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Review Article
Assessment of the equine neonate in ambulatory practice
S. M. Austin
Department of Veterinary Clinical Medicine, Equine Primary Care, University of Illinois at Urbana-Champaign,
Illinois, USA.
Corresponding author email: smaustin@illinois.edu
Keywords: horse; neonatal; foal; assessment
TABLE 1: Normal values for newborn foals Neonates should be examined for limb, joint or tendon
abnormalities. The umbilicus should be inspected and the
Age Heart rate Respiratory rate Temperature
abdominal wall examined for hernias (umbilical and inguinal).
(h) (beats/min) (breaths/min) °C (°F)
The umbilicus should be dipped in 0.5% chlorhexidine to
0–2 120–150 60–80 37–39 (99–100.5) decrease the risk of bacterial contamination. The addition
>2 90–120 20–40 37–39 (99–101.5) of surgical alcohol to the navel dip will speed drying and
help seal the umbilicus (Madigan 1990; Kavan et al. 1994). The
eyes should be examined for cataracts, corneal ulcers and
temperature, so hypothermia may be an early indication entropion; abnormal injection or colour of the sclera should
of potential problems (Stoneham 2006). Increased body be noted. The menace response is a learned behaviour and is
temperature is most frequently associated with sepsis or not reliably present between birth and 2 weeks of age
systemic inflammatory response syndrome (SIRS), although (Enzerink 1998).
both conditions may also be seen in foals with normal or low Signs of illness are usually quite nonspecific and typically
body temperatures and should prompt laboratory evaluation. include decreased activity, loss of suckle, decreased
Lung sounds are typically louder in foals than adults due to the interactions with the mare, increased sleepiness and a
thin body wall. However, there is poor correlation between decreased or increased body temperature. In many instances,
audible sounds and the presence of lung pathology, so to the first thing that is noticed is the mare streaming milk.
assess pulmonary function, close attention to the effort of In addition to the foal, both the placenta and mare should
breathing is necessary. Normal respirations are characterised be examined. The placenta should be examined to ensure the
by a gentle in and out motion. At birth, the respiratory rate may entire placenta has been passed and to identify abnormalities
be 60–80 breaths/min before decreasing to a rate of 20–40 suggestive of placentitis. Increased weight of the placenta has
breaths/min within the first 24 h after birth (Table 1). The thorax been associated with foal abnormalities (Whitwell and Jeffcott
should be carefully palpated to detect rib fractures which may 1975). Normal umbilical cords measure 36–83 cm in length and
click upon palpation. Subcutaneous swelling and oedema are cords measuring outside this range have been associated with
often found at the fracture site. Fracture of 3 or more ribs is increased foal abnormalities (Cottril 1991a; Cottril et al. 1991b).
associated with an increased risk of fatality (Schambourg et al. Examination of the mare should include temperature, pulse
2003). A ‘flail’ chest that moves in as the chest expands and respiration, mucous membrane colour, inspection of the
indicates that surgical intervention is necessary. An early sign udder and evaluation of perineum for foaling injuries.
of respiratory disease is a persistently elevated respiratory rate.
Signs of increasing respiratory difficulty include exaggerated
Ancillary diagnostic testing
intercostal movement with synchronous abdominal effort
and an expiratory grunt. Finally, paradoxical movement of Evaluation of passive transfer
the chest and abdomen are seen as the foal approaches Although foals are practically immunocompetent at birth,
respiratory failure (Stoneham 2006). they are immunologically naïve and must rely upon the
A grade 1–4 holosystolic murmur can be auscultated over absorption of maternal antibodies from the colostrum for
the left heart base for 24–48 h. Also, irregularities in heart rate protection until sufficient time has passed to mount a primary
may be transiently present immediately after birth due to high antibody response against environmental pathogens. Failure
vagal tone and hypoxia associated with delivery (Yamamoto to ingest adequate amounts of colostrum has been
et al. 1992). Murmurs grade 4 and louder, holosystolic associated with increased risk of sepsis and the incidence of
or pansystolic, bilateral, continuous, diastolic or right-sided failure of passive transfer (FPT) has been estimated to
murmurs are more likely to be associated with a pathological, between 3 and 38% of foals. Failure of passive transfer has
rather than physiological, cause (Chope 2006). Persistent been established as serum IgG at less than 4 g/l and levels
arrhythmias and murmurs detected beyond the first 96 h between 4 and 8 g/l have been termed partial failure of
should be investigated further. Normal heart rate may be high passive transfer (McGuire et al. 1977; Perryman and McGuire
(150 beats/min) when the foal first stands and will remain 1980; Morris et al. 1985; Kohn et al. 1989; Baldwin et al. 1991;
increased (90–120 beats/min) through the first 2 days of life, Clabough et al. 1991; Stoneham et al. 1991; Raidal 1996;
before decreasing to between 60 and 80 beats/min by McClure et al. 2003).
