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Equine LA Sx > Equine LA Sx > Flashcards

Equine LA Sx Flashcards

1
Q

Arthrocentesis in septic arthritis/tenosynovitis: WBC count

A
  • Increased WBC usually >30,000 cells/ µL
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2
Q

Arthrocentesis in septic arthritis/tenosynovitis: % of neutrophils

A
  • > 80% PMN
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3
Q

Arthrocentesis in septic arthritis/tenosynovitis: Total protein

A

> 3 g/dL

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4
Q

Normal Arthrocentesis value TP

A

<2.5 g/dL

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5
Q

Normal Arthrocentesis value: WBC count

A

<300 cells/µL

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6
Q

Normal Arthrocentesis Cell composition

A
  • Mononuclear cells
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7
Q

What three things do you need to do in all suspected cases of septic arthritis?

A
  1. ) Physical exam: clean the wound really well and explore it to see if it goes into the joint.
  2. ) Arthrocentesis and get a cell count/gram stain
  3. ) Distend the joint and pressurize it to see if it leaks out the wound (diagnostic), but make sure that you aren’t going through a really dirty layer
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8
Q

What is the most common bacteria associated with joint injections or surgery in septic arthritis?

A
  • Staphylococcus
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9
Q

What is the most common bacteria associated with wounds in septic arthritis?

A
  • Enterobacteriaeceae and anaerobes

- Often polymicrobial

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10
Q

What is the most common bacteria associated with foals in septic arthritis?

A
  • Enterobacteriaeceae, followed by E. coli
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11
Q

Will you always get a positive culture from arthrocentesis?

A
  • NO
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12
Q

Treatment for septic arthritis

A
  • Broad spectrum antibiotics based on most likely organisms
  • Joint lavage*** (Important to decrease numbers and contamination; also helps reduce inflammation by flushing out neutrophils and any inflammatory mediators)
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13
Q

How long should antibiotics continue post-infection with septic arthritis?

A
  • 2-3 weeks
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14
Q

Hyaluronan post-infection treatment with septic arthritis

A
  • Intra-articular or IV

- Can reduce inflammation and decrease likelihood of DJD

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15
Q

Survival rate of adults with septic arthritis

A

85%

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16
Q

Prognosis for return to racing in adults with septic arthritis

A
  • 56% of standardbreds and thoroughbreds released returned to racing
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17
Q

Prognosis for survival in foals with septic arthritis

A
  • 45-84% survival to discharge

- Depends on duration, comorbidities, and $$$$

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18
Q

Prognosis for performance in foals with septic arthritis?

A
  • 48% of TB foals that survived raced

- 33% of TB and SB foals

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19
Q

Joint lavage techniques

A
  • Through and through with needles
  • Arthroscopy (gold standard; can see what you’re doing)
  • Arthrotomy)
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20
Q

Joint lavage fluid type

A
  • sterile balanced electrolyte solution
  • LRS is preferred as saline can cause more inflammation
  • NEVER add chlorhexidine or iodine (pro-inflammatory)
  • No need to put antibiotics in the lavage solution
  • DMSO he doesn’t use because it will get everywhere
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21
Q

Antibiotics for septic arthritis

A
  • Very high local concentrations for > 24 hrs (can get a very high concentration)
  • Irritating to the joint
  • Careful about antibiotic resistance, but less risk due to local nature
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22
Q

Which antibiotic is most often used for joint infections?

A
  • Amikacin

- Also gentamicin, ceftiofur, timentin, methicillin, impipenem-cilastatin

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23
Q

When is open drainage technique indicated?

A
  • Cases of chronic septis or cases that don’t respond to lavage alone
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24
Q

Describe the open drainage technique for septic arthritis

A
  • 3-5 cm arthrotomy
  • Drain into a sterile bandage, which is changed aseptically 1-2x day
  • When upper joints are involved cross tie to prevent contamination
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25
Q

Regional perfusion antibiotics advantage

A
  • Maximizes tissue penetration of the antibiotic around the joint
  • Antibiotic levels >55x MIC for gentamicin
  • > MIC for 24 hours (MIC will stay the same, but they can get much higher than MIC)
  • May require general anesthesia
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26
Q

Antibiotic efficacy - is is concentration dependent or time dependent?

A
  • Concentration dependent
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27
Q

Technique for regional perfusion***

A
  • Tourniquet placed above and in some cases below target site
  • Abx injected into a vein distal to the site or into the medullary cavity
  • 1 gm gentamicin diluted to 30-60 mL delivered slowly (20 min)
  • Often need to be sedatedor need a twitch
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28
Q

Antibiotic impregnated PMMA - what are they?

