In medicine, we are taught to trust evidence. But evidence does not only come from laboratories and academic conferences. It also comes from observation at the bedside. A growing debate in wound care centers on whether skin failure and pressure injuries are distinct conditions. Some experts have proposed that skin failure represents a separate process that occurs in critically ill patients and that pressure may not be a causative factor. While the terminology continues to evolve, many clinicians find themselves returning to a simple principle—seeing is believing.
For more than a century, healthcare professionals have observed a consistent pattern. Patients who are critically ill, frail, dying, or burdened with multiple comorbidities often develop tissue breakdown over the sacrum, heels, buttocks, and other pressure-bearing areas. These wounds appear where the body is exposed to sustained mechanical loading. Whether the patient is in an ICU receiving vasopressors, a nursing home resident with advanced dementia, or a hospice patient nearing the end of life, the locations of skin lesions are similar.
The question is obvious: if pressure is not involved, why do these wounds consistently occur in areas subjected to pressure? If skin failure represents a fundamentally different process, one might expect a different anatomic distribution. Yet clinicians continue to observe lesions developing in the same pressure-bearing locations.
At the bedside, skin failure lesions appear in the same locations traditionally associated with pressure injuries. This observation raises important questions about attempts to separate the two conditions into entirely different categories.
It is an established fact that sustained mechanical loading causes tissue deformation, impaired blood flow, and cell death. At the same time, systemic illness including sepsis, shock, hypoxemia, malnutrition, organ dysfunction, and impaired perfusion make tissues more vulnerable to injury. These factors are not competing explanations. Rather, they work together. The presence of systemic vulnerability does not eliminate the role of pressure; it magnifies its effects.
This is what clinicians witness every day.
The danger of drawing rigid distinctions between skin failure and pressure injury is that it creates a false choice. Clinicians may feel pressured to classify wounds as either pressure-related or systemic, when the evidence suggests that both mechanisms are operating simultaneously.
Perhaps the more productive approach is to view these conditions along a continuum. Patients with robust health may tolerate prolonged loading without injury. Patients with severe illness may develop tissue breakdown after relatively short periods of pressure because their tolerance has been dramatically reduced. The underlying pathophysiologic factors may vary, but the interaction between mechanical forces and tissue vulnerability remain central.
Medicine advances when observation and science reinforce one another. Throughout the history of wound care, bedside observations have repeatedly guided scientific discovery. Today, those observations continue to tell a consistent story: patients develop tissue breakdown when pressure and systemic vulnerability converge. Regardless of the terminology ultimately adopted, the lesson from the bedside remains unchanged—seeing is believing.
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