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Biomedical subjects

C Strange

Publications and source records attributed to C Strange.

53 records · Page 3Linked to original sources

Double-lumen endotracheal tubes.

Double-lumen endotracheal tubes have revolutionized the anesthetic management of patients undergoing thoracic surgery. As experience with the techniques of DLT placement and monitoring progress, an increasing number of uses in the intensive care unit will evolve. Benefit from differential lung ventilation in patients with respiratory failure from unilateral lung diseases and bronchopleural fistulae has been documented in selected instances. Isolation of the lungs to prevent contralateral spread of hemoptysis is occasionally of assistance. Frequent monitoring of DLT position while understanding the physiology of differential lung ventilation will minimize complications with these tubes.

Humans↗

Management of parapneumonic pleural effusions and empyema.

Parapneumonic pleural effusions, the most common causes of exudative pleural fluid, are a frequent finding with bacterial pneumonia. Progression to empyema is related to delay in appropriate antimicrobial therapy. Once an empyema develops, therapy consists of early sterilization of the empyema space with appropriate antibiotics, early and adequate pleural space drainage, and obliteration of the empyema cavity by adequate lung expansion, surgical decortication, or enzymatic debridement.

Empyema, Pleural↗

Subglottic stenosis in Wegener's granulomatosis: development during cyclophosphamide treatment with response to carbon dioxide laser therapy.

A patient with Wegener's granulomatosis rapidly developed a circumferential subglottic stenosis while on a cyclophosphamide regimen that had caused resolution of systemic symptoms and pulmonary infiltrates. The stenosis developed in the area of previously noted tracheal ulceration and responded satisfactorily to carbon dioxide laser therapy.

Adult↗

Do chest radiographic findings reflect the clinical course of patients with sarcoidosis during corticosteroid withdrawal?

The use of serial chest radiographs to assess disease activity in patients with sarcoidosis is controversial. However, reliance on the symptomatic clinical course to assess disease activity may be misleading. As many patients being treated with corticosteroids have an abrupt clinical deterioration when doses of those medications are decreased, we questioned whether the chest radiograph could depict alterations in disease activity as measured by spirometry in this subset of patients. We retrospectively reviewed the clinical course of all patients with pulmonary sarcoidosis in whom the corticosteroid dose was reduced during a 6-month period. The 15 patients without fever, chills, or purulent sputum during that time were then examined to determine the presence (n = 10) or absence (n = 5) of a symptomatic relapse. All patients who had a symptomatic relapse also had a fall in forced vital capacity of at least 10%, suggesting an increase in disease activity. Serial chest radiographs were evaluated during and after corticosteroid dose reductions and after clinical recovery on higher steroid doses in the patients who had had a relapse. In eight patients, the disease was in radiographic stage 2 (hilar adenopathy and parenchymal lung disease); in seven patients it was in radiographic stage 3 (parenchymal lung disease alone). The disease did not change stage in any patient during the study. Chest radiographs worsened more frequently in patients who had a clinical relapse (seven of 10) than in those who did not have a relapse (zero of five, p less than .05). An alveolar chest radiographic pattern (n = 4) or reticulonodular pattern (n = 3) was noted in the seven patients who had a relapse, with worsening on radiographs often occurring before detection of relapse by symptomatology (four of seven) or spirometry (three of seven). Spirometry and radiographs improved or stabilized after an increase in corticosteroid dose in all 10 patients who had a relapse. We conclude that serial chest radiographs can reflect clinical relapse in patients with sarcoidosis during corticosteroid dose reduction. Furthermore, worsening seen on chest radiographs may be the first evidence of relapse.

Adrenal Cortex Hormones↗

The histology of experimental pleural injury with tetracycline, empyema, and carrageenan.

Models of pleural injury were established with intrapleural tetracycline, intrapleural carrageenan, and empyema in New Zealand White rabbits to evaluate histologically the pleural inflammatory response from 3 to 90 days. Both tetracycline and empyema models produced increases in the pleural connective tissue layers both above and below the fibroelastic membrane associated with angiogenesis and lymphangiogenesis. The influx of fibroblasts from the pleural surface into acellular fibrin strands formed adhesions between the visceral and the parietal pleurae. Injury to the mesothelial cell ranged from a cuboidal transition to total desquamation with the degree of mesothelial injury associated with the amount of fibrin adherence and the propensity toward fibrosis at 90 days. Intervention to promote the resolution of pleural inflammation without fibrosis should be directed toward preservation of the mesothelial surface, removal of pleural fibrin, and inhibition of fibroblast growth and chemotaxis.

