Navicular suspensory desmotomy in the treatment of navicular disease: technique and preliminary results


Wright, I.M.

Equine Veterinary Journal 18(6): 443-446

1986


The technique of navicular suspensory desmotomy for the treatment of navicular disease is described and the rationale behind its development is discussed. To date 16 horses involved in a clinical evaluation of the technique have been assessed six months after surgery. Thirteen of these horses are able to work without lameness.

EQUINE
VETERINARY
JOURNAL
443
Equine
vet.
J.
(1986)
18(6),
443-446
Navicular
suspensory
desmotomy
in
the
treatment
of
navicular
disease:
Technique
and
preliminary
results
I.
M.
WRIGHT
Department
of
Clinical
Veterinary
Medicine,
University
of
Cambridge,
Madingley
Road,
Cambridge
CB3
OES
Summary
The
technique
of
navicular
suspensory
desmotomy
for
the
treatment
of
navicular
disease
is
described
and
the
rationale
behind
its
development
is
discussed.
To
date
16
horses
involved
in
a
clinical
evaluation
of
the
technique
have
been
assessed
six
months
after
surgery.
Thirteen
of
these
horses
are
able
to
work
without
lameness.
Introduction
THE
pathogenesis
of
navicular
disease
remains
obscure
and
there
is
debate
whether
a
single
pathological
entity
exists
(Anon
1984).
Nevertheless,
in
the
past
decade
a
number
of
treatments
have
been
described
for
the
management
of
navicu-
lar
disease.
These
have
included
anticoagulant
therapy
(Colles
1979b;
Colles
1982),
peripheral
vasodilating
agents
(Rose,
Allen,
Hodgson
and
Kohnke
1983)
and
corrective
farriery
(Ostblom,
Lund
and
Melsen
1982;
Ostblom,
Lund
and
Melsen
1984).
Following
the
implication
of
the
ligamenta
sesamoidea
collateralia
(LSC)
(Anon,
1972)
in
the
aetiology
of
navicular
disease
(Badoux
1966;
Rooney
1969,
1974)
the
technique
of
desmotomy
of
the
LSC
(navicular
suspensory
desmotomy)
was
developed
by
Dr
Niels
Lowig
Larsen
(personal
com-
munication).
The
LSC
have
their
origins
proximal
to
the
medial
and
lateral
depressions
on
the
distal
extremity
of
the
first
phalanx
(Sisson
1975),
where
they
are
partly
blended
with
the
ligamenta
collateralia
of
the
proximal
interphalangeal
joint
(Fig
1).
They
are
broad
elastic
ligaments
which
continue
in
a
distopalmar
direction
across
the
proximal
interphalangeal
joint,
where
they
are
intimately
related
to
the
fibrous
joint
capsule,
before
traversing
the
body
of
the
second
phalanx
(Fig
3).
The
primary
Fig
1
(left).
Anatomical
model
of
distal
limb:
(a)
ligamentum
sesamoides
collateralia;
(b)
collateral
ligament
of
first
interphalangeal
joint;
(c)
lateral
palmar
ligament
of
first
inter-
phalangeal
joint;
(d)
extensor
branch
of
interosseous
ligament;
(e)
extensor
digitorum
communis
tendon
d
Fig
2
(right).
Limb
depicting
palpable
anatomical
landmarks:
(a)
extensor
digitorum
communis
tendon;
(b)
proximal
interphalangeal
joint;
(c)
extensor
branch
of
interosseous
ligament;
(--•)
medial
and
lateral
eminences
at
the
distal
extremity
of
the
first
phalanx
a
444
EQUINE
VETERINARY
JOURNAL
insertion
of
the
LSC
is
to
the
proximal
border
of
the
distal
sesamoid
bone
but
a
branch
of
each
ligament
also
inserts
on
the
axial
surface
of
the
adjacent
cartilago
ungularis
and
palmar
process
of
the
distal
phalanx.
