20. My Life as a Pediatric Resident in Montreal
I was given lots of responsibility at Montreal Children’s Hospital, and I thrived. At times, though, I was viewed as a bit strange, partly because of my peculiar status as a deserter but mainly because of my extensive experience at the pediatric hospital in Ethiopia.
Diphtheria Presents
At about 10 p.m. I was on duty in the emergency room. I was very new to Montreal. A child presented in extreme respiratory distress. She was near death. It was obvious to me that the child had diphtheria with a blocked airway. The child also probably had the cardiac failure secondary to cardiomyopathy (“floppy heart”) often seen with the disease. The other residents thought I was crazy. “We don’t have diphtheria here. We immunize against the disease. The DPT shot does that.” The D is for diphtheria; the P for pertussis, or whooping cough; and the T for tetanus. The child required an immediate tracheotomy. But the attending surgical staff was not in the building. I insisted on my diagnosis and asked the nurse to call the ENT (ear, nose and throat) surgeon on call. With the child in my arms, I made for the elevator to the tenth floor, where the operating suites were located.
The bad news is that, as a new staff member, I did not know the layout of the hospital. The bank of elevators that I took was on the wrong side of the operating suites. Instead of entering the front, I entered the back and found myself walking through all the operating rooms, contaminating everything with the lethal diphtheria bacteria as I went.
There was no time to wait for the pediatric surgeon to arrive. The anaesthesiology chief, who happened to be in the hospital, passed an endotracheal tube, and I did the tracheotomy. Together we saved the child’s life, in an endeavour that was eerily reminiscent of my experience with Haile Selassie’s grandson.
But the surgeons were not happy. All the operating rooms had to be closed for several days while the entire suite was decontaminated. Thus was born a story about that crazy draft dodger guy.
A month or so later, another child presented to the emergency room, this time with severe dehydration resulting from diarrhea and vomiting. The child was in such deep shock that no veins were visible for us to start an intravenous drip to administer fluids. This was a common event in Addis Ababa. We would rapidly warm a bottle of normal saline under hot water in the sink, put a large spinal needle into the abdomen at the umbilicus and rapidly infuse whatever it took to deal with the shock. The peritoneal lining of the abdomen is a huge membrane that rapidly absorbs the fluid and puts it into circulation. This solution was unheard of in Montreal.
It took more than a litre and a half of fluid before the veins finally appeared so that I could do a surgical exposure of the previously collapsed veins. I was then able to insert a catheter into a vein to administer the needed fluids.
Lead Poisoning
In the middle of the night, I was called to the emergency room of Children’s to see a two-year-old who was deeply comatose and pale with sluggish pupil responses, indicating severe brain injury. A smear of his anemic blood showed basophilic stippling and many fragmented red blood cells, typical findings in lead poisoning. His mother reported that he had been suffering from abdominal pain, which was treated with clear fluids. My previous experience in the Bronx with lead poisoning among poor children who were eating leaded paint chips had alerted me to the certainty of lead poisoning in this case, but it made no sense. Although anemia and basophilic stippling are certainly the tipoff to lead poisoning, this child came from a white middle-class family from the suburbs. We just did not see lead poisoning in Montreal.
I rapidly began a process of chelation, administering drugs that bind lead, a therapy unknown to the Children’s staff, as they did not see lead poisoning. I applied what we did in the Bronx to remove lead from blood and tissue, but before the treatment could take effect, the child died, his brain so swollen that life was unsustainable. While I questioned the distraught mother about possible sources of lead, we managed to get the four-year-old brother into the hospital. He also had suffered from abdominal pain, and the same pediatrician had been recommending clear fluids, with the same unfortunate result. He too was anemic and suffering from lead poisoning, but as he was bigger and older, he was not as sick. But what was the source of the lead?
In a joint sleuthing exercise with the mother, we finally determined the cause. The mother was an excellent amateur potter. She had fashioned a pot that she used to store apple juice in the refrigerator, topping it up when it got low. When the children began to have abdominal pain and cramping, a sign of lead poisoning but of many other things as well, their pediatrician recommended clear fluids. She gave the apple juice from the handcrafted jug that she had herself made, employing the glaze according to the formula recommended in her pottery manual. She had done everything right.
When she brought in the jug for me to examine, it was clear that the pot was lined with a white dusty powder, probably lead oxide. On our analysis, we found the pot released an amazing concentration of lead. Meanwhile, I had successfully chelated the four-year-old, who was recovering.
