Introduction
Medial shoulder instability (MSI) can cause pain and forelimb lameness in dogs.[1]
[2]
[3]
[4] It may be of traumatic origin when a single event results in tearing or laxity of
the shoulder's active and/or passive stabilizers that protect the joint.[1]
[5]
The medial glenohumeral ligament (MGHL) acts as passive stabilizer through its cranial
and caudal branches inserting on the glenoid and the third branch on the humeral head,
respectively.[1]
[6] Active stabilizers like the subscapularis muscle (SM) press the humeral head into
the glenoid fossa.[1] Their disruption causes dysfunction of the joint with medial shoulder luxation and
increased external rotation and abduction angle.[1]
[5] Grading of MSI depends on the degree of impairment of the structures involved.[7]
Manipulation of the joint and measurement of the abduction angle are essential for
the diagnosis of shoulder instability.[2] This test has good sensitivity but low specificity.[5]
[8] Other examinations like stress radiography may be required to assess pathological
joint laxity.[9] Magnetic resonance imaging (MRI),[10] computed tomography (CT),[11] and arthroscopy[8] allow to assess integrity of the stabilizers and cartilage.
Surgical management is particularly recommended to treat acute traumatic affection
with moderately to severely affected MGHL causing medial or multidirectional shoulder
instability.[3]
[7] Treatments include, among others, the imbrication of the SM[12] and prosthetic MGHL repair using synthetic implants fixed by suture anchors,[13] screws with spiked washers,[14] toggle sutures,[4]
[7] or knotless anchors.[15] Although interference screws (IS) associated with synthetic implants have already
been used in various ligament reconstructions,[16]
[17] they have never been explored to treat MSI. We thus report the surgical management
and long-term outcome of traumatic MSI in a small-breed dog treated by imbrication
of the SM and extra-articular stabilization using a synthetic implant and an IS.
Case Description
Clinical History
A 13-kg, 10-year-old sterilized female Fox Terrier was presented with a 1-month history
of nonweight-bearing right forelimb lameness following a fight with another dog.
Clinical Examination
The general examination and complete haematological and biochemical assessment were
normal.
Orthopaedic Examination
Severe muscle atrophy of the right shoulder was evident. The flexion of the shoulder
was painful. Shoulder dislocation could be elicited by humeral abduction and external
rotation, suggesting high-grade MSI. The neurological examination was normal. A complementary
orthopaedic examination was performed under anesthesia, during which an excessive
abduction angle of the shoulder joint compared with the contralateral limb was noted.
Diagnostic Imaging
All diagnostic imaging procedures were performed during a single session in anesthesia.
First, orthogonal radiographs (flat screen detector, Ibis, Italy) of the right forelimb
revealed mild new bone formation on the medial aspect of the neck of the scapula without
major signs of osteoarthritis. No fracture was identified. Stress radiographs confirmed
MSI with a 75-degree abduction angle at the intersection of the scapular and humeral
anatomical axes[9] ([Fig. 1A]).
Fig. 1 Preoperative diagnostic imaging. (A) Caudocranial stress radiograph of right shoulder showing a 75-degree abduction angle.
(B) Dorsal T2-weighted magnetic resonance imaging (MRI) showing lateral glenohumeral
ligament (arrow). Medial glenohumeral ligament and distal part of subscapularis muscle
are not visible (arrowheads). (C) Postcontrast transverse computed tomography showing swelling on medial aspect of
right shoulder (arrows). Complete examination of the right shoulder using MRI included
sagittal and transverse high-resolution turbo spin echo T2-weighted images, sagittal
and transverse spin echo T1-weighted images, transverse turbo 3D T1-weighted images,
and sagittal gradient echo T2-weighted images.
Second, an MRI (VetMR, 0.18T, Esaote, Italy) examination of the right shoulder highlighted
an increase in synovial fluid volume. The MGHL and the insertion of the SM were not
clearly identified. The lateral glenohumeral ligament, the insertion of the infraspinatus
and supraspinatus muscles, and the biceps tendon appeared normal ([Fig. 1B]).
