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Equine I > Wounds > Flashcards

Wounds Flashcards

1
Q

Mecahnical injuries

A

By far most common

Grazes, abrasions, erosions – heal relatively quickly by mitotic division and migration of underlying intact basal epithelium. Minimal involvement of inflammatory cells, capilleries etc.

Bruising, hematomas, contusions (=bruise + skin injury)

Puncture/penetrating wounds

Lacerations/incised wounds

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2
Q

Thermal injuries

A

Rare

Theramal burns

Friction rubs

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3
Q

Chemical injuries/irradiation

A

Rare

Acids - cause coagulation necrosis and protein precipitation

Alkalis - cause liquefaction necrosis

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4
Q

Clean wound

A

Elective/Surgical wounds created under aseptic conditions, primarily closed.

No break in technique or dirty space entered (i.e. respiratory, GI, UG)

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5
Q

Clean contaminated wound

A

GI, respiratory or UG tract (without urinary infection) entered without significant contamination.

Or minor break in aseptic technique

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6
Q

Contaminated wound

A

Traumatic wounds = always contaminated.

Or elective procedure with major break in aseptic technique

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7
Q

Dirty wound

A

> 1x10^5 bacteria.

Traumatic wound with devitalized tissues, FB, feces, chronic wound.

Transection of clean tissues to get to dirty (i.e. abscess, sinus surgery with pus in sinus)

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8
Q

Stages of wound healing

A

Inflammatory/debridement: haemostasis/acute inflammation

Proliferative/repair: tissue formation

Maturation/remodelling: tissue strengthens

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9
Q

Inflammatory/Debridement: hemostasis/acute inflammation

A

Immediate, lasting days to weeks

Neutrophils: removed damaged tissue and chemo attractants

Macrophages: Release O2 free radials, cytokines, tissue growth factors (thus initiating proliferative phase)

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10
Q

Proliferative/Repair: tissue formation

A

Day 3-14++

Angiogenesis, fibrous and granulation tissue formation, collagen deposition, epithelialization, wound contraction

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11
Q

Maturation/Remodeling: tissue strengthens

A

14 days++

Ends in the formation of scar tissue 1 to 2 years later

remains 15% to 20% weaker than the original tissue

Collagen fibers, which were once haphazardly arranged, are reestablished in bundles, cross-linked, and aligned along lines of tension by fibroblasts to progressively increase the tensile strength.

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12
Q

Most important history to check after a wound

A

Tetatnus status of the horse

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13
Q

How much blood can a horse loose without concern

A

A 500kg horse can lose up to 5 L without too much concern

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14
Q

How to control haemorrhage from superficial vessels

A

Tight pressure bandage for around 20 minutes

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15
Q

Surgical haemostasis

A

Applying a haemostat to the vessel

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16
Q

Topical agents for haemostasis

A

often expensive.

Include fibrin adhesives, Chitosan-based dressings (Celox gauze or granules) calcium alginate products, oxidised cellulose or collagen sponges (all of which provide a substrate for clot formation) and cyanoacrylate adhesives (e.g. vet-bond).

Most are suitable for surface use only.

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17
Q

What should you not use on the open wound surface?

A

Anti-septics that contain soap on the open wound surface

Hydrogen peroxide

Hypochloride

Salicylic or aceetic acid

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18
Q

What should you use for wound lavage?

A

Warm isotonic fluids

Povidine iodine solution

Chlorhexidine

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19
Q

Aseptic synoviocentesis

A

Mandatory to assess synovial structure involvement, provided that iatrogenic contamination can be avoided. i.e. don’t pass a needle directly through the wound to access the joint, access the joint from another point e.g. if the wound is on the medial fetlock, tap the joint from the lateral side.

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20
Q

Heel bulb laceration

A

Common injury (‘over-reach’)

ID structures involved (rule out coffin joint, DDFT, and navicular bursa involvement)

Primary or delayed primary closure best

Hoof cast reduces movement to allow faster healing and better comfort - Easy to apply, Horse must be box rested

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21
Q

Coronary band laceration

A

If deep can affect coffin joint/DFTS

Suture if possible to prevent healing with the CB misaligned -> hoof wall defects

Hoof cast also good

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22
Q

Eyelid injuries

A

Must be sutured to prevent deformities -> problems with tear distribution and secondary ulceration

Even if contaminated, usually heal primarily

Check globe and orbit

Close with small gauge suture material - keep knots away from cornea

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23
Q

Axilla injuries

A

Stake injuries common

Pneumomediastinum (+/- pneumothorax) can occur due to air being pumped up when foreleg moves

Box rest may prevent this

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24
Q

Thorax injuries

A

Check for rib fracture + pleural penetration (digital exploration will tell you a lot)

If pleural penetration, can hear air being sucked in or horse in respiratory distress; radiographs

