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LETTERS TO THE EDITOR |
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| Year : 2022 | Volume
: 25
| Issue : 6 | Page : 1218-1220 |
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Delayed reversible cortical blindness after spinal anesthesia with bupivacaine
Boby V Maramattom
Department of Neurology, Aster Medcity, Kochi, Kerala, India
| Date of Submission | 13-May-2022 |
| Date of Decision | 05-Jul-2022 |
| Date of Acceptance | 22-Jul-2022 |
| Date of Web Publication | 3-Dec-2022 |
Correspondence Address:
Boby V Maramattom
Department of Neurology, Aster Medcity, Kochi, Kerala
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/aian.aian_433_22
How to cite this article:
Maramattom BV. Delayed reversible cortical blindness after spinal anesthesia with bupivacaine. Ann Indian Acad Neurol 2022;25:1218-20 |
Sir,
We present an unusual neurological adverse reaction following spinal anesthesia with bupivacaine. Bupivacaine is an intermediate to long-acting amide-type local anesthetic that blocks Na+/K + channelsand action potential generation. It is used in obstetrics for spinal anesthesia (0.5%) as a hyperbaric solution (density >1.0037, compared to cerebrospinal fluid[CSF] density of 1.00003- 1.00023 mg ml −1 at 37°C). Baricity is a measure of the density of bupivacaine compared to CSF. After CSF instillation, hyperbaric bupivacaine remains within the lumbar dural sac and is rapidly metabolized with relief of anesthesia within 269 +/-53 minutes.[1] Bupivacaine is eliminated by vascular absorption into systemic circulation via the vessels in the subarachnoid and epidural spaces.
However, CSF bupivacaine concentrations can vary with an unpredictable half-life due to various factors.[2] Pregnancy increases intra-abdominal pressure, causing CSF redistribution, amplification of CSF oscillatory flow, and cephalad spread of bupivacaine.[3]
Acute cephalad spread above T4dermatome level blocks thoracic cardiac sympathetic fibers and produces hypotension, arrhythmias, cardiac arrest, respiratory muscle weakness, and vomiting.[4] However, late complications can occur. Spinal anesthesia or central neuraxial block (CNB) is usually associated with a low risk of neuraxial complications (NAC). Less than 0.04% of patients develop neurological complications.[5],[6] NAC includes transient neurologic symptoms, urinary retention, post-dural puncture headache, intracranial hypotension, intracranial or spinal hemorrhage, spinal epidural hematoma or abscess, and a cord or nerve root injury, transverse myelitis, spinal myoclonus, worsening of pre-existing neurological deficits, meningitis and delayed arachnoiditis.[7] Most NACs occur within a few hours to days after CNB, and transient neurologic symptoms can last up to 10 days.
A 25-year-old woman underwent an uneventful lower (uterine) segment Caesarean section under spinal anesthesia (2 ml 0.5% hyperbaric Bupivacaine with adjuvant fentanyl, 25 mcg) She was discharged on day two. On day four, she presented to the emergency department with complete blindness upon waking up from sleep. She also complained of weakness and numbness in both legs. An evaluation revealed only a perception of light in both eyes, preserved pupil reactions to light, normal fundus examination, and brisk tendon jerks with normal muscle power and sensations. Her blood pressures were normal (110/70 mm. Hg). Ocular ultrasound showed normal flow in both ophthalmic and central retinal arteries and normal optic nerve sheath diameters, suggestive of normal intracranial pressure. She also developed painless urinary retention (sensory-motor bladder) with an ultrasound estimated bladder volume of 750 ml. An indwelling foley's catheter was placed. Cortical blindness secondary to a posterior circulation infarct or posterior reversible encephalopathy syndrome (PRES) was considered. An urgent CT brain with a CT angiogram was normal. Flash visual evoked potentials (VEP) were absent bilaterally, on day four, suggestive of posterior visual pathway dysfunction. An MRI brain with MR angiogram and whole spine MRI was also normal on day 6. Routine blood tests were normal. EEG showed generalized low amplitude activity with intermittent 4-5 Hz theta waves. Transcranial doppler showed normal flow velocities in the basilar and PCA arteries. The possibilities included occipital seizures, acephalalgic or basilar migraine, and delayed toxicity of spinal anesthesia.
