Smith.16.17Manifestations And Management Of Neonantal Foals Flashcards
Fluid bolus rate and over what amount of time
20 ml/kg over 15 to 20 minutes
Max of number of fluid boluses to repeat within a short period of time?
80 ml/kg
**4L for a 50 kg foal
Essential laboratory data that can be collected during fluid resuscitation
Packed cell volume
Total plasma protein
Blood glucose
Blood gas (electrolyte & lactate)
Benefits of plasma
Improvement in osmotic pressure
Coaguation factors
Provides buffer base
Immunotherapy
Rate of plasma administration
10 ml/kg per hour
Dose of hetastarch for rapid fluid resuscitation in foals
3 ml/kg at rate of 10 ml/kg/hour
Foal that is moderately to severely sunken eyes is estimated to what percent dehdyration?
8 to 10%
When is inopressor therapy indicated?
If hypotension persists in the face of fluid resuscitation
**aim of therapy to raise MAP above 60 mmhg
Examples of inopressor drugs
Dobutamine
Dopamine
Norepinephrine
Vasopressin
Dobutamine
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
Norepinephrine mechanism of action
Alpha 1 & 2 receptors to mediate vasoconstriction
Beta1 adrenergic receptors causing pos inotropic & cardiotorpic effects
Norepinephrine dosing
CRI 0.05 to 5.0 microg/kg/min
Dopamine mechanism of action
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)
Dopamine dose
Lower rate improve renal/spanchnic perfusion: 0.5- 5 microg/kg/min
Higher infusion rate with severe septic shock: 10 - 25 microg/kg/min
Vasopressin mechanism of action
V1a receptors: in peripheral circulation causes vasoconstriction
V2 receptors: in kidney to facilitate water reposition
Vasopressin dose
0.25 to 1.0 mU/kg/min
Combination of vasporessin (low dose) and norepinephrine beneficial effects
Increase in MAP
Reduction in heart rate
Increased urine output
Why should boluses of glucose solutions be avoided?
Result in urinary losses of fluid, electrolytes & glucose
Can produce rebound hypoglycemia
Equation for replacement potassium supplementation
Replacement K (mEq)= 0.4 x body weight (kg) X K deficit (mEq)
Potassium can safely be added to fluids at what rate?
10 to 40 mEq/L
Potassium supplementation should not exceed what rate?
0.5 mEq/kg/hour
When is potassium supplementation in IV fluids usually indicated?
Critically sick neonates
Anorexic foals
Foals with diarrhea
Those receiving diuretic therapy
What is a situation when supplementation for sodium bicarbonate for an acidotic foal is not rewarding?
When acidosis is due to poor perfusion
Equation for bicarbonate deficit
Bicarb deficit (mEq)= 0.6 x body weight (kg) x base deficit (mEq)
How to make isotonic bicarbonate solution?
150 ml 8.4% bicarb solution to 850 ml sterile water
Plasma transfusion dose for failure of passive transfer
20 ml/kg
1 liter of plasma (with IgG>1200 mg/dL) raises serum IgG by
200 to 250 mg/dL (2 to 2.5 g/L)
Will the 20 ml/kg dose in septic foals attain a serum IgG concentration over 800 mg/dL?
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
Recumbency in foal increases the risk for:
Pneumonia
Predisposes to ileus & constipation
INc risk of milk aspiration
Exacerbates musculoskeletal weakness
Risk of decubital ulcers
Foals are more vulnerable to water loss than adults because
Inc basal metabolic rate
Greater surface area
Reduced urine concentrating ability
Normal caloric intake in foals
125 to 150 kcal/kg/day
20-30% of bwt in milk daily
Resting energy requirement (RER) in ill foals
50 kcal/kg/day
Benefits of enteral feeding a foal?
Stimulates normal gut maturation
Growth of intestinal villi
Production of crypt cells
Hepatic & biliary secretions
Brush border disaccharidase enzyme activity
Alternative species milk used for supplementing foals?
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
Ideal foal milk replacer
22% crude protein
15% fat
Less than 0.5% fiber on a dry matter basis
Can calf milk replacer be used to feed a foal?
If mixed with mares milk
Commonly used parenteral nutrition solution mixtures in foals
50% dextrose
8.5% or 10% amino acids
20% lipid emulsion
Simplified formula for 50 kg foal for parenteral nutrition
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
Foals should not receive over what percentage of calories from lipid?
