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Musculoskeletal disorders pdf

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Musculoskeletal disorders

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Musculoskeletal disorders pdf

  1. 1. 1 By: Getenet D(BScN, MSc in MSN, MSc student in Epidemiology at BDRU ) LECTURER at BDU-CHS, DEP’T OF NURSING Musculo skeletal system
  2. 2. MANAGEMENT OF PATIENT WITH MUSCULOSKELETAL SYSTEM  The musculoskeletal system includes:  bones,  joints, muscles, tendons, ligaments, and  bursae of the body.
  3. 3. Degenerative Joint Disease (Osteoarthritis)  joint disease that damages the articular cartilage leading to reactive new bone formation.  Osteoarthrites (OA) is described as progressive joint failure where all structures involved in joint function undergo pathologic changes.  Weight bearing joints (hips, knees), cervical and lumbar spine and the metacarpophalangeal and distal interphalangeal joints of the hands are commonly affected.
  4. 4. Degenerative Joint Disease (Osteoarthritis)  the most common and frequently disabling of the joint disorders.  The wrist, elbow and ankle joints are chacterstically spared or very raely involved.  It is more common in females than males.  OA is both over diagnosed and trivialized; it is frequently over treated or undertreated.
  5. 5. Degenerative Joint Disease (Osteoarthritis)  OA can be categorized into localized or generalized forms.  Generalized OA consists of involvement of three or more joint sites.  OA is generally a non inflammatory type of arthritis but some patients can have predominantly inflammatory arthritis characterized history of swelling, night pain, morning stiffness greater than 30 minutes, warm and tender joints on physical examination.
  6. 6. Degenerative Joint Disease (Osteoarthritis)  The functional impact of OA on quality of life, especially for elderly patients, is often ignored.  OA has been classified as primary (idiopathic), with no prior event or disease related to the OA, and secondary, resulting from previous joint injury or inflammatory disease.  The distinction between primary and secondary OA is not always clear.
  7. 7. Degenerative Joint Disease (Osteoarthritis)  Increasing age directly relates to the degenerative process in the joint, as the ability of the articular cartilage to resist micro fracture with repetitive low loads diminishes.  OA often begins in the third decade of life and peaks between the fifth and sixth decades.  By age 75 years, 85% of the population has either x-ray or clinical evidence of OA, but only 15% to 25% of these people experience significant symptoms.
  8. 8. Degenerative Joint Disease (Osteoarthritis) Risk Factors for Osteoarthritis  Increased age  Obesity  Previous joint damage  Repetitive use (occupational and recreational)  Anatomic deformity  Genetic susceptibility
  9. 9. Degenerative Joint Disease (Osteoarthritis) Clinical Manifestations  Pain at initiation of exercise (walking)  Morning stiffness which improves with exercise  Diminution of joint movement  Crepitus on moving affected joint(s)  Heberden's nodes and deformed joints in the hands  Joint swelling, warmth and effusions (knee especially)  If cervical and lumbar spine involved; muscle weakness in hands and legs respectively (myelopathy)
  10. 10. Degenerative Joint Disease (Osteoarthritis)  Characteristic bony nodes may be present; on inspection and palpation, these are usually painless, unless inflammation is present.  Tender and enlarged joints are common.  Investigations – CBC : high greater than 11,000 – ESR :usually >50 mm/h – X-ray of affected joints: osteophyte formation, joint space narrowing, subchondral sclerosis and cysts
  11. 11. X ray finding 52
  12. 12. X ray finding of OA…. 53
  13. 13. X ray finding of OA…. 54
  14. 14. Medical Management Osteoarthritis  Objectives – Relieve pain – Prevent and manage deformities – Educate patient  Although no treatment halts the degenerative process, certain preventive measures can slow the progress if undertaken early enough.  These include weight reduction, prevention of injuries, perinatal screening for congenital hip disease, and ergonomic modifications.
  15. 15. Degenerative Joint Disease (Osteoarthritis)  Conservative treatment measures include:  the use of heat,  weight reduction,  joint rest and avoidance of joint overuse,  orthotic devices to support inflamed joints (splints, braces),  isometric and postural exercises, and  aerobic exercise.  Occupational and physical therapy can help the patient adopt self-management strategies.
  16. 16. Degenerative Joint Disease (Osteoarthritis) PHARMACOLOGIC THERAPY  Pharmacologic management of OA is directed toward symptom management and pain control.  Medications are used in conjunction with non pharmacologic strategies;  Acetaminophen.  nonselective NSAIDs,  COX-2 inhibitors (cyclo-oxygenase- inflamatory enzyme).  opioids and  intra-articular corticosteroids
  17. 17. Pharmacologic mgt of osteoarthritis)  Pain management  Inflammatory osteoarthritis  First line-Ibuprofen, 200-400mg P.O., TID  Diclofenac, 50-75mg P.O., BID or rectal suppository 100mg/daily  Indomethacin, 25-50mg, P.O., 2-3 times/day; maximum dose is 200mg/day or rectal suppository 100mg/daily. Avoid indomethacin in hip OA.  Piroxicam, 10-20mg, P.O., once per day. Maximum dose is 20mg/day Dosage forms:
  18. 18. Degenerative Joint Disease (Osteoarthritis)  PLUS GI protection for high risk individuals  Omeprazole, 20mg, P.O., once daily or BID.  Esomeprazole, 20-40mg, P.O., once daily  Pantoprazole, 40mg, P.O., once daily  Alternative-H2 blockers,  Cimetidine, 400mg P.O., BID  Ranitidine, 150mg, P.O, BID 2.
  19. 19. Degenerative Joint Disease (Osteoarthritis)  Non inflammatory osteoarthritis  First line Paracetamol, 1g 4–6 hourly P.O., when required to a maximum of 4 doses per 24 hours  If ineffective: start NSAIDS as above Additional pain management –for both inflammatory and non infla mmmatory OA.  Third option  First line Tramadol, 50mg to 100mg, P.O., once to twice per day.  Alternative Codeine phosphate 30mg P.O., QID. USE CODEINE FOR SHORT DURATION ONLY.
  20. 20. Degenerative Joint Disease (Osteoarthritis)  Intra-articular steroids  osteoarthritis of the knee and shoulder that is refractory to NSAIDS  Not more than 2–3 injections per year per joint are recommended.  First line Methylprednisolone acetate, 20–80mg depending on joint size OR  Triamcinolone acetonide: Initial: Smaller joints: 2.5-5mg, larger joints: 5-15mg, up to 40mg for large joints.  methylprednisolone above Dosage forms: Injection, 10mg/ml, 40mg/ml in vial
  21. 21. Degenerative Joint Disease (Osteoarthritis) SURGICAL MANAGEMENT  In moderate to severe OA, when pain is severe or because of loss of function, surgical intervention may be used.  Procedures most commonly used are:  Osteotomy- to alter the force distribution in the joint and  Arthroplasty- diseased joint components are replaced with artificial products.
  22. 22. Degenerative Joint Disease (Osteoarthritis) SURGICAL MANAGEMENT  Viscosupplimentation- the reconstitution of synovial fluid viscosity.  Hyaluronic acid, that acts as a lubricant and shock absorbing fluid in the joint, may be used in this procedure.  Tidal irrigation/ (lavage) of the knee- introduction and then removal of a large volume of saline into the joint through cannulas.
  23. 23. Pyogenic Osteomyelitis  Pyogenic Osteomyelitis is an acute infection of the bone and its structures caused by bacteria.  Osteomyelitis occurs as a result of hematogenous spread, contiguous spread from adjacent soft tissues or direct infection from trauma or surgery.  Hematogenous osteomyelitis is usually monomicrobial, while osteomyelitis due to contiguous spread or direct inoculation is usually polymicrobial.  Staphylococcus aureus is the most common causative organism. Coagulase-negative staphylococci and aerobic gram-negative bacilli are also common causes.
  24. 24. Pyogenic Osteomyelitis  Clinical features Gradual onset varying from few days to weeks of local bone pain, swelling, low grade fever, malaise and weight loss.  Investigations - Clinical, CBC, ESR, C-reactive protein, X-ray of the affected bone - Culture of pus/sequester (if debridement is done)
  25. 25. Pyogenic Osteomyelitis  Treatment Objectives - Control infection - Prevent disability Non pharmacologic - Rest/immobilization - Surgical debridement
  26. 26. Pyogenic Osteomyelitis  Pharmacologic Empiric antibiotic – duration of antibiotics is for at least six weeks First line  Vancomycin, 30mg/kg/day, IV, in two divided doses PLUS  Ciprofloxacin, 750mg, P.O., BID  Alternative  Cloxacillin, 2gm, I.V. QID  PLUS  Ciprofloxacin, 750mg, P.O., BID
  27. 27. Pyogenic Osteomyelitis  Further treatment is guided by culture sensitivity tests  For pain and fever – Analgesic/antipyretic e.g. Paracetamol, 500-1,000mg P.O. as needed (4-6 times daily) can be given.
