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408 Cards in this Set
- Front
- Back
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What are the core vaccines given to horses in the US?
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EEE / WEE
WNV Tetanus Rabies |
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How much feed should a horse eat per day?
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1.5-2% of its body weight
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Using what arteries can you measure pulse pressure in the horse?
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Facial artery
Transverse facial artery Great metatarsal artery |
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What are the IM injection sites in the horse?
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The middle of the neck
The pectorals Semimembrinosus/tendiosus |
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What is the normal heart rate of a horse?
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24-44bpm
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What is S1?
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Closure of AV valves (lub)
(tricuspid & mitral) |
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What is S2?
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Closure of semi-lunar valves (dub)
(pulmonic & aortic) |
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What is S3?
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Early diastole/ rapid filling of ventricles
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What is S4?
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Atrial contraction
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What is the order of heart sounds in the horse?
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S4, S1, S2, S3
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What is the most common pathological arrhythmia in a horse?
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Atrial fibrillation
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What are some common physiological arrhythmias?
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Sinus block and 1st/2nd degree AV block. Non-pathologic at rest, should disappear with exercise
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What is the normal respiratory rate in the horse?
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8-16bpm
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What will encourage a horse to breath deeper for more detailed examination of lung sounds?
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A rebreathing bag
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What is the normal temperature for a horse?
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99-101.5F
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What would be a good order to start a physical exam?
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Start at the head, work down the left side and then back up the right side.
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FLUID THERAPY
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FLUID THERAPY
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How is total body water divided up?
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Total body water is 60% body weight
66% ICF 33% ECF |
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What is the main electrolyte in the ECF?
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Sodium
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ICF?
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Potassium
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What is the reflection coefficient of Starling's Equation?
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The efficacy of vessels to prevent leakage of protein verses passage of water. It decreases when disease damages the wall.
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Which space bears the brunt of pure water loss?
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The ICF replaces what is lost from the ECF
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What is an adult horses daily water requirement?
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50ml/kg/day ~ 25L for 500kg horse
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How does a diet high in protein and calcium effect water loss?
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An increase in water lost in the urine
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How does a diet high in fibre effect water loss?
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Increases faecal water output and decreases urine volume
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What electrolyte should be supplemented for a horse on prolonged fluid therapy?
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Potassium - horses have a high K output in their urine and can only get K from their diet. Fluids are normally high Na and low K
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What other electrolyte is excreted in urine?
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Calcium
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Hypernatremia is the hallmark of what?
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Dehydration
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Why is there no movement of water from the ICF in hypovolaemia?
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Because the loss is water and electrolytes therefore there is no change in tonicity
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Which homeostatic mechanisms are activated with decreased circulating volume
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Renin-angiotensin-aldosterone system (RAAS) - vasoconstriction and salt retention
Baroreceptors stimulater sympathetic neurons which increase heart rate Osmoreceptors cause release of ADH |
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What is the clinical expression of dysoxia?
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SHOCK
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What do DO2 and VO2 represent?
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DO2 - oxygen delivery to tissues
VO2 - oxygen required to sustain aerobic metabolism |
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What is the relationship between blood lactate and survival?
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As lactate increases survival decreases.
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At what point are the clinical signs of dehydration noticeable?
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5%
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What clinical signs make hypovolaemia stand out from dehydration?
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Tachycardia
Decreased pulse pressure,jugular fill Tachypnoea Cold extremities |
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What is the single best way to assess dehydration and response to therapy?
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Monitor weight gain once treatment has been started
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Other than haemoconcentration due to dehydration, what other reason is there for a raised PCV in a horse?
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Splenic contraction due to excitement
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A horse with colitis and hypovolaemia will have a total protein of what?
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Normal or low
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What is the normal Central Venous Pressure (CVP) in a horse?
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5-14mmHg
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What does an elevated CVP mean?
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Fluid overload
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Low CVP?
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Insufficient circulating volume
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What is a "shock dose" of fluids and how should it be administered?
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One blood volume - 8% body weight
Give 1/4 of this dose as a bolus and then reassess, give another 1/4 if signs persist. |
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What fluid should you administer if free water is the only thing you want?
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D5W or 5% dextrose
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How many litres of crystalloid should be given after 1L of hypertonic saline?
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10 litres
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What are the 2 most commonly used colloids in horses?
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Hetastarch
Fresh frozen plasma |
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What are the advantages of hetastarch?
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Relatively safe at <10ml/kg
No freezing No cross-matching Can be given quickly in an emergency |
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What are the disadvantages of hetastarch?
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Cannot test for it on a refractometer so cannot measure progress
Prolonged bleeding times at high doses (20ml/kg) |
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What are the advantages and disadvantages of fresh frozen plasma?
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Contains albumin, clotting factors and anti-endotoxaemic factos
However it can cause transfusion reactions and needs to be administered slowly |
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TRUE OR FALSE
It is not advisable to use the SQ space for fluid administration in horses |
TRUE
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How much fluid may be given via nasagastric tube?
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8-10L per hour
Should only give 4-6L per dose to prevent discomfort |
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Before giving enteral fluids what must you ALWAYS check for?
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Gastric reflux
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What should you add to enteral fluids?
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Electrolytes - table salt and lite salt for Na and K
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When is giving enteral pointless?
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When systemic perfusion is impaired, blood supply is rerouted from the gut to the heart and brain
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What size of catheter is normally used in the jugular vein?
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A 14 gauge
In an emergency 10-12 gauge can be used |
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ACID-BASE BALANCE
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ACID-BASE BALANCE
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What is the optimal pH?
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pH 7.40
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Ultimately what determines the hydrogen concentration in the ECF?
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A balance between the PCO2 and concentration of bicarb in the ECF
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What should happen when a primary acid-base disturbance alters one part of the PCO2/[HCO3-] ratio?
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The compensatory response alters the other component in the SAME DIRECTION to keep ratio constant. e.g. if there is a metabolic alkalosis (increase in bicarb), PCO2 should also increase to compensate
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When may a blood gas analysis be performed?
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To determine the acid-base status of the patient
To evaluate respiratory gas exchange of the patient |
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Is an arterial or venous sample most often used for blood:gas?
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Venous most often as it gives reflection of acid-base at cellular level and it is easier to get
Arterial is used when horse is under anaesthesia or has respiratory disease as it helps determine oxygen exchange at the alveolus |
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What is the first step of blood gas analysis?
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Determine if the pH is greater or less than 7.40
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What is the second step?
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Determine the changes in respiratory and non-respiratory components. Will help determine if the problem is metabolic or respiratory
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A gain in H+ if cause by what?
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Increased endogenous production of H+ - ketoacidosis, lacti acidosis
Toxins - Ethylene glycol Decreased renal excretion - Type 1 renal tubular acidosis |
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A loss in HCO3- can be caused by what?
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GI loss from V or D, loss from kidney - type 2 renal tubular acidosis
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An excess of H+ causes what to happen to bicarb conc?
