Oa Knee: Orthopedics Lecture PDF

OA KNEE PROF HATEM ELGOHARY  PROF OF ORTHOPEDIC SURGERY Kafr Elsheikh university Excutive director of Kafrelsheikh university hospitals Member of the international society of orthop. Surgery (SICOT)Paris Member of the pediatric orthopedic society (EG...

OA KNEE PROF HATEM ELGOHARY  PROF OF ORTHOPEDIC SURGERY Kafr Elsheikh university Excutive director of Kafrelsheikh university hospitals Member of the international society of orthop. Surgery (SICOT)Paris Member of the pediatric orthopedic society (EGPOS) Member of the arthroscopy society(EGAA) fellow of knee and shoulder surgery and sports injuries center. Safderjunk hospital. New Delhi. OA KNEE Chronic, degenerative disorder of multifactorial aetiology, characterised by loss of articular cartilage and periarticular bone remodelling,  particularly large weight- bearing joints Common in older patients but can occur in younger patients ( genetic mechanism , previous joint trauma ) Pathophysiology Degenerative alterations primarily begin in the articular cartilage External forces accelerate the catabolic effects of the chondrocytes and disrupt the cartilaginous matrix Enzymatic destruction increases cartilage degradation ↓ proteoglycans and collagen synthesis Pathophysiology Loss of cartilage results in the loss of the joint space Progressive erosion of the damaged cartilage occurs until the underlying bone is exposed Subchondral bone responds with vascular invasion and increased cellularity. Pathophysiology At areas of pressure the traumatized subchondral bone may undergo cystic degeneration At nonpressure areas along the articular margin → irregular outgrowth of new bone (osteophytes)  Surface layer of cartilage break down and wears away,causes the bones under the cartilage to rub together Pain, swelling, and loss of motion result formation of bone spurs Incidence Incidence increases with age After age 55 years, the prevalence increases in women in comparison with men Incidence Equivalent prevalence occurs in men and women aged 45-55 years Most adults older than 55 years show radiographic evidence of osteoarthritis No significant correlation exists between incidence of OA and race  Causes PRIMARY No (major) causative reason known i. genetic predisposition ii.Gender iii.Aging iv.Obesity v.Physical activity  Causes SECONDARY Articular gout Bone infarction Endocrine disorders (e.g., hyperparathyroidism) Hemophilia Intra-articular infections Joint instability (e.g., meniscus lesions) Neuropathy (e.g., Charcot’s joint) Overload causing excessive wear (work, sport, varus or valgus deformity) Paget’s disease Psoriatic arthritis Rheumatic disease Trauma  History Insidious throbbing arthralgias with activity Initially, resting relieves the pain Eventually, the pain occurs even at rest Morning stiffness ≥ 30 minutes Intermittent joint swelling Symptoms Pain Stiffness Instability  Signs Tenderness Swelling Effusion Crepitus Limitation of movement and muscle wasting  Imaging Plain radiographs Bone scans may be helpful in early diagnosis of OA.  The space between the bones is smaller Bony spurs (osteophytes) Increase bone density at the margin of the joint x-ray findings Joint space narrowing Osteophytes Subchondral sclerosis : ↑ bone density, frequently found adjacent to joint space Subchondral cysts : fluid-filled sacs which extrude from the joint Diagnosis On the basis of the initial history and examination X-rays Treatment Goals of managing OA Controlling pain Maintaining and improving the range of movement and stability of affected joints Limiting functional impairment  Treatment Education and behavioural intervention - Aim is to provide patients with an understanding of the disease process, its prognosis and the rationale and implications of managing their condition  Weight loss - Weight loss (5 kg) has significant short-term and long-term reduction in symptoms of OA  Mechanical aids :Wear shock-absorbing footwear Exercise:Aim of exercise is to reduce pain and disability by strengthening muscle, improving joint stability and increasing the range of movement. Treatment Medication - Acetaminophen is a mild pain reliever with few side effects Anti-inflammatory medication, such as ibuprofen and aspirin COX-2 inhibitors Glucosamine and Chondroitin sulfate Treatment Intra-articular injection - Glucocorticoids injection - Hyaluronic Acid (HA) Treatment Surgery Arthroscopy ( debridement) Proximal Tibial Osteotomy Artificial Knee Replacement Chondromalacia = soft cartilage  First described (1906) fissures occurring in the articular cartilage of the patella, may be traumatic in origin. The term chondromalacia developed in 1928 Other names: Patellofemoral overlaod syndrome Patellar pain syndrome AKP syndrome Runner’s knee  On examination Positive patellar facet tenderness test Positive patellofemoral compression tests Patellar crepitation: is the grater sound with manual transversal displacement of the patella.  Pathology The abnormality most commonly seen in chondromalacia patellae is fibrillation of the articular cartilage.  The cartilage changes are most commonly observed at the junction of the medial and odd facets of the patella Softening Swelling Fraying Fissuring Erosion of cartilage  Malalignment Abnormal loading Articular cartilage breakdown by repetitive shearing stresses leading to damage of the superficial chondrocytes which expose the innervated subjacent subchondral bone causing pain.  Radiological diagnosis Xrays CT scan MRI AP view Lateral Skyline Knee view in 30 view aligment flex Merchant Varus or Patellar valgus height view Arthroscopy  NON OPERATIVE TREATMENT 90% Restore muscle balance – Quad ex – VMO ex – Gluteal and hamstring – ITB stritching NSAIDs Restrict activities A knee brace Proper shoes  Surgery a conservative treatment programme lasting at least 6 months should be tried as a general rule before surgery is decided.  Surgery Arthroscopic debridement Correct malalignment If tight lateral retinaculum: lateral release or lengthening Trochleoplasty Patellofemoral replacement