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KNEE BRACES AND SPLINTING IN KNEE OSTEOARTHRITIs
Knee brace can be used to stabilize the joint thus reducing further damage and pain. Methods of preventing and treating knee injuries have changed with the rapid development and refinement of knee braces. Prophylactic knee braces are designed to protect uninjured knees from valgus stresses that could damage the medial collateral ligaments1. However, no conclusive evidence supports their effectiveness, and they are not recommended for regular use. Functional knee braces are intended to stabilize knees during rotational and anteroposterior forces. They offer a useful adjunct to the treatment and rehabilitation of ligamentous knee injuries2.
Types of Knee Braces:
Functional Knee Braces
Functional knee braces are designed to substitute for damaged ligaments. For example, a patient who sustains an ACL tear may be offered a knee brace to wear in efforts to allow certain activities without surgery. Most patients who are concerned about knee braces already have a knee ligament injury. These patients would be interested in the functional knee braces. These functional knee braces are designed to compensate for a torn knee ligament1.
Prophylactic Knee Braces
Prophylactic knee braces are used to prevent knee injuries. Prophylactic knee braces are worn by athletes who participate in some high-risk sports in an effort to minimize their risk of sustaining a knee injury1.

How Knee Braces are useful Osteoarthritic Patients?

While nothing can cure osteoarthritis, this brace can help a person return to the type of activities he or she loves2,3.


The Knee Brace for osteoarthritis knee support works by:
� Redistributing the weight and joint alignment. This is done by a process called �off-loading� which takes the direct weight off the joint. This allows the leg to move more naturally3,4.
� Bi-Axial hinge gives the brace more flexibility and the ability to better fit the leg comfortably.
� Load sensor helps the device to determine the forces being applied by the brace5.
� With the relief from pain and better stability, the brace allows for an increase in leg functions, which leads to building up the muscles around the joint5.
� More mobility reduces stiffness in the morning, allowing more activity during the day, and reduced pain when at rest4,5.
This knee brace is light weight and easily adjustable by the patient. It offers a 20 degree increase in range of motion and a 4-point dynamic leverage system. The knee support brace has many arthritis friendly features and is commended for its ease-of-use3,5.




An osteoarthritis patient should discuss using the brace or any other such appliance with his or her doctor first and understand what activities can be attempted before using such a device.7


What to expect from a Osteoarthritis (OA) knee brace?

� Braces cannot cure OA and may not be right for everyone. However, it is a viable solution for many people. The ideal candidates are typically active people who are motivated to strengthen their muscles and willing to wear a brace to realize the benefits of this form of treatment8.

� Discuss treatment goals with your doctor and others on your health care team before you get a brace5,7.

� Don�t expect a brace to feel good from the start. It may take from a week to a month to get used to how the brace feels on your leg. Be patient. It took a long time for your knee OA to develop9.

� Bracing has come close to eliminating pain for some people with knee OA, while others experience moderate relief2,6.
The Appropriate Knee Brace for You
There are different kinds of knee braces and it's important for your doctor or a health professional to help decide which knee brace might be appropriate for you10. Three knee components to consider are:
� medial (on the inside of the knee joint)
� lateral (on the outside of the knee joint)
� patellofemoral (behind the kneecap)
Usually knee braces are recommended for patients who have cartilage loss in one component of the knee, also known as unicompartmental knee damage. Osteoarthritis most commonly develops in the medial component8.
Types of Knee Braces Used in Knee OA
Single-piece sleeves made of neoprene, an elastic-rubbery material, are the most simple knee braces. The knee brace is pulled on over the foot of the affected leg and is placed over the knee where it provides compression, warmth, and support. This type of knee brace is for mild to moderate osteoarthritis and it is available over the counter in most drug stores. The fit should be snug9,10.
An unloader brace is a semi-rigid knee brace made from molded plastic and foam. Steel struts inserted on the sides limit lateral knee movement and add stability11. This brace is custom-fit to each individual patient for whom it is prescribed (usually patients with medial component osteoarthritis). Essentially, it relieves pain by transferring pressure from the inside to the outside part of the knee9.
The unloader knee brace can also be designed for patients with cartilage damage in the lateral component of the knee, as well as patients with severe osteoarthritis of the knee who are looking for temporary pain relief while they wait to have knee replacement surgery. To purchase an unloader knee brace, the patient must obtain a prescription from an orthopedic doctor, and the brace must be purchased at a store specializing in orthotics10.
Experts suggest that patients allow a week to one month to adjust to how the unloader brace feels. Right from the start, don't expect comfort. It takes a little time. Experts also warn patients about becoming too reliant on the unloader brace12. Take it off from time to time so you can exercise and strengthen muscles. It's also important to remember that a knee brace is just one part of a patient's treatment regimen. Don't disregard other aspects of your treatment regimen without first talking to your doctor

Splints in Knee Osteoarthritis..
The various types of knee splints differ in use, style, and complexity. The simplest knee brace is a neoprene sleeve. Neoprene sleeves are most useful if you have mild arthritis and your primary purpose is to reduce pain and swelling. This device does not provide alignment correction or structural support for the knee joint, although it may contribute some input to joint proprioception.
For realignment purposes, you can get several types of knee braces over the counter or custom fit by an orthotist. Custom fit braces are molded to your size and are usually of a higher quality; they are sometimes adjustable. Such braces are more expensive than over-the-counter braces, which have fewer options for adjusting fit11,13. Realignment goals vary because they are based on your personal biomechanics. They include bicompartment, patellofemoral, and tibiofemoral realignment 13.
For some people, the goal of using a knee brace may be ligament protection. I recommend that you see someone qualified to determine which type of brace meets your needs and to fit you properly11. Proper fit of a knee brace is essential, as an improper fit not only fails to realign the joint but also may lead to further joint damage. A gentleman I know used a brace for several years to reduce the pain in his knee during tennis, his preferred mode of exercise. Tennis puts lateral and torsional stresses on the knees, so a brace is a good way to reduce these stresses, which can damage arthritic knees7.

How Splinting Helps in Osteoarthritis KNEE ?
Many athletes wear braces or splints on their knee to help protect it from further injury. Wearing one may be all the knee needs, but only your ahead, a physical therapist can help you heal your knee and then teach you how to strengthen your knee after6,7,8.
Medications are an option that help many people. Your doctor may prescribe anti-inflammatories to reduce swelling inside the knee, reducing the irritation and pain. Analgesics, pain killers, may also be used. Depending on the injury, the knee may benefit from an injection of a corticosteroid directly into the joint6,7.
Immobilizing the knee is done in most traumatic knee injuries. By putting it in a splint, you can�t injure it any further through movement and the knee has a chance to heal6,8.

Hyaluronic acid in osteoarthritishttp://drgspatnaik.com

Hyaluronic acid in osteoarthritis
Osteoarthritis(OA) is a degenerative joint disease and is thought to be wear and tear of joint as part of an aging process.There are 2 types of OA,primary and secondary.Primary OA occurs in a joint de novo.It occurs in elderly and mostly in weight-bearing joints such as knee and hip.This is more common.Secondary OA occurs due to an underlying primary disease of the joint which leads to the degeneration of the joint.It can occur at any age and occurs commonly at the hip. Osteoarthritis is characterized by a loss of articular cartilage, which has a highly limited capacity to heal itself. Along with these cartilage changes, a reduction in the elastic and viscous properties of the synovial fluid occurs. The molecular weight and concentration of the naturally occurring hyaluronic acid decreases. Theoretically, this loss of elastoviscosity decreases the lubrication and protection of the joint tissues and is one postulated mechanism of pain production in osteoarthritis.1,2 Pharmacologic treatment generally consists of analgesics and/or nonsteroidal anti-inflammatory drugs (NSAIDs). Physical therapy can be used, with exercises to maintain range of motion and strength. Intra-articular corticosteroid injections are often used for transient symptom relief. When conservative measures fail, surgical treatments limited to arthroscopic debridement, osteotomies to redistribute load and total joint replacements have been the only options until recently.
Intraarticular injections of hyaluronic acid is a viscosupplementation that is newly available options for patients with symptomatic knee osteoarthritis.The increase in viscoelasticity of the synovial fluid seems to play a role.The indications for viscosupplementation can be considered for use in patients who have significant residual symptoms despite traditional nonpharmacologic and pharmacologic treatments.Patients who are intolerant of traditional treatments can be considered these injections.
Viscosupplementation
The concept of viscosupplementation is based on pathologic changes of synovial fluid hyaluronic acid with its decrease molecular weight and supplementation.Two hyaluronic acid products are currently available in the United States: naturally occurring hyaluronan (Hyalgan) and synthetic hylan G-F 20 (Synvisc). Hylans are cross-linked hyaluronic acids, which gives them a higher molecular weight and increased elastoviscous properties. The higher molecular weight of hylan may make it more efficacious than hyaluronic acid because of its enhanced elastoviscous properties and its longer period of residence in the joint space (i.e., slower resorption)3. The exact mechanism of action of viscosupplementation is not well known. Although restoration of the elastoviscous properties of synovial fluid seems to be the most logical explanation, other mechanisms must exist. The actual period that the injected hyaluronic acid product stays within the joint space is on the order of hours to days, but the time of clinical efficacy is often on the order of months.4 Other possible mechanisms to explain the long-lasting effect of viscosupplementation include anti-inflammatory and antinociceptive properties, or stimulation of in vivo hyaluronic acid synthesis by the exogenously injected hyaluronic acid.5
Clinical studies of hyaluronan
Multiple studies have been conducted to assess the efficacy of intra-articular hyaluronan injections. Initial studies6-8 in the 1970s and 1980s demonstrated benefits for hyaluronan-injected knees. More recently, Dahlberg and colleagues,9 and Henderson and coworkers,10 in randomized, double-blind placebo-controlled trials found no benefit from intra-articular hyaluronan over placebo. Lohmander and associates11 similarly found no significant differences between overall treatment and placebo groups; however, a subgroup analysis of patients more than 60 years of age with more severe symptoms revealed beneficial effects from the hyaluronan injections. In contrast to these recent trials, which demonstrated no or minimal beneficial effects from intra-articular hyaluronan, other randomized controlled studies12-14 suggest overall beneficial effects of hyaluronan over placebo. Another study15 demonstrated efficacy of hyaluronan in a randomized blinded trial, with the treatment group showing more improvement than the placebo group and a group taking oral naproxen.
Clinical studies of cross-linked hylan
A summary of four clinical trials performed in Germany using cross-linked hylan16 demonstrated excellent results in 71 percent of hylan-treated patients, compared with 29 percent of placebo-treated patients. After six months, 53 percent of hylan-treated patients still reported excellent pain relief, compared with 22 percent of the placebo-treated patients. In a double-blind, randomized placebo-controlled trial using hylan,17 it was found that 39 to 71 percent of hylan-treated patients were symptom free at 26 weeks compared with 13 to 45 percent of placebo-treated patients. Another study18 compared intra-articular hylan with NSAID therapy in a randomized blinded trial. Hylan was found to be as effective as NSAID therapy at 12 weeks and was superior to NSAID therapy at 26 weeks. In addition, findings from a clinical practice19 showed that 80 percent of 458 knees injected with hylan had a positive response, and the average duration of efficacy was 8.2 months.
Adverse effects of intraarticular hyaluronic acid
Rates of adverse reaction has been low.The most frequent adverse reaction to this treatment is transient localised pain or effusion which is resolved within one to three days.There were no systemic effects attributed to hyaluronic acid.There are also reports on cases of induced pseudogout20.No long term side effects have been reported21.
Indications
Intra-articular hyaluronic acid injections should be considered in patients with significantly symptomatic osteoarthritis who have not responded adequately to standard nonpharmacologic and pharmacologic treatments or are intolerant of these therapies (e.g., gastrointestinal problems related to anti-inflammatory medications).2,14,15 Patients who are not candidates for total knee replacement or who have failed previous knee surgery for their arthritis, such as arthroscopic debridement, may also be candidates for viscosupplementation. Total knee replacement in younger patients may be delayed with the use of hyaluronic acid22.
Injection technique
Hyalgan is supplied in 2-mL vials (one injection per vial) or prefilled syringes, and Synvisc is supplied in 2-mL prefilled syringes. The recommended injection schedule is one injection per week for five weeks for Hyalgan, and one injection per week for three weeks for Synvisc. Repeat courses of viscosupplementation can be performed after six months. A knee joint can be injected several ways. One approach is to have the patient lie supine on the examination table with the knee flexed 90 degrees. In this position, the anterior portions of the medial and lateral joint lines can easily be palpated as dimples just medial or lateral to the inferior pole of the patella. Often, the medial joint line is easier to palpate and define and can be chosen as the site of injection. Alternatively, the knee joint can be approached with the knee extended, again with the patient lying supin. Most commonly the superolateral edge of the patella is the site of injection, but other quadrants of the knee near the patellar edges can also be chosen. With this approach (knee in extended position), the needle is generally aimed under the patella.
Actual injection site can be marked with a fingernail imprint or the barrel of a pen. Next, sterile preparation with a povidone iodine preparation (Betadine) and alcohol can be performed. A 22- to 25-gauge needle can be used for the injection. Local anesthesia with lidocaine before the injection can be used, but with a small gauge needle this is not always necessary. Alternatively, an ethyl chloride spray can be used for local anesthesia. Following puncture through the skin and into the joint space, the injection is accomplished. If resistance is encountered, redirection of the needle may be necessary.
If effusion is present, aspiration of the joint is recommended before the injection to prevent dilution of the injected hyaluronic acid. The aspiration can be performed at the same site as the injection, as previously described. The same needle can be left in place and used for the aspiration and the injection. Aspiration may require a larger bore needle, such as an 18- or 20-gauge needle. Following local anesthesia with intradermal lidocaine or ethyl chloride spray, the needle can be placed into the joint for aspiration. When aspiration is completed, hemostat clamps can be used to grasp and stabilize the needle, while the aspiration syringe is detached from the needle. The syringe containing hyaluronic acid can then be attached to the same stabilized needle followed by injection. No excessive weight-bearing physical activity should take place for one to two days following injection

Medial Compartment Arthritis

Etiology
Osteoarthritis of the knee usually occurs secondary to mechanical factors, which include partial or complete meniscectomy, femoral osteonecrosis, lower extremity trauma, ligamentous laxity, obesity, and lower extremity malalignment.[1,2]
Pathophysiology
With removal of approximately one third of the meniscus, increased force is transferred directly to the tibial articular surface.[ 3]The joint also becomes less congruent and is not able to disperse the force across the joint. Both of these factors increase contact stresses, which can lead to articular cartilage damage and subsequent osteoarthritis.[3,4,5]
Results from multiple laboratory studies have shown that abnormal alignment also leads to abnormal contact stress. Ogata et al, Wu et al, and Reimann performed similar studies in which a varus stress was placed across the knee.[12] Each study documented degeneration of the articular cartilage in the medial compartment. The injury to the articular cartilage occurs in the deeper layers without any surface evidence of injury.[11,12]
Fractures of the tibial shaft and plateau may lead to subsequent lower extremity malalignment. Most clinicians accept less than 10� of angulation in tibial shaft fractures. For instance, residual varus angulation increases contact stresses across the medial compartment of the knee. Tibial plateau fractures also may lead to medial compartment osteoarthritis. The arthritis in this instance is due to direct articular cartilage damage caused by the intraarticular fracture.
Ligamentous laxity also is a cause of medial compartment osteoarthritis. Anterior cruciate and/or lateral collateral ligamentous laxity or incompetence has been implicated as causes for medial compartment osteoarthrosis. ACL-deficient knees allow for anterior subluxation of the tibia on the femur. This leads to increased shear force upon the articular cartilage, which leads to early degeneration of the articular surface.
Torsional deformities of the tibia and femur have a clinical association with the onset of medial compartment degenerative changes. The torsion may be present on the tibial or femoral side of the knee. This may lead to varus angulation and increased contact stresses across the articular cartilage of the medial joint space, which leads to accelerated medial compartment osteoarthritis.
Presentation
Patients generally present with a chief symptom of pain in the knee that has worsened over time. Patients state that the knee generally feels worse in the morning when they awaken and that the knee pain generally lessens with some activity. As their activity increases during the day, so does their pain. Patients may state that anti-inflammatory drugs help alleviate the pain. Patients frequently describe pain on the inside (genu varum) or outside (genu valgum) of the knee if unicompartmental arthritis is the cause of their symptoms.[9,10,11]
History and physical examination are crucial in making the diagnosis. It is important to ascertain whether trauma to the knee has occurred, indicating an old history of fracture, articular damage, and/or ligamentous injury and malalignment. A history of pain in other joints may alert the physician to an etiology of inflammatory arthritis or bilateral lower extremity malalignment.[9,10]
Physical examination may reveal varus or valgus alignment of the knee. Pain over the medial joint line may indicate a meniscus tear or degenerative changes within the medial compartment.[12] Patellar tendon tenderness also may indicate medial joint degeneration, as well as possible patellar tendon pathology. Patients may have crepitus in the knee. Range of motion (ROM) of the knee may be decreased compared to the opposite side. Fixed flexion contractures are uncommon but may occur in patients with tibiofemoral osteoarthritis. Evaluation of ligamentous stability is important. The integrity of the cruciate ligaments and collateral ligamentous stability may determine the feasible treatment options.[12,13,14,15]
Determining whether the patient with varus or valgus alignment of the knee can be passively corrected to neutral is of key importance.[14] Again, this aids in determining the surgical options for treatment of medial compartment disease.
Treatment Modalities
Multiple treatment options are available for isolated medial compartment osteoarthritis of the knee. Surgical intervention is indicated when conservative therapies have failed. Conservative therapies include nonsteroidal anti-inflammatory drugs (NSAIDs), joint viscosupplementation, unloading braces, and physical therapy.
Arthroscopy
The first operative procedure is knee arthroscopy. Arthroscopy is indicated for patients in whom conservative therapy has failed who want the most minimal surgical procedure available. Arthroscopy usually is used as a temporizing measure until definitive surgical treatment is undertaken. Knee arthroscopy sometimes is indicated as a diagnostic procedure to determine a treatment pathway or may be utilized in conjunction with a definitive procedure. Arthroscopy of the knee has not been shown to slow the course of osteoarthritis of the knee; however, it has been demonstrated to provide pain relief. The period of pain relief ranges from 6 months to a few years.[9 ]
Osteotomy
High tibial osteotomy (HTO) is indicated in patients younger than 60 years (ideally in their sixth decade of life) who are in labor-intensive fields and experience activity-related pain with a varus alignment of the knee. The arthritis in the medial compartment must be noninflammatory, and the patient should have no patellofemoral symptoms. Certain criteria regarding ligamentous stability and presence of minimal flexion contracture must be met. If this procedure is used alone, it should be considered a temporizing measure because joint resurfacing ultimately may be required.[5,13 ]
Arthroplasty
Unicompartmental knee arthroplasty is a surgical procedure used to relieve arthritis in one of the knee compartments in which the damaged parts of the knee are replaced. UKA surgery may reduce post-operative pain and have a shorter recovery period than a total knee replacements.[8] Also, UKA may have a smaller incision because the implants may be smaller.[8] Unicompartmental knee arthroplasty (UKA) is indicated in patients who are older than 60 years who have sedentary lifestyles, and were also performed for patients with age less than 60years noninflammatory arthritis, and pain with weight bearing[19]. Patients may have patellofemoral disease but usually are asymptomatic in that compartment. Symptomatic patellofemoral disease is a contraindication to the procedure. Ligamentous stability, weight, and coronal deformity of less than 15� also are considered. TKA is indicated in patients older than 65 years who have somewhat sedentary lifestyles and symptomatic arthritis in 2 or 3 compartments. The arthritis may be posttraumatic, degenerative, or inflammatory.[8,10,14,15,16,17 ,18, 19]Citation:
1. Birmingham TB, Kramer JF, Kirkley A, et al. Knee bracing for medial compartment osteoarthritis: effects on proprioception and postural control. Rheumatology (Oxford). Mar 2001;40(3):285-9. [Medline].
2. Dearborn JT, Eakin CL, Skinner HB. Medial compartment arthrosis of the knee. Am J Orthop. Jan 1996;25(1):18-26. [Medline].
3. Grelsamer RP. Unicompartmental osteoarthrosis of the knee. J Bone Joint Surg Am. Feb 1995;77(2):278-92. [Medline].
4. Gross AE, McKee NH, Pritzker KP, Langer F. Reconstruction of skeletal deficits at the knee. A comprehensive osteochondral transplant program. Clin Orthop. Apr 1983;(174):96-106. [Medline].
5. Jackson RW. Surgical treatment. Osteotomy and unicompartmental arthroplasty. Am J Knee Surg. Winter 1998;11(1):55-7. [Medline].
6. Kirkley A, Webster-Bogaert S, Litchfield R, et al. The effect of bracing on varus gonarthrosis. J Bone Joint Surg Am. Apr 1999;81(4):539-48. [Medline].
7. Lindenfeld TN, Hewett TE, Andriacchi TP. Joint loading with valgus bracing in patients with varus gonarthrosis. Clin Orthop. Nov 1997;(344):290-7. [Medline].
8. Borus T, Thornhill T (January 2008). "Unicompartmental knee arthroplasty". J Am Acad Orthop Surg 16 (1): 9�18. PMID 18180388
9. Marwin SE, Siegel JA. Unicompartmental Gonarthrosis of the Knee: The Role of Unicompartmental Knee Arthroplasty. Orthopedic Special Edition. 1999;5(2):57-60.
10. Moseley JB Jr, Wray NP, Kuykendall D, et al. Arthroscopic treatment of osteoarthritis of the knee: a prospective, randomized, placebo-controlled trial. Results of a pilot study. Am J Sports Med. Jan-Feb 1996;24(1):28-34. [Medline].
11. Squire MW, Callaghan JJ, Goetz DD, et al. Unicompartmental knee replacement. A minimum 15 year followup study. Clin Orthop. Oct 1999;(367):61-72. [Medline].
12. Bingham CO 3rd, Buckland-Wright JC, Garnero P, Cohen SB, Dougados M, Adami S, et al. Risedronate decreases biochemical markers of cartilage degradation but does not decrease symptoms or slow radiographic progression in patients with medial compartment osteoarthritis of the knee: results of the two-year multinational knee osteoarthritis structural arthritis study. Arthritis Rheum. Nov 2006;54(11):3494-507. [Medline].
13. Reimann I. Experimental osteoarthritis of the knee in rabbits induced by alteration of the load-bearing. Acta Orthop Scand. 1973;44(4):496-504. [Medline].
14. Niemeyer P, Koestler W, Kaehny C, Kreuz PC, Brooks CJ, Strohm PC, et al. Two-year results of open-wedge high tibial osteotomy with fixation by medial plate fixator for medial compartment arthritis with varus malalignment of the knee. Arthroscopy. Jul 2008;24(7):796-804. [Medline].
15. Bert JM. 10-year survivorship of metal-backed, unicompartmental arthroplasty. J Arthroplasty. Dec 1998;13(8):901-5. [Medline].
16. Fu FH, Harner CD, Vince KG. Knee surgery. Vol 2. Williams & Wilkins;1994:1061-255.
17. Kozinn SC, Scott R. Unicondylar knee arthroplasty. J Bone Joint Surg Am. Jan 1989;71(1):145-50. [Medline].
18. Emerson RH Jr, Higgins LL. Unicompartmental knee arthroplasty with the oxford prosthesis in patients with medial compartment arthritis. J Bone Joint Surg Am. Jan 2008;90(1):118-22. [Medline].
19. Frankowski JJ, Watkins-Castillo S, Sculco TP, et al.Primary total hip and total knee arthroplasty projectionfor the US population to the year 2030. AmericanAcademy of Orthopaedic Surgeons; John Wiley &Sons, Inc; 2002. Updated: Sep 12, 2008

 

Glucosamine in Osteoarthritis and other Food Supplements

Introduction

Osteoarthritis (OA) is the commonest form of arthritis found worldwide that can affect the hands, hips, shoulders and knees. It is responsible for the largest burden of joint pain and is the single most important rheumatological cause of disability and handicap.1,2 In Osteoarthritis, the cartilage that protects the ends of the bones breaks down and causes pain and swelling. Drug and non-drug treatments are used to relieve pain and/or swelling. Osteoarthritis commonly affects the hands, feet, spine and large weight-bearing joints, such as the hips and knees. Most cases of osteoarthritis have no known cause and are referred to as primary osteoarthritis. When the cause of the osteoarthritis is known, the condition is referred to as secondary osteoarthritis. These are food supplements show promise for helping people with osteoarthritis, those are Glucosamine sulphate, Chondroitin sulphate, SAMe (s-adenosylmethionine), Vitamin C ( ascorbic acid), Beta Carotene3 and many more.
Glucosamine
Glucosamine is almost synonymous with osteoarthritis as it has benefits for osteoarthritis. It can be found naturally in the body and is used by the body as one of the building blocks of cartilage.Glucosamine is an amino sugar produced from the shells of shellfish (chitin) and it is a key component of cartilage. Glucosamine (C6H13NO5) is an amino sugar and a prominent precursor in the biochemical synthesis of glycosylated proteins and lipids. Glucosamine is part of the structure of the polysaccharides chitosan and chitin, which compose the exoskeletons of crustaceans and other arthropods, cell walls in fungi and many higher organisms, glucosamine is one of the most abundant monosaccharides.3
Glucosamine is necessary for the construction of connective tissue and healthy cartilage. It is the critical building block of proteoglycans and other substances that form protective tissues. These proteoglycans are large protein molecules that act like a sponge to hold water giving connective tissues elasticity and cushioning effects. This also provides a buffering action to help protect against excessive wear and tear of the joints. Without glucosamine, our tendons, ligaments, skin, nails, bones, mucous membranes, and other body tissues can not form properly.

