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Chronic Pulmonary Disease
INTRODUCTION
Chronic respiratory problems include obstructive and restrictive lung diseases, obstructive sleep apnea (OSA), and pulmonary hypertension. Obstructive lung diseases are commonly divided into reactive airway disorders (asthma) and chronic obstructive pulmonary disease (COPD). However, many patients have more than one type of lung disease. Using regional or local rather than general anesthesia is preferable for patients with chronic respiratory diseases.
History
Common symptoms elicited in all patients include cough, wheezing, shortness of breath, chest tightness, sputum production, and reduced exercise tolerance. Important components of the history are recent exacerbations, current and previous therapies (including hospital admissions), emergency room visits, and tobacco use.
Physical Examination
Signs of chronic respiratory disease include tachypnea, cyanosis, use of accessory muscles of respiration, and clubbing of the fingers. Important examination findings are the presence of unequal breath sounds, wheezing, and rales during auscultation.
Laboratory Examination
Chest Imaging
A recent preoperative chest x-ray examination is not required for all patients but should be considered in any patient with a chronic respiratory disease or a patient with a recent change in respiratory symptoms or signs.
Spirometry
Simple spirometry (expired volume or flow vs. time), forced vital capacity (FVC), and forced expiratory volume in 1 second (FEV 1 ) ( Fig. 27.1 ) are not required in all stable patients but should be ordered if there is any doubt about the severity of disease, such as a recent change in symptoms, if the patient is unable to give a clear history, or if any patient with chronic lung disease is having lung surgery. Full pulmonary function tests (plethysmography) ( Fig. 27.2 ), including measurement of residual volume (RV), functional residual capacity (FRC), and measurement of the lung diffusing capacity for carbon monoxide (D lco ) are only indicated if the diagnosis or severity of the lung disease is unclear from the simple spirometry procedure.
Gas Exchange
Oxygen saturation (pulse oximetry: Sp o 2 %) should be documented preoperatively in every patient with a chronic respiratory disease. Arterial blood gases are required preoperatively in patients with moderate or severe chronic respiratory disease who are at risk of requiring postoperative mechanical ventilation (major abdominal, thoracic, cardiac, spine, or neurosurgery) or if symptoms have become more intense.
ASTHMA
Clinical Presentation
Asthma is a common form of episodic recurrent lower airway obstruction that affects 3% to 5% of the population. Sixty-five percent of people with asthma become symptomatic before age 5 years. Patients with childhood asthma often become quiescent with time but can have recurrences. Inflammation of the airways is a hallmark of asthma. Steroids (inhaled, oral, or both) are the most effective medications in controlling this inflammation. The inflamed airway is hyperresponsive to irritant stimuli with subsequent bronchospasm, small airway edema, and mucous secretions. Bronchospastic stimuli can include allergens, dust, cold air, instrumentation of the airways, and medications (nonsteroidal antiinflammatory drugs or histamine-releasing drugs). Patients with asthma are at risk for life-threatening bronchospasm during anesthesia, particularly during or recently after a respiratory tract infection. Elective surgery should therefore be delayed at least 6 weeks after a respiratory infection in these patients.
The severity of asthma, defined by the amount of treatment required to control symptoms, includes intermittent, mild persistent, moderate persistent, and severe persistent asthma , ( Box 27.1 ). Most patients will be in steps 1 or 2 of this treatment protocol. Caution is required when anesthetizing patients after step 3. A history of severe or life-threatening exacerbations, requiring endotracheal intubation or admission to intensive care, is indicative of patients at increased risk of major pulmonary complications. Peak expiratory flow (PEF) rate is a simple and useful measurement of asthma severity. Many patients measure their own PEF to guide their therapy. PEF rates less than 50% of the predicted value (corrected for age, gender, and height) indicate severe asthma. A PEF increase of more than 15% after bronchodilator administration suggests inadequate treatment of asthma.
