Keywords
calcific periarthritis - hydroxyapatite crystal deposition disease - HADD - carpal
tunnel - barbotage - ultrasound
Introduction
Hydroxyapatite crystal deposition disease (HADD) is a well-known systemic disorder
resulting from the abnormal periarticular and/or intra-articular deposition of calcium
hydroxyapatite crystals.[1] Its commonest presentation is calcific tendinopathy, also known as calcific tendinosis/tendonitis,
and typically involves the rotator cuff tendons (mainly supraspinatus),[1]
[2] a condition with a prevalence of up to 7.5% in adults and usually affecting middle
aged women. However, several other sites can be involved including bursae, joint capsules,
tendon sheaths, and ligaments.[3] Ultrasound-guided barbotage is a needling and lavage procedure and is an established
method of treating calcific tendinopathy of rotator cuff tendons.
Carpal tunnel syndrome (CTS) is a commonly encountered condition of the wrist resulting
from compression of the median nerve as it traverses the carpal tunnel, and is characterized
by pain, numbness, and paraesthesia of the hand in the distribution of the median
nerve.[4] While there are multiple risk factors associated with CTS including obesity, repetitive
activity of the wrist, pregnancy, genetics, and rheumatoid inflammation, the condition
is largely idiopathic.[4] Calcific deposits within the carpal tunnel resulting in median nerve compression
have been established as a rare cause of CTS, and several case reports exist in the
literature describing this entity.[3]
[5]
[6]
[7]
[8]
We described a case of a 45-year-old female patient who presented with excruciating
right wrist pain and symptoms of CTS. Ultrasound and radiographs demonstrated ill-defined,
mass-like calcification within the right carpal tunnel causing median nerve compression.
Ultrasound-guided barbotage was used as a first-line treatment, with a large amount
of milky, calcific material aspirated. The patient subsequently reported significant
improvement in her symptoms.
The case highlights the importance of recognizing HADD as a lesser-known cause of
CTS, and also outlines the valuable role of ultrasound-guided barbotage as a reliable
first-line management option, potentially negating the need for the conventional and
more invasive carpal tunnel surgery.
Case Report
A 45-year-old female presented with several days of excruciating right volar wrist
pain, resulting in marked restriction of wrist movements. There was also significant
pain in her hand in the distribution of the median nerve (thenar eminence and three
radial digits) with tingling and paraesthesia of the medial aspect of hand. She was
otherwise well, with no significant past medical or surgical history. There was no
history of trauma to the wrist. This was a first presentation, with no prior history
of CTS or arthropathy elsewhere.
On examination, there was markedly reduced range of movement of the right wrist. There
was no significant soft tissue swelling or erythema, and no palpable mass was evident.
An ultrasound was performed that revealed an amorphous mass-like calcification within
the carpal tunnel, deep to the flexor digitorum profundus tendons resulting in stretching
and compression of the overlying flexor tendons and the median nerve ([Fig. 1]) ([Video 1] and [2]). The mass was avascular on color Doppler. A radiograph was also obtained subsequently
which confirmed the presence of a lobulated soft calcification on the volar aspect
of the wrist joint ([Fig. 2]). The appearance of the calcification both on ultrasound and radiograph was typical
of that seen with calcific periarthritis and hence a provisional diagnosis of HADD
was made based on these features.
Fig. 1 Longitudinal sonographic view of the wrist demonstrating ill-defined, mass-like calcification
within carpal tunnel (white arrow), deep to the flexor tendons and median nerve (labeled). No significant
vascularity within the calcification. Also note the isoechoic-to-hyperechoic appearance
of calcification and absence of any appreciable acoustic shadowing, features which
are characteristic of type 3 calcification.
Video (1 and 2) Long axis (1) and short axis (2) cine clips demonstrating ill-defined, mass-like calcification within the carpal
tunnel deep to the flexor tendons and median nerve. Note the absence of appreciable
acoustic shadowing in relation to the calcification and isoechoic to hyperechoic appearance,
characteristic of type 3 calcification.
Fig. 2 Anteroposterior (A) and lateral (B) radiographs demonstrating soft, mass-like calcification within the carpal tunnel
(white arrows).
The patient was initially managed with ultrasound-guided barbotage of the calcific
deposits. After administering local anesthesia, an 18-gauge hypodermic needle was
introduced into the mass-like calcification in the carpal tunnel, taking care to avoid
the overlying flexor tendons and median nerve. Under direct visualization, the calcification
was simultaneously fragmented and flushed with approximately 5 mL of normal saline
([Video 3]). The contents were then aspirated into a 10 mL syringe via the same needle until
the calcification was substantially reduced in size; the latter was visualized in
real time ([Video 4]). A milky white solution was aspirated ([Fig. 3]). Following this, 40 mg of methylprednisolone acetate, a corticosteroid, was injected
into the carpal tunnel.
Fig. 3 Ultrasound-guided lavage procedure demonstrating patient and needle position. Note
the milky white aspirate of calcific material from the needle.
Video (3–4) Long axis cine clips demonstrating saline lavage of the calcification (3) followed by aspiration (4).
The procedure was performed in the outpatient department, and the patient was discharged
home on the same day after an uneventful 20-minute period of observation. On subsequent
follow-up several days later, the patient reported significant improvement of her
initial symptoms, and had regained the ability to move her wrist with minimal pain
and restriction. She received ongoing conservative management via her primary care
physician.
