National Board Examination Review

Equine Lameness and Surgery

Lameness Examination (Merck 777,813 Adams 134-141)

1. No lameness exam is complete without a history, physical exam, hooftester exam, jogging
or lunging, flexion tests and regional (perineural or intra-articular) anesthesia. Ancillary
diagnostics that may be indicated, based on the results of the initial exam include radiography,
ultrasonography, and nuclear scintigraphy, among others.

2. Lameness is commonly indicated by a headnod, hip hike, decreased cranial phase of

stride or height of stride, reduction in range of motion, tendency to veer to the left or right.
Signs of neurologic disease must be distinguished from lameness, if there is any doubt.

3. Once a limb has been identified as the source of lameness, regional anesthesia should proceed
from distal to proximal (in real-life, this is sometimes suspended based on physical and
historical findings like obvious middle carpal joint effusion).

• Palmar digital nerve block (heel block): Medial and lateral palmar digital nerves.
Blocks sensation of the heel, heel bulbs, navicular bone/bursa; the caudal third of the foot.
This will not block the lameness associated with laminitis. Horses with navicular disease,
septic navicular bursitis, or caudal subsolar abscess will improve significantly.
• Abaxial/basisesamoid block (foot block): Medial and lateral palmar digital nerves.
Blocks the whole foot, distal interphalangeal (coffin) joint, most of pastern region.
Horses with septic or arthritic disease of the coffin joint or navicular bursa, any subsolar
abscess, P3 fracture, or laminitis will improve significantly.
• Low four-point/low volar block: Palmar and palmar metacarpal nerves. Blocks the
metacarpophalangeal joint (fetlock), and everything distal to it. This may include condylar
fractures (distal cannon bone/MCIII), Pl or P2 fracture, sesamoid fractures, osteochondral
fragments (chip fractures) of Pl.
• High four-point/high volar block: More proximal palmar and palmar metacarpal nerves.
Blocks most of the superficial and deep digital flexor tendons, distal check (accesory)
ligament, splint bones (MC or MT II/IV). Horses with lameness from bowed tendons
(superficial digital flexor desmitis), distal check ligament desmitis, DDF tendon injury, splint
bone fracture, some suspensory lesions will improve. Injury to the origin of the suspensory or
proximal palmar avulsion of the cannon bone (MCIII) will not improve, if the lesion is
proximal to the blocking site.

4. Intra-articular anesthesia (Adams 145-150)

• Distal interphalangeal joint: Coffin. Lameness from DIP arthritis (low ringbone) or from
articular fracture of P3 will improve.
• Proximal interphalangeal joint: Pastern. Lameness from PIP arthritis (high ringbone)
will improve.
• Metacarpophalangeal joint: Fetlock. Lameness from MCP arthritis, condylar or
sesamoid fracture, or incomplete sagittal PI fracture will improve.
• Carpus: Sometimes referred to as the knee. There are three joints (antebrachiocarpal,
middle carpal, carpometacarpal); the bottom two communicate. Blocking either of the top
two will improve lameness associated with distal radial or carpal chip fractures
(osteochondral fragments) or intercarpal ligament injuries. We don't generally block the
CMC joint.
• Tarsus: The hock. There are four joints (tibiotarsal, proximal intertarsal, distal intertarsal,
tarsometatarsal); the top two communicate. It is most common to block the lower two
oints, because these are commonly prone to arthritis (known as bone spavin). Blocking the
top two joints will improve lameness associated with OCD of the distal intermediate ridge
of the tibia, medial malleolus of the tibia, trochlear ridges of the talus.
• Stifle: The true knee. There are three joints (femoropatellar, medial and lateral
femorotibial). The femoropatellar and medial femorotibial joint communicate. Blocking
the medial femorotibal will block lameness associated with arthritis, osseus cyst-like lesion
(osteochondrosis) of the medial femoral condyle, and lameness associated with trochlear
ridge OCD (cruciates and meniscus also blocked).

Lameness and Lay Terminology (Merck 820-7)

Working from distal to proximal

Conditions associated with the foot:

Remember, any foot lameness may cause increased digital pulses.
1. Foot abscess: Also referred to as a subsolar abscess, or if it breaks out at the coronary band
as a gravel. Most common cause of acute non-weight bearing lameness (every bit as lame as if
they had a fracture). Use hooftesters to locate site, and then pare with hoofknife, to establish
drainage. Treatment is daily soaking and bandaging until drainage and lameness resolve.

2. Pedal osteitis: Vague condition of P3 lysis/resorption/remodeling. Specific cause

unknown, but likely related to repetitive concussion or sole bruising. More common in
forelimbs, presentation is similar to navicular syndrome. Treatm nt is but /r st/shoein changes.

