Laminitis(Founder)
Inflammation of laminae of the foot.It is
peripheral vascular disease shown as decreased capillary perfusion, ischemic
necrosis of laminae and pain.
It is Complex systemic metabolic disease affected by
cardiovascular,renal,endocrinal,blood coagulation and acid-base status which results in acute degeneration of laminae.
Mostly fore limb affected
- Three phases of laminitis
- Developmental
phase -
initiation with trigger factor that lead to change in foot
- Acute
phase -
onset of clinical signs
- Chronic
phase -
48 hrs of continuous pain
- Etiology
- Carbohydrate overload
(grain founder)
- Lush grass over load (grass
founder)
- Obesity
- Endometritis (post
parturient laminitis)
- Severe systemic infection-altered
vasoactive process and coagulopathy with decreased perfusion and ischemic
necrosis.
- Colic
- Stress/exhaustion-with
concussion (Road founder)
- Drinking large amount of
cold water
- Toxins ingestion
- Hormone imbalance and
corticosteroid therapy.
- Over exercise on hard
ground
- Clinical signs
- Lateral recumbancy for long
period
- Increased respiratory rate
with muscle tremors, sweating
- Arched back condition
- Laminitic gait
- Hot to touch around
coronary band
- Digital pulsation
- Pain response to digital
pressure
- Dropped sole
- Laminitic ring around wall
- Diagnosis
- Clinical signs and history
- Radiography
- Treatment
o Medical treatment
with NSAIDS – phenylbutazone, acetylsalicyclate, flunixin meglumine
o Complete box rest
o Use of frog support
to reduce pressure on laminar band
o Removal of shoe
o Balanced diet
o Corrective trimming
and shoeing
o Realignment of
distal phalanx in pedal rotation.
Sand crack
- Fissure in the wall of the
hoof, parallel to the horn tubules, commencing at the coronet and
extending a variable distance down the wall, usually to its plantar
aspect. It may occur at any part of the wall and even in the bar, but its
commonest situations are the toes of the hind foot and the inner quarter
of the fore foot.
- Types
o Superficial or
deep, complete or incomplete, simple or complicated, straight, recent or old
- Etiology
- Thinness of the hoof wall
- Excessive rasping of the
wall
- Injury to the coronet
- Violent extension of the
corono-pedal joint
- Clinical signs
- Fissure in the hoof wall
- Oozing of blood, serum or
pus
- Swelling of coronet
- Necrosis of lamina
- Lameness depending on the
severity
- Spasmodic lifting of the
limb
- Diagnosis
- Clinical signs
- Radiography
- Ultrasonography
- Treatment
o Corrective shoeing
o Application of hoof
bandage or clasps or horseshoe nail
o Metal plate
screwing, wiring or lacing the hoof wall in shoe lace pattern overlaid with
fibreglass or acrylic patches
o Thinning/stripping
the horn wall and removal of necrotic tissues, pus and application of
antiseptic foot baths, hoof repair material
o Blistering the
coronet region to stimulate the growth of new horn
- Prognosis for
soundness
- Good – for superficial
cases
- Guarded in long standing
cases due to deformity of coronary band
Seedy toe
· It describes a
condition in which dermal and epidermal layers are separated in the toe region
of the foot. Newly formed horn follows the line of separation and perpetuates
the defect. After sometime the separation is visible in the white line in the
toe region and the dermal structures are exposed to ascending infection.
- Etiology
- Focal haemorrhage
- Seroma formation
- Failure of damaged laminae
to produce keratin
- Clinical signs
- Brown crumbly horn like
matter along the white line
- Lameness in severe cases
- Percussion of dorsal hoof
wall produces characteristic hollow sound
- Diagnosis
o Careful exploration
of the undermined wall with a blunt radio opaque allows radiological
documentation of the extent of separation.
o Gas shadow in the
soft tissues dorsal to the 3rd phalanx on lateromedial radiographs
of the foot.
