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CVSOH 4 > Equine Gastrointestinal > Flashcards

Equine Gastrointestinal Flashcards

1
Q

What are cyathostomes?

A
  • Small redworm
  • Can encyst in large intestinal mucosa for 2-3 years
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2
Q

What is larval cyathostomiasis?

A

Mass emergence of hypobiosed larvae causes massive inflammatory reaction that leads to severe diarrhoea, which is often fatal.

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3
Q

What is the effect of strongyles?

A
  • Cause problems during migration of larvae – direct migratory path
  • Verminous arteritis
  • From gastrointestinal tract to cranial mesenteric artery and back again
  • Can cause ischaemic areas of large intestine – fatal
  • Adults live in large intestine
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4
Q

What is the effect of strongyles westeri in foals?

A
  • Infects foal through dam’s milk or via skin penetration
  • Induces diarrhoea around 6 months later
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5
Q

What is unique about strongyles westeri?

A

Has free living reproductive cycle

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6
Q

What is the lifecycle of Dictyocaulus arnfieldi?

A
  • Lungworm lifecycle is not completed in horse
  • Adult worms do not attain sexual maturity here
  • Donkey is usual host
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7
Q

What is the effect of oxyuris equi?

A
  • Adults in colon
  • Female worm migrates down gastrointestinal tract
  • Deposits eggs around anus cemented to the skin with a thick sticky substance
  • Horse develops severe anal pruritus
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8
Q
A
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9
Q

What is the effect of tapeworms in equine?

A
  • Incidence of spasmodic colic increases with burden
  • Can cause intussusception
  • Thickened small intestine wall at ileo-caecal junction, leads to food impaction (due to narrowing)/ileal impaction – surgical colic
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10
Q

What is the effect of gastrophilus (bots)?

A
  • Not proven to cause any problem
  • Seen more with advent of gastroscopy
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11
Q

What is the clinical significance of stronyles, tapeworm and cyathosomes in equids?

A

Stronglyes are a rare cause of disease but resistance and tapeworm and encystsed cyathostomes are an important cause of disease that may be neglected.

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12
Q

What are refugia?

A
  • Refugia are those parasites in the horse’s environment that are not exposed to an anthelmintic at each dose
  • Pasture stages (eggs, L1, L2, L3) are not affected when you treat a horse
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13
Q

How do refugia affect resistance?

A

Increasing refugia is likely to slow development of resistance

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14
Q

How is resistance in alimentary parasites tested?

A

Faecal egg count reduction test

Doesn’t work for tapeworms

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15
Q

How are alimentary parasites controlled in horses?

A
  • Targeted worming (worm those that need it)
  • Poo-picking fields weekly
  • Not overgrazing
  • Consider needs of adults, foals, pregnant mares
  • Different things at different times of year
  • What to do when a new horse arrives
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16
Q

What anthelmintics are used for cyathostomes in horses?

A
  • Ivermectin will kill adults but you need to kill encysted ones too
  • Need moxidectin or 5 day course fenbendazole bits lots of resistance – as this kills adults and encysted
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17
Q

What anthelmintics against strongyles in horses?

A
  • Ivermectin
  • Moxidectin
  • Pyrantel
  • Fenbendazole
  • Try to use ivermectin
  • Save moxidectin for a resistance problem and encysted cyathostome
  • Pyrantel and fenbendazole not as effective (resistance)
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18
Q

When are horses wormed against strongyles?

A

It is okay to have a low level of strongyle infestation, as this helps against resistance. So FEC, de-worm for strongyles if greater than 200 eggs/gram faeces

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19
Q

What anthelmintics are used for parascaris in horses?

A
  • Most sensitive to pyrantel
  • Then avermectins
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20
Q

What anthelmintics are used against strongyloides westeri and when are horses wormed against this?

A
  • Ivermectin or fenbendazole
  • De-worm the mare a couple of weeks before due date
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21
Q

What anthelmintics are used against dictyocaulus and gastrophilus in horses?

A

Ivermectin (moxidectin)

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22
Q

What anthelmintics are used against oxyuris in horses?

A
  • Ivermectin
  • Pyrantel
  • Fenbendazole
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23
Q

What anthelmintics are used against tapeworm in horses?

A
  • Praziquantel
  • Double dose pyrantel
  • Twice a year
  • Now do tapeworm ELISA (blood or salivary)
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24
Q

In targeted dosing of horses, when are horses treated?

A
  • Treat when over 200 strongyle eggs/gram faeces
  • For middle-aged horses consider treating at 400epg?
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25
Q

What are the advantages of targeted dosing?

A
  • For some it will be cheaper than interval dosing
  • Can identify very high burdens
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26
Q

Describe the results of a blood test for tapeworm.

A
  • Looks for antibodies to tapeworm
  • Can tell if the animal has been exposed
  • But if then treated, antibodies will stay high for even up to 6 months
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27
Q

What pasture management is used to prevent alimentary parasites in horses?

A
  • Twice weekly manure removal
  • Increased stocking density increased helminth pasture burdens
  • Grazing with ruminants – will reduce number of strongyles, ascarids and tapeworms on pasture
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28
Q

What should happen in a typical suggested plan against alimentary parasites for non-gravid horses in Feb/March?

A

FEC (strongyles), de-worm with ivermectin if >200eggs/gram

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29
Q

What should happen in a typical suggested plan against alimentary parasites for non-gravid horses in May?

A
  • FEC (strongyles), de-worm with ivermectin if >200eggs/gram
  • Tapeworm ELISA
  • Praziquantel if tapeworm
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30
Q

What should happen in a typical suggested plan against alimentary parasites for non-gravid horses in August?

A

FEC (strongyles), de-worm with ivermectin if >200eggs/gram

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31
Q

What should happen in a typical suggested plan against alimentary parasites for non-gravid horses in Nov/Dec?

A
  • Tapeworm ELISA
  • Praziquantel for tapeworm if indicated
  • Cyathostome ELISA in low risk group, otherwise just treat
  • Moxidectin for encysted cyathostomes
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32
Q

How is a young horse between 1 and 4 years old prevented against alimentary parasites?

A
  • 3-4 treatments per year
  • Include one moxidectin/praziquantel late autumn/early winter
  • May need a second larvicidal treatment 3 months later
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33
Q

How is a new horse to the yard prevented against alimentary parasites?

