Answer:
Although initial theories regarding pressure sore development by Charcot (1879), Leyden (1874), and Munro (1940) all stressed the importance of neurologic impairment, we now know that pressure is the single most important etiologic factor. The compression of soft tissues results in ischemia and, if not relieved, will progress to cause necrosis and ulceration. In susceptible patients, this sequence of events may be accelerated owing to other endogenous sources such as infection, diabetes, or altered neurologic states.
Landis, in 1930, using a microinjection system, determined that capillary blood pressure in a single capillary ranged from 12 mm Hg on the venous end to 32 mm Hg on the arterial end. If the external compressive force exceeds capillary bed pressure, capillary perfusion is impaired and ischemia will ensue. However, this effect is not instantaneous. If it were, we all would suffer from pressure sores. An inverse relationship exists between the amount of pressure and the length of time required to cause ulceration. Early studies by Kosiak demonstrated that 70 mm Hg applied over 2 hours was sufficient to cause pathologic changes in dogs. Similarly, Daniel et al. also demonstrated ischemic changes in a paraplegic pig model. He showed that 500 mm Hg applied for 2 hours or 100 mm Hg for 10 hours was sufficient to cause muscle necrosis. Interestingly, it was not until 600 mm Hg was applied for 11 hours that ulceration of the skin could be seen. Not only did these results confirm the relationship between pressure and time, but they also demonstrated that the initial pathologic changes occurred in the muscle overlying the bone, and only subsequently in the surrounding area. Finally, they demonstrated that muscle is more susceptible than skin to ischemia. In a classic study Lindan used a compressible bed of springs and nails to measure the external distribution of contact pressure in patients in the supine and seated positions. He found that in the supine position the maximal recorded pressures were 40 to 60 mm Hg near the heels, buttock, and sacrum. In the sitting position, pressures were greatest near the ischial tuberosities, with measurements of up to 100 mm Hg. Husain et al. studied the effects of pressure and time to determine which had the greater impact on ulcer formation. Husain believed that low pressures maintained for long periods of time induced more tissue damage than did high pressures for short periods of time. Kosiak investigated dogs subjected to constant pressure for varying periods of time and noted an inverse parabolic relationship between the amount of pressure and duration of exposure. Dinsdale confirmed these results in a pig model, but he was also able to demonstrate minimal tissue injury if pressure could be relieved for as little as 5 minutes, even with pressures as high as 450 mm Hg.
As mentioned, Daniel demonstrated a resistance to ulceration of the skin in his studies in which only pressure and time were altered. In the clinical setting, we see skin involvement with nearly all of the pressure sores. Clearly, some other factor must be significantly involved for this to be the case. It has been proposed that the rapid rate of skin breakdown seen in pressure sore is suggestive of a bacterial process in which collagenolytic activity may be contributing to the acceleration in skin necrosis.
It has been shown that compressed skin has less resistance to bacterial invasion. In 1942, Groth demonstrated that bacteria would accumulate in areas of increased pressure. He simultaneously injected rabbits with bacteria while applying external pressure to the gluteal region. This resulted in localized collections of bacteria in the compressed sites. Robson and Krizek quantified the effect of pressure on bacterial count. They showed that surgical incisions created in areas of applied pressure and inoculated with known concentrations of organisms allowed for a 100-fold greater bacterial growth than in areas not subjected to pressure. The proposed mechanisms include impaired lymphatic function, ischemia, and impaired immune function.
The role of edema in promoting the infection process seen in pressure sores must not be overlooked. Compressed, denervated skin is known to become edematous by several processes. Landis demonstrated the pressure needed to overcome end capillary pressure in the skin. Once external pressures exceed 12 mm Hg, the veins become engorged, and total tissue pressure increases. As this process continues, end arterial pressure increases, and it is at this point that plasma extravasation occurs, leading to edema formation. Compounding this process is the fact that the tissues are denervated. The loss of sympathetic tone of the blood vessels causes vasodilatation and leads to greater engorgement of the vessels and further, greater edema. Denervation indirectly contributes to lymphatic edema, as demonstrated by Exton-Smith and Crockett. In their study of hemiplegic patients, edema was noted to be present 2 weeks after injury in 16% of the patients, and this persisted for as long as 6 months. They postulated that this was the result of injury to the lymphatic pump, which is dependent on the action of skeletal muscle to function. Edema formation in pressure sore patients is also the result of inflammatory mediators released in response to the trauma of compression. The normal homeostasis between PGF2a and PGE2 is disrupted in favor of PGE2 with increased leakage through the cell membranes and increased interstitial fluid accumulation. As interstitial plasma concentrations rise, the concentration of sebum on the skin surface is diluted. Sebum has been shown to be important in the defense against both streptococcal and staphylococcal infections.