Early recognition of abnormalities is of utmost importance for successful management of critically ill foals. (Also see Overview of Management of the Neonate in Large Animals.) Immediately after birth, the cardiovascular and respiratory systems of the foal must adapt to extra-uterine life. These critical events can be undermined by factors such as inadequate lung development, surfactant deficiency (primary or secondary), viral or bacterial infection, placental abnormalities, in utero hypoxia, and meconium aspiration.
Spontaneous breathing should begin within 1 min 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/min but should decrease to 30–40 breaths/min 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 newborn foal to appear slightly cyanotic during the adaptation period, but this should resolve within a few minutes of birth. Similarly, the heart rate of a healthy newborn foal has a regular rhythm and should be at least 60 bpm after the first minute. Occasionally, arrhythmias (atrial fibrillation, wandering pacemaker, atrial or ventricular premature contractions) may be ausculted but should resolve within 15 min after birth. A continuous holosystolic, or machinery, murmur heard for the first few days after birth over the left side of the heart is consistent with patent ductus arteriosis. Various other systolic murmurs, thought to be flow murmurs, may be heard during the first week of life. Murmurs that persist beyond the first week of age, those that are loud (>2/6), or murmurs that cause exercise intolerance or hypoxemia should be investigated more thoroughly.
Foals are normally nonresponsive to stimulation while in the birth canal. This lack of responsiveness has led to the presumption of fetal death during dystocia. Diagnostics, 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 the foal has died. If the foal's nose is accessible during parturition, nasotracheal intubation will allow measurement of CO2 tension in the expired gas. A long endotracheal tube (size 7–12 mm outer diameter) with an inflatable cuff should be used. The tube is passed blindly into the ventral meatus using a finger to guide the tube. Proper placement can be determined by palpation of the throat. The cuff is inflated, and manual ventilation is performed with either 100% oxygen or room air. CO2 tension is 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, but it should be consistently >20 mmHg and is usually closer to 30 mmHg. Once manual ventilation of a living foal is established, it must continue until the foal is delivered.
The righting reflex is present as the foal exits the birth canal, as is the withdrawal reflex. Cranial nerve responses are intact at birth, but the menace response may take as long as 2 wk to fully develop. Absence of a menace reflex should not be considered diagnostic of visual deficits in newborn foals. The suckle reflex should be strong by 10 min of birth. Within 1 hr of birth, healthy foals demonstrate auditory orientation with unilateral pinna control. The normal pupillary angle is ventromedial in the newborn; this angle gradually becomes dorsomedial throughout the first month of life. Foals may attempt to rise within 20 min of birth; most should stand on their own within 1 hr and nurse by 2 hr. Some foals defecate shortly after standing, but many will not attempt to defecate until after successfully suckling, about 3 hr after birth. First urination is more variable, with fillies usually urinating before colts. It is not unusual for colts not to “drop” their penis when urinating for the first few days of life because of the persistence of a normal tissue frenulum within the prepuce. The penis should not be forced from the prepuce; the frenulum will resolve without treatment.
The gait of the newborn foal is hypermetric, with a wide-based stance. Extreme hypermetria of the forelimbs, usually bilateral but occasional unilateral, has been seen in some foals associated with perinatal hypoxia and ischemia, but this gait abnormality usually resolves without specific therapy within a few days. Spinal reflexes tend to be exaggerated in the neonate. Foals also exhibit an exaggerated response to external stimuli (eg, noise, sudden movement, touch) for the first few weeks of life.
Dystocia and Resuscitation
Most newborn foals make the transition to extra-uterine life easily. However, for those with difficulties (eg, dystocia, premature placental separation), it is of utmost importance to recognize and institute appropriate resuscitation procedures. A modified Apgar scoring system has been developed as a guide to initiate resuscitation and estimate the level of fetal compromise (see Table 2: Modified Apgar Score for Equine Neonates). A brief physical examination should also be performed before starting resuscitation, because of humane issues concerning resuscitation of foals with serious birth deformities (such as severe limb contracture and hydrocephalus, among others).
