Exam 4 Flashcards
Lecture Objectives for Endocrine System
Describe and explain tests used to assess a horse for PPID, EMS, and insulin dysregulation
- PPID
-TRH
Mild cases
-TRH stimulation test
-Assess insulin status
-Refer to EEG recommendation for EMS
Severe or advanced cases
-Baseline ACTH
Baseline ACTH
-EDTA tube
-Keep samples cool
-Centrifuge
-Ship overnight
TRH stimulation test
0.5 mg-1.0mg of TRH IV
-Collect blood in EDTA tube exactly 10 minutes after TRH IV
-Submit plasma
Keep in mind
-changes in environment and health status
-Samples within 12 hours after a grain meal
-Should not be collected within 30 of stress signs
-Not ideal when laminitis, pain, or concurrent illness or malnutrition
-Avoid sedation for 24-48 hours prior
-Samples in Ice packs or refrigerated at all times
-Work with reputable labs
-Season: Severe cases ACTH high regardless of season.
-Larger variability in TRH ACTH responses in the fall FALL best time
-Assessing insulin status PPID cases: can be ID positive, lean or obese.
- EMS
- Insulin dysregulation
Oral sugar test protocol
-Fast 3-6 hrs
-Admin 0.15-0.45 ml/kg corn syrup orally via dose syringe
-Collect blood at 60 and/or 90 minutes
-Measure insulin and glucose
>45 uU/ml = dysregulation positive and RIA
-Assess baseline (fasting) glucose concentration to detect diabetes mellitus (rare)
Seasonal impact
Combined testing
-PPID TRH and immediately after OST
Pituitary Pars Intermedia Dysfunction
- Definition
-Age related dopaminergic neurodegenerative disease affecting the pars intermedia of the pituitary gland
-Inhibitory dopaminergic hypothalamic neurons
-Leads to hypertrophy, hyperplasia, and possibly microadenoma
Increased concentrations of hormones, ACTH
-Affects usually >15 years old animals
-Most common endocrine disease of older horses
-No breed or sex predilection - Etiology
-Progressive degenerative disease
-Early detection is critical - Epidemiology
- Identify, recognize, and interpret clinical signs
-Hypertrichosis
-Muscle atrophy
-Laminitis
-Depression or lethargy
-Weight loss
Early regional hypertrichiosis, later generalized
-PU/PD
-Muscle loss and patchy shedding possible
-Advanced: infections, hyperinsulinemia, laminitis, hair coat changes in color, retained guard hairs neck.
-Pot belly: severe cases - Discuss diagnosis and prognosis
-Early detection is critical
-Signalment, clinical signs, and history
-Incorporate diagnostic test, not test alone
-20% prevalence if >15 yo, 30% if >30 yo
Mild cases
-TRH stimulation test
-Assess insulin status
-Refer to EEG recommendation for EMS
Severe or advanced cases
-Baseline ACTH
- Develop a treatment plan
-Pergolide: is FDA approved, used as initial treatment
-Monitor through baseline ACTH along with clinical signs
Highlights
-Baseline ACTH (late stage)
-TRH stimulation test (early stage)
-Known when and when not to test
-Handling samples correctly matters
-Labs and assays are important
-Pay attention to season
-Combine PPID and ID is good
-Monitor PPID with treatment use baseline ACTH
Equine metabolic syndrome
- Definition
-Affects any age
-Pony breeds over-represented
-Spanish breeds, gaited breeds, miniature horses, warmbloods. - Etiology
Collection of risk factors: genetics, environment, insulin dysregulation is the core feature
-Diet and lack of exercise, excessive non-structural carbohydrates in diet.
