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Neonatalogy > Smith.16.17Manifestations And Management Of Neonantal Foals > Flashcards

Smith.16.17Manifestations And Management Of Neonantal Foals Flashcards

1
Q

Fluid bolus rate and over what amount of time

A

20 ml/kg over 15 to 20 minutes

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2
Q

Max of number of fluid boluses to repeat within a short period of time?

A

80 ml/kg

**4L for a 50 kg foal

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3
Q

Essential laboratory data that can be collected during fluid resuscitation

A

Packed cell volume
Total plasma protein
Blood glucose
Blood gas (electrolyte & lactate)

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4
Q

Benefits of plasma

A

Improvement in osmotic pressure
Coaguation factors
Provides buffer base
Immunotherapy

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5
Q

Rate of plasma administration

A

10 ml/kg per hour

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6
Q

Dose of hetastarch for rapid fluid resuscitation in foals

A

3 ml/kg at rate of 10 ml/kg/hour

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7
Q

Foal that is moderately to severely sunken eyes is estimated to what percent dehdyration?

A

8 to 10%

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8
Q

When is inopressor therapy indicated?

A

If hypotension persists in the face of fluid resuscitation
**aim of therapy to raise MAP above 60 mmhg

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9
Q

Examples of inopressor drugs

A

Dobutamine
Dopamine
Norepinephrine
Vasopressin

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10
Q

Dobutamine

A

Positive inotrope that improves cardiac output by improving stroke volume
Dose: CRI at 3-20 microg/kg/min

** not common to admin a vasopressor with dobutamin to improve tissue perfusion

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11
Q

Norepinephrine mechanism of action

A

Alpha 1 & 2 receptors to mediate vasoconstriction
Beta1 adrenergic receptors causing pos inotropic & cardiotorpic effects

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12
Q

Norepinephrine dosing

A

CRI 0.05 to 5.0 microg/kg/min

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13
Q

Dopamine mechanism of action

A

Alpha & beta adrenergic effects
— moderate to strong affinity for dopamine receptors (DA-1 & DA-2) and
— activity at dopaminergic recetors mediate vasodilation (renal, cerebral & splanchnic vasculr beds)

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14
Q

Dopamine dose

A

Lower rate improve renal/spanchnic perfusion: 0.5- 5 microg/kg/min

Higher infusion rate with severe septic shock: 10 - 25 microg/kg/min

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15
Q

Vasopressin mechanism of action

A

V1a receptors: in peripheral circulation causes vasoconstriction
V2 receptors: in kidney to facilitate water reposition

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16
Q

Vasopressin dose

A

0.25 to 1.0 mU/kg/min

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17
Q

Combination of vasporessin (low dose) and norepinephrine beneficial effects

A

Increase in MAP
Reduction in heart rate
Increased urine output

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18
Q

Why should boluses of glucose solutions be avoided?

A

Result in urinary losses of fluid, electrolytes & glucose

Can produce rebound hypoglycemia

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19
Q

Equation for replacement potassium supplementation

A

Replacement K (mEq)= 0.4 x body weight (kg) X K deficit (mEq)

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20
Q

Potassium can safely be added to fluids at what rate?

A

10 to 40 mEq/L

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21
Q

Potassium supplementation should not exceed what rate?

A

0.5 mEq/kg/hour

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22
Q

When is potassium supplementation in IV fluids usually indicated?

A

Critically sick neonates
Anorexic foals
Foals with diarrhea
Those receiving diuretic therapy

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23
Q

What is a situation when supplementation for sodium bicarbonate for an acidotic foal is not rewarding?

A

When acidosis is due to poor perfusion

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24
Q

Equation for bicarbonate deficit

A

Bicarb deficit (mEq)= 0.6 x body weight (kg) x base deficit (mEq)

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25
Q

How to make isotonic bicarbonate solution?

A

150 ml 8.4% bicarb solution to 850 ml sterile water

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26
Q

Plasma transfusion dose for failure of passive transfer

A

20 ml/kg

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27
Q

1 liter of plasma (with IgG>1200 mg/dL) raises serum IgG by

A

200 to 250 mg/dL (2 to 2.5 g/L)

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28
Q

Will the 20 ml/kg dose in septic foals attain a serum IgG concentration over 800 mg/dL?

A

Sometimes

Ill foals require more plasma b/c serum half-life of IgG is less and IgG may be sequestered in intravascular spaces or at sites of inflammation or be catabolized more readily

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29
Q

Recumbency in foal increases the risk for:

A

Pneumonia
Predisposes to ileus & constipation
INc risk of milk aspiration
Exacerbates musculoskeletal weakness
Risk of decubital ulcers

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30
Q

Foals are more vulnerable to water loss than adults because

A

Inc basal metabolic rate
Greater surface area
Reduced urine concentrating ability

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31
Q

Normal caloric intake in foals

A

125 to 150 kcal/kg/day

20-30% of bwt in milk daily

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32
Q

Resting energy requirement (RER) in ill foals

A

50 kcal/kg/day

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33
Q

Benefits of enteral feeding a foal?