  28. 28. Osteoporosis  Osteoporosis means ―porous bone.‖  Viewed under a microscope, healthy bone looks like a honeycomb.  When osteoporosis occurs, the holes and spaces in the honeycomb are much larger than in healthy bone.  Osteoporotic bones have lost density or mass and contain abnormal tissue structure. 69
  29. 29. Osteoporosis…..  One in two women and one in four  Osteoporosis is known as the “silent thief”  because it slowly and insidiously over many years robs the skeleton of its banked resources.  Bones can eventually become so fragile that they cannot withstand normal mechanical stress. 70
  30. 30. Why Osteoporosis is more common in women reasons:  lower calcium intake than men throughout their lives  have less bone mass because of their generally smaller frames;  bone resorption begins at an earlier age and accelerated at menopause;  pregnancy and breastfeeding deplete a woman’s skeletal reserve  longevity increases the likelihood of osteoporosis 71
  31. 31. Osteoporosis………  initial bone scan in women before the age of 65. If the results are normal and  the person is at low risk for osteoporosis, another scan is not needed for 15 years.  Testing should start earlier and be done more frequently if a person is at high risk for fractures (e.g., low body weight, smoker, prior fractures). Men should be screened before the age of 70 years old and by age 50 if at high risk for fractures  (e.g., low body weight, hypogonadism). 72
  32. 32. Osteoporosis……… 73
  33. 33. 74
  34. 34. Etiology and Pathophysiology  risk is associated with regular weight-bearing exercise and fuoride, calcium, and vitamin D ingestion.  Low testosterone levels are a major risk factor in men.  Peak bone mass (maximum bone tissue) is primarily achieved before age 20.  It is determined by a combination of four major factors: heredity, nutrition, exercise, and hormone function. 75
  35. 35. Etiology and Pathophysiology  Heredity may be responsible for up to 70% of a person’s peak bone mass.  Bone loss from midlife (ages 35 to 40 years) onward is inevitable, but the rate of loss varies.  At menopause, women experience rapid bone loss when the decline in estrogen production is the sharpest.  Tis rate of loss then slows, and eventually matches the rate of bone lost by men 65 to 70 years old.  Long-term use of corticosteroids, thyroid replacements, heparin, long-acting sedatives, or antiseizure medications 76
  36. 36. Etiology and Pathophysiology……  Bone is continuously being deposited by osteoblasts and resorbed by osteoclasts, a process called remodeling.  Normally the rates of bone deposition and resorption are equal to one another so that the total bone mass remains constant.  In osteoporosis, bone resorption exceeds bone deposition.  Many drugs can interfere with bone metabolism, including corticosteroids, antiseizure drugs (e.g., divalproex sodium [Depakote], phenytoin), aluminum-containing antacids, heparin, certain cancer treatments, and excessive thyroid hormones. 77
  37. 37. Osteoporosis Can Sneak up on You  Osteoporosis is often called a silent disease because one can’t feel bones weakening.  Breaking a bone is often the first sign of osteoporosis or a patient may notice that he or she is getting shorter or their upper back is curving forward.  experiencing height loss or your spine is curving, pre alarming sign 78
  38. 38. Clinical Manifestations of OP  Osteoporosis occurs most commonly in the bones of the spine, hips, and wrists.  Usual first manifestations are back pain or spontaneous fractures.  weakened bone and spontaneous fractures or fractures from minimal trauma.  Over time, wedging and fractures of the vertebrae  produce gradual loss of height and a humped back known as kyphosis,or ―dowager’s hump‖ 79
  39. 39. Clinical Manifestations of OP….. 80
  40. 40. General facts about OP 81
  41. 41. Diagnostic  conventional x-ray can not detect until more than 25% to 40% of calcium in the bone is lost.  Serum calcium, phosphorus, and alkaline phosphatase levels usually are normal, although alkaline phosphatase may be elevated afer a fracture.  Bone mineral density (BMD) :- quantitative ultrasound (QUS) and dual-energy x-ray absorptiometry (DXA). 82
  42. 42. Collaborative Therapy • Diet high in calcium Calcium supplements  Vitamin D supplements Exercise program  Drug therapy  Bisphosphonates, alendronate (Fosamax, Binosto)  clodronate (Bonefos), etidronate (Didronel)  Selective estrogen receptor modulator (e.g., raloxifene [Evista])  Recombinant form of parathyroid hormone (e.g., teriparatide [Forteo]), denosumab (Prolia)  Minimally invasive procedures, Vertebroplasty, Kyphoplasty 83
  43. 43. Rheumatoid arthritis (RA)  Systematic autoimmune inflammatory disease  Persistent inflammation of synovial tissue especially of the wrists, hands and feet.  long-term disease that can affect surrounding structures like the tendon sheath, the bursa and tendons.  Without treatment, RA can possibly lead to joint deformities and permanent function loss.
  44. 44. Rheumatoid Arthritis (RA)  RA is commonly used as the prototype for inflammatory arthritis.  The incidence rate is approximately 3%, with a two to three times greater incidence in women.  In RA, the autoimmune reaction primarily occurs in the synovial tissue.  Phagocytosis produces enzymes within the joint.
  45. 45. Rheumatoid Arthritis (RA)  The enzymes break down collagen, causing edema, proliferation of the synovial membrane, and ultimately pannus formation.  Pannus destroys cartilage and erodes the bone.  The consequence is loss of articular surfaces and joint motion.  Muscle fibers undergo degenerative changes.  Tendon and ligament elasticity and contractile power are lost.
  46. 46. Normal joint 87
  47. 47. Affected joint 88
  48. 48. Risk factors  Etiology is Unknown  Age: risky age groups; 40 - 60 .  Sex: more common among women than men.  Genetics  Weight  Smoking  Diet: Lower intake of vitamin D and antioxidants and higher intake of sugar, sodium, red meats, protein, or any food with much vitamin C 89
  49. 49. Factors decreased risk  Fish and omega-3 fatty acid consumption  Moderate alcohol intake  Healthy diet  Statin use  Oral contraceptive use/hormone replacement 90
  50. 50. Clinically Relevant Anatomy  inflammation and destructive erosion of bone and loss of joint integrity - disability.  Under normal circumstances, the synovium consists of 2 - 3 layers of cells.  In patients with rheumatoid arthritis, the synovium is strongly thickened and inflamed.  Due to the inflammation production of enzymes occurs, which breaks down the cartilage.  This can cause local damage to the bone-tissue and cartilage. 91
  51. 51. 92
  52. 52. Clinical Manifestations RA  The disease course typically follows three possible paths Monocyclic: Having one episode that does not reoccur. This usually ends within 2-5 years of initial diagnosis. Polycyclic: The disease severity varies over the course of the progression of the condition. Progressive: Condition continues to become more severe and non-remitting 93
  53. 53. Clinical Manifestations RA……  Clinical manifestations of RA vary, usually reflecting the stage and severity of the disease.  The three most important complaints are the pain, morning stiffness(>30 minute) and fatigue.  joint swelling, warmth and redness  a chronic, symmetrical inflammation of metatarsophalangeal joints (MTP), the wrists, the metacarpophalangeal joints (MCP) and the proximal interphalangeal joints (PIP).  Softening of the ligaments can lead to deformation of the fingers
  54. 54. Clinical Manifestations (RA)…….  Other symptoms can include:  a poor appetite (not feeling hungry)  weight loss  a high temperature, or a fever  sweating  dry eyes – as a result of inflammation  chest pain – as a result of inflammation.
  55. 55. Clinical Manifestations (RA)  Characteristically, the pattern of joint involvement begins with the small joints in the hands, wrists, and feet.  As the disease progresses, the knees, shoulders, hips, elbows, ankles, cervical spine, and temporomandibular joints are involved.  The onset of symptoms is usually acute.  Symptoms are usually bilateral and symmetric.  Deformities of the hands and feet are common in RA.  RA is a systemic disease with multiple extra-articular features.
  56. 56. 97 Stage Description Stage I Mild No destructive changes on radiographic examination Radiographic evidence of osteoporosis may be present Stage II Moderate Radiographic evidence of osteoporosis, with or without slight subchondral bone destruction; slight cartilage destruction may be present No joint deformities, although limitation of joint mobility may be present Adjacent muscle atrophy Extra-articular soft tissue lesions, such as nodules and tenosynovitis may be present Stage III Severe Radiographic evidence of cartilage and bone destruction in addition to osteoporosis Joint deformity, such as subluxation, ulnar deviation, or hyperextension, without fibrous or bony ankylosis Extensive muscle atrophy Extra-articular soft tissue lesions, such as nodules and tenosynovitis may be present Stage IV Terminal Fibrous or bony ankylosis Stage III criteria
  57. 57. Clinical Manifestations RA…… 98
  58. 58. Clinical Manifestations RA……99
  59. 59. Clinical Manifestations RA……100
  60. 60. Clinical Manifestations RA……101
  61. 61. X ray finding of RA…… 102
  62. 62. X ray finding of RA…… 103
  63. 63. Differential Diagnosis  There is no unique test or feature that is pathognomonic for RA. Common disorders to consider as differential diagnoses with RA are:  Osteoarthritis: the absence of systemic inflammatory signs and symptoms, onset in later life, and the pattern of joint involvement.  Infectious arthropathies: the important consideration in the setting of fever and polyarthritis. joint aspiration and synovial fluid cultures and blood cultures are often helpful in establishing the diagnosis. 104
  64. 64. Differential Diagnosis  Lyme disease: negative synovial fluid cultures. Apparent in endemic region where tick exposure was likely.  Seronegative spondyloarthropathies (reactive arthritis, ankylosing spondylitis, inflammatory bowel disease–associated arthropathy): muscle weakness and antibodies associated with these disorders most often readily distinguish these disorders from RA.  Fibromyalgia (FMS): absence of synovitis, the lack of pain on motion, and normal laboratory and imaging studies. 105
  65. 65. Other pathologies to consider as ddx  Osteoarthritis Paraneoplastic syndrome  Myelodysplastic syndrome  Polychondritis  Polymyalgia  Rheumatica Psoriatic Arthritis  Sarcoidosis Sjogren Syndrome  Systemic Lupus  Erythematous  Reiter Syndrome  Gout 106
  66. 66. Diagnosis of RA…..