Not over 50% of nonprotein calories from lipid
Disorders in foals that cause weakness/somnolence since birth
In utero acquired bacterial/viral infections
Birth asphyxia & trauma
Chronic placental problems
Congenital anomalies
Disorders of foals that display weakness/somnolence that have physical immaturity (ie tendon laxity)
Fatigue
Hypothermia
Hypoxia
Hypoglycemia
Disorders of weakness in foals (w/o somnolence)
Trauma
Pierpheral nerve or mucsle damage
Neuromuscular diseases that cause weakness without somnolence include:
Botulism
Nutritional myodegeneration (NMD, white muscle disease)
Congenital myotpahties
Botulism in foals is acquired via
GI tract
Wounds
Umbilicus
NMD associated with with selenium and/or vit E deficiency: 2 forms
- First year of life in rapidly growing large animals
- In utero form
Clinical signs associated with NMD include:
Localized signs (dysphagia)
Generalized paresis
Rhabdomyolysis precipitated by stress or periparturient hypoxia
Phenylbutazone given to a mare prior to foaling, is present in the foal in what form?
Oxyphenbutazone (active metabolite of phenylbutazone)
Severe electrolyte and metabolic derangements in foals that manifest as weakness
Hypoglycemia
Acidosis
Hyponatremia
Hypernatremia
Hyperkalemia
Compression of the spinal cord leading to paraplegia or tetraplegia can be due to
Vertebral body malformation
Osteomyelitis
Fractures
Vertebral body malformation occur sporadically in foals and are usually due to
Genetic
Nutrition
Environment
Normal gestation length: horses
~340 days (335 to 342 days)
Foals premature
<320 days
Foals dysmature
> 330 days with signs of prematurity
Prolonged gestation
> 360 days
**post-mature if large, thin foals
Stages of parturition
- Development of coordinated uterine contractions
- Expulsion of foal
- Passing of fetal membranes
Stage 1 parturition characteristics
Fetus plays active role in positions from dorsopubic to dorsosacral
Increased uterine pressure causes cervical dilation
Signs of restlessness, mild colic and patchy sweating
Stage 2 parturition characteristics
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
Stage 3 parturition characteristics
Passing of fetal membranes (w/in 3 hoours)
Normal respiratory-cardiac rhythm should be established in foals, how long after birth?
1 minute of birth
Righting and suckle reflexs are apparent within
5 minutes of birth
Foals should be starting to stand within:
30 minutes
Normal foal consumption of milk
20-25% bodyweight
When should foals pass meconium
1 to 4 hours after birth
When should foals urinate by?
8-12 hours
Differentials for lesion localization: cerebral
Neonatal maladjustment syndrome
Meningitis
Trauma
Sepsis
Metabolic derangements: hypoglycemia/electrolyte abnorm
Atlantoaxialoccipital malformation
Adequate passive transfer of immunity in foals
> 800 mg/dL
Partial failure of transfer of immunity in foals
400-800
Complete failure of passive transfer in foals
<400 mg/dL
Sepsis definition
Systemic inflammatory response (SIRS) caused by any circulating microorganisms and/or their products
Most common etiologic agents of sepsis in foals
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
Pre-hepatic differentials for icterus in foals
Neonatal isoerythrolysis
Hemolytic anemia (sepsis)
Anorexia
Hepatic differentials for icterus in foal
Sepsis
Ascending umbilical vein infection
Tyzzers
Actinobacillus equuli
Leptospira interrogans
Equine herpesvirus-1
NI cases receiving multiple blood transfusions (>4L)
Post-hepatic differentials for icterus in foals
Cholestasis/biliary obstruction
Causes of anemia
Hemorrahge
Hemolysis
Decreased production
Immune-mediated destruction
Oxidative destruction
Tests to determine immune mediated anemia
Auto-agglutination
Spherocytes
Coombs test
RBC surface antibody
What are the most common offending antigens in NI foals?
Aa
Qa
Donkey factor (mules)
Prevalence of NI
TB: 1%
STB: 2%
Mules (donkey sire, horse dam): 10%
Preventative tests for neonatal isoerythrolysis
Screen mares blood type and presence of anti-RBC antibody
Compare to stallions blood type prior to parturition
Jaundice foal agglutination test
In foals with neonatal encephalopathy, CNS as well as organs with high oxygen deman and metabolic activity may be affected, which organs are these:
GIT
Kidney
Liver
Heart
What are key functions of astrocytes?
