Intensive Care and Emergencies in Neonatal Foals

Early recognition of abnormalities is of utmost importance for successful management of critically ill foals. (Also see Management of the Neonate.) Immediately after birth, the cardiovascular and respiratory systems of foals must adapt to extrauterine life. These critical events can be undermined by factors such as inadequate lung development, surfactant deficiency, viral or bacterial infection, placental abnormalities, in utero hypoxia, and meconium aspiration.

Spontaneous breathing should begin within 1 minute of birth, and many foals attempt to breathe as soon as the thorax clears the mare’s pelvic canal. During the first hour of life, the respiratory rate can be > 60 breaths/minute; however, it should decrease to 30–40 breaths/minute within a few hours.

Auscultation of the thorax shortly after birth reveals a cacophony of sounds as airways are gradually opened and fluid is cleared. End-expiratory crackles are consistently heard in the dependent lung during and after periods of lateral recumbency.

It is not unusual for a neonatal foal to appear slightly cyanotic during the adaptation period; however, this condition should resolve within a few minutes of birth. Similarly, the heart rate of a healthy neonatal foal has a regular rhythm and should be > 60 bpm after the first minute. Occasionally, arrhythmias (atrial fibrillation, wandering pacemaker, atrial or ventricular premature contractions) are auscultated; however, they should resolve within 15 minutes after birth.

A continuous holosystolic (machinery) murmur heard for the first few days after birth over the left side of the heart is normal and consistent with patent ductus arteriosis. The ductus arteriosis closes without treatment, and the murmur resolves as the foal's circulatory system changes to an adult's. Various other systolic murmurs, thought to be flow murmurs, may be heard during the first week of life; they also resolve without intervention in that time frame.

Foals are typically nonresponsive to stimulation while in the birth canal. This lack of responsiveness can lead to a presumption of fetal death during dystocia. Diagnostic tests, including palpation of a pulse in the tongue, neck, or limb, or palpation and auscultation of the thorax for a heartbeat, should be performed to confirm whether the foal has died.

If the foal’s nose is accessible during parturition, nasotracheal intubation enables the measurement of CO₂ concentrations in expired gas. A long endotracheal tube (outer diameter 7–12 mm) with an inflatable cuff should be used. The tube is passed blindly into the ventral meatus, with a finger guiding it. Proper placement can be determined by palpation of the throat latch and neck. The cuff is inflated, and manual ventilation is performed with either 100% oxygen or room air.

Expired CO₂ concentrations are measured continuously with a capnograph or a single-use end-tidal CO₂ monitor. End-tidal CO₂ varies in foals during parturition, depending on cardiac output and ventilation frequency; however, it should be consistently > 20 mm Hg and is usually closer to 30 mm Hg. After manual ventilation of a living foal is established in the birth canal, it must be continued until the foal is delivered.

Both the righting reflex and the withdrawal reflex should be present as the foal exits the birth canal. Cranial nerve responses are intact at birth; however, the menace response can take up to 2 weeks to fully develop. Absence of a menace response should not be considered diagnostic of visual deficits in neonatal foals. The suckle reflex should be strong within 10 minutes of birth.

Within 1 hour of birth, healthy foals demonstrate auditory orientation with unilateral pinna control. The normal pupillary angle is ventromedial in the neonate; this angle gradually becomes dorsomedial during the first month of life. Foals can attempt to rise within 20 minutes of birth; most should stand on their own within 1 hour and nurse by 2 hours.

The gait of the neonatal foal is hypermetric with a wide-based stance. Extreme hypermetria of the forelimbs, usually bilateral but occasionally unilateral, has been observed in some foals in association with perinatal hypoxia and ischemia; this gait abnormality usually resolves without specific treatment within a few days.

Neonatal spinal reflexes tend to be exaggerated. Foals also exhibit an exaggerated response to external stimuli (eg, noise, sudden movement, touch) for the first few weeks of life.

Some foals defecate shortly after standing; many, however, do not attempt to defecate until after successfully suckling, approximately 3 hours after birth.

First urination is more variable; fillies usually urinate before colts. It is not unusual for a colt not to “drop” its penis when urinating for the first few days of life because of the persistence of a normal tissue frenulum in the prepuce. The penis should not be forced from the prepuce; the frenulum regresses without treatment.