Glucosamine works to stimulate joint function and repair. Everyone produces a certain amount of glucosamine within their bodies. Normally we generate sufficient amounts of glucosamine in our bodies to form the various compounds needed to generate connective tissue and healthy cartilage. But gradually the rate at which our bodies use glucosamine begins to gradually change with our increased athletic activity, injuries, burns, arthritis and other inflammatory disorders, age and other chronic degeneration.3 In such situations our bodies may not be able to keep up with the demand for glucosamine, leading to a decrease in the amount of proteoglycans produced. This can lead to a decrease in the amount of protective lubricating substances like the synovial fluids, which cushion our joints, and protects them from damage. In a nutshell, more glucosamine is needed but less is produced.
As the age advances, body loses the capacity to make enough glucosamine. Having ample glucosamine in the body is essential to producing the nutrients needed to stimulate the production of synovial fluid, the fluid which lubricates cartilage and keeps the joints healthy. Without enough glucosamine, the cartilage in weight-bearing joints, such as the hips, knees, and hands deteriorates. The cartilage then hardens and forms bone spurs, deformed joints, and limited joint movement. This is how the debilitating disease of osteoarthritis develops.4
Therefore, in short, glucosamine is a major building block of proteoglycans needed to make glycosaminoglycans, proteins that bind water in the cartilage matrix which also acts as a source of nutrients for the synthesis of proteoglycans and glycosaminoglycans. It is also a stimulant to chondrocytes and playing key factor in determining how many proteoglycans are produced by the chondrocytes needed to spur chondrocytes to produce more collagen and proteoglycans acts as a regulator of cartilage metabolism which helps to keep cartilage from breaking down. 5
Glucosamine is the supplement most commonly used by patients with osteoarthritis. It is an endogenous amino sugar that is required for synthesis of glycoproteins and glycosaminoglycans, which are found in synovial fluid, ligaments, and other joint structures. Exogenous glucosamine is derived from marine exoskeletons or produced synthetically.

Exogenous glucosamine may have anti-inflammatory effects and is thought to stimulate metabolism of chondrocytes.
Glucosamine is available in multiple forms. The most common are glucosamine hydrochloride and glucosamine sulfate. Some products contain a blend of these, and many combine one of the forms with a variety of other ingredients. Glucosamine has been safely used in long-term clinical trials Overall, the evidence supports the use of glucosamine sulfate for modestly reducing osteoarthritis symptoms and possibly slowing disease progression.
Chondroitin
Chondroitin, an endogenous glycosaminoglycan, is a building block for the formation of the joint matrix structure. Chondroitin sulfate is a sulfated glycosaminoglycan (GAG) composed of a chain of alternating sugars (N-acetylgalactosamine and glucuronic acid). It is usually found attached to proteins as part of a proteoglycan.6 Chondroitin sulfate is an important structural component of cartilage and provides much of its resistance to compression. Along with glucosamine, chondroitin sulfate has become a widely used dietary supplement for treatment of osteoarthritis. Chondroitin is a molecule that occurs naturally in the body. It is a major component of cartilage,the tough, connective tissue that cushions the joints. Chondroitin helps to keep cartilage healthy by absorbing fluid (particularly water) into the connective tissue. It may also block enzymes that break down cartilage, and it provides the building blocks for the body to produce new cartilage.
Chondroitin sulphate Chondroitin is the most abundant glycosaminoglycan in cartilage and is responsible for the resiliency of cartilage and it has various effects in relieving symptoms of osteoarthritis and those are its anti-inflammatory activity, the stimulation of the synthesis of proteoglycans and hyaluronic acid, and the decrease in catabolic activity of chondrocytes inhibiting the synthesis of proteolytic enzymes, nitric oxide, and other substances that contribute to damage cartilage matrix and cause death of articular chondrocytes. chondroitin sulfate reduced the IL-1β-induced nuclear factor-kB (Nf-kB) translocation in chondrocytes. In addition, chondroitin sulfate has recently shown a positive effect on osteoarthritic structural changes occurred in the subchondral bone.7 A number of scientific studies suggest that chondroitin may be an effective treatment for osteoarthritis
Therefore, overall effects of chondroitin sulphate are; reduces osteoarthritis pain, improves functional status of people with hip or knee osteoarthritis, reduces joint swelling and stiffness and ultimately provides relief from osteoarthritis symptoms for up to 3 months after treatment is stopped
S-Adenosyl methionine
S-Adenosyl methionine (SAM, SAMe, SAM-e) is a dietary supplement that has been clinically shown to support and promote joint health, mobility and joint comfort.It is a compound produced by our bodies from methionine. Methionine is an amino acid found in protein-rich foods and a common co-substrate involved in methyl group transfers. SAM-e is critical in the manufacture of joint cartilage and in the maintenance of neural cell membrane function.8
Administration of SAMe exerts analgesic and antiphlogistic activities and stimulates the synthesis of proteoglycans by articular chondrocytes with minimal or absent side effects on the gastrointestinal tract and other organs and improving pain and stiffness related to osteoarthritis
Vitamin C( ascorbic acid)

Vitamin C( ascorbic acid) may help reduce the progression of osteoarthritis. Vitamin C is involved in the formation of both collagen and proteoglycans (two major components of cartilage, which cushions the joints). Vitamin C is also a powerful antioxidant that helps to counteract the effects of free radicals in the body, which can damage cartilage. Ascorbic acid(vitamin c) is a sugar acid with antioxidant properties. Its appearance is white to light-yellow crystals or powder, and it is water-soluble. One form of ascorbic acid is commonly known as vitamin C. In human plasma, ascorbate is the only antioxidant that can completely protect lipids from detectable peroxidative damage induced by aqueous peroxyl radicals. Ascorbate appears to trap virtually all peroxyl radicals in the aqueous phase before they diffuse into the plasma lipids. Ascorbate is a highly effective antioxidant, as it not only completely protects lipids from detectable peroxidative damage, but also spares alpha-tocopherol, urate, and bilirubin.Ascorbic acid stimulates collagen synthesis and modestly stimulates synthesis of aggrecan (a proteoglycan present in articular cartilage), Sulfated proteoglycan biosynthesis is significantly increased in the presence of ascorbic acid thus it may offer some protective effect against the super oxide and free radicals and limiting and delaying the osteoarthritis progression

Beta-carotene
. Beta-carotene belongs to a family of natural chemicals known as carotenoids. Widely found in plants, carotenoids along with another group of chemicals, bioflavonoids, give color to fruits, vegetables, and other plants.
Beta-carotene is another antioxidant that also seems to help reduce the risk of osteoarthritis progression. Beta-carotene is a particularly important carotenoid from a nutritional standpoint, because the body easily transforms it to vitamin A. While vitamin A supplements themselves can be toxic when taken to excess, it is believed (although not proven) that the body will make only as much vitamin A out of beta-carotene as it needs. Assuming this is true, this built-in safety feature makes beta-carotene the best way to get your vitamin A. A high dietary intake of beta-carotene is associated with a significantly slower progression of osteoarthritis, according to a study in which researchers followed 640 individuals over a period of 8 to 10 years .10
Conclusion
In conclusion,there are nutrients and foods that may help to halt the progression osteoarthritis before it becomes severe as well as helping to reduce the pain and inflammation associated with it.
REFERENCES

1) Clinical Practise Guidelines. Management of Osteoarthritis http://www.msr.org.my/html/Bookleta.pdf accessed on 13 February 2010
2) Cochrane Library. Glucosamine Therapy for Treating Osteoarthritis http://www.cochrane.org/reviews/en/ab002946.html accessed on 13 February 2010
3) Spark People Life. Dietary Supplement for Osteoarthritis
http://www.sparkpeople.com/resource/nutrition_articles.asp?id=865 accessed on
14 February
4) Horton D, Wander JD (1980). The Carbohydrates. Vol IB. New York: Academic
Press. pp. 727�728.
5) Glucosamine and Osteoarthritis,How it works
http://www.arthritis-glucosamine.net/glucosamine-osteoarthritis.php accessed on
14 February 2010
6) Jamie G. Barnhill, Carol L. Fye, David W. Williams, Domenic J. Reda, Crystal L. Harris, and Daniel O. Clegg. Chondroitin Product Selection for the Glucosamine/Chondroitin Arthritis Intervention Trial. J Am Pharm Assoc. 2008; 46:14�24.
7) Davidson EA, Meyer K (2007). "Chondroitin, a mucopolysaccharide". J Biol Chem 211 (2): 605�11.
8) S-adenosyl methionine [SAMe]. Research Reports http://www.oralchelation.com/technical/SAM.htm accessed on 15 February 2010
9) McAlindon TE, Jacques P, Zhang Y, et al. Do antioxidant micronutrients protect against the development and progression of knee osteoarthritis? Arthritis Rheum. 1996;39:648-656.
10) iHerb. Com. Beta Carotene http://healthlibrary.epnet.com/GetContent.aspx?token=e0498803-7f62-4563-8d47-5fe33da65dd4&chunkiid=21547

Pathophysiolgy of Pathological Fracture

Pathological fracture is a fracture that occurs when a bone breaks in an area that is weakened by another disease process. Causes of weakened bone varies from genetic disorders , tumours , and even chronic infection , each having its own pathogenesis which leads to pathological fracture.
Pathological fractures occur usually during normal routine activities of the patient.He may rest his hand on table when it fractured,he may be playing with grandchildren when the fracture occurs.These are only few of the examples.The reason is that the underlying disease process weakens the bone to the point where the bone is unable to perform its normal function.
Here are some of the causes of pathological fracture,whereby the pathophysiology of few of the condition will be explained briefly.
Generalized cause which include osteogenesis imperfecta , postmenopausal osteoporosis , metabolic bone disease , myelomatosis , Polyostotic fibrous dysplasia, and Paget�s disease. Secondly , local benign condition including chronic infection , solitary bone cyst , Fibrous cortical defect , chondromyxoid fibroma , aneurismal bone cyst , Chondroma , monostotic fibrous dysplasia.There are also few primary malignant tumors leading to pathological fracture which are chondrosarcoma , Osteosarcoma , Ewing�s tumor.Lastly few of the metastatic tumors , including Carcinoma breast , lung , kidney , thyroid , Colon , and prostate.
In Osteogenesis Imperfecta,the pathology lies in the disturbance in the synthesis of type I collagen, which is the predominant protein of the extracellular matrix of most tissues. In bone, this defect of extracellular matrix causes osteoporosis, which leads to an increase in the tendency to fracture. Besides bone, type I collagen is also a major constituent of dentin, sclerae, ligaments, blood vessels, and skin; therefore, individuals with osteogenesis imperfecta may also have abnormalities of these structures.
The process of collagen molecule formation starts with the synthesis of procollagen, consisting of a long triple-helix protein flanked by 2 propeptides at its 2 terminals.It is then secreted into the extracellular compartment, where the amino- and carboxy-terminal propeptides are cleaved,thus forming the functional collagen molecule. Then,fibrils are formed.Any Mutations that interfere with expression of the collagen gene, formation of the triple helix , or procollagen secretion will affect the structure and function of collagen fibrils, leading to osteogenesis imperfecta.
A number of genetic defects cause the abnormal type I collagen synthesis that leads to osteogenesis imperfecta. It generally arises from mutations in 1 of 2 genes that encode for the synthesis and structure of type I collagen: the COL1A1 gene on chromosome 17, and the COL1A2 gene on chromosome 7. Mutations in these genes leads to decrease in normal collagen. Milder forms of osteogenesis imperfecta are caused primarily by a decrease in production of normal collagen, whereas more severe forms are caused primarily by the production of abnormal collagen. These abnormalities may be dominantly inherited, or they may be the result of sporadic mutation.
Next is Postmenopausal Osteoporosis.Underlying pathology : imbalance of bone resorption and bone formation.In normal bone, there is constant matrix remodeling of bone and up to 10% of all bone mass may be undergoing remodeling at any point in time. Bone is resorbed by osteoclast cells , after which new bone is deposited by osteoblast cells.The main mechanism by which osteoporosis develops are an inadequate peak bone mass (the skeleton develops insufficient mass and strength during growth), excessive bone resorption and inadequate formation of new bone during remodeling. An interplay of these three mechanisms underlies the development of fragile bone tissue.Moreover,hormonal factors , for example the lack of estrogen( as a result of menopause) increases bone resorption,and decreases the deposition of new bone that normally takes place in weight-bearing bones. The α-form of the estrogen receptor appears to be the most important in regulating bone turnover.
In bone structure,trabecular bone is the sponge-like bone in the ends of long bones and vertebrae. Cortical bone is the hard outer shell of bones and the middle of long bones. Because osteoblasts and osteoclasts inhabit the surface of bones, trabecular bone is more active, more subject to bone turnover, to remodeling. Not only is bone density decreased, but the microarchitecture of bone is disrupted. The weaker spicules of trabecular bone break ("microcracks"), and are replaced by weaker bone. Common osteoporotic fracture sites, the wrist, the hip and the spine, have a relatively high trabecular bone to cortical bone ratio. These areas rely on trabecular bone for strength, and therefore the intense remodeling causes these areas to degenerate most when the remodeling is imbalanced.
Next is the metabolic bone disease,in which rickets and hyperparathyroidism discussed here.As for rickets,it involves mainly dietary deficiency of Vitamin D and calcium.Vitamin D is required for proper calcium absorption from the gut. Sunlight, especially ultraviolet light, lets human skin cells convert Vitamin D from an inactive to active state. In the absence of vitamin D, dietary calcium is not properly absorbed, resulting in hypocalcemia, leading to skeletal and dental deformities and neuromuscular symptoms.(eg of food containing vitamin D are butter,egg,fish liver oil,margarine etc)
Next is Hyperparathyroidism.Osteoporosis associated with hyperparathyroidism is caused by the high parathyroid hormone secreted by overactive parathyroid gland. Excess parathyroid hormone acts indirectly on osteoclasts as they lack a PTH receptor. Instead, PTH stimulates osteoblasts, which in turn increases their expression of RANKL. RANKL is then able to bind osteoclasts which stimulates their activation which ultimately leads to the removal of calcium from the bones.
Moving on to the next cause of pathological fracture, which is Myelomatosis.Myeloma bone pain usually involves the spine and ribs, and worsens with activity. Persistent localized pain may indicate a pathological bone fracture. Myeloma bone disease is due to the release of RANKL by plasma cells and bone marrow stroma which binds to activatory RANK receptors on the osteoclast. These bone lesions are lytic in nature.(punced out lesion and pepper pot appearance on radiograph)


Next on the list is the Paget�s Disease/ Osteitis deformans.It is associated with genetic or viral etiology. Sir James Paget first suggested that the disease was due to an inflammatory process. New evidence suggests that he may have been correct and that a paramyxovirus infection is the underlying cause of Pagets Disease. No infectious virus has yet been isolated as a causative agent, however, and other evidence suggests that an intrinsic hyperresponsive reaction to Vitamin D and RANK ligand is the cause. The pathogenesis of Paget's disease involves 3 stages,which are : Osteoclastic activity , Mixed osteoclastic-osteoblastic activity and exhaustive (burnt out) stage. Initially, there is a highly increased rate of bone resorption at localized areas due to large and numerous osteoclasts (seen radiologically as an advancing lytic wedge in long bones or osteoporosis circumscripta in the skull ) .Then, the osteolysis is followed by a compensatory increase in bone formation which is induces by osteoblasts recruited to the area,leading to accelerated deposition of lamellar bone in a disorganized fashion ("mosaic" pattern), rather than the normal linear lamellar pattern. After that,the resorbed bone is replaced , marrow spaces are filled by fibrous connective tissue with a marked increase in blood vessels ( hypervascular bone ). The bone hypercellularity may then diminish leaving a dense pagetic bone ,also known as burned-out Paget disease.
As for chronic infection,osteomyelitis is one of the example.Osteomyelitis is the infection of bone or bone marrow. In general, microorganisms may infect bone through bloodstream, contiguously from local areas of infection (as in cellulitis), or penetrating trauma, including iatrogenic .Once the bone is infected, leukocytes enter the infected area, and, in their attempt to engulf the infectious organisms, release enzymes that lyse the bone. Pus spreads into the bone's blood vessels, impairing their flow, and areas of devitalized infected bone, known as sequestra form the basis of a chronic infection.Often, the body will try to create new bone around the area of necrosis. The resulting new bone is often called an involucrum.On histologic examination, these areas of necrotic bone are the basis for distinguishing between acute osteomyelitis and chronic osteomyelitis. Osteomyelitis is an infective process which encompasses all of the bone components, including the bone marrow. When it is chronic it can lead to bone sclerosis and deformity.Because of the particulars of their blood supply, the tibia, femur, humerus, vertebra, the maxilla, and the mandibular bodies are especially susceptible to osteomyelitis. Abscesses of any bone, however, may be precipitated by trauma to the affected area.
Chronic osteomyelitis can lead to pathological fracture.It is due to excessively large diapyseal separation and the formation of involucrum that is inadequate to stand the normal stress brought to bear upon the limb.Moreover,fracture is facilitated by imperfect immobilization and support of the diseased bone,and is therefore more found in single bone � humerus and femur , compared to those that have companion bone for support

The other cause of pathological fracture is Fibrous Cortical Defect ( FCD ) ,nonaggressive fibrous lesion of bone , considered to be developmental defects. It typically occurred within the metaphysis of growing long tubular bones in children, most commonly about the knee. FCDs are asymptomatic, small (<3 cm), eccentrically located, metaphyseal cortical defects; most of these spontaneously disappear. However, some evolve and enlarge into fibroxanthomas. Conversely, fibroxanthomas (>3 cm) are larger, eccentric, intramedullary lesions that abut the cortex; they have a typical, superficial, scalloping pattern in the adjacent cortex.While these lesions also can heal spontaneously (with reactive bone filling in the central lucent fibrous tissue component), they can also persist, with interval growth that continues into adulthood. Typically, fibroxanthomas are asymptomatic. However, the larger lesions may become symptomatic, with a risk of pathologic fracture. Steiner suggested that these 2 lesions are secondary to cellular proliferation due to aberrations in local development.

Next is the Solitary bone cyst ,a benign, fluid-filled, radiolucent lesion that may appear in virtually any bone, but typically, it is found in either the proximal humerus or proximal femur. This lesion is found almost exclusively in children.It often leads to thinning of adjacent areas of bone, such that fracture or pain from microfracture may occur. When such cysts are immediately adjacent to a growth plate, they are referred to as active cysts, and when they have achieved some distance from the growth plate, they are considered to be latent cysts. It usually presents as a unifocal (one bone) problem, affecting patients who are skeletally immature.
Then comes the aneurysmal bone cyst (ABC) , an expansile cystic lesion that most often affects individuals during their second decade of life and may occur in any bone in the body. Although benign, it may become locally aggressive causing extensive weakening of the bony structure and impinge on the surrounding tissues. The true etiology and pathophysiology remain a mystery. However,different theories about several vascular malformations were suggested, these include arteriovenous fistulas and venous blockage. The vascular lesions then cause increased pressure, expansion, erosion, and resorption of the surrounding bone. The malformation is also believed to cause local hemorrhage that initiates the formation of reactive osteolytic tissue , further leading to the pathological fracture.
Moving on with chondromyxoid fibroma (CMF) , a rare benign tumor of bone. The etiology is unknown however, one report has pointed to an error in chromosome 6.The tumor arises from the cartilage-forming connective tissue of the marrow space. Histologically, as its name implies, this benign cartilaginous neoplasm consists of chondroid, myxoid, and fibrous tissue in variable amounts.Osteoclast-like giant cells may also be present, as may small cysts and hemorrhagic zones. Focal calcification is found microscopically in approximately one fourth of patients, although any gross evidence of calcification is rare.
Next is the fibous dysplasia , which is the skeletal developmental anomaly of the bone-forming mesenchyme that manifests as a defect in osteoblastic differentiation and maturation. It can affect any bone in the body. It is a nonhereditary disorder of unknown cause.However , there are suggestion that it may be due to abnormal growth process is related to a mutation in the gene that encodes the subunit of a stimulatory G protein (Gsα) located on chromosome 20.As a consequence of this mutation, there is a substitution of the cysteine or the histidine�amino acids of the genomic DNA in the osteoblastic cells�by another amino acid, arginine. The osteoblastic cells will elaborate a fibrous tissue in the bone marrow instead of normal bone. In fibrous dysplasia, lesions are characterized by woven ossified tissue and extensive marrow fibrosis. Mechanical quality of bones is decreased. As a consequence of this bone fragility, patients have an increased risk of fracture. Incidence of fractures is around 50% of cases.The risk of fractures or bone deformity is higher in the long bones, such as the femur, tibia, and humerus, but all the bones can be affected. There are 4 disease patterns recognized which are monostotic,polyostotic,cherubism, and craniofacial form.The monostotic type most frequently occurs in the rib (28%), femur (23%), tibia or craniofacial bones (10-25%), humerus, and vertebrae, in decreasing order of frequency.This form may present with pain or a pathologic fracture in patients aged 10-70 years, but this form most frequently occurs in those aged 10-30 years.
Next is Chondrosarcoma , a malignant tumor of cartilaginous origin in which tumor matrix formation is entirely chondroid in nature. Chondrosarcomas are classified as central (originating within the intramedullary canal) or peripheral. Rarely, they arise as juxtacortical lesionsTumors are predominantly axial most commonly involving the pelvic bones, femur, humerus, ribs, scapula, sternum, or spine. In tubular bones, the metaphysis is the most common site of origin. The proximal metaphysis is more frequently involved than the distal end of the bone. Involvement of the distal humerus is most unusual. Chondrosarcoma rarely occurs in the hands and feet; such occurrences usually arise as a complication of a multiple enchondromatosis syndrome. Chondrosarcoma arising de novo in the hands and feet is extremely unusual.The tumor may occasionally occur as a pathologic fracture.
Then,there is also osteosarcoma, the most common primary malignancy of bone. It is a malignant connective tissue tumor whose neoplastic cells present osteoblastic differentiation.The tumour may be localised at the end of the long bone. Most often it affects the upper end of tibia or humerus, or lower end of femur. The tumor is solid, hard, irregular ("fir-tree," "moth-eaten" or "sun-burst" appearance on X-ray examination) due to the tumor spicules of calcified bone radiating in right angles (Codman�s triangle). Surrounding tissues are infiltrated.The characteristic feature of osteosarcoma is presence of osteoid (bone formation) within the tumour. Tumor cells are very pleomorphic. These cells produce osteoid describing irregular trabeculae (amorphous, eosinophilic/pink) with or without central calcification (hematoxylinophilic/blue, granular) - tumor bone. Tumor cells are included in the osteoid matrix. Depending on the features of the tumour cells present (whether they resemble bone cells, cartilage cells or fibroblast cells), the tumour can be subclassified. The affected bone is not as strong as normal bones and may fracture with minor trauma (a pathological fracture)

Next,the Ewing sarcoma , a malignant round-cell tumor. It is a rare disease in which cancer cells are found in the bone or in soft tissue. The most common areas in which it occurs are the pelvis, the femur, the humerus, and the ribs.Genetic exchange between chromosomes can cause cells to become cancerous, like these cells from metastasized Ewing sarcoma. Ewing sarcoma is the result of a translocation between chromosomes 11 and 22, which fuses the EWS gene of chromosome 22 to the FLI1 gene of chromosome 11.EWS/FLI functions as the master regulator.Other translocations are at t(21;2) and t(7;22)The radiographic appearance of Ewing sarcoma may vary highly from a lytic one to a dominantly sclerotic one,and patient may present with pathological fracture.
Lastly is the bone metastases.The behavior of bone metastases can be characterized as osteoblastic, osteolytic or mixed, based on the effect on surrounding bone. All are due to dysregulation of the normal bone remodeling mechanisms, caused by tumor-host cell interactions. Osteoblastic tumors cause an abnormal formation of bone by direct secretion of bone extracellular matrix (ECM) proteins and by indirect stimulation of osteoblasts.Osteolytic tumors cause abnormal resorption of bone by proteolytic enzymes and through actions on osteoclasts. Osteolysis can release sequestered growth factors from the ECM, resulting in a cyclical feedback loop that leads to further stimulation of osteoclasts and continued bone resorption. As bone mass is lost, tumors can then continue to proliferate in their place,grow in size,causing further weakening of bone and thus leading to pathological fracture.
It is important to look into the underlying causes of pathological fracture in order for the treatment to be effective and safe.Some pathologic fracture require the same treatment as the other fractures,while others may require a highly specialized care.In a nutshell,pathological fracture involves a spectrum of causes wherein lies the modality of the treatment and care we will be giving to our patients.

Reference:

Apley�s System of Orthopaedics and Fractures 8th Edition � Louis Solomon ,
David J. Warwick , Selvadurai Nayagam

http://orthopedics.about.com/cs/brokenbones/g/pathologic.htm

http://www.wheelessonline.com/ortho/pathologic_fracture

http://emedicine.medscape.com/article/411919-overview

http://en.wikipedia.org/wiki/Osteoporosis

http://en.wikipedia.org/wiki/Hyperparathyroidism

http://en.wikipedia.org/wiki/Myelomatosis

http://en.wikipedia.org/wiki/Paget%27s_disease_of_bone

http://emedicine.medscape.com/article/1254784-overview

http://emedicine.medscape.com/article/388738-overview

http://emedicine.medscape.com/article/389714-overview

http://emedicine.medscape.com/article/1255262-overview

http://emedicine.medscape.com/article/388869-overview

http://en.wikipedia.org/wiki/Osteosarcoma

http://emedicine.medscape.com/article/389464-overview

http://emedicine.medscape.com/article/1257331-overview

http://emedicine.medscape.com/article/389590-overview

Osteogenesis imperfecta


OI and sometimes known as Brittle Bone Disease, or �Lobstein syndrome�.Osteogenesis imperfecta is disorder of congenital bone fragility caused by mutations in the genes that codify for type I procollagen. It is a common heritable disorder of collagen synthesis that results in weak bones that are easily fractured and are often deformed. It is also known as Brittle Bone Disease, or �Lobstein syndrome�. This condition affects an estimated 6 to 7 per 100,000 people worldwide. Several distinct subtypes have been identified. All of them lead to micromelic (short-limbed) dwarfism of varying degree. Depending on severity, the bone fragility may lead to perinatal death or cause severe deformities that persist into adulthood. A wide array of clinical manifestations of the disease may be seen. These partly depend on the genetic subtype. Types I and IV are the most common forms of osteogenesis imperfecta, affecting 4 to 5 per 100,000 people.

The following 4 types of osteogenesis imperfecta have been reported. Type I - mild forms, type II - extremely severe, type III, severe type IV � undefined.

