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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary embolism is commonly fatal, yet notoriously difficult to detect. Diagnosis often relies on the ventilation-perfusion radionuclide scan, which itself is frequently equivocal. It has been suggested that if the equivocal ventilation-perfusion scan is interpreted in the light of clinical information, diagnostic accuracy can be improved. However, which features in the history should be considered? In this study of 197 patients undergoing ventilation-perfusion scanning, the clinical data of the 98 patients with either high-probability or normal scans were compared to the scan findings. The presence of a deep vein thrombosis was significantly associated with a high probability scan, whereas the presence of constant chest pain was significantly associated with a negative scan. Classical symptoms for pulmonary embolism, namely pleuritic chest pain and hemoptysis, were poor predictors of high-probability scans. Consequently, the authors advise considerable caution when using the clinical data to aid the interpretation of the equivocal lung scan in the individual case.
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PMID:Pulmonary embolism. Is the clinical history a useful adjunct to aid the interpretation of the equivocal lung scan? 884 64

Fever after a cardiac operation is commonly caused by myocardial infarction, postpericardiotomy syndrome, post-myocardial infarction syndrome (Dressler's syndrome), or postperfusion syndrome resulting from cytomegalovirus infection. Postpericardiotomy syndrome and post-myocardial infarction syndrome are autoimmune disorders characterized by eosinophilia, pleuritic chest pain, and pleural effusions. In contrast, the diagnosis of postperfusion syndrome caused by cytomegalovirus is suggested if the patient has a mild sore throat, no pleural component or chest pain, no eosinophilia, and atypical lymphocytosis. The syndromes of injury after cardiac surgical procedures are diagnoses of exclusion, but the diagnosis of postperfusion syndrome ("40-day postoperative fever") may be made on the basis of elevated cytomegalovirus IgM titers.
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PMID:Postpericardiotomy syndrome. 909 May 22

When faced with a patient with acute chest pain, clinicians must distinguish myocardial infarction (MI) from all other causes of acute chest pain. If MI is suspected, current therapeutic practice includes deciding whether to administer thrombolysis or primary percutaneous transluminal coronary angioplasty and whether to admit patients to a coronary care unit. The former decision is based on electrocardiographic (ECG) changes, including ST-segment elevation or left bundle-branch block, the latter on the likelihood of the patient's having unstable high-risk ischemia or MI without ECG changes. Despite advances in investigative modalities, a focused history and physical examination followed by an ECG remain the key tools for the diagnosis of MI. The most powerful features that increase the probability of MI, and their associated likelihood ratios (LRs), are new ST-segment elevation (LR range, 5.7-53.9); new Q wave (LR range, 5.3-24.8); chest pain radiating to both the left and right arm simultaneously (LR, 7.1); presence of a third heart sound (LR, 3.2); and hypotension (LR, 3.1). The most powerful features that decrease the probability of MI are a normal ECG result (LR range, 0.1-0.3), pleuritic chest pain (LR, 0.2), chest pain reproduced by palpation (LR range, 0.2-0.4), sharp or stabbing chest pain (LR, 0.3), and positional chest pain (LR, 0.3). Computer-derived algorithms that depend on clinical examination and ECG findings might improve the classification of patients according to the probability that an MI is causing their chest pain.
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PMID:The rational clinical examination. Is this patient having a myocardial infarction? 1005 39

A 29 year old white man presented to the emergency room with new onset pleuritic chest pain and shortness of breath. He was initially diagnosed as having viral pericarditis and was treated with non-steroidal anti-inflammatory drugs. A few weeks later he developed recurrent chest pain with cough and haemoptysis. Chest radiography, cardiac examination, transthoracic and transoesophageal echocardiography pointed to a mass that arose from the posterior wall of the right atrium, not attached to the interatrial septum, which protruded into the lumen of the right atrium causing intermittent obstruction of inflow across the tricuspid valve. Contrast computed tomography of the chest showed a right atrial mass extending to the anterior chest wall. The lung fields were studded with numerous pulmonary nodules suggestive of metastases. A fine needle aspiration of the pulmonary nodule revealed histopathology consistent with spindle cell sarcoma thought to originate in the right atrium. Immunohistochemical stains confirmed that this was an angiosarcoma. There was no evidence of extracardiac origin of the tumour. The patient was treated with chemotherapy and radiation. This case highlights the clinical presentation, rapid and aggressive course of cardiac angiosarcomas, and the diagnostic modalities available for accurate diagnosis.
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PMID:Primary right atrial angiosarcoma mimicking acute pericarditis, pulmonary embolism, and tricuspid stenosis. 1021 78

