Anesthetic considerations for obstructive lung disease

Signs and symptoms

Most common symptoms of acute URI include nonproductive cough, sneezing, and rhinorrhea. A history of seasonal allergies may indicate an allergic cause of these symptoms rather than an infectious cause. Symptoms caused by bacterial infections will usually present with more serious signs and symptoms such as fever, purulent nasal discharge, productive cough, and malaise. Such patients may be febrile, tachypneic, wheezing, or have a toxic appearance.

Diagnosis

Diagnosis is usually based on clinical signs and symptoms. Viral cultures and laboratory tests lack sensitivity, are time and cost consuming, and are therefore impractical in a busy clinical setting.

Management of anesthesia

Most studies regarding the effects of URI on postoperative pulmonary complications have involved pediatric patients. It is well known that children with a URI are at much higher risk of perioperative respiratory adverse events (PRAE) such as transient hypoxemia and laryngospasm, breath holding, and cough if they are anesthetized while suffering a URI. However, there are limited data about the adult population in this regard. There is evidence to show an increased incidence of respiratory complications in pediatric patients with a history of copious secretions, prematurity, parental smoking, nasal congestion, reactive airway disease, endotracheal intubation, and in those undergoing airway surgeries. Those with clear systemic signs of infection such as fever, purulent rhinitis, productive cough, and rhonchi who are undergoing elective surgery (particularly airway surgery) are at considerable risk of PRAE. Other risk factors that increase incidence of PRAE are airway surgery, secondhand smoke exposure, history of prematurity, and endotracheal intubation. Consultation with the surgeon regarding the urgency of the surgery is necessary. A patient who has had a URI for days or weeks and is in stable or improving condition can be safely managed without postponing surgery. If surgery is to be delayed, patients should not be rescheduled for about 6 weeks because some studies indicate that airway hyperreactivity may persist for that duration. The economic and practical aspects of canceling surgery should also be taken into consideration before a decision is made to postpone surgery. A scoring system for risk stratification of these patients has been proposed. The COLDS scoring system includes current signs and symptoms (higher risk with severe symptoms), onset of symptoms (higher risk <2 weeks ago), presence of lung diseases (higher risk with moderate or severe disease), airway device (higher risk with endotracheal tube [ETT]), and surgery (higher risk with major airway surgery). Initial studies demonstrate its utility in predicting PRAE and possibly as a decision aid in proceeding with surgery in a patient with URI.

Viral infections, particularly during the infectious phase, can cause morphologic and functional changes in the respiratory epithelium. The relationship between epithelial damage, viral infection, airway reactivity, and anesthesia remains unclear. Tracheal mucociliary flow and pulmonary bactericidal activity can be decreased by general anesthesia. It is possible that positive pressure ventilation could help spread infection from the upper to the lower respiratory tract. The immune response of the body is altered by surgery and anesthesia. A reduction in B-lymphocyte numbers, T-lymphocyte responsiveness, and antibody production may be associated with anesthesia, but the clinical significance of this remains to be elucidated.

The anesthetic management of a patient with URI should include adequate hydration, reducing secretions, and limiting manipulation of a potentially sensitive airway. Nebulized or topical local anesthetic applied to the vocal cords may reduce upper airway sensitivity. Use of a laryngeal mask airway (LMA) rather than an ETT may also reduce the risk of laryngospasm. URIs may increase the risk of PRAE during procedural sedation with an increased need for airway interventions in these patients. Considerations for induction and maintenance are similar to those for patients with asthma in this population of patients. When there are no contraindications, deep extubation may result in smoother emergence.

Adverse respiratory events in patients with URIs include bronchospasm, laryngospasm, airway obstruction, postintubation croup, desaturation, and atelectasis. Intraoperative and immediate postoperative hypoxemia are common and amenable to treatment with supplemental oxygen. Long-term complications have not been demonstrated.