People with this disease are born with defective connective tissue, or without the ability to make it, usually because of a deficiency of Type-I collagen. This deficiency arises from an amino acid substitution of glycine to bulkier amino acids in the collagen triple helix structure. The larger amino acid side-chains create steric hindrance that creates a "bulge" in the collagen complex. As a result, the body may respond by hydrolyzing the improper collagen structure. If the body does not destroy the improper collagen, the relationship between the collagen fibrils and hydroxyapatite crystals to form bone is altered, causing brittleness. Another suggested disease mechanism is that the stress state within collagen fibrils is altered at the locations of mutations. These recent works suggest that osteogenesis imperfecta must be understood as a multi-scale phenomenon, which involves mechanisms at the genetic, nano-, micro- and macro-level of tissues.
In osteogenesis imperfecta, the modes of inheritance, family history, clinical features, and radiologic findings vary.Four distinct types are identified: type I, which is the dominantly inherited form with blue sclerae; type II, which is the perinatal lethal form; type III, which is the progressively deforming form with normal sclerae; and type IV, which is the dominantly inherited form with normal sclerae.
In general, type I is the mildest form of disease; type IV, type III, and type II, respectively, increase in severity.
As a genetic disorder, Ti is an autosomal dominant defect. Most people with OI receive it from a parent but it can be an individual (de novo or "sporadic") mutation. Osteogenesis imperfecta is relatively rare. In some cases, the parent has osteogenesis imperfecta and the condition has been genetically transmitted to the child. But, the child's symptoms and the degree of disability could be very different from that of the parent. In some children, neither parent has osteogenesis imperfecta. In these cases, the genetic defect is a spontaneous mutation.
The primary pathology in osteogenesis imperfecta is a disturbance in the synthesis of type I collagen, which is the predominant protein of the extracellular matrix of most tissues. In bone, this defect of extracellular matrix causes osteoporosis, which leads to an increase in the tendency to fracture. Besides bone, type I collagen is also a major constituent of dentin, sclerae, ligaments, blood vessels, and skin; therefore, individuals with OI may also have abnormalities of these structures.
The process of collagen molecule formation starts with the synthesis of procollagen. This precursor consists of a long triple-helix protein flanked by 2 propeptides at its 2 terminals. Procollagen is synthesized and then secreted into the extracellular compartment, where the amino- and carboxy-terminal propeptides are cleaved; thus, the functional collagen molecule is formed. These molecules then assemble into an ordered fibril. Mutations that interfere with expression of the collagen gene, formation of the triple helix (amino acid sequencing), or procollagen secretion affect the structure and function of collagen fibrils, resulting in a form of OI.
Electron microscopic studies of OI demonstrate a decrease in the diameter of the collagen fibril, relative to the collagen fibril of healthy persons, and smaller-than-normal apatite crystals.
A number of genetic defects cause the abnormal type I collagen synthesis that leads to OI. OI generally arises from mutations in 1 of 2 genes that encode for the synthesis and/or structure of type I collagen: the COL1A1 gene on chromosome 17, and the COL1A2 gene on chromosome 7. Mutations in these genes may cause abnormal collagen to be produced and may lead to a decrease in the production of normal collagen. The varying degree to which these 2 factors manifest themselves results in the different phenotypic expressions of OI. Milder forms of OI are caused primarily by a decrease in production of normal collagen, whereas more severe forms are caused primarily by the production of abnormal collagen. These abnormalities may be dominantly inherited, or they may be the result of sporadic mutation.
Common causes of nonorthopedic morbidity in type I and type IV OI are joint hypermobility, which causes chronic joint pain, hearing impairment, and brainstem compression.Children with type III OI often require orthopedic care because of their progressive deformities. Standing and walking are often impossible because of spinal compression fractures and scoliosis. Progressive thoracic deformities are associated with recurrent pneumonias that often limit the patient's lifespan.
Type I: The life expectancy of patients with all forms of OI other than type III is often assumed to be shortened. However, according to Paterson et al, the life expectancy of patients with OI type IA is the same as that of the general population. Type IA is a subtype of type I OI in which dentinogenesis imperfecta (tooth abnormalities) does not occur. Type IB is a rare form of type I OI in which dentinogenesis imperfecta does occur. In types IB and IV, mortality is modestly increased in comparison with that of the general population; there is no statistically significant difference in life expectancy. Type II: This form of OI is fatal in the perinatal period.

Type III: Only in type III OI is life expectancy affected. However, patients with type III OI who survive beyond the age of 10 years have a better outlook than other patients with OI.
Osteogenesis imperfecta does not seem to have a predilection for any particular race. No known sex predilection is reported for osteogenesis imperfect. The onset of fractures and deformities varies according to the type of osteogenesis imperfecta (OI) that is present.
For type I, the age of onset is variable. This form most commonly appears during the preschool years when the child is starting to stand. Onset after puberty is uncommon, although fractures may recur in adulthood after menopause or after periods of inactivity, such as after childbirth. Type II occurs in utero. In type III, abnormalities are present at birth (ie, abnormalities develop in utero) in more than 50% of patients. Fractures are frequent during the first 2 years of life.Type IV abnormalities are present at birth in approximately 30% of patients. The onset of this form is during infancy or the preschool years.
The clinical features of osteogenesis imperfecta (OI) depend on the type, but bone fragility with multiple fractures and bony deformities are the common hallmark of all types.
The major presenting signs and symptoms of OI include blue sclerae, hearing loss, tooth abnormalities (dentinogenesis imperfecta), joint laxity, and abnormal skin texture (smooth and thin skin). Other features that are common to multiple OI types include bleeding diathesis (easy bruising) and respiratory distress.
OI is classified into 4 distinct types: I-IV. Some cases of OI do not fit easily into any of the 4 types. A type V category has been added to include patients with osteoporosis or interosseous membrane ossification of the forearms and legs, as well as patients who are prone to the development of hypertrophic calluses.




The type 1 prototypical and most common form of OI is associated with the best prognosis. The mode of inheritance is autosomal dominant. The distinguishing clinical features of type I are blue sclerae, which occurs in patients of all ages, and presenile conductive hearing loss; in addition, most patients with type I OI have a family history of hearing loss. Bone fragility is mild, and there are minimal bony deformities. The stature of patients with type I OI is often normal or near normal. Ligamentous hyperlaxity, resulting in joint hypermobility or subluxation, is common. Approximately 20% of patients have kyphoscoliosis.
Dentinogenesis imperfecta is present in some families but not in others.12 Therefore, type I OI is subclassified to distinguish patients without dentinogenesis imperfecta (type IA, more common) from those with dentinogenesis imperfecta (type IB, rare). Some investigators have suggested that these 2 subgroups are biochemically distinct and that individuals with OI type IB, whose bodies make structurally abnormal collagen, are more similar to those with OI type IV than to those with other types of OI, including type IA.
Type II is the most severe form of OI. It is characterized by extreme bone fragility that almost invariably leads to intrauterine or early infant death. The cause of death is most often respiratory failure. The mode of inheritance is autosomal recessive. The sclerae are blue and occasionally dark blue or black. Clinically distinguishing features include intrauterine growth retardation, thin and beaded ribs, crumpled long bones, and limited cranial and/or facial bone ossification. Limbs are short, curved, and angulated.
Type II OI can be further subdivided into types IIA, IIB, and IIC on the basis of the radiographic features of the long bones and ribs. Patients with type IIA or IIC inevitably die in the perinatal period; rarely, patients with type IIB survive into early childhood.
Type III is the next most severe form of OI after type II. It is the most severe form in which survival extends beyond the perinatal period.
Its hallmark feature is severe bone fragility and osteopenia, which is progressively deforming. The mode of inheritance is thought to be autosomal recessive. Multiple fractures and progressive deformity affect the long bones, skull, and spine and are often present at birth. Postnatal growth failure is severe. Kyphoscoliosis is common. Sclerae are either normal from birth, or they progress from pale blue in infancy to a normal appearance by adolescence.
Type III OI is probably the form that is best known to radiologists and orthopedic surgeons. Children with type II OI tend to have severe dwarfism caused by spinal compression fractures, limb deformities, and disruption of growth plates.
Type IV OI is distinguished from type I OI by the slightly increased, though still variable, severity of bone fragility and by the presence of normal sclerae. The mode of inheritance is autosomal dominant. Mild to moderate bony deformity of the long bones and spine is present; the incidence of fracture is variable. Basilar impression of the skull, with consequent brainstem compression, is common; it is reported in 70% of patients.

Hearing loss or a family history of hearing loss is noted in patients with this type of OI, as is dentinogenesis imperfecta. Type IV OI is also subclassified to distinguish patients without dentinogenesis imperfecta (type IVA) from those with it (type IVB). Compared with type I OI, hearing loss is less common in type IV, and dentinogenesis imperfecta (type IVB) is more common. Some authors have distinguished a self-limiting variant of OI, known as temporary brittle-bone disease. Its clinical features are identical with those found in cases of child abuse.
While there is no cure for osteogenesis imperfecta, there are opportunities to improve the child's quality of life. Treatment must be individualized and depends on the severity of the disease and the age of the patient. Care is provided by a team of health-care professionals, including several types of doctors, a physical therapist, a nurse-clinician and a social worker.
In most cases, treatment will be nonsurgical.
Medical bisphosphonates, given to the child either by mouth or intravenously, slow down bone resorption. In children with more-severe osteogenesis imperfecta, bisphosphonate treatment often decreases the number of fractures and bone pain. These medications must be administered by properly trained doctors and require close monitoring.
Casting, bracing, or splinting of fractures is necessary to immobilize the bone so that healing can occur. Movement and weight bearing are encouraged as soon as possible after fractures to increase mobility and decrease the risk of future fractures.
In surgical treatment, repeated fractures of the same bone, deformity, or fractures that do not heal properly are all indications that surgery may be necessary. Metal rods may be inserted in the long bones of the arms and legs. Some rods are a fixed length and must be replaced as the child grows. Other rods are designed like telescopes so they can expand along with the bone growth. However, other complications may occur with telescoping rods.
In many children with osteogenesis imperfecta, the number of times their bones fracture decreases significantly as they mature. However, osteogenesis imperfecta may become active again after menopause in women or after the age of 60 years in men. Scoliosis, or curvature of the spine, is a problem for many children with osteogenesis imperfecta. Bracing is the usual treatment for scoliosis, but it is often ineffective in children with osteogenesis imperfecta. Spinal fusion, in which the vertebrae are realigned and fused together, may be recommended to prevent excessive curvature.
At present there is no cure for OI. Treatment is aimed at increasing overall bone strength to prevent fracture and maintain mobility.
There have been many clinical trials performed with Fosamax (Alendronate), a drug used to treat women experiencing brittleness of bones due to osteoporosis. Higher levels of effectiveness apparently are to be seen in the pill form versus the IV form, but results seem inconclusive.

Bone infections are treated as and when they occur with the appropriate antibiotics and antiseptics.
Physiotherapy used to strengthen muscles and improve motility in a gentle manner, while minimizing the risk of fracture. This often involves hydrotherapy and the use of support cushions to improve posture. Individuals are encouraged to change positions regularly throughout the day in order to balance the muscles which are being used and the bones which are under pressure.
Children often develop a fear of trying new ways of moving due to movement being associated with pain. This can make physiotherapy difficult to administer to young children. With adaptive equipment such as crutches, wheelchairs, splints, grabbing arms, and/or modifications to the home many individuals with OI can obtain a significant degree of autonomy.
Spinal fusion can be performed to correct scoliosis, although the inherent bone fragility makes this operation more complex in OI patients. Surgery for basilar impressions can be carried out if pressure being exerted on the spinal cord and brain stem is causing neurological problems.
Because osteoporosis and multiple fractures are hallmark features of osteogenesis imperfecta (OI), other disorders that cause multiple fractures or decreased bone mineralization may be considered in the differential diagnosis. Such disorders including juvenile osteoporosis, steroid-induced osteoporosis, menkes (kinky-hair) syndrome, hypophosphatasia, battered child syndrome (syndrome X), temporary brittle-bone disease.

References:
http://emedicine.medscape.com/article/947588-overview

http://emedicine.medscape.com/article/411919-overview

http://ghr.nlm.nih.gov/condition=osteogenesisimperfecta

http://orthoinfo.aaos.org/topic.cfm?topic=A00051

http://hwmaint.jmg.bmj.com/cgi/content/abstract/16/2/101

Overuse Injuries in Orthopaedics practice

Posted by on Sunday, 12th September 2010

Overuse Injuries in Orthopaedics practice

INTRODUCTION

Overuse injuries are injuries of the musculoskeletal and nervous systems that may be caused by repetitive tasks, forceful exertions, vibrations, mechanical compression (pressing against hard surfaces), or sustained or awkward positions. It is also known as Repetitive Strain Injury or Cumulative Trauma Disorders. These are most commonly used to refer to patients in whom there is no discrete, objective, pathophysiology that corresponds with the pain complaints. Stress fracture is also a common overuse injury, which scientist already described it since 1855. Overuse injuries due to repetitive motion are common in occupational, recreational, habitual activities and elite athletes. [1] The examples of overuse injuries are Golfer's elbow, Tennis elbow, Baseball pitchers� elbow, Javelin throwers� elbow. These conditions have acquired names derived from activities in which they were encountered when they were first described.

PATHOPHYSIOLOGY
Normally, our tissues adapt to the stresses placed on them over time. Different types of stresses include shear, tension, compression, impingement, vibration, and contraction. Tendons, ligaments, neural tissue, and other soft tissues can undergo mechanical fatigue, resulting in characteristic changes depending on their individual properties. As a respond, the tissues attempt to adapt to the demands placed on them. In the process of adapting, they can incur injury unless they have appropriate time to heal. The rate of injury simply exceeds the rate of adaptation and healing in the tissue.
In stress fractures, it is resulted from recurrent and repetitive loading of bone. It differs from other types of fractures in that; most of them have no acute traumatic event preceding the symptoms. Usually, the patient has a history of an increase and/or change in the character of activity or athletic workouts, increase in frequency of doing activity, or change in posture during activity. Bones may be more prone to stress fractures if the bone is weakened, as in individuals with osteoporosis.
There are a lot of hypothesis as why does the injury happens in repetitive tasks. One of them is the depletion of adenosine 5�-triphosphate (ATP) in the muscle fibers, which leads to reduction of sarcoplasmic reuptake of Ca2+ resulting in high concentrations in the cytosol, allowing Ca2+ �dependent activation of phospholipase, the generation of free radicals, and damage to the muscle fibers involved. [1]
Other hypothesis involving Prostaglandin E2, which has been found to be present in high quantities in overuse tissues in rat and chicken models. [2] This mediator has been suggested to influence cell proliferation, increase collagenase, and decrease collagen synthesis. As the result of increasing loads on these tissues, nitric acid and prostaglandin amount are altered. However, a contradicting hypothesis based on rat-model observations shows that overuse of muscle may lead to an understimulation of tendon cells, rather than overstimulation.
In another study, alterations in regulation of genes within tendons undergoing overuse have been shown in the rat model, in which there is upregulation of genes associated with cartilage, and down-regulation of genes associated with tendon.[3] This might suggests that overuse may cause a morphologic alteration of tendon tissue, resulting in the cartilaginous changes in the tendons
From another point of view, psychosocial factors might play a role in overuse injuries for decades. This includes work satisfaction, perceived physical health, perceived mental health, coping mechanisms of the patient and his/her family, perception of work-readiness, and anxiety.
RISK FACTORS:
Risk factors for overuse injury are not only depends on the biomechanical changes of the action, but also intrinsic factor of the patient. Sex differences play a role in certain overuse injuries. For example, the incidence of carpal tunnel syndrome is higher among female compared to male. This has a variety of possible causes, including anatomical differences in the carpal tunnel, hormonal differences, differences in the activities performed by men and woman, biomechanical differences such as elbow carrying angles, Q-angles, femoral anteversion, and lean body mass. Stress fractures typically affect individuals who are more active, and the incidence probably increases with age due to age-related reduction in bone mineral density (BMD).
Although stress fractures result from repeated loading, some other causes such as menstrual disturbances and irregularities, lower dietary calcium intake, caloric restriction, less oral contraceptive use, muscle weakness, decreased testosterone level in male endurance athletes and leg-length differences are risk factors for stress fractures.[4] A study among military recruits has shown that recruits with stress fractures had significantly narrower tibiae and increased external rotation of the hip.
HISTORY:
It is important to obtaining complete information on the onset, timing, and frequency of symptoms; any associated symptoms; and alleviating and exacerbating factors. Information about specific activity or technique problem is also essential. Other relevant symptoms may include a history of popping, clicking, rubbing, erythema, or vascular phenomena. In athlete, specific attention must be paid to training details, equipment fit, and technique. The most salient historical feature in the diagnosis of stress fracture is the insidious onset of activity-related pain. In early stage, the pain is usually mild and felt toward the end of the inciting activity. As the disease progresses, the pain may worsen and occur earlier, limiting participation in sports activities. Rest may relief the pain in the early stages, but as the injury progresses, the pain may persist even after cessation of activity. Other than that, night pain is a frequent complaint. Usually, the patient has no recent history of trauma to the affected area.
Long-bone fractures usually lead to localized pain, while pain from injury of trabecular bone is more diffuse. Possible risk factors that precipitated or contributed to the injury should be identify. These include details of the athlete's training history both in terms of volume and intensity, intensive sustained muscular activity, muscle fatigue, structural malalignments, biomechanical inefficiencies, concurrent injury, or poor bone health status. Diagnosis is usually based on clinical findings and high index of suspicion because fracture site or new bone formation is visible on radiography maybe only after several weeks.
PHYSICAL EXAMINATION
The examination in case of overuse injury follows the basic method of orthopaedic examination; consist of inspection (including alignment and anatomical structure), palpation, and passive (including athlete's flexibility) and active range of motion (ROM). Usually, tenderness and guarding are present. During ROM examination, crepitus; painful or painless usually can be appreciated. On local examination, erythema, swelling, and anatomic derangement raise the possibility of an acute injury or infection, as well as the presence of an inflammatory disease. Some special test or maneuvers can be applied to help in making diagnosis, such as �Hop test� and �Fulcrum test�, or Tinel and Phalen tests at the wrist.[5] But, no single physical examination test is sufficiently sensitive and specific to permit the unequivocal diagnosis of a stress fracture. So, the doctor should correlate the history with examination, together with high clinical suspicion to consider the overuse injury as one of the possible diagnosis.

CAUSES

The primary factor leading to overuse injury is repetitive activity, although the specific type of force leads to different outcomes. Repetition is part of the definition of overuse injury. The concept is that overuse injury is associated with repeated challenge without sufficient recovery time. Another terms to describe repeated activities are cycles and fundamental cycles. While cycle is a large-scale activity that is repeated throughout the day, fundamental cycle is a small component of a cycle that may be repeated several times during the performance of a cycle. Repetitiveness and force exerted are features of a task that increase the risk of sustaining an overuse injury.

However, some studies have shown that cycle times and repetitive motions do not specifically lead to overuse injury in the upper extremity, but as possible causes for injury.[1] It is shown that vibration; especially over long periods is a factor in increasing the risk of many injuries such as lower back pain, intervertebral disk injury, and wrist injury. Apart from the above, malpositioning of limbs away from their neutral position increases the risk for overuse injury.


DIFFERENTIAL DIAGNOSIS
Differential diagnoses vary and depend on location, symptoms, history and physical examination.
o Shin splints (medial tibial stress syndrome) can mimic stress fractures ot the tibia. Shin splint pain tends to be present at the start of activity, while overuse injury at the end. Tenderness to palpation over a wide region of the tibia and the tibialis muscle, whereas the pain from stress fractures tends to be localized to a specific area on the tibia.
o True fractures can be differentiated from overuse injury by an obvious history, with a traumatic event being recalled by the patient with acute onset of pain.
� Muscle strains; may be acute or chronic. Chronic muscle strains can be differentiated from overuse injury by the location and by factors that exacerbate or worsen the injury.
� Costochondritis may mimic the pain seen in stress fractures of the ribs. Rib stress fractures should be suspected in athletes who participate in rowing sports, such as crew rowing. The pain of costochondritis may be more diffuse or widespread than the pain from stress fractures of the ribs. .[4]
� Nerve entrapment syndromes can also mimic overuse injury, but can be differentiated by presence of numbness in the former.[4]
� Popliteal artery entrapment syndrome is another cause of lower extremity pain. This also present with increased pain and/or swelling with exercise, which is more diffuse than the pain associated with stress fractures. Measurement of ankle blood pressures before and during exercise or an angiogram may help with the diagnosis.
DIAGNOSIS AND INVESTIGATIONS
Radiography
Stress fractures may not show up on radiographs for the first 2-4 weeks after injury. The first radiographic finding may be a localized periosteal reaction or an endosteal cortical thickening. The low sensitivity of radiographs for stress fractures gives advantage to bone scanning, magnetic resonance imaging (MRI), and computed tomography (CT).
Magnetic resonance imaging (MRI)
MRI not only provides information about bone integrity and fracture orientation, but also can demonstrate focal tissue damage and edema.
Technetium-99m bone scanning
It took 72 hours for Technetium bone scan findings to be positive in the case of a stress fracture. However, a positive bone scan finding is nonspecific, and it may be indicative of another diagnosis, such as an infection or a neoplastic process. In a study which compare conventional radiography and bone scanning for the initial detection of stress fractures, positive findings were reported in 96% of bone scans, whereas only 42% positive findings were reported on radiographs.
Electrodiagnostic testing
Electrodiagnostic testing (such as EMG, nerve conduction studies) can be very useful in cases of peripheral nerve compression or injury; such testing can provide evidence of the location and severity of the injury. However, EMG and nerve conduction studies are not tests with high specificity, although they can provide much-needed information when vague symptoms are the chief complaint. They are also very useful for documenting work-related injuries.
Laboratory Tests
These tests are relevant if the individual is discovered to have metabolic bone disease or another comorbidity such as inadequate nutritional status.

TREATMENT
Physical Therapy
Patient should have rest, particularly avoidance of the inciting activity. Total bed rest is virtually never advisable for these patients. Instead, participation in a carefully planned physical therapy program is important. The physical therapy program also offers the patient the chance to see that movement will not lead to ongoing tissue damage, thus preventing significant "sick behaviors" or kinesophobia. Ill-fitting equipment, overtraining, or technique flaws commonly cause overuse injury in athletes. So, specialized fitted equipments hould be provided, while sports psychology is worthwhile in combating overtraining, and sport-specific coaching is often invaluable. Coaches, athletes, and physicians must work together to correct these problems.
Occupational Therapy
Occupational therapists can help to identify workplace modifications. In cases of individuals who develop overuse injuries as a result of the interface with adaptive equipment, occupational therapy may be of great benefit. Simple modifications in the manner in which the patient performs activities of daily living or modifications in the equipment itself can provide relief.
 

Surgical Intervention
Surgical intervention is required only if conservative approaches fail, or if the injury is amenable to surgery. Most common problems that lead to surgery in overuse injury are decompression of nerves and repair of lax or failed ligaments. Surgical procedures most typically involve open-reduction internal fixation and pinning of the associated fracture sites. Surgeries that are performed solely to relieve pain in the absence of objective findings are notorious for suboptimal outcomes.
Medication
Combined injection of corticosteroids and local anesthetics is quite helpful in persons with overuse injury.[1] Pain relief enables more effective participation in therapy, and it may help to limit the likelihood that the patient will develop a chronic pain syndrome. Usually, injections should be performed after less invasive measures fail. In some rare condition, immediate relief of pain may be necessary to allow participation in an athletic or performing arts event, and this can be achieved through injection therapy.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are mainstays in the treatment of overuse injuries. However, there are evidences that revealed that true inflammation is rarely a component of these disorders, especially tendinopathies. So, the use of simple analgesics has become more prevalent in the treatment of such disorders. Muscle relaxants, opiates, corticosteroids, tricyclic antidepressants, and sleep medications have a role in the specific treatment of individuals with overuse injury.

PREVENTION
Nutritional measures: calcium supplementation
A study by Schwellnus and Jordaan found that there is no benefit with calcium supplementation (500 mg/d) beyond the usual dietary intake in male military recruits.[6]
Biomechanical measures: orthotics and shoe inserts
The use of orthotic devices and shoe inserts has been studied as a preventive measure for lower-extremity stress fractures. It is found that the incidence of lower-extremity stress fractures was lower in the group using semirigid orthoses (15.7%) or soft biomechanical orthoses (10.7%) than in the control group (27%). Additionally, the recruits better tolerated the soft biomechanical orthoses than the semirigid orthoses.[7]
In a prospective study of stress fractures, shock-absorbing orthotic device worn within military boots decreases the incidence of stress fractures. [8] There is a statistically significant decrease in the incidence of femoral stress fractures in the orthotic device group.
COMPLICATION
High-risk stress fractures
Even though nonunion of stress fractures is uncommon, but it can occur. To prevent this, stress injuries should be closely followed up for early surgical intervention. These include stress fractures of the neck of the femur, the anterior cortex of the tibia, the tarsal navicular, and the bases of the second and fifth metatarsals. Other high-risk stress fractures include stress fractures of the patella and medial malleolus.
Low-risk stress fractures
Low-risk stress fractures include most upper-extremity stress fractures, except for the fractures through the physis of the humeral head (little leaguer's shoulder) and fractures through the medial epicondyle (little leaguer's elbow), which may have complications due to the involvement of the growth plate.[9] Other low-risk stress fractures include stress fractures of the ribs, pelvis, femoral shaft, fibula, calcaneus, and the metatarsal shafts.

REFERENCES:
1. eMedicine. Scott R Laker, MD. Overuse Injury, Mar 12, 2008.

2. Flick J, Devkota A, Tsuzaki M, et al. Cyclic loading alters biomechanical properties and secretion of PGE2 and NO from tendon explants. Clin Biomech (Bristol, Avon). Jan 2006; 21(1): 99-106.

3. Archambault JM, Jelinsky SA, Lake SP, et al. Rat supraspinatus tendon expresses cartilage markers with overuse. J Orthop Res. May 2007; 25(5): 617-24.

4. eMedicine. John M Martinez, MD. Stress Fractures, Apr 17, 2008.

5. eMedicine. Vincent N Disabella, DO, FAOASM. Elbow and Forearm Overuse Injury, Feb 12, 2008.

6. Schwellnus MP, Jordaan G. Does calcium supplementation prevents bone stress injuries? A clinical trial. Int J Sport Nutr. Jun 1992; 2(2): 165-74.

