Approach to chronic colic & weight loss

What are the mechanisms of weight loss

List some common causes of weight loss

• Dental Disorders

• Parasitism

• Inadequate diet —> malnutrition, inability to compete for feed

• PPID (pituitary pars intermidia dysfunction)

• Liver dx

• Malabsorption & protein losing enteropathy —> parasitic, inflam bowel dx, neoplasia

Others for reference:

What physiological processes cause the intestinal pain in colic?

1. Stretch

2. Inflam

3. Ischaemia

4. M. spasm

lead to pain & altered contractility

Define chronic colic

Colic signs of variable intensity ≥ 48 hours

Define recurrent colic

Shorter periods of colic pain which recur @ variable intervals

NB. Chronic / recurrent & weight loss can present together & have common cause

What are the causes of recurrent colic?

• Tapeworms

• Cyathostomins

• Recurrent impactions due to dental disease

• Gastric disease (EGUS)

• Infiltrative bowel diseases

• Sand enteropathy

What are the causes of chronic colic?

Most things that can cause abdo pain, except strangulatng lesions —> would usually deteriorate to surgical level well before 48hrs

What is involved in obtaining the hx for recurrent colic?

• Characterise

• Investigate risk factors for ddx

• What has already been tried?

What is involved in a colic risk assessment?

What is the systematic approach when investigating colic / weight loss?

• Full clinical exam

• BCS

• Oedema present?

What preliminary clinical pathology tests would you do for a chronic colic and weight loss case?

• Blood and faecal tests

• Look for:

  • Specific organ disease – liver enzymes, creatinine etc.

  • Inflammatory processes – WCC, fibrinogen, globulins

  • Protein loss – esp. albumin

  • Occasionally indicators of malignancy e.g hypercalcaemia

• FEC

• ELISA test for cyathostominosis &tapeworms

What components of serum proteins can be interpreted in a weight loss case?

• Total protein

  • Decr may be masked by concurrent dehyd or incr. globulin

• Hypoalbuminaemia (GI loss > liver dx; severe peritoneal/pleural; lack of production due to malabsorption)

• Hypoglobulinaemia (GI loss)

• Hyperglobylinaemia (chronic inflam dx incl. cyathostominsosis; neoplasia)

• Fibrinogen / SAA (goes up quicker in response to inflam)

Why is the size of albumin compared to globulin relevant to oedema?

Albumin smaller molecule so losing a gram will have a bigger affect than globulin

What analysis can you perform of the peritoneal fluid?

• Nucleated cell count

• Protein

• Lactate

• Cytology

What can you identify on an abdominal U/S in horses?

• Peritoneal effusion

• Intestinal wall thickness

• Postion

• Lumen diameter

• Motility

• Abnormal structures

• Peritoneal structures

What other technique can be used to identify abdominal problems?

Gastroscopy

What further procedures can you do to diagnose the cause of a chronic colic/ weight loss?

• Oral glucose absorption test

  • Absorption test (indicated SI absortion) vs. tolerance

  • SI only

• Rectal mucosal biopsy

• Gastroscopy

• (Duodenal biopsy)

• Exploratory laparotomy / laparoscopy

Explain how an oral glucose absorption test is carried out?

• Fast overnight

• Baseline blood glucose

• 1 gm/kg glucose as 20% solution by nasogastric tube

• keep horse calm (do not sedate with alpha 2’s)

• Measure blood glucose q. 30mins

What are the parameters for a oral glucose absoprtion test? What is the limitaiton?

• Indicates SI absorption

• NORMAL absorption = >85% incr.

• PARTIAL malabsorption = 15 - 85% incr.

• COMPLETE malabsorption = < 15% incr.

Major issue w/ this test —> EMS status

How is rectal mucosal biopsy carried out?

• Mare uterine biopsy instrument

• 20-30cm inside rectum

• Submit for histo (in formalin)

• Single dose of penicillin & tetanus prophylaxis

What is the limiation of GI biopsies?

Does not reflect state of the entire GI tract

List some of the conditions associated with chronic colic and/or weight loss

• IBD

• Multi-systemic infiltrative bowel diseases

  • Multisystemic eosinophilic epitheliotropic disease (MEED)

  • Systemic granulomatous disease

• Equine Lymphoma

• Chronic infection

• Chronic parasitism

• Equine gastric ulcer syndrome (EGUS)

  • Equine squamous gastric dx (ESGD)

  • Equine glandular gastric dx (EGGD)

What are the different classifications of IBD?

• Lymphocytic-plasmacytic enteritis

• Eosinophilic enteritis

• Granulomatous enteritis

inflam cells in intestinal wall → malabsorption & protein loss

How is IBD diagnosed?

Poorly understood condition but thickened wall on U/S, serum biochem changes, biopsy histo

How is IBD treated?

• Manage underlying cause —> parasites? (anthelmintics), sand?, salmonella?, clostridia?, dietary allergy?

• Non specific treatment:

  • Prednilosone (monitor for signs of laminitis)

  • Dexamethasone

  • Dietary mangement

What are the multisystemic infiltrative bowel diseases that can affect horses?

• Multisystemic eosinophilic eptheliotropic disease (MEED)

  • also often involves skin, particularly around coronary bands, pancreas, liver

  • tx —> dexamethasone

• Systemic granulomatous dx

  • Skin & other organs may be affected

List some Ddxs for IBD

• cyathostomosis

• mixed strongyle infection

• idiopathic

• infiltrative bowel dxs

• Neoplasia

• Lawsonia (foals 3- 11 months)

What type of lymphoma affects the GI system?