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A decrease in bicarb as it buffers H+
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Metabolic alkalosis can only sustained if what occurs?
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If there is abnormal retention of HCO3- at the kidney i.e.e renal dysfunction as the kidney is normally incredibly efficient at bicarb regulation
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Metabolic alkalosis is usually accompanied by what?
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Hypokalaemia
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What are some examples of conditions causing metabolic alkalosis?
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Volume depletion - chronic V&D, diuretic therapy
Cushing's Disease |
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What is step 3 of determining and acid-base result?
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Is the compensatory response appropriate or not?
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How can you determine this?
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In a metabolic acidosis there should be a prompt decreased in pCO2
In a metabolic alkalosis there should be a rise in CO2 and visa versa |
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What happens when the analytes move in opposite directions?
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They have an additive effect on pH and a mixed acid-base disturbance is present
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How fast is the respiratory response compared to the metabolic response?
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It takes at least 24hrs for the kidney to respond metabolically.
Respiratory response is immediate |
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What is base excess (deficit) defined as?
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The amount of strong acid or base necessary to titrate 1L of blood to a pH of 7.40 at 37C while pCO2 is held at a constant 40mmHg
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What does a positive or negative BE mean?
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Positive base excess = alkalosis
Negative BE = acidosis |
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What is step 4?
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Determine if the diagnosis fits the patient's clinical condition. One way to do this is to measure the anion gap.
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How do you measure the anion gap?
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AG = (Na + K) - (Cl + HCO3)
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What is normal for anion gap?
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Normal = less than or equal to 15
High means there is an acidosis |
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What can make an anion gap calculation less useful?
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Abnormal phosphorus or protein
Hypoprteinamia with elevated lactate (AG can be normal) |
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How do you calculate amount of bicarb to administer?
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Body weight (kg) x 0.5 x bicarb deficit = amount of bicarb needed
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As a rule of thumb how is bicarb given?
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50% total as bolus and give the rest slowly while monitoring over 24hrs
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What care must be taken?
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Acute acidosis can have rebound alkalosis.
Better to correct volume depletion with fluids first before HCO3- Look out for iatrogenic hypernatraemia as bicarb is given as NaHCO3 |
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What is the leading cause of death in patients with colic, colitis or sepsis?
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Endotoxaemia
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What are some of the complications on endotoxaemia?
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Laminitis
Systemic Inflammatory Response Syndrome - leading to shock, multiple organ failure and death |
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What is an endotoxin?
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A heat stable lipopolysaccharide (LPS) structure
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What type of bacteria LPS as their major cell wall componant?
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Gram negative - even if not infectious
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Which part of the LPS is the toxic principle?
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Lipid A
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The O-specific chains, O-antigens define what about the LPS?
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The virulence factor
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O-chains also serve as what?
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Antigens for the production of host species-specific antibodies
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Gram negative live where in the horse?
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Very large amounts in the cecum and colon of GI tract
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What mechanisms are present to protect against small amounts of endotoxin?
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Mucous layer in the gut
Tissue macrophages and Kupffer cells |
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What are the clinical signs of endotoxaemia?
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Fever, leucopenia or leukocytosis, coagulopathy, hypotension, shock and death
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How can LPS get into the blood steam?
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Pentration through the GI wall
Inhalation Parental solutions Wounds Metritis |
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What first attacks free endotoxin?
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Lipopolysaccharide binding protein (LBP) which is synthesized in the liverand is an acute phase protein
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What is the main function of LBP?
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To carry LPS molecules to endotoxin-responsive immune cells
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What is CD14?
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A receptor found on macrophages, neutrophils and monocytes where the LBP-LPS complex is presented
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Which receptors are responsible for LPS signaling on innate immune cells?
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CD14 and toll-like receptor 4 (TLR4)
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How do they translocate the LPS signal to the immune cells?
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With MD-2 a transmembrane protein
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What does the CD14-TLR4-LPS signal mean?
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It upregulates nuclear transcription factors within the cell which leads to the immun cell producing loads of inflammatory cytokines
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What are some of the cytokines that get released?
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Interleukin 1 (IL1)
Tumour necrosis factor (TNF) IL6 IL8 Platelet activating factor (PAF) |
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Which cytokines are primarily responsible for mediation of the clinical signs of endotoxaemia?
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TNF and IL1
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TNF is central in the pathogenesis of what?
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Endotoxic shock
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Metabolites of the lipooxygenase pathway, which include leukotrienes, are responsible for what?
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Vasocontriction
Bronchospasm Increased vascular permeability |
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What are some of the potent vasodilatory agents that are produced?
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Free radicals
NO Histamine PGE2, PGI2, PGF2a These potentiate oedema formation |
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What do selectins do?
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They allow the PMNs to roll along the endothelial surface and interact with endothelial intercellular adhesion molecules (ICAMs)
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What does this do to the PMNs?
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Makes them exhibit less chemotactic sensitivity to interstitial mediators,
It is the lining of PMNs along vessel walls and their decreased extravasation which accounts for the moderate to severe neutropenia of patients |
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What comes from the PMNs that further damages vessels?
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Reactive oxygen species (ROS)
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What is it that leads to systemic hypotension and inadequate perfusion of tissues?
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The loss of vascular tone is the hallmark of endotoxaemic shock
Blood pools in the periphery and tissues no longer get oxygen |
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What is the hyperdynamic phase of endotoxaemia?
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15-45mins
Peripheral and systemic vasodilation, change in permeability = bright red mm and injected vasculature Fever, quick CRT |
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What happens 90mins after infection?
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Diarrhoea
Congested mm - dark red-purple with a purple "toxic" line Prolonged CRT 3rd spacing |
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What do most horses present with on bloodwork?
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Neutropenia
Lymphopenia Hyperglycaemia Hyperlactataemia |
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What can early, aggressive cardiovascular resuscitation do?
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Improve mortality
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What are the 5 goals of therapy?
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1) CVS resusitation
2) Laminitis prevention 3) Removal of cause/s 4) Neutralize free endotoxin 5) Inhibition of endotoxin-mediated inflammation |
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What does step one begin with?
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Hypertonic saline - suppresses degranulation of PMNs and cytokine release
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What else should be given in step one?
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Crystalloids
Colloids - hetastarch or plasma |
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When is prevention of laminitis most successful?
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Prior to development of clinical signs
ICE!!! Flunixin |
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How can removal of the cause be handled?
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Surgery to remove devitalised bowel
Broad-spectrum abx |
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Which situations indicate the use of systemic antimicrobials?
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1. Horse is <3mths, waning maternal antibody
2. Clostridium suspicion 3. Degenerative left shift or PMN or lymphocyte count of < 1000u/L 4. Clinical evidence of hyshemostasis (jugular thrombosis, abnormal coagulogram) |
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How can free endotoxin be neutralized?
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Combo therapy of hyperimmune plasma and Polymyxin B
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How does Polymyxin B work?
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Suppresses nuclear transcription - prevents inflammatory cytokines
CARE - nephrotoxic in large doses! |
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How can you inhibit endotoxin-mediated inflammation?
