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Bedsores
Last reviewed: 23.04.2024
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Decubitus (decubitus - decubitus ulcer) - chronic soft tissue ulcers that occur in patients with impaired sensation (usually in a stationary 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 hospitalized patients ranges from 2.7 to 29%, reaching 40-60% in patients who underwent spinal cord and spinal cord injury. Bedsores are formed in 15-20% of patients in nursing homes in England. Organization of quality care, which is specially trained nurses, can reduce the incidence of this complication to 8%.
Treatment of patients with bedsores is a serious medical and social problem. With the development of pressure ulcers, the length of hospitalization of the patient increases, there is a need for additional dressings and medicines, tools, equipment. In some cases, surgical treatment of decubituses is required. The estimated cost of treatment for decubituses in one patient in the United States ranges from $ 5,000 to $ 40,000. In the UK, the costs of caring for patients with bedsores are estimated at £ 200 million, they increase by 11% annually.
In addition to the economic costs associated with the treatment of bedsores, it is also necessary to take into account the non-material costs: severe physical and mental suffering experienced by the patient. The occurrence of pressure sores is often accompanied by severe pain syndrome, depression, infectious complications (abscess, purulent arthritis, osteomyelitis, sepsis). The development of pressure ulcers is accompanied by invariably high lethality. Thus, the mortality rate among patients admitted to nursing homes with bedsores is from 21 to 88%, according to various sources.
Why do bedsores occur?
The most commonly bedsores are found in long-stalled patients who are in a forced position after a trauma, with oncological and neurological pathology, in elderly and senile patients with severe therapeutic illnesses, as well as in patients who are long-term in intensive care units.
The main factors leading to the development of pressure sores, are the forces of pressure, displacement and friction, increased humidity. The risk factors include limited motor activity of the patient, malnutrition or obesity, incontinence of urine and feces, defects in care, concomitant diseases such as diabetes, paralysis and cancer. A significant risk factor is belonging to the male sex and age of the patient. In patients older than 70 years, the risk of bedsores increases dramatically. Of social factors, it should be noted the shortage of staff.
Ulcers that result from pressure sores are areas of tissue necrosis that occur in weakened individuals as a result of compression by the body of soft tissues directly adjacent to the bones and bony protuberances. Continuous exposure to continuous pressure leads to local tissue ischemia. It has been experimentally and clinically established that a pressure of 70 mm Hg "applied to the tissue continuously for two or more hours leads to irreversible changes in the tissues. However, with a periodic effect of pressure, even greater force, tissue damage is minimal.
The cumulative effect of pressure and displacement forces causes blood flow disorders with the development of irreversible tissue ischemia and subsequent necrosis. Muscular tissues are most sensitive to ischemia. In the muscles located above the bony protuberances, first of all, pathological changes develop, and only then they spread towards the skin. Attachment of infection aggravates the severity of ischemic tissue damage and promotes rapid progression of the necrosis zone. The resulting skin ulcer in most cases is a kind of tip of the iceberg, while 70% of all necrosis is located under the skin.
Risk factors for the development of pressure sores
One of the main stages of prophylaxis of bedsores is to identify patients at high risk. The risk factors for the development of pressure sores can be reversible and irreversible, internal and external. Internal reversible risk factors are depletion, limited mobility, anemia, poor nutrition, insufficient intake of ascorbic acid, dehydration, hypotension, urinary and fecal incontinence, neurological disorders, impaired peripheral circulation, thinned skin, anxiety, confused consciousness and coma. The external reversible risk factors include poor hygienic care, folds on bed and underwear, bed grips, use of patient fixation, spine trauma, pelvic bones, abdominal organs, spinal cord injuries, the use of cytostatic drugs and glucocorticoid hormones, improper technique of movement patient in bed. To external factors of risk of development of decubituses carry also extensive surgical intervention lasting more than 2 hours.
Various scales provide significant assistance in assessing the risk of developing pressure ulcers. The most widely used scale is J. Waterlow. In still patients, the risk of developing decubitus is assessed on a daily basis, even if the initial examination did not exceed 9 points. Anti-bedsore measures begin immediately when there is a high risk of their development.
