WM13 • Wound Management Special Offer

Table of Contents

WM13 • Wound Management Special Offer

How to Receive Credit

NetCE 5 Hour Course #34572 • Treating Pressure Ulcers and Chronic Wounds

34572 • Treating Pressure Ulcers and Chronic Wounds

1. INTRODUCTION

2. AN OVERVIEW OF PRESSURE ULCERS

3. PATIENT ASSESSMENT

4. WOUND ASSESSMENT

5. AN OVERVIEW OF WOUND HEALING

6. WOUND CLEANING

7. PAIN MANAGEMENT

8. WOUND DEBRIDEMENT

9. WOUND DRESSINGS

10. WOUND MONITORING

11. PREVENTION OF PRESSURE ULCERS

12. PROGNOSIS

13. CONCLUSION

14. RESOURCES

Works Cited

Evidence-Based Practice Recommendations Citations

NetCE 5 Hour Course #34343 • Pressure Ulcers and Skin Care

34343 • Pressure Ulcers and Skin Care

1. INTRODUCTION

2. GENERAL CHARACTERISTICS OF SKIN

3. PRESSURE ULCERS

4. PRESSURE ULCER RISK ASSESSMENT

5. SKIN AND PAIN ASSESSMENTS

6. INDIVIDUALIZED PROGRAM OF SKIN CARE

7. DOCUMENTATION

8. CONCLUSION

Works Cited

Evidence-Based Practice Recommendations Citations

NetCE 5 Hour Course #34372 • Hyperglycemia and Wound Management

34372 • Hyperglycemia and Wound Management

1. INTRODUCTION

2. CAUSES OF HYPERGLYCEMIA

3. AN OVERVIEW OF WOUND HEALING

4. DIABETES AND WOUND DEVELOPMENT AND HEALING

5. VASCULAR ULCERS

6. SENSORY-NEUROPATHIC ULCERS

7. PRESSURE INJURIES

8. SURGICAL WOUNDS

9. WOUND DOCUMENTATION

10. CASE STUDIES

11. CONCLUSION

Works Cited

Evidence-Based Practice Recommendations Citations

WM13 • Wound Management Special Offer

Maryam Mamou, BSN, RN, CRRN, CWOCN

www.netce.com

Copyright © 2026 NetCE, All rights reserved.

WM13 • Wound Management Special Offer

Expiration Date: 09/30/2020

How to Receive Credit

To complete this Special Offer for continuing education credit please go to http://www.netce.com/specials in your browser.

For assistance with receiving continuing education credit, please contact us at help@netce.com.

34572 • Treating Pressure Ulcers and Chronic Wounds

Maryam Mamou, BSN, RN, CRRN, CWOCN

www.netce.com

Copyright © 2018 NetCE, All rights reserved.

Implementation of early, state-of-the-art treatment is the key to effectively treating pressure ulcers and chronic wounds. However, this treatment must be holistic in its approach and take into consideration the patient's medical condition and the patient's/family's long-term goals. In this team effort, nursing staff of all levels play an important and decisive role in pressure ulcer treatment. This course will discuss how nurses can treat various types of pressure ulcers and wounds effectively and completely and will provide the information necessary to respond to patient and/or family queries about treatments used in wound care.

Table of Contents

34572 • Treating Pressure Ulcers and Chronic Wounds

Course Overview

Audience

Course Objective

Learning Objectives

Faculty

Faculty Disclosure

Division Planner

Division Planner Disclosure

About the Sponsor

Disclosure Statement

1. INTRODUCTION

2. AN OVERVIEW OF PRESSURE ULCERS

NPUAP PRESSURE INJURY STAGING

3. PATIENT ASSESSMENT

PATIENT HISTORY AND DATA COLLECTION

PHYSICAL EXAMINATION

NUTRITIONAL ASSESSMENT

OTHER COMORBIDITIES

ESTABLISHING APPROPRIATE GOALS

4. WOUND ASSESSMENT

HISTORY OF THE WOUND

WOUND PHOTOGRAPHY

WOUND MEASUREMENT

TUNNELING AND UNDERMINING

WOUND BED

SURROUNDING SKIN

WOUND PAIN

5. AN OVERVIEW OF WOUND HEALING

HEMOSTASIS

INFLAMMATION

PROLIFERATION

MATURATION/REMODELING

6. WOUND CLEANING

7. PAIN MANAGEMENT

8. WOUND DEBRIDEMENT

AUTOLYTIC DEBRIDEMENT

ENZYMATIC DEBRIDEMENT

MECHANICAL DEBRIDEMENT

CHEMICAL DEBRIDEMENT

9. WOUND DRESSINGS

HYDROCOLLOIDS

HYDROGEL

FOAM DRESSINGS

SILVER-IMPREGNATED DRESSINGS

CADEXOMER IODINE DRESSINGS

CALCIUM ALGINATE DRESSINGS

HYDROCOLLOID FIBER DRESSINGS

GAUZE

COMPOSITE DRESSINGS

COLLAGEN DRESSINGS

SPECIAL CONSIDERATIONS

10. WOUND MONITORING

DOCUMENTATION

11. PREVENTION OF PRESSURE ULCERS

12. PROGNOSIS

13. CONCLUSION

14. RESOURCES

Works Cited

Evidence-Based Practice Recommendations Citations

34572 • Treating Pressure Ulcers and Chronic Wounds

Education Category. Infection Control / Internal Medicine

Release Date. 08/01/2018

Expiration Date. 07/31/2021

Course Overview

Implementation of early, state-of-the-art treatment is the key to effectively treating pressure ulcers and chronic wounds. However, this treatment must be holistic in its approach and take into consideration the patient's medical condition and the patient's/family's long-term goals. In this team effort, nursing staff of all levels play an important and decisive role in pressure ulcer treatment. This course will discuss how nurses can treat various types of pressure ulcers and wounds effectively and completely and will provide the information necessary to respond to patient and/or family queries about treatments used in wound care.

Audience

This course is designed for nurses in all care settings who may care for patients with pressure ulcers or chronic wounds.

Course Objective

The purpose of this course is to provide nurses with information about the process of wound healing and interventions that may advance or hinder it in order to support the use of evidence-based practice and improve patient health.

Learning Objectives

Upon completion of this course, you should be able to:

1. Describe pressure injuries and ulcers and how they develop.

2. Accurately identify pressure injury stages.

3. List key points of patient history and physical examination, and describe how the different body systems impact pressure injury development and healing.

4. Perform a comprehensive wound assessment.

5. Discuss the stages of wound healing.

6. Describe the different approaches to wound debridement and cleansing.

7. List the different types of dressing materials available for wound care.

8. Outline the necessary components of evaluating and monitoring wound healing.

Faculty

Maryam Mamou, BSN, RN, CRRN, CWOCN, is an Irish-trained RN who has lived and worked in the United States for 20 years. During her career, she has completed a BSN and went on to become a certified rehabilitation nurse, a certified life care planner, and more recently a certified wound ostomy and continence nurse. She is a graduate of the wound ostomy and continence program at Emory University in Atlanta, Georgia, and is nationally certified in these areas.

Ms. Mamou has worked in various rehabilitation settings and has first-hand experience of how pressure ulcers impact patients' recovery and quality of life. She has held positions as staff nurse, unit coordinator, educator, and director of nursing in home health care. She has been involved in developing and implementing several staff education programs in a variety of settings. She was most recently employed as a wound ostomy and continence nurse at East Alabama Medical Center in Opelika, Alabama.

Faculty Disclosure

Contributing faculty, Maryam Mamou, BSN, RN, CRRN, CWOCN, has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

Division Planner

Jane C. Norman, RN, MSN, CNE, PhD

Division Planner Disclosure

The division planner has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

About the Sponsor

The purpose of NetCE is to provide challenging curricula to assist healthcare professionals to raise their levels of expertise while fulfilling their continuing education requirements, thereby improving the quality of healthcare.

Our contributing faculty members have taken care to ensure that the information and recommendations are accurate and compatible with the standards generally accepted at the time of publication. The publisher disclaims any liability, loss or damage incurred as a consequence, directly or indirectly, of the use and application of any of the contents. Participants are cautioned about the potential risk of using limited knowledge when integrating new techniques into practice.

Disclosure Statement

It is the policy of NetCE not to accept commercial support. Furthermore, commercial interests are prohibited from distributing or providing access to this activity to learners.

1. INTRODUCTION

Implementation of early, state-of-the-art treatment is the key to effectively treating pressure ulcers and chronic wounds. However, this treatment must be holistic in its approach and take into consideration the patient's medical condition and the patient's/family's long-term goals. Pressure ulcer management should incorporate comprehensive, holistic care so that all factors that contribute to the development and progress or lack of progress of the wound are equally addressed. The diagnosis and management of the wound should be seen in the context of the whole person.

Studies have shown that the most effective model for wound care management is a multidisciplinary team approach. Ideally, the team should include all disciplines with a role in promoting wound healing, including physicians, certified wound care nurses, nursing staff, physical therapists, dieticians, occupational therapists, social workers, utilization review specialists, and speech therapists [1]. In this team effort, nursing staff of all levels play an important and decisive role in wound treatment. However, it can be a daunting task for any nurse to be part of the decision-making process responsible for determining the wound care modality best suited to meet the needs of the patient. This course will provide the information necessary to properly treat various types of pressure ulcers and wounds effectively and completely.

As a result of the National Pressure Ulcer Advisory Panel (NPUAP) 2016 Staging Consensus Conference, the terminology changed from "pressure ulcer" to "pressure injury" to more accurately describe pressure injuries to both intact and ulcerated skin [18]. The staging system for pressure ulcers was also updated to clarify the definitions of various stages and reduce confusion. For the purpose of this course, the terms "pressure ulcer" and "pressure injury" are used interchangeably, except in defining and staging injury.

2. AN OVERVIEW OF PRESSURE ULCERS

According to the 2016 NPUAP guideline, pressure injuries are localized areas of injury to the skin or underlying soft tissue caused by sustained pressure or pressure in combination with shear or friction, including those related to a medical or other device. The tolerance of soft tissue for pressure and shear may also be affected by microclimate, nutrition, perfusion, comorbidities, and condition of the tissue. The injury can present as intact skin or an open ulcer and may be painful. They commonly develop in association with debilitating illness and injury that lead to immobility and gravity-dependent pressure over boney prominences, such as the sacrum, hip, heel, or ankle [1,14].

A pressure ulcer may also be referred to as a pressure injury, pressure sore, a bed sore, a dermal ulcer, or a decubitus ulcer. The ulceration is caused by compression of the soft tissue between two hard surfaces—the bone surface internally and the rigid surface of a bed, chair, or splint externally. According to the Centers for Medicare and Medicaid Services (CMS) guideline, a pressure ulcer can develop in at-risk patients within two to six hours of the onset of pressure [2]. Pressure ulcers can occur in all healthcare settings and affect all age groups. No healthcare specialty is immune from having a patient who will develop pressure ulcers [3]. The skin is the largest organ in the body, and preserving its integrity depends on the other organ systems for circulation, nutrition, and immune function.

The study of pressure ulcers began in recent times, although historical evidence suggests that wound problems have existed throughout humanity [4]. The oldest written documentation of wound management is from around 1500 B.C.E., in studies of ancient Egyptian medicine. These scripts show that Egyptians used oiled frog skins, honey, lint, and animal grease for wound care [4]. Attention to pressure ulcer prevention and treatment has grown in recent years, starting in the 1990s [4]. Historically, pressure ulcers were regarded as a nursing problem, but they are now recognized to be the result of deficits at multiple points of care [4].

An estimated 95% of pressure ulcers occur on the lower part of the body, with approximately 70% in the hip and buttocks area and 15% to 25% in the lower extremities [5]. There is a two to six times greater mortality risk for patients who develop pressure ulcers [5,6]. In acute care hospitals, patient risk for acquiring a pressure ulcer is estimated to range from 2.7% to 29% [1,5].

Pressure ulcers are one of the most recurrent medical complications of spinal cord injuries. The Model Spinal Cord Injury System reported that the risk of acquiring a pressure ulcer is approximately 15% in the first year after injury and increases steadily to about 27% at 25 years post-injury [7]. At any given time, 17% to 39% of the spinal cord injured population has a pressure ulcer [7].

The recurrence rate, or the number of patients who have had a pressure ulcer and develop another one, is highly debatable due to a lack of standardized nomenclature. One estimate for pressure ulcer recurrence ranges between 5% to 41%; another source indicates recurrence rates between 40% and 80%. Although rates are considered highly variable, all patients with existing pressure ulcers are considered at high risk for developing additional ulcers, regardless of the clinical setting [3,35].

NPUAP PRESSURE INJURY STAGING

In 2014, the NPUAP and the European Pressure Ulcer Advisory Panel (EPUAP) developed a common international definition and description system for pressure ulcers. As noted, the NPUAP further revised some of these definitions and staging efforts to reduce confusion and clarify terminology in 2016. The revised NPUAP guidelines for staging a pressure injury are [3,18]:

- Stage 1 Pressure Injury—Nonblanchable erythema of intact skin: Intact skin with nonblanchable redness in a localized area (usually over a bony prominence). Presence of blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes. Color changes do not include maroon or purple discoloration, as this may indicate deep pressure injury. Changes may appear differently in darkly pigmented skin.

- Stage 2 Pressure Injury—Partial-thickness skin loss with exposed dermis: The wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-filled blister. Adipose and deeper tissues are not visible. Granulation tissue, slough, and eschar are not present. These injuries commonly result from adverse microclimate and shear in the skin over the pelvis and shear in the heel. This stage should not be used to describe moisture-associated skin damage, including incontinence-associated dermatitis, intertriginous dermatitis, medical adhesive-related skin injury, or traumatic wounds (e.g., skin tears, burns, abrasions).

- Stage 3 Pressure Injury—Full-thickness skin loss: These wounds display full-thickness skin loss with adipose visible in the ulcer and granulation tissue and epibole (rolled wound edges) often present. Slough and/or eschar may be visible. The depth of tissue damage varies by anatomic location; areas of significant adiposity can develop deep wounds. Undermining and tunneling may occur. Fascia, muscle, tendon, ligament, cartilage, and/or bone are not exposed. If slough or eschar obscures the extent of tissue loss, it is considered an unstageable pressure injury.

- Stage 4 Pressure Injury—Full-thickness skin and tissue loss: Wounds of this stage have full-thickness skin and tissue loss, with exposed or directly palpable fascia, tendon, muscle, ligament, cartilage, or bone, often with sloughing or eschar on the wound bed and epibole, undermining, tunneling, and fistula formation. Depth varies by anatomic location. If slough or eschar obscures the extent of tissue loss, it is considered an unstageable pressure injury.

- Unstageable Pressure Injury—Full thickness skin and tissue loss in which the extent of tissue damage within the ulcer cannot be confirmed because it is completely covered by slough and/or eschar. If slough or eschar is removed, a stage 3 or stage 4 pressure injury will be revealed. Stable eschar (i.e., dry, adherent, intact without erythema or fluctuance) on the heel or ischemic limb should not be softened or removed.

- Deep Tissue Pressure Injury—Persistent non-blanchable deep red, maroon, or purple discoloration: This wound is characterized by intact or non-intact skin with localized area of persistent non-blanchable deep red, maroon, or purple discoloration or epidermal separation revealing a dark wound bed or blood-filled blister. Pain and temperature change often precede skin color changes. Discoloration may appear differently in darkly pigmented skin. This injury results from intense and/or prolonged pressure and shear forces at the bone-muscle interface. The wound may evolve rapidly to reveal the actual extent of tissue injury or may resolve without tissue loss. If necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle, or other underlying structures are visible, this indicates a full thickness pressure injury (Unstageable, stage 3, or stage 4). This term does not describe vascular, traumatic, neuropathic, or dermatologic conditions.

In addition to the revised staging definitions, the NPUAP Consensus Conference members agreed upon two new pressure injury definitions [18]:

- Medical device-related pressure injury: Medical device-related pressure injuries result from the use of devices designed and applied for diagnostic or therapeutic purposes. The resultant pressure injury generally conforms to the pattern or shape of the device. This term refers to etiology; the injury should be staged using the staging system.

- Mucosal membrane pressure injury: Mucosal membrane pressure injuries are found on mucous membranes with a history of a medical device use at the anatomic location. Due to the anatomy of the tissue, these injuries cannot be staged.

3. PATIENT ASSESSMENT

Assessment is the first and most critical step in wound care. It is important to keep in mind that treatment plans are based on the findings from the assessment, and one of the major goals is to prevent undirected and inappropriate care [6].

The two parts of the assessment are the physical examination and data collection, which includes past and present medical history, social environment, educational needs, and cultural norms [5,6]. These two components will enable the clinician to obtain an overall view of the patient's current health status [2].

PATIENT HISTORY AND DATA COLLECTION

A detailed history is usually gathered during an interview with the patient, significant others, family, caregivers, and other healthcare professionals involved in the patient's care. If a patient is admitted from another facility, it may be necessary to speak with the nursing staff at that facility in addition to reviewing the medical record.

The patient interview should be conducted in a private, quiet area and in an unhurried manner. One goal of the interview process is to begin to develop the therapeutic relationship with patients and those who are important in their care. The interview should not be merely a series of questions but should also include active listening and observation [6].

Health habits should be evaluated, including determination of how active the patient is, daily routines, diet, and sleep habits. Smoking, alcohol use, and illicit drug abuse can impair tissue profusion and delay wound healing [5,6].

A medication profile should be obtained, including prescription and over-the-counter medications. Certain medications will interfere with wound healing or interact with wound treatments [5,6]. For example, anti-inflammatory drugs can prolong the inflammatory phase of wound healing [2].

It is important to include a list of allergies in the medical history. For patients with latex allergy, wound care products that contain latex cannot be used. Sulfonamide antibiotics are common allergens, and silver sulfadiazine is a frequently used topical wound application. Before attempting any pharmacotherapy, the clinician must be aware of the patient's allergy history [6].

Social Environment

The patient should be evaluated within the context of his or her support system [5,6]. The strength or weakness of the support system will help determine the structure of the ongoing wound care plan. For example, is there someone who is willing to learn how to change dressings and perform procedures if the patient is discharged home? Is there someone available to take the patient to an outpatient wound treatment center after discharge? It is vital to determine which type of wound care is the safest, most efficient, and most cost effective for the patient and family and to evaluate the optimum environment in which to deliver this care [8].

Consequences of the wound for the patient and significant other/family must also be assessed [8]. Pressure ulcers have profound effects on the quality of life for patients and many times for caregivers also. Studies show that the psychologic impact of ulcers is greater among younger patients [8].

Caregiver guilt associated with the development of a pressure ulcer is common, and healthcare professionals should be aware of their own preconceptions related to pressure ulcers. Nonverbal responses, such as facial expressions, may be more important than the words that are said [8]. Patient and family reports suggest that, in many instances, healthcare professionals regard pressure ulcers as a sign of neglect [8]. In reality, most caregivers are family members willing to take on the responsibility but with little or no training or preparation for the role [8]. The emotional response of the patient and family to a pressure ulcer may range from anger, embarrassment, and shame to guilt and powerlessness [8].

The physical environment in the home setting must also be considered, especially if the patient will require the services of home health care to continue wound treatment postdischarge. Part of the assessment should include discussion of where the patient lives and if all the basic services are available to them after discharge, such as running water. If there is a lack of service for utilities and electricity, a social worker is an invaluable resource. It is important to recognize that these are issues that must be addressed from the moment of admission and not left until discharge is imminent. A patient with a poor or nonexistent support network or a challenging living environment will require a more in-depth discharge plan to ensure that the goals of wound treatment are met [6].

Educational Needs

Ascertaining the patient's educational status and ability to learn and retain new information is essential to the plan of care. Most of this information can be gathered by direct, nonthreatening questions, such as "What grade did you complete in school?" This simple question can elicit a direct answer and further information about the patient's level of education, literacy level, and language preferences. Knowledge of the significant other's/caregiver's level of education and comprehension is also important, especially for cognitively impaired or dependent patients.

In the clinical setting, the questions most frequently asked by patients and their families regarding wound care are [8]:

- Will the wound heal?

- How long will it take to heal?

- Will the treatment cause pain?

Both the patient's and the family's learning style should be assessed, including current understanding of wound prevention and wound care. Misconceptions may be addressed in a nonconfrontational manner. Many beliefs about appropriate wound care interventions are rooted in treatment modalities that were popular in the past. The clinician should be aware of current evidence-based practices and be able to explain them in simple, clear terms.

Finally, the patient's cognitive status should be assessed, including comorbidities that would adversely affect the patient's ability to care for him- or herself. For example, a patient who has experienced a cerebrovascular accident may have difficulties processing and retaining new information. The patient's coping patterns and willingness or ability to comply with treatment should be taken into consideration. Common issues that should be addressed are feelings of hopelessness, despair, depression, and anger. If any of these factors are present, referral to a mental health professional is advised.

Cultural Norms

In our multicultural society, patients have diverse healthcare beliefs, lifestyles, and practices. Respect for these differences is necessary for all healthcare providers. During the patient history, information should be gathered regarding the patient's and family's beliefs about health and wellness. If these beliefs are unknown, goals may be set that are not in keeping with the patient's priorities.

PHYSICAL EXAMINATION

The physical examination will include a systems review, and the clinician must assess how impairments in any body system will impact wound healing and help shape the plan of care [5]. Comorbid conditions play a part in this assessment. Diabetes and obesity, specifically, affect a large number of patients and can result in devastating impairment in wound healing.

Respiratory System

Many respiratory problems can lead to wound development, slow the process of wound healing, and require special wound care interventions. The respiratory system is partially responsible for delivering oxygen and nutrients to the tissues, both of which are necessary for wound healing.

Many patients with asthma require steroid therapy to control and relieve symptoms, and it is not unusual for individuals with asthma to have a prolonged history of steroid use [6]. While steroids are effective in suppressing the inflammation responsible for asthma attacks, they also block the inflammatory phase of wound healing, which is essential to wound resolution [6]. Oral or topical vitamin A may be used to decrease the anti-inflammatory effects of steroids; consultation with the treating physician on an individual basis for the possible use of vitamin A in the wound treatment plan of care is recommended [9].

Cardiovascular System

Patients with heart disease tend to have impaired pumping capacity, and all body tissues will suffer as a result of this. In patients with any cardiovascular disease, such as congestive heart failure and coronary artery disease, wound healing will be problematic [6].

Musculoskeletal and Neurologic Systems

Patients who have impaired movement in any part of their body are at high risk for pressure ulcer development [6]. This includes those with cerebrovascular accident, spinal cord injuries, multiple sclerosis, Parkinson disease, and arthritis [5,6]. These conditions can severely limit mobility (a risk factor for wound development) and make positioning for wound care difficult.

Gastrointestinal System

Gastrointestinal diseases that lead to poor digestion and malabsorption of nutrients will have a negative impact on wound healing [6]. Patients receiving enteral feedings via gastrostomy tubes frequently have loose stools, which can cause wound contamination. A dietician can make recommendations for altering the consistency of the existing formula or changing to another product. A key consideration for patients with diarrhea is the use of dressings that protect the wound from fecal contamination [6].

Genitourinary System

Approximately 10 to 13 million Americans are troubled with either transient or chronic urinary incontinence [10]. Urinary incontinence will lead to maceration (water logging) of the skin, potentiating the risk for further skin breakdown and contamination of existing wounds [6].

NUTRITIONAL ASSESSMENT

A full nutritional assessment and plan, preferably in consultation with a nutritionist, is an important part of wound care, as nutritionally compromised patients have greater difficulty achieving wound healing. The goal is to characterize the patient's current nutritional state, identify changes that have occurred in recent months or weeks, and predict the impact on the patient's overall functional level and prognosis for healing. This assessment should include protein and calorie intake, hydration status, and the measure of serum albumin and/or proalbumin. Dehydration impairs wound healing by decreasing the blood volume available to transport oxygen and nutrients to healing wounds [6].

Once the patient's nutritional needs and functional status have been clarified, an appropriate plan of care can be devised to ensure adequate nutritional and fluid intake. For some patients with late-stage pressure ulcers and documented nutritional deficiencies, a brief period of enteral or parenteral supplementation may be advisable, keeping in mind that the patient's and family's preferences play an important role in establishing a diet plan.

OTHER COMORBIDITIES

Diabetes

It is estimated that 7.2% of the American population has diabetes [11]. In these patients, elevated glucose levels can impair wound healing and negatively affect the immune system's ability to control infection. Wound healing in patients with diabetes is characterized by a decreased production and deposition of collagen and decreased strength of the healed tissue [1]. In addition, many patients with diabetes, particularly those whose disease is poorly controlled, will develop neuropathy, making the development of ulcers more likely and delaying healing.

Obesity

The number of individuals with morbid obesity continues to rise, and this in turn raises problems for wound healing. Adipose tissue is poorly vascularized, placing these patients at risk for prolonged healing [1].

ESTABLISHING APPROPRIATE GOALS

At the end of the interview and physical examination of the wound(s), it should be possible to formulate goals and develop a plan of care as a team, including the patient and family [6]. Clinicians should be aware that a completely healed wound may not be an attainable goal for all patients. For example, an appropriate goal for a hospice patient might be for the wound to remain stable and for wound pain and odor to be adequately controlled.

It may also be necessary to set separate short-term and long-term goals for wound care. The short-term goals are those that would be implemented immediately in the acute care setting, while long-term goals would continue after discharge [6].

4. WOUND ASSESSMENT

All wounds must be thoroughly assessed. Most facilities have their own guidelines regarding minimum frequency of wound assessments, but they should occur at least once a week [8]. Documentation of the cause of the wound is important, if this information can be obtained [8].

Evidence Based Practice Recommendation

According to the National Pressure Ulcer Advisory Panel, the European Pressure Ulcer Advisory Panel, and the Pan Pacific Pressure Injury Alliance, assessment and documentation of the physical characteristics of a pressure injury should include location, stage, size, tissue type(s), color, periwound condition, wound edges, sinus tracts, undermining, tunneling, exudate, and odor.

http://www.npuap.org/wp-content/uploads/2014/08/Quick-Reference-Guide-DIGITAL-NPUAP-EPUAP-PPPIA-Jan2016.pdf

Last Accessed: July 19, 2018

Level of Evidence: C (The recommendation is supported by indirect evidence and/or expert opinion.)

The wound assessment includes identifying the location of the wound; its size, shape, and depth; the condition of the wound edges; and the presence or absence of tunneling or undermining [8]. Assessment findings should also note the condition of the wound bed and how visible it is. For example, the entire surface of the wound may be visible or part or all of it may be obscured by necrotic tissue [6]. The location of the wound should be stated in a manner that is clearly understood [2]. Anatomical markings should be used, such as the sacrum or right or left ischium [2].

It is important to remember that an ulcer cannot be staged until the complete wound bed can be seen [2]. If necrotic tissue is present, determine its defining characteristics, including color (black, brown, yellow, or some combination) and density (hard and leathery or soft to the touch). Necrotic tissue may be attached to the wound bed, like a second skin, or it can be loosely adhered. Even if necrosis is present, visible wound size, length, and width must still be measured and documented.

It is necessary also to evaluate any exudate in the wound and again describe it; it may be clear, bloody, serosanguineous, thick yellow, or greenish. Note whether an odor is present [6].

