Code Blue Birth
By Deanna Isaacs

In the spring of 1992 Michael Benson got a potentially brilliant idea about a mysterious disease known as amniotic fluid embolism. AFE comes out of nowhere to kill women and their babies in the midst of childbirth. According to the medical literature, as many as half the women it strikes are dead within an hour of the first recognized symptom. Many of the rest die the same day or are reduced to a vegetative existence.
The idea came to Benson, an obstetrician and gynecologist practicing in Chicago's northern suburbs, as a result of his experience with three patients. I had come to Benson's office to pick up a copy of his first research paper. I was trying to make sense of my daughter's death in childbirth a few months earlier. Eleven days past her due date, she had gone to a major hospital in Phoenix for a routine induction of labor and come out dead.
In the days before the induction she'd had symptoms none of her caregivers seemed to notice and that she didn't know could be serious: shortness of breath, nosebleeds and bleeding gums, a bad taste in her mouth, a feeling of intense nervousness, lower abdominal tenderness, pain in her hands and legs, a rash of small red spots on the back of one hand and across her cheeks, swelling at her ankles, slightly bruised-looking toes, and a slight distention on the side of her neck. She was small, barely five feet tall, and had gained more than 40 pounds during the pregnancy. It looked like she was carrying a large baby, but her doctor made no special attempt to determine the size, in spite of a warning from one of his partners that if she carried to term she might not be able to have a vaginal birth.
At the hospital the morning she died, hours before her cardio respiratory collapse, she had prolonged bleeding at the IV-line puncture site, a relatively slow pulse that got significantly slower, a recurrence of the bad taste in her mouth, more shortness of breath, a cough, anxiety, chills, and severe, continuous pain, even between contractions. Neither her doctor nor any other obstetrician saw her during the six hours of induced labor that culminated in her death.
A little after seven that morning a young staff nurse came on duty. In words that haunt my family now, she announced to my daughter and her husband that she would be aggressive with the Pitocin so they "wouldn't have to be there all day." (Pitocin, used to stimulate contractions, is a synthetic hormone similar to the oxytocin the body produces.) She jacked up the dose repeatedly, until it was twice the manufacturer's generally recommended maximum though the contractions were already rapid and excessively painful, the baby failed to drop into place, and the cervix never dilated more than one to two centimeters. (Four days earlier my daughter had undergone a "cervical ripening" procedure: a prostaglandin tissue-softening gel had been placed inside her cervix three times at two-hour intervals, an unusually fast rate; the hospital would later change it to once every six hours.)
The nurse injected a narcotic, apparently without trying to figure out why her patient was having so much pain. Near noon a family-practice resident on obstetrics rotation came by to do a vaginal exam and unintentionally broke the amniotic sac. With my daughter flat on her back, a small amount of dark olive green, meconium-stained amniotic fluid ran out. (Meconium is the baby's first bowel movement; its presence in the amniotic fluid can be dangerous, though it's not uncommon.) The nurse lifted my daughter's hips to place a clean sheet under her. Within seconds, my daughter said she felt nauseated, stopped breathing, and had a convulsion. When they felt for a pulse, there was none.
A "code team" arrived, delivered her baby by cesarean section, and continued attempts to revive her, though they weren't sure what had gone wrong. About 45 minutes into the crisis, a doctor emerged to ask permission to do open-heart massage. "A blood clot must have traveled up from her legs," he said. The baby survived, but after an hour and a half of frantic efforts with staff rushing blood and equipment into the low-risk birthing area she'd been assigned to a wall of inscrutable strangers in green scrubs came out to tell us she was going to die.
By this time they'd settled on the cause, something we'd never heard of. She had amniotic fluid embolism, they said. Amniotic fluid somehow got into her bloodstream and traveled to her lungs, shutting them down. (Months later, poring over the hospital records, we would learn that when they opened her uterus for the C-section, they found bloody amniotic fluid and a placenta that had partially ripped away from the uterine wall.) They assured us nothing could have been done. "It's very rare and almost always fatal, and it happens in an instant," they said. "Tragic, but there's no way to see it coming or head it off."
No way to see it coming? We stared back at them, already thick with grief, and heard my daughter's voice as I had heard it on the telephone early that morning. "I'm having some discomfort already," she'd said. "High up, oddly enough. Like shortness of breath."
When we left the hospital I went to my daughter's home and pulled her well-read copy of What to Expect When You're Expecting from her bookshelf. There was no entry for amniotic fluid embolism in the index, no warning of any associated factors or possible symptoms. As far as anyone reading this book could tell, amniotic fluid embolism didn't exist.
By the time I got to Michael Benson's office four months later, I'd begun to read some of the numerous papers on amniotic fluid embolism in the medical literature. While estimates of its frequency are all over the map from 1 out of 5,000 to 1 out of 80,000 I realized that its characterization as an extremely rare occurrence was misleading. The hospital where my daughter died has about 6,500 deliveries each year. According to information provided by the hospital, during the five-year period from 1990 to 1995 it recorded five cases of AFE, or about 1 in every 6,500 births.
In America today AFE is the number one killer of women during or near the time of childbirth. It is, as one doctor put it, "every obstetrician's nightmare." It is also their best-kept secret.
Most accounts of the history of amniotic fluid embolism note that the syndrome was first described in a 1926 Brazilian medical-journal article by J.R. Meyer. It's hard to find anyone who's actually read that article, and it appears that little note was taken of it until 15 years later, when AFE burst into the English-language medical literature as a full-blown disease, "discovered" not by an obstetrician but by a pair of University of Chicago pathologists suspicious about an obstetric diagnosis.
The diagnosis was an old standby called "obstetrical shock," invoked whenever an apparently healthy woman died inexplicably during labor or soon after delivery. The understanding was that the woman had succumbed to shock (basically a collapse of the vascular system) brought on by hemorrhaging. If there wasn't any obvious sign of hemorrhaging, no matter; one could assume the bleeding had been internal. This was convenient for the attending doctor, who needed to be able to cite a cause of death.
But there was something odd about some of these cases. Paul Steiner, then a senior pathology department faculty member at the University of Chicago, had noticed that the patients seemed to have gone into shock before they started to hemorrhage. If this were true, the purported cause of death would be bogus. Steiner had been mulling this over for some time when Clarence Lushbaugh, a 24-year-old graduate student, tried to bluff his way through an autopsy by invoking the obstetrical-shock diagnosis.
Lushbaugh was working on a doctorate in pathology, supporting himself by doing weekend autopsies at Billings Hospital. Strapped for cash, he considered himself lucky when he was assigned a 26-year-old woman who'd died during labor. Since the woman had died without delivering, he would get paid for two autopsies.
