Sunday, March 27, 2011

Stress Fracture Update Part Two

Here are my images of the pelvic stress fracture. I have to be honest, even though told that these two images best show my fracture in the left pelvis, I can't really see what I am looking for! But I said I would share images when I got them. Maybe someone with a bit more experience can see them:

If you can't see the image, click here.

If you can't see the image, click here.

As I write today (March 27), the leg has greatly improved. I am almost walking normally and can even stand on one leg and do some very shallow one-legged squats. The pain has dropped substantially. I'm pretty upbeat about the improvement. I will be able to walk comfortably while on vacation in London. I would not consider the 10K unless I am completely pain free by 4/2. I put that chance at about 2% right now.

I am still going to get a bone density scan just to rule out osteoarthritis (OA). I'm 95% certain this was a overuse injury but as I turn 50 years young in April, I want to get a baseline bone density scan and rule out that possibility.

So, as a licensed drug dealer (pharmacist) I wanted to provide you with some information on OA, that you can tuck away for future reference and perhaps take some preventative measures. The following is summarized from notes taken from a continuing education course I took in 2010.

OA is becoming an increasingly common problem as the population ages. OA, the most common form of arthritis, is a rheumatologic disorder that is characterized by gradual loss of cartilage from the joints and, in some people, joint inflammation. OA was previously thought to be a normal consequence of aging, but we now realize that factors such as joint integrity, mechanical forces, local inflammation, and cellular and biochemical processes may all play a part in the diagnosis. Some symptoms of OA include pain, stiffness, and loss of motion.


In the United States, arthritis is considered one of the most common, expensive, and disabling diseases. OA is the most common arthritic condition, affecting nearly 27 million Americans. Its incidence rises substantially with age, resulting in 80% of persons having radiographic evidence of OA disorders by the age of 75 years. The Centers for Disease Control and Prevention estimate that the number of persons aged 65 years or older affected by arthritis will nearly double by the year 2030 because of the aging of the population.

The prevalence of OA is higher in women who usually present with more generalized proximal and interphalangeal joint inflammation. Approximately 17 million people are limited in their activities due to OA, resulting in 1.5 billion days of restricted activity per year. This has led patients with OA to have decreased social functioning and increased psychological distress as well as increased health care use. The annual cost associated with OA in the United States is more than $60 billion, and accounts for about 315 million provider visits and 8 million hospital admissions yearly.


OA is often referred to as degenerative joint disease because the weight-bearing joints simply wear out as a sign of advancing age. In addition, the degeneration of cartilage is a prominent pathologic aspect. However, we now realize that there is more to this disease than just “wearing and tearing” of the joints.

The pathophysiology of OA involves mechanical, biochemical, and cellular processes. The most common theory is that all of these processes change the composition and properties of articular cartilage. Synovial fluid along with articular cartilage permits almost frictionless movement of joint bones at their points of contact. Healthy cartilage allows internal remodeling as chondrocytes replace macromolecules lost in degradation. This process is disrupted in OA and is characterized by a progressive deterioration of cartilage, resulting in the formation of osteophytes and the loss of cartilage. This process may also lead to inflammation.

At the onset of OA, no symptoms of pain are noted in the joints because there are no nerve fibers in articular cartilage. Some subsequent potential sources of pain in OA are denuded bone, microfractures of bone, stress to ligaments as a result of loss of cartilage, low-grade synovitis, and spasming of surrounding muscles.


The precise cause of OA is unknown. Hypothesized causes include heredity, trauma, and obesity. OA is not a systemic disease and joint affectation often occurs in the knees, hands, and hips, although other joints can also be affected. OA tends to develop slowly and progresses over several years. The pain is often described as aching and is felt in the areas surrounding the affected joint. Bony enlargements and irregularities are common, especially in the hands at the distal interphalangeal joints (Heberden nodes) and less commonly in the proximal interphalangeal joints (Bouchard nodes). Alhough these bony enlargements are asymptomatic, many patients view them as a part of a disabling arthritic disorder or even an outward sign of aging.

The clinical presentation of OA depends on the number of joints affected and the duration and severity of the disease. Patients with OA of the hip may complain of gait problems. After periods of inactivity, hip stiffness is common and is usually a presenting factor. Patients with OA that affects the hands often have problems with manual dexterity. This is evident when the first carpometacarpal joint is involved. Instability or buckling of the knee is often noted in patients with OA of the knee. Some patients with erosive OA may have signs of inflammation in the interphalangeal joints of the hands.


Risk factors for OA include age, female gender, race, genetic susceptibility, obesity, joint overuse and injury, prior inflammatory joint disease, metabolic and endocrine disorders, and congenital and developmental abnormalities. Age is the greatest risk factor for OA, with a prevalence of 30% for women between 45 and 64 years of age and increasing to 68% in those greater than age 65. The female-to-male ratio associated with OA is 2:1 after age 65, so the prevalence is similar but somewhat lower in men. Occupations or hobbies that subject particular joints to repetitive trauma can predispose those joints to OA later in life.


The hallmark symptom of OA is joint pain. Primarily, patients will have pain only with the use of the affected joint, and this is what will bring them to a health care provider for treatment. This pain worsens with weight-bearing activity, but typically improves with rest. Patients with OA often experience gelling and morning stiffness of the involved joint after periods of inactivity. Patients may complain of morning joint stiffness that resolves within 30 minutes, which is a key factor in distinguishing OA from rheumatoid arthritis.

