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605 Cards in this Set
- Front
- Back
Water makes up what portion of a patient's body weight?
|
60%
|
|
What 2 major compartments is water distributed within?
|
ECF, ICF
|
|
The ECF is divided into what 3 compartments?
|
-intravascular
-interstitial -tanscellular |
|
The blood volume of most mammals comprises how much of total body water?
|
8%
|
|
What is plasma?
|
The non-cellular component of blood..communicates continuously with the interstitial fluid through a series of pores in the capillary cell membranes
|
|
Are proteins more highly concentrated in the ECF of the plasma?
|
Plasma
|
|
Plasma proteins are negatively charged and attract what?
|
Positively charged cations (NA, K)
|
|
What is the result of the attraction of NA and K?
|
Pulls water and lymph fluid from the interstitium into the vascular space
|
|
Plasma proteins are responsible for creating what pressure?
|
colloid oncotic
|
|
What are the forces that govern fluid movement across endothelial membranes?
|
Starling's forces (hydrostatic and oncotic)
|
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What is the primary ECF osmole?
|
cation Na+
|
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What is the primary ICF osmole?
|
cation K+
|
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Which space bears the brunt of the effects of pure water loss?
|
ICF
|
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What are the normal water requirements of a 500kg horse?
|
50ml/kg/day (6 gallons)
|
|
When doe most water intake occur in the horse?
|
Periprandial drinking
|
|
What are the electrolyte balances in horse fed a diet high in hay?
|
high K+
low Na+ |
|
Horses receiving IV fluids for more than one day are at risk for low levels of which electrolyte?
|
K+
|
|
Low K+ can lead to what clinical sign?
|
Muscle weakness
|
|
Unlike other species, horses absorb excessive amounts of Ca from feed, how is the excess Ca eliminated?
|
In the form of calcium crystals in the urine
|
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What is the cause of the turbid appearance of horse urine?
|
calcium carbonate crystals and mucus
|
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What condition is the hallmark of dehydration?
|
Hypernatremia
|
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What effect does pure water loss have on the tonicity of the ECF?
|
increases it
|
|
What effect does the increased tonicity of the ECF have on the ICF?
|
Fluid redistributes from the ICF to the ECF
|
|
How does the body correct for the elevation of Na+ resulting from dehydration?
|
Osmoreceptors trigger thirst
|
|
What is meant by the term hypovolemia?
|
Loss of water and electrolytes
|
|
If fluid lost from the ECF is isotonic, what effect will this have on the ICF?
|
None, no change in water balance
|
|
What are the cause of the loss of isotonic body fluid in the horse?
|
-hemorrhage
-diarrhea -vomiting -sweating |
|
Fluid deficits that affect the ECF (isotonic deficits) cause a compromise of which body system?
|
Circulatory
|
|
A patient with hypovolemia suffers from a decrease of volume in which compartment?
|
ECF
|
|
What are the events that occur as a result of hypovolemia?
|
-decreased return of venous blood to the heart
-decreased cardiac output -activation of homeostatic mechanisms |
|
Decreased effective circulating volume leads to the activation of what system?
|
Renin-Angiotensin-Aldoseterone System (RAAS)
|
|
Renin is released from where?
|
Juxtaglomerular cells of the afferent arteriole of the kidney
|
|
What is the effect of renin?
|
Causes converion of angiotensin I to angioternsin II (in the lungs)
|
|
What other chemical is needed for this conversion?
|
Angiotensin-converting enzyme (ACE)
|
|
What is the effect of angiotensin II?
|
AT II is a powerful vasoconstrictor...increase systemic blood pressure
|
|
ATII stimulates the release of aldosterone from where?
|
Adrenal cortex
|
|
What is the effect of aldosterone?
|
Enhances resorption of NA and CL, increasing vascular fluid volumes
|
|
What effect do baroreceptors have on decreased volume?
|
Stimulate sympathetic neurons in the CNS vis the vagus nerve, which increases heart rate and sympthetic vasoconstriction, improving CO and tissue perfusion
|
|
What is the purpose of the body's osomoreceptor's?
|
Monitor the tonicity of blood osmolalitiy
|
|
Changes in blood osmolality causes the release of what? From where?
|
Arginine Vasopressin AVP from the posterior pituitary
|
|
AVP is also know as what?
|
Anti diuretic hormone
|
|
What effect does AVP have on the collecting duct of the kidney?
|
Increases water resorption by placement of apical aquaporin channels (improves vasuclar volume and perfusion of tissues)
|
|
AVP can also effect the release of what hormone?
|
ACTH to release cortisol
|
|
Are the homeostatic mechanisms long lived or short lived?
|
Short lived
|
|
What is dysoxia?
|
The condition in which metabolic energy production is limited by the supply or utilization of oxygen
|
|
What is the term for the clinical expression of dysoxia?
|
Shock
|
|
The adequacy of tissue oxygenation is determined by the balance of what 2 values?
|
-oxygen delivered to the tissues (DO2)
-oxygen required to sustain aerobic metabolism (VO2) (rate of uptake of O2 into the tissues) |
|
When VO2 is sufficient, how many ATP are produced per mole of glucose?
|
36
|
|
When VO2 is not sufficient, some glucose is is diverted into the anaerobic production of what?
|
lactate
|
|
How many ATP are produced per mole of lactate?
|
2
|
|
What correlation has been shown, in humans, between lactate and survival?
|
As blood lactate increases, survival decreases
|
|
What determines the severity of hypovolemic shock?
|
-rate and amount of fluid lost
-age of patient -pre-existing disease |
|
Complications of decreased oxygen delivery to tissues include what conditions?
|
-decreased coronary and cerebral perfusion
-systemic metabolic derangements (including anaerobic metabolism) |
|
Hypovolemic shock may be secondary to hemorrhage, V/D, fluid loss into the 3rd space...these fluid loses come primarily from which fluid compartment?
|
ECF (vascular space)
|
|
What are the clinical signs of dehydration?
|
-tachycardia
-tacky mucus membranes -prolonged skin tent -sunken eyes -increased USG -irritable behavior (humans) -muscle cramping (humans) |
|
What are the clinical signs of hypovolemia?
|
-tachycardia
-decreased pulse pressure -reduced jugular fill -tachypnea -cold extremities -decreased urine output |
|
When do clinical signs of dehydration become evident?
|
At ~5% dehydration
|
|
What does 5% dehydrated mean?
|
Decrement in body mass due to fluid loss
|
|
Patients presenting with signs of hypovolemia may be ataxic, which may be confused with what condition?
|
Neurologic clinical signs
|
|
Dehydration and hypovolemia require immediate fluid therapy. What is the ideal measurement for assessing hydration?
|
Body mass
|
|
What are the 2 common lab parameters used for assessing hydration?
|
PCV, TA
|
|
Why is PCV not an accurate indicator of hydration in a horse?
|
PCV can be raised due to excitement and splenic contraction
|
|
Does plasma total protein increase with dehydration or with hypovolemia?
|
Increases with both
|
|
Horses with colitis will lose plasma protein from the GI tract. They present with increased PCV but normal to low protein. What typ eof fluids should they be given?
|
Colloids- when giving fluids a horse with colitis with drop in PCV and TS, colloids will help avoid a hypoproteinemic state.
|
|
Will a dehydrated horse have an increased or decreased USG?
|
Increased
1.025-1.040 |
|
What would you expect as a serum creatinine level in a hypovolemic horse?
|
Increased (in the absence of renal dysfunction)
|
|
Why would a dehydrated horse show a pre-renal azotemia?
|
Temporary renal insufficiency related to decreased GFR due to hypovolemia
|
|
What would you suspect if a patient has azotemia, but is isosthenuric?
|
Renal failure
|
|
Does measurement of lactate assist in determining dehydration or hypovolemia?
|
Hypovolemia- decreased DO2 leads to anaerobic metabolism- glucose converted to lactate
|
|
In vet med what should a normal L-lactate level be?
|
<1.0 mmol/L
|
|
The fraction of oxygen delivered to the capillaries that is actually taken up by the tissues is called what?
|
The oxygen extraction ratio
The ration of oxygen uptake to oxygen delivery (VO2/DO2) |
|
What should the normal oxygen extraction ratio be?
|
<25%
|
|
What would you suspect is the oxygen extraction ratio increases?
|
Dysoxia, or shock, is pending
|
|
What measurement is used to estimate the oxygen extraction ratio?
|
Central venous oxygen saturation (SvO2)
|
|
In a normal patient, Sv02 should be what?
|
> or = to 70%
|
|
In patients with shock, the oxygen extraction rises to 50%- 60%...what SvO2 will you see?
|
< 70%
|
|
What measurement is used to evaluate effective circulating volume?
|
Central venous pressure (CVP)
|
|
Central venous pressure is a measurement of what?
|
Right atrial pressure (pre-load)
|
|
In horses, what is a normal range for CVP?
|
5-14mm Hg
|
|
What does an elevated CVP indicate?
|
Fluid overload
|
|
What is the goal of fluid therapy in the hypovolemic patient?
|
Incease intravascular volume to improve venous return and cardiac output within 1-2 hours
|
|
A shock dose of fluids is considered to be what volume?