Signs and symptoms

Asthma is an episodic disease with acute exacerbations interspersed with symptom-free periods. Clinical manifestations of asthma include expiratory wheezing, productive or nonproductive cough, dyspnea, chest discomfort or tightness that may lead to air hunger, and eosinophilia. Most attacks are short lived, lasting minutes to hours, and clinically the person recovers completely after an attack. However, there can be a phase in which a patient experiences some degree of airway obstruction daily. This phase can be mild, with or without superimposed severe episodes, or much more serious, with significant obstruction persisting for days or weeks. Status asthmaticus is defined as life-threatening bronchospasm that persists despite treatment. When the history is elicited from someone with asthma, attention should be paid to factors such as previous intubation or admission to the intensive care unit (ICU), two or more hospitalizations for asthma in the past year, and the presence of significant coexisting diseases.

Diagnosis

The diagnosis of asthma depends on clinical history, symptoms, signs, and objective measurements of airway obstruction. Asthma is diagnosed when a patient reports symptoms such as wheezing, chest tightness, or shortness of breath and demonstrates airflow obstruction on pulmonary function testing that is at least partially reversible with bronchodilators. Classification of asthma severity depends on the clinical symptoms, pulmonary function test, and medication usage ( Tables 2.2 and 2.3 ).

TABLE 2.3

Classification of Asthma Severity in Youths Older Than 12 Years and in Adults

From National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma (EPR3). Bethesda, MD: National Heart, Lung, and Blood Institute; 2007.

Pulmonary function testing

Forced expiratory volume in 1 second (FEV ₁ ), forced expiratory flow (FEF), midexpiratory phase flow (FEF _25%–75% [also called maximum midexpiratory flow rate]), and peak expiratory flow rate (PEFR) are direct measures of the severity of expiratory airflow obstruction ( Fig. 2.1 ). These measurements provide objective data that can be used to assess the severity and monitor the course of an exacerbation of asthma. The typical asthmatic patient who comes to the hospital for treatment has an FEV ₁ that is less than 35% of normal. Flow-volume loops show characteristic downward scooping of the expiratory limb of the loop. Flow-volume loops in which the inhaled or exhaled portion of the loop is flat help distinguish wheezing caused by airway obstruction (i.e., due to a foreign body, tracheal stenosis, or mediastinal tumor) from asthma ( Figs. 2.2 and 2.3 ). During moderate or severe asthmatic attacks, the functional residual capacity (FRC) may increase substantially, but total lung capacity (TLC) usually remains within the normal range. Diffusing capacity for carbon monoxide is not changed. Bronchodilator responsiveness provides supporting evidence if asthma is suspected on clinical grounds. In patients with expiratory airflow obstruction, an increase in airflow after inhalation of a bronchodilator suggests asthma. Abnormalities in pulmonary function test (PFT) results may persist for several days after an acute asthmatic attack despite the absence of symptoms. Since asthma is an episodic illness, its diagnosis may be suspected even if PFT results are normal.

Arterial blood gas analysis

Mild asthma is usually accompanied by a normal Pao ₂ and Paco ₂ . Tachypnea and hyperventilation observed during an acute asthmatic attack do not reflect arterial hypoxemia but rather neural reflexes in the lungs. Hypocarbia and respiratory alkalosis are the most common arterial blood gas findings in the presence of asthma. As the severity of expiratory airflow obstruction increases, the associated ventilation/perfusion mismatching may result in a Pao ₂ of less than 60 mm Hg while breathing room air. The Paco ₂ is likely to increase when the FEV ₁ is less than 25% of the predicted value. Fatigue of the skeletal muscles necessary for breathing may contribute to the development of hypercarbia.

Chest radiography and electrocardiography

A chest radiograph in a patient with mild or moderate asthma even during an asthma exacerbation is often normal. Patients with severe asthma may demonstrate hyperinflation and hilar vascular congestion due to mucous plugging and pulmonary hypertension. Chest x-rays can be helpful in determining the cause of an asthma exacerbation and in ruling out other causes of wheezing. The electrocardiogram (ECG) may show evidence of right ventricular strain or ventricular irritability during an asthmatic attack.

