Chronic Bronchitis

Description

Chronic bronchitis is one of the two types of chronic obstructive pulmonary disease (COPD), the other being emphysema.
Defined as a productive cough > 3 months for two consecutive years.
- Additionally, it is characterized by irreversible airway obstruction, chronic airway irritation, hypersecretion of mucus, and bronchial inflammation.
- Diagnosis and treatment are guided by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) (1).
- Varying degrees of emphysematous disease are commonly present.
Postoperatively, patients with chronic bronchitis have an increased risk of bronchospasm, laryngospasm, atelectasis, wheezing, difficulty clearing mucous, and prolonged intubation. Additionally, preoperative pulmonary function tests (PFTs) do not reliably predict postoperative outcome.
In the ambulatory surgery setting, home discharge may be challenging and patients should be carefully selected and screened.

Epidemiology

Prevalence

In the US: 10–12 million
Women are twice as likely as men to have chronic bronchitis (2).
Highest prevalence in those >65 years of age

Morbidity

Treatment costs: $11.7 billion annually
Hospitalizations costs: $6 billion annually

Mortality

4^th leading cause of death in the US (2).
There is an increased risk of death within 5 years, following an episode of respiratory failure.
Overall mortality is associated with pack-year smoking history (average number of packs of cigarettes per day multiplied by total number of years smoking).

Etiology/Risk Factors

Smoking
Exacerbations can result from respiratory tract infections.

Physiology/Pathophysiology

Cough and chronic mucus production result from immune responses to inhaled toxic particles and gases in cigarette smoke. Inflammation in the epithelium of the central airways and mucous-producing glands result in increased mucous production, reduced mucociliary clearance, and increased permeability of the airspace epithelial barrier (3).
- Inflammatory cells release serine proteases that are potent secretagogues for mucous.
- Oxidant release from cigarette smoke induces the MUC5AC gene, causing overproduction of mucin.
During the early stages of COPD, it is unclear what the effects of mucus hypersecretion are. However, in the later stages of the disease, changes become apparent:
- Decreases in forced expiratory flow rates due to obstruction.
- Increases in residual volume (RV). Air trapping results in progressive hyperinflation with a resultant increase in total lung capacity (TLC) and flattening of diaphragms.
- Increases in the residual volume to total lung capacity ratio (RV:TLC).
Airway reactivity may be the result of smoking-induced inflammation or the airway narrowing that occurs with chronic disease (4).
Nonuniform distribution of ventilation causes ventilation/perfusion mismatch and an increase in dead space, leading to carbon dioxide (CO₂) retention. Some areas of the lung are underventilated in relation to perfusion because of airway obstruction. Air is forced from these areas to other parts of the lung, causing overventilation relative to perfusion.
Compensatory mechanisms
- Compensatory responses of the lungs changes their mechanical behavior. It decreases the tendency for alveoli to collapse and makes atelectasis less likely.
- Erythrocytosis, accompanied by an increase in blood viscosity, results from chronic hypoxemia.
- Chronic bronchitis "blue bloaters" have hypercarbia with resultant respiratory acidosis, which is metabolically compensated.
Cor pulmonale. Chronic alveolar hypoxemia causes pulmonary hypertension that becomes fixed over time due to changes in the pulmonary arterial vessels. High pressure in the pulmonary circulation causes right ventricular hypertrophy. Chronic findings can include right bundle branch block, right heart strain, and right heart failure.

Anesthetic GOALS/GUIDING Principles

Assess severity of disease
Optimize pulmonary function
Continue maintenance medications
Treat acute exacerbation
Avoid perioperative bronchospasm

Symptoms

Productive cough
Shortness of breath (SOB)

History

Age of onset
Current smoking status
Quality of current cough/mucus
Treatment history
- Frequency of exacerbations
- Bronchodilator use
- Steroid use
- ER visits
- Hospitalizations
- Intensive care unit (ICU) admissions
- Intubations

Signs/Physical Exam

Wheezing
Tachypnea
Prolonged expiration
JVD
"Blue bloaters"
Low baseline room air O₂ saturation with worsening on exertion.