Knowing nothing about pottery, I joined forces with Rosalie Namer, a well-known local potter, who studied the formula the mother had used from her pottery handbook, which was the book most used by hobbyists across North America. The formula was wrong. For lead to remain in the glaze, it required two parts of silica to one part of lead. The written formula was one to one, thereby allowing the lead to be released in the presence of acid solutions, like apple juice.
Abdominal pain from lead poisoning from pottery and pewter occurred often in the 1700s in the colonies of the American Revolution; it was known then as the dry gripes. It was also well known as far back as Greek and Roman times, with cases appearing occasionally to the present. It was thought to account for sterility, and even the fall of the Roman Empire. The theory was that the Roman upper patrician classes were storing wine in glazed pots, whereas the artisan class, who could not afford such luxury, flourished and reproduced.
That could have been the end of the story, but the potter and I needed to know how often this kind of event was occurring. The potter compounded many identical test pots. She applied different glazes according to the existing formulae in the texts of the day and exposed the pots to apple juice. Other faulty formulae were discovered.
I obtained a small grant and gave ten McGill medical students fifty dollars each to go shopping at Christmas time with instructions to buy whatever pottery containers caught their fancy, without telling them what was being studied. They returned with many pots—domestic, imported and handcrafted. Many released large amounts of lead. Earthenware was the most problematic, especially the brown, lightly glazed Mexican pottery that was ubiquitous.
The problem formula and many other incorrect formulae in the hobbyist texts had to be rewritten. With some difficulty, this was accomplished. Rosalie and I moved ahead with the project. The needed publicity was obtained. We then presented our findings to the appropriate authorities on both sides of the Canada-US border. We then worked with the appropriate governmental agencies in the US and Canada to change importation rules to stop the import of improperly glazed vessels and resolve the public health problem. And we worked with the appropriate authorities to develop legislation in the US and Canada to define safe glazes. Our findings were published in the New England Journal of Medicine.3
Trying to turn this terrible event into something as positive as possible, I spent a lot of time supporting the mother, who was blaming herself. She continued to stay in touch. The four-year-old developed normally. The family went on to adopt a child. I have tried several times since to have research published by the iconic New England Journal of Medicine and failed, whereas as a resident I had been successful. That’s the way it goes.
Prematurity and the Battered Child Syndrome
I was called to the emergency room to see a very small, very sick infant. It was immediately clear to me he had been severely battered. He was hugely bruised and had multiple fractures. He died of a ruptured stomach. The sad story could have ended there, the parents charged with murder.
The child had been a very small premature infant who was cared for on the newborn service at Children’s. He had spent many months in hospital, required weeks on a ventilator, experienced a variety of major crises but survived to be discharged to two young, immature parents. Whose fault was this? Well, everybody’s. Young parents are more likely to have a premature infant. And they are least able to care for a high-needs newborn. Teen mothers often get pregnant to have somebody to love and love them in return. This neurologically damaged baby, who had barely survived a variety of conditions and was unwell at discharge, was hardly able to do that. Did they have enough support? Certainly not.
Struggling to process this tragedy, I wondered what the prematurity itself might have had to do with the battering. The incidence of prematurity is about 6 per cent. In a rather simple study, I pulled all the hospital’s charts of children who had a diagnosis of battered child syndrome in a twenty-year period. I found that 26 per cent of them had been premature infants. Thus, prematurity clearly predisposed them to battering. And the sicker they were, the more likely they were to become battered. In fact, any child with a chronic disease or disability is more likely to be abused. While I was still a resident, I published the finding.4
These examples of my research illustrate that, beginning early in my career, I used a very eclectic approach. I studied what I needed to study. I felt compelled to think beyond the obvious to learn the underlying issues. I could not stop myself. These cases not only demanded diagnosis and resolution but raised questions of a systemic, even societal, nature that required answering. Why were these cases presenting? How could I not try to understand underlying causes? Later, as I began to focus on maternity and newborn care, the same approach characterized my work. Why was maternity care so resistant to change? Why were old and discredited approaches still in practice? Why was it so difficult to appreciate the obvious? What medical care did women really need?
I had completed my senior residency, and because I had been promoted rapidly through the postgraduate educational system, I still needed more total pediatric time to qualify to write the exams that would make me a Canadian and American pediatric specialist. I intended to stay in Canada, so I looked around Montreal to see what to study next. It boiled down to two good choices: Dr. Robert Usher, a well-known neonatologist who later became my mentor and whose work I regarded as seminal, or Dr. Charles Scriver, a world-renowned biochemical geneticist. I decided to do both. The paradox was that I never intended to become either a neonatologist or a biochemical geneticist, but as I had to remain in Montreal, I wanted to make the most of it.
