Elsevier

Early Human Development

Volume 90, Issue 10, October 2014, Pages 703-705
Early Human Development

Cerebral blood flow and oxygenation in infants after birth asphyxia. Clinically useful information?

https://doi.org/10.1016/j.earlhumdev.2014.06.007Get rights and content

Abstract

The term ‘luxury perfusion’ was coined nearly 50 years ago after observation of bright-red blood in the cerebral veins of adults with various brain pathologies. The bright-red blood represents decreased oxygen extraction and hence the perfusion is ‘luxurious’ compared to oxygen needs. Gradual loss of cellular energy charge during the hours following severe birth asphyxia was observed twenty years later by sequential cranial magnetic resonance spectroscopy. This led to the concept of delayed energy failure that is linked to mitochondrial dysfunction and apoptotic cell death. Abnormally increased perfusion and lack of normal cerebral blood flow regulation are also typically present, but whether the perfusion abnormalities at this secondary stage are detrimental, beneficial, or a mere epiphenomenon remains elusive. In contrast, incomplete reoxygenation of the brain during and following resuscitation is likely to compromise outcome. The clinical value of cerebral oximetry in this context can only be examined in a randomised clinical trial.

Section snippets

Historical perspectives on luxury perfusion and impaired oxygen metabolism

Niels Lassen coined the term luxury-perfusion syndrome in a hypothesis paper in the Lancet in 1966 [1]. It was based on three observations. First, two animal experiments demonstrating reactive hyperaemia lasting for several hours following hypoxia–ischemia had been presented at two conferences the same year. Second, the year before experience had been reported with bright-red blood in the veins on the surface of the brain during surgery for tumours and in cases of infarction. Finally, Lassen

Hyperperfusion

The first suggestion of cerebral hyperperfusion after birth asphyxia was obtained in 1979 by Doppler ultrasound as a reduced pulsatility in the anterior cerebral artery. The pulsatility of blood flow velocity in a distributory artery is an indicator of the vascular resistance distal to the point of measurement and pulsatility in the anterior cerebral artery is negatively correlated – although weakly – to cerebral blood flow in newborn infants. That cerebral blood flow really is increased – i.e.

Cerebral oxygen metabolism

Four small studies have attempted to measure cerebral oxygen metabolism in the asphyxiated newborn infant (Table 1). The standard method with blood sampling from the jugular vein was used in nine infants [7]. Oxygen extraction in the four who died or were handicapped was 2 ml O2 per 100 ml blood whereas it was 5 ml per 100 ml in the five who recovered. Cerebral blood flow was measured by the Kety–Schmidt method and found three times higher in those who died or were handicapped. Therefore cerebral

The prognostic value

A Doppler ultrasound pulsatility index of flow velocity in the anterior cerebral artery below 0.55 was highly predictive of poor neurodevelopmental outcome in term infants who had clinical hypoxic–ischaemic encephalopathy after severe birth asphyxia [11]. This prognostic value is reduced when therapeutic hypothermia is used [12]. Similarly, abnormally high StO2 predicts poor neurodevelopmental outcome [13], and this appears still to be true when therapeutic hypothermia is used [14].

But again,

Reducing brain damage

The concept of reperfusion injury implies that at least part of the damage is due to excessive oxygenation. In principle, this can be attributed to excessive oxygen content of arterial blood or to excessive reperfusion.

While it has now been generally accepted that there is no need to use supplementary oxygen during resuscitation, the use of a hypoxic gas mixture was tested in a piglet model [15]. An FiO2 of 12–18% was sufficient to achieve a sagittal sinus blood oxygen saturation of 17–23% 2 h

Conclusions

Cerebral hyperoxygenation, abnormally increased perfusion, and lack of normal cerebral blood flow regulation are typically present in severe hypoxic–ischaemic encephalopathy. This can be utilized for prognostication. Whether the perfusion abnormalities at this secondary stage are detrimental, beneficial, or a mere epiphenomenon remains elusive. In contrast, incomplete reoxygenation of the brain during and following resuscitation is likely to compromise outcome. The clinical value of cerebral

Key guidelines

  • Consider using Doppler ultrasound to diagnose cerebral hyperperfusion and/or near-infrared spectroscopy to diagnose cerebral hyperoxygenation, both indicators of secondary energy failure.

  • Caution is indicated when using this information for prognosis. Although it does have good prognostic value, this value is reduced during hypothermia. It is unclear how much it adds to information from other sources, such as clinical history, neurological state, EEG, or imaging.

Research directions

  • Cardiovascular compromise is common after birth asphyxia and it is possible that incomplete reoxygenation of the brain contributes to the primary injury. Cerebral oximetry in the first hours after resuscitation has potential to detect this and deserves testing in a clinical trial.

  • There are no guidelines or clear evidence that one must attempt to normalise hyperperfusion or hyperoxygenation. It is unknown if these contribute to the injury or constitute a compensatory mechanism and must be

I have no conflicts of interest regarding the contents of this article.

References (19)

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