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Perinatal Asphyxia Syndrome
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Summary
Predisposing factors are dystocia, requiring resuscitation at birth, birth by C-section, premature placental separation and illness of the mare prior to parturition. However, many cases occur without any of these predisposing factors being present.
There is a range of clinical signs, and foals may show any or all of them as they progress through the disease. In the mildest forms, there is reduced nursing activity and/or poor affinity for the mare. Incoordination of the suck response and “tongue-lolling” is also very common. General poor coordination, which can lead to inability to get up and down, and inability to walk can also be seen. The most severely affected foals are unable to rise, with either extensor rigidity or coma.
Seizure activity can occur with perinatal asphyxia syndrome, and is not always accompanied by other severe signs. A foal that is able to walk and nurse can show seizure activity. It is important to remember that, although it is the most common cause of seizures, it is not the only one. Head trauma, low plasma sodium concentrations (typically less than 108-110mmol/L) and kernicterus can all result in seizures or seizurelike activity.
Previously called Neonatal Maladjustment Syndrome or Hypoxic Ischaemic Encephalopathy
Causes
Thought to be primarily due to hypoxia and ischaemia during the birthing process. The syndrome is very common is foals resuscitated at birth, from emergency Caesarian sections and from premature placental separation (‘red bag’) deliveries. Other maternal conditions associated with perinatal asphyxia are endotoxaemia, anaemia, severe pulmonary disease and induced parturition. Other placental conditions associated with the syndrome are placentitis, hydrops and fescue-induced placental disease. Twinning, congenital cardiac defects, persistent foetal circulation, dystocia and meconium aspiration may also be causes.
Typical history
Two forms of perinatal asphyxia syndrome are recognised. In the first, the foal is obtunded from birth. In the second, the foal is apparently normal for a period of time and then starts to show clinical signs.
Clinical experience suggests that a foal will usually seizure within 72 hours of a hypoxic event, usually in the window between 18 and 36 hours after the event.
Clinical signs
Central nervous system: Generalized weakness, wandering away from mare, loss of suckle (tongue lolling is a typical sign), abnormal phonation (‘barking’), seizures, head tilt, coma, apnoea, blindness. Cardiovascular: Vasodilation, hypotension, capillary leak. Renal: Oliguria, anuria. Respiratory: Tachypnoea, dyspnoea, apnoea. Gastrointestinal: Colic, ileus, diarrhoea, necrotising enterocolitis. Hepatic: Icterus. Haematological: Coagulopathy, disseminated intravascular coagulation, anaemia, polycythaemia.
Laboratory signs
There are no specific laboratory signs of PAS. In some foals there may be laboratory evidence of placental insufficiency (markedly increased creatinine concentration, which can be as high as 1800 umol/L (normal range 35-185 umol/L)) and of asphyxial injury (markedly high calcium concentration; we recorded an ionized calcium of 3.71 mmol/L in one survivor (normal range 1.2-1.7 mmol/L)).
Treatment
Supportive care is the key for PAS. Mildly affected foals may need to be kept in a box with the mother, allowing them to be closely observed and to be helped to find the teat and nurse, if necessary. More severely affected foals will require nutritional support. In moderately affected foals, this can be by placing a feeding tube and giving milk. In severely affected foals, the intestine is also affected, and nutrition needs to be given intravenously as partial or total parenteral nutrition. Severely affected foals also require fluid therapy and sometimes inotrope or vasopressor support of the circulation. [...]
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