This is a large topic and so I have divided it up in the following way.
Anaesthesia and COPD
Chronic Obstructive Pulmonary Disease (COPD) is defined as incompletely reversible airway obstruction. It is usually progressive in nature and does not change significantly over several months. It is related to an abnormal inflammatory response to noxious particles or gases, most commonly due to smoking.
COPD is now the preferred terminology to cover the previous clinical conditions of chronic obstructive bronchitis and emphysema. Both these components may be present to a greater or lesser degree in patients with COPD.
Chronic obstructive bronchitis refers to chronic inflammation of the bronchi, with increased peribronchiolar inflammatory infiltrates, bronchial smooth muscle hypertrophy, mucus hypersecretion, and resulting airway obstruction from loss of airway calibre.
Emphysema refers to destruction of lung parenchyma. This results in loss of the elastic properties of the lung, with the loss of radial traction resulting in an increased tendency for airways collapse. This leads to lung hyperinflation and airway limitation. The destruction of alveolar septa results in reduced surface area for gas exchange, and sometimes consolidation into large bullae.
The consequences of these changes is impaired lung function, particularly from the effects of reduced airway calibre from mucus hypersecretion, bronchospasm and impaired elastic function. These impair respiratory mechanics and increase the work of breathing, as does the lung hyperinflation that results. This can lead to alveolar hypoventilation and impaired gas exchange. Destruction of lung parenchyma can also contribute to this. Both factors may result in impaired V/Q matching which can further impair respiratory function. With advanced disease, chronic respiratory dysfunction can develop, with hypoxia and hypercapnia. The patient’s respiratory centres can reset to tolerate these high levels of CO2, and instead the respiratory drive become dependent of blood oxygen tensions. Chronic hypoxia can result in increased pulmonary vascular tone, with resulting pulmonary hypertension and right heart strain.
Cigarette smoke is the main causative agent, although smoke from other fuels is an important factor in developing countries. Genetic factors contribute to the development of disease, and about 15% of smokers develop signs of COPD. The most well known specific genetic contributor is alpha1-antitrypsin deficiency (an antiprotease). An abnormality of the FAM13A gene has also been implicated in COPD development. In patients who are genetically susceptible, smoke inhalation triggers an inflammatory response in the airways and alveoli. This is thought to trigger an inflammatory mediated increase in proteases and decrease in the regulatory antiprotease activity. These proteases are secreted by immune cells, and their normal role is tissue breakdown as part of the repair process. There can be increased bacterial colonisation of the lower respiratory tract, with recurrent infections propagating the inflammatory damage.
There is often a multifactorial, systemic inflammatory process present with patients with advanced COPD. This is at least partly responsible for some of the extra-pulmonary effects such as weight loss, sarcopenia, osteoporosis, and cardiovascular disease.
An estimated 3 million people in the UK are diagnosed with COPD. It is estimated that 60-85% of patients with the disease actually remain undiagnosed.
Cigarette smoking is by far the biggest risk factor. Most patients are not diagnosed until their 50s. There is a strong association with other medical comorbidities: Lung cancer, cardiovascular disease, osteoporosis.
The onset of the disease is usually insidious. The most common features are:
Chronic productive cough
Frequent ‘bronchitis’ episodes
Acute exacerbations of the disease are common, and often increase in frequency with the progression of the disease.
A smoking history is almost always present. An assessment of the patient’s ‘Pack year history’ is important (number of cigarettes per day divided by 20). A pack year history of 40 or more is quite predictive. Clinical signs can include:
If advanced disease with cor pulmonale, there may be features of right heart failure.
In terms of assessing breathlessness, NICE recommend the use of the Medical Research Council (MRC) dyspnoea scale. This is as 5 point scale with increasing degrees of breathlessness at lower levels of activity:
Only breathless with strenuous exercise
Short of breath when hurrying or walking up a slight incline
Walks slower than contemporaries on the flat because of breathlessness.
