AVASCULAR NECROSIS DEFINITION Avascular necrosis (also osteonecrosis, bone infarction,[1] aseptic necrosis, ischemic bone necrosis,[2] and

AVN) is a disease where there is cellular death (necrosis) of bone components due to interruption of the blood supply.[3] Without blood, the bone tissue dies and the bone collapses.[2] If avascular necrosis involves the bones of a joint, it often leads to destruction of the joint articular surfaces (see Osteochondritis dissecans). Avascular necrosis (AVN) is defined as cellular death of bone components due to interruption of the blood supply; the bone structures then collapse, resulting in bone destruction, pain, and loss of joint function. AVN is associated with numerous conditions and usually involves the epiphysis of long bones, such as the femoral and humeral heads and the femoral condyles, but small bones can also be affected. In clinical practice, AVN is most commonly encountered in the hip. Recently, AVN of the jaw associated with bisphosphonate use has also been described. CLINICAL MANIFESTATION Joint pain under weight - initially only when putting weight on the joint Joint pain resting - then over time pain also on resting. Severe joint pain - if the disease progresses Limited joint mobility Bone pain Pain on standing Pain on walking Pain on lifting Progressive pain Muscle spasms Joint stiffness Limited range of motion PREDISPOSING FACTOR There are many theories about what causes avascular necrosis. Proposed risk factors include, chemotherapy, alcoholism,[4] excessive steroid use,[5] post trauma,[6][7] caisson disease (decompression sickness),[8][9] vascular compression,[10] hypertension, vasculitis, arterial embolism and thrombosis, damage from radiation, bisphosphonates (particularly the mandible),[11] sickle cell anaemia,[12] Gaucher's Disease,[13] and deep diving.[14] In some cases it isidiopathic (no cause is found).[15] Rheumatoid arthritis and lupus are also common causes of AVN. Prolonged, repeated exposure to high pressures (as experienced by commercial and military divers) has been linked to AVN, though the relationship is not wellunderstood. PATHOPHYSIOLOGY Although the pathophysiology of AVN is not fully understood, the final common pathway is interruption of blood flow to the bone. AVN affects bones with a single terminal blood supply, such as the femoral head, carpals, talus, and humerus. These bones have limited collateral circulation. Interruption of the vascular supply and resultant necrosis of marrow, medullary bone, and cortex are theorized to be caused by the mechanisms listed below. However, individual patients usually have more than one risk factor; this indicates that the pathogenesis of AVN is likely multifactorial.

Vascular occlusion: This is characterized by the interruption of the extraosseous blood supply via factors such as direct trauma (eg,fracture, dislocation), nontraumatic stress, and stress fracture. Altered lipid metabolism: Animal studies have led to the hypothesis that increased levels of serum lipids leads to lipid deposition in the femoral head, causing femoral hypertension and ischemia.[2] Lipid-level lowering drugs in animals reverse this process. Corticosteroid administration was associated with fat emboli in the femoral heads of rabbits.[3] Intravascular coagulation: Disorders of the coagulation system have been implicated in the pathogenesis of AVN. Typically, it is a secondary event triggered by a familial thrombophilia, hypercholesterolemia, allograft organ rejection, other disorders (eg, infection, malignancy), or pregnancy. Healing process: Necrotic bone triggers a process of repair that includes osteoclasts, osteoblasts, histiocytes, and vascular elements. Osteoblasts build new bone on top of the dead bone, leading to a thick scar that prevents revascularization of the necrotic bone, with resultant abnormal joint remodeling and joint dysfunction. Primary cell death: Osteocyte death without other features of AVN has been seen in renal transplant patients, as well as in patients receiving steroids and those who consume significant amounts of alcohol. Mechanical stress: Animal studies have shown an association between increased weight bearing and an increased incidence of AVN of the femoral head. DIAGNOSTIC TEST y X Ray An x ray is a common tool that the doctor may use to help diagnose the cause of joint pain. It is a simple way to produce pictures of bones. The x ray of a person with early avascular necrosis is likely to be normal because x rays are not sensitive enough to detect the bone changes in the early stages of the disease. X rays can show bone damage in the later stages, and once the diagnosis is made, they are often used to monitor the course of the condition. y Magnetic Resonance Imaging (MRI) MRI is quickly becoming a common method for diagnosing avascular necrosis. Unlike x rays, bone scans, and CT (computed/computerized tomography) scans, MRI detects chemical changes in the bone marrow and can show avascular necrosis in its earliest stages. MRI provides the doctor with a picture of the area affected and the bone rebuilding process. In addition, MRI may show diseased areas that are not yet causing any symptoms. y Bone Scan Also known as bone scintigraphy, bone scans are used most commonly in patients who have normal x rays. A harmless radioactive dye is injected into the affected bone and a picture of the bone is taken with a special camera. The picture shows how the dye travels through the bone and where normal bone formation is occurring. A single bone scan finds all areas in the body that are affected, thus reducing the need to expose the patient to more radiation. Bone scans do not detect avascular necrosis at the earliest stages. y Computed/Computerized Tomography A CT scan is an imaging technique that provides the doctor with a three-dimensional picture of the bone. It also shows "slices" of the bone, making the picture much clearer than x rays and bone scans. Some doctors disagree about the usefulness of this test to diagnose avascular necrosis. Although a diagnosis usually can be made without a CT scan, the technique may be useful in determining the extent of bone damage. y Biopsy A biopsy is a surgical procedure in which tissue from the affected bone is removed and studied. Although a biopsy is a conclusive way to diagnose avascular necrosis, it is rarely used because it requires surgery. y Functional Evaluation of Bone

