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Pericarditis as a complication of appendicitis is a rare event. In a 25-year period we encountered two pediatric cases with this severe complication due to (a)typical presentation of appendicitis resulting in small bowel obstruction, intraabdominal abscesses, constrictive pericarditis, and purulent pericarditis.
The cases of 17 patients with tuberculous pericarditis were reviewed. Thirteen patients had effusive pericarditis, and 10 had surgical drainage of the effusion. No deaths were due to pericardial tamponade; this appears to be related to earlier recognition of major pericardial effusions by echocardiography. In 2 patients clinical evidence of pericardial constriction developed while they were on a regimen of therapy, and in another 2 patients, echocardiography revealed pericardial thickening after resolution of the effusion. A pericardial window is recommended for the short-term management of patients suspected of having tuberculous pericarditis with a major pericardial effusion by echocardiography. If a thickened pericardium is found during the window procedure, early pericardiectomy is strongly encouraged.
Uremic pericarditis remains a significant cause of morbidity and mortality in most hemodialysis programs. A review of the literature and out own experience show that uremic pericarditis should be vigorously treated when detected. Usually an increase in the dialysis program with regional heparinization is sufficient to control the pericarditis. When signs of pericardial effusion are manifested, patients often progress rapidly to cardiac tamponade. A surgical anterolateral pericardiectomy is the most satisfactory measure in controlling pericardial effusion and preventing fatal cardiac tamponade. Although these patients have severely impaired renal function, the operation can be performed safely with a low morbidity and mortality.
Purulent pericarditis is rapidly fatal if untreated [1,2]. With increased development of bacterial resistance to antibiotics, severe bacterial infections in children are becoming more frequent [3,4]. We report two children with purulent pericarditis who presented in a 1-month period for evaluation of acute abdominal distention and signs of sepsis. In both, one evaluated with computed tomography (CT) and one with ultrasound, abdominal findings included periportal edema, gallbladder wall thickening, and ascites secondary to right heart failure from cardiac tamponade. Radiologists should be aware that children with purulent pericarditis may have a normal heart size on radiographs, present with acute abdominal symptoms, and demonstrate findings of right sided heart failure on abdominal imaging.
Stage One ST segment deviations are virtually diagnostic of acute pericarditis when typically distributed among limb and precordial ECG tracings. Atypical ECG responses include absence of ST deviations, which conceals the diagnosis, and restricted distribution of ST deviations, which suggests myocardial injury. Among 44 consecutive patients with acute pericarditis, 19 (43%) had atypical ECGs. Although all 19 had a pericardial rub, eight had no ST deviations in the limb leads and seven developed no ST changes, including three with no ECG abnormalities of any kind. Patients with typical ECGs by ST segment criteria were more likely to progress to T wave inversion. PR segment deviations occurred in 14 patients with typical, and 14 with atypical ECGs. In four of the latter, the PR segment shifts were the only ECG sign. Presence or absence of heart disease and etiology of pericarditis could not be statistically associated with particular electrocardiographic responses.
Acute pericarditis was recognized in six of 1,316 patients undergoing percutaneous transluminal coronary angioplasty (PTCA) between September, 1980 and December, 1984. "Atypical" chest pain different from the patients' usual exertional angina pectoris accompanied by a low grade fever and a pericardial friction rub on cardiac auscultation was considered diagnostic. Cardiac enzymes (CK-MB) were mildly elevated in three of six patients. None had perfusion defects on thallium-201 perfusion images. Serial ECG's showed minor ST-T abnormalities in five of six, while only one had the "classical" generalized ST elevation commonly expected with acute pericarditis. No patient had occlusion of the vessel undergoing PTCA nor compromise of any branch vessels in the region of the stenosis. All patients had significant dissection at the site of PTCA which may cause a regional, localized acute pericarditis not recognized by standard 12-lead ECG records.
In this report, we describe a patient who had purulent Nocardia asteroides pericarditis. In addition, we identified 13 previously suspected and reported cases of Nocardia pericarditis, but only 5 of these studies reported isolation of Nocardia from cultures of pericardial fluid or pericardium. Analysis of the clinical course of these five patients and our patient revealed the importance of long-term sulfonamide antibiotic therapy in combination with surgical pericardial drainage procedures. In our review, only patients who received antibiotics and underwent pericardiectomy survived. Our case substantiates the excellent penetration of sulfisoxazole into the pericardial fluid, even with oral administration of the drug, and provides evidence in support of aggressive management of Nocardia pericarditis.
