Equine emergencies, injuries, colic, liver Flashcards
Initial treatment of stable fire - burnt horse?
Stop any burning - cool with lukewarm water and remove rugs
Sedation/anziolytics if required
Flunixin IV
+/- Oxygen
Severe cases may need IV catheter placement +/- tracheostomy (URT inflammation, burn shock)
Referral/euthanasia may need to be considered
Less severe cases - cool skin with cold water, clip hair and lavage with chlorhexidine solution, apply water based antimicrobial ointment e.g. silver sulfadiazine
How to assess the severity of burns in stable fire etc?
Full clinical exam - check for involvement of eyes and other structure e.g. joints/tendon sheaths
Assess extent of burns injury = percentage of total body surface area, correlated with mortality
Assess depth of burns injury - 1st to 4th degree, correlated with morbidity
Determine if referral/euthanasia should be considered
Initial advice to an owner about wounds in horses?
Control any profuse haemorrhage by placing a dressing/any clean, dry material over site and maintaining pressure - if possible
Do not move horse if it is very lame unless in imminent danger
May only need telephone advice if minor wounds in low risk area
For more severe cases, tell them not to apply anything to the wound before you have assessed it
Clinical exam, history and what to initially do for a wound of a horse?
Initial first aid: control haemorrhage, stabilise limb Full history about circumstances of injury and when occurred, tetanus status Full clinical exam: - Assess for shock - Assess stance ability to bear weight - Check vital parameters - Check amount of blood lost - Check for other wounds
What to do more detailed assessment of horse wounds after initial clinical exam?
Poss sedation
Assess age of wound/degree of contamination, location
Apply sterile gel to wound and clip and clean area around it
Remove gel and lavage site with sterile polytonic fluids/chlorhexidine/povidone iodine with 35/60ml syringe and 18/19G needle
Wear sterile gloves and use finger/sterile probe to determine:
- depth and direction of wound
- presence of any foreign material
- subcutaneous pockets
- bone/tendon exposure
Is wound near joint/tendon sheath
Involves penetration of thoracic/abdominal organs or other vital areas e.g. trachea/oesophagus
Which wounds should be sutured? Things needed?
<8h old and have healthy looking tissue a the wound margins
Wounds around eyelids, nostrils and lips (full thickness)
May need:
- sedation
- GA
- local nerve blocks: mepivacaine/lignocaine (not with adrenaline), regional nerve block, ring/L block
- suture materials and equipment
- staples may be appropriate in some cases
- drains
- protection/bandaging of site
To do:
- remove necrotic/non-viable tissue (preserve issue flaps if possible, eyelids/nostrils/lips good anatomic reconstruction v important)
- skin staples only where no tension
- 3-3.5 metric monofilament for skin e.g. polypropylene, absorbable, similar size subcutaneous tissue
- +/- stenting
Ongoing management of horse wounds?
Analgesia and anti-inflammatories (IV then oral course)
Antibiotics (IV/IM then oral course e.g. trimethoprim sulphonamides)
+/- tetanus toxoid/tetanus booster
+/- box rest (beware colic due to no exercise -> reduced motility -> impaction)
Suture/staple removal - usually 10-14 days
Frequency of bandage changes depends on amount of exudation
Secondary intention healing for horse wounds - what dressing etc?
Apply sterile hydrogel and non-adherent, absorbent dressing initially
Bandaging of distal limb important (+/- splint or cast bandage)
Ongoing wound management important - can take a long time and can be expensive
Some wounds may be suitable for delayed primary closure (tertiary healing) or skin grafting techniques
Complications of horse wounds?
Synovial sepsis/fracture (missed initially)
Bone sequestrum formation - where cortex of bone exposed
Wound dehiscence
Foreign material remains in situ - be careful if wood involved
Sores associated with bandaging - bandaging performed by the owner may not be appropriate
Types of skin grafts for horses?
Pedicle grafts - rarely used, equine skin relatively inelastic
Free grafts - usually autografts, pinch/punch/tunnel grafts, solid or meshed sheets, meek micro grafts
Timing of skin grafting?
Can be applied to granulating wounds
Can also be applied to fresh injuries/surgically created defects
Wound bed requirements for a graft to be accepted in horses?
Vascularised
No necrotic tissue present
No evidence of overt infection
No evidence of delayed wound healing - sequestrum, foreign body
Acute wounds: rule out synovial involvement, bone/tendon/ligament pathology
Indications for skin grafts in horses?
Traumatic injuries Non- or slow healing granulating wounds Adjunct to management of skin neoplasia Extensive skin burns Deformity-causing scarring
How quick is epithelialisation of horse wounds?
<1mm/week
How to place grafts for horse wounds?
Start at the lowest site (prevents haemorrhage from obscuring sites) Make a pocket in the granulation bed No 15 scalpel blade Firmly tuck grafts into each pocket Non adhesive dressing, bandage Box rest Change bandage in 5-7 days
Full thickness graft donor site?
Pectoral region most commonly used
Complications with nasogastric intubation of horses? Tips to avoid this?
