EqMed F, Neonat I

  1. how does blood go from placenta to foal?
    through umbilical vein to portal vein to caudal vena cava into RA
  2. where does most blood go from after RA?
    80% from RA through foramen ovale to LA
  3. what critical info do you want to know about mare/gestation/foaling as red flags for FPT?
    • indications of placentitis, dystocia, mare previously ill
    • prematurity/dysmaturity
  4. During parturition, there is transient asphyxia as placenta separates. What should this cause in the foal?
    • incr. resistance in umbilical circulation - incr. sys. resistance
    • triggers gasping reflex in foal to clear airway
  5. when neonatal circulation is established, what happens to right atrium and pulmonary circulation?
    • decr. resistance in pulmonary circulation
    • decr. pressure in RA
    • leads to closure of foramen ovale/ductus arteriosus (may take up to 96hrs)
  6. what does the umbilical vein become? what about umbilical arteries?
    • u vein: falciform ligament
    • u aa: round ligaments of the bladder
  7. when is ideal time to test for FPT?
    as early as 12 hours, as late as 24-48
  8. what is adequate IgG transfer on stall side ELISA?
    • >400mg/dl
    • (200-400= partial FPT)
  9. what is gold standard diagnostic test for IgG passive transfer?
    radioimmunodiffusion assay (gives absolute number rather than color change as with ELISA)
  10. What do you do if foal has FPT (<400)?
    • plasma transfusion (1-2L)
    • *not to excede 20ml/kg per day
  11. how long will passive transfer last?
    ~8 weeks, then own immune system more sensitized to environment
  12. what are some other names for dummy foal syndrome?
    • neonatal encephalopathy
    • perinatal asphyxial syndrome
    • neonatal maladjustment syndrome
    • hypoxic ischemic syndrome
  13. How do dummy foals appear at birth? what manifests during first week?
    • normal at birth (takes time neurons to swell)
    • neurologic during first wk
    • -respiratory depression
    • -altered consciousness
    • -depressed reflexes
    • -seizures
  14. what is most common dysfunction seen with dummy foal syndrome?
    seizures (CNS dysfunction most common; any organ system can suffer too)
  15. what are risk factors for HIE?
    • *dystocia*
    • hypoxia in utero (placentitis, twins, fescue)
    • hypoxia during parturition (premature placental separation)
    • hypoxia in neonatal period
  16. what are some examples of hypoxia in neonatal period/immediately following birth?
    • following c-section
    • meconium aspiration
    • immature respiratory dev'l; congenital CV anomaly
    • anemia
    • premature
  17. Diazepam is useful first line treatment for seizures. Why can this treatment not be continued long term? what other drug can be used?
    • liver damage
    • phenobarbital (load over 20min IV, then oral)
  18. What are some anti-oxidant therapies commonly given to dummy foals?
    • vit E
    • Mg sulfate (NMDA receptor blockade)
    • ascorbic acid (vit. C as NMDA blockade)
    • thiamine (supports cerebral metabolism)
    • DMSO
  19. what is involved in respiration therapy?
    • nasal insufflation of O2 (FiO2 30-50%)
    • caffeine therapy to stimulate resp. activity
  20. if foals require fluids, what is maintenance rate?
    • 4-6ml/kg/hr
    • (initial bolus of 20ml/kg IV if "flat foal")
  21. how much milk should a foal be fed per day? Is IV or nasogastric feeding preferred?
    • maintenance = *20%* BW(kg)/day - feed q2h
    • *nasogastric* tube so can stay w/mare and nutrition for enterocytes
  22. how much wt should foal gain per day?
    1-2lbs per day (good indicator of progress)
  23. why are dummy foals often given antibiotics? what is often given?
    • risk of sepsis from FPT, premature; immature resp/GI
    • Amikacin (aminoglycoside) + B-lactam
    • or 3rd gen cephalosporin
  24. what is prognosis for dummy foals with CNS disease?
    very good - successful racing careers
  25. what is cellular debris, glandular secretions that can be swallowed by foals in utero? colts or fillies more often get impacted with this?
    • meconium
    • colts >fillies
  26. what are signs of meconium impaction?
    • colic signs within first 6-24 hours; straining
    • abdominal distention/ileus
    • no meconium passed by first 6 hours
    • flagging tail
  27. how is meconium impaction diagnosed?
    • PE/blood work= *healthy* foal
    • (no WBC elevations, may see hyperbilirubin)
    • digital rectal exam; absence of milk feces
    • contrast rads w/barium enema
  28. how is meconium impaction treated?
    • warm water/phosphorous enema (retain 20-40min)
    • analgesia/NSAIDs judiciously
    • (no xylazine; butorphanol ok)
  29. what are signs associated with urinary bladder rupture? how long after rupture are signs seen?
    • 24-72hr post rupture
    • colic, posture to urinate (may still pass urine)
    • abdominal distention
    • *sick*
  30. what is seen on blood work with uroabdomen?
    • hypoNa, Cl, K
    • azotemia
    • USG concentrated (foals should be hyposthenuric)
  31. how do you know fluid from abdominocentesis is urine?
    2-3x creatinine as that found in serum
  32. what is most pertinent danger of putting foal with ruptured bladder under GA too soon?
    hyperK can lead to sinus arrest if pt not stabilized quickly
  33. which fluids should you put uroabdomen pt on?
    NaCl - promotes diuresis
  34. how is uroabdomen treated?
    • place urinary catheter
    • drain peritoneal fluid (slowly to avoid shock)
    • correct e-lyte imbalances
    • surgery (NOT emergency, stabilize first)
  35. what condition is characterized by destruction of RBCs by alloantibodies of maternal origin? which blood types are highest risk?
    • neonatal isoerythrolysis
    • Qa/Aa
  36. what is pathophysiology of NI?
    mare negative for Ag then sensitized to Ag from previous pregnancy - foal acquired Ag from sire then drinks colostrum
  37. what are clinical signs of NI?
    • intravascular hemolysis - icterus, hemoglobinuria
    • decr. O2 carrying capacity- anemia and hypoxemia signs
  38. how is NI diagnosed? Treated?
    • Coomb's Test = agglutination
    • improve O2 carrying capacity via RBCs from mare
  39. how is NI prevented?
    • breed only to Ag negative sire (esp if mare is Qa/Aa)
    • screen mares prior to foaling to see what she has Ab for
  40. what should you do if you determine the foal is at risk for NI?
    • muzzle, prevent nursing from mare
    • tube feed donor colostrum/nutritional support
    • strip mare's colostrum
    • after about 36hr, mare/foal can nurse
  41. what is leading cause of death in foals <7 days old?
    sepsis dt *FPT*, unstable environment, gestation issues, etc.
  42. What are other triggers besides bacteria that can lead to sepsis?
    • viral, fungal
    • hypoxia
    • trauma/wounds
    • immunologic compromise
  43. what is seen on bloodwork with sepsis?
    • *leukopenia w/left shift*
    • hypoglycemia, azotemia
    • hyperlactatemia
  44. on sepsis score, what are two things that give foal higher score, thus worse prognosis?
    • toxic changes in neutrophils
    • FPT
  45. how is sepsis definitively diagnosed/gold standard? most common result?
    blood culture = + for e.coli
  46. what is a late term complication of sepsis?
    septic osteomyelitis, septic arthritis
  47. Today, 40-70% of septic foals can survive, but what are two parameters used for prognosis?
    • hypoglycemia (<60)
    • hypothermia (<100F)
  48. what is normal TPR in foal?
    • T: 99-102
    • P: 80-100 for first 30d; 60-70
  49. what is the most sensitive way to diagnose fractured ribs? how is this treated?
    • US
    • stall confined for 3-4wks
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EqMed F, Neonat I
EqMed F, Neonat I