MSK Flashcards
3 types of equine muscle disorders
primary - traumatic/metabolic/infectious - diffuse or focal pain
secondary - using muscles differently because of pain - localised, muscle enzymes often normal
neuromuscular - muscle atrophy - myogenic or neurogenic
muscle strain - equine
acute pain
localised pain and swelling
hard to isolate - large muscle mass
risk factors -
type of activity
surface terrain
poor warm up
mildly elevated muscle enzymes
Ultrasound - fluid accumulation and disrupted fibre pattern
treatment -
cold hosing/icing
NSAIDs
rest
gentle mobilisation and exercises
exertional myopathies - equine
very prevalent
signs -
poor exercise tolerance
muscle stiffness
shortened hind limb stride
reluctance to move
firm, painful, hindquarter muscles
anxiety
pain
sweating
increased resp rate
colic type signs - pawing, trying to lie down
myoglobinuria
elevated CK and AST
sporadic or recurrant
sporadic - one off extrinsic factors - overexercising, dietary imbalance, exhausted horse syndrome
recurrant - intrinsic factors - heritable factos, breed related, recurrent exertional rhabdomyolysis, polysaccharide storage myopathy
recurrent exertional rhabdomyolysis (RER) - equine
abnormal regulation of muscle contraction
issue in calcium kinetics
light or hot breeds - thoroughbreds
suggested heritability
more often in nervous females
risk factor - high grain diet
diagnosis -
signs and history
serum CK and AST increase
muscle histology - used to rule out concurrent conditions
polysaccharide storage myopathy (PSSM) - equine
accumulation of glycogen in muscle fibres
type 1 - mutation in glycogen synthesis gene
can test for mutation
type 2 - looks similar on biopsy but no gene identified
mutation most common in draft breeds, warmbloods, appaloosas, cobs, and ponies
diagnosis -
signs
muscle enzymes
muscle biopsies - only see changes over 2yo
genetic testing - on blood or hair roots
myofibrillar myopathy - equine
exercise intolerance
intermittent RER
warmbloods and arabs
warmbloods can have normal muscle enzymes - confirm on biopsy
arabs - high enzymes after exercise, myoglobinuria - tend to be less painful
exertional myopathies - treatment - equine
relieve pain
correct fluids
protect kidneys from effects of NSAIDs
stabling for acute stages then keep them working - days off can make it worse
diet -
low starch, high fat
adequate electrolytes
vitamin E supplementation
amino acid supplementation - less evidence
medications - dantrolene sodium (muscle relaxant)
clostridial myositis - equine
rare but nasty
usually iatrogenic - recent IM injection
necrotising infection of muscle
systemic illness - severe toxemia
swollen, painful muscle at injection site
subcutaneous emphysema
antimicrobials
multiple surgical debridements
delayed onset muscle soreness - equine
poor performance
diffuse pain
couple of days after unusual exercise
eccentric muscle contractions - contraction when muscle under tension
equine motor neurone disease
not common
generalised atrophy
oxidative damage to motor neurons
risk factors -
vitamin E/selenium deficiency
prolonged pasture access with high CHO diet
signs -
happy enough
normal appetitie
muscle weakness and atrophy
trembling
weight shifting on standing
walk better than they stand
low head carriage
exercise intolerance
“elephant on tub” stance
retinal changes - pigmentation at back of retina
diagnosis -
low vitamin E in plasma
elevated muscle enzymes
muscle biopsy of tailhead - definitive
usually need euthanising
vitamin E deficiency - equine
presents similar to motor neuron disease
responsive to treatment
immune mediated myositis - equine
rapid atrophy
moderate muscle enzymes elevation
usually quarter horses
MYH1 mutation - homozygous horses more affected
triggered by exposure to episode of strangles or other respiratory disease
diagnosis -
biopsy - epxial or gluteal muscles
genetic testing
treatment - steroids, antibiotics if concurrent infection
hip dysplasia - risk factors
weight
types of exercise
overexercising when young
breed - big dogs
ddx - hip dysplasia
arthritis
legg-calves perthes - avascular necrosis of femoral head
psoas injury
elbow dysplasia
cruiciate injury
luxated patella
nervous conditions - sciatic pathology
neoplasia - bone or joint
sepsis
hip dysplasia - pathophysiology
joint laxity –> femoral head subluxation
osteoarthritis changes - wear, cartilage thinning, fluid, osteophytes
most crucial time for hip development - before 8 weeks
hip scoring
each hip scored between 0-52 (overall out of 106)
lower score better
VD radiograph under GA
very straight
both limbs straight out and tied together
labelled
ID number and kennel club number
reviewed by 2 experts
patellar luxation - pathophysiology
bad conformation - muscle action pulls patellar ligament and displaces patella
not congenital - born normal, other abnormalities/deformities in limb causing them to turn inwards
grading 1-4
hip dysplasia - signs
difficulty rising
abnormal gait
bunny hopping
pelvic limb lameness
clicking of hips
assymetric muscle mass
sensitivity on hind quarters - esp on extension and abduction
reduced range of motion
crepitus
asymmetric pad wear
all non specific
hip dysplasia - testing
ortolani test
barden test
radiography - VD legs extended, VD frogleg, lateral (hip series) - measures of dorsal acetabular cover, norberg angle, distraction index
hip dysplasia - management
pain management
exercises - range of motion, muscle mass, strength
controlled activity level
weight management
nutraceuticals
physiotherapy
surgery - excision arthroplasty (joint fills with soft tissue to create false joint), total hip replacement, joint fusion (not hips but other joints)
cruciate injury - signs
frog sitting - external rotation of opposing stifle
sit test
loss of muscle mass
cranial draw
meniscal injury
seen secondary to cranial cruciate rupture (in most cases)
usually medial meniscus
heals poorly - usually needs taken out
if taken out - always end up with degenerative joint disease
cruciate injury - management
suture - loop round to create rotating force and hold in place
osteotomy - TPLO, TTA - good outcomes, expensive
cruciate injury
cruciate function - prevents cranial translation and internal rotation of tibia and prevents hyperextension of stifle
most common cause of hindlimb lameness
often eventually bilateral
changes can exist before ruptures
partial tears common
usually not a contact injury - different from in people
elbow dysplasia - pathopahysiology
osteochondrosis of humeral condyle - failure of endochondrial ossification
ununited anconeal process - failure of fusion of growth plate allows anconeal process to detach
fragmented coronoid process - medial coronoid fragments due to fissuring under the surface
radio-ulnar incongruity - step between radius and ulna instead of smooth gap
can have any of these concurrently - complicated joint
elbow dysplasia - signs
lameness
choppy forelimb gait
effusion
pain
crepitus
reduced range of motion
patellar luxation - surgery
wedge recession
block recession
abrasion
tibial tubercule transposition
distal femoral osteotomy - dramatic
angular limb deformity - equine
vargus - limb bending inwards
valgus - limb bending outwards
limbs turned in, knees out
happens as they grow
mild deformities - stall confinement
more dramatic - may need surgery - perioteal stripping or transphyseal bridging
corrective foot trimming
prognosis affected by - age at intervention, degree of deformity, joint affected and time that growth plate usually fuses, what the horse needs to eventually do
growth plate closure times - equine
P1 - long pstern - 2-3 months
MC3 - cannon bone - 6-9 months
distal radius - 9-12 months
osteochondrosis - equine
2 types -
osteochondrosis dessicans (OCD) - non loaded margin of high impact joints
sub chondral bone cysts (SBC) - high load margins, cysts develop within the joint
usually genetic with environmental factors
circulation not getting to cartilage as well as it should in rapidly growing young animals
cartilage doesn’t develop how it should
fracture classification
cause - intrinsic or extrinsic
open or closed - is skin breached
extent of damage
number of fractures
position
direction of fracture lines
location
