FAQ Category: General

There have been a few research studies trying to answer just this question. Pedersen et al looked at hip replacements and found some association with post operative pneumonia and death. Browne et al showed blood transfusions with total hip replacement to have increased mortality, length of stay in the hospital and total hospital charges. A more recent and larger study by Hart et al found that there was no increase in serious complications in the first thirty days after having a blood transfusion during a total knee or total hip replacement.

In a recent study by Hart et al, the authors looked into the risk factors associated with blood transfusion during total hip and knee replacements. They looked at information from the National Surgical Quality Improvement Program, which is a nationally validated, outcome based program that collects data about preoperative risk factors, variables during surgery, thirty-day postoperative complications and mortality rates. This database was used to identify patients undergoing elective primary hip and knee replacements in 2011. A total of 9362 hip replacements and 13,622 knee replacements were identified. For this set of patients the blood transfusion rate for hip replacement was 22.2 percent, and for total knee replacement 18.3 percent. Significant risk factors associated receiving a blood transfusion were similar for both knee and hip replacements and included (in order of importance) age, preoperative hematocrit (red blood cell count), BMI 2. These results were somewhat surprising, for example the authors did not expect lower BMI to be associated with increased transfusion requirement, and they also found that smoking was actually a protective factor against needing a transfusion. The authors hypothesize that with decreased BMI and lower red blood cell count before surgery, with too much loss of blood then a blood transfusion may more likely. They also hypothesize that smoking increases the red blood cell count over time to make up for less ability of the smokers red blood cells to carry oxygen, thus these patient may have more blood cells available to make up for blood loss during a surgery.

While this is ultimately a question for your surgeon, the decision to either reconstruct or amputate is based on multiple factors.  These include the complexity of the injury, the soft tissue damage, function following the accident, expected healing times, and chance of infection.

A sentinel event is a mistake that could have been avoided if proper procedures and techniques were followed that result in death, the risk of death, physical or psychological injury.  Examples include wrong side surgery or slips of the knife resulting in cut nerves, arteries, veins, bowels, etc. A surgical complication is an event that is not necessarily avoidable following surgery that does not seriously threaten a person’s well being.  Examples of these would be rejection of the hardware or poor healing.

The most basic explanation is that human blood plasma and platelets contain cells which cartilage uses for healing. Since cartilage is a poorly healing tissue on its own, it has been shown that providing the injured area with increased availability of these different cells can increase the ability of the cartilage to heal itself. More specifically plasma contains about 200 different types of proteins, which are involved in tissue healing, hormones, and human growth factors; the most significant one being IGF-1 which has been shown to assist in cartilage healing. Platelets also contain several types of growth factors and other bioactive molecules. There is also frequently addition of leukocytes, which are a source of cytokines and enzymes, which help prevent infection. Leukocytes also secrete molecules into the area of healing including interleukins, proteins, growth factors and interferon, which can help signal the bodies healing processes.

The successful treatment of muscle injuries depends on understanding what phase of healing is taking place. In the early days (first week) after an injury, the body mounts an inflammatory response. This is sometimes referred to as the destructive phase.

It is during this period of time that the macrophages are released. Macrophages are from the immune system and are designed to destroy damaged, bleeding, or injured cells. Application of the R.I.C.E. approach (Rest, Ice, Compression, Elevation) is the most often recommended treatment during this early acute phase of muscle injury.

But there is really no convincing evidence that this treatment is an effective way to treat soft tissue injuries. In fact, in animal studies, scientists have shown that applying ice too long can actually reduce blood flow to the area impairing recovery. And other studies using compression bandages right away after injury (within the first five minutes) does not decrease the amount of swelling or speed up healing.

Whether or not to immobilize the muscle (in a splint or cast) remains a point of debate and controversy. On the one hand, keeping the muscle from moving during the early healing (destructive) phase can minimize the gap that develops when the ruptured muscle stumps pull apart. As the body sets up a collagen scaffold that will be filled in with repair cells, a smaller gap between the injured tissue means a smaller scar.

On the other hand, immobilizing the damaged soft tissue too long can cause excessive scarring. Since scar tissue is less flexible, the muscle is at risk of reinjury under lower loads or force compared with normal, healthy muscles. And there is clear evidence that early movement aids the regenerating muscle fibers to heal in an organized fashion. With early mobilization and better tissue alignment, fewer adhesions can form.

Treatment also depends on the severity of muscle injuries (mild, moderate, or severe). Accompanying swelling, loss of motion, tearing of muscle fibers, and loss of function help determine how the muscle injury is classified. Mild injuries usually have only minor swelling and pain with no loss of motion or function. Complete rupture of a muscle will be obvious when the patient cannot contract or use that muscle to move the body part (e.g., arm, leg).