HISTORY OF THE WOUND

Aside from the physical condition of the wound, information about the history of the wound should be obtained. How the wound started and how long it has been present must be documented. Treatments used and the patient's wound response to these interventions should also be noted [6]. If noncompliance with treatments has been an issue, the underlying cause(s) must be ascertained. Lack of communication between the involved parties may have led to a misunderstanding on the part of the patient and/or caregiver(s) as to their role in wound care. For example, a bedbound patient in the home may require daily dressing changes by the designated family caretaker, with the home health agency monitoring wound progress on a weekly basis. To prevent inadequate care, the caretaker should be appropriately trained in the dressing technique and should understand the importance of completing the dressing changes on a daily basis. Economic strain can also contribute to noncompliance. Patients may not have the financial resources necessary to purchase dressing supplies.

WOUND PHOTOGRAPHY

With the growing awareness of the possibility of litigation in wound care, many facilities have instigated a policy of photo documentation. Wounds present on admission are photographed. In addition, some facilities require serial photographs to track wound progress and status at the time of discharge. Signed consent is required before wound photographs can be taken, and in most instances, the photographs become a permanent part of the patient's medical record. Approximately 75% of home health agencies in the United States now include wound photography as part of the patient's medical record [6]. The American Health Information Management Association recommends that consent for photography be included in the consent for treatment when photography is routinely used [12].

WOUND MEASUREMENT

Accurate measurement of the wound is probably the most important feature of wound assessment [6]. It provides information on the initial size and progression or non-progression of healing, allowing for valuable feedback on the effectiveness of clinical interventions [8]. Decreasing wound size is generally regarded as a sign of wound healing [8].

Wounds should always be measured in centimeters, using a plastic or paper ruler. Wound length is measured from head to toe; width is measured from hip to hip [1]. The depth of the wound can be obtained by gently inserting a sterile cotton-tipped applicator into the wound bed and marking it at skin level. The applicator is then measured using a metric ruler [1].

TUNNELING AND UNDERMINING

Sinus tracts and undermining impair healing, and it is important to immediately identify their presence [8]. A sinus tract is a tunnel that extends from any part of the wound and can bore through subcutaneous tissue and muscle [8]. This tunnel creates dead space, which can result in abscess formation and further impede the healing process [8]. A sinus tract can be measured using a sterile cotton swab [8].

Undermining is defined as destruction of the tissue under the skin around the edges of the wound. This frequently occurs in pressure ulcers that have been subjected to shear force as well as pressure. It is important to document the location and extent of undermining.

The easiest way to measure and describe undermining is by using the face of the clock [8]. With the patient's head representing 12 o'clock, sweep the area of undermining or probe the tunneling to ascertain the depth. For example, undermining along the right border would be recorded as extending from 1 o'clock to 5 o'clock with a depth of 4 cm [8]. It is important to check around the entire perimeter of the wound, as undermining can occur in more than one location.

WOUND BED

It is also vital to assess and document the appearance of the wound bed. If the wound bed has a mixture of tissue in it, this should be documented by an approximate percentage (e.g., the wound base is 75% granulation tissue and 25% slough). Granulation results in "beefy" red tissue with a shiny, moist granular appearance, while necrotic tissue is gray, brown, or black. Eschars are typically gray to black and dry or leathery in appearance [13]. Slough tissue is yellow/white to gray in color. It may be stringy or thick and appear as a layer over the wound bed [13]. Epithelial tissue will often begin to grow in from the edges over the wound surface. This tissue is generally pink and shiny. As a quick reference color guide, red is associated with normal healing, yellow indicates slough or dead tissue, and black is necrosis [8].

SURROUNDING SKIN

The condition of the surrounding skin surface up to 4 cm from the edge of the wound circumferentially must also be assessed and documented. Its characteristics should be noted, particularly color and integrity [9]. Maceration from excessive drainage may indicate that the dressing used is not appropriate and a different product is needed. Circumferential redness up to 2 cm from the wound is indicative of cellulitis.

WOUND PAIN

According to the NPUAP, pressure ulcers cause considerable pain and suffering [14]. Pressure ulcer pain has been described as ranging from sore to excruciating. In one study, 75% of patients rated their pain as mild, discomforting, or distressing; 18% rated their pain as horrible or excruciating [15]. Another study ranked pain according to stage of pressure ulcer and found that 50% of patients with stage 2 pressure ulcers indicated their pain was discomforting. All patients with stage 3 ulcers indicated pain was distressing, and 100% of patients with stage 4 injuries rated pain as horrible [16]. Pain and odor control are a major concern for patients, and studies have shown that patients rank pain control as more important than healing [8]. The level of pressure ulcer pain depends both on the stage of the ulcer and on manipulation of the area (e.g., if a dressing change is done at the time of assessment). The majority of patients report pressure ulcer pain at rest as well as with dressing changes. Pressure ulcer pain may be due to tissue trauma, inflammation, damaged nerve endings, infection, procedures such as debridement, and dressing changes [16].

The criterion standard for assessing pain intensity is self-report using standard pain intensity instruments. Two of the most widely used pain assessment scales are the numeric pain intensity scale and the Wong-Baker Faces Pain Rating Scale [17]. The numeric pain intensity scale consists of ratings from 0 (no pain) to 10 (worst possible pain). This scale can be used for pain assessment with adults and children older than 7 years of age [3]. Visual presentation of the numeric pain intensity scale is helpful with hearing impaired patients, and the scale has been translated into many languages.

The Wong-Baker Faces Pain Rating Scale consists of six faces ranging from a happy smiling face (no pain), to a crying, frowning face (worst pain). The patient is asked to choose the face that best reflects his or her pain. The Faces Pain Rating Scale is the preferred scale for use with children and may also be used with the geriatric population. It can also be used with cognitively impaired patients and those for whom English is a second language.

After the initial pain assessment has been completed, reassessment should be done at regular intervals. As noted, pain intensity should be rated by the patient, not a healthcare professional. The following questions may be used to help determine patients' pain levels:

- What kind of pain are you experiencing?

- What word(s) would you use to best describe it (e.g., burning, aching, shooting)?

- What makes the pain better?

- What makes it worse?

- Where is the pain located?

- Does the pain radiate?

- Would you describe your pain as none, mild, moderate, severe, or excruciating?

- How would you rate your pain on a scale of 0 to 10, with 0 representing no pain and 10 being the worst imaginable pain?

- What is the pain intensity at its worst, best, and now?

- Is the pain better or worse at any particular time of the day or night?

- When does it start and when does it stop?

5. AN OVERVIEW OF WOUND HEALING

Wounds heal by two possible mechanisms: regeneration or scar tissue formation [9]. The depth of the wound (i.e., the number of tissue layers involved) will determine whether the wound will heal by regeneration or by scar tissue formation [9].

Wounds can also be described as healing by primary or secondary intention. Wounds resolved by primary intention are surgically closed [9]. With secondary intention, wounds are left open and heal via the process of granulation, contraction, and epithelialization [9]. Pressure ulcers are an example of a wound that heals by secondary intention [9]. A third classification, wounds that heal by tertiary intention, includes cases in which healing starts by secondary intention but the wound is then surgically closed [9].

Wound healing can be conceptualized as a cascade of events, and the process will differ depending on many different factors, particularly whether the wound is partial thickness or full thickness [9]. A partial thickness wound involves loss of the epidermis and usually part of the dermis [1]. These wounds are shallow, superficial, and painful [9]. Healing of a partial thickness wound is usually a straight-forward process involving a brief inflammatory phase, cell migration, and re-establishment of normal skin layers [9]. The most important consideration with partial thickness wounds is to keep the area moist and clean. It is important to remember that a dry cell is a dead cell.

Full thickness wounds occur when there is destruction of the epidermis and the complete dermis [9]. At the base of the wound, subcutaneous tissue, fascia, muscle, or bone may be visible [9]. Healing of full thickness wounds occurs in four stages: hemostasis, inflammation, proliferation, and remodeling, with considerable overlap occurring among the stages [1]. The time frame for repair of a full thickness wound is considerably longer than that of a partial thickness wound [1]. Regardless of the cause, this biologic process of repair is the same for all acute wounds [6].

HEMOSTASIS

Hemostasis begins soon after a wound develops. This stage involves fibrin clot formation to stem blood loss and to protect the wound from bacterial infection. Studies have shown that substandard clot formation leads to poor wound healing, and individuals with impaired clotting have impaired healing [1,9]. Clotting activates degranulation of the platelets, which causes the release of growth factors called polypeptides into the wound [6]. Growth factors begin the process of wound repair by recruiting neutrophils and macrophages to the wound bed [9].

INFLAMMATION

The standard signs and symptoms of localized inflammation are erythema, swelling, warmth, and tenderness. In normal healing, these signs are only minimally noticeable [6]. During the inflammatory phase of wound healing, they are considered a normal response [6].

After hemostasis is established, the next stage in the process of natural healing is inflammation, which should result in the establishment of a clean wound bed [1]. During this phase, damaged tissue is broken down and, along with excessive bacteria, removed from the wound by white blood cells [1]. The two most important cells involved in the inflammatory phase are neutrophils and macrophages [8].

Neutrophils arrive in the wound immediately after injury, usually within the first hour [1]. For the first few days they lead the wound clean-up process [1]. They target the bacteria and debris in the wound, which is removed by the process of phagocytosis. Neutrophils have a very short life span, and around the third day after injury, they begin to disappear from the wound and are replaced by macrophages [8].

Macrophages perform multiple functions in wound repair and have been referred to as the regulators of wound repair. They are essential to the process of moving wound healing from the inflammatory phase to the proliferative phase [6]. Studies have shown that wound repair is limited or non-existent in the absence of macrophages [9].

When caring for a wound in the inflammatory phase, the goals are debridement and infection control. These wounds usually have a great deal of drainage, so absorptive dressings are normally used [9]. The end result of the inflammatory phase is a clean wound bed [1].

PROLIFERATION

The proliferative phase of wound healing overlaps and follows the inflammatory phase. During this process, the wound bed is filled with new granulation tissue and the wound is resurfaced with new epithelial tissue [9]. This stage can last for several weeks [6].

In full thickness wounds, the process of re-epithelialization occurs only from the wound edges [9]. Margin basal cells attached to the dermis eventually loosen and start migrating across the wound [6]. The horizontal movement comes to a halt when the cells meet [6]. This is called contact inhibition. Wound contraction is the final part of the proliferative phase. Fibers in the wound contract to bring the wound edges closer together.

MATURATION/REMODELING

Maturation and remodeling of the wound involves rearranging collagen fibers and increasing the tensile strength of the scar tissue [9]. Scar tissue regains about 80% of normal tissue strength within three months, but it is important to note that it never achieves the full strength of the original tissue [9]. Therefore, the healed site of an old wound is vulnerable to further breakdown.

6. WOUND CLEANING

The Institute for Clinical Systems Improvement (ICSI) recommends that all pressure ulcers be cleaned when first diagnosed and then with every dressing change [19,29]. The purpose of wound cleaning is to remove nonadherent debris from the wound bed in order to promote healing and make the wound less susceptible to bacterial overgrowth and infection [8]. While cleaning the wound, it is necessary to minimize trauma to the wound bed and healthy tissue [8]. Choosing the correct product for cleaning the wound is very important. Most wounds can be effectively cleaned with normal saline, a nontoxic and inexpensive product [6,29]. If used, saline must be applied to the wound with sufficient force to remove surface debris and contaminants while also minimizing trauma to the wound [1]. Normal saline used for wound cleansing should be room temperature and should be discarded within 24 to 48 hours after opening [6].

The most frequently used method for wound cleansing is irrigation [1]. Studies of the optimal irrigation pressure for effective wound cleaning have found that pressures less than 4 pounds per square inch do not remove wound debris and pressures greater than 15 pounds per square inch force the debris into the wound tissue rather than removing it [1]. The goal is to obtain pressures in the range of 8 to 15 pounds [9]. Irrigation should be done gently using a 35 cc syringe and a 19-gauge needle [9]. An angiocatheter can be used instead of a needle to decrease the risks of finger sticks [1].

If a large amount of debris is present in the wound, use of a commercial cleaning agent may be necessary [8]. Wound cleansers with surfactants in their composition are helpful when the wound is heavily burdened with surface debris. These cleansers break the chemical bonds that attach the wound debris and cause it to loosen from the wound bed [8].

Antimicrobial agents have usually been discouraged for wound cleansing, and they are not required for cleaning healthy, noninfected wounds [6,30]. However, research has shown that antiseptic agents such as sodium hypochlorite and povidone iodine (both at the strength of 0.25%) are safe to use in wound care for short periods of time (four to seven days) to decrease the bacterial burden [6,30]. Sodium hypochlorite should not be used for no longer than 10 days due to cytotoxicity of healthy cells and granulating tissues surround the wound [30,31,32]. Some studies show that infection rates using povidone iodine are similar to those when saline was used; saline may be as effective as and safer to use than povidone iodine [31,32]. The benefits of these products should be weighed against the possible risk of bacterial resistance. Skin cleansers (e.g., those used to remove feces from the skin) are much more toxic than wound cleansers and should not be used for wound care [8].

7. PAIN MANAGEMENT

The goals of pain management in the pressure ulcer patient are to provide analgesic relief and to eliminate the cause of pain. There are several interventions and practice modifications that can prevent or manage wound-associated pain.

Skin care and assessments should be performed at a time of day when the patient is least fatigued [2]. All procedures should be thoroughly explained before they are performed. If a patient has questions, this should be addressed, and healthcare professionals should be encouraging and provide positive reinforcement. It is important to avoid trauma (e.g., shearing, tear injuries) to fragile skin during transferring, positioning, or holding a patient. If necessary, adjunctive medications may be administered to improve sleep and reduce anxiety, which can contribute to experiences of pain.

Dressing changes are often very painful. An analgesic may be administered 30 minutes before dressing changes, and if possible, the number of daily dressing changes should be kept to a minimum. Tape should always be avoided on fragile skin. If patients are able, they should be allowed to remove their own dressings or set the pace of dressing changes. All patients should be assessed for pain before, during, and after dressing changes, and these findings must be documented [8].

Physical therapy and occupational therapy may be helpful to decrease contractures and muscle spasm. Of course, ensuring proper seating and positioning can improve pain scores and decrease the risk for further pressure injuries.

8. WOUND DEBRIDEMENT

Necrotic tissue compromises wound healing and can be a source of bacterial overgrowth [6]. It stalls wound healing in the inflammatory phase and prevents the natural progression of healing [9]. For a wound to heal, it must be free of nonviable tissue, and this is commonly achieved by debridement [8].

Necrotic tissue adheres to the wound bed more when the moisture level in the wound drops and the amount of tissue damage increases [6]. It can present in different forms, though most necrotic tissue is firm and dry [1]. Beneath the dry necrotic tissue is slough, the moist, soft, dead tissue often found loosely attached to the wound bed. Slough has a stringy appearance and may be brown, yellow, or gray in color [1].

In addition to helping move the wound through the stages of healing, debridement is often necessary to visualize the wound bed and stage the wound; a wound covered with necrotic tissue cannot be staged [8]. An exception is eschar on the heels, which acts as a natural biologic cover, and should not be removed unless infection is present.

Evidence Based Practice Recommendation

According to the National Pressure Ulcer Advisory Panel, the European Pressure Ulcer Advisory Panel, and the Pan Pacific Pressure Injury Alliance, mechanical, autolytic, enzymatic, and/or biologic methods of debridement should be used when there is no urgent clinical need for drainage or removal of devitalized tissue. Surgical/sharp debridement is recommended in the presence of extensive necrosis, advancing cellulitis, crepitus, fluctuance, and/or sepsis secondary to ulcer-related infection.

http://www.npuap.org/wp-content/uploads/2014/08/Quick-Reference-Guide-DIGITAL-NPUAP-EPUAP-PPPIA-Jan2016.pdf

Last Accessed: July 19, 2018

Level of Evidence: C (The recommendation is supported by indirect evidence and/or expert opinion.)

The method of debridement used depends on the amount of necrotic tissue present, the location of the wound, and the patient's overall condition [6]. By definition, stage 1 pressure injury does not require debridement. The wound should simply be covered with transparent film for protection and preventive measures taken to limit progression and reduce the risk for additional pressure injury elsewhere. Stage 2 and early stage 3 wounds can often be debrided effectively with autolytic and/or enzymatic debridement technique, as discussed in detail later in this section. Patients with stage 3 or 4 pressure ulcers who have undermining and/or tunneling or extensive necrotic tissue should have a surgical evaluation for possible surgical debridement of the wound, if this is consistent with their condition and the goals of care [3,18]. Infected wounds may require systemic antibiotic treatment and immediate surgical debridement [8]. Maintenance debridement should be continued until there is a covering of granulation tissue in the wound bed and the wound is free of necrotic tissue [3].

AUTOLYTIC DEBRIDEMENT

The body's own physiologic processes to remove necrotic tissue are referred to as autolytic debridement [6]. Studies have shown that autolytic wound debridement is more effective than wet-to-dry dressings because it removes only necrotic tissue and leaves healthy tissue intact [6]. For autolytic debridement to be successful there must be a moist environment and sufficient white blood cells available to the wound [1]. A layer of wound exudate should be kept in contact with the surface of the wound [9]. A moisture-retaining dressing may be used to keep the wound bed moist [6,8]. This allows fluid to accumulate in the wound, rehydrating necrotic tissue and making it possible for enzymes in the wound to digest the dead tissue [6]. For a wound covered with dry eschar, it is appropriate to crosshatch the eschar, as this allows a faster build-up of moisture in the wound [6]. In their clinical practice guidelines for pressure ulcer treatment, the ICSI recommends autolytic and enzymatic debridement as the preferred approach for patients in long-term care and home care and for patients who cannot tolerate other methods of debridement [6,19].

Choosing the correct product and dressing material for autolytic debridement is important to successful healing; a semiocclusive or occlusive dressing should be used [8]. In addition, amorphous hydrogels are effective in digesting necrotic tissue in wounds and may be used as an adjunct [6].

Transparent film dressings are the best choices for debriding dry eschar, as they are non-absorptive. These dressings establish a fluid environment [6]. For moist wounds with necrotic tissue, hydrocolloids are a good choice [6]. Hydrocolloids have the ability to absorb a certain amount of drainage while maintaining a moist wound environment [6].

There are several advantages to autolytic debridement. It is relatively inexpensive and harmless to healthy tissue [6]. Wound progress is usually seen within six days, and it can be used in combination with other debridement methods for enhanced effect [6]. It is generally a good option for patients whose condition does not permit surgical intervention.

The disadvantage of the autolytic approach is that lack of familiarity with the process can cause problems [1]. The breakdown of dead tissue and the subsequent odor and accumulation of exudate may cause clinicians/family members to wrongly infer that the wound is either infected or worsening [1].

Nursing staff and caregivers should understand that the accumulated fluid in the wound contains essential factors necessary for debriding the wound and promoting wound repair [1]. Education should also note that the wound will initially become larger with debridement, but this is not a sign that the wound is deteriorating [8].

ENZYMATIC DEBRIDEMENT

Enzymatic debridement is a safe and effective method that involves the application of a concentrated, commercially prepared enzyme to the surface of the necrotic tissue [8]. It is recommended when surgical debridement is not an option and the patient is not considered a good candidate for autolytic debridement [6,19].

Enzymatic debridement is a selective method that will not adversely affect healthy tissue [6]. Applied enzymes liquefy the necrotic tissue and destroy the bonds that attach it to the wound bed [2]. The advantages of enzymatic debridement are that it does not harm healthy tissue in the wound and can be effectively used in combination with other methods of debridement [6]. Eschar present in the wound should be crosshatched before application of enzymatic therapy to improve efficacy, as enzymes are not active on a dry surface [6].

Wound progress should be seen in 48 to 72 hours [9]. However, complete debridement of the wound may be a long process; therefore, whenever possible this method is used in conjunction with autolytic debridement and conservative surgical wound debridement (i.e., bedside removal of loosely adherent necrotic tissue) [9]. Conservative surgical wound debridement is completed by a physician or a wound care nurse.

Enzyme formulations available for debridement include collagenase (Santyl), papain (enzymes derived from papaya), and trypsin (Granulex, Vasolex, Xemaderm); only collagenase is available in the United States [2]. Collagenase is a derivative of Clostridium bacteria and acts by liquefying the collagen bonds that fasten necrotic tissue to the underlying wound bed. The time to effect ranges from several days to weeks.

Enzymatic debridement can be used in conjunction with most other dressings; however, it should not be used with silver or cadexomer iodine dressings. Silver dressings reduce the efficacy of collagenase by more than 50%; cadexomer iodine reduces its efficacy by 90% [20].

Studies indicate that enzymatic debridement is cost-effective, but it requires daily or twice daily dressing changes and the application of a secondary cover dressing, which should be factored into the cost [20]. When the wound bed is free from necrotic tissue and slough, the use of enzymatic debridement should be discontinued.

Enzymatic debridement is not generally indicated for the treatment of infected wounds due to the extended length of time required to achieve a clean wound [9]. If necessary, enzymes may be used in cases of infected wounds if antibiotic therapy has already been initiated [9].

MECHANICAL DEBRIDEMENT

Mechanical debridement is achieved by applying outside force to remove necrotic tissue in a wound [6,19]. One long-standing and widely used form of mechanical debridement is wet-to-dry gauze dressings, usually with normal saline. Although it is a commonly used treatment, the advantages of familiarity and simplicity of use are outweighed by the disadvantages. Studies indicate that wet-to-dry dressings remove healthy viable tissue as well as necrotic tissue [6]. In addition, the standard time frame for dressing changes, every eight hours, increases the associated costs of labor and supplies [6]. The dry, adherent dressings are painful to remove, and seepage of moisture from the dressing can lead to maceration of periwound tissue [6]. As such, the AHRQ advises cautious use of this method of debridement [6].

Whirlpool therapy is another form of mechanical debridement. It is most frequently used with larger wounds to remove debris and bacteria from the wound bed [1]. However, it does not remove dry eschar from the wound, and there are concerns about the likelihood of cross-contamination between patients [1].

The use of ultrasound waves to debride wounds has also been explored. With this technique, low-frequency ultrasound creates small bubbles in the wound that implode, causing the necrotic tissue to liquefy [2]. This method is generally less painful and less traumatic than traditional methods, with faster healing rates compared to other methods of mechanical debridement [21,33]. Studies show that low-frequency ultrasound is most effective when used three times per week [33]. However, further comparative evidence and large-scale studies are necessary before it can be recommended as a replacement for established treatment modalities [22,33].

Maggot Debridement Therapy

Maggot debridement therapy (MDT), an approach popular at the early 20th century, is finding a renewed place in wound care debridement [8,23]. Much of this interest is centered on the ability of maggots to ingest and destroy micro-organisms without inducing resistance among bacterial organisms [1]. It is believed that the larvae secrete enzymes, including collagenase, that break down the necrotic tissue; they also ingest and destroy micro-organisms [1]. Maggots have the ability to access moist tissue throughout the wound bed and clean small areas without harming healthy tissue [24]. The process involves the application of sterilized larvae from the green-bottle fly maggots to the wound bed every two to three days [8]. The maggots can be applied to the wound directly or in a containment pouch [8]. The most appropriate dressing for wounds treated with maggots is one that keeps the larvae in place, allows for a flow of oxygen, and is suitable for the characteristics of the wound [6].

MDT is indicated for pressure ulcers with necrotic tissue with or without infection [24]. It has also been shown to be an effective treatment of diabetic wounds [25]. Maggots work well in wounds in which moisture and oxygen are readily available and the pH is fairly stable [6]. The therapy is considered mainly for the treatment of wounds for which other forms of treatment are either not appropriate or not successful [9]. MDT is contraindicated in patients who have bleeding abnormalities or deep tunneled wounds [8]. Because there is no benefit in continuing MDT past one week, another type of dressing should be used after two or three applications of MDT [26].

Precautions should be taken to prevent the larvae from coming in contact with healthy skin, as there is a possibility of enzymatic damage [1]. Otherwise, there are no reported side effects from maggot therapy [1]. However, some patients complain of a crawling or tingling feeling [1]. Maggot therapy may also cause psychologic distress for many patients, and its use should be discussed thoroughly with the patient and/or family prior to commencing therapy [8]. This therapy should only be used with appropriately informed consent.

CHEMICAL DEBRIDEMENT

Chemical debridement utilizes nonenzymatic solutions to break down necrotic tissue in wounds [9]. The most widely used are sodium hypochlorite (bleach) solutions, including Dakin's solution, and oxychlorosene (Clorpactin WCS-90) [9]. Dakin's solution at the strength of 0.25% is nontoxic to healthy tissue, and gauze dressings soaked in Dakin's solution help to dissolve necrotic tissue and decrease the bacterial burden in the wound [9]. Regardless of the chemical used, the dressings must be changed every 12 hours. The periwound area should be protected from contact with the dressing, either with petrolatum ointment or strips of solid skin barrier around the edges of the wound [9].

Dakin's solution is normally stored in clear containers. It loses its potency in 24 to 48 hours and must be replaced at least every other day [9]. When first opened, containers should be labeled with the date and time. After the wound is free from necrotic tissue, the use of sodium hypochlorite or oxychlorosene should be discontinued [9].

9. WOUND DRESSINGS

Wound dressings are a pivotal aspect of wound care [3]. Dressings insulate the wound from the external environment, provide a barrier to prevent bacterial infection, maintain a moist environment, wick fluid from areas of tunneling, and absorb drainage [9]. Ideally, a wound dressing should also provide for gaseous exchange, allowing oxygen, carbon dioxide, and water vapor to pass in and out through the dressing [6].

When choosing a wound dressing, one of the most important factors to consider is the type of tissue in the wound bed—granulating or slick looking, moist or dry. Also consider the depth of the wound, whether tunneling or tracking is present, and the amount of drainage [9]. The condition of the skin surrounding the ulcer must also be determined [3].

Wound dressings can be divided into two main categories: those placed inside the wound in contact with the wound bed and those placed on top of the wound as a cover [9]. Shallow wounds with little drainage may only require a cover dressing [9]. However, wounds with a depth greater than 0.5 cm and/or with tunneling or undermining often require both an internal and a cover dressing [9]. As the wound changes, the type of dressing may also need to be changed [3].

Dressings can also be categorized according to their ability to introduce or wick moisture. Dressings that add moisture to the wound bed are referred to as hydrating; dressings that remove excess exudates from the wound surface are absorptive [9].

HYDROCOLLOIDS

Hydrocolloids are excellent dressings for the prevention of secondary infections [9]. In the past, hydrocolloids were considered occlusive dressings, but more recent versions have a backing of a semiocclusive film layer that is impermeable to fluids and bacteria but semipermeable to gas and water vapor [1]. Hydrocolloids can accommodate only moderate amounts of wound drainage and are therefore not used for heavily draining wounds [9].

Evidence Based Practice Recommendation

The National Pressure Ulcer Advisory Panel, the European Pressure Ulcer Advisory Panel, and the Pan Pacific Pressure Injury Alliance recommend using hydrocolloid dressings for clean stage 2 pressure ulcers in body areas where they will not roll or melt.

http://www.npuap.org/wp-content/uploads/2014/08/Quick-Reference-Guide-DIGITAL-NPUAP-EPUAP-PPPIA-Jan2016.pdf

Last Accessed: July 19, 2018

Level of Evidence: B (The recommendation is supported by direct scientific evidence from properly designed and implemented clinical series on pressure ulcers in humans.)

These dressings can produce an odor upon removal [8]. In the absence of other signs of clinical infection, this is not an abnormal finding and should be explained to concerned patients and staff [8]. Hydrocolloids may also leave a residual in the wound bed, which should be gently irrigated out at dressing change [1]. Hydrocolloids lose their effectiveness if they are changed too frequently and should not be used for wounds that need to be monitored daily [1].

