Ch. 40 Management of Clients with Musculoskeletal DisordersOsteoarthritis Etiology and risk factors Idiopathic or secondary Bone on bone action AKA degenerative bone disease Usually affects more males until age 55, then affects menopausal women Gradual onset Affects neck, hands, wrists, lower back, and hips Pathophysiology Process of cartilage matrix degradation accompanied by the bodys ineffectual attempts at repair Clinical Manifestations Worsening pain and stiffness Risk factors Idiopathic Increasing age Genetics Secondary Trauma Mechanical stress Inflammation of joint structures Joint instability Neurologic and endocrine disorders Selected medications Obesity Hormones Inactivity Athletes Overweight RA and Lupus Ligament and tendon issues with repetitive repair Medical management Goals Pain relief Functional independence: ADLs Maintenance of quality of life Approach Exercise Topical treatments and heat: Capsaicine cream is OTC Acetaminophen: Tylenol, Mobec NSAIDS, COX-2 inhibitors Dietary supplementsNursing Management of the Osteoarthritic Client Goal is promotion of a healthy, positive adaptation Decrease purines, caffeinated beverages, and carbs Moderate exercise: want active, but dont want to wear down bones Client education Collaborate with occupational therapist Reinforce and encourage client to notify physician of changes in condition Surgical management Osteotomy: incision into bone to realign joint, can delay total joint replacement Arthrodesis: debride bone Joint arthroplasty: total joint replacement Nursing diagnosis Pain: always primary Impaired physical mobility Risk for peripheral neurovascular dysfunction Risk for infection Ineffective tissue perfusionMetabolic Bone Disorders Osteoporosis Pagets disease Osteomalacia Gout and gouty arthritisOsteoporosis Etiology and risk factors Genetic and environmental Problems with hard and collagen bone Modifiable and Nonmodifiable risk factors Depends on how much bone mass is achieved between age 25-35 and how much loss later Modifiable risk factors Low estrogen Low testosterone Dietary: low lifetime calcium; Vit D deficiency Medication use: corticosteroids, some anticonvulsants Lifestyle: inactivity, cigarette smoking, excess alcohol Nonmodifiable risk factors Older age Family history History of fracture in first degree relative Being female especially Caucasian or Asian Being thin or having a small frame Pathophysiology Exact patho not clear Reabsorption of the bone is greater than new bone formation so there is bone loss, which is accelerated by risk factor such as Vit D deficiency or postmenopausal women with low estrogen. Clinical manifestations Diagnosed after fracture (most common) Loss of height Spine curvature Medical management Prevent loss of bone mass Prevention of bone resorption Medications Hormone replacement therapy Evista: without cancer risks, mimics effects of estrogen Decrease bone loss Side effects are risk of cancer Calcitonin Prevent bone loss Increase osteoblast Calcium supplements Vit D supplements Fluoride Increase the solubility (strength) Biphosphonates Fosamax, Actonel, Didronel, Boniva Inhibit bone resorption Preserves bone mass Nursing diagnoses Imbalanced nutrition: Less than body requirementsEncourage calcium intake (dairy, tofu, broccoli, spinach) and weight bearing exercise

Impaired physical mobility Pain related to fracturePagets Disease (Osteitis Deformans) Etiology Idiopathic Pathophysiology Progressive skeletal disorder that results form excessive metabolism activity in the bone Hypermetabolic Bones are large and softer Bone is replaced with disorganized bone Clinical manifestations Painful deformities Progresses slowly Demineralization of bone showing on x-ray (bone looks punched out) Familial tendency, usually males Common complaint is pain in long bones Pain most often at night Outcome management Control pain biophosphonates (Fosamax, Actonel), calcitonin, NSAIDs for inflammation and painOsteomalacia (Adult Rickets) Etiology Inadequate Vit D Most common cause is hypophosphatemia or hypocalcemia Pathophysiology Deficiency of phosphates, calcium, and Vit D Inadequate delayed mineralization of bone matrix Soft bones Clinical