Amniotic Fluid Embolism

Robert J. Miller, DO, Dorothy E. Dean, MD, Sarah Hamilton, MD, and Mark A. Gerhardt, MD, PhD

Distinguishing this life threatening obstetric emergency from other possible causes of hypotension and cardiovascular collapse is crucial to maximizing patient survival. This case illustrates the key role of transesophageal echocardiography in rapid diagnosis.

mniotic fluid embolism one of exclusion, and frequently it is Her obstetric history included one (AFE) is a rare, catastrophic not assigned until autopsy.6 previous pregnancy, four years earlier, complication of pregnancy In this article, we present a case of which culminated in a preterm deliv- A that occurs when the bar- AFE in which transesophageal echo- ery at 34 weeks gestation by cesarean rier between the amniotic fluid and cardiography (TEE) was used to ar- section (due to cephalopelvic dispro- maternal circulation is disrupted rive at a rapid and accurate diagnosis. portion). This delivery was success- (Figure 1).1,2 Although AFE was first While the patient in this case ulti- ful, with no complications. During reported in 1926 and expanded upon mately did not respond to resuscita- the current pregnancy, the patient in 1941,3,4 few advances in its diag- tive efforts, the ability of the team to had received no prenatal care until nosis and treatment have occurred rule out other entities in the differen- she presented to the obstetric clinic since then. To this day, AFE retains tial diagnosis spared her from ineffec- at 35 weeks gestation. At that time, a mortality rate of 60% to 80%, and tual treatment efforts that might have she was diagnosed with PIH, and she 50% of AFE survivors have perma- hastened her death or intensified her acknowledged her need for a repeat nent neurologic sequelae.2,5 suffering. cesarean section due to cephalopelvic While the clinical presentation of disproportion. The procedure was AFE is similar to that of pulmonary Initial exam scheduled, but the patient presented to thromboembolism and venous air A 34-year-old, white, pregnant the obstetric unit in labor prior to embolism, the etiology and treatment woman presented to the obstetric that date. options are distinctly different for unit of a university medical center at At the current presentation, her each entity. In order to provide the 39.43 weeks of gestation with sponta- medications consisted of prenatal appropriate treatment interventions neous onset of labor and pregnancy- vitamins, gentamicin for bacterial quickly enough to maximize chances induced hypertension (PIH). Her endocarditis prophylaxis (as recom- of recovery, therefore, prompt di- height was 114 cm (3 ft 9 in), her mended by her neurosurgeon fol- agnosis of AFE in parturients with weight was 65 kg (143 lb), and she lowing her VP shunt procedures), cardiovascular collapse is ideal—but had severe skeletomuscular abnor- rabeprazole for her GERD, and la- problematic. The diagnosis of AFE is malities. Her medical history was sig- betalol for her PIH. (She had been nificant for spina bifida (resulting in prescribed the beta-blocker labetalol

At the time of this writing, Dr. Miller was the di- paraplegia at the mid-thoracic level), rather than magnesium sulfate be- rector of obstetric anesthesia at the Ohio State seizure disorder, hydrocephalus, gas- cause magnesium sulfate can inter- University Medical Center, Columbus and an as- trointestinal reflux disorder (GERD), act with gentamicin to cause muscle sociate professor in the department of surgery at Wright State University, Dayton, OH. He is now a asthma, and tobacco use. She re- weakness.) The patient reported al- staff anesthesiologist at William Jennings Bryan ported no alcohol or drug abuse. Her lergies to intravenous pyelogram dye, Dorn VA Medical Center, Columbia, SC. Dr. Dean surgical history was significant for povidone-iodine solution, and ben- is a deputy director and forensic pathologist with the Franklin County coroner’s office in Columbus, Harrington rod placement, meningo- zoin—but said that she had no latex OH. Dr. Hamilton is a resident clinical instructor myelocele repair, ventricular-perito- allergy. There was no documentation in the department of obstetrics and gynecology neal (VP) shunt placement (multiple of a latex allergy in her records. She and Dr. Gerhardt is an assistant professor in the department of anesthesiology, both at the Ohio procedures), ureterostomy, ileostomy, had previously undergone radioal- State University Medical Center. colostomy, and knee arthroscopy. lergosorbent testing.

