The aim of the site is to offer clinicians a variety of mentorship opportunities, across a broad spectrum of clinical practice.
I am currently offering mentee focused clinical mentoring. The mentoring session are done online via Zoom and focus on the mentees specific needs. Sessions usually last for 60-90 minutes. Frequency is solely determined by the mentee and their specific needs.
The charge for each session is on average £100 in the UK and 100 Euro in Europe. Region specific charges are negotiable and I am cognisant of different financial constraints around the world.
I also offer clinical consults on Musculoskeletal issue, and I am happy to consult on specific cases with clinicians or see specific patients with clinicians if mutually agreed by the patient.
I also offer bespoke short courses for interested small groups on various topics surrounding patient self treatment and clinical reasoning.
For those interested here is a recent one hour webinar I did for a group in India. Link here
I have also done a recent blog and podcast on “Discs Don’t slip” you can access the podcast here
And the guest blog on all things Intervertebral Disc here “Intervertebral Discs are they jelly Donuts? ”
In my last blog post I highlighted that exercise is definitely not medicine in any shape or form for sufferers of Long-COVID (aka COVID Long Haulers), in fact for some long-COVID sufferers pushing through leads to complete breakdown and profound exhaustion.
Over the weekend I began to reflect on ponder, as the feedback and discussions around my blog developed on SoMe. It became apparent that long time advocates of exercise where finding it difficult to accept that graded exercise wasn’t the answer for long-COVID and played mental gymnastics with definitions of exercise, down to suggesting any activity of any sort was exercise and should be utilised to defend their stance.
Let me just place this in perspective, long-COVID sufferers commonly and almost universally are not suffering from a deficit of exercise, they are not exercise avoiders, they are not deconditioned. Their presentations do mimic deconditioning ie post exertion fatigue, general malaise, tachycardia, breathlessness. BUT, these are not due to deconditioned status they are symptoms of the effects of the the virus and it’s long term effects on cellular activity, chronic inflammation and organ damage, including heart, lungs, kidneys, liver and brain. Watch this video from 60 minute if you are still not convinced here
So why is it hard for clinicians to change their paradigm and accept that exercise is not the answer?
The answer lies in our difficulty to unlearn and relearn new information. I have labeled this “first in best dressed syndrome” meaning what we learn first and believe to be true, is much longer lasting , ingrained and harder to change, than new and conflicting information.
As a young educator I had to learn this the hard way, when I excitedly presented some new, controversial and conflicting ideas at a conference. I was overwhelmed by the negative response of the audience and the almost vitriolic attack on my newly presented knowledge. After the presentation someone gave me this paper as a message of support👇
Titled THE ROLE OF ANOMALOUS DATA IN KNOWLEDGE ACQUISITION: A THEORETICAL FRAMEWORK AND IMPLICATIONS FOR SCIENCE INSTRUCTION full text link here
The paper describes the way we handle conflicting information and highlights the seven different strategies that people adopt. All seven can be seen on SoMe discussing the role of graded exercise in the treatment of Long-COVID, as you will see if you read the paper six ways are used to discount the idea that exercise is not indicated and used to protect their original understanding of “exercise is medicine”
One of the hardest things to do is “unlearn” and then replace the old idea with new learning.
Most of use will try to use the six strategies highlighted in the paper above to maintain or previous notions and in some case appear to have adopted the new information.
in fact in some cases the more information that is provided for in support of the new idea, the greater the push back, which creates a back fire effect.
Unlearning is tough. But I would encourage clinicians to ponder on whose interest they serve, their own, or their patients? Believing that your ideas are sound and should be followed, rather than seeking to understand a new perspective from a patient focused point of view, seems futile.
I am striving for change and understanding, receive your patients narrative, listen to the sufferers of long-COVID, there are links to their stories here These narratives are not only sufferers of long-COVID they are your clinical peers.
There is so much we do not know or understand about the cause, and course of long-COVID, BUT making a change in your understanding and beliefs, doing some unlearning and releasing, listening to the narratives of long-COVID sufferers, may improve their care and journey.
Be part of the solution, not the problem.
As always I suggest Ethos (Gain Trust), Pathos (First seek to understand), Logos (the to be understood)
BUT, is exercise really medicine and should it be recommended for all that troubles us?
