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Rare but potentially catastroph-ic, amniotic fluid embolism(AFE) can occur suddenly andwithout warning. This poorlyunderstood condition carrieshigh maternal and neonatalmorbidity and mortality rates.In this article, I’ll describe AFEand its suspected pathophysiolo-gy, and discuss how to interveneif your patient develops AFE.

First identified in 1926, AFEdevelops in roughly 1 in 8,000to 80,000 pregnancies, and car-ries a maternal mortality rate ashigh as 80%.1,2 It occurs whenamniotic fluid and fetal cellsenter the maternal circulation,triggering a cascade of eventsthat can quickly lead to coagula-tion problems and organ failure.

About half of all women whodie from AFE die in the firsthour after symptom onset; the

rest succumb to coagulopathiessuch as disseminated intravas-cular coagulation (DIC).3 Of thewomen who survive AFE,about 85% have neurologicdamage.2 If AFE occurs duringlabor, most fetuses survive butabout 50% have neurologicimpairments.

What goes wrong?Amniotic fluid embolism candevelop during pregnancy,labor, cesarean section, or post-partum. To better understandAFE, researchers at theUniversity of Utah School ofMedicine created a nationalregistry in 1988.2 From thecases submitted to the registry,they concluded that exposure toeven small amounts of amnioticfluid might, in a susceptiblepatient, initiate a syndrome

Here’s how to respond when a patient developsthis rare pregnancy complication.

By Anne M. Schoening, RN, MSN

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similar to anaphylactic or septicshock. (See What triggers AFE?)

Although the syndrome ispoorly understood, it can bedescribed as a two-stage processcharacterized by varying degreesof hypoxia, hypotension, andcoagulopathy. If your patient alsohas DIC, you’ll see ecchymosisand bleeding from intravenous(I.V.) sites and other invasive lines;tachycardia; a weak or threadypulse; falling blood pressure (BP);cold, clammy, or cyanotic skin;decreased urine output; anddecreased level of consciousness.4

Any one of these clinical signsmay predominate, making itdifficult to recognize AFE. Forexample, in some cases, coagu-lopathy may be the initial oronly sign.5

In the first stage, amniotic fluidand fetal cells enter the maternalcirculation, triggering the releaseof endogenous mediators.2 Pul-monary artery vasospasm andpulmonary hypertension lead toelevated right ventricular pres-sure, and the resulting hypoxiadamages the heart and pulmonarycapillaries. Eventually, the left

side of the heart fails and thepatient develops acute respiratorydistress.3

About half of all patients whosurvive the first stage enter asecond stage characterized byhemorrhage and DIC. Amnioticfluid contains thromboplastin,which may initiate the clottingcascade.5

Postpartum cases of AFE(occurring 30 minutes or moreafter delivery) may be causedby various factors. Slow-releas-ing substance of anaphylaxis(leukotrienes) may delay the ini-tial signs and symptoms insome patients.2 Another theoryis that amniotic fluid lodges inthe uterine veins during deliv-ery and later is released into thecirculation during involution.6

Researchers speculate that signsand symptoms may occur morethan an hour after cesarean sec-tion if amniotic fluid becomestrapped in uterine veins and isreleased into the maternal cir-

culation with the return ofsympathetic tone and sponta-neous movement after spinalanesthesia.

Recognizing signs andsymptomsBecause no test can diagnosisAFE, your assessment skills arecritically important. Suspect thiscondition if a woman experiencessudden cardiovascular collapseduring pregnancy, labor, or post-partum, particularly if there’s noother explanation for her signsand symptoms. Many patientswith AFE develop acute dyspneafollowed by severe hypotension.Some women may developseizures or seizurelike activity.Other possible signs and symp-toms include cough, cyanosis,fetal bradycardia, pulmonaryedema, cardiac arrest, and uter-ine atony (if postpartum).3

If your patient develops AFE,your interventions during theacute phase are aimed at oxy-genating mother and fetus,maintaining cardiac output andBP, expediting delivery if neces-sary, correcting coagulopathies,and providing emotional supportfor the patient and family. Prepareto treat respiratory or cardiacarrest following advanced cardiaclife support guidelines. Be readyto assist with endotracheal intu-bation if necessary. Assess thepatient for signs of seizure activ-ity and take seizure precautions.Administer oxygen by face maskand monitor maternal oxygensaturation.