A
  • 12-24h before turnout, moxidectin plus praziquantel
  • Keep off pasture 3 days
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34
Q

You have had to refer a 2 year old colt to a hospital with surgical colic. An ileal impaction was found. What anthelmintic should you use on his pasture mates?

A

Praziquantel

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35
Q

What is the role of the equine large intestine?

A

100l fluid/24h enters GI tract and is reabsorbed in large intestine

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36
Q

Distinguish diarrhoea in foals and adult horses.

A

Diarrhoea in the adult horse is large intestinal

In foals can be small and/or large intestinal

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37
Q

What are the mechanisms of diarrhoea in horses?

A
  • Malabsorption
  • Increased secretion
  • Decreased transit time (abnormal motility)
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38
Q
A
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39
Q

What are the differentials of chronic diarrhoea in horses?

A
  • Genetic – granulomatous bowel disease
  • Infectious – chronic salmonellosis, strongylosis, cyathostomiasis, sand (inflammatory)
  • Autoimmune – inflammatory and granulomatous bowel diseases
  • Neoplasia – lymphoma most common
  • Chemical ad toxic/iatrogenic – NSAID use/abuse (right dorsal colitis), antibiotic induced
  • Some non-gastrointestinal causes, such as some liver diseases
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40
Q

What are the differentials of acute diarrhoea in horses?

A
  • Infectious – salmonella, clostridia toxins, rhodococcus in foals, cyathostomiasis, rotavirus in foals
  • Nutritional – sudden diet change (shouldn’t be sick)
  • Idiopathic
  • Chemical and toxic/iatrogenic – NSAID use/abuse (right dorsal colitis), antibiotic induced
  • Some non-gastrointestinal causes, such as some liver disease
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41
Q

How is dehydration in acute cases of diarrhoea tested?

A

PCV, TP, heart rate

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42
Q

How is endotoxaemia in cases of diarrhoea tested?

A

Clinical exam, heart rate, mmbs

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43
Q

How is inflammation in cases of diarrhoea tested?

A

Fever

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44
Q

How is protein loss in cases of diarrhoea tested?

A

TP and albumin (can have normal TP if high globulin from inflammation and low albumin, such as some cyathostomiasis), ventral oedema (if loss of protein, but if dehydrated won’t have enough fluid to create ventral oedema)

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45
Q

What can biopsies of the gastrointestinal tract diagnose?

A
  • Inflammatory bowel diseases (IBD)
  • Neoplasia
  • Culture (Salmonella)
  • Encysted cyathostomes
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46
Q

What are the advantages and disadvantages of rectal biopsies?

A

Easy, low risk, cheap but care with interpreting results (taking a rectal sample to tell you what is going on in the colon – not accurate)

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47
Q

What is intestinal biopsying?

A
  • Laparoscopy v. laparotomy
  • Standing v. GA
  • Consider if rectal biopsy was unrewarding
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48
Q

What can abdominoparacentesis diagnose?

A
  • Neoplasia – about ¼ lymphoma cases and ¾ squamous cell carcinoma cases shed cells
  • Inflammatory cells in IBD
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49
Q

What can abdominal ultrasound diagnose?

A

Thickened intestinal wall, may see in some cases:

IBD
Right dorsal colitis (NSAIDs)
Neoplasia

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50
Q

How is dehydration in horses treated?

A
  • Make a fluid plan – current dehydration + ongoing losses + maintenance
  • IV fluids usually best
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51
Q

How is electrolyte imbalance in horses treated?

A
  • Feed
  • Then spike fluid bags as required
  • Need to hydrate
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52
Q

How are acid base disturbances treated in horses?

A

Hydrate

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53
Q

How is hypoproteinaemia treated?

A
  • Plasma transfusion
  • May need to repeat
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54
Q

How is endotoxaemia in horses treated?

A
  • Flunixin, judicious as can give colitis in itself
  • Polymyxin B – binds LPS
  • Ice feet for laminitis – reduces perfusion of endotoxin down to the feet
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55
Q

How is colic in horses treated with medication?

A
  • Flunixin (care, as can cause colitis in itself)
  • May need opioids
  • Spasmolytics
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56
Q

How is bacteraemia and bacterial overgrowths in horses treated?

A
  • If sick/toxic – give penicillin, gentamicin (do TDM), metronidazole?
  • Take faecal and blood culture first
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57
Q

Why do you need to watch for thrombophlebitis in horses with bacteraemia or bacterial overgrowths?

A

Horses with diarrhoea have a lot of bacteria in the blood, which likes to sit at IV catheter where it is receiving IVFT and cause thrombophlebitis

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58
Q

What is transfaunation?

A
  • Filter faeces from a healthy horse from the sick horse’s home environment, mix with warm water
  • Nasogastric tube it
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59
Q

Why is blood flow to the colon wall encouraged?

A
  • For healing of inflamed colon
  • Including colonic ulceration
  • Will also help gastric ulceration
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60
Q

What are 2 drugs that can help gastric ulceration?

A

Oral sucralfate
Oral misoprostal

Both are PG agonists

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61
Q

What are some treatment extras for diarrhoea in horses?

A

Bio-Sponge
Yeasacc
Probiotics?
Nursing

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62
Q

What are the 4 clinical syndromes of salmonella enterica in horses?

A
  • Inapparent infections with latent or active carrier states (2%)
  • Depression, fever, anorexia, neutropenia without diarrhoea or colic
  • Acute enterocolitis with diarrhoea
  • Septicaemia with or without diarrhoea
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63
Q

What is the epidemiology of salmonella enterica in horses?

A
  • Faeco-oral transmission
  • Can persist in environment
  • If immune defences compromised (stress, illness) – carriers can get diseased, easier to get infected
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64
Q

What are the characteristics of acute enterocolitis caused by salmonella enterica in horses?

A
  • Severe inflammation, ulceration, even infarction
  • Fever and anorexia
  • Endotoxaemia - due to inflammation bacteria/LPS can cross to bloodstream
  • Diarrhoea 24-48 hours after onset of pyrexia - severe, very dehydrated, mild/moderate colic, protein losing enteropathy
  • Neutropaenic early on – low white cell count as lost form the gut
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65
Q

What are the consequences of endotoxaemia caused by salmonella enterica in horses?