Haemorrhage - common
Oesophageal perforation - uncommon, poor prognosis
Inhalation pneumonia - uncommon
Tips:
- use appropriate size, plenty of lube and ensure not roughened/damaged
- ensure horse is suitably restrained
- pass down ventral meatus
- never force tube, ensure placed properly in oesophagus/stomach before administering fluids
Problem with liquid paraffin via nasogastric tube?
Associated with severe lipoid pneumonia
Can be life threatening and difficult to treat
Even if small amount gets into lungs
Which horses have an increased risk of rectal tears during examination? Tips to avoid it?
Arabs, stallions/colts, horses with colic, fractious horses
Tips:
- ensure properly restrained
- sedate if fractious
- never push against rectum if horse strains: sedate +/- butylscopolamine
Initial action if blood on rectal sleeve (possible rectal tear) for horse?
Inform owner Sedate horse Give butylscopolamine \+/- epidural anaesthesia Evaluare integrity of rectal mucosa Protoscopy useful if endoscope available Determine the location and grade of the tear
Classification of horse rectal tears?
Grade 1: mucosa and submucosa
Grade 2: muscularis
Grade 3a: mucosa, submucosa and musculis (not midline)
Grade 3b: mucosa, submucosa and muscularis (midline)
Grade 4: all layers
Treatment of rectal tears?
Depends on grade of tear, location (extra/intraperitoneal rectum) and owner factors (economics etc)
Grade 1 - medical management/no treatment required
Grade 2 - medical management
Grade 3 and 4: medical/surgical management
Broad spectrum antibiotics - penicillin
Flunixin meglumine
Check tetanus status
+/- epidural anaesthetic and packing of rectum
Surgery - direct suturing, placement of rectal liner, temporary diverting colostomy
Horse level risk factors for colic?
No clear age, breed or sex predilection overall, specific types of colic do have specific age or sex risk factors
Crib biting/wind sucking - risk factor for EFE, SCOD, recurrent colic
Weaving - risk factor for recurrent colic
(can modify pasture access and diet)
Management level risk factors for colic?
Geography - sand colic, enteroliths, EGS, IFEE
Seasonal - spring and autumn peaks, EGS peaks in May, large colon impactions and EFE peak in winter
Change in feed within 2 weeks (association with weight of feed/concentrate feed, shifts in gut microbiota) - especially LCV
Coastal bermuda hay (not UK) - ileal impaction
Increased stabling/reduced pasture turnout - general colic, SCOD, colic in horses with CBWS behaviour
Pasture associated with Equine Grass Sickness
Dental care - SCOD:horses who had teeth checked less frequently, LCV:horses with known dental problem/seen quidding, LC impactions:donkeys with dental disease
Parasites and anthelmintic administration - measures to minimise parasite burdens reduces risk, Anoplocephala perfoliata associated with spasmodic impaction/ileal impaction/caecal intussusception
Access to water
Transport
Exercise
Owner/carer
Risk factors for colic recurrence?
Known dental problem
CBWS
Weaving
Time at pasture
Epidemiology of pedunculated lipoma strangulation?
Older horses and ponies (>8yo) Ponies>>>horses Geldings>mares Small intestine most common Occasionally small colon and other sites
Epidemiology of large colon volvulus (LCV) in horses?
Mares - post foaling Larger horses Increased stabling Dental disease Feed - especially changes
Epidemiology of large colon impaction in horses?
Change in management - stabling
Autumn/winter
Box rest e.g. hospitalised - motility, water balance
Straw bedding
Good prognosis (poss worse in donkeys and older animals)
Epidemiology of epiploic foramen entrapment?
Seasonal - Dec, Jan, Feb: increased stabling, feed
Crib biting/wind sucking behaviour
Predictors of whether a colic case is critical or not?
Pain
Cardiovascular signs
Absence of gut sounds
Post colic surgery survival?
High mortality in first few days after surgery
Slower rate of death in first 100 days
And then rate is constant
Risk factors for mortality after colic surgery?
Resection length
PCV
Duration of surgery
Potential postoperative complications of colic surgery?
Post-operative ileus (POI) Thrombophlebitis Post operative colic - SI strangulation, large colon torsion Diarrhoea Laminitis Incisional infection/dehiscence
What is grass sickness?
= Equine dysautonomia
Polyneuropathy affecting central and peripheral nervous systems of horses
Clinical signs related to neuronal degeneration in the autonomic and enteric nervous systems (severity depends on extent of degeneration)
Diagnosis of grass sickness?
Clinical signs
Histology - ileal biopsy (surgery), PM exam
Acute/subacute clinical presentation of grass sickness?
Colic Reflux Tachycardia SI distension Patchy sweating Salivation Difficulty swallowing Ptosis
Chronic clinical presentation of grass sickness?
Weight loss Dysphagia Tachycardia Patchy sweating Muscle fasciculations Rhinitis sicca (crusting around nares) 'Elephant on a barrel' stance
Epidemiology of grass sickness?
Previous outbreaks on premises increases risk
Regional - more common in North, Scotland
Young horses 2-7yo (particularly 3-5)
At pasture
Spring - especially April/May
Also peak in Autumn in certain years
Spatial clustering
Management risk factors for grass sickness?
