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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Re-expansion pulmonary oedema is an uncommon and potentially life-threatening complication after rapid expansion of a collapsed lung. Symptom onset (cough, chest pain, dyspnoea) is often sudden and the clinical picture may be dramatic. Pathogenesis is complex and partially unclear. A well-timed intensive therapy allows a better prognosis. To date, only one case of re-expansion pulmonary oedema following fenestration of a giant hepatic cyst has been reported in the literature. We here report a new case after surgical fenestration of a giant hepatic cyst.
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PMID:Re-expansion unilateral pulmonary oedema after surgical drainage of a giant hepatic cyst: a case report. 1731 36

Anthracycline cardiotoxicity is cumulative and can cause congestive heart failure. The cardiotoxicity caused by 5-fluorouracil (5-FU) is acute and is usually observed during the first cycle of chemotherapy. We present the case of a female patient operated on for colorectal cancer and receiving her first postoperative chemotherapy cycle. Three hours after the initiation of continuous 5-FU infusion she developed signs of acute heart failure (AHF) and pulmonary edema. The patient did not have any previous history of heart disease. Symptoms resolved 24 hours from the onset of the episode after the initiation of the relevant emergency therapy. One of the most common symptoms related to 5-FU cardiotoxicity is chest pain. In case of such a toxicity treatment should be switched to another antineoplastic agent.
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PMID:Acute heart failure after treatment with 5-fluorouracil. 1743 11

Few health care professionals realize that topical anesthetic spray can cause methemoglobinemia. We describe a 56-year-old woman who was transferred to our emergency department when severe cyanosis and chest pain developed after administration of topical oropharyngeal benzocaine and lidocaine during outpatient endoscopy. Investigations revealed a methemoglobin level of 51%. Despite rapid diagnosis and treatment with methylene blue, pulmonary edema consistent with adult respiratory distress syndrome developed, endotracheal intubation was required, and the patient suffered a lengthy course in the intensive care unit. This article presents a detailed discussion of the pathophysiology, diagnosis and treatment of methemoglobinemia, as well as a qualitative systematic review of the English literature on methemoglobinemia induced by topical anesthetic. The implications of this condition for emergency physicians are also outlined.
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PMID:Severe methemoglobinemia from topical anesthetic spray: case report, discussion and qualitative systematic review. 1761 44

We present a case of severe complication of myocardial infarction -- acute mitral regurgitation caused by papillary muscle rupture. A 69-year-old man was admitted with chest pain lasting 1 hour and pulmonary oedema. ECG revealed ST-segment depression in leads II, III, aVF, V2-V6. Soon after admission the patient experienced respiratory disorders and consequently arrest. The patient was transferred in shock to the Department of Cardiothoracic Surgery, where he underwent successful artificial mitral valve implantation. One year later the patient is in good condition (NYHA class I) and the valve is fully functional.
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PMID:[Acute mitral regurgitation caused by infarction-related papillary muscle rupture with successful surgical treatment: case report]. 1797 62

During an international breath-hold diving competition, 19 of the participating divers volunteered for the present study, aimed at elucidating possible symptoms and signs of pulmonary edema after deep dives. Measurements included dynamic spirometry and pulse oximetry, and chest auscultation was performed on those with the most severe symptoms. After deep dives (25-75 m), 12 of the divers had signs of pulmonary edema. None had any symptoms or signs after shallow pool dives. For the whole group of 19 divers, average reductions in forced vital capacity (FVC) and forced expiratory volume in the first second (FEV(1)) were -9 and -12%, respectively, after deep dives compared with after pool dives. In addition, the average reduction in arterial oxygen saturation (Sa(O(2))) was -4% after the deep dives. In six divers, respiratory symptoms (including dyspnea, cough, fatigue, substernal chest pain or discomfort, and hemoptysis) were associated with aggravated deteriorations in the physiological variables (FVC: -16%; FEV(1): -27%; Sa(O(2)): -11%). This is the first study showing reduced spirometric performance and arterial hypoxemia as consequences of deep breath-hold diving, and we suggest that the observed changes are caused by diving-induced pulmonary edema. From the results of the present study, it must be concluded that the great depths reached by these elite apnea divers are associated with a risk of pulmonary edema.
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PMID:Pulmonary edema after competitive breath-hold diving. 1821 6

Coronary heart disease is the principal cause of death in the industrialized world. Its most serious expression, acute myocardial infarction, causes 7.2 million deaths each year worldwide, and it is estimated that 20% of all people will suffer heart failure in the course of their lifetime. The control of risk cardiovascular factors, including arterial hypertension, obesity and diabetes mellitus is the best way to prevent such diseases. The most frequent and serious cardiovascular emergencies that can manifest during dental treatment are chest pain (as a symptom of underlying disease) and acute lung edema. Due to the high prevalence and seriousness of these problems, the dental surgeon must be aware of them and should be able to act quickly and effectively in the case of an acute cardiovascular event. In patients with a history of cardiovascular disease, attention must center on the control of pain, the reduction of stress, and the use or avoidance of a vasoconstrictor in dental anesthesia. In turn, caution is required in relation to the antiplatelet, anticoagulant and antihypertensive medication typically used by such patients.
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PMID:Cardiovascular diseases in dental practice. Practical considerations. 1844 13