-30 genes contribute to ID/EMS/HAL phenotype
-HAL can occur
-May be extremely insulin dysregulated
-May not be obese
-High risk for laminits - Epidemiology
-Welsh and Shetland ponies, Warmbloods more at risk - Identify, recognize, and interpret clinical signs
-Obesity
-Weight loss resistance
-Previous or subclinical HAL (hyperinsulinemia-associated laminitis)
-Divergent hoof rings
-Obesity usually mirrors ID in animals with typical obese EMS phenotype
-BCS 7-9/9
-Carter crest neck scoring system 1-5 (3-5/5 problem) - Discuss diagnosis and prognosis
- Develop a treatment plan
Obese (typical)
-Initial diet
-Restrict or eliminate grazing
-Do not feed grain
-Feed grass with low NSC content 1.5% of BW, reassess in 30 days, gradually lower to 1.2%
-House in dry lot or small paddock
-Avoid stress as much as possible
-NSC analysis highly recommended
-Soak hay in cold water
-Provide mineral/vitamin protein ratio
-Other: muzzle, strip grazing, turnout overnight/early morning, test hay, test pasture
Lean EMS (BCS 405/9)
-Consult with equine nutritionist
-Exercise ex: >5 times per week as canter to fast canter HR >130 BPM>30 mins
-Maintain low glycemic diet
-Restriction depending on postprandial insulin response.
-Low NSC, high fat, hight quality fiber
Medical
-Pergolide tablets
-Refer to EEG on PPID suspicion or concurrent
Exercise contraindicated when laminitis is present
Insulin dysregulation
- Definition
-Defined as any combination of basal (resting insulin) hyperinsulinemia, postprandial hyperinsulinemia (oral sugar test) or consumed feeds, tissue insulin resistance. - Etiology
-Excessive non-structural carbohydrates in diet
-Limited exercise
-Genetics
-Enviromental factors
-Obesity usually mirrors ID in animals with typical obese EMS phenotype
-BCS 7-9/9 - Epidemiology
- Identify, recognize, and interpret clinical signs
-Laminitis
-Divergent hoof rings
-Chronic lameness
-Generalized obesity
-Infertility
-Sheath swelling
-Suspicion of endocrine disease
-Obesity usually mirrors ID in animals with typical obese EMS phenotype
-BCS 7-9/9 - Discuss diagnosis and prognosis
-Withhold feed 3-6 hours, EDTA tube
overnight fasting no longer recommended
-Dynamic testing: Oral sugar test is the preferred and most practical field test
-Insulin tolerance test.
-Resting basal insulin concentration: false negatives are common - Develop a treatment plan
-Diagnosis and prevention via dietary management is key
-Diet and exercise
-Low NSC diet
Medical
-Metformin
-SGLT-2 inhibitors
-GLP-1 agonists and antagonists
-High dose levothyroxine for weight loss when weight loss resistance present
-Metformin hydrochloride loses efficacy over time
-Nutraceuticals, not much science facts
Important to monitor Insulin responses
-Individual response to diet
-Forage and complementary feed
-Throughout the year: when feed/forage changes, with change of BCS, BW, when re-introduced to grass, etc.
