Colorado VMA 2011
Food Animal Neurology: Examination and Localization of Lesions
Question 1: Is it a primary neurological disease?
Question 2: Is it rostral or caudal to foramen magnum?
Causes:
a. bacterial
b. viral
c. toxic
d. metabolic/nutritional
e. traumatic
f. neoplastic
g. congenital or hereditary
h. degenerative
History:
Very important!
a. Environment ie: hogs nearby?, junkyard?, plants?, feeding practices?, silage?
b. Past disease? ie: pneumonia?, diarrhea?, navel infection?, BVD?
c. Age of onset
d. Breed ie: Brown Swiss, Charolais, Saler
e. Length of illness
f. Therapy and response
g. Past vaccinations, dehorning, castrations, spraying
Neurologic Examination of the Ruminant
Broad View
Is it primary neurologic disease?
History
Gait
Posture
Mentation
Is it rostral or caudal to the foramen magnum?
Rostral to the foramen magnum
Cerebrum
Cerebellum
Vestibular system
Brain stem/cranial nerves
Caudal to the foramen magnum
Spinal cord
Peripheral nerves
Specific View
Overall Assessment (from a distance)
Gait – ataxia - focusing on coordination and strength
Posture – ie: head, body, limbs – animals with postural abnormalities may have normal
gaits, but animals with abnormal gaits will always have abnormal postural reactions
Mentation – is animal responding appropriately to environmental stimuli?
Does the history or above examination suggest neurologic disease?
Closer Examination (hands-on)
Cranial nerve examination:
Ocular exam
Palpebral, menace, papillary light reflex, corneal reflex
Ophthalmoscopic examination
Postural responses:
Proprioception, (adults), placing, hemistanding/walking (young or small
ruminants)
Spinal reflexes:
Panniculus, perineal, patellar and withdrawal (flexor)
Palpation:
Localized areas of pain, sweating, atrophy
Peripheral nerves:
Obturator, sciatic, femoral, peroneal, tibial, suprascapular, radial
Organization of the CNS
I.
Sensory – afferent nerves
II.
Brain and Spinal Cord – integration centers
III.
Motor – efferent nerves
a. Autonomic – Sympathetic, Parasympathetic
b. Somatic – Upper Motor Neuron
Initiates movement
Synapses on LMN
Signs – normal to hyperreflexic, hypertonic muscles
c. Somatic – Lower Motor Neuron
Brain stem- ventral horns of the spinal cord
Signs – loss of reflexes, hypotonic muscle tone, atrophy
Signs Associated With Lesions in the Head
Cerebrum:
Diffuse or Local
a. seizures
b. depression –Reticular Activating System
c. change in mentation
d. cortical blindness (normal PLR)
e. compulsive circling
f.
g.
h.
i.
opisthotonus
head pressing
yawning
bellowing (abnormal vocalization)
Cerebellum:
a. ataxia w/o paresis
b. intention tremors
c. wide based stance
d. hypermetria
e. strong muscle tone
f. falling over backwards
g. no conscious proprioception (CP) deficits
h. may lack menace reflex, but have normal vision (swelling in the cerebellar region
Vestibular:
Peripheral – usually not depressed (ie: Pasteurella, Histophilus., Mycoplasma, ear
ticks/mites
a. head tilt – to side of lesion
b. eye drop- “
“
c. leaning- “
“
d. circling – “
“
e. nystagmus – fast phase away from lesion – usually horizontal
f. ataxia w/o weakness
g. bright, alert, good appetite
Central – depression can occur
a. head tilt
b. eye drop
c. circling
d. hemiparesis
e. nystagmus – horizontal/vertical/rotary - fast phase any direction (changes direction
with movement of head)
f. ataxia w/weakness
g. lose appetite
h. change in mentation
Thalmus/Hypothalmus:
a. change in behavior
b. temperature regulation difficulties
heatstroke?
c. endocrine dysfunction
Brain Stem:
General: ataxia and paresis, depression to mania
pons and medulla – depression and irregular respiratory movements
Most cranial nerve deficits are due to disease in the brain stem on cranial n. nuclei (ie:
listeria, TEME)
Cranial nerves, signs of deficit and (sensory or motor designation)
1. Olfactory – can’t smell smoke (Sensory)
2. Optic – loss of vision (Sensory)
3. Oculomotor – pupil dilation, ventrolateral strabismus (Motor)
4. Trochlear – dorsomedial strabismus (Motor) ie: polio
5. Trigeminal – loss of sensation to head/tongue (Sensory), dropped jaw due to loss of
muscles of mastication, atrophy (Motor)
6. Abducens – medial strabismus, protrusion of eye (Motor)
7. Facial – loss of motor to the head (Motor), loss of sensation to tongue (taste)
(Sensory) – otitis interna/media
8. Vetibulo-Cochlear – loss of hearing, loss of equilibrium (Sensory)
9. Glossopharyngeal – loss of motor to the muscles of pharynx (Motor), loss of
sensation of pharynx, loss of parotid and zygomatic salivary glands (Sensory)
10. Vagus – loss of motor to pharynx, GI tract, heart, lungs, larynx (Motor), loss of
senstation to pharynx, larynx, esophagus, trachea, part of external ear (Sensory), loss
of afferent limb of many visceral reflexes
11. Accessory – loss of motor to trapezius, sternocephalicus, brachiocephalicus, larynx,
pharynx (Motor)
12. Hypoglossal – loss of motor to muscles of tongue (Motor)
Signs Associated with Lesions in the Spinal Cord:
Focal: General Causes
a. vertebral trauma
b. vertebral body abscess
c. vertebral fractures – ie: spondylosis in old bulls, malnutrition in young (Cu
deficiency, high P/low Ca
d. lymphoma
e. congenital malformation
Multifocal:
a. CAEV – young goats
b. Parelaphostrongylus tenuis – sheep, goats, llamas
c. Hypoderma bovis
Diffuse:
a. rabies
b. pseudorabies
c. O-P toxicity
d. botulism, tetanus
e. copper toxicity
f. progressive ataxia –Charolais and Brown Swiss (spinal muscle atrophy)
Gait Deficits:
a. paresis – flexor weakness – brain stem white matter or spinal cord
extensor weakness – spinal cord gray matter
limb dragging
worn hooves
buckling
no ataxia
trembling when bearing weight
b. ataxia
incoordination
swaying
abducted or adducted limb placement
limb crossing
pivots on inside limb and circumducts outside limb when circling
c. dysmetria
hypermetria
hypometria
Reflexes:
Panniculus reflex – cutaneous trunci (C8, T1)
hyperesthesia – cranial to lesion
anesthesia – at and caudal to lesion
Crossed extensor reflex – not normal except in young calves – lesion above reflex arc
Flexor reflex, Triceps reflex, Patellar reflex
Lesion Localization:
C1-C6 – Altered head and neck movements
Superficial sensation loss
CP deficits
Increased reflexes
Ataxia/weakness to all four
Recumbent – lesion side down can lift head, lesion up only lift head if caudal to
C4
Truncal sway
Knuckle, stumble, fail to lift inside limb when turning
C6-T2 – Hyperactive rear limb reflexes
Depressed fore limb reflexes
CP deficits- knuckle, stumble
Superficial sensation loss
Ataxia/weakness – forelimb can = rear limb
T2-L3 – Normal fore limb reflexes
Hyperactive rear limb reflexes
CP deficits in hind limbs
Superficial sensation loss
Ataxia/weakness – hind limbs
Dog sit
L4-S2 – Normal fore limb reflexes
Depressed rear limb reflexes
CP deficits in rear
Superficial sensation loss
Ataxia/weakness – hind limbs
S1-S2 – Bladder distention, loss of anal tone
“LMN Bladder” dribbles
S3-Cd5 – Flaccid tail, anus, loss of sensation to penis, vulva, perineum (caudal epidural)
Ancillary Diagnostics:
CSF fluid:
Collection
cisterna magnum – midline just cranial to a line connecting anterior edges of the wings
of the atlas
lumbosacral – midline in the lumbosacral space
Bovine Reference:
Protein: < 40 mg/dl
Nucleated cells: < 10/microliter – monocytes
Pandy: neg. for globulin
Glucose: 60-80% of blood
CPK: < or = 20 IU/dl
Sodium: 134-144 mEq/L
Colorado VMA
Food Animal Neurology Cases and Videos
CASE 1
Herd of 150 Angus crossbred cows, gave birth to these calves. A calf with similar signs
was born last year and died due to misadventure. Cows are normal in every way. Calves
usually somewhat improved. Postmortem on calf last year was grossly unremarkable.
