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When Simón Bolívar died on this day 185 years ago, tuberculosis was thought to have been the disease that killed him. An autopsy showing tubercles of different sizes in his lungs seemed to confirm the diagnosis, though neither microscopic examination nor bacterial cultures of his tissues were performed.
John Paul Jones died in Paris on this day in 1792, lonely and forgotten by the country he helped bring into existence. Shortly before his death, he began to lose his appetite. Then his legs began to swell, and then his abdomen, making it difficult for him to button his waistcoat and to breath.
On this day in 1863, General Thomas J. “Stonewall” Jackson, one of the wiliest military commanders this country ever produced, died eight days after being shot by his own men. He had lost a massive amount of blood before having his left arm amputated by Dr. Hunter Holmes McGuire, arguably the most celebrated Civil War surgeon of either side.
When Charles Darwin died at age 73 on this day 133 years ago, his physicians decided that he had succumbed to “degeneration of the heart and greater vessels,” a disorder we now call “generalized arteriosclerosis.” Few would argue with this diagnosis, given Darwin’s failing memory, and his recurrent episodes of “swimming of the head,” “pain in the heart”, and “irregular pulse” during the decade or so before he died.
Since Beethoven’s death on this day 188 years ago, debate has raged as to the cause of his deafness, generating scores of diagnoses ranging from measles to Paget’s disease. If deafness had been his only problem, diagnosing the disorder might have been easier, although his ear problem was of a strange character no longer seen. It began ever so surreptitiously and took over two decades to complete its destruction of Beethoven’s hearing.
The disease that carried Mozart off 224 years ago today was as sudden as it was mysterious. It struck during a year in which he was uncommonly healthy and also spectacularly productive. Only its essential elements are known, the most striking of which was progressive swelling (i.e., edema) of the entire body, ultimately so profound that a few days before Mozart died he was unable to make the smallest movement and had to be fitted with a gown that opened at the back to facilitate changing. By then, according to his son, Carl Thomas, he also had a stench so awful (likely due to retained urinary waste products), that “an autopsy was rendered impossible.” Although Mozart was the disorder’s most notable victim, he was by no means its only one. According to Dr. Eduard Vincent Guldener von Lobes, one of several consulting physicians: “A great number of inhabitants of Vienna were at this time laboring under the same complaint, and the number of cases which terminated fatally, like that of Mozart’s, was considerable. I saw the body after death, and it exhibited no appearances beyond those usual in such cases.” Von Lobes’ statement was recently confirmed by Zeger, Weigl and Steptoe, who found a marked increase in “deaths from edema among young men” recorded in Vienna’s official daily register in the weeks surrounding Mozart’s death compared with previous and following years.
Although over 100 different diagnoses have been proposed as the cause of Mozart’s fatal illness, none fits its character, course, and epidemiological characteristics better than acute glomerulonephritis – acute inflammation of the microscopic filters of the kidneys (the glomeruli) induced by a preceding streptococcal infection. Mozart, in fact, was no stranger to streptococcal infections and their complications. He had a series of severe illnesses as a child, which were almost certainly recurrent episodes of strep throat and streptococcus-induced acute rheumatic fever. Therefore, if his final, fatal illness was acute, post-streptococcal glomerulonephritis, it would have been just one of many times his life could have been cut short by an encounter with streptococci. However, unlike acute rheumatic fever, post-streptococcal glomerulonephritis is typically a benign disorder of young children, which virtually always resolves fully in a matter of weeks. How then, could acute, post-streptococcal glomerulonephritis explain not just Mozart’s death, but also those of the many other young Viennese men who died of “edema” during the winter of 1791/2?
