THE  ART  OF  MEDICINE  -  HEALING  AND  THE  LIMITS  OF  TECHNOLOGY

by  Herbert  Ho  Ping  Kong

LESSONS of the MONTREAL YEARS

He who studies medicine without books sails an uncharted sea, but he who studies medicine without patients does not go to sea at all. 

— Sir William Osier

The hard decision to emigrate having been made, I now faced another thorny question: where exactly to go. A number of friends and colleagues had happily moved to the United States, and I did receive a few informal American overtures. But my first preference was Canada, which I judged to be a gentler society.

Accordingly, I sent letters of introduction to the chiefs of medicine at hospitals in several major Canadian cities. General internists were not in high demand at the time, so I was not exactly deluged with offers. But I did receive replies about potential positions in Halifax, Edmonton and St. John's. I made a visit to Ottawa, but was discouraged by the February snowbanks that literally reached to the eaves of houses. And oneToronto physician-in-chief expressed interest, but with a caveat: he wanted me to effectively audition in private practice for a few years before applying for a staff position.

Then I received a one-line response from Montreal's McGill University, offering — sight unseen — to make me an assistant professor of medicine and consulting physician at the Royal Victoria Hospital. I waited one week and then accepted, without ever having set foot in Montreal. I arrived with my family in September 1973, a period of resurgent French nationalism in Quebec. A new adventure was about to begin.    

Our first weeks were spent in the Royal Terrace Hotel, not far from St. Joseph's Oratory, one of Montreal's famous landmarks. One day I took the family for a walk. Along the way, we met a francophone priest and stopped to chat. Noticing that my daughter was wearing a winter coat, even though it was still only September, he said, "You must be visitors."

We explained who we were and why we had come.

"Welcome,"  he   declared  with  genuine   enthusiasm.   "As Jamaicans, you and we Quebecois are fellow sufferers of colonialism. I'm glad you did not go to Ontario."

The faculty I joined at McGill was among the world's most distinguished. Its extraordinary constellation of medical talent included endocrinologist John Beck, chairman of the-department; Arthur Vineberg, the father of coronary artery surgery, famous for the invention of the Vineberg procedure, a precursor of cardiac bypass operations today; nephrologist John Dirks; endocrinologist Max McKenzie; hematologist Bernie Cooper and future palliative care specialist and nephrologist John Seely. John Meakins was to be my service chief and Peter Pare (who co-authored the Fraser and Pare chest radiology textbook, Diagnosis of Diseases of the Chest) was my unofficial guardian. I also remember fondly Martin Hoffman, at once a great physician and superb orator.

In earlier years, the renowned Wilder Penfield, Montreal's famed neurosurgeon and founder of the Montreal Neurological Institute and Hospital, had also taught there, as had anesthesiologist John Sanderson, (he'd previously been head of anesthesiology and the founder of the intensive care unit at the University Hospital in Jamaica), the legendary Sir William Osier and Norman Bethune. At that time, McGill ranked ahead of even Harvard or Johns Hopkins and produced genuine five-star physicians. More than a dozen future chiefs of medicine emerged from this extraordinary environment, taking their expertise to the wider world. For me, a mere country doctor from Jamaica, it was very heady stuff.

When I arrived in Montreal, I quickly made an appointment to see the chief of medicine, Dr. John Beck — who, like 20 percent of the staff, was an American.

"We're very pleased to have you here, Dr. Ho," he said.

"And I'm very pleased to be here. But tell me—what exactly is my job description?"

"Well," he said, "the truth is, we don't actually have a job description for you."

It was an odd arrangement, but entirely to my liking, allowing me to do what I thought I might do best — serve as a consulting general physician (known as a general internist in North America).

Two weeks later, I found myself supervising ward rounds with a group of residents, interns and medical students. At University Hospital in Jamaica (and most of the British Commonwealth), it had been the custom during rounds to actually spend time with the patient; in Montreal I found the team would simply gather in the corridor with the patient's file and discuss the case.

Outside one room, the resident informed me that this particular patient was a candidate for a liver biopsy.