A

Stimulates normal gut maturation
Growth of intestinal villi
Production of crypt cells
Hepatic & biliary secretions
Brush border disaccharidase enzyme activity

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34
Q

Alternative species milk used for supplementing foals?

A

Goats milk— higher in fat, total solids & gross energy than mare smilk
Cows milk— 2% skim with 20 g of dextrose per liter of milk

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35
Q

Ideal foal milk replacer

A

22% crude protein
15% fat
Less than 0.5% fiber on a dry matter basis

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36
Q

Can calf milk replacer be used to feed a foal?

A

If mixed with mares milk

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37
Q

Commonly used parenteral nutrition solution mixtures in foals

A

50% dextrose
8.5% or 10% amino acids
20% lipid emulsion

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38
Q

Simplified formula for 50 kg foal for parenteral nutrition

A

2.5 L of 8.5% amino acids
1 L of 20% lipid
1.5 L of 50% dextrose

**mixed into empty 5 liter fluid bag

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39
Q

Foals should not receive over what percentage of calories from lipid?

A

Not over 50% of nonprotein calories from lipid

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40
Q

Disorders in foals that cause weakness/somnolence since birth

A

In utero acquired bacterial/viral infections
Birth asphyxia & trauma
Chronic placental problems
Congenital anomalies

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41
Q

Disorders of foals that display weakness/somnolence that have physical immaturity (ie tendon laxity)

A

Fatigue
Hypothermia
Hypoxia
Hypoglycemia

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42
Q

Disorders of weakness in foals (w/o somnolence)

A

Trauma
Pierpheral nerve or mucsle damage

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43
Q

Neuromuscular diseases that cause weakness without somnolence include:

A

Botulism
Nutritional myodegeneration (NMD, white muscle disease)
Congenital myotpahties

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44
Q

Botulism in foals is acquired via

A

GI tract
Wounds
Umbilicus

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45
Q

NMD associated with with selenium and/or vit E deficiency: 2 forms

A
  1. First year of life in rapidly growing large animals
  2. In utero form
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46
Q

Clinical signs associated with NMD include:

A

Localized signs (dysphagia)
Generalized paresis
Rhabdomyolysis precipitated by stress or periparturient hypoxia

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47
Q

Phenylbutazone given to a mare prior to foaling, is present in the foal in what form?

A

Oxyphenbutazone (active metabolite of phenylbutazone)

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48
Q

Severe electrolyte and metabolic derangements in foals that manifest as weakness

A

Hypoglycemia
Acidosis
Hyponatremia
Hypernatremia
Hyperkalemia

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49
Q

Compression of the spinal cord leading to paraplegia or tetraplegia can be due to

A

Vertebral body malformation
Osteomyelitis
Fractures

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50
Q

Vertebral body malformation occur sporadically in foals and are usually due to

A

Genetic
Nutrition
Environment

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51
Q

Normal gestation length: horses

A

~340 days (335 to 342 days)

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52
Q

Foals premature

A

<320 days

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53
Q

Foals dysmature

A

> 330 days with signs of prematurity

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54
Q

Prolonged gestation

A

> 360 days
**post-mature if large, thin foals

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55
Q

Stages of parturition

A
  1. Development of coordinated uterine contractions
  2. Expulsion of foal
  3. Passing of fetal membranes
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56
Q

Stage 1 parturition characteristics

A

Fetus plays active role in positions from dorsopubic to dorsosacral
Increased uterine pressure causes cervical dilation
Signs of restlessness, mild colic and patchy sweating

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57
Q

Stage 2 parturition characteristics

A

Rupture of the chorioallantois
Strong abdominal contractions force expulsion of foal
Appearance of one hoof at vulva expected w/in 5 minutes of rupture of chorioallantois

**delivery w/in 20-30 minutes

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58
Q

Stage 3 parturition characteristics

A

Passing of fetal membranes (w/in 3 hoours)

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59
Q

Normal respiratory-cardiac rhythm should be established in foals, how long after birth?

A

1 minute of birth

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60
Q

Righting and suckle reflexs are apparent within

A

5 minutes of birth

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61
Q

Foals should be starting to stand within:

A

30 minutes

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62
Q

Normal foal consumption of milk

A

20-25% bodyweight

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63
Q

When should foals pass meconium

A

1 to 4 hours after birth

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64
Q

When should foals urinate by?