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The initial assessment begins during the presentation of the foal in the birth canal. Although the following 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. This also applies to a high-risk birth, although some disruption of normal bonding is inevitable.
The strength and rate of any palpable peripheral pulse should be evaluated as the foal presents. The apical pulse should be assessed as soon as the thorax clears the birth canal. Bradycardia (pulse <40 bpm) is expected during forceful uterine contractions, but the pulse rate should rapidly increase once the chest clears the birth canal. Persistent bradycardia is an indication for rapid intervention.
The fetus is normally hypoxemic compared with the newborn foal, and this hypoxia is largely responsible for the maintenance of fetal circulation by generation of pulmonary hypertension. During normal parturition, mild asphyxia occurs and results in fetal responses that lead to a successful transition to extra-uterine life. If more than mild asphyxia occurs, the fetus is stimulated to breathe in utero; this is known as primary asphyxia. If the initial breathing effort resulting from the primary asphyxia is not effective, a second gasping period occurs within several minutes known as secondary asphyxia. If asphyxia does not improve, the foal enters a stage called “secondary apnea,” which is irreversible unless resuscitation is initiated. Therefore, the first priority of neonatal resuscitation is establishing an airway and breathing for the foal. Foals that are not spontaneously breathing are assumed to be in secondary apnea.
The airway should be cleared of the fetal membrane as soon as the nose is presented. If meconium staining is present, the airway should be suctioned before delivery of the foal is complete, and before the foal breathes spontaneously to prevent aspiration. Suction should be continued to the level of the trachea if aspiration of the nasopharynx is productive. Suctioning should be brief and gentle; overzealous suctioning worsens hypoxia, which causes secondary bradycardia or cardiac arrest through vagal reflexes. Suctioning should stop once the foal begins to breathe spontaneously.
If the foal does not breathe or move spontaneously to right itself within seconds of birth, tactile stimulation is necessary (eg, drying with a towel). If tactile stimulation does not result in spontaneous breathing, the foal should be intubated immediately and manually ventilated. Mouth-to-nose ventilation can be used if nasotracheal tubes or a bag-valve-mask is not readily available. Hyperventilation with 100% oxygen is suggested to be the best choice to reverse fetal circulation; however, evidence from human medicine suggests there are no apparent disadvantages in using room air instead.
Almost 90% of foals requiring resuscitation respond to ventilation alone and require no additional therapy. Nasotracheal intubation can be started while the foal is in the birth canal if the foal is not delivered rapidly (eg, dystocia). This blind technique may require some practice but can be lifesaving. The nasotracheal tube also provides a convenient site for administration of intratracheal medications, such as epinephrine. Once breathing is spontaneous, humidified oxygen should be provided via nasal insufflation at 8–10 L/min.
Chest compressions should be started if the foal remains bradycardic despite ventilation or if a nonperfusing rhythm is palpated. The foal should be placed on a hard surface in right lateral recumbency with the topline against a wall or other support to keep the foal from sliding. The resuscitator's hands are placed over each other either directly over the heart (the cardiac method) or at the highest point of the chest (the thoracic method). The cardiac method is theorized to push blood forward by directly compressing the heart, whereas the thoracic method pulls blood forward by altering the intrathoracic pressure; both methods are valid in the foal. Compressions are provided at a rate of 80–120 per min, depressing the thorax 40% of its diameter, and allowing the chest to fully recoil. The first round of compressions should last 30–60 sec to allow for assessment of progress and addition of medications; after that, each round of compressions should last 2–3 min, followed by a 10-sec break to allow for assessment of heart rate, pulses, and rhythm. If the foal's heart does not start immediately after compressions cease, the resuscitator should switch out to prevent fatigue, and compressions are continued. Breaths should be provided by an assistant at a rate of 8–10 per min during cardiac compressions, or 2 breaths for every 30 compressions if the resuscitator is alone. If the foal is not resuscitated after 10–15 min of compressions, cerebral hypoxia is likely to have made further resuscitation efforts futile.