The answer lies with the particular species of streptococcus responsible for the cases of acute glomerulonephritis. Streptococcus pyogenes is the species of streptococcus responsible for the vast majority of acute post-streptococcal glomerulonephritis (also “strep throat’ and rheumatic fever) – those benign cases, involving children who recover completely after relatively brief illnesses. There is, however, another rarer form of post-streptococcal glomerulonephritis, a much severer form, which attacks and sometimes kills adults. It’s caused by a different species of streptococcus, Streptococcus equi, the agent responsible for “strangles,” a highly contagious infection of horses. The bacterium also attacks cows, and in rare instances in which humans are infected, consumption of milk or milk products from S. equi-infected cows is responsible. The infection produces an illness typical of acute glomerulonephritis, in which over 90% of the victims are adults. One in 50 dies, even with the best care available today. One in 20 requires renal dialysis to recover, which, of course, was not available in Mozart’s day.
In the final analysis, of the myriad diagnoses proposed to date, only an epidemic of acute post-streptococcal glomerulonephritis caused by milk or cheese contaminated with S. equi, explains both the clinical and the epidemiological features of Mozart’s fatal illness.
Headline image credit: Mozart family portrait, circa 1780. Public domain via Wikimedia Commons.
When Eleanor Roosevelt died on this day (7 November) in 1962, she was widely regarded as “the greatest woman in the world.” Not only was she the longest-tenured First Lady of the United States, but also a teacher, author, journalist, diplomat, and talk-show host. She became a major participant in the intense debates over civil rights, economic justice, multiculturalism, and human rights that remain central to policymaking today. As her husband’s most visible surrogate and collaborator, she became the surviving partner who carried their progressive reform agenda deep into the post-war era, helping millions of needy Americans gain a foothold in the middle class, dismantling Jim Crow laws in the South, and transforming the United States from an isolationist into an internationalist power. In spite of her celebrity, or more likely because of it, she had to endure a prolonged period of intense suffering and humiliation before dying, due in large part to her end-of-life care.
Roosevelt’s terminal agonies began in April 1960 when at 75 years of age, she consulted her personal physician, David Gurewitsch, for increasing fatigue. On detecting mild anemia and an abnormal bone marrow, he diagnosed “aplastic anemia” and warned Roosevelt that transfusions could bring temporary relief, but sooner or later, her marrow would break down completely and internal hemorrhaging would result. Roosevelt responded simply that she was “too busy to be sick.”
For a variety of arcane reasons, Roosevelt’s hematological disorder would be given a different name today – myelodysplastic disorder – and most likely treated with a bone marrow transplant. Unfortunately, in 1962 there was no effective treatment for Roosevelt’s hematologic disorder, and over the ensuing two years, Gurewitsch’s grim prognosis proved correct. Though she entered Columbia-Presbyterian Hospital in New York City repeatedly for tests and treatments, her “aplastic anemia” progressively worsened. Premarin produced only vaginal bleeding necessitating dilatation and curettage, transfusions temporary relief of her fatigue, but at the expense of severe bouts of chills and fever. Repeated courses of prednisone produced only the complications of a weakened immune system. By September 1962, deathly pale, covered with bruises and passing tarry stools, Roosevelt begged Gurewitsch in vain to let her die. She began spitting out pills or hiding them under her tongue, refused further tests and demanded to go home. Eight days after leaving the hospital, the TB bacillus was cultured from her bone marrow.
Eleanor Roosevelt with grandchildren Buzzie and Sistie Dall. Harris & Ewing, photographer, 1934. Public domain via Library of Congress.
Gurewitsch was elated. The new finding, he proclaimed, had increased Roosevelt’s chances of survival “by 5000%.” Roosevelt’s family, however, was unimpressed and insisted that their mother’s suffering had gone on long enough. Undeterred, Gurewitsch doubled the dose of TB medications, gave additional transfusions, and ordered tracheal suctioning and a urinary catheter inserted.
In spite of these measures, Roosevelt’s condition continued to deteriorate. Late in the afternoon of 7 November 1962 she ceased breathing. Attempts at closed chest resuscitation with mouth-to-mouth breathing and intra-cardiac adrenalin were unsuccessful.
Years later, when reflecting upon these events, Gurewitsch opined that: “He had not done well by [Roosevelt] toward the end. She had told him that if her illness flared up again and fatally that she did not want to linger on and expected him to save her from the protracted, helpless, dragging out of suffering. But he could not do it.” He said, “When the time came, his duty as a doctor prevented him.”
