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What can go wrong with bones? They can become infected Osteomyelitis They can become soft with decrease in mineralization Osteomalacia They can become porosis They can develop abnormal remodeling and functioning of osteoblasts & osteoclasts Osteoporosis Pagets Osteomyelitis A severe infection of the: bone bone marrow surrounding connective tissue Most common causative organism is Staphylococcus aureus Osteomyelitis How does a person get an infection? Indirect Direct Entry Route Development of Osteomyelitis Bacteria invade bone - inflammation Edema develops and Pressure within bone increases Bone abscess develops under the periosteum causing a decrease in blood supply with ischemia and bone necrosis. The dead bone tissue, called sequestrum The abscess cavity does not liquify or drain easily. The separated periosteum stimulates new bone growth = involcrum which surrounds the sequestrum. Infection trapped inside sequestrum causing recurring abscesses. Classification of Osteomyelitis Acute Chronic Clinical Manifestations of Osteomyelitis Systemic Local Signs of Chronic Osteomyelitis Chronic – an infection that persists for longer than 1 month Signs and Symptoms Constant bone pain Swelling Tenderness Warmth at site Continuous Drainage Osteomyelitis Diagnosis Biopsy of bone or soft tissue Cultures – blood and wound assessing for causative organism Erythrocyte sedimentation rate (ESR) – elevated WBC - elevated X-ray, no initial bone changes Radionucleotidetide bone scan MRI What test is the best way to determine the causative organism? Goals of Care Halt the Infection Relieve Pain Maintain Mobility Halt the Infection Intravenous Antibiotics Patient will need vigorous and prolonged treatment with antibiotics Start out in hospital with aggressive antibiotic therapy usually via PICC. Discharged to home with home health care follow up for up to 6 months Patient taught care of PICC site and side effects of antibiotics. Osteomyelitis Assorted IV antibiotics Penicillin, nafcillin (Nafcil) neomycin, vancomycin cephalexin (Keflex), cefazolin (Ancef) cefoxitin (Mefoxin) gentamycin (Garamycin) Oral Antibiotics ciprofloxacin (Cipro) Nursing Care Toxic effects: Aminoglycosides - Nephrotoxic, ototoxic, optic neuritis, fluid retention • Renal function tests (creatinine and BUN) should be done prior to administration and during therapy – therapy depends on test results. • Vestibular and auditory function are assessed prior to therapy and again 3-4 weeks after drug discontinued. Cephalosporins and Quinolones – jaundice, colitis, photosensitivity, crystalluria • C&S prior to beginning treatment Nursing Care / Patient Teaching Measure peak and trough levels Dosages are adjusted to maintain peak levels Preventive measures: Monitor I& O; Keep patient well hydrated to prevent nephrotoxicity or crystalluria Avoid direct sunlight, wear sunscreen Monitor urinary function, hearing, vision Assess for signs of yeast infections in genitourinary and mouth Relieve the Pain Immobilization of the affected limb Handle carefully , decreasing manipulation Give meds NSAID’S Opioid analgesics Muscle relaxants Maintain Mobility After the initial treatment and decrease of pain, need to make sure that limb mobility is maintained ROM Assist to stand and ambulate Provide assistive devices to help with ambulation Surgical Treatment and Nursing Care Debridement of the wound Insertion of antibiotic-impregnated polymethylmethacrylate bead chains to combat the infection Irrigation of wound with antibiotics Wound vac used to draw wound together – assess wound and drainage Treatment and Nursing Care Osteomyelitis Hyperbaric oxygen therapy – stimulates circulation and healing of infected tissue Bone grafts If all else fails – amputation Nursing Care – good body alignment, ROM, dressing changes, patient teaching about antibiotics and use of assistive devices, monitor patients response to antibiotic therapy. Try This Which of these manifestations should cause the nurse the MOST concern after treating a patient with osteomyelitis for two days with IV antibiotics? A. Sudden increase in temperature B. Complaints of pain at site of infection C. Drainage from wound D. Guarding of involved extremity Metabolic Bone Disease