✓ Appropriate management of intracranial pressure (ICP) in severely head injured patients depends in part on the cerebral vessel reactivity to PCO 2 ; loss of CO 2 reactivity has been associated with poor outcome. This study describes a new method for evaluating vascular reactivity in head-injured patients by determining the sensitivity of ICP change to alterations in PCO 2 . This method was combined with measurements of the pressure volume index (PVI), which allowed calculation of blood volume change necessary to alter ICP. The objective of this study was to investigate the ICP response and the blood volume change corresponding to alterations in PCO 2 and to examine the correlation of responsivity and outcome as measured on the Glasgow Outcome Scale. The PVI and ICP at different end-tidal PCO 2 levels produced by mild hypo- and hyperventilation were obtained in 49 patients with Glasgow Coma Scale scores of less than 8 and over a wide range of PCO 2 (25 to 40 mm Hg) in eight patients. Given the assumption that the PVI remained constant during alteration of PaCO 2 , the estimated blood volume change per torr change of PCO 2 was calculated by the following equation: BVR = PVI × Δlog(ICP)/ΔPCO 2 , where BVR = blood volume reactivity. The data in this study showed that PVI remained stable with changes in PCO 2 , thus validating the assumption used in the blood volume estimates. Moreover, the response of ICP to PCO 2 alterations followed an exponential curve that could be described in terms of the responsivity indices to capnic stimuli. It was found that responsivity to hypocapnia was reduced by 50% compared to responsivity to hypercapnia measured within 24 hours of injury (p < 0.01). The sensitivity of ICP to estimated blood volume changes in patients with a PVI of less than 15 ml was extremely high with only 4 ml of blood required to raise ICP by 10 mm Hg. The authors conclude from these data that, following traumatic injury, the resistance vessels are in a state of persistent vasoconstriction, possibly due to vasospasm or compression. Furthermore, BVR correlates with outcome on the Glasgow Coma Scale, indicating that assessment of cerebrovascular response within the first 24 hours of injury may be of prognostic value.
We evaluated the potential usefulness of the acetazolamide test by investigating whether acetazolamide vasoreactivity reflected the change in resting cerebral blood volume caused by compensatory vasodilation due to a decline in cerebral perfusion pressure.We measured resting and acetazolamide-activated cerebral blood flow with a stable xenon-enhanced CT system and resting cerebral blood volume with the subtraction technique using contrast-enhanced CT in 30 patients with various diseases. These parameters were measured in the anterior, middle, and posterior cerebral arterial territories of both hemispheres separately. We evaluated the statistical relationships between resting cerebral blood volume and vasoreactivity in these three territories, and the significance of the correlations was tested by ANOVA/ANCOVA to adjust for the double entries.Significant negative linear relationships were demonstrated between the resting cerebral blood volume and the change in cerebral blood flow, expressed as a percentage induced by acetazolamide activation, for the anterior (r = -.607, P = .0004), middle (r = -.551, P = .0015), and posterior (r = -.523, P = .0078) cerebral arterial territories and between the resting cerebral blood volume and the increase in cerebral blood flow (absolute values) for the anterior (r = -.512, P = .0164) and middle (r = -.523, P = .0001) but not the posterior (r = -.571, P = .0563) cerebral arterial territories.The acetazolamide test appears to be useful for the investigation of compensatory vasodilation: the vasoreactivity can be calculated as the increased cerebral blood flow expressed as a percentage or an absolute value, which both reflect cerebral blood volume directly.
✓ Cerebrospinal fluid (CSF) dynamics were correlated to the changes in ventricular size during the first 3 months posttrauma in patients with severe head injury (Glasgow Coma Scale score ≤ 8, 75 patients) to distinguish between atrophy and hydrocephalus as the two possible causes of posttraumatic ventriculomegaly. Using the bolus injection technique, the baseline intracranial pressure (ICP), pressure volume index, and resistance for CSF absorption (R0) provided a threedimensional profile of CSF dynamics that was correlated with ventricular size and Glasgow Outcome Scale (GOS) score at 3, 6, and 12 months posttrauma. Patients were separated into five different groups based on changes in ventricular size, presence of atrophy, and CSF dynamics. Group 1 (normal group, 41.3%) demonstrated normal ventricular size and normal ICP. Group 2 (benign intracranial hypertension group, 14.7%) showed normal ventricular size and elevated ICP. Group × (atrophy group, 24%) displayed ventriculomegaly, normal ICP, and normal R0. Group 4 (normal-pressure hydrocephalus group, 9.3%) had ventriculomegaly, normal ICP, and high R0. Group 5 (high-pressure hydrocephalus group, 10.7%) showed ventriculomegaly and elevated ICP with or without high R0. The GOS score in the nonhydrocephalic groups (Groups 1, 2, and 3) was better than in the hydrocephalic groups (Groups 4 and 5). It is concluded from these results that 44% of head injury survivors may develop posttraumatic ventriculomegaly. Posttraumatic hydrocephalus, as identified by abnormal CSF dynamics, was diagnosed in 20% of survivors and their outcome was significantly worse. This study demonstrates the importance of using CSF dynamics as an aid in diagnosis of posttraumatic hydrocephalus and identifying those patients who may benefit from shunt placement.
The cerebral blood flow (CBF) and mean stump pressure (MSTP) of 25 preoperative patients were measured during a 15 minute test occlusion of the ipsilateral internal carotid artery (ICA). CBF measurements were carried out by the Xenon/CT system adapted to the Toshiba 20A scanner with 4 min wash-in and 6 min wash-out of 30% Xe. Intra-arterial Xe concentration was calculated from endotidal tube-scanning. We selected two areas: the one fed by the middle cerebral artery (MCA), and the other defined as a unilateral cerebral hemisphere on the axial CT slice through the foramen of Monroe, to obtain CBF. We assessed the asymmetry ratio (AR) of CBF (AR = CBF in occlusion side/CBF in contralateral side) and investigated the correlation and regression of MSTP and AR in 25 cases. Furthermore, in 10 of the 25 patients, we measured the CBF with occlusion of the ICA 20 minutes after intravenous administration of acetazolamide. We evaluated the differences between before and after acetazolamide administration in MSTP and AR (paired t test), and investigated the correlation of and regression between MSTP and AR before and after acetazolamide administration again in these 10 patients.A) In 25 cases; In the cases where MSTP was below 40 mmHg, a straight correlation with significant correlation and regression coefficients (MCA: r = 0.834, P = 0.020; Hemisphere: r = 0.840, P = 0.018) between MSTP and AR recognized. However, this statistical correlation was not seen in the cases where MSTP exceeded 40 mmHg, indicating that relationship could be expressed as horizontal line. B) In 10 cases; (1) AR was found to be significantly decreased after acetazolamide administration (MCA: P = 0.007; Hemisphere: P = 0.004, paired t test), although MSTP remained unchanged. (2) Although the relationship between MSTP and AR could be expressed as horizontal lines without a significant regression coefficient before acetazolamide administration, after that their relationship became a straight correlation with a significant regression coefficient (MCA: r = 0.698, P = 0.025; Hemisphere: r = 0.826, P = 0.003).These results suggest that 40 mmHg of MSTP in the cases considered as almost normal is the lower limit of the autoregulatory range. In addition, an acetazolamide reactive mechanism might have a role in autoregulation, and in the lower range down to the lower limit of that the compensated CBF by this mechanism would increase as a progressive reduction of MSTP.
