Keywords
bicipital tenosynovitis - shoulder pain - bony exostosis - mineralization - ossification
Introduction
The transverse humeral ligament (retinaculum) runs from the lesser to the greater
tubercle of the humerus, preventing luxation of the biceps tendon from the intertubercular
groove, and it is a well-known anatomical structure in the dog and cat.[1]
[2] Gleason and colleagues[3] concluded that in humans this structure was not an actual ligament, but rather a
sling formed mainly by fibres of the subscapularis tendon, with contributions from
the supraspinatus tendon and the coracohumeral ligament. Complete ossification of
the transverse humeral ligament was described in a human cadaveric study in only one
specimen.[4] Clinical identification of mineralization of this structure in humans is limited
to a sonographic study of the biceps tendon in less than 1% of shoulders studied.[5] Calcification of the transverse humeral ligament and clinical manifestation of this
have not been reported in the veterinary literature. This is the first case report
of osseous metaplasia of the transverse humeral ligament in a cat treated surgically
with a successful outcome.
Case Description
History and Clinical Findings
A 10-year-old, neutered, male Bengal cat weighing 4.5 kg was presented to the University
of Liverpool Small Animal Teaching Hospital with a 1-month history of waxing and waning
right thoracic limb lameness. No specific traumatic event was witnessed by the owner
to trigger this lameness, which appeared to be more noticeable after exercise. Meloxicam
(0.05 mg/kg, per os [PO], q24h) was administered for 2 weeks prior to presentation
with no appreciable improvement. The patient was being medically managed for hypertrophic
obstructive cardiomyopathy with benazepril hydrochloride/spironolactone (0.25/2 mg/kg,
PO, q24h). On subjective gait analysis, a grade 4/10 right thoracic limb lameness[6] was elicited. Orthopaedic examination was limited due to the irritable nature of
the cat; however, a consistent pain response upon flexion of the right shoulder and
concurrent pressure over the bicipital groove could be identified. Neurological examination
was generally unremarkable.
Diagnostic Findings
The patient was sedated and positioned in sternal recumbency for computed tomography
(CT) of its thoracic limbs using an 80-slice multidetector CT scanner (Aquilion Prime,
Toshiba Medical Systems, Tokyo, Japan). Reconstructions were generated using standard
(soft tissue) and sharp (bone) kernel algorithms with a slice thickness of 0.5mm and
viewed in standard bone and soft tissue windows. The carpi and elbow joints were unremarkable.
A well-defined curvilinear bony exostosis was identified projecting from the distal
part of the greater tubercle of the right shoulder, which focally and completely encircled
the proximal biceps tendon ([Fig. 1]). The exostosis was smoothly marginated with no periosteal reaction. Mild osteophyte
formation was apparent at the margins of the scapulohumeral joint ([Fig. 2]). The left scapulohumeral joint was unremarkable.
Fig. 1 (A–C) Transverse computed tomographic images from distal (A) to proximal (C) through the proximal right humerus of a 10-year-old Bengal cat. Note the curvilinear
bone exostosis (arrowed) arising from the greater tubercle that fully encircles the biceps tendon in (B). (D–F) Transverse images of the proximal left humerus of the same cat at corresponding
locations. (G) A dorsal plane reconstruction of the left and right scapulohumeral joints; the bone
exostosis is arrowed. All images are sharp (bone) reconstructions displayed in a bone
widow.
Fig. 2 Three-dimensional computed tomography reconstruction of the glenohumeral joint showing
a curvilinear bony exostosis joining the greater and lesser tubercles of the right
humerus. Proximal is to the right and distal to the left of the image.
Ultrasonography of the shoulder region confirmed the presence of a well-defined mineralized
structure superficial to the right bicipital groove creating a distal acoustic shadow.
A moderate volume of anechoic fluid was present surrounding the tendon within the
bicipital tendon sheath ([Fig. 3]). These findings were consistent with right biceps tenosynovitis.
Fig. 3 Ultrasound images of the proximal brachial region of a 10-year-old Bengal cat. (A–C) Images aligned with the longitudinal axis of the bicipital tendon with proximal
to the left; (A) is the most proximal and (C) is the most distal. (D) is a transverse image of the tendon at approximately the same level as image (C) with medial to the left. The biceps tendon is marked with measuring callipers in
(A) and (B). Note the hyperechoic structure casting a distal acoustic shadow and obscuring the
tendon (arrowed in A and B) and the effusion surrounding the biceps tendon (arrowed in C and D).