The ethical standards of morally optimal care for the dying we hold dear today had not yet been articulated when Roosevelt became ill and died. Most of them were violated (albeit unknowingly) by Roosevelt’s physicians in their desperate efforts to halt the progression of her hematological disorder: that of non-maleficence (i.e., avoiding harm); by pushing prednisone after it was having no apparent therapeutic effect; that of beneficence (i.e., limiting interventions to those that are beneficial); by performing cardiopulmonary resuscitation in the absence of any reasonable prospect of a favorable outcome; and that of futility (avoiding futile interventions); by continuing transfusions, performing tracheal suctioning and (some might even argue) beginning anti-tuberculosis therapy after it was clear that Roosevelt’s condition was terminal.
Roosevelt’s physicians also unknowingly violated the principle of respect for persons, by ignoring her repeated pleas to discontinue treatment. However, physician-patient relationships were more paternalistic then, and in 1962 many, if not most, physicians likely would have done as Gurewitsch did, believing as he did that their “duty as doctors” compelled them to preserve life at all cost.
Current bioethical concepts and attitudes would dictate a different, presumably more humane, end-of-life care for Eleanor Roosevelt from that received under the direction of Dr. David Gurewitsch. While arguments can be made about whether any ethical principles are timeless, Gurewitsch’s own retrospective angst over his treatment of Roosevelt, coupled with ancient precedents proscribing futile and/or maleficent interventions, and an already growing awareness of the importance of respect for patients’ wishes in the early part of the 20th century, suggest that even by 1962 standards, Roosevelt’s end-of-life care was misguided. Nevertheless, in criticizing Gurewitsch for his failure “to save [Roosevelt] from the protracted, helpless, dragging out of suffering,” one has to wonder if and when a present-day personal physician of a patient as prominent as Roosevelt would have the fortitude to inform her that nothing more can be done to halt the progression of the disorder that is slowly carrying her to her grave. One wonders further if and when that same personal physician would have the fortitude to inform a deeply concerned public that no further treatment will be given, because in his professional opinion, his famous patient’s condition is terminal and further interventions will only prolong her suffering.
Evidence that recent changes in the bioethics of dying have had an impact on the end-of-life care of famous patients is mixed. Former President Richard Nixon and another famous former First Lady, Jacqueline Kennedy Onassis, both had living wills and died peacefully after forgoing potentially life-prolonging interventions. The deaths of Nelson Mandela and Ariel Sharon were different. Though 95 years of age and clearly over-mastered by a severe lung infection as early as June 2013, Mandela was maintained on life support in a vegetative state for another six months before finally dying in December of that year. Sharon’s dying was even more protracted, thanks to the aggressive end-of-life care provided by Israeli physicians. After a massive hemorrhagic stroke destroyed his cognitive abilities in 2006, a series of surgeries and on-going medical care kept Sharon alive until renal failure finally ended his suffering in January 2014. Thus, although bioethical concepts and attitudes regarding end-of-life care have undergone radical changes since 1962, these contrasting cases suggest that those caring for world leaders at the end of their lives today are sometimes as incapable as Roosevelt’s physicians were a half century ago in saving their patients from the protracted suffering and indignities of a lingering death.
Edgar Allan Poe died 165 years ago today in the early morning of 7 October 1849. Only a few details of the illness that extinguished his “bright but unsteady light” are known because his physician, Dr. John Joseph Moran, used the illness to promote his own celebrity and in the process denied posterity an accurate clinical description. One of his later accounts, one summarized by Charles Scarlett, Jr. in the Maryland Historical Magazine (1978; 73: 360-75) came to my attention shortly after returning to Baltimore after 14 years at the Dallas VA Hospital in 1988. I was so taken by Moran’s fascinating and detailed description of Poe’s final days, I decided to use it as the subject of a clinical conference that has long been my favorite – the Clinical Pathologic Case Conference (CPC) Conference. This would prove to be the first of an ongoing series of historical CPCs devoted to the likes of Alexander, Columbus, Mozart and Lenin, stretching over two decades and spawning too-numerous-to-count articles in the international press, scores of manuscripts published in medical journals, and two books.