A
  • Bone cement beads
  • Mix up and form a powder/liquid monomer
  • Mix up and add antibiotics
  • They do not dissolve; antibiotics will diffuse over time
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29
Q

Cautions of antibiotic impregnated PMMA

A
  • Moving joint?
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30
Q

What is the MOA of Antibiotic impregnated PMMA

A
  • Polymethylmethacrylate (PMMA)
  • Powdered polymer + liquid monomer
  • Elution of antibiotics (antibiotic release is based on diffusion concentration gradients)
  • Water enters cracks and pores of cement
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31
Q

How long do surface abx release over?

A
  • 24 hours
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32
Q

How long do antibiotics deeper in the beads release over?

A
  • Lower level sustained release (>24 hrs)
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33
Q

What determines abx diffusion rate with antibiotic impregnated PMMA beads?

A
  • Type of cement
  • Antibiotic selection
  • Antibiotic concentration
  • Size/surface area of implants
  • Environment
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34
Q

Antibiotic compatibility factors to consider

A
  • Stable at body temp
  • Water soluble
  • Heat stable
  • Bactericidal
  • Low incidence of hypersensitivity reactions
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35
Q

Epiphyseal osteomyelitis definition

A
  • part of the polyarthritis or polyosteomyelitis syndrome in young foals
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36
Q

What is more common: septic metaphysitis or epiphyseal osteomyelitis?

A
  • Epiphyseal osteomyelitis
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37
Q

Pathophysiology of epiphyseal osteomyelitis?

A
  • Pooling of blood in the venous sinusoid at the junction of the epiphyseal bone and cartilage is presumed to furnish conditions similar to those known to occur at the metaphysis
  • Sluggish blood flow encourages bacteria to lodge and establish at this site
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38
Q

Diagnosis of epiphyseal osteomyelitis

A
  • Accompanied by septic arthritis of the adjacent joint
  • Arthrocentesis (most commonly gram neg)
  • Radiographs (repeat in 7 days; not super sensitive in picking up bone infection)
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39
Q

What age of foals do you normally see epiphyseal osteomyelitis in?

A
  • <2 months
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40
Q

Advantage of plain x-ray films

A
  • Inexpensive

- readily available

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41
Q

Disadvantage of plain x-ray films

A
  • 30-50% mineral loss to detect lysis

- Not very sensitive

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42
Q

What findings on x-ray suggest osteomyelitis?

A
  • Deep soft tissue swelling
  • Periosteal reaction
  • Cortical irregularity
  • Demineralization
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43
Q

Advantages of CT

A
  • See changes earlier than plain films
  • Esepcially good for areas difficult to image with plain films
  • CT is better than x-ray in general
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44
Q

Findings suggestive of osteomyelitis

A
  • Increased marrow density early

- Sclerosis, demineralization, periosteal reaction (chronic)

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45
Q

MRI advantages

A
  • Better than plain films/CT
  • More sensitive for bone marrow abnormalities (marrow signal abnormalities on MRI more sensitive than lytic changes on plain films)
  • Direct few of intramedullary disorders
  • Findings may precede bone scan findings with bone marrow abnormalities
  • Multiple slices visualized
  • Better soft tissue contrast
  • better anatomic definition
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46
Q

Some consequences that can be seen with septic arthritis

A
  • Angular limb deformities
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47
Q

Septic implants impact on prognosis for survival

A
  • Significantly decreases prognosis
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48
Q

Septic implants impact on cost of treatment

A
  • Significantly increases it
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49
Q

What % of implants and screws get infected?

A
  • Approximately 50%
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50
Q

Etiology of infected implants

A
  • Open fractures
  • Contamination of the surgery site during open repair
  • Contamination through surgical incision (traumatized soft tissue)
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51
Q

Clinical signs of infected implant

A
  • Low grade persistent fever
  • Decreased use of limb
  • Inflammation or drainage from the incision site
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52
Q

Diagnosis of infected implant

A
  • CBC
  • Culture drainage
  • Ultrasound
  • Radiographs
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53
Q

Treatment of infected implant

A
  • removal of implants needed most often
  • Bacteria secrete a glycocalix (slime) that covers and protects them from antibiotics, antiseptics, antibodies, phagocytes, and mechanical removal
  • You usually don’t have an opportunity to put in another implant
  • They try to manage infection and give a bone callus time to form before taking out the implants
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54
Q

Treatment of infected implants

A
  • Broad spectrum antibiotics until culture results guide selection
  • Local abx with PMMA or regional perfusion
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55
Q

Prognosis of infected implants

A
  • Guarded to poor

- Depends on fracture type, age of patient, and virulence of the organism

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56
Q

Dfdx for an acutely non-weight bearing limb that have to do with the foot

A
  • Sole abscess (most often)
  • Laminitis (most often >1 limb)
  • Fracture (pretty uncommon)
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57
Q

In most lamenesses, where does the pain localize?

