Pressure ulcers


Epidemiology

A pressure ulcer is any wound that develops in the upper, outer layers of the skin as a result of sustained, external pressure. Pressure ulcers are serious complications among hospitalized patients. They increase healthcare costs, decrease patient quality of life, and often result in prolonged hospital stays. Hospital-acquired pressure ulcers are generally considered to be preventable, and if allowed to progress to full-thickness skin loss must be reported as “never events” to the Centers for Medicare & Medicaid Services. Current estimates of the prevalence of pressure ulcers among hospital patients are highly variable but have been decreasing across the United States. In the largest investigation to date, the incidence of hospital-acquired pressure ulcers is 4.5% and the prevalence of pressure ulcers on admission is 5.8%. More significantly, in those admitted with a previously acquired pressure ulcer, almost one in five patients developed an additional pressure ulcer at a different site during their hospital stay. , The prevalence of pressure ulcers is even higher among residents of long-term geriatric facilities, occurring in up to 30% of patients. Whereas the majority of the ulcers (50%) in hospitalized patients are stage I, the prevalence of stage III and IV ulcers is estimated to be as high as 4% in patients who reside in long-term care facilities.

Pressure ulcers result in a substantial financial burden, with an estimated cost ranging from $3.3 billion to $11 billion per year. , The Centers for Medicare & Medicaid Services has reduced the reimbursement for hospital-acquired pressure ulcers, with a single episode costing hospitals $500 up to $70,000.

Risk factors

There are multiple risk factors for the development of pressure ulcers; they can be categorized as intrinsic and extrinsic. Intrinsic risk factors are those related to the patient’s preexisting medical condition. Extrinsic factors are those related to the patient’s environment. Intrinsic risk factors include neurologic disease, motor impairment, cognitive impairment, sensory deficits, malnutrition, and hypoperfusion caused by peripheral vascular disease or congestive heart failure. Extrinsic risk factors include inadequate mobilization by care providers, trauma, sedation, application of physical restraints, improper positioning (especially among patients under general anesthesia), moisture, and shearing forces. Among these risk factors, failure to frequently change position is thought to be the biggest contributor to pressure ulcer formation. The combination of improper positioning and moisture at the skin surface is a frequent cause of pressure ulcer formation in critically ill patients.

Because of the underlying pathophysiology of pressure ulcer formation, there are several high-risk areas for the development of pressure ulcers. Pressure ulcers are more prone to develop in bony or cartilaginous areas. These include any area of the body that has limited soft tissue coverage such as the coccyx, spinous processes, heels, elbows, and ankles. In patients who are frequently positioned on their side, the iliac crest and trochanters are considered high-risk areas. Additionally, patients with malnutrition and subsequent cachexia have significant loss of soft tissue and are more prone to the development of pressure ulcers at any location. Medical devices can also be associated with the development of pressure ulcers. Examples include masks for noninvasive positive-pressure ventilation, cervical collars, endotracheal tubes, nasogastric tubes, and nasal cannula tubing.

Pathophysiology

Pressure ulcers form as a result of hypoperfusion to an area. The basic principle of pressure ulcer development is simple. When externally applied pressure exceeds the capillary perfusion pressure, flow becomes impaired and tissue ischemia occurs. If the hypoperfusion and ischemia are not reversed, necrosis of the involved tissue layers will occur. Ischemia to the area will initially present with erythema and induration. If this progresses to necrosis, tissue loss will occur. The critical duration of ischemia varies from patient to patient. However, it is generally accepted that pressure injury typically occurs between 30 and 240 minutes of hypoperfusion. In patients with preexisting peripheral vascular disease, the time to critical ischemia is shorter. Because of impaired arterial inflow, these patients experience significant delays in restoration of perfusion and reversal of tissue hypoxia after the external pressure has been removed. In addition, because of poor underlying tissue perfusion, these patients will experience longer healing times once pressure ulcers develop.

Classification

All pressure ulcers begin in the outer layers of the skin. With ongoing pressure, the ischemia progressively extends to deeper layers of the skin. Therefore the classification of pressure ulcers is based on the depth of skin involvement. Pressure ulcers are classified as stage I through IV, with stage I being the most superficial and stage IV being the deepest. The classification of pressure ulcers is listed in Table 154.1 . Having a uniform, well-defined classification system for pressure ulcers is critical. It not only allows for standardization of wounds for research purposes but also allows for accurate communication of wound staging among healthcare providers. Once a pressure ulcer develops, it is important to classify the wound and monitor the progress of the wound bed. Having a standard grading system allows for continuity of care and objective monitoring of the progression of the wound.

TABLE 154.1
Pressure Ulcer Staging
National Pressure Ulcer Staging System
Stage I Nonblanching erythema of intact skin.
Stage II Partial-thickness skin loss involving the epidermis and/or dermis. The ulcer is superficial and presents clinically as an abrasion, blister, or shallow crater.
Stage III Full-thickness skin loss with damage and/or necrosis of the subcutaneous tissue. The wound extends down to, but not through, the underlying fascia.
Stage IV Full-thickness skin loss with extensive destruction and necrosis of overlying structures, including muscles, bone, or tendon

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