Usually a referral case - the collapsed lung plugs mediastinum so horse can usually breath with unaffected lung while travelling

Emergency chest drain?
§ Chest tube/teat cannula with 60ml syringe and 3 way stop clock to evacuate air
§ Place in upper 1/3 chest - safest
Broad spectrum antibiotics

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25
Q

Abdomen injuries

A

Careful palpation will often help to decide whether abdominal wall has been fully penetrated

Abdominocentesis can help but changes take several hours (esp if a small penetration)

Often just monitor for CS of peritonitis e.g. colic, pyrexia, high HR

If large wound and risk evisceration, plug hole with damp gamgee pads and wrap with belly bandage before referral

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26
Q

Flexor tendon lacerations of the lower limb

A

If referring a horse with a tendon laceration, splinting of the leg (dorsal cortices aligned) and broad spectrum antibiosis are indicated prior to transport.

Postoperative external coaption for a prolonged period is likely to be involved in the treatment after surgical repair

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27
Q

Extensor tendon lacerations

A

in the absence of synovial sepsis of the extensor tendon sheath are frequently managed without primary surgical repair of the tendon.

Splinting should be applied for the first few days until the animal learns to accommodate for its gait deficit.

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28
Q

Radiographs of wounds

A

Fractures

Foot penetrations - radiograph with nail still in place

Osteomyelitis - old wounds

Foreign bodies - if radiopaque

Gas opacity to determine if wounds tracking near joints or bon

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29
Q

Ultrasound of wounds

A

Gas opacity from wound often inhibits use, but occasionally useful

Soft tissue damage - i.e. wound over flexor tendon

Foreign bodies

Gas opacity to determine if wounds tracking near joints or bones

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30
Q

Primary closure of wounds

A

Clean wounds with minimal contamination are good candidates.

Will give fastest healing time + best cosmetic result.

Partial closure can be used for large wounds and often speeds healing whilst allowing drainage.

Necrotic tissue should be debrided.

Upwards pointing ‘V’ skin flap often poorly vascularised, even if it subsequently dies it acts as a biological dressing - like a full thickness skin graft.

If wound edges are under tension, tension relieving suture patterns e.g. vertical or horizontal mattress or cruciates should be used.

Stent-supported sutures provide extra tension relief of the wound margin but not often needed.

Immobilisation with a bandage cast or splint will also help to stabilise the suture line in wounds that are closed under tension.

Degloving wound has good primary closure: proximal limb bandage placed to protect flap during transport.

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31
Q

Best suture material for equine wounds

A

Polypropylene is the least reactive suture material available and is therefore the best for equine skin, but other synthetic materials are also suitable (nylon, PDS).

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32
Q

Standing repair or GA

A

fractious horse, ££, other structures involved e.g. joints

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33
Q

In field or referral repair

A

your experience and comfort level, suspected/confirmed synovial sepsis/fracture etc., complexity of repair AND aftercare.

34
Q

Delayed primary closure

A

up to 5 days after the injury

a good option for contaminated wounds which are unsuitable for closure at the first visit.

Skin retraction usually occurs making it difficult to completely close wound.

35
Q

Delayed secondary closure

A

(after 5 days post injury i.e. after granulation tissue formed)

rarely used apart from certain areas e.g. heel bulbs– often skin is adherent to underlying granulation bed.

Granulation tissue is cut back and the skin is reapposed where possible.

Skin retraction occurs as above.

36
Q

Second intention healing

A

very common - for all contaminated wounds or if large amounts of tissue loss/devitalised tissue.

Heals primarily by proliferative/repair phase of wound healing – granulation then epithelisation and contraction.

Exudate is common and NORMAL.

Wound is usually bandaged during secondary intention healing (unless site is difficult to bandage .e.g. head, upper body)

37
Q

Topical medications for secondary intention healing

A

Hydrogel preparations

Silver sulfadiazine (gram negative bacteria and pseudomonas, contraindicated in pregnant animals)

Topical antibiotics: aminoglycoside (gram negative), soluble antibiotics lie penicillin, gentamycin etc.

Caustic agents (none proven to work)

Corticosteroids (reduces granulation tissue)

Manuka honey (contaminated/devitalised/non-healing wounds)

38
Q

Primary layer of a bandage

A

Adherent or non-adherent dressing

39
Q

Adherent dressing

A

these dressings stick to the wound surface and thus debride the surface when removed – often painful to remove – e.g. wet to dry swabs.

Not used much these days.

40
Q

Non-adeherent dressings

A

Cotton cellophane (melonin)

Polyurethane foam (advasorb, allevyn, biatain)

Polyurethane sheet (opsite)

Hydrocolloids (Tegasorb, replicare)

Petroleum impregnated gauze (vaseline)

Calcium alginate (algisate, algiderm)

Activated charcoal

41
Q

Cotton cellophane

A

Melolin
Cotton, coated with perforated polyethylene which is non-adherant.
Not very absorptive but when removed -> minimal trauma to the wound surface.

42
Q

Polyurethane foam dressings

A

Advasorb, Allevyn, Biatain

waterproof but gas permeable.

More absorptive than cotton cellophane and ideal for use with a hydrogel.

43
Q

Polyurethane sheet dressings

A

Opsite
Transparent adhesive film which is semi-occlusive, allowing passage of gases but not fluid.
Very little capacity for absorption therefore maintain a moist wound environment and promote epithelisation of partial thickness wounds or incisions which can not be easily bandanged e.g. on rump or thorax.

44
Q

Hydrocolloids

A

Tegasorb, Replicare

contain gel-forming agents, such as sodium carboxymethylcellulose (NaCMC) and gelatin.

In many products, these are combined with elastomers and adhesives and applied to a carrier - usually polyurethane foam or film, to form an absorbent, self adhesive, waterproof wafer.

Hydrocolloids absorb liquid and form a gel, which may be cohesive.

Expensive and do not stick to haired skin.

45
Q

Petroleum impregnated gauze

A

Vaseline
These allow passage of exudates into the secondary layer of the bandage.
May have antibiotics included in the dressing.
Innert and non-irritating but slow the rate of re-epithelisation.

46
Q

Calcium alginate dressings

A

Algisite, Algiderm
has haemostatic properties and is highly absorbent therefore suitable for exudative wounds.
Should not be used on dry wounds as will dessicate the site.

47
Q

Activated charcoal

A

designed primarily to control odour and absorb bacteria (especially burns patients).

Reported to have an inhibitory effect on granulation tissue.

48
Q

Compressive layer of bandage

A

Cotton wool/gamgee with a stretchy woven bandage on top
Can repeat the compressive layer several times -> more immobilisation, stabilisation and absorbtion if wound v exudative

49
Q

Protective layer of a bandage

A

Vet wrap , Elastoplast top and bottom

50
Q

Complications of wound healing

A

Infection/contamination

Excess tension on suture line

Loss of blood supply

Dead space (poor drainage)

Excessive motion

51
Q

Clinical signs of wound infection

A

Discolored granulation tissue

Oedema in and around the wound

Purulent exudate

Odor

Increased lameness and pain on palpation around the wound

52
Q

What to do if you get dead space in a wound

A

if large dead space when closing wound then use a drain.

○ Penrose drain most common in 1st opinion practice. Prevent skin scalding at drainage site - vaseline

○ Mesh the skin to allow drainage, pressure bandage - only for areas where will not compress important structure like the flexor tendons

53
Q

Causes of non-healing, chronic wounds - locally

A

Infection/necrotic tissue

Tension/motion

Poor vascular supply

Exuberent granulation tissue

Foreign body

Sequestrum

Large skin defect

54
Q

Definition of wound infection

A

> 10^5 bacteria/gram of tissue

55
Q

Exuberent granulation tissue

A

‘proud flesh’

Limbs&raquo_space; trunk wounds, Horses&raquo_space; ponies

Once granulation tissue protrudes higher than wound edge, v. difficult for epithelium to grow over it

Due to inefficient acute inflammatory phase and protracted chronic inflammatory response -> too much granulation tissue produced

56
Q

Factors that predispose to proud flesh

A

Chronic inflammation
◊ Infection - common cause

Motion

Bandages and casts

Size of horse

57
Q

Treatment of exuberent granulation tissue

A

Use treatments for excess motion, infection etc. as appropriate plus
◊ Bandage with moderate pressure
◊ Topical steroids

Excision of excess granulation tissue
◊ Can usually be done with sedation + local anaesthesia
◊ Bleeds a lot - cut from distal to proximal

58
Q

Sequestrum

A

due to exposed desiccated bone – may have lost some periosteum in original injury

Initial injury traumatises bone or blood supply to bone (periosteum stripped)

Stripping of periosteum + loss of blood supply -> necrosis of superficial bone -> walled off from the healthy intact bone

Suspect when see mature granulation bed but with a cleft or draining tract (‘cloaca’)

Take radiographs

59
Q

Causes of non-healing, chronic wounds - systemically

A

Has to be quite severe to affect wound healing

PPID (high endogenous cortisol)

Protein/nutrient deficient

60
Q

Involucrum

A

Reactive bone forms around the necrotic portion

61
Q

Cloaca

A

Draining tract to the skin connects with an opening to the sequestrum

62
Q

Indications for skin grafting

A

Too large (to suture or heal by secondary intention)
Slow healing

63
Q

Two basic types of skin graft

A

Pedicle graft - vasular and nerve supply

Free graft - devoid of vascular and nerve supply, full thickness or split thickness