Glutamate and GABA uptake
Glutamine synthesis
Energy generation (lactate production via aerobic glycolysis)
Water balance
Which receptors are involved in excitotoxicity associated with neonatal encephalopathy?
**all members of glutamate receptor family
—> specifically NMDA receptors
Which energy pathways are important to astrocyte energy generation?
Aerobic glycolysis
Lactate production (Warburg effect)
What energy pathways are important for neurons?
Mitochondiral oxidative phsopohyrlation (tricarboxylic cycle)
Pentose cycle
**important to produce energy & maintain antioxidant (NADPH) capacity
How do astrocytes provide a steady source of energy for neurons?
Neurons use pyruvate and lactate released by astrocytes to feed tricarboxylic cycle and oxidative phosphorylation to generate ATP
Glutamate effect on astrocytes
Glutamate accumulation stimulates glucose uptake and lactate production by astrocytes
Which cells have enzymatic machinery to produce neurosteroids from cholesterol?
Nuerons
Glial cells (astrocytes & oligodendrocytes)
What is the main receptor/target for neuroactive steroids?
GABA receptor
Activation of Gaba receptor facilitates:
Chloride entry
Hyperpolarizes the cell membrane
Decreases neuronal cell excitability
Modifies flial cell function
What neurosteroids are responsible for the sedated response of fetus in utero?
Allopregnanolone
Pregnanolone
What is the main source of pregnenolone throughout gestation?
Equine fetal gonads
What are the chief contributors to progesterone in fetal circulation?
Fetal adrenal glands
The fetal gonads produce pregnenolone, what other hormone do they produce?
Androgens (DHEA) that are converted to estrogens by the fetoplacental unit
What hormone changes are associated with fetal maturation of HPAA maturation?
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
Fetal risk factors for development of NE
Congenital anomalies
Twins
Prematurity/dysmaturity
Sepsis
Umbilical cord compression
Dystocia
what are physical characteristics of immaturity
low birth weight
small body size
short and shiny hair coat
doming of the head
periarticular laxity
droopy ears
Define prematurity in a foal
foals with shortened gestational period and signs of physical immaturity
Define dysmaturity in a foal
foals that are physically immature int eh face of an appropriate gestational length
Foals born after 365 days should be considered
post-term
Droopy ears can be a manifestation of:
systemic sepsis
thrombocytopenia caused by DIC or alloimmune thrombocytopenia
When is the menace response learned in a foal?
at approximately 14 days
What structure can be confused for cataracts?
posterior lens sutures
*8commonly seen in thoroughbred foals
Congenital cataracts are amenable to surgery with what conditions?
-absence of uveal tract inflammation
-normal retina
-appropriate demeanor
Episcleral injection is a prominent feature of
systemic sepsis
Iridocyclitis is associated with:
sepsis
– include hyphema, hypopyon and fibrin
**can be seen with inutero infection
Iridocyclitis can bee seen in older foals with infections involving
salmonella
rhodococcus equi
Icteric mucous membranes can be seen with what disease processes in neonatal foals
systemic sepsis
neonatal isoerythrolysis
liver disease
internal hemorrhage
mecnoium retention
infection with EHV1
Pale mucous membranes in a neonatal foal suggest anemia, which can occur with
external umbilical cord hemorrhage
internal hemorrhage from torn umbilical vessels
fracture ribs
hemorrhage w/in GIT or urinary tract
If observe overt cyanosis, what should be examined?
cardiovascular and respiratory systems
In term foals, when do incisors erupt
central: 5 to 7 days
middle incisors: 4 to 6 weeks
corner incisors: 6 to 9 months
When do the 12 temporary molars present in foals?
At birth or erupt within the ifirst week of life
Permanent premolars replace temporary premolars at what ages?
2.5, 3 and 4 years ofa ge
When do the molar teeth erupt?
1, 2, 3.5 years of age (for moalrs 1, 2, 3 repectively)
What is the most common congenital oral malformation of foals?
