Immediate Postpartum Care - The Merck Veterinary Manual

Immediate Postpartum Care

Hypothermia

Neonatal Hypoglycemia

Septicemia

Neonatal Diarrhea

Peripartum Asphyxia

Prematurity and Dysmaturity

After delivery, the neonate’s respiratory tract should be cleared immediately. A portion of the placenta may cover the nostrils, or inhaled amniotic fluid may block air passages. Meconium staining of the fetus or fluids is suggestive of birth stress and peripartum asphyxia. Meconium can physically obstruct the larynx and lower airways if inhaled, and it should be removed. Artificial respiration and elevation of the neonate’s hindquarters often assist in initiating respirations. Smaller animals can be held head down and, while carefully supported, swung through a small arc to promote drainage of the respiratory tract. Brisk rubbing with a towel and extension of the limbs also stimulates respiration.

Neonates experiencing postpartum apnea require artificial respiration using mouth-to-nose resuscitation or ventilation via an endotracheal tube. Prompt insertion of a cuffed endotracheal tube into the trachea and application of suction followed by positive-pressure ventilation can save some animals that would otherwise die. Calves and small ruminants can be intubated orally using a laryngoscope and an endotracheal tube with a rigid stylet. Calves can be intubated blindly via palpation of the larynx with the head and neck in an extended position. Foals can be intubated orally or nasally using a long, cuffed nasotracheal tube. Ideally, meconium or excessive amniotic fluid should be removed by suctioning of the nasal passages and nasopharynx, followed by positive-pressure ventilation administered via a handheld resuscitation bag. If spontaneous respirations are abnormally slow or labored and accompanied by bradycardia, oxygen supplementation is indicated. Oxygen can be administered using a face mask equipped with an exhalation valve or via an intranasal cannula placed up one nostril to a level just below the medial canthus of the eye. Oxygen flows of 3-7 L /min are usually adequate. Maintaining the neonate in sternal recumbency allows ventilation of both lung fields and reduces dependent lung atelectasis.

If cardiac arrest accompanies respiratory arrest, then chest compressions should be initiated after ventilation has been started. 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. If cardiac arrest persists, IV epinephrine should be given at an initial IV dosage of 0.01-0.02 mg/kg. If there is no response within 3 min, additional epinephrine can be given IV or intratracheally at a dosage of 0.1 mg/kg at 3- to 5-min intervals.

If birth was normal and the umbilical cord was not ruptured in the process, the cord should be left intact for ~5 min; contraction of the uterus forces placental blood into the neonate, thus increasing its chances of survival and reducing the risk of neonatal anemia. After the cord is broken, 2% iodine or chlorhexidine solution should be applied to the stump twice daily until the umbilical remnant is dry. All meconium should be passed within 24 hr of delivery. Foals are often given prophylactic gravity enemas to reduce the risk of meconium impaction. In areas where screw worms are a problem for ruminants, repellent should be applied. Because some dams, especially primiparous ones, may be apprehensive and injure their offspring by butting, striking, kicking, or biting, the attendant should protect the newborn from injury until the dam accepts it or remove it completely from the stall. Mares that attempt to kick or bite their newborn foals can be sedated with acepromazine. Hobbles and a grazing muzzle can be used on the mare to help prevent injury to her foal. Whenever there are signs of mismothering, it is important to reduce unnecessary traffic into and around the birthing stall while ensuring that calm, competent handlers are in attendance to facilitate bonding between dam and offspring.

All large animal neonates are born essentially without circulating γ-globulins due to the lack of in utero transfer of immunoglobulins to the fetus. Ingestion of colostrum that contains adequate amounts of IgG, IgM, and IgA is essential. When absorbed through the gut wall and when in the gut lumen, these immunoglobulins protect the neonate against systemic and enteric diseases. The effectiveness of colostrum in disease prevention and control is determined by the amount ingested, the concentration of specific immunoglobulins, and the absorptive capability of the neonate’s gut wall. Colostrum from primiparous animals may be deficient in immunoglobulins. Premature lactation in mares is another common cause of poor colostral quality.

