Bedsores

Bedsores (decubitus - decubital ulcer) are chronic ulcers of soft tissues that occur in patients with impaired sensitivity (usually in a motionless state) due to compression, friction or displacement of the skin, or as a result of a combination of these factors.

ICD-10 code

L89. Bedsores

Epidemiology

The incidence of pressure ulcers in hospitalised patients ranges from 2.7% to 29%, reaching 40-60% in patients who have suffered a spinal cord injury. In health and preventive care settings in England, pressure ulcers develop in 15-20% of patients. The provision of quality care, carried out by specially trained nurses, can reduce the incidence of this complication to 8%.

Treatment of patients with bedsores is a serious medical and social problem. As bedsores develop, the duration of the patient's hospital stay increases, and there is a need for additional dressings and medications, instruments, and equipment. In some cases, surgical treatment of bedsores is required. The estimated cost of treating bedsores for one patient in the United States ranges from $5,000 to $40,000. In the UK, the cost of caring for patients with bedsores is estimated at £200 million, increasing by 11% annually.

In addition to the economic costs associated with the treatment of bedsores, it is necessary to take into account the intangible costs: severe physical and mental suffering experienced by the patient. The occurrence of bedsores is often accompanied by severe pain syndrome, depression, infectious complications (abscess, purulent arthritis, osteomyelitis, sepsis). The development of bedsores is accompanied by an invariably high mortality rate. Thus, the mortality rate of patients admitted to nursing homes with bedsores, according to various sources, ranges from 21 to 88%.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ], [ 6 ], [ 7 ]

Why do bedsores occur?

Bedsores are most often found in patients who have been immobilized for a long time, who are in a forced position after an injury, with oncological and neurological pathology, in elderly and senile people with severe medical diseases, as well as in patients who have been treated for a long time in intensive care units.

The main factors leading to the development of bedsores are pressure, displacement and friction forces, high humidity. Risk factors include limited motor activity of the patient, malnutrition or obesity, urinary and fecal incontinence, defects in care, concomitant diseases such as diabetes, paralysis and cancer. A significant risk factor is the male gender and the age of the patient. In patients over 70 years of age, the risk of developing bedsores increases sharply. Among social factors, it is worth noting the shortage of service personnel.

Pressure ulcers are areas of tissue necrosis that occur in weakened individuals as a result of compression of soft tissues directly adjacent to bones and bony prominences by the body. Prolonged exposure to continuous pressure leads to local tissue ischemia. It has been experimentally and clinically established that pressure of 70 mm Hg applied to tissues continuously for two or more hours leads to irreversible changes in the tissues. However, with periodic exposure to pressure of even greater force, tissue damage is minimal.

The combined effect of pressure and displacement forces causes blood flow disturbances with the development of irreversible tissue ischemia and subsequent necrosis. Muscle tissues are most sensitive to ischemia. Pathological changes develop first in the muscles located above the bone protrusions, and only then do they spread towards the skin. The addition of infection aggravates the severity of ischemic tissue damage and promotes rapid progression of the necrosis zone. The resulting skin ulcer is in most cases a kind of tip of the iceberg, while 70% of all necrosis is located under the skin.

Risk factors for developing pressure ulcers

One of the main stages of pressure ulcer prevention is to identify patients at high risk. Pressure ulcer risk factors can be reversible and irreversible, internal and external. Internal reversible risk factors include exhaustion, limited mobility, anemia, poor nutrition, insufficient intake of ascorbic acid, dehydration, hypotension, urinary and fecal incontinence, neurological disorders, impaired peripheral circulation, thin skin, anxiety, confusion and coma. External reversible risk factors include poor hygiene, folds in bed and underwear, bed rails, use of patient restraints, injuries to the spine, pelvic bones, abdominal organs, spinal cord injuries, use of cytostatic drugs and glucocorticoid hormones, improper technique for moving the patient in bed. External risk factors for pressure ulcer development also include extensive surgery lasting more than 2 hours.

Various scales provide significant assistance in assessing the risk of developing pressure ulcers. The most widely used is the J. Waterlow scale. In immobile patients, the risk of developing pressure ulcers is assessed daily, even if it was no more than 9 points during the initial examination. Anti-pressure measures begin immediately when a high risk of their development appears.