Initial assessment of the possible need for resuscitation begins during presentation of the foal in the birth canal. Although the following discussion applies primarily to the birth of a foal from a high-risk pregnancy, quiet and rapid evaluation can be performed during any attended birth.

The goal in the normal birth of a healthy foal is to minimally disturb the bonding process between mare and foal. The goal is the same for high-risk births, although some disruption of normal bonding is inevitable.

Immediately after birth, foals must adapt to independent thermoregulation. Normal foals can generate heat through a metabolic surge after birth known as nonshivering thermogenesis. Nonshivering thermogenesis is impaired in hypoxic or asphyxiated neonates and in those ill at birth.

Human infants born to mothers sedated by benzodiazepines are similarly affected, which is a consideration in the choice of sedative and preanesthetic medications in mares with dystocia or undergoing cesarean section.

In addition to nonshivering thermogenesis, thermoregulation in healthy foals is supported by a high metabolic rate, thick hair, fat stores, and the ability to shiver within minutes of birth.

Heat losses by convection, radiation, and evaporation are quite high in most areas where foals are delivered, resuscitated, and managed, and care must be taken to ensure that cold stress is minimized in neonatal and critically ill foals. Foals should be dried and placed on dry bedding when resuscitation is complete. Supplemental heat in the form of radiant lamps or warm air-circulating blankets could be required.

Fluid therapy should be used conservatively in postpartum resuscitation. Neonates typically are not volume depleted unless excessive hemorrhage has occurred. Some compromised neonates are actually hypervolemic.

Because the renal function of the equine neonate is substantially different from that of adult horses, fluid therapy cannot simply be scaled down. If IV fluids are required for resuscitation and blood loss is identified, administration of 20 mL/kg of a polyionic, isotonic, glucose-free fluid over 20 minutes (approximately 1 L for a 50-kg foal) can be effective.

Indications for this shock bolus include poor mentation, poorly palpable peripheral pulses, and development of cold distal extremities compatible with hemorrhagic shock. The foal should be assessed after the initial bolus, with up to three additional fluid boluses administered as needed.

Dextrose-containing fluids can be administered after resuscitation at a rate of 4–8 mg of glucose/kg/minute (approximately 120 mL/hour of 10% dextrose in balanced electrolyte solution to the average 50-kg foal), particularly in obviously compromised foals. This treatment is indicated to maintain blood glucose concentrations, resolve metabolic acidosis, and support cardiac output, because myocardial oxygen stores have likely been depleted.

Prematurity, dysmaturity, and postmaturity can all be associated with high-risk pregnancy. Postmature foals are commonly born to mares that have summer fescue toxicosis from ingesting endophyte-infested fescue grass or hay.

Iatrogenic causes of prematurity include early elective induction of labor (based on inaccurate breeding dates) or misinterpretation of late-term colic or uterine bleeding as ineffective labor. Usually the cause is idiopathic. Even if undetermined, the cause can continue to affect the foal after birth.

• Physical examination

• Hematologic evaluation

• Blood culture

• Radiographic or CT examination

All body systems can be affected by prematurity, dysmaturity, and postmaturity, and comprehensive examination with laboratory analysis and diagnostic imaging is necessary.

• Oxygen therapy (potentially with mechanical ventilation)

• Fluid therapy with pressors or inotropes as needed

• Anticonvulsants

• Hyperimmune plasma

• Supportive care and physical rehabilitation

Respiratory failure is common in premature foals and is related to immaturity of the respiratory tract, poor control of respiratory vessel tone, and weak respiratory muscles, combined with poorly compliant lungs and a greatly compliant chest wall. It is usually not due to surfactant deficiency.

Most premature, dysmature, and postmature foals require oxygen supplementation and positional support for optimal oxygenation and ventilation. These “floppy foals” should be maintained in sternal recumbency, if possible. Some might require mechanical ventilation or high-flow oxygen therapy (> 40 L/minute) for respiratory support.

Premature foals also require cardiovascular support; however, they are frequently unresponsive to commonly administered pressors and inotropes, including dopamine, dobutamine, epinephrine, and vasopressin. Careful administration of these drugs and judicious IV fluid therapy are necessary.

