Berger watched them go. "Nine doctors," he says. "Four head doctors and five of the brightest young doctors in a big institution like Hershey Medical Center—and there wasn't one of them could tell me what was my trouble. And it worried them. I could tell they were really worried. So now I knew I'd really had it."
Dr. Jeffries completed his teaching rounds at about ten-thirty and dismissed his entourage. Dr. Field had a moment of leisure. He took the elevator down to the second floor—down to the laboratory. He sought out the technician to whom Berger's latest blood sample had been delivered for still another blood-gases assessment. The results were ready and waiting. They were very different from the two earlier sets of findings. Berger's blood pH was 7.41, or normal. His blood-carbon-dioxide pressure was 36.4, or normal. His blood-oxygen pressure was 109, or normal. And his blood-oxygen saturation was 98 per cent. Also normal. "That shouldn't have been surprising," Dr. Field says. "It was exactly what we would expect after a course of oxygen therapy. The oxygen balance in Berger's blood had been very nicely restored. But it was surprising. It didn't make sense. If Berger's blood gases were back to normal, how come he was still cyanotic? How come his hands were still blue? I had seen them less than half an hour before. There was something wrong somewhere."
Dr. Field went back up to the fourth floor. On the way, he decided to discontinue Berger's oxygen therapy. He wanted him breathing room air again. Then he would take another blood sample for another blood-gases study. Then he would see. He stopped in the corridor for a drink of water, and was joined by one of his colleagues, a resident named James E. Meyer. Dr. Meyer had also been a member of Dr. Jeffries' entourage. He said it had been an interesting round—particularly the Berger case. He said the look of Berger's hands had stuck in his mind. Those hands reminded him of something. And he had just realized what.
"What?" Dr. Field said.
"I don't know if I can explain it," Dr. Meyer said. "But you know how your hands look after you've been shoveling snow? I mean the way they look when you come in and take off your gloves. They have a certain look."
"Mmmm," Dr. Field said. "Yeah—I know what you mean."
But he didn't. He and Dr. Meyer walked together down the corridor. He had no idea what Dr. Meyer meant. But the thought of gloves stayed with him—gloves and skin discoloration. It hung on in the back of his mind. And suddenly it came alive. He stopped.
He said, "Wait a minute."
He cut off to the stockroom. He rummaged around and found a surgical acetone swab. He rejoined Dr. Meyer. Dr. Meyer looked at the swab.
"What's that for?"
"I just had an idea," Dr. Field said. "It was what you said. You gave me a brainstorm."
They came to Berger's room. Berger was alone and dozing. Dr. Field turned off the oxygen supply. He removed the nasal cannula. He asked Berger to hold out a hand. He took the hand by the wrist and gave the back a vigorous rub with the acetone swab. A pinkish pale streak appeared on the back of Berger's hand. The face of the swab turned blue.
Berger had been almost half asleep. Now he was fully, galvanically awake. He stared at the swab. Then he stared at his striped hand. "I didn't understand it," he says. "I just looked. My head was spinning. It was just too much too fast. Then I calmed down a little and saw something. The blue on the swab looked different from the blue on my hand. My hand looked dead. But the swab was simply blue, an attractive shade of blue. And blue is one of my favorite colors. I raised my head and looked across the room. My flannel shirt was hanging there on the back of a chair. It was the exact same shade of blue. The shirt was new—Cher had given it to me for Christmas. I looked at my shirt, and I didn't even have to think. I knew what had happened. I remembered sitting in the Distelfink and warming my hands in my armpits. And later on, during the night in the examining room. It was as simple as that. The dye had come off on my hands. But how? That stopped me for a moment. But I'm a chemist, not just a paint chemist. The answer was that the dye was fast by ordinary standards. It hadn't come off when I washed my hands. But it was soluble in what Dr. Field was using—in acetone. And in sweat. Sweat isn't just water and a little sodium chloride. It also contains certain solvents and acids. Acetic acid, for example. And butyric acid. And valeric acid.
"Dr. Field was reaching for my other hand. I gave it to him. And while he was scrubbing it back to normal, I told him what I thought had happened."
Dr. Field believed him. "It was weird," he says. "The whole thing was staggering. But I knew it was true. It had to have happened that way. The only trouble was that that only explained his hands —his cyanosis. It didn't explain those altered blood gases. Was possible that there actually was something wrong with his blood chemistry? Well, the way to make sure was to do what I had planned to do anyway. When he had been breathing room air for a sufficient length of time, I drew a sample of blood and took it down to the lab. The technician went to work. Blood gases don't take too long. Maybe ten or fifteen minutes. Then we went over the results. They weren't precisely the same as the previous study, but the differences were minimal. Insignificant. Berger's blood gases were normal. That was the answer I wanted, of course, but still—what about last night? What about those two other studies? No answer. There isn't any absolute explanation. My feeling— everybody's feeling—is that the lab had made a mistake. And that's the way it stands in the record: 'It was felt that evidently some error must have been made in the determination of the blood gases during the night, and it was felt that the patient's apparent hypoxemia was a lab error.' "
Dr. Trautlein says: "They told me that Dr. Field was looking for me. I found him, and he told me the story. Gulp!"
Berger was discharged from the hospital at five o'clock that afternoon. "I was ready to leave at noon," he says. "But that isn't the way they do things at Hershey. They wouldn't let me go until they had done a lung scan. It turned out normal. They expected it to be normal, but I guess they wanted to be absolutely certain. I didn't mind the wait too much. I was thankful just to be alive."
[1975]
* * *
author's note: Several readers of this piece found Mr. Berger's seeming cyanosis a more mysterious mystery than I intended it to be. The question that occurred to these readers was put with some succinctness by a gentleman from Kentucky. "Weren't Mr. Berger's armpits also blue?" he wrote. "If not, why not?"
Well, Mr. Berger's armpits were not blue. Nor, for that matter, were the underarms of his undershirt. And the reason for this, though chemically complex, is simply explained. The sweat evolved by the glands in the axilla, or armpit, was not the sweat that leached the dye from Mr. Berger's shirt. The sweat that drew the dye from his shirt and so alarmingly stained his hands was sweat evolved from his palms. These two glandular secretions are differently constituted. Dye—at least the dye of the sort contained in Mr. Berger's shirt—is fast to the sweat of the armpit. It yields, however, to that produced by the palms.
I am indebted to Dr. C. A. Hilgartner of the University of Rochester School of Medicine for a useful amplification of the sweating phenomenon. "Palmar sweating," he noted, "occurs more as a function of excitement of one kind or another than as a function of temperature—and probably the bridge tournament provided enough excitement to induce relatively profuse palmar sweating, at least at times."
CHAPTER 19
Antipathies
A young woman I'll call Sara Strong is sitting in the waiting room of the Tulsa Dermatology Clinic—a private group practice —on East Twenty-first Street in Tulsa, Oklahoma, and she is, of course, uncomfortable. The cause of Mrs. Strong's discomfort is an itchy rash on her elbows, on the backs of her legs, and here and there on her chest. She has had this rash for almost a month. When it first appeared, around the middle of April, her husband, an interne at St. John's Hospital, just down the street from the clinic, identified it as an eczematous allergic contact dermatitis, and treated it in the conventional manner—with an application of cortisone cream. The rash was then on her
elbows only, and the cream at first seemed effective. But a few days later, the rash had spread and worsened. It erupted first on her left leg, in the sensitive pocket behind the knee, and then on the other thigh. Mrs. Strong continued her husband's prescription of cortisone cream, and an added soothing lotion, but the rash continued to spread. It appeared on her chest, and Dr. Strong gave up. The proper treatment of her trouble was plainly beyond his professional powcrs. She needed more experienced and more specialized help. He put in a call to the Tulsa Dermatology Clinic and spoke to the appointments nurse. That was on the afternoon of May 15, a Saturday. The nurse responded with the sincerest form of professional courtesy: she gave Mrs. Strong the earliest possible appointment—Monday morning at eight o'clock.
The allergic condition—with its multiplicity of pains, gasps, fevers, sneezes, itches, nauseas, swellings, diarrheas, and strangulations—is at once the oldest and the newest of man's afflictions. There is no disease more ancient than asthma, and none more newly arrived than a flaming response to the latest creation of the cosmetics laboratory. Almost everything in the human environment (or, as the New York University dermatologist Alexander A. Fisher has put it, "everything under the sun, and even the sun itself') has the power to produce in some unfortunate person some form of allergic reaction. The list of allergens includes most common foods (wheat, corn, eggs, fish, milk, nuts, beans, chocolate), many popular drinks (cola, beer, orange juice), the most useful drugs (aspirin, quinine, codeine, the sulfonamides), the inescapable inhalations (dusts, spores, pollens, vapors, feathers, hair), the many kinds of injections (vaccines, penicillin, mosquito bites, bee stings, insulin), the infinite physical agents (poison ivy, chemicals, metals, soaps, dyes, paints, cosmetics, fabrics, furs, leather, plastics, rubber), and light and heat and cold.
The existence of the phenomenon now known as allergy was recognized long before there was any scientific understanding of its nature. It was too peculiar to be easily overlooked. The allergic phenomenon was probably first observed in what is still its most dramatic expression. Indeed, this manifestation forms the subject of the most celebrated aphorism of the pre-Christian Roman poet Lucretius: "What is food to one is to others bitter poison." Increase Mather, one of the more enlightened of the early Massachusetts clergymen, recorded it in larger scope. "Some men," he wrote in his treatise "Remarkable Providences," in 1684, "have strange antipathies in their natures against that sort of food which others love and live upon. I have read of one that could not endure to eat either bread or flesh; of another that fell into a swooning fit at the smell of a rose.... There are some who, if a cat accidentally come into the room, though they neither see it, nor are told of it, will presently be in a sweat, and ready to die away." Hay fever, which wrung from Sydney Smith the anguished cry "The membrane is so irritable that light, dust, contradiction, an absurd remark, the sight of a Dissenter—anything—sets me sneezing," was accurately described in the sixteenth century (by an Italian anatomist named Leonardo Botallo) and was given its misleading name in 1829 (by an English physician named Gordon), but it was not until 1873 that Charles H. Blackley, another English physician, demonstrated that the causative irritant was pollen. Black- ley's finding was accepted, after the usual exposure to derision and indifference, around 1906.
Allergy takes its name from the German Allergie—from the transliterated Greek alio ergon, which means, roughly, "altered reaction." The term was invented in 1906 by the Austrian investigator Clemens von Pirquet (1874-1929), who is also remembered as the inventor of the standard diagnostic skin test for tuberculosis. Von Pirquet developed the tuberculin test in the course of his explorations of allergy, and he came into that all but empty room through the then just opening door of immunology. This door (which legend recalls was first tried by Mithridates VI of Pontus when he attempted to gradually habituate himself to poison and thus confound his enemies) had suddenly yielded to the efforts of such men as Pasteur, von Behring, Kitazato, and Ehrlich. Standing on the shoulders of these and other giants (most notably those of Theobald Smith, of Harvard, and the subsequent Nobel laureate Charles Richet), von Pirquet observed that patients given a second injection of an immunizing serum a few days after a first injection sometimes developed outbreaks of hives, and even asthmatic attacks. Something had changed a protective serum into a hazard. He decided that what he had seen was an alteration in the immune reaction, and gave to the phenomenon the descriptive name by which it is now universally known.
The nature of allergy, though it has been the object of fifty years or more of increasingly sophisticated scrutiny, is still far from fully understood. There are, however, certain areas of at least translucent enlightenment. It is generally accepted that the phenomenon involves a perversion of the antigen-antibody reaction. The fundamental mechanics of immunity and allergy are much, if not entirely, the same. The effect of immunization—in its active, and most satisfactory, form—is to stimulate the natural defensive powers of the body. This is accomplished by first exposing the body to a safely bridled brush with a specific infecting agent, or antigen. The body instinctively reacts to the presence of this antigen by producing in certain tissues a specific chemical counter- agent, or antibody. The body thus armed is immune to that particular antagonist. In the event of a reexposure to that antigen, the sentinel antibody mobilizes in the bloodstream and destroys it. Allergy appears to be a blundering version of this beneficent process. The phenomenon has its beginning in a confusion of identity. A substance that is harmless to most people is identified as inimical by the body of a susceptible person, and (as in the development of the immune state) the body defensively elaborates a chemical weapon against its reappearance. This antibodylike material compounds the initial confusion into a kind of pandemonium. Through some constitutional derangement, it attacks not the allergen (as the antigen in allergy is called) but, in effect, the cells of the body itself. It is at this climactic moment that the scientific visualization of allergy begins to blur. It is not known what renders a person sensitive to one allergen or another—or to none at all. Nor is it known just how the damage in allergy comes about. It is accepted that the collision of allergen and antibody releases an irritating substance, but questions continue to loom. Is this substance totally toxic? Or are the affected tissues congenitally defective? About the most that can be said with any assurance is that susceptibility to allergy seems to be an inherited characteristic, and that the irritant involved may consist of one or more of several pharmacologically active substances. These substances include histamine, 5-hydroxytryptamine, and acetylcholine, all of which are natural and (within reason) necessary constituents of the body. "In this connection," E. B. French, Reader in Medicine at the University of Edinburgh, has observed, "it is worthy of note that the juice of the stinging nettle (Urtica dioica), from which is derived the name urticaria [hives], contains histamine, 5-HT, and acetylcholine."
Allergy differs from most other diseases in that its victims (including even most asthmatics) seldom die and almost as seldom recover. In this bittersweet respect, as well as in the fortitude with which its long embrace must be borne, it much resembles gout. But gout, though no longer considered a rarity, is nevertheless a disease of the unfortunate few. Allergy is a commonplace disaster. It is, in fact, the most common of all chronic complaints throughout the industrially developed World. The National Institutes of Health report that around eighteen million Americans are afflicted with one or another of the many chronic digestive diseases. Some twenty-two million, its records show, are afflicted with one or another of the several forms of arthritis, and about thirty-five million with hypertension. The allergic population of the United States is on the way to forty million. Almost fifteen million of these are hay-fever sufferers. Nine million are asthmatic, and another several million are allergic to some food or drink or drug. The rest, in whose company Sara Strong unhappily found herself on that spring morning, are victims of allergic eczematous contact dermatitis.
The Tulsa Dermatology Clinic
is an association of four young dermatologists. One member of the group is a former Mississippian named Vincent P. Barranco, and it was he who had arranged to see Mrs. Strong on that Monday morning in May. He found her to be a small, trim, dark-haired woman of twenty-six with the characteristic expression of a dermatitis patient. She looked dejected.
"And plain," Dr. Barranco says. "I could see that she was actually very attractive, but her trouble was wearing her down. There's nothing like a raw, itchy rash for taking the life out of a person. I've seen enough to know. And her history, when we got down to that, was disturbing. She suffered from hay fever. There were certain foods that she was allergic to. She had a sister with asthma. The sister was part of the record, because allergy is strongly familial. Now, all of this immediately suggested a diagnosis of atopic dermatitis. That's an eczema that occurs without any external or discernible allergic cause. It's an inherited constitutional state—very strange. But not at all uncommon. It differs from an allergic contact dermatitis in the matter of cause. In contact dermatitis, if you look hard enough, there is always a contactant—a cause. Well, Mrs. Strong's history and everything else she had to tell me seemed to indicate an atopic state. Except for one thing. This eczematous attack was her first, and atopic dermatitis usually begins in childhood and continues on through the years. But it still looked atopic to me. However, I took the usual precautions to eliminate any possible contactant. I gave her the usual instructions: no rings, no earrings, no bracelets, no jewelry of any kind. No cosmetics except those on this list of hypoallergenic products. No washing dishes or such without protective polyethylene gloves. And so on. I treated her rash as one would treat any allergic dermatitis—with topical cortisone cream. The same thing her husband had used, only a new and more potent type. Then, because her lesions were quite distinct and comparatively few, I injected each one of them with cortisone. Intralesional cortisone is a profound treatment. As a matter of fact, I thought twice before I decided to go ahead. I thought it might be more profound than the case called for. But she was so miserable. And she'd been miserable for almost a month—that made up my mind.
The Medical Detectives Volume I Page 33