First lets define what we mean by exercise. Simply put formal exercise is aimed at challenging bodily structures and systems to a point of controlled overload causing fatigue and or micro failure with the intent of stimulating adaptation of the structure or bodily system. Common types of exercises aim to strengthen muscles, improving flexibility, stimulate cardiovascular changes, improve general bodily endurance. Everyone is familiar with lifting a weigh to muscular fatigue, running until your pant and sweat, doing aerobic classes that make you pant and sweat, long runs and cycling that improve your endurance, climbing steep hill either by running or walking that challenge your heart rate and breathing. All are designed to push you to challenge the muscle or system followed by a period of rest to allow adaptation. Often the periods of effort/challenge followed by rest lead to increasing abilities in strength, power, improved cardiovascular responses and endurance. It is also recognised that these changes take several weeks and require regular challenging exercise and progression of load and intensity.
Yep exercise sounds great and yes it sounds like a great way to be healthy, almost a medicine in it’s self.
We are one year into the global pandemic caused by the SARS-Corona virus-2 commonly referred to as COVID-19. Many people have contracted the virus world wide and have recovered from the acute presentation, but many are still left suffering from the long term effect which present in multiple ways. This has lead to the term Long-COVID to describe the ongoing , often debilitating signs and symptoms, of post COVID infection.
One of the most common reported presentations with Long-COVID is post activity malaise and or extreme bodily fatigue which is immediate but often delayed by 24 hours. It can be unpredictable in nature. Also commonly reported are fluctuations in heart rate including tachycardia, and breathlessness, with minimal to no physical exertion.
The symptoms of Long-COVID seem to mirror those of Chronic Fatigue Syndrome (CFS) although no direct link has yet been shown.
So the question arises if exercise or even normal daily physical function causes irregular heart and breathing issues, followed by general malaise and or profound fatigue, how can exercise be the solution to long-COVID?
It may be time to adopt some of the strategies developed for the treatment of CFS such as activity pacing, rather than formalised “graded exercise”. It has been suggested that graded activities of daily living are exercise if they cause increased heart rate and fatigue, I would suggest this is not true in te case of long-COVID sufferers or CFS as the changes in heart rate and fatigue and often O2 saturation, are not due to deconditioning, but are unpredictable responses due to the the long post viral infection process, which at this point in time we do not fully understand. (Ref ) More on CFS and exercise here
So I propose that for long-COVID exercise per se or even graded activity may not be indicated as a therapy and in the case of long-COVID “exercise is NOT medicine.”
If you want to read more and understand the lived experience of many health professionals with long-COVID check out this blog (here)
At the current time we need to seek to understand the individual with long-COVID, there individual and unique presentation and give support and advice on management and perhaps pacing based on their own current understanding of their activity tolerance, triggers and long-COVID crashes. Employers, spouses, partners and society at large may need to be more understanding and accommodating, as people with long-COVID try to recover and restore their pre COVID health and lifestyles. There is a nice article/blog on pacing with long-COVID “Long covid and self-help pacing groups—getting by with a little help from our friends” found in the BMJ here
In conclusion it may be more important than ever to be a person focused therapist when managing people suffering from long-COVID. Exercise is NOT medicine, self directed activity pacing may be the best initial intervention, support and understanding are essential. Surgeries will have “crashes” we all need to be supportive and understanding.
As always thanks for reading I hope this was helpful.
Stimulated by my discussion with Jack Chew PT yesterday on his Chewing it over daily broadcast ( available here https://twitter.com/jackachew/status/1366365752974974977?s=21) I decided to write a short blog on my early experience as a freshly minted PT (actually Remedial Gymnast, I would transition to a PT in 1985 two years after initial graduation)
1984 was a big year for me for many reasons, I had been practicing for a year and had finally escaped from the OBGYN and special care baby unit, after nine months of anti natal classes, postpartum exercises and caring for little incubated humans. I transitioned to a new post on Batley Orthopaedic Hospitals rehab team.
the hospital is long abandoned and probably knocked down.
I remember my first day because it was raining and at this point in my life I still hadn’t learnt to drive ( yep aged 25 and unable to drive, partly due to being a cyclist and runner, and really because of fear ( long story ) and expense) I ran from my residence at Dewsbury Hospital as part of my triathlon training, two runs a day as a commute was great training on the hilly terrain of West Yorkshire.
