Why Do Patients Still Develop Pressure Injuries Despite Repositioning?

Pressure injury prevention has long been built around a simple principle: reduce prolonged pressure through regular repositioning. Across hospitals, aged care facilities and community settings, repositioning remains one of the most widely used interventions for protecting vulnerable patients.

Yet clinicians continue to encounter a familiar challenge. A patient is repositioned according to schedule, appropriate equipment is in place, and a pressure injury still develops.

If repositioning is considered best practice, why does this happen?

The answer lies in our evolving understanding of how pressure injuries form.

The Traditional Understanding of Pressure Injury Development

For many years, pressure injuries were primarily explained through tissue ischaemia.

The theory was straightforward. Sustained pressure compresses blood vessels, reducing oxygen and nutrient delivery to the affected tissue. Over time, cells become damaged and eventually die.

This understanding shaped modern prevention strategies. Repositioning schedules were designed to restore blood flow before damage occurred, while support surfaces aimed to redistribute pressure over a larger area.

These approaches remain important. However, research now shows that ischaemia is only one part of the story.

Pressure Injuries Develop Through Multiple Pathways

Current pressure injury guidelines recognise four mechanisms that contribute to tissue damage:

• Localised ischaemia
• Reperfusion injury
• Impaired lymphatic drainage
• Direct cell deformation

These processes occur simultaneously whenever soft tissue is loaded against a bony prominence.

Of these mechanisms, direct cell deformation is often the least understood and potentially the most important when considering why some pressure injuries develop despite appropriate repositioning.

Understanding Tissue Deformation

Unlike ischaemic injury, which develops as tissues are deprived of oxygen, tissue deformation is a mechanical process.

When tissue is compressed under sufficient load, cells can become physically damaged. Cell membranes stretch, internal structures are disrupted, and damage occurs regardless of oxygen supply.

Importantly, this process can occur much faster than traditional ischaemic injury.

Research suggests direct cell deformation may begin within minutes under significant loading conditions, whereas the metabolic effects of ischaemia typically develop over several hours.

This means tissue damage can begin long before a patient reaches their next scheduled repositioning interval.

Why Repositioning Doesn’t Eliminate Risk

Repositioning remains a cornerstone of pressure injury prevention, but it has limitations.

Firstly, repositioning redistributes pressure rather than eliminating it. Every position creates loading somewhere on the body. Even highly effective support surfaces primarily spread pressure across a larger contact area rather than removing it entirely.

Secondly, tissue tolerance varies significantly between individuals. Factors such as age, malnutrition, spinal cord injury, reduced muscle mass, vascular disease and critical illness can make some patients far more susceptible to tissue damage.

Finally, repositioning schedules are based on population-level recommendations rather than individual tissue tolerance. While two-hourly repositioning is common, healthy individuals naturally move much more frequently throughout the day and night. Patients who cannot reposition independently lose this protective mechanism.

Why Some Pressure Injuries Seem to Appear Overnight

Many clinicians have encountered pressure injuries that appear to develop suddenly.

In reality, the damage often begins beneath the skin before visible changes occur.

Research has shown that deep tissues, particularly muscle adjacent to bony prominences, are more susceptible to loading than the skin itself. By the time redness or skin breakdown becomes visible, tissue damage may already be well established beneath the surface.

This helps explain why some pressure injuries appear disproportionate to what was seen during earlier assessments.

What This Means for Clinical Practice

The key lesson is not that repositioning is ineffective. Rather, repositioning should be viewed as one part of a broader prevention strategy.

Effective pressure injury prevention requires consideration of:

• Patient mobility and tissue tolerance
• Support surface selection
• Shear and friction management
• Skin inspection and monitoring
• Nutrition and hydration
• Moisture management

No single intervention can address every pathway involved in pressure injury development.

Conclusion

Repositioning remains an essential component of pressure injury prevention. However, modern evidence suggests pressure injuries can develop through mechanisms that extend beyond prolonged pressure and reduced blood flow alone.

Understanding tissue deformation and the role of deep tissue loading helps explain why some patients continue to develop pressure injuries despite receiving appropriate care.

For clinicians, recognising these limitations is an important step towards developing more comprehensive prevention strategies and improving outcomes for patients at risk.