Third, CT (Canon Aquilion Lightning 32, 120 KVp, 120 mAs, 0.430 × 0.430 × 0.5 mm3 voxel size) of the right forelimb and cervicothoracic spine (C5 to Th3) was performed
before and after an intravenous injection of 600 mg I/kg of iodixanol (Visipaque,
GE, United States). Radiographic findings were confirmed as there was mild bone production
on the medial aspect of the scapular neck without fractures. Articular swelling was
present, particularly on the medial side of the shoulder ([Fig. 1C]).
Clinical and imaging findings (i.e., traumatic origin, absence of substantial radiographic
signs of osteoarthritis, disruption of two unique medial stabilizers of the shoulder)
indicated a grade 3 MSI[7] and the need for surgical stabilization.
Surgical Treatment
The patient received premedication and analgesia with 0.1 mg/kg/SC of morphine (morphine
chlorhydrate, Aguettant) and 0.1 mg/kg IV of meloxicam (Metacam, Boehringer Ingelheim).
Antibiotic prophylaxis consisted of 30 mg/kg/IV of cefazolin every 2 hours (Cefazolin,
Panpharma). Anesthesia was induced with 0.5 mg/kg/IV of diazepam (Valium, Roche) combined
with 2 mg/kg/IV of alfaxalone (Alfaxan, Dechra). After intubation, anesthesia was
maintained with isoflurane (Isoflurin, Axience).
The dog was positioned in dorsal recumbency. The procedure was performed through a
single craniomedial approach to the shoulder.[18] A remnant of the SM, the torn medial capsule, and a complete tear of the MGHL from
its glenoid insertion were identified. The optimal positioning of the two bone tunnels
was preplanned by CT scan. The entry point of the first tunnel was drilled at the
center of an estimated line connecting the insertions of the cranial and caudal branches
of the MGHL on the glenoid, near the articular surface ([Fig. 2A–C]).[6] A Kirschner wire secured the entry point of the tunnel. The tunnel was given an
oblique craniodorsal direction (i.e., the lateral exit was more cranial and dorsal
than the medial entry point). This increased its length, thus maximizing bone stock
to optimize anchorage, and avoided glenoid effraction. The orientation was validated
by subjective assessment. A 4.0-mm cannulated drill-bit was used for slow medial to
lateral drilling with constant irrigation. A second 3.5-mm tunnel was drilled perpendicular
to the axis of the humerus with a medial entrance close to the joint line and just
posterior to the lesser tubercle, to respect the insertion of the physiological MGHL
([Fig. 2A–C]).[6] This tunnel aimed to be bicortical to maximize screw purchase in the bone and increase
the surface in contact with the implant ([Fig. 2E]). After drilling, the entrances of the tunnels were flushed to avoid any bone debris.
Bone edges at tunnel entrances were smoothened with a countersink driver (DePuy Synthes)
to avoid damaging implant fibers. The humeral tunnel was pretapped.
Fig. 2 Reconstruction technique and preoperative surgical views. (A) Lateral, (B) medial, and (C–E) frontal view of shoulder joint showing position of scapular and humeral tunnels.
(D) Cortical button passed mediolaterally through scapular tunnel and flipped on lateral
aspect of scapula cranially to acromion. Implant then passed mediolaterally through
humeral tunnel, retrieved and tensioned with Mayo–Hegar needle holder. (E) Implant then secured by bicortical interference screw in humeral tunnel. (F) Placement of Novalig 4000 Platine implant. (G) Joint is held reduced (adduction and internal rotation) while implant is secured
with interference screw in humerus.
An ultra-high molecular weight polyethylene (UHMWPE) implant (Novalig 4000 Platine,
Novetech Surgery, France) with a preassembled cortical button was used to maintain
the reduction.