The differential diagnosis of asthma includes viral tracheobronchitis, sarcoidosis, rheumatoid arthritis with bronchiolitis, extrinsic compression (thoracic aneurysm, mediastinal neoplasm) or intrinsic compression (epiglottitis, croup) of the upper airway, vocal cord dysfunction, tracheal stenosis, chronic bronchitis, COPD, and foreign body aspiration. Upper airway obstruction produces a characteristic flow-volume loop (see Fig. 2.3 A). A history of recent trauma, surgery, or tracheal intubation may be present in patients with upper airway obstruction mimicking asthma. Congestive heart failure and pulmonary embolism may also cause dyspnea and wheezing.

Treatment

Aim of asthma treatment lies in controlling symptoms and reducing exacerbations. Short-acting inhaled β ₂ agonist (i.e., albuterol) is usually first-line treatment in patients with mild asthma. However, this is only recommended in patients with less than twice-a-month symptoms and who have no risk factors for exacerbations. Following short-acting β ₂ agonist, daily inhaled corticosteroids have been shown to improve symptoms, reduce exacerbations, and decrease risk of hospitalization. If symptoms remain uncontrolled, daily inhaled β ₂ agonist can be added to inhaled corticosteroids. Neither drug should be used in times of acute exacerbation. Other supplemental therapies include inhaled long-acting muscarinic antagonists, leukotriene modifiers, and mast cell stabilizers. Omalizumab, the first antiimmunoglobulin E (anti-IgE) monoclonal antibody approved for moderate to severe allergic asthma, has also been shown to reduce exacerbations and hospitalizations in adults and children. In patients with severe eosinophilic asthma, anti-interleukin-5 (anti-IL5) and anti-IL5 receptor medication can be used. Systemic corticosteroids are usually reserved for patients with severe asthma, uncontrolled with inhalational medication. Systematic reviews on the topic indicate that subcutaneous immunotherapy decreases use of long-term medications and may improve quality of life and subjective symptoms. A full list of pharmacologic therapy can be found in Tables 2.4 and 2.5 .

Bronchial thermoplasty (BT) is a recently approved and only nonpharmacologic treatment used for refractory severe asthma. BT uses bronchoscopy guidance to deliver radiofrequency ablation of airway smooth muscles to all lung fields except the right middle lobe. The procedure is performed in three sessions and uses intense heat, which carries a risk of airway fire. Loss of airway smooth muscle mass is thought to lessen rates of bronchoconstriction. Serial determination of PFTs can be useful for monitoring the response to treatment. When the FEV ₁ improves to about 50% of normal, patients usually have minimal or no symptoms.

Acute severe asthma

Acute severe asthma, previously called status asthmaticus, is defined as bronchospasm that does not resolve despite usual treatment and is considered life threatening. Emergency treatment consists of high-dose, short-acting β ₂ agonists and systemic corticosteroids. β ₂ agonists inhaled via a metered-dose inhaler (MDI) can be administered every 15 to 20 minutes for several doses without significant adverse hemodynamic effects, although patients may experience unpleasant sensations resulting from adrenergic overstimulation. Continuous administration of β ₂ agonists by nebulizer may be more effective for delivery of these drugs to relieve airway spasm. Intravenous (IV) corticosteroids are administered early in treatment because it takes several hours for their effect to appear. The corticosteroids most commonly used are hydrocortisone and methylprednisolone (e.g., 80 mg IV q8h). Supplemental oxygen is administered to help maintain arterial oxygen saturation above 90%. If respiratory failure occurs, mechanical ventilation should be initiated. Other drugs used in more intractable cases include magnesium and oral leukotriene inhibitors. The National Asthma Education and Prevention Program Expert Panel always has the most recent evidence-based guidelines for treatment of asthma on its website ( http://www.nhlbi.nih.gov/about/org/naepp/ ).

