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Large Animal Disease > Equine Neonatal Conditions and Care > Flashcards

Equine Neonatal Conditions and Care Flashcards

1
Q

what is the adaptive period

A

The perinatal period

the changes that a newborn foal is subjected to during the adaptation from intrauterine to freeliving environment

ability to adapt is crucial for survival in the wild

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2
Q

T/F: foals are just small adult horses

A

False

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3
Q

the prenatal period

A

gestation lenght where you are predicting the timing of foaling
and risk category of the foal

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4
Q

What is the gestational length of the horse

A

Mean: 340 days (many use 335 = 11 months) use shorter length so you are reading

significant variation
-breed, season
-more consistent between pregnancies

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5
Q

What is the best method in predicting specific gestation length in mares

A

what her gestational length last year was

really matters because normal foals at shorter of longer gestation
or dysmature at “normal” gestation lenght

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6
Q

Why is predicting a mare’s gestation important

A

unpredictable result when foaling is induced or when performing a c-section

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7
Q

Why is it important to predict the day of foaling

A

1) Increased vigilance
2) Be prepared
3) Recognize problems early
4) Intervene early

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8
Q

What is the most specific measure of predicting the day of foaling

A

milk calcium levels will increase 1-2 days before foaling

Mares with Ca concentration >200ppm have a 54% probability of foaling within 24 hours and 84% probability of foaling within 48 hours and 97% probability of foaling within 72 hours

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9
Q

What are general measures of predicting the day of foaling

A

Conformational changes: 1 week to 1 month

Teats fill (2d to 1 week)

Teat waxing (1d to 4d)

Increased calcium in milk (1d to 2d) * most specific

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10
Q

Gestational lengths shorter than _____ days in horses are considered premature

A

320 days

seasonal and breed factors impact gestational length

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11
Q

Males foaling during _____ days tend to have shortened gestation while mare foaling during ____ tend to have prolonged gestation

A

Long day: short gestation

Short days: long gestation

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12
Q

How do you determine calcium concentration in mammary secretions to determine foaling time

A

There are horse specific tests but a cheaper way is water hardness test stripes

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13
Q

What are the mare factors when determining the risk category of a foal

A

1) Mare with poor general health
2) Mare with poor confirmation (dystocia, ascending uterine infection)
3) mare with advanced age
4) Mare with prolonged transport prior to parturition (lower calcium concentrations and dystocia)

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14
Q

What are parturition factors when determining the risk category of a foal

A

1) Dystocia
2) Premature placental separation
3) Prolonged gestation (hypoxia, dystocia, placenta insufficency, no parturition trigger from foal)

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15
Q

What are the management factors when determining the risk category of a foal

A

1) Adverse environmental conditions
2) Poor hygiene
3) Inexperienced foaling attendant

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16
Q

What are the foal factors when determining the risk category of a foal

A

Any abnormality noted in the foal increases risk category

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17
Q

What does the normal foal heart sound like after parturition

A

1) 60-140 bpm (age dependent)- will later decrease
2) Up to 4 heart sounds
3) Murmurs heard for up to 72 hours (ductus arteriosis persists for several days after parturition) - pansystolic and pandystolic (continuous murmur)

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18
Q

What 2 things might pre-mature lactation in a mare tell you that is concerning

A

1) warning sign that there might not be colostrum ready for the foal when they are birthed
be prepared to treat failure of passive transfer

2) Placentitis

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19
Q

Why are you able to hear all 4 sounds in the foal

A

you are also able to do this in an adult but the chest wall is a lot thinner so you can hear all 4 sounds

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20
Q

The _________ closes typically at birth of a foal but the ________ remains intact for a couple days after parturition and creates a murmur

A

foramen ovale = closed at birth

ductus arteriosus = remains open for a couple days

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21
Q

You will hear a murmur in foals for up to

A

72 hours (3 days) after birth
you need to see if there is a decrease in intensity after 3 days but after 3 days there is still same intensity then it is concerning

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22
Q

What helps the foal clear the airways from excess fluid

A

the thoracic compression during the passage of the foal through the birth canal

beware during c-sections

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23
Q

What is the normal respiratory rate of a foal

A

At parturition typically around 70bpm but then will drop to around 20-35bpm but will still remain higher than adult rate for several days

