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

In 544 autopsy cases during the period from 1984 through 1990 at National Okura Hospital, there were 7 cases of fatal saddle pulmonary thromboembolism (1.3%). Pulmonary thromboembolism was included in the differential diagnosis, but not as a primary consideration. Therefore, no case was diagnosed antemortem. Saddle thromboembolus is defined here as a thromboembolus which impacted in the main pulmonary artery or lodged astride the bifurcation. The cases were 5 females and 2 males ranging in age from 53 to 76 years. During the clinical course of the initial disease, sudden symptoms including dyspnea, chest pain or tachypnea developed, and death occurred within one hour or in a relatively short period of time. In case 6, sudden death followed removal of a central venous catheter inserted in the inferior vena cava one week previously. In cases 2, 3, and 5, deep vein thromboemboli were detected at postmortem examination. In cases 3 and 4, the patients were 3- and 5-days postoperative, respectively. Laboratory data obtained before death showed no abnormalities of hematologic and coagulation profiles. At autopsy, the pulmonary artery trunk was completely occluded by embolus, and thromboemboli were detected in the femoral and iliac veins in 3 cases. These thromboemboli were composed of fibrin and red cells enmeshed with platelets. On microscopic examination, endothelial disruption was not observed at the levels of the large and smaller pulmonary vessels, which underlies thrombosis in situ or creates a procoagulant environment. Proximal pulmonary thromboemboli were demonstrated in only one out of seven cases (Case 1). Saddle thromboembolism, in our limited observation, resulted from the impact of large floating embolus, emanating from elsewhere, against the large pulmonary artery, rather than the propagation of a smaller pulmonary embolus originating in a peripheral artery.
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PMID:[Autopsy-proven cases of fatal saddle thromboembolism in the pulmonary artery]. 827 12

There is little information on the prevalence and clinical presentation of acid-base abnormalities associated with cocaine toxicity. To address these issues, arterial blood gas results were evaluated in 156 cocaine-associated emergency department patient visits. Arterial blood gas results were obtained as part of the patient's clinical assessment. The majority of patients (52%) had a normal pH (7.35 to 7.45). Thirty-three percent of patients were acidotic, with a pH between 6.4 and 7.35. In 33 patients the acidosis was metabolic, with a HCO3- of 14 +/- 6 mmol/L. The acidosis was primarily respiratory in 18 patients, with evidence of hypoventilation. Hypoventilation was generally secondary to chest trauma or decreased mental status. Alkalosis (pH > 7.45) was observed in 15% of patients, and was usually respiratory, as evidenced by tachypnea and a low PCO2. These results indicate that metabolic and respiratory acid-base abnormalities are common during cocaine toxicity. Acidosis and alkalosis were associated with numerous patient presentations, including chest pain, shortness of breath, decreased mental status, trauma, and seizures. Acid-base abnormalities do not appear to be associated with a specific route of cocaine self-administration. Patients with a history of potential cocaine toxicity should be evaluated for acid-base abnormalities.
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PMID:Acid-base abnormalities associated with cocaine toxicity in emergency department patients. 830 47

The clinical and laboratory features in 62 patients with acute pulmonary embolism were analized. There were 26 males, and 36 females with mean age of 63 +/- 11 (range 37 to 90). The clinical symptoms include: dyspnea (92%), chest pain and/or chest tightness (65%), cough (50%), wheezing (29%), leg swelling (32%), hemoptysis (24%), syncope (18%), leg pain (10%). Clinical signs include: tachypnea (respiratory rate > or = 20 per minute) (79%), tachycardia (37%), deep vein thrombosis (29%), cyanosis (8%), fever (> 38.5 degrees C) (2%). The possible predisposing factors include: immobilization (18%), surgery (5%), deep vein thrombosis, ever(5%), malignancy (5%), pulmonary embolism, ever (3%). Arterial blood gas analysis (while patients breathed room air) revealed mean PH of 7.46 +/- 0.06, mean PO2 of 64.5 +/- 12.1 mmHg, mean PCO2 of 35.3 +/- 4.6 mmHg, mean Alveolar-arterial O2 difference of 36.5 +/- 16.6 mmHg. The electrocardiographic changes include; nonspecific ST-T change (61%), sinus tachycardia (20%), S1Q2T3 pattern (15%), atrial fibrillation (16%), incomplete right bundle branch block (10%), complete right bundle branch block (8%), atrial premature contraction (7%), paroxysmal supraventricular tachycardia (2%). The chest x-ray findings include: cardiomegaly (48%), regional hypovascularity (31%), atelectasis (5%), pleural effusion (5%), wedge-shaped infiltrate (3%), elevated diaphragm (6%). Venous plethysmography was performed in 49 of 62 patients. Of these 49 patients, 28 patients revealed positive finding. Of these 28 patients with positive finding, 18 patients had clinical evidence of deep venous thrombosis. The in-hospital mortality rate was 10% (6/62).
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PMID:[Pulmonary embolism: clinical and laboratory features in 62 patients]. 904 62

