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

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Treatment

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Prevention

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Outcomes

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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.