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Ultrasound evaluation confirmed the gestational age of the fetus, a non- stress test was reactive, and amnio- centesis revealed mature fetal lungs. The obstetrician elected to perform a repeat, low-transverse cesarean delivery due to the patient’s worsening PIH and history of cephalopelvic dispro- Joe Gorman © 2007. portion. The patient also requested elective sterilization. She was not a candidate for regional anesthesia (spinal or epidural) due to her difficult anatomic configuration, spina bifida, Harrington rods, and her history of multiple VP shunt revisions. The de- cision was made, therefore, to proceed with general anesthesia.

hospital Course The patient received standard aspiration prophylaxis medications (meto- clopramide, famotidine, and sodium citrate). She was taken to the operat- ing room, where standard American Society of Anesthesiologists moni- tors were applied and positioned with left uterine displacement. The fetal heart rate was determined to be 122 beats/min prior to anesthetic induction. Fetal exposure to the anesthetic agents was limited by abdominal preparation with chlorhexidine prior Figure 1. Amniotic fluid embolism, in which the introduction of amniotic fluid into the ma- to rapid sequence induction of gen- ternal circulation triggers a series of events that can include pulmonary hypertension, ex- eral anesthesia. Endotracheal intu- treme hypoxia, heart failure, and disseminated intravascular coagulopathy. In up to 80% bation was accomplished without of cases, these events result in death. difficulty or complications. The patient received 100% oxygen with des- flurane for maintenance anesthesia. orized due to extensive adhesions in 26 mm Hg, and her pulse oximetry Uterine incision occurred six min- the abdominal cavity. This is impor- reading decreased from 100% to 92%. utes after skin incision. Abdominal tant because, theoretically, exterioriz- In addition, her end-tidal carbon di- delivery of a viable female fetus by ing the uterus could have entrapped oxide level was noted to be acutely double, footling breech through the air or amniotic fluid into the maternal decreased. Her temperature declined incision was accomplished three circulation. from 36.2ºC to 35ºC over the ensu- minutes later. The infant’s one- and ing five minutes. five-minute Apgar scores were both A crisis develops Ephedrine and a fluid bolus were 6, while the one- and five-minute One minute following delivery of administered to reverse the hypo- umbilical cord blood gas pH values the fetus, the patient began to show tension, and these measures were were 7.24 and 7.30, respectively. The signs of hypotension. Her blood pres- effective initially. The patient was patient’s vital signs had been stable to sure declined acutely to 66/20 mm observed to have skin mottling and this point. The uterus was not exteri- Hg, with a mean arterial pressure of cyanosis. Sinus bradycardia was

