False-Negative Responses to Diagnostic Analgesia

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

• Inaccurate injection

• Inadequate time for the local anesthetic solution to be effective

• Failure to appreciate improvement in the lameness

• Very severe pain

• Failure to alleviate subchondral bone pain after intraarticular injection

• Extraarticular pain

• Aberrant nerve supply

• Failure, in an unshod horse, to appreciate the extent of foot soreness contributing to lameness

• Failure to appreciate the degree of lameness fluctuation within an examination period

• Failure to abolish pain associated with a neuroma

• Neuropathic pain

The following are common case examples:

1 It is misleading to conclude that pain does not arise from the centrodistal and tarsometatarsal joints and the central and third tarsal bones after a negative response to intraarticular analgesia of the centrodistal and tarsometatarsal joints. Intraarticular analgesia has only a limited ability to alleviate subchondral bone pain. In moderate to advanced osteoarthritis, subchondral bone pain is a clinically significant contributor to pain. Hock pain may be missed if it is concluded that a negative response to intraarticular analgesia precludes the existence of hock pain and if there is a failure to desensitize the hock region using regional analgesia. It should also be recognized that perineural analgesia of the fibular and tibial nerves may result in only partial improvement in lameness associated with moderate-to-severe osteoarthritis of the centrodistal and or tarsometatarsal joints.

2 Laminitis, a fracture of either the distal phalanx or the navicular bone, and a subsolar abscess are all common causes of severe foot pain. Desensitization of the foot by perineural analgesia of the palmar (plantar) nerves at the level of the proximal sesamoid bones may have a negligible effect or result in only mild improvement in lameness. Foot pain in a hindlimb is often more difficult to alleviate than in a forelimb. If clinical signs point to foot pain, but apparent desensitization of the foot fails to markedly alter the lameness, further investigation of the foot should be performed with other means (e.g., radiographic examination).

The horse in Figure 12-1 was admitted with suspected back pain but showed obvious bilateral forelimb lameness, with right forelimb lameness predominating. Digital pulse amplitudes were increased in the right forelimb, but there was no response to hoof testers. Nonetheless, the horse appeared clinically to have foot pain typical of laminitis. Apparent desensitization of the foot, performed to convince the owner that the horse had foot pain, produced absolutely no change in the lameness. The horse responded rapidly to treatment for laminitis.

3 Inadvertent intrasynovial injection may result in misleading results. For example, accidental injection into the tarsal sheath when attempting to deposit local anesthetic solution around the plantar metatarsal nerves distal to the hock may result in proximal suspensory lesions being missed.

4 Failure to allow sufficient time for local anesthetic solution to be effective may result in a false-negative response in some circumstances. Premature assessment of the response to intraarticular analgesia of the femorotibial joints may result in a false-negative result in association with a cruciate ligament injury. These ligaments have an extrasynovial location, and it may take up to an hour after injection for cruciate ligament pain to be clinically significantly improved.

5 Subchondral bone pain in the condyles of the third metacarpal (metatarsal) bones, associated with extensive sclerosis, in young Thoroughbred and Standardbred racehorses is difficult to abolish in some horses, and responses to distal limb nerve blocks may add confusion.¹ There may be no localizing clinical signs suggestive of fetlock region pain. Improvement in lameness is sometimes seen after either palmar digital or palmar (abaxial sesamoid) nerve blocks; a “low four-point block” may further improve but not abolish lameness. The horse may be sound only after addition of a subcarpal block of the palmar metacarpal nerves. However, there may negligible response to intraarticular analgesia of the fetlock joint.

Fig. 12-1 A, Lateral and B, solar scintigraphic images of the front feet of a horse with suspected back pain but clinical signs of laminitis. There is reduced radiopharmaceutical uptake in the toe region (arrowheads). The horse showed no improvement in lameness after apparent desensitization of the lamer right front foot by palmar (abaxial sesamoid) nerve blocks, despite the firm focal pressure applied with artery forceps around the coronary band. However, the horse responded well to symptomatic treatment for laminitis.

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.

Failure to Perform the Appropriate Nerve Blocks

Failure to perform nerve blocks in a logical and complete sequence can lead to confusion. If the response to a low six-point block in a hindlimb is negative and is followed by a positive response to tibial and fibular nerve blocks, the clinician may conclude that pain arose from the hock. Lesions of the proximal aspect of the suspensory ligament (SL) may be completely overlooked.

Blocking the Wrong Limb

Failure to appreciate that a head nod reflects hindlimb lameness and is not always a sign of forelimb lameness may result in a blocking a forelimb with negative results, when the primary source of pain is in the ipsilateral hindlimb.

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.

Fig. 12-2 Lateral scintigraphic image of the shoulder region of a 6-year-old Warmblood with acute onset of moderate left forelimb lameness. Note the marked focal increased radiopharmaceutical uptake in the region of the deltoid tuberosity of the humerus. There was a slightly displaced fracture of the deltoid tuberosity of the humerus, which healed satisfactorily with conservative management.

Fig. 12-3 Caudocranial radiographic image of the left stifle of a general purpose riding horse with recent-onset, episodic, and transient severe left hindlimb lameness. There is a fracture of the proximal aspect of the fibula (large arrow). The lucent line separating the different centers of ossification further distally (small arrow) should not be confused as a fracture. There was little evidence of bony union after 6 weeks, but after 12 weeks the fracture healed satisfactorily.

Fig. 12-4 A, Dorsal oblique and B, caudal scintigraphic images of the tubera ischii of an 8-year-old Grand Prix show jumper with loss of hindlimb power and a tendency to jump to the right. There is increased radiopharmaceutical uptake in the right tuber ischium and a change of contour compatible with a fracture.

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.