x1899: Is asthma simply a "Nerve Storms"

Nerve Storm: Seizure, as in seizure of the entire body (epilepsy), seizure of the muscles of a certain joint (gout) or seizure of the respiratory bronchi (asthma). The seizure is caused by some imbalance either internal (emotion) or external that triggers the abnormal response of the brain.

I've read about asthma being described this way in many older journals, yet Dr. Joe Shoemaker, in his 1899 book, "The Monthly Encyclopedia of Practical Medicine" (Philadelphia, Vol. XIII), uses this term with force.

He further describes asthma as:

• A disease essentially due to some nervous change (this was the accepted dogma of the time)
• Partial hereditary (so we still think this)
• It's occurrence is largely in "neurotic" subjects
• It's occurrence in families subject to migraine (hmmm, where does this come from?)
• Attacks are characteristic of asthma (dyspnea due to bronchospasm)
• Pt inclined to hold to a chair or bed railing firmly to help expiratory muscles of expiration
• And all this is caused by a "nervous storm"
• Triggered by some unknown cause
• The cause of who has such a "nervous change" also remains a mystery
• It's seen in children and some adults
• It's rare
• Sudden in onset
• Occurs between 2-4 a.m. (remember, this is based on his observations)
• Accessory and natural muscles of respiration are contracting vigorously
• Dusky face shows embarrassment to circulation and deficient oxygen in the blood
• Sweating skin shows muscular exertion
• Lungs enlarged during paroxysm
• Yet auscultation shows little to no air entering them
• No normal respiratory murmur, instead expiratory whistle is heard upon austultation
• Sonorous rhonchi often heard (which is what we now call a wheeze)
• Duration of attack is variable, yet is often over by morning
• Duration may last 24 hours or longer
• Attack ends with expulsion of mucus
• No continued cough or expectoration

This is all part of the nervous storm we call asthma. What do you think?

My introduction to Albuterol

It's neat what memories a quick perusal of your medical records jogs.  For some reason I thought Ventolin was introduced to the market in the early 1990s, yet upon reading my National Jewish medical records I see the Albuterol inhaler was ordered for me to use as needed.  That was back in January of 1985. 

When I was on 7-Goodman we didn't get to carry our own meds, so when we went places, or if we had physical education, the PE instructor carried the only inhaler.  We kids would huddle around when he was giving out puffs like flies around maneur.

He would pass it from kid to kid until we all had our pre-exercise puffs.  We didn't even use spacers.  We were, however, taught to hold the inhaler two finger lengths from your mouth and inhale that way.  In fact, that's still how I use my inhaler to this day.

I don't remember one time anyone at National Jewish mentioning a spacer.  I don't think they even existed.  I had been informed about them prior to National Jewish, but there wasn't one on the market.  What I was taught to use was a toilet paper roll. 

Before I was at National Jewish the rescue medicine I used was Alupent.  Once at NJH it was Albuterol. To be honest, I have no idea why this was.  I know that Albuterol is supposed to have much fewer side effects, yet if that was the reason we used it, then why was I prescribed Alupent when I took nebulizer treatments?

You could also think it could be cost, yet, again, if cost was the reason, then why was I prescribed Alupent for my breathing treatments.  In fact, even when I was discharged from NJH/NAC I was still using alupent nebs and Albuterol inhaler.  That's how it was until 1991 when I learned about the Albuterol solution.  Is it possible Albuterol simply wasn't available as a solution in 1985? 

Either way, that's how it was.  And each time we had an event we'd all use the same inhaler.  We just passed it from one kid to the next until we were all finished puffing up.  Most of the time we used it this way before exercising, yet some of the times we used it this way when we were on excursions outside the hospital. 

For example, after we'd be roaming the mall for a few hours one of us asthmatics would say, "I'm a little short of breath.  Can we use the Albuterol now?"  If Jeff thought it was time for a scheduled dose, or if one of us really needed it, he would pass it around again.  That's just how we did it.

Another memory jogged here is that when we went on excursions outside the hospital we'd always have to lug an oxygen tank with us.  On my first trip to the mall I was told the newest patient had to pull it around.  Thankfully January was a busy month for admissions, because I only had to do it once.  Although I did volunteer to lug it around once or twice.

