Suprascapular nerve decompression for treatment of neuropathy in a bucking bull

Courtney Griffin 1Department of Clinical Sciences, College of Veterinary Medicine, Mississippi State University, Mississippi State, MS 39762.

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Cathleen A. Mochal-King 1Department of Clinical Sciences, College of Veterinary Medicine, Mississippi State University, Mississippi State, MS 39762.

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G. P. Grissett 2Department of Pathobiology and Population Medicine, College of Veterinary Medicine, Mississippi State University, Mississippi State, MS 39762.

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Andy Shores 1Department of Clinical Sciences, College of Veterinary Medicine, Mississippi State University, Mississippi State, MS 39762.

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Abstract

CASE DESCRIPTION

A 3-year-old 639-kg (1,406-lb) American bucking bull was examined because of a 4-day history of right forelimb lameness that began after the bull sustained an injury to the right shoulder region while exiting the chute during a rodeo.

CLINICAL FINDINGS

A 10 × 10-cm soft tissue swelling was present over the right shoulder region. Ultrasonographically, the contour of the scapular spine, bicipital bursa, bicipital tendon, and greater tubercle of the humerus appeared unremarkable; the swelling appeared to be a hematoma overlying the distal aspect of the scapula. No external wounds, palpable joint effusion, or swellings were noted on examination of the distal portions of the limbs. The bull developed atrophy of the supraspinatus and infraspinatus muscles with lateral abduction of the shoulder joint when walking. Electromyography revealed decreased innervation to the supraspinatus and infraspinatus muscles consistent with suprascapular neuropathy.

TREATMENT AND OUTCOME

The suprascapular nerve was surgically decompressed by removing the entrapping hematoma and periosteum and performing a notch resection of the scapula; dexamethasone (40 mg) was administered prior to closure. The bull was discharged 5 days after surgery; no lameness was evident at the time of discharge. The owner was instructed to restrict the bull to a stall or small pen for 6 weeks. Four months after surgery, the muscle atrophy had substantially improved, and the bull returned to bucking.

CLINICAL RELEVANCE

Findings suggested that suprascapular neuropathy can develop in bulls secondary to injury and that suprascapular nerve decompression may improve nerve function, muscle atrophy, and gait.

Abstract

CASE DESCRIPTION

A 3-year-old 639-kg (1,406-lb) American bucking bull was examined because of a 4-day history of right forelimb lameness that began after the bull sustained an injury to the right shoulder region while exiting the chute during a rodeo.

CLINICAL FINDINGS

A 10 × 10-cm soft tissue swelling was present over the right shoulder region. Ultrasonographically, the contour of the scapular spine, bicipital bursa, bicipital tendon, and greater tubercle of the humerus appeared unremarkable; the swelling appeared to be a hematoma overlying the distal aspect of the scapula. No external wounds, palpable joint effusion, or swellings were noted on examination of the distal portions of the limbs. The bull developed atrophy of the supraspinatus and infraspinatus muscles with lateral abduction of the shoulder joint when walking. Electromyography revealed decreased innervation to the supraspinatus and infraspinatus muscles consistent with suprascapular neuropathy.

TREATMENT AND OUTCOME

The suprascapular nerve was surgically decompressed by removing the entrapping hematoma and periosteum and performing a notch resection of the scapula; dexamethasone (40 mg) was administered prior to closure. The bull was discharged 5 days after surgery; no lameness was evident at the time of discharge. The owner was instructed to restrict the bull to a stall or small pen for 6 weeks. Four months after surgery, the muscle atrophy had substantially improved, and the bull returned to bucking.

CLINICAL RELEVANCE

Findings suggested that suprascapular neuropathy can develop in bulls secondary to injury and that suprascapular nerve decompression may improve nerve function, muscle atrophy, and gait.

A 3-year-old 639-kg (1,406-lb) American bucking bull was examined because of a 4-day history of right forelimb lameness. The owner reported that the bull had sustained an injury to the right shoulder region while exiting the chute during a rodeo and would not bear weight on the limb immediately after the injury. The lameness improved to the point that the bull would bear weight on the limb 24 hours after the injury, but right forelimb lameness persisted.