Renal function, reflected in low urine output, is often initially poor in foals because of a delay in making the transition from fetal to neonatal glomerular filtration rates. The delay can be due to true failure of transition or secondary to a hypoxic or ischemic insult. Fluid therapy should be used cautiously in these cases; an initial fluid restriction might be required to avoid fluid overload.

The Holliday-Segar formula is recommended to prevent excessive fluid administration. The formula is the sum of three parts, as follows:

• for the first 10 kg of body weight (1–10 kg), 100 mL/kg every 24 hours

• for the second 10 kg of body weight (11–20 kg), 50 mL/kg every 24 hours

• for foals > 20 kg, 25 mL/kg every 24 hours for the balance of the total body weight

Many premature, dysmature, and postmature foals have suffered hypoxic insult and present with all of the disorders associated with perinatal asphyxia syndrome, inducing neonatal encephalopathy (see Neonatal Encephalopathy below or the extended discussion in Management of the Neonate). Treatment is similar to that of term foals that exhibit these problems. Foals with this syndrome are also predisposed to secondary bacterial infections and must be examined frequently for clinical signs consistent with early sepsis or nosocomial infection.

The GI system of foals with prematurity or post-hypoxic syndrome is also commonly impacted: dysmotility, enterocolitis, and malabsorption are frequent clinical manifestations of GI dysfunction (see necrotizing enterocolitis image).

Necrotizing enterocolitis, foal

Image

Courtesy of Dr. Amelia Munsterman.

Hyperglycemia in premature and post-hypoxic foals is generally related to stress, increased concentrations of circulating catecholamines, and a rapid progression to gluconeogenesis. Hypoglycemia is associated with diminished glycogen stores, lack of gluconeogenesis, sepsis, and hypoxic damage. Endocrine function can be immature, particularly within the hypothalamic-pituitary-adrenal axis, and contributes to metabolic derangements.

When enteral feeding is provided, volumes given should be small at first and slowly increased throughout several days, depending on the response to treatment. Parenteral nutrition will be required until the foal is able to consume an adequate amount of milk.

In addition to multiple organ system dysfunction, premature or dysmature foals commonly have musculoskeletal abnormalities. Although not life-threatening, these abnormalities should be addressed promptly after the patient is stabilized.

With intensive care and attention to detail, the overall prognosis for premature, dysmature, and postmature foals is fair to good. Many such foals survive and become productive athletes. Complications associated with sepsis and musculoskeletal abnormalities are the most significant indicators of poor athletic outcome (1).

A wide spectrum of clinical signs are associated with neonatal encephalopathy in horses, ranging from mild lethargy with loss of suckle reflux to grand mal seizures. Affected foals are typically healthy at birth but show clinical signs of CNS abnormalities within a few hours. However, the onset of clinical signs varies; some foals show obvious signs at birth, and some show no signs until 24 hours after birth.

Neonatal encephalopathy is commonly associated with adverse peripartum events, including dystocia, placentitis, twinning, and premature placental separation. However, some foals show no evidence of a cause, suggesting that unrecognized in utero hypoxia occurred.

• Supportive care

• Anticonvulsants

• Fluid therapy

• Oxygen therapy

• Antimicrobials

• Pressor therapy

The following measures are taken to treat clinical signs of hypoxia and ischemia:

• control of seizures and cerebral edema

• support of cerebral perfusion

• correction of metabolic abnormalities

• maintenance of normal blood gas values, tissue perfusion, and renal function

• treatment of GI dysfunction

• prevention, recognition, and early treatment of secondary infections

• general supportive care

Seizures must be controlled because they increase cerebral oxygen consumption 5-fold. Diazepam (0.1–0.44 mg/kg, IV) and midazolam (0.04–0.1 mg/kg, IV, slowly) can be administered for emergency treatment; however, the foal must be monitored for respiratory depression. For severe or persistent seizures, phenobarbital (2–3 mg/kg, IV, every 8–12 hours), levetiracetam (32 mg/kg, IV or PO, every 12 hours), or a constant-rate infusion of midazolam (2–5 mg/hour for a 50-kg foal) can be instituted.

Sepsis in foals can be quite subtle initially, and the onset of clinical signs varies with the pathogen involved and the immune status of the foal. Common pathogens include gram-negative bacteria; some gram-positive infections have also been identified.