Animals↗

Biliopleural fistula as a complication of percutaneous biliary drainage: experimental evidence for pleural inflammation.

We describe 3 patients in whom biliopleural fistulae complicated percutaneous biliary drainage. All patients had complete obstruction of their biliary tree because of malignancy. Biliopleural fistulae developed as a complication of inadvertent catheter removal in 2 patients and of catheter dysfunction in the third. Early reinstitution of biliary drainage and successful drainage of the pleural space led to complete recovery in all patients. An animal model to evaluate the effects of bile in the pleural space in normal rabbits revealed rapid absorption of bilirubin, the production of a polymorphonuclear-predominant exudative effusion with extremely high LDH levels, and resolution with a macrophage influx. We conclude that biliopleural fistulae are heterogeneous in their presentation, depending upon the persistence of biliary drainage into the pleural space, the volume of exudative effusion, and the presence of suppurative complications.

Aged↗

Effect of patient positioning on distribution of tetracycline in the pleural space during pleurodesis.

Thoracostomy tube drainage with tetracycline (TCN) instillation is an effective technique for management of recurrent, symptomatic, malignant pleural effusions. Although patient rotation through various positions after instillation of TCN has been advocated empirically, it has not been shown scientifically to be necessary and is often uncomfortable for the patient and time-consuming for personnel. Five patients with symptomatic, malignant pleural effusions were studied during pleurodesis using radiolabelled TCN. Scintigraphic imaging was done immediately after TCN instillation prior to patient rotation. Patients were rotated through six positions and multiple images were obtained at 30 and 120 minutes. Tetracycline dispersed throughout the pleural space within seconds. Patient positioning had no effect on the intrapleural distribution of TCN in four of the five patients. In one patient with loculated hydropneumothorax and trapped lung, rotation minimally improved distribution of TCN to the apex. Rotation during pleurodesis does not appear to be necessary in patients with a relatively normal pleural space. However, patient rotation enhances distribution of TCN when the lung is separated substantially from the chest wall, as with trapped lung. Possibly, in this situation the properties of fluid mechanics and capillary action no longer apply.

Adult↗

Lidocaine concentrations in bronchoscopic specimens.

We measured lidocaine concentrations in bronchoscopic specimens and found that bronchoalveolar lavage (BAL) concentrations (16 +/- 7 micrograms/ml) were lower than those in bronchial washings (967 +/- 379 micrograms/ml [p less than 0.001]). Lidocaine concentrations in bronchial washings obtained "early" (991 +/- 505 micrograms/ml) compared with "late" (943 +/- 580 micrograms/ml) in the procedure did not differ (p = NS). High lidocaine concentrations sufficient to inhibit growth in culture of mycobacterial and fungal pathogens (greater than 5,000 micrograms/ml) occurred in one early and two late bronchial washings but no BAL specimens. No correlation between lidocaine dose and measured concentrations was noted in any specimen category; however, highest bronchial washing concentrations occurred with the use of greater than 250 mg of lidocaine. We conclude that BAL specimens are suitable for culturing pathogens that may be inhibited by lidocaine. Furthermore, collecting bronchial washings late in the procedure or limiting the lidocaine dosage do not reliably decrease measured lidocaine concentrations.

Bronchoalveolar Lavage Fluid↗

Systemic absorption of tetracycline and lidocaine following intrapleural instillation.

Seven patients with symptomatic pleural effusions (six) and recurrent pneumothorax (one) underwent attempted pleurodesis using tetracycline. Lidocaine (150 mg), followed immediately by tetracycline (20 mg/kg), was instilled into the pleural space through a chest tube. Venous blood was obtained at 0, 15, 30, 60, and 120 minutes following instillation in order to determine concentrations of lidocaine and tetracycline. The mean peak serum concentration of lidocaine was 1.3 mu/ml +/- 0.4 microgram/ml (mean +/- SE) (range, 0.3 microgram/ml to 3.2 microgram/ml), and the mean time to peak serum concentration of lidocaine was 86 +/- 13 minutes. The mean peak serum concentration of tetracycline was 3.6 microgram/ml +/- 0.9 microgram/ml (range, 1.0 microgram/ml to 5.0 micrograms/ml), and the mean time to peak serum concentration of tetracycline was 96 +/- 16 minutes. Therapeutic serum concentrations of lidocaine were found in four of the seven patients and therapeutic serum levels of tetracycline in four of five patients. With systemic absorption of lidocaine and tetracycline following intrapleural instillation, patients are at risk for potential toxic effects. If lidocaine is used in a dosage of less than 3 mg/kg, toxic levels of the drug are unlikely to occur. Furthermore, use of tetracycline or lidocaine in pleurodesis is contraindicated in patients with known sensitivity to the drugs.