Work-up on these is non-specific.
CASE 2
Group of 60 Holstein heifers raised as replacements out on pasture. Two heifers are
recumbent on farm, these were presented for examination. Nothing has died. Recumbent
heifers still eat, drink normally. On physical examination, no other remarkable findings
were noted. Cranial nerves were normal. These heifers still had an appetite. No
significant laboratory abnormalities were noted.
CASE 3
4-month old show heifer prospect presented for gradually worsening “lameness” or ataxia
of 10 days duration. No other abnormalities noted.
CASE 4
10-month old heifer presented for acute onset clinical signs. Recently increased feed. No
remarkable laboratory abnormalities.
CASE 5
Calf presented for acute onset clinical signs. The calf is 3-months old, and was out with
dam on pasture. No history of abnormal birth, or other disease problems prior to
presentation.
CASE 6
These calves were presented at 3 days of age. The signs you see were present at birth
according to the owner. The dam of these twins was part of a group of cows purchased
over the past 2 years. Supposedly, this cattle herd was well vaccinated. We came to find
out, however, that she had not been vaccinated on this particular farm.
CASE 7
This yearling heifer was presented for a two day history of ataxia. The owner thought
she may have been blind for a short period of time. When we got her off the trailer,
however, she appeared to have vision, although it was possibly limited. Another heifer at
the farm was recumbent and had been similarly affected prior to her progression to
recumbency. The owner treated with LA 200 on the first day they noticed clinical signs.
CASE 8
4 day-old calf born uneventfully. Herd is well vaccinated. Calf nursed and is bright and
alert otherwise.
CASE 9
Three week-old calf presented for the major clinical sign after it was noticed 1 week ago.
The calf was a product of dystocia, as it was “hip locked” for a period of time. The calf
did nurse and is normal in every other way.
CASE 10
Yearling heifer presented for history of recumbency for 7 days duration. Prior to going
down, heifer appeared healthy. Heifer maintained good appetite and drank water. On
physical and neurologic exam, heifer had slow palpebral reflexes and corneal reflexes
bilaterally, but was visual. No other cranial nerve problems noted. Generalized
hypotonia and hyporeflexia. Interpretation was generalized weakness.
Colorado VMA
The Basics of Medicine and Surgery of Camelids
The Species
Llama glama
Llama pacos
Llama guanaco
Llama vicugna
Uniqueness:
No gall bladder
Non-lobulated kidney
3 compartmentalized “stomachs”
I largest (most like rumen)
II and III (similar to reticulum, omasum and abomasum)
Terminal portion of III like abomasum
Upper lip is ‘prehensile’
Toenail rather than hoof
Female – 4 teats/4 quarters
Male – caudally pointing prepuce, non-dependent testicles
What are they used for?
Good question
Tax right-off?
To sell to other camelid owners
Fiber – rugs, etc.
Guard animals?
Pack animals
(the high mountains of Texas)
Normals?
Temperature
99 to 101.80 F
Heart rate
60 to 90 beats per minute
Respirations
10 to 30 breaths per minute
Compartmental motility
4 to 6 per minute
Things to keep in mind
Sensitive areas
Groin
Lower limbs
Ears
Approach and awareness
Stoic
Normal body functions are mostly un-observed
Camelid chute – If you get one, you are committed!!
Common Conditions/Diseases
Heat Stress
Risk factors
a. living in Texas
b. increased periods of activity (breeding, parturition)
c. maintaining the fiber coat (even alpacas!)
d. over conditioned!
e. stressors (parasites!, showing, weaning)
Clinical signs
a. droop lips, increased salivation
b. males have swelling around testicles and under hind limbs
c. temperature above 102 F, but may be NORMAL when examined
d. recumbent
e. laying around a lot
f. reluctant to move
h. stiffness
Tests we do to diagnose it
a. PCV/TP
b. chemistry panel with electrolytes
How do we prevent this?
a. sheer them
b. high shade
c. misters”
d. avoid activity
e. watch body condition!
What is involved with treatment?
a. at the farm – cool down body temperature, sheer them if not already, oral
electrolytes (Gatorade)
b. here – IV fluids, oral nutritional support, thiamine, rehabilitation with slings
How much will it cost?
a. initially about 4 to 500 and then roughly 75 to 100 per day after that
How do these turn out?
a. if they are recumbent more than 24 hours, prognosis goes down by a lot
b. improvement usually happens in “heat stress”, but they become down from
muscle damage and stay down
c. rehabilitation can last for a long time, with little to no results
d. as long as they eat and drink, we try to work with them based of course on
owner’s budget
e. unfortunately, often intensive, diligent treatment can not get these animals back
on their feet
Parasites
All of the common nematodes affect camelids. The big ones are Ostertagia, Haemonchus
and Trichostrongylus.
Anthelminthic resistance is a large concern just as it is in our sheep/goat population. The
same principles apply to camelids as those for sheep/goats in terms of management and
control.
Coccidia – there is one Eimeria spp. of coccidian that significantly affects camelids. This
will NOT show up with a standard fecal float. Only a sugar solution will show these,
therefore, if they are suspected, the sugar solution should be utilized.
Procedures/Techniques
Analgesia
Local
Lidocaine (toxic dose around 5 mg/kg – similar to small ruminants)
Epidural
Same location as in cattle
Lidocaine (1cc per 50 kg max.)
Xylazine (0.1 mg/kg)
Anesthesia
Llamas vs. alpacas
Llamas don’t require as much generally
Combinations for anesthesia
Llamas
0.5 to 0.6 mg/kg xylazine IM followed by, or in the same syringe with
5 to 6 mg/kg ketamine IM
Alpacas
0.6 to 0.7 mg/kg xylazine IM followed by, or in the same syringe with
6 to 7 mg/kg ketamine IM
Blood Draws
Right side
C2 to C3
C5 to C6
Vein is not deep, but skin is thick
Really important to place a good stab incision for catheter
J wire catheters work well
Food Trims
Have a nail, rather than a true hoof
Equipment
Hand-held Pruning shears work well
Small rasp
Procedure – cut flat with the pad
Castration
Procedure can be done standing with sedation with xylazine and a local block
I prefer to lay them down with xylazine and ketamine like a horse.
One or two pre-scrotal incisions, closed technique and leave the incisions open
Give pre-op penicillin G, banamine and a CDT vaccination.
COLORADO VMA
Food Animal Case Workups and Discussions
CASE 1
3 year-old bull presented for weight loss, chronic diarrhea of about one month’s
duration and some blood in the stool for the past week. The bull was on pasture with
cows and had maintained a good appetite throughout. He had been dewormed one
month prior to presentation. Vaccinations were current. The pasture was heavily
wooded. No other animals affected. The bull was raised from a calf on the farm.
