week 10

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nsnyderpotaczala
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146473
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week 10
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2012-04-08 22:53:52
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care of patients with burns
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  1. Introduction
    Pts who have burn injuries develop many physiologic, metabolic and psychological changes. Can range from sunburn to major injuries involving all layers of the skinWhen the skin is injured, inflammation and fluid loss change the function of most body systems. Burn pat needs comprehensive care for weeks to months to survive the injury, reduce complications and return to their best functional status. Multidiscplinary team needed for best care and patient outcomesInitial management affects long-term outcomesBurn centers- pg 521- table 28-2 classification of burn injury and burn center criteriaHighest morbidity- burns covering more than 50% of body surface; older patient; younger patient
  2. Pathophysiology of Burn Injury
    Problems include fluid and protein losses, sepsis, and changes in metabolic, endocrine, respiratory, cardiac,hematologic and immune functioning- related to the age, general health, extent of injury , depth of injury, and specific body injuredEven after healing burn injury may cause late complications such as contracture formation and scarring. Prevention of infection and closure of the burn wound is vitally important- lack of or delay in wound healing is a key factor for all systemic problems and a major cause of disability and death among patients who are burnedAnatomic changes- skin is the largest organ of the body- each of its 2 major layers- epidermis and dermis has several sublayers- epidermis which is the outer layer of skin is a layer of stratified epithelial cells – layer can grow back because the epidermal cells surrounding sweat and oil glands and hair follicles extend into the dermal tissue and regrow to heal partial –thickness wounds- together the sweat and oil glands and hair follicles are the dermal appendages and the depth varies from one body area to the next – epidermis has no blood vessels and nutrients to this layer diffuse from the second layer of skin( dermis)Dermis is sometimes called the “true skin” since it is not constantly shed and replaced- thicker than epidermisand made up of collagen, fibrous connective tissue and elastic fibers- within the dermis are the blood vessels, sensory nerves, hair follicles, lymph vessels, sebaceaous and sweat glandsWhen a burn injury occurs, skin can regrow as long as parts of the dermis are present- when entire layer of dermis is burned all epithelial cells and dermal appendages are destroyed and the skin can no longer restore itself. The subcutaneous tissue lies below the dermis and varies in thickness- with deep burns subcutaneous tissues may be damaged leaving bones, tendons and muscles exposedFUNCTIONAL CHANGES- protective barrier against injury and microbial invasion from the environment- - burn breaks this barrier which greatly increases risk of infection- skin also helps maintain delicate fluid and electrolyte balance- after burn injury massive fluid loss occurs through evaporation- evaporation through burn injured skin occurs 4x as rapidly as from intact skin- RATE OF EVAPORATION IS IN PROPORTION TO THE TOTAL BODY SURFACE AREA( TBSA) burned and the depth of injurySkin is an excretory organ- full thickness burns destroy the sweat glands reducing excretory abilitySense organ for pain, pressure, temperature and touch- sensations are triggered on the skin in normal daily activities which allows a person to react to changes in the environment- ALL BURN INJURIES ARE PAINFUL-with partial thickness burns nerve endings are exposed increasing sensitivity and pain – with full thickness burns nerve endings are completely destroyed so at first these wounds may not transmit sensation except at the wound edges when a sharp stimulus is applied- often patients have dull or pressure-type pain in these areasActivation of Vit D when exposed to sunlight- reduced with partial thickness and lost completely in full thickness Helps determne physical identity- cosmetic quality is part of each person’s unique appearance- with change in appearance psychological problems may developSkin can tolerate temps up to 104 F without injury- at temps of 158 and above cell destruction is so rapid that even brief exposure damages the skin and tissue below the skin- the internal body temp remains within a narrow range compared with the wide temp changes in the external environment- circulating blood both provides and dissipates heat efficiently
  3. Classification and Severity of Burn Injury