A
  • The foot
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58
Q

Sole abscess clinical signs

A
  • VERY sensitive to hoof testers
  • Foot will be warm
  • Increased digital pulses
  • Often quite acute
  • SEVERE lameness
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59
Q

How common are sole abscesses?

A
  • VERY SENSITIVE

- Look at the bottom of the foot

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60
Q

What is the definition of a foot abscess AKA sole abscess AKA hoof abscess?

A
  • Accumulation of fluid between the sensitive and insensitive laminae
  • Pressure is what will cause the pain
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61
Q

Etiology of sole abscess

A
  • Often unknown
  • Sole bruise (hemorrhage between sensitive and insensitive laminae that traps bacteria)
  • Penetrating injury
  • Farrier will often get blamed for this (if you’re pounding a nail, must stay in the insensitive tissues)
  • Most of the time goes from bottom up
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62
Q

Diagnosis of sole abscess

A
  • Based on clinical signs
  • Sometimes nerve blocks needed or useful
  • Radiographs often not needed initially
  • ID of abscess tract
  • Hoof testers are helpful (help you localize is, and then you can look for a little black tract)
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63
Q

When to do a radiograph with diagnosing foot lameness?

A
  • If you’re unable to localize it
  • If you have a recurrent abscess especially to make sure there isn’t osteomyelitis
  • Will most often see a gas pocket
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64
Q

Treatment of a sole abscess

A
  • DRAINAGE
  • Important to do enough but not too much
  • Follow the tract to its completion, e.g. the pus, blood, or end of the tract
  • If you can’t get exposure, pack with a poultice to soak the foot and let it break out on its own
  • Soaking with warm water, magnesium sulfate
  • Poultice (epsom salts; Mag sulfate)
  • Treatment plate (needed with extensive sole resection/undermining of sole, frog)
  • Flush tract with iodine or pack small amount of iodine soaked gauze to prevent contamination
  • +/- soak clean foot 1-2x daily for 2 days
  • Check tetanus status
  • anti-inflammatory drugs
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65
Q

What can happen if you make too big of a hole for a sole abscess?

A
  • Don’t want to expose too much solar corium which will prolapse and be a source of pain
  • Dig around the perimeter of the white line
  • Funnel shaped hole
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66
Q

Are antibiotics typically needed for a foot abscess?

A
  • No
  • Not typically for an abscess
  • Won’t allow it to break open if it hasn’t already
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67
Q

What is gravel?

A
  • Ascending infection of the white line

- Not a migration of gravel from the white line

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68
Q

What are signs of gravel?

A
  • Lameness, heat, pain, swelling, and drainage at the coronary band
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69
Q

Etiology of gravel?

A
  • Ascending white line infection

- Usually associated with pre-existing pathology of the white line

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70
Q

Diagnosis of gravel

A
  • Lameness, heat, pain, swelling, and drainage at the coronary band
  • X-rays are warranted as they often have a keratoma or osteomyelitis
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71
Q

Treatment of gravel

A
  • managed similar to a sole abscess
  • Appropriate debridement of the hoof
  • Radical hoof wall resection sometimes indicated
  • Trying to establish ventral drainage
  • He will sometimes do a nerve block and slide a canula down, then try to triangulate and dremel over
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72
Q

What is laminitis?

A
  • Inflammation or edema of the sensitive lamellae –> breakdown and degeneration of the union between the horny and sensitive lamellae
  • Pathological changes in hoof anatomy that result in crippling pain
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73
Q

Common sequelae of laminitis

A
  • Rotation of P3

- Sinking of P3

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74
Q

Which legs (front or rear) are most likely to be affected by laminitis?

A
  • Front leg
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75
Q

How common is laminitis?

A
  • Approximately 15% of adult horses will develop it
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76
Q

What % of horses with laminitis develop a chronic debilitating disease that often leads to euthanasia?

A
  • Approximately 75%
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77
Q

Seriousness of laminitis

A
  • Second leading killer of horses after colic
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78
Q

What are the two parts of the lamellae that interdigitate?