Physical examination abnormalities included bloody, watery diarrhea containing black
flecks of a hard material, oral and preputial erosions and a roughened, inflamed rectal
mucosa upon palpation.
Any other questions?
Differentials?
BVD, oak toxicosis, BTV, abomasal ulcer, enzootic lymhposarcoma, others?
Diagnostics?
BVD ELISA, BLV serology, CBC/electrolytes, chemistry panel, fecal, abdominal
ultrasound, others?
Results
BVD negative, BLV negative, fecal negative, normal abdominal ultrasound, mildly
decreased A/G ratio
Diagnosis
Treatment
CASE 2
3 year-old intact Boer goat presented for lameness of right rear limb of two weeks
duration that was worsening. The referring veterinarian radiographed the right stifle and
discovered effusion. He was placed on phenylbutazone with no response. Physical
examination abnormalities included pain upon manipulation of the right stifle and right
coxofemoral joints. The right stifle was palpably slightly larger than left but not warm to
the touch. Some crepitus was appreciated over the right coxofemoral joint. All other
findings were within normal limits.
Any other questions?
Differentials?
Trauma (fracture of the head of the femur, ruptured cruciate ligament, subluxation of
coxofemoral joint), others?
Diagnostics
Radiographs of stifle and coxofemoral joints
Results
Effusion of right stifle, mild. Lucency of right caudal acetabulum, increased joint space
and fracture of femoral neck. Suggestive of pathologic fracture from infection.
Further diagnostics: CT scan
Diagnosis
Treatment
CASE 3
5 year-old Brahman female presented for recumbency of 36 hours duration. She
had calved 6 days prior to presentation. Two weeks prior to presentation, she was
presented to the referring veterinarian for udder edema and vulvar edema. She was
treated with isoflupredone and a diuretic (furosamide) for one week until she calved. The
owner noted the edema went away completely following calving. Calving was
uneventful. Three days after she calved, the cow was noted to be down and reluctant to
stand. She progressively got weaker up to the point of presentation. She had continued to
eat and drink normally throughout. Physical abnormalities included recumbency,
moderate dehydration and her head and neck were flexed to the left toward her flank.
Neurologic examination revealed depressed reflexes in all limbs and generalized
decreased muscle tone and was interpreted as generalized paresis.
Any other questions?
Differentials?
Metabolic derangement (Ca, K, P), trauma, lymphosarcoma,
Diagnostics?
CBC, chemistry with electrolytes, cervical radiographs, BLV gp 51, others?
Results
Elevated CK, K of 2.5, metabolic alkalosis, cervical radiographs – no abnormalities, BLV
negative,
Treatment
CASE 4
Three 3 to 4 year-old cross breed does presented for recumbency and ataxia with
weakness for three days duration. These were 3 does from a group of 15 that were kept
in a 20 acre pasture. This pasture was one of 4 similar sized pastures and the owner
rotated these goats with two other groups of about 15 in each (always had one pasture
open). All 3 of these were from same pasture and none of the others in the other two
pastures were affected. One other goat in the same pasture was left as she had become
recumbent after a three day period of ataxia and weakness. Physical examination
abnormalities were: two of the does were recumbent and one was ambulatory but had
significant deficits. All three were bright, alert, eating, drinking and normal otherwise.
Neurologic examination abnormalities were: the two down does had no cranial nerve
deficits, however, one doe had markedly depressed withdrawal reflexes and patellar
reflexes while the other had a depressed patellar reflex of the left rear limb. The video
depicts the deficits in the ambulatory goat.
Lesion localization
Lower motor neuron disease with a lesion or lesions in the spinal cord, asymmetrical
distribution suggesting possible multiple lesions.
Any other questions?
Differentials?
Delayed OP toxicity, trauma?, meningeal worm?, others?
Diagnostics
CSF fluid analysis
Results
eosinophilic pleocytosis
Diagnosis
Treatment.
CASE 5
2.5 year-old Angus bull presented for weight loss, diarrhea and anorexia of
approximately 2 weeks duration. He was a show bull that had been weaned off full feed
and had been receiving 14% protein ration and alfalfa hay. When the diarrhea started, he
was placed on higher quality forage. Over the last few days he just picked at the hay and
had become more lethargic. He drank well and no problems were noted with urination.
No other animals were affected and he was from a well vaccinated herd. Physical
examination abnormalities included a 2/9 BCS, moderate dehydration and fecal staining
over the perineum and back legs.
Any other questions?
Differentials?
Parasitism, peritonitis, Johnes, ruminal acidosis, BVD, others?
Diagnostics
Abdominal ultrasound, CBC, chemistry panel/electrolytes, fecal with fluke finder, rumen
fluid analysis, Johnes ELISA, others?
Results
Multiple large hypoechoic regions in the liver surrounded by hyperechoic zones
suggestive of abscessation. Inflammatory leukogram with a low A/G ratio,
hypoproteinemia and hypoalbuminemia, fecal and fluke finder negative, rumen fluid
analysis normal, Johnes ELISA negative
Diagnosis
Treatment
CASE 6
2 year-old intact male Hampshire ram presented for breathing heavily and lack of
urination over the last 24 hours. The ram had been anorexic for about the last 3 days and
depressed. Upon physical examination, the patient was depressed and walked stiffly in
the rear legs. He had bilateral serous nasal discharge with increased respiration rate and
effort. Crackles were present in the right dorsal lung field. No signs of urination were
observed.
Differentials?
Pneumonia, urolithiasis (partial or complete), ruptured urinary bladder
Diagnostics: Radiographs; serum chemistry, abdominal ultrasound. urinalysis
Results
Bronchopneumonia of ventral lung fields, azotemia, distended urinary bladder, occult
blood in urine
Diagnosis
Treatment.
Ram developed red urine.
Further diagnostics
urine copper
Results
0.6 ppm copper (normal < 0.3)
Diagnosis part two
Treatment
CASE 7
15 month-old Angus bull presented for lethargy, partial anorexia and distended
abdomen. The lethargy started about 1 month, partial anorexia about 2 weeks and
abdominal distension about 10 days prior to presentation. The bull had been out on
pasture with cows. No prior history of illness. Urination and defecation not noted by
owner. Physical examination abnormalities included mildly pale mucous membranes,
tachycardia, tachypnea and marked bilateral ventral abdominal distention. Rectal
examination revealed the rumen was small and collapsed, there seemed to be a lot of
“space” and the caudal pole of the kidney was barely reachable. No feces were noted in
the rectum. The bull did not respond to withers pinch and actually bristled up to the
stimuli.
Any other questions?
Differentials?
Intestinal obstruction, uroabdomen, urolithiasis, hardware, others?
Diagnostics?
CBC/electrolytes, abdominal ultrasound, abdominocentesis, chemistry, rumen chloride,
others?
Results
Azotemia, free fluid in the abdomen, hyponatremia, hypochloremia, normal rumen
chloride, uroabdomen
Diagnosis
Treatment
CASE 8
5-year old Angus cow presented for stumbling/knuckling in both rear limbs and
ataxia that was progressively becoming worse over the last week. She calved 3 weeks
prior to presentation without assistance and they noticed some ataxia about ten day’s
post-partum. They thought she had lost weight since calving. She was reportedly febrile
at the referring veterinarian where she had been treated with flunixin meglumine and
florfenicol. Physical examination abnormalities included tachycardia, 103.5 F and
generalized lymphadenopathy. Neurologic examination revealed buckling of the rear
limbs and a rear limb ataxia with weakness. Tail and anal tone were normal. She had a
normal appetite and drank water. Within 36 hours of presentation, she became
recumbent.
Lesion localization?
L4 to L6
Any more questions?
