Acute exacerbations of COPD

Acute exacerbations of COPD (AECOPD) are a common cause of morbidity and mortality. There is a need for a standardised definition of an exacerbation of COPD. The common aetiological factors are bacterial, viral infection and air pollutants. Exacerbations of COPD may adversely affect the natural history of COPD. Several strategies are available now to prevent or reduce exacerbations of COPD including immunisation against influenza and inhaled corticosteroids in patients with moderate/severe disease. The mainstay of treatment involves increasing bronchodilator therapy, systemic glucocorticoids which have now been shown to have a beneficial effect. The circumstances for the use of antibiotic therapy is now established in patients with increased breathlessness, increased sputum production and/or sputum purulence. In those with respiratory failure, noninvasive ventilation has been shown to reduce intubation rates, shorten lengths of hospitalisation, and improve mortality. Early or immediate supported discharge for selected patients has been shown to be effective in the management of patients with COPD.     

The "COPD emergency 2003" study: a description of the hospital management of exacerbations of COPD

CURRENT SITUATION: Despite its impact on public health and numerous recommendations COPD remains under-diagnosed and its care pathways are not well known. Exacerbations are common presentations of the illness and contribute greatly to its impact on the health of the individual and the community. Despite this the methods of their management in hospital have not been precisely described. The purpose of the prospective study "COPD emergency 2003" is to describe these different aspects of the management of COPD and to study their determining factors. MATERIALS AND METHODS: It is a prospective, multicentre observational study of all the exacerbations of COPD managed as emergencies in public and private hospitals during a two-month period. Enrolment takes place between October 2003 and January 2004. The analysis will begin when the last patient has been discharged from hospital. EXPECTED RESULTS: The data obtained will allow identification of those aspects of the management of COPD and its exacerbations that are heterogeneous or in conflict with the current guidelines as well as the patient care pathways. In the future this study should help target the approaches aimed at improving the outcomes of patients suffering from COPD.     

Management of acute exacerbations of COPD

Exacerbations of COPD are common and cause a considerable burden to the patient and the healthcare system. To optimize the hospital care of patients with exacerbations of COPD, clinicians should be aware of some key points: management of exacerbations is broadly based on clinical features and severity. Initial clinical evaluation is crucial to define those patients requiring hospital admission and those who could be managed as outpatients. In hospitalized patients, the appropriate level of care should be determined by the initial severity and response to initial medical treatment. Medical treatment should follow recent recommendations, including rest, titrated oxygen therapy, inhaled or nebulized short-acting bronchodilators (Beta2-agonists and anticholinergic agents), DVT prevention with LMWH, steroids in most severely ill patients, unless there are contraindications and antibiotics in the case of a clear bacterial infectious aetiology. Severe exacerbations may lead to acute hypercapnic respiratory failure. Unless contraindicated, non-invasive ventilation (NIV) should be the first line ventilatory support for these patients. NIV should be commenced early, before severe acidosis ensues, to avoid the need for endotracheal intubation and to reduce mortality and treatment failures. Several randomised controlled clinical trials support the use of NIV in the management of acute exacerbations of COPD, demonstrating a decreased need for mechanical ventilation and an improved survival. In most severe cases, NIV should be provided in ICU. Although it has been shown that for less severe patients (with pH values>7.30), NIV can be administered safely and effectively on general medical wards, a lead respiratory consultant and trained nurses are mandatory. Mechanical ventilation through an endotracheal tube should be considered when patients have contraindications to the use of NIV or fail to improve on NIV. The duration of mechanical ventilation should be shortened as much as possible by an early weaning process, including preventive post-extubation NIV in hypercapnic patients. hospital stay could be shortened by non-invasive treatments. Future exacerbations should be avoided by respiratory specialist management of the patients, including education, optimization of long-term medical treatment, vaccinations, nutritional support, and pulmonary rehabilitation.     