We had to lug the oxygen around just in case one of us had a bad attack, although I don't ever recall it ever having to be used.  I never heard a story about it ever being used before I was admitted either.

Another thing we did back then was we all used the same vials of medicine solution for our breathing treatments.  We used a syringe to draw up the medicine, yet I'm sure this caused some contamination.  In fact, when I became an RT in 1995 we still used this method.  I think it was sometime in the 2000s that Albuterol and Alupent came premixed with normal saline in those nice little plastic amps.

Doctor anxiety

I've been seen by so many doctors in my life I can't even begin to count how many there's been.  And now, even while I work with my doctor, I still get doctor anxiety.  You'd think I'd be used to doctors by now, yet you'd be wrong.

As I sat on the crunchy paper on the exam table many things wafted through my mind that I wanted to talk to my doctor about, and then I'd talk myself out of it.  By the time he walked into the room all I said was, "Hey, how's it going?"

The doctor sat in his chair clicking on his little computer, spending most of his time trying to find out what medicines I was on.  Although had he asked I would have just told him.  Then he had me lie down and patted my abdomen, listened to my heart, and that was it.  Before I knew it he was walking out the door.

He stopped in the doorway and asked me if I thought Singulari did any good.  "My other patient's don't report any benefit from it," he said.  "You should experiment going off it and see if you notice a difference."

"I already did that," I said.  "When you're paying a dollar a pill you want to make sure it's worthwhile.  Yet I'll try it again sometime."

"Yeah," he said, "but after the allergy season is over."

"Sure thing."

The he asked me if I ever thought about trying Symbicort.  As I was walking out of the office he tossed a Dulera inhaler at me and said, "Try this, it's similar to Symbicort."

"I never heard of this one," I said.  Yet that was the anxiety talking.  I did hear about it.  Yet here I was leaving the doctor's office yet again not having discussed anything I wanted to discuss.

However, I wanted to talk to him about possibly adding another inhaled corticosteroid on top of the Advair to see if it gives me any benefit, yet I think the Dulera would be the next rational trial before taking that step anyway.

What is it about doctors and anxiety anyway?  They're humans.  And, worse, I work with my doctor every day, so why would I be uncomfortable with him as my doctor.

The answer, I think, is that guys like me don't like talking about themselves.  I hate being the center of attention.  So it only makes sense I'd hate a doctor asking me about... me.  Thoughts.

I'm trying Dulera

Dulera was approved in June 2010

My doctor recommended for kicks and grins I try Symbicort instead of Advair. Yet after searching his cupboard realized he didn't have any free samples left, so he grabbed a Dulera and tossed it at me. "Try this," he said. "It's basically the same as Symbicort."

Dulera was approved by the FDA as another option in the line of Advair and Symbicort. The LABA in it is the same as what's in Symbacort, and the inhaled corticosteroid is the same as Azmanex twisthaler, which was approved by the FDA in 2005.

I have read in a few places that the particle size of fluticasone (the inhaled steroid in Advair) is larger due to the fact it's a dry powder inhaler. The particle size of Dulera are smaller and may reach deeper into the lungs to provide a more even dispersion of the medicine.

However, I have not been able to set my eyes on any studies other than the initial studies completed by the company that prove that using Dulera is better than not using any asthma controller medications. I would like to see some studies proving that Dulera is better than Advair or Symbicort.

Formoterol, the LABA in Dulera and Symbicort, is faster acting than Salmeterol, the LABA in Advair. Other than that I'm not sure of any proven benefits of one of these combination inhalers over the others.

However, unlike Advair, Dulera is a metered dose inhaler, and therefore to get the maximum effect a spacer device must be used. That should make it a little more inconvenient because I think spacers are more of a bother than they're worth. Yet we'll see how that goes.

So if any of my readers has access to any further Dulera studies let me know. Other than that, I'll report back in a month when my sample of Dulera is used up, if the side effects of formoterol don't get to me first.

1818: Rostan claims asthma is cardiac, not nervous

Leon Louis Rostan (1790-1866) 

Writing as early as 1818 Professor Leon Louis Rostan (1790-1866) said that he did not believe in nervous asthma. In fact, he went as far to conclude in his writings that asthma was not even so much asthma but was nothing more than cardiac asthma.