Differentials?
Trauma, enzootic lymphosarcoma, others?
Diagnostics?
BLV gp 51 serology, BLV p24 antigen, peripheral lymph node aspirate, lumbar
radiographs, others?
Results
BLV gp 51 and p24 antigen positive, lumbar radiographs – no notable abnormalities,
cytology – predominately large lymphoblasts with multiple nucleoli and mitotic figures.
Diagnosis
Treatment
CASE 9
12 month-old Longhorn heifer clone presented for a 3 week history of diarrhea.
The heifer had lost a considerable amount of weight. She was dewormed when the
diarrhea started with ivermectin. She was eating 12% pelleted feed, alfalfa hay and free
choice Bermuda grass hay. Her appetite had been normal throughout. Physical
examination abnormalities included dehydration, fecal staining and matting over the hind
legs and tail, a 3/9 BCS, decreased rumen contractions and a few small oral erosions.
Any other questions?
Differentials?
BVD, parasitism, vesicular stomatitis, Salmonella, Johnes?, chronic hardware, others?
Diagnostics?
BVD ELISA, fecal, abdominal ultrasound, CBC, chemistry with electrolytes, Salmonella
screening, others?
Results
BVD negative, abdominal ultrasound within normal limits, hypoproteinemia and
albuminemia, Salmonella negative, fecal = over 8,000 Strongyle eggs per gram
Diagnosis
Treatment
Colorado VMA
Blood Transfusions of Ruminants
Why?
Anemia
Blood loss
Hemolytic event
Failure of passive transfer
Bovine plasma is expensive and is difficult to harvest due to the nature of the ruminant
blood. Whole blood has the IgG necessary to provide protection for the calf. Calves
greater than 24 hours of age that have not received colostrum, or those that are diagnosed
by other means to be failure (sodium sulfite test/refractometer)
Who is the best donor?
Adult from the same farm is ideal for either instance
For FPT, mother of calf has low circulating IgG
Adult ensures you can collect enough most of the time
Biosecurity issues – don’t want something from someone else’s herd (BLV,
anaplasmosis, BVD, etc.)
How much blood do we give?
BW(kg) x 0.1 x PCV desired – PCV patient
PCV donor
= L of whole blood
What about for failure of passive transfer?
BW(kg) x 0.1 x TP desired – TP patient
TP donor
= L of whole blood
For your average 100 lb. calf, this works out to be about 2 L.
How do we collect it?
Catheterize animals (donor and recipient) with 10 to 12 ga needle in cattle and 14 to 16
ga in small ruminants.
Glass bottles, ACD bags, commercial collection kits (don’t require catheter)
10 – 15 mL/kg can be safely removed from donor acutely
(About 20% of total blood volume)
Sodium citrate is the anticoagulant of choice if you will use it within hours
1 part sodium citrate; 9 parts blood
Acetate citrate dextrose required for longer storage of blood
1 part ACD, 9 parts blood
How do we give it?
Catheter placed, then blood is run through a transfusion set (filter).
Transfusion reactions are rare
Ruminants don’t have the tendency to form autoantibodies to red blood cells
However, I start at a slow rate for the first 10 to 15 minutes
0.5 mL/kg over this time
Signs:
Tremors
Tachypnea
Tachycardia
Then give at rate of 10 mL/kg/hr
What to expect?
Transfused cells only last about 4 days
If another transfusion is required, the same donor can be used as long as it is not after
about day 5. If after day 5, a different donor should be used to prevent a reaction.
Colorado VMA
Ruminant Lameness: Diagnostics, Treatment Modalities and Procedures
Lameness is a major cause of culling dairy cattle (10.5% as opposed to mastitis at 13.5%)
Data from 5 large western feedlots indicates that 16% of the animals treated for health
problems were treated for lameness. 5% of deaths were related to lameness. Total loss
per lame animal was $121.00 per head including drugs.
Foot lesions account for 85-90% of the lameness in cattle. Eighty to ninety percent of the
foot lameness occurs in the rear limbs and the same percentage of rear limb lameness
occurs in the lateral claw.
Lameness Examination
1. Signalment
Age
Breed
Sex
Weight
Body condition
2. History
Complaint
Number of animals affected
How long?
Onset?
Intended Use?
Other health problems?
Diet
Environmental conditions
Has the animal been treated with anything? If so, what? Did it improve?
3. Physical Exam
Begins by observing from a distance.
Symmetry
– muscle atrophy?
o Long standing lameness may lead to atrophy of the large muscle
groups. This may give you an idea of the true duration and the
location of the problem.
Conformation
– cow hocked, post legged, toe in or out
– select for claw angle >450 , hock angles 155-1600 , black or dark horn is 30%
harder
– normally the heel grows about 1cm/month, while the toe wall grows about
0.5cm/month
– axial and abaxial wall grow at similar rates
Obvious swelling
- joints
- tendons/sheaths
- coronary band
Stance
- where do they put the weight?
o In some cases, cattle will toe in or out depending on which claw is
affected.
Motion
- stride length
- break over point – center of foot?
o This is the point at which the animal flexes the fetlock joint as it is
moving. It should be when the weight has shifted to the front.
- exaggerated body movements to displace weight (ie:head bobs up when
bearing weight on affected front limb)
- reluctance to turn
Grades of lameness
I.
normal
II.
slight abnormality – uneven gait (tenderness)
III.
slight lameness-obvious lameness
IV.
obvious lameness – difficulty in turning
V.
non weight bearing
4. Hands on physical exam
Proper restraint – chute, foot ropes, chemical restraint, hydraulic chute, tilt table
Note conformational defects, hoof wear or lack thereof, toe angles/symmetry.
Most of the weight is carried on the medial claw of the forelimb and the lateral
claw of the hindlimb. It should also be primarily on the abaxial wall of the
hooves.
Always start with the foot!
Remember that most causes of lameness (85-90%) are in the foot.
Always thoroughly clean/scrub feet to remove distracting dirt, mud etc.
Look for heat, pain swelling
-hoof testers – differentiate pain from fighting restraint
-percussion – may show pain when hoof testers won’t
-hyper extend and flex digits – P3 fractures, joint pain may become more
evident
-digital palpation of interdigital space and coronary band area
Look for obvious sole lesions
-dark areas should be pared out to examine their extent
-bruises and ulcers usually in caudal third of sole
-heel erosion and interdigital dermatitis
-white line disease (separation of wall and sole) – laminitis, vertical wall
fissure
Sole is usually more thin at toe.
Palpation – heat?, swelling?
Anatomy Gems
The two flexor tendon sheaths do not communicate after bifurcation, therefore,
with tenosynovitis, don’t contaminate other side! The bifurcation occurs just
proximal to the fetlock joint on the plantar or palmar aspect.
The dorsal interdigital cruciate ligaments need to stay intact when amputating
digits (take off at 450 angle at distal 1/3 of P1)
Axial interdigital skin is the closest point to the DIP joint, therefore, infection can
easily extend into joint at this point.
Deep digital flexor tendon attaches to P3 at junction of heel and sole (important
for sole ulcers to be covered later)
Ancillary Diagnostics
1. ultrasound – good for joints, tendon sheaths
i. usually a 7.5 or 5.0 probe is sufficient to evaluate these
structures
2. radiographs – good obviously for bone, soft tissue swellings
i. joints can be somewhat evaluated (bone chips, effusion,
OCD lesions, etc.)
