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Equine Final > Foals > Flashcards

Foals Flashcards

1
Q

How long after being born should a foal take its first breath?

A

Within 30 seconds

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2
Q

How quickly should a foals mucous membranes turn pink after being born?

A

Within 1-2 minutes

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3
Q

How long after being born will a foal sit sternally?

A

10-15 minutes

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4
Q

How long after being born will a horse stand on its own?

A

About an hour

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5
Q

When does the umbilical cord break down?

A

When the mare stands up or when the foal stands up- don’t cut it, disinfect it

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6
Q

When should foals nurse after being born? How frequently should they nurse?

A

2 hours after being born, nurse 4-6 times/hour

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7
Q

What volume of milk should a foal ingest?

A

20% of their body mass daily (10L)

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8
Q

What are the normal TPR of a foal?

A

HR: 70-120, RR: 30-40, T: 99-102.5

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9
Q

What are clinical signs of fractured ribs in foals?

A

Soft swelling over the fractures site, crepitus, and pain on palpation, occasional respiratory distress from pneumothorax or hemothorax

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10
Q

What kind of treatment is used for fractured ribs?

A

Conservative treatment without intervention

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11
Q

What is meconium?

A

First poop- passed 1-2 hours post-partum, dark brown/black and consists of glandular secretions, swallowed amniotic fluid, and cellular debris

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12
Q

What do normal foal feces look like?

A

Semi-formed yellow paste

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13
Q

What does meconium staining on a foal or placenta suggest?

A

Hypoxia, intestinal ischemia, hyperperistalsis, anal sphincter relaxation, in utero passing of meconium

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14
Q

When does coprophagia occur in foals?

A

From weeks 1-9 eat mare’s feces

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15
Q

How much colostrum should the average foal consume?

A

2-3L

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16
Q

What does a Brix refractometer measure?

A

The concentration of dissolved solids in a solution (colostrum). >1.060 -> 3000mg/dl IgG

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17
Q

What defines failure of passive transfer?

A

<800mg/dl (400-800 is partial, <400 is complete failure)

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18
Q

How do you test for failure of passive transfer?

A

Radioimmunodiffusion, takes 24 hours to complete. ELISA and snap test- semi-quantitative, spectrophotometry- quick

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19
Q

What are causes of failure of passive transfer?

A

Foal being unable to rise and nurse, mare not producing enough or any colostrum, mare lost colostrum due to premature lactation, mare rejecting the foal

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20
Q

What is the treatment for a <12 hour old foal with failure of passive transfer?

A

Oral colostrum from the mare or from a bank, 2-3L recommended

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21
Q

What is the treatment for a >12 hour old foal with failure of passive transfer?

A

IV plasma (1-3L), observe for transfusion reaction, recheck IgG level 12-24 hours later

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22
Q

What complications are associated with failure of passive transfer?

A

Sepsis, pneumonia, infectious arthritis, omphalophlebitis, infectious diarrhea

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23
Q

Define a premature foal

A

Foal born <320 days of gestation, not fully phsyiologically developed

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24
Q

What are causes of prematurity?

A

Placental infection, placental insufficiency, fetal infection, inappropriate induction, prolonged or severe maternal illness, fescue toxicosis

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25
Q

What body systems of a premature foal might be compromised?

A

Decreased glycogen stores, insufficient surfactant production/development, immature skeletal system, abnormal adrenal function, immature GI tract and nervous system

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26
Q

Define dysmaturity

A

A foal born after normal gestational length that demonstrates signs of prematurity

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27
Q

What are causes of dysmaturity?

A

Placental infection, placental insufficiency, fetal infection, prolonged or severe maternal illness, fescue toxicosis

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28
Q

What are signs of inadequate development in a foal?

A

Short silky hair coat, floppy ears, soft lips, tendon and joint laxity, incomplete ossification of the cuboidal bone, poor suckle reflex, low birth weight/poor body condition and weak at birth, taking an abnormally long time to stand

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29
Q

What is the treatment for dysmaturity?

A

Oxygen, antibiotics, plasma, enteral/parenteral nutrition, pressors, nursing care, physical therapy, monitor blood glucose

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30
Q

How much should a foal gain daily on average?

A

2-3.5lbs/day

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31
Q

What complications are associated with dysmaturity? What is the prognosis?

A

Sepsis, neonatal maladjustment syndrome, musculoskeletal abnormalities. Prognosis is good.

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32
Q

What is red bag?

A

Premature placental separation that causes decreased oxygen transfer to the fetus- emergency, associated with placentitis, thickened placenta, twinning, inappropriate induction, or idiopathic

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33
Q

Describe fescue toxicosis

A

Neotyphodium coenophialum (ergopeptide alkaloid) is a dopamine agonist, inhibits prolactin release from pituitary, blocks corticotrophin releasing hormone in foal, blocks fetal cortisol increase which serves as signal for parturition in the mare, prolongs gestation. Signs include agalactia, prolonged gestation, abortion, thickened placenta, weak foal, and edema. Can administer domperidone to aid in lactation.

