**Pressure Injury in the ICU: Major Reconstructive Surgery Required**

Ashley Jordan

[35] Janzen J, Buurman BM, Spanjaard L, de Reijke TM, Goossens A, Geerlings SE. Reduction of unnecessary use of indwelling urinary catheters. BMJ Quality & Safety. 2013;**22**

[36] Blondal K, Ingadottir B, Einarsdottir H, Bergs D, Steingrimsdottir I, Steindorsdottir S.et al. The effect of a short educational intervention on the use of urinary catheters: A prospective cohort study. International Journal for Quality in Health Care. 2016;**28**(6):742-8

[37] Waters TM, Daniels MJ, Bazzoli GJ, Perencevich E, Dunton N, Staggs VS.et al. Effect of Medicare's nonpayment for hospital-acquired conditions: Lessons for future policy.

JAMA Internal Medicine. 2015;**175**(3):347-354

(12):984-988

108 Vignettes in Patient Safety - Volume 1

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.69904

#### **Abstract**

Pressure injury (PI) has replaced the former nomenclature pressure ulcer, a change initiated by the National Pressure Ulcer Advisory Panel (NPUAP) however, substitutes such as pressure ulcers, decubitus ulcers, and bedsores will continue to be used by many. Increased knowledge and awareness of PIs has lead to a decline in their overall prevalence. A review of the most common risk factors, including two risk factor assessment tools, the Braden scale and the Cubbin & Jackson are presented. Diagnosing PIs must be a methodical, meticulous process in order to accurately document and monitor their progression and improvement. In 2016 the NPUAP revised the definitions as well as the stages of PIs incorporating the etiology and anatomical features present or absent in each stage of injury. Treatment strategies such as managing co-morbidities, nutrition optimization, and pain management are important aspects to consider in treating PIs in addition to thorough wound care cleansing and debridement. Highlighted are the various effective debridement options such as surgical sharp, mechanical, autolytic, enzymatic and larval debridement. Wound dressing alternatives, their advantages, disadvantages, indications and contraindications are all are mentioned. Concluding the chapter are pressure injury rates of healing, prognosis and surgical indications.

**Keywords:** pressure injury, pressure ulcers, decubitus ulcers, bedsores, ulcer prevention, ulcer treatment

#### **1. Case introduction**

Cynthia is a 70-year-old retired African-American patient with a past medical history significant for anemia and lung cancer—now 10 years in remission. She initially presented to the hospital complaining fatigue and severe cough that she "just couldn't get rid of." She was

© 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

subsequently found to have severe pneumonia requiring intravenous antibiotics. She was transferred to the medical intensive care unit (ICU) due to hypoxia and rapid decompensation on the floor; before she knew it 2 weeks had gone by since her admission. She noticed increasing amounts of lower back pain, presumably from sitting in bed all day. While her family and nurses encouraged her to get out of bed and walk she refused, stating that she was just "too weak to walk." One day while repositioning Cynthia in order to change the bed sheets; her nurse noted a new dime sized, red mark right above her gluteal cleft. She knew that she was supposed to document all wounds but she did not think this small, little mark "counted" as it was pretty minor. The nurse finished her shift and did not think much about the lesion. As the days progressed the dime sized lesion became the size of a nickel, then a quarter and soon the wound was as large as your hand. The patient complained of very severe pain in that region. The once red tissue was now grayish-black and it occasionally it produced a yellow-green exudate. The nurses did their best to pad her sacral region with various dressings however she was so thin and malnourished that you could literally see the vertebrae along her spine; subsequently the tissue continued to break down. Eventually, Cynthia's pressure injury was so deep that a small piece of bone started to protrude from the wound base. The medical ICU team tried various modalities to simulate wound healing, once they had exhausted all options for pressure wound injuries, they felt it was necessary to ask the plastic surgery team to evaluate her. Due to the depth and size of the sacral lesion, the plastic surgeons determined that Cynthia was going to require an operation — more specifically a multistep, rotational flap procedure. The patient and her family cuold not believe the news. How could this have happened? Could this outcome have been prevented?

with many chronic, nonhealing wounds may impair patient's quality of life, lead them toward

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Pressure injuries most commonly affect the elderly ages 65–70 years old, those with limited mobility, including hospitalized patients, nursing home occupants, those with neurologic impairment and people with severe illnesses [10]. General facility demographic trends indicate that mean patient age acquiring pressure injuries has decreased, scores for the Braden Scale, a PI risk factor assessment tool have remained constant, and patient weight has

Increased knowledge and awareness of pressure injuries has lead to a decline in their overall prevalence (OP). A large sample sized study with data collection spanning from 2006 to 2015 showed that the OP of pressure injuries in all facilities declined from 13.5% (2006) to 9.3% (2015) [11]. The annual prevalence of pressure ulcers among patients 65 years and older in general medicine practice has varied from 0.31 to 0.7% [12]. An Australian study found that excluding Stage 1 ulcers, overall hospital-acquired pressure injury prevalence from 2012 to 2014 was 11% for intensive care patients and 3% for non-intensive care patients [13]. Intensive care patients were found to be 3.8 times more likely (RR 2.7–5.4, 95% CI) than non-intensive care patients to develop a pressure injury while in the hospital [13]. Prevalence varies according to the patient's residence or surrounding environment. Facility-acquired prevalence (FAP) declined from 6.2% (2006) to a range of 3.1–3.4% (2013–2015). Acute care OP was 13.3% in 2006 and declined to a range of 8.8–9.3% (2012–2015). Long-term acute care (LTAC) had the highest

The sacrum/coccyx is the most common site of hospital-acquired pressure injury in all patients (intensive care patients 22%; non-intensive care patients 35%) [13]. Stage 2 hospital-acquired pressure injury (HAPI) prevalence is the most common stage reported, 53% for intensive care patients compared to 63% for non-intensive care patients [13]. Mucosal tissue lines the tongue, gastrointestinal (GI) tract, nasal passages, urinary tract and vaginal canal. This type of tissue is vulnerable to pressure from medical devices, such as oxygen tubing, endotracheal tubes, orogastric and nasogastric tubes and urinary catheters. Mucosal pressure injuries have been found to be significantly higher in intensive care patients (22%) than in non-intensive

Incidence is a commonly reported measure; however it is computed by counting the number of patients with newly acquired pressure ulcers and dividing that number by the number of patients examined for pressure ulcers over a given period of time. Smaller facilities can appear to have a higher percentage of patients with ulcers because there are fewer patients in the denominator. For example, five patients with ulcers in a 100 patient facitlity equals a 5% incidence. The same number of patients with ulcers (5) in a 500 patient facility is only a 1% incidence. Incidence density is the best quality measure of pressure ulcer prevention programs, according to the NPUAP [14]. Pressure ulcer incidence density is a computation based on the number of in-patients who develop a new pressure ulcer(s) divided by 1000

isolation and can reduce their contact with family, significant others and care givers [9].

**3. Patient demographics, incidence and prevalence**

increased in most care settings [11].

care patients (2%) [13].

OP at 32.9% in 2006; it declined to 28.8% in 2015 [11].

#### **2. Introduction—what is a pressure injury?**

Pressure injury has replaced the former nomenclature pressure ulcer, a recent change initiated by the National Pressure Ulcer Advisory Panel (NPUAP). The change in terminology derives inception from past histopathological work, which indicates that small changes in pressure-related injuries start in the tissue prior to the changes being visible on physical examination [1–3].

A pressure injury is localized damage to the skin and/or underlying soft tissue usually over a bony prominence or related to a medical or other device [6]. An ulcer is defined as a break in skin or mucous membrane with loss of surface tissue, disintegration and necrosis of epithelial tissue, and often, purulent exudate [5]. Thus, a pressure injury can be present without an ulcer however an ulcer cannot be present without a prior injury [6]. While the new terminology, pressure injury is the more technically correct term; many have argued that the name change does nothing to add clarity, improve accuracy or correct patient outcomes [7, 8]. Regardless of the advisory panels' endorsed term substitutes such as pressure ulcers, decubitus ulcers, and bedsores will continue to be used by many.

Pressure injuries can present as intact skin or an open ulcer and may be painful. The injury occurs as a result of intense and/or prolonged pressure or pressure in combination with shear. The tolerance of soft tissue for pressure and shear can be affected by microclimate, nutrition, perfusion, co-morbidities as well as the condition of the soft tissue [4]. The foul odors associated with many chronic, nonhealing wounds may impair patient's quality of life, lead them toward isolation and can reduce their contact with family, significant others and care givers [9].

#### **3. Patient demographics, incidence and prevalence**

subsequently found to have severe pneumonia requiring intravenous antibiotics. She was transferred to the medical intensive care unit (ICU) due to hypoxia and rapid decompensation on the floor; before she knew it 2 weeks had gone by since her admission. She noticed increasing amounts of lower back pain, presumably from sitting in bed all day. While her family and nurses encouraged her to get out of bed and walk she refused, stating that she was just "too weak to walk." One day while repositioning Cynthia in order to change the bed sheets; her nurse noted a new dime sized, red mark right above her gluteal cleft. She knew that she was supposed to document all wounds but she did not think this small, little mark "counted" as it was pretty minor. The nurse finished her shift and did not think much about the lesion. As the days progressed the dime sized lesion became the size of a nickel, then a quarter and soon the wound was as large as your hand. The patient complained of very severe pain in that region. The once red tissue was now grayish-black and it occasionally it produced a yellow-green exudate. The nurses did their best to pad her sacral region with various dressings however she was so thin and malnourished that you could literally see the vertebrae along her spine; subsequently the tissue continued to break down. Eventually, Cynthia's pressure injury was so deep that a small piece of bone started to protrude from the wound base. The medical ICU team tried various modalities to simulate wound healing, once they had exhausted all options for pressure wound injuries, they felt it was necessary to ask the plastic surgery team to evaluate her. Due to the depth and size of the sacral lesion, the plastic surgeons determined that Cynthia was going to require an operation — more specifically a multistep, rotational flap procedure. The patient and her family cuold not believe the news. How could this have

Pressure injury has replaced the former nomenclature pressure ulcer, a recent change initiated by the National Pressure Ulcer Advisory Panel (NPUAP). The change in terminology derives inception from past histopathological work, which indicates that small changes in pressure-related injuries start in the tissue prior to the changes being visible on physical

A pressure injury is localized damage to the skin and/or underlying soft tissue usually over a bony prominence or related to a medical or other device [6]. An ulcer is defined as a break in skin or mucous membrane with loss of surface tissue, disintegration and necrosis of epithelial tissue, and often, purulent exudate [5]. Thus, a pressure injury can be present without an ulcer however an ulcer cannot be present without a prior injury [6]. While the new terminology, pressure injury is the more technically correct term; many have argued that the name change does nothing to add clarity, improve accuracy or correct patient outcomes [7, 8]. Regardless of the advisory panels' endorsed term substitutes such as pressure ulcers, decubitus ulcers, and

Pressure injuries can present as intact skin or an open ulcer and may be painful. The injury occurs as a result of intense and/or prolonged pressure or pressure in combination with shear. The tolerance of soft tissue for pressure and shear can be affected by microclimate, nutrition, perfusion, co-morbidities as well as the condition of the soft tissue [4]. The foul odors associated

happened? Could this outcome have been prevented?

**2. Introduction—what is a pressure injury?**

bedsores will continue to be used by many.

examination [1–3].

110 Vignettes in Patient Safety - Volume 1

Pressure injuries most commonly affect the elderly ages 65–70 years old, those with limited mobility, including hospitalized patients, nursing home occupants, those with neurologic impairment and people with severe illnesses [10]. General facility demographic trends indicate that mean patient age acquiring pressure injuries has decreased, scores for the Braden Scale, a PI risk factor assessment tool have remained constant, and patient weight has increased in most care settings [11].

Increased knowledge and awareness of pressure injuries has lead to a decline in their overall prevalence (OP). A large sample sized study with data collection spanning from 2006 to 2015 showed that the OP of pressure injuries in all facilities declined from 13.5% (2006) to 9.3% (2015) [11]. The annual prevalence of pressure ulcers among patients 65 years and older in general medicine practice has varied from 0.31 to 0.7% [12]. An Australian study found that excluding Stage 1 ulcers, overall hospital-acquired pressure injury prevalence from 2012 to 2014 was 11% for intensive care patients and 3% for non-intensive care patients [13]. Intensive care patients were found to be 3.8 times more likely (RR 2.7–5.4, 95% CI) than non-intensive care patients to develop a pressure injury while in the hospital [13]. Prevalence varies according to the patient's residence or surrounding environment. Facility-acquired prevalence (FAP) declined from 6.2% (2006) to a range of 3.1–3.4% (2013–2015). Acute care OP was 13.3% in 2006 and declined to a range of 8.8–9.3% (2012–2015). Long-term acute care (LTAC) had the highest OP at 32.9% in 2006; it declined to 28.8% in 2015 [11].

The sacrum/coccyx is the most common site of hospital-acquired pressure injury in all patients (intensive care patients 22%; non-intensive care patients 35%) [13]. Stage 2 hospital-acquired pressure injury (HAPI) prevalence is the most common stage reported, 53% for intensive care patients compared to 63% for non-intensive care patients [13]. Mucosal tissue lines the tongue, gastrointestinal (GI) tract, nasal passages, urinary tract and vaginal canal. This type of tissue is vulnerable to pressure from medical devices, such as oxygen tubing, endotracheal tubes, orogastric and nasogastric tubes and urinary catheters. Mucosal pressure injuries have been found to be significantly higher in intensive care patients (22%) than in non-intensive care patients (2%) [13].

Incidence is a commonly reported measure; however it is computed by counting the number of patients with newly acquired pressure ulcers and dividing that number by the number of patients examined for pressure ulcers over a given period of time. Smaller facilities can appear to have a higher percentage of patients with ulcers because there are fewer patients in the denominator. For example, five patients with ulcers in a 100 patient facitlity equals a 5% incidence. The same number of patients with ulcers (5) in a 500 patient facility is only a 1% incidence. Incidence density is the best quality measure of pressure ulcer prevention programs, according to the NPUAP [14]. Pressure ulcer incidence density is a computation based on the number of in-patients who develop a new pressure ulcer(s) divided by 1000 patient days. Using the larger denominator of patient days allows fair comparisons between institutions of all sizes and stabilizes results. Many state reporting systems and hospitalacquired conditions (e.g., CAUTI) currently use incidence density [14].

nurses, assess and reliably score a patient's risk of developing a pressure injury [22]. It consists of six categories: sensory perception, moisture, activity, mobility, nutrition, and friction/shear. Each category is rated on a scale of 1–4, excluding the 'friction and shear' category, which is rated on a 1–3 scale. The total score can range from 6 to 23. The scale is an inverse scoring system thus a lower score indicates a higher risk of developing an injury and vice versa. A score of 23 means there is no risk for developing a pressure ulcer while a score of six points represents the

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**5.2. The Cubbin & Jackson scale for predicting pressure sore risk in ICU patients**

likelihood of pressure ulcer development is [23] **Table 2**.

**Table 1.** Braden Scale [22].

The Cubbin & Jackson scale was specifically designed in 1991 for intensive care patients and is a modification of another assessment scale, the Norton scale. The scale consists of 10 items: age, weight, general skin condition, mental condition, mobility, hemodynamics, respiration, nutrition, incontinence, and hygiene. Each item has a 4-point scale; thus, a maximum of 40 points total. This is another inverse scale in that the lower the point total is, the higher the

most severe risk for developing a pressure ulcer [22] (**Table 1**).

#### **4. Risk factors**

There are a multitude of risk factors that can contribute to PIs. Literature has stated that the elderly, aged >60 years old are the most prone to the development of pressure injuries, due to changes in aging skin such as decreased skin elasticity, insufficient skin hydration, decreased sensitivity, and factors that are associated with chronic comorbid conditions [15, 16]. Conditions that interfere with peripheral circulation and tissue perfusion have also been linked to PIs, such as congestive heart failure (CHF), diabetes mellitus and smoking [16].

Limited mobility is considered a fundamental component of PI formation. A reduction in movement can be related to a spinal cord injury, progressive neurological disorders, stroke, pain, and fractures among other etiologies. Pressure from any hard surface (e.g. bed, wheelchair or stretcher), friction from a patient's inability to move well in bed and shear from involuntary muscle movements are also a major contributors toward pressure injuries. Moisture from bowel or bladder incontinence, excessive perspiration and wound drainage have also been found to be correlated with pressure injuries. Poor nutrition resulting in reduced body mass due to wasting or cachexia typically results in less subcutaneous fat. Less protection over areas of bony prominence can lead to increased risk of pressure injuries, thus optimizing patients' nutritional status is essential for skin protection as well as wound healing.

#### **5. Risk factor assessment tools**

The Braden Scale is one of the most common pressure injury risk scales used in the United States. It is valid and effective for assessing the risk of developing pressure ulcers [17]. The Braden and Cubbin & Jackson are valid scales for measuring the pressure injury risk in patients admitted to intensive care units (ICUs) [18]. The health status of ICU patients vastly differs from general hospital patients. ICU patients are more likely to have several comorbid conditions, be hemodynamically unstable, receive vasoactive medications, be ventilator- dependent and are often sedated [19]. Literature states that for every mmHg decrease in diastolic blood pressure, the odds of a deep tissue injury increases by approximately 7.5% (1/0.93 = 1.075) [20]. Some literature has shown that of the two ICU risk assessment tools, the Cubbin & Jackson scale is the most effective in predicting risk of decubitus ulcers in patients admitted in ICU with sensitivity of 99.3% and specificity of 55.5% [17]. The Cubbin and Jackson scale has been used for the ICU population with great results [19].

#### **5.1. Braden scale for predicting pressure sore risk: used on general hospital and ICU patients**

The Braden Scale is the most widely used pressure ulcer risk assessment system in the world [21]. It is a clinically validated tool that was developed to help all health professionals, especially nurses, assess and reliably score a patient's risk of developing a pressure injury [22]. It consists of six categories: sensory perception, moisture, activity, mobility, nutrition, and friction/shear. Each category is rated on a scale of 1–4, excluding the 'friction and shear' category, which is rated on a 1–3 scale. The total score can range from 6 to 23. The scale is an inverse scoring system thus a lower score indicates a higher risk of developing an injury and vice versa. A score of 23 means there is no risk for developing a pressure ulcer while a score of six points represents the most severe risk for developing a pressure ulcer [22] (**Table 1**).


**Table 1.** Braden Scale [22].

patient days. Using the larger denominator of patient days allows fair comparisons between institutions of all sizes and stabilizes results. Many state reporting systems and hospital-

There are a multitude of risk factors that can contribute to PIs. Literature has stated that the elderly, aged >60 years old are the most prone to the development of pressure injuries, due to changes in aging skin such as decreased skin elasticity, insufficient skin hydration, decreased sensitivity, and factors that are associated with chronic comorbid conditions [15, 16]. Conditions that interfere with peripheral circulation and tissue perfusion have also been linked to PIs, such

Limited mobility is considered a fundamental component of PI formation. A reduction in movement can be related to a spinal cord injury, progressive neurological disorders, stroke, pain, and fractures among other etiologies. Pressure from any hard surface (e.g. bed, wheelchair or stretcher), friction from a patient's inability to move well in bed and shear from involuntary muscle movements are also a major contributors toward pressure injuries. Moisture from bowel or bladder incontinence, excessive perspiration and wound drainage have also been found to be correlated with pressure injuries. Poor nutrition resulting in reduced body mass due to wasting or cachexia typically results in less subcutaneous fat. Less protection over areas of bony prominence can lead to increased risk of pressure injuries, thus optimizing

patients' nutritional status is essential for skin protection as well as wound healing.

The Braden Scale is one of the most common pressure injury risk scales used in the United States. It is valid and effective for assessing the risk of developing pressure ulcers [17]. The Braden and Cubbin & Jackson are valid scales for measuring the pressure injury risk in patients admitted to intensive care units (ICUs) [18]. The health status of ICU patients vastly differs from general hospital patients. ICU patients are more likely to have several comorbid conditions, be hemodynamically unstable, receive vasoactive medications, be ventilator- dependent and are often sedated [19]. Literature states that for every mmHg decrease in diastolic blood pressure, the odds of a deep tissue injury increases by approximately 7.5% (1/0.93 = 1.075) [20]. Some literature has shown that of the two ICU risk assessment tools, the Cubbin & Jackson scale is the most effective in predicting risk of decubitus ulcers in patients admitted in ICU with sensitivity of 99.3% and specificity of 55.5% [17].

The Cubbin and Jackson scale has been used for the ICU population with great results [19].

The Braden Scale is the most widely used pressure ulcer risk assessment system in the world [21]. It is a clinically validated tool that was developed to help all health professionals, especially

**5.1. Braden scale for predicting pressure sore risk: used on general hospital and** 

acquired conditions (e.g., CAUTI) currently use incidence density [14].

as congestive heart failure (CHF), diabetes mellitus and smoking [16].

**4. Risk factors**

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**5. Risk factor assessment tools**

**ICU patients**

#### **5.2. The Cubbin & Jackson scale for predicting pressure sore risk in ICU patients**

The Cubbin & Jackson scale was specifically designed in 1991 for intensive care patients and is a modification of another assessment scale, the Norton scale. The scale consists of 10 items: age, weight, general skin condition, mental condition, mobility, hemodynamics, respiration, nutrition, incontinence, and hygiene. Each item has a 4-point scale; thus, a maximum of 40 points total. This is another inverse scale in that the lower the point total is, the higher the likelihood of pressure ulcer development is [23] **Table 2**.


**Categories of scale Score Operational definition**

Spontaneous 4

 Mechanical ventilation 2 Breathless at rest/on exertion 1

Respiration

Nutrition

Incontinencea

Hygiene

Stable with inotropic support 3 MBP ≥ 65 mmHg with inotropic support

Critical with inotropic support 1 MBP ≤ 55 mmHg with inotropic support

inotropic support

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to the ICU

enteral nutrition

assessment form

or diets

scale

assessment form at the time of admission

liquid diets without regular or soft diets

Unstable with inotropic support 2 55 mmHg < MBP < 65 mmHg with

CPAP/T-piece 3 Airway and oxygen supply on the

 Full diet, fluids 4 Prescription of regular diets or soft diets Light diet/oral fluids/enteral feeding 3 Prescription of enteral nutrition, or full

Parenteral feeding 2 Prescription of TPN only without diets or

Clear intravenous fluid only 1 No prescription of TPN, enteral nutrition

None/anuric/catheterized 4 None/anuric/catheterized on clinical

Feces 2 More than two bowel movements per day

 Maintaining own hygiene with slight help 3 4 on position change score of Braden scale Requiring much assistance 2 3 on position change score of Braden scale Fully dependent 1 1 or 2 on position change score of Braden

Urine 3 Not applicable

Urine, feces 1 Not applicable

Competent in maintaining own hygiene 4 Not applicable

**Table 2.** Cubbin & Jackson Scale [23]. Used with Permission.


**Table 2.** Cubbin & Jackson Scale [23]. Used with Permission.

**Categories of scale Score Operational definition**

40–54 3 Age at the time of admission to the ICU

Obese 3 BMI on the medical record at the time of

Intact 4 No pressure ulcer, no sore or sore none on

Grazed/excoriated skin 2 Abrasion, or bullae on the nursing record

Agitated/restless/confused 3 Consciousness on the assessment form at

Very limited/chairbound 2 3 or 4 on position change score of Braden

Immobile/bedrest 1 1 or 2 on position change score of Braden

Stable without inotropic support 4 MBP ≥ 65 mmHg without inotropic support

scale

scale

Any of above and edema 1 Edema on the assessment form

Red skin 3 Redness on the nursing record

Necrosis/exuding 1 Necrosis on the nursing record

 Fully ambulant 4 Not applicable Walks with slight help 3 Not applicable

admission to the ICU

the nursing record

the time of admission to the ICU

<40 4

 55–69 2 >70 1

Average weight 4

Cachectic 2

Awake and alert 4

 Apathetic/sedated but responsive 2 Coma/unresponsive 1

Age (yr)

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Weight

General skin condition

Mental condition

Mobility

Hemodynamics

#### **6. Diagnosing pressure injuries**

Diagnosing pressure injuries must be a methodical and meticulous process in order to accurately document and monitor progression as well as improvement. Keen documentation of the physical examination including pictures should be established. Initially, a complete head to toe physical exam should be performed to assess the patient and identify all of his/her wounds and lesions. Look for signs of systemic infection including, fever, chills, fatigue, diaphoresis, hypotension and tachycardia.

**6.2. Assess for blanching**

stage the lesion [25].

**7. Staging pressure injuries**

adopted internationally [6].

numerals have caused less of an issue.

disc; access for blanching during the application

blanching

Finger pressure method: press on erythema for 3 seconds remove finger, then assess for

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Transparent disc method: apply pressure equally on all areas of erythema with a transparent

Of note, assessing for blanching in patients with dark skin may be challenging; in this patient population focus on skin temperature, skin tenderness, tissue consistency and pain levels. It is wise to rule out neuropathy in all patients by testing the skin's sensation at the level of the lesion. Do this by performing the Semmes-Weinstein monofilament exam. Once a thorough physical exam has been performed and documented, one can make the clinical diagnosis and

Attempts to classify pressure injuries date back to the 1975 staging system developed by J.D. Shea [26]. Since then, other staging systems have been proposed from the International Association of Enterostomal Therapy (now the Wound, Ostomy and Continence Nurses Society), [27] as well as the National Pressure Ulcer Advisory Panel (NPUAP). The NPUAP's initial 1989 pressure injury staging system was based on the International Association of Enterostomal Therapy's system. The NPUAP made revisions by incorporating deep tissue injury and also collaborated with the European Pressure Ulcer Advisory Panel to publish guidelines with category/stage differentiation [28]. NPUAP's staging system has been widely

Most recently in 2016, the NPUAP revised the definition as well as stages of pressure injury. The revision was undertaken to incorporate the current understanding of the etiology of pressure injuries, as well as to clarify the anatomical features present or absent in each stage of injury [6]. Each definition now describes the extent of tissue loss present and the anatomical features that may or may not be present in the stage of injury [6]. The nomenclature and staging changes have caused some uproar. Opponents stress concern that the existing staging system continues to perpetuate the fallacy that pressure induced skin damage presents as a top (epidermis) down (bone) sequence of evolution in severity, that can be accurately classified by simple visual assessment of the skin layers, which is not entirely true [8]. Other changes made by the NPUAP such as denoting the stages using Arabic numerals rather than Roman

Pressure injury staging is important as it has become the basis for treatment, comparison of outcomes, and, if applicable, reimbursement [6]. Regardless of the stage assigned by visual examination, the examiner must take into account all of the available information and incorporate their interdisciplinary clinical expertise into defining the pressure injury etiology and

development; he/she should then classifying the lesion [6] (**Figures 2** and **3**).

