The variety of rheumatoid disorders can be daunting, and pulling information together to tell them apart is challenging. In this episode, David covers osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, reactive arthritis, septic arthritis, and gout. After discussing each, the conditions are contrasted for easier recognition of clinical features.
For more information on rheumatoid disorders, we recommend hopkinsarthritis.org.
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Hello everyone and thanks for joining us again. Today’s episode will focus on providing an overview of how to distinguish between various forms of arthritis and inflammatory conditions. These are conditions that we see a lot as physical therapists, and as direct access is increasing, we need to be proficient at distinguishing between these conditions. Today we’re going to focus on the biggest rheumatoid disorders: osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis. At the end, we’ll briefly mention a couple others, including reactive arthritis, septic arthritis, and gout.
First, osteoarthritis. As orthopedic physical therapists, OA is probably what we are most used to seeing, and it is the most common form of arthritis. OA is characterized by degeneration of articular cartilage, reduced ability for chondrocytes to repair articular cartilage, inflammation of the synovium, and changes to the subchondral bone. It’s most common in the large, weight bearing joints of the body, like the knees and hips, but it can also occur in the hands and spine. It’s less common in the ankles, elbows, wrists, or shoulders, but it might present there if the individual has additional risk factors or a history of trauma in those joints. The presentation of OA is going to vary a bit depending on what joint it affects, and we have a whole CPG dedicated to hip OA, so we’re definitely going to come back to address OA more in the future. Right now, here are the highlights.
OA is typically asymmetric, so it’s not uncommon for someone to have OA and pain in the right knee but no problem in the left. Osteoarthritis becomes more common as people age, and it’s typically seen in men older than 50 and women older than 40. Female sex, obesity, history of occupation-related repetitive injury or trauma, and genetics are all risk factors. OA can either be primary with a gradual, insidious onset, or it can be secondary to an injury or an infection. People with OA tend to report pain and stiffness first thing in the morning that lasts less than 30 minutes, and they will report that the stiffness improves as they move around. You should know that this 30-minute stiffness is not a hard and fast rule, especially as the disease progresses, and the hip OA CPG uses “less than 1 hour” as the guideline for OA in the hip. Although there are therapeutic effects to movement and exercise with osteoarthritis, people with OA will typically report pain with activities, especially activities that are weight bearing. So those with hip and knee OA will report the pain is aggravated by activities like stairs, and those with hand OA will describe pain with fine motor or hand tasks. Pain is relieved by rest. Crepitus and joint effusion may be present, but effusion with OA is typically cool and not boggy, which makes it different from some other types of arthritis.
OA is typically diagnosed with a combination of exam findings and radiographs. Bone spurs are the most specific finding on radiographs for osteoarthritis, but it’s uncommon to see bone spurs early in the disease process. Joint space narrowing and subchondral cysts may also be noted on imaging in those with OA.
I’ll note one more key feature of OA and then we’ll move on. When OA affects the hands, it most often affects the 1st CMC joint. It can also affect the DIPs and the PIPs—but it typically spares the MCP joints. So, one more time: OA typically affects the 1st CMC, the DIPs, and the PIPs, but it rarely affects the MCPs.
We’ll definitely be returning to OA in future episodes, especially as we start to cover the hip CPGs. If you’re eager to do more review of OA, allow me to recommend Gail Deyle’s knee OA course on MedBridge. He really does a great job handling knee OA in that course.
Let’s move onto the second most common rheumatic disorder, RA. Rheumatoid arthritis is a chronic, systemic, inflammatory disease with spontaneous remissions and exacerbations. It’s an autoimmune disorder that, unlike OA, causes primary tissue inflammation. Although there is a form of RA that affects children, juvenile RA, rheumatoid arthritis usually first affects people in their 20s to 50s. Women are affected two to three times as often as men. RA typically involves swelling of the small joints, especially in the hands and feet, but it can affect most joints in the body. The most frequently involved joints are the PIP and MCP joints of the hands, while the DIP joints are typically spared. (Remember that this is different from OA, which affects the DIP but spares the MCP.) In RA, the wrists, shoulders, elbows, knees, ankles, and cervical spine—especially the AA joint—can also be affected, but the rest of the spine is often unaffected. (Speaking of the AA joint, you should recall from physical therapy school that RA is associated with upper cervical spine ligamentous instability, so watch out for cases of cerivical myelopathy in patients with RA, or complications following a poorly planned cervical manipulation.)