Management and Outcome
Meloxicam was discontinued for 8 days prior to re-admission to the hospital. The patient
was sedated with a combination of medetomidine (0.04 mg/kg, intramuscular [IM]), midazolam
(0.2 mg/kg, IM) and ketamine (2 mg/kg, IM) and placed in left lateral recumbency.
The lateral aspect of the right shoulder was clipped and aseptically prepared. Arthrocentesis
of the right shoulder using a 32-mm 23 G hypodermic needle was performed, which yielded
a mildly increased amount of macroscopically normal joint fluid. An in-house cytology
revealed a mild increase in number of mononuclear cells (3–4 cells per high power
field). Methylprednisolone acetate (4.4 mg/kg, intra-articular, once) was instilled
into the right glenohumeral joint. The patient was discharged with instructions on
strict cage rest.
Re-assessment after 4 weeks revealed an initial improvement of the lameness for approximately
3 weeks, with recurrence of the lameness after this period. At this stage, a grade
3/10 right thoracic limb lameness[6] was still present and pain was elicited on manipulation of the right shoulder. Surgical
management was discussed with the owner due to the only short-term relief of clinical
signs with conservative management, reiterating the lack of evidence on outcome after
surgical treatment.
Five weeks after steroid injection, the patient was anaesthetized and placed in left
lateral recumbency. A cranio-medial approach to the right glenohumeral joint was performed
through a 5-cm skin incision.[7] The deltoideus muscle was identified and an incision made on the brachiocephalicus
muscle elevating it from the proximal humerus. The thoracic limb was externally rotated
and the superficial and deep pectoral muscles were partially elevated from the humerus.
The area of ossification was identified over the tendon of biceps brachii muscle.
This area was subsequently demarcated with four 25G hypodermic needles and a 1-mm
round-tip high-speed burr was used to remove the calcified structure. After this was
elevated less than 50% of the fibres of the transverse humeral ligament were unaffected
and left intact. During manipulation of the shoulder, the biceps tendon was not luxating
and was sliding normally in the intertubercular groove even after challenging shoulder
joint motion. The pectoral and brachiocephalic muscles were sutured in two separate
simple continuous layers of three metric polydioxanone (PDS II, Ethicon). The subcutis
and cutaneous layers were closed routinely, and the patient was discharged the following
day with a 2-week course of meloxicam (0.05 mg/kg, PO, q24h) and further exercise
restriction. Histopathology of the calcified tissue confirmed a well-differentiated
bone formation that effaced normal ligament collagen fibres, with a transition between
fibrous dense tissue to bone structure which included osteoblasts, osteoclasts and
osteocytes and medullary cavities with blood vessels ([Fig. 4]). This was classified as a well-differentiated osseous metaplasia of the transverse
humeral ligament.
Fig. 4 Histology of the humeral ligament. There is a transition between normal tendon structure
(left) and progressive osseous metaplasia (haematoxylin and eosin, decalcified specimen;
scalebar = 200 microns). Inset: Higher magnification: evidence of formation of medullary
cavities with osteoblasts and osteoclasts and blood vessels (haematoxylin and eosin,
decalcified specimen; scalebar = 60 microns).
At follow-up appointment 8 weeks postoperatively, the cat was reported to have normal
ambulation without noticeable lameness at home, and being able to jump onto furniture
during the previous week without issues. No lameness could be elicited on subjective
gait analysis and right shoulder manipulation was non-painful with a normal range
of motion. Further imaging of the area was offered at this point and 1 year after
surgery; however, the owner declined due to full clinical recovery and the potential
risk of a further sedation procedure. On a telephone conversation with the owner 12
months after surgery the cat was reported to ambulate and jump normally with no identifiable
lameness.
Discussion
This case of osseous metaplasia of the transverse humeral ligament seems to be the
first reported in the veterinary literature. Limited information is available from
the human literature, where this condition was reported on autoptic specimen[4] and in a sonographic study in man where in four cases mineralization of this structure
was identified, with concurrent bicipital tenosynovitis.[5]
Bicipital tenosynovitis is a common cause of shoulder pain in humans[8] and in active, middle-aged or older, medium- to large-breed dogs.[9] In cats, it is only described in one case report and was believed to be secondary
to increased joint laxity associated with glenohumeral dysplasia and incongruity.[10] In the case we present here, bicipital tenosynovitis revealed to be the cause of
lameness as confirmed by the inflammation of the tendon on ultrasonographic assessment.
