Recognizing pressure injury in the darkly pigmented skin type.
Mrs. J., a 66-year old African-American, walked into the emergency department of a 600-bed urban hospital complaining of blood in her urine for the past 24 hours and mild suprapubic abdominal pain. She was widowed and lived independently in her own home after retiring 2 years ago after 31 years of service as a public school teacher. Mrs. J. was active in her church and community, and involved with her children and grandchildren who lived nearby. She had a history of chronic obstructive pulmonary disease, morbid obesity, hypertension, diabetes type 2, hyperlipidemia, and atrial fibrillation treated with war-farin (Coumadin[R]).
With the exception of the hematuria and abdominal discomfort, physical assessment was negative. Height was 5'6", weight 256 lbs, and calculated body mass index 41.3. Laboratory results supported a diagnosis of urinary tract infection with gross hematuria, acute renal failure with blood urea nitrogen of 32 mg/dL and creatinine 3.0 mg/dL, and hemoglobin of 9.9 g/dL.
A subsequent urology consult resulted in orders for computed tomography of the abdomen and pelvis, which demonstrated a right renal mass consistent with a neoplasm. An adrenal-sparing laparoscopic nephrectomy was performed the next morning.
After surgery, Mrs. J. was admitted to a renal-urology unit. Although hospital policy indicated every patient should have a complete skin assessment performed upon admission to the unit, this was not performed for Mrs. J. A clinical nurse documented a Braden score of 21 (range 6-23), indicating no interventions were needed to reduce risk for pressure injury. In spite of her obesity, Mrs. J. was placed on the standard hospital foam surface bed rather than a specialty bed designed to distribute pressure (Hyun et al., 2013).
The first 18 hours on the unit were unremarkable. When Mrs. J. complained of pain and some shortness of breath, the nursing staff placed the bed in high Fowler's position to facilitate patient comfort. Over the next 24 hours, Mrs. J. became hypotensive and had to be placed on vasopressors for hemodynamic support. Early in the morning, after 42 hours on the renalurology unit, she was transferred to the medical intensive care unit (MICU).
The admitting nurse on the MICU performed the required admission skin assessment and documented a "large bruised-like area" on Mrs. J's coccyx, a finding consistent with pressure injury. The nurse immediately initiated a consult with the wound-ostomy nurse, who examined the patient within 1 hour.
The wound-ostomy nurse documented a Braden score of 8 ([less than or equal to] 17 considered at risk for pressure injury) (Hyun et al., 2013). The patient had sustained deep tissue injury in a 15 x 18 cm area from her coccyx to her lower buttocks. The epidermis was intact but a small, fluid-filled blister was noted in the middle of the ulcer, and the color was documented as 100% deep purple. The entire ulcer felt boggy on palpation and was cool to the touch.
During the next 5 days, the epidermis over this area began to ulcerate; the area developed slough and became necrotic. The wound continued to break down over the next 2 weeks, with copious amounts of foul purulent exudate and a moderate amount of serosanguineous drainage. At week 3, the wound measured 15 x 18 x 8 cm. Bony prominences, tendons, and muscle were clearly visible. The deep tissue injury had progressed to a Stage IV pressure ulcer in less than 3 weeks after the patient's hospital admission.
Treatment of Pressure Ulcer
Mrs. J. underwent her first surgical debridement of this wound 3 weeks after its diagnosis as a deep tissue injury. The first excisional debridement included removal of devitalized areas of fat and tissue to the bone level; areas of bone were soft due to infiltrated purulent exudate. Sharp debridement at the bedside failed to establish stasis of necrosis, and eschar continued to develop. Hemostasis was achieved with electrocautery; the wound was irrigated and packed with saline gauze dressings.
Mrs. J. was discharged from the hospital 32 days after admission in stable condition to an extended care facility (ECF). After 4 days in the ECF, Mrs. J. became febrile and began to experience altered mental status. She was returned to the hospital by ambulance and was admitted to the MICU with a diagnosis of sepsis.