Whereas nonsteroidal antiinflammatory drugs (NSAIDs) were once routinely prescribed after muscle injury, more recent (animal) testing has brought about a change in thinking here as well. For example, there is evidence that these drugs can delay the destruction of damaged cells thus slowing repair and regeneration of the muscle tissue. Likewise, the use of steroids has been shown (again in animals only so far) to permanently impair healing.

Conservative care (applying the RICE principle) for the first two or three days may be all that’s needed. With time (typically four to six weeks, sometimes longer depending on your age, health, and severity of injury), the soft tissue will regenerate and remodel. The result will be a return to activity as before the injury.

If you think there is something more serious going on that might require surgery (or the conservative approach doesn’t work), don’t hesitate to seek medical evaluation and treatment. Your primary care physician, a sports medicine physician, or an orthopedic surgeon will be able to assess your condition and make the most appropriate recommendations.

There are three major types of muscles injuries: contusion, strain, or laceration. Contusion is caused by a direct and compressive force such as a direct blow. Muscle strain is more often the result of tensile force (tension) beyond what the muscle can stretch. And of course, a laceration or cut is the result of sharp trauma through the skin and fascia down to the muscle.

Strains are more common in muscles like the hamstrings that cross two different joints (in this case, the hip and the knee). Certain joint positions can put maximum strain on a muscle that is affected by two joints versus a muscle that is only affected by one joint.

You didn’t describe your injury but if it was one where you stretched the hamstring beyond its resting length, then you may very well have strained it. Full tears or ruptures cause the muscle to snap back away from the bone where it was attached. This separation is referred to as a retraction.

Most of the time, a full rupture with retraction will produce a ball of soft tissue somewhere along the muscle. You will also be more likely to lose strength and motion when the muscle is completely torn. The best way to find out is to see a physician for a full evaluation. Clinical exam may be all that’s needed to make the diagnosis. Imaging studies such as MRI or ultrasound may be ordered to confirm the diagnosis and to map out the full extent of the injury for treatment purposes.

A great deal of research is focused now on tissue regeneration for soft tissue and bone repair in humans. Stem cells from the person’s own bone marrow have two major advantages: the patient does not experience cell rejection and this source of stem cells avoids the controversy over the use of embryonic stem cells. Stem cells are useful because they can divide and develop into any type of cell in the body (including bone or cartilage).

Surgeons can remove or aspirate stem cells from the sternum (breast bone), vertebrae (spinal bones), and iliac crest (top of the pelvic bones). Studies are ongoing to investigate the effect(s) of removing stem cells from these areas and comparing results among the various harvest sites.

In a recent study from Italy, use of stem cells were compared between the anterior iliac crest and posterior iliac crest. Twenty-two adult donors (ages 18 to 72) participated in that particular study. A total of 20 mL of bone marrow was withdrawn using a collecting needle (skin puncture) in three places along the iliac crest.

The cells were taken to a lab and processed. The different types of cells were separated and counted in the first step of the process. Then the cells were prepared in such a way to allow them to replicate (grow and multiply) over a period of 14 days. The total number of cells was recounted with a particular focus on one type called connective-tissue progenitor cells. These cells are especially useful for repair of connective tissue.

The results of this study showed that bone marrow harvest of cells that become connective-tissue progenitor cells was better from the posterior iliac crest. In fact, there were 1.6 times more of these cells in the posterior compared with the anterior iliac crest. The recommendation made as a result of this study was for harvest of stem cells from the posterior iliac crest for bone repair.

There are many, many factors that can affect the total yield of the different cells produced from stem cells. Site of harvest in only one. The age and sex of the patient may make a difference. And although 14 days was the time period used in this study, it’s possible that other time periods would yield different results. The study you participated in could have been exploring any one of these factors. You can probably contact the study coordinator and find out more about the goal and results.

There has long been debate about the influence of weather on musculoskeletal symptoms. Many people who have injured a joint or other area of soft tissue (e.g., ankle sprain, bursitis, tennis elbow, broken bone) swear they can predict the weather. Their joints start to ache, throb, swell, or stiffen up.

The exact mechanism to explain these things remains under investigation. Some experts hypothesize that damage to the baroreceptors of the joint (tiny units that respond to changes in pressure) makes them more sensitive to changes in the weather. Or perhaps damage to the baroreceptors make it more difficult for the joint to adjust to changes in atmospheric pressure.