Newborns should receive colostrum as soon after birth as possible, preferably within the first 30-90 min. They should be observed closely and assisted if necessary to make certain that they nurse. If the neonate is too weak to nurse, colostrum should be fed via bottle or stomach tube. When colostrum from the dam is not available, it should be secured from another animal or from a previously frozen supply. Foals should receive a minimum of 1 L, and calves 2 L of colostrum. Following adequate colostrum ingestion, healthy foals and ruminants should have serum IgG concentrations >800 mg/dL and >1,600 mg/dL, respectively. Neonates >24 hr old with failure of passive transfer of colostral antibodies are unable to absorb immunoglobulins received PO due to a decrease in gut wall permeability. These older individuals must receive parenteral antibody supplementation using plasma from the dam or a commercial source. The minimal volume of plasma required is usually 20-40 mL/kg.

Early assessment of the newborn allows timely detection of illness and identification of potentially life-threatening congenital malformations. Early recognition of a hopelessly deformed neonate allows an owner to consider euthanasia versus prolonged care and treatment. Many birth defects are heritable, but it is often difficult to differentiate between those that are and those that are not. Surgical correction of some abnormalities is possible but usually not desirable if the animal will be used for breeding. Examples of potentially life-threatening congenital defects include severe craniofacial malformations, cleft palate, scoliosis, ventral septal defect, severe limb contracture, and atresia coli. Other defects such as umbilical or inguinal hernias are often self-correcting within the first few months of life.

Large animal neonates are precocious and should be able to stand and nurse within 1-3 hr of birth. Newborn foals and calves have a body temperature of 99-102°F (37-38°C) and a pulse of 80-110 bpm. Early signs of neonatal compromise include a weak or absent suckle reflex, inability to stand, depressed or somnolent attitude, and injected mucous membranes and/or sclera. Common periparturient conditions that result in reduced neonatal vigor include hypothermia, hypoglycemia, septicemia, diarrhea, peripartum asphyxia, and prematurity or dysmaturity. If newborn animals become sick, diagnosis and treatment must be prompt because they have little reserve and die quickly. Proper nursing care often determines whether a sick animal will live or die and should not be neglected.

Hypothermia:

Although most newborn livestock can withstand very cold temperatures once they are dried (except piglets, see below), their extremities may freeze if they are born into a cold environment. In climates where winter temperatures are low, protection should be provided. If economic conditions make this unfeasible, animals should be bred to give birth later in the winter or early spring.

Every effort should be made to maintain body heat during inclement weather. For large animals, it usually is not practical or advisable to heat a large barn to maintain the temperature during extremely cold weather. In such cases, it is advisable to partition small areas that can be more economically heated for severely stressed animals. If used, heat sources should be regulated to meet the needs of the species of animals being managed (eg, piglets require a much warmer environment than calves or foals). A radiant heat lamp placed beyond the animal’s reach probably is the most effective method of maintaining body heat in sick neonates.

Neonatal Hypoglycemia:

Hypoglycemia develops as a result of decreased caloric intake and/or increased catabolism. Decreased intake can be associated with inability to nurse due to neonatal factors such as weakness, prematurity, peripartum asphyxia, or competition between siblings, or it may be due to maternal factors such as agalactia, mastitis, or maternal rejection. Increased catabolism is often due to septicemia resulting in increased glucose consumption by bacteria and decreased glucose uptake by host cells due to peripheral insulin resistance.

Septicemia with secondary loss of nursing vigor is the most common cause of severe hypoglycemia (glucose <20-40 mg/dL) in newborn foals. Affected foals often exhibit temperature instability and varying degrees of hypovolemic and hemodynamic shock. In addition to parenteral glucose supplementation, septic foals require IV antibiotics, parenteral fluid therapy, and respiratory and nutritional support. Although the intraperitoneal route is used for glucose administration in piglets and small ruminants, it should not be used in foals.