The infectious disease service was consulted and wound cultures revealed anaerobic isolates. The wound was infected concurrently with Proteus and Escherichia coli; blood cultures revealed Proteus species, group D streptococci. Mrs. J. was treated with an empirical antibiotic regime and remained in MICU. After 3 weeks in the MICU, she was transferred to a medical-surgical unit.
Mrs. J. remained in the hospital for the next 4 months and underwent four more surgical debridements with weekly bedside debridements. She developed hypoproteinemia and hypoalbuminemia. Plasma cortisol values were high; electrolytes, especially potassium and magnesium, were depleted, and Mrs. J. required nutritional support.
This patient's hospital length of stay reached almost 1 year. Mrs. J. died from complications of sepsis related to the severity of her hospital-acquired pressure ulcer. The cost of treatment approached $500,000.
Scope of the Problem
The Centers for Medicare & Medicaid Services (2008; Jarrett, Holt, & LaBresh, 2014) no longer considers treatment of hospital-acquired pressure ulcers a reimbursable condition. The economic burden related to hospital-acquired pressure ulcers exceeds $3.6 billion annually (Miller, Parker, Blasiole, Beinlich, & Fulton, 2013). Federal regulations now indicate hospital leaders must create protocols and programs for the prevention of pressure injury (Ayello, 2011; Fyder & Ayello, 2012), but the protocols may not address the specific needs of patients with darkly pigmented skin types.
Pressure ulcer surveys across the country consistently reveal overall prevalence rates of pressure ulcers among dark-skinned individuals as higher than those of light-skinned individuals (Cai, Mukamel, & Temkin-Greener, 2010). In the most recent Nationwide Inpatient Sample, for example, African-American patients had an increased risk of pressure ulcers (odd ratio=2.3, 1.2) (Fogerty, Guy, Barbul, Nanney, & Abumrad, 2009). Additionally, some research indicates dark-skinned individuals have a tendency to develop more severe pressure ulcers (Clark, 2010); an emerging body of evidence further suggests patients with darkly pigmented skin have more pressure ulcer-associated mortality (Fyder, 2009). This increased risk is observed across all age groups in males and females, and does not correlate with any socioeconomic or hospital characteristics currently tracked by nationwide inpatient surveys (Fogerty et al., 2009).
Health care leaders across the country are trying to reduce the prevalence of pressure injury and implement evidence-based pressure ulcer prevention protocols. However, research illustrates existing standards apply only to patients with light skin (VanGilder, MacFarlane, Harrison, Fachenbruch, & Meyer, 2010). When assessing patients with darkly pigmented skin, however, clinicians are hampered by the lack of a universal, evidence-based guideline for skin assessment. When the case study patient Mrs. J. was admitted to the MICU, the nurse was unsure if the discol oration on the patient's coccyx was a bruise or pressure injury. The creation and adaptation of a simple concise tool would facilitate appropriate care for patients with dark pigmented skin.
State of the Science
The state of the science regarding pressure ulcers is described briefly. This includes current staging categories, the underlying pathophysiology of deep tissue injury caused by pressure, and difficulties associated with detection of pressure injury in darkly pigmented skin.
Current Staging System
A pressure ulcer is defined as a wound caused by incessant pressure or repeated friction that damages the skin and its underlying architecture (National Pressure Ulcer Advisory Panel, European Pressure Ulcer Advisory Panel, Pan Pacific Pressure Injury Alliance, 2014). Pressure ulcers are believed to begin in the subdermal tissue between the skin and bone, progressing by direct extension in the dermal tissue. Because epidermal tissue is denser than the dermal tissue, edema collects and pools within the dermis before it breaks through to the epidermis to become visible as a wound.
Pressure ulcers can occur in any anatomical region, but are found most frequently over bony prominences. Areas such as the sacrum, ischium, trochanter, coccyx (as in this patient's case), posterior iliac spine, and heel are the most common (National Pressure Ulcer Advisory Panel, European Pressure Ulcer Advisory Panel [NPUAP/ EPUAP], 2009). However, any area that sustains pressure is subject to a pressure injury.