Unlike with osteoarthritis, people who have rheumatoid arthritis will typically report morning stiffness lasting greater than 1 hour; in fact, the stiffness might last for several hours after waking or after a period of being sedentary. Early on in the disease, complaints may be isolated to one or just a few joints, but RA almost always progresses to involve five or more joints. Early on, presentation may be asymmetrical, but it typically progresses to a symmetrical presentation. During RA flare ups, individuals may have a low grade fever of 99 or 100 degrees Fahrenheit. These flare ups can also be associated with synovitis of the affected joints that presents with swelling and heat. Palpation of inflamed joints will often reveal spongy or doughy swelling, unlike the bony enlargement that is seen in OA.
RA is also different from OA in that it often involves multiple systems. Fatigue, malaise, and depression may commonly precede other symptoms of RA. Weight loss is common. Subcutaneous nodules occur in 20-30% of cases—usually on the extensor surfaces of the arms and elbows. RA may involve cardiac problems, including pericarditis and myocarditis. Atherosclerosis is the most common cardiac manifestation of RA, and it’s the leading cause of death among RA patients. There are also several possible pulmonary manifestations, including pleurisy and pulmonary fibrosis. Dry eyes is a common complaint. About 10-15% of RA patients also develop Sjogren’s syndrome, which is an autoimmune disorder that affects exocrine glands, leading to a decrease in tear and saliva production. Less commonly, RA can be associated with Felty’s syndrome, which is characterized by splenomegaly and leukopenia, leading to recurrent infections.
I know that’s a lot of information, so I’ll take a quick break to recap the highlights that make RA different from OA: RA is an autoimmune condition that involves primary tissue inflammation. Unlike OA, it typically starts with smaller joints, like the upper extremity joints, and is often symmetric in presentation. Often, five or more joints are involved, and RA can affect most joints in the body, but tends to spare the DIP joints and the lumbar and thoracic spine. Patients report stiffness that lasts greater than 1 hour, and multiple systems can be involved, including the cardiac and respiratory systems.
Like with OA, a diagnosis of rheumatoid arthritis is not made with a single lab test. 70-80% of patients with RA will have positive rheumatoid factor. A test for anti-CCP antibodies is actually more specific for RA than rheumatoid factor, though I personally see it less often. Rheumatologists may use other tests to aid in their diagnosis, but I would only expect positive rheumatoid factor or anti-CCP to possibly show up on the OCS exam. After all, we’re physical therapists, not rheumatologists.
And speaking of rheumatologists, let’s quickly address medical management of RA. Typically, medical management will involve the use of disease modifying anti-rheumatic drugs. The most commonly prescribed is methotrexate. NSAIDs may also be used for short-term pain relief.
And that about covers rheumatoid arthritis. Let’s move on to ankylosing spondylitis. Ankylosing spondylitis is a chronic inflammatory disease that primarily affects the axial skeleton. Individuals with AS are typically in their teens or twenties when symptoms first present; it is very rare for symptoms to first appear in individuals older than 40. Men are affected twice as often as women. One of the first symptoms is usually enthesis pain, so patients might initially complain of symptoms that resemble insertional Achilles tendonitis or plantar fasciitis. Ankylosing spondylitis almost invariably affects the thoracic spine, but it is also typically affects the lumbar spine, cervical spine, and SI joints. Individuals with AS will often present with a chief complaint of low back pain due to the spine arthritis or sacroiliitis. In AS, the sacroilitis is usually symmetrical. Although it’s less common, AS can progress to involve more peripheral joints as well, including the lower extremity joints and the shoulders. These peripheral joints are usually affected in an asymmetrical pattern, and when arthritis in these joints appears early in the disease progression, it is predictive of a poorer long-term prognosis. Ankylosing spondylitis may also cause uveitis, which is a type of eye inflammation that causes the eyes to appear red, and it can affect the aorta, causing aortitis, and, less commonly, cause cardiac arrhythmias.