7. Finestone A, Giladi M, Elad H. Prevention of stress fractures using custom biomechanical shoe orthoses. Clin Orthop. Mar 1999;360: 182-90

8. Schwellnus MP, Jordaan G, Noakes TD. Prevention of common overuse injuries by the use of shock absorbing insoles � A prospective study. Am J Sports Med. December 1990; 18:636-641.

9. Boden BP, Osbahr DC, Jimenez C. Low-risk stress fractures. Am J Sports Med. Jan-Feb 2001; 29(1): 100-11.


N.B. This article is excerpted from the Book : OVERUSE INJURIES IN ORTHOPEDIC PRACTICE: Diagnostic Enigma and Mananagement Principles

Editorial Reviews
Product Description
Overuse injuries are injuries of the musculoskeletal and nervous systems that may be caused by repetitive tasks, forceful exertions,vibrations,mechanical compression,or sustained or awkward positions.It is also known as Repetitive Strain Injury or Cumulative Trauma Disorders. These are most commonly used to refer to patients in whom there is no discrete,objective,pathophysiology that corresponds with the pain complaints.Physical activity is a great way for kids to build bone strength, prevent obesity and stay healthy,when paired with safety and prevention practices. With youth sports injuries rising at alarming rates,overuse injuries such as sore bones and muscles, and swollen or injured joints need prompt attention in child athletes to prevent chronic musculoskeletal problems later in life. Understanding overuse injuries can guide you to designing your training to reduce the risk of injury and help you to recognize and treat them as they inevitably occur.Overuse injuries can be defined as the product of "too much,too fast,too soon." The topics discussed in these chapters are conditions commonly seen by the author in his long stint as an orthopedic and sports medicine consultant.
About the Author
Prof Gourishankar Patnaik is internationally renowned orthopedic and Spinal surgeon. A topper throughout he has over two decades of teaching and research experience at various medical colleges in India, Oman, USA and Malaysia. A globe trotter he has authored many books. A gifted Surgeon his research interests include diabetes, Neurotrauma and E-learning.

Date Palm Synovitis

Date Palms
The date palm is common in the Sultanate of Oman and neighboring Gulf countries. The history goes back 600 years to Eridu in lower Mesopotamia where the first evidence of date cultivation has been found. Closer to this oasis, the Hilli settlements of Al-Ain in the Arabian Peninsula seems to be cultivated dates some 5000 years back. In Bidiyah, in the eastern region of the Sultanate of Oman, dates are the main-stay of the economy. Date growing is labor intensive in Oman and very traditional in its method.

To fertilize the female flowers (pistils), each date palm must be climbed and the pistils, which are clustered to the center of the leaves, pollinated. Each date palm provides the farmer with natural steps to climb the trunk. These are formed from the base of the previous season�s leaf stalks which were cut off. The technique of climbing is simple but since a date palm can be 30 meters tall, a key requirement is good head for height. The worker has to climb the tree once more in the later months in order to obtain the fruit that is now ready to be harvested.
Synovitis
Synovitis is the medical term for inflammation of the synovial membrane. This membrane lines joints which possess cavities, known assynovial joints. The condition is usually painful, particularly when the joint is moved. The joint usually swells due to synovial fluid collection.
Synovitis may occur in association with arthritis as well as lupus, gout, and other conditions. Synovitis is more commonly found in rheumatoid arthritis than in other forms of arthritis, and can thus serve as a distinguishing factor, although it can present to a lesser degree in osteoarthritis. Long term occurrence of synovitis can result in degeneration of the joint.

Date Palm Synovitis

Joint inflammation associated with intra-articular retention of a date palm thorn.

Synonyms

Date Palm Knee

Incidence

Uncommon in the northern hemisphere and in developed countries. It is much more common in Sultanate of Oman and neighbouring Gulf countries where traditional agricultural practices require climbing palm trees. Because the original injury may have been forgotten, this diagnosis should be considered in mono-articular inflammation in children.

Differential Diagnosis

Septic arthritis

( This can be differentiated by doing a simple blood investigation.
There will be normal WBC and ESR in Date Palm Synovitis, meanwhile in septic arthritis there will increase in both WBC and ESR)

Pathogenesis

A penetrating injury into the joint (usually the knee) results from a minor wound from a the thorn. The date palm tree bears thorns 10-15cm long, which can easily pierce the joint cavities.
If the thorn breaks off inside the joint, an acute, sub-acute or chronic inflammation of the joint may result. Many infective agents have been associated with date palm thorn. with no one predominating bacterium. Staphylococcus aureus has been found commonly but this is thought to be secondary infection following attempts at self-treatment.

Pathology

The arthritis may be either septic or sterile. It is unknown whether the primary features are due to infection or to an immune response to the foreign material in the vegetable matter. The reason for this is not clear, but alkaloids in the thorns are a possible cause (Stromqvist, Edlund and Lidgren 1985). The pathological features are those of acute inflammatory synovitis. Chronic synovitis develops if the condition persists.

Macroscopically,
� Redness, swelling, tenderness, loss of range of motion
� May settle to a chronic effusion with thickened boggy synovium
� May progress to a septic arthritis. There may also be a soft tissue infection leading to fasciitis. Examine for local, distant and systemic signs of infection � pyrexia, malaise, lymphadenopathy, cellulitis
� Rare presentation as locking, mimicking IDK with the thorn itself causing the locking

Microscopically,
Synovium from to two cases requiring partial synovectomy showed a non-specific synovitis. (Haematoxylin and eosin)
Synovial tissue from knee of patient with thorn-induced synovitis (hematoxyline- phloxine-saffron). Top: Heavy fibrin deposits (F) on surface and intenae infiltration of inflammatory cell (original maginification x 120, reduced approximately 25%). Bottom: Foreign material (arrow) in synovium, surrounded by numerous giant cells, seen under polarized light, material is highly refractile, consistent with plant thorn matter (original magnification x 540)

Stages

Acute
Infected
Inflammatory
Sub-acute (> 1 week)
Chronic
Non-specific

Classification

None encountered in the literature. Useful classifications could be devised using time, aetiological agent, infected/sterile or extent of the condition.

Clinical Features

Palm thorn synovitis is usually mild, the initial symptoms are often intolerated, delaying presentation for treatment.
The clinical features are:

� Puncture wound or history (may be absent)
� Redness, swelling, tenderness, loss of range of motion
� May settle to a chronic effusion with thickened boggy synovium
� May progress to a septic arthritis. There may also be a soft tissue infection leading to fasciitis. Examine for local, distant and systemic signs of infection � pyrexia, malaise, lymphadenopathy, cellulitis
� Rare presentation as locking, mimicking IDK with the thorn itself causing the locking

Investigation

CRP, aspiration and culture may identify an infective process and an organism but treatment of the infection may not resolve the problem unless the presence of the foreign body is detected. But normally, the WBC and ESR is within normal limits and no organisms was grown from any joint aspirate.

Depending on the stage fluid aspirated from the joint will have acute or chronic inflammatory cells but other rheumatological investigations will be negative.
Xrays are most often negative apart from a synovial effusion as thorns cannot be seen on radiographs. CT scan has been claimed to be diagnostic. MR scan is reliably diagnostic for this condition as the foreign body ( thorns) shows up well.

Prognosis untreated

In the acute infected case the prognosis is that of acute septic arthritis
For sterile cases and indolent infections the condition may settle to a chronic mono-arthritis with eventual secondary OA.
Since the condition is provoked by the presence of foreign material it will not settle completely until the foreign material is removed or eliminated.

Non-Operative Treatment

Appropriate antibacterial treatment.
Symptomatic treatment with analgesics and anti-inflammatory medication.
Steroid injection contra-indicated

Operative Treatment

Transarthroscopic excision of the loose body
Open or transarthoscopic synovectomy
Surgical treatment of septic arthritis

Complications

Chronic arthritis
Secondary OA
Sepsis

Outcomes

Favourable outcome after early recognition and surgical treatment
Literature suggests that synovectomy may be necessary after development of chronic synovitis i.e. that removal of the foreign body may not be enough.

Bibliography

1. Clough J.F.M. (1999) Cactus Knee Orthopaedic Rare Conditions Internet Database (ORCID) http://www.orthogate.org/orcid/aspercases.htm
Has an extensive bibliography on this subject

2. Maillot F, et al.
Plant thorn synovitis diagnosed by magnetic resonance imaging.
Scand J Rheumatol. 1994;23(3):154-5.


3. Doig SG, et al.
Plant thorn synovitis. Resolution following total synovectomy.
J Bone Joint Surg [Br]. 1990 May;72(3):514-5.

4. Klein B, et al.
Thorn synovitis: CT diagnosis.
J Comput Assist Tomogr. 1985 Nov-Dec;9(6):1135-6.


5. Ramanathan EB, et al.
Date palm thorn synovitis.
J Bone Joint Surg [Br]. 1990 May;72(3):512-3.

6. Olenginski TP, et al.
Plant thorn synovitis: an uncommon cause of monoarthritis.
Semin Arthritis Rheum. 1991 Aug;21(1):40-6.


7. Vaishya R.
A thorny problem: the diagnosis and treatment of acacia thorn injuries.
Injury. 1990 Mar;21(2):97-100.

8. Adams CD, Timms FJ, Hanlon M.
Phoenix date palm injuries: a review of injuries from the Phoenix date palm treated at the Starship Children's Hospital. Aust N Z J Surg. 2000 May;70(5):355-7.


9. Miller EB, Gilad A, Schattner A.
Cactus thorn arthritis: case report and review of the literature.
Clin Rheumatol. 2000;19(6):490-1.

10. Labbe JL, Bordes JP, Fine X.
An unusual surgical emergency: a knee joint wound caused by a needlefish. Arthroscopy. 1995 Aug;11(4):503-5.

FROZEN SHOULDER IN DIABETICS

Posted by on Sunday, 22nd August 2010

FROZEN SHOULDER IN DIABETICS
When we ponder upon diabetes mellitus and its complications, we might be imagining conditions like diabetic foot, renal failure, atherosclerosis, diabetic retinopathy and so on. Shoulder problems are not what come to mind when most people think of diabetes. But studies have found a link between both types of diabetes and a condition known as frozen shoulder.
The incidence of frozen shoulder has been estimated to be from 3% to 5% in the general population, with a significantly increased incidence amongst diabetics, on the order of
10% to 20%. It appears to be most common in adults between the ages of 40 to 70 years. Women appear to be at a slightly increased risk (4:1) and the non-dominant arm is most commonly affected. Idiopathic frozen shoulder is most strongly associated with insulin-dependent diabetes, in which the lifetime risk of developing adhesive capsulitis may be as high as 36%, with the first episode occurring at a significantly younger age than in the general population. Non-insulin-dependent diabetics also have an increased incidence of frozen shoulder, but not as high as in insulin users. Diabetics also have a tendency to develop bilateral shoulder involvement. Therefore, patients who present with a somewhat atypical set of findings should be screened for diabetes as part of their initial workup.
So, what is a frozen shoulder actually? A frozen shoulder is a shoulder joint with significant loss of its range of motion in all directions. The range of motion is limited not only when the patient attempts motion, but also when the doctor attempts to move the joint fully while the patient relaxes. A frozen shoulder is also referred to as adhesive capsulitis. The modern English words "adhesive capsulitis" are derived from the Latin words adhaerens meaning "sticking to" and capsula meaning "little container" and the Greek word itis meaning "inflammation". The shoulder is the most mobile joint in the body. Its function is to position the arm in space to reach out to objects and deliver them for other actions. The shoulder is a ball and socket joint formed by the upper end of the humerus (arm bone) and the socket formed by the glenoid of the shoulder blade. It is lined by a bag like capsule. The capacity of this joint is about 15- 20 cc. In frozen shoulder the capacity is reduced to 2- 3 cc. The movements at the shoulder joint occur synchronously with that at joint between the shoulder blade and the torso and are compensated to some extent by this.

A few theories had been put forth by a number of physicians and researchers to explain the link between frozen shoulder and diabetes mellitus. Dr. Aaron Vinik, MD, PhD who is the Director of Diabetes Research Institute in Eastern Virginia Medical School, Norfolk, Virginia said that certain compounds accumulate in the linings of joints in the collagen. The collagen fibers then stick together and limit the capacity for the joint and ligaments to stretch with movement. Ultimately this ends up as a frozen shoulder. Agreeing with the fact, Dr. Richard Bernstein of the Diabetes Center Mamaroneck, New York offers his perspective on frozen shoulder:
Muscular and skeletal problems are virtually universal among people with long-standing, poorly controlled diabetes. Sometimes the problems are very painful and even disabling. They probably stem from glycosylation of collagen (a protein in tendons).
Collagen fibers normally slide along one another during muscular movement. In glycosylation, they become glued together by glucose. This process can also occur in the skin, which becomes hard and tough (diabetic scleredema).
In another studies, Neviaser and Neviaser in 1945 coined the name "adhesive capsulitis" to suggest an adhesive process of the capsule to the humeral head and was first termed by. However, this name appears to be somewhat of a misnomer, as later shown by later arthroscopic evaluations. What has been found is a contracture that consists of thickening and fibrosis within the joint capsule itself. This process results in decreased intra-articular volume and diminished capsular compliance, so that glenohumeral motion is limited in all planes. Normal intra-articular volume is about 15 to 30 cc; in patients with adhesive capsulitis, the joint capacity is typically less than 10 cc.
Histologically there has been some controversy regarding the etiology of the fibrosis and contracture of the capsule. In original studies done by Neviaser there was evidence of synovial inflammation. In separate studies, however, Bunker suggested that the active pathologic process is that of fibroblastic proliferation. Interestingly, it appears that the histologic changes are very similar to Dupuytren's contracture, which is also associated with diabetes.
Meanwhile, recent advances discovered that the answer to frozen shoulder lies in the genes. These genes may also be associated with Diabetes mellitus. The alterations in these genes and chromosomes lead to a distorted response to wound healing and scar tissue formation. Exuberant scar tissue forms in response to trauma. The remodeling of scar tissue collagen is less. When more scar tissue forms in the capsule of the shoulder joint, the normally possible movements are grossly reduced. Diabetics also develop nodules in their palms and feet, another evidence of the exaggerated healing process.
Whatever it is, the pathophysiology of frozen shoulder in diabetics remains elusive. What can be said is that, there is a positive evidence to link the excessive level of glucose in the blood and the process of glycosylation of the collagen fibers to be responsible in the development of frozen shoulder.
Classically, the frozen shoulder has been described as occurring in 3 stages:
(1) painful, (2) stiff, and (3) resolving. The natural course of these phases
typically takes from 1 to 3 years to resolve. The first phase often begins
with pain in the shoulder. Patients will complain of pain while sleeping on
their side and will self-restrict the movement of their shoulder to their side
in order to avoid pain. They often complain of generalized pain in the deltoid
region. Often, patients will not seek medical attention during this phase,
expecting that the pain will resolve on its own. They may self-medicate with
analgesics, and will only present when the restriction of motion becomes problematic.
There is usually no inciting trauma or other event, although patients may remember
the specific moment when they were unable to do a particular activity due to
restricted motion. The painful phase may last from 2 to 9 months.
In the stiff or frozen phase, the shoulder is significantly
restricted, and patients note the inability to perform daily functions, especially
those that require significant internal or external rotation or elevation (e.g.
hair washing, reaching overhead). Patients often present at this point with
very specific complaints, such as an inability to scratch their back, fasten
their bra, or get an item from an overhead shelf. When moving within the limits
of their motion, the patient has little or no pain. It is only when the patient
attempts an activity that requires motion beyond their capability that they
develop "end-range pain." The frozen stage can last for 3 months
to 1 year.
In the resolution phase, the "thawing" begins and the patient gradually regains some range of motion. The ability to perform functional activities improves over 1 to 3 years; however, full range of motion is rarely recovered. On long-term follow-up (even up to 11 years later), up to 60% of patients appear to have persistent restriction. What is notable is that loss of less than 20% of the normal range of motion does not appear to affect activities of daily living, nor cause significant functional disability.
How a frozen shoulder is usually diagnosed? A frozen shoulder is suggested during examination when the shoulder range of motion is significantly limited, with either the patient or the examiner attempting the movement. Underlying diseases involving the shoulder can be diagnosed with the history, examination, blood testing to exclude any endocrine disorders e.g. hyperthyroidism, and x-ray examination of the shoulder.
If necessary, the diagnosis can be confirmed when an x-ray contrast dye is injected into the shoulder joint to demonstrate the characteristic shrunken shoulder capsule of a frozen shoulder. This x-ray test is called arthrography. Arthrogram contrasts are special x-rays that show details of the shoulder capsule, such as a decrease in size (in a normal shoulder the capsule is rounded, but in a frozen shoulder the capsule is squat, square and contracted).

The tissues of the shoulder can also be evaluated with an MRI scan. The MRI findings that suggest adhesive capsulitis include soft tissue thickening in the rotator interval, which may encase the coracohumeral and superior glenohumeral ligaments, and soft tissue thickening adjacent to the biceps anchor. Other findings that can be demonstrated on MRI include thickening of the inferior glenohumeral ligament greater than 4 mm and loss of definition of the inferior capsule secondary to edema and synovitis.
The aim of treatment for frozen shoulder is to alleviate pain and preserve mobility and flexibility in the shoulder. However, recovery may be slow, as symptoms tend to persist for several years. Treatment options for frozen shoulder include painkillers to relieve symptoms of pain. Nonsteroidal anti - inflammatory drugs (NSAIDs), such as ibuprofen, are over - the - counter (OTC, no prescription required) painkillers and may reduce inflammation of the shoulder in addition to alleviating mild pain. Acetaminophen (paracetamol, Tylenol) is recommended for extended use. Prescription painkillers, such as codeine (an opiate - based painkiller) may also reduce pain. Not all painkillers are suitable for every patient; be sure to review options with doctor.
Exercise which is frequent and gentle can prevent and even reverse stiffness in the shoulder. Vigorous activity involving shoulder joint should be hindered to prevent more injury from occurring at the site and thus slowed down the healing. Hot or cold compression packs may help to reduce pain and swelling. It is often helpful to alternate between the two.
Corticosteroid injection is a type of steroid hormone that reduces pain and swelling. Corticosteroids may be injected into the shoulder joint to alleviate pain, especially in the 'painful stage' of symptoms. However, repeated corticosteroid injections are discouraged as they could cause damage to the shoulder. It is also a diabetogenic hormone which is not so preferably good choice of treatment for frozen shoulder in diabetics.
Transcutaneous electrical nerve stimulation (TENS) numbs the nerve endings in the spinal cord that control pain and sends small pulses of electricity from the TENS machine to electrodes (small electric pads) that are applied to the skin on the affected shoulder.
Physical therapy or physiotherapy session can teach exercises to maintain as much mobility and flexibility as possible without straining the shoulder or causing too much pain. Physiotherapy in the form of gentle, firm stretching exercises in various planes of motion has been proven to be effective in the relief of pain and in recovery of range of motion in up to 90% of patients with idiopathic frozen shoulder.
Ultrasound can speed the recovery of a frozen shoulder injury significantly by breaking down the scar tissue around the shoulder joint. Using ultrasound on a regular basis or throughout the day will help relax the shoulder muscles, tendons and tissues, diminish pain and inflammation, soften scar tissue and contribute greatly to the healing of injury.
For a resistant frozen shoulder or if patient has poor compliance to the aforementioned regiments, shoulder manipulation can be used as an alternative. The shoulder joint is gently moved while patient is under a general anesthetic. Another way is shoulder arthroscopy - a minimally invasive type of surgery used in a small percentage of cases. A small endoscope (tube) is inserted through a small incision into the shoulder joint to remove any scar tissue or adhesions.
As a conclusion, most patients who present with a restriction of shoulder motion with history of diabetes mellitus and no significant history of trauma to the shoulder may fall under the category of frozen shoulder. This fact can help the clinician to choose an appropriate treatment regimen. Patients diagnosed with the idiopathic form of adhesive capsulitis should be put on a gentle stretching regimen, and counseled about the natural history of the disease, which can take many months to resolve. All of the above treatments absolutely work if properly performed with the right equipment. But, if blood sugar remains elevated, such problems will in all likelihood recur.

REFERENCES:
1. http://www.medicinenet.com/frozen_shoulder/article.htm
2. http://www.diabeteshealth.com/read/1999/11/01/1702/how-is-frozen-shoulder-associated-with-diabetes/
3. http://www.med.ucla.edu/modules/wfsection/article.php?articleid=233
4. http://EzineArticles.com/?expert=Alampallam_Venkatachalam
5. http://www.nlm.nih.gov/medlineplus/ency/article/000455.htm
6. http://www.deccanchronicle.com/health/diabetes-can-lead-frozen-shoulder-571
7. http://www.cnn.com/HEALTH/library/frozen-shoulder/DS00416.html
8. http://www.diabeteshealth.com/read/1999/11/01/1702/how-is-frozen-shoulder-associated-with-diabetes/
9. http://www.medicalnewstoday.com/articles/166186.php


This article is excerrpted from
: Orthopedic and Rheumatological afflictions in Diabetes Mellitus A review - Paperback (July 30, 2010) by Gourishankar Patnaikhttp://www.amazon.com/Musculoskeletal-Manifestations-Diabetes-Mellitus-Rheumatological/dp/363928089X/ref=sr_1_1?ie=UTF8&s=books&qid=1282478501&sr=8-1

ORTHOPEDIC MANIFESTATIONS DURING PREGNANCY

Posted by on Sunday, 22nd August 2010

ORTHOPEDIC MANIFESTATIONS DURING PREGNANCY

Almost all pregnant women experience musculoskeletal discomfort during pregnancy,
with a good portion of them suffering from severe disability. The enlarging gravid uterus alters
the maternal body's center of gravity, mechanically stressing the axial and pelvic systems, and compounds the stresses that hormone level fluctuations and fluid retention exert. While the pregnant woman
is prone to many musculoskeletal injuries, most can be controlled conservatively, but some require emergent surgical intervention.

Often, the source of these musculoskeletal problems can be traced to an endocrine disorder.
For example, carpal tunnel syndrome is not uncommon in patients who are pregnant or
have diabetes, hypothyroidism, or acromegaly. Joint problems and arthritis
are other common findings in diabetes, pregnancy, and hyperparathyroidism. Muscle weakness or stiffness is seen in both hypothyroidism and hyperthyroidism, and muscle wasting is a characteristic of adrenocorticoid insufficiency. Bone disorders are common with glucocorticoid excess, acromegaly, and hyperparathyroidism. Some presentations are a classic picture of a specific endocrine condition and are readily recognized if the index of suspicion is appropriately high.

During pregnancy, certain anatomical and hormonal changes occur that produce
increased stress on the pelvic
articulations resulting in the development of pelvic girdle relaxation. Pelvic girdle relaxation during pregnancy is physiological and is caused by hormonal and biomechanical factors. When a pregnant woman presents as
a patient with low back or pelvic pain, walking dysfunction and with reproduction
of pain with sacroiliac provocation, the diagnosis of symptomatic pelvic girdle relaxation can be madeThe gravid uterus
and the compensatory lordosis that it
causes create a tremendous mechanical
burden on the lower back. Joint laxity increases during pregnancy. The hormone relaxin has been identified as a major contributor to joint laxity during pregnancy. It decreases the intrinsic strength of the connective tissue allowing it to expand and lose its rigidity, resulting in increased widening and sliding mobility of the joints, thus causing potential instability. This occurs especially in the ligaments of the sacroiliac and pubic symphysis joints,
but may also occur in peripheral joint.
This may result in pubic symphysis pain,
low back pain or hip pain.

Pubic Symphysis Pain

Pathology: Separation of the pubic symphysis joint (diastasis or symphysiolysis), as a result of pelvic girdle relaxation, is thought to be the main cause of pubic symphysis pain. Relaxin levels were found
to be significantly higher in pregnant
women with pelvic pain and joint laxity.
The highest level was found in those women with the most severe clinical symptoms, who also took a longer time to recover after pregnancy. Swelling within the joint, ligament disruption and hemorrhage have
also been suggested to cause pubic symphysis pain. The severity of these conditions varies from mild self-limiting pain to a severe disabling condition. Lack of awareness and failure of recognition of these complications by obstetricians not only results in women feeling very lonely and misunderstood, but may also result in long-term morbidity.

Presentation: Patients may present during pregnancy (usually in the second or third trimester), during labour or 24-48 hours postpartum, with a sudden or insidious
onset of pain of variable severity in the pubic area or groin which may radiate to
the medial aspect of the thigh and increases on weight-bearing. Pain may occur also in the hips, suprapubic area or the lower back and be aggravated by walking, standing, stairs climbing, parting of the legs or turning in bed.

Clinically, a waddling gait or limp may be noticed. The woman may not be able to stand comfortably on one leg. Abduction of the thigh is usually painful. Point tenderness in the region of the pubic symphysis and pain on compression of the pelvis by simultaneous pressure on both trochanters are usually present. Care must be taken as exquisite pain may occur on palpation of
the pubic symphysis, which may also reveal
a gaping pubic defect and edema.

The symptoms (and their severity) experienced vary, but include:

. Present swelling and/or inflammation over joint.

. Difficulty lifting leg.
. Pain pulling legs apart.
. Unable to stand on one leg.
. Unable to transfer weight through pelvis and legs.

. Pain in hips and/or restriction of hip movement.

. Transferred nerve pain down leg.
. Can be associated with bladder and/or bowel dysfunction.

. A feeling of symphysis pubis giving way.
. Stand with a stooped over back.
. Mal-alignment of pelvic and/or back joints.

. Struggle to sit or stand.
. Pain may also radiate down the inner thighs.

. You may waddle or shuffle.
. Aware of an audible �clicking� sound coming from the pelvis.

Psychosocial impact - interferes with participation in society and activities of daily life; the average sick leave due to posterior pelvic pain during pregnancy is 7 to 12 weeks. In some cases patient may also experience emotional problems such as anxiety over the cause of pain, resentment, anger, lack of self-esteem, frustration and depression; she is three times more likely to suffer postpartum depressive symptoms. Other psychosocial risk factors associated with woman experiencing PGP include higher level of stress, low job satisfaction and poorer relationship with spouse.

Diagnosis of pubic symphysis separation is based on the clinical presentation and the response to therapy. Imaging (X-ray, ultrasound o r magnetic resonance [MRI])
may be useful in confirming the diagnosis. Ultrasound examination using a 7.5 MHz or 5 MHz linear array transducer may demonstrate widening of the interpubic gap in excess of 10 mm. Ultrasound has many advantages over conventional X-ray, as it can be done during pregnancy and can be repeated safely for follow-up. However, the amount of symphyseal separation does not always correlate with the severity of the symptoms, or the degree of disability, nor does it appear to
predict outcome.

