Monday, March 7, 2011

Perinatal Asphyxia

Perinatal Asphyxia

    
* Introduction
    
* Clinical Forms
    
Antepartum diagnosis *
    
* Changes postpartum laboratory
    
* Positive Diagnosis
    
* Postasfixic Syndrome
    
* Treatment
    
* Evolution and prognosis
Perinatal asphyxia is a syndrome that includes all the suffering that is the result of hypoxia and / or lactic acidosis associated with tissue ischemia, with or without hypercapnia, and can lead to hypoxic-ischemic encephalopathy as a result of oxygen deprivation, brain tissue or cerebral blood flow decrease or both.
Perinatal asphyxia complicated by hypoxic-ischemic cardiac injury, renal, gastrointestinal, neurological and respiratory representing the most important cause of morbidity and perinatal mortality in term newborn and premature. Recognition of perinatal asphyxia was defined long after the value of Apgar score and absence of breathing in the first two minutes installation of the expulsion of the head, but this criterion can not be correlated with respiration and asphyxia cause without installing an Apgar score below 7 can be given a series other causes. Asphyxia is defined indirectly by means of four parameters: the pH of cord blood <7, Apgar 3-1 minute that lasts less than 3 to 5, and 10 minutes, signs of hypoxic-ischemic encephalopathy (abnormal tone and reflexes) and changes in other organs (heart, kidney, liver, intestine).
Etiology:
A number of maternal diseases are incriminated in the etiology of perinatal asphyxia: gestational or maternal diabetes before pregnancy, maternal hypertension and toxemia pregnant mother's heart disease, lung disease in the mother, maternal infections, anemia, epilepsy, mother administered drugs (morphine, barbiturates , tranquilizers, reserpine, magnesium sulphate, alcohol). Utero-placental factors include: placenta praevia, cord compression, uterine malformations, infarcts, fibrosis placental abruption placentae, cord prolapsing. Fetal factors may be: genetic and congenital abnormalities, prematurity, intrauterine growth delay in, postmaturitatea, multiple pregnancy, hemolytic anemia by isoimmunization, fetal infections, hidramnios. Birth Factors include: abnormal presentations (transverse, face, breech), laborious birth, labor or ocitocice precipitated by administration of prostaglandin, applications of forceps, cesarean section, maternal sedation during labor, cord prolapsing, the upper and lower membership , amniotic fluid meconium
Pathogenic mechanisms:
The main mechanisms by which these factors are generating perinatal asphyxia: effect on maternal oxygenation, decreased placental blood flow and / or from the placenta to the fetus, impaired gas exchange at the placental or fetal tissue level, increased demand for oxygen to the fetus.

Pathophysiology: In terms of pathophysiology involves hypoxia asphyxia with hypoxemia, hipercarbie with or without metabolic acidosis. Decreased blood flow to placental hypoxia lead to hypoxemia, acidosis leads to cerebral edema, it will lead to decreased cerebral blood flow will lead to cerebral ischemia and consequently cortical necrosis, cerebral infarction. The degree of brain damage depends on the severity and duration of asphyxia, but not always a strict correlation. For example, a severe birth asphyxia leads to a severely affected child, which requires effective resuscitation followed or severe neurological complications, but a less severe asphyxia but longer duration may lead to subsequent severe brain damage without any neurological severe birth. Newborn brain has a high metabolic rate and relatively little energy reserves. In hypoxic brain energy sources decline sharply (ATP and phospho-creatine), glycolysis and thus increase the consumption of glucose, lactic acid production is all the worse. they aggravate asphyxia. Meanwhile occurring disorders pump Na and K, K efflux and influx of Na, Ca and Cl, as a result of neuronal membrane depolarization. It frees up the type of glutamate and aspartate neuroexcitatori will exacerbate neuronal damage Pathological changes observed in brain injury after asphyxia reflect a combination of various metabolic disturbances and cerebral hypoperfusion, the most frequent disturbance of selective neuronal necrosis was observed postasfixic

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