Pulmonology
Marvin I. Schwarz
Acute Respiratory Distress Syndrome
What is the definition of acute respiratory distress syndrome (ARDS)?
What are the principles of management of the patient with ARDS?
Discussion
What is the definition of ARDS?
Many acute medical conditions such as congestive heart failure, pneumonia, or the acute noninfectious interstitial pneumonias can mimic the clinical
picture of ARDS. A useful definition includes the following: relatively acute appearance of diffuse pulmonary infiltrates, profound hypoxemia (usually requiring mechanical ventilation), pulmonary compliance less than 20 mL/cm H2O (stiff lungs), and a pulmonary capillary wedge pressure less than 18 mm Hg (noncardiogenic edema). Causes include bacterial, viral, and protozoan pneumonias, all forms of shock, aspiration, high-altitude and neurogenic pulmonary edema, transfusion-related acute lung injury (TRALI) which is often postsurgical, trauma, and burns. The underlying histologic appearance is diffuse alveolar damage. This consists of two phases: the early exudative phase demonstrating alveolar edema and intraalveolar fibrin collective known as hyaline membranes and the fibroproliferative phase consisting of fibroblastic proliferative and collagen deposition.
What are the principles of management in the patient with ARDS?
There are few specific medical therapies for ARDS other than the treatment of the underlying cause. Trials of biologic modifiers have been generally disappointing, except in severe sepsis in which human recombinant activated protein C (activated drotrecogin α) reduces mortality rates. Management is mainly supportive and treating the underlying initiating cause in the hope that the lung can return to normal. The specific goals of therapy are to maintain tissue oxygenation (maximize oxygen delivery) while preventing complications resulting from mechanical ventilation, such as barotrauma (pneumothorax), and lung injury stemming from high airway pressures or oxygen toxicity. A recent National Institutes of Health (NIH)-supported study of mechanically ventilated ARDS subjects indicated a lower mortality for those ventilated with tidal volumes of 6 mL/kg versus the standard 12 mL/kg. There is evidence to support that higher respiratory pressures aggravate the lung injury.
Case
A 27-year-old white male motorcyclist is transported to the emergency room after he was involved in a high-speed, head-on collision with an oncoming automobile. At the accident scene, he was poorly responsive; his initial blood pressure was 70/40 mm Hg and injuries included a flail chest on the right, several pelvic fractures, an open fracture of the femur, and a closed, displaced fracture of the left tibia. A central and two peripheral catheters are inserted, and normal saline is administered at maximal rates. His blood is typed and crossmatched. He is also intubated in the emergency room, and a chest tube inserted on the right yields a bloody return. Suction is applied and no air leak is noted. Several units of blood are administered, and abdominal lavage fluid proves bloody. He is rushed to the operating room to undergo a laparotomy, and a liver laceration is found and repaired. During surgery he receives 8 units of whole blood, 5 units of platelets, and 8 units of fresh frozen plasma. His orthopaedic injuries are appropriately treated and he is transferred to the surgical intensive care unit in critical but stable condition. Chest radiographic study confirms that the endotracheal and chest tubes are in good position and reveals a right lower lobe infiltrate thought to be secondary to a pulmonary contusion. The ventilator is initially set at an inspired oxygen concentration (FIO2) of 40%, respiratory
rate of 12 per minute, and tidal volume of 90 mL in an assist-control mode. Arterial blood gas measurement reveals a pH of 7.46, a partial pressure of carbon dioxide (PCO2) of 3 mm Hg, and a partial pressure of oxygen (PO2) of 59 mm Hg, with an oxygen saturation of 92%. On the second hospital day, 12 hours after admission, he becomes agitated while on the ventilator, his respiratory rate rises to 25 per minute, his minute ventilation increases from 8.5 to 18 L per minute, and airway pressure rises from 20 to 60 cm H2O. A repeat chest radiograph now shows diffuse airspace pattern. Repeat arterial blood gas analysis reveals a PO2 of 39 mm Hg.
rate of 12 per minute, and tidal volume of 90 mL in an assist-control mode. Arterial blood gas measurement reveals a pH of 7.46, a partial pressure of carbon dioxide (PCO2) of 3 mm Hg, and a partial pressure of oxygen (PO2) of 59 mm Hg, with an oxygen saturation of 92%. On the second hospital day, 12 hours after admission, he becomes agitated while on the ventilator, his respiratory rate rises to 25 per minute, his minute ventilation increases from 8.5 to 18 L per minute, and airway pressure rises from 20 to 60 cm H2O. A repeat chest radiograph now shows diffuse airspace pattern. Repeat arterial blood gas analysis reveals a PO2 of 39 mm Hg.
What is the differential diagnosis of this patient’s clinical deterioration?