"We weren't supposed to have any predetermined ideas about what happened,  Lushbaugh said when I spoke with him in the fall of 1994. "The cause of death was supposed to be discovered in the course of the procedure." Still, he knew from the hospital records that this patient had gone through 31 hours of labor and that her water bag had broken, releasing amniotic fluid containing meconium. It looked as if she'd died from acute heart failure.
Lushbaugh scanned the body for irregularities. He saw the remains of a white froth around her mouth, but nothing else unusual. The lungs were bloated and heavy. When he cut into them a thin, pink, frothy fluid oozed out of the liverish surface. He noted this is a sign of pulmonary edema. He also saw that the heart was out of whack - the right side distended like a balloon, the left side contracted. The spleen was enlarged, but Lushbaugh knew this wouldn't be unusual in pregnancy. He removed the fetus. It weighed 3,500 grams and looked normal. The amniotic fluid that remained in the uterus was thick and dark with meconium. There was no sign of unusual bleeding.

The autopsy had revealed some fluid in the lungs, but it had failed to turn up a cause of death. "This woman didn't hemorrhage, so it was a dilemma as to what to put down on the death certificate," Lushbaugh recalled. He hesitated, then did what was usually done: attributed the death to obstetric shock.
On the Monday afternoon when Lushbaugh presented the case as obstetric shock, Paul Steiner was lying in wait.
"Did you see what is in the blood vessels?" Lushbaugh remembers Steiner asking. Over the course of a long career, a few incidents can burn themselves into memory so deeply they can be summoned up in their entirety decades later. When I spoke with Lushbaugh he could still hear his own flippant reply "Yes, blood" and the silence that followed.
"No," Steiner barked. "Look what's in the blood vessels of the lungs: squamous cells from the baby's skin, hair and foreign bodies that are reacted to by leukocytes. And this blood was all clotted up. This woman actually died of right-heart shock. The blood was stopped in the lungs. It's a cardiac death, death due to the fact that blood is not returned in sufficient quantity to the heart, and the heart, pumping it out, pumps itself dry."
In spite of Lushbaugh's gaffe, Steiner recruited him as his assistant, and the two began reviewing old cases of maternal death. "We got out eight cases of obstetrical shock from Chicago Lying-In Hospital," Lushbaugh recalled. "They had all been signed out as hemorrhage." As they read one case history after another, some patterns started to take shape. Several of the women had carried past their due dates, many had larger-than-average babies, and most had very hard labor before going into shock. They felt anxious and complained of chills (classic signs of pulmonary embolism, the obstruction of a blood vessel by an abnormal substance), had trouble breathing, and began to turn blue. Some vomited or were delirious. Blood pressure readings quickly fell; pulses became rapid and weak, then disappeared; hemorrhaging sometimes followed. In every case where the amniotic fluid had been observed, it contained meconium� something that immediately struck Steiner and Lushbaugh as significant.
When they put slides of lung tissue from each woman under a microscope they believed they'd hit the jackpot. Some arteries and many smaller capillaries were clogged. Globs of mucus, fat, and skin cells (squamous cells), which they assumed were from the fetus, had stuffed the tiny passageways. The clogging had been worsened by clusters of the mother's white blood cells sent to engulf the foreign material and destroy it; when these soldier cells attached themselves to the invading particles, they added to the bulk. Seeing nearly half of the arteries clogged in some sections, Steiner and Lushbaugh were convinced there was enough blockage to kill. "The amount of embolism certainly exceeds that which we have seen in some cases of fatal pulmonary fat embolism," they noted. There were two major questions left to answer. First, was an amniotic fluid infusion  the definite cause of death, or was this some sort of incidental finding that would show up in any pregnant woman? To address this, Steiner and Lushbaugh examined lung tissue from 34 women who'd died of other causes during or near childbirth. With the exception of a trace of mucus in a capillary from one of these patients, they found no sign of fetal debris. Second, would a dose of amniotic fluid in the bloodstream produce the syndrome these patients had exhibited? To test this, Steiner and Lushbaugh injected rabbits and dogs with human amniotic fluid and meconium. They found that filtered fluid (all particles removed) produced no reaction at all. But unfiltered fluid brought on the same symptoms seen in the eight dead women�and straight meconium produced them faster and with greater severity. Three cubic centimeters of meconium injected into a vein in a rabbit's ear brought on restlessness, gasping, convulsions, and death within ten minutes. The two pathologists were satisfied that they'd proved their theory.
At this point, Lushbaugh recalled, a confident Steiner sat down to write "the paper to end all papers" on this syndrome. Published in JAMA in April 1941, the article was so long it had to run in two issues. It made obstetric shock instantly obsolete, offering in its place a syndrome Steiner named amniotic fluid embolism.
Briefly, their paper said: Amniotic fluid embolism is shock coming on during or shortly after labor. Predisposing factors include exceptionally strong contractions, meconium in the amniotic fluid, a dead or unusually large fetus, previous pregnancies, and an older mother. Fatal cases seem to occur at the rate of 1 in 8,000 births (they revised this estimate to a lower frequency in a subsequent paper); nonfatal cases go unrecognized and probably occur more often. Indeed, Steiner and Lushbaugh wrote, mild AFE may be the cause of many instances of postpartum hemorrhage: "Instead of being considered a rarity among obstetric complications, this must be thought of as one of the commonest."
Steiner and Lushbaugh believed "excessively powerful" uterine contractions prepared a route for the embolism by tearing the placenta and other tissue and forcing the amniotic fluid into open maternal veins. But they also guessed that the result was more than just a mechanical obstruction of blood vessels by particles in the fluid. "Probably reflexes are initiated," they wrote, "which produce vascular spasm in the lung [a clenching of the blood vessels] and a depressant action on the heart."
Finally, they observed, these symptoms resemble "anaphylactic shock," with effects similar to a severe allergic reaction; to be sure of the diagnosis one would have to examine lung tissue under a microscope, which could be done only in fatal cases. As preventive measures, they advised: "Control those conditions which lead to the presence of meconium in the amniotic fluid, and those which prevent its free drainage once it is present." Exceptionally strong or long contractions "should be considered to be potentially dangerous." As treatment they recommended administering drugs to relieve vasospasms in the lungs and any slowing of the heart.
They also noted that "two measures commonly used to combat shock"�epinephrine and blood transfusions� tend to make matters worse because they increase the accumulation of fluid in the lungs.
