News Category: General

Have you ever heard of a problem called necrotizing fasciitis (NF)? It’s an infection of the soft tissues — primarily the fascia or connective tissue. It’s a rare condition but one that can have deadly consequences. That’s why physicians must be trained to recognize it early and treat it aggressively.

In this review article, the diagnosis and treatment of necrotizing fasciitis are explained in detail. Risk factors, bacteria that can cause the problem, and specific diagnostic tests needed to identify the condition are discussed. Treatment by a multidisciplinary team is required for successful outcomes.

Necrotizing fasciitis (NF) is caused by a bacteria or fungus — there are over 25 different types known to cause NF. Some of the more common names you may recognize: e coli, staphylococcus, streptococcus, enterococcus. Many times there is more than one organism present contributing to the problem.

There are certain risk factors associated with NF. Most people who develop NF have suffered some type of skin or soft tissue injury or trauma. It can be something as minor as a skin abrasion or scratch, insect bite, or cut. Necrotizing fasciitis can be a complication of chickenpox in children.

Chronic skin ulcers, severe burns, open wounds from surgery or other infections can also put a person at increased risk for this condition. Other known risk factors include diabetes or other chronic diseases, intravenous drug abuse, and immunodeficiency. Immunodeficiency refers to a depressed immune system — usually from something like AIDS, organ transplantation, arthritis, or autoimmune diseases.

How would you know if you or someone you know has this condition? The first sign may be tenderness and/or redness of the skin followed by skin blisters. Fever, elevated heart rate, and low blood pressure develop as the soft tissue starts to die (necrotize).

Without successful treatment, the tissue may die because the blood vessels supplying nutrients to the skin are damaged. The condition can progress to the point that the patient can even die.

Diagnosis is based on several things: patient history, clinical presentation (signs and symptoms), and diagnostic tests. X-rays, CT scans, MRIs, ultrasound studies, and lab work may be ordered. These tests offer information that help the physician rule out other problems like cellulitis (a less severe skin infection) or skin abscess.

That sounds very simple but the diagnosis can actually be very tricky. At first, there are no substantial changes in vital signs. Advanced imaging like CT scans or MRIs can take time to schedule and cause a delay in diagnosis and thus in treatment.

Some research is being done to find a more reliable lab test that can quickly and accurately predict who might be developing necrotizing fasciitis. The first of these tests is called the Laboratory Risk Indicator for Necrotizing Fasciitis (LRINF). Early studies suggest this is a useful test but further validation is required before it can be adopted as a routine and reliable diagnostic tool.

Right now for the fastest and most accurate diagnosis, a skin biopsy is required. The surgeon can do this right in the office or at the patient’s bedside for those who are already hospitalized. Results are obtained almost immediately including the type of organisms present.

The identification of the underlying bacteria or fungi is important in prescribing the most effective antibiotic. Because there are often polymicrobes (many different types), a broad spectrum antibiotic may be needed to inactivate all types and prevent further spread of bacteria.

The bacteria produce several toxins, causing severe breakdown of tissue in multiple organs. At least 50 per cent of affected individuals experience toxic shock syndrome with hypotension (low blood pressure), nausea, vomiting, and delirium. There is often renal (kidney), lung, and liver compromise as well. Death rate is as high 65 per cent of all patients affected by NF.

Many patients need more than an antibiotic. This is especially true if the infected tissue has lost its blood supply and the drug can’t get to the area. That’s when surgery may be needed. The surgeon removes as much of the pus and necrotic (dead) tissue as possible. This procedure is called debridement. In many cases, the process has to be repeated several times (serial debridement).

Along with antibiotics and debridement, there’s a third key part to successful treatment. This is referred to as adjunctive therapy and can include oxygen therapy, intravenous immunoglobulin therapy, and nutritional support.

In summary, necrotizing fasciitis is a serious medical condition that can cause death of skin, soft tissue, and organs. Mortality (death of the patient) is also a possibility. Early, accurate diagnosis and immediate intervention with antibiotics, surgery, and supportive therapy are essential to preventing loss of limb and ensuring full recovery.

According to the results of this systematic review, studies show that accuracy of joint injections can be improved. In the shoulder, coming in from behind (posterior approach) is more accurate than from the front (anterior approach).

Additionally, the surgeon who uses ultrasound, fluoroscopy, or magnetic resonance imaging to guide the needle to the right spot will also be more accurate. And that was true for all joints (elbow, knee, or shoulder).

What’s the purpose of these injections? Usually to reduce joint pain but also to improve function. The injection can be used to remove fluid from inside the joint (called aspiration) or to inject a numbing agent/steroid medication into the joint.

For this review, injection accuracy rates were the main focus. A secondary question was whether or not different joints can be accessed with greater accuracy than others. For example, is it easier to be more accurate injecting the knee or elbow compared with the more complex shoulder joint?

Turns out that needle placement accuracy is an issue only for the glenohumeral (shoulder) joint. Placement of the needle through portals (openings or channels through the skin down to the joint) for the knee, elbow, acromioclavicular (AC) joint, and subacromial space had the same accuracy rate.

The strength of the results of this review comes from the fact that when all other studies smaller in size but equal in measurement and design are combined, data can be compared and analyzed statistically. So for example, when comparing accuracy of needle placement for the shoulder, the results showed that accuracy improved from 45 per cent using the anterior approach to 85 per cent with the posterior injection.

Likewise, taking a look at a larger (combined) sample for accuracy with and without imaging to guide the surgeon showed differences of 79 per cent (without imaging) and 99 per cent (with imaging) for the knee. For the acromioclavicular joint, accuracy improved from 45 per cent (without imaging) to 100 per cent (with imaging). And for the subacromial space, accuracy improved from 63 per cent (no imaging) to 100 per cent with imaging.

But does improved accuracy mean better results? Accuracy and benefit in terms of patient outcomes are two separate things. Many studies have already shown evidence to support this idea.

People who receive joint injections often improve regardless of the accuracy of the needle placement. The placebo effect (patient expects to get better and does) may have as much of a role in results as accurate placement.

This particular systematic review did not include studies that reported patient results with location and/or accuracy of injection. Accuracy of results based on the type of imaging used was not evaluated either. The authors suggest future studies are needed to make such comparisons.

Compartment syndrome is a challenging problem to work with. Early diagnosis and proper treatment are required to save the affected limb. Without appropriate care, the patient with compartment syndrome could be at risk for death.

In this review article, orthopedic and hand surgeons from Duke University (North Carolina) bring us up-to-date on all aspects of this condition. They provide a brief history of compartment syndrome (first described in 1881). A definition for the condition and review of the anatomy of the various compartments of the arm are included.

Medical and surgical strategies for treatment based on pathophysiology (what went wrong at the cellular level) are a main feature in this review. Drawings, photos, MRIs, and X-rays are used to help the reader visualize the problem and the solution.

Just what is the problem? Compartment syndrome describes a condition in which fluid (swelling or blood) builds up inside one or more of the individual compartments of the arm.

Traumatic injuries, especially bone fractures that puncture the soft tissues are a common cause of compartment syndrome. A splint or cast that is too tight can also cause this problem. The use of a tourniquet during surgery (or with drug abuse) can contribute to compartment syndrome. Other causes include surgery for blood clots, bypass surgery, trauma from electrical or chemical burns, crush injuries, and snake bites.

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 and back of the upper arm, forearm, hand, and fingers.

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.

At the same time, 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. All of these effects can be irreversible (permanent).

Surgeons use several key tools to diagnose the problem. The patient history (what happened, when it happened, and how it happened) and clinical presentation (what the arm looks like) to get started. Various tools (catheter, manometer, Doppler flowmetry) are available to help measure the pressure inside the compartments.

Treatment hinges somewhat on the results of findings. For example, length of time since the injury, amount of pressure, and length of time soft tissues have been under increasing tissue pressure.

Research on this problem has shown that effects are reversible if stopped before eight hours of ischemia (loss of blood supply). Cells start to die at an alarming rate after four hours without blood delivering needed oxygen.

No one knows for sure exactly what level of tissue pressure must be sustained before permanent damage occurs. Based on current evidence and clinical experience, a general guideline is that surgery is needed when the compartment pressure is 20 to 30 mm Hg higher than the diastolic blood pressure. Just using the compartment pressures without comparing them to the blood pressure may be a less reliable method of determining when surgery is needed to release the pressure.

Treatment may begin with just taking pressure off the arm whenever and however possible (e.g., loosening bandages, splint, or cast if that’s the problem). Most of the time, early surgery is indicated.

The surgical procedure for this condition is called compartment decompression or fasciotomy. The surgeon slits open the skin and first layer of fascia called the epimysium. Once the upper layers of fascia have been released, the surgeon conducts a careful search of each compartment for any other areas of restriction.