What are the risk factors for ARDS in this patient?
How would you manage this patient’s hypoxemia?
What are the potential problems associated with positive end-expiratory pressure (PEEP)?
What is the mortality rate associated with ARDS?
Case Discussion
What is the differential diagnosis of this patient’s clinical deterioration?
Several possibilities need to be considered in this setting. First, an infection (pneumonia) must always be ruled out. It is possible that the patient aspirated gastric contents at the accident scene while his level of consciousness was impaired, and this could have injured the lung directly owing to acid aspiration or set the stage for an overwhelming pneumonia. Alternatively, a nosocomial (hospital-acquired) pneumonia could have been acquired in the surgical intensive care unit, although the early onset of his ARDS makes this unlikely. The massive fluid resuscitation could lead to a fluid-overload congestive heart failure syndrome, even despite a normal-functioning heart before the accident. If a cardiac contusion occurred, this would make him more susceptible to this complication. Pulmonary contusions are worth considering, but are usually more localized and develop within several hours. Airway hemorrhage, perhaps stemming from either bronchial fracture or a traumatic intubation, can occur, but is typically associated with bloody secretions when severe. The ARDS could also have resulted from prolonged hypotension or replacement of blood products or TRALI. Regardless, this patient has ARDS and under these circumstances, pathologic study would show diffuse alveolar damage consisting of hyaline membrane formation, alveolar wall edema, and inflammation.
What are the risk factors that put this patient at risk for ARDS?
This patient’s risk factors are: hypotension—usually prolonged and severe (systolic blood pressure <90 mm Hg); hypertransfusion—more than 10 units of blood products in a 24-hour period; aspiration—any patient with depressed mental status is at great risk for gastric aspiration (the resulting chemical injury is a common precursor for ARDS). Fat emboli syndrome—this syndrome consists of diffuse pulmonary infiltrates, mental status changes, thrombocytopenia, and conjunctival or axillary petechiae. It occurs most often in the presence of severe and multiple long
bone fractures, and is thought to result from fat emboli migrating from the bone marrow to the lungs. However, it occurs usually 24 to 72 hours after admission, making it unlikely in this patient.
Other risk factors include sepsis, pneumonia, drugs, pancreatitis, lung contusion, toxic fume inhalation, and oxygen toxicity.
How would you manage this patient’s hypoxemia?
Acutely, the FIO2 should be increased to 100%. However, the prolonged administration of 100% oxygen for 3 or more days is likely to lead to oxygen toxicity and further worsening of ARDS. Accordingly, the FIO2 should be decreased to the lowest level that achieves an oxygen saturation of 90% to 92%. There appears to be a threshold of 50% to 60%, below which oxygen toxicity is rare. The ventilator shows that tidal volume should be set at 6 mL/kg. If an FIO2 above this range is necessary, then a trial of PEEP is indicated. PEEP appears to improve oxygenation by recruiting collapsed gas-exchange units (atelectasis). Data indicate that placing the patient in a prone position also improves oxygenation, but not necessarily the outcome.
What are the potential problems associated with PEEP?
PEEP may be lifesaving by improving oxygenation and allowing the FIO2 to be lowered to “safe” levels; however, it is associated with several potential problems. The first is hypotension. High levels of positive intrathoracic pressure impede venous return to the heart and may be transmitted to the pulmonary arteries, causing pulmonary hypertension. Both these factors serve to decrease cardiac output, which precipitates hypotension.
The risk of barotrauma is greatly increased with PEEP because of the positive airway pressures and may result in pneumothorax or pneumomediastinum. Pneumothorax in a ventilated patient is often a medical emergency because a tension pneumothorax may evolve. PEEP levels above 15 cm H2O are particularly risky. The prophylactic administration of PEEP, before the onset of ARDS, has been shown to be of no value.
What is the mortality rate associated with ARDS?
In 1967, the mortality rate observed for ARDS was 60%. This has decreased to 30% to 40%, mainly due to improved ventilatory management as opposed to the treatment of the ARDS itself. In the survivors, pulmonary function can return to normal, and this usually occurs by 6 months. Persistent abnormalities past this time indicate pulmonary fibrosis and pulmonary impairment.
Suggested Readings
Calfee CS, Matthay MM. Recent advances in mechanical ventilation. Am J Med 2005;118:584–591.
Choc MK. Acute lung injury/adult respiratory distress syndrome: the third Pittsburgh international lung conference. Proc Am Thorac Soc 2005;2:181–245.
Vinant JL, Abraham E. The last 100 years of sepsis. Am J Respir Crit Care Med 2006;173:256–263.
Asthma
What is asthma, and how is it classified?
How is asthma diagnosed?
What conditions are associated with or may complicate asthma?
Discussion
What is asthma, and how is it classified?
Asthma is not a single entity, but rather a clinical syndrome consisting of (a) an increase in airway resistance to a variety of stimuli; (b) variable airflow obstruction, which is usually reversible, either spontaneously or with treatment; and (c) a chronic, multicellular inflammatory response within the airways that produces patchy bronchial epithelial denudation, submucosal edema, hypersecretion of mucus, and subbasement membrane collagen deposition. The asthmatic response to stimuli may be immediate, occurring within minutes and termed the early asthmatic response, or delayed, arising several hours after exposure and termed the late asthmatic response. The early asthmatic response primarily results from bronchial smooth muscle constriction and the late asthmatic response is characterized by inflammatory cell infiltration and activation. Both patterns may be triggered by exposure to the same stimuli, and may work in concert to produce sustained narrowing of the airway lumen.
Asthma may be classified on the basis of either the presumptive etiology or symptom severity and the pattern of airflow obstruction. Historically, attempts have been made to classify asthmatic subjects as having either intrinsic or extrinsic disease. Intrinsic asthmatics have no personal or family history of allergies, their immunoglobulin E (IgE) levels are normal, and they have no easily identifiable environmental precipitants of their symptoms. In contrast, extrinsic asthmatics have allergic or atopic histories, their IgE levels are typically elevated, and they have specific antigenic triggers to their asthma. This traditional etiologic classification is now probably obsolete because individual asthmatic subjects commonly exhibit both IgE- and non–IgE-mediated responses to broncho provocative stimuli. Therefore, a classification scheme that is instead based on the severity of symptoms and on lung function is more clinically relevant, and provides a framework on which to base a stepwise treatment approach. One proposed classification scheme is presented in Table 8-1.
Because the severity of an acute asthma attack may be underestimated by both patients and their families, patients are encouraged to use home expiratory flow rate devices, which can more objectively measure asthma severity. Factors that have been associated with an increased risk of asthma mortality include frequent emergency room visits, hospitalization within the previous year, prior life-threatening episodes, a previous need for intubation, a recent
reduction in the corticosteroid dosage or cessation of use, noncompliance with medical therapy, the presence of serious depression or psychosocial behavioral problems, and a lower socioeconomic status.
Table 8-1 Asthma Classification Scheme
Asthma Severity
Clinical Features
Pulmonary Function
Mild
Intermittent, brief symptoms (<1-2 times per week)
Expiratory flow rates >80% of predicted
Rare nocturnal symptoms (<2 times per week)
Expiratory flow rate variability <20%
Moderate
Exacerbations (>2 times per week)
Expiratory flow rates 60%-80% of predicted
Nocturnal symptoms (>2 times per week)
Expiratory flow rate variability 20%-30%
Severe
Almost daily bronchodilator use
Expiratory flow rate <60% of predicted
Frequent continuous symptoms
Expiratory flow rate variability >30%
Frequent nocturnal awakenings
Physical activities limited by symptoms
Hospitalization for asthma within the previous year
How is asthma diagnosed?
Because patients with asthma are a heterogeneous group, the diagnosis requires assessment of a patient’s pulmonary function and attention to select details revealed by the medical history, physical examination, and laboratory tests. Historical features important in establishing the diagnosis of asthma include the episodic and variable nature of the airflow obstruction and the reversibility of the obstruction. The most common symptoms—cough, wheezing, chest tightness, shortness of breath, and sputum production—are nonspecific and by themselves nondiagnostic. The pattern of symptoms may be suggestive, in that nocturnal (and early morning) symptoms are particularly characteristic of asthma. Commonly reported precipitants of bronchospasm include exercise, cold air, environmental allergens, exposure to occupational or chemical irritants, and upper respiratory tract infections. The differential diagnosis of adult wheezing or cough may include mechanical obstruction of the airway (e.g., foreign body, tumor mass, or granulomatous narrowing), vocal cord dysfunction, congestive heart failure, pulmonary embolus, aspiration injury, pulmonary eosinophilia syndromes, and other forms of chronic obstructive pulmonary disease (COPD) (e.g., cystic fibrosis, chronic bronchitis, and emphysema).
The physical examination findings may be either unremarkable or suggest the presence of air trapping and hyperinflation, with an increased anteroposterior thoracic diameter and a low diaphragm. Wheezing is the most characteristic breath sound of asthma but is an unreliable indicator of severity. Bronchospasm may produce a prolonged expiratory phase with reduced tidal volumes and minimal air movement. In this setting, faint wheezing paradoxically intensifies as airflow improves. Rhonchi and other adventitious
sounds may suggest the presence of secretions in the airways. Signs of severe airflow obstruction may include an increased pulsus paradoxus, supraclavicular retractions with accessory muscle use (sternocleidomastoid and intercostals), and thoracoabdominal paradox (the paradoxical retraction of abdominal musculature with inspiration).
Pulmonary function testing should be pursued in all patients with suspected asthma. Spirometric findings of reduced expiratory flow rates with a normal inspiratory flow–volume curve, lung volumes suggesting increased thoracic gas and residual volumes, and increased airway resistance are all characteristic signs of asthma and may be alleviated by bronchodilator treatment. After an acute exacerbation of asthma, however, pulmonary function may remain abnormal long after the symptoms have returned to their baseline status.
Additional studies and signs that may be useful in the evaluation of asthma include (a) bronchoprovocation testing with methacholine, histamine, or exercise to document increased airway responsiveness to stimuli; (b) peripheral eosinophilia; (c) increased IgE levels; (d) Charcot-Leyden crystals (crystallized cationic proteins), eosinophils, or Curschmann’s spirals (bronchiolar casts of mucus and cellular debris) in the sputum; and (e) a chest radiograph showing hyperinflation or the presence of barotrauma. No single test or battery of tests is appropriate for every suspected case. Selected studies may provide the objective evidence needed to confirm the diagnosis of asthma when the history and physical examination findings are only suggestive.
What conditions are associated with or may complicate asthma?
Several conditions may complicate the asthma syndrome, and they require special consideration.
Although a person’s clinical course is not predictable, unstable asthma develops during pregnancy in approximately one third of asthmatic women, one third experience no change, and symptoms are actually less severe in one third. Poorly controlled asthma during pregnancy may contribute to prenatal mortality, an increased likelihood of prematurity, and low birth weight. Therefore, using medications to obtain optimal control of asthma is appropriate, even if their safety in pregnancy has not been unequivocally proved. An inhaled corticosteroid preparation, selective β2 agonists, appropriately monitored theophylline use, and even systemic corticosteroids can be used when necessary to prevent fetal hypoxia. Medications that should be avoided include α-adrenergic compounds, brompheniramine, epinephrine, and some decongestants (oral α agonists), antibiotics (tetracycline and ciprofloxacin), and live virus vaccines.
The likelihood of asthma-related postoperative complications depends on the severity of the patient’s airway hyperresponsiveness, the degree of airflow obstruction, and the amount of excess airway secretions at the time of surgery. In addition, endotracheal intubation and the type of procedure performed (thoracic and upper abdominal) may pose an additional risk. Preoperative corticosteroids may be indicated if expiratory flow rates are reduced (<80% of personal best) or if corticosteroids have been required to control asthma in the previous 6 months.
Maintenance of nasal patency may improve lower airway function and asthma control. Although the mechanisms involved in this relationship are not completely understood, nasal obstruction, such as that caused by rhinitis, sinusitis, and nasal polyps, may lead to asthma instability and worsening of symptoms. Nasal β2 agonists and corticosteroids are sometimes useful in treating nasal obstruction.
Approximately 2% of all cases of asthma are due to occupational exposure to specific sensitizing substances. Proteins, organic compounds, and some inorganic chemicals (metal salts) have been implicated. Once the diagnosis is established, complete avoidance of exposure is mandatory because continued exposure to even minute concentrations may provoke severe and potentially fatal bronchospasm. Also, once well established, occupational asthma may not be completely reversible. The pharmacologic therapy used for this type of asthma is similar to that used for other forms of asthma, but is no substitute for diligent avoidance of exposure to the offending agents.
Chemical sensitivity may also provoke asthma attacks. Approximately 5% to 20% of adults with asthma sustain severe and potentially fatal exacerbations of asthma after taking aspirin or other nonsteroidal antiinflammatory drugs (triad asthma). Physical examination in these patients may reveal nasal polyps, and symptoms of vasomotor rhinitis may precede the development of aspirin-induced bronchospasm. Less commonly, sulfites, which may be used as a food preservative, and tartrazine, a yellow dye that may be used as a food coloring, have been linked to the occurrence of acute bronchospasm.
Although gastroesophageal reflux is more common in people with asthma, its relationship to bronchospasm is controversial. Most people with asthma and symptomatic gastroesophageal reflux have hiatal hernias, and the association between the two conditions may be best demonstrated by simultaneously monitoring the esophageal pH and pulmonary function. Medical management consisting of proton pump inhibitors is usually effective in these patients.
