Wound Care Quiz 1 – Flashcards

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Describe the role of the physical therapist in wound management ? What are some of the primary goals/ treatment objectives of physical therapy intervention?
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Role of the PT in Wound Care: • Assessment • Prevention***** • Treatment of wounds
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List members of the interprofessional wound care team and explain how they work together to best serve the needs of the patient.
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Psychiatry - People with psych issues (i.e. depression) are less likely to adhere to their patient education -Some people may not want to get better and/or purposely interfere with their healing process Pharmacy - some meds alter the rate and effectiveness of healing. Need to be evaluated. Certified Wound Specialist (CWS) [PT, RN, MD] - do the assessment and interventions Medicine - surgical wounds and comorbid conditions. Also deal with underlying systemic disease Podiatry (DPM) - deal with foot wounds such as ulcers. Orthotist/Prosthetist - need to fit orthotics correctly to ensure skin integrity, also can use braces and aids to improve body mechanics to prevent skin wounds Nutritionist/Dietary Personnel: Proper nutrition can aid in the healing process. Certain nutrients/minerals essential to proper healing. Case Management - Keeps track of prevalence/incidence of wounds in a healthcare setting. Helps identify trends and identify potential sources of injury
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How might a physical therapist use the Guide to Practice when working in the wound care arena?
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-Risk Reduction -Helping to Assess Wound type (i.e. superficial, partial thickness, full thickness, etc...) -Determine appropriate systems review/history -Identify Potential Interventions -Typical Duration of PT (number of visits)
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What are some of the interventions typically employed by physical therapists during wound management?
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***Patient/Family/Caregiver education Pressure Relief/redistribution -Positioning -offloading Wound debridement Hydrotherapy -Whirlpool -Pulsed Lavage -Wound Irrigation -Moist Wound Healing (via choice of dressing) -Physical Agents -Ultrasound, Diathermy, Estim, phototherapy, hyperbaric oxygen, compression therapy -Manual Techniques -Manual Lymphatic Drainage (MLD)
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5. Describe the functions of the skin.
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-Physical Barrier -Thermoregulation -Reduce Bacteria (skin is slightly acidic) - acid mantle -Homeostasis -Water Retention -Sensory Organ
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6. Explain why older patients are at greater risk of integumentary injury and delayed healing.
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-Thinning of epidermis and adipose layer -decrease in collagen and elastin (decreased turgor) -slower rate of regeneration -decreased moisture -Texture - "onion skin" ***This makes them more fragile and takes wounds longer to heal***
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7. What is the difference between healing by primary intention, and healing by secondary intention?
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Primary Intention: wound closure by the use of sutures or staples Secondary Intention: Natural wound closure by healing cascade (no medical intervention)
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8. What is tertiary healing, and when would this occur?
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Leaving wound to heal a little on its own - then cleaning it out and using sutures to close the wound. (used when there is a large possibility of contamination to prevent abscess from growing under sutures)
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9. Describe differences in clinical presentation and healing for partial thickness vs full thickness wounds.
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Partial Thickness: Part of dermis and/or basement membrane still intact. These wounds are very painful since pain receptors/nerve endings are still intact Hair follicles and pores still intact.. Heals primarily by epithelialization. Epithelial cells bud and migrate from wound margins and appendages. Cell division stops by contact inhibition Full Thickness: Epidermis AND dermis are no longer intact. Wound heals by contraction and scar tissue formation. Full-thickness wounds lack tensile strength when they heal. -only gain 60-70% of original skin turgor -scar tissue increases the risk of future breakdown
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10. Why do full-thickness wounds carry a higher chance of future skin breakdown, even after they are healed?
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-They lack the turgor of the original skin (only 60-70% of normal turgor)
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11. Describe the phases of wound healing. Be sure to include the important events that occur in each phase.
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Inflammatory Phase: 4-6 days Begins immediately after injury Signs of acute inflammation -swelling, redness, warmth, tenderness Histamine Reactions occur during this phase Histamine: released by mast cells. Makes capillaries more permeable which allows protein and fluid to flow out of the vessels. This causes swelling/edema -neutrophils increase capillary permeability as well hemostasis and blood clotting (platelet plug) occurs in this phase as well. Phagocytes remove debris and dead tissue -Macrophages help transition to proliferative phase through release of growth factors and chemical mediators. Fibroblasts: manufacture glycoproteins and mucopolysaccharides (Ground Substance) Proliferative Phase: 4-24 days -Formulation of the granulation tissue -migration of epithelial cells across granulation tissue (requires moist environment) -Exudate: moisture produced by wound -contains growth factors to aid in healing Remodeling Phase: 21 days - 2 years -Starts as granulation tissue is being formed (???) -Can continue up to 2 years post injury -Body's attempt to normalize scar tissue -Requires a balance between collagen formation and collagen lysis
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12. How does inflammation contribute to the healing process?
