Pulmonary Complications in Pregnancy
Suzanne McMurtry Baird
Betsy B. Kennedy
The frequency and significance of acute and chronic pulmonary complications in pregnant women has increased in recent years, making these complications one of the leading causes of maternal morbidity and mortality (Berg, Callaghan, Syverson, & Henderson, 2010; Clark et al., 2008; Kwon, Triche, Belanger, & Bracken, 2006; MacKay, Berg, Liu, Duran, & Hoyert, 2011). Some of the complications are unique to pregnancy (amniotic fluid embolism [AFE], preeclampsia, and tocolytic-induced pulmonary edema), whereas others are preexisting conditions that may worsen or be exacerbated (cardiomyopathy, thromboembolic disease, asthma, pneumonia, and HIV-related pulmonary complications). When pulmonary complications occur during pregnancy, an understanding of the normal physiologic changes of pregnancy and their implications for assessing maternal-fetal status is essential for developing appropriate interventions and treatment.
ANATOMIC AND PHYSIOLOGIC CHANGES OF PREGNANCY THAT AFFECT THE RESPIRATORY SYSTEM
Pregnant women are susceptible to respiratory compromise and injury for several reasons, including alterations in the immune system that involve cell-mediated immunity and mechanical and anatomic changes involving the chest and abdominal cavities. The cumulative effect is decreased tolerance to hypoxia and acute changes in pulmonary mechanics.
UPPER AIRWAY CHANGES
Increased estrogen levels result in mucosal edema, hyperemia, mucus hypersecretion, capillary congestion, and greater fragility of the upper respiratory tract (Hegewald & Crapo, 2011). These hormonal changes and mucosal changes result in rhinitis of pregnancy, characterized by nasal congestion during 6 or more weeks of pregnancy without other symptoms of respiratory tract infection and no known allergic cause. Rhinitis of pregnancy is experienced by 18% to 42% of pregnant women (Hegewald & Crapo, 2011). Epistaxis, sneezing, voice changes, and mouth breathing also are common (Hegewald & Crapo, 2011).
ANATOMIC CHANGES
Three important changes occur in the configuration of the thorax during pregnancy: (1) an increase in the circumference of the lower chest wall, (2) an elevation of the diaphragm, and (3) a 50% widening of the costal angle (Hegewald & Crapo, 2011; Norwitz & Robinson, 2010). These changes occur to accommodate the increase in uterine size and maternal weight gain, even though they appear in the first trimester prior to significant enlargement of the gravid uterus. The lower rib cage ligaments relax under hormonal influence to allow for a progressive widening of the subcostal angle and increased anterior-posterior and transverse diameters of the chest wall. Increased chest wall circumference accommodates elevation of the diaphragm such that total lung capacity is not reduced (Hegewald & Crapo, 2011).
RESPIRATORY CHANGES
Increased circulating levels of progesterone during pregnancy result in maternal hyperventilation and up to 50% greater tidal volume without corresponding changes in vital capacity or respiratory rate (Hegewald & Crapo, 2011; Norwitz & Robinson, 2010). Oxygen consumption and minute ventilation
increase as functional residual capacity (FRC) and residual volume decrease with expanding abdominal girth. Total lung capacity is preserved, however, because of rib flaring and unimpaired diaphragmatic excursion. The overall hemoglobin amount increases and allows for an increase in total oxygen-carrying capacity; however, the increase in blood volume is disproportionate to the increase in hemoglobin concentration, thus resulting in a physiologic anemia (Laibl & Sheffield, 2006).
increase as functional residual capacity (FRC) and residual volume decrease with expanding abdominal girth. Total lung capacity is preserved, however, because of rib flaring and unimpaired diaphragmatic excursion. The overall hemoglobin amount increases and allows for an increase in total oxygen-carrying capacity; however, the increase in blood volume is disproportionate to the increase in hemoglobin concentration, thus resulting in a physiologic anemia (Laibl & Sheffield, 2006).
The increase in minute ventilation that is associated with pregnancy is often perceived as a shortness of breath. Dyspnea usually starts in the first or second trimester and is reported by 60% to 70% of healthy pregnant women by 30 weeks of gestation (Hegewald & Crapo, 2011). Dyspnea occurs secondary to the respiratory stimulation of progesterone, greater hypercapnic ventilatory response, and altered chest wall proprioceptors (Hegewald & Crapo, 2011). Shortness of breath at rest or with mild exertion is so common during pregnancy that it is often referred to as “physiologic dyspnea.”
Pregnancy is characterized by a state of chronic compensated respiratory alkalosis. Normal maternal hyperventilation during pregnancy lowers maternal partial pressure of carbon dioxide (PCO2) and minimally increases blood pH. The increase in blood pH increases the oxygen affinity of maternal hemoglobin and facilitates elimination of fetal carbon dioxide but appears to impair release of maternal oxygen to the fetus. The high levels of estrogen and progesterone during pregnancy facilitate a shift in the oxygen dissociation curve back to the right, thereby stimulating oxygen release to a fetus that has an increased affinity for oxygen. These physiologic adaptations ensure fetal advantage from increased oxygen transfer across the placenta and adequate blood gas exchange.