HYDROGEL

Hydrogel dressings are used with shallow wounds with minimal amounts of drainage and are also a good option for painful ulcers [3]. Hydrogel dressings are usually hydrating and are either glycerin- or water-based [1]. These dressings are appropriate for use with topical medications and antibacterial agents [8].

Amorphous hydrogel dressings are especially useful for wounds with depth and contours [3]. However, these dressings provide only minimal absorption and should be used in wounds with small amounts of exudate [9]. Amorphous hydrogel dressings vary widely in their level of viscosity and are available in sheet dressing, tube, spray bottle, and ribbon gauze [1].

FOAM DRESSINGS

Foam dressings are a good choice for stage 2 and shallow stage 3 ulcers with drainage and for painful pressure ulcers. Foam dressings protect wounds at risk of further damage from shear and can be used along with topical treatments [3,8]. Foam dressings impregnated with ionic silver are available to reduce the risk of infection [1]. These dressings can also be used along with alginates to improve management of wound drainage [1]. Foam provides for thermal insulation, conforms to body shape, and leaves no residual in the wound [6]. Clinicians must be careful to place the correct side of the foam dressing in contact with the wound surface [8].

SILVER-IMPREGNATED DRESSINGS

Silver-impregnated dressings are a treatment option for infected or heavily colonized wounds or wounds that are at increased risk for infection [3]. Silver has an antimicrobial effect on a broad spectrum of organisms and has been shown to reduce the bacterial count in wounds [1]. Sustained-release silver dressings are toxic to bacteria and fungi but do not adversely affect healthy wound tissue [9]. However, silver-resistant organisms do exist, and the judicious use of silver is advised, similar to the approach adopted with antibiotics [1]. It is recommended that the use of silver dressings be limited to a two- to four-week period [1].

CADEXOMER IODINE DRESSINGS

Cadexomer iodine dressings are used for wounds with moderate-to-high amounts of drainage. They should not be used for patients who are sensitive to iodine or individuals with thyroid disease [3]. Cadexomer iodine dressings are antimicrobial and help fight bacteria while maintaining a moist environment for wound healing [8]. Although these dressings are capable of reducing bacterial counts in wounds, they do not replace the need for systemic antibiotic therapy and are regarded as an adjunct in the treatment of wound infections [8].

CALCIUM ALGINATE DRESSINGS

Calcium alginate dressings are highly absorptive dressings made from lightweight seaweed. They can absorb up to 20 times their weight in wound drainage, which makes them an excellent choice for heavily draining wounds [8]. There are two types of alginates: one that becomes a gel after coming in contact with the wound drainage and one that retains its original shape while absorbing exudates [9]. In addition to their absorptive abilities, calcium alginate dressings can aid in hemostasis, making them a good choice for bleeding wounds [8]. Wounds treated with alginate dressings made from seaweed may smell fishy or like "low tide" [8].

HYDROCOLLOID FIBER DRESSINGS

Hydrocolloid fiber dressings are used only in wounds with large amounts of drainage [9]. They are placed in the wound dry and transform into a gel after absorbing exudate [9]. These dressings are comfortable and easy to remove, but they usually require a secondary dressing to hold them in place [8].

GAUZE

Gauze packing was used frequently in the past, but it is now regarded as less effective in coping with wound drainage than calcium alginate or hydrocolloid fiber dressings [9]. Gauze dressings do not provide a barrier against bacteria, do not lower wound temperature, and can pull healthy granulating tissue out of the wound on removal [9]. Gauze dressings are also labor intensive, requiring several dressing changes daily, which adds to the cost of the overall care [8].

COMPOSITE DRESSINGS

Composite dressings are a combination of more than one material used to fulfill several important functions in the wound [8]. They provide an effective barrier to bacterial contamination of the wound and include an absorptive layer and foam, hydrocolloid, or hydrogel [8]. Composite dressings can have either a semi-adherent or non-adherent surface placed in contact with the wound bed [8]. Composite dressings are comfortable and are available in various shapes and sizes [1]. These dressings should not be cut, as this compromises the structure of the dressing [8].

COLLAGEN DRESSINGS

Some dressings incorporate collagen, which is an important protein involved in wound healing and repair [1]. The dressings can be 100% collagen or combined with other products, such as alginates [8]. They provide a high level of absorption while keeping the wound bed moist and are easily removed [8]. For wounds with very little drainage, collagen gel can be applied in a layer one-quarter inch thick [1]. Collagen used in most wound dressings is derived from cowhide [8]. Therefore, it should not be used in patients who are allergic to bovine products [8].

SPECIAL CONSIDERATIONS

Tunneling and Undermining

An occlusive dressing should not be placed over wounds with tunneling and undermining due to the danger of anaerobic micro-organism growth [8]. Ribbon gauze should be used to fill areas of narrow tunneling, with the end of the gauze placed securely in the wound base to allow for easy retrieval [2].

Wound Packing and Filling

Wounds are packed to fill dead space and eliminate the possibility of abscess formation caused by premature closure of the wound [1]. The materials used for packing should conform to the base and sides of the wound [1]. Wound packing material should be fluffed and placed loosely into the wound using a cotton swab [1]. It is important to ensure that the dressing material is in contact with all wound surfaces but also that the wound is not overpacked.

Wound fillers come in hydrated form, usually paste or gels, or dry form, which includes powder, granules, beads, and rope [1]. Wound fillers can contain collagen, alginate, foam, or hydrogel [1]. They are non-adherent and require a secondary dressing to hold them in place [1]. Dressing changes of packed wounds are normally done on at least a daily basis [1].

Frequency of Dressing Changes

The frequency with which a dressing will be changed depends on several factors, including the manufacturer's guidelines, the condition of the wound, and the amount of drainage present. Daily or every other day dressing changes are usually better for the patient, being less painful and more cost effective than dressings that must be changed two to three times per day [9]. This should be taken into consideration when selecting wound dressings.

10. WOUND MONITORING

Routine evaluation of wound treatments and wound progression is essential, and wounds should be assessed at each dressing change [1]. Clinical signs of improvement are expected to appear within two to four weeks [9]. When evaluating the wound, the most important factor to consider is whether the wound is progressing toward the goals established at the onset of treatment [1]. If the wound is not progressing, further assessment and adjustment of the treatment approach are warranted [1].

For nonhealing wounds, the first factor to evaluate is the quality of wound care. This includes determining if dressing changes are being carried out at the recommended intervals, if the dressings are applied appropriately, and if the manufacturer's instructions for product use are being followed [1]. Factors affecting the patient's condition should be taken into consideration and addressed appropriately [9]. Failure of a wound to improve is often due to systemic factors, such as ischemia, infection, or malnutrition, or continuation of the causative factors [9]. These issues must be addressed first to achieve optimum wound healing. A change in the dressing treatment is indicated if any of the following problems occur [9]:

- Maceration of the surrounding skin

- Inadequate control of wound drainage

- A change in the amount of drainage or the depth of the wound

Reverse staging of pressure ulcers is not an acceptable approach to gauging the level of wound healing. Healed pressure ulcers do not replace lost muscle, subcutaneous fat, or dermis [3]. Tools that do appropriately measure degrees of healing include the Bates-Jensen Wound Assessment Tool and the Pressure Ulcer Scale for Healing (PUSH) Tool [8,27]. The Bates-Jensen Wound Assessment Tool has thirteen variables that provide a composite picture of the status of the wound [8]. The PUSH tool uses scores in three domains (i.e., size, exudate amount, and tissue type) to indicate improvement or deterioration of the ulcer. A score of 0 on the PUSH tool indicates the wound has healed, whereas the highest score of 17 indicates wound degeneration [8].

DOCUMENTATION

Wound care documentation should be concise and frequent [8]. It should be based on nationally recognized standards of care; shortcuts should not be used, and only approved abbreviations should be included in the documentation [2]. Problems arise when there are numerous and different descriptions of a pressure injury [1]. If present, all wounds should be documented on admission to provide a baseline comparison for future assessments [8]. Subsequent wound care provided must be recorded, including accurate dates and times and the name of the clinician providing the care. All statements should be substantiated by objective clinical findings. The condition of the wound on discharge should be thoroughly documented and reported to the agency providing follow-up care. As noted, photography is becoming increasingly commonplace.

11. PREVENTION OF PRESSURE ULCERS

All persons who are bedfast or chairfast should be considered at risk of developing pressure ulcers. Specific potential risk factors include conditions that limit mobility, such as stroke, debilitating illness, frail elderly, and injuries that require external medical devices (e.g., fracture casting).

The 2014 NPUAP/EPUAP guideline and the 2016 NPUAP prevention points advocate attention to the following principles of preventive skin care for at-risk persons and for patients with an established pressure injury [3,34]:

- Skin should be examined within eight hours of admission, and a structured risk assessment (e.g., the Braden Scale) should be conducted as close to eight hours after admission to identify individuals at risk of pressure injury.

- Avoid positioning the individual on an area of skin redness whenever possible.

- Keep the skin clean and dry.

- Do not massage or vigorously rub skin zones at risk (i.e., over bony prominences).

- Develop and implement an individualized continence management plan.

- Protect at-risk zones of skin from excessive moisture with a barrier product.

- Consider prophylactic dressings, such as polyurethane foam dressing, to protect skin over boney prominences (e.g. back, sacrum) or in direct contact with medical devices.

Patients with any degree of pressure-induced skin injury/ulcer should be positioned and repositioned at frequent, regular intervals throughout the day, making use of foam mattresses or protective overlays designed to reduce pressure and avoid friction/shear.

12. PROGNOSIS

With appropriate care (i.e., careful and through assessment), treatment of comorbidities, diligent wound management, and maintenance of nutrition, the prognosis for complete healing of pressure ulcers is very good, especially if intervention occurs before late stage 3 progression. A two-year observational study of 1,626 patients with stage 2 through 4 pressure ulcers admitted to 51 nursing homes in all parts of the country found that with standard care 74% of stage 2, 60% of stage 3, and 33% of stage 4 ulcers had healed completely at six months [28]. Of surviving patients at one year of therapy, 87%, 80%, and 60% respectively had healed.

13. CONCLUSION

Wound care is an exciting and ever-evolving practice, and a coordinated team effort can bring about remarkable results. Healthcare professionals must keep abreast of the growing scientific research in this area, as newer or re-discovered treatments can impact nursing practice and expected patient outcomes. An improved knowledge and appreciation of wound development and healing will enhance patient care and ultimately quality of life.

14. RESOURCES

National Pressure Ulcer Advisory Panel (NPUAP)

Educational and Clinical Resources

http://www.npuap.org/resources/educational-and-clinical-resources

European Pressure Ulcer Advisory Panel (EPUAP)

Pressure Ulcer Guidelines

http://www.epuap.org/pu-guidelines

Agency for Healthcare Research and Quality (AHRQ)

Preventing Pressure Ulcers in Hospitals

https://www.ahrq.gov/professionals/systems/hospital/pressureulcertoolkit/index.html

Works Cited

1. Bryant RA, Nix DP. Acute and Chronic Wounds: Current Management Concepts. 5th ed. St. Louis, MO: Mosby Elsevier; 2016.

2. Medline Industries, Inc. The Wound Care Handbook. Mundelein, IL: Medline; 2007.

3. National Pressure Ulcer Advisory Panel, European Pressure Ulcer Advisory Panel, and Pan Pacific Pressure Injury Alliance. Prevention and Treatment of Pressure Ulcers: Quick Reference Guide. Available at https://www.npuap.org/wp-content/uploads/2014/08/Updated-10-16-14-Quick-Reference-Guide-DIGITAL-NPUAP-EPUAP-PPPIA-16Oct2014.pdf. Last accessed July 9, 2018.

4. Halfens RJ, Haalboom JR. A historical overview of pressure ulcer literature of the past 35 years. Ostomy Wound Manage. 2001;47(11):36-43.

5. Kirman CN. Pressure Ulcers and Wound Care. Available at https://emedicine.medscape.com/article/190115-overview. Last accessed July 9, 2018.

6. Sussman C, Bates-Jensen BM. Wound Care: A Collaborative Practice Manual for Health Professionals. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011.

7. Northwest Regional Spinal Cord Injury System. Pressure Ulcers Can Wreck Your Life! Preventing and Managing Skin Problems after SCI. Available at http://sci.washington.edu/info/forums/reports/pressure_ulcers_2012.asp. Last accessed July 3, 2018.

8. Baranoski S, Ayello EA. Wound Care Essentials: Practice Principals. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2015.

9. Emory University School of Medicine Wound, Ostomy and Continence Nursing Education Center. Skin and Wound Module. 6th ed. Atlanta, GA: Emory University WOCNEC; 2006.

10. Vasavada SP, Rackley RR, Carmel ME. Urinary Incontinence. Available at https://emedicine.medscape.com/article/452289-overview#a6. Last accessed July 9, 2018.

11. Centers for Disease Control and Prevention. National Diabetes Statistics Report, 2017: Estimates of Diabetes and Its Burden in the United States. Available at https://www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdf. Last accessed July 1, 2018.

12. Wound Ostomy and Continence Nurses Society. Photography in Wound Documentation: Fact Sheet. Available at https://c.ymcdn.com/sites/www.wocn.org/resource/resmgr/Publications/Photography_in_Wound_Documen.pdf. Last accessed July 9, 2018.

13. Kennedy KL. Gaymar Pictorial Guide to Pressure Ulcer Assessment. 2nd ed. Orchard Park, NY: Gaymar Industries; 2006.

14. National Pressure Ulcer Advisory Panel. NPUAP Pressure Injury Stages. Available at http://www.npuap.org/resources/educational-and-clinical-resources/npuap-pressure-injury-stages. Last accessed July 9, 2018.

15. Szor JK, Bourguignon C. Description of pressure ulcer pain at rest and at dressing change. J Wound Ostomy Continence Nurs. 1999;26(3):115-120.

16. Günes UY. A descriptive study of pressure ulcer pain. Ostomy Wound Manage. 2008;54(2):56-61.

17. Wong DL, Hockenberry-Eaton M, Wilson D, Winkelstein ML, Schwartz P. Wong's Essentials of Pediatric Nursing: Wong-Baker Faces Pain Rating Scale. 9th ed. St. Louis, MO: Mosby; 2012.

18. National Pressure Ulcer Advisory Panel. National Pressure Ulcer Advisory Panel (NPUAP) Announces a Change in Terminology from Pressure Ulcer to Pressure Injury and Updates the Stages of Pressure Injury. Available at http://www.npuap.org/national-pressure-ulcer-advisory-panel-npuap-announces-a-change-in-terminology-from-pressure-ulcer-to-pressure-injury-and-updates-the-stages-of-pressure-injury. Last accessed June 29, 2018.

19. Institute for Clinical Systems Improvement. Pressure Ulcer Prevention and Treatment Protocol. Health Care Protocol. Bloomington, MN: Institute for Clinical Systems Improvement; 2012.

20. Bryant RA, Nix DP. Acute and Chronic Wounds: Current Management Concepts. 5th ed. St. Louis, MO: Elsevier; 2016.

21. Butcher G. Low frequency ultrasonic debridement: a new tool in our armoury? J Foot Ankle Res. 2011;4(Suppl 1):P7.

22. Herberger K, Franzke N, Blome C, Kirsten N, Augustin M. Efficacy, tolerability and patient benefit of ultrasound-assisted wound treatment versus surgical debridement: a randomized clinical study. Dermatol. 2011;222(3):244-249.

23. Sherman RA. Maggot therapy takes us back to the future of would care: new and improved maggot therapy for the 21st century.J Diabetes Sci Technol. 2009;3(2):336-344.

24. Pearson C. Something old is new again: debriding and reducing local wound infection with maggots. Wound Care Canada. 2007;5(2):22-26.

25. Marineau ML, Herrington MT, Swenor KM, Eron LJ. Maggot debridement therapy in the treatment of complex diabetic wounds. Hawaii Med J. 2011;70(6):121-124.

26. Opletalová K, Blaizot X, Mourgeon B, et al. Maggot therapy for wound debridement: a randomized multicenter trial. Arch Dermatol. 2012;148(4):432-438.

27. Harris C, Bates-Jensen B, Parslow N, Raizman R, Singh M, Ketchen R. Bates-Jensen wound assessment tool: pictorial guide validation project. J Wound Ostomy Continence Nurs. 2010;37(3):253-259.

28. Brandeis GH, Morris JN, Nash DJ, Lipsitz LA. The epidemiology and natural history of pressure ulcers in elderly nursing home residents. JAMA. 1990;264:2905-2909.

29. Mayo Clinic. Bedsores (Pressure Ulcers). Available at https://www.mayoclinic.org/diseases-conditions/bed-sores/diagnosis-treatment/drc-20355899. Last accessed July 3, 2018.

30. Gabriel A, Windle ML, Schraga ED. Wound Irrigation. Available at https://emedicine.medscape.com/article/1895071-overview. Last accessed July 3, 2018.

31. De Luna V, Mancini F, De Maio F, et al. Intraoperative disinfection by pulse irrigation with povidone-iodine solution in spine surgery. Adv Orthop. 2017;10:7218918.

32. Ruder JA, Springer BD. Treatment of periprosthetic joint infection using antimicrobials: dilute povidone-iodine lavage. J Bone Jt Infect. 2017;2(1):10-14.

33. Chang YR, Perry J, Cross K. Low-frequency ultrasound debridement in chronic wound healing: a systematic review of current evidence. Plastic Surgery. 2017;25(1):21-26.

34. National Pressure Ulcer Advisory Panel. Pressure Injury Prevention Points. Available at http://www.npuap.org/wp-content/uploads/2016/04/Pressure-Injury-Prevention-Points-2016.pdf. Last accessed July 8, 2018.

35. Berg L. European Pressure Ulcer Advisory Panel Webinar: "Hard to Health Pressure Ulcers:" To Treat or Not to Treat. Available at http://www.epuap.org/wp-content/uploads/2017/03/epuap-webinar-hard-to-heal-pu.pdf. Last accessed July 8, 2018.

Evidence-Based Practice Recommendations Citations

1. National Pressure Ulcer Advisory Panel, European Pressure Ulcer Advisory Panel, Pan Pacific Pressure Injury Alliance. Prevention and Treatment of Pressure Ulcers: Clinical Practice Guideline. Washington, DC: National Pressure Ulcer Advisory Panel; 2014. Available at http://www.npuap.org/wp-content/uploads/2014/08/Quick-Reference-Guide-DIGITAL-NPUAP-EPUAP-PPPIA-Jan2016.pdf. Last accessed July 19, 2018.

34343 • Pressure Ulcers and Skin Care

Maryam Mamou, BSN, RN, CRRN, CWOCN

www.netce.com

Copyright © 2019 NetCE, All rights reserved.

A complete skin assessment and accurate documentation of the assessment findings are critical elements of the nurse's role in patient care. Nursing staff must be able to perform a thorough head-to-toe skin assessment and accurately document their findings. In order to do this, nurses should have a working knowledge of the general characteristics of the skin, its functions, and the changes that occur in the skin throughout an individual's life span. Identifying patients at risk for pressure ulcer development is vitally important, as presence of these wounds greatly increased morbidity and mortality. Use of a risk assessment tool, such as the Braden Risk Assessment, is recommended. Each patient deemed at risk for skin breakdown or with evidence of breakdown should have an individualized program of skin care, including nutritional support and patient and family education among other elements. Ongoing evaluation and documentation of the skincare program and whether or not it is meeting its goals is necessary.

Table of Contents

34343 • Pressure Ulcers and Skin Care

Course Overview

Audience

Course Objective

Learning Objectives

Faculty

Faculty Disclosure

Division Planner

Division Planner Disclosure

About the Sponsor

Disclosure Statement

1. INTRODUCTION

2. GENERAL CHARACTERISTICS OF SKIN

SKIN STRUCTURES

FUNCTIONS OF THE SKIN

SKIN THROUGHOUT THE LIFE SPAN

3. PRESSURE ULCERS

PRESSURE AND SHEAR

FRICTION

MOISTURE

STAGES OF BREAKDOWN

4. PRESSURE ULCER RISK ASSESSMENT

MAJOR RISK FACTORS IN PRESSURE ULCER DEVELOPMENT

RISK ASSESSMENT

5. SKIN AND PAIN ASSESSMENTS

ELEMENTS OF A BASIC SKIN ASSESSMENT

ASSESSING AND DOCUMENTING A PRESSURE ULCER

6. INDIVIDUALIZED PROGRAM OF SKIN CARE

POSITIONING IN BED

POSITIONING WHILE IN CHAIR

CLEANSING AND BATHING

MOISTURIZING THE SKIN

BOWEL AND BLADDER MANAGEMENT

SUPPORT SURFACES

PATIENT/FAMILY EDUCATION

STAFF EDUCATION

NUTRITIONAL SUPPORT

EVALUATION OF THE SKIN PROGRAM

7. DOCUMENTATION

8. CONCLUSION

Works Cited

Evidence-Based Practice Recommendations Citations

34343 • Pressure Ulcers and Skin Care

Education Category. Infection Control / Internal Medicine

Release Date. 06/01/2019

Expiration Date. 05/31/2022

Course Overview

A complete skin assessment and accurate documentation of the assessment findings are critical elements of the nurse's role in patient care. Nursing staff must be able to perform a thorough head-to-toe skin assessment and accurately document their findings. In order to do this, nurses should have a working knowledge of the general characteristics of the skin, its functions, and the changes that occur in the skin throughout an individual's life span. Identifying patients at risk for pressure ulcer development is vitally important, as presence of these wounds greatly increased morbidity and mortality. Use of a risk assessment tool, such as the Braden Risk Assessment, is recommended. Each patient deemed at risk for skin breakdown or with evidence of breakdown should have an individualized program of skin care, including nutritional support and patient and family education among other elements. Ongoing evaluation and documentation of the skincare program and whether or not it is meeting its goals is necessary.

Audience

This course is designed for nurses in all practice settings, particularly those caring for patients at high risk for developing pressure ulcers.

Course Objective

The purpose of this course is to provide nurses with the information necessary to accurately identify, treat, and manage skin breakdown (pressure ulcers), thereby improving patient outcomes and quality of life.

Learning Objectives

Upon completion of this course, you should be able to:

1. List the key structures and functions of the skin.

2. Describe skin changes throughout the life span.

3. Identify causative factors contributing to pressure ulcer occurrence.

4. Accurately identify each stage of pressure ulcer development.

5. Identify risk factors leading to the development of pressure ulcers.

6. Outline characteristics of a validated and reliable pressure ulcer risk assessment tool.

7. Complete thorough skin and pain assessments.

8. Outline an individualized program of skin care, including nutritional support, documentation, and patient education.

Faculty

Maryam Mamou, BSN, RN, CRRN, CWOCN, is an Irish-trained RN who has lived and worked in the United States for 20 years. During her career, she has completed a BSN and went on to become a certified rehabilitation nurse, a certified life care planner, and more recently a certified wound ostomy and continence nurse. She is a graduate of the wound ostomy and continence program at Emory University in Atlanta, Georgia, and is nationally certified in these areas.

Ms. Mamou has worked in various rehabilitation settings and has first-hand experience of how pressure ulcers impact patients' recovery and quality of life. She has held positions as staff nurse, unit coordinator, educator, and director of nursing in home health care. She has been involved in developing and implementing several staff education programs in a variety of settings. She was most recently employed as a wound ostomy and continence nurse at East Alabama Medical Center in Opelika, Alabama.

Faculty Disclosure

Contributing faculty, Maryam Mamou, BSN, RN, CRRN, CWOCN, has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

Division Planner

Jane C. Norman, RN, MSN, CNE, PhD

Division Planner Disclosure

The division planner has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

About the Sponsor

The purpose of NetCE is to provide challenging curricula to assist healthcare professionals to raise their levels of expertise while fulfilling their continuing education requirements, thereby improving the quality of healthcare.

Our contributing faculty members have taken care to ensure that the information and recommendations are accurate and compatible with the standards generally accepted at the time of publication. The publisher disclaims any liability, loss or damage incurred as a consequence, directly or indirectly, of the use and application of any of the contents. Participants are cautioned about the potential risk of using limited knowledge when integrating new techniques into practice.

Disclosure Statement

It is the policy of NetCE not to accept commercial support. Furthermore, commercial interests are prohibited from distributing or providing access to this activity to learners.

1. INTRODUCTION

A complete skin assessment and accurate documentation of the assessment findings are critical elements of the nurse's role in providing care for patients with pressure ulcers. In order to perform a thorough assessment, nurses should have a working knowledge of the general characteristics of the skin, its functions, and the changes that occur in the skin throughout an individual's life span.

Each patient deemed at risk for skin breakdown or with evidence of breakdown should have an individualized program of skin care, including nutritional support and patient and family education, among other elements. Ongoing evaluation and documentation of the skincare program and whether or not it is meeting its goals is necessary.

2. GENERAL CHARACTERISTICS OF SKIN

Skin is the largest organ in the body. In the average person it covers approximately 3,000 square inches [1]. In total, it weighs around six pounds, or up to 15% of the total adult body weight. Intact skin is dry, supple, and has a pH ranging from 4 to 6. It varies in thickness from 0.5 mm in the tympanic membrane to 6 mm on the soles of the feet and the palms of the hands. Frequent bathing and episodes of incontinence remove naturally occurring oils from the skin [2]. However, as an organ the skin is able to withstand limited mechanical and chemical assaults.

SKIN STRUCTURES

Human skin has two primary layers: the epidermis (outer layer) and the dermis (inner layer). The basement membrane separates the two layers. Beneath the dermis is the hypodermis, which is a layer of connective tissue also referred to as the subcutaneous tissue.

Epidermis

The epidermis is a thin layer that regenerates itself every four to six weeks. It contains no blood vessels and receives its blood supply from the inner (dermis) layer. Nerve fibers are located throughout the epidermis. It is divided into five layers—presented in order from the outermost layer inward: stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale.

The stratum corneum is composed of dead keratinized cells and is constantly being sloughed off and renewed from below [2]. It has an acid mantle, an oily layer with reduced pH, provided by sebum, the substance secreted by the sebaceous glands onto the skin surface via the hair follicles.

The stratum lucidum, also known as the clear layer, is found in areas where the epidermis is thicker, like the palms of the hands and the soles of the feet [1]. It lies directly below the stratum corneum. The next layer, the stratum granulosum, is composed of one to five layers. It is believed to help with keratin formation.

The stratum spinosum is referred to as the "prickly layer" because of the spine-like shape of the cells [2]. In this layer, skin cells begin to flatten as they are migrating toward the skin surface. The stratum basale, also known as the stratum germinativum, is the innermost layer of the epidermis. It is composed of a single layer of constantly dividing cells that form new cells. These new cells migrate to the stratum corneum [1]. Cellular migration usually takes 28 days, but this rate is affected by aging and chemotherapy.

Rete pegs and rete ridges are interlocking structures that extend down from the epidermis into the dermis. These finger-shaped downward projections on the epidermis interlock with upward projections from the dermis. Rete pegs and ridges ensure that all the skin layers move together.

The epidermis contains many specialized cells that affect patient health and appearance. The cells of the skin that provide immune protection (dendritic or Langerhans cells) are found in the stratum granulosum and the stratum spinosum. Melanocytes are found only in the epidermis and are responsible for differences in skin color. The number of melanocytes is approximately the same in normal skin regardless of skin color, but the amount of the pigment melanin produced varies from person to person and from one area of skin on the body to another.

