Reversible Pulmonary Edema Research Articles

Pulmonary toxicity of sodium dichloroisocyanurate after intratracheal instillation in sprague-dawley rats.

In water, sodium dichloroisocyanurate (NaDCC), a source for chlorine gas generation, releases free available chlorine in the form of hypochlorous acid, a strong oxidizing agent. NaDCC has been used as a disinfectant in humidifiers; however, its inhalation toxicity is a concern. Seven-week-old rats were exposed to NaDCC doses of 100, 500, and 2500μg·kg-1 body weight by intratracheal instillation (ITI) to investigate pulmonary toxicity. The rats were sacrificed at 1 d (exposure group) or 14 d (recovery group) after ITI. Despite a slight decrease in body weight after exposure, there was no statistically significant difference between the control and NaDCC-treated groups. A significant increase in the total protein level of the bronchoalveolar lavage fluid (BALF) was observed in the exposure groups. Lactate dehydrogenase leakage into the BALF increased significantly (p < 0.01) in the exposure groups; however, recovery was observed after 14 d. The measurement of cytokines in the BALF samples indicated a significant increase in interleukin (IL)-6 in the exposure group and IL-8 in the recovery group. Histopathological examination revealed inflammatory foci and pulmonary edema around the terminal bronchioles and alveoli. This study demonstrated that ITI of NaDCC induced reversible pulmonary edema and inflammation without hepatic involvement in rats.

Massive Inhalation of Desflurane due to Vaporizer Dysfunction

Massive Inhalation of Desflurane due to Vaporizer Dysfunction

Pulmonary injury after intravenous hydrocarbon injection

This report describes the case of a young man in whom an intravenous injection of a hydrocarbon led to reversible pulmonary edema. An 18-year-old male presented with chest pain, a cough and progressive dyspnea at a multidisciplinary paediatric intensive care unit in a tertiary care university hospital. Six hours after oxygen was given, blood gases were pH 7.16, partial pressure of carbon dioxide 43 torr (5.7 kPa), partial pressure of arterial oxygen 149 torr (19.9 kPa) and bicarbonate concentration 15 mEq/L. A chest radiograph suggested pulmonary edema. On day 3, the patient stated that he had injected himself with Varsol (Imperial Oil, Canada) - a mixture of straight and branched-chain hydrocarbons, naphthenes and alkyl derivatives of benzene - several hours before his admission. On day 5, the patient's respiratory rate returned to 20 breaths/min, and his chest radiograph was normal by day 7. The present case report suggests that the intravenous injection of hydrocarbons may lead to reversible pulmonary injury.

Reversible pulmonary edema due to bilateral renal artery stenosis

Reversible pulmonary edema due to bilateral renal artery stenosis

Evaluation of the respiratory tract after acute exposure to a pyrotechnically generated aerosol fire suppressant.

Fischer 344 rats (250-300 g) were exposed to the resulting aerosols from the pyrolysis of Spectrex Fire Extinguishant (SFE) Formulation A, a pyrotechnically generated aerosol fire suppressant, at a loading equivalent of 50 or 80 g m(-3) air for 15 or 60 min. Exposures were conducted in a 700-1 whole-body inhalation chamber under static conditions. The chamber atmosphere was analyzed for mass aerosol concentration and size distribution. Clinical observations were taken throughout the exposure. Animals were euthanized at 1 h, 6 h, 24 h, 7 days or 14 days post-exposure and underwent histopathological examination, enzyme analyses and wet/dry lung weight determination. No deaths occurred during the study. Animals exhibited signs of dyspnea, coughing, lack of coordination and lethargy during each exposure. These signs became more pronounced as the load and exposure length increased. No lesions were noted in the trachea, lung, heart or abdominal organs upon gross examination. A reversible pulmonary edema and olfactory necrosis were observed only in those animals exposed to an SFE loading equivalent to 80 g m(-3) for 60 min. Protein concentrations increased in the bronchoalveolar lavage but no changes in enzyme levels were observed. There was no significant difference between the control groups and the exposure groups for wet/dry lung weight determination.

Use of intravenous gamma globulin to passively immunize high-risk children against respiratory syncytial virus: safety and pharmacokinetics. The RSVIG Study Group

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.

Noncardiac pulmonary edema precipitated by tracheal intubation in patients with inhalation injury.

