Management of parapneumonic effusions.
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Biomedical subjects
Publications and source records attributed to R W Light.
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The objective of the study was to determine if residual pleural thickening after treatment for pleural tuberculosis could be predicted from the pleural fluid findings at the time of the initial thoracentesis. Forty-four patients initially diagnosed as having pleural tuberculosis between January 1986 and January 1988 were separated into two groups: the 23 patients in group 1 had residual pleural disease, while the 21 patients in group 2 had no residual pleural disease after treatment for their pleural tuberculosis was completed. The clinical characteristics of the two different groups did not differ significantly, but the patients in group 1 tended to be a little sicker in that the duration of their symptoms was longer, their hemoglobin values were lower, and weight loss and cough were more frequent. There were no significant differences in the pleural fluid findings in the two different groups. The mean pleural fluid protein level was 5.40 +/- 0.58 g/dl for group 1 and 5.17 +/- 0.80 g/dl for group 2, while the mean pleural fluid glucose level was 78.6 +/- 19.5 mg/dl for group 1 and 79.5 +/- 20.1 mg/dl for group 2. The mean pleural fluid lactate dehydrogenase (LDH) level in group 1 was 593 +/- 498 IU/L, while the mean level for group 2 was 491 +/- 198 IU/L. The presence of residual pleural thickening was not related to the chemotherapeutic regimen or the performance of a therapeutic thoracentesis. From this study we conclude that approximately 50 percent of patients with pleural tuberculosis will have residual pleural thickening when their therapy is completed, but that one cannot predict which patients will have residual pleural thickening from either their clinical characteristics or their pleural fluid findings.
The effect of ethanol ingestion on the efficacy of nasal continuous positive airway pressure (nasal CPAP) as a treatment for the obstructive sleep apnea (OSA) syndrome was studied in ten obese male subjects undergoing this therapy. On the first night of polysomnography, the lowest level of CPAP that maintained airway patency was determined (critical level). On the second (control) night (C), subjects slept the entire night on this level of CPAP. On the third night (E), subjects ingested either 1.5 ml/kg (part A, N = 6) or 2.0 ml/kg (part B, N = 4) of 50 percent ethanol (100 proof vodka) over one half-hour starting 1 h before bedtime. A serum ethanol level was obtained at bedtime (part A: 63.7 +/- 17.3 mg/dl; part B: 108.6 +/- 20.6 mg/dl), and subjects were monitored on the critical level of CPAP. Comparison of nights C and E for parts A + B showed no difference in total sleep time (TST) or the amount of different sleep stages as an absolute time or a percentage of TST except that there was more stage 2 (as a percent of TST) on E nights. The apnea + hypopnea index and C and E nights did not differ and was quite low (3.6 +/- 3.7/h vs 1.9 +/- 2.7/h). Similarly, ethanol ingestion did not increase the number of desaturations to at or below 90 and 85 percent, or lower the mean arterial oxygen saturation in NREM or REM sleep. Analysis of parts A and B separately also showed no differences with respect to the apnea + hypopnea index or the number of desaturations on control and ethanol nights. We conclude that acute moderate ethanol ingestion does not decrease the efficacy of an optimum level of nasal CPAP.
We have previously shown that the exercise performance of patients with severe chronic obstructive pulmonary disease (COPD) can be increased with the administration of oral morphine (0.8 mg.kg-1). The purpose of this study was to determine whether the administration of dextromethorphan (DXT), an antitussive structurally similar to codeine, would result in increased exercise performance and decreased dyspnoea in patients with COPD, without the side-effects of opiates. Six eucapnic patients (mean age = 66 +/- 3.8 yrs) with COPD (mean forced expiratory volume in one second (FEV1) = 1.01 +/- 0.07 l) underwent two incremental cycle ergometer tests to exhaustion (Emax) and assessment of their hypercapnic and hypoxic ventilatory responses and mouth occlusion pressure responses following first the oral administration of placebo (P) and then dextromethorphan (60 mg) in a single-blind fashion. There was no statistically significant difference in the maximal exercise performance, perceived dyspnoea (modified Borg scale), breathing pattern or expired gases after the two different treatments. In addition, the ventilatory response to CO2 production during exercise (delta VE/VCO2) and the ventilatory and mouth occlusion pressure responses to hypoxia and hypercapnia did not differ significantly after DXT as compared with after P. Indeed the exercise performance was poorer and the ventilatory responses were brisker after DXT. We conclude from this study that the administration of this opiate analogue does not improve the exercise capacity or decrease the ventilatory response of patients with COPD.