I began with Charles Scriver’s lab, spending six months working with patients with inborn genetic metabolic amino acid abnormalities, including phenylketonuria and tyrosinemia. What was interesting for me was not the biochemistry of the diseases but the lives of the families carrying the diseases. Hence, I visited them in their homes, collected specimens and ran the analyses. Although I learned a great deal, including appreciation for Dr. Scriver’s holistic approach to his patients, I knew that this was not to be my path.
The next period was as a chief resident with Robert Usher at the newborn intensive care nursery at the Royal Victoria Hospital. I greatly admired Dr. Usher’s research and the way he cared intensely about his little patients. But more importantly, I liked him as a person and I liked the way his neonatology unit worked. He gave the nurses great responsibility and engaged them in the research. He knew that I was not heading for neonatology as a career but some variety of community medicine. Nevertheless, I had determined that Dr. Usher had a lot to teach me about research methods as well as clinical care, regardless of where I would eventually wind up.
Dr. Usher appreciated my prior experience in Ethiopia and in the newborn nursery at Stanford. Therefore, unusual for him, he just oriented me for a couple of days and then left for a much-needed summer vacation, leaving me in charge of the neonatal intensive care unit. I was not completely alone, as Dr. Saroj Saigal arrived at about the same time. She was to be Dr. Usher’s research fellow, but she had good clinical skills, and we greatly enjoyed each other as colleagues. In practice we shared responsibility for the unit. She later became a well-regarded neonatologist and an expert in the long-term follow-up of very small premature infants.
Dr. Usher was a phone call away, but we tried not to call him. I felt that he was reassured that we would not get into too much trouble, as his head nurses were incredibly experienced and made sure that we stayed on course, and they were generous with their advice. Dr. Usher’s genius was in the way he gave his staff responsibility and appreciated them. He was also a wonderful debater, and I enjoyed the banter. I later learned that others thought him too argumentative and opinionated. I never felt that.
Dr. Usher was the father of the early effective treatment for hyaline membrane disease (respiratory distress syndrome) and the care of the very small premature infant. Many other neonatologists denigrated the excellence of his outcomes with comments like: “Nobody can get such good results because he is present on the unit all the time.” They called it the Usher Effect, which was a put-down, as in their units, care was passed on to residents and others down the food chain, and the chief was often remote from the shop floor. When we called Dr. Usher, he would even bicycle to the unit in the middle of the night. This was indeed the Usher Effect in action.
He taught me research methodology and critical thinking. For more than six months, I cared for one 615-gram baby, named baby Ho, a premature infant who at the time was among the smallest known survivors at such a low weight. In caring for this newborn, with Dr. Usher’s support, I was able to learn what he jokingly referred to as “all of neonatology.”
It began with a call for me, as resuscitation officer, to come to the delivery room for the birth of a very small infant. As I arrived, Mrs. Ho delivered the tiny girl. The mother was a new immigrant, and within minutes she said in broken English: “Too small. No good. No want.” She quickly got off the delivery table and left the hospital. The baby was both very premature and very malnourished. Over the next six months, this baby had multiple respiratory illnesses and cardiac failure, diabetes, multiple infections and a series of metabolic catastrophes.
By the end of six months, the baby looked beautiful, but I was convinced that she was deaf, and I was certain that the deafness was caused by the drugs that I had been forced to use to control her heart failure interacting with the drugs that I had to use to control her many infections. The literature showed much later that these drugs, used together, damaged hearing by destroying the eighth cranial nerve.
Somehow, we kept in touch with Mrs. Ho, who had never visited her baby. But at six months, she finally came to see her baby and said: “Nice baby. I keep.” And despite what we think we know about maternal-infant bonding, Mrs. Ho and baby Ho never looked back. Mrs. Ho had to learn English and sign language to be able to communicate with the audiologists and speech therapists. If not for baby Ho’s condition, Mrs. Ho might never have left her Chinese-speaking enclave in Montreal and learned to speak English. Baby Ho developed normally and did well in school. She attended a retirement party for Dr. Usher. She was studying to become a physiotherapist.
Baby Ho is a perfect example of the resilience of little babies when they’re treated fully for their condition. There was a time in the 1950s and ’60s when it was thought that such small babies ought to be left to die. Many of them did not die, but they were severely damaged by the lack of needed treatment. This approach is long gone.