Maxillary prognathism (parrot mouth)
mandibular prognathism is commonly associated with what:
congenital hypothyroidism
Campylorrhinus lateralis (wry nose, wry face) descirbes what onditon
where the premaxilla and nasal septum are deviated alterally
Wry nose can occur singularly in combination with what other deformities?
wry neck
cleft palate
maxillary or mandibular prognathism
What is the incidence of cleft palate in horses:
0.1 to 0.2% of all horse births
Where do a majority of clef palates occur in foals?
secondary palate– horizontal parition dividing oral and nasal cavities
What structures should be evaluated when milk is coming out of nose?
-palate (looking for cleft palate)
-tongue– looking for candidiasis– white plaques tan discoloration of the tongue)
Hypertrophy of the thyroid gland in foals is due to
-deficient or excess dietary iodine
-excess iodine supplementation during pregnancy
- seaweed in diet of mare
What hormone is important cofactor for the in maturation of the resipratory system?
thyroid hormone
Newborn foals have baseline T3 and T4 levels that are higher than adults, at what age do they decline?
12 days after birth
Functional obstruction caused by small intestinal ileus occurs more commonly in neonates secondary to range of diseases including:
hypoxic ischemic syndrome
sepsis
prematurity
enteritis
electrolyte derangements
overfeeding
Small intestinal intussusception in foals are most commonly in what location?
jejunojejunal
**visualize on ventral abdomen
Transit of barium through the GIT should occur in what time frame?
- Should clear SI in 3 hours
completely cleared by 36 hours
Cecum visible by 1 to 2 hours
Nucleated cell counts within abdominal fluid are considered abnormal at what level
> 1.5 x 10^9/L up to 4 molnths of age
heart rate in foals after birth should range between
36 and 80 betas per minute
reasons for bradycardia in a foal
hypothermia
electrolyte abnormalities
hypoglycemia
Arrhythmias in foals can persist normally up to what time frame?
up to 2 hours
**should be evaluated after this time period by ECG if persists
When should a murmur in a foal be referred for echocardiography?
-loud murmurs that persist beyond 7 dahs of age
- murmur accompanied by signs fo cardiac disease: poor growth, cyanosis, elthargy or exercise intolerance
PDA (patent ductus arteriosus) can be audible up to how many days?
3 to 4 days
**continuous washing machine murmur
paradoxical respiratory motion (thoracic wall moves inwards during inspiration and outwards during expiration) occurs in foals when
respiratory disease that is progressing to respiratory failure
**more commonly seen in premature foals
Pulmonary causes of increased respiratory rate in foals
meconium aspiration
bacterial or viral pneumonia
atelectasis d/t recumbency
congenital pulmonary disease
rib fracture or disolcation
pleural effsuion
Nonpulmonary causes of increased respiratory rate in foals
fever
pain
excitement
exercise
brain disease
compensatory response to metabolic acidosis
idiopathic or transietn tachypnea syndrome
Foals with erratic breathing patterns due to CNS disease, m ay require use of what?
respiratory stimulants (doxapram, caffeine)
mechanical ventilation
List uncommon causes of stertorous breathing or respiratory distress in foals to consider
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
crepitus of subcu tissues on the thorax is indicative of
leakage from respiratory tissues, most commonly from ruptured pulmonary bullae
**possible rib fracture
What are potential complications of rib fracture in a foal?
hemothorax
lung laceration
pneumothorax
pericardial/myocardial puncture
Causes of hypoxemia
- hypoventilation
- ventilation/perfusion mismatch
- right to left shuntting of blood
What are possible complications of umbilical herniations in foals, howver rare?
colic
enterocutaneous fistulae
umbilical abscessation
intesinal incarceration
Brix guidelines for colostrum quality in mares
- 0-15% Brix, 0 to 28 gm/L IgG= poor quality
- 15 to 20% brix, 28 to 50 gm/L IgG, borderline quality
- 20 to 30% Brix, 50 to 80 gm/L IgG, adequat quality
- > 30% BrIX, greaterthan 80 gm/L igG, very good quality
What is the recommended mimimum dose of colostrum in foals?
min dose of 60 to 90 gm/L of IgG in the first 6 hours after birth
baseline glucose values in foals should be what level after parturition?
Should be 50% of mares glucose and reach a low approx 2 hours after birth
How long can you wait to measure L-lactate measurements?
10 minutes
**otherwise red blood cells conitnue to rpoduce lactate in a lithium heparin tube
If foals have an elevated creatinine post birth associated with perinatal asphyxia syndrome (PAS), when should these decrease?
W/in 24 hours, and values should halve
Signs of clinical hypocalcemia:
tachycardia
sweating
tremor
muscular rigidity
stiff gait
recumbency
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?
30% with septic arthritis
48% with septic osteomyelitis
Prognosis for athletic performance with septic arthritis/osteomyelitis depends on what factors?
number of joints affected
numbe rof bones involved
age of the foal
presence of other medical problems
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?
2 weeks of age
common joints: carpus, stifle, hock
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?
3 to 4 weeks fo age
common sites: femoral condyles, distsal radius, distal tibia, patella
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
foals 1 to 12 weeks of age
common sites: distal radius or tibia, distal metacarpi/tarsi
Septic arthritis/osteomyelitis:
tarsal: classification describes osteomyelitis of what bones?
tarsus or carpus
What are common predisposing causes to joint and bone infections in neonates?
-persistent or transietn heamtogenous dissemination of bacteria from distant sites of infection:
-GI
-respiratory
-umbilical infection
-failure of passive transfer
Septic arthritis/osteomyelitis:
Common bacteria isolated
Enterbacteriaceae (E. coli_
Salmonella
Actinobacillus equuli
Klebsillaspp
Streptococcus
Rhodococcus equi
IN Septic arthritis/osteomyelitis, why do bacteria end up there?
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)
Why is physeal infection more likely to occur at 7 to 10 days of age?
closure of the transphyseal vessles
–> localization of the ifnection in metahphyseal vessel loops
Differentials for lameness in foals
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
Consistent and early clinical signs of joint sepsis is what:
effusion
other commonly reported: periarticular swelling, heat, pain on palpation of the bone or joint and restricted passive movement of the joint
Is hyperfibrinogenemia and leukocytosis sensitive for the septic arthritis/osteomyelitis?
No
Normal synovial fluid parameters:
TP <2.0 g/dL
TNCC <10,000 cells/microL
Neutrophils <10%
What can cause an increase in TNCC and TP of synovial fluid but percentage of neutrophils remains less than 80%?
sympathetic synovitis (fomr increase dblood flow to a region)
What is the percentage of bone infection in foals with septic arthritis?
38 to 80%
Radiographic changes of bone sepsis are not evident until how many days after the onset of infection?
7 to 10 days:
- joint space narrowing
-articular cartilage destruction
-periosteal reaction
-subchondral bone osteolysis
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?
62.4% gram negative
37.5% gram positive
If osteomyelitis is present, how long should foals be on antibiotic therapy for?
up to 2 months
Common antibiotics used for intraarticular injections in tx of septic arhtritis?
gentamicin (500 mg)
amikacin (125 to 250 mg)
ceftiofur sodium (125 to 500 mg)
For regional limb perfusion. How long should a tourniquet be left onf or?
at least 30 minutes wiht a max of 60 minutes total tourniquet application
What is the reported short term survival (to discharge) in foals with septic osteomyelitis?
71 to 81%
What is the prognosis for future athletic performance in foals with septic osteomyelitis
30 to 48%
What are common sites of fractures in the distal limbs of foals?
distal phalanx
physeal fractures of the first phalanx
proximal sesamoid bones
What is the most common fracture of the upper limb in foals?
olecranon
Signs of gastrocnemius rupture in foals
hyperflexion of the hock and extension of the stifle
Which foals are likely to have incomplete ossification of cuboidal bones at birth?
twins
premature foals
foals that are small for gestational age
foals with in utero acquired infection
hypothyroidism has been associated with what musculoskeletal abnormalities in foals?
angular limb deformities
contracted tendons
tarsal bone collapse
Foals have a higher or lower seizure threshold than adults?
foals lower than adults
Where are seizures generated?
by abnromal electrical acitivty w/inteh cerebral cortex
What are characateristics of generalized seizures:
recumbency
widespread involuntary muscle activity
paddling of the limbs
extensor rigidity
Differentiate REM sleep from seizure activity?
a foal in REM sleep should be easily aroused
Common bacterial agents of meningitis in foals?