3. arthrocentesis
coffin joint (DIP) – needle directed ventrally and medially just
lateral to common dig. extensor tendon
pastern joint (PIP) – needle in just lateral to extensor tendon
fetlock joint (metacarpal/tarsophalangeal) – between cannon
bone and suspensory ligament ventrally and axially
4. regional IV anesthesia
i. if pain disappears, source must be distal to tourniquet
5. intra-articular anesthesia
Synovial fluid normals
Character
Protein (g/dl)
WBC’s/mm3
Neut. %
Normal
Clear, no clot,
< 1.5
< 250
< 10
tacky
Aseptic
Slightly turbid,
3-4
3000
</> 10
inflammation
Septic
DJD
clot +/-, less
tacky
Turbid, clots,
thin
Clear, slightly
turbid
6 or >
70,000
90 or >
2-3
350
<10
Treatment Modalities
What can we do to address lame ruminants?
1. Trimming
Foot trimming takes practice and you should not be frustrated by not immediately
knowing how to do it. With that in mind, here are a few tips.
Start by thoroughly cleaning the foot. Remove sole with a Swiss knife or regular
hoof knife. When the sole begins to get “soft”, you have probably removed
enough. The outside hoof wall can then be removed with hoof nippers. You can
then grind, or file the surface to smooth things out.
We want the cranial wall angle with the ground to be 50-550 in front and
45-500 in rear
Heels should be high enough to keep softer areas of bulbs from bearing
weight and should also be even
Weight bearing should be on abaxial wall and axial wall of toe
Should be slightly concave toward axial wall
Trim larger claw first and match the other to it
Press on sole, when it gets soft, stop!
2. Curretage
You have to remove any unattached horn to provide drainage. You don’t want
any area to trap debris. Try to protect unaffected sensitive lamina.
Regional IV analgesia is useful for curretage – use dorsal digital vein, after apply
tourniquet – give 20 mls (2 mls/100 pound) 2% lidocaine on adult bovine via
butterfly catheter. You can leave this on for up to one hour.
3. Wooden or plastic blocks
Allows weight bearing surface to be perpendicular to the long axis of the cannon
bone to prevent strain or pressures on the sound digit.
Groove and clean claw prior to application. Make sure the sound digit has no
areas of trapped debris. Smooth out Technovit as it cures.
Remove in 3-4 weeks or it will wear off on its own.
4. Joint lavage
Goal is to remove bacteria, inflammatory mediators and leukocytes from joint.
The earlier, the better, before fibrin sets in.
Use regional IV anesthesia, general or intra-articular.
Surgical prep!
Distention irrigation – place LRS into joint, then remove it through same needle,
continue until fluid is clear, do it daily until cell count decreases.
Through and through lavage – needles on both sides of joint, large volume of LRS
under pressure, repeat as indicated, deposit antibiotic at end (ie: ceftiofur sodium)
5. Arthrotomy and /or Arthrodesis
Required for best results when joint contains fibrin
Very costly, intense
Needs to be a valuable animal to be practical
Sterile bandage and daily flushing
Brief description of artrotomy/arthrodesis of DIP joint
6. Amputation
Indicated when deeper structures of foot are severely affected
Longevity depends on use and environment (ie: lateral claw removal on the rear
limb of a breeding bull would not last long, however, front lateral claw removal
may last years in a bull used for collection and not natural service)
Use regional IV anesthesia, surgical prep, take off claw at distal end of P1 with
Gigli wire, ligate vessels, remove necrotic debris, bone, tendon, bandage
7. Topical therapy
Bandages – needed to control post surgical hemorrhage, to keep an area as sterile
as possible, support and allow for removal of exudates via dry over wet bandage
Antibiotics can be used under these bandages (terramycin, triple antibiotic
ointment, nolvasan cream) as well as disinfectants (iodine, formalin)
8. Systemic antibiotics
Consider withdrawl times and cost
If owner has already treated with an antibiotic (and they usually have), adding to
the withdrawl time may not be an issue depending on the condition. What you
don’t want to do is put an animal on a drug with a long withdrawl time that has a
poor prognosis (if things go south, you can always have a barbeque)
Procaine penicillin G – 20-40,000 IU/kg SID or BID – way off label dose! Have
to have a 45 day withdrawl time!
Ceftiofur sodium – more expensive, but no withdrawl time
Ceftiofur hydrochloride – more expensive, but 2 day slaughter withdrawl
Oxytetracycline (200mg/ml) – treatment of choice by owners – 28-day withdrawl
time
Florfenicol – good to get into joints, tendons, but has 28-day withdrawl time
Albon – sustained release bolus – long withdrawl time
9. Nonsteroidal Anti-inflammatory drugs
Flunixin meglamine – good for soft tissue, 4-day slaughter withdrawl, not
approved for use in lactating dairy cows
Phenylbutazone – better for musculoskeletal pain, but not approved for use in
food animals (illegal in dairy cattle greater than 20 months of age)
Need to have a valid veterinary-client patient relationship!
10. Prevention
Management – removal of organic material buildup
Aureomycin – off label use
Foot baths – zinc sulfate at 10 or 20%, copper sulfate at 5 or 10%, formalin at 5%
are common ingredients. Must keep fecal and soil contamination to a minimum
to avoid inactivation of ingredients. Needs to be recharged regularly. This can be
expensive.
Colorado VMA
Ruminant Lameness: Lower and Upper Limb , Infectious and Non-infectious
Causes
“Footrot” Interdigital necrobacillosis, infectious pododermatitis
An acute, subacute or chronic infection of the interdigital skin and deeper structures
Most popular owner diagnosis – only really accounts for 15-20% of lameness
Etiology
Maceration of interdigital skin, trauma, wet and muddy conditions
Fusobacterium necrophorium and Bacteroides melanogenicus (current
literature suggests this is now called Porphyromonas levii)
Both are gram negative, obligate anaerobic organisms
Both are normal inhabitants of the bovine GI tract
Require means of entry into skin (can’t penetrate intact epithelium)
Clinical signs
Occurs in all ages, may be sporadic or epidemic
May have sudden onset of lameness, usually one limb involved
Swelling, redness and pain in interdigital area
Skin fissures of skin in interdigital space into subcutaneous tissue
Necrotic tissue around edges of lesion
Swelling may extend up the limb
Commonly invades deeper structures ie: DIP joint
Pathogenesis
Integrity of interdigital skin compromised, entry of bacteria, diphtheric membrane
forms within 24-48 hrs
F. necrophorum is responsible for the necrosis and produces a leukotoxin that
protects both agents from phagocytosis. It can also produce an endotoxin as well.
B. melanogenicus (P. levii) produces proteolytic and collagenolytic enzymes that
attack subcutaneous tissues – spreads diseased tissue
Treatment
Systemic antimicrobials
Oxytetracycline – favorite choice among owners as well.
Remember that it has a 28 day withdrawal time
Ceftiofur – good choice for dairy cattle due to short withdrawal time
PPG – has a long withdrawal, but good for anaerobes
If no response, look for something more!
Clean area and remove necrotic material that is unattached
Can apply light bandages, but these usually just hold manure/urine up against the
lesion
Prevention
Management – reduce chances of interdigital trauma, constant fecal
contamination and contact
Foot baths – difficult to maintain properly
Trace mineral supplements
Aureomycin in “medicated feed”
Vaccinate?
Fusobacterium necrophorum bacterin
2 doses, 3-4 weeks apart followed by a yearly booster
Interdigital Dermatitis (Bovine Contagious Interdigital Dermatitis)
Acute to chronic inflammation of the interdigital skin. Does not extend into
subcutaneous tissues. Typically a chronic inflammation that can result in heel horn
erosion and undermining of the heel bulbs.
Etiology
Continuous wet and unhygienic conditions
Sequele to laminitis
Dichelobacter nodosus and probably a mixture of other organisms. (F.
necrophorum)
Clinical signs
Slight to moderate lameness – paddling?
