Australasian Anaesthesia 2011 - Australian and New Zealand ...

36 Australasian Anaesthesia 2011The disappointing spinal 37Pathology associated with previous surgery, spinal stenosis, and damage to nerve roots may also be contributory.Despite adherence to good technique and apparent uncomplicated administration, spinal blockade may fail dueto inability of spread and/or diffusion into neural structures. A published account of inadequate spinal anaesthesiaafter two apparently uncomplicated spinal punctures occurred in a male patient who had previously receivedintrathecal chemotherapy. 28 The authors suggested chemotherapy-induced nerve root changes may have beenresponsible. Pathological conditions of the spinal cord itself, such as syringomyelia, may render subarachnoid blockunsuccessful and have also been reported. 29 Adhesions between nerve roots or between the nerve root and thearachnoid membrane have been demonstrated by spinaloscopy and may hinder local anaesthetic action. 19 Diabeteshas also been suggested as a potential cause of failed subdural anaesthesia resulting from glycosylation of nerveroots in a manner similar to the well-recognised damage of autonomic and peripheral nerves in this condition.LOCAL ANAESTHETIC MALDISTRIBUTIONSpinal anaesthesia relies on the appropriate concentration of local anaesthetic acting on the appropriate neuralstructures. Introduction of a spinal needle, demonstration of free flow of csf, and the ability to aspirate confirmsinjection into the csf milieu. However, what concentration of local anaesthetic acts on nerve structures is indeterminate.As has been suggested in other reports 16 , csf volume, and presumably thereby local anaesthetic concentrations,play an important role in subarachnoid efficacy. One study reported on the csf concentrations of bupivacaine in 20patients following failed spinal injection and preceding a repeat injection. 30 Of these 20 patients, 60% had concentrationsgreater than 73µg/ml, this arbitrary threshold being the 5 th percentile of csf concentrations producing effective blockin another study by Ruppen and colleagues. 31 Of the 6 patients with a completely failed spinal, one had bupivacainecsf concentrations in excess of this threshold [106µg/ml]. Amongst the 14 patients with incomplete spinal anaesthesia,eleven were above this threshold with one demonstrating a csf bupivacaine concentration of 1020µg/ml!The authors of this study conjectured that given 60% of patients with either incomplete or totally failed spinalanaesthesia had csf bupivacaine concentrations above the threshold where one would expect satisfactory anaesthesia,maldistribution of local anaesthetic was a possible major factor. In particular, the patient with a concentration of≈1mg/ml after an injectate of 17.5mg of bupivacaine, would presuppose a csf volume of 17.5ml, well below thevolumes estimated in previous studies, 13 and unlikely given the expectation of a high block with such a small csfvolume. This particular case strongly suggests maldistibution and non-uniform spread of local anaesthetic wasresponsible.Certainly anatomical considerations as alluded to above, may hinder effective spread of local anaestheticthroughout the intrathecal compartment, and compartmentalisation would explain seemingly adequate csfconcentrations with inadequate block or even the absence of any block. Models of the intrathecal compartmenthave demonstrated this as a potential issue. 32Ruppen’s particular study involved bupivacaine concentration estimations in 60 patients subjected to a 2 nddiagnostic lumbar puncture, all of whom had had a successful initial spinal block. 31 He demonstrated highly variableconcentrations with no correlation between concentration and block extent at particular time points. Whilstinterpretation of their results is limited by methodology, the highly variable concentrations suggest non-uniformspread of local anaesthetic within the csf may be a normal occurrence. Multiple factors dictating this spread havebeen elaborated. 33 Fortunately, the factors most significant are largely under the control of the anaesthetist, thesebeing local anaesthetic baricity, patient positioning following deposition, and dosage.Aside from the development of a less than optimal block, the clinical significance of maldistribution of localanaesthetic within the subarachnoid space is the possibility of neurotoxicity associated with high concentrations.This potential is exacerbated with repeat injections since, if maldistribution is responsible and compartmentalisationhas resulted in high concentrations in restricted csf regions, a repeated injection could undergo the same processand elevate concentrations further. The potential for neurotoxicity is thus augmented.There is a longstanding concern within the anaesthetic community over neurotoxicity of local anaestheticsolutions. In vitro and animal research has demonstrated this toxicity convincingly 34,35,36 and many solutions havebeen implicated. The local anaesthetic agent used, the concentration and dose, and the time of exposure to theanaesthetic agent all appear significant. A higher concentration and dosage (presumably through a concentrationeffect) are more neurotoxic, whilst lignocaine, particularly at high concentration, may be worse than bupivacaine(although equipotent studies on neurotoxicity are lacking). Hyperbaricity may predispose to pooling and worsenconcentration-associated neurotoxicity.In the clinical literature there are numerous reports of significant neurotoxicity predominantly involving highconcentrations of lignocaine 37,38,39,40 through a continuous spinal catheter technique. A catheter may predispose toboth the use of higher doses than a single shot technique, and continuous or repeated delivery of local anaestheticthat undergoes maldistribution as a practitioner attempts to achieve a satisfactory block. However, cauda equinasyndrome has also been reported in cases involving single shot techniques using 5% hyperbaric lignocaine 41 andfollowing a repeat single shot of dibucaine. 42 Conus medullaris injury has been described following tetracaine and,subsequently, lignocaine spinal anaesthesia 43 , and numerous cases of severe neurologic deficits have been publishedinvolving multiple older spinal agents, tetracaine included. 