In addition to localizing pain to a certain joint with aide of diagnostic anesthesia, radiographs, ultrasound, computed tomography, magnetic resonance imaging (MRI) techniques and diagnostic arthroscopy have all be used to confirm causes of joint lameness. There is no “gold standard” for the diagnoses of preliminary joint disease in the horse as radiographic changes are usually indicative of irreparable harm.
Aggressive treatment in joint disease is indicated to decrease immediately soft tissue swelling and inflammation as well as to postpone the onset of permanent osteoarthritic changes. There is inherent difficulty in identifying joint pathology by any other means than subjective examination and lameness or “shortness of stride” reports from trainers.
Medications introduced into joints by human physicians that specialize in sports medicine are becoming more commonplace. Previous generalizations and perpetuation of myths about damage to joint environments caused by corticosteroids are primarily unfounded.
Damage may occur from excess corticosteroid injections or when there is cartilage fragmentation and bone alterations in a joint, usually associated with lameness. It has been proven that corticosteroids and HA together allows the natural synovial lining of a joint to make a more favorable environment.
All of these products are labeled for intra-articular use insuring purity and consistency with each individual manufacturer. Arteparon is the human equivalent to Adequate and the chemical structure of the two products is identical.
Chondroitin sulfate is the most commonly used GAG in these products and is harvested from bovine lung and trachea. Chondroitin sulfate, glucosamine, MSM and various other Gags can be found in many oral supplements, none of which are regulated by the Federal Drug Administration.
Small amounts of glucosamine can detect in the bloodstream of horses, but no deficiency has ever been reported, in any species. A number of test-tube studies have shown that glucosamine has biological activity, and various beneficial effects on cartilage cells.
While this should be great news, it should be noted that these studies have generally been conducted with levels of glucosamine that can’t be reached when the substance is fed to horses. Chondroitin sulfate (CS) is a sugar molecule found in cartilage, bone, tendons, and ligaments.
Some people have suggested indirect effects, due to elevated levels in the intestine, or in the liver, but this is just speculation, and hasn’t been demonstrated. This, of course, means that you unless you know specifically what’s in the product you’re feeding to your horse, you can’t anticipate any positive result.
While there’s a large amount of conflicting evidence, from many species, three clinical trials have looked at the combination of glucosamine hydrochloride and CS specifically in horses. This class of drug gained much fame, or infamy, as it is commonly used in racehorses with arthritis and has been blamed for many injuries post- injection.
As we mentioned earlier, enzymes that are produced by diseased or inflamed joints are very destructive to normal cartilage. Joints that are inflamed must be treated with anti-inflammatory medication, as well as HA in some instances, to allow them to return to their normal environment.
It was once said that a “human on corticosteroids can walk to the autopsy room” but now most orthopedic surgeons use these products in the most famous athletes in the world. Substantiation for a direct link between corticosteroid administration and arthritis has persistently been unable to prove by dozens of investigators.
U formation is becoming more recognized as a common occurrence in all breeds of horses due to stress and NSAIDs definitely can contribute to this process If the lameness resolves after injection, it is likely that the joint that was injected is the source of the horse's pain.
When your veterinarian makes a call to inject your horses' joints, they will go through several steps before they are ready for the procedure. Your veterinarian will find the location of the joint and quickly but carefully insert a needle.
(Figure 2) When using joint injections as a treatment for your horse, it is important to know the advantages and possible disadvantages of the procedure. Likewise, hyaluronic acid can be used with a steroid to protect the ever important cartilage within the joint.
There is a cost associated with joint injections, but it is often small compared to the effect they can have on your horse's performance. Sometimes a joint “flares” after injection, which is caused by inflammation that occurs secondary to the injection.
Any time you put a foreign object into the body there is a risk of infection, and this is possible with joint injections. However, your veterinarian uses precautions such as scrubbing the skin thoroughly and sometimes injecting antibiotics into the joint at the time of treatment to prevent infection from occurring.
Joint injection is a very important procedure used in veterinary medicine to localize lameness or medicate a joint associated with pain, swelling, and inflammation. Being aware of the uses and side effects of the procedure is vital information for any horse owner.
The most common complications encountered after joint injections are septic arthritis, flare reaction (aseptic acute synovitis) and particular cellulitis. Because of the overlap in changes in synovial fluid between septic arthritis and flare reaction, it is recommended to submit culture samples in all cases.
