The patterns on the electrocardiogram (ECG) screen trip over one another, degenerating once more from the essential electrical rhythm of life, becoming something more lethal. The patient is eighteen years old, and I don’t know what’s wrong. The nurses charge up the defibrillator again. We deliver the shock to try to escape this downward spiral. There is a pause. The cells of the heart reset themselves, and then a more normal rhythm returns.
We have taken blood, shot X-rays, and run CT scans in search of a diagnosis. There is little there to guide us. We have examined him from head to toe. His chest is clear, he is free from injury, and his kidneys appear to be working—at least for now. But his blood chemistry is a mess. Lactic acid—a toxic by-product of the body’s metabolism—is building up fast. Normally his kidneys and lungs would clear it from the circulation, but they are overwhelmed. Lying there in the bed, unconscious and ventilated, surrounded by the blinking lights of enough monitors to put a Christmas tree to shame, his heart driven by drugs, his lungs driven by a machine, he has the physiology of a man exhausted and on the verge of death. The ECG degenerates once more. We shock again.
His belly is slightly swollen. Perhaps there is a problem with his gut. Perhaps, somehow, a branch of the circulation that supplies the loops of bowel has become obstructed or compromised. That would be more than enough to make him critically unwell. But he’s really too young for that to be likely. We review the CT scan images. To our eyes they are unremarkable. None of it adds up. We call in the surgeons. They are reluctant to operate. If they take him to surgery, he’ll probably die on the table. But if we do nothing, he will die for sure. We debate the decision, and while we do so, I shock him again. It is perhaps the tenth defibrillation. I have lost count.
This is intensive care. We can support hearts, replace kidneys, ventilate lungs. We can resuscitate, render unconscious, and replenish. This is the sharp edge of all that can be done to support human physiology against illness and injury. This is everything we have, and still I cannot see how we can possibly win. When is enough enough? Perhaps the surgeons are right. It is, after all, absurd—extruding a man’s physiology to its very limits in this way, well beyond any realistic expectation of survival. Why should we set ourselves against these catastrophes, when there are other fights that might be more easily won?
The formidable systems of artificial life support at modern medicine’s disposal create new problems. The desire to find something more that we could do in the struggle to save life is sometimes replaced by the need to understand when to stop. To help understand why we try at all—and the events that gave birth to the first intensive-care units—we must first go back to a time and place where modern medical interventions would have seemed like the stuff of science fiction and technology presented little obstacle to death.
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THE VILLAGE OF GRAND GAUBE, on the tiny island of Mauritius, is set back inland only a few hundred feet from the Indian Ocean. In 1946 it was a ramshackle collection of the most basic dwellings, separated from the sea by a beach of brilliant white sand. My father, Ah Yoong, and his family lived in a single-roomed hut. He was nine years old and shared the floor space with his parents, his two brothers, Daniel and John, and three sisters, Angele, Pierrette, and Therese. The roof was made of corrugated iron, and the walls were made of stone with barred openings that served as windows. It was, in my father’s estimation, the best house in the village by far.
His parents, Li Moon Ki and Tang Tin Ying, were immigrants from China, finding their way from the southeastern Chinese province of Guangdong, via the oceangoing trade routes, to Mauritius. They were Hakka people—literally “the visitors”—nomadic over centuries, moving where the land was good, never limited by geographical boundaries. When the age of steam came, they boarded ships in search of prosperity. That journey ended in Mauritius, a tiny volcanic island maybe thirty miles wide and not much more in length, fringed by white beaches and a vibrant coral reef. Tang Tin Ying was by all accounts a woman of fierce character and intelligence, but she was illiterate. Li Moon Ki, however, was among the few men of the village who could read and write. The house doubled as a general store, selling everything from rice and spices to liquor and nails.
Grand Gaube was a fishing village, a ramshackle assembly of huts with wooden walls, thatched roofs, and cow-dung floors. There were outside standpipes bringing fresh water, but only the most basic sanitation.
For the residents of Grand Gaube, the sea was their life. They took its spoils and were hostage to its temperament. They were vulnerable to the tropical storms it brought, particularly its cyclones. In the summer of 1945, two cyclones passed near Mauritius and a third descended on the island directly. These spiraling winds, with gusts of over a hundred miles an hour, carried drenching rains and destroyed what little infrastructure villages like Grand Gaube had. Afterward my father and his siblings collected the fish freshly strewn along the beach and swam in newly formed pools brought by storm and tides that had run inland. But sewage had spilled into these waters, and disease swiftly followed.
That summer an epidemic of polio broke out on Mauritius, causing as much devastation as the cyclones. The virus causing the disease could be carried in the gut and then spread in feces. Poor hygiene, the destruction of infrastructure, and bouts of diarrheal illnesses following the cyclone all conspired to amplify the spread. A team of British epidemiologists tracked it as it moved from village to village, often carried by healthy adults who’d built up an immunity to the virus.
What followed is an example of what happens when a transmissible, disabling, and potentially fatal disease encounters a population with only the most rudimentary public health provisions. During that summer, there were more than a thousand cases of poliomyelitis on the island. The children were by far the worst affected. Of 851 cases identified and recorded by epidemiologists, around two thirds were under the age of five, and more than 90 percent were under ten. The virus was aggressive and unfettered by modern medicine. Almost every case identified by the epidemiology teams—nineteen out of every twenty—suffered paralysis and withering of one or more limbs.