Neonatal hypoglycemia is most common in piglets <1 wk old. It is a contributing factor that leads to death in many diseases and accounts for 15-35% of total piglet mortality. With only partial gluconeogenic ability, limited energy reserves, and essentially no brown fat, newborn piglets rely on glycogen reserves and, most importantly, frequent nursing. Piglets are predisposed to hypoglycemia if the sow has any disease that decreases or inhibits milk production or letdown. Large litter size with an inadequate number of teats precludes proper nursing. In addition, if the lower rail of the farrowing crate impairs access to the udder, inadequate milk intake and hypoglycemia can result.

Piglets have an effective metabolic response to cold and fully functional peripheral vasoconstriction, but their lack of insulating subcutaneous fat (until 1-2 wk old) allows marked heat loss. In drafty or wet environments, on cold floors, or in low ambient temperatures, maintenance of body temperature demands rapid glucose use, which depletes glycogen reserves; if milk intake is impaired, hypoglycemia and death result.

One or more piglets in a litter may be involved. Initially, behavior changes from vigorous sucking or play alternating with sleep to solitary lassitude. Affected piglets wander aimlessly with a faltering gait and cry weakly. The piglets are gaunt with poor muscle tone and pale, cold, clammy skin. They are hypothermic and unresponsive to external stimuli. As incoordination increases, piglets may stand with legs splayed, followed by sternal or lateral recumbency. Terminally, they exhibit convulsions with jaw champing, salivation, opisthotonos, nystagmus, forelimb and hindlimb contraction, coma, and death. Many affected piglets are crushed by the sow.

Blood glucose levels fall from a normal of 90-130 mg/dL to as low as 5-15 mg/dL; piglets usually manifest clinical signs when levels are <50 mg/dL. Any condition that impairs food intake by neonatal pigs can complicate the diagnosis. Generally, however, hypoglycemia can be diagnosed by examination of the sow and environment for predisposing factors and by the piglet’s response to glucose therapy.

Piglets should be treated with 15 mL of 5% glucose given IP and placed in a warm environment. A heat lamp can be used. Shivering and more activity should follow within 5-10 min. Severely hypoglycemic and hypothermic piglets may not respond. Sustained energy intake must be provided to avoid relapse. If oxytocin fails to promote milk letdown in the sow, 20 mL of 5% dextrose, cow’s colostrum, or evaporated milk diluted one-half with water can be administered intragastrically to each piglet through a small plastic cannula (with care, to avoid damage to the pharyngeal diverticulae), or treatment with glucose IP can be repeated every 4-6 hr. Active piglets learn quickly to drink from a dish. Foster-suckling of piglets is possible in batch farrowing units; most sows accept piglets during the milk letdown period if introduced quietly within the first 24 hr after farrowing. Redistribution of piglets from litters of uneven sizes may reduce mortality from starvation and hypoglycemia. Any primary disease of the sow should be treated, and any faults within the environment corrected. Piglets should be held in a draft-free creep area heated to 95°F (35°C) during the first week of life. Cold-stressed and marginally hypoglycemic piglets are more susceptible to other neonatal diseases.

Septicemia:

The most common routes of infection for large animal neonates are the placenta, the GI and respiratory tracts, and the umbilical remnants. Bacterial sepsis is most commonly associated with disseminated gram-negative bacterial infection. During sepsis, the release of bacterial endo- or exotoxins results in overactivation of the host’s immune system and uncontrolled release of endogenous mediators. This response precipitates a cascade of metabolic and hemodynamic changes that often culminates in multiple organ system failure. The endpoint is septic shock and is characterized by circulatory failure, perfusion deficits, and an inability of the body to use existing metabolic substrates effectively.