  67. 67. Rheumatoid Arthritis (RA) Note: RA diagnosed if at least four of these criteria are satisfied (the first four must have been present for at least six weeks). The major drawback of the criteria is insensitivity in identifying early disease which subsequently develop into typical RA .
  68. 68. Rheumatoid Arthritis (RA) Investigations - ESR/CRP - Rheumatoid factor - ANA (antinuclear antibody) – - X-ray of involved joints - Treatment - Objectives - Reduce pain, swelling and stiffness , Prevent deformities , Delay disease progression and onset of long term complications
  69. 69. Rheumatoid Arthritis (RA) Medical Management EARLY-STAGE RA  Begins with education, a balance of rest and exercise, and referral to community agencies for support.  Medical management begins with therapeutic doses of salicylates or NSAIDs.
  70. 70. Rheumatoid Arthritis (RA) Medical Management EARLY-STAGE RA  When used in full therapeutic dosages, these medications provide both anti-inflammatory and analgesic effects.  Several COX-2 inhibitors, another class of NSAIDs, have been approved for treatment of RA.  COX (cyclo-oxygenase) is an enzyme involved in the inflammatory process.
  71. 71. Rheumatoid Arthritis (RA) Medical Management Moderate, Erosive RA  For moderate, erosive RA, a formal program with occupational and physical therapy is prescribed  Educate the patient about principles of joint protection, pacing activities, work simplification, range of motion, and muscle-strengthening exercises.
  72. 72. Rheumatoid Arthritis (RA) Medical Management Persistent, Erosive RA  Reconstructive surgery and corticosteroids are often used.  Reconstructive surgery is indicated when pain cannot be relieved by conservative measures.
  73. 73. Rheumatoid Arthritis (RA) Medical Management Persistent, Erosive RA  Surgical procedures include  Synovectomy (excision of the synovial membrane),  Tenorrhaphy (suturing a tendon),  Arthrodesis (surgical fusion of the joint), and  Arthroplasty (surgical repair and replacement of the joint).
  74. 74. Rheumatoid Arthritis (RA) Medical Management Advanced, Unremitting RA  immunosuppressive agents are prescribed.  These include high-dose:  Methotrexate  Cyclophosphamide and  Azathioprine  These medications, however, are highly toxic and can produce bone marrow suppression, anemia, gastrointestinal disturbances, and rashes.
  75. 75. Rheumatoid Arthritis (RA)  Medical Management  Through all stages of RA, depression and sleep deprivation may require the short-term use of low-dose antidepressant medications.  They may include:  amitriptyline,  paroxetine , or  sertraline ,
  76. 76. MGT of RA….. Initiate early in the course First line Methotrexate, 7.5mg P.O., once per week. Increase dose gradually to a maximum of 25mg per week. N.B. Monitor: Liver function and CBC before and 12 weekly during treatment. PLUS Folic acid, 5mg P.O., per week with methotrexate at least 24 hours after the methotrexate dose. AND/OR Chloroquine phosphate, 150mg P.O., (as base) daily for 5 days of each week for 2–3 months.
  77. 77. MGT of RA…..  Then reduce dose if possible and administer 5 days a week with an annual medicine holiday for 1 month.  Do ophthalmic examination annually to monitor for ocular damage. AND/OR Sulfasalazine, 500mg P.O., 12 hourly.  Gradually increase over one month from 500mg to 1 g 12 hourly.  Liver function and CBCs monthly for first 3 months then every 3–6 months. 118
  78. 78. MGT of RA…..  Oral corticosteroids  Indications: - As bridging therapy while waiting for DMARDs to take effect. - The elderly if threatened by functional dependence and intolerant to NSAIDs. - Extra-articular manifestations, e.g. pleural effusion, scleritis. - Acute flare Prednisolone, 40mg P.O., daily for 2 weeks during acute flares. Thereafter gradually reduce the dose to < 7.5 mg daily. Maintenance low dose prednisolone may be needed in many patients  
  79. 79. MGT of RA…..  Joint pain management-NSAIDs  Use for active inflammation with pain.  NSAIDs are used for symptomatic control only, as they have no long-term disease modifying effects.  NSAID dose should be reduced and then stopped once the DMARDs have taken effect  Ibuprofen, 800mg, P.O.,TID with meals. If not tolerated: 400mg 8 hourly.
  80. 80. MGT of RA…..  An extra night-time dose of a NSAID may be added in some patients with severe nocturnal pain/morning stiffness OR  Diclofenac, Immediate or delayed release tablet: 150-200mg/day P.O., in 2-4 divided doses.  Rectal suppository, insert 50mg or 100 mg rectally as single dose to substitute for final daily dose OR  Indomethacin, 25-50mg P.O., BID TO TID; maximum dose: 200mg/day. Rectal suppository, insert 100mg, BID or once, at bed time. 121
  81. 81. Rheumatoid Arthritis (RA)  Nutrition Therapy  Patients with RA frequently experience anorexia, weight loss, and anemia.  Foods high in vitamins, protein, and iron for tissue building and repair are usually prescribed.  For the extremely anorexic patient, small, frequent feedings with increased protein supplements may be prescribed.
  82. 82. 3. GOUT  The deposition of microcrystals of uric acid in the joints and peri-articular tissues  May be present even when the level of uric acid in the blood is normal  Acute symptoms may precipitated by the consumption of alcohol and foods rich in purines e.g. red meat, sea foods, as well as trauma, surgery, starvation and infection.  The incidence increases with age and body mass index.  It occurs more commonly in males than females  not caused by the level of uric acid but by acute changes in the uric acid level
  83. 83. GOUT  Primary gout is related to underexcretion or overproduction of uric acid, which associated with dietary excesses or overuse of alcohol and metabolic syndrome.  Secondary gout is related to medications or conditions that cause hyperuricemia, such as myeloproliferative diseases and their treatment, hyperproliferative skin disorders, enzymatic defects, and renal failure  The prevalence of gout is reported to be 1.6 to 13.6 per thousand.
  84. 84. GOUT  Attacks of gout appear to be related to sudden increases or decreases of serum uric acid levels.  When the urate crystals precipitate within a joint, an inflammatory response occurs and an attack of gout begins.  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 urate lithiasis (kidney stones) with chronic renal disease secondary to urate deposition may develop.
  85. 85. Gout…..  Gout can be a manifestation or complication of other diseases such as;  metabolic syndrome,  hematological malignancies,  chronic kidney disease and  medicines like thiazide and loop diuretics, cytotoxic medicines and pyrazinamide 127
  86. 86. Gout….. Clinical Manifestations  Acute gouty arthritis (recurrent attacks of severe articular and periarticular inflammation),  Tophi (crystalline deposits accumulating in articular tissue, osseous tissue, soft tissue, and cartilage),  Gouty nephropathy (renal impairment), and  Uric acid urinary calculi.
  87. 87. GOUT……. Four stages of gout can be identified: 1. asymptomatic hyperuricemia, 2. acute gouty arthritis, 3. intercritical gout, and 4. chronic tophaceous gout.
  88. 88. GOUT………..  The subsequent development of gout is directly related to the duration and magnitude of the hyperuricemia.  Therefore, the commitment to lifelong pharmacologic treatment of hyperuricemia is deferred (delayed) until there is an initial attack.