In my father’s family, his older sister, Angele, was the first to fall sick. For days she suffered with high fevers and drenching sweats. Grand Gaube had no doctor of its own. Occasionally a physician would pass through the village, but he was seen as a charlatan and viewed with distrust by most of its residents. Ah Yoong was sent out by his father to pick the leaves of the lilac tree, from which a cool bed could be made, insulating Angele from the hot floor in the hope that this would somehow reduce the fever. But the fever continued, and Angele appeared to be getting weaker.
In the earliest days of the illness, Ah Yoong would take his older sister by the arm to help her walk. Later he resorted to carrying her on his back.
Eventually the fever passed, but Angele was left paralyzed, unable to walk. She was just nine years old.
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THE BASIS FOR THE CONSCIOUS PROCESS that triggers us to move a limb, speak a word, or register a thought remains elusive and likely will for some time to come. Consciousness is the last dark continent of life science. We are incapable of properly defining it, much less understanding how it works.
But the processes it sets in motion are better understood. When it comes to movement, we know that the motor cortex is the point of origin of signals that trigger voluntary movement.
You can get an idea of the location of this thin strip of brain by putting your thumb on your earlobe and then stretching your index finger up until it reaches the top of your skull. Below the quarter arc now made by your finger and thumb, beneath the layers of skin, bone, and tough protective tissues, lies a narrow strip of brain. It is less than a centimeter wide and penetrates to only a few millimeters below the brain’s surface. In this modest layer lies a population of pyramid-shaped cells from which the impulses that initiate movement are first fired. Those nerve cells are neurons, responsible for connecting thought to action, specialized for the task of transmitting signals from brain to muscle bed.
Most of us could have a good crack at drawing an animal cell. You’d start with an indefinite oval, and somewhere near its center, you’d plant a circle that you would shade in and call the nucleus. A couple of smaller scribbles around that nucleus would give you mitochondria, ribosomes, Golgi apparatus, and other organelles. But this is only the basic scheme. Not all cells are made equal. And when it comes to neurons, that sketch doesn’t quite cover it.
The word cell derives from cellula, the Latin word for a room. But the whole thing is built much more like a walled city. The important stuff—the executive decision making—is done in the nucleus, the town hall. Here densely packed double-stranded DNA is woven and stored—the blueprints from which your body, and indeed all life, is built. The surrounding clear cytoplasm is dotted with tiny organelles, much smaller than the nucleus, which function like a city’s utilities and amenities. Here the mitochondria serve as power stations, while ribosomes are industrial estates, given over to the execution of manufacturing orders handed down from the nucleus. Elsewhere in the cytoplasm, there are other microscopic structures that play structural roles or take part in waste disposal or defense.
The pyramidal nerve cells of the brain’s motor cortex stretch out over vast distances within the body. The extensions of the cell are called axons. For the longest neurons in the body, those axons can grow to be over a meter in length—an enormous distance, given the minute scale of the cell itself. To put that into context, consider this: If the cell body of the motor neutron were indeed a city, say about the size of London, its axon would be represented by a road that ran out into space for about twenty million miles (which would get you about halfway to Mars!)
The neuron sends its axon down through the brain, on into the brain stem, and through the spinal cord, running and converging with others, like individual telephone wires combining to form the main trunk. Most of them eventually cross over to the other side of the body (which is why a stroke on the left side of the brain can lead to paralysis on the right side of the body). In the front of the spinal cord, they end. This nerve cell, the first link in the path from brain to muscle, is called the upper motor neuron. It has so far carried a nerve impulse from the brain to what is essentially a junction box in the spinal cord.
Here in a location known as the anterior horn, it will form a synapse, connecting with a final neuron, completing the link between the events in the brain that provide the impulse to move and the physical means by which movement is achieved: the contraction of muscle. This second nerve cell, the lower motor neuron, runs from the spinal cord, and its axon finishes embedded in the substance of a skeletal muscle.
It is the junction of these two neurons in the anterior horn that is vulnerable to attack by the polio virus. If it invades and destroys the cell body of the neuron, then the entire cellular structure, from spinal cord to muscle, dies back too—for good.
The cells of the nervous system are the oldest in your body. In contrast to almost every other cell type in the human body, they lack the ability to divide and self-replicate. Unlike skin cells, which enjoy a hefty turnover, if neurons become irretrievably damaged or die, they are not replaced.
To partially compensate for this lack of ability to regenerate, the central nervous system is buried deep within the core of the body, encased within the column of bone that is your spine and protected in the vault of your skull.
Despite this, it remains vulnerable, especially in the face of modern threats like motor transport. And the armor of the skeleton is no protection against infection.
During an attack of poliomyelitis, many thousands of these lower motor neurons can be lost. Once deprived of their nerve supply, the muscles supplied begin to waste, giving the characteristic appearance of withered limbs that accompanies paralytic polio.
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WHEN YOU TALK TO VIROLOGISTS about viruses, they have a grudging respect for their foe. Incapable of independent existence, viruses rely upon entering more complex cells and hijacking both their metabolic and reproductive machinery. Their genomes are too restricted in information content to allow them to manufacture the means of their own survival. They have only the simplest instruction set—one that allows them to attach to and enter a cell and trick it into manufacturing further copies of the virus.
But these simple structures have the capacity to destroy the host cells they invade and then spread like wildfire—first from cell to cell and then from person to person. As a consequence, viral pandemics are capable of causing death, disease, and personal suffering in many millions.
By the time the epidemic in Mauritius had passed, my father’s older sister, Angele, was wheelchair bound. His younger sister, Therese, was less fortunate still. In her the polio virus had weakened the muscles responsible for breathing and those involved in swallowing. She went on to die of pneumonia.
