Care of the High Acuity Client Exam 2

Describe complications of fractures. How would the patient present? Identify medical treatments and nursing interventions for each- Compartment Syndrome

An anatomic compartment is an area of the body encased by bone or fascia (e.g., the fibrous membrane that covers and separates muscles) that contains muscles, nerves, and blood vessels. The human body has 46 anatomic compartments, and 36 of these are located in the extremities. Acute compartment syndrome, a time-sensitive surgical emergency, is characterized by the elevation of pressure within an anatomic compartment that is above normal perfusion pressure. Acute compartment syndrome arises from an increase in compartment volume (e.g., from edema or bleeding), a decrease in compartment size (e.g., from a restrictive cast), or aspects of both. When the pressure within an affected compartment rises above normal, perfusion to the tissues is impaired, causing cell death, which may lead to tissue necrosis and permanent dysfunction. The most common cause is fractures, with tibial fractures having the highest risk. Acute compartment syndrome is most common among young adults, and although it may take up to 48 hours for symptoms to present, it typically has a rapid progression of symptoms and signs over a few hours after the initial injury or fracture repair. Frequent assessment of neurovascular function after a fracture is essential and focuses on the "five Ps": pain, pallor, pulselessness, paresthesia, and paralysis. The patient with acute compartment syndrome typically presents with severe pain that is out of proportion to the injury, which is considered the cardinal symptom. Additionally, patients often describe this pain as deep and burning, and that it is unrelieved by medications. Exacerbation of pain on passive stretching of the muscles within the involved compartment is highly predictive. With continued nerve ischemia and edema, the patient experiences diminished sensation followed by complete numbness. Motor weakness may occur as a late sign of nerve ischemia. Motion is evaluated by asking the patient to flex and extend the wrist or plantar flex and dorsiflex the foot. Paralysis (no movement) is a late finding after prolonged ischemia and is associated with neurovascular injury. Peripheral circulation is evaluated by assessing color, temperature, capillary refill time, edema, and pulses. Cyanotic nail beds suggest venous congestion. Pallor or dusky and cold digits, prolonged capillary refill time, and diminished pulses suggest impaired arterial perfusion. Edema may obscure the function of arterial pulsation, and Doppler ultrasonography may be used to verify a pulse. Pulselessness is a late sign. A prompt diagnosis of acute compartment syndrome is based on clinical suspicion and repeated clinical examinations of the "five Ps"; however, it is important to keep in mind that pain is a subjective measure and may only be detected in patients who are conscious. As well, some of the clinical signs and symptoms may only present in the late stages of acute compartment syndrome. Palpation of the muscle, if possible, reveals it to be swollen and hard with the skin taut and shiny. The orthopedic surgeon may measure tissue pressure by inserting a tissue pressure-monitoring device, such as a handheld direct injection device (e.g., Stryker Intra-Compartmental Pressure Monitor), into the muscle compartment (normal pressure is 8 mm Hg or less). Nerve and muscle tissues deteriorate as compartment pressure increases. Prolonged pressure of more than 30 mm Hg can result in irreversible changes. Prompt management of acute compartment syndrome is essential and includes relieving all external pressure on the compartment. The orthopedic surgeon needs to be notified immediately if neurovascular compromise is suspected. Delay in treatment may result in permanent nerve and muscle damage, necrosis, infection, rhabdomyolysis with acute kidney injury, and amputation. If conservative measures do not restore tissue perfusion and relieve pain, a fasciotomy (surgical decompression with excision of the fascia) is considered the definitive treatment to relieve the constrictive muscle fascia. After fasciotomy, the wound is not sutured but is left open to allow the muscle tissues to expand; it is covered with moist, sterile saline dressings or with artificial skin. Negative-pressure wound therapy using a vacuum dressing has been shown to be effective to remove fluids and decrease times to primary closure (Modrall, 2019). The affected arm or leg is splinted in a functional position and elevated to heart level and prescribed intermittent passive ROM exercises are usually performed. In 2 to 3 days, when the swelling has resolved and tissue perfusion has been restored, the wound is débrided and closed (possibly with skin grafts). The nurse should frequently assess pain and neurovascular status of the affected limb and report any negative changes that may suggest compartment syndrome immediately to the primary provider. The limb should be maintained in a functional position at the level of the heart to promote optimal blood flow. Pain management is essential and is accomplished with opioid analgesia, as prescribed. Careful assessment of intake and output and urinalysis could alert the nurse to the development of rhabdomyolysis. Education is necessary for those patients discharged to home-based or community settings with fractures and casts and should include recognition of the unique characteristics of acute compartment syndrome (increasing, refractory pain and neurovascular manifestations) and instructions when to contact the primary provider for emergent follow-up. Acute compartment syndrome is managed by maintaining the extremity at heart level (not above heart level) and removing constrictive dressings by opening and bivalving the cast or opening the splint, if one or the other is present.

CHAPTER 34

Assessment and Management of Patients with Inflammatory Rheumatic Disorders

Identify nursing priorities in each phase of burn injury: Acute/intermediate

(From beginning of diuresis to near completion of wound closure) •Wound care and closure •Prevention or treatment of complications, including infection •Nutritional support The acute/intermediate phase of burn care follows the emergent/resuscitative phase and begins 48 to 72 hours after the burn injury. During this phase, attention is directed toward continued assessment and maintenance of respiratory and circulatory status, fluid and electrolyte balance, and GI and kidney function. Infection prevention and control, burn wound care (e.g., wound cleaning and débridement, topical antibacterial/antimicrobial therapy, application of dressings, wound grafting), pain management, modulation of the hypermetabolic response, and early positioning/mobility are priorities in the acute/intermediate stage of recovery. Nursing management of the patient in the acute/intermediate phase is focused on the following priorities: restoring fluid balance, preventing infection, modulating hypermetabolism, promoting skin integrity, relieving pain and discomfort, promoting mobility, strengthening coping strategies, supporting patient and family processes, and monitoring and managing complications.

Identify nursing priorities in each phase of burn injury: Rehabilitation

(From major wound closure to return to individual's optimal level of physical and psychosocial adjustment) •Prevention and treatment of scars and contractures •Physical, occupational, and vocational rehabilitation •Functional and cosmetic reconstruction •Psychosocial counseling (PTSD etc) Rehabilitation begins immediately after the burn has occurred and often extends for years after the initial injury. For nurses who care for patients with burns, this can be one of the more physically demanding and challenging phases. One important focus of the burn team is to evaluate the patient carefully for late complications related to burn injuries as described in Table 57-5. Burn rehabilitation is comprehensive, complex, and requires a multidisciplinary approach to optimize the patient's physical and psychosocial recovery related to the injury. As patients begin to recover, they become more aware of the injuries and challenges they face. Individualized plans of care that are specific to the severity and location of injury are developed and reevaluated frequently. The increased survival of patients with significant burn injuries has translated into the need for additional and comprehensive burn rehabilitation programs worldwide. The ultimate goal is to return patients to the highest level of function possible within the context of their injuries. Specially trained occupational and physical therapists are essential for optimal patient outcomes.

Identify nursing priorities in each phase of burn injury: Emergent/resuscitative

(From onset of injury to completion of fluid resuscitation) •Primary survey: A, B, C, D, E •Prevention of shock •Prevention of respiratory distress •Detection and treatment of concomitant injuries •Wound assessment and initial care The first step in management is to remove the patient from the source of injury and stop the burning process while preventing injury to the rescuer. Rescue workers' priorities include establishing an airway, supplying oxygen (100% oxygen if CO poisoning is suspected), inserting at least one large-bore IV catheter for fluid administration, and covering the wound with a clean, dry cloth or gauze. Continuous irrigation of chemical injury must begin immediately. The outward physical appearance of the person burned is often distracting, but the internal systemic effects pose the greater threat to life. An immediate primary survey of the patient is performed assessing the ABCDEs: airway (A) with consideration given to protecting the cervical spine, gas exchange or breathing (B), circulatory and cardiac status (C), disability (D) including neurologic deficit, and expose and examine (E) while maintaining a warm environment. The secondary survey focuses on obtaining a history, the completion of the total body systems assessment, initial fluid resuscitation, and provision of psychosocial support of the conscious patient. Nursing assessment in the emergent phase of burn injury focuses on the major priorities for any trauma patient; the burn wound is a secondary consideration to stabilization of airway, breathing, and circulation. The nurse monitors respiratory status closely, and pulses are evaluated, particularly in areas of circumferential burn injury to an extremity. Initially, cardiac monitoring is indicated if the patient has a history of cardiac disease, electrical injury, or altered respiratory conditions. The nurse should monitor vital signs with knowledge of expected abnormalities consistent with burn injury such as tachycardia, tachypnea. If all extremities are burned, determining blood pressure may be difficult. A clean dressing applied under the blood pressure cuff protects the wound from contamination. Because increasing edema makes blood pressure difficult to auscultate, a Doppler (ultrasound) device or a noninvasive electronic blood pressure device may be helpful. In patients with severe burns, an arterial catheter is preferred for blood pressure measurement and is helpful for collecting blood specimens. Peripheral pulses in burned extremities are checked frequently either by palpation or the use of a Doppler. Elevation of burned extremities above the level of the heart is indicated for edema reduction. Large-bore IV catheters (e.g., 16 to 18 gauge) and an indwelling urinary catheter are inserted, if not already in situ, and the nurse's documentation must include hourly assessment of fluid intake and urine output. Red-colored urine suggests the presence of hemochromogens from damage to red blood cells and myoglobin, the by-product of muscle damage (ABA, 2018). This anomaly is associated with deep burns caused by electrical injury or prolonged contact with heat or flame. Glycosuria, a common finding in the early postburn hours, results from the release of liver glycogen stores in response to stress. The nurse assists with calculating the patient's expected fluid requirements and monitoring the patient's response to fluid resuscitation. Nurse-driven resuscitation protocols have been shown to decrease the amount of fluid given and improve patient outcomes in the emergent/resuscitative phase (Stewart, Ladd, Kovler, et al., 2019). Nursing responsibilities consist of appropriate fluid administration, strict monitoring of intake and output, monitoring the patient's response, and notifying the treatment team of significant assessment findings and any abnormal laboratory values. To help guide treatment, the following are essential: documentation of body temperature, body weight, and pre-burn weight; history of allergies, tetanus immunization, past medical and surgical history, and current illnesses; and a list of current medications. The nurse performs a head-to-toe assessment, focusing on signs and symptoms of concomitant illness, associated trauma, or developing complications. Assessing the extent of the burn wound using the rule of nines or facilitated with anatomic diagrams (described previously) is performed. Additionally, the nurse works with the primary provider to clinically assess and document the initial areas of full- and partial-thickness injury. Psychosocial considerations of the patient and family and communication with the treatment team are imperative early in the course of care.

Identify and explain effects of major burn injury on the following: Cardiovascular Status

*cardiac depression, edema, hypovolemia When a burn injury occurs, there is an immediate decrease in cardiac output that precedes the loss of plasma volume. The systemic inflammation causes the release of free oxygen radicals that increase capillary permeability, causing increased plasma loss and subsequent peripheral edema as water migrates to the interstitium. As a compensatory response to intravascular fluid loss, the sympathetic nervous system releases catecholamines, resulting in an increase in peripheral resistance (vasoconstriction) and an increase in pulse rate that further decreases tissue perfusion. Due to vasoconstrictive compensatory responses secondary to plasma volume loss through capillary leak, the workload of the heart and oxygen demand increase. Hypovolemia is the immediate consequence of ensuing plasma volume loss and results in decreased perfusion and oxygen delivery to organs and tissues. As capillary leakage continues, vascular volume, cardiac output, and blood pressure decrease. This is the onset of early burn shock. Burn shock is initially a type of hypovolemic shock secondary to intravascular volume loss. Unlike traumatic injuries, often characterized by blood loss, only plasma is lost in the burn injury. Prompt, appropriate enteral or parenteral fluid resuscitation maintains the blood pressure in the low to normal range and improves cardiac output (see later discussion). However, even with adequate fluid resuscitation, cardiac filling pressures (central venous pressure, pulmonary artery pressure, and pulmonary artery wedge pressure) remain low during the initial burn shock period. Unless sufficient IV fluids are administered to maintain vascular volume, distributive shock occurs. Generally, the greatest volume of intravascular fluid leak occurs in the first 24 to 36 hours after the burn injury, peaking at approximately 6 to 8 hours after the initial burn injury. As the capillaries begin to regain their integrity, burn shock resolves and fluid shifts back into the vascular compartment. Intrinsic diuresis will begin and continue for several days to 2 weeks in the previously healthy adult.

Describe complications of fractures. How would the patient present? Identify medical treatments and nursing interventions for each- Avascular Necrosis of Bone

AVN occurs when the bone loses its blood supply and dies; the process eventually leads to bony collapse and destruction of the associated joint. It may occur after a fracture with disruption of the blood supply to the distal area. It is also seen with prolonged high-dose corticosteroid therapy, exposure to radiation, sickle cell disease, rheumatoid arthritis, and other diseases; chronic alcohol use and cigarette smoking are other atraumatic etiologies. The process is often progressive, and the patient develops pain with movement that progresses to pain at rest. Diagnostics include history and physical examination with x-rays, CT scans, and bone scans. AVN of the hip is the most commonly affected site; the knee is the second most common site. The goal of treatment is to preserve the native joint for as long as possible and includes both conservative and surgical interventions. Nonoperative management includes activity modification, administration of analgesics, and partial weight bearing of the affected region. Joint preserving procedures are aimed at revascularizing the affected area by drilling the avascular segment or using a bone marrow graft. In extreme cases, it is advisable to remove the fragment and reconstruct the joint.