On physical examination, the signs of OA may include limited range of motion, altered gait, crepitus (a cracking sound upon moving the joint giving the sensation of bone rubbing on bone), bone hypertrophy, and tenderness around the joint line. Crepitus is common in both OA and rheumatoid arthritis due to the irregularity of opposing cartilage surfaces. The American College of Rheumatology (ACR) has specific diagnostic criteria for OA at various sites, including the hip, knee, and hand. Notably, structural changes are not necessarily associated with clinical symptoms of pain and inflammation. Radiographic features and laboratory findings are not definitive for the diagnosis of OA. Radiographic features of the disease show loss of joint space and the presence of new bone formation (osteophytes). However, absence of these radiographic changes does not exclude a diagnosis of OA. Analysis of synovial fluid tends to reveal a white blood cell count of less than 2000/mm. Another helpful diagnostic laboratory test is the evaluation of the erythrocyte sedimentation rate. This test is part of the ACR’s Classification Criteria for Osteoarthritis. Many patients with radiographic changes are asymptomatic, and those with symptoms associated with OA may not have evidence of radiographic changes of the affected joint. Thus, an accurate diagnosis should consider the patient’s history, physical exam, and radiographic findings.

OA has been categorized as primary (idiopathic) or secondary, but the pathophysiology is indistinguishable. Primary OA is more common and its associated pain appears with no identifiable initiating event. Secondary OA results from a known cause such as a metabolic disorder, congenital joint deformity, and a joint or ligament injury. Distinguishing between the two forms is generally of little importance for the purposes of pharmacotherapy.

The goals of treatment for patients with OA are to reduce and control pain, decrease disability, educate patients about their role in disease management, and improve quality of life. Patients with OA rarely respond to drug therapy alone. First-line interventions are usually nonpharmacological; pharmacists should be ready to counsel patients on the importance of these options. Treatment should be individualized to patients’ level of function and activity, to their level of expectations, to their occupational needs, to the joints involved, to the severity of the disease, and to any coexisting medical problems.


Nonpharmacological treatment approaches appear to be the foundation for the management of OA. They encompass a three-prong approach, featuring patient education, lifestyle modification, and physical therapy.

Educational materials can be obtained from the Arthritis Foundation ( to help patients gain a better understanding of their disease when initially diagnosed. Patient education on the cause, effects, and symptoms of OA and a realistic understanding of what can be achieved with optimal therapy are essential. OA has both physical and psychological effects. The symptoms and limitations associated with OA may produce in patients with OA feelings of frustration, dependency, and even depression. The more patients learn about the disease, the more they can participate in their own care. Social support can be achieved by building an informal support team or by participating in formal OA groups.

Lifestyle modification revolves around exercising, weight reduction, and proper diet. The goals of an exercise program are to maintain joint range of motion and flexibility, enhance muscle strength, and increase aerobic cardiovascular conditioning. Patients with OA are often concerned that using an affected joint will “wear out” the already damaged area. However, evidence shows that patients with osteoarthritic joints did not increase the development of OA after regular low-impact exercise. Exercises to regain or maintain flexibility and range of motion can be achieved by low-intensity, controlled movements that do not cause increased pain. Patients should also be encouraged to participate in aerobic exercises such as swimming or walking to increase overall health. The benefits of exercise and activity may reduce the risk for several chronic diseases, may help to combat the depression that accompanies the chronic pain associated with OA, and may enhance quality of life and prevent disability associated with inactivity.

Although obesity appears to be a greater risk factor for women, there is an association between obesity and OA of the knee in both genders. The risk of OA increases by 10% for each kilogram of body weight over the ideal body weight. Weight loss has been shown to benefit patients with OA. Symptoms associated with arthritis in the hips, knees, and feet are exacerbated by obesity. In addition to reducing the risk of progression of OA, weight loss can produce improvement in joint pain and function. Primary prevention strategies should include measures to achieve weight loss or avoid weight gain in overweight patients.

Patients with OA should be mindful of their diet. Although there is little clinical evidence demonstrating a correlation between diet and the development of OA, it may be helpful to provide patients with certain dietary guidelines such as eating foods that contain omega-3 fatty acids, limiting use of polyunsaturated vegetable oils and partially hydrogenated oils, and avoiding refined and processed foods.

Physical and occupational therapy may be of benefit to patients with specific physical disabilities brought on by OA. Physical therapists can recommend use of modalities, advise patients of exercise programs, and recommend assistive devices to improve ambulation. Occupational therapists can teach patients proper joint protection and energy conservation, how to use assistive devices, and how to improve joint function. There are a variety of appliances that can help to relieve symptoms associated with OA by supporting the muscles that support the affected joint. Examples of assistive devices include crutches, various walking aids, shoe inserts, splints, braces, and special soles. Using special appliances may help patients to feel more comfortable, move around independently, and have better function. Other home medical supplies that are available in pharmacies are elevated seats for toilets, canes, walkers, grab bars for wall placement, and sitting stools for bathtubs and showers. Indeed, providing individualized exercise programs and teaching patients how to manage activities of daily living may enable patients to feel more independent and less affected by their disease.

Additional nonpharmacological therapies that may be of value in patients with OA include acupuncture, ultrasound, phonophoresis (the use of ultrasound to introduce medications transdermally to enhance the delivery of topical agents in OA), heat and cold treatment modalities, transcutaneous electrical nerve stimulation (TENS), and relaxation techniques.