- Treatment
o Regular cleaning of
the defect and shoeing with wide webbed, flat shoes.
o In more severe
cases the separated hoof must be removed from the solar margin of the toe to a
level where normal inter laminar band is present. The exposed laminae are
medicated under a dressing.
Fractures of 3rd phalanx(pedal bone,ospedis,coffin bone)
- Etiology: Acute
trauma due to kick
- Not common
- By exercise on hard surface
- More fore feet, left foot by
counter clockwise racing by twisting action.
- By penetrating foreign body
through sole.
- Improper shoeing.
- Nutrient deficiencies.
- Infections.
- Classification: Based on the anatomic location of the fracture
o Type I - Non
articular fractures of palmar or plantar process of the bone
o Type II - oblique
articular fracture from distal interphalangeal joint to solar margin of the bone
o Type III - mid
sagittal articular fracture that divide the distal phalanx in two equal parts
o Type IV - fracture
of the extensor process
o Type V - comminuted
fracture or secondary to foreign body penetration
o Type VI - Non
articular fracture of the solar and parietal cortices
o Type VII - Non
articular fractures of palmar or plantar process of the bone.
- Clinical signs: Acute supporting limb lameness.
- Sudden lameness after work.
- Increased digital pulse and Inc heat
in foot.
- Inc pain in entire sole, point of pain
known by hoof tester.
- Arthrocentesis of coffin joint-bloody
fluid within articular fracture.
- Diagnosis
- Radiography
- Local analgesia
- History and testing with
hoof testers before radiograph.
- Treatment: For
fracture of
o Chronic type I –
Palmar digital neurectomy to relieve the lameness
o Types I to V – Non
surgical management by applying bar shoe with quarter clips for 6-10 months
o Type VI - Rest and
application of shoe with pad
o Type VII - Complete
rest for 3 to 4 months
o If fractures are by
punctured wound, it will result in bone abscess and demineralization.Treat for
Abscess and correct shoeing.
o Sagittal and
oblique fracture
§ Should be treated
before fibrous union with internal fixation using 4.5 or 5.5 mm cortical or
shaft screws (ASIF cortical bone screws-association for the study of internal
fixation)
§ Pressure bandage
application with antiseptic soaked guaze dressing
§ Acrylics are used
for binding.
Prognosis: Good if
sufficient rest is given.
|
PEDAL OSTEITIS
|
- Pedal osteitis is an
inflammatory condition of the foot that results in demineralization of the
distal phalanx.
- Two recognized
classifications are
- non septic and
- septic
- Etiology
o Primarily it is
associated with severe or chronic sole bruising, concussion
o Secondary is most
common, caused by persistent corns, laminitis, puncture wounds, bruised wound
sole, conformational faults.
o Septic Pedal
osteitis develops from introduction of environmental microbes either into the
soft tissues of the foot or distal phalanx.
o It causes includes
chronic severe laminitis, sub solar abscess, solar margin fracture, deep hoof
wall cracks, avulsion of hoof injuries, penetrating wounds of the foot.
- Clinical signs
o Non septic PO
commonly affects forelimb and the condition can be either unilateral or
bilateral. Severity of the lameness depends upon on the cause and degree of
injury.
o Hoof tester
examination often reveals a focal or a diffuse region of increased sensitivity
when pressure is applied to the sole and to the hoof wall.
o Septic PO commonly
affects the forelimb; lameness grades ranging from 2-4.5 are common. On
palpation, increase in temperature and prominent digital pulses can often be
felt in the affected foot.
- Diagnosis
o Radiographic
assessment of distal phalanx for nonseptic PO includes atleast 3 views: 65º
dorsopalmar, medial and lateral oblique projections.
o Radiographic signs
include demineralization, widening of the nutrient foramina at the solar
margin, irregular bone formation along the solar margins of dorsal surface of
distal phalanx. Lateral border usually more roughened than medial.
o Radiographic signs
of septic PO are loss of trabacular detail with indistinct margins fading into
the surrounding bone, osteolysis at the margins of the distal phalanx.
- Treatment
- Non septic PO
§ Rest,
administration of NSAIDs, the avoidance of exercise on hard surfaces,
application of protective shoes should be useful.