For the next four and a half decades the papers on AFE that appeared sporadically in the medical literature followed Steiner and Lushbaugh's lead. Many were written by obstetricians who'd encountered a single case. Some were reports of animal studies. A few reviewed a collection of cases. None advanced knowledge about  the syndrome much beyond where the two pathologists had left it.
In 1986, on the 45th anniversary of Steiner and Lushbaugh's original paper, JAMA paid them an extraordinary tribute. The journal republished their paper in its entirety, designating it a "landmark" work and noting that the small gains that had come since were the result of advancing technology rather than any significant new insight. In an introductory essay pathologist Kris Sperry lauded the Steiner and Lushbaugh paper as one of those rare contributions to the medical literature that provide such a solid description of a disease that "subsequent decades of research and meticulous study fail to substantially improve on the original."
As Sperry pointed out, maternal death from other causes had been dramatically reduced in the years since Steiner and Lushbaugh first published. The advent of antibiotics all but eliminated the "childbed fever" infections that had long been the major cause of maternal deaths. Ironically, this near total victory over infection pushed AFE into a more prominent position in the lineup of pregnancy-related killers. Sperry found it "second only to pulmonary thromboembolism [blood clots] in most recent studies."
lark's work on AFE began in 1983, when he was just starting a fellowship at the University of Southern California. He'd gone there as an intern in 1979, after graduating with honors from the University of Wisconsin's medical school, and had stayed on for his residency. In a telephone interview in February 1995 he recalled his USC years as an exciting time. "We were just revving up a whole new area called critical-care obstetrics," he told me, adding that he'd had a role in the development of this specialty and had since edited a textbook on it. Before this, he said, "It was obstetricians writing about critical-care things they didn't quite understand."
The case that first caught Clark's interest was one he was called in on. A 21-year-old woman had come to USC's medical center to deliver her baby. Her water bag had broken, and she had thick meconium in her vagina. But she was dilated only one centimeter. According to the hospital records, after 12 hours of Pitocin-induced labor, she suddenly became agitated, started breathing rapidly, then stopped breathing altogether. After an emergency cesarean section she was taken to the intensive-care unit. Since she didn't die immediately, "we had a chance to do some special monitoring of her heart function," Clark said. An hour and ten minutes after she stopped breathing he placed a catheter in her pulmonary artery "a relatively new technique at the time" and performed a number of tests.
"Based upon what people had said in the books, I went in with a preconceived  notion of what I was supposed to find," Clark recalled. "I found something completely different."
Clark was looking for the clogged right heart and vasospasm in the lungs described by Steiner and Lushbaugh and corroborated in animal studies. Instead he found left-heart failure and no evidence of lung blood vessels clamping down. He also found that the patient had suffered cerebral hemorrhaging and swelling and was brain-dead. Thirty-six hours after her collapse she was removed from the respirator. Since blood drawn from her pulmonary artery contained fetal debris, the diagnosis of AFE was confirmed, though she never developed the coagulation problems common in AFE patients. There was no autopsy.
Surprised by his findings, Clark reviewed other cases in the medical literature in which pulmonary artery catheters had been used. There were just five of them, and in every case the crisis had occurred more than an hour (in most cases much more) before the catheter was put in place and the tests run. When Clark saw that these cases also suggested left-heart failure, things suddenly came together. "I saw quite clearly that everyone else had misinterpreted the data," he told me.
He then wrote his first paper on AFE, speculating that a two-phase process was involved in the reaction to an infusion of amniotic fluid. First, a brief period of vasospasm, right-heart failure, and serious loss of oxygen. Second, left-heart failure, loss of blood pressure, and ARDS (adult respiratory distress syndrome) - a condition in which blood leaks from the capillaries of the lungs. This, Clark said, had "important therapeutic implications."
"Then I started looking at all the other aspects of this condition and realized that many of the things that had been presupposed were wrong," Clark said. Over the next few years he and his colleagues published a string of papers on AFE that began to chip away at the associated factors (especially vigorous labor) and the course of the disorder described by Steiner and Lushbaugh. The third paper in the series was something of a bombshell.

For more than 40 years after Steiner and Lushbaugh's paper was published, a  finding of any fetal debris in the lung vessels of a woman who'd died in childbirth - even just a few skin cells - was taken as proof of amniotic fluid embolism. This wasn't quite what Steiner and Lushbaugh had intended. Their paper stipulated a finding of "widespread" and "rather massive the particulate matter found in amniotic fluid and by meconium." (Particulate matter could include fetal hair, fat, and mucus, as well as squamous cells.) But this standard got distorted, and the search for squamous cells became an all-or-nothing test. As Clark put it: "If you found any squam cells in a mother's circulation, that was amniotic fluid embolism. And if you didn't find them there, it could not be."
This was the prevailing assumption in 1983, when Warren Plauche, a physician at Louisiana State University Medical Center, dropped a note to the American Journal of Obstetrics and Gynecology, reporting that on two occasions he and his associates had found "fetal squames and other amniotic fluid detritus" in blood drawn from the pulmonary arteries of women who were delivering babies but didn't appear to have AFE. Plauche raised a basic question: He wondered if AFE "could be a common phenomenon in small quantities and only produce a clinical disorder when the inoculum is large?" (Plauche either didn't know or didn't think it relevant that Steiner and Lushbaugh had already postulated the existence of nonfatal,  undiagnosed cases with a minimal amount of embolism.)
In the highly competitive realm of medical research a letter like Plauche's is a call to action. Clark did his own analysis of pulmonary artery blood from a variety of  patients and got some extraordinary results. Not only were there squamous cells in the blood of non-AFE patients, but there were squamous cells in the blood of every patient�pregnant or not. Since researchers can't readily distinguish between an adult squamous cell and a fetal one, it looked like some of what was showing up was contamination from skin cells of the subject or the technician. Pregnant patients had a few more cells than nonpregnant patients, but didn't seem to have less than the apparent AFE case Clark compared them with. (Clark still believed that something in the amniotic fluid was causing AFE�some sort of "abnormal substance.")
On the basis of these findings, Clark took aim at what had long been the only solid factor in an AFE diagnosis. "Detection of squamous cells...may be a necessary, but not sufficient, condition for the diagnosis of amniotic fluid embolism," he wrote in a 1986 paper. In subsequent testimony as an expert witness he put it more bluntly. "We used to think we had a great test to see about amniotic fluid embolism. We know know that test is no good." Doctors were left with only a clinical diagnosis, that is, an educated guess based on the symptoms.
In our 1995 telephone interview Clark told me the assumption that squamous cells in the lungs were proof of AFE had been a "huge roadblock to progress" and had created "giant confusion." He explained, "People were dying from all kinds of things, and they were finding a few fetal cells at autopsy and publishing another report of a strange presentation of amniotic fluid embolism. What we found is that 90 percent of the cases of amniotic fluid embolism in the literature probably weren't amniotic fluid embolism. No wonder nobody understands it."
"Ninety percent? Really?" I asked. The figure was stunning. It would mean the literature was all but worthless.
He backed away. "Many. Put it that way. Many of the cases thought to be that [AFE] were not."
In 1988 Clark published a paper in the American Journal of Obstetrics and Gynecology announcing the opening of a registry for amniotic fluid embolism and inviting doctors to submit summaries of their cases. Any individual doctor writing a  case report goes in with a "preconceived bias," Clark told me. "So we said, everybody send your cases here, and maybe when we have one or two people looking at 40 cases consecutively we can begin to make some sense out of this clinically."
A little after eight o'clock on the morning of September 16, 1985, Janet Spiess entered Copley Memorial Hospital in Aurora. Spiess, a healthy 26-year-old, was just a week shy of her due date with her third child. Her husband, Tony, would later state in a deposition that they had just dropped off their two daughters, ages four and five, with his mother. Janet was leaking amniotic fluid, and her gut was periodically cramping; it seemed she was going into labor.
Janet's obstetrician examined her when she came into the hospital. Eleven days earlier he'd turned her baby around, manually nudging it from a breech to a head-down position - a procedure that sometimes causes the placenta to tear away from the uterine wall. Now he noted on her chart that the baby was large and very high, and that her cervix had barely dilated. He also noted that she might need a cesarean section because the baby could be too big for her to deliver vaginally.
An hour or so later he looked at Janet again. Her labor didn't seem to be progressing. According to Tony Spiess, he said that Pitocin might be useful to step up the contractions, but said it couldn't be used without a doctor present and he had to get to his office. Instead he ordered that Janet be stimulated with a breast pump, which would cause her body to produce extra oxytocin on its own. He looked in on her again at about 10:50, then left her in the care of the nurses. No doctor would see her again until 8:15 that night
Janet was hooked to an external fetal monitor, and an electronic pump was clamped to her swollen breast - 15 minutes on one side, 15 minutes on the other, several times over the next few hours. With the pump's yanking, the pain in her gut escalated, but the baby remained high. As the morning wore on, Janet began to believe something was wrong. By one o'clock, Tony would later testify, she was telling the nurses her contractions were too hard. She'd given birth twice before and knew this didn't feel right. The nurses reapplied the breast pump and went about their business. By mid afternoon Janet was in intense pain, a different kind of pain than any she'd experienced in her other labors. Around four o'clock she began to ask for a cesarean section, pleading for someone to summon a doctor. Tony stated that the nurse "just brushed it off. Called me over to the side and said it didn't seem that bad according to the [monitor] strips.
From that time on, Tony said, his wife repeated her plea for a C-section almost every time one of the nurses came into the room. None of them seemed concerned about her suffering or the fact that the fetal heart-rate tracings on the monitor strip looked erratic. A little after six o'clock, however, a pelvic X ray was taken. The nurse who looked at it told Tony the baby was "big." He asked if there would be a problem with vaginal delivery, and she gave him a response he later said he got  many times that day: "I can't answer that. I am not a doctor." When he asked the nurses to call a doctor, he was told none was available. Janet's obstetrician had gone home after office hours to baby-sit his own children while his wife went out. He would later testify that it wasn't his day to be on call.
Finally, at 8:15 that evening, one of the obstetrician's partners showed up and examined Janet. He found that the baby was still very high. Tony didn't know that a baby's failure to drop into position can be a signal that it's too big to deliver vaginally, but the doctor's words made an indelible impression on him anyway.
"The baby is somewhere in DeKalb County," the doctor announced. DeKalb is a county away from Copley Memorial Hospital.
"Jan was asking him to do a C-section," Tony testified, adding that she'd taken nothing for pain and "said she couldn't last any longer." Tony remembered the doctor replying, "You'll make it," then puncturing the amniotic sac so the remaining fluid would drain off. He'd told Tony there was a large amount of fluid and it could be dangerous if the water broke and came out rapidly. Tony saw him stab three times with a long metal needle, then make three cutting motions. After this there was "a great big gush of water, an abnormal amount," Tony said. The doctor attached an internal monitor to the baby's scalp, and he and the nurse left the room.
A few minutes after the doctor left, Janet told Tony she couldn't breathe. As she struggled for air, he rushed into the hall for help, feeling that each passing second could be critical. At the nursing station he found the doctor on the phone, deep in conversation. The subject appeared to be a Monday-night football game. Frantic, Tony turned to the nurse, who was talking with a coworker. "I said Janet was having problems breathing," he recalled. It seemed to him that the nurse wasn't terribly concerned, that from her point of view, his wife was a complainer. "She's probably hyperventilating," the nurse replied evenly. "No," Tony insisted, his anxiety mounting. "I've seen people hyperventilate. She is not hyperventilating." He ran back to the room alone. After an interminable moment the nurse appeared, walked to Janet's bedside, and told her to "do the Lamaze method." When Janet gasped that she couldn't breathe, the nurse advised her to "just keep on trying." As the color drained from his wife's face, Tony exploded. "She ain't hyperventilating," he shouted, pulling an oxygen mask from the wall and ordering the nurse to put it on.
She refused, relenting only when he tried to do it himself. Then she turned Janet on her side and left the room. Doubly frantic, Tony ran again to get the doctor, who was still on the phone. With Tony dancing in agitation before him, he took a moment to finish his conversation. By the time he got into Janet's room she'd torn the oxygen mask off. The doctor ordered it replaced, then, while she gasped for air, he decided to see what was happening in the birth canal. In the midst of this exam Janet went into a violent convulsion. Tony recalled that "her whole body was uncontrollable, flying up into the air. Everything was going haywire." And he remembered the doctor crying out, "Oh, shit, don't let this happen now." The doctor yelled for a tongue depressor as several nurses who'd run into the room stood by in "complete shock." Tony grabbed the cord from the bedside telephone and jammed it into Janet's mouth.

The convulsion lasted less than a minute, but after it was over Janet was as good as dead: unconscious, not breathing, with a pulse that rapidly dropped to zero. She was given CPR, intubated, and put on a ventilator. At 9:20, 30 minutes after she'd stopped breathing, an attempt was made to pull her baby out with forceps. But the relatively large baby had never settled into the birth canal, and Janet had never fully dilated. Not surprisingly, it didn't work. (During this attempt, the doctors would later write in their report, they found "a large amount of nonclotting blood in the uterus.") Half an hour later Janet's obstetrician, now on the scene, came out to the hallway where Tony had been sent to tell him his wife wouldn't make it and to ask if they should do a cesarean section "for the baby."
