Showing posts with label emphysema. Show all posts
Showing posts with label emphysema. Show all posts

Wednesday, February 1, 2017

1873: Berkart says asthma is merely a symptom

Dr. J.B. Berkart was Asistant-Physician to the Victoria Park Hospital for Diseases of the Chest.  So he was well acquainted with asthma.  Unlike his predecessor, Dr. Henry Hyde Salter, Berkart opposed the nervous and spasmotic theories of asthma.

Berkart understood that, as Dr. C.B. Williams proved in 1840, that the muscles surrounding the air passages could contract or spasm.  However, he believed that Paul Bert, who published the results of his own studies on the contractility of the lungs in 1870, proved that the lungs do not contract during an asthma attack.

Of Bert, Berkart wrote:
"In many of his experiments he failed to demonstrate the contractility of the lungs, but at last he succeeded in doing so; and he found, as the reason of his failure, that he "insufflated the lungs too much", which circumstance impedes their contraction.  But if Paul Bert has thus proven the contractility of the bronchial muscles, he has at the same time conclusively shown the impossibility that asthma can be due to a spasmodic stricture of the bronchial tubes in those cases in which it forms an integral part of the disease, namely, in emphysema. For that same cause which hinders the success of the physiological experiments fully exists under those pathological conditions. (1, page 537)
Berkart believed that Henry Hyde's theory that asthma is nervous simply because asthma leaves behind no physical signs was poppycock. (2, page 49-50) Of this, Berkart said:
For the absence of physical signs is no safe indicator of the absence also of pathological conditions, and all the positive evidence derived from experimental physiology only goes to show that the "bronchial muscles may contract"; but as to "how" and as to "when" nothing is known. (1, page 537)
Berkart likewise explained:
I  am prepared to show that, were even the entire nervous system bent upon producing a spasmotic contraction of the bronchial muscles, it would fail in its attempts, because they are in cases of asthma in such a state of nutrition as to be utterly incapable of contracting at all." (1, page 537)
Instead, asthma being the result of a neurosis that causes spasms of the air passages, Berkart postulated that asthma was merely a symptom that accompanies other diseases: (1, page 537)(2, page 110)
  1. Emphysema
  2. Bronchitis
  3. Other pulmonary affections 
  4. Cardiac affections (1, page 537)(2, page 110
Furthermore, he said asthma is most often secondary to emphysema and bronchitis, and "the rare cases in which these are supposed to be absent could only constitute an exception to the rule.  The exception, however, does by no means invalidate the rule." (1, page 438)

The proof that the exception "does by no means invalidate the rule," was proved, according to Berkart, by the experiments of Walshe.  Of this, Berkart wrote: 
So well has this fact been recognised by all clinical observers, that they more or less explicitly mention "an acute relaxation" (Walshe*, Diseases of the Lungs, 1871, page 209) of the bronchial walls in cases of acute bronchitis.  Therefore, what holds good in the acute, still more forcibly applies to the chronic affection.  Here indeed, are the bronchial muscles so completely soaked with serum, that, were this the sole change they undergo, it alone would surfice to render contraction of the muscles a matter of impossibility.  But very often the first outbreak  of an asthmatic attack is preceded by pathological changes of greater moment than bronchitis -- namely, by catarrhal pneumonia, the anatomical basis of whooping-cough, measles, etc; and that disease inflicts such injuries upon the bronchial walls, that their contraction is irrevocably lost." (1, page 538)
He therefore argued that there was no point in debating what causes the attack, as such debates were frivolous.  He said:
Gentlemen, we shall never arrive at the true nature of bronchial asthma if we continue to confine our attention to an attack itself, to its immediate causes, and to its peculiar type of respiration. In asthma, as well as in any other disease, the history of the case and its sequele will have to be carefully considered ; and then we shall find that, indeed, asthma is no independent disease, no dynamic affection of a nerve, but that it really forms a link in a chain of diseases, which commence with affections of the bronchi and terminate with emphysema, whilst asthma itself represents the stage intermediate between these two. (1, page 538)
As Salter was ultimately proved correct in his assertion that asthma was indeed a disease of bronchospasm, he was eventually proved wrong that asthma was a neurosis.  To the contrary, Berkart was ultimately proved wrong in his assertion that asthma was not a disease of bronchospasm, and was eventually proved correct that asthma was not a neurosis.