Mr. Rostan was the son of a wealthy family and received a good educat

A brief biography of Mr. Rostan was given by Harris L. Coulter.  He wrote:

He studied at Paris and graduated in 1812.  By 1814 he became (Philippe) Pinel's deputy at the Salpetriere where for eight months he administered a 2000-bed ward for Napoleon's army returning from Russia.  Four years later he was appointed physician at the same hospital where for the next fifteen years he gave heavily attended courses in "organicism."  A Zurich student noted in 1831 that Rostan's clinic was the most enlightening of all, being the only one given at the sickbed. (6, page 526)(also see 7)

As with many other physicians who studied asthma, he himself had the disease, suffering at one time a severe attack.  Perhaps this is what enticed him to study asthma during his tenure at Salpetriere.  (7)

After studying asthma in elderly women for many years at Salpetriere, and then performing autopsies on them once they passed away, he determined that what they actually had was heart disease, or what he called cardiac asthma. He published the results of his findings in a paper called "Is the asthma of old people a nervous affection?"  (3 pages 56-57)(5, pages 152-153)

The following are a couple examples of what he found (3, page 57):

• 61 years old idiot who suffered from periodic paroxysms of great oppression of breathing... a large aneurism of the left ventricle of the heart, and ossification of the parts surrounding the bronchiae, were the appearances observed after death.  3, page 57)
• A 74 year old woman, who had been asthmatic for 18 years: upon opening the body, he found an active aneurism of the left ventricle, with ossification of the aorta.  (3, page 57)

According to George Gregory, in his "Treaties on the theory and practice of physic, Rostan noted possible causes of asthma were "morbid alteration in the organs of respiration and circulation, producing an accumulation of blood in the lungs."  Examples include: (4, page 214)

• Thickening of the left ventricle of the heart
• Enlargement of the left ventricle
• Ossification (hardening) of the valves of the left ventricle
• Ossification of the valves of the aorta
• Thickening of the parieties of the aorta
• Adhesions between the lungs and the pleura
• Effusions of serum into the cavity of the chest
• The bronchia inflamed and filled with mucus
• The lungs converted to a substance resembling liver (4, page 214)

J.B. Berkart, in his book "On Asthma: It's pathology and Treatment," said Rostan always found some pathological explanation for dyspnea.  He said:

Rostan,  more especially, urged that in the numerous instances of it which had come under his notice he had always found pathological changes sufficient to account for the dyspnoea; and saw, therefore, no reason to assign this to a derangement of the nervous system. He appears, however, to have employed the term asthma in a manner too vague to give weight to his objections. So that the demonstration of the symptomatic nature of the disease in his own cases does not necessarily apply to all others. (1, page 22)

While some of the patients at Hospice de la Salpetriere were diagnosed with asthma, Rostan said "he never saw a case of purely nervous asthma." That all the cases that "commenced as nervous affections" were discovered to have some form of organic disease.  (3, page 57)

Armand Trousseau, in a 1858 lecture at Hotel Dieu, said the following of Rostan:

If my honorable colleague, Prof. Rostan, admits to-day the existence of purely nervous asthma, he has not always admitted it. There was a time when he did not believe in this peculiar neurosis of the respiratory organs, and he regarded it as being symptomatic of affections of the heart.  Influenced by the recollection of the laborious investigations which he had made on this subject in the case of the asthma of old men, while he was a physician of the Salpetriere, M. Rostan recognized no difference between asthma and dyspnoea. (2, page 517)

Trousseau, however, said he disagreed with Dr. Rostan.  He said:

To him, these two words (dyspnea and asthma) were synonymous; to me, this is far from being the case. Asthma is, in my eyes, a special, complete malady; it is a manifestation, a particular form of a general condition, having very different local expressions, manifesting itself sometimes by attacks of dyspnoea, of oppressed breathing, constituting asthma, but able, also, to exhibit itself in attacks of articular gout, or gout in a more diffused form, in attacks of gravel, or rheumatism... It is not the difficulty of breathing which constitutes asthma; for it would be necessary in this case to call by this name the dyspnoea which is symptomatic of diseases of the heart, or great vessels, the violent distress which goes to the verge of suffocation in patients suffering from oedema of the glottis, or children taken with croup. Now there is no one who would not shun such a confusion. Between dyspnoea and asthma the difference is immense. If asthmabe a dyspnoea of special form and character, every attack of dyspnoea is not asthma. (2, page 517)