A
  • Endotoxic shock – fever, tachycardia, congested mucous membranes, weakness, organ failure
  • Risk laminitis
  • Risk thrombophlebitis
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66
Q

When are horses isolated with salmonella enterica?

A

Any 2 of: pyrexia, depression, diarrhoea, leukopaenia – isolate, assume they are infectious until proven otherwise

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67
Q

How does clostrida affect the equine gastrointestinal tract?

A
  • Clostridia part of normal gut flora – but not those producing enterotoxin
  • Can be triggered by antibiotic administration
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68
Q

How can clostridia be diagnosed in horses?

A
  • Faecal culture – high numbers of clostridia, toxin
  • Presentation, similar to other causes of colitis
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69
Q

What is lawsonia intracellularis?

A
  • Obligate intracellular pathogen
  • Induces proliferative enteropathy in small intestine (gets very thick)
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70
Q

What is the proliferative response of the intestinal mucosa in response to lawsonia intracellularis?

A
  • Alters absorption of nutrients
  • Alters fluid secretion – by disrupting the architecture of the villi and altering maturation of epithelial cells into absorptive cells
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71
Q

What is the effect of lawsonia intracellularis?

A
  • Inflammatory response
  • Malabsorption – diarrhoea, severe weight loss, protein-losing enteropathy
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72
Q

What are the clinical signs of lawsonia intracellularis in foals 4-6 months old?

A

Ill-thrift
Weight-loss
Peripheral oedema
Diarrhoea
Colic

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73
Q

What is the clinical findings of lawsonia intracellularis?

A
  • Moderate-often severe hypoalbuminaemia
  • Hyperfibrinogenaemia
  • Anaemia
  • Marked thickening and oedema of intestinal wall
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74
Q

How is lawsonia intracellularis treated?

A
  • Supportive which may include plasma transfusion
  • Doxycycline until clinical signs, hypoproteinaemia, ultrasonographic evidence of intestinal thickening resolve
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75
Q

What are the clinical signs of cyathostomiasis?

A

Acute diarrhoea which can then become chronic
Weight loss
Ventral oedema
Intermittent pyrexia
Intermittent colic

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76
Q

How is cyathostomiasis diagnosed?

A
  • Larvae in faeces
  • Faecal sample
  • Rectal biopsy – large intestinal biopsy
  • Post mortem
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77
Q

How is cyathostomiasis treated?

A
  • As for colitis but need to deworm
  • Get massive inflammation when kill parasites, so then colitis worse
  • Moxidectin
  • Less inflammation and often more effective
  • Concurrent corticosteroids
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78
Q

What are the clinical signs of right dorsal colitis induced by NSAIDs?

A

Inflammation and ulceration
Anorexia
Lethargy
Colic
Diarrhoea – varying in severity, can be acute or chronic
Usually protein losing enteropathy causing ventral oedema

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79
Q

How is right dorsal colitis induced by NSAIDs diagnosed?

A

Thick colon wall on ultrasound – poor sensitivity and specificity

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80
Q

How is right dorsal colitis induced by NSAIDs treated?

A
  • Stop NSAIDs
  • Advice against NSAID use in the future
  • Opioids and buscopan, paracetamol?
  • Rarely, surgical resection
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81
Q

How is antibiotic induced colitis treated?

A
  • If antibiotics mild, just stop
  • Otherwise, may need penicillin, gentamycin, metronidazole (usually clostridial)
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82
Q

Distinguish large and small intestinal IBD in horses.

A

Can have weight loss – mostly with small intestine

Diarrhoea – large intestine

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83
Q

How is IBD in horses diagnosed?

A
  • Ultrasound – some will have thickened gut wall
  • Peritoneal fluid sample – inflammatory cells?
  • Biopsy - rectal biopsy first, small/large intestinal standing laparoscopy v. laparotomy
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84
Q

How is IBD in horses treated?

A

Corticosteroids
Resection?
Short fibre diet?
Yeasacc?

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85
Q

How is foal heat diarrhoea managed?

A

Mild, self-limiting

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86
Q

How is rotavirus in foals managed?

A

Common, vary in severity

Supportive treatment
Test for virus in faeces
Stable hygiene
Vaccinate

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87
Q

How is bacterial gastrointestinal disease in foals classified?

A

Up to 2 weeks old think gastroenteritis = failure of passive transfer or septic foals

3 months plus foals might be rhodococcus

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88
Q

You see a horse which is dull and has a fever. What must you do?

A

Isolate

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89
Q

What does a high heart rate indicate?

A

Pain, dehydration, endotoaxaemia

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90
Q

You see a horse with mild diarrhoea who does not seem systemically ill. Treatment?

A

Transfaunation, transfaunation and biosponge or nothing

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91
Q

What is done in the face of an obstruction?

A

Pass a tube – fluid builds up and cannot get past that point so builds up in the stomach, which needs emptying with a tube, as horse’s cannot vomit and will rupture stomachs

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92
Q

When can flunixin be used?

A
  • You have done a thorough investigation
  • You follow up the progress of your case
  • Pain despite full dose flunixin (1.1 mg/kg) = surgery
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93
Q

What analgesic medications are used in medical colic?

A
  • IV phenylbutazone for mild – moderate pain
  • Often I have given hyoscine (Buscopan) to aid rectal examination
  • Sedate with ideally xylazine (short-acting better if c-v compromised) for your own safety for rectal
  • If no access to bute then consider half dose flunixin
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94
Q

What is spasmodic colic?

A

Spasm of muscle layers in small intestine – causing pain

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95
Q

What are the predisposing factors of spasmodic colic?

A
  • Excitement
  • Physical exertion
  • Fatigue
  • Parasite migration
  • Mouldy feed
  • Changing diet
  • Excess grain, low fibre
  • Weather changes
  • Tapeworm infestation – risk increases proportionally to burden
96
Q

How is spasmodic colic characterised?

A
  • Fairly recent onset
  • Mild-moderate signs of pain
  • Passes all the Ps
  • Pulse < 60bpm
  • Hypermotile intestine - not very sensitive or specific
  • Response to treatment and always reassess
97
Q

How is spasmodic colic treated?