Highlight points
-ID is not only a problem for obese EMS horses
-Lean EMS and PPID ID
-Diagnostics are critical
-OST preferred, basal insulin use with caution
-Continue monitoring
-Management: team effort, vet, nutritionist, farrier/podiatrist
Avoid steroids
Thyroid disorders: Hypothyroidism in foals
- Definition
- Etiology
-Cold exposure can increase TRH release, enhanced thyroid hormone release
Blame it on the mare: develops in utero
-Prolonged gestation and dysmaturity: foals looks premature
-Skeletal immaturity: incomplete ossification, mandibular prognathism (monkey jaw) - Epidemiology
-Congenital hypothyroidism
-Excess consumption of iodine during pregnancy
-Fescue ingestion during pregnancy (Acremonium coephialum fungus) low thyroid hormones
-Idiopathic: foals born with goiter and no other signs
Hypothyroidism FYI
-Excess iodine in utero and milk
- Identify, recognize, and interpret clinical signs
-Delayed ossification of carpal and tarsal bones
+/- Goiter
-Respiratory distress
-Dysmaturity
-Mandibular prognathism (monkey jaw) - Discuss diagnosis and prognosis
- Develop a treatment plan
-Management: supplementation/confinement/supportive care
-Prevention: proper nutrition for mare
-No high iodine supplements, off fescue pasture, avoid goitrogens
Thyroid disorders: Thyroid gland neoplasia - Adults
- Definition
-Adult enlarged thyroid gland
-Common in older horses
-Benign adenoma most common
Does not affect thyroid function - Etiology
- Epidemiology
- Identify, recognize, and interpret clinical signs
- Discuss diagnosis and prognosis
-Ultrasound for measuring
-DO NOT biopsy - Develop a treatment plan
-Treatment not needed
Anhidrosis
- Definition
-Inability to sweat when appropriate
-Not an endocrine disease
-Unknown exact cause - Etiology
-Unknown cause
-Hot and humid weather
-When horses are moved to FL from NY, not adapted to heat
-When night time temperatures >70F - Epidemiology/Pathophysiology
-Sweating activated by alpha-2 receptors (neural or catecholamine stimulation)
-Sweat gland atrophy/higher circulation epinephrine, other factors - Identify, recognize, and interpret clinical signs
-Areas of residual sweat: neck, buttock, throat, flank, dilation of vessels.
-Exercise intolerance in hot humid weather
-Tachypnea during and after exercise
-Body temperature may reach dangerous levels
-Dry, thin hair coat
-Ddx: exercise intolerance and respiratory disease
-Dilated vessels crystals - Discuss diagnosis and prognosis
-Intradermal sweat test
-Serial dilutions of alpha-2 agonist Terbutaline
-Amount of sweat proportional to injected
-Delayed onset or insufficient amount
-TPR baseline record
-Lunged a trot for 30 min on a hot day
-TPR per 10 min for 30 min
-T and R correlate to ability to cool down (R back to baseline) - Develop a treatment plan
-Cool down: move to cooler environment, shade, fans, hose or sponge
-Stop workload and decrease stress
-Address concurrent DZ
-Supplements: KCl, L-thyrosine, ascorbic acid, ?dopamine precursors. Vitamin E, chinese herbs, acupuncture
-There is no One specific thing that helps
Meds
-Clenbuterol (alpha-2 adrenergic agonist). In particularly bad weather conditions, may precipitate DZ to complete anhidrosis
Prevention
-Work on CV fitness
-Supplements that were useful
-Control respiratory disease
-Avoid sedation in hot and humid weather
-Plan procedures during cooler weather
Prognosis
-Guarded for future athletic performance in hot weather
Hypocalcemia in Horses
C/S
-Increased neuromuscular excitability
-Tetany, stiff gait, excitability, anxiety
-Fasciculations, tremors, SDF (synchronous diaphragmatic falter)
-Tachycardia, cardiac arrhythmias
-Tremors, tetany, seizures, convulsions, death
-Decreased smooth muscle excitability: ILEUS
Associated Syndromes
-Synchronous diaphragmatic flutter
-Metabolic hypochloremic alkalosis