|
One blood volume, 8% of total body weight
|
|
In the horse, what is the rate for delivering a shock dose of fluids?
|
Administer 1/4 of the dose as a bolus, reasses, if signs persist continue until 1 blood volume is given
|
|
Correction of dehydration requires that fluids be given over what time period?
|
12-24 hours
|
|
What does the term crystalloid mean?
|
A substance in a solution that can diffuse through a semi-permeable membrane
|
|
What are the primary electrolytes in crystalloid fluids?
|
Na+ and Cl-
|
|
Crystalloids are designed to replace fluid in which compartment?
|
In the interstitium (leak from the vascular space)
|
|
What volume of administered crystalloids will remain in the vascular space 30 minutes after administration?
|
1/4 of the volume administered
|
|
Crystalloids are an excellent source for electrolyte replacement but can also be a cause of what?
|
Edema formation with fluid overload
|
|
What is tonicity?
|
The osmotic pressure of a solution based on the number of particles per kilogram of solution (osmolality)
|
|
What effect can a hypotonic solution have on RBC's?
|
Can cause them to swell and rupture
|
|
What effect can a hypertonic solution have on RBC's?
|
Can cause them to shrink (crenation)
|
|
What is the tonicity of plasma?
|
280 mOsm/L
|
|
What effect do isotonic fluids have when administered?
|
Temporary increase in plasma volume without causing electrolyte disturbances of fluid shift from the ICF
|
|
Which isotonic crystalloid is ideal for a hyperkalemic patient?
|
Normal saline (.9% NaCl)
isotonic but has greater amounts of Na and Cl do not use for resusciation due to potential development of hyperchloremic metabolic acidosis |
|
What is an example of a hypotonic solution?
|
0.45% NaCl (half-strength saline)
|
|
Why should half-strength saline be used with caution?
|
Is half the tonicity of plasma, can cause cells to swell
|
|
In patients with chronic hyponatremia, cells produce what to pull water into the cell?
|
idiogenic osmoles
|
|
Why is hypotonic saline given to these patients?
|
They must have Na+ replaced slowly with a solution that resembles the abnormal plasma tonicity to prevent cell swelling
|
|
Which solution provides no additional electrolytes?
|
Water (D5W)
|
|
Is D5W a good choice for resuscitation of hypovolemia?
|
No- less than 10% remains in the vascular space after 30 minutes, a bolus can cause severe hyperglycemia
|
|
What is an example of a hypertonic fluid?
|
7% NaCl, hypertonic saline
|
|
Hypertoninc saline quickly increases the tonicity of the ECF and interstitium. What effect does it have on the ICF?
|
Draws water from the interstitium and ICF into the vascular space
|
|
What is the general rule of thumb for giving additional fluids when hypertonic saline is used?
|
For every liter of hypertonic, 10 liters of isotonic should be given as replacement to the ICF
|
|
What are colloids?
|
Large branched molecules which exert substantial colloidal oncotic pressure and may act as capillary pore plugs preventing fluid from leaking from the vasculature
|
|
What are 2 commonly used colloids used in equine medicine?
|
-fresh frozen equine plasma
-hetastarch |
|
Why are colloids a good fluid choice for endotoxemia and ischemia-reperfusion injury?
|
Both conditions cxause capillary damage which allow plasma proteins to leak into the interstitium..proteins in the insterstitium draw water from the vascular space causing edema
|
|
What is a drawback to using hetastarch at high doses? (>20 ml/kg
|
Prolonged bleeding times
|
|
What is the drawback to measuring TS when using hetastarch?!
|
Doesn't measure on a refractometer
|
|
What are the benefits of using equine fresh frozen plasma in colitis patients?
|
-offers albumin
-clotting factors -anti-endotoxemic factors |
|
How is plasma administered to decrease the potential for a reaction?
|
Adminsiter slowly over the first 20 minutes, monitoring TPR and for signs of urticaria
|
|
What methods can be used to encourage a horse to increase their oral intake of fluids?
|
-electrolyte pastes
-salt slurries |
|
True or False. The SQ route of fluid administration for horses works well.
|
False
|
|
Which method of fluid administration is used to give large volumes of fluids easily?
|
Enteral (NG tube)
|
|
How much fluid can be safely given via NG tube?
|
4-6 L per dose repeated every 1-2 hours
|
|
What must be checked before administering any GI fluids to a horse?
|
Check for gastric reflux
|
|
What methods can be used to encourage a horse to increase their oral intake of fluids?
|
-electrolyte pastes
-salt slurries |
|
True or False. The SQ route of fluid administration for horses works well.
|
False
|
|
Which method of fluid administration is used to give large volumes of fluids easily?
|
Enteral (NG tube)
|
|
How much fluid can be safely given via NG tube?
|
4-6 L per dose repeated every 1-2 hours
|
|
What must be checked before administering any GI fluids to a horse?
|
Check for gastric reflux
|
|
True or False. The enteral route is not an adequate route for resuscitating a hypovolemic horse.
|
True- use the IV route
|
|
IV fluid administration in a horse usually requires the placement of catheters where?
|
Jugular veins
|
|
Physiologic processes of the body are optimized at what pH?
|
7.4
|
|
The hydrogen ion content of the ECF is determined by what?
|
The balance between the partial pressure of CO2 (PCO2) and the concentration of bicarb (HCO3-)
|
|
When a primary acid-base disturbance alters 1 component of the PCO2/HCO3 ratio, what direction does the compensatory mechanism move?
|
Same direction, to keep the ratio constant
|
|
What are the 2 reasons to perform a blood gas analysis?
|
-determine acid/base status
-evaluate respiratory gas exchange |
|
Which blood gas type is used for determining acid/base status?
|
Venous blood gas
|
|
Why is an arterial blood gas used to determine blood gas-oxygen exchange?
|
Arterial blood hasn't traveled through the systemic capillary network and subsequent exposure to cell uptake and waste
|
|
What anticoagulant is used in ABG collection?
|
Dry lithium heparin
|
|
What is the term for a disturbance that alters the amount of CO2 in the blood?
|
Respiratory acid-base alteration
|
|
As CO2 increases, what happens to pH?
|
It decreases
|
|
Aside from the lungs, what other body organs affect acid-base balance?
|
GIT & kidney
|
|
How quickly does the respiratory system compensate for acid-base alterations?
|
Minute by minute
|
|
What is the first step in evaluating a potential acid-base alteration?
|
determine the pH (acidosis/alkalosis)
|
|
What component on a blood gas report reflects the respiratory component of an altered acid-base balance?
|
PCO2
|
|
The normal respiratory components of a blood gas report include what?
|
HCO3 and base excess
|
|
Is PCO2 increased or decreased with a respiratory acidosis?
|
Increased
|
|
A metabolic acidosis is can be caused by what 2 conditions?
|
-gain of H+
-loss of HCO3 |
|
What conditions can cause a gain of H+?
|
-increased H+ production (ketoacidosis, lactic acidosis)
-metabolism of ingested toxins (ethylene glycol) -decreased reanl excretion of H+ (renal tubular acidosis) |
|
Loss of HCO3 is usually attributed to what?
|
Vomiting/diarrhea
loss from kidney |
|
Why is knowing the etiology of an acidosis important?
|
Determine is supplemental bicard is indicated
|
|
An increased in plasma HCO3- is termed what?
|
Metabolic alkalosis
|
|
How is a metabolic alkalosis generated?
|
Loss of H+ or gain of HCO3-
|
|
Because of the kidney's incredible efficiency of HCO3 excretion, metabolic alkalosis can only be sustained under what circumstance?
|
Renal dysfunction
|
|
Metabolic alkalosis is usually accompanied by what other imbalance?
|
Hypokalemia
|
|
Metabolic alkalosis can be brought on by volume depletion (ECF volume loss) or by what disease condition?
|
Cushing's
|
|
True or False. An acid-base derangements with compensation will show HCO3 and PCO2 moving in the same direction.
|
True
|
|
Where are the H+ chemoreceptors located?
|
Carotid bodies and lower brainstem
|
|
Metabolic acidosis (increased H+) creates what type of response from the chemoreceptors?
|
An increase in the respiratory rate and a secondary decrease in PCO2
|
|
An acid-base derangement on which the analytes move in opposite directions is termed what?
|
Mixed acid-base disturbance
|
|
Changes in the level of HCO3 by the kidneys can take how long to effect?
|
24 hours
|
|
How is base excess defined?
|
The amount of strong acid of base necessary to titrate 1 liter of blood to a pH of 7.4 @ 37 C while PCO2 remains at 40 mmHg
|
|
How is an anion gap calculated?
|
(Na + K) - (Cl + HCO3)
|
|
What is the value of a normal anion gap?
|
less than or equal to 15
|
|
Increased, unmeasured stray anions can indicate the presence of what conditions?
|
Lactic acidosis, ketoacidosis
|
|
Supplementation of bicarb can be calculated by what formula?
|
BWT (kg) x 0.5 x (HCO3 norm - HCO3 actual)
|
|
After calculating the amount of bicarb needed, how is it administered?
|
50% as a bolus, remainder slowly over 12-24 hours
|
|
ENDOTOXEMIA
|
ENDOTOXEMIA
|
|
Endotoxemia is a leading cause of death in horse with what condition?
