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Michaelmas 5th year > Equine colic > Flashcards

Equine colic Flashcards

1
Q

What chemical restraint is most commonly used for horses with colic any why

A

Xylazine because it is short acting; longer acting alpha 2 agonists will continue to have a negative effect on blood pressure i.e when going into surgery

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2
Q

When is nasogastric intubation essential in a colic case

A

When there is a SI obstruction (or rarely a gastric outflow issue)
Must do to avoid risk of stomach rupture

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3
Q

What is an abnormal amount of reflux to get back via nasogastric tube

A

> 2 L

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4
Q

Why might we give buscopan before a rectal examination

A

Because it is smasmolytic and anticholinergic therefore relaxes the rectum
This makes it easier to palpate organs + reduces risk of rectal tears

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5
Q

What effect of buscopan do we need to be aware of in terms of clinical monitoring

A

It causes a transient rise in heart rate

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6
Q

What colic cause might a horse which usually grazes full time but has been brought into box rest

A

Pelvic flexure impaction

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7
Q

How do we pass a nasogastric tube in a horse and how do we know we are in the right place

A

Pass tube up ventral meatus to nasopharynx, then flex chin to check to encourage swallowing
Suck on tube; should get negative pressure in oes (unlike trachea), watch down left neck, may have gurgle of gas in stomach

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8
Q

What might we feel when moving around during an equine rectal

A

12 o’clock feel aorta pulsing, on right feel caecum, large colon is ventral with pelvic flexure midline/left, spleen on left side body wall, left kidney caudal pole around 10 o’clock

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9
Q

What are 2 major red flags from rectalling a horse; i.e surgical or euthanasia are only options

A

Distended small intestine
Suspicion of colon torsion

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10
Q

What does serosanguinous fluid from abdominocentesis indicate

A

Devitilised small intestine; this is a surgical lesion

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11
Q

Where is it best to measure lactate concentration for predicting if lesion is surgical

A

Abdominocentesis is more sensitive than blood lactate

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12
Q

What abdominocentesis lactate level is associated with non-survival

A

> 16mmol/l
Indicates devitilised intestine

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13
Q

What does increased serum lactate indicate as compared to peritoneal fluid lactate

A

Serum: shows anaerobically respiring peripheral tissue
Peritoneal fluid lactate shows devitilised intestine

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14
Q

In what condition would GGT be especially elevated

A

Right dorsal displacement of the colon because this crushes the duodenum and causes bile duct obstruction and cholestasis

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15
Q

What heart rate would generally cause you to want to refer a colic case

A

> 60bpm

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16
Q

What basic treatment would you give for spasmodic/gas colic

A

Analgesia and buscopan

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17
Q

Treatment for pelvic flexure impaction

A

Enteral fluid (isotonic) therapy; at least 1L/100kg BW to overhydrate the mass and allow it to be passed

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18
Q

How can we reduce the risk of pelvic flexure impactions in hospitalised horses

A

Give water buffet to encourage drinking

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19
Q

What type of colic is tapeworm a risk factor for

A

Spasmodic/gas colic
Caecal impaction

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20
Q

What are the two types of caecal impaction

A

Type 1 = impaction with dry ingesta
Type 2 = due to underlying motility disorder

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21
Q

What do we need to be aware of when assessing the clinical signs of caecal impaction

A

Signs may be subtle up to the point of rupture
Gut content can still move through so still have some faecal output
Go to surgery quicker than pelvic flexure impaction but otherwise treat similarly

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22
Q

What is the most common cause of colic

A

Spasmodic/gas colic

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23
Q

What signs might we see with sand enteropathy

A

Diarrhoea due to abrasive action of sand
Weight loss
Acute colic

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24
Q

Treatment of sand enteropathy

A

Magnesium sulphate and psyllium together via nasogastric tube

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25
Q

Diagnosis of right dorsal displacement of the large colon

A

On rectal feel gas distended colon, tight taenial bands
On ultrasound see colonic mesenteric vessels against right body wall (which normally wouldn’t be seen)
Increased GGT concentration often

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26
Q

What happens in right dorsal displacement of colon

A

Pelvic flexure is displaced cranially towards diaphragm and colon moves cranially to sit either medially or laterally to the caecum

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27
Q

What happens in left dorsal displacement of the large colon

A

Pelvic flexure moves dorsally into the left nephrosplenic space

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28
Q

How would we diagnose left dorsal displacement of large colon

A

On rectal exam may feel colon in nephrosplenic space
On ultrasound find that large colon obscures the left kidney on the left paralumbar fossa