Because ~5% of foals are born with fractured ribs, assessment for the presence of rib fractures should be performed before starting chest compressions. Some of these fractures can be identified by palpation. Fractures typically occur between ribs 3 and 8, are usually multiple and consecutive, and are located in a relatively straight line along the part of the rib with the greatest curvature just dorsal to the costochondral junction. Unfortunately, their location over the heart can make chest compressions a potentially fatal exercise. Foals with rib fractures should be placed in lateral recumbency with the fractured ribs down for compressions. After resuscitation, ultrasound can be used to identify rib fractures that have escaped detection by palpation, or new fractures caused by compressions. Ultrasound is the most sensitive diagnostic tool to identify rib fractures.
Drug therapy should be started if a nonperfusing rhythm persists for >30–60 sec in the face of chest compressions. Epinephrine remains the drug of choice at a dosage of 0.01–0.02 mg/kg, IV. If given through the nasotracheal tube, the dosage should be 0.05–0.1 mg/kg. Epinephrine can be repeated every 2–3 min during compressions, coinciding with the 10-sec assessments between rounds of compressions. Vasopressin (0.6 U/kg, every 10–20 min) is gaining attention as a cardiovascular resuscitation drug, but experience in foals is limited. Atropine is not recommended in bradycardic newborn foals, because the bradycardia is usually secondary to hypoxia. Atropine can also increase myocardial oxygen debt if hypoxia is not corrected. Doxapram is not recommended for resuscitation of newborns, because it does not reverse secondary apnea.
Immediately after birth, the foal must adapt to independent thermoregulation. In response to the catecholamine surge associated with birth, uncoupling of oxidative phosphorylation occurs within the mitochondria, releasing energy as heat. This nonshivering thermogenesis is impaired in newborns undergoing hypoxia or asphyxiation, and in those ill at birth. Human infants born to mothers sedated by benzodiazepines are similarly affected, 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 the healthy foal is supported by a high metabolic rate, a thick hair coat, 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 newborn and critically ill foals. The foal should be dried and placed on dry bedding once resuscitation is compete. Supplemental heat in the form of radiant lamps or warm air circulating blankets may be required.
Fluid therapy should be used conservatively in postpartum resuscitation. The neonate is not volume depleted unless excessive hemorrhage has occurred. Some compromised newborns 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 min (~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, and additional boluses (up to three) administered as needed. Glucose-containing fluids can be administered after resuscitation at a rate of 4–8 mg of glucose/kg/min (~120 mL/hr, 10% dextrose in balanced electrolyte solution to the average 50-kg foal), particularly in the obviously compromised foal. This therapy is indicated to maintain blood glucose levels, resolve metabolic acidosis, and support cardiac output, because myocardial oxygen stores have likely been depleted.
Prematurity, Dysmaturity, and Postmaturity
Traditionally, prematurity in horses is defined as a birth at <320 days gestation. However, normal gestation length ranges from 310 days to >370 days in some mares, which makes it difficult to define maturity based solely on gestational age. Premature foals are small, with a fine, silky hair coat, generalized muscle weakness, joint and tendon laxity, incomplete cuboidal bone ossification, a domed forehead, and floppy ears. Foals born post-term, but small, are termed dysmature. These foals may also exhibit the characteristic signs of prematurity. Dysmature foals may have been classified in the past as “small for gestational age” and are thought to have suffered from placental insufficiency. A postmature foal is a post-term foal that has a normal axial skeletal size but is thin to emaciated. The hair coat is generally long, and the teeth may have erupted in utero. Postmature foals are usually healthy foals that have been retained too long in utero, perhaps due to an abnormal signaling of readiness for birth. Postmature foals become more abnormal the longer they are maintained in utero, and they may suffer from placental insufficiency. They are most commonly born to mares ingesting endophyte-infested fescue (see Summer Fescue Toxicosis).
Prematurity, dysmaturity, and postmaturity may all be associated with high-risk pregnancy. Iatrogenic causes include early elective induction of labor (based on inaccurate breeding dates) or interpretation of late-term colic or uterine bleeding as ineffective labor. Most often, the cause is idiopathic. Even if undetermined, the cause may continue to affect the foal after birth. All body systems may be affected by prematurity, dysmaturity, and postmaturity, and thorough evaluation is necessary.