|
-colic
-colitis -sepsis in foals |
|
Which disease is a complication of endotoxemia and is a co-factor for morbidity/mortality of many systemic diseases in horse?
|
Laminits
|
|
What is SIRS?
|
Systemic Inflammatory Response Syndrome
|
|
SIRS may follow development of endotoxemia and can lead to what conditions?
|
-endotoxemic/septoic shock and w/o resucitative measures, multiple organ dysfunction (MODS) and death
|
|
what type of structure is endotoxin?
|
heat-stabile LPS
|
|
LPS is a major structural cell wall component of which type of bacteria?
|
Gram negative (incl. non-infectious species)
|
|
In the LPS structure, which component is the toxic principle?
|
Lipid A
|
|
What is the function of the LPS D antigen?
|
Virulence
|
|
What innate barriers protect the horse fro endotoxins?
|
-enterocyte muscosal cells
-mucus layer for prostaglandins -tissue macrophages and Kupfer cells |
|
If endotoxin gains access to the bloodstream, what clinical signs may be seen?
|
-fever
-leucopenia or leucocytosis -coagulopathies -hypertension -shock, death |
|
Damage to the GI mucosa (and release of endotoxin into the system) can be caused by what?
|
-local tissue hypoxia (volvulus, infarct, incarceration, systemic hypoxia, mechanical trauma, intraluminal acidification (grain overload)
|
|
By what other methods can LPS enter the body?
|
-inhalation
-administration of parenteral solution |
|
Once LPS is in the blood, it is targeted by what?
|
Lipopolysaccharide Binding Protein (LBP) (synthesized in the liver, acute phase protein)
|
|
What is the function of LBP?
|
To carry LPS molecules to endotoxin-responsive immune cells (monocytes & macs), neutrophils, lymphocytes, endothelial cells
|
|
CD14 and which toll like receptor are responsible for signaling an innate immune response?
|
TLR4
|
|
CD14 and TLR4 cannot trabslocate the LPS signlal to the immune cells without what protein?
|
transmembrane protein MD2
|
|
Which 2 inflammatory cytokines are responsible for the mediation of clinical signs in endotoxemia?
|
TNF
IL1 |
|
The clinical signs of endotoxemia are mediated by TNF and IL and what other cascades?
|
-intravasucular coagulation pathway
-complement protein activation |
|
In the case of endotoxemia, what is the cause of moderate to severe neutropenia?
|
Margination of PMNs and decreased extravasation of PMNs
|
|
How can endotoxemia stimulate the extrinsic pathway of coagulation?
|
By causing endothelial damage and exposing tissue factor (III)
|
|
Loss of vascular tone (imbalance between vasoconstriction and dilation) leads to which 2 consequences?
|
-systemic hypotension
-inadequate perfusion of tissues |
|
Increased plasma TNF is associated with increased mortality w/ acute GI in foals with what condition?
|
Sepsis
|
|
LPS cleaves phospholipid membranes. As a result, what cascades respond?
|
-arachodonic acid cascade
-cycclooxygenase pathway (prostanoids, pg production) -lipooxygenase pathway |
|
Endotoxins also cause the release of what other inflammatory mediators?
|
-nitric oxide
-reactive oxygen species -tissue factor stimulation -complement -neutrophil activation |
|
All of the response meechanisms lead to the hallmark of endotoxemia, which is.....
|
Vascular permeability and endotoxemic shock
|
|
What clinical signs of endotoxemia in a horse can be seen during the hyperdynamic shock stage (15045 mins)?
|
-anorexia
-yawning -sweating -depression -colic -muscle fasiculation -fever -recumbency -altered vascular permeability -increased CRT |
|
What clinical signs are seen > 90 minutes post exposure to endotoxin?
|
-diarrhea
-prolonged CRT -dark red/purple mm -3rd space fluid -coagulopathy -obtunded mentation -hypothermia -circulatory failure -multi organ system failure -laminits -abortion |
|
What bloodwork results can you expect to see with endotoxemia?
|
-neutropenia
-lymphopenia -hyperglycemia -hyperlactatemia -thrombocytopenia -prolonged aPTT -prolonged PT -increased FDP, d dimers -decreased fibrinogen concentration |
|
What one potential drug looks promising for treating endotoxemia?
|
Acvtivated protein C
|
|
What is the best evidence for survival of endotoxemia?
|
-early aggressive cardiovascular resuscitation
-O2 -iv fluids -pressor tx -packed rbc's |
|
What are the goals of early endotoxemia therapy in horses?
|
-cardiovascular resusciation
-laminitis prevention -removal of causes of endotoxin -neutralization of fre circulating LPS -inhibition of LPS mediated inflammation |
|
Cardiovascular resuscitaion includes the use of which fluids?
|
-hypertonic saline
-colloids (hetastarch, plasma) -crystalloids |
|
What effects will hypertonic saline have in the tx of endotoxemia?
|
-transient increase in vascular volume
-suppressed degranulation of PMNs (decreased ROS) -prevents PMNs-endothelial adhesions -blocks nuclear transcription of inflammatory cytokines |
|
What benefit does hetastarch have in treating endotoxemia?
|
Higher COP than plasma, increases vascular volume
|
|
What must you be cautious about when using hetastarch?
|
prolonged aPTT when high doses are used
|
|
What benefits are there in using equine frozen plasma?
|
-excellent source of albumin
-anti-endotoxins -clotting factors |
|
What are the drawbacks to plasma?
|
-requires time to thaw
-requires time to administer -expensive |
|
Which fluid is used for resuscitation...colloids or crystalloids?
|
Both
|
|
What prophylactic steps can be taken to prevent laminitis?
|
-cryotherapy
-NSAIDs |
|
What is the advantage to cryotherapy?
|
50% reduction in the metabolic rate with a 10C drop in temp
|
|
True of False, cryotherapy is beneficial at all stages of endotoxemia?
|
False- before clinical signs are seen
|
|
What is the goal of low dose NSAID therapy?
|
Prevent LPS associated prostanoid production
|
|
What is the goal of high NSAID therapy?
|
Cox inhibitor, excellent visceral analgesia
|
|
What is the drawback to using NSAIDs?
|
-delayed muscosal healing
-toxicity (renal, gi) |
|
What causes of endotoxn can be removed?
|
-sx to remove ischemic bowel
-drainage of septic pleural/peritoneal/uterine fluid cavities |
|
Are broad spectrum antibiotics indicated for endotoxemia?
|
Yes, but with caution
|
|
Under what conditions do you need to be cautious when using antibiotics?
|
-horse < 3months old (maternal ab)
-suspicion of clostridial or antimicrobial associated enteritis -degenerative left shift or PMN/leukocytes < 1000uL -evidence of dyshemopoiesis |
|
What treatment would neutralize free circulating enodtoxemia?
|
-plasma tx
-polymixin B |
|
Polymixin B can have what toxic side effect?
|
-renal dysfunction
|
|
What drugs inhibit endotoxemia mediated inflammation?
|
-2% lidocaine CRI
-NSAIDs -pentoxyfylline -DMSO |
|
What effects does lidocaine have in the tx of endotoxemia?
|
-anti-inflammatory
-analgesic -prevents retardation of mucosal healing when used w/ Banamine |
|
What effects does pentoxifylline have?
|
Suppresses inflammatory cytokines, rheologic agent, inhibits TNFm promotes PGI1
|
|
What effect dose DMSO provide in the tx of endotoxemia?
|
-free radical scavenger
-anti inflammatory -prophylactic tx of laminitis |
|
What is a potential side effect of DMSO?
|
Hemolysis
|
|
What are the best steps to take in dealing with endotoxemia?
|
-recognize patients at risk
-restore perfusion/oxygenation -ameliorate clinical signs -prevent laminitis |
|
LAMINITIS
|
LAMINITIS
|
|
What is the definition of laminitis?
|
Inflammation of the laminae
|
|
What does laminitis cause?
|
Degeneration, necrosis and inflammation of the dermal and epidermal laminae of the hoof wall of horses
|
|
Which lamellae of the foot interdigitate?
|
Sensitive and insensitive lamellae
|
|
What is the function of the lamellae?
|
Hold PIII in close proximity to the hoof
-act as a suspension mechanism |
|
What kind of disease conditions initiate laminar changes?
|
Any disease that decreases laminar perfusion and protein synthesis
|
|
The rigidity of the hoof wall can lead to what complication with the swelling of the laminae?
|
Pressure necrosis
|
|
Hours before the onset of clinical signs, what happens to the sensitive and insensitive lamellae?
|
They separate
|
|
Failure of the laminae can lead to what disastrous condition?
|
MODS
|
|
What is the #1 risk factor for laminitis for patients in the ICU?
|
Endotoxemia
|
|
How can endotoxemia lead to laminitis?
|
GI disease may lead to translocation of endotoxin
|
|
What is the response of the body to LPS?
|
Up-regulation of inflammatory cytokines
|
|
True or False- endotoemia by itself can cause laminitis.
|
False- not by itself
|
|
What other systemic condition can lead to laminitis?
