Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CAEM Pt. 2 > Exam #4: Equine Neonatology > Flashcards

Exam #4: Equine Neonatology Flashcards

1
Q

Are dystocias more/less common in horses, compared to cattle?

A

Less common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What should you do during foaling and post-foaling?

A
  • Leave the mare alone during foaling, she may stop if you interfere
  • 2nd stage labor = only 15-30 min
  • Important time for bonding, placental passage, and umbilical blood transfer
  • At most = clear nostrils and remove amnion from head
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the 1-2-3 rule with foals? (and other standards)

A

> Standards for foals post-foaling

1) Standing with 1 HOUR
2) Nurse by 2 HOURS
3) Pass meconium by 3 HOURS
* Mares may be coprophagic and eat meconium

  • Lie sternal by 10 minutes
  • Suckle by 20 min
  • Urinate by 8 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Normal TPR of a newborn foal

A

> HR:

  • 1 min = 60-80 bpm
  • 15 min = 120-160 bpm
  • 12 hours = 80-120 bpm

> RR:

  • 1 min = rapid and shallow
  • 15 min = 40-60 bpm
  • 12 hours = 20-30 bpm

> Temp:

  • 1 min = 99-100 F
  • 12 hrs = 100-101 F
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Are twisted umbilical cords problematic after foaling?

A

No - only if there’s a large degree of twisting or active hemorrhage

Small amounts of bleeding comes from the PLACENTA, not the mare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Common foal behavior - activity level, nursing freq, urination

A
  • Very playful, usually by 2-4 hours of age
  • Spend 1/3 of life sleeping
  • Nurse frequently = 4-6 times/hr
  • Urinate often (clear in color)
  • Defecate up to 5-6 times per day
    • Mares are coprophagic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is APGAR scoring and why is it helpful?

A
  • Good SCREENING TOOL = only really used immediately post-foaling and for veterinarian-witnessed high risk foals
  • Done at birth, 5, 10, and 15 min post parturition
  • Based on HR, RR, muscle tone, nasal stimulation w/ straw up nose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Should you sever the umbilical cord quickly after foaling?

A

NO - approx. 1/3 of the foals blood is still transferring from the placenta following vaginal expulsion of the fetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

True or false - you should be concerned with hemorrhage from the maternal stump of the umbilical cord

A

FALSE - coming from the placenta, not the maternal circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What should you always do following placental expulsion?

A

Examine the fetus to ensure it passed, and weight it (edema and discoloring = signs of a high risk foal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What and how often should you dip the umbilical stump of a foal?

A
  • In 0.5-2% chlorhex (NO MORE than 10%)
  • No more than 2-3 days on first day

*Contamination of stump comes from dirty foaling environment or failure of passive transfer = what dipping CAN’T fix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Problems with maiden and older mares and colostrum production

A
  • Maiden mares = produce lower volumes, may be unruly, watch for foal safety
  • Older mares = may have dripped and lost quality/quantity (lowers IgG)
  • Systemic illness, fescue infestation may decrease colostrum volume (Southern US)

> Contains cells, complement, lactoferrin, fat, IgG, IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Quantity and suggestions for foal colostrum ingestion

A

> 2-3 L of good quality colostrum by 8 hours of age
Aim for IgG > 800 mg/dl
- Colostrum SG > 1.060
- Good idea to have frozen/banked colostrum
- Store at -20C for 1-2 seasons
*Tube if necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Things to include in a new foal exam

A

> Examine by 24-48 hours of age if apparently healthy (if not = sooner)
1) TPR
2) Full PE
3) Search for congenital defects = heart, palate, hernias (scrotal, inguinal, umbilical)
4) Semi-quantitative blood test for failure of passive transfer (> 800 mg/dl)
+/- Regional injections of Se/vit-E

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When do we sample for passive transfer and what are our cut-offs?

A

> Gold standard = RID (not done)
- 12-24 hours of age = before gut closes
> GOAL = IgG = 800 mg/dl
- IgG = 400-800 mg/dl = partial passive transfer
- IgG < 400 mg/dl - failure of passive transfer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the most common cause of death in the first week of a foal’s life?