#### **6.1. Skin assessment**

When diagnosing a pressure injury, it is essential to confirm the presence of pressure and/ or shear as a causative factor [6]. In order to perform an accurate visual assessment, pressure injury staging should take place only after the wound bed has been cleansed [6]. Have the patient in a neutral position when assessing the wound and use a consistent method when measuring the length, width and depth of the lesion. Note and document the number, location and size of the lesion(s) at each assessment, ideally with picture documentaiton. Look for accompanying edema, erythema, blanching response, warmth, tenderness, induration, exudate, purulence, odor, sinus tracts, necrosis, eschar formation, tunneling, undermining, wound margins, and possible exposed or palpable bone. Since the NPUAP pressure injury staging system is based on the extent of tissue damage, an understanding of anatomy is essential when evaluating the type of tissue present in the wound [4, 24] (**Figure 1**).

**Figure 1.** Skin Anatomy. [24] Used with permission. 2014 WebMD, LLC. All rights reserved.

#### **6.2. Assess for blanching**

**6. Diagnosing pressure injuries**

116 Vignettes in Patient Safety - Volume 1

phoresis, hypotension and tachycardia.

**6.1. Skin assessment**

Diagnosing pressure injuries must be a methodical and meticulous process in order to accurately document and monitor progression as well as improvement. Keen documentation of the physical examination including pictures should be established. Initially, a complete head to toe physical exam should be performed to assess the patient and identify all of his/her wounds and lesions. Look for signs of systemic infection including, fever, chills, fatigue, dia-

When diagnosing a pressure injury, it is essential to confirm the presence of pressure and/ or shear as a causative factor [6]. In order to perform an accurate visual assessment, pressure injury staging should take place only after the wound bed has been cleansed [6]. Have the patient in a neutral position when assessing the wound and use a consistent method when measuring the length, width and depth of the lesion. Note and document the number, location and size of the lesion(s) at each assessment, ideally with picture documentaiton. Look for accompanying edema, erythema, blanching response, warmth, tenderness, induration, exudate, purulence, odor, sinus tracts, necrosis, eschar formation, tunneling, undermining, wound margins, and possible exposed or palpable bone. Since the NPUAP pressure injury staging system is based on the extent of tissue damage, an understanding of anatomy is essen-

tial when evaluating the type of tissue present in the wound [4, 24] (**Figure 1**).

**Figure 1.** Skin Anatomy. [24] Used with permission. 2014 WebMD, LLC. All rights reserved.

Finger pressure method: press on erythema for 3 seconds remove finger, then assess for blanching

Transparent disc method: apply pressure equally on all areas of erythema with a transparent disc; access for blanching during the application

Of note, assessing for blanching in patients with dark skin may be challenging; in this patient population focus on skin temperature, skin tenderness, tissue consistency and pain levels. It is wise to rule out neuropathy in all patients by testing the skin's sensation at the level of the lesion. Do this by performing the Semmes-Weinstein monofilament exam. Once a thorough physical exam has been performed and documented, one can make the clinical diagnosis and stage the lesion [25].

#### **7. Staging pressure injuries**

Attempts to classify pressure injuries date back to the 1975 staging system developed by J.D. Shea [26]. Since then, other staging systems have been proposed from the International Association of Enterostomal Therapy (now the Wound, Ostomy and Continence Nurses Society), [27] as well as the National Pressure Ulcer Advisory Panel (NPUAP). The NPUAP's initial 1989 pressure injury staging system was based on the International Association of Enterostomal Therapy's system. The NPUAP made revisions by incorporating deep tissue injury and also collaborated with the European Pressure Ulcer Advisory Panel to publish guidelines with category/stage differentiation [28]. NPUAP's staging system has been widely adopted internationally [6].

Most recently in 2016, the NPUAP revised the definition as well as stages of pressure injury. The revision was undertaken to incorporate the current understanding of the etiology of pressure injuries, as well as to clarify the anatomical features present or absent in each stage of injury [6]. Each definition now describes the extent of tissue loss present and the anatomical features that may or may not be present in the stage of injury [6]. The nomenclature and staging changes have caused some uproar. Opponents stress concern that the existing staging system continues to perpetuate the fallacy that pressure induced skin damage presents as a top (epidermis) down (bone) sequence of evolution in severity, that can be accurately classified by simple visual assessment of the skin layers, which is not entirely true [8]. Other changes made by the NPUAP such as denoting the stages using Arabic numerals rather than Roman numerals have caused less of an issue.

Pressure injury staging is important as it has become the basis for treatment, comparison of outcomes, and, if applicable, reimbursement [6]. Regardless of the stage assigned by visual examination, the examiner must take into account all of the available information and incorporate their interdisciplinary clinical expertise into defining the pressure injury etiology and development; he/she should then classifying the lesion [6] (**Figures 2** and **3**).

Beware: Nonblanchable erythema may appear differently in darkly pigmented skin. Also, color changes do not include purple or maroon discoloration; these colors may indicate deep

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**Figure 4.** Stage 1 pressure injury lightly pigmented. Illustrations for figure is used with permission from Ref. [4].

**Figure 5.** Stage 1 pressure injury darkly pigmented. Illustrations for figure is used with permission from Ref. [4].

tissue pressure injury (DTPI) (**Figures 4** and **5**).

**Figure 2.** Heathy skin lightly pigemented. Illustrations for figure is used with permission from Ref. [4].

**Figure 3.** Heathy skin darkly pigemented. Illustrations for figure is used with permission from Ref. [4].

#### **7.1. Newly defined stages of pressure injury as defined by the National Pressure Ulcer Advisory Panel (NPUAP)**

#### *7.1.1. Stage 1 pressure injury*

Intact skin with a localized area of non-blanchable erythema. The presence of blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes [6].

Beware: Nonblanchable erythema may appear differently in darkly pigmented skin. Also, color changes do not include purple or maroon discoloration; these colors may indicate deep tissue pressure injury (DTPI) (**Figures 4** and **5**).

**Figure 4.** Stage 1 pressure injury lightly pigmented. Illustrations for figure is used with permission from Ref. [4].

**Figure 5.** Stage 1 pressure injury darkly pigmented. Illustrations for figure is used with permission from Ref. [4].

**7.1. Newly defined stages of pressure injury as defined by the National Pressure Ulcer** 

**Figure 3.** Heathy skin darkly pigemented. Illustrations for figure is used with permission from Ref. [4].

**Figure 2.** Heathy skin lightly pigemented. Illustrations for figure is used with permission from Ref. [4].

Intact skin with a localized area of non-blanchable erythema. The presence of blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes [6].

**Advisory Panel (NPUAP)**

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*7.1.1. Stage 1 pressure injury*

#### *7.1.2. Stage 2 pressure injury*

Partial-thickness skin loss of skin with exposed dermis. The wound bed is viable, pink or red, moist, and may present as an intact or ruptured serum-filled blister. Fat is not visible 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 [4] (**Figure 6**).

**Figure 6.** Stage 2 pressure injury. Illustrations for figure is used with permission from Ref. [4].

The revised definition of a Stage 2 pressure injury seeks to clarify the difference between moisture-associated skin damage and injury caused by pressure and/or shear [6]. Stage 2 injuries should not be used to describe moisture associated skin damage (MASD), incontinence associated dermatitis (IAD), intertriginous dermatitis (ITD), medical adhesive related skin injury (MARSI), or traumatic wounds such as skin tears, burns or abrasions [4].

#### *7.1.3. Stage 3 pressure injury*

Full-thickness loss of skin, in which fat is visible within the ulcer; granulation tissue and epibole (rolled wound edges) are often present. Slough and/or eschar may be visible. The depth of tissue damage varies by anatomical 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 then it should be classified as an unstageable pressure injury [4] (**Figures 7** and **8**).

may be visible as well as epibole (rolled edges). Undermining and/or tunneling often occur in Stage 4 wounds. Depth varies by anatomical location. If slough or eschar obscures the extent of tissue loss then it should be classified as an unstageable pressure injury [4] (**Figure 9**).

**Figure 8.** Stage 3 pressure injury with epibole. Illustrations for figure is used with permission from Ref. [4].

**Figure 7.** Stage 3 pressure injury. Illustrations for figure is used with permission from Ref. [4].

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Full-thickness skin and tissue loss in which the extent of the tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar. Once the slough or eschar is removed, a Stage 3 or Stage 4 pressure injury will be revealed. Stable eschar is often dry,

*7.1.5. Unstageable pressure injury*

#### *7.1.4. Stage 4 pressure injury*

Full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage or bone within the ulcer. Like in Stage 3 wounds, slough and/or eschar

**Figure 7.** Stage 3 pressure injury. Illustrations for figure is used with permission from Ref. [4].

**Figure 8.** Stage 3 pressure injury with epibole. Illustrations for figure is used with permission from Ref. [4].

may be visible as well as epibole (rolled edges). Undermining and/or tunneling often occur in Stage 4 wounds. Depth varies by anatomical location. If slough or eschar obscures the extent of tissue loss then it should be classified as an unstageable pressure injury [4] (**Figure 9**).

#### *7.1.5. Unstageable pressure injury*

*7.1.2. Stage 2 pressure injury*

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shear in the heel [4] (**Figure 6**).

*7.1.3. Stage 3 pressure injury*

*7.1.4. Stage 4 pressure injury*

Partial-thickness skin loss of skin with exposed dermis. The wound bed is viable, pink or red, moist, and may present as an intact or ruptured serum-filled blister. Fat is not visible 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

The revised definition of a Stage 2 pressure injury seeks to clarify the difference between moisture-associated skin damage and injury caused by pressure and/or shear [6]. Stage 2 injuries should not be used to describe moisture associated skin damage (MASD), incontinence associated dermatitis (IAD), intertriginous dermatitis (ITD), medical adhesive related skin

Full-thickness loss of skin, in which fat is visible within the ulcer; granulation tissue and epibole (rolled wound edges) are often present. Slough and/or eschar may be visible. The depth of tissue damage varies by anatomical 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 then it

Full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage or bone within the ulcer. Like in Stage 3 wounds, slough and/or eschar

injury (MARSI), or traumatic wounds such as skin tears, burns or abrasions [4].

**Figure 6.** Stage 2 pressure injury. Illustrations for figure is used with permission from Ref. [4].

should be classified as an unstageable pressure injury [4] (**Figures 7** and **8**).

Full-thickness skin and tissue loss in which the extent of the tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar. Once the slough or eschar is removed, a Stage 3 or Stage 4 pressure injury will be revealed. Stable eschar is often dry, adherent, and intact without erythema or it is commonly on the heel or on an ischemic limb and should not be softened or removed [4] (**Figures 10** and **11**).

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 there is necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle or other underlying structures visible, this indicates a full thickness pressure injury—Unstageable, Stage 3 or Stage 4. Do not use DTPI to describe vascular, traumatic, neuropathic, or dermatologic condi-

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**Figure 11.** Unstageable pressure injury—Slough and Eschar. Illustrations for figure is used with permission from Ref. [4].

**Figure 12.** Deep tissue pressure injury. Illustrations for figure is used with permission from Ref. [4].

tions [4] (**Figure 12**).

#### *7.1.6. Deep tissue pressure injury (DTPI)*

Intact or non-intact skin with a localized area of persistent non-blanchable deep red, maroon, purple discoloration or an epidermal separation revealing a dark wound bed or a blood filled blister. Discoloration may appear differently in darkly pigmented skin. Pain and temperature changes often precede the skin color changes. This injury results from intense and/or

**Figure 9.** Stage 4 pressure injury. Illustrations for figure is used with permission from Ref. [4].

**Figure 10.** Unstageable pressure injury—Dark Eschar. Illustrations for figure is used with permission from Ref. [4].

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 there is necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle or other underlying structures visible, this indicates a full thickness pressure injury—Unstageable, Stage 3 or Stage 4. Do not use DTPI to describe vascular, traumatic, neuropathic, or dermatologic conditions [4] (**Figure 12**).

adherent, and intact without erythema or it is commonly on the heel or on an ischemic limb

Intact or non-intact skin with a localized area of persistent non-blanchable deep red, maroon, purple discoloration or an epidermal separation revealing a dark wound bed or a blood filled blister. Discoloration may appear differently in darkly pigmented skin. Pain and temperature changes often precede the skin color changes. This injury results from intense and/or

and should not be softened or removed [4] (**Figures 10** and **11**).

**Figure 9.** Stage 4 pressure injury. Illustrations for figure is used with permission from Ref. [4].

**Figure 10.** Unstageable pressure injury—Dark Eschar. Illustrations for figure is used with permission from Ref. [4].

*7.1.6. Deep tissue pressure injury (DTPI)*

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**Figure 11.** Unstageable pressure injury—Slough and Eschar. Illustrations for figure is used with permission from Ref. [4].

**Figure 12.** Deep tissue pressure injury. Illustrations for figure is used with permission from Ref. [4].

#### *7.1.7. Additional terms of importance as defined by the NPUAP*

#### *7.1.7.1. 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. The injury should be staged using the staging system [4].

**8.2. Optimize nutritional status**

metabolic response triggered by the wound [29].

**a.** Daily Total Energy Expenditure Estimation

Normal Maintenance: 25–28 kcal/kg

equation:

**b.** Injury Factor (IF)

bers below as a guide:

Long Bone Fracture = 1.2

Poor nutritional status can be a contributing risk factor toward the formation of a pressure injury and can also contribute toward nonhealing. No matter what stage of pressure injury your patient is diagnosed with, if the patient's nutritional status is not optimized he/she will have a delayed healing evolution or even worse—never heal due to lack of energy. Serologic markers such as hemoglobin, serum albumin, prealbumin, transferrin and total lymphocyte count may be beneficial in assessing a patient's nutritional status. You should also use a valid

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One should determine the patient's daily caloric requirements to ensure they are obtaining enough fuel to support all of the patient's energy expenditures, known as the total energy expenditure (TEE) [29]. During illness, injury, or times of stress, the body may become hypermetabolic. Typically a patient with a wound requires additional calories to offset the hyper-

1) A simple way to calculate an estimate of caloric needs is by using a standard number of

Guidelines from the Agency for Health Care Policy and Research (now the Agency for Healthcare Research and Quality) state that approximately 30–35 kcals/kg/day are required for most patients with Stage 2 wounds or pressure injuries in risk of malnutrition. Increase to 35–40 kcal/kg/day if the patient is underweight or is losing weight; these estimates will likely

2) A more precise formula to determine caloric requirements is to use the three-component

IFs are variable and subjectively based according to the practitioner's judgment. Use the num-

Caloric Requirements = Harris Benedict Equation × Injury Factor × Activity Factor [29]

**a.** Daily Basal Energy Expenditure Estimate ( aka Harris Benedict Equation)

Males: 66.5 + (13.7 × Wt. in kg) + (5.0 × Ht. in cm) − (6.8 × age in Yrs.)

Females: 655 + (9.6 × Wt in kg) + (1.8 × Ht in cm) − (4.7 × age in Yrs.) [29]

and reliable nutritional screening tool to determine the patient's nutritional risk.

kcals/kg of body weight per day. Typical standards are listed below:

Mild-Moderate stress/illness, injury or malnutrition: 30–35 kcal/kg Severe major stress, critical illness or injury: 35–40 kcal/kg [25, 29].

achieve the desirable positive nitrogen balance [25, 29, 30].

Normal, minor Surgery, burn post graft = 1.0–1.2

#### *7.1.7.2. Mucosal membrane pressure injury*

Mucosal membrane pressure injury is found on mucous membranes with a history of a medical device in use at the location of the injury. Due to the anatomy of the tissue, these injuries cannot be staged [4].

#### *7.1.7.3. Important points*

The deterioration of a pressure injury does not predictably follow a linear evolution from Stage 1 to Stage 4 [6]. In addition, only pressure injuries should be staged with the NPUAP Pressure Injury Staging System. Many non-pressure-related ulcers and wounds are subject to unique staging or classification systems based upon the wound type for example: diabetic foot ulcers (Wagner Classification System), venous leg ulcers (Clinical Etiology Anatomy Pathophysiology), skin tears (International Skin Tear Advisory Panel), adhesive or tape injuries (medical adhesive related skin injury categories (MARSI)), and burn classification (total body surface area). It is essential that the intended staging or classification system be used for each type of injury to ensure appropriate treatment [6].

#### **8. Treatment of pressure injuries**

Managing and treating pressure injuries is only effective when a multidisiplinary team approach is utilized in the management of these patients. One must incorporate teams across several specialties and address the patient's issues as a whole in order for him/her to heal quickly and successfully. Below, we will briefly address some aspects in patient care to be mindful of when constructing treatment strategies; addressing these topics early in the management process will aid you in achieving positive outcomes.

#### **8.1. Manage co-morbidities**

Patients may have many comorbidities in addition to their pressure injury all of which need to be addressed and managed appropriately; for example stabilize glycemic control in diabetics and assess peripheral artery disease with a screening ABI ankle-brachial index (ABI) in vascular patients. An in depth discussion of the management of comorbid conditions will not be included in this chapter but be mindful to review all of the patient's comorbid conditions and assess whether or not there are correlations to wound care that need to be addressed.

#### **8.2. Optimize nutritional status**

*7.1.7. Additional terms of importance as defined by the NPUAP*

each type of injury to ensure appropriate treatment [6].

process will aid you in achieving positive outcomes.

**8. Treatment of pressure injuries**

**8.1. Manage co-morbidities**

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. The injury should be staged using the stag-

Mucosal membrane pressure injury is found on mucous membranes with a history of a medical device in use at the location of the injury. Due to the anatomy of the tissue, these injuries

The deterioration of a pressure injury does not predictably follow a linear evolution from Stage 1 to Stage 4 [6]. In addition, only pressure injuries should be staged with the NPUAP Pressure Injury Staging System. Many non-pressure-related ulcers and wounds are subject to unique staging or classification systems based upon the wound type for example: diabetic foot ulcers (Wagner Classification System), venous leg ulcers (Clinical Etiology Anatomy Pathophysiology), skin tears (International Skin Tear Advisory Panel), adhesive or tape injuries (medical adhesive related skin injury categories (MARSI)), and burn classification (total body surface area). It is essential that the intended staging or classification system be used for

Managing and treating pressure injuries is only effective when a multidisiplinary team approach is utilized in the management of these patients. One must incorporate teams across several specialties and address the patient's issues as a whole in order for him/her to heal quickly and successfully. Below, we will briefly address some aspects in patient care to be mindful of when constructing treatment strategies; addressing these topics early in the management

Patients may have many comorbidities in addition to their pressure injury all of which need to be addressed and managed appropriately; for example stabilize glycemic control in diabetics and assess peripheral artery disease with a screening ABI ankle-brachial index (ABI) in vascular patients. An in depth discussion of the management of comorbid conditions will not be included in this chapter but be mindful to review all of the patient's comorbid conditions and

assess whether or not there are correlations to wound care that need to be addressed.

*7.1.7.1. Medical device related pressure injury*

*7.1.7.2. Mucosal membrane pressure injury*

ing system [4].

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cannot be staged [4].

*7.1.7.3. Important points*

Poor nutritional status can be a contributing risk factor toward the formation of a pressure injury and can also contribute toward nonhealing. No matter what stage of pressure injury your patient is diagnosed with, if the patient's nutritional status is not optimized he/she will have a delayed healing evolution or even worse—never heal due to lack of energy. Serologic markers such as hemoglobin, serum albumin, prealbumin, transferrin and total lymphocyte count may be beneficial in assessing a patient's nutritional status. You should also use a valid and reliable nutritional screening tool to determine the patient's nutritional risk.

One should determine the patient's daily caloric requirements to ensure they are obtaining enough fuel to support all of the patient's energy expenditures, known as the total energy expenditure (TEE) [29]. During illness, injury, or times of stress, the body may become hypermetabolic. Typically a patient with a wound requires additional calories to offset the hypermetabolic response triggered by the wound [29].

1) A simple way to calculate an estimate of caloric needs is by using a standard number of kcals/kg of body weight per day. Typical standards are listed below:

**a.** Daily Total Energy Expenditure Estimation

Normal Maintenance: 25–28 kcal/kg Mild-Moderate stress/illness, injury or malnutrition: 30–35 kcal/kg Severe major stress, critical illness or injury: 35–40 kcal/kg [25, 29].

Guidelines from the Agency for Health Care Policy and Research (now the Agency for Healthcare Research and Quality) state that approximately 30–35 kcals/kg/day are required for most patients with Stage 2 wounds or pressure injuries in risk of malnutrition. Increase to 35–40 kcal/kg/day if the patient is underweight or is losing weight; these estimates will likely achieve the desirable positive nitrogen balance [25, 29, 30].

2) A more precise formula to determine caloric requirements is to use the three-component equation:

Caloric Requirements = Harris Benedict Equation × Injury Factor × Activity Factor [29]

**a.** Daily Basal Energy Expenditure Estimate ( aka Harris Benedict Equation)

Males: 66.5 + (13.7 × Wt. in kg) + (5.0 × Ht. in cm) − (6.8 × age in Yrs.)

Females: 655 + (9.6 × Wt in kg) + (1.8 × Ht in cm) − (4.7 × age in Yrs.) [29]

**b.** Injury Factor (IF)

IFs are variable and subjectively based according to the practitioner's judgment. Use the numbers below as a guide:

Normal, minor Surgery, burn post graft = 1.0–1.2

Long Bone Fracture = 1.2

```
COPD, Malnourished = 1.3
Severe Head Injury = 1.4
Cancer = 1.0–1.5
<50% Burns = 1.5
Ventilator = 1.6
Major Surgery, Multiple Traumas, 0–20% Burns Pre Grafting = 1.2–1.6
Acute Sepsis = 1.2–1.7
Severe infection = 1.4–1.8
20–40% Burn Pre Grafting 1.5–2.0
50% Burn = 2.0 [29, 31]
c. Activity Factor (AF)
1.2—Confined to bed
1.3—Out of bed
1.5—Normal, healthy activity [29, 31]
```
#### **8.3. High protein diet**

Provide a high protein diet (1.25–1.5 g/kg/day) to maintain a positive nitrogen balance for adults assessed to be at risk or with an existing pressure injury. A high protein diet in combination with arginine and micronutrient supplements is ideal. Arginine enriched mixed nutritional supplements have been shown to improve mean pressure ulcer healing time [32]. Literature has also shown that an arginine, zinc and antioxidant enriched nutritional formula increased the rate of healing in malnourished adults, [33] yet zinc supplementation alone appeared ineffective and was associated with adverse effects [34]. Thus, possibly it's the combination of both arginine and zinc that improves wound healing. Nutritional shakes in addition to vitamin and mineral supplements are strongly advised. If patients are unable to tolerate oral intake consider enteral or parenteral nutritional substitutions.

**9. Wound care: cleansing**

**10. Debridement**

and it will not revitalize [25].

**10.1. Infection**

Clean all pressure injuries at each dressing change to help facilitate removal of debris and bacteria. Water or normal saline are appropriate to use as cleansers and irrigation agents for most pressure ulcers. For compromised patients, wounds, or wound healing environments consider aseptic techniques. If there is debris, infection or high bacterial colonization, consider using a cleanser with surfactants and/or antimicrobials. Apply your choice of cleansing solution with ample pressure to clean the wound of debris without damaging the tissue, which may be friable. For each dressing change, a new, unopened container of cleansing solution

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If you are concerned about whether or not a wound needs to be debrided, a surgery consult should be placed. Surgeons have been exposed to a wide variety of wounds and are experts on assessing whether or not tissue debridement is indicated. All necrotic and nonviable tissue needs to be removed so that new granulation tissue may form; this includes the wound bed and edges. Maintenance debridement should occur frequently until all devitalized tissue is removed and the wound is covered with granulation tissue. There are no surgical indications to debride stable, hard, dry eschar in ischemic limbs because there is inadequate perfusion

One should always have a high index of suspicion for infection in pressure injuries especially if there is necrotic tissue present or if the wound is deep or large in size. Anatomic location also plays a large role in infection control particularly when the area is prone to exposure of contaminants (e.g., near the anus). Ulcers with signs of infection are in need of urgent surgical debridement—emergent surgical debridement if necrotizing fasciitis is suspected. Some signs of necrotizing fasciitis include rapidly spreading erythema, tenderness out of proportion to the physical attributes of the wound and crepitus. Beware of foreign bodies within wounds; they are commonly a nidus for infection. Patients at high risk of infection include those with

diabetes mellitus, malnutrition, autoimmune diseases and immunosuppression [25].

If there are clinical signs of spreading infection, such as extension of erythema beyond the wound, induration, purulence, increase in erythema, warmth or pain, obtain a quantitative culture via tissue biopsy or less preferably quantitate swab technique. An initial trial of antibiotics it is reasonable to administer. If you are dealing with a nonhealing pressure injury, needle aspiration or an ulcer biopsy for culture should be performed to determine bio-burden/ microbial load. In the absence of clinical signs of infection, the quantity of the organisms or microbial load is believed to be the best indicator of wound infection. Superficial wound cultures are not generally recommended due to the fact that all lesions are colonized with bacteria

should be used. Used irrigation solution should be appropriately discarded [25].

#### **8.4. Pain management**

While some pressure injuries lead to insensate tissue others injuries can be extremely painful. Pain management strategies should be addressed especially prior to any cleansing or debridement. An in depth discussion of pain management options will not be included in this chapter. However, the application of topical opioids such as benzydamine 3% or diamorphine gel (not available in the US) as well as topical anesthetics such as lidocaine-prilocaine should be considered [25].

#### **9. Wound care: cleansing**

COPD, Malnourished = 1.3

Major Surgery, Multiple Traumas, 0–20% Burns Pre Grafting = 1.2–1.6

Provide a high protein diet (1.25–1.5 g/kg/day) to maintain a positive nitrogen balance for adults assessed to be at risk or with an existing pressure injury. A high protein diet in combination with arginine and micronutrient supplements is ideal. Arginine enriched mixed nutritional supplements have been shown to improve mean pressure ulcer healing time [32]. Literature has also shown that an arginine, zinc and antioxidant enriched nutritional formula increased the rate of healing in malnourished adults, [33] yet zinc supplementation alone appeared ineffective and was associated with adverse effects [34]. Thus, possibly it's the combination of both arginine and zinc that improves wound healing. Nutritional shakes in addition to vitamin and mineral supplements are strongly advised. If patients are unable to tolerate oral intake consider enteral or parenteral nutritional

While some pressure injuries lead to insensate tissue others injuries can be extremely painful. Pain management strategies should be addressed especially prior to any cleansing or debridement. An in depth discussion of pain management options will not be included in this chapter. However, the application of topical opioids such as benzydamine 3% or diamorphine gel (not available in the US) as well as topical anesthetics such as lidocaine-prilocaine should

Severe Head Injury = 1.4

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Acute Sepsis = 1.2–1.7

Severe infection = 1.4–1.8

50% Burn = 2.0 [29, 31] **c.** Activity Factor (AF) 1.2—Confined to bed

1.3—Out of bed

substitutions.

**8.4. Pain management**

be considered [25].

**8.3. High protein diet**

20–40% Burn Pre Grafting 1.5–2.0

1.5—Normal, healthy activity [29, 31]

Cancer = 1.0–1.5 <50% Burns = 1.5 Ventilator = 1.6

Clean all pressure injuries at each dressing change to help facilitate removal of debris and bacteria. Water or normal saline are appropriate to use as cleansers and irrigation agents for most pressure ulcers. For compromised patients, wounds, or wound healing environments consider aseptic techniques. If there is debris, infection or high bacterial colonization, consider using a cleanser with surfactants and/or antimicrobials. Apply your choice of cleansing solution with ample pressure to clean the wound of debris without damaging the tissue, which may be friable. For each dressing change, a new, unopened container of cleansing solution should be used. Used irrigation solution should be appropriately discarded [25].

