Equine Medicine

3 categories of weight loss

1. Inadequate intake

2. Increased demand

3. Inappropriate utilization

Inadequate intake

-inadequate quantity

-inadequate quality

-inadequate uptake (dental/GI dz)

Increased demand

-illness

-pregnancy/lactation

-increased workload

-environmental factors

Inappropriate utilization

-liver dz

-GI dz (malabsorption/maldigestion)

What do you need to rule out first before doing you go looking?

-inadequate quantity

-dental dz

-malabsorption/maldigestion

LOOK AT CONCEPT MAP FOR CALORIC REQUIREMENTS

Forage caloric content

0.8Mcal/lb

Grain caloric content

1.3 Mcal/lb

What is the cornerstone of the equine diet?

Forage (hay)!!!! Should meet as much of horses protein, energy, and fiber needs. GRAIN IS NOT ESSENTIAL

Nutritional quality of hay depends on

Time of harvest! Want high CP and low acid detergent fiber and neutral detergent fiber

Alfalfa has high

Calcium! Can be beneficial for horses with ulcers but bad for horses that are predisposed to stones.

Examples of fat that you can add to horse diet

-vegetable oil

-linseeds

-rice bran

When to use fat in horses?

Use in athletes because it spares use of glucose/glycogen and increases use of body fat. It also decreases lactic acid/heat during exercise BUT needs 3 weeks to adapt.

Advantages of fat

-energy density

-no mastication required

-natural protection against GI ulceration

-behavioral benefits (less hot)

Disadvantages of fat

-weight gain

-low palatability

-expensive

-messy

-short shelf life

What is important to note when comparing fats?

They vary in proportions — Omega 3 > Omega 6

Grain digestive disturbances

-colic

-colitis

-diarrhea

-gastric ulcers

-laminitis

Grain metabolic conditions

-laminitis (insulin resistance)

-tying up

-obesity

-joint disease

-hyperlipemia

Sweet feed composition

-oats

-corns

-molasses

-+/- vitamins, minerals

Sweet feed characteristis

-palatable

-quickly consumed

-lower digestibility

-short shelf life

-expensive for nutrients they provide

Pelleted feed composition

-grains

-molasses

-vitamins, minerals

Sweet feed characteristics

-less messy

-longer shelf life

-more economical

-available as COMPLETE FEEDS

-good for horses with bad teeth

Oats

-palatable

-best nutrient balanced

-foregut digested

-high sugar

-makes horses "hot"

Corn

-denser than oats

-not nutrient balanced

-hindgut digested = hindgut acidosis = MUST BE PROCESSED

What is important to add to all diets?

Vitamin/minerals such as copper/zinc

DDX for esophageal dz

-inability to swallow (pharyngeal, neuromuscular)

-choke

-oral dz (ulcers)

-toxins (blister beetles)

Clinical signs of choke

-dysphagia

-frequent swallowing

-coughing

-ptyalism

-regurg of food in mouth/nostrils

-resp signs

-anxiety/neck stretch

-swelling/emphysema

Choke diagnostics

-naso-gastric tube

-endoscope

-radiographs

Naso-gastric tubes

-diagnostic

-therapeutic

-avoid damage! Difficult = do endoscopy

Endocscope

-may not show the primary blockage

-assesses motility, integrity, shape, and mucosa

Radiographs

-not as common or useful

-BARIUM (do not use if perfed)

Vital structures near esophagus

1. Vagosympathetic trunk

2. Recurrent laryngeal nerve

3. Carotid artery

Muscle structure of esophagus

2/3 striated and 1/3 smooth

Importance of serosa in the esophagus

The proximal 2/3rd does NOT have serosa! Serosa is helpful for healing. This means that this portion is susceptible to decreased healing.

Sedation options

-alpha 2 agonists = xylazine/detomidine

-acepromazine

Smooth muscle relaxant options

-buscapan

-methocarbamol

Why do we give sedation?

-lowers the head to decrease aspiration risk

-relaxes esophageal mm

3 common choke sites

1. Cervical portion

2. Thoracic inlet

3. Intrathoracic

Predisposing factors to choke

-poor dentition

-food that expands (beet pulp)

-meds

-corn cobs

Choke treatment

1. Sedation/mm relaxation

2. Lavage

3. Drugs

4. Support

5. Anesthesia

Do we use atropine or mineral oil?

No atropine cause can cause colic and esophagus is only smooth muscle for distal 1/3rd.

No mineral oil because can cause granulomatous pneumonia if aspirated.

Complications of choke

-fibrinous pleural pneumonia

-mucosa necrosis & stricture

Pathogenesis of gastric ulcers

-increase in aggressive factors

-decrease in protective factors

Aggressive factors

-HCl

-Pepsin

-Organic acids

Protective factors

-mucus

-bicarbonate

-mucosal perfusion

What is important about diet in regards to the pathogenesis?

HCl is constantly secreted. Feed and saliva buffers the acid build up. Access to food throughout the day helps to buffer HCl.

Which portion of the stomach has less protective factors?

