LA MS 10: Navicular Syndrome Flashcards
Navicular Bone Anatomy
Palmar or plantar aspect of P2 and P3 - coffin jt
Has 2 articulating surfaces - distal surface w/ P3, dorsal w/ P2
Lined with synovial fluid - synovial invaginations
Covered with hyaline cartilage
Flexor surface = fibrocartilage –> smooth surface for the tendon to run over
Fxn of the navicular bursa
Provides smooth surface for the DDFT to run over
Bursa Does not communicate with the coffin jt
2 collateral sesamoidinal ligaments - attach on the wings of the navicular bone
Blood supply, innervation
Medial and lateral palmar digital artery, vein, and nerve
Navicular Syndrome
Common FL lameness Syndrome vs disease Higher incidence in QH, WB, TB - rare in mules, donkeys M>F (not supported by research) Inherited??? --possibly DT conformation
Etiology
Poorly understood
2 theories
1- vascular
2 - biomechanical
Vascular Theory
Altered blood flow to navicular region
Theory lacks proof of concept support
In vivo data to support increased rate of bone remodeling and increased vascularization
Further in vivo data suggests active arterial hyperemia and passive venous congestion
Biomechanical theory
More accepted
Degen changes result from increased mechanical forces on the navicular bone and its supporting ligaments
–tension from DDFT
–tension from supporting ligaments
Origin of navicular pain
Intraosseous pressure
Damaged supporting ST structures
–collateral tears and DDFT tears often misdx’d as navicular
Bursa - bursitis
Predisposing Factores
Excessive body weight Small feet Upright pastern angles Hoof imbalances Work on hard surface --> concussion
Dx
Hx, CS Localization of lameness to palmar 1/3 of foot --perineural blocks - PD blocks --coffin jt --navicular bursa Imaging --RADS --Bone scan, CT, MRI
Hx, CS
Progressive, chronic unilat/bilat forelimb lameness
95% have asymmetric lameness
75% had extensor m atrophy
–chronic cases
–don’t want to extend all the way so decrease concussion on heel
CS: gait
Stiff, shuffling gait
Refuses leads, not willing to stride out
Lameness more obvious in a circle
Pointing of forelimb
Dx: hoof testers
+/- sensitive across heels, frog, possibly toe
Hoof abN
Low, under run, contracted or sheared heels Broken-back hoof pastern axis Medial-lateral hoof imbalance Small, upright foot Narrow foot
Dx Lameness Exam
Lameness variable Typically bilat but asymmetric - one limb more severely affected Stiff, shuffling, choppy gait Short cranial phase ***tend to land on toe***
Dx Lameness Exam: Lameness exacerbated when -
Hard surfaces Lower limb flexion Wedge test Frog pressure Worked in circle
Dx PD Nerve Block*
Small vol, small gauge needle --avoid block diffusing up the leg Desensitizes cd 1/3 of foot and ole Show marked improvement --> 80-90% Majority switch over to being lame on the other side
Dx Navicular bursa block
Aseptic technique
RADS control
Dx Coffin Jt Block*
IA ax of coffin jt NOT helpful in differentiating problems of coffin jt and navicular region
Dx RADS
Remove shoes
Clean feet
Pack feet - remove air artifacts
Bilateral
Dx RADS - views
Lateral
Dorsoprox-palmarodistal (60 degrees)
Palmaroproximal-palmarodistal: tangential or skyline view
Flat dorsopalmar
RADS findings: lat projection
Palmar, plantar angle
Bone production - prox and distal margins
Eval how P1, P2 and P3 line up
Normally toe should be tipped down just a bit
Rad findings: 60 degree dorsopalmar oblique
Increase in number, sz, abN shape of synovial invaginations - distal margin
RAD findings: skyline
(Aka palmaroprox-palmarodistal oblique)
Flexor cortex: erosions, roughening
Corticomedullary distinction - cortex should be more radioopaque than medullary cavity
–If hard to tell where medullary cavity ends and cortex begins, have sclerosis
RAD findings: flat DP projection
Eval whether have balance medial to lateral hoof
Other RAD findings
- loss of corticomedullary distinction
- medullary sclerosis
- mineralization of DDFT
- enthesophytes
Lameness with “toe up”
Fracture of navicular bone
–lost some of space so DDFT looser
Rupture of DDFT
Additional Imaging Modalities
Bone Scan
CT
MRI
MRI
Mainstay of dx problems in foot because presence of so many ST structures
If blocks out to the foot and RADS are inconclusive, move onto an MRI
3 mainstays of navicular tx
- Corrective shoeing
- Rest
- Bute
Treatment
Numerous tx modalities Usually combo --rest esp after shoeing --light work --corrective trimming/shoeing --drugs designed for tx of OA --Meds that improve blood flow Sx
Corrective shoeing
Basis for tx Goals --restore natural hoof balance --reduce biomechanical forces on the navicular region Egg Bars Shorten the toe --rolling, rockering, squaring of the toe and setting it slightly back on the front enhances breakover of the foot Raise the heel: shoe, wedge pads Reverse shoe - easier to bring leg back
Med Tx
NSAIDS
CS
HA
PSGAG
NSAIDS
Bute = best
CS
DIT jt, navicular bursa
Hyaluronic acid
IA, intramural, IV
PSGAG
PO, IM
Isoxsuprine hydroCl
Beta-adrenergic agent
VD/rheologic properties
Poorly proven - low SE so worth trying
Pentoxifylline
Synthetic xanthine derivate Increases erythrocyte flexibility Decreases fibrinogen Prevents aggregation of RBCs and platelets Inhibits action of IFM cytokines
Bisphosphonates
Ex: tildren, osphos Causes intracelluler, intercellular mediated cell death of osteoclasts --> decreased bone resorption Anti-IFM properties --decreased NO and cytokines released --Inhibits activity of MMPs SE: mild transient colic, renal failure No data on efficacy of Tildren as RLP
Palmar Digital Neurectomy
Not first line of defense
Performed in conjunction with corrective trimming, shoeing
Degree of response to pre-op block will predict response to neurectomy
Only lasts approx 2yr before nerve grows back
Tx Suspensory Branch (aka collateral ligament) desmotomy
Rationale - reduces forces on the navicular bone during WB phase of stride
