Large Animal

any change in the normal movement or gait; these changes are not always associated with pain.

any functional change that prohibits using the animal for a desired task (racehorses - lameness, infertility, breathing problems {Laryngeal Hemiplasia [Roarer], Allergies [Heaves]})

• 1. Walk - 4 beat gait - RF, LR, LF, RR
• 2. Trot - or jog. 2 beat diagonal gait - RF/LR, LF/RR
• 3. Canter - or lope. 3 beat gait (restrained gallop), "leads"
• 4. Gallop - or run. 4 beat gait.
• 5. Pace - 2 beat lateral gait - LF/LR, RF/RR

the period of time that the leg is bearing weight is shortened or absent - problem is usually from the carpus or tarsus distally and more likely bone related.

a lameness in which there is an alteration in stride, usually a shortening of stride - problem is usually muscular, tendon, or ligament in origin.

• Where in the air a particular leg is in
• comparison to the opposite leg

• front leg is behind opposite front leg
• (when viewed from the side) - posterior phase of flight (P)

• front leg is in front of opposite leg
• - anterior phase of flight (A)

• How high and how evenly the leg is picked
• up and advanced

• Ideally the highest point of the arc
• should be as the leg passes the opposite leg (entering the anterior phase)

• Arc of flight can be changed
• by trimming or shoeing the foot (long toes low heel, short toe long
• heel) or confirmation

• Signalment - age, sex ,and breed
• Length of time - chronic or acute
• Progressing, staying the same or getting better?
• What was the animal doing when the lameness first started?
• Use of animal
• Physical exam (temp, Hr,Rr)
• Medications/treatments to date

• 1. Conformation- standing still and square on flat, level surface (pointing one foot, attitude)
• 2. Walking – On hard and soft surfaces
• Stride length
• Medial to lateral hoof balance
• Twisting of the leg as it hits the ground
• Coordination
• 3. Trotting- straight line, in circles (longing),
• under saddle
• YOU MISS MORE FOR NOT LOOKING THAN NOT KNOWING!!!!

• 1. Hoof testers (80% of time problem is in the foot)
• 2. Palpate and manipulate all joints, tendons and muscles looking for heat, pain, swelling, differences from opposite leg
• 3. Flexion tests
• Front legs (fetlock, carpus, shoulder)
• Hind legs (fetlock, hock/stifle)
• 4. Neurological (cross leg, spin, tail pull, push, needle)

Front limb lameness - head goes down when sound limb hits the ground “DOWN ON SOUND”

• Hind limb - pelvis will hike up when the lame leg
• hits the ground (down when the sound leg hits the ground)

• Grade 0 - no lameness
• Grade 1 - lameness difficult to observe at the trot and not consistently apparent regardless of circumstances (circling, under saddle)
• Grade 2 - lameness difficult to observe at the trot in a straight line, but consistently seen under certain circumstances (circling, after flexion)
• Grade 3 - lameness consistently observable at the trot under all circumstances
• Grade 4 - lameness obvious at the walk
• Grade 5 - non-weight bearing or unwilling to move

Once you know which leg is the problem and have generalized an area, you can get more specific with diagnostic nerve blocks

• Extremely useful to localize the lesion to small area of the leg
• START AT THE FOOT AND WORK UP THE LEG
• Once the horse is sound, the lesion is between the last 2 blocks
• Once lesion is localized, then you can go to more advanced diagnostics

• AKA PD block, heel block
• Desensitizes just the caudal 2/3 of the foot
• Does not desensitize the coffin joint

Desensitizes the entire foot

• Desensitizes the limb from the fetlock down
• Must block 4 separate nerves - 2 just caudal to the splint bone and 2 underneath the splint bone

• *Behind distal carpus at origin of the check ligament 4 areas or ‘points’ to block
• *Blocks the deep and superficial tendons, check, suspensory ligaments, cannon bone, +/- fetlock

• Radiographs
• Ultrasound
• Thermography
• Nuclear Syntography
• CT Scan
• MRI

• inflammation of the lamina causing rotational change of the coffin bone
• Common in horses and cattle, can occur in any hoofed animal
• No matter what the cause of the problem, the initial physiologic event is an increase in systemic blood pressure

