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Equine > Lameness > Flashcards

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)

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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

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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)
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4
Q

what is lordosis and kyphosis

A

Lordosis = curved down (Swayback),
Kyphosis = arched up (Roach back)

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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

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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

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7
Q

most common location of hock effusion

A

most likely to find effusion in proximal medial joint (tibital tarsal)

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8
Q

drug used for nerve blocks

A

Mepivicaine

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9
Q

when should you work distally to proximally

A

when performing nerve blocks
synovial blocks are more specific so don’t need to

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10
Q

3 common fore limb blocks and what they desensitise (in order of when you do them)

A
  1. Palmar digital nerve block (Palmar digital nerves)
    * Removes sensation to palmar (back of) foot
  2. Abaxial sesamoid nerve block (Palmar digital nerves)
    * Removes sensation to foot, pastern and palmar (back of) fetlock
  3. Low four point (Palmar metacarpal and palmar nerves)
    * Removes sensation to fetlock and below
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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…)

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12
Q

how to perform the DBLPN block

A

o Flex limb and pull flexor tendons medially to reach suspensory with needle

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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
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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

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15
Q

what are the categories of triage priorities

A
  1. Immediate action (or might die): Hx of spinal or head trauma, haemorrhage
  2. Do not move (or could become unfixable): Fracture, tendon rupture, joint instability
  3. Requires urgent attention: Synovial/bone involvement, contaminated wounds
  4. Delay action. Doesn’t need emergency visit
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16
Q

duration of different alpha-2

A

Short duration = xylazine, medium = detomidine, long = romifidine

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17
Q

when to avoid ACP

A

Vasodilator so avoid in haemorrhage and hypovolaemia situations

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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

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19
Q

splinting in region 2

A

Between fetlock and carpus
o Splint placed laterally and palmar/planter

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20
Q

splinting in region 3

A

Between carpus and stifle/elbow
o Splint placed laterally (+/- medially if you can access)

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21
Q

splinting in region 4

A

o Can’t do much here
o Stabilsie above and below (carpus) for olecranon fractures

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22
Q

Where can DIP effusion be palpated

A

Dorsal coronary band

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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
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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

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25
Q

Where to centre upright pedal V upright navicular (and proper name)

A

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

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26
Q

What terms are given to a change pastern axis

A

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)

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27
Q

best place to feel digital pulses

A
  • Best to feel over neurovascular bundles (abaxial (out edge) margin of sesamoid bones)
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28
Q

pathophysiology behind laminitis

A
  • 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

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29
Q

clinical signs of laminitis

A
  • 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
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30
Q

diagnostic findings in laminitis

A
  • 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)
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31
Q

laminitis tx

A
  • 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
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32
Q

signs of a foot abscess

A
  • Acute onset lameness
  • Lameness severe
  • bounding digital pulses
  • may see discharging tract (or after exploring/paring)
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33
Q

Foot fracture clinging findings:
Small extra articular
Significan fractures
Articular fragments
Tendon involvement

A
  • 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)
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34
Q

presentation of solar bruising

A
  • 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

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35
Q

Tx of solar bruising

A

same as abscess (NSAIDs and box rest)

Prevention:
- Regular shoeing (6 wks)
- Padding to prevent concussion in at risk horse

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36
Q

what two conditions are predisposed by the long toe, low heel, broken back axis

A

Navicular degeneration
DIP osteochondrosis

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37
Q

Signs and Dx of DIP osteochondrosis

A
  • 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
Q

What intra-articular steroids can treat DIP ostechondrosis

A

Methylprednisolone or Triamcinalone. Potent and last 6 months

39
Q

What does Pentosan polysulphate do

A

reduces MMP production

40
Q

What commonly causes septic pedal osteitis

A

Nail

41
Q

signs of navicular degeneration on radiograph

A
  • 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
Q

clinical exam of navicular degeneration

A
  • 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
Q

Surgery that can be used to treat Navicular degeneration but risks

A

Neurectomy

neuroma and catastrophic DDFT breakdown, pedal osteitis/foot penetrations

44
Q

what condition lands toe first vs heel first

A

Navicular degeneration land toe first
Vs laminitis who land heel first

45
Q

what conditions benefit from heart shoes that support the pedal bone

A

laminitis, navicular syndrome, P3 fractures, teratomas, thin soles and low heels

46
Q

what ligaments can be injured in the hoof

A

Navicular suspensory (from dorsal P1 and palmar P2)
Impar (from navicular to palmar P3)
Collateral (attach P3 to P2, and P2 to P1)

47
Q

3 common foot soft tissue diseases and what they look like on MR

A

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
Q

name 4 conditions block to the foot but don’t have the typical localising signs (pulses, hoof testers, heat)

A

Subchondral cysts
pedal osteitis
mineralisation of collateral cartilage (side bone)
hoof imbalance
navicular bone degeneration
DIP osteoarthritis
fractures of P3 and navicular

49
Q

what is pedal osteitis

A
  • Irregular lysis of the solar margin
  • Due to chronic pressure or inflammation in the hoof
  • TB disease with thin soles
50
Q

implications of a sunken heal

A

DDFT has to travel further = more pressure no it and also puts crushing forces on navicular bursa

