You might expect the guidance on pressure ulcer prevention to have plenty to say about protecting the heels of larger patients, but that is not the case. In this article I want to show where the guidance goes quiet, what the research evidence really says about body size and heel ulcer risk (it is not what most people assume), and how I suggest thinking about the problem instead: as a question of equipment fit rather than a question of risk scores.

A note on language before we start. Following the Obesity UK "Language Matters" guidance, I use person-first phrasing for people, and I keep the word "bariatric" for equipment, pathways and products, where it remains the standard term. In manual handling circles, "plus-size" is the preferred word for the person, and I follow that convention here.

Clinical guidelines name pressure and shear as the cause of pressure ulcers, but rarely explain what the words mean. Drawing on thirty years in rehabilitation engineering, I unpack pressure, shear, stress and strain in plain language, show why the skin check can look normal while damage develops over the bone, and explain why the heels are so vulnerable. This one of our longer articles.

When I demonstrate an FES cycling system, spasticity is usually in the room before I have finished setting up. A leg that will not settle onto the pedal. A knee that pushes out straight at the wrong moment. A foot that starts bouncing the instant it takes any weight. The person in the chair rarely calls it spasticity. They say their legs have a mind of their own, or that everything goes rigid when they transfer, or that the spasms wake them at three in the morning. The clinical word comes later, if it comes at all.

This article is for the person who has just been introduced to that word, or who has lived with the thing itself for years without anyone quite explaining it. I want to cover what spasticity and spasms actually are, why they happen after a spinal cord injury, a stroke or with multiple sclerosis, what they do to daily life, and what genuinely helps, from medication through to electrical stimulation. I will try to be clear about what the evidence shows and what it does not; if different people have told you contradictory things, that is partly because the field itself contains genuine uncertainty.

After a neurological injury, whether a spinal cord injury, a peripheral nerve injury, or a period of enforced immobility, clients often ask: "Will electrical stimulation bring the muscle back?"

I have learned to pause before answering, because "back" hides two quite different questions. The first is about size: will the muscle get bigger again? Obviously, this is what people notice when they look down at their legs. The second is about substance: will the tissue that returns actually be muscle, in the working sense of the word, rather than a mixture of shrunken fibres, fat and scar? This is less obvious to a client, but it's what we actually need. Researchers call this second property muscle quality, and it is the more important of the two. It is also the one that almost nobody explains to patients.

In this article, I want to walk through what muscle quality means, how it is measured, what happens to it after injury, and what electrical stimulation has been shown to do about it. I will cover both of the situations we work with: innervated muscle, where the nerve supply is intact and conventional stimulation applies, and denervated muscle, where the nerve supply has been lost and an entirely different approach is needed. The evidence differs between the two, and so do the limits of what is possible, and I will be plain about both.

Physiotherapists inherit the consequences of the first weeks after a stroke, a brain injury or a spinal cord injury twice over.

The first consequence is at the ankle itself. A foot that has spent weeks driven into plantarflexion by tone and gravity arrives in the rehabilitation gym short of the range it needs. A foot that cannot reach plantigrade cannot take weight properly, and everything that needs attention (standing practice, transfers, gait work) gets harder.

The second inherited problem relates to the skin. A heel pressure ulcer acquired during the acute phase can halt weight-bearing for weeks or months, right at the point in recovery when time matters most. Every day that the patient remains in bed results in loss of muscle mass. We also know that such an ulcer, even when healed, is much more likely to recur due to changes in the tissue's mechanical properties.

Most writing about heel pressure relief devices treats these as separate problems, one belonging to tissue viability and one to physiotherapy. In my experience, if we want continuity of care, they are best considered as part of the same problem seen from two directions, and the device on the end of the bed is where they meet. This article is about that meeting point, including some evidence that does not say what many people assume it says.

In 1994, I was visiting the Cleveland Clinic and saw a product design I came to know as the PRAFO (pressure relief ankle-foot orthosis). I recognised this as a practical orthosis being used to reduce the risk of heel pressure ulcers developing in at-risk patients following orthopaedic procedures. It's true that I liked the concept so much that we created a company, Anatomical Concepts (UK), to bring the products to the UK. Thirty years have now gone by, and we still deal with the PRAFO range. We still see the challenge that heel pressure ulcers present to affected individuals and our healthcare systems. For decades, we've emphasised prevention, yet acquired ulcers remain a widespread problem. We have some understanding of the mechanical and medical factors that heighten risk and lead to pressure ulcers, but something is missing.