A

8-12 hours

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65
Q

Differentials for lesion localization: cerebral

A

Neonatal maladjustment syndrome
Meningitis
Trauma
Sepsis
Metabolic derangements: hypoglycemia/electrolyte abnorm
Atlantoaxialoccipital malformation

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66
Q

Adequate passive transfer of immunity in foals

A

> 800 mg/dL

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67
Q

Partial failure of transfer of immunity in foals

A

400-800

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68
Q

Complete failure of passive transfer in foals

A

<400 mg/dL

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69
Q

Sepsis definition

A

Systemic inflammatory response (SIRS) caused by any circulating microorganisms and/or their products

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70
Q

Most common etiologic agents of sepsis in foals

A

Gram neg most common:
E. Coli
Salmonella
Acitnobacillus equuli
Klebsiella spp
Enterobacter spp
Pseudomonas spp

Gram pos: enterococcus, Streptococcus, Stpahylococus spp
Fungal organisms: candida albicans

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71
Q

Pre-hepatic differentials for icterus in foals

A

Neonatal isoerythrolysis
Hemolytic anemia (sepsis)
Anorexia

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72
Q

Hepatic differentials for icterus in foal

A

Sepsis
Ascending umbilical vein infection
Tyzzers
Actinobacillus equuli
Leptospira interrogans
Equine herpesvirus-1
NI cases receiving multiple blood transfusions (>4L)

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73
Q

Post-hepatic differentials for icterus in foals

A

Cholestasis/biliary obstruction

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74
Q

Causes of anemia

A

Hemorrahge
Hemolysis
Decreased production
Immune-mediated destruction
Oxidative destruction

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75
Q

Tests to determine immune mediated anemia

A

Auto-agglutination
Spherocytes
Coombs test
RBC surface antibody

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76
Q

What are the most common offending antigens in NI foals?

A

Aa
Qa
Donkey factor (mules)

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77
Q

Prevalence of NI

A

TB: 1%
STB: 2%
Mules (donkey sire, horse dam): 10%

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78
Q

Preventative tests for neonatal isoerythrolysis

A

Screen mares blood type and presence of anti-RBC antibody
Compare to stallions blood type prior to parturition
Jaundice foal agglutination test

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79
Q

In foals with neonatal encephalopathy, CNS as well as organs with high oxygen deman and metabolic activity may be affected, which organs are these:

A

GIT
Kidney
Liver
Heart

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80
Q

What are key functions of astrocytes?

A

Glutamate and GABA uptake
Glutamine synthesis
Energy generation (lactate production via aerobic glycolysis)
Water balance

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81
Q

Which receptors are involved in excitotoxicity associated with neonatal encephalopathy?

A

**all members of glutamate receptor family
—> specifically NMDA receptors

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82
Q

Which energy pathways are important to astrocyte energy generation?

A

Aerobic glycolysis
Lactate production (Warburg effect)

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83
Q

What energy pathways are important for neurons?

A

Mitochondiral oxidative phsopohyrlation (tricarboxylic cycle)
Pentose cycle

**important to produce energy & maintain antioxidant (NADPH) capacity

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84
Q

How do astrocytes provide a steady source of energy for neurons?

A

Neurons use pyruvate and lactate released by astrocytes to feed tricarboxylic cycle and oxidative phosphorylation to generate ATP

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85
Q

Glutamate effect on astrocytes

A

Glutamate accumulation stimulates glucose uptake and lactate production by astrocytes

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86
Q

Which cells have enzymatic machinery to produce neurosteroids from cholesterol?

A

Nuerons
Glial cells (astrocytes & oligodendrocytes)

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87
Q

What is the main receptor/target for neuroactive steroids?

A

GABA receptor

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88
Q

Activation of Gaba receptor facilitates:

A

Chloride entry
Hyperpolarizes the cell membrane
Decreases neuronal cell excitability
Modifies flial cell function

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89
Q

What neurosteroids are responsible for the sedated response of fetus in utero?

A

Allopregnanolone
Pregnanolone

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90
Q

What is the main source of pregnenolone throughout gestation?

A

Equine fetal gonads

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91
Q

What are the chief contributors to progesterone in fetal circulation?

A

Fetal adrenal glands

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92
Q

The fetal gonads produce pregnenolone, what other hormone do they produce?

A

Androgens (DHEA) that are converted to estrogens by the fetoplacental unit

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93
Q

What hormone changes are associated with fetal maturation of HPAA maturation?

A

5-7 days prior to foaling enzymatic shift from progestogen to glucocorticoid synthesis
—> drop in progestogens with parallel increase in fetal corticotropin and cortisol concentrations

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94
Q

Fetal risk factors for development of NE

A

Congenital anomalies
Twins
Prematurity/dysmaturity
Sepsis
Umbilical cord compression
Dystocia

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95
Q

what are physical characteristics of immaturity

A

low birth weight
small body size
short and shiny hair coat
doming of the head
periarticular laxity
droopy ears

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96
Q

Define prematurity in a foal

A

foals with shortened gestational period and signs of physical immaturity

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97
Q

Define dysmaturity in a foal

A

foals that are physically immature int eh face of an appropriate gestational length

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98
Q

Foals born after 365 days should be considered

A

post-term

99
Q

Droopy ears can be a manifestation of:

A

systemic sepsis
thrombocytopenia caused by DIC or alloimmune thrombocytopenia

100
Q

When is the menace response learned in a foal?