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Histamine Reactions occur during this phase Histamine: released by mast cells. Makes capillaries more permeable which allows protein and fluid to flow out of the vessels. This causes swelling/edema -neutrophils increase capillary permeability as well hemostasis and blood clotting (platelet plug) occurs in this phase as well. Phagocytes remove debris and dead tissue -Macrophages help transition to proliferative phase through release of growth factors and chemical mediators. Fibroblasts: manufacture glycoproteins and mucopolysaccharides (Ground Substance)
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13. What are the hallmark signs of acute inflammation?
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swelling, redness, warmth, tenderness
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Give some examples of conditions and comorbidities that may diminish signs of inflammation in patients with open wounds.
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Steroid Therapy Diabetes Mellitus Older Patients Immunocompromised Patients
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15. How does histamine contribute to healing and the inflammatory response?
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. Makes capillaries more permeable which allows protein and fluid to flow out of the vessels. This causes swelling/edema
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16. What is the difference between primary tissue injury and secondary cell death?
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Primary Cell Death: occurs from trauma itself Secondary Cell Death: cell death after trauma - can occur partially to walling off response
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17. Describe the transition from inflammation to proliferation - i.e. - what cells help in the progression of the healing cascade?
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Macrophages help transition to proliferative phase through release of growth factors and chemical mediators.
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18. How do fibroblasts contribute to tissue repair in open wounds?
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manufacture glycoproteins and mucopolysaccharides (Ground Substance)
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19. Describe the clinical rationale for moist wound healing, including the current of injury.
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- Promotes Progression of healing cascade - Retains growth factors - Promotes autolytic debridement (self- cleansing of wound) - Supports current of injury -Current of Injury: Intact epidermis has a (-) charge Internal surface of skin has a (+) charge -Open wounds get a (+) charge from exposed underlying tissue The voltage gradient causes Galvanotaxis: charged tissues attracts ionized cells that are beneficial to healing
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20. What does granulation tissue consist of and how would you identify its presence?
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Granulation is red ("red carpet") due to developing blood supply. Granulation tissue contains the ECM and blood supply needed for proliferation of epithelial cells
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21. When does hypergranulation tissue develop? Why is it a problem, and how should it be addressed?
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-"proud flesh" -Can be caused by too much oxygen, chronic infection, repetitive trauma during proliferative phase -can be iatrogenic, from changing the dressing too often, or from presence of aerobic bacteria. Hypergranulation is a problem because it blocks the migration of epithelial cells from wound margins -epithelial cells wont travel uphill Management for hypergranulation: -Compressive dressings -Silver Nitrate (makes tissue look necrotic because it stains it black)
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22. How long does the remodeling phase last and in what ways does it contribute to healing?
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21 days - 2 years Body's attempt to normalize scar tissue Requires a balance between collagen formation and collagen lysis
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23. Compare and contrast the process of healing in partial vs full thickness wounds.
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Partial: Primarily by epithelialization full thickness: heal by contraction and scar tissue formation
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24. What are some of the factors that can contribute to delayed healing in chronic wounds? How would you distinguish between "intrinsic" and "extrinsic" factors?
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-Chronic Inflammation: wound possibly clogged by necrotic tissue or contaminated by debris and/or bacteria -Poor Circulation -Dry Wound Bed - no current of injury -Other complicating factors: - Smoking - Repetitive trauma - Poor nutrition - Old age - SCI, poor sensation, limited mobility - Venous or arterial insufficiency - Diabetes Intrinsic Factors: factors related to the patient's health and body's capacity to heal Extrinsic Factors: o Choice of Dressing o Support Surface/pressure distribution and relief o Mechanical stresses on wound site - pressure, friction, shear o Medications
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25. What are some of the medications that may contribute to delayed wound healing, and why?
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Chemotherapy Steroids (i.e. respiratory patients, RA...) Antibiotics Anticoagulants Certain Topical agents used in the wound (petroleum and oil based products can reduce current of injury)
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26. Why is it important to maintain an adequate fluid balance at the wound bed? How is this typically achieved?
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Need to prevent dessication or maceration (too much moisture) The balance is typically achieved by choice of dressing
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27. Describe signs of maceration. Explain how maceration can contribute to wound chronicity and explain how this can be addressed.
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Maceration is characterized by white, soft mushy tissue around the edges of the wound. It can extend the boundaries of the wound Maceration can be prevented by using absorbent dressing and/or a skin protectant at the wound margins.
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28. Describe some of the nutritional requirements for optimal wound closure.