Walk as if they are walking on eggshells
Typical lesions are heel horn erosions, undermined heel bulbs and superficial
erosions. See “melting” of horn. Not necrotizing like foot rot.
Treatment
Dry ground
Trim loose tissues
Frequent foot care/trimming
Cleanliness
Terramycin in “medicated” feeds
Foot baths
Difficult to maintain
Systemic antimicrobials are not as beneficial, but may inhibit “spread” to deeper
structures
Prevention
Management
Foot baths, topical spray
Contatious Foot Rot in Sheep “Contagious Digital Epidermatitis”
Interdigital dermatitis with extension into adjacent epidermal tissue underlying the hard
horn
All ages of sheep are affected, especially older
All breeds, but especially Merino
Etiology
Prolonged contact with moisture – soft macerated skin
Dichelobacter nodosus – infected sheep are the only source for non-infected
sheep
OBLIGATE PARASITE OF THE FOOT
Fusobacterium necrophorum – produces leukotoxin that protects agents from
phagocytosis
Actinomyces pyogenes – produces a factor that stimulates growth of F.
necrophorum
Transmission
Carrier sheep + warm environment + abundant moisture = spread of disease
through flock
Pathogenesis
Wet, inflamed interdigital skinnecrosisextension laterally and caudally
through layers underlying soft and hard hornseparation of axial bulb horn
underrunning bulb + sole + axial and abaxial wallsdeep pockets of necrosis
Clinical signs
Severe lameness
50-75% flock may be affected
Diagnosis
Clinical signs
Flock history
Find gram negative, club or barbell shaped rods
Therapy/control
Radical hoof trimming
Foot baths – ZnSO4
Beware of the CuSO4! (copper sensitive sheep)
Antibiotics
Procaine penicillin G
Oxytetracycline
Dry environment
Cull severe cases
Trim 2-4 times a year
Footvax
B. nodosus
2 doses 6 weeks to 6 months apart
boosters bi-annually
Volar – another vaccine
Papillomatous Digital Dermatitis (Hairy Heel Warts)
Transmissible dermatitis on the plantar/palmar surface of the pastern and on the heels.
There is complete erosion of the epidermis that is replaced by granulation tissue.
Etiology
Moisture
Spirochete (Treponema) appears to be the major factor in the disease
Zinc deficiency?
Thought to play a role in development.
Clinical signs
Lameness and weight shifting – one small lesion can be extremely painful
Painful to touch
Ulceration around the coronary band in the bulb area
Papillary hyperplasia of epidermis – fronds
(not Hans and Frons from Saturday Night Live)
Lesion is “washcloth” like in texture
Usually present in the interdigital space above the heel bulbs (however, they may
occur on the dorsal surface as well)
Not necrotizing like foot rot and more proliferative that bovine contagious
interdigital dermatitis
Treatment
Cleaning
Oxytetracycline or lincomycin spray – found to be useful prevention on dairies
(2.5% solution of oxytetracycline applied SID x 5 days, off 2, then repeat)
Oxytetracycline under a bandage
Foot baths (Agents in footbaths are frequently inactivated by organic debris,
therefore, the baths need to be fresh- can get expensive to properly maintain)
Injectable oxytetracycline – not very effective
However, one recent study in KS feedyards found that a single treatment of
ceftiofur crystalline free acid (Excede) or tulathromycin (Draxxin) resulted in
resolution of the lameness within about 10-14 days. Procaine penicillin G was
NOT effective, nor was oxytetracycline (as stated earlier). Topical treatment was
UNPRACTICAL IN THIS SETTING, therefore, they managed it with parenteral
antibiotics. Ceftiofur hydrochloride (two doses, 48 hours apart) also resolved the
lameness.
Prevention
Management of moisture and filth
Spray
Vaccine – available (anecdotal reports of efficacy) Treponema bacterin
One study in a California dairy found no benefit to vaccination.
Traumatic Pododermatitis-Subsolar abscess
Etiology
Puncture wounds
Concrete or grinder burns
White line disease
Bruise
Aseptic bruise – becomes infected
Anything that compromises the horn and allows access to the structures beneath.
Clinical signs
Pain – can be almost 3 legged lame!
Alteration of stance to shift weight
Usually no swelling unless there is joint or tendon involvement
Treatment
Curettage all undermined horn. Protect unaffected sensitive laminae.
Explore all tracts, especially those areas with erupting granulation tissue.
May need radiographs to evaluate deeper structures.
Wooden block on good claw
Bandage?
Systemic antibiotics if deep tissue is involved
Usually good prognosis if detected before deeper structures are involved.
Tenosynovitis
Etiology
Usually an extension of digital disease into the deep digital flexor tendon
sheath(s). This could be secondary to;
Foot rot
Subsolar abscess
White line disease – allows an opening that starts an infection that can
spread to the joints or tendon sheaths.
Others
Trauma- punctures and lacerations are common means of entry of organisms into
these deeper structures.
Clinical signs
Pain – severe lameness, non-weight bearing
Swelling and/or draining of synovial fluid from tendon sheath
This is usually pronounced and extends up the limb to above the hock in
some cases
Distended sheath – usually unilateral (remember, sheaths don’t communicate)
Ultrasound works well to differentiate between infection in sheath and
surrounding tissue
Treatment
Provide adequate drainage and flush
These should be treated as an abscess, however, it is essentially an open
joint once it has been opened and flushed. Therefore, once it is open and
been flushed, it should be covered with a sterile bandage and changed
daily for the first 5 days or so. Then realize that as it heals, fibrous tissue
now forms inside this sheath which used to be smooth. Residual lameness
commonly remains.
Wooden block on the good claw
Amputation if infection extends into other side or above fetlock
Traumatic lesions that are suspiciously close to the good stuff!
Early – flush wound
Thorough cleaning and debridement
Copious flushing – open up the sheath after regional IV anesthesia
Half limb bandage dry over wet, changed daily
This is a very time consuming expensive condition to address and most of the time,
after treatment at best (all things working for the good), the animal is left with some
mild residual lameness. Therefore, take this into consideration for selection of
antimicrobials (withdrawal times), economic issues and intended use.
Sequela
Tendon separation
Fibrosis/adhesions
Chronic lameness
Septic Arthritis/Physitis
Primary – penetration into joint, trauma
Secondary – extension into joint from adjacent infection
Tertiary – systemic or hematogenous spread (ie: navel ill, polyarthritis, endocarditis etc.)
Etiology
Viral
CAEV in goats
Bacterial
Mycoplasma – often follows respiratory disease, vaccine available
(efficacy?)
Histophilus somni. – often follows respiratory disease
Salmonella dublin
E. coli – neonates (most common agent isolated from foals and calves
with navel infection)
Erysipelothrix – pigs, sheep
Streptococcus
Staphylococcus
Chlamydia
Pseudomonas
Clinical signs
Pain, heat, swelling – articular and periarticular
Marked lameness – almost non-weight bearing
Systemic signs – we need to consider where this might have come from in older
animals
Endocarditis – jugular pulse, murmur, undulating fever
Pneumonia – fever, cough, may have happened 2 weeks ago
Diarrhea
Omphalophlebitis
Diagnosis
Physical exam
Leukogram – may suggest inflammatory process
Synovial fluid aspirate
Increased volume, cells, protein, clots, turbidity
Culture
Ultrasound
Blood culture?
Treatment
Joint lavage with antibiotics early (1-3 days) in course of disease
Through and through – sterile lactated Ringers is my favorite choice
Ingress/Egress – basically fill up the joint and then allow it to escape
The goal is to remove inflammatory mediators within the joint
Arthrotomy
This is sometimes the only way to address a chronically septic joint (signs
greater than 2-3 days) due to the fibrin build up in the joint and
subsequent inhibition of effective lavage
Systemic antibiotics – need to consider the ability to get there, and also,
withdrawal time so as to not “shoot yourself in the foot” (ie: give LA 200 and
have to wait 28 days to salvage animal if things go south).