Bartel,
Shryver,
Lowe
and
Parker
(1978)
claim
that
the
LSC
act
as
springs
to
resist
extension
of
the
distal
interphalangeal
joint
while
Badoux
(1966)
and
Leach
(1983)
believe
that
these
ligaments
are
under
severe
tension
at
the
end
of
the
stride
(immediately
prior
to
breakdown)
and
relax
at
the
beginning
of
the
stride
(at
break-
down).
Rooney
(1969,
1974)
suggests
that
the
LSC
anchor
the
distal
sesamoid
bone
thereby
preventing
its
descent
as
the
interphalangeal
joints
hyperextend
during
weight
bearing.
This
produces
vibratory
or
third
order
acceleration
forces
between
the
navicular
bone
and
flexor
digitorum
profundus
tendon.
Ostblom
et
a/
(1984)
consider
that
the
histological
and
radiographic
changes
of
navicular
disease
may
be
explained
as
adaptation
by
the
navicular
bone
to
mechanical
stress
and
so
removal
of
the
anchor
of
the
LSC
may
be
of
benefit
in
the
treatment
of
navicular
disease.
This
paper
describes
the
tech-
nique
of
navicular
suspensory
desmotomy
and
reports
the
initial
results
of
a
clinical
trial.
Materials
and
methods
Since
1984,
a
clinical
trial
has
been
in
progress
at
the
Department
of
Clinical
Veterinary
Medicine
of
the
University
of
Cambridge
to
assess
the
role
of
navicular
suspensory
desmotomy
in
the
treatment
of
navicular
disease.
The
criteria
for
diagnosis
and
inclusion
in
the
trial
are:
(1)
chronic
forelimb
lameness;
(2)
positive
response
to
local
analgesia
of
the
medial
and
lateral
palmar
digital
nerves;
(3)
radiological
evidence
of
significant
navicular
bone
pathology,
as
defined
by
O'Brien,
Millman,
Pool
and
Suter
(1975),
Colles
(1979a,
1982)
and
MacGregor
(1984),
assessed
by
an
independent
diplomate
in
veterinary
radiology.
Radiological
evaluation
is
based
upon
three
standard
projections;
dorsoproximal-palmarodistal
oblique
(upright
pedal),
lateromedial
and
palmaroproximal-dorsodistal
oblique
(flexor
view)
(Morgan
1972;
Smallwood,
Shively,
Rendano
and
Habel
1985).
Animals
which
complied
with
these
criteria
but
in
which
further
potentially
significant
clinical
or
radiological
lesions
were
detected
elsewhere
in
the
limb
were
not
included
in
the
trial.
Cases
were
assessed
clinically
and
radiographically
at
six
monthly
intervals
following
surgery.
The
first
clinical
assess-
ment
of
Cases
1
to
16
are
reported.
Technique
Surgery
was
performed
under
general
anaesthesia
with
the
horse
in
dorsal
recumbency.
Following
routine
surgical
preparation,
the
distal
limb
was
allowed
to
flex
and
lie
adjacent
to
the
thoracic
wall.
In
this
position
all
four
surgical
sites
were
readily
accessible
without
recourse
to
movement
of
the
animal
during
surgery.
The
anatomical
landmarks
were
the
extensor
digitorum
communis
tendon,
the
first
interphalangeal
joint,
the
medial
and
lateral
eminences
at
the
distal
extremity
of
the
first
phalanx
and
the
extensor
branches
of
the
interos-
seous
ligament
(Fig
2).
An
oblique
4
cm
skin
incision
was
made,
approximately
45°
to
the
long
axis
of
the
limb,
com-
mencing
over
the
eminence
at
the
origin
of
the
ligamentum
collateralia
of
the
proximal
interphalangeal
joint
and
termina-
ting
at
the
border
of
the
extensor
digitorum
communis
tendon
(Fig
4).
Following
division
of
the
subcutaneous
and
periliga-
mentar
fascia
along
the
line
of
the
skin
incision,
the
fibres
of
the
LSC
were
identified
running
at
90°
to
the
wound.
The
axial
border
of
the
ligament
was
readily
identified
and
separated
d
e
C
I
)
4
.--
--IF
Fig
3.
