women, sepsis and difuse infectious pneumonia are the two most common single-agent ARDS causes. Pyelonephritis, puer peral pelvic infection, and chorioamnionitis are the most frequent causes of sepsis. As discussed on page 917, severe preeclampsia and obstetrical hemorrhage are also commonly associated with permeability edema. Importantly, more than half of pregnant women with ARDS have some combination of sepsis, hemor rhage, shock, and luid overload. The contribution of tranosion related acute lung injuy (TAIl) is unclear (Chap. 41, p. 791).
Endothelial injury in the lung capillaries releases cytokines that recruit neutrophils to the inflammation site. Here, they elaborate more cytokines to worsen tissue injury. There are three stages of ARDS development. First, the exudative phase follows widespread injury to microvascular endothelium, including the pulmonary vasculature, and there is also alveolar epithelial injury. These result in increased pulmonary capillary perme ability, surfactant loss or inactivation, diminished lung volume, and vascular shunting with resultant arterial hypoxemia. Next, the ibroprolierative phase usually begins 3 to 4 days later and lasts up to day 21. Last, theibrotic phase results from healing, and despite this, the long-term prognosis for pulmonary func tion is surprisingly good (Herridge, 2003; Levy, 2015).
With pulmonary injury, the clinical condition depends largely on the insult magnitude, the ability to compensate for it, and the disease stage. For example, soon after the initial injury, physical findings are absent except perhaps hyperventilation. And at irst, arterial oxygenation usually is adequate. Pregnancy-induced mild metabolic alkalosis may be accentuated by hyperventilation. With worsening, clinical and radiological evidence for pulmonary edema, decreased lung compliance, and increased intrapulmonary blood shunting become apparent. Progressive alveolar and interstitial edema develop with extravasation of inflammatory cells and erythrocytes.
Ideally, pulmonary injury is identified at this early stage, and speciic therapy is directed at the underlying insult. Further progression to acute respiratory failure is characterized by marked dyspnea, tachypnea, and hypoxemia. Additional lung volume loss results in worsening of pulmonary compliance and increased shunting. Difuse abnormalities are heard by auscultation, and a chest radiograph characteristically demonstrates bilateral lung involvement (Fig.
At this phase, the injury ordinarily would be lethal in the absence of ventilatory support. When shunting exceeds 30 percent, severe refractory hypoxemia develops along with metabolic and respiratory acidosis that can result in myocardial irritability, dysfunction, and cardiac arrest.
Reduced ARDS mortality rates have resulted from advances in care of the critically ill (Levy, 2015). his requires close attention to: (1) recognizing and treating underlying medical and surgical disorders, (2) minimizing procedures and their complications, (3) administering prophylaxis against venous thromboembolism, gastrointestinal bleeding, aspiration, and central venous catheter infection, (4) promptly diagnosing nosocomial infections, and (5) providing adequate nutrition.
FIGURE 47-1 Anteroposterior chest radiograph of a secondtrimester pregnant woman with marked bilateral parenchymal and pleural opacification secondary to acute respiratory distress syndrome (ARDS) due to pyelonephritis.