Deep tissue injury (DTI) is a phenomenon that was added into the classification of pressure ulcers by the National Pressure Ulcer Advisory Panel,1 albeit with difficulty after a much prolonged debate. The question we need to ask is if DTI really belongs within chronic pressure ulcer management. Can we ponder the possibility that this injury has been incorrectly categorized and is not a chronic wound?
In the incidence of a deep pressure injury, blood flow to the area is absent or significantly diminished,1 which causes cell disruption, dematuration of plasma proteins,2,3 and hypertonicity,3 leading to cellular dehydration and cell death that may be similar to what happens to patients with frostbite. On relieving the pressure and restoring blood flow, reperfusion occurs with an accelerated microcirculatory injury caused by production of oxygen-derived free radicals. These events lead to more cell death in tissue,4 known as an ischemia-reperfusion (IR) injury.4 These oxygen-free radicals causing the damage are unstable with an unpaired electron in the outer shell.4 They are highly toxic and cause cell destruction by lipid peroxidation and propagation of more free radicals.4 Neutrophil adherence to the endothelium of arterioles4 seems to be the major culprit of this cascade, as the capillary vessels are broken through and the oxygen-free radicals leak out of the capillary system into tissue. As a further consequence of restoring blood flow, there is rouleaux formation of red blood cells (cells stack up in the vessel lumen),3 with stasis in the microcirculation and edema formation3 because of the leaky capillaries.
Ischemia-reperfusion is even more dangerous when present in skeletal muscle,4 and the damage from IR is proportional to the duration of the ischemia.4 During reperfusion, the demand for oxygen in tissue is the highest, while the delivery method of oxygen to tissue is simultaneously at its lowest.4 This is the disaster that puts the DTI into the situation where tissue damage may become irreversible. Left over time and because of the slow evolution of the injury,2 a clear demarcation line between viable and nonviable tissue will eventually occur, with the real extent of tissue loss visible only after surgical debridement.
The anatomical locations where DTIs are most prevalent are the heel (41%), the sacrum (19%), and, to a lesser extent, on the buttocks and ischial tuberosities (13%).5 All of these areas have a single blood vessel supply or a smaller collateral circulation. There is a paucity of thin vulnerable skeletal muscle on the deep lateral aspect of the heel toward the foot sole called the flexor digitorum brevis.6 Because its task lies mainly in stabilizing the foot, it is a very stiff and dense muscle covered with a rigid fascia. The rest of the layers of heel tissue are specialized tissue derived from fat and other components overlaying the implantation of the Achilles tendon on the crest of the calcaneous.6 This lateral compartment of the heel is also the area that is not supplied with a direct blood vessel system and receives its blood flow from collaterals in a dense capillary interwoven system.6
The midline of the sacrum, just as the heel, does not have a rich collateral blood supply. It is also not covered by huge compartments of superficial and intermediary muscles, but in the deepest part close to bone, the multifidus muscles extend from the sacrum to the cervical spine of the axis.6 The skin and soft tissue overlay an intricate ligament and tendon construction implanting on various areas over the sacrum and pelvis. Again, this deep muscle is small, stiff, and dense with a tight fascia.6 These 2 areas are where the highest incidence of this type of injury occurs.5
If clinicians examine the subgroup of conditions that fit the criteria for being classified as an acute traumatic ischemia,4 they will find compromised flaps and grafts, crush injury, compartment syndrome, traumatic amputations, frostbite, and burns. The theoretical common denominators of these injuries are hypoxia leading to ischemia in tissue, reperfusion with the damage from the free radicals, with a subsequent IR injury.4 The extent of tissue loss is dependent on the duration of the hypoxic incident, the amount of clotting in the microcir culation, and the extent of the edema that follows. Because of the devastating chemical chain reaction that follows the injury, tissue is nearly always lost in different degrees of depth severity.
When looking at a proposed pathway (Figure 1) from incident to injury, there may be a few factors at play. At first, there is an acute injury that involves hypoxia in the area compacted between a pressure point and a bony prominence that forms the epicenter of injury. This is followed by hypoxia in tissue, edema influx, and increased swelling, leading to subsequent ischemia in the epicenter, with progressive hypoxia spreading to the surrounding peri-injured area. Added to the hypoxic burden, a cascade of chemical reactions are also at work in the epicenter and peri-injured areas for the duration of the period of hypoxia. On relieving the incident, an attempt of restoration of blood flow occurs with an additional cascade of chemical active components, blood thrombi in the blood flow system, leaky capillaries, and edema. The injured deep tissue epicenter becomes irreversibly nonviable with the peri-injured area that progressively succumbs to this chemical onslaught and subsequent low supply of oxygen. The result of that is edema causing localized swelling in the deep muscle component. Within a nonelastic rigid fascia, that amount of swelling in the muscle will invariably lead to a deep compartment syndrome where muscle capacity exceeds fascia capacity.
The pressure incident in the deep muscle may well be coined as an infarct,7 but it may be that the rigidity of fascia surrounding the deep muscle where an infarct did occur, could be the one factor overlooked previously. Swollen muscle in a rigid fascia will lead to compartment syndrome either because of high-impact injury over a short time span or a lower-impact injury over a longer time span. Tissue succumbs to the hypoxic and subsequent chemical onslaught, with the skin the last and most resistant barrier before breaking down as well. This pathway depicts an injury from within that fits to a certain extent into the classic pattern of compartment syndrome. The extent of the subsequent chemical cascade, however, may be underestimated as a cause for these types of wounds to either break down completely or resolve on their own without skin breakdown.
Pressure does play a role,8 but it is more related to the physiological and metabolic state of the patient who sustains this type of injury. In the metabolically unstable patient, this injury may make patients more vulnerable to the chemical onslaught, despite standard precautions to prevent pressure ulcers as stated on the Braden Scale for Predicting Pressure Sore Risk© (sensory perception, moisture, activity, mobility, nutrition, friction, and shear).9
In summary, this commentary hypothesized that this type of injury in the future may be more correctly known as a hypoxic reperfusion ulcer rather than a DTI, which is not specific enough and opens the door for potential unfounded litigation issues.
2. Biem J, Koehncke N, Classen D, Dosman J. Out of the cold: management of hypothermia and frostbite. CMAJ 2003; 168: 305–11.
3. Zamboni W. The microcirculation and ischemia-reperfusion: basic mechanisms of hyperbaric oxygen. In: Kindwall EP, Whelan HT, eds. Hyperbaric Medicine Practice. Flagstaff, AZ: Best Publishing Company, 1999: 779–94.
4. Strauss M. Crush injury, compartment syndrome and other acute peripheral ischemias. In: Kindwall EP, Whelan HT, eds. Hyperbaric Medicine Practice. Flagstaff, AZ: Best Publishing Company, 1999: 753–78.
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6. Anderson JE. Grant’s Atlas of Anatomy. 7th ed. Baltimore, MD: Williams & Wilkins Co, 1978:Figure 4-11, Figure 4-101, Figure 5-28.
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9. Braden B. The Braden Scale for Predicting Pressure Sore Risk: reflections after 25 years. Adv Skin Wound Care 2012; 25: 61.