manifestations Fatigue Malaise Bone pain Some deformities in weight bearing bones Outcome management Daily Vit DGout and Gouty Arthritis Classifications Primary gout Elevated serum or blood level, uric acid level, from inborn error in a purine metabolism or decreased excretion of uric acid Have trouble breaking down purines Secondary gout Hyperuricemia from another disorder (ex. Tumor lysis syndrome) Can come from treatment More common in men 40-50 years old Not normally seen in women before menopause Clinical manifestations Develops in stages Can happen in any joint but most commonly in great toe Severe pain Build up of purines causing uric acid crystals in joints Stage 1 Client has asymptomatic hyperuricemia, excreting uric acid but no symptoms Stage 2 Acute vs chronic Affects a single joint= acute Chronic occurs when hyperuricemia that is not treated overtime leads to kidney disease or damage: crystals deposit in tubules or ureters Outcome management Management of the acute attack Long-term management of hyperuricemia Decrease ingestion of red meats and fishGout Diagnostic tests Serum uric acid levels (usually >7.5 mg/dL) WBC elevation: due to inflammation ESR (sed rate) elevation: to test inflammation, specifically eosinophils can be increased which can increase sed rate due to uric acid crystals depositing in joints 24-hr urine to assess for uric acid Aspiration of joint fluid: definitive way to diagnose Medications NSAIDs Colchicine Corticosteroids Analgesics Prophylactic (for chronic) Colchicine Uricosuric drugs (Probenecid, Anturane) Xanthine oxidase inhibitors (Allopurinol)Spinal Column Deformities Scoliosis Curvature of spine Kyphosis Humpback Lordosis Excessive inward curvature of lumbar spineScoliosis Etiology Congenital or neuromuscular Clinical manifestations Abnormal spinal curvature Outcome management Observation, braces, exercise Spinal fusionBone Infections: Septic Arthritis Etiology and pathophysiology Joint space becomes infected by a pathogen and then moves to blood Most common pathogen: staphylococcus aureus Risk factors: Persistent bacteremia Previous joint damage Surgery to joints Clinical manifestations Joint pain Swelling Tenderness Outcome management Medical management Nursing managementBone Tumors: Malignant Causes Unknown: past trauma? Diagnosis: needs to be prompt Serum AP level: will be increased (alkaline phosphate) Bone marrow biopsy Radiology (MRI, CT, X-ray)Disorders of the Foot Hallux valgus (bunion) Enlargement of joint or lump of bone at base or side of big toe Forms when toe moves out of place Mortons neuroma (plantar neuroma) Tumor like mass from tight fitting shoes Common problem associated is pain or swelling or nerve Usually at the ball of the foot on the third of fourth toe Hammer toe Toe contracture at middle joint Usually second toeMuscular Dystrophy Etiology and risk factors Genetic Death usually occurs at late teens or early adult Clinical manifestations Progressive weakness Skeletal muscle wasting Diagnosis Elevated Creatinine kinase Muscle biopsy Treatment Symptomatic and supportiveSjogrens Syndrome Autoimmune Causes inflammation and dysfunction of endocrine glands More common in women Artificial tears fix Manifestations Dry eyes Dry mouth Parotid gland enlargement Arthritis (systemic effect) Dysphagia (systemic effect)Fibromyalgia Common rheumatic syndrome Older women 9x more than men Musculoskeletal pain (dominant symptom), stiffness, and tenderness Resembles chronic fatigue syndrome Diagnosis given after three months of painScleroderma (hard skin) Rare, connective tissue disorder Causes Unknown- genetic, immune, environmental Starts with dry patches getting thicker and harder then spreads Persons antibodies directed against own tissues Affects ADLs CREST syndrome: abnormal calcium salt deposits seen around joints and tissues Medications are chosen based on symptomsRheumatoid Arthritis Chronic systemic autoimmune disease Cause Unknown- genetic, hormonal (sex hormones), reproductive, infectious factors (Epstein Barr) Insidious onset (may be precipitated by stressor) Manifestations Inflammation Fatigue Anorexia Weight loss Nonspecific aching and stiffness Persistent inflammation leads to joint deformity Synovial membrane is damaged Wrist involvement Visible swelling in the knees knock-knee Rest and exercise Walking and swimming Heat and cold Surgery Medications ASA and NSAIDs Low-dose corticosteroids Disease-modifying drugs Immunosuppressive therapy Nursing diagnoses Chronic pain Fatigue Ineffective role performance Disturbed body image