Hard to believe, but rickets seemed to be following me. In Montreal, Mayor Drapeau had declared that adding fluoride to the water and vitamin D to the milk was a “plot” to poison French Canadians. The result: terrible teeth cavities and rickets. The rickets story had been elucidated by Dr. Scriver. It was common in the Montreal long winters to find full-blown rickets, particularly among the poor, very young infants and children of the East End. These children would even appear in the hospital in winter with seizures because of low calcium, an effect of vitamin D deficiency. Under Dr. Scriver’s influence, when vitamin D was finally added to the milk, a process initiated decades earlier in the rest of North America, rickets disappeared in Montreal.
After my time with Dr. Usher, I was convinced by the retiring chief of pediatrics, Dr. Alan Ross, who had offered me the senior residency position that I needed to avoid deportation on arrival in Montreal, to become a chief resident at the children’s hospital. It was hard to refuse him, but I needed one more year before I took the specialist exams in pediatrics. Taking the chief residency would fulfil that need. Dr. Ross was determined to provide the incoming head of pediatrics, Dr. Mary Ellen Avery, who was arriving from Johns Hopkins, with an experienced chief resident. Dr. Avery was a world-famous neonatologist who had done outstanding fundamental work on the basis of hyaline membrane disease, elucidating the role of surfactant, the material that is synthesized by the developing lungs that is responsible for the lungs staying inflated.
In 1969–70, there were always two chief residents. Normally, they would split the year: six months in-patient and six months’ outpatient. My counterpart, Dr. Robert Williams, loved the in-patient and I preferred, at that point, the outpatient. Part of the reason I wanted to remain in the outpatient was that I really did not get on well with Dr. Avery. I enjoyed the community aspects of the outpatient department, but Dr. Avery made clear to me that she felt that the only true science was basic science. She told me that I had great potential as a scientist and that I was wasting my time in the outpatient department.
It actually worked out well, as we two chief residents supported each other and took turns covering the whole hospital on nights and weekends, in-patient as well as outpatient. The outpatient department provided a great opportunity. I was responsible for hundreds of patients per week, as well as teaching the interns and residents. I loved it.
But some tension between Dr. Avery and me developed as a direct consequence of the unfortunate resident strike of 1969. Within days of her arrival in Montreal, all of the Quebec interns and residents went on strike. The basis of the strike was the abysmal way that francophone residents were treated in Quebec teaching hospitals. The English residents at McGill felt that they had to support their francophone colleagues, even though their relationships with their own professors at McGill teaching hospitals were good. Hence, the anglophone residents reluctantly joined the strike.
This resident strike took place just after the strike of the Quebec physicians, a result of their opposition to the introduction of Medicare, which was being implemented when the resident strike took place. I was not at all supportive of the physicians’ strike against Medicare and found it hugely hypocritical that the professors were now criticizing residents for their similar action. But for Dr. Avery, a resident strike was incomprehensible. Dr. Avery came from Johns Hopkins, where residents, according to her, were on duty all the time except for an occasional holiday. She felt the Quebec residents, who were asking for duties to be limited to one in three nights, were spoiled. Moreover, she actually demanded that her two chief residents somehow force the children’s hospital residents to abandon the strike. “How can you strike against children?” she said.
I tried to explain to her that as chief residents, we had nothing to do with the strike. Chief residents are neither union nor management. It didn’t wash. She was adamant that we had the wherewithal to “get her residents back.” We felt that we had no power to do this. I felt our role as chief residents was to make sure that nobody died. With that in mind, we organized the attending staff to cover the wards and outpatient department on an emergency basis. We two chief residents organized teaching sessions for the attending staff, who had understandably lost some of the skills that they had not used for years. Pediatricians in office practice do not do procedures or start intravenous drips or engage in the many day-to-day tasks that hospitalized children need.
Although most of the attending staff respected what the residents were doing and realized the necessity, they were not happy, as it interfered with their office and specialist practices and income, so they hoped for a rapid resolution. They were so unhappy that after a few weeks some staff members got a bit threatening. Notable among them was Dr. Leo Stern, head of neonatology at Children’s, who somehow felt that I personally not only could but should stop the strike. He actually threatened me: “If you do not stop the strike, I will make sure that you never get a job anywhere in North America.” Years later, when I was job hunting, I was told that he was doing just what he promised. But I was also told not to worry, as he was recognized as a bad actor and would be ignored.