What considerations need to be considered when treating patients with acute pain?

Acute pain involves tissue damage as a result of surgery, trauma, burn, or venipuncture, and is expected to have a relatively short duration and resolve with normal healing. Nonopioid medications are analgesic agents used for a wide variety of painful conditions. They are appropriate alone for mild to some moderate nociceptive pain (e.g., from surgery, trauma, or osteoarthritis) and are added to opioids, local anesthetics, and/or anticonvulsants as part of a multimodal analgesic regimen for more severe nociceptive pain. Since acetaminophen and NSAIDs have different mechanisms of action, they may be administered concomitantly. Although there is no research supporting staggering the two medications, it may be helpful for some patients. Unless contraindicated, surgical patients should routinely be given acetaminophen and an NSAID in scheduled doses throughout the postoperati. Nonopioids are often combined in a single tablet with opioids, such as oxycodone or hydrocodone, and are very popular for the treatment of mild to moderate acute pain. They are traditionally a common choice after invasive pain management therapies are discontinued and for pain treatment after hospital discharge and dental surgery when an opioid is prescribed. Many people with persistent pain also take a combination nonopioid-opioid analgesic agent; however, it is important to remember that these combination medications are not appropriate for severe pain of any type because the maximum daily dose of the nonopioid limits the escalation of the opioid dose. Acetaminophen is versatile in that it can be given by multiple routes of administration, including oral, rectal, and IV. Oral acetaminophen has a long history of safety in recommended doses in all age groups. It is a useful addition to multimodal treatment plans for postoperative pain. Findings from one research study suggest that patients who receive scheduled acetaminophen with PRN opioids will use less opioids than if they receive PRN acetaminophen plus opioids. These results were supported in a more recent study evaluating opioid use among women who underwent Cesarean deliveries. IV acetaminophen is approved for the treatment of pain and fever and is given by a 15-minute infusion in single or repeated doses. It may be given alone for mild to moderate pain or in combination with opioid analgesic agents for more severe pain. The results of several research studies have been inconsistent regarding the opioid sparing effects of IV acetaminophen. Recommended dosing is 1000 mg every 6 hours for a maximum of 4000 mg in adult patients. A benefit of the NSAID group is the availability of a wide variety of agents for administration via noninvasive routes. Ibuprofen, naproxen, and celecoxib are the most widely used oral NSAIDs in the United States. When rectal formulations are unavailable, an intact oral tablet or a crushed tablet in a gelatin capsule may be inserted into the rectum. The rectal route may require higher doses than the oral route to achieve similar analgesic effects. Diclofenac can be prescribed in patch and gel form for topical administration, and an intranasal patient-controlled formulation of ketorolac has been approved for the treatment of postoperative pain. IV formulations of ketorolac and ibuprofen are available for acute pain treatment. Both have been shown to produce excellent analgesia alone for moderate nociceptive pain, and significant opioid dose-sparing effects when given as part of a multimodal analgesia plan for more severe nociceptive pain.

What role does nutrition play in burn healing?

Burn injuries produce profound metabolic abnormalities fueled by the exaggerated stress response to the injury. The body's response has been classified as hyperdynamic, hypermetabolic, and hypercatabolic. Hypermetabolism can affect morbidity and mortality by increasing the risk of infection and slowing the healing rate. Nutrition should be provided as soon as possible upon arrival to the burn center and may require placement of a nasogastric tube for adequate calorie delivery. Patients who are critically ill may even have their feedings continued intraoperatively if the airway is protected. Several formulas exist for estimating the daily metabolic expenditure and caloric requirements of patients with burn injuries. Carbohydrates are the most important energy source for patients who are severely burned. Fat, although a required nutrient, should be provided in more limited quantities. When the oral route is used, high-protein, high-calorie meals and supplements are given. Dietary consultations are useful in helping patients meet their nutritional needs. Daily calorie counts aid in assessing the adequacy of nutritional intake. Early excision and grafting of the burn wound is one of the most important factors in ameliorating hypermetabolism by removing eschar, thereby lessening the effects of inflammatory mediators. Appropriate manipulation of environmental temperatures decreases energy expenditure by the patient. Insulin therapy in patients with burns is required to treat the hyperglycemia that occurs from accelerated gluconeogenesis and is beneficial in muscle protein synthesis. Oxandrolone, an anabolic steroid, is commonly given to patients with burns because it improves protein synthesis and metabolism. Administration of propranolol (a beta-blocker) decreases heart rate and blocks harmful catecholamine effects.

How/why are compression devices used?

How/why are compression devices used: An early priority is prevention of the complications of immobility. Deep breathing, turning, and proper positioning are essential nursing practices that prevent atelectasis and pneumonia, control edema, and prevent pressure injuries and contractures. Specialty beds may be useful, and early mobility is strongly encouraged. If the lower extremities are burned, elastic pressure bandages should be applied before the patient is placed in an upright position to promote venous return and minimize edema formation. The burn wound is in a dynamic state for at least 1 year after wound closure. During this time, aggressive efforts must be made to prevent contracture and hypertrophic scarring. Both passive and active range-of-motion exercises are initiated from the day of admission and are continued after grafting within prescribed limitations. Splints or functional devices applied to the extremities may lessen contractures through compression and stretch. The nurse monitors the splinted areas for signs of vascular insufficiency, nerve compression, and skin breakdown. Occupational and physical therapists are consulted to develop a patient-specific plan of care throughout hospitalization and recovery. Preventive treatment modalities aimed at scar contractures and excess hypertrophic tissue are routinely employed. Compression is introduced early in burn wound treatment. Elastic bandage wraps used initially help promote adequate circulation, but they can also be used as the first form of compression for scar management, followed by elasticized tubular bandages until the patient can be measured for a customized garment. Application of elastic pressure garments loosens collagen bundles and encourages parallel orientation of the collagen to the skin surface. As pressure continues over time, collagen restructures and vascularity decreases. Although this therapy is somewhat controversial, pressure has shown to be beneficial in controlling scar formation over time. Recommended garment wear time is 23 hours per day; removing for bathing or wound care only. Many areas of the body are difficult to compress due to the contours or location of the injury. Inserts, such as silicone sheets, are helpful for these small troublesome areas and are placed beneath the garment or compression dressing to enhance scar compression. Gentle superficial scar massage can be performed with a moisturizer several times a day. Burn reconstruction is a treatment option after scars have matured and is discussed within the first few years after injury. This decision requires individualized planning, realistic expectations, and patience. The treatment team and the patient will ultimately decide on the best approach for long-term functionality and cosmesis. What patient education is essential with compression therapy: Wear compression garments 23 hours a day if instructed.

Describe complications of fractures. How would the patient present? Identify medical treatments and nursing interventions for each- Complex Regional Pain Syndrome

CRPS is a complex and rare disorder characterized by regional pain in a limb that is disproportionate; it typically begins following a fracture, soft tissue injury, or surgery. Dysfunctional peripheral and central nervous system responses that mount an excessive response to the precipitating event (e.g., fracture, surgery) are thought to be the cause of the pain. Women are affected more often than men, and the average age of diagnosis is 40 years. Two subtypes of CRPS have been recognized: Type I (formerly called reflex sympathetic dystrophy) applies to patients with CRPS without evidence of peripheral nerve injury, and Type II (formerly called causalgia) refers to patients with nerve injury. Clinical manifestations of CRPS include severe burning pain, local edema, hyperesthesia, stiffness, discoloration, vasomotor skin changes (e.g., fluctuating warm, red, dry and cold, sweaty, cyanotic), and trophic changes that may include glossy, shiny skin, and changes in hair and nail growth. This syndrome is frequently chronic, with extension of symptoms to adjacent areas of the body. Dysfunction of the affected limb may also be manifested in CRPS. The diagnosis is made through the history and physical examination and ruling out other organic causes. The primary objective of treatment is physical functional maintenance or recovery of physical function. Early effective pain relief is the focus of management. Pain may be controlled with analgesic agents. NSAIDs, topical anesthetics (e.g., lidocaine patches), corticosteroids, and opioids. Anticonvulsant agents (e.g., gabapentin) and antidepressant agents (e.g., amitriptyline) can be effective in treating neuropathic pain. Additional treatments may include sympathetic nerve blocks, neural stimulation, and intrathecal delivery of prescribed medications. Novel treatments under investigation include infusions of immunoglobulin (IVIG) and ketamine and the use of hyperbaric oxygen. The nurse evaluates the effectiveness of these interventions and therapies and helps the patient cope with CRPS manifestations through therapeutic listening, initiation of relaxation techniques and behavior modification, and referral for rehabilitation therapy. Rehabilitation initiated early can improve circulation to the affected area and maximize function. Depression and anxiety are often associated with severe pain disorders; therefore, the nurse should recommend a mental health referral as necessary. The nurse avoids using the affected extremity for blood pressure measurements and venipuncture in the patient with CRPS.

Compare and contrast chemical, thermal, and radiation burns

Chemical burns are tissue damage caused by strong acids, drain cleaners, paint thinner, gasoline and many other substances. The skin and the mucosa of the upper airways are the most common sites of tissue destruction, although deep tissues, including the viscera, can be damaged by electrical burns or prolonged contact with a heat or chemical source. The release of local mediators, changes in blood flow, tissue edema, and infection can cause progression in severity of the burn injury. Another potential mechanism of burn injury is radiation exposure. This has received increased attention because of threats of terrorism and recent world events. Radiation injuries produce two detrimental effects. The first is a thermal effect, which results in cutaneous burn injuries. The second effect is damage to the cellular DNA, which may be localized or affect the whole body. Morbidity and mortality are dose dependent. Treatment for the cutaneous injury is the same as other burns discussed in this chapter. The depth of a burn injury depends on the temperature of the burning agent and the duration of contact with the agent. In adults, exposure to temperatures of 54°C (130°F) for 30 seconds will result in burn injury. At 60°C (140°F), tissue destruction occurs in 5 seconds (this is a common setting for home water heaters. At 71°C (160°F) or higher, a full-thickness burn occurs instantaneously. It is important to recognize injuries that affect more than approximately 20% TBSA as severe injuries, as they produce both local and systemic effects. The systemic inflammatory response to a severe burn injury signals the release of proinflammatory and anti-inflammatory cytokines, prompting hypermetabolism effects that produce organ dysfunction, a pronounced catabolic response, systemic compromise and, potentially, mortality. Where radiation burns differ from thermal burns is the amount of time between contact and seeing the burn damage. A thermal burn is immediately apparent after contact with a hot object, but radiation burns may take even weeks to present. If you feel you have a radiation burn, seek immediate medical help.

What considerations need to be considered when treating patients with chronic pain? What about for occurrence of acute pain for patients with chronic pain?

Chronic or persistent pain is subcategorized as being of cancer or noncancer origin and can persist throughout the course of a person's life. Examples of noncancer chronic pain include peripheral neuropathy from diabetes, back or neck pain after injury, and osteoarthritis pain from joint degeneration. Chronic pain may be intermittent, occurring with flares, or it may be continuous. Some conditions can produce both acute and chronic pain.

Identify types of fractures (compression, compound, impacted, transverse, greenstick)

Compression: fracture in which bone has been compressed (seen in vertebral fractures) Compound: a fracture in which there is an open wound or break in the skin near the site of the broken bone. Impacted: fracture in which a bone fragment is driven into another bone fragment. Transverse: a fracture that is straight across the bone shaft. Greenstick: refers to a partial break. One side of a bone is broken and the other side is bent. Immediately after injury, if a fracture is suspected, the body part must be immobilized before the patient is moved. Adequate splinting is essential. Joints proximal and distal to the fracture also must be immobilized to prevent movement of fracture fragments. Immobilization of the long bones of the lower extremities may be accomplished by bandaging the legs together, with the unaffected extremity serving as a splint for the injured one. In an upper extremity injury, the arm may be bandaged to the chest, or an injured forearm may be placed in a sling. The neurovascular status distal to the injury should be assessed both before and after splinting to determine the adequacy of peripheral tissue perfusion and nerve function. With an open fracture, the wound is covered with a sterile dressing to achieve homeostasis as rapidly as possible at the injury site and to prevent contamination of deeper tissues. No attempt is made to reduce the fracture, even if one of the bone fragments is protruding through the wound. Splints are applied for immobilization. In the ED, the patient is evaluated completely. The clothes are gently removed, first from the uninjured side of the body and then from the injured side. The patient's clothing may be cut away. The fractured extremity is moved as little as possible to avoid more damage.