#### **10. Debridement**

If you are concerned about whether or not a wound needs to be debrided, a surgery consult should be placed. Surgeons have been exposed to a wide variety of wounds and are experts on assessing whether or not tissue debridement is indicated. All necrotic and nonviable tissue needs to be removed so that new granulation tissue may form; this includes the wound bed and edges. Maintenance debridement should occur frequently until all devitalized tissue is removed and the wound is covered with granulation tissue. There are no surgical indications to debride stable, hard, dry eschar in ischemic limbs because there is inadequate perfusion and it will not revitalize [25].

#### **10.1. Infection**

One should always have a high index of suspicion for infection in pressure injuries especially if there is necrotic tissue present or if the wound is deep or large in size. Anatomic location also plays a large role in infection control particularly when the area is prone to exposure of contaminants (e.g., near the anus). Ulcers with signs of infection are in need of urgent surgical debridement—emergent surgical debridement if necrotizing fasciitis is suspected. Some signs of necrotizing fasciitis include rapidly spreading erythema, tenderness out of proportion to the physical attributes of the wound and crepitus. Beware of foreign bodies within wounds; they are commonly a nidus for infection. Patients at high risk of infection include those with diabetes mellitus, malnutrition, autoimmune diseases and immunosuppression [25].

If there are clinical signs of spreading infection, such as extension of erythema beyond the wound, induration, purulence, increase in erythema, warmth or pain, obtain a quantitative culture via tissue biopsy or less preferably quantitate swab technique. An initial trial of antibiotics it is reasonable to administer. If you are dealing with a nonhealing pressure injury, needle aspiration or an ulcer biopsy for culture should be performed to determine bio-burden/ microbial load. In the absence of clinical signs of infection, the quantity of the organisms or microbial load is believed to be the best indicator of wound infection. Superficial wound cultures are not generally recommended due to the fact that all lesions are colonized with bacteria and superficial swab cultures are unreliable. The gold standard for determining microbial load is a quantitative culture of viable biopsied wound tissue [25].

Pulsed lavage as well as high- or low-pressure streams can be quite effective in removing loose necrotic tissue from the wound bed. A common practice after surgical wound debridement is pulsed lavage treatment for wound irrigation. Wound vacuum cleaning is thought to improve the healing of pressure injuries [36]. Ulcer irrigation pressures range from 4 to 15 psi of pressure; this range typically yields successful debridement yet does not cause trauma to the wound bed. Irrigation pressures below 4 psi may not be effective to cleanse the wound and pressures greater than 15 psi may cause trauma and drive the bacteria into the tissue [35]. Some pulsation devices allow copious amount of irrigation, which can be infused with antibiotics. These medical devices are certainly used in the operating room and portable versions are now available for bedside use in the appropriate setting. Normal saline "flushes" through a 60 cc Toomey syringe is another technique that works well to aid with debridement and a

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Whirlpools may be used initially to loosen and remove debris, bacteria, exudates, and necrotic tissue however prolonged use and periods of wetness may macerate the tissue or may be associated with bacterial contamination. NPUAP guidelines advise against whirlpool use for routine use in treating pressure ulcers due to the potential for contamination and the emergence of newer hydrotherapies [25]. In addition, individuals with dependent lower extremity edema or peripheral vascular disease, [37] immunocompromised individuals, those who are mechanically ventilated and lethargic, and incontinent individuals should never be immersed

Autolytic debridement uses the body's own endogenous enzymes and moisture to break down tough eschar and slough. This form of debridement is accomplished by moist interactive dressings, which allow the patient's natural wound fluid and endogenous enzymes to be kept in constant contact with the wound. The self produced fluid and endogenous enzymes soften and liquefy slough and promote granulation tissue formation [35]. The dressings used can be occlusive or semi-occlusive and consist of various materials such transparent films hydrogels and hydrocolloids. These dressings will be discussed more detail in the Wound Dressings section. Endogenous enzymes do not damage healthy skin however the wound will need to be cleaned after autolytic debridement in order to remove the necrotic debris. The time to break down dead and devitalized tissue can be slow and is quite variable. If tissue autolysis is not apparent in 1–2 weeks, another debridement method should be used [35]. Autolytic debridement is not recommended for infected wounds or very deep wounds that

Enzymatic debridement is achieved by topical application of exogenous enzymes to the wound surface to remove necrotic tissue [35]. The chemical agents are useful for debriding wounds with a large amount of necrosis and/or eschar. While enzymatic debridement effectively breaks down nonviable tissue, it also may damage nearby healthy tissue as well. In addition, these agents must be prescribed and a small tube can be quite costly. Enzymatic

copious amount of irrigation is possible with this technique.

in water [25, 38].

**11.3. Autolytic debridement**

require packing [35, 38].

**11.4. Enzymatic debridement**

The ulcer bed should be debrided if a biofilm is suspected. Be suspicious of biofilm formation if the wound has been present for >4 weeks, if healing still appears delayed after 2 weeks of attention and treatment, or if there is no response to antibiotics. Confirmation of a biofilm can be obtained once biopsy culture shows ≥ 10<sup>5</sup> colony forming units (CFU)/gram tissue. Beta hemolytic streptococci is a common culprit [25].

### **11. Debridement options**

The most common debridement options include: surgical sharp, mechanical, autolytic, enzymatic and larval. The method of debridement chosen depends upon the condition of the wound, the health status of the patient as well as the capabilities and confidence of the healthcare provider. More than one debridement method may be deemed appropriate for a given pressure injury and multiple modalities can be combined as well.

#### **11.1. Surgical-sharp debridement**

This type of debridement involves the use of instruments such as scissors, scalpels and forceps to remove necrotic, nonviable tissue from the wound [35]. Surgical debridement can be performed so that it extends into healthy tissue or conservative-sharp debridement can be performed which does not extend into or excise healthy tissue. Surgical debridement is an appropriate debridement option when a large amount of necrotic tissue needs to be removed from the wound bed. Surgical sharp debridement is indicated for extensive necrosis, advancing cellulitis, crepitus, fluctuance and/or when sepsis is related to the pressure injury. Perform urgent surgical debridement for ulcers with erythema, tenderness, edema, purulence, fluctuance, crepitus and malodor suggesting an infection around the injury. Most of the presentations listed above require operating room equipment, however, moderate surgical debridement may be performed by a competent medical professional at the bedside using a sterile scalpel or scissors. Extensive debridement should be executed in the operating room [25].

#### **11.2. Mechanical debridement**

Mechanical debridement physically removes nonviable, necrotic tissue with techniques such as wet-to-dry dressings, dry gauze and hydro-surgery such as wound irrigation and whirlpool techniques [35]. The wet-to-dry dressing system is one of the oldest forms of wound debridement. This method typically consists of applying moist to wet dressings to the wound, which are manually removed later once the dressings have dried. This causes non-selective debridement of necrotic tissue, eschar and slough; unfortunately sometimes viable, newly formed tissue is damaged and/or removed as well. This form of debridement can also be very painful to the patient if the dressings are very dry and hardened.

Pulsed lavage as well as high- or low-pressure streams can be quite effective in removing loose necrotic tissue from the wound bed. A common practice after surgical wound debridement is pulsed lavage treatment for wound irrigation. Wound vacuum cleaning is thought to improve the healing of pressure injuries [36]. Ulcer irrigation pressures range from 4 to 15 psi of pressure; this range typically yields successful debridement yet does not cause trauma to the wound bed. Irrigation pressures below 4 psi may not be effective to cleanse the wound and pressures greater than 15 psi may cause trauma and drive the bacteria into the tissue [35]. Some pulsation devices allow copious amount of irrigation, which can be infused with antibiotics. These medical devices are certainly used in the operating room and portable versions are now available for bedside use in the appropriate setting. Normal saline "flushes" through a 60 cc Toomey syringe is another technique that works well to aid with debridement and a copious amount of irrigation is possible with this technique.

Whirlpools may be used initially to loosen and remove debris, bacteria, exudates, and necrotic tissue however prolonged use and periods of wetness may macerate the tissue or may be associated with bacterial contamination. NPUAP guidelines advise against whirlpool use for routine use in treating pressure ulcers due to the potential for contamination and the emergence of newer hydrotherapies [25]. In addition, individuals with dependent lower extremity edema or peripheral vascular disease, [37] immunocompromised individuals, those who are mechanically ventilated and lethargic, and incontinent individuals should never be immersed in water [25, 38].

#### **11.3. Autolytic debridement**

and superficial swab cultures are unreliable. The gold standard for determining microbial load

The ulcer bed should be debrided if a biofilm is suspected. Be suspicious of biofilm formation if the wound has been present for >4 weeks, if healing still appears delayed after 2 weeks of attention and treatment, or if there is no response to antibiotics. Confirmation of a biofilm can

The most common debridement options include: surgical sharp, mechanical, autolytic, enzymatic and larval. The method of debridement chosen depends upon the condition of the wound, the health status of the patient as well as the capabilities and confidence of the healthcare provider. More than one debridement method may be deemed appropriate for a given

This type of debridement involves the use of instruments such as scissors, scalpels and forceps to remove necrotic, nonviable tissue from the wound [35]. Surgical debridement can be performed so that it extends into healthy tissue or conservative-sharp debridement can be performed which does not extend into or excise healthy tissue. Surgical debridement is an appropriate debridement option when a large amount of necrotic tissue needs to be removed from the wound bed. Surgical sharp debridement is indicated for extensive necrosis, advancing cellulitis, crepitus, fluctuance and/or when sepsis is related to the pressure injury. Perform urgent surgical debridement for ulcers with erythema, tenderness, edema, purulence, fluctuance, crepitus and malodor suggesting an infection around the injury. Most of the presentations listed above require operating room equipment, however, moderate surgical debridement may be performed by a competent medical professional at the bedside using a sterile scalpel or scissors. Extensive debridement should be executed in the operating

Mechanical debridement physically removes nonviable, necrotic tissue with techniques such as wet-to-dry dressings, dry gauze and hydro-surgery such as wound irrigation and whirlpool techniques [35]. The wet-to-dry dressing system is one of the oldest forms of wound debridement. This method typically consists of applying moist to wet dressings to the wound, which are manually removed later once the dressings have dried. This causes non-selective debridement of necrotic tissue, eschar and slough; unfortunately sometimes viable, newly formed tissue is damaged and/or removed as well. This form of debridement can also be very

colony forming units (CFU)/gram tissue. Beta

is a quantitative culture of viable biopsied wound tissue [25].

pressure injury and multiple modalities can be combined as well.

painful to the patient if the dressings are very dry and hardened.

be obtained once biopsy culture shows ≥ 10<sup>5</sup>

**11. Debridement options**

128 Vignettes in Patient Safety - Volume 1

**11.1. Surgical-sharp debridement**

**11.2. Mechanical debridement**

room [25].

hemolytic streptococci is a common culprit [25].

Autolytic debridement uses the body's own endogenous enzymes and moisture to break down tough eschar and slough. This form of debridement is accomplished by moist interactive dressings, which allow the patient's natural wound fluid and endogenous enzymes to be kept in constant contact with the wound. The self produced fluid and endogenous enzymes soften and liquefy slough and promote granulation tissue formation [35]. The dressings used can be occlusive or semi-occlusive and consist of various materials such transparent films hydrogels and hydrocolloids. These dressings will be discussed more detail in the Wound Dressings section. Endogenous enzymes do not damage healthy skin however the wound will need to be cleaned after autolytic debridement in order to remove the necrotic debris. The time to break down dead and devitalized tissue can be slow and is quite variable. If tissue autolysis is not apparent in 1–2 weeks, another debridement method should be used [35]. Autolytic debridement is not recommended for infected wounds or very deep wounds that require packing [35, 38].

#### **11.4. Enzymatic debridement**

Enzymatic debridement is achieved by topical application of exogenous enzymes to the wound surface to remove necrotic tissue [35]. The chemical agents are useful for debriding wounds with a large amount of necrosis and/or eschar. While enzymatic debridement effectively breaks down nonviable tissue, it also may damage nearby healthy tissue as well. In addition, these agents must be prescribed and a small tube can be quite costly. Enzymatic debridement is thought to be faster than autolytic debridement however it may cause increased wound pain and /or an uncomfortable burning sensation to the patient. Enzymatic debridement is most useful in patients who cannot tolerate sharp debridement and should not be used if an infection is present. Preparations available in the US include collagenase and papain/urea with or without chlorophyll [38].

(Dakin's solution) is cytotoxic at all concentrations and should be used with caution, at concentrations no greater than 0.025%, for short periods only when no other appropriate option

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New, less commonly used agents' effectiveness appear promising. Atorvastatin powder mixed with petroleum jelly and beeswax forms an ointment, which has been used as a topical agent resulting in a reduction in the size of Stage 1 and 2 pressure ulcers [51]. Recombinant human platelet-derived growth factor (rPDGF) has been shown to accelerate the healing of pressure ulcers [52]. Topical phenytoin may be more effective than DuoDERM dressing, saline dress-

Consider a systemic antibiotic only if clinical signs of systemic infection are present or there is a positive blood culture, cellulitis, fasciitis, osteomyelitis, systemic inflammatory response syndrome (SIRS) or sepsis. If systemic antibiotics are given, empiric antibiotics should cover methicillin-resistant *Staphylococcus aureus*, *anaerobes*, *enterococci* and Gram-negatives such as

There is insufficient evidence to support whether topical antimicrobials improve wound healing or reduce infection in patients with ≥Stage II pressure ulcers. Generally topical antibiotics are not recommended and should be limited or avoided if possible. Use is indicated in specific situations where the topical antibiotics' benefits outweigh the risks of antibiotic side effects and resistance. Consider topical Metronidazole for control of odor due to anaerobic bacteria

Osteomyelitis can be a detrimental finding in any patient thus rapid identification and treatment is necessary. If osteomyelitis is suspected in a patient's wound bed, obtain blood cultures and sensitivities, leukocyte count, erythrocyte sedimentation rate and a C-reactive protein level. Imaging should also be obtained. A plain X-ray is the initial imaging study of choice. Once osteomyelitis is confirmed, a CT scan is useful for needle guided biopsies, identifying necrotic bone and soft tissue extension. The gold standard test of choice for detection of early

Cultures at the time of presentation or first debridement may not be useful. Swabbing cultures from draining wounds and sinus tracts may not be reliable for predicting organisms

osteomyelitis and associated soft tissue disease is an MRI with gadolinium [25].

is available [25, 48–50].

**13.1. Systemic**

**13.2. Topical**

and protozoal infections [25].

**13.3. Osteomyelitis & abscesses**

**12.2. Other agents of interest**

ings and topical antibiotics for treating pressure ulcers [53].

**13. Antimicrobials: systemic & topical**

*Pseudomonas*, *Proteus* and *Providencia* species [25].

#### **11.5. Larval therapy/Medicinal maggot therapy**

Maggot debridement therapy is the intentional application of live, "medical grade" fly larvae to wounds. Medicinal maggots have been sited to perform major actions such as debridement, disinfection, stimulation of wound healing as well as biofilm inhibition and eradication [39]. Larval debridement is unique in that maggots selectively only engulf necrotic tissue—no healthy tissue is affected. This method is gaining in popularity due to its low cost, incredible effectiveness and expedited time for successful debridement. Some patients however find the method somewhat painful and their perception of maggots may stand in the way of using this highly effective method of debridement [38].

#### **12. Topical agents**

#### **12.1. Topical antiseptics**

When it comes to topical agents for pressure injuries the options are vast. Indications for specific topical agents can vary as the pressure stage progresses or the wound starts to heal. Antiseptic agents commonly used in wounds include: iodine (povidone, iodine or slow release cadexomer iodine), silver (silver sulfadiazine), polyhexanide and betaine (PHMB), chlorhexidine, sodium hypochlorite and acetic acid [25]. Topical antiseptics should be used for pressure ulcers that are not expected to heal, are critically colonized or topically infected. They should be used in conjunction with maintenance debridement. In managing biofilms, consider topical antiseptics to control bacterial bio-burden in wounds with delayed healing [25].

Be aware that some skin cleaners or antiseptics may destroy granulation tissue [10]. Avoid hydrogen peroxide as it is toxic to tissues even at low concentrations [40, 41]and should not be used as a preferred topical antiseptic. Its use should be completely avoided in cavity wounds due to the risk of surgical emphysema and gas embolus [28, 41–43].

Iodine products should be avoided in patients with impaired renal failure, history of thyroid disorders or known iodine sensitivity [44, 45]. There is a risk of acidosis when acetic acid is used for extended periods over large wound surface areas [46]. Silver may have toxic properties, especially to keratinocytes and fibroblasts; the extent of the toxicities however, is not fully described. Topical silver products should not be used on individuals with silver sensitivities, and silver sulfadiazine products are not recommended for people with sulfur sensitivities [47]. It is however appropriate to consider using silver sulfadiazine in heavily contaminated or infected pressure ulcers until definitive debridement is accomplished. Sodium hypochlorite (Dakin's solution) is cytotoxic at all concentrations and should be used with caution, at concentrations no greater than 0.025%, for short periods only when no other appropriate option is available [25, 48–50].

#### **12.2. Other agents of interest**

New, less commonly used agents' effectiveness appear promising. Atorvastatin powder mixed with petroleum jelly and beeswax forms an ointment, which has been used as a topical agent resulting in a reduction in the size of Stage 1 and 2 pressure ulcers [51]. Recombinant human platelet-derived growth factor (rPDGF) has been shown to accelerate the healing of pressure ulcers [52]. Topical phenytoin may be more effective than DuoDERM dressing, saline dressings and topical antibiotics for treating pressure ulcers [53].

### **13. Antimicrobials: systemic & topical**

#### **13.1. Systemic**

debridement is thought to be faster than autolytic debridement however it may cause increased wound pain and /or an uncomfortable burning sensation to the patient. Enzymatic debridement is most useful in patients who cannot tolerate sharp debridement and should not be used if an infection is present. Preparations available in the US include collagenase and

Maggot debridement therapy is the intentional application of live, "medical grade" fly larvae to wounds. Medicinal maggots have been sited to perform major actions such as debridement, disinfection, stimulation of wound healing as well as biofilm inhibition and eradication [39]. Larval debridement is unique in that maggots selectively only engulf necrotic tissue—no healthy tissue is affected. This method is gaining in popularity due to its low cost, incredible effectiveness and expedited time for successful debridement. Some patients however find the method somewhat painful and their perception of maggots may stand in the way of using this

When it comes to topical agents for pressure injuries the options are vast. Indications for specific topical agents can vary as the pressure stage progresses or the wound starts to heal. Antiseptic agents commonly used in wounds include: iodine (povidone, iodine or slow release cadexomer iodine), silver (silver sulfadiazine), polyhexanide and betaine (PHMB), chlorhexidine, sodium hypochlorite and acetic acid [25]. Topical antiseptics should be used for pressure ulcers that are not expected to heal, are critically colonized or topically infected. They should be used in conjunction with maintenance debridement. In managing biofilms, consider topical antiseptics to control bacterial bio-burden in wounds with

Be aware that some skin cleaners or antiseptics may destroy granulation tissue [10]. Avoid hydrogen peroxide as it is toxic to tissues even at low concentrations [40, 41]and should not be used as a preferred topical antiseptic. Its use should be completely avoided in cavity wounds

Iodine products should be avoided in patients with impaired renal failure, history of thyroid disorders or known iodine sensitivity [44, 45]. There is a risk of acidosis when acetic acid is used for extended periods over large wound surface areas [46]. Silver may have toxic properties, especially to keratinocytes and fibroblasts; the extent of the toxicities however, is not fully described. Topical silver products should not be used on individuals with silver sensitivities, and silver sulfadiazine products are not recommended for people with sulfur sensitivities [47]. It is however appropriate to consider using silver sulfadiazine in heavily contaminated or infected pressure ulcers until definitive debridement is accomplished. Sodium hypochlorite

due to the risk of surgical emphysema and gas embolus [28, 41–43].

papain/urea with or without chlorophyll [38].

**11.5. Larval therapy/Medicinal maggot therapy**

highly effective method of debridement [38].

**12. Topical agents**

130 Vignettes in Patient Safety - Volume 1

**12.1. Topical antiseptics**

delayed healing [25].

Consider a systemic antibiotic only if clinical signs of systemic infection are present or there is a positive blood culture, cellulitis, fasciitis, osteomyelitis, systemic inflammatory response syndrome (SIRS) or sepsis. If systemic antibiotics are given, empiric antibiotics should cover methicillin-resistant *Staphylococcus aureus*, *anaerobes*, *enterococci* and Gram-negatives such as *Pseudomonas*, *Proteus* and *Providencia* species [25].

#### **13.2. Topical**

There is insufficient evidence to support whether topical antimicrobials improve wound healing or reduce infection in patients with ≥Stage II pressure ulcers. Generally topical antibiotics are not recommended and should be limited or avoided if possible. Use is indicated in specific situations where the topical antibiotics' benefits outweigh the risks of antibiotic side effects and resistance. Consider topical Metronidazole for control of odor due to anaerobic bacteria and protozoal infections [25].

#### **13.3. Osteomyelitis & abscesses**

Osteomyelitis can be a detrimental finding in any patient thus rapid identification and treatment is necessary. If osteomyelitis is suspected in a patient's wound bed, obtain blood cultures and sensitivities, leukocyte count, erythrocyte sedimentation rate and a C-reactive protein level. Imaging should also be obtained. A plain X-ray is the initial imaging study of choice. Once osteomyelitis is confirmed, a CT scan is useful for needle guided biopsies, identifying necrotic bone and soft tissue extension. The gold standard test of choice for detection of early osteomyelitis and associated soft tissue disease is an MRI with gadolinium [25].

Cultures at the time of presentation or first debridement may not be useful. Swabbing cultures from draining wounds and sinus tracts may not be reliable for predicting organisms that will be isolated from infected bone, but might be helpful for infection control measures. Obtaining cultures of bone biopsies after an initial debridement is performed can be helpful in guiding therapy. Both aerobic and anaerobic cultures should be sent for culture; if within a few days there is no growth then fungal and mycobacterial cultures should be processed. Drain all local abscesses [25].

### **14. Types of wound dressings**

There are many factors to consider in choosing a wound dressing such as the ulcer size, depth and location, the ability to keep the wound bed moist, the need to address bacterial bio-burden, the nature and volume of wound exudate, the condition of the tissue in the ulcer bed, the condition of periulcer skin, the presence of tunneling and/or undermining as well as the goals of the individual with the pressure injury [25]. Ideally, one should choose a dressing that maintains a moist wound environment and controls exudate without desiccating the ulcer bed all while promoting wound healing. A moist wound environment physiologically favors migration and matrix formation while accelerating healing of wounds by promoting autolytic debridement [35]. It is also thought that moist wound healing reduces wound pain [35]. Keeping the wound environment clean may be a constant challenge especially when the ulcers are in unfavorable, not easily accessible locations however, any contaminated environment will make wound healing extremely difficult.

**14.2. Transparent film dressings**

**Figure 13.** Hydrocolloid dressings.

agents, gels, or ointments [25, 57].

friable skin in the periwound area.

**14.3. Hydrogel dressings**

Examples: 3 M Tegaderm, Mefilm [56] (**Figure 14**).

Transparent film dressings are semipermeable membranes, generally polyurethane, which are self-adhering, thin and waterproof. They allow gaseous exchange between the wound bed and the environment, but water, bacteria and other contaminants cannot penetrate the dressing. These dressings have a wide variety of uses because they are available in multiple shapes and sizes to conform to many different wounds. The transparency of the dressing allows for wound visualization, assessment of its healing progress and any drainage [25, 57]. Transparent film dressings are indicated for partial thickness wounds, Stage 2 ulcers and dry, necrotic wounds requiring debridement but should not be used in moderate to heavy exuding ulcers. These dressings help to maintain a moist wound surface and facilitate autolytic debridement. They should be avoided in immunocompromised individuals. They can be used as a secondary dressing with alginates or other wound fillers that will likely remain in the ulcer bed for 3 days or more however should not be used over enzymatic debriding

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Contraindications to transparent film dressing use include heavy exudating wounds, deep cavities, sinus tracts, undermining (unless used as a secondary dressing) and wounds with

Hydrogel dressings vary in composition but most are water or glycerin based, depending on the manufacturer and have a gel consistency. The non-occlusive dressing comes in sheets, beads, impregnated in gauze and in gel form. These dressings are indicated for shallow, minimally exuding pressure ulcers that are not clinically infected and are granulating. They may also be used on painful, dry wounds needing additional moisture such as burns and grafts because they will add additional moisture. These dressings work to provide moisture to a wound site while eliminating or preventing infection however their use is somewhat limited to dry and low exuding wounds because they can cause maceration to surrounding tissues when high volumes of the wound exudate is present [55, 58]. Hydrogel dressings work well on pressure injuries that have contours and/or on body areas that are at risk for wound

#### **14.1. Hydrocolloid dressings**

Hydrocolloid Dressings are a wafer-type dressing that contains hydro-active particles which, when in contact with wound exudate, forms a fluid/gel environment over the wound bed. Both occlusive and semi-occlusive dressings have been shown to provide and maintain a moist, hypoxic wound environment, provide protection and insulation to a healing wound and facilitate autolytic debridement [54, 55].

Hydrocolloid dressings can be self-adhering with a surface that repels water, bacteria and other outside contaminants. Various specific types of hydrocolloid dressings are on the market in sheet, paste, gel, and powder form. They may differ in size, shape, exudate absorption and intended use [55, 56]. Hydrocolloid Dressings are indicated for light to moderate exuding wounds, typically Stage 2 and shallow Stage 3 pressure injuries. They should be used in areas where they will not roll or melt. Filler dressings beneath hydrocolloid dressings can be used in deep ulcers in order to fill in the dead space. They can often be left on a wound for several days and can be used as a primary or secondary dressing [25, 57].

Contraindications to hydrocolloid dressing use include infected wounds, wounds with heavy exudate, deep cavities, sinus tracts (unless used as a secondary dressing over the packing), burns and grafts.

Examples: DuoDERM, Tegaderm Thin, Reliamed border sacral, Reliamed beveled, Flexicol bordered, Medihoney sheet (hydrocolloid with honey), Medihoney tube [57] (**Figure 13**).

**Figure 13.** Hydrocolloid dressings.

that will be isolated from infected bone, but might be helpful for infection control measures. Obtaining cultures of bone biopsies after an initial debridement is performed can be helpful in guiding therapy. Both aerobic and anaerobic cultures should be sent for culture; if within a few days there is no growth then fungal and mycobacterial cultures should be processed.