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Vitamin E: decreases inflammation, enhances immune function and may play a role in clot prevention Vitamin C: for collagen synthesis Vitamin A: collagen synthesis, aids in granulation and epithelialization, may enhance macrophage function Vitamin K: Needed for production of clotting factors B Complex: Needed for proper WBC function, contributes to tensile strength of healing wounds. Zinc: Assists in collagen formation and epithelialization, supports normal immune function Iron: Needed for healthy RBCs. Hemoglobin production, oxygen transport Calcium: needed for fibrin synthesis and blood clotting
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29. Within the wound care practice setting, what are some of the laboratory values the physical therapist may wish to gain when collecting data from the patient's medical chart? What types of helpful information do these values provide in terms of guiding treatment interventions?
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Creatinine: Kidney Function Serum Albumin: low levels reflect protein deficiency and malnutrition, looks for decreased plasma oncotic pressure Prealbumin: shorter half like than albumin - used to gauge effectiveness in interventions Fasting Blood Glucose: hypo/hyperglycemia can delay wound healing Electrolytes: Hemoglobin/hematocrit: checks for anemia TLC (Total Lymphocyte count): decreased levels indicate impaired immune function (delays healing) Serum Transferrin: low levels can indicate malnutrition
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30. What is the most common type of wound seen in the emergency department? Under what circumstances might these wounds require future treatment by the physical therapist?
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Laceration is most common wound High risk of contamination/Infection may require medical/PT intervention
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31. How do skin tears occur? Describe risk factors.
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Skin Tears occur via traumatic injury (minor trauma) - shearing, friction, blunt force, removal of adhesies Risk Factors are fragile skin (particular in elderly): Thinning of epidermis Less adherence b/w epidermis and dermis. Loss of collagen and elastin Decreased turgor and hydration
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How can skin tears be prevented? What is the best way to manage a skin tear?
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Prevention: assess and address environmental hazards Consider Use of protective clothing Management: - Control Bleeding (pressure and elevation) - Cleanse wound (warm water/saline, gently pat dry) - Approximate skin flap if possible - Use a barrier ointment to protect surrounding skin (not on granulation tissue)
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33. What is a "degloving" injury?
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Degloving is an avulsion injury where skin (and sometimes underlying tissue) are traumatically pulled from the body. (like pulling a glove off)
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34. Which factors determine the severity of an abrasion?
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Depth and Surface area
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36. Describe compartment syndrome - what is it's relevance in wound management?
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Increased pressure from accumulated fluid/blood within muscle fascia (usually in arms or legs) can compress blood supply and cause ischemic damage to tissue Treatment with fasciotomys create a giant gaping open wound that needs to be treated by CWS
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37. There is a high risk of infection with puncture wounds. Why?
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There is a high risk of infection from injection of contaminants deep into tissue
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38. What are some of the common agents responsible for infection in animal bites?
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-Pasteurellosis: from cat bites (travels up tendons and bones) -Strep and Staph infections -Proteus -Klebsiella -Rabies
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39. Describe factors that contribute to wound dehiscence.
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Factors: - Failure of sutures or staples to maintain primary wound closure - Infection - Excessive tension on wound (i.e. obesity or anatomic location of wound) - Contamination - Age and delayed healing
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40. Which factors contribute to high risk of sepsis and systemic infection in open wounds?
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The wound being open for too long, the wound being very deep, not fully debriding the wound, not packing the wound fully to the wound bed, allowing the wound to get too dry or too wet, not using sterile technique, not using clean technique, not using standard precautions, any type of immunosuppressant or inflammatory suppressant, any disease process that leads to immunosuppression or inflammatory suppression, dry/stable gangrene becoming wet gangrene.
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41. How does location and depth of wound contribute to risk of infection?
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Location: Pressure ulcers may occur in the sacral area if a patient's weight distribution is not adjusted at regular intervals, particularly if they have to remain in bed or in a certain seated position for an extended period of time. If they experience any issues with incontinence, the proximity of the sacral ulcer to the source of excrement poses greater risk for infection than a wound located more distally. Diabetic foot ulcers, if not properly dressed and covered while ambulating, are at increased risk for infection because they may come in direct contact with bacteria or other pathogens on the floor. Depth: The deeper the wound, the longer the expected healing time ("It generally takes 14-21 days for a keratinocyte to migrate from the base to skin surface"). The longer it takes the epithelium to close the wound and restore the protective barrier, the greater the risk of infection. If a wound is deep enough to reach subcutaneous tissue, like fascia, muscle, or bone, infection may then affect those tissues and be able to migrate to other parts of the body. Dr. Pignataro gave the example of streaking red marks caused by infection traveling along fascia. Bone does not generate its own immune response very well, therefore osteomyelitis is a concern for wounds that are deep enough to expose bone. A very superficial wound, as in the case of a skin tear, that just scrapes the epithelium but leaves a skin flap intact may be less prone to infection if the skin flap is replaced over the wound (using a dampened cotton swab, gloved fingers and tweezers) to help restore the protective barrier more quickly.
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