Ankylosing Spondylitis Chronic inflammatory arthritis primarily affecting the axial skeleton Sacroiliac joints of the spine Can lead to fusion of the spinal process More common in males Cause: unknown (genetic predisposition) 90% of patients were born with HLA B27 gene Onset is gradual Pain worse at night with morning stiffness that may radiate down the legs Treatment Physical therapy and exercise NSAIDs (Indocin) Topical or intra-articular corticosteroids SurgeryReactive Arthritis Acute, nonpurulent inflammatory arthritis that complicates a bacterial infection of the GU or GI tracts Often affects young men with HLA-B27 antigen Often found in HIV Usually asymmetric, affecting large weight-bearing joints Treated with NSAIDs Antibiotic to treat bacterial infectionSystemic Lupus Erythematosus Chronic inflammatory immune complex connective-tissue disease Type III hypersensitivity reaction Affects almost all body systems Cause: unknown (genetic, hormonal, and environmental factors) Manifestations mimic RA 90% have joint symptoms: painful swollen joints Muscle pain Red butterfly rash across cheeks Hair loss Edema Photosensitivity Can be difficult to diagnose May have increased SED Medications NSAIDs, ASA Plaquenil Corticosteroids Immunosuppressive agentsPolymyositis Systemic connective tissue disorder characterized by inflammation of connective tissue and muscle fibers Autoimmune relation Skeletal muscle weakness and atrophy Rash, arthralgias, fatigue Insidious or abrupt onset Be supportive and comfortingLyme Disease Inflammatory disease caused by Borrelia burgdorferi Transmitted by ticks Usually occurs in summer months: hunting season Manifestations are skin changes, musculoskeletal and CNS changes Over time develop flu-like symptoms Slightly red lesion at site of tick bite: bulls-eye shaped lesion Fatigue, malaise, fever, chills, myalgias, HA, and stiff neck

Ch. 39 Musculoskeletal Trauma and Disorders

Contusion, Strain, or Sprain Contusion Least serious Bleeding into soft tissue Strain Stretching injury to a muscle or a muscle-tendon unit Sprain Injury to a ligament surrounding a jointIce for 24-48 hrs and then use heat

Elevate above the heart

Fractures A disruption or break in the continuity of the structure of bone Traumatic injuries account for the majority of fractures Described and classified according to: Type Communication or noncommunication with external environment Anatomic locationClassification by Fracture LocationClassification by Fracture CommunicationType

Clinical Manifestations Patient history indicates a mechanism of injury associated with: Immediate localized pain Decreased function Inability to bear weight or use affected part Guarding May not be accompanied by obvious bone deformity Fracture healing Reparative process of self-healing (union) occurs in the following stages:1. Fracture hematoma: clotting factors form fibrin meshwork2. Granulation tissue: gradually replaces hematoma3. Callus formation: osteoblasts make collagen that unite bone fragments4. Ossification: spongy woven bone takes in calcium and starts to harden5. Consolidation: mature bone starting to form6. Remodeling: have bone resemble structure before it was injuredCollaborative care Overall goals of treatment: Anatomic realignment of bone fragments (reduction) #1 Immobilization to maintain alignment Restoration of normal function Fracture reduction Closed reduction Nonsurgical, manual realignment Open reduction Correction of bone alignment through a surgical incision Fracture immobilization Casts Temporary circumferential immobilization device Common treatment following closed reduction

