**4. Pathogenesis**

The development of a pressure ulcer is not solely dependent upon pressure [8]. Multiple factors that modify the effect of pressure on tissues play a role in the development of pressure ulcers. The tolerance tissues have to external load depends on the duration of the exerted load. High loads can be tolerated for short periods of time, while relatively low loads can be tolerated for longer periods of time. The internal load in the tissues, as a result of the external load, causes cell deformation, occlusion of blood and lymphatic vessels and ischemia. If the internal load could be measured a risk for pressure ulcer, development could potentially be quantified [8].

A pressure ulcer results from sustained compression of soft tissues [5]. This compression occurs most often between a bony prominence and an external surface. Blood flow supplies oxygen and nutrients to the tissues. If pressure is sustained, the blood supply to the tissues is interrupted. When the blood flow is interrupted, oxygen and nutrients are not delivered to the tissues. Without oxygen and nutrients, the tissue will be damaged and eventually die [5].

Not all types of pressure are equally damaging to tissues [9]. Hydrostatic pressure, the pressure exerted by a liquid, as is endured by divers for long periods of time does not result in pressure ulcer formation. Yet localized pressure, as is exerted on the sacrum of a bedbound patient in the supine position for an extended period of time, often causes tissue distortion and blockage of the blood vessels resulting in much more damage. Studies related to localized pressure have found that pressure applied over a bony prominence resulted in more damage to the muscle than to the skin causing the study team to conclude that the muscle is more sensitive to pressure than is the skin or subcutaneous tissue [9].

Further studies identified specific factors associated with the development of a pressure ulcer including; interface pressure, shear, moisture and friction [4]. The NPUAP, after investigating shear and friction which have long been associated with pressure ulcer development, has eliminated friction from its definition of a pressure ulcer the explanation of which will be discussed below [10].

*Interface pressure* contributes to pressure ulcer development, as it is the pressure that develops between the skin and a surface upon which an individual is sitting or lying. Interface pressure is a measure commonly used to evaluate the effectiveness of a support surface [11]. Pressure mapping measures interface pressures and helps to determine appropriate positioning [8].

Not all localized pressure results in a pressure ulcer. When the pressure of short duration is relieved, blood flow returns to the area. This occurrence is known as reactive hyperemia, blood vessels in the area of pressure dilate in an attempt to overcome the ischemia that occurs with the pressure. Reactive hyperemia is transient and is also described as blanchable erythema an area that becomes white when pressed with a finger and returns to erythema when the compression is removed [11].

Pressure that is not relieved and is of longer duration leads to further decreased capillary blood flow, occlusion of lymphatic vessels and tissue ischemia. Over a bony prominence, pressure of 20 mmHg can increase to as much as 300 mmHg. If this pressure is sustained, destruction of deep tissues can occur including destruction of muscle, subcutaneous tissue, dermis and epidermis [11].

**4. Pathogenesis**

326 Wound Healing - New insights into Ancient Challenges

than is the skin or subcutaneous tissue [9].

discussed below [10].

compression is removed [11].

The development of a pressure ulcer is not solely dependent upon pressure [8]. Multiple factors that modify the effect of pressure on tissues play a role in the development of pressure ulcers. The tolerance tissues have to external load depends on the duration of the exerted load. High loads can be tolerated for short periods of time, while relatively low loads can be tolerated for longer periods of time. The internal load in the tissues, as a result of the external load, causes cell deformation, occlusion of blood and lymphatic vessels and ischemia. If the internal load could be measured a risk for pressure ulcer, development could potentially be quantified [8].

A pressure ulcer results from sustained compression of soft tissues [5]. This compression occurs most often between a bony prominence and an external surface. Blood flow supplies oxygen and nutrients to the tissues. If pressure is sustained, the blood supply to the tissues is interrupted. When the blood flow is interrupted, oxygen and nutrients are not delivered to the tissues. Without oxygen and nutrients, the tissue will be damaged and eventually die [5].

Not all types of pressure are equally damaging to tissues [9]. Hydrostatic pressure, the pressure exerted by a liquid, as is endured by divers for long periods of time does not result in pressure ulcer formation. Yet localized pressure, as is exerted on the sacrum of a bedbound patient in the supine position for an extended period of time, often causes tissue distortion and blockage of the blood vessels resulting in much more damage. Studies related to localized pressure have found that pressure applied over a bony prominence resulted in more damage to the muscle than to the skin causing the study team to conclude that the muscle is more sensitive to pressure

Further studies identified specific factors associated with the development of a pressure ulcer including; interface pressure, shear, moisture and friction [4]. The NPUAP, after investigating shear and friction which have long been associated with pressure ulcer development, has eliminated friction from its definition of a pressure ulcer the explanation of which will be

*Interface pressure* contributes to pressure ulcer development, as it is the pressure that develops between the skin and a surface upon which an individual is sitting or lying. Interface pressure is a measure commonly used to evaluate the effectiveness of a support surface [11]. Pressure mapping measures interface pressures and helps to determine appropriate positioning [8].

