Bedsores

BEDSORES (Latin decubitus), as the name itself indicates, represent a trophic disorder, located mainly on the sacrum, buttocks, shoulder blades, elbows, heels, and characterized by gangrenous changes, significant spread along the periphery, and deep involvement of adjacent tissues. When a bedsore develops, the corresponding area of skin first begins to pale, then becomes cyanotic, peeling (dry gangrene), excoriation, and ulceration appear. Due to a secondary infection (from the bed, linen, excrement, etc.), the process quite rapidly takes on a gangrenous character (wet gangrene). Although a bedsore does not represent an independent disease, but is for the most part only a concomitant process in various diseases, in some cases it can still lead to a fatal outcome. By their origin, bedsores can be divided into two types: exogenous bedsores, originating from mechanical causes of a local nature (pressure, compression, pinching, etc.), and endogenous bedsores, the mechanism of development of which is connected with the localization of a disease in the nervous system or with a general weakening of trophic functions. 1. Exogenous bedsores can form from prolonged pressure on the skin or its compression by apparatuses, corsets, bandages, prostheses, and other objects of therapeutic influence or as a result of injuries of a traumatic nature. In these cases, under the influence of pressure or compression, local ischemia, nutritional disorder, and finally tissue necrosis develop. Usually, when using apparatuses and prostheses, bedsores develop on the dorsum of the foot, on the heel, above the Achilles tendon, on the trochanter, on the crest of the tibia, on the head of the fibula, and similar places. Of the mucous membranes, the mucous membrane of the trachea after tracheotomy (see Laryngostomy) and the mucous membrane of the urethra due to the pressure of a metal catheter are at risk of developing bedsores. Although with careless care the development of bedsores can lead to significant destruction of tissues, nevertheless, bedsores of exogenous origin are not so dangerous to life and are amenable to treatment. 2. Endogenous bedsores, in turn, can be divided into two types: 1) Bedsores forming as a result of a general weakening of the organism on the basis of an infectious or other suffering in severe patients who are forced mostly to lie in one position or are unable to change it due to weakness. In this case, the mechanical factor in the form of pressure gives an impetus to the formation of a bedsore, which develops further due to the lack of resistance and general weakness of the organism, including mainly trophic impulses, under the influence of general infection, intoxication, etc. 2) Another type of endogenous bedsore is the so-called neurotic bedsore, in the formation and development of which the lesion of the nervous tissue itself plays a direct role and which can develop not only in places subject to pressure. Samuel, who described this bedsore in 1860, notes the following three phases of development: the erythema phase, which is followed quite rapidly by the formation of vesicles (vesicular phase), the reddish-brown contents of which are emptied, exposing reddish and violet bleeding sores (necrosis phase), which connect with each other. During this period, usually due to the untidiness of patients, their bedding, incontinence of urine and feces, a purulent infection is added very quickly, and decubital gangrene, penetrating inward, captures the subcutaneous tissue, muscles, and in a few days reaches the bones. This whole process proceeds very rapidly: erythema sometimes appears after a few hours or within 3-4 days following the lesion of the nervous tissue; in 24 hours the process turns into necrosis, and after 48 hours it is already gangrene. Samuel, who described this bedsore, was at the same time the author of the theory of the trophic function of the nervous system, defending the existence of independent trophic nerves acting in a centrifugal way on tissues and regulating their nutritive processes. Somewhat later, in 1868, Charcot confirmed this opinion, localizing trophic centers in the anterior horns of the spinal cord. Kocher, Monakow, Oppenheim, Leyden, and others considered mechanical pressure and subsequent infection to be the source of the bedsore. Cassirer, Achard and Levy, L. Muller put forward causes for the formation of bedsores, but agreed mainly in the opinion that a lesion of the nervous system is mandatory for their formation. There were followers of the vasomotor theory, according to which vasodilation (neuroparalytic hyperemia of Schiff) plays the role of a predisposing factor for the development of inflammatory processes in the tissues; on the other hand, the influence of neuroirritative ischemia (Brown-Sequard) can lead to the development of gangrene. Dejerine and Leloire found changes in the nervous tissue in the vicinity of bedsores in the form of parenchymatous neuritis and believed that the cause of the occurrence of bedsores is a disturbance of the trophics of the central nervous system and that external pressure plays only the role of an accidental cause. In 1908, Jacobson discovered that the source of sympathetic fibers managing trophics are special cells of the spinal cord located in the lateral horns of the thoracic segments. Brusilovsky, on the basis of clinical observation and pathohistological examination on a large amount of material, established that in inflammatory diseases of the spinal cord, the pathological-anatomical equivalent of a bedsore in the sacrococcygeal region is a lesion of the sympathetic group of cells in the lateral horns of the spinal cord, with the side of the lesion of this group corresponding to the side of the bedsore, and the place of the lesion corresponding to the level of D_x-L_i and L_ii. Control cases confirmed these provisions. It is interesting to note that during pathohistological examination of cases of bedsores in multiple sclerosis, plaques were found precisely in the place of location of the sympathetic group of cells in the lateral horns. With high lesions of the spinal cord (traumatic injuries of the spinal cord, tumors), the formation of bedsores can be explained by a lesion of the pathways from the upper vegetative centers to the lateral horns of the spinal cord. Bedsores encountered in diseases of the brain (hemorrhage, softening) are explained by the existence of a special hypothetical trophic center with a presumed localization in the central convolutions. In hemiplegia, bedsores form on the buttock of the paralyzed side; in diseases of the