High prevalence of undiagnosed and severe chronic obstructive pulmonary disease at first hospital admission with acute exacerbation.

Chronic obstructive pulmonary disease (COPD) is a common cause of acute medical hospital admission, and the prevalence of undiagnosed COPD in the community is high. The impact of undiagnosed COPD on presentation to secondary care services is not currently known. We therefore set out to characterise patients at first admission with an acute exacerbation of COPD, and to identify potential areas for improvement in earlier diagnosis and further management. A retrospective case review of patients first admitted to a district teaching hospital with an acute exacerbation of COPD over a 1-year period was carried out. Forty-one patients with a first admission with an acute exacerbation of COPD were identified, 14 (34%) of whom had not been previously diagnosed and were diagnosed with COPD as a result of the admission. At presentation, this group of patients had severe disease, with mean (SD) FEV(1) 1.02 (0.32) L, and a respiratory acidosis in eight (20%) patients, even though this was their first admission for an acute exacerbation of COPD. Missed potential opportunities to intervene in community and inpatient management were identified, including earlier diagnosis, pre-hospital corticosteroid therapy, inpatient respiratory team input, provision of smoking cessation advice and consideration of pulmonary rehabilitation. Patients with a first hospital admission with an acute exacerbation of COPD frequently have severe disease at presentation. Despite having severe disease, a diagnosis of COPD had not been made in the community prior to admission in one-third of patients. Future work should be directed at earlier identification of patients who are symptomatic from COPD and ensuring that the interventions of proven benefit in COPD are systematically offered to patients in both primary and secondary care.

Platelet dynamics following allergen challenge in allergic asthmatics.

BACKGROUND: There is evidence that platelet activation occurs in allergic inflammation and asthma, but little is known about the role platelets play in airway inflammation associated with asthma. OBJECTIVES: In the present study, we have investigated the kinetics of platelet activation following allergen provocation of allergic asthmatics to determine the dynamics of platelet activation relative to changes in lung function and changes in airway inflammation. METHODS: Changes in platelet count and haematocrit from baseline were measured during the early asthmatic response (EAR), late asthmatic response (LAR; or at corresponding time points) and at 24 h were compared between allergen- and saline-challenged groups. A subgroup of allergen-challenged asthmatics, a group of 7 challenged asthmatics and 7 controls were bronchoscoped, and BAL fluid was collected and analysed for levels of histamine and eosinophil cationic protein. RESULTS: There was a fall in circulating platelet count, but not haematocrit after allergen challenge when compared with saline during the LAR or at 24 h. At 24 h FEV(1) had returned to within 20% of baseline in all subjects, although the thrombocytopaenia and airway inflammation persisted. CONCLUSIONS: Our results suggest that persistent thrombocytopaenia accompanies allergen exposure and persists beyond changes in airway obstruction at a time when airway inflammation is present. Our results provide further evidence that platelets may be involved in allergic disease.

Nasal ventilation in pregnancy: treatment of nocturnal hypoventilation in a patient with kyphoscoliosis.

The management of a young woman with congenital kyphoscoliosis, who developed symptomatic nocturnal hypoventilation during the third trimester of pregnancy, is described. Nasal intermittent positive pressure ventilation (NIPPV) was safely and effectively used to correct nocturnal hypoxaemia and hypercapnia from the 30th-36th week of gestation, when a healthy boy was delivered by Caesarean section. Following delivery, the mother no longer required NIPPV and returned to her prepregnancy level of activity.

Inulin as a marker of dilution of bronchoalveolar lavage in asthmatic and normal subjects.

Bronchoalveolar lavage (BAL) fluid is a variable mixture of instilled and lung fluid, which makes interpretation of solute concentrations difficult. We describe the use of inulin as a marker of dilution of BAL in human subjects. BAL, using saline containing 0.1 mM inulin, was safely performed in 13 subjects with mild asthma and 11 normal subjects. The dilution factor (DF: inulin concentration in BAL fluid/inulin concentration in instilled fluid) was measured spectrophotometrically, and it was used to calculate the volume of lung fluid in BAL fluid. There was no significant difference between the median (range) DF of 0.931 (0.825 to 0.952) in asthmatics and 0.907 (0.768 to 0.985) in control subjects (p = 0.77). There was wide individual variation in, but no significant difference between, the lung fluid volume of 8.1 ml (5.4 to 22.2) in asthmatics and 12.3 ml (1.9 to 30.6) in control subjects (p = 0.56), thus validating comparisons of concentrations per ml of BAL fluid. Alternatively, concentrations can be compared per ml of lung fluid. Inulin fulfilled the requirements for a marker of dilution of BAL, enabling the validation and standardization of comparisons of solute concentrations in BAL fluid.