"Perhaps, I should examine him then," I said, "since that's a potentially dangerous procedure."

"That won't be necessary," the resident assured me. "We examined him this morning."

"Look," I said, "where I come from, we examine patients. Give me 30 seconds."

So I examined him and, a minute later, declared that the liver they were about to biopsy was, in fact, a kidney. A murmur of surprise buzzed through the group.

"What did he say? What did he say?

"I said, this mass is a kidney, not a liver. It's a very large kidney and we need to find out why."

"How.do you know?"

"I know because that is what a kidney feels like. Where is the intravenous pyelogram?" I asked, referring to the gold standard imaging procedure for the kidney during that era.

"Rounds are finished until this afternoon," the chief resident promptly announced. An hour later, he emerged with the imaging result (IVP) confirming that it was indeed a kidney.

The story of this clinical encounter quickly spread through the Royal Victoria Hospital and the rest of the McGill system. This served as a much-needed impetus for significant changes in the teaching of clinical medicine in Montreal and the rest of Canada — the re-introduction of bedside teaching in the curriculum in those institutions that had discontinued this traditional approach.

Just how urgently reform was needed was borne out by a 1978 paper written for the Journal of Medical Education. It reported that while many physicians on rounds believed that they were spending considerable time teaching at patient bedsides, videotapes of these encounters indicated that, in fact, they were doing so only 16 percent of the time. For half the time, the presence of the patient was gratuitous. Most rounds were conducted in corridors, where medical students often confessed to being inattentive or having trouble hearing the teaching physician.

In time, I was able to change the way rounds were conducted at the Royal Victoria Hospital. Thereafter, they took place in the presence of patients with bedside examinations, where necessary.

I had been in Montreal a number of years when Gilbert, a 50-year-old star detective from the city's police force, appeared in my office. He was somewhat pale, complained of backache and had experienced a modest weight loss (less than 10 pounds) Physicians he had already seen suggested his problem was essentially mechanical, likely disc-related, and thought he might qualify for workmen's compensation.

Now, it was my turn for a little detective work. Although Gilbert's hemoglobin level was normal, his erythrocyte sedimentation rate (ESR) — the rate at which red blood cells tend to adhere — was 80. Normal would be less than 15. A high ESR rate is commonly taken to indicate the presence of inflammation in the body and can be an early clue to potentially serious organic disease.

That reading led me to the hypothesis that he could have a serious disease. I suspected multiple myeloma, a blood cancer arising from the bone marrow. Further testing, including protein electrophoresis and examination of the bone marrow, confirmed the diagnosis.

In the subsequent weeks and months, I came to know Gilbert quite well. One day, he appeared as a subject/patient case study for a clinic I was leading for a group of six medical students. I pointed out to them, as I always did, the value of observation —taking note, for example, of the importance of examining a patient's neck veins as potential indicia of cardio-vascular illness.

The detective stopped me right there.

"What you are doing is exactly the way I train my rookie detectives," he said. "It's all about paying attention to what you see."

Then, spontaneously, we devised a little experiment. We asked the students to close their eyes and tell us what objects were in the room. Most could accurately name only two or three out of 10. Then we let them keep their eyes open for two minutes and actively observe the objects in the room and repeated the test. Not surprisingly, by focussing harder, we recorded a five-fold increase in the number of items observed.

This was an important lesson, both for me and for them — not just to "see" or look at smoothing passively but to"look at it" actively. Sadly, although his illness was treatable, it was not curable. Gilbert succumbed to the disease a few years later. But three decades later, I am still using that same experiment with students.

And as I suggested in my Introduction, the same approach applies to hearing and touch.

Instead of just hearing (passive), physicians must listen (active). Instead of just feeling a lump in the neck, they must learn to palpate it. Ask yourself: this lump — how big is it? Is it hard or soft? What lies beside it? Is there a relationship to the surrounding tissue? Does it disappear if we change the head's position? Is it draining into the lymph nodes? These questions will help make the examination a more active process.

