Appropriate management in the peripartum period can substantially reduce morbidity and mortality for both large animal dams and their offspring. A key aspect of managing the large animal dam includes appropriate nutrition and body conditioning in the pre- and postpartum periods to reduce the risk of pregnancy-related diseases such as pregnancy toxemia, hypocalcemia, and vaginal prolapse, as well as to optimize colostrum quality and fetal and neonatal growth. Additionally, appropriate anthelmintic therapy and vaccination of the dam several weeks before parturition will help protect both dam and offspring from disease. Large animal neonates are born with limited energy reserves and without effective immunity because of a lack of transplacental antibody transfer during gestation; thus, ensuring the provision of good quality colostrum by the dam and adequate colostrum intake by the neonate are critical influences on neonatal survival. Hence, all factors that might compromise colostrum quality, volume, and delivery to the neonate should be considered. These can be grouped into maternal factors (disease during gestation, premature lactation, maiden dam), delivery factors (abnormal parturition, placental abnormalities), and neonatal factors (prematurity, dysmaturity, maternal rejection, multiple birth, and any other factor limiting neonatal mobility and strength). Additionally, environmental factors that may influence neonatal morbidity and survival include climactic conditions, attendant care and postpartum treatment, and the housing situation during the peripartum period.
Particular conditions affecting large animal neonates in the immediate postpartum period include peripartum asphyxia, hypoglycemia, hypothermia, septicemia, predation, mismothering, and various congenital diseases. Substantial losses can occur in flock or herd situations, and altering problematic aspects of management can therefore be of great benefit. Generally, equine and camelid neonates can be managed more intensively than neonatal calves, pigs, or lambs because of economic considerations. However, rapid assessment and appropriate management of all large animal neonates in the immediate postpartum period can substantially reduce the need for intensive and expensive measures in any species.
Dams should be present within their maternity location at least 3–4 wk before parturition to avoid transport stress in late gestation and to facilitate the production of colostral antibodies to pathogens within the local environment. Dams should be vaccinated for species-specific diseases, but modified live formulations generally should be avoided. Vaccines should be selected based on those diseases likely to pose a risk to the postpartum dam (eg, tetanus) and to the neonatal or juvenile animal; they should be administered 30–60 days before parturition to optimize colostral transfer of vaccine-induced antibodies. To reduce exposure to infectious diseases, the dam should be isolated from new arrivals, sick animals, and any transient animal populations. Other prepartum management techniques may include shearing of wool to encourage the dam to seek shelter, clipping and/or cleaning of the perineal region and/or udder, and preemptive adjustment of the housing situation and ration to avoid sudden changes in the peripartum period that may induce stress and anorexia.
If possible, the dam should be provided with separate quarters for delivery that are spacious, well lit, well ventilated, clean, disinfected, and that provide good footing. Flock animals can be divided into smaller groups to facilitate observation and feeding. If parturition occurs at pasture, then rotation of the birthing pasture should be practiced to avoid high concentrations of parasites and pathogens accumulating in the neonatal environment. Maternity stalls or pens with a high throughput should be thoroughly cleaned and freshly bedded after each use.
Induction of parturition should be avoided unless necessary because complications, especially retained fetal membranes, are common. Induction of parturition in the mare should be avoided because it frequently compromises foal viability, and complications in the mare can be particularly problematic. Parturition should be monitored if possible, especially for primiparous animals, to allow timely intervention should complications arise. Familiarity with the expected duration of parturition for each species facilitates understanding of when intervention is indicated. In general, fetal expulsion is rapid (~30 min) once active labor commences in horses, camelids, and small ruminants, and is slower in cattle (2–4 hr). A farrowing sow should deliver one piglet every 10–20 min. A dam in hard labor with no apparent progress in fetal expulsion within an appropriate period should be examined; in mares, this is an emergency because of the limited time a foal remains viable in the face of dystocia. Manual correction of fetal malposition is successful in most cases for all species, although the special circumstances of the mare mean that more drastic measures (fetal manipulation with general anesthesia and hoisting, cesarean section) may need to be pursued rapidly. Cesarean section is frequently indicated for dystocia not correctable by manipulation, for severe pregnancy toxemia, for uterine torsion that cannot be manually corrected, and for dead or malformed fetuses.
Immediate Postpartum Care
After delivery, the neonate's respiratory tract should be cleared immediately because it can be obstructed by a portion of the placenta or inhaled amniotic fluid, or in crias, by the fetal epidermal membrane that normally covers them at birth. The neonate and fetal fluids should be examined for meconium staining as an indicator of birth stress or peripartum asphyxia. Although minimal handling of the neonate is desirable to avoid disruption of maternal bonding, particularly in primiparous dams, respiratory efforts by the neonate can be stimulated by gently rubbing the thorax and extending the limbs.