Venous thromboembolism shows a high incidence and a significant mortality. Even if valid methods are available, thromboembolism is underdiagnosed. There are a number of diagnostic difficulties. They concern the time of the diagnostic suspicion, the patient selection for the various procedures and their combination. These difficulties may be overcome by team work where specialists of different disciplines (surgeons, internists, experts in nuclear medicine, radiologists) integrate their competence to attain the established objectives. The integration results in "synergism", namely an added value greater than the sum of competences of the team components. Thus, an operational unit active 24 hours over 24 must be formed to diagnose and treat the largest number of cases of thromboembolism. To establish the clinical suspicion of thromboembolism is the first indispensable step for patient selection. Thromboembolism should be investigated in all patients with chest pain, dyspnea and tachypnea in the absence of preexisting cardiorespiratory disease. The team should evaluate the impact of signs and symptoms to establish a definitive clinical probability which can direct towards the suitable, least invasive imaging procedure. Perfusion scanning, when highly suggestive or normal, is conclusive. However in 70% of cases it is indeterminate. Thus it should be combined with other procedures and with the clinical assessment. In practice, many dubious cases remain unsolved. The team work represents an organizational response to this diagnostic and therapeutic inadequacy. The real change in strategy which has revolutionized the diagnosis of thromboembolism was the widespread use of color Doppler US in the diagnosis of deep vein thrombosis. Since pulmonary embolism as well as deep vein thrombosis are treated with the same therapy, it is adequate to document the thrombosis also in the absence of a definitive demonstration of embolism. The old-fashioned approach should be reversed and the investigation should be centered on the assessment of deep vein thrombosis: site, emboligenic potential, floating extremity and extension. The integration of the clinical assessment, scanning finding and color Doppler US lowers by about 20% the number of indeterminate cases and indicates the patients for whom pulmonary spiral CT or pulmonary angiography is required. In all patients with cardiorespiratory insufficiency still unsolved after the combination of noninvasive exams, pulmonary angiography or spiral CT is mandatory because of the high risk for death. The remaining ones can be followed with serial color Doppler US exams. The cost/benefit ratio shows that the noninvasive strategy is the least expensive, the least hazardous and the most effective. At present, effective therapies are available for thromboembolism. Standard heparin and low molecular weight heparin fractions, fibrinolytic agents, surgery and recently caval filters are playing a major role in secondary prophylaxis of pulmonary embolism. The therapeutic approach is conditioned by various factors: the features of thrombosis, the presence and entity of pulmonary embolism, the patient cardiorespiratory condition, possible contraindications for anticoagulant and fibrinolytic agents. The presence of such a number of variables makes the use of a therapeutic algorithm, difficult. In this phase, based on our experience we believe that the present solution lies in the activity of an operational team of experts who establish the treatment to be performed.
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PMID:Multidisciplinary approach to venous thromboembolism. 906 64

This paper is a review of the patients with pulmonary thromboembolism hospitalized at General hospital in Teanj starting from the first case recorded in 1980 till now and 172 patients were subjects of this study. Thromboembolism was a direct cause of death in 43.7% (75 patients). Clinical and laboratory records, etiology, chest radiography, ECG data of 89 patients hospitalised and treated in the last five years were analyzed in detail. The most frequent symptoms were dyspnea and tachypnea, often accompanied with other symptoms (84.2%), chest pain (65.2%), cough (52.4%), tachycardia (40.5%), hemoptysis (25.8%). At 74% of patients with pulmonary thromboembolism a significant simultaneous increase of all examined enzymes, except CPK was found. Pulmonary insufficiency (global or partial) was found at 75% of patients. According to our results, in 57.2% of the subjects the pathologic changes on Radiography (infiltrates of the lung, with or without affection of the pleura and changed position of diaphragm) were found, and 70.9% had changes on the ECG.
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PMID:[Clinical aspects of pulmonary thromboembolism]. 1032 Oct 63