This prospective, multicenter, randomized, "unblinded," controlled clinical trial was designed to determine if the intrapleural instillation of 1500 mg of tetracycline hydrochloride would be effective in diminishing the ipsilateral rate of recurrence for spontaneous pneumothorax. During the 4-year enrollment period, 113 patients were assigned to the tetracycline group; 116 patients were assigned to the control group. During the 5-year study period, the recurrence rate in the tetracycline group (25%) was significantly less than that in the control group (41%). Use of tetracycline seemed to reduce the recurrence rates for patients with either primary or secondary spontaneous pneumothorax and for patients with either an initial or a recurrent pneumothorax. We conclude that the intrapleural administration of tetracycline in patients with spontaneous pneumothorax significantly reduces the rate of ipsilateral recurrence but is associated with intense chest pain. Intrapleural tetracycline therapy is indicated for patients with a spontaneous pneumothorax who are hospitalized and are treated with tube thoracostomy.
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PURPOSE: The pleural fluid that accumulates secondary to congestive heart failure is almost always a transudate based upon its level of protein and lactic acid dehydrogenase (LDH). Previous work has suggested that the characteristics of the fluid may change into those of an exudate with diuresis. The purpose of the present study was to determine whether aggressive diuresis does result in this change in pleural fluid characteristics. PATIENTS AND METHODS: Twelve patients with severe congestive heart failure (ejection fraction 23.9 +/- 9.6%) and pleural effusions were studied serially as they underwent diuresis. After an initial thoracentesis was performed, the patients then underwent aggressive diuresis for 12 to 48 hours with one or two follow-up thoracentesis. RESULTS: The mean weight loss during the study period was 4.5 +/- 2.8 kg. With diuresis the LDH level, LDH ratio, protein level, and protein ratio all increased significantly (p less than 0.05). All 12 patients had transudative pleural effusions at the onset of diuresis. However, despite the increases in the levels of protein and LDH with diuresis, only one patient's pleural fluid attained values compatible with an exudate. CONCLUSION: From this study we conclude that it is uncommon for a transudative pleural effusion due to congestive heart failure to develop the characteristics of an exudative pleural effusion with rapid diuresis.
The exercise capacity of polycythemic COPD patients has been shown to improve after phlebotomy, possibly because of reduction of ventricular afterload by decreased blood viscosity, resulting in increased cardiac output. Ten patients with polycythemic COPD and mean hematocrit 62% were studied at rest and during exercise before and after reduction of mean hematocrit to 50% by repeated phlebotomy. Pulmonary function was evaluated by physiologic exercise testing on a bicycle ergometer. Cardiac function was evaluated by rest and exercise RNVG. Significant increase in exercise tolerance and maximal oxygen uptake at peak exercise, with significant reduction in mean systemic BP, were demonstrated. Ejection fractions did not change, but dV/dt for ejection from the left ventricle at peak exercise improved significantly. Mean SV counts, ESV counts, and EDV counts were measured and the fractional increase with exercise compared for prephlebotomy and postphlebotomy, assuming that resting volumes would not change. ESV counts and EDV counts were both proportionately, though not significantly, reduced postphlebotomy. The data tend to support the hypothesis that the afterload on the left ventricle is reduced, with resulting improved myocardial contractility and left ventricular function. Improved peripheral oxygen uptake may also be a factor.
In 10 patients with stable severe chronic obstructive pulmonary disease (COPD) we evaluated the relationship between the degree of airway obstruction and hyperinflation, and the maximum inspiratory muscle endurance capacity during added inspiratory resistive loading. We measured the ratio of forced expiratory volume in 1 s to forced vital capacity (FEV1/FVC) and airway resistance (Raw) as indices of airway obstruction, and the ratio of functional residual capacity to total lung capacity (FRC/TLC) as an index of hyperinflation. The mean resting transdiaphragmatic pressure to its maximum (Pdi/Pdimax), the tension time index of the diaphragm, and the maximum transdiaphragmatic pressure (Pdimax) were also determined. Following 15 min of resting breathing, the patients breathed through added inspiratory resistances which were progressively increased every 3 min until exhaustion. Maximum endurance capacity (ECmax) was defined as the product of the esophageal pressure - time integral and frequency at the maximum load sustainable for 3 min. ECmax correlated significantly with Raw (r = -0.67, p less than 0.04). The addition of FRC/TLC to the analysis resulted in a significant increase in the correlation coefficient (r = 0.86, p less than 0.01). ECmax did not correlate with FEV1/FVC. Both resting Pdi/Pdimax and Pdimax independently influenced ECmax. In addition, Pdimax correlated significantly with FRC/TLC, and resting Pdi/Pdimax with Raw. We conclude that in stable patients with severe COPD, both airway obstruction and hyperinflation affect maximum inspiratory muscle endurance capacity during inspiratory resistive loading.
