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Anonymous User on January 5, 2018 at 11:31 am
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    • Anonymous UserAnonymous User
      Joined: Jan 5, 2018
      Posts: 0

      A few days ago I performed the procedure on a young woman (44) in good health but suffering from pain caused by a FBSS: the procedure was carried out without any problems, except for a motor block in the lower limbs probably caused by a subarachnoid diffusion of 2% lidocaine (2 ml) injected after the neuroplasty bolus consisting of hyaluronidase (1500 UI ) and non-particulate steroid (bethametasone 8 mg). I do not use hypertonic saline during the procedure. Probably a small dural lesion happened during neuroplasty (the first constrast bolus showed a subdural (?) appearance and so the catheter was repositioned , with a second contrastography showing a correct epidurography.

      The motor block regressed after two hours from the onset, but a few hours later (4 hours after the procedure) the patient started complaining headache and vomiting. For the persistence of the symptomatology an urgent brain CT was performed and a small right frontoparietal lesion with small air bubbles was found, therefore with a (suspected) diagnosis of little parenchymal hemorragic lesion in encephalomyelitis. Moreover, in a patient’s blood samples we have found high WBC (20.000) and a C-reactive protein, so the patient was transferred to the infectious disease ward, where cerebrospinal fluid was taken and brain MRI performed. At that moment she was awake, oriented, with severe headache, diplopia, dysarthia but no motor deficit.

      CSF was slightly hemorragic, with high number of leucocytes and proteins, but bacterioscopic examination was negative. The following results of bacterial coltures (even in the following days) showed no bacterial growth.

      The MRI results were catastrophic! Here the complete report:
      “At both the above and below the tentorial there are some areas of altered signal, located: in the right frontal-cortico-subcortical, cortico-subcortical temporo-insular posterior right, pontine antero-lateral right, center-pontine, at the level of the bulb, at the bulb-medullary passage, extended up to the apex of C2. All lesions take contrast and some of them are visible also in diffusion, characterized by mixed edema, cytotoxic and vasogenic.

      Finally, the lesions are more numerous and larger in the trunk, and cause swelling of the corresponding gyrations and of the trunk. Hypersignal FLAIR is highlighted in the subarachnoid spaces of both hemispheres, expecially in the fronto-parieto-occipital area. It is associated with pial peritruncal and fronto-basal level contrastographic enhancement . With the Gradient sequences some areas of net reduced signal are highlighted, one located in the context of the right temporo-insular lesion, in relation to the blood component, and the others at the level of the right-lateral insula sulcus and in the left fronto-basal site, in relation to gaseous coefficients. Moreover are evident some small areas of altered signal of the bilateral frontal and left parieto-temporal subcortical white matter, most likely referable to gliotic outcomes.”

      In the following 24 hours the patient developed in a progressive left hemiplegia and the clinical picture get progressively worst, with a plegia also of right lover limb developing in the following 24 hours.
      Fortunatly (!) even in the presence of a massive involvement of truncal structures, no signs of lesion of cranial nerves (except diplopia) or respiratory failure are present at the moment.
      We are trying to find out what could have been the causes of this catastrophic complication. Ruling out an infectious cause or a vascular injection (a vascular MRI was performed but no evident obstruction was noted) we are thinking to a “chemical” damage (but none of the drugs injected has reports of a such tremendous neurologic toxicity) or a type of hymmunological reaction : my neurologist is hypothesizing something similar to a ADEM desease (Acute Demyeliniziting Encephalomyelitis) triggered by the procedure or by the drugs injected.

      Has anyone never seen something similar? Have you any idea about the possible causes of this serious complication? I will be deeply grateful for any help you can give me.

      • Gabor B RaczGabor B Racz
        Joined: Mar 28, 2016
        Posts: 30

        Dear Dr.

        The examples used are from rather vivid memories just like your case shall remain with you for a very long time. The number one recognition when I looked at similar cases, makes one realize that these are extremely rare and secondly that we do not understand everything. A lot of the cases are beyond anyone physician’s potential experience because of the rarity, but because many of these cases have gone on to medical/ legal status. I have been an expert witness with information whatever was available to any party, was available to me.

        My first analysis of what has been done on this patient in terms of volumes of injected material, you have indicated 2 ml of 2% Lidocaine and 1 ml betamethasone, plus an unknown quantity of unknown hyaluronidase. In your discussion, you are talking about 2 boluses of an unknown quantity of contrast without being specific that it is safe for spinal administration. To be sure, please understand that I have never recommended 2% Lidocaine as the initial local anesthetic. The purpose of the local anesthetic, which should not by itself give a motor block, it is to indicate the appropriate tissue plane injection.

