ABSTRACT
Seven states now have laws requiring managed care plans to sign contracts with any primary care physician willing to meet contract terms. How do these laws affect patient care? Here's background on the issue, followed by the views of two physicians: one in favor of such laws and one opposed.
Subject(s)
Credentialing/legislation & jurisprudence , Physicians, Family/legislation & jurisprudence , Preferred Provider Organizations/legislation & jurisprudence , Contract Services/legislation & jurisprudence , Cost-Benefit Analysis , Patient Satisfaction , Practice Patterns, Physicians' , Preferred Provider Organizations/economics , Preferred Provider Organizations/standards , Quality of Health Care , State Health Plans/legislation & jurisprudence , United StatesABSTRACT
A 48-year-old woman had an 18-month history of malaise and chronic cough with intermittent episodes of fever, chills, and pneumonic infiltrates. Transbronchial biopsy findings were consistent with hypersensitivity pneumonitis. Cultures of fungus from a hot-tub room in her home were positive for Cladosporium species. Serum precipitins were weakly positive for Cladosporium cladosporioides. Removal of the patient from the home environment led to a resolution of symptoms within 1 week. Within 4 hours of re-exposure to the hot-tub room, symptoms and signs and changes in leukocyte count and spirometric values again occurred. Bronchial provocation with a commercial extract of C. cladosporioides led to a similar pattern 5 hours after the initial challenge. This case identifies a previously unreported etiologic agent and environmental site for hypersensitivity pneumonitis.
Subject(s)
Alveolitis, Extrinsic Allergic/etiology , Cladosporium/immunology , Mitosporic Fungi/immunology , Water Microbiology , Baths , Bronchial Provocation Tests , Dust , Female , Humans , Middle Aged , Precipitins/analysis , Skin Tests , Time FactorsABSTRACT
The response of the injured lung to hyperoxia is uncertain. In the present study, we evaluated the effects of 100% oxygen exposure for 120-168 h in mechanically ventilated baboons with or without previous diffuse alveolar damage (DAD) induced by oleic acid. These two groups were compared with another group of six baboons previously studied in our laboratory in which DAD induced with oleic acid was followed by ventilation with 40% oxygen. Oleic acid infusion caused a prompt reduction in total lung capacity, static compliance, and diffusion capacity and an increase in lung tissue volume. The magnitude and course of oleic acid lung injury was similar for 4 days in animals breathing 100% or 40% O2. Animals breathing 100% O2 without previous lung injury developed significant decreases in total lung capacity, oxygenation, and diffusion capacity after 72 h of hyperoxia. By 120 h, lung function was similarly impaired in both 100% O2-breathing groups, and rapidly worsening pulmonary edema appeared radiographically between 5.5 and 7 days in all O2-exposed animals. Subsequent weaning was successful in only three animals after 100% O2 exposure. All but one animal in the 40% O2 group were easily weaned. Histologic changes between 6 and 14 days in 100% O2 animals showed a marked proliferative response, particularly of type 2 cells; no differences were found due to prior oleic acid injury. Resolution of this process occurred in a surviving animal, resulting in focal fibrotic residua at 6 weeks, similar to that observed in 40% O2 oleic acid-treated survivors. Previous lung injury due to oleic acid did not modify the response of the baboon lung to hyperoxia.
Subject(s)
Lung Diseases/physiopathology , Lung/physiopathology , Oxygen/pharmacology , Animals , Lung/drug effects , Lung/pathology , Lung Compliance/drug effects , Lung Diseases/chemically induced , Lung Diseases/pathology , Lung Volume Measurements , Male , Oleic Acid , Oleic Acids , Papio , Pulmonary Alveoli/pathology , Pulmonary Diffusing Capacity/drug effects , Respiration, ArtificialABSTRACT
Lung repair after diffuse alveolar damage (DAD) may be modified by supportive therapy or the occurrence of complications. To provide a clinically relevant model of DAD, we studied the feasibility of long-term respiratory support of 5 normal baboons and 20 baboons with oleic-acid-induced lung injury. Oleic acid caused DAD, which evolved through exudative and reparative phases similar to those seen in human disease. Fibrotic residuals were present at 1 month but resolved by 6 months. Pulmonary function abnormalities, including reduction in total lung capacity and diffusing capacity, and hypoxemia occurred with DAD but resolved within 1 month. Bronchopulmonary infection with gram-negative bacilli was a common and frequently fatal complication. Revisions in management of the upper airway and the use of topical polymyxin B prevented this complication. Other complications included hemorrhagic gastritis, postextubation, upper airway obstruction, and pulmonary embolism. This model simulates many features of DAD in humans and should provide a valuable resource for future study.
