Esophageal obstruction (Choke), Equine gastric ulcer syndrome (EGUS), Equine Peritonitis

Question 1

3 anatomical reasons why horses choke

Answer 1

First 2/3 of the esophagus made up of striated muscle that can contract at will.
Last 1/3 of esophagus is horizontal and made up of smooth muscle that cannot contract at will.
Equine have tightest cardiac sphincter which needs stimulation to open (material pressing against it).

Question 2

Equine choke obstruction is caused by

Answer 2

Usually food (grain, pellet feeds, beet pulp, hay, carrots), sometimes foreign body.

Many pellets for horses NEED to be soaked (so that they wouldn’t stick and expand in the esophagus).

Question 3

Part of esophagus most commonly involved in choke.

Answer 3

most commonly occur proximally in the cervical esophagus

Question 4

4 Primary reasons for choke in equine.

Answer 4

‒ Dental problems (not chewing long enough)
‒ Eating behaviour (eating too fast, not chewing long enough)
‒ Dehydration and exhaustion
‒ Sedation (esophageal motility/contractility↓)

Question 5

7 Secondary reasons for choke in equine.

Answer 5

‒ Neuromuscular dysfunction
‒ Strictures
‒ Megaesophagus
‒ Diverticulum
‒ Tumors in the oesophagus
– Squamous cell carcinoma
‒ External compression of the oesophagus

Friesian horses are most prone to megaesophagus and thus choke.

Question 6

Tip to encourage horses to eat their grain slower.

Answer 6

Add a big rock (like cantaloupe sized at least) to their grain bucket. They are forced to fish around the rock to eat their grain.

Question 7

7 Clinical signs of choke.

Answer 7

• Dysphagia
• Intermittent flexion and extension of the neck
• Bilateral nasal discharge
  ‒ Foamy green froth (but can also be white foam)
• Excessive salivation
• Coughing and retching
• Focal swelling may be seen
• Dehydration

Owners may mistake the signs for respiratory issues.

Question 8

Ddx for choke.

Answer 8

• Dysphagia
  ‒ Teeth problems
  ‒ Strangles
  ‒ Oral foreign body
• Ptyalism
  ‒ Oral foreign body
  ‒ Strangles
  ‒ Stomatitis
  ‒ Parotitis
  ‒ Rabies
• Nasal discharge
  ‒ Strangles
  ‒ Sinusitis
  ‒ Ethmoidal hematoma
  ‒ Airway diseases
  ‒ Reflux

Question 9

Choke is an emergency. How should you advise the owner over the phone?

Answer 9

• Empty the stall so that it contains no food, water, or even bedding (muzzle if needed).
• Minimize the possibility of aspiration. Head down!
• Some esophageal obstructions may resolve spontaneously.

Equine choke is a common ailment.

Question 10

Diagnostics/ diagnostic procedures for equine choke. (5)

Answer 10

• Clinical signs, plus
• Inability to pass nasogastric tube to the stomach
  ‒ Lubrication
  ‒ Be gentle
• Sometimes external palpation (left side of neck)
• Esophageal endoscopy
  ‒ Sedation interferes with esophageal motility
  ‒ Can observe amount of damage after the obstruction
• X-ray (with contrast media)
  ‒ Gas proximal to obstruction, in the surrounding tissues, if ruptured
  ‒ If perforation suspected, do not use barium!

Question 11

Sedation and analgesia in equine with choke. (7)

Answer 11

• Romifidine
• Detomidine 0.01 – 0.02 mg/kg IV or 2 x dose IM
• Xylazine 0,25 – 0,5 mg/kg IV
• Butorphanol 0.02 – 0.03 mg/kg IV in combination with alpha2 agonists
• Flunixin (flunixine meglumin 50mg/ml) 1.1 mg/kg IV
• Acepromazine 0,04 – 0,1 mg/kg IV (15 – 20 min)
• Oxytocin 0.11 – 0.22 IU/kg IV for short-term esophageal relaxation.
  ‒ Proximal esophagus (striated muscles) In vitro distal esophagus
  ‒ Side effects: Colic, sweating
  ‒ Do not administer to pregnant mares

Triin does not recommend the use of oxytocin if you really don’t need it (due to side effects).