Reduction in leukotriene B4 generation by bronchoalveolar lavage cells in asthma.

BACKGROUND: Leukotrienes are inflammatory mediators implicated in the pathogenesis of asthma. The capacity of inflammatory cells within the airways to generate leukotrienes may be altered in asthma. This hypothesis was tested using bronchoalveolar lavage (BAL) to sample cells within the airways from atopic asthmatic and normal subjects, and by measuring their capacity to generate leukotriene B4 (LTB4) and leukotriene C4 (LTC4) in response to A23187, a potent stimulus of leukotriene generation. METHODS: Bronchoalveolar lavage was performed in 12 mild asymptomatic atopic asthmatic patients and 12 normal subjects. Mixed BAL cell aliquots (approximately 80% alveolar macrophages) were incubated with 0-20 microM A23187 for 10 minutes and with 4 microM A23187 for 0-30 minutes, and leukotrienes were measured by radioimmunoassay and high performance liquid chromatography. RESULTS: Mixed BAL cells from asthmatic subjects generated less LTB4 than cells from normal subjects in dose response and time course experiments (area under the curve 81.5 (0.0-228.5) ng.min.10(-6) cells in asthmatic subjects and 197.9 (13.9-935.6) ng.min.10(-6) cells in normal subjects. There were no differences in LTC4 generation between BAL cells from asthmatic and normal subjects. CONCLUSIONS: Generation of LTB4 by BAL cells from atopic asthmatic subjects in response to A23187 was reduced. As the alveolar macrophage is the major source of LTB4 in BAL cells, these results probably reflect reduced generation of LTB4 by alveolar macrophages from asthmatic patients. This may be a consequence of monocyte migration into the lung, or altered alveolar macrophage function in asthma, or both.

Assessment and follow up of patients prescribed long term oxygen treatment.

BACKGROUND: Prescription and use of long term oxygen treatment were audited in a large group of patients after more than five years of use of the guidelines for its prescription. METHODS: Patients with a concentrator were interviewed at home with a structured questionnaire in three family health service authorities in East London. Stable oxygen saturation (SaO2) breathing air and oxygen, forced expiratory volume in one second (FEV1) and current and previous dated concentrator meter readings were recorded. A further questionnaire was sent to each patient's general practitioner. Hospital case notes of patients who did not meet the criteria for long term oxygen treatment at reassessment were reviewed. RESULTS: A total of 176 patients were studied; 84% had chronic obstructive lung disease and 19% admitted to continued smoking; 140 patients had seen a respiratory physician but results of respiratory assessment were available to their general practitioner in fewer than 54 cases. FEV1 was < 1.5 1 in 158 patients but in 67 SaO2 was less than 91% breathing air, mainly in patients with chronic obstructive lung disease who had been inadequately assessed. Daily oxygen was prescribed for a median of 15 (range 4-24) hours and measured daily use was 15 (0-24) hours; 74% of patients used more than 12 hours. Only 35 patients had problems with oxygen treatment, but 29 had an undercorrected SaO2 of less than 92% when using their concentrator. CONCLUSIONS: Guidelines for prescription of long term oxygen treatment are largely followed and most patients complied with treatment. Increased communication about respiratory state is required between hospital doctors and general practitioners. Patients need regular reassessments to ensure that hypoxaemia is corrected and that oxygen is appropriately prescribed.

Percutaneous renal biopsy in the district general hospital.

This paper reports a retrospective study of the clinical value of percutaneous renal biopsy in secondary referral centres. Between 1984-90, 205 patients over the age of 16 had 218 biopsies at three district general hospitals. Adequate tissue was obtained in 194 patients (95%, 89% of the biopsies). Significant complications occurred in only four patients. In 170 patients (83%) the biopsy yielded information of diagnostic and prognostic value and influenced management. The main indications for biopsy were nephrotic syndrome, in 63 patients, and chronic renal failure, in 58 patients. The most frequent findings were minimal change disease, focal segmental glomerulosclerosis, IgA nephropathy, membranous glomerulonephritis and mesangiocapillary glomerulonephritis. The most obvious association between indication and histology was between haematuria and IgA nephropathy. Percutaneous renal biopsy in the district general hospital in patients selected by a nephrologist and performed by experienced or supervised operators is a safe procedure. There is a high yield of renal tissue which is of clinical value in patient care.

Nasal intermittent positive-pressure ventilation in weaning intubated patients with chronic respiratory disease from assisted intermittent, positive-pressure ventilation.

