Intermittent Electrical Stimulation as a Treatment Approach for Deep Tissue Pressure Injury after a Spinal Cord Injury

Intermittent Electrical Stimulation as a Treatment Approach for Deep Tissue Pressure Injury after a Spinal Cord Injury

Abstract

The main goal of this project is to use a novel technique known as the Intermittent Electrical Stimulation (IES) to improve the rate of healing after development of Deep Tissue Pressure Injury (DTPI) and prevent its progression into a stage 4 pressure injury. A DTPI is a serious form of pressure injury (PrI) that arise in muscle layers adjacent to the bony prominence because of prolonged mechanical loading. This type of injury is often unnoticed until an advanced stage, at which time treatment cannot reverse the deteriorating injury. Early intervention of DTPI can improve the healing process and even reverse the PrI. The present study was performed in an in vivo complete spinal cord injured animal model to determine the following: 1. Effect of IES on the progression of tissue edema i.e. caused by one time sustained loading using magnetic resonance imaging (MRI); 2. Time of IES intervention after development of DTPI. During the 2 second “ON” duration, intermittent electrical stimulation causes muscle contraction by targeting the muscles at risk of developing a DTPI; this followed by the 5 minute “OFF” period interval where the muscle relaxes. The “ON” and “OFF” cycles are repeated consecutively. IES induced muscle contractions aid in improving tissue oxygenation and reduce further inflammation after injury. In addition, this study investigated the rate of muscle regeneration after the development of DTPI using immunohistochemistry.

The MRI findings indicate that when IES is delivered on day 1 after the DTPI induction caused a significant decrease in the muscle volume exhibiting tissue edema, confirmed using immunochemistry. IES delivered on day 3 and day 5 after induction of DTPI did not show difference in the progression of the tissue edema compared to the groups that did not receive IES but received DTPI. This implied that early IES intervention could expedite the healing of DTPI and prevent from developing into a stage 4 pressure injury.

Table of Contents

Chapter 1 – Introduction

1. Problem definition………………………………………………………………………………………1
2. Significance of pressure injury after spinal cord injury……………………………………3
3. Classification of pressure injury…………………………………………………………………….3
   1.    Superficial Pressure Injury……………………………………………………………..4
   2.   Deep Tissue Pressure Injury……………………………………………………………4
4. Etiopathogenesis of Pressure Injury……………………………………………………………….5
   1.    Etiology of Pressure Injury………………………………………………………………5
   2.   Mechanism of Deep Tissue Pressure Injury………………………………………6
      1.                 Mechanical deformation……………………………………………………….7
      2.                Localized ischemia………………………………………………………………..9
      3.                Ischemia Reperfusion injury (IRI)…………………………………………10
         1.               Sequence of events after Deep Tissue Pressure Injury…………………………………………………………………………………10
5. Prevention of Deep Tissue Pressure Injury……………………………………………………..14
   1.    Risk factor assessment scales…………………………………………………………..14
   2.   Prevention strategies………………………………………………………………………15
      1.                  Repositioning………………………………………………………………………15
      2.                 Support surfaces…………………………………………………………………..16
      3.                 Novel techniques………………………………………………………………….18
6. Current treatment methods……………………………………………………………………………21
   1.    Wound management
   2.   Adjunctive therapy
7. Overview of Masters work………………………………………………………………………………25
8. Figures and tables………………………………………………………………………………………….28
9. Bibliography………………………………………………………………………………………………….34

Chapter 2

Chapter 3

List of tables and Figures

Figure 1-1: Classification of pressure injury

Figure 1-2: Mechanisms of Deep Tissue Pressure Injury

Figure 1-3: Ischemia pathway leading to DTPI

Figure 1-4: Reperfusion pathway leading to DTPI

Figure 1-5: Intermittent Electrical stimulation

Abbreviations

Chapter 1: Introduction

1.1 Problem definition

Pressure Injury (PrI), previously known as pressure ulcer [1], is a significant problem in Canada across the continuum of health care settings. These are serious secondary complications that occur in populations with reduced mobility [2] and/or sensation, including the elderly [3], patients in intensive care units [4], and in individuals with neurological insults [5][6]. PrI can also occur in individuals undergoing cardiac surgeries [7] and in those on orthoses and prostheses. A PrI can result in decreased quality of life [3], physical restrictions, loss of independence, social isolation, and financial stress [3]. Prolonged bed rest and restricted activity are among the other factors that can lead to clinical depression [8].