Severity - The severity and instability of the pelvis can be measured on a three level scale.

Pelvic type 1: The pelvic ligaments support the pelvis sufficiently. Even when the muscles are used incorrectly, no complaints will occur when performing everyday activities. This is the most common situation in persons who have never been pregnant, who have never been in an accident, and who are not hyperactive.
Pelvic type 2: The ligaments alone do not support the joint sufficiently. A coordinated use of muscles around the joint will compensate for ligament weakness. In case the muscles around the joint do not function, the patient will experience pain and weakness when performing everyday activities. This kind of pelvic often occurs after giving birth to a child weighing 3000 grams or more, in case of hyperactivity,
and sometimes after an accident involving the pelvis. Type 2 is the most common form of pelvic instability. Treatment is based on learning how to use the muscles around the pelvis more efficiently.

Pelvic type 3: The ligaments do not support the joint sufficiently. This is a serious situation whereby the muscles around the joint are unable to compensate for ligament weakness. This type of pelvic instability usually only occurs after an accident, or occasionally after a (small) accident in combination with giving birth. Sometimes a small accident occurring long before giving birth is forgotten so that the pelvic instability is attributed only to the childbirth. Although the difference between Type 2 and 3 is often difficult to establish, in case of doubt an exercise program may help the patient. However, if Pelvic Type 3 has been diagnosed then invasive treatment is the only option: in this case parts of the pelvic are screwed together.

Treatment: One of the main factors in helping women cope with the condition is with education, information and support. Other coping strategies include physical medicine and rehabilitation, physiotherapy, osteopathy, chiropractic, psychologist, prolo therapy or platelet-rich plasma therapy, massage therapy, acupuncture and alternative medicine. Mobility aids such
as a wheelchair, walker, elbow crutches
and walking stick can be very useful. Medication dispensed by a qualified health care provider can also be used to manage:

� Chronic pain
� Anxiety
� Depression
� Post Traumatic Stress Disorder (resulting from birth trauma/ pregnancy)
� Musculo-skeletal disorders.

Conservative treatment is effective in most cases, including those women with the most severe symptoms at presentati0n. A clear explanation of the condition and its management, to both the woman and her partner, is vital. The aim is to avoid abduction of the hip joint and encourage immobilization of the pubic symphysis joint. In cases presenting during pregnancy or after birth, women should be advised to rest as much as possible in the lateral decubitus position: avoid prolonged weight bearing and stairs and keep her legs together in activities such as turning in bed or getting into a car. Since immobilization is a primary risk factor for deep vein thrombosis, isometric exercises should be encouraged. Anti-embolism stockings and heparin may be required. Analgesics can be given on demand. If the above measures fail to improve the
symptoms, referral to an obstetric physiotherapist should be arranged. Pelvic support by a tight binder or tubular
bandage and the use of a walker or elbow crutches may be required. The maximum hip abduction possible without pain (pain-free gap) should be measured before labour, to avoid over-abduction of thighs in labour, especially when regional anesthesia is
used. Some pelvic joint trauma will not respond to conservative type treatments
and orthopedic surgery might become the
only option to stabilize the joints.

Surgery is rarely indicated, but may be considered for those who have inadequate reduction, recurrent diastases or
persistent symptoms. External skeletal fixation is the treatment of choice. The symphysis is compressed using a frame
which can be removed once stability has returned. Prognosis is uniformly good.
Mild cases typically resolve within 2 days to eight weeks of delivery with no lasting sequelae. However, some women require as much as eight months before they are free
of pain when walking. During this time the pain may be worse during the secretory phase of the menstrual cycle. In a recent survey of Norwegian women registered as having pregnancy-initiated pelvic joint pain, it was found that pelvic pain worsened with subsequent pregnancy in 81.4% of the responding. However, in the absence of specific obstetric indications, prior pubic symphysis separation should not be considered a strong indication for subsequent operative delivery.

Low Back Pain

Pathology: Symptomatic back pain in pregnancy is caused by the mechanical
burden created on the lower back by the pregnant uterus and compensatory lordosis. Relaxation of the sacroiliac joint and
pubic symphysis plays an important part.
The highest levels of relaxin during pregnancy have been found in women with incapacitating low back pain. Very occasionally, low back pain may be attributable to a herniated vertebral disc.
Presentation: The usual presentation is
that of low back pain or posterior pelvic pain that is aggravated by activity and relieved by lying down, sitting and the use of supportive pillow. The pain may radiate to the posterior aspects of the thighs. Examination reveals accentuation of the lumbar lordosis and the cephalad part of
the spine thrown backwards to compensate
for the increased size of the abdomen. Tenderness is usually greatest over the sacroiliac joints. Indirect bimanual compression over the iliac crest also produces discomfort in the sacroiliac
joints.

Management: Each patient should be questioned carefully about neurological compromise as very occasionally radicular signs or even a cauda equina syndrome may
be identified. Most patients with classic symptoms and signs limited to low back strain or sacroiliac instability can be managed without radiographic evaluation. Radiographic evaluation of patients with unusual or severe symptoms may be carried out after the first trimester and can include a three view spine series. However, MRI appears to be a safe way to image the pelvic regions during pregnancy and will give direct information about any disc prolapse without irradiation. This should now be the investigation of choice if indicated.

Treatment: Relief of symptoms of low back pain in pregnancy can be achieved by the patient limiting her physical activity, wearing low-heeled shoes, resting in bed with pillows under the knees and applying heat. Lying on the back with the feet propped approximately two feet above the hips for about 20 minutes four times a day usually relieves muscle spasm, decreases lumbar lordosis and relieves acute pain.
In addition, the pain can be partially relieved if the patient keeps the pelvis
in a flexed position, thereby improving spinal alignment. Exercise to increase the tone of the back and abdominal muscles should be commenced as soon as the pain decreases. A sacroiliac corset or trochanteric belt can relieve symptoms. Surgical treatment of low back pain is contraindicated in pregnancy, except when
a herniated disc is producing bowel or bladder incontinence. Pain relief can be achieved with simple analgesics but anti-prostaglandins are relatively contraindicated in pregnancy.

Hip Pain

Two relatively rare conditions, osteonecrosis of the femoral head and transient osteoporosis of the hip, both
seem to occur with somewhat greater frequency during pregnancy and present with pain in the hip or groin. The diagnosis of these conditions is often missed initially because pain is easily taken for pelvic girdle relaxation or round ligament pain. Early diagnosis and treatment are the keys for a successful outcome and prevention of secondary degenerative changes or fracture in the joints of these young women.

1) Osteonecrosis of the femoral head
Presentation: Symptoms usually begin in the third trimester or shortly after a difficult delivery, with sudden or gradually increasing pain of variable severity, usually unilateral and deep in the groin. The pain may radiate to the knee, thigh or back. Elderly primigravida are most at risk. On examination, painful limitation of
active or passive movements of the hip joint, especially with movement, can be noticed. The exact aetiology is not known. But it has been speculated that the rise in unbound cortisol, oestrogen and
progesterone in late pregnancy, the increased interosseous pressure and a
direct injury to the femoral joint by the compression of the growing uterus or during a difficult delivery may all act together
to produce insufficiency of blood supply
to the fernoral head at some point.

Management: Plain radiography may demonstrate arc-like subchondral
radiolucent areas and other pathological changes in the femoral head, but MRI has been used recently for earlier diagnosis with apparent safety during pregnancy.
Early diagnosis, rest and avoiding weigh-bearing are very important. Aspiration of the hip joint may occasionally be
required. The prognosis after early diagnosis and conservative treatment
seems to be good, although secondary degenerative or osteoarthritic changes
may develop and require surgical treatment at a later age.

Figure: Subchondral separation Figure: Osteonecrosis of femoral head on plain X-ray

2) Transient osteoporosis of the hip
Presentation: This is a poorly understood and frequently undiagnosed syndrome of unknown aetiology. It occurs in the third trimester and presents with pain in the
hip, anterior thigh or groin, which progressively increases and is made worse
by weight-bearing. The left hip is more frequently involved but bilateral involvement can also occur. On examination, pain and limitation of range of mobility on passive abduction and rotation of the affected joint is usually noticed.

Management: X-rays of the hip show advanced osteoporosis of the femoral head and neck and, occasionally, the acetabulum, but
with preservation of the joint space. These changes are present three to eight weeks after the onset of symptoms. MRI can be
use for early diagnosis. Bone mineral density (BMD) of the femoral neck of symptomatic women has been shown to be 20% lower than the average of age-matched controls. The great concern with regard
to this disorder is that continued unprotected weight-bearing can result in
a fracture of the femoral neck. The aim
of treatment is to avoid unprotected
weight bearing by the use of crutches until the symptoms resolve completely and radiography shows reconstitution of bone
in the proximal part of the femur. Given
the decrease in BMD that occurs during pregnancy and lactation, it might appear prudent to recommend cessation of lactation in these patients.

During pregnancy, circulating total calcium concentration drop slowly but consistently and parallel with decreasing albumin concentration. Reaching a nadir in the middle third of the third trimester. An early hypothesis was that pregnancy is a state of maternal physiologic hyperparathyroidism. According to this theory, transfer of calcium to the fetus induces secondary hyperparathyroidism
in the mother, which leads consequently
to increased 1,25-dihydroxyvitamin D production. Another theory says the
increase in circulating levels of 1, 25-dihydroxyvitamin D is the primary
event in calcium metabolism alterations during pregnancy, subsequently stimulating intestinal calcium absorption and possible additional effects on other target tissues. With these alterations in calcium metabolism, pregnancy may exacerbate or simply coexist with the number of
conditions that may result in maternal hypercalcemia. These conditions include primary hyperparathyroidism, vitamin A or
D intoxication, systemic sarcoid, hyperthyroidism, milk-alkali syndrome, familial hypocalciuric hyoercalcemia, immobilization, malignancy with or without bone metastasis or ectopic PTH secretion.
On the other hand, alterations in calcium and parathyroid hormone metabolism may
also results in hypoparathyroidism and hypocalcemia. Hypoparathyroidism results from inadequate secretions of PTH or defective production of biologically active PTH. Pseudohypoparathyroidism results from end-organ insensitivity to the hormone.
The diminished PTH activity in the kidney and bone leads to hypocalcemia and hyperphosphatemia. Patient with mild hypoparathyroidism may be asymptomatic or may experience only subtle manifestation
of the disease. In more severe forms of the disorder, symptoms and signs related to decreased serum ionized calcium concentrations may occur. Increased neuromuscular excitability, which can be elicited on physical examination by a positive result for Chovstek's sign
(tapping along facial nerve including contractions of the eye, mouth and nose)
or Trousseau's sign (inflating a blood pressure cuff above systolic pressure causing spasm of the hands within minutes), can uncommonly progress from weakness and paresthesia to the development of seizures, tetany, or laryngospasm. Papilloedema, elevated cerebrospinal fluid pressure and neurologic sign that mimic a cerebral
tumor may be found. A spectrum of mental status changes, from irritation to psychosis, can occur. Abnormalities in the cardiac conduction, particularly prolongation of
QT interval and T wave changes, may be present. Radiographs of the skull may demonstrate intracranial calcifications, which are sometimes associated with a parkinsonian-like syndrome. Additionally,
if the disease has been long standing, physical examination may reveal dental abnormalities or cataracts.
Untreated maternal hypoparathyroidism with its associated hypocalcemia leads to a high incidence of maternal, fetal and neonatal complications. Generalized skeletal demineralization, osteitis fibrosa cystica and fetal or neonatal death can occur. Although the secondary hyperparathyroidism is transient and generally resolves in the neonatal period, the infant may not
achieve normal bone mineralization until
6 months of age.

Deficiency of vitamin D and disorders of vitamin D absorption or metabolism can
lead to hypocalcemia and also to
subsequent disorders of bone
mineralization, such as osteomalacia and tetany. Derangements in vitamin D
metabolism may also explain the osteopenia associated with heparin treatment during pregnancy.

References:

1. Medical Complications During Pregnancy by Burrow and Duffy 5th edition

2. http://en.wikipedia.org

3. http://www.maitrise-orthop.com /corpusmaitri/orthopaedic/mo72_hernigou/index.shtml

4. http://www.ncbi.nlm.nih.gov/pubmed/18199383?dopt=AbstractPlus

5. http://www.ncbi.nlm.nih.gov/pubmed/1946104?ordinalpos=1&
itool=EntrezSystem2.PEntrez.Pubmed. Pubmed_ResultsPanel.Pubmed_ SingleItemSupl.Pubmed_ Discovery_RA&linkpos=4&log$=relatedreviews &logdbfrom=pubmed

Bed Sores:  A comprehensive review.

Introduction: One of the most nagging and frustrating problems in long term patient care is decubitus ulcer or commonly referred as Bed Sores. The problem becomes more compounded in cases of Diabetes Mellitus where there are problems ranging from delayed tissue healing to various biochemical changes that virtually frustrates every attempt to treat these patients. Proper Nursing Care is what is stressed up on.

According to www.medterms.com , Bed sore is defined as a painful often reddened area of degenerating, ulcerated skin caused by pressure and lack of movement, and worsened by exposure to urine or other irritating substances on the skin. Untreated bed sores can become seriously infected or gangrenous. Bed sores are a major problem for patients who are confined to bed or a wheelchair. They can be prevented by moving the patient frequently, changing bedding, and keeping the skin clean and dry. Synonyms include pressure sore, decubitus sore, or decubitus ulcer.

In a study conduced by the Healthcare Cost and Utilization Project (HCUP-USA) titled Hospitalizations Related to Pressure Ulcers among Adults 18 Years and Older in the year 2006 it was found that there were a total of 503,300 hospitalization with pressure ulcers noted as a diagnosis which is an increase in 78.9% since 1993 when there were about 281,300 hospitalization due to the same. Adult hospital stays bearing a diagnosis of pressure sores totaled up in 11.0 billion US Dollars in hospital bills in the year 2006 alone. (2)

Amongst others �highlighted� in the published report were: (2)

� Of the total admission, more than 90% of patient (among adults) with pressure ulcer related hospitalization were actually intended for other medical conditions like septicemia, pneumonia, and urinary tract infection to name a few.
� In comparison to hospital stays due to other medical conditions, pressure ulcers patients were more often discharged to a long-term care facility and are more likely to result in death in coming years.
� Almost every three out of four adult patients hospitalized with a secondary pressure ulcer diagnosis 72% were 65 years and older. On the contrary, adult patients with a principal diagnosis of pressures ulcers 56.5% of them are 65 or older.
� Moreover, the younger adults that are hospitalized primarily due to pressure ulcers often go hand in hand with paralysis and spinal cord injury.


Risk-factors

There are numerous risk factors listed below in development of pressure sores. (3)

� Prolong immobility :
Paraplegia
Arthritis
Operation and postoperative states
Plaster casts
Intensive care
� Decrease sensation :
Coma
Neurological disease or deficits
Diabetes Mellitus
Drug Induced Sleep
� Vascular Disease :
Atherosclerosis
Diabetes Mellitus
Scleroderma
Vasculitis
� Poor Nutrition :
Anaemia
Hypoalbuminemia
Vitamin C or Zinc deficiency

As the saying goes prevention is better than cure, after years of study on the topic per-say, several risk assessment tools have been devised for the immobile patient based on the known risk factor such as the �Norton scale�, and �Waterlow Pressure Sore Risk Assessment� are 2 validated systems which produce a numerical sore I while enabling staff to identify those at most risk. The table below depicts �Norton Scale�.
In recent days �Brandon Scale� for predicting risk for pressure ulcers is being used by many health care set-ups. Brandon�s scale is divided into six risk categories: sensory perception, moisture, activity, mobility, nutrition, friction and shear. The best possible interpretation is a score of 23 whilst the worst is a 6. If the total score is below 11, the patient is at risk for developing bedsores.
The patho-physiology & staging
Bedsores are predisposed by 5 main factors: pressure, injury, anaemia, malnutrition and moisture. (6) There are 3 main etiology for pressure ulcers to develop are namely:
1. Compression between bony prominences and contact surfaces, as when a patient remains in a single decubitus position for a prolonged period of time which will lead to decreased tissue perfusion, ischemia occurs and resulting in tissue necrosis
 rubbing against bed linen or patient�s gown.à2. Friction
3. Shearing forces. It�s the force that is created when skin of a patient stays in one place as the deep fascia and skeletal muscle slide down with gravity leading to pinching off of blood vessels which eventually ends up with tissue necrosis.
Infuriating the situation may be other conditions such as excess moisture from incontinence, perspiration or exudates where in elapse of time this excess moisture may deteriorate the bonds between epithelial cells resulting in the maceration of the epidermis.
At present there are two major theories about the development of pressure ulcers. The first and most accepted is the deep tissue injury theory which claims that the ulcers begin at the deepest level, around the bone, and move outward until they reach the epidermis. The second, less popular theory is the top-to-bottom model that says that skin first begins to deteriorate at the surface and then proceeds inward.
The results of all this will eventually lead to erosion, tissue ischemia, and finally infarction over the site. The most common sites where bed sores most frequently build up is over the sacrum, ischial tuberosities, trochanters, malleoli, and last but non the least the heels. It is not necessarily for the ulcers to only develop at these areas but they can develop elsewhere, including behind the ears when nasal cannulae are used for prolonged periods. Poorly fitting prosthetic devices are also grounds for pressure ulcers to develop over bony prominences. Increased force and duration of pressure directly influence risk and severity.
Pressure sores can as little as 3 to 4 hours to develope in some settings (for example trauma patients who are immobilized on rigid spine-immobilization boards) and these ulcers worsen when skin is overly moist and macerated (e.g., from perspiration or incontinence).
In February 2007 the National Pressure Ulcer Advisory Panel (NPUAP) added unstageable pressure ulcers on to the list of the already existing original 4 stages which are further described below.
Stage I: Intact skin, non-blanchable redness of a localized area usually over a bony prominence. The area may be painful, firm, and soft, with local temperature change as compared to adjacent tissue. It may be difficult to detect this stage in individuals with darker skin tones.
Stage II: Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. Patient in this stage may also present as an intact or open/ruptured serum-filled blister. Presentation is of a shiny / dry shallow ulcer without slough or with bruising which may very well be deep tissue injury. Conditions like skin tears, tape burns, perineal dermatitis, maceration or excoriation should not be mistaken and described in this stage.
Stage III: In this stage pressure ulcer varies by anatomical location. There is full thickness tissue loss with visible subcutaneous fat but bone, tendon or muscles are not exposed or palpable. Slough may be present but does not obscure the depth of tissue loss with possibility of undermining and tunneling. Areas that do not have subcutaneous tissue namely the nose-bridge, ear, occiput and malleolus shows shallow ulcer. On the contrary areas with significant adipose tissue can develop extremely deep stage III pressure ulcers.
Stage IV: In this stage there is full thickness tissue loss with exposed bone (visible and palpable), tendon or muscle with presence of slough over the wound bed with significant undermining and tunneling. Osteomyelitis may transpire in tandem of this stage as ulcers can extend into muscle and/or supporting structures namely fascia, tendon or joint capsule.
Unstageable: Full thickness tissue loss in which the base of the ulcer is covered by slough and/or eschar in the wound bed if and until the debris are removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined.
Prevention
One must bear in mind that bedsores are easier to thwart than to treat. A task is never easily achievable even if it�s the smallest of task need work, the same goes here although wounds can develop in spite of the most scrupulous care, it's possible to prevent them in many cases. First and foremost, the treating physician needs to devise a plan that is comprehendible and easy to follow by caregivers. The cornerstones of such a plan include position changes along with supportive devices, daily skin inspections and a maximally nutritious diet further explained below.
 As mentioned before it takes a mere 2-3 hours for a sore to develop over immobilized area hence changing of posture has to be frequent (experts claims to shift position every 15 minutes) and consistent as it�s crucial to prevent bedsores. If one is wheelchair bounded he/she should reposition 2 hourly. When night falls a caregiver should be there to assist a bed ridden patient to change position. Some guidelines that are readily available by some physician on position change are as listed:àPosition changes:
� Lie at a 30-degree angle so to avoid lying directly on hipbones..
� When in supine position a head size sleeping pillow should be kept from below knee onwards supporting calf and up to the heel.
� Try to avoid contact between knees and ankle using a foam pad or pillow..
� A higher incline head of the bed makes it more prone that one will slide down, where in there will be friction and shearing injuries.
� A pressure-reducing mattress / bed should be used as there are many options readily available in market stores including foam, air, gel or water mattresses.
� Pressure-release wheelchairs have recently been introduced in the market where in it functions to redistribute pressure hence making sitting for long periods easier and more comfortable. All wheelchairs need cushions in order to reduce pressure and provide maximum support and comfort.
 Skin should be inspected thoroughly at least once a day for pressure sores as its fundamental part of prevention. Inspect your skin thoroughly at least once a day, using a mirror if necessary. Special attention are to be paid to these areas hips, spine and lower back, shoulder blades, elbows and heels if a patient is bed ridden. When in a wheelchair, look especially for sores over the buttocks and tailbone, lower back, legs, heels and feet If an area of your skin is red or discolored but not broken, keep pressure off the sore, wash it gently with mild soap and water, dry thoroughly, and apply a protective wound dressing. If there is visible skin damage or any sign of infection such as drainage from a sore, a foul odor, and increased tenderness, redness and warmth in the surrounding skin, get medical help immediately.àSkin inspection
 Malnourished populaces are the ones highly predisposed to bed sores. It's crucial to get enough calories, protein, vitamins and minerals in preventing skin breakdown and in aiding wound healing. Markers of under nutrition include albuminàNutrition  < 3.5 mg/dL or weight < 80% of ideal. Protein intake of 1.25 to 1.5 g/kg/day is desirable for optimal healing. Zinc supplementation supports wound healing, and replacement at a dose of 50 mg thrice daily may be useful. Supplemental vitamin C 1 g/day may be provided. Providing a drink of water to patients at each repositioning may be useful to aid hydration.
Lifestyle changes including cessation of smoking as tobacco use damages skin and slows wound healing as on the other hand exercise improves circulation, helps builds up vital muscle tissue strengthen the body overall.

Treatment
The 1994 consensus guidelines provide a brilliant approach to the rational treatment of pressure ulcers. Listed below are the general summaries indicating steps necessary in management of this important issue.
Debridement of necrotic tissue can be done through a variety of potential techniques, which aids in healing of the wound. Several different debridement techniques are available.
� Sharp debridement is used in critical situations like cellulitis where in devitalized tissue are removed..
� Mechanical debridement where Hydrotherapy (whirlpool baths), ultrasound, medical maggots, wound irrigation, or dextranomers are to be used to remove thick exudates and loose necrotic tissue. Urgent debridement is indicated in advancing cellulitis or sepsis. Wounds with very loose exudates- debridement with wet-to-dry dressings can be done but only with utmost care as it is often painful and it may remove healthy tissue.
� Enzymatic debridement involves applying topical debriding agents to remove devitalized tissue using collagenase, papain, fibrinolysin, or streptokinase.
� Autolytic debridement requires the use of synthetic dressings that allow devitalized tissue to self-digest from enzymes present in wound fluids. DuoDERM or Contreet (which is impregnated with silver and thus offers antimicrobial effects) are commonly applied.
Wound cleansing using a 30 ml syringe and a 18 gauge angiocatheter will provide sufficient force to remove eschar, bacteria, and other debris from the wound site. Initially wound should be cleansed with normal saline and not using solutions that are cytotoxic in nature, such as povidone iodine, sodium hypochlorite solution and hydrogen peroxide, should be avoided to avoid further damage to tissue.
Treatment of Infected sites following the procurement of swabs from the area which are immediately sent for culture n sensitivity test. Conventionally first line therapy should cover gram-positive skin organisms, such as the use of a first-generation cephalosporin (e.g. Cephalexin 250-500 mg po qid). If the clinical picture is suggestive and/or swab results are confirmatory, consideration for antipseudomonal coverage should be made. Broader coverage should be emperically instituted in diabetic patients.
Dressing selection should be based on its ability to keep ulcer tissue moist and the surrounding intact skin, dry. Multiple types of dressings are available, and the choice should be based on clinical judgement. Objectives are to keep the ulcer bed moist to retain tissue growth factors while allowing some evaporation and inflow of oxygen, to keep surrounding skin dry, to facilitate autolytic debridement, and to establish a barrier to infection. Adjuvant therapy and /or operative repair are made on a case-by-case basis. Modes of operation include electrical stimulation, hyperbaric oxygen and laser irrigation. Electrical stimulation is only recommended for stage III and IV pressure ulcers. The table below tabulates the different options of dressing available for pressure ulcers.
Conclusion
Pressure ulcers are a preventable and treatable medical problem. Proper management of this problem can result in significantly improved quality of life and shorter hospital stays for elderly patients. When ulcers do develop, a multidisciplinary approach to treatment is recommended.