Osteomalacia Decalcification and softening of the bone Caused mainly by: vitamin D deficiency **Vitamin D is required for the absorption of calcium from the intestine and calcium is responsible for mineralization of bone Calcium Vitamin D Osteomalacia Who is at risk for developing osteomalacia? Someone with: lack of exposure to ultraviolet rays (sun) GI malabsorption, extensive burns, chronic diarrhea, pregnancy, drugs such as Dilantin. Osteomalacia Signs and Symptoms Most Common Bone pain Difficulty rising from a chair Difficulty walking Additional Signs and Symptoms Low back pain, muscle weakness Weight loss, progressive deformities Diagnosis Blood work – how do each of these tests assist in diagnosing Osteomalacia? serum calcium or phosphorus alkaline phosphatase X-Rays Show looser's transformation zone – (ribbons of decalcification in bone) Treatment and Nursing Care Osteomalacia Medication Therapy Vitamin D supplements Calcium salts or phosphorus supplements What would the nurse teach the patient to eat to increase vitamin D and calcium? What is the purpose of weight bearing exercises? What are examples of weight bearing exercises? Osteoporosis Characterized by low bone mass and structural deterioration Normal homeostatic bone remodeling is altered – the rate of bone resorption is greater than the rate of bone formation. Osteoporosis Osteoporosis is more common in women than men because? Diagnosis Bone Mineral Density Test (BMD) Dual-energy x-ray absorptiometry (DEXA) Treatment and Nursing Care Diet Therapy Weight bearing Exercises Encourage a diet high in calcium – see chart p.1636. ** Impact aerobics is NOT encouraged Decrease Risk Factors Quit smoking and decrease consumption of alcohol Medications used in Treatment of Osteoporosis Estrogen Replacement Therapy Calcium & Vitamin D supplements Calcitonin Bisphosphonates (Fosamax, Didronel, Actonel, Boniva, Aredia, Bonefos, Skelid) Selective Estrogen receptor modulator – Evista Medications used in treatment of Osteoporosis Hormone Replacement Therapy – Estrogen Controversy over use. Should discuss with health care provider Calcium There is a variety of calcium supplements available (See Table 64-15, p. 1636). • They should be taken with Vitamin D to aid in absorption. • Also if taking large doses i.e. 1000 mg. / day – take in divided doses of 500mg BID for better absorption Medications used in treatment of Osteoporosis Calcitonin A hormone made by the thyroid gland that helps keep calcium levels in the body from getting too high. It does this mainly by blocking the breakdown (absorption) of bone, which slows the release of more calcium into the blood What is needed to counter that effect? Medications used in treatment of Osteoporosis Bisphosphonates – (Fosamax, Boniva) Inhibit osteoclast-mediated bone resorption thereby increasing BMD and total bone mass. Side effects – anorexia, weight loss, gastritis Patient Teaching • • • Take on an empty stomach, in the morning, at least 30 minutes before any food, beverages or medications. Do not take within 2 hours of any calcium- containing food To decrease esophageal irritation - take with a full glass of water, and the patient must remain upright for at least 30 minutes after taking the medication. Medications used in treatment of Osteoporosis Selective Estrogen Receptor Modulators Mimic effect of estrogen on bone by reducing bone resorption without stimulating the breasts or uterus. Side effects • Leg cramps • Hot flashes Paget’s Disease Excessive bone resorption followed by replacement of normal marrow by vascular, fibrous connective tissue. The new bone is larger, disorganized, and weaker Most often affect the pelvis, long bones, spine, ribs, sternum, and cranium Paget’s Disease Clinical Manifestations Bone pain Fatigue CV disease (vasodilation of vessels in skin/tissues overlying affected bones) Waddling gait; bowing of legs; Hip or knee involvement can lead to limping, as well as pain and stiffness of the hip or knee. Headaches, visual deficits, loss of hearing occur as skull becomes enlarged and thickened Enlarged vertebrae cause spinal cord compression/ pinch of adjacent nerves causing tingling and numbness. Pagets Disease skull becomes enlarged and thickened Spinal cord compressed Loss of hearing Waddling