If nonpharmacological therapies fail to bring relief, a number of pharmacological approaches may be pursued. Patients who do not meet the exclusions from self-care can self-treat their pain. Used as directed, nonprescription products can be safe and effective for mild-to-moderate osteoarthritic pain. When self-care options have failed, appropriate prescription medications should be recommended. At present, there are no specific pharmacological therapies that can prevent the progression of joint damage due to OA. Because no medication has been shown to cure this disease, patients should clearly understand the risks and benefits associated with their treatment options.

Pain relief is the primary indication for the use of pharmacological agents in patients with OA who do not respond to nonpharmacological interventions. When quality of life becomes adversely affected by the disease, it would be a good time to initiate pharmacotherapy to minimize disability and control pain.


As an analgesic, acetaminophen works by simultaneously blocking peripheral pain impulse generation and inhibiting prostaglandin synthesis in the central nervous system. Acetaminophen has a long history of safe and effective use in the treatment of OA. Compared with placebo, acetaminophen 4000 mg/day was significantly more effective in showing decreased pain at rest, decreased pain on motion, and decreased tenderness in patients with OA in a randomized, double-blinded crossover study. Another study demonstrated acetaminophen 4000 mg/day to be comparable to ibuprofen 1200 mg/day and 2400 mg/day in relieving knee pain in patients with OA.20 Finally, acetaminophen at 4000 mg/day showed comparable efficacy to celecoxib 200 mg/day in relieving pain due to OA of the knee. The ACR has recommended that acetaminophen be used as a first-line agent for early treatment of OA that has been unresolved by other nonpharmacological approaches.

Acetaminophen is generally well tolerated, with mild side effects at therapeutic doses. Hepatotoxicity, a well-known adverse effect associated with acetaminophen, can occur if patients intentionally or unintentionally take more than the maximum daily dose of 4000 mg. Toxicity is increased in patients who have preexisting liver disease and/or drink alcohol. Prompt administration of N-acetylcysteine is used to prevent fatalities. Elevations in liver function test results (a sign of chronic acetaminophen toxicity) normally resolve when the drug is stopped. It is important for pharmacists to educate patients with OA taking maximum daily doses of acetaminophen to be aware of the potential effects of concomitant use of other prescription and OTC products that may contain acetaminophen.

Nonsteroidal Anti-Inflammatory Drugs

Nonsteroidal anti-inflammatory drugs (NSAIDs) act primarily on the cyclooxygenase (COX) enzyme system by blocking the formation of prostaglandins in normal and inflamed tissue. The COX enzyme system consists of two isoforms: COX-1 and COX-2. COX catalyzes the conversion of arachidonic acid to prostaglandins and other eicosanoids in the inflammatory pathway.

NSAID therapy is recommended for patients who are not responding to acetaminophen therapy and is an appropriate choice for treating moderate or severe arthritic pain and any associated swelling, stiffness, and inflammation. Patients with OA taking NSAIDs reported a 10% to 30% decrease in pain. A meta-analysis of randomized controlled trials involving NSAIDs for the treatment of OA of the hip found that there was a similar overall efficacy among the nonselective NSAIDs. NSAIDs carry a risk of gastrointestinal (GI) toxicity, even at low doses. GI toxicity is characterized by erosions, ulceration, perforation, and hemorrhage. The prevalence of gastric and duodenal ulcers associated with the use of NSAIDs ranges from 9% to 22%. Several risk factors appear to increase the risk of NSAID-induced toxicity including patients over age 65; previous ulcer or upper GI bleed; and concomitant oral corticosteroid, anticoagulant, or multiple NSAID therapy. Ibuprofen is a common NSAID used for the treatment of OA. The maximum dose of prescription ibuprofen is 3200 mg/day, whereas the maximum dose of OTC ibuprofen is 1200 mg/day.

Reduced prostaglandins in the gastric mucosa due to COX inhibition attributes to the GI side effects associated with NSAIDs. Proton pump inhibitors (PPIs) may be beneficial in helping to control the GI symptoms associated with chronic NSAID use. Misoprostol, a synthetic prostaglandin E1, may help to prevent gastric ulcers in patients on long-term NSAID therapy at a dose of 200 mcg four times daily. Usual doses of histamine-2 receptor antagonists (H2-blockers), such as cimetidine and ranitidine, may help with NSAID-associated GI side effects. NSAIDs can also impair platelet aggregation by inhibiting platelet COX, which then blocks thromboxane A2 and results in prolonged bleeding time. This is a potential concern for those at risk for bleeding such as patients on anticoagulation therapy, those undergoing surgery, or those with preexisting GI ulcers.

In addition, renal toxicity may develop in patients exposed to NSAIDs at a rate of 1% to 5%. This is because the kidneys synthesize prostaglandins to help maintain blood flow in situations in which perfusion is reduced. This needs to be considered in the elderly because of their age-related renal decline, illnesses, and concurrent medication therapy. NSAID selection should be based on frequency of administration, cost, efficacy and safety profiles, and patient response and acceptance. NSAIDs are the most frequently prescribed analgesics for the management of mild-to-moderate arthritic and musculoskeletal pain. An estimated 30 billion nonprescription doses of NSAIDs are consumed each year in the United States by 13 million individuals with osteoarthritis or rheumatoid arthritis.

Celecoxib, a specific COX-2 inhibitor, was designed to decrease the incidence of NSAID-associated adverse events. Discovering two distinct COX isoforms led to the hypothesis that specific inhibition of COX-2 would provide the anti-inflammatory and analgesic effects of NSAIDs, while preserving COX-1 and its important physiologic functions (gastric protection and normal platelet function). COX-2 inhibitors may be appropriate to initiate in therapy for patients with moderate-to-severe pain in whom nonselective COX inhibitors have proven ineffective or who have a history of GI disease. COX-2 inhibitors have at least a 200- to 300-fold selectivity for inhibition of COX-2 over COX-1 inhibitors.

