Bed support surfaces for preventing pressure injuries after spinal cord injury

Introduction

After a spinal cord injury (SCI), individuals often remain with limitations that will impede mobility and functional independence. Presence and severity of the neurological deficits associated with SCI represent important risks for developing pressure injuries (PI). During hospitalization, pain, associated injuries, medical complications, spasticity, joint contractures, and surgical interventions may further lead to prolonged bed rest and contribute to increased occurrence of PI. Achieving an optimal plan for preventing PI can be difficult in practice, particularly for individuals requiring total assistance for mobilization and repositioning in bed. The selection of a specialized support surface is thus a critical component of a comprehensive plan for PI prevention and treatment. Support surface refers to “a specialized device for pressure redistribution designed for management of tissue loads, micro-climate, and/or other therapeutic functions” as defined by the National Pressure Injury Advisory Panel ( ). In this document, support surface pertains to bed, mattress, overlay, and integrated bed system. At the end of this chapter, the reader will be able to:

• (1)

  Describe the different forces that are involved in the pathogenesis of PI in the SCI population.

• (2)

  Provide an overview of the main types and features of support surfaces to prevent and/or treat PI.

• (3)

  Propose a simple decision table for guiding healthcare providers to select a support surface for the prevention and treatment of PI in hospitalized SCI patients.

Pressure injuries (PI): Definition, epidemiology and impacts

Defined by the National Pressure Injury Advisory Panel (NPIAP) as a “localized damage to the skin and/or underlying tissue over a bony prominence,” pressure injuries (PI) (also called bedsores, decubitus ulcers, pressure sores) represent one of the most common medical complications experienced by hospitalized patients ( ). No other preventable event occurs as frequently as PI, occurring at a rate of 2%–40% of all acute care hospitalization in the United States and Canada ( ; ). PI can occur throughout the continuum of care, with a prevalence of 9.7%, 11.8%, and 12.0% for all patients hospitalized in acute care, in patient rehabilitation, and long-term care (nursing home), respectively ( ).

In the lying position, PIs usually develop at the sacrum (17%–27%), heel (9%–18%), malleoli (4.6%), trochanters (1.4%), and scapulae or occiput (< 5%) areas ( ; ; ). It is however proposed that prevention and management of heel PIs may be best managed independently from the bed support surface ( ). The occurrence of PI is particularly concerning for individuals with SCI as it interferes with rehabilitative care, community reintegration, and quality of life ( ; ; ). PIs are associated with higher morbidity and mortality and represent an enormous growing financial burden for healthcare systems, with a patient care cost per PI of 20,900 US$ to 151,700 US$, totalizing 26.8 billion US$ in 2019 ( ; ). Individuals with SCI are among the most vulnerable populations for PI, occurring in more than 95% of them during their lifetime ( ). Recent literature estimates that hospital-acquired PI among SCI patients ranges from 29.7% to 49.2% ( ). According to , the risk to develop PI is higher for individuals with severe spinal cord injury.

Pathogenesis of pressure injuries following spinal cord injury

The pathophysiology of PI involves different extrinsic factors, paralleling the severity of the neurological impairments related to the SCI. Pressure is acknowledged to be the main factor and is defined as the amount of force applied perpendicular to a surface per unit area of application ( ). In addition, shearing and friction represent stresses that are exerted parallel to the area of application and significantly contribute to the capillary damage ( ; ) ( Fig. 1 ). The resultant reduction in blood flow reduces the oxygen and nutrients being delivered to the tissues, while simultaneously limiting the removal of metabolic waste products ( ). Neurological impairments associated with severe SCI also lead to difficulties in identifying painful stimulus associated with prolonged and/or excessive compression, to which must be added the difficulty to make independent postural adjustments necessary to restore tissue perfusion ( ). Without the relief of compression on soft tissues, ischemia persisting for more than 2 hours may lead to necrosis of subcutaneous tissues ( ). Inadequate maneuvers while transferring, repositioning, and positioning in bed may also lead to excessive shearing and friction stresses to the skin, further contributing to the development of PI ( ). Immobility is also associated with the build-up of temperature at the interface, increasing local inflammation biomarkers, associated with PI occurrence ( ).

Dysfunction of the autonomic nervous system may also contribute the pathophysiology of PI following SCI, by altering the micro-vascular response below the level of the injury. Blood flow regulation relies on the rhythmic alteration of blood vessels constriction controlled by central neurogenic, local myogenic and metabolic mechanisms, which can be altered following SCI ( ). Impaired myogenic and neurogenic responses of the vascular smooth muscle due to chronic denervation also lead to an inappropriate local blood flow and metabolic responses to pressure load and unload. This phenomenon may be exacerbated in individuals with endothelial dysfunction (for instance, caused by smoking) and in the elderly, for which the loss of elastin and degradation of the collagen matrix put the skin at further risk of deformation of the blood vessels under loading pressure ( ).

Moreover, 70%–84% of individuals with SCI experience sphincter dysfunction (neurogenic bladder & bowel), which may lead to higher moisture and irritation of the skin, fostering the development of PI ( ). Nutrition status, comorbidities and body weight should also be assessed following SCI. Obesity and diabetes may reduce the skin ability to dissipate local heat and cutaneous temperature regulation under loading. On the other hand, muscle atrophy associated with SCI may make bony prominences to emerge, leading to increased local pressure and friction/shear in bed. Spasms and joint contractures associated with SCI should also be assessed, as a potential cause of excessive friction and shear and hindrance for proper positioning and repositioning in bed (increased pressure).

Support surfaces: An approach for prevention and treatment of pressure injuries

Biomechanical properties of support surfaces during loading

Support surfaces use three main mechanisms to prevent PI during loading: (1) pressure redistribution; (2) micro-climate, and (3) horizontal stiffness management. Their performance levels on these important features allow differentiating between the variety of available products and help in selecting a proper support surface that matches patient’s needs. During loading, the pressure at a specific location will decrease as the contact area increases. Based on this concept, support surfaces aim to redistribute the pressure by using two basic principles ( ; ; ; ) ( Fig. 2 ):

• (1)

  Envelopment , referring to the ability of a support surface to conform, so to fit and mold around irregularities in the body. It is generally measured in laboratories by indenter tests providing average pressures on each depth level (mm Hg).

• (2)

  Immersion , referring to the penetration (sinking) of the body into a support surface, measured by the depth of penetration (mm).

A higher envelopment and immersion performance of a support surface is associated with greater pressure redistribution, but at the expense of higher instability of the surface making it more difficult for a patient to reposition and/or get out of bed ( ).

The micro-climate is defined as the temperature and humidity at the body interface with the support surface and plays an important role in the development of PI, independently of the average peak pressure ( ). High skin temperature leads to an increased cutaneous stiffness under loading, higher inflammation, and metabolic activity, further leading to tissue damage ( ). Moisture can accumulate on the skin increasing the coefficient of friction at the interface while diluting the skin acidity, which was shown to reduce its antibacterial properties ( ; ). Micro-climate is measured in laboratories using the local temperature, relative humidity, evaporative capacity and/or dissipating properties of the support surface. However, support surfaces that provide great micro-climate management may also cause patients to feel cold or dehydrate.

The horizontal stiffness refers to shear and friction stresses that are generated when the gravity pulls the body down on a support surface, which reacts by pushing back. Horizontal stiffness is measured and reported in Newtons of force. A stiff support surface exerts high resisting forces on the tissues in response to a given amount of displacement, while this force is lower for softer support surfaces. However, the latter can contribute to sliding down in the bed and even to falls ( ).