Neonates displaying postpartum apnea require prompt treatment. In many situations, mouth-to-nostril resuscitation attempts are adequate to stimulate respiratory efforts. If not successful, an appropriately sized cuffed tube can be placed orotracheally with the assistance of a long laryngoscope or blindly with the head and neck held in an extended position during intubation. A cuffed nasotracheal tube can also be used in foals. Suction should be applied to remove any residual fluid in the airway before administration of positive-pressure ventilation via mouth-to-tube, handheld resuscitation bag, or oxygen demand valve techniques. The neonate should be placed in sternal recumbency during treatment to facilitate expansion of both lungs, and the chest should be seen to rise and fall with each breath. Abdominal distension that occurs and persists after a breath is administered is an indicator of esophageal intubation that should be immediately corrected. Respiratory efforts can be stimulated by the administration of doxapram (0.1–1 mg/kg, IV or sublingually) but should be accompanied by appropriate ventilation to avoid exacerbating hypoxia. Bradycardia is an additional indicator of hypoxia that suggests the need for oxygen supplementation. Oxygen can be administered intermittently by attaching an oxygen demand valve to the endotracheal tube, or continuously via face mask or placement of a small diameter cannula in one nasal cavity to the level of the medial canthus of the eye. Oxygen can be administered at a flow rate of 2–7 L/min, depending on the size of the neonate.
Cardiac arrest should be addressed by initiating chest compressions as soon as ventilation has been established. Larger neonates should be placed on their right side and cardiac compression applied just caudal to the left elbow and just above the costochondral junction. Return of cardiac function may be assisted by administration of epinephrine (0.01–0.02 mg, IV or 0.1–0.2 mg intratracheally at 3- to 5-min intervals) and atropine (0.05 mg/kg, IV or IM).
After an uncomplicated birth, the umbilical cord should be left intact for at least 5–10 min if it did not rupture during parturition to allow postpartum transfusion of blood from the dam to the neonate. Manual rupture can then be performed in a manner that avoids direct traction on the neonatal abdomen, and 2% iodine or 0.5% chlorhexidine solution should be applied to the stump twice daily until the umbilical remnant is dry. Excessive hemorrhage can be addressed by transient ligation with umbilical tape or a clamp. Neonates should pass meconium within 24 hr of delivery. Signs of meconium impaction include abdominal pain and straining; these frequently resolve after a warm soapy water enema. Multiple enemas can cause rectal edema and exacerbate straining and should be avoided. Primiparous dams in particular should be monitored for mismothering and even aggression toward their offspring. Maternal bonding is enhanced by a quiet maternity area with minimal handling of the offspring. Evidence of aggression may require sedation and/or restraint of the dam or removal of the offspring for special care if the problem cannot be resolved.
Neonates must ingest an adequate amount of good quality colostrum as soon as possible after birth, with attempts to nurse preferably commencing within 30–90 min. Manually stripping the teats of the dam to remove wax plugs and to check for the presence of colostrum will facilitate successful nursing attempts. The neonate should be inspected for any obvious congenital problems that may inhibit the ability to stand or to nurse effectively, including signs of prematurity, musculoskeletal abnormalities, cleft palate, and in crias, choanal atresia. Other abnormalities that are ultimately unlikely to be correctable include severe craniofacial malformations, spinal malformations, and atresia ani. Umbilical and inguinal hernias and mild musculoskeletal abnormalities are often self-correcting or readily addressed.
Weak or abnormal neonates that do not stand or nurse successfully within an adequate time (by 2–4 hr) with assistance should receive colostrum via bottle or stomach tube. If colostrum is not available from the dam, it should be secured from another animal of the same species or from a previously frozen (≤1 yr old) supply defrosted in warm water. Colostrum of other species can be used (such as cow colostrum for foals, kids, and lambs) but will not necessarily provide pathogen-specific immunity to the neonate. Commercial colostrum substitutes are also available but have similar limitations. Oral or IV administration of plasma or whole blood from the appropriate species can also be considered. Ideally, neonates should consume 5–12% of their body weight in colostrum in the first 12–18 hr, and healthy neonates frequently ingest considerably larger amounts (up to 27% of their body weight in 24 hr). Colostrum quality can be assessed by visual means (thick, sticky, yellow) and by sugar refractometry or use of a colostrometer.