There are many factors to consider in choosing a wound dressing such as the ulcer size, depth and location, the ability to keep the wound bed moist, the need to address bacterial bio-burden, the nature and volume of wound exudate, the condition of the tissue in the ulcer bed, the condition of periulcer skin, the presence of tunneling and/or undermining as well as the goals of the individual with the pressure injury [25]. Ideally, one should choose a dressing that maintains a moist wound environment and controls exudate without desiccating the ulcer bed all while promoting wound healing. A moist wound environment physiologically favors migration and matrix formation while accelerating healing of wounds by promoting autolytic debridement [35]. It is also thought that moist wound healing reduces wound pain [35]. Keeping the wound environment clean may be a constant challenge especially when the ulcers are in unfavorable, not easily accessible locations however, any contaminated environ-

Hydrocolloid Dressings are a wafer-type dressing that contains hydro-active particles which, when in contact with wound exudate, forms a fluid/gel environment over the wound bed. Both occlusive and semi-occlusive dressings have been shown to provide and maintain a moist, hypoxic wound environment, provide protection and insulation to a healing wound

Hydrocolloid dressings can be self-adhering with a surface that repels water, bacteria and other outside contaminants. Various specific types of hydrocolloid dressings are on the market in sheet, paste, gel, and powder form. They may differ in size, shape, exudate absorption and intended use [55, 56]. Hydrocolloid Dressings are indicated for light to moderate exuding wounds, typically Stage 2 and shallow Stage 3 pressure injuries. They should be used in areas where they will not roll or melt. Filler dressings beneath hydrocolloid dressings can be used in deep ulcers in order to fill in the dead space. They can often be left on a wound for several

Contraindications to hydrocolloid dressing use include infected wounds, wounds with heavy exudate, deep cavities, sinus tracts (unless used as a secondary dressing over the packing),

Examples: DuoDERM, Tegaderm Thin, Reliamed border sacral, Reliamed beveled, Flexicol bordered, Medihoney sheet (hydrocolloid with honey), Medihoney tube [57] (**Figure 13**).

Drain all local abscesses [25].

132 Vignettes in Patient Safety - Volume 1

**14.1. Hydrocolloid dressings**

burns and grafts.

**14. Types of wound dressings**

ment will make wound healing extremely difficult.

and facilitate autolytic debridement [54, 55].

days and can be used as a primary or secondary dressing [25, 57].

#### **14.2. Transparent film dressings**

Transparent film dressings are semipermeable membranes, generally polyurethane, which are self-adhering, thin and waterproof. They allow gaseous exchange between the wound bed and the environment, but water, bacteria and other contaminants cannot penetrate the dressing. These dressings have a wide variety of uses because they are available in multiple shapes and sizes to conform to many different wounds. The transparency of the dressing allows for wound visualization, assessment of its healing progress and any drainage [25, 57]. Transparent film dressings are indicated for partial thickness wounds, Stage 2 ulcers and dry, necrotic wounds requiring debridement but should not be used in moderate to heavy exuding ulcers. These dressings help to maintain a moist wound surface and facilitate autolytic debridement. They should be avoided in immunocompromised individuals. They can be used as a secondary dressing with alginates or other wound fillers that will likely remain in the ulcer bed for 3 days or more however should not be used over enzymatic debriding agents, gels, or ointments [25, 57].

Contraindications to transparent film dressing use include heavy exudating wounds, deep cavities, sinus tracts, undermining (unless used as a secondary dressing) and wounds with friable skin in the periwound area.

Examples: 3 M Tegaderm, Mefilm [56] (**Figure 14**).

#### **14.3. Hydrogel dressings**

Hydrogel dressings vary in composition but most are water or glycerin based, depending on the manufacturer and have a gel consistency. The non-occlusive dressing comes in sheets, beads, impregnated in gauze and in gel form. These dressings are indicated for shallow, minimally exuding pressure ulcers that are not clinically infected and are granulating. They may also be used on painful, dry wounds needing additional moisture such as burns and grafts because they will add additional moisture. These dressings work to provide moisture to a wound site while eliminating or preventing infection however their use is somewhat limited to dry and low exuding wounds because they can cause maceration to surrounding tissues when high volumes of the wound exudate is present [55, 58]. Hydrogel dressings work well on pressure injuries that have contours and/or on body areas that are at risk for wound

Of note, this dressing also comes in a silver added form for antimicrobial benefits. The silver form is not to be used with hydrogels and should not be used with products that create an ionic exchange in the wound site. Alginate dressings cannot be used with enzymatic prod-

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Examples: Maxorb Extra AG, Silverlon CA, Algicel AG, Reliamed AG-CMC (hydrofiber) [57]

The NPUAP's guidelines recommends avoiding use of gauze dressings for open pressure ulcers that have been cleansed and debrided because they are labor-intensive, cause pain when removed if dry, and can lead to desiccation of viable tissue. The association also advocates against the use of wet-to-dry gauze dressings. Gauze dressing is an economical means of debridement that can be effective when preformed often and appropriately. While the initial cost of moist gauze is less expensive than more advanced wound care products, the notion that moist gauze is more cost effective than all other wound care options may not be entirely true. When determining cost efficacy, one must look at all factors involved in the wound healing process. In addition to the product cost, one must take into account health care provider time, patient care goals and resources, ease of use and healing rate [35]. Once all of these aspects are accurately accounted for, gauze may not be the most economical wound care supply. When other forms of moisture retentive dressings are not available, continually applying moist gauze is preferable to dry gauze. Dry gauze dressings should only be used as the cover dressing to reduce evaporation when the tissue interface layer is moist. Consider using impregnated forms of gauze to prevent evaporation of moisture from continuously moist

If gauze is to be applied as your wound dressing it is recommended that loosely woven gauze be used to treat highly exuding ulcers so that a high volume of the exudate may be absorbed.

ucts. (ex Santyl Collagenase)

**14.5. Gauze dressings/"Wet-to-Dry Gauze"**

**Figure 15.** Sheet & strip alginate wound dressings.

gauze dressings [25, 57].

**14.6. Recommended gauze application technique**

Example: Kerlix [57].

(**Figure 15**).

**Figure 14.** Transparent film dressings.

dressing migration. The sheet form of hydrogel can be used for hastier healing of cosmetic procedures and/or scar reduction. These dressings typically have to be changed daily but are biocompatible with other dressings [57].

There are no specific contraindications to hydrogel dressings, however there is a risk that when hydrogel dressings are used on exuding ischemic ulcers a resultant shift from dry to wet gangrene within the wound can take place [55, 59]. Also, because of the moist nature of these dressings, care must be taken to observe the wound edges and protect the skin from maceration.

Examples: Skintegrity, SpanGel, Normlgel [57].

Of note, Hydrogel dressings are also available with additives such as silver for antimicrobial benefits. However, Hydrogel Silver dressings should not be used in conjunction with Tegaderm Matrix as the deactivation of both dressings will result [25, 57].

#### **14.4. Alginate dressings**

Alginate dressings are hydrophilic, non-woven fiber dressings that are derived from brown seaweed [55]. When the dressing contacts a wound's exudate it forms a gel mass in the wound. Alginate comes in a sheet or rope form and is absorbent. The dressing will absorb excess exudate while maintaining a moist wound environment. It facilitates autolytic debridement of loose, necrotic tissue and is indicated for partial thickness and full thickness wounds having moderate to heavy exudate. It is effective in filling cavities, tracts and undermining. A secondary dressing should be used to cover the alginate dressing. Irrigation will aid in its removal from the wound bed. Consider lengthening the interval between wound dressing changes or changing the type of wound dressing if the alginate dressing is still dry at the scheduled time for a dressing change. Alginate dressings are contraindicated in dry wounds [25, 57].

Examples: Maxorb, Algicel, Melgisorb, Reliamed, Sorbion Sachet S [57].

Of note, this dressing also comes in a silver added form for antimicrobial benefits. The silver form is not to be used with hydrogels and should not be used with products that create an ionic exchange in the wound site. Alginate dressings cannot be used with enzymatic products. (ex Santyl Collagenase)

Examples: Maxorb Extra AG, Silverlon CA, Algicel AG, Reliamed AG-CMC (hydrofiber) [57] (**Figure 15**).

**Figure 15.** Sheet & strip alginate wound dressings.

dressing migration. The sheet form of hydrogel can be used for hastier healing of cosmetic procedures and/or scar reduction. These dressings typically have to be changed daily but are

There are no specific contraindications to hydrogel dressings, however there is a risk that when hydrogel dressings are used on exuding ischemic ulcers a resultant shift from dry to wet gangrene within the wound can take place [55, 59]. Also, because of the moist nature of these dressings, care must be taken to observe the wound edges and protect the skin from

Of note, Hydrogel dressings are also available with additives such as silver for antimicrobial benefits. However, Hydrogel Silver dressings should not be used in conjunction with

Alginate dressings are hydrophilic, non-woven fiber dressings that are derived from brown seaweed [55]. When the dressing contacts a wound's exudate it forms a gel mass in the wound. Alginate comes in a sheet or rope form and is absorbent. The dressing will absorb excess exudate while maintaining a moist wound environment. It facilitates autolytic debridement of loose, necrotic tissue and is indicated for partial thickness and full thickness wounds having moderate to heavy exudate. It is effective in filling cavities, tracts and undermining. A secondary dressing should be used to cover the alginate dressing. Irrigation will aid in its removal from the wound bed. Consider lengthening the interval between wound dressing changes or changing the type of wound dressing if the alginate dressing is still dry at the scheduled time

for a dressing change. Alginate dressings are contraindicated in dry wounds [25, 57].

Examples: Maxorb, Algicel, Melgisorb, Reliamed, Sorbion Sachet S [57].

Tegaderm Matrix as the deactivation of both dressings will result [25, 57].

biocompatible with other dressings [57].

**Figure 14.** Transparent film dressings.

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Examples: Skintegrity, SpanGel, Normlgel [57].

maceration.

**14.4. Alginate dressings**

#### **14.5. Gauze dressings/"Wet-to-Dry Gauze"**

The NPUAP's guidelines recommends avoiding use of gauze dressings for open pressure ulcers that have been cleansed and debrided because they are labor-intensive, cause pain when removed if dry, and can lead to desiccation of viable tissue. The association also advocates against the use of wet-to-dry gauze dressings. Gauze dressing is an economical means of debridement that can be effective when preformed often and appropriately. While the initial cost of moist gauze is less expensive than more advanced wound care products, the notion that moist gauze is more cost effective than all other wound care options may not be entirely true. When determining cost efficacy, one must look at all factors involved in the wound healing process. In addition to the product cost, one must take into account health care provider time, patient care goals and resources, ease of use and healing rate [35]. Once all of these aspects are accurately accounted for, gauze may not be the most economical wound care supply. When other forms of moisture retentive dressings are not available, continually applying moist gauze is preferable to dry gauze. Dry gauze dressings should only be used as the cover dressing to reduce evaporation when the tissue interface layer is moist. Consider using impregnated forms of gauze to prevent evaporation of moisture from continuously moist gauze dressings [25, 57].

Example: Kerlix [57].

#### **14.6. Recommended gauze application technique**

If gauze is to be applied as your wound dressing it is recommended that loosely woven gauze be used to treat highly exuding ulcers so that a high volume of the exudate may be absorbed. Tightly woven gauze should be used for minimally exuding ulcers. Loosely fill ulcers with large tissue defects and dead space with salinemoistened gauze when other form of moisture retentive dressings are not available; this technique is preferred over tightly packing the wound which can lead to excessive pressure on the ulcer bed. Change gauze packing often enough to manage the exudate. It is preferable to use a single gauze strip or roll to fill deep ulcers rather than using multiple gauze dressings; as this will reduce the risk of retained gauze in the ulcer bed, which can serve as a nidus for infection [25].

has thermal insulation and protection properties. Removal of the foam often facilitates the removal of slough. Foam may be used as a primary or secondary dressing and is available in self-adhering or non-adherent forms although some may have adhesive border. Foam dressings are indicated for partial and full thickness wounds with moderate to heavy exudate. They also can be used to cover wounds containing packing material. Contraindications to its use are wounds with dry eschar as well as wounds with minimal to no exudate [25, 57].

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Examples: Mepilex (with Safetac technology), Mepilex Border (water resistant with Safetac

One can consider using silver-impregnated dressings for pressure ulcers that are clinically infected, heavily colonized or at high risk of infection. Prolonged use of silver-impregnated dressings should be avoided and silver dressings should be discontinued once the wound infection is controlled. As mentioned earlier, silver may have toxic properties but it is

Use of medical-grade honey as well honey impregnated dressings has been used in heavily contaminated or infected pressure ulcers. Honey impregnated dressings have been used on Stage 2 and 3 pressure ulcers until definitive debridement is accomplished. Before applying a honey dressing, ensure the individual is not allergic to honey. Individuals who have bee or

Consider using cadexomer iodine dressings in moderate to highly exuding pressure ulcers. Iodine products should be avoided in individuals with impaired renal failure, history of thyroid disorders or known iodine sensitivity [44, 45]. Iodine dressings are not recommended for individuals taking lithium or for pregnant or breast-feeding women. The risk of systemic absorption increases when iodine products are used on larger, deeper wounds or for prolonged periods of time. Iodine toxicity has been reported in a few case studies, especially in

Consider using platelet-derived growth factors for treatment of Stage 3 and 4 pressure ulcers

that have delayed healing. (Refer to topical agents section for more information) [25].

bee stings allergies are usually able to use properly irradiated honey products [25].

those individuals with large wounds, in whom dressings were changed often [25].

technology), Tegaderm foam, Polymem, Polymem Dot (with silver) [57].

**15. Special dressings**

**15.1. Silver-impregnated dressings**

unknown to what extent [25].

**15.2. Honey impregnated dressings**

**15.3. Cadexomer iodine dressings**

**16. Biologic dressings**

**16.1. Recombinant platelet-derived growth factor**

#### **14.7. Collagen matrix dressings**

A collagen matrix dressing is a naturally derived scaffold dressing. Scaffolds facilitate infiltration of cells such as fibroblasts and keratinocytes through pores of a controllable size while maintaining optimal healing conditions [55]. Ideally, a dermal scaffold mimics the tissue's natural extracellular matrix, allowing bioactive molecules to be incorporated while also being biocompatible [55]. Collagen matrix dressings are used for nonhealing Stage 3 and 4 pressure wounds. These dressings come in pads, gels or particles and promote the deposit of newly formed collagen into the wound bed. They can be used on any type of wound with minimal, moderate or heavy drainage. Some specific brands require the wound to be free of necrotic tissue but not all. The collagen provides a moist healing environment and promotes tissue granulation and epithelialization. Some brands reduce destructive elements within wound fluid to trigger healing while allowing the patient's growth factors to effectively heal the wound. No specific contraindications exist however, collagen may enable the transmission of infectious agents and thus it requires vigorous disinfection protocols [55, 57].

Examples: Pads—Prisma, Promogran (collagen with silver), BioPad, Fibracol Plus (alginate/ collagen combination); Gel—Stimulen Gel; Powder—Stimulen [57].

#### **14.8. Silicone dressings**

Silicone dressings can be considered as a wound contact layer to promote atraumatic dressing changes or as the contact layer within a dressing, for example, Mepilex, a polyurethane foam membrane is coated with a soft silicone layer [55, 60]. Consider silicone dressings to prevent periwound tissue injury when the surrounding tissue is fragile or friable. Silicone can be used on a range of acute and chronic wounds as it is incorporated in many different bandaging strategies [55, 57].

Examples: Mepitel, Mepliex Ag [57].

#### **14.9. Foam dressings**

Polyurethane foam dressings have an absorbent wound contact surface and typically also a moisture-repellant outer surface, which is non-occlusive. Polyurethane foam dressings are easy to use and customize as they can be cut to shape and come in a range of absorbencies [55]. Foam's ability to absorb exudate is dependent upon the thickness and density of the dressing. Foam dressings are designed to maintain a moist wound environment but absorb excess exudate thereby preventing maceration of the surrounding healthy tissue. Foam also has thermal insulation and protection properties. Removal of the foam often facilitates the removal of slough. Foam may be used as a primary or secondary dressing and is available in self-adhering or non-adherent forms although some may have adhesive border. Foam dressings are indicated for partial and full thickness wounds with moderate to heavy exudate. They also can be used to cover wounds containing packing material. Contraindications to its use are wounds with dry eschar as well as wounds with minimal to no exudate [25, 57].

Examples: Mepilex (with Safetac technology), Mepilex Border (water resistant with Safetac technology), Tegaderm foam, Polymem, Polymem Dot (with silver) [57].

#### **15. Special dressings**

Tightly woven gauze should be used for minimally exuding ulcers. Loosely fill ulcers with large tissue defects and dead space with salinemoistened gauze when other form of moisture retentive dressings are not available; this technique is preferred over tightly packing the wound which can lead to excessive pressure on the ulcer bed. Change gauze packing often enough to manage the exudate. It is preferable to use a single gauze strip or roll to fill deep ulcers rather than using multiple gauze dressings; as this will reduce the risk of retained

A collagen matrix dressing is a naturally derived scaffold dressing. Scaffolds facilitate infiltration of cells such as fibroblasts and keratinocytes through pores of a controllable size while maintaining optimal healing conditions [55]. Ideally, a dermal scaffold mimics the tissue's natural extracellular matrix, allowing bioactive molecules to be incorporated while also being biocompatible [55]. Collagen matrix dressings are used for nonhealing Stage 3 and 4 pressure wounds. These dressings come in pads, gels or particles and promote the deposit of newly formed collagen into the wound bed. They can be used on any type of wound with minimal, moderate or heavy drainage. Some specific brands require the wound to be free of necrotic tissue but not all. The collagen provides a moist healing environment and promotes tissue granulation and epithelialization. Some brands reduce destructive elements within wound fluid to trigger healing while allowing the patient's growth factors to effectively heal the wound. No specific contraindications exist however, collagen may enable the transmission of infectious agents and thus it requires vigorous

Examples: Pads—Prisma, Promogran (collagen with silver), BioPad, Fibracol Plus (alginate/

Silicone dressings can be considered as a wound contact layer to promote atraumatic dressing changes or as the contact layer within a dressing, for example, Mepilex, a polyurethane foam membrane is coated with a soft silicone layer [55, 60]. Consider silicone dressings to prevent periwound tissue injury when the surrounding tissue is fragile or friable. Silicone can be used on a range of acute and chronic wounds as it is incorporated in many different bandaging

Polyurethane foam dressings have an absorbent wound contact surface and typically also a moisture-repellant outer surface, which is non-occlusive. Polyurethane foam dressings are easy to use and customize as they can be cut to shape and come in a range of absorbencies [55]. Foam's ability to absorb exudate is dependent upon the thickness and density of the dressing. Foam dressings are designed to maintain a moist wound environment but absorb excess exudate thereby preventing maceration of the surrounding healthy tissue. Foam also

gauze in the ulcer bed, which can serve as a nidus for infection [25].

collagen combination); Gel—Stimulen Gel; Powder—Stimulen [57].

**14.7. Collagen matrix dressings**

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disinfection protocols [55, 57].

**14.8. Silicone dressings**

strategies [55, 57].

**14.9. Foam dressings**

Examples: Mepitel, Mepliex Ag [57].

#### **15.1. Silver-impregnated dressings**

One can consider using silver-impregnated dressings for pressure ulcers that are clinically infected, heavily colonized or at high risk of infection. Prolonged use of silver-impregnated dressings should be avoided and silver dressings should be discontinued once the wound infection is controlled. As mentioned earlier, silver may have toxic properties but it is unknown to what extent [25].

#### **15.2. Honey impregnated dressings**

Use of medical-grade honey as well honey impregnated dressings has been used in heavily contaminated or infected pressure ulcers. Honey impregnated dressings have been used on Stage 2 and 3 pressure ulcers until definitive debridement is accomplished. Before applying a honey dressing, ensure the individual is not allergic to honey. Individuals who have bee or bee stings allergies are usually able to use properly irradiated honey products [25].

#### **15.3. Cadexomer iodine dressings**

Consider using cadexomer iodine dressings in moderate to highly exuding pressure ulcers. Iodine products should be avoided in individuals with impaired renal failure, history of thyroid disorders or known iodine sensitivity [44, 45]. Iodine dressings are not recommended for individuals taking lithium or for pregnant or breast-feeding women. The risk of systemic absorption increases when iodine products are used on larger, deeper wounds or for prolonged periods of time. Iodine toxicity has been reported in a few case studies, especially in those individuals with large wounds, in whom dressings were changed often [25].

#### **16. Biologic dressings**

#### **16.1. Recombinant platelet-derived growth factor**

Consider using platelet-derived growth factors for treatment of Stage 3 and 4 pressure ulcers that have delayed healing. (Refer to topical agents section for more information) [25].

#### **16.2. Other growth factors**

Due to insufficient evidence to support or refute the use of growth factors (other than recombinant platelet-derived growth factor) in the treatment of pressure ulcers, they are not recommended for routine use at this time by the NPUAP guidelines [25].

use of HBOT as well as topical oxygen therapy in the treatment of pressure ulcers, these forms of oxygen therapy are not recommended for routine use according to the NPUAP guidelines

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Repositioning & offloading techniques as well as early mobilization are extremely important in the prevention and treatment of pressure ulcers. Repositioning so that pressure is relieved or redistributed will reduce the duration and magnitude of pressure over vulnerable areas of the body. All individuals at risk of or with existing pressure ulcers, should be repositioned often unless contraindicated; this will contribute to comfort, hygiene, dignity, and functional ability. Inspect the skin for changes and any new or developing transformations at every position. Frequent assessment will allow for early identification of signs of pressure damage such

If skin changes occur or the individual is not responding as expected to the repositioning regime then the frequency, method and technique of repositioning should be reassessed. Controlling the patients positioning contributes to maintenance of capillary circulation [62]. One should avoid positioning the patient on bony prominences with existing non-blanchable erythema as the pressure and/or shearing forces sustained will further occlude the blood supply to the skin, worsen the damage and result in more severe pressure ulceration [25].

Safe manual handling techniques should be utilized to ensure the safety of both the patient and the health professional. Use simple, manual handling aids such as lift sheets to help reduce friction and shear. Lift—do not drag the patient when repositioning. Do not leave moving equipment under the patient after use, unless the equipment is specifically designed for that purpose. Avoid positioning patients directly onto medical devices, such as tubes, drainage systems or other foreign objects. Patients should not be left on a bedpan longer than

The frequency of repositioning will vary from patient to patient. Pay close attention and consider the patient's tissue tolerance, level of activity and mobility, general medical condition, overall treatment objectives, skin condition, and comfort when determining a patient's frequency of off loading. While medical professionals primarily aid in repositioning, the patient and his/her family should be educated and taught pressure-relieving maneuvers to do them-

Position patients in the 30–40° tilted side-lying position (alternating, right side, back, left side) or the prone position if tolerable. Encourage patients who can reposition themselves to sleep

at this time [25].

**18. Physical treatment tactics**

as non-blanchable erythema [25].

necessary [25].

**18.2. Repositioning frequency**

selves throughout the day [25].

**18.3. Repositioning individuals in bed**

**18.1. Repositioning & offloading techniques**

#### **17. Biophysical agents**

A number of biophysical agents have been studied in the management of pressure ulcers. All provide some form of biophysical energy with the goal of promoting healing. Common forms of biophysical agents include energy from the electromagnetic spectrum (e.g., electrical stimulation, electromagnetic fields, pulsed radio frequency energy and phototherapy), acoustic energy (high and low frequency ultrasound) and mechanical energy (e.g., heric energy [hyperbaric and topical oxygen]) [25]. Many of the above mentioned biophysical agents are uncommon and are out of the chapter's scope of coverage. Only commonly used biophysical agents will be addressed.

#### **17.1. Mechanical energy—negative pressure wound therapy (NWPT)**

Consider negative pressure wound therapy (NWPT) as an early adjuvant for the treatment of deep, Stage 3 and 4 pressure ulcers. NWPT is not recommended in inadequately debrided, necrotic or malignant wounds; where vital organs are exposed; in wounds with no exudate, or in individuals with untreated coagulopathy, osteomyelitis or local or systemic clinical infection. Cautious use by an experienced health professional is recommended for individuals on anticoagulant therapy; in actively bleeding wounds; or when the wound is in close proximity to major blood vessels [25, 61]. Debride the pressure ulcer of necrotic tissue prior to the use of NPWT. Follow a safe regimen in applying and removing the NPWT system and evaluate the pressure ulcer with each dressing change. The optimal dressing change interval has not been well established, and should be based on characteristics of the individual and the wound. If pain is anticipated or reported consider tactics such as placing a nonadherent interface dressing on the wound bed, underneath the foam, lowering the level of pressure, changing the type of pressure (continuous or intermittent), and/or using a moist gauze filler instead of foam [25].

#### **17.2. Kinetic energy—hydrotherapy—pulsatile lavage with/without suction**

Refer to Debridement section 11 for more information

#### **17.3. Kinetic energy—hydrotherapy—whirlpool**

Refer to Debridement section 11 for more information

#### **17.4. Atmospheric energy—oxygen**

Hyperbaric oxygen therapy (HBOT) and topical oxygen therapy can both be used in the treatment of chronic wounds. Due to an insufficient amount of evidence to support or refute the use of HBOT as well as topical oxygen therapy in the treatment of pressure ulcers, these forms of oxygen therapy are not recommended for routine use according to the NPUAP guidelines at this time [25].

#### **18. Physical treatment tactics**

**16.2. Other growth factors**

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**17. Biophysical agents**

agents will be addressed.

Due to insufficient evidence to support or refute the use of growth factors (other than recombinant platelet-derived growth factor) in the treatment of pressure ulcers, they are not recom-

A number of biophysical agents have been studied in the management of pressure ulcers. All provide some form of biophysical energy with the goal of promoting healing. Common forms of biophysical agents include energy from the electromagnetic spectrum (e.g., electrical stimulation, electromagnetic fields, pulsed radio frequency energy and phototherapy), acoustic energy (high and low frequency ultrasound) and mechanical energy (e.g., heric energy [hyperbaric and topical oxygen]) [25]. Many of the above mentioned biophysical agents are uncommon and are out of the chapter's scope of coverage. Only commonly used biophysical

Consider negative pressure wound therapy (NWPT) as an early adjuvant for the treatment of deep, Stage 3 and 4 pressure ulcers. NWPT is not recommended in inadequately debrided, necrotic or malignant wounds; where vital organs are exposed; in wounds with no exudate, or in individuals with untreated coagulopathy, osteomyelitis or local or systemic clinical infection. Cautious use by an experienced health professional is recommended for individuals on anticoagulant therapy; in actively bleeding wounds; or when the wound is in close proximity to major blood vessels [25, 61]. Debride the pressure ulcer of necrotic tissue prior to the use of NPWT. Follow a safe regimen in applying and removing the NPWT system and evaluate the pressure ulcer with each dressing change. The optimal dressing change interval has not been well established, and should be based on characteristics of the individual and the wound. If pain is anticipated or reported consider tactics such as placing a nonadherent interface dressing on the wound bed, underneath the foam, lowering the level of pressure, changing the type of pressure (continuous or intermittent), and/or using a moist gauze filler instead of foam [25].

mended for routine use at this time by the NPUAP guidelines [25].