Berkart believed that asthma starts as a chronic catarrh, often in childhood, and over time develops into emphysema.  Since emphysema is rarely found in children, it usually gradually develops unnoticed into adulthood.

He said that even as the lungs become increasingly diseased, breathing is generally easy. "But when an obstacle arises," he said, "which for its removal requires a greater force than that of ordinary respiration, then the inability to effect the removal shows the deficient nutrition of the organ. It is this stage of developing emphysema-this stage of deficient elasticity of the lungs-which constitutes the anatomical basis of bronchial asthma." (1, page 538)

He thus explains asthma this way:
In typical bronchial asthma, the lungs are greatly distended, the thorax is in a position of extreme inspiration, and all the respiratory muscles are firmly contracted. Inspiration is short and abrupt, and the effort of the respiratory muscles, although prolonged and greatly increased, remains ineffectual. If an obstacle arise to the entrance and exit of air from the lungs, say the impaction of a tough pellet of mucus in a bronchus, a supplementary force is necessary in order to displace the obstacle and to effectually carry on the respiratory function. Such additional aid to expiration is obtained by deep inspiration; and this is easily effected, because it proceeds from the action of the inspiratory muscles, to which the lungs deficient in elasticity cannot offer any great resistance. Hence the easy and rapid overdistension of the lungs. (1, page 538)
As far as what triggers an asthma attack, Berkart noted both internal and extarnal "exciting causes," all of which "produce an obstacle to the interchange of gases, against which the deficient expiratory forces will for a long time labour in vain." (1, page 538-539)

These exciting causes were: (1, page 538-539)
  1. Tough and fibrinous sputa: The thicker it is, the harder the lungs have to work to expectorate it
  2. Inhalation of foreign bodies: Epecacuanha, pollen, etc. 
  3. Heat from ambient air:  It causes sputum to become crusty, forcing lungs to work extra hard
  4. Excitement, laughter: Sputum is displaced from one part of lung into another, diminishing the surface of respiration
  5. Edema (fluid) in lungs:  Occurs when kidney's become diseased
  6. Thrombosis and embolism (blood clot): Causes asthma symptoms (1, page 538-539)
In conclusion, Berkart wrote:
I may, therefore, in conclusion, state that asthma is a symptom which accompanies diseases of the lungs in which deficient elasticity is the prominent feature, and in consequences in which the existing expiratory forces are only able to overcome an obstacle to respiration after prolonged and increased efforts." (1, page 539)
Berkart, therefore, believed that asthma was not a disease entity of it's own, but rather was a symptom of, in most cases, bronchitis and emphysema. Therefore, despite physicians not being able to find physical signs that asthma exists, these signs do exist.  Berkart said:
A patient may daily expectorate several spittoonfuls of mucus, and yet the most practised and most careful observer may fail to detect, by means of percussion and auscultation, the least trace of disease. The reason is that the mucus forms and stagnates in a bronchus or bronchi, situated at some distance from the surface of the chest, in which position the adventitious sounds are, as the bronchial respiration is normally, obscured by the intervening healthy tissue of the lungs  (2, page 51-52)
Salter originally published his ideas in various articles throughout the 1950s, and later in the 1969 book: "On Asthma: It's Pathology and Treatment."  Berkart also published his ideas in various articles, and in 1978 published the book: "On Asthma: Its Pathology and Treatment."  While both authors used the same title for their respective books, the theories postulated were opposites.

Both Salter and Berkart are important to our asthma history in that they were both responsible for garnishing attention to our disease.  However, while their opinions were well established regarding the cause of asthma, the debate was ongoing.

*Walter Hayle Walshe (1812-1892)

References:
  1. Berkart, J.B., "On the Nature of the so-called bronchial asthma," British Medical Journal, November 8, 1873, 2 (671), pages 537-539
  2. Berkart, J.B., "On Asthma: It's pathology and treatment," 1878, London
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Wednesday, August 31, 2016

1837: Stokes defines chronic bronchitis

William Stokes (1804-1878)
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." (8, page 45)

He defined 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 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.