Similarly, with a heart murmur: what am I listening for? How loud is the murmur? What is its character? Does it change with respiration? Does it radiate in any direction? A sharper focus on what you are doing will almost certainly improve diagnostic accuracy.

I part company here with journalist Malcolm Gladwell's argument in his book Outliers: The Story of Success that great expertise is only acquired after 10,000 hours of experience. A good physician only needs to have seen a condition once before to commit its characteristics to informed memory, and to be able to diagnose it correctly if he or she encounters it again.

You have to develop effectively two separate skill sets — the intuitive talent of Sherlock Holmes, and the harder, more scientific approach of Dr. Watson.

I recall one Montreal case in which both observation and deduction were required. While on teaching rounds, my students and I came across Eleanor, a very sick 30-year-old woman. She had high fever, shortness of breath and tremor. It appeared to me to be a probable case of staphylococcus aureus septicemia (a blood infection). Physicians consider it the "cancer" of microbial agents because it spreads as quickly and as widely (metastasizing) as some aggressive cancers. Untreated, it can be lethal within two or three days.

As I was examining her, I noticed a series of four or five little dots, like puncture wounds, on her leg, just above the ankle.

"Where did you get those?" I asked.

"Oh," Eleanor replied. "I fell off my bicycle and the parts of the chain stabbed me."

I peered more closely at the wounds. The story was certainly plausible, but I suspected something else. The marks on her leg weren't sufficiently uniform, in shape or alignment, to have been caused by the bicycle's chain.

"Where are your needles;"'

The young woman immediately started to cry and, soon after, confessed to injecting herself with drugs (via the saphenous or leg vein). The contaminated heroin she was injecting had quickly been carried to the right side of the heart, formed a bacterial non-cancerous growth (a vegetation) on the valve, and subsequently embolized to the lungs, where it produced abscesses. I was thus able to say right then that she was suffering from staphylococcus endocarditis, a bacterial infection of the heart's lining. This is sometimes known as tricuspid endocarditis, common in places with high numbers of intravenous drug users. Fortunately for Eleanor, it was curable with antibiotics.

Inevitably, if you practise long enough, you will meet patients who lie in other ways. I recall the quiet of one Sunday morning in the emergency ward in Montreal disturbed by rising concern about Victor, a young man, also about 30, who worked in the hospital's emergency ward.

The chart showed that he was running a consistent fever of exactly 104.3 degrees and experiencing violent rigours, or whole body chills, as well as an accelerated heart rate and some blood in his urine. The ER doctors had already started him on a course of antibiotics, having diagnosed pyelonephritis, an infection of the urinary tract. Untreated, the condition could lead to septicemia and death.

I approached the bed, where Victor lay shaking violently under the white bed sheet (actually too violently, as you will see).

"Are you ready for this:"' I asked the doctors and nurses gathered around me. And with that, I suddenly yanked the bed sheet away from him and flung it on the floor. Simultaneously we heard the sound of glass hitting the concrete floor —clinkety, clink, clink, clink — a set of eight thermometers, all registering at exactly 104.3 degrees!

Deeply embarrassed, Victor promptly got up, dressed and left the hospital.

Although I had taken a risk with my dramatic approach to exposing him, I'd never seen a case where, in six consecutive readings, the temperature was always the same. That was the clue that this illness was not what it seemed. If you take a patient's temperature over a period of several hours, almost invariably, there will be slight variations. His were static, a straight line. Moreover, shaking chills or rigours are usually not as violent as this patient's shaking: his were like the violent shaking in a grand mal seizure attack.

This was a clear case of factitious fever, which is sometimes related to Munchausen syndrome. Its name derives from 18th-century German nobleman Baron Munchhausen, who had a great gift for embellishing the truth. The medical syndrome was named formally by British endocrinologist Richard Asher in 1951, to describe situations in which people fabricate histories, signs and symptoms of illness to get admitted to hospital.

In Victor's case, he had faked his body chills, fixed the temperature settings on the thermometers (by immersing all eight thermometers in hot water at the same time) and pricked his finger with a stylet to create blood in the urine. We later found the stylet that he used to prick his finger in the night table drawer beside his bed.