The procedure does involve direct release of all layers of fascia involved and debridement (removal of any tissue that has died). In some cases, it may be necessary to release tight tissues from around nerves passing through the compartments. The authors provide surgeons with detailed descriptions of their preferred surgical approaches for incisions, decompression, and debridement.

Serious complications can occur without treatment. Death of muscle tissue eventually leads to replacement with scar tissue called fibrosis. Fibrosis is stiff and unyielding. It can apply additional pressure on nearby soft tissue structures, including nerves. Tight tissues lead to contractures (muscles no longer stretch) and loss of joint motion. The final outcome can be chronic pain, loss of sensation, and loss of function.

With treatment, the results are generally good. Prognosis does depend on how soon an accurate diagnosis is made and treatment started. But there are some factors that affect the final outcomes including severity of injury (e.g., damage to the soft tissues from the injury) and length of time with elevated pressures.

Loss of blood supply, involvement of nerve tissue, and patient’s overall general health can also make a difference. The presence of other health problems (heart disease, diabetes, blood clotting disorders) can complicate matters.

There are many challenges for patients and surgeons when treating compartment syndrome. Patients with this condition must be prepared for a long course of treatment followed by months of rehabilitation. Repeated surgeries are often needed to clear out all dead tissue. Infection, poor wound healing, and open wounds in need of skin grafts further complicate recovery.

People with rheumatoid arthritis (RA) don’t have enough to worry about, there is the risk of developing more painful symptoms from fibromyalgia. In fact, one of the main characteristics of fibromyalgia is widespread pain throughout the body. Widespread body pain added to joint pain, heat, inflammation, and swelling from RA can be very disabling.

For that reason, scientists hope to be able to predict who among the patients with rheumatoid arthritis might be at risk for fibromyalgia. If predictive risk factors can be discovered, there may be a way to eliminate (or alter) the factors. The goal would be to prevent fibromyalgia in this already compromised patient group.

One way to do this is to collect as much information as possible on patients with rheumatoid arthritis (RA) who don’t already have fibromyalgia. Then the group is followed over time to see who develops fibromyalgia. An analysis of the two groups (group one with RA but no fibromyalgia and group two with RA and fibromyalgia) can help shed some light on why the group did develop fibromyalgia.

In a recent study, extensive data collected on 9739 patients with rheumatoid arthritis included their age, sex (male versus female), education level and occupation, income, and marital status. Number of years they had the arthritis was factored in along with their body mass index (BMI), smoking (tobacco use) history, and any psychologic problems such as depression, anxiety, or other mood disorders.

Symptoms (how many, what type, how intense, and how often) were tallied up. Any other illnesses (e.g., diabetes, heart disease, cancer), medications, activity level, previous surgeries, and patient reported (but not tested) fitness level were also recorded. Information on sleep and sleep disturbances and the number of visits to their doctors was also collected.

The authors of the study acknowledge up front that it is still unknown whether the many and varied symptoms associated with fibromyalgia cause the problem or are a result of the condition. We don’t know if risk factors are the same for healthy people as they are for patients already affected by rheumatoid arthritis. The results of this study might shed some light on these areas.

Here’s what they found. Men and women with rheumatoid arthritis (RA) developed fibromyalgia in equal numbers, so sex (male versus female) didn’t seem to be a factor. Other demographic factors (education, income, marital status and so on) by themselves did not predict fibromyalgia in RA patients. But if demographics were combined with severity of RA or risk factors for fibromyalgia (mood, BMI, fatigue, stress), then the odds increased for developing fibromyalgia for patients with RA.

Depression (mood), BMI associated with obesity, and poor fitness with limited exercise are predictive factors for fibromyalgia in patients with rheumatoid arthritis. These are all modifiable risk factors, which means there is something we can do to change the risk.

Two characteristics of patients with fibromyalgia bear further study in relation to people with rheumatoid arthritis. The first is the “chicken vs. the egg”: which came first, the depression and poor fitness level or the fibromyalgia, which then led to the depression and lack of physical activity?

The second is what is referred to as over reporting. People with fibromyalgia tend to seek medical care and report their symptoms more often than patients with other pain-related problems. Folks with fibromyalgia have more symptoms than anyone else, a variable called symptom count. How these pieces might fit into the rheumatology patient’s life in terms of developing fibromyalgia remains to be studied.

In summary, this study attempts to develop a fibromyalgia prediction model for patients with rheumatoid arthritis. Understanding how fibromyalgia develops in this patient group and what factors might be changed to prevent it will remain a key focus of future studies. Once the prediction model is complete, then testing will be done to see how accurate the model is before introducing it to the world at large.

You might not realize it but musculoskeletal injuries from explosions and gunshot wounds disable more soldiers than any other battlefield trauma. In fact, according to a study done by the United States Army, even when other bodily trauma occurs, it’s still the orthopedic injury that creates disability leading to discharge from the military. And that reduces our military’s fighting strength in the current Iraqi war.

In order to better understand the problem (and find a solution), the Army Physical Evaluation Board reviewed the records of all service members hurt in the line of duty over a four year period of time. They were collecting information to help identify patterns of injuries.

More then two-thirds of the injuries had an orthopedic component (damage to bones, skin, muscles, tendons, ligaments, and/or other soft tissues). A full 57 per cent were orthopedic only. All of the injuries reviewed left the soldier unfit for duty, which in turn, reduces our military strength and readiness.

Having a clear understanding of the types of injuries (musculoskeletal and nonmusculoskeletal) is important. Tallying up areas of the body affected most often and the mechanism of injury (how it happened) helps military health care officials prepare long-term treatment plans. They refer to this as combat casualty care.

Research like this to characterize wounded soldiers will help at every level. Care for the wounded soldier begins on the battlefield and continues as the combat veteran seeks services as a disabled civilian. Planning and allocating resources (personnel and programs and the money for both) to provide these services depends on information of this type.

As it turns out, orthopedic injuries that occur on the battlefield and lead to permanent disability happen more often than anyone in the military realized. For example, scar tissue affecting the arms or legs, pain, spinal cord injuries, nerve damage, and amputations are just some of the conditions that leave a soldier unfit for duty.

A closer look showed that degenerative arthritis was actually the most common condition, arm amputation created the greatest disability, and amputation of the leg affected the soldier in all areas the most (e.g., return to duty, long-term outcome). It’s very likely that the total cost of rehab for battlefield orthopedic conditions and long-term disability paid out is much greater than anyone anticipated.

In summary, this is the first study to look at battlefield injuries by type, severity, frequency, and impact. Combat casualty is high. Battle injuries and resulting disability are permanently affecting U.S. military strength.

Only one per cent of orthopedically injured soldiers involved in Operation Iraqi Freedom and Operation Enduring Freedom return to active duty. Future research must be directed toward improved outcomes including returning more service members to active-duty with fewer and less severe disabilities.

One of the biggest challenges soldiers face when wounded on the battlefield is infection. Explosives create a high-energy injury that can leave a wound open to the elements (dirt, debris). If the bone is broken and the skin laid open, the wound is at risk for tissue contamination.

In this article, surgeons from Walter Reed Army Medical Center discuss the diagnosis and medical/surgical management of chronic infection. In particular, the most common bone infection from severe war injuries called osteomyelitis is the main focus of their attention.

Treatment is usually débridement (irrigating and cleaning out the wound) and reconstruction. Surgeons have learned over the years that bacteria have a way of coating the bone and wound with a special covering called a biofilm.

It’s this thin layer of microorganisms that cling to the surface of the bone that must be cleaned out and removed. Any microscopic groups or colonies of bacteria left behind will just keep reproducing causing recurrent or chronic (ongoing) infection.

Scientists have shown that a single bacteria cell can make billions more like itself in a 24-hour period of time. As a result of this bacterial reproduction rate, debridement may have to be done more than once.

Antibiotics (medical treatment) help but the overuse of antibiotics has led to some pretty resistant bacteria. Instead of taking oral antibiotics or having antibiotics delivered directly through the blood stream via an IV (intravenous) method, it is better to put antibiotics directly inside the wound (local delivery).

This can be done using special antibiotic beads, sponges soaked in an antibiotic fluid, or antibiotic coated spacers. Any implant devices (rods, screws, metal plates, joint replacements) must be coated with an antibiotic as well.

Research is ongoing to find better, faster ways of delivering antibiotics to the affected tissue. The goal is to find a balance between the right amount of antibiotic to get rid of the bacteria but not so much the local tissue reaches toxic levels that prevent wound healing.

On the surgical side, surgery or a series of surgeries may be needed to restore the patient to full function again. This can take months to years to complete. During reconstructive surgery, the surgeon must put everything back together (bone, muscle, other soft tissues) and find enough skin to cover and close everything up.

