By: Jeff Smith, CRNA and Karen Ramsey, CRNA
There was recently an emergent case of amniotic fluid embolism (AFE) here at the hospital we cover. Fortunately—for everyone involved—the patient and baby both made a miraculous recovery thanks primarily to the efforts of the anesthesia team, OR team and surgeons. In light of the recent studies showing improved outcomes when using atropine, ondansetron and ketorolac (AOK) during these incidences, we will briefly outline some of those studies and explain our experience using AOK for AFE.
Our case of AFE was on a young, healthy woman who was having an uncomplicated pregnancy. While in the laboring room, she suddenly felt ill and became unresponsive. A code blue was called and resuscitation efforts began. A stat cesarean section was done at the same time the patient was being resuscitated. A bedside echocardiogram was performed and demonstrated right ventricular strain and septal bowing which suggests pulmonary embolism versus AFE. The patient was successfully resuscitated and transported to intensive care where she later made a full recovery and was discharged home after two weeks. The baby did great, as well, and was discharged after one week.
It was determined that the patient had an AFE. AFE is a complication of pregnancy in which amniotic fluid or other debris enters into the maternal pulmonary circulation causing cardiovascular collapse. This may occur during labor, during cesarean section, after abnormal vaginal delivery or during the second trimester of pregnancy. It may also occur up to 48 hours post-delivery. The pathophysiology of AFE is not completely understood (Kaur et al.).
AFE is the second leading cause of maternal mortality in the USA with an incidence of 1:15,200 births (Rezai et al.). Previously, it was documented that 50 percent of patients die within the first hour and about two-thirds experience a high incidence of severe and permanent neurological damage within five hours of the event among survivors, although mortality rates have declined (Kaur et al.). The current case fatality rate and perinatal mortality associated with AFE are 13–30 percent and 9–44 percent, respectively (Rezai et al.).
Symptoms of AFE vary and are often very sudden and may involve many organ systems. Acute dyspnea or sudden agitation, sudden chills, shivering, sweating, coughing and anxiety are common premonitory symptoms (Kaur et al.). Other symptoms include altered mental status, hypotension, decreasing pulse oximetry, cyanosis, fetal bradycardia, etc. Four criteria must be present to make the diagnosis of AFE:
- Acute hypotension or cardiac arrest.
- Acute hypoxia.
- Coagulopathy or severe hemorrhage in the absence of other explanations.
- All of these occurring during labor, cesarean delivery, dilation and evacuation, or within 30 minutes postpartum with no other explanation of findings (Kaur et al.).
Key factors in the management of AFE are early recognition, prompt resuscitation and delivery of the fetus. Current recommended treatment for AFE includes pulmonary vasodilators, prostaglandins, sympathomimetics and a host of other interventions. Along with these systemic mediators, large amounts of blood products such as fresh frozen plasma and packed red blood cells are rapidly infused to combat disseminated intravascular coagulation. Other management methods such as bypass and exchange transfusion by cardiovascular surgery have also been reported in several cases (Rezai et al).
Atropine, Ondansetron, and Ketorolac (AOK) is another up-and-coming treatment modality. Recent studies have shown better prognosis with patients that had emergent treatment with AOK. These studies recommend therapy that targets serotonin and thromboxane A2. Atropine is given for vagal response, Ondansetron is given for serotonin and Ketorolac is given for thromboxane A2 (Hicks, T.L.). Beneficial effects of atropine (1mg) for treatment include decreased vasoconstriction in pulmonary vasculature and it ameliorates symptomatic bradycardia and heart blocks commonly observed in Phase I of AFE. Ondasetron (8mg) contributes to vagotomy via 5-HT3 antagonism which can prevent cardiovascular collapse. Ketorolac (30mg) inhibits formation of clots and the extension of clots in situ and decreases the cascade of inappropriate clotting (Hicks, T, L.).
The AFE case recently experienced at our hospital has brought up several new learning opportunities for our staff and it has also shown that many providers were not familiar with these new studies. We hope that by providing some brief insight on this new treatment option that other anesthesia providers will be inspired to learn more about the AOK treatment modality.
Kaur, K., Bhardwaj, M., Kumar, P., Singhal, S., Singh, T., & Hooda, S. (2016). Amniotic fluid embolism. Retrieved April 16, 2021, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4874066/#:~:text=The%20prognosis%20after%20AFE%20is,between%20maternal%20arrest%20and%20delivery.
Hicks, T. L., DNP, CRNA. (2017, November 1). AOK for AFE. Retrieved April 16, 2021, from https://www.arkansascrnas.com/wp-content/uploads/2017/11/AOK-for-AFE-HANDOUTS-no-references.pdf
Rezai, S., Hughes, A., Larsen, T., Fuller, P., & Henderson, C. (2017, December 21). Atypical amniotic fluid embolism managed with a novel therapeutic regimen. Retrieved April 16, 2021, from https://www.hindawi.com/journals/criog/2017/8458375/