forces acting on the fracture - affects stability after fixed
involvement of other tissues - trapped nerves, vessels, soft tissues, puncture of organs
age of fracture
fracture geometry
transverse - straight across
oblique - line of break offset from right angle
comminuted - multiple peices
segmental - large segment blown out
femoral fracture
most common small animal appendicular fracture
access for surgery lateral - less vessels
radius/ulna fracture
usually distal of mid diaphyseal
usually just repair radius
little dogs jumping off things
can sometimes just use external fixator if sides of fracture well opposed
tibial fracture
high velocity injury
access for surgery from medial side - tension side, skin tighter over bone, less muscles to go through
external fixator may work if comminuted and open
salter-harris fractures
physeal (growth plate) fractures
S - straight across
A - above (along plate then up)
L - lower (along plate then down)
T - through (cutting down through plate)
ER - erasure of plate (crush)
always damage to growth plate
avoid putting in devices that compress or restrict bone lengthening - smooth k wires preferred
femoral head fracture
usually young dogs (3-10 months) and cats
fracture across growth plate
operate early, delayed action worsens prognosis
proximal tibial fracture
main growth plate is a complression plate but also a tension plate at tibial tuberosity (attachment for patellar ligament)
need a tension wire so tibial tuberosity doesn’t just pull off
mandibular symphyseal separation
common in cats
wire it shut - occlude sides but don’t overtighten and crush tissues
take wire out after about 6 weeks
can use heavy gauge PDS instead of wire so will absorb
check no other jaw fractures before fixing
pelvic fractures
referral
needs a significant impact, not easy to break
multiple fractures
check spine, bladder, sciatic nerve
MSK cancer types
primary -
osteosarcoma - most common - make bone
myeloma, lymphoma, chrondrosarcoma - don’t make bone
secondary -
metastasis to bone - squamous cell cancinoma, lung-digit - more common than primary
osteosarcoma
agreesive
osteoblast tumour
large and giant breeds
more in male than female
middle aged to older
usually appendicular
poor prognosis
needs amputation and chemo - amputation alone not enough
90% have micro mets at time of diagnosis
arthrodeisis
used in cases of untreatable fractures, chronic pain from degenerative joint disease, chronic luxation
fuse the joint
outcome dependent on joint
extensor tendon lacteration
not too serious - can sever whole way and still go back to work
usually from wound on front of leg
unable to extend joint
usually common digital and long digital extensor tendon
robert jone bandage if knuckling forwards
standard wound care
good prognosis
flexor tendon laceration
potentially life threatening - major support structure for distal limb
over reach injury
severe lameness
weight bearing can give indication which tendon
risk of synovial sepsis
Ultrasound to see which tendon
SDFT - fetlock drops on weight bearing
DDFT - toe off ground when weightbearing
SDFT, DDFT and SL - toe off ground and fetlock drop
treatment -
immobilise limb
debride wound
treat synovial sepsis
suture tendon ends - repair
prognosis good for life but bad for function
complete laceration - very poor prognosis
synovial sepsis - very poor prognosis
causes of recurrent abscess - equine
foreign body
insufficient drainage
sequestrum
keratoma
laminitis
quittor3
sequestrum and foreign body in foot - equine
persistently draining tract at coronary band
radiograph - classic sequestrum appearance (dead bone, black bit where there should be bone surround by involcrum)
can lead to infection in pedal bone
remove inciting cause for antibiotics to work
keratoma - equine
benign tumour - in keratinised tissue in hoof wall
noticable circular structure (keratinisation) in white line on base of foot
radiograph - circular radiolucent in P3
needs surgical removal
good prognosis but can reoccur
quittor - equine
mostly draught breeds
draining above coronary band
non healing wound
infection of collateral cartilages –> necrosis
