Biomedical subjects
Publications and source records attributed to N T Bateman.
A method to correct for background in lung DTPA transfer has been developed for use with a large field of view gamma camera. The method gives comparable values of T50 to those obtained by Jones et al. The correction factors vary from apex to base; therefore to allow intersegmental T50 comparisons each segment should be corrected for background using its own correction factor.
In order to measure regional lung 'leakiness' we have adapted a method developed by Jones et al., to correct for background in the estimation of regional lung transfer of DTPA. It is clear from our study that the half time transfer values (T50) alter from the apex to the base of the lungs in both smokers and nonsmokers. The mean apical T50 values are 56.0 and 56.7 min for the right and left lung respectively in nonsmokers and 12.5 and 12.6 min in smokers. The basal T50 values are 77.5 and 76.9 min for the right and left lung respectively in nonsmokers and 24 and 24.2 min in smokers. These figures suggest that cigarette smoke affects all lung regions and that the transfer values in the apices are more rapid than in the bases in both smokers and nonsmokers.
From July 1980, 104 consecutive patients with previously untreated small-cell lung cancer (SCLC) received vincristine 1.4 mg/m2, doxorubicin (Adriamycin) 40 mg/m2, and Etoposide (VePesid) 300 mg/m2 intravenously (as a single infusion) every 3 weeks. The overall response rate (complete response plus partial response) was 58%. In 47 patients with limited disease the response rate was 66% with 21/47 (45%) complete responders. Treatment was delivered on an outpatient basis. Toxicity was mild, and in 455 rapid infusions of etoposide, there have been no adverse reactions.
Ventilatory acclimatization, arterial acid-base status, brain stem and cortex metabolic acids, and high-energy phosphates were determined in rats during 2-h to 7-days exposure to two levels of hypoxia (O2 inspiratory pressure 75 and 58 Torr), and upon acute restoration of normoxia. Brain lactate concentrations increased during acute exposure to both moderate hypoxia (+52% in cortex and +61% in stem) and severe hypoxia (+211% in cortex and +163% in stem), and during chronic hypoxia remained unchanged or decreased, respectively, as hyperventilation progressed and arterial O2 content rose. Restoration of normoxia after chronic hypoxic exposure resulted in continued hyperventilation and elevated lactate concentrations. Brain intracellular pH was unchanged throughout moderate hypoxia and during severe hypoxia, became acid during acute exposure, but was completely compensated after 72 h of continued hypoxia. Preventing the hypocapnia (via increased inspiratory fraction of CO2) during acute hypoxia or restoring normocapnia during posthypoxic normoxia revealed the effects of hypocapnia independently of hypoxemia. Hypocapnia accounted for all of the changes in brain lactate concentration during moderate hypoxia but only 40-60% of the lactate changes during severe hypoxia. We speculate that the observed changes in plasma and brain tissue metabolic acids and in plasma [HCO-3] would acidify cerebral interstitial fluid (ISF) in chronic hypoxia; however, the time course of this change in ISF acid-base status would be quite different between the two levels of hypoxia and uncorrelated with the patterns of ventilatory acclimatization.
The PCO2 of tonometered human blood was measured with three different Radiometer PCO2 electrodes mounted in three different blood gas analysis systems. When the PCO2 electrode was calibrated with humidified gases it measured the PCO2 of gases accurately but showed a consistent error measuring the PCO2 of human blood. This error was reduced but not abolished by calibrating the electrodes over a wide range of PCO2 and by measuring each sample repeatedly. The PCO2 of human blood was measured accurately by electrodes calibrated with tonometered human blood or buffer. The electrode responded differently to gas and human blood. This could not be explained by an electrode memory effect or by exchange of CO2 between the sample and the electrode. When human, rat, dog and goat blood were tonometered and measured under identical conditions, the difference between gas and blood PCO2 varied. The error of measurement in all species was greatest at high PCO2.
Reports were made on combined ventilation-perfusion lung scans by three observers on three occasions and by another observer once. Reproducibility for each observer varied between 80 and 88%. There was complete agreement about the areas of scans reported as abnormal. Agreement between observes on whether or not the abnormality represented a pulmonary embolus averaged 77%. There was 86% agreement with the final clinical diagnosis. Our results show that reporting of ventilation perfusion lung scans by eye is reproducible. They support the claims that, under routine clinical conditions, the technique is 91% to 95% accurate for pulmonary emboli.
The incidence of pulmonary embolism and deep vein thrombosis was measured in 50 matched pairs of patients undergoing common surgical procedures with preoperative and postoperative ventilation-perfusion lung scans and the fibrinogen uptake test. One patient in each pair was treated with intravenous dextran 70 and pneumatic leggings. The incidence of pulmonary embolism among the treated patients was significantly reduced from 24% to 8%, but the incidence of deep vein thrombosis was not significantly reduced (34% to 24%).
It has been suggested that obliterative vasculitis in the lung might mimic pulmonary embolism on a ventilationperfusion scan. The combined scans of six patients with breast cancer who had undergone radiotherapy to the chest wall, which can induce pulmonary vasculitis, were therefore examined. Eleven of the 12 scans showed perfusion defects with ventilation-perfusion mismatch on the irradiated side. Special care is needed in interpreting the lung scans of patients who have received an appreciable tissue dose of radiation to the lungs; mismatch need not indicate pulmonary embolism.
Three clinically typical cases of multiple pyogenic liver abscesses are presented. In all three cases Streptococus milleri was isolated from the pus and in two cases it was isolated from blood cultures also. The patients were successfully treated by surgical drainage and antibiotics.
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Tissues require oxygen for survival. Its delivery depends on adequate ventilation, gas exchange and distribution in the circulation. Many causes of hypoxaemia can be corrected by adding oxygen to the inspired air but response is variable and must be measured.
Domiciliary oxygen is prescribed widely and often with benefit. However, patients with chronic lung disease, in whom its efficacy is proven, continue to be denied adequate assessment and treatment. It is time to ensure that this expensive treatment is given to those who will benefit in a manner that maximizes the improvement in the quality of life.