**17.1. Mechanical energy—negative pressure wound therapy (NWPT)**

**17.2. Kinetic energy—hydrotherapy—pulsatile lavage with/without suction**

Hyperbaric oxygen therapy (HBOT) and topical oxygen therapy can both be used in the treatment of chronic wounds. Due to an insufficient amount of evidence to support or refute the

Refer to Debridement section 11 for more information

Refer to Debridement section 11 for more information

**17.3. Kinetic energy—hydrotherapy—whirlpool**

**17.4. Atmospheric energy—oxygen**

#### **18.1. Repositioning & offloading techniques**

Repositioning & offloading techniques as well as early mobilization are extremely important in the prevention and treatment of pressure ulcers. Repositioning so that pressure is relieved or redistributed will reduce the duration and magnitude of pressure over vulnerable areas of the body. All individuals at risk of or with existing pressure ulcers, should be repositioned often unless contraindicated; this will contribute to comfort, hygiene, dignity, and functional ability. Inspect the skin for changes and any new or developing transformations at every position. Frequent assessment will allow for early identification of signs of pressure damage such as non-blanchable erythema [25].

If skin changes occur or the individual is not responding as expected to the repositioning regime then the frequency, method and technique of repositioning should be reassessed. Controlling the patients positioning contributes to maintenance of capillary circulation [62]. One should avoid positioning the patient on bony prominences with existing non-blanchable erythema as the pressure and/or shearing forces sustained will further occlude the blood supply to the skin, worsen the damage and result in more severe pressure ulceration [25].

Safe manual handling techniques should be utilized to ensure the safety of both the patient and the health professional. Use simple, manual handling aids such as lift sheets to help reduce friction and shear. Lift—do not drag the patient when repositioning. Do not leave moving equipment under the patient after use, unless the equipment is specifically designed for that purpose. Avoid positioning patients directly onto medical devices, such as tubes, drainage systems or other foreign objects. Patients should not be left on a bedpan longer than necessary [25].

#### **18.2. Repositioning frequency**

The frequency of repositioning will vary from patient to patient. Pay close attention and consider the patient's tissue tolerance, level of activity and mobility, general medical condition, overall treatment objectives, skin condition, and comfort when determining a patient's frequency of off loading. While medical professionals primarily aid in repositioning, the patient and his/her family should be educated and taught pressure-relieving maneuvers to do themselves throughout the day [25].

#### **18.3. Repositioning individuals in bed**

Position patients in the 30–40° tilted side-lying position (alternating, right side, back, left side) or the prone position if tolerable. Encourage patients who can reposition themselves to sleep in a 30–40° side-lying position. It is best to place the hip joint in the neutral position when the legs are in contact with the bed in order to distribute the pressure over the greater trochanter in the 30–40° laterally inclined positions. The 40° laterally inclined positioned has been shown to have lower average sacral peak pressure index (PPI) than the 30° (15 mmHg versus 20 mmHg) and should be strived for in patients with sacral pressure ulcers [63] (**Figures 16** and **17**).

Individuals should be positioned and supported to prevent sliding down in bed. If sitting in bed is necessary; avoid head-of-bed elevation or a slouched position that places pressure and shear on the sacrum and coccyx. Avoid lying postures that increase pressure, such as the 90° side-lying position, or the semi- recumbent position. Limit the head-of-bed elevation to 30° for an individual on bed rest unless it is contraindicated by medical condition or feeding and digestive considerations. Elevating the head of the bed may be medically necessary to facilitate breathing and/or prevent aspiration and ventilator associated pneumonia; in these cases the semi-Fowler's position is preferred [25, 64].

#### **18.4. Prone**

Use a pressure redistribution surface to off load pressure points on the face and body while in the prone position. At each rotation, assess other body areas (e.g., breasts, knees, toes, penis, clavicles, iliac crest, pubic symphysis) that may be at risk of bearing excessive pressure [25].

**Figure 17.** Turning and repositioning.

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**Figure 16.** 30°–40° side-lying position.

in a 30–40° side-lying position. It is best to place the hip joint in the neutral position when the legs are in contact with the bed in order to distribute the pressure over the greater trochanter in the 30–40° laterally inclined positions. The 40° laterally inclined positioned has been shown to have lower average sacral peak pressure index (PPI) than the 30° (15 mmHg versus 20 mmHg) and should be strived for in patients with sacral pressure ulcers [63] (**Figures 16** and **17**).

Individuals should be positioned and supported to prevent sliding down in bed. If sitting in bed is necessary; avoid head-of-bed elevation or a slouched position that places pressure and shear on the sacrum and coccyx. Avoid lying postures that increase pressure, such as the 90° side-lying position, or the semi- recumbent position. Limit the head-of-bed elevation to 30° for an individual on bed rest unless it is contraindicated by medical condition or feeding and digestive considerations. Elevating the head of the bed may be medically necessary to facilitate breathing and/or prevent aspiration and ventilator associated pneumonia; in these cases

Use a pressure redistribution surface to off load pressure points on the face and body while in the prone position. At each rotation, assess other body areas (e.g., breasts, knees, toes, penis, clavicles, iliac crest, pubic symphysis) that may be at risk of bearing excessive pressure [25].

the semi-Fowler's position is preferred [25, 64].

**18.4. Prone**

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**Figure 16.** 30°–40° side-lying position.

**Figure 17.** Turning and repositioning.

#### **18.5. Repositioning seated individuals**

Select a seated posture with an appropriate seat-to- floor height for the individual to avoid shear and friction. The seat should minimize pressure and shear exerted on the skin and soft tissues. Provide adequate seat tilt to prevent sliding forward in the wheelchair or chair, and adjust the footrests and armrests to maintain proper posture and pressure redistribution. Ensure that the feet are properly supported either directly on the floor, on a footstool, or on footrests when sitting upright in a chair or wheelchair. If the individual's feet cannot be positioned directly on the ground, footrest height should be adjusted so as to slightly tilt the pelvis forward by positioning the thighs slightly lower than horizontally. Limit the time an individual spends seated in a chair without pressure relief. One should limit sitting to ≤3 times a day and for ≤1 h each sitting period [25].

and a safe location for the pump/motor, including its ventilation. Proper selection and operation of support surfaces is the key to preventing complications. Repositioning is still required for pres-

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Pressure redistributing support surfaces are designed to either increase the body surface area that comes in contact with the support surface in order to reduce interface pressure or to sequentially alter the parts of the body that bear load, thus reducing the duration of loading at any given anatomical site. These support surfaces are especially helpful when frequent manual repositioning is not possible such as in morbidly obese patients. Describing the specifications of various mattresses and support surfaces is beyond the scope of this chapter however in general, one should use a high-specification reactive foam mattress rather than a non-high specification reactive foam mattress for all individuals assessed as being at risk for pressure

When pressure ulcers deteriorate or fail to heal, the clinician should consider replacing the existing support surface with one that will provide a properly matched support surface environment in terms of pressure, shear, and microclimate for the individual. Changing the support surface is only one of several strategies to consider. More frequent repositioning, preventive interventions and local wound care should also be intensified as needed. For all practical purposes, evolving deep tissue injury should be provided the same level of pressure redistribution as a Stage 3 or 4 pressure ulcer. Off loading and pressure redistribution may allow reperfusion of ischemic and injured tissue, limiting the extent of infarcted or dead tissue. Once the ulcer has fully evolved, the need for a support surface can be re-evaluated [25].

Individualize the selection of a seating support surface for posture and pressure redistribution with consideration to body size and configuration; the effects of posture and deformity on pressure distribution; mobility and lifestyle needs. Select a stretchable/breathable cushion cover that fits loosely on the top surface of the cushion and is capable of conforming to the patient's body contours. A tight, non-stretch cover will adversely affect cushion performance. Assess the cushion and cover for heat dissipation. Select a cushion and cover that permit air exchange to minimize temperature and moisture at the buttock interface. Provide complete and accurate training on use and maintenance of seating support surfaces, including wheelchairs and cushion devices delivered to the individual. If the patient already has an existing pressure injury, select a cushion that effectively redistributes the pressure away from the pressure ulcer [25].

Pressure injuries are difficult to resolve. After 6 months of appropriate treatment the rates of healing are >70% for Stage 2 ulcers, 50% for Stage 3 ulcers and 30% for Stage 4 ulcers [10]. In general, healing time increases with ulcer size. Therefore, it is extremely important to identify

**19.3. General recommendations on seating support surfaces**

**20. Rates of healing, prognosis & surgery**

sure relief and comfort when a support surface is used but typically not as often [25].

**19.2. Mattress and bed support surfaces**

ulcer development [25].

#### **18.6. Recommendations for individuals with existing pressure ulcers**

One should not be positioned directly on a pressure ulcer or on area(s) of suspected deep tissue injury with intact skin because pressure reduces perfusion to the injured tissue. Continued pressure on an existing pressure ulcer will delay healing and may cause additional deterioration. If repositioning cannot relieve pressure over the area, select an appropriate support surface and continue to turn and reposition the patient. Inspect the skin for additional damage each time the individual is turned or repositioned. Do not turn the individual onto a body surface that is damaged or still reddened from a previous episode of pressure loading, especially if the area of redness does not blanch. Ongoing assessment of the skin is necessary in order to detect additional skin damage.

#### **19. Relieving devices/support surfaces for pressure injury prevention**

Regular positioning is not possible for some individuals because of their medical condition, body habitus, etc. thus alternative prevention strategies such as providing a high-specification mattress or bed may need to be considered. Relieving devices or support surfaces play a major role in reducing compression on dependent tissue & preventing additional breakdown. Certain devices such as mattresses, integrated bed systems, mattress replacements, overlays, seat cushions, and seat cushion overlays have the ability to redistribute pressure for more effective tissue management and can serve other therapeutic functions as well [25].

#### **19.1. General recommendations for mattress and bed support surfaces**

Select a support surface that meets the individual's needs. Consider the individual's need for pressure redistribution based on the level of immobility and inactivity, the need for microclimate control, shear reduction, the size and weight of the individual, the risk for development of new pressure ulcers, and the number, severity, and location of existing pressure ulcer(s) [25].

Choose a support surface that is compatible with the care setting. Consider the weight of the bed, the structure of the building, the width of doors, the availability of uninterrupted electrical power, and a safe location for the pump/motor, including its ventilation. Proper selection and operation of support surfaces is the key to preventing complications. Repositioning is still required for pressure relief and comfort when a support surface is used but typically not as often [25].

#### **19.2. Mattress and bed support surfaces**

**18.5. Repositioning seated individuals**

142 Vignettes in Patient Safety - Volume 1

times a day and for ≤1 h each sitting period [25].

order to detect additional skin damage.

**18.6. Recommendations for individuals with existing pressure ulcers**

Select a seated posture with an appropriate seat-to- floor height for the individual to avoid shear and friction. The seat should minimize pressure and shear exerted on the skin and soft tissues. Provide adequate seat tilt to prevent sliding forward in the wheelchair or chair, and adjust the footrests and armrests to maintain proper posture and pressure redistribution. Ensure that the feet are properly supported either directly on the floor, on a footstool, or on footrests when sitting upright in a chair or wheelchair. If the individual's feet cannot be positioned directly on the ground, footrest height should be adjusted so as to slightly tilt the pelvis forward by positioning the thighs slightly lower than horizontally. Limit the time an individual spends seated in a chair without pressure relief. One should limit sitting to ≤3

One should not be positioned directly on a pressure ulcer or on area(s) of suspected deep tissue injury with intact skin because pressure reduces perfusion to the injured tissue. Continued pressure on an existing pressure ulcer will delay healing and may cause additional deterioration. If repositioning cannot relieve pressure over the area, select an appropriate support surface and continue to turn and reposition the patient. Inspect the skin for additional damage each time the individual is turned or repositioned. Do not turn the individual onto a body surface that is damaged or still reddened from a previous episode of pressure loading, especially if the area of redness does not blanch. Ongoing assessment of the skin is necessary in

**19. Relieving devices/support surfaces for pressure injury prevention**

effective tissue management and can serve other therapeutic functions as well [25].

**19.1. General recommendations for mattress and bed support surfaces**

Regular positioning is not possible for some individuals because of their medical condition, body habitus, etc. thus alternative prevention strategies such as providing a high-specification mattress or bed may need to be considered. Relieving devices or support surfaces play a major role in reducing compression on dependent tissue & preventing additional breakdown. Certain devices such as mattresses, integrated bed systems, mattress replacements, overlays, seat cushions, and seat cushion overlays have the ability to redistribute pressure for more

Select a support surface that meets the individual's needs. Consider the individual's need for pressure redistribution based on the level of immobility and inactivity, the need for microclimate control, shear reduction, the size and weight of the individual, the risk for development of new pressure ulcers, and the number, severity, and location of existing pressure ulcer(s) [25]. Choose a support surface that is compatible with the care setting. Consider the weight of the bed, the structure of the building, the width of doors, the availability of uninterrupted electrical power, Pressure redistributing support surfaces are designed to either increase the body surface area that comes in contact with the support surface in order to reduce interface pressure or to sequentially alter the parts of the body that bear load, thus reducing the duration of loading at any given anatomical site. These support surfaces are especially helpful when frequent manual repositioning is not possible such as in morbidly obese patients. Describing the specifications of various mattresses and support surfaces is beyond the scope of this chapter however in general, one should use a high-specification reactive foam mattress rather than a non-high specification reactive foam mattress for all individuals assessed as being at risk for pressure ulcer development [25].

When pressure ulcers deteriorate or fail to heal, the clinician should consider replacing the existing support surface with one that will provide a properly matched support surface environment in terms of pressure, shear, and microclimate for the individual. Changing the support surface is only one of several strategies to consider. More frequent repositioning, preventive interventions and local wound care should also be intensified as needed. For all practical purposes, evolving deep tissue injury should be provided the same level of pressure redistribution as a Stage 3 or 4 pressure ulcer. Off loading and pressure redistribution may allow reperfusion of ischemic and injured tissue, limiting the extent of infarcted or dead tissue. Once the ulcer has fully evolved, the need for a support surface can be re-evaluated [25].

#### **19.3. General recommendations on seating support surfaces**

Individualize the selection of a seating support surface for posture and pressure redistribution with consideration to body size and configuration; the effects of posture and deformity on pressure distribution; mobility and lifestyle needs. Select a stretchable/breathable cushion cover that fits loosely on the top surface of the cushion and is capable of conforming to the patient's body contours. A tight, non-stretch cover will adversely affect cushion performance. Assess the cushion and cover for heat dissipation. Select a cushion and cover that permit air exchange to minimize temperature and moisture at the buttock interface. Provide complete and accurate training on use and maintenance of seating support surfaces, including wheelchairs and cushion devices delivered to the individual. If the patient already has an existing pressure injury, select a cushion that effectively redistributes the pressure away from the pressure ulcer [25].

#### **20. Rates of healing, prognosis & surgery**

Pressure injuries are difficult to resolve. After 6 months of appropriate treatment the rates of healing are >70% for Stage 2 ulcers, 50% for Stage 3 ulcers and 30% for Stage 4 ulcers [10]. In general, healing time increases with ulcer size. Therefore, it is extremely important to identify and start treating pressure injuries as soon as they are discovered to avoid problems and complications as time progresses. Overall median time to heal an ulcer has been cited as 46 days, 33 median days to heal small ≤ 1 cm<sup>2</sup> ulcers, 53 days to heal medium, >1 to ≤4 cm<sup>2</sup> ulcers and 73 days for large ulcers >4 cm2 [65].

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[10] Bluestein D, Javaheri A. Pressure ulcers: Prevention, evaluation, and management.

[11] VanGilder C, et al, The International Pressure Ulcer Prevalenceª Survey: 2006-2015: A 10 year pressure injury prevalence and demographic trend analysis by care setting. Journal

[12] Margolis DJ, et al, The incidence and prevalence of pressure ulcers among elderly patients in general medical practice. Annals of Epidemiology. 2002;**12**(5):321-325 [13] Coyer F, et al, Pressure injury prevalence in intensive care versus non-intensive care

[14] Pressure Ulcer Incidence Density as a Quality Measure. Hot Topics - Press Releases - March 11, 2014. 2014 [cited 2017; Available from: http://www.npuap.org/pressure-ulcer-

[15] Moraes GLdA, et al. Evaluation of the risk for pressure ulcers in bedridden elderly at

[16] Borghardt AT, et al. Pressure ulcers in critically ill patients: Incidence and associated fac-

[17] Pattanshetty RB, Prasade PM, Aradhana K. Risk assessment of decubitus ulcers using four scales among patients admitted in medical and surgical intensive care units in a tertiary care set up: A crosssectional study. International Journal of Physiotherapy and

[18] Pancorbo-Hidalgo PL, et al. Pressure ulcers risk assessment: Clinical practice in Spain

[19] Hyun S, et al. Predictive validity of the Braden scale for patients in intensive care units.

[20] Kirkland-Kyhn H, Teleten O, Wilson M. A retrospective, descriptive, comparative study to identify patient variables that contribute to the development of deep tissue injury among patients in intensive care units. Ostomy Wound Management. 2017;**63**(2):42-47

and a meta-analysis of scales effectiveness. Gerokomos. 2008;**19**(2):84-98

The majority of pressure ulcer patients are frail and malnourished; some are too unstable to even be brought to the operating room, thus surgical intervention is only indicated for wounds refractory to less aggressive care or for use when rapid closure is indicated. Surgery is typically saved as a last effort measure once all other non-surgical options in wound management have been exhausted. Surgical procedures can be divided into those that prepare the patient for successful healing, and those that provide definitive closure [35]. Surgical intervention is the final invasive choice because unfortunately, for many large, nonhealing pressure injuries; a reconstructive flap procedure is indicated. Most of the reconstructive flap procedures are long, procedures are long, may have to be performed in several stages and have a high rate of morbidity. The overall complication rate after surgical intervention of pressure injures has been cited as almost 60%. Wound dehiscence is the most common complication seen in >30% of patients and pressure ulcer recurrence rate is slightly <30% [66]. The mortality rate in patients with a pressure ulcer has been found to be significantly higher than in patients without a pressure ulcer (9.1% versus 1.8%, OR = 5.08, CI: 5.03–5.1, P < 0.001) [67]. The importance of early identification cannot be stressed enough. All personnel involved in patient care should seek to minimize the risks of pressure ulcer injuries and address tissue breakdown early on so that ulcer formation can be prevented all together.

#### **Author details**

#### Ashley Jordan

Address all correspondence to: missashleyjordan@gmail.com

St. Luke's University Hospital, Bethlehem, PA, USA

#### **References**


[5] Webster M. Merriam-Webster Online Dictionary; 2006

and start treating pressure injuries as soon as they are discovered to avoid problems and complications as time progresses. Overall median time to heal an ulcer has been cited as 46 days,

The majority of pressure ulcer patients are frail and malnourished; some are too unstable to even be brought to the operating room, thus surgical intervention is only indicated for wounds refractory to less aggressive care or for use when rapid closure is indicated. Surgery is typically saved as a last effort measure once all other non-surgical options in wound management have been exhausted. Surgical procedures can be divided into those that prepare the patient for successful healing, and those that provide definitive closure [35]. Surgical intervention is the final invasive choice because unfortunately, for many large, nonhealing pressure injuries; a reconstructive flap procedure is indicated. Most of the reconstructive flap procedures are long, procedures are long, may have to be performed in several stages and have a high rate of morbidity. The overall complication rate after surgical intervention of pressure injures has been cited as almost 60%. Wound dehiscence is the most common complication seen in >30% of patients and pressure ulcer recurrence rate is slightly <30% [66]. The mortality rate in patients with a pressure ulcer has been found to be significantly higher than in patients without a pressure ulcer (9.1% versus 1.8%, OR = 5.08, CI: 5.03–5.1, P < 0.001) [67]. The importance of early identification cannot be stressed enough. All personnel involved in patient care should seek to minimize the risks of pressure ulcer injuries and address tissue

ulcers, 53 days to heal medium, >1 to ≤4 cm<sup>2</sup>

ulcers and

33 median days to heal small ≤ 1 cm<sup>2</sup>

[65].

breakdown early on so that ulcer formation can be prevented all together.

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[4] National Pressure Ulcer Advisory Panel. 2017 [cited 2017 March 16, 2017]; npuap.org]. Available from: http://www.npuap.org/resources/educational-and-clinical-resources/

Address all correspondence to: missashleyjordan@gmail.com

St. Luke's University Hospital, Bethlehem, PA, USA

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**Author details**

Ashley Jordan

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[54] Jones A, San Miguel L, Are modern wound dressings a clinical and cost-effective alternative to the use of gauze? Journal of Wound Care. 2006;**15**(2):65-69

**Chapter 9**

**Wrong Blood Type: Transfusion Reaction**

Blood products are frequently required in an inpatient setting for a number of serious conditions. It is of the utmost importance that providers are aware of the potential for adverse reactions and human error when ordering or administering these products. Patients who require blood products should have a signed informed consent form and a type and screen performed prior to transfusion. The patient's identity should be confirmed using two patient identifiers. There are two major categories for blood transfusion reactions, immune-mediated and nonimmune-mediated. Common manifestations of a transfusion reaction are nonspecific and may be attributed to a patient's other medical problems, so the index of suspicion must be high in order to identify and treat these reactions.

**Keywords:** blood transfusion, adverse reaction(s), hemolysis, immune-mediated, safety

A 28-year-old female is brought in by emergency medical services (EMS) following a motor vehicle collision in which she was the restrained driver. Her initial vital signs include a heart rate of 100 BPM, blood pressure of 90/68 mmHg, respiratory rate of 18/min, pulse ox of 96% on room air, and an oral temperature of 98°F. She complains of abdominal pain, especially in the left upper quadrant. Chest and pelvic X-rays are negative for acute traumatic injuries, and her FAST exam is positive. The patient's blood pressure drops to 76/50 mmHg and she is found to have a point-of-care hemoglobin of 5.8 g/dL. A massive transfusion protocol is started and she is given 2U packed red blood (PRBCs) and 1U of platelets. She is rushed to the operating room, and while she is being prepped for an exploratory laparotomy, she is found to have a temperature of 101.8°F and has dark urine draining from her Foley catheter. The operating room nurse is concerned about an acute transfusion reaction, and the blood transfusion is

> © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Holly Ringhauser and James Cipolla

http://dx.doi.org/10.5772/intechopen.69653

**Abstract**

**1. Introduction**

immediately stopped.

Additional information is available at the end of the chapter


## **Wrong Blood Type: Transfusion Reaction**

[54] Jones A, San Miguel L, Are modern wound dressings a clinical and cost-effective alterna-

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[57] Wound Care Resources - Wound Dressing Categories. [cited 2017 March 15, 2017];

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[64] Defloor T. The effect of position and mattress on interface pressure. Applied Nursing

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[66] Bamba R, et al. Flap reconstruction for pressure ulcers: An outcomes analysis. Plastic

[67] Bauer K, et al. Pressure ulcers in the United States' inpatient population from 2008 to 2012: Results of a retrospective nationwide study. Ostomy Wound Management.

tive to the use of gauze? Journal of Wound Care. 2006;**15**(2):65-69

Available from: http://www.woundcareresources.net/education.html

http://www.ahrq.gov/clinic/ta/negpresswtd/negpresswtd.pdf

sacrum and great trochanter. Journal of Wound Care. 2015;**24**(7)

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Library. 2013(7)

**1**(3):104-109

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Research. 2000;**13**(1):2-11

2016;**62**(11):30-38

Holly Ringhauser and James Cipolla

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.69653

#### **Abstract**

Blood products are frequently required in an inpatient setting for a number of serious conditions. It is of the utmost importance that providers are aware of the potential for adverse reactions and human error when ordering or administering these products. Patients who require blood products should have a signed informed consent form and a type and screen performed prior to transfusion. The patient's identity should be confirmed using two patient identifiers. There are two major categories for blood transfusion reactions, immune-mediated and nonimmune-mediated. Common manifestations of a transfusion reaction are nonspecific and may be attributed to a patient's other medical problems, so the index of suspicion must be high in order to identify and treat these reactions.

**Keywords:** blood transfusion, adverse reaction(s), hemolysis, immune-mediated, safety

#### **1. Introduction**

A 28-year-old female is brought in by emergency medical services (EMS) following a motor vehicle collision in which she was the restrained driver. Her initial vital signs include a heart rate of 100 BPM, blood pressure of 90/68 mmHg, respiratory rate of 18/min, pulse ox of 96% on room air, and an oral temperature of 98°F. She complains of abdominal pain, especially in the left upper quadrant. Chest and pelvic X-rays are negative for acute traumatic injuries, and her FAST exam is positive. The patient's blood pressure drops to 76/50 mmHg and she is found to have a point-of-care hemoglobin of 5.8 g/dL. A massive transfusion protocol is started and she is given 2U packed red blood (PRBCs) and 1U of platelets. She is rushed to the operating room, and while she is being prepped for an exploratory laparotomy, she is found to have a temperature of 101.8°F and has dark urine draining from her Foley catheter. The operating room nurse is concerned about an acute transfusion reaction, and the blood transfusion is immediately stopped.

© 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Whole blood, platelets, or plasma are collected from volunteer donors after a careful prescreening process. The prescreening process identifies volunteers with high-risk behavior, who use or have used certain medications, or who have recently traveled to areas affected by endemic diseases which may affect donated blood products. Following donation, these products are then screened by the blood bank for a battery of infectious diseases, undergo typing, and are stored until needed for patient use. Whole blood is separated into components, making it easy to transfuse only what a patient requires rather than whole blood. Packed red blood cells (PRBCs), platelets, fresh frozen plasma (FFP), and cryoprecipitate are the main blood components available in the USA, as well as individual clotting factors for specific disorders (for example, hemophilia A and B). In massive transfusion protocols, PRBCs, platelets, and FFP are given in a 1:1:1 ratio known as balanced resuscitation, which is close to giving the patient whole blood. There are many factors to take into consideration before deciding to transfuse a patient, which are outside the scope of this chapter.

have a different Rh status. If an Rh− mother is pregnant with an Rh+ fetus and is exposed to their blood (i.e., trauma, gynecologic procedures, etc.), she will develop anti-Rh antibodies that can cross the placenta. This will likely not affect the current pregnancy, but subsequent pregnancies with Rh+ fetuses are at risk for developing complications such as jaundice or hydrops fetalis [2]. This process can be prevented by administering rho(d) immune globulin to the mother when there is a concern or high risk for feto-maternal hemorrhage, even in

Wrong Blood Type: Transfusion Reaction http://dx.doi.org/10.5772/intechopen.69653 151

There are two major categories for blood transfusion reactions: immune-mediated and nonimmune-mediated. Immune-mediated reactions include all cellular and humoral responses to blood products, while nonimmune-mediated reactions include volume overload, electrolyte abnormalities, and hypothermia, among others [3]. Common manifestations of a transfusion reaction are nonspecific and may be attributed to patient's other medical problems. Signs and symptoms include fever, chills, back or flank pain, or changes in vital signs (specifically,

An acute hemolytic reaction is an immune-mediated event, which typically occurs within the first 24 hours of a transfusion [4, 5]. It is due to ABO incompatibility and is most commonly due to human error. Antigen-antibody complexes form between donor and patient blood, leading to complement fixation and catastrophic intravascular hemolysis, which in turn can

Delayed hemolytic reactions can occur days or even weeks after a blood transfusion and are caused by previously formed antibodies in the patient, which react with antigens on the surface of the donor cells [4, 5]. These are not ABO incompatibility reactions but are instead caused by minor antigen incompatibility. These reactions are difficult to diagnose due to their nonspecific symptoms and delayed onset after a transfusion. They are more common in

Febrile nonhemolytic reactions are also immune-mediated but do not result in the destruction of RBCs. These reactions are defined as an elevation in patient temperature of 1°C or more either during or following a transfusion, which is not explained by the patient's other medical issues [6]. A transfusion should be immediately stopped once there is a concern for a febrile reaction, and the remaining blood products and IV tubing should be returned to the blood bank to rule out acute hemolysis or bacterial contamination. If these tests are negative, a febrile nonhemolytic reaction can be diagnosed. These reactions can be caused by inflammatory cytokines or pyrogens in donor products or by preformed patient cytokines/pyrogens. A majority of patients who are diagnosed with this type of reaction will not have subsequent reactions in the future; however, if a second reaction does occur, the patient should then only be given leukocyte-reduced products and may benefit from receiving antipyretics prior to transfusion [6]. Posttransfusion purpura is an immune-mediated reaction to blood products which results in severe thrombocytopenia. This is a rare disorder caused by alloantibodies against a platelet antigen and is characterized as a precipitous drop in platelets approximately 1 week after blood product administration. Signs and symptoms include purpura, gastrointestinal (GI) bleeding, gross hematuria, or excessive wound bleeding. Treatment includes administration of

small quantities.

blood pressure and heart rate).

lead to shock, renal failure, and potentially death [6].

patients who have undergone multiple transfusions in the past.

corticosteroids and IV immunoglobulin or plasmapheresis.