Basement Membrane

The basement membrane's main function is to anchor the epidermis to the dermis. It contains several protein substances, including collagen, and is the layer that is affected in blister formation [1].

Dermis

The dermis is the most important part of the skin and is often referred to as the "true skin" [3]. It is the thickest layer of the skin, varying in thickness from 0.2 mm to 4 mm. The reticular dermis anchors the skin to the subcutaneous tissue and contains sweat glands, hair follicles, nerves, and blood vessels [1]. The dermis also contains the sebaceous glands, which secrete sebum, a substance rich in oil that lubricates the skin.

The major proteins found in the dermis are collagen and elastin [1]. Collagen gives skin its tensile strength, while elastin provides the skin with elastic recoil. This characteristic prevents the skin from being permanently reshaped. The dermis is divided into two areas: the papillary dermis, which contains capillaries for skin nourishment, and the reticular layer, which is comprised of thick collagen fibers. The dermis also contains Meissner and Vater-Pacini corpuscles, the receptors that sense pain and pressure.

Subcutaneous Tissue

Beneath the dermis lies subcutaneous tissue, which attaches the skin to the underlying structures. Subcutaneous tissue contains adipose tissue, connective tissue, blood vessels, lymphatics, and nerve endings. It is the adipose tissue that provides protection from pressure and shear. Elderly patients who may have inadequate subcutaneous tissue are at high risk for deep tissue injury due to pressure and shear [2].

Muscle and Fascia

Muscle and fascia are highly vascularized tissue that is most sensitive to ischemia. Pressure damage usually originates here [2]. The skin receives its blood supply from vessels that originate in the muscle tissue.

FUNCTIONS OF THE SKIN

The skin protects against mechanical and chemical trauma, pathogens, dehydration, and malignancy [2]. One of the most important functions of the skin is acting as a physical barrier to micro-organisms, protecting the body against infection. The acid mantle present in the epidermis also retards the growth of micro-organisms.

The skin immune system provides protection as well [1]. Macrophages found in the dermis are phagocytic cells that provide defense against pathogens for the skin and for open wounds. These macrophages also promote wound healing.

Mast cells are present in the skin and are the primary cells involved in allergic reactions. They also help protect against parasites.

The skin maintains heat regulation by the process of vasodilation and vasoconstriction, sweating and shivering [2]. Fluid evaporating from the skin allows for cooling to occur. The amount of sweat excreted can range from 100 mL to 2 liters in one hour [2]. As a result, the skin plays an important role in electrolyte balance and hydration.

Nerve endings in the skin provide information about the external environment and protection. Some areas of the skin are more sensitive than others (e.g., the fingertips are more sensitive than the back). Any loss of sensation increases the chances of injury.

The skin is also involved in the metabolism of certain vitamins. Specifically, the effect of ultraviolet B light on sterols in the skin causes synthesis of vitamin D. Certain drugs and some toxic substances (e.g., pesticides) can also be absorbed directly through the skin and into circulation.

Finally, skin provides for expression and body image [2]. Skin plays a vital role in self-esteem and social communication. Skin characteristics have an impact on how an individual communicates both verbally and nonverbally, and how the other person reacts to that individual. It also provides significant social cues regarding health and vitality.

SKIN THROUGHOUT THE LIFE SPAN

Fetal and Neonatal Skin

Fetal skin appears to have increased amounts of hyaluronic acid, which is associated with fetal scarless healing. Studies indicate that intrauterine surgery done late in the second trimester or early in the third trimester usually results in no scars [2].

Neonatal skin is more permeable due to the immature stratum corneum. During the first two weeks of life, topical administration can equal intravenous (IV) administration in terms of absorption [2]. Because infants have thinner skin and nails, epidermal stripping can occur easily.

Adult Skin

Adult skin shows a gradual increase in epidermal turnover time and decreasing dermal thickness. In young adults, epidermal turnover is around 21 days; by 35 years of age, this time doubles [2]. In addition, melanocytes decrease 6% to 8% each decade after 30 years of age. This loss of skin melanocytes is thought to increase the risk of skin cancer [1].

Elderly Skin

In elderly individuals, there is a 50% reduction in the cell turnover rate in the stratum corneum (outer most layer) and a 20% reduction in dermal thickness. Elderly patients experience an overall reduction in dermal vascularization and associated drop in blood flow to the skin. The collagen bundles in the dermis shrink, causing permanent wrinkles to develop [2].

Rete ridges and pegs flatten, resulting in decreased adhesion between the skin layers. The area of contact between the epidermis and the dermis is reduced by 50% [4]. There is increased capillary fragility; slight pressure can cause bruising. A decrease in subcutaneous tissue causes a reduction in thermal insulation and increases the risk of shear/pressure injury. Reduced activity of sweat glands and sebaceous glands can lead to dry skin.

Elderly individuals experience a drop in the number of Langerhans cells, a 50% decrease in the number of mast cells, and up to a 50% decrease in the function of the remaining cells. As a result, there is an increased risk of skin cancer and fungal and other infections [1].

Other age-related changes include decreased absorption, reduction in the skin's ability to synthesize vitamin D, and significantly marked reduction in the ability of the skin to sense pressure, heat, and cold. Decreased cellular competence and activity leads to a reduction in cell repair and the increased possibility of nonhealing wounds [2].

3. PRESSURE ULCERS

In 2016, the National Pressure Advisory Panel (NPUAP) released updated definitions for pressure ulcers and staging classification. In this revision, the term "pressure injury" replaced "pressure ulcer," to alleviate confusion between injury to intact skin and open ulcers. According to the NPUAP, a pressure injury is localized damage to skin and/or underlying soft tissue and usually occurs over a bony prominence. It is the result of prolonged pressure or pressure combined with shear and/or friction. A pressure injury can present as intact skin or an open ulcer. Patients at risk for pressure injury (e.g., immobile patients) are also at risk for friction and shear damage [5]. For the purpose of this course, the term "pressure ulcer" will encompass both injury of intact skin and an open ulcer, unless otherwise noted.

Pressure ulcers usually occur over a bony prominence such as the sacrum, the ischial tuberosity, the trochanter, and the heels, but they can occur anywhere on the body. In some cases, ulcers will develop around a tracheostomy tube or under a cast, splint, or cervical collar [1]. The most common locations for pressure ulcers are the sacrum and the heels because there is less soft tissue present between the bone and the skin in these areas. An estimated 95% of pressure ulcers occur on the lower body; of these, about 65% develop in the pelvic area and 30% in the lower extremities [6]. There is a two to six times greater mortality risk with pressure ulcer development. Many factors impact the level and extent of tissue trauma (Table 1) [7].

Table 1: FACTORS CONTRIBUTING TO THE FORMATION OF PRESSURE ULCERS

Extrinsic Factors

Undue, prolonged pressure

Shear

Friction

Moisture

Abnormal posture

Intrinsic Factors

Altered consciousness

Decreased or absent sensations

Nutritional factors (under- or over-nourished)

Anemia

Edema

Atherosclerosis

Aged-related changes

Acute illness

Sleep

Medications

Cardiovascular changes

Emotional stress

Source: [7]

PRESSURE AND SHEAR

Pressure that results in the development of ulcers is defined as compression of soft tissues between two rigid surfaces. For example, blood vessels, muscle, subcutaneous fat, or skin may be compressed between a bone and an external surface, such as a bed or chair. The end result is ischemia and necrosis. All the tissues between the two points of pressure are affected, but the tissue closest to the bony prominence suffers the greatest damage. It is important to note that low-intensity pressure over a long period of time can create tissue damage, just as high-intensity pressure over a short period of time can result in damage [2]. Application of high pressure for shorter duration not only causes tissue necrosis due to blockage of capillaries but also produces pressure effect on the larger vessels, causing thrombosis (usually venous). Hence, the deleterious effect of high pressure for short duration is much more than that of low pressure for a longer duration. This has been proven by the observation that when the high pressure is relieved, ischemia persists due to effects on the adjacent larger vessels; upon relief of low pressure, the normal hyperemic response compensates for the temporary ischemia and the tissue does not undergo degeneration [7].

Pressure ulcer pathogenesis has still not been clearly defined. Most reports indicate a "bottom-up" progression of tissue damage [2]. Muscle is more sensitive to pressure damage than skin because it is the most metabolically active layer and is at the greatest risk for ischemic injury [7].

The capillary level is the end point of circulation. From the capillaries oxygen and nutrients diffuse into the tissues, and carbon dioxide and waste products are removed. A collapsed capillary bed is nonfunctioning and useless to the tissues. The minimal amount of pressure required to collapse a capillary is referred to as the capillary closing pressure [1]. Studies have shown that an average of 32 mm Hg will collapse the arterial side of the capillary circulation, and 18 mm Hg of pressure will collapse the venous end. However, these values cannot be accepted as the universal; capillary pressures vary among persons, sites, and times [2]. Furthermore, the studies that elicited these values were done on healthy adult males, not debilitated or elderly patients. Other studies have shown that the functional capillary pressure, the pressure needed to the keep the capillary bed open, is around 17 mm Hg.

Shear is the result of gravity pushing down on the body and resistance (friction) between the patient and a surface, such as the bed or the chair, holding the skin in place [2]. For example, when the head of the bed is raised (e.g., high Fowler position), gravity facilitates forward slide, pulling the body down toward the foot of the bed. The skin on the patient's lower back and gluteal area resists the motion and is held in place by the bed's surface while the bones and tissues beneath the area begin to slide. This causes puckering of the skin, stretching and angulation of small vessels, impedance of blood flow, and traction on subcutaneous tissue and muscle. Left unchecked, the net effect may result in ischemic injury to tissues at the fascia layer. When the head of the bed is elevated more than 30 degrees, shear force occurs over the sacrum and coccyx. Shear injury is not usually visible at the skin level, but shear is responsible for much of the damage associated with initiation of pressure ulcers [4]. The areas of the body most vulnerable to shearing forces are shoulder blades, elbows, sacrum, ischial tuberosities, and heels. Signs of shear injury include irregular deep lesions, undermining, and tunneling.

Prevention of Pressure and Shearing

There are several steps that may prevent the damage resulting from pressure and shear. If possible, limit the head of the bed elevation to 30 degrees or less. If the head must be elevated, the patient's knees may be bent ("gatched") with his or her feet flat on the bed. Using lift sheets to reposition patients is also recommended. Support surfaces are often utilized, and a low-resistance, breathable, and waterproof surface helps to eliminate friction. Foam surfaces lock the patient into place and reduce sliding. However, foam is not an appropriate surface to use if maceration (damage due to moisture trapped against the skin) is a problem [2].

When the patient is in a chair in sitting position, he or she should place feet flat on the floor and the back should be in alignment with the back of the chair. Consider using wheelchair or chair cushions that are higher in the front than the back for patients who tend to slide out of their chairs.

FRICTION

Friction occurs when one surface moves across another surface, such as when a patient's skin slides across a bed sheet. This can result in the "sanding away" of the epidermal layer and upper part of the dermis, resulting in abrasions [2,7]. Friction injuries often present as erythema and tenderness followed by skin loss. Friction damage can be seen under restraints, braces, and on the elbows, or with repetitive rubbing or repetitive cleansing. Patients with uncontrollable movements or spasticity are also at high risk for friction injury, often referred to as "sheet burn." Friction injury occurs more frequently when the skin is fragile or macerated, and tissues subjected to friction are more susceptible to pressure ulcer damage, infection, and deeper ulceration [4,7].

Prevention of Friction

As with pressure and shear, there are steps to minimize friction in at-risk patients. The most common involve measures to prevent the patient sliding down in bed (e.g., use of knee gatch on bed). All skin care measures should be gentle, no scrubbing or aggressive rubbing, and heel and elbow protectors should be utilized. Cornstarch may help to reduce the impact of friction.

MOISTURE

Moisture weakens the resilience of the epidermis to external forces. Maceration causes softening of the connective tissue, and a macerated epidermis erodes more easily. Overhydrated skin has decreased tensile strength. Skin can appear "water-logged," with areas of denuded skin and fissure formation. Shear and friction are increased when there is a moderate amount of moisture present, but it has been reported that shear and friction decrease in the presence of high levels of moisture. The role moisture plays in pressure ulcer development is an area of on-going research [8].

Major sources of moisture are incontinence, wound drainage, tube leakage, and sweating. Urinary and fecal incontinence expose the skin to excessive amounts of moisture and chemical irritation. There is a higher risk for skin breakdown with fecal incontinence than urinary incontinence because of the pathogens in stool.

Prevention of Excessive Moisture

Research has shown that when properly assessed and treated, urinary incontinence can be corrected in about 30% of nursing home residents [9]. Depending on the severity of the incontinence, the patient may be initiated in a toileting program. This consists of prompted voiding; specifically, the patient is taken to the bathroom at regular intervals and instructed to use the bathroom.

When this is not feasible (e.g., if a patient is unable to respond to instructions), the patient should be checked for incontinence every two to three hours and repositioned every two hours, with skin checks. Moisture barrier creams/lotions offer good protection for patients with incontinence. A folded, clean pillow case between skin folds may also be used for moisture absorption.

For sweating, barriers are contraindicated, because they retain moisture against the skin. For patients for whom sweating is an issue, use non-caking powder or a non-occlusive moisture barrier [2].

Some patients will benefit from the use of absorptive products. All absorbent products are not equal, and their benefits must be evaluated according to the needs of the patient. Odor control, wicking properties, absorbency, comfort, and cost all must be considered.

The appropriate use of containment devices, such as condom catheters, should also be evaluated. Trauma related to incorrect application of condom catheters is common and correct sizing and application is important.

STAGES OF BREAKDOWN

Staging is an assessment system that classifies pressure ulcers based on anatomic depth of tissue damage. In 2016, the NPUAP updated the definitions of pressure injury stages (Table 2) [5]. As noted, in the 2016 revision to the NPUAP staging system, the term "pressure injury" replaced "pressure ulcer," to alleviate confusion between injury to intact skin (stages 1 and deep tissue injury) and open ulcers (stages 2–4 and unstageable pressure injury). In addition, the following changes were made [5]:

- Arabic numbers replaced Roman numerals in stages 1–4.

- The term "suspected" was removed from the deep tissue injury diagnostic label.

- Two additional pressure injury definitions, Medical Device-Related Pressure Injury and Mucosal Membrane Pressure Injury, were added.

Table 2: NPUAP PRESSURE INJURY STAGES

Stage

Definition

Stage 1

Intact skin with non-blanchable redness. Area may present with changes in sensation, temperature, or firmness, even before visual changes are noted. Darkly pigmented skin may not have visible blanching, but its color may differ from the surrounding areas.

Stage 2

Partial thickness loss of dermis presenting as a shallow open ulcer with a red/pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister.

Stage 3

Full thickness tissue loss. Subcutaneous fat may be visible, but bone, tendon, or muscle is not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling.

Stage 4

Full thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of the wound bed. Often include undermining and tunneling.

Unstageable pressure injury

Full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed.

Deep tissue pressure injury

Persistent non-blanchable, deep red, purple, or maroon area of discolored, intact or non-intact skin or blood-filled blister. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent tissue.

Medical device-related pressure injury

Describes the cause of a pressure injury resulting from and taking shape of a medical device. Use staging system to classify.

Mucosal membrane pressure injury

Injury found on mucous membranes in a location in which a medical device was used. Cannot be staged.

Source: [5]

Staging of a pressure injury can only occur after all necrotic tissue has been removed and it is possible to see the ulcer bed [1]. If this is not possible, the ulcer will be classified as unstageable. Pressure ulcer staging is not used to indicate pressure ulcer healing; a pressure ulcer should never be "down staged" or reverse staged (e.g., a pressure ulcer that is healing does not go from a stage 4 to a stage 3).

In pressure ulcer healing there is no regrowth of lost muscle, subcutaneous fat, or dermis; instead, the wound is filled in with scar tissue. Therefore, reverse staging does not accurately reflect the physiologic changes occurring in the pressure ulcer. When a stage 4 ulcer has healed, it should be classified as a healed stage 4 pressure ulcer [4].

Stage 2 pressure ulcers have a healing time that ranges from 8.7 to 38 days. Stage 3 and stage 4 pressure ulcers can take up to 69 days to heal. Healing rates are lower for stage 3 and stage 4 ulcers than for stage 2 ulcers in all healthcare settings [5]. Irreversible tissue damage can happen in as little as two hours in a patient with low tolerance; however, the ulcer may not become apparent for two to five days [10].

Stage 1

Stage 1 pressure injury presents as persistent redness in intact skin. If the area is pressed, it will not lighten in color (non-blanchable) [11]. It usually occurs in a localized area over a bony prominence, and this area can be painful, firm, soft, warmer, or cooler than the surrounding tissue [5]. This area of redness has a clear but possibly irregular boundary [11]. In darker skin tones, blanching may not be visible and the color may differ from the surrounding area [5]. In these instances, it is important to look for the other signs of pressure ulcers, such as pain, change in temperature, and changes in skin texture.

Stage 2

Stage 2 pressure injury presents as shallow, open wounds with partial loss of the dermis. The wound bed is pink/red and without slough. A stage 2 pressure ulcer may also present as a serous fluid-filled blister [5]. Fat and deeper tissues are not visible, and slough and eschar are not present. These injuries are most commonly seen on the sacrum due to moisture and shear, and on the heel due to shear [5]. Skin tears, tape burns, incontinence-associated dermatitis, maceration, or excoriation of the skin should not be classified as stage 2 pressure ulcers [4].

Stage 3

Stage 3 is full thickness tissue loss. Subcutaneous fat may be visible and rolled wound edges are often present, but bone, tendon, and muscle are not exposed. There may be slough in the wound, but it does not obscure observation of the wound bed; if slough or eschar obscures the observation, this is an unstageable pressure injury. Tunneling and undermining may be present [5]. It is important to remember that the depth of stage 3 pressure ulcers will differ from one location to another. For example, the bridge of the nose, ear, occiput, and malleolus do not have a subcutaneous layer, and in these areas a stage 3 pressure ulcer can be shallow [5].

Stage 4

Stage 4 ulcers are characterized by full thickness tissue loss with exposed bone, tendon, or muscle. These ulcers often include undermining and tunneling, and rolled wound edges are often seen [5]. Slough and eschar may be present in part of the wound bed; however, if slough or eschar obscures the observation, this is an unstageable pressure injury [11]. In some cases, stage 4 pressure ulcers can affect supporting structures and may lead to osteomyelitis. As with stage 3 ulcers, the depth of the injury will vary by anatomical location.

Unstageable Pressure Injury

A wound that is unstageable is defined as having full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) [5]. Until the base of the wound can be visualized, the wound will remain unstageable. A necrotic wound cannot be staged until the necrotic tissue has been debrided, and it is then that a stage 3 or stage 4 ulcer will be revealed [5]. It is also important to remember that it is clinically inaccurate to stage a granulating wound if it is the first assessment, as visualizing the depth of the actual pressure sore is not possible [4]. In addition, if stable eschar on an ischemic limb or the heel(s) is present, it should not be removed [5].

Deep Tissue Pressure Injury

Deep tissue pressure injury, previously suspected deep tissue injury, is a pressure-related injury, much like a bruise, that is characterized by persistent non-blanchable, deep red, maroon, purple discoloration or epidermal separation revealing a dark wound bed or blood-filled blister. Deep tissue pressure injuries can present on either intact or non-intact skin. This type of injury is caused by intense and/or prolonged pressure and/or shear. Deep tissue pressure injury may resolve without tissue loss or may rapidly change to reveal the extent of the tissue injury. If necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle, or other underlying structures are visible, this indicates a full thickness pressure injury (Unstageable, stage 3, or stage 4). The NPUAP does not recommend using deep pressure tissue injury to describe vascular, traumatic, neuropathic, or dermatologic conditions [5].

Color is the key to differentiating between deep tissue injury and a stage 1 pressure injury. Purple or maroon areas indicate deep tissue injury; non-blanchable redness is characteristic of stage 1 injuries. Deep tissue injury can become a stage 3 or a stage 4 pressure ulcer even with optimal care [5]. In general, the most common areas of involvement are the heels and sacrum [10]. In some patients, particularly those who are debilitated, deep tissue injury can develop rapidly [11].

Medical Device-Related Pressure Injury

Medical device-related pressure injuries describe injuries or ulcers that result from the use of devices designed and applied for diagnostic or therapeutic purposes. The injury is generally in the shape or pattern of the device and should be staged using the staging system [5].

Mucosal Membrane Pressure Injury

Mucosal membrane pressure injury is found on the mucous membranes. This type of injury is typically attributed to use of a medical device on a mucous membrane, and due to the nature of this type of tissue, these injuries cannot be staged.

4. PRESSURE ULCER RISK ASSESSMENT

Evidence Based Practice Recommendation

The National Pressure Ulcer Advisory Panel, the European Pressure Ulcer Advisory Panel, and the Pan Pacific Pressure Injury Alliance recommend the use of a structured approach to risk assessment that includes assessment of activity/mobility and skin status.

https://www.npuap.org/wp-content/uploads/2014/08/Quick-Reference-Guide-DIGITAL-NPUAP-EPUAP-PPPIA-Jan2016.pdf

Last Accessed: May 1, 2019

Level of Evidence: B (The recommendation is supported by direct scientific evidence from properly designed and implemented clinical series on pressure ulcers in humans, providing statistical results that consistently support the recommendation.)

Identifying patients at risk for pressure ulcers is vitally important as it allows for preventative measures to be initiated. Elements of prevention include identifying individuals at risk for developing pressure ulcers, maintaining skin integrity, treating the underlying causes of the ulcer, relieving pressure, assessing the total state of the patient to correct any deficiencies, and patient/family education.

MAJOR RISK FACTORS IN PRESSURE ULCER DEVELOPMENT

Decreased Mobility

Immobility is possibly the greatest risk factor for pressure ulcer development [4]. According to the United Spinal Association, up to 80% of patients with spinal-cord injuries will develop pressure ulcers during their lifetime and 30% will have more than one pressure ulcer [12]. Patients who have lost the ability to ambulate, either for physical or cognitive reasons, will commonly develop pressure ulcers while chair- or bedridden. The prevention of ulcers in these patients is a vital aspect of ensuring an optimal quality of life.

Contractures

Untreated contractures often lead to pressure ulcer development. Contracted limbs, usually caused by continued hypertonic muscle or tendon stress, can exert pressure on surrounding tissues and adjacent areas. Contracture of a leg or foot can result in pressure ulcer development in that extremity, because it exerts more pressure on the support surface than a normal extremity.

Decreased Sensation

The sensory receptors, cortex, and motor neurons/muscles act as a sort of "pressure ulcer prevention system." These sensations induce individuals to move or shift position when an uncomfortable sensation is experienced. Injury or disease to any component of this system results in a loss of these protective reflexes. Therefore, patients who cannot feel discomfort or cannot sense ischemia are at high risk for pressure ulcer development.

Perfusion Status

Adequate circulation is needed to maintain tissue health by delivering oxygen and nutrients to the cells and removing waste products. Edema reduces tissue perfusion by increasing the distance between the cells and the capillary network. Normal, healthy tissue (in a person with normal sensation and movement) can tolerate short periods of ischemia because tissues require intermittent rather than continuous blood flow [2]. However, extended periods of ischemia can result in tissue damage and, with regard to skin, can lead to pressure ulcers.

Hypotension

Low arterial blood pressure (hypotension), defined as systolic blood pressures less than 100 mm Hg and diastolic pressures less than 60 mm Hg, has been linked to increased risk for pressure ulcer development. In response to hypotension, the body redirects blood flow to the vital internal organs at the expense of the peripheral vascular system, which serves the skin. As the perfusion level drops so does the skin's ability to tolerate external pressure. Capillaries subsequently close at lower levels of interface pressure, and there is an increased risk of damage due to ischemia [1].

Hydration

Normal skin hydration is provided by an intact stratum corneum and sebum secretion. Factors that can decrease skin hydration are overly vigorous or frequent washing, low environmental humidity, and aging. The removal of sebum by frequent cleansing or bathing can cause dehydration. It is important to use moisturizing lotion, particularly immediately after bathing to moisten skin.

Cognition

Loss of cognition is also associated with increased risk for pressure ulcers. Impaired mental status leads to a lack of awareness of discomfort or pressure and may be associated with incontinence. The ability to respond appropriately or to inform others of the need for assistance is often lost completely.

Stress

Stress is a primitive response to injury or anticipated injury. Research has shown that during periods of stress, blood vessels in the peripheral tissues constrict. In a study designed to mimic the body's response to stress, healthy subjects were given an infusion of exogenous epinephrine [1]. The increased levels of epinephrine decreased the levels of subcutaneous tissue oxygen by 45%. Other studies have shown that psychologic stress has a negative impact on healing [1].

Depression

The National Institute of Mental Health estimates that 7.1% of adults in the United States are suffering from depression, and major depression is the leading cause of disability worldwide [13]. Depression is particularly under-recognized in the elderly. Depressed patients have little interest in self-care and nutrition, both of which may predispose an individual to pressure ulcers [4].

Age

Patients older than 65 years of age experience pressure ulcers most frequently [1]. With aging, the skin becomes more fragile. The skin layers adhere less securely to each other and often appear paper thin and almost transparent. There is also evidence of increased dryness, decreased vascularization, and increased vascular fragility.

In elderly individuals, there is a decrease in surface barrier function. The ability of the soft tissue to evenly distribute the mechanical load without compromising blood flow is impaired. There is less subcutaneous tissue to cushion boney prominences. This, in addition to decreased sensory perception, makes elderly skin more vulnerable to pressure, shear, and friction [2]. Research has shown that, in the geriatric population, blood flow in the area of the ischial tuberosity while sitting on an unpadded surface is lower than in younger adults [4].

Although much less common, children can also develop pressure ulcers. Most commonly, these ulcers develop in the occipital region in infants and toddlers and on the sacrum in young children [1].

Obesity

In the United States, approximately 78 million adults 20 years of age and older are obese and 15.5 million are morbidly obese [14,15]. Obesity is defined as a body mass index (BMI) of 30 or greater; severe or morbid obesity is defined as a BMI greater than 40 [14,16].

Factors that contribute to pressure ulcer development in obese individuals include decreased blood supply in adipose tissue, difficulty in turning and repositioning, moisture within skin folds, incontinence, skin-to-skin friction, immobility, and poor nutrition. Obese patients are particularly at risk for "unusual" pressure ulcers resulting from pressure within skin folds. Obese patients may have large panniculi ("aprons"), weighing up to 50 pounds. The abdominal panniculus must be regularly repositioned in order to prevent pressure injury. This may be accomplished by placing the patient in the side-lying position and lifting the panniculus away from the underlying skin surface, which allows air to the area and simultaneously relieves pressure.

Tubes or catheters can also cause pressure by burrowing into skin folds. Poorly fitting beds, chairs, or wheelchairs may also be a source of pressure [17].

Nutrition

Low body weight and impaired nutrition are also concerns. Weight less than 119 pounds or a BMI less than 20 are indicators of increased risk for pressure ulcer development [18].

Recent weight loss, decreased nutritional intake, inadequate dietary protein, and impaired ability to feed oneself have been identified as risk factors for pressure ulcer development. An estimated 50% of elderly patients admitted to the hospital have suboptimal protein nutrition [18]. When there is a sustained deficit of protein as an energy source, skin and soft tissues become more vulnerable to injury. Low protein levels also result in decreased resistance to infection. Older adults also have increased incidence of low calorie intake and low levels of zinc and vitamin B12.

