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Perinatal asphyxia



  • Asphyxia is a reduction of oxygen supply to the tissues, which can result from inadequate blood oxygenation (hypoxia) or inadequate blood flow through the capillaries (ischemia).
  • Perinatal asphyxia syndrome encompasses the syndrome variously known as hypoxic ischemic encephalopathy, neonatal encephalopathy, dummy foal syndrome or neonatal maladjustment syndrome. However, although neoatal maladjustment syndrome may be the most obvious clinical sign of perinatal asphyxia syndrome, perinatal asphyxia syndrome also affects organs other than the brain, such as the gastrointestinal tract and the kidneys, and may also affect cardiovascular, respiratory and endocrine systems.
  • Cause: occurs due to foals receiving an inadequate oxygen supply either during the birthing process (when the period between a functioning placenta and the foal breathing spontaneously is prolonged) or in utero. Early cessation of placental function occurs with:
  • Inadequate oxygen supply in utero may be caused by:
    • Placentitis.
    • Severe maternal illness, particularly associated with fever and sometimes with cytokinemia in the neonate, resulting from placental infection or insult.
    • Perinatal asphyxia can also occur with no obvious inciting cause.
  • Signs: apnea, respiratory arrest and death. Foals that have an asphyxial episode and survive are at greatly increased risk of subsequent (neonatal maladjustment syndrome) Foal: neonatal maladjustment syndrome.
  • Diagnosis: history of inadequate placental function in utero, early cessation of placental function at birth or late spontaneous breathing immediately after birth. Lack of spontaneous breathing within 30 sec of birth Foal: evaluation - neonate. Clinical signs of perinatal asphyxia syndrome Foal: neonatal maladjustment syndrome.
  • Treatment: cardiopulmonary resuscitation at birth, if appropriate. Anti-oxidative agents such as dimethyl sulfoxide, vitamin E and selenium.


Predisposing factors


  • May also result in neonatal maladjustment syndrome due to lack of oxygen.
  • Hemodynamic failure and maldistribution of blood flow may also → asphyxia and ischemia of major organs shortly after birth.


  • Asphyxia occurs either due to insufficient placental oxygen supply in utero, eg due to placentitis, impaired oxygen exchange across the placenta → fetal hypoxia, or during the birthing process when the period between having a functioning placenta and the foal breathing spontaneously is prolonged.
  • Early cessation of placental function may be due to:
    • Premature placental separation (Red Bag deliveries) Umbilical cord: premature separation can result secondary to placentitis, or more commonly, without any obvious underlying cause.  The allantochorion appears at the vulval lips as a red, velvety structure. The premature separation means that the foal is without an effective oxygen supply during the birthing process → asphyxia.
    • Torsion or early rupture of the umbilical cord Umbilical cord: torsion Umbilical cord: premature separation → an interruption of the supply of oxygenated blood to the foal during the birthing process and therefore → hypoxia. It may also → loss of blood or sequestration of fetal blood within the placenta and therefore ischemia.
  • Late spontaneous breathing may be due to:
    • Dystocia Reproduction: dystocia can delay the onset of spontaneous breathing after placental function has ceased. Hip locked foals may be most at risk, as there can be physical compression of the umbilical cord, preventing blood flow or natural separation of the placenta before the foal is successfully delivered.
    • Rib fractures Rib: fracture Rib: fracture 01 - pathologyRib: fracture 02 - radiograph- these can potentially prevent effective breathing in foals. However, most rib fractures do not have a substantial effect on breathing, and are only discovered incidentally.
    • Caesarean sections Uterus: caesarean section can result in asphyxia in two ways:
      • The anesthetic agents used during the Caesarean section can delay the onset of spontaneous breathing in the foal.
      • Secondly, emergency Caesarean sections are often performed for dystocia, and placental function may have ceased or have been compromised during the dystocia.
    • Obstruction of the airways with fetal membranes. Occasionally fetal membranes can block the airways in foals and prevent breathing.


  • Clinical signs may occur up to 72 h after the asphyxial event, but typically occur between 12 and 24 h.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Gold J R (2017) Perinatal asphyxia syndrome. Equine Vet Educ 29 (3), 158-164 VetMedResource.
  • Galvin N & Collins D (2004) Perinatal asphyxia syndrome in the foal: review and a case report. Irish Vet J 57 (12), 707-714 PubMed.
  • Jean D, Laverty S, Halley J et al (1999) Thoracic trauma in newborn foals. Equine Vet J 31, 149-152 PubMed.
  • Furr M (1996) Perinatal asphyxia in foals. Comp Cont Educ Pract Vet 18, 1342-1351 VetMedResource.
  • Hess-Dudan F & Rossdale P D (1996) Neonatal maladjustment syndrome and other neurological signs in the newborn foal: Part 1. Equine Vet Educ 8 (1), 24-32 VetMedResource.
  • Vaala W E (1994) Peripartum asphyxia. Vet Clin North Am Equine Pract 10 (1), 187-218 PubMed.

Other sources of information

  • Wilkins P A (2011) Perinatal Asphyxia Syndrome. In: Equine Reproduction. Eds: Mckinnon A O, Squires E L, Vaala W E & Varner D D. pp 147-153.

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