Lameness Flashcards
1
Q
What effect does hock conformation have on a particular cause of lameness
A
Significant effect on px for suspensory desmitis (bad if straight)
2
Q
Grades of lameness exam
A
o Grade 0: No lameness visible
o Grade 1: Difficult to observe and not consistent.
o Grade 2: Difficult to observe at a walk or straight trot but consistent under certain circumstances (weight-carrying, circling, inclines, hard surface).
o Grade 3: Consistently observable at a trot under ALL circumstances.
o Grade 4: Obvious at a walk
o Grade 5: Lameness is so significant the patient is minimally weight bearing
3
Q
what to look for in lameness exams
A
- Head nod: lift head up when weight bearing on painful limb
- Hip hike: like tuber coxae up more when weight bearing painful leg
- Also assess:
o Sound and rhythm
o Fetlock drop (drops more on sound leg at trot)
o Duration of stance (increased contact time on sound leg)
4
Q
what is lordosis and kyphosis
A
Lordosis = curved down (Swayback),
Kyphosis = arched up (Roach back)
5
Q
where to feel for femoral patella joint effusion Vs medial femoral tibial joint effusion
A
feel either side of patella ligament
Vs feel on medial aspect
6
Q
Two common causes of fetlock swelling and how to tell apart
A
o Fetlock joint effusion = Swelling dorsal to Suspensory
o DFT sheath effusion = Swelling plantar to Suspensory
7
Q
most common location of hock effusion
A
most likely to find effusion in proximal medial joint (tibital tarsal)
8
Q
drug used for nerve blocks
A
Mepivicaine
9
Q
when should you work distally to proximally
A
when performing nerve blocks
synovial blocks are more specific so don’t need to
10
Q
3 common fore limb blocks and what they desensitise (in order of when you do them)
A
- Palmar digital nerve block (Palmar digital nerves)
* Removes sensation to palmar (back of) foot - Abaxial sesamoid nerve block (Palmar digital nerves)
* Removes sensation to foot, pastern and palmar (back of) fetlock - Low four point (Palmar metacarpal and palmar nerves)
* Removes sensation to fetlock and below
11
Q
Most important hind limb block
A
DBLPN block (Deep branch of the lateral plantar nerve)
o Blocks the proximal suspensory ligament
(Said this is most important in PIE and then never mentioned it again…)
12
Q
how to perform the DBLPN block
A
o Flex limb and pull flexor tendons medially to reach suspensory with needle
13
Q
What points does the low 4 point block go into
A
- Buttons of splints (M + L) for the palmar metacarpal nerves
- Between DDFT and suspensory (M + L) for the palmar nerves
14
Q
what fractures should be euthanised
A
Open, comminuted fractures of long bones, complete fractures of scapula, humerus, radius, fermur and tibia
Also irreparable fx, poor QoL, poor return to work, finances
15
Q
what are the categories of triage priorities
A
- Immediate action (or might die): Hx of spinal or head trauma, haemorrhage
- Do not move (or could become unfixable): Fracture, tendon rupture, joint instability
- Requires urgent attention: Synovial/bone involvement, contaminated wounds
- Delay action. Doesn’t need emergency visit
16
Q
duration of different alpha-2
A
Short duration = xylazine, medium = detomidine, long = romifidine
17
Q
when to avoid ACP
A
Vasodilator so avoid in haemorrhage and hypovolaemia situations
18
Q
Splinting region 1 location
A
Fetlock and below
o Splint placed dorsally
o Align bones to stop fetlock hyperextension and bring bones into alignment. May need heel wedge
19
Q
splinting in region 2
A
Between fetlock and carpus
o Splint placed laterally and palmar/planter
20
Q
splinting in region 3
A
Between carpus and stifle/elbow
o Splint placed laterally (+/- medially if you can access)
21
Q
splinting in region 4
A
o Can’t do much here
o Stabilsie above and below (carpus) for olecranon fractures
22
Q
Where can DIP effusion be palpated
A
Dorsal coronary band
23
Q
What 5 views should be taken of the feet
A
- Latero-medial
- Standing dorso – palmar
- Dorsal proximal – palmar distal 60° oblique of pedal bone
o Aka upright pedal - Dorsal proximal – palmar distal 60° oblique of navicular bone
o Aka upright navicular - Palmar 45° proximal – palmar distal oblique of navicular bone
o aka flexor navicular
24
Q
How to take LM and what is it good for
A
Centre 1cm below coronary band
Good for: Assessing hoof-pastern axis, P3-sole angle, DIP osteoarthritis, Navicular D
25
Where to centre upright pedal V upright navicular (and proper name)
Dorsal proximal – palmar distal 60° oblique of pedal bone