COPD exacerbations: defining their cause and prevention

Exacerbations of chronic obstructive pulmonary disease (COPD) are episodes of worsening of symptoms, leading to substantial morbidity and mortality. COPD exacerbations are associated with increased airway and systemic inflammation and physiological changes, especially the development of hyperinflation. They are triggered mainly by respiratory viruses and bacteria, which infect the lower airway and increase airway inflammation. Some patients are particularly susceptible to exacerbations, and show worse health status and faster disease progression than those who have infrequent exacerbations. Several pharmacological interventions are effective for the reduction of exacerbation frequency and severity in COPD such as inhaled steroids, long-acting bronchodilators, and their combinations. Non-pharmacological therapies such as pulmonary rehabilitation, self-management, and home ventilatory support are becoming increasingly important, but still need to be studied in controlled trials. The future of exacerbation prevention is in assessment of optimum combinations of pharmacological and non-pharmacological therapies that will result in improvement of health status, and reduction of hospital admission and mortality associated with COPD.     

Pathogenesis of bacterial exacerbations of COPD

Acute exacerbations are significant events in the course of COPD. The pathogenesis of exacerbations was poorly understood, specifically, the role of bacteria was highly controversial. Recent observations have demonstrated that bacterial infection is involved in about half of the exacerbations. The predominant mechanism of bacterial exacerbation in COPD appears to be acquisition of new strains of bacterial pathogens from the environment that are able to establish infection in the tracheobronchial tree in COPD because of compromised innate lung defenses. These pathogens interact with airway cells, elicit an inflammatory response, which underlies the pathophysiology and symptoms characteristic of exacerbation. An immune response that can be mucosal, systemic or both develops to the infecting bacterial strain. This immune response contains the infectious process, could eradicate the infecting pathogen and prevent re-infection with the same strain. However, because of antigenic diversity among bacterial strains, this immunity tends to be strain-specific rather than widely protective. Other mechanisms, including increase in bacterial load and interaction with other etiologies such as viruses, also could contribute to bacterial exacerbations. Improved understanding of the host-pathogen interaction in the airways in COPD will lead to novel approaches to prevention and treatment of exacerbations.     

Urinary desmosine excretion in acute exacerbations of COPD: a preliminary report

Desmosine (DES) is an elastin-derived, cross-link amino acid, which is not metabolized; hence, its urinary levels reflect elastin breakdown. We hypothesized that elastin degradation should increase as a result of increased lung inflammation during an acute exacerbation of COPD and should decrease after recovery. To test this hypothesis we measured DES in three urine samples from nine COPD subjects during the first 5 days of an acute exacerbation and at 2 months after recovery. We also measured forced expiratory volume in 1 sec (FEV1) to monitor the effects ofthe exacerbation on ventilatory function. The mean (SD) FEV1 was 45 (15)% predicted during the exacerbation and 57.8 (16)% predicted 2 months later (P=0.00001).The mean (SD) DES excretion was 25.3 (9) microg g(-1) creatinine at day 1;23.5 (9) at day 3 and 24 (9) at day 5 of the exacerbation. The mean (SD) urinary DES excretion 60 days after discharge was 20.9 (7) microg g(-1) creatinine (P=0.049) in comparison with the mean of the three acute-phase values. The size of the increase in desmosine excretion during exacerbation is small, 3.2 microg g(-1) creatinine or 16% of the recovery desmosine value. We conclude that there is a small but statistically significant increase in lung elastin breakdown in the body during an acute exacerbation of COPD.     

Ileocolitis: The importance of a more precise definition

Summary We have reviewed our experience with 22 patients with nonspecific inflammatory involvement of the small and large bowel. Patients with this combination of lesions usually have long-standing and intractable illnesses, with many complications, frequently resulting in multiple operations. In long-term follow-up we found a mortality of 23%.A particularly troublesome combination is granulomatous disease of the small bowel accompanying or followed by ulcerative colitis. Some suggested guidelines as to therapy in the management of these difficult cases have been presented.The term ileocolitis should be qualified, whenever possible, by the more specific pathologic terms granulomatous or ulcerative as an aid in planning therapy and in making a prognosis. In the occasional case with both of these characteristics, we subscribe to the term mixed enterocolitis.