spinal cord, more often in the region of the sacrum and coccyx. Thus, the pathogenesis of bedsores is dependent on the state of the trophic centers; the lesion is caused by centrifugal influences, while mechanical factors in the form of pressure or compression are not the main cause, but a certain, although completely necessary, condition. In infectious and toxic diseases, the general weakening of the organism has an undoubted influence on trophic functions, contributing under unfavorable external conditions (pressure during the immobile lying of the patient) to the formation of bedsores. Bedsores of exogenous and endogenous character, besides the difference in the pathogenesis itself (centripetal and centrifugal character), also differ in the course of the process. With exogenous bedsores, a favorable outcome with proper preventive and therapeutic measures is the rule; with endogenous bedsores, a favorable outcome largely depends on the course of the underlying disease. That is why endogenous bedsores are essentially symptom-processes, while exogenous bedsores represent independent processes. The clinical picture of the latter is not as bright as that of endogenous bedsores, the course is not distinguished by such progressive capture of deep tissues; these bedsores proceed according to the type of dry gangrene, the treatment time is significantly shorter. The spread of bedsores depends to a significant extent on the course of the underlying disease and preventive measures. Sex has no significance in the development of bedsores; older ages predominate. Along with neurotic bedsores, other endogenous bedsores appear most often in severely ill and emaciated individuals who lie motionless on their backs, in septic processes, in the fall of cardiac activity, and in constitutional diseases, especially in diabetes. The clinical picture of neurotic and endogenous bedsores is expressed much more strongly and proceeds according to the type of wet gangrene. Mostly without any subjective phenomena on the areas of skin covering protruding bone parts facing the plane of the bed, first of all in the region of the sacrum and coccyx, as well as on the shoulder blades and heels, and in the lateral position above the greater trochanters of the femur, a deterioration of blood circulation occurs, manifesting as a pale spot that remains for a long time under finger pressure amidst a cold, bluish-purple colored zone. Sometimes the congestion goes so far that even a spot does not appear under finger pressure. In the dark-purple edematous focus and in any case in its upper macerated layers, after a few days or weeks, with an increasing febrile state, a blackening spot appears, which hardens and recedes into the depths.

XXVI, pp. 687-688), fig. 6]; when its edges are damaged, a dirty-brown, foul-smelling secretion, sometimes with fat droplets, appears. A probe inserted there finds significant cavities under the upper gangrenous covering, so that after the removal of the scab, a discolored focus filled with necrotic, foul-smelling masses is revealed, which spreads to neighboring areas of the skin and often reaches the bone. Only where these dead parts of the skin have not yet separated from their subcutaneous parts does slight bleeding occur upon their removal. The undermined edges of the wound dry out and turn a blackish color, while the adjacent parts take on the appearance of raw skin with bruising. Such bedsores can reach the size of 1-2 palms, especially in the sacral region, and depending on the general condition and the underlying disease, can be harbingers of death. The outcome of bedsores, depending on the underlying disease, is difficult to predict. Their toxic effect on the entire organism and the spread of local infection sometimes prove sufficient to cause a lethal outcome in a severely ill patient. Such an outcome is, however, a rare case. With proper attention and timely recognition and treatment, provided the tissues' resistance to the process is not too weakened, it is possible to stop the development of bedsores. If the organism has the strength to resist, then after the separation of the dead parts, fresh, abundant granulations develop, which can close even large defects in a relatively short time. A pale, flat, immobile scar marks the site of the former bedsore. Hardly in any other complication is prophylaxis as important as in bedsores. Parts of the body especially prone to bedsores must be protected by air rings (rubber circles inflated with air), water cushions, and pads that are moved from place to place. Once or twice a day, the patient's skin must be washed with cold water and soap, wiped with alcoholic solutions, and then powdered. If the patient complains of pressure from a splint or a hardened bandage, they must be replaced immediately. For long-term patients, lying on the back should be replaced by lying on the side for at least 1 hour during the day. In the event that, despite the preventive measures taken, bedsores still appear, it is under no circumstances recommended to use wet compresses, as they provoke moist gangrene. The above-mentioned preventive measures must be applied especially vigorously in such cases. If necrosis still occurs, only dry agents should be used, and it should be padded with a soft cotton cushion. If the necrosis becomes demarcated, the dead skin is removed with scissors and tweezers, and the resulting wound is treated with ointment dressings and soap baths. In the event of moist gangrene, recognized by the discharge of a foul-smelling secretion, the dead part of the skin is removed, and the undermined edges in the periphery are incised. The resulting wound is covered with gauze soaked in camphorated spirit, aluminum acetate, or 1% potassium permanganate solution. These dressings are changed twice a day and covered with impermeable (waxed, etc.) paper. If the dead parts have separated on their own and the wound has cleaned, it should be treated with ointment dressings. In all these cases, it is required that the patient leave the bed as early as possible, and it is necessary to induce an increase in blood circulation throughout the body with the help of baths and at least passive movements. Incidentally, it should be noted that a mysterious rise in temperature in the postoperative period, which finds no explanation in the underlying disease or the state of the surgical wound, often indicates poor care and an infected bedsore arising as a result. Therefore, it is the direct duty of the physician in such cases to keep a vigilant watch over the favorite sites of bedsores, especially over the sacral region.