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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 50-year-old male underwent successful percutaneous mitral valvuloplasty for restenosis after surgical commissurotomy. Trans-septal puncture was difficult. Following the procedure, the patient developed chest pain and signs of systemic venous congestion, yet no hemodynamic collapse. Echocardiographic evaluation revealed a cystic mass compressing the right atrium, not communicating with the atrial cavity, mostly an intramural hematoma. The case was managed conservatively, and serial echocardiographic follow-up showed gradual reduction in size until ultimate disappearance of the mass 1 month later. In conclusion, right atrial intramural hematoma is a possible complication of mitral valvuloplasty, readily detected by echocardiography, and amenable for conservative management.
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PMID:Right atrial wall hematoma following percutaneous mitral valvuloplasty. 1963 35

Diagnosing acute Stanford type A aortic dissection with the uncommon involvement of the left main coronary artery(LMCA) remains challenging for the emergency physician because it can resemble acute myocardial infarction with cardiogenic shock. The following case report illustrate this infrequent but critical situation. A 52-year-old woman with a history of hypertension awakened with acute retrosternal chest pain accompanied by nausea and vomiting. She was referred to our hospital for primary coronary intervention because of acute myocardial infarction with cardiogenic shock. Coronary angiography indeed revealed LMCA occlusion. Subsequently successful percutaneous coronary intervention with stent implantation was performed, followed by immediate clinical improvement of the patient. Soon after admission at the coronary care unit, severe chest pain, hypotension, and electrocardiographic signs of diffuse myocardial ischemia relapsed. Control coronary angiography,however, showed no in-stent thrombosis. Review of clinical examination revealed an aortic regurgitation murmur. Because of this dynamic pattern of (1) signs of acute myocardial ischemia, (2) relapse of hemodynamic collapse, and (3) unaltered control coronary angiography together with the confirmed aortic regurgitation at transthoracic echocardiography, the patient was suspected of having aortic dissection. Transesophageal echocardiography revealed Stanford type A aortic dissection with severe eccentric aortic regurgitation and no pericardial effusion. Emergent valve-sparing aortic replacement was performed. The patient recovered completely. In this case, the lifesaving element was primary coronary intervention with stenting of the LMCA preventing extensive myocardial damage followed by a surgical correction of the aorta.
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PMID:Acute myocardial infarction with cardiogenic shock in a patient with acute aortic dissection. 1968 31

A 71-year-old man who presented to hospital with chest pain and a history of cardiovascular disease was repeatedly hospitalised over the course of a month for care that included multiple investigations, intensive care, transfer to and from a metropolitan hospital, discharge, and readmissions for collapse, hemiparesis, and vision change. The medical team excluded underlying disease related to his initial chest pain and subsequent neurological symptoms. A search for (undisclosed) prior hospitalisations revealed multiple previous admissions and invasive investigations at hospitals across Australia, resulting in a diagnosis of Munchausen syndrome. Assuming that, despite interventions, patients with Munchausen syndrome or somatoform disorders often continue to seek care at other hospitals, we discuss the implications of this patient's behaviour for the health care system, society, and the risk to his own health. In our view, this case highlights conflicts between privacy legislation and doctors' mandates to protect the patient from harm, as well as their duty to attend to the financial viability of health services by communicating with other potential health care providers. The health care system and similar patients may benefit from efforts to educate doctors about this spectrum of disorders and from considering the implementation of a highly confidential, structured notification system.
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PMID:Patient privacy versus protecting the patient and the health system from harm: a case study. 1970 83