By means of two different IgM-capture assays, enterovirus-specific IgM responses were shown in 9 of 14 (64%) patients with chronic relapsing pericarditis. This finding suggests persistent enterovirus infection, particularly coxsackie B virus infection. IgM responses persisted for at least 1 year and for up to 10 years after onset of symptoms. In contrast, patients with acute enterovirus infections, including acute pericarditis, had transient responses. Among patients with acute pericarditis, the level of IgM antibody was significantly higher in those who subsequently relapsed (mean 1.21, range 0.6-2.0 optical density [OD] units) than in those who did not (0.4, 0.2-0.9 OD units; p less than 0.01). Of 86 patients with dilated cardiomyopathy, 28 (33%) showed enterovirus-specific IgM responses which were present for up to 19 months before transplantation and persisted up to 4 years afterwards. Although the distribution of HLA types in these patients was similar to that in the general population, the frequency of the HLA A2 haplotype was significantly higher in those who were IgM positive. IgM antibody was significantly more common in those who had had symptoms for longer than a year before transplantation than in those with a shorter duration of symptoms (1 of 21 vs 8 of 23; p less than 0.02). Persistent virus-specific serum IgA responses were also shown in patients with chronic cardiac disease.
Acute pericarditis is almost invariably associated with sinus tachycardia. Recent-onset chest pain in the presence of (sinus) bradycardia is considered to be associated with an acute ischemic syndrome rather than acute pericarditis. This report describes a patient with acute pericarditis initially presenting with sinus bradycardia, probably due to a vasovagal response to (chest) pain.
Pericarditis is a common but frequently subclinical entity. There are a number of causes, including infection, systemic illness, cardiac disease, trauma, and neoplasm. Iatrogenic causes include surgery, cardiac instrumentation, irradiation, and medications. The clinical presentation varies, depending on the cause. Chest pain and dyspnea are characteristic complaints. A typical progression of ECG changes occurs during the course of acute pericarditis. These changes occasionally require differentiation from those of acute myocardial infarction or normal variant ST segment elevation. Echocardiography is the most sensitive technique for detecting the presence of pericardial effusion. In addition, a number of echocardiographic findings are characteristic of larger effusions and cardiac tamponade. Any form of pericarditis may lead to the development of cardiac tamponade. Malignant effusion is probably the most common single cause.
Constrictive pericarditis is a rare complication of rheumatoid arthritis, with 78 published cases. We report a new typical case where the pericardial disease was associated with a severe seronegative rheumatoid arthritis of 17 years duration. Constrictive pericarditis generally occurs in men (62.8% of all cases) aged 52.4 +/- 11.5 years. Its clinical features are identical with those of constrictive pericarditis due to other causes. Diagnosis rests on echocardiography and, chiefly, on right heart catheterization. The arthritis is seropositive in 85.7% of the cases, frequently nodular (75%) and advanced. There is no relation between its duration (mean: 9.6 +/- 7.4 years) and the occurrence of the pericardial pathology. The pericardial fluid has no specific abnormality. Histology shows fibrosis and a non-specific inflammatory cell infiltrate. Immunoglobulin and complement deposits in the walls of the pericardial vessels are detected by immunofluorescence. The only treatment is pericardiectomy; without it the disease is constantly lethal.
A 59-year-old woman suffering from rheumatoid arthritis was admitted with pleural empyema and pericarditis due to non-encapsulated H. influenzae, and developed signs of cardiac tamponade. Purulent pericarditis resolved after ultrasound-guided percutaneous aspiration and systemic antimicrobial therapy. Serial echocardiographic examinations showed a slowly vanishing effusion. Long term follow-up revealed no evidence of pericardial constriction. This case illustrates that life-threatening purulent pericarditis in an immunocompromised patient may respond well to non-surgical treatment.
M-mode echocardiograms from 40 patients with proven constrictive pericarditis and 40 subjects without evidence of cardiac disease were reviewed for features previously described in constrictive pericarditis. In this large series, no single feature of the M-mode echocardiogram could be considered diagnostic, although a pattern of normal left ventricular size and systolic function, mild left atrial dilation, flattened diastolic left ventricular posterior wall motion and abnormal septal motion was found in most patients. It is concluded that the M-mode echocardiogram can provide findings suggestive of constrictive pericarditis but must be used in conjunction with hemodynamic and other studies to establish the diagnosis.