Female↗

The impact of respiratory failure on the diagnosis of tuberculosis.

Six patients with hypoxic respiratory failure (arterial PO2/alveolar PO2 less than 0.50) resulting from active tuberculosis were evaluated to assess the impact of respiratory failure on the diagnosis of the underlying tuberculosis. All patients demonstrated anemia (hematocrit [mean +/- SEM], 0.29 +/- 0.01 [29.0% +/- 1.0%]) and hypoalbuminemia (serum albumin, 22 +/- 2 g/L [2.2 +/- 0.2 g/dL]) and noted an illness longer than one week. Findings on chest roentgenograms varied from a miliary pattern, misinterpreted as congestive heart failure, to cavitary and noncavitary alveolar infiltrates, misdiagnosed as bacterial pneumonia. Tuberculosis was not considered as a diagnostic possibility on admission in any patient. The mean time from admission until consideration of tuberculosis was 4.7 +/- 1.0 days and the time to diagnosis was 7.2 +/- 1.7 days. In contrast, tuberculosis was considered on admission in 12 patients presenting with undiagnosed active tuberculosis without respiratory failure. We conclude that respiratory failure delays the diagnosis of active tuberculosis by suggesting nontuberculous pneumonia.

Adult↗

Pulmonary hemorrhage and air embolism complicating transbronchial biopsy in pulmonary amyloidosis.

We describe a fatal complication of transbronchial biopsy in a patient with pulmonary parenchymal amyloidosis. Hemorrhage after biopsy required intubation and positive-pressure ventilation that resulted in massive arterial air embolism. Postmortem findings suggested that the bleeding and air embolism were related to persistent patency of biopsied blood vessels infiltrated with amyloid. Patients with pulmonary amyloidosis may be at increased risk of major complications after transbronchial biopsy.

Aged↗

Use of pooled DNA samples to detect linkage disequilibrium of polymorphic restriction fragments and human disease: studies of the HLA class II loci.

A rapid method has been developed and used to search for restriction fragment length polymorphisms (RFLPs) that are in linkage disequilibrium with disease-associated loci. By using genomic blot-hybridization analysis with DQ beta-chain and DR beta-chain cDNA probes, we examined DNA polymorphisms within the HLA class II loci associated with susceptibility to insulin-dependent mellitus (IDDM). To facilitate the search for informative RFLPs, we compared pooled DNA samples from IDDM patients with pooled DNA samples from randomly selected control individuals, instead of using the conventional approach of examining DNA samples from individuals in two groups. (The conditions under which this approach is useful are treated theoretically in the Appendix.) Several specific polymorphic restriction fragments associated with IDDM were revealed by using this economical and rapid approach. The restriction enzymes and probes identified as informative in this screening were then used to analyze HLA-DR-typed IDDM families, homozygous typing cells, and unrelated individuals to determine the association of the specific restriction fragments with HLA-DR serological type and the frequency in control and IDDM populations. Some individual polymorphic fragments for which the IDDM population was enriched correlated strongly with HLA-DR3, whereas others correlated strongly with HLA-DR4. Some fragments (e.g., a 10-kilobase Taq I fragment detected with the DR beta probe) that were more prevalent in the IDDM population subdivided the serologically defined HLA-DR type and may be informative markers for IDDM susceptibility.

Cloning, Molecular↗

Massive pulmonary embolism: preliminary results of treatment with the Amplatz thrombectomy device.

PURPOSE: To determine the feasibility of using the Amplatz thrombectomy device (ATD) to treat massive pulmonary embolism (PE). PATIENTS AND METHODS: Five patients (four men, one woman; mean age, 45.2 years) with massive PE underwent mechanical thrombectomy with the ATD, which creates a vortex that pulverizes and recirculates the clots within the pulmonary circulation. The patients were followed up for 7-18 months after thrombectomy. RESULTS: Marked improvement in pulmonary perfusion was observed in three patients at angiography and ventilation-perfusion scanning. No changes could be assessed in one patient who died shortly after the procedure. One patient developed hemoptysis during the procedure, most likely because of a reperfusion syndrome. A reduction in pulmonary artery pressure was observed in only one patient; the remaining patients had increased pressure. The four surviving patients were discharged within 8 days. CONCLUSION: Mechanical thrombectomy with the ATD provides rapid debulking of thrombus in some patients with massive PE and has the potential to improve treatment and outcomes of the most sick patients.