Access to grass - longer time at pasture
Recent change in pasture (e.g. changed fields previous 2-4 weeks)
Pasture disturbances e.g. mechanical removal of droppings
Element levels in soil
Avoid turning out young horses to a pasture that has previously had GS in spring time, supplement with hay/haylage
Theory for cause of grass sickness?
Toxico-infection with C botulinum type C
Present in GIT, combination of risk factors triggers toxin production
Type C toxin found in ileum and faeces of GS cases
EGS cases have lower Ab to Clostridium type C than controls
Vaccination possibility?
How are parasites/anthelmintics a risk factor for colic?
No association with anthelmintic type/programme
Increased risk if not on a worming programme
Decreased risk if on a regular worming programme
Increased risk after anthelmintic administration
How can Strongylus vulgaris cause colic?
Thrombosis of the cranial mesenteric artery
Non strangulating infarction
Once was responsible for up to 90% of all colic cases - rarely seen since modern anthelmintic use
What causes post-worming colic?
Follows anthelmintic treatment of horses known to have high worm burdens
Inflammation of GIT subsequent to death of large numbers of parasites
Concurrent treatment with steroids sometimes undertaken in Cyathostominosis cases
Clinical signs of Cyathostominosis in horses?
Weight loss, hypoalbuminea
Diarrhoea
Intussusceptions - caecocaecal, caecocolic
Can be associated with high mortality
Colic from large burdens of Parascaris equorum - why? other signs? Which age affected?
Small intestinal impaction -> poss rupture
Weight loss/unthriftiness
Can be associated with high mortality despite surgical intervention
Relatively common in horses in first year of life
Strong acquired immunity
Pasture management for parasite management in horses?
Poo picking - twice weekly
Co-grazing with ruminants
Rotating pasture
Anthelmintics used for: - Anaoplocephala perfoliata - Strongylus vulgaris and Cyathostomins - Parascaris equorum - Fasiola hepatica? Resistance?
Anoplocephala perfoliata - pyrantel x 2 or praziquantel
Strongylus vulgaris and Cyathostomins - resistant to BZs, 50% resistant to pyrantel, MLs effective (ivermectin, moxidectin)
Parascaris equorum - resistant to ivermectin and moxidectin and some to pyrantel, use pyrantel or BZs
Fasciola hepatica - BZs?
Conclusions from horse parasite study?
Prevalence of strongyles and P equorum presence similar
Horses 1yo or less have high P equorum FEC
Youngstock <3yo have higher FEC
No evidence of increased prevalence or intensity of infection with S vulgaris
Poss increased prevalence of A perfoliata
Greater surveillance of parasitic infection is required
Timechart for when parasites in horses need to be controlled/treated?
May-Nov: P equorum when young, then Strongyles and tapeworm as matures
June-Nov: FEC monitoring/tapeworm ELISA
Nov-April: Larval cyathostome (+bot control)
Diagnosis of parasite burden in horses?
Cyathostomins: FEC for adult stages, larval stage ELISA
Large strongyles: FEC (indistinguishable from cyathostomins), larval culture and morphological identification is time consuming/needs specialist skills, ELISA
P equorum: FEC detection of spherical thick shelled eggs
A perfoliata: FEC (centrifugation flotation 60% se), ELISA, saliva based test
Oxyuris: adults in faeces, eggs in perianal region
Oxyuris equi?
Relatively common
Causes severe irritation
Wash peri-anal region and environment - power cleaning
Resistance/poor drug efficacy
Diagnose with adults in faeces/eggs in perianal region
Indications for medical treatment of colic (in general)?
Mild – moderate pain Good response to analgesia HR <50 bpm GI motility continuing / improving No net reflux Resolving / no abdominal distension Normal peritoneal fluid Normal PCV/TP and systemic lactate
Principles of medical treatment for colic?
Analgesia
+/- oral fluids (not if net reflux due to SI obstruction etc)
+/- IV fluids/phenylephrine/psyllium/epsom salts dependent on initial diagnosis
What to consider when choosing an analgesic for colic in horses? Groups to choose from?
Potency Duration of action Sedative/other effects e.g. smooth muscle relaxation Potential side effects NSAIDs, A2 agonists, Opiates
NSAIDs as analgesia for colic in horses - options? Potency? Duration of action? Cautions?
Phenylbutazone:
- moderate potency (good as won’t mask what’s going on)
- 12h duration
- beware perivascular administration (can cause irritation, sloughing etc)
- good first line analgesic for colic cases with mild/moderate pain
Flunixin meglumine
- potent analgesia
- 12h duration
- very effective in masking increase in HR with SIRS
- should be used with caution in colic cases showing mild/moderate pain where cause is unknown
Metimazole (Buscopan compositum)
Ketoprofen
Meloxicam
A2 agonists as analgesia for colic in horses - options? Potency? Duration of action? etc
Xylazine - good analgesia - short acting up to 30 mins duration - very useful in assessment of a painful colic case Romifidine - 2-4h duration - usually combined with butorphanol - can be administered IM - useful in colic cases showing moderate-severe pain Detomidine - potent analgesia for 2-4h - usually combined with butorphanol - useful in colic cases with moderate-severe pain
Opiates as analgesia for colic in horses - options?