This was presumed to be secondary to chronic chafing against the osseous bridge during
multidirectional movements such as jumping, playing and climbing as demonstrated by
the clinical improvement after removal of the osseous bridge. This chronic friction
was believed to cause inflammation and microtearing that could eventually lead to
degenerative changes in the tendon of the biceps, if untreated. Unfortunately, we
were unable to prove this with postoperative imaging of the shoulder joint and biceps
tendon due to the pet owner's denial.
In humans, genetic predisposition to calcification of other ligaments such as the
superior transverse scapular ligament has been postulated from a familial case that
affected father and son resulting in suprascapular nerve entrapment.[11] Other aetiologies such as repetitive strain on the subscapularis, supraspinatus
muscles and pectoralis major muscle, could result in microtrauma during biomechanical
movements of the shoulder and ultimately lead to calcification and ossification of
these fibres.[4] There is limited information regarding osseous metaplasia of other ligaments in
cats. A cadaveric feline study found similar metaplastic changes affecting the annular
ligament in several cats that was postulated to be a result of mechanical (tensile)
stress.[12] A similar etiopathogenesis can only be speculated in the case reported here; however,
no comparable lesions were identified on the thoracic limb joints of the same patient.
Thoracic limb lameness investigations in small animals have evolved in the past years
with the advent of advanced imaging modalities such as CT. Recent studies have shown
the increased sensitivity and specificity of CT for the detection of elbow and shoulder
pathologies,[13]
[14] with the addition of further information from CT arthrography in some shoulder pathologies.[15] An initial CT scan was elected for this case to characterize the thoracic limb lameness
and once pathology was confirmed in the shoulder, ultrasound of the bicipital groove
and tendon was considered the imaging modality of choice due to its non-invasive nature
and reliability in characterizing pathology of these structures.[5]
[8]
[9] Despite shoulder arthroscopy being the gold standard diagnostic procedure for shoulder
pathology, this would be unlikely to provide any further information to the case due
to inability to directly observe the transverse humeral ligament.[2]
Medical management of bicipital tenosynovitis has been successfully implemented, especially
as a first-line treatment in dogs,[9]
[16] involving the use of non-steroidal anti-inflammatory drugs, rest, physical therapy
and intra-articular injection of long-acting steroids. Medical management by intra-articular
corticosteroid administration was initially elected as previously recommended[17] due to the unreported nature of the condition and unknown surgical outcome. There
is continued controversy on the balance of beneficial or deleterious effects of intra-articular
corticosteroids on articular cartilage and the overall joint environment; however,
a systematic review suggested that there is not enough evidence about the effects
of corticosteroids on cartilage and inflammation.[18] In our case, this management failed to provide a long-term resolution of lameness,
which was attributed to the continuous presence of the inciting cause. Therefore,
surgical removal of the osseous bridge was elected in this case and resulted in a
successful outcome. Surgical removal of the transverse humeral ligament has been performed
with good success in cases of canine bicipital tenosynovitis[9] however, other surgical options such as tenotomy or tenodesis have also been reported
in dogs with equally good results.[9]
[16]
[19] In our case, once the ossified lesion was removed, we could grossly identify some
transverse fibres left in the region of the transverse humeral ligament, which could
suggest that the transverse humeral ligament in cats is also formed of fibres originating
from different tendons and ligaments of the area as it has been shown in humans[3] however, this cannot be concluded without a dedicated anatomical study and could
also be explained by partial mineralization of the transverse humeral ligament.
Conclusion
This is the first case report of osseous metaplasia of the transverse humeral ligament
resulting in bicipital tenosynovitis in a 10-year-old Bengal cat. Diagnosis of the
condition was achieved through orthopaedic examination, CT of the thoracic limbs and
ultrasonography of the bicipital groove. Conservative treatment failed to provide
long-term resolution of lameness, with surgical excision of the osseous lesion resulting
in fast resolution of clinical signs, as followed up 12 months after surgery.