References

  1. Qutayba Hamid, Joanne Shannon, James Martin, "Physiologic Basis of Respiratory Disease," 2005, Montreal, page 85-99
  2. Stokes, William, "The Diagnosis and Treatment of Diseases of the Chest," 1837, Dublin

Monday, July 11, 2016

1819: Laennec's treatment for emphysema and bronchitis

Laennec admitted himself to have been the first to accurately describe emphysema and bronchitis, and to note that they generally occur together.  While he offered no new remedies, he does offer an idea of how you would have been treated if you had COPD in the 1820s.

He referred to chronic bronchitis as chronic mucous catarrh.  If you were diagnosed with this, these would be your possible remedies.

In old persons:
  • Permanent drain in the arm or thigh
  • Use of aromatic bitters, such as hyssop, horehound, ground ivy, sage, veronica, &c.
If the expectoration suspended:
  • Oxymel of squills, or kermes mineral, in small doses
If cough becomes hard and returns by fits:
  • Peregorics are ordered
For long continuance of the disease: 
  • Emetics, repeated according to the patient's strength and his power in supporting their action
  • Tonics given in small doses after the emetic, such as barks and other bitters
  • Preparations of iron take away the complaint or greatly moderate it
  • Spirituous preparations particularly punch
  • Balsam of tulu and capaiba
  • Turpentine in 18-30 drops daily
  • Internal use of tar water 
  • Inhalation of fumes of tar water defused in the patient's chamber
When acute catarrh supervenes the chronic: 
  • Blisters
  • Cupping
When dyspnea becomes extreme: 
  • Narcotics, particularly the powder of belladonna or strammonium in doses of half a grain to a grain
  • Emetic of Squill, epecacuan, and kermes in small doses

He referred to emphysema as vesicular emphysema.  If you were diagnosed with this, these would be your possible remedies.

When caused by dry catarrh:

  • Friction with oil lessons catarrh
In cachectic subjects:
  • Subcarbonate of iron lessons catarrh, diminishes congestion of mucous membrane and diminishes spasmotic stricture of the bronchi
In severe asthmatic paroxysm:
  • Venesection to relieve congestion of blood in the lungs
  • Narcotics to diminish the necessary of respiration
If you became short of breath with either of these conditions, you would still be referred to as having a fit of asthma.  However, the cause, if your physician was observant enough, would be different.  Even the treatment might be different, at least to a slight degree

References:
  1. Laennec, Rene, "Mediate Auscultation," translated by John Forbes, Notes by professor Andral, 4th edition, 1838, New York, Samuel S. and William Wood, pages 84-87 for bronchitis treatment, and 175-177 for emphysema treatment
  2. Andras, author of the notes in the book, "Mediate Auscultation, by Rene Laennec," ibid
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Friday, July 8, 2016

1819: Laennec accurately groups emphysema and bronchitis

Laennec accurately described emphysema (13)
Dr. Rene Laennec was known as the father of chest medicine, and this is mainly due to the fact he was the first to have the tools necessary to compare what he learned upon assessment of the chest during life, with what he saw when inspecting the lungs during autopsy after life.

The tools he had access to were chest percussion and the monaural stethoscope he invented. He used these to perform complete assessments of the chest on any of his patients who complained of asthma or asthma-like symptoms, such as dyspnea, chest tightness, chest pain, increased phlegm, and coughing. By doing this he became the first physician to accurately distinguish asthma from chronic bronchitis and emphysema.

That said, here is how he described bronchitis and emphysema.

Bronchitis:  He defined it as "Chronic Mucous Catarrh."

He said bronchitic airways are sometimes present with a "general or partial dilation of the bronchi.  Pulmonary vessels are often congested, and this can often be diagnosed by sputum that is tinged with blood. In fact, while the amount expectorated varies from day to day, colorful sputum is almost always produced. However, when the person becomes weak, expectoration may become difficult. (2, page 81)

He said bronchitis usually occurs in the aging, and usually after a severe acute attack, and as it worsens often produces dyspnea.  (2, page 83)

He said if it does occur in the young, however, it usually disappears in a year or two.  However, the only time it disappears in the aging is during the summer months, only to return during the winter months. In such cases it usually returns with a fever and copious expectoration.  After a few times of this happening... (2, page 83)
...it terminates in a continual mucous catarrh... the great expectoration of which weakens and emaciates the patient." (2, page 83)
Since he had access to his stethoscope, he would use it to help him diagnose chronic mucous catarrh.  He would generally hear "mucous rhonchus, sometimes indeed pretty loud and abundant, but very rarely continuous, and still rarely general over the chest." (2, page 83-84)