§ A handmade, wide
web, egg bar shoe whose solar surface is deeply concave is more useful. In
horses in which the sole is thin and soft can be medicated topically with equal
parts of phenol, formalin and iodine to toughen them.
- Palmar
digital neurectomy recommended.
- Septic PO
§ Debridement of the
tract, removal of infected bone. Infected bone appears grayer and is softer
than the normal soft bone of the normal distal phalanx.
§ Tract is packed
with gauze soaked in dilute povidone iodine and protective bandage is applied.
Plastic or rubber boot can be applied to protect the bandage.
§ A shoe with a
removable metal plate can be applied.
· Prognosis
o Nonseptic PO: good if condition is primary and acute unfavourable, if chronic
o Septic PO: good if infection is controlled.
Ulceration of sole
· Commonly noticed in
grazing cattle and may occur in any digit but are more common in lateral claws
of hind limb and medial claws of forelimb. The seat of lesion is at the corium
that overlies the flexor process of the third phalanx
- Etiology
- Over trimming of toes
- As secondary to
interdigital dermatitis
- Clinical signs
o Slight haemorrhage,
necrosis of the corium and surrounding tissues
- Treatment
o Corrective trimming
and lowering the heel horn of the affected claw
o Application of hoof
block to healthy claw to avoid weight bearing on the affected limb
o If adequate heel
depth of healthy toe is available “heelless method of trimming”-removal of all
wall and sole from the posterior half of the digit to a depth with preservation
of thin layer of sole and application of hoof block on the healthy toe for a
period of four weeks.
Canker (Necrotic pododermatitis)
· Chronic
hypertrophic moist eczematous dermatitis involving the frog, sole and wall of
the foot.
- Common in the heavy draft
horses especially in the hind feet
- Etiology
- Unhygienic stable
- Poor foot care
- Prolonged exposure to
moisture
- Hereditary
- Clinical signs
o Peeling of horns as
soaked in oil
o Ergot formation -
finger like hypertrophic growth with foul smelling condition covered with
Friable crust over the frog
o Progressive
lameness
o Cheesy foul
smelling exudates from the frog
- Clinical signs
o Inflammation,
hypertrophy, necrosis, dyskeratosis at the frog region
- Treatment
o Removal of the
infected horns under general anaesthesia and application of triple sulph powder
(Zinc sulphate, Copper sulphate and Ferrous sulphate)
o Debridement and
dressing with noncaustic antiseptic sugar and iodine preparation
o Daily dressing with
dry sterile water proof pressure bandage
o Coverage of sole
with metal or leather
- Prognosis for
soundness
- Good – in early cases
- Unfavourable in long standing
cases
Corn
- Contusion of the sensitive
corium and sole at angle between the wall and the bar
- Types
- Moist , dry, suppurating or
festered and complicated corns.
- Etiology
- Defective conformation of
the foot
- Improper shoeing for long
period
- Excessive weight bearing on
the heel
- Secondary to side bone
formation
- Clinical signs
- Pointing of the limb
- Bilateral forelimb lameness
with shortened stride
- Bruised condition at the
angle between the wall and the bar
- Diagnosis
- Shoeing history
- Clinical signs
- Radiography
- Treatment
o Removal of improper
shoes
o Rest
o Foot bath and
antiseptic dressing
o Debridement of a
thin layer of sole horn over the corn
o Corrective shoeing
with full and long fitted heels or wide webbed egg-bar shoe
- Prognosis for
soundness
- Good at early stages
- Guarded – in collapsed heel
or pedal osteitis condition
Thrush
· It is a
degenerative condition of the central and collateral sulci of the frog,
characterized by disintegrating horn and the presence of grey to black material
in the affected areas.
- Etiology
- Unhygienic ,moist stabling
with poor foot care.
- Fusobacterium necrophorum
is mostly involved.
- Clinical signs
- Black discharge in the
sulci of the frog with very offensive odour.
- Only when sensitive
structures are involved lameness occurs.