But not everyone is affected by weather changes and for those who are affected, the changes aren’t the same for everyone. A recent study from Brazil has added some information to consider. Thirty-two (32) patients with known hand osteoarthritis (OA) filled out a survey answering questions about their hands. They did not know the study was about the influence of weather on hand arthritis.

In Brazil where this study was done, July has the lowest average temperature and higher relative humidity than any other month. November has the highest temperatures with low atmospheric pressure and humidity. Those features make these two months the most logical ones to select for a study on weather and arthritis affecting the hands.

They answered questions like, How much pain (or stiffness) have you had in your hands? They completed the same survey three times a week throughout the months of July (summer) and November (winter). The patients ranged in ages from 45 to 77 with half being younger than 60 years of age. There were men and women included from all levels of income. Some were underweight while others were overweight. In essence, the patients included came in all sizes, shapes, and backgrounds.

After each patient completed the surveys, they compared the patient responses about pain, stiffness, and function against meteorological (weather) records. The two weather factors that had the greatest effect on hand arthritis were temperature and humidity. In fact, there was a significant relationship between temperatures the day before and the day after changes in hand pain. Some patients (but not all) were affected by atmospheric pressure. The effect was most noticeable on hand function.

But the most interesting finding was that not everyone was affected in the same way. The lower the temperature, the more pain and stiffness with decreased function was experienced. But this wasn’t true for everyone or even the majority of patients. And remember, they did not know the study was about the influence of weather on their arthritic hands.

Some patients had improved symptoms when the temperature went up while others felt worse. It was the same with changes in humidity and atmospheric pressure. There were both positive and negative correlations between weather elements and arthritic effects. The question then becomes how to explain the variations in responses to weather?

The authors point out that whereas it is possible to measure changes in weather very specifically and accurately, patient perceptions of pain, stiffness, and function are subjective. Depending on mood, individual sensitivities, and what may be going on in the person’s life, ratings of pain, stiffness, and function could be over or under estimated. And the influence of medications being taken by the patients should be considered.

In summary, this study shows that weather does have a correlation with symptoms associated with hand arthritis. But as you and the women in your family have experienced, individual sensitivity is very different from one person to the next and cannot be predicted. Further study is needed before the exact relationship between weather and hand arthritis can be fully understood.

A recent study was done by surgeons from the United States Army reporting on the long-term results of 611 (mostly male) soldiers who had surgery for chronic exertional compartment syndrome of the lower leg. The information they reported may be of help to you in answering this question.

As you probably know by now, compartment syndrome describes a condition in which fluid (swelling or blood) builds up inside one or more of the individual compartments of the leg. The “compartments” are easier to understand if you think of each group of muscles and tendons as being surrounded by a protective sheath or lining of connective tissue called fascia. There are individual compartments on the front, sides, and back of the lower leg.

In each compartment, the fascia fits closely to the outer layer of the soft tissue it surrounds — like a sleeve or envelope. The structures are lubricated with a glistening fluid that allows everything to slide and glide against each other. There isn’t a lot of give or room for increased volume of fluid from swelling.

When an injury occurs that leads to swelling, the increased pressure inside the sleeve or envelope cuts off blood supply to the muscles. The muscle cells start to necrose or die. Left untreated, this necrosis can progress to the point of gangrene. Years ago, this problem was labeled “march gangrene” when it occurred in soldiers.

Compartment syndrome of the leg occurs in soldiers due to overexertion from exercise. Soldiers have daily, intense, high-demand physical requirements. Marching and running with heavy packs while wearing stiff boots along with routine weight training and aerobic exercise adds to the physical stress placed on the lower legs.

Treatment can be successful with a conservative approach including rest, activity modification, and antiinflammatory medications. But more often, surgery (fasciotomy) to cut the surrounding fascia and release the constrictive soft tissues is required. Even with surgical decompression, complete recovery doesn’t always happen.

As this study showed, almost half (44.7 per cent) of the patients had a recurrence of their painful symptoms after surgery. More than one-quarter (27.7 per cent) could not resume their previous level of activity. And a smaller group (5.9 per cent) had to have a second surgery because the first fasciotomy was not successful. Not all revision surgeries are successful either. In this study, only 14 per cent reported complete pain relief after the second operation.

In the military population, complications after surgery were the most likely reason for medical discharge. Infection, nerve pain, poor wound healing, blood clots, and complex regional pain syndrome were reported in 15.7 per cent of the soldiers.

The reality is (as this large study of the long-term results following surgical fasciotomy for chronic exertional compartment syndrome of the lower leg showed) there is a high chance of a poor outcome for many of the patients. Young, physically active soliders expecting to return to full active duty may be disappointed. One in five will have a failed surgery and ongoing pain and symptoms. It might be advised to expect the best but prepare for something less than optimal with this condition.

