How should transient neurologic symptoms (TNS) after spinal lidocaine be prevented and managed?

Management and Prevention of Transient Neurologic Symptoms After Spinal Lidocaine

Avoid spinal lidocaine entirely for short procedures by substituting prilocaine or bupivacaine, which carry significantly lower TNS risk while maintaining adequate anesthesia duration. 1

Understanding TNS vs. Permanent Nerve Injury

• TNS is a benign, self-limiting condition without structural neurological injury and must be distinguished from cauda equina syndrome, which causes permanent deficits. 2
• Permanent intrathecal nerve injury from lidocaine occurs only with high-concentration (5%), repeated-dose techniques through micro-catheters (<24 G), not with standard single-shot spinal anesthesia. 2
• Standard spinal lidocaine does not cause cauda equina syndrome—the pooling of concentrated lidocaine around nerve roots through continuous catheter techniques is the mechanism for permanent damage, not single-injection spinal blocks. 2

Prevention: Choice of Local Anesthetic

Primary Prevention Strategy

• Prilocaine 2% in 7.5% glucose is the preferred alternative to lidocaine for short surgical procedures, with TNS incidence of only 3% compared to 30% with lidocaine, while maintaining similar duration of action (ambulation at 165 vs. 150 minutes). 1
• Bupivacaine 0.5% in 7.5% glucose eliminates TNS risk entirely (0% incidence) but delays ambulation (200 minutes) and voiding (299 minutes) compared to lidocaine or prilocaine. 1

If Lidocaine Must Be Used

• Reducing lidocaine concentration from 5% to 2% does NOT reduce TNS risk—incidence remains 32-40% regardless of concentration when using hyperbaric preparations. 3
• Isobaric lidocaine 2% may have lower TNS incidence (2.5%) compared to hyperbaric preparations, though this requires confirmation. 4
• Hyperbaric 5% prilocaine shows similarly low TNS rates (1%) as an alternative hyperbaric preparation. 5

Risk Factors for TNS

• Older age is the only consistently identified risk factor—mean age of patients developing TNS is 58 years versus 48 years in those without symptoms. 5
• Lithotomy position and early ambulation have been implicated in some studies, though musculoligamental relaxation from profound motor blockade may contribute to postoperative musculoskeletal pain. 6
• The neurotoxic effect of lidocaine itself is the primary mechanism, not simply positioning or muscle relaxation, as TNS occurs in 27% of spinal lidocaine patients versus 3% of general anesthesia patients undergoing identical procedures. 6

Clinical Presentation and Natural History

• TNS presents as pain in the buttocks or symmetric radiating pain to lower extremities, with or without back pain, typically beginning within 24 hours postoperatively. 6, 4
• Symptoms have abrupt onset and relief, lasting 45 minutes to 24 hours, with complete resolution without sequelae. 4
• No neurologic examination abnormalities are present—TNS is a clinical diagnosis based on symptoms alone. 1

Management of Established TNS

• Reassurance is the cornerstone of management—patients should be informed that symptoms are self-limiting and will resolve completely without permanent effects. 2
• Symptomatic treatment with NSAIDs or acetaminophen for pain control during the brief symptomatic period is appropriate, though specific analgesic protocols for TNS are not established in the literature.
• No specific interventions alter the natural history—TNS resolves spontaneously regardless of treatment. 4

Common Pitfalls to Avoid

• Do not confuse TNS with cauda equina syndrome—TNS lacks the bowel/bladder dysfunction, saddle anesthesia, and permanent motor deficits that characterize true cauda equina injury. 2
• Do not assume lower lidocaine concentrations prevent TNS—both 2% and 5% lidocaine carry similar 30-40% TNS risk when hyperbaric. 3
• Do not use continuous spinal catheters with concentrated lidocaine—this is the only scenario associated with permanent neurologic injury. 2
• Do not delay evaluation of persistent symptoms beyond 24-48 hours—true neurologic injury requires urgent investigation, whereas TNS resolves within this timeframe. 4

Practical Algorithm

For procedures <60 minutes:

1. First choice: Prilocaine 2% in 7.5% glucose (40-60 mg)—provides adequate duration with 3% TNS risk. 1
2. Second choice: Bupivacaine 0.5% in 7.5% glucose—zero TNS risk but delayed discharge (acceptable for outpatient surgery with appropriate planning). 1
3. Avoid lidocaine unless no alternatives exist—if required, use isobaric 2% preparation and counsel patients about 30% TNS risk. 3, 4

For established TNS:

1. Confirm diagnosis by excluding cauda equina syndrome—verify absence of bowel/bladder dysfunction and saddle anesthesia. 2
2. Provide reassurance and symptomatic analgesia—NSAIDs or acetaminophen as needed. 4
3. Expect complete resolution within 24-48 hours—if symptoms persist beyond 72 hours, investigate for alternative diagnoses. 4