3. Street nail: Septic navicular bursitis from penetrating wound near middle of frog.
Frequently, no history of penetrating injury, and hole is difficult to find. Horses present non-
weightbearing lame with effusion of the digital sheath, increased digital pulse, painful on
hooftester exam. Workup includes identification of hole, and fistulogram to confin-n
communication with the navicular bursa. Submission of fluid from navicular bursa will rule
the diagnosis in or out (elevated WBC/TP). Prognosis is guarded (better in hindlimb than in
forelimb).

4. Sole bruise: Causes a focal area of pink sole, positive on hooftester exam. May have focal
pain on hooftester, without pink area (blood has not yet settled out from bruise on solar
corium). A bruise in the heel, between the bar and the wall is known as a corn.

5. Canker: Common in draft breeds in moist environments, canker is a proliferative disease

of the frog and sole for which there is no known cause (likely anaerobic or fungal etiology).
Treatment is resection of proliferative tissue, bandaging, maintenance in a dry environment.
 6. Sidebones: Ossification of the collateral (alar) cartilages of P3. These can be palpated and
seen radiographically, but do not cause lameness. Common in draft breeds. Perhaps related
to chronic imbalance in shoeing.

7. Laminitis (Founder): More common in front feet, but often all 4 feet are affected. Ponies
appear predisposed. May be idiopathic, but several things may cause it. These are
carbohydrate overload (sudden access to lush pasture or mischievous visit to the grain cart),
endotoxemia (from colic or retained placenta), bedding on black walnut shavings, pituitary
adenoma (equine Cushing's), hypothyroidism, corticosteroids, preferential weight bearing
from lameness in the contralateral limb. Inciting lesion is vasoconstriction (AVAs),
ultimately leading to separation of the sensitive and insensitive lamina, or at least severe
inflammation of the sensitive lamina. Radiographically, the dorsal surface of P3 may rotate
ventrally, with respect to the dorsal hoof wall, or P3 may appear to sink. Clinical signs
include a stance opposite that which is observed in horses with severe navicular syndrome
(focus of pain is heels in navicular syndrome, while focus of pain is toes in laminitis; this is
reflected by hooftester exam). They stand leaning all of their weight back, while navicular
horses lean forward, or are recumbent. Horses are extremely painful, with acute onset:
unwilling to pick up feet, or to turn in a small circle; digital pulses are bounding, may appear
"stuck in the mud", hooftesters reveal toe pain, though often pain is severe enough that it is
detected over entire sole; a cleft may form at the coronary band. Chronic cases are not
uncommon, and these horses may have the classic "slipperfoot" and hoof wall rings of
chronically foundered animals. Treatment is controversial, but it is safe to say that the
underlying problem should be addressed, and anti-inflammatory and analgesic therapy
initiated (bute, frog support). Bed stall deeply, don't make shoeing changes rapidly; feed only
hay. No steroids!

8. Navicular syndrome: Heel pain syndrome, or podotrochleosis. More common in horses

over 4 years old. Quarter Horses and Warmbloods appear predisposed. Very unusual in
Arabians. Usually bilateral in forefeet, and doesn't occur in hindfeet. May be associated with
DJD of DIP jt. Causes are unknown but likely have to do with conformation (small feet, big
horse), poor shoeing, repetitive concussion, with a possible heritable component (result may be
ischemia). Radiographically, can see lollipops on the distal margin of the navicular bone (best
seen on the dorsosolar aka standdown or down angled oblique projection). Clinical signs
include a leaning foreword stance, short strides with preference to place toe on ground first,
pain elicited over heels on hooftester exam. Lameness will improve following a palmar digital
nerve block in one leg, but may exacerbate the lameness in the contralateral limb ("switching").
Treatment is shoeing changes (wedge, improvement of breakover with shorter toes), bute,
possibly isoxsuprine. Cases refractory to conservative management may be treated with palmar
digital neurectomy, only if lameness resolves with PDN block. The most common
postoperative complication is painful neuroma formation, and reinnervation also occurs.

9. Quittor: Necrosis and or infection of the collateral (alar) cartilages of P3.

10. Buttress foot: Aka pyramidal disease. Necrosis of the extensor process of P3.
11. Thrush: Black/tarry foul smelling material found in the frog's central sulcus and abaxial
sulci, from anaerobic bacterial infection (Bacteroides or Fusobacterium necrophorum ). Only
severe cases are associated with lameness. Treatment is exposure to air, maintenance in a clean
dry environment, removal of decaying hom, and topical application of tincture of iodine, or
Koppertox.

12. Quartercrack: Hoof crack beginning at the coronary band and extending towards the
ground. Toecracks also occur. Dry, short feet (more common in racehorses) may be
predisposed. Treatment involves disinfection (if the crack is deep); shoeing changes, and
sometimes an acrylic hoof wall patch.

Lameness associated with any of the above should improve with a paimar digital nerve block.

13. White line disease: Also known as onichiomycosis, found in horses from damp
environments. The white line is seen, from the sole of the foot, and will be eroded. It is
different from seedy toe (hollow wall, dystrophia ungulae), but may appear similar. Lameness
is variable or absent.