A

at approximately 14 days

101
Q

What structure can be confused for cataracts?

A

posterior lens sutures
*8commonly seen in thoroughbred foals

102
Q

Congenital cataracts are amenable to surgery with what conditions?

A

-absence of uveal tract inflammation
-normal retina
-appropriate demeanor

103
Q

Episcleral injection is a prominent feature of

A

systemic sepsis

104
Q

Iridocyclitis is associated with:

A

sepsis
– include hyphema, hypopyon and fibrin
**can be seen with inutero infection

105
Q

Iridocyclitis can bee seen in older foals with infections involving

A

salmonella
rhodococcus equi

106
Q

Icteric mucous membranes can be seen with what disease processes in neonatal foals

A

systemic sepsis
neonatal isoerythrolysis
liver disease
internal hemorrhage
mecnoium retention
infection with EHV1

107
Q

Pale mucous membranes in a neonatal foal suggest anemia, which can occur with

A

external umbilical cord hemorrhage
internal hemorrhage from torn umbilical vessels
fracture ribs
hemorrhage w/in GIT or urinary tract

108
Q

If observe overt cyanosis, what should be examined?

A

cardiovascular and respiratory systems

109
Q

In term foals, when do incisors erupt

A

central: 5 to 7 days
middle incisors: 4 to 6 weeks
corner incisors: 6 to 9 months

110
Q

When do the 12 temporary molars present in foals?

A

At birth or erupt within the ifirst week of life

111
Q

Permanent premolars replace temporary premolars at what ages?

A

2.5, 3 and 4 years ofa ge

112
Q

When do the molar teeth erupt?

A

1, 2, 3.5 years of age (for moalrs 1, 2, 3 repectively)

113
Q

What is the most common congenital oral malformation of foals?

A

Maxillary prognathism (parrot mouth)

114
Q

mandibular prognathism is commonly associated with what:

A

congenital hypothyroidism

115
Q

Campylorrhinus lateralis (wry nose, wry face) descirbes what onditon

A

where the premaxilla and nasal septum are deviated alterally

116
Q

Wry nose can occur singularly in combination with what other deformities?

A

wry neck
cleft palate
maxillary or mandibular prognathism

117
Q

What is the incidence of cleft palate in horses:

A

0.1 to 0.2% of all horse births

118
Q

Where do a majority of clef palates occur in foals?

A

secondary palate– horizontal parition dividing oral and nasal cavities

119
Q

What structures should be evaluated when milk is coming out of nose?

A

-palate (looking for cleft palate)
-tongue– looking for candidiasis– white plaques tan discoloration of the tongue)

120
Q

Hypertrophy of the thyroid gland in foals is due to

A

-deficient or excess dietary iodine
-excess iodine supplementation during pregnancy
- seaweed in diet of mare

121
Q

What hormone is important cofactor for the in maturation of the resipratory system?

A

thyroid hormone

122
Q

Newborn foals have baseline T3 and T4 levels that are higher than adults, at what age do they decline?

A

12 days after birth

123
Q

Functional obstruction caused by small intestinal ileus occurs more commonly in neonates secondary to range of diseases including:

A

hypoxic ischemic syndrome
sepsis
prematurity
enteritis
electrolyte derangements
overfeeding

124
Q

Small intestinal intussusception in foals are most commonly in what location?

A

jejunojejunal

**visualize on ventral abdomen

125
Q

Transit of barium through the GIT should occur in what time frame?

A
  1. Should clear SI in 3 hours
    completely cleared by 36 hours
    Cecum visible by 1 to 2 hours
126
Q

Nucleated cell counts within abdominal fluid are considered abnormal at what level

A

> 1.5 x 10^9/L up to 4 molnths of age

127
Q

heart rate in foals after birth should range between

A

36 and 80 betas per minute

128
Q

reasons for bradycardia in a foal

A

hypothermia
electrolyte abnormalities
hypoglycemia

129
Q

Arrhythmias in foals can persist normally up to what time frame?

A

up to 2 hours
**should be evaluated after this time period by ECG if persists

130
Q

When should a murmur in a foal be referred for echocardiography?

A

-loud murmurs that persist beyond 7 dahs of age
- murmur accompanied by signs fo cardiac disease: poor growth, cyanosis, elthargy or exercise intolerance

131
Q

PDA (patent ductus arteriosus) can be audible up to how many days?