Case
A 26-year-old woman presents to the emergency room at 3:00 a.m. complaining of worsening cough with yellow-green sputum, shortness of breath, and wheezing of 5 days’ duration. Her symptoms began after an upper respiratory tract infection that was manifested as a low-grade fever, rhinorrhea with postnasal drip, and nasal congestion. She reports poor sleep quality for the last 2 days because of severe coughing and has used over-the-counter nasal sprays and cough suppressants, but without relief. She is 18 weeks pregnant, but has no significant past medical history. Her physical examination reveals that she is diaphoretic and unable to speak in sentences. Her vital signs reveal a respiratory rate of 30 breaths per minute, a heart rate of 120 beats per minute, a temperature of 37°C (98.6°F), and a pulsus paradoxus of 22 mm Hg. Spirometry is attempted but proves poorly reproducible, with a “best effort” forced expiratory volume in 1 minute (FEV1) of 30% of predicted. The remainder of her examination findings are noteworthy for the presence of supraclavicular retractions with inspiration, diffusely diminished breath sounds with
scattered, high-pitched inspiratory and expiratory wheezes, and a palpable subcutaneous crepitation over her anterior thorax. She is quite anxious, but alert and cooperative.
scattered, high-pitched inspiratory and expiratory wheezes, and a palpable subcutaneous crepitation over her anterior thorax. She is quite anxious, but alert and cooperative.
What additional studies may be important for the proper management of this patient?
What are the initial management considerations in this patient?
What are the treatment considerations for ongoing management in this patient?
Case Discussion
What additional studies may be important for the proper management of this patient?
The patient’s clinical presentation suggests acute, severe bronchospasm, and the immediate focus of the emergency room effort should be therapeutic rather than diagnostic. Although this is the initial episode of asthma for this patient, numerous factors suggest it is a dangerously severe attack. Dyspnea at rest, an inability to speak, and the use of accessory muscles are important observations. Objective measures of attack severity are an increased pulsus paradoxus and expiratory flow rates less than 40% of predicted. The intensity of wheezing is an unreliable indicator. The presence of subcutaneous emphysema suggests an associated pneumothorax or pneumomediastinum. On the basis of this presentation, chest radiography and arterial blood gas measurement are indicated, although treatment should not be delayed to do these. The chest radiographic findings may exclude the diagnosis of pneumonia and delineate the source of the subcutaneous emphysema. A pneumomediastinum can typically be watched without specific therapy, whereas a pneumothorax would likely require insertion of a chest tube with water-seal suction to bring about reexpansion. The arterial blood gas studies would likely show hypoxemia with hypocapnia. Hypoxemia with an elevated alveolar-arterial oxygen gradient is the result of mismatched ventilation and perfusion. Acute bronchospasm results in hyperventilation, and the arterial blood chemistry data should reflect a respiratory alkalosis with a reduced PaCO2. If the attack is severe and prolonged, the PaCO2 may rise as a result of increased dead space ventilation (high ventilation–perfusion ratio) and respiratory muscle fatigue. A normal or elevated PaCO2 in the setting of severe airway obstruction suggests impending respiratory failure and warrants intensive care unit observation, with consideration given to mechanical ventilation.
What are the initial management considerations in this patient?
The immediate goals of therapy are to ensure adequate oxygenation and gas exchange while reducing the bronchospasm and the work of breathing. In this case, the patient is “breathing for two” and fetal hypoxia is an important concern. At a minimum, adequate supplemental oxygen should be given immediately to ensure a PaO2 exceeding 65 mm Hg and an oxygen saturation greater than 90%. The decision to use ventilatory support consisting of intubation and mechanical ventilation is a difficult one, but may be lifesaving in patients with mental status deterioration, worsening respiratory distress from exhaustion, or progressively increasing PaCO2 levels with respiratory acidosis.
Frequent dosing with an inhaled β2-adrenergic agonist delivered by nebulizer or metered-dose inhaler is the most effective bronchodilator therapy for acute, severe
asthma (status asthmaticus). Asthmatic patients who are initially unresponsive to intensive inhaled therapy may respond to the subcutaneous delivery of β2 agonists, but oral administration is not indicated for acute management. Epinephrine should be avoided in this patient because it is a teratogen.
In addition to inhaled β2 agonists and supplemental oxygen, systemic corticosteroids should be instituted early in the emergency room management. Corticosteroids reduce airway obstruction by interrupting the inflammatory cascade at one or more critical steps in its genesis, and may also have a synergistic effect on β-adrenergic receptor activity. In general, systemic corticosteroids should be considered if significant improvement is not seen within the first 30 to 60 minutes of intensive bronchodilator treatment. Early corticosteroid use has been shown to lead to a reduction in both the rate of hospitalization and the rate of return to the emergency room after discharge. Inhaled corticosteroids are not indicated for the management of acute, severe asthma. Theophylline preparations offer little additional benefit when added to inhaled β2 agonist treatment in the emergency room, but they may augment respiratory muscle function during hospitalization. The use of inhaled β2 agonists, systemic corticosteroids, and even theophylline preparations (with serum levels kept at <12 μg/mL) may be considered appropriate in the setting of pregnancy and unstable asthma. Cautious hydration is also appropriate because insensible water losses increase with hyperventilation. The use of antibiotics is commonly reserved for objectively documented infections. The sputum production, although it is yellow-green, does not mandate antibiotic treatment unless there is Gram’s stain evidence of a dominant organism.
What are the treatment considerations for ongoing management in this patient?
The optimal management of chronic asthma relies on four interrelated principles: objective assessment of lung function, pharmacologic therapy, environmental control, and patient education. The goals of effective management are to maintain near-normal pulmonary function and physical activity levels, minimize symptoms and prevent exacerbations, and avoid the adverse effects of asthma medications. Spirometry, based on the peak expiratory flow rates or FEV1, provides an objective measure of asthma control and can be useful in adjusting medications (particularly tapering systemic corticosteroids) and assessing the need for intervention. Pharmacologic therapy is typically prescribed in a stepwise manner. In recognition that asthma is a chronic inflammatory disease, trends in therapy have placed a greater emphasis on the use of inhaled corticosteroids or cromolyn as first-line medications, with inhaled β2 agonists used to bring about acute relief of bronchospasm, as needed. Theophylline preparations and oral β-adrenergic agonists are often used as second-line agents, and are particularly useful for controlling the nocturnal worsening of asthma. Short “bursts” of oral corticosteroids are best used in the early treatment of acute, severe exacerbations, and every effort should be made to avoid chronic dependence on oral corticosteroids once the acute attack is controlled.
In selected cases, the identification and avoidance of specific triggers of bronchospasm may have significant impact on asthma control. Avoidance of aeroallergens (dust mites, cat dander, pollens, and molds), chemicals (sulfites and tartrazine),
certain medications (aspirin, β-blockers, and acetylcholinesterase inhibitors), and strong aeroirritants (tobacco smoke, household sprays, and wood smoke) may be helpful for certain patients. Although exercise is a common precipitating factor, the use of inhaled β2 agonists or cromolyn before exercise may minimize the associated bronchospasm. Last, patient education should begin at the time of diagnosis and be encouraged throughout the continued care. Learning to identify important signs and symptoms of asthma, the correct use of the peak expiratory flow rate meter and metered-dose inhaler, and addressing issues related to medication effects and environmental control may minimize patient misunderstandings regarding the ongoing management of asthma. In this patient, a warning regarding the avoidance of α-adrenergic agonists until the completion of the pregnancy is also warranted.
Suggested Readings
Busse WW, Lemansker F. Asthma. N Engl J Med 2001;344:350–362.
International report: international consensus report on diagnosis and treatment of asthma. Publication no. 923091. Washington, DC: U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, June 1992.
McFadden ER. Acute severe asthma. Am J Respir Crit Care Med 2003;168:740–759.
National Asthma Education Program. Executive summary: guidelines for the diagnosis and management of asthma. Publication no. 913042 A. Bethesda, MD: Office of Prevention, Education, and Control, National Heart, Lung and Blood Institute, National Institutes of Health, July 1991.
National Asthma Education Program. Executive summary: management of asthma during pregnancy. Publication no. 933279 A. Bethesda, MD: Office of Prevention, Education, and Control, National Heart, Lung and Blood Institute, National Institutes of Health, October 1992.
Chronic Obstructive Pulmonary Disease
What is chronic obstructive pulmonary disease (COPD)?
What are the epidemiologic trends in COPD?
What is the most commonly held theory explaining the development of emphysema?
What are the common signs and symptoms of COPD?
What are the common laboratory and radiographic findings in the setting of COPD?
Discussion
What is COPD?
The term COPD is commonly applied to two disorders: emphysema and chronic bronchitis. Most patients with COPD have a combination of these
two conditions. Some authors also include chronic obstructive asthma and other disorders associated with chronic airflow limitation (e.g., bronchiolitis obliterans and bronchiectasis) under the heading of COPD.
What are the epidemiologic trends in COPD?
There has been an approximate 60% increase in the prevalence of COPD since the late 1970s. Although emphysema is a common postmortem finding in adults, its prevalence is strongly correlated with smoking. COPD is more commonly diagnosed in men than women, but as more adolescent girls than boys are beginning to smoke, this trend may change. A heavy smoker exhibits an average decline in FEV1 of 40 to 45 mL per year; this decline is only 20 mL per year in a nonsmoking adult.
What is the most commonly held theory explaining the development of emphysema?
In part, on the basis of observations gleaned in people with α1-antitrypsin deficiency, most authorities believe that the destruction of the alveolar wall and the airspace enlargement seen in the setting of emphysema are due to an imbalance between the proteases and antiproteases in the lower respiratory tree (α1-antitrypsin being the major protein in this category). Cigarette smoke inactivates the normal antiproteases in people who do not have α1-antitrypsin deficiency.
What are the common signs and symptoms of COPD?
Although the initial complaint is usually dyspnea, some patients seek medical care because of chronic cough or sputum production, wheezing, recurrent pulmonary infections, or, in rare circumstances, weight loss or lower extremity swelling. Early in the disease, physical examination findings may be normal. Later, auscultation of the chest may reveal wheezing, rhonchi, or, in patients with predominant emphysema, decreased breath sounds. Percussion of the chest typically reveals hyperinflation and low diaphragms. In advanced cases, the point of maximal cardiac impulse may be felt in the subxiphoid area. Cyanosis, a right-sided third heart sound (S3), jugulovenous distention, and lower extremity edema are late findings.
What are the common laboratory and radiographic findings in the setting of COPD?
There are no specific laboratory values seen in the setting of COPD. The routine blood count is normal, although COPD patients with chronic hypoxia may show an elevated hematocrit. The finding of eosinophilia should raise the possibility of concomitant asthma. Typically in COPD the flow rates are reduced, the lung volumes are increased due to hyperinflation as measured by increased thoracic gas volume and functional residual capacity, and the diffusing capacity is decreased in emphysema. Reductions in both the FEV1 and forced vital capacity (FVC) are routinely seen, although the FEV1 is reduced out of proportion to the FVC. Early on, the chest radiograph is usually normal. As emphysema develops, the lungs show hyperinflation, flattening of the diaphragms, and an increased retrosternal airspace. Bullae can be seen. The electrocardiogram tends to be normal, except in advanced disease, when it may show low voltage in the limb leads, early R waves in V1 and V2, and peaked P waves (P pulmonale).
Case
A 65-year-old man is seen because of a 5-day history of progressive shortness of breath and dyspnea on exertion. He also complains of a cough productive of green sputum, as well as vague right-sided chest pain. He has felt feverish at home, but denies any shaking chills, sore throat, nausea, vomiting, diarrhea, edema, or exposure to anyone with a similar illness.
The patient has been smoking two packs of cigarettes per day for the last 30 years. However, he recently decreased his habit to one pack per day. He was seen by a physician approximately half a year ago and was told that he had emphysema. He has not been hospitalized previously. He is a retired bus driver and lives at home with his wife. They have no pets. Although he has noted some dyspnea on exertion over the last 3 to 4 years, he continues to maintain an active lifestyle and can still mow the lawn without much difficulty. He can walk 1 to 2 mi on a flat surface at a modest pace. The patient rarely drinks alcohol. He denies any other significant past medical history, including a history of childhood asthma or allergic diseases, significant cough, sputum production, or exposure to asbestos. His medications include sustained-release theophylline and over-the-counter vitamins.
On physical examination, the patient is found to be a somewhat thin but well developed and in moderate respiratory distress. His blood pressure is 150/98 mm Hg with a pulsus paradoxus of 20 mm Hg, his pulse is 110 beats per minute, his temperature is 37.9°C (100.22°F) orally, and his respiratory rate is 24 breaths per minute and labored. Head, eye, ears, nose, and throat findings are unremarkable. No adenopathy is found in his neck, and the neck veins are flat. His chest is hyperexpanded, and there is use of the accessory muscles of respiration. Hyperresonance to percussion is noted. His breath sounds are distant with an occasional scattered wheeze. During the cardiac evaluation, the point of maximal impulse is located in the epigastric area. There is a regular tachycardia with a systolic fourth sound (S4) heard best at the right lower sternal border. No murmurs or rubs are noted. His abdomen is scaphoid, bowel sounds are normal, and no tenderness or organomegaly is noted. His extremities are free of clubbing, cyanosis, and edema. Pulse oximetry shows a 91% saturation on room air.
What tests and studies would you order in this patient?
A chest radiographic study reveals the presence of hyperexpanded lung fields, a small cardiac silhouette, evidence of bullous disease in both lungs, and an alveolar infiltrate in the right middle lobe with some degree of volume loss. No effusions are seen.
Arterial blood gas measurement performed on room air reveals a pH of 7.50, a PaCO2 of 23 mm Hg, a PaO2 of 51 mm Hg, and an oxygen saturation of 92%. Respiratory alkalosis is present with hyperventilation. Results of a complete blood count are as follows: white blood cells, 14,300/mm3 with 8% band forms and 8.4% polymorphonuclear leukocytes; and the hematocrit reading is 44%. A chemistry panel reveals the following findings: sodium, 139 mEq/L; potassium, 4.1 mEq/L; chloride, 108 mEq/L; bicarbonate, 20 mEq/L; blood urea nitrogen, 21 mg/dL; and creatinine, 0.9 mg/dL. His theophylline level is 3.7 μg/mL. The electrocardiogram reveals sinus tachycardia with low voltage in the limb leads, and no acute changes.
