PRESSURE ULCERS: SYMPTOMS, CAUSES, RISK, PREVENTION - MEDICINE - 2025

The pressure ulcers or bedsores are ischemic skin lesions generated by pressure or shearing forces. An injury that is due to a failure of blood circulation in the injured area is called ischemic. This circulatory failure, in this case, is due to an external compression of the blood vessel.

These ulcers are also called decubitus (lying position) ulcers because they appear in people who are lying in that position for a long time. They are frequent in the elderly who remain in the same position for many hours a day.

Most common sites for pressure ulcers (Source: BruceBlaus via Wikimedia Commons)

Pressure ulcers usually develop over bony prominences, such as the sacrum, heel, ankle, ischium (hip), and greater trochanters of the femur. The little coverage of fatty tissue in the area and the muscular atrophies favor capillary pressure occlusion.

In people who use a wheelchair or those who sit for a long time, these ulcers can appear on the coccyx or buttocks, on the scapulae and spine, and on the back of the arms and legs, that is, in the places of support in contact with the chair.

Pressure ulcers are classified into various stages according to their depth, the involvement of the skin and the underlying tissues. Damage to the skin and tissues can appear as red intact skin, up to deep lesions of the deeper layers of the underlying skin, muscle and bone.

Symptoms

Initial symptoms include unusual changes in skin color or texture, swelling or edema, pus-like discharge, regions of the skin that feel cooler or warmer than others, and local pain or tenderness.

The pressure ulcer or eschar begins as a reddening of the skin that worsens over time, which can be a matter of hours. In the area of ​​redness, when the damage is superficial, the layer of dead tissue forms what looks like a blister or sore that acquires a whitish color.

If the damage is deeper, areas of reddish-blue discoloration appear and finally a deep depression with an open wound that exposes the muscle or, in extreme cases, the bone.

Tissue necrosis initially begins with an inflammatory response, with pain, fever, and leukocytosis (increased numbers of white blood cells). Although bacteria can colonize dead tissue, the infection is generally self-limited.

Enzymatic proteolysis (destruction of proteins by enzymes) caused by bacteria and macrophages dissolves necrotic tissue and causes a foul-smelling discharge that looks like pus.

In patients who do not have sensation problems or neuropathies, the ulcers are very painful. If the ulcerative lesions are extensive, the toxicity and pain produce loss of appetite, weakness and can lead to kidney failure.

Immunosuppressed patients or those suffering from diabetes mellitus can develop infections and inflammation of the adjacent tissues such as cellulitis, which are severe skin infections and, rarely, septicemia, a pathology in which microorganisms pass into the circulatory stream and spread.

Causes

The cause of the appearance of decubitus ulcers is the continuous pressure exerted in the areas of bone prominence where the layer of adipose tissue (fatty tissue) and the muscle layer are very thin.

The pressure exerted on the skin can be applied in two ways: 1) forces applied parallel to the skin that are called shear or friction and 2) forces that are applied perpendicular to the surface of the skin.

Superficial ulcers usually appear in the sacrum or gluteal area due to shear or friction forces (forces applied parallel to the skin).

Pressure perpendicular to the skin tends to produce deeper ulcerative lesions that are frequently seen in bedridden patients. The areas frequently affected under these conditions are the heels, ankles and hips, the back of the skull and the skin that covers the shoulder blades.

The tissue underlying the site of continuous pressure is without flow and therefore does not obtain the oxygen necessary to survive. If the pressure subsides within a few hours, a brief period of reactive hyperemia (redness) will occur without further tissue damage.

If the pressure persists continuously without yielding, the endothelial cells of the capillaries are injured and the smooth endothelial surface is disrupted, exposing the collagen. This promotes platelet aggregation, forming micro-clots or microthrombi that interrupt circulation and generate necrosis (tissue death) in the surrounding tissues nourished by these vessels.

People at risk of suffering them

Two groups are distinguished among people at risk of suffering from pressure ulcers, those with illnesses that require or not hospitalization and those who are in intensive care units due to their critical condition.

First group

- Elderly patients hospitalized or in nursing homes.