A
  • Intravenous
  • Spasmolytic agents - hyoscine/butylscolpolamine/Buscopan, butylscolpolamide + dipyrone
  • Analgesia - NSAID, an give alone or with hyoscine, phenylbutazone or half dose flunixin or (Carprofen/ketofen/meloxicam)
98
Q

What is gas colic?

A
  • Excess production of gas in all or part of large intestine
  • Pain from stretching intestinal wall
99
Q

What are the predisposing factors of gas colic?

A
  • Diet change
  • Rich grass
  • Rich haylage
  • > 2kg concentrate in any one meal
  • If repeated, consider inflammatory bowel disease
  • Parasites
  • Poor dentition
100
Q

How is gas colic characterised?

A
  • Passes the Ps – other than
  • Rectal – gas distended but still squishy viscus
  • But get this with a LI displacement or a large intestine torsion
  • And gas colic is often a precursor to developing these
101
Q

When might gas colic require surgery?

A
  • Displacements may need surgery
  • Torsions need surgery now
102
Q

How is gas colic treated?

A
  • Stomach tube with water may help as activates gastro-colic reflex
  • Check teeth, parasites
  • Check diet
  • If recurrent – change to wet hay, add Yeasacc/another hind gut supplement to feed, further investigation
103
Q

What is the pathophysiology of impactions in horses?

A
  • Tend to occur just oral to sites of intestinal narrowing and/or active pacemakers, such as pelvic flexure, ileocaecal junction
  • Impaction causes back-up of ingesta
  • Stretches mucosal wall, stimulating mural stretch receptors
  • Causing pain
  • If severe/prolonged potential vascular compromise – pressure on blood vessels
104
Q

What are the predisposing factors for large intestinal impactions?

A
  • Reduced water intake
  • Physical exertion (sweating)
  • Reduction in exercise
  • Parasite migration
  • Dental disease (don’t chew long fibre)
105
Q

What is associated with donkey large intestinal impactions?

A

Dental diastema

106
Q

How is large intestinal impaction characterised?

A
  • Mild to moderate signs of pain
  • Pass the Ps – peritoneal tap, other than abnormal rectal
  • Most large intestinal impactions are at the pelvic flexure
107
Q

Is a peritoneal tap taken for large intestinal impactions in horses?

A
  • Risk puncturing intestine if a large impaction
  • Gives you information on whether there is gut damage
108
Q

How is large intestinal impactions in horses treated?

A
  • Aim is to (over) hydrate ingesta so that gut peristalsis can clear the impaction
  • Pro-motility drugs contraindicated as may result in intestinal rupture
  • Main-stay is oral fluids
  • Can supplement with IV
  • Pass a stomach tube – always check for reflux, give water with/without additives. Give by gravity stop and think again if resistance
  • Analgesia – as for spasmodic
109
Q

What can be added to fluids for large intestinal impactions?

A
  • Lectade or similar, to make fluid isotonic
  • Magnesium sulphate - more effective
  • Dioctyl sodium sulphate – better than water alone, not as good as magnesium sulphate
  • Liquid paraffin – emollient, doesn’t help break up the impacted material, reasonably expensive, kills you if you mis-place the tube into the lungs
110
Q

What is done if there is no response to treatment

A

But if don’t respond (do not pass faeces or remain painful) or CV deterioration, reassess, may need peritoneal fluid sample. Might not just be an impaction, some impactions need surgery.

111
Q

Are ileal impactions medical or surgical?

A

Surgical

112
Q

What is the pathophysiology of ileal impactions?

A
  • Small intestine, usually at the ileocaecal junction, becomes blocked
  • With ingesta – usually due to hypertrophy of wall at ileocaecal junction secondary to tapeworm (anoplocephala)
  • With parascaris – often within 24 hours of deworming too effectively when have a high burden
113
Q

Describe anoplocephala ileal impactions.

A

Often under 4 years old, should de-worm with praziquantel or double dose pyrantel in the last 6 months

114
Q

Describe parascaris ileal impactions.

A

Often under 2 years old, should have had fenbendazole at 2-3 months, 6 months ivermectin, moxidectin or pyrantel, 9 months moxidectin and praziquantel, 12 months pyrantel

115
Q

How are ileal impactions diagnosed?

A
  • Sample small intestinal obstruction
  • Takes much longer for compromise to blood supply of gut wall than a strangulation
  • Present as for small intestinal strangulation
116
Q

How does small intestinal strangulation present?

A
  • Distended SI on rectal, scan
  • Pulse, PCV
  • Slow to reflux
  • Peritoneal tap slow to change
117
Q

How are ileal impactions in horses treated?

A
  • Whether you are sure of a diagnosis or not, the presenting signs indicate surgery is required
  • Clear impaction
  • May have to perform ileocaecal bypass if junction very thickened
118
Q

When may secondary caecal impactions occur?

A

Usually after unrelated surgical procedures that result in pain

119
Q

How are caecal impactions diagnosed?

A
  • Mild colic, or no colic
  • May just be dull
  • Reduced faecal output but still some
  • Can be very hard to detect – tend to blame depression and reduced faecal output on the original surgical procedure but can then rupture (fatal) without warning
  • Diagnosis by rectal – impaction over to the right side
120
Q

How are caecal impactions treated?

A
  • Treat as for LI impaction
  • Monitor peritoneal fluid for signs of caecal wall compromise
  • May need surgical evacuation with/without bypass
121
Q

What is the pathophysiology of sand impactions?

A
  • Irritates large intestine wall – irritation alone can cause recurrent colic. Hypertrophy, poor motility secondary to inflammation can lead to impaction
  • So present as recurrent colic or similar to large intestine impaction
122
Q

How are sand impactions treated?

A
  • As large intestinal impaction
  • Feed psyllium
  • May need surgery
123
Q

What are gastric impactions?

A
  • Aetiology not fully understood – motility disorder?
  • Often chronic, stomach can be huge
  • May rupture
124
Q

How are gastric impactions diagnosed?

A
  • Difficult to pass stomach tube
  • Spleen pushed caudally on rectal
  • Large stomach on ultrasound
  • Gastroscopy
125
Q

How are gastric impactions treated?

A

Try to lavage via stomach tube

126
Q

What are the causes of choke/oesophageal obstructions?

A
  • Usually primary impactions of food
  • Predisposed to by eating very quickly, having dental abnormalities
  • Rarely, secondary to oesophageal trauma, diverticulum, intra/extra mural masses
127
Q

What are the clinical signs of choke/oesophageal obstructions?