-Hypocalcemic tetany (e.g., lactation)
-Seizures
-Ileus, retained placenta
-Exhaustion
-Blister beetle toxicosis
-Colic, colitis
-Acute renal failure
Tx
-Calcium borogluconate: 250-500 ml 1:4 dilution slowly
-Monitor HR and rhythm
-May need to repeated/prolonged
Prevention
-Balanced diet
-Avoid bisphosphonates
Nutritional secondary hyperparathytoidism
- Definition
- Etiology
-Nutritional Ca:P ration <1 (normal 1.5-2:1)
-Diets low in calcium, high phosphorous, high oxalates
-Diets rich in grain
-Pastures/toxic with high oxalate levels
-Bran disease, miller’s disease, big head, osteodystrophia fibrous - Epidemiology
- Identify, recognize, and interpret clinical signs
-Increased bone resorption
-Unthriftyness
-Shiftning lameness, limb deformities, spontaneous fractures
-Facial changes, masticatory issues - Discuss diagnosis and prognosis
-Lab: hyperphosphatemia and hypocalcemia
-PTH, FE
-Radiographs: 30% decrease in bone density - Develop a treatment plan
-Diet evaluation
-Eliminate or reduce grain
-Avoid oxalates
-Recovery up to 9-12 months
-Confinement may be needed
Compare and Contrast Equine metabolic syndrome to pituitary pars intermedia dysfunction
Describe the 3 forms of equine metabolic syndrome
- Obese
- Lean
- Non-obese PPID
Summarize the mechanism by which horses with insulin resistance develop laminitis
Prolonged hyperinsulinemia induces laminitis
Laminar tissue damaged
Apoptotic epidermal cell death
Laminar elongation and weakening
Inflammation
Coffin bone rotation and/or sinks
Describe 3 diseases or abnormalities associated with the adrenal gland
Adrenal glands
- Differences exist in foals (immature)
-Late maturation (a few days before parturition)
-Decreased adrenocortical responsiveness
-Different cortisol binding, secretion, metabolism
-Premature foals: lower serum cortisol and higher ACTH, impaired ACTH response and/or cortisol synthesis - Critical illness related corticosteroid insufficiency
-Relative adrenal insufficiency (insufficient cortisol response for illness)
-2 Types of patients: septic foals and adult horses with colic
-Pathophysiology: poorly understood
-Clinical signs: TRIAD vague; related to primary disease
a. Persistent hypotension (resuscitation + volume support)
b. Hypoglycemia, hyperlactemia (glucose, perfusion)
c. Persistent signs of SIRS
-Diagnosis: not well defined (cortisol, ACTH stim)
-Treatment: ill-defined - Overtraining
-Training - fatigue - Rest - Fatigue - 2 weeks - Fatigue Overreaching, overtraining
-Pathophysiology: under research
-Clinical signs: Decreased BW, Increased HR, decreased Cortisol response, increased muscle enzymes, increased GGT. Alter behavior, susceptibility to infection
HPA
Key systemic effects
-Maintenance of blood pressure
-Immune and inflammatory regulation
-Metabolic effects
-Traget tissues: cardiac myocytes, vascular smooth muscle, hepatocytes, adipose tissue, muscle leukocytes
Stress - Hypothalamus - CRH -Anterior Pituitary - ACTH - Adrenal Cortex - Cortisol
Diseases of the Equine Immune System
Th1: cell-mediated immunity
(intracellular bacteria and viruses)
Th2: Humoral immunity
(extracellular parasites)
Th17: Cell mediated inflammation
Autoimmune diseases
(extracellular pathogens, fungi)
Treg: Immunoregulation
(peripheral tolerance)
Immunodeficiencies
Immunoglobulin deficiencies: Failure of Passive Transfer (also under foal diseases)
- Definition
-Secondary or acquired deficiencies: can occur at any age and be transient or chronic
- Etiology
-Secondary humoral deficiency in IgG antibodies due to premature lactation/colostrum loss, poor quality colostrum, or lack of nursing with ~24 hours of birth (2-4 liters)
-3Qs of colostrum: quickly, quantity, quality. - Epidemiology
- Identify, recognize, and interpret clinical signs
-Foal factors: weak and/or poor suckle reflex
-Unable to rise
