Keywords
sciatic - neuropathy - bursa - bursitis - MRI
Introduction
Neuropathy secondary to bursitis formation has not been reported in the dog but is
recognized in humans associated with rheumatoid and osteoarthritis, synovial chondromatosis[1] and synovial cysts.[2] Unilateral sciatic neuropathy is encountered in dogs and may occur secondary to
pelvic or femoral fractures[3]
[4] Iatrogenic sciatic nerve injury is reported following surgery of the pelvis,[4] femur[5] and hip joint[6] and following injections into the caudal proximal pelvic limb muscles.[7] Piriformis bursitis has been described as a cause of sciatic neuropathy in humans.[8]
Case History
A 4-year-old, male neutered, Dogue de Bordeaux was referred for evaluation of left
pelvic limb lameness of several months duration. No treatment had been given prior
to referral. The dog was diagnosed with cranial cruciate ligament disease of the left
stifle and a tibial plateau levelling osteotomy was performed. Recovery was uneventful
and at re-examination 6 weeks postoperatively the patient had excellent use of the
affected limb. Nine weeks postoperatively, the dog developed acute onset right pelvic
limb lameness, and re-presented 1 week subsequently.
Clinical Findings
On physical examination, the dog's clinical parameters were within normal limits and
body condition score was 5/9 (weight 65 kg). Orthopaedic examination revealed a semi-plantigrade
stance and occasional knuckling of the foot on the right pelvic limb. Mild gluteal
muscle atrophy was observed compared with the contralateral side. Assessment of proprioception
in this limb revealed delayed postural reactions. The right patellar reflex showed
pseudo-hyperreflexia and the cranial tibial reflex was absent. There was reduced stifle
flexion and absent flexion at the level of the hock on withdrawal reflex. Sensation
of the toes appeared normal. Localization was consistent with a peripheral sciatic
neuropathy. No pain response could be elicited on palpation or manipulation anywhere
in the right pelvic limb or lumbosacral spine.
Diagnostic Techniques
Radiographs of the right stifle showed a mild synovial effusion. Hock and lumbosacral
spinal radiographs were normal. A ventrodorsal radiograph of the pelvis showed mild
bilateral hip dysplasia. Five days after presentation, magnetic resonance imaging
(MRI) (Phillips Achieva Medical Systems 1.5 T, United Kingdom) was performed. Dorsal
T2w (weighted) and Short-TI inversion recovery (STIR) (repetition time—TR = 3900 ms,
echo time—TE = 15 ms, inversion time—TI = 160 ms), T1w (TR = 300–415 ms; TE = 8–11
ms) and T2w (TR = 5390–6607 ms; TE 100–110 ms) sagittal and transverse and post-contrast
(Gadolinium 0.1 mg/kg, Gadovist, Bayer plc) T1w sequences of all three planes of the
pelvis and lumbosacral junction were acquired. All images were acquired with a slice
thickness of 4 mm and an inter-slice gap of 4.4 mm aside from the dorsal sequences
(slice thickness 3.5 mm, inter-slice gap of 3.8 mm).
Surrounding the right coxofemoral joint and following the contour of the greater trochanter,
there was a well-demarcated round to crescent-shaped approximately 2 × 3 cm mass lesion.
The lesion extended mainly in a dorsal and caudal direction, mildly displacing the
gluteal and piriform muscles. Peripherally, this lesion was T1w isointense to muscle
([Fig. 1]) and T2w moderately hyperintense to surrounding muscles. Centrally, the lesion showed
a strongly T2w hyperintense signal and was faintly hypointense to the adjacent muscle.
On STIR sequences, the centre of the lesion was strongly hyperintense and its periphery
was isointense to adjacent muscles. On post-contrast images ([Fig. 2]), the periphery of the lesion had a layered appearance, with a thick inner rim of
contrast enhancement surrounded by a thinner outer rim showing no contrast uptake.
No contrast enhancement was seen in the centre of the lesion. The lesion was located
dorsal to the sciatic nerve and causing subjective compression of the nerve against
the ischium, although no contrast enhancement was seen in this nerve. No reactive
changes of the surrounding bones or soft tissues were noted. From these imaging characteristics,
the mass was determined to be a fluid-filled structure encapsulated by an area of
contrast-enhancing vascularized tissue and an outer non-contrast enhancing fibrous
capsule.
Fig. 1 T1w (weighted) transverse post-contrast image of the pelvis just caudal to the greater
trochanter of the femur. Pubis and pelvis are pointed out by the green arrows. Dorsal
is to the top of the image. The lesion is seen on the left side of the patient (red
circle) as a centrally T1w hypointense lesions surrounded by a thick contrast enhancing
rim (red asterisk) which itself is surrounded by a thin hypointense rim.
Fig. 2 T2w (weighted) sagittal image of the femur at the level of the greater trochanter
(green arrow). The lesion is visible dorsally to the greater trochanter as a strongly
T2w hyperintensity (red circle) encapsulated in an outer rim that is T2w isointense
to surrounding muscles.
Diagnosis/Treatment
Surgical exploration of the tissues caudal to the right hip joint was undertaken by
a standard caudodorsal approach.[9] This confirmed the presence of a firm soft tissue structure (∼3 cm in diameter)
in the location described above, causing sciatic nerve compression. It was originating
from the tissues underlying the caudal border of the middle gluteal muscle adjacent
to the joint capsule of the hip joint. Approximately 10 mL of straw-coloured fluid
of low viscosity was aspirated from the lesion for cytological examination. Careful
excision of the lesion was performed and exploration of the cavity of the bursa showed
no communication with the hip joint. Surrounding connective tissue was sutured with
several mattress sutures of 2–0 polydioxanone (PDS, Ethicon) and surgical closure
was otherwise routine. Buprenorphine 0.02 mg/kg three time a day was administered
intravenously for 24 hours following surgery. Oral amoxicillin-clavulanic acid 10
mg/kg BID (Synulox, Pfizer) was given for 5 days, and meloxicam 0.1 mg/kg SID (Metacam,
Boehringer Ingelheim) for 10 days, postoperatively.
Cytological examination of the fluid showed small numbers of large mononuclear cells
characterized by ovoid nuclei with prominent nucleoli and abundant cytoplasm, macrophage-like
cells and an absence of neutrophils and other inflammatory cells. Histological examination
of the lesion showed it to be composed of predominantly collagenous interstitial tissue,
with granulation tissue along one aspect. The granulation tissue bed demonstrated
progressive maturation characterized by immature congested capillaries lined by plump
endothelial cells progressing toward a defined capillary bed. Small capillaries were
frequently oriented perpendicular to the surface. Extravasated erythrocytes (haemorrhages)
were multifocally noted in these areas. The maturation of the vascular component was
associated with increased deposition of extracellular collagenous matrix and decreased
density of activated fibroblasts. On the contralateral aspect, papillary fronds composed
of activated fibroblasts and small capillaries embedded in moderate amount of collagen
rarely lined by synovial epithelial cells extended from the surface ([Fig. 3]). Small numbers of lymphocytes and plasma cells infiltrated perivascular spaces.
Histology was consistent with an inflamed bursa-like structure (bursitis).
Fig. 3 Histological findings consistent with Bursitis. Haematoxylin and eosin stain (100x).
Progress and Outcome
The dog was discharged the day after surgery and re-examined 6 weeks later. The semi-plantigrade
stance was persistent, but he no longer knuckled over on his toes when walking. Muscle
mass of the right pelvic limb had subjectively improved. Hock flexion was still absent
on testing of the withdrawal reflex and pseudo-hyperreflexia of the right patella
reflex was persistent. Re-examination 12 weeks following surgery showed resolution
of the plantigrade stance and mild hock flexion on withdrawal reflex testing. Patella
reflex was normal and previous muscle atrophy had almost completely resolved. There
was a mild cranial drawer on examination of the right stifle which was not deemed
clinically relevant. At last follow-up 6 months postoperatively, the dog was normal.