• Along with the hypertension, the blood vessels of the feet constrict and blood is shunted across the coronary band
• Since most of the blood is shunted from the foot, the laminae are oxygen deprived and die (ischemic necrosis). As the tissues die, they swell, cause more pressure and even less blood can enter the foot
• Once the cycle has begun, it can be very difficult to stop
• Once the lamina dies from ischemic necrosis the DDFT rotates the tip of the coffin bone down and back away from the hoof wall

• Metabolic-Increased carbohydrates (grain, lush pastures/grass, rich alfalfa hays) -Obesity, Cushings (Insulin resistance)
• Trauma - hard/frozen ground, injury to opposite leg, excessive exercise
• Poor hoof care
• Colic - endotoxin release
• Infections - metritis, PHF, any high fever
• Drugs – steroids
• Toxins-Black walnut shavings

• Shifting of weight to the hind legs - often mistaken for a hind limb lameness or neuro problem
• Reluctant to move or pick up feet
• Tender footed - “walking on eggshells”
• Reluctant to turn
• Pain at toe to hoof tester
• Increased heat in foot and a strong digital pulse

• Grade 1 - standing but incessant shifting of weight on front feet
• Grade 2 - willing to move, but difficult to pick up a leg
• Grade 3 - will not walk, very difficult to pick up a leg - irreversible damage has occurred within 12 hours of onset
• Grade 4 - recumbant

• Remove cause
• Reduce further damage - stall rest, trim feet or corrective shoes, hydrotherapy
• Anti-inflammatory drugs - bute
• Others - nitroglycerin, isoxsuprine, acepromazine
• Trental (pentoxyphyline)

• Bacterial and possibly fungal infection that eats away at the frog until you get down to sensitive tissues or lose support of the foot
• Fusiform necrophorus, other anaerobes
• Bacteria in mud and feces packs into medial and lateral sulci
• Sheared heels, contracted heels, underrun heels can result from chronic thrush

foul, black tarry discharge from sulci, frog seems softer than normal. As it progresses, the horse may become lame

• keep foot clean and dry -
• topical drying agents, turpentine, copper sulfate, salt, tea tree oil, sugardine poltice

one heel is higher than the other

• AKA scratches, mud fever, dew poisoning
• Moist dermatitis (hot spot) on pastern , heel bulbs, and occasionally above fetlock
• Etiology - constant contact with wet ground and microscopic “scratches” allow entry of bacteria into skin
• Almost exclusively on white haired areas
• Treatment - keep clean and dry, remove hair, topical medications
• Can be manifestation of greater systemic problems (Immune issues, infection etc.)

• bruising at the bars, caused by ill-fitting shoes or improper shoeing
• Especially predominant in draft horses (big feet) and Quarter Horses (little feet)

• Clinical signs - sensitive to hoof testers over bars, varying degrees of lameness
• Treatment - remove shoes and trim area well to relieve pressure

• can occur anywhere on the foot
• caused by trauma - kicking, stepping on stone, feet trimmed too short
• Clinical signs - acute lameness of varying degree, often right after exercising on rocky ground, after the ground freezes or in the first few days after having feet trimmed
• Treatment bruises – Initially soak foot in warm water and Epsom salts
• poltice (medicated mud)
• After Sound- pack foot in a mixture of sugar and betadine soap (sugardine) or paint with turpentine, strong iodine, bleach etc. to harden the foot.
• shoe, +/- pad

• *A bruise or trauma that becomes infected and creates an abscess pocket inside the hoof
• *Acute lameness causes increased pressure in the hoof
• #1 cause of acute non-weight bearing lameness

Clinical signs - acute lameness (can be non-weight bearing), heat in foot and increased digital pulse in the affected foot only, sensitive to hoof testers over abscess

• Drain the abscess through the bottom of the foot pare out with hoof knife
• Soak foot in warm water and Epsom salts or poultice for 3 days (15-20 minutes per tx.)
• Tetanus booster –(this is crucial if not current)
• Antibiotics +/- (Penicillin, tribrissen, etc)
• Sometimes the abscess can’t be opened from below and opens at the coronary band - called “gravel”