Pressure ulcers are categorized by severity, with a staging system that was defined first by Shea in 1975 and then by the National Pressure Ulcer Advisory Panel in 1987 (NPUAP/EPUAP, 2009). The NPUAP's four-stage pressure ulcer classification is based on clinical manifestations and the amount of exposed muscle and bone (see Table 1). In 2007, the NPUAP redefined the stages of pressure ulcers with the addition of two new categories: suspected deep tissue injury (DTI) and unstageable pressure ulcers. Deep tissue injury is an internal wound that deteriorates quickly. An unstageable pressure ulcer is described as full thickness tissue loss in which the base of the ulcer is covered by slough or eschar.
One of the most important factors in the development of pressure ulcers is unrelieved pressure. Pressure, over time, occludes blood and lymphatic circulation. The baseline pressure needed to keep capillaries open for tissue perfusion is 25-30 mm Hg in arterial skin capillaries and 5-10 mm Hg at the venous end. When external pressure exceeds tissue capillary pressure, tissue ischemia occurs and pressure ulcers develop. Thus, prolonged pressure deprives tissues of oxygen and nutrients, ultimately causing necrosis and ulceration (Anders et al., 2010). When the pressure on the tissue and capillaries exceeds the baseline pressures for 2 or more hours, or exceeds it excessively for a shorter duration of time, tissue damage and necrosis will occur (Agrawal & Chauhan, 2012; Flike, 2013). With the case study patient, the pressure injury likely started sometime after she was placed in high Fowler's position. The patient's obesity increased the pressure on her coccyx, thus contributing to her extensive injury.
If pressure is relieved before the critical time has elapsed, a normal compensatory mechanism (reactive hyperemia) will restore tissue nutrition and compensate for compromised circulation. If pressure is not relieved, the blood vessel collapses and resulting ischemia leads to impaired waste removal from the tissue (Bates-Jensen, McCreath, & Pongquan, 2009; Casey, 2013). The toxic byproducts of impaired waste removal cause increased cell membrane permeability, edema, and eventual cell death.
After cell death, the tissue becomes necrotic and a repair process known as autolytic digestion occurs to remove internal necrotic tissue. As autolytic digestion progresses, the area of pressure injury becomes cool in temperature. When palpated, the area may feel boggy or sponge-like as the tissue liquefies. Finally, as the necrotic tissue is sloughed, the extent of the pressure injury is revealed and the wound is identified and staged according to the amount of viable tissue lost (NPUAP/EPUAP, 2009).
Suspected Deep Tissue Injury Caused from Pressure
The NPUAP/EPUAP (2009) defined DTI as a pressure injury to subcutaneous tissue under intact skin. Evolution of the DTI may be rapid and exposes many layers of tissue (Flike, 2013; Gefen, Farid, & Shaywitz, 2013; Sullivan, 2013). Initially, DTI presents as a purple/ maroon nonblanchable area similar in appearance to a deep bruise. A thin blister roof, filled with blood or serous fluid, is observed commonly during the initial period of the DTI. Unlike the mechanics of a Stage I-IV pressure ulcer in which injury first occurs to subdermal tissue (Sullivan, 2013), DTI forms over the bony prominence from the inside to the outside. Superficial damage is not seen until later, when deep tissue has undergone necrosis. The necrotic tissue will reach the outer layer of the skin and appear as an external wound (NPUAP/EPUAP, 2009). The external wound then will be staged as a pressure ulcer according to the amount of tissue loss.
Mrs. J.'s pressure injury was typical of a DTI. The first purple/maroon area was large, with a popped blood blister in the center of the injury that appeared as a skin tear. The tissue was cool, soft, and boggy. As the internal tissue necrosed and liquefied, dead tissue started to slough. Daily, the wound worsened until all the damaged tissue was gone.
Difficult Detection in Darkly Pigmented Skin
Experts have identified the difficulty of classifying DTI on the dark-skinned patient because skin pigmentation affects the apparent color of a lesion. Hypoxic tissue under pale skin and necrotic tissue under darkly pigmented skin were found to look nearly identical to an observer when viewed directly from above. This suggests tissue necrosis such as DTI could be classified incorrectly as a Stage I pressure ulcer (VanGilder et al., 2010).
