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Navicular disease
or
Foot pain syndrome
What happen???
1990’s
“Degenerative changes in structure,
composition and mechanical function of the
cartilage, subchondral bone and surrounding
soft tissues, i.e. DDFT, impar ligament, collateral
ligaments, navicular bursa and distal
interphalangeal joint”
EQUINE VETERINARY JOURNAL
Review Article: Navicular disease: a review of what’s new
A. B. M. RIJKENHUIZEN
•
The navicular bone central role
•
Diagnosis: clinical examination, analgesia (DP, DIP
joint or bursa and Xr)
•
Etiopathogenesis: interaction of biomechanical
stress and circulatory disturbance
•
Treatment:
o
orthopaedic shoeing
o
intra-articular or intrabursal injection
o
peripheral vasodilators (e.g. isoxuprine,
pentoxifylline, warfarin)
1990’s
•
Surgical treatments:
o
Desmotomy of the navicular suspensory ligaments
o
Cutting the navicular suspensory ligaments
o
Perivascular sympathectomy for the digital arteries,
with or without fasciolysis
o
Palmar digital neurectomy
Troy Trumble
Nick Ernst
Today
•
Ultrasound
•
Nuclear scintigraphy
•
Computed tomography (CT)
•
Magnetic resonance imaging
•
Biomarkers
Diagnostic analgesia
•
Palmar digital nerves: No
desensitized dorsal part of the hoof,
DIP joint, bursa and tendon sheath
•
DIP joint or navicular bursa:
desensitizes joint  diffusion, the
associated structures
•
Palmar foot syndrome, a lameness
can remain due to pathology within
the palmar part of the foot.
RADIOGRAPHS
•
Only technique to evaluate the hoof.
•
Radiograph: limited assessment of mineralised
tissues, 40% change in bone density is required
before it can be identified
•
Navicular bursography identifying adhesions
between the DDFT and navicular bone
Ultrasound
•
Frogs were trimmed down to moist and soaked in
water for 12 hours
Results
Horses Bursitis Thicken Nav
bursa
Adhesion
DDFT to
navicular
Hypoechoic
to anechoic
areas DDFT
and DDAL
Navicular
lame (28)
Increase vol
fluid
yes 3 horses 5 fore feet
Navicular
No Lame (7)
None No No No
Nuclear Scintigraphy
Horse
/Path
ology
Increase
IRU nav
bone
IRU
pool
phase
DDFT
IRU
insertio
n DDFT
Focal IRU
insertion of
the medial
CL of the
DIP joint
Focal IRU
insertion of
the lateral CL
of DIP Joint
IRU in
the
medial
palmar
process
of the
distal
phalanx
Focal
IRU med
and lat
palmar
process
es
36.6% 13% 14.3% 9.4% 15% 7.6% 3.4%
•
Positive correlation between scintigraphy and total MRI
grades
MRI
•
15 horses no definitive diagnosis
(radiography, ultrasonography and nuclear
scintigraphy)
•
Lameness exam Perineural analgesia: palmar
digital and abaxial sesamoid, intra-articular
analgesia : DIP joint / navicular bursa
•
•
Lameness: PD or abaxial , analgesia DIP navicular
bursa, proximal interphalangeal and fetlock
•
Radiograph: Navicular views
•
US
•
Nuclear scintigraphy
•
MRI
•
Treatment:
1) Corrective trimming and shoeing,
2) Box-rest and controlled walking (1 h daily ) for 6
months for all primary soft tissue injuries.
3) Medication of the navicular bursa, DIP joint or
digital flexor tendon sheath: hyaluronan, with or
without triamcinolone.
4) Shockwave
Injury DDFT Desmitis
CL
Primary
injuries
middle
or distal
phalanx
DSIL Navicular
bone
abnormali
ties
primary
abnorm
alities
of the
DIP
3 or
more
structu
res
33% 15% 7% 6% 5% 2.5% 17%
Outcome of treatment
•
28% primary DDF tendonitis: Excellent
•
53% had persistent or recurrent lameness.
Prognosis:
o
Markedly worse: combined NB and DDFT 95%
suffering persistent lameness.
o
Abnormalities of the NB 22% resumed full work
fracture.
o
Collateral desmitis: 29% excellent
o
Lesions of the DIP joint: Poor.
•
DDFT: lesions 1 or more sites 82.6% of limbs.