Vitamin A, C, and E deficiencies have been associated with pressure ulcer formation. Vitamin A works in the body to maintain epithelial integrity and is involved in collagen synthesis. It also plays a role in protection against infection. A deficiency of vitamin A can inhibit collagen synthesis, delay re-epithelialization, and decrease cellular cohesion. Vitamin C is also involved in collagen synthesis, immune function, and wound repair. A deficiency of vitamin C can result in capillary fragility. Vitamin E deficiency often decreases the immune function of the skin.

Diabetes

It is estimated that 9.4% of the U.S. population has diabetes [19]. Alone, diabetes increases the risk for pressure ulcer development by 56% [18]. However, approximately 43% of diabetics in the United States are 60 years of age or older, which compounds the risks [20].

Elevated blood sugar levels characteristic of diabetes result in decreased phagocytic ability of neutrophils and diminished wound strength. Patients with diabetes are more prone to infection, and wound healing is slower in this population than in patients without diabetes. Hyperglycemia can also result in protein-energy malnutrition, dehydration, and alteration in microcirculation [1]. Peripheral neuropathy, a common complication associated with diabetes, results in decreased sensation, an established risk factor for pressure ulcers.

Smoking

Nicotine impedes blood flow to the tissues in two ways: it is a potent vasoconstrictor, and it increases the adhesiveness of platelets, resulting in clot formation. Carbon monoxide contained in cigarette smoke prevents oxygen from attaching to the hemoglobin molecule. This significantly reduces the amount of oxygen circulating in the blood stream. The same reaction occurs to some extent in people exposed to secondhand smoke. Studies have shown that cigarette smoking is associated with a higher incidence of pressure ulcer development in spinal cord-injury patients [21]. Patients who smoke also have a higher rate of recurrence of pressure ulcers [4].

Medications

Several medications can affect skin integrity. Normal skin flora can be altered by antibacterials, oral steroids, and hormones. Additionally, analgesics, antihistamines, nonsteroidal anti-inflammatory medications, and chemotherapy can alter inflammatory reactions. Of these, corticosteroids have been studied the most extensively. Corticosteroids interfere with collagen synthesis and epidermal regeneration at a dose of 40–60 mg per day [2].

Other Risk Factors

Areas of advanced pressure ulcers that have healed are more likely to have recurrent breakdown. Therefore, documentation of history of a healed ulcer and its stage, if known, is important. Several other conditions can interfere with systemic and peripheral oxygenations and nutrition, resulting in pressure ulcers. These conditions include:

- Respiratory problems

- Atherosclerosis

- Coronary artery disease

- Peripheral vascular disease

- Congestive heart failure

- Malignancies

- Human immunodeficiency virus/acquired immune deficiency syndrome

- Anemia

- End-stage renal disease

- Thyroid disease

- Terminal illness

- Patient refusal of some aspects of care and treatment

RISK ASSESSMENT

No step is more important in preventing pressure ulcers than understanding a patient's risk. Risk assessment is used to identify:

- Populations at risk

- Level of risk

- Type of risk

A risk assessment is a way of attaching numbers and specifics to identified risk factors. An informal risk assessment cannot take the place of a formal risk assessment, such as the one conducted using the Braden Scale. Research shows that without formal risk assessment, clinicians tend to intervene consistently only at the highest levels of risk [22]. In some studies, repositioning or turning, an important part of pressure ulcer prevention, was prescribed for fewer than 50% of the patients at mild-to-moderate risk for pressure ulcer development [4].

The Braden Scale

The Braden Scale was developed in 1987 by Barbara Braden and Nancy Bergstrom [22]. Since then, it has undergone testing in several clinical settings, and its validity has been established by expert opinion. It is considered one of the most reliable tools for identifying patients at risk for pressure ulcer development, and it is the most widely used. The Braden Scale scores factors that contribute to prolonged pressure and factors that result in diminished tissue tolerance for pressure [22]. There are six items scored in the assessment [22]:

- Sensory perception

- Moisture

- Activity

- Mobility

- Nutrition

- Friction and shear

Each item is scored on a scale between 1 and 4 with the exception of friction and shear, which is scored between 1 and 3. The lower the score, the more severe the impairment or problem in that area. Therefore, the lower the score, the higher the patient's risk for pressure ulcer development. Various studies have shown cut-off scores from 16 to 18 as being at risk [2]. Although cut-off scores vary, usually a score of 13–14 is considered moderate risk, 10–12 indicates high risk, and 9 or less is very high risk.

The Braden Scale should be used for assessment on admission to a care facility or after return from a hospital. Research shows that a repeat assessment done 48 hours to 72 hours after admission further defines pressure ulcer risk. In nursing home populations, the majority of pressure ulcers develop during the first two weeks following admission [1]. In addition, most facilities set their own policies regarding reassessment frequency (e.g., quarterly). However, it is important to note that any change in a patient's condition warrants reassessment.

Braden Scale assessment is completed by licensed personnel familiar with the patient and is shared with all staff caring for the patient; good communication is essential to ensure a meaningful assessment [4]. Licensed and unlicensed staff must have a basic knowledge of Braden scores and how it directs patient care. Accuracy of scoring is very important to determining the appropriate intervention.

5. SKIN AND PAIN ASSESSMENTS

Admission assessment is the foundation for effective prevention and initiation of a management program. All special garments, including shoes, heel and elbow protectors, orthotic devices, restraints, and protective wear, should be removed during a skin inspection. If immobilizers or splints are being used, the physician should be consulted to ensure that they may be safely removed. If they cannot be removed, this should be documented in the patient's record.

It is also important to incorporate a holistic assessment, evaluating the meaning and significance of skin breakdown and wound development to the patient and his or her caregiver. Does the patient view the ulcer as a sign of vulnerability, a loss of independence, or an unavoidable consequence of aging?

There are several goals of completing a skin assessment. Foremost, it is imperative to identify and assess areas of impending or actual skin breakdown and patients at risk for future skin ulcers and immediately begin appropriate management interventions. For patients at high risk for pressure ulcer development, a systemic skin assessment should be conducted at least daily and findings should be documented.

ELEMENTS OF A BASIC SKIN ASSESSMENT

A basic skin assessment includes evaluation of the temperature, color, moisture, turgor, and integrity of the skin. The skin's response to pressure indicates its condition. Pressure to soft tissue interrupts the blood flow to that area and results in pallor to the overlying skin. This pallor indicates tissue ischemia. When the pressure stops, the skin should quickly return to its normal color as blood flow returns [23]. In general, when pressure is relieved from an area, redness will resolve within 30 minutes if there is no tissue damage. Therefore, it is important to recheck areas of redness 30 minutes after pressure is relieved and to document findings.

All aspects of the assessment should be explained to the patient. Many people are shy about exposing their body to strangers, even to clinicians. Conduct the exam in a warm and private room with good lighting. It is vital not to rush or overlook part of the assessment, even if the patient is restless.

Although a head-to-toe assessment is often used, a toe-to-head assessment may result in less likelihood of missing areas of potential or actual breakdown, considering that a thorough inspection of the feet and heels is often overlooked. When completing a toe-to-head skin assessment, start with the tips of the toes, between the toes, soles of the feet, back and sides of the heels, and inner and outer areas of both ankles. Continue up the following assessment sites:

- Right and left lower legs

- Right and left knees' inner and outer surfaces

- Right and left thighs

- Right and left ischial tuberosity

- Right and left hip

- Right and left iliac crest

- Sacrum

- Coccyx

- Lower, mid, and upper back

- Right and left shoulders

- Right and left ears (particularly redness under oxygen tubing)

- Back of the head

ASSESSING AND DOCUMENTING A PRESSURE ULCER

Documentation of a pressure ulcer should include location, stage (per NPUAP definitions), wound description (e.g., size, color, drainage), and pain level. Wound size should always be recorded in centimeters. The length is the longest head-to-toe measurement, while the width is the longest hip-to-hip measurement. The best practice recommendation is to measure the wound at the point of greatest length and the point of greatest width. Wound depth is measured by gently inserting a pre-moistened, sterile cotton swab into the deepest part of the wound. The measurement from the tip of the applicator to the level of the skin surface is recorded as the depth [4].

Undermining and/or tunneling should also be recorded in centimeters. Undermining is defined as tissue destruction underlying the intact skin along the wound margins, meaning the wound margins have separated from the wound. Using the face of the clock as a reference for location, with the patient's head representing 12 o'clock, measure the extent of the undermining clockwise. For example, undermining along the right and bottom borders may be recorded as extending 1.5 cm from 2 o'clock to 7 o'clock [24].

Tunneling refers to channeling that extends from any part of the wound and may pass through subcutaneous tissue and muscle. It may result in dead space and abscess formation. The depth of the tunnel should be measured with a sterile cotton swab and recorded. The direction of the tunnel should be documented using the clock method (e.g., 4 cm at 5 o'clock). If there is more than one sinus tract/tunnel, number each one clockwise [4].

It is also vital to assess and document the appearance of the wound bed. If the wound bed has a mixture of tissue in it, this should be documented by an approximate percentage (e.g., the wound base is 75% granulation tissue and 25% slough). Granulation results in "beefy" red tissue with a shiny, moist granular appearance, while necrotic tissue is gray, brown, black, and moist. Eschars are typically gray to black and dry or leathery in appearance [24]. Slough tissue is yellow/white to gray in color. It may be stringy or thick and appear as a layer over the wound bed [24]. Epithelial tissue will often begin to grow in from the edges over the wound surface. This tissue is generally pink and shiny. As a quick reference color guide, red is associated with normal healing, yellow indicates slough or dead tissue, and black is necrosis [4].

Wound drainage is another important aspect of pressure ulcer assessment. The amount should be noted (scant, moderate, or copious). The color and consistency of the drainage may be serous (clear or light yellow in color, thin, watery), sanguineous (red, thin), serosanguineous (pink to light red, thin, watery), or purulent (creamy yellow, green, white, or tan, thick, opaque). The presence of any associated odor should also be documented. A non-infected wound produces little or no odor. The impact of wound odor can be quite devastating to the patient and his or her family.

The area up to 4 cm from the edge of the wound circumferentially should be assessed. Describe its characteristics, particularly color and integrity. Circumferential redness up to 2 cm is indicative of cellulitis [1]. The skin around the pressure ulcer should be palpated to determine if it is soft or indurated. Indurated (hard) tissue, even in the absence of redness, is an indication of infection.

ASSESSING PAIN

Pressure ulcers can cause considerable pain and suffering. Pressure ulcer pain has been described as ranging from sore to excruciating. In one study of patients with stage 2–4 pressure injuries, 74% of patients rated their pain as mild, discomforting, or distressing; 19% rated their pain as horrible or excruciating [25]. Pain and odor control are a major concern for patients, and studies have shown that patients rank pain control as more important than healing [4]. The level of pressure ulcer pain depends both on the stage of the ulcer and on manipulation of the area (e.g., if a dressing change is done at the time of assessment). The majority of patients report pressure ulcer pain at rest as well as with dressing changes. Pressure ulcer pain may be due to tissue trauma from sustained loads, inflammation, damaged nerve endings, infection, procedures such as debridement, and dressing changes [25].

The gold criterion for assessing pain intensity is self-reporting and the utilization of standard pain intensity instruments. Two of the most widely used pain assessment scales are the numeric pain intensity scale and the Wong-Baker Faces Pain Rating Scale [26]. The numeric pain intensity scale consists of ratings from 0 (no pain) to 10 (worst possible pain). This scale can be used for pain assessment with adults and children older than 7 years of age [27]. Visual presentation of the numeric pain intensity scale is helpful with hearing impaired patients, and the scale has been translated into many languages.

The Wong-Baker Faces Pain Rating Scale consists of six faces ranging from a happy smiling face (no pain), to a crying, frowning face (worst pain). The patient is asked to choose the face that best reflects his or her pain. The Faces Pain Rating Scale is the preferred scale for use with children and may also be used with the geriatric population. It can also be used with cognitively impaired patients and those for whom English is a second language.

After the initial pain assessment has been completed, reassessment should be done at regular intervals. Pain intensity should be rated by the patient, not a healthcare professional. The following questions may be used to help determine patients' pain levels:

- What kind of pain are you experiencing?

- What word(s) would you use to best describe it (e.g., burning, aching, shooting)?

- What makes the pain better?

- What makes it worse?

- Where is the pain located?

- Does the pain radiate?

- Would you describe your pain as none, mild, moderate, severe, or excruciating?

- How would you rate your pain on a scale of 0 to 10, with 0 representing no pain and 10 being the worst imaginable pain?

- What is the pain intensity at its worst, best, and now?

- Is the pain better or worse at any particular time of the day or night?

- When does it start and when does it stop?

Pain Management

The goal of pain management in the patient with pressure ulcer is to eliminate the cause of pain and to provide analgesia. There are several interventions and practice modifications that can prevent or manage pressure ulcer-associated pain.

Evidence Based Practice Recommendation

According to the National Pressure Ulcer Advisory Panel, the European Pressure Ulcer Advisory Panel, and the Pan Pacific Pressure Injury Alliance, adequate pain-control measures, including additional dosing, should be implemented prior to commencing wound care procedures.

https://www.npuap.org/wp-content/uploads/2014/08/Quick-Reference-Guide-DIGITAL-NPUAP-EPUAP-PPPIA-Jan2016.pdf

Last Accessed: May 1, 2019

Level of Evidence: C (The recommendation is supported by indirect evidence and/or expert opinion.)

Skin care and assessments should be performed at a time of day when the patient is less fatigued [11]. All procedures should be thoroughly explained before they are performed. If a patient has questions, this should be addressed, and healthcare professionals should be encouraging and provide positive reinforcement. It is important to avoid trauma (shearing and tear injuries) to fragile skin during transferring, positioning, or holding a patient. If necessary, adjunctive medications may be administered to improve sleep and reduce anxiety, which can contribute to experiences of pain.

Dressing changes are often very painful. An analgesic may be administered 30 minutes before dressing changes, and if possible, the number of daily dressing changes should be kept to a minimum. Tape should always be avoided on fragile skin. If patients are able, they should be allowed to remove their own dressings or set the pace of dressing changes. All patients should be assessed for pain before, during, and after dressing changes, and these findings must be documented [4].

Physical therapy and occupational therapy may be helpful to decrease contractures and muscle spasm. Of course, ensuring proper seating and positioning can improve pain scores as well as decreasing the risk for further pressure injuries.

6. INDIVIDUALIZED PROGRAM OF SKIN CARE

One of the most important steps to prevent pressure ulcers is physically repositioning the patient frequently. Repositioning should be done every one to two hours, depending on the patient's condition [2].

POSITIONING IN BED

Every time the patient is repositioned, look for areas of redness and make sure that the new position does not put weight on these areas. Avoid massaging reddened areas over bony prominences [11]. Donut-shaped supports or ring cushions that encircle the ischemic areas should not be used as they can reduce blood flow to an even wider area of tissue. To the degree that the patient is able, encourage activity. Even a few steps done frequently will help. It is important to maintain current activity level, mobility, and range of motion. When repositioning the patient in bed, it is essential to avoid the 90-degree side-lying position. This position puts intense pressure directly over the trochanter. Instead, use the 30-degree lateral position, utilizing a pillow or foam wedge to maintain the position [11]. Keeping the head of the bed at 30-degrees or less (if medically feasible) will help prevent shear. Place a pillow between the patient's knees or ankles to minimize pressure where one limb lies on top of the other. Lifting devices, such as an overhead trapeze or bed linen, are helpful when moving patients. It is important to minimize dragging during transfers and position changes. Minimize environmental factors leading to skin drying, such as low humidity (less than 40%) and exposure to cold [4]. Posting an individualized turning schedule in patient rooms can be helpful to healthcare professionals and patients.

Heel ulcers are especially painful and are among the most difficult to heal. Heel pressure ulcers can develop infection and, in extreme cases, may lead to amputation of the foot. To prevent the development of pressure ulcers on the heels, place a pillow under the calf to float the heels off the bed. There are also devices available that eliminate pressure on heels and prevent foot drop (e.g., suspension boots). Current guidelines state that heels are to be kept off the bed [2].

POSITIONING WHILE IN CHAIR

Pressure ulcers are a particular concern for patients who spend a significant amount of time in chairs. A patient is more likely to develop pressure ulcers from sitting than from reclining, as sitting puts the patient's weight on the relatively small surface areas of the buttocks, thighs, and soles of the feet. Much of this weight is focused over the small area of tissue covering the ischial tuberosities. It is important for patients who sit in a chair to regularly change position. A dependent patient must have his/her position changed in a chair at least every hour. Patients who are able to move themselves should shift their weight (even slightly) every 15 minutes.

Evidence Based Practice Recommendation

The National Pressure Ulcer Advisory Panel, the European Pressure Ulcer Advisory Panel, and the Pan Pacific Pressure Injury Alliance recommend using wheelchairs and chairs that are wide and strong enough to accommodate obese patients' girth and weight. A pressure redistribution cushion designed for the bariatric individual should be used on seated surfaces, and clinicians should check routinely for "bottoming out" of the cushion.

https://www.npuap.org/wp-content/uploads/2014/08/Quick-Reference-Guide-DIGITAL-NPUAP-EPUAP-PPPIA-Jan2016.pdf

Last Accessed: May 1, 2019

Level of Evidence: C (The recommendation is supported by indirect evidence and/or expert opinion.)

A patient should be properly positioned in a chair for postural alignment, distribution of weight, balance, and stability. Patients should sit with their back erect and against the back of the chair, thighs parallel to the floor, knees comfortably parted, and arms horizontal and supported by the arms of the chair. This position distributes weight evenly over the available body surface area. Slouching can cause shearing and friction and places undue pressure on the sacrum and coccyx. Feet should be kept flat on the floor to protect the heels from pressure and distribute the weight of the legs over the largest available surface area. The thighs and arms should remain parallel to ensure that weight is evenly distributed instead of being focused on the ischial tuberosities and elbows. Parting the knees will prevent the knees and ankles from rubbing together. If a patient uses a footstool, it is vital that his or her knees are not above hip level, because this shifts the weight from the back of the thighs to the ischial tuberosities. This same problem can occur if the chair is too short for the patient.

CLEANSING AND BATHING

Maintaining skin cleanliness and moisturizing frequently can protect skin integrity. The skin should be cleaned with water and a gentle soap, preferably a pH-balanced cleanser. Alkaline products remove skin lipids, which increases water loss and weakens the barrier function of the skin [11]. Avoid hot water for bathing and scrubbing or using harsh cleaning agents. A soft cloth should be used to pat rather than rub the skin dry. Thromboembolic deterrent (TED) stockings should be removed when bathing, and the nurse or physician should be notified of any redness, discoloration, or skin breakdown.

It is important to individualize the frequency of skin cleansing based on the patient's age, skin texture, and dryness or excessive oiliness of the skin. A daily bath may not be needed for all patients.

MOISTURIZING THE SKIN

The epidermis is about 30% water, but through a process called trans-epidermal water loss, skin can lose its natural moisture. Without sufficient moisture, skin can become dry, brittle, and vulnerable to breakdown [2]. Therefore, products should be used to keep the skin supple.

Emollients, such as mineral oil, petrolatum, and lanolin, penetrate into the stratum corneum to increase the lipid component and add softness to the skin. In addition, the oil film on the skin surface prevents water loss and helps to rehydrate the stratum corneum [11].

Moisture barriers such as dimethicone also help to prevent water loss and to retain lipids and water within the skin cells. These products maintain the "brick and mortar" configuration of the skin by replacing lost "mortar" [2].

Humectants, such as glycerin, urea, and Lac-Hydrin, increase the water content of the stratum corneum by pulling water from the environment. Normal hydration of the skin cells maintains normal cell shape and cell function. All moisturizers should be applied to clean, slightly moist skin. Special attention should be paid to bony prominences, heels, ears, and the back of the head.

BOWEL AND BLADDER MANAGEMENT

Urinary and Fecal Incontinence

According to the National Association for Continence, approximately 25 million Americans have transient or chronic incontinence. It is estimated that more than 90% of patients with urinary incontinence fail to seek medical intervention or treatment [28].

At least half of all nursing home residents experience urinary incontinence [28]. For patients who are cooperative and aware of bladder filling, a toilet program should be instituted, including planned voiding every two hours. For patients who are uncooperative or unaware of bladder filling, consider the use of absorptive products or condom catheters for men. It is important to use diapers and underpads that wick moisture away from patients' skin. These patients should be checked for incontinence every two hours. Incontinent patients should be cleaned as soon as possible after soiling using specialized incontinence skin cleansers or soaps.

For patients with fecal incontinence and severe diarrhea, all potential causative factors should be explored and addressed. A rectal pouch may be useful for these patients. In cases of chronic incontinence, an every-other-day suppository or enema may be considered. In addition, barrier ointments help protect the skin from incontinent episodes. If used, apply a thick coat of ointment, wipe off the soiled top layer, and apply another layer. Do not clean off the paste to skin level when bathing or cleaning.

SUPPORT SURFACES

There is a vast array of support surfaces and seating options available, but as helpful as these devices may be, they are no substitute for attentive care. Patients still require individualized turning schedules regardless of the equipment used.

Most support surfaces reduce pressure by conforming to the contours of the body so pressure is redistributed over a larger area rather than concentrated in one location [2]. There are many support options, including mattresses, overlays, and cushions.

Mattresses and Overlays

Most pressure relief mattresses use some form of foam, gel, or water to cushion the patient. Water mattresses and some air mattresses evenly distribute pressure under the patient. Low-air-loss and high-air-loss mattresses are specialized support devices that pass air over the patient's skin and promote evaporation [2].

The most common mattress overlays are foam, air, and gel. Foam overlays should be at least 3 inches thick for the average patient; even thicker is better. Two-inch foam overlays may add comfort, but they are not suitable for patients at risk for pressure ulcers. Standard egg-crate mattresses are used for comfort only [2]. All support surfaces, regardless of the medium, function best with less linen between the patient and the surface. If a patient's weight completely compresses a mattress overlay, it is not effective. To make sure that a mattress is not "bottoming out," slide one hand between the mattress overlay and the mattress. If the patient's body can be felt through the overlay, it should be replaced [8]. The weight limit for most support surfaces is about 350 lbs. Special low-air-loss mattresses are available for patients who weigh more than 350 lbs.

An important factor in air-filled overlays is inflation; they may not be effective in preventing pressure ulcers if they are over-inflated, under-inflated, or punctured. Therefore, inflation must be checked daily.

Patients must be comfortable and able to sleep on the support surface. Some surfaces produce noise that may not be tolerable for some patients.

Cushions

Products designed to help prevent pressure ulcers while sitting fall into two broad categories: those that relieve pressure and those that make repositioning easier.

Seat cushions may be used to distribute weight over the largest possible surface area. These are generally made of foam, gel, air, or a combination [2]. Wheelchair cushions for short-term use are foam, air, water, or gel. The goal of these products is to improve weight distribution cost effectively. Gel and air cushions have been shown to be the most effective [11]. Wheelchair-bound patients who require long-term solutions need cushions that fit the wheelchair, support seating stability, provide high-level pressure reduction, and reduce shear. All cushions should be checked and repaired or replaced on a regular basis.

PATIENT/FAMILY EDUCATION

A vital component of a pressure ulcer prevention program is education. If possible, pressure ulcer prevention should not be a passive process for the patient and his/her family members. Rather, it should be a dialogue in which the patient or family feels comfortable asking questions and discussing problems. Patients should have as much control as possible in the plan of care. Empowerment is very important in maintaining the patient's physical and emotional well-being. The plan of care should be explained thoroughly to cognitively aware patients and their family.

At the same time, it is vital to evaluate the patient's/family's existing knowledge regarding pressure and pressure ulcers. Healthcare professionals should show patients what they can do to facilitate pressure relief (e.g., how to make small position changes while in the chair). If possible, it is often beneficial to teach patients how to do simple range-of-motion exercises. Take time to train the patient as often as is appropriate; not everyone will absorb the information the first time it is heard [4]. It is important not to let noncompliance or a bad attitude from the patient or family discourage the teaching process. The subject should be approached as often as is reasonable. Include the family members and caregivers in the instructions. As well as assisting with care, they can encourage compliance. All efforts at patient and family/caregiver education should be documented, along with the patient's response (both verbal and behavioral).

STAFF EDUCATION

Education of caregivers is also a key factor in the prevention of pressure ulcers and in the successful management of existing pressure ulcers. All healthcare personnel providing care to the patient must appreciate the role that they play in pressure ulcer prevention. Materials should be prepared to meet the educational levels of different members of the interdisciplinary team [29]. Certified nursing assistants (CNAs) are an essential part of the nursing team, and their education regarding pressure ulcer prevention and pressure ulcer healing should not be neglected. Programs specifically geared towards CNAs may be developed and implemented.

NUTRITIONAL SUPPORT

Nutrition is important for maintaining skin integrity. A strong correlation exists between poor nutrition and pressure ulcer development [18]. Despite this fact, nutrition is often overlooked during treatment. It is of vital importance to address the nutritional needs of every individual with pressure ulcers [30].

Malnutrition is defined as undernutrition or overnutrition caused by a deficit or excess of nutrients in the diet. Undernutrition occurs because intake is inadequate or the individual is unable to absorb nutrients. Overnutrition is most commonly seen in obesity. Patients with nutritional compromise should receive nutritional support, with the possible exception of patients in the end of life. Evaluation of hydration status is also an integral part of the overall nutritional picture.

Nutritional Assessment

Weight is the cornerstone in the diagnosis of malnutrition [2]. An unplanned weight loss of more than 10% in the last six months indicates a serious nutritional compromise. Signs of malnutrition include:

- Loss of subcutaneous tissue

- Muscle wasting

- Generalized edema

- Dry, pluckable hair

- Dry, flaky, itchy skin

- Cracks in the mucous membranes

- Delayed wound healing/failure to granulate

Food and fluid intake should be continuously assessed. Pay attention to food preferences and tolerances; it is beneficial to optimize the eating environment by individualizing meal times and patterns as much as possible. Culture and religion often play a significant part in food choices and attitudes toward eating. It is often necessary to consider an interdisciplinary assessment of chewing and swallowing ability and dental problems.

Malnutrition is common in elderly individuals. Older people produce less saliva, which makes swallowing more difficult. Smell and taste diminish with age, and medication can affect taste buds, causing food to become less appealing. Patients' ability to self-feed should also be monitored. The use of finger foods, adaptive utensils, and feeding assistance should be considered if necessary.

Interventions to Promote Nutrition

For patients with inadequate nutrition, strategies must be employed to increase oral intake. The preferred route of nutritional support is oral; whenever possible, the gastrointestinal tract should be used for feeding. It is the easiest and most comfortable way to provide supplementation, and it is also the least expensive and most convenient way. Patients must have diets prescribed with protein and caloric content sufficient to meet metabolic needs. The diet should consider the patient's preferences and special needs (e.g., mechanical soft diets) [4]. Daily multivitamin supplementation may need to be implemented. Mouth care should be performed prior to eating. Additionally, toileting and hand washing should be offered prior to meals.

Provide an environment conducive to eating. Position the patient properly; an upright position is preferred. Make sure the food is at the right temperature for the patient. Do not rush eating, particularly if the patient is elderly and requires more time to be oriented. Many patients benefit from the inclusion of snacks high in calories and protein in the diet (e.g., a peanut butter sandwich with milk). Consider adding powdered milk to yogurt and pudding to maximize caloric intake and protein levels. Commercial nutritional supplements, such as breakfast shakes, are also a common adjunct.