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noted seven minutes after the senti- nel event, with a drop in heart rate from 90 to 42 beats/min. Pulseless electrical activity ensued 12 minutes after the inciting event and advanced cardiac life support resuscitative measures, consistent with the American Heart Association’s 2005 guidelines on cardiopulmonary resuscitation and emergency cardiovascular care,7 were instituted. Arterial and femoral central venous catheters were placed with difficulty. Initial resuscitative efforts resulted in restoration of an ac- Figure 2. Transesophageal echocardiography (TEE) of the cardiac chambers, performed ceptable blood pressure (143/55 mm to evaluate for pulmonary or venous air embolism. TEE examination of the right heart (left) Hg) with sinus tachycardia (heart and a five-chamber view of the heart in a coronal plane (right) show no mobile masses or air rate, 114 beats/min). The patient’s within the cardiac chambers. Abbreviations: AV = aortic valve; LA = left atrium; LV = left ven- core temperature continued to de- tricle; PA = pulmonary artery; RA = right atrium; RV = right ventricle; TV = tricuspid valve. cline to a nadir of 32.2ºC. A TEE probe was placed atrau- matically 20 minutes after the inciting event to assist with the differential diagnosis. There was no evidence of pulmonary thromboembolism in the right atrium and ventricle (Figure 2) or in the pulmonary arteries (Figure 3). The pulmonary artery was visu- alized along the entire length of the main artery and into the proximal left and right branches. Right ventricular dilation, right ventricular contractile dysfunction, and severe tricuspid regurgitation were noted consistent with (acute) pulmonary hypertension Figure 3. Transesophageal echocardiography (TEE) of the pulmonary artery bifurcation. and right ventricular failure (Figure Transverse plane TEE of the distal main pulmonary artery and bifurcation (left) demon- 4). There was no evidence of venous strates no saddle embolus. A close-up view of the bifurcation (right) is likewise devoid of air embolism. Moderate to severe cen- any echogenic signal. Abbreviations: Asc Ao = ascending aorta; PA = pulmonary artery; trally directed mitral regurgitation was L PA = left pulmonary artery; R PA = right pulmonary artery. noted and was consistent with acute left ventricular failure and papillary muscle dysfunction. The left ventricle found hypoxemia (pH, 7.16; partial dead 64 minutes after the initial epi- was dilated and demonstrated acute, pressure of carbon dioxide, 33 mm sode of hypotension. severe global hypokinesia, with an es- Hg; partial pressure of oxygen, 17 timated left ventricle ejection fraction mm Hg; bicarbonate level, 12 mmol/ Autopsy findings of 10% to 15% (Figure 5). L; base deficit, –15.8 mmol/L) despite Autopsy examinations confirmed the Resuscitative efforts were not suc- adequate ventilation and a fraction patient’s medical history and anatomic cessful in restoring viable hemody- of inspired oxygen level of 100%. abnormalities. Gross examination namics. Arterial blood gas analysis Hematologic analysis was consistent noted significant scoliosis; a “barrel- during resuscitative efforts demon- with disseminated intravascular coag- shaped chest”; lower extremities that strated metabolic acidosis and pro- ulation. The patient was pronounced were abnormally short and externally

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rotated; ileostomy, ureterostomy, and colostomy pouches; and a VP shunt extending from the left temporal lobe of the brain to the abdominal cavity, with clear cerebrospinal fluid. Chest radiographs confirmed the presence of Harrington rods. The skin was observed to be extremely pale, with no visual capillaries in the sclera (Figure 6), indicating profound blood loss. Of the conditions initially included in the differential diagnosis, pulmonary thromboembolism and venous air embolism appeared unlikely based on intraoperative TEE. Findings of the chest radiographs supported the exclusion of venous air embolism (as there were no radiolucent areas in the ventricles) and ruled out pneu- mothorax. The internal examination revealed a patent pulmonary arterial tree, with no thrombi or emboli, thus excluding pulmonary thromboembo- Figure 4. Color Doppler flow studies from transesophageal echocardiography of the car- lism as well. diac valve structures, showing severe tricuspid regurgitation (left) and moderate mitral The pericardium was smooth regurgitation (right). The patient’s lack of murmur on preoperative physical examination and intact. The coronary arteries suggests that these regurgitant lesions represent an acute change. were normal, without any stenosis or thrombosis. The pulmonary pa- renchyma exuded a marked amount The cause of death was deter- Both case reports and animal models, of blood but only a minimal amount mined to be disseminated intravascu- however, demonstrate that acute left of frothy fluid, and it was without lar coagulation secondary to AFE in ventricular dysfunction also occurs focal lesions. The abdominal cavity the immediate postpartum state. in the hemodynamic collapse that contained 1,300 mL of liquid blood, results from AFE. Specifically, case but no clotted blood was noted. This about the condition reports of AFE in humans have noted finding supported a terminal dissemi- Admixture of amniotic fluid into the acute left ventricle failure, which was nated intravascular coagulopathy. The maternal circulation is thought to be refractory to both inotropic and me- incision in the uterus was closed and commonplace following either vagi- chanical cardiac support.8,9 Release without exudate. There was no re- nal or cesarean delivery, but typically of systemic cardiac inhibitory factors tained placenta. it does not result in a physiologic appears to be responsible, in part, Microscopic examination of the problem. The clinical entity described for the left ventricle dysfunction. A lungs revealed squamous epithelial as AFE, on the other hand, results dose-dependent reduction in coro- cells in the maternal circulation, the in life threatening hypotension, hy- nary artery blood flow from human diagnostic feature of AFE (Figures 7 poxia, and disseminated intravascular amniotic fluid resulting in depressed and 8). There was no gross or micro- coagulation. cardiac function has been observed in scopic evidence of infection or inflam- Acute occlusion of the pulmonary a rat model.10 mation. Microscopic examination of vasculature with concomitant pul- The etiology of AFE and the the liver demonstrated portal triads monary hypertension, decreased oxy- physiologic disturbances responsible with normal hepatic cytoarchitecture gen exchange, and acute right heart for the extreme hypoxia, depressed and no evidence of fibrosis or inflam- failure initially was ascribed as the cardiac function, and coagulopathy mation, despite the diagnosis of PIH. pathogenesis of the AFE syndrome.4 are poorly understood. The entrain-