During labor and birth, hyperventilation is common due to pain, anxiety, and coached breathing techniques (Gei & Suarez, 2011; Hegewald & Crapo, 2011). Narcotics administered during labor and birth will act to decrease minute ventilation. In women with marginal placental reserves, hyperventilation and hypocarbia during labor and birth, leading to uterine vessel vasoconstriction and decreased placental perfusion, can have adverse effects on the fetus. Within 72 hours after birth, the minute ventilation rate decreases significantly with resumption of baseline in a few weeks. Lung volume changes normalize with decompression of the lungs and diaphragm after birth while FRC and residual volume are back to baseline within 48 hours (Hegewald & Crapo, 2011). Chest wall changes of pregnancy return to normal by 24 weeks postpartum, but the subcostal angle remains 20% of pregnancy width (Hegewald & Crapo, 2011).
RECOGNIZING RESPIRATORY COMPROMISE
A significant number of critical events are preceded by early signs of respiratory compromise. However, providers and patients often overlook or deny these signs and symptoms, leading to delays in communication and management. A woman with a pulmonary complication may present with a chief complaint of chest discomfort or tightness, persistant cough, unusual dyspnea or shortness of breath, or hemoptysis. If clinical history indicates a potential pulmonary complication, a thorough physical assessment should be conducted. Evidence-based guidelines that include early warning signs of maternal respiratory compromise should be used to improve communication between nurses and physicians, and to enhance clinical decision making regarding assessment parameters that fall outside defined normal values and that may indicate compromise. Physical signs of maternal respiratory compromise may include anxiety, increasing respiratory rate, wheezing, tachycardia, exertion with minimal activity, decreasing pulse oximetry values (trending below 96%), and/or adventitious breath sounds. Cyanosis, lethargy, agitation, intercostal retractions, and a respiratory rate greater than 30 breaths per minute indicate hypoxia and impending respiratory arrest.
FETAL SURVEILLANCE WITH MATERNAL PULMONARY COMPLICATIONS
In the presence of maternal respiratory compromise, which may include hypoxia, hypocapnia, or alkalosis, the fetus is at risk for impaired maternal-fetal gas exchange. Impaired gas exchange increases the incidence of fetal compromise and, if prolonged, will lead to intrauterine growth restriction (IUGR), oligohydramnios, meconium-stained amniotic fluid, preterm birth, and neonatal mortality (Beckmann, 2003; Coleman & Rund, 1997). The fetus depends on oxygen from maternal arterial oxygen content, venous return, and cardiac output, as well as from uterine artery and placental blood flow. Maternal hypoxia can cause fetal hypoxia directly, or the consequences of poorly controlled pulmonary conditions resulting in hypocapnia and alkalosis can cause fetal hypoxia indirectly by reducing uteroplacental blood flow (Cydulka, 2006). The fetus is sensitive to changes in maternal respiratory status, and decreases in maternal partial pressure of arterial oxygen (PaO2) may result in decreased fetal PaO2 and cause fetal hypoxia (Meschia, 2011). Rapid and profound decreases in fetal oxygen saturation and resultant fetal hypoxia occur with clinically significant decreases in maternal PaO2 below 60 mm Hg (Blaiss, 2004). Despite surviving in an environment of low oxygen tension, the fetus has very little oxygen reserve.
Administration of oxygen to the mother may produce only small increases in fetal PaO2, but this may increase fetal oxygen saturation significantly (Gardner & Doyle, 2004; Simpson & James, 2005). Oxygen should be administered as needed to maintain maternal oxygen saturation at 95% or higher (Cydulka, 2006).
Administration of oxygen to the mother may produce only small increases in fetal PaO2, but this may increase fetal oxygen saturation significantly (Gardner & Doyle, 2004; Simpson & James, 2005). Oxygen should be administered as needed to maintain maternal oxygen saturation at 95% or higher (Cydulka, 2006).
Fetal status may offer early warning of maternal pulmonary compromise. Because the uterus is physiologically a nonessential organ, when there is decreased blood volume, decreased cardiac output, or significant hypoxia, oxygenated blood flow will be directed to critical organs such as the brain, heart, and adrenal glands at the expense of uterine blood flow and, therefore, fetal well-being (Frye, Clark, Piacenza, & Shay-Zapien, 2011). Oxygenated blood flow will only be available to the uterus once other critical organs are perfused and oxygenated; therefore, a normal fetal heart rate (FHR) pattern excludes significant maternal hypoxia or hypotension, and an indeterminate or abnormal FHR pattern warrants close evaluation and intervention (Frye et al., 2011). Evaluation of the FHR pattern is an important element of assessment of maternal status and clinical decision making in the context of maternal respiratory disease (Frye et al., 2011). The frequency of fetal surveillance should be determined by gestational age, current maternal status, and fetal response to illness. If exacerbations of pulmonary complications occur, vigilant fetal surveillance is important. At each prenatal visit, confirmation that fundal height and fetal size are consistent with expected normal values based on current gestational age is crucial. In conjunction with nonstress testing, serial ultrasounds and biophysical profiles (BPPs) are used to monitor fetal status on an ongoing basis (Namazy & Schatz, 2006). Fetal movement counting may also be initiated based on provider preference.