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NSAIDs
Lidocaine - decreases inflammation, somatic analgesia, suppresses reperfusion injury Pentoxifylline - decreases cytokines Dimethyl sulfoxide (DMSO) |
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What is DMSO?
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The most widely used ROS scavenger - laminitis prophylaxis
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LAMINITIS
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LAMINITIS
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What is laminitis?
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It is an inflammation of the laminae causing necrosis and degeneration of the dermal and epidermal laminae in the hoof wall.
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What is the job of the laminae?
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They interdigitate and suspend the distal phalanx (P3) of the limb within the hoof capsule
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What happens when the laminae fail?
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It permits weight bearing forces e.g. pull from the deep digital flexor tendon, to drive P3 ventrally through the sole of the hoof
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What is the greatest risk factor?
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Systemic disorders that lead to endotoxaemia and eleboration of inflammatory mediators
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What are some common causes of laminitis?
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GI diseases, grain overload, pleuropneumonia, septic metritis and contralateral limb lameness
Equine Cushings, hyperinsulinaemia, black walnut shavings |
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What clinical sign often appears before the damage to the hoof occurs?
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Bounding digital pulses
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What are other signs of acute laminitis?
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Palpable heat in the hoof
Shifting weight Reluctance to move/pick up feet Rotation or sinking of P3 Tachycardia/pnoea Anorexia/depression |
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What scale is used to grade laminitis?
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Obel Scale
Grade 3 is most common for acute laminitis |
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When taking a radiograph of a laminitic foot where should markers be placed?
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Dorsal hoof wall
Coronary band Apex of frog These help to assess degree of rotation and depth of sole Place foot onto wooden block and take a lateral |
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What are the general principles of laminitis therapy?
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Eliminate the primary cause
Promote digital circulation Reduce tension on the laminae Minimise digital inflammation and pain |
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Cryotherapy and anti-inflammatory treatments are used for what?
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They are the primary means of prophylaxis - start them before there are any signs when a horse has a condition which could lead to laminitis
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What does flunixin meglumine (Banamine) do?
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It has been shown to scavenge free endotoxin
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What does lidocaine do and why would you want to use it concurrently with flunixin?
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Really good anti-inflammatory and when used with flunixin it decreases mucosal injury that occurs with use of NSAIDs
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What is the ideal bedding for laminitic horses?
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Deep sand
Peat moss can be used Can also provide sole support through use of styrofoam pads cut to fit each hoof |
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What happens in chronic laminitis?
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Chonic remodelling of the lamina produces changes in hoof growth from the coronary band
The sole is flat, white line widened and hoof wall shows signs of uneven growth |
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Osteomyelitis and deformation of P3 are typically observed in acute or chronic laminitis?
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Chronic
Recurring hoof abscess are also probable and changes in the lamina result in a misshapen foot |
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What methods are available for derotation of the coffin bone?
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Corrective shoeing - wedge shoe, rounding off the toe
DDF tenotomy to reduce tension |
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What will a venogram tell you?
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What the blood supply to the foot is doing
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Which is a worse prognosis rotation or sinking?
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SINKING!!
Really grave prognosis |
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GI
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GI
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What is the line of demarcation called in the horses stomach?
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The margo plicatus - divides the squamous mucosa and the glandular mucosa
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What commonly occurs at the margo plicatus?
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Ulcers
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How many litres of fluid can the equine stomach hold?
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On average ~8L
With chronic distension ~20L |
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How is the duodenum evaluated?
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By surgical palpation only
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How long is the jejunum?
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18-20 metres
It is freely moveable and most exteriorizable during ventral midline surgery |
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How is the ilium characterised?
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A non-vascular antimesenteric band - ileocecal fold which is contiguous with the dorsal band of the cecum. Landmark during surgery.
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Where is the cecum in the horse?
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Attached withing the dorsal right quadrant of the abdomen and apex is orientated cranioventrally
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How many bands does the cecum have?
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4
Dorsal band is avascular and is contiguous with antimesenteric band of ileum |
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What order does the ascending colon go by in the horse?
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Right ventral colon
Sternal flexure Left ventral colon Pelvic flexure Left dorsal colon Diaphragmatic flexure Right dorsal colon |
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Where are the most common areas of narrowing that are at risk of feed impaction?
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Pelvic flexure
Where the dorsal colon enters the transverse colon |
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Is the transverse colon palpable per rectum?
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No
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What is it about the descending colon that makes it distinct and palpable on rectal exam?
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A wide antimesenteric band and a thick and fatty mesentery
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NSAIDs induce colitis where?
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Right dorsal colon
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What drugs can be used in a rectal exam?
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Xylazine - (decreases HR & GI motility))
Buscopan - (increases HR decrease GI motility) |
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What must you do to try and prevent injury while performing a rectal exam?
|
Use a tail wrap
Copious amounts of lube |
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What might you be able to palpate in a normal abdomen?
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Spleen
Caudal pole of left kidney Nephrosplenic space Ventral band of cecum Pelvic flexure Faecal balls in small colon Caudal aorta Urogenital tract |
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What are the different grades of rectal tearing?
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I - Mucosa and submucosa
II - Muscularis only III - All layers except serosa IV - Full thickness |
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What is the treatment for these tears?
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I & II - laxatives and abx
III & IV - Get to a hospital, need surgery |
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What should you use when performing an abdominocentesis?
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U/S to avoid bowel
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What colour fluid can you get from the abdomen and what do they mean?
|
Orange = peritonitis
Serosanguinous = GI strangulation Green fluid with plant material and WBCs = GI tract rupture Green, plant material NO WBCs = Enterocentesis |
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What length of endoscope is needed to evaluate an adult horses stomach and proximal duodenum?
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3 metres
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How long should feed be withheld in order to decrease the size of the food bolus and visualize all aspects of the pylorus?
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12-18hrs
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What are the contraindications for laparoscopy?
|
Adherent viscera or adhesions at the site of trocar placement
Diaphragmatic hernias Extreme bloating |
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How are abdominal radiographs taken?
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In quadrants
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Which imaging modality has become a routine part of any colic work up?
|
Ultrasound
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What can a faecal examination tell you?
|
Efficiency of mastication
Colonic transit time Evidence of foreign material e.g. sand Cytological exam - GI parasites Culture - Salmonella and E. coli ELISA - Clostridium toxin |
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When is the best time to pass a stomach tube?
|
Acute colic - diagnostic and therapeutic
ANY reflux is ABnormal |
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When should you never administer anything orally?
|
If there is positive gastric reflux (>2L)
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What are the 9 'P's?
|
Physical exam/pulse
Passage of manure Perfusion Peristalsis Pain Palpation per rectum Pass stomach tube Peritoneal paracentesis Probe on the abdomen (U/S) |
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What muscle makes up the cranial 2/3 and the caudal 1/3 of the oesophagus?
|
Cranial 2/3 = Skeletal muscle
Caudal 1/3 = Smooth muscle |
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What does the oesophagus not have?
|
Serosa
(except b/w diaphragm and stomach) |
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What should examination of the oesophagus include?
|
Palpation
Plain and contrast radiographs Endoscopy Fluoroscopy |
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What things should you rule out when faced with a possible oesophageal problem?
|
Foreign body
Teeth issues Cranial nerves (Strangles) Gutteral pouch problems |
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What is the most common oesophageal disorder seen in horses?
|
Oesophageal choke
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What are the most common clinical signs of choke?