Laennec said emphysema has been described by some previous authors -- Bonetus, Morgagni, and Floyer,  who observed emphysema in a "broken winded mare" --although "none of these various authors appear to have been acquainted with the real character of the affection, viz -- dilation of the bronchial cells." (2, pages 161,165)

So he said it had never been accurately described. There were two exceptions to this, and these include Ruysh and Valsalva. (2, page 165)

Some might say that Dr. Ballie accurately described emphysema, but Laennec disagrees.  He said:
Dr. Baillie, author of the Morbid Anatomy, has correctly observed the three principal circumstances which constitute emphysema of the lungs, namely—the great size of these organs,—the dilatation of the cells,—and the vesicles formed by the extravasation of air under the pleura; but he does not appear to have been acquainted with the mutual dependence of these three states, and describes them as three different affections. (2, page 166)
In fact, he said that even he thought it was a rare disease until he started making use of the stethoscope.  Since then he said he has verified it in the living as well as the dead.  In fact, he became so adept at diagnosing it that he figured that many cases previously defined as asthma were actually emphysema.  (2, page 161, 163, 165)

He defined it simply as...
...dilation of the air cells... the cavity of these dilated cells descends some little way into the substance of the viscus, and there its walls do not collapse... the bronchial tubes, especially those of the small calibre, are sometimes very evidently dilated in those portions of the lung where the emphysema exists. (2, page 161-163)
He observed that while many of the cells were dilated, some were ruptured. Interestingly, Laennec said:
When we blow into an emphysematous lung, the dilated and projecting cells seem to become flatter the more they are distended, and fall down to the general level of the surface. This is owing to the greater relative extensibility and elasticity of the healthy cells, which in the first instance rise to the level of the dilated cells, and then fall below them, to their natural level. The continued projection of the dilated cells may be partly owing, also, to the difficulty with which the air escapes from them, more especially when the exciting cause of the emphysema is the dry catarrh. (2, page 163)
He also said:
On placing an emphysematous lung in a vessel of water, it sinks much less than a healthy lung; sometimes it floats on the surface with scarcely any obvious immersion."  (2, page 164) 
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.

He said the disease could be diagnosed upon autopsy, although he further stated it could be diagnosed in life by using the stethoscope. He said:
The respiratory sound is inaudible over the greater parts of the chest, and is very feeble in the points where it is audible... from time to time, while exploring the respiration or cough, a slight sibilous rhonchus... by the displacement of the pearly sputa. (2, page 172)
He also noted other signs that emphysema should be diagnosed over asthma: (2, page 172)
  • Diminished lung sounds
  • The long continuance of the disorder (chronic)
  • The severity of the habitual (chronic) dyspnea
  • The asthmatic paroxysm occasionally occurring
  • The cylindrical form of the chest (barrel chest)
  • The slight lividity of the skin
  • Occasional dry crepitous rhonchus on inspiration or with cough (inspiratory crackles due to secretions)
  • Occasional crackle where the rhonchus is heard
  • When the complaint is of long standing and the patient far advanced in life, the paroxysms become more frequent and severe
M. Andral suggests that the dry crepitous rhonchus described by Laennec was the first description of crackles "at the moment of rupture of the air cells."  In modern medical language, this would be crackles on inspiration due to the alveolar cells popping open.  This may have been the first description of this commonly heard lungsound. (3, page 173)

Interestingly, Laennec offers the following about the prognosis of this disease.
Pulmonary emphysema.  is not a disease of great severity.  Of all the varieties of asthma it is unquestionably that which affords to the patient the best prospect of long life. The long continuance and slow progress of the disease and the nature of its causes, render it possible to struggle against the organic lesion, and permit the functional disorders resulting from it to be kept within tolerable bounds (3, page 174)
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.