• Frog is eaten away
• The heels are narrower than normal - pinches on internal structures (like wearing shoes that are too tight)
• Due to improper shoeing, chronic disuse (due to pain), or conformation abnormalities
• Clinical signs - vague heel lameness, sensitive to hoof testers, shortened anterior phase of stride

• best treatment is to remove shoes and allow heels to expand naturally, but these horses become even more lame when shoes are removed
• Corrective shoeing - shoe “full in the heel” or “slipper the heel”
• Correction will occur gradually over time- could result in chronic lameness

• Calcification of the colateral cartilages of the foot - typically do not cause lameness
• If sidebones are large and are broken, can cause a true lameness
• Causes - trauma, injury, improper hoof balance
• Clinical signs - usually none; if very large there may be a noticeable lump on the medial and/or lateral aspect of caudal pastern above the coronary band; may be lame if extremely large and pinching on internal structures
• Treatment - try to remove fracture pieces

• AKA - caudal hoof disease
• Any pain originating in the heels - can be due to frog, sole, heels, navicular bone, navicular bursa, navicular ligaments, digital cushion, DDFT, collateral ligaments, coffin bone
• Usually affects large animals with small feet (Quarter Horses)
• Diagnosis- made based on a classic lameness and improvement after bilateral posterior digital nerve blocks (PDNB)
• Radiographs are important, for diagnosis and monitoring progression of the disease

• Short, choppy gait,
• Shortened anterior phase of stride
• Foot lands toe first
• Chronic stumbling
• Usually bilateral with one foot worse (Block lamest foot PDNB and horse goes lame on other foot Block it PDNB and horse goes sound)
• Excessive wear at toe

• Causes- arthritis, bursitis, trauma, conformation, chronic inflammation, genetics, etc.
• Regardless of theory,(Classically) there is excessive pressure and wear and tear on the navicular bone, leading to bone remodeling and lameness

• Primary Treatment - corrective shoeing; rocker toes, wedge pads to ease breakover and tension on DDFT
• NSAID
• Blood thinners (Isoxuprine, Trental, etc.)
• Reduce trauma, (change work load)
• Neurectomy as last resort
• This is a chronic disease that will not go away!

• Can occur anywhere on the hoof
• Are due to insufficient moisture in the hoof and trauma
• Once any crack reaches the coronary band, it will likely be there foreverMost cracks are superficial and cause no lameness
• Clinical signs - obvious crack, if deeper structures are involved it will be painful and may bleed or become infected

• Toe cracks - occur at toe
• Heel cracks - occur at heel
• Quarter cracks - occur anywhere in between
• Grass crack - starts at ground and goes up
• Sand cracks - go from the coronary band down

• Treatment - none if superficial
• supplements (biotin, methionine)
• Moisturize hooves, remember the periople is waterproof
• Farrier: (if crack dose not go to the coronary band) rasp line in hoof perpendicular to the crack deeper than crack (if to the coronary band) dermal and lace crack, unweight area, special shoes with clips, etc.

• Due to repetetive, concussive trauma, esp fast turning and stopping on hard ground, jumping
• Clinical signs - varying degree of forelimb lameness, increases in severity with fetlock flexion, worse with more exersize
• If exostosis is severe, there may be a visible change in the shape and appearance of the pastern or coronary band

• If periarticular, just cosmetic unless interfering with other structures (esp extensor tendon, collateral ligaments, etc.)
• If high or low and articular, may attempt joint injections, arthrodesis (only of PI/PII)

• periarticular – good
• (high) articular – fair may respond to steroid injections for a while arthrodesis is a possibility
• (low) articular - poor for return to function but may respond to steroids for a while

• Accumulation of fluid in the metacarpo(tarso) phalangeal [fetlock] joint pouches
• +/- flexor tendon sheath
• May or may not be associated with trauma
• More common in rear legs than front, especially warm bloods, increases with inactivity
• Clinical signs - variable sized fluid pouches on the dorsal palmar/plantar aspect of fetlock

• Not usually associated with pain or lameness
• Cosmetic problem only - indication of “milage”
• No treatment necessary