needs surgical debridment
antibiotics will hold it but if stop taking them draining will start again
white line disease - equine
sometimes pus
separation of horn sections
quite lame
crumbling of hoof wall
multifactorial - environmental, nutritional (biotin, calcium, vitamin A), mechanical (hoof maintenance), infection
can usually diagnose from separation of white line
aggressive debridement of hoof wall - remove enough but keep stable
manage triggering factors
canker - equine
hobby breeds
moist environment - predisposes to anaerobic bacterial infection (so bacterial but management related)
hypertrophy of dermis of horn of foot
shite soft moist tissue around heel and frog
usually smells bad
aggressive debridement needed
will bleed a lot - needs lots of packing
topical metronidazole
astringents - dry out tissue
address management issues - otherwise will reoccur
causes of foot pain - equine
foot balance
hoof wall
joint
collateral ligament
digital cushion
DDFT
navicular bursa
distal sesamoid ligament
food pain - presentation - equine
lameness - chronic and intermittent
inconsistent performance
loss of suppleness - not moving as usual
tripping or stumbling
unwillingness to go forwards - more likely to canter than trot
temporary improvement with rest
bilateral lameness signs - equine
worse on hard surfaces
worse when circling
mild to moderate
usually one limb worse
decreased cranial stride
unilateral lameness signs - equine
minimal external signs
insidious or acute onset
usually no digital pulse or swelling
improves with rest then gets worse when back to work
poor foot balance - equine
usually a contributing factor
address before looking to other ddx
foot trimming
navicular syndrome - equine
associated with navicular bone, bursa and soft tissues in that region
middle aged competition horses
bilateral shortened stride
worse on hard surface
resolves on rest then comes back
insidious onset
risk factors -
upright conformation
jumping
working on hard surfaces
radiograph - once signs visible usually quite advanced - abnormal synovial fossae, cysts in bone, osteophytes, decreased cortical meduallry definition
navicular syndrome - treatment - equine
change foot balance - decrease heel pressure, maximise surface area for weight
NSAIDs
steroids into bursa
stem cells - repair DDFT damage
polyacrimide hydrogel - support and cushioning for navicular bone
bisphosphonates
surgery - remove section of palmar digital nerve so can’t feel foot
progressive, not curable
manage pain and progression
DDFT tears - equine
unilateral forelimb lameness
acute onset
often can block with palmar digital nerve block
usually only shows on radiograph if very chronic tear
MRI best for diagnosis
articular pain - equine
DIP and PIP joints
mild lameness
loss of performance
reluctance to move forwards
nerve blocks to diagnose
acute joint damage –> synovitis (rapid) –> osteoarthritis (ongoing damage)
DIP joint - collateral ligament lameness - equine
worse when cicrcling
will block with abaxial sesamoid nerve block
usually acute
MRI to diagnose
side bone - equine
ossification of collateral cartilages –> extra bone formation at side of foot
rarely causes lameness unless fracture causing inflammation or concurrent cause of lameness
cob type horses
synovial disease - treatment - equine
NSAIDs -
chronic lameness
only effective if inflammation
bute - cheap, effective for synovitis, possible renal and GI side effects
flunixin meglumine - most effective for visceral pain, anti endotoxic, not usually first line for orthopedic pain
fibrocoxib - osteoarthritis, more expensive than bute but less side effects
paracetamol - human kind, analgesia for laminitis
bisphosphonates -
stop bone breakdown, alleviate pain and reduce lameness
good for some arthritis
significant side effects - renal, not with NSAIDs, colic (then can’t give flunixin with it)
tested for in doping - 30 day detection
intra-articular steroids -
reduced local inflammation
short acting or long acting
shorter acting - tramcinolone - high motion joints
longer acting - methyprednisolone - low motion joints
hyaluronic acid -
improved viscosity of synovial fluid
anti-inflammatory
polyacrimide hydrogel -
improved joint lubrication and cellular growth
high motion joints - more space to fit gel in
regenerative therapies -
stem cells - made from horse or off the shelp
reduction of mild to moderate degenerative joint disease
grow new cartilage
SDFT tendonitis - types
intrinsic - strain
extrinsic - injury
displacement
SDFT tendonitis - stages of damage
tendon matrix degeneration - cumulative, associated with aging
fibrillar spillage - crosslinks breakage
fibril rupture
complete rupture
most common injury of event horses
acute overload or degenerative
SDFT tendonitis - risk factors
previous inflammation
uneven surfaces
muscular exhaustion
foot imbalance
long sloping pasterns
reduced blood supply to mid SDFT region
SDFT tendonitis - signs
swelling
lameness
thickening of tendon
pain on palpation
oedema
heat
sinking fetlock stance
ultrasound - oedema, varying echogenicity, fibre allignment (scar tissue)
SDFT tendonitis - treatment
acute phase - days after injury -
limit inflammation
cold hosing
icing
NSAIDs
steroids
bandage - reduce oedema
supportive bandage, box rest - prevent further damage
subacute phase - reparative stage, some reduction in lameness and swelling
box rest
stem cells - promote angiogenesis, and quality repair
platelet rich plasma - promote quality repair
physio - therapeutic ultrasound, low level laser, hydrotherapy - reduce oedema and inflammation
chronic phase - remodelling (months)
controlled exercise programme - small amounts of hand walking then progressive increase
rescanning before and after changes in exercise level
mesenchymal stem cells
expensive and time consuming - have to harvest and grow them
off the shelf probably will be available eventually
autologous stem cells for tendon injuries
form tendon tissue instead of scar tissue
reduced re injury rate - better quality repair
platelet rich plasma
cheaper than stem cells
increased speed of healing
ultrasound guided injection
lacking long term studies around rate of reinjury
check ligament injury
common - forelimb
swelling in proximal 1/3 metacarpal
ultrasound - enlargement, focal abnormalities, fibre pattern disruption, concurrent SDFT tendonitis on margins
treatment -
acute - box rest, NSAIDs, cold hosing, bandaging
chronic - controlled exercise, NSAIDs, corrective foot trimming
suspensory ligament desmitis
proximal, body or branch types
proximal
forelimb - just below knee, some pain on deep palpation, some enlargement
treat with controlled exercise, box rest, stem cells
prognosis good
hindlimb - more chronic, bilateral, poor perofrmance
associated with striaght hindlimbs, worse on soft surface and with exercise
radiography - sclerosis, avulsion fracture
US - fibrosis, loss of striation, new bone laid down - US hard on hindlimbs
body
older event horses
variable lameness
further down leg
associated with the new bone laid down on splint bone after injury
diagnose on palpation
treat - controlled exercise, shockwave
branch
any limb
poor-fair prognosis
tenosynovitis
inflammation of tendon sheaths
mild to moderate lameness
minimal response to rest
intrasynovial analgesia to confirm
radiography - with contrast can see manica flexoria
manica flexoria
tendon ring that hold SDFT in place
marginal tears can drive chronic cases of tenosynovitis
tears caused by compression of tendon in overextension
capped hock
synovial fluid in cacaneal bursa (point of hock)
cosmetic
not usually lame
windgalls
fetlock or tendon sheath distension
with or without lameness
thoroughpin
synovial distension of tarsal sheath
cosmetic
tenosynovitis - treatment
acute -
rule out sepsis
rest
ice/cold hosing
NSAIDs
intrathecal steroids
hyaluronic acid
tenoscopy - if lack of response to conservative treatment
chronic -
tenoscopy - early exercise post surgery to reduce post op adhesions
rest and controlled exercise
address underlying issues
palmar annular ligament desmotomy - cut ligament to reduce constriction, good prognosis if desmitis has been controlled
carpal canal syndrome - equine
tenosynovitis of carpal sheath (carpal tunnel)