Not all apparent mysteries, of course, are so easily solved. One day, I was visited by Merle, a woman of about 34, who'd been referred by a family physician. She had a history of eye problems and was now complaining of fatigue and a general sense of unease. Her hemoglobin was 150 (normal is 120-130) — a possible indication of polycythemia, a disproportionate rise in the blood's red cells.

Six weeks later, Merle returned, still feeling unwell, with a hemoglobin reading of 160. More time passed, and the reading continued to climb, to 180. By then there were subtle differences in her neurological exam — i.e., minor changes in the tremor of her fingers on testing for coordination. This indicated a problem in her cerebellum, which is the part of the brain essential for normal coordination and balance. That minor signal — and the hemoglobin readings — got my attention. A high hemoglobin count is commonly caused by low oxygen levels. These can be caused either by chronic lung disease or shunts in the heart that divert blood from the lungs.

A high hemoglobin count can also be caused by excess erythropoietin, which is essential for the production of hemoglobin. It is erythropoietin (EPO) that has often been used — and abused — by professional athletes, especially cyclists, long-distance runners, speed skaters and cross-country skiers for blood doping, to increase oxygen-rich red cell counts. Many sports organizations have officially banned it, most famously the Tour de France and the Olympics.

Though rare, certain tumours can also produce erythropoietin in excess and thus cause high hemoglobin. There were only a few possibilities, among them renal cell carcinoma, or kidney cancer; thymoma; fibroids; liver cancer or a rare brain tumour, a cerebellar hemangioblastoma. A subsequent brain scan revealed the tumour, situated in her cerebellum (cerebellar hemangioblastoma).

Fortunately, the tumour could be removed by surgery and the young woman was able to fully recover. How rare is a cerebellar hemangioblastoma? I have not seen it since, which may help explain why the details of the case remain so vivid in my memory.

What I did see again, three decades later, was another case that involved elevated red blood cell counts. This time, the patient was a 68-year-old Asian woman who complained of mild headaches, fatigue, high blood pressure and a history of asthma. Her mucous membrane had a slightly reddish hue, which was explained by her hemoglobin reading — 180. The asthma suggested an oxygen deficiency, which can drive up hemoglobin levels. We commonly see this in patients with serious lung disease; in such cases, hemoglobin counts may be as high as 200, but her examination and tests for asthma were all normal.

Recalling the Montreal case from years before, I ordered a CT scan of the cerebellum, but there was no evidence of tumour. Other scans showed no lung damage, no abdominal tumours and no cirrhosis of the liver. Her erythropoietin level in the blood was high. The question that perplexed me was what explained the elevated levels of EPO?

Then I remembered that an ultrasound of the abdomen does not include the pelvis. A CT scan was ordered and a benign, grapefruit-sized fibroid was discovered. That was the source of her erythropoietin. It had made her blood too thick — the cause of her headaches and general fatigue and difficulty concentrating. A hysterectomy, removing the fibroid, cured her.

During my early years in Montreal in the 1970s, we did not yet have access to sophisticated ultrasound or CT technology. This made diagnoses more complicated, and I occasionally resorted to distinctly unconventional approaches. McGill, at that time, maintained a close medical relationship with the University of Nairobi. Personnel went back and forth regularly, working on aspects of infectious disease.

On one occasion, a colleague of mine returned from Kenya with a persistent fever. He was sweating frequently and losing weight, but tests ruled out both malaria and typhoid fever. My instinct was that he had developed a liver abscess, caused by amoebae he may have consumed in the Kenyan drinking water. To test my theory, I actually punched him — lightly — in the liver. His pained reaction told me I was right. We quickly drained the abscess, administered antibiotics and he made a complete recovery. Today, ultrasound or CT scans make diagnosis of these lesions precise, but you still have to make the clinical diagnosis before ordering those tests.