Points on the J. Waterlow scale are summarized. The degree of risk is determined by the following final values:
- no risk - 1-9 points;
- there is a risk of 10-14 points;
- high degree of risk - 15-19 points;
- a very high degree of risk - more than 20 points.
Symptoms of pressure sores
The localization of pressure sores can be extremely diverse. The frequency of the location of decubitus ulcers depends on the specialization of the clinic or department. In multidisciplinary hospitals, in the vast majority of patients, bedsores are formed in the sacrum. It is often enough to affect the area of a large trochanter, heels and sciatic tubercles. In more rare cases, a decubital ulcer occurs in the region of the scapula, the lateral surfaces of the thorax, the bony protrusions of the spine, the extensor surfaces of the knee joints and the occiput. Multiple bedsores occur in 20-25% of cases.
At the beginning of development of pressure sores, local pallor, cyanosis and puffiness of the skin appear. Patients complain of a feeling of numbness and a slight soreness. Later comes the detachment of the epidermis with the formation of bubbles filled with turbid serous-hemorrhagic exudate, necrosis of the skin and the glibrous tissues. Infection exacerbates the severity of necrotic tissue damage.
Clinically, pressure ulcers proceed according to the type of dry or wet necrosis (decubital gangrene). With the development of bedsores by the type of dry necrosis, the wound looks like a dense necrotic scab with a more or less distinct line of demarcation of nonviable tissues. In view of the weak pain syndrome and unexplained intoxication, the general condition of the patient does not substantially suffer. A more severe clinical picture is observed in the development of bedsores by the type of wet necrosis. The zone of deep irreversible tissue ischemia does not have a clear boundary, it rapidly progresses, spreading not only to the subcutaneous tissue, but also to the fascia, muscles, and bone structures. The surrounding tissues are edematous, hyperemic or cyanotic, sharply painful on palpation. From under the necrosis, a fetid, purulent discharge of gray color is abundantly supplied. There are symptoms of severe intoxication with a rise in body temperature to 38-39 ° C and higher, accompanied by chills, tachycardia, dyspnea and hypotension. The patient becomes drowsy, apathetic, refuses to eat, raves. When analyzing blood determine leukocytosis, increased ESR, progressive hypoproteinemia and anemia.
Classification
There are several classifications of pressure ulcers, but now the most widely accepted classification is the 1992 Agency for Health Care Policy and Research (USA), which most clearly reflects the dynamics of local changes in the area of decubitus ulcers:
- I degree - erythema, not extending to healthy skin areas; damage prior to ulceration;
- II degree - partial reduction of skin thickness, associated with damage to the epidermis or dermis; a superficial ulcer in the form of an abrasion, a bladder or a shallow crater;
- III degree - complete loss of skin thickness due to damage or necrosis of tissues located beneath it, but not deeper than the fascia;
- IV degree - complete loss of skin thickness with necrosis or destruction of muscles, bones and other supporting structures (tendons, ligaments, capsules of joints).
Classification of bedsores by size:
- fistulous form - a slight skin defect with a significantly deeper located cavity; often accompanied by osteomyelitis of the underlying bone;
- a small bedsore - a diameter of less than 5 cm;
- average decubitus - diameter from 5 to 10 cm;
- a large decubitus - a diameter of 10 to 15 cm;
- a giant decubitus - a diameter of more than 15 cm.
Exogenous bedsores, endogenous and mixed are distinguished by the mechanism of their appearance. Exogenous bedsores develop as a result of prolonged and intensive exposure to external mechanical factors leading to ischemia and necrosis of tissues (for example, bedsore as a result of tissue squeezing with a plaster bandage or a sacral sore from a patient permanently stationary). Eliminating the causes of bedsore, usually contributes to the development of reparative processes and its healing. Endogenous bedsores develop due to disruption of the body's activity, accompanied by neurotrophic changes in tissues due to diseases and injuries of the central and peripheral nervous system (for example, in patients with spinal trauma and stroke). Healing of such bedsores is possible with an improvement in the general condition of the body and trophic tissue. Mixed bedsores develop in patients weakened and emaciated by a serious illness, alimentary cachexia. The impossibility of self-altering the position of the body as a result of prolonged compression of tissues leads to ischemic damage to the skin in the region of the bony projections and the formation of pressure sores.
There are also external and internal pressure sores. External bedsores develop in the area of skin. Internal pressure ulcers occur in various parts of the mucous membranes that are subjected to prolonged compression by foreign bodies (drains, catheters, prostheses and stents) and endogenous formations (concrement of the gallbladder). Internal pressure sores can lead to perforation of the organ wall with the development of internal fistula, peritonitis, phlegmon and other complications.
Complications of decubituses heavier the condition of patients, worsen the prognosis of the disease, for the most part presenting a real threat to the life of the patient, becoming one of the main causes of death of patients. They include:
- contact osteomyelitis of the underlying bone;
- purulent arthritis and tendonitis;
- erosive bleeding;
- malignization;
- phlegmon;
- sepsis.
Osteomyelitis occurs in almost 20% of patients with bedsores. Most often, the sacrum, the bone of the coccyx, the ischial tubercle, the heel, the occipital bone are affected. The most severe bone-joint destructive changes occur in patients with bedsores of the large trochanter. Osteomyelitis of the large trochanter develops, and in more severe cases - purulent coke, osteomyelitis of the head of the femur and pelvic bones. The diagnosis is made on the basis of a visual evaluation of the bone, which becomes dull, has a gray color, is devoid of periosteum, impregnated with purulent exudate, becomes brittle on contact, bleeds little. In case of difficulties in diagnosis, radiographic examination, fistulography, CT and MRI are used. It should be noted that clear roentgenological data appear in the late periods of osteomyelitis with extensive bone lesions and sequestration.
Phlegmon is the most severe complication of decubitus. It develops in 10% of patients with bedsores, and is the main reason for emergency hospitalization of patients. Phlegmon in the main complicates the course of pressure ulcers, proceeding according to the type of moist necrosis. In this case, a significant deterioration in the condition of patients is noted, symptoms of systemic inflammatory reaction, pain syndrome, signs of organ dysfunction develop. Local changes have a negative dynamics. Significantly increased peri-focal inflammatory changes. Hyperemia, edema and infiltration of tissues spread over a considerable area; as on the skin around the decubitus, and in the distance from it appear cyanotic spots and blisters. When a large accumulation of pus can determine the fluctuation, and with the anaerobic nature of infection appears crepitation of tissues. Phlegmon usually develops as a result of delayed surgical treatment with the development of moist decubital gangrene. Purulent necrotic process begins in the deep layers of soft tissues, rapidly progresses and is accompanied by severe destructive changes in tissues with the development of necrotizing dermatocellulitis, fasciitis and myonecrosis. More than 80% of all cases of phlegmon it occurs in patients with ulcers of the sacrum. A purulent process can spread to the gluteal and lumbar regions, the perineum, the back of the thigh. In the vast majority of cases, a purulent-necrotic process causes a 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 infection. At exhausted weakened patients of elderly and senile age the lethality at occurrence of a phlegmon on a background of a decubitus exceeds 70%.
Sepsis occurs at some stage of development of deep bedsores (grade 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 a resistant bacteremia associated with bedsores, the prognosis for life becomes extremely unfavorable, and the lethality is not less than 50-75%.
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What prognosis are bedsores?
The prognosis and outcomes of treatment of pressure ulcers are closely related to the underlying disease, against which a decubital ulcer developed. In bedridden patients with severe somatic pathology or mental illness, the appearance of pressure sores becomes an unfavorable sign for life. In resuscitation patients who are on ALV, the formation of pressure ulcers 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 of ulcer closure with external exogenous bedsores is usually favorable, since after cessation of tissue compression and the appointment of 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 heavily burdened by the underlying disease. The development of an invasive infection reduces the chances of a favorable outcome. Spontaneous healing of decubitus ulcers occurs rarely, and in case of their independent or surgical closure, there is a high risk of recurrence of ulcers or the formation of new ones, since the risk factors for the development of pressure ulcers remain.