Alimentary —> can be generalised or solitary

(also cr. mediastinal & cutaneous)

What paraneoplastic syndromes can lymphoma cause?

• hypercalcaemia

• haemolytic anaemia

• cachexia

What are the clinical signs of lymphoma or other forms of disseminated neoplasia?

• fever

• wt. loss

• peritonitis

• pleural effusion

• abdo distension

• intra-abdominal mass palpable per rectum

• Hypercalcaemia/haemolysis/cachexia of malignancy

List the other intestinal neoplasia other than lymphoma that can affect the horse?

• Leiomyoma

• Myxosarcoma

• Gastric / Adenocarcinoma

• Melanoma

What are the causes of chronic parasitism and what dot they lead to?

• Large strongyles —> strongyus vulgaris:

  • overall luminal burden, wt. loss

  • verminous arteritis

  • thromboembolic colic

• Small strongyles —> cyathostomins:

  • submucosal inflam → wt. loss, D+, colic (can be recurrent)

• Parascaris equorum:

  • youngsters → wt. loss / ill thrift, SI impactions

What are the most common causative agents of chronic bacterial infection in the GI tract? ***

S. equi and R. equi

How do you diagnose and treat chronic infection of the GI tract? ***

Diagnosis

• inflam haemogram

Treat

• Long term antibiotics

What are the common haematological changes for parasitism? ***

• Neutrophilia, hypoalbuminaemia, and hyperglobulinaemia

• NOT eosinophillia

What are the features of equine gastric ulcer syndrome?

• Widespread & common (70% of horses in training)

• Hard to detect

  • Poor athletic perfromacne, recurrent colic/ poor behaviour, wt. loss, bruxism (involuntary grinding of teeth)

What is the most common site of gastric ulceration in horses?

Just dorsal to margo plicatus

What are the two forms of EGUS?

• Equine squamous gastric disease (blue)

• Equine glandular gastric disease (green)

What causes equine squamouse gastric dx? What are the two types?

Acid contact w/ squamous ep.

• 1° = ass. w/ management factors, rest of GI tract normal

• 2° = 2° to delayed emptying of stomach 2° to another problem in GI tract

  • E.g. glandular dx

Why are horses so susceptible to gastric ulceration?

• Performance horses —> incr. exercise intensity / freq

• Horses evolved to contunously graze & digest fibre; grains rapidly fermentable → production of acids

• If diet is high starch/ low roughage & intermittently fasted / lack of access to roughage → high risk

  • >2g/kg BW starch intake per day or 1g/kg BW starch per meal

What are the other risk factors of gastric ulceration?

• Hypertonic electrolyte solutions

• Increased stabling (?)

• Lack of contact with other horses

• Stress, (transport etc)

• Pain e.g. lameness

What are the grades of squamous ulcers?

Grades 1-4

• yellowing —> hyperkeritinisation

• Grade based on depth & extent of ulcer

What causes equine glandular gastric dx?

• It is a secretory surface of HCL & digestive enzymes

• Often this disease is not an ulcer but inflam

What are the risk factors for of EGGD?

• Lower prevalence than ESGD in thoroughbreds

• Sports/leisure horses

  • Warmblood

• Exercise > 5 days/week

  • Not intensity

• Recently started training

• Stereotypies

• Inflam bowel dx

• Reduced blood supply to stomach

• Feed —> unclear

What are the management changes to prevent gastric ulceration?

• High fibre, low starch diets —> incr. chewing = saliva

  • flax oil if needed for additional energy

• Cont. roughage access

• Concentrate meals should not be fed < 6hr apart

• Feed small chaff feed 20min before exercise (ESGD)

• Cont. access to water

• Electrolyte pastes in feed, not direct

• Min of 2 rest days / wk

• Minimise stressors

• Avoid high dose/ long courses of NSAIDs

Explain the general tx of gastric ulcers?

• Management (Diet & exercise)

• Medication —> acid suppression

  • Omeprazole (PO)

    • Mainstay for ESGS (supports EGGD healing)

What is the licensed dose for oral omeprazole in horses?

4mg/kg for 4wks q. 5d

• V. effective against squamous ulcers —> most effective tx for EGGD

• Give on empty stomach —> 30-60min before morning feed

• not effective as mono-therpy for glandular dx

Other than omeprazole what other drugs can you give for glandular dx?

• Oral Misoprostol

  • Prostaglandin E analogue —> CANNOT be handled by pregnant women & not for use in pregnant mare

  • Stimulates mucus and bicarb secretion

  • Improves blood flow to mucosa

  • Inhibits acid secretion

• Injectable omeprazole ± oral sucrulfate

• Oral esomeprazole (unlicensed) + sucralfate

• Oral omeprazole + oral sucralfate

List some additional therapies that you can add to omeprazole to treat equine gastric disease?

• Sucralfate

• Anatacids

• Pectin-lecitihin

• Yeast, probiotics, antioxidants, aloe vera, sea buckthorn

• Steroid drugs

• Antibiotics

  • If bacterial infection is suspected

What is the main mechanism of sucrulfate?

• Physical barrier to acid diffusion

• Stim of mucus secretion

• Incr. production of prostaglandin E

When would ABs be used to treat gastric ulcers?

Only where biopsy shows neutrophilic inflam & bacterial culture grows heavy growth of potensh relavent pathogen

Summarise the squamous and glandular medication

What can be done if treatment doesn’t work for gastric ulcers?

• Behaviour hasn’t improved? —> if stomach has healed = revisit diag

• Stomach lesions not resolves?:

  • squamous —> complete cure

  • glandular —> difficult to achieve pristine mucosa

• Long duration first line tx, second line tx?

• Management sufficiently changed?

• Underlying drive missed?