A
  • Epidermal lamellae (primary and secondary lamellae to increase the surface area)
  • Dermal lamellae
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79
Q

Characteristics of epidermal lamellae -

A

Avascular and aneural

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80
Q

Characteristics of dermal lamellae

A
  • Very vascular and very well innervated
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81
Q

Basement membrane of the lamellae

A
  • Tough sheet of connective tissue at the interface of the lamellar epidermis and dermis
  • Forms the receptor site for growth factors, cytokines, and adhesion molecules
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82
Q

What are the three phases of laminitis?

A
  1. Developmental phase
  2. Acute phase
  3. Chronic phase
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83
Q

Developmental phase of laminitis

A
  • Precedes appearance of clinical signs
  • 24-48 hours period during which laminar separation is triggered
  • Often times not recognized
  • Usually characterized by increased hoof wall temperature (increased blood flow?)
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84
Q

Example of case of horses that got into grain

A
  • Tubed with mineral oil to knock down the absorption
  • Acepromazine to increase circulation?
  • NSAIDs to knock down inflammation
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85
Q

Acute phase of laminitis

A
  • First signs of foot pain appear

- Lasts until clinical evidence of P3 displacement within the hoof capsule (rotation or sinking)

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86
Q

Chronic phase - when does it start?

A
  • Begins with displacement of P3 and lasts indefinitely
  • Clinical signs range from persistent, mild lameness to continued severe foot pain, to penetration of the sole of the hoof by the distal phalanx
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87
Q

When does the process initiating the destruction of the lamellar apparatus start relative to clinical signs?

A
  • Before first clinical signs of laminitis appear
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88
Q

What are the three theories of laminitis?

A
  1. Vascular theory (due to vasoconstriction and ischemic necrosis)
  2. Enzymatic theory says that there are enzymatic changes in the basement membrane (want to slow down reaction with cold)
  3. Glucose theory (haven’t talked about)
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89
Q

Etiology of laminitis

A
  • Biomechanical
  • Ingestion of excess carbohydrate (grain overload)
  • Grazing of lush pastures (ponies)
  • Excess exercise and concussion in an unfit horse
  • Endotoxemia
  • Corticosteroids?
  • Systemic disease (colic, pneumonia, colitis, enteritis, retained placenta)
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90
Q

Endotoxemia and laminitis

A
  • Seen as a trigger

- It’s endotoxin PLUS something else though

91
Q

Corticosteroids and laminitis

A
  • Triamcinolone is the most associated, but the association is loose at best
92
Q

Clinical signs of laminitis

A
  • Depend on severity and phase
  • Increased digital pulses**
  • Warm or cold feet
  • Characteristic stance (see picture; part their front legs far apart and put hind legs behind them)
  • +/- hoof tester sensitivity
93
Q

Nerve blocks for diagnosing laminitis?

A
  • Don’t work very well
  • Might assume palmar digital ring block (at pastern level) would work well, but most laminitic horses won’t improve at all
  • Other pain pathways go up the leg further
94
Q

Treatment for laminitis vs prevention

A
  • Prevention more successful

- Treatment in developmental stage may prevent laminitis

95
Q

Treatment for laminitis

A
  • Stall-rest (do NOT walk horses with damaged lamina)
  • Analgesia (NSAIDs, opioids, alpha 2 agonists)
  • Foam support pads until stable
  • Can do corrective trimming and shoeing when no longer in acute phase (especially if either rotation or sinking of P3 has occurred)
  • Will vary depending on the horse
96
Q

Prognosis for laminitis

A
  • Prognosis depends on degree of change and pain level

- High rate of recurrence

97
Q

Treatment during developmental phase

A
  • May prevent occurrence
  • 24-48 hours of cryotherapy (less useful once signs develop)
  • Banamine
  • Frog support
98
Q

Surgical treatment for laminitis

A
  • Inferior check ligament desmotomy

- Deep digital flexor tenotomy

99
Q

Deep digital flexor tenotomy description

A
  • lengthens deep digital flexor tendon and can get rid of some of the pull of the deep digital flexor tendon on the coffin bone
100
Q

Deep digital flexor tenotomy indications

A
  • When they are done rotating, if you palpate a taut deep digital flexor tendon
  • Cases that won’t respond to anything else
101
Q

Cons of deep digital flexor tenotomy

A
  • Performance limiting and performance ending
102
Q

Neurectomy for laminitis treatment

A
  • Results in sloughing of foot in many cases due to increased weight bearing
  • Low neurectomies are ineffective at relieving pain
103
Q

Palmar heel pain vs navicular disease/navicular syndrome

A
  • They are the same thing
104
Q

What is palmar heel pain?

A
  • Lameness originating from heel region
105
Q

Diagnosing palmar heel pain?

A
  • Often blocks out to a plmar digital nerve block
106
Q

Classic appearance of a horse with palmar heel pain

A
  • Bilateral, chronic, progressive forelimb lameness

- Horse often has small feet, underrun heels, long toe

107
Q

Breed predisposition for palmar heel pain

A
  • Quarter Horses, but all horses are susceptible
108
Q

Age of horses with palmar heel pain

A
  • 7-10 years old
109
Q

Why has palmar heel pain historically been challenging to treat, and what can be done to mitigate?

A
  • Most likely due to the fact that the heel region is very complicated and lameness was incorrectly assumed to originate from navicular bone
  • New imaging modalities (MRI) revealed injuries occur to all structures in this area
110
Q

Signs consistent with palmar heel pain

A
  • Lameness localized to the foot
  • No radiographic abnormalities
  • No evidence of bruising or abscessation
  • Further diagnostics usually required to ID specific structure (CT, MRI, ultrasound)
111
Q

CT advantages

A
  • Used a lot
  • Cheaper than MRI ($1000 compared to $2500) and much less time
  • Lets you look at things in very good detail (not as good as MRI, but still very good)
  • can see any fracture; DDF tendon where it crosses the surface
112
Q

Advantages of MRI for diagnosing palmar heel pain

A
  • Superior soft tissue detail
  • Excellent for imaging of bone
  • Yields a higher quantity and quality of information to aid in a diagnosis
113
Q

Disadvantages of MRI for diagnosing palmar heel pain

A
  • General anesthesia required
  • Cost to client
  • Some lesions can be missed due to section size
  • Availability of the technology
114
Q

What does treatment of palmar heel pain depend on?

A
  • The specific problem that is identified

- Helps give the owner a more accurate diagnosis

115
Q

Trimming and shoeing for palmar heel pain

A
  • Correct hoof imbalances
  • Rolled toe –> facilitate break-over
  • Correct hoof wall angles (should be same as the hoof wall)
  • Allow hoof expansion for shock absorption
  • SHort term reduction of biomechanical stress by raising the angle of the foot (heel wedges) –> altered pressure from DDFT
  • SHoeing can also provide a cushion and a mechanical barrier to protect the foot from trauma
116
Q

Medical treatments for palmar heel pain

A
  • Phenylbutazone

- Corticosteroid injection into the navicular bursa or the coffin joint

117
Q

Surgical treatment of palmar heel pain

A
  • palmar digital neurectomy
  • Navicular suspensory ligament desmotomy
  • Navicular bursoscopy
118
Q

Prognosis of palmar heel pain

A
  • Better if treated early in the course of the disease
119
Q

Treatment for an adhesion between DDF tendon and flexor sheath

A
  • Intrasynovial hyaluronic acid ,bilateral forelimb flexor tendon sheaths
  • Tenoscopy and debridement
120
Q

What does prognosis depend on often for young foals?

A
  • Level of ossification

- Take an x-ray right away even if they went to maturation

121
Q

Can you feel the bones that have not ossified?

A
  • No
  • Still feels firm
  • Cartilage feels lik ea bone
122
Q

What is the problem with a foal standing up on bones that have no ossified yet?

A
  • It will deform the bone until it ossifies

- Can lead to angular limb deformities

123
Q

What two things are super important for foals born early (or that are dysmature) with non-ossified bones?

A
  • Support to maintain axial alignment

- Restrict exercise until bones have formed (may involve tube feeding colostrum)

124
Q

Examples of support to maintain axial alignment

A
  • splints or casts
125
Q

What are five ways to correct angular limb deformities in foals (e.g. valgus, varus)

A
  • Controlled exercise
  • Corrective shoeing
  • Cast application
  • Growth acceleration
  • Growth retardation
126
Q

What side do you want to add a shoe on for valgus?

A
  • Medial side
127
Q

What side do you want to add a show on for varus deformity?

A
  • Lateral side
128
Q

What is important for determining if a varus or valgus deformity will correct itself over time?

A
  • Look at the limb perpendicular to the plane
  • Carpus and fetlock should be in alignment with each other
  • You don’t want the fetlocks to point in
129
Q

What two things can lead to angular limb deformities?

A
  • Crushed cuboidal bones vs physeal growth
130
Q

How to differentiate crushed cuboidal bones vs physeal growth on radiograph?

A
  • Draw a line from the two bones and see where they intersect
  • If it’s more on the epiphysis, likely an issue with the physeal growth plate
  • If it’s on the cuboidal bones, probably an issue with those
131
Q

How to differentiate crushed cuboidal bones vs physeal growth on physical exam?

