Factors contributing to pressure injuries in traumatic spinal cord injury


Abbreviations

ISNCSCI

International Standards for Neurological Classification of Spinal Cord Injury

NPIAP

National Pressure Injury Advisory Panel

PI

pressure injury

SCI

spinal cord injury

TSCI

traumatic spinal cord injury

Introduction

A pressure injury (PI), also known as pressure ulcer, pressure sore, bedsore, or decubitus ulcer, is defined as a circumscribed injury to the skin and/or underlying tissue due to pressure, or shear combined with pressure, causing ischemia, cell death, and tissue necrosis ( ; ). It may present as an open wound or intact skin. The most commonly used pressure injury classification system, based on the extent of tissue involvement, is the one developed by the National Pressure Injury Advisory Panel (NPIAP) ( Table 1 ) ( Fig. 1 ) ( ). In order to accurately describe PI, staging can only be done after proper cleansing of the wound and exposure debridement of slough or eschar, thus sometimes postponing final staging of certain PI where necrotic tissue is present in the wound bed ( ). PI assessment should also include dimensions, tissue quality, quantity and quality of exudate, wounds edges, presence of tunneling or undermining, peri-wound condition, odor and signs of infections, or other complications ( ).

Table 1
Pressure injury stages according to the National Pressure Injury Advisory Panel (NPIAP).
Stage 1 Intact skin with a circumscribed zone of non-blanchable erythema
Stage 2 Partial-thickness skin damage where the dermis is exposed
Stage 3 Full-thickness skin damage where the fat is exposed, granulation tissue is present and wounds edges are rolled
Stage 4 Full-thickness skin damage where fascia, muscle, tendon, ligament, cartilage, or bone is exposed
Unstageable Full-thickness skin damage where a Stage 3 or Stage 4 is suspected but cannot be determined due to presence of necrotic tissues
Deep tissue pressure injury Intact or damaged skin with a circumscribed non-blanchable purple or dark red zone, or presence of epidermal separation exposing a dark wound bed or blood-filled blister
Pressure injury classification system, based on the extent of tissue involvement, developed by the National Pressure Injury Advisory Panel (NPIAP) ( ).

Fig. 1, Pressure injury stages. Schematic drawings of the different pressure injury stages (illustrated by Bréval Le Mestique).

Due to risk factors inherent to their condition, such as decreased sensation and mobility limitations, spinal cord injury (SCI) patients are at higher risk of developing a PI when compared to the general population ( ; ). Their occurrence can have significant physical, psychological, and functional consequences and may hinder independence, self-esteem, social well-being, and overall quality of life ( ; ). Their prevention is therefore essential and should be an integral part of the medical and rehabilitation goals.

Pathophysiology of pressure injuries

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 ( ).

Prevalence, impact, and cost of pressure injuries in patients with SCI

Pressure injuries (PI) are one of the most common complications following SCI with up to 80% of patients developing a PI at some point during their lifetime ( ; ). Compared to other rehabilitation phases, the acute hospitalization represents the period with the highest PI risk ( ) with a prevalence ranging from 2.7% to 57% when compared to 15% to 54% in the chronic SCI stage ( ; ; ). Factors such as severe neurological deficits, altered level of consciousness, and multiple concomitant traumatic injuries lead to prolonged periods of immobility and decreased general health status, putting patients at higher risk of PI during acute care ( ).

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 ( ).

Structural and physiological changes following SCI

Following SCI, multiple structural and physiological changes occur, decreasing the body’s ability to maintain skin integrity, increasing the risk of tissue breakdown, and thus putting patients at higher risk of developing PI ( Table 2 ).

Table 2
Structural and physiological changes following SCI.
Skin changes
  • Skin thinning at load-bearing sites

  • Decrease in skin distensibility in the remaining skin tissues

  • Decreased fibroblast activity

  • Greater collagen catabolism

  • Decrease in type I to type III collagen ratio in skin below injury level

Disuse-induced muscle atrophy
  • Fibers thinning

  • Decrease in numbers of slow-twitch fibers and increase in fast-twitch fibers below the level of injury

  • Increase in intra-muscular fat causing greater intra-muscular shear stresses at interfaces between muscle and intra-muscular fat tissues

Bone changes
  • Flattening of ischial tuberosities due to chronic exposure to sitting mechanical loading coupled with cortical bone mass loss, shifting load transfer from weight-bearing ischial tuberosities to overlying soft tissues

Changes in macro- and micro-vasculature
  • Vasodilation and impairment in tissue perfusion below injury level

  • Decrease in the density of both alpha- and beta-adrenergic receptors in the skin below injury level resulting in abnormal vascular response

  • Decrease in number and size of capillaries feeding skeletal muscle fibers

  • Decrease in lower limbs cutaneous blood when sitting

Chronic inflammation and immune function
  • Decrease healing response by depression of immune system function

  • Chronic tissue inflammation decreases tissue tolerance and repair capacity further increasing tissue breakdown risk

Temperature dysregulation
  • Increase in resting skin temperature and decrease in skin temperature reactivity in lower limbs

Sensory impairments
  • Sensory deficits resulting in lack of protective response allowing the progression from ischemia to tissue breakdown and necrosis

Summary of the multiple structural and physiological changes occurring following SCI predisposing to pressure injuries ( ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ).

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