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

Ovarian hyperstimulation syndrome (OHSS) is the most serious complication of ovulation induction with exogenous gonadotropins, such as human menopausal gonadotropin and follicle-stimulating hormone. These hormones are considered to increase capillary permeability and cause third space fluid shift. We report an autopsy case of severe OHSS in a 28-year-old Japanese female. The patient developed bilateral chest pain and progressive dyspnea during the course of administration of human gonadotropins. Pleural effusion and hypouresis clinically disappeared 4 days after the onset of the symptoms, but the patient died suddenly of rapid respiratory insufficiency. Autopsy examination revealed massive pulmonary edema, intra-alveolar hemorrhage and pleural effusion without any evidence of pulmonary thromboembolism. Histopathological examination of the ovary demonstrated multiple well-developed follicle formations, consistent with OHSS. It is very important to recognize that massive pulmonary edema can occur in a patient with OHSS. To the best of our knowledge, this is the first autopsy report of a patient with severe OHSS.
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PMID:An autopsy case of ovarian hyperstimulation syndrome with massive pulmonary edema and pleural effusion. 1088 38

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

This prospective, observational study evaluated the safety of the Western Hospital admission protocol for patients with suspected acute coronary syndromes. The study included all patients admitted from the Emergency Department with an admission diagnosis of unstable angina, post infarct angina, atypical chest pain, or chest pain for evaluation. Data collected included demographic data, admission diagnosis, location of admission (bed with or without cardiac monitoring), past medical history and presenting chest pain history to determine Agency for Health Care Policy (AHCPR) and Western Hospital (WH) protocol classifications, cardiac enzyme assays, electrocardiogram analysis, adverse outcomes [death, myocardial infarction (MI), dysrhythmia, acute pulmonary edema, recurrent pain], diagnosis at hospital discharge, and length of stay-(LOS). There were 508 patients with a mean age of 63.7 years enrolled in the study. Three hundred nineteen (62.8%) were admitted to beds without any cardiac monitoring. There was one unexpected death in the unmonitored group, an 85 year-old patient who suffered a presumed dysrhythmia and whom the treating physician had decided was not for resuscitation. Twelve patients suffered nonfatal MI, and none suffered pulmonary edema. All MI patients made an uneventful recovery, and none required thrombolysis. If all patients had been admitted to an area of care based on AHCPR guidelines, an additional 310 admissions to monitored beds would have been required. The results of this study suggest that selected patients with suspected acute coronary syndromes can be safely managed in beds without continuous cardiac monitoring.
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PMID:It is safe to manage selected patients with acute coronary syndromes in unmonitored beds. 1160 75