Patients with idiopathic pulmonary fibrosis (IPF) are at risk for a variety of acute pulmonary complications, including pneumothorax and pneumomediastinum. Our aim was to describe the radiographic and CT findings and to determine the frequency of complicating spontaneous pneumothorax and pneumomediastinum in patients with IPF. A retrospective study was performed including 78 consecutive patients who underwent CT scanning of the chest and who had confirmed IPF. The chest radiographs and CT scans were reviewed by two chest radiologists and classified as showing features of extra-alveolar air collections. The CT scans showed extra-alveolar air in 9 (11.2 %) of 78 patients (six females and three males; age range 26-90 years, mean age 65 years). Pneumothorax was demonstrated in 5 patients and mediastinal air collections in 4 patients. All patients had dyspnea for 1-48 months (mean 14 months). Of the five cases with pneumothorax, four developed acute onset of dyspnea and pleuritic chest pain, whereas 1 patient had a relatively stable functional status. Of the 4 patients with pneumomediastinum, three presented with nonpleuritic chest pain and acute dyspnea. Chest radiographs showed extra-alveolar air in 6 patients. Three cases were predicted to be negative by chest radiographs. Follow-up CT showed that air collections had resolved completely in 5 patients. Two patients died of respiratory failure within 4 months after CT. Extra-alveolar air should be recognized as a relatively common IPF-related complication. Chest CT is a useful imaging method in determining air collections in patients with IPF that become acutely breathless and their chest radiograph fails to reveal the presence of extra-alveolar air.
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PMID:Spontaneous pneumothorax and pneumomediastinum in IPF. 1066 25

Pleuritic chest pain in patients on a rehabilitation unit may be caused by several conditions. We report 2 cases of postpericardiotomy syndrome (PPS) as a cause of pleuritic pain. PPS occurs in 10% to 40% of patients who have coronary bypass or valve replacement surgery. The syndrome is characterized by fever, chest pain, and a pericardial or pleural friction rub. Its etiology is believed to be viral or immunologic. The syndrome can be a diagnostic challenge, and an increase in length of hospitalization because of it has been documented. Identified risk factors for PPS include age, use of prednisone, and a history of pericarditis. A higher incidence has been reported from May through July. Many patients undergo a battery of expensive procedures before PPS is diagnosed. The pain is sharp, associated with deep inspiration, and changes with position. Pleural effusions may be present and tend to occur bilaterally. Pericardial effusions are a documented complication. A pericardial or pleural rub may be present and is often transient. Serial auscultation is important. Laboratory work provides clues with a mild leukocytosis and an elevated erythrocyte sedimentation rate. However, this does not provide the definitive diagnosis. Cardiac enzymes are not reliably related to the syndrome. An electrocardiogram will show changes similar to those associated with pericarditis. The patient may have a fever, but it is rarely higher than 102.5 degrees F. Complications include pericardial effusions, arrhythmias, premature bypass graft closure, and cardiac tamponade. Treatment consists of a 10-day course of nonsteroidal anti-inflammatory drugs.
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PMID:The postpericardiotomy syndrome as a cause of pleurisy in rehabilitation patients. 1076 45

Pericarditis should be considered in any patient complaining of chest pain and/or dyspnea who is taking a product that contains mesalamine or sulfasalazine. A 41-year-old woman was taking mesalamine 800 mg 3 times/day for 3 weeks before hospital admission. She complained of sharp, pleuritic chest pain that radiated down both arms and increased in intensity when lying down. She was diagnosed with pericarditis based on clinical presentation and electrocardiogram findings. Differential diagnoses for myocardial infarction, systemic lupus erythematosus, and viral or bacterial causes were ruled out based on subjective and objective data. Mesalamine-induced pericarditis was considered on hospital day 2, and the drug was discontinued at discharge on day 3. Clinicians should be aware of this potential drug-related complication, as the relationship between mesalamine or sulfasalazine and pericarditis has been reported rarely in the literature.
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PMID:Possible mesalamine-induced pericarditis: case report and literature review. 1189 96