  89. 89. Gout…..  Typical acute attack  Excruciating pain, redness, swelling, and disability.  Maximal severity of the attack is usually reached within 12 to 24 hours.  80% of initial attacks involve a single joint, most often at the base of the great toe (known as podagra), or the knee  - Affected joint is inflamed, swollen and tender 131
  90. 90. GOUT Diagnosis & Medical Management  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 within the fluid.  Investigations  - CBC, ESR,BUN, creatinine, Serum uric acid, Blood glucose, Serum lipids  - X-ray of affected joint
  91. 91. Positive finding of gout  Uric acid level in the blood >7.2 normal( 3.5 -7.2 mg/dl.  Uric acid urine test  A uric acid level > 750mg ( normal 250 - 750 mg) Joint x-ray: If there is chronic gout, to see if any joint damage.  Ultrasound: to look for urate crystals or tophi in your joints. 133
  92. 92. Positive x-ray finding in gout 134
  93. 93. Positive x-ray finding in gout….. 135
  94. 94. Treatment of gout  Objectives :-Relieve pain immediately ,Reduce joint inflammation ,Prevent recurrent attacks and joint damage, Prevent uric acid crystal deposition in soft tissues  Non Pharmacologic  Rest affected joint  Identify and manage underlying or predisposing factors  Weight reduction in obese or overweight individuals  Dietary modification (low purine diet) 136
  95. 95. Pharmacologic 1. Acute Gout  Ibuprofen, 800mg P.O.TID with meals. If not tolerated: 400 mg 8 hourly  An extra night-time dose of a NSAID may be added in some patients with severe  nocturnal pain/morning stiffness OR  Diclofenac, Immediate or delayed release tablet: 150- 200mg/day P.O., in 2-4 137
  96. 96. Pharmacologic mgmt…. OR  Indomethacin, 25-50mg P.O. BID or TID; maximum dose: 200mg/dayor Rectal  suppository, 100mg, BID or once at bed time  Alternative(when NSAIDS are not tolerated or contraindicated)  Prednisolone, 20-40mg P.O. for one to two wks and tapered over another one to 138
  97. 97. Pharmacologic mgmt.…. 2. Chronic gout  If possible, avoid known precipitants  Treat secondary causes when possible  Assess renal function and blood uric acid level  Uric acid lowering therapy  Indicated for  >2 acute attacks per year  chronic tophaceous gout  Uric acid renal stones  urate nephropathy 139
  98. 98. Pharmacologic mgmt.….  Allopurinol, 100 mg P.O. daily.  - Increase monthly by 100mg according to uric acid blood levels and eGFR.  - Most patients will be controlled with a dose of 300 mg daily  N.B. Do not stop uric acid lowering medicines during an acute attack 140
  99. 99. GOUT Nursing Management  While severe dietary restriction is not necessary, patients should be encouraged to restrict consumption of foods high in purines, especially organ meats, and to limit alcohol intake.  Maintenance of normal body weight should be encouraged.
  100. 100. GOUT Nursing Management  In an acute episode of gouty arthritis, pain management is essential.  During the intercritical period, the patient feels well and may abandon preventive behaviors, which may result in an acute attack.  Acute attacks are most effectively treated if therapy is begun early in the course.
  101. 101. 4. Septic (Infectious) Arthritis
  102. 102. Septic (Infectious) Arthritis  Joints can become infected through: Spread of infection from other parts of the body (hematogenous spread) (80-90%) Directly through trauma or surgical instrumentation (10-15%).  Previous trauma to joints, joint replacement, coexisting arthritis, and diminished host resistance contribute to the development of an infected joint.
  103. 103. Septic (Infectious) Arthritis  Some inflammation of joints, tendons, and bursae is directly related to infection caused by bacterial, viral, fungal, or parasitic agents.  Bacterial arthritis is the most rapidly destructive form of infectious arthritis.
  104. 104. Septic (Infectious) Arthritis  There are two major classes of bacterial arthritis:  arthritis caused by Neisseria gonorrhoeae and  Arthritis caused by non gonococcal bacterium.  The most prevalent of the non gonococcal organisms include Staphylococcus aurous and the various streptococcal variants.
  105. 105. Pathology of SA.. 147
  106. 106. Clinical Manifestations Septic Arthritis  Chills Fatigue and generalized weakness  The characteristic symptom is single swollen and painful joint.  The patient often immobilizes the joint and elevates the affected extremity because of pain and swelling.  Fever may be high or it may be absent.  Signs of systemic infection may be lacking in elderly patients, those with diabetes, and those with suppressed immune systems.
  107. 107. How Is Septic Arthritis Diagnosed?  CBC: usually very high  ESR>22 mm/hour for men and 29 mm/hour for women  CRP>3 mg/L  - synovial fluid analysis including Gram stain and culture will help to reach the right diagnosis.  X-ray of the affected joint should also be done.  MRI scanning is sensitive in evaluating joint destruction (not sensitive at early phase) 149
  108. 108. Positive x ray finding of SA 150
  109. 109. Treatment SA Objectives - Treat infection promptly and prevent joint destruction Non pharmacologic –  Aspiration/drainage when indicated  Splintage, but early immobilization if joints are mobile.  The joint must be splinted with a POP slab or skin traction to relieve pain and prevent contractures
  110. 110. Management SA  medical emergency : early diagnosis and treatment eliminate distribution of infection;  Otherwise, the joint may be destroyed relatively quickly.  Empiric antibiotics with duration of If synovial fluid gram stain is unavailable or negative:  At least the first two weeks of antibiotics should be through intravenous route.
  111. 111. Treatment of SA……  First line Vancomycin, 30mg/kg/day IV in two divided doses, not to exceed 2g per day PLUS  Ceftriaxone, 2gm, I.V, daily  Alternatives Cloxacillin, IV, 2g every 6 hr QID for 4-6 weeks OR  Ceftriaxone 2gm,IV, daily  If gram postive organism- vancomycin as first line and Cloxacillin as alternative.  If gram negative organism-use ceftriaxone with the above dose as first line.
  112. 112. Septic (Infectious) Arthritis Nursing Management  Nursing management focuses on providing pain relief, administering antibiotics, and assisting the patient with self-care activities.  If the patient is sent home on intravenous antibiotics, the nurse arranges home care and instructs the patient and care providers in safe administration and changes to report to a health care provider.
  113. 113. PYOMYOSITIS  Pyomyositis is a purulent infection of skeletal muscle that arises from hematogenous spread, usually with abscess formation.  By definition, it is not secondary to a contiguous infection of the soft tissue or bone, nor due to penetrating trauma.  Pyomyositis has a predilection for large-muscle groups and often results in localized abscess formation.  Pyomyositis often is called tropical myositis because of its prevalence in tropical areas, where pyomyositis accounts for 3% to 5% of hospital admissions 158
  114. 114. Predisposing factors for pyomyositis  Immunodeficiency; HIV infection, diabetes mellitus, malignancy, cirrhosis, renal insufficiency, organ transplantation, and administration of immunosuppressive agents.  trauma, injection drug use,  concurrent infection( Toxocariasis)  malnutrition. 159
  115. 115. MICROBIOLOGY  S. aureus is the most common cause of pyomyositis;  Methicillin-resistant S. aureus (MRSA), including community acquired strains, is also an increasingly important pathogen.  Group A streptococci ;second most common pathogen.  Less common causes ;non-group A streptococci, pneumococci and gram-negative enteric bacilli.  E. coli among patients with hematologic malignancy. 160
  116. 116. Clinical manifestation  Pyomyositis presents with fever and pain with cramping localized to a single muscle group.  usually affect lower extremity (sites include the thigh, calf and gluteal muscles),  but other muscles may be involved, including the iliopsoas, pelvic, trunk, paraspinal and upper extremity muscles. 161
  117. 117. Stage of Pyomyositis  Stage 1Characterized by  crampy local muscle pain, swelling, and low-grade fever  Mild leukocytosis and induration of the affected muscle may be present.  A deep abscess may not be discretely palpable, but the muscle may have a "woody" texture on palpation.  Fluctuation is not present, and aspiration of the muscle will not yield purulent material.  Only 2 percent of patients present at this stage. 162
  118. 118. Pyomyositis……. 163
  119. 119. Stage 2 of pyomyocities  Occurs 10 to 21 days after the initial onset of symptoms and is  characterized by fever, exquisite muscle tenderness, and edema.  A frank abscess may be clinically apparent, and aspiration of the affected muscle typically yields pus.  Marked leukocytosis is usually present.  More than 90 percent of the patients present at this suppurative stage 164
  120. 120. Stage 3 of pyomyocities  systemic toxicity.  The affected muscle is fluctuant.  bacteremia such as septic shock, endocarditis (S. aureus )  septic emboli, pneumonia, pericarditis, septic arthritis, brain abscess, and  acute renal failure can occur.  Rhabdomyolysis has also been described.  bacteremia, may cause endocarditis. 165
  121. 121. DIFFERENTIAL DIAGNOSIS  muscle strain, contusion, hematoma, cellulitis, deep vein thrombosis, osteomyelitis, septic arthritis, or neoplasm.  clostridial myonecrosis, necrotizing fasciitis, spontaneous gangrenous myositis, diabetic muscle infarction, septic arthritis, and other forms of myositis. 166
  122. 122. Case report of pyomyocities  A 58 year-old woman with type 2 diabetes was admitted with a one month history of increasing pain of the left thigh and the left arm. She complained for two months of polyuropolydipsic syndrome, weight loss and weakness. On presentation, the patient was febrile (38.5°C). Physical exam showed a firm and painful swelling of the left thigh with erythema . In the left arm we noticed an indurated painfull mass without erythema. There was no abdominal pain or vomiting. 167