Patients who require blood products should have a signed informed consent form and a type and screen performed prior to transfusion, whenever possible. If the patient is unstable and requires emergent uncrossmatched blood, a type and screen should still be sent for subsequent transfusions. A type and screen will indicate the patient's blood type (ABO and Rh status), whereas a type and cross tests a particular blood product against the patient's blood to confirm that they are compatible. If the patient has a previous type and screen on file with the blood bank, it should be the same ABO and Rh type as the current sample; otherwise, the suspicion for a mislabeled blood specimen should be high.

The patient's identity should be confirmed using two patient identifiers. Appropriate identifiers include the patient's name, date of birth, hospital identification number, or medical record number. Room number should never be used to identify a patient. Prior to administering blood products, two providers (usually RNs) should confirm the quantity and type of product, the ABO and Rh type, and the serial number of the product. Many centers have instituted a checklist to ensure compliance with each of these steps.

There are four major blood groups, A, B, AB, and O. These indicate the types of antigens present on the surface of the RBCs. A patient's immune system produces antibodies to the ABO antigens that are not present (**Table 1**) [1].

A second major surface antigen is the Rhesus factor or Rh factor. Administration of Rh+ blood to a patient who is Rh− typically causes little to no adverse reactions in a healthy adult. However, in women of childbearing age, it is a concern because the fetus and mother can


**Table 1.** ABO blood types.

have a different Rh status. If an Rh− mother is pregnant with an Rh+ fetus and is exposed to their blood (i.e., trauma, gynecologic procedures, etc.), she will develop anti-Rh antibodies that can cross the placenta. This will likely not affect the current pregnancy, but subsequent pregnancies with Rh+ fetuses are at risk for developing complications such as jaundice or hydrops fetalis [2]. This process can be prevented by administering rho(d) immune globulin to the mother when there is a concern or high risk for feto-maternal hemorrhage, even in small quantities.

Whole blood, platelets, or plasma are collected from volunteer donors after a careful prescreening process. The prescreening process identifies volunteers with high-risk behavior, who use or have used certain medications, or who have recently traveled to areas affected by endemic diseases which may affect donated blood products. Following donation, these products are then screened by the blood bank for a battery of infectious diseases, undergo typing, and are stored until needed for patient use. Whole blood is separated into components, making it easy to transfuse only what a patient requires rather than whole blood. Packed red blood cells (PRBCs), platelets, fresh frozen plasma (FFP), and cryoprecipitate are the main blood components available in the USA, as well as individual clotting factors for specific disorders (for example, hemophilia A and B). In massive transfusion protocols, PRBCs, platelets, and FFP are given in a 1:1:1 ratio known as balanced resuscitation, which is close to giving the patient whole blood. There are many factors to take into consideration before deciding to

Patients who require blood products should have a signed informed consent form and a type and screen performed prior to transfusion, whenever possible. If the patient is unstable and requires emergent uncrossmatched blood, a type and screen should still be sent for subsequent transfusions. A type and screen will indicate the patient's blood type (ABO and Rh status), whereas a type and cross tests a particular blood product against the patient's blood to confirm that they are compatible. If the patient has a previous type and screen on file with the blood bank, it should be the same ABO and Rh type as the current sample; otherwise, the

The patient's identity should be confirmed using two patient identifiers. Appropriate identifiers include the patient's name, date of birth, hospital identification number, or medical record number. Room number should never be used to identify a patient. Prior to administering blood products, two providers (usually RNs) should confirm the quantity and type of product, the ABO and Rh type, and the serial number of the product. Many centers have instituted

There are four major blood groups, A, B, AB, and O. These indicate the types of antigens present on the surface of the RBCs. A patient's immune system produces antibodies to the ABO

A second major surface antigen is the Rhesus factor or Rh factor. Administration of Rh+ blood to a patient who is Rh− typically causes little to no adverse reactions in a healthy adult. However, in women of childbearing age, it is a concern because the fetus and mother can

Antigens present A antigen B antigen A and B antigens None

Blood products they can receive A, O B, O AB, A, O

Antibodies present Anti-B Anti-A None Anti-A and Anti-B

**A B AB O**

Universal recipient

O

Universal donor

transfuse a patient, which are outside the scope of this chapter.

150 Vignettes in Patient Safety - Volume 1

suspicion for a mislabeled blood specimen should be high.

a checklist to ensure compliance with each of these steps.

antigens that are not present (**Table 1**) [1].

**Table 1.** ABO blood types.

There are two major categories for blood transfusion reactions: immune-mediated and nonimmune-mediated. Immune-mediated reactions include all cellular and humoral responses to blood products, while nonimmune-mediated reactions include volume overload, electrolyte abnormalities, and hypothermia, among others [3]. Common manifestations of a transfusion reaction are nonspecific and may be attributed to patient's other medical problems. Signs and symptoms include fever, chills, back or flank pain, or changes in vital signs (specifically, blood pressure and heart rate).

An acute hemolytic reaction is an immune-mediated event, which typically occurs within the first 24 hours of a transfusion [4, 5]. It is due to ABO incompatibility and is most commonly due to human error. Antigen-antibody complexes form between donor and patient blood, leading to complement fixation and catastrophic intravascular hemolysis, which in turn can lead to shock, renal failure, and potentially death [6].

Delayed hemolytic reactions can occur days or even weeks after a blood transfusion and are caused by previously formed antibodies in the patient, which react with antigens on the surface of the donor cells [4, 5]. These are not ABO incompatibility reactions but are instead caused by minor antigen incompatibility. These reactions are difficult to diagnose due to their nonspecific symptoms and delayed onset after a transfusion. They are more common in patients who have undergone multiple transfusions in the past.

Febrile nonhemolytic reactions are also immune-mediated but do not result in the destruction of RBCs. These reactions are defined as an elevation in patient temperature of 1°C or more either during or following a transfusion, which is not explained by the patient's other medical issues [6]. A transfusion should be immediately stopped once there is a concern for a febrile reaction, and the remaining blood products and IV tubing should be returned to the blood bank to rule out acute hemolysis or bacterial contamination. If these tests are negative, a febrile nonhemolytic reaction can be diagnosed. These reactions can be caused by inflammatory cytokines or pyrogens in donor products or by preformed patient cytokines/pyrogens. A majority of patients who are diagnosed with this type of reaction will not have subsequent reactions in the future; however, if a second reaction does occur, the patient should then only be given leukocyte-reduced products and may benefit from receiving antipyretics prior to transfusion [6].

Posttransfusion purpura is an immune-mediated reaction to blood products which results in severe thrombocytopenia. This is a rare disorder caused by alloantibodies against a platelet antigen and is characterized as a precipitous drop in platelets approximately 1 week after blood product administration. Signs and symptoms include purpura, gastrointestinal (GI) bleeding, gross hematuria, or excessive wound bleeding. Treatment includes administration of corticosteroids and IV immunoglobulin or plasmapheresis.

There are two immune-mediated allergic processes associated with transfusion reactions, which are urticarial and anaphylactic reactions. Urticarial reactions are immunoglobulin E (IgE)-mediated and consist of GI distress (nausea and vomiting, abdominal cramping, and diarrhea) and mild upper respiratory symptoms such as rhinorrhea. Treatment consists primarily of antihistamines. Anaphylactic reactions are IgA mediated and begin within seconds to minutes of the start of transfusion. These reactions include a sudden-onset cough, bronchospasm/laryngospasm, angioedema, severe hypotension, shock, or death. These reactions occur primarily in patients with selective IgA deficiency but can also occur in patients with antibodies to other donor plasma proteins. Treatment includes immediately stopping the transfusion, securing the airway (including intubation, if needed), and giving epinephrine, corticosteroids, and antihistamines [6].

from warmers or freezers or mechanical damage from cardiopulmonary bypass pumps, extracorporeal membranous oxygenation pumps, or continuous renal replacement therapy [9].

Wrong Blood Type: Transfusion Reaction http://dx.doi.org/10.5772/intechopen.69653 153

Other considerations regarding adverse blood transfusion reactions include hypothermia, electrolyte abnormalities, and infectious diseases. Trauma patients or patients who are already hypothermic prior to transfusion should ideally receive blood via a warmer. Patients with renal disease or preexisting electrolyte abnormalities should be closely monitored for signs of hyperkalemia or hypocalcemia, including cardiac monitoring during and after transfusion. Although rare, bacterial, or viral contamination of blood products can occur. Proper collection, storage, and administration of blood products are keys in limiting bacterial contamination. All blood products undergo vigorous screening for viral diseases including hepatitis B and C, cytomegalovirus (CMV) and human T-cell lymphotropic virus type 1 (HTLV-1) prior to administration. The overall incidence of blood-borne pathogen

Once an adverse reaction has been identified, the following actions should be performed:

**b.** Transfer blood product(s) and tubing back to the blood bank for analysis. Attach new IV

**c.** Recheck the patient's identity via their hospital assigned ID number, patient wristband,

**d.** Notify the blood bank immediately. In some hospitals, it may also be necessary to directly notify the pathologist on call as they will be evaluating the patient's posttransfusion blood

**e.** Transfusion reaction orders include repeat type and screen, Coombs' testing (direct antiglobulin), and plasma and urinalysis (in some cases, to check for hemolysis). Other tests that may be considered include a complete blood count, peripheral blood smear, bilirubin, serum haptoglobin, and lactate dehydrogenase (LDH), all of which can indicate hemolysis.

**f.** Specific therapies geared toward each type of transfusion reaction (diuretics, antihista-

**g.** Inform the patient of the error. Being honest with patients regarding medical errors is of

The patient was found to be blood type O-positive, but an error in the blood bank caused a unit of A-negative blood to be incorporated into the trauma blood container. She was aggressively resuscitated with IV crystalloid to maintain a urine output of at least 100 mL/hr and was found to have a grade IV splenic laceration. She had an emergent splenectomy performed and was subsequently given three additional units of O-positive blood. Postoperatively, she was found to have elevated blood urea nitrogen (BUN) and creatinine (indicating acute kidney injury), elevated indirect bilirubin, elevated serum LDH, and hemoglobinuria (indicating acute hemolysis), and persistent anemia (likely a combination of acute blood loss and

transmission during transfusion is low [9].

**a.** Immediate cessation of blood administration.

tubing that has been primed with saline.

the utmost importance and should be done promptly.

etc. as well as all blood products.

work.

mines, etc.).

Transfusion-associated acute lung injury (TRALI) is an immune-mediated transfusion reaction, which manifests as an inflammatory lung injury within the first 6 hours of transfusion. It is due to donor granulocyte-induced acute respiratory distress syndrome (ARDS). The chest X-ray findings are the same as in other causes of ARDS, namely, diffuse bilateral pulmonary infiltrates, and the treatment is the same (lung protective ventilation strategies and supportive care). TRALI is the leading cause of death due to blood transfusion reactions but is still relatively low around 10% [6].

Graft-versus-host disease can be seen in severely immunocompromised patients who receive blood products. It is an immune-mediated transfusion reaction caused by donor T lymphocytes, which attack patient human leukocyte antigen (HLA) antigens. Signs and symptoms include rash, elevated liver function test (LFTs), diarrhea, and bone marrow suppression and typically develop a week or more after transfusion. Treatment consists of supportive care, and prevention can be accomplished by giving irradiated PRBC or platelet transfusions to at-risk patients [8]. FFP and cryoprecipitate do not have to be irradiated; however, as this is a lymphocyte-mediated reaction and these products do not contain lymphocytes.

In addition to immune-mediated transfusion reactions, there are a number of nonimmune transfusion reactions which can occur, including transfusion-associated circulatory overload (TACO), nonimmune hemolysis, hypothermia, electrolyte abnormalities, and infectious diseases.

Transfusion-associated circulatory overload (TACO) is a nonimmune mediated transfusion reaction which is often confused with TRALI. Similar to TRALI, it also presents with respiratory distress following transfusion, but unlike TRALI, it is a type of acute cardiogenic pulmonary edema [7]. Several clinical features can separate this from TRALI such as elevated brain natriuretic peptide (BNP) and central venous pressure (CVP) and it is generally improved with diuresis. Patients with a history of heart failure, kidney insufficiency or failure, poor nutrition (leading to decreased intravascular oncotic pressure due to low albumin), and patients at extremes of age (pediatric and elderly patients) are at an increased risk of TACO [9]. Treatment consists of supportive care and diuresis, and prevention includes slower rates of infusion or infusing blood products in aliquots rather than whole units.

Nonimmune hemolytic transfusion reactions are due to red cell destruction by transfusing PRBCs at the same time as hypertonic or hypotonic IV fluids or medications, by thermal damage from warmers or freezers or mechanical damage from cardiopulmonary bypass pumps, extracorporeal membranous oxygenation pumps, or continuous renal replacement therapy [9].

Other considerations regarding adverse blood transfusion reactions include hypothermia, electrolyte abnormalities, and infectious diseases. Trauma patients or patients who are already hypothermic prior to transfusion should ideally receive blood via a warmer. Patients with renal disease or preexisting electrolyte abnormalities should be closely monitored for signs of hyperkalemia or hypocalcemia, including cardiac monitoring during and after transfusion. Although rare, bacterial, or viral contamination of blood products can occur. Proper collection, storage, and administration of blood products are keys in limiting bacterial contamination. All blood products undergo vigorous screening for viral diseases including hepatitis B and C, cytomegalovirus (CMV) and human T-cell lymphotropic virus type 1 (HTLV-1) prior to administration. The overall incidence of blood-borne pathogen transmission during transfusion is low [9].

Once an adverse reaction has been identified, the following actions should be performed:

**a.** Immediate cessation of blood administration.

There are two immune-mediated allergic processes associated with transfusion reactions, which are urticarial and anaphylactic reactions. Urticarial reactions are immunoglobulin E (IgE)-mediated and consist of GI distress (nausea and vomiting, abdominal cramping, and diarrhea) and mild upper respiratory symptoms such as rhinorrhea. Treatment consists primarily of antihistamines. Anaphylactic reactions are IgA mediated and begin within seconds to minutes of the start of transfusion. These reactions include a sudden-onset cough, bronchospasm/laryngospasm, angioedema, severe hypotension, shock, or death. These reactions occur primarily in patients with selective IgA deficiency but can also occur in patients with antibodies to other donor plasma proteins. Treatment includes immediately stopping the transfusion, securing the airway (including intubation, if needed), and giving epinephrine, corticosteroids,

Transfusion-associated acute lung injury (TRALI) is an immune-mediated transfusion reaction, which manifests as an inflammatory lung injury within the first 6 hours of transfusion. It is due to donor granulocyte-induced acute respiratory distress syndrome (ARDS). The chest X-ray findings are the same as in other causes of ARDS, namely, diffuse bilateral pulmonary infiltrates, and the treatment is the same (lung protective ventilation strategies and supportive care). TRALI is the leading cause of death due to blood transfusion reactions but is still

Graft-versus-host disease can be seen in severely immunocompromised patients who receive blood products. It is an immune-mediated transfusion reaction caused by donor T lymphocytes, which attack patient human leukocyte antigen (HLA) antigens. Signs and symptoms include rash, elevated liver function test (LFTs), diarrhea, and bone marrow suppression and typically develop a week or more after transfusion. Treatment consists of supportive care, and prevention can be accomplished by giving irradiated PRBC or platelet transfusions to at-risk patients [8]. FFP and cryoprecipitate do not have to be irradiated; however, as this is a

In addition to immune-mediated transfusion reactions, there are a number of nonimmune transfusion reactions which can occur, including transfusion-associated circulatory overload (TACO),

Transfusion-associated circulatory overload (TACO) is a nonimmune mediated transfusion reaction which is often confused with TRALI. Similar to TRALI, it also presents with respiratory distress following transfusion, but unlike TRALI, it is a type of acute cardiogenic pulmonary edema [7]. Several clinical features can separate this from TRALI such as elevated brain natriuretic peptide (BNP) and central venous pressure (CVP) and it is generally improved with diuresis. Patients with a history of heart failure, kidney insufficiency or failure, poor nutrition (leading to decreased intravascular oncotic pressure due to low albumin), and patients at extremes of age (pediatric and elderly patients) are at an increased risk of TACO [9]. Treatment consists of supportive care and diuresis, and prevention includes slower rates

Nonimmune hemolytic transfusion reactions are due to red cell destruction by transfusing PRBCs at the same time as hypertonic or hypotonic IV fluids or medications, by thermal damage

nonimmune hemolysis, hypothermia, electrolyte abnormalities, and infectious diseases.

lymphocyte-mediated reaction and these products do not contain lymphocytes.

of infusion or infusing blood products in aliquots rather than whole units.

and antihistamines [6].

152 Vignettes in Patient Safety - Volume 1

relatively low around 10% [6].


The patient was found to be blood type O-positive, but an error in the blood bank caused a unit of A-negative blood to be incorporated into the trauma blood container. She was aggressively resuscitated with IV crystalloid to maintain a urine output of at least 100 mL/hr and was found to have a grade IV splenic laceration. She had an emergent splenectomy performed and was subsequently given three additional units of O-positive blood. Postoperatively, she was found to have elevated blood urea nitrogen (BUN) and creatinine (indicating acute kidney injury), elevated indirect bilirubin, elevated serum LDH, and hemoglobinuria (indicating acute hemolysis), and persistent anemia (likely a combination of acute blood loss and  hemolysis). She required intubation and supportive care for 6 days postoperatively and was started on a course of plasmapheresis to remove any A antigen- anti-A antibody complexes that may still have been circulating in her blood stream. Additionally, she required several weeks of renal replacement therapy until her renal function recovered. She was ultimately discharged from the hospital with no long-term sequelae.

**References**

2016]

[1] Dean L. Blood Groups and Red Cell Antigens [Internet]. Blood Transfusions and the Immune System. Chapter 3. Bethesda (MD): National Center for Biotechnology Information (US); 2005. Available from: https://www.ncbi.nlm.nih.gov/books/NBK2265/

Wrong Blood Type: Transfusion Reaction http://dx.doi.org/10.5772/intechopen.69653 155

[2] Dean L. Blood Groups and Red Cell Antigens [Internet]. The Rh blood group. Chapter 7. Bethesda (MD): National Center for Biotechnology Information (US); 2005. Available

[3] The Department of Clinical Service, Research, and Teaching, University of Michigan at Ann Arbor. Chapter 7. Adverse Reactions to Transfusion. (n.d.). Available from: https:// www.pathology.med.umich.edu/bloodbank/manual/bbch\_7/ [Accessed: November 28,

[4] Sandler SG.. Transfusion Reactions. 2016. Available from: http://emedicine.medscape.

[5] Marx, JA, Hockberger RS, Walls RM, Adams J. Blood and blood components. In: Rosen's Emergency Medicine: Concepts and Clinical Practice. Chapter 7. St. Louis: Mosby; 2002

[6] Marino PL, Sutin KM. Anemia and red blood cell transfusions in the ICU. In: The ICU

[7] Criner, GJ, Barnette RE, D'Alonzo GE. Use of blood components. In: Critical Care Study

[8] Thomas K, MD, FCCP. Anemia and RBC transfusion in the ICU. In: ACCP Critical Care Medicine Board Review. Northbrook, IL: American College of Chest Physicians; 2012 [9] Ogedegbe H O. A review of non-immune mediated transfusion reactions. Laboratory

from: https://www.ncbi.nlm.nih.gov/books/NBK2269/

com/article/206885-overview [Accessed: November 28, 2016]

Book. Chapter 36. Philadelphia: Lippincott Williams & Wilkins; 2007

Guide: Text and Review. Chapter 55. New York: Springer: 2010

Medicine. 2002;**33**(5):380-385. DOI:10.1309/uyey-2cch-cump-ekrt

### **2. Analysis of errors**


#### **Author details**

Holly Ringhauser and James Cipolla\*

\*Address all correspondence to: james.cipolla@sluhn.org

Department of Trauma and Surgical Critical Care, St. Luke's University Hospital, Bethlehem, PA, USA

#### **References**

 hemolysis). She required intubation and supportive care for 6 days postoperatively and was started on a course of plasmapheresis to remove any A antigen- anti-A antibody complexes that may still have been circulating in her blood stream. Additionally, she required several weeks of renal replacement therapy until her renal function recovered. She was ultimately

**a.** The initial type and screen for the patient was waived prior to the first unit being administered because of her hemodynamic instability. In unstable patients with acute blood loss, it is appropriate to give O-negative blood (to women of childbearing age) or O-positive

**b.** Blood bank crossmatching was also waived prior to administration of the first unit of blood given the patient's mechanism of injury (major trauma) and hemodynamic instability. In most major trauma centers, a cooler of "trauma blood" arrives in the trauma bay for all of the highest level activation trauma patients. This cooler contains uncrossmatched packed red blood cells. This is also the case in massive transfusion protocols. The utmost level of care must be taken by blood bank staff to ensure that only O-negative or positive blood

goes into uncrossmatched containers to avoid an ABO incompatibility reaction.

**c.** The provider who is administering the blood transfusion must check the patient's hospital-issued wristband and identification number against the information listed on each blood product prior to administration. Many hospitals also require a second provider to

**d.** The patient should be reassessed and vital signs documented 15 minutes into a transfusion to ensure that they are not becoming febrile, hemodynamically unstable, or have complaints of itching, flank pain, chills, or other signs and symptoms concerning for a blood

**e.** If a transfusion reaction is suspected, the blood products should be stopped immediately

Department of Trauma and Surgical Critical Care, St. Luke's University Hospital, Bethlehem,

and appropriate actions should be taken to identify and treat the reaction.

discharged from the hospital with no long-term sequelae.

**2. Analysis of errors**

154 Vignettes in Patient Safety - Volume 1

blood (to all other patients).

verify this information to avoid errors.

transfusion reaction.

Holly Ringhauser and James Cipolla\*

\*Address all correspondence to: james.cipolla@sluhn.org

**Author details**

PA, USA


**Chapter 10**

**Provisional chapter**

**Patient Self-Harm in the Emergency Department: An**

Violence, deliberate self harm, and suicide in emergency departments and hospitals is likely to remain a significant problem for health care systems well into the future. Understanding how to confront, intervene, and manage episodes of patient deliberate self harm is extremely important, and can be life-saving. Here, through a clinical vignette, and a discussion of deliberate self harm we will highlight the importance of the direct observation of such patients, containment procedures (seclusion and physical restraints), and the use of pharmacological adjuncts. We hope that this concise, practically-oriented review will provide our readers with foundational understanding of the topic, including

**Keywords:** emergency department, evidence-based approach, patient safety, psychiatric

Violence in the hospital is not a new phenomenon, with health care and social service institutions being disproportionately affected by this serious problem [1, 2]. Also of major concern, every 16.6 min one American dies by suicide, amounting to over 30,000 suicides per year [3]. The prevalence of deliberate self-harm (DSH) in the hospitalized patient population is especially troubling, with one study reporting that DSH may be occurring in nearly 9% of hospital shifts on acute psychiatric wards [4]. Non-fatal DSH has also been called "parasuicide" a term we will not be using in this chapter for the sake of uniformity and consistency [5].

**Patient Self-Harm in the Emergency Department: An** 

DOI: 10.5772/intechopen.69640

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

© 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

and reproduction in any medium, provided the original work is properly cited.

**Evidence-Based Approach**

Ronya Silmi, Joshua Luster, Jacqueline Seoane, Stanislaw P. Stawicki, Thomas J. Papadimos, Farhad Sholevar and Christine

**Evidence-Based Approach**

Ronya Silmi, Joshua Luster, Jacqueline Seoane, Stanislaw P. Stawicki, Thomas J. Papadimos, Farhad Sholevar and Christine Marchionni

Additional information is available at the end of the chapter

the most important theoretical and clinical considerations.

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.69640

Marchionni

**Abstract**

emergency, self-harm

**1. Introduction**

**Provisional chapter**

#### **Patient Self-Harm in the Emergency Department: An Evidence-Based Approach Evidence-Based Approach**

**Patient Self-Harm in the Emergency Department: An** 

DOI: 10.5772/intechopen.69640

Ronya Silmi, Joshua Luster, Jacqueline Seoane, Stanislaw P. Stawicki, Thomas J. Papadimos, Farhad Sholevar and Christine Marchionni Seoane, Stanislaw P. Stawicki, Thomas J. Papadimos, Farhad Sholevar and Christine Marchionni

Ronya Silmi, Joshua Luster, Jacqueline

Additional information is available at the end of the chapter Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.69640

#### **Abstract**

Violence, deliberate self harm, and suicide in emergency departments and hospitals is likely to remain a significant problem for health care systems well into the future. Understanding how to confront, intervene, and manage episodes of patient deliberate self harm is extremely important, and can be life-saving. Here, through a clinical vignette, and a discussion of deliberate self harm we will highlight the importance of the direct observation of such patients, containment procedures (seclusion and physical restraints), and the use of pharmacological adjuncts. We hope that this concise, practically-oriented review will provide our readers with foundational understanding of the topic, including the most important theoretical and clinical considerations.

**Keywords:** emergency department, evidence-based approach, patient safety, psychiatric emergency, self-harm

#### **1. Introduction**

Violence in the hospital is not a new phenomenon, with health care and social service institutions being disproportionately affected by this serious problem [1, 2]. Also of major concern, every 16.6 min one American dies by suicide, amounting to over 30,000 suicides per year [3]. The prevalence of deliberate self-harm (DSH) in the hospitalized patient population is especially troubling, with one study reporting that DSH may be occurring in nearly 9% of hospital shifts on acute psychiatric wards [4]. Non-fatal DSH has also been called "parasuicide" a term we will not be using in this chapter for the sake of uniformity and consistency [5].

