Immediate care of the compromised foal for the field practitioner (Proceedings)
Perinatal Asphyxia Syndrome produces hypoxic ischemic encephalopathy (HIE) resulting in neurological deficits ranging from hypotonia to grand mal seizures. Foal's affected with perinatal asphyxia also experience gastrointestinal disturbances ranging from mild ileus and delayed gastric emptying to severe, bloody diarrhea and necrotizing enterocolitis (NEC). Renal compromise accompanied by varying degrees of oligouria is also a sequela to asphyxia.
Any discussion of the pathogenesis of perinatal HIE requires the definition of certain terms regarding variations in blood or tissue concentration of oxygen. Hypoxia is the partial (hypoxemia) or complete (anoxemia) lack of oxygen in the brain or blood. If the hypoxemia is severe enough, initially peripheral tissues and ultimately brain tissue will develop an oxygen debt, leading to anaerobic glycolysis and the production of lactacidosis. Asphyxia is the state in which placental or pulmonary gas exchange is compromised or ceases which typically progresses to hypoxemia. Ischemia is a reduction in or cessation of blood flow to an organ (brain), which compromises not only oxygen delivery to tissue but substrate delivery as well.
In utero the fetus adapts to a relatively hypoxic environment by increased oxygen affinity of fetal hemoglobin, increased ability to extract oxygen from the blood and a greater tissue resistance to acidosis. Similar to the redistribution of blood flow in a diving seal, the severely asphyxiated fetus and neonate are able to redistribute oxygenated blood away from less vital organs (lungs, kidneys, skin and bowel) to more vital organs (heart, brain and adrenals). As a result of this protective mechanism, multiple organs may sustain injury. The equine fetus appears to have an oxygen demand "reserve" in that, under conditions of reduced oxygen availability, it decreases its rate of growth and decreases it's oxygen consumption. This form of in utero growth retardation (IUGR) is termed disproportionate. The fetus is stunted and presents with a disproportionately large head, little muscle mass, small frail body and little to no fat. If the in-utero asphyxia is severe the fetus will not be able to sufficiently compensate and the CNS will be compromised. The compromise of the fetal CNS will lead to sequential loss of fetal reflexes with the most complex, oxygen demanding fetal activities affected first which begins with the fetal heart rate, followed by fetal breathing, generalized fetal movements, and fetal tone. Many factors including gestational age of the fetus, severity of hypoxia and duration determine the severity of clinical signs and CNS lesions.In utero passage of meconium could be normal or during hypoxia. In a hypoxic-ischemic event fetal reflex redistribution of cardiac output away from less vital organs such as the bowel results in intestinal ischemia followed by transient hyperperistalisis, anal sphincter relaxation, and meconium passage.
In the intact perinatal animal, and presumably in the human fetus or newborn, uncomplicated hypoxemia, no matter how severe, never causes brain damage.This is largely due to a redistribution of blood flow to the heart and brain during hypoxemia and also because of the preservation of cardiac function by the heart's high endogenous stores of glucose and glycogen. Studies in fetal animals do however support the notion that brain damage does occur when cerebral ischemia, secondary to systemic hypotension is superimposed on the hypoxemia.
Adenosine triphosphate (ATP) is the primary energy modulator of all cells including neurons. In tissue hypoxia ATP production by oxidative phosphorylation is curtailed, with concurrent increases in cellular adenosine disphosphate (ADP) and adenosine monophosphate (AMP). Of necessity, the loss of cellular ATP during hypoxia-ischemia severely compromises those metabolic processes that require energy for their completion. Thus, ATP-dependent NA+ efflux through the plasma membrane in exchange for potassium is curtailed with a resultant intracellular accumulation of sodium and chloride as well as water (cytotoxic edema). Intracellular sodium and chloride ions and water continue to accumulate, resulting in electrochemical gradients that cannot be re-established. Prolonged hypoxia-ischemia can also result in cell death of the capillary endothelium and tight junctions. Potentially this results in extracellular edema (vasogenic edema). How long a cell can survive in this situation is not known, as other factors are called into play that influence the ultimate cellular integrity. The role of extracellular edema and increased intracranial pressure in foals with HIE is still currently being debated with no consensus at this time.