References
1. Bedsores definition. http://www.medterms.com/script/main/art.asp?articlekey=11035
2. Russo C.A., Steiner C., Spector W. Statistical Brief # 64 Healthcare Cost and Utilization Project �Hospitalizations Related to Pressure Ulcers among Adults 18 Years and Older, 2006.� http://www.hcup-us.ahrq.gov/reports/statbriefs/sb64.jsp
3. Kumar P., Clark M. Kumar & Clark Clinical Medicine Textbook 6th edition. Elsevier Saunders 2005
4. Russel R.C.G., William N.S., Bulstrode C.J.K. Bailey & Love Short Practice of Surgery 24th Edition. Hodder Arnold 2004.
5. Wolff K., Goldsmith L. A., Katz S.I., Gilchrest B.A., Paller A.S., Leffell D.J., Fitzpatrick's Dermatology in General Medicine, 7th edition McGraw-Hill Professional 2008.
6. Niezgoda JA, Mendez-Eastman S (2006). "The effective management of pressure ulcers". Adv Skin Wound Care 19 Suppl 1: 3�15. doi:10.1097/00129334-200601001-00001. PMID 16565615. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00129334-200601001-00001
7. Support surfaces for pressure ulcer prevention by McInnes E, Cullum NA, Bell-Syer SEM, Dumville JC. http://www.cochrane.org/reviews/en/ab001735.html
8. Cervo FA, Cruz AC, Poscillico JA. Pressure ulcers: Analysis of guideline for treatment and management. Geriatrics. Mar 2000;55:55-60.
9. Pieper B. Mechanical Forces: Pressure, shear, and friction. In: Bryant RA. Acute and Chronic Wounds: Nursing Management, Second Edition. Mosby, Inc., 2000
10. Bergstrom N, Bennet MA, Carlson CE et al. Treatment of Pressure Ulcers. Clinical Practice Guideline, No 15. Rockville, MD. US Department of Health and Human Services. Public Health Service, Agency for Health Care Policy and Research. AHCPR Publication No. 95-0652. December, 1994.
11. Malone J.R., McInnes E. Pressure Ulcer Risk Assessment and Prevention. Royal College Of Nursing U.K. April 2001
12. Bedsores. Mayo Clinic. http://www.mayoclinic.com/health/bedsores/DS00570/DSECTION=symptoms
13. Encyclopedia for surgery. Bedsores. http://www.surgeryencyclopedia.com/A-Ce/Bedsores.html

Dietary supplements in Osteoarthritis Glucosamine , Chondrotin, S-adenosyl methionine Vitamin C, Beta carotene

INTRODUCTION:

Osteoarthritis (OA) is the commonest form of arthritis found worldwide that can affect the hands, hips, shoulders and knees. It is responsible for the largest burden of joint pain and is the single most important rheumatological cause of disability and handicap.1,2 In Osteoarthritis, the cartilage that protects the ends of the bones breaks down and causes pain and swelling. Drug and non-drug treatments are used to relieve pain and/or swelling. Osteoarthritis commonly affects the hands, feet, spine and large weight-bearing joints, such as the hips and knees. Most cases of osteoarthritis have no known cause and are referred to as primary osteoarthritis. When the cause of the osteoarthritis is known, the condition is referred to as secondary osteoarthritis. These are food supplements show promise for helping people with osteoarthritis, those are Glucosamine sulphate, Chondroitin sulphate, SAMe (s-adenosylmethionine), Vitamin C ( ascorbic acid), Beta Carotene3 and many more.
Glucosamine:
Glucosamine is almost synonymous with osteoarthritis as it has benefits for osteoarthritis. It can be found naturally in the body and is used by the body as one of the building blocks of cartilage.Glucosamine is an amino sugar produced from the shells of shellfish (chitin) and it is a key component of cartilage. Glucosamine (C6H13NO5) is an amino sugar and a prominent precursor in the biochemical synthesis of glycosylated proteins and lipids. Glucosamine is part of the structure of the polysaccharides chitosan and chitin, which compose the exoskeletons of crustaceans and other arthropods, cell walls in fungi and many higher organisms, glucosamine is one of the most abundant monosaccharides.3
Glucosamine is necessary for the construction of connective tissue and healthy cartilage. It is the critical building block of proteoglycans and other substances that form protective tissues. These proteoglycans are large protein molecules that act like a sponge to hold water giving connective tissues elasticity and cushioning effects. This also provides a buffering action to help protect against excessive wear and tear of the joints. Without glucosamine, our tendons, ligaments, skin, nails, bones, mucous membranes, and other body tissues can not form properly.

Glucosamine works to stimulate joint function and repair. Everyone produces a certain amount of glucosamine within their bodies. Normally we generate sufficient amounts of glucosamine in our bodies to form the various compounds needed to generate connective tissue and healthy cartilage. But gradually the rate at which our bodies use glucosamine begins to gradually change with our increased athletic activity, injuries, burns, arthritis and other inflammatory disorders, age and other chronic degeneration.3 In such situations our bodies may not be able to keep up with the demand for glucosamine, leading to a decrease in the amount of proteoglycans produced. This can lead to a decrease in the amount of protective lubricating substances like the synovial fluids, which cushion our joints, and protects them from damage. In a nutshell, more glucosamine is needed but less is produced.
As the age advances, body loses the capacity to make enough glucosamine. Having ample glucosamine in the body is essential to producing the nutrients needed to stimulate the production of synovial fluid, the fluid which lubricates cartilage and keeps the joints healthy. Without enough glucosamine, the cartilage in weight-bearing joints, such as the hips, knees, and hands deteriorates. The cartilage then hardens and forms bone spurs, deformed joints, and limited joint movement. This is how the debilitating disease of osteoarthritis develops.4
Therefore, in short, glucosamine is a major building block of proteoglycans needed to make glycosaminoglycans, proteins that bind water in the cartilage matrix which also acts as a source of nutrients for the synthesis of proteoglycans and glycosaminoglycans. It is also a stimulant to chondrocytes and playing key factor in determining how many proteoglycans are produced by the chondrocytes needed to spur chondrocytes to produce more collagen and proteoglycans acts as a regulator of cartilage metabolism which helps to keep cartilage from breaking down. 5
Glucosamine is the supplement most commonly used by patients with osteoarthritis. It is an endogenous amino sugar that is required for synthesis of glycoproteins and glycosaminoglycans, which are found in synovial fluid, ligaments, and other joint structures. Exogenous glucosamine is derived from marine exoskeletons or produced synthetically. Exogenous glucosamine may have anti-inflammatory effects and is thought to stimulate metabolism of chondrocytes.
Glucosamine is available in multiple forms. The most common are glucosamine hydrochloride and glucosamine sulfate. Some products contain a blend of these, and many combine one of the forms with a variety of other ingredients. Glucosamine has been safely used in long-term clinical trials Overall, the evidence supports the use of glucosamine sulfate for modestly reducing osteoarthritis symptoms and possibly slowing disease progression.
Chondroitin
Chondroitin, an endogenous glycosaminoglycan, is a building block for the formation of the joint matrix structure. Chondroitin sulfate is a sulfated glycosaminoglycan (GAG) composed of a chain of alternating sugars (N-acetylgalactosamine and glucuronic acid). It is usually found attached to proteins as part of a proteoglycan.6 Chondroitin sulfate is an important structural component of cartilage and provides much of its resistance to compression. Along with glucosamine, chondroitin sulfate has become a widely used dietary supplement for treatment of osteoarthritis. Chondroitin is a molecule that occurs naturally in the body. It is a major component of cartilage,the tough, connective tissue that cushions the joints. Chondroitin helps to keep cartilage healthy by absorbing fluid (particularly water) into the connective tissue. It may also block enzymes that break down cartilage, and it provides the building blocks for the body to produce new cartilage.
Chondroitin sulphate Chondroitin is the most abundant glycosaminoglycan in cartilage and is responsible for the resiliency of cartilage and it has various effects in relieving symptoms of osteoarthritis and those are its anti-inflammatory activity, the stimulation of the synthesis of proteoglycans and hyaluronic acid, and the decrease in catabolic activity of chondrocytes inhibiting the synthesis of proteolytic enzymes, nitric oxide, and other substances that contribute to damage cartilage matrix and cause death of articular chondrocytes. chondroitin sulfate reduced the IL-1β-induced nuclear factor-kB (Nf-kB) translocation in chondrocytes. In addition, chondroitin sulfate has recently shown a positive effect on osteoarthritic structural changes occurred in the subchondral bone.7 A number of scientific studies suggest that chondroitin may be an effective treatment for osteoarthritis
Therefore, chondroitin sulphate is effective as it reduces osteoarthritis pain, improves functional status of people with hip or knee osteoarthritis, reduces joint swelling and stiffness and ultimately provides relief from osteoarthritis symptoms for up to 3 months after treatment is stopped
S-Adenosyl methionine
S-Adenosyl methionine (SAM, SAMe, SAM-e) is a dietary supplement that has been clinically shown to support and promote joint health, mobility and joint comfort.It is a compound produced by our bodies from methionine. Methionine is an amino acid found in protein-rich foods and a common co-substrate involved in methyl group transfers. SAM-e is critical in the manufacture of joint cartilage and in the maintenance of neural cell membrane function.8
Administration of SAMe exerts analgesic and antiphlogistic activities and stimulates the synthesis of proteoglycans by articular chondrocytes with minimal or absent side effects on the gastrointestinal tract and other organs and improving pain and stiffness related to osteoarthritis
Vitamin C
Vitamin C( ascorbic acid) may help reduce the progression of osteoarthritis. Vitamin C is involved in the formation of both collagen and proteoglycans (two major components of cartilage, which cushions the joints). Vitamin C is also a powerful antioxidant that helps to counteract the effects of free radicals in the body, which can damage cartilage. Ascorbic acid(vitamin c) is a sugar acid with antioxidant properties. Its appearance is white to light-yellow crystals or powder, and it is water-soluble. One form of ascorbic acid is commonly known as vitamin C. In human plasma, ascorbate is the only antioxidant that can completely protect lipids from detectable peroxidative damage induced by aqueous peroxyl radicals. Ascorbate appears to trap virtually all peroxyl radicals in the aqueous phase before they diffuse into the plasma lipids. Ascorbate is a highly effective antioxidant, as it not only completely protects lipids from detectable peroxidative damage, but also spares alpha-tocopherol, urate, and bilirubin.Ascorbic acid stimulates collagen synthesis and modestly stimulates synthesis of aggrecan (a proteoglycan present in articular cartilage), Sulfated proteoglycan biosynthesis is significantly increased in the presence of ascorbic acid thus it may offer some protective effect against the super oxide and free radicals and limiting and delaying the osteoarthritis progression

Beta-carotene
Beta-carotene belongs to a family of natural chemicals known as carotenoids. Widely found in plants, carotenoids along with another group of chemicals, bioflavonoids, give color to fruits, vegetables, and other plants.
Beta-carotene is another antioxidant that also seems to help reduce the risk of osteoarthritis progression. Beta-carotene is a particularly important carotenoid from a nutritional standpoint, because the body easily transforms it to vitamin A. While vitamin A supplements themselves can be toxic when taken to excess, it is believed (although not proven) that the body will make only as much vitamin A out of beta-carotene as it needs. Assuming this is true, this built-in safety feature makes beta-carotene the best way to get your vitamin A. A high dietary intake of beta-carotene is associated with a significantly slower progression of osteoarthritis, according to a study in which researchers followed 640 individuals over a period of 8 to 10 years .10
Conclusion:
In conclusion,there are nutrients and foods that may help to halt the progression osteoarthritis before it becomes severe as well as helping to reduce the pain and inflammation associated with it.

REFERENCES

1) Clinical Practise Guidelines. Management of Osteoarthritis http://www.msr.org.my/html/Bookleta.pdf accessed on 13 February 2010
2) Cochrane Library. Glucosamine Therapy for Treating Osteoarthritis http://www.cochrane.org/reviews/en/ab002946.html accessed on 13 February 2010
3) Spark People Life. Dietary Supplement for Osteoarthritis
http://www.sparkpeople.com/resource/nutrition_articles.asp?id=865 accessed on
14 February
4) Horton D, Wander JD (1980). The Carbohydrates. Vol IB. New York: Academic
Press. pp. 727�728.
5) Glucosamine and Osteoarthritis,How it works
http://www.arthritis-glucosamine.net/glucosamine-osteoarthritis.php accessed on
14 February 2010
6) Jamie G. Barnhill, Carol L. Fye, David W. Williams, Domenic J. Reda, Crystal L. Harris, and Daniel O. Clegg. Chondroitin Product Selection for the Glucosamine/Chondroitin Arthritis Intervention Trial. J Am Pharm Assoc. 2008; 46:14�24.
7) Davidson EA, Meyer K (2007). "Chondroitin, a mucopolysaccharide". J Biol Chem 211 (2): 605�11.
8) S-adenosyl methionine [SAMe]. Research Reports http://www.oralchelation.com/technical/SAM.htm accessed on 15 February 2010
9) McAlindon TE, Jacques P, Zhang Y, et al. Do antioxidant micronutrients protect against the development and progression of knee osteoarthritis? Arthritis Rheum. 1996;39:648-656.
10) iHerb. Com. Beta Carotene http://healthlibrary.epnet.com/GetContent.aspx?token=e0498803-7f62-4563-8d47-5fe33da65dd4&chunkiid=21547 accessed on 16 February 2010
 

 

 

 

 

My Articles...

orthopedics articles

 

E - Learning in Medical Education

There is a growing debate in this knowledge hungry society that doctors have not updated themselves with recent trends and newer developments in medicine. There is some truth in their concern. The growing number of medical schools and the equally large number of quacks have not helped in improving the health care in our country. The goal of this article is to introduce many of the aspects of e-Learning as it pertains to medical education.
Traditionally, medical education had as its foundation a combination of didactic instruction in the classroom and integrated, hands-on "Socratic Method" learning in the clinical setting. Of late, there has been an increase in the use of problem-based learning discussions (PBLD's) in an effort to integrate basic science knowledge and clinical decision making with a goal of teaching critical decision making skills to upcoming physicians and other health care providers. Most Medical schools these days are realizing the importance of incorporating newer modalities of teaching. In countries where the patient outflow is poor for students learning simulation techniques are of increasing usage.
Medical education, especially in the advances stages of training, has many unique problems such as the temporal and geographic distribution of students, residents, and the physician instructors. Further complications result from unpredictable schedules that are present in most areas of medicine leading to poorly attended or cancelled lectures. Learning is the sharing or transfer of information between two parties. It is the phasing dispensation of knowledge from people of integrity and higher learning with zeal of transforming their realized knowledge to deserving souls who have similar intentions of propagating the sacred knowledge. Of course the definition of knowledge changes with increasing tends of materialism as seen by mushrooming of various so called temples of learning .Over the course of time, many modalities and theories about learning have been elucidated with varying degrees of effectiveness. With an increasing prevalence of computers in and out of the classroom and the development of more sophisticated web-based tools, knowledge transfer is increasing going high-tech. Similar to prior methods of teaching and learning, computer-based, e-Learning, has its own set of problems and potential. Medical education, especially in the advances stages of training, has many unique problems such as the temporal and geographic distribution of students, residents, and the physician instructors. Further complications result from unpredictable schedules that are present in most areas of medicine leading to poorly attended or cancelled lectures. E-learning adds many dimensions to the educational process and if utilized well, has the potential to enhance both the students and instructors educational experience. One of the problems with traditional didactic lectures is that they often present information that targets one of the many learning style of the students involved. In addition, the time and resources required to deliver the material is high and often does not completely meet the needs of those who are participating. One benefit of e-learning allows students to access the lectures and other material when they are most attentive. In addition, students have the ability to review the material to the degree they feel necessary. It is my hope this article touches the surface of some of the current web tools available for use in the area of education. Many of these tools are nonspecific and can be integrated well into medical education. Blogs, short for web logs, are also easy to update and maintain web pages with a layout that resembles a journal. Students and instructors can utilize these web resources to discuss topics and concepts. In addition to journaling, others can interact with the material and leave comments. For those that are interested, many sites have been set up to host these web resources and are very easy to manage, even for those who have relatively minimal computer sophistication.
Today, Continuous Medical Education (CME) becomes a crucial factor, because the life of knowledge and human skills in the field of medicine is shorter than ever. That causes the increasing pressure to remain at the forefront of medical education throughout doctors� career. E-learning comes with solutions and methods, which can be very helpful in supporting doctors with access to the up-to-date medical knowledge and achievements. It allows creation of interactive model of learning, which stimulates knowledge acquisition. Another advantage is that e-learning provides flexibility in both time and location, while accessing medical curriculum presented online. There is a possibility of collaboration between teachers and students from different universities, which allows exchange of knowledge and experiences.
Implementation of e-learning methods in medical education is needed to provide students with new ways of gaining knowledge. However certain steps must be taken to choose the solution, which is the best for the given learning area. To keep up to date with the latest scientific breakthroughs, current medical debates and state-of-the-art medical technology you don�t need to go on expensive further training seminars far away from your workplace. The only thing you need is a computer with online access � and the right links to e-learning (electronic learning) websites. These online resources offer a vast amount of possibilities in different medical fields tailor-made for a variety of users: Students can use it as well as trained physicians, employee workers or managers. Across the world many companies, universities and institutions maintain Virtual Academies. The providers strive for certification and international acknowledgment of this type of education.
We are just beginning to harness the power of the internet for the delivery and management of medical education. Even without a clear demonstration that e-learning is superior to traditional lectures; the use of online learning provides solutions that can overcome some problems with traditional education, especially in the area of medicine. With increasing constraints being placed on medical educators, one needs to explore other avenues for effective knowledge transfer to trainees in health care. The harnessing of computer technology, more specifically web-based tools open the door for collaboration amongst both students and teachers. One platform that harnesses the ability to deliver knowledge to students as well as collect information about the helpfulness of this information is the web-based Moodle e-learning platform.

Prof G S Patnaik is a consultant orthopedic and Trauma surgeon based in Bhubaneshwar.
 

 Emergency Department staffing

 

The Emergency Department (ED), sometimes termed Accident & Emergency (A&E), Emergency Room (ER), Emergency Ward (EW), or Casualty Department is a hospital or primary care department that provides initial treatment to patients with a broad spectrum of illnesses and injuries, some of which may be life-threatening and require immediate attention. In some countries, Emergency Departments have become important entry points for those without other means of access to medical care. Staff teams treat emergency patients and provide support to family members. The emergency departments of most hospitals operate around the clock, although staffing levels attempt to mirror patient volume, which in most ED's finds its nadir between 2:00 am and 6:00 am. Most patients seek the Emergency Department in the afternoon and evening hours, and staffing mirrors this phenomenon.
The vast array of people caring for patients in an emergency department can be quite confusing to the average health care consumer -- as confusing.
Additionally, most people are uncertain of the training and background necessary to become a member of the emergency-department team. Well, here's the scorecard.
Emergency Physician
Physician who specializes in the care of patients with acute injuries or with diseases that are an immediate threat to life or limb. A "board certified" specialist in emergency medicine is an emergency physician who has achieved certification by the American Board of Emergency Medicine (if an MD) or the American Osteopathic Board of Emergency Medicine
Emergency Nurse.
Nurses care for patients in the emergency or critical phase of their illness or injury. A specialist nurse who will independently assess, diagnose, investigate, and treat a wide range of common accidents and injuries working autonomously without reference to medical staff. They primarily treat a wide range of musculoskeletal problems, skin problems and minor illness, many are considered experts in wound management. They are trained in advanced nursing skills which though medical in nature - such as taking a full medical history and examination, x-ray interpretation, prescribing, suturing, & plastering, also encompass a holistic assessment of the patients needs, taking into account the need for health teaching and education, continuing care within the family and ongoing health support in the community.
PhysicianAssistant
Many emergency departments utilize physician assistants (PA). PAs work under the supervision of an emergency physician. They can examine, diagnose and treat patients (usually the less complicated ones) and review their findings with the physician.
EmergencyDepartmentTechnician
The tasks that performed may include taking your vital signs, drawing your blood, starting your IV, performing EKGs, transporting you to and from various tests, and providing aid and comfort to family and friends.
UnitSecretary
This essential member of the team is one you don't hear about very often. He/she often handles the communication needs of the ER. A few important examples of important communication needs include the emergency physician needing to speak to the patient's family physician, families calling about their loved ones, family physicians needing to inform the emergency department about patients being sent in, or patients calling in needing medical advice. Also, he/she coordinates the ordering of diagnostic tests.
Physicianintraining
An attending physician who usually has extensive experience in emergency medicine supervises these physicians. There are ways to bridge the nursing productivity gap, while improving staffing processes, improving efficiency, and creating a vision for the future. To improve staffing processes one has to increase forecasting accuracy, match staffing to demand, increase management vigilance, smooth the workload variation and enhance nurse efficiency in the emergency room.
In the hospital industry cost information plays a critical role in maintaining a competitive advantage. Strategic cost management allows us to provide low cost care. For example, reducing the cost of providing care by improving a process would allow the organization to reduce the cost to the patient, thus reducing customer sacrifice.
Managers will be forced to determine which activities are important if customer value is emphasized. The healthcare industry requires that managers be familiar with many functions of the financial end of business. Nurses have often looked the other way when it comes to finances and continually focused on patient care. In the year 2001 the attitudes and focus must shift to keeping the healthcare facility viable in the business world. Relating patient care, hours worked, and the number of nurses required to provide low cost, quality care is of extreme importance in today�s environment. This broader vision allows managers to increase quality, reduce the time required to service customers (both internal and external), and improve efficiency. Continuous improvement is fundamental for establishing a state of healthcare excellence.

Next-day productivity profiling holds each manager accountable for the outcome of his or her specific area and to manage his or her resources appropriately. Imprecise staffing standards and infrequent monitoring hinders flexing of staff and leaves managers unaccountable for productivity. The emergency department will be profiled daily on performance against productivity targets. They will use productivity standards and daily volumes to determine real-time, the amount of staff needed to meet the demand. In most cases, the core staff will already be in place, and only upward adjustments will prove necessary. Managers are being trained to look at the business, and to be able to forecast the needs of the units and react to the needs efficiently. It is the expectation that this process will become routine, requiring moderate effort to maintain.
To improve emergency department staffing a master schedule of worked hours is reviewed daily to determine the daily census and volume and the per shift census and volume. Then the total worked hours scheduled is evaluated along with the worked hours per shift per unit. Managers are actually evaluating labor on a shift-to shift basis. Real-time reporting of adherence to customized productivity standards enables more accurate matching of staffing to demand. This process prevents hiring unnecessary personnel and fosters a permanent focus on staff efficiency and cost control.
Study also shows that that between the hours of one am and ten am, historically the census is low and requires less staffing. The emergency department survey also reflected that the peak volume times in the emergency department were from 10am to 12 midnight and this has provided needed information on start times and these surveys were utilized in formulating the schedule. It is essential to obtain staff buy-in to effectively implement this process in any organization.
Implementation of the Emergency Department Productivity Profiling System will reduce the number of FTE'� needed per shift. This will further reduce cost associated with labor, as staff will be utilized more efficiently during peak arrival times. Thus, allowing to accurately plan for core and flexible staffing needs. Managers will be held accountable to department-specific hours-per-unit targets for flexible staffing. In turn, managers will be provided with timely, structured feedback on their performance against these targets. The staffing matrix developed for the Emergency Department will be adjusted periodically to further improve performance and reflect process or technology changes should they be needed.

References

Alba, T. (2000). Next-Day Productivity Profiling. Healthcare Advisory Board (Ed.), Nursing Cost Advantage, (Volume III, pp. 43-49). Washington, D.C.: The Advisory Board Company.
Ansari, S. (2000, March). Activity Based Management. Retrieved June 19, 2001 from the World Wide Web: http://www.wku.edu/~aldricr/.
Bellandi, D., Kirchheimer, B., & Galloro, V. (2001). Overall, not so bad. Modern Healthcare, Volume 31, pp. 36-37.
Coates, K. (2001, June). Trickle-down Effect. Nurse Week, Volume 6, p.13.
Covey, S. (1991). Managing Expectations. In Covey, S. (Ed.), Principle-Centered Leadership (pp. 204-205). New York, New York: Franklin Covey Co..
Hansen, D., & Mowen, M. (2000). Current Focus of Management Accounting. In Sears, M. (Ed.), Management Accounting (5th ed., pp. 10-15). Cincinnati, Ohio: South-Western College Publishing.
Nelson, D., & Quick, J. (2000). Forces for Change in Organizations. In J. Szilagyi (Ed.), Organizational Behavior (Third ed., p. 602). Cincinnati, Ohio: South-Western College Publishing.
Parker, C. (2001, June 11). AHA report shows staffing shortages threaten access to quality health care. AHA News, pp. 1, 2.
Pearson, C., & Barton, L. (2001). Vacancy Review Council. The Healthcare Advisory Board (Ed.), Liberating Hospital Economics, Volume I, pp. 37-43). Washington, D.C.: The Advisory Board Company.
Shaffer, F. (2001). On the Front Lines: A scan of the organizations that influence practice. Curtain Calls, Volume 3, p. 3.
Solovy, A. (2001). Mission Makes Wall Street. Hospitals & Health Networks, Volume 75, p. 38.

ORTHOPAEDIC MATTRESSES

In one episode of Merlin series whereby the Prince Arthur wanted to act like a normal citizen, whereby he stayed in his servant�s house. There was no double bed, only the bed for the servant. The prince has to sleep on the floor, but asked his another servant to get him his mattress from the palace. Why do you think a mattress is so important to him? It�s simple, because he do not want to get backache.
Nowadays, most of the people sleep on the bed or mattress, but why still many people suffer from backache? Maybe the mattresses they used are not good? How do you know that mattresses you are sleeping on are good enough? Just ask yourself how relaxed, rested or rejuvenated you feel immediately after you get up first thing in the morning? If the answer is not very, maybe it�s time to get a new mattress or change to orthopaedic mattress.
Why so many people suffer from back pain? There are of course many different answers to this question, but the quality of bed and mattress play a big role in this problem. Most people buy low quality mattress and kept them for too long. This bed already offer poor support and quickly goes off by time. Therefore they fail to provide support that the back need. This will avoided by orthopaedic mattresses.
The spine, along with the muscles and ligaments that enable it to work, can be easily aggravated, but the good news is that the back is also very robust and flexible and has great powers of recovery. This means that most back related problems can be rectified and that includes those caused by poor mattress support.
Do you wonder how mattresses can provide support to the back? The natural shape of the spine is double S. This shape needs to be maintained to keep the health of the back and ultimately the whole body. When this spine is not supported, the problem with back will arise.
In most of the people, the spine is poorly design structure which involve in many activities such as rotating and bending. During sleep, usually the spine get the opportunity to rest and recover. This is of course can be accomplish by a good and comfortable mattress which is designed as such to support the spine, skeletal structure and the muscles.
Nobody should use his mattress more than 10 years. This is because all mattresses that are 15-29 years old will be unable to provide an adequate support and will bring down the quality of the sleep ultimately to the health. However, the mattress does not need to be old to be changed. If you ever feel uncomfortable, achy and tense after waking up, It could be the sign to change the mattresses.
Unsuitable mattress usually manifest as minor aches or discomfort. Over time, it may progress into severe to the point that it irritates the daily activities. If the source of problem is not removed, the person has to suffer the pain forever. It is advisable to prevent the problem than to cure the disease. In order to prevent all this, orthopaedic mattress is highly suggested.

