Definition
“Asphyxia” (Greek: stopping of the pulse), i.e., the biochemical and clinical consequences of lack of oxygen and hypercarbia following antepartum or intrapartum interruption of respiration/perfusion. In addition to hypoxia, there is respiratory and metabolic acidosis that can lead to peripheral and pulmonary vasoconstriction and ultimately, if untreated, to myocardial failure, hypotension, and bradycardia.
The term “perinatal asphyxia” should be used with constraint, not only for medical-legal reasons, but also due to the lack of a broadly accepted definition. According to Carter et al. (1993), perinatal asphyxia is defined as a combination of:
Severe umbilical arterial acidosis with a UA pH value <7.00
Persistently low Apgar score <4 for at least 5 min after birth
Neurological symptoms, such as seizures, unconsciousness or muscle hypotonia, and
Cardiac, pulmonary, intestinal or renal dysfunction
The American College of Obstetrics and Gynecology defines an acute intrapartum hypoxic event meeting the following combined criteria as sufficient to cause spastic quadriplegic or dyskinetic cerebral palsy:
Severe umbilical arterial acidosis with a UA pH value <7.00 and base deficit ≥12 mmol/l
Early onset of moderate to severe encephalopathy in an infant ≥34 weeks' gestation
Exclusion of other identifiable etiologies
! It is inappropriate to use the term “birth asphyxia” based on a single low Apgar score or a single low pH value (obtained from the umbilical artery) in the absence of neurological signs or symptoms.
Epidemiology
Delayed postnatal adaptation occurs in approx. 5%–10% of all births; thus, in about 2–3/1000 births, birth asphyxia is possible.
Etiology/pathophysiology
Impairment of the feto–placental gas exchange:
Preplacental: lack of oxygen supply due to uterine rupture, maternal anemia, shock, embolism, sepsis, respiratory insufficiency, or conditions causing chronic placental insufficiency
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