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ment of a foreign substance (fetal tissue) into the maternal circulation and release of endogenous mediators causes a profound myocardial depres- sion with resultant hypotension and decreased cardiac output. The exact mechanism by which this occurs, however, has remained elusive. Likewise, no established management strategy has been shown to improve fetal or maternal outcome. Supportive therapy is the primary method utilized to date. In this case, we directed our resuscitative efforts toward support of the acutely failing right and left heart and inadequate oxygenation. Figure 5. Transesophageal echocardiographic (TEE) evaluation of myocardial contractility. The role of TEE in diagnosis Transgastric TEE examination of the left ventricle (LV) at the mid-papillary muscle level demonstrates severe contractile dysfunction. The LV is shown in systole (left) and dias- Although our resuscitative efforts did tole (right); note that there is minimal change in the intraventricular cavity. The estimated not succeed, they were directed ap- LV ejection fraction is 10% to 15%, despite inotropic support with epinephrine. Abbrevia- propriately because of a rapid, defin- tions: A = anterior; L = lateral; P = posterior; S = septal. itive diagnosis made possible largely by TEE. The differential diagnosis in this case, based on the clinical presen- Some types of primary cardiogenic a hyperdynamic, empty heart— tation, included anaphylaxis, primary shock also were determined to be in- rather than an acutely failing heart with cardiogenic shock (arising, for exam- consistent with the patient’s presen- enlargement of all four chambers. ple, from acute myocardial infarction tation. The patient’s age and lack of Of the potential mechanical causes or massive hemorrhage), and mechan- risk factors for coronary artery dis- of the patient’s initial arrest, pneumo- ical etiologies (such as pneumotho- ease (such as familial dyslipidemia) rax, venous air embolism, pulmonary made infarction unlikely. And while thromboembolism, and AFE). TEE the physiologic stress of pregnancy helped us to exclude all of these pos- usually results in decompensation of sibilities except AFE within 15 min- undiagnosed chronic heart failure, utes of cardiovascular collapse. especially during the second trimes- Some potential causes of the pa- ter, the patient’s physical examination tient’s hypotension were excluded findings and term intrauterine preg- prior to TEE. Anaphylaxis, for in- nancy argued against a primary car- stance, was ruled out because the diac cause. clinical features of this case were not Hypovolemic shock could have consistent with the diagnosis. Spe- precipitated the initial hypotension, cifically, the care team avoided all tachycardia, and decreased end-tidal known allergens (including latex, carbon dioxide level, but the surgeons even though the patient had no his- did not note any dramatic hemorrhage Figure 6. The patient’s sclera at autopsy, tory of latex allergy), the timing of in the operative field. Occult hemor- showing a lack of vascular markings, the arrest was not associated with the rhage was a distinct possibility, given which suggests massive hemorrhage. This administration of any medications, the surgical challenges posed by this is a rare finding in amniotic fluid embolism. and the patient’s rapid development patient’s adhesions and skeletomuscu- In this case, it was most likely a result of of hypothermia is not a feature asso- lar abnormalities. If this were the case, disseminated intravascular coagulopathy. ciated with anaphylaxis. however, TEE would have shown