Various reconstructive techniques include bone grafting, limb shortening, skin or bone flaps, and internal or external fixation are common. The goal is first, to preserve the limb and second, to maintain as much limb length as possible to match the other side.

Treatment does depend on an accurate diagnosis and gathering as much information as possible about the amount of bone loss, edema or swelling, and the presence of bone abscess.

X-rays, MRIs, and other imaging studies are very helpful. Blood tests must be done to assess the amount of immune system response and the presence of bacteria or fungi in the tissues or fluids.

The authors conclude by exploring future research directions in the treatment of chronic combat-related bone infection of the limbs. Efforts to understand how bacteria signal one another and grow will provide more specific ways to stop their reproductive cycle.

Right now, scientists are just in the experimental stage with more theories than solutions. They expect it may be quite some time before any major breakthroughs change the way chronic osteomyelitis (bone infection) is managed.

Soldiers returning from the field with battle wounds often have severe trauma affecting the leg. All efforts are made to save the leg but constant severe pain may lead the soldier to opt for amputation. The two topics highlighted in this article are: 1) what causes pain during limb salvage and 2) what can be done about it.

First, what is the etiology or cause of this type of chronic pain? Most likely there isn’t a single cause. Instead, there can be multiple different reasons why pain develops and persists. Just the damage to the soft tissues alone is enough to cause severe suffering.

Things happen during the course of healing that can contribute to the pain as well. For example, sometimes the body forms bits of bone in damaged muscles called ossification. The bone embedded in the muscle decreases its flexibility and alters muscle function as it can no longer contract-relax normally.

Joints that have been injured in traumatic accidents, explosions, or other combat-related injuries often develop painful posttraumatic arthritis. Nerve pain from pressure placed on it by scar tissue or ossification can be a big factor in chronic pain for these wounded warriors.

You may have heard of phantom limb pain — the leg (or arm) has been amputated but the patient still feels it and it hurts! The remaining stump can also be extremely painful. Physicians think that failure to control pain early on when surgeries are being done to save the limb may be a contributing factor in stump and phantom pain.

Soldiers with severe battlefield injuries involving the limbs experience two other significant problems. The first is a condition called complex regional pain syndrome (CRPS). CRPS can occur anytime soft tissues are damaged, cut, or injured.

The affected patient has severe burning pain along with a host of other symptoms. There are often skin temperature changes, change in hair growth patterns, numbness or hypersensitive skin, swelling (edema), and stiffness. All of these symptoms create an impaired limb.

And for amputees who use a leg prosthetic (artificial leg), chronic low back pain becomes an issue. Using extra energy and effort to hold, lift, and carry the prosthetic all day everyday takes its toll on the rest of the body.

What can be done to prevent this painful suffering or at least manage it for our returning soldiers? Pain relieving medications are the first line of treatment. Sometimes more than one drug is used in combination called multimodal pharmacology. Tylenol still remains a very effective nonnarcotic pain reliever.

Nonsteroidal antiinflammatory drugs (NSAIDs), antineuropathic (nerve pain) medications, antidepressants, along with opioids (narcotics) are available tools used for pain control. The idea of getting early control over pain is to prevent chronic pain from imprinting nerve pathways with a permanent pain signal.

Other management tools for chronic pain in this group of combat casualties can include physical and occupational therapy, biofeedback therapy, relaxation training, and counseling. Complex regional pain syndrome has its own treatment protocol prescribed and supervised by the physical therapist.

Various methods are used in an effort to stop the pain signals at the level of the nerve. Injections of numbing agents and steroids may be helpful. Nerve blocks, pulsed radio waves to the nerve plexus (place where nerves converge together), and various types of electrical stimulation have been used with varying levels of success.

Many times it takes a concentrated effort of many team members to help suffering soldiers find the right mix of medications and management techniques to gain control of their pain. This type of program is referred to as a comprehensive interdisciplinary pain protocol.

Experts in pain medicine work together using any and all tools that might help the soldier or veteran. Complementary modalities such as acupuncture, Reiki, touch, BodyTalk, massage, hypnosis, as well as many other alternative approaches are often tried and incorporated into the program.

In conclusion, it’s clear now from the many wounded soldiers coming back from Iraq with traumatic limb injuries that early pain control is essential. Pain clinics staffed by pain experts near the battle zone have helped improve outcomes. Pain conditions treated early and aggressively result in fewer cases of chronic pain, disability, and amputation.

What does it take to get a damaged nerve cell to repair itself? Scientists are still shaking their heads because we simply don’t know. Oh, a small injury to a single nerve takes time but it can regenerate. But the process is very slow and doesn’t always result in normal function.

Take that scenario and multiply it many times over with major nerve injuries. Add a stretch or traction injury to the nerve plexus and the outcome can be very poor indeed. The nerve plexus is an area where many nerves join together before separating and going to their individual destinations.

Multiple and/or major nerve injuries occur as a result of birth trauma, gunshot wounds, explosions, crush injuries, tumors, and motor vehicle accidents. Treatment may depend on the type of injury, severity, and location.

In some cases, time and support are all that can be offered patients. In patients with transected nerves (cut all the way across), surgery to stitch the ends back together or graft nerve (or other) tissue between the two ends may be necessary. But patients are warned ahead of time that they may only get partial control back.

Nerve transfers are another way to manage some major nerve injuries. A donor nerve taken from the same limb or another area is used to restore valuable function in the affected arm or leg. But nerves are very delicate and disturbing them to move them or surgically repair them has its own downfalls and complications.

Whether a patient is waiting for a return of function from nerve graft or nerve transfer, the process is slow. Many other factors can get in the way and prevent full functional repair.

For example, nutrition is a key factor. But even more important are the changes the tissues supplied by the damaged nerve are experiencing because of the loss of nerve impulses. Fat and fibrous scar tissue can get in the way of the regenerating nerve bridging the gap from one side to the other. And without the nerve signals, the muscles start to waste (atrophy) and get weaker and weaker.

The need to speed up nerve healing and recovery has led scientists to explore molecular and cell-based therapies. The body does have a protein called nerve growth factor. There’s just not enough of it to quickly or adequately repair a major nerve injury. So maybe there’s some way to use stem cells to grow more growth factor and thus stimulate faster nerve re-growth.

Other researchers are looking for ways to deal with the atrophy that occurs when nerve tissue is off-line. They are taking a look at the space between the nerve and muscle called the myoneural junction.

This space is where all the biochemical action takes place. Electrical signals passing down the length of the nerve turn into chemical signals that cross the gap between nerve and muscle and instruct the muscle to contract.

With a nerve injury, no messages are being sent down the nerve. No chemical changes occur in the junction. The muscle remains quiet. Perhaps there’s a way to artificially stabilize the neuromuscular junction and stimulate the muscle until the nerve can take over. This could possibly prevent the degeneration that occurs around the nerve cells and perhaps help prevent atrophy as the muscle waits for nerve signals to resume.

What does all this mean? Basically, that we need a breakthrough in our understanding of nerves in order to find better ways to treat nerve injuries. If scientists can break the code of the molecular biology involved in nerve injury and repair, it might be possible to find alternate ways to help the regenerative healing process along.

Until then, surgery remains inadequate and patients are at risk for a poor prognosis following major nerve injuries. That’s the bad news. But the good news is that scientists are indeed busily researching and investigating many different ways to approach this problem from all sides. It’s only a matter of time before we have the information needed to guide faster and more effective nerve regeneration.

In wartimes, military surgeons have their work cut out for them. More than 75 per cent of all injuries are to the limbs from explosions. Fractures, bone infections, and loss of soft tissue mass create chronic disability. In this report, experts from the military-based Skeletal Trauma Research Consortium bring us up-to-date on the problem of volumetric muscle loss or VML.

Volumetric muscle loss (VML) is defined as the loss of skeletal muscle and function from trauma or surgery. Although the focus is on combat-related extremity wounds, nonmilitary personnel (i.e., civilians) can experience the same type of injuries from high-energy trauma.

Even with the best of care, sometimes these injuries still create many disabling problems. With so many war injuries affecting the lower extremity (limb), military medicine is taking a closer look at volumetric muscle loss.

They have discovered that even after extensive reconstructive surgeries, many soldiers choose to have the leg amputated. They find that living without the weak, painful leg is actually easier than trying to work around all the functional deficits.

Now the task becomes how to evaluate volumetric muscle loss (VML) and track patient progress. That sounds easy enough until you try to do it. The VML injuries can be very different in type, severity, and location from patient to patient. But it’s important to find a way to characterize, describe, and measure VMLs so that members of the treatment team can communicate effectively with one another.