If the patient hasn’t delivered,have an experienced obstetricnurse perform electronic fetalmonitoring. Notify the obstetricand neonatal teams, includinganesthesia, and prepare for sur-

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Amniotic fluid embolism

What triggers AFE?When amniotic fluid enters thebloodstream, researchers thinkthat the body regards it as a for-eign substance and releasesendogenous mediators such ashistamine, bradykinin, cytokines,prostaglandins, leukotrienes, andthromboxane. These mediatorsare responsible for the clinicalsigns and symptoms of AFE. Theconcept of AFE as an immunolog-ic reaction is supported by the factthat more than half of the womenin the national registry were carry-ing a male fetus, and many hadknown drug allergies or atopy.2

Because no test candiagnose AFE, your

assessment skills arecritically important.

gical delivery and neonatalresuscitation. Collect samplesfor lab tests as ordered. Thesemay include a complete bloodcell count with platelets, typeand crossmatch (if not done previously), and DIC panelincluding prothrombin time,activated partial thromboplastintime, d-dimer, and antithrombinIII levels.8

Prepare to administer bloodproducts and coagulation factorsif ordered. Have pressor agentssuch as dopamine, norepineph-rine, and dobutamine ready fortreating hypotension. To treatanaphylactic-like signs and symp-toms, be prepared to administerI.V. corticosteroids and histamine1and histamine2 agents.3,4

Teach survivors about thedisorder and the long-termplan for recovery and rehabili-tation. Women also may havequestions about future preg-nancies, but limited researchis available on this. One studyfound six cases of successfulpregnancy after AFE, with norecurrence of AFE. In one case,the patient was treated withcorticosteroids before deliveryto reduce the theoretical riskof recurrence.9 Women shoulddiscuss the risks of future preg-nancies with their healthcareprovider and obstetrician.

Future hope?The AFE registry in the UnitedStates has closed, but a similarregistry in the United Kingdomis tracking cases. A worldwideregistry that would include post-partum cases and information ontreatments may help identifyeffective therapies for AFE. Forexample, drugs that block thesuspected mediators of AFE

(such as leukotrienes) may holdpromise for the future.

In the meantime, by knowinghow to intervene for a patientwith AFE, you can give her andher baby a better chance atsurvival. ❖

REFERENCES1. Benson MD. Nonfatal amniotic fluidembolism: Three possible cases and a newclinical definition. Arch Fam Med. 2(9):989-994, September 1993.

2. Clark SL, et al. Amniotic fluid embolism:Analysis of the national registry. Am J ObstetGynecol. 172(4 Pt. 1):1159-1167, April 1995.

3. Moore LE, Ware D. Amniotic fluidembolism. http://www.emedicine.com/med/topic122.htm. Accessed August 31, 2005.

4. Gilbert ES, Harmon JS. Manual of HighRisk Pregnancy and Delivery, 3rd edition.St. Louis, Mo., Mosby, Inc., 2003.

5. Gei A, Hankins G. Amniotic fluid embolus:An update. Contemporary OB/GYN. 45:53-66,January 2000.

6. Courtney LD. Coagulation failure inpregnancy (letter). BMJ. 1(5607):691, March14, 1970.

7. Margarson MP. Delayed amniotic fluidembolism following cesarean section underspinal anesthesia. Anaesthesia. 50(9):804-806,September 1995.

8. Mansen T, McCance K. Alterations ofhematologic function. In Huether S, Mc-Cance K (eds), Understanding Pathophysiology,3rd edition. St Louis, Mo., Mosby, Inc., 2004.

9. Stiller RJ, et al. Successful pregnancy af-ter suspected anaphylactoid syndrome ofpregnancy (amniotic fluid embolus): A casereport. J Reprod Med. 45(12):1007-1009,December 2000.

Anne M. Schoening is an assistant professor inmaternal/child nursing at Creighton UniversityMedical Center School of Nursing in Omaha, Neb.This article was adapted and updated fromSchoening AM, Amniotic fluid embolism:Historical perspectives and new possibilities,Maternal Child Nursing, March/April 2006.

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