Pulmonary edema complicates 1 in 500 to 1000 deliveries and is associated most commonly with preeclampsia, preterm labor, fetal surgery, and infection. The use of β-agonists to forestall labor is associated with pulmonary edema, often in the setting of occult chorioamnionitis and sepsis. When tocolytic therapy is not used, most cases of pulmonary edema develop in older, usually obese women with chronic hypertension that is further complicated by preeclampsia. These cases are often precipitated by operative delivery with acute blood loss, anemia, and infection.
There are three general causes of acute pulmonary edema: (1) heart failure, (2) permeability edema from alveolar-capillary injury (ARDS, or adult respiratory distress syndrome) and (3) combination of these two problems. Permeability edema from acute pulmonary injury has been associated with a number of disorders listed in Table 45-1. Although most are coincidental, some are unique to pregnancy.
TABLE 45-1. Some Causes of Acute Lung Injury and Respiratory Failure in Pregnant Women
Adult respiratory distress syndrome (ARDS) is the most common cause of respiratory failure in pregnancy. It includes both pulmonary alveolar epithelial injuries sustained via the airways and endothelial injuries sustained via the pulmonary vasculature. After recruitment to the site of inflammation by chemokines, neutrophils accumulate and initiate tissue injury by secretion of cytokines. This results in increased pulmonary capillary permeability, loss of lung volume, and shunting with resultant arterial hypoxemia. Pregnant women with ARDS have a mortality rate of 25 to 40 percent, with perinatal mortality rates.
With pulmonary injury, the clinical condition depends largely on the magnitude of the insult, the ability to compensate for it, and the stage of the disease. For example, if the woman presents soon after the initial injury, there commonly are no physical findings except hyperventilation, and arterial oxygenation usually is adequate. With continued insult, or with time, auscultatory and radiological evidence for pulmonary disease becomes more obvious. There will usually be decreased lung compliance and increased intrapulmonary blood shunting. Progressive alveolar and interstitial edema develop with extravasation of inflammatory cells and erythrocytes.
Further progression results in acute respiratory failure characterized by marked dyspnea, tachypnea, and hypoxemia. Further loss of lung volume results in worsening of both pulmonary compliance and increasing intrapulmonary shunts. There are diffuse abnormalities by auscultation, and the chest radiograph characteristically demonstrates bilateral lung involvement. At this phase, injury has progressed to a point that ordinarily will be lethal in the absence of treatment with high concentrations of inspired oxygen. Positive airway pressure, whether by mask or by intubation, is frequently necessary at this stage for airspace recruitment.
During the final phase of the respiratory distress syndrome, intrapulmonary shunts in excess of 30 percent result in severe and refractory hypoxemia. The marked increase in dead space, often exceeding 60 percent of tidal volume, leads to hypercapnia and an inability to provide ventilation and oxygenation. Metabolic and respiratory acidosis can result in myocardial irritability, dysfunction, and cardiac arrest.
In acute and severe lung injury, attempts are made to provide adequate oxygenation of peripheral tissues while ensuring that therapeutic maneuvers do not further aggravate lung injury. Support of systemic perfusion with intravenous crystalloid and blood is imperative. Pulmonary artery catheterization does not improve outcomes. Because sepsis is commonplace in lung injury, empirical antimicrobial therapy is given.
Reasonable goals in caring for the woman with severe lung injury are to obtain a PaO2 of 60 mm Hg or 90 percent oxyhemoglobin saturation at an inspired oxygen content of less than 50 percent, and with positive end expiratory pressures of less than 15 mm Hg. Delivery of the fetus does not improve maternal oxygenation.
Treatment of critically ill women with acute respiratory failure also requires assiduously detailed attention to fluid balance, because fluid overload further compromises pulmonary status. Intake and output records should be supplemented with daily weights. A mechanically ventilated patient retains an extra liter of fluid daily. Because respiratory distress syndrome is characterized by a pulmonary permeability defect, fluid leaks into the interstitium, even at normal pressures. Thus, it is best to maintain the lowest pulmonary capillary wedge pressure possible while avoiding decreased cardiac output.
For further reading in Williams Obstetrics, 23rd ed.,
see Chapter 42, “Critical Care and Trauma.”