- Mainly hind limbs affected.
- Treatment
- Debridement of affected and
separated horn .
- Daily topical astringent
medication under dressing. Sterile bandaging after each debridement and
continue treatment under plate shoe.
· Monday Morning
Sickness (or disease) is an old slang term used for a condition properly known
as Azoturia. It is also referred to as Exertional Myopathy. It is a potentially
fatal condition that makes it very difficult and painful for the horse to move
and can cause failure of the kidneys. Azoturia is most commonly found in horses
that are heavily exercised on a regular basis, and then not worked for one or
two days but still fed the same amount of food. This results in glycogen (a
carbohydrate) building up in the muscles. When the horse returns to work, this
glycogen breaks down quickly and produces an overload of lactic acid. The
lactic acid damages skeletal muscles, releasing muscle enzymes and myoglobin,
which can lead to acute kidney failure.
· Tying-up is a
milder form of the condition that is usually seen in race and performance
horses after a hard workout. While cooling down, the muscles stiffen and
tremor. The muscles of the hindquarters are particularly tense, hard and
painful. The pain causes anxiety and sometimes sweating.
· The horse, is
subject to muscle problems due to abnormal metabolism of energy. The byproducts
of abnormal metabolism cause inflammation of muscle cells, which leads to
painful spasms of the large muscles of the back and hindquarters. The clinical
result is a horse that can’t move due to these painful muscle spasms.
o Causes
o Symptoms
· The most common
cause of Monday morning sickness or Azoturia is from a carbohydrate overload
combined with time off. This used to be very common with draught horses who
would have Sunday off and then have an episode of Azoturia on the Monday, hence
the term Monday Morning Sickness.
· The glycogen in the
hard feed builds up in the muscles and produces an excess of lactic acid to be
produced when the horse resumes work, the lactic acid in turn damages the
muscle tissue and subsequent blood flow to the muscles. As the Lactic Acid
cannot be dispersed quickly enough it causes an episode of Azoturia to occur.
· These can vary
depending on the severity of the attack.
o Horse will show a
reluctance to move.
o Horse will refuse
to move, hence the term tying-up.
o The muscles will
tighten up and go hard and often be quite hot.
o The urine will be
dark brown in colour due to the muscle pigment myoglobin going into the blood
stream and subsequently being urinated.
o The horse may show
signs of repeatedly trying to urinate with no affect.
o The horse may sweat
up.
o The horse will be
distressed.
· The use of pain
killers and anti inflammatory drugs are used initially to make the horse more
comfortable Fluids are often administered to help flush out the toxins.
· The horse should
then have box rest followed by gentle exercise and a new feeding program that
is appropriate for the level of work. If you are riding when the horse develops
symptoms then dismount immediately and place rugs over the horse to keep the
horse warm.
· Put them directly
into a warm stable with plenty of bedding and water and do not want to ride
them as this will only further damage muscles and cause more pain.
· Carefully warm up
your horse and use an exercise blanket on cold days.
· Ensure that if the
horse has a rest day that the hard feed is reduced.
· On rest days ensure
that the horse is turned out as this will allow them to gently exercise.
· Feed according to
the work being done and if the horse is prone to Rhabdomyolysis reduce the
carbohydrate in the feed, the use of soya oil for energy can be a useful
addition in the diet.
· The use of some
supplements may be of value, for example the addition of Selenium and vitamin E
are known to be good at reducing free radicals and the correct balance of
electrolytes is essential to provide a natural balance.
Cording up
· Myopathy that
occurs after active muscular exertion. Horses affected are usually on high
grain ration and tested for one or two days.
Painful condition of iliopsoas muscle that occurs within minutes after exertion of race.
Painful condition of iliopsoas muscle that occurs within minutes after exertion of race.
· Signs
o Stiffness after
racing
o Back is rigid
o Palpation of
iliopsoas muscle- painful.
o Muscles hard to
touch.
o Involvement of
gluteal and quadriceps
o Mild myoglobinuria
· Diagnosis
o Clinical signs and
history.