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24
Q

The foal’s chest wall is very compliant, what must they do during adaptation

A

foals must make active respiratory movements for both inspiration and expiration

dystocia might fracture ribs and make it hard for them to breathe

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25
Q

If the foal’s lungs are immature then

A

they will develop acute respiratory distress syndrome (ARDS) and result in significant mortality

fetal lungs develop the capacity for gas exchange relatively late in gestation

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26
Q

How do you assess fractured ribs in a foal after birth from dystocia

A

ultrasound

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27
Q

Foals need to pass ___________ very soon after parturition

A

Meconium
(dark, sticky, patent GI tract)

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28
Q

What is meconium

A

the first defecation of a horse that is pelleted, dark, brown, sticky feces

the passage of meconium indicates that the gut is fully patent and there is no physical or neurological (lethal white syndrome) obstruction

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29
Q

What does the passage of meconium indicate

A

the passage of meconium indicates that the gut is fully patent and there is no physical or neurological (lethal white syndrome) obstruction
also colostrum deprived foals will get meconium obstruction

most foals will pass meconium within the first few hours (often within minutes of the first feed)

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30
Q

What does milk feces look like vs meconium

A

Milk feces: pasty, yellow

Meconium: dark, sticky, pelleted, hard

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31
Q

What is the #1 colic in foals less than 48 hours is

A

meconium impaction

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32
Q

What are the urinalysis differences noted in foals

A

1) Some protein + (up to 72 hours)
2) Lower SG (lower ability to concentrate, first urine, dehydration) - 1.010

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33
Q

What might help to mature the lungs in premature fetuses

A

Glucocorticoids- premature fetuses has been shown to increase their survival and decreased the incidence of ARDS after delivery

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34
Q

Normal foals should stand to their feet and move within

A

1-2 hours after birth and move rapidly by 2-4 hours

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35
Q

T/F: menace response in foals are weak at birth and might remain that way for several days to months

A

True

beware, you do not want to diagnose them of being blind

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36
Q

Hypothermia in a foal is indicated when it is below

A

98F

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37
Q

Foals might have higher _____ liver values

A

GGT

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38
Q

What is the immunity status of foals

A

immunologically naive but immunocompetent

it is functioning but it hasnt come across what it needs to

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39
Q

The innate immune system is composed of

A

1) anatomical (skin, mm)
2) Physiological (acidic pH in stomach, fever)
3) Phagocytic (monocytes, macrophages)
4) Inflammatory barriers (leakage of serum proteins with antibacterial activity into areas of tissue damage and inflammation

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40
Q

What is true of the foals innate immune system

A

Antiviral response: Type I interferons
Cytokines, antiviral proteins

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41
Q

What is true of the foal’s adaptive immunity

A

Humoral: little produced, need passive transfer

Cell mediated response: poorly developed, requires maturation

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42
Q

How does passive transfer occur

A

High MW: take up by pinocytosis and go to lymphatics and systemic blood

Low MW: absorbed by duodenal cells into portal blood and systemic

both go to urine (why proteins all enter the urine

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43
Q

What is the foal’s absorption kinetics of colostrum

A

the foal is only able to absorb colostrum for some time but then the gut closes at 24-48 hours so after 24 hours, you have a bad window of opportunity

closes because pathogens can enter. it closes faster if there is adequate passive transfer

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44
Q

When adequate colostrum ingestion occurs then IgG blood levels reach there peak by ______- hours after birth

A

18 hours after birth

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45
Q

How do you ensure adequate passive transfer

A

Mare
1) Healthy
2) Good body condition
3) udder/teat health
4) exposure to antigens
5) vaccinations
6) age

Foal
1) healthy
2) ability to stand
3) strong suckle
4) mature GI tract
5) timing

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46
Q

What kind of placenta does the horse have

A

Epitheliochorial- prevents transfer in utero.

the foal may begin devleoping IgM in utero

foal develops some immunoglobulin at birth but it isnt apparent until 10-14 days

therefore most of humoral is from ingestion of colostrum

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47
Q

How might you determine the colostral IgG concentration

A

1) Radial immunodiffusion (RID) - direct
2) Colostrometer via specific gravity - indurect

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48
Q

The horse would

Stand by ____- after birth
Nurse by _____ after birth
Mare pass placenta by _____ hours after birth

A

1 hr: stand
2 hr: nurse
3 hr: placenta

draft foals may take a little too long, might need to let them up

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49
Q

How do you assess passive transfer in foals

A

1) Single radial immunodiffusion (SRID): most accurate, requires time (18h) and laboratory