Celecoxib is recommended in doses of 200 mg per day for the treatment of osteoarthritic pain. The most common adverse effects associated with celecoxib are abdominal pain, diarrhea, and dyspepsia. COX-2 inhibitors are associated with lower gastroduodenal toxicity, but increased risk of cardiovascular events has lead to the withdrawal of two agents, rofecoxib and valdecoxib, from the market.

Celecoxib may be the NSAID of choice in patients who have a history of GI bleeds or ulcers, are at least 65 years of age, or are currently on ulcerogenic therapy. Since celecoxib contains a sulfonamide group, it should be used cautiously in patients with sulfa allergies. Pharmacists should also warn patients not to combine celecoxib with OTC NSAIDs.

Black-box warnings about the risk of myocardial infarction, ischemic stroke, and GI bleeding have been added to the labels for celecoxib and some NSAIDs. Acetaminophen, celecoxib, and NSAIDs have all been observed to show increases in the incidence of new hypertension.

Nonacetylated Salicylates

Nonacetylated salicylates work by inhibiting prostaglandin synthesis and have similar efficacy to NSAIDs. Choline magnesium trisalicylate and salsalate are two common drugs in this class. Nonacetylated salicylates do not demonstrate the antiplatelet effects and the nephrotoxicity that are associated with NSAIDs, but they are not without risk. Ototoxicity and central nervous system adverse effects may develop with long-term use and salsalate has been shown to cause agranulocytosis. Tinnitus has been seen in adults using these agents for treating inflammatory diseases; it may subside gradually with a reduction in dose. Other symptoms of overdose include headache, dizziness, and confusion. If these occur, treatment should be stopped immediately.

Other Analgesics

Codeine, oxycodone, propoxyphene, and other opioid analgesics work by binding to opiate receptors in the central nervous system and causing inhibition of the ascending pain pathways. These agents may be useful for short-term flairs of osteoarthritic pain or when other medications are not able to be used or are not tolerated. Long-term use of these agents, particularly in the elderly, should be avoided due to associated side effects that include constipation, confusion, and sedation. Chronic narcotic use is controversial due to the potential for inducing physical and psychological dependence. A decision to use narcotics in treating OA should be based on the severity of pain, a clear understanding of the maximum daily doses, and a lack of effect from other drugs.

Tramadol is a centrally acting analgesic that exerts dual action by binding to the opioid receptor site in the central nervous system and also weakly inhibiting the reuptake of biogenic amines. It is contraindicated in patients taking monoamine oxidase inhibitors. Compared with narcotics, tramadol does not cause significant constipation and respiratory depression. Tramadol is usually given as a rescue medication for symptomatic relief and may be considered as a treatment option if NSAID therapy fails. As a centrally acting oral analgesic, tramadol allows for a lower dose of an NSAID in combination therapy. The recommended dose of tramadol is 50 mg given every four to six hours, with a total daily dose not to exceed 400 mg. Dizziness, nausea, vertigo, constipation, and lethargy are the common adverse effects asociated with tramadol that may particularly exclude its use in elderly patients. It has also been added to acetaminophen to augment analgesia in patients with OA. Tramadol is a reasonable therapeutic option in patients with OA who cannot tolerate NSAIDs or who have had poor responses with other treatment regimens.

Topical Agents

Topical capsaicin, a pepper-plant derivative, has been shown to more effectively relieve the pain associated with OA compared with placebo. Capsaicin works by depleting local sensory nerve endings of substance P, a neuropeptide mediator of pain. Capsaicin cream 0.025% applied four times a day was effective in the management of pain caused by OA of the knee, ankle, wrist, and shoulder in a double-blind, randomized, controlled trial. One common side effect associated with capsaicin use is a localized burning sensation; patients should be advised to wash their hands after application to avoid spreading capsaicin to the eyes or other mucous membranes. Capsaicin is available OTC in concentrations of 0.025%, 0.075%, and 0.25%.

Methyl salicylate, also known as oil of wintergreen, is a natural product of plants. It is used as a rubefacient (shows redness of the skin by dilation of the capillaries and increases blood circulation) in deep healing liniments. Application to the affected area should not exceed three to four times daily. As with the use of capsaicin, proper hand washing techniques after application should be stressed in patients using methyl salicylate.

The FDA has approved a 1% diclofenac gel for the treatment of OA. After topical application, system exposure of diclofenac is limited (only 6% of the same oral dose). There have been no reports of any associated GI effects or nephrotoxicity. There is currently no safety information for use of the gel in patients with ulcers or who are on anticoagulation therapy. For OA of the knees, feet, and ankles, four grams of the gel applied to the affected joint up to four times daily is recommended. For the upper extremities, including wrists, elbows, and hands, two grams of the gel applied four times daily is recommended. The manufacturer recommends that no more than 32 grams daily should be applied over the affected joints. To help administer correct amounts, each prescription comes with a dosing card to ensure proper amount and application of the product. The most frequent adverse effects associated with this agent have been application site reactions including dermatitis. The product labeling also recommends not exposing the treated area to sunlight. Patients should avoid bathing for at least one hour after applying the product.