  123. 123. Case report of pyomyocities ….  Laboratory findings shows a high white blood cell count of 17910/mm3, hemoglobin 12.4 g/dL, platelets count 458000/mm3, erythrocyte sedimentation rate 107 mm, C reactive protein: 213 mg/L, serum creatinine: 77µmol/L, serum glucose: 27.5 mmol/L, CPK: 208 U/L, LDH: 265 U/L. The urine dipsticks demonstrate ketosis and glucosuria. Blood gases parameters showed metabolic acidosis: PH: 6.98, PaO2: 64 mmHg, PCO2: 27 mmHg, HCO3-: 17 mmol/L. The culture of urine analysis was negative. Three serial blood cultures were negative. Ultrasonography of the painful areas was in favor myositis. 168
  124. 124. Case report of pyomyocities …. 169
  125. 125. DIAGNOSIS  Radiographic can defining the site(s) of infection and for ruling out other entities.  Computed tomography (CT) is helpful for detecting muscle swelling and well-delineated areas of fluid attenuation that display rim enhancement with contrast, as well as for radiographic-guided drainage of purulent material  CT is preferable if available, ultrasonography is also a potentially useful  Magnetic resonance imaging (MRI) can be helpful for identification of the extent of infection 170
  126. 126. DIAGNOSIS………  Cultures:- Bacteriologic diagnosis can be made by cultures of drainage prior to antibiotic therapy.  Laboratory data:- leukocytosis with left shift, elevated ESR and C-reactive protein.  Eosinophilia for a concomitant parasitic infection.  Counterintuitively , creatine kinase levels are often normal. 171
  127. 127. TREATMENT  Although stage 1 pyomyositis can be treated with antibiotics alone, most patients present with stage 2 or 3 disease and therefore require both antibiotics and drainage for definitive management  In the setting of deep infection or extensive muscle involvement with significant necrosis, surgical intervention may be required. 172
  128. 128. TREATMENT…….  For immunocompetent individuals, initial empiric parenteral antibiotic therapy should be directed against staphylococci and streptococci.  Empiric therapy for MRSA should be initiated for patients with a previous episode of proven MRSA infection, patients with risk factors for MRSA, and patients with systemic toxicity.  In addition, it should be considered in communities where the prevalence of MRSA is greater than 30 percent. 173
  129. 129. TREATMENT…….  For immunocompromised cover both gram-positive, gram-negative and anaerobic organisms with vancomycin  The course of therapy for patients with other sequelae of bacteremia (such as endocarditis or osteomyelitis) should be adjusted based on the nature of infection at these other sites. 174
  130. 130. Necrotizing fasciitis  A progressive life-threatening softtissue infection (with liquifactive necrosis of subcutaneous fat and fascia) ± skin . 175
  131. 131. Necrotizing fasciitis has also been referred to as  Hemolytic streptococcal gangrene  Meleney ulcer  Acute dermal gangrene  Hospital gangrene  Suppurative fasciitis  Synergistic necrotizing cellulitis 176
  132. 132. CAUSITIVE ORGANISMS  Group A Hemolytic streptococci (Streptococcus pyogenes) and Staphylococcus aureus, alone or in synergism, are frequently the initiating  other aerobic and anaerobic pathogens  Bacteroides fragilis  Clostridium perfringens  Peptostreptococcus  Enterobacteriaceae  Pseudomonas  Klebsiella 177
  133. 133. Pathophysiology 178 This deep infection causes vascular occlusion, ischemia, and tissue necrosis. Superficial nerves are damaged, producing the characteristic localized anesthesia
  134. 134. Types of necrotizing fasciitis  Type I:- Polymicrobial (aerobic and anaerobic;enterobacter +Non Group A streptococi)  Common with DM and PVD, after surgical procedures  Type II:- Monomicrobial (primarily by GAS,  occasionally caused by community associated MRSA).  TYPE 3:- Gas Gangrene by clostridial myo necrosis  TYPE 4 (recently placed under of classification)  Fungal cause 179
  135. 135. Sign and symptoms  Small, red, painful lump or bump on the skin- Changes to a very painful bruise-like area and grows rapidly, sometimes in less than an hour  The center may become black and die  The skin may break open and ooze fluid  Severe pain  Bullae formation (thin walled fluid filled blisters)  Other symptoms may include:  Fever, Chills, Sweating, Nausea, Weakness, Lightheadedness or dizziness 180
  136. 136. Sign and symptoms 181
  137. 137. Sign and symptoms… 182
  138. 138. DIAGNOSIS  Laboratory Testing:  elevated WBC, azotemia, abnormal coagulation profiles, and decreased platelet and fibrinogen levels.  elevated lactate and blood glucose levels, hypocalcaemia, hypoalbuminemia, and anemia are also commonly found.  Imaging studies:  Plain radiography, ultrasonography, CT, and MRI have all been used to help diagnose NSTI. 183
  139. 139. X ray findings of necrotizing fasciitis 184
  140. 140. Positive findings of necrotizing fasciitis 185
  141. 141. Differential Dx 186
  142. 142. Treatment  Intravenous antibiotic :Chloramphenicol, Erythromycin.  Process of debridement is done for removal of heavily contaminated tissue and all devitalized tissues by surgery.  Amputations of affected limbs, in some cases.  Hyperbaric oxygen therapy (HBO): Increased oxygen partial pressure has been associated with the reversal of basic pathophysiologic mechanisms of necrosis 187
  143. 143. 8.OSTEOMYELITIS
  144. 144. OSTEOMYELITIS  Osteomyelitis is an infection of the bone.  The bone becomes infected by one of three modes: Extension of soft tissue infection (e.g., infected pressure or vascular ulcer, incisional infection) Direct bone contamination from bone surgery, open fracture, or traumatic injury (e.g., gunshot wound) Hematogenous (bloodborne) spread from other sites of infection (e.g., infected tonsils, boils, infected teeth, upper respiratory infections).
  145. 145. OSTEOMYELITIS  Patients who are at high risk for osteomyelitis include: Poorly nourished, Elderly Obese Impaired immune systems, Chronic illness (e.g., diabetes, rheumatoid arthritis), Long-term corticosteroid therapy
  146. 146. OSTEOMYELITIS  Bone infections are more difficult to eradicate than soft tissue infections because the infected bone becomes walled off.  Natural body immune responses are blocked, and there is less penetration by antibiotics.  Osteomyelitis may become chronic and may affect the patient’s quality of life
  147. 147. OSTEOMYELITIS Clinical Manifestations  If bloodborne sudden onset of the ff manifestations of septicemia like:  chills, high fever, rapid pulse, general malaise  pain, swellining, and extreme tenderness.  Constant, pulsating pain that intensifies with movement as a result of the pressure of the collecting pus.
  148. 148. OSTEOMYELITIS Clinical Manifestations  If from spread of adjacent infection or from direct contamination:  No symptoms of septicemia  Swollen, warm, painful, and tender to touch.  Chronic osteomyelitis Presents with a continuously draining sinus or Recurrent periods of pain, inflammation, swelling, and drainage.
  149. 149. OSTEOMYELITIS Medical Management  IV antibiotic therapy  An antibiotic to which the causative organism is sensitive is prescribed after results of the culture and sensitivity studies are known.  IV antibiotic therapy continues for 3 to 6 weeks.  After the infection appears to be controlled, the antibiotic may be administered orally for up to 3 months.
  150. 150. OSTEOMYELITIS SURGICAL MANAGEMENT  If the patient does not respond to antibiotic therapy, the infected bone is surgically exposed, the purulent and necrotic material is removed, and the area is irrigated with sterile saline solution. Nursing Interventions  Reliefing pain  Improving physical mobility  Controlling the infectious process
  151. 151. OSTEOMYELITIS Prevention  Elective orthopedic surgery should be postponed if the patient has a current infection (e.g., urinary tract infection, sore throat) or a recent history of infection.  Use of aseptic surgical environment and other techniques to decrease direct bone contamination.  Prophylactic antibiotics 24 hours before and after surgery  Aseptic postoperative wound  Prompt management of soft tissue infections
  152. 152. ANKYLOSING SPONDYLITIS  It is a form of arthritis that primarily affects the spine, although other joints can become involved.  It causes inflammation of the spinal joints (vertebrae) that can lead to severe, chronic pain and discomfort.  In more advanced cases this inflammation can lead to ankylosis new bone formation in the spine  causing sections of the spine to fuse in a fixed, immobile position.  AS can also cause inflammation, pain, and stiffness in other areas of the body such as the shoulders, hips, ribs, heels, and small joints of the hands and feet.
  153. 153. ANKYLOSING SPONDYLITIS….  Sometimes the eyes can become involved rarely the lungs and heart can be affected.  The hallmark sign is the involvement of the sacroiliac (SI) joints during the progression of the disease.  The SI joints are located at the base of the spine, where the spine joins the pelvis
  154. 154. 199
  155. 155. Ankylosing Spondylitis  Ankylosing spondylitis affects the cartilaginous joints of the spine and surrounding tissues.  Occasionally, the large synovial joints, such as hips, knees, or shoulders, may be involved.  Ankylosing spondylitis is usually diagnosed in the second or third decade of life.
  156. 156. Ankylosing Spondylitis  Mainly affects men than women.  Back pain is the characteristic feature.  As the disease progresses, ankylosis (stiffness) of the entire spine may occur, leading to respiratory compromise and complications.
  157. 157. Newer SpA Classification System  Axial Spondyloarthritis (AxSpA)  Axial SpA causes inflammation in the spine and/or pelvis that typically brings on inflammatory back pain.  Peripheral Spondyloarthritis (pSpA)  causes inflammation in joints and/or tendons outside the spine or sacroiliac joints. Commonly involved sites include joints in the hands, wrists, elbows, shoulders, knees, ankles, and feet.  Many people with SpA have or will develop both axial SpA and peripheral SpA. Others will have only axial SpA or only peripheral SpA. 202
  158. 158. Ankylosing Spondylitis Medical Management of Spondylitis  Focuses on treating pain and maintaining mobility by suppressing inflammation.  Good body positioning and posture are essential, so that if ankylosis (fixation) does occur, the patient is in the most functional position.  Maintaining range of motion with a regular exercise and muscle-strengthening program is especially important.