External fixation Metallic device composed of pins that are inserted into the bone and attached to external rods For hip, use abduction pillow and isometric exercises. Dont cross legs Internal fixation Pins, plates, intramedullary rods, and screws Surgically inserted at the time of realignment Fracture reduction Traction Application of a pulling force to an injured part of the body while counter traction pulls in the opposite direction Magic number is 6 lbs or less Types of traction: Skin traction (short-term) Bucks traction: pre-surgery Skeletal traction (longer periods) Manual traction Balanced suspension: pulling at two different places Purpose of traction: Prevent or reduce muscle spasm Immobilization Reduction Treat a pathologic condition Drug therapy Muscle relaxant: Soma, Flexeril, Norflex Narcotics: IV for severe injuries PCA and epidural: serious injuries following surgery; watch O2 sat NSAIDs Tetanus-diphtheria toxoid or immunoglobulin Bone-penetrating antibiotic CephalosporinNursing Management Nursing assessment Brief history of the accident: driver, passenger, seatbelt? Mechanism of injury Special emphasis focused on the region distal to the site of injury: check for circulation Neurovascular assessment: #1 is pain Color Temperature Capillary refill Peripheral pulses Edema Sensation Motor function pain Nursing diagnoses Risk for peripheral neurovascular dysfunction Acute pain Risk for infection Risk for impaired skin integrity Impaired physical mobility Ineffective therapeutic regimen management Planning Overall goals: Physiologic healing with no associated complications Pain relief Achieve maximal rehabilitation potential Nursing implementations Health promotion Safety precautions Use of seat belts Stretching before exercising Participate in moderate exercise Acute intervention Preoperative management Inform of immobilization device and expected activity limitations Skin preparation Normal pre-op checklist Postoperative management Monitor vital signs Frequent neurovascular assessments Limitations of movement Other measures Activity Maintenance of high fluid intake Diet high in bulk Never medicate before getting a culture Traction Ensure proper functioning of tractioning equipment Pin site care Ambulatory and home care Cast care Frequent neurovascular assessment Teach patient signs of complications Elevation of extremity above level of the heart Exercise joints above and below the cast Psychosocial problems Assist patient to adjust to any problems caused by injury Ambulation Usually started in mobility training when able to sit in bed and dangle feet over the side Assistive devices Cane Walker Crutches Evaluation Expected outcomes: Normal neurovascular examination Tolerable or no pain No evidence of infection No evidence of skin breakdown Ambulation devices used correctly Minimal loss of muscle bulk of affected extremityComplications of Fractures Infection Collaborative care Open fractures and soft tissue injuries have increased incidence Osteomyelitis can become chronic Open fractures require aggressive surgical debridement Post-op IV antibiotics for 3-7 days Compartment syndrome Condition in which elevated intracompartmental pressure within a confined myofascial compartment compromises the neurovascular function of tissues within that space Manifestations (6 Ps) Paresthesia Pain Pressure Pallor Paralysis Pulselessness Venous thrombosis Veins of the lower extremities and pelvis are highly susceptible to thrombus formation after fracture, especially hip fracture Precipitating factors: Venous stasis caused by incorrectly applied cast or traction Local pressure on a vein Immobility Lovanox, Coumadin, Heparin Fat embolism syndrome (FES) Characterized by the presence of fat globules in tissues and organs after a traumatic skeletal injury Tissues most often affected: lung, brain, heart, kidney Fractures that most cause FES: Long bones Ribs Tibia Pelvis Manifestations: Interstitial pneumonitis Chest pain Tachypnea Cyanosis Decreased PaO2 Dyspnea Apprehension Tachycardia Rapid and acute course Feeling of impending doom Patient may become comatose in a short time Collaborative care Treatment directed at prevention Careful immobilization of a long bone fracture (most important) Symptom management Fluid resuscitation Oxygen Reposition as little as possible Corticosteroids for inflammation in tissues and