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W Sandritter

Publications and source records attributed to W Sandritter.

At least 19 recordsLinked to original sources
PubMed1979

Morphologic development of human shock lung.

In the initial phase of shock, edema spreads throughout the alveolar interstitium even before injury occurs in the alveolar epithelium and endothelium. The endothelium and the epithelium are damaged only subsequently, causing reduction in the average barrier thickness of the epithelium and the endothelium. A point of irreversibility is reached by the end of the first week. While early cell regeneration may be observed within the alveolar endothelium and epithelium, proliferation of fibroblasts and fibrosis of the alveolar wall occur in addition to edema which spreads within the interstitium. This widening of the gas exchange barrier may be considered as the anatomic substrate of respiratory insufficiency induced by shock. This enlargement continues up to the moment when thickening of the alveoli impedes satisfactory functioning of the lung, and, as consequence, threatens the life of the patient.

Cell Division↗
PubMed1978

Surveillance, prevention and control of hospital-acquired infections. III. Nosocomial infections as cause of death: retrospective analysis of 1000 autopsy reports.

One thousand post-mortem reports were analysed retrospectively to see whether the patient had had a nosocomial or community-acquired infection and whether this led directly to or contributed to the patient's death. In 7.4% of all autopsies nosocomial infection was the direct cause of death. In 6.3% of the patients, nosocomial infection was a contributory factor leading to death. The most common hospital infections were pneumonia, septicaemia, peritonitis, meningitis, and hepatitis B. Most infections which led to or contributed to death were acquired in surgical wards. Patients with nosocomial infections, however, were more endangered by factors predisposing to infections (1.8 factors per patient) than patients without nosocomial infections (0.67 factors per patient). Sixty-three patients acquired an infection outside the hospital; in 70% of these patients, the infection was the main or contributory cause of death.

Adolescent↗
PubMed1978

The pulmonary air-blood barrier of human shock lungs (a clinical, ultrastructural and morphometric study).

Interstitial edema in the alveolar septa is the first morphologically recognisable change to be observed in cases of shock. It is brought about by the altered function of the membranes of the damaged epithelium and endothelium in the alveolar wall. At the same time there is an impairment of gaseous exchange, which is rendered more difficult by the exudative process in the interstitium. Pari passu with these events there is injury to the cells of both the alveolar epithelium and the alveolar capillary endothelium. Both these processes are still reversible. The point of irreversibility appears to be reached--so far as time is concerned--at the end of the first week, after which the injurious effects on the cell are established, since the thin alveolar wall necessary for the exchange of gases becomes overgrown with bulky alveocytes (Tpye II), and the fibroblasts in thealveolar interstitium push the capillaries away from the surface of the alveolus. In most of the advanced cases of shock this process of thickening of the alveolar wall exceeds the critical value, and respiratory exchange is so impaired that satisfactory functioning of the lungs is no longer possible.

Adult↗
PubMed1978

[Shock lung].

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Humans↗