On day 4, an 18FDG-PET CT showed severe occipital hypometabolism. Following the PET CT, a lumbar puncture was performed. CSF opening pressure (15 cms of H20) and parameters were normal. A lumbar drain was placed and 100ml of CSF was drained per 24 hours for 3 days. By day five, her vision had improved to finger counting at 2 meters. On day five, her pattern evoked VEP showed prolonged P100 latencies. Serum/CSF NMDA and paraneoplastic workup were negative. Her urinary catheter was removed and she was able to void normally. By day six, she regained normal vision. She had no history of exposure to sedative drugs or alcohol. CSF bupivacaine levels could not be estimated. A repeat MRI brain with MR angiogram was normal on day 8. On day nine, her VEP showed normal P100 latencies. A repeat brain PET-CT at 1 month showed normalization of occipital PET activity [Figure 1]. | Figure 1: Panel A-Axial diffusion weighted MRI image. Panel B- MR intracranial angiogram showing normal vasculature. Panel C. Repat MRI DW imaging, again showing normal brain parenchyma. Panel D- visual evoked potentials on day 5 showing prolonged P100 potential latencies bilaterally. Panel E- Axial 18FDG PET CT images at admission showing significant occipital hypometabolism. Panel F; Axial 18FDG PET CT images at one month, showing normalisation of occipital metabolism. Panel G- visual evoked potentials on day 9 showing normalisation of P100 potential latency
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The combination of reversible cortical blindness, crural sensorimotor symptoms, urinary retention, absent VEP, reversible occipital hypometabolism on 18FDG-PET CT, normal MRI and MR angiograms with the exclusion of other causes, suggested the possibility of delayed post-spinal anesthesia bupivacaine toxicity.
Mild sensorineural hearing loss is encountered in almost 10% of patients after CNB. It is thought to occur due to abrupt changes in CSF pressure or due to cephalad CSF bupivacaine spread into the cochlea [as the subarachnoid space is contiguous with the cochlear aqueduct of the ear] or other factors.[8],[9] Similar to this, we hypothesize that slow cephalad spread of intrathecal bupivacaine and redistribution over the dependent occipital cortex (in the supine position) might have resulted in cortical blindness. Local anesthetic effects might have suppressed occipital cortical function (reduced alpha amplitude on EEG, absent VEP, occipital hypometabolism on 18FDG PET CT), resulting in cortical blindness. Mild residual spinal anesthetic effects could have also resulted in subjective crural sensorimotor impairment and urinary retention.
Normally, the frontal, parietal and occipital cortices show higher 18FDG uptake. However, exposure to caffeine, alcohol, benzodiazepines, or anesthetic agents (propofol, isoflurane, benzodiazepines, and barbiturates), and corticosteroids can produce global cerebral hypo-metabolism on 18FDG PET CT.[10] Inhaled anesthetic gases and most intravenous anesthetic agents (with the exception of propofol, fentanyl, and remifentanil) also abolish VEP. Intra-operatively, cortical potentials such as VEP are affected earlier than brainstem or spinal potentials.
With immediate postoperative visual loss (POVL), the differential diagnosis includes central retinal artery occlusion, an ischaemic optic neuropathy (due to intraocular 'compartment syndrome' with hypo-perfusion of the optic nerve), transient ocular ischemia, and cortical blindness [due to cerebral embolism, hypoperfusion or PRES syndrome]. Immediate and persistent cortical blindness due to occipital infarction has also been reported after thoracic epidural anesthesia with bupivacaine.[11] However, delayed post spinal anesthesia cortical blindness is as yet unreported.
Similar to post CNB reversible hearing loss, delayed cortical neurotoxicity of bupivacaine should be considered with cortical blindness occurring within a few days of CNB and normal structural neuroimaging. Lumbar CSF drainage might speed up clinical improvement by reducing CSF bupivacaine concentrations. Neurologists should be cognizant of unusual delayed adverse events of spinal anesthesia.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
 References | |  |
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| 10. | Probasco JC, Solnes L, Nalluri A, Cohen J, Jones KM, Zan E, et al. Decreased occipital lobe metabolism by FDG-PET/CT. Neurol Neuroimmunol Neuro inflamm2018;5:e413. |
| 11. | Visser WA, Kolling JB, Groen GJ, Tetteroo E, van Dijl R, Rosseel PMJ, et al. Persistent cortical blindness after a thoracic epidural test dose of bupivacaine. Anesthesiology 2010;112:493-5. |
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