A
  • Palpate
  • Hold onto the proximal part of the leg and straighten out the carpus
  • If the carpus can straighten out by pressing on it, it’s more likely a periarticular injury or crush injury
  • If the physis is the issue, you pushing on it won’t help you straighten it out anymore
132
Q

When is the end of the rapid growth phase for the fetlock joint?

A
  • ~2 months
133
Q

When is timeline for growth acceleration on fetlock joint?

A
  • Within 2 months
134
Q

When is timeline for growth retardation on fetlock joint?

A

2-3 months

135
Q

When is the end of the rapid growth phase for the distal tibia?

A
  • 4-6 months
136
Q

When is timeline for growth acceleration on distal tibia?

A
  • 4 months
137
Q

When is timeline for growth retardation on distal tibia?

A

4-6 months

138
Q

When is the end of the rapid growth phase for the distal radius?

A

~6 months

139
Q

When is timeline for growth acceleration on distal radius?

A
  • 4-6 months
140
Q

When is timeline for growth retardation on distal radius?

A

4-6 months

141
Q

What happens if you try growth acceleration to correct an angular limb deformity after the end of the rapid growth phase?

A
  • WON’T DO ANYTHING
142
Q

Description of periosteal stripping

A
  • Incision down to skin down to bone
  • T-shaped incision on the periosteum
  • Peel it and literally put it right back
  • Initiating growth factors
143
Q

For a valgus limb deformity, which side is growing faster, and which side should you do periosteal stripping on?

A
  • Growing faster on the inside

- Do the periosteal strip on the outside

144
Q

For a varus limb deformity, which side is growing faster, and which side should you do periosteal stripping on?

A
  • Growing faster on the outside

- Do the periosteal strip on the inside

145
Q

Benefits of periosteal stripping

A
  • Outpatient procedure
  • Tiny incision
  • No implants
  • Impossible to over-correct
146
Q

Downsides of periosteal stripping

A
  • May not be as effective
  • Often have shoe application and bandaging
  • May have corrected anyways
147
Q

What are the two major rules of growth retardation?

A
  1. ) Don’t want to go into the joint (bridge it)

2. ) Want screws to be above and below the joint

148
Q

What can happen if you accidentally cross the physis?

A
  • SImilar to a Type V Salter Harris
149
Q

Transphyseal bridge description

A
  • Two screws
  • One above and one below the physis
  • Dig some tunnels and wrap a wire around them
  • Slows down growth on that side to allow it to grow
150
Q

Transphyseal screw description

A
  • Going across the physis vertically
151
Q

At what point should you remove a transphyseal screw?

A
  • When the limb is straight
152
Q

What are disadvantages of transphyseal screws?

A
  • You CAN over-correct
153
Q

What side would you put a transphyseal bridge/screw on for valgus deformation?

A
  • Inside
154
Q

What side would you put a transphyseal bridge/screw on for varus deformation?

A
  • Outside
155
Q

What side would you put a transphyseal bridge/screw on for varus deformation?

A
  • Outside
156
Q

What are options if you miss your window to do growth acceleration or growth retardation?

A
  • Remove a portion of the bone (e.g. osteotomy or osteoectomy)
157
Q

What are some issues with osteotomy or osteoectomy?

A
  • Have to make a fracture

- Forces they are placing on them will alter how they heal

158
Q

Can you treat an angular limb deformity for a cannon bone deviation?

A
  • NOPE

- Deviation of the cannon bone rather than an issue across the joints

159
Q

When should you start seeing changes with angular limb deformities?

A
  • WIthin a few weeks
160
Q

Congenital factors that can lead to angular limb deformities?

A
  • Teratogenic agents
  • Intrauterine positioning
  • Genetic predisposition
161
Q

Acquired factors that can lead to angular limb deformities?

A
  • Nutrition (excessive intake or abrupt changes in quality and quantity of intake leading to rapid growth; or mineral imbalance)
  • Infectious polyarthritis
  • Trauma (e.g. paralysis or true tendon contracture)
  • Can lead to pain and prolonged overload of other limbs
162
Q

Digital hyperextension

A
  • Walking on the back of their foot

- Laxity of the flexors

163
Q

Treatment for digital hyperextension?

A
  • Build up the muscle so that they can contract the muscles back
  • Don’t want to put on full limb bandages because that will worsen it (can do put little band-aids so they have pressure sores)
  • Controlled exercise treatment
  • Can do shoeing changes (heel extension)
164
Q

Congenital contracted tendons appearance

A
  • Hyper-flexion
165
Q

What should you deal with first: angular limb deformity or contracted tendons?

A
  • Contracted tendons are more of a thing to deal with first
166
Q

Treatment for contracted tendons (management)

A
  • Analgesics (painful)
  • Oxytetracycline (relaxes tendons; 3 g IV)
  • Toe extensions to increase the lever arm in front of the foot
  • Splints and casts (can be painful; do on for 12 hours and off for 12 hours)
167
Q

What do you have to worry about with oxytetracycline for contracted tendons?

A
  • Nephrotoxicity

- 3 g IV is often more than what you give adults

168
Q

Surgery for contracted tendons

A
  • Flexor carpi ulnaris and ulnaris lateralis
  • More severe
  • Last resort
169
Q

Coffin joint flexural limb deformity cause

A
  • Acquired deformity
  • Bone is growing too fast for tendon to keep up
  • Can also be a distal interphalangeal joint
170
Q

Club foot

A
  • Coffin joint flexural deformity
171
Q

Diagnosis of club foot or coffin joint flexural limb deformity

A
  • Get an idea of the angle of the distal limb and the hoof
172
Q

Inferior check ligament desmotomy indication

A
  • Flexural deformity of the distal interphalangeal joint (AKA club foot)
173
Q

What is the inferior check ligament?

A
  • Deep digital flexor accessory ligament
174
Q

Age of patient and inferior check ligament desmotomy

A
  • If the bone and soft tissue surrounding the coffin joint have deformed, it doesn’t matter how much of this ligament we cut, it won’t go back to normal
175
Q

What else needs to be done with inferior check ligament desmotomy?

A
  • Concurrent hoof trimming
  • They want to bear weight towards the toe
  • Bear more weight on the heel and lengthen the toe
  • Also put on bandages or splints
  • Lots of follow up treatment
176
Q

What is the difference between the medial and lateral approach for inferior check ligament desmotomy?

A
  • Medial is more cosmetic (little artery in the way but will scar on the inside)
  • Lateral has less wrap around of the check ligament, and you worry about the medial palmar artery
177
Q

Shoeing changes for inferior check ligament desmotomy

A
  • Took some of the heel off to increase the length of the heel
  • Put a toe extension on to increase the lever arm
178
Q

Osteochondrosis definition

A
  • Disease pathology of the bone in the cartilage
179
Q

Osteochondritis definition

A
  • Inflammatory process
180
Q

OCD definition

A
  • Condition in which a flap can be demonstrated
181
Q

What is endochondral ossification?

A
  • Process of bone formation over a cartilage template responsible for postnatal long bone growth at the physeal cartilage and epiphyseal growth at the epiphyseal cartilage
  • Chondrocytes are arranged in the 4 orderly histologic zones from proliferation to hypertrophy
182
Q

Where is the growth cartilage of the epiphysis?

A
  • Interposed between the metaphysis and the separate center of ossification of the epiphysis
  • Surrounded peripherally by perichondrium (blood supply)
183
Q

What is the articular-epiphyseal cartilage complex?

A
  • Cartilage covering the end of a long bone in a growing animal is actually composed of bone epiphyseal growth cartilage and articular cartilage and is referred to as the articular-epiphyseal (A-E) cartilage complex
  • Epiphyseal cartilage will transform into bone
184
Q

Pathophysiology of osteochondrosis

A
  • Abnormal chondrocyte differentiation and formation of defective intercellular matrix
  • Histologically lesions contain persistent chondrocytes in the mid- to late hypertrophic zone with failure of vascular invasion and subsequent osteogenesis
  • Island of cartilage separate from subchondral bone
185
Q

Where does nutrition of the growth cartilage happen?

A
  • Through vessels in the cartilage canals
186
Q

When do cartilage canals disappear?

A
  • 7 months
187
Q

Where does articular cartilage receive nutrition?

A
  • From synovial fluid

- Avascular

188
Q

What happens to retained plugs of cartilage?

A
  • They starve and die

- Get soft and necrotic

189
Q

Etiology of osteochondrosis (5 theorized causes) ?

A
  • Growth rate
  • Dietary mismanagement
  • Genetic predisposition
  • Trauma
  • Hormonal imbalance
190
Q

Growth rate and OCD

A
  • In some species rapid growth rates have been associated with increased incidence of osteochondrosis
  • Increased dietary energy is associated with lesion development rather than growth rates per se

-

191
Q

Dietary management/mismanagement and OCD: dietary energy vs protein

A
  • Dietary energy was what mattered (high concentrate fed horses)
  • Horses fed 126% of NRC crude protein had no increase in lesions
192
Q

Dietary management and OCD: Phosphorus, calcium, zinc

A
  • Phosphorus: high levels had increased incidence
  • Calcium levels do not associate
  • Zinc levels high enough to induce copper deficiency can induce lesions
193
Q

Genetic predisposition for osteochondrosis

A
  • Standardbreds!
  • progeny of Standardbred stallions with osteochondrosis have 3x the incidence of osteochondrosis than do the progeny of stallions without it
  • Definitely a risk
194
Q

What are the three categories of OCD lesions?

