Frederick Henry Horatio Akbar Mahomed (11 April 1849 – 22 November 1884) was an internationally known British physician from Brighton, England.
Contents
Frederick Henry Horatio Akbar Mahomed (11 April 1849 – 22 November 1884) was an internationally known British physician from Brighton, England.
Frederick Henry Horatio Akbar Mahomed was born on 11 April 1849 in Brighton. [1] He was the eldest son of Frederick Mahomed (1818–1888) and his second wife, Sarah Hodgkinson (1816–1905). He was also the grandson of the pioneering Indian traveller, author and entrepreneur Sake Dean Mahomed who was born in the city of Patna. [2] Frederick Akbar Mahomed's father, Frederick Mahomed, ran a fencing, gymnastics and callisthenics academy in Hove, which included boxing instruction. [2] Cameron and Hicks [2] dispute the suggestion that he ran Turkish baths at Brighton [3] attributing this to a confusion of Mahomed's father Frederick with his uncle, Arthur. Mahomed had three brothers (Arthur George Suleiman, James Deen Kerriman and Henry), and one sister (Adeline). He was educated privately in Brighton prior to attending medical school. [4]
On June 14, 1873, at the parish church of St Nicholas', Brighton, Mahomed married Ellen (Nellie) Chalk. The couple had two children, a son, Archibald in 1874 [5] and a daughter, Ellen in 1876. [6] Only a month after the birth of Ellen in 1876, his wife, Ellen, died suddenly of sepsis [7] and Mahomed and his family moved in with his uncle, Horatio, also a widower, in Seymour Street near Portman Square, London. [2] In 1879 Mahomed married Ada Chalk, the younger sister of his first wife. As such a marriage was not legal under English law, the couple married in Switzerland. [8] They lived at 12 St Thomas Street, close to Guy's Hospital. The couple had two daughters, Dorothy in 1880, [9] and Janet in 1881, [10] and a son, Humphry in 1883. [11] In 1884 the family moved from St Thomas' Street into a six-story Georgian house at 24 Manchester Square. Sadly, later that year, Mahomed contracted typhoid fever, presumably from a patient at the London Fever Hospital, where he was working. He died on 22 November 1884 from an intestinal hemorrhage and a perforated intestine. [2] He was buried on the western side of Highgate Cemetery. [12] On his death a subscription was set up to assist his family and several notable physicians, including Sir William Gull, Sir Samuel Wilks, Sir James Paget and Elizabeth Garrett Anderson, contributed. His oldest son, Archibald, later became a doctor, and in 1914 Archibald and the rest of the family changed their name to Deane (possibly acknowledging Frederick's grandfather's name, Deen) to lessen the impact of the xenophobia and racial prejudice associated with the outbreak of the World War I. [2]
In 1867, aged 18, Mahomed began to study medicine at the Sussex County Hospital, Brighton. Two years later in October 1869, he entered Guy's Hospital, London as a medical student. [13] He was an outstanding student and, in 1871, won the student Pupils' Physical Society prize for his work on the sphygmograph, having been runner-up the previous year. [2] Mahomed qualified as a Member of the Royal College of Surgeons in 1872. Following qualification, Mahomed worked at Highgate Infirmary (St Pancras' North Infirmary, Central London Sick Asylum) for a year. In 1873, he was appointed as resident medical officer at the London Fever Hospital in Liverpool Street, Islington. In 1874 Mahomed became a member of the Royal College of Physicians and was appointed as Student Tutor and Pathologist at St Mary's Hospital, Paddington. In 1875, Mahomed gained a doctorate (M.D.) from the University of Brussels. In 1877, he returned to Guy's Hospital as a Registrar (Senior Resident). He was elected as a Fellow of the Royal College of Physicians in 1880, and in 1881, he was awarded an M.B. from Cambridge University for his thesis on "Chronic Bright's disease without albuminuria". In the same year, he was appointed Assistant Physician at Guy's Hospital and, in 1882, he was appointed as a Demonstrator in Morbid Anatomy at Guy's Hospital.