Some three decades later, I received a call from a family physician, Dr. David Greenberg, who asked me to examine one of his patients, a desperately ill man of about 50. He came in with fever and chills, slightly jaundiced. I punched him — not too hard — in the liver and, based on his wincing reaction, was convinced he had a liver abscess. I sent him for an ultrasound the same day, which confirmed the diagnosis.

Despite the time it requires, the critical importance of documenting a patient's full history—personal and professional—was underscored to me in one fascinating Montreal case. Two members of the city's police department paid me a visit. They did not come to interrogate me. They came separately, each describing a similar set of symptoms — decreased appetites, mild abdominal pain and reduced energy levels. The malaise was non-specific; they just didn't feel quite right. When I saw them, each had been ill for more than six months. Curiously, I learned, they had often worked together.

Even though I had no indication of why, one of the early differential diagnoses was lead poisoning. After a series of non-conclusive tests on the first patient, we decided to test lead levels in his blood. They proved to be far above the normal range. So the diagnosis was now clear: lead poisoning. The question was why.

Lead plays an interesting role in the history of disease. Affecting several organs and tissues, toxic levels can produce symptoms that range from mild confusion and abdominal pain to coma and death. Its effects were observed as early as the second century BC by the Greek botanist Nicander, who described its consumption as leading to colic and paralysis. Some academics maintain that lead, used widely in Roman aqueducts for 800 years, may have contributed to the fall of the Roman Empire, its toxins seeping into the water supply via lead plumbing.

In the modern era, lead mixed into paint has been blamed for lead poisoning in children. Children and adults exposed to lead poisoning typically show impaired intellectual ability.

In the 1980s,  Canadian researchers  conducted tests  on the cadavers of victims of the ill-fated Franklin expeditions of the 19th century, British explorers famously lost in the Arctic. Examination of their bones revealed lead content of 228 parts per million, versus only 22-36 ppm in the bones of Native Canadians accompanying the mission. The villain: cans of meat (bully beef) that the explorers had stocked on board their ships. The tins were the product of a then novel technology, soldered by lead and tin. I doubted whether that was the cause of lead levels in the blood of the first police officer who came to me, but something was.

As I often do, I began with a few questions about his work.

"You're a policeman, I see."

"Yes."

"How long have you been on the force?"

"Twenty years."

"Do you live near a battery-making plant or a battery dump?"

Lead in such waste facilities has been known to leech into the water supply.

"No," he said.

"What are your responsibilities on the force?"

"I've done various things, but for several years I taught other officers how to shoot guns."

"At an outdoor shooting range?"

"Indoors. And underground."

Bingo, as they say. The air in that subterranean facility would have been filled with microscopic fragments of lead. My patient would have breathed it into his lungs every day and had it on his hands when he ate lunch. Repeated exposure had produced the effects of lead poisoning.

When his colleague came to see me with similar symptoms, that mystery was even more quickly resolved. He had also spent many hours in the indoor shooting range.

Both men were successfully treated with the drug, dimercaprol, which leeches lead out of the system via the urine.

So while it is sometimes suggested that getting to know your patient is a waste of time, my own experience is that it is essential. At a minimum, it helps cement the connection between doctor and patient, establishing a bond of trust likely to make treatment more effective. And, as with the Montreal police officers, it can yield the answer to the origins of disease and distress.

One day in Montreal, I was asked to attend to Colette, a 79-year-old woman who had broken her arm. Apparently, she had been kneeling in church, at prayer, when she collapsed, falling onto her limb. We started chatting and she related the terrible experience. I took her pulse — a normal 70 beats per minute. Then I put my finger on her carotid sinus, located in the neck just below the angle of the jaw. The pace was 40 beats per minute, a disturbingly low pace. Carotid sinus pressure can cause the heart to slow, by increasing what is known as the vagal tone (relating to the vagus nerve).

By chance, visiting my office was Dr. Maurice McGregor, a professor of cardiology and at that time the chief of medicine at Royal Victoria Hospital.

"What are you doing!" he asked.