boneAmputation Partial or total removal of a body part Acute Chronic Goals of amputation Alleviate symptoms Maintain healthy tissue Increase functional outcome Types Open (guillotine) Closed (flap) no infectionPost-amputation Site healing Stump molding Dressings Prosthesis selectionComplications Infection Delayed healing Pain ContracturesProsthesis Level of amputation Selection of prosthesis Timing Nursing diagnoses Pain Disturbed body image Risk for dysfunctional grieving Risk for infection Risk for impaired skin integrity Impaired physical mobility Ineffective coping Disturbed personal identity HopelessnessOsteomyelitis The most common infecting microorganisms are: Staphylococcus aureus (most common) Escherichia coli Pseudomonas Salmonella Fungi, mycobacteria Klebsiella Proteus Direct contamination Complication of surgery Adjacent soft-tissue infectionsHematogenous Osteomyelitis Caused by pathogens carried in the blood from other sites of infection Primarily affects older adultsAcute Osteomyelitis An infection of less than one month in duration Manifestations are both systemic and localChronic Osteomyelitis A bone infection that persists for longer than one month OR an infection that has failed to respond to the initial course of antibiotic therapy Either a continuous, persistent problem or a process of exacerbations and remission Over time, granulation tissue turns to scar tissue providing an ideal site for further microorganism growth Systemic signs may be diminished, with local signs of infection more common Constant bone pain and swelling, tenderness, and warmth at the siteDiagnostic studies Bone or soft tissue biopsy Blood and/or wound cultures Elevated WBC and ESR Radionuclide bone scans (gallium and indium) MRI CTCollaborative Care Vigorous and prolonged IV antibiotic therapy is the treatment of choice of acute osteomyelitis, as long as bone ischemia has not yet occurred Home care with a central venous catheter or PICC 4-6 weeks or as long as 3-6 months Surgical treatment Needle aspiration or percutaneous biopsy Removal of the poorly vascularized tissue and dead bone Antibiotic-impregnated polymethymetharcrylate bead chains may be implanted at this time to aid in combating the infection After debridement the wound may be closed, and a suction irrigation system is inserted Intermittent or constant irrigation of the affected bone with antibiotics may also be initiated Hyperbaric oxygen therapy of 100% oxygen may be administered in chronic osteomyelitis Orthopedic devices may need to be removed Myocutaneous flaps or skin and bone grafting may be necessary if destruction is extensive Amputation of the extremity may be necessary to preserve life and improve the quality of life Long-term and mostly rare complications of osteomyelitis include septicemia, septic arthritis, pathologic fractures, squamous cell carcinoma, and amyloidosisAntibiotics Penicillins Nafcillin (Nafcil) Cephalexin (Keflex) Cefoxitin (Mefoxin) Gentamycin (Garamycin) Tobramycin (Nebcin) Cefazolin (Ancef) Ciprofloxacin (Cipro) Vancomycin FluoroquinolonesNursing diagnoses Acute pain Impaired physical mobility Infection Altered peripheral tissue perfusion AnxietyPlanning Overall goals: Satisfactory pain and fever control No complications Cooperation with treatment plan Maintenance of a positive outlook on the outcome of the diseaseNursing implementation Health promotion Control existing infections to prevent osteomyelitis Instruct patients on local and systemic manifestations of osteomyelitis Inform families of their role in monitoring the patients health Symptoms of bone pain, fever, swelling, and restricted limb movement should be reported immediately to the health care provider Acute intervention Bed rest in the early stages for an acute infection Good body alignment and frequent position changes Avoid activities such as exercise or heat application Uninvolved joints and muscles should continue to be exercised Ambulatory and home care Instruct on proper care and management of the venous access device Instruct on antibiotic administration If there is an open wound, dressing changes are often necessary Family needs to understand the infection is not contagious