PrI can initiate at the skin layer and progress towards the deep layers. These injuries are evaluated based on their involvement of the layers of the skin, subcutaneous tissue, and muscles [9]. Deep Tissue Pressure Injury (DTPI) is a more recently studied form of pressure injury that originates at deep bone-muscle interface progressing towards the epidermis [1]. For example, in the recumbent position, the soft tissue between the support surface and the sacral region is entrapped [4]. The tissue deformation and local obstruction in the blood supply can cause discomfort. If the individual were to be able-bodied, then the individual would subconsciously reposition to relieve the discomfort. The same would not be possible in individuals with disorders causing immobility or reduced sensation. In the seated position, the common sites affected are the region adjacent to the ischial tuberosities, shoulder blades, and posterior aspect of arm and legs. The compression of the tissue near the bony prominence over time can develop into a DTPI. This injury to deep structures puts patients at risk for complications such as septicemia [10], osteomyelitis [11], and premature death.

The incidence rates of PrI in acute settings range from 5 – 9 % [12][13]. The acute care facilities include those who are severely ill or had a recent surgery. These individuals experience decreased mobility and loss of sensory perception after anesthesia. Whereas, critical care settings have incidence rates as high as 20.7% [12]. The increasing aging population in developed countries has shown an increase in the incidence rates of PrI [14]. One study shows that more than two-third of hospitalized patients developing a PrI were 70 years or older [15][16]. The overall prevalence rate in all health facilities in USA, Canada, Europe range between 8% – 26% [17][18]. The prevalence in the non-acute care facilities (long-term care and nursing homes) across Canada is the highest among all the hospital settings with a rate of 29.9% [18]. The prevalence rates in the acute care facilities and community care are 25.1% and 15. 1 %, respectively [18].

The average length of hospital stay after developing a PrI is 14.1 days [19][20]. During this single episode of hospitalization, the average cost to treat a stage 4 PrI in the United States was $ 129, 248 [21]. In 2006, the minimum annual cost to treat a hospital acquired PrI was $9.2 – 11 billion in the United States [22][23]. These costs are attributed by the presence of complications and the involved diagnostic tests, monitoring, extended in-patient stay and re-hospitalisation [2][24]. The lengthy hospital stay and the costs associated with the management are a significant concern in the Canadian health care system [24]. In spite of the advancements in the knowledge underlying the etiology and the emergence of standard care interventions prevalence shows no change over the last two decades [25].

1.2 Significance of Pressure Injury on Spinal Cord Injury (SCI)

The incidence rates of PrI are higher among the people with chronic SCI than in the general population. In the United States, at least 35% of the people with SCI will develop a PrI during the initial hospitalization and the incidence rates rise with every year post-injury [6]. The prevalence of PrI in SCI in the first year was 8% and this can increase up to 32% a few years after SCI [26][5]. Individuals with SCI are especially more vulnerable to PrI because of loss of sensory, motor, and autonomic function. They experience a change in the anatomical and physiological properties of the skin and the muscles after injury. This can cause health related complications, including pressure injury. Some of the predisposing factors in SCI that lead to development of a PrI are duration after SCI, completeness of injury, spasticity, advancing age, urinary incontinence, and difficulty in performing routine skin care [27]. These factors contribute to life time risk of developing a PrI to 85% in individuals with SCI [28][29][26].

1.3 Classification of Pressure Injury

A pressure injury is defined by the National Pressure Ulcer Advisory Panel (NPUAP), “as a localized damage to the skin and/or underlying soft tissue usually over a bony prominence or medical device, as a result of pressure in combination with shear and/or friction.” This injury can present as intact skin or open ulcer. Based on where the injury originates the PrI is classified into two main types – superficial pressure injury and Deep Tissue Pressure Injury (DTPI).

1.3.1 Superficial pressure injury

Superficial pressure injury initiates at the epidermis and progress to underlying fat and muscle if unnoticed. These injuries are primarily formed as result of friction, shear stresses between the body and the support surface leading to a skin breakdown. The current numerical system by the NPUAP classifies superficial pressure injury into five stages based on the anatomical depth and extent of tissue damage. Stage 1 injury is characterized by an intact skin with a localized area of non blanchable erythema. Stage II (partial thickness skin loss) is caused by excessive moisture and shear in the skin. Inadequate care to the skin may progress into a stage 3 (full thickness skin loss) or stage 4 (full thickness skin and tissue loss), wherein deep structures such as fascia, muscle, tendon, ligaments are visible. A newer addition to the 4-stage system is the unstageable pressure injury, in which slough, eschar can make the staging of PrI difficult. In the past, the focus of prevention and treatment of the PrI stages was concentrated on the skin to prevent a stage 1 from progressing into a full thickness and skin loss.