Has to stop after 100m of a few minutes of walking on the flat.
Breathless on dressing/undressing. Unable to leave the house.
There is no gold standard test for COPD. The diagnosis is based on a combination of history, examination and spirometry evidence of airflow obstruction. As such, spirometry is a key investigation for the disease.
Other investigations may include:
CXR - to assess for alternative disease or look for features of COPD
FBC - to look for anaemia (as a cause of symptoms) or polycythemia.
Alpha1-antitrypsin - This may be used in patients presenting very young with the disease.
ECG - as part of the assessment of other disease. May show features of right heart strain.
NICE provides useful guidance on the diagnosis of COPD. The definition they use for ‘airway obstruction’ is an FEV1/FVC ratio of <0.7.
Spirometry In most patients reversibility testing isn’t required. This is because it can be difficult to use results to help with the diagnosis. The exact details of spirometry are discussed elsewhere but are important to understand
Assessment of Severity Severity of airway obstruction can be defined by the result of spirometry. This table describes the increasing levels of severity, based on the patient’s FEV1 compared to predicted values. Of note, functional severity of COPD may not be accurately reflected by the severity of airway obstruction. NICE recommend a more global assessment based on
MRC dyspnoea scale
Exercise capacity e.g. 6 minute walk test
Presence of cor pulmonale
They recommend calculation of the BODE index (BMI, airway Obstruction, Dyspnoea score, Exercise tolerance) to aid with prognostication. There is a link to a calculator here: https://www.mdcalc.com/bode-index-copd-survival
The management of chronic COPD has several key areas:
Advice on exacerbations
Smoking Cessation This is the key factor in reducing further progressive deterioration lung function. Patients will often need support in stopping smoking which should be offered e.g. nicotine replacement therapy. The use of ‘teachable moments’, such as around a major operation, can provide the impetus to quit.
Inhaled Bronchodilator therapy The use of either beta2-agonist or muscarinic antagonist agents can help improve symptoms in patients with COPD. Their effectiveness shouldn’t be assessed on the basis of improvement in improvements in test of obstruction, but more on symptomatic relief. The choice of bronchodilator class is not thought to be important. A staged inhaler approach is recommended, escalating as needed:
Short acting bronchodilator
+ Long acting bronchodilator if FEV1 >50%
+ Long acting bronchodilator and corticosteroid combination if FEV1 <50%
+ additional long acting bronchodilator (the alternative class to what the patient is already on)
The use of inhaled corticosteroids is controversial, with evidence of an increased incidence of serious pneumonia. This should be discussed with patients. They have a role in decreasing the frequency of exacerbation, so may be more appropriate in this cohort who have regular exacerbations.
If breathlessness remains severe and debilitating despite optimal inhaler therapy, then nebulised bronchodilator therapy should be considered. There should be a clear assessment to show that they provide some benefit to the patient.
Oral steroids These are not usually indicated in patients with COPD. Some patients with advanced COPD may struggle to have them withdrawn following an exacerbation. In these cases the dose should be kept as low as possible and protection against the adverse effects considered.
Vaccinations Patients should receive vaccination against pneumococcal disease. They should also receive annual influenza vaccination.
Long Term Oxygen Therapy Oxygen therapy may provide a mortality benefit to patients with COPD who have severe hypoxaemia. This benefit require O2 therapy for at least 15 hours a day, with greater benefit at 20 hours a day usage.
LTOT is indicated in patient who (when well) have:
PaO2 <7.3 kPa
PaO2 7.3-8 kPa and:
Secondary polycythemia, or
It can be considered in patients with other signs of severe COPD e.g. severe airway obstruction.
Assessment requires 2 arterial blood gases at least 3 weeks apart. LTOT can not be prescribed to patients who continue to smoke due to the very real risk of fire or explosion. In general, an oxygen concentrator is used rather than oxygen cylinders.