The aim of this audit was to determine a baseline for timing, numbers and case mix of detainees referred to hospital for medical assessment in order to review the effectiveness of existing custody procedures for the management of medical emergencies. Data was examined for the 3-month period January to March 2006. A total of 12015 detainees were processed during this period, 188 patients identified as requiring hospital assessment, a hospital transfer rate of 1.57% for the period, 80 cases (0.65%) were for potentially life threatening conditions. The health care team assessed 37.7% of all detainees and were recorded as involved in 151 of the 188 cases transferred (80%). The categories of patients sent to hospital included head injury (26/188 or 13.8%), overdose and poisoning (20/188 or 10.6%); chest pain (17/188 or 9.0%), collapse (12/188 or 6.4%), unrousable intoxicated (10/188 or 5.3%), possible drug swallowers (7/188 or 3.72%), breathing problems (4 or 2.12%), acute confusional state (3/188 or 1.6%), 2/188 had a query deep vein thrombosis, one diabetic problem and one acute allergic reaction. The largest category of all was for a miscellany of minor injury unit care.
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PMID:Audit of hospital transfers January to March 2006 from Sussex police custody. 2008 49

A 27-year-old weight lifter developed mild chest pain and dyspnea after 'bouncing' a 250-lb barbell off his chest. A plain radiograph revealed a large, right-sided pneumothorax with collapse of the lung. He underwent an emergency tube thoracostomy. One month later, he resumed lifting without recurrence. This case report demonstrates the need to be responsive to dyspnea and chest pain in healthy, young athletes. Pneumothorax in sports is uncommon, but cases of spontaneous and trauma-induced pneumothorax have been reported. Initial symptoms may be minimal, but prompt recognition can help prevent respiratory and cardiovascular compromise. Treatment depends in part on the size of the pneumothorax.
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PMID:Pneumothorax in a weight lifter: the importance of vigilance. 2008 37

Thrombolysis with intravenous tissue (IV) plasminogen activator (tPA) is considered for patients with acute ischemic stroke falling within the described inclusion criteria defined by The National Institute of Neurological Disorders and Stroke (NINDS) rtPA trial. Complications of IV thrombolysis with tPA are commonly related to hemorrhage, anaphylaxis, or arterial occlusion. We describe two cases of acute myocardial infarction (MI) following IV tPA infusion for acute stroke. One of the patients had underlying ischemic heart disease (IHD) while the other did not have any prior IHD. Both had presented with acute ischemic stroke within the window period of thrombolysis and had no contraindications for thrombolysis. Both the patients succumbed due to myocardial infarction and cardiovascular collapse due to new onset arrhythmias. Acute MI immediately following IV tPA for stroke is a rare but serious complication. The disruption of intracardiac thrombus and subsequent embolization to coronary arteries may be an important mechanism in the occurrence of MI after administration of tPA for acute ischemic stroke. As both the patients succumbed before the arrangement for coronary angiography, the demonstration of intracardiac or intracoronary thrombus was not possible. But clinically, the presence of chest pain with elevated troponin levels and ST segment elevation pointed to MI. We suspect that fragmentation and lysis of intracardiac thrombus may result in MI after use of tPA for acute ischemic stroke, though the remote possibility of simultaneous occurrence of two atherosclerotic events MI and stroke exists.
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PMID:Acute myocardial infarction following intravenous tissue plasminogen activator for acute ischemic stroke: An unknown danger. 2043 51

Pulmonary sarcomas constitute only 0.1-0.5% of all primary lung malignancies. These tumors may derive from the lung parenchyma, bronchial tree or pulmonary arteries. The most important entity in the differential diagnosis is metastatic synovial sarcoma. A 76-years-old woman was admitted for investigation of a fever, productive cough, dyspnea, weight loss and left-sided chest pain which had been present for one month. A chest computerised tomography showed enlarged mediastinal lymph nodes were observed, as well as a left-sided pleural effusion. Thoracentesis revealed hemorrhagic pleural effusion which was exudate and lymphocyte predominant, closed pleural biopsy showed chronic inflammation. Left sided thoracoscopy was performed under local anesthesia, total collapse of left lung and multiple pleural nodules were observed on the visceral pleura multiple biopsies were obtained from those nodules. Pathologic examinations revealed "synovial sarcoma". As skeleton single photon emission tomography was unremarkable, primary pleuropulmonary synovial sarcoma was decided as diagnosis and chemotherapy was planned for the patient. Primary pleuropulmonary synovial sarcoma is a rare neoplasm of lung and pleura but it is rare entity.
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PMID:An old woman with weight loss and chest pain. 2051 34

