A Country Doctor Writes:

Every patient is unique, with some common basic and measurable features and parameters. For a couple of decades now, healthcare has professed to be patient centered. But the prevailing culture of “quality” (and the reality of getting paid for what you do) has us spending at least half our time documenting for outsiders, who are non-clinicians, the substance and value of our patient interactions. That means our patients get half of our attention and others get half.

But of course, if you really wanted to be patient centered, you’d have to ask what patients actually care about, like their blood pressure or their cholesterol, their anxiety or their sore knees. Their answers may not align with the payers’ priorities. And then what…

Parents raise their children and never have to file any reports on how they do it. I believe clergy can still counsel their parishioners without filing reports. But doctors, nurses, nurses aides and physical therapists are trapped in the tyrannical dichotomy of “If you didn’t document it, it didn’t happen”, which actually forces us to do less for our patients just so we will have time to document what we did do. We are, to varying degree, robotniks in a big, inhumane corporate and federal healthcare billing machine these days.

Perhaps the most striking example of the micromanaging and patient-uncentered mandates we are subjected to is the Medicare Annual Wellness Visit: Miss one thing, like offering HIV screening to 80 year old devout French speaking, monogamous Catholics in Van Buren, Maine and risk getting your payment retracted. But we are not mandated to ask about personal life goals or how to balance seniors’ independence with reliance on their children.

Which is more real? The work we do, face to face or even screen to screen, behind closed doors with our patients, or the EMR documentation we produce as a result of those encounters? I know many providers generate voluminous notes that don’t reflect in any way what happened in the visit. That is where the money is.

Right now I am reading a Swedish book by philosopher Jonna Bornemark, titled (my translation) RENAISSANCE OF THE UNMEASURABLE – battling the pedants’ world domination. Much of it is about how the professions of caring for others have been reduced to protocols and reporting systems that make it harder to do what we were trained and developed a passion for. It talks about how checklists and workflows devalue and discourage the powerful creativity that arises when professionals interact with their unique clients and with each other. She anchors all this in the writings of philosophers Cusanus, Bruno and Descartes. It talks about the unknowable, which is something pedants usually don’t want to think about.

Basically, according to Cusanus, there are two models of knowledge, Ratio and Intellectus. Ratio is the possession of measurable and definable information, which basically fits with generalizations we humans make. Beyond that is what is not known. Our modern way of thinking is perhaps that this is simply what we don’t know yet, but eventually can learn or understand. Intellectus is a form of curiosity that scans the horizon of the known or knowable. It asks “what is” and can thereby sometimes make classification and counting possible, but far from always.

People who have Ratio but completely lack Intellectus, Bornemark describes as pedants.

Pedant is a common word in the Swedish language, but not so common here. It means someone with superficial knowledge, focused on perfection of form rather than substance. Words like stickler, nitpicking and OCD reverberate with the notion of the pedant. The Intellectus archetype is what professionals have always strived to emulate.

(Bornemark has a few books available in English that I know of. She is the editor of one with a title that really intrigued me, EQUINE CULTURES IN TRANSITION – Ethical Questions.)

Henrik Sjövall, professor emeritus at Gothenburg’s department of molecular and clinical medicine (that sounds like the title of a man who knows both Ratio and Intellectus) writes:

Bornemark’s discussion of Cusanus’s concept of Intellectus centers on the distinction between the unknown and that which is not yet known. She notes that Ratio accepts only the latter, because according to Ratio, everything can be measured and weighed provided you have sufficiently good methods, which in principle can replace the “flummery” of Intellectus. Intellectus responds with the circle metaphor: a polygon will never be the same as a circle. Oh yes, it can be, provided there are enough of sectors, Ratio responds… Then tell me what a patient’s narrative weighs, says Intellectus. It simply consists of the answer to a lot of yes and no questions, Ratio retorts, and it is dead easy to measure.

He continues:

Bornemark writes that Ratio has, in principle, already won that battle and Intellectus is in retreat, as most people consider him difficult. A manifestation of this is all these algorithms and patient care plans with checklists that inundate us. Triaging in the emergency room is part of the same way of thinking, a rough sorting based on the outcome of a number of objectively measured vital parameters. The next step in that chain is, of course, the introduction of artificial intelligence as interrogator and information sorter, and maybe eventually as a decision-maker without the patient having to meet a doctor at all…

It would be cheap and good, right?

What are the counterforces to this development? I am active in the Swedish Association for Narrative Medicine (anyone interested is welcome to join), an association that wants to focus on something that cannot be measured and weighed, namely the patient’s story. We are making an effort to stop or ideally reverse this development. In other words, to train Intellectus doctors.

I read in the Wall Street Journal about a forthcoming book about living with autism – not being able to fully understand the nuances of facial expressions and intonation, for example. It seems to me that those things are exactly what good clinicians excel in. Such things make them Intellectus practitioners and elevate their work to a level beyond Ratio, the territory some hope will ultimately be the domain of Artificial Intelligence. I, for one, don’t think AI will ever move beyond Intelligence to Intellectus.

I must say I was a little surprised to see my post on doxepin generate well over 6,000 views in three days. I guess there is interest out there in using old drugs for some of their less well known therapeutic effects.

So here are some other pearls I have collected since I graduated from medical school in 1979. Some may be more well known than I think they are, so please skip over the obvious ones:

SEX: TOO SLOW, TOO FAST, TOO LITTLE OR TOO MUCH

SSRIs like fluoxetine, sertraline, citalopram and escitalopram can cause delayed ejaculation. Citalopram was falsely marketed as having fewer side effects than other SSRIs, but actually had the most. The new version, escitalopram, is better than the others, but can still cause this frustrating side effect. There is a long list of drugs that can counter this. I personally have had the best luck with periactin, an antihistamine, taken PRN for hot dates or even with supper every night for steadier relationships. I have also had good luck with adding daily Wellbutrin (bupropion). This drug can also restore female libido suppressed by SSRIs.

Some men just can’t help themselves and climax way too soon. I give them an SSRI and take advantage of the side effect that others try to counteract.

Men with dementia and frontal lobe brain injuries can have inappropriate sexual desires and behaviors. A desperate 80 year old wife lead me to ask my esteemed colleague, Dr.Google, for advice. With his help I achieved great success with low dose buspirone for her husband, who admitted to me that he felt restless most of the time. My prescription took care of both his restlessness and his outsized libido.

FOOD, ALCOHOL AND BEDTIME RUMINATIONS

Topiramate is an also-ran as seizure medicines go, and it is the weakest of mood stabilizers. But it’s a pretty good migraine prophylactic. It has won FDA approval as a weight loss drug and I have had huge success using it for alcohol cravings: One dose right after work can eliminate the need for that first drink walking through the door and another dose by suppertime is a common dosing time. A bedtime dose often works really well for people who can’t fall asleep because their mind keeps churning about the day’s events, what went wrong, what they should have done or said and so on. Remember that a history of kidney stones is a relative contraindication.

THIS IS YOUR BODY ON STEROIDS

Prednisone is truly a multipurpose miracle drug. Here are some of the indications I use it for:

Gout attacks: Safer than indomethacin, better tolerated than colchicine, can be used independent of kidney function and hardly ever affects warfarin’s effect on INR.

Asthma flareups, COPD exacerbations, hives and allergic reactions.

Nasal polyps and rhinitis medicamentosa (nasal decongestant overuse).

Status migrainosus (protracted migraine): 20 mg twice daily for 10 days almost always works.

Acute back pain with sciatica or cervical radiculopathy. The literature suggests oral steroids work 30% of the time. In my experience they work most of the time.

AN OPIOID DRUG TO CONSIDER

Buprenorphine, the main ingredient in Suboxone, is a good pain medication with less euphoria and lower addiction potential than traditional opiates. This is because of its different affinity for the Mu receptor, less effect on the Kappa receptor and so on. But the best thing of all is that the only approved pain version of it is as a once-a-week skin patch. Four patches per 28 days makes “pill counts” pretty straightforward and removes the temptation to take more than prescribed. And if someone were to try to get a buzz from taking other opiates, their effect is blunted by buprenorphine’s strong binding to the Mu receptor.

A PECULIAR APPETITE STIMULANT

Mirtazapine is a powerful appetite stimulant. It is also an antidepressant, increasing serotonin receptor activity. It can be used by itself or as an adjunct to combat “serotonin burnout” from long term SSRI use. As a sleep aid, it has the peculiar property of being more effective in its lowest dose than in higher doses. I still can’t wrap my head around that one.

These are some of the pharmaceuticals that come to mind right now. I might be back with more some day. I haven’t thought of cataloguing my Black Bag like this before; I’ve just tossed things in over time without keeping inventory, so to speak. They just come to mind when I need them. But now I’ll try to be more organized.

A “frozen shoulder” can be manipulated to move freely again under general anesthesia. The medications we use to put patients to sleep for such procedures work on the brain and don’t concentrate in the shoulder joints at all.

An ingrown toenail can be removed or an arthritic knee can be replaced by injecting a local anesthetic – at the base of the toe or into the spine – interrupting the connection between the body and the brain.

An arthritic knuckle can stop hurting and move more freely after a steroid injection that dramatically reduces inflammation, giving lasting relief long after any local anesthetic used for the injection has worn off.

The experience of pain involves a stimulus, nerve signaling and conscious interpretation.

Our brains not only register the neurological messages from our sore knees, shoulders, snake bites or whatever ails us. We also interpret the context or significance of these pain signals. Giving birth to a long awaited first baby has a very different emotional significance from passing a kidney stone, for example.

I have written before about how we introduce the topic of pain to our chronic pain patients in Bucksport. Professor Lorimer Moseley speaks entertainingly of he role of interpretation in acute pain and also explains the biochemical mechanisms behind chronic pain.

TREATING PAIN WITH ANALGESICS

Even when we are awake, we can reduce orthopedic pains with medications that work on the brain and not really in our joints. A common type of arthritis, such as that of the knees, is often treated with acetaminophen (paracetamol), nonsteroidal anti-inflammatory drugs (NSAIDS) like ibuprofen or even opioids.

NSAIDS reduce inflammation, and reach the tissues inside our knees, but also have an effect on our nervous system’s signaling and perception of pain in the absence of serious inflammation. Their main action is inhibiting cyclooxygenase (COX) enzymes that are involved in prostaglandin release, which happens in the brain to a large extent. Prostaglandins do bad things like causing pain, swelling and fever, but they also do good things, like repair stomach ulcers.

Acetaminophen (paracetamol) also inhibits COX enzymes, but doesn’t reduce inflammation. By itself it does relatively little for pain, but when added to an NSAID, it can greatly improve pain control.

Opiates work mostly centrally for pain, helping our brains filter out the pain messages from different kinds of receptors throughout our bodies. The most well studied are Mu, Delta and Kappa receptors. Less well understood is the nociceptin opioid peptide receptor (NOP).

While Mu, Delta and Kappa receptor stimulation all decrease pain perception, there are other effects, too. Mu simulation contributes to addiction.

Mice without Mu receptors don’t get pain relief from opiates and also don’t get addicted to them. They do show increased pain sensitivity in general and are less likely to develop addictions to non-opioid drugs of abuse.

Mice without Delta receptors demonstrate more anxious and depressive behaviors than normal mice.

Kappa receptor stimulation in pain patients can cause depression and may have a primary role in depression, unrelated to pain, as well. Experimental drugs that stimulate or block only Kappa receptors interestingly have different effects in men and women. This may deepen our understanding of older opioid medications. New Kappa receptor blockers are on the horizon as possible antidepressants.

CHRONIC PAIN

Chronic pain is like a self perpetuating bad habit: Nerve signals from damaged tissue can continue to fire, even if there is no further damage occurring. The frightening thing with treating chronic pain with opioid drugs is a phenomenon called opioid induced hyperalgesia. By blocking the usual nerve signaling in our modern, human, fast transmitting and precise nervous system, our bodies can rely more, an “up-regulation”, on a primitive system of nerve fibers I think of as a lizard system, that tells us something is wrong, as in tissue damage, but with less specificity about type and location. Physicians see this when a person with a bad back on oxycodone treatment winces when you pump up the cuff to take their blood pressure or reports they just plain hurt “everywhere”.

Non-opioid medications for chronic pain that are viewed as safer, like gabapentin, Lyrica (pregabalin) and duloxetine, have their own dependence potential.

Pregabalin produced a “buzz” in some of the patients who took it in early testing, and was therefore made a federally “controlled substance”. Gabapentin is classified as such in the UK and some US states. It is often misused and is more and more often mixed with opiates, benzodiazepines and alcohol by substance abusers.

Duloxetine is related to the serotonergic antidepressants, SSRIs, but also has an effect on norepinephrine. Just like the SSRIs, it is associated with a sometimes severe withdrawal syndrome. I had one new patient who was on duloxetine for fibromyalgia suffer severe symptoms when she tapered herself off duloxetine. She went through a year of seizure-like phenomena, causing a neurologist to put her on anti-seizure drugs to control her twitching muscles and electric shock sensation in her limbs. There are now doctors and clinics specializing in helping people get off SSRIs. There is a growing concern, perhaps especially in Sweden, about the permanent brain changes these drugs can cause and how they can actually prevent full recovery from depression.

Given all this, it seems as if we need to move further and further away from the old pharmacocentric (Hey, I think I just made up a new word!) view that pain is a vital sign and something that deserves and always should be treated with medications.

But if drugs can change the brain’s perception of pain, are there non-drug options for doing the same? The context of pain can be altered: We are hardwired to associate pain with danger, tissue damage. But that isn’t always the case. If we know that use of a joint won’t change how fast our arthritis will progress, perhaps we will still choose to do some of the things we enjoy. We know that poor sleep doubles self-reported pain levels. Stress can increase pain perception as well as cause muscle spasm and a host of other health issues. We also know that hypnosis can change our pain experience. And, let’s not forget that we have naturally occurring opiate-like endorphins that work on same of the same receptors as the opiate drugs. Endorphins are naturally released in response to pain or stress. They can also be released in response to exercise, sex, dark chocolate, chili peppers and acupuncture.

FUTURE DIRECTIONS

There is research that holds the promise of safer centrally acting drugs, but we don’t know just how safe they will be. There are interesting studies on peripherally acting opioids, injected into joints, that actually have both pain relieving and anti-inflammatory properties. But will they be safe? How long will it take to find out and know for sure?

There is some hope for the future but a great deal to worry about today when it comes to treating pain. For too long, pain has been viewed too simplistically as easily and objectively quantifiable and treatable with drugs. Now we know that opiates can ultimately cause more pain and prevent us from releasing our own endorphins. As so often in medicine, a seemingly brilliant shortcut can lead us astray, down a treacherous road, where more pain, addiction and depression affects so many patients.

A holistic, multimodal approach to pain may sound like a lot of work, but since such a strategy boosts our natural biochemical abilities to overcome both acute and chronic pain, it is worth the effort.

A while back I was able to completely stop my mastocytosis patient’s chronic hives, which the allergist had been unable to control.

I did it with a drug that has been on the market since 1969 and is taken once a day at a cost of 40 cents per capsule at Walmart pharmacies.

Hives are usually treated with antihistamines like diphenhydramine (Benadryl). My super drug has a 24 hour duration of effect and is about 800 times more potent than diphenhydramine, which has to be taken every fours hours around the clock.

Histamine is involved in allergic reactions, but it also plays a role in stomach acid production. The allergic response happens mostly through stimulation of Histamine 1 receptors and the stomach acid output is regulated mostly via Histamine 2 receptors. Typical antihistamines are blockers of the H1 receptor, or binding site; they don’t do anything except sit there and prevent the real histamine from attaching and starting the allergic chain reaction. While diphenhydramine sits there for 4 hours, loratadine and the other modern, nonsedating (and less itch-decreasing) antihistamines work for 24 hours. Because there is some overlap between H1 and H2 blocking effects, H2 blockers like famotidine can boost the antiallergy effect of the typical H1 blockers. My mastocytosis patient still had hives on diphenhydramine, loratadine and famotidine combined.

But, wait, there’s more…

A much less well known effect of H1 receptor stimulation happens in the central nervous system. An interesting 2013 article explains:

Histamine is an excitatory neurotransmitter in [the] central nervous system. It plays an important role in the regulation of the sleep-wake cycle. Antidepressants with sleep-promoting effects, for example, doxepin, promote sleep not through a sedative action but through resynchronisation of [the] circadian cycle. The stimulation of the H1 receptor is thought to play an important role in mediating arousal. Doxepin has a high affinity for the H1 receptor, making it a selective H1 antagonist at low dose and it has been shown to display sedating properties. Compared to other sedative antidepressants, low dose doxepin is the only tricyclic drug which has been evaluated by well-designed, randomised, double blind, placebo controlled studies in both adult and elderly patients.

American Family Physician writes “Controlled-release melatonin and doxepin are recommended as first-line agents in older adults.” Yet, at least in this country, trazodone is much more commonly used, even though it is less specific in how it helps people sleep.

Doxepin definitely deserves more attention than it is getting.

The woman had a bleeding ulcer and required a blood transfusion. The hospital discharge summary said to see me in three days for a repeat CBC. But she had a late Friday appointment and there was no way we would get a result before the end of the day. She also had developed diarrhea on her pantoprazole and had stopped the medication. As if that wasn’t enough, her right lower leg was swollen and painful. She had been bed bound for a couple of days in the hospital and sedentary at home after discharge.

She could still be bleeding and she could have a blood clot. There were no openings for an ultrasound until almost a week later. Normally, with the modern blood thinners, we can just start anticoagulation until the diagnosis of a blood clot can be confirmed or disproven. But you don’t do that when somebody has a bleeding ulcer.

The radiology department solved my dilemma by pointing out that the emergency room can order an ultrasound and the department will call in an on-call technician. So that is where my patient had to go. Her blood count was stable and the ultrasound was negative. So now we just have to hope that lansoprazole, which she had taken in the past, but stopped because she didn’t have heartburn, would be effective.

Not long ago, a Friday evening telephone call from a patient with severe nasal pain and a clear discharge after a Covid swab made me think she might have a cerebrospinal fluid leak. She, too, went to the emergency room on my recommendation.

Sometimes I over-explain the reasons I recommend the ER. I will list the types of tests that could help make the diagnosis, the patient only hears “head CT” or “wrist X-ray” and shows up at radiology with no order.

In this part of the country, with sketchy cell phone reception and people not always equipped with land line answering machines, let alone cell phone voice mail, I don’t want to have someone get an imaging test done and be on their way home when I get an abnormal result without being able to reach the patient. I’ve been burned before. And writing “WET READ, PLEASE” doesn’t always result in a call while the patient is still at the hospital.

As so often in medicine, getting the test is only the first step, then there are decisions, interventions and patient education to handle.