Box 27.1
Stepwise Therapy for the Treatment of Asthma
prn , As needed.
*Formoterol is a long-acting inhaled β 2 -agonist (LABA); there are several formulations of formoterol combined with an inhaled corticosteroid in a single inhaler.
†Long-acting muscarinic antagonists include tiotropium bromide and aclidinium bromide.
Stepwise approach for asthma management according to the National Asthma Education and Prevention Program Coordinating Committee. Step 1 is for patients with intermittent asthma only; the remaining steps are for patients with persistent asthma. Alternative management steps and additional treatment recommendations are available in Expert Panel Working Group of the National Heart, Lung, and Blood Institute (NHLBI) administered and coordinated National Asthma Education and Prevention Program Coordinating Committee (NAEPPCC), Cloutier MM, Baptist AP, Blake KV, et al. 2020 Focused updates to the asthma management guidelines: A report from the National Asthma Education and Prevention Program Coordinating Committee Expert Panel Working Group. J Allergy Clin Immunol. 2020;146(6):1217–1270.
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Step 1: Inhaled short-acting β 2 -agonists (SABA) PRN (e.g., salbutamol [aka albuterol] 100–200 μg prn)
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Step 2: Daily low-dose inhaled corticosteroids (ICS) and SABA PRN, or PRN concomitant with ICS and SABA (e.g., inhaled fluticasone 88 mcg twice daily)
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Step 3: Daily and PRN combination low-dose ICS-formoterol*
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Step 4: Daily and PRN combination medium-dose ICS-formoterol
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Step 5: Daily medium-high dose ICS-LABA plus long-acting muscarinic antagonist † (LAMA) and PRN SABA
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Step 6: Daily high-dose ICS-LABA plus oral systemic corticosteroids plus PRN SABA
Suppression of the hypothalamic-pituitary-adrenal (HPA) axis may occur with corticosteroid therapy. Adrenal crisis may be precipitated by the stress of surgery. Short courses of oral prednisone used to treat asthma exacerbations can affect HPA function for up to 10 days, but dysfunction is unlikely to be prolonged. Large doses, prolonged therapy (>3 weeks), evening dosing, and continuous (as opposed to alternate day) dosing all increase suppression of the HPA axis and may take up to a year before returning to normal. Inhaled steroids are less likely to cause suppression of the HPA axis.
Management of Anesthesia
The adequacy of asthma control should be assessed during preoperative evaluation and symptoms uncharacteristic of asthma excluded ( Table 27.1 ). Principles of perioperative management of patients with asthma are outlined in Box 27.2 . Volatile anesthetics, particularly sevoflurane, reduce bronchomotor tone and produce a degree of bronchodilation (except desflurane) that may be helpful in patients with obstructive lung disease or bronchoconstriction.
Table 27.1
Preoperative Assessment for Asthma
| History Suggestive of Inadequate Asthma Control | |
| Frequency of symptoms | |
| Use of β 2 -agonist medications/relievers frequently | |
| Hospital attendances (e.g., emergency department, physician office visit) | |
| Hospital/intensive care unit (ICU) admissions | |
| Use of oral steroids/high-dose inhaled steroids | |
| Features Uncharacteristic of Asthma | Differential Diagnosis |
| Unremitting wheeze/stridor | Suggestive of fixed airway obstruction |
| Persisting wet cough/productive cough | Suggestive of suppurative lung disease |
| Wheeze present from birth (rare with asthma) | Tracheomalacia/bronchomalacia |
| A monophonic wheeze loudest over the glottis | Vocal cord dysfunction |
Box 27.2
Principles of Perioperative Management of Asthma
LMA , Laryngeal mask airway.
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Usual inhalers per normal on day of surgery. Inhaled β 2 -agonists before anesthesia.
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Avoid lower airway manipulation (e.g., endotracheal intubation) if possible. Use regional anesthesia or an LMA/mask for general anesthesia if possible.