• Inflammation of the interosseus ligaments between cannon (MC/TIII) and splint bones (MC/TII or MC/TIV)
• n+/- fracture of the splint bone
• Traumatic - kicks, falls, excessive work on hard ground/pavement especially in circles (longing)
• Medial/lateral imbalance of foot/leg

• acute – firm swelling over splint bone hot and painful to palpation, mild lameness in direction of splint
• chronic - ossification of MC/TII or MC/TIV to MCIII results in hard, cold, non-painful “popped splint”, no lameness

• acute - stall rest {Cold (water, ice, frozen peas) , poultice, Heat (sweats), anti-inflammatory cream} under a pressure bandage
• Injection with steroids to reduce inflammation
• NSAID systemically
• chronic - blister, pin fire, freeze fire, shock wave, ultrasound (make chronic injury acute)
• If fracture is present, may remove fracture piece if small and distal, if large and proximal, leave it in
• Once acute phase is over, the remaining lump is cosmetic and will cause no lameness
• Size of lump will reduce by 1/2 over the next year

• Inflammation of dorsal cortex of the Cannon Bone ( MCIII or MTIII )- “shin splints” remodeling of the cannon bone to accommodate activity
• Repeated concussive trauma causes subperiosteal bleeding, micro fractures, and remodeling (can progress to cortical fractures)
• Affects young horses in training
• #1 cause of lameness in 2 year old horses
• Clinical signs - variable lameness; heat over dorsal cannon bones, painful to palpation -Stripe test -When at bleeding microfracture remodeling stage, there are no radiographic abnormalities

• acute - rest (30 days), NSAIDS cold water, sweats, poltice, etc.
• chronic - pin firing, shock wave, Ultrasound, etc. (make chronic acute)
• Cortical fractures - Surgery

• Inflammation and arthritis of proximal fetlock (MC/T-PI ) metacarpo(tarso)phalangeal joint)
• Repetitive, concussive, traumatic in origin, Injury of exhaustion, racing with toe grabs (dorsal proximal PI hits caudal proximal MCIII)
• Clinical Signs – soft tissue swelling of proximal fetlock, forelimb lameness, increases with fetlock flexion,
• Treatment - steroid injections, NSAID, topical treatments (sweat, poultice, etc) oral supplements

• “Bowed Tendon”
• Can involve SDFT, DDFT
• Most often SDFT
• Caused by hyperextension of the tendon (racing, riding, fatigue plays major role)
• Is an injury that develops over time
• Clinical signs - hot, painful, swollen behind cannon - leg appears “bowed” backward can also occur below fetlock but won’t be as obvious
• Lameness depends on severity (lame left front going to the right on longe)

Diagnosis and Prognosis - Ultrasound

• Conservative- 2-3 months stall rest then turnout 24 hrs in large field, cold water, poultice, sweats, NSAIDS initially until sound in stall
• Aggressive- Platelet rich plasma, Stem Cells, IRAP, Tendon splitting etc
• Return to training is very gradual depending on ultrasound evidence - never 100% as strong

• “Pulled suspensory”
• Suspensory ligament, Check ligament
• Same causes as bowed tendons
• Clinical signs - not as obvious as bowed tendons, lameness depends on severity of lesion (lame left front going to right)
• Diagnosis, Prognosis, and Monitoring of repair - ultrasound
• Treatment same

• Elbow hygroma - “water on the elbow”
• Traumatic injury to the elbow causes accumulation of fluid in the bursa
• Shoe hitting elbow, lying on hard ground
• Clinical signs - fluid filled pouch over olecranon - nonpainful, does not usually cause lameness

• Treatments usually ineffective
• Draining and injection with steroids, radiographic contrast material
• “Boil boot” to prevent worsening

• Damage to the suprascapular nerve
• Caused by damage to the shoulder, esp kicks to the point of the shoulder, falls, pulling collars
• Leads to atrophy of supraspinatus and infraspinatus muscles which are responsible for advancing the limb
• Atrophy of these muscles leads to prominence of the scapular spine and inability to advance the leg, though it can bear full weight
• Treatment - rest , steroids, electro-stimulation
• Salvageable with time (1 year +)

