EditorI read with interest the review by Hocking and Wildsmith1 on intrathecal drug spread. I feel they omitted to mention an important aspect of drug spread that could have a bearing for all blocks.
They quite rightly stated that vasoconstrictors added to intrathecal local anaesthetic could prolong the duration of a block, although not affect the height of block. They failed to mention the effect of i.v. vasopressors on spinal block height. An article by Cooper and Mowbray2 in 2003 first mentioned the affect of choice of i.v. vasopressor on the rostral spread of spinal anaesthetic. He conducted a formal study that was published in 2004,3 which showed that when using phenylephrine as the hypotensive rescue drug, the block height, when assessed to cold and light touch sensation, was on average two dermatomes lower compared with ephedrine.
Given the increasing use of phenylephrine; particularly in obstetric anaesthesia, to treat sympathetic blockade related hypotension, it should certainly have been mentioned.
Leeds, UK
EditorIn their review of intrathecal drug spread, Hocking and Wildsmith state that pulse and blood pressure are related to block height.1 This relationship however is not precise, as there are other more significant influences.4
Although later, the authors stress the importance of venous return for the maintenance of blood pressure, they omitted the clinically highly significant relationship between a dropping venous return to the right heart and bradycardia.4
I accept that the cardiovascular responses to spinal blockade formed only a small incidental part of this review. Unfortunately, however, this short sentence relating pulse and blood pressure solely to cephalad spread of spinal anaesthesia could encourage the anaesthetist erroneously to attribute a slowing heart exclusively to the height of the spinal block, so inducing a false sense of security.
In 1988, Caplan and colleagues5 demonstrated the serious consequences of failing adequately to appreciate the significance of bradycardia during spinal anaesthesia. This warning sign must alert the anaesthetist to the possibility and hence the consequences of a dropping venous return, and cannot be passed off as a side-effect of cephalad spread of spinal anaesthesia.
Nottingham, UK
EditorWe thank Drs Akerman and Hutter for their interest in our review, and are grateful for the opportunity to respond.
Dr Akerman raises an interesting point, but should recognize the various dynamics involved. These are both relevant and important. First, the definitive paper by Cooper and colleagues3 did not appear until our review was well advanced in the publication process. Second, Cooper and colleagues3 only studied their patients for 20 min after intrathecal injection, and it is well recognized that intrathecal spread will continue for at least 30 min. Thus, the third issue, that this was the first description of a previously unreported association, was made in a dynamic clinical situation. Before an influence of systemic vasopressor on intrathecal drug disposition can be accepted as definitive it will need confirmation, and preferably confirmation in patients whose blocks are followed for at least 30 min, if not longer. Type 2 error is not just a theoretical possibility; it happens.
Dr Hutter is correct in stating that extent of block is not the only factor that may contribute to perioperative bradycardia, but it is a major factor and we stand by our wording, particularly given the subject matter of this paper. The other issues have been discussed elsewhere,68 including some thoughts on the series from Caplan and colleagues.5
1 Oxford, UK
2 Dundee, UK
References
1 Hocking G, Wildsmith JAW. Intrathecal drug spread. Br J Anaesth 2004; 93: 56878
2 Cooper DW, Mowbray P. Can choice of vasopressor therapy affect the rostral spread of spinal anaesthetic? Anesthesiology 2003; 98: 1524[CrossRef][ISI][Medline]
3 Cooper DW, Jeyeraj L, Hynd R, et al. Evidence that intravenous vasopressors can affect rostral spread of spinal anaesthesia in pregnancy. Anesthesiology 2004; 101: 2833[CrossRef][ISI][Medline]
4 Greene NM, Brull SJ. Physiology of Spinal Anesthesia. Baltimore: Williams and Wilkins, 1993; 1324
5 Caplan RA, Ward RJ, Posner K, Cheney FW. Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing factors. Anesthesiology 1988; 68: 511[ISI][Medline]
6 McCrae AF, Wildsmith JAW. Prevention and treatment of hypotension during central neural block. Br J Anaesth 1993; 70: 67280[Abstract]
7 Burke D, Wildsmith JAW. Severe vaso-vagal attack during regional anaesthesia for Caesarean section. Br J Anaesth 2000; 84: 8234[Medline]
8 Wildsmith JAW. Perioperative bradycardia. Br J Anaesth 2001; 87: 649[Medline]