Respiratory failure is common in these 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 a surfactant deficiency. Most foals require oxygen supplementation and positional support for optimal oxygenation and ventilation. Effort must be expended to maintain these “floppy foals” in sternal recumbency. Some may require mechanical ventilation.
These foals also require cardiovascular support but are frequently unresponsive to commonly used pressors and inotropes, including dopamine, dobutamine, epinephrine, and vasopressin. Careful use of these drugs and judicious IV fluid therapy are necessary. Renal function, reflected in low urine output, is often initially poor 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 may be required to avoid fluid overload.
Many premature, dysmature, or postmature foals have suffered a hypoxic insult and present with all of the disorders associated with perinatal asphyxia syndrome, inducing neonatal encephalopathy (see Neonatal Encephalopathy). Treatment is similar to that of term foals with these problems. These foals are also predisposed to secondary bacterial infections and must be examined frequently for signs consistent with early sepsis or nosocomial infection.
The GI system of these foals is not usually functionally mature because of a primary lack of maturity or secondary to hypoxia. Dysmotility and varying degrees of necrotizing enterocolitis are common, as are hyperglycemia and hypoglycemia. Hyperglycemia is generally related to stress, increased levels of circulating catecholamines, and a rapid progression to gluconeogenesis, whereas hypoglycemia is associated with diminished glycogen stores, the inability to engage gluconeogenesis, sepsis, and hypoxic damage. Endocrine function may be immature, particularly regarding the hypothalamic-pituitary-adrenal axis, and contributes to metabolic derangements. If possible, enteral feeding should be delayed until metabolic and cardiorespiratory parameters are stable, and parenteral nutrition provided. When enteral feeding is initiated, small volumes should be provided first and slowly increased throughout several days.
Musculoskeletal problems are frequent, particularly in premature foals, and include significant flexor laxity, periarticular ligament laxity, and decreased muscle tone. Premature foals frequently exhibit flexor laxity combined with decreased cuboidal bone ossification that predisposes them to crush injury of the carpal and tarsal bones if weight bearing is not strictly controlled. Physical therapy, in the form of assisted standing and controlled exercise, is indicated in the management of these problems; however, care should be taken to ensure that the foal does not become fatigued and stand in abnormal positions. Splints and casts only increase laxity in the limbs, although light bandages over the fetlock may be necessary to prevent injury if flexor laxity is severe. Glue-on shoes may help improve the weight-bearing axis. If tube casts are used, they should not extend below the fetlock to minimize laxity, and they should be changed regularly to prevent sores. These foals are also predisposed to angular limb deformities and must be closely monitored for development of this problem as they mature. Postmature foals may be affected by flexural contracture deformities, most likely due to decreased intrauterine movement as they increase in size (Also see Flexion Deformities in Horses.)
The overall prognosis for premature, dysmature, and postmature foals remains good with intensive care and attention to detail. Many foals survive and become productive athletes. Complications associated with sepsis and musculoskeletal abnormalities are the most significant indicators of poor athletic outcome.
A wide spectrum of clinical signs is associated with neonatal encephalopathy, ranging from mild depression with loss of suckle reflux to grand mal seizures. Affected foals are typically healthy at birth but show signs of CNS abnormalities within a few hours. However, the timing of onset of clinical signs varies; some foals are obviously abnormal at birth, and some do not show clinical signs until 24 hr of age. Neonatal encephalopathy is commonly associated with adverse peripartum events, including dystocia, placentitis, twinning, and premature placental separation. However, some foals have no known evidence for the cause of the hypoxic event, suggesting that unrecognized in utero hypoxia occurred. (Also see Neonatal Encephalopathy.)