First, the cortical button was inserted blindly from the medial to the lateral side
of the scapula through the bone tunnel, using a Mayo–Hegar needle holder ([Fig. 2F]). It was gently pushed through the tunnel using a passing tube (Novetech Surgery,
France), ensuring that it fully exited the tunnel laterally and trying to avoid penetrating
overlying fascia or muscle. To secure the button in contact with the lateral cortex
of the scapula, it was flipped like a toggle by exerting tension on the implant. A
suture passer was used to push the implant through the humeral tunnel in a medial
to lateral direction. The implant was maintained in a flat position. The suture passer
was retrieved laterally without any additional approach. The implant was grabbed at
the lateral side ([Fig. 2D]) using a Mayo–Hegar needle holder and brought back cranially to the humerus medial
side where tension was applied ([Fig. 2G]). The latter was adjusted and temporarily secured by pulling the implant and rolling
it around the Mayo–Hegar needle holder ([Fig. 2G]). Restrained abduction, maintenance of joint coaptation, and normal range of motion
in all plans were the criteria for validating optimal tension. Final fixation was
achieved with a 4.5 × 20-mm titanium IS placed medially to laterally in the humeral
tunnel ([Fig. 2E, G]). We reconstructed the remnants of the joint capsule and reattached the SM by imbrication
with a horizontal mattress suture pattern of 2–0 polydiaxonones.[12] The implant was positioned under the SM and outside the joint capsule. Owing to
capsular tear, its complete reconstruction was unachievable, and part of the implant
was in contact with humeral head cartilage. Rinsing and plane-by-plane closure were
performed.
Immediate Postoperative Examination
A slightly reduced range of flexion of the shoulder with maintenance of joint coaptation
was observed. Abduction was reduced due to the transfixation ([Fig. 3]). The abduction angle was −11 degrees (indicating excessive adduction) owing to
an inversion of the scapular and humeral anatomical axes at their intersection on
stress radiographs ([Fig. 4B]). Radiographs and CT confirmed the appropriate position of the implant and bone
tunnels and correct restoration of the articulating surfaces ([Fig. 3]).
Fig. 3 Immediate postoperative imaging. (A) Mediolateral and (B) caudocranial radiographs of right shoulder. Multiplanar computed tomography reconstructions
([C] Sagittal, [D] dorsal, and [E] transverse) of right shoulder showing position of implant, interference screw, and
tunnels. The angulation of the scapular tunnel (α) was 19 degrees from the glenoid
surface on the sagittal plan.
Fig. 4 Measurement of abduction angle. (A) Preoperative abduction angle of the right shoulder measured at 75 degrees, (B) at −11 degrees immediate postoperatively, (C) −4 degrees at 2 months, and (D) 31 degrees at 2.5 years postoperatively. The stress radiographs are oriented with
the scapula in similar position to facilitate comparison. Abduction angles were measured
at the intersection of the scapular and humeral anatomical axes as described in Livet
methodology.[9] The measurement of abduction angle is subjected to approximation because of difficulty
of scapula positioning. Negative values are due to the inversion of scapular (purple)
and humeral (green) axis indicating excessive adduction.
Postoperative Management
Nonsteroidal anti-inflammatory drugs (Meloxicam, Metacam, Boehringer Ingelheim) were
prescribed for 21 days. Hobbles were placed around the shoulder for 15 days. Gentle
mobilization of the limb (passive range of motion of the shoulder three time a day)
was thereafter prescribed with regular short walks for 1 month.
Long-Term Postoperative Examination
Postoperative examinations were performed at 1, 2, 4.5 months, and 2.5 years postoperatively.
Each included orthogonal radiographs under sedation and CT.
The dog bore weight after surgery and resumed normal gait at 2 months postoperatively,
while presenting increased joint amplitude with full recovery of shoulder flexion.
At 2.5 years, the owner reported slight lameness after exercise, which spontaneously
resolved with rest. Full restoration of the periscapular muscle mass was observed
compared with the contralateral limb during the follow-up.