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29
Q

What is equine grass sickness

A

Equine dysautonomia due to enteric and autonomic neuronal degeneration
Get functional obstruction which can lead to secondary impactions
Pathogenesis unclear; may be related to C botulinum and neurotoxin spread

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30
Q

Risk factors for equine grass sickness

A

Strongly associated with particular paddocks
Recent movement to new pasture = main risk; recent anthelmintics, disturbance of pasture

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31
Q

What are the categories of equine grass sickness and which might survive

A

Acute is fatal within 48 hours
Subacute is fatal within a week
Chronic has 50% survival rate

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32
Q

Diagnosis of equine grass sickness

A

Ileal biopsies is gold standard

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33
Q

How to treat chronic EGS and which cases would not be suitable for treatment

A

If very dysphagic probably not suitable as high risk of aspiration pneumonia

Nutritional support, analgesia, hydration

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34
Q

Signs of post-operative ileus

A

Nasogastric reflux, distended small intestine, discomfort, tachycardia

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35
Q

Management of post operative ileus

A

nasogastric intubation, early feeding post surgery if done, analgesia

Don’t overload with fluids
Stop NSAIDs early since these can stop mucosal healing
Give prokinetics

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36
Q

Rules of thumb with using prokinetics after surgery to stop ileus

A

Give lidocaine for 24 hours
If still has ileus then give metoclopramide; then could double metoclopramide if needed

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37
Q

Diagnosis of peritonitis

A

Pyrexia of unknown origin, anorexia, half of them colic
Increased inflammatory markers
On abdominocentesis see turbid colour fluid with increased cell count and total protein, often high lactate low pH

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38
Q

Treatment of peritonitis

A

Use broad spectrum antibiotics until culture results come through
Supportive treatment INCLUDING ICING FEET CONTINUOUSLY to prevent laminitis

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39
Q

Indications for referring for colic surgery

Rectal fndings
Peritoneal tap findings

A

On rectal: feeling distended small intestine, colonic displacement evidence (tight taenial bands, gas filled distended viscus)

> 2L fluid from nasogastric fluid

On peritoneal tap: high WBCs, serosanguinous fluid (RBC leaking from strangulated gut), high peritoneal lactate

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40
Q

A combination of colic and pyrexia might be an indication to…

A

Not go into surgery
Probably peritonitis

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41
Q

How does the prognosis vary with by surgical lesion location for colic surgery

A

Small colon best, then large intestine, then small intestine, then caecum

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42
Q

What is pyloric/duodenal stenosis

A

Rare congenital condition seen in foals

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43
Q

Non-strangulating lesions of the small intestine

A

Simple impaction; ascarids, poor feed, motility issue, muscle hypertrophy

Intestinal neoplsia

Anterior enteritis

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44
Q

Where can small intestinal entrapment occur

A

Anywhere
- Natural locations: epiploic foramen, inguinal ring, umbilicus

  • Through tears made in mesentery, diaphragm, gastrosplenic ligament
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45
Q

Why would we do a caecal bypass in surgical cases of caecal impaction

A

To prevent recurrence as this may be due to a primary hypomotility issue

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46
Q

Preventative measures for recurrent large colon displacement

A

Left dorsal displacement: laparoscopic closure of the nephrosplenic space
In right dorsal displacement: do a colopexy to suture colon to body wall

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47
Q

Risk factors for colon volvulus/torsion

A

Large horses, post-foaling, diet change

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48
Q

Important viral cause of diarrhoea in horses

A

Coronavirus

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49
Q

Signs of coronavirus infection in horses

A

Pyrexia, lethargy, anorexia, diarrhoea, leukopenia

50
Q

How can be diagnose coronavirus in horses

A

Via faecal PCR transported on ice; don’t get background shedding so if we see a positive this ikely means it is clinically relevant

51
Q

Signs of salmonella in horses

A

Variable
May be severe, acute colitis
Or just generally sick

52
Q

What type of pathogen is salmonella and how does it transmit

A

Inracellular; faeco oral transmission and lives in enterocytes

53
Q

Diagnosis of salmonella in horses

A

5 daily faecal samples
- PCR is much more sensitive than culture

54
Q

When might we use antimicrobials in salmonella cases

A

If very neutropenic i.e <1 x 10^9

55
Q

Treatment of clostridia

A

Metronidazole, symptomatic treatment

56
Q

Diagnosis of clostridia

A

Must detect toxin; faecal sample and toxin ELISA

57
Q

Which clostridia species are we thinking about in horses

A

C difficule (makes A and B toxnis)
C perfringens (makes enterotoxin and beta toxin)

58
Q

When do we see lawsonia cases

A

Mostly in foals 4-7 months (weanlings)