Irukandji syndrome is usually characterized by delayed severe abdominal, back and chest pain associated with autonomic effects including diaphoresis, hypertension and, in severe cases, myocardial injury and pulmonary oedema. It is most often associated with envenoming by the jellyfish Carukia barnesi, but a number of other jellyfish, including Alatina mordens, are now known to produce Irukandji syndrome. In the present study, nematocyst-derived venom from A. nr mordens (150-250 microg/kg, i.v.) produced a long-lasting pressor effect in anaesthetised rats. This pressor response (250 microg/kg, i.v.) was significantly inhibited by prior administration of the alpha-adrenoceptor antagonist prazosin (200 microg/kg, i.v.) but not by CSL box jellyfish antivenom (300 U/kg, i.v.). A. nr mordens venom 250 microg/kg (i.v.) caused marked increases in plasma adrenaline and noradrenaline concentrations following administration in anaesthetised rats. The venom did not contain appreciable amounts of either adrenaline or noradrenaline. A. nr mordens venom (25 microg/ml) produced a contractile response in rat electrically stimulated vas deferens which was markedly reduced in tissues pre-treated with reserpine (0.1mM) or guanethidine (0.1mM). Sodium dodecyl sulphate (SDS)-PAGE analysis showed that A. nr mordens venom is comprised of multiple protein bands ranging from 10 to 200 kDa. Western blot analysis using CSL box jellyfish antivenom indicated several antigenic proteins in A. nr mordens venom, however, it did not detect all proteins present in the venom. This study characterizes the in vitro and in vivo effects of A. nr mordens venom and indicates that the cardiovascular effects are at least partially mediated by endogenous catecholamine release.
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PMID:An examination of the cardiovascular effects of an 'Irukandji' jellyfish, Alatina nr mordens. 1854 53

Takotsubo is a reversible cardiomyopathy, often triggered by a stressful event. It combines clinical features mimicking a myocardial infarction, transient apical ballooning of the left ventricle, normal coronary arteries and a small rise in troponin level. There is a striking female predominance with mean age ranging from 65 to 76 years among series. Preceding stressful event is documented in 50 to 100% of patients. The most common clinical presentation is an angor-like chest pain with ST-segment elevation on the electrocardiogram (70%). The prognosis is excellent even if serious complications may occur: pulmonary oedema, cardiogenic shock, transient dynamic intraventricular gradient, life-threatening arrhythmias. In-hospital mortality is in the range of 0 to 10%. The recurrence rate is low. The precise physiopathology of the syndrome remains unknown but catecholamine mediated myocardial stunning is the most favored explanation.
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PMID:[Takotsubo cardiomyopathy or transient left ventricular apical ballooning syndrome]. 1893 23

Takotsubo cardiomyopathy, also known as stress induced cardiomyopathy and transient left ventricular apical ballooning syndrome, is a rare syndrome that is characterized by a transient decrease in ejection fraction. This is accompanied by hypokinesis of the left ventricle and ballooning of the apex, with hypercontractile base and non-obstructive coronary artery disease. Takotsubo was first described in Japan in the early 1990's. It was named such due to the morphology of the apical ballooning that is similar in shape to a 'takotsubo', which is a pot with a round bottom and narrow neck used for trapping octopuses. Though most often described in Asians, reports of Takotsubo in Caucasian populations is becoming more common, possibly due to heightened awareness and detection. The most common presenting symptom of Takotsubo is acute chest pain mimicking myocardial infarction. Patients may also present with dyspnea, pulmonary edema and, more rarely, cardiogenic shock. Clinical symptoms are accompanied by transient left ventricular dysfunction. Despite clinical symptoms consistent with acute myocardial infarction, normal coronary arteries are usually detected upon cardiac catheterization. The case presented here is of an Asian woman who developed symptoms of acute myocardial infarction during a stressful hospital stay.
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PMID:Takotsubo cardiomyopathy: case report and review of the literature. 1954 75

This report describes the case of a young man in whom an intravenous injection of a hydrocarbon led to reversible pulmonary edema. An 18-year-old male presented with chest pain, a cough and progressive dyspnea at a multidisciplinary paediatric intensive care unit in a tertiary care university hospital. Six hours after oxygen was given, blood gases were pH 7.16, partial pressure of carbon dioxide 43 torr (5.7 kPa), partial pressure of arterial oxygen 149 torr (19.9 kPa) and bicarbonate concentration 15 mEq/L. A chest radiograph suggested pulmonary edema. On day 3, the patient stated that he had injected himself with Varsol (Imperial Oil, Canada) - a mixture of straight and branched-chain hydrocarbons, naphthenes and alkyl derivatives of benzene - several hours before his admission. On day 5, the patient's respiratory rate returned to 20 breaths/min, and his chest radiograph was normal by day 7. The present case report suggests that the intravenous injection of hydrocarbons may lead to reversible pulmonary injury.
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PMID:Pulmonary injury after intravenous hydrocarbon injection. 2017 61


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