-Mare factors: recently moved to a new area, not enough time to develop antibodies. Sick, placentitis. Running milk pre-parturition
- Explain the pathophysiology
- Develop a treatment plan
- Describe and explain common methods used to examine and assess the equine immune system in the horse
Dx/Tx
-Test under 24 hrs of age
-May supplement with oral colostrum
-Intravenous plasma over 24 hrs
Immunodeficiencies
Immunoglobulin deficiencies: Combined immunodeficiencies: severe combined immunodeficiency (SCID)
- Definition
-Primary and humoral and cellular immunodeficiency
-Cause: autosomal recessive, inherited condition in Arabian and Arabian-crosses + report in an Appaloosa - Etiology
- Epidemiology
- Identify, recognize, and interpret clinical signs
-Typically start around 3 months of age
-Generalized signs of infection
-Respiratory, GI, musculoskeletal, etc. - Explain the pathophysiology
- Develop a treatment plan
-Highly susceptible to infections and unable to recover
-Lifespan <6months
-Avoid breeding carriers (25% chance of SCID foal when 2 carriers bred) - Describe and explain common methods used to examine and assess the equine immune system in the horse
-Persistent lymphopenia and low IgM in affected foals
-Genetic testing is available
Immunodeficiencies
Immunoglobulin deficiencies: FYI Foal immunodeficiency syndrome and common variable immune deficiency
- Definition
- Etiology
- Epidemiology
- Identify, recognize, and interpret clinical signs
- Explain the pathophysiology
- Develop a treatment plan
- Describe and explain common methods used to examine and assess the equine immune system in the horse
Hypersensitivity diseases
Anaphylaxis
- Definition
-Type I hypersensitivity reaction to an allergen
-IgE mediated, bound to mast cells
-Systemic signs caused by large release of histamine
-Previous sensitization is NOT required
Most commonly caused by vaccines, Vit E/Selenium and plasma
-Can be caused by penicillin, iron, anesthetics, but usually not immunological in origin
-Expiration dates important - Etiology
- Epidemiology
- Identify, recognize, and interpret clinical signs
-Urticaria
-Sweating
-Respiratory distress (dyspnea)
-Cardiovascular collapse and hypotension (weak pulse and or pale mucous membranes) - Explain the pathophysiology
- Develop a treatment plan
-Respiratory distress: 1:100 Epinephrine 3-6ml/450 kg IV (severe), can be IM, or intracardiac
-Temporary tracheostomy
-Furosemide
CV collapse and hypotension
-Epinephrine
-Hypertonic saline
Prognosis
-Variable
Prevention
-Avoid administering known allergens in the future as the response could be worse
- Describe and explain common methods used to examine and assess the equine immune system in the horse
Hypersensitivity
Immune mediated hemolytic anemia
- Definition
-Type II hypersensitivity
-IgG targets (directly/indirectly) RBCs - Etiology
- Epidemiology
- Identify, recognize, and interpret clinical signs
-Anemia manifests as pale/white mucous membranes
-Fever, lethargy, and weight loss
+/- hemoglobinuria (intravascular hemolysis only) - Explain the pathophysiology
-RBC membrane changed by viral, bacterial, or neoplastic disease processes
-Antigen-antibody complex deposition on RBC surface
-Drug-induced hemolysis - Develop a treatment plan
- Describe and explain common methods used to examine and assess the equine immune system in the horse
Dx
-Coombs’ test
-EIA/Piroplasmosis negative
-Regenerative response on bone marrow cytology
-Improvement following removal of drug, if drug-induced
Ddx
-Infectious: piroplasmosis & EIA
-Immune mediated: Autoimmune, bacterial (C. perfringes, Streptococcal)
-Neoplasia: lymphoma
-Drug reaction: Penicillin
-NI
-Iatrogenic Hypo/Hypertonic Soln.
-Oxidative injury: phenothiazine, onion, red maple leaf, familial methemoglobinemia
-Miscellaneous: hepatic disease, DIC, DMSO, OAK, Burn injury.
