Pericarditis Acute Publications (2847)
Pericarditis Acute Publications
It was relieved by sitting up straight and did not radiate to her left arm or jaw. Computed tomography (CT) scan of the chest, posteroanterior and lateral views, showed a mild left pleural effusion with adjacent left basilar atelectasis/infiltrate. CT angiography of the chest with axial contrast showed mild left pleural effusion as well as a small pericardial effusion with bilateral lower lobe interstitial infiltrates. There was no evidence of pulmonary embolism. Electrocardiogram (EKG) showed no apparent ST segment elevation or depression that would be consistent with pericarditis, or acute ischemia or infarct. There was non-specific T wave abnormality. The patient was prescribed prednisone on a tapering dose. On follow-up visit, her condition significantly improved.
4 mg/dl) and elevated glutamic oxaloacetic transaminase (GOT; 1,050 U/L). Radiographs demonstrated an enlargement of the cardiac silhouette. The bird died 7 days after presentation, despite treatment with enrofloxacin, allopurinol, a preparation of hepatorenal protectors, and complex B vitamins with dextrose. Necropsy revealed severe fibrinohemorrhagic pericarditis with a 15 mm long and 2.5 mm diameter, rigid foreign body in the pericardial exudate. Microscopically, this foreign body was of vegetal origin.
Such cases have occurred predominantly in younger males, and involved a single causative species, namely Campylobacter jejuni. We report the first case of myopericarditis following Campylobacter coli enterocolitis, with illness occurring in an immunocompetent middle-aged female.
A 51-yo female was admitted to a cardiology unit with a 3-days history of chest pain. The woman had no significant medical history or risk factors for cardiac disease, nor did she report any recent overseas travel. Four days prior to the commencement of chest pain the woman had reported onset of an acute gastrointestinal illness, passing 3-4 loose stools daily, a situation that persisted at the time of presentation. Physical examination showed the woman's vital signs to be essentially stable, although she was noted to be mildly tachycardic. Laboratory testing showed mildly elevated C-reactive protein and a raised troponin I in the absence of elevation of the serum creatinine kinase. Electrocardiography (ECG) demonstrated concave ST segment elevations, and PR elevation in aVR and depression in lead II. Transthoracic echocardiogram (TTE) revealed normal biventricular size and function with no significant valvular abnormalities. There were no left ventricular regional wall motion abnormalities. No pericardial effusion was present but the pericardium appeared echodense. A diagnosis of myopericarditis was made on the basis of chest pain, typical ECG changes and troponin rise. The chest pain resolved and she was discharged from hospital after 2-days of observation, but with ongoing diarrhoea. Following discharge, a faecal sample taken during the admission, cultured Campylobacter spp. Matrix assisted laser desorption ionization time-of-flight (Bruker) confirmed the cultured isolate as C. coli.
We report the first case of myopericarditis with a suggested link to an antecedent Campylobacter coli enterocolitis. Although rare, myopericarditis is becoming increasingly regarded as a complication following campylobacteriosis. Our report highlights potential for pericardial disease beyond that attributed to Campylobacter jejuni. However uncertainty regarding pathogenesis, coupled with a paucity of population level data continues to restrict conclusions regarding the strength of this apparent association.
Surgical lung, pericardial, and pleural specimens yielded TB from a nodule in the right upper lobe and lung adenocarcinoma from the pericardium and pleura. Anti-tuberculous therapy was administered and gefitinib was subsequently started after the positive identification of epidermal growth factor receptor (EGFR) mutation (exon 19 deletion). The patient's general condition gradually improved with the anti-tuberculous and the EGFR-tyrosine kinase inhibitor (EGFR-TKI) treatment. Dual pathology is important to consider in patients with atypical radiological appearances. In those with proven EGFR mutation positive for lung cancer and pulmonary TB, sequential anti-tuberculous medication followed by EGFR-TKI treatment is advised.
We report a case of a 65-year-old man who presented with a 3-week history of fever with chills, non-productive cough and dyspnea. The case was diagnosed by positivity of acid-fast staining, culture and polymerase chain reaction (PCR) of the aspirated pericardial fluid and treated promptly with antituberculosis drugs. The patient showed complete recovery.
These clinical and paraclinical aspects were: stasis hepatomegaly with hepatojugular reflux, pulmonary congestion with stasis rales, peripheral edema, transudative polyserositis - pericarditis, hydrothorax, ascites, dilatation of inferior vena cava and suprahepatic veins, decrease of arterial blood pressure, tissue and cutaneous vasoconstriction. Anatomical and clinical aspects, with major alterations (Vth degree hepatomegaly, polyserositis, peripheral edema, tachyarrhythmic heart contractions, hypotension, pallor accentuated by vasoconstriction) acutely installed in a previously healthy young person, require a rapid lesions diagnosis and emergency treatment due to vital risk, control of acute heart failure manifestations remission and proper monitoring. Differential diagnosis was focused on determining possible aspects like: acute heart failure (of various etiology), internal post-traumatic lesions or hemorrhages, tuberculosis polyserositis, collagenosis, nephrotic syndrome, protein deficiencies, neoplasia with hepatic determinations, hematological diseases (lymphomas, leukemias), considered in young patients. Severe visceral, vascular and tissular pathological alterations were reactively induced in a young person, by stasis and hypoperfusion due to hypodiastolic heart failure caused by persistent supraventricular tachyarrhythmia triggered post-traumatic, on a proarrhythmic structural heart.
Among TNFRSF1A variants, the low-penetrance p.Arg92Gln variant represents the most commonly detected, and is typically associated with mild and short episodes, with a higher tendency to spontaneous resolution, and less familial association than the structural TNFRSF1A mutations. Pericardial involvement is rare but a well-known clinical feature of TRAPS, with a significant increased rate in those adult patients in whom the onset of the disease occurred during adulthood. Moreover, idiopathic recurrent acute pericarditis has also been occasionally described as a clinical presentation of TRAPS. However, cardiac tamponade is an unusual initial manifestation of the disease. Herein, we present a brief review based on the description of the exceptional case of a 35-year-old female patient who presented with recurrent pericardial effusions and cardiac tamponade. TNFRSF1A analyses showed a heterozygous genotype for the low-penetrance p.Arg92Gln variant. Due to disease severity, the patient was treated with the anti-interleukin-1 drug anakinra, showing a prompt resolution of her clinical manifestations.
The treatment of ACS consists of an immediate anti-ischemic therapy, anti-thrombotic therapy and invasive coronary diagnostics with subsequent interventional or operative revascularization therapy. The timing of invasive management is essentially determined by the individual patient risk, with the exception of STEMI where interventional revascularization must be undertaken within 120 min of diagnosis. In this context the GRACE 2.0 and TIMI risk score have become established as reliable tools. Another rare but fatal cause of acute chest pain is aortic dissection. An abrupt onset of tearing and sharp chest pains, deficits in pulse as well as the presence of high-risk factors, such as advanced age, arterial hypertension, atherosclerosis, known collagenosis and previous aortic or coronary artery procedures are highly indicative for aortic dissection and additional diagnostic imaging and the highly sensitive D‑dimer should be undertaken. Additionally, inflammatory diseases, such as pericarditis and myocarditis can be associated with chest pains and mimic the character of ACS and should also be considered in the differential diagnostics.
In routine clinical practice, acute pericarditis can be associated with myocarditis due to their overlapping etiologies.