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Persistent Paralysis after Spinal Anesthesia for Cesarean Delivery
Abstract Number: F 51
Abstract Type: Case Report/Case Series
Anterior spinal cord ischemia has rarely been reported as a cause of permanent neurologic complications after neuraxial anesthesia in obstetric patients. We describe a parturient that developed anterior spinal cord ischemia after spinal anesthesia (SA) for cesarean delivery (CD).
We present the case of a 32-year-old G4P2A1 parturient of Ethiopian origin, who presented at 41(2/7) weeks for primary elective CD for breech presentation. This current pregnancy was uncomplicated and she had no significant medical history. Preoperative BP was 98/70 mmHg and haemoglobin (Hb) 108. Uncomplicated SA was performed at L3-4 with clear CSF on the first pass. Bupivacaine 12mg (0.75% hyperbaric), fentanyl 20mcg, and preservative-free morphine 150mcg were administered. Phenylephrine was then infused at 50 mcg/min. Block height was T4 at 5 min. Intraoperative course was uneventful except for symptomatic bradycardia (37-40 bpm) and hypotension (SBP 85mmHg) 15 min post SA, treated by decreasing the phenylephrine infusion, intravenous ephedrine 10mg and atropine 0.6mg. Blood loss was estimated at 750 ml and the lowest intraoperative SBP recorded (Innovian® Anesthesia, Draeger Medical) was 85 mmHg.
Initial postoperative vitals were BP 107/65, HR 82, SpO2 97%. Over 3 hours, 3 episodes of mild hypotension (SBP 85-90) were treated with fluid boluses. Clinical assessments revealed no excessive bleeding and postoperative Hb was 82. Seven hours after SA, the patient had persistent motor block, despite pain from her surgical incision. At nine hours, diffusion-weighted unenhanced MRI of the lumbosacral region was normal, finding no spinal cord compression or cord lesion. Fifteen hours after SA, Neurology found leg strength 0/5 bilaterally, decreased sensation to T6, no sensation to void, intact bowel function, vibration sense and proprioception. The deficits were consistent with a lesion above T6, impacting the anterior spinal cord while sparing the posterior tracts. Two more unenhanced spinal cord MRI studies within 48 hours failed to identify the pathology. Normal echocardiogram ruled out patent foramen ovale and a negative sickle cell screen ruled out vaso-occlusive crisis. Daily neurologic improvement was observed on postpartum days 7-14. At one year, persistent neurologic deficits included mild left hip flexor weakness, persistent T10-12 dyesthesia and left leg neuropathic pain.
Possible etiologies of anterior spinal cord ischemia include severe hypotension, arteriosclerosis, or mechanical interference with aortic blood flow (emboli or vasospasm). Three cases report spinal artery syndrome after neuraxial anesthesia in the obstetric population. Mild hypotension combined with a vasoconstricting agent and the hypercoagulable state of pregnancy may be contributory. Our case report highlights the importance of the clinical examination in parturients with a prolonged block after neuraxial anesthesia.
Int J Obstet Anesth 2000; 9: 99–124
South Med J 1990; 83: 695–697