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

A young, pregnant woman with angiographically proved pulmonary emboli developed pulmonary edema and wheezing without evidence of left ventricular failure. This cast study points out the unusual association of pulmonary embolism with pulmonary edema, wheezing, and hyper-reactive airways in a patient with a positive family history of allergy, but no antecedent history of bronchospasm. Mechanisms for the occurrence of noncardiogenic pulmonary edema and wheezing after pulmonary embolism are reviewed.
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PMID:Pulmonary edema and wheezing after pulmonary embolism. 116 36

Upper respiratory and pulmonary complications of cocaine addiction have been increasingly reported in recent years, with most of the patients being intravenous addicts, users of freebase, or smokers of "crack." The toxicity of cocaine is complex and is exerted via multiple central and peripheral pathways. Recurrent snorting of cocaine may result in ischemia, necrosis, and infections of the nasal mucosa, sinuses, and adjacent structures. Pulmonary complications of cocaine toxicity include pulmonary edema, pulmonary hemorrhages, pulmonary barotrauma, foreign body granulomas, cocaine related pulmonary infection, obliterative bronchiolitis, asthma, and persistent gas-exchange abnormalities. Respiratory manifestations are nonspecific and include shortness of breath, cough, wheezing, hemoptysis, and chest pains. Severe respiratory difficulties have been reported in neonates of abusing mothers. In the absence of a cocaine-abuse history, it may be difficult to recognize the etiological role of cocaine, especially in the absence of needle tracks pointing to previous intravenous drug abuse and/or negative toxicology.
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PMID:Respiratory complications of cocaine abuse. 158 7

Infants with cardiopulmonary disease develop severe illness from respiratory syncytial virus (RSV) infection. Safety, feasibility, and pharmacokinetics of intravenous gamma globulin (IVIG) to prevent RSV illness were studied in 23 high-risk infants in a phase I trial. IVIG with an RSV neutralizing antibody titer of 1:1,100 in 5% solution was given monthly over a 2- to 4-h period in a clinical setting during the RSV season. The first group (n = 7) received 500 mg/kg of body weight, the second group (n = 9) received 600 mg/kg, and the third group (n =7) received 750 mg/kg. Serum was drawn prior to infusion and 2, 14, and 30 days after infusion. Total immunoglobulin G and RSV A2 and RSV B neutralizing antibody levels were obtained after the first IVIG infusion. Two children developed mild reversible pulmonary edema (group receiving 600 mg/kg per dose), and one developed hives and wheezing during one infusion (group receiving 500 mg/kg per dose). Twelve children developed subsequent RSV infection during two RSV seasons (November to April) over a 2-year follow-up period; 9 of 12 developed infection during the infusion year. Eleven illnesses were mild; one child died of progressive RSV illness (group receiving 500 mg/kg per dose). A cumulative infusion effect was not observed. IVIG appears safe and feasible in an outpatient setting, and at 750 mg/kg per dose, a target RSV antibody level of greater than or equal to 1:100 was achieved.
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PMID:Use of intravenous gamma globulin to passively immunize high-risk children against respiratory syncytial virus: safety and pharmacokinetics. The RSVIG Study Group. 171 13

The clinical hallmarks of asthma are wheezing and reversibility. Any disease that impairs air flow through obstructed airways may cause wheezing. Patients with true asthma may give a history of allergy and past attacks of dyspnea and wheezing occurring when exposed to allergens, inhaled irritants, upper respiratory infection, cold and humid air, exercise, and emotional stress. When encountering a wheezing dyspneic patient who does not report such a history, it behooves the physician to entertain the possibility that the patient may have a disease other than asthma. Chronic bronchitis, pulmonary emphysema, cardiogenic pulmonary edema pulmonary emboli, aspiration of gastric contents, and upper airway obstruction are the common causes of nonasthmatic wheezing. In almost every instance a wide spectrum of easily obtainable data, particularly historical, are available to alert the physician that the patient's dyspnea and wheezing are not due to asthma. Laboratory data are also readily available to buttress the correct diagnosis.
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PMID:The differential diagnosis of asthma. 176 18

A patient presented with wheezing, evidence of vascular congestion on physical examination, and leukocytosis. A chest x-ray film suggested pneumonia. When unilateral pulmonary edema was revealed on a repeat chest film, the patient was given diuretic therapy and responded favorably. This case thus differs from the usual pattern of symmetrical homogeneous density on the chest roentgenogram in pulmonary edema of cardiac origin.
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PMID:Spontaneous unilateral pulmonary edema. 378 62

Air embolism--the most dangerous complication of central venous catheterization--may occur in several ways. The most frequent is from disconnection of the catheter from the related intravenous tubing. An embolism may present with a sucking sound, tachypnea, air hunger, wheezing, hypotension and a "mill wheel" murmur. A later manifestation is severe pulmonary edema. In a review of 24 patients, the mortality was 50 per cent. Among the survivors, five (42 per cent) had neurologic damage. Immediate treatment includes placing the patient in the left lateral and Trendelenberg positions, administration of oxygen and aspiration of air from the heart. Cardiac massage and emergency cardiopulmonary bypass may be necessary. Most instances can be prevented by inserting the cannula with the patient in the Trendelenberg position, occluding the cannula hub except briefly while the catheter is inserted, fixation of the catheter hub to its connections and occlusive dressing over the track after removal of the catheter.
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PMID:Air embolism after central venous catheterization. 643 96

