Problems of the Pregnant Mare Flashcards

1
Q

describe the pathogenesis of placentitis

A
  1. entrance of pathogen: via service or hematogenous or diffuse into placenta
    -pathogen can enter fetus through umbilicus or mouth and cause amnion inflammation
  2. pathogen causes inflammation, which causes hypoxia and growth retardation, as well as production of cytokines and prostaglandins, which can cause premature contractions and premature fetal development (fetus releases cortisol before actually ready to be born)
  3. can lead to fetal death or fetal septicemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe ascending placentitis

A
  1. most common; localized around cervical star
  2. due to strep equi zooepidemicus and E. coli most commonly!! and aspergillus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

describe diffuse placentitis

A
  1. affects entire placenta:
    -amnionitis
    -funisitis
    -changes in choroallantois
  2. most commonly due to:
    -leptospira interrogans
    -if live with skunks, raccoon, or cattle, other lepto serovars can also cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe focal mucoid placentitis

A
  1. also called nocadioform
    -located at horn-body junction
  2. caused by nocardioform actinomycetes and also by strep species
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

describe diagnosis of placentitis

A
  1. external signs:
    -vaginal discharge
    -premature udder development
  2. ultrasonographic eval:
    -CTUP (combined thickness of uterus and placenta); thickness can help decide if ascending placentitis (usually increase by 1mm per month)

-amnion: usually very thin

-fluid echogenicity

-assess fetus: check heartrate for distress; on transabdominal US (should be between 60-120bpm; hypoxia can bring out of this range)

  1. blood progestin levels:
    -should be >4ng/mL throughout pregnancy
    -sudden drop could indicate placentitis bc placenta takes over for progesterone production once CLs regress
  2. blood estrogen levels:
    - should be >1000pg/mL
    -drop could indicate placentitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

describe treatment of placentitis

A
  1. antibiotics:
    -pen K, gentamicin, TMS
  2. altrenogest: to prevent prostaglandin-mediated abortion
  3. NSAIDs if sick: flunixin meglumine
  4. +/- acetylsalyicylic acid to increase blood flow to uterus
  5. foal from placentitis mom is prone to problems so:
    -strict foal watch! for dystocia and placental detachment
    -intense neonatal care likely needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe twins

A
  1. 1-15% of preg result in 1-2 live foals
    -thoroughbreds: 19-31% double ovulation
    (we bred for this bc increases pregnancy rate)

-more prone to twins: maidens or mares barren for a season with a great BCS

-ovulation inductors also make prone to double ovulation

  1. complications:
    -early embryonic death
    -late-term abortions
    -premature delivery
    -birth of weak foals
    -dystocia
    -retained placenta
    -decreased fertility, loss of breeding season = frustration
  2. twin versus cyst: hard to tell!
    -embryos migrate throughout the uterus
    -cysts stay in same spot
    -so if reeval 2 days apart, embryo will look different (grow 2-4mm per day in 1st 15 days) or be in dif spot, cyst will be same
  3. diagnosis: ultrasound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

describe reduction of twins

A
  1. manual technique: if find early and can separate (squish)
  2. transvaginal ultrasound guided aspiration: if already fixated (stabby stabby)
  3. cranio-cervical dislocation: when fetus >45d
    -transrectally
    -transabdominally (flank)
    -colpotomy
  4. thoracic compression: when fetus >4 months
    -put repeated weight on thorax of foal; causing hypoxia
  5. transabdominal ultrasound fetal cardiac puncture: when fetus approx 120d
    -inject heart with potassium or insulin

success rate decreases the bigger the fetus gets

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

describe ventral ruptures

A

a serious complication!!

  1. types:
    -oblique abdominal muscles
    -transverse abdominal muscles
    -prepubic tendon
    -rectus abdominis muscle
  2. risk factors:
    -more common in draft and old mares
    -in cases of hydrops or twins (increased uterine weight)
  3. clinical presentation:
    -abdominal pain
    -reluctance to walk
    -pendent or bulging abdomen
    -ventral edema
  4. management:
    -abdominal support
    -stall rest
    -assisted foaling (induction, more recommended) or C section when fetus is visible (C section more complications)
    -pain mgmt
    -diet (reduce hay and oil)
    -antibiotics: to prevent abscesses on hematoma areas
    -progestin to keep uterus quiescent
    -fetal monitoring
    -CAN carry further pregnancies (this baby was just hella big for some reason, may be at risk)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe hydrops of fetal membranes

A
  1. hydroallantois:
    -more common
    -rapid abdominal enlargement over 10-14d after 7 months of gestation
    -caused by placental abnormality affecting fluid absorption or increased transudate production
  2. hydroamnion:
    -rare condition, thought to be of fetal origin
    -fluid originates from amnionic epithelium, fetal salivary glands, and nasopharynx secretions

diagnosis:
-clinical signs
-rectal palpation
-ultrasound

treatment:
-pregnancy termination and slow drainage
-supportive fluid therapy
-uterine inertia means oxytocin does not work so manual cervix dilation and extraction

prognosis: poor

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

what are 7 complications of hydrops of fetal membranes?

A
  1. uterine rupture
  2. ventral rupture
  3. inguinal herniation
  4. abortion, stillbirth
  5. retained placenta
  6. uterine inertia
  7. hypovolemic shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly