I am sure many of you won’t want to know about the underbelly of living with advanced MS. As pwMS become more disabled, complications of being immobilised start to appear. The one that worries all HCPs working with patients who have MS is pressure sores or ulcers.

Pressure ulcers remain a devastating clinical challenge encountered in the management of people with advanced MS. Pressure ulcers, pressure sores, bedsores, decubitus ulcers, or pressure injuries, are localised areas of cellular necrosis and tissue damage occurring in the skin and underlying soft tissues. They almost exclusively develop over bony prominences such as the sacrum, ischial tuberosities (hips), heels, and occiput (back of head). The following image from Wikipedia illustrates the most common sites for pressure ulcers.

MS does not intrinsically or directly cause skin breakdown; however, motor and sensory loss, autonomic dysfunction, spasticity, and cognitive impairment associated with advanced MS are risk factors for pressure sores.

The economic burden of pressure sores is very high and continues to escalate globally. In the UK, pressure ulcers rank among the top 10 harms in the NHS, affecting hundreds of thousands of patients annually. In 2004, pressure ulcers were estimated to cost the NHS between £1.4 billion and £2.4 billion per year, representing approximately 4% of total NHS expenditure at the time. More recent estimates indicate that the management of pressure ulcers costs the NHS over £3.8 million every single day. At an individual level, pressure ulcers diminish a patient’s health-related quality of life. The condition frequently confines individuals to strict bed rest, exacerbates social isolation, causes pain, and introduces the risk of life-threatening complications such as osteomyelitis and septicemia.

I recall when I was a very junior neurology trainee looking after a young woman with MS and a large cavitation pressure ulcer over her sacrum. She spent more than 6 months on the ward having the pressure sore managed. Sadly, shortly after discharge, she developed recurrent septicaemia and passed away from infection. Whenever I see a patient with a pressure sore, I have flashbacks to my experience with this patient.

The management of pressure ulcers within the MS population is complex and requires a multidisciplinary team to manage spasticity, pain and frequently immobility. Care pathways have shifted away from reactive wound care toward highly proactive, multidisciplinary prevention strategies integrated within frameworks like the National Wound Care Strategy Programme (NWCSP). The intersection of clinical care, patient safety, and legal accountability in the UK has transformed the reporting and management of severe pressure ulcers. Regulatory bodies, such as the Care Quality Commission (CQC), alongside legislative frameworks such as the Care Act 2014, have established notification and safeguarding protocols. These legal mechanisms are designed to determine whether severe tissue damage represents an unavoidable consequence of terminal clinical decline or a physical manifestation of systemic neglect and institutional failure. Yes, pressure sores are a notifiable condition under the NHS and must be investigated.

Mechanisms of tissue failure

The aetiology of pressure ulcers in pwMS is multifactorial. The injury involves prolonged mechanical loading on soft tissues compressed between an external support surface—such as a mattress, wheelchair seat, or orthotic device—and an internal skeletal structure. The continuous pressure, friction, and shear forces are responsible for tissue injury. Under normal conditions, capillary closure pressure is approximately 32 mmHg. When external mechanical pressure exceeds this threshold for a sustained period, localised tissue perfusion is severely compromised. This results in hypoxia, the accumulation of metabolic waste products, and subsequent cellular necrosis. Vulnerable individuals lacking the capacity for spontaneous movement, irreversible ischaemic damage can commence in as little as 20 minutes.

Shear forces represent a particularly insidious and destructive mechanism. Shearing occurs when the epidermal layer remains stationary against a support surface, anchored by friction, while the underlying skeletal structures and deep fascial layers shift or slide. This dynamic is frequently observed when a patient with poor core control slides down the incline of a hospital bed or assumes a slumped posture within a wheelchair. This parallel, opposing force severely distorts, stretches, and ultimately ruptures deep fascial blood vessels, initiating ischaemia from the deep muscle tissues outward toward the skin. This mechanism frequently results in suspected deep tissue injuries that cause massive subdermal necrosis while initially presenting only as intact, discoloured skin on the epidermal surface. Friction, conversely, acts directly on the epidermal layer. Functioning like sandpaper, friction physically strips away the protective stratum corneum during transfers or spasms, drastically lowering the tissue’s threshold for pressure-induced necrosis and exposing deeper layers to bacterial colonisation.