A 16-year-old boy was hospitalized for fever, chest pain, and cardiovascular collapse. Transthoracic echocardiography revealed a 30-mm circumferential echogenic "porridge-like" pericardial effusion with signs of cardiac tamponade. Tuberculosis (TB) was suspected because of its prevalence in Djibouti. Emergency pericardiocentesis was attempted, but only 10 ml of pericardial fluid was obtained. Subxiphoid pericardiotomy and drainage were then performed, and pericardial fibrinous pockets were surgically collapsed. Antituberculosis chemotherapy was given, and the pericardial effusion progressively disappeared without corticosteroids. The diagnosis of TB was subsequently confirmed by cultures of the pericardial fluid. A pericardial biopsy was normal. After 3 months of follow-up, there was no sign of constrictive pericarditis. Pericardiocentesis may fail in cases of advanced-stage fibrinous TB pericardial effusion. Thus, pericardiotomy with complete open draining is the only lifesaving procedure.
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PMID:Porridge-like tuberculous cardiac tamponade: treatment difficulties in the Horn of Africa. 2054 56

Pericardial effusion may be detected as an incidental finding during echocardiography or following a diagnostic imaging study for a symptomatic patient. When a pericardial effusion is detected the first step is to assess its size, hemodynamic importance, and possible associated diseases. The more common causes of pericardial effusions include infections (viral, bacterial, especially tuberculosis), cancer, connective tissue diseases, pericardial injury syndromes, metabolic causes (i.e. hypothyroidism), myopericardial and aortic diseases. The relative frequency of different causes depends on the local epidemiology, the hospital setting and the diagnostic protocol that has been adopted. Many cases still remain idiopathic in developed countries, whereas tuberculosis is the dominant cause in developing countries. Specific testing should be performed according to clinical suspicion. The presence of elevated inflammatory markers and other criteria (chest pain, pericardial rubs, ECG changes) suggest pericarditis and management should be directed accordingly. Treatment should be targeted at the etiology as much as possible. Nevertheless, when diagnosis is still unclear, or idiopathic and inflammatory markers are elevated, empiric anti-inflammatory therapy may be worthwhile. A true isolated effusion may not require a specific treatment if the patient is asymptomatic, but large ones have a theoretical risk of progression to cardiac tamponade (up to one-third) if subacute with signs of right-sided collapse, and especially chronic (>3 months). Pericardiocentesis alone may be curative for large effusions but recurrences are also common and pericardiectomy or less invasive options (i.e. pericardial window) should be considered whenever fluid re-accumulates (especially with tamponade), becomes loculated, or biopsy material is required.
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PMID:Triage and management of pericardial effusion. 2081 14

Unexpandable lung is the inability of the lung to expand to the chest wall allowing for normal visceral and parietal pleural apposition. It is the direct result of either pleural disease, endobronchial obstruction resulting in lobar collapse, or chronic atelectasis. Unexpandable lung occurring as a consequence of active or remote pleural disease may present as a post-thoracentesis hydropneumothorax or an effusion that cannot be completely drained because of the development of anterior chest pain. Pleural manometry is useful for identifying unexpandable lung during initial pleural drainage. Unexpandable lung occurring as a consequence of active or remote pleural disease may be separated into two distinct clinical entities termed trapped lung and lung entrapment. Trapped lung is a diagnosis proper and is caused by the formation of a fibrous visceral pleural peel (in the absence of malignancy or active pleural inflammation). The mechanical effect of the pleural peel constitutes the primary clinical problem. Lung entrapment may result from a visceral pleural peel secondary to active pleural inflammation, infection, or malignancy. In these cases, the underlying malignant or inflammatory condition is the primary clinical problem, which may or may not be complicated by unexpandable lung due to visceral pleural involvement. The recognition of trapped lung and lung entrapment as related, but distinct, clinical entities has direct consequences on clinical management. In our practice, pleural manometry is routinely performed during therapeutic thoracentesis and is useful for identification of unexpandable lung and has allowed us to understand the mechanisms surrounding a post-thoracentesis pneumothorax.
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PMID:The unexpandable lung. 2117 37


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