Compartment syndrome describes a condition in which fluid (swelling or blood) builds up inside one or more of the individual compartments of the leg. The “compartments” are easier to understand if you think of each group of muscles and tendons as being surrounded by a protective sheath or lining of connective tissue called fascia. There are individual compartments on the front, sides, and back of the lower leg.

In each compartment, the fascia fits closely to the outer layer of the soft tissue it surrounds — like a sleeve or envelope. The structures are lubricated with a glistening fluid that allows everything to slide and glide against each other. There isn’t a lot of give or room for increased volume of fluid from swelling.

When an injury occurs that leads to swelling, the increased pressure inside the sleeve or envelope cuts off blood supply to the muscles. The muscle cells start to necrose or die. Left untreated, this necrosis can progress to the point of gangrene. Years ago, this problem was labeled “march gangrene” when it occurred in soldiers.

Treatment can be successful with a conservative approach including rest, activity modification, and antiinflammatory medications. But more often, surgery (fasciotomy) to cut the surrounding fascia and release the constrictive soft tissues is required. Even with surgical decompression, complete recovery doesn’t always happen.

Patients with compartment syndrome of the lower leg do face the possibility of symptoms coming back after treatment, complications from surgery, and the need for a second operation. Long-term results can even include an inability to return to full participation in previous activities.

Other soft tissue structures inside the compartment such as nerves can get pinched or compressed. The effect is like a crush injury with damage to the nerves resulting in neuritis, which may be what has happened to you. Treatment is with conservative measures such as physical therapy and medications. All of these effects (including the neuritis) can be transient (temporary) or irreversible (permanent).

You can try a very direct approach by asking your physician this very question in as tactful a way as possible. Consumers have a right to the most up-to-date services and should be able to ask any of their health care providers how they keep abreast of the latest ideas for the particular problem at hand.

Physicians have at their disposal a variety of ways to keep up with the latest knowledge and understanding of the diseases, illnesses, and conditions they treat. It could be as simple as reading an article on elbow arthritis that has been approved as a continuing education course. Anyone who reads the material and answers the questions correctly can earn continuing education credits. In the process, the reader will gain an understanding of current thinking and orthopedic practice in the treatment of elbow arthritis.

For example, in a recent publication of The Journal of Hand Surgery (March 2013), recent developments in the treatment of elbow arthritis were presented. Learning objectives for the reader included understanding function of the elbow and forearm, causes of elbow arthritis, types of patients who have this condition, and treatment (nonsurgical and surgical) of the problem.

The following is a brief summary of the contents of that article to give you an idea of what crosses physicians’ desks these days just through their professional literature. The review was broken down into two major sections: diagnosis and management. As with all medical conditions, the diagnosis of elbow arthritis requires a careful patient history and clinical examination.

Special tests (neurologic exam, examination of alignment, blood work) and imaging (X-rays, CT scans, or MRIs) are part of the evaluation process. X-rays are usually enough to identify joint damage, loss of joint space, and the presence of bone spurs or any “loose bodies” (fragments of bone or cartilage) inside the joint. More advanced imaging such as CT scans or MRIs are more likely ordered when surgery is being planned.

The physician must differentiate between rheumatoid (inflammatory) arthritis and osteoarthritis (degenerative disease). Recognizing differences in the signs and symptoms and patient history/patient type is important in making this distinction. For example, someone with rheumatoid arthritis of the elbow will have pain and stiffness throughout the full elbow range-of-motion.

A patient with osteoarthritis is more likely to have difficulty at the point of full elbow flexion or elbow extension. Pain through the entire range of elbow motion doesn’t develop with osteoarthritis until the condition is very severe (considered “advanced” disease).

The patient’s history can be very telling. Trauma to the elbow or a history of heavy use of the arm (e.g., weight lifting, construction work, throwing athletes) is linked with osteoarthritis. Patients with rheumatoid arthritis (RA) may have a family history of RA but no history of overuse to suggest osteoarthritis (OA).

The plan of care for anyone with elbow arthritis is to relieve pain and improve or restore function for daily activities. That sounds simple enough but there are many ways to approach this. The first is always with conservative (nonoperative) care. This can include medications, rest, physical therapy, and modification of activities. Treatment of osteoarthritis in manual laborers can be more challenging as they are unable to stop working or even change the way they use the arm because of the job requirements.

In the case of rheumatoid arthritis (RA), 10 per cent of patients will get full recovery with early diagnosis and aggressive treatment with disease modifying anti-rheumatic drugs (DMARDs) and other biologic therapies. Surgery for elbow arthritis is only recommended when patients fail to improve with nonsurgical care. Surgical options include synovectomy, arthroscopic debridement, and joint replacement (called arthroplasty).