•
Most frequently
1) level of CSL and NB: 59.4%
2) level of the DSIL or insertion 35.1%,
3) level PIP joint 29.1%
4) level of the proximal phalanx 6.2%.
•
Type of lesions:
o
Level proximal phalanx: core lesions 90.3%
o
PIP joint core lesions 43.1% alone or in
combination.
o
DSIL : 38.2%
o
CSL: 10.5%
o
Medial and lateral CLs of the DIP joint: 28.2% and
12.4%
o
DIP joint and navicular bursa: 42.3% and 49.4%
•
Clinical examination, Xr, BS, and MRI ( aspect NB,
spongiosa, dorsal, palmar, proximal and distal
border was graded on a scale of 0–3)
•
(22 horses) 3 clinical categories
-Group 1, navicular pathology pain and lameness
Group 2, navicular pathology association with other
lesions
Group 3, horses with other causes of foot lameness.
Increased signal in the spongiosa of the NB MRI
may occur in association with lesions of the
fibrocartilage with or without subchondral bone or
reflecting a variety of alterations of trabecular
bone
Synovial fluid biomarkers
•
Pathology develops and a change in pattern of
the biomarkers will be detectable.
•
Joint damage: Decrease GAG, lower
GAG/cartilageoligomeric matrix protein ratios,
increased HA and relative increase in the
activity of the matrix and MMP
•
COMP: No significant changes between horses with
navicular disease and control horses.
•
DIP: navicular disease less GAG and lower
GAG/COMP ratio
•
HA, HA/COMP ratio, MMP-2/COMP ratio and
MMP-9/COMP ratio higher DIP of horses with
navicular disease.
•
Navicular bursae (navicular disease): lower GAG
GAG/COMP ratio and HA/COMP ratio was increased
and no difference HA. Higher relative activities of
MMP-2 and MMP-9 and the MMP-2/COMP ratio
and the MMP-9/COMP ratio.
Conclusion
“It is currently unknown what biomechanical
factors predispose to the lesions of the
podotrochlear apparatus and DDFT. It has been
proposed that reduction in the angle of the distal
phalanx within the hoof capsule may be related to
increased strain on the DDFT and navicular bone
and thus predispose to injury”
1990 2015
US
CT
MRIBS
Treatments
•
Therapeutic trimming and shoeing to reduce
biomechanical forces on the navicular/heel:
•
Of 30 (73%) horses with clinical signs of navicular
pain improved one grade of lameness within 6
weeks of corrective shoeing.
•
There is no standard shoeing technique for horses
with navicular pain
Shoes:
o
Arim shoe or half-round shoe has a rounded edge that
enhances breakover
o
The Natural Balance Shoe has a rockered toe
o
Egg bar shoe: heel support and more surface-to-ground
contact.
•
Raised heels: Heel wedge pad, reduces the tension between
the DDFT and navicular bone
•
Acute ligamentous injuries: 3 to 4 wedge pad decrease
tension of these soft tissue structures and gradually
decreases the quantity of heel elevation over time.
•
There were detectable concentrations of
triamcinolone acetonide in navicular bursa synovial
fluid of all groups after injection
•
All horses were treated with corticosteroids (40 mg
of methylprednisolone acetate) and hyaluronan (10
mg of sodium hyaluronate)
•
Rest 6 months
Force Plate 3000 pulses/ 10Hz 1/2 the pulses
between the heel bulbs, and the other were applied
over the middle third of the frog with the limb
elevated  FP
•
ESWT did not produce immediate analgesia or any
such effect during the week after treatment.
•
Corrective shoeing: wedge full pad, egg bar, heart
bar, open wide webbed or natural balance shoes
•
Injection: DIJ or DFTS, NB.
•
4–8 weeks of stall rest, control exercise
•
shock wave therapy: 1500 impulses per treatment
every 2 weeks for 3 treatments.
•
Only 22 of 56 (39.3%) horses had a successful
outcome.
•
Unsuccessful outcome (44.1%) had concurrent
DDFT, NB and NBU lesions, poor response
•
Therapeutic protocol for horses with combined
DDFT and NB lesions was not greatly
•
Single injection of BTXB: Alleviate
lameness for at least 14 days without
causing systemic adverse effects
Inclusion examination  FP Foot trim
 Wide
•
Web aluminum horseshoes (3o wedge)
•
Heel-elevation shoeing and
phenylbutazone
•
The DIPJ was injected 6 mg
triamcinolone
1990 2015
US
CT
MRIBS
SHOE
NSAID
TA+HA
SHOE
NSAID
TA+HA
QUESTIONS???