59
Q

Treating lawsonia in foals

A

Oxytetracycline, doxycycline

60
Q

Two manifestations of NSAIDs causing iatrogenic diarrhoea and what is the mechanism

A

Inhibition of prostaglandin production, loss of mucosal defence so ulcerated mucosa and protein losing enteropathy

Manifestations = right dorsal colitis, or generalised NSAID toxicity

61
Q

What sign might horses with NSAID toxicity present with before diarrhoea

A

Ventral oedema; due to protein losing enteropathy from mucosal ulceration

62
Q

Treating diarrhoea caused by NSAID use

A

Misoprostol to replace prostaglandins, sucralfate?
Use more COX2 selective NSAIDs moving forward

63
Q

How can macrolides directly cause diarrhoea and how might this affect who we give them to

A

Agonism on motilin receptors so get increased motility which causes diarrhoea
Don’t give to horses older than 5 months

64
Q

How does carbohydrate overload cause diarrhoea

A

Spill over of undigested carbohydates into large intestine; rapid fermentation by gram +ve lactic acid producing bacteria
Fall in pH kills gut microbial population
Lactic acid acts via osmotic draw

65
Q

What is chronic diarrhoea

A

Diarrhoea that has gone on for longer than 7-14 days

66
Q

Treatment of acute diarrhoea

A

Fluids: monitor electrolytes, correct metabolic acidosis
Analgesia
May give anyto-endotoxxins e.g polymyxin B

67
Q

What is di-tri-octahedral smectite

A

Biosponge used to bind bacterial toxins

68
Q

How can psyllium help in diarrhoea cases

A

Provides short chain fatty acids for enterocytes to use

69
Q

Causes of crhonic diarrhoea

A

Diet
IBD
Sand enteropathy
NSAID use
Peritonitis
Chronic infection

70
Q

Signs of prepharyngeal dysphagia

A

dropping feed, hypersalivation, can’t prehend food

71
Q

Signs of pharyngeal or post-pharyngeal dysphagia

A

Coughing, nasal discharge of eed and water, neck extension when following

72
Q

What drug choice might we make depending on whether obstruction thought to be proximal or distal in choke case

A

If more proximal: use oxytocin to act on smooth muscle of prox oes
If more distal: use buscopan to act of smooth muscle of distal oes

73
Q

Risk factors for choke

A

Key ones = poor dentition, rapid ingestion of dry feed
Also: eating when sedated, oesophageal disaese e.g abscess, functional disease, diverticula

74
Q

Approach to a case of choke

A

Sedate heavily with long acting alpha-2 agonist
Keep head low to reduce aspiration pneumonia risk
Can use buscopan/oxytocin to relax smooth muscle of oesophagus
Pass nasogastric tube and lavage with pain water

75
Q

Which side of the neck does the oesophagus run down

A

Left side; palpate here in choke

76
Q

Presenting signs with choke

A

Head and neck outstretched
Coughing
Food coming from nostrils
Distressed or very quiet

77
Q

Signs of equine gastric ulceration syndrome

A

Fussy eaters, reacting to girth tightening, poor condition, grumpy etc

78
Q

Two types of EGUS

A

Equine squamous gastric disease
Equine glandular gastric disease

79
Q

Which type of EGUS is it appropriate to use a grading system for

A

Just equine squamous gastric disease

80
Q

Risk factors for ESGD

A

Exposure of the squamous mucosa to acid; increased likelihood with starchy diet, stress, fasting

81
Q

Dietarry management for EGUS

A

low starch diet
- High fibre + oil for calorie replacement

82
Q

Treatment for ESGD

A

Omeprazole orally for 28 days then re-scope
+ hold off exercise during this time

83
Q

Treatment for EGGD

A

Omeprazole and sucralfate for 28 days then rescope
This can be harder to treat than ESGD; may want to use injectable omeprazole off license, can try misoprostol
Reduce exercise to twice per week during this time

84
Q

What is it important to remember when perscribing misoprostol for managing EGGD

A

Cause abortion in humans; must make this very clear to owner

85
Q

How does using injectable omeprazole work and what should we be aware of

A

INject every 5-7 days
Causes swelling at injecting site and very painful

86
Q

What things can lead to gastric impactions in horses

A

Usually eating feedstuff that swells or lots of bedding
Can also be due to dysmotility disorders or outflow tract obstructions

87
Q

How can we diagnose IBD

A

Biopsy
Glucose absorption test

88
Q

How does the oral glucose absorption test work

A

Starve and take bloods for baseline glucose
Stomach tube with 1g/kg 20% glucos solution; then blood sample every 30 mins to look at increase in glucose level
–> Total failure when <15% increase in glucose levels