I remember arriving wet and disheveled to discover there was no shower in the Physiotherapy department, a brisk cold wash in the men’s it was then. ( this became my routine for over a year, thank goodness for scented body spray)
My ne role on the Physiotherapy team as to prescribe exercise, at this point in my career I didn’t have the “skill” of “training” to work the banks of magic SWD machines (and knit at the same time, wooden needles only) or make circles with the US machine, or supervise wax dipping and mass puppet show, no i was just there to dispense “movement” (which ironically is now the number one go to PT modality 😊)
My day was split in two, mornings were spent on in-patinet care and afternoons on outpatient care in the small back room rehab gym.
Inpatient care involved ward rounding with the Gods (in my early days most surgeons ruled the hospital and their word was the rule of law) Imagine patients had to be washed, fed and sitting quiet in bed or bedside chair for the Orthopeadic surgeon to do his (rarely if ever (and never) in my early days a she).
Rounds involved following Mr X (no longer referred to as Doctor as now one has reached the lofty height of being called Mister again) around like a line of quiet ducks and ducklings, only allowed to speak if asked to.
the picture above is an exact replica of the ward I worked on. Patients were generally acute trauma orthopeadic injuries or suffering from “sciatica” , the treatment for all seemed to be the same, forced bed rest and traction.
It’s hard to believe that probably 60% of the ward beds were filled with young males, often post motorbike crash, with fractured femurs placed in a Thomas splint and steinmann pin through their tibia to offer a traction point attachment. They would be in bed for up-to 12 weeks to allow good callous formations and alignment of their fracture.
As I joked yesterday, being a young PT on a ward full of relatively healthy young men, (rarely if every young women, the perils of male youth and stupidity) was more like being a Butlin’s Redcoat, chief exercises encourager, motivational clown, listener and hopefully prevent or of bed sores and infections.
Movement is life has never been such an important concept. These guys needed to be as active as possible in all respects apart from literally being tied to a bed, so yes straight leg raises, ankle pumps single leg cycling glute squeezes, you name it we did it.
Yo may think, thank good ness we don’t tie people to bed s for up-to 12 weeks these days, thank goodness we have modern surgical techniques that have moved us into an age were patients are moved/ mobilised early and sent home to avoid hospital based super bugs.
Well this depends where you live and what resources are available. I spent some time in Niger (hard to believe it was 6 years ago) Niger is one of the poorest nations on the planet. it is not unusual for developing countries like Niger to still practice orthopeadics similar to what I experienced as a young therapist.
Hard to believe this quote “Conservative management of femur fractures with traction remains the best and very often the only option for cost-sensitive developing countries”
Remember when we talk about the social determinants of health, this also involves care. What we believe to be old, updated ramblings of an old PTs reflections are actually still a recognised standard of care.
What we call our history some call their present reality. As we discussed yesterday, it’s not what was old is new, it’s just that we have suddenly discovered someone else’s reality and common knowledge.
Thanks for reading my rambling reflections. Here is to another 38 years.
From a patient centered to a person focused paradigm.
(picture source Google images)
I have recently been on a journey trying to understand the philosophical terms, thoughts and underpinnings involved in the Cause Health series on Dispositional thinking and Causation.
I am a self confessed “numpty” I see the world from a simplistic view point, mainly self taught with little if any philosophy back ground. It has been a struggle to gain understanding of the complex and new world.
After reading the blog I went for a walk and let it ruminate in the back of my mind and allow my subconscious to reflect and create.
I ponder, do we over complicate things? I have proposed in a recent blog that the Biopsychosocial model is misunderstood and when you look at the human condition and suffering from a ‘whole-istic” view, you see that humans are more like a complex ecosystem where the individual parts interact, no longer possessing the qualities of individual players, but produce a new functioning, often complex, whole.
When we talk about causation, and dispositions, do we make a basic error in assumption, that we can identify the players (in this case dispositions) and their assumed causal role. Do we miss sight of the fact that the multiple dispositions we identify, may be selected based on our biased external view, and our assumptions of the role they may play in causality of the persons’ current presentation.
I am trying to get my head around mutual manifestation partners , the phrase is attractive to me and I ponder that in a person who is suffering and we try to identify the dispositional properties that may be part of the causation, we make assumptions that all of the players are having an active role?