Factors predisposing to the development of septicemia include overcrowding; poor ventilation and sanitation; inappropriate umbilical disinfection; and periparturient stresses including premature delivery, dystocia, cesarean section, peripartum hypoxia, severe maternal illness, and failure of passive antibody transfer. Early signs of neonatal sepsis include lethargy, hypotonia, decreased nursing vigor, loss of suckle reflex, hyperemic mucous membranes with rapid capillary refill time associated with peripheral vasodilation, increased cardiac output, tachycardia, bounding peripheral pulses, extremities that are still warm, tachypnea, and variable body temperature. Increased vascular permeability contributes to the development of petechial hemorrhages on the gums, sclera, coronary bands, and inside the ears. During late sepsis, signs of shock develop. Affected neonates are usually recumbent, dehydrated, and moribund. Clinical signs include severe hypotension; tachycardia; cold extremities; dry, injected mucous membranes with a toxic ring; and prolonged capillary refill time. Gut motility is reduced or absent and is accompanied by gastric reflux, abdominal distention, and diarrhea or constipation. Tachypnea, dyspnea, rib retractions, and expiratory grunting characterize respiratory failure. One of the earliest laboratory signs of sepsis is the development of leukopenia, neutropenia, and a degenerative left shift accompanied by dehydration.

Successful treatment of neonatal sepsis depends on early recognition and aggressive support using systemic, broad-spectrum, bactericidal antibiotics, IV fluids (crystalloids and colloids), plasma, enteral and/or parenteral nutritional support, and oxygen therapy.

Neonatal Diarrhea:

Diarrhea is a common problem for all large animal neonates. In ruminants, causes of neonatal diarrhea include rotavirus, cryptosporidia, coronavirus, Campylobacter spp , enterotoxigenic Escherichia coli , and Salmonella . In calves, bovine viral diarrhea virus is another important etiologic agent. Causes of diarrhea in newborn foals include rotavirus, Salmonella , Clostridia spp , Strongyloides , and necrotizing enterocolitis. Therapy for neonatal diarrhea focuses on maintaining hydration and preventing electrolyte imbalances such as metabolic acidosis, hyponatremia, and hypochloremia, while treating the underlying cause.

Peripartum Asphyxia:

Asphyxia is the result of impaired oxygen delivery to cells and usually results from a combination of hypoxemia—decreased oxygen concentration in the blood—and ischemia—decreased tissue perfusion. Periparturient asphyxia can result from any event that impairs uteroplacental perfusion prepartum or intrapartum or disrupts normal distribution of blood flow postpartum. Neonatal asphyxia has been associated with normal deliveries, dystocias, induced deliveries, cesarean sections, placentitis, premature placental separation, meconium-stained foals, the birth of multiple fetuses, severe maternal illness, and post-term pregnancies.

Neonates with periparturient asphyxia display a wide spectrum of neurologic signs that include jitteriness, hyperalertness, stupor, somnolence, lethargy, hypotonia, seizures, extensor rigidity, tonic posturing, aimless wandering, head pressing, loss of affinity for the dam, inability to find the udder, abnormal vocalization (barking, high pitched cry), loss of suckle, dysphagia, odontoprisis, central blindness, anisocoria, nystagmus, eye deviation, head tilt, head and neck turn, irregular respiration, apnea, abnormally slow respiratory rate, dysmetric gait, and proprioceptive deficits. Hypoxic neonates may also experience gut stasis and renal ischemia. Therapy includes anticonvulsants to stop seizures (eg, diazepam, phenobarbital), medication to control cerebral edema (eg, IV dimethyl sulfoxide, IV mannitol), antibody administration to prevent secondary sepsis, nutritional support to prevent hypoglycemia, and vigilant nursing care to prevent injury while the neonate is recumbent or disoriented.

Prematurity and Dysmaturity:

Possible causes of prematurity or dysmaturity include the following: 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.

Clinical signs include low birth weight; generalized muscle weakness; inability to maintain sternal recumbency or stand unassisted; short, silky hair coat; domed forehead; floppy ears and soft lips; diminished suckle reflex and ineffective swallow; delayed time to nurse; periarticular ligamentous laxity and flexor tendon laxity; delayed time to stand; hypothermia due to poor thermoregulatory control; intolerance to oral feeding due to immature GI function resulting in colic, gastric reflux, abdominal distention, and diarrhea; increased work of breathing; tachypnea and respiratory distress due to lung and chest wall immaturity; and incomplete ossification of cuboidal bones. Premature neonates require good nursing care and excellent nutritional support until they are able to stand and nurse normally. Until that time, premature newborns are at increased risk of respiratory distress and septicemia.