To evaluate the persistence of medial shoulder stability over time, the abduction
angle was measured on stress radiographs.[9] The abduction angle was −4 degrees at 2 months ([Fig. 4C]) and 31 degrees at 2.5 years ([Fig. 4D]) postoperatively on the stress radiographs. Radiography at 1 month postoperatively
did not allow comparable measurement. CT revealed a widening of the medial entrance
of both the scapular and humeral tunnels after 1 month, which slightly increased up
to the 2-month visit and then remained stable ([Fig. 5]). Only mild bone remodeling of the lateral parts of the tunnels was observed during
the entire follow-up, with no apparent signs of loosening of the IS and the cortical
button ([Fig. 5]). Comparable measurements were available only for the medial entrance of the glenoid
tunnel and indicated 4.1 mm immediately after the operation ([Fig. 5I]), 5.6 mm at 1 month ([Fig. 5J]), 6.2 mm at 2 months ([Fig. 5K]), 6.1 mm at 4.5 months ([Fig. 5L]), and 6.7 mm at 2.5 years ([Fig. 5M]) postoperatively. At the 2.5-year visit, no contrast enhancement of the joint capsule
or regional lymph node enlargement was observed on CT. The humeral screw seemed covered
by bone ([Fig. 3]) and no signs of screw intolerance were observed. Minor signs of osteoarthritis
were present on the radiographs at 2.5 years.
Fig. 5 Evolution of tunnels over time. Immediate postoperative computed tomography (CT)
multiplanar reconstruction (MPR) ([A] sagittal, [B] frontal, and [C] transverse) of right shoulder. Sagittal CT imaging of right shoulder (D) immediate postoperatively, and at (E) 1 month, (F) 2 months, (G) 4.5 months, and (H) 2.5 years postoperatively. Frontal CT imaging of right shoulder (I) immediate postoperatively, and at (J) 1 month, (K) 2 months, (L) 4.5 months, and (M) 2.5 years postoperatively. MPR was used to acquire appropriate planes to perform
standardized approximation of measurements of largest diameter of scapular tunnel
during follow-up:• Yellow line is parallel to medial cortex of scapula (B, I–M).• Purple line passes through center of the two tunnels (A, D–H).• Medial entrance of glenoid tunnel (green line symbolized by the letter “a” overlapping
yellow line) was + 36.6% at 1 month (J), + 51.2% at 2 months (K), + 48.8% at 4.5 months (L), and + 63.4% at 2.5 years (M) postoperatively.Deformation percentage expressed relatively to immediate postoperative
measure. MPR did not provide satisfactory planes to measure humeral tunnel.
A cytopathological analysis of the synovial fluid (microscopic observation of three
smears) was performed at 2.5 years postoperatively. The paucicellular smears showed
90% of mononuclear cells of synoviocyte type and no granulocyte cells.
Discussion
Medial shoulder instability is a diagnostic[1]
[2]
[8] and therapeutic[7]
[12]
[14]
[15] challenge. In this traumatic case, painful shoulder instability was associated with
excessive abduction of the shoulder along with major amyotrophy. A 75-degree abduction
angle on stress radiography confirmed MSI.[9] This test seems to be sensitive for values above 53 degrees and correlated with
shoulder abduction angles measured clinically under sedation.[9] However, it remains unspecific,[8]
[9]
[19] especially in the event of severe amyotrophy.
Magnetic resonance imaging and normal neurological examination confirmed the anatomical
structures involved in the MSI[10] and excluded other major causes of neurological shoulder amyotrophy inducing “root
signature” (i.e., plexus sheath tumor, brachial plexus avulsion).[20]
[21] It confirmed the disruption of the MGHL and the SM, with joint effusion compatible
with a traumatic injury.
Computed tomography completed the evaluation of the joint[11] and confirmed the absence of fractures. It provided a 3D reconstruction of the joint,
which helped to plan tunnel drilling for a safe placement of the implant. During the
follow-up, CT helped to monitor and measure the enlargement of the tunnels.
However, we did not perform an arthroscopic evaluation of the joint, which could have
provided information on cartilage integrity and intra-articular stabilizers. The small
size of the joint and its disruption could have been risk factors for damage or fluid
extravasation around it.
These findings justified surgical stabilization. The reconstruction and imbrication
of the SM alone can be moderately effective to stabilize the shoulder.[12] Owing to the severe amyotrophy and grade 3 MSI in our case, we were concerned that
SM imbrication might have been insufficient.
