Medical Colic 2

Question 1

Equine dysautonomia.

Answer 1

Grass sickness.
Acquired degenerative polyneuropathy.
Affects neurons of the autonomic enteric NS.
Clinical signs are variable.
3 forms - no clear divide.

Question 2

Risk factors predisposing horses to equine dysautonomia.

Answer 2

Young horses between 3 and 5.
Outbreaks.
Contact with but no disease makes horse 10x less likely to develop it.
Higher risk if recently moved to the premises.
Suggests a possibility to develop immunity from subclinical exposure.
Geographical variation.
Some premises have history of cases.
Usually, but not always, access to pasture.
Soils disturbance due to short grass / mechanical faeces collection / recent rain.
Spring / autumn.

Question 3

Equine dysautonomia clinical signs and Pathogenesis.

Answer 3

CS related to damage of autonomic NS.
Most severe lesions in plexi of ileum then celiacomesenteric ganglion.
Dysphagia from cranial nerve / brainstem involvement.
Numerous suggested causes.
- most likely is a clostridium botulinum toxicoinfection?
— organism ingested, usually in soil, then produces toxin directly inside gut.
—> but more recent moves away from this thought.
But something happens with soil disturbance, spring, geographics, and can get immunity to it.

Question 4

Acute form of equine dysautonomia.

Answer 4

Fatal.
Course of disease usually <48hrs.
Acute onset GI ileus.
- very dehydrated due to no fluid absorption.
— hypovolaemia —> tachycardia, High PCV/TP.
- leads to SI and gastric distension.
— leads to severe abdominal pain (but pain may then reduce).
— feel SI distension on rectal.
— may feel small ‘corrugated’ LI impaction.
Other signs: generalised/patchy sweating, muscle fasciculations, pyrexia, dysphagia, ptosis (cannot open eyelids properly).
Death from: cardiac failure from reduced circulating volume or gastric rupture.
Treatment as for distended SI.
- surgery — empty stomach with stomach tube, flunixin, hospital.
BUT needs repeated gastric emptying and cannot eat so need euthanasia.

Question 5

Subacute form of equine dysautonomia.

Answer 5

Course of disease 3-7 days.
Clinical signs less severe than with acute form.
Usually do not reflux, at least initially.
Large colon impactions (often fairly small, ‘corrugated’).
May have: intermittent colic, patchy sweating, rhinitis sicca, weight loss, dysphagia, muscle fasciculations.
May be euthanised / die as start to reflux / can’t eat.
May progress to chronic.
- forms overlap.

Question 6

Chronic form of dysautonomia.

Answer 6

Disease course weeks to months.
Rapid severe weight loss.
May have mild recurrent colic.
GIT empty.
Rhinitis sicca.
Sweating.
Muscle fasciculations.
Base-narrow stance.

Question 7

Diagnosis of equine dysautonomia.

Answer 7

Exclusion based dx without biopsy or PM.
Index of suspicion from CS, Hx, signalment, geography, time of year.
Definitive Dx has important need health (and financial) implications.
Phenylephrine eye test if ptosis present.
- 0.5% phenylephrine eye drops may reverse ptosis in <30 mins in non seated horse.
- Variable results, but non-invasive and may add to body of evidence.
In theory, tongue biopsy.
Ileal biopsy (rapid process if poss).
- almost but not quite 100%.
- sub-acute / chronic cases may be suitable for standing laparoscopic assisted biopsy.
Ex lap, in particular acute cases because of differential diagnoses.
PM.

Question 8

Differential diagnoses for equine dysautonomia.

Answer 8

SI ileus, reflux.
- strangulating or simple SI obstruction.
- anterior enteritis.
LI impaction.
- primary impaction.
Dysphagia.
- FB.
- choke.
- pharyngeal paralysis.
Chronic weight loss.
- other causes of wasting.

Question 9

Tx of equine dysautonomia.

Answer 9

Acute:
- can treat while waiting for histology results.
— so rapid process these (results in 12-24hrs but not as reliable).
- IV fluids, gastric decompression.
- positive result — PTS.
- negative result — will need to PTS if doesn’t improve with supportive therapy.
Similar for sub-acute.
Chronic:
- approx. 50% Horses survive with appropriate care.
- may return to work.
Some have residual abnormalities such as mild dysphagia, sweating.
When to treat:
- committed owner, horse wants to eat and is able to eat (mild dysphagia, no reflux), horse not suffering persistent colic.
How to treat:
- mainstays are:
— high energy, easily swallowed and palatable food.
— lots of care.

