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

Almost one mountain trekker or climber out of two develops several symptoms of high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. Individual susceptibility is the most important determinant for the occurrence of high altitude pulmonary oedema (HAPE). Symptoms associated with HAPE are incapacitating fatigue, chest tightness, dyspnoea at the slightest effort, orthopnoea, and cough with due to haemoptysis in an advanced stage of the disease pink frothy sputum. The hallmark of HAPE is an excessively elevated pulmonary artery pressure (mean pressures of 35 and 55 mm Hg), which precedes the development of pulmonary oedema. Elevated pulmonary capillary pressure and protein- as well as red blood cell-rich oedema fluid without signs of inflammation in its early stage are characteristic findings. Furthermore, decreased fluid clearance from the alveoli may contribute to this non-cardiogenic pulmonary oedema. Immediate descent or supplemental oxygen and nifedipine are recommended until descent is possible. Susceptible individuals can prevent HAPE by slow ascent: an average gain of altitude not exceeding 400 m/day above an altitude of 2500 m. If progressive high altitude acclimatization is not possible, a prophylaxis with nifedipine should be recommended.
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PMID:High altitude-induced pulmonary oedema. 1690 89

We present the case of a 71-year-old woman with a 7-year history of a giant left atrial myxoma. The myxoma was attached to the atrial septum and occupied almost the entire left atrial cavity. The patient was hospitalized 4 times because of dyspnea on exertion, palpitations, fatigue, general asthenia, and weight loss. During prior hospitalizations, the patient had refused cardiac surgery. She developed several complications, including atrial fibrillation, mitral and tricuspid regurgitation, mesenteric embolism, pulmonary edema, and thrombotic stroke. We herein describe the natural history of left atrial myxoma in an elderly patient over a 7-year period.
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PMID:Giant left atrial myxoma in an elderly patient: natural history over a 7-year period. 1702 71

Headache is the cardinal symptom of acute mountain sickness (AMS). The headache normally worsens, with increased cerebral affection and the development of high-altitude cerebral edema (HACE). A Norwegian expedition aimed to climb Baruntse (7129 m) in Nepal in 2003. At 5400 m a 35-year-old man felt exhausted. The next day he aborted his attempt at further climbing as a result of extreme fatigue. Over the next 24 hours he developed cough, dyspnea, and severe hypoxia before progressing to ataxia and blurred vision. At no point did he experience headache or nausea. The patient was evacuated by helicopter. He improved immediately after descent and recovered completely within a week. The speed of progression from AMS to HACE varies. Abrupt onset of HACE is occasionally reported. High-altitude pulmonary edema (HAPE) may induce severe hypoxia that can lead to rapid development of HACE. High-altitude cerebral edema in the setting of HAPE was the most likely diagnosis despite the unusual lack of headache. Rapid onset of HAPE with subsequent severe desaturation should raise awareness of the development of HACE, even in the absence of headache.
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PMID:High-altitude cerebral edema with absence of headache. 1744 14

Reported here is a rare case of babesiosis with pulmonary complications followed by a review of the literature. Babesiosis presents clinically as a malaria-like illness with fever, chills, headache, fatigue with lymphopenia, atypical lymphocytes, mildly or transiently elevated serum transaminases, thrombocytopenia, and increased lactate dehydrogenase (LDH) levels. The diagnosis of babesiosis is based on identification of Babesia spp. on a peripheral blood smear. Babesiosis is usually mild in normal hosts, but it may be severe or even fatal in asplenic patients. Pulmonary manifestations are rare in babesiosis, but non-cardiogenic pulmonary edema (NCPE) is the most frequent manifestation. NCPE in babesiosis does not appear to be related to the degree of parasitemia or splenic function and its onset may be early or late. NCPE usually resolves rapidly with supportive treatment; it is rarely fatal. Clinicians should suspect NCPE in patients with babesiosis who acutely develop shortness of breath and have chest radiograph findings compatible with acute pulmonary edema without cardiomegaly or pleural effusions.
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PMID:Pulmonary complications of babesiosis: case report and literature review. 1755 89

In response to questions about the safety of ephedra-based dietary products, ephedra-free products are now available. Many contain synephrine, a sympathomimetic amine with structural similarities to ephedra. We present a 22-year-old, previously healthy, African American male with sickle cell trait who developed rhabdomyolysis after ingestion of a synephrine-containing dietary supplement. The patient developed fatigue, dehydration, and myalgias while exercising. He developed severe rhabdomyolysis, with a peak creatine phosphokinase level of 2.8 million U/L, complicated by pulmonary edema, acute renal failure, disseminated intravascular coagulation, and bilateral compartment syndromes in his lower extremities. He required prolonged hospitalization for hemodialysis, multiple wound debridements, hyperbaric oxygen therapy, and physical therapy. He has permanent sensory and motor neurological deficits in his distal lower extremities. Military physicians should routinely inquire about the use of dietary supplements, educate patients about the potential adverse reactions associated with these agents, and encourage healthy diets and exercise for weight loss.
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PMID:A case of severe exercise-induced rhabdomyolysis associated with a weight-loss dietary supplement. 1761 52