1.3.2 Deep Tissue Pressure Injury (DTPI)

Deep Tissue Pressure Injury was previously known as suspected deep tissue injury (sDTI). This injury arises from prolonged entrapment or compression of soft tissue between a bony prominence and an external support surface. DTPI is a serious form of injury due to its late detection and rapid deterioration. In the year 2016, NPUAP added DTPI into the revised staging. These injuries are challenging to detect at the time of initiation. As the DTPI progresses towards the skin it presents as non blanchable purple or localized maroon areas or blood-filled blisters. This clinical presentation is often labeled as a stage 1 or stage 2 PrI, resulting in the management at the level of skin. However, by then, the injury has involved the deep tissue and is approaching the epidermis. Other challenges are the skin changes on a darkly pigmented skin make the detection and differentiation difficult. Various research studies have suggested the use of biomarkers in sweat or blood using infrared spectroscopy. Imaging with MRI and ultrasound are other methods used for early detection. Still, these diagnostic techniques under research are not in use in the hospital settings. Inappropriate management and late detection affect the healing, progressing into a stage IV pressure injury or an irreversible injury.

In a prevalence study conducted in the US population in the year 2006 – 2009 showed a decrease in the proportion of stage I and stage II pressure injury. In contrast, there was a 3-fold increase in the proportion of DTPI. This increase is due to staging education among the health care staff.

1.4 Etiopathogenesis of Pressure Injury

1.4.1 Etiology of Pressure Injury

The predisposing factors to the development of a PrI are broadly classified into mobility/activity related factors, sensory perception, extrinsic factors, and patient related factors [30]. Immobility is a major contributing factor to the PrI formation. The consequences of prolonged immobilization affect the various systems. Cardiovascular manifestations include the orthostatic hypotension, change in body fluid composition, and impairment in the peripheral blood flow. Disuse of the muscles can cause the affected muscle groups to atrophy over time. Individuals who are immobilized have decreased appetite affecting their nutrition requirements leading to weight loss and malnutrition [24]. The general health status and nutrition intake are affected in cognitively impaired increasing the risk of developing a PrI.

Some of the extrinsic factors are the pressure shearing force, friction, moisture, and the stiffness of the support surface [30]. Friction is defined as the force that resists two surfaces. For instance, individual moving on the wheelchair without being completely lifted can result in a friction between the skin and the supporting surface. A shear stress is generated when the externally applied load causes the tissue to move in the direction opposite and parallel to the supporting surface. Friction and shear stresses are primarily responsible for the development of superficial pressure injury and maybe a predisposing factor to the DTPI formation. Moisture caused by urinary incontinence, fecal incontinence, and dual incontinence can exacerbate the stage I/II injury to a stage IV injury.

The intrinsic biomechanical factors that determine the risk of developing DTPI are the anatomy of the bone and the mechanical properties of the soft tissue affected by illness or age. These biomechanical factors make certain individuals more susceptible than the other individuals [30]. Premorbid conditions such as hypotension, anemia and diabetes mellitus have also shown an increase in the risk of PrI.

1.4.2 Mechanisms of Deep Tissue Pressure Injury

Muscle tissue is comprised of 3 components – bundles of muscle fibers (fascicles), connective tissue, and blood and lymph vessels. Each muscle fibers is a multinucleated syncytium made of the myoblasts. Traditionally, the pathophysiology of DTPI was explained using the vascular and lymphatic components of the muscle tissue. A recently emphasized mechanism is the role of mechanical tissue deformation in the development of DTPI. It is difficult to separate these two mechanisms in understanding their effects on tissue damage.

1.4.2.1 Mechanical deformation

In the last decade, studies have focused on cell deformation within the tissue as critical factor for cell damage after prolonged mechanical loading. Nonetheless, the development of DTPI is considered to be caused by combined effects of cellular deformation and ischemia.

It was believed that if the pressure between the contact area i.e. skin and the support surface (interface pressure) exceeded the critical capillary closure pressure (32 mm Hg), ischemia occurs [31]. If this pressure is sustained for a sufficient period of time a tissue break down could occur. Conversely, a study published in 1953 indicated the interface pressure cause the blood vessels in the skin and the subcutaneous tissue to be occluded and not the blood vessels in the muscle. The surface pressure (friction/shear) and the interface pressures are not solely responsible for the internal mechanical conditions that occur inside the tissue, which are important for the tissue break down. The internal mechanical conditions are a consequence of the tissue internal stresses/strain caused by the compression of the tissue between the support surface and bony prominence.

The relationship of the external load to local internal stresses/strain were studied using the theoretical and numerical models. One such model is the finite element model proposed by Oomens et al., provides the magnitude and the location of the internal stresses/strain. An empirical model was used to demonstrate the relationship using intact and SCI pigs. The levels of strain were quantified in the pig muscle around the ischial tuberosity during the external loading (25 % BW and 50% BW). The strain measurements were performed at the center of ischial tuberosity (IT), dorsal, and ventral IT. The muscle tissue located between the apex of IT and edge of the skin, moves the tissue towards the IT known as the tissue compression. Muscle tissue located laterally from the IT was displaced away from the bone is referred as the shear deformation. It was found that the high peak strain magnitudes were present ventral to the bony prominence in comparison to the central IT. The compression of the tissue near/adjacent to an irregular shaped bony prominence results in an internal pressure to exceed the external surface pressure at the skin level leading to tissue deformation.

The threshold value of a cell indicates the effect of deformation and the time for the cell damage to occur. If the level of deformation is below this threshold level – cells are not affected at all. These cells are able to adapt to the physical deformation. However, if the cell deformation exceeds the adaptive capacity of the cell – cell damage occurs by apoptosis (programmed cell death) or necrosis (final cell death). Tissue deformation can result in apoptosis within 10 minutes.  A study performed to determine the relationship between the cell deformation and cell damage indicated a high compressive strain (50%) showed a higher percentage of damaged cells in comparison to 30% gross compression.

Intact cells utilize circulating ATP as energy to maintain a normal homeostasis. The energy is generated by a cytoplasmic pathway known as the glycolysis, converts glucose into two pyruvates. During this pathway 2 moles of ATP are generated. If a cell lacks mitochondria or oxygen, glycolysis occurs anaerobically. In the presence of cell mitochondria and oxygen, the pyruvate enters the citric acid cycle leading to the oxidation of acetyl-CoA to carbon dioxide, generating energy in the form of ATP. Enzymes in the mitochondria and those that are responsible for the citric acid cycle produce nicotinic amide dehydrogenase (NADH). Oxidation of NADH to release NAD are reutilized by the mitochondrial enzymes as required. This oxidation reaction delivers electrons to the electron transport chain (ETC). The mitochondrial electron transport chain functions capture chemical energy to convert into electricity through the transport of electrons in the chain. The energy generated in this process can run proton pumps which drive the protons from the matrix space into intermembrane space. It also helps in the transport of Na+ ions, across the membrane to create a concentration gradient.

1.4.2.2 Ischemia

Muscle tissue is highly vascularized making it susceptible to perfusion changes during sustained loading. The animal studies have demonstrated that muscle tissue is tolerant to ischemia for 4 hours. The resulting decrease in blood supply leads to a state of ischemia and tissue hypoxia, wherein there is a deprivation in the transport of nutrients and oxygen to the cell and removal of metabolic wastes away from the cell in the tissue. Irreversible muscle cell damage starts with 3 hours of ischemia and is complete at 6 hours.

Tissue hypoxia deprives the ETC of sufficient oxygen, further decreasing the rate of ETC and ATP production. As the metabolic demands of the tissue exceed the availability, cells switch to anaerobic metabolism. This leads to a faster depletion of glucose stores, and an accumulation of lactic acid as a by-product. Lactic acid compromises cellular viability, and induces a state of lactic acidosis, which can lead to apoptosis and necrosis [7]. In this cell acidosis state, functioning of Na⁺/K⁺-ATPase pumps fail, causing intracellular accumulation of Na⁺ and Ca²⁺ and in exchange K⁺ to diffuse out of the cell. This electrolyte imbalance changes the concentration gradient within the cell, and therefore induces water to enter the cell through diffusion, causing cellular swelling and eventual cell rupture. An increase in Ca²⁺ by the mitochondrial permeability transition pore causes the Ca²⁺ in the cytosol to increase. This leads to an increase in the Ca²⁺ dependent proteases, nucleases, and production of toxic reactive oxidative species [9]. The activation of Ca²⁺ dependent proteases causes the extracellular matrix to undergo degradation. The phospholipase enzyme activation increases the cell and organelle membrane permeability. The presence of endonucleases leads to denaturation of proteins, clumping of nuclear chromatin, and inactivation of DNA and enzymes leading into an irreversible cell death.