Measurements of lung function can be very helpful in assessing the severity of disease and the response to treatment. Patients whose FEV ₁ or PEFR is decreased to 25% of normal or less are at risk of developing hypercarbia and respiratory failure. The presence of hypercarbia (defined as a Paco ₂ >50 mm Hg) despite aggressive antiinflammatory and bronchodilator therapy is a sign of respiratory fatigue that requires tracheal intubation and mechanical ventilation. The pattern of mechanical ventilation can be particularly important in the patient with acute severe asthma. The expiratory phase must be prolonged to allow for complete exhalation and to prevent self-generated or intrinsic positive end-expiratory pressure (auto-PEEP). To prevent barotrauma, some recommend a degree of permissive hypercarbia. When the FEV ₁ or PEFR improves to 50% of normal or higher, patients usually have minimal or no symptoms; at this point, the frequency and intensity of bronchodilator therapy can be decreased, and weaning from mechanical ventilation can ensue.

When asthma exacerbation is resistant to therapy, it is likely that the expiratory airflow obstruction is caused predominantly by airway edema and intraluminal secretions. Indeed, some patients may be at risk of asphyxia due to mucous plugging of the airways. In rare circumstances when life-threatening hypoxia persists despite aggressive pharmacologic therapy, it may be necessary to consider general anesthesia to produce bronchodilation. Isoflurane and sevoflurane are effective bronchodilators in this situation. Treatment of severe acute asthma is summarized in Table 2.6 .

Management of anesthesia

The occurrence of severe bronchospasm has been reported in 0.2% to 4.2% of all procedures involving general anesthesia performed in asthmatic patients. Factors that are more likely to predict the occurrence of severe bronchospasm include the type of surgery (risk is higher with upper abdominal surgery and oncologic surgery) and the proximity of the most recent asthmatic attack to the date of surgery.

Several mechanisms could explain the contribution of general anesthesia to increased airway resistance. Among these are depression of the cough reflex, impairment of mucociliary function, reduction of palatopharyngeal muscle tone, depression of diaphragmatic function, and an increase in the amount of fluid in the airway wall. In addition, airway stimulation by endotracheal intubation, parasympathetic nervous system activation, and/or release of neurotransmitters of pain such as substance P and neurokinins may also play a role.

Preoperative evaluation of patients with asthma requires an assessment of disease severity, the effectiveness of current pharmacologic management, and the potential need for additional therapy before surgery. The goal of preoperative evaluation is to formulate an anesthetic plan that prevents or blunts expiratory airflow obstruction.

Preoperative evaluation begins with a history to elicit the severity and characteristics of the patient’s asthma ( Table 2.7 ). History of symptom control, frequency of exacerbation, need for hospitalization and endotracheal intubation, and previous tolerance of anesthesia and surgery should be noted. A list of asthma medications may also provide insight into asthma severity and control. On physical examination the general appearance of the patient and any use of accessory muscles of respiration should be noted. Auscultation of the chest to detect wheezing or crepitations is important. Blood eosinophil counts often parallel the degree of airway inflammation, and airway hyperreactivity provides an indirect assessment of the current status of the disease. PFTs (especially FEV ₁ ) performed before and after bronchodilator therapy may be indicated in patients scheduled for major surgery. A reduction in FEV ₁ or forced vital capacity (FVC) to less than 70% of predicted, as well as an FEV ₁ :FVC ratio that is less than 65% of predicted, is usually considered a risk factor for perioperative respiratory complications.

Chest physiotherapy, antibiotic therapy, and bronchodilator therapy during the preoperative period can often improve reversible components of asthma. Measurement of arterial blood gases is indicated if there is any question about the adequacy of ventilation or oxygenation.

Antiinflammatory and bronchodilator therapy should be continued until the time of anesthesia induction. If the patient is currently on or has been treated with high doses of systemic corticosteroids within the past 6 months, supplementation with stress-dose hydrocortisone or methylprednisolone may be indicated. However, hypothalamic-pituitary-adrenal suppression is very unlikely if only inhaled corticosteroids are used for asthma treatment. In selected patients a preoperative course of oral corticosteroids may be useful to improve overall lung function. Patients should be free of wheezing and have a PEFR of either greater than 80% of predicted or at the patient’s personal best value before surgery.

During induction and maintenance of anesthesia in asthmatic patients, airway reflexes must be suppressed to avoid bronchoconstriction in response to mechanical stimulation of these hyperreactive airways. Stimuli that do not ordinarily evoke airway responses can precipitate life-threatening bronchoconstriction in patients with asthma.