14. Keratoma: Possibly from chronic inflammation, keratomas are masses associated with
the inner wall of the hoof. Radiographically, a large circular area of erosion can be seen in the
third phalanx. Treatment is surgical resection of affected wall. Horses may be very lame.

15. Coffin bone fracture: Fractures of' the third phalanx come in six forms (the most common
is type 2, which is articular, so horses may be very lame). Most common in forelimb of
Standardbreds. Treatment of articular fractures involves a bar shoe with clips + pad, stall rest
for at least 6-8m, and screw fixation or neurectomy may be indicated in some cases.

Conditions associated with the pastern:

16. Scratches: Also known as grease heel or dermatitis verrucosa. This is seborrheic
dermatitis of the palmar/plantar aspect of the pastern. Foulsmelling, occasionally associated
with lameness. Concern is that it may progress to cellulitis. Treatment is disinfection, soaking,
dry/clean environment. Horses that are lame with suspected scratches should not be blocked
through the irritated skin.

17. Low ringbone: Osteoarthritis (degenerative joint disease) associated with the distal
interphalangeal joint (coffin joint). Exacerbated by distal limb flexion. On radiographs, there
is proliferation of bone on distal P2, and proximal P3/extensor process of P3. This may be
visible/palpable externally. Upright pastern conformation may predispose. Improves with
basisesamoid block or with intra-articular anesthesia of the DIP joint. Treatment is intra-
articular steroids and or HA.

18. High ringbone: OA/DJD of the proximal interphalangeal joint (pastern joint). Similar
radiographic findings, but associated with the PIP jt. Conformation implicated in pathogenesis.
High ringbone may be primary joint disease or may develop secondary to fracture involving the
PIP jt, or possibly secondary to deep lacerations of the pastern area. Also exacerbated by distal
limb flexion and improved by basisesamoid or IA block. Proliferative bone is again evident
radiographically, and can be palpated or seen externally. Treatment is similar to low ringbone.
Conservative mangement will allow progression to ankylosis. Particularly in hindlimb, PIP jt
arthrodesis may restore athletic function (though disease occurs more commonly in forelimb).

19. P2 fracture: Primarily a Quarter Horse injury (cutting, reigning, barrel racing). Different
configurations, all are articular. Occasionally, management may be distal limb cast and stau
rest, but PIP jt arthrodesis provides best prognosis for return to function (prognosis for athletic
function is good in hind limb, fairly good in forehmb).

Lameness associated with any of the above should improve with a basisesamoid nerve block.

Conditions associated with the fetlock:

20. Proximal P1 fragment: Most commonly found at proximal dorsomedial aspect of PI,
more commonly in forelimbs (hyperextension injury). There may be effusion of the fetlock
(metacarpophalangeal joint). Lameness is vaiiable. Another type of fragment occurs most
commonly in Standardbred racehorses: the plantar or palmar process PI fragment. These are
less likely to be associated with any effusion or lameness. To be sure these are the source of
lameness, anesthesia of the metacarpophalangeal joint or scintigraphic exam should be
performed. Definitive treatment is arthroscopic removal.

21. Sagittal PI fracture: Fracture of proximal PI that occurs in racehorses. Treatment is lag
screw fixation. Horses may not be acutely or severely lame at first.

22. Proximal sesamoid fracture: Common racehorse injury as another type of hyperextension
injury. Many types (apical, basilar, midbody, axial, sagittal, comminuted) with apical 1/3
articular most common. Prognosis in part determined by degree of associated suspensory
ligament injury. Horses are lame at a walk with palpable heat and swelling in the fetlock
region, with pain on manipulation of the joint, and obvious positive response to fetlock flexion.
Any horse lame at a walk with PE findings clearly pointing to a specific source should not be
blocked, since those with incomplete fractures may worsen after block--radiograph first.
Surgical options depend on the type of fracture and include removal of small fragments, lag
screw fixation, or wire fixation. Best prognosis is with apical fractures.

23. Sesamoiditis: Associated with lysis/prominent vascular channels seen on radiographs.

May predispose to sesamoid fracture. Prognosis guarded, even with 6 months of rest.
Treatment is rest and bute.

24. Osselets: Proliferative periostitis of the distal dorsal cannon bone, usually bilateral in
forelimb. They can be seen radiographically and may be old and inactive, or they may be an
ongoing source of lameness progressing to DJD. Treatment is rest, bute, intraarticular
medication.

25. Villonodular synovitis: Inflammation of the synovial membrane (almost like a soft polyp
at times) in the region of the reflection of the metacarpophalangeal joint capsule (the distal
dorsal aspect of the cannon bone). Radiographic changes may be seen in this area. Effusion
and or soft tissue swelling associated with the fetlock joint. Treatment involves arthroscopic
excision of the tissue.