"How long has it been since Jan got oxygen?" Tony remembered asking.
"Over an hour."
"How much brain damage would she [the baby] have?"
"Total and irreversible."
At ten o'clock that night Janet Spiess, a normal, eight-pound daughter still in her uterus, was declared dead of a presumed amniotic fluid embolism. The attending physician's report stated that "the husband requested that an agonal C-section not be performed since it was felt that the baby had expired very quickly after the mother's cardiovascular and respiratory arrest." There was no mention of the hour they'd waited before putting the question to him, no mention of the many times that afternoon that Janet had called for a doctor or tried to tell the nurses something was wrong. Reading the physician's report, you would never know that while she could still breathe and talk, Janet had begged repeatedly for a C-section.
Tony Spiess sued the doctors and the hospital. On January 9, 1990, Steven Clark was deposed as an expert witness in defense of the physicians. Although no doctor had seen Janet for at least nine hours of what turned out to be the last day of her  life, he testified that there had been "no negligence involved in the care of this patient," that everything had been "in compliance with the standard of care." No mention was made of studies in the medical literature showing that breast stimulation to bring on contractions produces unpredictable results, including uterine hyperstimulation (excessively hard, fast, and long contractions) in about half the cases.
Spiess's attorney, John Lamont, asked Clark whether Janet's AFE might have been triggered by the needle that ruptured her amniotic sac. Clark replied that it would not; such a rupture, he said, "is, if anything, going to decrease the pressure on the amniotic fluid, let it out another way other than going into veins."
Lamont also asked about the failure to do a C-section before the baby was brain damaged. For this, Clark had an authoritative response. A C-section is done, he said, "only if the mother is stable enough." He added that Spiess was not.
The jury found the hospital, though not the doctors, to be at fault. They awarded Tony Spiess $200,000 for the death of his daughter, but nothing for the loss of his wife. They apparently believed Clark's testimony that her fatal AFE had been, in effect, inevitable, that nothing the nurses and doctors did had brought it on, and that nothing they might have done would have saved her�an opinion he would repeat testifying in numerous other AFE cases.
Lamont filed a motion asking for a new trial on the issue of damages. The motion stated, "It can only be speculation to state what influenced the jury to award '0' damages for Janet. But we suggest that Dr. Clark's inappropriate and prejudicial assertion that Janet was 'destined to die' may have had something to do with it."
The motion was denied.
Five years later, in 1995, Clark would publish a paper in which he offered a different opinion on a couple of things he'd testified to. AFE "appears to be initiated after maternal intravascular exposure to fetal tissue," he would write. Arguing that some such exposure is inevitable, he nevertheless allowed that "actions by the  health care providers...may affect the timing of the exposure." In a significant number of cases he saw "a striking temporal relationship between artificial rupture of the membranes or placement of an intrauterine pressure catheter and acute cardiovascular collapse."
In the same paper he also concluded, "We recommend that peri-mortem cesarean section be initiated as soon as possible after maternal cardiac arrest in patients with clinical amniotic fluid embolism." In addition to offering a chance to save the child, he noted, a prompt C-section might "actually be of benefit to the mother undergoing cardiopulmonary resuscitation."
Michael Benson told me it was a third brush with death that got him thinking obsessively about amniotic fluid embolism. At four o'clock on a Sunday morning in the spring of 1992, in the posh labor and delivery ward of north-suburban Highland Park Hospital, Benson's patient struggled to push her baby the final few inches to life. Her labor had begun the previous day; she'd been stalled at this excruciating juncture for an hour.
Benson thought she could use some help. He applied the suction cup of a vacuum extractor to the matted circle of scalp that periodically mooned into view at the vaginal opening. With each of the next few contractions a nurse squeezed the trigger of the pump, building the vacuum. Suddenly, in a rush of fluid and blood, the infant's head popped out. The skull showed the temporary elongation that comes with molding and suction, but it was a healthy boy. The placenta followed spontaneously ten minutes later. It seemed like a successful, routine delivery, but a minute or two after expelling the placenta the patient turned pale and said she felt nauseated. Her blood pressure took a nosedive, and her heart rate jumped. So did Benson's. His patient was crashing.
He cut off the epidural anesthetic she'd been receiving, increased her IV fluid, and called for help. But within five minutes, just as suddenly as it had come on, the situation appeared to resolve itself. The patient felt better, and her blood pressure returned to normal.
"The whole thing was such a fluke," Benson told me. "So strange. It was as though the angel of death had slipped into the room and slipped out." For an instant, he was reminded that he'd seen something like this twice before, and the thought made his blood run cold. In both cases, shortly after the birth of a child the patient had developed a nightmarish complication called disseminated intravascular coagulation. When DIC sets in, the patient's blood loses its ability to clot. The patient begins to hemorrhage, blood oozing from surgical incisions, IV sites, and every natural orifice. Benson pushed the thought from his mind. What did it have to do with a patient who now looked fine? He took a bed in the ward to catch a few hours of sleep before morning rounds. When he awoke and headed for his patient's room to see how she was doing, he found her hooked up to a cardiograph, her pulse alarmingly fast - more than 140 beats per minute. He ordered an immediate blood workup. The results hit him with a thud: his patient had a mild case of DIC.
A hematologist Benson conferred with offered an intriguing explanation. "He said he had seen this before," Benson told me. "He said it's just a little amniotic fluid gets  into the bloodstream." The hematologist was casual about it, but to Benson, who hadn't thought his patient had AFE, this was startling, "quite in contrast with medical dogma." As far as he knew, the medical literature didn't include many nonfatal AFE cases (though DIC was known to be linked with AFE). His patient recovered spontaneously, but Benson, "tired of having people get very sick on me" and  nursing a hunch that wouldn't be ignored, began to study the literature in earnest.
Benson, now 38, is one of those people who will always look younger than he is, a short guy with a cowlick and an impish grin. Nothing about his benign appearance suggests the often abrasive onslaught of fact, opinion, and theory that comes rushing at you when he opens his mouth and seems like it would keep
coming forever if there weren't a baby to be delivered or a patient waiting to be examined in the next room.