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IN 1952 THE POLIO VIRUS ARRIVED in northern Europe. But the pattern of attack was very different from that seen in Mauritius. Poliomyelitis, the inflammation and destruction of the motor nerves brought about by the polio virus, is also known as infantile paralysis because in earlier epidemics it was almost invariably young children who were most severely affected.
That pattern of attack and disability continued in developing countries like Mauritius, but in Europe polio had for some time been confined to small outbreaks because of improved sanitation, so there was little in the way of natural immunity to the virus among the wider community. When the epidemic arrived in Copenhagen in the summer of 1952, the disease ran rife in adults and children alike. The manifestation of the disease in adults was far more severe with a much higher risk of paralysis of the muscles involved in breathing and swallowing. This form of the disease—hitherto rarely seen in polio epidemics—was commonly fatal.
In 1952 there was no drug or vaccine that physicians could set against polio. When outbreaks hit major cities, they created tragedies of the grandest proportion. Thousands were infected and many hundreds left paralyzed or dead. Clinicians in general became nihilistic in their attitudes to the disease. Medicine, it seemed, had little or nothing it could offer.
But there was a distant hope—that the respiratory system could be supported artificially with ventilators, as a temporary bridge to survival, while the virus ran its course. For this the world of medicine would turn to the fledgling specialty of anesthesia.
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DURING AN INTERVIEW FOR A JOB with a cardiothoracic unit, an anesthetist was once asked by a rather pompous surgeon what she thought her role was within the surgical team. “Oh, that’s easy,” she replied. “It’s like an aircraft. I fly the plane, and you do the in-flight entertainment.” Apparently she still got the job.
There’s much more to the art of anesthesia than injecting a drug and making the patient count backward from ten. Anesthetists fly human physiology as pilots fly planes. While you’re awake and conscious, your physiology is largely under automatic control, just like a passenger airliner on autopilot. The intricacies of your cardiovascular and respiratory systems are held neatly in balance with your kidneys, gut, liver, and the enormous complexity of your brain. Your body’s autopilot—its system of autonomic control and feedback loops—is pretty good at the job. In health it keeps things running on an even keel, night and day, beat to beat, even when you’re asleep. Evolution has allowed thousands of biological processes to be seamlessly integrated and orchestrated under automatic control, so that you can go about your business and do the stuff of conscious thought without having to be bothered by pesky things like stopping to remember to make yourself breathe or keep your heart beating with the right rate and force.
But the unconsciousness of anesthesia is something other than sleep. It’s a little bit like rebooting that autopilot midflight and giving the aircraft over to someone else for manual control. In the same way that the captain of the plane takes over control to gently navigate around bad weather, so the anesthetist must wrest control of physiology from the patient in order to navigate the hazards presented by surgery, injury, and disease.
This ability of anesthetists to support and replace the function of organ systems artificially was vital to the creation of the new specialty of intensive-care medicine.
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THE SCALE OF THE 1952 DANISH polio epidemic was unprecedented. In Copenhagen over three thousand people were infected, among whom more than a third showed signs of paralysis. The number of these patients suffering with respiratory failure was higher than in any other European outbreak. Copenhagen boasted several large municipal hospitals, but there was only one, the five-hundred-bed Blegdam Hospital, that was equipped to deal with infectious diseases.
Toward the end of the summer, the polio epidemic was in its fullest throes. Henry Cai Alexander Lassen, professor of epidemiology at Blegdam, charted the progress of the outbreak and was shocked by the tidal wave of disease and death that flowed through the hospital’s doors. Among the facility’s staff, there was frank desperation; the disease appeared to defy any conventional treatment. In the first three weeks of August, thirty-one patients suffering with paralysis of the muscles of breathing and swallowing were treated at Blegdam. Despite the hospital’s best efforts, all but four died. Desperate for a measure that might turn the tide against the virus, one of Blegdam’s physicians, Mogens Bjørneboe, recalled the work of an innovative young doctor named Bjørn Ibsen, who was interested in anesthesia and artificial ventilation. Ibsen was a freelancer among the hospitals in Denmark, and Bjørneboe had worked briefly with him earlier that year in treating and ventilating a newborn suffering with tetanus. The child did not survive, but the intervention itself appeared to Bjørneboe to have worked, at least briefly. Ibsen was promptly summoned.
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THREE YEARS EARLIER, in 1949, Bjørn Ibsen had traveled to Boston to train as an anesthetist at Massachusetts General Hospital. He spent a year there and returned to Denmark with new skills and insight. He was nothing if not unconventional. He chose anesthesia over more traditional careers—a bold move in a world that wasn’t yet ready to acknowledge that this was a specialty worthy of the attention of qualified doctors.
He returned to Copenhagen in 1950 to find his former tutors scornful of his experience. The University Hospital of Copenhagen regarded Ibsen’s sojourn abroad as though it were time spent in the wilderness. “You have been away from the fountain of life for one year,” remarked a professor of surgery. “Let us hope you can catch up with what you have missed.” Despite these verbal assaults, Ibsen thought that the anesthetist might find a role well beyond the walls of the operating theater. After all, the experience of resuscitating a patient bleeding to death from a brisk hemorrhage or managing the life-threatening side effects of primitive anesthetic agents gave the anesthetist fraternity an appreciation of real-time applied physiology that was otherwise lacking in medical practice.
But Ibsen—having witnessed isolated cases of polio and with firsthand experience of the slow suffocating death that it brought—was most interested in the anesthetist’s ability to take over a temporarily compromised organ system.
