by Lewis Thomas
I have had a fair amount of firsthand experience with the issue, having been an apprehensive patient myself off and on over a three-year period on the wards of the hospital for which I work. I am one up on most of my physician friends because of this experience. I know some things they do not know about what nurses do.
One thing the nurses do is to hold the place together. It is an astonishment, which every patient feels from time to time, observing the affairs of a large, complex hospital from the vantage point of his bed, that the whole institution doesn’t fly to pieces. A hospital operates by the constant interplay of powerful forces pulling away at each other in different directions, each force essential for getting necessary things done, but always at odds with each other. The intern staff is an almost irresistible force in itself, learning medicine by doing medicine, assuming all the responsibility within reach, pushing against an immovable attending and administrative staff, and frequently at odds with the nurses. The attending physicians are individual entrepreneurs trying to run small cottage industries at each bedside. The diagnostic laboratories are feudal fiefdoms, prospering from the insatiable demands for their services from the interns and residents. The medical students are all over the place, learning as best they can and complaining that they are not, as they believe they should be, at the epicenter of everyone’s concern. Each individual worker in the place, from the chiefs of surgery to the dieticians to the ward maids, porters, and elevator operators, lives and works in the conviction that the whole apparatus would come to a standstill without his or her individual contribution, and in one sense or another each of them is right.
My discovery, as a patient first on the medical service and later in surgery, is that the institution is held together, glued together, enabled to function as an organism, by the nurses and by nobody else.
The nurses, the good ones anyway (and all the ones on my floor were good), make it their business to know everything that is going on. They spot errors before errors can be launched. They know everything written on the chart. Most important of all, they know their patients as unique human beings, and they soon get to know the close relatives and friends. Because of this knowledge, they are quick to sense apprehensions and act on them. The average sick person in a large hospital feels at risk of getting lost, with no identity left beyond a name and a string of numbers on a plastic wristband, in danger always of being whisked off on a litter to the wrong place to have the wrong procedure done, or worse still, not being whisked off at the right time. The attending physician or the house officer, on rounds and usually in a hurry, can murmur a few reassuring words on his way out the door, but it takes a confident, competent, and cheerful nurse, there all day long and in and out of the room on one chore or another through the night, to bolster one’s confidence that the situation is indeed manageable and not about to get out of hand.
Knowing what I know, I am all for the nurses. If they are to continue their professional feud with the doctors, if they want their professional status enhanced and their pay increased, if they infuriate the doctors by their claims to be equal professionals, if they ask for the moon, I am on their side.
8
NEUROLOGY
During my second year in medical school I took an elective course in “advanced” neuroanatomy, taught by Professor David Rioch, a member of the Department of Anatomy. The course consisted entirely of the construction, by each member of the class of a dozen or so students, of a plasticene model of the human brain. It was child’s play, in several senses: building an engrossing sort of toy, made up of dowels fitted to each other and adorned with wire extensions upon which the various nuclear structures in the brain were molded in clay of various colors; putting together an esthetic experience so that it came out right without falling apart; and, in the end, regarding in puzzlement an altogether primitive and naïve conception of the immense and, at that time, unimaginable complexity of the brain. Even so, in 1934, when we had no idea that we had no idea, the finished model seemed to make a certain kind of sense. Our wires arranged themselves to represent the great sensory tracts entering the base of the brain from the spinal cord, intermeshed with the bundles of motor fibers on their way down from the brain stem, and, higher up, the fanning out of intercommunicating fibers linking the basal ganglia, the cerebellum, the thalamus, and some smaller globules of clay representing structures in the hypothalamus, all neatly wired to each other and out and up into the highest reaches of the cerebral cortex, from which, as our models were intended to demonstrate, everything else was governed and run, like a wonderful electric apparatus. When the models had been completed, and checked in detail by the professor, we sprayed the things with varnish and took them back to our rooms. Mine pleased me so much that I kept it for nearly fifteen years, until it finally dried up and fell to pieces on the back shelf of a closet.
This simple mechanical exercise, requiring only three months, provided lasting enchantment. During the next two years of school, while I was clerking in the various teaching hospitals of Boston, the patients that interested me the most, and on whom I spent the most time on the wards and back in the library, were cases of neurological disease.
The making of a neurological diagnosis was itself a kind of game. All you needed to play were three implements, a rubber hammer for eliciting reflexes over tendons and muscles, a pin for testing pain receptors, and a wisp of cotton (some neurologists carried around a feather) for testing light touch. One’s thumbnail served for scratching the soles of the feet to see if the toes extended and spread; this reflex, the Babinski, was probably the most important single feature of the neurological examination, signifying that damage had been done to the long motor pathways and, always, real trouble.