Butorphanol
- usually combined with a2 agonist
- an be used on its own
- useful in colic cases that are moderately/severely painful
Pethidine
- preparation licenced for use in horses with colic but uncommonly used
Morphine
- potent analgesia but not appropriate for use in colic cases seen in first opinion practice (other analgesics are available and are more suitable)
Butylscopolamine/hyoscine for colic in horses? When used?
Smooth muscle relaxant
Buscopan and Buscopan composites (combined with metimazole)
Indicated in spasmodic colic/mild colic pain
Useful when performing rectal examination where horses are strain - reduces risk of rectal tears
Why must flunixin meglumine be used with caution for colic?
Potent analgesia so signs of colic pain masked - owners may not appreciate severity of situation/may delay contacting vet again
Masks effects of SIRS (endotoxaemia) - increases in HR and PCR are delayed
Makes decision making in early stages of strangulating lesions difficult
When is flunixin acceptable for colic? When to be cautious?
Acceptable:
- when referral is not an option and horse is exhibiting moderate/severe pain (if no response seen euthanasia is appropriate)
- when an exact diagnosis is known and medical treatment is appropriate (e.g. pelvic flexure impaction)
- when the decision to refer has already been made
Be cautious:
- mild/moderate pain of unknown cause and where referral is an option
Oral fluids for colic - benefits? How much>
Easy and inexpensive?
Stimulates gastrocolic reflex
Provides hydration provided horse not refluxing
Hydrates ingesta assisting resolution of large colon impactions
4-6L (500kg horse)/electrolytes every 4h by nasogastric intubation
IV fluids for colic - downsides?
Expensive
Rarely indicated in medical colic cases
What is spasmodic colic? Signs? Treatment?
Pain due to intestinal spasm
Undiagnosed/spasmodic colic is most frequent diagnosis in first opinion
Mild pain
Normal CV parameters
Butylscopolamine +/- NSAID (metimazole/phenylbutazone) effective in most cases
Pelvic flexure impaction colic - when seen? signs? Treatment?
More common in horses stabled more than normal e.g. box rest, or during winter months
Very rare in horses our at grass all the time
Mild/moderate signs of pain
Classic findings on rectal exam - doughy, firm structure on LHS of caudal abdomen
Treatment:
- oral fluids every 4h until faeces passed
- can add epsom salts to water on first occasion
- no evidence liquid paraffin is of any use
- surgery may be required in some cases - progressive deterioration in pain/clinical parameters
Nephrosplenic entrapment colic (left dorsal displacement) - treatment? Diagnosis?
More common in warmblood type/large horses
Specific medical management indicated if:
- CV parameters normal
- pain not severe
- no marked gaseous distention of large colon
Surgical management indicated in some cases:
- severe pain/gas distention of colon
- deteriorating CV parameters
- non-response to treatment
Diagnosis - ultrasound: failure to image left kidney and spleen (gas distended large colon seen instead)
Analgesia - PBZ, a2 agonst
Phenylephrine infusion:
- administered over 15 mins
- reduces size of spleen
- horse lunged for 10 mins
- assess if LC has repositioned itself
- *increased risk of haemorrhage in older horses
Large colon distension/other displacements colic - signs? Treatment?
Mild – moderate signs of pain initially
Medical therapy indicated initially and light exercise can be helpful
Surgical management may be needed in some cases - severe / worsening pain, deteriorating CV parameters
Sand colic - when seen? Why happens? What happens? Diagnosis and treatment?
Potential to ingest sand when sandy soil, poor grazing, turnout on sand arenas
Sand irritates colon, sometimes causing diarrhoea/recurrent mild colic
Can cause impactions within colon and colon displacement/torsion
Diagnosis - confirmed by finding sand in faeces, seashore sound on auscultation, sand retrieved on abdominocentesis (accidental enterocentesis)
Treatment:
- remove source of sand
- provide plenty of forage
- +/- psyllium added to feed (efficacy debated)
Meconium retention colic in neonatal foals - signs? Treatment?
Failure to pass normal black/tarry faeces
Common cause of colic in neonates
Treatment:
- soapy water/commercial (phosphate or acetylcysteine) retention enema
Sedate foal & keep HQ elevated for 30 min
Advice to owners for colic?
Remove feed & leave water with horse
Ask owners to provide an update in 2 hours, sooner if signs of colic recur
If horse responds to treatment: offer small amounts of food once faeces passed (and increase back to normal over around 24h)
If horse does not respond to treatment perform repeat visit - repeat tests, look for improvement / deterioration in clinical parameters and keep an open mind
When to consider euthanasia for colic?
Uncontrollable pain despite potent analgesia
Severe CV compromise - HR >90bpm, PCV >60%, purple mucous membranes
Gastrointestinal rupture
Signs of gastrointestinal rupture following colic? Prognosis?
Frequently due to stomach rupture along greater curvature (nasogastric intubation can be life-saving)
Hopeless prognosis even if surgery attempted
Brown/red ingesta contaminated peritoneal fluid
Profuse sweating
Sudden reduction in pain
Marked progressive increase in HR/PCV
Deterioration of mms
‘Boarding’ of abdomen
Indications for potential need for surgery of a colic cases?