Other physicians, however, agreed with Rostan that asthma was not nervous, including Beau, Crozant, Budd, and Louis.  (1, 30-31,

Berkart said Beau and his pupil Crozant, instead of believing asthma was nervous or spasmotic, thought it was a disease of "chronic bronchial catarrh, accompanied with very viscid secretion.  Such sputa, they maintain, are capable of obstructing the bronchi, and of thus producing the dyspnoeal attacks, as well as the sonorous sibilant rhonchi -- their 'rales vibrants' (sound of mucus moving through narrowed air passages).  With the displacement of the mucous plug into a larger bronchus, or on its expulsion by means of a fit of coughing, the dyspnea ceases, and with it also the rales disappear. This form of bronchitis, in their opinion, due partly to an idiosyncrasy of the patient, partly to exciting causes, which greatly vary in different individuals.  ."  (1, page 30-32) (8, page 52)

However, Berkart said Beau's opinion was not well supported, mainly because the nervous theory of asthma "was so well rooted to be readily abandoned upon the mere denial of its foundation. Beau omitted to offer and proof that a bronchial spasm was impossible or improbable" (1, page 31)

Of Budd, Berkart said he believed asthma was a tonic spasm of the diagram or glottis  (1, page 34-35)  Of Louis, Berkart said he believed "emphysema was a disease of gradual and insidious development, it therefore seemed to them highly probable that the asthmatic paroxysm were merely its precursory symptom."  (1, page 32)

Rostan's theory arose from the fact he studied older men and women with dyspnea, and determined the cause was not asthma but heart failure (cardiac asthma).   So most of Rostan's cases probably weren't even asthma to start with, but cases of heart failure.

Regardless of the views of Rostan, Beau, Constant, Budd and Louis, the nervous theory of asthma won the era.  It would remain a main asthma theory until it was disproved in the 1950s.

References:

1. Berkart, J.B., "On asthma: its pathology and treatment," 1878, London, J. & A. Churchill
2. Trousseau, Armand, "Lectures on Asthma: Lecture III, Examination of the opinions of the profession of this disease," delivered at Hotel Dieu and translated from the Gazette de Hospiaux on Sept. 16th, 1858, for the Boston Medical and Surgical Journal, published in the Medical and Surgical Journal, 1859, edited by W.W. Morton, page 517
3. "Historical sketch of the progress of medical science, from January to July, inclusive, 1819," The London Medical and Physical Journal, Volume XLII, no. 245, July 1819, J. Souter, pages 56-57
4. Gregory, George, S. Colhoun, "Treaties on the theory and practice of physic, with notes and additions adapted to the practice of physic in the University of Maryland, ," volume 2, 1826, Philadelphia, J.H. Cunningham
5. Wood, John, "On some effects of inflammation of the membranous lining of the larynx; with suggestions relative to the operation of bronchotomy and incidental remarks on spasm and wounds of the throat," pages 138-157,  Volume XVII, London, 1832, Published by the Royal Medical Chirurgical Society of London,
6. Coulter, Harris L., "Divided history of the schism in medical thought," volume II, 1977, Berkeley, California, North Atlantic Books
7. Rostan, Leon Louis, "encyclopedia.com, http://www.encyclopedia.com/doc/1G2-2830903744.html, accessed 12/30/13
8. Fox, Wilson, writer, Sidney Coupland, editor,"A treaties on the diseases of the lungs and pleura," London, 1891, J. & A. Churchill

Can I excel despite asthma?

I've done this with quite a bit of success on my other blogs, so I thought I'd try it here at Hardluck Asthma. I like to check my statcounter to see what searches are leading readers here. Assuming the queries were not answered, I provide here my humble responses.

1. Can I smoke even though I have asthma? Yes you can, yet why would you want to. Smoking is linked to worsening asthma, and can even cause severe asthma. If you smoke and have asthma, here's 20 incentives to quit.

2. I have asthma and I can't smell:  Seventy five percent of asthmatics are believed to have allergies, and about 75 percent of asthmatics also have a history of rhinitis and sinusitis. All of these cause inflammation of the nasal passages which in turn can effect your sense of smell. I've had this problem in the past, and still do at times. The best treatment is to work with your doctor to find a good medicine regime to help you out.