• Most common forelimb sites - distal radius, midcannon and phalangeal (P1 and P2)
• In a horse > 450 pounds, any fracture above the carpus/tarsus is irreparable
• Anything distal can be repaired providing the fracture is not open, grossly contaminated and the animal will tolerate a cast, $$$$$$
• Prognosis- usually poor, esp if involves a joint or multiple pieces

• Spavin = hock
• Arthritis of the hock, esp the distal intertarsal and tarsometatarsal joints
• Caused by normal wear and tear, trauma, infection
• Clinical signs - constant or intermittent hind limb lameness that gets better as the horse works, reluctance to flex hock
• 1st thing owners will report is “feels rough” while being ridden, back is sore, or has trouble with maintaining the proper lead at the canter, short strided in hind, drags toes
• Diagnosis - lameness increases with hock flexion tests and has radiographic changes to distal intertarsal and tarsalmetatarsal joints

• Treatment depends on severity
• Early joint disease (Prevention) - oral joint supplements, (chondroitin sulphate, glucosamine, hyaluronic acid), Legend (IV), Adaquqn (IM), Polyglycan, etc.
• NSAID
• Moderate to severe disease - joint injections with corticosteroids +/- hyaluronic acid, plus above tx.
• It is important to keep working these horses!

• Accumulation of fluid in the tibiotarsal joint pouches - causes distention on the proximomedial and plantarolateral side of the hock
• Causes - joint disease (chip fractures, OCD, arthritis), traumatic synovitis, idiopathic
• Clinical signs - obvious swelling on hock
• +/- lameness depending on cause

• aimed at underlying cause
• Usually there is no radiographic changes and just a cosmetic issue, or it may away on its own

• Blood spavin - traumatic synovitis with bleeding into the joint capsule - almost always traumatic
• Blind spavin - horse shows characteristic lameness of spavin (+ hock flexion test), but has no bog, no blood and no radiographic changes

• Desmitis of the plantar ligament
• Almost exclusively an injury of Standardbred racehorses
• Causes - repetetive trauma (same as bowed tendons)
• Clinical signs - very lame in the acute stages with much heat over hock and pain on palpation
• Variable sized swelling 4-6” below the hock on the plantar surface of the leg
• Treatment – Cold: water initially, then heat, bandaging and stall rest with NSAIDS
• Chronic cases - “pin firing”

• Not a bone, refers to the gluteal muscles and their bursa over the trochanter of the femur
• Almost exclusively in Standardbred racehorses
• Trauma induced - strained during race, kick or falls
• Clinical signs - pain on palpation of the trochanter area, shorter stride with the affected leg, gluteal atrophy if chronic
• Diagnosis - made by clinical signs - rule out bone spavin too
• Treatment - rest, NSAIDS and injection of bursa with corticosteroids

• Inflammation of the stifle
• Causes – same as bog spavin in the hock, esp OCD
• Clinical signs - pronounced effusion of the stifle joint pouches, often will not be lame until horse begins training
• Treatment - aimed at underlying cause

• Neurologic dysfunction that causes the horse to snap the leg up abnormally (may kick itself in the stomach)
• Cause is unknown
• Clinical signs - characteristic movement
• Treatment - depends on severity - ranges from nothing to transection of the lateral digital extensor

• Tying up, Azoturia (Asotemia), Monday Morning Disease
• Severe cramping of all skeletal muscles, but esp the gluteals and semimembraneous and semitendenous muscles
• Causes of ER - lactic acidosis, electrolyte imbalances, overexertion, heat exhaustion, myopathies, abnormal Ca regulation, hormonal

• Sporadic ER - occurs infrequently, due to extrinsic factors (overexertion, CHO overload, excessive sweating)
• Recurrent ER - TB, Stb, fillies - due to intrinsic muscle defect

• Clinical signs - often mistaken for colic - profuse sweating, intense tachycardia and tachypnea, panicked expression, rock hard muscle groups and inability to walk, +/- myoglobinuria and acute renal failure
• Treatment- DO NOT MOVE THE HORSE!
• Keep warm with blankets, sedation, NSAIDS , muscle relaxants, IV fluids, Vitamin E and Se