Jumping back to the Biopsychosocial (BPS) model, one of my contentions is that it is a like a fully cooked pancake, one the person arrives the constituent parts and their properties are long gone and a new whole “the suffering person” presents as their own unique, fully cooked, BPS pancake. I would also like to propose that some of the constituent ‘players” of causation may in fact be nearly “catalyst’ that play no active causal part but are responsible for amplifying the clinical presentation. Is it possible that some dispositions are in fact catalysts? (Does it matter?)
We often talk about “the social determinate of health” (SDH), they have been a visible topic of conversation during the COVID-19 pandemic. Many have argued that they are a involved in the causation of poor health and outcomes. What is the social determinate of health are viewed as a catalyst not an active causal disposition? It is well known that changing the SDH is far beyond the scope of most PTs or clinicians. Should we focus on what we can affect, and if the SDH are a catalyst, their effect will diminish once the persons health improves. In simple terms SDH may not be causative but contributors as catalysts. (I could be wrong, of course)
My last pondering and reflection relates to the so called power dynamic that may still occur even in a dispositional approach to causation, as suggested in the blog by @nakedphysio, there is still a suggestion that the clinician is the one in charge making the decisions on which dispositions are possibly causal.
I propose that we switch from a patient centered view to a person focused view, where we are responsible to the person by providing our knowledge, expertise and clinical skills in a synergistic relationship, NOT responsible for the person, that responsibility lies with the individual.
The clinicians focus should be on the “macroscopic” view, we are in fact a clinical catalyst to the resolution solution, not the solution it’s self. Being person focused and viewing ourselves as catalyst may also decrease our need to act on people, it will also allow the person who is suffering to become their own causal solution, acting on proactively, rather than being acted on “reactively”.
I hope some of this makes some sense. If not nothing wasted but a bit of reading time.
As always thanks for taking the time to read my ramblings.
There are a plethora of clinical guidelines published around the world on various clinical presentations from low back pain to managing multiple medical conditions. The intent of a guideline is to offer clinicians evidence based information on the most effective way to diagnose, manage and implement treatment for the target condition. They are simply put, evidence summations and sign posts for the best current care. Ref: https://en.m.wikipedia.org/wiki/Medical_guideline
There have been many papers written on the lack of adoption or “adherence” to the published clinical guidelines amongst clinicians. Some of the lack of adoption is based on lack of awareness of the existence of the guidelines, but a lot of clinicians fail to follow them because they patients they see do not fit the inclusion criteria for the evidence base used to write the guidelines. It is common for RCT to exclude people with multiple co-morbidities, law suits, workers compensation claims, those undergoing current therapy, previous surgery etc. The average patient seen in daily practice, often has one or more of these exclusion criteria.
I have consistently suggested that clinical guidelines reflect a “perfect” world situation using the average outcomes from RTCs and Systematic reviews, where in everyday clinical practice patients come with complex issues, often with co-morbidities and related complex social determinants of health. It is obvious to most clinicians that no one necessarily needs what the average of all of us might need.
So what use are the guidelines if clinicians are not following them and the do not reflect the real world situation of everyday clinical practice?
A recent review by Lin et al looked at the best advice across the board from multiple guidelines and came up with 11 common recommendations. These recommendations are reasonable and can be applied across multiple clinical disciplines and seem to apply to most if not all patients. 👇
As a clinician the paper is an important read, the recommendations are easy to apply in everyday practice.
It appears that a lot of clinicians don’t follow the guidelines because they are unaware, feel their patients aren’t represented, stuck in a treatment belief that they believe in but lacks evidential support, or (dare I say it), they believe they know better.
I have to admit, I’m not a guideline follower, but I do believe I am pretty close to the 11 recommendations from the Lin et al paper.
Over the last few days I’ve been having several discussions on twitter, about clinical tests including the reliability, validity and accuracy of said tests. During the discussions, with some very clever clinicians, it became evident that clinicians may not have a good grasp on what constitutes a valid test, or how to test with intent using a Bayesian Conditional Probability approach, for testing a clinical hypothesis.
So I decided to write a numpties (that’s me) guide to clinical testing. So strap in and enjoy the journey.