Short burst oxygen therapy (10-20 mins) is an option for symptomatic treatment of patients with severe breathlessness with COPD that is unrelieved by other treatment.
Mucolytic therapy can be considered in patients with chronically productive cough. Again, a they should be reassessed to ensure that they derive a benefit from it. Other management options of chronic COPD include pulmonary rehabilitation and lung surgery for resection of significant bullous disease.
Acute Exacerbations of COPD
This is defined as “sustained worsening of the patient's symptoms from their usual stable state which is beyond normal day-to-day variations, and is acute in onset”
The trigger of the exacerbation is often not clear. There can be a number of infective and non-infective triggers.
Bacterial - strep pneumoniae, H. influenzae, Moraxella Catarrhalis, Staph aureus
Other medical condition e.g. pneumonia, pulmonary embolism
There is an increased inflammatory response of the airways, with bronchospasm, increased mucus production and retention. These can lead to increased airways obstruction, with increased work of breathing, collapse of lung units and impaired gas exchange.
The worsening symptoms usually involves:
Worsening cough, including increased volume and purulence of sputum
Reduced exercise tolerance
Increased chest tightness/wheeze
There can also be:
Clinical signs can vary from signs of wheeze and airway obstruction, through to extreme respiratory distress.
The diagnosis is generally a clinical one, but investigations can help assess for alternative diagnoses and management. Some cases can be managed in the community, whereas others require hospital admission.
As with other potentially acutely ill patients, a systematic A to E assessment should be undertaken.
Investigations in hospital include:
Bloods - FBC, U&E as minimum
Sputum cultures if producing sputum
Blood cultures if considering sepsis
The basic principles of management are:
High dose bronchodilators
Antibiotics if bacterial infection likely
Further management options may include:
Non invasive ventilation
High dose bronchodilators These can often help with the breathlessness associated with an exacerbation. Beta agonists and muscarinic antagonist can both be used with similar efficacy. The method of administration (nebulised vs inhaled) depends on the required dose and ability of the patient to effectively use. Inhaled delivery using a spacer can provide equivalent drug delivery. Nebulised therapy should usually be driven by air rather than oxygen to allow control oxygen delivery, especially in any patient with hypercapnia.
Systemic Steroids Systemic steroids should be given to all patients with an exacerbation unless there is a strong contraindication. Prednisolone 30mg OD orally for 7-14 days is recommended. Early administration within the course of the exacerbation is preferable. Patients may have ‘rescue packs’ at home if they have had education on their exacerbations to try and allow community management. Protection against complications (particularly osteoporosis) should be considered for patients receiving regular courses of steroids. Advice needs to be provided on discontinuing the course.
Antibiotics The decision for antibiotics should generally be based on the presence of increased purulent sputum. Their use may also be indicated if there is a coexisting pathology e.g. pneumonia. Cultures should ideally be sent before commencing treatment. Choice of antimicrobials should be based on local guidance, following the principles of initial empirical therapy and then targeted therapy as the organism is identified.
Theophylline It is recommended that theophylline should only be considered in cases of an inadequate response to nebulised bronchodilators.
Oxygen It is important that an oxygen delivery is done in a controlled manner, to target patient specific SpO2 targets. Uncontrolled oxygen therapy is strongly implicated with worsening of patient’s clinical state, increasing the degree of acidosis and mortality.
Critical Care Management
Acute exacerbations of COPD can lead to a need for critical care support due to organ failure. Of particular note is the risk of hypercapnic respiratory failure. This cohort of patients may require increased levels of care, although there has been increased management within general medical or specific respiratory ward environments.
Acute hypercapnic respiratory failure (AHRF) complicates around 20% of COPD exacerbations. It is a marker of severe disease and poor long term prognosis. It is defined as:
PaCO2 > 6.5kPa
pH < 7.35
When persisting despite optimal medical treatment, it is an indications for non-invasive ventilation (NIV).
