Field approach to treating the sick neonatal foal

Equine NICUs have greatly improved our knowledge and understanding of the normal and abnormal physiology of the equine neonate, resulting in an improvement in our ability to successfully treat the critically ill equine neonate and save lives. The success rate has increased tremendously since the early 1980s from a little over 50% to 80% or more for most facilities; some of best success has been in the treatment of ‘dummy foals’ that have a greater than 80% rate of survival to discharge in most hospitals. We have also been able to translate many treatments from the referral hospital to the field with good success for the practitioner. This lecture provides information on how to translate many specific and supportive treatments from the NICU to the field situation.

Neonatal Encephalopathy: The ‘Dummy’ Foal

Neonatal encephalopathy (NE) is one of the most common diseases of the equine neonate and is also described as dummy foal syndrome and neonatal maladjustment syndrome (NMS). A wide spectrum of clinical signs are associated with NE ranging from mild depression with loss of the suck reflex to grand mal seizure activity. The majority of affected foals are normal at birth but show signs of central nervous system (CNS) abnormalities within a few hours following birth although some will not show signs until 24 hours of age. NE is the most common clinical presentation and management of foals presenting with signs consistent with a diagnosis of NE requires complete examination of other body systems and provision of specific and supportive therapies of all affected body systems. Although PAS is most clinically obvious as NE, the gastrointestinal tract and kidneys are also frequently affected; complications associated with these systems should be anticipated, in addition to cardiovascular, respiratory, and endocrine disorders.

Pathophysiology:

The underlying pathophysiologic details of PAS and NE in the foal are unknown and likely multifactorial and equine neonatologists have long looked to human studies and models of the human disease for understanding of the syndrome in the equine neonate. NE is commonly associated with adverse peripartum events, including dystocia and premature placental separation, but a fair number of foals have no known peripartum period of hypoxia, suggesting that these foals result from unrecognized in utero hypoxia. Severe maternal illness may also result in foals born with PAS. There is increasing evidence that cytokinemia, resulting from placental infection or insult, is a major contributor to NE in infants, and probably foals, with incidence of NE increased with the presence of maternal fever, something veterinarians have suspected for the last decade or so.

Treatment:

Therapy for the various manifestations of PAS involves control of seizures, general cerebral support, correction of metabolic abnormalities, maintenance of normal arterial blood gas values, maintenance of tissue perfusion, maintenance of renal function, treatment of gastrointestinal dysfunction, prevention/recognition/ early treatment of secondary infections and general supportive care. It is important that seizures be controlled as cerebral oxygen consumption increases five-fold during seizures. Diazepam and midazolam can be used for emergency control of seizures. If seizures are not readily stopped with diazepam or midazolam, or more than two seizures are recognized, then diazepam should be replaced with a midazolam constant rate infusion (CRI).

Probably the most important therapeutic interventions are aimed at maintaining cerebral perfusion. Thiamine and vitamin C supplementation in the intravenous fluids can be administered to support metabolic processes. The author rarely uses DMSO, has not used it at for the last decade and has not recognized any change in outcome by discontinuing its use. GABAergic agonists (gabapentin) are being used by some practitioners in the managements of PAS/NE in foals, based on evidence showing neuroprotection when used in ischemia, both alone and in combination with NMDA antagonists like magnesium.

Foals suffering from PAS will also have frequent recurrent bouts of hypoxemia and occasional bouts of hypercapnia. INO2 is generally needed in these cases both as a preventative therapy and as direct treatment, as the appearance of the abnormalities can be sporadic and unpredictable. Additional respiratory support, particularly in those foals with centrally mediated hypoventilation and periods of apnea or abnormal breathing patterns, include caffeine (per os or per rectum) or doxapram CRI and finally positive pressure ventilation.

Maintaining tissue perfusion and oxygen delivery to tissues is a cornerstone of therapy for PAS in order to avoid additional injury. Oxygen carrying capacity of the blood should be maintained; some foals will require transfusions to maintain a PCV > 20%. Adequate vascular volume is important, but care should be taken to avoid fluid or sodium overloading. Early evidence of fluid overload is subtle accumulation of ventral edema between the front legs and over the distal limbs. Perfusion is maintained by supporting cardiac output and blood pressure by judicious use of intravenous fluid support and inotrope/pressor support. We do not aim for any ‘magic’ systolic, mean or diastolic pressure. Instead we monitor urine output, mentation, limb perfusion, gastrointestinal function and respiratory function as indicators that perfusion is acceptable.

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