Discussion
Possibility of estimating of ICP has appeared at us as a result of the introduction of ophthalmodynamometry of central retinal vein. Over the past 10–15 years, several studies have confirmed the clinical relevance of ophthalmodynamometry in determining of intracranial pressure. Motschmann M., et al. showed a linear relationship between ICP and pressure in central retinal vein assessed invasively with a correlation coefficient of 0.968.[14] So, authors concluded that the ophthalmodynamometry is valuable and accurate method of assessment of intracranial pressure, it can be used in patients with various neurological disorders such as hydrocephalus, brain tumor and head injury. Ophthalmodynamometry can be successfully used in the diagnosis of idiopathic intracranial hypertension.[15] A more recent study showed that the increase of pressure in central retinal vein in patients with idiopathic intracranial hypertension correlated with the direct measurement pressure of cerebrospinal fluid through a lumbar puncture.[16] In 2010, a group of researchers conducted a blind research of ophthalmodynamometry in neurological hospital patients and healthy volunteers at high altitudes.[17] Ophthalmodynamometry showed a significant correlation with ICP determined by a ventricular sensor. The correlation coefficient was 0.85, the accuracy of the method - 89 %. In 2011, a group of German collaborators published a paper on the definition of accuracy of ophthalmodynamometry in the evaluation of intracranial pressure. The study included 102 patients with diseases of the brain. Ophthalmodynamometry has proved to be an accurate noninvasive method for the diagnosis of intracranial hypertension with a sensitivity of 84.2 % and a specificity of 92.8 %.[11] The main limitation of this method is its discrete nature. Thus, it allows us to estimate only the trend, abrupt changes in intracranial pressure may remain unnoticed.
We observed a moderate decrease in intracranial pressure during anesthesia with propofol which is consistent with the work carried out earlier showed that propofol significantly reduces ICP in patients with intracranial hypertension. Such dynamics is connected with the fact that propofol reduces the cerebral metabolic rate,[18,19] and also causes cerebral vasoconstriction and proportional decrease in cerebral blood flow.[20] There are a number of publications, showing an increase of this indicator on application of epidural anesthesia,[21–23] which is more pronounced in patients with an initial tendency to intracranial hypertension.[6] It is primarily resulted from the dural sac external compression reducing its capacity.[5] These changes can lead to the inadequate epidural anesthesia and make complications more frequent.[24] According to our data, no increase in intracranial pressure with epidural anesthesia, and no effect of the elevated ICP on the efficiency of epidural anesthesia can be explained by methodological differences between researchers. The bolus injection of the main dose of the local anesthetic solution was used in all studies that showed an increase in intracranial pressure whereas we used a method of the continuous infusion in our research. This is supported by the studies claiming that the epidural anesthesia with the infusion administration of solutions with the low concentration of local anesthetics is safe in patients with increased intracranial pressure.[9,24] BPS was significantly reduced, which is specific for a sympathetic blockade and vasodilation inherent to propofol, however, the simultaneous reduction of intracranial pressure allowed us to maintain CPP at a safe level in all cases. However, it should be noted that maintaining a minimum safe level of CPP at 60 mm Hg,[25,26] required more frequent use of vasopressors in patients with initially elevated ICP. Thus, in the absence of monitoring of intracranial pressure in patients with elevated ICP there is a risk of reduction of CPP below a safe level even at normal BPS.
BMC Anesthesiol. 2015;15(76) © 2015 BioMed Central, Ltd.