During the polio epidemic in Copenhagen, the most fortunate among the patients were treated with artificial ventilators called iron lungs, which assisted breathing by helping the patient’s chest expand. These devices were half-cylindrical vacuum chambers, large enough to accommodate an adult. They were constructed so that a patient could lie sealed inside with only the head protruding through a hole in the top, sealed around the neck with rubber. The pressure inside the cylinder, and therefore inside the patient’s lungs, could be reduced to below that of the outside air, creating a partial vacuum in the patient’s chest and sucking air into his or her lungs through the mouth and nose. In this way the iron lung devices mimicked the normal mechanism of the lungs, using reduced pressure inside the chest cavity to suck air in from outside. This became known as negative-pressure ventilation.
Ibsen realized that iron lungs were effective but cumbersome, expensive, and, when it came to the hospitals of Copenhagen, in desperately short supply. Their use was severely rationed, and during the polio outbreaks, doctors had the unenviable task of deciding who, among the dozens of victims, should be given this chance of life and who should be left to die. So scarce was the resource that even when the iron-lung ventilators were employed, they were often used too late to make a difference.
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WHILE THE WORST CASES OF POLIO in the Copenhagen epidemic were proving almost invariably fatal, Ibsen was nevertheless confident that the skills and knowledge he had acquired while in the United States could save lives. Ibsen believed that the early failures seen at Blegdam were partly attributable to clinicians’ poor understanding of both the disease and its effect on human physiology.
No one seemed sure why these patients were dying. The sickest patients were drowsy and febrile, to the point where some of the doctors assumed that polio was causing infection and inflammation of the brain.
But Ibsen disagreed. The drowsiness and rapid heart rate, he believed, were not the result of encephalitis caused by polio but the consequence of high levels of carbon dioxide accumulating in the bloodstream.
In addition to bringing fresh oxygen into the body, the lungs are also responsible for expelling carbon dioxide. Deficient levels of oxygen in the bloodstream can, in part, be treated by increasing the amount of oxygen inhaled. The expulsion of carbon dioxide from the lungs depends much more heavily upon the rate and depth of breathing. Ibsen measured the levels of carbon dioxide in the bloodstreams of the sickest polio patients. Levels of oxygen appeared to be normal in these patients, but carbon dioxide had, in contrast, accumulated to many times its normal level.
Artificial ventilation was the answer, Ibsen was sure of it. He had taken great interest in the work of Dr. Albert Bower and his colleagues in Los Angeles, who had described their ventilation of polio sufferers with iron lungs and how this had reversed their prognosis from 90 percent mortality to nearly 80 percent survival in less than four years. If the Danish polio patients suffering with paralysis of the muscles responsible for breathing and swallowing could be similarly ventilated, then perhaps they could hope for the same success rates.
But iron-lung machines were bulky and hugely expensive—about the same price as the average 1950s family home. Blegdam Hospital possessed only three.
A cheaper, more widely available alternative would have to be sought. Here Ibsen fell back upon his experience in the operating room. He knew that patients could be ventilated by passing a tube into the trachea, connecting a rubber bag to the end of the tube, and then allowing oxygen to run into the assembly. When squeezed, the bag would push fresh oxygen into the lungs, thereby inflating them. When released the elastic recoil of the lungs expelled air laden with carbon dioxide through a valve. This method of ventilation moved air into the lungs by applying positive pressure from the outside rather than trying to replicate the work performed by the respiratory system in generating negative pressure within the chest. Ibsen was sure that this would work outside of the operating room, too. The scheme required little equipment and so could offer a lifeline to dozens of patients rather than the few who could be serviced by the handful of iron lungs that the hospital possessed. But Ibsen’s method would first have to be demonstrated and proved before his physician colleagues would accept it. He would not have to wait long for the opportunity.
Just a few days after Ibsen first arrived at Blegdam Hospital, he was referred the case of a twelve-year-old girl whose limbs and chest were paralyzed and who could not swallow. Breathless and unable to deal with the saliva in her mouth, she was choking on her own secretions. Her case was nearly identical to that of the twenty-seven patients who had died in the previous month. Without intervention, it seemed certain that she, too, would die.
Ibsen took her to the operating room and persuaded a surgeon to perform a tracheostomy, making a hole in the neck, around an inch below the Adam’s apple, which could admit a breathing tube.
The surgery proved difficult. They had injected a local anesthetic agent into the skin where the incision had been made, but the girl was agitated and fought against the medical team. The surgical wound bled back into her airway, soiling her lungs and adding to her distress. By the time the tracheostomy was complete and Ibsen’s rubber breathing tube had been inserted through the new opening, she was in extremis, with Ibsen wrestling to retrieve the situation. His colleagues, who had gathered to observe his efforts, assumed that they were merely witnessing the futile efforts of a physician to revive yet another patient dying of poliomyelitis. One by one they turned their backs and left the room.
Ibsen had to think quickly. The girl on the operating table before him was suffocating. The tube connecting her lungs to Ibsen’s rubber bag was in place and free of obstruction. But she was now distressed and fighting against Ibsen’s efforts to squeeze air into her lungs. With no air entering or leaving her chest, the oxygen in her bloodstream was dwindling while carbon dioxide was on the rise. If she was to survive, he would have to stop her from fighting against him and take over her breathing completely. Ibsen injected sodium thiopental, an anesthetic agent, and within seconds her body had gone limp. Now for the first time able to squeeze air into her lungs, Ibsen could make headway. Asleep and unable to resist Ibsen’s efforts, she was finally breathing—albeit artificially and with his assistance. The color returned to her face, and as the carbon dioxide fell, her heart rate stabilized.