The military rehab team recommendations the following for evaluating volumetric muscle loss and its effects:

From the outside you wouldn’t know by looking at the forearm that there are three separate compartments. Each section is separated by connective tissue called fascia. The hand has 10 of these compartments. There are a total of 15 compartments in the entire upper extremity (arm) from shoulder to hand. Any condition that changes the pressure in a compartment can reduce blood flow (called ischemia) and cause death of the tissues (necrosis).

Injuries that increase pressure in any one of these compartments can result in a condition called acute compartment syndrome (ACS). The most common cause of ACS is a bone fracture. Repetitive exercise (muscle contractions over and over) is another potential risk factor for ACS. Other causes of ACS of the upper extremity include dressings, tourniquets, or casts that are too tight. Bleeding disorders and burns can also increase the amount of fluid (called fluid volume) inside a compartment. And remember, these compartments are tightly packed with very little room for extra fluid. In a smaller number of cases, swelling from a spider or snake bite can also lead to ACS.

In this review article, hand surgeons bring us up to date on the diagnosis and treatment of ACS of the upper extremity. They begin by brushing up on the anatomy and descriptions of the compartments. Drawings help show the various compartments and the contents of each one. Muscles, tendons, nerves, and blood vessels are clearly labeled.

For the surgeon, a clear understanding of where each compartment begins and ends is important when making incisions to release pressure in the affected compartment. The necessary procedure to restore circulation and save the arm is called a fasciotomy. The surgeon makes long slits in the fascia to allow it to open and spread. Without release of the pressure within the compartment, the loss of blood flow can result in serious loss of arm and hand function. In severe cases, amputation may be the recommended treatment.

The decision to perform a fasciotomy is based on patient symptoms, clinical presentation (how the arm looks when examined), and pressure measurements taken inside the compartments. For mild to moderate increases in pressure, the patient is closely monitored by taking serial measurements. These same measurements are used to confirm that the compartments have returned to normal after surgical decompression. Each compartment must be measured separately. Special monitoring devices are used. Sometimes more than one compartment needs releasing.

The authors provide step-by-step drawings and descriptions of fasciotomies of the forearm and hand. Where to make the incisions with length and depth at each location are provided. How successful is this procedure? That depends on a number of different variables. For example, the patient’s age and medical condition can affect outcomes.

Likewise, the type of injury, cause, and severity all play a role in the results. Early treatment has the best chance for good results with fewer complications. The longer a patient waits between injury and treatment, the greater the risk of problems such as infection, nerve damage, amputation, and even death.

One other serious problem that can develop is called Volkmann ischemic contracture. The long period without blood to the soft tissues inside the affected compartment(s) can cause irreversible damage. The muscles go into full contraction and cannot let go or relax. The patient’s hand, forearm, and/or upper arm assume a telltale position, which is called Volkmann contracture.

Patients who progress to the point of having a Volkmann contracture are not likely to regain full use of the affected area even with surgical treatment. Additional surgeries such as muscle or tendon transfers may be needed.

In summary, any cause of increased pressure inside one or more of the 15 separate compartments of the upper extremity can be a very serious, even life threatening condition. Symptoms of pain, swelling, and tense tissue (especially with muscle contractures) are red flag findings. An early diagnosis of acute compartment syndrome (ACS) and immediate treatment are essential for a good outcome. In severe cases, patients should be counseled not to expect full recovery of motion, strength, or function of the involved arm.

Having trouble getting up out of a chair? Going up and down stairs? Getting in and out of a car? If so, you may be experiencing the effects of muscle weakness. Muscle weakness is a fairly common problem as we get older and in those who are physically deconditioned (i.e., “couch potatoes”). Another term for anything that’s wrong with the muscles is myopathy (myo = muscle and pathy = pathologic or diseased).

But muscle weakness or myopathy could also be caused by a wide range of medical problems such as infections, endocrine diseases, muscular dystrophies, cancer, and neurologic conditions. Other causes of muscle weakness include drug toxicity, rheumatologic diseases (e.g., fibromyalgia, sarcoidosis), and vitamin deficiency.

In this report, a rare cause of muscle weakness is discussed: inflammatory muscle disease. Doesn’t ring any bells for you? That’s because it only affects one in five million adults in the United States. But for those individuals, early diagnosis and treatment is important for the best outcomes.

Who is affected? Inflammatory muscle disease is actually age- or gender-linked depending on what type of muscle disease is involved. There are three basic types of inflammatory muscle disease: 1) polymyositis, 2) dermatomyositis, and 3) inclusion body myositis.

Polymyositis only affects adults, whereas dermatomyositis is seen in children and adults. Inclusion body myositis is rare in anyone younger than 50 and occurs most often in men over the age of 60.

People who develop any of these three inflammatory muscle diseases develop symptoms slowly over months to years. Muscle weakness affecting the shoulders and hips is first. That’s when patients with this disease start to notice difficulty sitting up and down from the toilet, putting something up on a high shelf, or brushing the hair.

No one really knows what brings this inflammatory muscle disease on. That’s why they are referred to as idiopathic (unknown cause). And because there are so many other potential causes of muscle weakness, it can take quite a while to figure out what’s going on. Dermatomyositis is the only one that has a characteristic facial rash to help point the right direction in searching for a diagnosis. It’s also the only one to be associated with a history of cancer.

Just how does the physician make the final diagnosis? It requires a number of different steps starting with a thorough history (personal and family history) and timeline for symptoms. Lab tests help sort out infections from inherited muscle diseases and from endocrine disorders such as Addison disease, Cushing syndrome, and thyroid problems.

There are some specific lab tests just for muscle diseases. For example, measuring blood levels of an enzyme called creatine kinase (CK) may be helpful. CK is elevated in all three types of inflammatory myopathies. An increase in CK doesn’t always point to inflammatory muscle disease(s).

High levels of CK can occur as a result of trauma, medications, and even exercise. There are even times when the CK levels are normal but the person really does have an inflammatory muscle disease.

Whenever the lab values come back normal, it’s back to the diagnostic drawing board so-to-speak. The physician will recheck for other subtle signs and symptoms such as difficulty swallowing or speaking, heart or lung problems, and skin rash. Some additional lab studies may be ordered. And imaging studies (MRIs), X-rays (chest and abdomen) electromyography (EMGs), and muscle biopsy may be ordered.

By themselves, none of the tests and measures can diagnose inflammatory muscle diseases. The physician must really rely on all the diagnostic clues and information provided by each one. All put together, it is possible to rule out other causes of the muscle weakness until the only reasonable possibility is inflammatory myopathy.

At that point, treatment is the next step. Most often, the patient is referred to a specialist who sees more than an occasional case now and then. Medical therapy begins with antiinflammatory drugs (e.g., corticosteroids) to reduce inflammation. If one drug doesn’t work, it may be necessary to combine several drugs together to get the intended result.

Exercise (aerobic or cardio and strength training) is a key feature of treatment. Exercise will not make the disease worse and has been shown to make things much better. Exercise will help keep the weakness from getting worse rapidly. It’s still likely that strength will continue to decline but it will happen at a much slower pace.

Physical activity and exercise are also important in keeping the joints moving and preventing muscle and joint contractures (soft tissues get stuck on one position and can’t stretch or move). Patients must be educated to understand that exercise has its own anti-inflammatory effects and should be a part of each day.

For anyone who would like a detailed review of inflammatory muscle diseases, this article provides some helpful tables, photos, and descriptions of each one. Patient evaluation, diagnosis, and treatment are discussed in detail as well.

Trigger fingers, De Quervain syndrome, and intersection syndrome are the topic of this review article. These three conditions have one thing in common: they all cause painful forearm, wrist, and/or hand symptoms. Although these problems all fall under the category of tenosynovitis (inflammation of the synovial lining around the tendons), they aren’t all really inflammatory conditions.

How do we know this? Scientists have examined cells taken from painful tendons, tendon sheaths, the synovial lining, and other supportive soft tissue structures. By looking at them under a microscope, they have been able to see that very few (sometimes no) inflammatory cells are even present. So what’s going on?

It’s more likely that repetitive motions (using the finger or hand over and over) have caused the lining around the tendon (called the tendon sheath) to form extra fibers and then start to thicken. Thickening of the tendon sheath is referred to as hypertrophy.

The fingers and hand are delicate structures and carefully put together. Every layer of tissue (tendon, sheath, synovium) and each layer of space between have just the right amount of room for smooth sliding and gliding of the tendons. Even a small amount of thickening can cause a problem called stenosis. Stenosis is a narrowing of the normal space allowed for the tendons to move through the tendon sheath.

Over time, with thickening and stenosis, the tendon gets “stuck” while trying to move through the narrow space available in the tunnels created for them. As the tendon passes over boney bumps normally there to help fulcrum them (acting like a pulley system), tendon gliding is restricted. That’s when the patient feels like the finger is catching or locking up on them — a perfect description of trigger finger.

