Early recognition of abnormalities is of utmost importance for the successful management of critically ill foals. (Also see Management of the Neonate.) Immediately following birth, the cardiovascular and respiratory systems of the foal must adapt to extrauterine life. These critical events are 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 their thorax clears the pelvic canal. During the first hour of life, the respiratory rate of a healthy foal can be as high as 80 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 opened and fluid is cleared. End-expiratory crackles are consistently heard in the dependent lung during and following lateral recumbency. It is not unusual for a newborn foal to appear slightly cyanotic during this initial adaptation period, but this should resolve within minutes of birth. Similarly, the heart rate of a healthy newborn foal has a regular rhythm and should be at least 60 bpm at the first minute. A continuous murmur can usually be heard over the left side of the heart, although its loudness may vary with position. Variable systolic murmurs, thought to be flow murmurs, may be heard during the first week of life. Murmurs that persist beyond the first week of life in an otherwise healthy foal should be more thoroughly investigated, as should any murmur associated with persistent hypoxia.
Foals are normally nonresponsive while in the birth canal. This lack of responsiveness has lead to presumption of fetal death during dystocia. Other tests should be attempted before determining that a foal has died during birth, eg, detection of pulses in the tongue, neck, or any presented limb; or palpation of the thorax for a heartbeat.
If the foal's nose is accessible, nasotracheal intubation will allow measurement of CO2 tension in the exhaled gas. Nasotracheal intubation of foals under these circumstances can be quite readily performed with minimal practice. Long endotracheal tubes of several sizes (7–12 mm outer diameter) with an inflatable cuff should be available. The tube can be passed blindly using a finger in one nostril for guidance; position can be checked by palpation of the throat. The cuff is inflated, and manual ventilation with either 100% oxygen or room air is begun. CO2 tension is measured continuously using a capnograph or single-use disposable end-tidal CO2 monitor. End-tidal CO2 varies in foals during birth, depending on cardiac output and ventilation frequency, but it should be consistently >20 mm Hg and is usually closer to 30 mm Hg. Once manual ventilation of a living foal is established, it must be continued until the foal is completely 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, and its absence should not be considered diagnostic of visual deficits in a newborn foal. Within an hour of birth, normal foals demonstrate auditory orientation with unilateral pinna control. The normal pupillary angle is ventromedial in newborn foals; this angle gradually becomes dorsomedial over the first month of life. Foals should be able to stand on their own within 2 hr of birth and nurse unaided by 3 hr postpartum. Some foals may defecate shortly after standing, but others may not attempt defecation until after successfully suckling from the dam. Urination is more variable, with fillies usually urinating before colts. It is not unusual for colts to fail to “drop” their penis when urinating over the first few days of life.
The gait of newborn foals is hypermetric, with a base-wide stance. Extreme hypermetria of the forelimbs, usually bilateral but occasionally unilateral, has been observed in some foals associated with perinatal hypoxic/ischemic insults, but this gait abnormality usually resolves without specific therapy within a few days. Spinal reflexes tend to be exaggerated. Foals also exhibit an exaggerated response to external stimuli (eg, noise, sudden visual changes, touch) for the first few weeks of life.
Dystocia and Resuscitation
Most newborn foals make the transition to extrauterine life easily. However, for those in difficulty, it is of utmost importance to recognize the condition immediately and institute appropriate resuscitation. A modified Apgar scoring system has been developed as a guide for initiating resuscitation and determining probable level of fetal compromise. A brief physical examination should be performed prior to initiating resuscitation, as there are humane issues concerning foals with serious problems such as severe limb contracture, microophthalmia, and hydrocephalus, among others.
The initial assessment begins during presentation of the fetus. While 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 a normal birth of a healthy foal is to minimally disturb the bonding process. This also applies to high-risk births, although some disruption of normal bonding is inevitable.
The strength and rate of any palpable peripheral pulse should be evaluated. The apical pulse should be evaluated as soon as the chest clears the birth canal. Bradycardia (pulse <40 bpm) is expected during forceful contractions, and the pulse rate should increase rapidly once the chest clears the birth canal. Persistent bradycardia is an indication for rapid intervention.