Intra-Articular Glucocorticoids and Hyaluronic Acid

Patients who suffer from painful flares associated with OA of the knee may benefit from intra-articular injections of corticosteroids such as methylprednisolone or triamcinolone. Short-term pain relief can be obtained with aspiration of the joint fluid followed by intra-articular injection of the corticosteroid when the joint is painful and swollen. Joints should not be injected more than three or four times a year to prevent possible cartilage damage. Patients may need to be considered for surgical intervention if they are requiring more than three to four shots per year to control symptoms.

Hyaluronic acid, a glycosaminoglycan polysaccharide compound, provides viscoelastic and lubricating properties to joints. It is a major nonstructural component of the synovial and cartilage matrix makeup. The molecular weight and concentration of hyaluronic acid is thought to be decreased in patients with OA. The FDA has approved hyaluronic acid intra-articular injections for the treatment of pain caused by OA of the knee. A treatment cycle consists of three to five injections given at weekly intervals depending on the specific product used. The injections are well tolerated, although local skin reactions and pain with injection have been shown.

Intra-articular injections need to be carried out using aseptic techniques and the aspirated joint fluid needs to be examined to rule out infections. It is recommended that patients should minimize activity and stress on the joint for several days following an intra-articular injection.


OA often progresses to a degree where no cartilage remains and bone is rubbing on bone. For those patients whose symptoms are not controlled with pharmacological and nonpharmacological therapy and who experience moderate-to-severe pain and functional impairment, orthopedic surgery may be a treatment option. Depending on the joint involved, some replacement procedures have become commonplace. Patients need to be made aware of the risks and benefits associated with orthopedic surgery before making a decision to have it.


Patients often seek alternative therapies for treating OA after experiencing side effects or incomplete relief of symptoms from conventional medications. Because the herbal and supplement industry is not regulated by the FDA, supplement composition can vary. Even though glucosamine, chondroitin, or the combination of the two have been used for the treatment of OA since the 1960s, recent data have suggested that they may not be more effective than placebo. However, an analysis has suggested that a subset of patients experiencing moderate-to-severe knee pain may benefit from the combination.

Glucosamine sulfate, a popular treatment for treating the symptoms associated with OA, is derived from oyster and crab shells. The American Pain Society (APS) recommends that adults with OA take glucosamine sulfate 500 mg three times daily based on evidence that it may have a role in decreasing joint space narrowing. However, based on data that indicate glucosamine sulfate provides no benefit over placebo, patients should be advised to limit taking glucosamine sulfate after three months if no improvement in symptoms is seen.

Chondroitin sulfate has demonstrated efficacy by acting as a building block of proteoglycan molecules to improve the symptoms associated with OA. Chondroitin is derived mostly from shark and cow cartilage. Chondroitin is usually dosed at 1200 mg/day in three divided doses. Data have shown that at least one month of therapy is needed to achieve results.
S-adenosylmethionine (SAMe) is a naturally occurring compound found in all living cells that is commercially produced in yeast-cell cultures. Studies have found SAMe to be more effective than placebo in improving pain and stiffness related to OA. Dosages range from 400 to 1200 mg/day.

Other modalities that are showing promise for the treatment of OA include shea nut triterpenes, methylsulfonylmethane (MSM), and peppermint. Since these products are not FDA approved, patients need to be reminded of their limitations.


In addition to the treatments previously listed, other experimental therapies seek to modify and/or reverse the course of OA. A few of these disease-modifying OA drugs (DMOADs), whose mechanism of action is directed at slowing the progression of radiographic changes of OA, have shown promise in animal models. No treatment has yet been clearly demonstrated to have structure modifying DMOAD activity in humans.


At present, there is no cure for OA. However, pharmacological therapies that offer the promise of reversing OA are under investigation. As research continues, we will gain a greater understanding about concepts related to OA such as biologic markers and genetic factors.

When used properly, a combination approach to treatment can provide the best therapeutic outcomes. Millions of dollars are spent yearly on nonmedical therapies for the treatment of OA, and patients need to be educated about the risks and benefits of such treatments. When patients have an appropriate understanding of their disease, they are more likely to follow a treatment plan that will enable them to maintain joint function and have an improved quality of life.

Tuesday, March 22, 2011

Stress Fracture News

Elvis Aaron Presley had the nickname "Elvis the Pelvis" because of the way he would back off the microphone and gyrate his lower body.

I wonder had Elvis lived to see his golden years, would he have experienced any issues with his pelvis? As he died suddenly in 1977 at the age of 42, we'll never know. I rather think Elvis....young Elvis, not fat Elvis....would have been a pretty good endurance/multi-sport athlete. Again, we'll never know but I'm pretty confident he would have had a really cool speed suit.

Well, I have a stress fracture now. A nasty one. On a scale of 1-5, with 5 being the worst, I was told this ranks as a 4 or 5. Let me remind everyone, as you read the report below, that I ran a 19:36 5K with this injury. I say that again to state my Neanderthal-like pain tolerance and my Neanderthal-like stupidity in even running it. Click on image for larger view of the reports below:

I hope to be able to display some actual MRI images later this week as soon as they release those to me.