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Avoid medications that release histamine (e.g., thiopental, morphine, atracurium).
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Use anesthetic drugs that promote bronchodilation (propofol, ketamine, sevoflurane).
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If instrumentation of the lower airway is necessary, it should be performed after attaining a deep level of general anesthesia to decrease airway reflexes.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Clinical Presentation
The pathologic hallmarks of COPD include inflammation of the small airways and destruction of lung parenchyma. The FEV 1 /FVC ratio will be less than 70%, and the RV will be increased. The severity of COPD is assessed by the percent of FEV 1 : stage I, more than 50% predicted (this category includes both mild and moderate COPD); stage II, 35% to 50%; and stage III, less than 35%. Stage I patients should not have significant dyspnea, hypoxemia, or hypercarbia. Specific complications of COPD to be considered preoperatively are described next.
Carbon Dioxide Retention (Baseline Pa co 2 >45 mm Hg)
Some patients with stage II or III COPD have an elevated Pa co 2 at rest. Patients with CO 2 retention cannot be differentiated from patients without retention on the basis of history, physical examination, or spirometry. When these patients are given supplemental oxygen, their Pa co 2 values increase because of an increase in alveolar dead space from a decrease in regional hypoxic pulmonary vasoconstriction and the Haldane effect. However, supplemental oxygen must be administered to these patients to prevent the hypoxemia associated with the postoperative decrease in FRC. Increased CO 2 concentrations above baseline lead to respiratory acidosis, which causes cardiovascular changes (tachycardia, hypertension, and pulmonary vasoconstriction). Pa co 2 levels more than 80 mm Hg can cause a decreased level of consciousness. The increase in Pa co 2 in these patients postoperatively should be anticipated and monitored. To identify these patients preoperatively, patients with stage II or III COPD should have an analysis of arterial blood gas performed.
Right Ventricular Dysfunction
Right ventricular dysfunction occurs in up to 50% of patients with severe COPD. Chronic recurrent hypoxemia is the cause of right ventricular dysfunction and subsequent progression to cor pulmonale. Cor pulmonale occurs in 70% of adult COPD patients with an FEV 1 less than 0.6 L. Mortality risk in these patients is primarily related to chronic hypoxemia. Administration of oxygen is the only therapy that improves long-term survival and decreases right-sided heart strain associated with COPD. Patients who have a resting Pa o 2 less than 55 mm Hg should receive supplemental oxygen to maintain Pa o 2 at 60 to 65 mm Hg at home.
Bullae
Many patients with moderate or severe COPD develop cystic air spaces in the lung parenchyma known as bullae . These bullae will often be asymptomatic unless they occupy more than 50% of the hemithorax, in which case the patient will present with findings of restrictive respiratory disease in addition to their obstructive disease. A bulla is actually a localized loss of structural support tissue in the lung with elastic recoil of surrounding parenchyma. The pressure in a bulla is the mean pressure in the surrounding alveoli averaged over the respiratory cycle. Whenever positive-pressure ventilation is used, the pressure in a bulla will become positive in relation to the adjacent lung tissue and the bulla will expand, with the attendant risk of rupture, tension pneumothorax, and bronchopleural fistula. Positive-pressure ventilation can be used safely in patients with bullae, provided the airway pressures are low and adequate expertise and equipment are immediately available to insert a chest drain and obtain lung isolation if necessary. Nitrous oxide will diffuse into a bulla more quickly than the less soluble nitrogen can diffuse out and may lead to rupture of the bulla. The presence of bullae should be ascertained by examination of the chest imaging of any patient with COPD preoperatively.