On initial examination, the bull had a grade 3/5 right forelimb lameness that progressively worsened to grade 4/5 lameness during evaluation. A 10 × 10-cm soft tissue swelling was apparent over the right shoulder region, proximal and caudal to the greater tubercle of the humerus.

The bull was not amenable to physical examination. Therefore, it was restrained with a hydraulic squeeze and tilt table and sedated with xylazine (0.05 mg/kg [0.023 mg/lb], IV) and acepromazine (0.08 mg/kg [0.036 mg/lb], IV). Ultrasonography of the right shoulder region was performed with a 7.5-MHz linear probe. The contour of the scapular spine, bicipital bursa, bicipital tendon, and greater tubercle of the humerus appeared unremarkable. The soft tissue swelling in the shoulder region consisted of an approximately 5 × 7-cm, hypoechoic, fluctuant mass with a honeycomb appearance that was overlying the distal aspect of the scapula and was considered to most likely represent a hematoma with edema of the triceps brachii muscle.

The bull was tilted into lateral recumbency, and the claws and distal portions of the limbs were thoroughly evaluated to rule these regions out as potential sources of the lameness. No external wounds, palpable joint effusion, swellings, or sensitivity to hoof testers was noted on examination of the distal portions of the limbs.

Radiography of the right shoulder region was recommended. However, because of the bull's demeanor, general anesthesia was required. Therefore, the bull was hospitalized so that medical management could be attempted first. Acepromazine (0.15 mg/kg [0.068 mg/lb], PO, q 12 h, applied to the feed) was administered, and the bull was allowed to acclimate to the hospital. Medical management of the lameness consisted of meloxicam (0.5 mg/kg [0.23 mg/lb], PO, q 24 h for 3 days, then 0.5 mg/kg, PO, q 48 h). In addition, the bull was restrained in a squeeze stall twice daily for 20-minute hydrotherapy treatments of the right shoulder region. Over the next 48 hours, the soft tissue swelling decreased substantially, and the right forelimb lameness became intermittent.

Four days after medical management was initiated (ie, 8 days after the injury), the bull was no longer improving and began to have noticeable atrophy of the right supraspinatus and infraspinatus muscles (Figure 1). Intermittent right forelimb lameness was still present; however, the gait had changed dramatically so that abduction of the limb occurred with each step (ie, a so-called sweeny-type gait). Radiographic evaluation and electromyography were elected at this time. Food was withheld for 24 hours prior to anesthesia.

Figure 1—
Figure 1—

Photographs of a 3-year-old 639-kg (1,406-lb) American bucking bull that was examined because of a 4-day history of right forelimb lameness that began after the bull sustained an injury to the right shoulder region while exiting the chute during a rodeo. A—Notice that the right shoulder region appears slightly lower and rolled slightly outward, compared with the left shoulder region. B—Notice the loss of muscle over the scapula, as evidenced by the dipped appearance and lack of rounding over the scapula. C—The loss of muscle was even more evident following clipping of the hair to allow notch resection of the scapula and suprascapular nerve decompression.

Citation: Journal of the American Veterinary Medical Association 255, 5; 10.2460/javma.255.5.591

The bull was premedicated with xylazine (0.05 mg/kg, IV) and butorphanol (0.025 mg/kg [0.011 mg/lb], IV), and anesthesia was induced with ketamine (2.2 mg/kg [1 mg/lb], IV) and maintained with isoflurane. Because of the bull's size, a complete radiographic evaluation of the shoulder region could not be performed. However, radiography of the shoulder joint, greater tubercle of the humerus, and proximal portion of the humerus did not reveal any evidence of fractures.

While the bull was still anesthetized, electromyography was performed on the supraspinatus, infraspinatus, biceps brachii, triceps brachii (lateral and long heads), extensor carpi radialis, and flexor carpi ulnaris muscles. Ground, reference, and recording electrodes were placed, and each muscle was evaluated multiple times. Both the supraspinatus and infraspinatus muscles had obvious signs of muscle atrophy, as evidenced by various degrees of coarse fibrillation potentials with occasional positive sharp waves (Figure 2). Insertion of recording electrodes in the biceps brachii, triceps brachii (lateral and long heads), extensor carpi radialis, and flexor carpi ulnaris muscles yielded short insertion potentials followed by electrical silence, characteristic of the normal muscle response. Application of electrical pulses to a stimulation electrode placed near the suprascapular nerve resulted in mild contraction of the supraspinatus and infraspinatus muscles. Recordings were consistent with polyphasic motor unit action potentials, which were interpreted as evidence of a mild degree of reinnervation. Electromyographic findings were consistent with a diagnosis of suprascapular neuropathy, and suprascapular nerve decompression was recommended.