Treatment History

Supplemental O₂ is indicated when baseline O₂ saturation is <88% or <90% when there are signs of pulmonary hypertension or right heart failure. It is used to maintain PaO₂ between 60 and 80 mm Hg and is the only current treatment that reduces mortality.

Medications

Corticosteroids
- Inhalational route has minimal systemic effects and scheduled dosing has been shown to decrease exacerbations.
- Oral route causes more side effects with little improvement in benefit; may be prescribed to treat an acute exacerbation or prophylactically in patients with severe disease prior to a surgical procedure.
Bronchodilators reduce exacerbations and improve symptoms.
- Anticholinergics (ipratropium bromide)
- Beta-adrenergic agonists (salmeterol, albuterol)
Theophylline is a methylxanthine used to improve ventilation by relaxing bronchial smooth muscle. It is a phosphodiesterase inhibitor and adenosine receptor antagonist. Because of the narrow therapeutic window and adverse cardiac effects, it is used infrequently. High levels can cause tachycardia, arrhythmias, hypotension, and CNS excitation.
Antibiotics are useful in treating acute exacerbations triggered by infection; scheduled, prophylactic antibiotics have not shown benefit.
Bupropion or nicotine replacement
Diuretics for cor pulmonale

Diagnostic Tests & Interpretation

Labs/Studies

Baseline room air O₂ saturation
EKG may show right axis deviation as a result of right ventricular hypertrophy.
Chest x-ray (CXR) should be performed if infection is suspected. May show hyperinflation, bullae, blebs, and increased pulmonary vascular markings.
ABGs (often PaCO₂ >45 mm Hg and PaO₂ <65 mm Hg)
Sputum sample (neutrophils, bacteria)
Pulmonary function (FEV₁/FVC <0.7 and not reversible with bronchodilator)

CONCOMITANT ORGAN DYSFUNCTION

Cor pulmonale
Emphysema

Circumstances to delay/Conditions

Acute exacerbation as demonstrated by dyspnea, increased O₂ requirement, increased mucous production, fatigue or lethargy, or a PaCO₂ increased from baseline (or an acute respiratory acidosis where metabolic compensation has not yet occurred).
Pneumonia or upper respiratory infection
Pulmonary edema

Classifications

Based on spirometric measurements. Diagnosis requires an FEV₁/FVC ratio <0.7. Severity is gauged by the postbronchodilator FEV₁ (1):

Mild: FEV₁80% predicted
Moderate: FEV₁ 50–80% predicted
Severe: FEV₁ 30–50% predicted
Very severe: <30% predicted

PREOPERATIVE PREPARATION

Premedications

Antibiotics if sputum quality or quantity suggests infection.
Bronchodilator use for symptom improvement should be continued perioperatively via puffs or nebulizer.
Inhaled corticosteroids should be continued.
Smoking cessation for any length of time is beneficial, but optimally should be initiated 8 weeks before surgery. Abrupt discontinuation may actually increase mucus production.
Anxiolytics are appropriate if care is taken to avoid hypoventilation and CO₂ retention. These patients are more sensitive to the respiratory depressant effects of sedatives and opioids.

INTRAOPERATIVE CARE

Choice of Anesthesia

Consider regional techniques to avoid airway instrumentation, mechanical ventilation, and systemic opioid administration.
A combination of regional and general anesthesia may assist with early ambulation, decrease in opioid use, and return of respiratory function.

Monitors

Standard ASA monitors.
Arterial line placement for frequent ABG draws may be considered. A large gradient may exist between the arterial and end-tidal CO₂ due to an increase in dead space. PaO₂ measurements may aid with ventilator settings.