Non Invasive Ventilation NIV in this cohort of patients has been shown to clearly improve outcome, and also demonstrates improved outcomes compared to invasive mechanical ventilation. Compared with standard care, NIV produces lower mortality (RR 0.41), lower rates of intubation (RR 0.42) and improvements in physiological parameters (including pH and pCO2). However, there is still a need to identify the cohort of patients who are failing NIV and when need IMV, as a failure to do this actually increases mortality.
The British Thoracic Society recommends the following points for NIV:
Pressure targeted mode ventilation is preferred
The presence of adverse features or contraindications should not necessarily completely preclude use of NIV because of its many benefits. Instead it should be trialed in a highly monitored environment to detect for failure/complications.
Oxygen therapy should be targeted at an SpO2 of 88-92% in these patients.
Bronchodilator therapy should preferably be given during breaks from NIV rather than via the circuit.
Agitation with NIV is not uncommon. Sedation may be indicated to allow the patient to tolerate the support (e.g. if I&V is not appropriate) but should be done in a highly monitored environment.
NIV can be stopped once the respiratory parameters have returned to the normal range and the patient’s general clinical condition has improved.
The target is as much NIV as tolerated in the first 24 hours, with gradual reduction over 48-72 hours
Indications and Contraindications The indications for NIV will be patient specific, but some specific respiratory parameters of AHFR are noted about. There is advice that more severe respiratory failure, for instance impending respiratory arrest or a pH <7.15, should indicate a need to progress straight to IMV. However, the BTS guidance notes that as the use of NIV is often associated with a better outcome in these patients, there should be fairly strong efforts made to at least trial this. With patients that are this unwell, this clearly needs to be done in a highly monitored critical care environment, with preparation to intubate if needed. They note that sometimes, even the brief support provided whilst preparing to intubate e.g. via hadn ventilation, can be enough to provide some stability to trial NIV first.
Similarly, the benefits derived from NIV, mean that many of the contraindications are only relative, as longer as NIV can be delivered in a safely monitored environment, with rapid initiation of IMV if needed. Indeed, some disturbances such as hypotension are better suited to NIV. Conditions that need careful consideration or other intervention prior to NIV include:
Vomiting - dependent on patients ability to respond to need to vomit
Pneumothorax - will need an intercostal drain before any positive pressure support.
Notable acidosis or hypercapnia - will likely be helped by NIV
Some conditions are almost certain to be absolute contraindications:
Fixed upper airway obstruction
Severe facial deformity
NIV is not indicated in the case of a co-existing pneumonia.
Delivery of NIV The use of a full face mask is recommended by the BTS. Pressure targeted ventilation by machines specifically designed for NIV are recommended. Appropriate initial settings are an EPAP of 3 and an IPAP of 15. IPAP should be uptitrated over 10-30 minutes to achieve good chest expansion and a reduction in respiratory rate. A target IPAP of between 20-30 Oxygen therapy should be titrated to target a SpO2 of 88-92%.
Continuous oxygen saturation monitoring is essential. Episodic measurement of blood gases is also essential to assess effectiveness. Capillary gases are often employed to this end, though invasive arterial lines may be used in critical care areas.
Humidification of NIV circuits is not necessary unless significant upper airway dryness or dry secretions becomes problematic. Bronchodilator therapy is not as effective when delivered via the NIV circuit. It is therefore advised that they are administered during breaks from NIV. They can be given via the circuit of the patient is dependent on NIV.
Patient distress and agitation is common in AHRF and may impact on the success of NIV. Concerns about further CNS or respiratory depression are reasonable, but treating the patient’s distress is an important ethical consideration, as well as a factor that may improve the AHRF through better toleration of NIV. If IMV remains a possible intervention, then cautious, titrated sedation should be employed if necessary to optimise tolerance of NIV. If IMV is not deemed a suitable intervention, then anxiolysis is still an important therapeutic goal, and is likely to increase the chances of success of NIV. The BTS guidance notes that an opioid may be the preferred drug of choice, as there is theoretically less obtundation of upper airway reflexes than with benzodiazepines.