The objective of this study was the prospective evaluation of the relationship between serum and pleural fluid antibody levels to mycobacterial antigens and their role in the diagnosis of tuberculous pleuritis. The setting was a tertiary care medical center. Thirteen patients with tuberculous pleuritis and 53 control subjects with pleural effusion (22 with carcinoma, 17 with cardiac failure, and 14 with empyema or parapneumonic effusion) were studied. The level of IgG was measured by ELISA. The median titers of antibody to both Mycobacterium tuberculosis and M avium were significantly higher in the serum and pleural fluid of the patients with tuberculosis than in the control patients. There was a very close relationship between the levels of M tuberculosis (r = 0.95) and M avium (r = 0.94) antibodies in the serum and pleural fluid. We concluded that the levels of antimycobacterial IgG in pleural fluid, adjusted to constant protein concentration, are very closely related to the serum levels. Therefore, these antibodies in the pleural fluid probably result from passive diffusion from serum and not local production. Measurement of pleural fluid antibody levels will not add diagnostic sensitivity or specificity to that achieved with serodiagnosis.
The purpose of this study was to determine the effects of phlebotomy on the exercise tolerance and right and left ventricular ejection fraction of polycythemic patients with chronic obstructive pulmonary disease. Ten patients with COPD (mean FEV1 = 1.32 +/- 0.55 L) and polycythemia (mean Hct = 62 +/- 3 percent) were studied before and after their hematocrits had been reduced to approximately 50 percent. Post-phlebotomy the maximal oxygen consumption increased from 1.09 +/- 0.34 L/min to 1.26 +/- 0.43 L/min (p less than 0.05) and the maximum workload increased from 56.5 +/- 32.6 watts to 74.5 +/- 23.4 watts (p less than 0.05). The increase in the exercise tolerance appeared to be primarily due to an increased cardiac output at Emax. There was no relationship between the increases in the upright exercise capacity and changes in the supine ejection fractions of the right or left ventricular either at rest or during exercise.
CPPV is an accepted standard of treatment in patients with acute respiratory failure. Because of rapid technologic advancements, new modes of ventilation have been developed. Unfortunately, this occurs at a time when there are still many controversies about the relative benefits and modes of action of CPPV. Before the proliferation of use of these newer modes in the intensive care units, documentation of the beneficial effects and safety of these modalities under controlled condition is of utmost importance. Although some of the "new" ventilatory modes (PSV, PAV) improve patient comfort and synchrony, and PAV has the potential to replace CPPV, the superiority of the "new" ventilatory modes over that of CPPV remains to be established, particularly in the area of patient survival, morbidity, and cost.
Continuous positive airway pressure (CPAP) breathing can be delivered using the demand-flow (DF) or continuous-flow (CF) system. A modified CF system, the flow-by (FB) system, operates with preset base-flow (BF) values between 5 and 20 L/min. The DF depends on changes in pressure for opening the pneumatic valve of the system (pressure sensitivity). In contrast, the FB depends on changes in flow (flow sensitivity). In six healthy male subjects, we determined the mechanical inspiratory work of breathing (WI, J/L) and the inspiratory work rate (J/min) on the DF and the FB systems at a BF of 5 and 20 L/min, at CPAP levels of 0, 5, and 10 cm H2O. In comparison to DF, on the FB system both WI and inspiratory work rate were significantly less at a CPAP of 10 cm H2O (p less than .01). This was most likely due to the smaller drop in airway pressure at the onset of inspiration with the FB system. Varying the BF values in the FB system had no effect on WI or inspiratory work rate.
Previous studies have shown that opiates increase the maximal external work performed at exhaustion in patients with chronic obstructive pulmonary disease (COPD). The mechanism responsible for this improvement in exercise tolerance is unknown. The purpose of this study was to determine the effects of an oral morphine solution (0.8 mg/kg) on the exercise tolerance, perception of dyspnea, and arterial blood gases of patients with COPD. Thirteen eucapnic patients with stable COPD (FEV1 = 0.99 +/- 0.48) underwent duplicate incremental cycle ergometer tests to exhaustion (Emax) after the ingestion of placebo and after the ingestion of morphine. After the ingestion of morphine, the maximal workload increased by 18% (p less than 0.001) and the VO2 increased by 19.3% (p less than 0.001). Ten of the 13 patients had a higher ventilation at Emax after morphine ingestion. Despite the higher ventilation at Emax after morphine, the mean Borg score was not significantly higher. At Emax after morphine ingestion, the PaO2 (65.8 +/- 11.6 mm Hg) was significantly lower and the PaCO2 (43.5 +/- 8.3 mm Hg) was significantly higher than at Emax after placebo (71.9 +/- 15.5 and 38.3 +/- 8.5, respectively). When data at the highest equivalent workload were analyzed, the ventilation and the Borg scores were significantly lower, whereas the VO2 and VCO2 were comparable. From this study, we conclude that the administration of opiates can substantially increase the exercise capacity of patients with COPD. The improved exercise tolerance appears to be related to both a higher PaCO2 resulting in lowered ventilation requirements for a given workload and also to a reduced perception of breathlessness for a given level of ventilation.