51
Q

at what level does the Al-DDFT join the DDFT

A

mid metacarpus/tarsus

52
Q

typical region of SDFT injuries

A

Mid metacrpus
clasic palmar bow appearance

53
Q

typical region of DDFT injuries

A

hoof or DFT sheath

54
Q

typical region of Al-DDFT injuries

A

Very specific
proximal third of metacarpus, laterally

55
Q

typical region of suspensory injuries

A

origin or insertion
o = palmar of 3rd metacarpal/tarsal
I = proximal sesamoids

56
Q

why are tendons prone to re injury

A

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
Q

initial treatment of tendon injuries

A

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
Q

when can tendon intra-lesional therapy be used

A

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
Q

Explain stem cell intralesional therapy

A

Collected from bone marrow
Stem cells collected  cultured in lab  injected  differentiate into tenocytes
3 weeks to culture

60
Q

explain platelet rich plasma therapy

A

blood sample collected
Centrifuged or filtered  high number of platelets collected and injected  promote angiogenesis  loads more healing factors (IGF, platelet GR etc)

61
Q

explain bone marrow aspirate concentrate

A

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
Q

tendon surgery examples for
- Annular ligament desmtitis
- SDFT tendonitits
- Manica flexoria tear
- DDFT tear

A
  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
Q

where is Extracorporeal shockwave therapy most effective

A

bone-soft tissue interface (proximal suspensory ligament, suspensory branches, thoracolumbar spine)
for chronic cases, not acute injury

64
Q

what is a pathogenomic sign of DTF sheath effusion

A

Marked swelling palmar to suspensory ligament

65
Q

Preferred cleaning method for wounds

A

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
Q

how to check if wound has communicated with joint

A

insert needle into joint away from wound
fill with saline and apply pressure
if no leak = no communication

67
Q

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
  • 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
Q

What is typing up or sporadic rhabdomyolysis (Acquired) caused by

A
  • Overexertion (strenuous ex.)
  • Dietary imbalances (especially low electrolytes and forage)
  • Exhaustion (TB and endurance horses training in hot, humid)
69
Q

Signs of tying up

A
  • Stiff, stilted gait
  • Excessive sweating
  • Increase respiratory rate after exercise
  • Firm painful muscles (hindquarters, back),
  • Reluctant to move
  • Occasional dark urine
70
Q

Dx of tying up

A
  • Clinical signs
  • Elevated CK and AST (often off the scale) and linked to exercise
  • Pigmenturia
  • Look for signs of renal damage (creatinine)
71
Q

name two muscle relaxants

A

Methocarbamol (also pain relief) or Dantrolene (Dantrium)

72
Q

What is recurrent exertional rhabdomyolysis (RER)

A

Genetic
- Intermittent rhabdomyolysis (TBs and SBs)
- Linked to abnormal calcium regulation in myofibers with SERCA receptors

73
Q

Muscle biopsy for recurrent rabdomyolysis

A

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
Q

What is PSSM

A

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
Q

signs of PSSM

A
  • Most asymptomatic except performance drafts
  • Stiffness after a short period of exercise
  • Reluctance to move
  • Poor performance
  • Sweating
  • Maybe myoglobinuria
76
Q

Dx for PSSM

A
  • 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
Q

Diet for RER, SER and PSSM

A
  • Diet is key: High protein + fat, low starch + sugar (haylage bad)
  • Also consistent exercise
78
Q

What is myofibril myopathy

A
  • Abnormal Desmin protein
  • Poor performance
  • Lack of hindlimb engagement
79
Q

Dx of myofibril myopathy

A
  • Muscle biopsy and desmin stain
  • Abnormal accumulations of desmin
80
Q

What is Hyperkaliaemic periodic paralysis (HYPP)

A
  • Leaking sodium channels = prolonged depolarisation and abnormal action potentials
  • High potassium contributes to even more depolarisation = opens sodium channels = more depolarisation
81
Q

Cs and TX for HYPP

A
  • 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
Q

Toxic atypical myopathy cause

A

Toxic rhabdomyolysis from Hypoglycin A ingestion
(Sycamore in Autumn

HGA converted into MCPA carnitine (toxic metabolite) in horses amino acid cycle

83
Q

Signs of toxic rhabdo

A
  • 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
Q

Dx of toxic rhabdo

A
  • 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
Q

Tx for toxic rhabdo

A

No antidoate
- IVFT, Vitamin B2, Anti-oxidants (VE, V12) , oral toxin binders
- If dysphagia give IV dextrose of karyosyrup
- Monitor heart

86
Q

What can cause immune mediated myositis

A
  • 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
Q

What are the kinetics of CK and ALT? And how should you overcome this?

A

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
Q

What is a dynamic CK test

A

sample  trot (15-20 mins)  take second sample 6 hours later
* Significant finding if sample 2 is double sample 1

89
Q

3 muscle biopsy stains and what to use them for

A

H&E = RER
Periodic acid schiff = PSSM (add amylase first)
Desmin stain = myofbirbialr myopathy

90
Q

What muscle to biospy

A

semimembranosus

Equine (11 decks)

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