64
Q

Island grafts - pinch/punch grafts

A

Most common type of grafting in horses

Purpose is to increase area of epidermis from which epithelization proceeds

Implanting grafts in the granulation bed, rather than applying them to surface, is better

Punch: full-thickness plugs of skin harvested with skin biopsy tool, and implanted into granulation tissue using another skin biopsy tool, one size smaller

Pinch: small discs of skin harvested by hand using scalpel blade

Elevate skin with hypodermic needle with bent tip

65
Q

Donor sites for island grafts

A

Neck beneath mane

Ventral abdomen (thick skin here)

Perineum

66
Q

Tunnel grafts

A

Useful for large skin defects
§ Highly mobile sites
§ Sites that are difficult to bandage
□ Thorax/abdomen/gluteal

Technically simple

Donor site = neck, leaves more of a scar than pinch/punch

67
Q

Split thickness grafts

A

Very painful to harvest

Needs specialist equipment (dermatome)

Technically difficult but higher % ‘take’

68
Q

Disadvantages of full thickness sheet grafting

A

Not accepted as readily as split-thickness grafts
□ Have fewer exposed vessels available for imbibition or inosculation
□ Requirement for nourishment is greater

Epidermis usually sloughs

69
Q

Synovial sepsis

A

potentially fatal in horses and must be treated as an emergency.

Survival rate (to discharge from hospital)= 89% , return to previous athletic function = 69%

If synovial contamination has occurred, immediate parental antibiotics (penicillin + gentamicin) should be administered and the horse should be for arthroscopic lavage under general anaesthesia.

70
Q

Where can synovial sepsis occur?

A

Joints

Tendon sheaths – lower rate of return to athletic function -circa 50%

Bursae

71
Q

What is synovial sepsis caused by?

A

Traumatic wound (most common)

Iatrogenic i.e. after joint injection (or inadvertent puncture of joint during nerve block) or after joint surgery (arthroscopy)

Haematogenous (rare in adult horse, common in foal)

72
Q

Pathophysiology of synovial sepsis

A

Contamination of synovial cavity

Marked inflammatory response = marked lameness
§ Fibrin accumulates + bacteria + inflammatory cells -> synovial thickening/pannus
§ Continues inflammatory process may lead to irreversible articular cartilage, tendon and/or subchondral bone damage/infection

73
Q

Aetiologies of synovial sepsis

A

Penetrating traumatic injury - most common in adults

Haematogenous spread - most common in foals

Iatrogenic infection

Extension of local infection

74
Q

Clinical signs of synovial sepsis

A

Lameness typically acute and severe

Open joints/acute wounds with synovial involvement may initially be mildly/not lame

Osteomyelitis in foals may present first with mild, intermittent lameness

Synovial effusion and/or periarticular oedema

TPR
○ Adults typically WNL
○ Foals typically febrile, but not always

75
Q

DIagnosis of synovial sepsis

A

Synoviocentesis
§ Collection of synovial fluid
§ Number 1 test for diagnosis no matter the aetiology
§ Fluid analysis (gross and microscopic) – WBC count, % of neutrophils and TP most important
§ Culture and sensitivity – takes days to get result – often not performed

Synovial distension/pressure leak test
§ Sterile saline injected into joint under pressure to see if any communication present with wound
§ Always collect joint fluid if possible before distending joint

76
Q

Synoviocentesis technique

A

Aseptic prep

Aseptic technique using landmarks to enter

Collection/aspiration of synovial fluid (for analysis and C/S)

If wound present enter at a different site and do leak test

77
Q

Normal synovial fluid

A

straw yellow, translucent, viscous

WBC: <10 x 109/L, Total Protein: <10 g/L, usually <15% neutrophils, but can increase after e.g. joint injection up to 50-60%

78
Q

Septic synovial fluid

A

Varies (Florescent yellow-cream coloured, serosanguinous), turbid or flocculent material, decreased viscosity

WBC: >20 x 109/L , Total Protein: >30 g/L

> 90% neutrophils

79
Q

Treatment of synovial sepsis

A

Rapid (ideally <24hrs) and aggressive

Synovial lavage

Antibiotics (penicillin and gentamycin systemically, Aminoglycosides locally)

Additional treatments e.g. stall rest, NSAIDs, bandaging

80
Q

Prognosis of synovial sepsis

A

Good for vast majority of horses with prompt treatment (<24 hrs)

Excellent for survival (90%)

Good for athletic use (50-70% reported—lower with foals)

Prognosis decreases with:
○ increased time from inoculation to lavage
○ degree of damage to sheath /joint, surrounding structures, or infection into the bone
○ Specific synovial structures known to have worse outcomes than others

OA is a sequellae to septic arthritis—especially if prolonged treatment

Equine I (21 decks)

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