Because it avoids instrumentation of the airway and tracheal intubation, regional anesthesia is an attractive option when the operative site is suitable. Concerns that high sensory levels of anesthesia will lead to sympathetic blockade and consequent bronchospasm are unfounded.

When general anesthesia is selected, induction of anesthesia is most often accomplished with an IV induction drug. Propofol is often used for induction in a hemodynamically stable asthmatic patient. It produces smooth muscle relaxation and contributes to decreased airway resistance. Ketamine is a preferred induction drug in a hemodynamically unstable patient with asthma.

After general anesthesia is induced, the lungs are often ventilated for a time with a gas mixture containing a volatile anesthetic. The goal is to establish a depth of anesthesia that depresses hyperreactive airway reflexes sufficiently to permit tracheal intubation without precipitating bronchospasm. Sevoflurane is the preferred inhalational anesthetic agent as it produces more profound bronchodilation compared to isoflurane and desflurane. An alternative method to suppress airway reflexes before intubation is IV or intratracheal injection of lidocaine (1–1.5 mg/kg) several minutes before endotracheal intubation.

Opioids should also be administered to suppress the cough reflex and to achieve deep anesthesia. However, prolongation of opioid effects can cause postoperative respiratory depression. Remifentanil may be particularly useful because it is an ultrashort-acting opioid and does not accumulate. Most opioids have some histamine-releasing effects, but fentanyl and analogous drugs can be used safely in asthmatic patients. Administration of opioids prior to intubation can help prevent increased airway resistance, but muscle rigidity caused by an opioid could decrease lung compliance and impair ventilation. Opioid-induced muscle rigidity can be decreased by the combined use of IV anesthetics and neuromuscular blocking drugs.

Insertion of an LMA is less likely to result in bronchoconstriction than insertion of an ETT. Therefore use of an LMA is often a better method of airway management in asthmatic patients who are not at increased risk of reflux or aspiration. Supraglottic airway devices can be especially useful during airway-sharing procedures in severe asthmatics such as BT. Here, LMA combined with controlled ventilation and low Fio ₂ to minimize airway fire from intense procedural heat may confer a significantly better safety profile. During maintenance of general anesthesia, it may be difficult to differentiate light anesthesia from bronchospasm as the cause of a decrease in pulmonary compliance. Administration of a neuromuscular blocker will relieve the ventilatory difficulty resulting from light anesthesia but has no effect on bronchospasm.

Intraoperatively the desired level of arterial oxygenation and carbon dioxide removal is typically provided via mechanical ventilation. In asthmatic patients, sufficient time must be provided for exhalation to prevent air trapping. Humidification and warming of inspired gases may be especially useful in patients with exercise-induced asthma in whom bronchospasm may be due to transmucosal loss of heat. Adequate administration of fluids during the perioperative period is important for maintaining adequate hydration and ensuring that airway secretions are less viscous and can be removed easily. Skeletal muscle relaxation is usually provided with nondepolarizing muscle relaxants. Neuromuscular blockers with limited ability to evoke the release of histamine should be selected.

Theoretically, antagonism of neuromuscular blockade with anticholinesterase drugs could precipitate bronchospasm due to stimulation of postganglionic cholinergic receptors in airway smooth muscle. However, such bronchospasm does not predictably occur due to the protective bronchodilation effects provided by the simultaneous administration of anticholinergic drugs. The newest neuromuscular blockage reversal agent, sugammadex, does not possess any muscarinic properties and may be used as an alternative to anticholinesterase drug reversal. However, bronchospasm has been reported in 2.6% of patients in this population as well.

At the conclusion of surgery it may be prudent to remove the ETT while anesthesia is still sufficient to suppress hyperreactive airway reflexes, a technique referred to as deep extubation . When it is deemed unwise to extubate the trachea before the patient is fully awake, suppressing airway reflexes and/or the risk of bronchospasm by administration of IV lidocaine or treatment with inhaled bronchodilators should be considered.

