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Abstract

  1. Top of page
  2. Abstract
  3. DIFFERENTIAL DIAGNOSIS:DR JACKSON T. WRIGHT, JR
  4. HISTORICAL DISCUSSION: DR W. FITZHUGH BRUNDAGE
  5. COMMENT: DR PHILIP A. MACKOWIAK
  6. Acknowledgements:
  7. References

This case discussion was presented originally in an open forum on May 5, 2006, in Baltimore, MD, sponsored by the Department of Veterans Affairs Maryland Health Care System and the University of Maryland School of Medicine as part of an ongoing series of historical clinicopathological conferences.

This patient was one of the most influential and controversial Americans of his time. Born a slave 150 years ago, he was to become the successor of Frederick Douglass as leader and spokesman for African Americans in the aftermath of the Civil War. For more than 50 years he relentlessly pursued the Puritan ethic of hard work, cleanliness, and thrift. By his mid-50s, however, he was wasted by a disease that his physician claimed was due, at least in part, to “racial characteristics,” raising in some peoples' minds the suspicion that he might have had syphilis. Shortly before he died on November 15, 1915, at age 59, he was hospitalized in New York City. The following is an abridged version of his hospital record:

November 1, 1915

Complaint: Headache, sleeplessness, fatigue and dyspnoea on climbing stairs. Palpitation, slight cough, occasional indigestion, loss of weight, loss of appetite, failing vision.

Family History: Nothing known of father. Mother died forty years ago, probably of dropsy. One sister died this year of apoplexy.

Past History: About twenty years ago patient had malaria. He has always been troubled with dyspepsia … gets up two or three times at night to urinate for the past two or three years. He drinks a great deal of water. Vision has been failing somewhat. He takes about two tablespoonfuls of Scotch whiskey daily; no beer or wine. He smoked one or two cigars a day up to six months ago; since then, none. Patient denies all venereal infections.

Present Illness: Up to one year ago patient was quite well except for occasional [frontal] headaches that he called bilious headaches … In February he was acutely ill with gastro-intestinal upset, and since that time has noticed increasing ease of fatigue and dyspnoea on exertion [Two weeks prior to admission, he had palpitations]. He has never had any oedema. Memory is good; no evidence of any mental symptoms.

Physical Examination: Patient is a middle-aged African American man variously described as having “medium brown skin of a mulatto … luminous eyes … short, wiry and forceful … a rather Irish face … and the odd look of an Italian.” He lies in bed rather restless, moving constantly.

Head: Temporal arteries are dilated, tortuous and non-compressible.

Eyes: Pupils are equal and regular; react promptly to light. Eyeballs prominent. Ophthalmoscopic examination–Right Eye, margins of disc cannot be made out. Arteries narrow, veins dilated. There are a few flame-shaped hemorrhages. The retina is pale. Left Eye, disc slightly better outlined than other eye, but temporal margin cannot be made out. There are several flame-shaped hemorrhages. Arteries very narrow [A second examiner also detected a “great many yellowish spots (fatty degeneration) around the posterior pole of the eye.”].

ENT: Negative.

Lungs: There are a few fine râles over both bases.

Heart: No impulse is visible over the precordium. Area of cardiac dulness is 14.0 cm from the midline in the fifth interspace. Apex is palpable in the fifth interspace 10.5 cm from the mid-line. A blunt first sound, followed by an accentuated and reduplicated second sound. At the left of the lower end of the sternum a low-pitched [intermittent] systolic murmur follows the first sound. Regular rapid rhythm.

Pulses: Two pulses are equal in volume and in time. Blood pressure is 225 systolic, 145 diastolic, right arm, lying down.

Abdomen: Liver palpable 5 cm from the costal margin in the mid-clavicular line [not felt by a second examiner].

External Genitalia: Negative.

Extremities: No oedema. Knee jerks present, not exaggerated. Radial arteries not easily compressible.

Laboratory Studies:Wassermann negative

Figures 1 and 2 are replicas of data in the patient's actual hospital record. Normal ranges for the results listed were not included.

image

Figure 1. From the hospital record.

image

Figure 2. From the hospital record.

DIFFERENTIAL DIAGNOSIS:DR JACKSON T. WRIGHT, JR

  1. Top of page
  2. Abstract
  3. DIFFERENTIAL DIAGNOSIS:DR JACKSON T. WRIGHT, JR
  4. HISTORICAL DISCUSSION: DR W. FITZHUGH BRUNDAGE
  5. COMMENT: DR PHILIP A. MACKOWIAK
  6. Acknowledgements:
  7. References

This patient could only have been Booker T. Washington. As indicated in the hospital record, he presented with severe, symptomatic hypertension; grade IV hypertensive retinopathy (hemorrhages, exudates and papilledema); cardiac dysfunction; and renal insufficiency. Although lacking hematuria, this presentation was classic for malignant hypertension. The negative result of the Wasserman test contradicts speculation that he might have had syphilis.

The diagnosis of malignant hypertension introduces the need to consider secondary causes of hypertension. Had today's diagnostic resources been available in 1915, a secondary cause might have been identified in up to one third of patients with this presentation. In Mr Washington's case, the hypertension might have been due to a primary renal disorder, although most likely the renal failure was the result, rather than the cause, of his hypertension. His palpitations, gastrointestinal symptoms, and headaches raise the possibility of a pheochromocytoma. Although a calcium value is not available, hypercalcemia (eg, due to hyperparathyroidism alone or associated with one of the multiple endocrine neoplasia syndromes) might also explain the hypertension, gastrointestinal symptoms, renal dysfunction, and polyuria. The diagnosis of secondary hypertension is often not pursued in black patients because the major screening criteria (early age of onset and severe disease) are more likely to result in the diagnosis of essential hypertension in this population. Despite the above, untreated progressive essential hypertension is, by far, the most probable cause of Mr Washington's hypertension and associated findings.

The patient died 2 weeks after entering the Rockefeller Hospital in New York City in early November of 1915. Despite the extent of his renal insufficiency, blood pressure reduction might have prolonged his life. There were no effective antihypertensive therapies then, however, and the 5-year survival in cases of malignant hypertension was fewer than 1%.1,2 Furthermore, the importance of treating elevated blood pressure was not yet recognized and would not be generally accepted until the latter half of the 1900s.3,4 Although blood pressure measurements were routinely performed in 1915, and an elevated blood pressure was often seen in patients with heart disease, stroke and renal (Bright's) disease, few appreciated the causal role of hypertension in these disorders.3–5 When hypertension was treated, the interventions generally consisted of warm salt baths, rest, potassium iodide, nitrates, and/or barbiturates.3,6

Hypertension arises more often and at an earlier age, is more severe, and causes more target organ damage in African Americans than whites, for reasons that are nearly as uncertain in 2007 as in 1915. Many hypotheses have been proposed to explain the predilection of African Americans for hypertension, including lower socioeconomic status, exposure to certain environmental factors, increased sleep apnea and sympathetic activity, deficiency of renal vasodilators, lower nephron number due to a higher rate of premature births, increased salt sensitivity, and a yet-to-be-characterized genetic susceptibility.7–11

The first effective antihypertensive drugs (agents like ganglionic blockers, Veratrum alkaloids, and peripheral sympatholytics) did not become available until the 1940s, and thiazide-type diuretics were not released until the 1950s.4 With the parenteral medications and follow-up therapy currently available, Mr Washington might have expected some return of his renal and cardiac function, but his disease was near end stage by the time of his final admission. Some treated cases of malignant hypertension have, however, survived for many years.4 Even today, the challenge, especially in black populations, is outpatient blood pressure control and prevention of progression of hypertension and its complications before they become clinically significant.

Mr Washington, at a weight of less than 64 kg, was not overweight. This contrasts with recent surveys reporting that more than 60% of non-Hispanic African American men and 77% of non-Hispanic African American women are overweight, with a body mass index of at least 25 kg/m2.12 African Americans exercise less than whites, with almost half of African American adults (44.1% of men and 55.2% of women) reporting no participation in any leisure activity.13 A program of lifestyle modification, including salt and caloric restriction, and increased physical activity (less of an issue in Mr Washington's time), as well as moderation of alcohol intake, may be effective in lowering blood pressure in hypertensive African Americans.14 In the Dietary Approaches to Stop Hypertension (DASH) study15 (which included 459 participants, 60% of whom were African American), African Americans randomized to the DASH eating plan had average decreases in blood pressure of 13/6 mm Hg. Combining the DASH diet with sodium restriction resulted in an additional decrease in blood pressure that was also most pronounced in African Americans.16