When I originally trained and on continuing education courses, early in my career, I remember learning clinical tests on a simple level. Instructors would say “here is a test for shoulder impingement (ie Hawkins Kennedy or Neer’s test), if it’s positive your patient has a shoulder impingement.” Despite evidence against this being correct, you can still find this information with a simple Google search on “shoulder impingement tests” 👇
Clinical tests should not be used to prove a hypothesis or diagnosis, they should be used with the sound clinical intent of assessing the shift in probability of your clinical hypothesis.
It is important to choose the best tests, that will improve the probability of your clinical hypothesis being correct. It is also important to remember that your clinical hypotheses should be based on sound clinical reasoning and on receiving the patient historical narrative. Here is a link to a webinar I did on clinical reasoning in low back pain which give examples of this https://youtu.be/8KZvRbmQu7s
So what do we need to be aware of when choosing a clinical tests?
For most clinical tests we need them to have good clinical utility, based on good reliability and validity. Sounds complicated and technical. Simply put reliability is the ability for agreement, validity is the ability of the test to do what it says on the tin, ie how good is is at finding the target pathology (the tests sensitivity) and how good is it at detecting when you don’t have the target condition (the tests specificity)
Sensitivity of a test is basically a description of the true positive rate.
Specificity of a test is basically a description of the true negative rate.
The aim of a good test is to have both high Sensitivity (Sn) and high Specificity (Sp)
An old pneumonic was used to indicate that Sn and Sp could be used to rule conditions in an out, SnNout and SpPin. In simple terms if a test has a high Sn it will be very goo at detecting the target, so counter intuitively it could be used to rule a target out if the test result was negative. Conversely Sp when high would be good at saying you don’t have the target hence when a test with high Sp was positive it could thus be used to rule in the target. I would propose that this simple view of testing doe snot improve your ability to test your Clinical hypothesis. A combination of Sn & SP can be used to calculate a ratio known as the likelihood ratio, which can then be used to calculate the change in probability when you perform your test when it is both positive and negative.
Likelihood ratios are useful as they are a combination of the true positive and true negative rates of the test. Once calculated they can be used with a Bayesian nomogram or online calculator to calculate the post test probability of your clinical hypothesis give you know the pre test probability, which is generally available looking at population data or the occurrence in your clinical population of the target condition.
Calculation likelihood ratios: 👇
Once you have calculated the likelihood ratios of you test (here is a link to an online calculator http://getthediagnosis.org/calculator.htm ) you can use them as a rough guestimate of how a positive or negative test may alter the post test probability of your clinical hypothesis. See the table below 👇
if you know the pre test probability of the target hypothesis you can also get an accurate post test probability using a Fagan or Bayesian nomogram. I speak to this in the blog I posted earlier.
The nomogram is easy to use (but you can use the free online calculator posted above) find the pre test probability on the right, find the Likelihood ration in the middle and dram a line from one through the other extending to the post test probability on the right.
It is important to note that due to Bayesian conditional probability the post test result of your test now becomes the new pre test probability of you next test. Hence be aware that if you use a test that has a positive likelihood ratio below 1 you are lowering your new pre test odds. See the example below.
Conditional probability is also why a cluster of average test can produces a better post test odds than a single test average test. Each test shifts the pre test probability for the next test.
I hope this all makes sense? It highlights that in the old way of thinking when a test came up negative you may just have chosen a new tests or several new tests until several, until one came up positive “confirming” your hypothesis. It is important to remember that every test has an effect on the starting point of the next test.
Look at the data set below, it can bee seen that in the case of testing for SI joint pain we should be aware that many of the listed tests have poor clinical utility.
Any test with a +LHR below one is basically a useless test as it lowers the post test probability and thus the new pre test probability for the next test.
It is also important to remember that if you have a very high pre test probability of a target condition, based on the history findings received from the patient, it is important to be cognizant that a poor clinical test may not shift the probability post test enough for you to reject the diagnosis. An example of this is with COVID-19 and testing. 👇 this is why we should seek to understand the basics of clinical tests and their application to clinical scenarios.
I have tried to simplify testing to allow understanding of the complexity and affect testing can have on probability. I propose that we should use clinical tests sparingly and that all clinical tests should be seen as ‘special”. Ask your self “well the test I am about to perform shift the probability of my clinical hypothesis significantly in a positive direction?” If the answer is “No” then why perform the test?
I have been talking about patient empowerment for over half of my career. Terms like “Patient Centered Care” and “Therapeutic Alliance” have become more more common place than they were 20 years ago.