Pleuropulmonary amebiasis is the common and pericardial amebiasis the rare form of thoracic amebiasis. Low socioeconomic conditions, malnutrition, chronic alcoholism, and ASD with left to right shunt are contributing factors to the development of pulmonary amebiasis. Although no age is exempt, it commonly occurs in patients aged 20 to 40 years, with an adult male to female ratio of 10:1. Children rarely develop thoracic amebiasis: when it does occur there is an equal sex distribution. The infection usually spreads to the lungs by extension of an amebic liver abscess. Infection may pass to the thorax directly from the primary intestinal lesion through hematogenous spread, however. Lymphatic spread is one possible route. Inhalation of dust containing cysts and aspiration of cysts or trophozoites of E histolytica in the lungs are some other hypothetical routes. The lung is the second most common extraintestinal site of amebic involvement after the liver. Usually the lower lobe, and sometimes the middle lobe of the right lung, are affected, but it may affect any lobe of the lungs. The patient develops fever and right upper quadrant pain that is referred to the tip of the right shoulder or in between the scapula. Hemophtysis is common. The diagnosis of thoracic amebiasis is suggested by the combination of an elevated hemidiaphragm (usually right), hepatomegaly, pleural effusion, and involvement of the right lung base in the form of haziness and obliteration of costophrenic and costodiaphragmatic angles. Infection is usually extended to the thorax by perforation of a hepatic abscess through the diaphragm and across an obliterated pleural space, producing pulmonary consolidation, abscesses, or broncho-hepatic fistula. Empyema develops when a liver abscess ruptures into the pleural space. Rarely, a posterior amebic liver abscess can burst into the inferior vena cava and develop an embolism of the inferior vena cava and thromboembolic disease of the lungs with congestive cardiac failure or corpulmonale. Diagnosis by finding E histolytica in stool specimens is of limited value. In a limited number of cases amebae might be found in aspirated pus or expectorated sputum. "Anchovy sauce-like" pus or sputum may be found. Presence of bile in sputum indicates that the pus is of liver origin. Serological tests are of immense value in diagnosis. Liver enzymes are usually normal and neutrophilic leucocytosis may or may not be found. ESR is invariably elevated. Anti-amebic antibodies can be detected by ELISA, IFAT, and IHA. Amebic antigen can be detected from serum and pus by ELISA. Detection of Entamoeba DNA in pus or sputum may be a sensitive and specific method. Pleuropulmonary amebiasis is easily confused with other illnesses and is treated as pulmonary TB, bacterial lung abscesses, and carcinoma of the lung. A single drug regimen with metronidazole with supportive therapy usually cures patients without residual anomalies. Aspiration of pus from empyema thoracis may be needed for confirmation and therapeutic purposes. The pericardium is usually involved by direct extension from the amebic abscess of the left lobe of the liver, sometimes from the right lobe of the liver, and rarely from the lungs or pleura. An initial accumulation of serous fluid due to reactive pericarditis followed by intrapericardial rupture may develop either (1) acute onset of severe symptoms with chest pain, dyspnea, and cardiac tamponade, shock, and death, or (2) progressive effusion with thoracic cage pain, progressive dyspnea, and fever. Chest radiograph, ultrasound examination, and CT scan usually confirm the presence of a liver abscess in continuity with the pericardium and fluid within the pericardial sac with or without the fistulous tract. Echocardiography may demonstrate fluid in the pericardial cavity. Patients should be cared for in the ICU and ambecides should be started without delay. Pericardiocentesis usually confirms the diagnosis and improves the general condition of the patient. Aspiration of the accumulated fluid should be performed urgently in cardiac tamponade; repeated aspiration may be needed. Surgical drainage should be done if needed. Acanthamoeba, a free-living ameba, may also infect the lungs in the form of pulmonary nodular infiltration and pulmonary edema in association with amebic meningoencephalitis in immunocompromised patients. It usually spreads to the meninges of the brain by way of the blood from its primary lesion in the lung or skin. Early diagnosis and institution of treatment may be life saving for these patients. A literature review shows that HIV/AIDS patients are not prone to infection with E histolytica. It is now clear that there are an increasing number of HIV-seropositive patients among amebic liver abscess patients, however, which suggests that although the incidence of intestinal infection is not high among HIV-seropositive or AIDS patients they are more susceptible to an invasive form of the disease.
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PMID:Thoracic amebiasis. 1209 41

We report a case of spontaneous intramural left atrial hematoma with chest pain and pulmonary edema as the primary clinical manifestations. Echocardiographic techniques revealed obstruction of the left atrial cavity by cyst-like masses attached to the posterior and anterior atrial wall. A large intramural hematoma due to extensive atrial wall dissection was observed by magnetic resonance imaging. Surgery confirmed the diagnosis of intramural left atrial hematoma with no complications. We review the clinical and diagnostic profile of the three cases of spontaneous intramural left atrial hematoma reported in the world medical literature.
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PMID:[Diagnosis by magnetic resonance imaging of a case of intramural left atrial hematoma]. 1219 85

Cocaine use has increased considerably during the last twenty years and several related complications can be identified. Clinical features of cocaine intoxication are variable, but predominantly involve cardiovascular events. Chest pain is the most main complaint; myocardial ischemia must be ruled out. Other cardiovascular manifestations are left ventricular dysfunction, arrhythmia, endocarditis and aortic dissection. Non-cardiac complications include neurological (seizures, stroke, cerebral hemorrhage), respiratory (asthma, interstitial pneumonitis, pulmonary edema), renal (acute renal failure, rhabdomyolysis) and obstetrical disorders. Detection of cocaine in the urine provides the diagnosis. Symptomatic treatment is generally given, combining conventional treatment of the complication and broad use of benzodiazepines.
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PMID:[Acute complications in cocaine users]. 1221 80

A 45-year-old patient developed shortness of breath, intensive cough, hemoptysis, chest pain and acute bilateral pulmonary infiltrates following the inhalation of crack-cocaine. The bronchoalveolar lavage and transbronchial biopsy revealed infiltrations of polymorphonuclear neutrophils and the formation of foreign body granulomas. The diagnosis of a crack-syndrome was made and the patient rapidly improved under temporary discontinuation of cocaine inhalation and symptomatic therapy. Crack-cocaine is the free-base of cocaine-hydrochloride and its chemical properties allows it to be inhaled tobacco-like. Therefore the lungs become the principal organs exposed and affected. In addition to our findings, diffuse damage of the alveolar wall and capillary injury due to vasoconstriction and toxic action were reported, in some cases rapidly progressing into pulmonary oedema and ARDS. As the consumption of crack cocaine in Germany has markedly increased over the past decade, a higher prevalence of the reported syndrome has to be assumed.
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PMID:[Crack-syndrome: the pulmonary complications of inhaled cocaine. A review a propos a case report]. 1244 9

A 68-year-old female was admitted for sudden onset of chest pain. She received a successful percutaneus coronary intervension for total occlusion in the diagonal artery, but continued to develop progressive heart failure. A chest X-ray showed right pulmonary edema without cardiomegaly, and an echocardiogram revealed massive mitral regurgitation with prolapse in the anterior mitral leaflet due to a rupture in the papillary muscle. An emergency operation was conducted using routine cardiopulmonary bypass. There was complete rupture in the anterior papillary muscle. Mitral valve replacement with posterior mitral leaflet preservation was performed using a size 25 mm Carbomedics prosthetic valve. The postoperative course was uneventful, and she was discharged on postoperative day 29 in New York Heart Association class I. Postoperative pathological findings showed necrosis in the papillary muscle with inflammatory changes. Early diagnosis, prompt medical stabilization, and aggressive surgical intervention are essential to save such a group of patient.
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PMID:Acute mitral regurgitation due to total rupture in the anterior papillary muscle after acute myocardial infarction successfully treated by emergency surgery. 1277 54

Re-expansion pulmonary oedema is a well-recognized rare complication of the treatment of spontaneous pneumothorax. It has been associated with death in 20% of cases. A fit 20-year-old man who had returned from holiday 2 days previously presented with a large left-sided pneumothorax of 10 days' duration. He had exhibited symptoms of chest pain and shortness of breath during the return flight. He showed no signs of respiratory distress at presentation to the Accident and Emergency Department, but after treatment with a chest tube in the ensuing 90 min developed severe unilateral re-expansion pulmonary oedema and circulatory collapse. Factors in the aetiology of the condition and prevention are considered.
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PMID:Re-expansion pulmonary oedema and circulatory shock in a 20-year-old man. 1278 75

Clinical reports on unintentional mass exposure to extreme concentrations of carbon dioxide are rare. We describe an industrial incident caused by a container of liquid carbon dioxide that was unintentionally opened in an enclosed working environment. Twenty-five casualties reached our emergency department. Symptoms included dyspnea, cough, dizziness, chest pain, and headache. ECGs (n=15) revealed ST-segment changes in 2 (13.3%) patients, atrial fibrillation in 2 patients, and non-Q wave myocardial infarction in 1 patient. Chest radiographs (n=22) revealed diffuse or patchy alveolar patterns, consistent with pneumonitis, in 6 (27%) patients and pulmonary edema in 2 (9%) patients. Eleven (44%) patients were admitted to the hospital: 8 were discharged 24 hours later and the others within 8 days. No patient died. Exposure to high concentrations of carbon dioxide resulted in significant but transient cardiopulmonary morbidity with no mortality when victims were promptly evacuated and given supportive therapy. Cardiac complications were frequently observed and should be actively sought.
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PMID:Exposure to extremely high concentrations of carbon dioxide: a clinical description of a mass casualty incident. 1474 8


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