Routine utilization of the transient hyperaemic response test after aneurysmal subarachnoid haemorrhage.

In order to explore the applicability of daily cerebral autoregulation monitoring through routine utilization of the transient hyperaemic response (THR) test in patients after aneurysmal subarachnoid haemorrhage (SAH), we performed THR tests daily in 50 consecutive patients with verified SAH. Out of 1167 studies, the test results were acceptable during 954 procedures (81.5%). 310 negative (32.5%; range 0.75-1.099; mean 1.03) and 644 positive (67.5%; range 1.10-1.77; mean 1.19) test results were obtained. Multiple logistic regression analysis revealed that the registration of negative THR in a middle cerebral artery (MCA) during the period of critical care was related to the patients' poor clinical grade (p-0.02) and Fisher CT-grade (p-0.04) on admission, to the development of vasospasm (p-0.003) and to the detection of ipsilateral intracerebral haemorrhage and/or cerebral infarction (p-0.01). The frequent registration of negative THR tests (negative results in > 30% of all the tests in an MCA) was independently related to the detection of ipsilateral intracerebral haemorrhage and/or cerebral infarction (p-0.0001). THR tests provide information about intracranial alterations and can be safely performed as a routine monitoring tool after SAH.

The possible role of CSF hydrodynamic parameters following in management of SAH patients.

It is suggested that reduced intracranial compliance may be present even when measured ICP is normal and may precede clinical deterioration. Our findings reflect a decompensation of hydrodynamic parameters more pronounced 4-7 postictal days, when compliance is reduced not only in patients with poor clinical condition, but also in patients with Hunt-Hess grade I-III. Increased CSF outflow resistance in the first few days is not surprising; it is thought to be due to the blockage of flow of CSF through the basal subarachnoid cisterns and clogging of the arachnoid villi with erythrocytes and fibrin. Enlargement of ventricles seen on CT scan at the same time suggests the development of acute hydrocephalus. During the first days after SAH, our data reflects evidence of ventricular enlargement in patients presenting with both poor and better clinical condition. We conclude that the monitoring of ICP and dynamic measuring of CSF hydrodynamic parameters is important for longer than the generally accepted few days for selected cases after SAH.

Correlations between brain oedema volume on CT and CSF dynamics in severely head injured patients.

The CSF dynamics were studied in 18 patients with severe head injury who remained comatose over 6 hours after trauma (GCS less than 8). Amount of brain oedema was estimated by CT tomodensitometry. In addition, CSF parameters of PVI. Elastance (E), compliance (C) and resorption resistance (R) were calculated from serial bolus infusion tests. We observed a decrease in viscoelastic parameters as indexed by PVI, however, no increase in resistance to CSF outflow. It was noted that patients with lower PVI developed more severe brain oedema during the 3-5 day post traumatic period. From these data, we conclude that buffering capacity in severe head injury is mainly affected by the volume of brain oedema and not by the haematoma volume.

Quantitative analysis of CT visualized periventricular and perifocal brain oedema by means of CSF dynamics infusion test.

Brain oedema of different pathogenesis cannot be differentiated with CSF infusion tests. In cases with periventricular oedema the CSS viscoelastic parameters are changed more towards the decompensated state than in cases with perifocal oedema.