Severe, unrelenting pain Recurrence of pain despite moderate-potent analgesia HR >60bpm Net reflux >2L Deteriorating CV parameters Reduced intestinal motility Increased abdominal distension Deteriorating peritoneal fluid values
Common types of surgical colics?
SI - pedunculated lipoma, epiploic foramen entrapment
Caecum
Large colon - displacements, torsion
Small colon
What parts of the GIT can’t be exteriorised in midline laparotomy for colic surgery?
Stomach Duodenum Base caecum / terminal part of ileum Parts of right ventral and dorsal colons Transverse colon Very proximal and distal parts of small colon Rectum
Post-op recovery procedures for colic surgery?
Place in stable
Belly bandage
Confirm medication - antibiotics, analgesia, others e.g. lidocaine infusion
Oral or IV fluids
Colic checks usually every 4 hours
Decompression of stomach if needed (post-op ileus)
In hand walking every 4h in day
Gradual increase in feeding once on oral fluids
Colic checks?
Observation - attitude/signs of pain, defaecation/urination
Full clinical exam - TPR, GIT sounds, digital pulses
PCV/TP
Incision checked
Catheter site checked
Post operative (colic) care at home?
6 weeks box rest with in-hand walking 2-3 times per day
Skin sutures removed 10-14d post-op by referring vet
8 weeks turnout in small yard/paddock
Normal turnout and gradual return to normal exercise over 6-8 weeks
Complications that can occur following discharge home after colic surgery?
Colic - occurs in around 30% of cases, most episodes respond to medical therapy, may need surgery or euthanasia
Incisional infection - occurs in around 20% of cases, increased risk of incisional hernia
Incisional hernia development - relatively uncommon ~4%, often don’t cause problem
What is ‘Choke’? Clinical signs?
Oesophageal obstruction
Feed becomes impacted within oesophageal lumen - proximal cervical region or distal cervical (thoracic inlet) region
Coughing, ptyalism, dysphagia (food and saliva at nostrils), repeated flexion and extension of neck
Signs usually sudden in onset and associated with eating
Advice to owner for choke?
(most episodes will clear spontaneously)
Take all feed and water away
Monitor for 30 minutes - if no improvement, veterinary examination required
If does resolve spontaneously, provide water but wait 1-2h until feeding (and start with sloppy feeds / grass)
Ask about horse’s dental history/any evidence of quidding behaviour as dental problems should be ruled out
Treatment of choke after not improved for 30 mins?
Full clinical exam - palpate left cervical region
Sedation (a2 agonist/butorphanol +/- butylscopolamine) - calms horse and lowers head (reduces aspiration of fluid) +/- oxytocin (efficacy not proven)
Nasogastric tube - confirm diagnosis, identify level of the obstruction
Lavage oesophagus - warm water, stirrup pump better than gravity flow, *single ended stomach tube
Repeat lavage until obstructed material all removed and tube can be passed into stomach
Aftercare of choke?
Decide if antibiotics needed - risk of aspiration pneumonia
Provide water and gradually reintroduce feed over 24-48 hours - sloppy feed/grass then gradually onto forage
Owner should monitor for nasal discharge/coughing/dullness
Rule out underlying cause - dental exam
Endoscopic evaluation if 2 or more episodes of choke occur - rule out underlying problem e.g. stricture
What if choke cannot be cleared after initial lavage?
If feed is known to have been involved may be appropriate to repeat lavage again in 4-8 hours - left no longer than this (risk of inhalational pneumonia/dehydration)
Endoscopic evaluation required - determine underlying cause, may be required to remove foreign bodies
Occasionally lavage under GA may be indicated
Rarely is oesophageal surgery required (usually best avoided as high risk of complications)
What is the problem with carbohydrate overload (e.g. horse breaking into feed shed)?
Intestinal bacterial fermentation and absorption of endotoxins
- > Colic and severe abdominal distension
- > SIRS, laminitis, diarrhoea +/- death
Initial information needed and clinical exam for carbohydrate overload (e.g. horse breaking into feed shed)?
How much and type of feed they ingested
When occurred
If other horses could have accessed this
If there are other additives in the feed (feed for other species - may need them to get feed label)
Initial clinical examination
Assess vital signs & digital pulses
Check for evidence of colic / abdominal distension
Pass a stomach tube to check for reflux
Treatment for carbohydrate overload (e.g. horse breaking into feed shed)?
Initial management (early stages):
- lavage gastric contents with warm water (within 1-2h of ingestion occuring) and continue until only water is retrieved
- +/- administer activated charcoal (1-3g/kg as slurry)
- administer Flunixin 0.25mg/kg IV q.8h
- perform cryotherapy (ice therapy) of feet (preventing laminitis development)
Later stages once signs of SIRS have developed:
- referral or intensive medical or occasionally surgical management indicated
- prognosis generally poor if signs of colic/laminitis develop
Causes of dysphagia?
Pain: - buccal/lingual abscess - strangles - retropharyngeal abscess - dental pathology - mouth pain/trauma e.g. mandibular fracture - foreign body - masseter myositis - atypical myopathy Neurogenic: - head trauma - guttural pouch disease - pharyngeal paralysis - lead poisoning - botulism - hepatoencephalopathy - EGS - Equine Viral encephalomyelitis Obstructive: - oesophageal obstruction/stricture - neoplasia
Approach to diagnosis for dysphagia?
