(1)
Division of Pulmonary and Critical Care Medicine, Eastern Virginia Medical School, Norfolk, VA, USA
A COPD exacerbation is defined as an increase in the symptoms of COPD (dyspnea, cough, sputum production, sputum purulence) of a magnitude greater than the normal day-to-day variability [1, 2]. An increase in airway inflammation is considered central to the pathogenesis of a COPD exacerbation. A stimulus that acutely increases airway inflammation results in increased bronchial tone, increased bronchial wall edema and increased mucus production. These processes worsen ventilation–perfusion mismatch and expiratory flow limitation. Corresponding clinical manifestations would include worsening gas exchange, dyspnea, cough, sputum production and sputum purulence, which are the cardinal manifestations of an exacerbation. The in-hospital mortality rate for acute COPD exacerbations is approximately 10 %, and approximately 25 % of patients require admission to an ICU [3].
Patients with chronic obstructive pulmonary disease (COPD) who acutely decompensate may benefit from admission to the ICU. Patients with COPD admitted to an ICU for an acute exacerbation of COPD have a hospital mortality between 10 and 25 % with a 1-year mortality of about 40 % [4, 5]. Long-term survival of patients with COPD who required mechanical ventilation for an acute exacerbation of their disease cannot be predicted simply from data available at the time of intubation. Furthermore, the need for mechanical ventilation appears not to influence either short- or long-term outcome; therefore, the need for mechanical ventilation should not be used as a reason for not offering respiratory support [4, 5]. Noninvasive positive-pressure ventilation (NPPV) should be considered prior to endotracheal intubation in suitable candidates (see Chap. 20).
Patients with COPD often have risk factors for cardiac disease and it is often difficult to distinguish cardiogenic pulmonary edema from a COPD exacerbation. A BNP (or pro-BNP) may help distinguish between these two conditions however the BNP may be mildly increased in patients with a COPD exacerbation [6, 7]. Furthermore patients with the Malignant Obesity Hypoventilation Syndrome (MOHS) are frequently misdiagnosed as having a COPD exacerbation; these patients do not benefit from COPD therapy [8].
Common Precipitating Events
Precipitating factors must be determined in patients with COPD who present with an acute deterioration in respiratory status [4]. While chest infection is the most common precipitating factor, other readily treatable factors (e.g, atrial fibrillation, cardiac failure) should actively be investigated, including the following:
Upper respiratory tract infection
Chest infection: acute bronchitis or pneumonia
Pneumothorax
Pleural effusion
Pulmonary embolus
Heart failure
Arrhythmias
Atelectasis/mucous plugging
Use of sedative agents
Lower airway colonization by bacteria is common in patients with stable COPD. Haemophilus Influenzae, Streptococcus pneumonia and Moraxella Catarrhalis are the most common colonizing organisms. Exacerbations of COPD are frequently associated with viral infections; influenzae, parainfluenzae, and respiratory syncytial virus are the most common etiological agents. Studies using invasive diagnostic testing suggest that between 50 and 70 % of exacerbations of COPD are related to bacterial infection [2]. Approximately 25 % of patients admitted to hospital with an exacerbation of COPD have co-infection with bacteria and viruses [9]. It is not possible to differentiate clinically those patients whose exacerbation of COPD is caused by a bacterial infection. H. Influenzae, S. pneumoniae, M. Catarrhalis, and Chlamydia pneumoniae are the most common pathogens; however, multi-drug resistant (MDR) gram negative rods (including Pseudomonas aeruginosa) are not uncommon [10–12]. Risk factors for MDR gram –ve’s include previous antimicrobial treatment and previous intubation [10]. Gram-stain and culture should therefore be performed in all patients admitted to the ICU with an exacerbation of COPD (not to diagnose infection but to identify the potential pathogens).