Squamous epithelium (non-glandular)

Causes of gastric ulcers

-strenuous exercise

-stress/illness

-NSAIDs

-feeding

Clinical signs of choke

-colic

-poor body condition

-poor hair coat

-poor performance

-changing appetite

-attitude changes

-girthiness

-back pain

Foal clinical signs different from adult horse

-D+

-more prone to perforation cause thin stomach

Management of gastric ulcers

-avoid stress

-24hr access to feed

-alfalfa (high Ca2+)

-oil added to diet

Medical management of gastric ulcers

-Antacids

-PPIs (omeprazole)

-Antihistamines

-Misoprostol (synthetic PGE2)

-Sucralfate (bandaid for pain relief)

Good prognosis

-squamous mucosa

-management changes

Fair prognosis

Glandular mucosa

Poor prognosis

Perforation

Clinical signs of liver disease

-hepatic encephalopathy

-photosensitization

-coagulopathy

-icterus

-weight loss

-edema/ascites

Hepatic encephalopathy

-ACUTE but can be chronic

-decreased BUN, increased NH4

Photosensitization

-pathophys = chlorophyl is fermented to produce phylloerythrin that the liver cannot process = photo activated in vasculature

-CHRONIC

-non-pigmented areas

Coagulopathy — which clotting factor is prolonged first?

Factor VII has shortest half life = PT prolonged first

Icterus in food animals

More often hemolytic than hepatic or biliary

Icterus in horses

MOST often due to anorexia followed by hepatic/biliary disease

Icterus in foals

Neonatal isoerythrolysis

Weight loss

CHRONIC

Edema/ascites

-hypoproteinemia and portal hypertension

-CHRONIC

Liver specific enzymes

SDH (hepatocellular) & GGT (biliary)

Liver associated enzymes

AST/LDH (hepatocellular) & AP (biliary)

Acute liver disease enzyme

Severe elevation

Chronic liver disease enzyme

Mild elevation

Hypoalbuminemia is a chronic or acute indicator?

Chronic because has a long half life

Liver function tests

-BUN

-albumin

-glucose

-cholesterol

-bilirubin

Two acute liver disease causes in the horse

1. Theiler's disease

2. Tyzzer's disease

Theiler's disease

-poss viral etiology

-acute hepatic necrosis

-consequence of equine biological products like plasma/tetanus vax

Tyzzer's disease

-foals

-peracute, no signs of dz

-culture, histopath

-usually well-nursing foals

Chronic liver disease causes in the horse

1. Pyrollizidine alkaloid toxicity

2. Cholangitis/cholangiohepatitis

3. Cholelithasis

4. Neoplasia

Pyrollizidine alkaloid toxicity

-weight loss, photosensitization, icterus, HE

-4-6 months post ingestion

-cirrhosis

-no tx, sheep are resistant

Cholangitis/cholangiohepatitis

-icterus

-colic

-fever

-ascending infection, proximal enteritis can predispose

-tx = TMS, supportive care, sx

Chronic liver disease diagnostics

-ultrasound but hard to see cause runs across diaphragm

-liver biopsy to look for fibrosis, inflammation, location, culture

Prognosis of chronic liver disease

Poor if extensive fibrosis

Acute ruminant liver disease

1. Clostridium novyi type D

2. Black dz (C novyi type B)

C. Novyi type D

-anaerobic conditions allows for activation of spores

-liver flukes can create this condition

-necrosis, hemolysis, DIC, ischemic hepatic infarcts

-top DDX = ANTHRAX

Black disease

-sheep

-hepatic necrosis, endothelial damage

-usually found dead with no hemolysis/signs of DIC

Chronic ruminant liver disease

Liver abscess!

Liver abscess cause

High amounts of readily fermentable carbohydrates causing ruminal acidosis then bacterial load overwhelms liver! Subclinical is common but may see laminitis

Caudal vena cava syndrome types

1. Obstruction from abscess results in portal hypertension and pulmonary hemorrhage

2. Rupture into cd vena cava = septic shock and death

Diagnostic liver abscess

Rumenocentesis

Liver abscess prevention

Gradual change of carbohydrates

Pathogenesis of endotoxemia

1. Impairment of mucosal barrier

2. Pro/anti-inflammatory mediators

3. Endotoxin makes microvasculature sticky/leaky/soggy

4. Blood pooling in microvasculature

Pro-inflammatory

TNF alpha and TF

Anti-inflammatory

IL-10

Will you see neutropenia or neutrophilia at first in endotoxemia?

Neutropenia

Clinical signs of endotoxemia

-increase HR/RR

-ileus

-mild to moderate colic

-congested mm/injected vessels

-increased CRT

-decreased peripheral pulses

-DIC

Complication of endotoxemia

Laminitis! May progress after systemic signs approve. Can help by icing the limbs

Causes of endotoxemia

-intestinal inflammation/ischemia

-bacterial infection of pleural/peritoneal cavity

-cattle = gram neg mastitis/metritis

Endotoxemia treatment

1. Prevent uptake

2. Neutralize endotoxin

3. Inflammatory mediators release

4. Prevent activation

Prevent uptake

-remove source of endotoxin

-bind in the GI (sponge/charcoal)

Neutralize endotoxin

-antiendotoxin serum (enhance opsonization)

-polymyxin B (NEPHROTOX)

Inflammatory mediator release

-glucocorticoids = increase risk of laminitis = DO NOT USE

-NSAIDS (good but careful nephrotoxicity)

Prevent activation

-anti CD14 antibody

-allopurinol scavenges ROS from neutrophils

Pathophys of infiltratize disease

Inflammation thickens mucosa and leads to protein/fluid leakage and villi blunting/ulceration

Malabsorption

Mucosa thickens and villi blunts = weight loss and lethargy