Placenta: placental insufficiency in Horses (Equis) | Vetlexicon
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Placenta: placental insufficiency

ISSN 2398-2977


Introduction

  • The equine placenta comprises the choriallantois, the amnion and the placental vasculature that constitutes the umbilical cord.
  • The placenta is considered diffuse, microcotyledenary and epitheliochorionic in character.
  • The placenta is fetal in origin and functions to allow transfer of nutrients and oxygen from the dam's blood to the fetus and a diffusion of waste products from the fetus to the dam's blood.
  • The placenta also synthesizes steroids, peptides, glycoproteins and eicosanoids, and inactivates other hormones such as catecholamines, glucocorticoids, thyroxine and prostaglandins.

Presenting signs

  • Premature mammary gland development.
  • Premature lactation.
  • Vulval discharge.
  • Abortion.
  • Stillbirth.
  • Birth of a weak/anoxic/meconium stained foal.
  • Grossly abnormal fetal membranes.

Geographic incidence

  • No particular geographical incidence although nocardial placentitis   Placenta: placentitis  occurs in North America.

Age predisposition

  • Older (in-foal) mares predisposed due to age-related endometrial degeneration   Endometrium: fibrosis  .

Breed/Species predisposition

  • No particular breed predilection.

Cost considerations

  • Significant cost for breeder due to production of weak foal that requires significant treatment and may have implications for athletic future or due to death of fetus or newborn foal.

Pathogenesis

Etiology

Predisposing factors

General
  • Mares in poor bodily condition.
  • Older mares.
  • Poor biosecurity on studs predisposes to viral infection.

Specific

  • Poor vulval/perineal conformation.

Pathophysiology

  • Pathology of placenta (etiology as above) causes an interruption to the maternal/fetal transfer of nutrients and causes either in-utero growth retardation of the fetus or death of the fetus, and may initiate parturition resulting in abortion or premature birth.

Timecourse

  • Dependent on etiology (rapid abortion in EHV-1 infection, insidious for villous atrophy).

Epidemiology

  • Important to rule out EHV-1 and 4 in mcases of abortion/stillbirth/neonatal death.
  • Following abortion/stillbirth/neonatal death all movements off and onto a stud should be suspended whilst the cause is identified. If EHV is diagnosed in a mare which has aborted or given birth to a weak or dead foal, remaining in-foal mares should be split into small groups and managed to minimize the risk of spread of EHV.

Diagnosis

Presenting problems

  • Premature mammary gland developemnt.
  • Premature lactation.
  • Vulval discharge.
  • Abortion   Abortion: overview  .
  • Stillbirth.
  • Birth of weak/anoxic/meconium stained foal.

Client history

  • Signalment of mare.
  • Previous reproductive history.
  • Vaccination status, particularly EHV-1/4.
  • History of problems with in-contact mares.
  • Any recent movements of mares on premises prior to clinical signs.

Clinical signs

  • As for presenting problems.

Diagnostic investigation

  • Maternal bloods:
    • Hematology/biochemistry - can be normal; NB placenta is fetal in origin.
    • Estone sulfate - confirms live fetus from 120-280 days.
    • Serum relaxin concentrations may be measured as an indicator of placental insufficiency - where placental function is impaired serum relaxin concentrations are low.
  • Mammary secretions:
    • Electrolyte levels initially similar to plasma - Na = ~135 mmol/l; K = ~3-4 mmol/l; Ca = ~1-2 mmol/l.
    • Na decreases and K rises crossing at approx. 24-48 h before foaling.
    • Ca rises and is >10 mmol/l within last 24 h of pregnancy.
  • Vulval discharge: culture and senstivity.
  • Transrectal ultrasonography   Ultrasonography: reproductive tract - female  :
    • Cervical pole combined uteroplacental thickness (CUPT) - normal >300 d = ~7-13 mm.
    • Uteroplacental contact.
    • Fetal motility, assessment of fetal fluids:orbit size.
  • Transabdominal ultrasonography:
    • CUPT assessment.
    • Uteroplacental contact.
    • Fetal motility, fluid, orientation and heart rate.
    • Assessment of aortic diameter as indicator of fetal size.
  • Vaginoscopy: visualize cervix re tone/discharge.
  • Fetal ECG (telemetric?).

Confirmation of diagnosis

Discriminatory diagnostic features

  • Premature mammary gland development and lactation, vulval discharge.
  • Fetal ECG showing constantly elevated heart rate   Heart: ECG - fetal  maternal  .

Definitive diagnostic features

  • Transabdominal and transrectal ultrasound.
  • Abortion.
  • Histology of placenta.