A

3 to 4 days
**continuous washing machine murmur

132
Q

paradoxical respiratory motion (thoracic wall moves inwards during inspiration and outwards during expiration) occurs in foals when

A

respiratory disease that is progressing to respiratory failure
**more commonly seen in premature foals

133
Q

Pulmonary causes of increased respiratory rate in foals

A

meconium aspiration
bacterial or viral pneumonia
atelectasis d/t recumbency
congenital pulmonary disease
rib fracture or disolcation
pleural effsuion

134
Q

Nonpulmonary causes of increased respiratory rate in foals

A

fever
pain
excitement
exercise
brain disease
compensatory response to metabolic acidosis
idiopathic or transietn tachypnea syndrome

135
Q

Foals with erratic breathing patterns due to CNS disease, m ay require use of what?

A

respiratory stimulants (doxapram, caffeine)
mechanical ventilation

136
Q

List uncommon causes of stertorous breathing or respiratory distress in foals to consider

A

stenotic nairs
choanal atresia
subepiglottic cysts
colapsing trachea
lung lob agenesis
tearing of idaphragm during birth
dorsally dispalced soft palate (neurologic or anatomyc dysfunction)
guttural pouch tympany

137
Q

crepitus of subcu tissues on the thorax is indicative of

A

leakage from respiratory tissues, most commonly from ruptured pulmonary bullae
**possible rib fracture

138
Q

What are potential complications of rib fracture in a foal?

A

hemothorax
lung laceration
pneumothorax
pericardial/myocardial puncture

139
Q

Causes of hypoxemia

A
  1. hypoventilation
  2. ventilation/perfusion mismatch
  3. right to left shuntting of blood
140
Q

What are possible complications of umbilical herniations in foals, howver rare?

A

colic
enterocutaneous fistulae
umbilical abscessation
intesinal incarceration

141
Q

Brix guidelines for colostrum quality in mares

A
  1. 0-15% Brix, 0 to 28 gm/L IgG= poor quality
  2. 15 to 20% brix, 28 to 50 gm/L IgG, borderline quality
  3. 20 to 30% Brix, 50 to 80 gm/L IgG, adequat quality
  4. > 30% BrIX, greaterthan 80 gm/L igG, very good quality
142
Q

What is the recommended mimimum dose of colostrum in foals?

A

min dose of 60 to 90 gm/L of IgG in the first 6 hours after birth

143
Q

baseline glucose values in foals should be what level after parturition?

A

Should be 50% of mares glucose and reach a low approx 2 hours after birth

144
Q

How long can you wait to measure L-lactate measurements?

A

10 minutes
**otherwise red blood cells conitnue to rpoduce lactate in a lithium heparin tube

145
Q

If foals have an elevated creatinine post birth associated with perinatal asphyxia syndrome (PAS), when should these decrease?

A

W/in 24 hours, and values should halve

146
Q

Signs of clinical hypocalcemia:

A

tachycardia
sweating
tremor
muscular rigidity
stiff gait
recumbency

147
Q

Manifestation of sepsis with survival rates to discharge being 42 to 80% reported. What percentage of these horses had septic arthritis/septic osteomyelitis that achieved long -term athletic soundness?

A

30% with septic arthritis
48% with septic osteomyelitis

148
Q

Prognosis for athletic performance with septic arthritis/osteomyelitis depends on what factors?

A

number of joints affected
numbe rof bones involved
age of the foal
presence of other medical problems

149
Q

Septic arthritis/osteomyelitis involving just the Synovial membrane of one more joints joints with no radiographic change, at what age group is this form seen and what joints are involved?

A

2 weeks of age
common joints: carpus, stifle, hock

150
Q

Septic arthritis/osteomyelitis:
Epiphysial classification involving the joint and osteomyelitis of the adjacent subchondral bone is most commonly seen in what age group and what common sites?

A

3 to 4 weeks fo age

common sites: femoral condyles, distsal radius, distal tibia, patella

151
Q

Septic arthritis/osteomyelitis:
physeal type, osteomyleitis of the physis on the metaphyseal side of the growth plate, common seen in what age group and what common sites

A

foals 1 to 12 weeks of age
common sites: distal radius or tibia, distal metacarpi/tarsi

152
Q

Septic arthritis/osteomyelitis:
tarsal: classification describes osteomyelitis of what bones?

A

tarsus or carpus

153
Q

What are common predisposing causes to joint and bone infections in neonates?

A

-persistent or transietn heamtogenous dissemination of bacteria from distant sites of infection:
-GI
-respiratory
-umbilical infection
-failure of passive transfer

154
Q

Septic arthritis/osteomyelitis:
Common bacteria isolated

A

Enterbacteriaceae (E. coli_
Salmonella
Actinobacillus equuli
Klebsillaspp
Streptococcus
Rhodococcus equi

155
Q

IN Septic arthritis/osteomyelitis, why do bacteria end up there?

