The process of labor and delivery is considered to be a joyous event in women’s lives, and most of the time it is. However, practitioners have to be aware of potential complications that can have dire adverse outcomes, causing maternal morbidity and mortality as well as severe consequences for the baby.
In considering such complications, physicians usually think of women who have serious underlying comorbidities. However, the three complications discussed here – amniotic fluid embolism, ruptured uterus, and peripartum cardiomyopathy – are conditions that can happen to otherwise young, healthy women. Fortunately these complications are rare. However, when they do happen, early recognition and prompt intervention are critical to optimizing the outcome. This means we must continually keep a high index of suspicion for all such complications so that we are ready in the event that labor and delivery does not proceed normally.
Amniotic Fluid Embolism
By Dr. Valerie E. Whiteman
This complication is a leading cause of maternal morbidity and mortality in the United States and other developed countries. It should be considered in any patient who has sudden, unheralded cardiopulmonary collapse followed by profuse hemorrhage associated with disseminated intravascular coagulation (DIC).
While the hallmark presentation of amniotic fluid embolism (AFE) is this profound cardiopulmonary collapse with severe hemorrhage, it is important to note that published definitions of the condition state that coagulopathy may occur in isolation. In a 2011 review, Dr. Michael Benson points out that at least six case reports have described coagulopathy alone as the sole clinical sign of AFE (Clin. Dev. Immunol. 2012:946576 Epub 2011 Sept. 29 [doi:10.1155/2012/946576]).
AFE is a diagnosis of exclusion, and one that is based on symptoms and clinical presentation rather than on laboratory testing or histopathologic examination. There is broad consensus that a clinical diagnosis of AFE can be made based on one or more of four key signs/symptoms (in the absence of other medical conditions or explanations): cardiovascular collapse (hypotension and/or cardiac arrest); respiratory distress; DIC; and coma and/or seizures.
The condition can occur suddenly and unpredictably at any point during labor and delivery or in the immediate postpartum period. It also has been reported to occur as late as 48 hours after delivery.
Pulmonary thromboembolism often may be suspected, and indeed, it is part of the differential diagnosis. Patients with thrombotic pulmonary embolism do not usually develop the classic DIC type of coagulopathy, however, while patients with AFE are coagulopathic and often hemorrhage profusely.
The incidence of AFE has been difficult to determine. The authors of a 2009 evidence-based review of AFE reported that the estimated incidence based on large population-based studies is 1 in 15,200 deliveries in North America and 1 in 53,800 deliveries in Europe (Am. J. Obstet. Gynecol. 2009;201:445.e1-13). The incidence in an Australian population-based cohort was recently reported to be 3.3 per 100,000 deliveries (BJOG 2010;117:1417-21).
Other published reports and reviews have described an extremely broad range of estimated incidence. For instance, a report in the journal Anesthesia and Analgesia, published by the International Anesthesia Research Society, stated that AFE may occur between 1 in 8,000 and 1 in 80,000 deliveries (Anesth. Analg. 2009;108:1599-602).
The pathophysiology of AFE also is poorly understood, causing us great uncertainty as to why some apparently stable patients undergo such a profound, life-threatening collapse. When AFE was first described more than 70 years ago, it was thought to result from amniotic fluid entering the maternal circulation and obstructing the pulmonary blood flow – thus the name "amniotic fluid embolism." However, research over the decades has consistently discounted this view. As Dr. Benson states, current thinking has shifted away from embolism and toward a maternal immune response to the fetus.
Investigators have suggested possible immunologic mechanisms such as complement activation and reactions similar to anaphylaxis, but more research needs to be done. In the meantime, we must recognize that the name AFE probably does not accurately reflect what actually occurs in these patients.
Management is usually first directed at getting the patient through the initial cardiovascular insults – often hypotension and cardiac arrest – and at treating hypoxia and rapidly correcting maternal hemodynamic instability. Significant teamwork is required for the mother and baby to survive – and to survive neurologically intact. Anesthesia is needed for development and control of the airway, for instance, and critical care is essential for inotropic support. Cardiology also must be involved, as continuous cardiac, respiratory, and blood pressure monitoring – and aggressive respiratory and circulatory support – are key.
The nursing staff also can play a critical role in preventing subsequent pulmonary edema by keeping meticulous records of the intake and output of fluids. The overwhelming insult of AFE to the heart and lungs leaves patients at high risk of developing pulmonary edema, and meticulous record-keeping can help ensure that these patients are not overloaded.