During surgery, bronchospasm may be due to light anesthesia rather than asthma itself ( Table 2.8 ). Signs may include high peak airway pressure, upsloping of the end-tidal carbon dioxide (ETCO ₂ ) waveform, wheezing, and desaturation. Treatment of intraoperative bronchospasm and wheezing will depend on its cause. Deepening anesthesia with either volatile agents or IV injections of propofol and administration of a rapid-acting β ₂ agonist such as albuterol via the ETT are common first steps. Because the vast majority of albuterol delivered into an ETT by MDI does not reach the patient, other methods of delivery should be considered. These include increasing the number of puffs and delivery via nebulizer attached to the circuit. If bronchospasm continues despite these initial therapies, other drugs (e.g., IV corticosteroids, epinephrine, magnesium) may be necessary.

Emergency surgery in the asthmatic patient introduces a conflict between protection of the airway in someone at risk of aspiration and the possibility of triggering significant bronchospasm. In addition, there may not be sufficient time to optimize bronchodilator therapy prior to surgery. Regional anesthesia may be a good option in this situation if the site of surgery is suitable.

Signs and symptoms

Signs and symptoms of COPD vary with disease severity but usually include dyspnea at rest or on exertion, chronic cough, and chronic sputum production. COPD exacerbations are periods of worsening symptoms as a result of an acute worsening in airflow obstruction. As expiratory airflow obstruction increases in severity, tachypnea and a prolonged expiratory time are evident. Breath sounds are likely to be decreased, and expiratory wheezes are common. As the disease progresses, patients get exacerbations more frequently, and these are often triggered by respiratory infections with a bacterial component.

Diagnosis

Providers should have a high degree of suspicion and low threshold to test for COPD in patients with symptoms such as dyspnea and chronic cough and/or lifestyle and environmental exposures, which places them at risk (Singh et al, 2019). Definitive diagnosis of COPD is made with spirometry.

Pulmonary function tests

Results of PFTs in COPD reveal a decrease in the FEV ₁ :FVC ratio and an even greater decrease in the FEF between 25% and 75% of vital capacity (FEF _25%–75% ). An FEV ₁ :FVC less than 70% of predicted, an increased FRC and TLC, as well as reduced diffusing capacity for carbon monoxide (DLCO) are usually seen in these patients ( Fig. 2.4 ). Slowing of expiratory airflow and gas trapping behind prematurely closed airways are responsible for the increase in residual volume (RV). The pathophysiologic advantage of an increased RV and FRC in patients with COPD is related to an enlarged airway diameter and increased elastic recoil for exhalation. The cost is the greater work of breathing at the higher lung volumes.

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) works with healthcare professionals and public health officials around the world to raise awareness of COPD and improve treatment. GOLD was launched in 1997 in collaboration with the National Heart, Lung, and Blood Institute of the US National Institutes of Health and the World Health Organization. GOLD developed a classification/severity grading system that is now widely used by physicians around the world ( Table 2.9 ).

Chest radiography

Radiographic abnormalities may be minimal even in the presence of severe COPD. Hyperlucency due to arterial vascular deficiency in the lung periphery and hyperinflation (flattening of the diaphragm with loss of its normal domed appearance and a very vertical cardiac silhouette) suggest the diagnosis of emphysema. If bullae are present, the diagnosis of emphysema is certain. However, only a small percentage of patients with emphysema have bullae.

Computed tomography

Computed tomography (CT) is much more sensitive at diagnosing COPD than chest radiograph. Airspace enlargement and alveolar destruction accompanied by loss of bone, muscle, and fat tissue are suggestive of the multiorgan loss of tissue (MOLT) phenotype, which is associated with higher rates of lung cancer, while bronchiolar narrowing and wall thickening indicate the bronchitic phenotype that is usually accompanied by metabolic syndrome and high rates of cardiac disease. CT also has the ability to reveal other disease states such as pulmonary fibrosis and coronary artery disease, which may affect COPD treatment. Although CT scan is not routinely used for COPD diagnosis, the plethora of information it can gather has prompted some to advocate its use in all patients with COPD.