The choice of which surgical procedure to perform depends on whether the condition is inflammatory (rheumatoid) arthritis or degenerative (osteoarthritis). Other considerations include type of work (use or physical demands placed on the elbow), severity of the arthritis, and the age of the patient.

This continuing education review includes a detailed section on each surgical treatment option — how to perform the procedure, when to use it, and what to expect in terms of outcomes or results. It is readily recognized that treatment is different for each person. The authors of this review and continuing education tool were clear in stating that the material was not intended to represent the only methods or best procedures for elbow arthritis. Rather, it provides a helpful review of current approaches used successfully by many orthopedic surgeons.

Other ways to stay current on arthritis available to your physician include other on-line peer reviewed (high quality) publications, on-line webinars, and continuing education at conferences held periodically around the United States. Your physician will likely be able to let you know what kinds of continuing education he or she has pursued over the last one to two years.

Your father has suffered what is referred to as a fragility fracture. A fragility fracture is a bone break that occurs without significant trauma, which makes it a low-energy fracture. The person could just be lifting a cup of coffee, turning a key in the door lock, or picking up a small book when the bone fractures. Osteoporosis (decreased bone mineral density or “brittle bones”) is usually the reason for these fractures.

Half of all bone fractures that occur each year in the United States are related to osteoporosis. More than 300,000 hip fractures occur in the United States every year. A person with a hip fracture has a 20 percent chance of dying within six months as a result of the fracture. Osteoporotic-related fragility fractures can also affect just the arm. In fact, each year in the United States, one-quarter of a million adults (250,000) experience bone fractures of the arm from this condition.

One-third (34 per cent) of fragility bone fractures of the arm affect the wrist for women. In men, this figure is closer to 17 per cent. But even one osteoporosis-related fracture increases the risk two to four times for another fracture later. This is serious because many people who have a fracture related to osteoporosis spend considerable time in the hospital and in rehabilitation.

As you have discovered, treatment is with dietary supplementation (e.g., calcium and vitamin D), hormones, bisphosphonates (e.g., Boniva, Fosamax, Reclast), and biologic therapy (e.g., monoclonal antibodies). And some patients may want to pursue alternative therapies such as additional drug therapy with calcitonin, strontium, hormone replacement therapy, and/or estrogen receptor modulators.

Contraindications (reasons NOT to prescribe certain drugs) vary for each treatment recommended. For example, anyone with kidney disease, parathyroid disorders, or bone tumors is not a good candidate for dieatry supplementation with calcium and vitamin D. Bisphosphonates (used to prevent bone loss) are not advised for patients who cannot sit up for at least 30 minutes. And hormone therapy may be contraindicated in patients who have had prior radiation treatment to the skeleton or who have mets to the bone from cancer.

Anyone with a low-energy or fragility fracture associated with osteoporosis may be best served by coming under the care of a specialist with advanced knowledge of osteoporosis. This could be a primary care physician, a rheumatologist, or an endocrinologist. They will be familiar with the appropriate medications to prescribe and any contraindications. Having one physician supervise all aspects of care and management of this condition is important to prevent future fractures from occurring.

For more information (especially detailed information on pharmacologic and other treatment), see our document Patient Guide to Osteoporosis.

Although obesity is a known, direct factor in joint arthritis, osteoarthritis (OA) is considered a multifactorial disease. There’s more than meets the eye on this one. In other words, many factors contribute to the damage and destruction of the joint that leads to arthritis.

For example, increasing age, sex (female), family history, race, previous injury, and lifestyle are all known risk factors for osteoarthritis (OA). Of all those risk factors, only obesity is considered modifiable (in other words, a risk factor you can do something about).

Though you share the same family history with your brother, you may not share the same personal history (e.g., past injuries) or even lifestyles. Exercise is known to help keep the joints lubricated and helps combat arthritic changes. Even being overweight, if you have a regular exercise routine, you may be able to hold off some of the arthritic changes that develop over time.

Obesity does, in fact, cause local biomechanical changes in the joint reducing shock absorbing ability and increasing load and force on the joint cartilage. Eventually the joint starts to break down. It is possible to have changes present that even show up on X-rays but no symptoms. Without an X-ray to know for sure, this could be your situation.

But even if nothing shows up on an X-ray you should be aware that fat cells (referred to as adipose tissue) also activate inflammation that is system-wide (throughout the entire body). This low-grade inflammation has a direct and pathologic effect on the musculoskeletal system (especially bone and cartilage). Fat is not just a store house of energy. It is also a very active endocrine (hormone producing) gland. Blood tests confirm that this is the case with elevated levels of inflammatory markers measured in obese people.

