Navicular disease
or
Foot pain syndrome

What happen???

1990s

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 JOURNALReview Article: Navicular disease: a review of whats newA. 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:

orthopaedic shoeing

intra-articular or intrabursal injection

peripheral vasodilators (e.g. isoxuprine, pentoxifylline, warfarin)

1990s

Surgical treatments:

Desmotomy of the navicular suspensory ligaments

Cutting the navicular suspensory ligaments

Perivascular sympathectomy for the digital arteries, with or without fasciolysis

Palmar digital neurectomy

Troy TrumbleNick 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

HorsesBursitisThicken Nav bursaAdhesion DDFT to navicular Hypoechoic to anechoic areas DDFT and DDAL

Navicular lame (28)Increase vol fluidyes3 horses5 fore feet

Navicular No Lame (7)NoneNoNoNo

Nuclear Scintigraphy

Horse/Pathology Increase IRU nav boneIRU pool phase DDFTIRU insertion DDFTFocal IRU insertion of the medial CL of theDIP jointFocal IRU insertion of the lateral CL of DIP JointIRU in the medial palmar process of the distal phalanxFocal IRU med and lat palmar processes

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

In 2 weeks: MRI

Lameness: PD or abaxial , analgesia DIP navicular bursa, proximal interphalangeal and fetlock

Radiograph: Navicular views

US

Nuclear scintigraphy

MRI

Treatment:

Corrective trimming and shoeing,

Box-rest and controlled walking (1 h daily ) for 6 months for all primary soft tissue injuries.

Medication of the navicular bursa, DIP joint or digital flexor tendon sheath: hyaluronan, with or without triamcinolone.

Shockwave

Injury

DDFTDesmitis CL Primary injuries middle or distal phalanx DSILNavicular bone abnormalities primary abnormalities of the DIP 3 or more structures

33%15%

7%

6%

5% 2.5%

17%

Outcome of treatment28% primary DDF tendonitis: Excellent

53% had persistent or recurrent lameness.

Prognosis: Markedly worse: combined NB and DDFT 95% suffering persistent lameness.

Abnormalities of the NB 22% resumed full work fracture.

Collateral desmitis: 29% excellent

Lesions of the DIP joint: Poor.

DDFT: lesions 1 or more sites 82.6% of limbs.

Most frequently

level of CSL and NB: 59.4%

level of the DSIL or insertion 35.1%,

level PIP joint 29.1%

level of the proximal phalanx 6.2%.

Type of lesions:

Level proximal phalanx: core lesions 90.3%

PIP joint core lesions 43.1% alone or in combination.

DSIL : 38.2%

CSL: 10.5%

Medial and lateral CLs of the DIP joint: 28.2% and 12.4%

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 03)

(22 horses) 3 clinical categories

-Group 1, navicular pathology pain and lameness Group 2, navicular pathology association with other lesionsGroup 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

USCTMRIBS

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: Arim shoe or half-round shoe has a rounded edge that enhances breakover

The Natural Balance Shoe has a rockered toe

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

Follow up: returning to exercise

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.

48 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

USCTMRIBS

SHOE
NSAIDTA+HA

SHOE
NSAIDTA+HA

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