A 55-year-old man presented with a 3-week history of dry cough and left pleuritic chest pain with a new exudative pleural effusion. Sixteen years earlier, he was diagnosed with sarcoidosis presenting with hilar lymphadenopathy, erythema nodosum, mildly disturbed liver function tests and noncaseating granulomata on liver biopsy, with no evidence of pulmonary parenchymal disease. He was treated with prednisone and in recent years maintained at a low daily dose, until it was eventually discontinued two years prior to his present illness. There was no evidence of infection or malignancy, and the fluid resolved following treatment with naproxen. Three weeks later the patient presented with sudden onset of dyspnea and left chest pain. After starting intravenous heparin for suspected pulmonary emboli, the patient developed hemodynamic instability which was accompanied by abdominal tenderness and decreasing hematocrit. Splenic rupture was diagnosed, and the patient underwent splenectomy. Pathology specimens revealed a hemorrhagic infarct with subcapsular hematoma, and numerous noncaseating granulomata within the splenic tissue. This patient had recurrent sarcoidosis with two rare manifestations of the disease, 2 years after withdrawing low dose prednisone, given for a prolonged time. The possibility of reemergence of the disease in organs other than the organs involved in the initial presentation should always be considered in sarcoidosis.
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PMID:Pleural effusion with splenic rupture as manifestations of recurrence of sarcoidosis following prolonged remission. 1258 4

A 69-year-old white woman presented at our emergency room with right-side pleuritic chest pain, fever, and tachycardia. Results of the physical examination, routine laboratory tests, and chest radiography were unexceptional. An electrocardiogram showed ST elevation in leads V(1) through V(3) with T-wave inversion. Because of the chest pain and the ST elevation, the patient underwent emergency cardiac catheterization, which showed no coronary artery stenosis. A computed tomographic scan of the chest showed pulmonary infiltration in the right middle lobe and the lingula of the left upper lobe; pneumonia was diagnosed, and appropriate antibiotic therapy was started. The electrocardiographic changes met the criteria for type-1 Brugada pattern. Brugada syndrome is an arrhythmogenic disease caused in part by mutations in the cardiac sodium channel gene SCN5A. When the sodium current is disrupted, the outward transient current at the end of phase 1 of the action potential becomes unopposed. This creates a voltage gradient between the epicardium and endocardium, especially in the right ventricular wall, which leads to J-point elevation in leads V(1) through V(3). Fever exaggerates this defect in sodium channels. In our patient, the pleuritic chest pain was caused by the pneumonia, and the ST elevation was probably related to Brugada syndrome, unmasked by the febrile episode. Brugada syndrome can be associated with ventricular tachycardia or fibrillation; the only treatment proven to prevent sudden death is placement of an implantable cardioverter defibrillator, which is recommended in symptomatic patients or in those with ventricular tachycardia induced during electrophysiologic studies.
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PMID:Brugada syndrome unmasked by pneumonia. 1721 81

Pleural effusion is an uncommon manifestation of amiodarone toxicity and is usually associated with amiodarone-induced interstitial pneumonitis. We describe a 70-year-old woman who came to the emergency department with bilateral pleuritic chest pain and malaise 4 weeks after her amiodarone dose was increased from 200 mg/day to 600 mg/day. She had bilateral exudative pleural effusions without associated pneumonitis. She was diagnosed with amiodarone-induced pleural effusions after a thorough workup during her hospitalization excluded other causes for the effusions. Due to intractable arrhythmias, the patient's amiodarone was not discontinued, and she was discharged home. Four days later at a follow-up visit at the pulmonary clinic, the patient complained of worsening chest pain as well as dyspnea and cough. A computed tomography scan showed left-sided pleural effusion with multiple loculations. She underwent a pulmonary vein isolation procedure, and amiodarone was discontinued. She was treated with prednisone 40 mg/day, tapered over the next 2 weeks. Three weeks after the amiodarone was stopped, the patient was asymptomatic, and a chest radiograph showed complete resolution of the effusions. Review of the patient's medical records revealed that she had experienced similar symptoms and exudative pleural effusions 2 years earlier after a similar dose escalation of amiodarone; the symptoms and pleural effusions resolved after the amiodarone dosage was reduced. Use of the Naranjo adverse drug reaction probability scale indicated that the association between the pleural effusions and amiodarone was highly probable (score of 9). This case report emphasizes that amiodarone should be considered in the differential diagnosis of patients with exudative effusions after a thorough workup has excluded other causes. Amiodarone should be replaced with alternative antiarrhythmic therapy if clinically feasible, and corticosteroids may be beneficial.
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PMID:Amiodarone-induced loculated pleural effusion: case report and review of the literature. 2009 96


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