The choice of a UHMWPE implant was based on the biocompatibility of its fibers[22] as well as the ex vivo biomechanical strength[23]
[24]
[25] and clinical versatility it demonstrated in various applications.[16]
[17] In the reported case, its flat and wide shape (compared with other implants[7]) helped to restore stability while reconstructing a single arm of the MGHL, previously
shown to be sufficient for maintaining shoulder stability in young beagles.[26] Covering the joint with an implant fixed on a single point on the glenoid to stabilize
MSI has previously been described with various implants and materials (spiked washers
and screws, buttons and UHMWPE tape, anchors).[7]
[14]
[27] These reports seem to have obtained good clinical outcomes.[7]
[14]
The flat and wide section of the implant was expected to increase the contact area
and the stability of the joint, especially by increasing stiffness.[28] A previous ex vivo study on hip stabilization has demonstrated the mechanical superiority of tape-type
implants over string-like ones when using a toggle rod fixation to limit luxation.[28] In the shoulder, the TightRope system has shown 20% of reluxation (2/8 dogs presented
with luxation or subluxation).[7]
The stiffness of the UHMWPE implant is close to that of the physiological ligament
and joint capsule on feline hip cadaver models.[25] It seems to persist in the long-term follow-up, as suggested by the abduction angle,
which remains below 53 degrees (i.e., the threshold value indicating an affected shoulder
on stress radiographs).[9] However, these may be approximate measures as they depend on the reproducible orientation
of the scapula during radiograph acquisitions. The implant is placed flush with the
joint surface, thus limiting its working length and increasing its stiffness.[29] This was expected to limit an excessive range of motion of the joint.[29]
With the cortical button placed through a bone tunnel, it was possible to fix the
implant on the scapula, which has limited bone stock. This positioning seemed appropriate
to preserve the integrity of the glenoid rim, especially in a small dog. The safety
implantation of anchors has only been studied in dogs above 20 kg,[30]
[31] whereas sutures with buttons have been used for scapular fixation in small dogs
under 10 kg.[7]
[15] The wide flat implant required broad tunnels, which could be a limitation for the
safety of the implantation and a risk for glenoid integrity. Using a cortical button
avoided any concerns about the safety angle of the anchor or screw insertion and the
associated risks of loosening.[15]
[27]
[30]
[31] Suture toggles have been suggested to have biomechanical advantages over knotless
anchors, owing to the difficulty to implant and angulate anchors.[27]
[31] Indeed, reaching the optimal anchor insertion angle for the greatest pullout resistance
(i.e., “deadman's angle”) is difficult yet essential to achieve satisfactory implantation
and decrease the risks of loosening.[31]
Medial implantation without a minimal lateral approach (as discussed in[7]) could be advantageous. In theory, careful implantation without penetrating the
overlying soft tissues should limit the risk of entrapping the suprascapular nerve
with the button.[7] It also helps to place the button tightly against the bone since it only needs to
be flipped and pushed down just after having exited the scapular tunnel.[7] Finally, it limits the risk of seroma on the lateral part of the shoulder and the
subsequent risk of sepsis on a pressure point when the patient lies down.[7] However, entrapping soft tissues is a risk in this procedure, which could lead to
an early change in implant tensioning.
The IS placed in the humerus provided a fixation system with an important pull-out
strength.[24] It avoided the use of a knot fixation that tends to slip with UHMWPE,[32] which might be a limitation of toggle pin implants. It also had the advantage of
being totally embedded inside the bone allowing to fix the implant near the humeral
insertion of the MGHL[6] and the articular space. It avoided any conflict with the joint or abrasion risks
for the implant and surrounding tissues, unlike with eyelet anchors.[33] It avoided the use of screws associated with spiked washers, which have a tendency
to loosen in this area.[14] The use of an IS could be an advantage over knotless anchors or spiked washers and
screws as the tension can be preadjusted. In our case, tension was adjusted with a
Mayo–Hegar needle holder. This surgical instrument provided an optimal grip of the
implant due to the tungsten carbide, which prevented UHMWPE slipping,[32] when tensioning by rolling the implant around it. Joint mobility was then tested
before securing the final tension with the IS.
Follow-up examinations revealed a widening of the medial part of both tunnels at implant/tunnel
interface, associated with recovery of normal flexion amplitude at the 2-month visit.