gait Hip or knee involvement can lead to limping bowing of legs Paget’s Disease Diagnosis Elevated serum alkaline phosphatase X-ray will show increase in bone size Will the bone return to normal size and shape following treatment? Goal of Treatment Relieve the Pain Drug Therapy for Paget’s Human calcitonin (Cibacalcin) or Calcitonin-salmon (Miacalcin) NSAIDS Bisphosphonates Paget’s Disease Other treatments and Nursing Care Back support by firm mattress Teaching about use of Splints or braces to support bones and joints and help prevent weakened bones - skin care, circulation, etc. Teach how to correctly use canes or walkers Physical Therapy Etiology and Pathophysiology of Rheumatoid Arthritis Rheumatoid arthritis is an autoimmune disease. This means that the body's immune system mistakenly attacks the tissues it is supposed to protect. RF antibodies are formed in synovium against body’s IgG antigens. This leads to formation of immune complexes which cause inflammation of synovium –synovitis. 1. Synovitis causes release of WBC and enzymes which damage the bone and breakdown cartilage of the joint and the surrounding tissues. 2. Vascular granulation tissue grows across the surface of the cartilage (pannas) with loss of cartilage beneath the expanding pannas 1 2 Etiology and Pathophysiology of Rheumatoid Arthritis 3. Inflammatory pannus causes cartilage destruction and bone erosion. Loss of Bone Density Joint Deformity 3 4. This leads to joint deformities. Destruction of bone cartilage Erosion o f edges o f bone Increased soft tissue swelling due to Inflammation and thickening of synovium Rheumatoid Arthritis Signs and Symptoms Fatigue Anorexia Weight loss Generalized stiffness Joints are tender, painful, and warm to touch Rheumatic nodules Multi-system involvement Rheumatoid Arthritis Deformities Synotenovitis Ulnar Drift Boutonniere Swan neck Rheumatoid Arthritis Deformities Mutlans deformity (rapidly progressing RA) Hammer Toe Hitch-hiker thumb Genu valgus (knee away from midline) Hallux valgus (bunion) Extraarticular Manifestations Nodules See page 1652 in Lewis Diagnostic Testing Blood Studies ↑ Rheumatoid factor (RF) – 80% ↑ Erythrocyte sedimentation rate (ESR) ↑ C-reactive protein (CRP) Synovial fluid analysis X-rays Will not diagnosis – only show bone changes Goals of Care Control disease activity Relieve pain Maintain functionality and activities of daily living (ADLs) Maximize quality of life Treatment and Nursing Care for Rheumatoid Arthritis See Table 65-3 for meds used for arthritis p. 16461647. Salicylates NSAIDs Antibiotics Topical analgesics Corticosteroids DMARDs Gold compounds Antimalarials Immunosupressants Biologic/Targeted therapy Drug Therapy Disease-Modifying Antirheumatic Drugs Methotrexate (Rheumatrex)is know as the cornerstone medication in treating RA – explain. What are the side effects? What are important nursing implications? Drug Therapy Antimalarials – Plaquenil and Azulfidine Second choice of drug treatment May suppress formation of antigens Side effects: • Ocular toxicity - changes in vision, • Ototoxicity - changes in hearing or tinnitus, • Peripheral neuritis - muscular weakness Nursing Care • Monitor CBC and hepatic function • Tell patient to report any above changes immediately Drug Therapy Gold Compounds Parenteral – Myochrysine, Solganal Oral - Ridaural Side effects: • Common - Stomatitis, dermatitis, photosensitivity, proteinuria • Serious - Leukopenia, thrombocytopenia, anemia Nursing Care: • Observe for pruritis, rash, sore mouth, metallic taste • Monitor CBC, UA Drug Therapy Immunosuppressant's – Imuran, Cytoxan Used to decrease DNA. RNA, protein synthesis Assess for GI irritation Advise patient to report unusual bleeding or bruising Avoid during pregnancy Biologic/ targeted therapy Used to decrease inflammatory process and slow disease process Report persistent fever; it may be the only sign of an infection. Assess for signs of CHF. The response to a PPD may be suppressed and a false negative may result Giving a live vaccine could result in contracting disease Relieve Pain NSAID’s DMARD’s Non-Pharmacological Heat or Cold applications Rest Relaxation techniques Treatment and Nursing Care Diet Therapy Rest Heat and cold applications Exercise Patient and Family Teaching