Benson read more than 50 papers on AFE, including ones by Steiner and Lushbaugh and by Clark, then began to draft his own. He was troubled by the fact that for so many years a positive diagnosis could be had only for dead patients. He was sure this had created a bias that led doctors to underestimate the prevalence of AFE and to overestimate how lethal it was. I n his paper, the one he would send to Clark to read he described what had happened to his three patients and listed conditions for a diagnosis in survivors. He suggested that since the very name of the ailment was misleading, it should be called "amniotic fluid embolism syndrome." He warned that placing a catheter in the pulmonary artery (a measure promoted by Clark) could be dangerous. He also suggested that AFE might not only resemble a severe allergic or anaphylactic reaction (an extreme immune response to an antigen) (as Steiner and Lushbaugh and others had written) but might actually be  an anaphylactic reaction. If it were, that could change how women with AFE were treated. He concluded that AFE "may be an immunologically mediated response to some type of pregnancy-associated antigen leaking into the maternal circulation."
When Benson contacted Clark in January 1993 he hoped Clark would make comments on his paper and allow him to cite Clark's registry, which he knew would give the paper credibility with editors. He waited eagerly for Clark's response and was crushed when Clark wrote back that he didn't think any of Benson's patients had had AFE and that Benson should therefore rethink his conclusions.
When the paper was published that September in the Archives of Family Medicine, Benson, working with researcher Roger Lindberg, had already come up with a practical way to test whether he was on the right track. If AFE victims were having allergic reactions, their blood would show elevated levels of a substance called tryptase. If he could get blood samples from these patients, perhaps as few as 10 or 20, he could test for tryptase. The problem was getting the samples. He would need the cooperation of a broad network of obstetricians who, in the midst of an emergency, would think about drawing blood and sending it to him. He knew that would happen only if he got the word out in one of the major journals serving the specialty. But his second paper, which explained his theory and how he intended to test it and asked for blood samples, had already been turned down by the Journal of Reproductive Medicine as too speculative. He conceded that this was a fair criticism. "Medical journals aren't in the business of publishing speculation," he said. But this left him in a catch-22: he couldn't prove his theory until he published and got the blood samples - and he couldn't publish before the theory was proved. Aware that Clark, one of very few AFE researchers, would be a likely peer reviewer for any AFE manuscript submitted to the major obstetric journals, Benson sat on his second paper. A year and a half went by. During that time, if the record at the hospital where my daughter died is representative, more than 900 women went to American hospitals to have babies and developed cases of AFE serious enough to be recognized. Benson's idea remained in limbo. Had it been proved, he and other researchers could have pursued the implications; had it been disproved, they would have known to take a different tack.
When I met him in July 1994 Benson was still trying to figure out how to get this paper published. He said he was planning to send a personal letter requesting blood samples to the heads of obstetrics at 2,000 hospitals, but said he didn't expect much response. Without the credibility lent by publication it was unlikely that many doctors would cooperate.
I continued reading the medical literature through the fall of 1994. By December I thought I had a sufficient grasp of Steven Clark's publications to do a telephone interview. When I called him I told him I thought he'd reviewed my daughter's case, though I had no intention of discussing it with him and was calling for general information. (No lawsuit was filed in my daughter's case.) He thought he remembered the case, said it was a classic instance, and told me he'd written a new paper that would soon be published in the American Journal of Obstetrics and Gynecology. He said his recent research had produced a breakthrough on the cause of AFE. He offered to send me a draft, and I assured him I wouldn't write or talk about it until the paper appeared in the journal.

Clark's draft was a review of what he'd learned from studying 46 cases of AFE that had been reported to his registry since 1988. His major new finding turned out to be a "striking" similarity between the symptoms of AFE and those of anaphylactic shock. I found that strange, since Steiner and Lushbaugh had made this observation in their 1941 paper, and they'd credited an earlier writer. But when Clark went on to discuss the dynamics of AFE in terms of a break in the "immunologic 'barrier' between the mother and the antigenically different products of conception," I started to think he wasn't just echoing Steiner and Lushbaugh.
Nor did he seem to be building on previous papers of his that I'd read, which mostly referred to "abnormal" amniotic fluid. To me, admittedly no scientist, Clark's breakthrough sounded a lot like Michael Benson's hypothesis.
There was no mention of Benson or his paper in Clark's draft, nor did Clark mention Benson in the two telephone conversations I had with him. When the paper appeared with 25 references but no citation for Benson in the April 1995 issue of the American Journal of Obstetrics and Gynecology, I wondered if my impression was wrong. I called Benson to ask if he'd seen the article.
"No," Benson said. "What does he say?"
"He says it's an allergic reaction."
"Anaphylactic?" Benson asked.
"Well, he calls it anaphylactoid."
"What was the basis of your idea that it was an anaphylactic reaction?" he asked. "These patients were well one moment and very sick the next," Benson said, adding that he looked in the literature for similar reactions.
This was consistent with what Clark had told me in February 1995, when he described his major new finding, discovered through a review of the registry cases in the summer of '93 (a review he'd done five to seven months after reading Benson's paper). He'd said AFE is "like a bee-sting reaction," then explained, "A thousand women are stung by a bee, and it's a minor irritant. Number 1,001 is stung by the very same bee with a very small amount of venom, and suddenly it's shock, cardiac arrest, can't breathe, and die. And that's exactly what we're dealing with here. Most women get some amniotic fluid in their circulation at some point during their pregnancy mostly during labor and delivery, or maybe at the time of a C-section. You just can't avoid it....In most cases it's nothing, no big deal. But in rare cases, for unknown reasons, there is simply a mismatch, a genetic mismatch, and that fetal tissue getting in the mother's circulation sets off a reaction very much like a bad penicillin allergy, a bee-sting allergy, or something like that, and the mother collapses and in most cases dies."
He continued, "The frightening thing about this is that if [you're pregnant and] you've got the mismatch, you're going down. Y ou can have an abortion, you can not, you can deliver vaginally, you can have a C-section, you're not getting out of this pregnancy without getting some fetal tissue in you, in your blood mix. And if you've got the wrong mismatch, as I say, you're goin' down. And there's not a cotton-pickin' thing, as of yet, that we can do, unfortunately, to predict it."
Severe reactions to bee stings and penicillin are immunoglobulin-mediated anaphylactic events - exactly what Benson had proposed as the cause of AFE.
Letters from Benson and Clark, as well as the tryptase paper, were published in he September 1996 issue. Clark's letter offered two reasons why Benson might be wrong: an immunoglobulin reaction would likely produce rashes and upper-airway swelling and would require exposure prior to the acute episode. He didn't explain why he'd referred to foreign antigen and breaches of the immunologic barrier in his own article, or why he'd compared AFE to an allergic reaction to bee stings, which also requires a previous exposure, in the OBG Management interview.