Florfenicol
Oxytetracycline (LA 200)
Tilmicosin
Ceftiofur – not necessarily the best choice, but good for withdrawal times
NSAID’s – absolutely required
Flunixin meglumine (1.1 mg/kg IV)
Prognosis for septic arthritis
Guarded – if less than 7 days duration and one joint
Poor – longer than one week
Dig a hole – multiple joints
Osteomyelitis
Etiology
Hematogenous
Salmonella, Pasteurella, Streptococcus
Archanobacter
Neonates get physitis, which subsequently spreads to adjacent bone
Most commonly secondary to failure of passive transfer
Infection from navel can also establish itself in the vertebral bodies
Sequela to trauma
Open fractures and deep wounds, or extension of infection to deeper
structures
Clinical signs
Pain, heat, swelling and sometimes a draining exudate
Neurological signs if in vertebral bodies If you encounter an open, raised, hard wound on a long bone that does not
heal and periodically drains, ask yourself, do we have a sequestrum?
Treatment
Aggressive bone debridement
Culture and sensitivity
Long term antibiotic treatment – local and systemic
Regional IV infusion, bone screws into the marrow cavity, antibiotic beads
NSAID’s
Make sure and check function of other organs for involvement (ie: kidneys)
Prognosis
Guarded at best
Non-Infectious Conditions of the Digits/Distal Limb
Fractures
It is sometimes important to stabilize (distal limb fractures) during travel – use sedation
upon arrival if required
P2 and P3 fractures
Clinical signs
No swelling
Lameness – may be more mild and vague than you would think
Diagnosis
Pain may not be detected with hoof testers
Percussion with hoof testers may, however, reveal pain
Hyperextend and hyperflex the fetlock joint – may tip you off
Regional IV analgesia
Radiographs
Treatment
Wooden block on sound claw – 6-8 weeks
Prognosis
Good
P1 fracture
Clinical signs
May see some swelling
Lameness – more severe than P2 and P3
Diagnosis
Radiographs
Treatment
With these, a cast is required
Cast – enclose foot to carpus unless comminuted fracture of P1.
Comminuted fractures of P1 require a full limb cast to prevent
collapse of fragments
Cast for 8 – 12 weeks
Prognosis
Guarded due to involvement of a high-motion joint.
Sole Ulcers (Rusterholz ulcer) – ulceration through horn at junction of heel and sole
Very distinct location
Etiology – the following factors predispose and contribute either directly or indirectly to
the formation of a sole ulcer:
Low heels and/or long toes
Corkscrew claw
Excessive trimming – not leaving enough sole
High concentrate, low roughage diet – can lead to chronic laminitis, poor horn
production and erosion of horn in distinct location
Standing in slurry (manure/urine, etc.)
The cubicles in freestall barns are too short
Clinical signs
Pain – lameness can be severe
Presence of swelling depends on extent of involvement and duration, but usually
in the beginning there is none
Ulcer at junction of heel and sole
Granulation tissue erupting like a volcano with or without draining tract
May involve P3, DIP joint, navicular bone and deep flexor tendon
Treatment
Radiographs to determine extent – bony involvement?
Foot trim and pare out all undermined horn
Trim out granulation tissue
Block healthy claw
Antibiotic bandage to control granulation tissue
Footbaths
Salvage – involvement of deeper structures
Amputate claw
Arthrodesis/arthrotomy of DIP joint
Prognosis is guarded depending on extent; it is usually good however, if no
deeper structures are involved.
Sand Crack – vertical hoof fissure
Occurrence
85% of cases occur in front lateral claw
Rodeo bulls
Heavier cows/bulls 1.5 y old
Etiology
Dry weather – drying of horn
Laminitis – inferior quality horn leads to cracking
Stress separations
Coronary band trauma – leads to inferior quality horn as it grows down
Clinical signs
Vertical hoof fissures from coronary band going toward the weight-bearing
surface
Pain depends on depth and presence of infection
Treatment
Trimming – shorten and roll toe to quicken “break over” and put less pressure on
toe
Keep hooves soft – various ointments, however, these are usually impractical
Curettage – provide drainage, prevent packing of soil and manure, leave
keratinized layer if possible
Wooden block – rebuild hoof wall with Technovit and wire
Wire – drill holes, lace it up
Thimble Claw – Horizontal Hoof Fissures
Etiology
Systemic illness or laminitis
Interference with normal hoof growth
Hardship or stress lines due to interrupted horn growth at the coronary band
Clinical signs
Usually “stress lines” are present in all four feet, but only one or more “crack”
and result in pain
Horizontal fissures that are usually over half way grown out from the top
Starting to separate from the new hoof growth
Treatment
Trimming – remove all unattached hoof wall
Prognosis
Good if no deeper structures are involved
Laminitis
“Founder”
Etiology
Usually in cattle < three years old
High concentrate diets with minimum long stem roughage
Parturition – stress, endocrine changes, new diet, udder edema
Secondary to mastitis, metritis
Pathogenesis
hyperemia  hemorrhage thrombosis vasculitishypoxiaedema and
necrosis of sensitive laminaeseparationrotationwhite line disease
Clinical signs
Pain and heat – acute
Assume a stance to remove pressure from affected feet
Weight shifting
Lateral recumbency
Muscle tremors
Walking stiffly (on eggshells) – hardware?
Increased heart and respiratory rate
Pain – chronic
Results from secondary conditions occurring in the foot
Hoof changes
Hemorrhages and bruising beneath the sole
White line separation
Heel horn erosion
Wide, flat hooves
Stress rings
Dropped sole
Yellowish, waxy, soft hoof horn – inferior quality
Treatment
Acute
Correct the cause
Laxatives – magnesium oxide
Non-steroidal anti-inflammatory drugs (endotoxemia)
Antihistamines early
Soft bedding
Chronic
Foot care and regular trimming
White Line Disease
Separation of area between sensitive and insensitive laminae where hoof wall joins sole.
The white line is the junction of the horn of the wall and sole.
Most often affects abaxial walls of the rear limb lateral claw, or the front limb medial
claw
Etiology
Sequele to laminitis – inferior horn, leads to separation
Thin walls
Wet conditions
Overgrown hoof
Clinical signs
Uncomplicated
Pain – due to movement along junction of wall and sole
Dark areas at white line – due to “packing” of fecal material/dirt into
separation
Severe – lateral penetration
Navicular bursitis and drainage above the coronary band
DIP joint infection
Treatment
Remove affected sole and wall
Self cleaning – make a groove to allow manure and/or other material to e
scape
Systemic antibiotics if deeper structures are involved.
Block the unaffected claw
Toe lesions that extend to P3 can lead to osteomyelitis, which may lead to
fractures
Heritable Conditions
1. interdigital skin hyperplasia (corns) – don’t always cause lameness
2. imbalances in the convexity of the axial surfaces of the medial claw of the
thoracic limb vs. that of the lateral claw
3. imbalances in the convexity of the axial surfaces of the lateral claw of the
pelvic limb vs. that of the medial claw
4. hoof hypoplasia – mainly lateral claw on hind limb
longer and narrower than the normal claw
may curve medially and interfere with medial claw
may produce excessive horn due to increased pressures
5. corkscrew claw – primarily lateral claw of hind limb, but also medial claw of
front
hoof rotates toward the axial plane
Corkscrew Claw
Corkscrew claw is the rotation of the lateral hoof wall toward the axial plane.
