Esophageal obstruction (Choke), Equine gastric ulcer syndrome (EGUS), Equine Peritonitis Flashcards
3 anatomical reasons why horses choke
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).
Equine choke obstruction is caused by
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).
Part of esophagus most commonly involved in choke.
most commonly occur proximally in the cervical esophagus
4 Primary reasons for choke in equine.
‒ Dental problems (not chewing long enough)
‒ Eating behaviour (eating too fast, not chewing long enough)
‒ Dehydration and exhaustion
‒ Sedation (esophageal motility/contractility↓)
7 Secondary reasons for choke in equine.
‒ 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.
Tip to encourage horses to eat their grain slower.
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.
7 Clinical signs of choke.
- 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.
Ddx for choke.
- Dysphagia
‒ Teeth problems
‒ Strangles
‒ Oral foreign body - Ptyalism
‒ Oral foreign body
‒ Strangles
‒ Stomatitis
‒ Parotitis
‒ Rabies - Nasal discharge
‒ Strangles
‒ Sinusitis
‒ Ethmoidal hematoma
‒ Airway diseases
‒ Reflux
Choke is an emergency. How should you advise the owner over the phone?
- 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.
Diagnostics/ diagnostic procedures for equine choke. (5)
- 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!
Sedation and analgesia in equine with choke. (7)
- 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).
Lavage for choke.
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
If the esophageal obstruction is not resolved in 6 hours…
refer to the clinic/hospital.
- For Transportation
‒ Head as low as possible
‒ Safety first
‒ Sedation
At the clinic, choke cases should be worked up with the following: (6)
- Hematology/biochemistry
- Sedation and analgesia
- IV-catheter
- Fluid balance
- Endoscopy
- Treatment of the aspiration pneumonia
IV catheter and fluids for choke cases
- 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
What is this and how is it treated?
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
Why are triglycerides measured from a choke case horse?
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.
Which AB do you need to be careful about monitoring the kidneys with?
gentamicin
you may be able to use enrofloxacin instead
First part of lungs to receive aspiration of fluids or other?
right cranial lobe
What is ACC (Equimucin) for post-esophageal obstruction?
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.
Tx of aspiration pneumonia in clinic.
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.
Tx of aspiration pneumonia at home.
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!
Complications of esophageal choke. (6)
- 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)
Feeding after esophageal obstruction.
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
How long should you not feed a horse after sedation for?
2 hours
Equine gastric ulcer syndrome (EGUS) is super common. What is it?
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.
Prevalence of EGUS.
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
Describe the parts of the horses’ stomach.
Non-glandular stomach: fundus (acts as a storage area).
Glandular stomach: body, pylorus
Horses have continuous gastric acid secretion!
What secretions does the glandular portion of the equine stomach produce or are otherwise found there? (6)
HCl
pepsin
bile caids
organic acids
bicarbonate
mucus
The pH is lowest near margo plicatus in adult horses. There’s no pH gradient in nursing foals.
Describe Prostaglandin E2. (5)
- 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
Stress and NSAIDs disrupt its action.
Equine gastric ulcer syndrome is caused by: (7)
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.
Diagnosis of EGUS. (4)
Diagnosis of gastric ulcer disease is based on:
* Clinical signs
* Endoscopic examination
* Response to treatment
* Post mortem
Clinical signs of EGUS. (7)
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
Gastric ulcers in foals
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.
Sick foal imaged: abnormal sleeping position that indicates colic.
Endoscopic examination for equine gastric ulcer syndrome.
- 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.
14-16 hour fast before scoping. A 3m scope is needed for adult horses, 1.1- 1.5 m for foals.
Grading system for equine squamous gastric disease.
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.
Tx of EGUS. (6)
- Antacids
- H2-receptor antagonists (considered ineffective these day)
- Sucralfate
- Omeprazole
- Misoprostol
- Esomeprazole
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.
Describe antacids for EGUS.
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)
Describe H2- receptor antagonists for EGUS.
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
Describe sucralfate for EGUS.
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.
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.
Describe omeprazole for EGUS.
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.
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.
Describe misoprostol for EGUS.
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
contraindicated in pregnant mares
Describe esomeprazole for EGUS.
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
Before ending tx for EGUS, you must
Recheck before the treatment period is over!
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.
Environmental, nutritional, and dietary management for EGUS. (5)
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
Feeding after EGUS.
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!
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.
If after adjusting the horses’ diet to life after EGUS, is additional energy is required, what can you add?
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.)
Image shows some hyperkeratinization because its yellowish.
healthy pylorus
How many piles of feces should horses pass in 24 hours?
10-12 in 24 hours
interpret these:
fib 4,7 g/l
Lac 1.11 mmol/L
fibrinogen slightly increased, normal 2.0–4.0 g/L
lactate still WNL, normal 0.5–1.5 mmol/L
Decreased fibrinogen (<200 mg/dL or <2.0 g/L) Can indicate liver disease (reduced production) or disseminated intravascular coagulation (DIC).
Describe Normal Peritoneal fluid (3)
- 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.
Peritonitis in horses is usually secondary to another condition.
Classification of peritonitis in horses. (4)
- 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.
Describe Primary peritonitis
bacterial infection without an obvious intraperitoneal
source.
extremely Rare in adult horses
Secondary peritonitis may caused by: (4)
– External trauma
– GIT-diseases
– Breeding and foaling injuries
– Intra- and postoperative infections
E.g. even a horse getting kicked by another and getting an internal bleed can then develop peritonitis.
Most common Peritonitis in the horse is… (4)
secondary, acute, diffuse and septic.
- Mixed bacterial infections usually.
Clinical signs of peritonitis in horses. (10+)
- 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.
Diagnostic procedures for equine peritonitis. (4)
- Abdominal paracentesis aka abdominocentesis
- Hematology/biochemistry
- Rectal palpation
- Ultrasonography
Peritoneal fluid processing:
- 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.
Hematology results in equine peritonitis cases. (4+)
- 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
Rectal palpation findings may be non-specific!
U/S in equine peritonitis cases. (2)
- You’ll find an excessive quantity of peritoneal fluid.
- Fibrin tags or adhesions between bowel and parietal peritoneum or between the abdominal organs.
Tx of equine peritonitis. (5)
- 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.
Prognosis for equine peritonitis.
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
Why should enrofloxacin not be administered to young, growing horses?
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
How does flunixin meglumine help to prevent endotoxemia in ailing horses?
(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.