· Treatment
o Walking horse for
30-40 minutes.
o Calcium gluconate
intravenous injection.
o Tranquilizers.
o Alkalization of
blood with sodium carbonate.
|
MYOSITIS OF PSOAS
|
· Inflammation of
muscle is known as myositis, especially a voluntary muscle
· This type of muscle
disease (myopathy) represents a group of different diseases which all share the
feature of inflammatory cells within the muscle.
· Myositis is the
early stage of muscular infection.
· A psoas abscess is
defined as a purulent infectious collection within the psoas muscle
- Myositis can affect
- One muscle
- Groups of muscles
Etiology
· Infection,
autoimmune conditions, genetic disorders medication adverse events, electrolyte
disturbances, and diseases of the endocrine system.
· Some idiopathic cases
of polymyositis are suspected to be related to infectious agents, especially
viruses such as the paramyxoviruses or enteroviruses .
Signs
- Pain
- Tenderness
- Swelling
- Weakness
Diagnosis
· Laboratory
evaluation reveals leukocytosis with a left shift and an elevated erythrocyte
sedimentation rate.
· In cases of
secondary psoas abscesses, pyuria and positive urine cultures may be found when
the genitourinary tract is the originating site of infection. The diagnosis is
established by radiological imaging. A psoas abscess may be detected on
ultrasound evaluation, but this test is not as sensitive as CT or MRI scans.
Treatment
· Surgical drainage
and intravenous antibiotics are recommended.
· Drainage may
involve either CT-guided percutaneous drainage or an open surgical procedure.
· This is the
thrombosis in the iliac arteries - the vessels into which the abdominal aorta
breaks up beneath the lumbar spine, and whose branches are distributed to the
hind-quarters and extremities.
o Causes
o Symptoms
Causes
· The causes of
thrombosis are chiefly injuries such as wounds, severe contusion, and
stretching , diminish its vitality may determine the coagulation of blood
within it. It is also a consequence of degenerative changes in the structure of
the vessel, and of arrest of the circulation from aneurism or any other cause
which induces the blood to stagnate.
·
For the most part thrombosis of
the iliac vessels is the result of sprain inflicted by violent backward
stretching of the hind legs, would result when a horse falls short in jumping
and slips down, or when his legs fly back from under him, or "
spread-eagle", while drawing a heavy load over a slippery surface, or out
of deep heavy ground.
· In all these
positions there would be sudden and severe stretching of the vessels and injury
to their coats.
· Thrombosis from
stagnation of blood
· Thrombosis from
alteration of the wall
· There are cases in
which coagulation occurs by transfusion of blood from lower animals.
Symptoms
· Slight stiffness of one or both hind-limbs,
more especially on rising from the recumbent posture, slight swelling of the
limbs are the initial sign.
· When the animal is
made to move, the blood disappears from the veins, and returns but slowly.
· In the more
advanced stages of the disease exertion brings on a rolling gait behind, and,
if continued, results in paralysis of the posterior part of the body. At this
time the animal breaks out into a profuse perspiration, the breathing is
hurried, the muscles quiver, and the pulse is much accelerated. In some cases
the affected animal strikes the belly, looks round to the flank, and shows
signs of acute pain, as if the subject of colic.
· After a short
period of rest the symptoms subside, and the horse resumes his normal
condition, and will most likely continue in apparent good health until the
exertion is again repeated.
· Although the
symptoms described are very indicative of iliac thrombosis, the diagnosis may
be rendered still more complete by a careful manipulation of the affected
vessels.
· The iliac arteries
are to be found striking off right and left beneath the lumbar spine, and quite
within reach of the hand when pushed well forward into the rectum.
· In carrying out
this examination the hand and arm must be well anointed with oil or vaseline,
and after entering the bowel the arm is turned so that the palm is presented
upward; the fingers are then directed to that part of the spine where the loin
joins on to the quarters, immediately beneath which the great iliac vessels -
two on either side - will be felt branching off right and left from the
posterior aorta.
· Treatment in these
cases is of no avail.
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