08/04/2023
Encefalopatía neonatal en potrillos
Neonatal Encephalopathy in Foals
Brian S. Burks, DVM
Diplomate, ABVP
Board Certified Equine Specialist
Neonatal encephalopathy (NE) is a common, noninfectious CNS disorder of neonatal foals. This disorder has also been known as neonatal maladjustment syndrome, hypoxic-ischemic encephalopathy, and dummy foal syndrome, etc.
Clinical signs of NE begin by 36 hours of age and vary from mild to severe, depending upon the part and how much of the brain is affected. Central nervous system signs include:
• Loss of suckle
• Loss of tongue curl
• Depression/lethargy
• Somnolence, difficult to arouse, coma
• Dysphagia
• Loss of affinity for the mare
• Disorientation
• Wandering
• Head pressing
• Abnormal vocalization (barking)
• Hyperesthesia
• Abnormal breathing patterns
• Weakness and recumbency
• Fading
• Head tilt
• Nystagmus
• Seizures
Affected foals often have renal and GI issues, though the latter are most obvious, ranging from mild colic to severe diarrhea. These may appear several days after the CNS signs.
Risk factors for perinatal asphyxia include maternal and fetal causes. The former include respiratory disease, endotoxemia, hemorrhage, anemia, cesarean delivery or other surgery, placentitis, and chronic or acute uteroplacental separation. Fetal causes include twinning,, congenital abnormalities, dystocia, meconium aspiration, sepsis, and prematurity/dysmaturity. These factors induce hypotension and reduced tissue oxygenation. Placental pathology impairs uteroplacental perfusion. Chronic fetal hypoxia results from areas of chronic placental separations. The most acute cause of perinatal asphyxia is complete premature placental separation during parturition (“red bag” delivery).
This condition is associated with perinatal asphyxia, resulting from unrecognized in-utero or peripartum hypoxia, affecting multiple organ systems. There is impaired oxygen delivery to cells due to hypoxemia or anemia and ischemia (decreased blood perfusion).
True hypoxic ischemic encephalopathy can occur during events such as prolonged umbilical cord compression, birth asphyxia from prolonged stage 2 labor and cardiopulmonary failure. Foals with true hypoxic disease typically have histologic lesions in their brain consistent with the insult. There is little evidence that most foals with neonatal encephalopathy sustain a hypoxic-ischemic insult. There is increasing evidence for the role of inflammation in NE. The most common cause of NE is placentitis, but any inflammatory focus can cause NE, such as laminitis or cellulitis.
Inflammation in the mare can lead to maternal systemic inflammatory response syndrome (SIRS) and subsequently fetal systemic inflammatory response syndrome (FIRS). Once pro-inflammatory cytokines are stimulated, they can cross the fetal blood-brain- barrier, leading to neuroinflammation, which causes a cascade of events leading to CNS dysfunction.
Neurosteroids are protective of the fetal brain and are responsible for somnolence of the fetus in utero. The placenta supplies substrates for the formation of neurosteroids in the fetal brain. Once the placental stimulus is removed at birth, there is a decline in neurosteroid concentrations, allowing the foal to awaken. In foals with NE, neurosteroid levels do not decline.
Progestagens (progesterone, epitestosterone and androstenedione) are neurosteroids that have the ability to cross the blood brain barrier and have neuromodulatory effects and could be involved in the etiology of neonatal encephalopathy.
Differential diagnoses for NE include bacterial meningitis, equine herpesvirus 1 infection, metabolic abnormalities (eg, hypoglycemia, electrolyte derangements), acid-base disturbances, kernicterus subsequent to massive hemolysis (i.e, neonatal isoerythrolysis), brain or spinal trauma, congenital defects (eg, hydrocephalus, hydranencephaly), and nutritional myodegeneration (white muscle disease).
Diagnosis of NE is based upon compatible clinical findings and exclusion of differential diagnoses. A history of dystocia, premature placental separation, or placentitis support a diagnosis of NE related to perinatal asphyxia.
Treatment of NE is largely supportive. Maintenance of adequate blood pressure and tissue perfusion is vital to ensure cerebral blood flow and avoid further ischemic injury. This is accomplished by the use of intravenous fluids and vasopressors. Mild hypothermia and barbiturates are sometimes used to decrease cerebral metabolic rate and preserve energy. Intravenous glucose may be needed to maintain normal blood glucose concentrations. If the foal is unable to nurse, nutrition is supplied by an indwelling nasogastric tube; total parenteral nutrition is given to foals with GI dysfunction.
Seizure control is important to prevent not only injury, but because seizures increase oxygen and metabolic demands and worsen NE. Oxygen delivery is important and changes in respiratory function should be addressed promptly. Foals may suffer from ARDS, aspiration pneumonia, infectious pneumonia, fractured ribs, etc.
Prevention of sepsis is also important. Colostrum provides immunoglobulins, but also promotes local gastrointestinal immunity and helps form a barrier between luminal bacteria and the foal. Colostrum contains numerous biologically active substances including important pro and anti-inflammatory cytokines, immune modulators and other proteins. Foals that cannot be given colostrum should be given plasma. Appropriate antibiotics should also be used.
Stress experienced during parturition and the pressure of passing through the pelvic canal signals the decrease in neurosteroids that lead to quiescence in utero. As foals with NE have elevated levels of neurosteroids, mimicking the birth canal ‘squeeze’ to signal a decrease in neurosteroids has had some success.
Foals with NE can make full recoveries, but often require intensive management. They require constant nursing care and regular veterinary monitoring.
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