While these mechanical forces are the direct forerunners of ulceration, the intrinsic neurological deficits imposed by MS render the tissues susceptible to injury, stripping away the body’s natural defensive mechanisms. Advanced MS is usually associated with paraparesis or quadriparesis, which is associated with a lack of spontaneous micro-movements and weight-shifting behaviours that healthy individuals continuously utilise to redistribute weight and permit capillary reperfusion during sitting or sleeping. At the same time, damage to the ascending sensory pathways results in significant hypoaesthesia or complete anaesthesia. The loss of protective pain feedback, which would normally alert the brain to impending tissue ischaemia and a change in posture, is reduced or lost in advanced MS.

Spasticity (hypertonia), muscle spasms, and joint contractures alter resting posture, often forcing limbs into unnatural and asymmetrical positions, and create friction and shear forces as the patient’s body rubs against support surfaces during movement of spasms.

Comorbid bladder and bowel dysfunction leads to frequent urinary and faecal incontinence. Prolonged exposure to moisture, along with bacterial and fungal overgrowth, macerates the epidermis. Moisture accelerates frictional damage and introduces the complicating factor of moisture-associated skin damage (MASD), which frequently co-occurs with pressure ulceration.

Advanced MS is often accompanied by dysphagia, fatigue, and severe depression, all of which contribute to reduced caloric and protein intake. This leads to malnutrition and low albumin levels. Skin integrity is intrinsically linked to nutritional status; malnourished, hypoalbuminaemic tissues lack the amino acid substrates required for repair, collagen synthesis, and maintenance of interstitial oncotic pressure, resulting in oedema and diminished resistance to hypoxic stress.

Epidemiology

Pressure ulcers are a pervasive, escalating global health crisis, exacerbated by ageing populations, increasingly fragmented care networks, and the rising prevalence of complex chronic diseases. In the Global Burden of Disease (GBD) Study, report that the incident cases of pressure ulcers more than doubled from 1,142,594.8 in 1990 to 2,468,317.5 in 2021, and the resultant mortality attributed to pressure ulcers rose from 16,741.1 to 37,032.7 globally, and DALYs surged from 408,887.0 to 803,747.4 over the same period.

Despite these increases in absolute burden driven by population growth and ageing, the age-standardised incidence rate (ASIR) decreased slightly, indicating that, while the total number of patients suffering is higher, the per-capita risk, when adjusted for age, has stabilised or marginally improved due to preventive measures.

Sadly, the burden of pressure ulcers correlates with the socio-demographic index (SDI), with significantly higher burdens observed in elderly females and a rising incidence in elderly males.

In a prospective cohort study of 185 pwMS without existing skin breakdown, the incidence rate of developing a new pressure ulcer was documented at 10.8% (20 patients) (see paper below). The development of pressure ulcers was not random; predictors of tissue failure included a history of previous stroke, being bed- or chair-bound, poor nutrition and urinary or faecal incontinence.

In the UK, pressure ulcer prevalence in highly dependent populations ranges from 11 to 13%. However, when looking strictly at wheelchair users—who constitute a large and vulnerable proportion of patients with advanced MS—registry studies indicate varying prevalence rates heavily dependent on the underlying neurological pathology. Among young wheelchair users overall, 55% experience at least one pressure ulcer a decade post-injury or disease onset. Specifically within the MS sub-population of chronic wheelchair users, the cross-sectional prevalence of current pressure ulcers is estimated at 4%.

Within intensive care units (ICUs) and orthopaedic surgical wards where MS patients may be admitted during severe disease relapses or for unrelated acute pathologies, incidence rates peak dramatically. General ICU prevalence averages 6.8%, with an incidence rate of 3.8%. Orthopaedic surgery wards have alarmingly high incidence rates of 18.5%, emphasising the danger of prolonged surgical immobilisation.

The sacrum is overwhelmingly the most affected area, accounting for up to 68% of ulcers, followed closely by the heels, left and right trochanters, and ankles. When analysing severity across generalised hospital populations, stage 1 and stage 2 ulcers account for the vas...