3. Can I excel despite asthma?  Yes you sure can. Asthma wisdom and medicine has improved so much in the past 20 years to the point where most asthmatics should be able to live a normal active life. You'll have to work with your doctor though, and continue reading about asthma and how to control it. For good tips on how to control your asthma click here.

4. What's the 18th century name for asthma? Actually, in the 18th century asthma was called asthma. Nasal inflammation was called catarrh. Allergies were described yet not yet identified. Chronic bronchitis, cystic fibrosis, allergies, and many other causes of wheezes and shortness of breath were often all associated with asthma. There were often various classifications of asthma, yet these classifications were usually different from doctor to doctor.  For the most part, 18th century doctors described any condition that caused dyspnea or a wheeze as asthma.  For more click here.

5. Have you achieved excellence despite asthma? I have five blogs, a great job, a wonderful wife, great kids, and an overall wonderful life. To learn how asthma has benefited my life, click here and here

6. Is asthma a nervous condition? No. It was believed to be in the 19th century, yet by 1950 that theory was proven wrong. Stress and Depression may be linked to asthma, and may trigger asthma, but asthma is a real physical condition, not a mental disorder. Click here for more.

7. What are asthma organs? Asthma is more than just a lung disease. I write about this here.

8. Can a barrel chest go away with asthma? Yes it can. It's caused because air gets trapped in your lungs. Once you gain control of your asthma it will go away. I know because mine went away.

So there you have it. If you have any further questions you are free to email me absolutely any time. Thanks.

x1851-1913: The history of asthma sputum

Ernst Victor von Leyden (1832-1910 discovered
crystals in asthmatic sputum, and suspected these
to be the cause of asthma. During his era, he was
the closest supporter of Dr. Robert Bree's
bronchitic theory of asthma. (9, pages 14-15)
He believed these crystals somehow irritated the
"vagus in the mucus membrane of the bronchials,
and hereby caused by reflex action a spasm
of the muscles of the small bronchial tubes."
(10, page 8)

Most people find sputum disgusting, and so will have nothing to do with it. But as far back as 400 B.C. the medical significance of it was observed by ancient Greek physicians, and probably even earlier than that.

If you mention it at the dinner table your mother might smack your hand. But for the sake of gaining a complete grasp on the history of asthma and respiratory disease, we must delve into the topic of sputum.  Sorry, but we must.

It must have been observed at an early date in history that people with breathing issues produce sputum, sometimes consisting of a putrid smell, often consisting of many varied colors such as red, yellow, brown and white.

Yet rather than being petrified by the grossness of the substance, Greek philosophers became fascinated by it. They even gave it its own classification as one of the four humors that, along with determining ones personality, also determined whether was healthy or sick.

Prior to the philosophical medicine of the ancient Greeks, other ancient societies, and the primitive clans and families that roamed the lands before them, believed sputum was the production of some evil spirit, demon or god. When a person expectorated the substance, they were in essence expectorating an evil substance that caused the symptoms they were suffering from.

From the ancient world to the scientific revolution there were few changes in the way physicians viewed diseases and treated their patients.  In 1799 Dr. Robert Bree speculated that sputum contained a poison that it was trying to get out of the body, and asthma was the result.  This theory wasn't much different than any idea Hippocrates might have postulated.

Since the sputum preceded the asthmatic fit, Bree essentially speculated that asthma was essentially bronchitis, and thus created the bronchitic theory of asthma.  Others, without much more evidence, speculated sputum was the effect of asthma rather than the cause.

Such speculation gradually tapered off, but never really came to an end, during the scientific revolution, and mainly due to the inventions of the microscope, which allowed physicians to see that the human body was made up of substances too small to be seen by the unassisted eye, and the stethoscope, which allowed physicians to hear changes that occurred inside the chest and to diagnose diseases with accuracy prior to autopsy.

The microscope allowed physicians to learn that air passages were surrounded by smooth muscle, and that it was capable of spasming when stimulated.  The stethoscope allowed them to hear when sputum accumulated in the chest, and learn that it was the effect and not the cause of asthma.

So, pretty much, prior to the 1850s asthma was basically considered to be a disease of excess sputum, mainly because this was all physicians could observe with the unaided eye and ear.

