Join now to get access to this content and more.
Become a SOAP member and have access to our benefits.
- Sample Centers of Excellence Applications
- ACOG Documents
- SOAP Policy and Procedure Manual (P&P Manual)
- SOAP Neuraxial Morphine Consensus Statement for Membership Review
- SOAP's Learning Modules
- ASA Corner
- 2019 Annual Meeting Lecture Videos
- December 2018 - SOAP Unofficial Guide to ASA Committees Webinar
- Submit a Position
- View Job Postings
- Search our Patient Safety Archive
- Ask SOAP a Question
- Our Bylaws
- Previous Meeting Archives
- Newsletter Archives
- Newsletter Clinical Articles
- Annual Meeting Publications
- CMS Guidelines
- Clinician Education
- And more…
Partial Paralysis after Spinal Anesthesia
Abstract Number: SU-42
Abstract Type: Case Report/Case Series
CASE: A 24 yo G2P1 pt at 26 2/7 wks EGA presented with chronic abruption. On day 3 she underwent CD for non-reassuring fetal status. Hgb was 13.6, platelet count 195, INR 1.2, fibrinogen 417. She had prior uncomplicated epidural labor analgesia. Spinal anesthesia was administered via 24-g needle at the L4-L5 interspace without paresthesia/complications. On POD 1 pt had LLE weakness (3/5 throughout) and decreased propioception, temperature, sensation to light touch, and had bilateral LE clonus. She denied pain and bowel/ bladder problems. MRI L-spine w/wo contrast showed hyperintense area at L1-L2 consistent with small blood collection without cord/nerve root compression; MRI T-spine w/wo contrast, CT head wo contrast, MRI brain w/wo contrast, MRA brain wo contrast were normal. Pt was admitted to NICU. On POD 6 follow up MRI, L-, T- and C-spine w/wo contrast showed resolution of hyperintense signal and no pathology. Pt had minimal improvement but was able to ambulate with walker and was discharged to rehabilitation on POD 11. She is scheduled for EMG in 2 weeks.
DISCUSSION: The etiology of this patient’s neurologic deficit remains unclear. Although the majority of neurologic injuries after delivery are of obstetric origin; our patient’s CD makes obstetric palsy less likely.1 Anesthesia-related etiologies include direct trauma, but it is usually preceded by paresthesia.2,3 The incidence of direct nerve trauma after spinal is ~1/10,000.3 Permanent injury is less common at 2.0-4.2/100,000 with 2/3 of initially disabling injuries resolving within 6 months.4 It is notable that blood was present at L1-L2, indicating puncture may have occurred above the estimated L4-L5 level, which may increase risk. Inaccurate interspace estimation is well-described.5 There was no evidence of a space-occupying lesion as the small amount of blood present was non-compressive; a hematoma is more common after epidural than spinal anesthesia2 and is rare in OB pts, especially in the absence of coagulopathy.6 Absence of cord or nerve root abnormality makes neurotoxic injection, chemical irritation, adhesive arachnoiditis, ischemia from vascular trauma, MS, or infectious causes unlikely. Negative imaging ruled out intracranial pathologies (e.g., hemorrhage, thrombosis). Confusing the picture further, bilateral clonus seems to indicate a spinal cord lesion; however, presence of motor and sensory symptoms in the same leg rather than opposite legs indicates a brain or peripheral injury. EMG studies may help delineate lesion level but several weeks must pass before results are valid; an EMG is still pending. Postpartum neurologic deficits are only rarely due to neuraxial procedures but require vigilance on the part of the healthcare team.
1. Wong: Ob Gyn 2003;101:279
2. Moen: Anesthesiology 2004;101:950
3. Auroy: Anesthesiology 1997;87:479
4. Royal College of Anaesthetists. NAP3. 2009.
5. Broadbent: Anaesthesia 2000;55:1122
6. Bateman: Anesth Analg 2013;116:1380