Gross autopsy findings

  • Twins.
  • Placenta:
    • Excessively edematous and twisted umbilical cord.
    • Excessive edema and thickened placenta.
    • Posterior pole avascular necrosis.
    • Marked villous atrophy.
  • Fetus:
    • State of carcass - body condition, autolysis.
    • Straw colored pleural or peritoneal fluid (?EHV).

Histopathology findings

  • PCR: fetus and placenta for EHV.
  • Placenta:
    • Marked inflammatory infiltration (placentitis).
    • Viral inclusion bodies (EHV).
    • Villous atrophy.
  • Fetus: viral inclusion bodies (EHV).

Differential diagnosis

  • For vulval discharge: urine staining, varicose vaginal veins, vaginitis.
  • For premature mammay gland development - mastitis; twinning.
  • For abortion - often involves some form of placental insufficiency, though can be iatrogenic, eg due to drug administration.
  • For stillbirth/weak neonate - dystocias/congenital anomaly, premature placental separation; twinning.

Treatment

Initial symptomatic treatment

  • Dependent on etiology.
  • For infectious placentitis:
  • Abortion:
    • Ascertain EHV status.
    • Monitor mare for signs of toxic endometritis and treat as necessary - uterine flush, antibitoics, NSAIDs, etc.
  • Weak foal: neonatal intensive care.

Monitoring

  • For subsequent pregnancies, monitor high risk mares via transabdominal and/or transrectal ultrasonography.
  • Increased CTUP gives indication for early intervention with antibiotics, altrenogest and pentoxifylline.

Prevention

Control

  • Progesterone/altrenogest:
    • Can be used throughout pregnancy.
    • Mares with placentitis will foal through altrenogest.
    • If the mare reaches full-term (320 days min), and mammary electrolytes indicate that parturition is imminent, altrenogest may be discontinued.
    • Helpful in reducing ascending placentitis by aiding cervical tone and may have some effect on uterine quiescence, preventing the cascade that initiates expulsion of the fetus.
  • Antibiotics:
    • Some authors advocate a 1 week/month course of trimethoprim/sulfonamide antibiotics for the last 5 months of pregnancy for high risk mares.
  • Hypoglycemia in the pregnant mare can have adverse effects on placental function via an increase in placental PGFM. For this reason, pregnant mares that have to be starced, eg due to surgery, should be maintained on a glucose drip. Pregnant mares that are anorexic should be supplemented parenterally or via nasogastric tube.

Prophylaxis

  • EHV-1/4 vaccination.
  • Meticulous attention to vulval conformation and treat as necessary, ie Caslick or Pouret's operation, etc.
  • Care with regard to movement of mares prior to foaling - mares should be resident where they are due to foal a minimum of 1 month before their due date. Also, pregnant mares should be isolated from other animals, particularly youngstock, if possible.

Group eradication

  • Difficult to eradicate all types of placental insufficiency.

Outcomes

Prognosis

Breeding prognosis

  • Dependent on etiology.
  • For EHV abortion: unlikely (not impossible) to recur in future pregnancies.
  • For bacterial placentitis: perform thorough barren mare examination and monitor carefully during future pregnancies. Correct any predisposing abnormalities, eg poor vulval conformation before re-breeding the mare.
  • For umbilical torsions: some authors argue that there appears some genetic involvement so advocate using a different stallion for subsequent pregnancies.
  • For twins: ultrasound scanning at 16 days post-cover (manual reduction) and again before 32 days should allow diagnosis and reduction of twin pregnancy avoiding problems later in pregnancy.
  • For villous atrophy due to endometrial degeneration: perform careful barren mare examination, including a uterine biopsy to ascertain the likelihood of the mare carrying a pregnancy to term.

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Bucca S (2006) Diagnosis of compromised equine pregnancy. Vet Clin North Am Eq Pract 22, 749-761 PubMed.
  • Fowden A L & Forhead A J (2004) Endocrine mechanisms of intrauterine programming. Reproduction 127 (5), 515-526 PubMed.
  • Troedsson M H T (2001) Ultrasonographic evaluation of the equine placenta. Pferdeheilkunde 17 (6), 583-588 VetMedResource.

Other sources of information

  • Robinson N E & Sprayberry K A (2008) Current Therapy in Equine Medicine. Saunders Elsevier. pp 834-847.
  • MacPherson M L (2007) Identification and Management of the High-Risk Pregnant Mare. In: Proc 53rd AAEP Congress. pp 293-303.
  • Samper J C, Pycock J & McKinnon A O (2006) Current Therapy in Equine Reproduction. Saunders Elsevier. pp 389-416, 435-440.
  • Knottenbelt D (2003) Equine Stud Farm Medicine & Surgery. Saunders. pp 325-342.
  • Ryan P, Vaala W & Bagnell C (1998) Evidence that Equine Relaxin is a Good Indicator of Placental Insufficiency in the Mare. In: Proc 44th AAEP Congress. pp 62-63.