Therapy for the various manifestations of hypoxia and ischemia involves 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; and general supportive care. Seizures must be controlled, because they increase cerebral oxygen consumption by 5-fold. Diazepam (0.1–0.44 mg/kg, IV) and midazolam (0.04–0.1 mg/kg, IV slow) can be used for emergency therapy, but the foal must be monitored for respiratory depression. For severe or persistent seizures, phenobarbital (2–3 mg/kg, IV, bid-tid) or a constant-rate infusion of midazolam (2–5 mg/hr for a 50-kg foal) may be instituted.
Sepsis in foals can be quite subtle initially, and the onset of clinical signs is variable depending on the pathogen involved and the immune status of the foal. Common pathogens include gram-negative bacteria, although gram-positive infections have been identified. Failure of passive transfer of immunity can contribute to development of sepsis in foals at risk. The current recommendation is that foals have an IgG level >800 mg/dL for passive transfer to be considered adequate. Other risk factors for development of sepsis include any adverse event at the time of birth, maternal illness, or any abnormalities in the foal. Although the umbilicus is frequently implicated as a major portal of entry for infectious organisms, the GI tract may be the primary site of entry. Other portals of entry include the respiratory tract and wounds.
Early signs of sepsis include depression, decreased suckle reflex, increased recumbency, fever, hypothermia, weakness, dysphagia, failure to gain weight, increased respiratory rate, tachycardia, bradycardia, injected mucous membranes, decreased capillary refill time, shivering, lameness, aural petechiae, and coronitis. Survival rates of foals treated for sepsis have improved, but infection must be recognized early for the possibility of a good outcome. The pathogen involved can also affect survival. Gram-negative species are more commonly diagnosed, but gram-positive septicemia is being recognized more frequently, and multiple organisms may 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 signs are present. Until antimicrobial sensitivity patterns for the pathogen involved are obtained, broad-spectrum antimicrobial therapy should be started. IV amikacin (25–30 mg/kg/day, IV) and penicillin (22,000–44,000 U/kg, IV, qid) are good first-line choices, but renal function must be monitored closely. Other first-line antimicrobials include high-dose ceftiofur sodium (2–10 mg/kg, IV, tid-qid) or ticarcillin/clavulanic acid (50–100 mg/kg, IV, qid).
Failure of passive transfer should be treated, if present, with hyperimmune plasma. Intranasal oxygen insufflation at 5–10 L/min should be provided even if hypoxemia is not present, to decrease the work of breathing and provide support for the increased oxygen demands associated with sepsis. Mechanical ventilation may be necessary in cases of severe respiratory involvement seen with acute lung injury or acute respiratory distress syndrome. If the foal is hypotensive, pressor agents or inotropes may be administered by constant-rate infusion. Inotrope and pressure therapy is generally restricted to referral centers, where the infusions and the foal's blood pressure can be closely monitored. NSAIDs are used by some practitioners, as are corticosteroids in specific circumstances. Use of these drugs should be judicious, because they may have several negative consequences, including, but not limited to, renal failure and gastric or duodenal ulceration. Antiulcer medications are controversial, because critically ill, recumbent foals typically have an alkaline gastric pH but may be useful once the foal is ambulatory.
Supportive care is important in treatment of septic foals. Foals should be kept warm and dry, and turned at 2-hr intervals if recumbent. Every attempt should be made to keep the foal sternal to improve respiratory function and reduce atelectasis. Feeding septic foals can be a challenge if GI function is abnormal; total parenteral nutrition may be needed. If at all possible, foals should be weighed daily and blood glucose levels monitored frequently. Some foals become persistently hyperglycemic on low glucose infusion rates. These foals may benefit from constant-rate infusions of insulin. Recumbent foals must be examined frequently for decubital ulcers, corneal ulcers, and for heat and swelling associated with the joints and physes. Physical therapy or passive range of motion exercises should be provided.
The prognosis for foals in the early stages of sepsis is fair to good. Once the disease has progressed to septic shock, the prognosis becomes less favorable, although short-term survival rates are similar to those seen in human patients. Long-term survival and athletic outcomes are fair. Racing-breed foals that make it to the track perform similarly to their age-matched siblings.
Last full review/revision September 2014 by Amelia S. Munsterman, DVM, MS, DACVS, DACVECC