It is vital to maintain patient control as far as medically feasible. Some patients may not like ice in their water, others may prefer soup lukewarm. Patient preferences should be accommodated as much as possible.

Remind the patient to chew food thoroughly. If necessary, liquids may be offered between bites; some patients require this to help swallow their food.

Keeping patients hydrated is vitally important, and healthcare professionals should take all available opportunities to improve patients' hydration if it is medically indicated. Patients at risk of becoming dehydrated should be listed on assignment/report sheets as a reminder to monitor these patients. Fluids should be scheduled between meals at least three times a day. Patient preferences for fluids (e.g., straws, temperature, ice) should be observed and noted. Refill water pitchers frequently and keep them within reach of patients, especially those with restricted mobility. Patients should be offered something to drink at every interaction. Ambulatory patients should be provided with a water bottle. As with nutrition and positioning, it is necessary to educate patients/families about the importance of hydration. When, despite these measures, patients are unable to consume adequate levels of water or nutrients, tube feeding or parenteral feeding should be considered. Patient and family preferences and the overall goals of treatment guide these decisions [18].

EVALUATION OF THE SKIN PROGRAM

Patients at risk for skin breakdown should have a daily inspection at every interaction, including during bathing, dressing, and repositioning. Every time the patient is repositioned, the skin surfaces should be checked. This will help determine if the turning schedule is appropriate for the patient or if it should be modified. Particularly, patients should be assessed to determine if episodes of incontinence are being adequately controlled. Differential diagnosis for fecal incontinence includes infection (e.g., Clostridium difficile), impaction, and dietary deficits. Ongoing evaluation of interventions in use is essential to ensure that they are effective.

Assessment is a team effort and should include all members of the interdisciplinary team, including physicians, nurses and nurse assistants, physical therapists, occupational therapists, dieticians, and social workers. If an intervention is determined to be ineffective, it should be modified or changed completely. Possible modifications of a skincare plan include physical therapy to assess current level of mobility, changing seating surfaces, and correcting inappropriate body alignment when sitting.

7. DOCUMENTATION

Documentation of skin assessments provides information for those involved in the patient's care; it is a communication tool between the disciplines. To determine if an ulcer is improving, documentation of the various states of the ulcer is necessary. This allows for evidence that the ulcer has improved [8]. Therefore, observations and interventions should be presented clearly and concisely. Another purpose of documentation is for a legal record of the assessment, interventions, and outcomes [6]. The individualized interventions for skin care should be documented, with specific details regarding who provided care, how often, what supplies and equipment are needed, and how the care should be undertaken. This information should be readily available to all of the patient's caretakers.

There are several tips to facilitate the complete documentation of pressure ulcers. A good rule for documentation is to keep a record of the initial evaluation, interventions, patient's response, and any follow-up. All changes or complications identified should be noted. It is important to write clearly so anyone reading the chart will understand the language and the terms used.

Efforts to educate patients and/or families should be documented, including instructions given and responses from the patient/family. If a patient refuses or is unwilling to engage in certain interventions, this should become part of the documentation.

8. CONCLUSION

A thorough, holistic assessment of each patient at admission, with factual, concise documentation of findings, is a clear starting point for treating and/or preventing pressure injuries. Daily skin assessments for high-risk patients and informal assessment with every patient contact are recommended to ensure optimal patient care. A reliable tool, such as the Braden Scale, should be utilized to identify patients at high risk for skin breakdown, and the NPUAP guidelines should be used to stage skin breakdown appropriately. The establishment of goals consistent with the values and lifestyle of the patient and his/her family can facilitate greater patient involvement in care and adherence to prescribed interventions. A team approach in deciding appropriate individualized interventions for each patient has proven advantages. Team members should be aware of their roles in implementing the plan of care. Ongoing assessment of the interventions in place and modification/change of the plan of care as needed is the final step in implementing an individualized skincare plan. Of course, this should be supported by timely, accurate documentation.

Works Cited

1. Bryant RA, Nix DP. Acute and Chronic Wounds: Current Management Concepts. 5th ed. St. Louis, MO: Elsevier-Mosby; 2016.

2. Emory University School of Medicine Wound, Ostomy and Continence Nursing Education Center. Skin and Wound Module. 6th ed. Atlanta, GA: Emory University WOCNEC; 2006.

3. Barber P, Parkes J, Blundell D. Further Essentials of Pharmacology for Nurses. Maidenhead: McGraw-Hill International; 2012.

4. Baranoski S, Ayello EA. Wound Care Essentials: Practice Principles. 3rd ed. China: Lippincott Williams & Wilkins; 2012.

5. National Pressure Ulcer Advisory Panel. Press Release. National Pressure Advisory Panel (NPUAP) Announces a Change in Terminology from Pressure Ulcer to Injury and Updates the Stages of Pressure Injury. Available at http://www.npuap.org/national-pressure-ulcer-advisory-panel-npuap-announces-a-change-in-terminology-from-pressure-ulcer-to-pressure-injury- and-updates-the-stages-of-pressure-injury. Last accessed April 10, 2019.

6. Fenstemacher PA, Winn P (eds). Post-Acute and Long Term Medicine: A Pocket Guide. 2nd ed. Geneva: Springer International Publishing; 2016.

7. Agrawal K, Chauhan N. Pressure ulcers: back to the basics. Indian J Plast Surg. 2012;45(2):244-254.

8. Wound, Ostomy, and Continence Nurses Society. Guideline for Prevention and Management of Pressure Ulcers. Mt Laurel, NJ: Wound, Ostomy, and Continence Nurses (WOCN); 2010.

9. Newman DK, Palmer MH. Incontinence and PPS: a new era. Ostomy Wound Manage. 1999;45(12):32-49.

10. Wound, Ostomy and Continence Nurses Society. WOCN Society Response to NPUAP White Papers: Deep Tissue Injury, Stage I Pressure Ulcers, and Stage II Pressure Ulcers. Ninth National NPUAP Conference. February 2005.

11. Medline Industries, Inc. Pressure Ulcer Prevention Program. Mundelein, IL: Medline Industries, Inc.; 2008.

12. United Spinal Association. Health and Wellness after SCI: Skin Breakdown, Pressure Ulcer Prevention with SCI-RRTC. Available at http://www.spinalcord.org/resource-center/askus/index.php?pg=kb.page&id=2396. Last accessed April 10, 2019.

13. National Institute of Mental Health. Major Depression. Available at https://www.nimh.nih.gov/health/statistics/major-depression.shtml. Last accessed April 10, 2019.

14. Hamdy O. Obesity: Epidemiology. Available at https://emedicine.medscape.com/article/123702-overview#a5. Last accessed April 10, 2019.

15. Sturm R, Hattori A. Morbid obesity rates continue to rise rapidly in the US. Int J Obes (Lond). 2013;37(6):889-891.

16. Centers for Disease Control and Prevention. Overweight and Obesity: Defining Adult Overweight and Obesity. Available at https://www.cdc.gov/obesity/adult/defining.html. Last accessed April 10, 2019.

17. Institute for Clinical Systems Improvement. Pressure Ulcer Prevention and Treatment Protocol: Health Care Protocol. Bloomington, MN: Institute for Clinical Systems Improvement; 2012.

18. Stasik L. Hospital-Acquired Pressure Ulcers: Making the Nutrition Connection. Columbus, OH: Abbott Nutrition; 2008.

19. Centers for Disease Control and Prevention. National Diabetes Statistics Report: Diabetes Fast Facts. Available at https://www.cdc.gov/diabetes/data/statistics/statistics-report.html. Last accessed April 10, 2019.

20. Centers for Disease Control and Prevention. National Center for Chronic Disease Prevention and Health Promotion: Division of Diabetes Translation. National Diabetes Statistics Report, 2017: Estimates of Diabetes and Its Burden in the United States. Available at https://www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdf. Last accessed April 10, 2019.

21. Smith BM, Guihan M, LaVela SL, Garber SL. Factors predicting pressure ulcers in veterans with spinal cord injuries. Am J Phys Med Rehabil. 2008;87(9):750-757.

22. Bergstrom N, Braden BJ, Laguzza A, Holman V. The Braden Scale for predicting pressure sore risk. Nurs Res. 1987;36(4):205-210.

23. Family Health Media. Pressure Ulcer Prevention: What Caring People Need to Know [DVD]. 2nd ed. Charlottesville, VA: Family Health Media; 2008.

24. Kennedy KL. Gaymar Pictorial Guide to Pressure Ulcer Assessment. 2nd ed. Orchard Park, NY: Gaymar Industries; 2006.

25. Günes UY. A descriptive study of pressure ulcer pain. Ostomy Wound Manage. 2008;54(2):56-61.

26. Wong DL, Hockenberry-Eaton M, Wilson D, Winkelstein ML, Schwartz P. Wong's Essentials of Pediatric Nursing: Wong-Baker Faces Pain Rating Scale. 6th ed. St. Louis, MO: Mosby; 2001.

27. Bergstrom N, Allman R, Alvaraz O, et al. Treatment of Pressure Ulcers: Clinical Guideline Number 15. Publication No. 95-0652. Washington, DC: Agency for Healthcare Policy and Research; 1994.

28. National Association for Continence. Incontinence Conditions From A–Z. Available at https://www.nafc.org/conditions-overview. Last accessed April 10, 2019.

29. Armstrong, Ayello EA, Capitulo KL, et al. New opportunities to improve pressure ulcer prevention and treatment: implications of the CMS inpatient hospital care present on admission indicators/hospital-acquired conditions policy: a consensus paper from the International Expert Wound Care Advisory Panel. Adv Skin Wound Care. 2008;21(10):469-478.

30. Dorner B, Posthauer ME, Thomas D. The Role of Nutrition in Pressure Ulcer Prevention and Treatment: National Pressure Ulcer Advisory Panel White Paper. Available at https://www.npuap.org/wp-content/uploads/2012/03/Nutrition-White-Paper-Website-Version.pdf. Last accessed April 19, 2019.

Evidence-Based Practice Recommendations Citations

1. National Pressure Ulcer Advisory Panel, European Pressure Ulcer Advisory Panel, Pan Pacific Pressure Injury Alliance. Prevention and Treatment of Pressure Ulcers: Clinical Practice Guideline. Washington, DC: National Pressure Ulcer Advisory Panel; 2014. Available at https://www.npuap.org/wp-content/uploads/2014/08/Quick-Reference-Guide-DIGITAL-NPUAP-EPUAP-PPPIA-Jan2016.pdf. Last accessed May 1, 2019.

34372 • Hyperglycemia and Wound Management

Diane Thompson, RN, MSN, CDE, CLNC

www.netce.com

Copyright © 2017 NetCE, All rights reserved.

Hyperglycemia is commonly detected in hospitalized patients, and it can result in increased mortality and morbidity. One major area of concern is the relationship between hyperglycemia and wound healing. Reduction in wound healing and associated hyperglycemic state is well documented in recent literature. The prevention of delayed, inadequate, and incomplete healing of surgical, accidental, vascular, venous, and/or pressure wounds is the goal of therapy. The relationship between hyperglycemia and delayed wound healing is merely touched upon in the academic setting, leaving the professional nurse to find his or her own way in the care and understanding of the relationship between the two phenomenons. This course reviews the impact of hyperglycemia on wound healing and interventions that may improve the prognosis for these patients.

Table of Contents

34372 • Hyperglycemia and Wound Management

Course Overview

Audience

Course Objective

Learning Objectives

Faculty

Faculty Disclosure

Division Planner

Division Planner Disclosure

About the Sponsor

Disclosure Statement

1. INTRODUCTION

2. CAUSES OF HYPERGLYCEMIA

DIABETES

HOSPITAL HYPERGLYCEMIA

3. AN OVERVIEW OF WOUND HEALING

ACUTE WOUNDS

CHRONIC WOUNDS

4. DIABETES AND WOUND DEVELOPMENT AND HEALING

DIABETIC NEUROPATHY AND ULCERATIONS

MICROVASCULAR DISEASE

5. VASCULAR ULCERS

6. SENSORY-NEUROPATHIC ULCERS

7. PRESSURE INJURIES

STAGING

TREATMENT

PRESSURE ULCER INFECTIONS

8. SURGICAL WOUNDS

9. WOUND DOCUMENTATION

10. CASE STUDIES

CASE STUDY 1

CASE STUDY 2

11. CONCLUSION

Works Cited

Evidence-Based Practice Recommendations Citations

34372 • Hyperglycemia and Wound Management

Education Category. Infection Control / Internal Medicine

Release Date. 10/01/2017

Expiration Date. 09/30/2020

Course Overview

Hyperglycemia is commonly detected in hospitalized patients, and it can result in increased mortality and morbidity. One major area of concern is the relationship between hyperglycemia and wound healing. Reduction in wound healing and associated hyperglycemic state is well documented in recent literature. The prevention of delayed, inadequate, and incomplete healing of surgical, accidental, vascular, venous, and/or pressure wounds is the goal of therapy. The relationship between hyperglycemia and delayed wound healing is merely touched upon in the academic setting, leaving the professional nurse to find his or her own way in the care and understanding of the relationship between the two phenomenons. This course reviews the impact of hyperglycemia on wound healing and interventions that may improve the prognosis for these patients.

Audience

This course is designed for nurses in all practice settings with a desire to better understand the relationship between diabetes/hyperglycemia and wound management.

Course Objective

The impact of hyperglycemia as a comorbidity in delayed wound healing is well documented. The purpose of this course is to provide nurses with a working knowledge of preventative strategies of skin breakdown, identification of types of skin breakdown, and steps for appropriate care of wounds in patients with diabetes.

Learning Objectives

Upon completion of this course, you should be able to:

1. Identify causes of and risk factors for hyperglycemia in the clinical setting.

2. Describe acute and chronic wounds, and discuss the impact of hyperglycemia on both wound types.

3. Evaluate the pathologic effects of diabetes as it relates to wound development and healing.

4. Differentiate between arterial and venous ulcers.

5. Analyze characteristics of sensory-neuropathic ulcers.

6. Illustrate differences between pressure injuries of various stages.

7. Recognize hyperglycemia's role in delaying surgical wound healing.

8. Review significant aspects of wound documentation.

Faculty

Diane Thompson, RN, MSN, CDE, CLNC, has an extensive history in nursing and nursing education. She possesses a strong background in diabetes and cardiac care, starting her professional career at the cardiac care area of the Cleveland Clinic in Cleveland, Ohio. Ms. Thompson took the knowledge and experience she learned from the Cleveland Clinic and transferred it into the home health arena in rural Ohio, after which she moved to Florida and obtained further knowledge while working as a PRN nurse in all areas, including medical/surgical, intensive care, emergency, critical care, and cardiology. With a desire to have a specific area to concentrate her profession, Ms. Thompson accepted a position as a pneumonia case manager, which led into a diabetes case manager career.

Ms. Thompson has been employed in diabetes care since 2001, when she was hired as a diabetes case manager. After the completion of 1,000 hours of education to diabetes patients, Ms. Thompson earned her certification as a diabetes educator in 2003. From 2006 to 2018, Ms. Thompson was the Director of Diabetes Healthways at Munroe Regional Medical Center in Ocala, Florida. As the director of the diabetes center, Ms. Thompson was responsible for the hospital diabetes clinicians, hospital wound care clinicians, and out-patient education program. Today, she is the nurse manager of a heart, vascular, and pulmonary ambulatory clinic at Metro Health System in Cleveland, Ohio. Ms. Thompson has also lectured at the local, state, and national level regarding diabetes and the hospital management of hyperglycemia. Ms. Thompson is a member of the ADA, AADE, Florida Nurses Association, and the National Alliance of Certified Legal Nurse Consultants.

Ms. Thompson acknowledges her family as her greatest accomplishment. She is a wife of more than 30 years and a mother of a daughter and son, of which she is very proud. Ms. Thompson credits her husband for the support needed to set a goal and achieve it. He has been by her side through nursing school and completion of her Bachelor's degree and Master's degree, which she was awarded in 2015 from Jacksonville University in Florida.

Faculty Disclosure

Contributing faculty, Diane Thompson, RN, MSN, CDE, CLNC, has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

Division Planner

Jane C. Norman, RN, MSN, CNE, PhD

Division Planner Disclosure

The division planner has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

About the Sponsor

The purpose of NetCE is to provide challenging curricula to assist healthcare professionals to raise their levels of expertise while fulfilling their continuing education requirements, thereby improving the quality of healthcare.

Our contributing faculty members have taken care to ensure that the information and recommendations are accurate and compatible with the standards generally accepted at the time of publication. The publisher disclaims any liability, loss or damage incurred as a consequence, directly or indirectly, of the use and application of any of the contents. Participants are cautioned about the potential risk of using limited knowledge when integrating new techniques into practice.

Disclosure Statement

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1. INTRODUCTION

Hyperglycemia, often the result of poorly controlled diabetes, is commonly detected in hospitalized patients and can result in increased mortality and morbidity. The presence of hyperglycemia significantly impacts various aspects of patient care regardless of diagnosis; however, as the number of patients with type 2 diabetes increases, excessive blood glucose is becoming a significant public health issue. A major area of concern is the relationship between hyperglycemia and wound healing. The reduction in wound healing associated with a hyperglycemic state is well documented in the literature, and it is exceedingly evident in cardiovascular patients. The prevention of delayed, inadequate, and incomplete healing of surgical, accidental, arterial, venous, and/or pressure wounds is the goal of therapy. This course will review the impact of hyperglycemia on wound healing and interventions that may improve the prognosis for these patients.

2. CAUSES OF HYPERGLYCEMIA

There are three main causes of hyperglycemia: diabetes, certain medications, and physiologic or psychologic stress. Diabetes is by far the most common cause of chronic hyperglycemia and is associated with many adverse effects on a patient's health, including impaired wound healing and increased risk for lower extremity ulcers and amputation. However, medication use and physiologic/psychologic stresses are also important contributors to hyperglycemia, particularly among hospitalized patients. When all of these factors are combined, a patient can be at significantly heightened risk for wound complications and poor outcomes.

DIABETES

Diabetes, known clinically as diabetes mellitus, is a progressive disease process affecting the fuel metabolism functioning within the body [1]. According to the Centers for Disease Control and Prevention (CDC), the prevalence of diabetes has increased 900% since 1958, when 0.93% of Americans had diabetes, with the sharpest increase occurring in the 2000s [2]. As of 2015, 9.4% of the United States population, or 30.3 million Americans, had diabetes [3]. Unfortunately, 7.2 million of these individuals are unaware of their diabetes diagnosis. Diabetes has been considered epidemic since the 1970s, and the percentage of Americans expected to have diabetes or prediabetes is estimated to reach 15.5% and 30%, respectively, by the year 2030 [4].

The scope of the problem is vast and diverse, particularly among geographical regions. The CDC has identified a "diabetes belt" in the United States, consisting of 644 counties in 15 states, where 11.7% of the adult population has diagnosed diabetes, compared with an 8.5% average in other counties (Figure 1) [5]. Although this represents a particularly dense geographic concentration of disease, there are many other counties and groups of counties outside of this belt with prevalences as high or higher. Many of the counties outside of the "diabetes belt" with especially prevalent diabetes have high Native American populations; one such example are several counties in northeastern Arizona, northwestern New Mexico, and southern Utah [3].

Figure 1: THE DIABETES BELT

Source : [5]

Genetics, race, age, and lifestyle significantly influence the onset and progression of the disease process [6]. Although all races and ethnicities can develop diabetes, the prevalence is greatest among non-Hispanic blacks, Mexicans, and Native Americans/Alaska Natives [3,7,8,9]. The incidence of diagnosed diabetes is estimated to be 12.7% among non-Hispanic blacks 18 years of age and older, compared with the overall U.S. rate of 9.4%. The prevalence of diabetes among persons of Hispanic descent who are 18 years of age or older is 12.2% [8]. Among the subdivisions of Hispanic groups, diabetes prevalence rates are 8.5% for Central/South Americans, 9% for Cubans, 12% for Puerto Ricans, and 13.8% for Mexicans. In addition to being at high-risk for diabetes, Mexican Americans are 40% more likely to die from the disease than their non-Hispanic white counterparts [3]. However, Native Americans/Alaska Natives present the greatest risk for the development of type 2 diabetes; their risk is nearly three times greater than that of white Americans [9]. It is estimated that approximately 17.6% of Native Americans/Alaska Natives 18 years of age and older have type 2 diabetes. The highest prevalence of diabetes in the United States is observed in certain Native American groups of the Southwest, where an estimated 22.2% of the population has the disease [3]. The highest rate of diabetes for any population (worldwide) has been reported to occur in the Pima Indians of Arizona [10].

The most rapid increase in diabetes prevalence in the last decade has been among adolescents. Historically, children and adolescents with hyperglycemia have been diagnosed with type 1 diabetes, a result of the body being unable to produce adequate amounts of insulin. However, it is now estimated that as many as 46% of juvenile-onset cases of diabetes are type 2 [11]. Furthermore, it has been predicted that children born in this millennium will have a one in three chance of developing diabetes in their lifetime; among high-risk ethnic groups, the estimate is as high as one in two [12].

Pathogenesis

Individuals with type 1 diabetes typically present to their primary care office or hospital emergency department with a sudden weight loss and severe hyperglycemia [13]. The consequences of the disease can take years to impact the body if optimally controlled. In contrast, an individual with type 2 diabetes may be unaware of the disease process for years prior to being diagnosed. The onset of type 2 diabetes is insidious, with the loss of first-phase insulin response to postprandial levels. The first elevation may be detected at the time of screening as prediabetes or impaired glucose tolerance (IGT) [14]. During this time, the disease progression and hyperglycemia are ravaging the body's micro- and macrovascular systems [1].

In a healthy body, carbohydrate consumption results in an initial swell in serum glucose levels and hyperglycemia. In response to this escalation, the body releases insulin from pancreatic beta cells into the circulatory system to assist with glucose transport into muscle, liver, and adipose tissues; this causes a lowering of the blood glucose levels.

In the case of type 1 diabetes, pancreatic beta cells fail to produce and release insulin, and the only treatment option is exogenous insulin and other appropriate injectables [14].

The pathogenesis of type 2 diabetes is more complex. Virtually all individuals diagnosed with type 2 diabetes have insulin resistance in conjunction with some degree of insulin deficiency [15]. In response, the body's inability to react to the mounting glucose level is magnified by insulin deficiency in the functioning pancreatic beta cells, insulin resistance in the muscular tissue, or both [1]. Unlike the therapy for type 1 diabetes, type 2 diabetes is initially treated with lifestyle modification therapy (e.g., medical nutrition therapy, exercise, behavior change) and frequently with an oral medication, such as a biguanide. Within five years of type 2 diabetes diagnosis, it is estimated that as many as 90% of people will fail this initial therapy and require further oral medications or injectables to achieve adequate glucose control. As a result of this failure rate, medication therapy is initiated early (in the prediabetes stage) in diabetes medical treatment algorithms [16].

Diagnosis

As discussed, the most common types of diabetes are type 1 and type 2. However, gestational diabetes is also relatively common and is a source of significant morbidity and mortality. Gestational diabetes is first recognized in pregnancy, usually around the 24th week of gestation, and typically resolves after the birth of the child [13]. Other less common types of diabetes do occur and include [14,15]:

- Maturity-onset diabetes of the young (MODY): A genetic, autosomal-dominant defect of the pancreatic beta cells results in insulin deficiency and decreased insulin release without the presence of insulin resistance and obesity. This form of diabetes typically develops in patients younger than 25 years of age. It is a different clinical entity than type 2 diabetes of the adolescent, which presents with insulin resistance.

- Diabetes related to diseases of the exocrine pancreas, such as cystic fibrosis, and various endocrine diseases, such as Cushing syndrome, acromegaly, and chromocytoma

- Drug-induced diabetes resulting from the use of certain medications, particularly high-dose corticosteroids

All adults older than 45 years of age should be screened for diabetes every three years or every two years if they have any risk factors for type 2 diabetes [15,17]. In addition, individuals of any age who are at risk for or are suspect of having diabetes should be screened. Established risk factors for type 2 diabetes include:

- Age older than 45 years

- Body mass index (BMI) greater than or equal to 25 kg/m^2

- Family history of type 2 diabetes

- Habitual physical inactivity

- Race/ethnicity (e.g., African American, Hispanic American, Native American, Alaska Native, Pacific Islander)

- IGT or elevated fasting glucose

- Previous history of gestational diabetes or giving birth to a child weighing more than 9 pounds

- Hypertension (i.e., blood pressure greater than 140/90 mm Hg in adults)

- Abnormal lipid levels (i.e., high-density lipoprotein [HDL] level <35 mg/dL and/or triglyceride level >250 mg/dL)

- Polycystic ovarian syndrome

- History of vascular disease

- Acanthosis nigricans (most common among individuals of African descent)

The diagnostic criteria for type 2 diabetes are fairly straightforward and are based on fasting plasma glucose and postprandial plasma glucose levels (Table 1). After a diagnosis of type 2 diabetes has been definitively made, education on self-care management is necessary in order to obtain euglycemia and prevent complications related to the detrimental effects of hyperglycemia [13]. As previously stated, it is estimated that as many as 90% of patients with type 2 diabetes will require oral medications to achieve adequate glucose control within five years of diagnosis [13]. When glucose levels cannot be adequately controlled with oral medications, the use of injectable medications is necessary. If elevated blood glucose levels are untreated and continue to rise, the result can be hyperosmolar hyperglycemia syndrome (HHS) and ultimately death [18].

Table 1: DIAGNOSTIC CRITERIA FOR TYPE 2 DIABETES

Stage

Fasting Plasma Glucose Levels

Two-Hour Postprandial Plasma Glucose Levels

Euglycemia

<100 mg/dL

<140 mg/dL

Prediabetes

>100 mg/dL but <126 mg/dL

>140 mg/dL but <200 mg/dL

Diabetes

≥126 mg/dL

≥200 mg/dL

Source: [14,18]

HOSPITAL HYPERGLYCEMIA

In the past, hyperglycemia was considered an inevitable consequence of acute illness in some patients, and glycemic control was not a focus of hospital care. However, as it has become clear that hyperglycemia is linked to a number of adverse hospital outcomes, controlling inpatients' glucose levels has become a key part of the care of acutely ill patients [20]. A number of features suggest that individuals with newly diagnosed hyperglycemia tend to be more severely ill than individuals with known diabetes [21]. Hospital hyperglycemia, in patients with and without diabetes, has been identified as a marker of poor clinical outcomes, particularly in cardiac surgery patients. However, adverse effects, such as extended length of stay, complications, and increased mortality, have been noted among general and noncardiac surgical patients as well. The impact appears to be greater among patients without a history of diabetes compared to those with a diabetes diagnosis [22].

According to observational studies, 32% to 38% of hospitalized patients are admitted with hyperglycemia or diabetes, and 70% to 80% of diabetic patients with critical illnesses or undergoing cardiac surgery experience hyperglycemia during their stay [23]. A number of serious complications are associated with long-term diabetes, including macrovascular complications, microvascular complications, neuropathies, alterations of skin integrity, and infection [24]. Stress hyperglycemia is frequently recognized as a complication related to hospitalization for individuals with or without diabetes [14]. Often, hospitalized patients are treated with medications that can affect elevation of blood glucose levels. Most commonly, glucocorticoids can induce hyperglycemia resulting from stimulation of alpha cells, leading to hyperglucagonemia and increased glycogenolysis [14]. Admission hyperglycemia has been associated with increased hospital mortality in critically ill individuals, specifically those with myocardial infarction and cerebrovascular accidents [21,23].