ASTHMA
SIGNIFICANCE AND INCIDENCE
Asthma is the most common chronic medical condition, affecting up to 8% of women during pregnancy (American College of Obstetricians and Gynecologists [ACOG], 2008; Dombrowski et al., 2004). The effects of pregnancy on asthma symptoms vary, with 23% of women improving, 30% experiencing worsening of their symptoms, and 47% remaining unchanged (Dombrowski et al., 2004). Overall, if asthma symptoms worsen, it is more likely to occur between 17 and 24 weeks’ gestation, and it is less severe in the last 4 weeks of pregnancy (Belfort & Herbst, 2010; Gluck, 2004). Severe asthmatics, even those under good control prior to pregnancy, are more likely to experience severe exacerbation requiring hospitalization (Belfort & Herbst, 2010; Dombrowski et al., 2004; Gluck & Gluck, 2006). Exacerbations during labor and birth are unusual (Frye et al., 2011). After birth, 75% of asthmatic women return to their prepregnancy asthmatic status. In most women, asthma severity is the same as prepregnancy status within approximately 3 months postpartum (Gluck & Gluck, 2006).
Asthma has a variable natural history, creating a wide range of symptom expression during pregnancy. History of asthma severity in previous pregnancies may predict the severity of asthma in subsequent pregnancies (Blaiss, 2004). The relationship between asthma and pregnancy outcomes can also be influenced by risk behaviors and demographics. Smoking, age extremes, and Hispanic and African-American races have been shown to increase perinatal risk in asthmatic women (Beckmann, 2003). Maternal complications reported among asthmatics include hyperemesis, vaginal bleeding, placenta previa, preeclampsia, hypertensive disorders, a predisposition to infections, gestational diabetes, preterm rupture of membranes, preterm labor, cesarean birth, an increased length of hospital stay, and having a low-birth-weight infant (ACOG, 2008; Alexander, Dodds, & Armson, 1998; Beckmann, 2003; Cydulka, 2006; Dombrowski, 2006; Gardner & Doyle, 2004; Källén, Rydhstroem, & Aberg, 2000; Kwon et al., 2006; Minerbi-Codish, Fraser, Avnun, Glezerman, & Heimer, 1998; National Asthma Education and Prevention Program [NAEPP], 2005; Pereira & Krieger, 2004). Severe or uncontrolled asthma can be life threatening for a woman and her fetus during pregnancy. Potentially life-threatening complications of severe asthma include pneumothorax, pneumomediastinum, acute cor pulmonale, and respiratory arrest (Belfort & Herbst, 2010; Cydulka, 2006; Gardner & Doyle, 2004). Maternal mortality is reported as high as 40% when a pregnant woman with asthma requires mechanical ventilation (Gardner & Doyle, 2004). Asthma has been associated with a fetal death rate twice that of pregnant women without asthma (Blaiss, 2004; Silver, 2007). However, effective control can optimize pregnancy outcomes close to that of the general population (ACOG, 2008). The NAEPP’s (2005) suggested steps for asthma control, as discussed in its publication, Working Group Report on Managing Asthma During Pregnancy: Recommendations for Pharmacologic Treatment—Update 2004, are listed in Table 10-1.
PATHOPHYSIOLOGY
Asthma is a chronic inflammatory disease of the airways in which the tracheobronchial tree is hyperresponsive to a multitude of stimuli (Dombrowski & Schatz, 2010). Asthma is one of the specific disease entities that is included in the general category of obstructive lung disease, which is characterized by limitation of airflow that generally is marked more during
expiration than inspiration and results in a prolonged expiratory phase. Asthma has varying degrees of airway obstruction, bronchial hyperresponsiveness, and airway edema that are accompanied by eosinophilic and lymphocytic inflammation (Belfort & Herbst, 2010; Gardner & Doyle, 2004). This results in edema of the bronchial wall, airway diameter reduction, and secretions that are thick and tenacious. Asthma involves a complex interplay of inflammatory cells, cellular mediators, and external triggers (Gluck & Gluck, 2006). It is a chronic disease with acute exacerbations that are characterized by recurrent bouts of wheezing and dyspnea that result from airway obstruction (Frye et al., 2011). The airway of an asthmatic patient is hyperresponsive to stimuli such as allergens, viral infections, air pollutants, smoke, food additives, exercise, cold air, and emotional stress (Dombrowski & Schatz, 2010). Common triggers of asthma exacerbations are listed in Table 10-2.