Hip fractures (whose most at risk, describe hip precautions, identify nursing interventions)

Identify those most at risk: Annually, more than 300,000 adults older than 65 years of age sustain a hip fracture requiring hospitalization; 95% of these result from falls. Populations at higher risk of hip fracture include older adults (particularly women) who have decreased bone density and muscle mass and those with chronic conditions (e.g., endocrine and intestinal disorders) that lead to weakened bones or who have cognitive impairment which increases the risk of falling. Stress and immobility related to the trauma predispose the older adult to atelectasis, pneumonia, sepsis, VTE, pressure injuries, and reduced ability to cope with other health problems. Many older adults hospitalized with hip fractures are vulnerable for delirium as a result of stress of the trauma, pain, unfamiliar surroundings, sleep deprivation, and medications. In addition, delirium that develops in some older adult patients may be caused by mild cerebral ischemia or mild hypoxemia. Other factors associated with delirium include frailty, malnutrition, dehydration, infectious processes, mood disturbances, and blood loss. In older patients with hip fractures who have dementia, the same factors that may cause delirium may exacerbate their dementia, further complicating recovery and increasing the risk for adverse outcomes. To prevent complications, the nurse must assess the older patient for chronic conditions that require close monitoring. Examination of the legs may reveal edema due to heart failure or absence of peripheral pulses from peripheral vascular disease. Similarly, chronic respiratory problems may be present and may contribute to the possible development of atelectasis or pneumonia. Coughing and deep-breathing exercises are encouraged. Frequently, older adults take cardiac, antihypertensive, or respiratory medications that need to be continued. The patient's responses to these medications should be monitored. Dehydration and poor nutrition may be present. At times, older adults who live alone cannot call for help at the time of injury. A day or two may pass before assistance is provided, and as a result, dehydration and debilitation occur. Nutritional status may have been poor prior to admission, so the nurse should monitor for complications of dehydration and malnutrition (e.g., pressure injuries, etc.). Screening for malnutrition and high-protein nutritional supplementation may be effective in improving outcomes in older adults with hip fractures and should be incorporated into the plan of care. Muscle weakness may have initially contributed to the fall and fracture. Bed rest and immobility cause an additional loss of muscle strength unless the nurse encourages the patient to move all joints except the involved hip and knee. Patients are encouraged to use their arms and the overhead trapeze to reposition themselves. This strengthens the arms and shoulders, which facilitates walking with assistive devices. Describe hip precautions: Identify nursing interventions: The immediate postoperative care for a patient with a hip fracture is similar to that for other patients undergoing major surgery. Attention is given to pain management, prevention of secondary medical problems, and early mobilization of the patient so that independent functioning can be restored. During the first 24 to 48 hours, relief of pain and prevention of complications are important, and continuous neurovascular assessment is essential. The nurse encourages deep breathing and dorsiflexion and plantar flexion exercises every 1 to 2 hours. Thigh-high anti-embolism stockings or pneumatic compression devices are used, and anticoagulants are given as prescribed to prevent the formation of VTE. The nurse administers prescribed analgesic medications and monitors the patient's hydration, nutritional status, and urine output.

Orthopedic surgery Post-operative care (describe suction drain assessment and care, identify potential complicaitons) Expected drainage is 200 to 500 ml in the first 24 hours and by 48 hours postoperatively the total expected drainage in 8 hours usually decreases to 30 ml or less. To decrease the homologus blood transfusions, autotransfusion drainage system may be used.

Describe suction drain assessment and care: Identify potential complications: VTE, infections, pain, blood loss, nerve injury, shock.

Identify and explain effects of major burn injury on the following: Fluid and Electrolytes

Edema forms rapidly after a burn injury. A superficial burn will cause localized edema to form within 4 hours, whereas a deeper burn will continue to form edema up to 18 hours post injury. The increased perfusion to the injured area in the presence of increased capillary permeability reflects the amount of microvascular and lymphatic damage to the tissue. In burns greater than 20% TBSA, inflammatory mediators stimulate local and systemic reactions resulting in extensive shift of intravascular fluid, electrolytes, and proteins into the surrounding interstitium. Treatments for edema may include elevation of the extremity or, in severe cases, cutting of the eschar (i.e., devitalized tissue) via escharotomy (i.e., surgical incision through eschar), or decompression of edema formation via fasciotomy (i.e., surgical incision through fascia to relieve constricted muscle) to restore tissue perfusion. Reabsorption of edema begins about 4 hours post injury and is complete approximately 4 days postburn injury. However, the rate of reabsorption depends on the depth of injury to the tissue. Although adequate fluid resuscitation is paramount to maintaining tissue perfusion, excessive fluid administration increases edema formation in both burned and unburned tissue causing ischemia and necrosis. Immediately after burn injury, hyperkalemia (excessive potassium) may result from massive cell destruction. Hypokalemia (potassium depletion) may occur later with fluid shifts and inadequate potassium replacement. Serum sodium levels vary in response to fluid resuscitation. Hyponatremia (serum sodium depletion) may be present from plasma loss or may occur during the first week of the acute phase, as water shifts from the interstitial space and returns to the vascular space. At the time of burn injury, some red blood cells may be destroyed, and others damaged. Despite this, the early hematocrit may be elevated due to plasma loss (hemoconcentration). Abnormalities in coagulation, including a decrease in platelets (thrombocytopenia) and prolonged clotting and prothrombin times also occur. For patients in the emergent/resuscitative phase, nurses should do a primary survey and closely monitor circulation. As the taut, burned tissue becomes unyielding to the edema beneath its surface, it begins to act like a tourniquet, especially if the burn is circumferential. As edema increases, pressure on small blood vessels in the distal extremities obstructs blood flow resulting in consequent tissue ischemia and potentially acute compartment syndrome. Patients in the acute/intermediate phase must be closely monitored for the development of venous thromboembolism (VTE).

Describe complications of fractures. How would the patient present? Identify medical treatments and nursing interventions for each- Fat Embolism

Fat embolism syndrome (FES) describes the clinical manifestations that occur when fat emboli enter circulation following orthopedic trauma, especially long bone (e.g., femur) and pelvic fractures. FES is more frequent in closed fractures than in open fractures. At the time of fracture, fat globules may diffuse from the marrow into the vascular compartment. The fat globules (e.g., emboli) may occlude the small blood vessels that supply the lungs, brain, kidneys, and other organs. The onset of symptoms is rapid, typically within 24 to 72 hours of injury, but may occur up to a week after injury. FES occurs more frequently in males than in females, with its highest incidence in those between the ages of 10 and 40 years. The classic triad of clinical manifestations of FES includes hypoxemia, neurologic compromise, and a petechial rash. The typical first manifestations are pulmonary and include hypoxia, tachypnea, and dyspnea accompanied by tachycardia, substernal chest pain, low-grade fever, crackles, and additional manifestations of respiratory failure. Chest x-ray may show evidence of acute respiratory distress syndrome (ARDS) or it may be normal. Petechial rash may develop 2 to 3 days after the onset of symptoms. This rash is secondary to dysfunction in the microcirculation and/or thrombocytopenia and is typically located in nondependent regions (e.g., chest, mucous membranes) of the body. There may be varying degrees of neurologic deficits that can include restlessness, agitation, seizures, focal deficits, and encephalopathy. There are no universal criteria for diagnosis of FES; diagnosis relies on clinical suspicion based upon the classic triad of symptoms and imaging findings. Subtle personality changes, restlessness, irritability, or confusion in a patient who has sustained a fracture are indications for immediate arterial blood gas studies. Prevention is the most important aspect of treatment; immediate immobilization of fractures, including early surgical fixation, minimal fracture manipulation, and adequate support for fractured bones during turning and positioning, and maintenance of fluid and electrolyte balance are measures that may reduce the incidence of fat emboli. There is no specific treatment for FES; the treatment is supportive. Fluid resuscitation, oxygenation, vasopressors, mechanical ventilation, and sometimes corticosteroids are used as supportive therapy.

Identify the four classifications of burns

First-degree burns are superficial injuries that involve only the outermost layer of skin. These burns are painful and erythematous, but the epidermis is intact; if rubbed, the burned tissue does not separate from the underlying dermis. This is known as a negative Nikolsky's sign. A typical first-degree burn is a sunburn or superficial scald burn. Second-degree (partial-thickness) burns involve the entire epidermis and varying portions of the dermis. They are painful and typically associated with blister formation. Healing time depends on the depth of dermal injury, typically ranging from 2 to 3 weeks. Hair follicles and skin appendages remain intact. The wound bed is moist due to serous leakage from the peripheral microcirculation. Third-degree (full-thickness) burns involve total destruction of the epidermis, dermis, and, in some cases, damage of underlying tissue. Wound color ranges widely from pale white to red, brown, or charred. The deeply burned area lacks sensation because the nerve fibers are damaged. The wound appears leathery and dry due to the destruction of the microcirculation. Skin organelles such as hair follicles and sweat glands may be affected. The severity of this burn is often deceiving to patients because they have no pain in the injury area. Fourth-degree burns (deep burn necrosis) are those injuries that extend into deep tissue, muscle, or bone. Burn depth determines whether spontaneous reepithelialization will occur. Determining burn depth can be difficult even for the experienced burn care provider. The following factors are considered in determining the depth of a burn: how the injury occurred, causative agent (such as flame or scalding liquid), temperature and duration of contact with the causative agent, and thickness of the skin at the injury site.

Identify and explain effects of major burn injury on the following: Thermoregulation

Integumentary loss also causes an inability to regulate body temperature resulting in various complications. Patients with burn injuries often exhibit low body temperatures in the early hours after injury not necessarily due to initial first aid, which may include cooling of the wounds, but more likely from the amount of TBSA involved, the IV resuscitation fluids administered, and exposure resulting in increased evaporative heat loss. Burn centers often have additional heating sources to help maintain the patient's body temperature through environmental warming.

CHAPTER 57

Management of Patients with Burn Injury

CHAPTER 36

Management of Patients with Musculoskeletal Disorders

CHAPTER 37

Management of Patients with Musculoskeletal Trauma

What considerations need to be considered when treating patients with neuropathic pain management?

Neuropathic pain is caused by either a lesion or a disease involving the somatosensory nervous system. Injuries to peripheral nerves can either be traumatic or nontraumatic, such as diabetic or compression neuropathies. Although specific causes may vary based on the underlying pathology, it is theorized that there are changes in the ion channels; imbalance of the stimuli processing between excitatory and inhibitory somatosensory signals; activity of glial cells; or potential differences in modulation of pain that occur with neuropathic pain. Recent research findings suggest that dysfunction in autophagy (i.e., cellular degradation of unnecessary materials) is involved with neuropathic pain. Research is ongoing to better define the peripheral and central mechanisms that initiate and maintain neuropathic pain. Deafferentation pain: Injury to either the peripheral or central nervous system; burning pain below the level of a spinal cord lesion reflects injury to the central nervous system Examples: Phantom pain as a result of peripheral nerve damage; poststroke pain; pain following spinal cord injury Sympathetically maintained pain: Associated with dysregulation of the autonomic nervous system Example: Complex regional pain syndrome Peripherally Generated Pain Painful polyneuropathies: Pain is felt along the distribution of many peripheral nerves. Examples: Diabetic neuropathy; postherpetic neuralgia; alcohol-nutritional neuropathy; some types of neck, shoulder, and back pain; pain of Guillain-Barré syndrome Painful mononeuropathies: Usually associated with a known peripheral nerve injury; pain is felt at least partly along the distribution of the damaged nerve Examples: Nerve root compression, nerve entrapment; trigeminal neuralgia; some types of neck, shoulder, and back pain. Co-analgesic agents, such as antidepressants, anticonvulsants, and local anesthetics, but there is wide variability in terms of efficacy and adverse-effect profiles.

What considerations need to be considered with the older adult population and pain management?