Trigger fingers may be painful but just as often there may be no pain — just the locking or catching sensation. Locking is more common as the patient tries to extend or straighten the affected finger but triggering can occur with flexion (bending) the finger, too. Sometimes the patient has to physically use the other hand to “unlock” the finger that is stuck. In chronic cases, the finger gets stuck in the locked position and can’t be pulled out of it.

What can be done about this trigger finger condition? Many times a simple treatment formula of rest, change in activity and use of the fingers/hands, and use of ice and ibuprofen does the trick. Symptoms slowly go away and full hand motion and function are restored. Studies show that the most successful treatment may be the use of steroid injection. Finger and hand splints have also been used with good results.

But steroid injections have complications of their own so physicians are studying patient factors to see who might be the best candidates for this type of treatment. Studies are also being done to compare type of injection given (e.g., dexamethasone, triamcinolone) and location (e.g., into or around the tendon sheath). So far, they’ve discovered that it is easier to tell who won’t do well with steroid injections rather than who will benefit from them.

Patients with diabetes, a previous history of trigger fingers, more than one finger affected, and a long history of symptoms are not likely to get the desired results with steroid injections. These patients seem to do better with surgical release. The surgeon cuts through fibrotic tissue to release the tendon pulley mechanism. This procedure must be done carefully to avoid cutting into the tendon. It is not advised for trigger thumb or trigger index finger because of the danger of cutting blood vessels and nerves in the area.

In this article, the authors give equal time and focus to De Quervain and intersection syndromes. Both of these conditions occur as a result of overuse of the thumb or wrist. Pain and swelling on the thumb side of the hand with clicking during thumb and wrist movement are the main symptoms. The main differences between these two syndromes are the cause and pain location.

Intersection syndrome is more often seen in athletes such as tennis players (or other racquet sports), weight lifters, and rowers. The painful symptoms are above the wrist (more toward the elbow side rather than down by the thumb where symptoms of De Quervain syndrome occur). De Quervain syndrome is seen more often in older women (40 years old and older), African Americans, and members of the military.

Treatment is the same for both De Quervain and intersection syndromes (and very similar to trigger finger). Rest from aggravating activities, steroid injections, and splinting may be helpful. Steroid injections seem to have the best results for nonoperative care, providing pain relief lasting at least a full year for 78 per cent of patients. There are some studies that show splinting offers no extra help and may not really be needed for De Quervain syndrome. Splinting seems to be more useful for intersection syndrome.

As with trigger fingers, if conservative (nonoperative) care (including one or two steroid injections) doesn’t work, then surgery may be needed. An open incision is made and the affected tendon sheath(s) are split from top to bottom. The surgeon makes every effort to avoid cutting the tendon or nearby nerves and blood vessels. The surgeon is more likely to remove tissue during surgery for intersection syndrome, especially when there is active inflammation.

In summary, trigger finger, De Quervain syndrome, and intersection syndrome make up a group of painful conditions referred to as stenosing tenosynovitis of the hand, wrist, and forearm. The surgeon who understands how the individual anatomical parts (tendon, sheath, synovium) are affected will have a better idea how to successfully manage these conditions. Every effort is made to treat the problem conservatively. Surgery is the treatment of choice only after nonoperative care has failed to provide pain relief and/or improve thumb, hand, wrist, or forearm function.

Stress fractures were once most common among military personnel who marched and ran day after day. But today, stress fractures are on the rise in athletes, from distance runners and sprinters to skaters, hurdlers, and tennis, volleyball, soccer, and basketball players. Dancers and gymnasts are not immune either. Men and women in these two sports who train more than five hours a day have been shown to be 16 times more likely to develop a stress fracture.

A stress fracture is a hairline crack in the bone that can grow larger over time if not treated properly. There are two types of stress fractures. Insufficiency fractures are breaks in abnormal bone under normal force.

Fatigue fractures are breaks in normal bone that has been put under extreme force. Fatigue fractures are usually caused by new, strenuous, very repetitive activities, such as marching, jumping, or distance running. The main focus of this update (review) article is on fatigue stress fractures among athletes.

Besides being a soldier or an athlete, being a female in either of these groups increases the risk of a stress fracture. Other risk factors include biomechanics (alignment of the foot, ankle, and lower leg), muscles mass and strength, and bone density and bone geometry (shape, thickness).

One of the new findings in risk factors is the cross-sectional diameter of the long bones of the leg. For example, a smaller cross-sectional area of the tibia (lower leg bone) has been linked with stress fractures in male runners. The cross-section of a bone is the width of the bone you would see if that bone was cut straight across (sideways not length-wise). The thickness of the bone seen this way represents the bone strength.

There’s not much a person can do to change the cross-sectional area of the bone or gender (male versus female). But there are ways to prevent stress fractures by modifying other risk factors. For the athlete with flat feet, forefoot malalignment, excessive hip internal rotation, uneven leg length, or other biomechanical factors, an insert placed inside the shoe can make a big difference.

For women who are overtraining while also limiting calories, a better balance of eating and nutrition may be helpful. Females who have an eating disorder or disordered eating are common among athletes where “lean is mean” (a desired state of body and mind) in some sports. In such cases, nutritional and behavioral counseling are advised.

Training schedules can also be reviewed and altered if training is too much, too often, too long, or too intense. A sudden change in the athlete’s training routine (increased intensity and/or duration) is the biggest training error leading to stress fractures. Gradual increases in training may be able to avoid this mistake.

Muscle mass and muscle strength can be increased with a strength training program. Smaller muscles and muscle fatigue may result in an increase in the force placed on the bone with activity. Women may be at increased risk of tibial (lower leg bone) stress fractures because the female’s calf muscle just isn’t as large as the male’s.

And with excessive training, muscle fatigue may result in a change in postural alignment and body mechanics — all adding up to more force transmitted from the ground up the leg and into the bone. But athletes worry that they will lose their edge in fitness if they decrease their training volume. They are not gung-ho about backing off their training schedule.

A review of training surface and shoe wear may be all that’s needed before altering the training schedule. And for those who do need to pull back a bit, studies show for the already fit athlete, reducing the training volume temporarily does not affect athletes’ ability to perform and compete effectively. Lower levels of fitness may actually be a risk factor for stress fractures. So for some athletes, bumping up the fitness portion of their training may be a good idea.

These prevention ideas are all very good but how does an athlete with various aches and pains know when a stress fracture has already developed? The most common symptom is increased pain with specific sport activities (e.g., increased shin bone pain when running or jumping). If the athlete presses on through the pain, then typically, pain will be present at rest as well.

Pressure on the painful area increases the pain. Hopping on that leg also reproduces the severe pain often present with activity. There may be swelling around the painful site. The physician or other examiner can perform a tuning fork test (pain is reproduced when a vibrating tuning fork is placed over the painful area). But the fastest and most accurate way to diagnose a stress fracture is with an MRI.

Once it is certain that the problem is, indeed, a stress fracture, then treatment becomes a matter of management. Rest and avoiding activities that cause pain are the first two steps. The athlete can still participate in a fitness program so long as it does not cause any pain. Swimming, pool-running, and bicycling are usually safe bets.

Tibial stress fractures seem to respond faster when the athlete wears a special pneumatic leg brace. A cast on the foot and ankle may be needed for foot stress fractures. In those cases, the athlete is non-weight-bearing (using crutches) and cannot continue with training that involves the fractured foot/leg.

Surgery is not a main line of treatment for most stress fractures. Fracture fixation with screws, wires, and/or a metal plate may be needed for stress fractures that progress to a full fracture with displacement (ends of the fractured bone separate) or for stress fractures of the hip.

Regardless of the treatment provided, there should always be a re-evaluation of the athlete and gradual return to sports activities, fitness regimens, and training schedules. All risk factors should be assessed and modified wherever possible. Nutrition is a vital key for all athletes but especially women who are already at greater risk for stress fractures than their male counterparts.

Athletes are always in a hurry to get back into action whether that’s on a football field, tennis court, or baseball diamond. For professional athletes, time is money and a place in the limelight. Tendon injuries are common among sports participants. And tendons are notorious for being slow to heal and quick to reinjure.

Efforts are being made to find ways to speed up and enhance the healing process. Scientists have discovered that human blood contains key ingredients for healing. The plasma portion of human blood (the clear liquid) has parts called components that may come to our aid.

In particular, tiny platelets circulate every minute of every day in the blood — they are always there in case of an injury. Platelets help form blood clots to stop bleeding. When the body signals that there is a need for platelets, they become activated and rush to the area of injury. Once there, they clump together to form a clot and then release tiny chemicals called growth factors.