The points on the J. Waterlow scale are summed up. The degree of risk is determined by the following final values:

• no risk - 1-9 points;
• there is a risk - 10-14 points;
• high risk - 15-19 points;
• very high risk - more than 20 points.

Symptoms of Bedsores

The localization of bedsores can be extremely diverse. The frequency of detection of the location of bedsores depends on the specialization of the clinic or department. In multidisciplinary hospitals, the vast majority of patients develop bedsores in the sacrum area. Quite often, the area of the greater trochanter, heels and ischial tuberosities is affected. In rarer cases, a decubital ulcer occurs in the area of the shoulder blades, lateral surfaces of the chest, bony protrusions of the spine, extensor surfaces of the knee joints and on the back of the head. Multiple bedsores occur in 20-25% of cases.

At the beginning of the development of bedsores, local pallor, cyanosis and swelling of the skin appear. Patients complain of a feeling of numbness and minor pain. Later, the epidermis peels off with the formation of blisters filled with turbid serous-hemorrhagic exudate, and necrosis of the skin and underlying tissues occurs. Infection aggravates the severity of necrotic tissue damage.

Clinically, bedsores occur as dry or wet necrosis (decubital gangrene). When a bedsore develops as dry necrosis, the wound looks like a dense necrotic scab with a more or less distinct demarcation line of non-viable tissue. Due to the weak pain syndrome and mild intoxication, the general condition of the patient does not suffer significantly. A more severe clinical picture is observed when a bedsore develops as wet necrosis. The zone of deep irreversible tissue ischemia does not have a clear boundary, progresses rapidly, spreading not only to the subcutaneous tissue, but also to the fascia, muscles, and bone structures. The surrounding tissues are edematous, hyperemic or cyanotic, and are sharply painful upon palpation. A foul-smelling purulent gray discharge comes from under the necrosis. Symptoms of severe intoxication with a rise in body temperature to 38-39 °C and higher, accompanied by chills, tachycardia, shortness of breath and hypotension are noted. The patient becomes drowsy, apathetic, refuses to eat, and is delirious. Blood tests reveal leukocytosis, increased ESR, progressive hypoproteinemia and anemia.

Classification

There are several classifications of pressure ulcers, but at present the most widely used is the classification adopted in 1992 by the Agency for Health Care Policy and Research (USA), which most clearly reflects the dynamics of local changes in the area of pressure ulcers:

• Grade I - erythema that does not spread to healthy areas of the skin; damage preceding ulceration;
• Grade II - partial decrease in skin thickness associated with damage to the epidermis or dermis; superficial ulcer in the form of an abrasion, blister or shallow crater;
• Grade III - complete loss of skin thickness due to damage or necrosis of the tissues located underneath it, but not deeper than the fascia;
• Grade IV - complete loss of skin thickness with necrosis or destruction of muscles, bones and other supporting structures (tendons, ligaments, joint capsules).

Classification of bedsores by size:

• fistula form - a small skin defect with a significant, deeper cavity; often accompanied by osteomyelitis of the underlying bone;
• small bedsore - diameter less than 5 cm;
• medium bedsore - diameter from 5 to 10 cm;
• large bedsore - diameter from 10 to 15 cm;
• giant bedsore - diameter more than 15 cm.

According to the mechanism of occurrence, bedsores are classified as exogenous, endogenous and mixed. Exogenous bedsores develop as a result of prolonged and intense exposure to external mechanical factors leading to tissue ischemia and necrosis (for example, a bedsore as a result of tissue compression by a plaster cast or a bedsore of the sacrum in a patient who has been immobile for a long time). Elimination of the causes that caused the bedsore usually promotes the development of reparative processes and its healing. Endogenous bedsores develop due to disruption of the body's vital functions, accompanied by neurotrophic changes in tissues as a result of diseases and injuries to the central and peripheral nervous system (for example, in patients with spinal cord injury and stroke). Healing of such bedsores is possible with an improvement in the general condition of the body and tissue trophism. Mixed bedsores develop in patients weakened and exhausted by a serious illness, alimentary cachexia. The inability to independently change the body position as a result of prolonged tissue compression leads to ischemic damage to the skin in the area of bony protrusions and the formation of bedsores.