Figure 2—
Figure 2—

Representative electromyographic recording obtained from the supraspinatus muscle of the bull in Figure 1. Notice the coarse fibrillation potentials (FP) and positive sharp waves (PSW) consistent with muscle atrophy secondary to suprascapular neuropathy.

Citation: Journal of the American Veterinary Medical Association 255, 5; 10.2460/javma.255.5.591

The bull recovered from anesthesia without any complications. Two days later, feed was again withheld for 24 hours and water was withheld for 12 hours. Flunixin meglumine (1.1 mg/kg [0.5 mg/lb], IV) and florfenicol (20 mg/kg [9.1 mg/lb], IM) were administered prior to surgery. The bull was anesthetized as previously described and positioned in left lateral recumbency. Hair was clipped from the right shoulder region, and the site was prepared for surgery. A 30-cm curvilinear incision was made that began over the spine of the scapula and continued craniodistally toward the greater tubercle of the humerus. The incision was deepened to transect the cutaneous trunci muscle. The hematoma overlying the spine of the scapula was debrided until the fascia covering the spine of the scapula could be identified and incised. The brachiocephalicus muscle was elevated from the spine of the scapula with a periosteal elevator and retracted cranially. The suprascapular neurovascular bundle was then identified and carefully dissected free from the scapula and surrounding fascia with a small periosteal elevator. Once the neurovascular bundle was elevated from the scapula, notch resection of the cranial margin of the scapula was performed by creating a 10-mm-wide, approximately 5-mm-deep groove with a Maltz bone rasp. Care was taken to ensure the groove was smooth and free from sharp edges. The neurovascular bundle and brachiocephalicus muscle were replaced, and a 3.5-inch, 18-gauge spinal needle was placed through the brachiocephalicus muscle overlying the nerve. The fascia was closed with size-1 polyglactin 910. Dexamethasone (40 mg) was then instilled through the preplaced spinal needle, which was subsequently removed. The remaining surgical incision was closed routinely. While recovering from general anesthesia, the bull experienced a large volume of regurgitation.

Four days after surgery, the bull became febrile (40°C [104.0°F]) and developed bilateral mucopurulent nasal discharge. Aspiration pneumonia was suspected, and treatment with florfenicol (40 mg/kg [18.2 mg/lb], SC, once) was initiated. The muscle atrophy was especially apparent after surgery because of the hair removal (Figure 1), but did not appear to get any worse during the remainder of the hospitalization period. Moderate swelling of the incision was present 48 hours after surgery.

The bull recovered from the aspiration pneumonia and was discharged 5 days after surgery with instructions that it be returned in 14 days for suture removal. No lameness was evident at the time of discharge. The owner was advised to restrict the bull to a stall or small pen for the next 6 weeks and to continue treatment with meloxicam (0.5 mg/kg, PO, q 48 h) for 14 days. The owner was informed that, on the basis of information from the Food Animal Residue Avoidance Databank, a slaughter withdrawal time of 40 days after the last dose of meloxicam was recommended.

The bull was returned in 14 days for suture removal. There was still a small amount of swelling at the distal aspect of the incision, but no residual lameness. The bull was reevaluated by video examination 4 and 12 months after surgery. Four months after surgery, the muscle atrophy had improved by approximately 90%, and the bull was returned to bucking. Twelve months after surgery, the muscle atrophy had resolved, and the bull was able to perform competitively, with no evidence of problems associated with shipping to various events. However, the bull had a minor decrease in performance if it competed on consecutive weekends.

Discussion

Suprascapular neuropathy is a relatively common injury in horses,1 but to our knowledge, only 2 cases of suprascapular neuropathy involving cattle have been reported in the literature. In the first case,2 suprascapular neuropathy developed secondary to streptococcal meningoradiculitis in a cow, and treatment was not attempted. The second case3 involved a 1.5-year-old Angus bull; treatment consisted of application of a counterirritant, but outcome was not reported.