26. Windpuffs: Also known as windgalls, these are effusion of the palmar/plantar pouch of
the fetlock and not usually associated with lameness. They represent an inconsequential
abnormality of the older equine athlete. More common in hindlimbs; more common in
showhorses. No treatment necessary.

27. Condylar fracture: Fracture of the distal cannon bone that occurs in racehorses almost
exclusively. The medial or the lateral condyle may be affected. Medial fractures are more
likely to spiral proximally constituting a more serious fracture. With internal fixation, simple,
nondisplaced lateral (or perfectly reduced displaced) condylar fractures carry an excellent
prognosis for complete return to athletic function. Displacement and palmar comminution
worsen the prognosis. Concurrent sesamoid fractures may occur.

28. Breakdown injury: Refers to a "racetrack breakdown". This means that the suspensory
apparatus/plamar support of the fetlock (metacarpophalngeal joint) is destroyed. It must
involve one or several of the following structures: cannon bone, sesamoids, suspensory
ligament, superfical or deep digital flexor tendons, distal sesamoidean ligaments. Management
is arthrodesis or euthanasia.

29. Soft tissue injury: The superficial digital flexor tendon (bowed tendon), distal check
ligament, annular ligament and suspensory are common sites of soft tissue injury in the distal
limb, diagnosed on PE/LE and using ultrasound. Often, lameness will be worse when the
affected leg is to the outside of the circle while jogging (this is the opposite of most
lamenesses). They often take longer to heal than fractures (4 bone, 6 tendon, 8 ligament, at
least).

Lameness associated with any of the above conditions should improve with a low volar nerve
block.

Conditions associated with the cannon bone region:

30. Splints: More than one thing may be referred to in this way, by laypeople. Splint bone
(MCII/IV or MT II/IV) fractures typically involve the distal 1/3 of the splint, medial more
common. Pain elicited on palpation; swelling is apparent if chronic. May be seen
radiographically as a fracture or as fracture with periosteal reaction. Treatment (surgical
removal of fractured end) is indicated if local infiltration of the area with anesthetic confirms it
as the source of lameness. Inflammation of the ligament between the cannon bone and the
splint bone is a "blind/occult splint". In both conditions, lameness is mild, and U/S is indicated
to evaluate degree of injury to the suspensory (important for the prognosis).

31. Bucked shins: Occur almost exclusively in TB racehorses, and are characterized by a
warm, extremely painful dorsomedial aspect of the front cannon bone; usually in the left before
the right, and seen radiographically as smooth subperiosteal proliferation, or as thickened
dorsal cortex. Treatment is rest, NSAIDS, coldhosing. Horses with bucked shins may develop
dorsal cortical stress fractures (saucer fractures), usually on the dorsolateral aspect of MCIII.
Treatment is screw fixation and or osteostyxs.

32. Bowed tendon: SDF tendonitis, usually in the midmetacarpal region, often seen in
racehorses and showhorses. Horses are lame, with palpable heat and swelling, in the affected
area. U/S may reveal a core lesion (hole seen best in transverse section). Treatment is rest for
6-12 months, with hydrotherapy, sweat/poultice and support bandage for first two weeks.
Surgical intervention after rest may include resection of the distal annular ligament (for low
bow), proximal check ligament desmotomy (to allow lengthening of the tendon), tendon
splitting. There are conformational features that may predispose to bowed tendons including
long sloping pasterns, long toes, underrun heels, and also toe grabs. Based on this, you can
imacine why horses with bowed tendons may have their lameness exacerbated by a wedge toe.

33. Suspensory desmitis: There are three typical sites. These include the proximal suspensory
ligament (sometimes associated with avulsion fracture of the paimar or plantar cortex of the
cannon bone MCIII/MTIII, so radiographs or scintigraphy may be helpful in these cases). The
body is most commonly affected in racehorses, and diagnosis is based on ruling out other
possibilities and on the clinical finding of pain elicited on palpation of that area. Desmitis of
one or both of the extensor branches of the suspensory ligament can be seen using U/S, and
may be treated with tendon splitting. Treatment includes NSAIDS, hydrotherapy, stall rest for
6-12 months, and the prognosis may be fair to guarded for return to athletic function.

34. Check ligament desmitis: Refers to the distal (inferior) check. Jumpers.

Lameness associated with any of the above should improve with a high volar nerve block.

Conditions associated with the carpus:

35. Carpal hygroma: Usually not associated with lameness, hygroma is a large soft (fluid
filled) mass associated with the dorsal aspect of the campus. The etiology may be bursitis or
tenosynovitis of the extensor carpi radialis sheath. The hygroma is a "new" bursa, i.e. one that
has developed secondary to trauma, and the lining must be surgically resected (some will elect
to leave in drain), in order to resolve the problem. Centesis and decompression of the hygroma,
followed by injection of corticosteroid may lead to temporary reduction of swelling, but
surgery is the treatment of choice. This is the carpus'version of capped elbow or capped hock,
sometimes called popped knee.