It’s those growth factors that turn stem cells into tendons. Stem cells are basic cells that haven’t formed a specific type of cell (e.g., heart, muscle, joint, organ). The body can turn a stem cell into any kind of cell needed including tenocytes (tendon cells). In this study, blood and tendons were taken from rabbits and used together in the lab to see what the effect of platelet-rich plasma would be on the damaged tendon.

Actually, from previous experiments, they already know that platelet-rich plasma injected into injured tissues (such as ligaments and tendons) does help promote healing. The question now is: how does it do so? That’s the focus of this study. By examining the process in the laboratory under a microscope, scientists hope to unravel the mysteries of this healing helper.

By using different dosages of the platelet-rich plasma (two per cent and 10 per cent), they were able to measure the effects of each on the injured tendon cells. Using gene analysis, they could examine cells produced in the damaged tendons and see how many and what type of tissue was forming (e.g., collagen fibers, scar tissue, healthy tenocytes). The experiment included a control group — damaged tendons that did not receive the platelet-rich plasma.

They found that the platelet-rich plasma did indeed cause tendon stem cells to form into tenocytes. They were interested to note that once stimulated, these stem cells didn’t form other types of cells like fat cells, bone cells, or cartilage cells. That’s good because a mix of all those types would impair tendon healing rather than stimulate it.

Using platelet-rich plasma not only causes stem cells to form tenocytes, it also increases the number of tendon cells formed. Not only were there more tenocytes, but there was plenty of the right kind of collagen (the basic building block of all soft tissues) needed for healthy tendon tissue rather than weak scar tissue.

In summary, this study helps shine some light on how tendon stem cells fit into the picture of tendon healing and how platelet-rich plasma as a treatment might aid in that healing process. It is a safe procedure but one that will require further study to find the right concentration of platelet-rich plasma to get the ideal healing response.

There are far more “unknowns” about tendon healing and the role of platelet-rich plasma in tendon healing than we currently have answers. Questions that remain to be answered include:

Some of the best minds in the world of rehabilitation have come together to formulate a scoring system for complex regional pain syndrome (CRPS). Until now, patients were diagnosed with this condition as either “yes you have CRPS” or “no, you don’t have CRPS”. [That’s what is called a dichotomous diagnosis]. Until now, there has been no way to give it a description such as mild, moderate, or severe that conveyed to everyone just what the condition looked like.

Like its name, complex regional pain syndrome (CRPS) is a complex problem. CRPS is a disorder that can cause severe pain and disability. However, as painful and disabling as the condition is, there is not a lot that doctors know about it. More women get it than men. It occurs after about one to two percent of all bone fractures. It is most common (up to 35 percent) after certain types of wrist fractures.

Complex regional pain syndrome more commonly affects the hand or foot, but may spread further up the affected limb and even into the opposite limb. The common symptoms of CRPS are unrelenting burning or aching pain, skin sensitivity, swelling, discoloration, sweating, and temperature changes. If the condition becomes chronic, dystrophy or deterioration of the bones and muscles in the affected body part may occur.

What they don’t know is why it happens, who it will happen to, and how severe it will be. And, because treatment of CRPS depends on the symptoms, a severity scoring system like this Complex Regional Pain Syndrome Severity Score (CSS) may help.

The CSS is a simple test that can be given easily yet still reflects diagnostic features of CRPS (e.g., pain, sweating, skin color changes). It was put together and tested by experts from well-known rehabilitation centers such as Rehabilitation Institute of Chicago, Vanderbilt University School of Medicine, Trauma Related Neuronal Dysfunction Consortium in The Netherlands, Rush University Medical Center in Chicago, Stanford Medical Center (California), and two universities in Germany.

It was tested on 114 people with a known diagnosis of CRPS and compared with 41 patients with nerve pain that was not caused by CRPS. Most of the CRPS patients had a history of fracture or crush injury leading to the development of CRPS.

The test consisted of a checklist of signs and symptoms common with this condition. Self-reported symptoms included differences in temperature, skin color, sweating, and swelling from one side (involved side) to the other (uninvolved side). A second section of the test evaluates signs observed by the examiner such as exaggerated levels of pain with pinprick test, differences in skin temperature felt by the examiner, and decreased range-of-motion of the involved part (hand, foot).

Higher test scores meant more severe pain and other symptoms. Patients with CRPS had much higher test scores than the patients in the nerve pain but non CRPS group. Statistical analysis showed that this new scoring system for severity of CRPS is reliable and valid. In other words, it can be used dependably to identify people with CRPS and provide a picture of the severity of their condition. Used over time, it can also show changes or fluctuations in individual cases.

The authors conclude that this type of tool will help health care professionals plan and modify treatment for patients with CRPS. Having a consistent severity score will help improve communication among all the health care professionals working with people who have CRPS.

Researchers involved in this project do not see this tool as a replacement for current pain scales in use to measure treatment outcomes. But the scoring system may be helpful when conducting research on this condition as it can show changes in symptoms with treatment. It may even function as a predictor of who will get better with different types of treatment.

Are you a physician with a busy practice? Do you tend to medicate rather than educate patients with arthritis? Are you a patient with osteoarthritis? Would you rather be educated than medicated? If you fall into either of these categories, then the information in this article is for you.

The authors of this article make it clear that their goal is to help physicians provide thorough but efficient management of osteoarthritis (OA). But today’s busy consumers who happen to have osteoarthritis are also interested in this information. Armed with the knowledge we have about osteoarthritis, you will be able to discuss these points with your physician.

Forming a plan of care that is evidence-based, complete, and do-able is an essential part of managing osteoarthritis. It starts with an accurate diagnosis and the understanding that osteoarthritis isn’t just wear and tear on the joints.

Scientists have come to see that the joint is like an entire organ system in its own right. It is a very complex organ with multiple different structures like synovium, bone, nerves, muscles, and blood supply. There are mechanical parts and there is a neurologic road map to provide movement of those mechanical parts.

There are a few basic things that haven’t changed in our understanding of this disease. First, age is the biggest risk factor. The older you get, the greater your chances for developing this condition. Second, the joints affected most often are the large ones: hips, knees, hands, and sometimes shoulders.

The symptoms tend to be the same no matter what joint is involved: pain, decreased joint movement, morning stiffness that gets better after 30 minutes of gentle movement, joint tenderness, and decreased function. There are certain risk factors that point to osteoarthritis as the cause of these symptoms including trauma, surgery, repetitive use or excessive use (usually work-related), and family history.

Your physician will rely on three tools when making the diagnosis: clinical findings, imaging studies (usually X-rays), and lab results. Many times, your verbal report of what’s wrong is enough to make a diagnosis. X-rays can be helpful to guide treatment but aren’t always necessary. Taking a sample of the fluid from inside the joint (called synovial fluid) may provide some additional clues.

The American College of Rheumatology has specific criteria physicians use to make the diagnosis for hand, hip, or knee osteoarthritis. They have updated their traditional format for diagnosis based on continued evidence from studies. Now they use a technique called the tree format.

The tree format combines various symptoms to determine how likely it is the patient has osteoarthritis (OA) of the joint in question. For example, when diagnosing hand osteoarthritis, instead of looking for hand pain, aching, or stiffness plus some other determining factors (the traditional format), now they look for hand pain, aching, or stiffness AND specific other clinical findings (tissue enlargement, deformity, swelling). Similar changes have been made for the diagnosis of hip and knee OA.

The idea of treatment of osteoarthritis has really been replaced with the notion that it is a disease that is managed. That means there isn’t one single treatment for everyone. It’s more of a plan that involves multiple different approaches.

Today’s research evidence calls for a nonpharmacological approach first. Simply stated, that means “without drugs”. This approach requires more time to educate the patient about the process and about his or her choices and responsibilities. There is much less focus on a magic pill to cure-all.

More and more, patients are being called upon to be proactive for themselves. They are encouraged to learn about the disease and find ways to protect their joints. But patients don’t have to do this all alone. A team approach is advised with orthopedic surgeon, primary care physician, and physical and occupational therapists to offer advise, counsel, and guidance.

Some of the tools shown to make a difference include various types of joint braces, shoe inserts or shoe modifications, supportive neoprene sleeves, exercise, and weight loss. Modalities such as heat, cold, electrical stimulation, and acupuncture can be helpful during acute flare-ups. Assistive devices such as a walking stick, cane, or walker may be helpful to off-load the joint and protect the joint surface from further damage.

When medications are indicated, acetaminophen (Tylenol) is the first choice. When used as directed, it is a safe and effective pain reliever. Acetaminopehn does not have any antiinflammatory effects. There is a danger of liver damage with too much acetaminophen so patients must be advised carefully and monitored closely to prevent any adverse effects from occurring.