Ibsen’s physician colleagues returned to the room, incredulous that he had rescued a child who a few minutes earlier had been so clearly at the point of death.
The hospital wasted no time. Ibsen’s technique was adopted, and within eight days, the wards were filled with patients being ventilated using this technique. Armies of medical students and nurses were recruited to assist in the task; standing by bedsides, squeezing bags in shifts, day and night, they provided artificial ventilation to dozens of patients at a time.
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UP UNTIL THE MIDDLE OF THE twentieth century, medicine was mostly about the treatment of chronic illness: consumption, cancer, syphilis, arthritis, and the like. Short, severe illness was generally fatal. Survival was rarely attributable to heroic medical intervention. With the exception of a few genuine medical emergencies that could be solved with a knife, there was little that the art of medicine could put in the way of critical illness. The idea that medicine might be in the business of buying the patient time by supporting their vital organs against the onslaught of overwhelming disease was almost entirely alien. But Ibsen’s pioneering work in the field was to have far-reaching consequences. What Ibsen started by organizing patients into intensive wards of care during the Copenhagen polio epidemic came to underpin the frontiers of modern medicine. In time, intensive care allowed us to stretch and protect human physiology well past the previously accepted limits of survival—paving the way for more ambitious surgeries and more aggressive medical therapies.
And poliomyelitis was by no means the last viral epidemic to threaten the world.
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ON MARCH 11, 2003, CARLO URBANI was on his way from Hanoi to Bangkok, attempting to relax after what had been a frenetic and exhausting fortnight.
Based in Vietnam with the World Health Organization, Urbani had been called in to advise physicians at the French Hospital in Hanoi on February 28. There a Chinese-American businessman named Johnny Chen had been admitted, suffering with an unusual and serious flulike illness. Urbani was unsure of the identity or nature of the disease; it behaved unlike anything he had seen before. As Chen’s condition deteriorated, Urbani’s concern at the strangeness of his illness grew. Within days, members of the medical team who had been in contact with Chen were also falling ill and exhibiting the same constellation of symptoms. It was clear to Urbani that they were dealing with a new and potentially dangerous infectious disease.
Chen, a man in his midforties, had a high fever and what looked like severe pneumonia. But other organ systems were also involved: His blood pressure was dropping, and his kidneys were showing signs of compromise. The medical team investigated further, but none of the usual suspects was present; bacteria were absent from his bloodstream, and the course was too aggressive to be ordinary viral influenza in a reasonably young, previously healthy man. The disease was a mystery. It was without a name, a known cause, or a point of origin. Without these it would remain without a treatment, a vaccine, or a means of containment. And if, as seemed likely, it proved lethal to Chen, then Urbani would be looking at an unknown, fatal, and highly infectious disease in a man who had traveled halfway across the world aboard a sealed jet aircraft, making countless contacts on the way.
Reports of a severe and atypical pneumonia sweeping across the southern provinces of China had been circulating for some months, but details and reliable data had been frustratingly hard to come by. Chinese officials had initially played down the scale of the outbreak, stating that the number of cases ran to little over three hundred, with only five deaths among these. This implied that the mystery illness was of little concern and would most likely burn itself out. But the true extent of the outbreak had been disguised. Later the world would learn that over eight hundred people had become infected in China in those early months, and more than thirty had died. But in February 2003, Urbani and the medical team at the French Hospital in Hanoi knew nothing of this.
Urbani spent the next eleven days working closely with the French Hospital in Hanoi. He first told the staff how best to protect themselves with the equipment they had available. At this time, they had little more than gloves, hand basins, and medical masks, but Urbani impressed upon them the vital importance of these basic measures. As concern grew among the hospital staff, Urbani provided reassurance through his continued presence. He returned every day and worked late into the night. Through these efforts, he built trust and later persuaded the hospital to take the difficult step of quarantining those members of staff with symptoms away from the wider Hanoi public. Shortly afterward, the French Hospital was closed to the public and armed guards were posted outside its front doors.
Urbani’s instincts told him that this was something very strange and very dangerous—something other than flu. He pursued lines of inquiry relentlessly, working long days at the French Hospital, taking samples, running tests, and making sure that infection-control protocols were properly enforced. Containment and proper identification of the causative organism were his priorities. The war against this infectious disease, whatever it was, would turn on these simple measures.
Pascale Brudon, the head of the World Health Organization’s regional office in Hanoi, witnessed Urbani’s efforts and was in touch with him throughout. She was concerned for his safety and anxious that he should take proper steps to protect himself. Urbani understood the risks he ran but regarded it as his duty to help the clinicians at the French Hospital amid this terrifying outbreak. Between them Urbani and Brudon saw to it that the WHO’s headquarters in Geneva was alerted. If their instincts were correct, then the fallout from this disease would be felt all over the world.
Over the next few days, international experts, summoned by the Vietnamese government on Urbani’s recommendation, arrived in droves. By this point, Brudon could see that Urbani was exhausted. He had for that past fortnight been alone in the fight to identify and contain this disease and now clearly needed to rest. Brudon suggested that Urbani could now afford to take a break and attend a conference in Bangkok, where he was due to give a lecture. Fatigued, Urbani accepted, and on March 11, 2003, after handing over to the incoming teams from the WHO and the United States’ Centers for Disease Control (CDC), he boarded a plane at Hanoi airport.
Aboard the flight, Urbani developed a fever, a dry cough, and a headache. In those hours, confined aboard that aircraft, he could have been under no illusions about his ailment’s likely cause. After the plane touched down, Urbani found his way through to the arrivals hall, where a colleague from the CDC was waiting to greet him. Fearing the worst, Urbani urged him not to approach. While they waited for an ambulance to arrive, the two men sat apart in silence. The paramedic team arrived wearing masks and protective clothing and took Carlo to the hospital. He died eighteen days later.