Question 12

Lavage for choke.

Answer 12

There’s a high risk of aspiration of fluids, so:

• 2 Nasogastric tubes:
  1 short endotracheal tube through a nostril to block the trachea.
  A 2nd, but longer and thinner tube is fed through the short one so that is for sure bypasses the trachea. Since it’ll be sheathed by the shorter tube, you can move it back and forth more freely without damaging the meatus mucosa. LOTS of lubrication!
• Only lavage via tube if heavily sedated
  ‒ First DO NO HARM
  ‒ Small volumes of water
  ‒ Keep the head lowered (gravity)
  ‒ NEVER use paraffin oil during lavage
• Can leave in stable for 6 hours
  ‒ No food or water
  ‒ Heavy sedation is the key

even only 100 ml of paraffin oil can destroy the horses’ lungs

Question 13

If the esophageal obstruction is not resolved in 6 hours…

Answer 13

refer to the clinic/hospital.

• For Transportation
  ‒ Head as low as possible
  ‒ Safety first
  ‒ Sedation

Question 14

At the clinic, choke cases should be worked up with the following: (6)

Answer 14

• Hematology/biochemistry
• Sedation and analgesia
• IV-catheter
• Fluid balance
• Endoscopy
• Treatment of the aspiration pneumonia

Question 15

IV catheter and fluids for choke cases

Answer 15

• Long standing cases (> 12 hours)
• Salivary loss (dehydration, electrolyte imbalances)
• Intraflon IV catheters 12 G (pictured)
• Maintenance rate 65ml/kg/day
• If dehydrated ≥ 1.5 x maintenance

Triin says can bolus using maintenance x 1.5- 2, e.g. 500 kg horse 48.75- 65L / 24 = 2- 2.7 Liters

Question 16

What is this and how is it treated?

Answer 16

Aspiration pneumonia

• Give Antibiotics if obstruction is there > 1 hour
• First signs of aspiration pneumonia can appear in 24 h of obstruction, but sometimes it takes several days.

Antibiotics
* Penicillin against gram pos. 22 000 – 44 000 IU/kg IV q6h
* Gentamicin against gram neg. 6,6 mg/kg IV q24h (check renal function due to nephrotoxicity)
* Metronidazole against anaerobics 15 – 25 mg/kg PO q8h

Nebulisation
* NaCl vapor mixed with gentamicin

Question 17

Why are triglycerides measured from a choke case horse?

Answer 17

checking triglycerides in a choke case horse is crucial because prolonged fasting due to the choke can trigger dangerous fat metabolism imbalances, leading to hyperlipemia and potentially serious complications.

Hyperlipemia can lead to fatty liver disease and organ failure, which can be fatal if not treated.

Treatment focuses on getting them eating again, providing IV fluids with glucose or oral molasses, and sometimes medications to control fat metabolism.

Question 18

Which AB do you need to be careful about monitoring the kidneys with?

Answer 18

gentamicin

you may be able to use enrofloxacin instead

Question 19

First part of lungs to receive aspiration of fluids or other?

Answer 19

right cranial lobe

Question 20

What is ACC (Equimucin) for post-esophageal obstruction?

Answer 20

ACC = Acetylcysteine

Acetylcysteine is a mucolytic, meaning it helps break down thick mucus. This can be useful in choke cases where mucus buildup in the esophagus makes swallowing difficult.

Is also a powerful antioxidant that helps reduce oxidative stress and inflammation.

Equimucin (NAC powder) can be given by mouth to help thin secretions in the esophagus and airways.

Question 21

Tx of aspiration pneumonia in clinic.

Answer 21

Equivet IV catheter 12- 14G

Combo ABs, gentamicin, flunixin, metronidazole + molasses orally + ACC was added (Equimucin)

Also give many liters of Ringer’s as a bolus (due to illness and gentamicin, trying to avoid kidney failure). E.g. a horse might get 10 L but it depends on weight.

Nebulisation with gentamicin.

Question 22

Tx of aspiration pneumonia at home.

Answer 22

The pleura is painful in aspiration pneumonia.

• Drug choices for analgesia
  – Flunixin 1.1 mg/kg IV or PO q12h
  – Phenylbutazone 2 - 4.4 mg/kg PO q12h
  – Meloxicam 0.6 mg/kg PO q24h
  – After 3 – 5 days reduce doses
• Antibiotics
  – Procaine pencillin 22 000 IU/kg IM q12h or
  – TMS 30 mg/kg PO q12h
• Check rectal temperature daily for 2 weeks!

Question 23

Complications of esophageal choke. (6)

Answer 23

• Esophageal mucosal ulceration, necrosis
• Stricture formation (usually in 30 days)
• Esophageal perforation
• Aspiration pneumonia
• Chronic recurrent obstruction (usually has underlying problem)
• Megaesophagus (Result of chronic or recurrent obstruction, develops Proximally to the obstruction and has a poor prognosis)

Question 24

Feeding after esophageal obstruction.

Answer 24

Simple obstructions without mucosal damage or with mild damage can be fed after 12 – 24 hrs.
* Small amounts of pelleted feed or grass every 4 – 6 hours
* No hay for 4 – 5 days. Start to feed hay gradually.

If esophagal ulceration or strictures occur, feed should not be provided 48 – 72 hrs.

Minimally abrasive feed
* Greenline
* Mash
* Grass or chopped hay

Question 25

How long should you not feed a horse after sedation for?

Answer 25

2 hours

Question 26

Equine gastric ulcer syndrome (EGUS) is super common. What is it?

Answer 26

EGUS - Equine gastric ulcer syndrome is An umbrella term. EGUS = ESGD and/or EGGD: ESGD - Equine squamous gastric disease EGGD - Equine glandular gastric disease Ulceration can be in the terminal part of esophagus, non-glandular (squamous mucosa) or glandular gastric mucosa, or proximal duodenum. So, squamous (non-glandular fundus) is more common. Glandular ulcers (affecting the lower stomach and pylorus) are less common.

Question 27

Prevalence of EGUS.

Answer 27

Is extremely prevalent condition and an economically significant disease. Varies with breed, use, level of training but, * up to 90% of Race horses in training have it * up to 60% of Show/sport horses have it * 66% of Pleasure horses have it * up to 70% of Broodmares have it

Question 28

Describe the parts of the horses' stomach.

Answer 28

Non-glandular stomach: fundus (acts as a storage area). Glandular stomach: body, pylorus Horses have continuous gastric acid secretion!

Question 29

What secretions does the glandular portion of the equine stomach produce or are otherwise found there? (6)

Answer 29

HCl pepsin bile caids organic acids bicarbonate mucus ## Footnote The pH is lowest near margo plicatus in adult horses. There's no pH gradient in nursing foals.

Question 30

Describe Prostaglandin E2. (5)

Answer 30

* Promotes secretion of the mucus-bicarbonate layer * Enhances mucosal blood flow * Mucus and bicarbonate production * Stimulation of production of the surface-active protective phospholipids * Mucosal repairment ## Footnote Stress and NSAIDs disrupt its action.

Question 31

Equine gastric ulcer syndrome is caused by: (7)

Answer 31

Exercise (any movement at a speed greater than a walk) which then: * causes Gastric compression * causes Decreased gastric pH (more acidic) Intermittent feeding Diet Transport stress Stall confinement Drugs All The above can cause Prolonged exposure to hydrochloric acid, pepsin, bile acids and organic acids. The fundus has no mucus production for protection thus it Responds to irritation by increasing the thickness of the keratin layer.

Question 32

Diagnosis of EGUS. (4)

Answer 32

Diagnosis of gastric ulcer disease is based on: * Clinical signs * Endoscopic examination * Response to treatment * Post mortem

Question 33

Clinical signs of EGUS. (7)

Answer 33

They are vague colic signs which are usually: * Mild * Recurrent * After eating Inappetence Poor body condition Weight loss Diarrhea (a more rare sign) Changes in behavior: cribbing, head nodding, stall wall kicking, stall pawing, wood chewing, flehmen, and stall weaving. Poor performance

Question 34

Gastric ulcers in foals

Answer 34

Affected foals are often 2 to 6 months of age * Lethargy * Colic * Frequent recumbency * Bruxism * Ptyalism * Frothing or drooling of milk from the mouth * Tongue lolling * Diarrhea (present or recent) * Frequent rolling into dorsal recumbency. The most common in foals is silent gastric ulceration. ## Footnote Sick foal imaged: abnormal sleeping position that indicates colic.

Question 35

Endoscopic examination for equine gastric ulcer syndrome.

Answer 35

* The definitive diagnosis of gastric ulcers is based on endoscopic visual evidence of gastric erosion, ulceration, or other lesions. Assess the lesion severity via scope. * A presumptive diagnosis of the disease can be made based on history, clinical signs, and response to treatment with a therapeutic trial. The stomach is filled with air while scoping in order to visualize the stomach surfaces properly. ## Footnote 14-16 hour fast before scoping. A 3m scope is needed for adult horses, 1.1- 1.5 m for foals.

Question 36

Grading system for equine squamous gastric disease.

Answer 36

0-4 0 – intact epithelium, no mucosal changes or appearance of hyperkeratosis (makes it look yellow) 1 – the mucosa is intact, but there are areas of hyperkeratosis 2 – small, single or multifocal lesions 3 – large single or extensive superficial lesions 4 – extensive lesions with areas of apparent deep ulceration Can be very subjective! There is minimal data on the validity of grading glandular lesions.

Question 37

Tx of EGUS. (6)

Answer 37

* Antacids * H2-receptor antagonists (considered ineffective these day) * Sucralfate * Omeprazole * Misoprostol * Esomeprazole ## Footnote The duration of treatment is 28 days. The stomach needs to be scoped again before the end of the treatment (ideally after week 3) to assess the degree of improvement. Sometimes the treatment needs to continue past 4 weeks.

Question 38

Describe antacids for EGUS.

Answer 38

Antacids: * Aluminium hydroxide * Magnesium hydroxide * Mixtures of both aluminium hydroxide and magnesium hydroxide. (Maalox) * Calcium carbonate (Rennie tablets contain this) They Neutralize acid, but do not have a long duration of effectiveness. 180 ml mixture of aluminium/magnesium hydroxide combination (Maalox) increases the pH of the gastric fluid to greater than 3.0 for 15 – 30 minutes in the horse. (so not very long)

Question 39

Describe H2- receptor antagonists for EGUS.

Answer 39

H2- receptor antagonists Suppress HCl secretion by binding the parietal cell histamine H2 receptor. Efficiacy debatable these days. * Ranitidine 6,6 mg/kg q8h PO * Cimetidine 20 – 25 mg/kg q8h PO

Question 40

Describe sucralfate for EGUS.

Answer 40

Product Antepsin as tablet or fluid. * Sucralfate 12 mg/kg PO q12h Is Sulfated polysaccharide that Adheres to ulcerated mucosa. Stimulates increased prostaglandin E1 synthesis and mucus secretion. Sucralfate may best be used in addition to omeprazole treatment. ## Footnote E.g. Antepsin (sucralfate) 10 tablets twice a day (approximately 12 hours apart) for 4 weeks. Omeprazole and Antepsin should be given at least 30 minutes apart.

Question 41

Describe omeprazole for EGUS.

Answer 41

Is a proton pump inhibitor that blocks secretion of H+ at the parietal cell membrane. Result is long-term blockade of acid secretion. Is 10 times more potent than ranitidine (H2-antagonist). Give SID. * Omprazole 4 mg/kg PO q 24h for 28 days * Omeprazole 4 mg/kg IM q 7 days * Omeprazole 0,5 – 1,5 mg/kg IV q 12-24h Not all types are avail. in all countries. ## Footnote E.g. Peptizole (omeprazole) paste 600 kg dose once a day for 4 weeks. One tube contains 700 kg dose, so the remaining 100 kg dose can be saved. This saves 1 tube per 7 days. Peptizole can be given at any time during the day. Omeprazole and Antepsin should be given at least 30 minutes apart.

Question 42

Describe misoprostol for EGUS.

Answer 42

Misoprostol is a prostaglandin E1 analogue Used in humans to induce labour and abortions as well as treat gastric ulceration. Main use in horses is in the treatment of glandular ulcers. helps treat equine gastric ulcers by mimicking the protective effects of endogenous prostaglandins. Absorption when given per os is higher when the horse is unfed. Some studies have shown misoprostol to be more effective for treating equine gastric glandular disease than even omeprazole. * Misoprostol 5 mcg/kg PO, PR q 8h for 28 days ## Footnote contraindicated in pregnant mares

Question 43

Describe esomeprazole for EGUS.

Answer 43

S – enantiomer of omeprazole (Nexium) Reported to be the most efficacious proton pump inhibitor in humans. The drug can be given with feed. * Esomprazole 0,5 – 2 mg/kg PO q24h

Question 44

Before ending tx for EGUS, you must

Answer 44

Recheck before the treatment period is over! ## Footnote The duration of treatment is minimum 28 days. The stomach needs to be scoped again before the end of the treatment (ideally after week 3) to assess the degree of improvement. Sometimes the treatment needs to continue past 4 weeks.

Question 45

Environmental, nutritional, and dietary management for EGUS. (5)

Answer 45

Without alterations in management, squamous ulcers quickly return if horses are maintained in training. Glandular ulcer recurrence on the otherhand, has not been evaluated. Modification of exercise intensity and duration Pasture turnout Change in management

Question 46

Feeding after EGUS.

Answer 46

The diet needs to be modified to maximise treatment efficacy. The dietary change needs to be permanent to minimise the risk of ulcer re-occurrence. * Hay or dry haylage needs to be available at all times. * Any additional feed needs to be grain-free (not just oat-free) and rich in fiber, protein and oil. The sugar and starch content should not exceed 10%. * Straw should not be fed as the only or primary feed, because it was found to be at least 4.4 times more likely to increase squamous gastric ulcer severity scores! ## Footnote Alfalfa cubes/ hay can be added because theyre rich in calcium and protein, which helps in buffering gastric acid. All changes in feeding have to be implemented gradually.

Question 47

If after adjusting the horses' diet to life after EGUS, is additional energy is required, what can you add?

Answer 47

vegetable oil can be added to the ration. * Maximum digestible amount is 1gr of oil per kg BWT (500 ml per 500 kg horse). * Start from 100 ml/day and adding 100 ml every week. * When oil is given, the horse requires additional vitamin E 100-150 IU per day/100ml oil. (High-fat diets can sometimes displace other vitamin E-rich feedstuffs (e.g., fresh pasture), reducing overall vitamin E absorption.) ## Footnote Image shows some hyperkeratinization because its yellowish.

Question 48

Answer 48

healthy pylorus

Question 49

How many piles of feces should horses pass in 24 hours?

Answer 49

10-12 in 24 hours

Question 50

interpret these: fib 4,7 g/l Lac 1.11 mmol/L

Answer 50

fibrinogen slightly increased, normal 2.0–4.0 g/L lactate still WNL, normal 0.5–1.5 mmol/L ## Footnote Decreased fibrinogen (<200 mg/dL or <2.0 g/L) Can indicate liver disease (reduced production) or disseminated intravascular coagulation (DIC).

Question 51

Describe Normal Peritoneal fluid (3)

Answer 51

* The peritoneal cavity normally contains a small volume of fluid (100 to 300 ml). * A pure transudate that contains solutes in the same concentration as serum. * Absorbed from the abdominal cavity by lymphatic vessels. ## Footnote Peritonitis in horses is usually secondary to another condition.

Question 52

Classification of peritonitis in horses. (4)

Answer 52

* Primary or secondary: indicating the origin of the disease (usually secondary though). * Peracute, acute or chronic: depending of the onset and duration. * Diffuse or localized: indicating the region affected. * Septic or non-septic: bacteria present or not.

Question 53

Describe Primary peritonitis

Answer 53

bacterial infection without an obvious intraperitoneal source. extremely Rare in adult horses

Question 54

Secondary peritonitis may caused by: (4)

Answer 54

– External trauma – GIT-diseases – Breeding and foaling injuries – Intra- and postoperative infections ## Footnote E.g. even a horse getting kicked by another and getting an internal bleed can then develop peritonitis.

Question 55

Most common Peritonitis in the horse is... (4)

Answer 55

secondary, acute, diffuse and septic. * Mixed bacterial infections usually.