On September 14, 1996, Feder and Stewart completed their final report, which  was 79 pages long and had nearly 200 pages of attachments. They analyzed the two articles and published letter Clark had cited as evidence that he'd had the idea first; they determined that none of them held up. In addition, they examined all other AFE papers published by Clark and found no evidence that he'd proposed an immune-mediated allergic response as the cause of AFE in any paper published prior to his reading of Benson's draft.
Over the last several years hundreds of hours that might have been spent researching AFE have been ground up in the Clark-Benson misadventure. What's been gained? The tryptase paper finally got into the obstetric literature, and Benson  is beginning to get the blood samples he needs. He's now collaborating with doctors here and in Japan on an expanded testing program that will check blood and urine for tryptase and several additional factors that might mark an immune response. He says he'll pay for it out of his own pocket if necessary. An abstract presented by Benson at the first World Congress on Maternal Mortality (held in Morocco in March 1997) announced that he and his collaborators "hope to collect several dozen specimens over the next five years and intend to make this specimen pool available to other investigators should AFE prove to be a nonimmunologic illness."
And indeed there's a good chance Benson and Clark have been galloping down the wrong path together. In the end, AFE may prove not to be the result of a rare allergy. There's plenty of evidence in the medical literature to suggest that a significant volume of amniotic fluid (especially the fluid of a woman in labor) carrying meconium, vernix, or other chemical or particulate material is toxic if it gets into the woman's bloodstream. It hardly seems necessary to postulate an unusual allergic sensitivity or "genetic mismatch" to explain the havoc such fluid can raise. Whatever the cause, discovering it would be easier if a way were found to weed out the cases of air embolism, surgical or anesthetic accident, and hemorrhage from other causes that are presented as AFE and continue to cause confusion about the circumstances in which it occurs.
he huge 20th-century reduction in maternal deaths, the movement to reclaim childbirth as a natural event, and insurers' efforts to cut medical expenses have combined to lull us into a casual attitude about giving birth. But no matter what euphemisms or anesthetics it's cloaked in, childbirth is a bloody, dangerous process. Researchers at the Centers for Disease Control say maternal deaths due to pregnancy are significantly underreported. Their best guess is that in the United States (it's much worse in many other countries) pregnancy and childbirth bring death to 1 out of every 5,000 mothers. Yet as obstetrics is now practiced, women entering labor are often left in the hands of strangers, whichever nurse or doctor-in-training happens to be on duty in the labor and delivery ward on the climactic day. If a woman's own doctor is on call and gets to the hospital in time to "catch" the baby, she can consider herself lucky.
At its worst, this is a situation that combines maximum intervention with minimal care. A labor induced with synthetic oxytocin, for instance, is chemically and functionally different from a natural labor. Until recently it required the on-site supervision of the attending physician. Why doesn't it still? The doctor who wrote the book on labor, Emanuel Friedman, was chairman of the obstetrics and gynecology department at the Chicago Medical School and Michael Reese Hospital in 1967 when the first edition of his groundbreaking text, Labor: Clinical Evaluation and Management, was published. Friedman applied statistical methods of observation and analysis to labor, described its stages, and devised a simple method for charting its course that was widely adopted. In this and later editions of his work he was unequivocal about induction, writing, "It is absolutely essential that the attending physician be present at all times." I wondered if this was still his standard. Now a professor emeritus at Harvard and still teaching at Albert Einstein Medical College in New York City, Friedman told me he hadn't changed his mind. "The attending physician should be on the labor and delivery unit," he said, "within earshot."
According to the obstetric literature, oxytocin is barely present in the mother's blood in a natural labor until she's fully dilated, and even then only at a fraction of the levels commonly used in induction. Parke-Davis, the manufacturer of Pitocin, warns that the dose of this drug that individual women can tolerate varies in unpredictable ways. An overdose can produce unusually strong and frequent contractions that stress the fetus, which may cause it to dump meconium into the amniotic fluid. This kind of hyperlabor can also rip the margins of the placenta and other tissue, exposing veins, releasing clotting factors, and opening the fast route to the mother's bloodstream described by Steiner and Lushbaugh. While no one would argue that synthetic oxytocin is involved in every case of AFE, it seems reasonable to suspect that misuse of this drug may be at least a contributing factor in some cases.
On the basis of my family's experience and my subsequent reading, I'm convinced that in some cases AFE has a gradual onset and early symptoms that are likely to  be overlooked by hospital staff. While it's not unusual to experience some of these symptoms in a normal pregnancy and labor, they should never be ignored. The assumption that one can't see AFE coming assures that no one will be watching for it. (Just as the assumption that AFE was always fatal gave credence for years to the opinion that any patient who survived what looked like AFE probably hadn't had it.) And once a crisis occurs, no attending physician or nurse will be eager to point out danger signals they missed.
Pregnant women should be aware that a large baby can be a problem during delivery, particularly if the mother is of small stature. If there's a chance the head i too large to pass through the mother's pelvis, an overdose of oxytocin with an intact or semi-intact amniotic sac might spell trouble. Shortness of breath during or around the time of labor can be a danger signal and should be checked out. So should any unusual bad taste in the mouth or easy or prolonged bleeding from any site. Signs of petechiae, a frecklelike rash caused by bleeding into the skin, should be reported to a doctor immediately, as should pain in hands or legs. A combination of intense anxiety, coughing, chills, and extreme pain during early labor, especially chest or abdominal pain that continues between contractions, should be a red flag. So should a somewhat slow or faint pulse or a pulse rate that drops 10 or 20 percent during labor (the normal pulse rate for a pregnant woman is faster than her nonpregnant rate). A simple blood-coagulation test given early in labor would probably be a good idea. If there's any reason to suspect trouble, an oximeter (a blood-gas monitor) could be helpful; there have been cases in which an oximeter warned of an AFE-caused fall in oxygen level before there was any apparent sign of it. Most books for pregnant women are designed to reassure them and reduce the number of questions they put to their physicians. What these women really need is the opposite advice. Don't try to be a "good" patient, especially in the hospital. Never be stoic. Communicate everything and be sure it's understood. If your doctor won't make a reasonable commitment to be there for your labor, think about hiring your own labor nurse or finding a different doctor or a midwife. Don't assume you'll be in good hands, and don't assume the tests and care your insurance company will pay for are all you'll need.
In medicine, as in every other human endeavor, experience counts. Beware the resident unaccompanied by his or her board-certified supervisor. And having a father, especially a first-time father, as the "birth coach" is a well-intentioned new concept with questionable ramifications. In today's labor and delivery wards it often means that he's the one providing the laboring mother's minute-to-minute observation and care. Historically women have known better and have been attended at birth by as many experienced females as they could gather.