Tests to measure the pressure inside a bone may be used when the doctor strongly suspects that a patient has avascular necrosis, despite normal results of x rays, bone scans, and MRIs. These tests are very sensitive for detecting increased pressure within the bone, but they require surgery. MEDICAL INTERVENTION AVN is staged from 0 to stage VI. Medical management depends upon the stage of disease being treated. However, no medical management has been demonstrated to prevent and arrest AVN. Limited weight bearing and pain control can be used if the involvement is less than 15% and removed from a weight bearing region. Immobilization is sometimes used. Preliminary studies have been done on the use of bisphosphonates. Statin use is also being investigated. There is really no consensual surgical treatment of AVN. In those stages that are precollapse, core decompression and possibly bone graft is the most common surgical procedure. Later in the disease, femoral head necrosis is most commonly treated with arthroplasty SURGICAL INTERVENTION Avascular necrosis is especially common in the hip joint. A variety of methods are now used to treat avascular necrosis,[21] the most common being the total hip replacement, or THR. However, THRs have a number of downsides including long recovery times and short life spans. THRs are an effective means of treatment in the geriatric population, however doctors shy away from using them in younger patients due to the reasons above. A new, more promising treatment is hip resurfacing or metal on metal (MOM) resurfacing. It is a form of a THR, however in this procedure, only the head of the femur is removed as opposed to a THR in which the entire neck is removed. MOM resurfacing is still experimental in America but has been endorsed in Great Britain as an excellent alternative to a THR. A MOM Resurfacing may not be suitable in all cases of Avascular Necrosis, its suitability depends on how much damage has occurred to the femoral head of the patient, bone is always undergoing change or remodelling.[25] The bone is broken down by osteoclasts and rebuilt by osteoblasts.[25] Some doctors also prescribe bisphosphonates (e.g. alendronate) which reduces the rate of bone breakdown by osteoclasts, thus preventing collapse (specifically of the hip) due to AVN.[26] Other treatments include core decompression, where internal bone pressure is relieved by drilling a hole into the bone, and a living bone chip and an electrical device to stimulate new vascular growth are implanted; and the free vascular fibular graft (FVFG), in which a portion of the fibula, along with its blood supply, is removed and transplanted into the femoral head.[27] Progression of the disease could possibly be halted by transplanting nucleated cells from bone marrow into avascular necrosis lesions after core decompression, although much further research is needed to establish this technique.[28]