A

Septicemia (usually due to failure of passive transfer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Treatment of failure of passive transfer

A
  • Best option = hyperimmune plasma
  • Whole blood transfusions
    +/- Prophylactic antibiotics for 5-7 days

*MONITOR CLOSELY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Dx? Lethargic foal, increased lying time and apparent sleeping, diminished nursing frequency/vigor, petechiation, systemic signs (seizures, hypopyon, diarrhea, pneumonia, joint swelling, lameness)

A

Septicemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

True or false - TPR is a reliable clinical sign of septicemia in foals

A

FALSE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

True or false - mucous membrane color and CRT is a reliable clinical sign of septicemia in foals

A

FALSE - variable, look for petechiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What organ system(s) should you always exam (that is often missed) in foals? (2)

A

1) OPHTHO EXAM - looking for hyphemia, hypopyon, uveitis (miosis, aqueous flare)
2) JOINT exam - examine elbows/stifles (joint dz occurs late in septicemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Clin path abnormalities with foal septicemia (9)

A

> HELPFUL info for septic foals

  • Leukogram = leukopenia, neutropenia, degenerative left shift
  • Hyperfibrinogemia
  • Low to absent IgG levels
  • Positive blood cultures (aerobic and anaerobic)
  • Azotemia = keep an eye on RENAL function
  • Hypoglycemia = glucose metabolism dysfunction
  • Electrolyte abnormalities
  • Elevated muscle enzymes
  • Liver function tests (uncommon cause of death)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Antibiotic choices for septicemic foals based on creatinine levels

A
  • Creatinine < 5 mg/dl = K penicillin (beta lactam, gram + and anaerobes), amikacin (aminoglycoside, gram -)
  • Creatinine > 5 mg/dl = K penicillin and cefazolin
    • Requires a greater gram neg coverage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Septicemic therapy for foals

A

> Hospitalization!!

  • Antibiotics = broad spectrum, IV (< 5 Cr = K pen and amikacin, > 5 Cr = K pen and cefazolin)
  • PLASMA = 1-2 L = critically important
  • Fluid therapy
  • Enteral therapy = lytes, acid/base correction, glucose
  • Anti-endotoxic flunixin banamine
  • Adjunct tx = seizure control, eye meds (commonly hurt w/ seizures), cardiac/respiratory support
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Prognosis for septicemia

A

> POOR

  • Average = 65%
  • Truly bacteremic = 50/50
  • Expensive - PREVENT, DON’T TREAT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Cause of dummy foal syndrome

A

> Hypoxic ischemic encephalopathy , perinatal asphyxia syndrome, neonatal maladjstment syndrome

  • Due to hypoxia and ischemia during birth = impaired perfusion to cells or tissues
  • Many are due to dystocia, but can occur in unwitnessed deliveries
  • BE SUSPICIOUS of other organ involvement = brain (muscle can use anaerobic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Pathology of HIE or dummy foal syndrome

A

> Hypoxia initiates metabolic cascades in brain
- Decreased energy production
- Ion dysregulation
- Increased concentrations of excitatory NT’s (glutamate, asparate)
- Impaired protein synthesis
Increased in intracellular Ca++ = leads to neuronal injury
Others = pro-inflam cytokines, O2-free radicals, nitric oxide
*Inflammatory cytokines can initiate similar cascades, like in meningitis or brain injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Clinical signs of hypoxic ischemic encephalopathy

A
  • Foals often appear normal at birth
  • Signs begin several hours –> 2 hrs after delivery
    + Can’t find udder or suckle inanimate objects
    + Loss of recognition of mare
    + Odd tongue movements
    + Wanders/walks into walls
    + Can’t/won’t lay down
    + Seizures - generalized, local
    + Anuria or colic if intestinal or kidney involvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Tx of hypoxic ischemic encephalopathy (6)

A

> Supportive = minimize hypoxia and neuronal edema
Prevent hypoglycemia, sepsis, self trauma
(1) CONSERVATIVE fluid tx = maintain hydration and renal perfusion, acid-base, lyte levels
(2) Glucose admin = decrease cerebral infarct, neuroprotective (stimulates insulin release and decreases glycosis and injury
(3) Control seizures = benzodiazepines or barbituates (if irresponsive
(4) Reduce cerebral edema = thiamine, Mg sulfate (decreased secondary neuron death), +/- mannitol (CAREFUL if you suspect head injury), +/- DMSO
(5) O2 supplementation = target 100-150 mm Hg PaO2
(6) Vit-C = antioxidant
+/- Parenteral feeding = rests GI tract, reduce ileus complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Prognosis for dummy foals