• HYPP
• Genetic defect of QH, Appaloosa and Paints with “Impressive” in their pedigree
• Affected horses can have periodic attacks
• Caused by genetic defect in the Na/K pump
• [Na] in the blood >[Na] cell
• [K] in blood < [K] cell
• (Na is trying to get into cell and K is trying to get out.) This is the pump and it is responsible for waste products leaving the cell and nutrition entering. In HYPP the K leaks out shutting down the pump

• Diagnosis -DNA test (need sample of horses mane hairs including the follicles), and pedigree. Is done at U C Davis.
• It is a recessive trait with results reported as HH, HN, or NN
• HH – severe
• HN – mild
• NN - normal
• Clinical signs - sweating (may be focal), muscle tremors that begin at the head and gradually spread throughout the body, anxiety, prolapse of 3rd eyelid, recumbency and possible death
• Attacks brought on by stress or halothane anesthesia

• Treatment of attacks - IV calcium solutions
• Prevention of attacks - low potassium diets (no alfalfa hay or sweet feeds)oats and 1st cut, potassium wasting diuretics, reduce stress levels
• This disease could be eliminated with selective breeding

• Complex of musculoskeletal diseases that affect the growing foal
• Epiphysitis
• Contracted tendons
• Lax tendons
• OCD
• Wobblers syndrome

• Inflammation of the growth plates, esp the distal radius, tibia and MC/TIII
• Caused by trauma, improper Ca/P ratio in diet, high protein and fast growth
• Clinical signs - variable lameness, enlarged physes - “hourglass”,”Figure 8” legs +/- heat and pain on palpation
• Treatment - reduce exercise (reduce trauma), no grain in diet, grass hay only, balanced mineral supplement to give proper Ca/P ration (2:1), increase zinc and copper, mild NSAIDS

• Can be congenital or acquired
• Bones grow faster than the tendons and the limb cannot be fully extended
• If congenital (seen from birth), treat with IV oxytetracycline - binds calcium and relaxes muscles Needs to be done in first 12 hours after birth for maximum effect
• If acquired, treat cause and hope for the best
• Superior check ligament desmotomy

• If the tendon contracture affects just the pastern and/or fetlock, it is termed a club foot
• Grade 1 - dorsal hoof wall is vertical or in front of vertical
• Grade 2 - dorsal hoof wall is behind vertical
• Treatment - inferior check ligament desmotomy
• Corrective hoof care: trimming and shoeing is essential for success of the surgery and long-term soundness
• Treatment must be accomplished while horse is still young

• Normal in the neonate and stalled foals, it should resolve with the beginning of exercise
• Joints are very loose and unstable - bandage for support and protection of skin
• Treatment usually not required, may splint or tube cast if very severe

• Developmental defect of subchondral bone
• Failure of subchondral bone to calcify - soft spots in joint surface
• Cartilage can either break off in pieces and float around in joint (true OCD) or develop into a cyst in the subchondral bone (SBC)
• Occurs most often in the hock, stifle and fetlock but can be in any joint

Clinical signs vary with the joint affected

• Hock - moderate lameness, prominent bog spavin, + hock flexion test, changes seen radiographically
• Stifle - no lameness until training begins, then very lame, prominent gonitis, + hock flexion test
• Ankle - often an incidental finding on pre-purchase exam

Treatment - removal of joint mice, curettage of SBC or nothing other than rest

Prognosis with hock OCD good with surgery, stifle poor even with surgery

• Neurologic disorder caused by pinching of the spinal cord in the neck
• Form of neck OCD
• Seen in young, fast growing horses - esp 12-18 month old TB colts
• Sudden onset or slowly progressive hind limb ataxia, may progress to forelimbs
• Diagnosis - myelogram, radiographs
• Treatment - rest and steroids (wait and see), cervical vertebral arthrodesis ($$$)

• Cervical instability - spinal cord is pinched intermittently with neck flexion and extension; horse can be normal one minute, throw its head up and immediately become recumbant
• Cervical stenosis - bone growth in spinal canal causes constant pressure on spinal cord; horse is always neurologic