Discussion
While HADD commonly affects the rotator cuff tendons, in particular the supraspinatus
tendon, a range of other periarticular soft tissues can be involved. Calcific deposits
may be seen within tendons, tendon sheaths, joint capsules, ligaments, bursae, periarticular
connective soft tissues and rarely within the joints[3] and retinacula.[9] While the rotator cuff tendons, particularly the supraspinatus tendon, is most commonly
involved, other tendons in less common locations, such as the rectus femoris, can
also be involved.[10] Intramuscular involvement has also been reported.[11]
HADD, when occurring within tendons, can present in three distinct phases, namely
precalcific, calcific and postcalcific, as described by Uhthoff and Loehr.[12] The calcific stage is further subdivided into formative, resting and resorptive
stages. In the pre-calcific phase, fibrocartilaginous metaplasia, probably related
to decreased oxygen tension, leads to the formation of calcification, giving rise
to the formative stage. In the resorptive phase, cellular reaction around the calcific
deposits, and increased vascularity can result in growth of the deposits, which can
become poorly defined. This can also result in migration of the calcific deposits
to surrounding tissues, and hence it is this phase of the disease that is most painful
and symptomatic.[2]
[12] Postcalcific phase involved formation of granulation tissue and tendon remodeling.
Bianchi and Becciolini[2] described three distinct types of calcification which can be seen in the disease,
based on the percentage of calcium within the deposits; type 1 which is calcium rich
and correspond to formative and resting phases, and these present as hyperechoic foci
with acoustic shadowing on ultrasound; type 2 calcifications which are hyperechoic
but only show faint acoustic shadowing, and type 3 calcifications which are isoechoic
to tendons, appear ill-defined and show no acoustic shadowing. Types 2 and 3 usually
correspond to the resorptive phase and hence more likely to be encountered in acutely
symptomatic patients. While the pathogenesis described by Uhthoff and Loehr[12] and calcification types described by Bianchi and Becciolini[2] specifically refer to calcific tendinopathy, similar parallels can be drawn to patients
with calcific periarthritis as both conditions result from deposition of hydroxyapatite
crystals. The patient described in this report had typical type 3 calcifications,
which appeared poorly defined on ultrasound without any acoustic shadowing, and her
acute excruciating symptoms at time of presentation suggested the disease was in the
resorptive phase.
While the imaging features seen in this case are typical of HADD, it is nonetheless
important to consider other potential etiologies in a patient presenting with calcification
within the carpal tunnel. These include gout, pseudogout, vascular malformations,
tumoral calcinosis, and heterotopic ossification.[13] The latter can be seen with malunited fractures of the distal radius.[13] Neoplasms, particularly synovial sarcoma, which can present as a calcified mass,
should also be considered,[14] and when suspected based on preliminary imaging and clinical history, should be
investigated further with magnetic resonance imaging prior to attempting any intervention.
Ultrasound-guided barbotage is an established procedure utilized for the treatment
of painful calcific tendinopathy and periarthritis of the rotator cuff tendons.[15] It involves a needling and lavaging technique. The procedure has been shown to be
effective in the treatment of calcific tendinopathy of the rotator cuff.[10] With ultrasound guidance, a needle is used to fragment the calcific deposits, which
attempts to break down the hydroxyapatite crystals, and subsequently flushed with
normal saline.[16] The mixture of fragmented calcium hydroxyapatite and the saline mixture is then
aspirated, and the contents usually appear as a milky white mixture due to the presence
of calcium. A relatively large gauge needle (typically at least an 18-G) needle is
used to ensure the fragmented calcifications can be satisfactorily aspirated. The
procedure can either be performed as a single- or double-needle technique, the latter
utilizing separate needles for fragmentation / saline flush and aspiration.[17] The procedure is often followed by an injection of a corticosteroid into the area,
as the anti-inflammatory properties of the steroid can help with analgesia, and improve
function.[18]
Excellent results have been reported in calcific tendinopathy following partial removal
of calcific deposits, due to sufficient disruption and localized bleeding, which facilitates
spontaneous resorption of the remaining calcium or its dispersion, in addition to
the benefits of directly lavaging the deposits. Better response has been reported
with ill-defined calcifications showing faint acoustic shadowing, and when there is
measurable reduction in calcium size and echogenicity post-procedure,[19] as was the case with our patient. While no reports of the utility of this procedure
in treatment of CTS due to HADD can be found in the existing literature to the best
of our knowledge, satisfactory results have been reported with the use of barbotage
for the treatment of HADD in unusual locations other than rotator cuff, such as the
spring ligament.[20] Given that it is the same entity causing carpal tunnel in this scenario, a similar
approach can be used with successful outcomes as demonstrated in this case.
While it is generally a safe procedure, one also needs to be aware of potential complications
that may arise from ultrasound-guided barbotage. The complications may be related
to the barbotage itself, or secondary to the corticosteroid injection that often accompanies
the procedure. Complications related to barbotage include infection, bleeding, tendon
rupture, and temporary exacerbation of the inflammation.[21] In cases involving the carpal tunnel, risk of damage to neurovascular structures
including the median nerve, radial artery, and anatomical variants such as a persistent
median artery[22] should also be considered and discussed with the patient. Performing the procedure
under aseptic conditions, and sound procedural technique with adequate needle visualization
under ultrasound guidance, taking precautions to avoid critical structures can mitigate
these risks. The use of corticosteroid and local anesthetic during the procedure can
minimize the exacerbation of symptoms from the procedure. Corticosteroid-related adverse
effects are well described in the existing literature that are beyond the scope of
this discussion.
Conclusion
HADD can be a rare cause of CTS. Ultrasound and radiographs prove to be valuable tools
in diagnosing the condition with a high degree of confidence. Ultrasound-guided barbotage
of the calcific deposits is a reliable alternative to surgery in managing these patients
and relieving symptoms, potentially negating the need for surgery in some patients.