Since we are most likely to see these patients with a chief complaint of back pain, let’s talk about that back pain for a minute. In ankylosing spondylitis, back pain follows an inflammatory pattern where it is worse at rest and improves with activity. Those with AS will often wake up during the second half of the night—between 2 and 5 AM—due to back pain. Morning stiffness usually lasts longer than 30 minutes, and exercise relieves the symptoms. Symptoms typically start at the low back and progress to the thoracic and cervical spine. The vertebrae gradually fuse together, causing a characteristic “bamboo spine” finding on radiographs. Fusion can affect the ribs at the thoracic spine and at the sternum, so chest excursion is limited. When taking a deep breath, chest excursion—which is measured at the 4th intercostal space—should be at least 5 cm. A finding of less than 2.5 cm is highly specific for ankylosing spondylitis.
The treatment of choice for those with AS is combination of physical therapy and NSAIDs. Other medications, such as disease-modifying anti-rheumatic drugs, may be used as well. Since people with AS will typically end up with a fused spine with decreased lumbar lordosis and excessive thoracic kyphosis, physical therapy is focused on maintaining as much mobility as possible—and especially maintaining thoracic extension. As the disease progresses, PT will focus less on mobility and more on maximizing function with ADLs.
Before I move on to psoriatic arthritis, I want to summarize a couple ways that ankylosing spondylitis is diagnosed. I expect this material to show up at least once on your exam, so if you missed everything I just said about ankylosing spondylitis, pay attention to this.
Ankylosing spondylitis does not have a single lab test that confirms the diagnosis. However, there is a strong association between AS and the human leukocyte antigen B27 gene, also called HLA-B27. To be clear, most people who are positive for HLA-B27 do not have ankylosing spondylitis. But if a person is HLA-B27 positive and has symptoms that fit ankylosing spondylitis, the positive test greatly aids diagnosis. When rheumatologists are making a diagnosis of ankylosing spondylitis, one of the criteria they use involves the following: back pain for at least 3 months, less than 45 years old, HLA-B27 positive, and at least one feature of spondyloarthropathy, such as inflammatory back pain, enthesitis, family history, or a few other less important features. So if, on the exam, you have a case that causes you to suspect ankylosing spondylitis, and the question asks you what lab test you want to request from the physician, you’re looking for HLA-B27.
And what would that case look like on the exam? Well we have two validated clinical prediction rules to help recognize ankylosing spondylitis. The first has four criteria: morning stiffness greater than 30 minutes, improvement in back pain with exercise but not with rest, awakening because of back pain during the second half of the night only, and alternating buttock pain. If you see three or four of these criteria, you should increase your suspicion of AS. The second clinical prediction rule has five parts: age at onset less than 40 years old, insidious onset, improvement with exercise, no improvement with rest, and pain at night with improvement on getting up. We’re looking for at least four positives here. You can see how we’re basically just describing the unique features of ankylosing spondylitis in these clinical prediction rules, so if you know the key features of the condition, you know the clinical prediction rule, and vice-versa.
Okay, that’s enough about ankylosing spondylitis. Let’s talk about psoriatic arthritis. Psoriatic arthritis is an autoimmune disease associated with the chronic skin condition psoriasis. The cause of psoriatic arthritis is unknown, but there’s a clear genetic component. The same genetic marker seen in those with ankylosing spondylitis, HLA-B27, is present in about 60% of people with psoriatic arthritis. Psoriatic arthritis is equally common in men and women, and peak age for developing psoriatic arthritis is between 30 and 40 years old. Psoriatic arthritis can manifest in a number of patterns. I don’t think you need to know these specifically, but I’ll mention a few of them. It can manifest as distal joint disease, primarily affecting the DIPs of the hands and feet but also affecting the PIPs; it can present as asymmetric oligoarthritis, affecting several peripheral joints in an asymmetrical pattern; or as polyarthritis, affecting many joints still in an asymmetrical pattern about half the time; or as arthritis mutilans, which is a severe and destructive form of psoriatic arthritis that causes bone breakdown and joint dissolution, particularly in the hands. Arthritis mutilans has some characteristic radiological findings, which we will talk about in a minute.