Pathophysiology

Acute illness can trigger hyperglycemia in susceptible individuals. Furthermore, hyperglycemia can induce changes that allow an acute illness to proliferate (Figure 2).

Figure 2: THE RELATIONSHIP BETWEEN ACUTE ILLNESS AND HYPERGLYCEMIA

Source : [20]

The endocrine system acts together with the nervous and immune systems to respond to stressors, initiating the stress response [24]. Psychologic and physiologic stress have considerable effects on metabolism in individuals without diabetes, resulting in increased counter-regulatory hormones and elevations in blood glucose levels [25]. During stress, the general adaptation syndrome includes the development of three successive stages:

- The alarm stage: The central nervous system is aroused, and the body's defenses are mobilized.

- Resistance or adaptation: Mobilization contributes to the fight-or-flight response.

- Exhaustion: Continuous stress causes the progressive breakdown of compensatory mechanisms and homeostasis.

The alarm stage impacts glucose levels by inducing increased secretion of glucocorticoids and activation of the sympathetic nervous system, including the adrenal medulla gland, with increased release of epinephrine [24].

Critically ill individuals are at risk for a combination of starvation and the physiologic stress resulting from injury, trauma, major surgery, and/or infection. Starvation may occur as a result of the individual being classified as "nothing by mouth," or NPO, in preparation for surgical interventions, being unable to eat due to disease-related factors, and/or being hemodynamically unstable and unable to eat. This physiologic stress results in an increased metabolic rate (hypermetabolism), which in turn causes an increase in oxygen consumption and energy expenditure [26].

The stress response directly influences the immune system through hypothalamic and pituitary peptides and through the sympathetic branch of the autonomic nervous system. There is a direct innervation of the thymus, spleen, lymph nodes, and bone marrow. Endogenous opiates are released during stress and have concentration-dependent enhancing and suppressive effects on various immune cells [24].

Hypermetabolic processes are the result of increased catabolic hormone changes caused by the stressful event. The sympathetic nervous system is stimulated, causing the adrenal medulla to release epinephrine, norepinephrine, and glucocorticosteroids, which increase blood glucose levels [26]. Increased levels of circulating glucocorticosteroids are an important mechanism in the stress-related immune structure alterations and in the suppression of the immune response. The release of immune inflammatory mediators (e.g., interleukin-1, tumor necrosis factor-α [TNF-α], interferon) is triggered by infection, cancer tissue injury, and other insults that in turn initiate a stress response through the hypothalamic-pituitary-adrenal pathway [24]. This results in nutrient substrates, primarily amino acids, moving from peripheral tissue, such as skeletal muscle, to the liver for gluconeogenesis [26]. Enhanced systemic production of cytokines also induces additional central nervous system and behavior changes during an acute infectious episode [24].

Neutrophil chemotaxis and phagocytosis are defective in poorly controlled glycemia related to diabetes or stress-induced hyperglycemia. Cell-mediated immunity may also be abnormal. In addition, vascular lesions can hinder blood flow, preventing an inflammatory response in wounds or other possible sources of infection. Therefore, individuals with diabetes are more prone to develop infections and may have more severe infections [27].

Management

Management of critically ill patients requires healthcare professionals to be responsive to the effects of medications and the impact of the effects of hyperglycemia on outcomes [6]. The goals of medical management are to administer vasopressor therapy and corticosteroids and to provide an adequate level of nutrition, including enough protein to maintain optimal cellular and tissue growth [26].

Discontinuation of the offending medication is often necessary in cases of drug-induced hyperglycemia. Epinephrine and norepinephrine are commonly utilized to control hypotension in critically ill individuals. Healthcare professionals should be aware that these medications stimulate gluconeogenesis, increase skeletal muscle and hepatic glycogenolysis, increase lipolysis, suppress insulin secretion, and increase peripheral insulin resistance. All of these actions function to increase the serum glucose levels [26]. Healthcare professionals can correct vasopressor-induced hyperglycemia with an infusion of insulin and dextrose [6].

The incidence of hyperglycemia in the hospital has increased significantly along with increased diagnoses of diabetes, prediabetes, and metabolic syndrome. The more frequent use of steroid therapy for the treatment of other chronic conditions has also contributed to hyperglycemia [28]. Glucocorticoids are the most common cause of drug-induced hyperglycemia [14]. Individuals with decreased insulin secretory reserve and the use of high glucocorticoid doses are risk factors for significant hyperglycemia, including the development of HHS [6]. Mechanisms that contribute to the development of hyperglycemia include a decrease in peripheral insulin sensitivity, increased hepatic glucose production, and inhibition of pancreatic insulin production and secretion [14].

Glucocorticoids that are oxygenated, such as hydrocortisone, and/or have a double bond ring, such as prednisone and prednisolone, have the greatest diabetogenic effect. Glucocorticoids can also produce hyperglycemia through stimulation of alpha cells, leading to hyperglucagonemia and increased glycogenolysis. Mineralocorticoids do not directly influence carbohydrate metabolism, although hypokalemia associated with their use may reduce insulin secretion [14].

Interestingly, both beta-agonists and antagonists are associated with the development of hyperglycemia through the stimulation of an increase in plasma glucose via an increase in glycogenolysis and lipolysis, despite increased insulin secretion. Beta-agonists' diabetogenic potential is dose dependent and more pronounced with intravenous and oral routes than with the subcutaneous route. Multiple mechanisms for this action have been identified, including an increase in hepatic glucose production, peripheral insulin resistance, and plasma glucagon following beta-2 agonist administration [14].

3. AN OVERVIEW OF WOUND HEALING

ACUTE WOUNDS

The pathophysiology of acute wound healing has been characterized as a hierarchical progression through four distinct phases. The first phase is coagulation and occurs immediately at the time of tissue injury [29]. The key cell activated in this phase is the platelet, which aggregates at the area of injury and binds with thrombin to form a plug. Vasoconstriction occurs, and cytokines and growth factors, including platelet-driven growth factors and fibroblast growth factors, are released [29]. These reactions initiate healing and act as chemoattractants for circulating polymorphonuclear cells and macrophage [30].

With vasodilatation, cells enter the wound and initiate the inflammation phase. During this phase, the inflammatory cells phagocytose bacteria and macrophages produce a greater amount of cytokines and growth factors such as interleukins-6, fibroblast growth factor, and transforming growth factor-β [29,31]. The inflammatory cells produce matrix metalloproteases, enzymes that digest collagens and elastins, and components of the fibrin clot, also known as the provisional matrix [32]. Through paracrine and autocrine mechanisms, the growth factors serve as a call to action for fibroblasts, which infiltrate the provisional matrix and begin to produce fibronectin and collagen [30].

The matrix metalloproteases also clear the way for endothelial cells and new vessel formation, or angiogenesis. In a sense, they are "drilling for oxygen" to accelerate wound healing. When this process finally occurs, the proliferation phase begins [29,30]. During this phase, fibroblasts and endothelial cells are recruited locally and from circulating precursors from the bone marrow, drawn in by multiple angiogenic growth factors present in the wound [31]. The recently formed matrix, with its rich arcade of new vessels, appears to the naked eye to be fine, red granules termed "granulation" [30]. This granulation tissue provides a supporting lattice to allow the migration of keratinocytes across the surface of the wound to create a new epidermis. After re-epithelialization, endothelial cells undergo apoptosis, and the granulation tissue is replaced by collagen and dermal structure [29].

Simultaneously, scar tissue formation and collagen shortening occur, and fibroblasts are transformed into myofibroblasts, causing the wound to react and contract [30]. When the wound is completely covered with epithelium and not draining, it is considered healed. The entire process typically takes 10 to 14 days to complete in an acute wound [31]. This is followed closely by the remodeling phase, during which collagen fibrils in scar tissue are remodeled in a turnover process resulting from the interplay of degradation of the matrix metalloproteases and the production of matrix components from the fibroblasts. This final phase may continue for the next 6 to 12 months [30].

CHRONIC WOUNDS

Unlike the orderly healing process described for acute wounds, chronic wounds are stuck in a disorderly mix of inflammation and failed eruptions of proliferation [30]. Dysfunctional wound healing may occur during any phase of the healing process and may involve insufficient repair, excessive repair, or infection. The causes can be related to a predisposing disorder, such as diabetes, an acquired condition, such as hypoxia, or one of many potential medication interactions or alterations in nutrition [24].

The chronic wound is characterized by several primary defects [30]. Healing may be prolonged if bleeding is not stopped during the acute inflammation phase. A clot increases the quantity of space that granulation tissue may fill and serves as a mechanical barrier to oxygen diffusion. The accumulation of excess blood cells resulting from hemorrhage prolongs the inflammation phase, creating an excellent medium for bacterial growth and infection [24]. Excessive inflammation occurs as a result of overproduction of inflammatory cytokines, such as interleukin-6, TNF-α, and matrix metalloproteinases, particularly matrix metalloproteinase-1, matrix metalloproteinase-8, and matrix metalloproteinase-13. This allows the accumulation of altered matrix substances, such as fibronectin, that have been rendered ineffectual by protein degradation [30].

Hypovolemia also inhibits inflammation, as the physiologic response is vasoconstriction rather than the dilatation required to deliver inflammatory cells to the site of injury. Anti-inflammatory steroids prevent macrophages from migrating to the site of injury and inhibit the release of collagenase and plasminogen activator. Anti-inflammatory steroids also inhibit fibroblast migration into the wound during the reconstructive phase [24].

Optimal nutrition is important during all phases of healing because metabolic needs are increased. The substances most vital to healing include glucose, oxygen, and protein [31]. Because leukocytes require a glucose-rich environment to produce the adenosine-5 triphosphate (ATP) needed for chemotaxis, phagocytosis, and intracellular killing, individuals with poorly controlled diabetes heal poorly, mainly because of infection [33]. Individuals with diabetes are also at an increased risk for ischemic wounds, because they are likely to have both microvascular diseases that impair the microcirculation and altered glycosylated hemoglobin affinity for oxygen, with oxygen not readily released into the tissue. Oxygen delivery is also compromised by the hypoxemia state. Ischemic tissue is susceptible to infection, which in turn prolongs the inflammatory process.

Along with hypoxemia, hypoproteinemia lengthens inflammation by impairing fibroblast proliferation [24]. Most of the factors that interfere with the production of collagen in healing tissues are nutritional [24]. Scurvy, for example, is caused by a lack of ascorbic acid (vitamin C), which is one of the cofactors required for collagen formation by fibroblasts. As a result, patients with scurvy have poorly formed connective tissue and greatly impaired healing. Protein and other nutrients, including iron, oxygen, β-ketoglutarate, manganese, copper, and calcium, are required for collagen synthesis [34]. However, minute amounts of these substances are usually required as cofactors, so deficiencies are not generally clinically significant. Dysfunctional collagen overwhelming the surface of a wound is manifested by a keloid or hypertrophic scar, both of which are related to increased collagen synthesis and decreased collagen lysis [35].

Regulated expression of the gap junction protein connexin 43 plays a pivotal role in wound healing. Connexin 43 is normally down-regulated and protein connexin 26 is upgraded in keratinocytes at the edge of the wound as they adopt a migratory phenotype [36]. However, alterations in this action may result in chronic wounds. Individuals who have diabetes have been found to have decreased protein connexin 43 and 26 communication within the intact epidermis and increased protein connexin 43 communication within the intact dermis. Within 24 hours of injury in patients with diabetes, protein connexin 43 is upregulated in a thickened bulb of keratinocytes at the edge of the wound; in contrast, a healthy individual with normal down-regulation will form a set of thin migratory cells. In the presence of diabetes, protein connexin 43 is delayed for up to 48 hours after re-epithelialization has begun. Furthermore, although protein connexin 26 is upregulated as normal after tissue injury in the skin of an individual with diabetes, the skin at the edge of the wound appears abnormal [36].

4. DIABETES AND WOUND DEVELOPMENT AND HEALING

The public health impact of wounds is immense. An estimated 2.5 million inpatients develop pressure injuries each year, particularly older and malnourished individuals [37]. Furthermore, 10% to 15% of the 30.3 million individuals with diabetes in the United States will develop diabetic ulcers; many more will have venous ulcers or wounds that result from vascular disease [38]. The annual cost of treating wounds of this nature is estimated to be more than $12 billion, which has led to specific guidelines based on specialist organization consensus [37,39,40,41]. In patients with diabetes, neuropathy and microvascular disease are the greatest contributors to impaired wound healing, both of which can be improved with optimal management of blood glucose levels.

DIABETIC NEUROPATHY AND ULCERATIONS

Diabetic neuropathies are the most common form of neuropathy in developed countries, and it is estimated that 60% to 70% of individuals with diabetes have some form of nervous system damage [3,42]. These disorders are among the most widespread complications of diabetes and are a significant source of morbidity and mortality. The most frequent complication is diabetic foot ulcerations, which, if poorly treated, can result in gangrene and ultimately loss of limb [17]. In fact, diabetes is the underlying cause of 50% to 75% of all nontraumatic amputations in the United States [17]. In the United States, 86,000 amputations are performed on individuals with diabetes each year; up to 75% of the procedures are considered to be preventable [17].

Neuropathy refers to the impaired effectiveness of the nerves in conducting pain, pressure, or movement sensations. In many patients with diabetes, the development of neuropathy in the lower extremities leads to loss of protective sensation, resulting in undetected trauma and infection. The most common type of neuropathy in patients with diabetes is peripheral neuropathy, which affects the ends of the longest nerves first; the toes and feet are the most severely affected. Other types or neuropathy include autonomic neuropathy, mononeuropathy, and diabetic amyotrophy (also referred to as radiculoplexus neuropathy). In patients with peripheral neuropathy, the development of foot ulcers and even foot deformities is common, and the healing of these ulcers can be complicated by the presence of hyperglycemia [42].

Foot ulcerations are rarely caused by a single pathology and typically result from two or more contributing factors. Insensitivity resulting from neuropathy combined with either extrinsic factors (e.g., trauma caused by walking barefoot or stepping on a sharp object) or intrinsic factors (e.g., bunions, calluses) ultimately results in ulceration [6]. Neuropathy is the most common cause of lower extremity ulcerations. However, in approximately one-third of all cases, peripheral ischemia resulting from proximal arterial disease is a contributing factor in ulceration. The ischemic foot appears red, dry, and often neuropathic, so it is susceptible to pressure from footwear [30].

Foot deformities, such as claw toes or prominent metatarsal heads, are a proven risk factor for ulceration [26,42]. One cross-sectional study demonstrated that plantar callus accumulation was associated with an 11-fold increase in formation of diabetic foot ulceration [30]. In follow-up with these individuals, plantar ulceration occurred only at sites of callus in neuropathic feet. Other risk factors include a past history of foot ulcers or amputation, the presence of other microvascular complications, long duration of poorly controlled diabetes, increase in plantar foot pressures, and peripheral edema [30,43]. The most common triad leading to breakdown of the diabetic foot is peripheral neuropathy (insensitivity), deformity (claw toe), and trauma (from ill-fitting footwear, repetitive stress, or thermal damage) [30,42,44].

Symmetric polyneuropathy is a potentiating factor in the development of foot ulceration in individuals with diabetes; it manifested at clinical examination as diminished or absent vibratory and cutaneous pressure sensation and absence of ankle reflexes. This type of neuropathy is present in 75% to 90% of patients with current diabetic foot ulcerations [45]. In addition to symmetric polyneuropathy, peripheral vascular disease is an important contributory factor in the development of diabetic foot ulcerations in 10% to 30% of all cases [30]. The location of ulceration on the foot provides indications of the causative factors and assists in the determination of the most effective treatment approach [30].

Diabetic foot ulcers often lead to amputation due to ischemia and impaired immune response related to macrovascular disease (present in 30% to 40% of diabetic foot ulcers) and microvascular disease [27]. Intermittent claudication and pain at rest may be presenting symptoms of major vessel disease. Ulceration is a common feature of the neuroischemic foot [43]. This type of ulceration is usually painless, and there is typically an area of necrosis surrounded by a rim of erythema. Common locations of these ulcerations are the great toe, the medial surface of the first metatarsal head, and the heel [24].

MICROVASCULAR DISEASE

Individuals with diabetes and neuropathy also have significant microvascular defects. Hyperglycemia is associated with a ubiquitous involvement of the microvasculature manifested by capillary sclerosis and dropout, particularly in individuals with type 1 diabetes [30]. This can be seen with capillaroscopy and measurement of elevated capillary pressures. For individuals with type 2 diabetes and neuropathy, functional microvascular abnormalities develop, especially endothelial dysfunction and impaired vasoreactivity [6]. These abnormalities are best demonstrated by laser Doppler imaging of the microcirculation, which demonstrates defective vasodilatory response to heat (generalized defect), acetylcholine (endothelial defect), and sodium nitroprusside (vascular smooth muscle defect). In addition, neuropathy affects the neuron-inflammatory microvascular vasodilatation in response to injury or noxious stimuli [30]. Angiogenesis is also seen in patients with diabetes. Among many contributors to angiogenesis are neural mediators such as acetylcholine, substance P, and neuropeptide Y, all substances involved in the impaired neuron-inflammatory response in patients with diabetes. The presence of peripheral neuropathy may contribute to impaired angiogenesis and wound healing on a cellular basis [31].

Hyperglycemia may slow neutrophil chemotaxis, primarily through a hyperosmotic effect [30]. Studies of fibroblasts in individuals with diabetes demonstrate an alteration in functioning and in response to stimulatory challenges [35]. A vast body of literature suggests that the altered blood glucose levels and free fatty acid metabolism associated with diabetes result in oxidative stress, endothelial dysfunction, and activation of inflammatory cytokines. Additionally, there is an increased expression of TNF-α, transforming growth factor-β, interleukin-6, and other inflammatory factors. These factors are overexpressed in chronic wounds and most likely amplified in the inflammatory milieu of diabetes [30].

5. VASCULAR ULCERS

Vascular ulcers may develop in the arterial, venous, or lymphatic systems from a variety of causes [33]. Patients with diabetes are at an increased risk for both arterial and venous ulcers. The pathophysiology of venous (or stasis) ulcers is related to venous hypertension that develops as the result of inadequate calf muscle pump action and either primary or secondary valvular incompetence [46]. Arterial ulcers, on the other hand, are wounds that will not heal due to compromised or inadequate arterial blood flow [33]. Arterial calcification is commonly detected in radiographs of diabetic feet and hands. This is related to calcification of the media on muscular arteries [43]. Differentiating between arterial and venous ulcers involves careful patient history and evaluating the appearance of the ulcer and surrounding skin (Table 2) [32].

Table 2: CHARACTERISTICS OF ARTERIAL AND VENOUS ULCERS

Aspects

Venous Ulcers

Arterial Ulcers

Location

Superior to medial malleolus

Medial aspect of the leg and ankle

"Gaiter" region of the legs

Areas exposed to excessive pressure or repetitive trauma

Lateral malleolus

Mid-tibial

Phalangeal heads

Toe tips or web spaces

Surrounding skin

Erythemic

Scaling

Crusting

Brown staining

Lipodermatosclerosis

Normal skin temperature (warm to touch)

Pitting or nonpitting edema, with possible induration and cellulitis

Scarring from previous ulcers

Ankle flare

Dependent rubor

Shiny

Taut

Dry, thin, hairless

Atypical edema

Decreased skin temperature (cool to touch)

Atrophy of subcutaneous tissue

General appearance

Ruddy red base

Yellow adherent or loose slough

Granulation tissue present

Vary in size (small to full circumference of the leg)

Pale, sloughy base

Granulation rarely present

Necrosis, eschar, gangrene (wet or dry)

Smaller, but deep

Tendon or bone may be visible

Depth

Usually shallow

Deep

Margins

Irregular

Undermining or tunneling uncommon

Edges rolled

Punched out

Smooth and undermining

Exudate

Moderate to heavy

Minimal

Infection

Less common

Frequent, but signs may be subtle

Source: [32,46]

Studies have proven that individuals with diabetes possess an abnormally thickened vascular basement membrane in the capillaries, but the membrane does not appear to be associated with gangrene [30]. Impairment, calcification, and thickening of these vascular capillaries can lead to impairment of blood flow to the lower extremities, as evidenced by diminished dorsalis pedis and/or posterior tibial pulses [14]. The results include ischemia in the vasculature, skin, and supporting tissues. Symptoms include chronic pooling of blood in the lower extremities and hyperpigmentation of the skin around the feet and ankles. Circulation to the extremities becomes increasingly sluggish, to the point that the metabolic demands of the cells are scarcely met. Any trauma or pressure can therefore result in a further lowering of oxygen supply, leading to cell death and necrosis [24].

In patients with diabetes, venous ulcers predominantly occur on the foot, but may arise on the lower leg or ankle as well. Venous ulcers and venous insufficiency in general often occur in patients with reduced mobility and/or a history of obesity, deep vein thrombosis, traumatic injury, phlebitis, orthopedic procedures, or congestive heart failure [32].

The precipitating events for arterial ulcers vary. Limbs with arterial compromise may have minimal but adequate blood flow to maintain tissue viability. Ischemic lower extremity ulcerations are often precipitated by trauma or infection [33]. Infection can occur as a result of poor circulation impairing the delivery of cells and biochemicals essential for the immune and inflammatory responses [24].

Evidence Based Practice Recommendation

The Infectious Diseases Society of America states that no adjunctive therapy has been proven to improve resolution of diabetic foot infection, but for selected wounds that are slow to heal, clinicians might consider using bioengineered skin equivalents, growth factors, granulocyte colony-stimulating factors, hyperbaric oxygen therapy, or negative pressure wound therapy.

https://www.guideline.gov/summaries/summary/37220

Last Accessed: September 15, 2017

Strength of Recommendation/Level of Evidence: Weak/Moderate (Alternative approaches likely to be better for some patients under some circumstances)

Treatment and management of vascular ulceration include the following approaches [30,31,47]:

- Pressure off-loading, utilizing crutches, wheelchairs, therapeutic footwear, half shoes, and removable cast walkers to relieve pressure on the affected area.

- Debridement of necrotic tissue from the ulceration to allow for healing. This can be accomplished by surgical or nonsurgical means and allows for viable skin to be produced and adhere to the surface of the ulcer. This therapy is commonly utilized in the mid- or chronic stages of ulceration.

- Adjunctive wound therapy, including low-adherent dressings, interactive (occlusive) hydrocolloid dressings, semi-permeable films, hydrogels, and alginate dressings. Synthetic foams work as healing agents, and antimicrobial barriers are commonly utilized in all stages of acute and chronic ulceration.

- Growth factor, in combination with a platelet releasate or delivered through recombinant platelet-derived growth factor technology, is utilized in early and involved diabetic ulcerations.

- Hyperbaric oxygen therapy. Intermittent inhalation of pure oxygen at a pressure greater than one atmosphere absolute (15 pounds pressure/in^2) increases the percentage of oxygen available to produce adequate wound healing. This therapy is utilized in the chronic stages of diabetic ulcerations when other therapies have lost their efficacy. Authors of a 2012 Cochrane review concluded that hyperbaric oxygen therapy is significantly beneficial in the short term but not in the long term.

- Electrical stimulation to increase the blood flow. Utilizing asymmetric biphasic stimulation is associated with increased healing of nearly 60%. This form of therapy can be utilized in early or involved stages of diabetic ulceration therapy.

- Low-intensity ultrasonic stimulation improves the rate of wound healing.

- Topical radiant heat. This therapy optimizes the enzymatic processes involved in wound healing and can be utilized in early or involved stages of diabetic ulceration therapy.

6. SENSORY-NEUROPATHIC ULCERS

Diabetes may affect both the central and peripheral nerves. The most common cause of lower extremity ulcers in patients with diabetes is chronic sensory-motor neuropathy [43]. Diabetic neuropathy alters the mechanics of the foot, which causes increased shear and pressure on the sole and results in an increased risk for injury and complication [33]. The prevalence of sensory-neuropathic ulcers approaches 30% in patients with diabetes and increases with age and duration of diabetes [43].

Sensory neuropathy contributes to an inability to perceive injury to the foot due to the loss of protective sensation [33]. Individuals with sensory loss are seven times more likely to develop foot ulcers compared to those without neuropathic disorders [30]. Loss of sensation is the result of demyelination of the peripheral nerves (particularly the distal nerve endings) [27]. Presentation of this loss of sensory sensation typically begins with numbness or paresthesia of the toes and progresses upward to create a "stocking" effect to the extremity [48].

With neuropathies of the foot, an individual will initially experience loss of pain and heat perception as a result of the changes in the small and large myelinated nerve fiber. This leads to a loss of touch, vibration, and proprioception sense [43]. Neuropathy can further progress to fragility and wasting of the intrinsic musculature of the lower extremity, with consequential deformities of the foot and toes [33].

Prevention of neuropathic ulcerations of the leg and foot consists of frequent inspection, controlling blood glucose levels, and patient education regarding proper care and maintenance of the foot and lower extremities [48]. It is important to educate the individual with diabetes to remove footwear and socks when at the physician's office [6]. This will allow examination of the foot and identification of any deformities and evidence of neuropathy, vascular disease, plantar calluses, edema, or other risk factors [27]. A simple foot pressure mat can assist in the identification of high pressures under the diabetic foot, and these pressure maps can be utilized to educate patients regarding their risk for development of subsequent ulcerations and the care required to prevent this occurrence [30].

7. PRESSURE INJURIES

Evidence Based Practice Recommendation

According to the American College of Physicians, risk assessment is often part of bundled care and multicomponent interventions for preventing pressure ulcers. Risk factors for pressure ulcers include diabetes, impaired microcirculation, and malnutrition. Clinicians should make individualized decisions based on risk assessment on whether to use a single or multicomponent intervention to prevent pressure ulcers in patients.

https://www.guideline.gov/summaries/summary/49050

Last Accessed: September 15, 2017

Strength of Recommendation/Level of Evidence: Weak recommendation, low-quality evidence

The public health impact of chronic wounds is staggering, with an estimated 3 million individuals in the United States believed to have pressure injuries [49]. Treating these wounds is associated with an estimated cost of an estimated $11 billion each year [49]. Estimates of the incidence of pressure injuries range from 0.4% to 38% in acute care hospitals, from 2% to 24% in long-term care facilities, and up to 17% in the home care setting, with an overall prevalence in the United States of 13.5% in 2008 and 12.3% in 2009 [49]. Pressure injury-related hospitalizations are longer and more expensive than many other hospitalizations. The length of hospitalizations for patients with pressure injuries is nearly three times longer than hospitalizations without a diagnosis of pressure injuries [49].

Although diabetes is not a cause of pressure injuries, the altered nutritional state, poor circulation, and impaired healing associated with the disease places patients with diabetes at greater risk for pressure injuries. Furthermore, pressure injuries that develop in patients with diabetes tend to be more severe and heal more slowly. It has been hypothesized that the structure of the collagen network in the skin of patients with diabetes may lower its tolerance of external pressure and delay skin reconstruction [50].

Pressure ulcers or injuries primarily develop over a bony prominence when pressure or shearing forces occlude cutaneous and subcutaneous blood flow. In patients with diabetes, pressure injuries often occur on the heel. Cutaneous pressure on the tissue between the bony prominence and a resistant outside surface distorts capillaries and prevents adequate blood from circulating to the area [33]. Unrelieved pressure on the skin constricts capillaries that supply the skin with nutrients and oxygen. This can be exacerbated by existing arterial disease and neuropathy. When skin is starved of nutrients and oxygen for an extended period, the tissue dies and a pressure injury forms. The affected area may feel warmer than surrounding tissue. Skin reddening that disappears after pressure is removed is normal and is not a sign of a pressure injury [51]. If pressure is relieved within a few hours, a brief period of reactive hyperemia may occur with no lasting tissue damage [24].