I had it in the back of my mind, all through the last years of medical school and my internship in medicine, that one day I would study neurology seriously. Hopkins, McGill, Columbia, the University of Pennsylvania, and Harvard were the places to try for, I had been told, but I had no idea whether one was better than another, or whether they were good at different things. Then, one day in 1938, partway through my internship, I was told that Dr. Robert F. Loeb was taking on the directorship of the Neurological Institute of New York and that I should look into the possibility of a residency there. Loeb was a youngish but already famous member of the faculty in the Department of Medicine at P & S, recognized internationally for his work on Addison’s disease, the metabolic functions of the adrenal cortex, and the new field of salt and water control in physiology. He had never done neurology, but had been persuaded to leave his position at Presbyterian Hospital, where he was a full professor, to reorganize and modernize the Neurological Institute and, especially, to try to introduce more contemporary research into what had always been a prestigious clinical facility but had had very limited scientific interests.
This was a piece of exciting news. Neurology had always been an entirely descriptive branch of medicine. Once the clinician had figured out the precise location of the lesion (or lesions) in the brain or spinal cord—and the exactitude with which this localization could be accomplished, when you knew enough neuroanatomy, was the challenge of the field—there was nothing much to be done for therapy because of so little understanding of how the structures really worked. The principal exceptions were pernicious anemia, often associated with destruction of the long sensory and motor pathways in the spinal cord, which could be treated with liver extract; neurosyphilis, for which fever therapy was marginally useful; and pellagra, by this time a rare disease seen only in chronic alcoholics, in which widespread lesions of both the central and peripheral nervous systems occurred because of vitamin B deficiency. A few brain tumors could be successfully removed by the neurosurgeons, but the commonest ones were almost always inoperable. The great need in neurology in the 1930s was obviously to introduce some proper research laboratories devoted to the study of brain disease.
The Neurological Institute was dominated at that time by a large a
ttending staff, almost all of whom were in private practice and carried the professional title of “neuropsychiatrist”; one couldn’t make a living doing just neurology, so most of the clinicians did psychiatry as well, and many of the private rooms in the institute were occupied by “nervous” patients, not sick enough to be confined next door in the New York State Psychiatric Institute, but certainly without real neurological disease either. Some were unhappy neurotics, needing rest and comfort, others alcoholics in for drying out, and a few barbiturate addicts admitted for what usually turned out to be unsuccessful efforts at withdrawal.
The real neurological diseases were out on the open wards, twenty beds to a ward, and these beds were governed with considerable autonomy by the neurology residents, guided by a carefully selected group of attending neurologists who made ward rounds each morning with the residents, along with clusters of Columbia medical students on neurology elective clerkships. Once a week Dr. Loeb came down from his new office on the top floor of the institute to make his own grand rounds on one ward or another. These were state occasions, involving not only the neurologists but also a large entourage of residents, students, and visitors from the medical service across the street in Presbyterian Hospital. We spent a lot of time selecting the cases to be presented at these rounds; they had to be interesting combinations of complex neurological and medical illnesses, and we always hoped to have a few patients in whom the diagnostic problems would be sufficiently obscure to baffle Loeb himself, but this, so far as I can recall, never happened. Loeb was a master diagnostician. He had the gift I had observed earlier in Hermann Blumgart at the Beth Israel Hospital at Harvard: he could walk on a ward and recognize, by some kind of instinct, each of the patients in whom something deeply serious was going on. He was also a master at the art of raising interesting questions, unanswerable but nevertheless interesting, about the possible mechanisms that underlay the diseases with which we were confronted. What did we think was going on, really going on, in such a disease as multiple sclerosis (this was one of the commonest of all problems on our wards)? It begins in young adults with a series of sudden, small neurological defects: double vision, slurring speech, unsteadiness of gait, weakness in one extremity or another, areas of numbness here or there, then progresses in cyclic episodes of new and equally sudden impairments, all due to patches of destruction of the myelin sheaths around nerve fibers in one or another region of the brain and spinal cord. The disease goes on for years in most patients, but not all; some have only one or two brief attacks and then, unaccountably, are finished with the disease, while others go on to total incapacitation for the rest of their lives. It was during Loeb’s rounds, and the long discussions resulting from his questions, that I became convinced that multiple sclerosis was an autoimmune disease, caused by the presence within the brain of antibodies directed against a component of brain tissue itself. It was a new idea in the 1930s. Thomas Rivers, George Packer Berry, and Francis Schwentker had shown five years earlier at the Rockefeller Institute that monkeys developed brain lesions resembling multiple sclerosis after being injected repeatedly with extracts of monkey brain tissue; their observation had been an accidental one, made in the course of attempts to develop vaccines against various viruses known to cause brain disease. The problem in the ward rounds discussions was how to extrapolate from this experimental model to the spontaneous human disease; how to explain this disease, progressing with one destructive lesion after another over many years, in terms of an antibrain antibody? The matter remains almost as much an unsolved problem today; there are, however, new sources for clues: it is suspected that long-latent viruses, measles for example, may become lodged in brain tissue and later give rise to antibodies simultaneously directed at the virus and a component of brain tissue; it is also known that multiple sclerosis patients differ as a group from other people with respect to the HLA gene locus, which governs immunologic reactivity. Perhaps these patients have an inborn error of immunologic perception, which permits the elaboration of antiself antibodies in the brain in response to the presence of an otherwise irrelevant virus, and thus the disaster.