A
  1. ) Those showing clinical and radiographic signs (Classic; often have joint effusion)
  2. ) Those showing cliniacl without radiographic (but arthroscopic lesions)
  3. ) Those showing radiographic but no clinical signs
195
Q

How do you diagnose horses showing radiographic but not clinical signs?

A
  • Pre-purchase exam
  • Pick and choose which areas to radiograph
  • Pre-sales films
196
Q

Subchondral bone cysts etiology

A
  • Similar to OCD

- Abnormal cartilage development predisposes to the development of both lesions

197
Q

What type of force causes flap development?

A
  • Shear forces
198
Q

What type of force causes cyst development

A
  • Weight bearing

- May have a cyst lining

199
Q

What is the most common clinical signs of OCD?

A
  • Joint effusion
200
Q

What is the difference between joint effusion and joint swelling?

A
  • Swelling is SC edema
201
Q

What are the most common locations of OCD of the tarsocrural joint?

A
  1. ) Distal intermediate ridge of the tibia
  2. ) Lateral trochlear ridge
  3. ) Medial malleolus
202
Q

When are most OCD lesions identified?

A
  • by 3 years of age
203
Q

Do most horses with OCD present lame?

A
  • Nope
204
Q

What is prognosis if you take out OCD lesions when young?

A
  • Effusion will resolve
205
Q

What is prognosis if you wait to take out OCD lesions?

A
  • Chance of healing is significantly decreased
206
Q

What to do with an OCD lesion in the tarsocrural joint with mild effusion that is seen before 3 months?

A
  • Can wait to see if it will heal
  • Can heal by 7-8 months; if not healed by then, often need surgery
  • If severe effusion or lameness, be careful
207
Q

How does size of DIRT lesion affect prognosis?

A
  • it doesn’t!
208
Q

For DIRT and lateral trochlear ridge lesions, what is best radiograph to take?

A
  • Dorsomedial-plantarolateral oblique radiographs
209
Q

DMPLO radiograph

A
  • look at it on the slide (page 29)
210
Q

Treatment for DIRT lesion

A
  • Surgical removal if clinical signs are present

- Medical doesn’t work well

211
Q

Prognosis for resolution of synovitis and soundness with a DIRT lesion

A
  • Good
  • May have athletic careers that are good!
  • Must take it out early
212
Q

What to do if you find an incidental OCD lesion on radiographs of a 7-12 month old horse?

A
  • Probably want to take it out

- Effusion or lameness likely to happen eventually

213
Q

Osteochondrosis of the femoropatellar joint - what age will they show signs by?

A
  • Three years of age
214
Q

What is most common sign for osteochondrosis of the femoropatellar joint?

A
  • Joint effusion
  • Harder to see
  • Palpate them
215
Q

Lameness with osteochondrosis of the femoropatellar joint

A
  • Varies

- None to severe lameness

216
Q

% of osteochondrosis of the femoropatellar joint that is bilateral

A
  • 50-60%
217
Q

What is most common location for an OCD lesion in osteochondrosis of the femoropatellar joint?

A
  • Lateral trochlear ridge!

- Also can be found on medial trochlear ridge and patella

218
Q

Prognosis of osteochondrosis of the femoropatellar joint

A
  • Extent of damage in the trochlear groove, not the length of the defect in the ridge
219
Q

What is most common location for a subchondral bone cyst?

A
  • Medial femoral condyle is the most common site

- May be seen in the lateral condyle or in the proximal tibia

220
Q

Subchondral bone cysts: more often unilateral or bilateral?

A
  • Usually bilateral

- If you see it in one, radiograph the other

221
Q

Clinical signs of subchondral bone cysts

A
  • Usually not until the horses enter training, when they will become lame
  • Not a lot of effusion
  • Can result from trauma
222
Q

What does the cystic lining of a subchondral bone cyst secrete?

A
  • Inflammatory mediators
223
Q

Treatment options for subchondral bone cysts (4)

A
  1. ) Surgical debridement (may not resolve well) - try to leave it open
  2. ) Injection of cyst with steroids (may or may not have an effect)
  3. ) Rest
  4. ) Stem cells? (medium success or less)

Equine LA Sx (4 decks)

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