ECR 2018 / C-0153
Certificate of Merit
Hypoxic-ischemic encephalopathy review: mechanisms of injury and patterns of cerebral involvement in both children and adults
Congress: ECR 2018
Poster No.: C-0153
Type: Educational Exhibit
Keywords: Neuroradiology brain, MR, MR-Diffusion/Perfusion, Imaging sequences, Ischaemia / Infarction
Authors: A. Hilario Barrio, E. Salvador, L. Koren, P. Martín Medina, A. Martinez de Aragon, C. Liebana de Rojas, G. Ayala, J. M. Millan, A. Ramos; Madrid/ES
DOI:10.1594/ecr2018/C-0153

Background

 

It is now well established that hypoxic-ischemic brain injury is a syndrome that evolves over days, even weeks, and reflects the evolution of a delayed cascade of molecular events triggered by the initial insult.

 

During normal conditions, the human brain has a high requirement for oxygen and glucose, normally used in oxidative phosphorylation to produce adenosine triphosphate (ATP).

 

During a hypoxic-ischemic episode, oxidative phosphorylation is rapidly reduced leading to primary energy failure in glutamatergic neurons Fig. 2 .

 

 

PHASE I (0-6 HOURS)

 

Represents one of the first phases that results in CHANGES IN THE VASCULATURE.

 

If placental blood flow is disrupted a period of asphyxia occurs, causing a loss in auto-regulation and the development of cerebral blood flow being dependent on systemic arterial pressure.

As a result of this change in regulation of cerebral blood flow, a decrease in systemic arterial blood pressure increases the risk for tissue acidosis and ischemic brain injury Fig. 3 .

 

This is a PRIMARY ENERGY FAILURE phase that occurs at the cellular level.

Since there is a loss of oxygen that is readily available to the brain, cellular energy metabolism shifts to a dependency upon anaerobic metabolism.

Then a collection of lactic acid and depletion of adenosine triphosphate occurs. There is also an intracellular accumulation of sodium, calcium, water and excitatory neurotransmitter release causing an EXCITOTOXIC-OXIDATIVE CASCADE.

 

Further influx of calcium also leads to increased activation of lipase, causing a release of fatty acids, and increased activation of neuronal nitric oxide synthase giving rise to free radical production and MITOCHONDRIAL DYSFUNCTION.

 

Mitochondrial dysfunction ultimately signals pathways of APOPTOTIC AND NECROTIC CELL DEATH.

 

 

PHASE II (6-48 HOURS)

 

The second energy failure phase occurs 6-48 hours after an episode of hypoxia ischemia.

 

This phase results in:

1. Detrimental release of excitatory neurotransmitters and free radicals.

2. Depletion of high phosphate reserves.

 

Second phase differs from the primary energy failure phase since it is INDEPENDENT OF CEREBRAL ACIDOSIS Fig. 4 .

 

 

PHASE III (AFTER 48 HOURS)

 

The third phase is though to include mechanisms of inflammation and epigenetic changes that lead to an impairment or alteration of axonal growth, neurogenesis and synaptogenesis.

 

In summary, the principle pathogenic mechanism underlying neurological damage in hypoxic-ischemic encephalopathy resulting from hypoxemia, ischemia, or both, is deprivation of glucose and oxygen supply that causes a energy failure and initiates a cascade of biochemical events leading to cell dysfunction or death Fig. 5 .

 

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