In 1940 Dr. Loeb went back to the Department of Medicine at P & S and soon thereafter became its chairman. Dr. Tracy Jackson Putnam arrived from Harvard to become director of the Neurological Institute. Putnam was primarily a neurosurgeon, but he had a long and distinguished record in research; the discovery for which he is still remembered today, along with his collaborator Houston Merritt, was the Dilantin class of anticonvulsive drugs for the treatment of epilepsy.
Putnam promptly organized a laboratory for work on a method for producing brain abscesses in experimental animals, so that better methods could be devised for treating such abscesses by combining surgery with chemotherapy, using one or another of the new sulfonamide drugs. I began working on this during the summer of 1940, when the residents’ duties on the wards were relatively light.
We devised a method that worked beautifully and with reproducibility, providing chronic brain abscesses that could be observed for many weeks and that resembled in detail the counterpart lesions in the brains of human beings, and I wrote my first scientific paper. Very soon thereafter, penicillin became available, then other more powerful antibiotics, and there was no need for an animal model for studying brain abscesses. The disease itself became a rarity, and still is.
I finished my residency and then became the first Tilney Fellow in Neurology at the institute, thus assured of an income of $1800 for the year 1941, with the understanding that I would spend the year at Harvard and then return to New York as chief resident at the Neurological Institute. I was twenty-seven years old, and for the first time in my life I was independent enough, and solvent enough, to undertake marriage. Beryl and I were married in the chapel of Grace Church in Manhattan on the morning of New Year’s Day, 1941, and that afternoon we headed for Boston. We had an extremely small but absolutely perfect apartment on Longwood Avenue, just across the street from the Children’s Hospital and down the road from the medical school quadrangle, and settled in after New Year’s Day. A few days later we learned that John Dingle’s laboratory was being mobilized for a trip to Halifax, Nova Scotia, where a meningitis epidemic had just been recognized and the health authorities, shorthanded because of the war, had requested help from Harvard. So we packed again and flew to Halifax, where I went to work on the treatment of meningococcal meningitis with a new sulfonamide called sulfadiazine, of which I had never heard, and Beryl was recruited as a laboratory assistant to keep the records and carry cultures from one place to another.
We were in Halifax for about a month, culturing the spinal fluids of several hundred patients with meningitis, collecting samples of serum from these patients and other people who did not develop meningitis but were in close contact, in order to study the possible role of antibodies in protection against the disease, and recording with care the clinical course of the illness under treatment with sulfadiazine, which was administered to all patients with an established diagnosis. Sulfadiazine was wonderfully effective. The only patients who failed to recover were those with a rapidly developing and overwhelming infection—some of them became comatose within a few hours and were brought to the hospital in deep shock, their skin surfaces covered everywhere by areas of hemorrhagic necrosis (looking very much like the Shwartzman phenomenon which I was to study several years later), and these patients were dead before we could start treatment. All the rest, the majority, recovered promptly when given sulfadiazine, and we saw none of the late complications—blindness, deafness, mental confusion—which had occurred in earlier epidemics of untreated meningococcal meningitis.
We came back to Boston with crates of cultures and sera, and my laboratory was committed to the problem of the meningococcus and the mechanism of its peculiar affinity for the surfaces of the brain and spinal cord in human beings. None of the conventional laboratory animals were particularly vulnerable to this organism: rabbits, guinea pigs, rats, and mice co
uld tolerate the intravenous injection of huge numbers of live meningococci without turning a hair, and the bacteria disappeared from their bloodstreams within ten minutes or so. It was evident that the animals possessed a highly effective mechanism for their protection, and I settled down to find out more about this. The first and simplest possibility, that they were able to kill off the injected meningococci by means of an already-existing “natural” antibody, was easiest to test in rabbits, so rabbits became the laboratory’s routine animal. We quickly learned that the serum of a normal adult rabbit was capable of destroying almost any number of meningococci; when up to a million organisms were added to a single milliliter of freshly obtained rabbit serum, and the mixture then incubated for a few hours at 37 degrees Centigrade, the specimens became sterile. If the serum samples were heated at 56 degrees Centigrade for an hour before adding the bacteria, the bactericidal action was completely lost, indicating that the killing power depended on the presence of complement (a sequence of proteins, still incompletely understood, which makes possible the action of antibodies against antigens on the surface of bacteria).