A
  • Anxious
  • Head and neck extended
  • Gagging
  • Frothy nasal discharge with saliva, food, water
  • May see distension LHS jugular furrow if obstruction in cervical
128
Q

If choke/oesophageal obstructions are prolonged/severe, what are the signs of secondary problems that may follow?

A
  • Dehydration
  • Electrolyte imbalance
  • Acid-base imbalances
  • Aspiration pneumonia
  • Oesophageal rupture – crepitus, cellulitis, systemic inflammation
129
Q

How are choke/oesophageal obstructions treated?

A
  • Need to sedate as you want the horse’s head down to try to reduce the risk of aspiration
  • Aim of treatment is to lavage the obstruction back out of the oesophagus
  • Consider NSAIDs and starve for a few hours, then slow re-introduction to feeding with short fibre food
  • Check for aspiration pneumonia (auscultate, temperature)
  • Check teeth/other reasons why might have choked
130
Q

How is the obstruction lavaged in choke/oesophageal obstructions?

A
  • Not to force it through into the stomach
  • Take care not to rupture oesophagus
  • Take care to reduce risk of aspiration pneumonia
  • Pass a nasogastric tube
  • Gently, up to the obstruction and then pull back a little
  • Pour 1 litre of water in, then tube down to the floor to empty back out
  • Water coming out will be food contaminated
  • Repeat
131
Q

What is equine dysautonomia/grass sickness?

A
  • Acquired degenerative polyneuropathy
  • Affects neurons of autonomic and enteric nervous system
132
Q

What are the risk factors of equine dysautonomia/grass sickness?

A
  • Young horses between 3 and 5
  • If been in contact with EGS cases but did not develop the disease, 10 x less likely to develop it
  • Geographical variation
  • Some premises have a history of cases
  • Soil disturbance
  • Peak in Spring (Autumn)
133
Q

What is the pathogenesis of equine dysautonomia/grass sickness?

A
  • Related to damage to the autonomic nervous system
  • Most severe lesions in plexi of ileum then celiacomesenteric ganglion
  • Dysphagia from cranial nerve/brainstem involvement
  • Most likely is a Clostridium botulinum toxicoinfection

More recent moves away from this thought

134
Q

What is the acute form of equine dysautonomia/grass sickness?

A
  • Fatal
  • Ileus leads to small intestine and gastric distension
  • Distension causes severe abdominal pain
  • Hypovolaemic (fluid sequestered in GI tract)
  • Distended small intestine on rectal
  • Death from cardiac failure from reducing circulating volume or gastric rupture
135
Q

What are the clinical signs of acute equine dysautonomia/grass sickness?

A

Generalised/patchy sweating
Muscle fasciculations
Pyrexia
Dysphagia
Ptosis

136
Q

What is the subacute form of equine dysautonomia/grass sickness?

A
  • Clinical signs less severe
  • Large colon impactions
  • May be euthanised/die as start to reflux/can’t eat
  • May progress to chronic – overlap
137
Q

What are the clinical signs of the subacute form of equine dysautonomia/grass sickness?

A

Intermittent colic
Patchy sweating
Rhinitis sicca
Lose weight
Dysphagic
Muscle fasciculations

138
Q

What is the chronic form of equine dysautonomia/grass sickness?

A
  • Usually present as rapid, severe weight loss
  • May have mild, recurrent colic
139
Q

What are the clinical signs of the chronic form of equine dysautonomia/grass sickness?

A

GI tract empty
Rhinitis sicca
Sweating
Muscle fasciculations
Base-narrow stance

140
Q

How is equine dysautonomia/grass sickness diagnosed?

A
  • Exclusion based diagnosis without biopsy or post-mortem
  • Phenylephrine eye test if ptosis present – may reverse ptosis
  • Ileal biopsy
  • Sub-acute/chronic - standing laparoscopic assisted biopsy
  • Ex-lap – may have to ex-lap in particular acute cases
  • Post-mortem
141
Q

What are the differential diagnoses of equine dysautonomia/grass sickness?

A
  • Small intestine ileus, reflux – strangulating or simple small intestine obstruction
  • Large intestine impaction – primary impaction
  • Dysphagia – foreign body, choke, pharyngeal paralysis
  • Chronic weight loss – other causes of wasting
142
Q

How is acute equine dysautonomia/grass sickness treated?

A
  • IV fluids, gastric decompression
  • If result positive, PTS
  • If negative, will need to PTS if doesn’t improve with supportive therapy

Similar for subacute

143
Q

How is chronic equine dysautonomia/grass sickness treated?

A
  • Appropriate care
  • Residual abnormalities such as mild dysphagia, sweating
144
Q

What is anterior enteritis/duodenitis-proximal jejunitis (DPJ)?

A

Inflammation and oedema of the duodenum and proximal jejunum

145
Q

What is the pathophysiology of anterior enteritis/duodenitis-proximal jejunitis (DPJ)?

A
  1. A toxigenic strain of Clostridium difficile may be the cause. Recent dietary change with increase in dietary concentrate level is a risk factor
  2. Inflamed small intestine
  3. Inflammation has impact on motility
  4. Ileus/no peristalsis
  5. Fluid you secret in stomach that is absorbed into small and large intestines backs up in the stomach
  6. Must come out stomach tube or stomach ruptures
  7. Dehydration
146
Q

What does the inflammation in anterior enteritis/duodenitis-proximal jejunitis cause?

A
  • Ileus
  • Excess fluid and electrolyte secretion into small intestine
  • Pyrexia
  • Elevated peritoneal fluid protein (inflammation)
147
Q

What can be caused by excess fluid and electrolyte secretion in the small intestine in anterior enteritis/duodenitis-proximal jejunitis cause?

A
  • Distended small intestine
  • Gastric overfilling
  • Reflux (often a lot)
  • Colic
  • Hypovolaemia – tachycardic, high PCV
  • Endotoxaemia – tachycardic
148
Q

What are the differential diagnoses for anterior enteritis/duodenitis-proximal jejunitis?

A

Small intestinal obstruction, simple or strangulating

149
Q

How is anterior enteritis/duodenitis-proximal jejunitis treated?