Discussion
Bursae are simple connective tissue sacs containing viscous fluid that serve to reduce
friction of one tissue over another. Bursae are lined by synovial tissue which produces
the lubricating fluid. Most bursae differentiate concurrently with synovial joints
during embryogenesis; however, new bursae may develop in response to local stress
(such as inflammation or trauma) and pre-existing bursae may hypertrophy.[10] Pre-existing bursae may also develop communications with local joints in response
to stress. In the canine hip joint, bursae may be found deep to the tendon of insertion
of the deep gluteal muscle, where the internal obturator glides over the lesser ischiatic
notch, and deep to the internal obturator and gemelli tendons in the trochanteric
fossa between the trochanter major and joint capsule.[11] Bursitis associated with the piriformis muscle has been reported as a cause of sciatic
neuropathy in humans,[8] but no such bursa appears to be associated with this muscle in the dog.
The dog had a mild joint effusion of the right stifle and mild cranial drawer on examination
at 12 weeks of follow-up. This was not considered relevant in this case because no
pain or lameness was present and these signs would not explain the neurological deficits
seen in this case. It is likely that the dog had early cranial cruciate ligament disease
that was not clinically significant at this time. At the last follow-up, the dog was
back to normal after conservative management.
Histological appearance of the lesion in this case was more suggestive of bursitis
than a synovial cyst, as synovial cells were not identified along the granulation
bed. Bursitis is defined as inflammation of the bursa. Repetitive injury within the
bursa results in local vasodilatation and increased vascular permeability, stimulating
the inflammatory cascade. Bursitis occurs when the synovial lining becomes thickened
and produces excessive fluid, leading to localized swelling and pain.[12] Bursitis has been shown to be painful in humans[8] and horses but unusually was not the case in this dog. Synovial cysts have been
reported in dogs and arise from synovial joints and tendon sheaths. They have a synovial
lining but do not always communicate with the joint space.[13] If they develop from synovial joints along the spine, they may contribute to nerve
root compression.[14] Although rarely reported in dogs, they occasionally develop from joints in the limbs,[15] but to the authors' knowledge, there are no reports of synovial cysts arising from
the hip joint.
It is unclear why bursitis developed in this dog. It is possible that it occurred
secondary to increased weight-bearing by the limb following contralateral stifle surgery.
The large size of this dog may have been a contributory factor. In humans, bursitis
has many causes, including autoimmune disorders, crystal deposition (gout and pseudogout),
infectious diseases, traumatic events and haemorrhagic disorders, as well as occurring
secondary to overuse.[10] Penetrating trauma as a cause was deemed unlikely in this case given the lack of
haemosiderin and/or inflammatory infiltrate. Although small numbers of plasma cells
and rare lymphocytes were identified in the granulation tissue bed and small numbers
of lymphocytes cuffed vascular spaces in the interstitium, their presence was more
consistent with mild chronic irritation or inflammation, supporting the authors' hypothesis
that bursitis was stress-induced due to increased weight-bearing in this dog. No communication
with the hip joint was observed on MRI or during surgical exploration; however, prior
traumatic rupture of the synovial pouch with leakage into the surrounding tissue and
subsequent development of a granulation tissue capsule is possible.
In this case, MRI of the pelvis enabled lesion identification. It is also possible
that ultrasonography could have enabled a diagnosis; however, ultrasound was unavailable
and given the neurological deficits an MRI was opted for. The authors propose that
an alternative approach to similar cases may be to drain fluid under ultrasound guidance
and if cytological examination is consistent with bursitis, conservative treatment
(with rest and non-steroidal anti-inflammatories) may be considered. Surgical excision
could then be pursued if the lesion was to recur. In this instance, a decision was
taken to excise the bursa to allow the nature of the pathology to be fully characterized
given how unusual the clinical and imaging findings were.
In conclusion, bursitis caudal to the hip joint should be considered as a differential
diagnosis for unilateral sciatic neuropathy in the dog. Surgical excision leads to
successful recovery in this case.