To determine the success of colostral antibody transfer, measurement of serum IgG concentration at 18–24 hr of age is frequently practiced in foals and crias, in which values of >800 mg/dL and >1,200 mg/dL, respectively, are ideal. Although measuring serum IgG is less commonly practiced in ruminants, concentrations >1,600 mg/dL are ideal. Serum total protein can also be used as a rough estimate of colostral transfer and should exceed 5.0 mg/dL, and ideally 5.5 mg/dL.
Neonates that reach 18–24 hr of age with suspected or known failure of passive transfer require parenteral antibody supplementation because of negligible remaining ability to absorb intact antibodies from the intestine. Plasma can be obtained from the dam, a local donor of the same species (although llama plasma can be given to alpacas), or from a commercial source. Plasma should be administered at a minimum volume of 20–40 mL/kg, preferably IV, although intraperitoneal administration is frequently practiced in crias. Healthy neonates with partial failure of passive transfer and for which transfusion is not considered feasible can be maintained in a clean environment with close monitoring. The umbilicus should be disinfected regularly, and prophylactic broad-spectrum antibiotics may be administered to prevent sepsis.
Large animal neonates are precocious and should be able to stand and nurse within 1–3 hr of birth. Body temperature is usually ≥100ºF (37.8ºC) (≥102ºF [38.9ºC] in crias and small ruminants), and heart rate is usually >80 bpm. Early signs of neonatal compromise include a weak or absent suckle reflex, inability to stand, lethargy, abnormal behavior, and injected mucous membranes and/or sclera. Reduced neonatal vigor may reflect hypothermia, hypoglycemia, septicemia, peripartum asphyxia, and prematurity or dysmaturity. Identification of problems resulting in reduced viability must be investigated promptly because neonates have little reserve and can deteriorate rapidly with lack of appropriate care or disease.
Most newborn large animal neonates are fairly resistant to cold ambient temperatures, particularly once their coat is dry. Piglets, however, are a notable exception and require their environment to be maintained at approximately 85–90ºF (29.4–32.2ºC). This is usually best achieved by providing heat lamps or heat pads in a location that minimally impacts the sow. However, in very cold climates or during bouts of severe inclement weather, shelter must be provided to avoid neonatal mortality due to hypothermia. Shearing of ewes in late gestation may encourage shelter seeking, which protects the lambs. If shelter cannot be reliably provided to animals birthing outdoors, then breeding should be timed to allow parturition in late winter or early spring.
Hypothermia causes weakness, reduces suckling activity, and impedes digestion of ingested milk, all of which promote hypoglycemia and further weaken the neonate in a vicious cycle. Hypothermic neonates can be managed by providing an external heat source (eg, heat lamps, heating pads, heating box) or submersion in warm water (for small ruminants). Neonates should be wrapped in a plastic bag before submersion to help keep the coat and navel dry. Heat lamps should be carefully positioned, especially when used for compromised neonates, because thermal skin injury and hyperthermia can result if the neonate is incapable of moving away. Body temperature should be monitored periodically, and colostrum or another glucose source provided to the neonate once body temperature rises to at least 98ºF (36.7ºC).
Hypoglycemia in the neonate usually reflects inadequate caloric intake or increased glucose utilization as a result of disease. Any factor that prevents the neonate from nursing adequately can promote hypoglycemia, including neonatal weakness or disease, competition between siblings, and failure of the dam to provide milk as a result of agalactia, mastitis, or rejection of the offspring. Hypoglycemia often accompanies septicemia as a result of increased catabolism. Hypoglycemia is readily exacerbated by cold ambient temperatures, which increase neonatal energy requirements.
The significance of hypoglycemia varies to some degree between species. In ruminants, hypoglycemia frequently reflects inadequate caloric intake from poor mothering and/or competition with siblings, and is often exacerbated by cold ambient temperatures in pastured animals. These problems can be addressed to some degree through management changes. However, in crias and foals, hypoglycemia should raise strong suspicion of septicemia, necessitating more intensive treatment and diagnosis of the underlying problem. In Quarter horse neonates in particular, recurrent hypoglycemia may also indicate glycogen branching enzyme deficiency, a fatal hereditary condition that limits the ability to produce glucose from endogenous glycogen stores. Neonatal piglets are very susceptible to hypoglycemia because of their sensitivity to environmental temperature, limited energy reserves and brown fat deposits, and competition for food within a large litter. Furthermore, hypoglycemic piglets are at great risk of being crushed by the sow, whereas trauma to the compromised neonate by the dam is considerably less frequent in other species.