Yet by the 1850s it was looking pretty clear that asthma was also a disease associated with spasms of the air passages, particularly by the wheezes heard by air flowing through narrowed air passages, and rhonchi heard as air flowed through sputum lined air passages.  (1, pages 592-595)

In 1851, Dr. Beau, along with his assistant Cozart, observed that fits of asthma usually ended with a wad of sputum being coughed up. Beau used this observation as evidence to support his theory that asthma was a disease of chronic catarrh, and that asthma was caused by increased sputum in the air passages.  (3, page 31)

When this sputum dried out mucus plugs formed that were capable of blocking the air passages, thus resulting in dyspnea and other symptoms of asthma, including the "sonorous and sibilant rhonchi -- their 'rales vibrants' heard upon auscultation with a stethoscope."  (3, page 31)

The fit, therefore, was resolved when mucus plugs were broken up with a fit of coughing.  (3, page 31)

Then, in 1878, at a time when most physicians had accepted the nervous and spasmotic theories,  J.B. Berkart used Beau's research as evidence of the bronchitic theory of asthma.

Berkart said:

With the displacement of the mucous plug into the larger bronchus, or on its expulsion by means of a fit of coughing, the dyspnea ceases, and with it also the rales disappear.  This form of bronchitis is, in their (Beau and Crozant's) opinion, due partly to an idiosyncrasy of the patient, partly to exciting causes, which greatly vary in different individuals."

Tiny crystals were first observed in sputum in 1851 by Jean Martin Charcot, but it wasn't until 1872 that these crystals were linked to asthma by Ernst Victor von Leyden. So history has given credit for this discovery to both men by calling the crystals Charcot-Leyden crystals.

Leyden, whose asthma theories were similar to Dr Bree's bronchitic theory, believed Charcot-Leyden crystals caused asthma by irritating...

...the peripheral extremities of the vagus nerve, and produce reflex spasm of the bronchial muscle."  

The asthma attack, as Bree and Beau observed, ended when a wad of sputum was coughed up during a fit of coughing. (4, page 14-15

However, it was the discovery of these Charcot-Leyden crystals that would ultimately put an end to the bronchitic theory of asthma.  This was noted by Dr. John Charles Thorowgood in 1878.  He said that these crystals were found in sputum obtained from patients with "ordinary catarrh and croupus bronchitis."  (4, page 15)

Thorowgood said:

The asthmatic patient while in a fit presents abundance of symptoms distressing enough to endure or to witness; and yet, when things seem to be at their worse, and the patient well-nigh at his last gasp, a remission comes on, the spasm yields, air enters the lungs, and the attack subsides, coincidentally often with access of cough and mucous expectoration." (4, page 16)(9, page 1,2)

In 1879, bacteriologist Paul Erlich discovered the eosinophil, and it was soon discovered that elevated levels of eosinophils (eosinophilia) was commonly found in asthmatics. (5)

In 1882 Heinrich Curshmann observed other spirals in asthma sputum and believed they were associated with causing asthma. He believed since Leyden's crystals didn't cause asthma, perhaps his crystals did. (5)

Later Curshmann's crystals were determined to be fragments of mucus plugs associated with asthma, and Leyden crystals were determined to be fragments of eosinophils. Eosinophils were later learned to be a type of white blood cell that, along with mast cells, are involved in the allergic reaction.

In 1911 Hermann Sahli described eosinophils in asthmatic sputum. Yet Sahli noted another author from 1891 who described eosinophils in asthmatic blood, and he concluded that these must be pathological with asthma. Yet he also noted that neither the cause of the eosinophils nor their origin was known. (7)

Sahli could isolate the area where the sputum came from based on epithelial cells in it, yet he did not understand the mechanisms of its production as we do today. (7)

Dr. James Adams describes asthma sputum in 1913: (8)

"Asthmatic sputum varies. Often there is none till the end of the attack; then it is in the typical form of small, tough pellets expelled by laborious coughing. The attack may then cease, or it may go on till a more free and profuse expectoration occurs."

He also wrote:  (8)

"The sputum does not readily decompose, and is said to be wonderfully free from microbes; but this is not always so, as I have occasionally found it teeming with them."

The true purpose of sputum is to ball up microbes inside the lungs and haul them out, and in this way the lungs stay sterile.  Surely asthma can be caused by inhaling a microbe, such as a bacteria, but it's also caused by asthma triggers (dust mites, smoke, fumes, chemicals, pollution, animal dander) that are innocuous to most people, and non infecting agents.