36. Carpitis: Term mostcommonly used by racehorse trainers to describe any knee
pain/disease (evident as effusion, jogging basewide). Injury to the joint capsule early may be
seen radiographically as distal radial, third carpal, and radiocarpal enthesiopathy, later. This
may be found in conjunction with other more specific diseases of the carpus (C3 slab fracture,
osteochondral fragments, arthritis).

37. Carpal bone fractures: Most of the fractures are "chips", more appropriately referred to
as as osteochondral fragments. The most common sites for these vary according to breed, but
 in general the distal dorsolateral radius, distal radiocarpal bone, proximal third carpal bone,
proximal intermediate carpal bone are most commonly affected. The third carpal bone is also
subject to proximal corner fractures and to slab fractures (remember, a true slab must extend
from one articular surface to another). Large slabs can be repaired using a single cortical bone
screw (3.5 mm) placed in lag fashion.

38. Coronation

Conditions associated with the elbow:

38. Olecranon fracture: Often articular, olecranon fractures through the semilunar notch lead
to non-weightbearing lameness. Dropped elbow (as with radial nerve paralysis).
Surgical treatment is application of a plate to the tension surface. With good
reduction/fixabon, prognosis is good for athletic soundness.

Conditions associated with the shoulder:

39. Sweeney: Damage to the suprascapular nerve will lead to atrophy of the supraspinatus
and infranspinatus muscles. This is often caused by a kick; may also have brachial plexus
injury. In acute cases, creation of a notch in the scapular spine may decrease pressure on the
nerve and halt progression of signs. Shoulder abduction and atrophy are classic signs.
Prognosis after atrophy has occurred is guarded. May monitor with EMG.

Conditions associated with the hock, stifle, upper hindlimb:

40. Bog spavin: Effusion of the tarsocrural joint (secondary to chonic synovitis), seen best
medially (so, bog spavin is really a sign of underlying disease, and not a primary problem, so
not a diagnosis by itself). The most common condition associated with bog spavin is OCD of
the distal inten-nediate ridge of the tibia. Often not lame. Radiographs are indicated.

41. Bone spavin: May refer to osteoarthritis of either or both the distal intertarsal joint or the
tarsometatarsal joint, and occurs in many breeds including QH and warmbloods. The changes
are more prominent on the dorsomedial aspect of the joint, so the DLPMO is the best
radiographic view to take for this condition. Horses will be positive to hock flexion, and
lameness will improve with intraarticular anesthesia. Treatment is NSAIDS and joint
injections of HA and or steroid. The DIT and TMT may ankylose, and this will not lead to any
reduction in range of motion, but will usually mean the end of lameness. Surgical methods to
promote ankylosis include forage and MIA.

42. Jack spavin: Older layterm used to describe a condition of the medial aspect of the hock
that may be from irritation to the cunean tendon or cunean bursitis. Cunean tenectomy is called
"cutting the jacks". This is fairly unusual today.

43. Rupture of the peroneus tertius: Normally, the stay apparatus dictates, "as goes the stifle,
so goes the tarsus". When this is not true, and the stifle can be flexed while the hock is
extended, the horse must have at least a ruptured peroneus tertius. Horses can bear weight
normally, but there is a mechanical lameness. Treatment is stall rest and handwalking.
44. Stringhalt: Usually bilateral, involuntary hyperflexion of the hind limb. The etiology is
unknown, though some think that it may be caused by a peripheral neuropathy (peroneal, tibial,
or sciatic), lathyrism (Sweet pea poisoning), or focal spinal cord disease. Diagnosis is made by
recurrent observation of the characteristic gait abnormality (EMG to confirm). Ddx fibrotic
myopathy. Treatment is lateral digital extensor tenectomy (standing), and the prognosis is
good to excellent, though resolution of signs may take 23 weeks.

45. Capped hock or elbow: Acquired bursitis (chronic repetitive trauma, fibrosis leading to
inflammation/swelling of subcutaneous rather than anatomically normal bursae that is palpable
as a fluid filled swelling). No lameness. Treatment is surgical, as for hygroma, but some acute
cases treated early with cold hydrotherapy decompression and injection of steroids may
resolve. Capped elbow is also known as shoeboil.

46. Curb: Desmitis of the long plantar ligament, usually seen in young STB. Horses with
sickle hocked conformation may be predisposed. Painful/lame initially, though swelling may
persist after lameness resolves. Problem may be self limiting. Counterirritation is often used
at the racetrack.

47. Thoroughpin: Effusion of the tarsal sheath (sheath of the DDF) best seen just proximal to
the hock. It is usually unilateral and can be seen on both the medial and lateral sides, while
bog spavin is more obvious medially and more frequently bilateral. Usually no lameness,
though traumatic origin is possible. To treat, withdraw fluid, inject HA and/or steroid;
recurrence is common.