    Iggy- pg 521- table 28-1 classification of burn depthThe American Burn Association describes burs as minor, moderate or major depending on the depth, extent, and location of injury and describes the criteria for referral to a burn centerWe have burn centers around the country but typically patients are seen in Ers first
  4. žSuperficial
    Have the least damage because the epidermis is the only part of the skin that is injured-epithelial cells and basement membrane( needed for total regrowth) remains presentSuperficial thickness wounds are caused by prolonged exposure to low-intensity heat( sunburn) or short( flash) exposure to high intensity heatRedness with mild edema, pain and increased sensitivity to heat occurs as a result- DESQUAMATION (peeling of dead skin) occurs for 2-3 days after 2-3 days after the burn- area heals rapidly in 3-5 days without a scar or other complication
  5. žSuperficial Partial- thickness
    Caused by heat injury to the upper third of the dermis leaving a good blood supply- these wounds are red and moist and BLANCH when pressure is applied- small vessels bringing blood to this area are injured resulting in leakage of large amounts of plasma which in turns lifts off the heat-destroyed epidermis causing blister formation- the blisters continue to increase in size after the burn as cell and protein breakdown occur- sm blisters are often left intact if they are not present over a joint- larger blisters are usually opened to promote healing-Superficial-partial-thickness wounds increase pain sensation. Nerve endings are exposed and any stimulation(touch or temp changes) causes intense pain. With standard care, these burn heal in 10-21 days with no scar but some minor pigment changes may occur
  6. žDeep- Partial Thickness
    Extend deeper into the skin dermis and fewer healthy cells remain- blisters usually do not form because the dead tissue layer is so thick and sticks to the underlying dermis that it does not readily lift off the surface- the wound surface is red and dry with white areas in deeper parts( dry because fewer blood vessels are patent) when pressure is applied to the burn, it may blanch slowly or not at all- edema is moderate and pain is less than with superficial burns because more of the nerve endings have been destroyed –Blood flow to these areas is reduced by blood vessel constriction- progression t odeeper injury can occur from hypoxia and ischemia- adequate hydration, nutrients and oxygen are needed for regrowth of skin cells and prevention of conversion to deeper burns. These wounds can convert to full-thickness wounds when tissue damage increases with infection,hypoxia or ischemiaDeep partial-thickness wounds generally heal in 3-6 weeks but scar formation results. Surgical intervention with skin grafting can reduce healing time.
  7. žFull-Thickness
    Occurs with destruction of the entire epidermis and dermis, leaving no true skin cells to repopulate- this wound does not regrow and whatever area of the wound is not closed by wound contraction will require graftingHas a hard, leathery eschar that forms from coagulated particles of destroyed dermis-eschar is dead tissue that must slough off or be removed from the burn wound before healing can occurWound may be waxy white, deep red,yellow, brown or black0 thrombosed vessels may be visible beneath the surface of the burn- sensation is reduced or absent because of nerve ending destruction- healing time depends on establishing a good blood supply in the injured area-process can range from weeks to months
  8. žDeep Full-Thickness
    Extend beyond the skin into the underlying fascia and tissues- these injuries damage muscle, bone, and tendons and leave them exposed- occur with flame, electrical or chemical injuriesWound is blackened and depressed and sensation is completely absent- need early excision and grafting- grafting decreases pain and length of stay and hastens recovery- amputation may be needed when an extremity is involved
  9. Changes Resulting From Burn Injury
    With vascular changes- circulatory disruption occurs at the burn site immediately after the burn injury- blood vessels to the burned skin are occluded and blood flow is reduced or stopped- blood vessel constriction is caused first by damaged macrophages with the tissues releases chemicals> blood vessel thrombosis may occur causing necrosis which can lead to deeper injuries in the already damaged areas
  10. Vascular Changes
