We thank Dr. Lambert for his comments, which add interesting aspects to the discussion.
The difficulties of controlling local anesthetic (LA) spread during “isobaric” subarachnoid block in daily practice are well-known. As Dr. Lambert states, there is a manifold of influencing factors whereof several are unknown to the practitioner before LA injection (e.g. , lumbosacral cerebrospinal fluid volume).
Former studies have confirmed that pharmacokinetic action of cold and warm LA is quite different in the subarachnoid space1–5in terms of faster onset and higher maximum level of sensory block when using the warmed solution. Moreover, prolonged analgesia was reported by Dr. Lambert.6
After equilibration of the injected LA to cerebrospinal fluid (body) temperature, with the exception of articaine and mepivacaine, all commercially available LA solutions will behave hypobarically. This means that LA after injection at room temperature will initially descend and, after passing the isogravimetric point, ascend. This is supported by the fact that by keeping the patient in a sitting position during and after administration of warmed LA, a higher maximum level of sensory blockade is obtained.3–5Shortening the period of sitting or puncturing in the lateral decubitus position masks the hypobaric effect of warmed LA.2This may, likewise, be illustrated by Dr. Lambert's study,6where no difference in maximum level of sensory blockade was found in patients punctured in the lateral decubitus position and then immediately turned to the supine horizontal position. The clinical impact of positioning during “isobaric” subarachnoid block is further supported by the effect of (un)intended late posture change.7,8Further, cerebrospinal fluid density is lower in women.9Therefore, the absolute effect of warming LA on individual baricity must be considered smaller in females than in males at a given body temperature and may bias the results.6
From the available data, we conclude that the sitting position during puncture is a prerequisite for obtaining clinical impact of the hypobaricity concept of warmed LA solutions in terms of higher maximum level of sensory blockade, and a smaller variability of the number of blocked segments. Whether those observations are clinically transferable into lower doses of warmed LA in the sitting position must be evaluated in forthcoming trials.
With regard to puncturing in the lateral decubitus position, another point of view deserves discussion. Because the sensory nerves derive from the dorsal horn of the spinal cord and the roots are located posterior, in the supine position hypobaric (37ºC) LA will ascend ventrally apart from these target structures and may even have less analgesic effect. In this regard, it would have been of particular interest if in his work6Dr. Lambert observed differences between anterior or posterior nerve roots. Because motor neurons and sudomotor output derive from the anterior roots, in their setting the usual difference of two segments between sensory and (sudo)motor block may have been lost in the hypobaric (37ºC) group. This hypothesis is supported by data in a comparable setting (lateral decubitus puncture) from Higuchi et al. ,10who found a trend to correlation between motor block onset and cerebrospinal fluid density—not, however, between time to peak sensory block level and cerebrospinal fluid density.
The discussion on pKa values of LA in conjunction with subarachnoid block, as already addressed elsewhere,6,11should not be overemphasized. LAs gain body temperature within 2 min12when injected at room temperature, and pKa values are then equilibrated with those LAs injected at 37ºC. Therefore, the decreased pKa values of LAs injected at 37ºC6are comparatively effective for 2 min and may account for earlier onset of blockade but not, however, for the prolonged LA effects more than 2 h later.
Taken together, the discussed effects carry uncertainty for daily practice but may, besides others, explain the high interindividual ranges in maximum level of sensory blockade reported in many studies using “isobaric” solutions. In vitro studies and modeling as performed in our work11always observe and depict a limited part of reality. They never allow conclusions on the reality itself; rather, they may be hypothesis generating or may improve existing hypotheses, which then must be verified (or falsified) in reality. The problems associated with the complex physiology of subarachnoid block may not be solved with simple physics. The intention of our study was to identify isobaric temperatures and, thus, make the course of LA within the subarachnoid space more predictable to improve the nonprecise anesthetic .
*University Hospital Carl Gustav Carus, Dresden, Germany. email@example.com