Scientists haven’t fully unraveled how obesity, systemic inflammation, and joint changes are all connected. But they are finding out more and more each day that may eventually help find a drug to prevent or at least manage osteoarthritis. This proinflammatory state of the obese body is also suspected as a contributing cause of hypertension, insulin resistance, and high cholesterol levels.

If you are overweight to the point of being considered obese, you know that weight loss isn’t easy. Many health care professionals recommend education to prevent weight gain first. But for those whose body mass index (BMI) indicates they are already past ‘normal’ and in the overweight or obese zone, weight loss is still advised.

Strategies for successful weight loss include diet and exercise, behavioral counseling and incentive programs, and/or possibly bariatric surgery. Slow, gradual, but steady weight loss is always preferred because maintaining weight loss is just as challenging as losing the weight in the first place. Negative side effects of bariatric surgery (e.g., decreased bone mass, increased risk of bone fractures, failure with weight gain) make this approach less desirable.

Don’t wait until you start to experience joint pain. Talk with your doctor soon and get on a plan that can work for you to change your diet, lifestyle, and body mass index. Encourage your brother to do the same. In the long-run, you will both benefit in more ways than one.

It is true that scientists have made some remarkable discoveries about fat in the last 10 years. Brown adipose tissue (BAT) (or “brown fat”) and white adipose tissue (WAT) or “white fat” are real phenomenon in the body.

Brown fat is found in larger amounts in new born babies and hibernating mammals. Its main purpose is to generate body heat in animals or newborns because they do not shiver. The brown color comes from a higher number of mitochondria that contain iron.

White fat cells are found in abundance in obese adults. It serves as a storage unit for energy but has also been discovered to be a powerful endocrine gland (producing hormones). These hormones are proinflammatory causing a low-grade inflammation throughout the body (not just the joints). This proinflammatory state of the obese body is also suspected as a contributing cause of hypertension, insulin resistance, and high cholesterol levels.

As a result of these discoveries and this new knowlege, joint osteoarthritis is no longer considered just a “wear-and-tear” type of arthritis. Obesity and the excess weight and load associated with obesity are major factors. But now we know there are inflammatory effects of adipose (fat) tissue that also contribute to joint destruction. Weight loss and exercise aren’t always easy solutions but they are the most successful in addressing all of the local and systemic effects of obesity.

There has been much debate around the issue of Worker Compensation, failure to recover due to the possibility of financial gain, and predictable worse outcomes for workers injured on-the-job compared with those who are not covered by Worker Compensation.

In fact, studies do show that results after surgery for worker compensation patients are worse than for non-worker compensation patients. Worker compensation patients take longer to recover after shoulder/arm surgery compared with non-worker compensation patients treated for the same thing. And worker compensation patients are much slower to return to their jobs at a preinjury level compared with non-worker compensation patients.

It’s also true that more worker compensation patients change jobs because of continued pain after surgery compared with non-worker compensation patients. And fewer worker compensation patients return to employment at all compared with non-worker compensation patients.

What’s behind these differences? Recovery from work-related injuries can be complicated by the fact that workers are financially compensated for bodily injury in the
work place. It is tempting to assume that financial gain is the reason for unfavorable outcomes and worse prognoses for these workers.

But from a review of studies done in this area, several factors have come to light that might help explain the differences in results. First, worker compensation patients tend to be younger and expected to be more physically active on-the-job compared with non-worker compensation patients with the same injuries.

Returning to preinjury levels of activity may differ between these two groups. Workers must get back to their preinjury level of work activities (e.g., pushing, pulling, or lifting heavy objects, operating heavy equipment). Non-worker compensation patients may be having trouble performing less difficult tasks (e.g., brushing teeth, caring for a child, dressing). Of course, your point is well-taken that it doesn’t matter what the level of skill or work that self-employed individuals who are injured on-the-job face — they have to get back to work no matter what if they want a paycheck.

From a historical perspective, Worker Compensation was first started in Prussia back in the late 1800s. Until the United States enacted similar laws, injured workers were on their own when injured, maimed, or even killed on the job. The average worker simply could not afford to bring a lawsuit on his or her behalf — even when the injury was a direct result of their employer’s negligence.

And employers hid behind beliefs that they were not legially liable for injuries resulting from actions, inactions, or outright negligence of other workers. Employees were told “you knew the risks when you signed on” for this job. Some employers even had their employees sign a contract agreeing that the job gave them the right to be killed without compensation. This was referred to as a death contract.