I explained that I had just examined an elderly patient who had fallen in church, broken her arm, had a very slow pulse and was likely suffering from what is known as carotid sinus syndrome, the cause of her syncope or fainting spell. She probably needed to have a pacemaker implanted in her heart, I suggested. "I don't believe you," he said. "Let me have a look." Together, we went to visit the patient. McGregor placed his fingers on her carotid artery. Now, the heart rate was 38 beats per minute.

Still, he was unconvinced. "This doesn't prove anything, Herbert." "Maybe not, but do you want to wait until it's 30 and she falls and breaks a hip?" I think he was annoyed that I was telling him, a cardiologist, what needed to be done.

Finally, with a twinkle in his eye, he graciously conceded the point. McGregor was no ordinary cardiologist. He later went on to integrate South Africa's Witwatersrand medical school, even before the release of Nelson Mandela.

Sometimes known as Stokes-Adams attacks, cardiac syncope is not rare. The cause may be electrical — the heart's natural pacemaker may fail, leading to heart block (i.e., a very slow heart rate). Or it may beat too fast. It can also be mechanical, precipitated by organic disease of some kind, aortic valve stenosis or hyper-tropic cardiomyopathy. If the heart beats too slowly (30 beats per minute or less), not enough blood flows to the brain, so it shuts down the system and you faint. If the heart beats too fast — say, 200 beats per minute—the same thing will happen. On occasion, the beat may alternate between too fast and too slow in the same person, the so-called tachybrady syndrome.

In a typical cardiac syncope episode, everything is fine until it isn't. You lose balance then consciousness, usually leading to a fall to the floor and, frequently, injuries. This is part of what distinguishes it from vasovagal attacks, which usually come with some warning — dizziness, nausea or tinnitus (ringing in the ears). Epilepsy may also induce syncope, though again there are distinguishing features such as flashing lights (prodrome) or twitching. Or you may have a grand mal seizure, usually followed by disorientation.

Physicians must therefore be careful to determine which form of syncope they are treating. With cardiac syncope, recovery — if you survive — is usually spontaneous, with full memory of the event. Regardless, it is critically important to understand the precise circumstances that led to syncope because it is a potentially serious and life-threatening problem.

Jeremy, a man of about 45, came to see me after fainting on a beautiful summer day at his cottage. He was sitting on a dock by the lake when, without warning, he suddenly fainted. It lasted only 25 seconds and then he came to. He thought he had fallen asleep.

I saw Jeremy a few months later and he seemed otherwise healthy. We did an echocardiogram and outfitted him with a Holter, a monitor that measures and records the heart's electrical competence. The latter told us he was suffering from intermittent but complete heart block in the conduction system. In lay terms, his wiring was defective. Causes of this potentially lethal condition include coronary artery disease, fibrosis or sarcoidosis, a non-infectious TB-like illness. Jeremy needed a pacemaker, which corrected the problem.

So did Fern, a 42-year-old woman who fainted while driving, crashing her car into a tree. Shaken but not badly injured, she went to an emergency room. Tests there turned up nothing definitive, and she was then sent to a neurologist to see if the blackout had been caused by epileptic seizure. Again, her brain function was normal. At that point, they asked for my opinion. I took her history, which included a bout of sarcoidosis some 15 years earlier. We outfitted her with a Holter, which proved normal, but an MRI revealed a lesion on her left ventricle.

Her history of pulmonary sarcoid, the syncopal event and the MRI of her heart showing the nodule all suggested susceptibility to heart block and the need for a pacemaker. One was implanted and Fern has experienced no recurrence of syncope.

The pacemaker, in most cases, can successfully address problems of syncope caused by brachycardia (heart beating too slowly). But it should be remembered that the pacemaker, too, is a machine and can malfunction, adding complications. And not every incident of cardiac syncope needs to be treated with a pacemaker.

Lawrence, an Anglican priest of about 64 years, had experienced recurrent syncopal episodes for a year. His palpitations and flushing were so severe that he had rushed off to an emergency room on four or five occasions. Cardiologists and internal medicine specialists had examined and tested him with electrocardiograms, an echocardiogram and a Holter device, but were unable to find any organic problem.

When I saw him, he complained that his tachycardia was making his life miserable.

"Tell me," I said, "are you high church Anglican or low church?

"High church," he said.

In the high church, priests take communion, the symbolic re-enactment of the Last Supper, by eating a wafer and drinking wine.

I said, "Maybe you are having these attacks because you are allergic to the sulfites in red wine. Stop drinking it completely and see what happens.

For the first year, Lawrence had no further attacks. But after that, every now and then, he would attend a celebration and drink a glass of wine, beer or half a glass of champagne — and another attack would ensue. But as long as he remained abstinent, he was fine.

Both PERSONALLY and PROFESSIONALLY, my years in Montreal were happy and successful. But by the early 1980s, I was in my early 40s: if I were ever going to make another career move, it was certainly the time.

……….

AN  EDUCATOR'S  PERSPECTIVE

Dr. BRIAN HODGES

Brian Hodges graduated from Queen's University School of Medicine in 1989, completed a psychiatry residency at the University of Toronto in 1994, a masters of Higher Education in 1995 and a Ph.D, in 2007. Since 2003, he has been the director of the University of Toronto Wilson Centre, one of the largest centres for health professional education research in the world. From 2004 to 2008, he was chair of evaluation at the Royal College of Physicians and Surgeons of Canada, overseeing assessment of the 62 specialty programs. He was named full professor and the Richard and Elizabeth Currie chair in Health Professions Education Research at University of Toronto in 2009 and vice president education at the University Health Network (UHN) in 2010.

It's likely that few physicians are more in sync with the teaching philosophy of Dr. Herbert Ho Ping Kong than Dr. Brian Hodges, the University Health Network's vice president for education. In various roles, he has spent the last 20 years trying to inculcate the principles of humane practice. Just how essential they have become in an age of transcendent technologies was brought home to him a few years ago: he became a patient in his own hospital system when he suffered a ruptured appendix while on the job.

"I would say my own experience was mixed," he says, reflecting on the event. "I didn't know it was happening to me. There were some good clinical skills on display, but there was also a little bit of 'let's see what the CT scanner says' kind of thinking. And appendicitis is still a clinical diagnosis, by and large."

The incident, Hodges says, solidified his conviction that educators must be careful not to "deskill in the art and humane practice side of medicine."

More than psychiatry, he says, medicine needs "to continue to emphasize the physical examination and basic clinical skills. What I love about Herbert's message is that he makes the case that medicine rests on the basic contact between patient and doctor. But there's no doubt we have drifted away from it." Hodges' own specialty, psychiatry, is not exempt from these principles.

Although most of Hodges' time is now devoted to administration, when he's on call, he heads for the emergency ward. His first question to residents is '"Which patients have had a physical exam?' And if they haven't done it, I'll say, 'Let's go do it.' Sometimes they'll look at me like I have three heads. But until you've done a comprehensive clinical assessment, you don't know anything about anybody."

Advocates for the traditional patient-centric approach, Hodges concedes, often confront a challenge from other doctors —the argument that there is not sufficient evidence to justify huge expenditures of time interviewing patients when technology, in the form of the CT scan or an ultrasound machine, can often do a better diagnostic job.

It was in part to answer such critiques, he says, that "Herbert set up his Centre for Education in Excellence and Practice [CEEP] at Toronto Western, to conduct research that would not only prove the value of the physical exam, but demonstrate that the empathic relationship formed between doctor and patient pays health dividends. There's some great work in diabetes that shows that people with strong doctor-patient bonds live longer and have better outcomes. So he's using science, evidence-based medicine, to prove his case."

The MRl, CT scanner and other marvels of technology represent a great set of tools, he allows. "But if you are building a house, you don't start with the circular saw. You start with a plan, with a design. We could send every person in the emergency room to get a CT scan when they arrived, but there is no brain activity for that. It's like trying to build a house without an architect, without a plan."

