In many cases, the surgery results in the death of one or both of the twins, particularly if they are joined at the head or share a vital organ. This makes the ethics of surgical separation, where the twins can survive if not separated, contentious. Alice Dreger of Northwestern University found the quality of life of twins who remain conjoined to be higher than is commonly supposed. Lori and George Schappell and Abby and Brittany Hensel are notable examples. The first record of separating conjoined twins took place in the Byzantine Empire in the 900s. One of the conjoined twins had already died, so the doctors of the town attempted to separate the dead twin from the surviving twin. The result was partly successful as the remaining twin lived for three days after separation. The next case of separating conjoined twins was recorded in 1689 in Germany several centuries later. The first recorded successful separation of conjoined twins was performed in 1689 by Johannes Fatio. In 1955, neurosurgeon Harold Voris (1902-1980) and his team at Mercy Hospital in Chicago performed the first successful operation to separate craniopagus twins (conjoined at the head), which resulted in long-term survival for both. The larger girl was reported in 1963 as developing normally, but the smaller girl was permanently impaired.In 1957, Bertram Katz and his surgical team made international medical history performing the worlds first successful separation of conjoined twins sharing a vital organ.
The characteristic pulmonary function finding in asbestosis is a restrictive ventilatory defect. This manifests as a reduction in lung volumes, particularly the vital capacity (VC) and total lung capacity (TLC). The TLC may be reduced through alveolar wall thickening; however, this is not always the case. Large airway function, as reflected by FEV1/FVC, is generally well preserved. In severe cases, the drastic reduction in lung function due to the stiffening of the lungs and reduced TLC may induce right-sided heart failure (cor pulmonale). In addition to a restrictive defect, asbestosis may produce reduction in diffusion capacity and a low amount of oxygen in the blood of the arteries. Cause
The cause of asbestosis is the inhalation of microscopic asbestos mineral fibers suspended in the air. In the 1930s, E. R. A. Merewether found that greater exposure resulted in greater risk. Pathogenesis
Asbestosis is the scarring of lung tissue (beginning around terminal bronchioles and alveolar ducts and extending into the alveolar walls) resulting from the inhalation of asbestos fibers. There are two types of fibers: amphibole (thin and straight) and serpentine (curly). All forms of asbestos fibers are responsible for human disease as they are able to penetrate deeply into the lungs. When such fibers reach the alveoli (air sacs) in the lung, where oxygen is transferred into the blood, the foreign bodies (asbestos fibers) cause the activation of the lungs local immune system and provoke an inflammatory reaction dominated by lung macrophages that respond to chemotactic factors activated by the fibers.