  159. 159. Ankylosing Spondylitis Pharmacologic therapy  Salicylates, NSAIDs, and corticosteroids often produce marked improvement in back, skin, and joint symptoms. Surgical management  Surgical management may include total hip replacement. Nursing Management of Spondylitis  Manage symptom and maintain optimal functioning.
  160. 160. 6. ACUTE LOW BACK PAIN
  161. 161. ACUTE LOW BACK PAIN Most low back pain is caused: Acute lumbosacral strain due to lifting heavy objects Unstable lumbosacral ligaments and weak muscles, Osteoarthritis of the spine, Spinal stenosis, Herniated disk Intervertebral disk problems, and Unequal leg length
  162. 162. ACUTE LOW BACK PAIN  In older patients it is associated with osteoporotic vertebral fractures or bone metastasis.  Other causes include: ◦ Kidney disorders, ◦ Pelvic problems, ◦ Retroperitoneal tumors, ◦ Abdominal aneurysms, ◦ Obesity, ◦ Stress,
  163. 163. Causes of low back pain  chemical substances are released in response to tissue irritation.  ―stimulate‖ the surrounding pain sensitive nerve fibers, resulting in the sensation of pain.  Some of these chemicals trigger the process of inflammation, or swelling, which also contributes to pain.  The chemicals associated with this inflammatory process feed back more signals which perpetuate the process of swelling.  The inflammation attributable to this cycle of events may persist for days to weeks. 208
  164. 164. Causes of low back pain…..  Muscular tension (spasm) in the surrounding tissues may occur resulting in a ― trunk shift‖ (the body tilts to one side more than the other) due to muscular imbalance.  Additionally, a relative inhibition or lack of the usual blood supply to the affected area may occur  nutrients and oxygen are not optimally delivered and removal of irritating byproducts of inflammation is impaired. 209
  165. 165. ACUTE LOW BACK PAIN Clinical Manifestations  Acute back pain or  Chronic back pain (lasting more than 3 months without improvement) and  Fatigue.  Pain radiating down the leg, which suggests nerve root involvement.
  166. 166. ACUTE LOW BACK PAIN Clinical Manifestations  The patient’s gait, spinal mobility, reflexes, leg length, leg motor strength, and sensory perception may be altered.  Paravertebral muscle spasm (greatly increased muscle tone of the back postural muscles) with a loss of the normal lumbar curve and possible spinal deformity.
  167. 167. Diagnosed Of back pain  In most cases of acute low back pain, diagnostic testing is not required.  X-ray : in cases of pain associated with severe trauma, history of cancer, fever, diabetes, other medical problems, illicit IV drug use, age over 50, bowel or bladder dysfunction, nocturnal pain or osteoporosis.  CT scan and magnetic resonance imaging (MRI). 212
  168. 168. ACUTE LOW BACK PAIN Medical Management  Most back pain is self-limited and resolves within 4 weeks with analgesics, rest, stress reduction, and relaxation.  Management focuses on relief of pain and discomfort, activity modification, and patient education.  Heat or cold therapy frequently provides temporary relief of symptoms.
  169. 169. Treatment of back pain  Remain active ―as tolerated‖- cardiovascular activities, such as walking,  stretching muscles and tissues in the legs and back during an acute episode, but stretching should not cause more severe pain.  Local application of heat or ice can temporarily reduce pain and heat may facilitate stretching, 214
  170. 170. 7.OSTEOMALACIA
  171. 171. OSTEOMALACIA  Osteomalacia is a metabolic bone disease characterized by:  Inadequate mineralization of bone.  softening and weakening of the skeleton,  causing pain, tenderness to touch, bowing of the bones, and pathologic fractures.  Skeletal deformities (spinal kyphosis and bowed legs) give patients an unusual appearance and a waddling or limping gait.  As a result of calcium deficiency, muscle weakness, and unsteadiness, there is an increased risk for falls and fractures.
  172. 172. OSTEOMALACIA Causes  Deficiency of activated vitamin D (calcitriol),  Failed calcium absorption (e.g., malabsorption syndrome) or from excessive loss of calcium from the body.  Liver and kidney diseases can produce a lack of vitamin D because these are the organs that convert vitamin D to its active form.  Hyperparathyroidism  Deficiency in vitamin D often associated with poor intake of calcium (malnutrition)
  173. 173. OSTEOMALACIA Medical Management  Correcting underlying cause of  If osteomalacia is caused by malabsorption, increased doses of vitamin D, along with supplemental calcium.  Exposure to sunlight for ultraviolet radiation to transform a cholesterol substance (7-dehydrocholesterol) present in the skin into vitamin D may be recommended.
  174. 174. OSTEOMALACIA Medical Management  If osteomalacia is dietary in origin, a diet with adequate protein and increased calcium and vitamin D is provided  Dietary sources of calcium and vitamin D (eg, fortified milk and cereals, eggs, chicken livers) are recommended
  175. 175. 9. Bone Tumors
  176. 176. Bone Tumors  Neoplasms of the musculoskeletal system are of various types, including osteogenic, chondrogenic, fibrogenic, muscle (rhabdomyogenic), and marrow (reticulum) cell tumors as well as nerve, vascular and fatty cell tumors.  They may be primary tumors or metastatic tumors from primary cancers elsewhere in the body (e.g., breast, lung, prostate, kidney).  Metastatic bone tumors are more common than primary bone tumors.
  177. 177. Bone Tumors Benign Bone Tumors  Benign tumors of the bone and soft tissue are more common than malignant primary bone tumors.  Benign bone tumors generally are slow growing and well circumscribed, present few symptoms, and are not a cause of death.
  178. 178. Bone Tumors Benign Bone Tumors  Benign primary neoplasms of the musculoskeletal system include: Osteochondroma (tumor of bone), Enchondroma (tumor of hyaline cartilage), Osteoid osteoma (painful tumor in children and young adults), Rhabdomyoma, and Fibroma  Some benign tumors, such as giant cell tumors, have the potential to become malignant.
  179. 179. Bone Tumors Malignant Bone Tumors  Primary malignant musculoskeletal tumors are relatively rare.  Malignant primary musculoskeletal tumors include: Osteosarcoma, Chondrosarcoma, Ewing’s sarcoma, and Fibrosarcoma.
  180. 180. Bone Tumors Malignant Bone Tumors  Soft tissue sarcomas include: Liposarcoma, Fibrosarcoma of soft tissue, and Rhabdomyosarcoma.  Bone tumor metastasis to the lungs is common.
  181. 181. Bone Tumors Metastatic bone disease  Metastatic bone disease (secondary bone tumor) is more common than any primary bone tumor.  Tumors arising from tissues elsewhere in the body may invade the bone and produce localized bone destruction (lytic lesions) or bone overgrowth (blastic lesions).
  182. 182. Bone Tumors Metastatic bone disease  The most common primary sites of tumors that metastasize to bone are: The kidneys, Prostate, Lung, Breast, Ovary, and Thyroid.
  183. 183. Bone Tumors Metastatic bone disease  Metastatic tumors most frequently attack the: Skull, Spine, Pelvis, Femur, and Humerus and involve more than one bone (polyostotic).
  184. 184. Bone Tumors Clinical Manifestations  Some may be symptom free or  have pain (mild and occasional to constant and severe),  varying degrees of disability and,  at times, obvious bone growth.  Weight loss, malaise, and fever may be present.  The tumor may be diagnosed only after pathologic fracture has occurred.
  185. 185. Bone Tumors Clinical Manifestations  With spinal metastasis, spinal cord compression may occur.  It can progress rapidly or slowly.  Neurologic deficits (eg, progressive pain, weakness, gait abnormality, paresthesia, paraplegia, urinary retention, loss of bowel or bladder control)
  186. 186. Bone Tumors Medical Management PRIMARY BONE TUMORS  The goal of primary bone tumor treatment is to destroy or remove the tumor.  Surgical excision (ranging from local excision to amputation and disarticulation),  Radiation therapy if the tumor is radiosensitive,  Chemotherapy (preoperative, intraoperative, postoperative, and adjunctive for possible micrometastases).
  187. 187. Bone Tumors Medical Management METASTATIC BONE DISEASE  The treatment of metastatic bone cancer is palliative.  The therapeutic goal is to relieve the patient’s pain and discomfort while promoting quality of life.
  188. 188. Bone Tumors Nursing Interventions  Similar in many respects to that of other patients who have had skeletal surgery.  Vital signs are monitored;  Blood loss is assessed; and  Observations are made to assess for the development of complications.
  189. 189. Trauma and Soft Tissue Injuries
  190. 190. 1, Contusions, Strains, and Sprains
  191. 191. Contusions, Strains, and Sprains  Contusion: is a soft tissue injury produced by blunt force, such as a blow, kick, or fall.  Many small blood vessels rupture and bleed into soft tissues (ecchymosis, or bruising).  A hematoma develops when the bleeding is sufficient to cause an appreciable collection of blood.  Local symptoms (pain, swelling, and discoloration) are controlled with intermittent application of cold.  Most contusions resolve in 1 to 2 weeks.