- Neurological pathologies that occur with loss of mobility and / or sensitivity such as damage to the spinal cord, dementia and cerebrovascular diseases.

- Immobilization.

- Incontinence.

- Debilitating diseases.

- Patients who lie in bed without mobility or changes in position for long periods.

- Staying for hours or days in operator jobs or in front of computers.

- Chronic diseases that present with anemia, edema, kidney failure, malnutrition, sepsis, and fecal and / or urinary incontinence.

- Very thick sheets used on the bed that increase friction.

Second group

Risk factors for the appearance of pressure ulcers in critical or serious illnesses that require treatment in intensive care units (ICU) are included.

- Infusions of norepinephrine (drug that causes vascular constriction).

- Fecal incontinence.

-Anemia (decrease in red blood cells).

- Length of stay in the ICU, the longer the ICU hospitalization, the greater the risk.

- APACHE score II (Acute Physiology, Age, Chronic Health Evaluation II). It is a classification system for evaluating the severity of a disease used in many intensive care units.

Types

Ulcers can be staged according to the severity of the lesions on the skin and underlying tissues.

Stage I

Non-bleachable erythema on intact skin. It means that when the reddened skin is pressed it does not turn white. This is the first sign of the appearance of an eschar.

Stage II

Partial loss of skin thickness involving the epidermis or dermis. At this stage, a blister or an area of ​​skin abrasion appears.

Stage III

Total loss of thickness of the skin with damage or necrosis that involves the subcutaneous tissue and can extend to the underlying fascia, but does not exceed it. In this period an open lesion appears.

Stage IV

Total loss of skin thickness with extensive destruction, tissue necrosis, or damage to underlying tissues such as muscle, bone, and supporting structures such as tendons.

Stages of pressure ulcers (Source: Nanoxyde).push ({});

The prevention of bedsores consists of reducing the pressure avoiding prolonged support in the same position. Certain general measures are very useful, among them the following can be highlighted:

- Patients in bed should change position every two hours. If the patient is immobilized, he must be mobilized periodically in different positions.

- Pillows, foam pads and talcum powder can be attached to cushion the pressure.

- Maintain a balanced diet high in calories.

- Maintain good hydration.

- Keep the skin clean, dry and well lubricated.

-Use special mattresses called anti-decubitus mattresses.

Therefore, frequent mobilization with changes in position in bed, use of pressure reducing surfaces, maintenance of a good caloric and fluid intake are effective prevention techniques. Nutrition, oxygenation and water balance must be maintained.

If the patient can still move, it is necessary to motivate him and help him to change position and preferably stand up and walk, even for short periods. Walking and exercising, even if it is little, is essential for circulation, for the delay of muscular atrophies and to improve the quality of life of the elderly.

Treatment

The surface of the ulcers should be covered with flat, non-bulky, non-wrinkle dressings so that they do not increase friction or pressure. Spontaneous healing will occur faster if the ulcer is kept moist with an occlusive dressing. Applying tension for a range of mobilization can promote healing.

Antibiotic treatment is rarely required. Antiseptics such as hydrogen peroxide (hydrogen peroxide, H2O2) or iodine cause tissue granulation damage and should not be used. Successful healing requires continuous pressure relief.

Extensive and deep ulcers may require surgical debridement of necrotic tissue and placement of skin grafts to close the wound and promote effective healing.

References

1. Allman, RM, Goode, PS, Patrick, MM, Burst, N., & Bartolucci, AA (1995). Pressure ulcer risk factors among hospitalized patients with activity limitation. Jama, 273 (11), 865-870.
2. Ganong, WF, & Barrett, KE (2012). Ganong's review of medical physiology. McGraw-Hill Medical.
3. Lyder, CH (2003). Pressure ulcer prevention and management. Jama, 289 (2), 223-226.
4. McCance, KL, & Huether, SE (2002). Pathophysiology-Book: The Biologic Basis for Disease in Adults and Children. Elsevier Health Sciences.
5. Reddy, M., Gill, SS, & Rochon, PA (2006). Preventing pressure ulcers: a systematic review. Jama, 296 (8), 974-984.