        Recommended Local Anesthetics are .2% Ropivacaine or 0.25% Bupivacaine. Either of these local anesthetics, if injected in the subdural space will develop a motor block usually in 14 or so minutes, but will not produce a motor block in the epidural space. Whereas, Lidocaine will give a motor block every time in the subdural and epidural space.

        The catheter virtually should never go through the dura to the subdural space, but you must remember to put a 2.5 cm 15 degree bend near the tip and slow-down in advancing and make sure you navigate to the target which is the ventral lateral epidural space. The subarachnoid space on aspiration inevitably gives cerebrospinal fluid and to review other points regarding dealing with technical issues recommend the chapter 9 in Techniques of Neurolysis 2nd edition, editors G.B. Racz: Carl Noe.

        Answering your questions:
        Every single one of what you have injected except possibly betamethasone can have disastrous consequences. Anaphylaxis is usually followed by edema and circulatory cardiovascular consequences. Most of the medications are drawn up by the nursing staff and the physician does not always check every medication given. A prime example is ionized versus non-ionized contrast material. A very small volume of ionized contrast can be lethal in the spinal canal.
        A male in his 50’s after multiple back surgeries with significant arachnoiditis causing lower extremity weakness, bowel/bladder dysfunction and pain. The patient was being evaluated for a morphine pump and was scheduled for a myelogram. 30 – 45 minutes later developed tonic-clonic movements with circulatory collapse. He was rapidly resuscitated but remained in a coma. Several hours later he had a repeat circulatory arrest and died. It had taken two years later to discover the explanation which was the substitution of the contrast to an ionized contrast. No catheter was used, the hyaluronidase was of bovine extract. Dani Moore published some 1200 epidural use of hyaluronidase in the 1950’s and suggested a high incidence of anaphylactic reactions, including death. His findings have not been substantiated. Recommended reading – Hyaluronidase: a review of approved formulations, indications and off-label use in chronic pain management. Dunn AL1, Heavner JE, Racz G, Day M.

        Example 1:
        Cervical epidural single shot steroid: Uneventful single shot epidural steroid injection was done initial 2 ml’s Omnipaque 240 2ml’s local anesthetic and 1ml 40mg Depomedrol. After observation 15 – 20 minutes post procedure the patient was getting dressed when it was noted that he lost consciousness and stopped breathing. The nursing staff called the patients physician who was talking to the family about how good the procedure went. Following resuscitation and intubation, the MRI showed a subdural and intracranial spread of the injected fluids. The following days CAT Scan showed contrast still visible in the cerebral ventricular system and lighting up the central canal of the spinal cord showing the draining of intracranial contents. Touhy needles have a long bevel and can easily cut through the dura to be in multiple spaces at the same time, such as subdural and epidural. The subdural space communicates with intracranial structures. The local anesthetic used was .25 Bupivacaine and it will not give motor block in the epidural space but will give motor block in 14 minutes or so in the subdural space. The patients must be closely observed especially the first 30 minutes.

        Example 2:
        A young patient with non-specific back pain had a lumbar single shot epidural steroid injection. The procedure went very well having an injection of contrast followed by local anesthetic .25% bupivacaine steroid 40 ml’s Depomedrol. The patient was observed to be sitting in the recovery area eating an orange. Attention for further recovery was relaxed, 15 minutes or so after this he was found to be in respiratory and cardiovascular arrest. Resuscitation failed. All patients need to be intently observed and monitored especially in the first 30 minutes. Once again the Touhy needle was used, the total volume injected was 8 ml’s.

        Example 3:
        An Elderly patient had failed back surgery, lower extremity and back pain, bowel/bladder dysfunction and significant arachnoiditis. The catheter entered the subdural space and following the injection of contrast, 10 ml’s of .25% bupivacaine and 1 ml of triamcinolone. The patient developed a post-procedure motor block that recovered in a few hours but had a loss of rectal tone function and ended up with a permanent colostomy. The urinary bladder sphincter control remained intact. The patient reported excellent recovery of severe pain. This is the reason we must not go into patients with arachnoiditis and the subdural space with any kind of volume injection as it loculates and interferes with blood flow. The patient was so pleased with the pain relief they never filed a lawsuit.

