Williams Manual of Pregnancy Complications, 23 ed.

CHAPTER 50. Asthma

Asthma is a chronic inflammatory airway disorder with a major hereditary component that affects about 8 percent of the general population. The hallmarks of asthma are reversible airway obstruction from bronchial smooth muscle contraction, mucus hypersecretion, and mucosal edema. There is airway inflammation and responsiveness to a number of stimuli, including irritants, viral infections, aspirin, cold air, and exercise. The smaller functional residual capacity and increased effective shunt of normal pregnancy render the gravid woman more susceptible to develop hypoxemia. There is no evidence that pregnancy has a predictable effect on underlying asthma. Indeed, about one-third of asthmatic women can expect worsening of disease at some time during pregnancy, while the remainder either improve or remain unchanged. Because F-series prostaglandins and ergonovine exacerbate asthma, these commonly used obstetrical drugs should be avoided if possible.

Generally, unless there is severe disease, asthma has relatively minor effects on pregnancy outcome. Increased incidences of preeclampsia, preterm labor, low-birth weight infants, and perinatal mortality have all been associated with severe asthma. Life-threatening complications include status asthmaticus, pneumonia, pneumomediastinum, acute cor pulmonale, cardiac arrhythmias, and muscle fatigue with respiratory arrest. Maternal and perinatal mortality are substantively increased when mechanical ventilation is required.


Clinically, asthma represents a broad spectrum of illness ranging from mild wheezing to severe bronchoconstriction capable of causing respiratory failure, severe hypoxemia, and death. The functional result of acute bronchospasm is airway obstruction and decreased airflow. The work of breathing progressively increases and patients present with chest tightness, wheezing, or breathlessness. Subsequent alterations in oxygenation primarily reflect ventilation–perfusion mismatching, as the distribution of airway narrowing is uneven.

The clinical stages of asthma are summarized in Figure 50-1. With mild disease, hypoxia initially is well compensated by hyperventilation, as reflected by a normal arterial oxygen tension and decreased carbon dioxide tension with resultant respiratory alkalosis. As airway narrowing worsens, ventilation–perfusion defects increase and arterial hypoxemia ensues. With severe obstruction, ventilation becomes impaired sufficiently because of respiratory muscle fatigue to result in early CO2 retention. Because of hyperventilation, this may only be seen initially as an arterial CO2 tension returning to the normal range. Finally, with critical obstruction, respiratory failure follows, characterized by hypercapnia and acidemia.


FIGURE 50-1 Clinical stages of asthma. (Reproduced, with permission, from Cunningham FG, Leveno KJ, Bloom SL, et al (eds). Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010.)

The subjective impression by the patient of the severity of asthma frequently does not correlate with objective measures of airway function or ventilation. Clinical examination also is inaccurate to predict severity, but useful signs include labored breathing, tachycardia, pulsus paradoxus, prolonged expiration, and use of accessory respiratory muscles. Signs of a potentially fatal attack include central cyanosis and altered level of consciousness.

Arterial Blood Gas Analysis

Measurement of blood gases provides objective assessment of maternal oxygenation, ventilation, and acid–base status. Care must be taken to interpret the results in relation to normal values for pregnancy. For example, a pCO2greater than 35 mm Hg with a pH less than 7.35 is consistent with hyperventilation and CO2 retention in a pregnant woman.

Pulmonary Function Testing

Pulmonary function testing has become routine in the management of chronic and acute asthma. Sequential measurement of the forced expiratory volume in 1 second (FEV1) from maximum expiration is the single best measure to reflect severity of disease. The peak expiratory flow rate (PEFR) correlates well with the FEV1, and it can be measured reliably with inexpensive portable peak flow meters. These two measurements are the most useful tests to monitor airway obstruction. An FEV1 less than 1 L or less than 20 percent of predicted correlates with severe disease as manifest by hypoxia, poor response to therapy, and a high relapse rate.


Effective management of asthma during pregnancy includes objective assessment of pulmonary function, avoidance or control of environmental precipitating factors, pharmacological therapy, and patient education. In general, women with moderate to severe asthma are instructed to measure and record PEFRs twice daily. Predicted values range from 380 to 550 L/min, and each woman has her own baseline value. Recommendations for therapy adjustments can be made using these measurements.

Outpatient treatment depends on the severity of disease. Shown in Table 50-1 are medications and suggested doses for outpatient management of asthma in the pregnant woman. For mild asthma, β-agonistsgiven by inhalation as needed are usually sufficient. Inhaled corticosteroids are the preferred treatment for persistent asthma. Inhalations are administered every 3 to 4 hours as needed. The goal is to reduce the use of β-agonists for symptomatic relief. Cromolyn sodium (category B) and nedocromil inhibit mast-cell degranulation. They are ineffective for acute asthma and are taken chronically for prevention.

TABLE 50-1. Step Therapy of Chronic Asthma during Pregnancy



Theophylline is a methylxanthine, and its various salts are bronchodilators and possibly anti-inflammatory. Some of its derivatives are considered useful for oral maintenance therapy of outpatients who do not respond optimally to inhaled corticosteroids and β-agonists (see Table 50-1).

Leukotriene modifiers inhibit their synthesis and include zileuton, zafirlukast, and montelukast. They are given either orally or by inhalation for prevention and are not effective with acute disease. There is little experience with their use in pregnancy.


Treatment of acute asthma during pregnancy is similar to that for the nonpregnant asthmatic. An exception is a significantly lowered threshold for hospitalization of the pregnant woman. Most will benefit from intravenous hydration to help clear pulmonary secretions. Supplemental oxygen is given by mask. The therapeutic aim is to maintain the pO2 greater than 60 mm Hg, and preferably normal, along with 95-percent oxygen saturation. Baseline pulmonary function testing includes FEV1 or PEFR. Chest radiography is usually indicated. Continuous pulse oximetry and electronic fetal monitoring may provide useful information.

First-line pharmacological therapy of acute asthma includes use of a β-adrenergic agonist—epinephrine, isoproterenol, terbutaline, albuterol, isoetharine, or meta-proterenol. Corticosteroids should be given early to all patients in the course of severe acute asthma. Intravenous methylprednisolone, 40 to 60 mg, is usually given every 6 hours. Equipotent doses of hydrocortisone by infusion or prednisone orally can be given instead. Because their onset of action is several hours, it is emphasized that corticosteroids, whether given intravenously or by aerosol, are given along with β-agonists for treatment of acute asthma.

Further management depends upon the response to therapy. If initial therapy with β-agonists is associated with return of the PEFR to above 70 percent of baseline, then discharge is considered. Some women may benefit from longer observation. Alternatively, for the woman with obvious respiratory distress or in whom the PEFR is less than 70-percent predicted after three doses of β-agonist, admission is advisable. The woman should then be given intensive therapy to include inhaled β-agonists, intravenous corticosteroids, and close observation for worsening respiratory distress or fatigue in breathing.

Status Asthmaticus and Respiratory Failure

Severe asthma of any type not responding after 30 to 60 minutes of intensive therapy is termed status asthmaticus. During pregnancy, consideration should be given to early intubation when the maternal respiratory status continues to deteriorate despite aggressive treatment (see Table 50-1). Fatigue, CO2 retention, or hypoxemia is an indication for intubation and mechanical ventilation.


Regularly scheduled asthma medications are continued throughout labor and delivery. Stress-dose corticosteroids are administered to any woman given systemic steroid therapy within the preceding 4 weeks. The usual drug therapy is 100 mg of hydrocortisone given intravenously every 8 hours during labor and for 24 hours after delivery. The PEFR or FEV1 should be determined on admission. If asthma symptoms develop, then serial measurements are made after treatments.

In choosing an analgesic for labor, a nonhistamine-releasing narcotic, such as fentanyl, may be preferable to meperidine or morphine. Epidural analgesia for labor is ideal. For surgical delivery, conduction analgesia is preferred because tracheal intubation can trigger severe bronchospasm. In the event of refractory postpartum hemorrhage, prostaglandin E2 and other uterotonics should be used instead of prostaglandin F, which has been associated with significant bronchospasm in asthmatic patients.

For further reading in Williams Obstetrics, 23rd ed.,

see Chapter 46, “Pulmonary Disorders.”