Finally, some women actually do need C-sections. And for some of those women,  the "trial of labor" through induction is a dangerous exercise. If your doctor is  thinking more about his C-section rate than about your particular situation, look out. Whatever the abuses of the recent past, there's a knee-jerk avoidance of cesarean delivery in this country right now. Kieran O'Driscoll and Declan Meagher describe a radically different attitude toward induction in their manual Active Management of Labour (first published in 1980). These Dublin doctors have had an international impact as advocates of oxytocin to speed up delivery when spontaneous labor is well under way in first-time mothers, so it's all the more compelling that their standard for induction is extremely cautious: "Induction is not attempted in this hospital unless the head is engaged and the cervix is, at the very least, reasonably favourable," they write. "Whenever the need to terminate pregnancy arises before these basic conditions are fulfilled, caesarean section is performed on the grounds that induction is not the correct method of treatment in these circumstances. Prostaglandin, to ripen the cervix, is rarely used."
The same text also warns that "oxytocin may increase the risk of amniotic fluid infusion into the maternal circulation unless free drainage has been established....In no circumstances is oxytocin used when the membranes are intact."
The bible of the specialty of obstetrics in America is the venerable textbook Williams Obstetrics, first published in 1903. For the last couple of decades it has been written by doctors at the University of Texas Southwestern Medical School and the affiliated Parkland Memorial Hospital. F. Gary Cunningham is one of its senior authors. When Texas obstetrician Gary Hankins presented a study of induced AFE in pregnant goats (with Steven Clark listed as a coauthor) at a medical meeting in 1992, Cunningham led the follow-up panel discussion. He said he'd been practicing obstetrics for a quarter century and had seen a number of fatal cases of amniotic fluid embolism. Here's what he thought about it: "Over the years I have concluded that amniotic fluid embolism has a spectrum of clinical presentations dependent on the amount of fluid absorbed and, perhaps more importantly, the degree of contamination with meconium. The 'milder' cases (if there is such a thing) are characterized by activation of the coagulation mechanism with consumptive coagulopathy. Probably in most cases of women delivered vaginally these are clinically insignificant, but with extensive lacerations or with cesarean section there is clinical evidence for abnormal clotting. As the amount of meconium contamination increases, so does the evidence for cardiorespiratory dysfunction, and in the most severe cases death is by cor pulmonale [right-heart failure caused by problems in the lung]."
Cunningham's summary seemed congruent with what I'd observed in my daughter's case, and it stuck with me. I put him on a mental list of people to call before I published this story, thinking he might be an authoritative source for an alternative to the allergy theory being pursued by Benson and Clark. A year ago, preparing to make a call to Cunningham, I pulled the new, 1997 edition of Williams Obstetrics from the reserve shelf of the medical library to see if there'd been any change in the section on AFE since the previous edition. Before I opened the book I had my answer. The list of seven authors on the cover now included Steven Clark.
The AFE section was written by Clark and echoes his 1995 paper. It perpetuates the idea that an abrupt crisis is the first sign of AFE. There's no suggestion that there might be any symptoms to look for before a patient stops breathing, has a convulsion, or begins to hemorrhage. It also makes the sweeping claim that amniotic fluid "itself is innocuous" in the maternal bloodstream.
The new Williams credits Clark with the idea that AFE is similar to anaphylaxis and with the suggestion that the name amniotic fluid embolism (or "amnionic," as Williams puts it) is a misnomer. It also credits Clark with the theory that mediators such as those activated in an allergic event are the culprits.
More important, the book presents AFE as something that happens to "certain women" (ostensibly those with a rare sensitivity) rather than in certain circumstances (as previous editions suggested). This is contrary to what Cunningham thought in 1992, and contrary to a good deal of experimental evidence, including the Hankins goat study, where the goat given the highest concentration of meconium died so fast the researchers couldn't get data on it. Curiously, Williams cites the Hankins goat study as a relevant model, even though AFE symptoms were a universal response to any infusion of meconium and didn't  require any special allergy on the part of the goats.
Williams also declares that a "breach in the physiological barrier that normally exists between maternal and fetal compartments" is the means by which AFE occurs. However, it goes on to state that hyper stimulation and synthetic oxytocin have nothing to do with AFE. The fact that hyper stimulated labor can stress the fetus, increase the chance of meconium in the fluid, and rip the placenta and other tissue, causing a large or early "breach in the physiological barrier" is not addressed (previous editions cited hard labor as an associated factor).
Williams now asserts that the frequency of oxytocin use in AFE victims is no greater than in the general obstetric population. The source Clark gives is a brief passage he wrote for a continuing-medical-education workbook. The source given in the workbook is a 1979 review of previous AFE articles by a British anesthesiologist, M. Morgan. But there was little consistency of reporting in the articles Morgan read, and Morgan himself cautioned that "not all facts [were] mentioned in every case," explaining that obvious discrepancies in his numbers were due to this problem. There's no reason to assume that his data on hyper stimulation or uterine stimulants was complete. Moreover, it's clear that any such study of the literature would be distorted by the large numbers of inaccurate AFE diagnoses Clark complained of in my phone interview with him in '95. How then can Morgan's article constitute a basis for a blanket refutation of any relationship between oxytocin use (or misuse) and AFE?
Clark himself provided what looks like evidence to the contrary when he reported that 50 percent of patients in the cases he reviewed for his 1995 study had been  given oxytocin during labor. He said this was about the rate of oxytocin use at the hospital where he practiced, so he assumed it was representative. But the National Center for Health Statistics reported in the same year that only 26 percent of obstetric patients had any kind of induction or augmentation. If NCHS is right, oxytocin use would have to be less than 26 percent, since it's only one of several methods used for these purposes.
No mention is made in the new Williams of the high number of placental abruptions (in which the placenta pulls away from the uterine wall) associated with AFE, though Clark previously reported that they were apparent in up to 50 percent of cases. (And it doesn't take much insight into human nature to guess that abruption, and the hyperstimulation that can cause or exacerbate it, is likely to be underreported when the information comes from the physician responsible for the patient's care.) According to the American College of Obstetricians and Gynecologists, the reported incidence of placental abruption for the general obstetric population is only about 1 percent.
This version of Williams is the book the current crop of obstetricians-in-training will study to learn about AFE. It may be useful to them if they have to defend themselves against a malpractice charge. But how much help will it be to their patients?
This article originally appeared May 15, 1998 in Chicago Reader - 1998 Deanna Isaacs.

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