Question 10

Equine dysautonomia - what next?

Answer 10

Major implications for other horses in premises.
Major implications for a business.
Take other horses off field now?
No horse ok that field in spring and autumn?

Question 11

Equine dysautonomia - the future.

Answer 11

Know horses can develop immunity even though do not know the Pathogenesis well.
Ongoing work to develop vac but hasn’t had a breakthrough, sparking thoughts it might not be a clostridium botulinum toxicoinfection.

Question 12

1. What is anterior enteritis?
2. Anterior enteritis pathophysiology.

Answer 12

1. Inflammation and oedema of the duodenum and proximal jejunum.
2. Underlying aetiology cannot be determine in most cases.
   Salmonella spp. or clostridium spp. can be cultured from reflux in some cases.
   A toxigenic strain of clostridium difficile may be the cause.
   Recent dietary change with increase in dietary concentrate level is a risk factor.

Question 13

What are the consequences of anterior enteritis?

Answer 13

Inflammation causes ileus and excess fluid and electrolyte secretion into SI,
- distended SI, gastric overfilling, reflux (often a lot), colic, hypovolaemia (tachycardia, high PCV), endotoxaemia (tachycardia).
Pyrexia.
Elevated peritoneal fluid protein (inflammation).

Question 14

Anterior enteritis differential diagnoses.

Answer 14

SI obstruction (simple or strangulating).
Simple or strangulating SI obstruction would be more common.

Question 15

Anterior enteritis tx.

Answer 15

Refer.
For ex-lap?
- may need this to be sure of you dx where the disease is uncommon.
- find v red, ‘angry’ SI, poor motility.
- no strangulation.
- manual decompression of SI helpful.
Cases having Sx may have poorer Px.
Medical/surgical after care.
- IV fluids.
- analgesia.
- frequent gastric decompression.
- anti-endotoxin therapy.
- nutritional support.
- nursing care.
Antibiotics:
- metronidazole.
- penicillin.

Question 16

Anterior enteritis Px.

Answer 16

Up to 80% survival.
May be worse if surgical (worse cases and post Sx risks).
Can be expensive to treat.

Question 17

Peritonitis.

Answer 17

Can occur with any insult - mechanical, chemical, infectious - that results in:
- disruption or irritation of the peritoneal lining.
- inflammation or infection of abdominal organs.
- compromise of intestinal wall.

Question 18

Considerations for a horse with peritonitis.

Answer 18

Origin (primary or secondary).
Onset (peracute, acute, chronic).
Distribution (localised or diffuse).
Presence of bacteria (septic vs non-septic).

Question 19

Peritonitis clinical signs.

Answer 19

Depend on:
- primary disease process.
- duration of disease.
- extent of disease.
Peracute:
- e.g. intestinal rupture, rectal tear.
— severe toxaemia.
— weakness —> reluctant to walk, but stagger.
— colic.
— tachycardia.
— tachypnoea.
— circulatory failure.
— pouring / sweating.
— purple MMs.
— muscle fasciculations.
— pain in palpation.
— rectal exam ‘gritty’ from fibrin.
— fever?
More mild or chronic.
- chronic or intermittent colic.
- intermittent fever
- depression.
- anorexia.
- weight loss.
- ventral oedema.
- exercise intolerance.

Question 20

Peritonitis dx.

Answer 20

Fever + colic.
Peritonitis - peritoneal fluid sample.
— needed!
— needle or cannula, but if suspect intestinal rupture use a cannula .
— collect plain (culture) then EDTA (cytology). .
Colitis - D+, or very dehydrated — v high HR.
- grossly cloudy fluid +/- gut content.
- perform white cell count, diff-Quik, can be difficult to interpret after recent celiotomy.
Other causes of SI distended more likely than anterior enteritis.
Some info from Hx, clinical signs, haematology, serum amyloid A / fibrinogen.
Abdo U/S can add info.

Question 21

Peritonitis tx.

Answer 21

Depends on cause.
Rupture intestine - euthanasia.
Acute phase:
- arrest endotoxic, septic, hypovolaemia shock (if are this bad, need referral)
- treat pain.
— fluids, flunixin, polymyxin B.
Penicillin, gentamicin, metronidazole.
Reassess once culture results back.
- and once had 5 days gentamicin.
— care with kidneys.
— often follow with TMPS if suitable.
Continue until fluid normal (check weekly).
Peritoneal lavage?
Surgery?
- case-by-case.
- try avoid as increased risk of adhesions (and the rest).
- may need to allow dx/ resolution.
- if doesn’t respond to tx / recurs.
- laparoscopy/laparotomy.