Protection of joints – page 1658. Causes of Gout Inflammatory response related to: increase in the production uric acid underexcretion of uric acid increase consumption of foods that contain purines Thereby causing high levels uric acid in blood (hyperuricemia) Causes of Gout Urate salts deposited in articular, periarticular and subcutaneous tissue Primary gout – related to heredity error of purine metabolism in 90% of cases Secondary gout - to increased cell turnover and related to medications, diseases, leukemia, etc. Clinical Manifestations of Gout Stage 1: asymptomatic; hyperuricemic Stage 2: acute gouty arthritis; affect single joint due to trauma, stress; high level uric acid; joint hot, red swollen; generally metatarsophalangeal joint great toe. Gout Stage 3: Chronic Tophi occur if gout untreated >urate pool increases > develop in multiple areas (esp. ear, bursae, toes) > compress nerves and erode through tissues. Diagnostic Tests Serum Uric acid – elevated; usually above 6 mg/dl; not specifically diagnostic of gout WBC- elevated as high as 20,000/mm3 during acute attack ESR: elevated 24 hour urine collection-determine uric acid production and excretion (evaluate if from decreased renal excretion or overproduction of uric acid) Most commonly diagnosed via clinical symptoms such as Tophi seen – indicator of chronic disease Drug Therapy for Gout Colchicine NSAIDs Corticosteroids Uricosuric Agents Probenecid (Benemid) Sulfinprazone (anturan) Drug Therapy Xanthine-oxidase inhibitors Decrease uric acid production Allopurinal (zyloprim) – can lead to agranulocytosis ULORIC (febuxostat) Force Fluids while on these medications!! to keep urine alkaline Treatment and Nursing Care Diet Therapy Avoid foods high in Purine such as? Treatment and Nursing Care Bedrest and position for comfort Joint immobilization and protect joint from pressure Local application of heat or cold Assess for complications Formation of kidney stones Hypertriglyceridemia Hypertension Chronic multisystem disease involving vascular and connective tissue Pathophysiology of SLE Lupus is an autoimmune disease characterized by acute and chronic inflammation of various tissues of the body. Patients with lupus produce abnormal antibodies in their blood that target tissues within their own body rather than foreign infectious agents. Because the antibodies and accompanying cells of inflammation can affect tissues anywhere in the body, lupus has the potential to affect a variety of areas Causes of SLE The precise reason for the abnormal autoimmunity that causes lupus is unknown. Inherited Dozens genes, viruses, ultraviolet light, of medications have been reported to trigger SLE. Clinical Manifestations of SLE Fatigue; Low-grade fever Loss of appetite Muscle aches; arthritis; polyarthralgia Ulcers of the mouth and nose Facial rash ("butterfly rash") Photosensitivity Pleuritis and pericarditis, tachypnea, Poor circulation to the fingers and toes with cold exposure (Raynaud’s syndrome) Proteinuria and development of glomerulonephritis Focal seizures, peripheral neuropathy, organic brain syndrome Diagnosis Autoantibody Testing: Anti-DNA- specific Anti- smith antibody (Anti-Sm) Anti nuclear antibody (ANA) ESR – elevated C-reactive protein – elevated These are not diagnostic for SLE, but help in the diagnosis Treatment and Nursing Care What is the single most important medication used in the treatment of SLE? Other Medications : Anitmalarial Immunosuppressive agents Treatment and Nursing Care Relieve pain and discomfort and Fatigue Application of heat and cold Encourage to alternate Rest and activity Support devices – braces, splints, firm mattress Analgesics and anti-inflammatory medications Nursing Care Maintain Skin Integrity Apply topical anti-inflammatory Avoid direct sunlight. Use sunscreens and protective clothing, sun hats Increase Mobility ROM Assistive devices – walkers, canes, crutches Treatment and Nursing Care Facilitate self care Improve body image Provide adaptive equipment for eating, bathing, toileting, dressing Allow patient extra time to complete care Encourage patient to verbalize feelings, perceptions, and fears Monitor for complications Assess for serious adverse effects of medications used in treatment Avoid immunizations with live viruses