Signs of clinical hypoglycemia include weakness, lethargy, incoordination, abnormal behavior, and seizures and other neurologic signs. Hypothermia is frequently present. The diagnosis can be confirmed by measurement of blood glucose concentration, which is frequently <50 mg/dL, although species-specific reference ranges should be observed. The neonate and dam should be examined for possible predisposing causes (eg, mismothering, agalactia, udder abnormalities, sepsis in the neonate), and treatment of the neonate instituted rapidly. Hypoglycemic animals should be checked for hypothermia and warmed if appropriate to reduce glucose requirements. Glucose can be administered as a 5% or 10% dextrose solution (2–10 mL/kg, IV) to foals, crias, and calves. Piglets and small ruminants can be administered glucose via IP injection of warmed dextrose (15 mL of 5% glucose for a piglet; 20–40 mL of 10% or 20% solution for lambs or kids). Glucose and/or colostrum sources can also be administered via stomach tube if it is more convenient to do so. If continuous IV infusion of glucose constitutes part of ongoing treatment, blood glucose concentrations should be monitored periodically to avoid hyperglycemia, which crias are particularly susceptible to developing.
Treatment of hypoglycemia in any neonate must be accompanied by diagnosis and management of underlying disease, (eg, sepsis) and by correction of any predisposing factors. This helps ensure effective and ongoing caloric intake by the neonate after treatment and prevents relapses of hypoglycemia. If a maternal factor is identified that prevents the dam from successfully supporting her offspring, steps should be taken to redistribute one or all of the offspring to more effective foster dams, or to establish appropriate feeding of the orphaned neonate using alternative milk sources or milk replacer products appropriate for the species.
Sepsis is a highly problematic condition in large animal neonates. It typically has an insidious onset, a fulminant course, and a high mortality rate; furthermore, it often results in chronic complications that are detrimental to longterm productivity or performance. Sepsis is usually the result of a gram-negative septicemia, although gram-positive and anaerobic agents can also invade the systemic circulation. Invasions can occur via the placenta, the GI and respiratory tracts, and umbilical remnants. Bacterial endo- or exotoxins promote a profound inflammatory response, resulting in a cascade of metabolic and hemodynamic changes that often culminates in multiple organ failure. The endpoint is septic shock, which is characterized by circulatory failure, perfusion deficits, and inability to effectively utilize existing metabolic substrates.
The single most important factor behind the development of sepsis in large animal neonates is failure of adequate passive transfer, and the various factors (maternal, neonatal, and delivery) that predispose to failure of passive transfer have been previously mentioned (see Immediate Postpartum Care). However, in production systems in particular, overcrowding, poor ventilation and sanitation, inappropriate umbilical disinfection, and exposure to the elements may be additional contributing factors. Early signs of neonatal sepsis include lethargy, weakness, decreased nursing vigor, and/or frequency, loss of suckle reflex, tachypnea, tachycardia, hyperemic mucous membranes, and bounding peripheral pulses. Petechial hemorrhages may be observed on the gums, sclera, coronary bands, and inside the ears. Fever is not a reliable indicator of sepsis, and body temperature of affected neonates may be normal, subnormal, or increased. As sepsis progresses, signs of hypoperfusion, metabolic acidosis, and shock develop. Affected neonates frequently become recumbent and display signs of dehydration and hypotension, including tachycardia; cold extremities; dry, injected mucous membranes with a toxic line along the margin of the teeth; and a prolonged capillary refill time. Gut motility is frequently reduced, which may result in gastric reflux, abdominal distention and pain, and diarrhea or constipation. Laboratory tests often reveal hypoglycemia, hyperlactatemia, azotemia, and leukopenia associated with neutropenia and a degenerative left shift.
Successful treatment of neonatal sepsis depends on early recognition and aggressive support using systemic, broad-spectrum, bactericidal antibiotics; appropriate IV fluid support (crystalloids and colloids); and plasma transfusion when feasible. Generally, most neonatal large animal species have a fluid requirement of 90–120 mL/kg/day, although this can increase substantially if complications such as diarrhea arise. Nutrition is a critical aspect of care that is easily neglected, and neonates should receive enteral and/or parenteral nutritional support to maximize the chances of recovery. Crias and ruminants should be given at least 10–12% of their body weight in milk or an appropriate milk substitute per day if they are not suckling adequately, and foals should receive at least 20%. Parenteral nutrition is required in animals that cannot tolerate their milk requirement orally and may consist of dextrose, amino acids, and possibly lipids in a crystalloid fluid base. Oral fluid intake should be accounted for when calculating IV fluid volumes to avoid complications of excessive fluid administration. Daily monitoring for complications of sepsis should be performed, including assessment of the lungs and eyes and palpation of the joints and external umbilicus, which are common sites of complications.