When psoriatic arthritis affects the sacroiliac joints, it tends to be asymmetric. This distinguishes psoriatic arthritis from ankylosing spondylitis, which tends to affect the SI joints symmetrically. Individuals with psoriatic arthritis tend to have less tenderness to palpation on the affected joints than is seen in RA, which helps distinguish it from rheumatoid arthritis. Additionally, more than 80% of individuals with psoriatic arthritis have nail lesions, which further aids in diagnosis. Other clinical features that may be present include dactylitis (or swelling of the fingers or toes), tenosynovitis, enthesitis (like is seen in ankylosing spondylitis), iritis (inflammation of the iris, which sometimes leads to vision loss), urethritis (inflammation of the urethra causing painful urination), cardiac arrhythmias, and gastrointestinal problems, including inflammatory bowel disease.
The diagnosis of psoriatic arthritis is complex, so we’re not going to get into all the specific criteria, but you should be able to pick up on psoriatic arthritis based on the information we just discussed. A combination of psoriasis, nail lesions, polyarthritis affecting the DIPs, and any of the other features we listed should help you recognize this form of arthritis. Also remember that, like with ankylosing spondylitis, enthesitis may be present, so you might need to recognize when psoriatic arthritis could be the underlying cause behind Achilles tendon or plantar fascia complaints.
Treatment is also complicated since there are so many different presentations. Anti-inflammatory and disease-modifying medications may be used. PT is often used for strengthening, anti-inflammatory purposes, and to manage the tendon and tenosynovitis issues that pop up.
I think that covers most of what you need to know about psoriatic arthritis. I want to talk for a second about radiological findings seen with arthritis mutilans. Now we discussed that arthritis mutilans is one presentation of psoriatic arthritis, but you should also know that it can occur with severe rheumatoid arthritis as well. The bone breakdown at the finger joints in arthritis mutilans causes specific radiological findings. The OCS exam occasionally likes to throw some radiological terms at you to see if you know what condition the terms are associated with. In arthritis mutilans, the bone breakdown and joint dissolution in the fingers can cause a “pencil-in-cup” deformity, where the eroded and collapsing IP joint looks like a pencil going into a cup. This collapse can cause a telescope-like recession of the fingers, called, “telescoping fingers,” or, “opera glass hands.” You should know that these terms are characteristic findings in of arthritis mutilans, which may be present with severe psoriatic or rheumatoid arthritis.
So we’ve covered OA, RA, ankylosing spondylitis, and psoriatic arthritis. Before we wrap up, I want to give very brief summaries of a few other types of arthritis you might see.
First, reactive arthritis. Reactive arthritis is an inflammatory arthritis that follows a bacterial infection. Most often, the infection is a GI infection or a urogenital infection. These infections are commonly—though not always—acquired from tainted food, such as a salmonella infection, or through a sexually transmitted infection, like chlamydia. Typically, the inflammatory reaction occurs 2 to 4 weeks after infection, and it can affect one or a few joints. Presentation is typically asymmetric, and the most commonly affected joints are the knees, ankles, and feet, but fingers and wrists can sometimes be affected as well. One form of reactive arthritis is Reiter syndrome, which is a triad of arthritis, conjunctivitis, and urethritis. One mnemonic device that has been proposed to help recall the symptoms of Reiter syndrome is, “Can’t see, can’t pee, sore knee.” These individuals also tend to be positive for HLA-B27 and have enthesis inflammation. So reactive arthritis shares some features with ankylosing spondylitis and psoriatic arthritis, except that it is connected to an infection, it doesn’t present with thoracic and rib stiffness like ankylosing spondylitis, and it shouldn’t involve psoriasis or nail lesions like in psoriatic arthritis.