Obtain a full history
Watch horse trying to eat to determine what phase the problem appears to be in - oral, pharyngeal, oesophageal
Perform full clinical examination
Perform neurological assessment - especially cranial nerves
+/- perform intra-oral examination - in rabies endemic areas do not perform where rabies is a potential cause
+/- Imaging required - radiography, endoscopy
Haematology/biochemistry
Other laboratory tests (based on suspected cause)
Treatment for dysphagia?
Depends on underlying cause Referral may be warranted in some cases NSAIDS Slurry feed/nasogastric intubation \+/- IV fluids General nursing care & ongoing careful observation
Difference in treating partial thickness and full thickness tongue lacerations?
Partial - conservative management
Fill - suturing required (may need referral)
Treatment of incisive plate mandibular fractures in horses?
Can be treated in the field
Sedation and nerve blocks
Intra-oral wiring
Causes of rectal prolapses in horses? Treatment?
Usually secondary to prolonged straining
Diarrhoea
Colic
Heavy parasite burden
Proctitis/mass in rectum
Other causes of repeated straining – dystocia, retained foetal membranes
Grades I, II & III - reduce prolapsed tissue, address underlying cause
Grade IV - surgical management (poor prognosis)
Possible consequences of abdomen trauma in horses?
Rupture of abdominal viscus Body wall tears / rupture Diaphragmatic tears Abdominal haemorrhage Peritonitis
Treatment of incisional hernias post colic surgery?
Conservative treatment initially
- prolonged box rest in some cases
- use of a commercial hernia belt (e.g. CM belly band)
Surgical repair may be required in some
- repair not performed until 4-6 months after initial surgery
- prosthetic mesh placement
Mechanisms of weight loss and causes for each?
Reduced intake
- inappropriate feeding, unable to obtain feed, competition, dental disorders, dysphagia
Reduced digestion, absorption or assimilation of nutrients
- dental disorders, malabsorption syndromes, liver disease
Increased losses
- protein losing enteropathy
Increased requirements
- pregnancy, lactation, sepsis, neoplasia etc
Common causes of weight loss in horses?
Dental disorders Parasitism Inadequate diet PPID Liver disease Malabsorption and protein losing enteropathy (idiopathic, parasitic, infiltrative bowel disease, neoplasia)
What % of its BW should a typical horse eat? Racehorses?
2-2.5%
Racehorses: 1% BW roughage, 4-6kg concentrates
Less common causes of weight loss in horses?
Chronic diarrhoea Abdominal abscess Renal disease Cardiac disease Chronic thoracic disease Non‐GI neoplasia Equine grass sickness
Define chronic and recurrent colic?
Chronic colic = colic signs of variable intensity >/= 48h
Recurrent colic = shorter period of colic pain which recur at variable intervals
Why is colic painful?
Intestinal pain:
- stretch
- inflammation
- ischaemia
- muscle spasm
Interpreting serum proteins from biochemistry in horses?
TP - decreases may be masked by concurrent dehydration
Hypoalbuminaemia - GI loss far more common than renal, effusions (peritoneal/pleural), liver disease rarely a cause
Hypoglobulinaemia - GI loss
Hyperglobulinaemia - chronic inflammatory disease
Hyperfibrinogenaemia - infection, inflammation, neoplasia (stays high for couple of weeks after)
Serum Amyloid A - acute phase protein, more acute marker (better for monitoring)
What does it mean if lymphoblasts in peritoneal fluid? What do they look like?
Lymphoma
Large lymphocytes - >2x size of normal lymphocytes
Diagnostic approach to chronic weight loss?
History and initial clinical exam Rectal exam Diet Teeth Worming history/faecal test Faecal sand test Poss Feed comptetition Biochemistry Peritoneal fluid analysis - cytology Oral glucose absorption test Rectal biopsy Duodenal biopsy Transabdominal/transrectal ultrasound - intestinal ultrasound
Oral glucose absorption test?
Fast overnight
1g/kg in 20% solution via nasogastric tube
Keep horse calm (don’t sedate with a2s)
Normal: >85% increase in blood glucose concentration at 2 hours
Partial: 15-85% increase in blood glucose concentration at 2 hours (SI/LI disease or normal)
Complete: <15% increase in blood glucose concentration at 2 hours (SI disease)
Rectal biopsy for chronic weight loss work up in horses?
Correlation with GI pathology in 50% cases
Mare uterine biopsy instrument
20-30cm inside rectum
Small piece of mucosa from floor at around 4 or 8 o’clock
Submit for histology and culture
Antibiotics and tetanus prophylaxis
What is assessed in intestinal ultrasonography?
Wall thickness
Lumen diameter
Motility
Anatomy
Differential diagnosis for malabsorption and protein-losing enteropathy syndromes?
Cyathostomosis Mixed Strongyle infection Idiopathic Infiltrative bowel diseases Neoplasia Lawsonia (foals 3-11 months)
Infiltrative bowel diseases in horses?
Granulomatous enteritis
Lymphocytic-plasmacytic enteritis
Eusinophilic enteritis
Aetiology unknown - parasites, genetic, food allergy, immune response, infectious agents
Presence of inflammatory cells in intestinal wall lead to malabsorption and protein loss
Treatment for infiltrative bowel diseases?