Older adults often live with chronic pain, yet physiologic changes and comorbidities make management more complicated among them. Older adults are often sensitive to the effects of co-analgesic agents that produce sedation and other CNS effects, such as antidepressants and anticonvulsants. Since they are also at risk for undertreatment of pain, therapy should be initiated with low doses, and titration should proceed slowly with systematic assessment of patient response. Older adults are also at increased risk for NSAID-induced GI toxicity. Acetaminophen should be used for mild pain and is recommended as first line for musculoskeletal pain (e.g., osteoarthritis). If an NSAID is needed for inflammatory pain, it is recommended that a COX-2 selective NSAID (if not contraindicated by an increased CV risk) or the nonselective NSAID least likely to cause a peptic ulcer should be used. The addition of a proton pump inhibitor to NSAID therapy, or opioid analgesic agents rather than an NSAID, is recommended for high-risk patients. The American Geriatric Society (AGS) recommends using extreme caution when prescribing NSAIDs among older adults. NSAIDs are safest when used for short-term pain flares that may occur during transient worsening in severity of chronic diseases or conditions (e.g., osteoarthritis, fibromyalgia, low back pain). A number of NSAIDs are available in topical formulations which may be preferred for older adults. Age is considered an important factor to consider when selecting an opioid dose. The starting opioid dose should be reduced by 25% to 50% in adults older than 70 years because they are more sensitive to opioid adverse effects than younger adults; the number of subsequent doses is based on patient response

CHAPTER 9

Pain Management

Osteomyelitis (what should you anticipate, differentiate the types and cause of each (hematogenous, continuous, vascular insufficiency, traumatic injury) potential signs and symptoms)

Patho: More than 50% of bone infections are caused by Staphylococcus aureus and increasingly of the variety that is methicillin resistant (i.e., MRSA). Surgical site ink markers have been linked to infections by cross contamination between preoperative patients who use their markers; therefore, these items are now considered one patient or one-time use items. Other pathogens include the gram-positive organisms streptococci and enterococci, followed by gram-negative bacteria, including pseudomonas. The initial response to infection is inflammation, increased vascularity, and edema. After 2 or 3 days, thrombosis of the local blood vessels occurs, resulting in ischemia with bone necrosis. The infection extends into the medullary cavity and under the periosteum and may spread into adjacent soft tissues and joints. Unless the infective process is treated promptly, a bone abscess forms. The resulting abscess cavity contains sequestrum (i.e., dead bone tissue), which does not easily liquefy and drain. Therefore, the cavity cannot collapse and heal, as it does in soft tissue abscesses. New bone growth, the involucrum, forms and surrounds the sequestrum. Although healing appears to take place, a chronically infected sequestrum remains and produces recurring abscesses throughout the patient's life. This is referred to as chronic osteomyelitis. What should you anticipate in regards to activity/ mobility orders: Treatment regimens restrict weight-bearing activity. The bone is weakened by the infective process and must be protected by avoidance of stress on the bone. The patient must understand the rationale for the activity restrictions. The joints above and below the affected part should be gently moved through their range of motion. The nurse encourages full participation in ADLs within the prescribed physical limitations to promote general well-being. Caution around external fixation devices is required. Hematogenous (cause and S&S): (i.e., due to bloodborne spread of infection). Contiguous focus (cause and S&S): from contamination from bone surgery (especially with hardware insertion), open fracture, or traumatic injury (e.g., gunshot wound). Vascular insufficiency (cause and S&S): seen most commonly among patients with diabetes and peripheral vascular disease, most commonly affecting the feet Patients who are at high risk for osteomyelitis include older adults and those who are poorly nourished or obese. Other patients at risk include those with impaired immune systems, those with chronic illnesses (e.g., diabetes, RA), those receiving long-term corticosteroid therapy or immunosuppressive agents, and those who use illicit IV drugs. Traumatic injury (cause and S&S):

Gout (pathophysiology, common medications and their side effects/complications)

Pathophysiology: Gout is the most common form of inflammatory arthritis. More than 8.3 million Americans self-report the diagnosis of gout. The prevalence is reported to be about 3.9% and appears to be on the rise. Men are three to four times more likely to be diagnosed with gout than women. The incidence of gout increases with age, body mass index, alcohol consumption, hypertension, and diuretic use. Evidence links the consumption of fructose-rich beverages with the risk of gout for both men and women. Patients with gout have an increased risk of cardiovascular disease. Comorbid conditions such as hypertension, dyslipidemia, diabetes, osteoarthritis, kidney disease, and depression may be present in patients with gout. Gout is caused by hyperuricemia (increased serum uric acid). Uric acid is a by-product of purine metabolism; purines are basic chemical compounds found in high concentrations in meat products. Urate levels are affected by diet, medications, overproduction in the body, and inadequate excretion by the kidneys. Hyperuricemia (serum concentration greater than 6.8 mg/dL) can, but does not always, cause urate crystal deposition. However, as uric acid levels increase, the risk becomes greater. The initial cause for the gout attack occurs when macrophages in the joint space phagocytize urate crystals. Through a series of immunologic steps, interleukin-1β is secreted, increasing the inflammation. This process is exacerbated by the presence of free fatty acids. Both alcohol and consumption of a large meal, especially with red meat, can lead to increases in free fatty acid concentrations; they also are implicated as triggers to acute gout attacks. With repeated attacks, accumulations of sodium urate crystals, called tophi, are deposited in peripheral areas of the body, such as the great toe, the hands, and the ear. Renal uratelithiasis (kidney stones), with chronic kidney disease secondary to urate deposition, may develop. Primary hyperuricemia may be caused by severe dieting or starvation, excessive intake of foods that are high in purines (shellfish, organ meats), or heredity. In secondary hyperuricemia, gout is a clinical feature secondary to any of a number of genetic or acquired processes, including conditions in which there is an increase in cell turnover (leukemia, multiple myeloma, some types of anemias, psoriasis) and an increase in cell breakdown. Altered renal tubular function, either as a major action or as an unintended side effect of certain pharmacologic agents (e.g., diuretics such as thiazides and furosemide), low-dose salicylates, or ethanol can contribute to uric acid underexcretion. The finding of urate crystals in the synovial fluid of asymptomatic joints suggests that factors other than crystals may be related to the inflammatory reaction. Recovered monosodium urate crystals are coated with immunoglobulins that are mainly IgG. IgG enhances crystal phagocytosis, thereby demonstrating immunologic activity Common medications (What are they, What are the side effects, Potential complications): Given that the incidence of gout increases with age, its management can be complicated by other medical conditions, medications, and age-related changes. A definitive diagnosis of gouty arthritis is established by polarized light microscopy of the synovial fluid of the involved joint. Uric acid crystals are seen within the polymorphonuclear leukocytes in the fluid during a disease flare up. Acute attacks are managed with colchicine (oral or parenteral), an NSAID such as indomethacin, or a corticosteroid. Management of hyperuricemia, tophi, joint destruction, and renal disorders is usually initiated after the acute inflammatory process has subsided. Once the acute attack has subsided, uric acid lowering therapy should be considered. Xanthine oxidase inhibitors, such as allopurinol and febuxostat, are the agents of choice. Given the role of IL-1 in the pathogenesis of gout, some experts suggest that there may be a role for anakinra, an IL-1 receptor antagonist in the management of acute gout. Management between gout attacks needs to include lifestyle changes such as avoiding purine-rich foods, weight loss, decreasing alcohol consumption, and avoiding certain medications. Uricosuric agents, such as probenecid, may be indicated in patients with frequent acute attacks. Uricosuric medications correct hyperuricemia and dissolve deposited urate. Corticosteroids may also be used in patients who have no response to other therapy. In patients with refractory chronic gout who are not controlled with the regimens mentioned earlier, pegloticase, a newer agent, has been shown to be effective in lowering uric acid levels. Specific treatment is based on the serum uric acid level, 24-hour urinary uric acid excretion, and renal function. Colchicine: Lowers the deposition of uric acid and interferes with leukocyte infiltration, thus reducing inflammation; does not alter serum or urine levels of uric acid; used in acute and chronic management. Acute management: Administer when attack begins; dosage increased until pain is relieved or diarrhea develops, then stop medication. Chronic management: Causes gastrointestinal upset in most patients. Probenecid: Uricosuric agent; inhibits renal reabsorption of urates and increases the urinary excretion of uric acid; prevents tophi formation. Be alert for nausea and rash. Allopurinol, febuxostat: Xanthine oxidase inhibitors; interrupt the breakdown of purines before uric acid is formed; inhibit xanthinoxidase because uric acid formation is blocked. Monitor for side effects, including bone marrow depression, nausea, vomiting, diarrhea, abdominal pain, or rash. Avoid starting medication or increasing dose if active flare present. Nursing: Research indicates that providers overestimate patient knowledge of gout and that patients prefer the use of both written and verbal materials. Therefore, the nurse takes every opportunity to educate and reinforce knowledge of gout verbally and in writing. Severe dietary restriction is not necessary; however, the nurse encourages the patient to restrict consumption of foods high in purines, especially organ meats, and to limit alcohol intake. Maintenance of normal body weight should be encouraged. In an acute episode of gouty arthritis, pain management with prescribed medications is essential, along with avoidance of factors that increase pain and inflammation, such as trauma, stress, and alcohol. Medication adherence is critical but poor among patients prescribed urate lowering therapies. The nurse reinforces the importance of taking prescribed medications. Between acute episodes, the patient feels well and may abandon medications and preventive behaviors, which may result in an acute attack. Acute attacks are most effectively treated if therapy begins early.

Septic arthritis (pathophysiology, treatments)

Pathophysiology: Joints can become infected through spread of pathogens from other parts of the body (hematogenous spread) or directly through trauma, injection, or surgical instrumentation, causing septic arthritis. People at greatest risk include older adults, particularly those older than 80 years; people with comorbid conditions such as diabetes, RA, skin infection, or alcoholism; and people with a history of a joint replacement or other joint surgery or IV drug abuse. S. aureus is the most common cause of joint infections in all age groups, followed by other gram-positive bacteria, including streptococci. Gonococcal infection may cause septic arthritis through hematogenous spread. Pseudomonas aeruginosa is a commonly implicated pathogen in those who use illicit IV drugs. Single knee or hip joints are most commonly infected in patients with septic arthritis, although up to 20% of cases involve more than one joint (i.e., polyarticular disease). Prompt recognition and treatment of an infected joint are important because accumulating purulent material may result in chondrolysis (destruction of hyaline cartilage), and continued hematogenous spread may lead to sepsis and death. See Chapter 11 for further discussion of sepsis. The overall mortality rate for single joint infections is about 11%, but it approaches 50% in patients with polyarticular disease or in those who are immunocompromised. Treatments: Prompt treatment is essential and may save the prosthesis for patients who have had joint replacement surgery or may prevent sepsis. Broad-spectrum IV antibiotics are started promptly and then changed to organism-specific antibiotics after culture results are available. The IV antibiotics are continued until symptoms resolve. The synovial fluid is aspirated and analyzed periodically for sterility and decrease in WBCs. Aspiration of the joint with a needle to remove excessive joint fluid, exudate, and debris promotes comfort and decreases joint destruction caused by the action of proteolytic enzymes in the purulent fluid. Arthrotomy or arthroscopy is used to drain the joint and remove dead tissue. The inflamed joint is supported and immobilized in a functional position by a splint that increases the patient's comfort. Analgesic agents are prescribed to relieve pain. The patient's nutrition and fluid status is monitored. Progressive range-of-motion exercises are prescribed as soon as the patient can begin movement without exacerbating symptoms of acute pain. If septic joints are treated promptly, recovery of normal function is expected. If the articular cartilage was damaged during the inflammatory reaction, joint fibrosis and diminished function may result. The patient is assessed periodically for recurrence over the next year. The nurse educates the patient and family about the septic arthritis physiologic process and explains the importance of supporting the affected joint, adhering to the prescribed antibiotic regimen, inspecting the skin under any splints that may be prescribed, and observing weight-bearing and activity restrictions. The patient must understand that recurrence of infection in the near and far future is possible and is educated about signs and symptoms to observe and report to the primary provider. The same interventions used for the patient with osteomyelitis are planned for the patient with septic arthritis. See previous discussion.

Osteomalacia (pathophysiology, potential causes, treatment)

Pathophysiology: Osteomalacia is a metabolic bone disease characterized by inadequate mineralization of bone. As a result, the skeleton softens and weakens, causing pain, tenderness to touch, bowing of the bones, and pathologic fractures. On physical examination, skeletal deformities (spinal kyphosis and bowed legs) give patients an unusual appearance and a waddling gait. These patients may be uncomfortable with their appearance and are at risk for falls and pathologic fractures, particularly of the distal radius and the proximal femur. The major defect in osteomalacia is a deficiency of activated vitamin D, which promotes calcium absorption from the GI tract and facilitates mineralization of bone. The supply of calcium and phosphate in the extracellular fluid is low and does not move to calcification sites in bones. Osteomalacia may result from failed calcium absorption or from excessive loss of calcium from the body (e.g., kidney failure). GI disorders (e.g., celiac disease, chronic biliary tract obstruction, chronic pancreatitis, small bowel resection) in which fats are inadequately absorbed are likely to produce osteomalacia through loss of vitamin D (along with other fat-soluble vitamins) and calcium, the latter being excreted in the feces with fatty acids. In addition, liver and kidney diseases can produce a lack of vitamin D because these are the organs that convert vitamin D to its active form. Severe renal insufficiency results in acidosis. The body uses available calcium to combat the acidosis, and PTH stimulates the release of skeletal calcium in an attempt to reestablish a physiologic pH. During this continual drain of skeletal calcium, bony fibrosis occurs, and bony cysts form. Chronic glomerulonephritis, obstructive uropathies, and heavy metal poisoning result in a reduced serum phosphate level and demineralization of bone. Hyperparathyroidism leads to skeletal decalcification and thus to osteomalacia by increasing phosphate excretion in the urine. Prolonged use of anticonvulsant medication (e.g., phenytoin, phenobarbital) poses a risk of osteomalacia, as does insufficient vitamin D (dietary, sunlight). Osteomalacia that results from malnutrition (deficiency in vitamin D often associated with poor intake of calcium) is a result of poverty, poor dietary habits, and lack of knowledge about nutrition. It occurs most frequently in parts of the world where vitamin D is not added to food, where dietary deficiencies exist, and where sunlight is rare. Treatment: Physical, psychological, and pharmaceutical measures are used to reduce the patient's discomfort and pain. If the underlying cause of osteomalacia is corrected, the disorder may resolve. If kidney disease prevents activation of absorbed vitamin D, then supplementation requires the activated form (calcitriol). If osteomalacia is caused by malabsorption, increased doses of vitamin D, along with supplemental calcium, are usually prescribed. Exposure to sunlight may be recommended; ultraviolet radiation transforms a cholesterol substance (7-dehydrocholesterol) present in the skin into vitamin D. If osteomalacia is dietary in origin, the interventions are akin to those discussed previously in the discussion on osteoporosis. Long-term monitoring of the patient is appropriate to ensure stabilization or reversal of osteomalacia. Some persistent orthopedic deformities may need to be treated with braces or surgery (e.g., osteotomy may be performed to correct long bone deformity).