A

Refer if feel distended small intestine

Exploratory laparotomy?
- You may need this to be sure of your diagnosis where the disease in uncommon
- Find very red, ‘angry’ SI, poor motility
- Manual decompression of SI helpful

150
Q

What is the medical and surgical aftercare needed for anterior enteritis/duodenitis-proximal jejunitis?

A
  • IV fluids
  • Analgesia
  • Frequent gastric decompression
  • Anti-endotoxin therapy
  • Nutritional support
  • Nursing care
  • Antibiotics – metronidazole, penicillin
151
Q

What are the consequences of peritonitis in horses?

A
  • Disruption or irritation of the peritoneal lining
  • Inflammation or infection of abdominal organs
  • Compromise of the intestinal wall
152
Q

What must you consider about peritonitis?

A
  • Origin (primary or secondary)
  • Onset (peracute, acute, chronic)
  • Distribution (localised or diffuse)
  • Presence of bacteria (septic versus non-septic)
153
Q

What are the clinical signs of peracute peritonitis?

A

Intestinal rupture
Rectal tear
Severe toxaemia
Weakness - stagger
Colic
Tachycardia
Tachypnoea
Circulatory failure
Sweating (pouring)
Purple mucous membranes
Muscle fasciculations
Palpation of abdomen is painful
Rectal exam ‘gritty’ from fibrin deposition
Fever?

154
Q

What are the clinical signs of more mild/chronic peritonitis?

A

Chronic or intermittent colic
Intermittent fever
Depression
Anorexia
Weight loss
Ventral oedema
Exercise intolerance

155
Q

How is peritonitis diagnosed in horses?

A
  • Fever and colic
  • Peritonitis – peritoneal fluid sample
  • Colitis – diarrhoea, or so dehydrated (would have high heart rate) that it can’t show diarrhoea
  • Collect in a plain first for culture and then EDTA for cytology
  • Grossly – cloudy, may see/smell gut content
  • White cell count, diff-quik – can be difficult to interpret after recent celiotomy
156
Q

How is peritonitis in horses treated?

A
  • Ruptured intestine – euthanise
  • Acute phase – arrest endo toxic, septic, hypovolaemic shock and treat pain – fluids, flunixin, polymyxin B?
  • Penicillin, gentamicin, with/without metronidazole
  • Reassess once culture results
  • And once had 5 days gentamicin – care with kidneys
  • Often follow with TMPS if suitable
  • Continue until peritoneal fluid normal
157
Q

When is surgery used to treat peritonitis in horses?

A
  • May need to allow diagnosis/resolution
  • If doesn’t respond to treatment/recurs
  • Laparoscopy/laparotomy
158
Q

What is the cause of IBD in horses?

A

Immune mediated disease
Unknown cause

159
Q

What are the clinical signs of IBD in horses?

A
  • Can present with acute, surgical colic
  • Or chronic/recurrent colic
  • And/or diarrhoea (but not usually fever) if colitis
  • And/or weight loss if enteritis
160
Q

How is IBD diagnosed with biopsy?

A
  • Ideally ex-lap and biopsy – but surgery a big deal and long time off work
  • Start with a rectal biopsy
  • May be suitable for laparoscopic exploration and laparoscopic assisted biopsy – standing, can’t always sample the large intestine
161
Q

How is IBD treated in horses?

A

Corticosteroids (prednisolone) – lowest dose possible

162
Q

What are ESGD and EGGD?

A

Equine glandular gastric disease (EGGD)
Equine squamous gastric disease (ESGD)

= Equine gastric ulcer syndrome

163
Q

What is the aetiology of equine gastric ulcer syndrome?

A
  • ESGD graded 1-4
  • EGGD graded descriptively
  • ESGD – acid exposure: exercise, periods with an empty stomach, concentrate feeds lowering pH
  • EGGD – we don’t know
164
Q

What are the clinical signs of equine gastric ulcer syndrome?

A

None
Poor performance
Recurrent colic
Poor appetite
Weight loss
Discomfort on girthing
Change in behaviour/attitude
Crib-biting

165
Q

How is equine gastric ulcer syndrome diagnosed?

A
  • Gastroscopy (starve 12-16h)
  • Need a 3m long scope to visualise all stomach, and if possible go through pylorus into proximal dudodenum
166
Q

How is equine gastric ulcer syndrome treated?

A

Proton pump inhibitor – omeprazole. Blocks acid production from parietal cells

167
Q

How is equine gastric ulcer syndrome managed?

A
  • Grazing
  • No long periods without food
  • Less concentrate
  • Roughage
  • Oil
  • Mat of chaff 30 mins before exercise
168
Q

What are the behavioural symptoms of colic in horses?

A

Rolling
Kicking abdomen
Looking at abdomen
Recumbency
Anorexia
Stretching
Yawning
Urination

169
Q

What are the Ps of colic?

A

Pain
Progression
Pulse
Pass a tube
Palpate per rectum
Peritoneal fluid
PCV
Pyrexia
Per abdominal ultrasound

170
Q

How are gastrointestinal and cardiovascular signs used to diagnose colic?

A

Gastrointestinal system for indications of the nature and site of the problem. Cardiovascular system for indicators of the severity of systemic disturbance produced by the GI tract problem.

171
Q

What are the core basic parameters needed to investigate colic?

A
  • Heart rate
  • Pulse quality
  • Respiratory rate – puffing, tachypnoea
  • Temperature
  • mmbs and CRT
  • Abdominal auscultation – percussion, assess all 4 quadrants
  • Rectal palpation?
  • Nasogastric reflux – pass a tube?
172
Q

What are the extra investigations that can be used for colic?

A
  • Rectal palpation?
  • Nasogastric reflux – pass a tube?
  • Haematology, biochemistry – PCV and TP or percentage dehydration
  • Per abdominal ultrasound
  • Abdominal paracentesis
  • Gastroscopy
  • Exploratory laparotomy
173
Q

What are the reasons heart rate might increase in colic?

A

Increases due to pain, endotoxaemia, haemoconcentration, reduced venous return

174
Q

What are the heart rate ranges and what do they indicate in colic?

A

20-40 bpm Normal
40-60 bpm Mild pain
60-80 bpm pain with likely circulatory collapse
80 + bpm likely surgical

175
Q

What does pulse quality tell us about colic?