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IN THE SAME WEEK that Carlo Urbani left Hanoi, Johnny Chen, the forty-eight-year-old businessman whom Urbani had first been called to see, died in intensive care after having been transferred to Hong Kong.
Days later, Jean-Paul Derosier, a sixty-five-year-old French anesthetist who had treated Chen, along with a nurse who had been involved in his care, also died of the same disease. By March 15, authorities were aware of forty-three cases in Hanoi. Of these, forty-two were health-care workers who had looked after Johnny Chen. The exception was the son of one of the infected hospital staff. Among these, five had deteriorated rapidly, eventually needing intensive care and artificial ventilation.
The WHO had also become aware of new cases worldwide, in Singapore, Taiwan, Canada, and Hong Kong. In the week that Carlo Urbani was admitted to an intensive-care unit in Bangkok, the WHO issued a global health warning for the first time in its fifty-year history. The disease, whose precise nature was still a mystery, would finally get a name: severe acute respiratory syndrome, or SARS.
By the time of the WHO’s health warning, this much was known: The disease was infectious, highly transmissible, and deadly. Health workers on the front line and their families were most at risk.
Due in large part to the efforts of Urbani in the early days of the outbreak, the origins of SARS were rapidly established. It emerged that Johnny Chen had traveled from Hong Kong; there he had stayed on the ninth floor of the Metropole Hotel. Here he and seventeen other guests had acquired SARS from a single individual. Dr. Liu Jianlun, a sixty-four-year-old Chinese medical professor, had unknowingly contracted SARS in Guangdong while treating patients. He had traveled to Hong Kong to attend his niece’s wedding. This journey from the southeastern provinces of China to Hong Kong was the triggering event in the global outbreak that followed. Room 911, the room occupied by Dr. Liu, became the centerpiece of the investigation, and the ninth floor of the Metropole became ground zero for SARS.
The virus had circulated in animals for many months. Virologists chased its origins back to civet cats. In the food markets of Guangdong, with their exotic animal husbandry, it had moved from animal species to animal species before finally making the jump into humans.
Precisely how it did this remains a fundamental question for the science community. The limited repertoire of genes that the virus possesses is able to mutate and reassort. It is like the badly copied blueprint for a curious device, handed down from one generation to the next. Offspring are able to share new innovations or spontaneously improvise, until finally enough of those alterations align and sum to produce a terrible weapon. Nature, as our virologists are fond of reminding us, is the best and most efficient bioterrorist.
But SARS would have likely remained endemic within the southern provinces of China, had it not been for the fateful journey of Dr. Liu Jianlun. Taking it to Hong Kong, to an international business hotel, provided the most efficient vehicle for the spread of disease. At that nodal point, Jianlun was confined and in contact with dozens of travelers, all of them passing through, many on their way to other international destinations. From the moment Jianlun checked in to the Metropole Hotel, SARS was set to go global.
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SARS, AS ITS NAME SUGGESTS, first affects the respiratory system. But unlike polio it does not target the mechanics of breathing but the substance of the lung itself. The virus binds to cells in the tissues of its fragile air sacs and the branching network of airways. The virus enters and forces these cells to start churning out millions of new copies, like a printing press turned over to the production of quick and dirty war propaganda. The cells are not entirely without response. They are able to signal that they are compromised and summon the immune system to attack. But the virus is buried deep within the structure of the cell, and so destroying it means destroying the cell in its entirety: collateral damage in the wider fight against disease.
A combination of the death of these infected cells and the scarring and inflammation that accompanies the immune system’s attack leaves the substance of the lungs compromised. The once tissue-thin membranes, capable of expanding and collapsing like a supple balloon, become more rigid and less compliant. The exchange of oxygen and carbon dioxide across their surfaces is obstructed, and the force needed to expand the chest and perform the work of breathing is massively increased.
To the physician called to see a patient deteriorating in the face of SARS, the signs are all too clear. Effortless healthy breathing is replaced by a rapid, shallow pattern. Other muscles not usually involved in expanding the chest are recruited to overcome the stiffness brought by the viral infection. All of this additional mechanical effort needs to be paid for. The body’s demand for oxygen increases at the same time as its ability to grab those molecules of oxygen from the outside air and exchange them through the thickened, diseased membranes of the lung worsens.
Hemoglobin, the molecule in the blood cells that carries oxygen, is bright red in appearance when fully laden. Once stripped of this oxygen load, it becomes duller and bluer—accounting for the difference in appearance between arterial and venous blood. But if arterial blood cannot acquire a new, full load of oxygen in the lungs, it loses its rosy hue. The skin through whose capillaries these blood cells course acquires a shade more akin to thundercloud gray.
It is that vision—of the gray, breathless patient with the thousand-yard stare—whose first glimpse, even in the half-light of a hospital ward at night, signals real trouble and the need for interventions that can be provided only by intensive care. When the supply of oxygen is outstripped by demand, critical illness and death will inexorably follow. In these circumstances, the bridge to survival is provided by modern intensive care.
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CHARLES GOMERSALL WAS at the end of another shift as consultant in charge of the intensive-care unit at the Prince of Wales Hospital in Hong Kong. He had worn his hard-shell mask all day; its metal pinch clip had dug itself into his face, leaving a reddened dent in the bridge of his nose. But even now, striding across the car park, away from the ward and main hospital building, he kept it in place. The past fortnight had been punishing. The SARS outbreak was now at its height, and the unit was under strain from the constant flow of cases in need of critical care.
