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

Clinical experience with five patients exposed to phosgene is described. The treatment of phosgene poisoning was focused upon the presenting problem, pulmonary edema. Arterial hypoxemia was treated with a face mask with 10 cm CPAP with the FiO2 adjusted as needed or with a volume ventilator with controlled ventilation. Ventilation was controlled to reduce the work of breathing. Metabolic acidosis was treated with NaCHO3 to produce a normal pH. A vigorous program of diuresis was used to treat the pulmonary edema. Lasix was administered to produce a negative fluid balance while maintaining a good urinary output. The negative fluid balance correlated well with reduced oxygen requirements.
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PMID:Phosgene: a practitioner's viewpoint. 302 27

The case of an 8-year-old boy is reported, who developed acute pulmonary edema associated with acute subglottic swelling and subsequent partial upper airway obstruction after extubation and recovery from anaesthesia. The main factors responsible for the formation of pulmonary edema presumably are a large subatmospheric transpulmonary pressure gradient and hypoxia leading to translocation of circulating blood volume into the pulmonary vasculature and fluid shift across the alveolar-capillary membrane. Application of oxygen and CPAP or PEEP plus diuretic therapy will promote rapid clearance of the pulmonary edema.
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PMID:Pulmonary edema due to partial upper airway obstruction in a child. 318 93

1. With improvements in treatment of burn shock and wound sepsis, inhalation injury has emerged as the number one cause of fatality in the burn patient; it accounts for 20 to 84 per cent of burn mortality. 2. Only steam is capable of inflicting direct thermal damage; most injury is caused by incomplete products of combustion, the most important being aldehydes. 3. More accurate diagnostic techniques, including fiberoptic bronchoscopy and 133Xe scanning, have been added to the traditional clinical signs of inhalation injury, such as facial burns, singed nasal vibrissae, and closed space injury, and have led to a new estimation of a 30 per cent incidence among patients with major burns. 4. Patients with inhalation injury typically pass through three stages, those of acute pulmonary insufficiency, pulmonary edema, and bronchopneumonia. 5. The major early pathophysiologic changes seen in the lungs of burned patients related to edema. With inhalation injury this is probably mediated by the products of activated neutrophils. Later changes are the result of the reduction of surfactant and thus lung compliance. 6. Treatment consists of intubation at the first hint of respiratory distress; the issue of tracheostomy versus endotracheal intubation has not been scientifically resolved, but most centers employ prolonged nasotracheal intubation. Prophylactic antibiotics or steroids are not of benefit. Further care is only supportive and includes CPAP, PEEP, vigorous pulmonary toilet, humidification of inspired air, and antibiotics for documented infection. 7. Further advances await the development of pharmacologic methods of affecting the lung's response to injury, which includes altered capillary permeability and decreased immune function.
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PMID:Pulmonary injury in burned patients. 391 76

Adult respiratory distress syndrome is becoming more frequent in pediatric age. There are several factors involved in its' etiology. Sepsis is almost invariably present in all patients. Basic mechanism is an increase of pulmonary capillary permeability with production of acute non cardiogenic oedema. The decrease in compliance and functional residual capacity produce a respiratory failure with hypoxemia non-responsive to the increase in FiO2. Pulmonary hypertension and low cardiac output appear once the syndrome has developed. In its' management, cardiorespiratory monitoring is essential. Prophylaxis is based on early treatment of the essential pathological process. Corticoids are only effective if they are administered before development of pulmonary oedema. The treatment is based on: a) Moderate water restriction. b) Early respiratory assistance using PEEP or CPAP. c) Maintenance of adequate oxygen transport. The extracorporeal oxygenation guarantees the oxygen exchange but it does not affect survival. Mortality is 95%. Patients who survive have minimal pulmonary sequelae.
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PMID:[Adult respiratory distress syndrome in childhood]. 681 14

This report describes a case of paraquat poisoning, treated with continuous positive airway pressure. After an initial phase of acute respiratory failure with diffuse pulmonary edema, we observed radiologically a complete clearing of both lungs, associated with an aspect of overdistension. Surprisingly, FRC was above normal, as was total quasi static compliance. The patient died on the 15th day, with intractable hypoxemia. Pathologic analysis revealed large zones of parenchyma with overdistended airspaces, explaining the emphysematous-like aspect of the lungs. We propose that the attempts to increase lung volume with CPAP, at an early phase of diffuse epithelial disorganization, may have, partially at least, dilated the remaining distal airspaces.
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PMID:PEEP-induced airspace overdistension complicating paraquat lung. 704 28