Not all localized pressure results in a pressure ulcer. When the pressure of short duration is relieved, blood flow returns to the area. This occurrence is known as reactive hyperemia, blood vessels in the area of pressure dilate in an attempt to overcome the ischemia that occurs with the pressure. Reactive hyperemia is transient and is also described as blanchable erythema an area that becomes white when pressed with a finger and returns to erythema when the

Pressure that is not relieved and is of longer duration leads to further decreased capillary blood flow, occlusion of lymphatic vessels and tissue ischemia. Over a bony prominence, pressure of 20 mmHg can increase to as much as 300 mmHg. If this pressure is sustained, destruction When capillaries are occluded metabolic waste begins to accumulate in the surrounding tissues due to the lack of oxygen and nutrients. Capillaries that are damaged become more permeable and leak fluid into the interstitial space‐causing edema. Perfusion is slowed through the edematous tissue; therefore, hypoxia worsens. Hypoxia increases cell death that results in an increased metabolic waste released into the surrounding tissues [11]. The ensuing edema further compresses small vessels causing increased edema and ischemia. Local tissue death occurs, which results in a pressure ulcer [7].

*Shear* is an applied force that causes an opposite yet parallel sliding motion such as when an individual slides in a bed or chair. The individual's skeletal structure slides in one direction yet the skin layer is restrained in the original position secondary to friction forces. In these situations, when shear is involved, multiple studies have found the pressure needed to occlude the blood vessels is much less than in an area where shear force is not involved [5, 8]. Elderly individuals are at higher risk for the effects of shear due to the decreased amount of elastin in their skin which is a normal consequence of aging [5].

*Moisture*, another factor associated with the development of pressure ulcers, alters the resiliency of the epidermis to external forces [11]. The effects of friction and shear are increased in the presence of moisture. Increased moisture is often associated with incontinence, perspi‐ ration or wound exudate [5].

*Friction* was originally determined to be a causative factor in the development of pressure ulcers after a study by Sidney Dinsdale was published in 1974 [10]. The results of this study showed that significantly less pressure was needed to stimulate the development of a full or partial thickness wound when the pressure was applied in conjunction with friction.

There are several forms of friction as they relate to the development of pressure ulcers. Friction, as a general term, is the rubbing of two body parts together. It is also a force that resists the motion of two bodies and/or material elements sliding against each other. In relation to skin breakdown, the type of friction, that is of concern is dry friction, of which there are two types, namely static and kinetic. Static friction is the force that resists the motion between two bodies when there is no sliding. There are multiple aspects that impact the amount of static friction at the skin surface including an individual's hydration level and what the individual is in contact with, for example bed linen. Moisture is an important factor relative to static friction as humidity and liquid moisture increases the friction and may cause an individual to adhere to a surface. Dynamic friction, also known as kinetic friction, is the force between two bodies relative to one another as they are sliding. Dynamic friction occurs when an individual slides downward in bed or rubs a foot in a shoe causing a blister. Such a blister may be misdiagnosed as a pressure ulcer.

In relation to the Dinsdale study, the type of friction applied during the study was not noted. The results of this study showed that the blood flow to the epidermis in a given area was not significantly different when pressure and friction were applied together and when pressure was applied alone. Investigators concluded that increased susceptibility of lesions with friction was not due to ischemia in the epidermis. Three decades later, it has been hypothesized that the friction used in Dinsdale's study was creating shear strain or deformation in deeper layers of tissue. Current hypothesis is that friction causes mechanically damaging shear strain of superficial tissue cells and tissue damage results directly from excessive deformation not ischemia as previously thought.

Friction is an important factor as it leads to shear stress and strain yet does not alone lead to the development of a pressure ulcer. Friction contributes to the development of a pressure ulcer due to the shear forces it can create. In other words, friction causes the shear forces in the tissue, which can increase the risk of tissue breakdown and lead to the development of a pressure ulcer. Therefore, shear remains in the current NPUAP definition of a pressure ulcer yet friction is eliminated. Including friction would be redundant as friction is now thought to be a cause of shear. Also, eliminating friction may decrease the number of wounds that are misdiagnosed as pressure ulcers when they are caused solely by friction [10].