This condition is a result of a malalignment of the middle and distal phalanx. The third
phalanx is often curved on its abaxial margin. These abnormalities result in a lateral to
medial deviation of the abaxial wall causing the wall to curl under the sole. Claws most
severely affected and most commonly recognized as the first claws affected are the lateral
claws of the hind limb. The condition becomes evident usually by 1 to 3 years of age and
is associated with many complications such as lateral collateral ligament strain, localized
periostitis, subsolar abscess, sole ulcers and bruising. In addition, a lifetime of corrective
trimming goes along with the condition. Corkscrew claw has a low degree of heritability,
but greater expression results from feeding for increased performance. I tell my clients
not to use these animals unless they are for a terminal cross. Obviously, owners don’t
want to hear this sometimes, but all you can do is lay down the facts. It’s hard to tell
someone who just purchased a 2 year-old breeding bull for a handsome price that his feet
are bad, will always be bad and he can pass that to his progeny!
Treatment is by regular trimming only and addressing the various complications as they
arise.
Interdigital Fibroma (Corns)
Hyperplasia and fibrosis of interdigital skin. Lameness depends on whether there is
trauma to weight bearing surface or whether it is being pinched by the claws
Etiology
Inherited predisposition – incomplete penetrance (may not show up in some
progeny)
Overfeeding
Wet and filthy conditions
Clinical signs
Front feet of bulls and hind feet of cows generally most common areas
Look for other causes of lameness!
You don’t want to remove corns and discover they weren’t the problem
Treatment
Hoof trimming, management and feeding changes
Surgical removal
Surgical prep
Axial digital nerve block or regional IV analgesia
Remove all hyperplastic tissue
Wire claws together
Bandage with antibiotic dressing
Antibiotics for 3 days
Prevention
Genetic selection
Hoof trimming
Weight control
Dry conditions
Upper Limb Lameness
Fractures:
Metatarsal/metacarpal
Cast to upper 1/3 of limb to immobilize joint above and below fracture
Immobilize 4-6 weeks in calves ( may need to remove in 2 weeks to reapply)
6-12 weeks in animals over 6 months of age
Shaft of the ileum – “knocked down hip”
may not be that lame, do a rectal to potentially palpate fracture line
future natural births?
Salter- Harris fractures
Usually distal physis of metacarpus or metatarsus
Not as lame as you would expect
Cast up to the carpus or tarsus
Compound fractures and fractures above carpus and tarsus – some can be treated
External fixation
Pins
Plate
Trauma
Sometimes due to conformation problems, over time, joints can undergo “wear
and tear”
This leads to joint effusion.
Straight legged bulls especially
Not warm, painful, lame
Femoral nerve paralysis
Occurrence
Occurs most commonly in calves that experience a difficult birth. History often
reveals that the calf was “hip locked” for a period of time. (sometimes hard for
owners to admit) In this position in the pelvis of the cow, the femoral nerve is
damaged due to pressure, or if the calf is pulled too hard, the nerve can be
damaged at the spinal root.
Clinical signs
Can’t extend stifle – stand with limb “dropped”, or if bilateral, they are crouched
like a rabbit
If bilateral, may not be able to stand
Prognosis
Give them about 4 weeks – physical therapy required in most cases
Guarded
Main differentials are bilateral hip luxation and lateral luxation of the patella!
Sometimes the patella can be more movable with femoral nerve paralysis, so
you have to carefully palpate them.
Stifle injuries
Etiology – one of the most common “traumatic” injuries we see in the upper limb
Mounting injuries
Fighting
Poor footing and falling
Degenerative joint disease
Ataxia from metabolic disease (ie: low calcium)
Clinical signs
Avoids flexing the stifle
Hock and stifle are often held in a fixed position
Puts most of weight on toe
Legs camped under body to take weight off affected leg
Periarticular and joint swelling – may be difficult to appreciate due to size of
animal
Heat may indicate infection (gonitis)
Diagnostics
If stifle lameness is suspected, but joint effusion is not present, intra-articular
analgesia may help localize lameness.
Lateral femorotibial compartment – insert behind the lateral
patellar ligament and direct backwards
Femoropatellar space – insert between medial and middle patellar
ligaments directing up and back
Stifle anatomy
Medial femoropatellar, lateral femoropatellar and medial femorotibial joints
communicate
However, lateral femorotibial joint usually does not communicate
Joint instability – abnormal movement in joint can be palpated at a walk or drawer
movement
Quadriceps and gluteal muscles atrophy
Lameness in foot may resemble stifle lesion – use hoof testers
Crepitation in hip can appear as if its coming from the stifle – check the hip
internally and externally
Collateral ligament injury
Etiology
Trauma to medial collateral ligament
Clinical signs
Stifle signs
Widening of medial femorotibial joint space with abduction of lower limb
Effusion of lateral femorotibial joint (lateral collateral ligament)
Treatment
Salvage
Confinement for 6-8 weeks
Surgery – imbrication of periarticular tissues
Cranial cruciate ligament rupture
Etiology
Trauma (fighting, falling)
Conformation may predispose (straight hocks)
Clinical signs – acute onset, lameness is usually 3-4/5.
Stifle signs (toe on the ground at rest) – if weight is born, it is on the toe
Joint instability
Drawer signs, “clicking” or crepitation may be appreciated
Joint effusion – damage occurs in medial femorotibial joint (medial
meniscus, medial collateral ligament, cranial cruciate ligament)
Muscle atrophy – takes about 2 weeks for disuse atrophy
Diagnosis
History, clinical signs
Radiographs – cranial displacement of tibia relative to femur, degenerative
joint disease may be evident as well as effusion and small pieces of
avulsed bone within joint.
Treatment
Salvage
Stall rest
Collect semen or embryos
Surgery – need to find someone that has done several of these (moderate
success)
Imbricate tissue
Implants
“over the top technique”
Upward fixation of the patella
Etiology – medial femoral condyle is larger than lateral
This can be due to:
Trochlear malformation
Decreased muscle tone of the quadriceps
Conformation – heritable?
Nutritional – malnutrition
Neurologic – deficit (femoral nerve)
Clinical signs
Usually no swelling
Either limb fixed in extension at end of propulsion and beginning of anterior
phase of stride
Jerking motion at end of propulsion to anterior phase of stride
Treatment
Determine underlying cause and correct if possible
Correct genetics
Medial patellar desmotomy
Lateral luxation of the patella
Usually happens in younger animals
Etiology – medial condyle is larger than lateral
Trauma to medial patellar ligament or the femoropatellar ligament
Congenital malformation of trochlea and or patella
In calves, you have to rule out the possibility of femoral nerve paralysis –
dystocia?
If bilateral, looks like a rabbit in hind limbs
Treatment
Imbrication of femoropatellar ligament and joint capsule
Salvage
Coxofemoral luxation
Cranio dorsal
Etiology
Trauma
Clinical signs
Usually younger cattle
Ambulatory usually
Toe and stifle rotate outward
Pelvic asymmetry
Increased distance between greater trochanter and tuber ischii
Biggest differentials are a capital physeal fracture or femoral neck fracture
Might differentiate by feeling crepitance upon palpation over hip while
manipulating leg
Evaluate relationships between 3 structures: greater trochanter, tuber ischii and
tuber coxae – compare to other side
Treatment
General anesthesia to reduce if very early
Get semen, embryos
Salvage
Coxofemoral luxation
Cranio ventral
Etiology
Trauma
Post calving
Lightning strike
Clinical signs
Usually older cattle
Down and won’t get up
Palpate femoral head in obturator foramen or at brim of pelvis
Always do rectal
Treatment
Salvage or euthanasia