An improvement in physiological parameters (particularly pH, pCO2 and resp rate) within the first 1-2 hours of NIV is a positive predictor for outcome. Conversely, a deterioration in these parameters is associated with a worse outcome and indicate a need to change management, including the possibility of intubation.
The common cause of failure in NIV are:
Excessive mask leak
Invasive Mechanical Ventilation Invasive mechanical ventilation (IMV) may be required in some patients with a severe AECOPD with AHRF. This may be immediately apparent because of the severity of the patient’s illness, or because an NIV approach has failed or is contraindicated.
Indications for IMV include:
Failure of NIV or contraindicated
Depressed GCS (often using 8 as a cut off)
As previously noted, the BTS note that experienced clinicians may wish to trial NIV in these conditions whilst monitoring very closely.
The decision to proceed to IMV is a challenging one. This is because of the significant morbidity and mortality associated with critical care admission in these circumstances, coupled with the often poor long term outcomes of patients with COPD of this severity. This can lead to ceilings of care being set at the level of NIV, on the grounds of futility or a greater risk of harm than benefit to the patient. However, the BTS guidance notes that clinicians are often overly pessimistic about the outcome of this cohort of patients. They note that outcome for these patients is probably actually better than in many other conditions where IMV is instigated.
Tailored decision making for each patient must be undertaken to help makes decisions such as this. There are no perfect criteria to help guide this decision making. Instead factors such as patient’s wishes, baseline functional status, previous exacerbations (including ICU admissions), other comorbidity, and markers of physiological severity of this exacerbation should be used. Several scoring systems can be used to help in his way:
APACHE score - a marker of general physiological derangement but applicable to patients with AECOPD.
BOSE index - provides an idea of prognosis when stable
COPD and Asthma Physiology Score (CAPS)
Factors associated with a worse prognosis include:
Long term oxygen therapy
BMI < 22
Age > 75 years
Higher scores of physiological severity (e.g. APACHE, CAPS)
CAPS Full link to initial paper is available here: https://www.ncbi.nlm.nih.gov/pubmed/17616454 This is a score of 0-100 based on the physiological disturbance of the patient. A higher score indicates a higher mortality. The score was derived from a large cohort of patients and prospectively validated in a similarly large cohort. The AUROC curve was 0.718, suggesting it was slightly better than the APACHE score (version 3) in this cohort. The score is better for asthma than COPD though.
DECAF This score is based on 5 easy to derive parameter:
Dyspnoea at baseline - MRC dyspnoea scale 5
Eosinopenia (<0.05 x 10^9/L)
Consolidation on CXR
Acidaemia (pH < 7.30)
Fibrillation (atrial) - on admission ECG
The dyspnoea can be either 1 point if 5a on the scale (can dress and bathe self) or 2 if 5b on the scale (requires assistance with dressing and bathing. The other criteria get 1 point. They can be then categorised into different risk cohorts:
This seems a useful score and demonstrated high AUROC curve score on both the initial study (0.86) and on validation (0.83)
Delivering IMV The initial period of IMV often requires a controlled ventilation approach to be taken, due the the physical challenges of ventilation. This allows a period of time for the administered treatment (bronchodilators, steroids, antibiotics) to have effect, as well as allow mechanical removal of secretions. After this period, ventilatory strategy should switch to a pressure support approach, to allow reduction in sedation and get the patient’s respiratory muscles working to reduce wasting.