  192. 192. Contusions, Strains, and Sprains  Strain: is a ―muscle pull‖ caused by overuse, overstretching, or excessive stress.  Strains are microscopic, incomplete muscle tears with some bleeding into the tissue.  The patient experiences soreness or sudden pain, with local tenderness on muscle use and isometric contraction.
  193. 193. Contusions, Strains, and Sprains  Sprain: is an injury to the ligaments surrounding a joint that is caused by a wrenching or twisting motion.  The function of a ligament is to maintain stability while permitting mobility.  A torn ligament loses its stabilizing ability.  Blood vessels rupture and edema occurs; the joint is tender, and movement of the joint becomes painful.
  194. 194. Contusions, Strains, and Sprains  Sprain:  The degree of disability and pain increases during the first 2 to 3 hours after the injury because of the associated swelling and bleeding.  An x-ray should be obtained to rule out bone injury.  Avulsion fracture (in which a bone fragmented is pulled away by a ligament or tendon) may be associated with a sprain.
  195. 195. Contusions, Strains, and Sprains Management  Treatment of contusions, strains, and sprains consists of resting and elevating the affected part, applying cold, and using a compression bandage.  (The acronym RICE Rest, Ice, Compression, Elevation—is helpful for remembering treatment interventions.)
  196. 196. Contusions, Strains, and Sprains Management  Rest prevents additional injury and promotes healing.  Moist or dry cold applied intermittently for 20 to 30 minutes during the first 24 to 48 hours after injury produces vasoconstriction, which decreases bleeding, edema, and discomfort.  Care must be taken to avoid skin and tissue damage from excessive cold.
  197. 197. Contusions, Strains, and Sprains Management  An elastic compression bandage controls bleeding, reduces edema, and provides support for the injured tissues.  Elevation controls the swelling.  If the sprain is severe (torn muscle fibers and disrupted ligaments), surgical repair or cast immobilization may be necessary so that the joint will not lose its stability.  The neurovascular status (circulation, motion, sensation) of the injured extremity is monitored frequently.
  198. 198. 2, Joint Dislocations
  199. 199. Joint Dislocations  A dislocation of a joint is a condition in which the articular surfaces of the bones forming the joint are no longer in anatomic contact.  The bones are literally ―out of joint.‖  A subluxation is a partial dislocation of the articulating surfaces.
  200. 200. Joint Dislocations  Traumatic dislocations are orthopedic emergencies because the associated joint structures, blood supply, and nerves are distorted and severely stressed.  If the dislocation is not treated promptly, avascular necrosis (tissue death due to anoxia and diminished blood supply) and nerve palsy may occur.
  201. 201. Joint Dislocations  Dislocations may be congenital, or present at birth (most often the hip); spontaneous or pathologic, caused by disease of the articular or periarticular structures; or traumatic, resulting from injury in which the joint is disrupted by force.
  202. 202. Joint Dislocations  Signs and symptoms of a traumatic dislocation are: pain, change in contour of the joint, change in the length of the extremity, loss of normal mobility, and change in the axis of the dislocated bones.  X-rays confirm the diagnosis and demonstrate any associated fracture.
  203. 203. Joint Dislocations Medical Management  The affected joint needs to be immobilized while the patient is transported to the hospital.  The dislocation is promptly reduced (ie, displaced parts are brought into normal position) to preserve joint function.  Analgesia, muscle relaxants, and possibly anesthesia are used to facilitate closed reduction.  The joint is immobilized by bandages, splints, casts, or traction and is maintained in a stable position.
  204. 204. Joint Dislocations Medical Management  Neurovascular status is monitored.  After reduction, if the joint is stable, gentle, progressive, active and passive movement is begun to preserve range of motion (ROM) and restore strength.  The joint is supported between exercise sessions.
  205. 205. Joint Dislocations Nursing Management  Nursing care is directed at:  Providing comfort,  evaluating the patient’s neurovascular status, and  protecting the joint during healing  Teaching the patient how to manage the immobilizing devices and how to protect the joint from reinjury.
  206. 206. 3. Fractures
  207. 207. Fractures  A fracture is a break in the continuity of bone and is defined according to its type and extent.  Fractures occur when the bone is subjected to stress greater than it can absorb.  Fractures are caused by direct blows, crushing forces, sudden twisting motions, and even extreme muscle contractions.
  208. 208. Fractures  When the bone is broken, adjacent structures are also affected,  Resulting in soft tissue edema, hemorrhage into the muscles and joints, joint dislocations, ruptured tendons, severed nerves, and damaged blood vessels.  Body organs may be injured by the force that caused the fracture or by the fracture fragments.
  209. 209. Types of Fractures  Based on cross-section of the bone involved: 1. Complete fracture: involves a break across the entire cross-section of the bone and is frequently displaced (removed from normal position). 2. Incomplete fracture (eg, greenstick fracture): the break occurs through only part of the cross-section of the bone. 3. Comminuted fracture: is one that produces several bone fragments.
  210. 210. Types of Fractures  Based on involvement of the skin: 1. Closed fracture (simple fracture): is one that does not cause a break in the skin. 2. Open fracture (compound, or complex, fracture): is one in which the skin or mucous membrane wound extends to the fractured bone.
  211. 211. Types of Fractures  Open fractures are graded according to the following criteria: ◦ Grade I: is a clean wound less than 1 cm long. ◦ Grade II: is a larger wound without extensive soft tissue damage. ◦ Grade III: is highly contaminated, has extensive soft tissue damage, and is the most severe.  Fractures may also be described according to the anatomic placement of fragments, particularly if they are displaced or nondisplaced.
  212. 212. Fracture Clinical Manifestations  The clinical manifestations of a fracture are: ◦ pain, ◦ loss of function, ◦ deformity, ◦ shortening of the extremity, ◦ crepitus (a grating sensation palpation), and ◦ local swelling and discoloration.  Not all of these clinical manifestations are present in every fracture.
  213. 213. Emergency Management of Fractures  Immediately after injury, whenever a fracture is suspected, it is important to immobilize the body part before the patient is moved.  If an injured patient must be removed from a vehicle before splints can be applied,  The extremity is supported above and below the fracture site to prevent rotation as well as angular motion.
  214. 214. Emergency Management of Fractures  With an open fracture, the wound is covered with a clean (sterile) dressing 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.
  215. 215. Medical Management of Fractures 1. REDUCTION  Reduction of a fracture (―setting‖ the bone) refers to restoration of the fracture fragments to anatomic alignment and rotation. 1. Closed Reduction: closed reduction is accomplished by bringing the bone fragments into apposition (ie, placing the ends in contact) through manipulation and manual traction. 2. Open Reduction. Through a surgical approach, the fracture fragments are reduced. Internal fixation devices (metallic pins, wires, screws, plates, nails, or rods) may be used to hold the bone fragments in position
  216. 216. Medical Management of Fractures 2. IMMOBILIZATION  After the fracture has been reduced,  The bone fragments must be immobilized, or held in correct position and alignment, until union occurs.  Immobilization may be accomplished by external or internal fixation.
  217. 217. Medical Management of Fractures 3. MAINTAINING AND RESTORING FUNCTION  Reduction and immobilization are maintained as prescribed to promote bone and soft tissue healing.  Swelling is controlled by elevating the injured extremity and applying ice as prescribed.  Neurovascular status (circulation, movement, sensation) is monitored, and the orthopedic surgeon is notified immediately if signs of neurovascular compromise are identified.  Isometric and muscle-setting exercises are encouraged to minimize disuse atrophy and to promote circulation.
  218. 218. Complications of Fracture  Complications of fractures fall into two categories—early and delayed.  Early complications include:  Shock,  Fat embolism,  Compartment syndrome,  Deep vein thrombosis,  Thromboembolism (pulmonary embolism),  Disseminated intravascular coagulopathy (DIC), and  Infection.
  219. 219. Complications of Fracture  Delayed complications include: Delayed union and nonunion, Avascular necrosis of bone, Reaction to internal fixation devices, Complex regional pain syndrome (formerly called reflex sympathetic dystrophy), and Heterotrophic ossification.
  220. 220. Care of the Patient in a Cast 267
  221. 221. Care of the Patient in a Cast 268  A cast is a rigid external immobilizing device that is molded to the contours of the body.  It permit mobilization of the patient while restricting movement of a body part.  The purposes of a cast are:  To immobilize a body part in a specific position,  To apply uniform pressure on encased soft tissue,  To immobilize a reduced fracture,  to correct a deformity,  To apply uniform pressure to underlying soft tissue, or  To support and stabilize weakened joints.
  222. 222. Types of Cast 269  Short arm cast: Extends from below the elbow to the palmar crease, secured around the base of the thumb. If the thumb is included, it is known as a thumb spica or gauntlet cast.  Long arm cast: Extends from the upper level of the axillary fold to the proximal palmar crease. The elbow usually is immobilized at a right angle.  Short leg cast: Extends from below the knee to the base of the toes. The foot is flexed at a right angle in a neutral position.
  223. 223. Types of Cast 270  Long leg cast: Extends from the junction of the upper and middle third of the thigh to the base of the toes. The knee may be slightly flexed.  Walking cast: A short or long leg cast reinforced for strength.  Body cast: Encircles the trunk.  Shoulder spica cast: A body jacket that encloses the trunk and the shoulder and elbow.  Hip spica cast: Encloses the trunk and a lower extremity. A double hip spica cast includes both legs.