Chest pain can arise from cardiovascular or noncardiovascular causes. Among the latter are the skin, the chest wall, intrathoracic structures, or subdiaphragmatic organs. The problem to attribute the chest discomfort to either the heart or extracardiac organs arises because the heart, pleura, aorta, and esophagus are all supplied by sensory fibers from the same spinal segments. In contrast to the diseases mentioned above, angina pectoris in sensu strictu is defined as chest pain or discomfort of cardiac origin that arises because of temporary imbalance between myocardial oxygen supply and demand. The metabolic oxygen requirements of the myocardium are essentially dictated by myocardial contraction since only a fraction of the consumed oxygen is needed by the quiescent heart. Therefore, the factors that primarily influence myocardial oxygen consumption include heart rate, the force of cardiac contraction, and myocardial wall tension, as determined by pressure (afterload), volume (preload), and wall thickness. Extracoronary diseases, e.g. hypertensive heart disease, aortic stenosis or cardiomyopathies, can influence these factors and induce angina pectoris (Figure 1). On the other hand, different diseases influencing the oxygen supply, e.g. anemia, can cause angina pectoris, too. In addition, the modulation of the coronary tone by mediators and cytokines can cause angina, coronary spasm being one example. The neurophysiological substrate of angina pectoris are ganglia which are present within the heart, particularly in epicardial fat. The sympathetic nervous system is the main conveyer of afferent pain fibers from the heart and pericardium, but many fibers may travel by the vagus and the phrenic nerves. Therefore, multiple thoracic structures may cause similar pain syndromes in the distressed patient. The blood supply of intrinsic cardiac ganglia arises primarily from branches of the proximal coronary arteries. Adenosine, among a number of substances, can modulate the activity generated by cardiac afferent nerve endings and intrinsic cardiac neurones. During myocardial ischemia adenosine is released in large quantities into the interstitial space. Given as an intravenous bolus to healthy volunteers or to patients with ischemic heart disease and angina pectoris, adenosine provokes angina pectoris-like pain, which is similar to habitual angina pectoris with regard to quality and location. But other mediators (e.g. bradykinin, histamine, prostaglandins, potassium, lactate) can be involved in the development of angina pectoris, too. As most emphasis should be given to the most serious causes first, the cardiologist has to consider ischemic cardiac disease in the differential diagnosis of nearly every case of acute chest pain. The differential diagnosis contains several causes of nonischemic cardiac chest pain. Dissecting aortic aneurysm may cause severe anterior chest pain that can be mistaken for myocardial infarction. Patients frequently will note the sudden onset of the pain rather than the relatively slower onset of ischemic pain. Furthermore, they feel as a tear and describe it as the most severe pain they have ever had. Pericarditis can be characterized as a sharp precordial knife-like pain that is often increased by lying down, breathing, swallowing, or any other thoracic motion. Radiation of pericardial pain is often relieved by sitting up or leaning forward. It may involve the shoulders, upper back, and neck because of the irritation of the diaphragmatic pleura. Acute pulmonary embolism is associated with severe chest pain. It may mimic acute myocardial infarction. Pulmonary embolism should be suspected when dyspnea or tachypnea seems to be disproportionate to the severity of the chest pain. Diffuse esophageal spasm is the extracardiac condition that is confused most often with ischemic cardiac chest pain. This pain presents as a deep thoracic pain that may be present over most of the thorax. It may extend down the anterome
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PMID:[Angina pectoris in extracoronary diseases]. 1037 99

