usefulness of the electrocardiographic sign of "low voltage" in the diagnosis of pericardial effusion was investigated in 122 patients comprising three study groups. Sixty-four patients (group 1) had a pericardial effusion detected and measured by echocardiographic studies. The volume of the effusion showed no correlation with electrocardiographic voltage. A second group of 36 patients was identified as having low voltage on routine electrocardiograms. Only 13 (36 percent) had echocardiographically demonstrable pericardial effusion. Group 3 consisted of 22 patients who required pericardiocentesis. The ECGs obtained immediately after pericardiocentesis showed an increase in average voltage of 0.48 mm in the limb leads and 0.83 mm in the precordial leads for each 100 ml of fluid removed. This study demonstrates that a single ECG with "low voltage" is not useful in the diagnosis of pericardial effusion but that a reduction in the voltage of serial ECGs may suggest the development of pericardial effusion.     

Massive parapneumonic effusion caused by Mycoplasma pneumoniae in a child: a case report

Mycoplasma pneumoniae infection is usually mild course and self-limited. Parapneumonic effusion is not a common feature of M. pneumoniae. The treatment of parapneumonic effusion is macrolides and chest tube with adequate pleural drainage. We report here on a child with M. pneumoniae infection complicated by massive parapneumonic effusion. Protracted course of fever and respiratory distress was noted in patient. Pneumothorax was occurred subsequent to chest tube drainage.     

糖皮质激素辅助治疗原发性甲状腺功能减退症大量心包积液一例

原发性甲状腺功能减退症(甲减)是临床常见的一种内分泌疾病，心包积液是其临床表现之一，但大量心包积液少见。传统的治疗方法为以小剂量甲状腺激素替代治疗开始，再逐步增加剂量。若患者能耐受，心包积液一般可以逐渐消退；若患者不能耐受，就会出现严重的心绞痛症状。为此，改变原有的思维模式，从自身免疫性疾病的角度理解大量心包积液产生的     

Massive pericardial and pleural effusion with anasarca following allogeneic bone marrow transplantation

A 10-year-old girl presented with massive pericardial/pleural effusion with anasarca 216 days after an allogeneic bone marrow transplantation from her HLA-matched sibling for relapsed acute lymphoblastic leukemia. She did not show any other symptoms of chronic graft-versus-host disease (GVHD). The antinucleolar antibody was elevated in the blood and the pleural fluid. The lymphocytes in the fluid were mostly CD8+/HLA-DR+, and a majority of CD8+ cells in the blood expressed CD57. These data suggested that she had chronic GVHD. Immunosuppressive therapy including prednisolone, cyclosporin A, high-dose methylprednisolone, tacrolimus (FK506), and methotrexate had no effect, and the patient died of Aspergillus pneumonia 183 days after the presentation of the disease. Although it has not been described before, isolated serositis with edema should be recognized as a clinical feature of chronic GVHD.     

Ultrasonography in pericardial effusion

Four cases of pericardial effusion diagnosed by echocardiography are reported. While one of the four cases was referred for echocardiography with a diagnosis of pericardial effusion, the other three patients were selected for echocardiography on the basis of cardiomegaly demonstrated in plain x-ray chest examination. Real time echocardiography was considered to be most rapid, safe, convenient, accurate and least invasive method of diagnosing pericardial effusion.     

Procainamide-induced pericardial effusion

A case of hemodynamically significant pericardial effusion due to a procainamide-induced SLE-like syndrome is reported. This case emphasizes that the acute pleuropericardial syndrome seen after procainamide therapy is potentially dangerous. Close follow-up of patients taking procainamide is warranted.     

Purulent pericardial effusion

A fatal case of purulent pericardial effusion in which the patient was treated with sulfadiazine and penicillin is presented.     

Neoplastic pericardial effusion

Neoplastic pericardial effusion is a serious and common clinical disorder encountered by cardiologists, cardiothoracic surgeons, oncologists, and radiation oncologists. It may develop from direct extension or metastatic spread of the underlying malignancy, from an opportunistic infection, or from a complication of radiation therapy or chemotherapeutic toxicity. The clinical presentation varies, and the patient may be hemodynamically unstable in the setting of constrictive pericarditis and cardiac tamponade. The management depends on the patient's prognosis and varies from pericardiocentesis, sclerotherapy, and balloon pericardiotomy to cardiothoracic surgery. Patients with neoplastic pericardial effusion face a grave prognosis, as their malignancy is usually more advanced. This review article discusses the epidemiology and etiology, pathophysiology, clinical presentation, diagnosis, management, and prognosis of neoplastic pericardial effusion.     

Incidence of pericardial effusion in pulmonary tuberculosis.

Tuberculosis (TB) is one cause of pericardial disease. In order to know the incidence of tuberculous pericardial effusion (TPE) in patients with pulmonary tuberculosis (PT), the factors associated with their presence and whether human immunodeficiency virus (HIV) patients have a higher risk, we analyzed different parameters and performed an echocardiography to evaluate the presence of TPE. The incidence of TPE was 14.1%, and the presence of pleural effusion was associated with TPE (OR 24.39). HIV patients do not have a higher risk of TPE, independently of immunosuppression. It is necessary to eliminate the presence of TPE in patients with PT, mainly in those with pleural effusion.