Autohemotherapy Saved My Brother

In 1940, my older brother, Albert, was born prematurely, with a severe case of ichthyosis (skin with scales like fish.)

Due to Albert’s prematurity, at birth his entire body fit in the palm of my father’s hand. Albert had no suckling reflex, and so the pediatrician said there was nothing that could be done to save him. The newborn was doomed.

Based on the above information, I would place the baby’s fetal development at roughly 2/3rds of the way through the second trimester, perhaps at 22 weeks, close to a pound in weight and at most eight inches from the top of his head to his rump. He would have been below the now standard 24 week “age of survivability.” Survival at that stage of prematurity was unlikely.

Dr. Albert S.J. Clarke, an orthopedic surgeon, was my Dad. The infant at risk was Dad’s first child, named after him (Albert Sidney Johnston Clarke III.) Being a physician, Dad was not going to give up on his son without a fight.

Due to Albert’s small size, and the condition of his skin, they were unable to start an I.V., which is the standard of care in today’s medical world. So, as my Mother explained it, as a last resort, Dad withdrew his own blood and injected it into the gluteal muscles of the baby. That blood carried nutrition and sustenance to Albert; e.g., water, minerals, protein, sugar.

That was not as crazy as it seems, since Autohemotherapy was used in the early 20th century to treat dermatological cases, starting in 1913. The following abstract is an example of a 1928 article after the method gained some medical acceptance.

Quoting from the abstract, “Autohemotherapy, first used in dermatologic conditions by Ravaut (1913), closely followed by Spiethoff (1913), consists in the withdrawal of blood … and its injection into the patient’s gluteal muscles, preferably.”

By the 1940’s, Dr. Clarke was no doubt aware of the questionable therapeutic efficacy of the old method, but as a means of delivering fluid and nutrition to an infant otherwise shut-off from the world, there was nothing to lose. Their blood types matched, so in theory, a blood injection would not hurt.

Although the Rh factor was just discovered that year (1940), Albert’s odds of survival were likely assured by the fact that most people are Rh positive.

At the beginning of the 20th century, there was virtually no standard of care for premature infants. Julius H. Hess (1876–1955) published the first book on the subject of medical care for the premature infant in 1922.

In that book, Hess described tube feeding, or gavage, as in the illustration below. However, in the following years, infants often died from aspiration pneumonia induced by early feeding after birth, and early-applied gavage fell out of favor.

A year after my father successfully salvaged my brother, Hess amended his guidance in his 1941 text, writing “Small premature babies (those weighing under 1200 g) were not fed for 24–48 h …. During this time the premature baby receives physiologic salt solution, subcutaneously in the thighs, one to three times daily.”

Obviously, physiological saline solution avoids the risk of incompatible blood reactions, but in the case of that baby and his father-physician, God had blessed them with fully compatible blood types.

I don’t know if Hess had been made aware of my Dad’s lifesaving treatment conducted a year before Hess made his latest recommendation, but that is certainly possible.

I never discussed with Dad the details of his saving intervention, but from what I’ve read about babies with ichthyosis, my brother’s survival and thriving until age 73 is a bit of a miracle. His pediatricians gave him zero chance of surviving his first days. They didn’t know just how determined my Father could be.

Due to my brother’s genetic skin disease, he shed skin in large flakes; his bed sheets were always covered in them. He had to be lathered in Vaseline to keep his brittle skin from cracking too deeply, and bleeding. He also had very poor tolerance to heat because he had few if any functioning sweat glands.

In spite of his disability, Albert was one of the nation’s first Respiratory Therapists. He trained other Respiratory Therapists in west coast colleges, and ran several Respiratory Therapy Departments in hospitals across the country.

With unlimited medical research libraries at his disposal, he discovered on his own that a drug used for treating psoriasis helped him control his own skin condition. As a result, his quality of life in his last decades greatly improved. He fulfilled a dream of remarrying, all made possible by a determined physician willing to take a chance when the “experts” had given up hope.

Dr. A.S.J. Clarke, M.D. in his later years.

Today, thanks to advances in the medical management of premature infants, autohemotherapy is medically unnecessary. In fact, many doubters question its efficacy. However, I have the physical scars from growing up with a rambunctious big brother to prove that, in at least one case, it was a lifesaver.