Osteoporosis (pathophysiology, potential causes, prevention strategies)

Pathophysiology: Osteoporosis is the most prevalent bone disease in the world. More than 1.5 million osteoporotic fractures occur every year. Fractures requiring hospitalization have risen significantly over the past two decades. More than 10 million Americans have osteoporosis, and an additional 33.6 million have osteopenia (i.e., low bone mineral density [BMD])—the precursor to osteoporosis. The consequence of osteoporosis is bone fracture. It is projected that one of every three women and one of every five men over the age of 50 will have an osteoporosis-related fracture at some point in their lives. Osteoporosis is characterized by reduced bone mass, deterioration of bone matrix, and diminished bone architectural strength. Normal homeostatic bone turnover is altered; the rate of bone resorption that is maintained by osteoclasts is greater than the rate of bone formation that is maintained by osteoblasts, resulting in a reduced total bone mass. The bones become progressively porous, brittle, and fragile. They fracture easily under stresses that would not break normal bone. This occurs most commonly as compression fractures of the thoracic and lumbar spine, hip fractures, and Colles fractures of the wrist. These fractures may be the first clinical manifestation of osteoporosis. Potential causes: Small-framed women are at greatest risk for osteoporosis. In terms of ethnicity, Asian and Caucasian women are at highest risk. Although African American women tend to have higher mineral mass when younger, they are still at risk due to the prevalence of sickle cell and autoimmune diseases in this population. In addition, many African American women also have poor calcium intake due to lactose intolerance. The use of aromatase inhibitors is an additional risk for women with breast cancer. Men have a greater peak bone mass and do not experience a sudden midlife estrogen reduction. As a result, osteoporosis occurs about one decade later, but one in four men still sustain an osteopenic fracture. It is believed that both testosterone and estrogen are important in achieving and maintaining bone mass in men, although the risk profile for men is not as well established as it is for women. Nutritional factors contribute to the development of osteoporosis. A diet that includes adequate calories and nutrients needed to maintain bone, calcium, and vitamin D must be consumed. Patients who have had bariatric surgery are at increased risk for osteoporosis as the duodenum is bypassed, which is the primary site for absorption of calcium. Patients who have gastrointestinal (GI) diseases that cause malabsorption (e.g., celiac disease, alcoholism) may benefit from additional magnesium supplements. However, in adults who follow a strict gluten free diet, magnesium supplements are currently not recommended. Autoimmune diseases also contribute to poor bone health. Many of them are associated with nutritional deficiencies (e.g., celiac, autoimmune liver disease). Furthermore, many patients with autoimmune diseases are prescribed corticosteroid medications and, as a consequence of their disease processes, are relatively sedentary. These factors also can cause weak bones. Bone formation is enhanced by the stress of weight and muscle activity. When immobilized by casts, general inactivity, paralysis, or other disability, the bone is resorbed faster than it is formed, and osteoporosis results. Immobility contributes to the development of osteoporosis. Resistance and impact exercises are most beneficial in developing and maintaining bone mass. Prevention strategies: Peak adult bone mass is achieved between the ages of 18 and 25 years in both women and men and is affected by genetic factors, nutrition, physical activity, medications, endocrine status, and general health. Men typically develop larger, heavier bones than women; therefore, they manifest osteoporosis at more advanced ages. Primary osteoporosis occurs in women after menopause (usually by age 51) but it is not merely a consequence of aging. Failure to develop optimal peak bone mass and low vitamin D levels contribute to the development of osteopenia without associated bone loss. Early identification of at-risk teenagers and young adults, increased calcium and vitamin D intake, participation in regular weight-bearing exercise, and modification of lifestyle (e.g., reduced use of caffeine, tobacco products, carbonated soft drinks, and alcohol) are interventions that decrease the risk of fractures and associated disability later in life. Secondary osteoporosis is the result of medications or diseases that affect bone metabolism. Men are more likely than women to have secondary causes of osteoporosis, including the use of corticosteroids (especially if they receive doses in excess of 5 mg of prednisone daily for more than 3 months) and excessive alcohol intake. Specific disease states (e.g., celiac disease, hypogonadism) and medications such as anticonvulsants (e.g., phenytoin), thyroid replacement agents (e.g., levothyroxine), antiestrogens (e.g., medroxyprogesterone), androgen inhibitors (e.g., leuprolide), selective serotonin receptor inhibitors (SSRIs; e.g., fluoxetine) and proton pump inhibitors (e.g., esomeprazole) place patients at risk; these diseases and medications need to be identified and therapies instituted to halt the development of osteoporosis. The degree of bone loss is related to the duration of medication therapy. When the drugs are discontinued or the metabolic problem is corrected, the progression is halted but restoration of lost bone mass may not occur.

Total hip arthroplasty (what are the precautions and why are they important)

Pathophysiology: THA is the replacement of a severely damaged hip with an artificial joint. Indications for this surgery include OA, as well as RA, femoral neck fractures, failure of previous reconstructive surgeries, such as a failed prosthesis with osteotomy, and conditions resulting from developmental dysplasia or Legg-Calvé-Perthes disease (avascular necrosis of the hip in childhood). A variety of total hip prostheses are available. Most consist of a metal femoral component topped by a spherical ball made of metal, ceramic, or plastic that is fitted into a plastic or metal acetabular socket. The surgeon selects the prosthesis that is best suited to the individual patient, considering various factors including skeletal structure and activity level. The patient has irreversibly damaged hip joints, and the potential benefits, including improved quality of life, outweigh the surgical risks. With the advent of improved prosthetic materials and operative techniques, the life of the prosthesis has been extended, and today younger patients with severely damaged and painful hip joints are undergoing total hip replacement. Describe hip precautions (What are they and Why are they important): For patients undergoing a posterior or posterolateral approach for THA, maintenance of the femoral head component in the acetabular cup is essential. The risk for dislocation is more common with this approach and may occur when the hip is in full flexion, adducted (legs together), and internally rotated. Therefore, correct positioning is maintained at all times. The patient should be in a supine position with the head slightly elevated and the affected leg in a neutral position. The use of an abduction splint, a wedge pillow (see Fig. 36-10), or two or three pillows placed between the legs prevent adduction beyond the midline of the body. A cradle boot may be used to prevent leg rotation and to support the heel off the bed, preventing development of a pressure injury. When the nurse turns the patient in bed to the unaffected side, it is important to keep the operative hip in abduction (movement away from the center or median line of the body). The patient should not be turned to the operative side, which could cause dislocation, unless specified by the surgeon. The patient's hip is never flexed more than 90 degrees. When using a fracture bedpan, the nurse instructs the patient to flex the unaffected hip and to use the trapeze to lift the pelvis onto the pan. The patient is also reminded not to flex the affected hip. Limited flexion is maintained during transfers and when sitting. When the patient is initially assisted out of bed, an abduction splint or pillows are kept between the legs. The nurse encourages the patient to keep the affected hip in extension, instructing the patient to pivot on the unaffected leg with assistance by the nurse, who protects the affected hip from adduction (movement toward the center or median line of the body), flexion, internal or external rotation, and excessive weight bearing. High-seat (orthopedic) chairs with arm rests, semi-reclining chairs, and raised toilet seats are used to minimize hip joint flexion. When sitting, the patient's hips should be higher than the knees. The patient's affected leg should not be elevated when sitting. The patient may flex the knee. The nurse educates the patient about protective positioning, which includes maintaining abduction and avoiding internal and external rotation, hyperextension, and acute flexion, as described previously. At no time should the patient cross the legs or bend at the waist past 90 degrees (e.g., to put on shoes and socks). Occupational therapists can provide the patient with devices to assist with dressing below the waist. Hip precautions for patients who had a posterior or posterolateral approach for THA should be enforced for 4 months or longer after surgery (see Chart 36-7). A patient who has had an anterior surgical approach may not need these precautions. Several studies have reported an anterolateral approach to THA results in a lower rate of dislocation than a posterior approach owing to its ease of access, superior visualization, and a predictable healing pattern. Using a less restrictive mobility protocol in these patients can lead to earlier and better resumption of ADL, earlier return to work, a shorter length of hospital stay, and improved patient satisfaction. Dislocation may occur with positioning that exceeds the limits of the prosthesis. The nurse must monitor for signs and symptoms of dislocation of the prosthesis, which include: •Increased pain at the surgical site, swelling, and immobilization •Acute groin pain in the affected hip or increased discomfort •Shortening of the affected extremity •Abnormal external or internal rotation of the affected extremity •Restricted ability or inability to move the leg •Reported "popping" sensation in the hip If any of these clinical manifestations occur, the nurse (or the patient, if at home) immediately notifies the surgeon, because the hip must be reduced and stabilized promptly so that the leg does not sustain circulatory and nerve damage. After closed reduction, the hip may be stabilized with Buck's traction or a brace to prevent recurrent dislocation (see Chapter 37, Fig. 37-11). As the muscles and joint capsule heal, the chance of dislocation diminishes. Stresses to the new hip joint should be avoided for the first 8 to 12 weeks, when the risk of dislocation is greatest

What education needs to be provided to those with a PCA

Patient-controlled analgesia (PCA) is an interactive method of pain management that allows patients to treat their pain by self-administering doses of analgesic agents. It is used to manage all types of pain by multiple routes of administration, including oral, IV, subcutaneous, epidural, and perineural. Current guidelines from the APS, the American Society of Regional Anesthesia and Pain Medicine, and the American Society of Anesthesiologists strongly recommended IV PCA for postoperative pain management when it is necessary to use the parenteral route to deliver analgesic medications. A PCA infusion device is programmed so that the patient can press a button (pendant) to self-administer a dose of an analgesic agent (PCA dose) at a set time interval (demand or lockout) as needed. Patients who use PCAs must be able to understand the relationships among pain, pushing the PCA button or taking the analgesic agent, and pain relief, and must be cognitively and physically able to use any equipment that is necessary to administer the therapy. A basal rate (continuous infusion) may be used for patients who are opioid tolerant, and when PCEA is used. It is discouraged for patients who are opioid naïve and receiving IV PCA due to the risk of oversedation with subsequent respiratory depression. Essential to the safe use of a basal rate with PCA is close monitoring by nurses of sedation and respiratory status and prompt decreases in opioid dose (e.g., discontinue basal rate) if increased sedation is detected. The primary benefit of PCA is that it recognizes that only the patient can feel the pain and only the patient knows how much analgesic will relieve it. This reinforces that PCA is for patient use only and that unauthorized activation of the PCA device by anyone other than the patient (PCA by proxy) should be discouraged. However, for some patients who are candidates for PCA but unable to use the PCA equipment, the nurse or a capable family member may be authorized to manage the patient's pain using PCA equipment. This is referred to as Authorized Agent Controlled Analgesia; guidelines are available for the safe administration of this therapy. Staff, family, and other visitors should be instructed to contact the nurse if they have concerns about pain control rather than activating the PCA device for the patient.

Identify and explain effects of major burn injury on the following: Metabolism

Patients who are critically ill, especially those with burns, are predisposed to altered gastrointestinal (GI) motility. Impaired enteric nerve and smooth muscle function, inflammation, surgery, medications such as vasopressors, and inadequate tissue perfusion are some causes of GI dysfunction. Indicators of GI organ ischemia include increased bladder pressure, increasing serum lactate, and feeding intolerance. Three of the most common GI alterations in patients with burns are paralytic ileus (absence of intestinal peristalsis), Curling's ulcer, and translocation of bacteria. Decreased peristalsis and bowel sounds are manifestations of paralytic ileus. Gastric distention and nausea may lead to vomiting; therefore, gastric decompression is advised. Gastric bleeding secondary to massive physiologic stress may be signaled by occult blood in the stool, regurgitation of "coffee-ground" material from the stomach, or bloody vomitus. These signs suggest gastric or duodenal erosion (Curling's ulcer). Probiotics may be useful in maintaining intestinal barrier function through avoidance of colonization of pathogenic microorganisms. Thermal injury damages the liver through induction of hepatic edema, apoptosis, insulin resistance associated with metabolic derangements, and development of a fatty liver. In addition, with severe burn injury, acute pancreatitis is common and may result in a threefold increase in amylase or lipase, feeding intolerance, or abdominal pain. Patients with large TBSA burns are also at risk for life-threatening abdominal compartment syndrome (ACS) due to large volumes of fluid required for resuscitation, fluid shifts to the interstitium causing edema formation, and decreased abdominal wall compliance due to eschar formation. Increased pressure in the abdominal cavity contributes to GI tract and abdominal organ ischemia. Ramirez, Palmieri, Greenhalgh, and colleagues reviewed 10 years of cases of ACS in patients with burns and found support for early laparotomy as definitive treatment of ACS.

Nursing Roles- What education needs to be provided about using non-pharmacological/ alternative pain-relief measures?