A

Hypermetric bounding pulse – circulatory shock

Weak thready pulse – circulatory failure

176
Q

Why might respiratory rate increase with colic?

A

Increases with pain, attempt to correct metabolic disturbances, watch effort too.

177
Q

What can temperature tell us about colic?

A
  • Mild pyrexia with pain
  • Marked pyrexia with infection – salmonellosis, aspiration pneumonia, peritonitis
  • Hypothermia in profound circulatory shock
178
Q

What does mucous membrane colour tell us about colic?

A

Salmon pink - normal
Red – congested, circulatory shock
Purple rings – endotoxaemia
Pale - anaemia, unlikely

179
Q

What can CRT tell us about colic?

A

<2s normal
>2s circulatory compromise

180
Q

What can abdominal auscultation tell us about colic?

A
  • Increased in hyperperistalsis/spas
  • Decreased/intermittent – hypoperistalsis
  • None – ileus
  • Tinkling – tympany
  • Toilet flushing – caecal emptying
181
Q

Which pathologies can be identified rectal examination that could cause colic?

A
  • Distended Small Intestine (DSI) – “sausages”
  • Impaction – often pelvic flexure
  • Displacement – taenial band orientation
  • Tympany –taught, balloon like
  • Mesenteric mass
182
Q

Where per rectum can you palpate the pelvic flexure of the horse?

A

Left ventral quadrant

183
Q

How can nasogastric intubation be used in colic cases?

A
  • Normally get 1-2L
  • Anything over this is abnormal – large quantity discoloured and malodorous, indicates obstruction
  • Also releases gas
  • Decompression reduces pain
184
Q

How does colic present on haematology and biochemistry?

A
  • PCV/TP – both elevate with dehydration and shock
  • Lactate – demonstrates tissue ischaemia
  • Blood gas – before/during GA to identify acidosis and electrolyte disturbances
  • Basic profile – if suspect alternative or concurrent pathology, such as WBC or muscle/liver enzymes
185
Q

Where can you visualise the duodenum of the horse?

A

Right dorsal quadrant

186
Q

How is abdominal paracentesis done in horses?

A
  • Ventral midline
  • 4th caudal to sternum or most dependent part of abdomen
  • Cannula (local anaesthesia, stab in the linea alba) or needle
187
Q

How would you know that a sample from abdominal paracentesis was septic?

A

< few mls of coloured cloudy fluid
TP > 50 g/L
CCC > 50 x 10^9 cells/L
Lactate > 5mmol/L

188
Q

What does the colour and transparency of an abdominal paracentesis sample tell us?

A
  • Normal clear and straw coloured
  • Amber/orange indicates vascular compromise
  • Red/black indicates necrosis
  • Gut content indicates rupture or accidental lumen penetration
  • Transparent/clear – acellular
  • Opaque/cloudy – cellular
189
Q

What are the reasons for failing to achieve a diagnosis with abdominal paracentesis and how are these resolved?

A
  • Dehydration = rehydrate and repeat
  • Splenic tap = use US guidance
  • Extensive fat layer = US and long cannula
  • Enterocentesis = consider US
  • Not penetrated peritoneum = sharper movement
190
Q

What are the reasons for euthanasia in colic cases?

A
  • Financial constraints
  • Poor prognosis
  • Perceived need for additional surgery
  • Repeat colic episodes
  • Post op complications
  • Concurrent issues
  • Anticipated behaviour non-compliant for box rest
191
Q

What are the usual causative lesions of abdominal crisis in horses?

A

Obstruction of the small intestine (ileal impaction)
Obstruction of the blood supply to the gut (strongylus vulgaris infarcts)
Or both (strangulating lipoma)

192
Q

Describe simple obstructions in horses.

A
  • Lumen only obstructed
  • Vasculature intact so intestine minimally compromised
  • Prognosis usually good (many won’t need surgery) – ileal/pelvic flexure impaction
193
Q

Describe functional obstructions in horses.

A
  • Peristalsis fails to propel ingesta (ileus) leading to distension
  • Vasculature intact so intestine minimally compromised
  • Pressure necrosis may follow particularly with non-ingesta impactions such as ascarids and faecoliths
194
Q

Describe the progression of strangulation cases in horses.

A
  • Compromise of vasculature resulting in ischaemia of intestine
  • Veins obstructed before arteries, causing oedematous thickening of gut wall
  • Bacterial death by changes in environment as it is now anaerobic and acidic releases LPS
  • As mucosa is damaged it becomes permeable to endotoxin, which leaks into peritoneum
  • Peritoneal LPS absorbed into systemic circulation
  • Endotoxaemia, causes systemic compromise or shock
195
Q

What are 2 secondary problems of strangulation cases that further worsen prognosis?

A
  • Bacteria translocate from lumen as barrier ineffective, setting up potential for peritonitis
  • Endotoxaemia may lead to DIC or laminitis
196
Q

What are surgical options for abdominal crisis in horses?

A

Emergency colic surgery – exploratory laparotomy

Elective surgery – exploratory laparoscopy/laparotomy

Focussed elective surgery
- Nephrosplenic space obliteration
- Biopsy collection in chronic weight loss case
- Hernia repair
- Non-GI – mass excision

197
Q

What should be the first structure visible as you enter the peritoneum?

A

Caecum

198
Q

How do you do abdominal exploration of the small intestine?

A

Trace the dorsal taenial band of the caecum to the ileum, then exteriorise this and continue orally until obstruction reached. Obstruction may be exteriorisable or not. Palpate the duodenocolic ligament

199
Q

How do you do abdominal exploration of the large intestine?

A

Identify pelvic flexure and exteriorise this, extend it maximally from incision. May require deflation and/or correction to exteriorise

200
Q

How is the abdomen closed after abdominal exploration?

A
  • Ensure all swabs removed – count
  • Replace intestines in normal anatomical position – a logical sweep around the abdomen
  • Lavage with sterile saline
  • Anti adhesion treatments carboxymethylcellulose
201
Q

What artery supplies the jejunal arteries?

A

Cranial mesenteric

202
Q

Describe the circulation of the small intestine.

A
  • Cranial mesenteric artery supplies jejunal arteries
  • Caecocolic artery branches to form ileal artery
  • Blood supply needs to determine the site of any anastomosis
203
Q

What are the clinical characteristics of simple and functional obstructions?