Adult↗

Electron microscopic analysis of the normal and the activated pleural macrophage.

Despite an apparent role in pleural pathophysiology, little information is known about pleural macrophage morphology. Intrapleural tetracycline (TCN) results in pleural macrophage influx and pleural fibrosis; intrapleural carrageenan (CAR) induces macrophage influx without ensuing fibrosis. Pleural macrophages collected from normal (NL) and TCN- or CAR-exposed rabbit pleural spaces were examined with electron microscopy. Cellular size; number of microvilli; pseudopods; coated pits (CP) and coated vesicles (CV); and prevalence of golgi, rough endoplasmic reticulum (RER), and intermediate filaments (IF) were determined. The means of each variable in each group were assessed by one-way analysis of variance, with post hoc testing performed by Scheffe F test; p < or = .05 was considered significant. TCN-stimulated pleural macrophages were characterized by their small perimeters. CAR-induced pleural macrophages were marked by their large size and abundant intracellular amorphous material. They had larger perimeters, areas, and diameters than the TCN-induced or normal macrophages and thus smaller numbers of CV + CP per area. The normal pleural macrophages were characterized by more IF, microvilli, and microvilli per perimeter than either the CAR- or TCN-induced pleural macrophages. No differences between groups were found in nuclear cytoplasmic ratios, number of pseudopods, and content of golgi or of RER. The results suggest that normal pleural macrophages and TCN- and CAR-induced pleural macrophages differ morphologically and that these morphologic differences reflect functional differences.

Animals↗

Pleural macrophages differentially alter pleural mesothelial cell glycosaminoglycan production.

Glycosaminoglycans are produced in abundance by the pleural mesothelium and likely participate in the inflammatory response to pleural injury. Because intrapleural tetracycline (TCN) results in pleural macrophage influx and pleural fibrosis, this study attempted to define the role of pleural macrophage products on mesothelial glycosaminoglycan (GAG) production. Pleural macrophages were isolated 72 h after intrapleural TCN or intrapleural carrageenan (CAR), a substance that recruits pleural macrophages without producing pleural fibrosis. Macrophage cultured for 24 h produced a conditioned medium that was added to pleural mesothelial cell culture containing [3H]-glucosamine and was compared to control cultures treated with RPMI culture media alone or with the addition of TCN or CAR. After 72 h, GAGs were isolated by pronase digestion, cetyl pyridinium precipitation, and MgCl2 and ethanol extraction. The majority of GAGs were found in the culture media as compared to the combined mesothelial cell and basement membrane fractions of control mesothelial cells (883 +/- 33 vs. 216 +/- 16, cpm, counts per minute), TCN-treated (792 +/- 48 vs. 204 +/- 18 cpm), CAR-treated (849 +/- 45 vs. 223 +/- 13 cpm), and macrophage-conditioned media-treated mesothelial cells (TCN macrophage-conditioned media: 1420 +/- 42 vs. 356 +/- 11 cpm; CAR macrophage-conditioned media: 1241 +/- 38 vs. 339 +/- 10 cpm) (all p < .05). Media samples were enzymatically digested and individual GAG species were separated by Sephadex G-50 column chromatography. TCN macrophage-conditioned media induced more GAG production by the mesothelial cell into the cell media (1420 +/- 42 cpm) than CAR macrophage-conditioned media (1241 +/- 38 cpm) (p < .05), which was predominantly a difference in hyaluronate production (342 +/- 53 cpm vs. 186 +/- 7 cpm) (P. < .05). The results show that pleural macrophages modulate mesothelial GAG production during tetracycline pleural injury. Increases in mesothelial cell hyaluronate production may be important in the fibrotic response to chemical pleural injury.

Animals↗

Amiodarone-cyclosporine interaction in a heart transplant patient.

We report the case of a heart transplant patient whose cyclosporine clearance decreased by more than 50% after the institution of amiodarone therapy. This interaction necessitated a significant dosage reduction to maintain cyclosporine concentrations within the therapeutic range. To investigate the mechanism of the interaction, a cyclosporine-lipoprotein-binding determination was performed. The results suggest that drug displacement from competitive lipoprotein-binding sites is not responsible for the alterations in cyclosporine pharmacokinetics. Clearance data suggests, however, that the primary mechanism for the interaction is the inhibition cyclosporine metabolism by the cytochrome P-450 system. This report emphasizes the importance of reevaluating therapeutic drug regimens when new agents are added to prevent complications caused by drug interactions. If amiodarone and cyclosporine must be used concomitantly, cyclosporine levels must be monitored frequently, in anticipation of this interaction.

Amiodarone↗