Physical modalities Proper body alignment; application of heat and/or cold; massage; transcutaneous electrical nerve stimulation (TENS); acupuncture; physical therapy; and aqua therapy Be aware that some of these methods require a prescription in the inpatient setting, as inappropriate use can cause harm (e.g., burns or frostbite from extreme temperatures and prolonged thermal application). Cognitive and behavioral methods Relaxation breathing; distraction; listening, singing, or rhythmic tapping to music; imagery; humor; pet therapy; prayer; meditation; hypnosis Prior to use, evaluate patient's cognitive ability to learn and perform necessary activities. Movement therapy Yoga, T'ai chi Prior to use, evaluate patient's physical ability to perform necessary activities. Biologically based therapies Taking herbs, vitamins, and proteins; aromatherapy; diet modifications Evaluate use to identify potential adverse effects. Energy therapies Therapeutic touch, Reiki, and healing touch Obtain patient's permission before using intervention.

Amputation (reasons for amputation, complications, Syme amputation, patient education on mobility post-surgery)

Reasons for: Amputation is the removal of a body part by a surgical procedure or trauma. The majority of amputations are often consequences of vascular disease, especially from diabetes; trauma is the second most common indication. African Americans are at heightened risk of having amputations. An amputation is performed to control pain or disease process, to improve function, and to save or improve the patient's quality of life. If the health care team communicates a positive attitude, the patient adjusts to the amputation more readily and actively participates in the rehabilitative plan, learning how to modify activities and how to use assistive devices for ADLs and mobility. The level of amputation is performed at the most distal point that will heal successfully and should take into account the ability of the patient to achieve a successful rehabilitation. The site and extent of amputation is determined by circulation in the area (and whether or not necrosis is present), the degree of tissue loss and viability of the tissues, functional usefulness (i.e., meets the requirements for the use of a prosthesis) and the presence of infection. The circulatory status of the limb is evaluated through physical examination and diagnostic studies. Muscle and skin perfusion are important for healing. Doppler flow studies with duplex ultrasound, segmental pressure determinations, and transcutaneous oxygen measurements of the limb are valuable diagnostic aids. Angiography is performed if revascularization is considered an option. The objective of surgery is to conserve as much limb length as needed to preserve function and possibly to achieve a good prosthetic fit. Preservation of knee and elbow joints is desirable. Figure 37-23 shows the levels at which a limb may be amputated. Most amputations involving limbs eventually can be fitted with a prosthesis. The amputation of toes and portions of the foot can cause changes in gait and balance. A Syme amputation (modified ankle disarticulation amputation) is performed most frequently for extensive foot trauma and aims to produce a durable residual limb that can withstand full weight bearing. Below-knee amputation (BKA) is preferred to above-knee amputation (AKA) because of the importance of the knee joint and the energy requirements for walking. A knee disarticulation (e.g., amputation through the joint) is most successful with a young, active patient who can develop precise control of the prosthesis. When AKAs are performed, all possible length is preserved, muscles are stabilized and shaped, and hip contractures are prevented to maximize ambulatory potential. Most people who have a hip disarticulation amputation must rely on a wheelchair for mobility. Upper limb amputations are performed with the goal of preserving maximal functional length. The prosthesis is fitted early to ensure maximum function. A "staged" amputation may be used when gangrene and infection exist. Initially, a débriding amputation in the form of a guillotine amputation (i.e., transfemoral, transtibial) is performed to remove the infected and necrotic tissue. Once the infected limb is removed, systemic antibiotics are administered, and the wound is left open and allowed to drain. In a few days, after the infection has been controlled and the patient's condition has stabilized, a definitive amputation with skin closure is performed; a drain may be left in place Potential complications: Complications that may occur with amputation include hemorrhage, infection, skin breakdown, phantom limb pain, and joint contracture. Because major blood vessels have been severed, hemorrhage may occur. Infection is a risk with all surgical procedures. The risk of infection increases with contaminated wounds after traumatic amputation. Antibiotic prophylaxis prior to surgery is recommended. Skin irritation caused by the prosthesis may result in skin breakdown. Phantom limb pain (pain perceived in the amputated section) is caused by the severing of peripheral nerves. Joint contracture is caused by positioning and a protective flexion withdrawal pattern associated with pain and muscle imbalance. Associated comorbidities such as ischemic disease and psychological disorders such as depression and anxiety must also be monitored closely as they can contribute to further complications and chronic limb pain. Syme amputation: See above. Patient education on mobility post-surgery: The objective of treatment is to achieve healing of the amputation wound, the result being a nontender residual limb with healthy skin for prosthetic use. Healing is enhanced by gentle handling of the residual limb, control of residual limb edema and pain, and the use of aseptic technique in wound care to avoid infection. The primary postoperative dressings to support soft tissues, control pain and edema, and prevent joint contractures include nonremovable rigid dressings, removable rigid dressings, soft dressings (elastic and crepe), and weight-bearing immediate postoperative prostheses. The type of dressing used in patients with lower limb amputations varies. A reduction in edema, pain, contractures, healing time, time to prosthetic fitting, and injury due to falls has been shown for certain types of amputations (e.g., transtibial) with the use of removable rigid dressings as compared to soft dressings. However, a soft dressing with or without compression may be used if there is significant wound drainage, frequent inspection of the residual limb is required, and the patient has poor skin integrity. An immobilizing splint may be incorporated in the soft dressing. Good clinical judgment over which dressing to use should consider the risks and benefits for each individual patient. A wound drain can be placed to remove excess blood and drainage from the surgical site. Staples or sutures maintain closure at the operative site and are typically removed approximately 3 weeks postoperatively. The multidisciplinary rehabilitation team (patient, nurse, primary provider, social worker, physical therapist, occupational therapist, psychologist, prosthetist, vocational rehabilitation worker) helps the patient achieve the highest possible level of function and participation in life activities (see Fig. 37-24). Prosthetic clinics, amputee support programs, and peer visits (face-to-face, telephone, digital) for patients with a limb amputation facilitate the rehabilitation process, both physically and psychosocially. Patients who undergo amputation need support as they grieve the loss and change in body image. Their reactions can include anger, bitterness, and hostility. Psychological issues (e.g., denial, anxiety, avoidance) may be influenced by the type of support the patient receives from the rehabilitation team, the effectiveness of pain management, and by how quickly ADLs and the use of the prosthesis are learned. Providing education about the full options and capabilities available with the various prosthetic devices, as well as the recovery of walking capacity, if appropriate, can give the patient a sense of control over the resulting disability and promote independence

Identify the three methods used to determine Total Body Surface Area (TBSA) burned

Rule of Nines The most common method of estimating the extent of burns in adults is the rule of nines (see Fig. 57-3). This system is based on anatomic regions, each representing approximately 9% of the TBSA, allowing clinicians to rapidly estimate percent of body burned. If the burn affects only a portion of an anatomic area, the TBSA is calculated accordingly—for example, if approximately half of one arm were burned, the TBSA burned would be 4.5%. Lund and Browder Method A more precise method of estimating the extent of a burn is the Lund and Browder method, which recognizes the percentage of surface area of various anatomic parts, especially the head and legs, as it relates to the age of the patient. By dividing the body into very small areas and providing an estimate of the proportion of TBSA accounted for by each body part, clinicians can obtain a reliable estimate of TBSA burned. The initial evaluation made on arrival of the patient to the hospital should be revised within the first 72 hours, because demarcation of the wound and its depth present themselves more clearly by this time. The Lund and Browder chart is readily available in both printed and electronic formats. Palmer Method In patients with scattered burns, or very large burns with minimal sparing, the palmer method is an expeditious method to determine extent of injury. The size of the patient's hand, including the fingers, is approximately 1% of that patient's TBSA.

SLE (clinical manifestations, nursing management)

SLE: While the exact cause is not known, SLE starts with the body's immune system inaccurately recognizing one or more components of the cell's nucleus as foreign, seeing it as an antigen. The immune system starts to develop antibodies to the nuclear antigen. In particular, B cells begin to overproduce antibodies with the help of multiple cytokines such as B-lymphocyte stimulator (BLyS), which is overexpressed in SLE. The antibodies and antigens form antigen-antibody complexes and have the propensity to get trapped in the capillaries of visceral structures. The antibodies also act to destroy host cells. It is thought that those two mechanisms are responsible for the majority of the clinical manifestations of this disease process. The immunoregulatory disturbance is thought to be brought about by some combination of four distinct factors: genetic, immunologic, hormonal, and environmental. Research into the genetic origins of SLE has thus far revealed that multiple genes are likely implicated in the development of SLE. The large majority of SLE cases, however, remain sporadic and unrelated to family medical history. Given the high number of women with SLE compared with men, it is hypothesized that female sex hormones (estrogen) play a role in the predisposition to SLE. Estrogen may contribute to the body's response of overreacting to the body's own tissues. Although genetics and hormones likely play a role in the predisposition of SLE, it is hypothesized that exogenous or environmental triggers are also implicated in the onset of the disease process. These triggers may include cigarette smoke, ultraviolet rays, exposure from sunlight and fluorescent light bulbs, medications (hydralazine, minocyline, or procainamide), viral infections, emotional stress, stress on the body (e.g., surgery, pregnancy), and silica dust exposure in the occupational setting. Clinical manifestations: SLE is an autoimmune, systemic disease that can affect any body system. The disease process involves chronic states where symptoms are minimal or absent and acute flares where symptoms and lab results are elevated. Symptoms most often include fever, fatigue, skin rashes, as well as joint pain and swelling. The mucocutaneous, musculoskeletal, renal, nervous, cardiovascular, and respiratory systems are most commonly involved. Less commonly affected are the gastrointestinal tract and liver as well as the ocular system. Some type of cutaneous system manifestation is experienced in up to 85% of patients with SLE. Several skin manifestations may occur in patients with SLE, including subacute cutaneous lupus erythematosus, which involves papulosquamous or annular polycyclic lesions, and a discoid rash, which is a chronic rash with erythematous papules or plaques and scaling and can cause scarring and pigmentation changes. In some cases, the only skin involvement may be a discoid rash. In some patients with SLE, the initial skin involvement is the precursor to more systemic involvement. The lesions often worsen during exacerbations (flares) of the systemic disease and possibly are provoked by sunlight or artificial ultraviolet light. Oral ulcers, which may accompany skin lesions, may involve the buccal mucosa or the hard palate, occur in crops, and are often associated with exacerbations. Other cutaneous manifestations include splinter hemorrhages, alopecia, and Raynaud's phenomenon. Joint pain and swelling occur in more than 90% of patients with SLE. Joint swelling, tenderness, and pain on movement are also common. Frequently, these are accompanied by morning stiffness. The cardiac system is also commonly affected in SLE. Pericarditis is the most common cardiac manifestation. Patients may present with substernal chest pain that is aggravated by movement or inspiration. Symptoms can be acute and severe or last for weeks at a time. Other cardiac symptoms may involve myocarditis, hypertension, cardiac arrhythmias, and valvular incompetence. Nephritis as a result of SLE, also referred to as lupus nephritis, occurs due to a buildup of antibodies and immune complexes that cause damage to the nephrons. Serum creatinine levels and urinalysis are used in screening for renal involvement. Early detection allows for prompt treatment so that renal damage can be prevented. Renal involvement may lead to hypertension, which also requires careful monitoring and management. Central nervous system involvement is widespread, encompassing the entire range of neurologic disease. The varied and frequent neuropsychiatric presentations of SLE are now widely recognized and include psychosis, cognitive impairment, seizures, peripheral and cranial neuropathies, transverse myelitis, and strokes. These are generally demonstrated by subtle changes in behavior patterns or cognitive ability. Nursing Management (Emotional support & Coping): Nursing care of the patient with SLE is based on the fundamental plan presented earlier in the chapter. The most common nursing diagnoses include fatigue, impaired skin integrity, body image disturbance, and lack of knowledge for self-management decisions. The disease or its treatment may produce dramatic changes in appearance and considerable distress for the patient. The changes and the unpredictable course of SLE necessitate expert assessment skills and nursing care with sensitivity to the psychological reactions of the patient. The patient may benefit from participation in support groups, which can provide disease information, daily management tips, and social support. Because sun and ultraviolet light exposure can increase disease activity or cause an exacerbation, patients should be instructed to avoid exposure or to protect themselves with sunscreen and appropriate clothing. Because of the increased risk of involvement of multiple organ systems, patients should understand the need for routine periodic screenings as well as health promotion activities. A dietary consultation may be indicated to ensure that the patient is knowledgeable about dietary recommendations, given the increased risk of cardiovascular disease, including hypertension and atherosclerosis. In the healthy population, smoking and using electronic nicotine delivery systems (ENDS) including e-cigarettes, e-pens, e-pipes, e-hookah, and e-cigars clearly poses health risks. Smoking increases the incidence of respiratory infections, lung cancer, risk of coronary artery disease; increases blood pressure, which can worsen kidney function; inhibits liver function (which can also inhibit treatment medications from working appropriately, such as hydroxychloroquine); increases the risk for skin diseases; and increases the risk for osteoporosis. The health risks of ENDS use is under investigation. Patients diagnosed with SLE are at even higher risk of developing lung cancer and other rare cancers. Therefore, smoking cessation programs should be offered to all patients who report smoking habits. The nurse educates the patient about the importance of continuing prescribed medications and addresses the changes and potential side effects that are likely to occur with their use. The patient is reminded of the importance of monitoring because of the increased risk of systemic involvement, including renal and cardiovascular effects. Because of the immunosuppression associated with systemic corticosteroid usage, the nurse must watch for signs and symptoms of infection, especially with patients who are acutely ill. The nurse should also screen the patient for osteoporosis, because long-term use of corticosteroids increases the incidence of osteoporosis. Patients should have a bone mineral density test performed at diagnosis and prior to beginning steroid use to determine a baseline status and then every 2 years thereafter. Educating the patient regarding calcium and vitamin D supplementation daily is encouraged, along with the benefits of weight-bearing activities to support bone health.