Escherichia coli
Enerobacter spp
Salmonella sppsreptococcal spp
Definitive diagnosis of meningitis
CSF analysis: neutrophilic pleocytosis
Antibiotic recommendations for treatment of meningitis?
3rd generation cephalosporins (cefotoxaime or ceftriazone)
**base don culture adn sensitivty
Prognosis for survival of bacterial meningitis?
fair- if signs are limited to hyperesthesia and neck stiffness
poor-otherwise
Benign juvenile epilepsy is described in what breed?
Arabian foals of Eqgyptian origin
Benign juvenile epilepsy resolves after what age?
usually by 12 months of age in all foals
Benign juvenile epilepsy can be treated with what medications?
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)
Seizure disorders should have rule outs of
hypoglycemia
electrolyte abnormalities (Low Ca, Na, or High Na)
What is the msot common congeital brain disease in foals?
hydrocephalus
Clinical signs of tetanus are not likely before what age of foal?
prior to 7 days
Clinical signs of tetanus in foals?
difficulty lcoating and latching onto the teat
dysphagia
gait siffness
elevation fo the tail head
anxious facial expression
prolapse of third eyelid
tachycardia
sweating
When is it recommended that mares receive a booster of tetanus toxoid?
approximately 28 days before esitmated parution
What are reported signs of ivermectin toxicity
obtudnation
blindness
ataxia
head pressing
seizure
Clinical signs of ivermectin toxicity are caused by:
opening of the GABA-gated chloride channels with resultant membrane hyperpolarization and blockage of neuronal impulses
Successful management of ivermectin toxicosis incldues:
IV lipid emulsions (20% soybean oil in water, 1.5 ml/kg bolus, followed by 0.25 ml/kg/min for 30 minutes)
kernicterus results from deposition of what in the brain?
**particularly within the basal ganglia , cornua ammonis and substantia nigra
bilirubin IX alpha
At what serum bilirubin concentration are foals at risk for devvelopment of kernicterus?
> 27.0 mg/dL
Lavender foal syndrome is also referred to as
coat color dilution lethal (CCDL)
Describe lavender foal syndrome
autosomal recessive gene disorder of Arabian foals of Egyptian bloodlines
Lavender foal syndrome is caused by what gene mutation?
frameshift single base mutation in exon 30 of the myosin-Va gene (mYO5a) resulting in premature termination of transcription
**primary homozygous foals
foals affected with lavender foal syndrome have clinical signs of:
unable to achieve sternal recumbency
severe neuro signs: frequent episodes of opisthotonus, limb paddling, rapid eye movements
death (w/in 72 hours of age)
What is the carrier frequency of LFS in teh US
10.3% in Egyptian Arabians
1.8% in non-Egyptian Arabians
Glycogen storage disease IV
**describe the disease
auosomal recesive disease of Quarter Horses adn PainHorse breeds
Glycogen storage disease mutation occurs where?
glycogen branching enzyme, encoded by the GBE1 gene
Clinical signs of foals with Glycogen storage disease
still born or aborted
profound muscular weakness and hypothermia
hypoglycemic seizures or cardiopulmonary failure
**all foals died or euthanized by 18 wks of age
causes of anemia in foals: hemolysis
neonatal isoerythrolysis
less common causes:
-non-NI immune mediated hemolysis
-intracellular RBC parasites
-rapid administration of hypotonic or hypertonic solutions (DMSO)
-equine infectious anemia
A syndrome of anemia and B-cell lymphopenia reported in what breed?
Fell ponies
A foal is considered premature at what age of gestation?
born before 320 days
premature foals typically have problems maintaining what:
body temperature
blood pressure
blood glucose
The average relative weight of the term foal to its dam is around what percentage?
10%
postterm or post mature foals will have
erupted incsors
long hair coat
pregnant mares consumption of tall fescue pasture infected with Neotyphodium coenophialum leads to a range of abnormal signs including:
prolongation of gestation
perinatal mortality
agalactia
What hormone is critical for organ maturation in the fetus?
cortisol
**too much– or too early= intrauterine growth restriction
How is the fetus protected from cortisol during gestation?
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
During the majority of gestation the major produts of seroidogenesis are:
progesterone
5alpha-reduced progestagens
**not cortisol
What are the triggers for the process that results in fetal cortisol production, organ maturation and birth?
unkown
Which hormones are critical for lung maturation in the new born (particularly reabsorption of lung liquid)?