Costing data for intensive care admissions is important, not only for unit funding, but also for cost outcome analysis of new therapies. This paper presents an intensive care episode costing methodology using the example of a cost-benefit analysis of mask CPAP for severe cardiogenic pulmonary oedema (CPO). This analysis examines the intervention of admitting all patients with severe CPO to the intensive care unit for mask CPAP, compared with the previous practice of admitting only patients failing conventional non-CPAP treatment and requiring mechanical ventilation. The episode costs were determined from a prospective study which showed mask CPAP reduced the need for mechanical ventilation from 35% to 0%. The mean cost of a mask CPAP episode was $1,156, with a mean stay of 1.2 days, compared with ventilated patients, $5,055 and 4.2 days. The major contributors to cost in both groups were nursing and medical salaries, and hospital overheads. The cost of previous estimated yearly caseload of 35 ventilated patients ($176,925) was greater than the cost associated with an increased caseload of 100 mask CPAP patients ($115,600). We conclude that, despite an increase in admissions, mask CPAP for severe CPO is cost-effective.
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PMID:Intensive care costing methodology: cost benefit analysis of mask continuous positive airway pressure for severe cardiogenic pulmonary oedema. 821 20

In patients who have experienced near-drowning, hypoxemia is the major clinical consequence. We report two cases of patients who have experienced near-drowning in freshwater who were successfully treated with nasal-continuous positive airway pressure (N-CPAP) plus oxygen therapy. Both patients presented a radiographic appearance of bilateral pulmonary edema. We suggest the use of N-CPAP as an easier and less costly alternative to tracheal intubation for treating near-drowning in patients who are breathing spontaneously and who have not experienced loss of consciousness.
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PMID:Nasal-continuous positive airway pressure in the treatment of near-drowning in freshwater. 887 83

Noninvasive mechanical ventilation has been suggested for the treatment of patients with respiratory failure. We describe the case of a patient affected by bilateral cystic bronchiectasis and acute hypercapnic respiratory failure, due to a cardiogenic pulmonary edema, successfully treated with bi-level nasal-CPAP. This report suggests that in some cases noninvasive ventilatory support may mean avoiding tracheal intubation, even with critically ill patients.
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PMID:Pulmonary edema and acute hypercapnic respiratory failure treated with bi-level nasal-CPAP: case report. 917 22

Six cases of post-extubation pulmonary oedema in otherwise healthy patients are reported. All were preceded by an episode of laryngospasm and followed a clinical course similar to that previously documented in cases of post-obstructive pulmonary oedema. Frank haemoptysis was a feature of five of the presentations. One patient was reintubated and ventilated, two were admitted to the intensive care unit for mask CPAP, one was managed with CPAP in the recovery ward and two with supplemental oxygen only. All cases resolved fully within 24 hours. Some evidence points to the syndrome being the result of airway bleeding rather than true pulmonary oedema. The literature suggests that it occurs more commonly than is generally thought, with a frequency of 0.05 to 0.1% of all anaesthetics, and is often unrecognised or misdiagnosed. Most cases occur in the early postoperative period, so anaesthetists are well placed to witness, investigate and manage this interesting condition.
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PMID:Postobstructive pulmonary oedema--a case series and review. 1126 21

Pulmonary edema following acute or chronic upper airway obstruction is a threatening complication. A case is presented in which a 15 year old boy developed a massive pulmonary edema after a acute endotracheal tube obstruction during emergence from anesthesia. Leading pathophysiologic cause for the formation of the edema is a markedly negative intrapleural pressure due to the forceful inspiration against the obstructed airway. Treatment modalities include the instantaneous solution of the obstruction, a rapid reoxigenation and the ventilation with PEEP or CPAP. Sound knowledge of the disease increases the vigilance of the caring anaesthesiologist and helps to identify patients at risk. Preventing measures may further reduce the risk of occurrence of the postobstructive pulmonary edema.
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PMID:[Post-obstructive pulmonary edema as a complication of endotracheal tube obstruction]. 1113 Jan 39


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