"I can no longer do this," she decided, working hard to stop the tears. The children stood around her silent and concerned. These episodes were happening more frequently now, so often that she could barely stand it. "I'm fine," she said. It was a lie.
Looking into our prism we can see the woman obviously suffered from Cronic Obstructive Pulmonary Disease (COPD), although back then the disease she suffered from was poorly understood. In Alaska there may have been no treatment at all other than rest.
We know she probably acquired the disease gradually over time as she continued to inhale smoke from the same fires she used to cook food for the children and their parents. We know she probably died slowly from lack of oxygen.
Nearly 1,600 years later, a Greek physician named Hippocrates described asthma for the medical community, describing it as dyspnea, or shortness of breath. He was not aware of different causes of dyspnea, so they were all included under his umbrella term asthma.
Yet somewhere, tucked nicely under this umbrella, were patients who had inhaled some microscopic substances, perhaps a chemical, that caused changes of some airway tissue and destruction of others. The end result were diseases we now refer to as chronic bronchitis and emphysema, and that we lump under the umbrella term chronic obstructive pulmonary disease.
It would be another 2,000 years before emphysema would be described around 1650 A.D. The 17th century was well known as a time when physicians were performing autopsies in order to match symptoms observed in life with changes that occurred within the body.
Emphysema became a term that would be used to describe lungs that were larger than normal due to the fact they held abnormal amounts of air. The term would come from the Greek term physe, which means "to blow into." They did not, however, understand why the lungs had extra air blown into them, so this resulted in much speculation.
|Theophile Bonet (1620-1689)|
Giovanni Morgagni (1682-1771) wrote how he respected the works of Bonet, and he himself described several cases of "turgid" lungs in his classic work "On the seats and causes of disease."
Dr. James Arthur Wilson was only 19 when he performed the autopsy on Dr. Johnson, and he described the following:
In 1721 Ruysh provided the first detailed description of emphysema coupled with pictures.
"On opening into the cavity of the chest, the chest did not collapse as they usually do when the air is admitted, but remained distended, as they had lost the power of contraction; the air cells on the surface of the lungs were also very much enlarged... the heart was exceedingly large and strong."
Dr. Samuel Johnson
Matthew Ballie was a prominent British physician who inherited his father's anatomy school in 1783. Throughout his career he studied the bodies of diseased patients, including some specimens handed down to him, such as the lungs of Dr. Samuel Johnson.
|Matthew Ballie (1761-1823)|
He published a book in 1793, "The Morbid Anatomy of Some of the Most Important Parts of the Human Body." It's believed to be the first book on pathology.
He described the lungs of emphysema patients, which included the following description of Dr. Johnson's lungs:
"The lungs are sometimes, though I believe rarely, formed into pretty large cells to resemble the lungs of an amphibious animal. Of this I have seen three instances. It is not improbable that this accumulation (of air) may break down two or three contiguous cells into one, thereby, form a cell of very large size." (5, page 2)
|Charles Badham (1813-1884)|
Bronchitis would soon "supercede" the term chronic catahrr when referring to chronic inflammation of the respiratory tract that resulted in a chronic cough and the spitting up of yellow or otherwise colorful phlegm. (9)
Catahrr was a blanket term used to describe swelling of mucus membranes that resulted in excessive secretions. Throughout the remainder of the 19th century, catahr would continue to be used to describe inflammation of the nasal passages. Another term that caught on around the 1820s was or hay fever. The terms allergy and colds would not be coined for another 80-plus years. (9)
|Laennec accurately described emphysema (13)|
He defined bronchitis as "chronic mucous catahrr," and "filled with mucous fluid." (3)
He defined emphysema as "lungs (that) do not collapse. But they fill up the cavity completely on each side of the heart." (3)
Laennec became the first to describe emphysema due to aging, and he was the first to define emphysema as tissue damage in the peripheral air passages. He further defined emphysema as a breakdown of tissue in the parynchema of the lungs as opposed to air trapped in the alveoli due to an obstruction such as occurs in asthma and bronchitis.
