Lund Therapy – pathophysiology-based therapy or contrived over-interpretation of limited data?

Excerpt

There have been few concepts in critical care that have polarised views in the way that the “Lund Therapy” has consistently done over the past 14 years. Proponents fiercely defend the comparable results from their case series with similar series managed according to the evolving Brain Trauma Foundation guidelines [1, 2]. Indeed, the most recent evolution of these guidelines has moved closer to Lund Therapy goals [3, 4, 5], but not in the recommendations on how to achieve them [6, 7]. Both Lund Therapy and Brain Trauma Foundation guidelines have prevention of secondary injury as their cornerstone, with Lund Therapy focused on brain volume regulation [3, 4]. Current strategies are limited, but aim to reduce ischaemia- induced secondary injury by maintaining the delicate balance between cerebral perfusion (oxygen and substrate delivery) and metabolic requirement. Historically, autopsy data have consistently demonstrated a significant burden of ischaemic damage in non-survivors after traumatic brain injury. More recently, using contemporary data from PET scans, evidence has been constructed to show that managing traumatic brain injury patients according to Brain Trauma Foundation guidelines does not eliminate “ischaemic” brain volume. These data, however, require careful interpretation. Ischaemia assessed by PET is classified by the authors according to measures of oxygen extraction fraction, and not metabolic correlates of anaerobic metabolism. The same group has also shown that hyperventilation does increase oxygen extraction fraction, but none of the ischaemic brain volume data are PaCO₂ corrected [8, 9, 10]. It is plausible that the more severely damaged patients were hyperventilated to a greater extent and thus evidenced a larger ischaemic brain volume. The conclusion must be that therapies that reduce cerebral perfusion should be avoided. …