Fetus is in an aquatic environment. There is no air in the lungs only pulmonary fluid. Amniotic fluid (which contains keratin squames) is not breathed but it is swallowed and is therefore in the abomasum only. Meconium, containing bile pigment, desquamated epithelial cells and squames of keratin from amniotic fluid that was swallowed, is in the colon and rectum. Hooves have eponychia. The lamb is wet and 'slimy'. Loss at this stage is called an abortion or stillbirth depending on whether the lamb is independently viable (stillbirth) or not (abortion).

If the lamb is stressed en utero, it will defecate meconium, gasp for air but inhale amniontic fluid (with squames and meconium), and it may 'struggle'.

At birth, the fetus enters the terresterial enviroment. It is freed from its membranes, it gasps to breath air and the umbilical cord breaks. The cord is pulled and stretched and the ends constrict. The lamb struggles to rise, stands and the eponychia are are torn off in the process. The lamb then finds the mother/mammary gland and drinks. Milk enters the abomasum, and the gastrocolic reflex operates to cause the meconium to be passed. Milk, rich in lipids, passes into the duodenum and jejunum where it is absorbed. Fat as chyle is visible in the lymphatics. Brown fat acts as a ready source of energy if there is any delay in milk uptake or if there is increased energy requirement. In extreme conditions of cold and wet, this supply can last only several hours, otherwise it is present for many days.

Is this

• an abortion (expelled prior to age of viability, small fetus, did not breath, amniotic fluid in abomasum and meconium in colon and on the coat)
• a stillbirth (parturition at normal gestation lengh, did not breath, usually meconium stained coat)
• postnatal death (born at normal time, did breath, cord constricted)

Is the umbilicus constricted? If so, go on, otherwise go back to stillbirth.

Is there air in the lungs? If so go on, otherwise go back to stillbirth.

Is there eponychia on the hooves.

If so, is there trauma, hemorrhage or evidence of anemia - investigate this further. If not go back to stillbirth.

If not, go on

Is there metabolism of pericardial or perirenal fat?

If so, is there a reason for weak lamb, mismothering, very cold temperatures, brain hemorrhage/dystocia. If not, go on.

Is there milk in the stomach? If so, is there trauma, hemorrhage or evidence of trauma - investigate this further. If not go and look at all tissues.

 

Perinatal mortality in horses

E.J. Dickey, S.N. Long and R.W. Hunt (2011) Hypoxic Ischemic Encephalopathy—What Can We Learn from Humans? J Vet Intern Med 2011, 25: 1231–1240

Hypoxic ischemic encephalopathy (HIE) is a condition
in foals that is known by many names,
including neonatal maladjustment syndrome (NMS)
and perinatal asphyxia syndrome (PAS). The incidence
in foals is reported to be 1–2% of all births.1 There
have been no direct studies of HIE in foals, and hence,
knowledge of the condition has been extrapolated
from studies in humans and other animal models with
attendant limitations. Because the basic pathophysiology
of brain injury in many species shares common
features, the purpose of this review is to summarize
the pathophysiology, diagnosis, and treatment of HIE
in human neonates. Current protocol in the human
neonatal intensive care unit (NICU) and ongoing
research in this area have raised important points for
discussion regarding our approach to and management
of the condition in foals.
Incidence and Consequences
HIE affects 3–5 per 1000 human live births, with
moderate or severe hypoxia affecting 0.5–1.0 per 1000
live births.2 HIE has very important sequelae with 10–
60% of affected infants dying in the newborn period
and with at least 25% of survivors having important
long-term neurodevelopmental impairment.3 The most
important long-term complication is development of
cerebral palsy, which is defined as a group of permanent
motor disorders that are attributed to nonprogressive
disturbances which occur in the developing
fetal or infant brain.4
Etiology
The origin of hypoxic ischemic brain injury results
from a reduction in cerebral blood flow and oxygenation
during the antepartum, peripartum, or postnatal
period. Evidence suggests that approximately 70–80%
of cerebral palsy cases are the result of antepartum
injury, with birth asphyxia responsible for only 20%.5
Hypoxia can develop during labor because of compression
of the umbilical cord, insufficient uteroplacental
circulation, cord prolapse, uterine rupture, shoulder
dystocia, or vaginal breech delivery.6 Most preventative
measures and therapies target the birth asphyxia
group, as there is a limited time period after insult to
prevent or reduce injury, and often with antepartum
injury that period has passed by the time the infant is
born.7 Risk factors for the development of hypoxic
brain injury in foals include prolonged dystocia, premature
placental separation (red bag delivery), and
need for resuscitation after cesarean section.8 Recently,
the term neonatal encephalopathy (NE) has been used
to encompass all neonatal foals that exhibit neurological
abnormalities. It is important to note that HIE is a
specific type of NE, and not all NE cases are caused
by hypoxia ischemia. An example of NE without true
hypoxic brain injury is evident in human infants born
From the Neonatal Research, Murdoch Children's Research
Institute, Melbourne, Australia (Dickey); Faculty of Veterinary
Medicine, University of Melbourne, Australia (Long); and
Director of Neonatal Medicine, Royal Children's Hospital,
Neonatal Research, Murdoch Children's Research Institute,
Melbourne, Australia (Hunt).