centre over coronary band
Dorsal proximal – palmar distal 60°oblique of navicular bone
centre 1-2cm above coronary band
26
What terms are given to a change pastern axis
Normally P3 and hoof wall should be parallel
Broken forward =PIP joint bulges forwards (Pastern bones create shallower angle)
Broken back = PIP joint bulges back
(pastern bones created wider angle)
27
best place to feel digital pulses
* Best to feel over neurovascular bundles (abaxial (out edge) margin of sesamoid bones)
28
pathophysiology behind laminitis
- Laminae of P3 (epidermal) and hoof (dermal) strongly bonded and interdigitate
- Hoof growth: MMP enzyme breaks bond to allow growth
- Too much MMP = more breakdown + failure of interdigitation = more separation = laminitis
excess MMP due to high insulin, high ACTH, enodotoxaemia
29
clinical signs of laminitis
- Stance: leaning backwards, weight shifting
- Pain: High RR and HR, temperature, sweating
- Feet: hot feet with increased digital pulses. May be all 4, or just front 2 (rarely just hind or unilateral)
- Presence of growth rings indicate previous episodes
30
diagnostic findings in laminitis
- Hoof testers: Just in front of point of frog (where P3 contacts sole)
- Depression at coronary band = bones sinking
- Dynamic exam: Lameness, land on heels first, worse on hard, high stepping (HL)
31
laminitis tx
- Pain: NSAIDs (bu), paracetamol, opioid if bad
- ACP: vasodilator and anxiolytic
- Support feet: Deep hay, rubber frog supports, remove shoes?
- Diet: Soak hay to remove sugar
32
signs of a foot abscess
- Acute onset lameness
- Lameness severe
- bounding digital pulses
- may see discharging tract (or after exploring/paring)
33
Foot fracture clinging findings:
Small extra articular
Significan fractures
Articular fragments
Tendon involvement
- Small fragments = low grade lameness with minimal localising signs
- Significant fractures = acute and severe with localising signs (digital pulses, heat in hoof, positive to hoof testers)
- Articular fragments – DIP effusion (palpate at coronet)
- Tendon involvement = digital flexor tendon sheath effusion (navicular bone fx)
34
presentation of solar bruising
- Acute, severe unilateral lameness (Ddx – subsolar abscess, pedal bone fracture)
- Mild bilateral (or quadrilateral) pain (Ddx – laminitis, forelimb lameness)
Examination findings:
- Increased digital pulses
- Increased hoof temperature
- Sensitivity to hoof testers
35
Tx of solar bruising
same as abscess (NSAIDs and box rest)
Prevention:
- Regular shoeing (6 wks)
- Padding to prevent concussion in at risk horse
36
what two conditions are predisposed by the long toe, low heel, broken back axis
Navicular degeneration
DIP osteochondrosis
37
Signs and Dx of DIP osteochondrosis
- Mild lameness, often bilateral once threshold of disease reached
- Worse on hard
- Moderate positive response to distal limb flexion
- CE: Coffin joint effusion
On X-rays:
osteophyte formation and long toe, low heel, broken back conformation
38
What intra-articular steroids can treat DIP ostechondrosis
Methylprednisolone or Triamcinalone. Potent and last 6 months
39
What does Pentosan polysulphate do
reduces MMP production
40
What commonly causes septic pedal osteitis
Nail
41
signs of navicular degeneration on radiograph
- Loss of the medullary architecture + sclerosis
- Fibrocartilagenous change of the flexor surface (Stops DDFT gliding smoothly)
- May have adhesions between tendon + bone
- Enthesiophyte formation (bony spur where ligament inserts)
42
clinical exam of navicular degeneration
- Slow onset BILATERAL forelimb lameness
- Initially intermittent
- Sound in straight line as condition is bilateral
- Lame on lunge (inside leg). Often obvious in contralateral limb if nerve block applied
43
Surgery that can be used to treat Navicular degeneration but risks
Neurectomy
neuroma and catastrophic DDFT breakdown, pedal osteitis/foot penetrations
44
what condition lands toe first vs heel first
Navicular degeneration land toe first
Vs laminitis who land heel first
45
what conditions benefit from heart shoes that support the pedal bone
laminitis, navicular syndrome, P3 fractures, teratomas, thin soles and low heels
46
what ligaments can be injured in the hoof
Navicular suspensory (from dorsal P1 and palmar P2)
Impar (from navicular to palmar P3)
Collateral (attach P3 to P2, and P2 to P1)
47
3 common foot soft tissue diseases and what they look like on MR
DDFT core lesions
- Focal lesion with surrounding aystemetry due to enlargement of tissue