44 In a prospective study of complications related toregional anaesthesia, 12 cases of cauda equina syndrome were identified following uncomplicated subarachnoidblock. 45 Nine of these had received hyperbaric lignocaine, and 3 had received hyperbaric bupivacaine. These latterthree however, had only transient neurological deficits.Many of such reported cases have demonstrated clinical evidence of local anaesthetic maldistribution with arestricted block. In the instance of a failed spinal if a repeat injection is to be is performed, it would seem prudentto limit the total dose of local anaesthetic to that which is reasonable for a single injection. Furthermore, testing ofthe sacral dermatomes in the circumstance of a ‘totally’ failed block may give an insight into the problem ofmaldistribution and the potential for neurotoxicity with repeat injection.LOCAL ANAESTHETIC RESISTANCELocal anaesthetic resistance is an intriguing postulated cause of spinal failure. Despite the lack of definitive molecularor genetic evidence, there are multiple anecdotal reports within the literature that suggest resistance exists as atrue phenomenon.Case reports within the literature vary in the local anaesthetic used, techniques, and attempts to redress failure.Reports where patients have demonstrated failure to one type of anaesthetic and success subsequently with anothertype and/or skin anaesthesia to the original local anaesthetic are more tenuous for complete resistance. This variableresponse may suggest either technical failure, a selective resistance, or possibly a site concentration problem aspreviously elaborated.One report described the case of a 77 year old man who underwent continuous spinal anaesthesia for cystoscopywith an end-hole catheter inserted without incident. 46 Despite being able to freely aspirate csf and injection of atotal of 125mg of hyperbaric lignocaine in two aliquots over 25 minutes, the patient failed to develop any demonstrableblock. Csf was aspirated from the catheter following lignocaine injection and subsequent failure, and analysisdemonstrated concentrations too high to measure. 0.75% bupivacaine however was able to provide an adequateblock at a conventional dose. The patient returned a second time for a transurethral resection of the prostate andagain underwent continuous spinal anaesthesia. Lignocaine was used as before, and again failed to result in anyblock, with successful anaesthesia achieved with bupivacaine. Interestingly, subcutaneous lignocaine from thesame vial resulted in skin anaesthesia. The authors concluded that the most likely explanation was the existenceof local anaesthetic resistance to lignocaine. However this conclusion would need to be explained by failure withinthe same class of local anaesthetic since bupivacaine was used as the ‘rescue’ drug after lignocaine. Additionally,their conclusion does not explain why skin anaesthesia was achieved.Another author published a case report of a 48 year old male who underwent continuous spinal anaesthesia ontwo occasions with intrathecal tetracaine. 47 Despite apparent successful insertion of the catheter, no sensory ormotor blockade resulted. On the second occasion following failure of the spinal anaesthetic, radiographic contrastwas injected through the catheter and demonstrated dispersion of the contrast throughout the csf. Subcutaneoustetracaine was effective in producing anaesthesia, with the author concluding that anaesthetic resistance wasexcluded by such means. However, as demonstrated by the previous case, complete failure of spinal anaesthesiahas been reported where the same anaesthetic agent produced skin anaesthesia.A case report was published of a 55 year old female who presented with lower limb and perianal numbness andan abnormal magnetic resonance imaging study suggestive of transverse myelitis. 48 Attempts at lumbar puncturewere hampered by inability to produce skin anaesthesia with up to 15ml of 1% lignocaine being used. The procedurewas abandoned and performed under general anaesthesia. On further questioning the patient gave a history offailure of local anaesthesia with dental treatments and a similar problem with her father.Reports of the failure of patients to achieve demonstrable subarachnoid block using multiple forms of localanaesthetics on multiple occasions and in multiple settings, is more convincing for true resistance to local anaesthetics.Reports of such failure are summarised:In a series of 71 patients, hyperbaric 5% lignocaine was used in 30 patients and in five of these there wascomplete absence of motor or sensory block. 49 In four of these five, csf lignocaine levels where measured andfound to be at high enough concentration to warrant a successful block. Successful anaesthesia was achievedwhen 0.75% bupivacaine was used in four patients. However, one patient failed to develop any subarachnoid blockwith neither hyperbaric lignocaine (csf concentrations adequate when tested) nor 0.75% bupivacaine and also gavea history of multiple regional anaesthetic failures including failed brachial plexus and wrist blocks, and multiplefailures of local anaesthetics used for dental restorations.In a further case report a female parturient failed to achieve any sensory or motor block with a single shot spinalanaesthetic for a caesarean section despite evidence of technical proficiency. 50 The local anaesthetic agent usedwas 0.75% bupivacaine. Interestingly, she also failed to develop skin anaesthesia with 1% lignocaine sourced fromtwo different lots preventing attempts at a combined spinal-epidural technique as originally planned. Generalanaesthesia was performed and no block was discernable on wakening. Subsequent history revealed the sameproblems with her previous caesarean in which attempts to achieve skin anaesthesia were unsuccessful, the regionalblock failed, and reversion to general anaesthesia was necessary. Furthermore, the patient related repeated failuresof local anaesthetics for intravenous line placement, and a series of dental procedures despite three different typesof anaesthetics being used. A published letter responded to this relating a case of a failed spinal in a patient havinga history of repeated failures of local anaesthetics for dental and dermatological procedures. 51