2) Zinc sulfate turbidimetric assay: accurate, IgG to precipitate in a 20% zinc sulfate solution

3) ELISA based: fast, can be done stall-side
assess to the calibration spots
can really only tell if it is High or Low

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50
Q

What is the gold standard for assessing passive transfer

A

Single Radial Immunodiffusion (SRID) - more sensitive

annoying because it takes 24 hours to get results

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51
Q

How do most people assess passive transfer

A

ELISA based
fast, can be done stall slide

can only tell if high or low, cant quantify numerically

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52
Q

What might cause failure of passive transfer

A

1) premature lactation
2) mare failing to transfer sufficient IgG from colostrum
3) Delayed suckling by foal
4) ingestion of too little colostrum or failure of the foal to absorb IgG from colostrum

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53
Q

What level of IgG dictates adequate transfer, vs partial and complete failure

A

Adequate transfer >800 mg/dl

Complete <400 mg/dL at 24 hours of age

numbers dont matter as much: need to have high levels until the foal’s IgG takes over, bridge the gap with colostrum immunity

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54
Q

By definition, what is failure of passive transfer in foals

A

<400 mg/dl IgG at 24 hours of age

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55
Q

there is a 3-25% partial or complete failure of passive transfer, why is the incidence of septicemia in foals even lower?

A

management practices

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56
Q

How do you treat foals with failure of passive transfer

A

1) Colostrum:
-useful up to 24 hours (maybe even longer?)
-local mare preferred (hard to find)
-oral serum product

2) Plasma
-Does not rely on GI absorption/function
-No “local” immunity
-Hyperimmune for certain pathogens
-Hypersensitivity

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57
Q

What is a major downside of treating failure of passive transfer with colostrum administration

A

hard to obtain
need to ensure IgG adequate levels
need to rely on GI absorption/function

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58
Q

What is a major downside of treating

A

1) No local immunity
2) Hypersensitivity - make sure the client knows

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59
Q

The foal’s umbilical stump should be dry within

A

1-2 days

dip in dilute chlorhexidine

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60
Q

What should you dip the foal’s umbilical stump in?

A

dilute chlorhexidine

never straight iodine

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61
Q

What are the risk categories of the foal to have failure of passive transfer

A

1) Maternal/ prenatal factors
2) Poor general health
3) Poor perineal conformation- ascending placentitis
4) Advanced age - lower foaling rate, scarring of uterus and chronic endometritis
5) Premature lactation - colostrum is produced once and only once, low immunoglobulin within 24 hours of onset of lactation
6) Prolonged transport: hypocalcemia

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62
Q

How can you assist in the passage of meconium to avoid impaction in foals

A

prophylactic enema

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63
Q

What should you consider when doing prophylactic enemas in foals

A

1) only do once by owner, 2) never against resistance
3) be careful using potentially irritating solutions

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64
Q

What does meconium straining of the newborn or fetal fluids indicate

A

fetal distress in utero and if present the foal should immediately be classified as high risk

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65
Q

What should you do when evaluating the placenta

A

early detection of potential problems with mare and foal
observe
-body
-gravid horn
-umbilical cord
-non-gravid horn
-cervical star (chorioallantoic)
-weight (10-11% body weight)
-chorionic surface
-allantoic surface

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66
Q

What should you do for the foal within the first day of birth

A

Check colostrum
Examine placenta
Dip umbilicus
Clinical exam
+/- determine early IgG

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67
Q

What should you do for the foal on the second day of birth

A

Dip umbilicus
Determine IgG
+/- Hematology
+/- Chemistry

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68
Q

Weakness and abnormal behavior in a foal might be associated with

A

1) Endotoxemia
2) Hypoxia
3) Trauma
4) Acid/base abnormalities
5) Hypovolemia
6) Hypoglycemia
6) Birth defects

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69
Q

What are the 3 most common causes of weakness or abnormal behavior in a foal

A

1) Prematurity/dysmaturity
2) Septicemia
3) Neonatal Asphyxia Syndrome

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70
Q

Assessing prematurity and dysmaturity in a foal

A

assessing the level of maturity based on both gestational length and clinical presents
-Significant variation
-Unpredictable results induced birth
-Premature <320 days
-Dysmature at normal length
-Clinically similar

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71
Q

Prematurity is assessed by _____ while dysmaturity is assessed by

A

Prematurity: gestational length

Dysmaturity: condition of the foal- foal born within the normal or even prolonged gestational range but shows the clinical signs normally associated with prematurity