1.4.2.3 Ischemia Reperfusion Injury (IRI)

The perfusion and nutrients to the cells are restored when the load is removed. For example, when an individual is turned towards the opposite side or is lifted from the wheelchair to relieve the pressure. Although restoration of blood flow causes some of the ischemic muscle to be salvaged but a series of complex reactions occur in the blood vessels and adjacent tissue.

1.4.2.3.1 The sequence of events occurring after reperfusion –

• Microvascular disruption
• Neutrophil accumulation
• Edema formation

If the ischemic skeletal muscle is exposed to normoxic blood, microvascular disruption ensues leading to increased permeability and tissue damage. In contrast, reperfusion of the skeletal muscle with anoxic blood generates a less tissue damage. Therefore, limiting the availability of oxygen to ischemic tissue during reperfusion can reduce the tissue necrosis. The reperfusion of ischemic tissue produces an acute inflammatory response that causes necrosis and irreversible cell death to both vascular endothelium and tissue. Injury caused by 3 hours of ischemia followed by reperfusion was found to be higher than ischemia alone. In fact, IRI is a severe cause of DTPI thus making it an important underlying mechanism.

During the sustained loading (~3 hours) ischemia causes the cell to lose the ability to produce ATP from ADP. There is a substantial increase of ADP which is converted to hypoxanthine in a series of reactions. Hypoxanthine and xanthine is accumulated in ischemic conditions leading to an oxidative damage. Xanthine Dehydrogenase (XDH) is an enzyme present in the non-ischemic healthy cells. Hypoxic stress results in the production of xanthine oxidase (XO) from Xanthine dehydrogenase (XDH). By then, some cells have passed the point of recovery and are progressing to necrosis.

When the load is removed reperfusion introduces molecular oxygen into the tissue. This molecular oxygen reacts with hypoxanthine and XO to produce a burst of reactive oxygen metabolites (ROM) such as superoxide anions and hydrogen peroxide. Histochemical tests indicated the localization of XO in microvascular endothelial cells making it susceptible to oxidant damage. In the presence of iron the superoxide anion and hydrogen peroxide are converted to highly reactive hydroxyl ions (Haber Weiss reaction).

The ROM degrade the structural, contractile, transport proteins, enzymes, and nucleic acids. The cytotoxic hydroxyl ions cause lipid peroxidation of cell membrane. In turn, there is a release autolytic enzymes, apoptotic factors, and reactive ions into the extracellular space. Lipid peroxidation of the cell membrane affect the cell permeability. This can cause increase Ca⁺² influx associated with loss of K⁺ ions. The increase in intracellular Ca⁺² activates Ca⁺² dependent proteases, phosphatases, and phospholipases causing cell death.

In response to IRI the neutrophils (primary leukocytes) are recruited in the capillaries to post ischemic tissue. The neutrophils are subdivided into the circulating pool and a marginating pool. The neutrophils migrating along the central axial column of the capillary contribute to the circulating pool. Whereas the neutrophils migrating close to the capillary wall are referred to as the marginating pool. The rolling of the neutrophils in approximation to vascular endothelium is mediated by P-selectin and E-selectin at the site of injury. The neutrophils bound to the vascular endothelium are exposed to cytotoxic compounds to form activated neutrophils. The activated leukocytes contain NADPH oxidase which oxidizes NADP⁺ and reduces molecular oxygen to superoxide and hydrogen peroxide. The activated neutrophils contain -2 integrin modulating the adhesion between the neutrophil and the vascular endothelium. The vascular endothelial cells also contain adhesion molecules – Intracellular adhesion molecule (ICAM) and Vascular cell adhesion molecule (VCAM). These adhesion molecules aid in firm adhesion of neutrophils and vascular endothelial cells. The -2 integrin /ICAM interaction lead to microvascular barrier disruption further increasing the filtration of trans capillary fluid into the interstitial space known as the edema.