His first week on duty during the epidemic had been sobering. As an experienced intensivist, he was familiar with destructive pneumonias and deranged physiologies and used to holding the line in the face of adversity, but SARS had a different character. The clinical course was so fierce that at first Gomersall wondered if any of his infected patients would manage to survive.
The damage to the respiratory system wrought by the virus was severe. Artificial ventilation had to be applied with care. Forcing stiffened lungs open with external pressure from a ventilator was not without its hazards. Titrating the volumes and pressures applied by the mechanical ventilators precisely against the needs of each individual patient was an art. Getting it wrong could rupture delicate membranes, causing pneumothorax and a life-threatening collapse of the lungs. Ventilating too hard, with overzealous volumes, could further inflame the lungs and the situation. But it was the impact of SARS upon the rest of the body that presented the biggest challenge.
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THE CELLS OF THE IMMUNE SYSTEM roam the bloodstream and tissues, like policemen pacing the beat. They detect potentially harmful microbes, attack them, and then beckon other immune cells to enter the fray. When activated appropriately, this system puts a stop to trouble before it has a chance to get out of hand. But this system can be all too responsive. Some infections—SARS among them—overstimulate the immune response, giving rise to widespread inflammation that in turn can harm the body, an inappropriate response that causes more damage than the original infection itself ever could have.
Because of this, Gomersall’s SARS patients endured more than simple respiratory failure. The storm of immune response damaged kidneys and livers and caused hearts to fail, which meant multiorgan failure also had to be supported.
In the years since Ibsen’s first intensive-care unit was established, medical technology has moved on to allow the carefully nuanced support of many organs besides the lungs.
Now the failing circulation can be supported with noradrenaline, which raises sagging blood pressure. The heart can be driven with infusions of adrenaline, boosting its contractile force and ejecting greater volumes of blood needed to perfuse the rest of the body. Medicine has learned how to replace the work of the kidneys, using dialysis machines and blood filters. Even a malfunctioning gut can be augmented with a feeding tube or replaced by running calories and nutrients directly into veins. Today all of this can be achieved artificially and, in the most dangerous days of the disease, with patients in a state of anesthesia and unaware of their plight.
But Gomersall, along with other doctors and nurses on the intensive-care unit, was fast becoming fatigued. It was unheard of to have so many patients dependent on such high levels of artificial support for such a prolonged period of time. At this point, the outbreak had been raging for weeks, and there was no end in sight. What’s more, SARS was threatening the lives of the very frontline medical professionals who were struggling to keep its victims alive.
Protecting the clinical team had become a priority, one that Gomersall’s intensive-care unit had found itself initially ill prepared for. The high-filtration masks, so essential to prevent droplets laden with virus from penetrating into the health-care workers’ respiratory tracts, were in short supply. They also had to be tested for a precision fit: a poorly fitting mask was worse than no mask at all. This procedure could take up to twenty minutes for each person—a frustrating delay in the middle of the frantic battle against death and disease.
There were other, unanticipated problems. It was the beginning of the Hong Kong summer. Ambient temperatures ran at close to 30°C. (86°F.) with humidity at nearly 80 percent. The personal protection equipment covered the ICU team members from head to toe, leaving only a few square inches of skin exposed. The heat stress was stifling, even with the unit’s air-conditioning set to a usually bone-chilling 17°C. (63°F.). But despite fastidious attempts to avoid infection, the intensive-care staff found that even their cumbersome masks, gloves, and protective clothing couldn’t keep them safe from SARS. In all, five of their team contracted the disease, and one was later admitted to the intensive-care unit. But despite the dangers to themselves and their families, the doctors and nurses of the Prince of Wales Intensive Care Unit continued to show up for work, week in, week out.
Gomersall got into a routine. As soon as the severity of the situation became clear, he moved out of the family home, away from his wife, Carolyn, and two young daughters. He rented an apartment nearer the hospital and traveled to work by car. The act of getting in and out of the protective garb, to eat, drink, or go to the toilet, was time-consuming and left him vulnerable to infection. Gomersall took to waking early in the morning to breakfast and take on a decent load of water to hydrate himself. He then worked through the day without having to get undressed or remove his mask. Only when safely back inside his own car did he finally take the mask from his face. Each day, when he got back to his flat and closed the door, he felt a sense of overwhelming relief to be away from the ward and in his own space again. There, alone, he was in no danger of infection. More important, he was at no risk of passing the virus on to anyone else.
Gomersall would work for five days in a row on the unit. Before he could go home, he had to make sure that he wasn’t incubating SARS. To do this, he would spend ten days away from the ward, teaching and doing administrative tasks in his office—still staying at the apartment. At the end of that time, if he wasn’t sick and hadn’t developed a fever, it would be safe to go back to his family. Gomersall went through this cycle of work, self-imposed quarantine, and brief family reunion three times.
He got only four days at home between each shift. His family would studiously avoid talking about the elephant in the room. SARS dominated the news. Hong Kong had been paralyzed by it. But Charles didn’t much want to talk about what he’d seen, and Carolyn didn’t want to hear about it. Should he fall ill at work, Charles had told Carolyn that she should not come and visit. To lose one parent to SARS would be tragic; to lose two—as some families in China already had—would be insupportable.
Every day the teams faced the same set of problems: an intensive-care unit full of people ravaged by SARS, hopelessly unwell, propped up by a constellation of machines and drugs. These weren’t much more than a way of buying time in the hope that the disease would abate. That is all intensive care ever is: an extraordinary effort on the part of medicine to stretch human physiology well beyond its survivable limits in the hope that the patient can stay alive until something changes for the better.