The fetus is normally hypoxemic when compared with the newborn foal, and this hypoxemia 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 extrauterine life. If more than mild transient 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, the secondary asphyxia response, occurs in several minutes. If asphyxia does not improve, the foal enters secondary apnea, which is irreversible unless resuscitation is initiated. Therefore, the first priority of neonatal resuscitation is establishing an airway and breathing pattern. Foals that are not spontaneously breathing are assumed to be in secondary apnea. The airway should be cleared of membranes as soon as the nose is presented. If meconium staining is present, the airway should be suctioned before delivery of the foal is completed and before the foal breathes spontaneously. Suction should be continued to the trachea if aspiration of the nasopharynx is productive. Overzealous suctioning worsens bradycardia, as it worsens hypoxia. Suctioning should end once the foal begins breathing spontaneously because hypoxia will worsen with continued suction. If the foal does not breathe or move spontaneously within seconds of birth, tactile stimulation is necessary. If tactile stimulation does not result in spontaneous breathing, the foal should be immediately intubated and manually ventilated. Mouth-to-nose ventilation can be used if nasotracheal tubes or an ambu bag (or equivalent) are not available. Hyperventilation with 100% oxygen is the best choice to reverse fetal circulation. However, evidence from human medicine suggests that there are no apparent clinical disadvantages in using room air rather than 100% oxygen for ventilation of asphyxiated human neonates.
Almost 90% of foals requiring resuscitation respond to hyperventilation alone and require no additional therapy. Nasotracheal intubation can be initiated 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 initiated if the foal remains bradycardic despite ventilation and a nonperfusing rhythm is present. The foal should be placed on a hard surface in right lateral recumbency with the topline against a wall or other support. Because ~5% of foals are born with fractured ribs, an assessment for the presence of rib fractures should be done before initiating chest compressions. Many of these fractures can be identified by palpating the ribs. They are usually multiple and consecutive on one side of the thorax, located in a relatively straight line along the part of the rib with the greatest curvature dorsal to the costochondral junction. Unfortunately, ribs 3–5 are frequently involved, and their location over the heart can make chest compression a potentially fatal exercise. Auscultation over the ribs during breathing results in a recognizable “click,” identifying rib fractures that may have escaped detection by palpation.
Drug therapy should be started if a nonperfusing rhythm persists for >30–60 sec in the face of chest compression. Epinephrine is the drug of choice, although the best dose and frequency of administration for resuscitation are controversial. Vasopressin is gaining attention as a cardiovascular resuscitation drug, but experience with it is limited. Atropine is not recommended in bradycardic newborn foals, as the bradycardia is usually due to hypoxia and atropine can increase myocardial oxygen debt if the hypoxia is not corrected. Doxapram is not recommended because it does not reverse secondary apnea, the most common apnea in newborns.
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 mitochondria, releasing energy as heat. This nonshivering thermogenesis is impaired in newborns undergoing hypoxia or asphyxiation and in those that are ill at birth. 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 caesarian section. 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 cold stress is minimized in both newborn and critically ill foals. The foal should be dried and placed on dry bedding once resuscitation is complete. Supplementary heat, in the form of radiant heat lamps or warm air circulating blankets, may be required.
Fluid therapy should be used conservatively during postpartum resuscitation. The neonate is not volume depleted unless excessive bleeding has occurred. Some compromised newborn foals are actually hypervolemic. Because the renal function of the equine neonate is substantially different from that of adult horses, fluid therapy cannot be simply scaled down. If IV fluids are required for resuscitation, and blood loss is identified, administration of 20 mL/kg of a nonglucose-containing polyionic isotonic fluid over 20 min (∼1 L for a 50-kg foal) can be effective. Indications for this “shock bolus” therapy include poor mentation, poorly palpable peripheral pulses, and the development of cold distal extremities, compatible with hemorrhagic shock. The foal should be reassessed after the initial bolus, and additional boluses administered as necessary. Glucose-containing fluids can be administered after resuscitation at a rate delivering 4–8 mg/kg/min glucose (∼240 mL/hr 5% dextrose or 120 mL/hr 10% dextrose to the average 50-kg foal), particularly in the obviously compromised foal. This therapy is indicated to help resolve metabolic acidosis, support cardiac output as myocardial glycogen stores have likely been depleted, and prevent postasphyxial hypoglycemia.
Prematurity, Dysmaturity, and Postmaturity
Traditionally, prematurity is defined as a birth at <320 days gestation in the horse. Because gestation length ranges from 310 days to >370 days in some mares, it is possible for a mare whose usual gestation length is 315 days to have a term foal at 313 days, while a mare whose usual gestation length is 365 days may have a premature foal at 340 days. Foals that are born post-term but small are termed dysmature. A postmature foal is a post-term foal that has a normal axial skeletal size but is thin to emaciated. Dysmature foals may have been classified in the past as “small for gestational age” and are thought to have suffered placental insufficiency; postmature foals are usually normal foals that have been retained too long in utero, perhaps due to an abnormal signaling of readiness for birth, and have outgrown their somewhat aged placenta. Postmature foals become more abnormal the longer they are maintained and may also suffer from placental insufficiency. They are most commonly born to mares ingesting endophyte-infested fescue (see Summer Fescue Toxicosis).