RICKETS DEFINITION Rickets is a pediatric disorder not commonly encountered by physicians in the US. Nevertheless, the podiatric physician should be aware that it persists and may exist in children who initially present with gait disturbances or failure to thrive. By using routine plain film radiography of the child's foot, the podiatric physician can screen one of the child's most rapid sites of secondary osseous growth, ie, the distal tibia. A brief overview of the rachitic and osteomalacic disorders is presented, followed by a discussion centered primarily on the plain film radiologic diagnosis of rickets. CLINICAL MANIFESTATION Rachitic children are apathetic, irritable, with a height and weight below the 3rd percentile Dentition is delayed, often they have severe caries and defective enamel Spine often has long, smooth dorsal kyphosis (rachitic catback) and the chest shows enlargement of the costal cartilages (rachitic rosary) The extremities are most profoundly affected. Long bones are shortened and deformed, ligamentous laxity is common, and fractures are common. PREDISPOSING FACTORS Deficiency- vitamin D intake is inadequate which causes diminished absorption of Ca from the gut. Gastrointestinal- interference with bile salt production which interferes with absorption of the fat soluble vitamin D. Ingested Ca forms an insoluble soap with free fatty acids and is lost in the feces. Vitamin D-Resistant Rickets- four main types. Phosphate diabetes- vit D and Ca are normal but are hypophosphatemic and cannot mineralize skeleton. Decrease in 1,25-dihydroxyvitamin D production- cannot convert 25-hydroxyvitamin D to 1,25 form and thus cannot absorb Ca. End-organ insensitivity- gut cell is insensitve to 1,25 vit D Renal tubular acidosis- excretes excessive amounts of Ca Renal Osteodystrophy- Damage to the glomerulus causes retention of PO4 while tubular injury reduces the production of 1,25 vit D. Hyperphosphatemia further suppresses the production of 1,25 vit D andinhibits renal reabsorption and GI absorption of Ca.. Renal osteodystrophy is characterized by rickets, osteitis fibrosa (severe lysis of the skeleton due to secondary hyperparathyroidism), osteosclerosis (20%),and ectopic calcification. PATHOPHYSIOLOGY This type occurs in infants and children, which is a result of a lack of sun exposure and vitamin D in their diet. Vitamin D deficiency Rickets is not very common in the present day and is most commonly seen in breastfed babies that have a limited exposure to sunlight. Premature babies may form neonatal rickets, which results in spontaneous fractures, impaired growth, and respiratory distress. Neonatal rickets is usually seen within the first 8 to 10 weeks of life and is diagnosed with a chest x-ray. The radiographic appearance could show fractured ribs or just softened which would result in the ribs having an irregular and frayed appearance. Vitamin D deficiency rickets may appear in patients that have disorders of the small bowel, abnormalities of the hepatobiliary system, or gastrointestinal malabsorption problems. Intestinal surgery can also cause rickets by decreasing the mineralization of the bones. A related deficiency is the deficiency of 25(OH) Vitamin D that occurs in patients with neonatal hepatitis, biliary atresia, liver disease, anticonvulsant therapy, and vitamin-D-dependent rickets. A patient with renal osteodystrophy may develop rickets due to the deficiency of 1,25(OH2) vitamin D.

Rickets is caused by a lack of Vitamin D and other factors contribute to the cause of the disease. The main factors are the ratios and quantities of calcium and phosphorus available in the body, the speed and growth of the individual, and the ultraviolet ray filtering power of the atmosphere (Evans, 1994). Vitamin D has three different forms: vitamin D, 25(OH) vitamin D, and 1,25(OH2) vitamin D. These vitamins come from sunlight therefore, if a person receives an insufficient amount of sunlight, they could be at risk for developing Rickets. DIAGNOSTIC TEST The most effective way to diagnose Rickets is through the evaluation of x-rays. The early stages of the disease will be noticeable in the distal ends of the radius and ulna. The ulna will show significant changes will the radius appears to be normal. The main changes are the irregular fraying of the provisional zone of calcification. It is normally sharply defined, however, with Rickets it becomes fuzzy and fades into the soft tissue density of the adjacent cartilage (Evans, 1994). Radiographic findings will show abnormal increased axial height of the cartilaginous portion of the epiphyseal plate while cupping and widening of the ends of the long bones. Flat bones such as the skull or sternum may have an appearance of decreased density and become deformed and thin in children MEDICAL MANAGEMENT Measurements of BUN, Creatinine, Ca, PO4, alk phos, 1,25 and 25 vit D, PTH, and urine Ca and PO4 to help establish the diagnosis and categorize the type. First step is ALWAYS treat the underlying metabolic abnormality first. Often after proper medical therapy the patient will go onto normal growth and lifestyle. The limb malalignment is often dependent upon when the metabolic abnormality occurred. If it is before two years old a varus deformity will occur, after two years old a valgus deformity is most likely. If malalignment fails to improve after the underlying metabolic abnormality is corrected, bracing and/or surgery may be indicated. NO SURGICAL MANAGEMENT NURSING MANAGEMENT Continued medical therapy as indicated Continued orthopaedic observation No surgical intervention needed at this time since the patient's deformities continue to improve.