Mahomed‘s earliest contribution, while still a medical student, was to improve the sphygmograph, a device for measuring blood pressure that had originally been devised by Karl von Vierordt and further developed by Étienne-Jules Marey. Mahomed’s major innovation was to make the sphygmograph quantitative, so that it was able to measure arterial blood pressure (in Troy ounces). The description of the modified instrument was published in 1872. [14] Following his graduation in the same year, Mahomed took up an appointment at the Central London Sick Asylum, where he worked with Sir William Broadbent, who became a strong supporter and friend. [2] Several of Mahomed’s pulse tracings are contained in Broadbent’s classic book, The Pulse. [15] Mahomed used the new sphygmograph to measure arterial tension (blood pressure) in Bright's disease and a range of other conditions, including pregnancy, scarlet fever, gout, alcohol and lead poisoning. [16] He found that in some individuals blood pressure was elevated before there was evidence of kidney disease, assessed by measurement of protein in the urine (proteinuria). He also made the association between the elevated blood pressure and various post-mortem changes, including enlargement of the heart (cardiac hypertrophy), thickening and fibrosis of the arterial wall, aneurysm formation, and damage to the microcirculation (arterio-capillary fibrosis). In effect, Mahomed was describing most of the key pathological effects of essential hypertension for the first time. Initially he termed this condition "Bright's disease without albuminuria" but later he described it as “high pressure diathesis”. His description of the condition is worth citing:
‘…the existence of this abnormally high pressure does not necessarily mean disease, but only a tendency towards disease. It is a functional condition, not necessarily a permanent one, though it is generally more or less so in these individuals. These persons appear to pass on through life pretty much as others do… As age advances the enemy gains accessions of strength; perhaps the mode of life assists him—good living and alcoholic beverages make secure his position, or head work, mental anxiety, hurried meals, constant excitement, inappropriate or badly cooked food, or any other of the common but undesirable circumstances of everyday life, tend to intensify the existing condition, or, if not previously present, perhaps produce it. Now under this greatly increased arterial pressure, hearts begin to hypertrophy and arteries to thicken; what has previously been a functional condition tends to become more of the nature of an organic one…’ [16] : 400
Mahomed also proposed that reducing blood pressure would prolong life, [16] although the means of doing that in his era were in the main limited to lifestyle advice.
In 1880 Mahomed made a first foray into public health. [17] He wrote to the British Medical Journal to advocate undertaking the comprehensive systematic documentation of disease in Britain; he termed this idea, Collective Investigation. Mahomed’s proposals were warmly supported by Sir George Murray Humphry, the President of the British Medical Association, and a Collective Investigation Committee was formed in 1881 with Mahomed as secretary. Around this time Mahomed became acquainted with the British polymath, Francis Galton, who shared an interest in factors predisposing to disease. Mahomed and Galton collaborated to produce composite photographs of over 400 patients with phthisis (tuberculosis), which they compared with composite photographs based on 200 individuals without evidence of phthisis to test whether, as was widely believed, appearance or looks indicated a predisposition to disease. They found no evidence of a characteristic facial appearance associated with tuberculosis beyond some evidence of emaciation.
In 1882 Mahomed advocated expanding Collective Investigation to include a general collection of detailed family life histories: [17]
'for encouraging patients to keep carefully prepared records of their lives and of the chief incidents therein, both medical and otherwise. These records would prove of very great value, alike to the patient, to the doctor, and to medical science.'
A life-history subcommittee of the Collective Investigation Committee, including both Mahomed and Galton was formed in 1882. [17]
Initially the Collective Investigation Committee was very successful with 54 local Collective Investigation Committees being formed to collect data. Their preliminary findings were published in 1883 as a 76-page single volume called 'The Collective Investigation Record' and included results based on more than 2000 patients. [17] In 1884, a Life History Album was published to allow parents to record details of family circumstances and child development. It was advertized in Nature and Galton offered prizes of £500 to people who submitted the most complete family records - within 5 months he had received in excess of 150 records. [17] Over the subsequent 5 years data based on over 300 family records were published, with the main findings summarised in Galton’s book, Natural Inheritance. [17] However, Mahomed would not see these achievements as he died in November 1884 from typhoid fever. [18]
Michael F. O'Rourke summarizes the contributions of Frederick Akbar Mahomed as follows: [19]
In detailed clinical studies, he separated chronic nephritis with secondary hypertension from what we now term essential hypertension. He described the constitutional basis and natural history of essential hypertension and pointed out that this disease could terminate with nephrosclerosis and renal failure. His clinical studies were done without the benefit of a sphygmomanometer but with the aid of a quantitative sphygmogram that he had initially developed while a medical student. He described characteristic features of the pressure pulse in patients with high blood pressure and in persons with arteriosclerosis consequent on aging. These pressure wave changes have recently been verified and explained. He contributed to a number of other advances in medical care, including blood transfusion and appendectomy for appendicitis. He initiated the Collective Investigation Record for the British Medical Association; this organization collected data from physicians practicing outside the hospital setting and was the precursor of modern collaborative clinical trials.
Blood pressure (BP) is the pressure of circulating blood against the walls of blood vessels. Most of this pressure results from the heart pumping blood through the circulatory system. When used without qualification, the term "blood pressure" refers to the pressure in a brachial artery, where it is most commonly measured. Blood pressure is usually expressed in terms of the systolic pressure over diastolic pressure in the cardiac cycle. It is measured in millimeters of mercury (mmHg) above the surrounding atmospheric pressure, or in kilopascals (kPa). The difference between the systolic and diastolic pressures is known as pulse pressure, while the average pressure during a cardiac cycle is known as mean arterial pressure.
Hypertension, also known as high blood pressure, is a long-term medical condition in which the blood pressure in the arteries is persistently elevated. High blood pressure usually does not cause symptoms. It is, however, a major risk factor for stroke, coronary artery disease, heart failure, atrial fibrillation, peripheral arterial disease, vision loss, chronic kidney disease, and dementia. Hypertension is a major cause of premature death worldwide.
Pulse pressure is the difference between systolic and diastolic blood pressure. It is measured in millimeters of mercury (mmHg). It represents the force that the heart generates each time it contracts. Healthy pulse pressure is around 40 mmHg. A pulse pressure that is consistently 60 mmHg or greater is likely to be associated with disease, and a pulse pressure of 50 mmHg or more increases the risk of cardiovascular disease. Pulse pressure is considered low if it is less than 25% of the systolic. A very low pulse pressure can be a symptom of disorders such as congestive heart failure.
Pulmonary hypertension is a condition of increased blood pressure in the arteries of the lungs. Symptoms include shortness of breath, fainting, tiredness, chest pain, swelling of the legs, and a fast heartbeat. The condition may make it difficult to exercise. Onset is typically gradual. According to the definition at the 6th World Symposium of Pulmonary Hypertension in 2018, a patient is deemed to have pulmonary hypertension if the pulmonary mean arterial pressure is greater than 20mmHg at rest, revised down from a purely arbitrary 25mmHg, and pulmonary vascular resistance (PVR) greater than 3 Wood units.
Essential hypertension is the form of hypertension that by definition has no identifiable secondary cause. It is the most common type affecting 85% of those with high blood pressure. The remaining 15% is accounted for by various causes of secondary hypertension. Primary hypertension tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors. Prevalence of essential hypertension increases with age, and individuals with relatively high blood pressure at younger ages are at increased risk for the subsequent development of hypertension. Hypertension can increase the risk of cerebral, cardiac, and renal events.
Eisenmenger syndrome or Eisenmenger's syndrome is defined as the process in which a long-standing left-to-right cardiac shunt caused by a congenital heart defect causes pulmonary hypertension and eventual reversal of the shunt into a cyanotic right-to-left shunt. Because of the advent of fetal screening with echocardiography early in life, the incidence of heart defects progressing to Eisenmenger syndrome has decreased.
Cushing reflex is a physiological nervous system response to increased intracranial pressure (ICP) that results in Cushing's triad of increased blood pressure, irregular breathing, and bradycardia. It is usually seen in the terminal stages of acute head injury and may indicate imminent brain herniation. It can also be seen after the intravenous administration of epinephrine and similar drugs. It was first described in detail by American neurosurgeon Harvey Cushing in 1901.
Edward D. Freis was an American physician and researcher, who received the Albert Lasker Award for his studies of the treatment of hypertension.
Dean Mahomed (1759–1851) was a British Indian traveller, soldier, surgeon, entrepreneur, and one of the most notable early non-European immigrants to the Western World. Due to non-standard transliteration, his name is spelled in various ways. His high social status meant that he later adopted the honorific "Sake" meaning "venerable one". Mahomed introduced Indian cuisine and shampoo baths to Europe, where he offered therapeutic massage. He was also the first Indian to publish a book in English.
Hypertensive kidney disease is a medical condition referring to damage to the kidney due to chronic high blood pressure. It manifests as hypertensive nephrosclerosis. It should be distinguished from renovascular hypertension, which is a form of secondary hypertension, and thus has opposite direction of causation.
Vital signs are a group of the four to six most crucial medical signs that indicate the status of the body's vital (life-sustaining) functions. These measurements are taken to help assess the general physical health of a person, give clues to possible diseases, and show progress toward recovery. The normal ranges for a person's vital signs vary with age, weight, sex, and overall health.
A hypertensive emergency is very high blood pressure with potentially life-threatening symptoms and signs of acute damage to one or more organ systems. It is different from a hypertensive urgency by this additional evidence for impending irreversible hypertension-mediated organ damage (HMOD). Blood pressure is often above 200/120 mmHg, however there are no universally accepted cutoff values.
The sphygmograph was a mechanical device used to measure blood pressure in the mid-19th century. It was developed in 1854 by German physiologist Karl von Vierordt (1818–1884). It is considered the first external, non-intrusive device used to estimate blood pressure.
Robert Wallace Wilkins was an American medical investigator and educator. He made many contributions in the research of hypertension and cardiovascular disease. He was the president of the American Heart Association in 1957 and received its Gold Heart Award in 1962. Wilkins received the Albert Lasker Award in 1958 for his research.
Nathan W. Levin is an American physician and founder of the Renal Research Institute, LLC., a research institute dedicated to improving the outcomes of patients with kidney disease, particularly those requiring dialysis. Levin is one of the most prominent and renowned figures in clinical nephrology as well as nephrology research. He has authored multiple book chapters and over 350 peer-reviewed publications, including articles in leading journals such as Nature, the New England Journal of Medicine, and The Lancet.
The modern history of hypertension begins with the understanding of the cardiovascular system based on the work of physician William Harvey (1578–1657), who described the circulation of blood in his book De motu cordis. The English clergyman Stephen Hales made the first published measurement of blood pressure in 1733. Descriptions of what would come to be called hypertension came from, among others, Thomas Young in 1808 and especially Richard Bright in 1836. Bright noted a link between cardiac hypertrophy and kidney disease, and subsequently kidney disease was often termed Bright's disease in this period. In 1850 George Johnson suggested that the thickened blood vessels seen in the kidney in Bright's disease might be an adaptation to elevated blood pressure. William Senhouse Kirkes in 1855 and Ludwig Traube in 1856 also proposed, based on pathological observations, that elevated pressure could account for the association between left ventricular hypertrophy to kidney damage in Bright's disease. Samuel Wilks observed that left ventricular hypertrophy and diseased arteries were not necessarily associated with diseased kidneys, implying that high blood pressure might occur in people with healthy kidneys; however, the first report of elevated blood pressure in a person without evidence of kidney disease was made by Frederick Akbar Mahomed in 1874 using a sphygmograph. The concept of hypertensive disease as a generalized circulatory disease was taken up by Sir Clifford Allbutt, who termed the condition "hyperpiesia". However, hypertension as a medical entity really came into being in 1896 with the invention of the cuff-based sphygmomanometer by Scipione Riva-Rocci in 1896, which allowed blood pressure to be measured in the clinic. In 1905, Nikolai Korotkoff improved the technique by describing the Korotkoff sounds that are heard when the artery is ausculted with a stethoscope while the sphygmomanometer cuff is deflated. Tracking serial blood pressure measurements was further enhanced when Donal Nunn invented an accurate fully automated oscillometric sphygmomanometer device in 1981.
The article reviews the evolution of continuous noninvasive arterial pressure measurement (CNAP). The historical gap between ease of use, but intermittent upper arm instruments and bulky, but continuous “pulse writers” (sphygmographs) is discussed starting with the first efforts to measure pulse, published by Jules Harrison in 1835. Such sphygmographs led a shadowy existence in the past, while Riva Rocci's upper arm blood pressure measurement started its triumphant success over 100 years ago. In recent times, CNAP measurement introduced by Jan Penáz in 1973 enabled the first recording of noninvasive beat-to-beat blood pressure resulting in marketed products such as the Finapres™ device and its successors. Recently, a novel method for CNAP monitoring has been designed for patient monitoring in perioperative, critical and emergency care, where blood pressure needs to be measured repeatedly or even continuously to facilitate the best care for patients.
Sir James Murray (1788–1871) was an Irish physician, whose research into digestion led to his discovery of the stomach aid Milk of Magnesia in 1809. He later studied in electrotherapy and led the research into the causes of cholera and other epidemics as a result of exposure to natural electricity. He was the first physician to recommend the breathing in of iodine in water vapour for respiratory diseases.
Thomas G. Pickering was a British physician and academic. He was a professor of medicine at College of Physicians and Surgeons, Columbia University Medical Center in New York City. He was an internationally renowned expert in clinical hypertension and a leader in the fields of hypertension and cardiovascular behavioral medicine. He coined the term "white-coat hypertension" to describe those whose blood pressure was elevated in the doctor's office, but normal in everyday life. He later published the first editorial describing "masked hypertension". He also discovered and gave his name to the Pickering Syndrome, where bilateral renal artery stenosis causes flash pulmonary edema.
Harriet Pearson Dustan (1920–1999) was an American physician who is known for her pioneering contributions to effective detection and treatment of hypertension. She was the first woman to serve on the Board of Governors of the American Board of Internal Medicine.
{{cite book}}: CS1 maint: multiple names: authors list (link)