Narrow airway calibre can result in challenges with ventilation, including high airway pressure, dynamic hyperinflation, and the adverse consequence of these. An initial management approach should therefore consider:
Lung protective volumes - 6-8ml/kg
Lower respiratory rate - 10-15 bpm
Prolonged expiratory time - I:E ratios of 1:2-1:4
SpO2 target 88-92%
Permissive hypercapnia if peak inspiratory pressures > 30cmH2O
Positive end expiratory pressure (PEEP) is often required when ventilating these patients. AECOPD results in collapsed lung units and globally impaired ventilation. Application of extrinsic PEEP can improve lung compliance (shifting the compliance curve to the right), improve expiratory airflow (by preventing dynamic airway collapse) and improve alveolar ventilation. Intrinsic PEEP can occur in AECOPD. Setting extrinsic PEEP above this level can be deleterious, and thus it is recommended that ePEEP is set no higher than 50-80% the calculated value of iPEEP.
Recovery Regular clinical assessment should be undertaken to ensure response to treatment. Regular blood gas monitoring will be required in patients with hypercapnia, to monitor response to treatment. Regular assessment of airway obstruction (e.g. PEFR) is not required due to the high variability and slow recovery of such parameters, limiting their usefulness. Assessment with spirometry is recommended in all patients prior to discharge though. Patients should be established on their optimal bronchodilator regime and have clear return of their normal physiology parameters. Follow up arrangements should be made with patients prior to discharge.
Exacerbations of COPD are associated with a decrease in lung function and quality of life, as well as an increased mortality. Symptoms and recover slowly (median time 7 days) and objective evidence of airway obstruction even more slowly (75% of patients returned to baseline at 35 days). In patients who developed AHRF, the median survival time was 1 year, and around 12% of patients died during the hospital admission. Such events should prompt discussions about end of life planning.
Anaesthesia and COPD
COPD has a significant impact on the delivery of anaesthesia for patients. It is a relatively common disease and is associated with greater perioperative morbidity and mortality than in patients without the disease. Patients with severe COPD undergoing surgery are at particular high risk of complications, including the need for unanticipated intubation perioperatively.
History A preoperative assessment will include a full history from the patient, with specific enquiry about important factors related to their COPD. This should include:
Exercise tolerance (MRC dyspnoea scale can be useful)
Frequency of exacerbation
Previous critical care treatment (NIV or IMV)
Most recent exacerbation (including antibiotic and steroid treatment)
A clear history of the patient’s medications is important and can also provide an indication of severity. Of particular note:
Home nebulisers - indicate severe disease
Oral steroids - may mean a degree of adrenal suppression
Theophylline - multiple interactions and narrow therapeutic window
In patients with severe disease, discussions about ceilings of care and end of life plans may be appropriate e.g. in high risk cases. These patients may already have made plans about limits of intervention e.g. @I don’t want to go on a ventilator’.
Investigations Some investigations will likely have been done in the regular care of the patient’s disease, but important ones to review or repeat include:
Spirometry - provides more objective evidence of airway obstruction
ECG - assessing for evidence of right heart changes or IHD
CXR - not indicated preoperatively, but if they have been performed can show evidence of bullous disease
Blood gas - can help identify severe disease at baseline. pO2 < 8 and pCO2 >6 kPa are both markers of severity.
Formal assessment of functional state can be very useful e.g. 6 minute walk test, stair climbing.
Examination A thorough clinical examination preoperatively is important. Clinical signs of airways disease before surgery (wheeze, reduced breath sounds) are predictors of complications post op and warrant aggressive bronchodilator treatment and possibly steroids. Features of a exacerbation of COPD, particularly infective features, really mandate postponement of the surgery.
Preoperative intervention Stopping smoking is the most effective intervention in reducing the ongoing decline of lung function in COPD. Similar advice is given regarding the impact of stopping smoking on improving perioperative care. Although there have been some studies that suggest an increased risk of complications if smoking is stopped less that 8 weeks before surgery, this has not been convincingly borne out on further investigation. Support with nicotine replacement therapy may help with this.
Anaesthetic technique It is widely accepted that a general anaesthetic technique has a greater risk of complications in this group of patients. The risks of a GA in this cohort include an increased risk of bronchospasm, laryngospasm, barotrauma, and mucous plugging. This can lead to increased challenges intra-operatively and an increased rate of postoperative complication e.g. respiratory failure, pneumonia. One study has shown a 50% reduction in postoperative pneumonia when a GA was avoided.
