Perinatal hypoxic-ischemic encephalopathy (EHIP)

Perinatal hypoxic-ischemic encephalopathy (EHIP)

    * Introduction
    * Clinical signs
    * Diagnosis
    * Treatment
Hypoxic-ischemic encephalopathy is one of the most common brain injury in the neonatal period and the most common cause of long-term neurological disability. Hypoxic-ischemic encephalopathy is actually a variety of clinical entities that share a decrease in oxygen for brain and neurological damage is defined by occurring in newborns due to cerebral hypoxia and ischemia secondary chronic or acute fetal distress.
Epidemiology:
The incidence of hypoxic-ischemic insult in newborns is 2-4% a newborn infant at term and higher incidence of premature infant who presents a serious risk of injury due to hypoxic-ischemic cardio-pulmonary instability, labile self-regulation of cerebral blood flow, increased frequency of sepsis and metabolic disorders. Hypoxic-ischemic insult occurs mostly in antepartum and intrapartum, and long-term neurological damage such as cerebral palsy may be associated with a rate of 10-15% with intrapartum hypoxic-ischemic insult.
Etiology:
Incriminated in the etiology of the disease are three types of factors: factors antepartum, intrapartum factors and neonatal factors. From vategoria antepartum factors include: pregnant toxemia, maternal diabetes, disease-specific obstetric incompetent cervix, placenta previa, abruptio placentae, polihidramnios, multiple pregnancy. Intrapartum factors may be the following: abnormal presentations, prolonged labor. Neonatal factors are prematurity, idiopathic respiratory distress syndrome, cardiopulmonary abnormalities, infectious diseases, hemolytic diseases, convulsions, ventilatory alkalosis.
Pathophysiology:
Brain injury is the result of an association of hypoxia with ischemia, which increases the rate of cellular anaerobic metabolism, with low-phosphate products produced macroergici and accumulation of anaerobic metabolism, lactic, As intracellular free radicals, excitatory neurotransmitters. Changing cerebral blood flow is the main change induced by asphyxia postasfixica. Normal cerebral blood flow varies between 80-100 ml/100 g tissue / minute and depends on the quantity of blood pumped by the heart, the pressure difference between arteries and veins of the cerebral vascular resistance of the vessels involved. Following the installation of asphyxia, cardiac output is redistributed compensatory response, which leads to increased cerebral blood flow. The relationship between cerebral perfusion pressure and cerebral blood flow is governed by the principle of self-regulation, which represents the tendency of the brain to maintain a steady flow in terms of variations in cerebral perfusion pressure. As the hypoxia persists, this mechanism is not effectively self leads to a decrease in cardiac output with systemic hypotension and decreased cerebral flow, cerebral lesions. In turn, acidosis, hypercapnia and hypoglycaemia can disrupt brain mechanisms of self-regulation.