In addition to diabetes and hyperglycemia, there are many risk factors for the development of pressure injuries, including [24]:

- Older age

- Neurologic disorders, such as spinal cord injuries, dementia, or cerebrovascular disease, resulting in decreased sensation and/or mobility

- Immobilization

- Incontinence

- Fractures (e.g., hip or femur)

- Coarse bed sheets

- Reduced tissue perfusion (e.g., as from edema or hypotension)

- Obesity

- Skin dehydration

- Stress

- Depression

- Low body weight and impaired nutrition

- Smoking

- Certain medications

There are many scales to validate and predict risk for the development of pressure injuries. The most commonly utilized in the United States is the Braden Scale, which takes into consideration sensory perception, moisture, activity, mobility, nutrition, friction, and shear [33,49]. Each item is scored on a scale between 1 and 4, with the exception of friction and shear, which is scored between 1 and 3. The lower the score, the more severe the impairment and the greater the patient's risk for pressure injury development. Studies have shown scores of 16 to 18 as indicative of increased risk [52]. Although cut-off scores vary, usually a score of 13 to 14 is considered moderate risk, 10 to 12 indicates high risk, and 9 or less is very high risk.

When a patient with diabetes or hyperglycemia is found to be at risk for pressure injury formation, preventive steps should be taken, including an individualized program of skin care. This can include [24,53]:

- Scheduled repositioning every one to two hours, depending on the patient's condition

- The use of assistive devices to ensure correct position in beds (e.g., floatation mattresses, cushions, suspension boots) or chairs (e.g., cushions, correct size chair)

- Maintaining skin cleanliness and moisturizing frequently

- Bowel and bladder management

- Maintenance of adequate nutrition, oxygenation, and fluid balance

- Enhanced patient and caregiver education

- Strict control of blood glucose levels

Research supports the findings that undernourishment on admission to a healthcare facility increases the potential of an individual developing a pressure injury [33,54]. In one prospective study, high-risk individuals who were malnourished upon admission had two times greater risk of developing a pressure injury compared to individuals who were adequately nourished [33]. Maintaining an adequate level of nutrition is paramount for successful wound healing [53]. This includes addressing any vitamin and/or mineral deficiencies that may be present (e.g., zinc deficiency in patients with diabetes). Repair of the wound requires proteins, carbohydrates, fats, vitamins, and minerals to ensure the energy demands for cellular proliferation, phagocytosis, and the production of connective, endothelial, and epithelial tissues are met [54]. Each of these components plays a specific and irreplaceable role in the continuum of healing. A delay in, or absence of, any one of these components can result in a prolongation or even a prohibition of healing [34].

STAGING

Staging is an assessment system that classifies pressure injuries based on anatomic depth of tissue damage. In 2016, the National Pressure Ulcer Advisory Panel (NPUAP) updated the definitions of pressure injury stages [55]. In the 2016 revision to the NPUAP staging system, the term "pressure injury" replaced "pressure ulcer," to alleviate confusion between injury to intact skin (stages 1 and deep tissue injury) and open ulcers (stages 2–4 and unstageable pressure injury). In addition, the following changes were made [55]:

- Arabic numbers replaced Roman numerals in stages 1–4

- The term "suspected" was removed from the deep tissue injury diagnostic label

- Two additional pressure injury definitions, Medical Device-Related Pressure Injury and Mucosal Membrane Pressure Injury, were added

Staging of a pressure injury can only occur after all necrotic tissue has been removed and it is possible to see the ulcer bed [56]. If this is not possible, the ulcer will be classified as unstageable.

Pressure injury staging is not used to indicate healing; a pressure injury should never be "down staged" or reverse staged (e.g., a pressure ulcer that is healing does not go from a stage 4 to a stage 3). In pressure ulcer healing, there is no regrowth of lost muscle, subcutaneous fat, or dermis; instead, the wound is filled in with scar tissue. Therefore, reverse staging does not accurately reflect the physiologic changes occurring in the pressure ulcer. When a stage 4 ulcer has healed, it should be classified as a healed stage 4 pressure ulcer [33].

Stage 2 pressure ulcers have a healing time that ranges from 8.7 to 38 days. Stage 3 and stage 4 pressure ulcers can take up to 69 days to heal. Healing rates are lower for stage 3 and stage 4 ulcers than for stage 2 ulcers in all healthcare settings [55]. Irreversible tissue damage can happen in as little as two hours in a patient with low tolerance; however, the ulcer may not become apparent for two to five days [57].

Stage 1

Stage 1 pressure injury presents as persistent redness in intact skin. If the area is pressed, it will not lighten in color (non-blanchable) [58]. It usually occurs in a localized area over a bony prominence, and this area can be painful, firm, soft, warmer, or cooler than the surrounding tissue [55]. This area of redness has a clear but possibly irregular boundary [58]. In darker skin tones, blanching may not be visible and the color may differ from the surrounding area [55]. In these instances, it is important to look for the other signs of pressure ulcers, such as pain and changes in skin temperature and/or texture.

Stage 2

Stage 2 pressure injury presents as shallow, open wounds with partial loss of the dermis. The wound bed is pink/red and without slough. A stage 2 pressure ulcer may also present as a serous fluid-filled blister [55]. Fat and deeper tissues are not visible, and slough and eschar are not present. These injuries are most commonly seen on the sacrum due to moisture and shear, and on the heel due to shear [55]. Skin tears, tape burns, incontinence-associated dermatitis, maceration, or excoriation of the skin should not be classified as stage 2 pressure ulcers [33].

Stage 3

Stage 3 is full thickness tissue loss. Subcutaneous fat may be visible and rolled wound edges are often present, but bone, tendon, and muscle are not exposed. There may be slough in the wound, but it does not obscure observation of the wound bed; if slough or eschar obscures the observation, this is an unstageable pressure injury. Tunneling and undermining may be present [55]. It is important to remember that the depth of stage 3 pressure ulcers will differ from one location to another. For example, the bridge of the nose, ear, occiput, and malleolus do not have a subcutaneous layer, and in these areas a stage 3 pressure ulcer can be shallow [55].

Stage 4

Stage 4 ulcers are characterized by full thickness tissue loss with exposed bone, tendon, or muscle. These ulcers often include undermining and tunneling, and rolled wound edges are often seen [55]. Slough and eschar may be present in part of the wound bed; however, if slough or eschar obscures the observation, this is an unstageable pressure injury [58]. In some cases, stage 4 pressure ulcers can affect supporting structures and may lead to osteomyelitis. As with stage 3 ulcers, the depth of the injury will vary by anatomical location.

Unstageable Pressure Injury

A wound that is unstageable is defined as having full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) [55]. Until the base of the wound can be visualized, the wound will remain unstageable. A necrotic wound cannot be staged until the necrotic tissue has been debrided, and it is then that a stage 3 or stage 4 ulcer will be revealed [55]. It is also important to remember that it is clinically inaccurate to stage a granulating wound if it is the first assessment, as visualizing the depth of the actual pressure injury is not possible [33]. In addition, if stable eschar on an ischemic limb or the heel(s) is present, it should not be removed [55].

Deep Tissue Pressure Injury

Deep tissue pressure injury, previously suspected deep tissue injury, is a pressure-related injury, much like a bruise, that is characterized by persistent, non-blanchable, deep red, maroon, or purple discoloration or epidermal separation revealing a dark wound bed or blood-filled blister. Deep tissue pressure injuries can present on either intact or non-intact skin. This type of injury is caused by intense and/or prolonged pressure and/or shear. Deep tissue pressure injury may resolve without tissue loss or may rapidly change to reveal the extent of the tissue injury. If necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle, or other underlying structures are visible, this indicates a full thickness pressure injury (unstageable, stage 3, or stage 4). The NPUAP does not recommend using deep pressure tissue injury to describe vascular, traumatic, neuropathic, or dermatologic conditions [55].

Color is the key to differentiating between deep tissue injury and a stage 1 pressure injury. Purple or maroon areas indicate deep tissue injury; non-blanchable redness is characteristic of stage 1 injuries. Deep tissue injury can become a stage 3 or a stage 4 pressure ulcer even with optimal care [55]. In general, the most common areas of involvement are the heels and sacrum [57]. In some patients, particularly those who are debilitated, deep tissue injury can develop rapidly [58].

Medical Device-Related Pressure Injury

Medical device-related pressure injuries describe injuries or ulcers that result from the use of devices designed and applied for diagnostic or therapeutic purposes. The injury is generally in the shape or pattern of the device and should be staged using the staging system [55].

Mucosal Membrane Pressure Injury

Mucosal membrane pressure injury is found on the mucous membranes. This type of injury is typically attributed to use of a medical device on a mucous membrane, and due to the nature of this type of tissue, these injuries cannot be staged [55].

TREATMENT

Over the years, the initial care of pressure injuries has commonly involved innovative mattresses, ointments, creams, solutions, dressings, ultrasonography, ultraviolet heat lamps, sugar, and surgery, depending on the degree of ulceration and condition of the ulcer base exposed and the purpose of the treatment (e.g., protection, moisture, removal of necrotic tissue) [59]. Overall, there are four principles for successful medical management of pressure injuries [24,59]:

- Debridement of necrotic tissue as needed on initial and subsequent assessments

- Cleansing the wound initially and with each dressing change, and using a dressing that keeps the ulcer bed continuously moist and the surrounding intact tissue dry

- Prevention, diagnosis, and treatment of infection

- Reduction of pressure

Ulcer healing should be assessed at least weekly, with a focus on the efficacy of the basic ulcer care plan. If the ulcer is healing, monitoring for continued progression should continue. If the ulcer is not healing, the treatment plan should be reassessed and the level of adherence to the plan scrutinized [33]. The plan and implementation strategy should be modified as necessary for optimal outcome. Close monitoring of serum blood glucose levels is necessary. Adjunctive therapies may include hyperbaric oxygen therapy, electrical stimulation therapy, electromagnetic therapy, growth factor therapy, and negative-pressure wound therapy; however, these adjuncts may not offer significant benefits and should be used according to clinical protocol [39,53,59]. Protein or amino acid supplementation may accelerate healing in certain patients, particularly those who are malnourished; these patients should receive nutritional support that is consistent with their medical condition and personal desires [39].

In cases in which an ulcer lacks progression in the healing process, operative repair may be an option for selected patients [24,53]. Information regarding available operative procedures and the anticipated benefits and harms of each should be part of patient counseling and the decision-making process. In the presence of obesity, longer surgical times (more than five hours) can adversely impact the patient's skin integrity, increasing the risk for deep tissue injury and necrosis. Furthermore, the presence of excess adipose tissue can prolong surgical time and increase the need for forceful retraction, potentially leading to tissue trauma [60]. In general, patients who are poor surgical candidates should not undergo pressure ulcer reconstruction due to the extremely high risk of complication [59]. Vigilance in regard to postoperative follow-up care is crucial to a successful operative outcome [33]. Educate patients and caregivers that measures to promote healing and prevent recurrence are lifelong [53].

PRESSURE ULCER INFECTIONS

For appropriate healing of any acute or chronic wound, infections should be prevented or treated aggressively. All pressure ulcers will become colonized with both aerobic and anaerobic bacteria; they are not sterile [33]. Infections within the wound must be addressed before healing is possible, but it can be challenging to distinguish an infected wound from one that is not [38]. Potential signs and symptoms of pressure ulcer infection include [24]:

- Erythema

- Localized pain

- Periulcer edema

- Increased skin temperature surrounding the ulcer

- Leukocytosis

- Purulent and/or foul-smelling exudate

As discussed, individuals with diabetes are at a greater risk for infection, with greater severity in relation to the level of blood glucose control [27]. This increased potential for infection in patients with diabetes can be attributed to physiologic alterations precipitated by inadequate glucose control [61].

8. SURGICAL WOUNDS

Several observational studies point to a strong association between hyperglycemia and poor surgical outcomes, including on measures of length of stay, infection rates, posthospitalization disability, and mortality [62]. One well-studied population is cardiovascular surgery patients, partially because individuals with diabetes are at increased risk for cardiovascular disease and frequently require coronary artery bypass and grafting. Hyperglycemia, whether related to diabetes or stress, is associated with suboptimal outcomes when experienced on the first post-operative day after cardiovascular surgery [63]. However, the impact of diabetes on the risk of cardiothoracic surgical site infection and other poor outcomes may not simply be related to alterations in glucose control. Patients with diabetes are more likely to possess other factors associated with poor surgical outcomes, including obesity [61].

When hyperglycemia is present, there is an impact on fibroblast function during the period of granulation tissue formation and maturation. Decreased levels and cross-linking of collagen may impair wound healing and strength [14]. For these reasons, patients with diabetes preparing for a surgical intervention should maintain as close to normal metabolic functioning as possible. Therapeutic goals should include avoidance of hypoglycemia, hyperglycemia, lipolysis, ketogenesis, proteolysis, dehydration, and electrolyte imbalance [14].

Evidence Based Practice Recommendation

The Institute for Clinical Systems Improvement asserts that determination of a patient's glycemic control status is an important factor in preventing surgical-site infection. In patients with diabetes, glycemic control should be directed at achieving blood glucose levels between 140 and 180 mg/dL, and not be directed at more intensive goal targets (80–110 mg/dL).

https://www.guideline.gov/summaries/summary/48408

Last Accessed: September 15, 2017

Strength of Recommendation/Level of Evidence: Strong recommendation, high-quality evidence

There is significant research regarding the benefit of glycemic control after surgery, specifically after cardiac surgical interventions. One study revealed that improvements in postsurgical cardiac surgery glucose control were linked to a reduction in mediastinitis [60]. Some reviews recommend target presurgical glucose levels in the 100–180 mg/dL range because this level of glycemia has been shown to prevent infection, risk of hypoglycemia, and dehydration as a result of osmotic diuresis [14]. Although hyperglycemia is associated with adverse patient outcomes, controversy remains as to the appropriate levels required to prevent adverse outcomes while also avoiding potentially detrimental hypoglycemia [62,64]. A 2017 study of 300 patients with hyperglycemia (50% with diagnosed diabetes) who underwent cardiac surgery, found that intensive (100–140 mg/dL) and conservative (141–180 mg/dL) glucose control regimens produced similar circulating markers of acute inflammatory and oxidative stress response [63].

In addition to hyperglycemia, obese patients with or without diabetes have a significantly increased risk of impaired wound healing than those of normal weight [60]. Severe obesity is associated with venous stasis disease, pitting pretibial edema, bronze edema (a result of extravasation of red blood cells into the skin), cellulitis, and obesity hypoventilation [65]. Furthermore, obesity is a known risk factor for surgical-site infection. Patients with diabetes have been shown to have increased carriage rates for Staphylococcus aureus colonization, a leading cause of surgical-site infection [61]. These conditions impact the body's ability to heal an incision, potentially leading to wound dehiscence, rhabdomyolysis, and complications of the skin and underlying tissue [60].

Wound dehiscence is a serious complication for all obese patients whether or not they have diabetes. However, as previously stated, when hyperglycemia is present, wound healing and strength is impaired; when both are present, the risk of delayed healing is even greater [14]. In the early postoperative period, wounds stay approximated due to the strength of the sutures or the normal healing process as the muscle regains its strength. Consequently, obesity, heavy coughing or retching, and ascites can strain the wound and result in dehiscence [33].

A wound is at greatest risk of dehiscence in the first two weeks following surgery, when the wound is still fresh and very fragile. When dehiscence does occur, it can be mild (e.g., a small area of the incision begins to pull apart and leave a gap) or severe, causing the sutures, staples, or surgical glue to completely give way and the entire incision to open. In severe cases, the open incision is a surgical emergency and medical attention should be obtained immediately [66].

When wound dehiscence occurs, swift detection and action is critical. Interventions include antibiotic therapy and analgesics [67]. When appropriate, exposing the wound to air may accelerate healing by allowing growth of new tissue from below and preventing infection. Surgical removal of contaminated and dead tissue may also be necessary. A temporary or permanent piece of mesh may be placed to bridge the gap in the incision or wound. Vacuum-assisted wound closure may be used to increase granulation tissue and remove excess drainage. When appropriate, frequent changes in the incisional dressing are required to prevent infection.

9. WOUND DOCUMENTATION

Documentation is an imperative part of caring for the patient with wounds. Not only are nurses caring for patients, identifying adverse reactions, and taking appropriate actions, they are also responsible for documenting all findings, actions, treatments, and response to any interventions [26]. Wound assessments are required to be extremely detailed and complete. The well-documented history of pressure injuries and other wounds is a valuable communication tool between disciplines and a historical document to evaluate past care and efficacy and guide future care [33]. A factual record may be utilized in lawsuits to determine the quality of care rendered to serve as evidence of physical harm. Experts have suggested using the Nine Cs of Wound Assessment as a guide to the assessment and documentation process. This consists of [33]:

- Cause(s) of the wound

- Clear picture of what the wound looks like

- Comprehensive picture of the patient

- Contributing factors

- Communication to other healthcare practitioners

- Continuity of care

- Centralized location for wound care information

- Components of the wound care plan

- Complications from the wound

The etiology of a lesion must be correctly identified in order to provide the most appropriate and effective care and treatment [33]. A thorough assessment of the ulcer involves evaluating its appearance, the wound location and size, the wound bed tissue, the wound edges, the periwound skin, and wound exudate [68]. It is important to document the location of ulcers and wounds, as this will assist in identifying the etiology [32]. Pressure injuries are typically located over bony prominences (particularly the heel in patients with diabetes) and should be documented as occipital, sacral, scapular, or malleolus [32]. Unlike pressure injuries, venous stasis and neuropathic ulcers are located primarily on the lower extremities [33]. Incisions are obviously in the operative area, but it is important to document the exact location (e.g., distal, lateral, mediastinal) [24].

The size of an ulcer or wound is important to assess and document as it will provide vital information regarding the efficacy of the treatment and advancement of infection or necrosis [32]. Documentation of the sizes of any ulcers should include [68]:

- An accurate length in centimeters, typically measured from head to toe or from twelve o'clock to six o'clock from wound edge to wound edge

- An accurate width in centimeters, typically measured from left to right or from nine o'clock to three o'clock from wound edge to wound edge

- An accurate depth in centimeters in the center of the wound or the deepest area within the wound

- The location and extent of any undermining and tunneling, measured using a cotton probe

The optimal time interval between wound measurements is approximately seven days. More frequent measurement is unlikely to demonstrate clinically relevant differences in wound dimension [24]. Weekly documentation should minimally include a reassessment of wound appearance. The NPUAP recommends the use of digital photography in documenting changes in dimension and base of wounds over time. These photographs may be used to supplement written documentation, but they should never be used as a replacement for clearly written documentation [69,70]. As noted, the face of a clock can be used to provide additional accuracy to the description of wound characteristics [71]. The terms used in documentation should represent objective data rather than subjective findings [24]. When documenting wounds, descriptive words such as "huge" or "deep" and diagnostic terms such as "infected" should be avoided. Instead, the objective descriptors such as "perierythema" or "induration" should be used [68].

Clean wound beds may or may not have granulation tissue. An agranular, friable wound bed (that may bleed easily) can indicate a high bacterial load that must be controlled before granulation occurs. Granulation tissue is composed of new capillary buds that should be supported by moist wound healing techniques [33]. Documentation should include the presentation of abnormal growth, such as slough and eschar. Slough is necrotic tissue and may be identified as a moist, stringy, yellow tissue in the base of the wound. In addition to slough, it is essential to document the presence of eschar tissue [71]. Thick, black, and leathery eschar indicates that wound bed has become dehydrated [33]. It is also essential to document the percentage of each type of tissue on the wound bed, such as "50% yellow slough" [68].

The skin surrounding the wound also provides a wealth of information to the practitioner and is an important piece of the documentation process [33]. Wound edges should be open to allow for epithelial migration (not rolled or hardened). Erythema and induration of the periwound skin is common in the inflammatory phase but can indicate infection if it is accompanied by increased drainage, size, pain, or odor [68]. Erythema and warmth may denote inflammation or infection and should be communicated in the documentation record and monitored closely [33]. Interruption of the periwound area may indicate an allergy or sensitivity to dressing adhesives or tape products [24]. Maceration or desiccation may be an indication that the dressing is too moist or too dry for the amount of exudate [33]. Maceration present in periwound tissue is a significant indication of poorly controlled exudate, which could impair wound healing [32].

Assessment of the wound bed is completed with visualization and devices such as wound rulers and cotton swabs [32]. These devices can be utilized for assessment of the periwound areas as well, although palpitation is often a significant part of the assessment process. Palpitation can reveal induration or fluctuance, an abnormal accumulation indicative of further tissue damage or an abscess [33].

Drainage amount and quality should also be noted. If drainage strikes through the dressing, dressing absorption is inadequate. Moisture seepage can facilitate bacterial spread from either the wound or the environment [68]. Observance of yellow purulent drainage may indicate staphylococcal involvement within the wound or ulcer. Green drainage may indicate the presence of pseudomonal involvement. Estimating the amount of drainage present can help determine increases or decreases on subsequent assessments [71]. The type of exudates, such as serous, serosanguineous, sanguineous, or purulent, is an essential aspect of documenting a wound and should be reflected consistently and accurately [68,71]. The odor of the wound and drainage can offer clues as to potential infections in the wound. An acrid, fruity odor is indicative of staphylococcal organisms; a musty odor is indicative of Pseudomonas aeruginosa; a foul (fecal-like) odor is consistent with other gram-negative bacteria [68,71].

Healthcare professionals may be following several ulcers simultaneously, making it difficult to recall individual wound progression. Accurate, objective documentation provides a timeline of the wound progression on which to base changes in ulcer care [33]. An accurate depiction of the wound is also important legal protection. Ambiguity can be risky [24]. Documentation is legal evidence of the quality of wound care that has been provided [68]. When present, diabetes may cause profound difficulties in wound healing. Identifying and understanding these comorbidities will guide more effective interventions and assist in establishing realistic expectations for the healing process.

10. CASE STUDIES

CASE STUDY 1

Patient M is a white man, 67 years of age, with type 2 diabetes who is admitted to the hospital with a fever, two-day history of lethargy, and a rapid decrease in level of consciousness. His vital signs on admission are: temperature, 39.7 degrees Celsius; heart rate, 112 beats per minute, regular rate and rhythm; 26 respirations per minute and shallow; blood pressure, 88/40 mm Hg; blood glucose level, 329 mg/dL. The patient is complaining of a severe pain, reported at a 7 on a scale from 1 to 10. Physical assessment indicates:

- Height: 5 feet 10 inches

- Weight: 239 pounds without shoes

- Body mass index: 34.4 kg/m^2

- Lungs: Crackles upon auscultation

- Heart sounds: Clear without rubs or murmurs auscultated

- Abdomen: Soft and non-tender all quadrants

- Peripheral pulses: Present upon Doppler assessment at the lower extremities

- Feet and lower extremities: Cool to touch, hairless and shiny, taut, and thin bilaterally. Toes mottled.

- Capillary refill: Absent

Two lesions are present on the left lateral lower extremity, approximately 4 cm distal to the malleolus. The lesions are 5 cm in length, 3 cm in width, superficial depth, with yellowed edges, pale red base, and weepy.

Laboratory values reveal:

- Blood cultures positive for S. aureus

- White blood cell count: 21,000/mcL

- Glycated hemoglobin (HbA1c): 8.5%

- pH: 7.29

Patient M is admitted to the hospital with a diagnosis of septicemia secondary to a venous stasis ulcer, peripheral vascular disease, and uncontrolled hyperglycemia related to infection. He is started on antibiotic therapy, pain management, and dressing changes.

On day three of therapy, Patient M's temperature has been stabilized for the past 24 hours. Laboratory values are normalizing. His blood glucose levels remain elevated, with measurements between 276 mg/dL and 310 mg/dL. His pain is fluctuating between a 1 and a 5 and is being controlled with analgesics. Patient M's wound drainage is scant and yellow in color, with a slightly foul odor. His treatment plan consists of a moist, non-adherent dressing, and improvements have been noted. After three weeks of treatment, the wound assessment documentation indicates one lesion present on the left lateral lower extremity, approximately 4 cm distal to the malleolus. It is 4.6 cm in length, 2.8 cm in width, and superficial depth. The lesion is dry with irregular, yellowed edges and a reddened base. The surrounding tissue remains shiny and ruddy in color.

Patient M is discharged with orders for home health care for wound assessment and antibiotic therapy via a midline catheter.

CASE STUDY 2

Patient J is a white female patient, 54 years of age, with a history of uncontrolled insulin-dependent diabetes for the past 10 years. She is obese, with a body mass index of 41 kg/m^2. She reports a history of shortness of breath with minimal exertion and severe bilateral osteoarthritis of the knees. She was a two-pack-per-day smoker but has been cigarette-free for the past six months. She is scheduled for gastric bypass surgery in two days. Presurgical teaching includes:

- Incisional support and care to prevent infection

- Techniques for turning, coughing, and deep breathing after surgery

- The need to turn/change position at least every two hours to prevent pressure injuries

The surgery is completed without incident, and Patient J appears to be recovering as expected. However, two weeks postoperative she begins to cough uncontrollably, neglecting to support her incision. This occurs a total of four times throughout the night. At approximately 4:00 a.m., Patient J feels her incision "let go" and begins to bleed profusely; her incision has dehisced. She is rushed into surgery to resecure the incision and stop the bleeding. Although the bleeding can be cauterized, the periwound is too friable and further suturing will not adhere.

Patient J's incision measures 15 cm from twelve o'clock to six o'clock, 10 cm from three o'clock to nine o'clock, and 6 cm in depth. It is beefy red in color and appears to be healthy, with granulation tissue present. The surgeon prescribes treatment of the dehisced incision with a vacuum-assisted closure. She is premedicated for pain prior to dressing initiation and for subsequent dressing changes every 48 to 72 hours. After three weeks of vacuum-assisted closure therapy, Patient J's incision measures 12 cm from twelve o'clock to six o'clock, 9 cm from three o'clock to nine o'clock, and 4 cm in depth. It continues to look healthy and show signs of granulation. No odor is present within the wound. Wound edges are healthy, without maceration or rolling. The vacuum-assisted closure therapy is continued. At Patient J's next appointment eight weeks after the surgical procedure, her incision is assessed to be 8 cm from twelve o'clock to six o'clock, 5 cm from three o'clock to nine o'clock, and 2 cm in depth, with healthy color and edges. Vacuum-assisted closure therapy is discontinued, and a saline dressing is applied. Patient J's surgery is a success for both weight loss and the healing of her dehisced wound.

11. CONCLUSION

The impact of hyperglycemia as a comorbidity in delayed wound healing is well documented, and it can impact a wide variety of wounds, including pressure injuries. The Centers for Medicare and Medicaid Services identifies nosocomial pressure injuries as a "never" event [72]. As a result, hospital staff is required to have a working knowledge of preventative strategies of skin breakdown, identification of types of skin breakdown, and steps for appropriate care. This course has provided a thorough explanation of the pathophysiology of hyperglycemia and its impact on healing and wound management. With an understanding of these points, healthcare providers should be in a position to ensure that their patients receive optimal care, resulting in decreased healthcare costs and improved quality of life.

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