A
  • Good with proper support (70-75%)
  • Poorer prognosis with sepsis, no neuro improvement w/in 5 days of life, dysmature/premature foals with prolonged hypoxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

CNS sequelae to CNS hypoxia

A
  • Docile in nature
  • Decreased vision
  • Seizures = can grow out of it
  • Spasticity = can grow out of it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

DDx for foal seizuring (3)

A

1) Hypoglycemia
2) Septicemia
3) Dummy foal - hypoxia ischemic encephalopathy

  • Hypoxia
  • Encephalitis
  • Fever
  • Hyponatremia
  • Hypernatremia
  • Prematurity
  • Neonatal isoerytholysis
  • Liver disease
  • Head trauma
  • Congenital malformation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Things to keep in mind about the menace response in foals (and other neuro exam in foals)

A

Menace reflex = ABSENT until 2 weeks of age (may or may not have vision)

  • Normally hypersensitive to stimuli or face/nose
  • Mentation
  • General behavior
  • CN exam
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Dx? Normal foal at birth, then at 24-36 hours = weak, depressed, decreased suckling, profound icterus, rapid/shallow breathing, tachycardia, seizures (kernicterus), anemia, +/- dark urine, death

A

Neonatal isoerythrolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What causes the dark urine in neonatal isoerythrolysis cases?

A

Pigment nephropathy from the hemoglobin pigment after hemolysis

36
Q

What causes the rapid/shallow breathing and tachycardia in neonatal isoerythrolysis cases?

A

Progressive anemia from hemolysis

37
Q

Pathology behind neonatal isoerythrolysis

A

> Hemolytic anemia of the newborn foal = most common cause of jaundice in the foal
- Foal’s RBC’s are destroyed by the alloantibodies received from the dam’s colostrum
*Occurs with multiparous (sensitized at birth) or previously sensitized dams (previous plasma transfusions)
- Most commonly occurs in mules (10%), STB (2%), TB (1%)
RBC antigen inherited from sire = donkey factor or Aa Qa blood type in horse

38
Q

Treatment of neonatal isoerythrolysis

A
  • Prevent stress = already anoxic/anemic
  • Blood transfusion if PCV is severly low (>20% = not necessary)
    • 1-2 L whole blood, mare/gelding not previously bred
  • Fluid therapy for pigment nephropathy
  • Alternative parenteral nutrition (not suckling)
  • Milk out mare and discard the remaining colostrum = dilutes out any remaining colostrum
  • Keep foal from nursing for 24-36 hours
  • Steroids = not helpful, process has already occurred
39
Q

Prevention of neonatal isoerytholysis

A

> Plan ahead = test parents before breeding
- Mare-side test = agglutination between umbilical blood and mare’s colostrum (not a great test, doesn’t test for hemolysis)

> If you know there will be a problem:

  • Don’t allow the foal to drink the colostrum
  • Use donor colostrum or plasma
  • Discard mare colostrum
  • Feed foal milk replacer for the first 24-36 hours of life

*Do not totally separate = they need to BOND

40
Q

Dx? Petechiation, ulcerative skin lesions (commonly on the head), oral ulcers –> in a foal commonly 7 days or older

A

Alloimmune thrombocytopenia (rarer than NI)

41
Q

Pathophysiology behind alloimmune thrombocytopenia

A

Alloimmune antibiodies directed against the foal’s platelets, risk spontaneous hemorrhage < 30,000

Rare - but more common in TB’s, Arabians, and QH

42
Q

Treatment of alloimmune thrombocytopenia

A
  • Whole blood transfusions (RBC’s and platelets)
  • Corticosteroids = older foals are more resilient to the immunosuppression of steroids (usually don’t get better w/o it)
43
Q

Congenital malformations to keep in mind in neonatal foals

A

> Craniofacial = palate defects (milk out nose), wry nose
CNS = an/hydrocephaly (Mini horses), cerebellar malformation (heritable in Arabs, intention tremors)
Ophtho = cataracts, entropion (can be acquired in sick foals, catabolize orbital fat pad), Rocky Mountain horses
GI = atresia ani/recti/coli, Lethal White syndrome (colicky, agangliosis)
Hernias = scrotal, inguinal, umbilical
M/S = angular limb deformities, etc
Skin = epitheliogenesis imperfecta, hyperelastosis cutis (HERDA in QH’s)
Cardiac = VSD, any murmur that persists and is high grade, on the right
Urinary = ectopic ureters, polycystic kidneys, renal cysts
Repro = intersex, hermaphroditism

