4.1 Pressure Injury Pathophysiology and Risk Tools

Pressure Injury Pathophysiology and Risk Tools

Pressure injuries form when mechanical load exceeds what skin and soft tissue can tolerate. For the Certified Wound Care Nurse (CWCN) exam, you must explain how injury develops, not only name the sacrum. The same mechanics that produce a sacral ulcer produce a nasal-bridge injury under a mask: intensity, duration, shear, and the local microclimate interact with perfusion, sensation, and mobility. This OpenExamPrep chapter uses the clinical names of risk tools and of National Pressure Injury Advisory Panel (NPIAP) categories because those are the terms wound teams document with; it is independent teaching, not a claim of sponsorship by WOCNCB or NPIAP.

Tissue deformation, ischemia, and reperfusion

Older bedside teaching emphasized capillary occlusion and ischemia. That still matters, but current pathophysiology also emphasizes tissue deformation. Over a bony prominence, external load compresses and distorts cells, the extracellular matrix, and small vessels. Cytoskeletal strain can kill cells even before a classic ischemic infarct is complete. Muscle and adipose deform more readily than skin, which is why a small surface finding can sit over a much larger deep injury—the pattern you will later recognize when a deep tissue pressure injury (DTPI) declares itself.

Ischemia-reperfusion injury is the second wave. When pressure is relieved, blood returns to hypoxic tissue. Reperfusion delivers oxygen and inflammatory cells that generate reactive oxygen species, capillary leak, and further necrosis. That is why a purple or boggy area may look worse hours after a long operating-room case even though the patient is now on a support surface. Offloading prevents the next cycle; it does not instantly reverse damage already triggered.

Perfusion modifiers change the threshold. Hypotension, vasopressors, shock, peripheral arterial disease, edema, anemia, and nicotine-related vasoconstriction all reduce the load a tissue can survive. Fever and inflammation raise metabolic demand, so the same pressure becomes more injurious. In the intensive care unit (ICU), a routine turning interval can still be catastrophic if mean arterial pressure has collapsed.

Intensity times duration

Injury risk is not a single pressure number. High intensity for a short time (a hard table edge, a tight cast, a folded sling) can injure as surely as moderate intensity for a long time (hours of unrelieved sacral pressure). This product of intensity × duration is why operating rooms, emergency stretchers, and interventional radiology tables are high-risk even for patients who scored well on a unit Braden Scale yesterday.

There is no universal safe number of minutes at a given millimeters of mercury for every patient. A well-perfused mobile person may tolerate a load that injures a hypotensive, insensate, malnourished patient in far less time. Use intensity × duration as a clinical reasoning frame, not as a calculator you can plug into an exam answer.

Pressure, shear, and friction

These three forces are not interchangeable on the exam or at the bedside.

Pressure is the perpendicular load. Shear occurs when bone moves one way and skin is held by the mattress or chair, stretching and angulating perforating vessels. Sliding down in bed with the head of bed well above 30 degrees is the classic shear setup. Friction damages the epidermis; it is a cofactor, not the full explanation for a Stage 3 or Stage 4 injury. The Braden friction-and-shear subscale exists because dragging, spasticity, and agitation repeatedly add epidermal injury on top of deep load.

Microclimate: heat and moisture

Microclimate is the temperature and humidity at the skin–support-surface interface. Moisture from urine, stool, wound drainage, or sweat macerates stratum corneum, reduces tensile strength, and increases friction. Heat raises local metabolic demand and sweating. Occlusive pads, plastic-backed linens, non-breathable chair cushions, and febrile diaphoresis all worsen microclimate. Moisture-associated skin damage can coexist with pressure injury; they are not the same diagnosis, but moisture lowers the threshold for pressure damage.

Bony prominences and typical positions

Always inspect skin under and around medical devices, not only these landmarks.

Medical devices as an etiology

Any object that concentrates load can cause a pressure injury: nasal cannulas, oxygen tubing, noninvasive-ventilation masks, nasogastric tubes, endotracheal-tube holders, pulse-oximetry probes, sequential-compression sleeves, antiembolism stockings, casts, traction, restraints, fecal-management systems, and tracheostomy ties. Device-related injuries may sit on soft tissue that is not a classic bony prominence. Pathophysiology is the same—deformation, ischemia, and microclimate—but the concentrating object is often the device pressing tissue against another structure rather than body weight against bone.

Scenario: the overnight injury after a reassuring score

A 68-year-old after vascular surgery has a Braden score of 19 on the floor. Overnight he is hypotensive on a vasopressor, remains on a non-breathable overlay, and is not turned because of a femoral sheath. By morning the sacrum is boggy and darker than surrounding skin. The score did not capture an acute perfusion and duration insult. Clinical judgment should have escalated prevention despite the number.

The Braden Scale

The Braden Scale for Predicting Pressure Sore Risk is the named adult tool you must know. Six subscales:

Each subscale is scored; lower totals mean higher risk. A common hospital at-risk cutoff is 18 or below. Some intensive-care protocols use 16. Know the tool by name and remember that the facility sets the protocol cutoff—do not treat 18 as a biologic constant. A score of 18 is not a milder wound than a score of 12; it is a screening threshold that should increase prevention intensity (turning, surfaces, moisture control, nutrition support), which later chapters develop.

Braden Q and Norton Plus

Braden Q is the pediatric adaptation. It retains the Braden logic and adds developmental and tissue-perfusion considerations used in infants and children. Do not apply the adult cutoff numbers blindly to a neonate; use the pediatric tool your facility specifies.

Norton Plus (an expanded Norton Scale) scores physical condition, mental condition, activity, mobility, and incontinence, then adds extra clinical items. Local forms may add points for diabetes, hypertension, or other comorbidities. Like Braden, lower scores indicate higher risk. Know the named domains; do not memorize every local extra-item list as if it were universal.

Timing and what a score cannot do

Reassess on admission, at regular intervals defined by policy, and with any significant condition change—transfer, operating room, shock, new device, new incontinence, drop in nutrition, or new immobility. Tools do not replace clinical judgment. A high score does not grant immunity during a four-hour procedure. A low score does not by itself prove that an existing wound is a pressure injury.

Limitations to respect:

• Over-prediction and under-prediction. Screening tools generate false positives and false negatives.
• Darkly pigmented skin. Visual erythema is an unreliable early cue; compare with adjacent skin and use temperature, induration, pain, and moisture change.
• Operating room and ICU. Acute hypotension, vasopressors, devices, and duration of immobility can injure tissue between scheduled scores.
• A score is not a stage. Risk tools estimate likelihood; they do not classify wound depth.

Scenario: pediatric transfer after a spine board

A 4-year-old is admitted from an outside emergency department after six hours on a spine board. Adult Braden is in the chart with a score of 20. Occipital skin is boggy. The correct tool is Braden Q, and a high adult number does not erase the intensity × duration load already delivered to the occiput.