Pressure and shear

Pressure and shear forces, especially over bony prominences or due to medical devices or other objects, are the principal factors associated with the development of PI. As a result of these forces, the loaded soft tissues will deform, causing strains and stresses which, if sustained, may lead to tissue damage ( ). Sustained soft tissue deformation leads to hypoxia, reduced lymphatic flow as well as reduced nutrient supply and removal of metabolic waste products which in turn causes cell death and tissue damage ( ; ; ). Pressure intensity and duration as well as tissue tolerance and vascular perfusion also play a significant role ( ).

Both low mechanical load for a long period and high load for a short period of time may result in tissue damage ( ; ; ). To date, no universal safe tissue interface pressure threshold has been established, thus highlighting the importance of evaluating and addressing all possible PI risk factors as tissue interface pressure measurement alone is insufficient ( ; ; ).

Tissue tolerance

Different tissue types have varying degrees of tolerance to deformation with muscle tissues being more susceptible to damage than fat and skin ( ). The orientation of shear forces is also important as skin is more resistant to forces occurring in alignment with collagen fiber bundles than when they are applied perpendicular to fiber bundles ( ).

In addition, soft tissue tolerance may be affected by many factors such as perfusion, micro-climate as well as patients and tissue characteristics ( ). For example, trauma victims have an increased risk of developing PI, with 45.8% of them developing within 48 h of admission ( ). Because of the risk factors inherent to their condition, such as immobility, decreased autonomic control, hyper catabolic responses, and lack of protective response due to sensorimotor deficits ( ; ), patients with traumatic spinal cord injury (TSCI) are almost 14 times more likely to develop a PI than other trauma patients ( ).

Most common locations and severity

During acute care and rehabilitation, when patients spend more time in a supine position, the most commonly affected areas include the ischium (28%), the sacrum (17%–27%), trochanters (12%–19%), and heels (9%–18%) ( ). During the chronic stage, when patients spend more time in a sitting position, the ischium or perineum (48.3%), sacrum (37.2%), and trochanters (14.5%) are more susceptible to PI ( ).

Molano et al. have shown that in their cohort, the majority of PIs occurring during acute care were stage 2 and 3 ( ). For their part, Powers et al. have shown a predominance of stages 1 and 2 ( ). In a recent study, Ham et al. suggested that the number of stage 1 PI may be underestimated due to the absence of skin loss, making their identification sometimes more difficult and by the fact that they rapidly progress to more severe stages if not addressed ( ).

Impact

Patients with TSCI who develop a PI during acute hospitalization have higher complication rates, significantly longer length of stay, and higher risk of recurrence ( ; ; ). Complications of PI such as wound infection, cellulitis, septic arthritis, osteomyelitis, sepsis, and malignant transformation (Marjolin’s ulcers) may also occur ( ). In some cases, PI can lead to surgical procedures, amputation, and sometimes even death due to an infection ( ). Indeed, 7%–8% of patients with TSCI who develop a PI die from associated complications ( ). PI also limit long-term functional outcome by interfering with rehabilitation ( ; ). Following the acute hospitalization, patients are at higher risks of developing a PI during the first year post-SCI or more than 25 years post-injury ( ). After urinary tract infections, PI represent the second most common cause of re-hospitalization during the first year post-TSCI as well as in the following years, accounting for 11.3% of re-hospitalizations at 1 year, 14.6% at 5 years, 17.5% at 10 years, and 21.3% at 20 years post injury ( ).

Cost

It has been estimated that one-quarter of the cost of care for patients with SCI is associated with PI and thus represent a significant preventable financial burden. In 2013, in Canada, the occurrence of PI resulted in an additional $18,758 to the cost of acute hospitalization following TSCI ( ). In the United Kingdom, PI treatment ranges from $2000 to $18,000 ( ) while in the United States, annual health care costs per patient was estimated to be $73,021 higher for patients with PI when compared to patients without PI ( ). Finally, a recent systematic review showed that interventions to prevent PI occurrence were considerably less expensive than the interventions for their treatment ( ).

Skin

Thinning of skin at load-bearing sites, decrease in skin distensibility in the remaining skin tissues, decrease in fibroblast activity, and increase in collagen catabolism are seen in patients with SCI with greater changes in skin distensibility, elasticity, and viscoelasticity observed in patients with longer time elapsed since SCI ( ; ). A decrease in type I to type III collagen ratio is also seen in the skin below the level of injury which may further contribute to skin fragility following SCI by decreasing tensile strength ( ).

Muscle and bone

In addition to normally occurring age-related muscle atrophy ( ), patients with SCI undergo significant disuse-induced muscle atrophy below the level of injury ( ) with greater atrophy seen at the level of ischial tuberosities ( ). Muscle atrophy decreases natural protective cushioning over bony prominences, increasing PI risk ( ). Thinning of the fibers, decrease in the numbers of slow-twitch fibers, and increase in fast-twitch fibers may be seen as early as 4–6 weeks following TSCI ( ). An increase in intra-muscular fat is also observed ( ), causing greater intra-muscular shear stresses at interfaces between muscle and intra-muscular fat tissues ( ; ), thus further increasing PI risk. In addition, due to chronic exposure to sitting mechanical loading coupled with cortical bone mass loss, ischial tuberosities tend to flatten, shifting load transfer from weight-bearing ischial tuberosities to overlying soft tissues ( ).

Macro- and micro-vasculature

Changes in macro- and micro-vasculature also occur partly due to alteration in autonomic control. First, a loss of vascular tone is seen below the lesion resulting in vasodilation and thus decreasing vascular resistance and impairing tissue perfusion ( ). Also, a decrease in the density of both alpha- and beta-adrenergic receptors is observed in the skin below the level of injury in patients with longer-standing injuries resulting in abnormal vascular response ( ). When compared to patients without SCI, lower limbs cutaneous blood flow has been shown to decrease by at least 50% in patients with SCI when sitting ( ). A decrease in number and size of capillaries feeding skeletal muscle fibers is also seen, making these muscles more susceptible to ischemia, especially during episodes of low blood pressure ( ; ). Moreover, when compared to healthy controls, patients with SCI tend to have significantly higher sitting pressure and significantly lower transcutaneous oxygen tension levels, followed by slower reactive hyperemia when unloaded, translating into a lower rate of reperfusion ( ; ). This therefore suggests a longer recovery time is required for patients with SCI following loading periods to allow appropriate tissue re-oxygenation before reloading the area.

Inflammation and immune function

A chronic systemic inflammatory response occurs following trauma and may predispose patients with SCI to PI and decrease healing response by depressing immune system function ( ; ). Compromise in tissue perfusion paired with chronic tissue inflammation decrease tissue tolerance and repair capacity further increasing tissue breakdown risk ( ).

Temperature

Due to loss of autonomic control, temperature dysregulation is also common in patients with SCI. Cotie et al. have shown that an increase in resting skin temperature and a reduced skin temperature reactivity are seen in the lower limbs of patients with SCI ( ). In addition, urinary and/or fecal incontinence is common in patients with SCI further increasing the risk of moisture and maceration ( ; ). An increase in body temperature, especially when coupled with excessive humidity and maceration, has a profound effect on tissue tolerance to damage and thus must not be overlooked especially when addressing support surfaces and medical devices ( ; ; ).

Sensory impairments

Finally, sensory deficits associated with SCI results in a lack of protective response due to decreased awareness of tissue injury thus allowing the progression from ischemia to tissue breakdown and necrosis ( ; ; ).