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

High altitude sickness is a common name for illnesses that can occur at high altitude, usually above 3000 meters from sea level. The cause is hypoxia but the pathophysiology of the diseases is a complex mixture of multiple factors, involving the human response to hypoxia. The most common symptom is headache, but loss of appetite, nausea and sleep disturbances are also common complaints. With rapid or high ascent there is increased risk of acute mountain sickness, with severe headache that responds poorly to pain medications, nausea, vomiting and extreme fatigue as the most common symptoms. The most severe forms of high-altitude sickness are high altitude cerebral edema and high altitude pulmonary edema. High altitude sickness can be prevented by slow ascent and avoiding overexertion. Medications can also be used to reduce symptoms. In this overview high altitude physiology and acclimatisation are reviewed. The main types of high altitude sickness are described with special emphasis on symptoms and diagnosis, but treatment and prevention are also reviewed.
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PMID:[High altitude sickness - review]. 1949 9

Metformin is a biguanide. Due to its effects in decreasing the hepatic production of glucose and in increasing insulin sensitivity in peripheral tissues, such as adipose tissue and skeletal muscle, the agent is used in metabolic syndrome and type 2 diabetes mellitus and, in which insulin resistance is especially pronounced. Eighty-one-year old male patient was admitted to the emergency unit with sudden vertigo, tiredness, dyspnea, cyanosis, and lethargy. He had had type 2 diabetes mellitus for 10 years and was taking glargin 12 U/kg once daily and metformin (glucophage) 850 mg thrice daily. The patient showed no cooperation and orientation. Metabolic acidosis, hypoxemia, and hypercapnea were detected in arterial blood gases (ABG). The patient was transferred to an intensive care unit of the hospital; endotracheal intubation was applied and mechanic ventilation was started. On the following day, his ABG got better; he was disconnected and weaning was applied. Lung X-ray study revealed no signs of pneumonia or pulmonary edema. On the same day, extubation was ended and O2 was given by mask at a rate of 4 L/min. After the patient's vital signs, blood sugar, and lactate levels were stabilized; his treatment regimen was arranged again and the patient was discharged on day 4 of his admission. Dyspnea, acidosis, and hypoxia seen in the patient were thought to be due to lactic acidosis which may rarely occur when metformin is used.
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PMID:[A clinical case of lactic acidosis development in a diabetic patient taking metformin]. 1951 47

Peripartum cardiomyopathy (PPCM) is a rare life-threatening cardiomyopathy of unknown cause that occurs in the peripartum period in previously healthy women.[1] the symptomatic patients should receive standard therapy for heart failure, managed by a multidisciplinary team. The diagnosis of PPCM rests on the echocardiographic identification of new left ventricular systolic dysfunction during a limited period surrounding parturition. Diagnostic criteria include an ejection fraction of less than 45%, fractional shortening of less than 30%, or both, and end-diastolic dimension of greater than 2.7 cm/m(2) body surface-area. This entity presents a diagnostic challenge because many women in the last month of a normal pregnancy experience dyspnea, fatigue, and pedal edema, symptoms identical to early congestive heart failure. There are no specific criteria for differentiating subtle symptoms of heart failure from normal late pregnancy. Therefore, it is important that a high index of suspicion be maintained to identify the rare case of PPCM as general examination showing symptoms of heart failure with pulmonary edema. PPCM remains a diagnosis of exclusion. No additional specific criteria have been identified to allow distinction between a peripartum patient with new onset heart failure and left ventricular systolic dysfunction as PPCM and another form of dilated cardiomyopathy. Therefore, all other causes of dilated cardiomyopathy with heart failure must be systematically excluded before accepting the designation of PPCM. Recent observations from Haiti[2] suggest that a latent form of PPCM without clinical symptoms might exist. The investigators identified four clinically normal postpartum women with asymptomatic systolic dysfunction on echocardiography, who subsequently either developed clinically detectable dilated cardiomyopathy or improved and completely recovered heart function.
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PMID:Emergency management of decompensated peripartum cardiomyopathy. 1956 73

From 1998 to 2008 we noticed 3 cardiac deaths in male teenagers aged 18-19 during or after physical exercise. The first was working at the site recreatively, the second was engaged in soccer recreatively and the third was professional soccer player. One felt general tiredness and was exhausted of a heavily physical effort, the other after physical exercise became septic and the third was without symptoms. One died suddenly during physical exercise at the field and two died in the hospital. At the forensic autopsy the first had bilateral bacterial pneumonia, possible high-altitude non-cardiogenic pulmonary edema and cerebral edema. The second had bilateral bacterial pneumonia, adult respiratory distress syndrome, disseminated intravascular coagulation, suprarenal bleeding, cerebral edema, hypoplastic right coronary artery and myocardial fibrosis. The third had bilateral bacterial pneumonia, fibrinous pericarditis, cerebral contusion with edema, thickenning of the left ventricle 20 mm and hypoplastic ascending aorta. In Croatia the death rate among athletes reached 0.15/ 100,000, in athletes suffered of acute pneumonia 0.28/ 100,000, in others who practice exercise recreatively 0.57/ 100,000 (p = 0.0068), in all males who practice exercise recreatively 0.75/ 100,000 (p = 0.0014). Physical exercise is contraindicated in acute respiratory tract infections. Every such case has to be treated by physician. When to start with physical training after bacterial pneumonia depends on disappearing of clinical and X-ray signs of pneumonia, normalization of erythrocite sedimentation rate and of white cell count.
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PMID:Physical exercise and cardiac death due to pneumonia in male teenagers. 1966 54


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