Non specific
Prednisolone
Dexamethasone - given i morning, monitor for signs of laminitis and infection
Anthelmintics
What is multisystemic infiltrative bowel disease in horses?
Multisystemic eosinophilic epitheliotropic disease
- also often involves skin, particularly around coronary bands, pancreas, liver
- treatment - dexamethasone
Systemic granulomatous disease - skin and other organs may be affected
Forms of equine lymphoma? Age of horses affected?
Alimentary - juveniles and aged horses
Generalised - particularly aged horses, often involves GIT
Solitary - any age group
Cranial mediastinal - any age group
Cutaneous - any age group
Paraneoplastic syndromes - hypercalcaemia, haemolytic anaemia
Clinical signs of lymphosarcoma and other forms of disseminated neoplasia in horses?
Fever Weight loss Peritonitis Pleural effusion Abdominal distension Intra-abdominal mass palpable per rectum Hypercalcaemia/haemolysis/cachexia of malignancy
Treatment of IBD in horses?
Anthelmintic responsive
Steroid responsive in some cases
Common cause of chronic infection of GIT causing weight loss? Treatment?
S equi and R equi
Long term antibiotics
Haematological changes for parasitism in horses?
Neutrophilia
Hypoalbuminaemia
Hyperglobinaemia
Not eusinophilia
Divisions of Equine Gastric Ulcer Syndrome (EGUS)?
EGGUS (glandular) - risk factors not well known poss stress, NSAID related
ESGUS (squamous) - risk factors related to acid injury
Signs of EGUS?
Sometimes subtle and not very evident Vague - weight loss, poor performance Selective appetite, slow eating, eat roughage in preference for grain Bad/cranky behaviour Girthy? Overt colic unlikely
Portions of equine stomach?
Squmaous portion - prone to acid injury, pH 5.4
Glandular acid secreting portion - protected from acid injury by mucous layer, pH 1.8
Why are horses susceptible to EGUS? Predisposing factors for acid injury?
Stomach anatomy - poor mixing, grain portion rapidly fermentable, production of acids
Intermittent feeding v trickle feeding over 18+ hours - continuous gastric acid secretion not associated with meals
High concentrate diets - VFAs -> acid injury, low fibre concentrations -> reduced saliva production - acid buffer
Exercise - gastrin production, increased abdominal pressure can promote acid ‘splashing’ injury due to unprotected upper regions of stomach
Stress - transport, confinement, restriction from exercise or social interaction by stabling
Diagnosis of EGUS?
Gastroscopy
Faecal occult blood not reliable
Treatment for EGUS?
Proton pump inhibitor omeprazole
ESGUS more responsive at lower doses
EGGUS less responsive and requires higher doses
Reduce exposure to risk factors - diet, exercise, stress
Long term dietary supplements
Functions of the equine liver?
Digestive and secretory Metabolic Detoxification/excretory Synthetic Storage
Main causes of jaundice (retention of bilirubin) in horses?
Anorexia (ddx if <120umol/l)
Haemolysis
Sepsis - masks e.g purple mms
Potential clinical signs of liver disease?
Jaundice Weight loss Depression/CNS signs Photosensitisation (phylloerythrin accumulation) Haemorrhage (liver failure) Colic Oedema Diarrhoea Dyspnoea - usually ragwort, laryngeal paralysis Anorexia/inappetance
Diagnosis of liver disease in horses with clinical pathology?
Liver enzymes
- GGT: mainly biliary tree and liver (and pancreas) specific (hepatic and cholestatic), rapid increase, sustained levels over a month
- AST: hepatocellular, similar half life, not organ specific
- SDH: hepatocellular, acute enzyme - rapid increase and short half life
Serum bilirubin
- difficult to interpret
- if increased conjugated portion, likely hepatocellular or cholestasis
Bile acids
- good liver function test
- continuous production so no need to fast
- correlated with severity
Blood ammonia
- failure of gut detoxification
- may predict encephalopathy (not correlated well with cause)
Viral screening, aflatoxins
Liver fluke ELISA
Clotting times
Triglycerides
Where to ultrasound liver in horses?
14th ICS (have 18 ribs)
Risks of taking a liver biopsy from a horse?
Haemorrhage - don’t perform if clinical coagulopathy (but no association found between an abnormal coagulation profile and biopsy complications)
Inappropriate sample e.g. focal lesions
Negative culture >50%
Infections - cover with antibiotics if septic hepatitis
Pneumothorax - rare
Advantage of a liver biopsy?
Biopsy score is the best indicator of prognosis in liver disease >6 poor prognosis Assesses presence of: - fibrosis - irreversible cytopathology - inflammatory ilfiltrate - haemosiderin accumulation - biliary hyperplasia
What is the toxin in ragwort? Why does it cause liver failure?
Pyrrolizidine alkaloid
Alkylates DNA
Anti-mitosis - megalocytosis, fibrosis, persistent toxic effects
5% BW can be lethal
Presentation of ragwort poisoning?