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Navicular disease

  • 3. 1990’s “Degenerative changes in structure, composition and mechanical function of the cartilage, subchondral bone and surrounding soft tissues, i.e. DDFT, impar ligament, collateral ligaments, navicular bursa and distal interphalangeal joint” EQUINE VETERINARY JOURNAL Review Article: Navicular disease: a review of what’s new A. B. M. RIJKENHUIZEN
  • 4. • The navicular bone central role • Diagnosis: clinical examination, analgesia (DP, DIP joint or bursa and Xr) • Etiopathogenesis: interaction of biomechanical stress and circulatory disturbance • Treatment: o orthopaedic shoeing o intra-articular or intrabursal injection o peripheral vasodilators (e.g. isoxuprine, pentoxifylline, warfarin)
  • 5. 1990’s • Surgical treatments: o Desmotomy of the navicular suspensory ligaments o Cutting the navicular suspensory ligaments o Perivascular sympathectomy for the digital arteries, with or without fasciolysis o Palmar digital neurectomy
  • 7. Today • Ultrasound • Nuclear scintigraphy • Computed tomography (CT) • Magnetic resonance imaging • Biomarkers
  • 8.
  • 9. Diagnostic analgesia • Palmar digital nerves: No desensitized dorsal part of the hoof, DIP joint, bursa and tendon sheath • DIP joint or navicular bursa: desensitizes joint  diffusion, the associated structures • Palmar foot syndrome, a lameness can remain due to pathology within the palmar part of the foot.
  • 10. RADIOGRAPHS • Only technique to evaluate the hoof. • Radiograph: limited assessment of mineralised tissues, 40% change in bone density is required before it can be identified • Navicular bursography identifying adhesions between the DDFT and navicular bone
  • 12. • Frogs were trimmed down to moist and soaked in water for 12 hours
  • 13. Results Horses Bursitis Thicken Nav bursa Adhesion DDFT to navicular Hypoechoic to anechoic areas DDFT and DDAL Navicular lame (28) Increase vol fluid yes 3 horses 5 fore feet Navicular No Lame (7) None No No No
  • 15. Horse /Path ology Increase IRU nav bone IRU pool phase DDFT IRU insertio n DDFT Focal IRU insertion of the medial CL of the DIP joint Focal IRU insertion of the lateral CL of DIP Joint IRU in the medial palmar process of the distal phalanx Focal IRU med and lat palmar process es 36.6% 13% 14.3% 9.4% 15% 7.6% 3.4% • Positive correlation between scintigraphy and total MRI grades
  • 16.
  • 17. MRI
  • 18. • 15 horses no definitive diagnosis (radiography, ultrasonography and nuclear scintigraphy) • Lameness exam Perineural analgesia: palmar digital and abaxial sesamoid, intra-articular analgesia : DIP joint / navicular bursa •
  • 19.
  • 20.
  • 21. • Lameness: PD or abaxial , analgesia DIP navicular bursa, proximal interphalangeal and fetlock • Radiograph: Navicular views • US • Nuclear scintigraphy • MRI
  • 22. • Treatment: 1) Corrective trimming and shoeing, 2) Box-rest and controlled walking (1 h daily ) for 6 months for all primary soft tissue injuries. 3) Medication of the navicular bursa, DIP joint or digital flexor tendon sheath: hyaluronan, with or without triamcinolone. 4) Shockwave
  • 23. Injury DDFT Desmitis CL Primary injuries middle or distal phalanx DSIL Navicular bone abnormali ties primary abnorm alities of the DIP 3 or more structu res 33% 15% 7% 6% 5% 2.5% 17%
  • 24. Outcome of treatment • 28% primary DDF tendonitis: Excellent • 53% had persistent or recurrent lameness. Prognosis: o Markedly worse: combined NB and DDFT 95% suffering persistent lameness. o Abnormalities of the NB 22% resumed full work fracture. o Collateral desmitis: 29% excellent o Lesions of the DIP joint: Poor.
