Page 1369 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

1344 CHAPTER 14

VetBooks.ir Management NMS for foals that have no history or suspicion of
birth hypoxia.
If diagnosed early, attempts should be made to suc-
tion as much meconium-contaminated fluid from
Recent evidence suggests that NMS occurs when
the airways as possible, but care must be taken not to foals fail to adapt fully to extrauterine life. In a nor-
induce further lung damage. Humidified intranasal mal foal, the hypothalamic–pituitary–adrenal (HPA)
oxygen can be used to reduce the work of breathing. axis produces a large number of progestagen-based
The use of corticosteroids remains controversial. steroids that reach high concentrations shortly before
There is some evidence in children that a single dose birth. In a healthy foal, the final maturation of the
of dexamethasone early in the course of the condi- HPA axis causes activation of enzymes that con-
tion may be beneficial. High levels of supportive care vert these compounds to cortisol and its derivatives,
may be required, and broad-spectrum bactericidal which are responsible for the final maturation of
antibiotics should be given. Mechanical ventilation many organ systems. Concentrations of progestagens
can be used in severe cases. Intravenous or nebu- then fall rapidly after foaling. In foals with NMS,
lised N-acetylcysteine may be beneficial owing to its progestagen concentrations remain high after foal-
mucolytic and anti-inflammatory properties, as well ing, or begin to fall and then rise again sharply. The
as its ability to alter the physical properties of meco- exact trigger for dysfunction in these pathways is not
nium (breakage of disulphide bonds). yet known but factors such as systemic inflammation,
hypoxia, abnormal delivery and placental abnormali-
NEONATAL MALADJUSTMENT ties may play a role. In some NMS foals, it has been
SYNDROME observed that foaling is unusually rapid and this has
raised the possibility that the physical pressure of the
Definition/overview birth canal may be an important stimulus for these
NMS affects foals less than 3 days of age. Synonyms normal maturational pathways. In foals that recover
include perinatal asphyxia syndrome, neonatal from NMS, progestagen concentrations fall in line
encephalopathy, hypoxic/ischaemic encephalopathy, with their recovery. Many of the progestagen com-
‘barker’ foals, ‘dummy’ foals and convulsive foals. pounds can cross the blood–brain barrier and have
The most common clinical signs are neurological, neuroactive effects. These compounds, or the imbal-
but the syndrome can affect many body systems and ance of these compounds, may directly cause some of
in severe cases lead to multiorgan dysfunction. Foals the observed neurological signs. Experimental infu-
with this condition exhibit a wide range and severity sion of certain progestagen compounds can cause
of clinical signs. sedation and reduced consciousness in healthy foals.
In foals that suffer from perinatal asphyxia syn-
Aetiology/pathophysiology drome, hypoxic–ischaemic insults produce cellular
Historically, the syndrome has been attributed to damage to a variety of organ systems. The central
hypoxic–ischaemic injury that occurs around the nervous system (CNS), kidneys and gut tend to be
time of foaling. This is undoubtedly the underly- most severely affected. On post-mortem examina-
ing cause for some foals with the condition and is tion, evidence of hypoxic injury can be seen in these
often easy to diagnose, based on a history of a dif- tissues. In foals that die following NMS, evaluation
ficult delivery or prolonged dystocia. Foals that have of the neurological system is usually unremarkable
experienced a severe hypoxic event often show the with the exception of changes related to secondary
most severe clinical signs and have a worse progno- sepsis and perfusion abnormalities.
sis. However, many foals with NMS make a rapid
and complete recovery with 2–5 days of supportive Clinical presentation
care, which suggests a different aetiology. In the Affected foals may be normal at birth and then go
authors’ opinion, this condition may be better split on to develop clinical signs within 12–48 hours.
into two syndromes: perinatal asphyxia syndrome These foals tend to be the less severely affected.
for foals that have experienced a hypoxic event; and Some foals show signs of the syndrome immediately