This report describes the case of a young woman who presented to an emergency department with severe abdominal pain and shock. The patient was found to have pericardial tamponade due to a massive pericardial effusion. On further evaluation, the etiology of this effusion was considered to be secondary to hypothyroidism with concominant acute viral pericarditis leading to a fulminant tamponade. The presentation, differential diagnosis, and management of pericardial effusion and tamponade secondary to hypothyroidism and viral pericarditis are discussed. The diagnosis of hypothyroidism in conjunction with acute viral pericarditis should be considered in patients presenting with unexplained pericardial effusion and tamponade.
This case reports coccidiomycosis presenting as pericarditis with tamponade rapidly progressing to effusive-constrictive pericarditis and death over 72 hours. Coccidiomycosis pericarditis is a rapidly progressing disease requiring early and complete pericardiectomy to avoid the hemodynamics of constriction. We illustrate the use of echocardiography in this case and demonstrate the histopathology. We review the literature and discuss therapy and management. Coccidiomycosis is often clinically unsuspected and unrecognized by the health care worker unfamiliar with the disease process.
Chylous ascites due to constrictive pericarditis is an extremely rare clinical entity, possibly caused by the augmented lymph production and high impedance to lymph drainage due to central venous hypertension. The authors describe a patient with chylous ascites caused by constrictive pericarditis in the absence of lymphatic obstruction. Cardiac catheterization is essential for the confirmation of accurate diagnosis of constrictive pericarditis. Magnetic resonance imaging of the heart is also very helpful in the diagnosis. The patient was symptom free and his ascites and edema completely resolved after pericardiectomy.
We report a case of pneumococcal pericarditis in a 13-year-old boy following allogeneic BMT from an HLA-identical unrelated donor. The post-transplant course was complicated by chronic GVHD which led to reinstitution of immunosuppressive therapy. Eight months after BMT the patient developed pericarditis with cardiac tamponade, and Streptococcus pneumoniae was isolated in the pericardiocentesis fluid. This is the first reported case of pneumococcal pericarditis after BMT. Although pericardial effusions after allogeneic BMT are often sterile and related to conditioning therapy or associated with chronic GVHD, rapid microbiological investigation and empirical treatment with antibiotics are necessary. Prophylaxis for pneumococcal infection in patients with chronic GVHD is recommended.
UNLABELLED: Effect of JTV-519 on AF. INTRODUCTION: A new cardioprotective drug, JTV-519, blocks Na+ current and inwardly rectifying K+ current and inhibits Ca2+ current. However, its role in atrial electrophysiology is unknown. We investigated the antiarrhythmic effects of JTV-519 on atrial fibrillation/flutter in the canine sterile pericarditis model. METHODS AND RESULTS: In nine dogs with sterile pericarditis, 38 episodes of sustained (>30 sec) atrial fibrillation (8 dogs) and 24 episodes of sustained atrial flutter (7 dogs) were induced by rapid atrial pacing. When atrial fibrillation or atrial flutter was sustained >15 minutes, it was cardioverted and reinduced. The inducibility of atrial fibrillation/flutter, the atrial effective refractory period, and the intra-atrial conduction time were compared before and after the continuous infusion of JTV-519 (0.03 mg/kg/min). JTV-519 significantly decreased the mean number of sustained atrial fibrillation episodes (from 4.2 +/- 2.9 to 0 +/- 0, P < 0.01). In contrast, atrial flutter was still inducible in 4 dogs after JTV-519 (from 2.7 +/- 2.5 to 1.6 +/- 2.1, P = NS). JTV-519 significantly prolonged effective refractory period (from 123 +/- 18 to 143 +/- 14 msec, from 127 +/- 18 to 151 +/- 12 msec, and from 132 +/- 13 to 159 +/- 9 msec at basic cycle lengths of 200, 300, and 400 msec, respectively, P < 0.01), but it did not affect the intra-atrial conduction time (from 47 +/- 11 msec to 48 +/- 11 msec, P = NS). CONCLUSION: JTV-519 had significant protective effects on atrial fibrillation in the canine sterile pericarditis model, mainly by increasing effective refractory period, suggesting that it may have potential as a novel antiarrhythmic agent for atrial fibrillation.