Next, septic arthritis. Septic arthritis is also caused by a pathogen in the blood stream. But while reactive arthritis is an inflammatory response to an infection somewhere else, septic arthritis is an infection that has moved into the joint itself. It is more common in people who already have another form of arthritis and in those on immunosuppressive drugs. It occurs more often in children than in adults. The infection can start in a variety of ways, including through surgery, through skin puncture, as secondary to a GI infection, or as secondary to a nearby skin infection. In septic arthritis, pain is usually severe and accompanied by spasms. Individuals may have a fever, and joint swelling, redness, and tenderness. Joints are often held in an open packed position; for example, in children with septic arthritis of the hip, it’s very typical to find them maintaining hip abduction and external rotation. Individuals with septic arthritis may be unwilling or unable to bear weight on the joint. Septic arthritis is potentially life-threatening, so it’s important to catch it quickly. To help confirm the presence of septic arthritis, physicians may look for an elevated ESR or elevated white blood cell count.
Finally, let’s cover gout. Gout is possibly the oldest documented form of arthritis. It used to be known as “the disease of kings” because of its association with rich food. Gout is an inflammatory response to uric acid crystals that form due to high uric acid levels in the blood. Onset is usually sudden and occurs during the night or in the early morning. The affected joint is typically warm, swollen, red, and painful. Fever, chills, and malaise may accompany an episode of gout. The first MTP joint—meaning the MTP joint of the large toe—is most commonly affected, though the shoulder, knee, wrist, ankle, elbow, or fingers can be affected as well. The high levels of uric acid which cause gout can either be due to decreased renal clearance—for example, in the case of kidney disease—or increased uric acid synthesis due to diet. Foods that may contribute to high levels of uric acid include: alcohol, hearts, herring, mussels, yeast, smelt, sardines, sweetbreads, anchovies, grouse, mutton, veal, bacon, liver, salmon, turkey, kidneys, partridge, trout, goose, haddock, pheasant, and scallops. In other words, if you can imagine a 12th Century European king eating it, then it’s probably something that can cause elevated levels of uric acid.
Okay, as we wrap up, let’s tie some of this together by comparing the major forms of arthritis side by side.
One differentiating feature is where the arthritis occurs. OA typically occurs in the weightbearing joints or in the DIPs and PIPs—but it spares the MCPS—and it typically presents in an asymmetrical pattern. RA more frequently affects the small joints, like the wrist, and it affects the PIPs and MCPs—but spares the DIPs. Also, RA often presents symmetrically, and joints tend to be more swollen, doughy, and tender during a flare up. Ankylosing spondylitis primarily affects the SI joints and spine, though it can often affect the lower extremity joints and the shoulders as well. It tends to affect the SI joints symmetrically, while psoriatic arthritis tends to affect the SI joints in an asymmetrical pattern. When psoriatic arthritis affects the hands, it tends to affect the DIPs and the PIPs, like OA does.
Another way to help distinguish types of arthritis is by the pain pattern. People with OA report morning stiffness that improves in less than 30 minutes or less than an hour—depending on the joint or disease progression. People with RA report stiffness that takes longer than an hour to improve. And individuals with ankylosing spondylitis report stiffness that tends to wake them up during the second half of the night, takes longer than 30 minutes to improve, and is relieved by exercise.
And lastly, you should recognize extra-articular signs and symptoms associated with each type of arthritis. With OA, we don’t see many symptoms outside of the affected joint. In RA, we may see fever, fatigue, cardiac conditions, and lung conditions. In both ankylosing spondylitis and psoriatic arthritis, we see enthesis pain, potentially some aorta inflammation or cardiac arrhythmias, and potentially some eye conditions causing eye redness. In psoriatic arthritis specifically, we can also see nail lesions, dactylitis, and tenosynovitis.
I know this was a lot of information, and there’s always more to learn and know. But I think this is more than enough to get you ready for what you might see on the OCS exam. If you really want to learn more, I want to particularly recommend the Johns Hopkins Arthritis Center, which can be found at hopkinsarthritis.org. It has a lot of great, straightforward information written at a level that is appropriate for a healthcare provider like yourself. And if you’d like a chart summarizing this information, I’m going to be working on getting one posted to our Physio Field Guide Patreon page. As always, thanks for your attention and support, and you can expect to hear from us again soon.