Effects of subdural hemorrhage, mass lesion and controlled cortical impact on multi-parametric neuromonitoring in pigs

Abstract

A common problem in traumatic brain injury (TBI) is the effect of acute subdural hemorrhage (ASDH), especially if accompanied by contusion, leading to a high mortality rate. Little is known about the acute pathophysiological mechanisms of such an injury type and the role of blood constituents or shear volume. Therefore, the goals of this study were to establish a porcine model of acute subdural hematoma (ASDH), to study the effect of ASDH as secondary injury after controlled cortical impact (CCI) and to distinguish the effects of blood from sole mass effects (paraffin oil). 43 pigs were used. and intravenously anaesthetised by alpha-chloralose. After cannulation of femoral artery and vein animals were fixed in a stereotaxic frame for drilling a large craniectomy (20 mm) for application of TBI and small burr holes for oxygen (Licox), temperature and microdialysis probes (CMA/70). A SEP (somatosensory evoked potential) electrode and an intraventricular ICP sensor were also applied [Alessandri et al., J. Neurotrauma 20(12), 2003]. Measurements were made at least every 15 minutes throughout the experiment. After a baseline period (60 min), TBI was initiated by: (a) CCI at 2.5 m/s, 9 mm injury depth; (b) subdural infusion of 2 mL, 5 mL or 9 mL venous blood (0.5 mL/min); (c) 5 mL paraffin oil and (d) a combined CCI and ASDH trauma (2 mL, starting 10 min after CCI). Sham pigs received all interventions, but no TBI. Twelve (12) hours after TBI, brains were removed and analysed histologically. Subdural infusion of 9mL blood elevated ICP to 34.73 mmHg (peak: 463 mmHg at 20 min) during the first post-TBI hour and remained close to 30 mmHg throughout the study, whereas ICP after 2 mL and 5 mL blood recovered quickly from peak 22.34 and 29.45 mmHg. Ipsilateral tissue oxygen decreased acutely to 40-60% of baseline (23.31.1 mmHg) after ASDH, but except for 9 mL, oxygen recovered within several hours. Glutamate was long-lasting increased only in the 9 mL group, adding to the large histological damage. The assessed contusion index [Adams, 1985] did not differ between the 2- and 5 mL-group. A 2 mL ASDH as secondary injury affected neuromonitoring parameters as well as histology only slightly when compared to CCI trauma. Peak ICP was 13.72 (CCI) and 173.4 mmHg (CCI+2 mL blood) and ptiO2 decreased to 70% of baseline in both cases. In both CCI-groups, but not the 2 mL ASDH group SEP amplitude declined below 50% (CCI 37.8%, CCI+2 mL: 36.9%, 2 mL: 80.3% at 120 min post-TBI) throughout the entire experiment. Comparison of 5 mL subdural blood and paraffin oil infusion revealed no differences in neuromonitoring and contusion index. A porcine model of ASDH could be established with a threshold blood volume for long lasting neuromonitoring effects between 5 and 9 mL (7-13% of brain volume). A volume of 2 mL blood was insufficient to potentate the effects of brain contusion. Furthermore, the similar effects of 5 mL blood or paraffin indicate that the acute increase of ICP determines processes leading to a 'subacute' histological damage found after 12 hours, and that additional effects due to blood contact with brain tissue (e.g. inflammation) may be detected only at later time-points.