The present report generally supports many of the previous recommendations published in the 1999 Canadian Asthma Consensus Report and provides higher levels of evidence for a number of those recommendations.

No abstract

Chronic obstructive pulmonary disease (COPD) is a common medical disorder, which causes considerable morbidity and mortality. Given the chronic and symptomatic nature of the disease, the patient is often seen in the physician's office with complaints of dyspnea. However, more than 50% of COPD patients also have sleep complaints characterised by longer latency to falling asleep, more frequent arousals and awakenings, and/or generalised insomnia. Sleep disturbance tends to be more severe with advancing disease and substantially reduces the COPD patients' quality of life. In approaching the COPD patient who complains of insomnia it is important to take a complete sleep history. Having characterised the degree and duration of the problem, medical management of the underlying COPD must first optimise oxygen saturation while minimising the effects of many of the medications used for COPD. While aerosol therapies may be systemically absorbed and contribute to sleep disruption, anticholinergics, such as ipratropium bromide, are the least likely to do so and indeed have been shown to improve sleep quality in this population. Many of the traditional sedatives and hypnotics have been used in the COPD population including benzodiazepines, imidazopyridines, pyrazolopyrimidines and, less commonly, antidepressants and phenothiazines. Clinical trials support the role of numerous agents in treating insomnia in this population but do not always provide reassurance that these therapies can be used safely, particularly in the patient with severe COPD with hypercarbia. Benzodiazepines are among the most commonly employed agents, but case reports and series continue to describe adverse pulmonary events. Although the newer pyridine derivatives also have the potential to worsen pulmonary function, they appear less likely to do so. Data to date are limited with the tricyclic antidepressants and phenothiazines, although they appear to be very well tolerated from a respiratory point of view. Since sleep disturbances are often long-standing and associated with maladaptive behaviours towards sleep, cognitive/behavioural approaches are often useful and are more effective in the long-term than are hypnotics. When prescription of a sedative is to be made, extra caution is required for those patients at increased risk of adverse respiratory effects, such as those with advanced disease and hypercarbia in whom pharmacological therapy is often best avoided. Selection of the various options will depend upon the degree of underlying disease and the patient's specific complaints of insomnia. Finally, it is important to remember that while most hypnotics work in an acute setting, the long-term management will require an integrated approach.

Dalteparin was effectively and safely used for the thromboprophylaxis of a patient with mechanical heart valves whose anticoagulation was previously difficult to manage with warfarin. Dalteparin deserves further study in patients who are unable to tolerate warfarin.

High-dose pentobarbital infusion has been advocated as an effective adjunct in controlling persistent intracranial hypertension after severe head trauma in patients refractory to conventional therapy. Pentobarbital disposition was assessed in 10 adults with severe nonpenetrating head injury after an intravenous loading dose of sodium pentobarbital, 10 mg/kg, infused over 1 hour, followed by a continuous infusion at 0.5 to 3.0 mg/kg/hr provided the cerebral perfusion pressure remained greater than 50 torr. Pharmacokinetic parameters of volume of distribution at steady state (Vss), total body clearance (CL), and t1/2 for the patients with trauma were statistically compared with similar estimates reported for seven adult subjects without head injury. On discontinuation of the pentobarbital infusion, serum concentrations in the patients followed a monoexponential decline with a mean (+/- SD) t1/2 and Vss that were significantly less than values reported for the control subjects (15.6 +/- 3.9 vs. 22.3 +/- 4.0 hours and 44.0 +/- 11.7 vs. 63.4 +/- 15.2 L, respectively). However, there was no significant difference between the mean pentobarbital CL of the patients (2.0 +/- 0.7 L/hr) and the subjects (2.0 +/- 0.4 L/hr). To our knowledge this is the first report on the disposition, elimination, and intrasubject variability of high-dose pentobarbital infusion in adult patients with head trauma.