The failure in restoration of blood flow on reperfusion to ischemic tissue is known as no – reflow phenomenon. The mechanism underlying this phenomenon is un clear. Various mechanisms have been proposed to explain the pathogenesis of this perfusion defect. One potential mechanism is the adhesion of activated neutrophils to the vascular endothelium. The partial occlusion of the capillary by the adherent leucocytes affects the blood flow dynamics in the capillaries at the ischemic site. Another mechanism is the release of ROM by the activated neutrophils cause the endothelial cell to swell. This can decrease the caliber of the capillary lumen. Use of antioxidant can decrease the neutrophil and endothelial cell adhesion hence improving the perfusion. Treatment with hyperosmotic saline dextran has shown to decrease the no reflow effect. A third mechanism is the leucocyte adhesion leading to microvascular disruption. Increasing capillary permeability causes the transcapillary fluid filtration into the interstitial space. The increasing interstitial fluid pressure compresses the capillaries preventing the blood flow therefore impairing the cell nutrition during the reperfusion.

1.5. Prevention of Deep Tissue Pressure Injury

1.5.1 Risk assessment scales

Pressure injury risk assessment is a part of screening process to identify individuals who are at risk. Early identification of the risk factors is essential for prevention of DTPI. They help in the prediction of a prevention plan among the high-risk populations. The literature describes various scales for PrI. Of these scales, the commonly used risk assessment scales in the clinics are the Braden, Norton, and Waterlow scales.

The Norton scale, first risk assessment scale was developed in 1962, comprises of 5 subscales. This is a 4-point scale used to grade the general physical condition, cognition, activity, mobility, and incontinence. Even though the subscales have equal weights, few factors have a significant role in the formation of PrI. The cut off score defines those who are at risk from those who are not. A score less than 12 indicates an inevitable risk of PrI. Another scale is the Braden scale used in research studies. The Braden scale consists of 6 subscales – sensory perception, skin exposure to moisture, mobility, ability to change position, nutrition intake, and presence of friction and shearing force. The total score ranges from 6 – 23. A low score indicates a greater risk of developing a pressure injury.

A review study was conducted to determine the effect of the risk assessment scales on the patient outcomes. The results indicate the Braden and Waterlow scales showed no additional benefit in comparison to routine clinical tests. The prevention of pressure injury requires early detection and an appropriate plan. A failure in one of these can lead to the development of a new pressure injury.

1.5.2 Prevention strategies

The preventive strategies aim at reducing the magnitude and duration of pressure between the body surface and the external support. The interface pressure is decreased by manual repositioning and the use of pressure relieving support surfaces. Other newer interventions are introduced to modify the internal mechanical conditions around the bony prominences. Prevention of DTPI is critical to avoid progression into an open wound and the use of expensive interventions for its treatment.

1.5.2.1 Repositioning

A commonly used preventive strategy to redistribute the pressure from particular parts of the body. The Cochrane review for prevention of pressure injury using repositioning showed a 3-hourly repositioning in a 30-degree tilt can improve tissue oxygenation and relieve/redistribute the pressure [32]. A less frequent change in the position results in higher incidence of PrI.

There is no fixed optimal repositioning regime [33][34]. The determining factors for a repositioning schedule are the health status of the individual and the costs associated with the nurse time. The number of turns for an individual, number of nurses required for the turn, and the time for one turn vary with every individual. The clinical guidelines for prevention of PrI requires two-hourly repositioning. The wheelchair users are advised to perform push-ups, side – side leans or back – back leans depending on the nature of the injury. A minimum duration of 2 minutes of unloading is necessary to restore the tissue perfusion and oxygen. Partial unloading can replenish the oxygen to tissues, but the tissue deformation leads to an irreversible injury. Much of the prevention depends on the efficiency of the patient, care providers, and healthcare staff. The health care staff experience musculoskeletal symptoms while performing frequent repositioning impacting their work.

One of the disadvantages of frequent repositioning is sleep deprivation. The alteration of sleep-wake cycle affects the regulation of immune function. In turn, slowing the healing process and recovery. The presence of wounds, stiff joints, and bony pain can cause additional discomfort on repositioning.

