Differentiating haematoma with the R2' relaxation rate

Introduction Subdural haematoma (SDH) is a form of traumatic brain injury that can be classified as acute, subacute or chronic, based upon time from injury. When acute, it is a medical emergency in which surgical decompression is the only option to prevent mortality. Small subdurals and those that are no longer actively bleeding may be left to re-absorb spontaneously and clinical decision-making is aided by an accurate assessment of size and age of the haematoma. MR could potentially be used to differentiate the stages of SDH based on the accumulation and spatial position of methaemoglobin. The acute phase of SDH may be characterised by increasing concentrations of intracellular methaemoglobin, while in the subacute phase, methaemoglobin is released as red cells begin to lyse [1]. Methaemoglobin provides a magnetic susceptibility effect through dipole-dipole interaction. In vitro studies using canine blood show that an increase R2 (=1/T2) relaxation rate correlates with increased methaemoglobin accumulation within clot. We hypothesise that the local field inhomogeneity created by methaemoglobin (containing Fe) compartmentalised by intact red blood cells demonstrates a greater effect in R2*. This is based on literature demonstrating the compartmentalisation of iron-oxide contrast agents into the static dephasing regime [2]. It follows from this effect that intracellular methaemoglobin can be differentiated from extracellular methaemoglobin with R2’ imaging [3]. In the subacute phase, when red cells containing methaemoglobin begin to lyse, R2 becomes low [4]. We examine this phenomenon in an in vitro system of SDH using human blood, and show potential for a more accurate method to diagnose onset of the subacute phase.