48. Upward fixation of the patella: Usually unilateral, hindleg appears in rigid extension and
limb is pulled foreword with toe dragging. Push horse backwards to correct. Cause is
intermittent locking of the middle and medial patellar ligaments proximal to the medial
femoral trochlea. Conservative treatment involves exercise to increase strength of quadriceps.
Surgery is medial patellar ligament desmotomy, done standing.

49. Fibrotic myopathy: Fibrosis of the semimembranosus or tendinosus causing decreased

cranial phase of hindlimb movement. Muscles are firm, non painful. Sugery to correct this
involves transaction of the semitendinosus at its insertion on the caudomedial aspect of the
tibia.

50. Gonitis: Uncommonly used term to describe arthriti-s/djd of the stifle. Nonspecific, so
may be caused by anything that would produce arthritis, like OCD, upward fixation of the
patella (or medial patellar ligament desmotomy), injury to the meniscus or cruciates or to the
medial or lateral collateral stifle ligaments. Horses are severely lame, whereas with carpitis,
lameness is variable. Prognosis is guarded.

Developmental orthopedic diseases (Merck 837, 765)

Osteochondrosis: (Merck 838)

 1. Very common condition in which there is failure of endochondral ossification, and
retention of embryonic cartilage within the hypertrophied zone. Classic dessicans lesions
involve a dissecting cartilage flap, while cysts (osteochondrosis) are structures penetrating
deeper into the subchondral bone. Often minimal or no lameness; most common sign is joint
effusion. Sites vary with breed.
Stifle: Lateral trochlear ridge of the femur, medial femoral condyle, medial trochlear ridge of
the femur, distal patella; present at 1-3 yrs old; prognosis good for all but MFC
Hock: Distal intermediate ridge of the tibia, lateral and medial trochlear ridges of the talus,
medial malleoulus of the tibia; present with TCJ effusion at <2yrs old; prognosis good.
Shoulder: Like the dog, the most common site is the caudal glcnoid. Can have a
subcondral cyst or a flattened humeral head or both. Prognosis is fair to poor; horses
present at 6-12m very lame.

Angular limb deformities: (Merck 765)

1. Valgus (knockkneed): Carpi or tarsi. Feet lateral to proximal limb (lateral deviation). Can
also occur in fetlocks (MCP of MTP). Deviation is from the level of the metaphysis, epiphysis
or cuboidal bones. Treatment is HCPT/E, transphyseal bridging. For fetlocks, treatment must be
performed before 4 weeks of age. Many young foals will correct with no therapy. Eg for carpus
valgus, strip lateral and bridge medial.

2. Varus: Opposite of valgus; var-us deformities are less common. Same possible treatments.

Flexural deformities: (Merck 840)

Deviate in the sagittal plane, while valgus indicates deviation in the vertical plane. Flexural
deformities may be congenital or acquired. Chronic pain, sometimes from physitis, is the most
common cause. Etiology is related to imbalanced Ca:P, overfeeding of concentrates (rapid
growth), and other causes of chronic pain. Horses 3-12 months old are more likely to have club
foot; flexural deformity at the level of the distal interphalangeal joint. Radiographs should be
taken to evaluate for djd of the DIP jt. Treatment is based on severity and type of flexural
deformity. Mild cases may be managed with toe extension shoes, lowered heels, NSAIDS and
altered diet. More severe cases may require a distal check ligament desmotomy, in addition.
Knuckling at the fetlock occurs in slightly older horses, 1-2 yrs old. Definitive treatment is
proximal check desmotomy. In sever cases, or those in which origin of deviation is obscure,
proximal and distal checks may be cut. Newbom foals may have contracted tendons and these,
like flexor tendon laxity, may resolve without intervention. Contracted tendons can be treated
with oxytetracycline.

Selected Surgical Topics

Dentistry (Merck 133)

Deciduous teeth: 2(Di 3/3 Dc 0/0 Dp 3/3) = 24

Permanent teeth: 2(13/3 C 1/1 P3-4/1 M 3/3) = 40-42
 Females will not have canine teeth. The wolf tooth is a small first upper premolar that is often
removed because of potential interference with the bit.
Eruption:
Deciduous 7d 7w 7m
Permanent 2.5 yrs 3.5 yrs, 4.5 yrs
Dental Star (gone at) 6 yrs(I1), 7 yrs(I2), 8 yrs(I3)
Float the maxillary teeth on the buccal side, and the mandibular on the lingual side.

Management of colic (Merck 165)

1. Take a history: What is the duration and intensity of pain? Has it responded to sedation,
analgesia, gastric decompression? Have there been any changes in management (diet or
activity level)? Recent dewonning? Is the patient pregnant? Is the patient an intact male?
Features of the history should guide your thinking.

Case 1. After questioning, you find that the horse is 30 yrs old, has not had her teeth floated in
the last ten, eats poor quality hay, has had mild intermittent colic for 3 days, and may not have
had access to as much water because of a recent cold spell. This spells large colon impaction
(and differentials include fecalith, enterolith, and any other intraluminal obstruction). A rectal
exam is needed to confirm the diagnosis.