44
Q

Things to remember about the hearts of newborn foals

A

> All foals are born with a PDA
- Closes during the first 48 hours of life
+ Left heart base, soft systolic murmur (grade I or II)

45
Q

Pathophys behind SCIDS

A

> Severe combined immunodeficiency syndrome
- Lack IgG and IgM synthesis = susceptible to infection
- Lack protein kinase = deficiency in B/T lymphocytes
- Autosomal recessive condition of foals to two heterozygote Arab carriers (usually asymptomatic)
+ Normal at birth, but diet by 3-5 months of age, may die sooner if FPT occurs (sepsis, recurrent bacterial/viral infections)

46
Q

Diagnosis of SCIDS

A

> Blood tests

  • Absent IgM after 3 weeks of age (ensure they’re not maternal Ab’s) or pre-colostrum admin
  • CBC = severe and persistent lymphopenia
  • Genetic testing to ID/confirm foals or carrier adults
47
Q

Causative organisms of diarrhea, in a foal 7-10 days old (4-5)

A

1) Part of neonatal septicemia = both a manifestation of sepsis or a cause of sepsis
2) Clostridial enteritis
3) Salmonellosis (any age)
4) Others = Bacteroides fragilis, E. coli (rare)
5) Foal heat diarrhea

48
Q

Causative organisms of diarrhea, in a foal > 10 days old (6)

A

1) Salmonellosis (any age)
2) Rotavirus = 1-6 weeks
3) Lawsonia intracellularis = proliferative enteropathy, common if co-housed near pigs
4) Rhodococcus equi = 3-6 mo, commonly manifests as resp dz but can uncommonly show GI signs
5) Antibiotic-induced
6) Others = nutritional, protozoal, parasites

*Often difficult to ID the causative organism as the animal gets older

49
Q

Source and serotype of Salmonella in neonates (< 7 days) and older foals

A

> Foals < 7 days = from dam or foaling environment, can be any serotype, passive transfer doesn’t guarantee the foal won’t be infected
*High risk for true bacteremia = SIRS, MODS, DIC, death

> Older foals > 10 days = from mares, other horses, environment (can be endemic), any serotype (enterica Typhimurium is most common)
*Still potentially fatal, but mortality risk decreases with age

50
Q

Diagnosis of Salmonellosis

A
  • Blood culture
  • Joint culture
  • Series of fecal cultures
  • Use the correct media = doesn’t grow well in competition with other bugs

*PCR isn’t helpful = don’t know if it’s a viable/contagious pathogen if positive

51
Q

Treatment of neonatal salmonellosis

A

> Approach like any other septic foal

  • Fluids
  • Plasma
  • Antibiotics
  • Anti-endotoxic banamine
  • Usually requires hospitalization
52
Q

Treatment of older foal salmonellosis (not a neonate)

A

> Lower mortality rates, but still at risk for bacteremia and sepsis

  • Fluids
  • NSAID’s, Ex banamine
  • Plasma
  • Antibiotics
  • Anti-ulcer meds, Ex: omeprazole
53
Q

Do we have a vax for Salmonella in foals?

A

No - no licensed or available vax, may borrow from food animal but no proven efficacy

*Can try autogenous vax for Salmonella or Clostridial pathogens, vax pregnant mares and vax foals > 3-4 months when they’re not getting colostrum anymore

54
Q

How long is a horse shedding Salmonella when infected?

A

Minimally 1 month, but up to 6 months

55
Q

Is there host adapted form of Salmonella in horses (Ex: dublin in cattle)?

A

No

56
Q

Prevention of salmonellosis on endemic arms

A
  • Ensure passive transfer
  • Impose biosecurity
  • Disinfect with phenols, quaternary ammonium compounds w/ adequate drying time
  • Manure disposal (NOT ON THE FIELDS) - burn or throw in trash
57
Q

Dx? Colic and abdominal pain in a neonatal foal (7-10 days), ileus, GI distension, rapid progression to bloody diarrhea

A

Clostridial diarrhea

58
Q

Etiology of Clostridial infections in foals

A

> Clostridium perfringens type A «< C
- Type C = more common, higher mortality

> C. diff = not a commensal org, but not all animals that are infected develop enteritis
Other anaerobes = Bacteroides fragillis

59
Q

Why are HIE foals at risk for necrotizing enterocolitis?