A

b/c of vascular pattern of neonates

main arteriole– blood supply to synovial membrane and epiphysis
nutrient artery– blood supply to the metaphysis

Transphyseal vessels connect epiphyseal and metaphyseal blood supplys

–> bacterial deposition occurs as epihyseal vssel branch twoard articular surface, hairpin bends ending in venous sinuosoids (synovial membrane lacks a basement membrane–> bacteria easily cross sybsunovial capillaries)

156
Q

Why is physeal infection more likely to occur at 7 to 10 days of age?

A

closure of the transphyseal vessles

–> localization of the ifnection in metahphyseal vessel loops

157
Q

Differentials for lameness in foals

A

septic arthritis/osteitis/osteomyelitis
fracture
common sites: PIII, physis of P2, proximal sesamoid bones, olecranon
Hemarthrosis
cellulits
felxural deformity
rupture of the common digital extensor tendons
rupture of the gastrocnemius mm
subsolar/solar bruising of the foot
laminitis
peripheral nerve injury

158
Q

Consistent and early clinical signs of joint sepsis is what:

A

effusion

other commonly reported: periarticular swelling, heat, pain on palpation of the bone or joint and restricted passive movement of the joint

159
Q

Is hyperfibrinogenemia and leukocytosis sensitive for the septic arthritis/osteomyelitis?

A

No

160
Q

Normal synovial fluid parameters:

A

TP <2.0 g/dL
TNCC <10,000 cells/microL
Neutrophils <10%

161
Q

What can cause an increase in TNCC and TP of synovial fluid but percentage of neutrophils remains less than 80%?

A

sympathetic synovitis (fomr increase dblood flow to a region)

162
Q

What is the percentage of bone infection in foals with septic arthritis?

A

38 to 80%

163
Q

Radiographic changes of bone sepsis are not evident until how many days after the onset of infection?

A

7 to 10 days:
- joint space narrowing
-articular cartilage destruction
-periosteal reaction
-subchondral bone osteolysis

164
Q

a retrospective study of foals with septic arthritis reported that 85.7% of synovial fluid samples cultured that yielded growth, what percentage were gram negative and gram positive?

A

62.4% gram negative
37.5% gram positive

165
Q

If osteomyelitis is present, how long should foals be on antibiotic therapy for?

A

up to 2 months

166
Q

Common antibiotics used for intraarticular injections in tx of septic arhtritis?

A

gentamicin (500 mg)
amikacin (125 to 250 mg)
ceftiofur sodium (125 to 500 mg)

167
Q

For regional limb perfusion. How long should a tourniquet be left onf or?

A

at least 30 minutes wiht a max of 60 minutes total tourniquet application

168
Q

What is the reported short term survival (to discharge) in foals with septic osteomyelitis?

A

71 to 81%

169
Q

What is the prognosis for future athletic performance in foals with septic osteomyelitis

A

30 to 48%

170
Q

What are common sites of fractures in the distal limbs of foals?

A

distal phalanx
physeal fractures of the first phalanx
proximal sesamoid bones

171
Q

What is the most common fracture of the upper limb in foals?

A

olecranon

172
Q

Signs of gastrocnemius rupture in foals

A

hyperflexion of the hock and extension of the stifle

173
Q

Which foals are likely to have incomplete ossification of cuboidal bones at birth?

A

twins
premature foals
foals that are small for gestational age
foals with in utero acquired infection

174
Q

hypothyroidism has been associated with what musculoskeletal abnormalities in foals?

A

angular limb deformities
contracted tendons
tarsal bone collapse

175
Q

Foals have a higher or lower seizure threshold than adults?

A

foals lower than adults

176
Q

Where are seizures generated?

A

by abnromal electrical acitivty w/inteh cerebral cortex

177
Q

What are characateristics of generalized seizures:

A

recumbency
widespread involuntary muscle activity
paddling of the limbs
extensor rigidity

178
Q

Differentiate REM sleep from seizure activity?

A

a foal in REM sleep should be easily aroused

179
Q

Common bacterial agents of meningitis in foals?

A

Escherichia coli
Enerobacter spp
Salmonella sppsreptococcal spp

180
Q

Definitive diagnosis of meningitis

A

CSF analysis: neutrophilic pleocytosis

181
Q

Antibiotic recommendations for treatment of meningitis?

A

3rd generation cephalosporins (cefotoxaime or ceftriazone)
**base don culture adn sensitivty

182
Q

Prognosis for survival of bacterial meningitis?

A

fair- if signs are limited to hyperesthesia and neck stiffness
poor-otherwise

183
Q

Benign juvenile epilepsy is described in what breed?

A

Arabian foals of Eqgyptian origin

184
Q

Benign juvenile epilepsy resolves after what age?

A

usually by 12 months of age in all foals

185
Q

Benign juvenile epilepsy can be treated with what medications?

A

phenobarbital (5 to 20 mg/kg PO as loading dose, then 2 to 5 mg/kg PO bid)

potassium bromide (100 mg/kg PO as loading dose, followed by 25 mg/kg PO q24h)

186
Q

Seizure disorders should have rule outs of

A

hypoglycemia
electrolyte abnormalities (Low Ca, Na, or High Na)

187
Q

What is the msot common congeital brain disease in foals?