A protocol for treatment of scorpion sting based mainly on antivenom therapy was applied nation-wide in Saudi Arabia. At least 5 x 1 ml ampoules of antivenom diluted in 20-50 ml saline were injected slowly i.v. in all patients confirmed to have scorpion stings or suspected stings with systemic manifestations. A list of drugs was specified to be used in adjunctive therapy, when required. Analysis of 1033 cases at Al-Baha region, 791 cases at Al-Qassim region and more than 600 cases from 12 central and specialist hospitals in the Central Province revealed impressive results. Except for a 12-year-old boy who was inadequately treated with antivenom and died from pulmonary oedema, haematemesis, severe neurotoxicity and circulatory failure, no other fatalities occurred. The incidence of pulmonary oedema, hypertension, hypotension, cardiac dysrhythmias and neurological symptoms requiring drug therapy following antivenom administration was very slight. The period of stay in the hospital was reduced; most patients were symptom-free within 1-2 days. The early reaction to antivenom administration was lower than expected, amounting to 6.6% and 1.7% among Al-Qassim and Al-Baha victims, respectively. The severity of the reaction in both groups was low, consisting mainly of skin rashes, urticaria, wheezing and bronchial secretion, but no anaphylaxis. About 13.8% of Al-Baha victims were previously treated with antivenom but only 1.7% of the patients showed positive skin tests. This might be due to the low protein content of the antivenom and the action of the venom in releasing massive amounts of catecholamines.
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PMID:The treatment of the scorpion envenoming syndrome: the Saudi experience with serotherapy. 780 36

Pulmonary edema is a frequent and common cause of death in patients in critical care settings. It is seen as a complication of myocardial infarcts, hypertension, pneumonia, smoke inhalation, and high-altitude pulmonary edema. Pulmonary edema occurs when there are alterations in Starling forces and capillary permeability, opposition to lymphatic flow in the lungs, decreased plasma oncotic pressure, central nervous system lesions, and following some types of strenuous exercise. Pulmonary edema presents initially with crackles, wheezing, and dry cough and progresses to tachypnea, dyspnea, orthopnea, pink frothy sputum, and cyanosis. Treatment involves supportive therapy, reduction in blood volume, and oxygen therapy.
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PMID:Pathophysiology of pulmonary edema. 800 Sep 33

In this two year retrospective review, 86 cases of chlorine gas inhalation from 49 medical facilities were treated with nebulized sodium bicarbonate on the recommendation of the Kentucky Regional Poison Center. Typical manifestations included cough, chest discomfort, shortness of breath, and wheezing. No patients developed pulmonary edema or respiratory insufficiency requiring ventilatory support. Sixty-three cases (73.3%) were exposures to chlorine producing acid/hypochlorite mixtures. Six (7.0%) were exposed to chlorine gas in industrial settings. Twelve (14.0%) were exposed to chlorine gas in swimming pool settings. Sixty-nine (80.2%) were treated and released from the emergency department. In 53 patients, clinical condition was clearly improved on emergency department discharge. Seventeen (19.8%) were admitted to the hospital. All admitted patients gradually improved and had a mean hospital stay of 1.4 days (range 1 to 3 days). No patients in this study deteriorated clinically after nebulized sodium bicarbonate use. Nebulized sodium bicarbonate appears safe and merits prospective evaluation in the therapy of chlorine gas inhalation.
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PMID:Nebulized sodium bicarbonate in the treatment of chlorine gas inhalation. 800 31

To determine if spirometric changes reflect early high-altitude pulmonary edema (HAPE) formation, we measured the FVC, FEV1, and FEF25-75 serially during the short-term period following simulated altitude exposure (4,400 m) in eight male subjects, four with a history of HAPE and four control subjects who had never experienced HAPE. Three of the four HAPE-susceptible subjects developed acute mountain sickness (AMS), based on their positive Environmental Symptom Questionnaire (AMS-C) scores. Clinical signs and symptoms of mild pulmonary edema developed in two of the three subjects with AMS after 4 h of exposure, which prompted their removal from the chamber. Their spirometry showed small decreases in FVC and greater decreases in FEV1 and FEF25-75 after arrival at high altitude in the presence of rales or wheezing on clinical examination and normal chest radiographs. One of the two subjects had desaturation (59 percent) and tachycardia during mild exercise, and excessive fatigue and inability to complete the exercise protocol developed in the other at 4 h. The six other subjects had minimal changes in spirometry and did not develop signs of lung edema. Further, we measured each subject's ventilatory response to hypoxia (HVR) prior to decompression to determine whether the HVR would predict the development of altitude illness in susceptible subjects. In contrast to anticipated results, high ventilatory responses to acute hypoxia, supported by increased ventilation during exposure to high altitude, occurred in the two subjects in whom symptoms of HAPE developed. The results confirm that HAPE can occur in susceptible individuals despite the presence of a normal or high ventilatory response to hypoxia.
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PMID:Pulmonary function and hypoxic ventilatory response in subjects susceptible to high-altitude pulmonary edema. 841 62


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