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Biomedical subjects

S A Sahn

Publications and source records attributed to S A Sahn.

At least 127 records · Page 7Linked to original sources
PubMed1987

Aspergilloma in sarcoid and tuberculosis.

The presentation, treatment, and outcome of 28 patients with aspergilloma and cavitary tuberculosis (14) and sarcoidosis (14) were compared. Patients with tuberculosis had localized disease (12 of 14, 86 percent), whereas patients with sarcoidosis had diffuse disease (1 of 14, 7 percent localized). Results indicated that patients with either sarcoid or tuberculosis who developed an aspergilloma had a poor prognosis over the next decade. Patients with sarcoid appeared to have a worse short-term prognosis; surgical resection in the tuberculosis patients may have contributed to their better short-term survival.

Aspergillosis↗
PubMed1986

Mycosis fungoides presenting as ARDS and diagnosed by bronchoalveolar lavage. Radiographic and pathologic pulmonary manifestations.

A patient with mycosis fungoides involving the lung, presenting with ARDS, and diagnosed by bronchoalveolar lavage, is described. A review and correlation of chest radiographic manifestations and pathologic observations are presented. We stress the importance of obtaining a specific diagnosis in light of the tenuous radiographic-pathologic correlation and discuss procedures for diagnosis and the inclusion of bronchoalveolar lavage as a previously undescribed diagnostic modality. The dismal prognosis of these patients, once pulmonary involvement is diagnosed, is noted.

Adult↗
PubMed1986

Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction. Are certain patients at increased risk?

Pulmonary edema due to upper airway obstruction can be observed in a variety of clinical situations. The predominant mechanism is increased negative intrathoracic pressure, although hypoxia and cardiac and neurologic factors may contribute. Laryngospasm associated with intubation and general anesthesia is a common cause of pulmonary edema in children. However, only seven cases of pulmonary edema presumably due to laryngospasm have been reported in adolescents and adults. Five of the seven had other risk factors for upper airway obstruction, and in four, the diagnosis of "laryngospasm" could be explained by other factors. Patients with underlying risk factors for upper airway obstruction, such as a forme fruste of sleep apnea or nasopharyngeal abnormalities, appear to be at increased risk for the development of pulmonary edema in the setting of intubation and anesthesia. This form of pulmonary edema usually resolves rapidly without the need for aggressive therapy or invasive monitoring.

Airway Obstruction↗
PubMed1985

The pathogenesis of low glucose, low pH malignant effusions.

Possible mechanisms to explain the finding of a low pH, low glucose, malignant pleural effusion include: use of glucose and acid production by pleural fluid constituents including leukocytes and free malignant cells; pleural membrane metabolism, especially by malignant cells; abnormal transfer of glucose, carbon dioxide, and hydrogen ion across a diseased pleural membrane. To determine the pathogenesis of low glucose, low pH effusions, we performed incubation and glucose and gas transport studies in 5 patients with malignant effusions, 3 with a low pH (less than 7.30) and 2 with a pH greater than 7.30 (control patients). After 24 h of incubation, there was no significant difference in the metabolic activity of pleural fluid between low pH fluids and control fluids. Transport studies confirmed impaired glucose transfer both into and out of the pleural space and impaired efflux of CO2 from the pleural space in patients with low pH effusions, whereas control patients demonstrated free transfer across the pleural membrane. It appears that an abnormal pleural membrane (tumor or fibrosis), rather than increased acid production, results in a low glucose concentration from impaired glucose transfer from blood to pleural fluid and a low pH from impaired hydrogen ion efflux in some malignant effusions.

Adenocarcinoma↗
PubMed1985

Bacillus Calmette-Guérin-stimulated neutrophils release chemotaxins for monocytes in rabbit pleural spaces and in vitro.

Neutrophils are often seen first at sites of granulomatous inflammation but their contribution to monocyte recruitment and granuloma formation is unknown. We tested the hypothesis that neutrophils release chemotaxins which attract monocytes. We found that rapid accumulations of fluid and influxes of neutrophils followed by monocytes occurred in bacillus Calmette--Guérin (BCG)-sensitized rabbits given BCG intrapleurally but did not occur in nitrogen mustard-treated (neutropenic) BCG-sensitized rabbits given BCG intrapleurally--unless the rabbits were also given intrapleural injections of neutrophils. We also found monocyte chemotaxins in pleural spaces of control and neutrophil-reconstituted neutropenic but not in neutropenic rabbits given BCG intrapleurally. Moreover, pleural fluid monocyte chemotaxins had molecular weights (12,000-15,000 and 1,000) that were similar to molecular weights of monocyte chemotaxins present in supernatants from mixtures of neutrophils and BCG in vitro. In addition, intrapleural injection of neutrophils and BCG or supernatants from in vitro mixtures of neutrophils and BCG (but not neutrophils or BCG alone) increased the numbers of monocytes and 3H cell pellet activity in pleural fluids from untreated neutropenic rabbits or neutropenic rabbits previously injected intravenously with 3[H]methyl thymidine-labeled monocytes. Furthermore, fewer BCG were recovered from pleural fluids of BCG-sensitized control compared to neutropenic rabbits given BCG, and at autopsy 10 d after instillation of BCG, control but not neutropenic rabbits had well-defined granulomas without adhesions on their pleural surfaces. Our results suggest that BCG stimulates neutrophils to release chemotaxins that recruit monocytes, and that these responses might contribute to granuloma formation in tuberculous pleurisy.

