Blog with interesting cases and/or problems related to anesthesia with discussion based on best evidence in the literature.

June 11, 2013

The neuromonitoring Technician: Friend or Foe?

A couple of days ago I took over a posterior lumbar interbody fusion from L2 to S1.  The case had started at 7:45 am that morning, and I came into the room at 3pm.  The report I received from the CRNA was that the patient had been stable for the entire case until just recently when the blood pressure began to sag.  The CRNA had already checked a Hgb and ordered two units of blood which were on there way.  It was clear from a brief glance at the surgical field that this case had a ways to go and there was continual bleeding from the field.  A cell saver machine was working and the patient had received about 300 mL from the cell saver machine already.  I checked the UO and it was low and appeared to be concentrated.  The patient was being maintained on Desflurane at 4% with a dexmedetomidine infusion at about 0.15 mcg/kg/hr which had been discontinued due to low blood pressure.  The patient had a history of COPD and was 68 years old, but other wise had no significant medical history that would impact his anesthetic.  Neuromonitoring consisted of SSEPS, MEPS and running EMGS.  No paralysis was being used. 

The patient had already received 4.5 L of crystalloid and 1 L of Hespan.  Due to the prolonged case and the prone position, this patient was at some risk for perioperative visual loss (POVL).  An ASA task force on perioperative blindness (consisting of 12 ASA members) recently published guidelines to help clinicians better deal with this potential outcome.  The task force culled the most recent literature to make recommendations.  They identified several preoperative risk factors which include: hypertension, glaucoma, carotid artery disease, smoking, obesity and diabetes.  This patient was mildly obese and had a prolonged smoking history having ceased just 6 weeks prior to surgery.  The task force also identified surgery lasting longer than 6.5 hours, preoperative anemia, large volume blood loss (i.e. 44% of blood volume) and also prolonged procedures combined with large blood loss cases.  The task force also identified several intraoperative events that are linked to POVL.  These included intraoperative hypotension, anemia, hypovolemia, hypoxia, hemodilution, edem of face and use of vasopressors, infusion of large amounts of fluid, pressure on the eyes, prone positioning (or head down), and increased venous pressure. This case included several of the above risk factors including long duration procedure with large volume fluid ressuscitation, intraoperative and preoperative anemia.  There was ongoing blood loss and it wasn't clear the total volume that would ultimately be lost during the procedure.

At this point all clinical indicators were that the patient was hypovolemic due to blood loss.  I focused on giving blood and volume while attempting to avoid phenylephrine as much as possible. During this time the Neuromonitor technician notified the surgeon that MEPs on the left lower leg had decreased significantly.  The blood pressure was low (MAP of 60s) at this time so I continued to work on increasing this with rapid blood transfusion (3 units) and crystalloid. (2L).  After this volume the blood pressure improved slightly but began sagging again.  It was clear that the patient was still hypovolemic.  I drew more labs and started pumping in more fluid.  During this time the neuromonitoring technician told the surgeon that we needed to put the patient on 3% Desflurane and start a propofol infusion.  I immediately told the neuromonitoring tech I would not be starting a propofol infusion under any circumstances at this point.

He disagreed with me and began telling me why I was wrong to believe that we shouldn't do as he suggested.  He indicated that I was derelict in my duties because I was not following the established protocol for neuromonitoring and that if he should decide, he could write me up and bring me before peer review for my refusal to follow the protocol.

A brief discussion of the current recommendations for anesthetic technique during neuromonitoring is warranted.  Also, I would recommend looking over previous posts on this topic. 1) MEPs with dexmedetomidine and 2) MEPS in AIDCF.