Flow Limitation
Severe COPD patients are often flow limited, even during normal breathing. Flow limitation occurs when any increase in expiratory effort will not produce an increase in flow at that given lung volume. Flow limitation is present in normal patients only during a forced expiratory maneuver and in patients with COPD as a result of the loss of lung elastic recoil. During positive-pressure ventilation, this can lead to the development of an intrinsic positive end-expiratory pressure (auto-PEEP). Severely flow-limited patients are at risk of hemodynamic collapse during positive-pressure ventilation because of dynamic hyperinflation of the lungs leading to obstruction of pulmonary blood flow.
Perioperative Management
Four treatable complications of COPD must be actively sought and managed at the time of preoperative assessment: atelectasis, bronchospasm, respiratory tract infections, and congestive heart failure. Atelectasis impairs local lung lymphocyte and macrophage function, predisposing to infection. Wheezing may be a symptom of both airway obstruction and congestive heart failure. Patients with COPD should receive bronchodilator therapy as guided by their symptoms. If sympathomimetic and anticholinergic bronchodilators provide inadequate therapy, a trial of corticosteroid therapy should be instituted.
COPD patients have fewer postoperative pulmonary complications when intensive chest physiotherapy is initiated preoperatively. Even in patients with severe COPD, exercise tolerance can be improved with physiotherapy of at least 1 month or more. Among COPD patients, those with excessive sputum benefit the most from chest physiotherapy. A comprehensive program of pulmonary rehabilitation involving physiotherapy, exercise, nutrition, and education has been shown consistently to improve functional capacity for patients with severe COPD. These programs typically have a duration of several months and are generally not an option in resections for malignancy.
INTERSTITIAL LUNG DISEASE
Interstitial lung disease (ILD) is a chronic restrictive pulmonary disease (i.e., FEV 1 <70% predicted, FEV 1 /FVC ratio normal or increased, and RV decreased). Approximately 35% of ILD cases are attributable to an identifiable cause, such as exposure to inorganic dust, organic antigens, drugs, or radiation. The inciting agent in the remaining 65% of patients is unknown. In many of these patients, the lung is part of an autoimmune disorder.
Elastic recoil of the lungs increases as a consequence of inflammation and fibrosis of the alveolar walls, which results in decreased lung volumes. Early in the disease, patients adapt to smaller tidal volumes by increasing their respiratory rate. As the disease progresses, increased respiratory effort and energy are required to maintain sufficient tidal volumes to prevent alveolar hypoventilation. Uneven disease distribution throughout the lung can cause significant ventilation/perfusion mismatch and is the primary cause of hypoxemia in patients with ILD.
Controlled ventilation via an endotracheal tube is often the most reliable and safest approach to optimizing oxygenation and ventilation in patients with ILD when a general anesthetic is required. The goal of mechanical ventilation in patients with ILD is to maintain adequate ventilation and oxygenation while minimizing the risks of barotrauma and acute lung injury. Potential strategies to minimize airway pressures include the use of long durations of inspiration compared with the duration of expiration ratios (e.g., ratios of 1:1 to 1:1.5), small tidal volumes, and rapid respiratory rates. In contrast to obstructive lung disease PEEP can be used safely in ILD.
CYSTIC FIBROSIS
Cystic fibrosis is an autosomal recessive disorder that results in impaired transport of sodium, chloride, and water across epithelial tissue. This leads to exocrine gland malfunction with abnormally viscous secretions, which can cause obstruction of the respiratory tracts, pancreas, biliary system, intestines, and sweat glands. It presents as a mixed obstructive and restrictive lung disease. Inability to clear the thick purulent secretions enhances bacterial growth and leads to bronchiectasis as the disease advances.
The early mortality of cystic fibrosis is primarily the result of pulmonary complications, including air-trapping, pneumothorax, massive hemoptysis, and respiratory failure. Effective sputum elimination is a key goal in the long-term management of cystic fibrosis. To optimize patients with cystic fibrosis for anesthesia, chest physiotherapy should be performed immediately before surgery. Endotracheal intubation with a large endotracheal tube is preferred, as it facilitates endobronchial toileting with a suction catheter, bronchoscopy, or both.
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