And no single machine — or even constellation of machines — he notes, can do pattern recognition the way a human can. "And pattern recognition remains the heart of diagnostic medicine. It rests entirely on a doctor sitting down with a patient, looking at them, listening to them, talking to them, assembling the story and then using the technological tools as an adjunct to confirm suspicions or a hypothesis."

In Hodges' experience, medical students in their early years broadly accept the importance of learning and practising the art of medicine. Often, it's a validation of the idealistic thinking that may have brought them to the profession in the first place. But as they move through the system, they become exposed to the so-called hidden curriculum, which begins to undo their instincts and hardens them.

"Remember that as third-and fourth-year students, as clinical clerks, they not only see humane, caring role models like Herbert and his disciples," says Hodges. "They see other faculty members who take shortcuts and look for efficiencies. And they see conflicts between different medical services over what constitutes the right approach or what's important. If it's not handled well, the student begins to stop doing things they once did, because he's hearing that it's not really important. And if too many of those factors impinge at the same time, they may take a very rudimentary approach and fall into the trap of relying on technology, or stop thinking — just refer the problem to someone else."

In fact, he says, it's a fallacy that humane medicine takes a huge amount of time. "Being empathic and making a connection does not take an hour. My best role model for this, when I was an intern, was actually a surgeon. I was at Toronto's St. Joseph's Hospital and in those days, we had short three-week rotations. He sat down with me and said, 'Brian, most of my patients are dying of cancer and we only have about five minutes with each of them, but you must make a connection with them in that time. Yes, the x-rays are important. Yes, the follow-up is important. The time is short, but there's no reason you can't build a relationship in five minutes.' And he was absolutely right."

Is there a protocol to follow in the process? Absolutely, says Hodges. "Rule number one would be not to look at your watch."

Not long ago, an advocate from Toronto General Hospital's office of patient relations related an instructive anecdote to Hodges. A doctor walked into a patient's room and immediately began talking. The patient interrupted him and said, "Excuse me, would you mind if we began by you telling me who you are, and I'll tell you who I am, and we can chat for a minute before discussing what my MRI says?"The doctor apologized and said, "Of course, you are right." "So a lot of this is simple human communication skills," says Hodges.

Nothing is going to change the current paradigm of subspecialization, Hodges believes, but "if I'm a diabetes specialist or if I only treat patients with schizophrenia, or if I deal with post-partum hemorrhage, I need to constantly remind myself that medicine is larger than this. A lot of the responsibility rests on those who train sub-specialists — to challenge them to understand the generalist's perspective and communicate their thoughts to the generalist, which is often the family practitioner." But there are, he acknowledges, weaknesses in the system. "There need to be more conversations. The specialists have to reach out to the generalists and say, 'What do you think? You know the whole person."'

To counteract the tendency to reductionism, the sub-specialist has to approach the patient and his or her family with humility, Hodges contends. "The opening conversation should not be about the blood sugar levels but 'How are you? What's the big picture?"'

Every patient, he says, is a unique canvas and thus requires a custom-made approach. "The art in the art of medicine is not just a generic 'be nice to people.' It's like any other art, a set of refined skills that can be learned and need mentorship and modelling. How I talk to someone in the emergency ward who is depressed is quite different than how I'd talk to someone who is dying and needs palliative care."

The medical historian Edward Shorter, Hodges says, has documented the decline of the art of medicine. "There was more art when there was less science and fewer drugs, when doctors made house calls and saw patients in their homes. We've slid from that longitudinal relationship." Now, some medical schools are attempting to revive the longitudinal approach, with students spending a year with one mentor/doctor, instead of two weeks.

Hodges himself chairs the management committee of the Phoenix Project, a multi-year initiative that aims to give doctors and nurses a better balance between human compassion and technical expertise. The project was launched by the charity Associated Medical Services, which felt medicine was drifting away from the model of compassionate care. If that care were measured today on a scale of 10, our current performance, Hodges maintains, would be below average.

"A lot of it is our fault," he says. "Medical students come in with those values and we undo them in our institutions. You can make people better or worse, depending on the environment they work in."

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TO  BE  CONTINUED