Pulmonary embolism has been implicated in up to 25 % of patients with a COPD exacerbation who require hospitalization [13]. Based on this data all patients with a COPD exacerbation requiring admission to the ICU should undergo lower extremity Doppler studies. D-dimer levels have a high negative but a low positive predictive value for PE in COPD exacerbations because a multitude of different inflammatory and infectious etiologies can cause blood D-dimers to rise [14]. A CTPA should be considered in those patients with –ve Doppler’s, a +ve D-Dimer and an intermediate to high pretest probability of PE.
Classic teaching suggests that treatment with β-blockers should be avoided in patients with COPD. However many patients with COPD have cardiovascular diseases that may benefit from the use of such agents. Paradoxically, treatment with β-blockers may reduce the risk of exacerbations and improve survival in patients with COPD [15]. The benefit β-blockers may be related to the fact that many patients with COPD have unrecognized heart failure. Furthermore, β-blockers may upregulate β2-receptors in the lung and thus improve the bronchodilator responsiveness and effectiveness of inhaled β2-agonists. These data suggest that patients with COPD may be treated with β-blockers (β1 selective preferred) [15].
Indications for Hospitalization
Co-morbid conditions
Pneumonia
Heart failure
Renal or liver failure
Inadequate response of symptoms to outpatient management
Marked increase in dyspnea
Worsening hypoxemia
Worsening hypercapnia
Changes in mental status
In ability for patient to care for her/himself
Indications for ICU Admission
Impending or actual respiratory failure
Hemodynamic instability
Increasing confusion or obtundation
Treatment
Correct hypoxia; this usually requires only small increases in FiO2 A high PaO2 may cause an increase in CO2; the mechanisms of this phenomenon are complex and include an increase in V/Q mismatching, the Haldane effect and possibly a suppression of the “hypoxic drive.” Patients with severe COPD develop chronic compensatory mechanisms for a low PaO2 and therefore do not require a “normal” PaO2; a PaO2 between 50 and 60 mmHg is usually well tolerated. An elevated PaCO2 is acceptable as long as the patient is alert and cooperative and the arterial pH >7.2.
The results of RCT’s demonstrate that NPPV reduces the need for intubation, reduces in-hospital mortality, and shortens hospital stay during acute COPD exacerbations. NPPV should be considered in all patients who are alert and cooperative and able to tolerate NPPV (see Chap. 20) [3, 16].
Empiric antibiotics are usually given even in the absence of clinical features of infection. A meta-analysis demonstrated that antibiotics significantly reduced treatment failures in hospitalized patients (RR, 0.34; 95 % CI, 0.20–0.56) and mortality (RR, 0.22; 95 % CI, 0.08–0.62) [3]. More recent data suggests that that the addition of antibiotics to systemic corticosteroids has a limited and short-lived effect on clinical outcome and symptoms and no effect on lung function and systemic inflammation [17]. In this RCT the authors found no significant difference in clinical outcome on Day 30 among patients with a COPD exacerbation who were randomly assigned to doxycycline as compared to placebo. The antibiotic of choice in a patient with a COPD exacerbation should be guided by knowledge of the local pathogens and their sensitivity patterns. Ampicillin/clavulanate, doxycycline or respiratory fluoroquinolones (levofloxacin, moxifloxacin) are suitable choices. The antibiotics may need to be changed, guided by sputum/lower respiratory tract sampling culture results. Antipseudomonal/ extended spectrum B-lactams will be required in patients “colonized” with Pseudomonas aeruginosa or other MDR gram –ve’s and vancomycin/ linezolid in those with MRSA [12]. Procalcitonin has been used to guide the use of antibiotics in patients with a COPD exacerbation. This approach is however controversial. Stolz et al performed a RCT in which patients were randomized to standard care (which included antibiotics) or a group in which the use of antibiotics was guided by the admission PCT level [18]. A procalcitonin level of >0.25 ng/mL was used as an indication for antibiotics. Clinical outcome and improvement in FEV1 at 14 days and 6 months did not differ between groups. Within 6 months, the exacerbation rate, the rehospitalization rate, and meantime to the next exacerbation were similar in both groups. We suggest that the decision to treat with antibiotics be based on the patients’ clinical features, severity of illness, chest radiograph as well as the PCT level.Related posts:
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