Tunnel widening has been described after 1 month postoperatively in feline[34] and canine hip surgeries[35] after the use of a toggle rod and UHMWPE implant. In human knee surgery, the use
of IS and cortical buttons with tendinous grafts can also be associated with bone
tunnel widening.[36]
[37] Biological etiologies may explain this phenomenon, which includes thermal bone necrosis
due to drilling,[38] immune response to UHMWPE,[39] and influx of synovial fluid containing cytokines into tunnels.[36]
A cannulated drill bit was used. It is known to produce more heat than regular drill
bits.[40] Despite an appropriate drilling technique, potential thermal cell damage causing
an enlargement of the bone tunnels cannot be completely excluded.
Biomechanical forces may also be a cause for tunnel deformation. A “bungy cord” effect
due to excessive tension and/or micromovements of the implant during bone healing
might cut into the bone.[36]
[41] The asymmetry of the tunnel deformation supports the biomechanical hypothesis.
The flat shape of the implant may have limited this deformation since it has lower
risks of cutting into the bone than a round suture, as described in stifle surgery.[41] The orientation of the scapular tunnel might also have influenced the deformation.
The angulation of the scapular tunnel was done at 19 degrees from the glenoid surface
to avoid a sharp exit angle ([Fig. 3D]). In stifle joint surgery, an angulation of 30 to 45 degrees was recommended to
optimize implant transition, which could be an improvement of the technique.[41]
During surgery, the joint was held in excessive adduction when tensioning the implant
to maintain joint coaptation and facilitate SM imbrication. On the one hand, this
may have resulted in excessive tension on the implant, which may then have exerted
pressure on the bone. Excessive tension could lead to immediate damage to the bone
tunnel. On the other hand, potential initial overtensioning might have compensated
for any subsequent loss of tension during recovery, as it did not negatively influence
the outcome in terms of abduction angle, which remained in the physiological value
range.[9] Overtensioning may help to protect the soft tissues during healing as the implant
acts as a mechanical brace. Reconstructing the two arms of the MGHL could also help
distribute the pressure exerted by a single implant and limit tunnel deformation.
Tunnel deformation might have contributed to a loss of tension of the implant, which
may partly explain the increased abduction angle observed at 2.5 years postoperatively.
However, since the abduction angle increased by 35 degrees between 2 months and 2.5
years postoperatively despite the stabilization of the scapular tunnel deformation,
other causes such as loss of tension due to implant slippage at the IS/bone interface
is possible. It is the most common mode of failure of this fixation system.[42] Alteration in the mechanical properties of the implant due to cyclic load is another
possible cause.[24]
Determining the appropriate tension, tunnel angulation and rest period should limit
the biomechanical stress exerted on the tunnel bone, thus limiting the widening effect.[41]
Two major differences between the reported procedure and human surgery should be highlighted.
First, tunnel deformation seems uniform along the tunnel axis in humans, suggesting
biological causes.[36]
[37] Second, fixation with a cortical button seems to be associated with lesser tunnel
deformation than with IS in humans.[36]
[37] However, this comparison has limitations since the grafts, the IS material and the
joints are different.[36]
[37]
Despite tunnel deformation that may compromise the mechanical integrity of the fixation,[41] the patient's long-term outcome was satisfactory from a clinical functional aspect
(i.e., joint stability, muscle mass recovery). Long-term shoulder stability may result
from the combination of the stabilization provided by the implant, SM imbrication,
and partial capsular reconstruction. The procedure allowed the patient to quickly
resume limb weight-bearing, thus leading to muscle mass and active stabilizers recovery,
and to the development of periarticular healing structures.[14]
Further investigations are needed to determine whether this satisfactory outcome in
one case is reproducible, to define the causes of tunnel widening and to determine
the optimal tension of the implant. A cutoff tunnel deformation value that could affect
clinical outcome should also be established.[37] Finally, since this outcome is in line with previously published results,[7]
[13]
[14]
[15] this modified stabilization method using an IS could be considered as a possible
improvement for the treatment of MSI.
Corrigendum: A corrigendum has been published for this article (DOI: 10.1055/s-0044-1788640).