Orthopaedic mattress is a mattress is design as such to provide support to the double S shaped human spine. In a recent studies that tested mattress ergonomics, 12 women were the subjects were tested by lying on an incompressible wooden surface was compared with various mattresses. All of the mattresses were judged as significantly more comfortable that the wooden surface, but there were no differences between the mattresses type, even these included orthopaedic mattress. Measure of shoulder, elbow, hip, knee, body ankle pressures showed few significant differences and surprisingly, there were no significant associations between measures and comfort ratings.
However, how hard or soft the mattress feels is thought to be an important factor in reducing or preventing back pain. Comparison of sleeping on a futon or softer air mattress showed that sleep onset latency, waking after sleep onset and the sleep efficiency index were comparable for both mattress, but subjective sleep evaluation tended to be offer for air mattress. A study of sleep quality and bed firmness showed that 4 of 9 male subjects slept significantly better on the softer mattresses, while 2 slept better on the harder mattresses. The greatest difference in quality occurred when changing from the subject�s own mattress to one of the test mattresses, and the authors concluded that it may take several days to adapt to a new sleep surface. This is may be why business travelers often report sleep difficulties.
The Cornell University�s Ergonomics group suggests that if you are to look for a mattress, then here is the guidelines:
- Designed to conform to the spine�s natural curves and to keep the spine in alignment when you lay down
- Designed to distribute pressure evenly across the body to help circulation, decrease body movement and enhance sleep quality
- Designed to minimize the transfer of movement from one sleeping partner to the other.
- Design with perimeter edge support
The orthopaedic mattresses are of course fulfill all the guidelines above as they are designed as such to provide support to spine, skeletal structures and muscles. There are few types of this mattress which are designed differently in their structure and how they function.
There are 2 basic type of orthopaedic bed, a divan bed and bed constructed with a frame. A divan bed has under bed storage with draws or compartments and the mattress is supported by a sprung or platform topbase. These bed are therefore consider as multipurpose.
In the other hand, orthopaedic bed comprising of frame, can be constructed from any number of materials including timber and steel. There is no separate storage and can neither have a void beneath them or sit closer to the floor than a divan. These beds can also be made in such a way to be adjustable through the addition of electric motor and a remote control unit.
The mattresses are further classified according to their support and springing system. They are achieved either through one or a combination of different systems. They primary spring and support methods used today are �spring systems�, memory foam, latex foam and air cushioning.
Within the category of spring system, there are 3 slightly different construction approaches which are �posture spring� (Slumberland, Silentnight and Sealy), �open coil� (Airsprung, Silentnight and Sealy) and �pocket sprung�
Posture spring are made from a continuous single wire which enables all the spring to be interlinked. This creates support system that allow every spring to act together with other spring.
Open coils bed have a frame of springs that are linked together by further horizontal or vertical coils to create a tight and interconnected mesh of springs. They are very firm and been regarded for their orthopaedic qualities.
Pocket sprung have individual springs that are placed in separate pockets which run in rows along and across the mattress.
Memory foam beds able to contour themselves to unique shape of anyone who sleeps on them and offer superior support by balancing out weight distribution across the body. The ability to give orthopedic characteristic made them highly popular.
Latex foam beds is fairly new, but offers many advantage of memory foam and the natural rather than synthetic latexes have the additional advantage of sleeping cool, hypoallergenic and no noticeable odor.
There is also a type called gel bed which is relatively new innovation. Contrary to the name, it is not a viscous liquid like material, rather something that resembles rubber and it is usually manufactured in a nest or honeycomb with large air voids between the small sections. The benefits of gel bed is that it is multi fold and offer same characteristic as memory and latex foam.
An air mattress is an inflatable mattress that is typically made of plastic, textile reinforced plastic or rubber. The support is achieved by means of filling the mattress with compressed air. Therefore, it can be easily stored and transported, so suitable for camping of travelling.
As mention earlier, the orthopedic mattresses are solely to provide support to the spine especially in elderly and those who work hard in the day and need good sleep at night. As more and more people suffering from back pain, so this mattress is recommended for all.
It is the lifeline to heath of spine and back as it is benefit body as a whole by providing supportive and restful sleep so that we recover from busy activities day to day. It helps to avoid stiffness, aches, muscular discomfort and back pain by allowing the back to retain its natural position without the build of unnecessary tension or pressures.
However, there is also an advantage of this mattress that it is rigid attachment of big diameter springs , therefore it reduce the orthopedic properties of the mattress.

ORTHOPEDIC CHAIR
As with the mattress, the orthopedic chairs are also design as such to support the body and the back thus promote a good and comfortable sitting posture. They have different designs to suit the activities done using it. Such as, one chair is suitable for rest and the other suitable for office job.
Usually the orthopedic or also known as �ergonomic� chairs are design to suit 2 conditions � home and office.
At home of course is the place to run away from a hectic life outside. Sitting on the orthopedic chair can provide relaxation by providing massage and or vibratory motion or even heat from controllable embedded heat pads.
In an office environment, orthopedic chair function primarily to attain good posture while using the office equipment, such as computers. It takes account for users who need to use have free and unrestricted hand movement, at the same time with good back support.
There are three main categories of orthopedic chair � support chair, lift chair or �rise and recline� and massage chair. All three of them have their particular function but still share same characteristic to make the user comfortable. And it is possible to combine all the three function in one chair.
The support chair is designed to make sure that your spine is in the possible best condition when you are sitting down. As mention before, spine is double S profile, in the same boat with the orthopedic mattress to provide comfortable to the back and to prevent back ache. This chair also minimize the chances of your position to slip away.
The lift chair helps to user to make transition from a seated position to a standing posture easy in some less-able members in the community. This involves an automated system built into the chair itself, as it lift and tilts to help them get up or even help them to get into the chair. Elderly man, injured or those with back issues can make use out of this characters.
While massage chair, as the name depict, it gives pleasure by providing vibratory, mechanical air or water muscle stimulation. Originally, it was used as medical aid, but nowadays it is more to luxury item.
In office environment, especially if the job need you to focus to the equipment for entire day, so it is easy to get weary. Maybe quite some time needed to restore the energy back, so kind of time wasting going on in the office. It looks simple, but productivity tends to slide if people are distressed or if they got sore due to bad posture, I recommended that employers should purchase this chair so the employees remain healthy.
These chair usually don�t have many accessories attached to them, the important thing is the worker�s hand are free while their back are taken care of. Due to different atmosphere between home and office, the office chair tend to have more Spartan design philosophy and more focus on support than decorating and the most common options are height and tilt adjustment, so it can be considered part of a comfortable and productive working environment.
Of course, none of this chair works if people don�t know how to sit properly. The bottom part of your back should be in contact with the chair�s back, that is the proper technique of sitting. For those who could not afford the expensive orthopedic chair, a lumbar pillow or spine support can be put on the chair, but the result is not as good as the chair itself.
 

STEM CELL TRANPLANT IN SPINAL CORD INJURY

INTRODUCTION
Stem cell research is advancing knowledge about how an organism develops from a single cell and how healthy cells replace damaged cells in adult organisms. This promising area of science is also leading scientists to investigate the possibility of cell-based therapies to treat disease, which is often referred to as regenerative or reparative medicine.
WHAT ARE STEM CELLS?
Stem cells are cells found in most multi-cellular organisms. They have two important characteristics that distinguish them from other types of cells. First, they are unspecialized cells that renew themselves for long periods through mitotic cell division and differentiation. The second is that under certain physiologic or experimental conditions, they can be induced to become cells with special functions such as the beating cells of the heart muscle or the insulin-producing cells of the pancreas.

The two broad types of mammalian stem cells are: embryonic stem cells that are isolated from the inner cell mass of blastocysts, and adult stem cells that are found in adult tissues.

Stem cells are important for living organisms for many reasons. In the 3- to 5-day-old embryo, called a blastocyst, stem cells in developing tissues give rise to the multiple specialized cell types that make up the heart, lung, skin, and other tissues. In some adult tissues, such as bone marrow, muscle, and brain, discrete populations of adult stem cells and progenitor cells act as repair system for the body, replenishing specialized cells, but also maintaining the normal turnover of regenerative organs, such as blood, skin, or intestinal tissues.
Stem cells can now be grown and transformed into specialized cells with characteristics consistent with cells of various tissues such as muscles or nerves through cell culture.
Highly plastic adult stem cells from a variety of sources, including umbilical cord blood and bone marrow, are routinely used in medical therapies. Embryonic cell lines and autologous embryonic stem cells generated through therapeutic cloning have also been proposed as promising candidates for future therapies.[3
UNIQUE PROPERTIES OF STEM CELLS
Stem cells differ from other kinds of cells in the body and regardless of their origin have three general properties. They are capable of dividing and renewing themselves for long periods; they are unspecialized; and can give rise to specialized cell types.
Stem cells do not have any tissue-specific structures that allow it to perform specialized functions. A stem cell cannot work with its neighbours to pump blood through the body (like a heart muscle cell); it cannot carry molecules of oxygen through the bloodstream (like a red blood cell), nor can it fire electrochemical signals to other cells that allow the body to move or speak (like a nerve cell), but, more importantly, it can give rise to the development of these specialized cells by a process known as differentiation.
The internal signals are controlled by a cell's genes, which are interspersed across long strands of DNA, and carry coded instructions for all the structures and functions of a cell. The external signals for cell differentiation include chemicals secreted by other cells, physical contact with neighbouring cells, and certain molecules in the microenvironment.
Unlike the above mentioned specialized cells, stem cells are capable of proliferating for long periods. A starting population of stem cells that proliferates for many months in the laboratory can yield millions of cells. If the resulting cells continue to be unspecialized, like the parent stem cells, the cells are said to be capable of long-term self-renewal.
Adult stem cells typically generate the cell types of the tissue in which they reside. A blood-forming adult stem cell in the bone marrow, for example, normally gives rise to the many types of blood cells such as red blood cells, white blood cells and platelets. Until recently, it had been thought that a haematopoietic stem cell in the bone marrow could not give rise to the cells of a very different tissue, such as nerve cells in the brain. However, a number of experiments over the last several years have raised the possibility that stem cells from one tissue may be able to give rise to cell types of a completely different tissue, a phenomenon known as plasticity. Examples of such plasticity include blood cells becoming neurons, liver cells that can be made to produce insulin and haematopoietic stem cells that can develop into heart muscle.


HISTORY OF STEM CELL RESEARCH
� 1908 - The term "stem cell" was proposed for scientific use by the Russian histologist Alexander Maksimov (1874�1928) at congress of hematologic society in Berlin. It postulated existence of haematopoietic stem cells.
� 1960s - Joseph Altman and Gopal Das present scientific evidence of adult neurogenesis, ongoing stem cell activity in the brain; like Andr� Gernez, their reports contradict Cajal's "no new neurons" dogma and are largely ignored.
� 1963 - McCulloch and Till illustrate the presence of self-renewing cells in mouse bone marrow.
� 1968 - Bone marrow transplant between two siblings successfully treats SCID.
� 1978 - Haematopoietic stem cells are discovered in human cord blood.
� 1981 - Mouse embryonic stem cells are derived from the inner cell mass by scientists Martin Evans, Matthew Kaufman, and Gail R. Martin. Gail Martin is attributed for coining the term "Embryonic Stem Cell".
� 1992 - Neural stem cells are cultured in vitro as neurospheres.
� 1997 - Leukemia is shown to originate from a haematopoietic stem cell, the first direct evidence for cancer stem cells.
� 1998 - James Thomson and coworkers derive the first human embryonic stem cell line at the University of Wisconsin�Madison.[60]
� 2000s - Several reports of adult stem cell plasticity are published.
� 2001 - Scientists at Advanced Cell Technology clone first early (four- to six-cell stage) human embryos for the purpose of generating embryonic stem cells.[61]
� 2003 - Dr. Songtao Shi of NIH discovers new source of adult stem cells in children's primary teeth.[62]
� 2004�2005 - Korean researcher Hwang Woo-Suk claims to have created several human embryonic stem cell lines from unfertilised human oocytes. The lines were later shown to be fabricated.
� 2005 - Researchers at Kingston University in England claim to have discovered a third category of stem cell, dubbed cord-blood-derived embryonic-like stem cells (CBEs), derived from umbilical cord blood. The group claims these cells are able to differentiate into more types of tissue than adult stem cells.
� 2005 - Researchers at UC Irvine's Reeve-Irvine Research Center are able to partially restore the ability of mice with paralyzed spines to walk through the injection of human neural stem cells.
� August 2006 - Rat Induced pluripotent stem cells: the journal Cell publishes Kazutoshi Takahashi and Shinya Yamanaka.[63]

� October 2006 - Scientists at Newcastle University in England create the first ever artificial liver cells using umbilical cord blood stem cells.[64][65]
� January 2007 - Scientists at Wake Forest University led by Dr. Anthony Atala and Harvard University report discovery of a new type of stem cell in amniotic fluid.[66] This may potentially provide an alternative to embryonic stem cells for use in research and therapy.[67]
� June 2007 - Research reported by three different groups shows that normal skin cells can be reprogrammed to an embryonic state in mice.[68] In the same month, scientist Shoukhrat Mitalipov reports the first successful creation of a primate stem cell line through somatic cell nuclear transfer[69]
� October 2007 - Mario Capecchi, Martin Evans, and Oliver Smithies win the 2007 Nobel Prize for Physiology or Medicine for their work on embryonic stem cells from mice using gene targeting strategies producing genetically engineered mice (known as knockout mice) for gene research.[70]
� November 2007 - Human induced pluripotent stem cells: Two similar papers released by their respective journals prior to formal publication: in Cell by Kazutoshi Takahashi and Shinya Yamanaka, "Induction of pluripotent stem cells from adult human fibroblasts by defined factors",[71] and in Science by Junying Yu, et al., from the research group of James Thomson, "Induced pluripotent stem cell lines derived from human somatic cells":[72] pluripotent stem cells generated from mature human fibroblasts. It is possible now to produce a stem cell from almost any other human cell instead of using embryos as needed previously, albeit the risk of tumorigenesis due to c-myc and retroviral gene transfer remains to be determined.
� January 2008 - Robert Lanza and colleagues at Advanced Cell Technology and UCSF create the first human embryonic stem cells without destruction of the embryo[73]
� January 2008 - Development of human cloned blastocysts following somatic cell nuclear transfer with adult fibroblasts[74]
� February 2008 - Generation of pluripotent stem cells from adult mouse liver and stomach: these iPS cells seem to be more similar to embryonic stem cells than the previous developed iPS cells and not tumorigenic, moreover genes that are required for iPS cells do not need to be inserted into specific sites, which encourages the development of non-viral reprogramming techniques.[75]
� March 2008-The first published study of successful cartilage regeneration in the human knee using autologous adult mesenchymal stem cells is published by clinicians from Regenerative Sciences[76]
� October 2008 - Sabine Conrad and colleagues at T�bingen, Germany generate pluripotent stem cells from spermatogonial cells of adult human testis by culturing the cells in vitro under leukemia inhibitory factor (LIF) supplementation.[77]
� 30 October 2008 - Embryonic-like stem cells from a single human hair.[78]
� 1 March 2009 - Andras Nagy, Keisuke Kaji, et al. discover a way to produce embryonic-like stem cells from normal adult cells by using a novel "wrapping" procedure to deliver specific genes to adult cells to reprogram them into stem cells without the risks of using a virus to make the change.[79][80][81] The use of electroporation is said to allow for the temporary insertion of genes into the cell.[82][83][84][85]
� 28 May 2009 Kim et al. announced that they had devised a way to manipulate skin cells to create patient specific "induced pluripotent stem cells" (iPS), claiming it to be the 'ultimate stem cell solution'.[86]
DEVELOPMENT OF STEM CELL RESEARCH

The spinal cord needs more protection then any other organ or system because unlike other organs, the spinal cord once damaged, cannot regenerate. While the majority of cells found in the central nervous system are born during the embryonic and early postnatal period, scientists recently discovered that new neurons are continuously added to two specific regions of the adult mammalian brain (Reynolds and Weiss 1992). Neural stem cells were isolated from the dentate gyrus of the hippocampus and the walls of the ventricular system called the ependymal layer. The progeny of these stem cells differentiate in the granule cell layer, meaning neurogenesis continues late into adult rodent life. These stem cells also migrate along the rostral migratory stream to the olfactory bulb, where they differentiate into neurons and glial cells (Luskin, 1993). Nerve cell differentiation has been witnessed in vivo, as well as in vitro when stimulated with an epidermal growth factor (Gage, 1995).
Along with pluripotent stem cells progenitor cells, a more restricted type of stem cells, are found in the hippocampus and ependymal layer. These cells are immature cells that are predetermined to differentiate into neurons, oligodendrocytes, and astrocytes. In 1995 Frissen observed that the presence of nestin increases in response to spinal cord injury. Nestin is a protein expressed by stem cells: presence of it indicates neural stem cells are much more active then previously believed. Our brain naturally increases the production of stem cells to aid an injured CNS. In 1999, Johansson and Momma observed that the only active progenitor cells were differentiating into astrocytes. They labeled ependymal cells with a Dil injection so migration could be followed. After making lesions in the spinal cord they waited four weeks and then observed the progress of the ependymal cells. They tested the cells found in the scar tissue around the site of injury and found that all DIL marked cells were astrocytes. This indicates that the progeny from ependymal cells had only differentiated to astrocytes. Stem cells do respond to spinal cord injury, just not for the purpose of reestablishing connection between neurons.
This realization sparked scientist�s interest in understanding what triggers these progenitor cells to proliferate. Scientists began to focus on neurotrophic factors that triggered this differentiation, specifically the presence of brain derived neurotrophic factors (BDNF) and neurotrophin 3 and 4 (NT-3 and NT-4). In the early 90�s these trophic factors were targeted as what triggered axon growth during early development. NT-3 also is expressed in greater amounts in response to spinal cord injury. In 1994 Schwab reported dramatic increase in function, and regrowth of a partially severed cord of rats after treatment with NT-3. In 1997 Grill, Gage, and colleagues published a paper examining the effects of transplanted NT-3 on motor skills and morphology after induced spinal injury in mice. They focused on the corticospinal tract, the pathway in charge of making voluntary movements. NT-3 has been previously observed to promote regrowth of corticospinal axons, and preserves degenerating motor neurons.
Grill and colleagues induced lesions in the dorsal hemisection of adult rat�s spinal cord, resulting in severely limited motor ability. Next grafts of syngenic fibroblasts, genetically altered to produce NT-3, were transplanted into the lesion cavity of the experimental group. These rats were kept alive for three months and put though a series of tests to monitor motor improvement. These tests examined coordination, ability to walk on inclined surfaces and precision of foot placement. After three months these rats were killed for the purpose of a quantitative cell count.
Recipients of the NT-3 secreting grafts showed significant improvement in motor skills over the control group, although they did not recover to the full ability they had before injury. After three months recipients of the NT-3 grafts demonstrated growth of corticospinal axons up to 8 mm from where the stem cells were transplanted. Only the injured axons at the lesion site showed any sign of regrowth. Uninjured axons showed no effort to reestablish connections across the site of injury. This suggests that NT-3 only responds when corticospinal axons are injured. If scientists could pinpoint signals triggering this response there is potential to manipulate the process in a manner causing neural cells to differentiate.
Triggering neurotrophic factors in hopes of inducing progenitors to proliferate is one of two major areas of study in spinal cord regeneration. Scientists also can derive undifferentiated embryonic stem cells (ES cells) from foetal spinal cord tissue and then mature them into cells that are suitable to implant into the damaged spinal cord. When using ES cells, researchers have two options: they can treat ES cells, allowing them to mature into CNS cells in vitro before transplantation, or they can directly implant differentiated cells and depend on signals from the brain mature the cells. This technique became possible when Reynolds and Weiss found that stem cells taken from the brain could be propagated in vitro. This allowed labs to duplicate what occurs naturally in the brain, and attempt to use the product to re-grow the damaged cells.
In December of 1999 McDonald and colleagues from Washington University School of medicine successfully implanted ES cells in laboratory rats. McDonald induced thoracic spinal cord injury in rats using a metal rod 2.5 mm in diameter resulting in paralysis. Nine days after the injury McDonald and colleagues transplanted roughly 1 million ES embryoid bodies pre-treated with retinoic acid into the syrinx that had formed around the contusion. During the nine days that passed between injury and transplantation, all the standard events following a spinal cord injury occurred. At the time of injury some cells died immediately, followed by a second wave of apoptosis within the first 24 hours. The centre of the bruised spine filled with fluid becoming a cyst referred to as syrinx. McDonald injected the ES cells into this cavity.
Two weeks after the transplantation ES stem cells filled the area normally occupied by glial scarring. After five weeks the stem cells had migrated further away from the implantation site. Although a number of them had died, there was still enough for the rats to have a growing supply of neurons and glial cells. Most of the surviving cells were oligodendrocytes and astrocytes, but some neurons were found in the middle of the cord. The rats regained limited use of their legs. Paralysis had been cured!!
McDonalds work in 1999 represented new successes in stem cell technology but this technology is yet to be tested in humans. A major obstacle remains: although scientists are achieving results, they don�t understand the factors responsible for what occurs. In McDonalds study, the regaining of functions could result from the few differentiated neurons. Another possibility could be that the high differentiation of oligodendrocytes re-myelinated enough axons to reestablish communication. Or perhaps functions regained due to ES cells producing growth factors�more research will have to be done before these options are narrowed down. Additional to unclear understanding of the process, other complications exist. Any introduction of foreign cells into the body triggers the immune system. ES cells would not simply be accepted into the host CNS. McDonald used cyclosporine to prevent rejection in the rats, but things get more complicated when testing begins on humans. The brain and spinal cord is complex, mysterious realms of the body�until science can predict the exact affect of evolving technologies, no testing on humans can occur.
A major motivation behind spinal cord research has been Christopher Reeve. Injured in a horseback riding incident, Christopher Reeve suffered a cervical spinal cord injury that left him quadriplegic. Christopher Reeve began the Christopher Reeve Paralysis Foundation (CRPF). CPRF funds research to treat or cure paralysis resulting from spinal cord injury or other CNS disorders. CPRF supports a Research Consortium, which collaborates the work of nine laboratories, as well as funds an international individual grants program. Several of the labs involved in the Research consortium focus on stem cells, making a lot of progress. The Salk Institute, run by Dr. Fred Gage examines the progenitor cells differentiating into glial cells. Someday they hope to manipulate these progenitor cells, inducing differentiation into neural cells.
STEM CELL TRANSPLANT VS ETHICS
There are a lot of people who find stem cell research extremely unethical. Scientists have found the most success with ES cells taken from embryoid spinal cords: although the ES cells are taken from embryos consisting at most of 64 cells, they still have potential to develop into a human being. People who believe life begins at conception remain morally against stem cell research. Justification is that the stem cells are derived from embryos discarded from fertility clinics. These embryos would be wasted if not used for stem cell research. Christopher Reeve published a position paper in response to the moral concerns and President Bush's decisions on stem cell researching. CPRF supports responsible stem cell research, recognizing the fine ethical boundaries existing in this technology.
TRANSPLANTATION OF STEM CELLS INTO SPINAL CORD
The original cell transplantation technology has been developed in the Centre for treating SCI patients. After surgically disrupting an intramedullary cyst (see Figure 1), the spinal cord defect is entirely filled up with the special gel containing foetal-derived, immature stem cells (see Figure 2). Moreover, during several months after the surgery each patient is subarachnoidally grafted with foetal-derived cells one or more times. The donor cell combination that is highly effective in generating regenerative processes in an adult nervous tissue has been previously determined by special experimental studies.

Figure 1. Dissection of the connective tissue cyst and opening access to the cord defect.
FUTURE OF STEM CELLS
It has been hypothesized by scientists that stem cells may, at some point in the future, become the basis for treating diseases such as Parkinson's disease, diabetes, and heart disease.
As scientists learn more about stem cells, it may become possible to use the cells not just in cell-based therapies, but also for screening new drugs and toxins and understanding birth defects.

STRESS : A lifestyle Disease

Stress is the condition that results when person-environment transactions lead the individual to perceive a discrepancy, whether real or not, between the demands of a situation and the resources of the person's biological, psychological or social systems. In medical terms, stress is the disruption of homeostasis through physical or psychological stimuli. Stressful stimuli can be mental, physiological, anatomical or physical reactions.
Millions of people are looking for a magic supplement and herb combination that will increase their health and vitality. People are ingesting Coenzyme Q, pycnogenol, magnesium, Vitamin C, Gingko, Echinacea and thousands of other products and combinations. In many cases, these supplements give a slight energy and health boost. In some cases, the body needs both healthy foods and supplements to help recover from an illness. However, for most people, much of the increased need for nutrients is due in a significant part to a high level of daily physical and/or psychological stress.

Taking steps to relax and body and mind (in addition to getting adequate sleep) can be enormously healing and is highly recommended for those interested in healing acute or serious chronic illnesses or preventing future illnesses. Relaxation techniques can add enormous power to other holistic healing techniques. I hope that you take the time to make gradual changes which will allow deep relaxation and the healing and vitality that comes with it to become an increasing part of your life
Some Common Signs and Symptoms of Excess Stress
� Regularly walking, eating or working in a rushed way.
� Regularly thinking and worrying about the past or future.
� Frequent tension in the body (esp. neck, face, shoulders, back and chest, and stomach) which often goes unnoticed until one slows down, breaths deep and carefully surveys the body.
� Feeling of the "weight of the world" on your shoulders.
� Emotionally "on edge."
� Regular tiredness during the day.
� Significant need for outside stimulation to feel good (coffee, sweeteners, food, sex, TV, alcohol, money, accomplishments, etc.)
The Goal
Occasional challenges, both physical and psychological, are not unhealthy for most people. Occasional challenging projects, arguments, difficulties with children, difficulties at work/school, etc. are a normal part of life. These types of stresses are normal and can actually be strengthening. The goal is not necessarily to avoid all stressful events, but to develop the ability to relax during day-to-day activities and during challenging occurences (such as those mentioned above). Persons who are recovering from an illness should attempt to keep challenging situations to a minimum but not necessarily avoid them totally unless they are extremely weak.
Strategies For Stress Relief
As part of the process of curing an illness, promoting health & vitality and preventing illness and premature aging, it is important to gradually move towards a daily life that less stressful.
Some Strategies to Avoid
� Attempting to make everything in life stress-free.
� Focusing on every event and constantly reminding yourself to relax.
� Regularly avoiding the feeling of emotions (e.g., sadness, anger, joy, fear, etc.).
� There are a number of other things which will not work in the long run when used by themselves only -- long vacations, execise, etc.
The type of strategy which tends to work is the combination of gradually and gently trying to change one's habits plus regular practices or situations which help put the body in a relaxed state. Both types of strategies are important in promoting stress reduction.