Acute lung embolism is an uncommon but recognised complication of deep venous thrombosis. The parameters RTG, ECG, PaO2, PaCO2, LDH, CPK, SGOT, SGPT and pulmonary ventilation/perfusion scan have been examined in 200 patients with pulmonary thromboembolism. For that purpose discrimination values of synopticly relevant RTG findings, arterial blood gas and enzymes analysis results and pulmonary ventilation/perfusion scintigraphy, were observed in a comparative analysis of numerous data that could be integrated as an unique finding in sense of qualitative diagnosis. The most frequent symptom was dyspnea and tachypnea, often accompanied with other symptoms (84%), chest pain (65%), cough (53%), tachycardia (41%), hemoptysis (26%). In 74% of patients pulmonary thromboembolism the significant simultaneous increase of all the mentioned enzymes, except CPK, was found 75%. However, according to the results in 58% of the examined persons the pathologic changes on RTG (infiltrates of the lung, with or without affection of the pleura and changed position of diaphragma) were found, and 71% on ECG. Pulmonary ventilation/perfusion scintigraphy is the precise examination for acute lung embolia. For the routine clinical examination measurement of PaO2, PaCO2, LDH, ECG, x-rays is sufficient (correlation test + 0.56). In this paper we have presented our own diagnostic-therapeutic protocol in of lung emboly.
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PMID:[Diagnosis and treatment of acute pulmonary embolism]. 1054 64

Twenty children, aged 6 months to 13 years, with acute pericarditis admitted between 1987 and 1997 to a university hospital were analyzed retrospectively for their etiology, presentation, management, and prognosis. The most common types of pericarditis were purulent (40%), collagen vascular disease (30%), viral (20%), and neoplastic disease (10%). Most children presented with chest pain, fever, and tachypnea, but cardiac tamponade was not seen in any children. Staphylococcus aureus was the most frequent causative organism of purulent pericarditis and septic arthritis was the most common concurrent infection in the patients. Surgical drainage was performed for 11 cases, 9 underwent subxiphoid pericardial window, and 2 underwent thoracotomy. There was no constrictive pericarditis or reaccumulation of fluid after surgery. Two children died, one of staphylococcal septicemia and the other had a malignant mediastinal tumor. The remaining 18 made a complete recovery. We conclude that subxiphoid pericardial drainage is a simple, safe, and quick procedure and can be done easily in general hospitals by pediatric surgeons. The expensive facilities of cardiac surgeries are not needed.
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PMID:Acute pericarditis in childhood: a 10-year experience. 1086 14

Pulmonary oedema with severe, dramatic course following CNS injury was termed neurogenic pulmonary oedema (NPO). NPO was mainly described as a consequence of grand mal seizures, subarachnoid bleeding, intracranial bleeding or head injury. However, the pathogenesis of NPO is not entirely clear yet. In the majority of cases, early or classic symptoms of pulmonary oedema are evident from several minutes up to several hours after CNS damage. Dyspnoea, chest pain, bloody expectoration are observed shortly after consciousness disorders, although NPO may occasionally be diagnosed on the basis of chest x-ray in patients with no clinical symptoms. Tachypnoea, tachycardia, rales without any changes in cardiac system are usually observed during physical examination. The ailments withdraw quickly in the majority of patients, who may require oxygen therapy at most. NPO has been well-known in adults, but our knowledge of its occurrence in children is still rather sparse. The current work presents a case of a 13-year-old boy with pulmonary oedema as a post-seizure complication.
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PMID:Neurogenic pulmonary oedema in a 13-year-old boy in the course of symptomatic epilepsy--case report. 1120 46

Two men, aged 52 and 57 years, had vomited and then developed chest pain, dyspnoea and tachypnoea. After a myocardial infarction had been excluded in the cardiac emergency room, further examination revealed a rupture of the oesophagus. This was treated surgically with the ultimate creation of a tubular stomach. Both patients then recovered well. The Boerhaave's syndrome, a 'spontaneous' perforation of the oesophagus, is a rare and potentially lethal condition which should be diagnosed at an early stage. Pain in the chest, dyspnoea and vomiting are frequent symptoms. A cardiac cause is sometimes erroneously suspected. Subcutaneous emphysema is a major indication for a perforation of the oesophagus. The chest X-ray shows also mediastinal emphysema and infiltrative abnormalities; in case of doubt a second X-ray should be made some hours later.
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PMID:[Boerhaave's syndrome: also in the emergency room]. 1126 4


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