Tx
-Discontinue any previously administered drugs
-Treat any underlying, primary diseases
+/- Blood transfusion
+/- IV fluids with hemoglobinuria
-Dexamethasone
Prognosis
-Dependent on underlying cause
List common etiologies of laminitis
Definition
-Inflammation of the lamina
-Result: loss of adherence between the hoof wall and the coffin bone
Types
- Rotational: dorsal detachment, more common, better prognosis
- Distal displacement (sinking): circumferential detachment
Causes
- Endocrine
-EMS
-IR
-PPID
-Corticosteroid administration - Inflammation
-Endotoxemia
-Sepsis
-SIRS
-Colitis
-Retained placenta
-Endothelial/vascular dysfunction
-Toxic plants: black walnut - Mechanical
-Compensatory
-Excessive concussion
Steroid Induced Laminitis
-High dose of glucocorticoids can cause laminitis in horses, can occur at lower levels as well
-Mechanism: unknown, probable effect on lamina mediated by insulin
Normal dose of Dexamethasone
-Hyperinsulinemia in insulin sensitive ponies
-No increase in insulin in normal ponies
Triamcinolone
-Hyperglycemia and hyperinsulinemia
-Divergent hoof rings growth
Administering steroids without known laminitis risk does NOT induce laminitis
How to handle these cases
-Low risk: should discuss with client.
-Test for PPID, EMS, IR and get under control before intra-articular injections
-Use the LOWEST dose possible
-Consider other treatment options: Equinox (Firocoxib), ProStride, IRAP.
Laminitis and Endotoxemia/Sepsis
-Endotoxemia: systemic inflammatory response to gram negative bacteria: leads to organ and circulatory failure
-Sepsis may lead to marked inflammatory response distant to source of infection = SIRS. Laminar endothelium as “end organ”
-Tissue damage amplifies inflammatory response: continuation of response after resolution of “infection”
-Horse seems to be getting better and then laminitis
Experimentally inducing laminitis
-Black walnut toxicity
-Oligofructose overdose
Compensatory laminitis
-Vascular dysfunction from mechanical overload
Describe clinical signs associated with the development of laminitis
Stages of Laminitis
Prodromal
-No signs: laminitis not showing the day before on x-rays, can happen quickly
Acute
-Heat in hoof
-Increased digital pulse
-NO rotation
Subacute
-Start rotation of P3
Chronic
-Clear rotation of P3
-Reduction in pain as inflammation resolves
C/S
Bad: heat in hooves, shifting weight, elevated Digital pulse
Worse: Founder stance, reluctant to move, walks heel to toe
Ugly: P3 comes out bottom of foot
Define and apply Obel grading to horses with laminitis
Grade 1
-At rest, horse shifts weight between forelimbs; the horse is sound at the walk, but gait is stilted at the trot and when turning
Grade 2
-Gait is stilted at the walk and the horse turns with difficulty, but one forelimb can be lifted
Grade 3
-The horse is reluctant to walk, and one forelimb can only be lifted with great difficulty
Grade 4
-The horse will only move if forced
Describe how to take radiographs and a venogram of a horse with laminitis, including measurements on radiology used to diagnose laminitis and determine prognosis
Radiographs
Correct laterals & Dis of P3 = 2 views
-Marker on dorsal hoof wall
-Distal P3 alignment in all planes, not coffin joint!!
-Level surface: can tell if sinking medially
-Include entire hoof capsule
-Do not have to remove shoes or pack foot
- Sole Depth
- Palmar angle
- Angle of dorsal hoof wall vs. angle of dorsal P3
- Coronary band to extensor process of P3 “founder distance” measure of “sinking”
- Distance of P3 to dorsal hoof wall “wall thickness” measure of “rotation”
Monitor case progression
-Founder distance: not influenced by trimming
-P3 rotation: can be influenced by trimming
Venogram
-Helps determine prognosis
-Visualize blood flow within the foot
-Filling defects indicate a lack of perfusion
Procedure
- Sedation
- Inject contrast
- Tourniquet on the leg to keep contrast in the foot
- Radiographs taken within 45 minutes
Venogram
Lots of ways to mess up and make your image look worse than the patient is
-Inadequate contrast injection
-Wait too long to take the radiograph