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Fortunately, the vast majority of self-harm events are classified as minor [4]. **Figure 1** shows various factors that may, alone or in combination, result in violent behavior and DSH in the health care setting.

obvious DSH tends to be fragmented and incomplete, with currently employed triage methods in need of significant improvement [17]. This *status quo* is not acceptable, as statistics have shown that a single episode of DSH is associated with 6-fold increase in future suicide risk [15, 18]. The type of DSH, as well as the patient's response to treatment also influence the risk and patterns of subsequent DSH [9, 19]. Finally, the authors believe that the topics of DSH and violent patient behavior are interrelated, and that it is difficult to speak of one without

Patient Self-Harm in the Emergency Department: An Evidence-Based Approach

http://dx.doi.org/10.5772/intechopen.69640

159

Detailed behavioral health assessment following DSH episodes should commence as soon as the patient is deemed medically stable [20]. There should be an evaluation to determine the presence of any comorbid psychiatric disorders (e.g., depression, substance abuse, personality disorders) [21, 22]. This is critically important because certain psychiatric diagnoses are associated with significant lifetime risk of DSH [23–25]. Specific factors that strongly correlate with risk of future suicide include serious acts of DSH and the associated degree of potential lethality of the self-harming act [26, 27]. The list of proposed risk factors for DSH include young age, male sex, the presence of depression and psychosis, substance misuse, medical comorbidity, impulsivity, aggression, and/or loneliness [22, 28]. There is also evidence suggesting the involvement of specific neurotransmitter imbalances in the overall genesis of DSH [29]. While some factors contributory to DSH may be more readily modifiable (e.g., the availability of effective management of underlying psychiatric condition), some others may be difficult or impossible to influence (e.g., substance abuse, demographic factors). The following case describes a sequence of events secondary to a woman's Emergency Department (ED) admission for an acute psychotic depressive episode. Despite specific precautions being implemented during her ED stay, the patient

A 35-year-old Caucasian female presented to her primary care physician (PCP) on several occasions within the previous 6 months, complaining of increasing fatigue, loss of interest in daily activities, lack of energy, and "feelings of worthlessness". Her husband prompted her to seek treatment after a recent violent episode in which she threatened to harm herself. Following an initial evaluation, the patient revealed that she had contemplated suicide on several occasions and was threatening to ingest a bottle of "sleeping pills" when she returned home later that day. The patient's PCP called emergency medical services for urgent transport to the nearest ED for further evaluation and possible admission. Her husband was noti-

Upon arrival, the patient was found to be irritable and aggressive towards hospital staff. She refused to provide a thorough history. Initial vital signs showed hypertension (160/90 mmHg). A toxicology screening was ordered to rule out substance abuse, and was later reported to be negative. The patient was placed in an isolation room due to her increasing agitation and

violent behavior. A dedicated chaperone was placed in her room.

mentioning or discussing the other.

succeeded in inflicting significant DSH.

**2. Clinical vignette**

fied of the transfer.

DSH is defined as the intentional act of self-directed injury, irrespective of motivation. Important distinction is drawn between intentional self-directed injury without suicidal intent and an act of attempted suicide [6]. It is important to recognize that hospitalized patient population differs from individuals who engage in DSH across other settings, both in terms of impulsivity and the degree of violence involved during self-harm attempts [7–10]. It has also been noted that certain forms of DSH tend to result in patterns of escalation over time, up to and including suicidal acts [7–12]. The resultant long- and short-term burden is significant, with approximately 20–25% of individuals treated for DSH reporting previous self-inflicted injury [13], and a similar percentage of patients presenting with repeated DSH within 1 year [14]. Among adult patients who seek emergent treatment for self-inflicted injury, about half require admission for behavioral health evaluation and treatment [15, 16]. Despite the grave consequences, there are few standardized ways to reliably determine individual risk of DSH. Furthermore, the assessment of patients who present to the emergency department (ED) with

**Figure 1.** Factors that may contribute to violence and self-harm in the health care setting.

obvious DSH tends to be fragmented and incomplete, with currently employed triage methods in need of significant improvement [17]. This *status quo* is not acceptable, as statistics have shown that a single episode of DSH is associated with 6-fold increase in future suicide risk [15, 18]. The type of DSH, as well as the patient's response to treatment also influence the risk and patterns of subsequent DSH [9, 19]. Finally, the authors believe that the topics of DSH and violent patient behavior are interrelated, and that it is difficult to speak of one without mentioning or discussing the other.

Detailed behavioral health assessment following DSH episodes should commence as soon as the patient is deemed medically stable [20]. There should be an evaluation to determine the presence of any comorbid psychiatric disorders (e.g., depression, substance abuse, personality disorders) [21, 22]. This is critically important because certain psychiatric diagnoses are associated with significant lifetime risk of DSH [23–25]. Specific factors that strongly correlate with risk of future suicide include serious acts of DSH and the associated degree of potential lethality of the self-harming act [26, 27]. The list of proposed risk factors for DSH include young age, male sex, the presence of depression and psychosis, substance misuse, medical comorbidity, impulsivity, aggression, and/or loneliness [22, 28]. There is also evidence suggesting the involvement of specific neurotransmitter imbalances in the overall genesis of DSH [29]. While some factors contributory to DSH may be more readily modifiable (e.g., the availability of effective management of underlying psychiatric condition), some others may be difficult or impossible to influence (e.g., substance abuse, demographic factors). The following case describes a sequence of events secondary to a woman's Emergency Department (ED) admission for an acute psychotic depressive episode. Despite specific precautions being implemented during her ED stay, the patient succeeded in inflicting significant DSH.

#### **2. Clinical vignette**

Fortunately, the vast majority of self-harm events are classified as minor [4]. **Figure 1** shows various factors that may, alone or in combination, result in violent behavior and DSH in the

DSH is defined as the intentional act of self-directed injury, irrespective of motivation. Important distinction is drawn between intentional self-directed injury without suicidal intent and an act of attempted suicide [6]. It is important to recognize that hospitalized patient population differs from individuals who engage in DSH across other settings, both in terms of impulsivity and the degree of violence involved during self-harm attempts [7–10]. It has also been noted that certain forms of DSH tend to result in patterns of escalation over time, up to and including suicidal acts [7–12]. The resultant long- and short-term burden is significant, with approximately 20–25% of individuals treated for DSH reporting previous self-inflicted injury [13], and a similar percentage of patients presenting with repeated DSH within 1 year [14]. Among adult patients who seek emergent treatment for self-inflicted injury, about half require admission for behavioral health evaluation and treatment [15, 16]. Despite the grave consequences, there are few standardized ways to reliably determine individual risk of DSH. Furthermore, the assessment of patients who present to the emergency department (ED) with

**Figure 1.** Factors that may contribute to violence and self-harm in the health care setting.

health care setting.

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A 35-year-old Caucasian female presented to her primary care physician (PCP) on several occasions within the previous 6 months, complaining of increasing fatigue, loss of interest in daily activities, lack of energy, and "feelings of worthlessness". Her husband prompted her to seek treatment after a recent violent episode in which she threatened to harm herself. Following an initial evaluation, the patient revealed that she had contemplated suicide on several occasions and was threatening to ingest a bottle of "sleeping pills" when she returned home later that day. The patient's PCP called emergency medical services for urgent transport to the nearest ED for further evaluation and possible admission. Her husband was notified of the transfer.

Upon arrival, the patient was found to be irritable and aggressive towards hospital staff. She refused to provide a thorough history. Initial vital signs showed hypertension (160/90 mmHg). A toxicology screening was ordered to rule out substance abuse, and was later reported to be negative. The patient was placed in an isolation room due to her increasing agitation and violent behavior. A dedicated chaperone was placed in her room.

Once onsite, the husband was able to provide a thorough past medical history, revealing episodes of postpartum depression after the birth of their first and second child with symptoms mirroring her current presentation. These post-partum depressive episodes occurred 5 and 8 years prior to the current presentation, respectively. He also explained that the patient's mother has been battling major depressive disorder for several years after the death of her husband. The patient's PCP had previously prescribed Fluoxetine for each depressive episode resulting in complete symptom resolution within 6 months. She is currently not taking any medications, with the exception of a daily multivitamin. The husband reports no other illnesses. Past hospitalizations include the births of her three children during which there were no complications.

this definition as an "act with a nonfatal outcome, in which an individual deliberately initiates a non-habitual behavior that, without intervention from others, will cause self-harm… and which is aimed at realizing changes which the subject desired via the actual or expected physical consequences" [6]. The mode of injury can include cutting, stabbing, burning, skin carving, ingestion, and self-medicating, with more severe episodes of DSH resulting in serious secondary manifestations, such as traumatic brain injuries, infections, skeletal fractures, and even unintended death [30, 31]. In this chapter's clinical vignette, the patient sustained significant injuries secondary to violent, self-destructive pattern of behavior. While establishing intent is an essential determinant for differentiating non-suicidal self-injury from a suicide attempt, understanding which populations are at greatest risk for DSH is crucial for properly allocating treatment resources and establishing appropriate patient management [31, 32]. The importance of objective and constructive approach by healthcare providers toward patients

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The prevalence of DSH in the United States among adults (regardless of gender or pre-existing mental illness) is estimated to be between 1 and 4%, and this figure is projected to increase [35]. Previous episode of DSH continues to be the primary predictive factor for future DSH, although other parameters must be considered when determining the risk for each individual patient [6]. More specifically, it has been reported that up to 40% of psychiatric patients, independent of illness severity or disorder classification, have reported an episode of DSH [35]. Borderline personality disorder (BPD), marked by patterned instability of moods, behavior, and functioning, is one such condition, with as many as 75% of these patients engaging in selfinjury [35]. In addition, it has been estimated that over 40% of patients engaging in DSH also meet the criteria for major depressive disorder (MDD) [35]. Our clinical vignette demonstrates this point well, with the patient having a documented history of depression. Furthermore, more than 75% of patients with substance abuse disorders are estimated to engage in DSH [36]. In the acute setting, a thorough understanding of a patient's history of psychosis will be

The need for prompt and effective management of DSH in the healthcare setting stems from the pattern of escalation and the high-risk of mortality among hospitalized patients [12, 37]. Of concern, suicide and DSH are among the leading causes of death in the United States, and their incidence is projected to increase over the next 2 decades [38]. The associated long- and short-term burden is also substantial, with approximately 1 in 4 individuals who are admitted for DSH reporting a previous self-inflicted injury [13]. Among adult patients who seek emergent treatment for self-inflicted injury, approximately half are admitted for further evaluation and treatment [15, 16]. Despite hospital admission, this patient population continues to be at high-risk for subsequent episodes of DSH and suicide attempts following discharge. Nearly 20% of patients who were admitted for DSH-related injury will be evaluated within a year for a repeated self-inflicted injury [14]. Although EDs are usually well equipped to manage acute presentations of patient self-harm, significant risk exists for discharge into the community without a mental health assessment [15, 16]. Furthermore, of those patients who were discharged directly, little more than half seek treatment in an outpatient facility within 30-days of their self-inflicted injury [15, 16]. Because previous DSH is among the strongest predictors of future DSH, inadequate clinical management and/or

instrumental in preventing severe self-injury as well as DSH occurrences.

who present with DSH must be emphasized [33, 34].

The patient's current ED clinical course was complicated when she became increasingly agitated and began hitting her head against the padded wall of the isolation room. Her husband's attempts at intervention were unsuccessful. Meanwhile, the chaperone alerted the nearest nursing station and the patient was sedated with 2.0 mg haloperidol intravenously. While under sedation, the patient was restrained using a four-point restraint system. Of note, the initial ECG showed no abnormalities, and telemetry monitoring was implemented during the initial 24 h following haloperidol administration. A physical examination of the patient following this episode of self-harm revealed a large cephalohematoma at the site of the selfinflicted traumatic injury. A cranial computed tomogram (CT) was obtained, revealing a small right subdural hematoma.

As the effects of the sedative abated, the patient became acutely agitated again and attempted to free herself from the previously placed restraints. During the struggle, the patient suddenly cried out in pain and cradled her right arm within the limits of the restraints. The chaperone immediately notified the nursing station of the patient's pain. Upon further examination by the ER resident, there appeared to be a deformity of the right shoulder. Radiographic workup revealed an anterior dislocation of the patient's right shoulder. During the struggle, the patient also managed to chip her left central maxillary incisor. Her injuries were immediately treated by the Trauma service, including shoulder relocation. Plans were also made for dental reconstruction after patient stabilization.

During the subsequent 24 h, the patient's mental condition improved significantly. She was started on Fluoxetine and did not require any additional active therapy. Within 2 days of admission, the patient was transitioned to routine hospital care, with discharge to home 3 days later. Her post-injury clinic visit at 2 weeks showed uneventful recovery, and she continued to follow-up with her psychiatrist on monthly basis for the first 3 months, then quarterly for the remainder of the initial post-discharge year. After that, her care was transitioned to the PCP and she was continued on long-term maintenance Fluoxetine therapy.

#### **3. Discussion**

Self-harm is defined as the intentional act of an individual to cause self-directed injury or poisoning irrespective of motivation. The World Health Organization (WHO) further qualifies this definition as an "act with a nonfatal outcome, in which an individual deliberately initiates a non-habitual behavior that, without intervention from others, will cause self-harm… and which is aimed at realizing changes which the subject desired via the actual or expected physical consequences" [6]. The mode of injury can include cutting, stabbing, burning, skin carving, ingestion, and self-medicating, with more severe episodes of DSH resulting in serious secondary manifestations, such as traumatic brain injuries, infections, skeletal fractures, and even unintended death [30, 31]. In this chapter's clinical vignette, the patient sustained significant injuries secondary to violent, self-destructive pattern of behavior. While establishing intent is an essential determinant for differentiating non-suicidal self-injury from a suicide attempt, understanding which populations are at greatest risk for DSH is crucial for properly allocating treatment resources and establishing appropriate patient management [31, 32]. The importance of objective and constructive approach by healthcare providers toward patients who present with DSH must be emphasized [33, 34].

Once onsite, the husband was able to provide a thorough past medical history, revealing episodes of postpartum depression after the birth of their first and second child with symptoms mirroring her current presentation. These post-partum depressive episodes occurred 5 and 8 years prior to the current presentation, respectively. He also explained that the patient's mother has been battling major depressive disorder for several years after the death of her husband. The patient's PCP had previously prescribed Fluoxetine for each depressive episode resulting in complete symptom resolution within 6 months. She is currently not taking any medications, with the exception of a daily multivitamin. The husband reports no other illnesses. Past hospitalizations include the births of her three children during which there were

The patient's current ED clinical course was complicated when she became increasingly agitated and began hitting her head against the padded wall of the isolation room. Her husband's attempts at intervention were unsuccessful. Meanwhile, the chaperone alerted the nearest nursing station and the patient was sedated with 2.0 mg haloperidol intravenously. While under sedation, the patient was restrained using a four-point restraint system. Of note, the initial ECG showed no abnormalities, and telemetry monitoring was implemented during the initial 24 h following haloperidol administration. A physical examination of the patient following this episode of self-harm revealed a large cephalohematoma at the site of the selfinflicted traumatic injury. A cranial computed tomogram (CT) was obtained, revealing a small

As the effects of the sedative abated, the patient became acutely agitated again and attempted to free herself from the previously placed restraints. During the struggle, the patient suddenly cried out in pain and cradled her right arm within the limits of the restraints. The chaperone immediately notified the nursing station of the patient's pain. Upon further examination by the ER resident, there appeared to be a deformity of the right shoulder. Radiographic workup revealed an anterior dislocation of the patient's right shoulder. During the struggle, the patient also managed to chip her left central maxillary incisor. Her injuries were immediately treated by the Trauma service, including shoulder relocation. Plans were also made for dental

During the subsequent 24 h, the patient's mental condition improved significantly. She was started on Fluoxetine and did not require any additional active therapy. Within 2 days of admission, the patient was transitioned to routine hospital care, with discharge to home 3 days later. Her post-injury clinic visit at 2 weeks showed uneventful recovery, and she continued to follow-up with her psychiatrist on monthly basis for the first 3 months, then quarterly for the remainder of the initial post-discharge year. After that, her care was transitioned

Self-harm is defined as the intentional act of an individual to cause self-directed injury or poisoning irrespective of motivation. The World Health Organization (WHO) further qualifies

to the PCP and she was continued on long-term maintenance Fluoxetine therapy.

no complications.

160 Vignettes in Patient Safety - Volume 1

right subdural hematoma.

**3. Discussion**

reconstruction after patient stabilization.

The prevalence of DSH in the United States among adults (regardless of gender or pre-existing mental illness) is estimated to be between 1 and 4%, and this figure is projected to increase [35]. Previous episode of DSH continues to be the primary predictive factor for future DSH, although other parameters must be considered when determining the risk for each individual patient [6]. More specifically, it has been reported that up to 40% of psychiatric patients, independent of illness severity or disorder classification, have reported an episode of DSH [35]. Borderline personality disorder (BPD), marked by patterned instability of moods, behavior, and functioning, is one such condition, with as many as 75% of these patients engaging in selfinjury [35]. In addition, it has been estimated that over 40% of patients engaging in DSH also meet the criteria for major depressive disorder (MDD) [35]. Our clinical vignette demonstrates this point well, with the patient having a documented history of depression. Furthermore, more than 75% of patients with substance abuse disorders are estimated to engage in DSH [36]. In the acute setting, a thorough understanding of a patient's history of psychosis will be instrumental in preventing severe self-injury as well as DSH occurrences.

The need for prompt and effective management of DSH in the healthcare setting stems from the pattern of escalation and the high-risk of mortality among hospitalized patients [12, 37]. Of concern, suicide and DSH are among the leading causes of death in the United States, and their incidence is projected to increase over the next 2 decades [38]. The associated long- and short-term burden is also substantial, with approximately 1 in 4 individuals who are admitted for DSH reporting a previous self-inflicted injury [13]. Among adult patients who seek emergent treatment for self-inflicted injury, approximately half are admitted for further evaluation and treatment [15, 16]. Despite hospital admission, this patient population continues to be at high-risk for subsequent episodes of DSH and suicide attempts following discharge. Nearly 20% of patients who were admitted for DSH-related injury will be evaluated within a year for a repeated self-inflicted injury [14]. Although EDs are usually well equipped to manage acute presentations of patient self-harm, significant risk exists for discharge into the community without a mental health assessment [15, 16]. Furthermore, of those patients who were discharged directly, little more than half seek treatment in an outpatient facility within 30-days of their self-inflicted injury [15, 16]. Because previous DSH is among the strongest predictors of future DSH, inadequate clinical management and/or follow-up is likely to result in substantial financial and human burden for the community. The best way to improve the *status quo* and prevent repeated DSH events (including hospital readmissions) to proactively reform the medical delivery system. Greater availability of mental health specialists in our EDs, combined with protocols to better transition patients to outpatient treatment can help bridge the gap between acute and long-term management. However, without standardized protocols and procedures, even the best designed infrastructure will be unable to meet the enormous need that currently exists in this clinical arena.

**5. Direct observation**

special observation [4].

restraints or seclusion.

**6. Seclusion**

The use of patient observation assistants (PtOA) or the so-called "sitters" has been utilized to facilitate safer patient environment [39]. Despite the widespread use of PtOAs, there are no clearly defined industry standards regarding key metrics of safety, quality, and effectiveness of this practice [39, 40]. Neither is there firmly established evidence that special observation using PtOAs is efficacious [41]. Nonetheless, the continued need for PtOAs is highlighted by the fact that the other mainstay approaches to preventing DSH—physical restraints and pharmacological interventions—both carry significant rate of complications and a non-trivial risk of mortality [42, 43]. Consequently, the use of PtOAs is considered an important component of the multi-pronged approach consisting of close monitoring and prevention of recurrent self-harm. Of importance, there is evidence to suggest that intermittent observation may be associated with reduced self-harm when compared to constant

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Seclusion in management of severe agitation and/or violence first started in the mid-nineteenth century as an alternative option to mechanical restraint [44, 45]. In brief, seclusion represents involuntary confinement of the patient alone in a room (or another designated area) where the patient is physically prevented from leaving. In 2001 the UK Central Council for Nursing, Midwifery and Health Visiting determined there were no studies of value in using restraints and seclusion in mentally ill patients and could not recommend their effectiveness or use [46]. The fact is that since 2000 the use of what are termed "containment procedures," i.e., seclusion and restraints, in US psychiatric hospitals has been trending downward [47]. Over the past 10 years best practices have been instituted to limit use of containment procedures in the US to assist mental health professionals in their clinical practices [48, 49]. Additionally, the National Association of State Mental Health Program Directors (NASMHPD) had released its six core strategies for reducing seclusion and restraint use to assist in the development of safe and effective mental health programs [50]. Nonetheless, there have been some reports that show a correlation between reduced use of seclusion and restraints and an increase in patient related violence [51, 52]. However, recent work demonstrated that the implementation of better sound leadership practices, the use of accurate clinical data, developing and training a good workforce, evidence based policies and procedures, along with the use of specialized response teams, behavioral therapy, and the discontinuation of nursing "as needed" orders for restraint and seclusion use resulted in better patient outcomes and more favorable behavioral patterns [44, 53]. When the above mentioned educational, clinical, and administrative best practices are combined with sensory modulation there can be marked reductions in disturbances and a dramatic drop in the use of seclusion [54]. It is critical to ensure both safety and dignity of the patient when using

#### **4. Management of patients who engage in self-harm**

The primary objective in the clinical management of a patient who engages in DSH in the acute setting is to prevent further injury to self and others. In addition to cognitive strategies and direct patient supervision, methods typically employed include both physical restraints and pharmacological agents. Caution must be exercised in the use of all of the above interventions in this population due to the complexity of the patient's mental state and the degree of clinical unpredictability. General management pathway for patients who pose acute risk of self-harm is shown in **Figure 2A**–**C**.

**Figure 2.** General management pathway for patients who pose acute risk of deliberate self-harm; [Part A] Patient risk stratification; [Part B] Management algorithms based on overall risk / acuity; [Part C] Interventional considerations based on suspected / established etiology.

#### **5. Direct observation**

follow-up is likely to result in substantial financial and human burden for the community. The best way to improve the *status quo* and prevent repeated DSH events (including hospital readmissions) to proactively reform the medical delivery system. Greater availability of mental health specialists in our EDs, combined with protocols to better transition patients to outpatient treatment can help bridge the gap between acute and long-term management. However, without standardized protocols and procedures, even the best designed infrastructure will be unable to meet the enormous need that currently exists in this clinical arena.

The primary objective in the clinical management of a patient who engages in DSH in the acute setting is to prevent further injury to self and others. In addition to cognitive strategies and direct patient supervision, methods typically employed include both physical restraints and pharmacological agents. Caution must be exercised in the use of all of the above interventions in this population due to the complexity of the patient's mental state and the degree of clinical unpredictability. General management pathway for patients who pose acute risk of self-harm is shown in **Figure 2A**–**C**.

**Figure 2.** General management pathway for patients who pose acute risk of deliberate self-harm; [Part A] Patient risk stratification; [Part B] Management algorithms based on overall risk / acuity; [Part C] Interventional considerations

based on suspected / established etiology.

**4. Management of patients who engage in self-harm**

162 Vignettes in Patient Safety - Volume 1

The use of patient observation assistants (PtOA) or the so-called "sitters" has been utilized to facilitate safer patient environment [39]. Despite the widespread use of PtOAs, there are no clearly defined industry standards regarding key metrics of safety, quality, and effectiveness of this practice [39, 40]. Neither is there firmly established evidence that special observation using PtOAs is efficacious [41]. Nonetheless, the continued need for PtOAs is highlighted by the fact that the other mainstay approaches to preventing DSH—physical restraints and pharmacological interventions—both carry significant rate of complications and a non-trivial risk of mortality [42, 43]. Consequently, the use of PtOAs is considered an important component of the multi-pronged approach consisting of close monitoring and prevention of recurrent self-harm. Of importance, there is evidence to suggest that intermittent observation may be associated with reduced self-harm when compared to constant special observation [4].

#### **6. Seclusion**

Seclusion in management of severe agitation and/or violence first started in the mid-nineteenth century as an alternative option to mechanical restraint [44, 45]. In brief, seclusion represents involuntary confinement of the patient alone in a room (or another designated area) where the patient is physically prevented from leaving. In 2001 the UK Central Council for Nursing, Midwifery and Health Visiting determined there were no studies of value in using restraints and seclusion in mentally ill patients and could not recommend their effectiveness or use [46]. The fact is that since 2000 the use of what are termed "containment procedures," i.e., seclusion and restraints, in US psychiatric hospitals has been trending downward [47]. Over the past 10 years best practices have been instituted to limit use of containment procedures in the US to assist mental health professionals in their clinical practices [48, 49]. Additionally, the National Association of State Mental Health Program Directors (NASMHPD) had released its six core strategies for reducing seclusion and restraint use to assist in the development of safe and effective mental health programs [50]. Nonetheless, there have been some reports that show a correlation between reduced use of seclusion and restraints and an increase in patient related violence [51, 52]. However, recent work demonstrated that the implementation of better sound leadership practices, the use of accurate clinical data, developing and training a good workforce, evidence based policies and procedures, along with the use of specialized response teams, behavioral therapy, and the discontinuation of nursing "as needed" orders for restraint and seclusion use resulted in better patient outcomes and more favorable behavioral patterns [44, 53]. When the above mentioned educational, clinical, and administrative best practices are combined with sensory modulation there can be marked reductions in disturbances and a dramatic drop in the use of seclusion [54]. It is critical to ensure both safety and dignity of the patient when using restraints or seclusion.

#### **7. Physical restraints**

Approximately 50% of intensive care unit patients [55], 20% of patients on neurologyneurosurgery wards [56], and 25% of individuals admitted to mental health facilities experience at least one type of "control intervention" during acute hospitalization [57]. One method of such "control intervention" is the use of physical restraints (PhyR), defined as any device, material or equipment attached to or near a person's body, which is intended to prevent a person's free body movement to a position of choice and/or a person's normal and unrestricted access to their body [58]. The use of PhyR is relatively common, with some authors suggesting that it is overused [43, 59]. As a consequence, there are numerous initiatives to reduce the reliance on PhyR, especially among the most vulnerable patient populations [60–62]. As mentioned in this chapter's clinical vignette, restraints may not eliminate the risk of DSH. Therefore, the choice to use PhyR continues to be controversial and should only be entertained as a last resort option when there exists a real possibility of serious physical injury to self or others [63–65]. There is therefore a need for caution and balanced judgment on part of the treatment team, beginning with a well-informed understanding of potential complications and safety procedures designed to prevent adverse outcomes [63–65].

Published guidelines provide a framework for the use of PhyR in a variety of settings [66, 67]. The initial criteria for instituting PhyR should be based on a thorough evaluation of a patient's mental status. An individual at risk for DSH, who is cognitively aware of this risk of harm to themselves, is less likely to become violent while in restraints and can therefore be placed in a soft restraint apparatus [56]. However, in the event that a patient becomes increasingly violent when actively restrained, there is an increased risk of limb injury due to a tendency for the device to tighten [68]. Moreover, patients who are restrained and sustain secondary trauma are prone to more serious injuries because part(s) of their body is/are physically tied, which may render normal protective, instinctive responses ineffective. Other complications of soft restraints include abrasions, contusions, immobility, and dislodgement of various devices (e.g., intravenous lines, feeding tubes) [68–71]. In some cases, leather restraints can be utilized if the patient becomes increasingly combative; however, appropriate precautions are critical when using leather PhyR because device removal can be challenging in emergent situations [70].