Case 2 After questioning, you find that the horse is a 5 year old American Quarter Horse who is
in show training. The horse is fed very little hay and is bedded on shavings or saw dust
(alternatively, the horse is fed coastal Bermuda hay), and the owners think that they may have
seen him eating some of his grain from the floor. Furthermore, the horse's pain improved quite
a bit, after the RDVM siphoned 8L of reflux from the stomach. This spells ileal impaction (and
differentials include other small intestinal intraluminal obstructions, enteritis with which the
horse may be febrile with a left shift or a leukopenia, and stangulating obstruction may also be
possible).
A horse with pneumonia, laminitis, or rhabdomyolysis may present as colic.

2. Perform diagnostics as indicated, based on history and PE: It is always indicated to pass a
nasogastric tube and perform a rectal exam. Abdominal U/S will help in some cases.
Hematology and chemistry. Abdominal paracentesis is contraindicated in enormously
distended horses, is useful in other circumstances (eg serosanguinous fluid is often consistent
with a surgical lesion), and not strongly indicated if the horse's pain is mild and of short
duration appears to have resolved. Hanging manure in a rectal sleeve with water is a simple
cheap test that is indicated if the horse cats off of sand, and has sand auscultable in the
abdomen.

3. Initial pain management: This usually means sedation. The alpha-2 agonists are the
analgesics of choice.

Alpha-2 agonists
• Xylazine (Rompun®) takes about 5 minutes to have an effect, lasts for 15-20 minutes, also
has analgesic properties, can be given either IV or IM, may promote ilcus with several
doses. It is a good choice in most circumstances.
• Detomidine (Dormosedan®) has a longer duration of action, and is a more potent analgesic
(also more expensive).
Others
• Butorphanol (Torbugesic®) is an opiate, and so has some analgesic properties. It also has
a longer duration of action than xylazine. It is often used in combination with detomidine.
• Acepromazine isn't used in colics anymore, and should never be used on intact males.
Causes hypotension, so is not a good choice in horses that may be in shock. It has no
analgesic properties.

For analgesia without sedation, phenylbutazone and flunixin meglumine are the principal
choices, though ketoprofen is also used. Flunixin is the best choice because it is very effective,
lasts up to 12 hours, and has been proven beneficial in horses with endotoxemia. Controversial,
but banamine may mask surgical pain.

Horses require referral and possibly surgery if pain persists despite appropriate medical therapy,
or if a diagnosis has been made that requires surgical correction (e.g.
intussusception, right dorsal displacement of the large colon).

Foals with colic are more likely to have certain conditions:

• Intussusception (Merck 175): The intussusceptum goes into the intussuscipiens. Small
intestine. Any intussuseption in an older horse is more likely to involve the cecum and is
therefore likely to be involved with Anoplocephala perfbliatti.
• Ruptured bladder (Merck 1156): Occurs more commonly in colts, and usually presents
within the first couple of days of life. Abdominal distention with urine
(uroperitoneum) and hyponatremia, hypochloremia, hyperkalemia are hallmarks (don't
forget that the fluid in nthe abdomen will have a creatinine 2X or greater than that found in
the blood).
• Gastric ulceration (Merck 219): Uclers occur most commonly along the margo plicatus, in
the nonglandular stomach, and may also occur in the proximal duodenum. They are often
asymptomatic, but some horses show intermittent mild abdominal pain, lie on their backs
grind their teeth (bruxism).

Old horses:
• Stangulating lipoma (Merck 176): Don't have to be overweight. Pedunculated lipoma
strangulates small intestine.
• Colonic impactions (Merck 177,180): Poor dentition predisposes to improper chewing, and
may therefore lead to impaction of feed material. Small colon impactions have been
associated with Salmonella.
• Epiploic foramen entrapment (Merck 176): Due to atrophy of the liver lobes with aging.

Broodmares:
• Colon torsion/volvulus (Merck 180): Typically several weeks after fooling.

Stallions:
 • Scrotal hernia: Particularly common in younger horses (Standardbreds in particular though
draft horses, Saddlebreds, and Walking Horses are also predisposed).

Lacerations and wound management (Merck 1260)

1. Once again, history is important. How old is the laceration? What type of material
caused the laceration? How has the horse been managed since the laceration? All horses with
lacerations should receive a tetanus toxoid, and NSAIDS.

2. Lacerations are like real estate, location is everything. The MOST important thing to
asses is involvement of synovial structures. How close is the laceration to a joint, and is there
any drainage? Is the patient lame enough to have a septic joint? Vessels involved?

3. Workup almost invariably involves radiographs. If there is an osseus abnormality, you

need to know (management, prognosis, cost ... ). Foreign bodies may be identified (though
wood will not be).