expiration than inspiration and results in a prolonged expiratory phase. Asthma has varying degrees of airway obstruction, bronchial hyperresponsiveness, and airway edema that are accompanied by eosinophilic and lymphocytic inflammation (Belfort & Herbst, 2010; Gardner & Doyle, 2004). This results in edema of the bronchial wall, airway diameter reduction, and secretions that are thick and tenacious. Asthma involves a complex interplay of inflammatory cells, cellular mediators, and external triggers (Gluck & Gluck, 2006). It is a chronic disease with acute exacerbations that are characterized by recurrent bouts of wheezing and dyspnea that result from airway obstruction (Frye et al., 2011). The airway of an asthmatic patient is hyperresponsive to stimuli such as allergens, viral infections, air pollutants, smoke, food additives, exercise, cold air, and emotional stress (Dombrowski & Schatz, 2010). Common triggers of asthma exacerbations are listed in Table 10-2.
Table 10-1. STEPWISE APPROACH FOR THE PHARMACOLOGIC MANAGEMENT OF CHRONIC ASTHMA DURING PREGNANCY | ||||||||||||
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The precise cause of airway inflammation and hyperresponsiveness is not well understood. When triggered by external stimuli, inflammatory cells infiltrate bronchial tissue and release chemical mediators such as prostaglandins, histamine, cytokines, bradykinin, and leukotrienes. Ultimately, airway smooth muscle responsiveness is increased because of these mediators. Narrowing of the airway lumen and airway hyperresponsiveness may be a result of the development of bronchial mucosal edema, excess fluid and mucus, inflammatory cellular infiltrates, and smooth muscle hypertrophy and constriction. During asthma exacerbations, there is decreased expiratory airflow, increased FRC, increased pulmonary vascular resistance, hypoxemia, and hypercapnia. The fetus can be negatively affected during acute episodes of asthma in which there is maternal arterial hypoxemia and the potential for uterine artery vasoconstriction (Dombrowski et al., 2004; Frye et al., 2011).
Table 10-2. COMMON TRIGGERS OF ASTHMA EXACERBATIONS | ||||||||||
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CLINICAL MANIFESTATIONS
Women may have one or a combination of asthma symptoms, which include shortness of breath, wheezing, nonproductive coughing, flaring nostrils, chest tightness, and use of accessory respiratory muscles. There may be scant or copious sputum, which is usually clear. Reports of nocturnal awakenings with asthma symptoms are common. An increase in cough, the appearance of chest tightness, dyspnea, wheezing, decrease in fetal movement, or a 20% decrease in peak expiratory flow rate (PEFR) may signal worsening of asthma and should warrant immediate clinical attention (Cydulka, 2006). Women with the following symptoms should be considered for intubation and mechanical ventilation: (1) worsening pulmonary function tests; (2) decreasing PaO2, increasing PaCO2, or progressive respiratory acidosis, despite vigorous bronchodilator therapy; (3) declining mental status; and (4) increasing fatigue (Cydulka, 2006).
Guidelines for assessing the severity of asthma before initiating therapy have been developed by the National Heart, Lung, and Blood Institute, a division of the National Institutes of Health (Scheffer, 1991). This classification system, like many others, was developed without specific consideration of pregnancy, but it may be helpful when assessing an adult patient with asthma. Patients are identified as mild, moderate, or severe asthmatics. Mild asthmatics experience exacerbations with coughing and wheezing no more than two times each week. There may be an intolerance of vigorous exercise. Women with moderate asthma experience infrequent exacerbations, with emergent care required
less than three times each year. Severe asthmatics experience daily wheezing and require emergency treatment more than three times per year. Women with severe asthma have poor exercise tolerance.
less than three times each year. Severe asthmatics experience daily wheezing and require emergency treatment more than three times per year. Women with severe asthma have poor exercise tolerance.
DISPLAY 10-1 Management Plan of Care for Pregnant Women with Exacerbations of Asthma
Obtain initial blood gas and pulmonary function tests to gather baseline data.
Continuously monitor maternal pulse oximetry.
Oxygen therapy to maintain SpO2 >95%.
Monitor fetal status as determined by estimated gestational age.
Tocolytic of choice for preterm labor management is magnesium sulfate. Use of magnesium sulfate therapy may enhance bronchodilation. Nonsteroidal anti-inflammatory medications, such as indomethacin, may exacerbate asthma and are contraindicated.
β-agonist inhalation therapy is the initial pharmacologic therapy.
If initial bronchodilator treatments fail to result in adequate response, high-dose intravenous corticosteroids may be considered.
Antibiotics may be used to cover secondary bacterial infection.
Measure and record intake and output. Observe for fluid volume imbalances.
Observe for signs and symptoms of hydrostatic pulmonary edema due to tocolytic therapy and intravenous steroids.
Ongoing care based on response to initial management.
Identification of the pregnant woman with severe asthma is important so that a plan of care and intensive treatment can be initiated early. See Display 10-1 for a management plan of care for pregnant women with exacerbations of asthma. Characteristics of maternal history that should alert healthcare providers to an increased risk of a potentially fatal asthma exacerbation are listed in Display 10-2. Nursing evaluation of the symptoms of asthma begins with clinical assessment of signs of respiratory distress. Significant findings include dyspnea, cough, wheezing, chest tightness, nasal flaring, presence of sputum, and tachycardia. Intercostal retractions or a respiratory rate greater than 30 breaths per minute indicates moderate to severe asthma. Pulsus paradoxus of more than 15 mm Hg is an indication of severe asthma. If pulsus paradoxus is present, blood pressure is audible only during expiration. To make this assessment, carefully observe the woman’s breathing, noting when systole first appears, and the millimeter level of mercury until pulsations are heard during inspiration and expiration. Lung auscultation usually reveals bilateral expiratory wheezing. Occasionally, on inspiration or expiration, only rhonchi are heard. Rales are rarely auscultated in asthmatics. Detailed clinical findings are listed in Display 10-3.
DISPLAY 10-2 Markers for Potentially Fatal Asthma
History of systemic steroid therapy >4 weeks
Three recent emergency room visits for asthma
History of multiple hospitalizations for asthma
History of hypoxic seizure, hypoxic syncope, or intubation
History of admission to an intensive care unit for asthma
The most beneficial tools to determine the severity of asthma is a pulmonary function test such as peak expiratory flow. Predicted values of PEFR are unchanged during pregnancy and range from 380 to 550 L/min. An individual baseline value should be established for each woman when her asthma is under control. Evaluation of exacerbations can be made by comparing baseline values with current peak flow values. Peak expiratory flow values that are more than 50% below personal baseline values require immediate attention.
Evaluations of arterial blood gases can help to establish severity of an asthma attack, with attention focused primarily on the pH and PCO2 to define severity. A mild attack is characterized by an elevated pH and a PCO2 below normal for pregnancy. The combination
of normal pH, low PO2, and normal PCO2 for pregnancy indicates a moderate asthma attack. A low PO2, low pH, and a high PCO2 are most significant for severe respiratory compromise. When maternal arterial PO2 falls below 60 mm Hg, the fetus is in severe jeopardy, and risk of fetal demise is increased.
of normal pH, low PO2, and normal PCO2 for pregnancy indicates a moderate asthma attack. A low PO2, low pH, and a high PCO2 are most significant for severe respiratory compromise. When maternal arterial PO2 falls below 60 mm Hg, the fetus is in severe jeopardy, and risk of fetal demise is increased.
DISPLAY 10-3 Clinical Findings in AsthmaSIGNS AND SYMPTOMS
Shortness of breath, chest tightness, productive or nonproductive cough
Increased respiratory rate (>20 breaths/min)
Tachycardia
Nasal flaring
Exertion with minimal activity
Recurrent episodes of symptoms
Nocturnal awakenings from symptoms
Waxing and waning of symptoms
AUSCULTATORY FINDINGS
Diffuse wheezes
Diffuse rhonchi
Longer expiratory phase than inspiratory phase
SIGNS OF RESPIRATORY DISTRESS
Rapid respiratory rate (>30 breaths/min)
Pulsus paradoxus >15 mm Hg
Retractions intercostally or supraclavicularly
Lethargy
Confusion or agitation
Cyanosis
Potentially fatal asthma includes a history of any one of the factors listed in Display 10-2. During pregnancy, monthly evaluations of pulmonary function and asthma history are important. These evaluations should include the following assessments: pulmonary function testing, ideally spirometry; detailed symptom history (symptom frequency, nocturnal asthma, interference with activities, exacerbations, and medication use); and physical examination with specific attention paid to the lungs (Namazy & Schatz, 2006).
CLINICAL MANAGEMENT
The goals when managing the woman with asthma during pregnancy include educational support, maintaining optimal respiratory status and function, objective assessment of maternal and fetal status, avoiding triggers, and pharmacologic treatment to control symptoms and prevent exacerbations and/or adverse effects of medication (ACOG, 2008; NAEPP, 2007). Fetal surveillance for women with asthma begins early in pregnancy. Women who have moderate or severe asthma during pregnancy should have ultrasound examinations and antenatal fetal testing (ACOG, 2008). If possible, first-trimester ultrasound dating should be performed to assist with subsequent evaluations of fetal growth restriction and determine risk of preterm birth. Serial ultrasound examinations to monitor fetal activity and growth should be considered (starting at 32 weeks of gestation) for women who have poorly controlled asthma or moderate to severe asthma and for women recovering from a severe asthma exacerbation (ACOG, 2008).
PATIENT/FAMILY EDUCATION
Education should be designed to assist the woman and her family to gain motivation, confidence, and skills to keep asthma symptoms under control and to understand the potential adverse effects of uncontrolled asthma on the woman and the fetus. Although some women may be reluctant to take prescribed medications for fear they may harm the developing fetus, the woman needs to be reassured that risks to the fetus from hypoxia-related, untreated asthma are greater than risks of medications (ACOG, 2008; Namazy & Schatz, 2006). All patients should be taught to be conscientious of fetal activity and to report concerns to their healthcare provider (ACOG, 2008). Also, it is critically important that the pregnant woman be able to recognize symptoms of worsening asthma and have the knowledge of how to treat them appropriately. Correct inhaler technique should be reinforced, and the patient should know how to reduce her exposure to, or control, those factors that exacerbate her asthma (Namazy & Schatz, 2006). Educational topics (NAEPP, 2005) include the following:
Signs and symptoms of asthma
Airway changes
Avoiding asthma triggers
Effects of pregnancy on the disease and the disease on pregnancy
Peak flow meters and metered dose inhalers
Role of medications
Correct use of medications
Adverse effects of medications
Managing exacerbations
Emergency care
Individualized education throughout pregnancy should be guided by assessment of the woman’s understanding of her asthma assessment management plan and her level of cooperation. It is essential to highlight the changes that pregnancy has on asthma and treatment. When there is active participation by the healthcare provider, the pregnant woman, and her family, asthma control can be maximized.
NONPHARMACOLOGIC CONTROL
Identification of triggering factors for asthma in each woman is an important aspect of management that may improve clinical status, prevent acute exacerbations, and decrease the need for pharmacologic intervention. Asthma is associated with allergies, with 75% to 85% of patients reporting positive testing to common allergens (Dombrowski, 2006). Historic information and prior skin testing may give important information regarding common triggers such as pollens, molds, house-dust mites, animal dander, and cockroach antigens. Other common asthma irritants include air pollutants, strong odors, food additives, and tobacco smoke. It is particularly important for the pregnant asthmatic woman to stop smoking during her pregnancy (Gluck & Gluck, 2006). Education about the risks of smoking, including an increased severity of her asthma, bronchitis, or sinusitis and the need for increased medication, can be helpful in motivating the woman to stop smoking.
Viral respiratory infections, vigorous exercise, and emotional stress may also cause severe asthma exacerbations. Medications such as aspirin, beta-blockers, nonsteroidal anti-inflammatory drugs (NSAIDs), radiocontrast media, and sulfites have been implicated as asthma triggers as well. Once the woman has been assisted to identify common asthma triggers, exposure to allergens or irritants can be minimized, thereby lessening exacerbations.
PHARMACOLOGIC THERAPY
Pharmacologic therapy plays an essential role in optimizing maternal and fetal outcomes by providing protection for the respiratory system from irritant stimuli, prevention of pulmonary and inflammatory response to allergen exposure, relief of bronchospasm, resolution of airway inflammation to reduce airway hyperresponsiveness, and improvement of pulmonary function. Undertreatment is an ongoing problem in the care of pregnant asthmatic women. Medications commonly used in asthma management are generally considered safe and effective during pregnancy and lactation. It is safer for pregnant women with asthma and their fetuses to take prescribed medications than to experience an exacerbation (ACOG, 2008). The effectiveness of medications for the treatment of asthma during pregnancy is assumed to be the same as in nonpregnant women (NAEPP, 2007). Inhalation therapy is usually more effective than systemic treatment because asthma is an airway disease. Aerosolized medications are ideal because they deliver the drug directly to the airways, minimizing systemic side effects and decreasing exposure to the fetus.
Pharmacologic therapy for asthma is divided into two categories: (1) rescue (medications that provide symptomatic relief of acute bronchospasms without treating the cause of the bronchospasm) and (2) maintenance (medications that control airway hyperreactivity and treat underlying inflammation) (Belfort & Herbst, 2010). Generally, a stepwise approach to the pharmacologic management of chronic asthma is preferred (see Table 10-1).
Rescue Medications
Short-Acting Beta-Agonists
The use of inhaled short-acting beta-2-agonists provides bronchodilation and is recommended for acute and mild intermittent asthma therapy (Chambers, 2006). The onset of action is rapid with demonstrated safety profiles for mother and fetus, making short-acting beta-2-agonists the preferred rescue medication for acute exacerbations of asthma. Medications in this group include metaproterenol (Alupent), terbutaline (Brethine), and albuterol (Ventolin, Proventil). This group of drugs has minimal side effects, such as maternal tachycardia, tremors, restlessness, anxiety, and palpitations (Lehne, 2010). If symptoms disappear and pulmonary function normalizes, these medications can be used indefinitely. Prolonged use may result in rapid tolerance and limited usefulness. Women are candidates for anti-inflammatory therapy if they require the use of a beta-2-agonist more than three times each week. In the management of moderate to severe persistent asthma, long-acting beta-agonists may be added to a regimen of inhaled corticosteroids for greater asthma control (Blaiss, 2004; NAEPP, 2005).
Long-Acting Beta-Agonists
Salmeterol (Serevent Diskus) and formoterol (Foradil) are newer long-acting beta-agonists with limited published data regarding safe use in pregnancy. Therefore, the use of these medications are limited to women with moderate to severe asthma who report relief of symptoms with use of these agents prior to pregnancy or as an add-on therapy for women who are currently on inhaled steroids and need additional therapy for symptom relief.
Anticholinergics
Ipratropium (Atrovent) is an anticholinergic medication that may be used in combination with inhaled beta-agonists to promote bronchodilation. Even though published reports show safe use, the combination of these medications is rarely used in pregnancy (NAEPP, 2005). If prescribed during pregnancy, nebulized forms of anticholinergics may be considered for additional therapy in cases of acute asthma exacerbations that are not controlled after initial beta-agonist therapy (Namazy & Schatz, 2006).
Maintenance Medications
Methylxanthines
Because of the success of inhalation therapy, systemic aminophylline and theophylline are rarely used today. Sustained-release theophylline may be helpful for the pregnant woman whose symptoms are primarily nocturnal because of its long-acting properties. Although safe at recommended doses during pregnancy, theophylline treatment is associated with a higher incidence of maternal side effects than inhaled beta-agonists (NAEPP, 2005).
Cromolyn Sodium
Cromolyn and nedocromil are nonsteroidal anti-inflammatory agents that work by preventing the release of inflammatory mediators through stabilization of mast cells. Neither produces any side effects. Both are FDA category B drugs (Schatz, 2001), and cromolyn data have demonstrated long-term safety (Blaiss, 2004). Neither is as effective as inhaled corticosteroids in preventing asthma symptoms.
Inhaled Corticosteroids
One of the greatest advances in asthma treatment in the past decade has been the availability of inhaled corticosteroids (ACOG, 2008). For women with persistent mild asthma, these medications are currently the treatment of choice because they reduce the risk of asthma exacerbations associated with pregnancy and have not been related to any increases in congenital malformations or other adverse perinatal outcomes (NAEPP, 2005). To minimize systemic effects and improve respiratory tract penetration, inhaled corticosteroids are administered with a spacer. At recommended doses,
these medications act without systemic side effects to effectively reduce mucus secretion and airway edema. They may increase bronchodilator responsiveness while inhibiting many of the mediators of inflammation. Studies suggest that beclomethasone or budesonide are the inhaled steroids of choice for use during pregnancy due to reassuring safety data (ACOG, 2008).
these medications act without systemic side effects to effectively reduce mucus secretion and airway edema. They may increase bronchodilator responsiveness while inhibiting many of the mediators of inflammation. Studies suggest that beclomethasone or budesonide are the inhaled steroids of choice for use during pregnancy due to reassuring safety data (ACOG, 2008).
Unlike the immediate-acting bronchodilators, the effects of inhaled corticosteroids are gradual. After 2 to 4 weeks of use, full effects of symptom suppression and PEFR improvement are seen. Patient education is vital to ensure that the woman will continue her anti-inflammatory therapy until the medication achieves maximum effectiveness. The most common side effect of inhaled steroids is hoarseness, which disappears when therapy is discontinued. Other uncommon side effects include throat irritation, cough, and oral thrush. Infrequent effects such as easy bruising, skin thinning, and low serum cortisol levels have been reported. Published data have shown no evidence of teratogenicity with use of inhaled corticosteroids (Blaiss, 2004). Intranasal corticosteroids have not been studied during human pregnancy, but because their systemic effects are minimal, continued use during pregnancy appears to be safe (ACOG, 2008; NAEPP, 2005).
Systemic Corticosteroids
Due to associated fetal and pregnancy complications, systemic oral corticosteroids may be prescribed when maximum doses of bronchodilators and anti-inflammatory agents fail to control asthma. Conflicting reports show possible association of increased cleft lip and palate formation with exposure (Park-Wyllie et al., 2000; Reinisch, Simon, Karow, & Gandelman, 1978; Robert et al., 1994). Consistently, reports of pregnancy-associated complication have been shown with corticosteroid use. These complications include gestational hypertension, preeclampsia, gestational diabetes or worsening of diabetes mellitus, preterm birth, and low birth weight (ACOG, 2008; NAEPP, 2005). However, if needed for short-term therapy to control exacerbations of asthma symptoms or long-term management, the benefits of using oral corticosteroids outweigh the risks and are recommended as needed (ACOG, 2008; NAEPP, 2005).
Leukotriene Modifiers
Leukotriene modifiers are a new class of drugs that limit the inflammatory action of leukotrienes—chemical mediators that cause bronchoconstriction and mucus hypersecretion and stimulate microvascular leakage, edema formation, and eosinophil chemotaxis (Belfort & Herbst, 2010). Examples of these drugs include zileuton (Zyflo), zafirlukast (Accolate), and montelukast (Singulair). Due to limited data, ACOG (2008) recommends that, with the exception of zileuton, leukotriene modifiers may be used during pregnancy if women show resistance to other classes of safety-proven medications.
Combination Drugs
Combination drugs, such as Advair Diskus and Combivent, may be prescribed for continued use during pregnancy if symptoms are well controlled. However, because these medications contain a combination of medications, it is not recommended to initiate these drugs during pregnancy unless the benefits outweigh the risks of the individualized medications contained in these combination formulas (ACOG, 2008).
Immunotherapy
Pregnant women with asthma who have allergens responsive to desensitization may benefit from allergen immunotherapy. Pollens, dust mites, and some fungi are aeroallergens that have been effectively suppressed with the use of allergy injections. Maintenance dose injections may continue for a pregnant woman who is not reacting regularly and continues to benefit from the immunotherapy (Blaiss, 2004). Because there is a 6- to 7-month interval before clinical benefits are seen and a significant risk of a systemic reaction, pregnancy is not a time for initiation of immunotherapy.
Other Pharmacologic Therapies
Antihistamines may be useful in the woman with a clear allergic stimulus to her asthma. The safest decongestant for use during pregnancy appears to be pseudoephedrine, although it has recently been linked to the birth defect gastroschisis (ACOG, 2008). Pseudoephedrine has been routinely used in the treatment of rhinitis, although intranasal corticosteroids are currently the most effective medications for this condition and carry a low risk of systemic effects. Avoidance of oral decongestants in the first trimester is suggested unless absolutely necessary. Pregnant women with asthma should be cautioned about use of over-the-counter medications because many of the medications contain vasoconstrictors that may cause fetal abnormalities and decreased uterine blood flow (NAEPP, 2005). The influenza vaccine is indicated for women with chronic asthma after the first trimester. Because it is an inactivated virus, the influenza vaccine poses no risk to the fetus.
LABOR AND BIRTH
Approximately 10% to 20% of women with asthma experience an exacerbation during the intrapartum period (Gluck & Gluck, 2006; Namazy & Schatz, 2006). The risk of dyspnea or wheezing can be minimized through ongoing asthma medication during labor and the postpartum period. An exacerbation
during labor is treated no differently than at any other time. Control of the asthma is a priority for safety of the mother and her fetus. Intravenous (IV) access should be established on admission (Gardner & Doyle, 2004). A peak flow rate should be taken on admission and then every 12 hours (Gardner & Doyle, 2004). If the woman develops symptoms of asthma, peak flows should be measured after treatments (Gardner & Doyle, 2004). If a systemic steroid has been administered in the past month prior to birth, additional rescue-dosed steroid therapy should be given during labor to prevent maternal adrenal crisis (Belfort & Herbst, 2010). IV hydrocortisone 100 mg every 6 to 8 hours should be administered for 24 hours or until oral medications are tolerated (Belfort & Herbst, 2010).
during labor is treated no differently than at any other time. Control of the asthma is a priority for safety of the mother and her fetus. Intravenous (IV) access should be established on admission (Gardner & Doyle, 2004). A peak flow rate should be taken on admission and then every 12 hours (Gardner & Doyle, 2004). If the woman develops symptoms of asthma, peak flows should be measured after treatments (Gardner & Doyle, 2004). If a systemic steroid has been administered in the past month prior to birth, additional rescue-dosed steroid therapy should be given during labor to prevent maternal adrenal crisis (Belfort & Herbst, 2010). IV hydrocortisone 100 mg every 6 to 8 hours should be administered for 24 hours or until oral medications are tolerated (Belfort & Herbst, 2010).
Air exchange is enhanced through patient positioning in a semi-Fowler’s or high-Fowler’s position. Potential for fluid overload can be avoided through strict intake and output measurements. Oxytocin is the drug of choice for the induction of labor because prostaglandin F2α is a known bronchoconstrictor (Frye et al., 2011; Towers, Briggs, & Rojas, 2004). The use of prostaglandin E2 for cervical ripening intracervically or intravaginally has not been reported to result in a clinical exacerbation of asthma (Namazy & Schatz, 2006). The pain relief method of choice for women in labor with asthma is epidural analgesia (Gardner & Doyle, 2004). Epidural analgesia can reduce oxygen consumption and may enhance the effects of bronchodilators (NAEPP, 2005). Meperidine and morphine sulfate are contraindicated because of their actions on smooth muscle and the potential for respiratory depression, and they may result in bronchospasm through histamine release (Belfort & Herbst, 2010). Butorphanol and fentanyl are appropriate substitutes (Belfort & Herbst, 2010).
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