Regular Practices and Situations to Promote Stress Relief

Note: The positive effects of these techniques vary from person to person.
Examples of Powerful and Healing Regular Practices
Taking a class and going to regular group practices can be crucial in promoting a regular practice. Some people have moved into teaching centers in order to be certain they will have a regular practice and promote healing and transformation.
� Yoga -- This is a wonderful practice for stress reduction and profound healing.
� Meditation
� Tai Chi
� Conscious Breathing Routine
� Pranayam
� Dancing
� Bioenergetics Classes
� Holistic Healing Retreat
� Vacation
� Massage (Some people practice regularly by exchanging with a partner.)

Daily Stress Reduction Tips

Note: As mentioned earlier, there will naturally be times when these tips are not used, but try to gradually incorporate them into your life where possible.
1. Add something beautiful to your life on a daily basis (e.g., flowers).
2. Do some enjoyable activities whenever possible.
3. Walk, work, and eat at a relaxed pace.
4. Take a short break after meals to relax.
5. If possible, go outside at least once per day and notice the simple things such as the weather, scenery, etc.
6. During the day, whenever you remember, notice and tension in your body (jaw, neck, diaphram, shoulders, etc.). Breath deeply and gently stretch and relax any tense areas.
7. If you notice your mind racing or worrying about the past or future, take a minute to breath deeply and gently focus on something in the moment such as your breath, scenery, birds.
8. Take breaks during the workday to relax.
9. Wear comfortable and loose clothing when possible. Take off your shoes when you can.
10. Avoid holding in feelings day after day, but instead, find a safe place to feel, express and embrace them.
Please be gentle with yourself. Some people find themselves falling back into excessively stressful habits from time to time. That is perfectly normal. Simply notice that change in a non-judgemental way and move back to the stress reduction practices and tips that promote a healthy way of life.
Stress Relief Ideas in Specific Situations
On many ocassions there are situations that come up which can cause significant amounts of stress. Listed below are a few such situations along with some ideas that I have found useful in addressing the situation. As in all of the idea listings on the Holistic Healing Web Page, please do not try to do everything at once.
� Financial Difficulties

Financial difficulties can be enormously stressful for some people because our goals and our security is wrapped up in the need to have sufficient finances. Such difficulties often don't magically disappear, but there are some steps that can be taken to reduce or eliminate the stress and worry while working one's way through these difficulties. A few suggestions include:
o Steps -- Carefully follow the plan outlined in the book, "Your Money or Your Life." This book will take you step by step towards financial independence. Following the program in the book can also be useful in helping to find your goals and make career decisions.
o Share -- Tell at least one close friend, family member or religious leader (e.g., minister, priest , guru) about your difficulties. Keeping the difficulties secret will often add stress and eventually cause inner turmoil.
o Faith -- Persons who have a regular Meditation Practice or Spiritual Practice often develop enormous faith that difficulties can be worked through successfully. The potential stress can be reduced many-fold through these types of practices. While it doesn't directly effect the financial situation, these practices can improve health, reduce stress, make it easier to see worthwhile opportunities and make it easier to change habits that may, in some cases, contribute to financial difficulties.
o Acceptance -- While it may seem strange, having a loving acceptance of oneself in the current situation is often an important key to making a permanent change in the situation. This goes hand-in-hand with having a strong faith. If you look at people who successfully turn their lives around, you will usually notice both a loving acceptance of who they are as well as a strong faith. The opposite end of the sprectrum are the unfortunate souls who have lost their faith and their self-esteem (or never had it).

o Inner transformational tool that addresses the situation. Some such tools are Meditation Practice, Spiritual Practice etc
o Persons suffering from psychological illnesses which are contributing in some way to the financial difficulties can, if possible, have these health problems treated by a Holistic Healthcare Professional
o Tasks and Time Constraints

There are situations where there is constant time and work pressure and which adds significant stress to one's life. Sometimes these situations are not easily avoidable. In order to start a medical training program with friends (who had planned to start at a specific date), I chose to continue to work full-time, take prerequisite classes nearly full-time and to continue to serve as the webmaster for the Holistic Healing Web Page. In order to come out of situations like these with one's health, it is helpful to consider a few ideas which I have related below.
o Small Tasks -- Spliting projects and assignments into small pieces and doing a small amount of work on a regular basis on these projects is perhaps one of the very best ways to prevent becoming overwhelmed with work.
o Priorities -- Choosing appropriate priorities for tasks is an important way to avoid stress. Is it better to performs A+ (4.0 grade) in school and study all of the time or to get a B average and spend the extra time having fun, exercising, etc.? Is it better to work overtime completing projects to earn extra money or job prestige and not see your family much or to somehow avoid overtime work and spend alot of time with your family? These are the types of decisions which are important and can have a significant effect on stress levels. The decisions should be made while keeping in mind what it important in life. In my case mentioned above, I chose to work extra hard for a year in order to start a medical program with my friends. But if such a decision would cause extreme stress that would lead to health problems, I would not have decided to work so hard.
o Stress Reduction Practices -- Continuing a regular practice of stress reduction techniques such as yoga, bioenergetics or meditation can help one get through busy times with one's sanity. It can be many times easier to develop a regular practice by going to a class. Most people can spare at least 15-30 minutes per day to perform a short routine.

� "I Hate My Job" Syndrome

Job stress can be one of the biggest sources of stress for many people. In many cases, people feel hopeless when thinking about solving serious problems on the job, dissatisfaction with the job, or making career choices. In fact, a large percentage of the people I have met have had this situation at one time in their life. It can be difficult to heal a chronic illness if you are experiencing a large amount of stress on the job. In addition, chronic illnesses may become more likely if the excessive on-the-job stress is not addressed. Below are a few ideas which may prove helpful.
o Program -- The first four ideas suggested for Financial Difficulties above are highly recommended in this situation.
o Improving the Job -- A couple of excellent resources for making the very best of a difficult situation are 1) the book, "The Corporate Mystic: A Guidebook for Visionaries With Their Feet on the Ground" by Gay Hendricks & Kate Ludeman
o Personnel Office -- The Personnel Office in most companies is responsible for helping resolve conflicts with other employees and for resolving and problems you are having with job responsibilities. If discussing the situation with your boss does not resolve the situation or if you do not feel comfortable discussing the situation with your boss, please consider whether the Personnel Office in your company can help find solutions for the problem.
o Exploration -- Pursuing creative expression in various ways can be helpful in finding goals that may one day become a career. While it may not seem possible upon initial evaluation, many exciting hobbies can eventually become careers. Therefore, it can be helpful to take classes and explore various endeavors while paying attention to what excites you as a possible hobby or career.
o Bioenergetics -- One of the goals with Bioenergetic Analysis is to help the student "find their own movement." By learning to find my own movement physically and expressing myself vocally using Bioenergetic techniques, I gained confidence and skills in both identifying and pursuing my own career goals. Others have seen similar effects. The classes can be helpful in this regard, but one-on-one work can be even more effective.
Difficulty Making Changes !!
Many people say I am having difficulty keeping a regular practice of yoga/meditation as well as eliminating habits that cause stress. I keep falling back into the same old patterns of stressful living and not taking care of myself. Do you have any ideas?

Having difficulty making changes can have a number of possible causes. Below are a few suggestions to consider:
o Class -- Taking a class can make an enormous difference in one's ability to keep a yoga or meditation practice going. I know some practitioners who give classes because it is easier for them to keep up a practice by doing so. Try to find a class near your home if possible.
o Friends & Family -- It can be much easier to make changes and sustain those changes you get regular support and love from close friends and family.
o Positive Influences -- Spend time around positive, cheerful people whenever possible. There's little that can drag a person down more easily than a lack of positive attitudes in one's life or excessive exposure to negative attitudes. Some people move to yoga or meditation centers or take retreats regularly at such centers in order to learn and to be around people who are positive and taking care of themselves.
o Programs -- Two different and very simple programs that people have found helpful are described in the following books. I would suggest only doing one program at a time.
o Meditation -- Inner Transformation techniques such as meditation has proven extremely helpful for many people in making changes.


Prof. G S Patnaik is a consultant orthopedic and spinal surgeon with advance degrees in orthopedic and trauma surgery ,sociology , economics,public administration.presently he is pursuing courses in management and international law. His interests includes study of scriptures of all faith and is a well known columnist and a gifted public speaker He can be contacted at Web Page: www.drgspatnaik.com
 

 

KNOWLEDGE DISSEMINATION: CONTINUED MEDICAL EDUCATION

Key words: Knowledge, Medical Knowledge , hoarding , dissemination

Introduction:

At the simplest level, dissemination is best described as the delivery and receipt of a message, the engagement of an individual in a process, or the transfer of a process or product. It is also helpful to think about dissemination in three broadly different ways, viz., dissemination for awareness, for understanding , and for action. Indeed, effective dissemination of a knowledge product will most likely require that it satisfy all three in turn: utilization is the goal. Knowledge is a "thing" that simply needs to find a good home� Nowhere is this more apparent than in the worthy effort to define dissemination as consisting of four activities: spread, exchange, choice, and implementation.

Definitions of dissemination also reflect differing assumptions and beliefs about the ways in which knowledge is used, indeed about the very nature of knowledge itself. The focus varies from perceiving dissemination and utilization as linear, mechanical processes of "transfer," in which knowledge is packaged and moved from one "place" to another, much as an appliance might be packaged and shipped, to characterizing the process as highly complex, nonlinear, interactive, and critically dependent on the beliefs, values, circumstances, and needs of intended users.

Scholarly research makes a profound contribution to the social, cultural and economic wealth of a country. The results of research, referred to here as "scholarly knowledge", is created, organized, preserved and disseminated within the scholarly communication system. Many countries are undertaking national research strategies aimed at understanding and navigating these changes. In order to optimize the dissemination of scholarly knowledge, it is critical that we develop a comprehensive research strategy to examine the future of scholarly communication in this country.

Creation, manipulation, management and dissemination of knowledge cannot go on forever without determining what impact it is having on those who create it and those who use it. This paper explores methods of determining the impact of disseminated Knowledge. It does this by first defining what knowledge is. This is followed by a discussion on different mediums through which knowledge may be disseminated. It then discusses two questions � when do we know when to disseminate knowledge and how do we know when it has been disseminated.(1)


MEDIUMS OF KNOWLEDGE DISSEMINATION

Contrary to Plato and Foskett�s definition of knowledge, it is postulated that knowledge is information that is acceptable to a norm about a subject. In treating different mediums that may be used to disseminate knowledge, it is argued that mediums of disseminating knowledge can be grouped into two main categories, namely natural and man made mediums. Natural mediums of knowledge dissemination include audio and gestures, which are performed by all leaving beings whereas; man-made mediums include all mediums of communication that man has developed out of transforming matter.

Knowledge itself cannot be monitored, only presence in its carrier can. Ipso facto, analyzing different carriers of it or usethereof, not knowledge itself, can do evaluation of knowledge because an indisputable truth is that presence of knowledge is only manifest in its application. In monitoring and evaluating knowledge as transformed matter, the criteria of process and progress; relevance, efficiency, effectiveness, impact and sustainability may be used respectively. Techniques of analyzing applied knowledge data abound. For something to count as knowledge, it must actually be true. I see knowledge as information that is acceptable to a norm about a subject. As long as the information that you have conforms to an established and acceptable societal norm, it is knowledge it does not have to be true. If it conforms to an established norm, it will always be believed. As soon as the norm changes, what you know becomes information. When people do not believe you, it is simply because what you say to them is not acceptable to their norm. Good knowledge is useful knowledge. It permits man�s survival by allowing him to use it to solve his problems.

When we attend schools or listen to priests preach to us and accept what they tell us as reasonable and pass it on to other people or use it to solve our problems, what we are doing is simply accepting new norms about new or existing subjects. According to Polanyi, ��tacit knowledge is what is in our heads and explicit knowledge is what we have codified� Given that tacit knowledge is knowledge that is in our heads the easiest and the only way to disseminate this type of knowledge is through organs of the body. We can communicate it through voice. This method of communication is largely applied in schools from primary to tertiary. Besides explicit communication, a lot of information and knowledge is passed on from one person to another through gestures. Laughing is a simple sign of happiness. Shrugging your shoulders indicates that you do not know. Of unique interest to note though is that gestures are not universal, they are unique to societies. Nodding one�s head means that one is in agreement with what is being said after the European fashion. The converse is true in the Asian culture. In the Asian culture when you shake you head from side to side this means concurrence with what is being said. One of the notable efforts to try to address the problem of different norms and standards on gestures is what has come to be known as the sign language which came into being as an effort to address different human beings impairments such as speech and hearing. This confirms the definition made earlier on that knowledge is that which conforms to a norm about any subject.

The second type of knowledge is explicit knowledge. This is knowledge that has been codified. How can knowledge be codified? Codification of knowledge came as a result of man�s application of tacit knowledge to transform matter into various useful objects for his survival. Writing is the oldest form of codifying knowledge. Most of the world�s knowledge is in written form in the form of books. With further transformation of matter through application of tacit knowledge other ways of codifying knowledge have emerged over time. We now find knowledge in medium such as recorders, the INTERNET and others. Of particular interest to me is knowledge that is manifest in transformed matter.

HOARDING KNOWLEDGE

There is no stipulated rule on where and when knowledge should be disseminated. The simple answer to this question is knowledge is ready to be disseminated when the holder of it feels it is ready to be. Besides, it does not make sense to acquire knowledge to hoard it. In fact, it is impossible to hoard knowledge because we need to constantly exchange it for survival. Hoarding of knowledge makes sense only when one does it in order to gain comparative advantage over other human beings. Even this is not eternal. Overtime, the hoarded knowledge gets known and is further exchanged. Dissemination of knowledge is often done with a certain intention in mind. When this is the key reason for knowledge dissemination, it is important to determine whether knowledge dissemination has really taken place. This is important for a number of reasons. One, it allows for learning on whether knowledge was successfully disseminated so that if not other means of disseminating it successfully could be devised. For example, at institutions of learning gauging of knowledge dissemination is done through tests and examinations as we all know and two, for accountability purposes. (4) However, the key gauge of whether knowledge has been disseminated is its application. As indicated earlier, as tacit knowledge, knowledge application is seen in the development of different solutions in the form of products and services. In a codified form, knowledge dissemination is seen in the use of the products and services to solve societal problems. Note before, knowledge use does not only lead to useful solutions to societal problems, at times it creates more problems and leads to societal ills. A clear epitome of this is the atomic bomb that was dropped by the Americans on Hiroshima and the current nuclear age in which nuclear bombs, which are an epitome of man�s application of his knowledge, are a threat to humanity.


MEDICAL KNOWKEDGE

Medical doctors claim that their discipline is founded on scientific knowledge. Yet, although the ideas of evidence-based medicine are widely accepted, clinical decisions and methods of patient care are based on much more than just the results of controlled experiments. Clinical knowledge consists of interpretive action and interaction�factors that involve communication, opinions, and experiences. The traditional quantitative research methods represent a confined access to clinical knowing, since they incorporate only questions and phenomena that can be controlled, measured, and counted. (2)
Biomedical knowledge is expanding at an unprecedented rate-one that is unlikely to slow anytime in the future. While the volume and scope of this new knowledge poses significant organizational challenges, it creates tremendous opportunities to release and direct its power to the service of significant goals. One can achieve those by integrating numerous resource-intensive, technology-based initiatives-including personnel, services and infrastructure, digital repositories, data sets, mobile computing devices, high-tech patient simulators, computerized testing, and interactive multimedia-in a way that enables the center to provide information tailored to the needs of students, faculty and staff on the medical center campus and its surrounding health sciences colleges.
Emphasis must be made on discovering, applying, and sharing new knowledge, information assets, and technologies in this way is a collaborative process. This process creates open-ended opportunities for innovation and a roadmap for working toward seamless integration, synergy, and substantial enhancement of the academic medical center's research; educational, and clinical mission areas (5)
Continuing Medical Education
Continuing medical education (CME) plays a key role in test ordering, while pharmaceutical manufacturers� representatives are important sources of information concerning new therapeutic agents. The dissemination of information is a complex process. Physicians frequently use multiple sources of information in the decision making process. Physicians and planners of CME must be aware of what types of educational activities are best suited for their needs (6)
The tacit knowing of an experienced practitioner should also be investigated, shared, and contested. Qualitative research methods are strategies for the systematic collection, organization, and interpretation of textual material obtained from talk or observation, which allow the exploration of social events as experienced by individuals in their natural context. Qualitative inquiry could contribute to a broader understanding of medical science. The Internet is a convenient but complex source for health information used by an increasing number of health consumers. Especially for people suffering from a chronic illness (e.g., diabetes), information seeking forms a part of the daily management of the disease, a �project of life.� The study of Web texts examines the citation patterns for a specific and controversial health issue: the beneficial or hazardous use of dietary chromium supplementation in diabetes self-management. Texts from different categories of Web sources (scientific, professional, educational, and commercial sources, as well as diabetes discussion groups) were analyzed in order to study how knowledge is transferred between sources, and how diabetics participating in discussion groups refer to and make sense of the information from different sources on the Internet. The citation patterns suggest that deviations from the traditional models of scientific knowledge dissemination can occur in the Internet environment (1).
It is beyond argument that Continued Medical education (CME) should play a very significant role in the changing health care environment. There are various types of literature (e.g., concerning learning and adult development principles, problem-based/practice-based learning, and other topics) that contribute to ways of thinking about and understanding CME. It is gratifying that the Association of American Medical Colleges (AAMC) has made a commitment to helping CME be more effective in the professional development of physicians.
The professional development of physicians is a lifelong commitment that builds on formal and informal opportunities to learn emerging science, apply innovations in clinical settings, and expand understandings of caring for patients. One essential element in that commitment has been continuing medical education (CME), the final part of the education continuum. Although CME has a long history in supporting physicians as lifelong learners, it has become increasingly important and focused during the past ten to 15 years as a result of the impact of changing educational, social, and political forces on medical practice. People in academic medicine can support continuing medical education to respond to the changed and changing health care environment, and suggest new directions for individuals and institutions involved with continued learning.
CONCLUSION
As far as medical knowledge dissemination it is imperative that collaboration among the appropriate academic groups, professional associations, and health care institutions, with leadership from the state bodies, is essential to create the best learning systems for the professional development of physicians.
Building new knowledge-based systems today usually entails constructing new knowledge bases from scratch. It could instead be done by assembling reusable components. System developers would then only need to worry about creating the specialized knowledge. New systems should interoperate with existing systems, using them to perform some of its reasoning. In this way, declarative knowledge, problem- solving techniques, and reasoning services could all be shared among systems. This approach would facilitate building bigger and better systems cheaply. The infrastructure to support such sharing and reuse would lead to greater ubiquity of these systems, potentially transforming the knowledge industry. One sees a vision of the future in which knowledge-based system development and operation is facilitated by infrastructure and technology for knowledge sharing. It is believed that newer initiatives currently under way to develop these ideas would pave a long way in the complex yet simpler process of knowledge sharing and dissemination. The future is looking expectantly to realize this vision.

References:

1. Enabling Technology for Knowledge Sharing
Robert Neches, Richard E. Fikes, Tim Finin, Thomas Gruber, Ramesh Patil, Ted Senator, William R. Swartout AI Magazine, Vol 12, No 3


2. Health discussions on the Internet: A study of knowledge communication through citations: Marianne Wikgrenv Department of Information Studies, �bo Akademi University, Tavastgatan 13, FIN-20500 �bo, Finland
3.Continuing Medical Education: A New Vision of the Professional Development of Physicians
Bennett, Nancy L. PhD; Davis, Dave A. MD; Easterling, William E. Jr. MD; Friedmann, Paul MD; Green, Joseph S. PhD; Koeppen, Bruce M. MD, PhD; Mazmanian, Paul E. PhD; Waxman, Herbert S. MD Academic Medicine: December 2000 - Volume 75 - Issue 12 - p 1167-1172

4. Www.researchutilization.org/matrix/resources/review/ -

5. Managing Knowledge and Technology to Foster Innovation at The Ohio State University Medical Center
Cain, Timothy J. PhD; Rodman, Ruey L. MLS; Sanfilippo, Fred MD, PhD; Kroll, Susan M. MLSAcademic Medicine:
November 2005 - Volume 80 - Issue 11 - pp 1026-1031

6. Information sources and clinical decisions: journal of General Internal Medicine Jeoffrey K. Stross Vol 2., No.3 May, 1987, 155-159


NB: This was a lecture delivered at the KNOWLEDGE GLOBALIZATION conference at Dhaka May 2010.Dr Patnaik was invited to chair the session on session of Education. The key note was delivered by Noble Laurate Dr Mohd Yunus. The conference was aimed at sharing knowledge with scholars and researchers across geographic and academic boundaries. It was a
global multidisciplinary conference with delegates from across the world.

 

avoidable tragedy: spurious liquor

Posted by on Sunday, 18th December 2011

Avoidable Tragedy: Spurious Liquor


With more than half of all alcohol drinkers in India falling into the criteria for hazardous drinking, alcohol abuse is emerging as a major public-health problem in the country. The problem becomes more compounded especially where we find the urban poor and rural peasants flocking to the liquor shops with a 10 rupee note and buying death in a sachet as seen in the recent Calcutta tragedy India's reputation as a country with a culture of abstinence especially in matters regarding alcohol is underserved, say experts. The country, which has seen a rapid proliferation of city bars and nightclubs in recent years, is fast shedding its inhibitions about alcohol as a lifestyle choice.
This situation has led to fears of an undocumented rise in alcohol abuse not only among poorer classes but also in sections of society that were previously considered dry. The entire policy regarding the pricing and trading of state sponsored liquor outlets with singular aim of generating revenue needs to be questioned by concerned citizens. The increasing production, distribution, and promotion of alcohol have already seen drink-related problems emerging as a major public-health concern in India. Sales of alcohol have seen a growth rate of 8% in the past 3 years. Officially, Indians are still among the world's lowest consumers of alcohol�government statistics show only 21% of adult men and around 2% of women drink. But up to a fifth of this group�about 14 million people�are dependent drinkers requiring �help�.

The concern, say experts, is that there has been a rapid change in patterns and trends of alcohol use in India. Chief among them is people are beginning to drink at ever-younger ages. The percentage of the drinking population aged less than 21 years has increased from 2% to more than 14% in the past 15 years, according to studies in the southern state of Kerala by Alcohol and Drugs Information Centre India, a non-governmental organization (NGO). Alarmingly, the study found that the �average age of initiation� had dropped from 19 years to 13 years in the past two decades.
The centre points out that a �powerful international and domestic alcohol lobby� is purposely targeting young Indians. The local industry has introduced flavored alcohol drinks to attract previously non-drinking women and young men. Multinational companies have identified India with its vast unexploited markets as one of the worlds most sought after places for investment.
Many alcohol adverts now feature spirited groups of young people having a good time. Although alcohol advertising is banned in the electronic and print media, surrogate advertising is rife, �Drinking water and apple juice is packaged by alcohol companies. It's all about getting young people to start early and be life-long consumers. Bollywood films now glorify alcohol where the good guys drink.�
The shifting composition of Indian drinkers has seen a rise in the number of Indian women drinking regularly and heavily. One recent study in the southern state of Karnataka found young women consumed similar amounts of alcohol to young men on any typical drinking occasion.
What is of particular concern�and an important indicator of health risks�is that the signature pattern of alcohol consumption in India is frequent and heavy drinking. More than half of all drinkers fall into the criteria for hazardous drinking, which is characterized by bingeing and solitary consumption to the point of intoxication. Moreover, spirits account for 95% of the beverages drunk in India.
There is evidence even to suggest that the poor are beginning to drink more than they earn�a deadly spiral of alcohol and debt. Although the Indian constitution includes the prohibition of alcohol among its directive principles, alcohol policy is devolved to individual states�as is the levying of taxes on it. Since most states derive around a fifth of their revenue from alcohol taxation�the second largest source after sales tax�they are generally ambivalent towards stemming its flow. Moreover, there is a long history in India of a powerful alcohol lobby with industry figures influencing the political process, both in the form of party donations and as representatives. But experts argue that Indian society is losing considerably more than it gains.
According to a recent study by researchers from NIMHANS it is shocking to know that the direct and indirect costs attributable to alcohol addiction is more than triple the profits of alcohol taxation and several times more than the annual health budget of Karnataka. These included the tangible costs of health care, occupational, financial, social, and legal factors.
Indian Alcohol Policy Alliance, an NGO aiming to prevent alcohol-related harm through evidence-based policy intervention, says that the key is to break the stranglehold of state revenue departments who see increasing consumption of alcohol as a boon to treasury coffers.
In less than a week after more than 90 women, men, and children died in a calamitous fire at the AMRI hospital in Kolkata, illicit brew has claimed the lives of about 150 people, at Sangrampur in the South 24 Parganas district of West Bengal. The hooch was sold in sachets, priced between Rs.7 and Rs.20, virtually opposite a police post in the area. Starting with a couple of deaths early in the morning, the toll kept rising through the day and touched 80 by daybreak next day. Most of the victims complained of body pain, stomach cramps, vomiting, and a burning sensation. The recurrence of heart-rending tragedies caused by the killer brew only lends credence to the thinking among political parties and State governments that it might be better to introduce legal sale of licensed liquor than let addicts go for the illicit stuff. There is a demand from sections in government to suggest monopolizing sale of government controlled liquor as the Tamil Nadu Model .Of course the protagonist will feel that this step might be catastrophic. But the evidence from across India shows that prohibition just doesn't work; in fact, it brings on all sorts of ill effects, social as well as medical. Although States that still implement prohibition, full or partial, have set up separate wings in the police department to handle cases arising out of prohibition offences and illicit brewing, it is common knowledge that connivance between the brewers and sections of the police makes the hooch flow, particularly in festival season. Most, if not all, victims tend to be poor laborers, and the families end up paying a terrible price. Alcoholism is a social menace that needs to be tackled in a sensitive, intelligent, multi-pronged way. Driving it underground, to dangerous devices, is clearly not the way.


(Prof Gourishankar Patnaik is a senior Consultant in orthopedics based in Bhubaneswar. He can be contacted at www.drgspatnaikcom)

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