A

hydrocephalus

188
Q

Clinical signs of tetanus are not likely before what age of foal?

A

prior to 7 days

189
Q

Clinical signs of tetanus in foals?

A

difficulty lcoating and latching onto the teat
dysphagia
gait siffness
elevation fo the tail head
anxious facial expression
prolapse of third eyelid
tachycardia
sweating

190
Q

When is it recommended that mares receive a booster of tetanus toxoid?

A

approximately 28 days before esitmated parution

191
Q

What are reported signs of ivermectin toxicity

A

obtudnation
blindness
ataxia
head pressing
seizure

192
Q

Clinical signs of ivermectin toxicity are caused by:

A

opening of the GABA-gated chloride channels with resultant membrane hyperpolarization and blockage of neuronal impulses

193
Q

Successful management of ivermectin toxicosis incldues:

A

IV lipid emulsions (20% soybean oil in water, 1.5 ml/kg bolus, followed by 0.25 ml/kg/min for 30 minutes)

194
Q

kernicterus results from deposition of what in the brain?
**particularly within the basal ganglia , cornua ammonis and substantia nigra

A

bilirubin IX alpha

195
Q

At what serum bilirubin concentration are foals at risk for devvelopment of kernicterus?

A

> 27.0 mg/dL

196
Q

Lavender foal syndrome is also referred to as

A

coat color dilution lethal (CCDL)

197
Q

Describe lavender foal syndrome

A

autosomal recessive gene disorder of Arabian foals of Egyptian bloodlines

198
Q

Lavender foal syndrome is caused by what gene mutation?

A

frameshift single base mutation in exon 30 of the myosin-Va gene (mYO5a) resulting in premature termination of transcription

**primary homozygous foals

199
Q

foals affected with lavender foal syndrome have clinical signs of:

A

unable to achieve sternal recumbency
severe neuro signs: frequent episodes of opisthotonus, limb paddling, rapid eye movements
death (w/in 72 hours of age)

200
Q

What is the carrier frequency of LFS in teh US

A

10.3% in Egyptian Arabians
1.8% in non-Egyptian Arabians

201
Q

Glycogen storage disease IV
**describe the disease

A

auosomal recesive disease of Quarter Horses adn PainHorse breeds

202
Q

Glycogen storage disease mutation occurs where?

A

glycogen branching enzyme, encoded by the GBE1 gene

203
Q

Clinical signs of foals with Glycogen storage disease

A

still born or aborted
profound muscular weakness and hypothermia
hypoglycemic seizures or cardiopulmonary failure
**all foals died or euthanized by 18 wks of age

204
Q

causes of anemia in foals: hemolysis

A

neonatal isoerythrolysis

less common causes:
-non-NI immune mediated hemolysis
-intracellular RBC parasites
-rapid administration of hypotonic or hypertonic solutions (DMSO)
-equine infectious anemia

205
Q

A syndrome of anemia and B-cell lymphopenia reported in what breed?

A

Fell ponies

206
Q

A foal is considered premature at what age of gestation?

A

born before 320 days

207
Q

premature foals typically have problems maintaining what:

A

body temperature
blood pressure
blood glucose

208
Q

The average relative weight of the term foal to its dam is around what percentage?

A

10%

209
Q

postterm or post mature foals will have

A

erupted incsors
long hair coat

210
Q

pregnant mares consumption of tall fescue pasture infected with Neotyphodium coenophialum leads to a range of abnormal signs including:

A

prolongation of gestation
perinatal mortality
agalactia

211
Q

What hormone is critical for organ maturation in the fetus?

A

cortisol

**too much– or too early= intrauterine growth restriction

212
Q

How is the fetus protected from cortisol during gestation?

A

type 2 isoform of enzyme 11 beta-hydroxysteroid dehydrogenase converts excess biologically active cortisol into the inactive cortisone in the placenta

enzymes (3 betaHSD, P450 scc and P450C17) required conversion of cholesterol and pregnolone to synthesize cortisol are inhibited or deficient during pregnancy

213
Q

During the majority of gestation the major produts of seroidogenesis are:

A

progesterone
5alpha-reduced progestagens
**not cortisol

214
Q

What are the triggers for the process that results in fetal cortisol production, organ maturation and birth?

A

unkown

215
Q

Which hormones are critical for lung maturation in the new born (particularly reabsorption of lung liquid)?

A

**cortisol

**T3

216
Q

What are factors that can induce premature maturation of the fetal HPA axis?

A

hypoxemia
exogenous glucocorticoids
poor nutrition before/after conception
placenta and/or fetal infection

** stimuli in foals has not been well described

217
Q

What does HPA stand for?

A

Hypothalamic-Pituitary-Adrenal Axis

218
Q

lung surfactant is usually fully developed in foals at what gestational age?