The clinicopathological conference is a standard medical conference designed to teach physicians and physicians-in-training basic medical concepts and clinical problem-solving techniques. It is a case-based exercise, in which the featured speaker and the audience struggle together to diagnose a particularly challenging illness of some patient using only the information included in a clinical summary prepared especially for the conference. That clinical summary, distributed well in advance of the conference, typically contains all of the medical information pertaining to the case in question, except for the definitive, diagnostic test result. That result, known only to the conference organizers, is revealed at the very end of the conference as a validation or repudiation of the presenter’s conclusions. To my knowledge, our “Poe Historical CPC” was the first to use an historical, rather than a current, patient as the subject of the conference.
Illustration for Edgar Allan Poe’s story “Descent into the Maelstrom” by Harry Clarke (1889-1931), published in 1919. Public domain via Wikimedia Commons.
In 1995, during this first Historical CPC at the University of Maryland, Dr. R. Michael Benitez concluded that Poe died of rabies resulting from an unrecorded and most likely unrecognized animal exposure prior to his hospitalization in Baltimore. His diagnosis became a media sensation covered in venues as diverse as Science magazine and the answer to the final Jeopardy question of the TV show of the same name. Benitez based his diagnosis on evidence of autonomic instability (dilating and contracting pupils and an irregular pulse which alternated between rapid and slow), fluctuating delirium, and hydrophobia (suggested by Poe’s adamant refusal of alcohol and difficulty swallowing water) included in Moran’s later descriptions of the terminal illness.
Rabies, in fact, has much in common with Moran’s later description of Poe’s final illness. It is a viral encephalitis (i.e., an infection of the brain) marked by acute onset of confusion, hallucinations, combativeness, muscle spasms and seizures, all of which tend to wax and wane during the course of the illness. Autonomic instability marked by alternating tachycardia (racing pulse) and bradycardia (slow pulse), profuse sweating, lacrymation, and salivation are also characteristic. The infection is virtually always fatal, with a median survival time after the onset of symptoms of four days. Poe died four days after being admitted to the hospital.
Moran gave no such indication of autonomic instability or hydrophobia in the letter he wrote to Mrs. Clemm a month after her son-in-law’s death. Only decades later, most likely relying on memory alone, does he mention a “very low pulse” and that his famous patient’s “pulse which had been as low as fifty was rising rapidly, though still feeble and variable.”
Many diagnoses have since been offered to explain Poe’s death. The earliest and most persistent has been that of alcohol-induced delirium tremens. Moran’s later case summary, one almost certainly written to satisfy his public’s appetite for ever more moving and ironic details of his patient’s final hours, has generated several more. These include homicide, carbon monoxide poisoning, suicide, syphilis, and mercury intoxication, reflecting more an unwillingness on the part of the proposers to accept an ordinary disease as the cause of Poe’s death than any convincing clinical evidence of such disorders.
Given numerous well-documented instances of Poe’s refractory alcohol abuse and its adverse effects on his physical and mental health prior to his departure from Richmond in late September of 1849, and the nature of the illness described by Moran in his letter of 15 November 1849 to Poe’s mother-in-law, one need look no further than delirium tremens as an explanation for his death. Whether his last bout with alcohol was the result of “cooping,” his own inability to control the craving that had for so many years driven him to drink, or a second (successful) attempt at suicide will never be known. However, if one ignores Moran’s later expanded description of Poe’s final illness, which deviates so spectacularly from his initial description in his letter to Maria Clemm a month after his patient’s death, neither rabies, homicide, mercury intoxication, nor, for that matter, any of the myriad other explanations proposed in the century and a half since Poe’s death, offers a better fit than delirium tremens.
Headline image credit: A photograph (taken by C.T. Tatman in 1904) of a daguerreotype (taken by Edwin H. Manchester in 1848) of Edgar Allan Poe. Public domain via Wikimedia Commons.