Dissected
specimen:
(a)
ligamentum
sesamoidea
collateralia;
(b)
proximal
interphalangeal
joint
capsule;
(-k)
capsular
vein;
(c)
dorsal
branch
of
proximal
phalangeal
vein;
(d)
extensor
branch
of
interosseous
ligament;
(e)
extensor
digitorum
communis
tendon
from
the
tendon
of
the
extensor
digitorum
communis
by
sharp
dissection.
A
small
but
distinct
pouch
of
the
proximal
inter-
phalangeal
joint
capsule
accompanied
by
a
capsular
vein
was
identified
in
the
angle
between
these
two
structures
(Fig
3).
At
the
palmar
extremity
of
the
incision
the
dorsal
branch
of
the
proximal
phalangeal
vein
should
be
identified
and
preserved
(Fig
3).
A
tenaculum
was
used
to
separate
the
LSC
from
the
under-
lying
joint
capsule.
It
was
directed
to
emerge
at
the
eminence
on
the
first
phalanx
which
marks
the
poorly
defined
junction
of
the
LSC
and
ligamentum
collateralia
of
the
proximal
inter-
phalangeal
joint
(Fig
4).
This
procedure
was
facilitated
by
extension
of
the
foot
and
pastern.
Following
division
of
the
ligament
with
a
tenotomy
blade
the
area
was
inspected
to
ensure
complete
transection.
At
the
palmar
aspect
this
was
done
by
palpation
of
the
eminence
at
the
origin
of
the
liga-
mentum
collateralia
while
dorsally
visual
appraisal
was
possible.
The
skin
wound
was
coapted
with
interrupted
sutures
of
the
non-absorbable
material
(Fig
4)
before
the
procedure
was
repeated
to
divided
the
opposite
LSC
of
the
ipsilateral
limb.
Postoperative
management
Protective
dressings
were
applied
from
hoof
to
midmeta-
carpus.
Postoperative
medication
consisted
of
tetanus
EQUINE
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JOURNAL
445
Fig
4.
Surgical
procedure:
(left)
oblique
skin
incision;
(centre)
isolation
of
the
LSC
with
a
tenaculum;
(right)
wound
closure
prophylaxis
and
five
days'
parenteral
penicillin.
The
horses
were
hand
walked
for
20
mins
twice
a
day
and
dressings
changed
at
48
to
72
h
intervals
until
suture
removal
10
to
14
days
after
surgery.
The
hooves
could
be
dressed
and
reshod
at
anytime
following
surgery
when
care
was
taken
to
balance
the
foot
before
fitting
a
standard
concave
fullered
shoe.
Walking
in
hand
continued
for
the
first
three
weeks
when
light
ridden
exercise
was
begun
and
the
horse
turned
out
if
required.
Following
an
ascending
exercise
programme,
full
work
could
be
resumed
three
months
after
surgery.
The
importance
of
regular
exercise
regimes
was
stressed
to
owners.
Results
A
bilateral
desmotomy
was
performed
in
each
of
the
first
16
cases
of
the
clinical
trial
(Table
1).
The
period
of
lameness
prior
to
surgery
varied
from
one
to
48
months
with
a
mean
of
15.4
months.
During
this
time
a
variety
of
treatment
regimes
had
been
attempted.
The
clinical
outcome
is
that
recorded
six
months
after
surgery,
ie,
three
months
after
resumption
of
full
work.
Case
4
had
been
in
its
present
ownership
for
six
months
and
on
inquiry
had
been
lame
in
the
same
forelimb,
albeit
without
investigation,
for
the
previous
12
months.
Case
8,
although
lame,
has
continued
showjumping
while
receiving
oral
phenyl-
butazone.
Neurectomy
of
the
palmar
digital
nerves
was
alleged
to
have
been
performed
on
two
cases
before
surgery.