Question 22

Peritonitis Px.

Answer 22

Depends on cause.
— from fatal to excellent.
— if ‘idiopathic’, usually do v well.

Question 23

IBD.

Answer 23

Immune-mediated.
Unknown cause.
Several different types, characterised by cell types e.g. eosinophilic.
Can consider on a spectrum - from ‘irritable bowels’ even up to lymphoma.
SI (enteritis) and/or LI (colitis) (enterocolitis of both).
Some types have multi-systemic involvement.

Question 24

IBD clinical signs.

Answer 24

Acute, surgical colic, or chronic/recurrent colic.
And/or D+ (but not usually fever) if colitis.
And/or weight loss if enteritis.

Question 25

IBD Dx.

Answer 25

Think of differentials framework.
Abdominal U/S may find thickened intestinal walls.
Abdominocentesis may show inflammation.
But need a biopsy!

Question 26

IBD biopsy.

Answer 26

Ideally ex lap and biopsy.
- but Sx a big deal and long time off work.
Start with rectal biopsy (for colitis):
- easy.
- low risk.
- can do in field.
- CARE with interpretation.
— rectum is not colon!
May be suitable for laparoscopic assisted biopsy.
- no GA — safer.
- standing.
-.only needs 2w off work.
- can’t always sample LI.
- should not do on painful horse
— long time to stand still.

Question 27

IBD tx.

Answer 27

Corticosteroids (preds).
- lowest dose possible.
- continuous vs pulse treat vs single treatment.
- i.e. Px variable, often not closely linked to dx of type or severity.

Use of repeat peritoneal fluid sample / rectal biopsy / laparoscopic biopsy to determine course of tx.

Diet.
- v important in tx of people.
— lack of published evidence in horses.
- hay not haylage?
- Yeasacc.
- pro- and pre- biotics.
- reduced long fibre.
- increased short fibre.
Resection of inflamed intestine (rare).

Question 28

Equine gastric ulcer syndrome.

Answer 28

Covers both squamous and glandular disease.
Glandular ulcers like to be in the pylorus.

Question 29

Equine gastric ulcer syndrome aetiology.

Answer 29

Adults vs foals.
Squamous:
- acid exposure.
— exercise.
— periods with an empty stomach.
— concentrate feeds lowering pH.
— But broodmares at grass also affected.
Glandular:
- equine Helicobacter?
- don’t know.
Squamous - graded 1-4.
Glandular - graded descriptively.

Question 30

Equine gastric ulcer syndrome prevalence.

Answer 30

Racehorses in training 93-100%.
Racehorses not in training 36%.
Broodmares 70%.

Question 31

Equine gastric ulcer syndrome clinical signs.

Answer 31

Variable.
None?
Poor performance.
Recurrent colic.
Poor appetite.
Weight loos.
Discomfort on girthing.
Change in behaviour / attitude.
Crib-biting? (cause/effect?).

Question 32

Equine gastric ulcer syndrome effect on performance.

Answer 32

80% elite performance horses have ulcers.
50% have clinical signs.
- CS often non-specific so presence of ulcers can be coincidental.
- treat — if ulcers gone and CS resolved then ulcers were the cause of those clinical signs.
50% appear asymptomatic.
- treat:
— 50% improve performance and consistency.
— 50% no change.

Question 33

Equine gastric ulcer syndrome Dx.

Answer 33

Gastroscopy (starve 12-16hrs).
Need ~3m long scope to visualise all stomach and if possible go through pylorus into proximal duodenum.
Grade severity 0-4 for squamous.
Grade descriptively for glandular.
- ACVIM consensus statement.

Question 34

Equine gastric ulcer syndrome tx.

Answer 34

Proton pump inhibitor.
- Omeprazole:
— 1-4mg/kg.
— start at 4mg/kg then may be able to reduce to 1mg/kg.
— Gastroguard or generic Ulcergold, Peptizole.
— bioavailability:
—> 16% in generic.
—> formulation vital.
— blocks acid production from parietal cells.
— may need to use for maintenance (1mg/kg).
— check competition rules.
— expensive but v effective.
Histamine antagonists e.g. ranitidine.
Antacids.
Pectin - Lecithin Complex (Pronutrin).
— some benefit from these but they are used more for maintenance.
Management:
- diet.
— grazing.
— no long periods without food (small hole Haynes, soak hay over 1 hour).
— less concentrate.
— roughage.
— oil.
— mat of chaff 30 mins before exercise.