Prematurity, dysmaturity, and postmaturity may be associated with high-risk pregnancy. Iatrogenic causes include early elective induction of labor, based on inaccurate breeding dates or misinterpretation of late-term colic or uterine bleeding as ineffective labor. The majority of causes are 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 not usually due to 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 due to 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 hypoxic or ischemic insult. Fluid therapy should be used cautiously in these cases, and initial fluid restriction may be necessary 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 asphyxial syndrome, including hypoxic ischemic encephalopathy. Treatment is similar to that of term foals with these problems. These foals are also predisposed to secondary bacterial infection 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 due to a primary lack of maturity or secondary to hypoxia. Dysmotility and varying degrees of necrotizing enterocolitis are common. Both hyperglycemia and hypoglycemia are frequently encountered. Hyperglycemia is generally related to stress, increased levels of circulating catecholamines, and rapid progression to gluconeogenesis, while hypoglycemia is associated with diminished glycogen stores, inability to engage gluconeogenesis, sepsis, and hypoxic damage. Immature endocrine function may be present, 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. When enteral feeding is initiated, small volumes should be provided at first and slowly increased over several days.
Musculoskeletal problems are frequent, particularly in premature foals, and include significant flexor laxity and decreased muscle tone. Postmature foals may be affected by flexural contracture deformities, most likely due to decreased intrauterine movement as they increase in size.
Premature foals frequently exhibit flexor laxity and decreased cuboidal bone ossification that predisposes them to crush injury of the carpal and tarsal bones if weightbearing is not strictly controlled. Physical therapy, in the form of standing and 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. Bandaging of the limbs only increases laxity, although light bandages over the fetlock may be necessary to prevent injury if flexor laxity is severe. These foals are predisposed to angular limb deformity and must be closely monitored for development of this problem as they mature.
The overall prognosis for premature, dysmature, and postmature foals remains good with intensive care and attention to detail. Many foals (up to 80%) survive and become productive athletes. Complications associated with sepsis and musculoskeletal abnormalities are the most significant indicators of poor athletic outcome.
Hypoxic Ischemic Encephalopathy
A wide spectrum of clinical signs is associated with hypoxic ischemic encephalopathy (HIE), ranging from mild depression with loss of the suck reflex to grand mal seizures. Affected foals are typically normal at birth but show signs of CNS abnormalities within a few hours. However, some foals are obviously abnormal at birth, and some do not show signs until 24 hr of age. HIE is commonly associated with adverse peripartum events, including dystocia and premature placental separation, but some foals have no known peripartum period of hypoxia, suggesting that unrecognized in utero hypoxia occurred. (Also see Hypoxic Ischemic Encephalopathy.)
Therapy for the various manifestations of hypoxia and ischemia involves control of seizures; general cerebral support; correction of metabolic abnormalities; maintenance of normal arterial 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 and midazolam can be used for emergency control of seizures. If seizures are not readily stopped with diazepam, or >2 seizures are recognized, then treatment using a midazolam constant rate infusion can be instituted or phenobarbital therapy initiated.
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. Failure of passive transfer of immunity can contribute to the development of sepsis in a foal at risk. The current recommendation is that foals have IgG levels ≥800 mg/dL for passive transfer to be considered adequate. Other risk factors for the development of sepsis include any adverse advents 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 suck 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. The survival rate of foals treated for sepsis has improved. If sepsis is recognized early, foals may have a good outcome, depending on the pathogen involved. Gram-negative sepsis is more commonly diagnosed, but gram-positive septicemia is being recognized more frequently. It is important to isolate the organism involved early in the course of the disease. Blood cultures and, if localizing signs are present, samples should be obtained as appropriate. Until antimicrobial sensitivity patterns for the pathogen involved are obtained, broad-spectrum antimicrobial therapy should be initiated. IV amikacin and penicillin are good first-line choices, but renal function should be monitored closely. Other first-line antimicrobials include high-dose ceftiofur sodium or timentin. Failure of passive transfer should be treated if present. 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 pressor therapy is generally restricted to referral centers, where these drugs can be given as constant rate infusions and blood pressure can be closely monitored. NSAID are used by some practitioners, as are corticosteroids in specific circumstances. Use of these drugs should be judicious, as they may have several negative consequences including, but not limited to, renal failure and gastric or duodenal ulceration.
Supportive care is important in the treatment of septic foals. Foals should be kept warm and dry and turned at 2-hr intervals if they are recumbent. 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 low-dose insulin infusions. Recumbent foals must be examined frequently for decubital ulcers, corneal ulcers, and for heat and swelling associated with joints and physis.
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 as good as those seen in human patients. Longterm 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 March 2012 by Pamela Anne Wilkins, DVM, MS, PhD, DACVIM-LA, DACVECC