Tissue hypoxia from pressure usually is detected first by the presence of nonblanching erythema. This early stage of vibrant red reversible damage, while easily observed in the light-skinned patient, is not distinguished readily on dark skin because it is difficult to visualize erythema in the presence of a great deal of skin pigment. In the darkly pigmented patient, the hypoxic area appears darker than the surrounding skin (Sommers, 2011).
Current Assessment Criteria
The most commonly used tool to assess risk for skin impairment is the Braden Scale for Predicting Pressure Sore Risk (Bergstrom, Demuth, & Braden, 1987). Universally accepted in health care as a valid and reliable assessment tool, the Braden Scale is familiar as most nurses use it to identify patients at risk for pressure ulcers. The Braden Scale is a summated rating scale comprised of six subscales; five subscales are scored from 1-4, with the friction and shear subscale scored 1-3. Total point range is 6-23 (Bergstrom & Braden, 2002). The lower the total score, the higher the predicted risk of acquiring a pressure injury.
Evidence about the sensitivity and validity of the Braden Scale is conflicting when used for people with darkly pigmented skin. A large multi-site study of the predictive validity of the Braden Scale (Bergstrom & Braden, 2002) among Black and White subjects was conducted in nursing homes, tertiary care, and Veterans Administration Centers to determine if the Braden Scale predicts pressure ulcer risk similarly for both racial groups. The Braden Scale score was the best predictor of pressure risk (Bergstrom & Braden, 2002). In contrast, Lyder and coauthors (1999) suggested the Braden Scale score was a significant predictor of pressure ulcer development for Blacks age 75 or older, but it under-predicted the risk of pressure ulcers for Blacks and Latinos/ Hispanics age 74 and younger. Further research is needed for a risk assessment tool validated for patients with darkly pigmented skin (Sommers, 2011).
Education Reduces Adverse Events
Wound experts agree a need exists for increased education focused on darkly pigmented skin. Current assessment techniques are not sensitive enough to make an early diagnosis of tissue breakdown in dark skin (Black et al., 2010).
Consensus Panel Recommendations
A multidisciplinary panel of wound experts in the United States examined current literature to determine if a standardized, accurate process was available to facilitate clinicians' accurate identification and documentation of pressure ulcer stages and tissue types (Black et al., 2010). They examined the curricula of 50 medical schools and found students received an average of only 4 hours of instruction on wound-related topics, including the anatomy and physiology of wounds and wound healing. Nurses received similar minimal instruction during their basic education. The convened panel identified a need for accurate assessments with a common standardized language. Members supported added education concerning wound healing and pressure ulcers in curricula as well as in professional staff education. The panel also concluded a need exists for research to determine reliability of the staging system revised by the NPUAP in 2007 as it pertains to darkly pigmented skin.
Proposed Assessment for Patients with Darkly Pigmented Skin
The following guidelines are proposed for use in patients with darkly pigmented skin:
1. Use a pocket guide. Pocket reference (see Table 2) should be used by any clinician unfamiliar with darkly pigmented skin.
2. Image data base in the electronic health record. Clear, accurate photographs of various stages of pressure ulcers should be readily available to the staff for quick reference.
3. Know the normal variations in dark skin. See Table 3.
4. Ensure excellent lighting when assessing darkly pigmented skin. Use a penlight or flashlight to aid in distinguishing color changes. Avoid fluorescent lighting as it casts blue tones on dark skin.
5. Ongoing education. Risk prevention for pressure injury for the darkly pigmented skin type should be incorporated into a yearly updated educational session for every member of the multidisciplinary team.
Skin Assessment Components
Review of the difference in skin assessment methods for the patient with darkly pigmented skin should be included in the orientation of new staff members. Listed below are specific guidelines for darkly pigmented skin for the bedside clinician.
* Assess for a history of pressure ulcers. A healing or healed pressure ulcer in an individual with darkly pigmented skin will assume a hypopigmented (lighter) color before returning to the original pigmentation (Clark, 2010). During this period of hypopigmentation, the healed ulcer is extremely fragile and prone to reulceration (Hess, 2012).
