摘要
I thank Dr. Tighe for his excellent comments about the potential value of using low-dose spinal anaesthesia during hip fracture repair, to try and avoid hypotension and associated mortality 1. It is curious that anaesthetists continue to use similar doses of spinal anaesthesia for older, sicker hip fracture patients who need an effective block to T11 unilaterally, to those known to cause hypotension and bilateral block to T4 in younger, fitter obstetric patients. Although published research points to very low doses providing cardiostable surgical anaesthesia for up to two hours duration, I do not think that it is necessary to reduce intrathecal doses of bupivacaine as low as 5 mg (i.e. 1 ml 0.5%). Data from ASAP show that 7.5 mg bupivacaine (1.5 ml, either hyper- or normobaric) is associated with a mean fall in systolic blood pressure from baseline to lowest recorded of 20%, well above thresholds associated with increased mortality in other observational studies 2, 3. Importantly, this fall is relatively more predictable in magnitude than when using larger volumes of bupivacaine. From my own experience of using similar volumes (1.3 ± 0.3 ml), not only is a small fall predictable, but it tends to occur at a slower rate than with higher volumes, and so avoids ‘saw-toothing’ of the patient's blood pressure during surgery, with persistent hypotension corrected intermittently with intravenous vasopression. It remains uncertain whether relative or absolute blood pressure values, duration or rate of development of hypotension (or combinations of these) are important in increasingly apparent links between hypotension, mortality and morbidity 4, 5, but, as Dr. Tighe points out, intra-operative blood pressure is an anaesthetic problem that would seem to be treatable in part just through the simple action of giving less spinal anaesthetic. I understand anaesthetists’ concerns about reduced doses of spinal bupivacaine providing shorter durations of surgical anaesthesia. Dr. Tighe suggests using local anaesthesia infiltration if the cephalad end of the wound regains sensation at the end of prolonged surgery. Instead, I propose that patients should be administered a fascia iliaca nerve block before spinal administration. This has several theoretical advantages: analgesia is provided during positioning for spinal anaesthesia reducing the need for sedation; lower doses of spinal anaesthesia can be used without concern for pain occurring during skin closure after prolonged surgery; and analgesia is extended for 6–10 h after surgery, avoiding the need for intrathecal opioid co-administration (and therefore the associated side-effects of these). I would encourage anaesthetists who are currently using ‘obstetric’ doses of spinal bupivacaine 0.5% to consider reducing doses by 0.05 mg (0.1 ml) during subsequent anaesthetics, towards 7.5 mg (1.5 ml) for all procedures except total hip arthroplasty, for which 9 mg (1.8 ml) should provide a sufficient duration of anaesthesia. Dr. Tighe is absolutely right: this is a fertile area for research involving older, frailer hip fracture patients, particularly in describing the cardiovascular effects of lower dose spinal anaesthesia in observational trials, and comparing cardiovascular stability using lower dose (~1.5 ml) compared with higher dose (~2.5 ml) spinal anaesthesia. Readers may be interested in further information about the rationale behind using low dose spinal anaesthesia for hip fracture surgery, together with relevant references and options for future research, which can be found at www.hipfractureanaesthesia.com.