The Detroit Tigers medical staff revealed that perennial quick-bat/quick-bat Gary Sheffield had two cortisone injections in both his shoulders earlier this week to help alleviate pain. He had a second injection in his right shoulder on Wednesday in an effort to help the healing process, according to baseball injury analyst Rick Wilton.
If the latest injection does not provide relief, perhaps he will get a third or face a trip to the disabled list. In any event, Sheffield's outlook does not appear good.
It's uncommon for a player to receive two injections in such short time period, intimating that Sheffield's shoulder discomfort and limited range of motion of the right shoulder is more serious initially assumed. There is some hearsay intimated in the Detroit area that he is considering retirement.
If one cortisone injection is good, and two are better, why not three, or four, or six? Like prunes for constipation, "two may not be enough, six may be too many" as the Hailey's MO commercial tagline used to go.
Cortisone is a popular word for a wide variety of injectable corticosteroids (e.g., triamcinolone, dexamethasone, betamethasone, methylprednisolone), anti-inflammatory medications that, when delivered by needle from a steady hand into the correct pinpoint area of the body, when clinically indicated, has the benefit of ostensibly producing maximum drug effect over a small concentrated area, avoiding adverse systemic effects.
To get the same effect systemically, taking the medication orally, one would have to ingest large doses of the same drugs, risking a wide variety of systemic effects.
Systemic corticosteroids cause weight gain. They elevate the blood sugar. They thin the bones, cause gastrointestinal bleeding, produced cataracts, atrophy the skin, and, in some people, result in florid psychosis. But injectable corticosteroids are not risk free and are no panacea for what ails you.
Because of the lack of well-controlled outcome studies, the multitude of target organs, and the complex interactions in the body, little is actually known about the exact mechanism of action of corticosteroids in each of the many disease states and conditions for which they are presently used. Even less is known for treatment of sports injuries because of the lack of accepted and reviewed studies. Corticosteroids have either a direct or an indirect effect on the metabolism of most tissues in the body. Their high lipid solubility allows their effect to occur systemically. This effect is mediated by the ability of corticosteroids to bind to appropriate receptors in cell nuclei and to initiate messenger ribonucleic acid translation.
During administration of a corticosteroid, it is found in all cells in the body, but effects are induced only in those cells that have its receptor. Corticosteroids usually reach a maximal effect at about 4 to 6 hours when administered orally and intravenously. Intra-articular administration, such as that applied to Sheffield's shoulder, yields an immediate maximal response with varying durations.
As illuminated by DeLee: DeLee and Drez's Orthopaedic Sports Medicine, Second Edition, one well-known mechanism is the role of cortico-steroids as anti-inflammatory agents. The inhibitory action of corticosteroids on inflammatory mediators is similar to that of NSAIDs (nonsteroidal anti-inflammatory drugs, e.g., ibuprofen). The site of action is one step before cyclooxygenase and lipoxygenase. Phospholipase A2 is responsible for the release of arachidonic acid from phospholipids. Corticosteroids inhibit this release by inhibiting phospholipase A2. The synthesis of prostaglandin, leukotriene, and thromboxane is inhibited by the administration of corticosteroids. Because of this blanket inhibition, corticosteroids are much more effective at decreasing inflammation than NSAIDs are. With this increased short-term efficacy, however, the corticosteroids cause more adverse effects.
Corticosteroids influence immunologically mediated disease states. Most notable is the ability to produce monocytopenia, lymphocytopenia, and neutrophilic leukocytosis. Two broad categories of effects on white blood cells are alterations in cell function and changes in their trafficking through the circulatory system. Transient cell movement occurs in lymphocytes and monocytes as the corticosteroids induce their redistribution out of the circulation and into their respective lymphoid compartments. 'T' lymphocytes are preferentially depleted over other lymphocytes. Cell function can be compromised in three ways: (1) depletion of a cell type can occur; (2) accessory cells are suppressed; and (3) direct suppression of the functional capacity of the cell occurs. Translation? The body's immune system is rendered incompetent resulting in an inability to respond to stress and disease.
Of the two means of delivery of corticosteroids—oral administration and local injection—sports injuries are mostly treated with local injections. Although they are excellent anti-inflammatory agents, oral corticosteroids do not have a proven efficacy for sports injuries because of the systemic effects and risks when they are used frequently. Two studies of intra-articular corticosteroid injections showed a decrease in the migration of labeled neutrophils (white blood cells) to inflamed joints. The exact mechanisms are unknown, but it is speculated that corticosteroids block the action of macrophage-inhibiting factor, which accounts for reduced vascular permeability, cell adhesion, and migration. Synovial membranes were also found to decrease secretion of interleukin-1 after the administration of corticosteroids. All this medical gobbly-gook and gibberish is not good (read: bad).
Orthopaedic surgeons frequently use intra-articular and extra-articular applications of injectable corticosteroids in an effort to treat both acute and chronic inflammatory conditions and pain related to sports injuries. Treatment foci have included cartilage, bursae, ligaments, and tendons. Additional targets are nerves and the joints in rheumatoid and osteo arthritis.
Intra-articular injections of corticosteroids are most commonly used in arthritis treatment, both inflammatory and noninflammatory (degenerative) types. The injections decrease both inflammation and concomitant swelling, which decreases pain and increases joint mobility. Specific results are based on the degree of weight-bearing that the joint withstands.
The larger weight-bearing joints, like the hip and the knee, do not react as well in the long term to corticosteroid injections because pain is usually derived from gravitational forces sustained by the joint in osteoarthritis. The injections do, however, provide some short-term relief in these conditions. The application sites for corticosteroid injections in ligaments are questionable but most commonly are the collateral ligaments of the elbow, the extra-articular ligaments of the knee, and the ligaments of the ankle. Actual injection is applied around the ligament and not directly into it.
Corticosteroid injections are used for their anti-inflammatory properties to reduce pain, to decrease recovery time, and to allow earlier mobilization. The inherent composition of ligaments poses a problem, considering that approximately 70 to 80 percent of their dry weight is composed of collagen, and corticosteroids are known to inhibit collagen synthesis.
Long-term studies have shown that there is no appreciable difference in treatment efficacy with or without injections. Short-term use decreases pain but does not sustain pain relief and in fact could cause weakening of the ligament and possible rupture. Again, there is no consensus on corticosteroid injection in ligaments, but it is usually not recommended.
Tendon injuries, including tenosynovitis and tendinitis, are common ailments that plague athletes and warrant corticosteroid treatment. The most common form is tendinitis, with inflammation usually occurring at the insertion site to bone. Tenosynovitis is inflammation of the fatty tissue or synovium between the tendon and the tendon sheath called the paratenon. Risk of tendon rupture after corticosteroid injections locally makes such use significantly less desirable.
The subacromial, greater trochanteric, olecranon, prepatellar, and retrocalcaneal bursae are common sites of corticosteroid treatment. Results depend on the site of application. Trochanteric and olecranon bursitis both respond well to injections. Injections into retrocalcaneal (Achilles tendon) and prepatellar (patellar tendon) bursae have had less promising efficacy and have been associated with tendon rupture. Nerve compression syndromes (e.g., carpal tunnel syndrome) and stenosing tenosynovitis (e.g., de Quervain's disease and trigger fingers) are also treated with injectable corticosteroids, usually after a trial of NSAIDs has failed.
The efficacy and the application of each corticosteroid preparation have been differentiated only by the solubility of each preparation in water. The more soluble the preparation, the shorter half-life the drug maintains; thus, for more chronic conditions, water-insoluble corticosteroids are more applicable for treatment. In addition, because of proximity to another potential source of inflammation and pain, like the patellar tendon and the prepatellar bursa, it is sometimes difficult to know which tissue is being treated. This is a problem intrinsic to injection therapy. In contrast, when corticosteroids are injected directly and accurately into an anatomic structure and complete pain elimination results, the diagnostic usefulness of local injection of corticosteroid preparations is clear.
Although corticosteroid injections are widely used by physicians, a consensus on applications, techniques, and dosages has not been reached. Most physicians rely on past experience as a guide. Much more investigation is needed in this area. The primary contraindication to corticosteroid injections is local infection of the area of concern. In such an instance, it is necessary to avoid direct inoculation of the affected joint and to allow the innate immune response to initiate clearance of the bacteria.
Because corticosteroids have an inhibitory effect on leukocyte function and the normal healing response, their use can be a problem in the presence of early or established infection. Other contraindications include true hypersensitivity to corticosteroids, existence of a joint prosthesis, and hemorrhagic diathesis.
Direct injection into a tendon or a ligament should always be avoided owing to the risk of tendon rupture. Poorly compliant patients should not receive corticosteroids because they have an inherent propensity to fail to follow any portions of a treatment plan. In the case of corticosteroids, rest is just as important as rehabilitation. Joint instability, anticoagulation therapy, poorly controlled diabetes, and adjacent abraded skin are also reasons to avoid corticosteroid treatment.
Adverse effects include local and systemic manifestations. Initial findings supporting systemic absorption of locally administered corticosteroids included beneficial effects in distant joints, increased metabolites in the urine, and transient eosinopenia. The most serious of the potential side effects is that at higher doses, such as would occur during treatment of multiple joints at the same time, the corticosteroids can inhibit the hypothalamic-pituitary-adrenal axis. This suppression occurred anywhere from two to seven days after injection. The stress response to hypoglycemia was also suppressed for 48 hours.
Some of the local effects have been alluded to in the section on indications; namely, both ligament and tendon ruptures can occur despite peritenon placement of the medication. Arthropathy, another result of injection treatment, is related to the reduction or elimination of pain with subsequent increased activity at the joint. The clinical presentation improves subjectively, but the objective evaluation shows further progression of the disease. This is why compliance of the patient is important in the use of corticosteroid treatment.
Other effects are avascular necrosis at the site of injection and distant joints, infection, postinjection flare, hypersensitivity reactions, cutaneous atrophy at the site of injection, and calcification of the joint capsule. Rare cases of necrotizing fasciitis and visual hallucinations have also been documented.
One relatively new manifestation is osteoporosis, which has been found secondary to the use of corticosteroids. Corticosteroids have been found to increase osteoclastic activity and inhibit osteoblastic activity, thus decreasing bone mass. The only differences from normal osteoporosis that occurs with age are that it occurs faster and in all ages. Because injectable corticosteroids are not administered in a constant manner, as oral corticosteroids are, they have not yet been implicated as the cause of osteoporosis.
We project that the reach for potentent corticosteroid medications, and for additional medications, for Mr. Sheffield does not bode well for his longevity. In 2008, if he does return to duty, Sheffield will be reduced to pinch hitting and occasional DH roles. His remaining days in uniform are most definitely numbered.