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Hypersalivation and froth nasal discharge containing feed and saliva
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What additional signs might be seen?
|
Gagging/retching
Coughing Distention of oesophagus cranial to obstruction Dehydration, weight loss, aspiration pneumonia and oesophageal rupture |
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What would indicate an oesophageal rupture?
|
Crepitus palpable along the neck
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What should be the first thing you do?
|
Sedate the horse, allowing the head to hang below the point of the shoulder
Prevents aspiration |
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What drug may relax oesophageal motility?
|
Buscopan
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After the horse has been sedated what should then happen?
|
Using an NG tube at the level of the obstruction, gently lavage the oesophagus and attempt to gently push the bolus into the stomach
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If the impaction doesn't respond to levage what else can be tried?
|
Put the horse on IV fluids and try to hydrate it that way
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What must NOT be given to the a choked horse?
|
Feed or water
Stable should also be stripped of bedding to make sure the animal is NPO |
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How many horses re-obstruct?
|
40%
Re-slowly with soft mashed food and only after confirming mucosal healing with an endoscope |
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What are some of the complications of choke?
|
Metabolic alkalosis
Oesophageal ulceration Stricture Perforation Aspiration pneumonia Megaoesophagus |
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When should antibiotics be given?
|
If the initial lavage didn't help as aspiration pneumonia is likely
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How long after the initial insult to the oesophagus does it take for the maximum amount of stricture tightening to occur?
|
30 days post-obstruction
Remodelling of mucosa continues for 60 days after ulceration |
|
|
Is an oesophageal stricture a good or bad prognosis in a horse?
|
Guarded
Ballooning or anastomosis are not well tolerated in horses |
|
|
What tends to happen when the oesophagus is perforated?
|
Extensive necrosis of tissues due to drainage of saliva and feed material within the facial planes
Significant SQ emphysema, cellulitis and endotoxaemia are common |
|
|
How can it be treated?
|
Extensive debridement
Lavage of tissues Broad spectrum abx Tetanus prophylaxis Oesophageal rest |
|
|
Are most cases of megaoesophagus acquired or congenital?
|
Acquired
|
|
|
How does acquired megaoesophagus develop?
|
Primary or secondary oesophageal obstruction
|
|
|
What is the outcome?
|
Megaesophagus after choke that was solved quickly - usually reversible
However if it takes a long time to correct the choke it may cause permanent motility problems |
|
|
What other diseases can cause megaesophagus?
|
Reflux oesophagitis
EPM Equine herpes myeloencephalitis Botulism Pleuropneumonia Grass sickness |
|
|
What is the treatment?
|
Slurries or pelleted feed to improve transit time
If reflux oesophagitis may respond to metoclopramide or bethanecol to lower oesophageal tone, gastric emptying time and reduce gastroeophageal reflux |
|
|
What is the prognosis?
|
Megaoesophagus related to reflux oesophagitis may respond well
Other forms have a poor prognosis |
|
|
THE STOMACH
|
THE STOMACH
|
|
|
How does the stratified squamous mucosa protect itself from the stomach acid as it has no mucous layer?
|
It is extremely impermeable until pH falls below 2.5
|
|
|
Why do horses maintain a feed bolus in the stomach?
|
To help protect the gastric mucosa
|
|
|
What is EGUS?
|
Equine Gastric Ulcer Syndrome
|
|
|
Where are most stomach ulcers found?
|
Adults - squamous mucosa
Foals - Glandular and pyloric regions |
|
|
What are the risk factos for EGUS?
|
An increase in exercise intensity
Feeding practises (meal fed) Management (stall confinement) NSAIDs |
|
|
When is acidity highest?
|
When horse is off feed as acid is continually produced
|
|
|
Why is the use of NSAIDs a problem?
|
They disable the production of endogenous vasodilators like PGE2 and PGI2, decreasing gastric mucosal blood flow and the protective mucous barrier.
|
|
|
What are the signs?
|
Losing weight
Poor hair coat and BCS Poor appetite Intermittent colic Other signs - attitude, stiffness, tucked up abdomen, poor performance |
|
|
What are some of the risk factors for foals?
|
#1 = hypoxaemia
NSAIDs Stress, hospitalisation Mild-severe pain |
|
|
How is EGUS diagnosed?
|
Clinical signs
Endoscopy Response to treatment |
|
|
Will a horse with an ulcer be anaemic or hypoproteinaemic?
|
No - if so look for something else
|
|
|
What is the primary goal of therapy?
|
Reduce discomfort - best done by neutralising acid secretion
H2 antagonists - ranitidine Proton pump inhibitors - omeprazole |
|
|
Which is the drug of choice as it treats and prevents gastric ulcers?
|
Omeprazole
|
|
|
What else does sucralfate do other than bind to exposed endothelium?
|
Stimulates gastric mucous secretion
Enhances mucosal blood flow and PGE2 synthesis |
|
|
What other conditions can affect the stomach?
|
Gastric impaction
Gastric rupture Gastric tumours - SCC |
|
|
SMALL INTESTINE
|
SMALL INTESTINE
|
|
|
What is characteristic of the ileum?
|
Non-vascular antimesenteric band - ileocecal fold, contiguous with dorsal band of cecum
|
|
|
What cells define the sort of inflammatory bowel disease a horse may have?
|
The granulocytic cells - eosinophils, basophils, lymphocytes and macrophages
|
|
|
How does a horse with Idiopathic Focal Eosinophilic Enteritis (IFEE) differ from one with IBD?
|
They present with acute colic pain and no evidence of protein losing enteropathy
|
|
|
What are the clinical signs of traditional IBD?
|
Progressive weight loss despite good appetite and intermittent signs of colic
+/- diarrhoea (none if only SI involved) May have peripheral oedema from protein losing enteropathy |
|
|
With which form of IBD does the horse also present with dermatitis?
|
Multisystemic eosinophilic epithliotropic enterocolitis (MEED)
|
|
|
What are the IBD abnormalities with clin path?
|
Anaemia
Hypoalbuminaemia Hypoproteinaemia Malabsorption of glucose |
|
|
How is IBD definitively diagnosed?
|
Biopsy of small or large intestine via laparoscopy or celiotomy
|
|
|
How can IBD be treated?
|
Often unsuccessful even with aggressive steroid therapy
|
|
|
What are the differenct types of IBD?
|
Granulomatous enteritis (GE)
MEED Eosinophilic enteritis (EE) Lymphocytic/plasmocytic enteritis (LCPC) |
|
|
What are the cells responsible in each?
|
GE - macrophages, unknown cause, 1-5yo, Standardbreds, poor Px
MEED - young, dermatitis, tissue eosinophilia, diarrhoea, eosinophils, lymphs and macs LCPC - rare lymphocytes and plasma cells |
|
|
What bacterium will cause a proliferative enteropathy of the small intestine?
|
Lawsonia intracellularis - obligate intracellular bacteria
|
|
|
How is it transmitted?
|
Fecal-oral and affects weanling foal populations
|
|
|
What increases the risk of catching L. intracellularis?
|
Overcrowding, ration changes, transport and weaning
|
|
|
What are the hallmarks of the proliferative enteropathy (PE)?
|
Chronic wasting with severe hypoproteinaemia accompanied by grossly thickened SI with mucosal ulceration
|
|
|
Where in the SI does the profound proliferation of crypt cells occur?
|
Terminal jejunum and ileum
|
|
|
Decreased brush border activity and therefore decreased absorptive capacity causes what conditions?
|
Weight loss
Diarrhoea Hypoproteinaemia |
|
|
What is the primary differential for PE?
|
Rhodococcus equi
- often has concurrent respiratory infection |
|
|
What clinical signs do you see with PE?
|
Seen in 4-6mth foals
Unthrifty - poor coat, small Weight loss Peripheral oedema Diarrhoea Colic |
|
|
What are some of the secondary complications of a Lawsonia intracellularis infection?
|
Lethargy, gastric ulcers, dermatitis, bronchopneumonia and intestinal parasitism
|
|
|
What is the gold standard of diagnosis?
|
Isolation and culture from tissue
This is difficult and requires specialised media and stains. It also needs sugical tissue biopsy Also tissue and fecal PCR |
|
|
What is the treatment?
|
Abx - tetracyclins or macrolides w/ rifampin
Supportive care - fluids etc. Good Px |
|
|
What is the other name for anterior enteritis?
|
Duodenitis-proximal jejunitis (DPJ)
|
|
|
What is DPJ?
|
A syndrome of inflammation and oedema of the duodenum and proximal jejunum, excessive fluid and electrolyte secretion into the small intestine and consequently high volumes of enterogastric reflux
|
|
|
Do horses with DPJ have a mechanical or a functional obstruction of the bowel?
|
A functional obstruction - inflammation causes dysregulation of the myenteric plexus. Most horses have SI distension, copious reflux and pain
|
|
|
What is a common gross lesion with DPJ?
|
Serositis - petechial and ecchymotic haemorrhages on the serosal surfaces.
|
|
|
What is the precise cause of DPJ?
|
Unknown
|
|
|
What are the major differential diagnoses?
|
All SI obstructions
Hard to differentiate - degree of pain, response to gastric decompression, presence of fever and changes in blood work and peritoneal fluid parameters may help. |
|
|
What would happen if you passed an NG tube in a DPJ horse?
|
Large volume of smelly, orange/brown fluid
|
|
|
What are some of the clinical signs?
|
Distended loops of SI
Pain Dehydration Endotoxaemia/hypovolaemia Decreased gut sounds Tachycardia/pnoea |
|
|
What are the fluid parameters for a belly tap on a DPJ horse?
|
Turbid, dark yellow - orange
Mildly elevated cell count and elevated TP |
|
|
What is the treatment?
|
Aggressive supportive therapy - frequent gastric decompression and IV fluids
Colloids, antiinflammatories, antiendotoxin, analgesia, Abx, nutrition and prokinetics |
|
|
What are some of the complications?
|
Abdominal adhesions
Peritonitis Pharyngitis/oesophagitis Cardiac arrhythmias due to electrolyte abnormalities $$$ |
|
|
What is the difference between a functional vs a mechanical obstruction?
|
Functional - neuromuscular in nature, lack of propulsive force
Mechanical - physical obstruction of the lumen |
|
|
What is the difference between a strangulation and obstruction?
|
Obstruction - occlusion of bowel lumen with NO compromise to blood supply
Strangulation - occlusion to BOTH lumen and blood supply |
|
|
What is the severity of pain related to?
|
The degree of obstruction and the intestinal distension proximal to obstruction
|
|
|
What happens typically to a horse with a strangulating lesion?
|
Moderate - severe pain
Endotoxin release Haemoconcentration Dehydration |
|
|
When is surgical correction necessary for survival?
|
In a strangulating lesion
|
|
|
What is the ascarid (round worm) that causes problems like obstruction in horses?
|
Parascaris equorum
|
|
|
What age of animal does ascarid impaction typically occur?
|
Foals between 3-6mths old that are heavily parasitised which then get oral paste dewormed.
|
|
|
When should foals be dewormed by?
|
Prior to 8 weeks old as the prepatent period for the worm is 8-12 weeks
|
|
|
What happens in the gut after the animal is dewormed?
|
Adult worms live in the small intestinal lumen and once exposed to anthelmintic they begin to die enmass. The carcasses of all these worms block the lumen.
|
|
|
What are the clinical signs?
|
Mild-moderate colic
Gastric reflux Fever and signs of endotoxaemia (toxins released when worms die) |
|
|
How can ascarid impaction be treated?
|
Gastric decompression and lavage, antiinflammatory drugs, fluids Abx and GI protectants
Surgery may be necessary |
|
|
What are the foals at risk of?
|
Intestinal necrosis
Rupture Peritonitis Intra-abdominal adhesions |
|
|
Which treatment carries the best prognosis?
|
Medical treatment
|
|
|
If you suspect a foal has a large worm burden what should you treat with?
|
A less effective anthelcide as it will avoid mass killing and get rid of them slowly
|
|
|
What is the most likely thing that will cause an ileal impaction?
|
Dry feed matter e.g. Bermuda grass hay
|
|
|
When performing a rectal exam on a horse with suspected ileal impaction how will time be play a part?
|
Early - may palpate a firm mass
8-10hrs later - won't be able to feel ileum but jejunum will be distended with gas (at this point it is more common to have reflux also) |
|
|
When is medical therapy encouraged?
|
As long as peritoneal fluid remains normal and pain is manageable - mineral oil, analgesics, fluids
|
|
|
What can be done surgically?
|
Massage impaction into the cecum
SI enterotomy |
|
|
What is one of the complications?
|
Post-op ileus
|
|
|
Post-operative ileus (POI) occurs most commonly following SI surgery, what is a risk factor?
|
Handling of the bowel
Distension of bowel proximal to obstruction Also associated with general anaesthesia - cecal dysfunction |
|
|
What things influence whether an animal will develop POI?
|
Length of resection
Age PCV at admission Duration of anaesthesia |
|
|
What are the clinical signs to recognise?
|
Increased heart rate/breathing
Colic Decreased manure and gut sounds. Signs develop 24-96hrs post surgery |
|
|
What other things must you rule out?
|
Mechanical re-obstruction
Peritonitis |
|
|
How is it treated?