Animals↗
PubMed1985

Pleuropulmonary complications of enteral tube feedings. Two reports, review of the literature, and recommendations.

Enteral tube feeding is an attractive alternative to intravenous alimentation for nutritional support. As previously used nasogastric tubes have been replaced with narrow-bore nasogastric tubes, the spectrum of complications seen with these devices has changed. We report a previously undescribed event associated with narrow-bore nasogastric tube feeding, review the literature, noting predisposing factors and complications, and suggest guidelines to avoid pitfalls of insertion and the ensuing adverse effects.

Aged↗
PubMed1985

Malignant pleural effusions.

Various diseases of the gastrointestinal tract at times are accompanied by an exudative pleural effusion. The exudative pleural effusions resulting from esophageal perforation, pancreatic disease, subphrenic abscess, intrahepatic abscess, splenic abscess, abdominal operations, and diaphragmatic hernia are discussed in this article.

Adenocarcinoma↗
PubMed1985

Immunologic diseases of the pleura.

This heterogeneous group of immunologic causes of pleural effusions includes connective tissue diseases, a syndrome related to tissue injury (postcardiac injury syndrome), a disease of unknown etiology (sarcoidosis), a malignancy, and adverse reactions to drugs. Except in rheumatoid pleurisy and lupus pleuritis, the pleural fluid findings are either nonspecific or have not been characterized fully. The clinical presentation is essential in the presumptive diagnosis of these causes of pleural effusions.

Adult↗
PubMed1984

Pathogenesis of pleural plaques. Relationship of early cellular response and pathology.

To study the initial pleural cellular response to asbestos and to determine the relationship between this response and the development of pleural plaques, a model of asbestos pleurisy was developed in both normal and nitrogen-mustard-treated (neutropenic) New Zealand white rabbits. Animals were rendered neutropenic, as it has been shown that neutropenic rabbits do not develop a macrophage influx in the pleural space after the administration of either BCG or bacteria and that the pathology is different from that in normal rabbits treated in a similar fashion. Intrapleural asbestos induced an exudative effusion in normal animals within 4 h, and there was increased metabolic activity through 120 h, with a fall in pleural fluid pH and PO2 and a rise in pleural fluid PCO2. Neutropenic animals similarly developed an exudative pleural effusion but showed no change in metabolic activity of pleural fluid. Normal rabbits showed a marked cellular influx into the pleural space after asbestos treatment, with a peak total cell count of 27,208/microliters at 24 h; the majority of these cells were polymorphonuclear leukocytes. A macrophage influx occurred at 48 h and peaked at 72 h. By 120 h, lymphocytes were the predominant cell. Nitrogen-mustard-treated animals reached a peak of only 5,442 cells/microliters in the pleural space at 24 h, with a small percentage of polymorphonuclear leukocytes. A macrophage peak did not occur in these animals. There was a marked contrast between groups noted at autopsy. Normal animals developed pleural plaque formation, which was evident by 7 days and completely developed by 1 month.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Dimethyl sulfoxide inhibits phagocyte influx into infected pleural spaces and phagocyte locomotion in vitro.

Influx of polymorphonuclear leukocytes (PMNs) and monocytes (MNs) into pleural spaces was decreased in dimethyl sulfoxide (DMSO)-treated rabbits infected intrapleurally with Staphylococcus aureus. In addition, pleural fluids contained S. aureus longer and marked pleural thickening with fibrosis occurred in DMSO-treated rabbits. DMSO also inhibited stimulated locomotion of PMN and MN in vitro, suggesting that the aforementioned responses in vivo may have occurred because of DMSO-mediated inhibition of the locomotion of PMN and MN.

Animals↗
PubMed1983

The pathogenesis of the low pleural fluid pH in esophageal rupture.

To determine the possible mechanisms responsible for the low pH pleural effusion associated with esophageal rupture we evaluated the following possibilities: (1) gastric acid reflux, (2) bacterial metabolism, and (3) leukocyte metabolism. Neither elimination of gastric hydrogen ion contribution by distal esophageal ligation nor elimination of bacteria with antibiotics prevented the progressive fall in pleural fluid pH after esophageal rupture. Only elimination of polymorphonuclear leukocytes from the pleural space by rendering animals leukopenic with nitrogen mustard, prevented a low pH effusion after esophageal rupture. It appears that pleural fluid leukocyte metabolism is primarily responsible for the low pH effusion associated with esophageal rupture.

Animals↗