**cortisol
**T3
What are factors that can induce premature maturation of the fetal HPA axis?
hypoxemia
exogenous glucocorticoids
poor nutrition before/after conception
placenta and/or fetal infection
** stimuli in foals has not been well described
What does HPA stand for?
Hypothalamic-Pituitary-Adrenal Axis
lung surfactant is usually fully developed in foals at what gestational age?
300 days
** but could be delayed until after 340 days in some foals
What is the most severe form of respiratory failure in neonatal foals?
neonatal respiratory distress syndrome (RDS)
– characterized by progressive resp failure, sever hypoxemia, hypercapnia and death
The effects of dopamine are dose dependent, including:
- 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
- moderate doses (4 to 10 microg/kg/min) simulate Beta1 adrenergic receptors and result in chronotropy
- High dose dopamine (>10 microg/kg/min) cause agonist of alpha 1 adrenergic receptors lead to widespread vasoconstfction
Dobutamine at 3 to 20 microg/kg/min acts primarily on what receptors?
beta 1 adrenoreceptors– producing an improvement in myocardial contractility without vasoconstriction
Thermogenic mechanisms develop late in gestation and are rleated to circulating levels of?
T3
Problems with thermogenesis are exacerbate din preterm foals because of what?
incomplete adrenal function
Why is coughing uncommon in neonatal foals with respiratory disease?
postnatal delay in maturation of irritant receptors w/in airways
delayed onset of laryngopharyngeal cough reflex
What is the danger of giving of giving foals sodium bicarboante to foals with pulmonary disease?
can exacerbate hypercapnia
Chornic hypercapnia vs acute hypercapnia
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
Congenital defects of the upper respiratory tract include
collapsed trachea
stenotic anres
choanal atresia
epiglottal cyst
guttural pouch tympany
causes of laryngeal paralysis in foals
nutritional myodegeneration
hyperkaelmic periodic parlaysis
botulism
In foals with HYPP what clinical signs are seen
exercise and excitement induced respiratory stridor
Collapsed trachea is a rare congenital or acquired condition most commonly reported in what breed?
American miniature horses
The most common bacterial isolates that are associate with pulmonary diseasein foals include
E coli
Klebsiella pneumoniae
Pasturella sppactinobacillus spp
Streptococci spp
Why does positioning foals in sternal vs lateral recumbency better in foals with respiratory disease?
the neontal foal readly develops depedent atelectasis in lateral recumebncy
**imporved ventilatory acapacity and higher arterial oxgyen tension
Outcome for neonatal pneumonia due to EHV-1?
frequently fatal
meconium aspiration can result in
regional air trapping
chemical pneumonitis
alveolitis
alveolar edema
displacement of surfactant–> dec lung compliance, small airway obstruction and focal atelectasis
When is the best time to suction airways if known meconium impaction?
in the birth canal prior to taking its first breath
**nasotracheal intubation and carefuls uction reocmmended
Radiographs of a foal that has aspirated meconium show:
ventrocranial distribution of pulmonary infiltrate characteristic of aspiration
Milk aspiration can occur in foals with what dz processes
cleft palate
persistent dorsal displacement of the soft palate (DDSP)
botulism
neonatal encpalopathy
generalized weakness d/t sepsis
prematurity
iatreogenic (bottle feeding)
Causes of pneumothorax in foals
positive pressure ventilation of dzed lungs
birth trauma
rif fracture
ruptured bullae w/in lung parenchyma
During mechanical ventilation, if the a foals respiratory condition suddenly worsens, what should be considered
uneven alveoalr ventilated that leads to aolveolar rupture and dissection fo air into the interstitium
What is required to confirm diagnosis of pneumothorax?
radiographs
Why after removal the abdominal fluid from a uroperitoneum can foals develop tachypnea, tachycardia, hypercapnia and hypoxemia?
due to re-expansion pulmonary edema
**if thoracic fluid is present with uroperitoneum
What is transient tachypnea in teh neonate?
self limiting and speculated to be associated with central or peripheral control of thermoregulation and or respiratory rate and pattern
Transtracheal O2 delivery may be beneficial in which foals?
-larger foals
-hypoxemia in neonatal foals with a rapid, shallow breathing pattern
-foals with severe pulmonary disease that are unresponsive to nasal insufflation