What considerations need to be considered when treating patients with breakthrough pain?

Some patients with cancer have continuous chronic pain and also experience more intense acute exacerbations of pain periodically, which is called breakthrough pain (BTP).

Identify and describe types of debridement (surgical, mechanical, natural debridement)

Surgical: Early surgical excision to remove devitalized tissue along with early burn wound closure has long been recognized as one of the most important factors contributing to survival in a patient with a major burn injury. Surgical débridement occurs before the natural separation of eschar transpires from bacterial lysis of collagen fibers at the dermal-eschar junction. This may be performed as soon as possible after the burn, once the patient is hemodynamically stable and edema has decreased. Ideally, the wound is covered immediately with a skin graft (if necessary) and a dressing. If the wound bed is not ready for a skin graft at the time of excision, a temporary biologic or synthetic dressing may be applied until an autograft can be successfully applied during a subsequent surgery. The use of surgical excision carries with it risks and complications, especially with large burns. The procedure creates a high risk of extensive blood loss with lengthy operating and anesthesia times. Blood losses sustained during surgical procedures, wound care, and ongoing hemolysis exacerbate anemia. Blood transfusions may be required periodically to maintain adequate hemoglobin levels for oxygen delivery to the myocardium. When conducted in a timely and efficient manner, surgical excision results in shorter lengths of stay and decreased risk of complications from invasive burn wound sepsis. Once débrided, granulation tissue fills the void created by the wound, creates a barrier to bacteria, and serves as a bed for epithelial cell growth. A wound covering is applied to keep the wound bed moist and promote the granulation process. Mechanical: Mechanical débridement involves the use of surgical tools to separate and remove the eschar. This technique, performed by primary providers, specially trained nurses, or physical therapists, is usually performed with routine dressing changes. If bleeding occurs, hemostatic agents or pressure may be applied to achieve hemostasis. Dressing changes and wound cleaning aid the removal of wound debris. Wet-to-dry dressings are not advised for burn care because of the possibility of removing viable epithelial cells along with necrotic tissue. Wet-to-wet or wet-to-moist dressings may be used instead. Natural debridement: With natural débridement, the devitalized tissue separates from the underlying viable tissue spontaneously. Bacteria present at the interface of the burned tissue and healthy viable tissue gradually liquefy the fibrils of collagen, a protein present in skin, tendon, bone, cartilage, and connective tissue, that hold the eschar in place. Proteolytic and other natural enzymes cause this phenomenon. The process may take weeks to months to occur.

Differentiate between opioid tolerance and addiction

Tolerance is also a normal physiologic response that can occur with regular administration of an opioid and consists of a decrease in one or more effects of the opioid (e.g., decreased analgesia, sedation, or respiratory depression). Although it may occur in conjunction with SUD, it cannot be equated with SUD. It may be treated with increases in dose to attain the previous effect. With the exception of constipation, tolerance to the opioid adverse effects develops with regular daily dosing of opioids over several days. Substance Use Disorder (SUD) was historically known as addiction or addictive disease, and defined as a chronic, relapsing, treatable neurologic disease. The APA has since described SUD as the impaired use of a substance, such as opioids, even while experiencing major problems, characterized by impaired control over use, compulsive use, continued use despite harm, and craving for the substance. With SUD, use of the opioid is for nontherapeutic reasons and is thus independent of pain relief. The development and characteristics of SUD are influenced by genetic, psychosocial, and environmental factors.

Identify the nociception pain process (transduction, transmission, perception, modulation)

Transduction: Transduction refers to the processes by which noxious stimuli, such as a surgical incision or burn, activate primary afferent neurons called nociceptors, located throughout the body in the skin, subcutaneous tissue, and visceral (organ), and somatic (musculoskeletal) structures. These neurons have the ability to respond selectively to noxious stimuli generated as a result of tissue damage from mechanical (e.g., incision, tumor growth), thermal (e.g., burn, frostbite), chemical (e.g., toxins, chemotherapy), and infectious sources. Noxious stimuli cause the release of a number of excitatory compounds (e.g., serotonin, bradykinin, histamine, substance P, and prostaglandins), which move pain along the pain pathway. In addition, sodium, calcium, and potassium ion channels are stimulated to open, resulting in electrical impulses that are transmitted through the large, rapid conducting A-delta and smaller, peripheral C-fiber nociceptors. Prostaglandins are lipid compounds that initiate inflammatory responses that increase tissue swelling and pain at the site of injury. They form when the enzyme phospholipase breaks down phospholipids into arachidonic acid. In turn, the enzyme cyclo-oxygenase (COX) acts on arachidonic acid to produce prostaglandins. COX-1 and COX-2 are isoenzymes of COX and play an important role in producing the effects of the nonopioid analgesic agents, which include the nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen. NSAIDs produce pain relief by mediating inflammation at the site of trauma, primarily by blocking the formation of prostaglandins. The nonselective NSAIDs, such as ibuprofen, naproxen, diclofenac, and ketorolac, inhibit both COX-1 and COX-2, and the COX-2 selective NSAIDs, such as celecoxib, inhibit only COX-2. As Figure 9-2 illustrates, both types of NSAIDs produce anti-inflammation and pain relief through the inhibition of COX-2. Acetaminophen is known to be a COX inhibitor that has minimal peripheral effect, is not anti-inflammatory, and can both relieve pain and reduce fever by preventing the formation of prostaglandins in the CNS. Other analgesic agents work at the site of transduction by affecting the flux of ions. For example, sodium channels are closed and inactive at rest but undergo changes in response to nerve membrane depolarization. Transient channel opening leads to an influx of sodium that results in nerve conduction. Local anesthetics reduce nerve conduction by blocking sodium channels. The calcium channel blocking anticonvulsants that are used to treat neuropathic pain facilitate analgesia by reducing the flux of calcium ions and limiting glutamate, norepinephrine, and substance P release Transmission:Transmission is another process involved in nociception. Effective transduction generates an action potential that is transmitted along the lightly myelinated rapid conducting A-delta fibers and the unmyelinated slower impulse conducting C fibers. The endings of A-delta fibers detect thermal and mechanical injury, allow relatively quick localization of pain, and are responsible for a rapid reflex withdrawal from the painful stimulus. Unmyelinated C fibers respond to mechanical, thermal, and chemical stimuli. They produce poorly localized and often aching or burning pain. A-beta fibers are the largest of the fibers and respond to touch, movement, and vibration but do not normally transmit pain. The action potential impulse with the noxious information passes through the dorsal root ganglia, then synapses in the dorsal horn of the spinal cord, and then ascends up to the spinal cord and transmits the information to the brain, where pain is perceived. Extensive modulation occurs in the dorsal horn via complex neurochemical mechanisms. The primary A-delta fibers release glutamate and C fibers release substance P and other neuropeptides. Glutamate is a key neurotransmitter because it binds to the N-methyl-D-aspartate (NMDA) receptor and promotes pain transmission Perception: An additional process involved in nociception is perception, which is the result of the neural activity associated with transmission of noxious stimuli. It requires activation of higher brain structures for the occurrence of awareness, emotions, and impulses associated with pain. Although the physiology of pain perception continues to be studied, it can be targeted by nonpharmacologic therapies, such as distraction, which are based on the belief that innate brain processes can strongly influence pain perception. Modulation: Modulation is another process involved in nociception. Modulation of the information generated in response to noxious stimuli occurs at every level from the periphery to the cortex and involves many different neurochemicals. For example, serotonin and norepinephrine are inhibitory neurotransmitters that are released in the spinal cord and the brain stem by the descending (efferent) fibers of the modulatory system. Some antidepressants provide pain relief by blocking the body's reuptake (resorption) of serotonin and norepinephrine, extending their availability to fight pain. Endogenous opioids are located throughout the peripheral and central nervous systems, and like exogenous opioids, they bind to opioid receptors in the descending system and inhibit pain transmission.

Sprains/ strains (what are they, what are the different classifications, and how are they treated)

What are they (Know the classifications of strains): A strain is an injury to a muscle or tendon from overuse, overstretching, or excessive stress; it is commonly known as a muscle pull. Tendons are fibrous cords that attach muscle to a bone; strains often occur in tendons of the foot, leg (e.g., hamstring), and back. Strains can be categorized as acute or chronic and are graded along a continuum based on postinjury symptoms and loss of function. Acute strains can result from a single injurious incident; whereas, chronic strains result from repetitive injuries. Chronic strains can result from improper management of acute strains. Depending on the severity of muscle fiber damage, three degrees of strains can be classified: •A first-degree strain is mild stretching of the muscle or tendon with no loss of ROM. Signs and symptoms may include the gradual onset of palpation-induced tenderness and mild muscle spasm. •A second-degree strain involves moderate stretching and/or partial tearing of the muscle or tendon. Signs and symptoms include acute pain during the precipitating event, followed by tenderness at the site with increased pain with passive ROM (PROM), edema, significant muscle spasm, and ecchymosis. •A third-degree strain is severe muscle or tendon stretching with rupturing and complete tearing of the involved tissue. Signs and symptoms include immediate pain described as tearing, snapping, or burning, muscle spasm, ecchymosis, edema, and loss of function. An x-ray should be obtained to rule out bone injury, because an avulsion fracture (in which a bone fragment is pulled away from the bone by a tendon) may be associated with a third-degree strain. X-rays do not reveal injuries to soft tissue or muscles, tendons, or ligaments, but magnetic resonance imaging (MRI) and ultrasound can identify tendon injury. A sprain is an injury to the ligaments and tendons that surround a joint. It is caused by a twisting motion or hyperextension (forcible) of a joint. While tendons connect muscle to bone, ligaments connect bone to bone. The function of a ligament is to stabilize and support the body's joints while permitting mobility. An injured ligament causes joint instability, with the most vulnerable areas of the body being the ankles, knees, and wrists. The severity of a sprain is graded according to how badly the ligament has been damaged and whether or not the joint has been made unstable: •A Grade I sprain is stretching or slight tearing in some fibers of the ligament and mild, localized hematoma formation. Manifestations include mild pain, edema, and local tenderness. •A Grade II sprain is more severe and involves partial tearing of the ligament. Manifestations include increased pain with motion, edema, tenderness, joint instability, ecchymosis, and partial loss of normal joint function. •A Grade III sprain is a complete tear or rupture of the ligament. A Grade III sprain may also cause an avulsion of the bone. Symptoms include severe pain, edema, tenderness, ecchymosis, and abnormal joint motion. How are they treated: The treatment for contusions, strains, and sprains is guided by the severity of injury and the goal of protecting from further injury. Protection from further injury is accomplished through support of the affected area (e.g., sling, brace) and/or splinting, taping, or compression bandages. To control pain, bleeding, and inflammation, most contusions, strains, and sprains are managed with the RICE method, an acronym that refers to rest, ice, compression, and elevation. Rest prevents additional injury and promotes healing. Intermittent application of cold or ice packs during the first 24 to 72 hours after injury produces vasoconstriction, which decreases bleeding, edema, and discomfort. Cold packs should not be in place for longer than 20 minutes at a time, and care must be taken to avoid skin and tissue damage from excessive cold. An elastic compression bandage controls bleeding, reduces edema, and provides support for the injured tissues. Elevation at or just above the level of the heart controls the swelling. If the sprain or strain is the most severe grade or degree, immobilization by a splint, brace, or cast may be necessary so that the joint will not lose its stability (see later discussions). Nonsteroidal anti-inflammatory drugs (NSAIDs) may be prescribed for pain management. The neurovascular status, a type of focused assessment of the neurologic (motor and sensory) and vascular function of the injured extremity, is monitored at frequent intervals (e.g., every 15 minutes for the first 1 to 2 hours after injury) and then at lesser intervals (e.g., every 30 minutes) until stable. Decreases in sensation or motion and increases in pain level should be documented and reported to the patient's primary provider immediately so that acute compartment syndrome can be prevented.

Pain Assessment

What data should be collected for someone in pain? Location of pain, intensity using a pain tool/scale, quality, onset, duration, effect of pain on function and quality of life, pain goal, what makes it feel better/worse. What needs to be considered when considering pain relief measures: Achieving optimal pain relief is best viewed on a continuum, with the primary objective being to provide both effective and safe analgesia. The quality of pain control should be addressed whenever patient care is passed on from one clinician to another, such as at change of shift and transfer from one clinical area to another. Optimal pain relief is the responsibility of every member of the health care team and begins with titration of the analgesic agent, followed by continued prompt assessment, analgesic agent administration, and nonpharmacologic interventions during the course of care to safely achieve pain intensities that allow patients to meet their functional goals with relative ease. Although it may not always be possible to achieve a patient's pain intensity goal within the short time the patient is in an area like the PACU or emergency department, this goal provides direction for ongoing analgesic care. Important information to provide during transfer report is the patient's comfort-function goal, how close the patient is to achieving it, what has been done thus far to achieve it (analgesic agents and doses and/or nonpharmacologic interventions), and how well the patient has tolerated administration of the analgesic agent (adverse effects). There is growing interest among both clinicians and researchers in linking pain management to functional goals. One effort in this work is the Clinically Aligned Pain Assessment (CAPA) Tool, which is used to assess various degrees of comfort, pain control, function, and sleep. Pain management interventions should improve and not inhibit progress toward healing and rehabilitation. Pain is a complex phenomenon involving multiple underlying mechanisms that requires more than one analgesic agent to manage it safely and effectively. The recommended approach for the treatment of all types of pain in all age groups is called multimodal analgesia or multimodal pain management. A multimodal regimen intentionally and simultaneously combines medications with different underlying mechanisms, along with nonpharmacologic interventions, which allows for lower doses of each of the medications in the treatment plan, reducing the potential for adverse effects. Furthermore, multimodal analgesia can result in comparable or greater pain relief with fewer adverse effects than can be achieved with any single analgesic agent.

Polymyalgia rheumatica (what is it and how would the patient present)

What is it: PMR involves stiffness of muscles and pain in the neck, shoulder, and pelvic girdle. GCA is a form of vasculitis affecting the medium-sized and large arteries of the body. GCA is also sometimes referred to as temporal arteritis. PMR and GCA represent a spectrum of one disease. Both primarily affect individuals older than 50 years and are associated with the same HLA haplotype genetic markers. PMR and GCA occur predominately in Caucasians and often in first-degree relatives. PMR has an annual incidence rate of 52 cases per 100,000 people older than 50 years. GCA varies by geographic location and has the highest incidence in Scandinavian countries. PMR is two to three times more common than GCA. The underlying mechanism of action involved with PMR and GCA is unknown. It is clear, however, that the immune system is abnormally activated in both disease processes with increases in circulating monocytes that produce IL-1 and IL-6. These circulating monocytes make the endothelial linings of blood vessels more vulnerable to vasculitis. Immunoglobulin deposits in the walls of inflamed temporal arteries suggest that an autoimmune process is at work. How would the patient present: PMR is characterized by severe proximal muscle discomfort with mild joint swelling. Severe aching in the neck, shoulder, and pelvic muscles is common. Stiffness is noticeable most often in the morning and after periods of inactivity. This stiffness can become so severe that patients struggle putting on a coat or combing their hair. Systemic features include low-grade fever, weight loss, malaise, anorexia, and depression. Because PMR usually occurs in people 50 years and older, it may be confused with, or dismissed as, an inevitable consequence of aging. Nursing: Nursing care of the patient with PMR is based on the fundamental plan of nursing care presented earlier. The most common nursing diagnoses are pain and lack of knowledge of medications. A management concern is that the patient will take the prescribed medication, frequently corticosteroids, until symptoms improve and then discontinue the medication. The decision to discontinue the medication should be based on clinical and laboratory findings and the prescription. Nursing implications are related to helping the patient prevent and monitor adverse effects of medications (e.g., infections, diabetes, gastrointestinal problems, and depression) and adjust to those side effects that cannot be prevented (e.g., increased appetite and altered body image.

Scleroderma (what is it, identify CREST syndrome)

What is it: Scleroderma is a rare autoimmune disease affecting the connective tissue of the skin, blood vessel walls, and internal organs. There are two general types: localized (affecting only the cutaneous system) or diffuse (routinely referred to as systemic sclerosis and affecting multiple organ systems). Similar to other autoimmune diseases, women are affected four times more than men, and the onset occurs typically between the ages of 25 and 50 years. Scleroderma has a variable course with remissions and exacerbations. The pathogenesis is poorly understood. Scleroderma commonly begins with skin involvement. Mononuclear cells cluster on the skin and stimulate lymphokines to stimulate procollagen. Insoluble collagen is formed and accumulates excessively in the tissues. Initially, the inflammatory response causes edema, with a resulting taut, smooth, and shiny skin appearance. The skin then undergoes fibrotic changes, leading to loss of elasticity and movement. Eventually, the tissue degenerates and becomes nonfunctional. This chain of events, from inflammation to degeneration, also occurs in blood vessels, major organs, and body systems. Identify CREST syndrome: The skin and subcutaneous tissues become increasingly hard and rigid due to excess collagen and cannot be pinched up from the underlying structures. Wrinkles and lines are obliterated. The skin is dry because sweat secretion over the involved region is suppressed. The extremities stiffen and lose mobility. The condition spreads slowly; for years, these changes may remain localized in the hands and the feet. The face appears masklike, immobile, and expressionless, and the mouth becomes rigid; referred to as "stone facies". The changes within the body, although not visible directly, are vastly more important than the visible changes. The esophagus hardens, interfering with swallowing. The lungs become scarred, impeding respiration. Digestive disturbances occur because of sclerosing (hardening) of the intestinal mucosa. Vascular involvement of the kidneys leads to malignant hypertension and renal insufficiency. Cardiac disorders include pericarditis, heart block, and myocardial fibrosis. The patient may manifest a variety of symptoms referred to as the CREST syndrome. CREST stands for calcinosis (calcium deposits in the tissues), Raynaud's phenomenon, esophageal dysmobility, sclerodactyly (scleroderma of the digits), and telangiectasia (capillary dilation that forms a vascular lesion) Nursing: Nursing care of the patient with scleroderma is based on the fundamental plan of nursing care presented earlier. The primary nursing diagnoses are impaired skin integrity; self care deficits; impaired nutritional status; and disturbed body image. The patient with advanced disease may also have impaired gas exchange, impaired cardiac output, impaired swallowing, and constipation. Providing meticulous skin care and preventing the effects of Raynaud's phenomenon are major nursing challenges. See Chapter 26 for further discussion of Raynaud's phenomenon.

Rheumatoid arthritis (pathophysiology, diagnostic tools, pharmacological treatments, non-pharmalogical treatments)

What is it? (pathophysiology): Rheumatoid arthritis is an autoimmune disease of unknown origin that affects 1% to 2% of the population worldwide, with females having a three times greater incidence than males. It may occur at any age but the onset commonly occurs between the third and sixth decade of life. The incidence of RA increases after the sixth decade of life. RA that occurs after the age of 65 is referred to as elderly onset RA. Additional risks that have been identified include family history, environmental influences such as diet or geographic location, nulliparity, as well as the modifiable factors of smoking and obesity. The exact mechanism of action for the etiology of RA is unknown. Evidence points to a genetic predisposition and the development of immunologically mediated joint inflammation. An autoimmune reaction occurs in the synovial tissue. RA synovium breaks down collagen, causing edema, proliferation of the synovial membrane, and ultimately pannus formation. Pannus destroys cartilage and erodes the bone. The consequence is the loss of articular surfaces and joint motion. Muscle fibers undergo degenerative changes. Tendon and ligament elasticity and contractile power are lost. The RA inflammatory process has also been implicated in other disease processes (i.e., arteriosclerosis). It is hypothesized that the RA disease process somehow interferes with the production of high-density lipoprotein cholesterol, which is the form of cholesterol responsible for decreasing cellular lipids and, therefore, is considered antiatherosclerotic. The nervous system is also affected by the RA inflammatory process. The synovial inflammation can compress the adjacent nerve, causing neuropathies and paresthesias. Axonal degeneration and neuronal demyelination are also possible due to the infiltration of polymorphonuclear leukocytes, eosinophils, and mononuclear cells, causing necrotizing or occlusive vasculitis. Diagnostic tools: Several assessment findings are associated with RA: rheumatoid nodules, joint inflammation detected on palpation, and certain laboratory findings. The history and physical examination focus on manifestations, such as bilateral and symmetric stiffness, tenderness, swelling, and temperature changes in the joints. The patient is also assessed for extra-articular changes; these often include weight loss, sensory changes, lymph node enlargement, and fatigue. Symptoms and examination findings are often recorded using a disease activity score, a variety of which are in use, to evaluate disease activity, help guide treatment decisions, and monitor treatment efficacy. Rheumatoid factor is present in many patients with RA, but its presence alone is not diagnostic of RA, and its absence does not rule out the diagnosis. Antibodies to cyclic citrullinated peptide (anti-CCP) have a specificity of approximately 95% at detecting RA. The ESR and CRP tend to be significantly elevated in the acute phases of RA and are therefore useful in monitoring active disease and disease progression. The complete blood count (CBC) should be assessed to establish a baseline count especially prior to starting medications. Patients may exhibit anemia, and platelets may be elevated due to the inflammatory process. A tuberculin (TB) skin test should be done prior to the initiation of certain medications to rule out tuberculosis. In the event the patient has latent TB and has never been treated, the infection can be reactivated. The patient should also be assessed for hepatitis B and hepatitis C, which could impact treatment strategies if positive. If the client tests positive for hepatitis, the infection should be treated prior to starting medication. Liver and kidney monitoring are recommended for most DMARD therapy because it can cause elevation of the liver enzymes and can also affect kidney function. X-ray, ultrasound, or both of the hands, wrists, and feet can be useful in establishing a baseline for joint evaluation, and assessing the joints for erosions and synovitis. Joint damage may occur within the first 6 to 12 months of diagnosis and should be followed as indicated. Plain x-ray is the most common radiographic study used to track disease progression as it is inexpensive, reliable, and reproducible. MRI can also be useful to detect small erosions that may not be visible on x-ray or ultrasound. Pharmacological treatments: begins with nonbiologic or biologic DMARD to prevent inflammation and joint damage. After initiating treatment with a DMARD, patients generally report a beneficial effect within 6 weeks and tolerate the medication relatively well. However, some patients may take longer to see improvement. Corticosteroids are recommended as a "bridge" in the early treatment but are not recommended for long-term therapy due to side effects. newer class of drugs, the Janus Kinase (JAK) inhibitors, bind to the active JAK enzyme sites, inhibiting autophosphorylation and thus inhibiting cytokine production and decreasing the immune response. JAK inhibitors are used in combination with methotrexate or other nonbiologic DMARDs. They may also be used as monotherapy. NSAIDs and specifically the cyclo-oxygenase 2 (COX-2) enzyme blockers are used for pain and inflammation relief. NSAIDs, such as ibuprofen and naproxen, are commonly prescribed because of their low cost and analgesic properties. They must be used with caution, however, in long-term chronic diseases because of the possibility of gastric ulcers. Several COX-2 enzyme blockers have been approved for treatment of RA. Cyclo-oxygenase is an enzyme that is involved in the inflammatory process. COX-2 medications block the enzyme involved in inflammation (COX-2) while leaving intact the enzyme involved in protecting the stomach lining (COX-1). As a result, COX-2 enzyme blockers are less likely to cause gastric irritation and ulceration than other NSAIDs; however, they are associated with increased risk of cardiovascular disease and must be used with caution. The nurse should be aware that NSAIDs do not prevent erosions or alter disease progression and, consequently, are medications useful only for symptom relief. Additional analgesia may be prescribed for periods of extreme pain. Opioid analgesic agents are avoided because of the potential for continuing need for pain relief. Nonpharmacologic pain management techniques (e.g., relaxation techniques, heat and cold applications) are taught. Nonpharmacological treatments: In patients with established RA, a formal program with occupational and physical therapy is prescribed to educate the patient about principles of pacing activities, work simplification, range of motion, and muscle-strengthening exercises. The patient is encouraged to participate actively in the management program

Giant Cell Arteritis (what is it, how is it diagnosed and how would the patient present)

What is it? GCA is a form of vasculitis affecting the medium-sized and large arteries of the body. GCA is also sometimes referred to as temporal arteritis. PMR and GCA represent a spectrum of one disease. Both primarily affect individuals older than 50 years and are associated with the same HLA haplotype genetic markers. PMR and GCA occur predominately in Caucasians and often in first-degree relatives. PMR has an annual incidence rate of 52 cases per 100,000 people older than 50 years. GCA varies by geographic location and has the highest incidence in Scandinavian countries. PMR is two to three times more common than GCA. How is it diagnosed? Assessment focuses on musculoskeletal tenderness, weakness, and decreased function. Careful attention should be directed toward assessing the head (for changes in vision, headaches, and jaw claudication). An MRI scan may be used in the assessment of extra-articular synovitis in patients with PMR, regardless of symptoms. Often, diagnosis is difficult because of the lack of specificity of tests. A markedly high ESR is a screening test but is not definitive. The CRP level and platelet count also provide valuable data. In fact, simultaneous elevation in the ESR and CRP has a sensitivity of 98.6% and a specificity of 75.7% in making the diagnosis of GCA when coupled with clinical findings. Diagnosis of both GCA and PMR is more likely to be made by eliminating other potential diagnoses. The dramatic and immediate response to treatment with corticosteroids is considered by some to be diagnostic. In the case of GCA, biopsy of the temporal artery is the definitive diagnostic tool. High-resolution MRI is an alternative or adjunct to the traditional temporal artery biopsy. How would the patient present? GCA may cause headaches, changes in vision, and jaw claudication. These symptoms should be evaluated immediately because of the potential for blindness and stroke if left untreated. PMR and GCA have a self-limited course, lasting several months to several years.