1.5.2.2. Support surfaces

Pressure relieving and redistributing devices such as cushions, mattresses, overlays, and bed replacements are used in conjunction with repositioning to reduce the magnitude and the duration of pressure. They mold around the shape of the body to distribute the weight over greater surface area or mechanically alter the interface pressure. The support surfaces are divided into low technology/non-powered surfaces and high technology surfaces based on their mode of operation. The low technology surfaces have a static relief of pressure whereas the high technology surfaces have a dynamic pressure relief.

The standard hospital mattresses are used on initial admission. However, individuals at risk of developing a PrI are moved from standard mattresses to non-powered/static relief devices. During long surgical procedures and postoperative period these devices are laid on the bed to reduce a development of PrI. Few examples of non-powered/static relief devices are the sheep skin, static air-filled supports, gel-filled supports, water-filled, and bead filled supports. Similarly, specialized cushions are prescribed for the wheel chair users for preventing PrI. These devices fit around the body surface so that the pressure is distributed over the larger area. Many studies compared the incidence and severity of PrI with the use of these devices. One of the study showed a significant decrease in the incidence of stage 1 PrI from 26.3 % to 19.9% in the group that used the specialized cushions/mattresses. There was no significant decrease in the incidence of stage 2 or stage 4 PrI.

A specialized device in the dynamic group is the alternating pressure system. These devices are connected to an external power source to generate an alternating inflation and deflation of the cells in the mattress/cushion. The most commonly available devices are made of air and water. The disadvantages with these systems are seasickness like sensation and sleep disruption in the users. A newer device is comprised of variable density of foam in the air cells to avoid these unpleasant sensations. These systems focus on reducing the interface pressure, but have a minimal role on internal mechanical conditions around the bony prominence. Although, prevention of superficial pressure injury may be possible with these interventions. So far, there is no established evidence that these preventive methods are able to reduce the occurrence of DTPI.

1.5.3.3. Electrical stimulation

The use of electrical stimulation to reduce the seating pressure was studied by Simon Levine and the coworkers. This group was among the first in the literature to quantify the tissue deformation and shape on electrical stimulation using eight transducer ultrasound imaging system. The second paper published in the same year studied the change in the blood flow with electrical stimulation in able bodied and SCI individuals. The study concluded that the SCI individuals had an increase in the blood flow between rest and electrical stimulation. The experiments were performed in the absence of pre-muscle conditioning hence the effect of muscle fatigue cannot be ruled out.

Ferguson et al. (1992) continued Levine’s work by conducting experiments in nine SCI individuals. The electrical stimulation was applied for 10 second intervals with a 20 second rest period to the quadriceps muscle by the restricting the knee extension. The periodical muscle contractions were able to relieve the ischial pressures during sitting. Another study also reported a decrease in the ischial tuberosity pressures with gluteus muscle stimulation.

In addition, paralyzed muscles undergo a change in the cross-section area and enzymatic properties after a complete SCI. Long term application of low frequency (  10 Hz) electrical stimulation to the tibialis anterior muscle showed an increase oxidative enzyme activity and fatigue resistance. The electrical stimulation was delivered for 6 weeks with subsequent increase in the duration stimulation per day. This study showed no change in the muscle fiber size and endurance with training. However, another study showed that electrical stimulation when applied for a duration of eight weeks increased the muscle bulk with a significant decrease in the ischial tuberosity pressures during the stimulation. The improvement in the muscle properties provide a cushioning effect leading to a static pressure relief around the ischial tuberosities.

Mushahwar lab, developed a novel technique known as Intermittent Electrical stimulation (IES) for prevention of the DTPI. The principal idea behind this technique is periodical IES induced muscle contractions are able to mimic the voluntary or assisted repositioning. Two paradigms were tested in the able-bodied individuals (10 seconds of electrical stimulation every 10 mins vs 5 mins). The study investigated the role of IES in changing the tissue shape to reduce the IT pressures. In turn, addressing the first biochemical pathway i.e. mechanical deformation. Secondly, IES induced contraction were able to improve tissue perfusion and oxygenation. The animal study conducted by the same lab showed a significant reduction of muscle volume exhibiting tissue edema with IES, confirming less tissue damage.

In summary, the work by various researchers indicate electrical stimulation could reduce the pressure adjacent to the bony prominences. Thus, reducing tissue deformation and necrosis. By improving the tissue perfusion, electrical stimulation help maintain the tissue viability and properties. With its ablity to target the etiology of DTPI this could be a potential intervention for prevention of DTPI.

Treatment of DTPI

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