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72
Q

Dysmature foals often associated with

A

placental pathology

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73
Q

What are the clinical signs of foals with prematurity/dysmaturity *

A

1) Weakness- decreased muscle tone
2) Floppy ears (pliant)
3) Dome-shaped forehead
4) Silky hair coat
5) Tendon laxity
6) Incomplete ossification small carpal and/or tarsal bones
7) Immature lungs, ARDS- very low or high resp rates
8) Small body size for age
9) Immature GI tract, postprandial colic

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74
Q

Foals that are premature/dysmature have an immature GI tract making them more susceptible to

A

1) Postprandial colic
2) Failure of passive transfer

75
Q

How do you diagnose foal prematurity/ dysmaturity

A

Based on physical characteristics +/- history
1) Weakness- decreased muscle tone
2) Floppy ears (pliant)
3) Dome-shaped forehead
4) Silky hair coat
5) Tendon laxity
6) Incomplete ossification small carpal and/or tarsal bones
7) Immature lungs, ARDS- very low or high resp rates
8) Small body size for age
9) Immature GI tract, postprandial colic

Do confirmation by various tests (ACTH stimulation)

76
Q

What test can you do to diagnose foal fetal prematurity / dysmaturity

A

ACTH stim

77
Q

How do you treat foal fetal prematurity / dysmaturity

A

1) Nursing care *
2) Nutritional support (milk or parenteral)
3) Antibiotics (anticipate issues)
4) Additional therapy based on clinical signs (oxygen, fluid)
5) Incomplete ossification- wrap limbs to maintain positioning and minimize negative effect on nonossified bones.

78
Q

What is the prognosis of

A

Decreased lung function = short term prognosis

Ossification = long term prognosis (may warrant euthanasia)

good prognosis if >310 days

79
Q

foal fetal prematurity / dysmaturity has good prognosis if

A

> 310 days of gestation and ossification is close to complete

80
Q

Half of foals that become septic are infected ____

A

in utero

81
Q

What is the number one killer in horses <7 days of age

A

septicemia

82
Q

How do foals typically get septicemia

A

1) In utero (placentitis) 50%
2) Respiratory infection
3) Oral Infection
4) Umbilical infection

83
Q

What bacteria typically cause septicemia in foals

A

Gram negative
-E. coli
-Actinobacillus
-Salmonella
-Klebsiella

Gram positive
-Streptococcus
-Staphylococcus
-Clostridium (anaerobe)

gram negative are more common

84
Q

What are the clinical signs of septicemia in foals

A

Often unspecific
1) Nurse less (distention of the mare’s udder and dripping of milk)
2) Sleeps more and progressively more depressed
3) Death (multiple system involvement develop- joints, lungs, brains, eyes)

85
Q

In foals, bacteremia can spread to what common sites

A

Eyes
Joints
Lungs

86
Q

How do you diagnose sepsis in foals

A

definite: isolation of bacteria from blood

Supporting findings:
hypoglycemia
acidosis
azotemia
neutropenia (left shift)

87
Q

What CBC/CHEM results will you see with sepsis in foals

A

hypoglycemia
acidosis
azotemia
neutropenia (left shift)

88
Q

What samples should you take for sepsis evaluation in foals

A

1) Blood cultures
2) Hematology - bacteremia
neutropenia (left shift)
3) Chemistry - azotemia
4) Blood glucose - hypoglycemia
5) Blood gas - acidosis

89
Q

What antibiotic considerations should you have when choosing an antibiotic for treating sepsis in foals

A

1) Broad spectrum - both gram + and -
2) Bactericidal
3) Penetrate the tissue of concern (e.g CNS)

commonly a penicillin and aminoglycoside combination (caution aminoglycoside nephrotoxictiy)

90
Q

What supportive care should you do for foals with sepsis

A

1) Colloids
2) Add dextrose
3) Plasma
4) Nutrition - enteral, parenteral (dextrose)
5) Gastroprotectants
6) Pressure support
7) NSAIDs

91
Q

What should you beware of when treating foals with sepsis with penicillin and aminoglycoside

A

aminoglycoside nephrotoxicity!

if nephrotoxicity present, might want to stay away

92
Q

a syndrome to describe fewborn foals that exhibit behavioral or neurological abnormalities that are not caused by infectious or toxic agents, metabolic disorders or due to congenital/ developmental abnormalities