secondary to tendonitis of SDFT and DDFT, or fracture in that region, or osteochondroma
need to remove the osseous impingment
Wooden tongue
actinobacillus lignaressi - gram -ve, oral commensal, gains entry through breaks in buccal mucosa
sudden onset salivation
dysphagia
protrusion of tongue
firm, swollen, painful tongue - not moving as much as usual
enlarged lymph nodes
submandibular swelling
diagnosis - exam and bacterial c&s
wooden tongue - ddx
stomatitis
lumpy jaw
dental disease
oral foreign body
pharyngeal trauma
wooden tongue - management
isolate animal - makes sure get enough food an water
ensure adequate food and water
antibiotics
oral potassium iodide or IV sodium iodide - not licensed in UK food animals
lumpy jaw
actinomycosis
pyogranulomatous osteitis
seen when young cattle teething - entry through mucosa when teeth erupting
infects bone
usually bright seeming
enlargement of horizontal ramus of jaw
soft tissue swelling
irregular swelling and bone remodelling
tooth displacement
fractures
discharging sinus tracts
pain and inability to eat –> weight loss
diagnosis - exam, impression smear from discharging tracts, radiography (extent of bone remodelling, doesn’t change treatment options)
lumpy jaw - ddx
tooth root abscess
fracture of mandible
neoplasia
foreign body
feed impaction
lumpy jaw - treatment
food and water to reduce weight loss
antibiotics
mandibular fracture - farm
usually due to trauma - kick, hit by tractor, dystocia
dysphagia
weight loss
excess salivation
swelling at fracture site
protruding tongue
diagnosis - palpate misalignment at site, radiography
management -
slight displacement - will heal over time
wire
external fixator
euthanasia/emergency slaughter
(if don’t have time for aftercare then just euthanise)
ramus in calf will heal better than mandibular symphysis
dental disease - farm
not commonly reported
leads to inefficient chewing –> decreased intake –> decreased productivity
tooth root abscess - from infection from periodontal disease or penetration of crown of tooth by commensal bacteria
jaw swelling
salivation
halitosis
discharging sinus tracts
inappetence
weight loss
diagnosis - inside mouth exam (use a gag), external palpation, radiography
tooth root abscess - treatment - farm
remove infected tooth (could flush or suture after but hard to get it clean enough
will cause overgrowth or malocclusion of opposing tooth
antibiotics - long term if bone infection, can have negative effects on gut microflora
NSAIDs
dietary change - high energy concentrate that doesn’t need as much chewing
choke
oesophageal obstruction
can be proximal cervical, at thoracic inlet or in thoracic oesophagus
usually due to access to large lumps of root vegetables
distress
extended neck and lowered head
salivation
regularly trying to swallow
lower obstruction - large amounts of clear viscous saliva
over time - rumen bloat from not being able to ruminate
may be able to feel or see blockage if very cranial
pass stomach tube - won’t go down if blocked
choke - ddx
frothy bloat
gassy bloat
tetanus
choke - management
relieve bloat - trocar or needle
hyoscine - relaxes oesophagus
massage obstruction further cranial
manually remove if very cranial
pass form stomach tube to push block into reumen
probang - device that dislodges or slices obstruction
if not too distressed can just leave it until it degrades a bit and can be swallowed
bovine papular stomatitis
parapoxvirus
zoonotic
usually calves under 1yo
papules in mouth
anorexia
salivation
mild pyrexia
lesions
most severe - raised lesions
ddx -
foot and mouth
BVD
vesicular stomatitis
bovine herpes
blue tongue
foot and mouth
picornavirus
notifiable
very contagious
lesions in mouth and on feet
anorexia
depression
pyrexia
salivation
milk drop
vesicles on tongue and dental pad and hard palate - rupture to leave shallow ulcers
lesions on coronary band later - pathopneumonic
calf diptheria
fusobacterium necrophorum
necrosis in mouth
young calves - see outbreaks
associated with poor hygiene
lesions caused by trauma to mucosa
wet lower jaw - excess saliva
firm swellings in cheeks
necrosis in mouth mucosa
halitosis
swelling in submandibular lymph nodes
pyrexia
if infection in larynx - anorexia, pyrexia, coughing inspiratory stridor (roaring), dyspnoea
death - due to asphyxiation/respiratory distress
treatment -
penicillin
steroids if in respiratory distress
NSAIDs
tracheotomy - if really struggling to breathe
laryngeal chondritis
texel throat (sheep)
unable to breath properly
more in tups
infection of mucosal abrasions –> abscess in larynx –> exacerbates existing issue with larynx in predisposed breeds
acute respiratory distress
inspiratory effort and stertor - snoring sound
neck extended, head lowered, nostril flare
open mouth breathing
diagnose by signs and breed predisposition
laryngeal chondritis - management
steroids - reduce swelling
NSAIDs - more long term
antibiotics - long term, prevent abscessation
euthanasia
tracheotomy - in severe cases
usually doesn’t fully resolve and often recurs
hypocalcemia - signs
loss of smooth muscle tone
recumbant
s shaped neck
hypocalcemia - management
calcium sub cut - takes a few hours to work because impaired peripheral circulation
calcium borogluconate (with magnesium) - into jugular
slow calcium if heart irregularities
don’t give too much calcium - spike
thick bedding with lots of grip
food and water in easy reach
remove calf for 24 hours
lift and turn every 6 hours if recumbent - so not laying on muscle groups too long
bloods - test if need also magnesium or phosphorus
may need further calcium - bolus, electrolyte fluid, oral gels
prevention -
high calcium concentrate at calving
assess forage component in diet
prophylactic calcium for at risk coews - 3rd lactation on, twins
keep in calving box for an extra day
remove calf
not milk for first few days
hand feed colostrum and don’t milk out whole udder
D3 injection before calving
control BCS
calcium restriction last 3 weeks of gestation
magnesium supplementation
calcium binding products last 2 weeks gestation
diet cation:anion balance manipulation - low sodium and potassium, high chloride and sulphates - monirot using urine pH
straw or maize silage better low calcium
hypocalcemia - sheep
late pregnancy/early lactation
older sheep
associated with stress
passive reflux of ruminal contents down nose when lying down
blood sample pre treatment - calcium under 1mmol/litre
treatment - slow IC calcium borogluconate
prevention - feed adequate but not excessive calcium (5-10g/day), avoid stressful conditions/events
hypomagnesia
majority magnesium locked in bone, can only use the part from rumen and omasum (or intestines in calf)
needed for milk and tissue production
spring and autumn lactating cows without enough supplementation
types -
peracute
acute
subclinical
chronic
calf milk tetany
hypomagnesia - signs
nervous and aggressive
hyperaesthesia
convulsions
death
hypomagnesia - management
emergency - treat ASAP
calm - surprises can cause convulsions
keep in lateral while treating then move to sternal
calcium borogluconate - has magnesium in, IV in tail vein
control seizures - xylazine, ACP, pentobarbitone
food and water nearby
food with magnesium ongoing
clinical cases usually tip of iceberg, check herd for subclinical
lick blocks
bolus magnesium
concentrated
magnesium in water
spray pasture
check soil magnesium levels
good grasses that translate magnesium to their leaves
ensure good daily dry matter intake
reduce stress
hypomagnesia - sheep
first 6 weeks after lambing
ewes with multiple lambs
convulsion and sudden death
ddx - acute mastitis (also presents as sudden death)
treatment - IV calcium borogluconate, reduced stress (provide shelter)
hypophosphatemia
down cows
high production cows in periparturient period or if reduced feed intake around calving
decreased GI motility
young cows - slow growth, rickets
adult - lethargy, weight loss, anorexia, muscle weakness, muscle and bone pain, rhabdomyolysis, intravascular hemolysis
later stages - pica
usually seen with milk fever
diagnosis - blood sample for phosphorus, watch reaction to calcium treatment (try and get up but just shuffle about)
oral or injectable phosphorus