-Difficult finding peripheral vessel
-Tourniquet not tight enough
-Practice normal
Prognosis
-Take radiographs every few days
-If better then every 6-8 weeks at shoeing appointments
-Serial venograms: can be repeated to help determine if treatment is working or if you need to be more aggressive
-Loss of contrast in lamellar zone, circumflex vessels & terminal arch = grave prognosis
Describe how to treat a horse with acute laminitis
- Eliminate underlying cause
- Cryotherapy best for prevention
-Profound anti-inflammatory effect
-Causes vasoconstriction: prevents hematogenous delivery of laminitis triggers
-Suggested protocol: immersion of limb up to the carpus/tarsus
-IV fluid bags taped to feet
-Jack’s Ice boots modified $400 - Support the bony column
-Axial support
-Decreases lever on lamina at toe
-Decreases pull of DDFT
Take weight off the wall and put it on frog and sole
a. Pull shoes
b. Impression material or styrofoam
c. Wooden clogs +/- impression material: reduce pull of DDFT, screwed on less painful than nails
d. Other orthotics
e. Sand stall or deep bedding: >6inches deep, more pressure on sole of hoof - Pain control
- Inflammation
- Nociceptive
-Biochemical disruption
-Remodeling of structures - Neuropathic
NSAIDs - Injectable or oral
-Flunixin meglumine
-Phenylbutazone
-Firocoxib
Opioids
-Butorphanol Injectable
-Morphine: can cause colic and excitation at high doses
GABBA
-Gabapentin: used for neuropathic pain, used in conjunction with other meds, not good alone
Develop an analgesic plan for a horse with acute and chronic laminitis
Continuous therapeutic recommendations
CRI
-Ketamine
-Butorphanol
-Alpha-2 agonist
-Lidocaine
Continuous nerve block
-Catheter and local anesthetic
Microvascular Dysregulation Drugs
-Nitroglycerine (topical): increases digital blood flow??
-Pentoxyfylline: reduces laminar changes in OGF model
-Isoxsuprine: vasodilation
-Acepromazine: IM increases digital blood flow for short time
-NSAIDs: platelet effect via thromboxane, anti-inflammatory
Insulin Resistance Cases
-Levothyroxine or Metformin
-Reduced calorie diet PLUS low intensity exercise is helpful
Develop a therapeutic trimming/shoeing plan for a horse with acute and chronic laminitis
Chronic Laminitis
-Reduce the horse’s weight
-Corrective shoeing
Short toe to ease breaker and reduce pull of DDFT
-Elevated heel
-Reduce weight bearing on walls and toe
-Leave the sole!
Point A: furthest dorsal the shoe should be set
Point B: ideal point of breaker
May end up with 2 planes of weight bearing surface
Type of shoes
-Egg bar
-Heart Bar
-Backward shoe
-Wide web aluminum +/- rocker or wedge
Hoof Wall Resection
-Chronic abscessation
-Chronic Band Prolapse
Surgical Options
DDF Tenotomy
-Rotation despite best efforts
-Persistent pain despite radiographic stabilization
-Correct secondary flexural deformities
-Perform mid-carpal region: above sheath, leaves distal sites an option
-Prognosis: salvage procedure
Equine Pain management
Assess pain in an equine patient
Adaptive pain
-Protective
-Necessary part of life
Maladaptive pain
-Result of a disease or surgical trauma (e.g., amputation)
-Can affect peripheral and central pain centers
Goal: keep adaptive pain and get rid of maladaptive pain
Golden Rules for Pain Assessment
- Prevent: predictable tissue trauma whenever possible. Preemptive multimodal therapy, minimizing neuroplasticity and heightened pain
- Be proactive: Behavior should override pain scores if animal in signs of distress
- Be observant: frequently check for signs of pain
Frequent Pain Assessment
-Every 2 hours
-Helps detect subtle changes
-Goal: determine if analgesics need to be increased, changed or tapered. NOT to withhold pain medications
- Undisturbed observation: Position in stall, body expression, degree of awareness (curious, dissociated, annoyed)
- Observation through interaction
-Owner’s input valuable
-Get to know the animals personality before surgery
-Know “normal” behaviors for that horse
Apply non-traditional analgesic methods to a clinical case
Develop a pain management plan for a horse with laminitis