A distinction is also made between external and internal bedsores. External bedsores develop in the area of the skin. Internal bedsores occur in various areas of the mucous membranes that are subject to prolonged compression by foreign bodies (drainages, catheters, prostheses and stents) and endogenous formations (gallstones). Internal bedsores can lead to perforation of the organ wall with the development of an internal fistula, peritonitis, phlegmon and other complications.

Bedsore complications aggravate the condition of patients, worsen the prognosis of the disease, in most cases posing a real threat to the patient's life, becoming one of the main causes of death of patients. These include:

• contact osteomyelitis of the underlying bone;
• purulent arthritis and tendonitis;
• erosive bleeding;
• malignancy;
• phlegmon;
• sepsis.

Osteomyelitis occurs in almost 20% of patients with bedsores. The most commonly affected areas are the sacrum, coccyx, ischial tuberosity, calcaneus, and occipital bones. The most severe bone-articular destructive changes occur in patients with bedsores in the greater trochanter area. Osteomyelitis of the greater trochanter develops, and in more severe cases - purulent coxitis, osteomyelitis of the femoral head and pelvic bones. The diagnosis is established based on a visual assessment of the bone, which acquires a dull appearance, has a gray color, lacks periosteum, is saturated with purulent exudate, becomes fragile upon contact, and bleeds little. If diagnostic difficulties arise, X-ray examination, fistulography, CT and MRI are used. It should be noted that clear X-ray data appear in the late stages of osteomyelitis with extensive bone lesions and sequestration.

Phlegmon is the most severe complication of bedsores. It develops in 10% of patients with bedsores and is the main reason for emergency hospitalization of patients. Phlegmon mainly complicates the course of bedsores, which occur as wet necrosis. In this case, a significant deterioration in the patient's condition is noted, symptoms of a systemic inflammatory reaction, pain syndrome progress, signs of organ dysfunction develop. Local changes have negative dynamics. Perifocal inflammatory changes increase significantly. Hyperemia, edema and tissue infiltration spread over a significant area; cyanotic spots and blisters appear both on the skin around the bedsore and at a distance from it. With a large accumulation of pus, fluctuation can be determined, and with an anaerobic nature of the infection, tissue crepitation appears. Phlegmon usually develops as a result of delayed surgical treatment during the development of wet decubital gangrene. The purulent-necrotic process begins in the deep layers of soft tissues, progresses rapidly and is accompanied by severe destructive changes in the tissues with the development of necrotic dermatocellulitis, fasciitis and myonecrosis. In more than 80% of all cases of phlegmon, it occurs in patients with sacral bedsores. The purulent process can spread to the gluteal and lumbar regions, perineum, and back of the thigh. In the vast majority of cases, the purulent-necrotic process is caused by polyvalent microflora. The main role is played by microbial associations consisting of Staphylococcus aureus, Streptococcus spp., Enterococcus spp., bacteria from the genus Enterobacteriaceae, Pseudomonas aeruginosa, anaerobic clostridial and non-clostridial infections. In exhausted weakened elderly and senile patients, the mortality rate in the event of phlegmon against the background of a bedsore exceeds 70%.

Sepsis occurs at one or another stage of deep pressure ulcers (grades III-IV) in approximately 70% of patients. In 24%, it is accompanied by bacteremia, which is polyvalent in more than 50% of cases. In the group of patients with persistent bacteremia associated with pressure ulcers, the prognosis for life becomes extremely unfavorable, and the mortality rate is at least 50-75%.

[ 8 ], [ 9 ]

What is the prognosis for bedsores?

The prognosis and treatment outcomes of bedsores are closely related to the underlying disease against which the decubital ulcer developed. In bedridden patients with severe somatic pathology or mental illness, the appearance of bedsores becomes an unfavorable sign for life. In intensive care patients on mechanical ventilation, the formation of bedsores adequately reflects the unfavorable course of the underlying disease with the progression of multiple organ failure and serves as a poor prognostic sign.

The prognosis for ulcer closure in external exogenous bedsores is usually favorable, since after stopping tissue compression and prescribing appropriate therapy, it is possible to achieve a cure relatively quickly. The prognosis for endogenous and mixed bedsores is usually serious, since the patient's condition is significantly aggravated by the underlying disease. The development of invasive infection reduces the chances of a favorable outcome. Spontaneous healing of bedsores is rare, and in the case of their spontaneous or surgical closure, the risk of ulcer relapse or the formation of new ones is high, since the risk factors for the development of bedsores remain.