Pendelluft—The Beast Within

It was dark, the only light coming from the red glowing numerals of my digital alarm clock. I hadn’t set it to alarm—I needed to sleep as long as I could.

It was also quiet in my bedroom, quiet enough for me to hear my breathing as I lay still, trying to sleep. The breath sounds were rhythmic and calming, breathing in with a hiss, and out with a coarser and louder “huh,” endlessly repeated.

I had just been released from our local hospital after five days on oxygen, diagnosed with “respiratory failure” of unknown origin. The medical term for unknown origin is “idiopathic,” but that word added no clarity to what had happened.

What had happened has been described in a previous blog post, a post that correctly warned that if the illness that almost killed me was any indication, we should NOT expect COVID-19 to abate during the hot and humid months in the American South.

Whatever virus I picked up in Thailand in July, seemed to have a predilection for the hot and humid summer weather of Florida. In other words, it had made itself right at home in my lungs. The result was a puzzling but treacherous case of silent hypoxia, or as some have called it, happy hypoxia. In that regard, my respiratory failure was every bit as inexplicable and potentially deadly as COVID-19.

Thankfully, my viral infection had not yet reached the level of transmissibility of COVID-19. Otherwise, my wife of fifty years would certainly have been affected as she sat by my side for those long and frustrating days in the hospital.

But now, it was time for celebration. By sheer willpower and some tricks of the respiratory physiology trade, I had gotten myself discharged from the hospital. But that’s another story.

At home once again, my finger-tip pulse oximeter showed I was oxygenating reasonably well on air (in the low 90 percentile), but I was not back to normal (the high 90s). My lungs still had some healing to do before I could claim I was 100% normal.

As I now lay quietly as night enveloped me, entering almost a meditative state listening to my breathing, I noticed a strange sound. Alerted, I listened more intently. And what I heard scared the hell out of me.

There was something alien in my body. I couldn’t feel it, but I could hear it. When I breathed in, it breathed out. When I breathed out, it breathed in. It was clear as day, something was breathing in my chest, and it wasn’t me.

I had a monster in my chest.

At times like that, it is hard to be objective. But with years of training as a scientist, I forced myself to collect data and analyze the results before, well, FREAKING OUT!   

The first thing I noticed, was that the asynchrony between my breathing and the other’s breathing, was invariant. They were 180 degrees out of phase, and that never changed.

Professionally, I’ve dealt with probability my entire scientific career. So, if there were in fact some other living thing in my chest, the odds that it would never change its breathing rhythm seemed unlikely. Unless—it was waiting for my lungs to have a full “tidal” breath” before IT took a breath.

Of course! That is exactly what I would do if I was in some giant’s chest. I’d wait until their lungs were full before I’d steal air from them. After all, how else could I, as a little monster, breathe?

But wouldn’t X-rays at the hospital have shown its presence? Well, yes, and no. They didn’t do an MRI. If IT was soft bodied, and growing, it might not have been detected. And going an analytical step further, that could explain why my arterial oxygen saturation levels were not back to normal. IT was stealing oxygen from me.

My heart rate was increasing, which was the last thing I wanted it to do. The more blood I sent the thing, the faster IT would grow. I had to stay calm. But how?

I began thinking about physiology text books. That would put anybody to sleep. But that was also the magic moment. That was when I put a name on the creature in my chest.

I called it, Pendelluft.

Until that night, Pendelluft had been to me of little more than academic interest. I’d read about it, but I knew it is primarily found in patients with chronic obstructive pulmonary disease (COPD); which I do not have. I’ve also never been a smoker or asthmatic.

I knew of the diagrams which explain it, but I never thought that I would be able to hear it, in my body, and especially without a stethoscope.

An illustration of the mechanism of Pendelluft from a humorously named web site, Deranged Physiology.

After I explored the medical literature, I’m not sure anyone in the medical field thinks it possible for a patient to hear his own Pendelluft. But it must be true, since the monster never reared its ugly head, and my arterial oxygen level regained its expected normal value only after the “monster” faded away.

 According to a 1985 paper in the Journal of Applied Physiology, the experimental evidence and theoretical aspects of Pendelluft are attributable to varied pulmonary (lung) airway resistance and compliance (the opposite of stiffness), and were first described in a classic paper by Otis et al. in 1956.  

