What is the pathophysiology of reduced cerebral blood flow (CBF) in hypoxic-ischemic encephalopathy (HIE)?

Updated: Jul 18, 2018
  • Author: Santina A Zanelli, MD; Chief Editor: Dharmendra J Nimavat, MD, FAAP  more...
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Answer

Limited data in the human fetus and the newborn infant suggest that CBF is stable over much narrower range of BPs. [10, 11] Some experts have postulated that, in the healthy term newborn, the BP range at which the CBF autoregulation is maintained may be only between 10-20 mm Hg (compared with the 40 mm Hg range in adults noted above). In addition, the autoregulatory zone may also be set at a lower level, about the midpoint of the normal BP range for the fetus and newborn. However, the precise upper and lower limits of the BP values above and below which the CBF autoregulation is lost remain unknown for the human newborn.

In the fetus and newborn suffering from acute asphyxia, after the early compensatory adjustments fail, the CBF can become pressure-passive, at which time brain perfusion depends on systemic BP. As BP falls, CBF falls below critical levels, and the brain injury secondary to diminished blood supply and a lack of sufficient oxygen occurs. This leads to intracellular energy failure. During the early phases of brain injury, brain temperature drops, and local release of neurotransmitters, such as gamma-aminobutyric acid transaminase (GABA), increase. These changes reduce cerebral oxygen demand, transiently minimizing the impact of asphyxia.


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