References:
  1. Petty, Thomas L, "The History of COPD,"Int. J. Chron. Obstruct. Pulmon. Dis., 2006, March; 1(1): 3-14
  2. Laennec, Rene, "Mediate Auscultation," translated by John Forbes, Notes by professor Andral, 4th edition, 1838, New York, Samuel S. and William Wood
  3. Andras, author of the notes in the book, "Mediate Auscultation, by Rene Laennec," ibid
  4. Laennec, Rene, "A Treaties on the Diseases of the Chest and on Mediate Auscultation, " 1834, London (copius notes by John Forbes)
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Friday, April 15, 2016

1784: Emphysema is further defined

Charles Badham (1813-1884)
After the term emphysema was coined in 1679 the quest was on to learn more about this disease. Perhaps some best knowledge was gained from an unexpected source in Dr. Samuel Johnson, although not until he was dead, and his autopsy was performed

In 1721 F. Ruysh provided the first detailed description of emphysema coupled with pictures in his book "Observations anatomica-chirirgicae."  (1, page 85)

In 1764, W.Watson described a case of emphysema in "On account of what happened upon opening the body of an asthmatic person."  He was quoted in "Physiologic Basis of Respiratory Disease" as saying:  (1 page 85)
"The lungs were enormously distended with air... this air was extravasate and had burst through the extremities of the bronchi and vesicular substance...  In a word the lung was truly emphysematous.  In several parts this had formed large bladders... The air getting loose in the substance in the lungs cannot be parted with expiration; it subsequently is retained there and the space it occupies prevents as much of the external air being received into the lungs as its own quantity.(1 page 85)(13, pages 145-147)
Watson also described the diseased condition of the heart.
The figure of the human heart is that of a cone, divided through its axis; but in this case, the heart's figure was altered, and was more compressed than usual; and its ventricles distended with grumous blood. Every other part of the body was in its natural state. (13, page 145)
He added:
From this examination we find that in this instance respiration was greatly disturbed... The varices of the pulmonary vein not only retarded the blood in its passage to the left auricle of the heart, but, occupying a much larger space in the lungs than they naturally should, they left less room for the minute ramifications of the bronchia to extend themselves and consequently a less quantity of air was taken in at every inspiration than was necessary for the ordinary purposes of life...  But the disorder of the lungs from the varices was made infinitely worse by the emphysema. For by the extravasated air possessing so large a portion of the lungs, and which the patient could by no means part with in expiration, very little room was left for fresh air in inspiration; the lungs, from the emphysema, and from the diseased state of the pulmonary vein, filling almost the whole cavity of the thorax. (13, pages 145-146)
He said that in life the man was seized with a troublesome cough, and shortness of breath with minimal exertion.  He said there was no cure for the man because there was "no method of discharging the extravasated air from the lungs." (13, page 146)

Dr. Samuel Johnson (1709-1784)
By 1784 Dr. Samuel Johnson was well known for his medical skills,  and he also well known for his breathing trouble. He was thought to have suffered from asthma since birth, and later he was determined to have died of fibrosis of the lungs.  (6)

At any other time in history this information would have gone down as a fact and that would have been the end of it.  However, Dr. Johnson was born into a time when the medical community was searching for answers about diseases, and so, before he died he gave permission for his lungs to be preserved and studied for science.  (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."
Based on this autopsy report, later physicians, upon examining it, determined that Dr. Johnson did not die of asthma, nor fibrosis, but of a disease that was barely known at the time: emphysema. He was also found to have suffered from cor pulmonale, which would have been the result of his heard working so hard for many years to pump blood through his stiff lungs. (6)

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)
In 1799 and 1807, Ballie  described emphysema with detailed pictures.  He described the condition as "enlarged air spaces" in the lungs, and lungs that did not collapse.

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)
In 1814 British Physician Charles Badham became the first to use the term "bronchitis" to denote "inflammatory changes in the mucous membrane." (9?)

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)

In 1819 a French physician would invent a device called the stethoscope that would forever change the landscape of medicine, allowing for a more precise means of diagnosing pulmonary diseases in life, as opposed to waiting for an autopsy to take place.  The inventor would be Dr. Rene Laennec.

References:
  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.
  13. Wilson, W., "An account on what appeared on opening the body of an asthmatic person," The Philosophical Transactions of the Royal Society of London, from their commencement, in 1665, to the year 1800, abridged with biographical illustrations by Charles Hutton, George Shaw, Richard Pearson, Volume XII, 1809, London, Printed by and for C. and R. Baldwin, pages 145-147
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Wednesday, January 20, 2016

1679: The term emphysema is coined

Theophile Bonet (1620-1689)
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 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.

So it was in the year 1679  that a Swiss physician named Theophile Bonet 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 19 cases of "turgid" lungs in his classic work "On the seats and causes of disease." (3)

About 200 years after the death of Morgagni, 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).

References:
  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.
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