|
Same as DPJ
- Decompression, fluids, anti-inflammatories, prokinetics |
|
|
What is peritonitis?
|
An inflammatory condition of the mesothelial lining of the peritoneal cavity
|
|
|
What is the pathophysiology for peritonitis?
|
Insult
Macrophage and mast cell degranulation Release of vasocative mediators - histamine and serotonin Increase vascular permeability Transudation of fluid, protein and cells |
|
|
What happens when macrophages stimulate an inflammatory process?
|
Leads to lysosomal degranulation, fibrin deposition and translocation of bacteria
Ultimately leads to endotoxaemia, bacteraemia and shock |
|
|
What are the different classifications of peritonitis?
|
Primary or secondary
Acute or chronic Septic or non-septic Localised or diffuse |
|
|
Do we know what causes primary peritonitis?
|
No
|
|
|
Aseptic peritonitis can be what?
|
Mechanical or chemical irritation
|
|
|
What are the clinical signs of peritonitis?
|
Pyrexia, diarrhoea, abdominal pain, ileus, abnormal rectal, tachycardia/pnoea
|
|
|
What will blood work look like?
|
Acute = neutropenia with toxic left shift and normal fibrinogen
Chronic = neutrophilia, increased fibrinogen Septic = hypoproteinaemia and electrolyte imbalance |
|
|
What will peritoneal fluid look like?
|
Orange, cloudy, increased TP and WBC count
|
|
|
Why does recent surgery complicate diagnosis?
|
It is not uncommon for WBCs and TP to still be high up to 6 days post-op
|
|
|
What is another way to help you diagnose peritonitis?
|
Compare the peritoneal fluid to the horses blood gas results
Glucose lower than blood glucose Elevated lactate Very low pH |
|
|
How is peritonitis treated?
|
Abx (include metronidazole), Anti-inflams, anti-endotoxin/laminitis, fluids and electrolytes, nutrition
Poss peritoneal lavage |
|
|
What is the prognosis?
|
Variable
Complications - laminitis, adhesions |
|
|
When there is an intussusception, the proximal part telescopes into the distal segment, what are the names of the segments?
|
Proximal - intussesceptum
Distal - intussuscipiens |
|
|
Where is the most common place for intussusceptions to occur?
|
Ileocecal
|
|
|
Who gets this condition?
|
Young horses <3yo
Can occur after deworming, abrupt dietary changes or ascarid/tapeworm infestations |
|
|
When a horse gets an acute intussusception what are the signs?
|
Severe pain, reduced borborygmi, dilated SI, gastric reflux and abnormal peritoneal fluid.
Surgery is needed due to compromised/devitalised bowel - often resection and anastamosis |
|
|
What might a horse with a chronic intussusception look like?
|
Poor BCS, colic after meals, low appetite and low grade fever. Peritoneal fluid may be normal and may have no signs of obstruction
|
|
|
In an acute ileocecal intussusception why is there a guard prognosis?
|
As necrosis of the distal ileal stump may result in septic peritonitis, abscessation or adhesions
Jujunal and chronic cases have good Px |
|
|
What does the intussusception look like on U/S?
|
Classic "bull's eye"
|
|
|
In a small intestinal volvulus where does the SI twist?
|
Around the root of the mesentary, resulting in complete interruption of the intestinal blood supply
Most common cause of colic in the foal |
|
|
What parasite has been implicated in the cause?
|
Anaplocephala perfoliata - horse tapeworm and also ascarids
|
|
|
Definitive diagnosis is not possible until surgery but what are the clinical signs?
|
Abdominal pain, reflux, poor tissue perfusion, decreased gut sounds and distended SI.
Peritoneal fluid will become serosanguinous and WBCs and TP will increase. Lactic acidosis is common |
|
|
Why should horses with a SI volvulus receive aggressive fluid therapy before surgery?
|
They display physical and clinicopathologic evidence of CVS compromise
Hypertonic saline and balanced IV fluids given straight away |
|
|
What is done at surgery?
|
If caught early - reposition the intestines
If late - resect affected part If 50% or more of the SI is affected the horse will not be salvaged |
|
|
What is SI incarceration?
|
The SI gets entrapped through a mesenteric rent, inguinal ring, gastrosplenic ligament or epiploic foramen
|
|
|
In stallions with inguinal hernia what will the area look like?
|
Testicle on affected side will be enlarged, swollen, cold and painful. Intestines will be palpable entering the ring during rectal exam.
|
|
|
When do epiploic foremen entrapments occur?
|
In horses older than 8yo and typically involve the ileum or distal jejunum. Most cases occur in Jan and cribbing horses are most at risk
|
|
|
Colic is the most common complication from what?
|
Adhesions, POI, incisional infection and/or ventral body wall hernias
|
|
|
Is a pedunculated lipoma neoplastic?
|
No
|
|
|
A lipoma arises from which tissue?
|
Mesenteric adipose tissue
Over time the pedicle gets longer and stalk-like and can entrap the SI. Leading to mechanical obstruction of the bowel |
|
|
At what age are lipomas a problem?
|
Older horses >9yo and occur more commonly in arabs and geldings
|
|
|
Why might clinical signs be confusing?
|
Many tend be depressed rather than in severe pain.. Most are painful early on. Reflux may occur, distended SI.
|
|
|
Can you palpate the lipoma?
|
Rarely palpated however dessicated feed in the colon is a common finding
|
|
|
What might it be misinterpreted as?
|
Large colon feed impaction
|
|
|
How can you tell between them?
|
Older horses rarely get feed impactions but they do get lipomas. Feed impactions generally do not cause deterioration in CVS parameters as occur with devitalised bowel.
|
|
|
How are strangulating lipomas treated?
|
Surgery must be performed to free the intestine from pedicle. Ischemic portion requires resection and anastamosis. Generally good Px
|
|
|
What is colitis and what is the cardinal sign?
|
Inflammation of the colon wall
Cardinal sign is diarrhoea |
|
|
What is the most common serotype of Salmonella isolated from horses?
|
Salmonella typhimurium
|
|
|
1-17% of healthy horses shed salmonella in the faeces. What factors influence infectivity?
|
Serotype
Exposure dose Host immunity Younger, older and sick horses are more susceptible |
|
|
What are some of the risk factors?
|
Stress, hospitalization, diet change, surgery, anaesthesia and antibiotic use
|
|
|
Transmission is faecal-oral, what does infection result in?
|
Intestinal wall inflammation
Hypersecretion Ulceration Protein and electrolyte loss |
|
|
Why is the horse likely to suffer from endotoxaemia?
|
Intestinal inflammation inpairs the mucosal barrier allowing luminal endotoxin to be absorbed
|
|
|
What are the most common clinical signs?
|
Fever, diarrhoea and endotoxaemia
Pain can be mild to severe In rare cases it affects the SI |
|
|
What are the common complications?
|
Laminitis
Coagulopathy Thrombophlebitis |
|
|
How can you diagnose it?
|
Intense neutropenia with a toxic left shift
Hypoproteinaemia Metabolic acidosis and electrolyte loss Confirm diagnosis via bacterial culture or PCR of faeces, tissue or body fluids (blood in foals as often septicaemic) |
|
|
When can you say that salmonellosis is unlikely?
|
When at least 5 faecal cultures or 3 PCRs taken 12-24hrs apart are negative
|
|
|
How is salmonellosis treated?
|
Most important treatment is fluid therapy!