We evaluated the effect of radiation therapy in 57 patients with obstruction of a large bronchus with NSCC. Response with aeration of the atelectatic lung was seen in 12 patients (21 percent). Three patients (5 percent) showed partial response with persistent partial atelectasis, and nine patients (16 percent) showed good response with complete aeration of the atelectatic lung. In these patients the response appeared to be related to the dose of radiation. All of the patients who responded received more than 50 Gy. The difference in the response rate related to the dose of radiation was statistically significant (p less than 0.05). The rates were similar with all histologic types of NSCC. Regardless of the clinical response observed, bronchoscopy performed two to four months after completion of radiation therapy in 14 patients revealed persistent endobronchial tumor. There was no significant relationship between the persistence of endobronchial tumor, the dose of radiation therapy, and the tumor's histologic type. Of the 12 patients with radiographic improvement in atelectasis, fibrotic changes developed in four (33 percent) patients and pneumonitis in two (17 percent). Progression of disease with distant metastases occurred in 58 percent (seven) of the 12 patients who showed a clinical response of their bronchial obstruction. The median time to survival was nearly identical in responders and nonresponders.
The purpose of this study was to determine if there is a relationship between improvement in exercise capacity with supplemental oxygen and the magnitude of hypoxic ventilatory drive in patients with CAO. We hypothesized that those patients with the highest hypoxic drives would be the most likely to have increased exercise tolerance with supplemental oxygen. Seventeen patients with CAO (mean FEV1 = 0.99 +/- 0.45 L) underwent identical maximal cycle ergometry exercise tests on two occasions 45 minutes apart while breathing either air or 30 percent oxygen in a randomized single-blind fashion. With supplemental oxygen, the ventilation decreased and the PaCO2 increased significantly at rest. The patients had a significantly greater exercise tolerance on supplemental oxygen (76.7 vs 69.1 watts, p less than 0.005) but no increase in the maximal ventilation. When the nine patients who improved were compared to the eight patients who did not improve, the two groups were basically identical. Specifically, there were no significant differences in the mean ventilatory or mouth occlusion responses to hypoxia or in the blood gases. The patients who did improve tended to have a greater reduction in their ventilatory response to exercise while exercising on oxygen as compared to when they were exercising on room air. From this study, it was concluded that measurements of hypoxic ventilatory drive are not helpful in predicting which patients with CAO are likely to have improved exercise capability while breathing supplemental oxygen.
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Elevated endorphin levels in patients with COPD may act to diminish the sensation of dyspnea. Exogenous opioids decrease exertional dyspnea and increase exercise capacity in COPD patients. The purpose of this study was to determine the effects of endogenous opioids on the exercise capacity and control of breathing in patients with COPD. We hypothesized that naloxone, an opioid antagonist, would block the endogenous endorphins and decrease the exercise capacity of our patients. Six patients (mean age, 58.8 +/- 3.2 years) with COPD (mean FEV1, 1.28 +/- 0.46 L) underwent identical incremental cycle ergometer tests to exhaustion (Emax) and assessment of their hypercapnic and hypoxic ventilatory responses and mouth occlusion pressure responses following the IV administration of naloxone (0.4 mg/kg) (N) or placebo (P) in a randomized, double-blind fashion. Perceived dyspnea (modified Borg scale), breathing patterns, and expired gas levels were compared at rest and at maximal workload (WL). There was no significant difference after N compared with after P in the WL or the duration of work. At Emax there were no significant differences after N compared with after P in ventilation, the level of dyspnea, P0.1, VO2, or VCO2. The ventilatory response to CO2 production during exercise (delta VE/delta VCO2) and the ventilatory and mouth occlusion pressure responses to hypoxia and hypercapnia did not differ significantly after N compared with after P. This study does not support the hypothesis that endogenous opioids play a significant role in dampening dyspnea and facilitating exercise in patients with COPD.