Frequently may only see signs of liver failure just prior to death
Can be delayed disease over a year of exposure
Early clinical signs difficult to detect and non specific e.g. inappetence, weight loss, mild depression
Weight loss, behavioural change and anorexia predominant
Inspiratory dyspnoea - laryngeal paralysis
Severe CNS signs - hepatic encephalopathy, usually depression
Colic - gastric impaction
Photosenstisation
Haemorrhages e.g. epistaxis post tubing
Icterus
Diagnosis of ragwort poisoning?
History
Clinical presentation
Clinical pathology - GGT, alkaloid measurement may be available soon
Ultrasound - non specific
Biopsy - may not always see megalocytosis
Treatment for ragwort poisoning?
Can try supportive - fluid therapy, electrolytes, glucose
Reduce hepatic encephalopathy - moderate-low protein diet, high BCAAs, decrease enteric ammonia - neomycin or metronidazole
Presentation of cholangiohepatitis and cholelithiasis?
Fever, jaundice, colic
Anorexia, photosensitisation
Marked elevations in GGT
What is cholangiohepatitis and cholelithiasis?
Ascending bile duct infection from GIT
G-ves deconjugate bilirubin -> unconjugates precipitates -> choleliths
Diagnosis and treatment of cholangiohepatitis and cholelithiasis?
Ultrasound
Biopsy useful - histo (neutrophils) and culture
Long term antibiotics
Biopsy findings for chronic active hepatitis? Treatment?
Plasmacytic-lymphocytic
Corticosteroids or other immunosuppressive medications e.g. azathioprine
Causes of acute hepatitis in horses? Signs?
Theiler's disease associated virus Other viruses - parvovirus, hepacivirus Aflatoxins Liver fluke Range from mild to severe CNS signs, jaundice, discoloured urine
Hyperlipaemia risk factors in horses?
Breed Obesity Females Age vs insulin resistance Underlying disease Transport, stress, lactation Starvation
Pathogenesis of hyperlipaemia?
Breakdown of stored fat
FAs to liver - energy
Liver poor ketogenic capability, energy production overwhelmed
Triglycerides accumulate in liver and in plasma
Ideally want to promote re-uptake in periphery by LPL to clear plasma, but LPL can’t keep up with HSL and liver
Presentation of hyperlipaemia?
Non specific - anorexia, lethargy, weakness
Can progress to more severe CNS and other signs
Signs may be underlying disease, hyperlipidaemia or secondary liver disease
Hyperlipaemia diagnosis?
Cloudy serum
- TGs > 5mmol/l = hyperlipaemia
- TGs < 5 but > 1.5mmol/l = hyperlipidaemia
Test for liver disease, azotaemia
Treatment for hyperlipaemia?
Treat underlying disease and parasites
Positive energy balance
Correction of dehydration, electrolyte imbalances, acidosis
Other symptomatic therapy
Normalisation of lipid metabolism - insulin? risk of laminitis, avoid if insulin already very high
Prognosis of hyperlipaemia?
Guarded to poor
Mortality >50%
Worse if female, other organ involvement, poor initial response, failure to eat
Get them out of the box especially if used to being out
What types of colic is Anoplocephala perfoliata associated with?
Spasmodic colic
Ileal impactions
Caecal intussusceptions
What is a vet’s role in a horse rescue situation?
Provide triage - assess injury severity
Provide restraint
Provide euthanasia
Advise on welfare
How long do a2 agonists take for onset and duration for horse rescue?
Xylazine: max effect in 2 mins, 20-30 mins duration
Detomidine: max effect in 5 mins, 45 mins duration
Romifidine: max effect in 5-10 mins, 40-60 mins duration
How much to increase an a2 sedation dose if giving IM in a rescue situation rather than IV? What if very excited horse e.g. at end of a race?
IM: double the dose
Excited: double the dose IV
GA for horse rescue?
Sedation with a2 agonist
Induction with ketamine (2.2mg/kg, 11ml of 100mg/ml prep for 500kg horse)
Duration anaesthesia: 15-30 mins
Maintenance:
- top of up 1/4 - 1/2 original dose of sedative and ketamine either at timed intervals or as required
- too much = ataxic recoveries
Constant infusion e.g. xylazine/guaifenesin/ketamine ‘triple drip’ - can use for up to 90 mins (ataxic recoveries if longer)
What medication to use post-colic surgery if refluxing/ileus?
Lidocaine and metaclopramide
Treatment for liver disease -> hepatic encephalopathy?
Prednisolone
+/- Antibiotics (ideally dependent on C + S) - TMPS good empiric choice as activity against G-ves and its high concentration in bile
Low protein, high carbohydrate diet: e.g. grass, oat hay, concentrate grains, sugar beet, linseed (avoid alfalfa, beans and leguminous grass/hay)
High BCAAs
Neomycin or metronidazole - decreases enteric ammonia
In feed supplements containing milk thistle extracts, SAMe, vitamin E, selenium
Frequent small meals (3-6/day) to reduce peaks of high serum ammonia due to reduced intensity of hindgut fermentation (may prevent clinical signs)
What does it mean if lymphoplasmacytic on liver biopsy?
Immune mediated
Differentials for foal with encephalopathy?
Intestinal hyperammonaemia - parasitic most common, colitis
Hepatic - PSS, Tyzzer’s, herpesvirus