    After the initial vasoconstriction as a result of blood vessels near the burn, dilating and leaking fluid into the interstitial space-it is a continuous leak of plasma from the vascular space into the interstitial space- loss of plasma fluids and proteins decreases blood volume and blood pressure- leakage of fluid and electrolytes from the vascular space continues,causing extensive edema, even in areas not burned- fluid shift with excessive weight gain usually occurs in the 1st 12 hrs after the burn and can continue 24-36 hrsHyperkalemia as a direct result of cell injury that releases lg amounts of cellular potassium. Sodium is retained by the body as a result of the endocrine stress response. Aldosterone secretion increases leading to increased sodium reabsorption by the kidney. This sodium, however quickly passes into the interstitial spaces of the burned area with the fluid shift, therefore despite the increased amount in the body, most of the sodium is trapped in the interstial space and sodium deficit occursHemoconcentration-develops from vascular dehydration and blood viscosity increases, reducing flow through small vessels and increasing tissue hypoxiaFluid remobilization- during this phase hyponatremia develops because of an increase renal sodium excretion and loss of sodium from wounds and hypokalemia results from potassium moving back into the cells and also from being excreted in urine outputProtein continues to be lost from the wounds – metabolic acidosis is possible because loss of sodium bicarbonate in the urine and increased fat metabolism that occurs because of decreased carbohydrate intake
  11. Cardiac Assessment
    Loss of volume decreases cardiac output and oxygen deliveryCatecholamine release causes tachycardia and vasoconstrictionMyocardial depression with negative inotropic effectCardiac output may remain low until 18-36 hours after the burn injury- increase 48 hours after injury leads to diuresisDecrease oxygen delivery to body tissues Purpose of post burn fluid resuscitation is to aid in restoring normal cardiac outputInflammatory compensation can trigger healing- sympathetic nervous system compensation occurs when any physical or psychological stressors are present
  12. Pulmonary Changes
    Direct injury to the lung from contact with flames rarely occurs- respiratory changes usually are caused by superheated air, steam, toxic fumes or smoke- such problems are a major cause of death in patients with burns and are most likely to occur when the burn takes place indoors- respiratory failure with burn injuries can result from airway edema during fluid resuscitation, pulmonary capillary leak, chest burns restrict chest movement Upper airway often cause a reflex closure of smoke and toxic gases entering the lungs- some heat does reach the upper airway, causing an inflammatory response that leads to edema of the mouth and throat with the potential of airway obstructionMore airway is caused by chemicals and toxic gases rather than heat that are produced during combustion- the ciliated membranes lining the trachea normally trap bacteria and foreign materials- lining of the trachea and bronchi may slough 48-72 hrs after injury, enter the airway, narrow the tracheal lumen and obstruct the lower airwaysLung tissue injuries result from toxic irritant damage to the alveoli and capillaries- leaking capillaries cause alvelor edema- can occur immediately or as late as 1 week after the injury- progressive pulmonary failure develops leading to acute pulmonary insufficiency and infectionCarbon Monoxide poisoning- leading causes of death from a fire- colorless, ordorless, tasteless released in process of combustion- oxygen-carrying capacity of the hemoglobin is reduced, blood-gas value of PaO2 is normal-Thermal usually limited to upper airway above the glottis- heat damage of the pharynx is often severe enough to produce edema and upper airway obstruction especially the epiglottis- Inhaled steam can injure the lower respiratory tract because water holds heat better than dry air does- respiratory tract down to the major bronchioles can be damaged by steam- ulcerations, redness and edema of the mouth and epiglottis are the 1st manifestations with rapid swelling leading to upper airway obstruction- stridor, hoarseness and shortness of breath resultSmoke poisoning- is a common type of inhalation injury- Pulmonary overload- pulmonary edema- can occur even when lung tissue have not been damaged directly- circulatory overload from fluid resuscitation may cause left-sides congestive heart failure- this creates high pressure within pulmonary blood vessels that pushes fluid into lung tissue-pt is SOB, has dyspnea in the supine position, crackles are heard on auscultation- elevate HOB to at least 45degrees, apply humidified oxygen, and notify the burn team or Rapid Response Team
  13. Gastrointestinal Changes
    The fluid shifts and decreased cardiac output divert blood flow to the brain,heart and liver- as a result other organs have decreased blood flow- gastric, mucosal integrity and motility are impairedSympathetic nervous system stress response increases secretion of epinephrine and norepinephrine which inhibit GI motility and further reduce blood flow to the area- parastalsis decreases and a paralytic ileus may develop- secretions and gases collect in the intestines and stomach, causing abdominal distentionCURLING’s ULCER- acute gastroduodenal ulcer that occurs with the stress of severe injury- caused because of reduced GI blood flow and mucosal damage- mucous lining the stomach acts as a barrier but with the decreased gastric mucus production disrupts the barrier and hydrogen ion production is increased and ulcers may develop as a result- less common because of the use of H2 histamine blockers,drugs that protect GI mucosal tissue and early enteral feedingLook for decreased bowel sounds, gastric distention and N/VPts with burns 25% TBSA or who are intubated generally require a NG tube inserted to prevent aspiration and remove gastric secretions- assess tube for placement and patency- because potential for ulcer formation in GI tract each stool and vomitus are examined for the presence of gross blood or “coffee ground” emesis( partially digested blood) Test for the presence of occult blood on any vomit or stool
  14. Metabolic Changes
    A serious burn injury greatly increases metabolism by increasing secretion of catecholmines, antidiuretic hormone, aldosterone, and cortisol- increase patient’s oxygen use and calorie needs are highCatecholamines active stress response- increase production and loss of heat breaks down protein and fat(catabolism),rapidy uses glucose and calores and increases urine nitrogen loss- heat and water lost from burn also increase metabolic and catabolic rates which increase calorie needs- burn patients have a metabolic rate 100 -200 times their basal rate and some degree of elevation continues for 9-12 months occurs post resuscitation(48-72hr after burn) – reduces with wound closure, may last for months as stated above, muscle wasting, weight loss: degree of response is based on % tbsa, age, sex, nutritional status and preexisting medical conditions – depending on extent of injury pt’s calorie needs double or triple normal energy needs.Increase rates peak 4-12 days after burnIncreases core body temp- pt loses heat through the burned skin because the protective barrier is lost- core body temp increases as a response to the adjustment in temp regulation by the hypothalmus- a central body temp control change occcurs to adapt to the hypermetabolic state resulting in the development of a low-grade fever- this change is a “resetting” of the body’s normal termp-control systme to a higher baseline body temp
  15. Immunologic Changes
    All types of immunity are suppressed- topical and systemic antibiotics, general anesthesia, blood transfusion and the stress of surgery further reduce immune functionInflammatory response and the sympathetic nervous system stress response provide immediate benefit- together these responses cause changes that result in many of the manifestations seen in the firs 2-3 days after a burn injuryInflammatory compensation can be helpful by triggering healing in the injured tissues- also responsible for some of the serious problems that occur with the fluid shift- causes blood vessels to leak fluid into the interstitial space and WBC cells to release chemicals that trigger local tissue reactions- responses cause massive fluid shifts, edema and hypovolemia seen in the first 48hrs- extent of the inflammatory response depends on the burn severity- inflammatory compensation is immediately helpful to the body when injury occursSympathetic nervous systme compensation is the stress response that occurs when any physical or psychological stressors are present- changes caused by sympathetic compensation are most evident in the cardiovascular, respiratory and GI systems
  16. Etiology of Burn Injury
    Fires and burns are the 5th most common cause of unintentional injury deaths in the US and the 3rd leading cause of fatal home injuries- although the number of fatalities and injures caused by residential fire-related deaths has gradually declined over the past several decades they remain preventable and continue to pose a significant public health problemAn estimated 4000 fire and burn injuries occur each year-includes deaths from fires,and motor vehicle or aircraft crashes, electricity,chemicals, hot liquids and substances and any other sources of burn injuryMost deaths occur at the scene of the accident or during transportMen experience more burn injuries than women; death from burn injuries decreases with the appropriate interventionFactors that increase the risk for death include age older than 60 yrs, a burn greater than 40% TBSA; and the presence of inhalation injury- when patient has all three risk factors, the risk of death is very high – better outcomes from burn injuries occur because of many therapeutic advances such as vigourous fluid resuscitation, early burn wound excision, improved critical care monitoring, early enteral nutrition, antibiotics and the use of specialized burn centers.
  17. Chemical Burns
    Alkalis found in oven cleaners, fertilizers, drain cleansers, and heavy industrial cleaners damage the tissues by causing the skin and its proteins to liquefy- allows for deeper spread of the chemical and more severe burns. Acids found in bathroom cleaners, rust removers, chemicals for swimming pools, and industrial cleaners damage tissues by coagulating cells and skin proteins which can limit the depth of tissue damage. Organic compounds are found in chemical disinfectants and gasoline- cause damage because they are fat soluble and are easily absorbed by the skin- once absorbed they produce toxic effects on kidneys and liver
  18. Electrical Injuries
    Skin is the most resistant organ- greatest resistance is in the epidermis of the skin- various underlying tissues have different resistance to current flow – once skin resistance is overcome- body acts as a conductor and current flows throughout the involved body partBone has a very high resistance because of its density- current flows along the surface of the bone and the heat generated damages the attached muscle- as a result deep muscle injury may present even when superficial muscles appear normal or uninjuredThe longer the electricity is in contact with the body the greater the damage- duration of contact is increased by tetanic contractions of the strong flexor muscles in the forearm which can prevent the person from releasing the electrical sourceDifficult to know the exact path a current takes in the body- the course of flow is first defined by the locations of the “contact sites”-which are the entrance and exit wounds- at first the mounds may not be obvious- path of the injury may involve many internal tissues between the 2 contact sites.
  19. Burn Injuries
    Thermal burns occur when clothes ignite from heat or flames produced by electrical sparksExternal burn injuries can occur when the electrical current jumps or “arcs” between two body surfaces- injuries are usually severe and deepTrue electrical injury occurs when direct contact is made with an electrical source. Internal damage results and the injuries can be devastating- damage starts on the inside and goes out- deep –tissue destruction may not be apparent immediately after the injury- organs on the path of the current may become ischemic and necrotic
  20. Health Promotion and Maintenance
    Leaving and not going back in to a burning building is critical to preventing injury or deathFor smoke detectors recommendation is for each bedroom have a separate one and at least one detector in the hallway of each story, at least one detector for the kitchen , each stairwell, and each house/home entranceLaw about CO2 detectors-SUMMARY OF PROVISIONS : Section 1. Section 378 of the executive law is amended by adding a new subdivision 5-a which states standards for installation of carbon monoxide detectors requiring that every one or two-family dwelling or any dwelling accommodation located in a building owned as a condominium or cooperative in the state, constructed or offered for sale after the effective date of this subdivision, shall have installed an operable carbon monoxide detector of such manufacture, design and installation standards as are established by the council.Mckinney pg 1366 prevention and management of emergency
  21. Resuscitation/ Emergent Phase
    Burns can be devastating and dehumanizing- events within the 1st hour after the injury can make the difference between life and deathImmediate care focuses on maintaining an open airway, ensuring adequate breathing and circulation, limiting the extent of the injury and maintaining the function of vital organsNeed to secure the airway, give fluid replacement, keep pt comfortable with analgesics, provide careful wound care
  22. Renal/ Urinary Changes
    Renal system is sensitive to decreased cardiac output- initial decrease in urinary output related to decreased glomerular filtration rate and then is followed by diuresis as fluid shiftsRENAL-sodium and water are retained to preserve intravascular fluid. Oliguria occurs, urine becomes concentrated, if fluid resuscitation is not adequate renal failure can occur. With fluid resuscitation diuresis occurs approximately 48 hrs after injury secondary to an increased cardiac output
  23. Skin Assessment
    Except with electrical burns initial size assessment usually can be made accurately with specific assessment tools and chartsMost rapid method for calculating the size of the burn injury in adult patients whose weights are in normal proportion to their heights is the rule of nines- using multiples of 9% of total body surface areaTo sum up smaller area,scattered burns the patient’s palm method is used- size of the patient’s palm plus the fingers=1% of TBSAAnother method the Lund-Browder Rules of nines varies from adult to children because children have proportionately larger head size
  24. Laboratory Assessment
    • žDuring resuscitation/emergent phase and before start of fluid resuscitation›Venous blood analysis reflects fluid shift and direct tissue damage›Changes in WBC count and differential count reflect immune function and inflammatory responses–Total WBC 1st rises and then drops rapidly as immune system becomes unable to sustain its defenses–Total WBC count may be as low as 2000cells/mm3 if sepsis occurs
    • Changes in lab test values are found in different phases of postburn recovery and reflect tissue damage or compensatory responses- other changes in specific lab findings may suggest complications
  25. Resuscitation/Emergent Phase
    Interventions are aimed at increasing blood fluid volume, supporting compensatory mechanisms and preventing complications- surgical interventions is required most often for full thickness burnsFluid volume and tissue blood flow are restored through IV therapy and drug therapy- priority nursing interventions are carrying out fluid resuscitation and monitoring for indication sof effectiveness or complicatons
  26. Fluid Resuscitation
    Rapid infusion of IV fluids is needed to maintain sufficient blood volume for normal cardiac output, mean arterial pressure and tissue oxygenation- many formulas for calculating fluid requirements – types and amounts of electrolytes, crystalloids and colloids vary the purpose of all formulas is to prevent shock by maintaining circulating blood fluid volume- optimal formula and infusion schedules remain controversialResuscitation for a severe burn requires large fluid loads in a short time to maintain blood flow to vital organs- all common formulas recommend that ½ of the calculated fluid volume for 24hrs be given in the 1st 8 hrs after the injury- the other ½ is given over the next 16 hrs for a total of 24hrs- fluid boluses are avoided because they increase capillary pressure and worsen edema- fluid replacement formulas are calculated from the time of the injury not from the time of arrival at the hospital-if burn injury occurred at 8am but not admitted to the hospital until 10 am the 1st 8 hr would be completed at 4pm or 8 hrs after the injury- calculated fluids would need to be given over 6hr period rather than 8hr- all burn resuscitation formulas are used as a guide –pt response determines exact fluid guidesIn the 2nd 24 hr period after a burn injury, the volume and content of the IV fluids are based on the pt’s specific fluid volume and electrolyte imbalances and response to treatment- usually this resuscitation involves hourly infusion amounts that are greatly in excess of the 125-150 ml per hour commonly infused for other conditions
  27. Fluid Guidelines for Adults
    Parkland- total of 16,500 ml, 8,250 in first 8 hours or 1031.25 ml/hr and 8,250 or 515.6 mL/hr in the next 16 hours
  28. žSurgical management: Escharotomy
    Incision through the burn eschar relieves pressure caused by the constricting force of fluid buildup under circumferential burns on the chest or extremity and improves circulation- if the pressure isn’t relieved arterial compression can occur with a loss of blood flow to the extremity leading to ischemia and possible necrosis- if the tissue pressure remains elevated after escharotomy, a fasciotomy( deeper incision extending through the fascia) may be neededEscharotomy may be performed at the bedside – no anesthesia is needed since nerve endings have been destroyed by burn injury but sedation and analgesia are fiven to reduce anxiety- reassure pt that they will be made as comfortable as possible- remove dressing and cleanse areas to be incised. After the procedure apply topical antimicrobial drugs and dressings to the area. Carefully monitor sites for bleeding Fasciotomy should be performed in the OR and pt should be under general anesthesia
  29. Acute Phase of Burn Injury
    Continue with assessments performed during resuscitative phaseRespiratory- signs of respiratory compromise;chest xrays, fever, respirations and secretions; wbcCardio- maintain fluid requirement; monitor intake and output; monitor weightNeuro status- changes in level of consciousnessReanl status- urine outputGI- stress ulcer; nutritional considerationIntegumentary – infection- pg 538- table 28-6Neuroendocrine- increase metabolic demands placed on the body after a severe burn can severely deplete nutritional storesOpen wounds and reduced immune function make patient at high risk for infection and sepsis
  30. Non Surgical Managment
    Autolysis rarely used in North America for lg burns because it is slow and results in long hospital stay- increases risk if infection- it is the disintegration of tissue by action of the patient’s own cellular enzymesTopical enzyme agents such as collangenase are applied directly to the wound in a once a day dressing change, the enzymes digest collagen in necrotic tissues- need a most environment within a specific pH range to be activePolysporin powder- often used with the topical agent to prevent infection
  31. Nonsurgical Management:
    –Standard wound dressings
    žBiologic dressings
    Generally changed and reapplied every 8-24 hours after thoroughly cleaning the areas. Biological dressing are skin or membranes obtained from human tissue donorsHomografts also called allografts are human skin from a cadaver, fresh or frozen, obtained from a skin bank,( expensive and has a risk of blood borne infections)Heterografts- also called xenografts, skin from another species, pigskin most often usedAmniotic membrane – large skize, low cost, and availability help with success- require frequent changes, does not develop a blood supplyCultured skin-grown from a small specimen of epidermal cells from an unburned area of the patient’s body- very costly and takes awhile to growArtificial skin- created from beef collagen and shark cartilage

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