  • 25. • DDFT: lesions 1 or more sites 82.6% of limbs. • Most frequently 1) level of CSL and NB: 59.4% 2) level of the DSIL or insertion 35.1%, 3) level PIP joint 29.1% 4) level of the proximal phalanx 6.2%.
  • 26. • Type of lesions: o Level proximal phalanx: core lesions 90.3% o PIP joint core lesions 43.1% alone or in combination. o DSIL : 38.2% o CSL: 10.5% o Medial and lateral CLs of the DIP joint: 28.2% and 12.4% o DIP joint and navicular bursa: 42.3% and 49.4%
  • 27. • Clinical examination, Xr, BS, and MRI ( aspect NB, spongiosa, dorsal, palmar, proximal and distal border was graded on a scale of 0–3) • (22 horses) 3 clinical categories -Group 1, navicular pathology pain and lameness Group 2, navicular pathology association with other lesions Group 3, horses with other causes of foot lameness.
  • 28.
  • 29. Increased signal in the spongiosa of the NB MRI may occur in association with lesions of the fibrocartilage with or without subchondral bone or reflecting a variety of alterations of trabecular bone
  • 31. • Pathology develops and a change in pattern of the biomarkers will be detectable. • Joint damage: Decrease GAG, lower GAG/cartilageoligomeric matrix protein ratios, increased HA and relative increase in the activity of the matrix and MMP
  • 32. • COMP: No significant changes between horses with navicular disease and control horses. • DIP: navicular disease less GAG and lower GAG/COMP ratio • HA, HA/COMP ratio, MMP-2/COMP ratio and MMP-9/COMP ratio higher DIP of horses with navicular disease. • Navicular bursae (navicular disease): lower GAG GAG/COMP ratio and HA/COMP ratio was increased and no difference HA. Higher relative activities of MMP-2 and MMP-9 and the MMP-2/COMP ratio and the MMP-9/COMP ratio.
  • 33. Conclusion “It is currently unknown what biomechanical factors predispose to the lesions of the podotrochlear apparatus and DDFT. It has been proposed that reduction in the angle of the distal phalanx within the hoof capsule may be related to increased strain on the DDFT and navicular bone and thus predispose to injury”
  • 36. • Therapeutic trimming and shoeing to reduce biomechanical forces on the navicular/heel: • Of 30 (73%) horses with clinical signs of navicular pain improved one grade of lameness within 6 weeks of corrective shoeing. • There is no standard shoeing technique for horses with navicular pain
  • 37. Shoes: o Arim shoe or half-round shoe has a rounded edge that enhances breakover o The Natural Balance Shoe has a rockered toe o Egg bar shoe: heel support and more surface-to-ground contact. • Raised heels: Heel wedge pad, reduces the tension between the DDFT and navicular bone • Acute ligamentous injuries: 3 to 4 wedge pad decrease tension of these soft tissue structures and gradually decreases the quantity of heel elevation over time.
  • 38. • There were detectable concentrations of triamcinolone acetonide in navicular bursa synovial fluid of all groups after injection
  • 39. • All horses were treated with corticosteroids (40 mg of methylprednisolone acetate) and hyaluronan (10 mg of sodium hyaluronate) • Rest 6 months
  • 40.
  • 41. Force Plate 3000 pulses/ 10Hz 1/2 the pulses between the heel bulbs, and the other were applied over the middle third of the frog with the limb elevated  FP • ESWT did not produce immediate analgesia or any such effect during the week after treatment.
  • 42. • Corrective shoeing: wedge full pad, egg bar, heart bar, open wide webbed or natural balance shoes • Injection: DIJ or DFTS, NB. • 4–8 weeks of stall rest, control exercise • shock wave therapy: 1500 impulses per treatment every 2 weeks for 3 treatments.
  • 43. • Only 22 of 56 (39.3%) horses had a successful outcome. • Unsuccessful outcome (44.1%) had concurrent DDFT, NB and NBU lesions, poor response • Therapeutic protocol for horses with combined DDFT and NB lesions was not greatly
  • 44. • Single injection of BTXB: Alleviate lameness for at least 14 days without causing systemic adverse effects
  • 45. Inclusion examination  FP Foot trim  Wide • Web aluminum horseshoes (3o wedge) • Heel-elevation shoeing and phenylbutazone • The DIPJ was injected 6 mg triamcinolone
  • 46.