As such there is an increased push to use regional techniques to facilitate surgery. These can be complemented by gentle sedation if needed. Intraoperative NIV may be beneficial if patients have significant difficulty with the necessary surgical positioning e.g. lying flat. Whereas the use of interscalene blocks in these patients was controversial (because of the impact of phrenic nerve paralysis) the benefits of avoiding a GA may actually favour this approach. Careful, low volume, ultrasound guided techniques can further minimise the impact on the phrenic nerve.
General Anaesthesia Particular issues associated with general anaesthesia include:
Impaired expiratory flow can lead to gas trapping and development of intrinsic PEEP.
This can result in cardiovascular instability and barotrauma.
Increased alertness to the possibility of these needs to be maintained, e.g. observation of capnography trace, measurement of intrinsic PEEP.
A more prolonged inspiratory time can be useful in managing this - using higher I:E ratios with lower resp rates
Application of external PEEP can oppose small airways collapse and reduce gas trapping
changes in intrathoracic pressure on induction can result in cardiovascular instability.
An arterial prior to induction is recommended (especially as blood gas monitoring is likely to be needed.
Can be precipitated by several factors, including airway manipulation
Management involves use of bronchodilator agents and ensuring appropriate depth of anaesthesia
There should be awareness of the risk for pneumothorax. Preoperative nebulisers may be considered.
Extubation Transitioning back from anaesthesia can be challenging. It is essential that all factors are optimised prior to extubation being attempted (though this is important for all extubations) e.g. nueromuscular blockade, temeparture. Extubation straight on to NIV may be indicated in some patients with severe disease.
Analgesia Effective analgesia is essential to ensure optimal respiratory function i.e. not limited by pain. However, the sedative effects of opioids are also not desirable. An analgesia plan will need to be tailored to each placement, but the goal should be effective analgesia with minimal respiratory side effects. Effective regional techniques can be very effective to this end e.g. epidural analgesia.
Close observation of these patients postoperatively is essential to prevent, detect and manage any complications. This will clearly be tailored to the severity of their COPD, their comorbidities and the extent of the surgery. For patients with severe COPD, especially if anything but minor surgery, a critical care environment is likely to be needed. The use of perioperative NIV will be based on the individual patient’s case. Effective sputum clearance should be optimised through aggressive physiotherapy and consideration of pharmacological support where needed e.g. saline nebs.
An escalation of bronchodilator therapy may be beneficial during the postoperative period i.e. to nebulised therapy, additional agents. Features of postoperative infection (e.g. purulent sputum, pyrexia) should be treated aggressively.
Links & References
Beers, M et al (eds). Chronic Obstructive Pulmonary Disease. The Merck Manual (18th ed). 2006.
Lumb, A. Biercamp, C. Chronic obstructive pulmonary disease and anaesthesia. CEACCP. 2014. 14(1): 1-5.
Chronic obstructive pulmonary disease (COPD) in Allman, K. Wilson, I. (eds) Oxford handbook of anaesthesia (3rd ed). 2012
Wildman, M. et al. A new measure of acute physiological derangement for patients with exacerbations of obstructive airways disease: the COPD and Asthma Physiology Score. Respiratory Medicine. 2007. 101(9): 1994-2002. Available at: https://www.ncbi.nlm.nih.gov/pubmed/17616454
Steer, J. Gibson, J. Bourke, S. The DECAF Score: predicting hospital mortality in exacerbations of chronic obstructive pulmonary disease. Thorax. 2012. 67: 970-976. Available at: http://thorax.bmj.com/content/67/11/970.info
Echevarria C, Steer J, Heslop-Marshall K, et al. Validation of the DECAF score to predict hospital mortality in acute exacerbations of COPD. Thorax. 2016. 71:133-140. Available at: http://thorax.bmj.com/content/71/2/133