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thorax was excluded based on physical examination findings (bilateral breath sounds and a nondeviated trachea), observation of normal peak airway pressures during mechanical ventilation, and the absence of any significant risk factors (such as central line placement or attempts to place an epidural or spinal anesthetic) other than administration of Figure 7. Histopathologic image showing Figure 8. Histopathologic image of the ma- positive pressure ventilation. Venous fetal squamous epithelial cells in the maternal lung tissue, showing intravascular air embolism, pulmonary thrombo- ternal pulmonary tissue, which is highly thrombosis, consistent with disseminated suggestive of amniotic fluid embolism. embolism, and AFE, on the other intravascular coagulation. hand, were all considered strong pos- sibilities prior to TEE. lism. The hormones that support to prevent additional air entrainment. Venous air embolism can result pregnancy result in a hypercoagu- Once the diagnosis is made, venous when uterine venous structures are lable state. And since this patient was air embolism is treated with central exposed to the atmosphere and nega- bedridden due to her spina bifida, line placement for aspiration of air tive pressure allows the entrainment of stasis of blood within the lower ex- and with hyperbaric therapy. Pulmo- air into the vasculature. Cesarean deli- tremity veins was likely. Further- nary thromboembolism is treated by very is known to increase the risk more, her short stature and limitation thrombolysis and, rarely, pulmonary of venous air embolism. When a suf- of uterine mobility due to adhesions artery embolectomy or mechanical ficient air bolus is delivered to the might have resulted in significant cardiorespiratory support (extra- heart, an “air lock” can occur in the caval compression, which would be corporeal membrane oxygenation). right ventricle, impeding the transit expected to increase blood return In our patient, all of these therapies of blood from the great veins into the from the pelvic veins. would have been, at best, useless or, pulmonary system. Occasionally, the Acute right heart failure associated at worst, needlessly harmful. Throm- surgeon notes a sucking air sound in with acute pulmonary hypertension bolytic therapy, in particular, carries the field. and hypoxia are the hallmarks of pul- a significant risk in surgical patients A sudden increase in the end- monary thromboembolism. The left and might have had the effect of has- tidal nitrogen level is a sensitive and ventricle is hyperdynamic and under- tening death in this patient. Because specific indicator of venous air em- filled (decreased preload) because the TEE excluded venous air embolism bolism. On cardiac auscultation, a failing right heart is unable to deliver and pulmonary thromboembolism, mill-wheel murmur is noted. Other blood through the pulmonary vascu- we were not forced to consider any of signs and symptoms of venous air lature. In our patient, however, TEE these options. embolism are nonspecific and in- demonstrated that this was not the In summary, we believe that, de- clude hypoxia, cardiovascular col- case, which effectively excluded pul- spite the patient’s death, this case lapse, a decreased end-tidal carbon monary thromboembolism. This left shows TEE to be an important and dioxide level, and elevated cardiac only one option—AFE—to explain potentially lifesaving tool in cases of filling pressures (central venous pres- the patient’s condition, and autopsy acute hemodynamic instability. ● sure) and pulmonary artery systolic confirmed this diagnosis. and diastolic pressures, but not pul- It is important to note that, while Author disclosures monary capillary wedge pressure). venous air embolism, pulmonary The authors report no actual or poten- TEE is exquisitely sensitive to the thromboembolism, and AFE are tial conflicts of interest with regard to detection of intracardiac air, particu- all embolic in nature, their presen- this article. larly as it enters the right side of the tation and treatment strategies dif- heart.11 In this case, findings of TEE fer significantly. Whenever the Disclaimer excluded venous air embolism. diagnosis of venous air embolism is The opinions expressed herein are The patient also was at very high suspected, the obstetrician should those of the authors and do not risk for pulmonary thromboembo- flood the surgical field immediately necessarily reflect those of Federal

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