Neonatal Maladjustment Syndrome
Also know as: NMS — Perinatal Asphyxia Syndrome — Hypoxic Ischaemic Encephalopathy — Dummy Foal — Barker Foal
Neonatal maladjustment syndrome is a multisystemic disease affecting the nervous, cardiovascular, gastrointestinal and renal systems of the neonatal foal. The central nervous signs are noticed first and are the most overt.
Typically, affected foals are normal at birth but show signs within a few hours. Some are obviously abnormal at birth and some take 24 hours to show signs.
A variety of foetal and maternal conditions are associated with NMS:
Foetal factors include: twinning, meconium aspiration, sepsis, prematurity or dysmaturity and severe anaemia.
Maternal factors include: conditions that cause hypotension or impaired tissue oxygenation, maternal surgery or cesaerean section, dystocia and placental abnormalities (premature placental separation for example).
Initially, the foal responds to asphyxia by shunting blood away from non-vital organs (gut, kidney, bone...) to vital organs (brain, heart, adrenal glands). Continued asphyxia leads to cerebral ischemia. The brain's stores of glucose are depleted by anaerobic metabolism and glutamate uptake is impaired leading to accumulation and overstimulation of receptors.
Free-radicals are produced which overwhelm the scavenging systems and lead to the release of neurotransmitters and inflammatory mediators.
This goes on to affect all body systems leading to fluid and electrolyte derangements and abnormal acid-base due to central respiratory depression.
Signs can be present at birth but usually develop over the first few hours of life. Initially, behaviour changes may be all that is apparent: depression, wandering, loss of affinity for mare, head pressing. Other possible neurologic signs include: bruxism, hyperexcitability, extensor spasm of the limbs, head, tail and convulsions alternating with a semicomatose state. Dysphagia, central blindness, head tilt and nystagmus have also been reported.
Signs of trauma associated with seizure activity can also be apparent: traumatic blepharitis, eyelid trauma, trauma to bony prominences.
Respiratory signs include varying degrees of tachypnoea and dyspnoea and erratic breathing patterns.
Cardiovascular signs present as tachycardia, hypotension, or murmurs associated with valve dysfunction.
Renal signs, oliguria and peripheral oedema may occur if fluid therapy is not adjusted for decreased urine output.
Gastrointestinal signs such as ileus, poor feeding, loss of suckle reflex, colic, abdominal distension, gastric reflux and diarrhoea can be present.
The clinical signs associated with the condition are usually sufficient to make the diagnosis.
There are no definitive blood chemistry or white blood cell abnormalities that aid in diagnosis, but these tests are helpful in eliminating other causes of the clinical signs. Other clinical syndromes that can present with similar signs and must be differentiated from NMS include hypoglycemia, electrolyte and acid-base derangements, septic meningitis, head trauma, cerebral bleeding, and congenital CNS defects.
Intensive supportive care is critical for the support of the affected foal. Providing warmth and nutrition is essential. An indwelling nasogastric tube can be placed if the foal is not suckling, and mare's milk should be given.
Isotonic fluids with added glucose should be given intravenously, and urine output monitored to avoid overhydration.
Seizure control is imperative, and diazepam should be administered if needed, with long term control using phenobarbital.
Respiratory support with flow-by oxygen, or positive-pressure ventilation if necessary.
Cardiac dysfunction can be treated with dopamine to increase cardiac output, and diuretics to reduce oedema.
Renal dysfunction should be treated with dopamine infusions to increase renal blood flow and urine output.
General supportive care includes: immunologic support with plasma infusions if the foal's IgG levels are below 800mg/dl. Antibiotic therapy should be considered because sepsis commonly accompanies ischemic bowel damage, and broad-spectrum antibiotics should be administered intravenously. Anti-ulcer medication such as ranitidine and sucralfate are recommended as gastric ulcers are a common complication.
Prevention of further self-trauma by placing a padded head-collar and paying attention to corneal ulceration is vital.
Prognosis is usually good for a foal delivered without obvious complications, especially if it is able to stand after delivery and has a normal immunoglobulin concentration. Approximately 75% of foals with good prognostic indicators survive with intensive nursing care. Clinical signs usually stabilise within 3 days but full recovery may take as long as 2 weeks.
A poor prognosis is associated with foals which have concurrent septicaemia, fail to show neurological improvement within 5 days or suffer from repeat seizures and are persistently comatose.
Long-term neurological deficits might be seen: unusually docile behaviour, prolonged vision impairment, residual spasticity, recurrent seizures.
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Carleton, C. (2011) Blackwell's Five Minute Consult Clinical Companion: Equine Theriogenology Wiley-Blackwell
Ogilvie, T. (1998) Large animal internal medicine Wiley-Blackwell
Synder, J. (2006) The equine manual Elsevier Health Sciences
Maggs, D. (2008) Slatter's fundamentals of veterinary ophthalmology Elsevier Health Sciences
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