A

Neonatal Asphyxia Syndrome / Hypoxic-Ischemic Encephalopathy / Neonatal Maladjustment Syndrome

93
Q

What are other names for Neonatal Asphyxia Syndrome (NAS)

A

1) Hypoxic-Ischemic Encephalopathy
2) Neonatal Maladjustment Syndrome

94
Q

Why is it called Neonatal Asphyxia Syndrome

A

because the majority of neonatal foals that exhibit CNS signs have suffered from lack of cerebral oxygen delivery (either due to ischemia or hypoxemia)

95
Q

Why are the hypotheses behind the etiology of Neonatal Asphyxia Syndrome

A

1) Anything that interferes with O2 delivery during parturition (placentitis, dystocia, red bag, foal resuscitation)
Hypoxemia and ischemia leading to decreased PaO2, then cell death, swelling, and increased intracranial pressure

2) Abnormal levels of neurosteroids (sedative effect)- stress during normal parturition (e.g passage through birth canal) signals the decrease in neurosteroids

96
Q

Are the clinical signs of Neonatal Asphyxia Syndrome acute or delayed

A

Delayed

foals appear normal for first few hours up to >2 days

onset and severity of signs depend on the degree and duration of oxygen deprivation (and sequelae)

97
Q

What is the typical history for doals with Neonatal Asphyxia Syndrome

A

1) Gestational problems (vaginal discharge- placental infection, premature lactation, prolonged or shortened gestational length) in the mare
2) Dystocia and premature placental separation
3) Delivery through emergency c-section

all result in development of hypoxic insult before or shortly after delivery

98
Q

What is the hypothesis of neurosteroids in Neonatal Asphyxia Syndrome

A

Abnormal levels of neurosteroids (sedative effect)- stress during normal parturition (e.g passage through birth canal) signals the decrease in neurosteroids
but these levels stay high and have a sedative effect to the foal

99
Q

What is the typical onset of Neonatal Asphyxia Syndrome

A

foals appear normal for first few hours up to >2 days
could be as late as 4-5 days after birth

100
Q

What are the clinical signs of Neonatal Asphyxia Syndrome / Hypoxic-Ischemic Encephalopathy

A

Inability to find udder
wandering
head-pressing
lip smacking
loss of coordination
seizures
coma
death

101
Q

How do you diagnose Neonatal Asphyxia Syndrome / Hypoxic-Ischemic Encephalopathy

A

1) Diagnosis of exclusion (history and clinical signs) - eliminate other possible causes of CNS disease in a newborn foal

2) Increased creatinine, CK, AST may be suggestive

102
Q

Increases in ______
_____
_____
might be indicative of
Neonatal Asphyxia Syndrome / Hypoxic-Ischemic Encephalopathy

A

Increased creatinine
CK
AST

103
Q

How do you treat Neonatal Asphyxia Syndrome / Hypoxic-Ischemic Encephalopathy

A

Symptomatic
1) Adequate ventilation: Intranasal oxygen, caffeine, mechanical ventilation

2) Maintain perfusion: IV fluids, colloids, pressure agents

3) Maintain adequate glucose levels: IV dextrose admin, PPN/TPN, oral nutrition

4) Controlling seizures: diazepam, midazolam, phenytoin, phenobarbital

5) Reduce cerebral edema and neuroprotection: DMSO, mannitol, hypertonic saline, hypothermia, allopurinol, magnesium, vitamin C, vitamin E, thiamine, melatonin, xenon

6) Madigans foal squeeze procedure for abnormal neurosteorids

104
Q

What is Madigan’s foal squeeze procedure for?

A

re-enact the foaling procedure, aims to decrease the neurosteroids amount
might have beneficial effects if minor brain damage

105
Q

the prognosis for survival of premature/dysmature foals is usually dependent on ________ while the prognosis for future use is strongly dependent on _______

A

Survival: lung maturation

Future use prognosis: cuboidal bone ossification

106
Q

What is a common, often deadly sequelae of primary infections such as enteritis and pneumonia in the foal

A

sepsis

107
Q

What is the prognosis of Neonatal Asphyxia Syndrome / Hypoxic-Ischemic Encephalopathy

A

dependent on the severity of the initial insult and the progression of cellular damage. If cerebral damage results in fixed, dilated, and non-responsive pupils then the prognosis is grave

108
Q

What causes icterus

A

Increased level of bilirubin (indirect, direct, or both)