Failure of transfer of passive immunity (often shortened to "failure of passive transfer") can contribute to the development of sepsis in foals at risk. An IgG concentration > 800 mg/dL is adequate for the transfer of passive immunity to foals. Other risk factors for development of sepsis include any adverse event at the time of birth, maternal illness, or any abnormality in the foal.

Although the umbilicus is frequently implicated as a major portal of entry for infectious organisms, the GI tract can be the primary site of entry. Other portals of entry include the respiratory tract and wounds.

Early clinical signs of sepsis in foals can involve any tissue or organ system (see Coronitis image) and often include the following:

• lethargy

• weakness, recumbency

• dysphagia, decreased suckle reflex

• failure to gain weight

• tachypnea

• tachycardia or bradycardia

• fever or hypothermia

• injected mucous membranes, petechiae, increased capillary refill time

• lameness

Coronitis, foal

Image

Courtesy of Dr. Amelia Munsterman.

• Clinical evaluation of the affected organ

• Bacteriological culture

• PCR assay

• Evaluation of response to treatment

Survival rates of foals treated for sepsis have improved; however, infection must be recognized early for the possibility of a good outcome. The pathogen involved can also affect survival. Gram-negative species are commonly diagnosed, but gram-positive septicemia is being recognized more frequently, and multiple organisms can be involved.

It is important to identify the organism early in the course of the disease. Blood cultures should be obtained, as well as samples from synovial fluid, CNS, peritoneal fluid, urine, and tracheal aspirates if localized clinical signs are present.

• Antimicrobials

• Hyperimmune plasma

• Oxygen therapy

• Pressors or inotropes

• Supportive care

Until antimicrobial susceptibility patterns for the pathogen involved are obtained, broad-spectrum antimicrobial treatment should be started. Amikacin (25–30 mg/kg, IV, every 24 hours) and penicillin (22,000–44,000 U/kg, IV, every 6 hours) are good first-line choices; however, renal function must be monitored closely. Therapeutic drug monitoring might be needed to ensure adequate drug concentrations.

Other first-line antimicrobials include ceftiofur sodium (5–10 mg/kg, IV, every 12 hours) and ticarcillin/clavulanic acid (50–100 mg/kg, IV, every 6 hours).

Failure of passive transfer should be treated with administration of hyperimmune plasma (1–2 L for the average 50-kg foal). Intranasal oxygen insufflation at 5–10 L/minute should be provided, even if hypoxemia is not present. If hypoxemia or hypercapnea develops, high-flow oxygen therapy (40 L/minute) can decrease the work of breathing and provide support for the increased oxygen demands associated with sepsis.

Mechanical ventilation can be necessary in cases of severe respiratory involvement that occur with acute lung injury or acute respiratory distress syndrome. If the foal is hypotensive, pressor agents or inotropes can be administered by constant-rate infusion. Treatment with inotropes and pressors is generally restricted to referral centers, where infusions and the foal’s blood pressure can be closely monitored.

NSAIDs and corticosteroids are used to treat sepsis in foals in specific circumstances. For example, NSAIDS provide excellent pain management, and corticosteroids are important in the treatment of adrenal insufficiency. These drugs should be administered judiciously because they can have severe negative consequences, including, but not limited to, renal failure and GI ulceration.

Proton pump inhibitors are controversial for treating sepsis in foals because critically ill, recumbent foals typically have an alkaline gastric pH. These medications can be more useful once the foal is ambulatory.

Supportive care is important in the treatment of sepsis in foals. If recumbent, foals should be kept warm and dry and turned at 2-hour intervals. Foals should be maintained in sternal recumbency to improve respiratory function and decrease the risk oflung atelectasis.

Feeding septic foals can be a challenge if GI function is abnormal; total parenteral nutrition could be needed. If possible, foals should be weighed daily and blood glucose concentrations monitored frequently. Some foals become persistently hyperglycemic on low rates of glucose infusion. These foals can benefit from constant-rate infusions of insulin.

Recumbent foals must be examined frequently for decubital and corneal ulcers, as well as for heat and swelling associated with the joints and physes. Physical rehabilitation or passive range-of-motion exercises should be provided.

The prognosis for foals in the early stages of sepsis is fair to good. If sepsis progresses to septic shock, the prognosis becomes less favorable. Longterm survival and athletic outcomes are fair. Racing-breed foals perform on the track similarly to their age-matched siblings (2).