The
owner
reported
that
a
unilateral
neurectomy
had
been
performed
six
TABLE
1:
Case
histories
of
horses
undergoing
navicular
suspensory
desmotomy
and
clinical
outcome
Case
Age
Period
of
Previous
treatment
(years)
lameness
months
Clinical
outcome
1
7
4
Farriery
No
lameness,
hunting
2
12
24
Farriery,
phenylbutazone
isoxuprine,
neurectomy
No
lameness,
showjumping
(unilateral),
pulsating
electromagnetism
3
7
5
Farriery,
warfarin
No
lameness,
eventing
4
9
5
I+
121
Farriery,
phenylbutazone
No
lameness,
showjumping
5
9
5
Phenylbutazone
No
lameness,
showjumping
6
8
12
None
No
lameness,
hacking
7
7
12
Farriery
No
lameness,
hacking
8
12
36
Farriery,
phenylbutazone,
Lame,
showjumping
9
8
1
Phenylbutazone
No
lameness,
eventing
10
10
48
Farriery,
phenylbutazone
Lame
11
6
12
None
No
lameness,
hacking
12
10
12
Farriery,
warfarin
No
lameness,
endurance
13
6 6
Corticosteroids
Lame
14
18
36
None
No
lameness,
hacking
15
13
10
Warfarin
No
lameness,
riding
club
activities
16
8
18
Phenylbutazone,
neurectomy
No
lameness,
showjumping
months
before
referral
in
Case
2.
Skin
scars
were
present
but
no
sensory
deficit
was
demonstrable.
Bilateral
scar
tissue
was
present
in
Case
16
following
`neurectomy'
at
least
18
months
earlier
but
again
no
deep
or
cutaneous
sensory
loss
could
be
detected.
Discussion
The
16
horses
reported
in
this
paper
exhibited
evidence
of
bilateral
navicular
disease
and
thus
in
every
case
desmotomy
of
the
LSC
was
performed
on
both
forelimbs.
No
tourniquet
is
necessary
for
this
procedure,
indeed
in
the
author's
opinion
valuable
anatomical
landmarks
are
lost
with
its
use.
In
this
series,
an
escape
of
synovial
fluid
was
noted
in
approximately
25
per
cent
of
cases
on
division
of
the
LSC
owing
to
its
intimate
relationship
with
the
underlying
joint
capsule.
No
attempt
was
made
to
repair
these
perforations
and
no
dif-
ferences
in
wound
healing
or
clinical
outcome
have
been
noted
to
date.
Careful
interposition
of
the
tenaculum
between
the
LSC
and
dorsal
pouch
of
the
first
interphalangeal
joint
should
limit
the
number
of
synovial
cavities
breached.
No
deep
or
cutaneous
sensory
loss
has
been
demostrated
in
any
horses
following
navicular
suspensory
desmotomy.
Post-
operative
analgesia
has
not
been
considered
necessary
either
on
humane
grounds
or
to
enable
horses
to
begin
walking
exercise.
Animals
frequently
exhibit
a
stiff
gait
when
beginning
exercise
but
this
progressively
improves
during
convalescence.
The
regime
outlined,
although
empirical
and
open
for
modifi-
cation
as
experience
dictates,
has
so
far
produced
satisfactory
results.
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(1972)
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T.
and
Habel,
R.
E.
(1985)
A
standardized
nomenclature
for
radiographic
projections
used
in
veterinary
medicine.
Vet.
Radio!.
26,
2-9.
Received
for
publication
24.2.86
Accepted
15.7.86
ABSTRACT
Anaesthesia,
pharmacology
and
therapeutics
Effects
of
multiple
intramuscular
injections
and
doses
of
dexamethasone
on
plasma
cortisol
concentrations
and
adrenal
responses
to
ACTH
in
horses
MACHARG,
M.
A.,
BOTTOMS,
G.
D.,
CARTER,
G.
K.
and
JOHNSON,
M.
A.
(1985)
Am.
J.
vet.
Res.
46,
2285-2287.
DEXAMETHASONE
and
other
synthetic
analogues
of
the
major
circulating
glucocorticosteroid,
hydrocortisone
(cortisol),
are
widely
used
to
treat
allergic,
immune-mediated
and
other
inflammatory
disorders
in
the
horse.
In
some
countries
these
agents
are
also
used
illegally
to
dope
racehorses
in
the
hope
of
improving
performance.
A
potential
problem
associated
with
prolonged
glucocorticosteroid
therapy
is
that
the
suppression
of
the
pituitary-adrenal
axis
which
occurs
during
a
course
of
treatment
may
precipitate
adrenocortical
insufficiency
when
therapy
is
discontinued.