* Conduct a visual skin assessment of the entire body. Assess skin from side and frontal views to facilitate identification of a color change in darker skin.
* Inquire about pain or discomfort in an area predisposed to pressure.
* Texture changes will occur as pressure injury progresses. In the patient with darkly pigmented skin, nonblanchable tissue usually is deep purple in color, may have a blistered top layer, and may present bilaterally as a mirror image (NPUAP/EPUAP, 2009). Skin also will appear taut and shiny as edema intensifies. Blisters appear due to localized friction that separates the epidermis and creates pockets of superficial serous fluid, indicating the first sign of tissue loss (NPUAP/ EPUAP, 2009).
* Assess nutrition. Compromised nutritional states, such as protein malnutrition and dehydration, are risk factors for pressure injury (Landau, 2014). Diets of ethnic populations differ from the diets of Whites (August & Sorkin, 2010) and may affect hospitalized patients who are accustomed to traditional foods. Risk factors are altered significantly for a person who is not eating for any reason (Landau, 2014).
Palpate for changes in temperature. As tissue devitalizes, the intact area will feel cool to the touch. A circumscribed area may feel soft and boggy, or hard. Induration is a clinical sign of excessive inflammation and necrosis. As autolysis occurs, the site may feel boggy (Sommers, 2011).
The following methods increase the detection of pressure injury in the patient with darkly pigmented skin:
* Take photographs of the skin, as the instant flash increases visualization of dark skin (Sommers, 2011) and provides an objective record of the patient's condition. Ensure adherence to hospital policy and government regulations concerning privacy of patient information.
* The use of newer technologies such as high-resolution ultrasound or laser Doppler should be considered in darker pigmented, high-risk individuals because they provide images of tissue damage that cannot be seen with the naked eye (Porter-Armstrong et al., 2013).
Events described in the case study may have been prevented if staff had been educated appropriately in assessment of patients with darkly pigmented skin. Because Blacks acquire pressure injury at a significantly increased rate than Whites (Fogerty et al., 2009; Li, Yin, Cai, Temkin-Greener, & Mukamel, 2011), all health care personnel should be educated concerning variances in skin type and prepared to practice in a multi-ethnic society.
Mary Steven, MS, RN, ACNP-BC, is Clinical Instructor, University of Michigan School of Nursing, Ann Arbor Ml.
Laura Struble, PhD, GNP-BC, is Clinical Assistant Professor, University of Michigan School of Nursing, Ann Arbor, MI.
Janet L. Larson, PhD, RN, FAAN, is Professor, University of Michigan School of Nursing, Ann Arbor, MI.
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TABLE 1. International NPUAP-EPUAP Pressure Ulcer Definition: A pressure ulcer is localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure or pressure in combination with shear. A number of contributing or confounding factors are also associated with pressure ulcers; the significance of these factors is yet to be elucidated. Pressure Ulcer Stages Stage 1 Nonblanchable erythema Intact skin with nonblanchable redness of a localized area usually over a bony prominence Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area may be painful, firm, soft, warmer, or cooler as compared to adjacent tissue. Category 1 may be difficult to detect in individuals with dark skin tones. May indicate "at risk" persons. Stage II Partial thickness Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ ruptured serum-filled or serosanguineous filled blister. Presents as a shiny or dry shallow ulcer without slough or bruising (bruising indicates deep tissue injury). This category should not be used to describe skin tears, tape burns, incontinence- associated dermatitis, maceration, or excoriation. Stage III Full-thickness skin loss Full/thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle is not exposed. Slough may be present but does not obscure the depth of tissue loss. May include under/mining and tunneling. The depth of a Category/Stage III pressure ulcer varies by anatomical location The bridge of the nose, ear, occiput, and malleolus do not have (adipose) subcutaneous tissue and Category/Stage III ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep Category/Stage III pressure ulcers. Bone/tendon/is not visible or directly palpable. Stage IV Full-thickness tissue loss Full/thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present. Often includes