Ben Friis-Hansen

Bio: Ben Friis-Hansen is an academic researcher. The author has contributed to research in topics: Respiratory distress & Cerebral blood flow. The author has an hindex of 1, co-authored 1 publications receiving 622 citations.

Cerebral intravascular oxygenation correlates with mean arterial pressure in critically ill premature infants.

Abstract: Objectives. Premature infants experience brain injury, ie, germinal matrix–intraventricular hemorrhage (GMH-IVH) and periventricular leukomalacia (PVL), in considerable part because of disturbances in cerebral blood flow (CBF). Because such infants are susceptible to major fluctuations in mean arterial blood pressure (MAP), impaired cerebrovascular autoregulation would increase the likelihood for the changes in CBF that could result in GMH-IVH and PVL. The objectives of this study were to determine whether a state of impaired cerebrovascular autoregulation could be identified reliably and conveniently at the bedside, the frequency of any such impairment, and the relation of the impairment to the subsequent occurrence of severe GMH-IVH and PVL. Patients and Methods. To monitor the cerebral circulation continuously and noninvasively, we used near-infrared spectroscopy (NIRS) to determine quantitative changes in cerebral concentrations of oxygenated hemoglobin (HbO2) and deoxygenated hemoglobin (Hb) from the first hours of life. Our previous experimental study showed a strong correlation between a measure of cerebral intravascular oxygenation (HbD), ie, HbD = HbO2 − Hb, determined by NIRS, and volemic CBF, determined by radioactive microspheres. We studied 32 very low birth weight premature infants (gestational age: 23–31 weeks; birth weight: 605-1870 g) requiring mechanical ventilation, supplemental oxygen, and invasive blood pressure monitoring by NIRS from 1 to 3 days of age. MAP measured by arterial catheter pressure transducer and arterial oxygen saturation measured by pulse oximetry were recorded simultaneously. The relationship of MAP to HbD was quantitated by coherence analysis. Results. Concordant changes (coherence scores >.5) in HbD and MAP, consistent with impaired cerebrovascular autoregulation, were observed in 17 of the 32 infants (53%). Eight of the 17 infants (47%) developed severe GMH-IVH or PVL or both. Of the 15 infants with apparently intact autoregulation, ie, coherence scores .5. Conclusions. We conclude that NIRS can be used in a noninvasive manner at the bedside to identify premature infants with impaired cerebrovascular autoregulation, that this impairment is relatively common in such infants, and that the presence of this impairment is associated with a high likelihood of occurrence of severe GMH-IVH/PVL.

Assessment of cerebral pressure autoregulation in humans - a review of measurement methods

Abstract: Assessment of cerebral autoregulation is an important adjunct to measurement of cerebral blood flow for diagnosis, monitoring or prognosis of cerebrovascular disease. The most common approach tests the effects of changes in mean arterial blood pressure on cerebral blood flow, known as pressure autoregulation. A 'gold standard' for this purpose is not available and the literature shows considerable disparity of methods and criteria. This is understandable because cerebral autoregulation is more a concept rather than a physically measurable entity. Static methods utilize steady-state values to test for changes in cerebral blood flow (or velocity) when mean arterial pressure is changed significantly. This is usually achieved with the use of drugs, shifts in blood volume or by observing spontaneous changes. The long time interval between measurements is a particular concern in many of the studies reviewed. Parallel changes in other critical variables, such as pCO2, haematocrit, brain activation and sympathetic tone, are rarely controlled for. Proposed indices of static autoregulation are based on changes in cerebrovascular resistance, on parameters of the linear regression of flow/velocity versus pressure changes, or only on the absolute changes in flow. The limitations of studies which assess patient groups rather than individual cases are highlighted. Newer methods of dynamic assessment are based on transient changes in cerebral blood flow (or velocity) induced by the deflation of thigh cuffs, Valsalva manoeuvres, tilting and induced or spontaneous oscillations in mean arterial blood pressure. Dynamic testing overcomes several limitations of static methods but it is not clear whether the two approaches are interchangeable. Classification of autoregulation performance using dynamic methods has been based on mathematical modelling, coherent averaging, transfer function analysis, crosscorrelation function or impulse response analysis. More research on reproducibility and inter-method comparisons is urgently needed, particularly involving the assessment of pressure autoregulation in individuals rather than patient groups.

Implications of the Blood-Brain Barrier and Its Manipulation

Abstract: As a neurologist and student of the microvasculature, I find great pleasure in introducing this treatise Presented here is a view of brain pathophysiology and therapy from the perspective of the blood-brain barrier (BBB) Virtually every disease process that affects the brain-traumatic, neoplastic, infectious, inflammatory, toxic, metabolic, degenera tive, vascular, and epileptic-affects the BBB Damage to this homeostatic system often leads to disruption of the composition and volume of brain fluid compartments, thereby contributing to neurologic symptoms and pathology Furthermore, in disorders in which the integrity of the barrier is not breached, its normal restrictive nature may limit therapeu tic approaches For example, the barrier appears to function normally in Parkinson dis ease, but its ability to compensate for striatal dopamine depletion is in part determined by the activity of transporters and enzymes operative in the brain microvasculature of antibiotics, anticonvulsants, antineoplastic agents, and neurolep Similarly, the choice tics requires attention to these drugs' interaction with the BBB Thus, the barrier inter faces with virtually all nervous system diseases and therapies Future brain treatments with regulatory peptides, immune mediators, and gene components will require selective methods to deliver these agents to specific brain regions The second volume of this text successfully provides a thorough review of BBB function and failure in a variety of clinical situations"

Fluctuating pressure-passivity is common in the cerebral circulation of sick premature infants.

Abstract: Cerebral blood flow pressure-passivity results when pressure autoregulation is impaired, or overwhelmed, and is thought to underlie cerebrovascular injury in the premature infant. Earlier bedside observations suggested that transient periods of cerebral pressure-passivity occurred in premature infants. However, these transient events cannot be detected reliably by intermittent static measurements of pressure autoregulation. We therefore used continuous bedside recordings of mean arterial pressure (MAP; from an indwelling arterial catheter) and cerebral perfusion [using the near-infrared spectroscopy (NIRS) Hb difference (HbD) signal) to detect cerebral pressure-passivity in the first 5 d after birth in infants with birth weight <1500 g. Because the Hb difference (HbD) signal [HbD = oxyhemoglobin (HbO2) - Hb] correlates with cerebral blood flow (CBF), we used coherence between MAP and HbD to define pressure-passivity. We measured the prevalence of pressure-passivity using a pressure-passive index (PPI), defined as the percentage of 10-min epochs with significant low-frequency coherence between the MAP and HbD signals. Pressure-passivity occurred in 87 of 90 premature infants, with a mean PPI of 20.3%. Cerebral pressure-passivity was significantly associated with low gestational age and birth weight, systemic hypotension, and maternal hemodynamic factors, but not with markers of maternal infection. Future studies using consistent serial brain imaging are needed to define the relationship between PPI and cerebrovascular injury in the sick premature infant.