A

Foals are already hypoxemic/ischemic = have low circulating O2 levels that make them at risk for anaerobes to proliferate (Bacteroides, Clostridium, etc)

60
Q

Diagnosis of Clostridial diarrhea

A

> Difficult to say if it’s pathogenic or commensal

  • Fecal grams stain w/ gram + rods
  • Toxin assays (esp for C. diff)
  • Anaerobic culture

*Fecal stain + clinical signs = presumptive diagnosis for tx

61
Q

Tx of Clostridial diarrhea

A
  • Oral metronidazole TID
  • High doses of crystalline penicillin IV
  • Sepsis tx = anti-endotoxin, fluids, enteral therapy, plasma transfusion
62
Q

Dx? Foal > 1 week of age, watery/green/bubbly diarrhea, no blood, low mortality, fever, depressed –> may grow out of it but have ill thrift or weakness

A

Rotavirus diarrhea - HIGHLY CONTAGIOUS

63
Q

When does rotaviral diarrhea commonly occur in foals?

A

1-6 weeks - HIGHLY CONTAGIOUS

64
Q

Dx of rotaviral diarrhea

A
  • Gold standard = electron microscopy
  • Viral particles only present in feces for 48-72 hours (not widely shed)
  • PCR&raquo_space; sensitive than ELISA
65
Q

What clin path values are common with rotaviral diarrhea?

A
  • Significant hyponatremia (enteral and fluid loss)
  • Hypochloremia
  • Mild pre-renal azotemia
  • Marked metabolic ACIDOSIS
66
Q

Tx of rotaviral diarrhea

A
  • IV fluids = crystalloids + KCl + BICARB, given bolused QID then BID
    +/- Oral bicarb (cheaper than IV)
    *ANTI-ULCER meds = Ex: raniditine, omeprazole
  • Keep the perineum clean
67
Q

Prevention and control of rotaviral diarrhea

A
  • Strict biosecurity - VERY CONTAGIOUS, change clothing between patients
  • Disinfect with phenols (works with organic material)
  • Consider phase 2 = detergent first, dry, then disinfectant
  • Minimum 20-min contact time = MAKE SURE IT DRIES

> Vax dam at 8, 9, 10 mo of gestation = prob only helpful on endemic farms

68
Q

Protozoal etiologic agents in diarrhea, tx?

A

> Cryto parvum = outbreaks in mixed animal hospitals, usually self-limiting
- Tx = none, nitrazoxanide?

> Giardia and Eimeria in normal foals = cause problems in immunocompromised foals
- Tx = fenbendazole, sulfas for Eimeria

69
Q

What is foal heat diarrhea?

A

> Occurs at 11-12 days of age
+ Self limiting and mild diarrhea
+ Usually DON’T go off feed or stop nursing
*Associated with when the mare is going through her first postpartum heat
- Tx = no need

70
Q

Are parasitic, nutritional, or antibiotic-induced diarrhea common in foals?

A
  • Parasitic = not an issue w/ enteritis, Strongyloides westeri = historical problem
  • Nutritional = plausible, but self-limiting
  • Antibiotic-induced, usually after R. equi treatment (affects the MARE more than the foal)
71
Q

General timeline of diarrhea etiologic agents over time in foals

A
  • First week (< 7 days) = Salmonella, anaerobes (Bacteroides, Clostridia)
  • Older (> 10 days) = Salmonella, rotaviral
  • Even older (> 1 month) = difficult to find a cause
72
Q

What diagnostic tool is helpful in differentiating obstructive versus infectious enteritis in foals?

A

Ultrasound

73
Q

General treatment of neonatal diarrhea in foals (9)

A

1) Fluids = isotonic +/- dextrose, KCl, bicarb
2) 1 L of plasma (PLE w/ diarrhea)
3) Antibiotics = pencillin (K pen) + aminoglycosides empirically, then culture based later, metronidazole
4) Anti-endotoxin banamine
5) Feeding = may not allow to nurse if colicky, if not = feeding tube or enteral nutrition
6) Anti-ulcer meds (proton pump inhibitors > H-antagonists)
7) +/- Probiotics
8) Lactase = lactose intolerance (common with rotavirus)
9) Plasma if septic
- People use bismuth subsalicylate and kaolin/kaepectate as an adsorbent, no evidence

Smectite = biosponge, adsorbing power against Clostridia and rotaviral infections

74
Q

Essential portions of the respiratory exam in a neonate, other non-essential tests

A

1) Palpation of ribs along costochondral junction for fractures (widest portion in violent 2nd stage labor)
2) Demo of bilateral nasal flow
3) Palpation of cervical trachea - collapsed? induces a cough?
4) Pulmonary auscultation - preferred in sternal/standing (lateral can show false congestion)
5) Rebreathing = hold off nostril then relisten, accentuates subtle differences

Others = imaging (x-ray w/ FL’s extended forward, U/S), arterial blood gas (lateral metatarsal a.)

75
Q

Causes of respiratory disease in neonates

A

1) Pneumonia = hematogenous/septic, primary bacterial or viral
2) Atelectasis in premature foals
3) Pulmonary hemorrhage from rib fractures
4) Hyaline membrane disease - insufficient or consumed surfactant (chronic/severe lung dz = surfactant gets used up)
4) Aspiration of meconium or milk = common in sick/weak neonates
* LET THEM NURSE, unless they’re sick tachypneic and dyspneic foals have a hard time protecting their airway

Rare = pulmonary edema or pneumothorax

76
Q

General tx of neonatal respiratory dz

A
  • Broad spectrum antibiotics (like in sepsis)
  • NSAID’s
  • Supportive fluid and colloid tx
  • Plasma if you suspect failure of passive transfer
  • Feeding tube or parenteral feeding if you fear aspiration
  • O2 therapy = shooting for 70-120 mm Hg
  • Surfactant in premature animals
  • Nursing care = constant turning, sternal support, coupage, nebulization
  • RARE = ventilation
77
Q

Common cause of pneumonia in foals 2-5 months of age (infection begins much early, but this is when they should clinical signs)

A

Rhodoccus equi - occurs worldwide, endemic in some areas

*Hot and dusty places (not really WI)

78
Q

Dx? Tachypnea, tachycardia, fever, diarrhea, uveitis (aqueous flare, miosis), synovitis, polyarthritis (joint effusion), abscesses (likes lungs, LN’s, abdomen)

A

Rhodoccus equi

79
Q

Diagnostics for R. equi

A

+ Clinical signs, esp from endemic farms
- Transtracheal wash via endoscope or percutaneous
+/- Rads = not very helpful, may see interstitial fluffy/cotton infiltrates
**U/S = easy to see peripheral abscesses, discontinuity in pleural shadowing

  • Serology = NOT helpful
80
Q

Treatment of R. equi

A
  • Antibiotics = clarithryomycin + rifampin
    • Others = azi/erythromycin (macrolides)
  • Treat until resolution of leukocytosis and hyperfibrinogenemia, rad or U/S resolution, or COMBOS
  • Mean tx = 6-7 weeks
  • Tx until clinical signs resolve = NOT a good idea, improve clinically before medically
81
Q

Control of R. equi on endemic farms

A

> Decreasing environmental challenge = avoid dry/dusty environments, overcrowding, remove manure, wet paddock, rotate pastures
Early recognition and tx = WBC is the most sensitive indicator (> 14,000)
PASSIVE TRANSFER, often with hyperimmune plasma before 1 mo of age (BEFORE exposure)
*1 L in first week
*1 L between 30-50 days old

82
Q

Prognosis of R. equi foals

A

If they get over it = return to performance is good

83
Q

When do foals first become infected with R. equi?

A

First 1-2 weeks of life

*Don’t develop signs until 2-5 months

84
Q

Do we have R. equi vax?

A

NO - foals can’t develop a sufficient response < 2 weeks of age, also usually diagnosed at > 2 mo of age

85
Q

Things field practitioners can do if they suspect sepsis in a foal

A
  • Consider them an emergency (< 1 week of age) = respond promptly because they progress quickly
  • Assume sepsis is likely if < 96 hours old
  • Don’t hesitate to refer
  • DON’T let neonates ride with dam in trailer = consider bringing foal first, mare later
  • Keep them warm
  • Give them glucose support (dextrose IV)

CAEM Pt. 2 (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions