Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary edema of water immersion, which is not associated with aspiration or a closed glottis, is infrequently described in the literature. Swimming-induced pulmonary edema is a syndrome whose pathophysiologic characteristics have not been fully elucidated. Immersion alone has marked effects on central vascular volume, redistribution of pulmonary blood flow, and lung volumes. These changes are more prominent in cold water. These changes, coupled with an elevated cardiac output, may expose regions of the capillary bed to high pressures that favor the extravasation of fluid by hydrostatic forces and potential stress failure of the capillaries. Patients with swimming-induced pulmonary edema present with dyspnea, cough, hypoxemia, and occasionally hemoptysis. Physical examination and chest radiographs usually reveal evidence of pulmonary edema. Treatment is symptomatic and conservative. Improvement and resolution of symptoms are usually rapid, with radiographic normalization in 24 to 48 hours. We describe here 3 cases of swimming-induced pulmonary edema.
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PMID:Swimming-induced pulmonary edema. 1254 77

Non-invasive positive pressure ventilation (NIPPV) has been discussed comprehensively in the last years, but usage of non-invasive ventilation in Intensive Care Units is rare. The reasons may be uncertainty in indications and difficulties in handling the masks and ventilators. In the last years the introduction of full face masks and respiratory helmets has made it possible to ventilate patients with unusual facial forms and to avoid problems of pressure necrosis. Software components designed for NIPPV are available for standard respirators. Indications for NIPPV (neuromuscular diseases, spinal abnormalities, chest wall malformations, COPD, cardiogenic pulmonary edema) have been ensured in clinical trials. No sufficient data are available for the application of NIPPV in weaning and respiratory failure following extubation. Indication for NIPPV becomes apparent when therapy starts in early stage with sufficient ventilation pressure. Compared to standard therapy, no reliable advantage has been seen for NIPPV in hypoxic hypercapnia respiratory failure except for malignant diseases. However, prophylactic use in patients with high risk might be conceivable. For these patients strict criteria of termination are required to avoid missing the time point for intubation. Gas exchange disturbances in advanced lung fibrosis, pneumonia and ARDS are not amenable to NIPPV. Contraindications for NIPPV are non-compliant patients, absence of cough- and pharyngeal reflexes as well as retention of secretions and malignant ventricular arrhythmia. Relative contraindications are catecholamine-dependent circulatory collapse and acute myocardial infarction, since sufficient data for NIPPV are missing.
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PMID:[Noninvasive ventilation in the intensive care unit -- is it still negligible?]. 1267 84

A 64-year-old man complained of irritable cough of 3 months' duration and 1 episode of hemoptysis and dyspnea related to effort. The radiograph revealed a mass in the upper right lobe. Adenocarcinoma of the lung was diagnosed by mediastinoscopy. After removal of the right lung, the patient was admitted to the recovery unit for 36 hours and transferred out without complications. The clinical course in 48 hours on the ward included increasing dyspnea, tachypnea and greater respiratory effort with hypoxemia in spite of increased FiO2. A radiograph showed pulmonary edema and the patient was readmitted to the recovery unit. We describe this case of postpneumonectomy edema and discuss the possible origins of the clinical picture, differential diagnosis, preventive measures and possible treatments.
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PMID:[Post-pneumonectomy edema]. 1270 11

Noninvasive ventilation (NIV), i.e. without tracheal intubation, has been reintroduced for the treatment of respiratory failure to reduce the complications of mechanical ventilation. Nowadays, NIV with positive pressure is the preferred method, applied through a mask held in place by a harness. Several masks can be used (nasal, bucconasal facial) and a variety of means can be used to keep them in place. Many respirators can be selected, ranging from those traditionally used in the intensive care unit(ICU) to specific NV respirators and conventional ICU respirators with specific software for NIV. Many respiratory modalities can be used according to the respirator (biphasic positive airway pressure [BIPAP], proportional assist ventilation, pressure support, synchronized intermittent mandatory ventilation [SIMV], etc.). NIV is mainly indicated in exacerbations of chronic respiratory failure: neuromuscular diseases, pretransplantation cystic fibrosis, and obstructive sleep apnea syndrome. It is also indicated in acute respiratory failure: pneumonia, status asthmaticus, and acute lung edema. The main contraindications are a weakened airway protection reflex(absent cough reflex) and hemodynamic instabiity. The advantages of NIV derive mainly from avoiding the complications associated with invasive ventilation. NIV also presents some disadvantages, especially the greater workload involved to ensure good patient adaptation to the respirator. The most common sequelae of NIV are skin lesions due to pressure on the nasal bridge.
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PMID:[Mechanical ventilation in pediatrics (III). Weaning, complications and other types of ventilation. Noninvasive ventilation]. 1456 42

A 33 years old woman was admitted to the hospital after four days with cough, dyspnea, orthopnea and hemoptysis. Blood pressure was 170/90 mmHg, pulse was 112 and temperature was normal. She had cyanosis and a left ventricular gallop, without heart murmurs. A chest radiograph revealed pulmonary edema and echocardiogram showed a global left ventricular systolic disfunction. Oxygen and furosemide were started, but cardiopulmonary collapse ensued. The patient was supported with mechanical ventilation and treated with inotropic drugs. A right sided cardiac catheterization showed pulmonary wedge pressure of 18 mmHg and a cardiac index of 3 l/min/m2. The levels of creatinine and urea nitrogen were elevated and a urine protein was 97 mg/dl. Coagulation tests were normal except by a positive lupic anticoagulant. Markers of connective tissue diseases or vasculitis were negatives. The clinical evolution suggested that a catastrophic antiphospholipid syndrome was ongoing. Intravenous corticoids, gammaglobulin and cyclophosphamide were administered with transient improvement. On her fourth day of treatment, the patient presented sudden pulmonary bleeding and embolism. A plasmapheresis was performed with improvement of renal, cardiac and pulmonary function. After this episode, the patient has been treated with prednisone and oral anticoagulants treatment for the last two years, without further clinical events.
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PMID:[Catastrophic antiphospholipid syndrome and acute heart failure. Report of a case]. 1463 91

As increasing numbers of people choose to sojourn or retire to the mountains, high-altitude illness is becoming a pathological phenomenon about which healthcare providers should have greater awareness. Hypoxia is the primary cause of high-altitude illness, but other stressors on the sympathetic nervous system, such as cold and exertion, also contribute to disease development and progression. Although variable across persons, symptoms of high-altitude disorders usually occur at altitudes over 7000 feet, and typically in 1 of 3 forms: acute mountain sickness (AMS), high-altitude cerebral edema (HACE), or high-altitude pulmonary edema (HAPE). Major symptoms include nausea, poor sleep, headache, lassitude, cough, dyspnea on exertion and at rest, ataxia, and mental status changes. As a rule, illness occurring at high altitude should be attributed to the altitude until proven otherwise. Treatment is best accomplished by descent and by oxygen or pharmacologic intervention if necessary. Under no circumstances should a person with worsening symptoms of high-altitude illness delay descent. As will be discussed in part II of this article, gradual ascent and subsequent acclimatization to altitude is the most effective prevention, though acetazolamide (Diamox) may be a useful prophylactic measure in some.
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PMID:High-altitude-related disorders--Part I: Pathophysiology, differential diagnosis, and treatment. 1513 83

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

A-23-year-old medical student, resident of an altitude of 700 meters, developed dyspnea and cough during a temple visit at an altitude of 2200 m within 10 hours of arrival and his symptoms improved on descending and with 100% oxygen. Chest skiagram and CT scan chest revealed soft fluffy shadows on the left side with small right lung and absent right pulmonary artery. Absent right pulmonary artery was responsible for development of pulmonary oedema at moderate altitude.
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PMID:Life threatening unilateral pulmonary oedema at moderate altitude. 1507 26

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

Acute pulmonary oedema has been described in individuals participating in three aquatic activities: (i) scuba diving; (ii) breath-hold diving; and (iii) endurance swimming. In this review, 60 published cases have been compiled for comparison. Variables considered included: age; past medical history; activity; water depth, type (salt or fresh) and temperature; clinical presentation; investigations; management; and outcome. From these data, we conclude that a similar phenomenon is occurring among scuba, breath-hold divers and swimmers. The pathophysiology is likely a pulmonary overperfusion mechanism. High pulmonary capillary pressures lead to extravasation of fluid into the interstitium. This overperfusion is caused by the increase in ambient pressure, peripheral vasoconstriction from ambient cold, and increased pulmonary blood flow resulting from exercise. Affected individuals are typically healthy males and females. Older individuals may be at higher risk. The most common symptoms are cough and dyspnoea, with haemoptysis also a frequent occurrence. Chest pain has never been reported. Radiography is the investigation of choice, demonstrating typical findings for pulmonary oedema. Management is supportive, with oxygen the mainstay of treatment. Cases usually resolve within 24 hours. In some cases, diuretics have been used, but there are no data as to their efficacy. Nifedipine has been used to prevent recurrence, but there is only anecdotal evidence to support its use.
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PMID:Pulmonary oedema of immersion. 1573 Mar 35


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