So why do I have a stress fracture? And just out of the blue with no other warning signs? I can think of three possible reasons. The reason for my stress fracture may be a combination of all three. Let's break these down:

  1. Over Training: The later half of the 2010 season I was really on fire and competing at the best level yet in my comeback to the sport which started in 2007 after being diagnosed with low testosterone. I took a few weeks off in November and then started up base building training in December incorporated with some speed work. When February hit, my running mileage increased from the 25-30 mile/week range to 50-55 mile/week range. Yes, this is way above the "Don't Increase by More than 10% per week" rule. However, I was experiencing no issues with fatigue or muscle soreness. The pain first surfaced the Monday after a 10.5mi Saturday run and a 8mi Sun run/30mi bike. Could the heavier run mileage have done me in?
    1. Assessment: High probability. But it is damn disappointing if this is indeed the case. I'm a guy who ran 100+ mile weeks through college at the high end and 70+ miles routinely. Being in the 50-mile range should not have proved to be a detriment for me now. Especially since I was thinking about concentrating solely on running during the 2012 season and let triathlons take a back burner for one year. Now, I wonder if I just need to keep the multi-sport lifestyle and keep my running to a minimum.
  2. Endurance Athletes & Bone Density: There was a recent article on this topic in which researchers have studied endurance athletes and whether or not they have a higher rate of osteoporosis (thinning of bone tissue) than the average sedentary person. Studies have shown that perhaps cyclists develop more instances of low bone density than sedentary people and suggest that the lack of weight bearing activity is the cause.
    1. Assessment: Probable, but not sure this is in direct proportion to my issue. I had a bone density scan in 2007 and it was perfectly normal. Yes, I should probably get another as a lot can change in ones body in four years. However, the reason I feel this my be a indirect, rather than direct cause of my pelvis stress fracture is this. When reading the research behind the aforementioned article it states: Activities that produce high strain magnitudes and high strain rates distributed unevenly across the bone provide the greatest osteogenic stimulus. Furthermore, the degree of mechanical strain applied to bone in weight-bearing activities increases proportionally with increased ground reaction forces. Evidence from cross-sectional studies of athletes from a variety of sports, including gymnastics, volleyball, karate and running, supports the notion that bone undergoes a positive adaptive response to high impact activities. Intervention studies, most of which are reported for women, have shown increases in bone mass induced by high strain activities such as jumping and running in children as well as older adults. In stark contrast, weightless environments experienced by astronauts or individuals participating in bed-rest studies cause rapid and marked bone loss. Similarly, non-weight-bearing activities such as swimming and cycling afford few, if any, benefits to bone health in young adults. So, two of the three activities that we train for in triathlons are non-weight bearing and afford no benefit to bone health. How much of this is offset by running? I would like to see a study of bone health for triathletes.
  3. Low Testosterone: Osteoporosis is a significant problem in older men, 30% of all hip fractures occur in men and the mortality rate following hip fracture exceeds that of women. Testosterone is thought to be important in the development of peak bone mass but its role in age-related bone loss is not established. What is known is that osteoporosis is a significant complication of low testosterone. As mentioned before (and long time readers know), I was diagnosed with low testosterone in 2007. Normal total serum testosterone levels for a person of my age are 600 - 900 ng/dL. Mine in 2007? 70 ng/dL.
    1. Assessment: Probable and the most worrisome. A bone density test should be able to confirm or alleviate my worries with this possibility. Am I destined for a life of stress fractures? I think I should be able to stave off any such worry with the right amount of exercise, testosterone & calcium replacement therapies. But this possibility certainly will never be eliminated. To be honest, my physical therapist stated he is 95% certain this fracture was not related to bone density as he saw no indications of osteoporosis. So, I may be worrying over this possibility a little too much. We'll see if my primary physician is agreeable to scheduling a bone density scan and we'll go from there.
So, what are the steps anyone can take to help prevent bone loss? Let us start with dairy products. There exists a direct relationship between dietary calcium and bone health. The best source of bioavailable (highly absorbed by the body) calcium is from dairy products such as milk, yogurt and cheese. In fact, 1 cup of fat free milk has 86 calories and a whopping 302 milligrams of calcium! Three cups of milk per day supplies almost all of the dietary calcium most of us need. The recommended intakes of calcium are:

It is possible to acquire calcium from other food sources but remember that milk, specifically, also contains vitamin D, vitamin A, protein, potassium, riboflavin, niacin, vitamin B12 and phosphorus. Each of these 9 essential nutrients play a different role in your body to help regulate body processes and maintain good health.

For those of you not too keen on milk, here are some other food sources that contain calcium:

This means the 10K in London I have been looking so forward to, is to be missed. Additionally, the following events are in jeopardy of being missed this season:

Apr 30 - Iron Mountain Du; Arkadelphia, Arkansas (USAT) 2mi run, 11mi bike, 2mi run

May 1 - Iron Mountain Tri; Arkadelphia, Arkansas (USAT) - 880 yard swim, 16.2mi bike, 3mi run

May 14 - Lakes to Pines Triathlon; Park Rapids, MN 500 yard swim, 14.7mi bike, 5K run

May 28 (signed up) - Apple Duathlon; Sartell, MN (USAT) - 5k run, 33k bike, 5k run

Jun 5 (signed up) - Pigman Sprint Triathlon; Cedar Rapids, IA (USAT) - Swim .5K, Bike 25K, Run 5K

If my recovery is to be 6-8 weeks, then I would be able to start training again sometime in mid-May. So realistically my possible first event back would be:

Jul 2 (signed up) - Minneman Triathlon; Oak Grove, MN (USAT) - 0.3 Mile Swim, 13mi bike, 3 mi run

There will certainly be up days and down days as I struggle through this setback. I know I will be blogging about progress, and such as that is all I can do. And frankly, I could use any helpful comments from people who have suffered from stress fractures as well as positive input to keep me sane. I received a nice Tweet from Mr. William Jenks that lays down my approach to this injury: Bummer about stress fracture. Recover like you train.

Well said.