|
Septic metritis
|
|
What is contra-lateral limb laminitis?
|
Excess weight bearing on a limb due to injury in the opposite limb (support limb laminitis)
|
|
What type of dietary changes can lead to laminitis?
|
Increase in CHO, grain overload (incomplete pre-cecal digestion), grazing lush spring grass
|
|
What types of horses can get laminitis from grazinf lush spring grasses?
|
Ponies
Horses w/ metabolic syndrome |
|
Laminitis can be caused by what types of endocrinopathies?
|
-equine Cushing's
-equine metabolic syndrome -glucocorticoid excess -insulin resistance -impaired glucose utilization -inflammatory up-regulation -hyperinsulinemia |
|
Ingesting what plant/tree can lead to clinical signs of laminitis?
|
Black walnut
|
|
Where might a horse encounter black walnut?
|
In shavings for bedding
|
|
What are the clinical signs of ACUTE laminitis?
|
-bounding digital pulses
-heat in the hoof capsule -softness of coronary band -shifting weight -refusal to pick up feet/or walk -pain -tachycardia/tachypnea -anorexia/depression |
|
What grading system is used to rank the severity of laminitis?
|
Obel grading
|
|
What is the importance of radiographs during an acute laminits?
|
Can be used as a baseline
|
|
Radiographically, what may be the only indication of laminitis inflammation?
|
Thickening of the dorsal foot wall
|
|
What are the effects of laminitis on PIII?
|
Leads to the detachment of P3 from the hoof wall
rotation sinking |
|
Ideally, when should laminitis treatment begin?
|
Prophylactically
|
|
What are the goals of laminitis treatment?
|
-eliminate the primary cause
-promote digital circulation -reduce tension on the laminae -minimize digital inflammation and pain |
|
True or false...the acute phase of laminitis is a medical emergency.
|
TRUE!
|
|
Prophylactic treatment for laminitis includes what 3 components?
|
-cryotherpy
-anti-inflammatories -sole support |
|
When should cryotx be started?
|
before the clinical signs of laminitis
|
|
Which drugs are sued as anti-inflammatory prophylaxis?
|
2% lidocaine CRI
NSAIDs |
|
What type of sole support is used for laminitis?
|
-removal of metal shoes
-apply styrofoam cushion |
|
What type of bedding should be used for horses with laminitis?
|
-deep sand
-peat moss |
|
Pain management for laminitis should take what approach?
|
Multi-modal
|
|
CHRONIC laminitis is a result of what?
|
Abnormal hoof conformation
|
|
What are some conditions that lead to mis-shapened feet?
|
-growth at toe (ski shoes)
-lack of growth at heel -growth rings prominent, not parallel -sole flattened |
|
What radiographic changes might be seen in a case of chronic laminitis?
|
-osteomyelitis
-deformation of PIII |
|
What types of lifetime foot problems can be expected with chronic laminitis?
|
-recurring foot abscessation
-hoof cracks and chips -tendency towards sole bruising |
|
What treatment can be used to reduce rotation of the coffin bone?
|
raise the heel
|
|
Therapy for chronic laminitis includes what?
|
-good foot care
-balances shoeing -sole pads -tx of thrush -good environment |
|
What is the prognosis for laminitis?
|
It is for a lifetime
|
|
What is the capacity of the equine cecum?
|
30 liters
|
|
What is the capacity of the equine large colon?
|
60 liters
|
|
What are some of the clinical signs of colic?
|
-kicking at belly
-pawing -lying down -looking at sides -curling lips -playing in water -grinding teeth -refusing feed -change in attitude -decreased fecal output |
|
What are the clinical signs of severe, acute colic?
|
-down and rolling
-evidence of rolling -breathing hard -sweating -abdominal distention |
|
Why do you inspect the feces in reference to a case of colic?
|
For amount and consistency
|
|
Why is a rectal palpation performed on a horse with colic?
|
Identify changes in visceral organs
|
|
What are 2 additional steps to take prior to performing a rectal?
|
Wrap tail
Use copious lube |
|
What is a potential serious complication of rectal palpation?
|
Rectal tear
|
|
How many grades of rectal tears are there?
|
I- IV
|
|
A grade I tear includes what?
|
Mucosa and submucosa
|
|
What constitutes a Grade II tear?
|
Muscularis only
|
|
A rectal tear with a grade IIIa/b includes which layers?
|
All layers except serosa
|
|
What constitutes a grade IV rectal tear?
|
Full thickness, all layers
|
|
What color is normal peritoneal fluid?
|
Clear transudate to straw/yellow
|
|
TP of peritoneal fluid should normally be what?
|
< 2g/dl
|
|
Serosanguinous fluid from an abdominocentesis indicates what conditions?
|
-bowel devitilization
-splenic puncture -sub cu blood vessel |
|
In the case of a bowel rupture, you would expect peritoneal fluid to have what color?
|
Green
|
|
What color is peritoneal fluid in the case of peritonitis?
|
Thick orange
|
|
What lenght of endoscope is needed for a horse?
|
1 M and 3 M
|
|
True or False. Laporoscopy is considered a diagnostic tool.
|
True
|
|
A routine GI examination should include what imaging modality?
|
U/S
|
|
Which U/S probe is used for equine GI?
|
3-5 mHz
|
|
Where do you place the U/S probe to located the stomach?
|
-right side
-9-13 ICS |
|
Where is the duodenum located?
|
-right side
-ventral to the caudal pole of the right kidney |
|
How do you distinguish the large colon from other organs on U/S?
|
look for the hautra/ sacculations
|
|
Which imaging modality is useful for diagnosing bone disease?
|
Nuclear medicine
|
|
How are full thickness biopsies obtained?
|
-ventral midline celiotomy
-laporoscopy |
|
Along with evaluating the amount and consistency of feces, what else do you examine the feces for?
|
Sand
Parasites |
|
When is an absoprtion test indicated?
|
In chronic weight loss
|
|
What shape does a normal absorption uptake curve have?
|
Inverted V
|
|
True or False. The equine esophagus is covered by a thin serosa.
|
False.,..not covered at all except for a short distance between the diaphragm and stomach
|
|
What is the benefit of the esophagus being attached to surrounding tissues?
|
Allows movement of the esophagus during swallowing
|
|
What types of muscle comprise the equine esophagus?
|
Cranial 2/3 is skeletal
Caudal 1/3 smooth |
|
What muscle forms the cranial esophageal muscle?
|
Cricopharyngeus
|
|
Why can't horses vomit?
|
-poorly developed vomition center
-high interluminal pressure of the distal esophagus |
|
What is a primary clinical sign of esophageal disease in a horse?
|
Ptyalism -hypersalivation
|
|
What should you be aware of when palpating the esophagus?
|
-creptius (emphysema)
-swelling |
|
What is the value of plain radiographs in evaluating the esophagus?
|
-localize evidence of obstruction
-gas opacity between fascial planes indicating perforation |
|
Why would you perform barium studies?
|
To outline intraluminal obstruction/strictures
|
|
A complete esophageal exam will include what procedure?
|
Endoscopy
|
|
What imaging procedure would you use to evaluate the motility of the esophagus?
|
Fluoroscopy
|
|
What is primary choke?
|
Simple luminal obstruction
|
|
What are some causes of primary choke?
|
-roughage
-foreign bodies: corn cobs, potatoes, apples |
|
What are some intramural causes of choke?
|
-tumor
-strictures -diverticula -cysts, -vascular ring anomalies |
|
What is the most common clinical sign of esophageal obstruction?
|
Ptyalism and frothy nasal discharge with feed and saliva
|
|
What other signs of obstruction may be seen?
|
-may stand with head and neck extended
-gagginr -retching -coughing |
|
Why would you see an electrolyte imbalance in a horse with choke?
|
Loss of saliva
|
|
Definitive information about the cause of esophageal obstruction can be made with what technique?
|
Endoscopy
|
|
Where do most esophageal obstructions occur?
|
At the sites of narrowing
-cervical esophagus -heart base/thoracic inlet -terminal esophagus |
|
What is the primary goal in the treatment of choke?
|
To relieve the impaction
|
|
Why is the horse sedated to treat for choke?
|
To prevent aspiration
|
|
An attempt to dislodge the obstruction is made with what?
|
A NG tube
|
|
If the NG tube/lavage method does not clear the obstruction, what method is tried?
|
Chemically relax the esophagus and provide isotonic IV fluids
|
|
Why is a horse at risk for re-obstruction?
|
-dilatation of the esophagus proximal to the site of obstruction
-traumatic mucosal injury -esophagitis |
|
What percentage of horses will experience re-obstruction post resolution of the choke?
|
40%
|
|
True or False. Complications of choke include metabolic acidosis from prolonged losses of Na and Cl.
|
False, metabolic alkalosis
|
|
What other complications might be encountered?
|
-esophageal ulceration
-stricture -perforation -aspiration pneumonia -mega esophagus |
|
Why are broad spectrum antibiotics indicated when lavage alone doesnt resolve a choke?
|
Due to possible aspiration pneumonia
|
|
Some clinicians recommend the administration of what drugs to reduce the development of strictures?
|
NSAIDs (Banamine, Bute)
|
|
What is the cause of esophageal sticture?
