Ulkus Dekubitus

01Pathophysiology

Pressure ulcers develop when sustained external pressure exceeds capillary closing pressure (approximately 32 mmHg in arteriolar limbs). When a patient lies or sits on a bony prominence without relief, the tissue between the bone and the external surface is compressed. This compression occludes capillary blood flow, leading to local tissue ischemia. If the pressure is not relieved, ischemia progresses to cell death and tissue necrosis.

The injury pattern is often described as an inverted cone or iceberg model: the greatest pressure and earliest damage occur at the bone-tissue interface (deep tissue), while the skin surface may initially appear intact. This is why a small surface wound can overlie a much larger area of deep tissue destruction. This concept is tested frequently because it explains why Stage 4 ulcers can present with deceptively small openings.

Shear forces contribute significantly. When the head of the bed is elevated, gravity pulls the body downward while the skin remains adhered to the bed surface. The underlying fascia and deep tissue slide relative to the skin, distorting and tearing blood vessels in the subcutaneous plane. This is why the sacrum is the single most common location for pressure ulcers in bedridden patients, and the ischial tuberosity is the most common location in wheelchair-bound patients.

Friction damages the epidermis directly (dragging a patient across bed sheets). Moisture from incontinence causes skin maceration, lowering the threshold for mechanical breakdown. These factors act synergistically with pressure to accelerate ulcer formation.

Malnutrition is a critical modifiable risk factor. A serum albumin below 3.5 g/dL or a prealbumin below 15 mg/dL indicates protein-calorie malnutrition, which impairs collagen synthesis, immune response, and wound healing. On the exam, a vignette describing a malnourished, immobile patient with a wound over a bony prominence is pointing directly at this diagnosis.

02Classification and Clinical Manifestation

The staging system used is the National Pressure Injury Advisory Panel (NPIAP) classification. This is the standard framework tested on licensing exams.

Key testing points about staging:

Stage 1 is the only stage where the skin remains intact. If a vignette describes broken skin, it is at minimum Stage 2. Stage 3 and Stage 4 are differentiated by whether bone, tendon, or muscle is visible. If you can see bone, it is Stage 4. If you see fat but no bone, it is Stage 3. An unstageable ulcer is not "worse" than Stage 4; it simply means the wound bed is covered and the true depth cannot yet be assessed. Pressure ulcers do not "reverse stage" during healing. A healing Stage 4 ulcer does not become Stage 3, then Stage 2. It is documented as a "healing Stage 4" ulcer. This is a commonly tested principle.

03Diagnostic Workup

Pressure ulcer is fundamentally a clinical diagnosis. No lab test or imaging study is needed to make the diagnosis. You look at the wound, identify its location over a bony prominence, and stage it based on tissue involvement.

The diagnostic workup beyond inspection focuses on two key questions the exam will test:

First: Is the patient malnourished? Serum albumin (half-life approximately 20 days) reflects chronic nutritional status. Prealbumin (half-life approximately 2 to 3 days) is more sensitive to acute changes and is the better marker to track whether nutritional interventions are working. If a vignette gives you a low albumin in a patient with a non-healing wound, the tested answer is nutritional optimization.

Second: Is there underlying osteomyelitis? This is the critical complication to evaluate in Stage 3 and Stage 4 ulcers. If bone is visible at the wound base, or if a sterile metal probe can touch bone (positive "probe-to-bone" test), the likelihood of osteomyelitis is high. The best initial imaging test is a plain radiograph, which may show cortical erosion or periosteal reaction. However, X-ray changes lag behind the actual infection. MRI is the most accurate non-invasive test for osteomyelitis, with high sensitivity and specificity. Bone biopsy with histopathology and culture is the definitive gold standard for both confirming osteomyelitis and identifying the pathogen to guide antibiotic selection.

Do not order wound cultures routinely. All chronic wounds are colonized with bacteria, and a positive surface swab does not mean infection. Cultures are indicated only when there are clinical signs of infection. When cultures are needed, deep tissue biopsy or quantitative wound cultures are preferred over superficial swabs.

