I understood my colleague’s thinking, but something about this situation made me uneasy with the idea that it was time to give up and withdraw her support. I wasn’t yet sure what I would do differently during my week on call, but it just seemed that we were not yet at the end of the line.
Our hospital was located on the edge of Chinatown, and many of our patients were recent immigrants from the Far East. This girl’s family was one of them. Her mother spoke barely any English, and we relied on interpreters for virtually all communication. After completing rounds with the interns and residents, I called an interpreter and sat with the girl’s mother to tell her what I thought we might change medically, to reiterate the gravity of the situation, and most of all to hear her thoughts. Speaking to parents through an interpreter is always difficult—all of the nuances that can be appreciated by face-to-face communication become diluted and difficult to discern. The cultural barriers become magnified, too. The mother listened attentively to everything I told her and replied, “I appreciate all that you are doing, but I would like to have a Chinese healer come in to help treat my daughter.”
Admittedly, I am not exactly a believer in what has come to be termed “alternative medicine,” but our scientific, “evidence-based” medicine had not been a rousing success either. To be honest, I was somewhat skeptical that this little girl had much of a chance of survival anyway, no matter what the treatment philosophy. We were stuck, having tried everything in our armamentarium, and despite our best efforts she was deteriorating before our eyes. It took little insight to realize that this mother needed to know that she had tried everything possible for her daughter, and that a crucial part of the formula for her included intervention by a Chinese healer.
I told her mother that we could administer the Chinese remedies only if they could be dissolved in a solution to pass through the child’s feeding tube that went directly into her stomach (because of the breathing tube in her throat, she hadn’t been getting food or water by mouth for many days), and only if the healer could tell us all of the ingredients. I was very concerned, because many of the ingredients in “traditional” medicines can have numerous different effects on the body, and some of those could be dangerous to a patient already in such a precarious state. Additionally, the healer’s medicines could interact with drugs we were administering and cause harm. I had no objection to trying to allow the mother to feel she had done all that was possible, but I did not want the healer—and my assent to his involvement—to be the direct instrument of this girl’s demise.
The next morning her condition was unchanged. The healer arrived and met with our ICU pharmacist and, through an interpreter, went over all of the ingredients. But despite extensive searching and consultation, we couldn’t figure out the chemical identity of the majority of them. We decided, with much trepidation, to go ahead anyway, moved by our desire to give this mother the sense of having tried everything to save her daughter, even if her efforts were in vain.
The healer said prayers for the little girl and the Chinese medicines were flushed into the feeding tube. The rest of the day and evening passed without much change. Her oxygen and carbon dioxide levels were relatively stable with the ventilator strategy I had implemented, but her situation was still tenuous and she still required maximal support, both from our drugs and the ventilator.
By the next morning, however, we couldn’t believe what was happening. She began to rally, and we were able to drop the level of breathing support we were giving her by machine for the first time in more than a week. The herbalist arrived again, and under our supervision administered a second dose of his Chinese medicines. And more prayers. By the second morning there was clear improvement, and by the end of my week on duty she had success-
fully weaned off the breathing machine and no longer needed the tube in her windpipe. She was now able to receive sufficient breathing support simply with an oxygen mask. The next time I came on call, two weeks later, she was no longer in the ICU at all. Several weeks after that she walked out of the hospital, fully recovered!
I learned a lot from this patient and her mother, and I think about them often, whenever I’m faced with a critically ill child. The primary lesson, of course, is that physicians should never have too much confidence in our abil-ity to predict the future. There are surely many situations where the outcome is not hard to predict, but many where uncertainty still remains. We should never mistake one for the other, and we must have the wisdom and humility to discern between the two. The second lesson for me at this early stage in my career was to listen carefully to our patients and their families, even when you do not speak their language—both literally and figuratively.
And finally—the obvious lesson—not everything we see in our clinical practices can be explained. I will never know whether it was the passing of time, my manipulations of the ventilator settings, or the herbalist’s potions and prayers that played the critical role in this girl’s recovery. It doesn’t really matter. In the end, all that matters is that she came back from the brink and into the arms of her family.
Date of event: 2004
It’s Alive!
Robert J. Buys, MD
I am an ophthalmologist subspecializing in diseases of the retina (the light-sensing organ lining the back of the eye) and vitreous (the fluid-filled chamber at the very back of the eye, just in front of the retina). At the time of this case, I had been in practice for twenty-one years and privileged to have participated in the care of thousands of patients both in the office and the operating room. I met incredible people, from the very young to aging World War II heroes. Of all those cases there is one that still haunts me; it can wake me up at night with a shudder. It’s still the one I cannot fully explain or understand.
If you read on, it may have the same effect on you.
It all started innocently enough with a phone call. As a doctor in a referral practice, I was always happy to speak with any other physician. This one was unusual because it came from out of state and the doctor, also an ophthalmologist, seemed nervous and incredibly excited. More like talking to a kid after Christmas than hearing a calm case presentation.