Other medications can be used if acetaminophen in combination with the management program isn’t enough to reduce pain and improve function. These include nonsteroidal antiinflammatory drugs (NSAIDs), capsaicin (topical agent rubbed on the skin to produce a counter irritant), steroid injections, hyaluronic acid injections, and glucosamine and chondroitin sulfate (supplements).

If nothing works and the patient is still experiencing intolerable pain, then narcotic pain relievers may be prescribed or surgery may be recommended. In the case of severe knee osteoarthritis, there are several different surgical procedures that might help before going to a full joint replacement. Joint alignment can be corrected with an osteotomy (removing a wedge-shaped piece of bone to shift the weight bearing load). Or a unicompartmental replacement is possible (just replacing the side of the joint that is affected).

In summary, osteoarthritis is more than just a disease of wear and tear. The entire joint complex is involved with advancing age and multiple other risk factors as part of the picture. Treatment should be a program of self-management directed by a team of health care professionals.

Patient education and nonpharmacologic treatment are the first steps. The goal is to preserve and protect the joints while maintaining motion and function. It’s not that medications can’t be used — they just shouldn’t be the first thing patients are given. There’s plenty of evidence that the approach described here for osteoarthritis works well and prevents unnecessary exposure to drugs and surgery.

Can you name the most common venomous snakes in the U.S.? Did you know snakes have a bite reflex? They can still strike even when the head has been separated from the body! What about first aid for a snake bite — any idea what to do? Don’t worry; the authors of this article on snake bites have included all that information and much more. Read on!

It might surprise you to know that out of 6,000 snake bites reported (many are never reported) in the United States, only 12 result in death each year. But one out of three people are bitten by venomous snakes like rattlesnakes, cottonmouths, copperheads, and coral snakes.

Symptoms may develop right away up to hours later. They can be mild to severe and include nausea, vomiting, pain, numbness (even paralysis), and bruising and swelling of the area. More serious symptoms such as difficulty breathing, blood clot formation, and drop in blood pressure require immediate medical treatment.

What will the medical personnel do for a snake bite? Emergency medical techs (EMTs) are always taught to use the A, B, Cs first. A is for airway — make sure the person’s mouth and trachea are clear. B for breathing. If the patient is not breathing, a special emergency device can be used to pump air into the lungs. And C for circulation or compression. C reminds the EMT to check for a pulse or heartbeat and/or start applying chest compression if necessary.

In some situations, once the patient has been transported to a medical facility and evaluated, there may be nothing else required. Those patients are just kept under observation for eight to 12 hours. During that time, the local site of the bite will be cleaned and then monitored for any changes in size, color, swelling, or bleeding. When antivenin is available, this antidote to the snake bite is given to the patient right away.

What should you do if either you or someone with you gets bitten by a snake? Well, one thing you shouldn’t do is follow the old Western cowboy movies. DON’T put a tourniquet around the arm or leg. DON’T cut around the bite and suck out the venom. Get medical help as quickly as possible. With cell phones and GPS units, fast emergency aid is often just minutes away.

Most people do alright after a snake bite. The worry about gangrene setting in and losing a limb or life is real but extremely rare. Antibiotics are not routinely used unless there are signs of skin or wound infection. Surgery is only required when there is damage to the deep structures such as the blood vessels, nerves, tendons, or muscles.

Every effort is made to keep the limb from swelling up. Reaction to the snake venom can create what looks like a compartment syndrome. Pressure from fluid inside the arm or leg stretches the soft tissues and layers of skin so much, surgery is required to cut the skin and release the pressure. The procedure is called a fasciotomy.

You don’t have to worry about snake bites at all times and in every state. Of course, being outdoors in areas where snakes are sunning themselves on rocks or sleeping under leaves is a red-flag situation. Most snakes are hibernating and nowhere to be seen between November to March. The prime months for snake sightings and encounters are between April and October. And if you want to vacation in states where there are no native venomous snakes, try Hawaii, Maine, and Alaska!

You’ve probably heard it before. We’ll have to repeat it here. Spiders are really good guys. They eat mosquitoes, flies, and other annoying bugs. They reportedly save us billions of dollars in pest control — and that’s especially helpful in the agricultural business.

In some countries, spiders are considered good food. But admittedly, they are ugly to the human eye. We are more inclined to kill them than to escort them outside. And some of them do bite.

But there are only two species in the United States that can cause bodily harm with their bites: the black widow spider (Lactrodectus) and the brown recluse or fiddleback spider (Loxosceles). “Fiddleback” refers to the violin shaped back of this spider.

The brown recluse is considered by some experts to be the most dangerous spider to humans. But in their defense, remember they eat cockroaches, silverfish and other soft-bodied insects. Not all states even have this type of spider. They are most common in the western, central, and southern states.

As the name suggests, the brown recluse spider tries to avoid contact with humans. They tend to hide out in basements and dark corners. You are most likely to get bitten when putting on clothes or shoes that were left on the floor.

The spider crawls into the warm, dark material (or shoe). You put the article of clothing on without thinking to check for unwanted guests. And the spider reacts to the sudden movement with its only defense: a bite. Spider bites that are present when you wake up in the morning occur when the spider climbs up covers that touch the floor. If you move or roll onto the spider, you get the same defensive response: a bite.

The female black widow is commonly recognized by its black color, hour glass shape and red markings. Males are smaller, usually have yellow and red bands and spots over the back, and don’t bite. Although they live in warmer climates (and desert areas), they can be found in states with cooler temperatures.

The female black widow spider is probably the most venomous spider in North America. But it injects a very small amount of venom (poison) when it bites. Very few people actually die of spider bites.

The bite of the brown recluse or black widow can cause local effects (pain, redness of the skin, an open wound) or systemic effects. In a very small number of people, deep wounds can develop from infection. The result can be necrosis (tissue death). For those patients, surgery might be needed to help deep wounds heal.

The systemic symptoms are caused by the neurotoxic effects of the venom. Neurotoxins primarily target the nervous system. Systemic symptoms can include muscle cramping, sweating, nausea, vomiting, fever, chills, and dehydration. In less than one per cent of cases, the reaction can be severe enough to cause paralysis, respiratory arrest, and even death.

Whenever dealing with spider bites, the best advice is to capture the spider (if possible) for identification and seek medical advice right away. Most of the time, local treatment of the skin is all that’s required. A tetanus shot may be needed. Hospitalization is only necessary when there is a severe reaction with dehydration and/or compromise of the heart or lungs. Antibiotics are not used unless infection develops.

Antivenin (an antidote to the poison) is not given routinely because symptoms go away quickly (within several hours to several days). Although there is a specific antivenin for brown recluse spider bites, it is not available in the United States. There aren’t very many studies on the subject, but research evidence does not support the use of antivenin to prevent skin necrosis.

To avoid spider bites, the best advice is to keep all clothes and bedclothes off the floor. To keep spiders out of bed with you, don’t use a dust ruffle around the bottom of the bed. This just gives the spider a “leg up” so-to-speak. And don’t throw the sheets, blankets, or covers on the floor.

Check your shoes before putting them on. When working outdoors, wear gloves and beware of spiders when picking up those gloves or other tools if they have been sitting in a shed, garage, or other dark storage area.

Despite all the photos you can find on-line of the severe local effects of some spider bites, these cases are really rare. Death from spider bites is even more unusual.

Gout has been around for thousands of years. We know this from evidence seen in Egyptian mummies and written reports from ancient kings before the time of Christ. Although it is caused by a disorder of purine metabolism, it is often brought on by dietary excesses. In ancient days, only the wealthy could “afford” to have gout, but today, many more people (with access to the same foods) are affected.

Gout is a disease that involves the build-up of uric acid in the body. About 95 percent of gout patients are men. Most men are over 50 when gout first appears. Women generally don’t develop gout until after menopause. But some people develop gout at a young age.

In gout, excess uric acid causes needle-shaped crystals to form in the synovial fluid of the joints. Synovial fluid is the fluid that the body produces to lubricate the joints. Uric acid is a normal chemical in the blood that comes from the breakdown of other chemicals in the body tissues.

The first symptom of gout is often a pain at the base of the big toe (the metatarsal phalangeal joint). The joint becomes swollen, warm, and red within eight to 12 hours. The attacks occur most often at night. Patients say the pain is so bad the joint can’t even stand the slightest touch. Even the weight of a sheet causes excruciating pain. Walking and standing are almost impossible if the legs or feet are affected. Many patients have flu-like symptoms, including fever and chills. The pain may go away on its own in a few hours, or it may take a few weeks.