Sagittal splits
- Hyperintesnive lines through DDFT
- Often at the level of the navicular bone
dorsal border fibrillation
- Irregular invaginations of the DDFT dorsal surface
48
name 4 conditions block to the foot but don't have the typical localising signs (pulses, hoof testers, heat)
Subchondral cysts
pedal osteitis
mineralisation of collateral cartilage (side bone)
hoof imbalance
navicular bone degeneration
DIP osteoarthritis
fractures of P3 and navicular
49
what is pedal osteitis
- Irregular lysis of the solar margin
- Due to chronic pressure or inflammation in the hoof
- TB disease with thin soles
50
implications of a sunken heal
DDFT has to travel further = more pressure no it and also puts crushing forces on navicular bursa
51
at what level does the Al-DDFT join the DDFT
mid metacarpus/tarsus
52
typical region of SDFT injuries
Mid metacrpus
clasic palmar bow appearance
53
typical region of DDFT injuries
hoof or DFT sheath
54
typical region of Al-DDFT injuries
Very specific
proximal third of metacarpus, laterally
55
typical region of suspensory injuries
origin or insertion
o = palmar of 3rd metacarpal/tarsal
I = proximal sesamoids
56
why are tendons prone to re injury
Repaired core lesion is weaker T3 collagen that doesn’t stretch as much
o Surrounding tendon has to stretch more to compensate = extra strain
57
initial treatment of tendon injuries
key is stopping inflammation
o NSAIDs asap (as inflammation worsens injury) and continue for weeks
o Single dose of IV steroid (dexamethasone) to stop inflammatory cascade
o External support: Bandage +/- splint or cast to compress
o Cold therapy (hosing or ice bandages) to reduce inflammation
o Confinement stops injury worsening too
58
when can tendon intra-lesional therapy be used
o Use end of inflammatory phase and start of repair (2-3 weeks after injury)
o Only suitable if there is a core lesion (Hole), not for swelling lesions
o Done under ultrasound guidance supra-physiological healing
59
Explain stem cell intralesional therapy
Collected from bone marrow
Stem cells collected cultured in lab injected differentiate into tenocytes
3 weeks to culture
60
explain platelet rich plasma therapy
blood sample collected
Centrifuged or filtered high number of platelets collected and injected promote angiogenesis loads more healing factors (IGF, platelet GR etc)
61
explain bone marrow aspirate concentrate
Bone marrow sample collected with Jamshidi needle
Fluids + cells collected (inc mesenchymal stem cells, platelets and growth factors) centrifuged injected
Less stem cells and less platelets than others BUT has both
62
tendon surgery examples for
- Annular ligament desmtitis
- SDFT tendonitits
- Manica flexoria tear
- DDFT tear
1. Annular ligament desmitis = if medical therapy unsuccessful, it constricts and squashes tendons. Transect to release pressure (desmotomy)
2. SDFT tendonitis = usually mid-cannon region. To release tension and weight bearing, do a superior check ligament desmotomy. This cuts the check ligament from about the carpus to release pressure
3. Manica flexoria tear = can be removed arthroscopically
4. DDFT tear = Often occur adjacent to the navicular bursa and in the DFT sheath synovial fluid. Remove torn fibres arthroscopically
63
where is Extracorporeal shockwave therapy most effective
bone-soft tissue interface (proximal suspensory ligament, suspensory branches, thoracolumbar spine)
for chronic cases, not acute injury
64
what is a pathogenomic sign of DTF sheath effusion
Marked swelling palmar to suspensory ligament
65
Preferred cleaning method for wounds
o Clean, potable tap water can be used to grossly lavage
o Chlorhexidine preferable as not inactivated by organic material
Dilute first as can be irritant
o Use of povidone may be beneficial to lavage contaminated wounds
Inactivated by organic material so clean first
66
how to check if wound has communicated with joint
insert needle into joint away from wound
fill with saline and apply pressure
if no leak = no communication
67
Which ligament is transected with the following limb positions:
dropped fetlock
dropped fetlock and toe elevated
fetlock on floor and toe elevated
dragging foot
* A: Only SDFT transected. Fetlock drop but toe on ground
* B: SDFT and DDFT. Fetlock drop and toe elevated
* C: SDFT, DDFT and suspensory transected. Fetlock on floor
* Dragging foot = think about extensors too
68
What is typing up or sporadic rhabdomyolysis (Acquired) caused by
- Overexertion (strenuous ex.)