Diarrhea can be problematic in the neonatal period of most domestic large animal species and should also be viewed as a possible indicator of sepsis. Significant causes of neonatal diarrhea in ruminants include rotavirus, coronavirus, Cryptosporidium, enterotoxigenic Escherichia coli, and Salmonella; most of these pathogens are also problematic in piglets. Neonatal foals may develop diarrhea as a result of rotavirus, Salmonella, Clostridium spp, and Strongyloides infection. Crias are susceptible to infection with Cryptosporidium, Giardia, coronavirus, and Eimeria. Other causes of diarrhea that should be considered include nutritional diarrhea, resulting from inappropriate formulation of milk substitutes, and “foal heat” diarrhea in foals that are 5–14 days old. Therapy for neonatal diarrhea focuses largely on maintaining hydration and preventing or treating acid-base and electrolyte disorders. When the underlying cause is amenable to treatment with anthelmintics, coccidiostats or antibiotics should be administered, and the neonate monitored carefully for hydration, adequate caloric intake, and signs of sepsis.
Asphyxia results from impaired oxygen delivery to cells and is usually the consequence of a combination of hypoxemia (decreased arterial oxygen concentration) and decreased tissue perfusion. Periparturient asphyxia can result from any event that impairs uteroplacental perfusion before or during parturition, or that disrupts normal distribution of blood flow in postpartum neonates. Neonatal asphyxia can occur in apparently normal deliveries, dystocias, induced deliveries, cesarean sections, placentitis, premature placental separation, the birth of multiple fetuses, severe maternal illness, and post-term pregnancies.
Neonates with periparturient asphyxia display a wide spectrum of neurologic signs that may include hyperesthesia, somnolence, lethargy, weakness, seizures, extensor rigidity, aimless wandering, head pressing, loss of affinity for the dam, inability to find the udder, abnormal vocalization, loss of suckle, dysphagia, central blindness, anisocoria, nystagmus, strabismus, head tilt, irregular or abnormal respiration, dysmetric gait, and proprioceptive deficits. Hypoxic neonates may also have gut stasis and renal ischemia. Neonates sometimes appear normal at birth and develop neurologic signs 24–48 hr later. Therapy frequently includes pharmacologic control of seizures (diazepam for individual seizures which may be followed with phenobarbital to control recurrent seizures), medications to reduce cerebral edema (IV dimethyl sulfoxide and/or mannitol), and plasma transfusion to provide oncotic support and prevent secondary sepsis. Provision of oxygen is controversial but should be performed if hypoxemia is documented. Enteral or parenteral nutritional support is critical because affected animals usually have suboptimal voluntary intake, which can lead to hypoglycemia and worsening of clinical signs. Vigilant nursing care is required to prevent injury while the neonate is recumbent or disoriented. Respiratory function is assisted by maintaining recumbent neonates in a sternal position; periodic administration of eye lubricant should be considered to prevent corneal ulceration from incomplete lid closure or corneal trauma related to recumbency.
Prematurity and Dysmaturity
Prematurity is delivery of the neonate before the end of normal gestation, whereas dysmaturity describes neonates born after an appropriate duration of gestation that display aspects of prematurity. The normal gestation length varies significantly among large animal species but is ~340 days in mares, alpacas, and llamas; 280 days in cattle, 150 days in small ruminants, and ~114 days in sows. Possible precipitating causes of prematurity and dysmaturity can include in utero viral infection, acute or chronic bacterial placentitis, congenital fetal abnormalities, maternal endocrine abnormalities, chronic placental insufficiency, maternal hydrops allantois/amnii, incompetent cervix, severe maternal illness, and prolonged maternal fasting.
Physical characteristics of the premature or dysmature animal can include low birth weight; thin condition; a short, silky hair coat; domed forehead; floppy ears and soft lips; an absence of incisor teeth; closed eyes; incompletely ossified cuboidal bones; and an absence of hair in extreme prematurity. Functional disabilities that can occur include weakness, inability to maintain sternal recumbency or to stand unassisted, diminished suckle reflex and ineffective swallow, ligament and tendon laxity, hypothermia due to poor thermoregulatory control, and tachypnea and respiratory distress due to lung and chest wall immaturity. Frequently these neonates display a delayed time to stand and nurse, which compromises passive transfer. Additionally, immature GI function can further compromise absorption of the ingested antibodies, and intolerance to oral feeding can result in signs of colic, gastric reflux, abdominal distention, and diarrhea.
Premature neonates require good nursing care and excellent nutritional support until they are able or allowed to stand and nurse normally. Major complications that can affect premature neonates include respiratory compromise (reflected by respiratory distress, hypoxia, and hypercapnia) and the development of septicemia as a result of inadequate passive transfer.
Last full review/revision July 2011 by Erica C. McKenzie