Pathophysiology of Birth Asphyxia

Birth Asphyxia: A Review of the Clinical Problem

Pathophysiology of Birth Asphyxia

The review of Joseph Volpe of Harvard University, Boston, U.S.A., stemmed from the thesis that approach to therapy should be based, as far as possible, on an understanding of the pathophysiology and neuropathology of birth asphyxia.

Dr. Volpe introduced the topic pointing out that several major processes were responsible for the brain damage in birth asphyxia. He described in detail the various types and locations of cell damage that result from asphyxia. These include selective neuronal necrosis (in the cerebral cortex, brain stem and basal ganglia) as well as parasagittal cerebral injury and strokes with focal lesions (Figures 2.1, 2.2, 2.3, 2.4, 2.5 and 2.6).



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Dr. Volpe discussed the pathophysiology leading to the above lesions. The first was interference with blood flow to the brain due to systemic hypotension and by a failure of autoregulation of flow (Figure 2.7). Normally blood flow to the brain is kept constant despite changes in blood pressure. However in asphyxia this regulation may be lost so that as blood pressure drops, flow to the brain also drops (Figure 2.8). These changes produce ischemia, a major factor in the causation of brain damage. Ischemia then causes neuronal and oligodendogrial damage via excitoxicity (Figure 2.9). The latter is a process initiated by ischemia. It causes reduced energy production and a fall in ATP, resulting in glutamate release, which in turn reacts with glutamate receptors (Figure 2.10), causing changes in membrane function and especially an accumulation of calcium within the cell (Figure 2.11). This causes damage by interfering with mitochondrial function and other direct effects resulting in the release of free radicals and cell death (Figure 2.12).


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Dr. Volpe pointed out that these steps take time after the ischemic event. This is an important concept because preventive therapy may be directed during those few hours. The observation that final cell death is related to oxidative damage may relate to the observations presented by Dr. Saugstad indicating that resuscitation with oxygen may be harmful. Dr. Volpe also dissected the pathway of cell damage and pointed out several sites at which therapy may be directed (
Figures 2.12, 2.13).

 

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