        Example 4:
        Single Shot Epidural Steroid severe C6 Radiculopathy. Previous fusion at C4-5 and C6-7. The first epidural steroid for this patient gives two weeks pain relief, three weeks later second injection 1ml contrast 3 ml’s local steroid consisting of .25% bupivacaine and 40mg triamcinolone. The procedure performed under propofol anesthesia. The intra-operative epiduragram shows a posterior left sided near midline dye spread to the C6 level. Post-procedure, the patient develops pain of the left arm and continues on to numbness and weakness along with loss of function. Three weeks later the patient was seen by his physician who immediately ordered an MRI that showed a syrinx in the C6 area of the spinal cord. The lesson is that the patient noting pain, numbness progressive weakness should notify their physician or designate. But equally important, the emergency room or rehab facility staff need to know that the patient has had an injection procedure which could be causing pressure, vascular compression and secondary ischemia and numbness. This could be reversed by flexion rotation exercises.

        Almost every single one of the reasons I listed above could have caused some of the problems to your patient. I would most certainly not give up on Hypertonic Saline, but would give up on 2% Lidocaine. Single shot epidural steroids because of the Touhy needle can cause respiratory arrest if it spreads into the subdural space. Interesting to note that at one time the primary neurotoxic insult was one-sided which implies that the injected material is the primary potential explanation and it may very well be the wrong type of contrast or absolutely any other liquid believing it was contrast unless you drew it up yourself.

        There have been well over 2 million Lysis cases done worldwide and even if it was a low-frequency occurrence, I would have heard about it. My deepest sympathies for the moment and wishing you a bright future ahead of you.

        Dr. Gabor B. Racz

          • Anonymous UserAnonymous User
            Joined: Jan 5, 2018
            Posts: 0

            Dear Dr. Racz,


            First of all I want to thank you for your detailed answer. I absolutely agree that you post your response on PainCast as I think that this clinical report could be of great importance for many physicians, making them aware of a possible rare but severe complication during neuroplasty procedure.

            As you said I must specify the exact amount of volumes that I used during the procedure: the first administration was of 2 ml of contrast (iopamidol 300); after the uncorrect intrathecal spreading the catether was repositioned and again 1 ml of the same contrast was administered, followed by 2 ml of lidocaine 2% and then 8 mg of Betamethasone (1 ml) plus 1500 UI of Hyaluronidase. I used this steroid since in Italy there is no longer any authorization to administer triamcinolone both epidural and in the subarachnoid space and so we have any non-particulate long acting steroid available for spinal procedures.

            I agree completely with your consideration about the fact that the recommended local anesthetics for neuroplasty procedure are bupivacaine or ropivacaine , but in my clinical practice it is also important and to be considerated the longest motor block of these two drugs compared to lidocaine, that could be a substantial problem in case of a subarachnoid spreading.

            Regarding this specific case, it is undoubted that the drugs have been administrated uncorrectly in the subarachnoid space and that probably the use of different local anesthetic and a different timing of administration could have avoided this, but in my opinion the key point is why and with which mechanism the administration of lidocaine, hyaluronidase, betamethasone or iopamidol caused such severe and extended CNS lesions.
            Indeed the MRI and vascular MRI scans performed at 24 and 72 hours showed no signs of vascular obstructions, but a cytotoxic and vasogenic edema located in frontal-cortico-subcortical, cortico-subcortical temporo-insular posterior, pontine antero-lateral, center-pontine regions on the right and also at the level of the bulb, at the bulb-medullary passage, extended up to the apex of C2. Moreover, lesions are present also at the spinal cord with signs of myelitis from C1 to C4 and from C7 to D7 Ruling out an infection or a vascular mechanism, the more consistent hypothesis is about a direct toxic effect of one of the injected drugs or an immune-mediated reaction. During the review of the medical database that I performed after the event I didn’t find report of such severity after administration of any of the cited drugs.

            I think that excluding as possible responsible agent both lidocaine than betamethasone we have to focus our attention to hyaluronidase and contrast medium. The database search on toxic effects of intrathecal hyaluronidase did not highlight anything relevant, while the toxicity of contrast media is well known and I found several case reports of neurological complications after myelography (1- it is only one of the most relevant case reports) and also one after epiduroplasty (2). In both cases the contrast media was a non-ionic water-soluble one but the reported MRI aspect was of a reversible brain edema, wich unfortunately it is not the case of my patient.