I was pleased when I read that one of my mentors, Dr. Arthur Otis, the one time Department Head of the Physiology Department at the University of Florida School of Medicine, had done the pioneering research on the subject.

However, I found no reference to breath sounds until I came across the 2012 article in the journal Pulmonary Medicine. That study used very complex instrumentation and statistical methodology to detect Pendelluft.

I have to admit that I smiled when I read that 2012 article. I was questioning how much money was spent on that very elaborate medical investigation. Arguably, it was fine work and contributed nicely to the field.

But, I wondered, did they try asking the patient, “Do you hear a monster in your chest?”

For what it’s worth, I did.

And it was scary as hell.

Warning Order

“Consider this a warning order.”

The voice on the other end was from the Pentagon. That was the last thing I’d expected to hear on Saturday morning, March 21st, 2020.

On October 1, 2018, I had happily retired after forty years of Federal service. I had remained engaged with the Naval Sea Systems Command and the Navy Experimental Diving Unit as their one and only Volunteer Scientist Emeritus, until I received that call.

Within 90 minutes, I had been reinstated with full security clearance and told to pack my bags.

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The next day as I was flying on government orders in an almost empty plane to New Hampshire, I had no idea that the company I was sent to help would begin a ventilator design effort from scratch, that same day. I also couldn’t imagine that the resulting ventilator would receive FDA approval 41 days later. 

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 The company, Wilcox Industries, in Newington, New Hampshire, has for twenty years built hybrid self-contained breathing apparatus (SCBA) for the military. In fact, twenty years ago, with full Navy support, I helped them design and test their first Scout (now Patriot), life-support system for Tier One operators. But when the COVID Task Force phoned me, Wilcox had no experience with medical devices, especially ventilators. But with the can-do attitude so typical of military support manufacturers, they were willing to learn. In fact, no one I met at Wilcox questioned that it could be done.

In the middle, Jim Teetzle, CEO of WilcoX Industries
Jim Teetzel (center) and Gary Lemire showing me the latest Hybrid Patriot 5510 Life Support System.

 All it took was the drive and leadership of Jim W. Teetzel (center of the photo), a brilliant engineer, businessman and CEO who holds more patents than he can probably remember, young engineers who never considered failure being a possibility, a nimble supply system that provided needed parts within 24 hours, and the magic words which opened every door. Those words were, “COVID Task Force.”

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Through the Wilcox network of friends and family, patient ventilation circuit parts almost magically appeared, as did the world’s best mechanical Test Lung.

Michigan Instruments Training Test Lung

There was nothing I asked for that did not appear almost as soon as I requested it.

Most important for me was the opportunity to teach by showing, by taking pieces of patient tubing circuits and arranging them in a way that would work with a totally new ventilator concept, the Patriot SAVR (Synchronous Automatic Ventilating Resuscitator.)

Mechanical Engineer, Nick Mercurio, "The Magician."
The Mechanical Engineer, Nick Mercurio, who I call “The Magician,” is working his engineering magic.

Our tasking from the COVID Task Force was not to produce multiple copies of existing sophisticated ventilators that cost as much as a nice car, but to have all hands engaged in producing small, cheap ventilators built to exacting engineering and medical standards. The proof that Wilcox accomplished that goal was the hard won stamp of approval from the Federal Drug Administration (FDA.)

Software Engineer, Jansen Habriel, "The Wizard."
The Software Engineer, Jansen Habrial, or the “Wizard,” makes the SAVR do things I never could have imagined.

While we want Americans to have the finest medical care money can buy, to include BMW-priced ventilators if the need arises, the fact is that during a world pandemic there simply are not enough of those deluxe models to go around. In the most populous nations of the world where per capita income is low, the availability of hundreds of such ventilators are a luxury few if any outlying hospitals can afford. However, low-cost ventilators like the Patriot SAVR fill that need.

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Wilcox is blessed with a retired Marine Corp Colonel, Kevin Dodge (on the left side of this photo), Jim Teetzel’s Chief Strategy Officer. Dodge not only has the experience of managing production and testing programs as complex as that for the V-22 Osprey, but has an understanding of the need for strategically placed world markets.

Together, Jim Teetzel, Kevin Dodge, the “wicked” smart Executive Director of International Programs and Lebanese-born Roula Assadi, and Jim’s senior engineers (Nic Goupil, Gary Lemire, Stan Carter) and their Maestro of Quality Assurance, Lorena Grol, have succeeded in turning a small but wealthy Arab nation into a manufacturing center for the Middle East and North African Region, as well as the huge Indo-Asian continent.

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A photo of the first Patriot SAVR Q made overseas by the Barzan Industrial Group in Doha, Qatar. It is being held by John Bousquet, one of the young designers from Wilcox Industries.

Considering the tactical pedigree of this ventilator, and the company which built it, I foresee that eventually every U.S. military medic or independent duty corpsman will have one or more of the Patriot SAVR units available at their aid station, just in case any Patriots need saving.

Happy Hypoxia – A 2018 Warning

“Happy hypoxia,” or more properly, silent hypoxia, has been one of the most puzzling signs and symptoms of patients presenting to Emergency Rooms with COVID-19. The patient’s arterial oxygen saturation can be in the fifties instead of the normal values in the upper 90s, and yet the patient can be cheerful, fully coherent, and even chatty. Normally, with that low an oxygen concentration in the blood stream, a patient would be in severe respiratory distress.

I experienced silent hypoxia after a visit to Thailand in July of 2018, which makes me wonder: was there a coronavirus lurking in Southeast Asia in 2018 that later mutated to become the killer SARS CoV-2? Did I have SARS CoV-1.5? 

Summertime was everything you would expect in Thailand. It was warm and humid, but not uncomfortably so. I had twelve hours ahead of me in the Bangkok Airport waiting for my return flight to Taiwan, then the long leg across the Pacific to Los Angeles. Eventually, I would make my way back to my home in Panama City, Florida, which would also be hot and muggy. No surprises there. 

What was a surprise, was that a young lady wandering the airport asked if she could interview me for the Thai Ministry of Tourism. She had official looking IDs, and a load of interview questions. I wasn’t interested, and I was busy, I offered, already tired before the twelve hours of dead time even began.  

In truth, I wasn’t that busy, but felt it best not to mingle. I seemed to be the only person not speaking Thai, except for that young lady. Surprisingly,  she had no detectable accent and could pass for a Southern California blond.

After a couple of hours, she returned when I could no longer claim to be busy. She had a simple, youthful attractiveness and an unassuming manner. So, tiring of the boredom of waiting, I allowed her to sit beside me while she started running down her list of tourism related questions. 

She wanted to know why I came to Thailand. It was to give a talk at a medical and scientific conference on sports medicine. My subject was “Oxygen,” a fact that would soon become ironic. I discovered later that my travel, ostensibly paid for by the Thai Sports Authority, was bankrolled by Beijing. But I didn’t know that at the time. 

For 45 minutes the questions continued. They were business-like, the type of questions I would expect from a Tourist Bureau. But one thing caused me concern, her occasional hacky cough. She insisted it was nothing, and I was not alarmed. I thought no more about it as I finally boarded the plane for the first leg of my long journey home.

Eight hours after my arrival in Panama City, I felt ill as I lay in bed, trying to sleep after being exactly twelve hours time-shifted. I felt sicker by the minute. Jet lag doesn’t do that.

By morning, I had suffered chills and sweats, and my physician son insisted I be taken to the closest Emergency Room. As we neared the ER I felt I was going to vomit, and I leaned into a trash can that my wife brought for that purpose. 

The next thing I heard was her screaming at me.

I yelled back, completely confused and annoyed. “Why are you yelling at me?”

“I thought you’d died,” she said. “You sighed, threw your back into the seat, and your arms were stiff and shaking.”

Apparently I had passed out from a drop in blood pressure.  (I had not yet thought about hypoxemia.)

As I was being monitored in the ER, I felt OK. I conversed with my wife, and was half-joking and half-irritated at my unexpected welcome home event.

After awhile, I began to pay attention to the finger tip pulse-oximeter that was monitoring my arterial oxygen saturation. The reading was slipping lower than I had ever seen before, but neither the nursing staff nor the attending physician seemed the least bit concerned. My wife and I continued to chat. I was not in any discomfort, and ignored the monitors until I caught sight of the updated pulse-ox reading. It had plummeted down to a horrifically low 55%. 