  224. 224. CASTING MATERIALS 271  Nonplaster (fiberglass casts): they are water- activated polyurethane materials and have the versatility of plaster but are lighter in weight, stronger, water resistant, and durable.  Plaster (POP): Rolls of plaster bandage are wet in cool water and applied smoothly to the body.  The plaster cast requires 24 to 72 hours to dry completely, depending on its thickness and the environmental drying conditions.
  225. 225. Management of undried cast 272  While damp (wet), the cast can be dented. Therefore, it must be handled with the palms of the hand and not allowed to rest on hard surfaces or sharp edges should be exposed to circulating air to dry and should not be covered with clothing or bed linens
  226. 226. Management of undried cast 273  Cast dents may press on the skin causing irritation and skin breakdown.  A wet plaster cast appears dull and gray, sounds dull on percussion, feels damp, and smells musty.  A dry plaster cast is white and shiny, resonant, odorless, and firm.
  227. 227. POTENTIAL COMPLICATIONS OF CAST AND THEIR MANAGEMENT 274 Compartment Syndrome  Compartment syndrome occurs when there is increased tissue pressure within a limited space (eg, cast, muscle compartment) that compromises the circulation and the function of the tissue within the confined area.
  228. 228. POTENTIAL COMPLICATIONS OF CAST AND THEIR MANAGEMENT275 Compartment Syndrome  Management: To relieve the pressure, the cast must be bivalved (cut in half longitudinally) while maintaining alignment, and the extremity must be elevated no higher than heart level.  If pressure is not relieved and circulation is not restored, a fasciotomy may be necessary to relieve the pressure within the muscle compartment.  The nurse records neurovascular responses and promptly reports changes to the physician.
  229. 229. POTENTIAL COMPLICATIONS OF CAST AND THEIR MANAGEMENT276 Pressure Ulcers  Pressure of the cast on soft tissues may cause tissue anoxia and pressure ulcers.  Lower extremity sites most susceptible to pressure are the heel, malleoli, dorsum of the foot, head of the fibula, and anterior surface of the patella.
  230. 230. POTENTIAL COMPLICATIONS OF CAST AND THEIR MANAGEMENT277 Pressure Ulcers  Management: To inspect the pressure area, the physician may bivalve the cast or cut an opening (window) in the cast.  If the physician elects to create a window to inspect the pressure site, a portion of the cast is cut out.  The portion of the cast is replaced and held in place by an elastic compression dressing or tape.  This prevents the underlying tissue from swelling through the window and creating pressure areas around its margins.
  231. 231. POTENTIAL COMPLICATIONS OF CAST AND THEIR MANAGEMENT278 Disuse Syndrome  While in a cast, the patient needs to learn to tense or contract muscles (eg, isometric muscle contraction) without moving the part.  This helps to reduce muscle atrophy and maintain muscle strength.
  232. 232. POTENTIAL COMPLICATIONS OF CAST AND THEIR MANAGEMENT279 Disuse Syndrome  Management: The nurse teaches the patient with a leg cast to ―push down‖ the knee and teaches the patient in an arm cast to ―make a fist.‖  Muscle-setting exercises (e.g., quadriceps-setting and gluteal setting exercises) are important in maintaining muscles essential for walking.  Isometric exercises should be performed hourly while the patient is awake.
  233. 233. Managing the Patient in Traction 280
  234. 234. Managing the Patient in Traction 281  Traction is the application of a pulling force to a part of the body.  Traction is used: to minimize muscle spasms; to reduce, align, and immobilize fractures;  to reduce deformity; and  to increase space between opposing surfaces.
  235. 235. Managing the Patient in Traction 282  Traction must be applied in the correct direction and magnitude to obtain its therapeutic effects.  As muscle and soft tissues relax, the amount of weight used may be changed to obtain the desired effect.  The effects of traction are evaluated with x-ray studies, and adjustments are made if necessary.  Traction is used primarily as a short-term intervention until other modalities, such as external or internal fixation, are possible.  At times, traction needs to be applied in more than one direction to achieve the desired line of pull.
  236. 236. PRINCIPLES OF EFFECTIVE TRACTION 283 1. Whenever traction is applied, counter-traction (forces in opposite direction) must be used to achieve effective traction. 2. Traction must be continuous to be effective in reducing and immobilizing fractures. 3. Skeletal traction is never interrupted. 4. Weights are not removed unless intermittent traction is prescribed. 5. Any factor that might reduce the effective pull or alter its resultant line of pull must be eliminated.
  237. 237. TYPES OF TRACTION 284  Straight or running traction: applies the pulling force in a straight line with the body part resting on the bed. E.g. Buck’s extension traction  Balanced suspension traction (Fig. 67-5): supports the affected extremity off the bed and allows for some patient movement without disruption of the line of pull.  Skin traction: Traction applied to the skin.
  238. 238. TYPES OF TRACTION 285  Skeletal traction: traction directly applied to the bony skeleton.  The mode of application is determined by the purpose of the traction.  Manual traction: Traction applied with the hands.  This is temporary traction that may be used when applying a cast, giving skin care under a Buck’s extension foam boot, or adjusting the traction apparatus.
  239. 239. 286
  240. 240. Potential Complications of Skin Traction287  Skin breakdown,  nerve pressure, and  circulatory impairment
  241. 241. Nursing Interventions 288  Monitor and prevent skin breakdown  Regularly assess sensation and motion.  Immediately investigate any complaint of burning sensation under the traction bandage or boot.  Promptly report altered sensation or motor function.  Circulatory assessment consists of the following:  Peripheral pulses, color, capillary refill, and temperature of the fingers or toes  Indicators of DVT, including calf tenderness, and swelling.
  242. 242. Nursing Interventions for Skin Traction289  Maintaining effective traction  Maintaining positioning  Preventing skin break down  Monitoring neurovascular status  Promoting pin site care  Promoting exercise (iso-metric excersice for immobilized parts)
  243. 243. Amputation 290
  244. 244. Amputation 291  Amputation is the removal of a body part, usually an extremity.  Amputation of a lower extremity is often made necessary by progressive peripheral vascular disease (often a sequela of diabetes mellitus), fulminating gas gangrene, trauma (crushing injuries, burns, frostbite, and electrical burns), congenital deformities, chronic osteomyelitis, or malignant tumor.  Of all these causes, peripheral vascular disease accounts for most amputations of lower extremities.
  245. 245. Purposes of Amputation 292  Amputation is used to: relieve symptoms, improve function, and save or improve the patient’s quality of life.
  246. 246. Levels of Amputation 293  Amputation is performed at the most distal point that will heal successfully.  The site of amputation is determined by two factors: 1. circulation in the part, and 2. functional usefulness (ie, meets the requirements for the use of the prosthesis).  The objective of surgery is to conserve as much extremity length as possible.  Preservation of knee and elbow joints is desired. Almost any level of amputation can be fitted with a prosthesis.
  247. 247. 294
  248. 248. Levels of Amputation 295  Upper extremity amputations are performed to preserve themaximum functional length.  The prosthesis is fitted early for maximum function.  A staged amputation may be used when gangrene and infection exist. Initially, a guillotine amputation is performed to remove the necrotic and infected tissue.  The wound is débrided and allowed to drain. Sepsis is treated with systemic antibiotics.  After the infection has been controlled and the patient’s condition has stabilized, a definitive amputation with skin closure is performed.
  249. 249. Complications of Amputation 296  Complications that may occur with amputation include: hemorrhage, infection, skin breakdown, phantom limb pain, and joint contracture
  250. 250. Medical Management 297  The objective of treatment is to achieve healing of the amputation wound, the result being a non tender residual limb (stump) with healthy skin for prosthesis use.  Healing is enhanced by gentle handling of the residual limb, control of residual limb edema through rigid or soft compression dressings, and use of aseptic technique in wound care to avoid infection.
  251. 251. Medical Management 298  A closed rigid cast dressing is frequently used to provide uniform, to support soft tissues, to control pain, and to prevent joint contractures.  Immediately after surgery, a sterilized residual limb sock is applied to the residual limb.  Felt pads are placed over pressure-sensitive areas.  The residual limb is wrapped with elastic plaster-of- paris (POP) bandages while firm, even pressure is maintained.  Care is taken not to constrict circulation.
  252. 252. Medical Management 299  A removable rigid dressing may be placed over a soft dressing to control edema, to prevent joint flexion contracture, and to protect the residual limb from unintentional trauma during transfer activities.  This rigid dressing is removed several days after surgery for wound inspection and is then replaced to control edema.  The dressing facilitates residual limb shaping.
  253. 253. Medical Management 300  A soft dressing with or without compression may be used if there is significant wound drainage and frequent inspection of the residual limb (stump) is desired.  An immobilizing splint may be incorporated in the dressing.  Stump (wound) hematomas are controlled with wound drainage devices to minimize infection.
  254. 254. Medical Management 301  Rehabilitation: Because the amputation is the result of an injury, the patient needs psychological support in accepting the sudden change in body image and in dealing with the stresses of hospitalization, long-term rehabilitation, and modification of lifestyle.  Patients who undergo amputation need support as they grieve the loss, and they need time to work through their feelings about their permanent loss and change in body image.
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Musculoskeletal disorders


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