Current explanations describe disruption of the maternal-fetal interface, which allows material from the fetal compartment to enter maternal circulation. This leads to abnormal activation of proinflammatory mediator systems, similar to the systemic inflammatory response syndrome (SIRS), and causes initial, transient pulmonary vasoconstriction and hypertension. Acute right ventricular failure is then followed by hemodynamic collapse from right ventricular infarction coupled with interventricular 300A Platelets x 103/lL septum displacement to the let and ultimately decreased let sided cardiac output. This right and now let ventricular dysfunc250 tion is followed by cardiogenic pulmonary edema and systemic hypotension. Concurrently in this process, acute respiratory fail ure with severe hypoxemia from shunting develops. Notably, the resulting multiorgan dysfunction is an interrelated process, with both the cardiac and pulmonary systems afecting each other. Women who survive beyond these first phases invariably have the third component of the classic triad-a consumptive coagulopathy. Similar to the coagulation process described earlier, the material from the fetal compartment containing tissue 50 factor activates factor VII. This leads to the development of DIC (see Fig. 41-29).
In those who succumb, postmortem histopathological ind1100 1200 ings may be obvious (Fig. 41-31). However, detection of such B Time(hours) material may require special stains, and even then, debris may not be seen. In one study, fetal elements were detected in 75 findings of fetal squames (arrows) packed into a small pulmonary percent of autopsies and in 50 percent of specimens prepared artery. B. Results of coagulation studies from the same woman from concentrated buy coat aspirates taken antemortem from with abruptly decreased fibrinogen levels and platelets and a pulmonary artery catheter (Clark, 1995). simultaneously increased fibrin split products.
Medicine, 2016). Additional supportive care measures such as intubation are usually necessary. During the phase of right ventricular failure, inotropic agents such as dobutamine may improve right heart output, and later systemic hypotension should be treated with vasopressors such as norepinephrine.
Excess fluid administration is discouraged due to risks of wors ening dilation of an already engorged right ventricle, which of the inteventricular septum.
lapse or during the ensuing phases of injly, a coagulopathy develops in most cases from activation of factor VII and X. This may be exacerbated by ongoing hemorrhage. A common source of obstetrical bleeding is uterine atony. herefore, immediate evaluation of coagulation parameters is prudent with concur rent clinical management of bleeding.
Clinical Outcomes. Most reports describe dismal outcomes with amnionic fluid embolism. his is likely influenced by underdiagnosis and reporting biases that favor the most severe cases with the highest mortality rates. Several reports are illustrative. From a California database of 1.1 million deliveries, the mortality rate with amnionic fluid embolism was 60 percent (Gilbert, 1999). In a report of34 mothers from China, 90 percent died (Weiwen, 2000). Death can be amazingly rapid, and 12 of the 34 died within 30 minutes. he mortality rate was somewhat better in the largest study from Canada. Of 120 women with an amnionic luid embolism, only a fourth died. Survivors commonly have profound neurological impairment. Clark (1995) observed that only 8 percent of women who lived despite cardiac arrest survived neurologically intact. Overall, prognosis appears to be more associated with disease severity and the attendant cardiac arrest than with any speciic treatment modality (Clark, 2014).