89
Q

Clinical signs of IBD

A

Weight loss despite good appetite, mild recurrent colic, diarrhoea (chronic or intermittent)

90
Q

What is duodeneitis-proximal jejunitis and how can we differentiate it from strangulating SI lesions

A

Inflammation of proximal SI, mimics obstructive disease in presentation (distended SI, gastric reflux)
BUT peritoneal tap fluid has lower cell count that strangulating lesions do

91
Q

What are cyathostomins

A

Small red round worms = nematodes
(strongyles)

92
Q

Larval cyathostominosis characteristics

A

Sudden diarrhoea in young horses (mainly)
Due to emergence of late stage larvae from cysts causing inflammation of large intestine following arrested development
= ubiquitous parasite but only causes disease where there is a heavy burden

History of lethargy, failure to gain weight

93
Q

Signs and pathogenesis of larval cyathostominosis

A

Damage to large intestine causing protein losing enteropathy
Get low albumin on bloods and see dependent oedema
Weight loss, diarrhoea, lethargy

Anaemia of chronic disease

94
Q

Treatment of larval cyastominosis

A

PLasma transfusion to replace lost albumin
Steroids to reduce inflammation
Worming treatment

95
Q

How to monitor resistance to wormers

A

Do faecal egg count reduction tests yearly
Give de-wormer and then do egg count two weeks later; expect no strongyle eggs

96
Q

What is a good cut off for deciding to worm (cyastomes)

A

200-500epg

97
Q

PPPof cyathostomins

A

Depends on length of arrested development; can be from 5 weeks to 2 years

98
Q

PPP of parascaris univalens

A

75-90 days

99
Q

Signs of parascaris univalens

A

diarrhoea or constipation
colic
lethargy
weight loss
rough coat
pot belly

100
Q

Why do we only see parascaris univalens in foals <1 yr

A

Strong protective immunity

101
Q

Resistance to wormers in cyathosomes vs parascaris univalens

A

Cyathostomes: v high resistance to benzimidazoes, pyrantel
–> Macrocylic lactones still work

Parascris univalens: v high resistance in macrocyclic lactones
–> less in bendendazole and pyrimidines

i.e opposite of each other

102
Q

What is the intermediate host of the tapeworm in horses

A

Oribatid mite

103
Q

Which tapeworm species is found at the ileocaecal valve

A
  • Anoplocephala perfoliata
104
Q

Clinical disease caused by tapeworm

A

inflammation, necrosis and reddening at site of attachment, thickening of area
Assocaition with intusussecption, impaction, gut rupture

105
Q

How can we use ELISAs in tapeworm diagnostics

A

Best for herd management levels; about EXPOSURE not infection

106
Q

What do we look for on. a post-treatment 24hr faecal analysis (tapeworms)

A

A high number of eggs shows that there was an active infection before deworming (tapeworm has exploded due to wormer)

107
Q

Strongylus vulgaris life cycle

A

Horses eat infective L3 on pasture –> migrates along arteries and congregates at root of mesentery; returns to GI tract as adult
PPP 6-7 months

108
Q

How does strongylus culgaris causes disease

A

Migration along arteries irritated endotherlium; thrombi develop along this and travel down to smaller vessels on GI tract
Get non-strnagulating infarction of intestines –> colic

109
Q

What is unique about the lifecycle of strongyloides westeri

A

Half the lifecycle is done in the adult horse; arrest in mammary tissue and devilvered in milk to foals
Then finish life cycle
So can be shed from foal within just 5 days

110
Q

What worm egg looks small and thin shelled with larvae inside

A

Strongyloides westeri

111
Q

What is ‘frenzy’ with strongyloides westeri infection

A

Skin infection due to larvae present in heavily infested bedding

112
Q

Do gastrophilus bots cause issues

A

No

113
Q

Which type of caecal impaction is more likely to rupture so should be taken to surgery sooner

A

Due to underlying motility disorder

114
Q

What makes a caeco-colic intussusception strangulating

A

Obstruction of the caecocolic artery

115
Q

Medical treatment for left dorsal displacement of the colon

A

Phenylephrine and lunging
- Avoid phenylephrine in older horses>15years due to risk of fatal haemorrhage

116
Q

What GI disorder is salmonella implicated in

A

Small colon impaction

117
Q

Are post-surgical adhesions more common in foals or adults

A

Foals
Need careful tissue handling and use of fluids in the area

118
Q

Which parasite has thick walled eggs

A

Parascaris univalens
It is eggs that are eaten when grazing

119
Q

Treatment of larval cyathostominosis

A

PLasma transfusion to replace lost albumins
Steroids for inflammatino
Worming to remove burden

120
Q
A

Michaelmas 5th year (41 decks)

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