04Management and Treatment

Acute stabilization begins with pressure offloading. The single most important step in managing any pressure ulcer is to relieve the pressure causing it. Patients must be repositioned at least every 2 hours. Pressure-redistribution mattresses (alternating-pressure or low-air-loss) should replace standard hospital mattresses for at-risk patients. For wheelchair-bound patients, pressure relief every 15 minutes and use of specialized cushions is recommended.

Wound management follows the principle of maintaining a moist wound environment. A moist (not wet, not dry) wound bed promotes granulation tissue formation and epithelial migration. The dressing choice depends on wound characteristics: hydrocolloids for clean, minimally exudative wounds; alginates or hydrofibers for wounds with heavy drainage; foam dressings for moderate exudate; and hydrogels for dry wound beds that need hydration. Wet-to-dry dressings are considered outdated for routine wound care because they cause non-selective tissue damage during removal.

Debridement is required when necrotic or devitalized tissue is present, as dead tissue serves as a medium for bacterial growth and physically blocks wound healing. Sharp surgical debridement is the fastest method. Enzymatic debridement (e.g., collagenase) is an alternative for patients who are not surgical candidates. The one critical exception: stable, dry, intact eschar on the heel should be left in place as a biological cover unless there are signs of infection (fluctuance, erythema, drainage, odor). This exception is a high-yield testing point.

Nutritional optimization is not optional. It is a required component of the management plan. Protein supplementation (1.25 to 1.5 g/kg/day) and correction of vitamin C and zinc deficiencies are standard. If a vignette describes a non-healing wound and a low albumin, the next best step is to address nutritional status.

Surgical flap closure is reserved for large, deep (Stage 3 or 4) ulcers that have failed conservative management. Prerequisites include adequate nutrition, absence of active infection, and the patient being a reasonable surgical candidate. This is a definitive treatment but carries a recurrence rate if the underlying risk factors (immobility, malnutrition) are not addressed.

05Differential Diagnosis and Distractors

The most commonly tested distractor is the venous stasis ulcer. Both conditions affect elderly, relatively immobile patients. The discriminating feature is location: pressure ulcers occur over bony prominences subjected to sustained pressure (sacrum, heel, ischium), while venous ulcers occur over the medial malleolus in the gaiter zone with surrounding skin changes from chronic venous insufficiency.

The second common distractor is the arterial ulcer. The key differentiator is the presence of peripheral arterial disease signs: absent pulses, claudication history, and an abnormal ankle-brachial index. Arterial ulcers have a punched-out appearance and are exquisitely painful, often worse with leg elevation.

06Traps and High-Yield Pearls

The most common trap with pressure ulcers on an exam involves staging errors. Students frequently confuse Stage 3 and Stage 4 because they focus on wound size rather than depth of tissue involvement. The distinction is straightforward: if bone, tendon, or muscle is exposed or palpable, it is Stage 4. If subcutaneous fat is visible but deeper structures are not, it is Stage 3. Size is irrelevant to staging.

A second common mistake involves the unstageable ulcer. Students sometimes assume that if a wound is covered in eschar, it must be the most severe stage. Unstageable simply means the base cannot be visualized due to slough or eschar, so the true stage is unknown. The next best step is debridement to reveal the wound bed and allow accurate staging, with the heel eschar exception described above.

Another frequently tested concept is the "reverse staging" error. Pressure ulcers do not heal by progressing backward through the stages. A Stage 4 ulcer heals by filling with granulation tissue and contracting, but it remains classified as a "healing Stage 4 ulcer." Calling it a Stage 2 because it looks shallow during healing is incorrect.

The core competency being tested across questions on this topic is the ability to identify the modifiable risk factors (pressure, nutrition, moisture, friction) and sequence the management correctly. The tested logic is: relieve the pressure first, assess and optimize nutrition, manage the wound with appropriate moist dressings and debridement, evaluate for osteomyelitis in deep ulcers, and consider surgical intervention only when conservative measures have failed and the patient is optimized. Questions will reward you for recognizing that a non-healing wound with low albumin requires nutritional support before (or in addition to) any procedural intervention.