With good reason. He told me that he was seeing a thirty-five-year-old healthy male who happened to work in the same building as his office. The patient was sent directly to this ophthalmologist’s office when he reported to his employer he had totally lost his vision in his right eye. Examination of the eye revealed a complete blockage of the central retinal artery, causing the retina to become swollen and white. The patient’s vision was barely enough for light perception, the pressure inside his eye was normal, and his eye was not inflamed. The patient reported that a similar event had occurred the night before, lasted fifteen minutes, then resolved. That history, coupled with the exam, convinced the referring doctor that a clot or a piece of calcium (called a plaque) had become dislodged and traveled through the bloodstream to the eye. He felt this “embolus” (the term for any kind of substance that shouldn’t be there traveling through the bloodstream) most likely came from one of the carotid arteries, the major arteries in the neck and the source of blood supply to everything in the head, including the eyes.
That would have made sense except carotid artery clots, plaques, and emboli (plural for embolus) do not typically happen to healthy, young patients. So something was wrong with this picture, very wrong. Could this complete blockage of the central retinal artery be due to a plaque breaking off from a diseased heart valve? A normal heart exam ruled that out. Did he have some unusual disease that predisposed him to such an event? He was completely healthy and took no medications.
What was really incredible was the patient had been able to get to an ophthalmologist only minutes after the occlusion occurred because they worked in the same building. The occlusion itself is painless and can happen at any time. Once it happens, studies show you have about ninety minutes before permanent vision loss occurs. So for a patient
to get proper care quickly is very rare. In all the years I practiced, the best I saw was twenty-four hours afterward. This was too late to alter the final result, which is usually vision of 20/200 or worse (considered to be legal blindness; normal vision is 20/20). That meant, for this patient, there was hope to get the presumed embolus out of the central artery and move it further downstream and preserve his eyesight. The way this is done is to lower the pressure in the eye—either by medicines, massage, or letting a small amount of fluid out of the front of the eye. With the artery facing lower pressure from the eye, it can flow more freely and hopefully push the embolus to a smaller artery, thereby creating less damage to the retina.
Then things got weird. The referring doctor said after he lowered the pressure in the eye, the embolus “emerged” from the artery, was visible for just a second, and then blood squirted into the vitreous, obscuring the view to the retina. I have never been witness to such a thing—it must have been incredible to have a front-row seat like my colleague had. What kind of clot or plaque bursts forth from a blocked artery? None that I had ever heard of!
By the time I saw the patient, about twelve hours later, my exam revealed his vision was still poor, around 20/400. There was a large clot in the vitreous which prevented me from seeing the macula, the center of vision located in the retina. But I could see the outer portions of the retina. That is when I saw what I had never seen before—and gratefully never since—a meandering, dark, narrow trail carved out beneath the retina. There is only one type of entity that can cause such a finding . . . an entity that was alive!
This was not just a piece of clot or plaque; it was a moving, living organ-ism! Was it a parasite of some sort. A worm?
I quickly called back the referring ophthalmologist. That is when he told me the whole crazy story, one he could not believe himself. In the rush to get the patient to me and the excitement of all that had occurred, this part of the story was not originally communicated to me. He had seen some thing slither up from the optic nerve (where the central retinal artery emanates from). It had black and white stripes, and when it broke through the artery it looked directly at him, opening its mouth in a silent scream. He could see what looked like whiskers at the edge of the mouth, and then the blood squirted out into the vitreous obliterating his further viewing.
The phone went silent. I was shocked. I did my best to sound professional, like we see this all the time. A slithering, striped thing with whiskers around a gaping mouth creeping around the retina. Truth is, I was completely stunned and, between you and me, I was freaked out! How do I treat this? Do I operate? I’m the retinal expert after all, and I’m supposed to know what to do.
I went back to the patient and explained to him what I thought was the diagnosis. As you might imagine, that was the last thing he expected to hear from me.
We talked at great length and three potential sources of parasitic infection emerged as possible explanations: 1) he had been fishing three weeks earlier and got bitten by an insect in the eyelid; 2) he ate sushi a week before; 3) he lived in the country, near horses.
At first my concern was an infection in addition to the parasite. Clearly, this thing was from the outside world and whatever it was must have carried bacteria with it. But with no definite evidence of infection yet, I opted to wait and see what came next. Of course, I had no clue what to expect.
The next day the patient returned to my office, his eye red and with a small collection of white blood cells in the front of the eye. White blood cells are a sign of inflammation, the body’s response to infection and other foreign substances. A tough call to be sure, but upon close examination I came to the conclusion the parasite had died and created an inflammatory response. The vitreous fluid in the back of the eye did not seem to have any white cells in it so I opted for conservative treatment and simply injected an antibiotic and steroid below the eye. No surgery for now.