The specific placement of restraints and number of application points are important in ensuring the balance between satisfactory outcomes and minimizing complications [56, 58, 72]. If the patient poses a low risk of violence, a two-point restraint system can be utilized safely [70, 73]. Four-point restraints should be reserved for combative and violent patients in the acute setting to maximally prevent uncontrolled movements [70]. Again, applicable guidelines should be followed to reduce restraint-related complications (e.g., self-injury, overturning of the stretcher) while ensuring adequate immobilization of the patient [70, 74]. Belt and jacket restraints can serve as adjunct to extremity restraints, but mandate special precautions, such as the concurrent use of full side rails [75, 76].

be provided with adequate space for free chest expansion and his or her respiratory and airway status must be closely monitored [77, 78]. If restrained while supine, patients are at risk for aspiration [79]. Thus, the patient's head should be positioned at 30° with the ability to rotate freely in order to avoid this complication [70, 79]. Moreover, optimal configuration of 4-point restraints calls for one arm being directed up toward the patient's head and the other arm down toward the patient's hip. Aside from these positional considerations, additional precautions must be instituted regarding prolonged immobilization due to the risk of pressure ulcers, focal neurovascular compression, and deep vein thrombosis [70, 80]. In addition to various potential physical complications inherent in the use of restraints, patients may experience significant emotional trauma from the ordeal, such as feelings of powerlessness, humiliation, and/or the sensation of terror seen with PhyR [81]. Common manifestations of restraint-related psychological trauma include "flashbacks" to the emotional ordeal (e.g., retraumatization), hopelessness and helplessness (e.g., "broken spirit"),

**Table 1.** Important considerations for placement and maintenance of mechanical restraints.

Detailed documentation of all restraint-related clinical decisions and procedures should be made in the medical

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In all instances of mechanical restraint use, an individualized clinical management plan should be established and

Periodic re-evaluation, as frequent as every 30 min, should be performed to determine the need for continuation of

Restraints should be placed and removed in team setting by sufficient number of staff members to prevent patient

Facilitation of diagnosis through behavioral control under conditions requiring minimal or no medication use

Duration of restraint use should be firmly justified and continue for the least amount of time applicable

Mechanical restraints should be utilized in "last resort" capacity when all other interventions have failed

Restraints should always be utilized under the supervision of a qualified physician/practitioner

Information regarding the restraint procedure should be given to the patient

The use of restraints for discipline or staff convenience is forbidden an illegal Vital signs should be monitored at all times during mechanical restraint period

Facilitation of the development of a therapeutic alliance with the patient

Protection of the patient, other patients, staff, and/or property

**Specific indications for mechanical restraints**

Provision of a respite for regaining control

Mitigation of staff fears/anxiety

Reduction of overall stimuli Repression/control of aggression

Physical containment

**General considerations**

record

followed

restraints

harm

Consideration must also be given to the immobilized patient's positioning, including appropriate contingency plans if complications occur. If restrained while prone, patients may be in danger of suffocation. Consequently, if this position is utilized, the patient must

#### **General considerations**

**7. Physical restraints**

164 Vignettes in Patient Safety - Volume 1

[70].

as the concurrent use of full side rails [75, 76].

Approximately 50% of intensive care unit patients [55], 20% of patients on neurologyneurosurgery wards [56], and 25% of individuals admitted to mental health facilities experience at least one type of "control intervention" during acute hospitalization [57]. One method of such "control intervention" is the use of physical restraints (PhyR), defined as any device, material or equipment attached to or near a person's body, which is intended to prevent a person's free body movement to a position of choice and/or a person's normal and unrestricted access to their body [58]. The use of PhyR is relatively common, with some authors suggesting that it is overused [43, 59]. As a consequence, there are numerous initiatives to reduce the reliance on PhyR, especially among the most vulnerable patient populations [60–62]. As mentioned in this chapter's clinical vignette, restraints may not eliminate the risk of DSH. Therefore, the choice to use PhyR continues to be controversial and should only be entertained as a last resort option when there exists a real possibility of serious physical injury to self or others [63–65]. There is therefore a need for caution and balanced judgment on part of the treatment team, beginning with a well-informed understanding of potential complica-

Published guidelines provide a framework for the use of PhyR in a variety of settings [66, 67]. The initial criteria for instituting PhyR should be based on a thorough evaluation of a patient's mental status. An individual at risk for DSH, who is cognitively aware of this risk of harm to themselves, is less likely to become violent while in restraints and can therefore be placed in a soft restraint apparatus [56]. However, in the event that a patient becomes increasingly violent when actively restrained, there is an increased risk of limb injury due to a tendency for the device to tighten [68]. Moreover, patients who are restrained and sustain secondary trauma are prone to more serious injuries because part(s) of their body is/are physically tied, which may render normal protective, instinctive responses ineffective. Other complications of soft restraints include abrasions, contusions, immobility, and dislodgement of various devices (e.g., intravenous lines, feeding tubes) [68–71]. In some cases, leather restraints can be utilized if the patient becomes increasingly combative; however, appropriate precautions are critical when using leather PhyR because device removal can be challenging in emergent situations

The specific placement of restraints and number of application points are important in ensuring the balance between satisfactory outcomes and minimizing complications [56, 58, 72]. If the patient poses a low risk of violence, a two-point restraint system can be utilized safely [70, 73]. Four-point restraints should be reserved for combative and violent patients in the acute setting to maximally prevent uncontrolled movements [70]. Again, applicable guidelines should be followed to reduce restraint-related complications (e.g., self-injury, overturning of the stretcher) while ensuring adequate immobilization of the patient [70, 74]. Belt and jacket restraints can serve as adjunct to extremity restraints, but mandate special precautions, such

Consideration must also be given to the immobilized patient's positioning, including appropriate contingency plans if complications occur. If restrained while prone, patients may be in danger of suffocation. Consequently, if this position is utilized, the patient must

tions and safety procedures designed to prevent adverse outcomes [63–65].

Detailed documentation of all restraint-related clinical decisions and procedures should be made in the medical record

Duration of restraint use should be firmly justified and continue for the least amount of time applicable

In all instances of mechanical restraint use, an individualized clinical management plan should be established and followed

Information regarding the restraint procedure should be given to the patient

Mechanical restraints should be utilized in "last resort" capacity when all other interventions have failed

Periodic re-evaluation, as frequent as every 30 min, should be performed to determine the need for continuation of restraints

Restraints should always be utilized under the supervision of a qualified physician/practitioner

Restraints should be placed and removed in team setting by sufficient number of staff members to prevent patient harm

The use of restraints for discipline or staff convenience is forbidden an illegal

Vital signs should be monitored at all times during mechanical restraint period

#### **Specific indications for mechanical restraints**

Facilitation of diagnosis through behavioral control under conditions requiring minimal or no medication use

Facilitation of the development of a therapeutic alliance with the patient

Mitigation of staff fears/anxiety

Physical containment

Protection of the patient, other patients, staff, and/or property

Provision of a respite for regaining control

Reduction of overall stimuli

Repression/control of aggression

**Table 1.** Important considerations for placement and maintenance of mechanical restraints.

be provided with adequate space for free chest expansion and his or her respiratory and airway status must be closely monitored [77, 78]. If restrained while supine, patients are at risk for aspiration [79]. Thus, the patient's head should be positioned at 30° with the ability to rotate freely in order to avoid this complication [70, 79]. Moreover, optimal configuration of 4-point restraints calls for one arm being directed up toward the patient's head and the other arm down toward the patient's hip. Aside from these positional considerations, additional precautions must be instituted regarding prolonged immobilization due to the risk of pressure ulcers, focal neurovascular compression, and deep vein thrombosis [70, 80].

In addition to various potential physical complications inherent in the use of restraints, patients may experience significant emotional trauma from the ordeal, such as feelings of powerlessness, humiliation, and/or the sensation of terror seen with PhyR [81]. Common manifestations of restraint-related psychological trauma include "flashbacks" to the emotional ordeal (e.g., retraumatization), hopelessness and helplessness (e.g., "broken spirit"), negative general psychological impact, and perceptions of unethical healthcare practices [82, 83]. All of the above factors must be considered when implementing PhyR, although they should not prevent the use of restraints if clinically justified and necessary [84, 85].

[103]. It has been reported that droperidol can be given intramuscularly at a dosage up to 10 mg to have the same efficacy as other sedatives [103]. Of note, a prior history of cardiac disease is a contraindication due to a black box FDA warning for fatal cardiac arrhythmias when intravenous doses exceed 2.5 mg [104]. This warning carries a strong recommendation to precede the use of droperidol with an ECG to screen for any cardiac abnormalities. Other side effects include the risk of developing dystonia or akathisia [105]. These symptoms can be ameliorated through the co-administration of histamine (H1) antagonists such as Diphenhydramine or Promethazine [106]. Importantly, precautions should be taken when using droperidol (and other similar agents) as adjunctive therapy to mechanical restraints due to potentially elevated risk of suffocation or posi-

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167

There is a paucity of research on acute manifestations of DSH in patients under the influence of cocaine. The existing literature recommends the use of lorazepam as the primary agent of choice for physiological alterations secondary to cocaine use [108]. This medication can also be used as first-line therapy for patients experiencing withdrawal from alcohol or recreational stimulants, as it has been shown to be more effective than neuroleptic drugs, such as haloperidol [109]. However, due to its CNS depressive effects and long-duration, Lorazepam should not be used if a patient appears intoxicated or if he/she has ingested other sedatives [104]. Further precautions should be taken in patients of childbearing age as this medication is a class D agent

Olanzapine, a second generation thienobenzodiazepine antipsychotic, may also be considered in cases of acute psychosis with associated DSH [110]. This medication, which antagonizes dopamine and serotonin, is equally as effective as lorazepam and haloperidol in the acute setting [70]. However, a thorough history is necessary before using this drug as it can lead to hypotension when combined with anti-muscarinic medications [70]. Currently, there is limited understanding of the use of this medication in patients presenting with acute psychosis,

Midazolam (a benzodiazepine) is indicated for situations where short duration of action is desired [113, 114]. Midazolam has similar efficacy to lorazepam or haloperidol and may therefore be beneficial in patients who do not require long term management and whose risk of DSH may be related to substance abuse and acute intoxication [109]. Furthermore, due to its short action, its systemic effects on the patient quickly wear off, allowing subsequent evaluations, discharge from the ED, and transition to outpatient setting in a more

Other agents have been described in the management of acute behavioral disturbances, including DSH, but the limited scope of this chapter does not permit a more in-depth discussion [103, 104, 114–119]. In all similar cases, the goal is to medically stabilize the patient and then prevent recurrent episodes of self-harm [115]. It is important to note that while our discussion describes largely a local pattern of practice, a number of effective professional guidelines have been published in this general area. Consequently, the reader is referred to those guidance documents for further information regarding the

tional asphyxia [107].

in the setting of pregnancy [70].

as well as substance abuse [111, 112].

timely fashion [70].

Due to the potential for severe complications and even mortality associated with PhyR use, the Joint Commission established protocols pertaining to the usage of restraints in the healthcare setting [86]. Restraints need to be justified, well documented, and monitored at all times to help minimize the risk of iatrogenic injury [87]. Current guidelines recommend the restraint use for children ages < 9 years be limited to 1 h; 2 h for adolescents ages 9–17 years; and 4 h for adults before mandatory clinical re-evaluation [70, 88]. These precautions are necessary to minimize both the physical and psychological complications of PhyR use [89, 90]. Details regarding indications and maintenance of mechanical restraints are provided in **Table 1**.

### **8. Pharmacological "restraints"**

The high complication risk of PhyR has led to the increased use of pharmacological agents, as either monotherapy or polytherapy, in the management of high risk patients at risk for DSH. In fact, the prevalence of chemical restraints in certain settings exceeds 33% [91]. At times, pharmacological approaches are used in conjunction with PhyR [92]. Some of the most common pharmacological agents used in psychiatric emergencies include haloperidol, droperidol, lorazepam, olanzapine, and midazolam [93–95]. Due to the ethical considerations of PhyR, these pharmacological agents are often first line therapy in a patient who is at acute risk for self-harm. Multi-modality, high intensity, or combined therapy is often employed when a patient becomes acutely violent or combative, thus posing as an immediate danger to both themselves and others [95, 96].

Haloperidol is a butyrophenone antipsychotic agent with onset of action within 30–60 min of administration and clinical effect lasting up to 24 h [97]. Haloperidol is commonly used in the setting of psychosis and self-harming behaviors because of its minimal drug interactions with non-psychiatric medications, which is essential due to the challenge of obtaining a medical history from acutely agitated patients. In a study of ED patients with agitated, threatening, or violent behaviors, haloperidol resulted in significant clinical improvement within 30 min of administration in 83% of patients [98]. Furthermore, due to the lack of interactions and relatively favorable safety profile, this medication is used as first-line therapy for patients at risk for DSH [99, 100]. Caution is nonetheless necessary due to some rare, yet potentially serious adverse events associated with haloperidol use. The most prominent side effect includes extrapyramidal syndrome and dystonia, which can occur in up to 20% of patients [97]. Haloperidol can also increase the QTc interval, cause torsade de pointes, and even sudden death. Consequently, patients should optimally undergo an ECG prior to haloperidol administration [101].

Another agent, droperidol, may be considered when immediate sedation is required [102]. Droperidol has a rapid onset of 15–30 min, making it more suitable for acute situations [103]. It has been reported that droperidol can be given intramuscularly at a dosage up to 10 mg to have the same efficacy as other sedatives [103]. Of note, a prior history of cardiac disease is a contraindication due to a black box FDA warning for fatal cardiac arrhythmias when intravenous doses exceed 2.5 mg [104]. This warning carries a strong recommendation to precede the use of droperidol with an ECG to screen for any cardiac abnormalities. Other side effects include the risk of developing dystonia or akathisia [105]. These symptoms can be ameliorated through the co-administration of histamine (H1) antagonists such as Diphenhydramine or Promethazine [106]. Importantly, precautions should be taken when using droperidol (and other similar agents) as adjunctive therapy to mechanical restraints due to potentially elevated risk of suffocation or positional asphyxia [107].

negative general psychological impact, and perceptions of unethical healthcare practices [82, 83]. All of the above factors must be considered when implementing PhyR, although they

Due to the potential for severe complications and even mortality associated with PhyR use, the Joint Commission established protocols pertaining to the usage of restraints in the healthcare setting [86]. Restraints need to be justified, well documented, and monitored at all times to help minimize the risk of iatrogenic injury [87]. Current guidelines recommend the restraint use for children ages < 9 years be limited to 1 h; 2 h for adolescents ages 9–17 years; and 4 h for adults before mandatory clinical re-evaluation [70, 88]. These precautions are necessary to minimize both the physical and psychological complications of PhyR use [89, 90]. Details regarding indications and maintenance of mechanical restraints

The high complication risk of PhyR has led to the increased use of pharmacological agents, as either monotherapy or polytherapy, in the management of high risk patients at risk for DSH. In fact, the prevalence of chemical restraints in certain settings exceeds 33% [91]. At times, pharmacological approaches are used in conjunction with PhyR [92]. Some of the most common pharmacological agents used in psychiatric emergencies include haloperidol, droperidol, lorazepam, olanzapine, and midazolam [93–95]. Due to the ethical considerations of PhyR, these pharmacological agents are often first line therapy in a patient who is at acute risk for self-harm. Multi-modality, high intensity, or combined therapy is often employed when a patient becomes acutely violent or combative, thus posing as an immediate danger to both

Haloperidol is a butyrophenone antipsychotic agent with onset of action within 30–60 min of administration and clinical effect lasting up to 24 h [97]. Haloperidol is commonly used in the setting of psychosis and self-harming behaviors because of its minimal drug interactions with non-psychiatric medications, which is essential due to the challenge of obtaining a medical history from acutely agitated patients. In a study of ED patients with agitated, threatening, or violent behaviors, haloperidol resulted in significant clinical improvement within 30 min of administration in 83% of patients [98]. Furthermore, due to the lack of interactions and relatively favorable safety profile, this medication is used as first-line therapy for patients at risk for DSH [99, 100]. Caution is nonetheless necessary due to some rare, yet potentially serious adverse events associated with haloperidol use. The most prominent side effect includes extrapyramidal syndrome and dystonia, which can occur in up to 20% of patients [97]. Haloperidol can also increase the QTc interval, cause torsade de pointes, and even sudden death. Consequently, patients should optimally undergo an ECG prior to halo-

Another agent, droperidol, may be considered when immediate sedation is required [102]. Droperidol has a rapid onset of 15–30 min, making it more suitable for acute situations

should not prevent the use of restraints if clinically justified and necessary [84, 85].

are provided in **Table 1**.

166 Vignettes in Patient Safety - Volume 1

**8. Pharmacological "restraints"**

themselves and others [95, 96].

peridol administration [101].

There is a paucity of research on acute manifestations of DSH in patients under the influence of cocaine. The existing literature recommends the use of lorazepam as the primary agent of choice for physiological alterations secondary to cocaine use [108]. This medication can also be used as first-line therapy for patients experiencing withdrawal from alcohol or recreational stimulants, as it has been shown to be more effective than neuroleptic drugs, such as haloperidol [109]. However, due to its CNS depressive effects and long-duration, Lorazepam should not be used if a patient appears intoxicated or if he/she has ingested other sedatives [104]. Further precautions should be taken in patients of childbearing age as this medication is a class D agent in the setting of pregnancy [70].

Olanzapine, a second generation thienobenzodiazepine antipsychotic, may also be considered in cases of acute psychosis with associated DSH [110]. This medication, which antagonizes dopamine and serotonin, is equally as effective as lorazepam and haloperidol in the acute setting [70]. However, a thorough history is necessary before using this drug as it can lead to hypotension when combined with anti-muscarinic medications [70]. Currently, there is limited understanding of the use of this medication in patients presenting with acute psychosis, as well as substance abuse [111, 112].

Midazolam (a benzodiazepine) is indicated for situations where short duration of action is desired [113, 114]. Midazolam has similar efficacy to lorazepam or haloperidol and may therefore be beneficial in patients who do not require long term management and whose risk of DSH may be related to substance abuse and acute intoxication [109]. Furthermore, due to its short action, its systemic effects on the patient quickly wear off, allowing subsequent evaluations, discharge from the ED, and transition to outpatient setting in a more timely fashion [70].

Other agents have been described in the management of acute behavioral disturbances, including DSH, but the limited scope of this chapter does not permit a more in-depth discussion [103, 104, 114–119]. In all similar cases, the goal is to medically stabilize the patient and then prevent recurrent episodes of self-harm [115]. It is important to note that while our discussion describes largely a local pattern of practice, a number of effective professional guidelines have been published in this general area. Consequently, the reader is referred to those guidance documents for further information regarding the overall diagnostic framework and the associated implementation of both physical and pharmacological restraints [120–123].

**Author details**

Farhad Sholevar4

Sciences, Toledo, OH, USA

13 March 2016]

2008;**193**(5):395-401

, Joshua Luster<sup>1</sup>

, Jacqueline Seoane1

1 Temple University School of Medicine, St. Luke's University Hospital Campus, Bethlehem,

2 Department of Research and Innovation, St. Luke's University Health Network, Bethlehem,

3 Department of Anesthesiology, The University of Toledo College of Medicine and Life

[1] Rothaus C. Violence Against Health Care Workers. 2017. Available from: http://blogs. nejm.org/now/index.php/violence-against-health-care-workers/2016/04/28/ [Accessed:

[2] Jacobson R. Epidemic of Violence against Health Care Workers Plagues Hospitals. 2017; Available from: https://www.scientificamerican.com/article/epidemic-of-violence-

[3] Mitchell AM, et al. Suicide assessment in hospital emergency departments: Implications for patient satisfaction and compliance. Topics in Emergency Medicine. 2005;**27**(4):302

[4] Bowers L, et al. Relationship between service ecology, special observation and selfharm during acute in-patient care: City-128 study. The British Journal of Psychiatry.

[6] de Cates AN, et al. Are neurocognitive factors associated with repetition of self-harm? A

[7] Winchel RM, Stanley M. Self-injurious behavior: A review of the behavior and biology of

[8] Wyder M. Understanding deliberate self harm: An enquiry into attempted suicide. 2004; Available online at: http://researchdirect.westernsydney.edu.au/islandora/object/

systematic review. Neuroscience & Biobehavioral Reviews. 2017;**72**:261-277.

self-mutilation. The American Journal of Psychiatry. 1991;**148**(3):306

uws%3A644/datastream/PDF/view (Last Access on June 9, 2017)

against-health-care-workers-plagues-hospitals/ [Accessed: 13 March 2014]

[5] Skegg K. Self-harm. The Lancet. 2005;**366**(9495):1471-1483

4 Department of Psychiatry, St. Luke's University Health Network, Bethlehem, PA, USA

 and Christine Marchionni<sup>4</sup> \*Address all correspondence to: stanislaw.stawicki@sluhn.org

, Stanislaw P. Stawicki2

Patient Self-Harm in the Emergency Department: An Evidence-Based Approach

\*, Thomas J. Papadimos3

http://dx.doi.org/10.5772/intechopen.69640

,

169

Ronya Silmi1

PA, USA

PA, USA

**References**

#### **9. Management and prevention of deliberate self-harm: key points**

Emergency management of acutely violent patients, especially those involved in DSH, can be challenging [124]. Similar to many other medical conditions, prevention of DSH should be given the highest priority. This includes prevention of both initial and recurrent episodes of DSH [125, 126], especially since repeated self-harm is associated with long-term, cumulative risk of death [127]. Many patients who inflict self-harm can be treated quickly and effectively, without the need for clinical escalation. The initial approach to escalation usually involves close direct observation [39–41] and the provision of an injury-proof, secluded environment [128, 129]. However, individuals who continue to exhibit behaviors that constitute danger to self or others may require the implementation of physical or pharmacological restraints, i.e., containment procedures [70, 72, 117]. Because of the significant risk for potentially serious complications associated with the use of restraints, special care and attention is required in such situations [129–131]. Additionally, we highlighted progressive views regarding containment procedures and how they can be implemented effectively, while at the same time referencing their drawbacks. Once the patient has stabilized clinically, a combination of psychosocial and pharmacological approaches is utilized to prevent repetitive self-harming behaviors [125, 132]. Multidisciplinary teams including primary care practitioners, community and behavioral health experts provide the best framework for long-term recovery [133, 134].

#### **10. Conclusions**

DSH will continue to be a challenging problem that confronts health care providers in the ED (and other areas of the hospital). The approach to such patients must be multidisciplinary and occur in an evidence-based environment. Practitioners must be aware of their hospital protocols used to address patients who present with DSH. Detailed behavioral health assessment following DSH episodes should be completed as soon as the patient is medically stable. Specifically, an inventory of comorbid psychiatric disorders that put a patient at risk for DSH, especially suicide, must be catalogued as well as a determination of the presence of associated risk factors that may contribute to an escalation of illness severity. The practitioner must also become well versed in the use of direct observation, containment procedures (seclusion and physical restraints), and pharmacological restraints, as well as an appreciation as to the direction of new clinical evidence regarding care and the promulgation of new legislation. Clinical approaches and legal perspectives in this field will continue to evolve.

### **Author details**

overall diagnostic framework and the associated implementation of both physical and

Emergency management of acutely violent patients, especially those involved in DSH, can be challenging [124]. Similar to many other medical conditions, prevention of DSH should be given the highest priority. This includes prevention of both initial and recurrent episodes of DSH [125, 126], especially since repeated self-harm is associated with long-term, cumulative risk of death [127]. Many patients who inflict self-harm can be treated quickly and effectively, without the need for clinical escalation. The initial approach to escalation usually involves close direct observation [39–41] and the provision of an injury-proof, secluded environment [128, 129]. However, individuals who continue to exhibit behaviors that constitute danger to self or others may require the implementation of physical or pharmacological restraints, i.e., containment procedures [70, 72, 117]. Because of the significant risk for potentially serious complications associated with the use of restraints, special care and attention is required in such situations [129–131]. Additionally, we highlighted progressive views regarding containment procedures and how they can be implemented effectively, while at the same time referencing their drawbacks. Once the patient has stabilized clinically, a combination of psychosocial and pharmacological approaches is utilized to prevent repetitive self-harming behaviors [125, 132]. Multidisciplinary teams including primary care practitioners, community and behavioral health experts provide the best framework for

DSH will continue to be a challenging problem that confronts health care providers in the ED (and other areas of the hospital). The approach to such patients must be multidisciplinary and occur in an evidence-based environment. Practitioners must be aware of their hospital protocols used to address patients who present with DSH. Detailed behavioral health assessment following DSH episodes should be completed as soon as the patient is medically stable. Specifically, an inventory of comorbid psychiatric disorders that put a patient at risk for DSH, especially suicide, must be catalogued as well as a determination of the presence of associated risk factors that may contribute to an escalation of illness severity. The practitioner must also become well versed in the use of direct observation, containment procedures (seclusion and physical restraints), and pharmacological restraints, as well as an appreciation as to the direction of new clinical evidence regarding care and the promulgation of new legislation. Clinical approaches and legal perspectives in this field

**9. Management and prevention of deliberate self-harm: key points**

pharmacological restraints [120–123].

168 Vignettes in Patient Safety - Volume 1

long-term recovery [133, 134].

**10. Conclusions**

will continue to evolve.

Ronya Silmi1 , Joshua Luster<sup>1</sup> , Jacqueline Seoane1 , Stanislaw P. Stawicki2 \*, Thomas J. Papadimos3 , Farhad Sholevar4 and Christine Marchionni<sup>4</sup>

\*Address all correspondence to: stanislaw.stawicki@sluhn.org

1 Temple University School of Medicine, St. Luke's University Hospital Campus, Bethlehem, PA, USA

2 Department of Research and Innovation, St. Luke's University Health Network, Bethlehem, PA, USA

3 Department of Anesthesiology, The University of Toledo College of Medicine and Life Sciences, Toledo, OH, USA

4 Department of Psychiatry, St. Luke's University Health Network, Bethlehem, PA, USA

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## *Edited by Michael S. Firstenberg and Stanislaw P. Stawicki*

It is clearly recognized that medical errors represent a significant source of preventable healthcare-related morbidity and mortality. Furthermore, evidence shows that such complications are often the result of a series of smaller errors, missed opportunities, poor communication, breakdowns in established guidelines or protocols, or systembased deficiencies. While such events often start with the misadventures of an individual, it is how such events are managed that can determine outcomes and hopefully prevent future adverse events. The goal of Vignettes in Patient Safety is to illustrate and discuss, in a clinically relevant format, examples in which evidencebased approaches to patient care, using established methodologies to develop highly functional multidisciplinary teams, can help foster an institutional culture of patient safety and high-quality care delivery.

Vignettes in Patient Safety - Volume 1

Vignettes in Patient Safety

Volume 1

*Edited by Michael S. Firstenberg* 

*and Stanislaw P. Stawicki*

Photo by pittawut / iStock