Gouty arthritis attacks come and go. There may be months between attacks. Over time the attacks happen more often, last longer, and involve more joints. Eventually the pain doesn’t ever completely go away. The joints stay swollen and tender even between flare-ups, and the flare-ups start to happen every few weeks. Eventually, some patients develop tophi (visible crystals) on joints or pressure points and kidney stones.

We mentioned food in association with gout –what does food have to do with it? The breakdown of purines in the body releases uric acid. Purines are ingested through certain types of food such as sweetmeats (e.g., liver, kidney, brain, lunch meat, bacon, salami) and seafood. The increased intake of fructose-sweetened soft drinks has also been linked with an increased risk of gout. Alcohol (especially beer) also raises uric acid levels in the body and impairs the kidneys’ ability to excrete the buildup.

Everyone has some uric acid in his blood. Usually the excess uric acid is then passed out of the body through the urine. As your immune system tries to get rid of the crystals, inflammation develops. For the person with too much uric acid, this inflammation can cause painful arthritis.

More than 90 percent of people with gout have kidneys that don’t effectively get rid of uric acid. Sometimes this is caused by certain kinds of drugs, such as diuretics, cyclosporine, and low-dose aspirin. Other medical conditions, such as obesity, hypertension, and diabetes, can also make some people more likely to develop gout.

What can be done for those who suffer this disease? The first step is to make sure the person with painful joint symptoms has been properly diagnosed. Other joint diseases such as septic (infectious) arthritis or pseudogout can look like gout. In fact, it’s possible to have both gout and one of these other joint problems.

An accurate diagnosis depends on removing fluid from the joint and examining it under a microscope. The presence of urate crystals is the “gold standard” for making the diagnosis. Other imaging studies may be ordered such as X-rays, ultrasound, CT scans or MRIs. Each of these tests offers a little piece of information that helps define the location, severity, and extent of disease.

In many cases, a change in diet is enough to resolve the symptoms and the patient never has another attack. But untreated acute attacks can become chronic (long-lasting) with joint inflammation leading to joint destruction. Besides the metatarsal phalangeal joint (big toe), the ankles, knees, elbows, and small joints of the fingers can be affected.

What happens if symptoms don’t go away? The main goal of treating gout is to reduce the amount of urate in the blood. Joint crystals will not dissolve or go away unless the serum urate concentration is below six mg/dL.

Nonsteroidal antiinflammatory medications (NSAIDs) are used to combat the inflammatory process. Steroid-based anti-inflammatories called corticosteroids (oral by mouth or injected into the joint) can also be used to decrease swelling and relieve pain.

Another common medication that has been found effective with gout is called colchicine. Colchicine has an anti-inflammatory effect. It also inhibits urate crystal from forming deposits. Studies show that low-doses of this drug within 12 hours of an acute attack are very successful.

One other group of medications available to lower urate levels in the body is allopurinol. This drug is one of the serum uric acid (SUA)-lowering therapies. It works by inhibiting a substance called xanthine oxidase, which then reduces the production of urate.

Zyloprim is the brand name for allopurinol. Zyloprim does not take away the acute attacks of gout. But it is useful in preventing recurrence. Other allopurinol drugs on the market include Allohexal, Allosig, Progout, and Zyloric. As with all drugs, there are some patients who can’t tolerate allopurinol. They develop an itchy skin rash, severe diarrhea, and fever.

What’s new on the market for the pharmaceutical (drug) treatment of gout? New understanding of the exact mechanisms behind gout has led to the development of new agents for patients with refractory gout. Refractory means the symptoms won’t go away and the condition has become chronic and unmanageable.

These new treatments called uricase therapy aren’t available for use in the general public. They are just in the experimental stages. Drug companies are looking to find ways to use enzymes that convert uric acid into an acid that will be readily absorbed and passed out of the body. One of these enzymes is uricase. Humans don’t have this enzyme naturally but other animals do. The use of pig and baboon uricase called pegloticase therapy is under investigation and pending FDA approval.

Some researchers are using medications already on the market but used for other problems. This practice is referred to as off-label use. One drug in particular (rasburicase) normally used to break down cancerous tumors has been tested. It seems to work but it is very expensive ($8000) per dose so that won’t work if a patient is supposed to take it for a long time.

Right now uricase (biologic) therapy is an induction therapy, which means it is administered intravenously. Infusion reactions are holding things back a bit. At least 10 per cent of the patients receiving induction therapy experience severe adverse reactions including flushing, hives, low blood pressure, chest pain, and muscle cramping. It may be possible eventually to start with an intravenous dose, get the symptoms under control, and then switch to a pill form of the same medication to maintain results.

The future looks promising for gout sufferers. It seems certain that better understanding of purine metabolism will come to light in the very near future. Experts feel sure that it’s only a matter of time before scientists hit upon a pharmaceutical “cure” for cases of gout that can’t be managed otherwise with diet and exercise.

Do you suffer from the painful effects of rheumatoid arthritis (RA)? Or do you know someone who does — perhaps a close friend, loved one, or family member? If you answered ‘yes’ to either of those questions, then you will be interested in this update on medications to treat this problem.

Many new drugs are out on the market now specifically for rheumatoid arthritis. These medications have made it possible for many, many arthritis sufferers to experience remission.

Remission refers to the absence of any signs of the disease. No symptoms means improved function and increased activity. That is good news for anyone who previously couldn’t even zip up their own pants or pick up a cup of coffee.

Treatment for RA has changed quite a bit in the past 10 to 15 years. Studies show that patients get better results if their disease is treated early and aggressively. Early is easy to understand. What does ‘aggressively’ mean?

Aggressive treatment starts with the use of medications called disease modifying anti-rheumatic drugs or DMARDs. Many patients are familiar with the most commonly prescribed DMARD: methotrexate or MTX. MTX has been around since the mid-1980s. But it wasn’t always recommended right away because of concerns about toxicity. Only those patients with severe, advanced disease were given this drug.

Now we know that adverse responses to methotrexate (MTX) are much less than feared and the drug offers enough benefit to make it worth taking. Improved symptoms means better quality-of-life all the way around. And even better than that, disease modifying anti-rheumatic drugs (DMARDs) have been shown to slow and even stop joint destruction.

Today’s best care starts patients on methotrexate (MTX) right away. Aggressive treatment requires taking methotrexate (MTX) at increasing dosages over a period of three to six months until the patient has gotten the best (maximum) response. Response is monitored closely. Anyone who is not getting the desired or expected results by the end of six months’ time will be given another DMARD or possibly one of the newer biologic agents (more on biologic agents in a minute).

Monitoring patient response is considered a key part of the management process. Aggressive treatment calls for getting results early and quickly. The best way to know if the desired results are achieved involves measuring seven areas: number of tender joints, number of swollen joints, function, pain, patients’ perception of their own health, physician assessment of the patient’s progress, and lab values.

Lab values are useful because blood tests show levels of inflammation and changes in those markers as a result of taking meds. Physicians also have a tool called the disease activity score (DAS) to help monitor disease activity. It’s a bit cumbersome and complicated to use, so a newer (easier-to-use) tool called the RAPID3 instrument is being tested for validity and reliability.

In the past, a lack of response or less than optimal response would have meant stopping the MTX and starting a new drug. The approach taken was called monotherapy (one drug at a time). Now, physicians know the best next step is to combine drug therapies (combination therapy). The patient keeps taking MTX but adds a second DMARD such as sulfasalazine (SSZ) or hydroxychloroquine (HCQ).

If that doesn’t work, a biologic agent may be added to the mix. Biologic agents include etanercept, infliximab, adalimumab, and abatacept. These drugs fall into a category called tumor necrosis factor-alpha inhibitors or TNF-alpha inhibitors.

Many studies have shown that combining methotrexate (MTX), plus one other DMARD along with one of these biologic agents gives much better results than monotherapy with just one or the other. Taking all three types of medications is referred to as triple therapy.

About 85 to 90 per cent of all patients with rheumatoid arthritis are helped greatly by monotherapy with MTX, combination therapy with MTX plus another DMARD, or triple therapy with MTX, DMARD, and a biologic agent. That still leaves 10 to 15 per cent of patients who don’t respond facing a future of painful disability.

That sounds discouraging but the good news is that there are new medications coming out that have a different mode of action (MOA). New TNF-alpha inhibitors (abatacept, rituximab) and an interleukin-6 blocker (tocilizumab) are now available to try. And if those don’t work, more new medications are in the pipeline soon to be on the market.

In summary, rheumatologists and primary care physicians have new and improved tools to help treat patients with rheumatoid arthritis. Best care defined as “care you would give your mother” is the motto.

With the new disease modifying anti-rheumatic drugs and biologic agents on the market, Mom (and everyone else with this disease) can remain pain-free, active, and even disease-free for much longer than ever before. And that is the new “gold standard” of care!