Severe hypoproteinaemia may need to have plasma/hetastarch Endotoxaemia protection - NSAIDs |
|
|
When would you use antibiotics?
|
Evidence of extraintestinal infection
Foal less than 3mths Severe or persistent neutropenia Concurrent disease |
|
|
How long will it take for a horse to stop shedding salmonella?
|
Days to months
|
|
|
Can humans catch it?
|
Yes!
|
|
|
What is the prognosis?
|
Mortality rate is variable - severe diarrhoea, intense colic, extra-intestinal infection and coagulopathy have a poor prognosis
|
|
|
What is the organism that is a gram +ve spore forming anaerobic rod that may be considered normal intestinal flora?
|
Clostridium perfringes/difficile
|
|
|
Why might these organisms overgrow and colonise colonic mucosa?
|
Stress, immunosuppression or changes in normal flora due to Abx therapy
|
|
|
How can clostridium harm the horse?
|
It releases toxins that cause enterocyte damage and increased intestinal permeability
|
|
|
Clinical signs are similar to salmonellosis, how can clostridium be diagnosed?
|
Difficult but suspect if it can be cultured from faeces. C. difficile toxin A or B can be identified by ELISA, cytotoxin assay or PCR
|
|
|
How is it treated?
|
Discontinue antimicrobials if they are the cause
Start horse on metronidazole Additional supportive care for fluid, protein loss and endotoxin protection |
|
|
What drug can be used to help bind clostridial toxin?
|
DTO-smectite is a biosponge
Mortality is high with clostridium |
|
|
What is the agent that causes Potomac Horse Fever?
|
Neorickettsia risticii
A rickettsial-like organism that has a trophism for monocytes and enterocytes |
|
|
How is it transmitted to horses?
|
Organism is carried by flukes that infest snails thus horses grazing near freshwater during warm seasons are susceptible
|
|
|
What are the clinical signs?
|
May be subclinical or it might look like salmonellosis. Abortion may occur. Biphasic fever
|
|
|
PHF can be detected with a PCR to find the antigen in blood or faeces, how is it treated?
|
Oxytetracyclin is the drug of choice
Additional supportive care for fluid, protein and electrolyte loss |
|
|
What is a Cyanthostome?
|
Small strongyles which are highly resistant to anthelmintics
|
|
|
How do they cause a problem in horses?
|
The L3 stage get ingested and they then encyst in the wall of the colon and cecum where they mature to L4. Months - years later they excyst releasing the worm and excretory/secretory products that have built up over time. This results in focal oedema, congestion and haemorrhage
|
|
|
What is "larval cyanthostominosis"?
|
A seasonal condition when large numbers of encysted nematodes emerge at once. Leading to massive damage of colonic mucosa
|
|
|
What are the clinical signs?
|
Severe diarrhoea, rapid weight loss, marked hypoproteinaemia and passage of large numbers of cyanthostomins in faeces. SImilar to acute colitis
|
|
|
How can it be treated?
|
Fenbendazole and moxidectin are the only two licensed
Can also use daily pyrantel as prophylactic treatment |
|
|
Which antimicrobial should never be used in horses?
|
Lincomycin - causes a nasty colitis in adult horses
|
|
|
Essentially all antimicrobials can cause colitis but which ones are more frequently associated with it?
|
Erythromycin
Ceftiofur Tetracyline Ampicillin Metronidazole Neomycin Trimethoprim sulfas |
|
|
What is toxin contained in Blister beetles?
|
Cantharidin - a mucosal irritant
|
|
|
How many beetles need to be eaten for clinical signs to show?
|
4-5
|
|
|
What are the clinical signs?
|
Ulceration of mouth - salivation
GI tract - colic and diarrhoea Urinary tract - haematuria, stranguria Myocarditis may also be present |
|
|
In additional to signs of colitis what may also happen resulting in signs in tetany and bizarre behaviour?
|
Hypocalcaemia
|
|
|
How can you diagnose cardiac damage?
|
Increase in CK and cardiac troponin I
|
|
|
Cantharidin can be detected where?
|
In gastric contents and urine
|
|
|
What is the treatment?
|
Supportive only, mortality rate 50%
|
|
|
What bacterial growth does grain overload encourage?
|
Bacillus, lactobacillus and strep
|
|
|
What do these bacteria produce which subsequently lowers intestinal pH?
|
Lactate and proprionate
|
|
|
What happens when there is a low pH?
|
Decreases fermentation by impairing normal flora
This results in cecal/colic dysmotility = gast distension = colic pain Mucosa also gets "burned" by the low pH leading to endotoxaemia |
|
|
How is grain overload treated?
|
If caught early:
Gastric lavage, +/- mineral oil, activated charcoal. Endotoxin and laminitis prophylaxis Cecal trocharisation to combat bloat |
|
|
What level of feed increases a horses risk of this?
|
Feeding greater than 2.7kg per day of oats increases risk x6
Normal is <200g/100kgbw per meal |
|
|
What is the main cause of sand impaction?
|
Horses grazing on sandy soils pick up sand while they eat
|
|
|
What are the clinical findings?
|
Mild to severe pain if the right dorsal colon or transverse colon is acutely and completely obstructed.
Horses stretch out or lie down a lot. Often they pass a large amount of watery stool before/after passage of normal manure |
|
|
How is it diagnosed?
|
Sand may be palpable in the faeces or if the faeces is mixed with water and allowed to settle
|
|
|
What might be seen on ultrasound?
|
The houstra of the intestine disappears with the weight of the sand - CARE with abdominocentesis!
|
|
|
What is the therapy?
|
Mild pain - remove sand from colon via repeated use of Metamucil in water via NG tube. Oral and IV fluids and analgesics
|
|
|
What if the pain is severe and unrelenting or there is severe bloat?
|
Surgery may be necessary - perform a pelvic flexure enterotomy
If bloat is severe perform cecal trocharization to relieve gas distension prior to surgery |
|
|
Where in the colon is the most common site of colitis as a result of NSAID toxicity?
|
Right dorsal colon
|
|
|
How does toxicity occur?
|
NSAIDs cause mucosal ulceration through inhibition of COX.
This suppresses prostaglandin production which is critical for maintenance of normal blood flow and mucosal health of GI tract |
|
|
When is damage most commonly reported?
|
When excessive doses are given in the face of water deprivation
|
|
|
What NSAID is most commonly associated with toxicity?
|
Phenylbutazone
|
|
|
Clinical signs are similar to salmonellosis, what happens if the toxicity is chronic?
|
Fibrosis may develop in the right dorsal colon and cause strictures to form
|
|
|
How is it treated?
|
STOP NSAIDs and supportive care. May need to alter diet to more easily digestible fibre. Can include some corn oil and psyllium to increase production of anti-inflammatory fatty acids. Possibly use synthetic prostaglandin misoprostol or metronidazole to reduce inflammation
Butorphanol or lidocaine for pain |
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LARGE COLON
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LARGE COLON
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Where are the sites of luminal narrowing that are most likely to become obstructed?
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Pelvic flexure and left ventral colon
Junction between the right dorsal colon and transverse colon |
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Most affected horses show intermittent colic signs unless impaction has a prolonged course without treatment so what is the treatment?
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Oral and IV fluids
Mild analgesics Laxative - mineral oil, DSS, Magnesium sulfate) Ideally remove feed and give 2-4x maintenance fluids |
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What is the goal of treatment?
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To overhydrate. Fluid absorbed from SI redistributes to distal large intestine. This softens the feed such that normal motility may resolve the impaction
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Why is giving isotonic enteral fluids better?
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Stimulates gastrocolic reflex which improves motility
Cost effective Can leave a tube in and give enteral fluid over several days for large, firm impactions |
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Prognosis is excellent what do you need to be aware of?
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Re-impaction can occur, take care when re-feeding
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What is the difference between primary and secondary cecal impaction?
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Primary - similar to large colon feed impaction
Secondary - cecum becomes dilated with fluidy digesta. It is a motility dysfunction |
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What are the risks that contribute to secondary cecal impaction?
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General anaesthesia
Hospitalization NSAIDs |
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What are the presenting signs?
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Acute fluid retention = severely painful and rupture of cecum is common
Large feed impactions have minimal deterioration unless impaction has prolonged course |
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When do cecal impactions tend to occur?
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In middle aged horses and they are more often associated with rupture than any other site in the tract
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Surgery must be discussed with the owner as spontaneous rupture may occur. What is the prognosis?
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Guarded
This disease should be high on the differential list for any post-op patient that has colic following general anaesthesia |
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What condition is also know as nephrosplenic entrapment of the large colon?
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Left dorsal displacement of the large colon
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How is it caused?
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The pelvic flexure or the entire left colon moves over the renosplenic ligament. As colonic distension occurs the spleen contracts in response to pain, the gas-filled colon displaces more dorsally and the spleen re-engorges trapping the displaced colon
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When might the result of a paracentesis lead you to suspect this?
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If you get blood from puncturing the engorged spleen
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What are the 4 possible treatments?
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1. Restrict feed and see if colon corrects itself as it empties
2. Treat horse with phenylephrine - causing vasoconstriction and splenic contracture. Then jog the horse and see if colon "bounces" back 3. Short term IV anaesthesia and rolling the horse - start with horse on right side and roll 4. Surgery |
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What are the options for repeat offenders?
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Colopexy and colonic resection
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What are enteroliths?
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Concretions of magnesium ammonium phosphate crystals which form around a nidus in the gut
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Recurring bouts of acute pain which can be severe is the obstruction is complete and marked distension of the colon proximally are the main signs but what is normal?
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Mucous membranes remain pink although heart and respiratory rates are increased.
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Where are the stones found most often?
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They can cause an obstruction from the right dorsal colon and the transverse colon. The are rarely palpable rectally
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Surgery needs to be done to decompress the colon and remove the stone. What should be done if the enterolith is polyhedral in shape?
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Look for more stones!
The flat sides are made when the stones rub against each other. Singular stones are spherical |
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Which large strongyles are responsible for causing Thromboembolic Colic?
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Strongylus vulgarus or S. edentatus
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Why do these parasites create thrombi?
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L3 is ingested and swallowed into intestinal tract. Parasite moves through intestinal wall and migrates into the cranial mesenteric artery, where it attaches and moults from L4 to L5. Disruption of the arterial wall causes turbulent blood flow and creates thrombi. These thrombi flow downstream and obstruct the smaller vessels within the large intestinal tract
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Which parts of the intestine are at greatest risk of ischemic death?
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The colon and the cecum as they have little to no collateral circulation
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What are the clinical findings?
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Varying amounts of pain
Large intestinal gas distension Abdominal fluid depends on the size of bowel ischemia Fremitus when Cr. mesenteric artery is palpated |
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What type of congestion is typically seen with Right Dorsal Displacement of the Large Colon?
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Venous congestion as it is only a 180 degree twist
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What happens?
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The pelvic flexure displaces laterally around the base of the cecum and ends up near the diaphragm. Called "right" displacement as colon is trapped to the right of the colon
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Most horses have a slow development of systemic deterioration as blood supply to the colon is usually maintained. How is it treated?
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Medically - remove feed, fluids and analgesia. Once colon empties it may resolve itself
Surgery if this doesn't work Good Px |
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What condition is a MAJOR emergency?
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Large Colon Volvulus
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What is it?
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A twist of the large colon near the attachment of the colon to the cecum. The colon twists on the mesentary between the dorsal and ventral colons
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What is it most often associated with?
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Impending or recent parturition
A grass diet and/or highly fermentable feeds |
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At what degree of twist will there be a strangulating lesion?
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If volvulus is 360 degrees or greater
<270 degrees may not result in tissue ischemia |
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What are the clinical findings?
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Sudden onset of severe colic, often non-responsive to analgesics - this is the hallmark of LCV
Tachycardia and rapid deterioration of CV parameters Great distension of the colon resulting in depression in ventilation as well as venous return |
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This is an emergency that requires surgery. How can you tell if the colon is dead?
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Look at the mucosa
Colon starts dying in 30mins! |
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There is a chance that this can recur especially in brood mares, what is done to help prevent this?
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A colopexy or colonic resection
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What can cause an impaction of the small colon?
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Dehydrated faeces, very fibrous faecal material or foreign body
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Can you palpate the obstruction?
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Possibly if caught early otherwise you will just feel distension of proximal colon
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Which breed does this usually affect?
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Miniature horses
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What sort of signs can be present?
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May have diarrhoea, abdominal distension, signs of endotoxaemia.
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What is the treatment?
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Can treat medically with fluids and laxatives
However surgery is often indicated due to the severity of pain and gas distension |
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How is surgery performed?
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Massage to break down impaction or enterotomy at the pelvic flexure to remove obstruction if it is too hard
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What is the most common complication?
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Diarrhoea
Re-feed with care to avoid re-impaction |
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What are faecaliths?
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Concretions of feed material that form larger than normal faecal balls that most commonly obstruct the small colon and occasionally the large colon
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What type of horses are most involved?
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Miniature horses and ponies
Horses <1yo but can be in older animals |
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What is the clinical sign that can help distinguish this disease?
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There will be no manure passed once colic develops
Severe abdominal distension may be present |
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What can be done if distension is severe?
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Cecal trocharization
Otherwise just perform the pevlic flexure enterotomy to evacuate the colon Px is excellent |