109
Q

Pre-hepatic causes of icterus in foals

A

Septicemia
Neonatal isoerythrolysis
Neonatal HGB turnover
others

110
Q

Hepatic causes of icterus in foals

A

Tyzzer’s Disease
Sepsis
In utero EHV-1 infection
others

111
Q

Post-hepatic causes of icterus in foals

A

1) Bile duct aplasia (congental)
2) Duodenal ulcers (bile duct obstruction)

112
Q

caused by a blood group incompatibility between the foal and the dam
results from absorption of maternal antibodies against fetal erythrocytes (alloantibodies) from the colostrum and subsequent loss of RBCs by both intravascular hemolysis

A

Neonatal isoerytholysis

113
Q

What are the prerequisites for neonatal isoerythrolysis

A

1) Foal must express erythrocyte antigen (alloantigen) that the mare does not possess (most blood groups arent antigenic)

2) Mare must become sensitized to the incompatible alloantigens and produce antibodies to it - likely occurs from transplacental hemorrhage during a previous pregnancy

114
Q

foals most typically associate with what times of RBC antigens in neonatal isoerythrolysis

A

Type Aa
factor Qa
C occasionally (milder disease)

115
Q

What antigen has a milder outcome of neonatal isoerythrolysis than Type A and factor Q

A

neonatal isoerythrolysis

116
Q

What is the pathogenesis of neonatal isoerythrolysis in horses

A

after the mare becomes sensitived to her foal’s isoerythrolysis, the alloantibodies concentrate in the colostrum.
Foals are protected to these antibodies prior to birth
thus, in foals neonatal isoerythrolysis only develops after ingestion and absorption of colostrum containing alloantibodies specific for the foal’s alloantigens

117
Q

Are alloantibodies worse for Aa or Qa?

A

alloantibodies against Aa are potent hemolysins and are generally associated with more severe clinical disease than antibodies against Qa

118
Q

Why is there a neonatal isoerythrolysis frequency in mules as high as 8-10%

A

because in donkey sire X horse mare mating ALL are incompatible matings
-donkey factor

119
Q

Dam that is Qa-
Sire is Qa +

Foal will be

A

Qa+

the foal will have neonatal isoerythrolysis after ingesting colostrum

alloantibodies could have developed during mating

120
Q

Dam is Aa+
Sire is Aa-

the foal will be

A

Aa+

the foal will not have neonatal isoerythrolysis

121
Q

What are the clinical signs of neonatal isoerythrolysis

A

born normal then become depressed and weak

secondary signs: tachycardia, tachypnea, dyspnea

pale mucous membranes and then icteric (although not always present)

hemoglobinuria is not common but may be observed in severe cases

122
Q

What are other differential diagnoses for neonatal isoerythrolysis in foals

A

blood loss anemia due to birth trauma

icterus due to sepsis or liver dysfunction (Tyzzer’s)

should all be considered

123
Q

How do you treat neonatal isoerythrolysis in foals

A

<24 hours of age: withhold dam’s milk and strip out mare and feed different source

> 24 hours: alloantibody levels are minimal because gut is closed

Supprotive care: Fluids- Hydration to minimize nephrotoxicity

Blood transfusion is warranted if PCV<12%

124
Q

How do you diagnose neonatal isoerythrolysis

A

tentative: lethargy, anemia, icterus during first 4 days of life

definitive: alloantibodies in the dam’s serum or colostrum that are directed against the foal’s erythrocytes

125
Q

In neonatal isoerythrolysis, when PCV is ________ then you should consider transfusion to prevent cerebral hypoxia

A

PCV< 12%

126
Q

Donor RBC vs Recipient serum

A

Major cross match

127
Q

Recipient RBC / Donor serum

A

Minor cross match

128
Q

What is the issue with doing a crossmatch prior to blood transfers for neonatal isoerythrolysis

A

it takes lab and about 1 hour of time

129
Q

How do you choose a blood donor for neonatal isoerythrolysis

A

1) Cross match
2) Prescreened donor that is negative for Aa, Ca, Qa

if none available use washed RBCs of the foal’s dam or a young gelding - removing the plasma and just giving the blood

130
Q

What are typically not good blood donors for neonatal isoerythrolysis

A

1) Broodmares
2) Horses that had a transfusion
3) Unusual breeds

131
Q

How do you prevent neonatal isoerythrolysis

A

blood group of a mare can be checked at any time

Ab titer in mares can be checked during late pregnancy
Test is relatively inexpensive and just requires serum from mare to complete the test

muzzle the foal and milk out the mare until antibody in colostrum is depleted, must provide alternate source of colostrum and nutrition

132
Q

What is the prevalence of neonatal isoerythrolysis

A

typically 1-2% prevalence of NI causing antibodies in mares

typically seen in pluriparturient mares

133
Q

Tyzzer’s disease causes

A

acute hepatitis in 7 to 42 days in foals
no signs of disease (variable: fever, anorexia, icterus, seizures, coma)

often peracute (sudden death)

134
Q

What is the causative agent of Tyzzer’s disease

A

Clostridium pilifrome
-filamentous gram negative pleomorphic rod

135
Q

How do you treat Tyzzer’s disease in foals

A

usually unsuccessful - no reports of successful treatment in foals

136
Q

It is uncommon for Tyzzer’s disease to cause non peracute disease (not death) in foals. But if you do, what do you see

A

Fever
Anorexia
Icterus
Seizures
Coma

clinicopathological: hyperbilirubinemia, hyperfibrinogenemia, hypoglycemia, and metabolic acidosis

137
Q

How do you diagnose Tyzzer’s disease

A

Definitive: made only on portmortem examination
organism is demonstrated on Warthin-Starry stained sections

138
Q

T/F: Tyzzer’s disease often cause sudden death in foals with no known signs

A

True

139
Q

What is the prognosis of Tyzzer’s disease in foals

A

Extremely poor

140
Q

What might cause a newborn foal with a distended and painful abdomen

A

1) Meconium impaction
2) Uroperitoneum
3) Enteritis
4) GI ulcers

141
Q

What is the key finding of distinguishing neonatal isoerythrolysis from other causes of icterus (ie Tyzzer’s) is _______ *

A

the patient will be anemic

142
Q

Most commonly meconium becomes impacted in the

A

rectum and small colon

143
Q

What are the clinical signs of meconium impaction

A

affected foals have abdominal distension with gas which may be percussed
foals will stain frequently to defecate evidenced by a humped back, the rear limbs placed under the body, swishing of the tail and restlessness

144
Q

How do you diagnose meconium impaction

A

digital examination often reveals a rectum packed with hard fecal material

x-rays or ultrasound may be warranted if located more proximally (large or small colon)

145
Q

How do you treat muconium impaction

A

enema with mild soap and warm water, commercial enma, a small amount of dioctyl sodium sulfosuccinate

146
Q

Commonly uroperitoneum results from

A

a tear in the urinary bladder or urachus
usually present at birth, despite looking normal

147
Q

What are the clinical signs of uroperitoneum in foals

A

1) Stranguria
2) repeated posturing to urinate
3) Depression
4) Cardiac arrhythmias - bradycardia
5) Abdominal distension

presence of urine DOES NOT rule out uroperitoneum

148
Q

T/F: the presence of urine rules out uroperitoneum in foals

A

False - it could be a small leak

149
Q

How do you diagnose uroperitoneum in foals

A

1) Clinical signs
2) Hyponatremia
3) Hyperkalemia
4) Hypochloremia
5) Ultrasound
6) Creatinine ratio >2:1
7) ECG changes

150
Q

What Creatinine ration of abdominal fluid : blood makes you confirm uroperitoneum

A

Fluid : Blood ratio of > 2:1

151
Q

How do you treat uroperitoneum

A

Usually surgically
stabilize foal: correct electrolyte, fluid and acid / base disturbances (saline, dextorse, sodium bicarbonate) to correct potassium

152
Q

What might cause diarrhea in foals

A

Foal heat
Parasites
Bacteria
Antibioitcs
Nutrition
Viruses
Mechanical obstructions

153
Q

What causes intestinal clostridiosis in foals

A

1) Cl perfringens Type A, C
2) Cl difficile

154
Q

What is the clinical presentation of intestinal clostridiosis in foals

A

Neonatal foal with acute to peracute lethargy, anorexia, colic, diarrhea (with blood)

155
Q

Neonatal foal with acute to peracute lethargy, anorexia, colic, diarrhea (with blood) likely is caused by

A

Intestinal Clostridiosis

156
Q

diarrhea that occurs between age 5 and 14 days and diarrhea is usually mild, transient, and requires no treatment
frequently coincides with the mare’s post-foaling estrus, hormonal or constitutional changes in milk composition but the cause is unknown

A

Foal heat diarrhea

157
Q

condition where an animal ingests its own feces

A

Coprophagy

158
Q

the most common parasitic infection in young foals

A

Strongloides westeri

159
Q

How is strongloides westeri transmitted to foals?

A

transmammary

160
Q

What are your top 2 differentials for a foal that presents with hemorrhagic diarrhea

A

1) Intestinal clostridiosis
2) Salmonella

161
Q

With intestinal clostridiosis, what do the potent exotoxins result in

A

Gi wall necrosis
sepsis
death

162
Q

How do you diagnose Intestinal Clostridiosis in foals

A

1) Clinical signs (think hemorrhagic diarrhea)
2) Demonstration of bacterium
3) Presence of exotoxins *
-Culture (anerobic)
-PCR on toxins

163
Q

How do you treat intestinal clostidiosis in foals

A

1) Antibiotics (Metronidazole)
2) Anti-inflammatory agents
3) Biotype C antitoxin
4) Bio-Sponge to bind clostridial toxins in luimen of tract
5) Supportive care

164
Q

What antibiotic is used to treat intestinal clostidiosis in foals

A

Metronidazole

165
Q

How do you prevent intestinal clostidiosis in foals

A

foal out in pasture
separate cows from horses
wash udder prior to foal nursing
vaccinate mares
reduce grain feeding
administer antitoxin
prophylactic use of antibiotics and Biosponge

166
Q

What does Bio-Sponge do

A

binds clostridial toxins in the lumen of the intestinal tract

167
Q

What is the pathogenesis of Rotavirus in foals

A

1) Destroy epithelial cells at tips of villi in small intestine
2) Decrease absorptive surface area
3) Malabsorptive diarrhea because cells normally produce lactose
4) Secretory diarrhea

maldigestion, malabsorption, and osmotic forces _ secretory viral protein

168
Q

What are the clinical signs of Rotavirus in foals

A

1) Profuse watery diarrhea that can sometimes scald the skin
2) Weight loss
3) Stunted growth
4) Anorexia

foals less than 2 months of age

169
Q

How does rotavirus cause diarrhea

A

1) Maldigestion
2) Malabsorption
3) Osmotic forces and secretory viral protein

170
Q

How do you diagnose Rotavirus in foals

A

Electron microscopy and PCR to rule out other causes

171
Q

How do you treat rotavirus in foals

A

supportive care (lactase?)

172
Q

T/F: E coli is pathogenic in foals

A

False - it has not been found to be

173
Q

How do you prevent rotavirus in foals

A

reduce crowding
vaccination
hygiene

174
Q

Is mortality in foals higher with C perfringens type A or type C

A

Type C

175
Q

Gastric ulcers occur in ______% of sick foals <90 days of age

A

50%

176
Q

Where do gastric ulcers typically occur in foals

A

in the glandular region of the stomach

177
Q

What are the clinical signs of gastric ulcers in foals

A

1-4 months: bruxism, excessive salivation, colic, diarrhea

Neonatal foals: gastric perforation, pyloric obstruction

178
Q

What is controversial in the treatment of equine neonates with gastric ulcers

A

Proton pump inhibitors
1) Stomach acid provides barrier function
2) Gastric acid assists digestion of milk
3) Glandular ulcer formation most likely not a function of increased HCl production

179
Q

Why are proton pump inhibitors controversial in the treatment of equine neonates with gastric ulcers

A

1) Stomach acid provides barrier function
2) Gastric acid assists digestion of milk
3) Glandular ulcer formation most likely not a function of increased HCl production

180
Q

How do you treat gastric ulceration in foals

A

histamine Ha2 receptor antagonists (ranitidine, cimetidine)
mucosal protectants (sucralfate, bismuth) and anticacids

treatment of perforated ulcers is unsuccessful

use of proton pump inhibitors is controversial

181
Q

What is the prognosis of gastric ulceration in foals

A

depends on stage and location

not good if perforated

might affect duodendal scarring and bile duct obstruction

182
Q

what species has a high prevalence of neonatal isoerythrolysis

A

mules

183
Q

concurrent finding of icterus and moderate to severe anemia in a neonatal foal is suggestive of

A

NI

184
Q

Prior to surgical intervention, what should be done in foals with uroperitoneum

A

electrolyte, fluid and acid/base disturbances should be corrected

Large Animal Disease (7 decks)

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