Ten patients with body surface burn and clinical evidence of inhalation injury developed transient, reversible pulmonary edema within 5 min after endotracheal intubation. Hemodynamic studies within 1 hr after intubation revealed normal cardiac output and pulmonary artery wedge pressure (WP). Additionally, in the latter 4 patients, protein concentration of edema fluid (EF) aspirated from the trachea was 58-104% of plasma (P) total protein. These findings suggest that altered capillary permeability was responsible for this transient pulmonary edema. It is postulated that glottic generated expiratory retard may increase alveolar pressure, thus preventing pulmonary edema. Bypass of glottis by tracheal intubation may render alveolar pressure atmospheric and facilitate edema formation.

HEMODYNAMIC AND ALVEOLAR PROTEIN STUDIES IN NONCARDIAC PULMONARY EDEMA

Hemodynamic data were obtained within 15 hours of admission in 11 previously healthy patients (20 to 51 years of age, 7 men and 4 women) who had developed transient, reversible pulmonary edema without cardiac dilation in association with near-death from freshwater drowning (2 cases), pentobarbital overdose, heroin overdose (2 cases), smoke inhalation, chest trauma, sepsis (2 cases), pancreatitis, or prolonged abdominal surgery with suspected sepsis. Using a balloon-tipped flow-directed catheter, the pulmonary artery systolic/diastolic pressures (in mm Hg) were 25/12, 22/9, 31/11, 26/15, 20/10, 35/15, 40/15, 32/18, 20/10, 24/10, and 20/7; the corresponding pulmonary capillary wedge pressures (in mm Hg) were 8, 9, 6, 14, 6, 6, 15, 15, 10, 10, and 5, respectively. Plasma colloidal osmotic pressures measured in the latter 5 cases were 26, 18, 18, 18, and 15 mm Hg, respectively. In addition, the protein content of the alveolar fluid was 5.1, 3.4, 4.0, and 7.1 g per 100 ml in 4 patients. The concentration and distribution of the protein in plasma and alveolar fluid were very similar. These findings provide strong efidence that altered capillary permeability is responsible for the pulmonary edema.

Hemodynamic and alveolar protein studies in noncardiac pulmonary edema.

Hemodynamic data were obtained within 15 hours of admission in 11 previously healthy patients (20 to 51 years of age, 7 men and 4 women) who had developed transient, reversible pulmonary edema without cardiac dilation in association with near-death from freshwater drowning (2 cases), pentobarbital overdose, heroin overdose (2 cases), smoke inhalation, chest trauma, sepsis (2 cases), pancreatitis, or prolonged abdominal surgery with suspected sepsis. Using a balloon-tipped flow-directed catheter, the pulmonary artery systolic/diastolic pressures (in mm Hg) were 25/12, 22/9, 31/11, 26/15, 20/10, 35/15, 40/15, 32/18, 20/10, 24/10, and 20/7; the corresponding pulmonary capillary wedge pressures (in mm Hg) were 8, 9, 6, 14, 6, 6, 15, 15, 10, 10, and 5, respectively. Plasma colloidal osmotic pressures measured in the latter 5 cases were 26, 18, 18, 18, and 15 mm Hg, respectively. In addition, the protein content of the alveolar fluid was 5.1, 3.4, 4.0, and 7.1 g per 100 ml in 4 patients. The concentration and distribution of the protein in plasma and alveolar fluid were very similar. These findings provide strong efidence that altered capillary permeability is responsible for the pulmonary edema.

Letter: Reversible pulmonary edema following cyclophosphamide treatment.

To the Editor.— I would like to report the occurrence of a case of acute reversible pulmonary edema with circulatory and renal failure following intravenous use of cyclophosphamide. A 60-year-old man presented with night sweats, weight loss, and abdominal discomfort of several weeks' duration, and hematemesis and melena of several hours' duration in October 1973. At laparotomy, diffuse histiocytic lymphoma involving the retroperitoneal lymph nodes and mesenteric lymph nodes with invasion of the duodenojejunal flexure was found. Staging with bone scan, liver scan, liver function tests, chest x-ray examination, lymphangiogram, and blood and bone marrow examination revealed no other areas of involvement. Radiation in an inverted mantle field to a dose of 4,000 rads over a four-week period was given in November and December 1973. Chemotherapy with orally given prednisone, 50 mg twice daily for five days, and one dose each of cyclophosphamide, 500 mg intravenously, and vincristine, 2 mg