But has much changed on a day to day basis in the practice of Physical Therapy(Physiotherapy) or do we just pay lip service to the terms?
On the average day in a busy clinic, with a packed schedule, several new evals, one or two re-evals, several patients turning up late, how do your “motivational interviewing” and relationship building skills fare?
If you have a consistent patient interaction skill set, then even on the busiest day, with all the hiccups that may ensue, you will still be able to give each and every patient the understanding and empathy they deserve.
One simple and consistent method of patient interaction is to practice Ethos, Pathos, Logos. The original concept developed by Aristotle to win people over to his arguments during debate. This was later expanded on by Stephen Covey (of Seven Habits fame).
Ethos, is the root word for Ethics and Covey explains it is the essence of developing a good relationship, simply put it means “gain trust.”
During the initial encounter with a patient everything matters, patients are assessing your clinic, the staff, and you, as much as you are assessing them. It is important they feel safe and listened to. Gaining their trust is key to a good therapeutic alliance. Without trust as a foundation everything else may start to fail.
Pathos, is the root word for empathy, Covey suggests that this implies “seeking to understand”, without judgement, truly listening to another, seeing things from their point of view. The emphasis is on empathetic listening, where one listens not with the intent to prepare to answer, but to understand the patient’s narrative. (This synergies with Ethos, as it is a powerful tool for building trust)
Logos, is the root word for logic, here Covey suggests that after truly listening then one can “seek to be understood” again this synergies with Pathos and Logos, seeking to be understood requires one to utilize the patient’s narrative, to form an individualized assessment and treatment plan, based on shared decision making with the patient. Education is not simply an add on to the end of a treatment session it is part of the fabric of the whole patient encounter. Allowing patients to reflect during the clinical encounter leads to a more patient centered learning experience.
Ethos, Pathos, Logos is a simple framework which can be utilized to make each clinical, encounter meaningful for both the clinician and the patient.
On social media recently there are numerous discussions on placebo, placebo effect contextual effects, non specific effects and specific effects. Some are proposing as clinicians we should #bebetterthanplacebo, or suggesting we should be more than the sum of the contextual effect, often created around a therapeutic alliance.
So are we better than placebo? Well true placebos are inert substances with no known active effect, so hopefully our treatments are truly better than “nothing”. The problem arises when we ask are we better than the sum of the contextual effects created during the therapeutic encounter? (See the milk bottle model)
What are the differences between “nonspecific” treatment effects or so called “placebo responses” and specific effects? If you are just reducing pain with your intervention is this a specific or a non specific effect?
Kory Zimmer Ref has suggested that to understand the specific effects of an intervention you should replace the word “specific” with “unique” ie what responses are unique to the intervention?
With this in mind I would ask you to ponder, what effects are unique to your interventions, that are not attributable to contextual effects?
There is still a lot of confusion regarding the word “biopsychosocial”. Yes it’s a compound word made up of three other words “biological (physical) , Psychological (of the mind) and Social (of the environment)
The trouble is that just like the word biopsychosocial is all one, so are humans. Clinicians constantly talk about the three elements as separate drivers of pain and health, whilst forgetting that they all apply and are often intimately connected in a causal relationship that can not be found by separating them.
Humans experience distress, often manifested as “yellow flags, this can be in response to multiple drivers. We talk about self efficacy (the belief you can do something) and locus of control ( the belief you have control in yourself, internal locus, or that external factor control your situation an external locus.
These measures are part of the human experience and are a reflection of human suffering. It is normal to be distressed when experiencing ill health or pain. Everyone, bar non, will display some degree of psychological manifestation during times of suffering.
The hard part for clinicians is to realise distress responses are normal and are all part of the human condition.
I have proposed the analogy that trying to separate biopsychosocial into it’s composite part to find causation is like trying to separate water in to hydrogen and oxygen to find out the properties of water.
As clinicians it may be time to utilize a “whole-istic” approach to understanding patient who present for treatment of painful conditions. Considering their social determinants of health, their coping strategies, their level of distress, including kinesiophobia, catastrophizing, self efficacy and locus of control, their physical and functional impairments, is all part of the big picture contributors of the clinical condition.
We can not understand the whole by dissecting it into it’s constituent parts, just like we can’t uncook a pancake.