Nasal intermittent positive-pressure ventilation (NIPPV) has been used for domiciliary ventilatory support, and to avoid intubation for acute respiratory failure in patients with chronic airflow limitation (CAL). Its role in weaning patients from assisted ventilation in intensive care has not been defined. We have used NIPPV to wean 14 patients with respiratory disease who were referred either because of predicted difficulty in weaning or failure to wean using standard techniques. Twelve patients were ventilated for acute respiratory failure; eight patients had CAL and four had chest wall or neuromuscular disease. Two further patients with chest disease were difficult to wean following surgery. Weaning was successful in 13 patients. NIPPV corrected hypoxia, reduced hypercapnia and was well tolerated. Weaning from NIPPV was achieved in all patients with CAL, although three patients with chest wall disease later required domiciliary ventilatory support. All but one of the patients survived to leave hospital. NIPPV may have an important role in weaning from assisted ventilation, particularly in patients with underlying chronic respiratory disease. This preliminary report needs to be followed by a controlled study comparing NIPPV with established weaning methods.

Comparison of nasal pressure support ventilation with nasal intermittent positive pressure ventilation in patients with nocturnal hypoventilation.

Nasal intermittent positive pressure ventilation (NIPPV) provides effective ventilatory support in patients with nocturnal hypoventilation. Nasal pressure support ventilation (NPSV), which only provides ventilation in response to patient triggering, may also be effective, simpler, and cheaper, but has not been evaluated. NIPPV and NPSV were compared in 12 patients with nocturnal hypoventilation, requiring domiciliary ventilatory support. The patients were studied on three consecutive nights, in random order: a control night without ventilation and a night on each mode of ventilatory support using the bilevel positive airway pressure (BiPAP) ventilator. Both NIPPV and NPSV significantly increased mean arterial oxygen saturation (SaO2) compared to the control night (NIPPV mean increase 4.1%; 95% confidence interval (CI) 2.2 to 6.1, NPSV 4.4%; CI 2.1 to 6.6) with no significant difference between the two modes. The percentage of the study night spent below 90% SaO2 was significantly reduced by both ventilator modes compared to the control night (median reduction on NIPPV 37%; CI -54 to -10, reduction on NPSV 31%; CI -53 to -9, with no significant difference between NPSV and NIPPV. NPSV was as effective as NIPPV in patients with nocturnal hypoventilation, which suggests that these patients are able to trigger the ventilator adequately. The lower cost of NPSV will make it accessible to more patients with chronic lung disease.

Comparison of nisoldipine and nifedipine as additional treatment in hypertension inadequately controlled by atenolol.

Twenty-eight patients (11 Caucasian, 17 black) whose blood pressure was more than 160/96 mmHg after 4 weeks on placebo added to atenolol 100 mg/day were randomly given, in addition, nisoldipine 10 mg or nifedipine 20 mg each twice a day for 8 weeks in a double-blind cross-over study. There was a statistically significant (P < 0.001) fall in blood pressure with no change in heart rate, both supine and erect, on both drugs. There were no significant differences between nisoldipine and nifedipine. Adverse effects were recorded in 15%, 17% and 35% of the patients available for safety comparison for placebo, nisoldipine and nifedipine, respectively. There were no significant differences between the black and Caucasian patients in blood pressure responses, although the study had only a low power to detect these. However, the fasting serum triglyceride levels at the end of both calcium antagonist treatment periods were highly significantly lower in the black patients compared with the Caucasian patients. Nisoldipine, which has a higher coronary vascular selectivity and less negative inotropism than nifedipine, is as effective and as well tolerated as nifedipine in patients whose hypertension is inadequately controlled on atenolol. It may have a special role in hypertensive patients with impaired left ventricular function.

Ambulatory oxygen in chronic heart failure.

Ambulatory oxygen therapy may be of benefit in bicycle exercise tests. We have assessed the effects of ambulatory oxygen during walk tests in 12 patients with chronic heart failure. In 6 min walks with the patient breathing air, mean (SD) arterial oxygen saturation (SaO2) fell from 94.4 (3.7)% at rest to 90.1 (6.1)% (p = 0.014) on exercise. 21/min oxygen increased resting SaO2 from 93.7 (4.0)% (air cylinder) to 96.5 (3.0)% (p < 0.001) with no effect on minimum SaO2, distance, or breathlessness. During endurance walks, 4 l/min oxygen increased minimum SaO2 from 90.4 (5.6)% to 93.5 (4.7)% (p = 0.011) but also had no effect on breathlessness or distance. Ambulatory oxygen in currently available cylinders cannot be recommended for patients with chronic heart failure.

Primary malignant retroperitoneal germ cell tumour presenting with accelerated hypertension.

A 42 year old man presented with accelerated hypertension and an abdominal mass that proved to be a primary malignant retroperitoneal germ cell tumour involving renal vessels. The hypertension resolved with chemotherapy. To our knowledge this is the first case of a primary malignant retroperitoneal germ cell tumour to present with accelerated hypertension.