|
Circumferential mucosal erosion related to choke (also from corrosive medicinal agents and trauma, congenital strictures have been reported
|
|
In what timeframe does maximal esophageal stricture occur?
|
Within 30 days post obstruction
|
|
Is Bougienage helpful?
|
No, not in horses
|
|
Esophageal perforation can occur as a result of choke, but also from what other related conditions?
|
-external trauma
-iatrogenic perforation from exccesive force using a NG tube |
|
How are perforations treated?
|
-debridement and lavage
-antibiotics -tetanus prophylaxis -esophageal rest (use wound for esophagotomy) |
|
Hypomotility of the esophagus results in what condition?
|
-dilation
-megaesophagus |
|
Acuqired megaesophagus is a result of what?
|
Primary or secondary esophageal obstruction
|
|
Megaesophagus has also be associated with reflux esophagitis and what types or neuro disease?
|
-equine protozoal myeloencephalitis
-equine herpes virus myeloencphalitis -idopathic vagal neuropathy also with pleuropneumonia, C. botulinum and grass sickness |
|
Is megaesophagua a functional or mechanical obstruction?
|
Functional
|
|
Definitive dx of esophageal hypomotility requires what technique?
|
barium fluoroscopy
|
|
What exam can rule out a myopathy as a cause of megaesophagus?
|
EMG
|
|
Treatment of megaesophagus can include giving metaclopramide or bethanecol (if reflux eosphagitis is present) to have what effect?
|
-increase the tone of the lower esophageal sphincter
-reduce reflux |
|
What is the prognosis of congenital megaesophagus?
|
Poor
|
|
The equine stomach is divided into 4 regions based on what?
|
Type of mucosal lining
|
|
What are the 4 types of stomach mucosa?
|
-non-glandular stratified squamous epithelium (continuous w/the esophagus)
-cardiac epithelium -gastric mucosa -pyloric mucosa |
|
What structure separates the non-grandular and cradiac regions from the glandular mucosa?
|
Margo plicatus
|
|
Which cells of the gastric mucosa secrete HCL?
|
Parietal cells
|
|
What 3 receptors must bind concurrently for the production of HCL?
|
-gastrin
-ACH -histamine 2 |
|
The stratified squamous epithelium layer is impermeable to HCL until the pH falls below what level?
|
2.5
|
|
Which cells secrete mucus and bicarb that form a gel-like substance to titrate HCL before it reaches the gastric lumen?
|
Goblet cells
|
|
Additional gastric mucosal protection is provided by what secretions?
|
Prostaglandins
|
|
What is the benefit of horses being constant grazers?
|
Maintains a feed bolus which helps protect the mucosa from HCL
|
|
Lesions found in the gastric squamous or glandular mucosa, ulcerations, gastritis, gastic-emptying disorder and reflux disorders as all grouped under what heading?
|
Equine Gastric Ulcer Syndrom (EGUS)
|
|
In adult horses, ulcer dz is commonly associated with which mucosa?
The foal? |
Adult- squamous mucosa
Foals- glandular and pyloric regions |
|
The prevalence of EGUS is high in horses, especially under what conditions?
|
Training--- 70-90% in racehorses
|
|
Along with increased exercise, what other factors contribute to EGUS?
|
-feeding pratices
-management -NSAIDs |
|
What feeding practice exposes the horses mucosa to HCL?
|
Meal feeding (2 X day), stall confinement
|
|
What effect do NSAIDs have in EGUS?
|
Disables production of protective prostaglandins
|
|
Does H. pylori contribute to EGUS?
|
The antibody has recently been reported as being present in horses
|
|
What are the clinical signs of EGUS?
|
-loss of body weight
-poor hair coat -poor body condition -poor appetite -intermittent colic |
|
The dx of EGUS is based on what?
|
-age-related clinical signs
-edoscopic exam -response to tx |
|
Where do most ulcers form in adult horses in training?
|
Along the margo plicatus
|
|
Does EGUS cause anemia or hypoproteinemia?
|
No
|
|
What is the goal of EGUS tx?
|
Alleviate discomfort by neutralizing acid secretion
Avoid NSAIDs |
|
What drug class is used to suppress acid production?
|
H2 antagonist
ranitidine, cimetidine, famotidine and nizatidine |
|
What is the mechanism of action of H2 antagonists?
|
Interfers with histamine stimulation of HCL secretion from partietal cells of gastric mucosa
|
|
What is another method of supressing HCL secretion?
|
Proton-pump inhibition
|
|
How do proton pump inhibitors work?
|
Block the H+ K+ ATPase pump on the parietal cells
|
|
Which drug is a proton pump inhibitor?
|
Omeprazole
|
|
Is Sucralfate helpful in healing gastric ulcers in horses?
|
No
|
|
Why is true gastric impaction an infrequent diagnosis in a horse?
|
It is a difficult dx to make
|
|
Which foodstuffs are particularly indicated in gastric impaction?
|
Beet pulp and bran..become dessicated in the stomach
|
|
other than a surgical dx, how is gastric impaction diagnosed?
|
Endoscopic documentation of a feed bolus in the stomach 12-24 hours following ingestion
|
|
What is the tx for gastric impaction?
|
Lavage via NG tube, also give dioctyl sodium succinate (DSS) as a detergent
|
|
Gastric impaction may be a result of which more severe disease see in Britain and South America?
|
Grass sickness (equine dysautonomia)
|
|
What can potentially gas a gastric rupture?
|
Secondarily to gastric distention from ingesta, fluid or gas
|
|
Is gastric rupture in the adult horse treatable?
|
No-a catastrophic injury with excessive contamination
|
|
What is the most common neoplasm to affect the equine stomach?
|
Squamous cell carcinoma
|
|
What are the presenting clinical signs of neplasm of the stomach?
|
-weight loss
-anemia -nasal reflux -colic |
|
What are the components of the equine small intestinal tract?
|
-duodenum
-jejunum -ileum |
|
What is the approximate total length of the equine small intestine?
|
70 feet
|
|
How much of the small intestine can be surgically resected?
|
roughly 1/2
|
|
What additional GI structures are located within the duodenum?
|
Major and minor papilla of common bile duct
|
|
Which small intestine segment is the longest?
|
Jejunum
|
|
What structure is located at the distal end of the ileum?
|
Cecum
|
|
How is the ileum differentiated from other segments of small intestine?
|
Non-vascular, antimesenteric band (ileocecal fold) which is contiguous with the dorsal band of the cecum
|
|
Which diagnostic technique is most useful in evaluating the small intestines?
|
U/S
|
|
How does IBD in horses differ than in humans?
|
Humans- neutrophilc inflammation
Horses- neutrophil is the primary effector cell but the dz is defined by other granulocytic cells (eosinophils, bashophils, lymphos, macs) |
|
Horses with IBD present with weight loss and diarrhea. How do horse present with (a new condition) idiopathic focal eosinophilic enteritis (IFEE)?
|
Signs of acute colic pain but no protein losing enteropathy
|
|
True or False, a horse with traditional IBD of the SI will not have diarrhea.
|
True
|
|
Why would a horse with IBD present with peripheral edema?
|
Hypoproteinemia- enteric protein loss
|
|
What change might U/S show in a case of IBD?
|
increased intestinal wall thickness (>5mm)
|
|
What would a glucose absorption test curve look like in the case of IBD?
|
Flat- malabsorption
|
|
In IBD, inflammatory cells infiltrate the intestinal tract, making what procedure a useful tool in indentifying IBD?
|
Rectal mucosal bx
|
|
How is a definitive dx of IBD made?
|
Bx of small or large intestine via laparoscopy or celiotomy
|
|
How successful is tx of IBD in horses?
|
Largely unsuccessful
|
|
Do horses with IBD or IFEE have a better chance at recovery?
|
IFEE- typically respond to surgical decompression
|
|
Granulomatous enteritis tends to affect which horses?
|
Young, standardbred
|
|
On hisotpath, what cells are primarily seen in granulomatou enteritis?
|
macrophages
|
|
What is the prognosis of a horse with granulomatous enteritis?
|
Poor
|
|
Which non-infectious inflammatory bowel dz of young horses has dermatological effects?
|
MEED
Multisystemic Eosinophilic Epitheliotropic Enterocolitis Dz |
|
True or False...lymphocytic/plasmacytic enteritis is a common disease of horses of all ages?
|
False- it's rare
|
|
Lawsonia intracellularis causes what disease of the intestine of mammals and avian species?
|
Proliferative enteropathy
|
|
In pigs, what name is Lawsonia as it causes proliferation of the SI?
|
garden hose gut
|
|
How does the Lawsonia bacterium infection occur, and in what horses?
|
Fecal-oral
affects weanling foals |
|
What factors increase the chances of infection?
|
-overcrowding
-ration changes -transport -weaning |
|
What are the 2 hallmarks of Lawsonia?
|
-hypoproteinemia
-grossly thickened SI with mucosal ulceration |
|
Mucosal proliferation of the SI crypt cells typically affect which areas of the SI?
|
Terminal jejunum and ileum
|
|
What is the appearance of the SI epithelium in an infection with Lawsonia?
|
Thickened, corrugated
|
|
What effect does this thickening have on the SI function?
|
-decreased brush border enzyme activity
-decreased absorptive capacity -weight loss -malabsorption diarrhea -hypoproteinemia |
|
What is the primary differential dx for Lawsonia?
|
R equi
|
|
What are the clinical signs of Proliferative Enteritis seen in foals 4-6 months of age?
|
-Ill thrift: poor hair coat, pot bellied, dimished stature, poor grwoth rate
-weight loss -peripheral edema -diarrhea -colic |
|
Why do horses affected with PE show hyperfibrinogenemia?
|
Chronic inflammation
|
|
What other blood results would you see in a case of PE?
|
-modearte hypoproteinemia
-hypoalbuminemia -mild anemia -hypoglobulinemia -neutrophilic leukocytosis -pre reanal azotemia |
|
U/S exam of the abdomen may show what sign of PE?
|
Thickened walls of SI tract (>5mm)
|
|
When are most cases of Lawsonia PE seen?
|
August to January
|
|
What is the gold standard dx for Lawsonia?
|
Isolation and culture from tissue
|
|
What stain is used to visualize Lawsonia?
|
Warthin-Starry stain
|
|
What is the tx for PE?
|
-antimicrobial tx targeting intracellular pathogens and supportive care
-tetracylcine (Ocytet/Doxy) |
|
What is the prognosis for a foal with Lawsonia?
|
Good, 93% recovry, may be small in stature compared to other foals
|
|
What does enteritis mean?
|
Inflammatory condition of the small intestine.
|
|
What are the cardinal signs of inflammatory lesions?
|
-fever
-endotoxemia -depression |
|
Acute pain is due to what?
|
-intestinal wall inflammation
-edema -necrosis -infarction |
|
What are the cardinal clinical findings of enteritis?
|
-fluid distended loops of small intestine on U/S exam
-on rectal palpation -gastric reflux |
|
How is duodentitis-proximal jejunitis (DPJ) characterized?
|
-inflammation and edema of the duodenum and proximal jejunum, excessive fluid and electrolyte secretion into the small intestine and consequently, high volumes of enterogastric reflux
|
|
True or false with DPJ horses have copious reflux and abdominal discomfort without mechanical obstruction to flow of ingesta.
|
True
|
|
Inflammation within in the SI causes what kind of obstruction?
|
A functional obstruction of motility due to dysregulation of the myenteric plexus )or enteric nervous system)
|
|
What is a common finding of DPJ in sx or necropsy?
|
Serositis: bright red to dark red petechial and ecchymotic hemorrhages on the serosal surface of the proximal SI
|
|
What factors are used to help determine which horses with SI obstruction need sx intervention or medical tx?
|
-degree of pain and response to gastric decompression
-fever -changes in bloodwork and peritoneal fluid parameters |
|
Horses with DPJ have what type of results when an NG tube is passed?
|
-Large amounts of typically odrous fluid, orange-brown in color
|
|
What hallmark of DPJ is seen when a NGT is passed?
|
-horses are less colicky and appear depressed
|
|
Horses with DPJ have what other clinical signs?
|
-fever
-mild to moderate colic -dehydration -signs of endotoxemia, hypovolemia, increased borborygmi, elevated heart and respiratory rates |
|
What is the appearance of the SI with DPJ as seen on U/S?
|
Variable sized and shaped distended loops of SI, typically with increased wall thickness (>5-6mm)
|
|
Horses with ischemic/necrotic bowel have abnormal peritoneal fluid parameters such as elevated total solids, elevated nucelated cell count and abnormal color (serosanguinous). How does DPJ compare to this?
|
DPJ abdominal fluids may be turbid, dark yellow to orange but rarely serosanguinous, mild elevated cell count and elevated total solids
|
|
DPJ may have an infectious cause such as what?
|
Salmonella spp, Clostridium spp.
|
|
When is definitive confirmation of DPJ made?
|
At sx or necropsy
|
|
What is the tx for DPJ?
|
-support tx centered of frequent gastric decompression (indwelling NGT) and IV fluid replacment
also tx for hypoproteinemia, antiendotoxin, antiinflammatory tc, analgesia etc |
|
What are the 2 causes of GI Ileus?
|
-DPJ (most common)
-POI post op ileus following general anesthesia |
|
How does SI sx cause ileus?
|
-handling of the bowel
-distention of the bowel proximal to obstruction |
|
Non-abdominal can result in GI ileus....how?
|
Cecal dysfunction for general anesthesia
|
|
30% of hoses undergoing SI sx will have POI, what factors affect this situation?
|
-length of resection
-age -PCV at admission -duration of anesthesia |
|
Why does POI increase morbidity and mortality?
|
-adhesion formation (chr. colic)
-lamintis also a big financial burden |
|
POI can occur in any post op pt, how soon after sx do clinical signs of POI develop?
|
24-96 hours post op
|
|
What clinical signs of POI should you watch for?
|
-tachycardia
-tachypnea -colic -decreased manure production -decreased borborygmi |
|
How can you monitor a horse for POI development?
|
Serial U/S exams
|
|
How do you dx POI?
|
-serial U/S exam
-rectal exam -peritoneal fluid -pass NG tube (20L in 24 hrs or 8L at any one time) -volume of reflux should taper -attempt to r/o mechanical obstruction |
|
What factors would make you suspicious of POI?
|
-hx of sx intervetion
-/+ resection -degree of inflammation of of GI tract -distention of proximal bowel also concern about mechanical re-obstruction development of peritonitis |
|
What is the TX for POI?
|
Same as for DPJ:
-gastric decompression -monitor fluids in and out -anti-inflammatory tx -prokinetic Tx |
|
What is one of the serious complications of POI?
|
Adhesion formation
|
|
What is peritonitis?
|
An inflammatory condition of the mesothelial lining of the peritoneal cavity
|
|
Where is the mesothelial lining located?
|
-1 cell layer thick
-visceral/parietal surfaces -lines internal organs -has a large surface area |
|
What is the pathophysiology of peritonitis?
|
-initial insult
-release of vasoactive mediators: histamine & serotonin -increased vascular permeability -transudation -protein, fluids, cells |
|
Macrophages stimulate the inflammatory process leading to what?
|
-lysosomal degranulation
-fibrin deposition -translocation of bacteria |
|
The increased peritoneal permeability leads to shifting of fluid and electrolytes which can cause what?
|
-dehydration
-hypovolemia |
|
Endotxoemia, bacteremia and shock can result from what component of peritonitis?
|
Intravascular re-entry of pro-inflammatory substances and bacteria
|
|
What is the difference between primary and secondary peritonitis?
|
Primary: no identifiable inciting cause
Secondary: caused by -infection -trauma -chemical -parasitic -visceral disease -abdominal surgery -neoplasia |
|
Aseptic peritonitis is defined as what?
|
-mechanical or chemical irritation
(urine/bile/foreign material) -surgery |
|
What does septic peritonitis imply?
|
-bacterial foci within the peritoneum
|
|
What are some of the sources of septic peritonitis?
|
-bowel perf
-penetrating wounds -rectal tears -dehiscence -uterine rupture -breeding accident -bacetremia |
|
What is the most common cause of septic peritonitis?
|
Surgical contamination
|
|
What are the clinical signs of peritonitis?
|
-pyrexia
-diarrhea -anorexia -dehydration -abdomen pain -tachycardia/pnea -ileus -depression -abd distention -abnormal rectal exam findings |
|
How would you Dx peritonitis?
|
-CBC and fibrinogen
-rectal exam -abd U/S -peritonel paracentesis |
|
On a CBC what is the difference between an acute and a chronic peritonitis?
|
-acute: neutropenia w/ toxic left shift, normal fibrinogen
chronic: neutrophilia w/ increased fibrinogen |
|
What would you expect to see on the analysis of peritoneal fluid from peritonitis?
|
-color/clarity altered
-markedly elevated WBS -increased TP do C&S and cytology |
|
Recent surgery complicates the dx of peritonitis, what test would you run to help?
|
Blood gas analysis of the peritoneal fluid
|
|
How does the blood gas of septic peritoneal fluid compare to serum blood gas?
|
-glucose < 50 points lower than serum
-elevated lactate -very low pH |
|
What cause these changes in the blood gas values of peritoneal fluid?
|
Bacteria metabolize glucose and produce lactate as by-product, lowering pH
|
|
What is the Tx for peritonitis?
|
-Abx
-anti-inflammatory tx -anti-endotoxemic/laminitis tx -maintain hydration -e-lyte balance -consider nutrition -monitor protein loss into the abd |
|
What controversial tx is sometimes used to tx peritonitis?
|
Peritoneal lavage
|
|
What is the prognosis of peritonitis?
|
-variable
-depends on underlying etiology -complications (laminits, adhesions) |
|
What is meant by the term small bowel obstruction?
|
-occlusion of the small bowel lumen of the instestine without compromise to the associated blood supply (non-strangulating lesion)
|
|
What is a functional obstruction?
|
Simple obstructions which are nueromuscular in nature and result in the lack of propulsive muscle activity (ie DPJ)
|
|
What is a mechanical obstruction?
|
Physical occlusion of the intestinal lumen
|
|
The severity of pain from an obstruction is related to what?
|
-degree of obstruction and the amount of intestinal distention proximal to the obstruction
|
|
What is a strangulating obstruction?
|
Occlusion of the intestinal lumen as well as the blood supply to that segment of SI
|
|
Horse with strangulating obstructions often develop what conditions?
|
-endotoxemia
-hemoconcentrated -dehydration |
|
What is the course of action for a horse with a strangulating obstruction?
|
Surgery
|
|
Which ascarid impaction occurs in horses < 1 year of age?
|
Parascaris equoroum
|
|
How do foals become impacted?
|
Following oral paste deworming with an antihelmintic in heavily parasitized individuals...adult worms live in Si lumen and die en masse, causing luminal obstruction
|
|
What are some of the clinical signs of impaction?
|
-mild to moderate colic pain
-gastric reflux -fever, endotox -inflammatory mediators lead to fever, tachcardia/pnea, poor perfusion, shock |
|
What is the goal of tx for ascarid impaction?
|
Medical
-gastric decompression -gastric lavage -anti-inflammatory meds |
|
What conditions might a foal with ascarid impaction develop?
|
-intestinal necrosis
-rupture -peritonitis -adhesion |
|
What is the prognosis for a foal with ascarid impaction?
|
Guarded due to the sever inflammatroy response from the death of the parasite. Medical tx is a better prognosis than sx
|
|
How can ascarid impaction be avoided?
|
use a slow kill antihelmentic
|
|
Where, geopgraphically, does ileal impaction occur, and why?
|
Southeast US due to luminal obstruction of the ileum with dry feed matter
|
|
Which feed is most likely to cause ileal impaction?
|
Coastal Bermuda grass hay
|
|
Ileal impaction has also been associated with what other condition?
|
Tapeworm infestation due to irritation at the ielocecal junction
|
|
What clinical signs are associated with ileal impaction?
|
SI obstruction signs
-colic that is acute, mild to severe -not all will show reflux -reduced intestinal sounds -distended bowel loops on rectal exam |
|
What medical tx might be of use early in the impaction?
|
-mineral oil (via NGT)
-analgesics -IV fluids |
|
What sx approach can be taken for ileal impaction?
|
Removal via SI enterotomy
|
|
What is the term for the proximal (oral) segment of an SI intussusception?
|
Intussusceptum
|
|
What is the term for the distal segment of an SI intussusception?
|
Intussuscipiens
|
|
What is the most common location for a SI intussusception?
|
ileocecal
|
|
In what age of horse is intussusception seen?
|
< 3 years, foals and weanlings
|
|
Sx manipulation of an intussusception may be possible except in the ileocecal region....how is this handled?
|
resection or baypass of the ileum
|
|
What is the U/S appearance of an intussusception?
|
Bull's-eye, 2 concentric rings in a circular area
|
|
Necrosis of the distal ileal stump may result in what conditions?
|
-septic peritonitis
-abscessation -ahesions |
|
What is a SI volvulus?
|
twisting of the intestines around the root of the mesentary
|
|
What is the cause of volvulus in a young horse?
|
change in feeding habit--shift to forage
-GI parasitism |
|
What are the clinical signs of SI volvulus?
|
-abd pain
-reflux -poor tissue perfusion -decreased intestinal sounds -distended SI on rectal |
|
How should a horse with SI volvulus be tx until sx?
|
Aggressive fluid tx
|
|
What is SI incarceration?
|
A segment of the SI is entrapped through a rent in the mesentary, inguinal ring, gastro splenic ligament or epiploic foramen
|
|
What can cause a mesenteric rent?
|
Blunt abd trauma (trailer accident, kick)
|
|
What is the gastropslenic ligament?
|
Lesser omenrum that connects the stomach to the spleen
|
|
What clinical might you see in a stallion with an inguinal hernia?
|
-testicle on affected side with by enlarged, swollen, cold, painful
SI will be palpable entering the inguinal ring on rectal exam |
|
When do most cases of epiploic formane entrapment occur?
|
Winter months
in horses 8+ year cribbing is a factor |
|
How are SI incarcerations Tx?
|
SX resection and anastomosis of strangulated section
|
|
From where do pendunculated lipomas arise?
|
Mesenteric adipose tissue
|
|
As the lipoma stalk lengthens it can entrap the SI causing what type of obstruction?
|
Mechanical
|
|
Pedunculated lipomas occurs in horses > 9 and particularly of which breed?
|
Arabs (and geldings)
|
|
How do you distinguish feed impaction from pedunculated lipoma?
|
--older horses rarely get feed impaction
-feed impactions generally do not lead to a cardiovascular parameters as with devitilized bowel |
|
Is diarrhea a primary sign of SI or LI dz?
|
LI
|
|
In horses, diarrhea is what type of condition?
|
Emergency
|
|
What is colitis?
|
Active inflammation of the colon wall
|
|
What is the cardinal sign of colitis?
|
Diarrhea
|
|
Which cell is the acute colitis effector cell?
|
PMN- neutrophil
|
|
What are the clinical signs of colic?
|
-fever
-endotoxemia -diarrhea -peripheral edema -colic pain +/- reflux |
|
What can occur if diarrhea is severe or prolonged?
|
Hypovolemia, shock
|
|
What changes in bloodwork can indicate colitis?
|
-neutropenia
-metabolic acidosis -hyponatremia |
|
What might be seen on U/S in a horse with colitis?
|
-swirling fluid within cecum/colon
-may also see dilated SI/stomach -may see excess peritoneal fluid |
|
What would you expect the results to be of a peritoneal paracentesis for colitis?
|
Normal fluid
|
|
Which factors help in making a definitive dx of colitis?
|
-fecal cultures
-bacterial toxins in feces -PCR -use of signalment/history -use of season/time of year |
|
Regardless of the cause of colitis, how is it tx?
|
Supportive care
|
|
What are the first steps in colitis tx?
|
-fluids to ocmbat dehydration, electrolyte loss and acidosis
-crystalloid/colloid to tx hypoproteinemia |
|
Why is hypertonic saline used with caution in colitis patients?
|
-many are dehydrated and have volume depletion, hypertonic saline can lead to blindness and cerebral signs
|
|
What are the components of anti-endotoxemia tx?
|
-Nsaids
-equine plasma -polymixin B (binds LPS) -cryotherapy |
|
What additonal meds are given to tx colitis?
|
-oral anti-diarrheal agents
-antimicrobials (beta lactam) -TPN |
|
What are the potential complications of colitis?
|
-endotoxemia (laminitis)
-thrombophlebitis -coagulopathy prolapsed rectum -infarcted bowel |
|
Which is the most common serotype of Salmonella in horses?
|
S typhimurium
|
|
Which age of horse is more susceptible to Salmonella?
|
younger
older sick |
|
Transmission of Salmonella is by the fecal-oral route an causes what reactions?
|
-intestinal wall inflammation
-hypersecretion -ulceration -protein and e-lyte loss resulting inflammation impairs the mucosal barrier allowing luminal endotoxin to be absorbed |
|
What are the common clinical signs of salmonellosis?
|
-fever
-diarrhea -endotoxemia |
|
What clinicopathology results are seen with a Salmonella infection?
|
-intense neutropenia with left shift
-toxic changes -azotemia -hypoproteinemia -metabolic acidosis -e-lyte loss |
|
How is a dx of Salmonellosis confirmed?
|
-bacterial culture or PCR of feces, tissues or body fluid
|
|
What is the most important tx for Salmonellosis?
|
Fluid Tx
|
|
What is the prognosis for Salmonella infection?
|
variable- positive horses should be isolated while shedding the bacterium
|
|
How does Clostridium overgrow and colonize the colonic mucosa?
|
-stress
-immunosuppression -changes in the normal flora from abx tx |
|
How is a dx of Clostridium infection confirmed?
|
-fecal culture
-identicification of C difficle toxin A or B by Elisa or PCR |
|
How is Clostridum treated?
|
-if infection is associated wtih antimicrobile tx, discontinue abx
-metronidazole is the first-line abx mortality rate is high |
|
What is the causative agent of Potomac Horse fever?
|
Neorickettsia risticii
has tropism for monocytes and enterocytes |
|
What is the intermediate host for N. risticii?
|
A fluke that infests snails
snails are eaten by horses grazing pasures near freshwater in warm season |
|
What are the clinical signs of Potomac Horse Fever?
|
can be sub clinical but signs same as Salmonella
|
|
How is PHF dx?
|
within 4-10 days of clinical signs, large rise in titers is see
|
|
What is the tx of choice for PHF?
|
Oxytetracycline
|
|
What are the complications of PHF?
|
-laminitis
-abortion |
|
What are cyathostomes?
|
Small strongyles
|
|
On the L3 larvae are ingested where do the migrate?
|
Mucosa of the cecum and colon where they mature to L4
|
|
What happens when the L4 excyst?
|
The submucosal capsule ruptures, releasing the nematode larvae as well as excretory and secretory products that have accumulated over time
|
|
What effect does this excystment have?
|
Massive damage of the colonic mucosa
|
|
What are the clinical signs of cyathostomiasis?
|
-severe diarrhea
-rapid weight loss -marked hypoproteinemia -passage of larvae in the feces |
|
How is cyathostomiasis dx?
|
Larvae may be seen in feces or fecal egg counts are high. Adult worms may be seen on the rectal sleeve of the examiner
|
|
What is the tx for cyathostomiasis?
|
-fenbendazole
-moxidectin |
|
Which abx should never be used in horses?
|
Lincomycin
|
|
Which abx are most associated with causing colitis in horses?
|
-erythromycin
-ceftofur -tetracycline -ampicillin -metronidazole -neomycin -trimethroprim sulfates |
|
Which insect carries the toxin cantharidin, a mucosal irritant?
|
Blister beetles
|
|
How do horses consume blister beetles?
|
While eating alfalfa hay
|
|
What are the clinical signs of cantharidin toxicosis?
|
-ulceration, salivation of oral cavity
-colic -diarrhes -hematuria -stranguria -myocarditis |
|
Cantharidin can also cause what other condition resulting in signs of tetany and bizarre behavior
|
Hypocalcemia
|
|
How is cantharidin toxicosis dx?
|
-suspected in hypocalcemia horses with oral, GI and urinary ulceration after consuming alfalfa hay
|
|
What is the tx for cantharidin toxicosis
|
-supportive care
-mineral oil my evacuate beetles from the intestinal tract prognosis is poor with 50% mortality |
|
What is the cause of grain overload?
|
Grazing on lush pasture
Feeding too much concentrate to much CHO to cecum, lowers cecal pH |
|
What effect does decreased cecal pH have?
|
-decreased fermentation
-cecal/colic dysmotility -gas distention -colic pain |
|
What is the tx for grain overload?
|
-lavage, mineral oil, charcoal NGT
-anti-endotoxemia tx -laminitis prophylaxis -cecal trocar |
|
What is sand enteropathy?
|
Horses on pasture with sandy soil consume sand as they graze or eat hay off the ground
|
|
What are the clinical signs of sand enteropathy?
|
-mild abd pain
-or severe pain if the right dorsal colon or transverse colon is acutely or completely obstructed -horse mat stretch out or lie down -may have diarrhea |
|
How is sand enteropathy dx?
|
-fecal float in water for sand
-rads to see sand in ventral colon -U/S guided bx of peritoneal fluids, disappearance of haustra with weight of sand |
|
What is the tx for sand enteropathy?
|
-Metamucil in water vis stomach tube
-oral and IV fluids -analgesics -sx may be necessary to remove sand for right dorsal and transverse colons (via pelvic flexure enterotomy) |
|
Why do Nsaids cause mucosal ulceration?
|
They suppress prostaglandin production which is necessary for bloodflow to the mucosa
|
|
Nsaid induced colonic damage occurs when?
|
Excessive doses in the face of water deprivation
|
|
which segment of the colon is most sensitive to Nsaid toxicosis?
|
Right dorsal colon
|
|
With Nsaid toxicity, fibrosis may develop in the right colon leading to what condition?
|
Stricture
|
|
How do you dx Nsaid toxicosis?
|
Clinical signs and a hx of recent nsaid use, elimination of other etiologies
|
|
What U/S evidence can support the dx of nsaid toxicity?
|
Thickening of the right dorsal colon wall
|
|
What is the tx for nsaid toxicity?
|
-Discontinue nsaids
-supportive care for colitis -feed corn oil and psyllium to increase production of anti-inflammatory short chaon fatty acids |
|
What drugs should be used for pain management if Nsaids are to be avoided?
|
-Butorphanol
-Lidocaine- cri |
|
Obstruction of the large intestinal lumen may occur due to what?
|
-ingestion of coarse feed
-inadequate mastication -insufficient water supply -reduced intake of water |
|
What are the most common sites for impactions?
|
Where luminal narrowing occurs
-pelvic flexure and left ventral colon -junction between the right dorsal and transverse colon |
|
What are the clinical signs of large colon impaction?
|
-mild intermittment colic
-minimal systemic deterioration -heart rate may be slightly increased |
|
What is the tx for impaction?
|
-oral and IV fluids
-mild analgesics -laxatives -overhydration -isotonic solution should be used -no feed until impaction is resolved..slow return to feed |
|
Cecal impaction can have the same causes as large colon impaction an what additional risk factors for cecal atony or motility dysfunction.
|
-pts that have had general anesthesia
-tx w/ Nsaids |
|
What are the clinical findings in the case of cecal impaction?
|
-severely painful, rupture is common
|
|
Cecal impactions occur in horses of what age?
|
8 years
|
|
What is the tx for cecal impaction?
|
Discuss sx correction with client due to rupture in 50% of cases
|
|
Left dorsal displacment of the large colon is also referred to as what?
|
Nephrosplenic entrapment of the large colon
|
|
How does Nephrosplenic entrapment occur?
|
-colonic distention
-spleen contracts in response to pain -gas filled colon displaces dorsally -spleen re-engorges and hooks colon |
|
What are the clinical signs of Nephrosplenic entrapment?
|
-mod to severe abd pain
-heart rate varies -pelvic flexure may be palpated over the ligament |
|
What are the treatment for Nephrosplenic entrapment?
|
1. restrict feed intake and see if the condition corrects itself
2. tx w/ phenylephrine to induce splenic contraction 3. short-time IV anesthesia and roll horse 4. sx intervention |
|
What is an enterolith?
|
Concretions composed of magensium, ammonium phosphate crystals around a nidus
|
|
Geographically, where do enteroliths occur?
|
Southwest US
CA Fl IN |
|
Which breeds are most affected by enterolith?
|
Arabians/Arabian mix, adults
|
|
What are the clinical signs of enterlithiasis?
|
-recurring bouts of pain
-distention of the colon |
|
How can you dx an enterolith?
|
Rads
|
|
What is the tx for enteroliths?
|
Sx: decompress the colon, remove enterolith
|
|
Where is the enterotomy made to remove a transverse colon -right colon enterolith?
|
At the pelvic flexure
|
|
If an enterolith has a flat or polyhedral side, what should you do?
|
Look for a second enterolith
|
|
Strongylus vulgarus and S edentatus migrate to where in the horse?
|
Cranial mesenteric artery
|
|
What is the result of these larvae attaching to the arterial wall?
|
Cause turbulent blood flow and creation of a thrombus that flows downstream and obstruct smaller vessels in the large intestine
|
|
Arteritis of the cranial mesenteric artey leads to what condition?
|
Thromboembolic colic
|
|
Why are the cecum and colon at greater risk of ischemia from Thromboembolic colic?
|
little or no collateral circulation
|
|
What are the clinical signs of Thromboembolic colic?
|
-mild to severe colic
-large intestine gas distention |
|
What is the tx for Thromboembolic colic?
|
Sx resection of the ischemic bowel
|
|
What is right dorsal displacement of the large colon?
|
Pelvic flexure becomes displaced laterally around the base of the cecum and ends up near the diaphragm
|
|
Why is this condition called right displacement?
|
Colon is trapped to the right of the cecum
|
|
How are horses with mild abdominal pain from right dorsal displacement treated?
|
-remove feed
-fluid tx -analgesia |
|
Where does a large colon volvulus occur?
|
At the attachment of the colon to the cecum (near the cecocolic fold)
|
|
Large colon volvulus is most often associated with what conditions?
|
-impending or recent parturition
-a grass diet and/or highly fermentable feeds |
|
True or False....if the volvulus is < 270 degrees, there may be obstruction to the bowel lumen with tissue ischemia.
|
True
|
|
What is the hallmark clinical sign of large colon volvulus?
|
When resulting in strangulation pain is severe and non-responsive to analgesics
|
|
What other clinical signs are seen with large colon volvulus?
|
-increased heart rate
-rapid deterioration of CV parameters -distention of colon -depression of ventilation and venous return -reflux |
|
What time of year is small colon impaction more common?
|
fall and winter
|
|
What are the clinical signs of small colon impaction?
|
-mild to moderate pain
-diarrhea -distention -endotoxemia |
|
What causes a small colon impaction?
|
-dehydration of feces
-inspissated fibrous fecal material -foreign body |
|
What exam should be performed on any horse presenting with diarrhea/colits?
|
A rectal exam
|
|
How is a small colon impaction treated?
|
Medically: fluids and laxatives
Surgically: massage to break down the impaction or an enterotomy to remove the obstruction |
|
Where is an enterotomy performed in the case of a small colon impaction?
|
pelvic flexure
|
|
50% of horses that have sx for impaction have cultured positive for what organism?
|
Salmonella
|
|
What might be administered post op to help feed move through the small colon?
|
Mineral oil
|
|
What is a fecalith and where in the colon do they occur?
|
Concentrations of feed material that form larger than normal fecal balls
Commonly obstruct the small colon, sometimes the large colon |
|
Which horse species is over represented in the occurrence of fecaliths? Why?
|
Miniature horses and ponies
dietary indiscretion and breed associated dental problems |
|
What are the clinical signs of a fecalith?
|
-mild to moderate colic
-usually no manure is passed once colic develops -sever abdominal distention may be seen |
|
What is the tx for fecaliths?
|
Sx removal of fecaliths- pelvic flexure enterotomy
|