Additional Reading:

Evaluation and Management of Stress Fractures of the Pelvis and Sacrum (Ortho Super Site)

Osteoporosis -Maybe You Have It But Don't Know It (John Post, MD)

Monday, March 14, 2011

Race Result: Chase a Leprechaun 5K; Becker, MN

Event: Chase a Leprechaun 5K; Becker, MN
Goal: Survive. With MRI coming Wednesday (3/16) to check out possible stress fracture in left femur
Actual: 19:36 (6:16 per mile pace) official. Official results.
Overall: Second (est, 90+ total)
AG Overall: First (41 and over Male AG)
Weather: 16F, winds 30-35 MPH, windchill at -4

The year is 1979. It is late March in Jamestown, North Dakota and one week before the North Dakota State Indoor track meet at the North Dakota State Fieldhouse. The Jamestown Blue Jays have just wrapped up a Monday practice. Everyone is feeling good, as well they should under the tutelage of head coach Russ Schmeichel.

I've showered and about to give a ride home to fellow track buddies Brad Braunberger and Joe Bennett. Twelve years later, Joe would be my best man at my wedding to the Well Kept Wife. Brad would go on to become the  3000-Meter Steeplechase National Champion (Division III) in 1982. We are a tight bunch. The team is loaded with sprinters, middle distance and long distance runners. As I approach the car, I hit a piece of ice. My right kneecap slams into my car door. Not a nice sound.

I'm unable to run the rest of the week. My knee is swollen. I can't put pressure on it. There is some talk about me sitting the meet out. I talk Coach Schmeichel into letting me make the trip and allow me to warm up and see how I feel. Friday comes, and we're off to Fargo.

I'm warming up and the pain is there. Especially on the tight turns of the 200-meter indoor track. But I want to run. I get cleared by two assistant coaches who speak to Coach Schmeichel.

My first event is the prelims of the 400-meter dash. Two laps. Its going to be hell. Can't really feel my knee but something deep inside me is just putting off the pain. I'm not ranked anywhere near the top 12 in the state in this event. Coach Schmeichel has been working with me to hang back instead of charging from the gun. He reminds me of this again just prior to my heat.

Gun goes off. There is a little pain, but the adrenaline is kicking in. I'm in dead last as we come down the stretch for the bell lap. But then everything changes. This is were I was told to let loose. Hold back, and then let loose. I win the heat going away. It's not even close. I'm going to the state finals of the 400 on a bum knee with 7 others.

Friday night is spent with ice on the knee. Basically, we dump tons of ice in the bathtub as some other people are a bit stiff as well. My knee is stiff and throbbing. And the 400-meter finals are up first Saturday morning.

I'm able to loosen up enough to be able to move around the corners with just a noticeable limp. Again, I'm told to hang back. Gun goes off. I'm dead last again as we move into the straight before the bell lap. I'm wanting to turn the jets loose, but I'm boxed in by 3 people.

I see a very tiny sliver of daylight and my right elbow buries itself into the chest of a runner next to me. I'm free and roaring out of turn 2 and down the back straight. As I head to home, I'm in 3rd but get nipped at the wire by team mate Miles Pederson and another runner. An indoor PR at :53.40. Fifth place in state is not too bad for a unranked runner with a bad knee I tell myself.

I have a few hours break and then we are up for the mile relay. The knee is really, really stiff now. But the adrenaline is still pumping and I'm full of confidence. Miles leads off and comes into the exchange with me in 3rd. I'm not even in contact with the front two runners. I don't hold back this time.

Coming out of turn 2 on the first lap there is a row of team mates to my left screaming at me. The bleachers are on the right full of people on their feet and screaming. I don't hear them. I see them, but all I hear is my breathing and my heart.

Coming into the bell lap, I do something I'm still a little bit ashamed of. As I pass the lead two runners I turn slightly, wave and mouth "bye-bye"......and I'm gone. My team mates have seen this and are now going ape shit. I came into my exchange with Brad Braunberger and I've given him a 15-yard lead. He adds to it. Bill DaBill anchors and he brings home the win. Mile relay state champions. Top of the podium.

I had shoved aside the pain. I had won the mind vs. body war that would come back to me so many more times. But having won this first battle meant I could do it again.

I share this story as it was mind vs. body again this past Saturday. Just a small town 5K fun run. I had signed up for this as a precursor to the 10K I have in London on April 2. But little more than 15 days ago, I developed pain in my left leg right below the groin. Pain which radiates thru the back of the ham and across to the hip. I had two sessions at the locally renowned Sport and Spine Institute where I received conventional treatment to see if it could be muscle related. Dr. Justin Thielke looked at me during the first session and basically shook his head and uttered, "Brian, I don't like how this is looking."

It looks like I have a stress fracture in my femur. At the best of times, I simply have trouble trying to snap the leg forward. At the worst, I can barely put weight on it. But after two treatments we had located the spot where the pain radiates. So could it be muscle afterall? My mobility was much, much better after each session. We decided to have me run over the weekend. This was carefully thought out and considered.

Saturday morning came and the leg felt pretty darn good. Not perfect, but I decided to go and race. Conditions were cold, blustery, and icy. Gun goes off, and I'm back in April, 1979. Not much of anyone cheering, but the adrenaline has set in. Only a half-mile in there are only three of us running in front. Then there are just two. Eventual race winner, Wade Kruser, separated himself from me by 60-yards by the one mile mark.

I'm doing OK. Yeah, the leg hurts on every stride but its tolerable. We're going along at sub-6 pace. By mile two, the leg is starting to hurt more. In the few training runs I have been able to do in the last 2+ weeks, it has been two miles when the leg refuses to go any further. But a glance at the watch still reads sub 6:20 so I'm just trying to keep the leg loose and the stride easy. Any one can run one more mile, right?

