Pulmonary failure as a cause of death in COPD.

Data on the outcome of patients with chronic obstructive pulmonary disease (COPD) are limited. We know that the prognosis is poor when respiratory insufficiency develops, but we have little information on the actual cause of death. Epidemiological studies are suitable for the assessment of the prevalence of the disease, but give no details on the actual cause of death. Age and forced expiratory volume in one second (FEV1) have been recognized as the best predictors of mortality in studies designed to quantify survival of COPD patients, particularly when the post-brochodilator value is used, as this provides a better estimate of airway and parenchymal damage. Data from Intensive Care Units on acute respiratory failure have several significant limitations. Firstly, it is probable that some patients elect not to undergo intensive treatment for a terminal bout of respiratory failure, particularly if it is not first episode. Secondly, the actual cause of death is often not described in adequate detail. Hypoxaemia and acidaemia are the main risk factors in acute exacerbation of the disease and the presence of pulmonary infiltrates on chest radiographs worsens the prognosis. A single bout of respiratory failure appears to have no effect on the prognosis of COPD patients after recovery, but there is a consistent increase in mortality after the second episode. It seems possible to manage the majority of episodes of acute respiratory failure with mechanical ventilation administered with noninvasive techniques. When endotracheal intubation is necessary, the prognosis is usually poor and the survival after 1 yr is usually lower than 40%. The role of long-term home mechanical ventilation is still unclear. Results from pivotal studies have been encouraging, although survival is far less impressive than in neuromuscular disorders. In patients with end-stage lung disease, lung transplantation can be considered the only possibility of increasing pulmonary functional capacity. However the technique is reserved only for a highly selected group of patients and data on the long-term outcome are awaited.

Overnight urinary uric acid: creatinine ratio for detection of sleep hypoxemia. Validation study in chronic obstructive pulmonary disease and obstructive sleep apnea before and after treatment with nasal continuous positive airway pressure.

During hypoxia ATP degradation to uric acid is increased in animal models and humans. To assess the reliability of an overnight increase in uric acid excretion as a marker of nocturnal hypoxemia, we selected 10 normal volunteers (7 males and 3 females), 29 COPD patients (26 males and 3 females), and 49 subjects with obstructive sleep apnea (OSA) (43 males and 6 females). The patients underwent standard polysomnography, which was repeated in 14 subjects with nasal continuous positive airway pressure (CPAP), and were subdivided into two groups: Group D included desaturating subjects who spent at least 1 h at SaO2 < 90% and 15 min below 85%, and Group ND were nondesaturating subjects. The overnight change in the uric acid:creatinine ratio (delta UA:Cr) was negative in normal subjects (-27.5 +/- 9.1 [mean +/- SD]) and ND groups: -19.7 +/- 14.3 in COPD, -16.1 +/- 13.0 in OSA. In both COPD and OSA Group D, the ratio was usually positive: delta UA:Cr was 17.9 +/- 31.4 in Group D COPD (p < 0.001 versus ND) and 10.1 +/- 30.7 in Group D OSA (p < 0.001 versus ND and versus normal subjects) despite 4 of 15 false negative results in COPD and 8 of 20 in OSA. CPAP effective treatment induced a marked reduction ((p = 0.0024) in delta UA:Cr, leading to a negative value. We conclude that delta UA:Cr seems to be a promising index of significant nocturnal tissue hypoxia, with good specificity but poor sensitivity (about 30% false negative), which might be useful for the long-term follow-up of outpatients on nasal CPAP with a positive ratio at baseline.