I told my wife to alert the nurse. They finally started me on a nasal cannula with oxygen. (For those who know, that was an incredibly delayed reaction.) I also knew enough to realize I should be almost stuporous, yet I wasn’t. I was content, except for my circumstances.

Within a few minutes, an ambulance transported me to a real hospital. Being aware of my overseas travel, they assumed I had a pulmonary embolism, which if detected, would have required immediate surgery. But after a perfusion scan, nothing abnormal was revealed. 

After settling into a room, I had zero desire for any of the food they brought me. It was all tasteless, and remained that way for two days.

Initially they kept me on 3 liters of oxygen per minute by nasal cannula, which still wasn’t bringing my oxygen saturation above 84 percent. That was a problem.

At the urging of the CDC, the nursing staff came to my room fully gowned and face-shielded, and stuck that infamously long sampling swab up my nose. They tested me for the most recent viral illness in Southeast Asia at the time, the H7N9 Bird Flu virus of 2017. The results were negative.

In spite of my growing displeasure with being in the hospital, and not tolerating the taste, or lack thereof, of their food, I was happy and chatty with the nursing staff. But neither I, a respiratory physiologist, nor the medical staff could figure out what was wrong. My X-rays showed some consolidation in my lingula, a small lobe in the middle of my lungs, but that was not enough to cause hypoxia of the level I was experiencing. 

After a while, I began to get a few signs of pneumonia in my lower lung lobes, but not enough to cause any discomfort, or difficulty breathing. While physicians clobbered the growing infection with antibiotics and steroids, I remained happily hypoxic.

After five days in the hospital, and slowly watching my oxygen saturation rise, a respiratory therapist snuck behind me and turned off the oxygen. My saturation remained low, at 88%, but it didn’t drop further. 

That meant, I would remain on air until discharge. That encouraged me enough to call for a walking test, walking down the hospital corridor breathing nothing but air. Unfortunately, I failed that test, and was sent back to bed.

About that time, a pulmonologist came by and told me I had a good bit of atelectasis (collapsed alveoli or lung sacs) in my lower lobes. Finally, something I could fix. I knew what to do.

I wore out my incentive spirometer over the next couple of hours, and then called for another walking test. The Respiratory Therapist chided me…I would just fail again, she said. But I do love a challenge. With her by my side, I moved slowly down the hall, refusing to talk, and that time my oxygen saturation did not drop. 

Due to that walking test, I was discharged from the hospital with an oxygen saturation of 92% and returned home to fully recover. (That is in itself an interesting story which I’ll write about next.)

However, the point of this post is that as I read about COVID-19, I’m finding that physicians are puzzled about some of the same bizarre symptoms I experienced in 2018,  notably  a silent hypoxia. I was never “short of breath” as would be expected with an arterial saturation in the fifties. 

From my studies of respiratory physiology, I knew that what had happened to me in 2018 should not have happened, according to the text books. I did not have the SARS virus identified in 2017. But viruses mutate constantly. Could my symptoms have been the signs of a predecessor or cousin to COVID-19? Could it have been an unrecognized COVID-18?

When lungs are not filled with fluid from rampant pneumonia, the most likely way to become hypoxic breathing air is through something called ventilation-perfusion (V-Q) mismatch. A pulmonary embolus can cause massive V-Q mismatch, and can quickly kill if untreated.

However, a recent Science article suggested that COVID-19 might cause microemboli resulting in silent hypoxia. It seems reasonable that enough microemboli, if that’s what it was, could have caused my symptoms in the summer of 2018 without being detected on a pulmonary perfusion scan. 

And that worries me for the current pandemic. Summer heat and humidity might not kill this virus. It certainly didn’t kill the virus that I presumably caught from a pretty young girl with a “nothing” of a cough in late July of 2018. It may have been nothing for her, but it was sure something for me.

None of my friends at the medical conference got sick upon returning home. I was the only one spending 45 minutes less than a foot away from that coughing girl. I feel pretty confident where I got it. My only question is, did I pick up a version of coronavirus that was beginning to mutate towards the destructive potential of SARS CoV-2 which erupted just over a year later?

I will provide an update on the results of my antibody test for COVID-19. That could prove interesting.