By 2.5 the leg is shot. My endurance, from lack of any real run training, is starting to show as my breathing is very audible. My mind is saying, "just keep it loose. Keep the stride easy." But the pace is falling off. I'm peeking over my shoulder now. A big no-no. But at least the final turn and the finish line awaits. Hey, second overall not so bad for a nearly 50 year old man with a bad leg!

While waiting for awards, the leg turns into basically a solid sheet of immovable object. I know I've probably done some damage. The drive home is painful. I can't even get into the vehicle without sitting down first and lifting the leg with my arms.

When I get home the Well Kept Wife has to help me inside and get me undressed. She's half concerned, half laughing. That sort of, "you stupid old man" laugh that I expect I will be getting more and more in the coming years. Trouble is, I can't do this in London as I'll ruin the trip. The afternoon of the race, we are to be on a train to Stonehenge for a private tour where we actually get to be inside the sacred stones. I'm sure she does not want to pushing me in a wheelchair. But its three weeks away. And for me, there is still a whole lot of the boy from April, 1979 raring to tackle another race.

Pain be damned.

Event Review: I can best sum up this event thusly: Where else are you going to get a quality T-shirt and a super medal for $12!?! That is simply unheard of these days. I really push and recommend for people to jump into your local fun run events. Support your local community. I recommend this race....big thumbs up!

Super nice medal from the Becker fun run!

Next Events:

Mar 19 - Get Lucky 7K, MPLS - 7K (4.52mi)

This is so not going to happen. I need to make sure that I can walk and enjoy London.
Apr 2 - Miles for Missing People 10k; London, England 10K run and 2 mile fun run

At this time, I very much doubt I will be doing this event. I may just go and cheer on the family in their 2-mile run. I just can't take the chance to compete and then be unable to walk for the remainder of the vacation.

Thursday, March 3, 2011

Shoreview Community Center Tri-Performance Triathlon Clinic

Just passing along information about an upcoming Triathlon Clinic.

On Saturday, April 9, 2011 the Shoreview Community Center has Tim Hola, who is one of the best amateur triathletes in the country, coming to conduct a one day Tri-Performance Triathlon Clinic. Tim will have a number of giveaways from Powerbar and Timex, which includes a Timex Heart Rate Monitor. The clinic begins with the swim training portion from 7:00-8:15 AM and ends with an interactive session from 8:45 – 10:30 AM.

Below is a poster with more information about the clinic (click for larger size). They would love to have you join us for this great event! Register online here.

If you have any additional questions, please contact Bri Bachrach, Aquatic Coordinator, at 651-490-4766.

Wednesday, March 2, 2011

Totals: Month Ending February 2011

I had a good month going. Nay, a great month going. All my targets as well as comparisons to same-time-last-year were well ahead of plan. Then the wheels sort of fell of the proverbial bus.

We had a whole week of spring like 50-degree weather. I took full advantage and had a streak of outdoor runs giving me 54.8 miles over a 8-day period. I was feeling great. I had also just completed planning our spring trip. No, not Arizona this time around but to London. I had even found a 10K run I could fit into while there (April 2).

To further make sure I was going to be able to run with the international crowd, I signed up for a local 5K on March 12 and a 7K on March 19. I would use these as tune-up races to make sure I was race ready. Man, I was living the high life.

After the big week of mileage, I cut back a tad. The weekend came, more nice temps. I did a 10.5 mile run on a Saturday and followed that with a 7.8 miler the next day after which I hopped on the bike to crank out a 30 mile bike on the trainer.

The next day, I woke up and the left leg is sore way high up, right under the glute. I think nothing of it, just take the day as a rest day. Nearing 50 years old, I'm getting to use to the occassional pain and ache and usually they resolve themselves in 1-2 days.

The next day I go out for a run and about a mile in I'm hardly able to pull the leg forward. I'm panicking as that is never good a good sign. I take 5 days COMPLETELY off. No run, no bike, no swim.

The leg comes along nicely using compression sleeves and various ointments and using the Stick, roller, etc. On the last day of February I'm feeling good enough to try an easy run. All is well for first two miles. I'm keeping it easy...very like 8:20 pace. Last two miles, same thing happens. I can feel the leg tighten up and I crawl home.

The area is right below my left glute and radiates over to the groin (right off my left testicle). So probably some injury trifecta of ham, groin and glute with a sprinkle of IT band. All I know, this is going to be one that will be slow to heal and probably nag at me all year.....if I am even able to get back out and train. Depressed cannot even begin to describe my feelings at the moment.

February 2011 Total Numbers

Total Workout Hours: 28:01:31
Total training days missed to plan rest day or injury: 9
Swim Yards - 12000
Bike Miles - 203.47
Run Miles - 97.77 (7:45 per mile avg)

Compare to last year -

February 2010 Total Numbers

Total Workout Hours: 30:00.17
Swim Yards - 22600
Bike Miles - 159.21
Run Miles - 90.77 (8:18 per mile avg)

Compare to last month -

January 2011 Total Numbers

Total Workout Hours: 36:16:58
Swim Yards - 17000
Bike Miles - 317.83
Run Miles - 100.42 (7:53 per mile avg)

March Events (provided injury allows it) -

Mar 12 (signed up) - Chase a Leprechaun 5K; Becker, MN
Mar 19 (signed up) - Get Lucky 7K, MPLS - 7K (4.52mi)