Question 56

Clinical signs of peritonitis in horses. (10+)

Answer 56

* depression * colic * inappetence * pyrexia (usually >39,5º C) * tachycardia * tachypnea * ileus or decreased gut sounds * decreased fecal output * sweating * diarrhea * abnormal rectal findings * Mucous membrane color is usually red or hyperemic with a toxic gum line.

Question 57

Diagnostic procedures for equine peritonitis. (4)

Answer 57

* Abdominal paracentesis aka abdominocentesis * Hematology/biochemistry * Rectal palpation * Ultrasonography

Question 58

Peritoneal fluid processing:

Answer 58

* EDTA and plain containers for cytology, gram stain, protein + blood culture bottles. * A diagnosis of peritonitis can frequently be made by direct visual examination of the fluid. * Bacterial cultures are frequently negative despite the presence of bacteria in peritoneal fluid. * The definitive diagnosis of equine peritonitis is usually made by examination of peritoneal fluid.

Question 59

Hematology results in equine peritonitis cases. (4+)

Answer 59

* Fibrinogen can be normal or low in the early stages of acute peritonitis because it takes 48 hours for it to peak. * Endotoxemia will be present ‒ Leukopenia ‒ Neutropenia ‒ Degenerative left shift * Hypoproteinemia * Electrolyte imbalances ‒ Hyponatremia ‒ Hypokalemia ‒ Hypochloremia ## Footnote Rectal palpation findings may be non-specific!

Question 60

U/S in equine peritonitis cases. (2)

Answer 60

* You'll find an excessive quantity of peritoneal fluid. * Fibrin tags or adhesions between bowel and parietal peritoneum or between the abdominal organs.

Question 61

Tx of equine peritonitis. (5)

Answer 61

* Antibiotic therapy needs to be started before results of culture is available. – Na⁺ or K⁺ penicillin 22 000 – 44 000 IU/kg IV q6h – Gentamicin 6,6 mg/kg IV q24h or – Enrofloxacin 5 mg/kg IV or 7,5 mg/kg PO q24h (not for young horses!) – TMS 30 mg/kg PO or 20 mg/kg IV q12h – Metronidazole 15 – 25 mg/kg PO q8h * Analgesic and anti-inflammatory therapy. – Flunixin 0,5 - 1,1 mg q12h, Also used to prevent endotoxemia. * Heparin therapy to prevent adhesion formation. ‒ In theory, heparin decreases thrombin production. ‒ 10 – 120 IU/kg SC q6 - 24h * Abdominal drainage and lavage – Cases with purulent effusion. – If poor response to medical treatment. – 10-30 liters of warmed lavage solution used.

Question 62

Prognosis for equine peritonitis.

Answer 62

Guarded. Life-threatening problem. * Horses with bacteria observed on cytologic examination of the peritoneal fluid have a guarded or poor prognosis. * Mortality rates for peritonitis in the horse range from 30% to 67%. * Mortality rates are dependent on the cause of course. * Intra abdominal adhesions may develop which can cause – Recurrent colic – Poor weight gain – Poor performance

Question 63

Why should enrofloxacin not be administered to young, growing horses?

Answer 63

because it can cause cartilage damage in developing joints. Enrofloxacin is a fluoroquinolone antibiotic, and this class of drugs has been shown to cause chondrotoxicity, leading to erosions and lesions in articular cartilage. This effect is particularly concerning in growing horses, as their joints are still developing and are more susceptible to damage. safer alternatives are trimethoprim-sulfamethoxazole (TMS), ceftiofur, or penicillin

Question 64

How does flunixin meglumine help to prevent endotoxemia in ailing horses?

Answer 64

(commonly known as Banamine) helps prevent the harmful effects of endotoxins released by Gram-negative bacteria. reduces inflammation, pain, and fever associated with endotoxemia. Flunixin helps prevent the harmful cardiovascular effects of endotoxemia, such as hypotension and tissue damage. Flunixin helps stabilize blood vessels, preventing excessive leakage and maintaining circulatory stability. It reduces the production of thromboxane and other inflammatory mediators that contribute to coagulation abnormalities and organ failure.