- Dietary imbalances (especially low electrolytes and forage)
- Exhaustion (TB and endurance horses training in hot, humid)
69
Signs of tying up
- Stiff, stilted gait
- Excessive sweating
- Increase respiratory rate after exercise
- Firm painful muscles (hindquarters, back),
- Reluctant to move
- Occasional dark urine
70
Dx of tying up
- Clinical signs
- Elevated CK and AST (often off the scale) and linked to exercise
- Pigmenturia
- Look for signs of renal damage (creatinine)
71
name two muscle relaxants
Methocarbamol (also pain relief) or Dantrolene (Dantrium)
72
What is recurrent exertional rhabdomyolysis (RER)
Genetic
- Intermittent rhabdomyolysis (TBs and SBs)
- Linked to abnormal calcium regulation in myofibers with SERCA receptors
73
Muscle biopsy for recurrent rabdomyolysis
H&E stain
- Internalised nuclei (should be peripheral)
- Marked variation in fibre sizes (should be uniform)
- Infiltration of macrophages
- +/- caffeine sensitivity on fresh samples (hyperresponsive)
74
What is PSSM
Polysaccharide storage myopathy 1
- Abnormal storage of glycogen in muscle fibres (difficult to metabolise)
- Draft horses
- PSSM1: Genetic mutation in glycogen synthase enzyme = overactivity
- PSSM2: Unknown aetiology but glycogen accumulation in all conditions
75
signs of PSSM
- Most asymptomatic except performance drafts
- Stiffness after a short period of exercise
- Reluctance to move
- Poor performance
- Sweating
- Maybe myoglobinuria
76
Dx for PSSM
- Signs, high AST + CK
- +/- pigmenturia
- Genetic testing: PSSM1 test is used and validated
definitive. Run on whole blood or hair plucks with follicles
- Muscle biopsy in Periodic acid Schiff shows glycogen accumulation. Add amylase to sample first to remove non-resistant glycogen
77
Diet for RER, SER and PSSM
- Diet is key: High protein + fat, low starch + sugar (haylage bad)
- Also consistent exercise
78
What is myofibril myopathy
- Abnormal Desmin protein
- Poor performance
- Lack of hindlimb engagement
79
Dx of myofibril myopathy
- Muscle biopsy and desmin stain
- Abnormal accumulations of desmin
80
What is Hyperkaliaemic periodic paralysis (HYPP)
- Leaking sodium channels = prolonged depolarisation and abnormal action potentials
- High potassium contributes to even more depolarisation = opens sodium channels = more depolarisation
81
Cs and TX for HYPP
- Sporadic attacks of stiffness, muscle tremors, weakness and collapse
- Breathing difficulties: Paralysis of laryngeal muscles = stridor
- Prolapse of third eyelid
limit potassium intake (no clover or alfalfa)
Severe = Adrenaline, calcium gluconate, dextrose
82
Toxic atypical myopathy cause
Toxic rhabdomyolysis from Hypoglycin A ingestion
(Sycamore in Autumn
HGA converted into MCPA carnitine (toxic metabolite) in horses amino acid cycle
83
Signs of toxic rhabdo
- Stiffness, muscle fasciculations, weakness,
- Sweating, myoglobinuria (~90%)
- Colic, tachycardia, tachypnea, recumbency, distended bladder, reduced/Absent GI sounds
- Dysphagia (25%)
- Cardiac arrest ==> euthanasia
Patients feel: Nausea, weak
84
Dx of toxic rhabdo
- Muscle enzymes extremely high with no link to post-exercise. High even after dilution (Highest)
- Pigmenturia
- High RR and HR as toxin effects contractility
Toxin testing:
- On blood or vegetation
- For Hypoglycin A or MCPA
85
Tx for toxic rhabdo
No antidoate
- IVFT, Vitamin B2, Anti-oxidants (VE, V12) , oral toxin binders
- If dysphagia give IV dextrose of karyosyrup
- Monitor heart
86
What can cause immune mediated myositis
- Associated with previous respiratory infections (Strep. Viral (Flu + EHV)
- Purpura haemorragica: 10 days after S. equi infection = severe vasculitis with muscle infarction
- Streptococcal myopathy: occurs at the same as classical strangles signs: stiffness and recumbency
87
What are the kinetics of CK and ALT? And how should you overcome this?
CK: rises rapidly, peaks at ~ 6 hours, stays here ~6 hours, rapidly declines. Back to normal at ~ 24 hours
AST: rises gradually and peaks ~18-24 hours, decline is gradual. Back to normal at ~20 days
2 serial samples (24 hours apart)
* If CK is decreasing, AST is increasing, we can localise samples to just after acute myopathy
* If CK is continuing to increase, it shows we have ongoing muscle damage
88
What is a dynamic CK test
sample trot (15-20 mins) take second sample 6 hours later
* Significant finding if sample 2 is double sample 1
89
3 muscle biopsy stains and what to use them for
H&E = RER
Periodic acid schiff = PSSM (add amylase first)
Desmin stain = myofbirbialr myopathy
90
What muscle to biospy
semimembranosus
