A brief history of COPD

The 42-year-old Alaskan woman sat by the crackling fire 1,600 years before the birth of Christ.  She was severely winded after just a short walk with the children.  Her chest heaved up and down, occasionally interrupted by a dry, hacking, painful cough.

“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 names Hippocrates included every disease that causes shortness of breath, what he called dyspnea, under the umbrella term of asthma.  The term comes from the Greek word Aezean which literrally means gasping or panting.

It would be another 2,000 years, about 1,650 A.D, before the term emphysema was used in autopsies to describe lungs that were larger than normal because they held extra air.  The term comes from the Greek physe which means “to blow into.”  Emphysema would become a word to describe lungs inflated with extra air.

In 1679 a Swiss physician named Theophile Bonet (1620-1689) performed over 3,000 autopsies on patients he followed, and was among the first to describe emphysema as a medical condition of “voluminous lungs” in his book Sepulchretum. (2) (3) (4)

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. Samuel Johnson

In 1784 Dr. Samuel Johnson was a well known physician, and he also became well known for his breathing trouble. He was thought to have suffered from asthma from birth, and later he was determined to have died of fibrosis of the lungs.  Although from autopsy results future historians have concluded that what he died of was emphysema and cor pulmonale and not asthma.  (6)

Dr. James Arthur Wilson was only 19 when he performed the autopsy on Dr. Johnson, and he described the following:

“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.”

In 1721 Ruysh provided the first detailed description of emphysema coupled with pictures.  In 1799 and 1807 Matthew Ballie also provided a description of emphysema with detailed pictures.  He described the condition as “enlarged air spaces” in the lungs, and lungs that did not collapse.  He is beleived to have had the lungs of Dr. Samuel Johnson to help him with his descriptions. 


Matthew Ballie (1761-1823) was a prominent British physician who inherited his father’s anatomy school in 1783.  Throughout his career he studied the bodies of diseases patients, including some specimens handed down to him, such as the lungs of Dr. Samuel Johnson.  


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 beleive 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)

In 1814 British Physician Charles Badham became the first to use the term “bronchitis” to denote “inflammatory changes in the mucous membrane.”  Bronchitis would soon “supercede” the term chronic catahrr when referring to this condition.  Catahrr was a blanket term used to describe swelling of mucus membranes that resulted in excessive secretions. Throughout the 19th century catahr continued to be used to describe inflammation of the nasal passages (or hay fever).  (9)

Laennec accurately described emphysema (13)

In 1821 Dr. Rene Laennec — known as the father of chest medicine in part due to his invention of the stethescope — accurately described both emphysema and bronchitis as related conditions.  He defined bronchitis as “chronic mucous catahrr,” and “filled with mucous fluid.”  He defined emphysema as “lungs (that) do not collapse.  But they fill up the cavity completely on each side of the heart.”  (3)

Laennec also became the first to describe emphysema due to aging.  He also was the first to define emphysema as tissue damage in the peripheral air passages, and 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 1837 Dr. William Stokes became the first to use the term “chronic bronchitis” in his book ”The Diagnosis and Treatment of Diseases of the Chest.”  He defines bronchitis as “inflammation of the mucous membrane,” and that this condition may give rise to “dilations of the air cells and tubes, and to pulmonary emphysema.”  (8, page 45)

He also noted that bronchitis is evident in nearly all diseases of the lungs.  In noting this, he is drawing a similarity with bronchitis, pneumonia and asthma.  Bronchitis and emphysema were initially considered diseases under the umbrella of asthma, and now these diseases are slowly branching off as diseases of their own as more wisdom is learned about these diseases.

Like Laennec, Stokes was likewise among the first to explain the relationship between chronic bronchitis and emphysema, and believed bronchitis lead to emphysema.  He also was the first to describe different types of sputum, such as mocoid and mucopurulent.  (1, page 86).  He also mentioned increased secretions and chronic cough as part of the condition.

John Hutchinson’s spirometer

In 1846 John Hutchinson invented the spirometer, which ultimately was used to perform many tests on the lungs.  While he believed his device was limited in its purpose, it would become the perfect device for diagnosing and treating many diseases of the lungs.

His device was limited in that it could only measure vital capacity, which is the total amount of air that can possibly be exhaled.

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.  Emphysema was now clearly defined as “dilation of the alveoli of the lungs and atrophy of the alveolar walls.”   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. Because the chest was already expanded the regular muscles of inspiration would be of little use and this would require use of accessory muslces during regular breathing.  (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.

 In 1944 he suggested that because the lungs were always expanded due to loss of elastic recoil, expiration would have to be passive.  He wrote:

“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)

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.

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 was now 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 patients may be partially reversible.  As with emphysema, both may result in a barrel chest, although emphysema results in a chronic barrel chest.

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.  By the 1980s pulmonary function testing would become commonplace in diagnosing COPD, with the measurement of FEV1 as the most important measurement in diagnosing diseases of airflow obstruction like COPD and asthma..

While physicians like Dr. Wilson keenly observed the large heart in those suffering from lung diseases, physicians now understand diseased lungs make the lungs stiff, and this causes the right heart to work extra hard to pump blood through it.  The extra work causes the heart to become enlarged, like the muscles of someone who pumps iron.

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).

1. 
   Qutayba Hamid, Joanne Shannon, James Martin, “Physiologic Basis of Respiratory Disease,” 2005, Montreal, page 85-99
   


2. 
   Bhatia, K. Sujata, “Biomaterials for Clinical Application,” 2010, London, page 100
   


3. 
   Petty, Thomas L, “The History of COPD,”Int. J. Chron. Obstruct. Pulmon. Dis., 2006, March; 1(1): 3-14
   


4. 
   
   
   

   Crellin, J. M.D., “Selected Items from the history of pathology,” Am J Pathol. 1980 January; 98(1): 212.
   

   
   

   
   

   
   
   
   


5. 
   Thurlbeck, Wright, “Thurlbeck’s Chronic Airflow Obstruction,” 1999, Canada, pages 1-6
   


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
   


7. Laennec, Rene, “Treaties of the diseases of the chest,” 1821


8. 
   Stokes, William, “The Diagnosis and Treatment of Diseases of the Chest,” 1837, Dublin
   


9. 
   Gee, Samuel, “Bronchitis, Pulmonary Emphysema and Asthma, ” The Lancet, March 18, 1899, page 51
   


10. 
    Klotz, Oskar, Wm. Charles White, ed., ”Papers on the Influence of Smoke on Health,”  Bulletin #9, 1914, page 36
    


11. Christie, Ronald V, “Emphysema of the Lungs: Part II, British Medical Journal, Jan. 29, 1944, page 143-146


12. Cleveland, Geo. Henry, “The Clinical Review: AJournal of Practical Medicine and Surgery,” Vol. VIII, April-Sept. 1898, Chicago.

Photos:  

1. http://library.medicine.yale.edu/about/adopt/laennec