In mid-June 2003, something did change. For the first time since the SARS epidemic began, no new cases were being admitted from outside the hospital. The only infections now were happening on the wards, between patients and health-care staff. SARS, for all its ferocity, had a peculiar pattern of behavior that had limited its spread. Some viruses, influenza for example, are highly transmissible very early in the infection, long before the patient becomes incapacitated and unwell. This is why flu spreads so quickly and so widely. Many people infected with flu remain well enough to go about their business, shedding virus to the outside world all the while.
But in most cases of SARS, the peak of contagiousness occurs only once the victim has become critically unwell, usually in the second week after infection. By this time, most of the patients had already been admitted to a hospital. This was why health-care staff had been so badly affected. Though the virus was both highly transmissible and deadly at this point, this limited SARS’s spread in the world outside the hospitals. By mid-July 2003, a little over four months after Carlo Urbani had first been called to the French Hospital in Hanoi, the SARS outbreak was firmly in decline, and the last of the travel restrictions to affected areas, recommended by the WHO, had been lifted. Worldwide, there had been more than 8,000 cases with 916 deaths among these. By the following May, no new cases were being reported to the World Health Organization. The chain of spread from human to human had finally been broken.
It could have been far worse. Carlo Urbani’s heroic efforts in the early identification of the disease and his swift actions in notifying the World Health Organization’s headquarters in Geneva led to a series of events that contained outbreaks and limited the overall spread of the disease.
Urbani first reported his concerns in early March 2003. After tracking rapid dissemination to three other countries, the World Health Organization issued its global warnings a fortnight later. Before the month was out, Malik Peiris’s laboratory at the University of Hong Kong had identified a new coronavirus, SARS-CoV, as the probable causative agent, and within a month of that, a Canadian laboratory succeeded in sequencing its genome. This provided information vital to the development of diagnostic tests and vaccines. But with travel to affected areas restricted and quarantine measures in place, the virus burned itself out.
The fight against epidemics and global pandemics is won not by high-tech interventions but by public-health measures. In this context, the work of intensive-care units may appear as little more than a gesture: the symbolic fighting of brush fires in a world under threat of being engulfed by a massive conflagration.
Indeed, the polio epidemic, which gave birth to the specialty of intensive care, was defeated not by ventilators, adrenaline pumps, or dialysis machines but by a program of vaccination—a campaign so effective that today the polio virus stands on the brink of eradication from the world. Since then, intensive care has retooled and repurposed itself. But the question remains: What is the value of intensive-care medicine—a specialty that invests so many resources for such marginal gains in the face of critical disease?
We can reassure ourselves that it is more than just a futile gesture. Of the sickest patients admitted to intensive-care units during the SARS epidemic, three out of four survived. Without the battery of artificial support, none would have lived. Mortalities in the worst-afflicted patients of Copenhagen’s polio epidemic of 1952 fell from 90 percent to less than 20 percent as soon as Ibsen’s innovations were implemented.
Today intensive care is a branch of medicine that allows other specialties to undertake more ambitious surgeries and interventions than ever before, safe in the knowledge that intensivists have successfully redefined the limits of human life when challenged by disease and injury.
At times of great crisis, the polio and SARS outbreaks included, intensive care has provided medicine with a much needed bulwark against illness, a means of buying precious time. It also does this for any given patient, on any given day, in any intensive-care unit. Intensive care exists in the hope that time enough might be bought for a disease to abate or for clinicians to successfully intervene.
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WE ARRIVE IN THE OPERATING ROOM and administer another shock before the surgeons begin. The ventilator is running. The patient’s lungs, too, are now beginning to fail—becoming stiffer and demanding more oxygen. The acidosis in his bloodstream is worsening, and his kidneys are deteriorating. We increase the adrenaline and the noradrenaline. The doses are now so high that their side effects are becoming a real problem. The drugs make his heart more irritable, more prone to fatal arrhythmias. We can hold his blood pressure up, but we must defibrillate more often now. Each time the ECG flips into a shockable rhythm, the defibrillator spits out an inch-wide strip of paper on which the jagged trace is printed in hard copy, like a seismograph beating out the lines of an earthquake. Several feet of this strip have now collected on the floor. An alarm goes off. I nod at the surgeons. They step back from the table. We fire the defibrillator again.
This is absurd. Sooner or later the rhythm of his heart will degenerate into something we can’t treat, something that electricity can’t reset. Perhaps, realistically, that is all we’re waiting for.
But then the surgeons call out. They’ve found a section of dead bowel, its arcade of vessels blocked by something—a blood clot perhaps. Deftly, the surgeons snip out the gangrenous tissue and join healthy ends of bowel together. Things do not change immediately, but with the diseased bowel gone and no longer leaking toxins into the circulation, my patient’s physiology will get better rather than worse. Surviving the next few days will be no mean feat, but the surgeons have given us the means to turn the corner. They are the change that we have been hoping for. We are far from out of the woods, but at least the woods are no longer on fire.
Back on the intensive-care unit, in the hours after the operation, the support we need to provide steadily decreases. We still deliver shocks, but they are fewer in number and less frequent. Slowly the patient is weaned off the drugs and the artificial ventilator. Over the next few days, we gradually hand control back to the patient, shutting off our machines as his normal physiology reasserts itself. Precisely how his body is able to recover and knit itself back together after such an insult is unclear. But he is young, and the young are remarkably resilient.
Less than four weeks later, that eighteen-year-old walks out of the hospital.