What is your diagnosis based on the information you have, and how would you manage this patient?
What therapy should you institute while the patient is in the hospital?
The patient is started on inhaled β2 agonists and intravenous ampicillin. After 2 days of treatment, his condition fails to improve and respiratory fatigue requiring emergent endotracheal intubation and ventilation develops. His wife states that she does not want to prolong the patient’s life “by artificial means” and is worried that the patient will require indefinite mechanical ventilation. Another option would be the use of noninvasive ventilation with BiPAP (i.e., nasal positive airway pressure during inspiration and expiration).
How would you respond to his wife’s concern about the need for indefinite mechanical ventilation?
The patient’s sputum culture grows Haemophilus influenzae that is resistant to ampicillin. His antibiotics are changed, and 4 days later he is successfully extubated. After 14 days in the hospital, he is ready to be discharged.
After the patient is discharged, how would you provide follow-up, and what are your treatment options now?
Case Discussion
What tests and studies would you order in this patient?
A chest radiographic study should be obtained. Although the value of a routine chest radiographic study in patients with an exacerbation of COPD has been debated, this patient has a productive cough, low-grade temperature, and localizing chest pain, all of which indicate the existence of an intrathoracic abnormality, stressing the importance of a chest radiograph.
Despite a pulse oximetry reading of 91%, arterial blood gas measurements are indicated for in this patient. There are several factors that can cause a poor correlation between the pulse oximetry value and the PaO2, as measured by arterial blood gas determinations. It is poor in patients with jaundice or dark skin pigmentation, as well as in those with poor peripheral circulation. Furthermore, under various physiologic and pathologic conditions (e.g., changes in the pH or 2,3-diphosphoglyceric acid level), the oxyhemoglobin dissociation curve can be shifted to the right or left. Therefore, the oximeter can either underpredict or overpredict the actual PaO2. Finally, in a patient with a moderately severe pulmonary process, knowledge of the PaCO2 and pH is imperative.
A complete blood count and chemistry panel should be obtained. The complete blood count can provide useful information regarding the severity of the infectious process (e.g., leukocytosis). Furthermore, significant polycythemia may indicate the existence of long-standing hypoxia, which signifies the chronicity and severity of the disease. The chemistry profile can provide valuable information concerning electrolyte imbalance (e.g., hyponatremia in the syndrome of inappropriate antidiuretic hormone secretion) or volume depletion. Knowledge of the serum bicarbonate level is useful in conjunction with the arterial blood gas findings to assess the chronicity of any respiratory acid–base disorders.
In a patient of advanced age with risk factors for coronary artery disease (tobacco abuse and hypertension) and chest pain, an electrocardiography is indicated. Furthermore, many types of arrhythmias (e.g., multifocal atrial tachycardia) are seen predominantly in the setting of decompensated pulmonary disease.
The theophylline level must be determined. Because this drug has a narrow therapeutic index, close monitoring of the serum levels is essential in acutely ill patients.
What is your diagnosis based on the information you have, and how would you manage this patient?
The patient has a right middle lobe pneumonia and, as a result, an exacerbation of his COPD. Given the lack of cough and sputum production in his past history, as well as the bullae noted in the chest radiographic study, his clinical picture is consistent with emphysema, as opposed to chronic bronchitis. Most patients have a combination of both disorders. He should be admitted to the hospital.
What therapy should you institute while the patient is in the hospital?
Blood and sputum cultures should be obtained. A Gram’s-stained sputum specimen should be examined both by the primary physicians and by the laboratory technician.
Inhaled β-adrenergic agonists (e.g., 0.5 mL of albuterol in 1.5 mL of saline) are the mainstay of treatment for a COPD exacerbation. The initial dosing frequency of this medication depends on the severity of the disease; it can be administered every 1 to 3 hours. As the patient’s condition improves, the dosing frequency can be reduced to every 4 to 6 hours. Although metered-dose inhalers can be used with a similar degree of success, their efficacy depends on the ability of the patient to coordinate the timing of the inhalation and the activation of the inhaler, making them a less-than-optimal tool in an acutely ill patient.
The role of theophylline in the management of an acute exacerbation of COPD remains controversial. Most authorities agree that theophylline is a weak bronchodilator with a low therapeutic index. In a randomized, controlled study, the addition of aminophylline to a well formulated therapeutic regimen in hospitalized patients with COPD failed to show any benefit in terms of improvement in lung function or on the dyspnea scale. If used, theophylline levels should be monitored closely and the patient observed for any signs or symptoms of toxicity.
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