So this might explain why Adams most often found asthmatic sputum without an infecting agent, and sometimes "teeming with them."

Backing up a moment to 1906, Australian pediatrician Clemons van Pirquet coined the term allergy when he observed that some of his patients were hypersensitive to substances that did not bother other people (what we now refer to as allergens, or asthma triggers).  This was the first time asthma was linked with allergies.

By 1910 Histamine was discovered and found to be a major component in the allergic response.  So some went on to speculate that finding a way to block histamine would cure both allergies and asthma.

By 1946 antihystamines hit the market, and within a decade they were among the most commonly prescribed medicines.

Yet as time went by, it was learned that there was more to asthma and allergies than just histamine.  It was learned that asthmatic and allergic immune systems respond irrationally to allergens and asthma triggers by increasing production of eosinophils and this spearheads inflammation of the bronchial muscles.

Another weapon of the immune system is mast cells that line the respiratory tract and eyes, and these were discovered in 1953.  .

In 1967 Immunoglobulin E antibodies (IgE) were discovered.  It was later learned IgE has a significant role in the asthmatic and the allergic response.  The first time asthmatics are exposed to asthma triggers (allergens), say dust mites, their immune systems develop dust mite IgE antibodies that attach to mast cells that line the epithelial layer of the skin or respiratory tract.

The second time that person is exposed to that allergen (dust mites in this case), a mast cell that has a dust mite IgE antibody attached to it explodes and releases its contents:  the mediators of inflammation.  A mediator of inflammation called histamine was discovered in 1910, and others called cytokines and leukotrienes were discovered in the 1970s.

These mediators, when released into the blood stream, cause inflammation of the respiratory tract, thus causing the allergic and asthmatic responses.

In the allergic person, they can also cause inflammation of the upper respiratory tract, which includes the back of the throat and nose.  The offending substance (dust in our case) is recognized by the immune system, trapped in the mucus layer, absorbed by the mucus, balled up by the mucus, and sent on it's way up the respiratory track to be coughed up.

So this would explain what Dr. Bree, Beau, and Berkart observed. While hacking up a wad of sputum may have been related to the fit of asthma, it was not the cause, and had nothing to do with the cure.

Later it was learned that asthmatic lungs tended to produce an abnormal number of goblet cells, this results in an abnormal increase in mucus production during an asthma attack.  While some of this sputum may be coughed up, some becomes trapped in obstructed air passages, dries out to form mucus plugs, and this further blocks the air passages, thus compounding the asthma response.

When the fit ends, when the air passages relax and dilate, which may be a result of time or medications, the asthmatic will probably expectorate this sputum, which will usually be, if no bacteria or virus is balled up within it, white and sterile.  It will also have IgE and eosinophils in it, hence your Charcot-Leyden and Curshmann crystals.

So it's easy to understand how this production of sputum at the end of an attack could easily be misinterpreted as the cause, rather than the effect, of asthma.

References:

1. Lotval, J., "Contractility of Lungs and air tubes: experiments performed in 1840 by Charles J.B. Williams, European Respiratory Journal, 1994, (7) pages 592-595
2. Bree, Robert, "A Practical Inquiry into Disordered Respiration Distinguishing the Species of Convulsive Asthma, their Causes and Indication for a Cure," 4th ed, 1810, London, page pages 117-118
3. Berkart, J.B., "On Asthma: Its Pathology and Treatment," 1878
4. Thorowgood, John C., "Asthma and Chronic Bronchitis: A New Edition of Notes on Asthma and Bronchial Asthma," 1894, London, Bailliere, Tyndall, & Cox
5. Lipkowitz, Myron, Tova Navarra, "Encyclopedia of Allergies," 2001
6. Brenner, Barry E, "Emergency Medicine, 1998, page 10
7. Sahli, Hermann, "A treatise on diagnostic methods of examination," 1911
8. Adams, James, Asthma and it's Radical Treatment, 1913
9. Thorowgood, John C., "Notes on Asthma," 1878, 3rd edition, London, J & A Churchill
10. Shmiegelow, Ernst, "Asthma, considered specially in relation to nasal disease," 1890, London, H.K. Lewis