Rationalising tuberculosis contact tracing in low prevalence areas.
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Biomedical subjects
Publications and source records attributed to A G Leitch.
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We report the case of a head-injured patient with spontaneous hyperventilation who had recurrent episodes of relative hypoventilation associated with increases in intracranial pressure. Detailed ventilatory studies were performed during the 2nd week after injury. Our findings in this patient prompted us to review the possible mechanisms underlying the observed changes. We suggest that spontaneous hyperventilation in head injury is secondary to a decrease in cortical inhibitory influences on respiratory control mechanisms and that the transient episodes of relative hypoventilation observed in our patient may reflect modified ventilatory responses dependent on the altered state of consciousness. (Neurosurgery, 5: 701--707, 1979).
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In a double-blind placebo controlled trial in 24 patients fulfilling the MRC criteria for chronic bronchitis, ipratropium bromide 40 microgram and salbutamol 200 microgram produced similar and significant (P less than 0.001) increases in forced expiratory volume in one second (FEV1) and forced vital capacity (FVC). A greater increase in FEV1 and FVC was seen when both drugs were used together, but this increase did not differ significantly from that produced by either drug alone. Salbutamol increased 12-minute walking distance significantly (P less than 0.001) by 62 +/- 15 metres, whereas the increase of 43 +/- 15 metres observed after ipratropium was not significant (P less than 0.05). With both drugs in combination 12-minute walking distance increased by 72 +/- 15 metres, but this change was not significantly different from that observed with salbutamol alone. If aerosol bronchodilators in the doses used in this study are to be given with a view to improving exercise tolerance in such patients than salbutamol would appear to be the aerosol of choice.
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Mediators of immediate-type hypersensitivity were studied in the sputum of patients with chronic bronchitis. The same mediators were also measured in early-onset, skin-test-positive asthmatics, in late-onset, skin-test-negative asthmatics, and in patients with bronchial carcinoma, bronchiectasis, and pneumonia. Sputum eosinophilia was a feature of bronchitics and asthmatics, whereas raised blood eosinophil levels were found only in the early-onset, skin-test-positive asthmatics. Histamine and IgE were present in considerable amounts in the sputum of bronchitics and early-onset, skin-test-positive asthmatics. Smaller amounts were found in the other groups. The sputum in all the groups contained material giving an "S.R.S (slow-reacting substance) like" induced contraction of the guinea pig ileum. "Classical" S.R.S.-A., determined by arylsulphatase IIB susceptibility, was present only in bronchitics and both types of asthmatics. Since the bronchitics were, in general, skin-test negative and had normal concentrations of circulating IgE and eosinophils, it is suggested that the findings in the sputum indicate an element of local immediate-type (type I) hypersensitivity in bronchitis although its significance for pathogenesis is not known.
Intravenous infusion of salbutamol 10 mug/min in seven healthy subjects significantly increased their ventilatory responses to inhaled CO2 in both hypoxia and hyperoxia. These changes in chemical control of breathing are unlikely to be significant when the drug is used in severe asthma but may benefit patients with acute exacerbations of chronic ventilatory failure. The infusion also increased heart rate, which was most pronounced when hypoxia was combined with hypercapnia. The infusion produced an average fall in plasma potassium from 3-99 to 3-10 mmol/l, which was associated with an increase in plasma glucose and serum insulin, suggesting that this arose from a shift of potassium from the extracellular to the intracellular space. Routine monitoring of plasma potassium and the electrocardiogram is indicated when an intravenous salbutamol infusion is used to treat severe asthma as the drug may predispose to cardiac dysrhythmias.
Studies in identical twin athletes, using a wide range of methods of measuring chemical control of breathing, have demonstrated identity of ventilatory responses to hypoxia and hypercapnia in such subjects. This suggests that, when the effect of a major environmental factor, physical activity, is removed, genetic factors predominate in determining the ventilatory responses to carbon dioxide and hypoxia.
We have studied maximal oxygen uptake, maximal heart rate, maximal exercise ventilation and the ventilatory response to exercise in 24 male and 14 female Scottish athletes. The values for maximal oxygen uptake are similar to those reported in other international studies. In eight athletes repeat measurements of maximal oxygen uptake 7-11 months after the initial study showed no change from the initial values. The values for the ventilatory response to exercise in our athletes were normal. The relationship is discussed between maximal oxygen uptake and ventilatory responses to exercise, hypoxia and hypercapnia and it is suggested that these may be related to athletic event.
Ten patients with cor pulmonale complicating severe chronic bronchitis and emphysema have been treated with 2 litres/min of oxygen for prolonged periods in the day, at home, over 12 to 62 months. Two patients died after 12 and 36 months of treatment. Pulmonary arterial pressure was reduced in seven patients, and red cell mass in eight, when the oxygen was given for over 15 hours in the day. Hospital inpatient treatment was greatly reduced following the start of long-term oxygen treatment in all patients. This treatment is expensive, and a controlled trial is necessary to establish its definitive place and cost-effectiveness, but the results of such a current Medical Research Council trial will not be available for a further two years.
We have studied arterial PO2, PCO2, and hydrogen ion and electroencephalogram during sleep in 10 patients with stable severe chronic respiratory failure. As a group the patients slept badly. Sleep was associated with a worsening of hypoxia and no significant change in PCO2 and H+. Two patients were restudied, receiving oxygen therapy overnight. Both had improved sleep but one, who had an intact hypoxic drive to breathing, developed marked hypercapnia and acidosis when his PO2 was restored to normal during sleep; the other, who had no hypoxic drive to breathing, developed no more hypercapnia or acidosis during sleep when breathing oxygen than when breathing air. Oxygen therapy may improve sleep disturbance in these patients, but its effect on the drive to breathing during sleep should be considered if severe hypercapnia and acidosis are to be avoided.
Seven patients admitted to hospital during or immediately after status epilepticus or recurrent episodes of grand-mal seizures had very high concentrations of uric acid in their blood at a time when the blood-urea was normal in five of them. The blood-lactic-acid was high in the five patients in whom it was measured. All of the patients developed reversible renal failure, and two required haemodialysis. The blood-uric-acid should be measured in patients who have had prolonged seizures, and the measures which might be taken in hyperuricaemic patients to prevent the development of acute renal failure include rehydration, alkalinisation of urine, and, where alkalinisation is impossible, haemodialysis.
1. Maximal oxygen uptake (VO2 max), lung volumes, and ventilatory responses to carbon dioxide and hypoxia have been measured in identical twin athletes, who were trained to a similar high degree. 2. The results confirm previous findings for VO2 max. and lung volumes in identical twins, and are in keeping with the suggestion that genetic factors play a major part in determining the ventilatory response to carbon dioxide and hypoxia.