4. Copius ravage of the laceration, and debridement of dead fissue. In order to evaluate
communication of a laceration with a joint, the area must be prepared aseptically. Perform
arthrocentesis and collect fluid, then inject saline and see if discharge comes I - rom the
laceration. If the laceration involves a joint, tendon sheath, any synovial
structure, the prognosis is fair or poor. The synovial structure must be ravaged with LRS, and
injection of Ab is indicated.

5. Lacerations involving flexor tendons require general anesthesia for repair. Though you
may have seen tendons sutured, many books say not to suture. Flexor tendon lacerations
MUST be managed in a cast (6 weeks is goal).

6. Any area of bone that loses skin coverage will develop a sequestrum, and it takes 2-3
weeks to see one radiographically. If the laceration is old, primary closure is not indicated.

7. Often, in equine distal limbs, there is not enough skin to close. Skin grafting takes place
only in referral hospitals, but seems to come up on the NBE. There are several types of skin
grafts. These include split thickness (epidermis + 75% of dermis), and full thickness
(epidermis and dermis, Wolfe). There are meshed sheet grafts, punch, pinch etc and all must be
placed into a healthy bed of granulation tissue (no fat, no denuded bone). The sequence of
graft acceptance is adherence, plasmatic imbibition, revascularization (inosculation),
organization, contraction. The reasons for graft failure include fluid accumulation (purpose of
mesh), infection, and movement. In horses, autografts are used (from same animal). Allograft
is from same species, and xenograft is from a different species.

8. Systemic antibiotics are indicated, if a synovial structure is involved, or if there is dead

space. Prophylactic antibiotics are indicated in most traumatic wounds that are contaminated,
and many will become infected despite prophylaxis. NSA]IDS are used to minimize
inflammation and pain. Wounds are cleaned daily with water, and a clean bandage applied. The
most common complication is exuberant granulation tissue, and this may have to be trimmed
daily, while the wound is healing.
Other topics that have come up in the past

I. Castration: Open involves incision into the parietal vaginal tunic, closed does not. The
most common postoperative complications are preputial swelling and bleeding. A scirrhous cord
is a chronic infection by pyogenic organisms (Staphylococcus sp. ) in the remaining spermatic
cord (botryomycosis). A horse that is cut proud (false rig) is one that continues to behave as
though intact (historically believed to be caused by remaining epidydimal tissue).

2. Cryptorchidism (Merck 986): Condition is considered heritable. Both testicles should be

descended before birth. A "high flanker" is a horse whose retained testicle is in the inguinal ring;
the testicle can also be retained within the abdomen and abdominal retention is associated with
increased incidence of seminomas. A gelding with stallion-like behavior can be evaluated using
estrogen assay: if high, he is a cryptorchid; if low, there is no remaining testicular tissue.
Alternatively, hCG is given, and testicular tissue must be present, in order for serum testosterone
to increase. It is considered unethical to show a horse that was cryptorchid.

3. Hernias (Mcrck 177): Inguinal is repaired by surgical reduction and possibly closure of
the external inguinal ring. Present with colic. Umbilical hernias are common in foals and may
be managed in the field using bands, repeated manual reduction, or hernia clamps (clamps are
no longer considered safe, and are not used). The most common contents are small intestine or
intestine, though they may contain cecum or ventral colon. Surgical correction involves
hemiorrhaphy.

4. Surgical diseases of the throat presen6ng for exercise intolerance and noise, and requiring
upper airway endoscopic exam. Differentials are lameness and heart disease.
• DDSP: Cannot see the epiglottis, palate may be ulcerated. Soft palate displaces above the
epiglottis, causing expiratory stridor. Treatments include stemothyrohyoidectomy,
staphylectomy, epiglottic augmentation.
• Epiglottic entrapment: Can see the epiglottis, though the scalloped border is smooth;
entrapment is by aryepiglottic tissue. Treatment is laser division, or transoral axial
division using a hook.
• Left laryngeal hemiplegia: Left arytenoid cartilage (comiculate process) hangs into the
airway causing roaring noise and exercise intolerance. Treatment is left laryngoplasty and
bilateral sacculectomy.
• Chondritis: Inflammation of arytenoid cartilage, asymmetrical. Partial, subtotal or
complete arytenoidectomy is treatment.

5. Cribbing surgery: Forssell's operation involves transaction of the stemothyrohyoideus,

omomhyoideus, stemomandibularis, and neurectomy of the ventral branches of the spinal
accessory nerve. Unreliable results.

6. Cryosurgical techniques: Treatment of sarcoids, squamous cell carcinoma, habronemiasis.

Optimal sequence is rapid cooling to -20C twice, with slow thaw.
7. Differential diagnoses for epistaxis or nasal discharge: Guttural pouch mycosis (acute/severe
bleeding predominantly unilateral), ethmoid hematoma (mild, chronic, unilteral), sinusitis
secondary to tooth root infection, paranasal sinus cyst (may have mucopurulent discharge, facial
swelling), neoplasia (squamous cell carcinoma). In practice, trauma or sinusitis most common.