In a review article on intraoperative monitoring (IOM), it states, "These findings support the current position of propofol being the standard anesthetic approach for IOM recording of MEPs." [1].  "These findings" in the above quote refers to a study done in 1998 by Pechstein et al.[2].  In fact, this study is the  basis for the recommendations made and thus serves as the basis for propofol being the automatic "go to" anesthetic for IOM with MEPS during spine surgery.  It should be noted that in the study by Pechstein et al. there were two study groups of 17 (group A) and 13 (group B) patients.  Group A received TIVA (total intravenous anesthesia) with propofol and alfentanil.  In Group B, patients received Nitrous oxide (66%), isoflurane and fentanyl.  MEPS could be recorded in 88% vs. 8% of group A patients vs. Group B patients.  Therefore, this small study was able to show that mixing nitrous oxide with isoflurane is likely to make it difficult to record MEPs.  It certainly does not allow us to conclude that propofol is the gold standard anesthetic for IOM.  It has been well demonstrated that nitrous oxide can also suppress completely MEPs when given with propofol as well [4]. Another study found that both 50% nitrous or doubling the propofol dose both could decrease the amplitude of tc MEP [5].  Zentner [6] found that using 66% nitrous oxide reduced the recorded MEPS to 6% of baseline.  Todd Sloan, in a review of motor evoked potential monitoring stated, "when compared at equipotent anesthetic concentrations, nitrous oxide produces more profound changes in myogenic tcMEP than any other inhalational anesthetic agent.
 On the other hand, more recent work, has found that desflurane can be utilized effectively when IOM is required. Lo et al. successfully measured MEPS in 9/10 patients undergoing scoliosis surgery with Desflurane (mean 3.3%) + 60% nitrous oxide [3].   In fact, Desflurane + nitrous oxide was compared to a propofol narcotic technique when measuring MEPS [7].  They compared 20 consecutive patients randomly  assigned to one of the two groups (10 in each group).  The Desflurane group received a mean ET concentration of 3.4% + 66% nitrous oxide.  MEPS were adequate in all 20 cases. In fact, prior to instrumentation, amplitudes were higher in the Desflurane group (85 mV vs. 59.1 mV).    These studies (done with nitrous) combined with the evidence that nitrous oxide is a potent inhibitor of MEPS recording, supports the technique of using Desflurane without nitrous oxide with minor effect on MEPS.
Published results suggest that to accomplish the 1 MAC equivalent with propofol, it is required to achieve plasma levels of 6 mcg/mL.  This requires an infusion of approximately 200 mcg/kg/min.  Other authors have already shown that MEPS are reduced when propofol is given at much lower dosages than this. Therefore, on a dose equivalent basis, propofol's advantage over Desflurane is likely very small.  Additionally, most studies using propofol for MEPS recording used infusion rates of around 100 mcg/kg/min.
       Propofol does indeed provide for easy recording of MEPS, and in particular, with pulti pulse stimulation, seems to allow very good signals.  However, when dealing with a hypovolemic patient with multiple risk factors for POVL, adding propofol to the equation in to improve MEPS is risky.  Furthermore, as propofol will likely worsen MAP, in reality, the signals are likely not to improve or worsen as low MAP is particularly inhibitory to the recording of MEPS.
       In reality, the key is to obtain good baseline readings, and then maintain a steady anesthetic state.  Whether propofol or desflurane is used is less important than keeping the baseline anesthetic stable. If during a procedure, attenuation of the signal occurs in one part of the body, it is important to find the source of this inhibition.  Any changes to the anesthetic would be important to note. However, anesthetics will result in global signal reduction, not focal.  Other causes of global signal reduction include, severe anemia, hypotension, and hypoxia.  Focal reduction of signal is most likely related to focal ischemia or mechanical trauma..  If this can be ruled out, then lead placement or other mechanical issues related to the measuring process such as impedance should be ruled out first.  In the above presented case, the patient had significant ongoing bleeding with decreased blood pressure.  He had significant anemia (nadir of about 7 gm/dL) and his blood pressure was suppressed (MAP of 58 to 62 mmHg).   I was running desflurane at a steady concentration of 4% which had not changed during the case.  Dexmedetomine was being titrated to effect and had been decreased due to the patients decreased blood pressure.  The technician's request to switch to 3% desflurane + a propofol infusion was not logical for a number of reasons.  First, as mentioned, a stable anesthetic level will aid in the intepretation of MEPS.  Decreasing the desflurane and adding propofol (he didn't specify what dose he wanted) would disrupt this.   Propofol also suppresses the MEPS to a degree not much less than desflurane if you consider the dose equivalent amount.  Another important factor is the risk for sudden patient movement.   As referenced in a previous post, patients are far more likely to move suddenly during propofol anesthesia than when receiving volatile anesthetics.  Of all the potent inhaled anesthetics, some evidence suggests Desflurane is the most effective in the prevention of patient movement [8].  Therefore, despite that propofol is the best from a neuromonitoring stand point, it is not that much better than desflurane and has the disadvantages of not effectively inhibiting patient movement, inability to monitor real time plasma concentration levels, and causing profound hypotension in anemic hypovolemic patients.  There is one other major disadvantage of propofol.  In the setting of spinal surgery with instrumentation, the whole goal with neuromonitoring is to avoid causing injury to the spinal cord or roots.  The injury is often ischemic in nature although mechanical trauma is also a possibility.  The potent inhalational agents have the beneficial property of anesthetic preconditioning which protects organs against ischemic reperfusion damage. This would be pertinent not only for spinal cord/nerve root ischemic protection, but also, retinal  ischemic protection.

