Unexplained Lameness

Chapter 12 Unexplained Lameness



Lameness diagnosis is a never-ending challenge, even for an experienced clinician, because despite a logical and thorough investigation it still may prove difficult to reach a satisfactory conclusion. This chapter discusses some of the reasons why a definitive diagnosis may remain elusive. In some horses it may be possible to isolate the source of pain reasonably accurately, but it may not be possible to determine the cause of pain. In other horses the source of pain cannot be determined (see Chapter 97).



False-Negative Responses to Diagnostic Analgesia


A false-negative response to local analgesic techniques may occur for a variety of reasons, including the following:













The following are common case examples:








Failure to allow sufficient time may in some circumstances result in a false-positive response and then confusion. The tibial and fibular nerves are relatively large, and it takes time for the local anesthetic solution to diffuse into them and to take effect. This time requirement, combined with the deep location of the deep fibular nerve and thus difficulty in precisely locating the site for injection, may result in a response delayed for up to an hour after injection. Testing the efficacy of these blocks through evaluation of cutaneous sensation is unreliable. If the response is deemed to be negative after 30 minutes, and intraarticular analgesia of the compartments of the stifle is then performed and the lameness improves, it may be wrongly inferred that pain originated in the stifle. However, the improvement in lameness may reflect alleviation of pain arising from the hock region. Much wasted time and money may then be spent trying to establish a cause of stifle pain.


Blocking each compartment of the stifle joint separately (e.g., the medial femorotibial joint) may not result in substantial clinical improvement in the lameness, despite the presence of stifle pain. A considerably better response is frequently seen after blocking the medial and lateral femorotibial joints and the femoropatellar joint in combination.


The importance of the clinical examination and repeated observations of a horse cannot be overemphasized. Each clinician has to learn how much to trust nerve blocks. This depends on experience and the frequency of performing blocks. An inexperienced clinician is far more likely to encounter false-negative responses. The results of nerve blocks must be compared with the clinical signs, and if the interpretation is doubtful, the block should be repeated or the area desensitized with a different technique. The clinician must develop experience in the interpretation of improvement in lameness compared with complete alleviation of pain and lameness. This contrast depends to some extent on the degree of the baseline lameness and whether the forelimbs or hindlimbs are involved.





Sources of Pain That Cannot Be Desensitized by Nerve Blocks


Many regions of the limbs proximal to the carpus and tarsus cannot be satisfactorily desensitized. In young horses, stress fractures are now well-recognized causes of lameness that pain from which in many circumstances cannot be blocked out. In young or older horses, fractures of the deltoid tuberosity of the humerus (Figure 12-2), the proximal aspect of the fibula (Figure 12-3), the third trochanter of the femur, and the tuber ischium (Figure 12-4) are all causes of lameness that are unaffected by nerve blocks.





Muscle injuries, such as tearing or fibrosis of brachiocephalicus or the pectoral muscles, may have no localizing signs (see page 152). Associated lameness cannot be influenced by nerve blocks. Atypical equine rhabdomyolysis can cause hindlimb lameness without any other clinical signs typical of tying up.


Periarticular lesions of the otifle such as collateral ligament injury are usually associated with detectable soft tissue swelling, but injuries of the patellar ligaments can occur with no localizing clinical signs, and associated pain is often unresponsive to intraarticular analgesia (see Chapter 46). I have also examined five horses with acute onset of severe lameness and mild swelling on the craniomedial aspect of the femoropatellar joint resulting in loss of palpable definition of the patellar ligaments. Lameness was characterized by a markedly shortened cranial phase of the stride at the walk, but less severe lameness at the trot. Ultrasonographic examination revealed the presence of a periarticular hematoma surrounding the patellar ligaments, which themselves were structurally normal.




Potentially Confusing Responses to Local Analgesic Techniques


Improvement without complete alleviation of lameness after perineural analgesia is not always easy to interpret. It may reflect failure to completely alleviate pain from a single source, or there may be additional sources of pain. Sometimes lameness improves with each successive block (e.g., palmar digital, palmar [abaxial sesamoid], low four-point, and subcarpal nerve blocks). However, the lameness is not associated with any detectable radiological, ultrasonographic, or scintigraphic abnormalities. Sometimes additional useful information can be obtained by performing intraarticular analgesia of the interphalangeal and metacarpophalangeal joints, but if the response is negative the diagnosis remains inconclusive.


Isolation of pain to a region but failure to define the cause is particularly frustrating. For example, intraarticular analgesia of the femorotibial joints may be positive, but no radiological or ultrasonographic abnormalities may be detectable. Nuclear scintigraphy may reveal a generalized increased uptake of the radiopharmaceutical in the distal aspect of the femur and proximal aspect of the tibia compared with the contralateral limb. Medication of the joints may result in no improvement. Exploratory arthroscopy may reveal minor findings (e.g., mild fibrillation of the cranial meniscal ligaments) of questionable relevance, but evaluation of all the joint surfaces and meniscal cartilages is impossible. The definitive diagnosis for the cause of pain remains elusive. Computed tomography (CT) and magnetic resonance imaging (MRI) may permit the identification of subchondral bone injuries and meniscal and ligamentous injuries not accessible to arthroscopic inspection.


The importance of subchondral bone pain as a cause of lameness must not be overlooked. Such pain frequently is present without associated radiological change. A comparison of the responses to intraarticular analgesia and perineural analgesia (and the response or lack thereof to intraarticular medication) may be helpful. With subchondral pain, intraarticular analgesia may have a limited effect. Nuclear scintigraphy is a sensitive indicator of increased modeling in the subchondral bone. MRI has the potential to show subtle structural changes in the subchondral bone.


Until recently, soft tissue lesions within the hoof capsule have proved elusive to definitive diagnosis. Diagnostic ultrasonography, although possible, has marked limitations. Pool-phase scintigraphic images sometimes are helpful. Examination of the navicular bursa may yield useful information about the bursa, the deep digital flexor tendon, and the distal sesamoidean impar ligament. Advanced imaging techniques such as CT and particularly MRI have the best potential to demonstrate soft tissue pathological conditions, although determining the clinical significance of lesions is not necessarily easy.


False-positive results may be obtained if the horse is only mildly lame at investigation but has a history of a more obvious lameness. The detectable mild lameness may not necessarily reflect the original cause. Lameness that is induced when a horse is lunged in small circles on a concrete surface may not reflect the primary cause of lameness. Thus eliminating this lameness by nerve blocks may be misleading. Lameness induced by flexion also may not reflect the principal cause of lameness. Blocking the flexion response does not necessarily identify the primary cause of lameness.


A pony had moderate forelimb lameness that was markedly accentuated by lower limb flexion. The response to flexion was eliminated by either regional or intraarticular analgesia of the fetlock joint. However, the baseline lameness was unchanged and did not respond to any of the nerve blocks that were repeated on several occasions. Surgical removal of a large osseous fragment from the fetlock joint did not improve the lameness.






Jun 4, 2016 | Posted by in EQUINE MEDICINE | Comments Off on Unexplained Lameness
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