In horses, damage to the suprascapular nerve most commonly occurs as a result of direct trauma and may cause paralysis and subsequent atrophy of the supraspinatus and infraspinatus muscles.4,5 Lateral stability of the shoulder joint is compromised, resulting in a characteristic gait deficit commonly referred to as “sweeny.” Medical and surgical management have both provided successful outcomes; however, surgical decompression reportedly results in a faster return to athletic function and an improved cosmetic outcome.6

The reflection of the suprascapular nerve around the cranial border of the scapula makes it predisposed to inflammation secondary to traumatic injury.7 Arising from the sixth and seventh cervical spinal cord segments, the suprascapular nerve innervates the supraspinatus and infraspinatus muscles via the brachial plexus. Accompanying the suprascapular artery, it passes between the subscapularis and supraspinatus muscles before its reflection around the cranial border of the scapula. At this site of reflection, a small tendinous band extends over the nerve.8 Damage to the suprascapular nerve likely occurs less commonly in ruminants than in horses because anatomically the nerve lies deeper within the musculature, potentially serving as protection against injury.3 However, findings for the bull described in the present report demonstrate that suprascapular nerve injury can occur in cattle.

A systematic approach to lameness evaluation is important in the assessment of cattle with potential suprascapular neuropathy, especially in patients that do not have clinically apparent atrophy of the supraspinatus and infraspinatus muscles at the time of initial evaluation. Typically, atrophy of these muscles and subsequent prominence of the scapular spine are not documented until 7 to 10 days after injury.8 A history of direct trauma to the shoulder region is helpful in making the diagnosis, but damage to the sixth or seventh cervical spinal cord segments and injury to the brachial plexus should also be considered in light of clinical signs.1

Because approximately 90% of cattle with lameness have lesions localized to the foot, it is important to rule out more common conditions such as sole abscesses, sole ulcers, septic arthritis of the distal interphalangeal joint, fractures of the third phalanx, interdigital phlegmon (foot rot), and heel warts.9–13 Other important considerations include bicipital bursitis, fracture, shoulder joint luxation, and septic arthritis of the shoulder joint.1,8 Careful evaluation of the distal portions of the limbs and claws is necessary to rule out foot conditions in cattle. Radiographic evaluation of the limb will facilitate fracture diagnosis and evaluation of joint spaces.

Spontaneous activity of the suprascapular nerve during electromyographic evaluation of the supraspinatus and infraspinatus muscles 5 to 7 days after an injury is confirmatory for a diagnosis of suprascapular nerve paralysis. Careful evaluation of additional muscles of the limb should be considered to distinguish suprascapular nerve injury from injury to the brachial plexus.8

Medical management recommended for horses with suprascapular neuropathy consists of strict stall confinement until resolution of lateral instability of the shoulder joint. This is typically followed with 2 to 4 months of pasture confinement before returning to work. Resolution of the lameness is achieved in most cases; however, mean time to resolution can range from 2 to 12 months.5,6

Surgical decompression of the suprascapular nerve has been well described in horses with suprascapular neuropathy. Scapular notch resection, or suprascapular nerve release, involves subtotal ostectomy of the cranial border of the scapula at the level of the scapular notch. The nerve is freed from the overlying tendinous band and gently retracted before an osteotome or wire saw (both methods have been described) is used to remove a small section of bone. The suprascapular nerve is then returned to the notched section of bone, minimizing entrapment and subsequent compression.4,14 Postoperative treatment routinely includes administration of NSAIDs and stall rest, and results are reportedly good, with 80% of patients attaining normal muscle function following surgery.14

The bull described in the present report had classic signs of suprascapular neuropathy with subsequent muscle atrophy and lameness associated with the injury. The lameness improved with medical management but did not resolve completely until surgery was performed. After surgery, the bull was able to be returned to its intended use. Findings for this case suggested that suprascapular neuropathy can develop in bulls secondary to injury and that suprascapular nerve decompression may improve nerve function, muscle atrophy, and gait.

Acknowledgments

Supported by the Departments of Clinical Sciences and Pathobiology and Population Medicine, College of Veterinary Medicine, Mississippi State University.

References

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