Slowly, steadily he improved. Eventually he regained 20/40 vision. Only the remaining track of the parasite through the macula caused some visual loss. Many questions remain as I think of this: Where and how did this thing get into his body and eventually to the eye? Was there more than one? Perhaps the trail I saw was from a second parasite, the one that caused the first set of symptoms the day before he saw the referring ophthalmologist? Was there a collection of these creatures hidden somewhere else in the body? Was there a shower of these wormy creepers circulating around his body that only became apparent when one got trapped in the small retinal artery? If it had not happened the way it did, would he have ever known he was infested with parasites?
After consulting a parasite expert I concluded the most likely culprit was that a “botfly” bit him, depositing a fertile egg. Over the next two to four days, an embryo would have emerged, the textbook pictures of which match what my referring ophthalmologist had seen. From there the embryo(s) must have entered the bloodstream. But the patient gave no history of a bite in that time frame; recall the one he reported was several weeks earlier.
This is the only time I have ever seen a complete central retinal artery occlusion treated and end up with a great visual result (all credited to the rapid treatment by the referring physician who lowered the pressure in the eye and allowed the creepy crawler to move along the artery and burst through it). These occlusions almost always result in blindness. Miraculous, right? If the ophthalmologist had not lowered the pressure in the eye just in the nick of time for the little wormy parasite—striped and with whiskers around its gaping mouth—to burst forth, there would surely have been more permanent retinal damage.
Without a doubt, the most haunting, eerie, and weird case I ever treated.
Editor’s note: To see disturbing pictures of botfly embryos (imagine these in your eye!), see:
http://www.wired.com/2013/10/absurd-creature-of-the-week-botfly/
Date of event: December 1982
The Short Discharge Summary
Joann N. Bodurtha, MD, MPH
Following my pediatrics residency at a large, medically sophisticated East Coast children’s hospital, I joined the Indian Health Service and moved to a very cold and geographically isolated Native American reservation. Overnight I went from having the best medical services in the country available to me to become a “rural medical doctor,” a minimum 500-mile drive from the nearest high-level care center. My basic pediatri-
cian’s desire never to miss a diagnosis followed me, but my ability to rely on technology had changed. At night, if a patient needed an urgent blood test, I had to call a janitor to come in to drive the sample to a hospital in the next town as our testing machines weren’t staffed at night. Equipment we take for granted today, like finger clip meters to measure blood levels of oxygen, wasn’t available in rural hospitals.
I had previously seen this eighteen-month-old boy once in clinic. He had “failure to thrive,” a condition in which growth and body weight are far below normal. This toddler was below the third percentile in weight—meaning, on a weight-for-age-and-gender growth chart, he weighed less than 97 percent of similarly aged boys—and not much interest in eating. On the very stormy night his mother brought him into our small ER, he was limp and listless, showing signs of total body failure from lack of fluids and nutrition. I knew he needed an intravenous (IV) infusion of sugar and minerals, but starting an IV line in a child this shriveled is very difficult. I tried three times, stepped away to drink a cola and regain my bearings, and tried the IV again. No luck. I was sure he was going to die, and I knew his only chance was leaving our small reservation hospital and getting somewhere where a team could start an IV surgically and provide intensive care.
I called the children’s hospital in the next state, but the storm was too severe for a small medical transport plane to come. I needed to find a nurse and get our ambulance driver prepared for the twelve-hour drive with potential stops for stabilization along the way. His mother came over and held my hand
several times as she saw me desperately making phone calls from our small emergency room. Our lab technician came in to help me run tests, from which I confirmed what I had already concluded from the child’s deathly appearance: his blood was life-threateningly acidic. I suspected an inherited metabolic condition (a chemical imbalance caused by a genetic defect) and called the priest. The child’s mother understood that he could die but wanted to try the drive, so we packed her in the ambulance with her son, the nurse, and the driver, with a map of small hospitals where they could stop along the way if he needed a final safe place.
As the ambulance pulled away, I looked up in the sky and no stars were visible through the clouds. The little boy could not possibly survive, and I knew to expect the phone call from some hospital somewhere along the way that he had died.
No call came that night, and two days later the nurse arrived back with the ambulance driver. The child’s mother was staying with him in the big city. I braced myself, assuming I would hear through the reservation grapevine when he died. This would be my first pediatric death since I had arrived on the reservation. My sense of destiny and anguish about his death overrode my deep curiosity about his diagnosis and what had happened. We had no cell phones or Internet back then to facilitate communication.
It wasn’t until I received the short hospital discharge summary in the mail three weeks after that starless night that I learned of the miracle. The discharge diagnosis was listed as methylmalonic acidemia (MMA). MMA is an inherited metabolic disorder that can be successfully managed through life with medicines and diet—but only if the patient can survive the initial crisis. Indeed, many patients don’t survive the initial crisis because their deterioration has gone too far and efforts to resuscitate them are too late. This child’s desperate condition that night, coupled with the prolonged delay in reaching a facility with adequate resources, put him well beyond what seemed a survivable crisis.
Miracles We Have Seen Page 11