But as the industrialization of America took hold, individual states started passing legislation to protect its workers. The first one (called the American Worker Compensation law) was passed in Wisconsin in 1911. Over time, each state passed its own law governing protection of workers involved in work-related injuries.

Most recently, deaths and injuries in the workplace have started to decline. Better safety measures have helped. The high cost of injuries (medical as well as work place) is a driving force behind the push to reduce work-related accidents. Your point is well taken about the motivation and impetus behind return-to-work for the self-employed versus employees protected by Worker Compensation. But with laws passed in each state to protect workers, it’s not likely the system will be abolished.

Many studies have been done comparing results of injury for treatment of Worker Compensation patients compared with non-compensation employees. Until recently, the number one reason workers were out was always low back pain. Now, the number of claims from leg and arm injuries has increased dramatically. And shoulder injuries (e.g., rotator cuff tears) can keep a worker off the job twice as long as a back injury.

We do know that results after upper extremity (shoulder or arm) surgery for worker compensation patients are worse than for non-worker compensation patients. Worker compensation patients take longer to recover after shoulder/arm surgery compared with non-worker compensation patients treated for the same thing.

Worker compensation patients are sl oftenower to return to their jobs at a preinjury level compared with non-worker compensation patients. And more worker compensation patients change jobs because of continued pain after surgery compared with non-worker compensation patients. In fact, fewer worker compensation patients return to employment at all compared with non-worker compensation patients.

Recovery from work-related injuries can be complicated by the fact that workers are financially compensated for bodily injury in the work place. It is tempting to assume that financial gain is the reason for unfavorable outcomes and worse prognoses for these workers.

But from a review of studies done in this area, several factors have come to light that might help explain the differences in results. First, worker compensation patients tend to be younger and expected to be more physically active on-the-job compared with non-worker compensation patients with the same injuries.

Returning to preinjury levels of activity may differ between these two groups. Workers must get back to their preinjury level of work activities (e.g., pushing, pulling, or lifting heavy objects, operating heavy equipment). Non-worker compensation patients may be having trouble performing less difficult tasks (e.g., brushing teeth, caring for a child, dressing).

The type of surgery performed may vary from study to study. Results from arthroscopic shoulder surgery are not always the same compared with other surgical techniques (e.g., open surgery or mini-open approaches). The use of alcohol and/or tobacco (known to delay wound healing and recovery) are additional factors to be considered. It is possible that ongoing pain, shoulder stiffness, and lower function after surgery may be worse in some
patients as a direct result of these lifestyle factors.

Sometimes pinpointing results after surgery can be difficult. For example, some worker compensation patients do return-to-work but are unable to meet the higher work demands or end up at a lower functional level than before their injury.

And sometimes the type of injury and surgery required affect outcomes (e.g., results after elbow surgery are usually worse than after rotator cuff (shoulder) surgery). Worker compensation patients are also more likely to need a second surgery but whether or not this is to regain a higher level of physical function was not reported.

So, you can see the issues around work-related injuries and Worker Compensation are complex and varied and not easily understood. Hopefully, this quick review will broaden your understanding of these issues. Putting into place and enforcing safety measures in the workplace is the number one way to decrease occupational injuries. As a manager, this is something you can pay particular attention to.

Yes! In fact several studies have been done confirming low vitamin D levels as a possible contributing factor to soft tissue and bone injuries. For example, blood tests taken in preparation for surgery to treat sports injuries show that more than half of the athletes tested were vitamin D insufficient. One-third of that group wasn’t just vitamin D insufficient — they were in the deficient zone. And maybe that’s why they injured themselves in the first place.

Several individual studies of National Football League players also showed lower levels of vitamin D (if not insufficient levels) among players with muscle injuries. And a study of elite Australian gymnasts came up with the same findings.

Without adequate levels of vitamin D in the blood stream, anyone (young, old, althetic or not) can suffer low bone mass, decreased immune function, and altered physical performance. Any of those (and especially all in combination) can pose serious problems for athletes.

Bone fractures and muscle injuries associated with low vitamin D can sideline athletes for an entire season. Frequent colds, flus, and other more serious illnesses from a compromised immune system can lead to days without practice and poor performance. The athlete may not miss a day but still isn’t at the “top of their game” so-to-speak.