34
Q

What is omphalophlebitis?

A

Infected umbilical structures, can cause ascending infection, may be associated with patent urachus, may become systemic with bacteremia and sequela such as infected joints, hepatic abscess, uveitis, sepsis, septic arthritis

35
Q

What are the clinical signs of omphalophlebitis?

A

Fever, depression, loss of suckle, moist exudative umbilicus, pain heat and swelling of umbilical stump, signs of sepsis, swollen joints

36
Q

How is omphalophlebitis diagnosed?

A

Clinical signs and CBC with fibrinogenemia and leukocytosis. Umbilical U/S definitive diagnosis. Can do blood culture, aspiration, or swab of umbilicus

37
Q

How is omphalophlebitis treated?

A

Based on culture if possible, otherwise broad spectrum antibiotics (penicillin/aminoglycoside), treat patent urachus with chlorhexidine, dip umbilicus if less than 3 days old, consider surgery if abscessed, septicemic, peritonitis, or danger of rupture

38
Q

What is lethal white syndrome?

A

Solid white foals born to overo-overo mating of American paint horses may suffer from congenital aganglionosis of the ileum, cecum, and colon. No treatment.

39
Q

What are causes of meconium retention?

A

Meconium impaction, obstructive colic, perforation

40
Q

What are signs of meconium retention?

A

Restless, tail swishing, kicking, colic, persistent non-productive straining to defecate, depression, anorexia

41
Q

How is meconium retention diagnosed?

A

Clinical signs, U/S and rads with contrast

42
Q

How is meconium retention treated?

A

Low enema, phosphate enema (can cause hyperphosphatemia), warm soapy water. Can use high retention enema if refractory. Acetylcysteine can be used to decrease viscosity of meconium

43
Q

Define sepsis

A

Life threatening organ dysfunction caused by dysregulated host response to infection

44
Q

Define septic shock

A

Subset of sepsis with circulatory and cellular/metabolic dysfunction associated with higher risk of mortality

45
Q

Define bacteremia

A

Presence of bacteria within the bloodstream, confirmed by culture

46
Q

What is the mortality rate of equine sepsis?

A

50%

47
Q

Sepsis is SIRS + what

A

Bacteremia

48
Q

Septic shock is sepsis plus what

A

Refractory hypotension

49
Q

What organisms are most prevalent in sepsis?

A

G-enteric organisms, opportunistic (E. coli), pathogenic (Salmonella)

50
Q

What are risk factors for sepsis and septic shock?

A

Lack of good colostrum, delayed gut closure, illness (omphalophlebitis, enteritis, pneumonia), maternal illness, dystocia, hypoxia, placentitis, twins, prematurity, adverse environmental conditions

51
Q

What are clinical signs of sepsis?

A

Weakness, depression, coma, fever/hypothermia, tachycardia, tachypnea, dehydration, colic, diarrhea, uveitis, hypopyon, petechia, sclera injection, toxic line, umbilical infection, septic arthritis, sometimes neuro signs

52
Q

What bloodwork abnormalities are associated with sepsis?

A

Hypoglycemia, hyperlactemia, hyponatremia, hypochloremia, pre-renal azotemia, acidosis, high liver enzymes, inflammatory leukogram (luekopenia, neutropenia- toxic changes, bands, increased fibrinogen, increased serum amyloid A, thrombocytopenia)

53
Q

How is sepsis diagnosed?

A

Positive bacterial culture of blood sample- gold standard, takes 24-48 hours, but some foals have negative blood culture. Use clinical signs and clinicopathologic data as well.

54
Q

What pathogens are associated with sepsis?

A

E. coli, Klebsiella, Enterobacter, Salmonella, Actinobacillus, Proteus, Pseudomonas, Strep, Enterococcus, Staphylococcus

55
Q

What is the treatment for a septic shock foal?

A

If <12 hours old feed colostrum, provide antibiotics (Beta lactams, aminoglycosides, metronidazole; amikacin + ampicillin or penicillin usually best choice), fluid therapy (shock resuscitation), anti-inflammatories (flunixin), prevent gastric ulcers, provide nutrition

56
Q

What are signs of neonatal encephalopathy? How does it occur?

A

Dissociation with the mare, aimless wandering in stall, circling, weak or absent suckle reflex, abnormal nursing behavior, coma, seizures, opisthotonus, nystagmus. Occurs from hypoxia and ischemia. Can cause necrotizing enterocolitis and renal failure as well.

57
Q

How is neonatal encephalopathy diagnosed?

A

Based on history and signalment, no definitive test.

58
Q

What is the prognosis of neonatal encephalopathy?

A

75% recover and are normal with adequate support

59
Q

How is neonatal encephalopathy treated?

A

Anti-inflammatories and anti-oxidants (flunixin, vitamin C and E, magnesium, mannitol, DMSO), supportive therapy, Madigan squeeze technique- mimics birth canal

60
Q

Define uroperitoneum- what causes it?

A

Presence of urine within foal’s abdominal cavity. Can be caused by ruptured bladder, ruptured urachal remnants, or ruptured ureter (less common)

61
Q

What is the classic signalment and history for uroperitoneum?

A

Usually colts, tear noted at dorsal aspect of bladder, normal parturition and apparently healthy for first 24-48 hours

62
Q

What clinical signs are consistent with uroperitoneum?

A

Progressive depression, anorexia, and abdominal distension, dysuria/stranguria, tachypnea and/or dyspnea

63
Q

What clinicopathologic abnormalities are associated with uroperitoneum?

A

Stress leukogram, hyperkalemia, hyponatremia, hypochloremia, azotemia, metabolic acidosis, hypocalcemia, excessive free fluid on abdominocentesis

64
Q

How do you diagnose uroperitoneum?

A

Abdominal ultrasonography- free fluid. Compare abdominal fluid with systemic creatinine, if greater than 2:1 then highly suggestive of uroperitoneum

65
Q

How is uroperitoneum treated?

A

Treat electrolyte derangements (fluid therapy without potassium, IV calcium, dextrose, sodium bicarbonate, insulin), drain uroperitoneum, surgical correction if torn bladder or removal of infected urachus, urinary catheter to keep bladder drained

66
Q

What are the clinical signs of a ruptured urachal remnant?

A

Urachus may be infected, sepsis, signs similar to uroperitoneum (progressive depression, anorexia, abdominal distension, dysuria, tachypnea)

67
Q

How is ruptured urachal remnant treated?

A

Surgical excision or urachal remnant, treat peritonitis with broad-spectrum antimicrobials and anti-inflammatories

68
Q

What is the treatment for a patent urachus?

A

Frequent (2-4x daily) chemical cauterization with iodine or chlorhexidine solution, +/- antimicrobials, or no treatment at all, or surgical excision

69
Q

What is the etiology of neonatal isoerythrolysis?

A

Mare makes antibodies against foals RBCS that are then ingested by the foal via colostrum

70
Q

What are clinical signs of neonatal isoerythrolysis?

A

Normal foal at birth, onset of weakness, lethargy, icterus, hemoglobinuria, kernicterus, and liver failure followed by sepsis +/- thrombocytopenia, occurring 6-96 hours later

71
Q

What clinicopathologic abnormalities are associated with neonatal isoerythrolysis?

A

Anemia, increased bilirubin, hypoglycemia

72
Q

How is neonatal isoerythrolysis diagnosed?

A

Positive hemolytic crossmatch between foal and dam, coomb’s test, liver function tests

73
Q

How is neonatal isoerythrolysis treated?

A

Supportive care, muzzle foal and feed milk replacer, blood transfusion, dexamethasone if immune-mediated thrombocytopenia is concurrent (NOT if platelets are normal)

74
Q

How can neonatal isoerythrolysis be prevented?

A

Test mares for presence of Aa, Qa, and Ca late in gestation- use jaundice foal agglutination test to determine if colostrum will react to foal’s RBCs

75
Q

What are causes of foal enterocolitis?

A

Nutrition (overfeeding, grains, sand consumption), infection (Clostridium perfringens- 3 days, hemorrhagic; Salmonella- 3 days, hemorrhagic; Clostridium difficile <3 days, may be hemorrhagic, not usually bacteremic; Rotavirus-2, Coronavirus-2, Rhodococcus equi, Cryptosporidium, Lawsonia intracellularis, parasitism)

76
Q

What is foal heat diarrhea?

A

Physiologic diarrhea between 7-14 days, etiology unknown, treatment not usually necessary

77
Q

What are clinical signs of foal enterocolitis?

A

Diarrhea, depression, stupor, coma, dehydration, sepsis, fever, tachycardia or bradycardia, tachypnea, hyperemic mucus membranes, abdominal distension and/or colic pain

78
Q

What clinicopathologic abnormalities are consistent with foal enterocolitis?

A

Hyponatremia, hypochloremia, hypokalemia, hypocalcemia, hypoproteinemia, metabolic acidemia, pre-renal/renal azotemia, neutropenia +/- band neutrophils

79
Q

How is foal enterocolitis diagnosed?

A

Blood culture if signs of sepsis, fecal ELISA for Clostridium perfringens, fecal PCR for Clostridium difficile, fecal float for parasitism

80
Q

How is foal enterocolitis treated?

A

Fluids (isotonic crystalloid), gastric ulcer prevention (omeprazole, sucralfate, ranitidine), antibiotics (broad spectrum if sepsis, penicillin or metro for clostridiosis, cephalosporin or ampicillin with aminoglycoside or chloramphenicol for salmonellosis, oxytetracycline, doxytetracycline, or chloramphenicol for lawsonia), supplemental nutrition, absorptive agent (Bismuth subsalcylate or bio-sponge)

Equine Final (5 decks)

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