Authors: Sherwin B Nuland
How We Die (12 page)
Such a one was Thomas Browne, who lived in that extraordinary seventeenth century when the scientific method and inductive reasoning first began to affect the thinking of educated people and made them question the truths so dear to their fathers. In 1643, Browne published a small literary jewel of contemplation,
Religio Medici
, “The Religion of a Doctor,” which he described as “a private exercise directed to myself.” That little masterpiece is usually published together with a compilation on the lingering agonies of a dying man, entitled “A Letter to a Friend,” in which the author writes: “He came to be almost half himself and left a great part behind him which he carried not to the grave.” How often have I stood with families at a deathbed and witnessed their disbelief at this process unfolding its too-often-agonizing panorama before them. They question why it is different from their expectation and why seemingly they alone should have to endure what they conceive to be a uniqueness of suffering. It was that uniqueness I thought I had been forced to live through with Bubbeh’s death and then later with the image of that alien corpse.
Religio Medici
, “The Religion of a Doctor,” which he described as “a private exercise directed to myself.” That little masterpiece is usually published together with a compilation on the lingering agonies of a dying man, entitled “A Letter to a Friend,” in which the author writes: “He came to be almost half himself and left a great part behind him which he carried not to the grave.” How often have I stood with families at a deathbed and witnessed their disbelief at this process unfolding its too-often-agonizing panorama before them. They question why it is different from their expectation and why seemingly they alone should have to endure what they conceive to be a uniqueness of suffering. It was that uniqueness I thought I had been forced to live through with Bubbeh’s death and then later with the image of that alien corpse.
The force of life fills out our tissues with its pulsing vibrancy and puffs them up with the pride of being alive. Whether it departs with a bang, as it did for Irv Lipsiner, or a prolonged whimper, as it did for Bubbeh, it often leaves behind an object of shrunken unrealness. When Charles Lamb beheld the corpse of the popular English comedian R. W. Elliston, he was moved to write, “Bless me, how
little
you look. So shall we all look—kings, and kaisers—stripped for the last voyage.” Browne himself wrote, “I am not so much afraid of death, as ashamed thereof; ‘tis the very disgrace and ignominy of our natures, that in a moment can so disfigure us, that our nearest friends, wife, and children, stand afraid and start at us.”
little
you look. So shall we all look—kings, and kaisers—stripped for the last voyage.” Browne himself wrote, “I am not so much afraid of death, as ashamed thereof; ‘tis the very disgrace and ignominy of our natures, that in a moment can so disfigure us, that our nearest friends, wife, and children, stand afraid and start at us.”
Thomas Browne’s words, or Lamb’s, might have reassured me at my grandmother’s coffin. That day would surely have been a lot easier for me, and its memory less painful, had I but known that not only my own grandmother but indeed everyone becomes littler with death—when the human spirit departs, it takes with it the vital stuffing of life. Then, only the inanimate corpus remains, which is the least of all the things that make us human.
Reviewing those years just ended, I might also have recognized the commonality of death’s experience in a sentence to be found a few pages earlier in Browne’s book: “With what strife and pains we come into the world we know not, but ‘tis commonly no easy matter to get out of it.”
IV
Doors to Death of the Aged
M
Y GRANDMOTHER HAD
chosen a way “to get out of it,” to use Thomas Browne’s expression, that is hardly unique. Stroke is the third most common cause of death in the developed countries of the world, as listed by the World Health Organization. More than one hundred and fifty thousand Americans die of it each year, representing approximately one-third of all those who suffer a stroke. Another third will be left with permanent severe disability. Only cardiac disease and cancer exceed its marauding power. Following a long period during which its incidence declined, a plateau has been reached in recent years: approximately 0.5–1.0 stroke per 1,000 population each year. But that figure represents the entire spectrum of our citizenry. As people age, their propensity to stroke naturally increases. There are no probability estimates for sedentary Jewish ladies who have kept themselves on a high-cholesterol kosher diet for almost a century, but we do know that of a random group of one thousand American or Western European men and women over the age of seventy-five, between twenty and thirty will suffer a stroke each year—among our eldest elders, the risk is some thirty times as great as it is for the rest of us.
Y GRANDMOTHER HAD
chosen a way “to get out of it,” to use Thomas Browne’s expression, that is hardly unique. Stroke is the third most common cause of death in the developed countries of the world, as listed by the World Health Organization. More than one hundred and fifty thousand Americans die of it each year, representing approximately one-third of all those who suffer a stroke. Another third will be left with permanent severe disability. Only cardiac disease and cancer exceed its marauding power. Following a long period during which its incidence declined, a plateau has been reached in recent years: approximately 0.5–1.0 stroke per 1,000 population each year. But that figure represents the entire spectrum of our citizenry. As people age, their propensity to stroke naturally increases. There are no probability estimates for sedentary Jewish ladies who have kept themselves on a high-cholesterol kosher diet for almost a century, but we do know that of a random group of one thousand American or Western European men and women over the age of seventy-five, between twenty and thirty will suffer a stroke each year—among our eldest elders, the risk is some thirty times as great as it is for the rest of us.
Stroke
is such a ubiquitous term that there is sometimes a little fuzziness about the way it is used. To a physician, a stroke is a deficit in neurologic function resulting from a decrease in blood flow through some specific artery supplying the brain. Further, the deficit must last longer than twenty-four hours for the episode to be called a stroke. Anything else is classified as a transient ischemic attack, or TIA. Although TIAs usually clear up within an hour, a few do last somewhat longer before their symptoms disappear.
is such a ubiquitous term that there is sometimes a little fuzziness about the way it is used. To a physician, a stroke is a deficit in neurologic function resulting from a decrease in blood flow through some specific artery supplying the brain. Further, the deficit must last longer than twenty-four hours for the episode to be called a stroke. Anything else is classified as a transient ischemic attack, or TIA. Although TIAs usually clear up within an hour, a few do last somewhat longer before their symptoms disappear.
If all of this has a familiar ring, there is good reason. It is basically the same mechanism by which the heart’s deficit is produced when one of its arteries fails to deliver the required volume of blood. It is that universal mechanism of ischemia, the quenching of blood flow and the parching of tissues, that is so common a denominator in the killing off of cells in so many parts of the body. It carried off James McCarty, it carried off my Bubbeh, and, in one form or another, it will carry off most of us now living. It does its work by suffocating the tissues of its victim. The blood flow stops for much the same reason it does in the coronary arteries of the heart. The buildup of atheroma has reached the critical point at which a branch of one of the internal carotid arteries becomes completely occluded. The occlusion may be due to a completion of the atherosclerotic process in that branch itself, or it may occur because a bit of plaque has separated from the wall of a larger artery and been propelled as an embolus up into the brain, plugging an already-compromised vessel.
Or the stroke and its attendant ischemia may be caused by quite another manifestation of this vast syndrome of cerebrovascular disease, namely a hemorrhage into the substance of the brain, which in the elderly is almost always due to long-standing hypertension. Its wall already weakened by the long years of abnormally high pressure against it, the fragile atherosclerotic vessel finally gives way at some specific point, resulting in an outrush of blood into the surrounding brain tissue. Such an intra-cerebral bleed carries a mortality rate of twice the 20 percent that is usually estimated for occlusive strokes. Hemorrhage accounts for approximately 25 percent of strokes, and vascular occlusion for the rest.
It takes a great deal of energy to keep the brain’s engine functioning efficiently. Almost all of that energy is derived by the tissue’s ability to break down glucose into its component parts of carbon dioxide and water, a biochemical process that requires a high level of oxygen. The brain does not have the capacity to keep any glucose in reserve; it depends on a constant immediate supply being brought to it by the coursing arterial blood. Obviously, the same is true of the oxygen. It takes only a few minutes for the ischemic brain to run out of both before it suffocates. Neurons are extremely sensitive to ischemia; irreversible destructive changes begin within fifteen to thirty minutes of the onset of the deprivation. After no more than an hour of the beginning of ischemia, infarction of significant segments of brain tissue becomes inevitable.
The symptoms caused by the cell destruction vary, depending upon which vessel is occluded. Although at least half a dozen branches of the internal carotid are particularly susceptible to obstruction, most frequently involved in ischemic stroke is one of the paired middle cerebral arteries. The middle cerebral (MCA) supplies blood to most of the lateral surface of the cerebral hemisphere and some of the centers that lie deep beneath the cortex. The MCA feeds the major sensory and motor areas of the cortex—areas that are involved in hand and eye movement, and also the specialized sensory tissue for hearing. It nourishes the region involved in what are called the “higher mental functions,” such as perception, organized thought, voluntary movement, and the integrated coordination of all these abilities. On the dominant side of the brain (the right side for lefties and the left for the other 85 percent of us), the MCA supplies the sensory and motor areas for language. This particular bit of geographic distribution explains why so many stroke victims lose their powers to express and comprehend spoken and written language.
Many MCA strokes are caused not by actual occlusion at the site but by bits of material broken off from the crusted atheroma in the main internal carotid artery, or from the heart itself in the form of small bits of old organized clot. The released particle then becomes an embolus. Here we encounter another of those terms contributed by Rudolf Virchow, from the Greek
embolos
, signifying a wedge or plug, which in turn is derived from two words meaning “to cast or throw in.” Literally, then, a plug has been thrown into the artery and will be propelled by the bloodstream until it wedges itself into a narrowed portion of the vessel, which it will completely block off. In the more common cases where the plugging is not caused by an embolus, it results from the final completion of atheroma buildup. In either situation, the tissue supplied by the vessel instantly loses its source of oxygen and glucose, and within a few minutes becomes wounded enough to cause symptoms. If the blockage is not relieved rapidly, the area of brain dies by infarction.
embolos
, signifying a wedge or plug, which in turn is derived from two words meaning “to cast or throw in.” Literally, then, a plug has been thrown into the artery and will be propelled by the bloodstream until it wedges itself into a narrowed portion of the vessel, which it will completely block off. In the more common cases where the plugging is not caused by an embolus, it results from the final completion of atheroma buildup. In either situation, the tissue supplied by the vessel instantly loses its source of oxygen and glucose, and within a few minutes becomes wounded enough to cause symptoms. If the blockage is not relieved rapidly, the area of brain dies by infarction.
If one were to name the universal factor in all death, whether cellular or planetary, it would certainly be loss of oxygen. Dr. Milton Helpern, who was for twenty years the Chief Medical Examiner of New York City, is said to have stated it quite clearly in a single sentence: “Death may be due to a wide variety of diseases and disorders, but in every case the underlying physiological cause is a breakdown in the body’s oxygen cycle.” Simplistic though it may sound to a sophisticated biochemist, this pronouncement is all-encompassing.
Many strokes are so small that there are few or no immediate significant symptoms to indicate what has taken place. But with time, such little strokes accumulate, and the evidence of gradual deterioration becomes clear to even the most casual observer. Walter Alvarez, the great Chicago clinician of a generation ago, once quoted “a wise old lady” who said to him, “Death keeps taking little bits of me.” As his clinical description so clearly states:
She saw that with each attack of dizziness or fainting or confusion she became a little older, a little weaker, and a little more tired; her step became more hesitant, her memory less trustworthy, her handwriting less legible, and her interest in life less keen. She knew that for 10 years or more, she had been moving step by step towards the grave.
Of those so betrayed by their cerebral circulation, William Osler is reported to have said, “These people take as long to die as they did to grow up.”
Almost 10 percent of elderly people diagnosed with dementia owe their situation to a series of such small strokes, a concept popularized by Alvarez in 1946, after observing it in his own father. Now called multi-infarct dementia, the process is characterized by an irregular series of abrupt little worsenings. Interestingly, this form of cerebral arteriosclerosis was first described by Alois Alzheimer in 1899, eight years before he introduced the quite different type of intellectual decline that we now call by his name.
The subtle process of infarcting brain may go on and on, accumulating irregular stepwise degenerations in cerebral function for as long as a decade or more, until a major stroke or some other lethal process intervenes to bring abrupt fulfillment of the slow progression’s ultimate purpose.
Major infarction by MCA stroke results in sensory loss and weakness that are most prominent in the part of the face and in the extremities opposite to the side of the brain where the stroke has occurred; such infarction causes as well a condition called aphasia—the loss of power of expression—although comprehension tends to remain reasonably well preserved. Occlusion of other vessels produces a whole range of symptoms, determined not only by the area served by the vessel but also by the amount of nutrition brought in by a collateral blood supply that may be available from nearby unscathed vessels. Language and visual disturbances, paralysis, sensory losses, difficulties in balance—all of these are the more common manifestations of stroke.
Large strokes often result in coma. If the stroke is extensive enough or if further complications ensue, such as decreased blood pressure or cardiac output due to failure or arrhythmia, recovery is prevented and the area of ischemia may actually increase. If it becomes large enough, the brain tissue begins to swell. Being compressed in the unyielding confines of the skull, a swollen brain is further damaged by being pushed up against its covering membranes and bony encasement, and part of it may actually be forced down through a fold in those membranes that separates the “higher” brain from the “lower,” or brain stem—the part that thinks from the part that is involved with more automatic mechanisms such as cardiac and respiratory control, digestive and bladder function, and a group of others. When this happens, the pressure causes so much damage to the brain stem’s centers controlling the heart and breathing that death follows soon thereafter, from either arrhythmia or cardiac and respiratory failure.
Collapse of vital function is only part of the array of possible mechanisms by which strokes kill approximately 20 percent of their victims, or even more when the cause is hypertensive hemorrhage. If brain damage is massive enough, all kinds of normal controls go awry. Preexisting diabetes sometimes goes so much out of control that blood acidity rises enough to be incompatible with life; the functioning of the lungs is sometimes impaired by paralysis of the muscles of the chest wall; the blood pressure may become elevated to dangerous levels—these are among the most common lethal complications of major strokes.
And then there is my Bubbeh’s way—pneumonia. More than any other organ system excepting skin, the lungs of elderly people are subjected to every insult our polluted environment is capable of inflicting. Whether elasticity is lost for that reason or simply by the ordinary process of aging, the passage of time results in a decreased ability to inflate or deflate completely. Mechanisms for clearing mucus are weakened, and the already-narrowed airways are more prone to become filled with debris-laden material. The situation is worsened by an inability to maintain proper humidity and temperature in the finer bronchial branches. These strictly physical debilities are complicated by a depressed production of local antibodies as part of the old person’s generally lessened immune response.
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