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On the value of umbilical cord blood base deficit measurement
Summarized from Knutzen L, Svirko E, Impey L. The significance of base deficit in acidemic term neonates. Am J Obstet Gynecol 2015; 213,3: 373.e1-7h
A clinical requirement for determination of the pH and base deficit (BD) of umbilical-cord arterial blood has ensured a role for the blood gas analyzer in the delivery suite of obstetric units.
The principal objective of this testing in the minutes immediately after birth is to identify those babies who have been deprived of oxygen for one reason or another and are therefore at risk of the potentially life-threatening or life-changing consequences of hypoxia. This testing of umbilical cord blood is aimed at identifying metabolic acidosis, a consequence of hypoxia.
Metabolic acidosis arises in hypoxic individuals because of the accumulation of lactic acid that inevitably occurs during anaerobic metabolism of glucose (i.e. metabolism in the absence of sufficient oxygen). The accumulating acid overwhelms the normal buffering capacity of blood and blood pH falls as BD rises.
The normal (reference) range for arterial cord blood pH is 7.12-7.35, and for arterial cord BD it is +9.3 to –1.5 mmol/L. In obstetrics, metabolic acidosis is most widely defined as cord arterial blood pH <7.0 and BD >12.0 mmol/L, although some suggest the threshold pH should be higher (<7.1).
The finding of cord-blood metabolic acidosis is important because it identifies those babies at increased risk of hypoxic brain-cell injury and associated hypoxic-ischemic encephalopathy (HIE). HIE is a condition of brain/neurological dysfunction. Symptoms among affected neonates include hypotonia, poor feeding, respiratory difficulties, seizures and reduced level of consciousness.
Eventual outcome depends on severity/site of brain injury; those with mild HIE survive with usually little or no long-term consequences, but most of those with moderate/severe HIE either die during the neonatal period or survive with severe and permanent neuro/psychological deficit, cerebral palsy is an outcome for some. HIE is thus a significant cause of perinatal death and birth-related permanent disability.
A recent UK clinical study of cord-blood metabolic acidosis was designed to examine the comparative value of pH and BD to predict outcome for neonates with metabolic acidosis. The hypothesis tested by this study was that BD provides no more prognostic information than that provided by the severity of the fall in pH.
From a database of 8797 deliveries in which validated cord-blood pH and BD had been determined, the authors identified 436 cases of moderate acidosis (pH <7.1 but >7.0) and 84 cases of severe acidosis (pH <7.0). Five adverse outcome measures were chosen for study: severe HIE (i.e. grade 2/3 encephalopathy or death; admission to neonatal intensive care; 5 min Apgar score <7; composite adverse neurological outcome, e.g. seizures, abnormal brain imaging, etc.); composite adverse systemic signs (e.g. need for ventilation, renal/liver dysfunction, etc.).
Retrieval of the case records from the 520 neonates with metabolic acidosis confirmed that those with severe acidosis (pH < 7.0) were much more likely to have suffered all five of the adverse outcomes than those with moderate acidosis (pH <7.1 but >7.0).
So for example, 8.5 % of patients with severe acidosis suffered severe HIE or death compared with just 1.2 % of those with moderate acidosis; and 46.4 % of those with severe acidosis required admission to intensive care compared with 14.9 % of those with mild acidosis. For all five outcomes the predictive value of pH was statistically determined and for all five outcomes the extra information provided by BD values did not alter this predictive value.
The authors were able to conclude that, in line with their hypothesis, knowledge of cord-blood BD value adds no prognostic information beyond that provided by severity of pH reduction.
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