Several major clinical trials (eg, the Hypertension Detection and Follow-Up Program [HDFP], the African American Study of Kidney Disease and Hypertension [AASK],17 and the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial [ALLHAT]18) have shown that rational antihypertensive therapy lowers blood pressure to desired levels, even in the most difficult-to-manage African American patients.17–20 Most patients with hypertension require 2 or more antihypertensive medications to reach their blood pressure goal, and failure to titrate therapy is a major cause of the poor blood pressure control.18,19

Although multiple studies have shown that all of the available antihypertensive agents are effective in lowering blood pressure in African Americans, monotherapy with drugs that inhibit the renin-angiotensin system (ie, angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), and β-blockers) are consistently less effective in lowering blood pressure in this population; ACEIs and ARBs are less effective in preventing clinical events than thiazide-type diuretics (and calcium channel blockers) in black patients.21–24

My diagnosis based on the evidence is that Mr Washington had malignant (essential) hypertension complicated by renal failure and hypertensive cardiomyopathy. Hypertension shortened the life of Booker T. Washington, just as it continues to do in poorly treated hypertension patients. Modern therapy should prevent progression of hypertension and the occurrence of malignant or accelerated hypertension.

HISTORICAL DISCUSSION: DR W. FITZHUGH BRUNDAGE

  1. Top of page
  2. Abstract
  3. DIFFERENTIAL DIAGNOSIS:DR JACKSON T. WRIGHT, JR
  4. HISTORICAL DISCUSSION: DR W. FITZHUGH BRUNDAGE
  5. COMMENT: DR PHILIP A. MACKOWIAK
  6. Acknowledgements:
  7. References

In 1903, the prominent African American, W.E.B. Du Bois, observed that “easily the most striking thing in the history of the American Negro since 1876 is the ascendancy of Mr Booker T. Washington.”25 Few contemporaries were likely to disagree with Du Bois or to fail to be impressed by the heroic rise of the former slave to international prominence as an orator, educator, and racial spokesman (Figure 3).

image

Figure 3. Booker T. Washington, ca. 1890. From the Prints and Photographs Division of the Library of Congress, Washington, DC. Available at: http://lcweb.loc. gov/rr/print. Reproduction No. LC-USZ62-25624 (6–2).

The son of a slave mother and an unidentified white father, he experienced deprivation and hard-ship; of slavery's cruelties, none so rankled him as enforced ignorance. As soon as emancipation allowed him, he began to teach himself to read. In 1876, when he was 16, he made his journey, by foot, across Virginia to the Hampton Normal and Agricultural Institute, a school founded in 1868 to educate former slaves. After graduation, he was invited to teach at his alma mater. In 1881, at the age of 25 years, he was hired to oversee the school that was to become the Tuskegee Institute.26 In 2 decades, Washington raised the endowment and attracted black students from all over the world. Tuskegee offered a regimen of supervised work, classes in the trades, and clean living. In 1892, Washington founded the Tuskegee Negro Conference, which annually brought hundreds of blacks to the campus to discuss programs for social welfare, economic development, and educational reform; he advocated self-help and racial cooperation.

Northern philanthropists ranging from industrialists Andrew Carnegie and John D. Rockefeller to Sears and Roebuck magnate Julius Rosenwald sought Washington's advice about the best means to promote black advancement. Presidents Theodore Roosevelt and William Howard Taft discussed race relations with him and solicited his advice regarding patronage appointments.

Any consideration of Washington's rise to power must take into account the circumstances in which he and other former slaves encountered in the South after the Civil War. When emancipated, most southern blacks were impoverished, landless, and illiterate. Recognizing the importance of education to their aspirations, freed people flocked to the newly established public schools in the South. The rate of illiteracy among southern blacks dropped steadily across the late 19th century, but black schools in the South remained woefully underfunded and faced ongoing threats from both white legislators and vigilantes.

Booker T. Washington did not rise to his position as the leader of his race by a democratic process. Instead, connections, ambition, and circumstances enabled him to achieve prominence. After the death of Frederick Douglass in 1895, there was no obvious black leader of national stature to assume his role as the voice of black aspirations. Seven months later, Washington delivered a speech at the Atlanta Exposition and caught the attention of whites. He capitalized on his national acclaim and displayed skill in building an expanding network of white patrons. Yet his power remained tenuous because it ultimately derived from white patronage. Simply put, if he alienated his patrons, he lost his power.

In his final years, he remained as active as ever, maintaining a punishing regimen of speaking engagements, meetings, and fund-raising tours despite his deteriorating health. But his influence with white Americans waned with the election in 1912 of Woodrow Wilson, a southern-born Democrat who rapidly expanded the segregation of federal offices. No longer was Washington able to use his influence in the nation's capital to reward allies and punish critics, or to control the black press as he once had. As his end drew near, he came under increasing attack by black challengers who founded the National Association for the Advancement of Colored People (NAACP) in 1909 and were mustering into their ranks growing numbers of white racial liberals, reform-minded social workers, socialist radicals, and black militants.

When Washington succumbed to his malignant hypertension, the United States lost a remarkable public figure. His death at the comparatively young age of 59 years also abruptly ended the evolution of his program.

COMMENT: DR PHILIP A. MACKOWIAK

  1. Top of page
  2. Abstract
  3. DIFFERENTIAL DIAGNOSIS:DR JACKSON T. WRIGHT, JR
  4. HISTORICAL DISCUSSION: DR W. FITZHUGH BRUNDAGE
  5. COMMENT: DR PHILIP A. MACKOWIAK
  6. Acknowledgements:
  7. References

When news of Booker T. Washington's illness finally broke on November 10, 1915, Dr Walter A. Bastedo, who had taken charge of his case, announced to a worried public that he had “made an examination of Dr Washington a few days ago and found him completely worn out … aging rapidly. Racial characteristics … are in part responsible for Dr Washington's breakdown.”27 Just what he meant by “racial characteristics” is uncertain. Mr Washington's long-time physician in Chicago, Dr George C. Hall, believed the expression meant “a syphilitic history when referring to Colored people and…a doctor making such a diagnosis isn't the right kind to treat this patient.”26

Mr Washington did not have syphilis. His negative Wassermann test proves that. Rather, as indicated in the hospital record made public for the first time in this conference, he had malignant hypertension, which destroyed his kidneys, damaged his heart, and eventually killed him. Were “racial characteristics…in part responsible”?

The data reviewed for us by Dr Wright suggest that, indeed, there might be endogenous factors peculiar to African Americans that are responsible, at least in part, for the common occurrence of hypertension and its adverse consequences. As Dr Wright has also pointed out,27 however, genetics are not likely the key to differences in disease presentation between African Americans and whites. Because human genetic variation is continuously distributed, humans do not cluster discretely by continent of origin, and any attempt to allocate races of individuals into discrete genetic groups according to the origin of their ancestors is difficult, if not patently arbitrary. Mr Washington was the product of an African (slave) mother and a white father. If his “rather Irish face” or “odd look of an Italian” were indicative of his father's heritage, would he not have been as much an Irish American or Italian American as an African American in terms of his genetic composition (ie, his “racial characteristics”)? In view of such ambiguities, it is no wonder we are not much closer today than we were in 1915 to understanding why hypertension singled out this prominent American or why it continues to be so severe a problem for African Americans.

Acknowledgements:

  1. Top of page
  2. Abstract
  3. DIFFERENTIAL DIAGNOSIS:DR JACKSON T. WRIGHT, JR
  4. HISTORICAL DISCUSSION: DR W. FITZHUGH BRUNDAGE
  5. COMMENT: DR PHILIP A. MACKOWIAK
  6. Acknowledgements:
  7. References

We are indebted to Dr Barry S. Coller for locating Mr Washington's hospital record, Mrs Margaret Washington Clifford (Mr Washington's granddaughter) for permission to make the record public, Mr Larry Pitrof for assistance in organizing the conference on which the manuscript is based, and Dr Morton D. Kramer for financial support.

References

  1. Top of page
  2. Abstract
  3. DIFFERENTIAL DIAGNOSIS:DR JACKSON T. WRIGHT, JR
  4. HISTORICAL DISCUSSION: DR W. FITZHUGH BRUNDAGE
  5. COMMENT: DR PHILIP A. MACKOWIAK
  6. Acknowledgements:
  7. References
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