undermining and tunneling. The depth of a Category/Stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have (adipose) subcutaneous tissue and these ulcers can be shallow. Category/Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon, or joint capsule), making osteomyelitis or osteitis likely to occur. Exposed bone/muscle is visible or directly palpable. Additional Categories/Stages for the United States Unstageable Full-thickness skin or tissue loss--depth unknown Full/thickness tissue loss in which actual depth of the ulcer is completely obscured by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed. Until enough slough and eschar are removed to expose the base of the wound, the true depth cannot be determined; it will be either a Category/Stage III or IV. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels serves as "the body's natural (biological) cover" and should not be removed. Suspected Deep Depth unknown Tissue Injury Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and-or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent tissue. Deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may evolve further and become covered by thin eschar. Evolution may be rapid, exposing additional layers of tissue even with optimal treatment. Source: Adapted from NPUAP, EPUAP, 2009 TABLE 2. Clinician Pocket Guide: Assessment of Dark Skin This skin assessment was devised from review of the literature to aid in the assessment of dark skin. 1. Be aware of normal variations in dark skin types. 2. Ensure excellent lighting. Use a penlight or flashlight to distinguish color changes. 3. Avoid fluorescent lighting as it casts blue tones on dark skin. 4. Assess patient nutrition. 5. Inquire about pain or discomfort in areas predisposed to pressure. Inquire if patient has a history of pressure injury. 6. Physical assessment always accompanies visual assessment. Observe entire body, and assess skin from both side and frontal views. Examine for changes in appearance. * Edema, induration: tissue damage * Boggy, taut or shiny, deep purple in color: deep tissue injury * Fluid-filled blisters: separation of epidermis and pocket of serous fluid are occurring; this is first sign of tissue loss 7. Palpate for changes in temperature with back of hand. Circumscribed area warmer than surrounding skin: inflammation; cooler than surrounding skin: ischemia 8. Take photographs of the questionable area in accordance with facility policy. 9. Determine correct pressure reduction surface. Use standards such as Braden Scale in assessing risk of pressure ulcer development. 10. Determine if technological intervention is needed. 11. Consult Wound Care Nurse as needed. [c] 2012 Mary Steven Note: The pocket guide has yet to be tested for validity and reliability. Sources: Hess, 2014; Landau, 2014; NPUAP/EPUAP, 2009; Sommers, 2011; Wake, 2010 TABLE 3. Normal Variations in Black Skin Futcher's Sharp, bilateral, pigmentary demarcation lines (Voights) lines usually on the extremities * Correspond to underlying spinal nerves at dermatome * Incidence of 25% reported in heavily pigmented Black persons. * 79% of Black females have at least one type of line. * Benign condition Midline Linear band overlying the sternum hypopigmentation * Unknown etiology; may be inherited in an autosomal dominant pattern * Incidence approximately 30%-40% in Black persons * Black males primarily affected; becomes less noticeable with age Mongolian spot A congenital blue-gray patch * Usually located lumbosacrally * Patches are devoid of scale. * May appear as a bruise to the untrained eye Nail pigmentation Linear hyperpigmented nail streaks * Represents a normal variant in over 50% of Black people * Melanin deposited in nail plate/matrix, possibly due to trauma or ultraviolet light. * Positive correlated with advancing age * Thumb and index nails most commonly involved * Often distributed bilaterally * Drugs (e.g., antimalarials, bleomycin [Blenoxane[R]], doxorubicin [Adriamycin[R]], zidovudine [Retrovir[R]]) may cause nail pigmentation. * Associated with systemic diseases (e.g., Addison's disease, Peutz-Jeghers syndrome) Palmoplantar Due to localized hypermelanosis hyperpigmentation * Polymorphous brown macules with sharp or indistinct borders * Creases on the palms often present with hyperpigmentation; may contain hyperkeratotic papules or pits. Source: Adapted from Connolly & Bikowski (2010) with permission of Merit Publishing International.
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|Author:||Steven, Mary; Struble, Laura; Larson, Janet L.|
|Article Type:||Case study|
|Date:||Sep 1, 2015|
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