2 days of age (Table 1) (Rossdale 1967). The most common causes of FPT are poor quality
Prolonged capillary refill time (>2 s) with cool ears and colostrum, loss of colostrum before suckling, failure to ingest
distal extremities is indicative of decreased peripheral adequate amounts before 24 h of age and insufficient
perfusion and must be further evaluated. In addition, the absorption of colostral antibodies. Mares produce between
mucous membranes should be examined for potential 1.8–2.8 l of colostrum late in gestation (Kohn et al. 1989).
abnormalities. Pale mucous membranes are suggestive of Colostrum quality appears to increase in the later parts of the
anaemia or decreased perfusion, while sepsis is associated foaling season as the amount of solar radiation increases;
with mucous membrane, sclera, ear (pinnae) and coronary however, antibody concentration declines in the face of mare
band hyperaemia and/or petechiation. Yellow mucous illness during pregnancy, ingestion of endophyte-infected
membranes may be seen with elevations in bilirubin secondary fescue and mares greater than 10 years of age (Clabough
to liver disease or haemolysis. Dehydration may be associated 1990; LeBlanc et al. 1992). Colostral quality can be assessed
with tacky mucous membranes, sunken eyes, decreased by measurement of specific gravity with a ‘colostrometer’
urination and a prolonged skin tent. Tenting the skin of the (Equine Colostrometer)1; good quality colostrum should have
eyelids is more reliable than the skin on the neck for assessing a specific gravity of at least 1.060 (LeBlanc et al. 1986).
hydration status. Frequent urination with dilute urine is Absorption of colostrum in the neonatal gut occurs
associated with normal hydration. by nonselective pinocytosis through specialised intestinal
epithelial cells. Normal foals begin absorbing colostral TABLE 2: Normal reference values for neonatal foals
antibodies at first nursing and capacity declines rapidly to 22%
Parameter 1 day 2–7 days
by 3 h after birth and reaches less than 1% by 20 h (Jeffcott
1971, 1974). A delay in nursing does not appear to delay Red blood cells (¥1012/l) 9.5–11.5 8.46–10.6
closure of the equine neonatal gut (Raidal et al. 2005). Haemoglobin (g/l) 13.3–15.5 12.0–14.4
Therefore, foals slow to nurse will have a decreased ability Packed cell volume (%) 38–46 33–40
to absorb intact immunoglobulin from the gastrointestinal MCV (fl) 36.6–43.8 37.1–41.6
tract and are at risk for the development of FPT. Premature MCHC (%) 31.8–35.8 35.1–37.5
or dysmature foals may actually ingest adequate amounts Total WBC (¥109/l) 6.1–11.2 6.9–11.3
Neutrophils (¥109/l) 4.2–8.6 4.5–8.5
of colostrum but fail to absorb antibodies through the
Lymphocytes (¥109/l) 1.0–2.2 1.6–2.8
gastrointestinal tract. Numerous studies have demonstrated a
Monocytes (¥109/l) 0.05–0.4 0.05–0.5
link between foals with failure of passive transfer and an Eosinophils (¥109/l) 0 0–0.2
increased risk for the development of sepsis (McGuire et al. Neutrophil:lymphocyte ratio 3.2 3.0
1977; Perryman and McGuire 1980; Kohn et al. 1989; Baldwin Platelets (¥109/l) 100–3250 140–315
et al. 1991; Clabough et al. 1991; LeBlanc et al. 1992; Raidal Total plasma protein (g/l) 54–69 58–70
1996; Raidal et al. 2005). Since sepsis is recognised as among Albumin (g/l) 25–34 25–34
the leading causes of foal mortality (Cohen 1994), all foals Fibrinogen (g/l) 1.7–3.1 2.2–4.0
should be evaluated for FPT. Serum amyloid A (mg/l) <30 <50
Maternal antibodies peak in the foal at 18–24 h of age Sodium (mmol/l) 134–146 135–144
Potassium (mmol/l) 3.5–5.3 4.1–4.9
(Sheoran et al. 2000), so foals can be tested as early as 12–18 h
Chloride (mmol/l) 100–107 97–105
of age (LeBlanc 2001). There are numerous commercial
Calcium (mmol/l) 2.7–3.2 2.7–3.1
tests available that have been shown to be suitable as Phosphate (mmol/l) 1.3–1.9 1.8–2.3
screening tests for detection of FPT (Davis and Giguere 2005). Magnesium (mmol/l) 0.8–1.0 1.0–1.2
All commercial tests have a sufficient sensitivity to correctly Bicarbonate (mmol/l) 23 24
identify foals with failure of passive transfer, but at higher Glucose (mmol/l) 5.3–9.8 6.7–10.0
antibody concentrations between 4–8 g/l, the commercial Urea (mmol/l) 3.5–4.0 2.3–4.0
tests kits may underestimate serum IgG levels and result in the Creatinine (mmol/l) 150–256 88–150
unnecessary treatment of a few foals that actually had Total bilirubin (mmol/l) 19–111 16–94
adequate serum immunoglobulin levels. Determination of Congugated bilirubin (mmol/l) 5–12 7–20
Bile acids (mmol/l) 0–8.0
serum total protein, although simple, is not accurate enough
Glutamate dehydrogenase (GLDH) (iu/l) 8–43
to determine if adequate transfer of antibodies has occurred Alkaline phosphatase (iu/l) 1182–3382 849–590
(Davis and Giguere 2005). It is recommended that healthy, Gamma glutamyltransferase (iu/l) 15–45 11–26
vigorous foals with complete failure and high risk foals with Aspartate aminotransferase (iu/l) 99–209 165–285
either partial or complete failure of passive transfer should be Lactate dehydrongenase (iu/l) 387–487 390–590
treated to increase serum immunoglobulin to greater than
8 g/l.
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