In
this
study
adrenocortical
function
was
assessed
in
two
groups
of
six
horses
given
dexamethasone
(0.044
mg/kg
and
0.088
mg/kg
bodyweight
[bwt])
intramuscularly
(im)
every
fifth
day
for
a
total
of
six
treatments.
Blood
samples
were
collected
daily
and
plasma
cortisol
concentrations
were
later
measured
using
a
radioimmunoassay
kit
procedure.
ACTH
response
tests
were
performed
using
repositol
corticotrophin
two
days
before
the
first
injection
of
dexamethasone
and
again
eight
days
after
the
last
injection.
Mean
plasma
cortisol
concentrations
before
each
dexamethosone
injection
were
generally
in
the
range
of
90
to
180
ng/ml.
Cortisol
concentrations
were
maximally
suppres-
sed
24
h
after
each
injection
with
mean
concentrations
generally
less
than
40
ng/ml
at
this
time.
Cortisol
concentrations
rose
progressively
on
each
succeeding
day
and
had
returned
to
pre-
treatment
values
in
all
horses
by
four
days
after
each
dexamethasone
injection.
The
response
of
the
horses
to
repository
ACTH
(1
iu/kg
bwt)
was
the
same
eight
days
after
the
course
of
dexamethasone
treatment
as
the
response
observed
before
treatment.
Mean
plasma
cortisol
concentrations
were
about
150
ng/ml
before
ACTH
administration.
Concentrations
were
significantly
increased
by
2
h
and
reached
a
plateau
approximately
twice
the
baseline
concentration
betwen
2
and
8
h
after
ACTH
administration.
The
authors
concluded
that
the
two
commonly
used
doses
of
dexamethasone
employed
in
this
study
(0.044
mg/kg
and
0.088
mg/kg
bwt
at
five
day
intervals)
did
not
induce
measurable
adrenal
atrophy
although
they
did
induce
marked
but
temporary
suppression
of
adrenocortical
output.
Abstractor's
comments.
This
work
provides
documentation
to
support
the
clinical
impression
of
a
number
of
veterinarians
that
horses
do
not
readily
develop
adrenal
atrophy
in
response
to
intermittent
treatment
with
therapeutic
doses
of
dexametha-
sone.
However,
the
maintenance
of
adequate
endogenous
adrenal
function
is
likely
related
to
the
dosage
and
interval
between
doses.
If
the
clinical
situation
demands
a
prolonged
course
of
therapy
then
the
minimum
dose
needed
to
control
the
clinical
signs
should
be
administered
at
the
longest
possible
dosage
interval.
Whenever
possible,
short
acting
steroids
such
as
prednisone
or
prednisolone
administered
orally
should
be
used
instead
of
the
more
adrenal
suppressive
agents
such
as
dexamethasone,
triamcinolone
and
flumethasone.
Adrenal
suppressive
effects
can
be
reduced
further
by
the
administration
of
short
acting
glucocorticosteroid
drugs
in
the
morning
and
at
intervals
of
more
than
24
h.
The
authors
point
out
that
the
cyclic
and
day
to
day
fluctuations
in
plasma
cortisol
concentrations
makes
the
interpretation
of
the
results
of
isolated
samples
difficult.
If
adrenal
dysfunction
is
suspected
an
ACTH
stimulation
test
can
prove
useful
diagnostically.
The
number
of
samples
and
time
required
for
this
test
can
be
reduced
by
using
synthetic
ACTH
in
aqueous
solution
(1
mg/horse
im
or
intravenously)
rather
than
repository
corticotrophin.
Samples
can
be
collected
before
and
2
h
after
ACTH
administration
rather
than
at
2
h
intervals
up
to
10
h
as
used
in
this
paper.
The
wide
disparity
in
plasma
cortisol
concentrations
reported
by
different
laboratories
reflects
the
different
assay
methods
used
and
emphasises
the
need
to
estab-
lish
'normal
ranges'
in
each
laboratory
before
the
results
of
cor-
tisol
assays
on
clinical
cases
can
be
interpreted.
W.
DAVID
WILSON