A

300 days

** but could be delayed until after 340 days in some foals

219
Q

What is the most severe form of respiratory failure in neonatal foals?

A

neonatal respiratory distress syndrome (RDS)
– characterized by progressive resp failure, sever hypoxemia, hypercapnia and death

220
Q

The effects of dopamine are dose dependent, including:

A
  1. low doses (0.5 to 5 microg/kg/in) provide agonism of dopaminergic receptors and possible renotubular effects along with vasodilation of coronary and intestinal vasculature
  2. moderate doses (4 to 10 microg/kg/min) simulate Beta1 adrenergic receptors and result in chronotropy
  3. High dose dopamine (>10 microg/kg/min) cause agonist of alpha 1 adrenergic receptors lead to widespread vasoconstfction
221
Q

Dobutamine at 3 to 20 microg/kg/min acts primarily on what receptors?

A

beta 1 adrenoreceptors– producing an improvement in myocardial contractility without vasoconstriction

222
Q

Thermogenic mechanisms develop late in gestation and are rleated to circulating levels of?

A

T3

223
Q

Problems with thermogenesis are exacerbate din preterm foals because of what?

A

incomplete adrenal function

224
Q

Why is coughing uncommon in neonatal foals with respiratory disease?

A

postnatal delay in maturation of irritant receptors w/in airways

delayed onset of laryngopharyngeal cough reflex

225
Q

What is the danger of giving of giving foals sodium bicarboante to foals with pulmonary disease?

A

can exacerbate hypercapnia

226
Q

Chornic hypercapnia vs acute hypercapnia

A

acute hypercapnia– associated with substantial drop in blood pH, lead to circulatory collapse and coma (if accompanied by acute hypoxemia)

Chronic hypercapnia– permits adaptation, drop in pH is less dramatic d/t enhanced bicarb reabsorption in the PCT of the kidney

227
Q

Congenital defects of the upper respiratory tract include

A

collapsed trachea
stenotic anres
choanal atresia
epiglottal cyst
guttural pouch tympany

228
Q

causes of laryngeal paralysis in foals

A

nutritional myodegeneration
hyperkaelmic periodic parlaysis
botulism

229
Q

In foals with HYPP what clinical signs are seen

A

exercise and excitement induced respiratory stridor

230
Q

Collapsed trachea is a rare congenital or acquired condition most commonly reported in what breed?

A

American miniature horses

231
Q

The most common bacterial isolates that are associate with pulmonary diseasein foals include

A

E coli
Klebsiella pneumoniae
Pasturella sppactinobacillus spp
Streptococci spp

232
Q

Why does positioning foals in sternal vs lateral recumbency better in foals with respiratory disease?

A

the neontal foal readly develops depedent atelectasis in lateral recumebncy
**imporved ventilatory acapacity and higher arterial oxgyen tension

233
Q

Outcome for neonatal pneumonia due to EHV-1?

A

frequently fatal

234
Q

meconium aspiration can result in

A

regional air trapping
chemical pneumonitis
alveolitis
alveolar edema
displacement of surfactant–> dec lung compliance, small airway obstruction and focal atelectasis

235
Q

When is the best time to suction airways if known meconium impaction?

A

in the birth canal prior to taking its first breath

**nasotracheal intubation and carefuls uction reocmmended

236
Q

Radiographs of a foal that has aspirated meconium show:

A

ventrocranial distribution of pulmonary infiltrate characteristic of aspiration

237
Q

Milk aspiration can occur in foals with what dz processes

A

cleft palate
persistent dorsal displacement of the soft palate (DDSP)
botulism
neonatal encpalopathy
generalized weakness d/t sepsis
prematurity
iatreogenic (bottle feeding)

238
Q

Causes of pneumothorax in foals

A

positive pressure ventilation of dzed lungs
birth trauma
rif fracture
ruptured bullae w/in lung parenchyma

239
Q

During mechanical ventilation, if the a foals respiratory condition suddenly worsens, what should be considered

A

uneven alveoalr ventilated that leads to aolveolar rupture and dissection fo air into the interstitium

240
Q

What is required to confirm diagnosis of pneumothorax?

A

radiographs

241
Q

Why after removal the abdominal fluid from a uroperitoneum can foals develop tachypnea, tachycardia, hypercapnia and hypoxemia?

A

due to re-expansion pulmonary edema
**if thoracic fluid is present with uroperitoneum

242
Q

What is transient tachypnea in teh neonate?

A

self limiting and speculated to be associated with central or peripheral control of thermoregulation and or respiratory rate and pattern

243
Q

Transtracheal O2 delivery may be beneficial in which foals?

A

-larger foals
-hypoxemia in neonatal foals with a rapid, shallow breathing pattern
-foals with severe pulmonary disease that are unresponsive to nasal insufflation

Neonatalogy (5 decks)

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