Before anything can be done about low vitamin D, it is essential to know what your vitamin D levels are. This can be done with a simple blood test. But that’s where simplicity ends because experts say there is no clearly known optimal level of vitamin D to shoot for. Right now, the various levels are determined by measuring total serum 25-hydroxyvitamin D (25(OH)D3) and defined as:

Deficient: 25(OH)D3 is less than 20 ng/mL
Insufficient: level is 20 to 31 ng/mL
Intoxication: blood levels are higher than 150 ng/mL
Sufficient: at least 30 ng/mL up to 50 ng/mL

Having “sufficient” blood levels of vitamin D means the body can absorb calcium from our diet to keep bones healthy. And sufficient levels prevent the cascade of biologic events that occur in the body when vitamin D drops too low. For athletes, the end-result can be protection from stress fractures, bone fractures, and soft tissue injuries of muscles, tendons, and ligaments.

Not everyone needs to rush out and start taking Vitamin D supplements. Treatment should be applied to those individuals with low (insufficient or deficient) vitamin D. Taking large (supraphysiologic) doses of Vitamin D supplements is NOT recommended as a way to enhance athletic performance. There are an equal number of studies that show higher levels of vitamin D could lead to kidney (and other tissue) damage.

Before doing anything, ask your doctor what you need to do (if anything) at this time. Even in a young and healthy athlete, a blood test to establish your current (baseline) level of vitamin D may not be a bad idea. He or she will know if this is appropriate for you based on your level of risk factors.

Most likely your son’s coach has heard something about the perils of low vitamin D. Without it, we can suffer low bone mass, decreased immune function, and altered physical performance. Any of those (and especially all in combination) can pose serious problems for athletes.

For example, bone fractures and muscle injuries associated with low vitamin D can sideline athletes for an entire season. Frequent colds, flus, and other more serious illnesses from a compromised immune system can lead to days without practice and poor performance. The athlete may not miss a day but still isn’t at the “top of their game” so-to-speak.

The biggest known risk factors for vitamin D deficiency are: 1) limited sun exposure (based on where athletes live), 2) the use of sunscreen, and 3) athletes with dark skin pigmentation. Does your son fit any or all of these descriptions?

To elaborate just a bit, these factors limit the skin’s absorption of ultraviolent B (UVB) rays from the sun needed for vitamin D production in the body. Living, practicing and playing indoors (especially in the northern latitudes) is a direct cause of low UVB radiation. But living in a sunny climate may be thwarted by the increased use of sunscreen products. We use these to keep UVB rays from contributing to skin cancer.

Before anything can be done about low vitamin D, it is essential to know what the vitamin D levels are. This can be done with a simple blood test. But that’s where simplicity ends because experts say there is no clearly known optimal level of vitamin D to shoot for. Right now, the various levels are determined by measuring total serum 25-hydroxyvitamin D (25(OH)D3) and defined as:

Deficient: 25(OH)D3 is less than 20 ng/mL
Insufficient: level is 20 to 31 ng/mL
Intoxication: blood levels are higher than 150 ng/mL
Sufficient: at least 30 ng/mL up to 50 ng/mL

Having “sufficient” blood levels of vitamin D means the body can absorb calcium from our diet to keep bones healthy. And sufficient levels prevent the cascade of biologic events that occur in the body when vitamin D drops too low. For athletes, the end-result is protection from stress fractures, bone fractures, and soft tissue injuries of muscles, tendons, and ligaments.

Experts in this area do recommend a blood test to determine levels of total serum 25(OH)D3 for at-risk athletes before attempting any vitamin D supplementation. Treatment should be applied to those individuals with low (insufficient or deficient) vitamin D. Taking large (supraphysiologic) doses of Vitamin D supplements is NOT recommended as a way to enhance athletic performance. High levels of vitamin D can lead to kidney (and other tissue) damage.

Talk with your son’s (or your) primary care physician about this recommendation. Your physician can advise you as to the medical necessity of baseline Vitamin D testing. Any deficiencies requiring supplementation must be treated under his or her supervision and guidance anyway.

You wouldn’t think athletes with their strong bones and muscles would need any Vitamin D supplementation. But according to a recent report, there are sports health benefits to taking Vitamin D supplements. Some of those benefits actually come in the form of prevention. That is — preventing the musculoskeletal events that can occur when someone is Vitamin D deficient (e.g., bone fractures, musculoskeletal pain, frequent illness).

Vitamin D is made in the body when the skin is exposed to ultraviolet B rays from the sun. But fears about skin cancer have reduced sun exposure through the use of sunscreen products. People living in certain (Northern) regions of the globe don’t receive enough of the essential sun rays even without sunscreen.

Because very little Vitamin D comes from natural food sources, some products like cereals and milk are Vitamin D fortified. But even with these dietary sources, most people (children and adults) are considered Vitamin D deficient and in need of supplementation. Athletes and sports participants are no exception. In the report we referred to, results of studies suggest the following for athletes: