Pressure Ulcers: Etiology, Demographics, and Risk Factors

A Detailed Report on Pressure Ulcers
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Pressure Ulcers
Etiology
Many etiologies have been identified as the root cause or preceding event following the formation of pressure ulcers. Typically, these form due to the increased pressure over the skin, especially over the bony prominences and the increased weight of the individual, leading to the decrease in blood flow in the area. The friction damages the skin, and the reduced blood flow decreases the healing process due to the lack of oxygen and nutrient delivery. Conversely, in patients with reduced sensory inputs, the lack of feedback due to pain results in prolonged exposure to pressure then the exact pathogenesis follows. The risk is enhanced by increased arteriole pressure, shearing forces, friction, and moisture (Mondragon & Zito, 2021).
Demographics
In the United States alone, the disease concerns over three million individuals annually, and the differences in the number of patients vary per institution. The disease is common in long-term care facilities and intensive care units (Mondragon & Zito, 2021). Studies revealed that after surgery, its overall prevalence is high at 18.96%. The gender difference revealed slightly more common in females than in males at 12.8% and 10.1%, respectively. This illustrated a 2.7% overall discrepancy (Shafipour et al., 2016). According to the meta-analysis conducted by Shiferaw et al. (2020), the disease is more common in Africa and Europe than in the other continents, with a 41.94% and 37.47% prevalence, respectively.
Risk Factors
Grada & Phillips (2021) enumerated the following risk factors for pressure ulcer formation: 1) The older population ages 65 and above are more likely to suffer from it secondary to the low amount of subcutaneous fat and reduced capillary blood flow. The former results in a decreased cushion of the skin, increasing the friction when in contact with a surface, while the latter results in reduced oxygen and nutrient delivery, slowing down the healing process.; 2) Lack of mobility is typically observed in patients in long-term care, critical care, or palliative care. This also involves patients who underwent surgery that required a prolonged hospital stay and bed rest and patients with cognitive and musculoskeletal impairment.; 3) Contact with skin irritants such as urine and feces in patients with incontinence; 4) Impaired sensation; 5) Compromised wound healing process.
Pathophysiology
The primary trigger for pressure ulcer formation is the prolonged pressure to the skin surface secondary to prolonged contact of the skin and another surface. The pressure typically exceeds the normal capillary pressure, which is between 12 to 32 mmHg. The soft tissues under the skin are injured due to ischemia in the area. The lack of pressure relief eventually leads to tissue death, significantly if the compression exceeds 4 hours. The effect is enhanced by the lack of oxygen and nutrient delivery for tissue repair (Mondragon & Zito, 2021; Grada & Phillips, 2021).
Consequently, the damaged area can also suffer more progressively from tissue reperfusion injury, where reactive oxygen species are formed when the blood supply is re-established after a period of ischemia. These substances stimulate an inflammatory response, enhancing the effect of ischemia. The lack of oxygen and nutrients in the area also predisposes the skin to infection, especially after wound formation (Mondragon & Zito, 2021; Grada & Phillips, 2021).
Clinical Presentation
Mayo Clinic (2020) enumerated the signs and symptoms of pressure ulcers, including the uncommon skin discoloration or changes in skin texture, warmth, swelling with tenderness upon palpation, redness, and yellowish discharges in a wound in areas where pressure sores are common.
It has six stages. Stage 1 can be seen as an area of non-blanchable redness that persists an hour after pressure relief. Stage 2 refers to the partial thickness of skin loss with the visible dermis. Stage 3 is illustrated by the subcutaneous tissue and/or muscle exposure with full-thickness skin loss. Stage 4 is the same as stage 3 but exposes deeper body parts such as the bones and tendons. The disease is unstageable when there is a presence of eschar, and it is difficult to assess the depth of the ulcer while it is classified as deep tissue when the skin is constantly non-blanchable or with evident purple discoloration even with pressure relief (Mondragon & Zito, 2021).
As mentioned, it affects between one to three million people in the United States yearly (Mondragon & Zito, 2021). Studies have shown that its prevalence is lower in the outpatient setting at 1.61% of the 75 168 elderly who consult the clinics. The prevalence increases with age, and the studies show that 4.2% of them are ages 85 and above. In Canada, the prevalence rate is higher in the hospitals at 4.5%, but it is highest in long-term care facilities at 36.8 to 53.2%. From these, the incidence rate ranges from 11.6% to 11.7% (Jaul et al., 2018).
Consequently, mortality is highly associated with age, existing comorbidities, and the length of stay in the facility. Typically, a pressure ulcer is not the ultimate cause of death. However, it compounds the risk of individuals and results in many complications. For instance, 40% of patients with advanced dementia suffer from pressure ulcers, which increase their risk of infection, ultimately leading to death (Jaul et al., 2018).
The prognosis of the disease varies per stage. Early-stage decubitus ulcers have excellent recovery with proper and timely treatment. The early stages heal in a few weeks or less. More than 70% of stage 2 ulcers, approximately 50% of stage 3 ulcers, and around 30% of stage 4 ulcers heal after six months of treatment. However, if proper treatment is significantly delayed and the patient suffers from complications, short-term and long-term prognoses are poor (Grada & Phillips, 2021).
Differential Diagnosis
The differential diagnoses are venous insufficiency, arterial insufficiency, diabetic ulcer, ulcer due to a malignancy, and hypertensive ulcer (Mondragon & Zito, 2021).
Diagnostic and Laboratory Tests: Rationale and Comparison Between Normal and Abnormal Test Results
The disease can be diagnosed clinically by inspection, palpation, and depth measurement via the National Pressure Injury Advisory Panel staging system. History and physical examination would also suffice in differentiating this from its differential diagnosis. Glycated hemoglobin (HbA1c) and the comprehensive metabolic panel are significant in ruling in or out diabetic and/or hypertensive ulcers. The components of the latter are as follows: 1) Fasting blood glucose. This should be done to know if the patient has diabetes.; 2) Fluid and electrolytes must be quantified to know the nutritional status of the patient...