Induction/Airway Management

A slow and controlled induction should be performed to allow for attainment of an adequate depth of anesthesia and onset of muscle relaxation prior to airway instrumentation.
Agents
- Propofol does not bronchodilate the airways but blunts the laryngeal response.
- Ketamine can provide bronchodilation; however, its side effect of increasing secretions is often undesirable.
- Volatile agents may be introduced after IV induction to bronchodilate the airways. Alternatively, mask induction may be chosen.
- Lidocaine 1–1.5 mg/kg IV or 4% sprayed topically prior to intubation may reduce intraoperative or postoperative coughing.
Avoid hyperventilation while bag masking if the patient is a CO₂ retainer.

Maintenance

The patient should be adequately anesthetized to avoid laryngospasm and bronchospasm.
Nitrous oxide can increase pulmonary artery pressures and is often avoided.
Ventilation
- Maximize oxygenation to avoid increases in pulmonary hypertension.
- Correct severe hypercapnia without hyperventilating (can result in respiratory alkalosis due to chronic increase).
- PEEP may prevent airway closure and improve lung compliance.
- I:E ratio should allow sufficient time for expiration and avoid auto-PEEP.
Mucus can be softened with adequate IV fluid maintenance and warm, humidified inspiratory gases.

Extubation/Emergence

Suction the endotracheal tube prior to extubation.
Consider deep extubation when appropriate.
The use of IV lidocaine prior to extubation may help to suppress airway reflexes.

Bed Acuity

Vigilance for bronchospasm
Supplemental O₂ (nasal cannula, face mask) without suppressing hypercarbic drive
Thoracic and upper abdominal surgeries are associated with atelectasis, hypoxemia, and slow return to baseline respiratory function. FRC may not return to baseline following these procedures until 2 weeks postoperatively.
Pulmonary care
- Chest physiotherapy
- Incentive spirometry
- CPAP

Complications

Acute respiratory failure
Atelectasis
Bronchospasm
Pneumonia

Rabe KF , Hurd S , Anzueto A , et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. Am J Respir Crit Care Med. 2007;176:532–555.
American Lung Association Epidemiology and Statistics Unit Research and Program Services Division . Trends in COPD (Chronic Bronchitis and Emphysema): Morbidity and Mortality. February 2010.
MacNee W. Pathogenesis of chronic obstructive pulmonary disease. Proc Am Thorac Soc. 2005;2(4):258–266.
Warner DO , Warner MA , Offord KP , et al. Airway obstruction and perioperative complications in smokers undergoing abdominal surgery. Anesthesiology. 1999;90(2):372–379.

Blanchette CM , Roberts MH , Peterson H , et al. Economic burden of chronic bronchitis in the United States: A retrospective case-control study. Int J Chron Obstruct Pulmon Dis. 2011;6:73–81.
www.aafp.org Management of Chronic Bronchitis

See Also (Topic, Algorithm, Electronic Media Element)

Cor Pulmonale
Pulmonary Function Tests
Cigarette Smoking
Pulmonary Hypertension
Postoperative Pulmonary Complications

ICD9

491.9 Unspecified chronic bronchitis
496 Chronic airway obstruction, not elsewhere classified

ICD10

J42 Unspecified chronic bronchitis
J44.9 Chronic obstructive pulmonary disease, unspecified

Assess the severity of disease in order to plan appropriate preoperative medications and intraoperative technique, as well as postoperative extubation, level of acuity, and pulmonary rehabilitation.
Evaluate for respiratory tract infections by noting fever, mucus quality or quantity greater than normal, and increase in SOB.
Baseline O₂ saturation and review of home O₂ dependence aid in PACU management and discharge plan.

Jennifer Wu , MD, MBA

section name header

Basics ⬇

Prevalence

Morbidity

Mortality

Diagnosis ⬆ ⬇

History

Signs/Physical Exam

Labs/Studies

Treatment ⬆ ⬇

Premedications

Choice of Anesthesia

Monitors

Induction/Airway Management

Maintenance

Extubation/Emergence

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