            So, in my opinion, there are some aspects that we need to clarify to reduce the risk of such serious complications

            • Is it correct to continue neuroplasty procedure when the first administration of contrast spread in the subdural/subarachnoid space or it is better to considerate interrupting the procedure?
            • Does this possible interruption of the procedure make sense, since that all the iodinated contrasts (included the non-ionic water-soluble ones) even in small volumes could be neurotoxic and therefore also the first administration could lead to a neurologic damage? (I know that this assertion is really provocative..)
            • Could it be more correct to inject the anesthetic bolus first to exclude a subdural/intrathecal spreading and only later the contrast media?

            Kindest regards

            1)            Brian C. Kelley, Simon Roh, Philip L. Johnson and Paul M. Arnold. Case Report Malignant Cerebral Edema following CTMyelogramUsing Isovue-M 300 Intrathecal NonionicWater-Soluble Contrast: A Case Report. Radiology Research and Practice. Volume 2011, Article ID 212516, 6 pages

            2)            Chang Hyun Oh, Seong Dae An, Seung Hyun Choi and Gyu Yeul J. Contrast mimicking a subarachnoid haemorrhage after lumbar percutaneous epidural neuroplasty: a case report. Journal of Medical Case Reports 2013, 7:88 .

            • Gabor B RaczGabor B Racz
              Joined: Mar 28, 2016
              Posts: 30

              Dear Dr.

              Thank you for opening this case up to open discussion. I suspected from the beginning some of the injected materials that went into unplanned locations. Iopamidol* is not an agent that I have ever been exposed to, looking up the attached Google abstract describes a patient who had seizures, tonic-clonic movement which is a rather unique hallmark of ionized contrast, but no contrast is immune from it. Very commonly tiny amount is fatal if injected into the subarachnoid space. The only remedy at the time of this occurring is twenty to forty minutes after the injection, but the subarachnoid space must be washed and rinsed out with preservative free normal saline. I had one of these patients were I used to think injecting through the surgical scar will free up the scar tissue. On that day, I watched the contrast dissect and burst into a chimney like structure which later, I understand, was subarachnoid contrast. The patient was seizuring, a moving target, but I was able to get a needle, extension tubing, 3-way stop cock and a liter of preservative-free normal saline and rinse the subarachnoid space out. The patient had a stormy recovery with 2-3 days in the intensive care unit, but survived. This was approximately in 1982-1983 . I believe this comes closest to the mechanism of action in your patient. Especially in view of the repositioned, possibly subdural catheter, where the fluid entered through the foramen magnum, intracranial space and drained through the foramen of Luschka and Magendi to the ventricular system.

              1. If you get the catheter to the wrong space, I would remove it and cancel the case and reschedule for 3-4 weeks. Patients understand caution.
              2. The Lydocaine vs. Ropivacaine should be to rule out subdural spread. It may not be induced during the procedure, but spreads through a surgical tear. In the presence of arachnoiditis and tight spinal stenosis you need to know if the spread occurred and there are no shortcuts. A fully trained ACLS certified nurse in the holding area can respond if there is a motor block.
              3. A small volume of contrast can tell you which space you have injected into which will prevent a bigger problem.

              Just as you can see I have been through problems over the last 38 years, my technique has improved through very careful selection of the safest approach and equipment. I do not feel the pressure, neither do I have the complications as I did at the beginning. Remember the incidence of complication is somewhere in 8 – 12000 and you may go a lifetime without any or you may have 2 in 2 weeks.

              My best regards,

              Gabor B. Racz, M.D.

              *Iopamidol, a water-soluble contrast agent, has been rarely associated with seizures. We describe a case of generalized tonic-clonic seizure after cervical myelography with iopamidol in a previously healthy young man. In patients presenting with seizures, a history of recent myelography should be considered as an etiology. Iopamidol myelography may be associated with a risk of seizures. Clinicians need to be aware of this complication and inform their patients about such risk. 

            • John SwicegoodJohn Swicegood
              Joined: Apr 20, 2017
              Posts: 0

              What a terrible case. I think your neurologist is right, I had a case of transverse myelitis after a simple blood patch for a uncomplicated dural puncture. Onset was very quick worsening into paraplegia and extensive cord myelomalacia within days. The literature referenced cases of which the onset was triggered by neurologic interventions or events. I just do not see any of the drugs doing this if, as Gabor mentioned, that in fact they were what they were supposed to be. I saw one case of a myelogram with suspected ionic contrast, it was the worst death over 3 weeks I’ve ever witnessed. We all knew what happened, but the radiologist denied it.

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