So, if propofol is a poor choice in this setting, what are some other options.  Todd Sloan reports in his review on MEPS that in addition to use a mulit pulse technique, the interstimulus interval (ISI) made need to be varied until the optimal response is found.  For example, he states that at low concentrations of Isoflurane (i.e. 0.2%) a wide ISI  (i.e. 2-5 ms).  However, at higher concentrations (i.e. 0.4-0.6%), a wider ISI is better (i.e. 4-5 ms). At even higher concentrations (1%), the most effective ISI was 1 ms.  In short, its likely best to optimize the ISI to the concentration early on in the case.  Other considerations when its difficult to record MEPS are other anesthetics.  Ketamine and Etomidate are both ideal in that do not effect MEPS to any appreciable degree and also increase SSEP recordings.  Both of these also have positive hemodynamic profiles. Unfortunately, etomidate as an infusion suppresses adrenal function and, therefore, has fallen out of favor.  Ketamine at appropriate dosages (0.25 mg/kg/hr to 0.5 mg/kg/hr), is less likely to cause the negative psychological side effects (hallucinations). Several studies have found ketamine to have a protective analgesia effect in general surgical cases and one study in particular found that intraoperative ketamine reduces post operative morphine consumption in patients on chronic opioid pain therapy undergoing spinal surgery [9].  Todd Sloan reports in a review of IOM that in patients where MEPS are "very sensitive" to inhalational agents and neuromuscular blockers, he uses propofol and then adds ketamine if this isn't sufficient.  His typical protocol calls for:  Mix ketamine into propofol 50 cc's at 2mg ketamine to 1 cc (10mg/cc) Propofol.  He then titrates down on the ketamine concentration for each subsequent 50 cc syringe infused over the duration of the case; i.e. 1st syringe 2mg Ketamine/cc Propofol, 2nd syrine 1.5 mg Ketamine/cc Propofol, 3rd syringe; 1mg Ketamine/cc Propofol infused. etc.  The lasty syringe contains only Propofol.  Of course, Propofol can be avoided altogether in many cases.

In conclusion; IOM is becoming very prevalent and in particular, Motor Evoked Potentials are ever more common.  The anesthesiologist needs to be aware of those things that will affect the IOM and how to adjust the anesthetic so that IOM can be successful while considering the other important aspects of the anesthetic: Immobility, Anesthesia, and Amnesia.

1. Pajewski TN, Arlet V, Phillips LH.  Current approach on spinal cord monitoring: the point of view of the neurologist, the anesthesiologist and the spine surgeon.  Eur Spine J. 2007:18. 115-129.

2.  Pechstein U et al.  Isoflurane plus nitrous oxide vs. propofol for recording of motor evoked potentials after high frequency repetitive electrical stimulation.  Electroencephalogr Clin Neurophysiol. 1998: 108(2): 175-81.

3. Lo YL, Dan YF et al.  Intraoperative monitoring in scoliosis surgery with multi-pulse cortical stimuli and desflurane anesthesia.  Spinal Cord. 2004;42: 342-5.

4.  Kunisawa T et al.  A comparison of the absolute amplitude of motor evoked potentials among groups of patients with various concentrations of nitrous oxide.  J Anesth. 2004;18:181-4.
5.  van Dongen EP. et al.  The influence of nitrous oxide to supplement fentanyl/low-dose propofol anesthesia on trancranial myogenic motor-evoked potentials during thoracic aortic surgery.  J cardiothorac Vasc Anesth.  1999; 13:30-4.
6.  Zentner J et al. Influence of anesthetics-nitrous oxide in particular-on electromyogrphaic response by tc electrical stimulation of the cortex.  Neurosurgery. 1989; 24:253-6.
7.  Lo YL et al. Intraoperative motor-evoked potential monitoring in scoliosis surgery: comparison of desflurane/nitrous oxide with propofol total intraenous anesthetic regimens.  J Neurosurg Anesthesiol. 2006; 18:211-4.
8.  Wulf H. et al. Neuromuscular blocking effects of rocuronium during desflurane, isoflurane, and sevoflurane anaesthesia.  Can J Anaesth. 1998;45: 526-32.
9. Loftus R et al.  Intraoperative Ketamine reduces Perioperative Opiate Consumption in Opiate-Dependent Patients with Chronic Back Pain Undergoing Back Surgery. Anesthesiology. 2010;113: 639-46.


Joe Hartman said...

I can't believe that the neuromonitoring tech was demanding/threatening you to change to TIVA with propofol. Not only is that out of line with their scope of practice (assuming they aren't an anesthesiologist), but wouldn't solve the reason why the MEPs (most likely) changed in the first place.

Excellent write up for professionals on both sides.

- Joe

Tony K said...

As a Neurophysiology Technologist I would say that TIVA works better in all cases for SSEP and MEP and that if inhalational anaesthetic is used Desflurane has less effects that other volatiles in reducing amplitude, particularly below 0.3MAC, it tends just to take the edge off.

However I would agree with the anaesthetists point of view here. A change to TIVA, while it might make a trace a little clearer, is not appropriate at the time given the patients physiological state. Taking the volatile out, in the technicians mind, would eliminate that as a possible cause of inhibition and may enhance signals enough to make a diagnosis clearer, however if this is a sudden change and is isolated to one side (particularly if the upper reference remained in tact and the signals had been stable up till then) then it is not related to a global issue such as anaesthesia and is more likely related to the surgery or to a peripheral issue involving the reduced leg. Could also be a contralateral cerebral issue.

Best option in this case is if the anaesthetist can treat the hypovolemia and increase the MAP to ensure blood flow, check the effected leg for perfusion issues or compression issues (have had an leg fall off the bed slightly causing the same issues) and inform the surgeon that there may be an issue with the nerve roots effecting the leg (particularly if this is a sudden change after a surgical maneuverer). No mention of the SSEP changing as well which would be helpful in nailing down the issue.

It's a shame that we get all riled up like this, we all need to work together, it is in the patients best interest.