The overall incidence of post- injection septic arthritis has recently been reported to be 0.092% based on a large sample size of cases, which includes a 0.091% incidence for local anesthetic, 0.161% for corticosteroids, 0.159% for hyaluronic acid (HA) and 0.394% for polysulfide glycosaminoglycans (e.g. Adequan-Luitpold Pharmaceuticals).1 Despite the low incidence, septic arthritis can have potentially devastating effects on the patient, making early recognition and treatment of great importance. Post- injection septic arthritis is diagnosed based on clinical signs, radiography and ultrasonography (if indicated), and cytology and culture of the synovial fluid.
Chemical synovitis, often referred to as joint flare, can occur in response to the injection of corticosteroids, local anesthetics, HA and polysulfide glycosaminoglycans. After serial arthrocentesis and injection of local anesthetic, gentamicin sulfate, ceftiofur sodium or niacin, clinicopathologic values (NCC, percentage of neutrophils and total protein concentration) in the synovial fluid of equine joints increase to greater than reference ranges and can approach values suggestive of septic arthritis.5 Thus, prior sampling and treatment may complicate interpretation of synovial fluid analysis.
Early onset of clinical signs (around 24 hours), a synovial NCC less than 30 × 109/L, and resolution within one to three days have been suggested to be helpful in differentiating chemical synovitis from septic arthritis.8 Clearly, overlap with the findings expected with septic synovitis may still occur, and repeated lameness examinations and follow-up sampling are appropriate. Marked lameness and synovial effusion can occur with a nonseptic flare, so acute synovitis after arthrocentesis is best treated as septic arthritis if doubt exists.
The overlap among clinicopathologic values in septic synovitis with a low NCC (as may occur in early septic arthritis), septic arthritis resulting from corticosteroid injection into a synovial structure or infection with an organism of low virulence, and nonseptic arthritis that can occur secondary to trauma or therapeutic intervention (e.g. synoviocentesis alone, injection of medications) can make differentiating among these diagnoses impossible. My and others' clinical experience suggests that concurrent systemic NSAID administration helps reduce the risk of flare reactions after joint injections.
Occurrence of particular cellulitis is rare afterjointinjection, but it should not be overlooked when diffuse swelling of the area surrounding the injection site develops. Typically, horses with cellulitis have marked swelling around the area of injection that may spread to surrounding regions and lameness of the affected limb.
The swelling is normally hot and painful on palpation, and sometimes pitting occurs when digital pressure is applied to the affected area. On ultrasonographic examination there is marked thickening and increased echogenicity of the subcutaneous tissue, sometimes accompanied by fluid pockets associated with the injection sites.
Conservative treatment consisting of supportive local treatment (bandages, cold water therapy) and systemic NSAIDs and antibiotics (selected based on bacterial culture and susceptibility testing of the fluid obtained from the fluid pockets identified with ultrasound) should result in gradual improvement over five to seven days. The three most common problems associated with intra-articular injection in horses are septic arthritis, flare reactions and particular cellulitis.
These conditions can be difficult to differentiate from one another, but early recognition, use of the appropriate diagnostic aids and prompt treatment will result in an increased likelihood of successful outcome. In addition to surgery, he also enjoys the challenges of lameness diagnosis, sports medicine and multiple types of imaging.
Infectious arthritis following intra-articular injection in horses not receiving prophylactic antibiotics: A retrospective cohort study of 2833 medical records, in Proceedings. Alamo RM, Rampage LR, Label AA The influence of corticosteroids on sequential clinical and synovial fluid parameters in joints with acute infectious arthritis in the horse.
Schneider OK, Rampage LR, Moore RM, et al. A retrospective study of 192 horses affected with septic arthritis/tenosynovitis. A good understanding of distal limb anatomy is necessary to successfully place and interpret intrasynovial anesthesia.
Accuracy of needle placement can be ensured in most cases by aspirating synovial fluid before infusion; if this is not possible, local anesthetic solution should be instilled slowly with minimal resistance and, when pressure is released from the syringe, it occasionally refills. Skin preparation is critically important when undertaking intrasynovial diagnostic anesthesia to minimize the risk of iatrogenic sepsis.
The needle should be introduced at approximately 80 degrees to the skin in a proximodistal direction into the proximal recess of the joint to avoid damaging the articular cartilage. Synovial fluid should be appreciated in the needle hub and the injection of local anesthetic should be without resistance (Fig 1 a).
The author prefers the midline approach into the coffin joint, where synovial fluid is commonly obtained (Passage and Ross 2011). Palmer/plantar approach With the limb flexed, the landmarks for injection are the palmarolateral/anterolateral aspect of the middle phalanx, proximal and dorsal to the apex of the lateral collateral cartilage.
The needle should be advanced in a proximolateral to medial–distal direction so that it stays close to the Palmer/plantar middle phalanx and avoids the particular bursa (Fig 1 b). It is thought that, after five minutes, the effect of the block is specific to the DIP, but the author has seen cases with particular bursa pathology that have improved five minutes after the injection, so it is important to compare the response to DIP anesthesia with the response to anesthesia of the particular bursa.
The proposed explanation for this is that the Palmer/plantar digital nerves pass close to the Palmer/plantar pouch of the DIP joint. After 30 to 40 minutes, maximal diffusion to surrounding structures (particular bursa, deep digital flexor tendon and sole) will have occurred and any further improvement is unlikely.
It provides lubrication and cushioning to the DDT as it passes around the particular bone to insert on the Palmer/plantar aspect of the distal phalanx. The skin at this site is desensitized first with a subcutaneous blew of local anesthetic; the author also routinely uses a twitch.
The spinal needle is introduced with the limb held up, aiming 1 cm distal to the coronary band halfway between the dorsal and Palmer/plantar walls of the hoof (Fig 2). As the needle is advanced and passes through the DDT, resistance can be appreciated; the horse can show resentment at this stage.
If the needle is in the correct location, the Palmer/plantar aspect of the particular bone should be encountered with firm resistance. The needle is introduced 1 cm proximal to the coronary band, between the heel bulbs in a Palmer to dorsal direction, aiming slightly distally to a point 1.5 cm distal to the coronary band, halfway between the dorsal and Palmer hoof walls.
Interpretation The horse should be re-evaluated promptly after the injection (within 10 minutes) when the block has the highest specificity to the bursa only. Dorsal approach With the limb in a weight bearing position, the needle should be introduced from the lateral aspect in an axial and slightly distal direction at the level of the lateral condole of the proximal phalanx, approximately 3 cm proximal to the coronary band (Fig 4 a).
Palmer/plantar approach With the limb held in flexion, the needle should be introduced immediately Palmer/plantar to the condole of the proximal phalanx, in an axial/distal direction in a small angle formed by the Palmer/plantar border of the proximal phalanx and the superficial digital flexor tendon branch (Fig 4 b). It is important to introduce the needle immediately Palmer/plantar to the proximal phalanx to avoid inadvertent penetration of the digital flexor tendon sheath (DOTS).
This approach also runs the risk of inadvertent anesthesia of the biaxial Palmer/plantar nerve as a result of back leakage from the joint. Interpretation As with any intrasynovial anesthesia, the horse should be re-evaluated 10 and 40 minutes after the injection before further nerve blocks are applied.
The needle is directed distally and axially under the common digital extensor tendon (Fig 5 a). It is often tempting to perform synoviocentesis and inject local anesthetic into the distended fetlock joint at this prominent out pouching.
However, the adjacent large venous plexus frequently results in intra-articular hemorrhage and joint sample contamination (Fig 5 a). With time, particular structures become desensitized, including DeSantis of the suspensory ligament branches (particularly when these involve dorsal tears or avulsions from the apex of the sesamoid bone).
Fig 6:Four commonly used injection sites for diagnostic anesthesia and synoviocentesis of the digital flexor tendon sheath With the limb in a non-weightbearing position, the needle should be introduced into the out pouching at the abaxial aspect of the base of the sesamoid bone in a palmarodistal/plantarodistal to dorsoproximal direction and 1 cm Palmer/plantar to the neurovascular bundle.
Interpretation A recent study compared these sites for their ease of injection into the sheath and their proximity to the Palmer/plantar nerve (Jordana and others 2012). The authors note that regional anesthesia of the Palmer/plantar nerves is frequently required to completely abolish lameness originating from tears to the Manila Flexeril.
Fiske-Jackson and others (2013) also aimed to predict Manila Flexeril tearing by injecting contrast material into the sheath at the time of intrathecal analgesia and subsequently evaluating a anteromedial radiograph of the DOTS to establish the Manila Flexeril's silhouette relative to the proximal sesamoid bones and DDT. Fig 7:Lateral radiograph of the fetlock joint and contrast genogram of the digital flexor tendon sheath.
(a) The radio dense line (arrows) indicates the correct position of the Manila Flexeril within the proximal sheath. If the lameness is localized to the foot, a complete blocking profile (including anesthesia of the DIP joint and particular bursa) is recommended before advanced imaging to allow better interpretation of the detailed findings provided by these modalities.
This should be performed a minimum of 10 days after diagnostic anesthesia to prevent artefactual increases in radio pharmaceutical uptake.