A
  • Distension (orally) causes more ileus
  • Surgery to decompress SI/remove obstruction
  • Vascular supply intact
  • No anastomosis needed
  • May biopsy
204
Q

What are the possible causes of simple and functional obstructions?

A
  • Grass sickness
  • Eosinophilic enteritis
  • Anterior enteritis
  • Ileal impaction
  • Ascarid impaction
205
Q

What do strangulating lesions cause?

A

Simultaneous vascular occlusion and luminal obstruction

206
Q

What are the potential causes of strangulating lesions?

A
  • Lipoma
  • Intussception
  • Epiploic foramen entrapment
  • Adhesion
  • Mesenteric band/rent/torsion
  • Gastrosplenic ligament tear with incarceration
  • Scrotal herniation
  • Diaphragmatic herniation
207
Q

What is the pathogenesis of strangulating lesions?

A
  • Often veins occluded first, arteries later
  • Congestion, haemorrhage, oedema
  • Due to increased hydrostatic pressure and microvascular permeability
  • Creating a thick black walled friable necrotic intestine
  • 4-5h mucosa completely necrotic
  • 7+hours then affecting serosa too
  • Spontaneous rupture may follow
  • These cases will be severely endotoxaemic
208
Q

What type of suture is used in an intestinal anastomosis?

A

Inverting – larger lumen width to work with, in order to maintain seal

209
Q

An example of an inverting suture pattern is?

A

Connels, cushings, lemberts

210
Q

How do lipomas cause colic?

A
  • Fatty deposits in SI mesentery, grow to form a lipoma, the weight of this encourages formation of a peduncle
  • Acts like a ball and chain to loop around a piece of intestine strangulating it
  • Acute colic signs for surgical colic
211
Q

Distinguish internal and external hernias in horses.

A

Internal hernias – through an aperture within the abdomen

External hernias – through an aperture to exit the abdominal cavity

212
Q

What vices predispose a horse to epiploic foramen entrapment?

A

Crib biting and wind sucking

213
Q

What is epiploic foramen entrapment?

A
  • Slit like opening into omental bursa in RD abdomen – bordered by caudate lobe of liver, Cd vena cava, pancreas, hepatoduodenal ligament and portal vein
  • Small intestine passes left to right to sit above duodenum
214
Q

What are the risk factors of epiploic foramen entrapment?

A

Crib biting/windsucking
Tall horses
History of colic in last 12m
Increased time in stable in previous 4w

215
Q

What is the clinical significance of umbilical hernias in horses?

A
  • Very rarely cause GI pathology
  • Repair when >3cm diameter or if not resolved at 1yo – options rubber elastrator rings, hernia clamps or herniorrhaphy
216
Q

Describe indirect inguinal/scrotal congenital hernias.

A

Common in young colts, usually reducable, rarely obstructed or ischaemic

217
Q

Describe direct inguinal/scrotal congenital hernias.

A
  • Tear in peritoneum/vaginal tunic
  • Intestine lies in subcutaneous tissue
  • Severe local swelling and skin necrosis
  • Rarely strangulates but acutely painful condition requiring correction and repair
218
Q

What causes acquired inguinal/scrotal hernias?

A

Post mating, castration complication, spontaneous

219
Q

What is caused by acquired inguinal/scrotal hernias?

A
  • Acute strangulation
  • Testicle becomes oedematous and congested due to local pressure on testicular vessels
220
Q

What are the complications for strangulating lesion R&As?

A
  • Contamination, and peritonitis
  • Endotoxic shock
  • Ileus
  • Post-operative adhesions
  • Recurrent colic
  • Incisional wound healing
  • Jugular vein thrombosis
221
Q

What is thought to cause nephroplenic entrapment/left dorsal displacement of the colon in horses?

A

Excess gas production and altered motility

222
Q

What happens with nephrosplenic entrapment/left dorsal displacement of the colon?

A
  • Initially a non-strangulating lesion
  • The weight of the colon causes the spleen to displace medially and ventrally and to become congested
  • Oedematous wall at risk of rupture
  • The left colon can become impacted because of impaired flow of ingesta over time
223
Q

What are the treatment options for nephrosplenic entrapment/left dorsal displacement of the colon?

A
  • Starve/restricted feed (all cases)
  • Fluids and analgesics
  • With/without phenylephrine – splenic contraction
  • With/without surgical correction – most ventral midline, standing flank possible
224
Q

How does right dorsal displacement of the colon present?

A
  • Moderate degrees of pain α gaseous distension
  • Progressive dehydration
  • Bands on the distended colon run transversely across the pelvic inlet and caecum cannot be identified
  • High GGT
225
Q

How is right dorsal displacement of the colon medically managed?

A
  • If mild pain and gaseous distention minimal
  • Starve, natural evacuation
226
Q

How is right dorsal displacement of the colon surgically managed?

A
  • When significant pain
  • Identify pelvic flexure
  • Relocate colon to normal position by rotating it around the caecal base
227
Q

What happens in large colon volvulus?

A
  • Strangulating obstruction with ischaemia of a huge section of the horse’s GI tract
  • Rapid and extreme gaseous distension
228
Q

Where does large colon volvulus occur in the horse?

A

Sternal flexure or close to the attachment of the right ventral colon to the cecum

229
Q

How does large colon volvulus present?

A
  • Severe pain is sudden
  • Very distended large colon
  • Tachycardia and poor peripheral perfusion due to endotaxaemia
230
Q

How do caeco-caecal and caeco-colic intussusceptions appear on ultrasounds?

A

Bullseyes

231
Q

What is the risk factor for caeco-caecal and caeco-colic intussusceptions?

A

Anoplocephala infestation

232
Q

What happens in caeco-caecal and caeco-colic intussusceptions?

A
  • Tip of caecum invaginates into body
  • May then continue so entire caecum invaginates and is inside out in the colon
  • Initially can be reduced manually
  • Once oedematous and ischaemic the devitalised bowel will need resecting
  • Prone to rupture
  • May/may not be reducible
233
Q

What are enteroliths?

A

Mineralised concretions of food material

234
Q

What do enteroliths cause?

A

Obstruction at sites where large intestine narrows – transverse colon, pelvic flexure, small colon

235
Q

How are enteroliths treated?

A

Surgical excision via enterotomy

CVSOH 4 (13 decks)

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