In this way, it was Laennec who became the first to distinguish chronic bronchitis and emphysema as separate entities from asthma. He was the first to speculate that they ought to be extricated from the umbrella term asthma, to become disease entities of their own with their own treatments.
|William Stokes (1804-1878)|
He also said bronchitis is evident in nearly all diseases of the lungs. In noting this, he was drawing a similarity with bronchitis, pneumonia and asthma.
Like Laennec, Stokes was among the first to explain the relationship between chronic bronchitis and emphysema, and believed bronchitis lead to emphysema. He was also the first to describe different types of sputum, such as mucoid and mucopurulent. (1, page 86).
He also mentioned increased secretions and chronic cough as part of the condition.
|John Hutchinson's spirometer|
His device was limited in that it could only measure vital capacity, which is the total amount of air that can possibly be exhaled. Yet this measurement would become useful in helping a physician distinguish between bronchitis, emphysema and asthma.
In 1861 Dr. Henry Hyde Salter described in his book, "On Asthma: It's Pathology and Treatment," that he had never performed an autopsy on an asthmatic when he didn't see evidence of emhysema. Other doctors would make similar statements. Salter also described the barrel chest common with asthmatic children.
However, Salter and other physicians of his day didn't have the ability to differentiate from true asthma as we know it today and true emphysema and chronic bronchitis. Yet to their credit, emphysema was a rare disease until after WWI when cigarette smoking became common place.
By 1870 emphysema and chronic bronchitis were clearly noted as related diseases, and descriptions were present regarding the breakdown of lung tissue that resulted in progression of the disease that resulted in hyperinflation of the lungs.
In 1885 a physician by the name of Mendelssohn "stated that he had met many persons dying from tuberculosis whose symptoms never showed themselves until they worked with coal dust and smoke." (10)
He was therefore among the first to observe the relationship between environmental inhalents and lung disease.
By 1898 the air sacs in the lungs were no longer called simply "cells," they were referred to as alveoli in books and magazines such as The Clinical Review. (12)
Emphysema was now clearly defined as "dilation of the alveoli of the lungs and atrophy of the alveolar walls." (12)
Doctors such as Joseph M. Patton started differentiating overdistention of alveoli due to obstructive diseases such as asthma with excessive air in the lungs due to tissue "atrophy." (12)
By 1930 a plethera of descriptions of the conditions started to show up. One physician described enlarged goblet cells in bronchitic lungs that resulted in increased secretions. Another performed tests that showed airflow limitations in patients with emphysema, and explained that this was due to lost of lung elasticity.
By the 1930s emphysema was clearly understood to be a disease of loss of elasticity of the lungs that results in enlargement of the thoracic cage, which resulted in the appearance of a barrel chest, such as what was previously described by Salter. (11)
Because the chest was already expanded, the regular muscles of inspiration would be of little use in drawing in more air. So, in order to take a deeper breath, the patient would have to make a conscious effort and use his accessory muscles. At first these muscles would become sore, although over time, as they were used with increased frequency, they would become strong, and therefore hypertrophied, and would therefore be no longer sore. (11)
In 1933 Ronald V. Christie, a professor of medicine at the University of London who specialized in emphysema, performed a study that showed the relationship between loss of lung elasticity and airflow limitations. (1, page 87)
With breakdown of tissue of the alveolar walls excess air enters this space and the result is overdistention. This can also result in bulla, which are large areas of tissue breakdown and air trapping, meaning this entire portion of the lung will not be involved in the process of ventilation. The end result is increased dyspnea.
In 1944 Christis suggested, that because the lungs were always expanded due to loss of elastic recoil, expiration would have to be passive. He said:
"With loss of elasticity there must be loss of elastic recoil, so that if the lung is to be deflated it has to be squeezed. The respiratory musculature was not built for this task, and the intercostals have to be assisted by the accessory muscles on expiration: the muscles of the abdominal wall can often be felt to contract on expiration, which is prolonged as it is in other conditions, such as asthma and tracheal obstruction, in which the lungs have to be compressed by an active muscular effort. With so extensive an impairment of both inspiration and expiration it is not surprising that the vital capacity and chest expansion are reduced." (11)In other words, he is describing the conscious use of accessory muscles.
He describes lungsounds as faint except for in the bases where they may appear to be absent. Diagnosis could be made by observation of the physical signs, such as a barrel chest, vital capacity measurements with spirometry, and obvious dyspnea on exertion not attributable to other conditions.
He also suggested diagnosis should be made based on signs of chronic cough or asthma, meaning dyspnea.
By the 1950s physicians had learned so much about the lungs that they pretty much wiped the slate clean and redescribed both emphysema and chronic bronchitis for the medical community.
Experts determined there were various disease processes that could result in excessive air in the chest or overdistention of the alveoli such as acute asthma or chronic bronchitis. This "overdistention" was no longer considered emphysema. True emphysema would now be considered air in the interstitial spaces due to breakdown of parychemal lung tissue such as the pores of Kahn and the walls of the alveoli.
Air trapping in asthmatics was determined to be completely reversible, and air trapping in chronic bronchitis patient only partially reversible. As with emphysema, both may result in a barrel chest, although a barrel chest in asthma is only temporary, and the barrel chest in emphysema is chronic.
During the 1960s and 1970s pulmonary function testing was used with increased frequency to study lung diseases, and it was during this era that the term FEV1 was first used to measure expiratory flow. This is a test result that could not be faked, and that could easily be used to differentiate asthma from chronic bronchitis, emphysema, and other lung diseases.
By the 1980s pulmonary function testing would become commonplace in diagnosing COPD, with the measurement of FEV1 being the most significant measurement.
While physicians like Dr. Wilson keenly observed the large heart in those suffering from lung diseases, by the 1980s physicians understand that diseases like chronic bronchitis and emphysema, now lumped under the umbrella term COPD, became still.
In an effort to force blood through stiff lungs, the right heart is overworked and becomes enlarged over time, resulting in a condition called cor pulmonale. Physicians now understood that when this occurred, the disease was in it's final stages, or end stages.
It was at time time dyspnea would become increasingly worse, and might be caused by infections such as pneumonia in the lungs, or it might be caused by heart failure.
In 1972 the mummy of a 1,600 year old woman was discovered in Alaska. The woman was found to have evidence of emphysema, and this may be the oldest reported case of COPD. (1, page 85).
- Qutayba Hamid, Joanne Shannon, James Martin, "Physiologic Basis of Respiratory Disease," 2005, Montreal, page 85-99
- Bhatia, K. Sujata, "Biomaterials for Clinical Application," 2010, London, page 100
- Petty, Thomas L, "The History of COPD,"Int. J. Chron. Obstruct. Pulmon. Dis., 2006, March; 1(1): 3-14
- Crellin, J. M.D., "Selected Items from the history of pathology," Am J Pathol. 1980 January; 98(1): 212.
- Thurlbeck, Wright, "Thurlbeck's Chronic Airflow Obstruction," 1999, Canada, pages 1-6
- Reich, Jerome M, "Convulsion of the lung: an historical analysis of the cause of Dr. Johnson's fatal emphysema," Journal of the Royal Society of Medicine, Vol. 87, December, 1984, page
- Laennec, Rene, "Treaties of the diseases of the chest," 1821
- Stokes, William, "The Diagnosis and Treatment of Diseases of the Chest," 1837, Dublin
- Gee, Samuel, "Bronchitis, Pulmonary Emphysema and Asthma, " The Lancet, March 18, 1899, page 51
- Klotz, Oskar, Wm. Charles White, ed., "Papers on the Influence of Smoke on Health," Bulletin #9, 1914, page 36
- Christie, Ronald V, "Emphysema of the Lungs: Part II, British Medical Journal, Jan. 29, 1944, page 143-146
- Cleveland, Geo. Henry, "The Clinical Review: AJournal of Practical Medicine and Surgery," Vol. VIII, April-Sept. 1898, Chicago.